FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Nieminen-von Wendt, T Metsahonkala, L Kulomaki, T Aalto, S Autti, T Vanhala, R von Wendt, L AF Nieminen-von Wendt, T Metsahonkala, L Kulomaki, T Aalto, S Autti, T Vanhala, R von Wendt, L TI Changes in cerebral blood flow in Asperger syndrome during theory of mind tasks presented by the auditory route SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Asperger syndrome; theory of mind; PET; cerebellum ID SHORT-TERM; AUTISM; CEREBELLUM; BRAIN; CHILDREN; MEMORY; ADULTS; INVOLVEMENT; ACTIVATION; FMRI AB Lack of theory of mind (TOM) has been considered to be a key feature in Asperger syndrome (AS). The main aim of the present study was to determine whether an exclusively auditory input of ToM stories activated the same brain areas as demonstrated previously using visual stimuli. Eight right-handed otherwise healthy men with AS and eight healthy right-handed male controls participated in a PET activation study using auditory given TOM stories and stories about physical events for induction. Both subjects with AS and controls showed increased activation in the occipitotemporal area bilaterally and in thalamus during ToM tasks. Both groups also showed activation in the medial frontal area during ToM tests. However, this activation was more intensive and extensive in the control group, especially when a more sensitive analysis method was used. As a group, unrelated to the tasks, the AS subjects showed increased activation of the cerebellum. It was concluded that the activation pattern was mainly in agreement with earlier studies using comparable stimuli administered differently. There was no support for a right hemisphere specific dysfunction. C1 Univ Helsinki, Cent Hosp, Dept Child Neurol, Hosp Children & Adolescents, Helsinki 00029, Finland. 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PD AUG PY 2003 VL 12 IS 4 BP 203 EP 203 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 703GP UT WOS:000184271900007 ER PT J AU Luharuka, R Gao, RX Krishnamurty, S AF Luharuka, R Gao, RX Krishnamurty, S TI Design and realization of a portable data logger for physiological sensing SO IEEE TRANSACTIONS ON INSTRUMENTATION AND MEASUREMENT LA English DT Article; Proceedings Paper CT 19th IEEE Instrumentation and Measurement Technology Conference (IMTC/2002) CY MAY 21-23, 2002 CL ANCHORAGE, AK SP IEEE Instrumentat & Measurement Soc DE autism; data logger; galvanic skin response (GSR); microcontroller; physiological sensing AB A microcontroller-based data logger has been designed, prototyped, and field-tested for recording galvanic skin response data and relaying them to a computer for physiological analysis. 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PD AUG PY 2003 VL 52 IS 4 BP 1289 EP 1295 DI 10.1109/TIM.2003.816808 PG 7 WC Engineering, Electrical & Electronic; Instruments & Instrumentation SC Engineering; Instruments & Instrumentation GA 723EQ UT WOS:000185419800049 ER PT J AU Fombonne, E AF Fombonne, E TI Epidemiological surveys of autism and other pervasive developmental disorders: An update SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorder; epidemiology; prevalence; incidence; childhood disintegrative disorder; Asperger disorder ID INFANTILE-AUTISM; TUBEROUS SCLEROSIS; CHILDHOOD AUTISM; PRESCHOOL-CHILDREN; CONGENITAL-RUBELLA; MEDICAL DISORDERS; TOTAL POPULATION; SOCIAL-CLASS; FIELD TRIAL; URBAN AREAS AB This paper was commissioned by the committee on the Effectiveness of Early Education in Autism of the National Research Council (NRC). It provides a review of epidemiological studies of pervasive developmental disorders (PDD) which updates a previously published article (The epidemiology of autism: a review. Psychological Medicine 1999; 29: 769-786). The design, sample characteristics of 32 surveys published between 1966 and 2001 are described. Recent surveys suggest that the rate for all forms of PDDs are around 30/10,000 but more recent surveys suggest that the estimate might be as high as 60/10,000. The rate for Asperger disorder is not well established, and a conservative figure is 2.5/10,000. Childhood disintegrative disorder is extremely rare with a pooled estimate across studies of 0.2/10,000. A detailed discussion of the possible interpretations of trends over time in prevalence rates is provided. There is evidence that changes in case definition and improved awareness explain much of the upward trend of rates in recent decades. 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Autism Dev. Disord. PD AUG PY 2003 VL 33 IS 4 BP 365 EP 382 DI 10.1023/A:1025054610557 PG 18 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800002 PM 12959416 ER PT J AU Rivers, JW Stoneman, Z AF Rivers, JW Stoneman, Z TI Sibling relationships when a child has autism: Marital stress and support coping SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE marital stress; siblings; support coping ID MENTALLY-RETARDED CHILDREN; YOUNG-CHILDREN; CHRONIC DISABILITIES; EARLY ADOLESCENCE; MIDDLE CHILDHOOD; SOCIAL SUPPORT; FAMILY STRESS; ADJUSTMENT; MOTHERS; ADAPTATION AB Family systems theory was employed to study sibling relationships in 50 families with a child with autism. Typically developing siblings expressed satisfaction with their sibling relationships. Parents were somewhat less positive about the sibling relationship than were the siblings themselves. 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E, 1980, AM J MENT DEFIC, V84, P354 YOUNG DM, 1994, TOP EARLY CHILD SPEC, V14, P488 NR 70 TC 48 Z9 52 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 2003 VL 33 IS 4 BP 383 EP 394 DI 10.1023/A:1025006727395 PG 12 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800003 PM 12959417 ER PT J AU Jarbrink, K Fombonne, E Knapp, M AF Jarbrink, K Fombonne, E Knapp, M TI Measuring the parental, service and cost impacts of children with autistic spectrum disorder: A pilot study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; cost; burden of illness; informal care ID CARE; SCHIZOPHRENIA; ADULTS AB The aim of this study was to carry out a preliminary examination of a research instrument developed specifically to collect cost information for individuals with autistic spectrum disorder. There is very little cost information on children or adults with autism or autism-related disorder, and no study appears to have carried out a specific cost collection in this area. Although some global cost estimates can be made, little is known about the cost implications of parental burden. By using different techniques to collect indirect costs, the study outlines a functional methodology. Results from this small pilot study point to considerable economic burden for parents and give some indication of the associated costs of autistic spectrum disorder. C1 Inst Psychiat, David Goldberg Ctr, Hlth Serv Res Dept, Ctr Econ Mental Hlth, London SE5 8AF, England. Montreal Childrens Hosp, Montreal, PQ H3Z 1P2, Canada. RP Knapp, M (reprint author), Inst Psychiat, David Goldberg Ctr, Hlth Serv Res Dept, Ctr Econ Mental Hlth, De Crespigny Pk, London SE5 8AF, England. 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Autism Dev. Disord. PD AUG PY 2003 VL 33 IS 4 BP 395 EP 402 DI 10.1023/A:1025058711465 PG 8 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800004 PM 12959418 ER PT J AU Miles, JH Takahashi, TN Haber, A Hadden, L AF Miles, JH Takahashi, TN Haber, A Hadden, L TI Autism families with a high incidence of alcoholism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism; alcoholism; genetics ID PERVASIVE DEVELOPMENTAL DISORDERS; NCB-20 NEUROBLASTOMA-CELLS; SEROTONIN REUPTAKE INHIBITORS; EMPIRICALLY DERIVED TYPOLOGY; DOPAMINE-BETA-HYDROXYLASE; PSYCHIATRIC-DISORDERS; HEAD CIRCUMFERENCE; 5-HT3 RECEPTOR; DIAGNOSTIC INTERVIEW; SUBSTANCE DEPENDENCE AB To determine the significance of neuropsychiatric disorders in autism families, we analyzed 167 pedigrees ascertained through an autistic child; 39% had alcoholism in patterns consistent with transmission of a genetic trait. Children from high alcoholism families were more likely to have the onset of their autistic behavior occur with a loss of language (52.5% vs. 35.8%, p = 0.04). This occurred primarily in families where the mother was alcoholic (80% vs. 40%, p = 0.05), suggesting an association between maternal alcoholism and regressive onset autism. Children from high alcoholism families were less likely to be macrocephalic (14.7% vs. 40.6%, p = 0.0006). Children from high alcohol and low alcohol families did not differ in dysmorphology status, IQ, sex ratio or sib recurrence risk. C1 Univ Missouri Hosp & Clin, Div Med Genet, Columbia, MO 65212 USA. RP Miles, JH (reprint author), Univ Missouri Hosp & Clin, Div Med Genet, 1 Hosp Dr, Columbia, MO 65212 USA. 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The Social Responsiveness Scale (SRS-formerly known as the Social Reciprocity Scale) is a new instrument that can be completed by parents and/or teachers in 15-20 minutes. We compared the SRS with the Autism Diagnostic Interview-Revised (ADI-R) in 61 child psychiatric patients. Correlations between SRS scores and ADI-R algorithm scores for DSM-IV criterion sets were on the order of 0.7. SRS scores were unrelated to I.Q. and exhibited inter-rater reliability on the order of 0.8. The SRS is a valid quantitative measure of autistic traits, feasible for use in clinical settings and for large-scale research studies of autism spectrum conditions. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, Campus Box 8134,660 S Euclid Ave, St Louis, MO 63110 USA. 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PD AUG PY 2003 VL 33 IS 4 BP 427 EP 433 DI 10.1023/A:1025014929212 PG 7 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800007 PM 12959421 ER PT J AU Mount, RH Charman, T Hastings, RP Reilly, S Cass, H AF Mount, RH Charman, T Hastings, RP Reilly, S Cass, H TI Features of autism in Rett syndrome and severe mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Rett syndrome; autism; PDD; diagnosis; mental retardation; behavioral phenotype ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIOR CHECKLIST; SPECTRUM DISORDERS; DIFFERENTIAL-DIAGNOSIS; MECP2 MUTATIONS; CHILDREN; INDIVIDUALS; DISABILITY; CLASSIFICATION; PHENOTYPE AB It has long been recognized that there is phenotypic overlap between Rett syndrome (RS) and autism. Advances in our clinical and genetic understanding of RS over the past decade have made clear that the cause and course of RS and autism are distinct (except perhaps in a few cases). Despite this, further delineation of the phenotypic overlap between RS and autism is warranted to enhance clinical decision-making and to further understanding of neuropathological development in both disorders. The present study measured autistic symptoms using the Autism Behavior Checklist (ABC) in a sample of girls with RS and a comparison group of girls with severe and profound mental retardation (SMR). Controlling for developmental level and motor ability, girls with RS scored more highly than those with SMR on the Sensory and Relating subscales. In contrast, there were no group differences on the Body and Object use, Language and Social and Self-help subscales. Further work on the characterisation of the behavioral phenotype of genetic disorders such as RS and autism may aid in identifying the neuropathogenic processes that lead from gene-to-brain-to-behavior. C1 UCL, Inst Child Hlth, Brain & Behav Sci Unit, London WC1N 1EH, England. 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Autism Dev. Disord. PD AUG PY 2003 VL 33 IS 4 BP 435 EP 442 DI 10.1023/A:1025066913283 PG 8 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800008 PM 12959422 ER PT J AU Curin, JM Terzic, J Petkovic, ZB Zekan, L Terzic, IM Susnjara, IM AF Curin, JM Terzic, J Petkovic, ZB Zekan, L Terzic, IM Susnjara, IM TI Lower cortisol and higher ACTH levels in individuals with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; cortisol; ACTH ID PLASMA BETA-ENDORPHIN; INFANTILE-AUTISM; YOUNG-ADULTS; DOUBLE-BLIND; CHILDREN; DISORDER; BRAIN; ABNORMALITIES; ADOLESCENTS; NALTREXONE AB Blood concentrations of pituitary hormones adrenocorticotropin (ACTH), prolactin, growth hormone, and adrenal hormone-cortisol were measured in 36 autistic and 27 control individuals. Individuals with autism had significantly lower serum concentrations of cortisol (p < 10(-6)), and significantly higher concentrations of ACTH (p = 0.002) than control age- and sex-matched subjects. Also, prolactin concentrations in autistic patients with epilepsy were significantly higher when compared with normal subjects. The observed hormonal changes may indicate dysfunction of the hypothalamo-pituitary-adrenal axis in individuals with autism. C1 Univ Split, Sch Med, Dept Physiol, Split, Croatia. Ctr Autism, Zagreb, Croatia. Clin Hosp, Dept Nucl Med, Split, Croatia. RP Terzic, J (reprint author), Sch Med Split, Dept Physiol, Soltanska 2, Split 21000, Croatia. 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Autism Dev. Disord. PD AUG PY 2003 VL 33 IS 4 BP 443 EP 448 DI 10.1023/A:1025019030121 PG 6 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800009 PM 12959423 ER PT J AU Arnold, GL Hyman, SL Mooney, RA Kirby, RS AF Arnold, GL Hyman, SL Mooney, RA Kirby, RS TI Plasma amino acids profiles in children with autism: Potential risk of nutritional deficiencies SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE plasma amino acid profile; gluten restricted diet; casein restricted diet; autism; protein nutrition deficiency ID CHILDHOOD AUTISM; DIAGNOSIS; SEROTONIN; BEHAVIOR AB The plasma amino acid profiles of 36 children with autism spectrum disorders were reviewed to determine the impact of diet on amino acid patterns. Ten of the children were on gluten and casein restricted diets administered by parents, while the other 26 consumed unrestricted diets. No amino acid profile specific to autism was identified. However, children with autism had more essential amino acid deficiencies consistent with poor protein nutrition than an age/gender matched control group. There was a trend for children with autism who were on restricted diets to have an increased prevalence of essential amino acid deficiencies and lower plasma levels of essential acids including the neurotransmitter precursors tyrosine and tryptophan than both controls and children with autism on unrestricted diets. These data indicate that larger, more focused studies of protein nutrition in children with autism are needed in order to determine the extent to which restricted diets might place the developing brains of children with autism at risk from protein malnutrition. The high rate of tryptophan and tyrosine deficiency in this group is also of concern given their role as neurotransmitter precursors. C1 Univ Rochester, Med Ctr, Dept Pediat, Rochester, NY 14642 USA. 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The daytime administration of oral melatonin to those people, in doses that raise their plasma melatonin levels to the nocturnal range, can accelerate sleep onset. We examined the ability of similar, physiological doses to restore nighttime melatonin levels and sleep efficiency in mentally retarded subjects with sleep deficits. In a double-blind, placebo-controlled study, mentally retarded subjects (n = 20) received, in randomized order, a placebo and two melatonin doses (0.1, and 3.0 mg) orally 30 minutes before bedtime for a week. Treatments were separated by 1-week washout periods. Sleep data were obtained by polysomnography on the last three nights of each treatment period. The physiologic melatonin dose (0.3 mg) restored sleep efficiency (p < 0.0001), acting principally in the midthird of the night; it also elevated plasma melatonin levels (p < 0.0008) to normal. The lowest dose (0.1 mg) also improved sleep. C1 Chrisitan Doppler Klin, A-5020 Salzburg, Austria. RP Niederhofer, H (reprint author), Chrisitan Doppler Klin, A-5020 Salzburg, Austria. 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Autism Dev. Disord. PD AUG PY 2003 VL 33 IS 4 BP 469 EP 472 DI 10.1023/A:1025027231938 PG 4 WC Psychology, Developmental SC Psychology GA 708UK UT WOS:000184587800013 PM 12959427 ER PT J AU Seeman, C AF Seeman, C TI The boy who loved windows: Opening the heart and mind of a child threatened with autism. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo, Libs, Toledo, OH 43606 USA. RP Seeman, C (reprint author), Univ Toledo, Libs, 2801 W Bancroft St, Toledo, OH 43606 USA. CR Stacey Patricia, 2003, BOY WHO LOVED WINDOW 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 AUG PY 2003 VL 128 IS 13 BP 110 EP 110 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 710VG UT WOS:000184703100228 ER PT J AU Seeman, C AF Seeman, C TI The gift of autism: The unexpected joy of parenting a challenging child. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo, Libs, Toledo, OH 43606 USA. RP Seeman, C (reprint author), Univ Toledo, Libs, 2801 W Bancroft St, Toledo, OH 43606 USA. CR SHARP M, 2003, GIFT AUTISM UNEXPECT 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 AUG PY 2003 VL 128 IS 13 BP 110 EP 110 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 710VG UT WOS:000184703100227 ER PT J AU Padhye, U AF Padhye, U TI Excess dietary iron is the root cause for increase in childhood Autism and allergies SO MEDICAL HYPOTHESES LA English DT Article ID DECLINING PREVALENCE; ANEMIA; HEMOCHROMATOSIS AB Autism is a profoundly and poorly understood developmental disorder that impairs a person's social and communication abilities. I propose a hypothesis that the excessive dietary iron consumed by today's infants is the root cause of increased cases of Autism, allergies and other childhood diseases. Iron is a powerful immune system modulator. Excess iron causes hyperactive immune system. This hyperactive immune system attacks undigested food peptides. The chemicals released during these intense allergic reactions can damage surrounding tissue. Neurodegeneration is caused by combination of, oxidative stress induced by free iron radicals and intense immune reactions. Iron chelators have shown beneficial results in Autism and allergies. (C) 2003 Elsevier Science Ltd. All rights reserved. RP Padhye, U (reprint author), 2990 River Meadows, Canton, MI 48188 USA. 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Hypotheses PD AUG PY 2003 VL 61 IS 2 BP 220 EP 222 DI 10.1016/S0306-9877(03)00126-9 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 713YM UT WOS:000184885600014 PM 12888307 ER PT J AU Keller, F Persico, AM AF Keller, F Persico, AM TI The neurobiological context of autism SO MOLECULAR NEUROBIOLOGY LA English DT Review DE autism; development; genetics; serotonin; GABA; acetylcholine; oxytocin; reelin; wnt-2; hoxa1; ARX; animal models ID HETEROZYGOUS REELER MOUSE; X MENTAL-RETARDATION; PURKINJE-CELL SIZE; SEROTONIN TRANSPORTER; SPECTRUM DISORDERS; PLATELET SEROTONIN; CEREBRAL-CORTEX; LINKAGE-DISEQUILIBRIUM; EXTRACELLULAR-MATRIX; TUBEROUS SCLEROSIS AB Autistic disorder (AD) is a complex neuropsychiatric disorder of neurodevelopmental origin, where multiple genetic and environmental factors may interact, resulting in a clinical continuum. The genetic component is best described by a multilocus model that takes into account epistatic interactions between several susceptibility genes. In the past ten years enormous progress has been made in identifying chromosomal regions in linkage with AD, but moving from chromosomal regions to candidate genes has proven to be tremendously difficult. Neuroanatomical findings point to early dysgenetic events taking place in the cerebral cortex, cerebellum, and brainstem. At the cellular level, disease mechanisms may include altered cell migration, increased cell proliferation, decreased cell death, or altered synapse elimination. Neurochemical findings in AD point to involvement of multiple neurotransmitter systems. The serotoninergic system has been intensively investigated in AD, but other neurotrasmitter systems (e.g., the GABAergic and the cholinergic system) are also coming under closer scrutiny. The role of environmental factors is still poorly characterized. It is not clear yet whether environmental factors act merely as precipitating agents, always requiring an underlying genetic liability, or whether they represent an essential component of a pathogenetic process where genetic liability alone does not lead to the full-blown autism phenotype. A third potential player in the pathogenesis of autism, in addition to genetic and environmental factors, is developmental variability due to "random" factors, e.g. small fluctuations of gene expression and complex, non-deterministic interactions between genes during brain development. These considerations suggest that a non-deterministic conceptual framework is highly appropriate for autism research. C1 Lab Dev Neurosci & Neural Plast, Rome, Italy. Lab Mol Psychiat & Neurogenet, Rome, Italy. RP Keller, F (reprint author), Lab Dev Neurosci & Neural Plast, Univ Campus Biomed, Rome, Italy. 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Neurobiol. PD AUG PY 2003 VL 28 IS 1 BP 1 EP 22 DI 10.1385/MN:28:1:1 PG 22 WC Neurosciences SC Neurosciences & Neurology GA 727MC UT WOS:000185661700001 PM 14514983 ER PT J AU Gerlai, J Gerlai, R AF Gerlai, J Gerlai, R TI Autism: a large unmet medical need and a complex research problem SO PHYSIOLOGY & BEHAVIOR LA English DT Article; Proceedings Paper CT 11th Annual Meeting of the International-Behavioral-Neuroscience-Society (IBNS) CY JUN 23, 2002 CL CAPRI, ITALY SP Int Behav Neurosci Soc DE autism; autistic spectrum disorder; Asperger syndrome; mouse; rat; social behavior ID DIAGNOSTIC OBSERVATION SCHEDULE; SEROTONIN TRANSPORTER GENE; FRAGILE-X-SYNDROME; INFANTILE-AUTISM; LANGUAGE DISORDER; ASPERGER-SYNDROME; KNOCKOUT MICE; ANIMAL-MODEL; PHARMACOTHERAPY; OXYTOCIN AB Autism has been becoming the focus of attention as its apparently increasing prevalence is better appreciated. According to some estimates, the frequency of children with autistic spectrum disorder (ASD) can be as high as I in 150. The diagnosis can be made as early as 2 years of age, and autistic patients often have a normal life span. Thus, in terms of the number of "patient years," ASD represents a market that is as large as that of the biggest neurological indication, Alzheimer's disease. Despite the clear unmet medical need, no effective treatment is available. This may be because the mechanism of ASD is not understood. The aim of the present paper is to review recent advances in autism research and to discuss some of the most stressing problems mainly from a preclinical research standpoint. We hope to draw attention to the need to study this devastating disease that places an enormous burden on the society in general and the relatives and caregivers of autistic patients in particular. (C) 2003 Elsevier Inc. All rights reserved. C1 Eli Lilly & Co, Lilly Corp Ctr, Neurosci Discovery Res, Indianapolis, IN 46285 USA. RP Gerlai, R (reprint author), Eli Lilly & Co, Lilly Corp Ctr, Neurosci Discovery Res, Indianapolis, IN 46285 USA. 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Through his research and visionary conceptualizations, current investigators can legitimately study social behavior from a neurobiological perspective. His research and writings provided three important contributions. First, he emphasized the importance of evolution as an organizing principle that shaped both the structure of the nervous system and the adaptive social behavior. Second, by defining the limbic system, he legitimized the biological perspective in the study of emotion. Third, he recognized the important role of the vagal afferents in the regulation of higher brain structures. The paper will focus on the Polyvagal Theory. The Polyvagal Theory is a new conceptualization of the role of vagus and employs several features that MacLean emphasized including the importance of evolution, limbic structures and vagal afferents. 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Behav. PD AUG PY 2003 VL 79 IS 3 BP 503 EP 513 DI 10.1016/S0031-9384(03)00156-2 PG 11 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 720YY UT WOS:000185291300018 PM 12954445 ER PT J AU Harris, JC AF Harris, JC TI Social neuroscience, empathy, brain integration, and neurodevelopmental disorders SO PHYSIOLOGY & BEHAVIOR LA English DT Article; Proceedings Paper CT 11th Annual Meeting of the International-Behavioral-Neuroscience-Society (IBNS) CY JUN 23, 2002 CL CAPRI, ITALY SP Int Behav Neurosci Soc DE MacLean; isopraxis; empathy; autism; Lesch-Nyhan syndrome ID LESCH-NYHAN-SYNDROME; MATERNAL-BEHAVIOR; MIRROR NEURONS; TRIUNE BRAIN; AUTISM; MIND; IMITATION; RESPONSES; MONKEYS; SYSTEM AB Paul MacLean has investigated integrated brain functioning through selected brain lesions in animals that disturb circuits necessary for complex behaviors, such as social displays. MacLean is unique in his comparative neurobehavioral approach that emphasizes the evolutionary origins of parenting and social behaviors and the implications of brain changes in the evolution from reptiles (social displays) to mammals (nursing, audiovocal communication, play) to man (self-awareness, intentionality, social context) that link affect and cognition. Subjectively, how "looking with feeling toward others," the basic element in empathy, evolved has been a central concern of his. Neuroimaging studies of social cognition, mother-infant communication, moral behavior, forgiveness, and trust are consistent with particular brain systems being activated in cooperative social behaviors. The identification of mirror neurons is pertinent to MacLean's model of isopraxis and studies of thalamocortical resonances may be pertinent to his neurobehavioral models. Studies of behavioral phenotypes in human neurodevelopmental disorders are consistent with MacLean's model of brain circuits being linked to complex behaviors during development. In autistic disorder, the behavioral phenotype involves disrupted social communication, deviant imaginative play, and motor stereotypies. In Lesch-Nyhan syndrome (LNS), self-injury occurs in individuals with normal sensory systems intact who require and request physical restraint to prevent self-injury; they ask for assistance from others to prevent them from harming themselves. Autism involves the lack of subjective awareness of others intentions and LNS involves a failure in self-regulation and self-control of self-injurious behavior. MacLean's models laid the groundwork for studies focused on understanding brain functioning in these conditions. (C) 2003 Elsevier Inc. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21287 USA. 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Behav. PD AUG PY 2003 VL 79 IS 3 BP 525 EP 531 DI 10.1016/S0031-9384(03)00158-6 PG 7 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 720YY UT WOS:000185291300020 PM 12954447 ER PT J AU Ruggieri, VL Arberas, CL AF Ruggieri, VL Arberas, CL TI Behavioural phenotypes. Biologically determined neuropsychological patterns SO REVISTA DE NEUROLOGIA LA French DT Review DE autism; behavioural phenotypes; fragile X syndrome; Rett syndrome ID DUCHENNE MUSCULAR-DYSTROPHY; SMITH-MAGENIS-SYNDROME; LESCH-NYHAN SYNDROME; IDIOPATHIC INFANTILE HYPERCALCEMIA; PHENYLALANINE-HYDROXYLASE GENE; EARLY-TREATED PHENYLKETONURIA; PRADER-WILLI SYNDROME; NANCE-HORAN-SYNDROME; FRAGILE-X SYNDROME; TUBEROUS-SCLEROSIS AB Introduction and aims. A behavioural phenotype (BP) is a characteristic pattern of motor, cognitive, linguistic and social abnormalities that are associated in a way that is compatible with a biological disorder, while environmental factors are also known to be important in their development. Taking these concepts into account, we have analyzed several entities with acknowledged BP, which were selected according to the frequency of presentation, the compatibility of the association between BP and the underlying disease, and the importance of recognizing the entity, so as to enable suitable therapeutic guidance and proper genetic counselling. Development. They were organized by dividing them into three groups according to the biological characteristics recognized to date: a) BP associated to genetic diseases with an identified biological basis (syndromes such as Lesch-Nyhan, Rett, fragile X, tuberous sclerosis complex, Noonan, Sotos, Aicardi, Angelman, Prader Willi, Williams, Down, Smith Magenis, Di George, Pallister Killian and Turner, among others; b) BP associated to agenetic disease with an unidentified biological basis (Cornelia de Lange syndrome); and, c) BP with an as yet unidentified biological basis associated to diverse causations (autism). In all the entities phenotypic, clinical, cognitive, behavioural and biological aspects were analyzed from the way they are inherited to the molecular bases. C1 Hosp JP Garrahan, Serv Neurol, RA-1245 Buenos Aires, DF, Argentina. RP Ruggieri, VL (reprint author), Hosp JP Garrahan, Serv Neurol, Combate Pozos 1881, RA-1245 Buenos Aires, DF, Argentina. 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Autism is a neurobiological, life-long disorder characterized by abnormal social skills, deficient verbal and not verbal communication, symbolic and imaginative play, reasoning and related complex behaviour. Autism is 4 times more frequent in males. 70% are mentally retarded (30% mild and the rest moderate and severely retarded). Approximately 25% have convulsions and around 65% inespecific EGG. abnormalities. Other conditions like ADHD, anxiety, depression may be associated. RMN: increased subarachnoidal spaces, moderate ventricular enlargement, 20% have megalencephaly. PET and 31 PMMR show increased glucose metabolism and decreased functional links with association cortex. Mental level and language are de best prognostic indices for outcome. Pathology: reduced size of nerve cells in hippocampus, subiculum, sections of the amygdala, mamillary bodies, medial septal nucleus, decreased size of cerebellar hemispheres, posterior vermis, VI-VII neocerebellar lobules. 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Neurologia PD AUG 1 PY 2003 VL 37 IS 3 BP 259 EP 266 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 722LF UT WOS:000185375700010 PM 12938058 ER PT J AU Peretz, I Hyde, KL AF Peretz, I Hyde, KL TI What is specific to music processing? Insights from congenital amusia SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID AUDITORY AGNOSIA; PITCH; AUTISM; RECOGNITION; PERCEPTION; DEFICITS; DISCRIMINATION; DISSOCIATIONS; ORGANIZATION; IMPAIRMENT AB Musical abilities are generally regarded as an evolutionary by-product of more important functions, such as those involved in language. However, there is increasing evidence that humans are born with musical predispositions that develop spontaneously into sophisticated knowledge bases and procedures that are unique to music. Recent findings also suggest that the brain is equipped with music-specific neural networks and that these can be selectively compromised by a congenital anomaly. 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PD AUG PY 2003 VL 7 IS 8 BP 362 EP 367 DI 10.1016/S1364-6613(03)00150-5 PG 6 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 714TL UT WOS:000184929500014 ER PT J AU Lawrence, D AF Lawrence, D TI Scientists discover link between brain growth and autism SO LANCET LA English DT News Item CR Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Lainhart JE, 2003, JAMA-J AM MED ASSOC, V290, P393, DOI 10.1001/jama.290.3.393 NR 2 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD JUL 19 PY 2003 VL 362 IS 9379 BP 220 EP 220 DI 10.1016/S0140-6736(03)13959-1 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 702PJ UT WOS:000184232000021 ER PT J AU Courchesne, E Carper, R Akshoomoff, N AF Courchesne, E Carper, R Akshoomoff, N TI Evidence of brain overgrowth in the first year of life in autism SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HEAD CIRCUMFERENCE; MENTAL-RETARDATION; INFANTILE-AUTISM; BASAL FOREBRAIN; YOUNG-CHILDREN; ABNORMALITIES; CORTEX; AGE; DISORDER; VOLUME AB Context Autism most commonly appears by 2 to 3 years of life, at which time the brain is already abnormally large. This raises the possibility that brain overgrowth begins much earlier, perhaps before the first clinically noticeable behavioral symptoms. Objectives To determine whether pathological brain overgrowth precedes the first clinical signs of autism spectrum disorder (ASD) and whether the rate of overgrowth during the first year is related to neuroanatomical and clinical outcome in early childhood. Design, Setting, and Participants Head circumference (HQ, body length, and body weight measurements during the first year were obtained from the medical records of 48 children with ASD aged 2 to 5 years who had participated in magnetic resonance imaging studies. Of these children, 15 (longitudinal group) had measurement at 4 periods during infancy: birth, 1 to 2 months, 3 to months, and 6 to 14 months; and 33 (partial HC data group) had measurements at birth and 6 to 14 months (n=7), and at birth only (n=28). Main Outcome Measures Age-related changes in infants with ASD who had multiple-age measurements, and the relationship of these changes to brain anatomy and clinical and diagnostic outcome at 2 to 5 years were evaluated by using 2 nationally recognized normative databases: cross-sectional normative data from a national survey and longitudinal data of individual growth. Results Compared with normative data of healthy infants, birth HC in infants with ASD was significantly smaller (z= -0.66, P<.001); after birth, HC increased 1.67 SDS and mean HC was at the 84th percentile by 6 to 14 months. Birth HC was related to cerebellar gray matter volume at 2 to 5 years, although the excessive increase in HC between birth and 6 to 14 months was related to greater cerebral cortex volume at 2 to 5 years. Within the ASD group, every child with autistic disorder had a greater increase in HC between birth and 6 to 14 months (mean [SD], 2.19 [0.98]) than infants with pervasive developmental disorder-not otherwise specified (0.58 [0.35]). Only 6% of the individual healthy infants in the longitudinal data showed accelerated HC growth trajectories (>2.0 SDs) from birth to 6 to 14 months; 59% of infants with autistic disorder showed these accelerated growth trajectories. Conclusions The clinical onset of autism appears to be preceded by 2 phases of brain growth abnormality: a reduced head size at birth and a sudden and excessive increase in head size between 1 to 2 months and 6 to 14 months. Abnormally accelerated rate of growth may serve as an early warning signal of risk for autism. C1 Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Psychiat, La Jolla, CA 92093 USA. Childrens Hosp Res Ctr, Ctr Autism Res, San Diego, CA USA. 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Am. Med. Assoc. PD JUL 16 PY 2003 VL 290 IS 3 BP 393 EP 394 DI 10.1001/jama.290.3.393 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 699WK UT WOS:000184078800034 PM 12865381 ER PT J AU Hung, CC Yeh, JI Fang, JS Chen, CH AF Hung, CC Yeh, JI Fang, JS Chen, CH TI No association of a dodecamer duplication in the human opposite paired (HOPA) gene with mental retardation and schizophrenia in Chinese patients from Taiwan SO PSYCHIATRY RESEARCH LA English DT Article DE genetics; prevalence; mental illness; selection; migration ID HOPA(12BP) POLYMORPHISM; HYPOTHYROIDISM; EXPRESSION; VARIANT; AUTISM; XQ13 AB The human opposite paired-containing (HOPA) gene is believed to be a co-activator of the thyroid hormone receptor and involved in thyroid hormone signal transduction. The gene consists of 45 exons and includes a dodecamer duplication in exon 43, which has been reported to be associated with mental retardation, autism, psychiatric disorders and hypothyroidism. We were interested to know if the 12-bp duplication variant of the HOPA gene is a risk factor for mental retardation and schizophrenia in the Chinese population. We investigated the prevalence of the 12-bp variant in a sample of Chinese mental retardation and schizophrenic patients from Taiwan by PCR-based genotyping. None of the mentally retarded and schizophrenic patients were found to have this dodecamer duplication variant. Our results indicate that the HOPA polymorphism might be very rare in our population and is unlikely to be a major risk factor for mental retardation and schizophrenia in the Chinese population. (C) 2003 Elsevier Ireland Ltd. All rights reserved. C1 Tzu Chi Uni, Grad Inst Human Genet, Hualien 970, Taiwan. Tzu Chi Uni, Dept Family Med, Hualien 970, Taiwan. Tzu Chi Uni, Dept Psychiat, Hualien 970, Taiwan. RP Chen, CH (reprint author), Tzu Chi Uni, Grad Inst Human Genet, Hualien 970, Taiwan. RI Chen, Chia-Hsiang /E-3939-2010 CR Beyer KS, 2002, AM J MED GENET, V114, P110, DOI 10.1002/ajmg.1613 DeLisi LE, 2000, AM J MED GENET, V96, P398, DOI 10.1002/1096-8628(20000612)96:3<398::AID-AJMG30>3.0.CO;2-Z Friez MJ, 2000, HUM GENET, V106, P36, DOI 10.1007/s004390051006 Ito M, 1999, MOL CELL, V3, P361, DOI 10.1016/S1097-2765(00)80463-3 Kirov G, 2003, AM J MED GENET B, V118B, P16, DOI 10.1002/ajmg.b.10065 Michaelis RC, 2000, J AUTISM DEV DISORD, V30, P355, DOI 10.1023/A:1005583517994 Philibert RA, 1999, HUM GENET, V105, P174, DOI 10.1007/s004390051084 Philibert RA, 1998, MOL PSYCHIATR, V3, P303, DOI 10.1038/sj.mp.4000442 Philibert RA, 2000, GENE, V246, P303, DOI 10.1016/S0378-1119(00)00049-4 Philibert RA, 2001, AM J MED GENET, V105, P130, DOI 10.1002/1096-8628(20010108)105:1<130::AID-AJMG1076>3.0.CO;2-P NR 10 TC 4 Z9 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JUL 15 PY 2003 VL 119 IS 1-2 BP 163 EP 166 DI 10.1016/S0165-1781(03)00135-5 PG 4 WC Psychiatry SC Psychiatry GA 704FX UT WOS:000184329300016 PM 12860370 ER PT J AU Bejerot, S Nylander, L AF Bejerot, S Nylander, L TI Low prevalence of smoking in patients with autism spectrum disorders SO PSYCHIATRY RESEARCH LA English DT Article DE obsessive-compulsive disorder; obsessive-compulsive personality disorder; autistic disorder; smoking; nicotine; catatonia; schizophrenia ID OBSESSIVE-COMPULSIVE DISORDER; ASSESSING AXIS II; PERSONALITY-DISORDERS; DIAGNOSTIC INTERVIEW; NICOTINE DEPENDENCE; ASPERGER-SYNDROME; SCHIZOPHRENIA; TRAITS; ANXIETY AB Psychiatric patients are significantly more often smokers than the general population, the only known exception being obsessive-compulsive disorder (OCD) and catatonic schizophrenia. We have investigated nicotine use in subjects with autism spectrum disorders (ASD). Ninety-five subjects (25 females and 70 males) consecutively diagnosed with any ASD and of normal intelligence were included in the study. Only 12.6% were smokers, compared with 19% in the general population and 47% in a control group of 161 outpatients diagnosed with schizophrenia or a schizophreniform disorder. The results suggest that smoking is rare among subjects with ASD, while the opposite was shown for schizophrenia. If replicated, this finding could suggest biological differences between non-catatonic schizophrenia and ASD, and support the theory of a biological link between ASD and a subtype of OCD, and between ASD and catatonic schizophrenia. (C) 2003 Elsevier Ireland Ltd. All rights reserved. C1 Karolinska Inst, Dept Psychiat, St Gorans Hosp, Inst Clin Neurosci, SE-11281 Stockholm, Sweden. Univ Hosp, Dept Neurosci, Lund, Sweden. RP Bejerot, S (reprint author), Birger Jarlsg 131B, SE-11356 Stockholm, Sweden. CR Bejerot S, 1999, COMPR PSYCHIAT, V40, P268, DOI 10.1016/S0010-440X(99)90126-8 Bejerot S, 2001, NORD J PSYCHIAT, V55, P169 BEJEROT S, 2000, THESIS UPPSALA U UPP Bejerot S, 2000, EUR PSYCHIAT, V15, P395, DOI 10.1016/S0924-9338(00)00509-5 Beratis S, 2001, COMPR PSYCHIAT, V42, P393, DOI 10.1053/comp.2001.26273 Black D W, 1999, Ann Clin Psychiatry, V11, P129, DOI 10.3109/10401239909147061 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Buitelaar J K, 2000, Paediatr Drugs, V2, P67 Farde L, 1997, NATURE, V385, P590, DOI 10.1038/385590a0 GILLBERG C, 1995, CLIN CHILD NEUROPSYC, P54, DOI 10.1017/CBO9780511570094.007 Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Gillberg C, 2000, ACTA PSYCHIAT SCAND, V102, P321, DOI 10.1034/j.1600-0447.2000.102005321.x Gillott A, 2001, AUTISM, V5, P277, DOI 10.1177/1362361301005003005 GLASS RM, 1990, JAMA-J AM MED ASSOC, V264, P1583 GOFF DC, 1992, AM J PSYCHIAT, V149, P1189 Gross-Isseroff R, 2001, World J Biol Psychiatry, V2, P193 HEATHERTON TF, 1991, BRIT J ADDICT, V86, P1119 Laakso A, 2000, AM J PSYCHIAT, V157, P290, DOI 10.1176/appi.ajp.157.2.290 Leekam SR, 2002, J CHILD PSYCHOL PSYC, V43, P327, DOI 10.1111/1469-7610.00024 MCKENNA K, 1994, J AM ACAD CHILD PSY, V33, P636, DOI 10.1097/00004583-199406000-00003 Michell L, 1997, SOC SCI MED, V44, P1861, DOI 10.1016/S0277-9536(96)00295-X Noble EP, 2000, EUR PSYCHIAT, V15, P79, DOI 10.1016/S0924-9338(00)00208-X Pich EM, 1997, SCIENCE, V275, P83 POHL R, 1992, PSYCHIAT RES, V43, P253, DOI 10.1016/0165-1781(92)90058-B Poirier MF, 2002, PROG NEURO-PSYCHOPH, V26, P529, DOI 10.1016/S0278-5846(01)00304-9 RUTTER M, 1987, BRIT J PSYCHIAT, V150, P443, DOI 10.1192/bjp.150.4.443 Sonntag H, 2000, EUR PSYCHIAT, V15, P67, DOI 10.1016/S0924-9338(00)00209-1 *STAT SWED, 2001, CONS TOB SWED THAKER G, 1993, AM J PSYCHIAT, V150, P66 Westen D, 1999, AM J PSYCHIAT, V156, P258 Westen D, 1999, AM J PSYCHIAT, V156, P273 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WING L, 1981, PSYCHOL MED, V11, P115 NR 33 TC 19 Z9 19 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JUL 15 PY 2003 VL 119 IS 1-2 BP 177 EP 182 DI 10.1016/S0165-1781(03)00123-9 PG 6 WC Psychiatry SC Psychiatry GA 704FX UT WOS:000184329300019 PM 12860373 ER PT J AU Kemner, C van Engeland, H AF Kemner, C van Engeland, H TI Autism and visual fixation SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Letter ID CHILDREN CR Haxby JV, 2002, BIOL PSYCHIAT, V51, P59, DOI 10.1016/S0006-3223(01)01330-0 Klin A, 2002, AM J PSYCHIAT, V159, P895, DOI 10.1176/appi.ajp.159.6.895 van der Geest JN, 2002, J CHILD PSYCHOL PSYC, V43, P669, DOI 10.1111/1469-7610.00055 van der Geest JN, 2002, J AUTISM DEV DISORD, V32, P69, DOI 10.1023/A:1014832420206 NR 4 TC 9 Z9 9 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 2003 VL 160 IS 7 BP 1358 EP 1359 DI 10.1176/appi.ajp.160.7.1358-a PG 2 WC Psychiatry SC Psychiatry GA 697RN UT WOS:000183957200034 PM 12832263 ER PT J AU Klin, A Jones, W Schultz, RT Volkmar, F AF Klin, A Jones, W Schultz, RT Volkmar, F TI Autism and visual fixation - Dr. Klin and colleagues reply SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Letter ID INDIVIDUALS CR Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 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 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 NR 4 TC 3 Z9 3 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 2003 VL 160 IS 7 BP 1359 EP 1360 DI 10.1176/appi.ajp.160.7.1359 PG 2 WC Psychiatry SC Psychiatry GA 697RN UT WOS:000183957200035 ER PT J AU Horton, PC AF Horton, PC TI Autism and visual fixation - Dr. Horton replies SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Letter CR BREGER L, 2000, DARKNESS MIDST VISIO Esman AH, 2003, AM J PSYCHIAT, V160, P801, DOI 10.1176/appi.ajp.160.4.801 Horton PC, 2002, AM J PSYCHIAT, V159, P511 NR 3 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 2003 VL 160 IS 7 BP 1360 EP 1360 DI 10.1176/appi.ajp.160.7.1360 PG 1 WC Psychiatry SC Psychiatry GA 697RN UT WOS:000183957200036 ER PT J AU Newson, E Le Marechal, K David, C AF Newson, E Le Marechal, K David, C TI Pathological demand avoidance syndrome: a necessary distinction within the pervasive developmental disorders SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Review AB A proposal is made to recognise pathological demand avoidance syndrome (PDA) as a separate entity within the pervasive developmental disorders, instead of being classed under "pervasive developmental disorder not otherwise specified" (PDDnos, DSM-IV).(10) Discriminant functions analysis shows PDA to be significantly different on many counts from classic autism and Asperger's syndrome, both separately and together, including an equal sex ratio (150 cases). Demand avoidance using social manipulation is seen in all children, which strongly contrasts with the features of autistic spectrum disorders. A criterial structure is described, supported by statistical data from a random sample of 50 children diagnosed with PDA, together with a follow up sample of 18 young adults. C1 Early Years Diagnost Ctr, Nottingham NG15 9AH, England. RP Newson, E (reprint author), Early Years Diagnost Ctr, 272 Longdale Lane, Nottingham NG15 9AH, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barber MA, 2002, ARCH DIS CHILD, V86, P230, DOI 10.1136/adc.86.4.230 DAVID C, 1999, THESIS U WALES DENT K, 1996, THESIS U NOTTINGHAM NEWSON E, 1998, PSYCHOBIOLOGY AUTISM NEWSON E, 2000, DEFINING CRITERIA DI NEWSON E, 1999, RES INTO THERAPY NEWSON E, 1998, ED HANDLING GUIDELIN NEWSON E, 1996, THERAPEUTIC INTERVEN NEWSON E, 1990, PATHOLOGICAL DEMAND NR 10 TC 8 Z9 8 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD JUL 1 PY 2003 VL 88 IS 7 BP 595 EP 600 DI 10.1136/adc.88.7.595 PG 6 WC Pediatrics SC Pediatrics GA 692KM UT WOS:000183660300014 PM 12818906 ER PT J AU Gurney, JG Fritz, MS Ness, KK Sievers, P Newschaffer, CJ Shapiro, EG AF Gurney, JG Fritz, MS Ness, KK Sievers, P Newschaffer, CJ Shapiro, EG TI Analysis of prevalence trends of autism spectrum disorder in Minnesota SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; RUBELLA VACCINE; MMR-VACCINE; CAUSAL ASSOCIATION; NO EVIDENCE; MEASLES; MUMPS; IMMUNIZATION; POPULATION; EPIDEMIOLOGY AB Background: Alarming increases in the prevalence of autism spectrum disorder have been reported recently in the United States and Europe. Objectives: To quantify and characterize prevalence trends over time in autism spectrum disorder in Minnesota. Methods: We conducted an age-period-birth cohort analysis of special educational disability data from the Minnesota Department of Children, Families & Learning from the 1981-1982 through the 2001-2002 school years. Results: Prevalence rates of autism spectrum disorder rose substantially over time within single-age groups and increased from year to year within birth cohorts. Autism spectrum disorder prevalence among children aged 6 to 11 years increased from 3 per 10000 in 1991-1992 to 52 per 10000 in 2001-2002. All other special educational disability categories also increased during this period, except for mild mental handicap, which decreased slightly from 24 per 10000 to 23 per 10000. We found that federal and state administrative changes favoring identification of autism spectrum disorders corresponded in time with the increasing rates. Conclusions: We observed dramatic increases in the prevalence of autism spectrum disorder as a primary special educational disability starting in the 1991-1992 school year, and the trends show no sign of abatement. We found no corresponding decrease in any special educational disability category to suggest diagnostic substitution as an explanation for the autism trends in Minnesota. We could not assess changes in actual disease incidence with these data, but federal and state administrative changes in policy and law favoring better identification and reporting of autism are likely contributing factors to the prevalence increases and may imply that autism spectrum disorder has been underdiagnosed in the past. C1 Univ Minnesota, Dept Pediat, Div Pediat Epidemiol & Clin Res, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Pediat, Dept Pediat Clin Neurosci, Minneapolis, MN 55455 USA. Minnesota Dept Children Families & Learning, Dept Special Educ, St Paul, MN USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Ctr Autism & Dev Disabil Epidemiol, Baltimore, MD USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. RP Gurney, JG (reprint author), Univ Minnesota, Dept Pediat, Div Pediat Epidemiol & Clin Res, Mayo Mail Code 715,420 Delaware St SE, Minneapolis, MN 55455 USA. CR Accardo P, 1999, J PEDIATR-US, V135, P533, DOI 10.1016/S0022-3476(99)70045-4 American Psychiatric Association, 2000, DIAGN STAT MAN MENT 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 Black D, 1998, LANCET, V351, P905, DOI 10.1016/S0140-6736(05)70316-0 Bonde E, 2000, EUR CHILD ADOLES PSY, V9, P7 Boyle CA, 1999, INFANT YOUNG CHILD, V12, P75 Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DeLong GR, 1999, NEUROLOGY, V52, P911 Edwards KP, 2000, JAMA-J AM MED ASSOC, V284, P3171, DOI 10.1001/jama.284.24.3171 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 Feikin DR, 2000, JAMA-J AM MED ASSOC, V284, P3145, DOI 10.1001/jama.284.24.3145 Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 Gill AR, 2001, JAMA-J AM MED ASSOC, V286, P670, DOI 10.1001/jama.286.6.670 Gillberg C., 1998, AUTISM, V2, P423, DOI 10.1177/1362361398024007 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Gresham FM, 1998, J AUTISM DEV DISORD, V28, P5, DOI 10.1023/A:1026002717402 Halfon N, 1999, J AM ACAD CHILD PSY, V38, P600, DOI 10.1097/00004583-199905000-00023 Halsey N A, 2001, Pediatrics, V107, pE84, DOI 10.1542/peds.107.5.e84 Hillman R E, 2000, Mo Med, V97, P159 Jacobson JW, 2000, J AUTISM DEV DISORD, V30, P585, DOI 10.1023/A:1005691411255 Juul-Dam N, 2001, PEDIATRICS, V107, part. no., DOI 10.1542/peds.107.4.e63 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Koegel RL, 2001, J CLIN CHILD PSYCHOL, V30, P19, DOI 10.1207/S15374424JCCP3001_4 Lauritsen M, 1999, J CHILD PSYCHOL PSYC, V40, P335, DOI 10.1017/S0021963098003710 Lee JW, 1998, LANCET, V351, P905, DOI 10.1016/S0140-6736(98)26012-0 Liu JJ, 2001, AM J HUM GENET, V69, P327, DOI 10.1086/321980 London E, 2000, ENVIRON HEALTH PERSP, V108, P401 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Makela A, 2002, PEDIATRICS, V110, P957, DOI 10.1542/peds.110.5.957 Marwick C, 2001, BRIT MED J, V322, P1083 Mayes SD, 1999, INFANT YOUNG CHILD, V12, P90 Morris DL, 2000, AM J GASTROENTEROL, V95, P3507 NASH M, 2002, TIME 0429 Patel R, 1997, AM J PREV MED, V13, P74 Peltola H, 1998, LANCET, V351, P1327, DOI 10.1016/S0140-6736(98)24018-9 Ramsay S, 2001, LANCET, V357, P290, DOI 10.1016/S0140-6736(05)71737-2 SILBERMAN S, 2001, WIRED MAGAZINE DEC Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Vastag B, 2001, JAMA-J AM MED ASSOC, V285, P2567, DOI 10.1001/jama.285.20.2567 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Wakefield Andrew J., 2000, Adverse Drug Reactions and Toxicological Reviews, V19, P265 YAZBAK FE, 2003, AUTISM 99 NATL EMERG Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 2002, CDC ACTIVITIES RELAT 1999, CHANGES POPULATION P 2002, AUTISM EPIDEMIC IS N 2000, LANCET, V355, P1379 NR 58 TC 95 Z9 100 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD JUL PY 2003 VL 157 IS 7 BP 622 EP 627 DI 10.1001/archpedi.157.7.622 PG 6 WC Pediatrics SC Pediatrics GA 699EZ UT WOS:000184044800003 PM 12860781 ER PT J AU Lattimore, LP Parsons, MB Reid, DH AF Lattimore, LP Parsons, MB Reid, DH TI Assessing preferred work among adults with autism beginning supported jobs: Identification of constant and alternating task preferences SO BEHAVIORAL INTERVENTIONS LA English DT Article ID MULTIPLE SEVERE DISABILITIES; CHILDREN; PERFORMANCE; INDIVIDUALS; CHOICE AB We evaluated a multiple-stimulus assessment for identifying work preferences among adults with autism prior to beginning supported jobs. Initially, a prework assessment focused on identifying preferences across different work tasks. Eight preference assessments involving office-cleaning tasks were conducted with five supported workers. Results of five assessments involving three individuals indicated respective workers had a strong preference for one work task. On three assessments involving three workers and different cleaning tasks, weak preferences for given tasks were identified. Next, choices between more- and less-preferred tasks were provided during the daily job routine. Workers who had a strong preference on the prework assessment consistently chose the previously assessed, more preferred task during the daily job. Workers who had a weak preference always chose the more preferred task on the first choice of the work day, and then alternated between tasks on 71% of subsequent choice opportunities. Results appear to support the utility of the prework, multiple-stimulus assessment for predicting preferred tasks among supported workers with autism when the assessment identifies strong preferences. Results also offer some support for predicting a preference to alternate tasks when the assessment identifies weak preferences for respective work tasks. Implications of the results are discussed in terms of developing work routines within community jobs for adults with autism that are more in accordance with their work preferences than traditional job placement practices. Copyright (C) 2003 John Wiley Sons, Ltd. C1 Carolina Behav Anal & Support Ctr, Morganton, NC 28680 USA. Western Carolina Ctr, Morganton, NC USA. RP Reid, DH (reprint author), Carolina Behav Anal & Support Ctr, POB 425, Morganton, NC 28680 USA. 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Intervent. PD JUL PY 2003 VL 18 IS 3 BP 161 EP 177 DI 10.1002/bin.138 PG 17 WC Psychology, Clinical SC Psychology GA 702ER UT WOS:000184212200001 ER PT J AU Heering, PW Wilder, DA Ladd, C AF Heering, PW Wilder, DA Ladd, C TI Liquid rescheduling for the treatment of rumination SO BEHAVIORAL INTERVENTIONS LA English DT Article ID FOOD SATIATION; QUANTITY AB A pre-intervention assessment was conducted to determine the conditions under which rumination by a 19-year-old man with autism was most and least likely to occur. The results of the assessment suggested that rumination was least likely when the participant did not consume liquids with meals and when he consumed peanut butter during meals. Based upon the results of the assessment, an intervention consisting of rescheduling access to liquids (i.e., no liquids during meals) was evaluated across both breakfast and lunch at the participant's school placement. Results suggest that the intervention was effective in reducing rumination. Copyright (C) 2003 John Wiley Sons, Ltd. C1 Univ Pacific, Dept Psychol, Stockton, CA 95211 USA. Tuolumne Cty Off Educ, Sonora, CA USA. RP Wilder, DA (reprint author), Univ Pacific, Dept Psychol, Stockton, CA 95211 USA. CR Barton L. 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We report the near-elimination of automatically reinforced pica in a 7-year-old boy diagnosed with autism by having him practice an alternative response (discarding objects) contingent on attempted or actual pica. Intervention was implemented 6 hours per day, under naturalistic conditions in a school setting, with outcome maintained through a 4 month follow-up phase of evaluation. Copyright (C) 2003 John Wiley Sons, Ltd. C1 May Inst Inc, Norwood, MA 02062 USA. May Ctr Appl Res, Norwood, MA USA. RP Ricciardi, JN (reprint author), May Inst Inc, 1 Commerce Way, Norwood, MA 02062 USA. 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PD JUL PY 2003 VL 18 IS 3 BP 219 EP 226 DI 10.1002/bin.135 PG 8 WC Psychology, Clinical SC Psychology GA 702ER UT WOS:000184212200006 ER PT J AU Levitt, JG Blanton, RE Smalley, S Thompson, PM Guthrie, D McCracken, JT Sadoun, T Heinichen, L Toga, AW AF Levitt, JG Blanton, RE Smalley, S Thompson, PM Guthrie, D McCracken, JT Sadoun, T Heinichen, L Toga, AW TI Cortical sulcal maps in autism SO CEREBRAL CORTEX LA English DT Review ID INFERIOR PREFRONTAL CORTEX; POSITRON-EMISSION-TOMOGRAPHY; SPATIAL WORKING-MEMORY; HUMAN EXTRASTRIATE CORTEX; HUMAN NEURAL SYSTEMS; CEREBRAL BLOOD-FLOW; FUSIFORM FACE AREA; SENTENCE COMPREHENSION; CHILDHOOD AUTISM; TEMPORAL CORTEX AB This study presents the first three-dimensional mapping of cortical sulcal patterns in autism, a pervasive developmental disorder, the underlying neurobiology of which remains unknown. High-resolution T-1-weighted MRI scans were acquired in 21 autistic (age 10.7+/-3.1 years) and 20 normal control (age 11.3+/-2.9) children and adolescents. Using parametric mesh-based analytic techniques, we created three-dimensional models of the cerebral cortex and detailed maps of 22 major sulci in stereotaxic space. These average maps revealed anatomic shifting of major sulci primarily in frontal and temporal areas. Specifically, we found anterior and superior shifting of the superior frontal sulci bilaterally (Pless than or equal to0.0003), anterior shifting of the right Sylvian fissure (P=0.0002), the superior temporal sulcus (P=0.0006 right, P=0.02 left) and the left inferior frontal sulcus (Pless than or equal to0.002) in the autistic group relative to the normal group. Less significant sulcal shifts occurred in the intraparietal and collateral sulci. 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Cortex PD JUL PY 2003 VL 13 IS 7 BP 728 EP 735 DI 10.1093/cercor/13.7.728 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 695NG UT WOS:000183836600004 PM 12816888 ER PT J AU Chawarska, K Klin, A Volkmar, F AF Chawarska, K Klin, A Volkmar, F TI Automatic attention cueing through eye movement in 2-year-old children with autism SO CHILD DEVELOPMENT LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Academy-of-Child-and-Adolescent-Psychiatry CY OCT, 2002 CL SAN FRANCISCO, CALIFORNIA SP Amer Acad Child & Adolescent Psychiat ID JOINT ATTENTION; SPECTRUM DISORDER; VISUAL-ATTENTION; GAZE DIRECTION; LISTENING PREFERENCES; DEVELOPMENTAL-CHANGES; MENTAL-RETARDATION; FUNCTIONING AUTISM; PRESCHOOL-CHILDREN; INFANT SENSITIVITY AB Automatic attention cueing by perceived changes in gaze direction was studied in 2-year-old children with autism and typically developing (TD) controls using a visual attention cueing paradigm. In Experiments I and 2 the cue consisted of an eye movement (Eyes) and a nonbiological movement (SimEyes), respectively. The results suggest that visual attention in children with autism and their TD counterparts is cued by perceived eye movement. Thus, although in naturalistic situations toddlers with autism do not follow the gaze of others, they are sensitive to directional cues inherent in eye movement. Cue-specific differences in performance related to the level of engagement and cue-processing time may suggest reliance on different underlying strategies for gaze processing in autism. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. RP Chawarska, K (reprint author), Yale Univ, Sch Med, Ctr Child Study, 333 Cedar St, New Haven, CT 06520 USA. 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PD JUL-AUG PY 2003 VL 74 IS 4 BP 1108 EP 1122 DI 10.1111/1467-8624.00595 PG 15 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 706EB UT WOS:000184438900015 PM 12938707 ER PT J AU Lohmann, H Tomasello, M AF Lohmann, H Tomasello, M TI The role of language in the development of false belief understanding: A training study SO CHILD DEVELOPMENT LA English DT Article; Proceedings Paper CT Meeting of the Society-for-Research-in-Child-Development CY APR, 2003 CL TAMPA, FLORIDA SP Soc Res Child Dev ID APPEARANCE-REALITY DISTINCTION; MIND DEVELOPMENT; CHILDREN; REPRESENTATIONS; DEAFNESS; AUTISM AB The current study used a training methodology to determine whether different kinds of linguistic interaction play a causal role in children's development of false belief understanding. After 3 training sessions, 3-year-old children improved their false belief understanding both in a training condition involving perspective-shifting discourse about deceptive objects (without mental state terms) and in a condition in which sentential complement syntax was used (without deceptive objects). Children did not improve in a condition in which they were exposed to deceptive objects without accompanying language. Children showed most improvement in a condition using both perspective-shifting discourse and sentential complement syntax, suggesting that each of these types of linguistic experience plays an independent role in the ontogeny of false belief understanding. C1 Max Planck Inst Evolutionary Anthropol, Leipzig, Germany. RP Tomasello, M (reprint author), Deutsch Blatz 6, D-04103 Leipzig, Germany. CR Appleton M, 1996, SOC DEV, V5, P275, DOI 10.1111/j.1467-9507.1996.tb00086.x Astington J. 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It is characterized by the early regression of acquired language, cognitive functions, social skills, and purposeful hand function. Patients with Rett syndrome are often misdiagnosed as autistic. Recent reports of minicolumnar abnormalities in the brains of autistic and Asperger's syndrome prompted us to search for similar pathology in Rett syndrome. Material: The patient population consisted of 5 Rett syndrome patients (mean age = 14.4 +/- 4.0 years) and 17 controls (mean age = 14.6 +/- 9.5 years). Tissue was celloidin embedded, sectioned at 35 um and Nissl stained. Images (100x) were taken from Brodmann's areas 9, 21, and 22 from layer III of the left hemisphere. Method: Columnar width measurements for these images were obtained with computerized image analysis using previously published algorithms. Each area was analyzed separately with univariate ANOVA, including diagnosis as a fixed factor and age (linear and quadratic terms), and sex as covariates. 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Neuropathol. PD JUL-AUG PY 2003 VL 22 IS 4 BP 163 EP 168 PG 6 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA 702MD UT WOS:000184226900001 PM 12908751 ER PT J AU Platek, SM Critton, SR Myers, TE Gallup, GG AF Platek, SM Critton, SR Myers, TE Gallup, GG TI Contagious yawning: the role of self-awareness and mental state attribution SO COGNITIVE BRAIN RESEARCH LA English DT Article DE contagious yawning; mental state attribution; self-awareness; Schizotypal personality; schizophrenia; emotional contagion; self ID MIRROR NEURONS; SEX-DIFFERENCES; MIND; RECOGNITION; IMITATION; SCHIZOPHRENIA; AUTISM; CHIMPANZEES; PERSPECTIVE; SCHIZOTYPY AB Contagious yawning is a common, but poorly understood phenomenon. We hypothesized that contagious yawning is part of a more general phenomenon known as mental state attribution (i.e. the ability to inferentially model the mental states of others). 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Brain Res. PD JUL PY 2003 VL 17 IS 2 BP 223 EP 227 DI 10.1016/S0926-6410(03)00109-5 PG 5 WC Computer Science, Artificial Intelligence; Neurosciences; Neuroimaging SC Computer Science; Neurosciences & Neurology GA 735MY UT WOS:000186120200003 ER PT J AU Hooker, CI Paller, KA Gitelman, DR Parrish, TB Mesulam, MM Reber, PJ AF Hooker, CI Paller, KA Gitelman, DR Parrish, TB Mesulam, MM Reber, PJ TI Brain networks for analyzing eye gaze SO COGNITIVE BRAIN RESEARCH LA English DT Article DE superior temporal sulcus (STS); amygdala; fMRI; social cognition; emotion; face perception; joint attention; theory of mind; autism; schizophrenia ID HUMAN NEURAL SYSTEM; FACE PERCEPTION; TEMPORAL CORTEX; SPATIAL ATTENTION; BIOLOGICAL MOTION; VISUAL-ATTENTION; JOINT ATTENTION; HUMAN AMYGDALA; DIRECTION; IDENTITY AB The eyes convey a wealth of information in social interactions. This information is analyzed by multiple brain networks, which we identified using functional magnetic resonance imaging (MRI). Subjects attempted to detect a particular directional cue provided either by gaze changes on an image of a face or by an arrow presented alone or by an arrow superimposed on the face. Another control condition was included in which the eyes moved without providing meaningful directional information. Activation of the superior temporal sulcus accompanied extracting directional information from gaze relative to directional information from an arrow and relative to eye motion without relevant directional information. Such selectivity for gaze processing was not observed in face-responsive fusiform regions. Brain activations were also investigated while subjects viewed the same face but attempted to detect when the eyes gazed directly at them. Most notably, amygdala activation was greater during periods when direct gaze never occurred than during periods when direct gaze occurred on 40% of the trials. 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Brain Res. PD JUL PY 2003 VL 17 IS 2 BP 406 EP 418 DI 10.1016/S0926-6410(03)00143-5 PG 13 WC Computer Science, Artificial Intelligence; Neurosciences; Neuroimaging SC Computer Science; Neurosciences & Neurology GA 735MY UT WOS:000186120200021 ER PT J AU Peterson, C Slaughter, V AF Peterson, C Slaughter, V TI Opening windows into the mind: mothers' preferences for mental state explanations and children's theory of mind SO COGNITIVE DEVELOPMENT LA English DT Article DE Maternal Mental State Input Inventory; mothers; children; theory of mind ID INDIVIDUAL-DIFFERENCES; FALSE BELIEF; LANGUAGE; SIBLINGS; EMOTIONS; AUTISM; BLIND; TALK; 1ST AB A new questionnaire, the Maternal Mental State Input Inventory (MMSII) was created to measure mothers' preferences for introducing and elaborating on mental states in conversation with their young children. In two studies, the questionnaire was given to mothers of young children, and the children's theory of mind (ToM) development was assessed with standard tasks. In both studies, the questionnaire exhibited good internal reliability, and significant correlations emerged between mothers' self-reported preferences for elaborated, explanatory talk about the mental states and children's theory of mind performance. Further, mothers' conversational preferences, as measured by the MMSII, were the best predictors of children's theory of mind development when relevant control variables were included in the analyses. These results converge with naturalistic observational research that has demonstrated links between mothers' conversational styles and their children's theory of mind. They go further in suggesting that mothers' tendencies toward elaborated, explanatory talk about a range of mental states is particularly beneficial to children's theory of mind development. (C) 2003 Elsevier Inc. All rights reserved. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Peterson, C (reprint author), Unit 124,6 Oxford St, Darlinghurst, NSW 2010, Australia. CR Astington JW, 2001, CHILD DEV, V72, P685, DOI 10.1111/1467-8624.00305 BARONCOHEN S, 1995, BRIT J DEV PSYCHOL, V13, P379 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen S, 1995, MINDBLINDNESS Brown JR, 1996, CHILD DEV, V67, P836, DOI 10.1111/j.1467-8624.1996.tb01767.x BROWN JR, 1991, BRIT J DEV PSYCHOL, V9, P237 Cutting AL, 1999, CHILD DEV, V70, P853, DOI 10.1111/1467-8624.00061 DUNN J, 1995, COGNITION EMOTION, V9, P187, DOI 10.1080/02699939508409008 Dunn J, 1998, COGNITION EMOTION, V12, P171 Dunn J, 1996, J CHILD PSYCHOL PSYC, V37, P507, DOI 10.1111/j.1469-7610.1996.tb01437.x DUNN J, 1994, ORIGINS UNDERSTANDIN, P297 Dunn L. 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Jiminez (2000) proposed that weak central coherence is a primary cognitive deficit in autism and speculated that it may even account for theory of mind impairments. The current study investigated whether weak central coherence could account for deficits in 2 behaviors purported to tap capabilities fundamental to a theory of mind: joint attention and pretend play. Twenty-one children (ages 3-5 years) with autism spectrum disorders were matched to 21 control: children on chronological age, nonverbal ability, and gender. Pretend play did not differentiate the groups. Weak central coherence, poor joint attention, and low verbal ability contributed significantly and independently to the prediction of autism group membership, a finding consistent with 3 independent cognitive deficits underlying autism. C1 Univ Western Australia, Sch Psychol, Nedlands, WA 6907, Australia. RP Morgan, B (reprint author), Univ Western Australia, Sch Psychol, Nedlands, WA 6907, Australia. 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Psychol. PD JUL PY 2003 VL 39 IS 4 BP 646 EP 656 DI 10.1037/0012-1649.39.4.646 PG 11 WC Psychology, Developmental SC Psychology GA 693XE UT WOS:000183743000002 PM 12859119 ER PT J AU Bailly, D De Lenclave, MBD Lauwerier, L AF Bailly, D De Lenclave, MBD Lauwerier, L TI Hearing impairment and psychopathological disorders in children and adolescents. Review of the recent literature SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE children; deafness; mental disorders ID DEAF SCHIZOPHRENIC-PATIENTS; MANUAL COMMUNICATION; COCHLEAR IMPLANTS; BEHAVIOR PROBLEMS; ORAL DEAF; AUTISM; ATTENTION; PREVALENCE; ADJUSTMENT; SCHEDULE AB Objective - Hearing impairment is a multifaceted condition with medical and social aspects. If the neuropsychiatric impact of deafness on children has been investigated by researchers from a variety of fields and backgrounds, their conclusion is that children with hearing impairment follow many different developmental pathways. The aim of this paper is to examine the relationships between hearing impairment and mental health and the effect of impaired communication on family development. Method - From a review of the literature, the authors examine the relationships between hearing impairment and mental disorders in children and adolescents in terms of prevalence, clinical features and etiological factors. The family dynamics and the parents-child interactions were also explored. Results - The assessment of psychiatric disorders in hearing-impaired children sets some methodological problems. Accurate evaluation is hampered by the immature language exhibited by many hearing-impaired children and by the difficulties that may be encountered in establishing rapport if the child does not understand the examiner's verbal exchanges. Several authors point out the lack of communication skills and experiences with hearing-impaired children on the part of many examiners. In addition, delays have been observed for the development of social maturity in hearing-impaired children and the parents' descriptions may reflect their own worries, rather than the emotional-behavioral functioning of the child. The measurement of psychiatric symptoms is then compromised insofar as many of the assessment procedures are highly verbal and were standardized for normal-hearing children. These difficulties may explain that the prevalence rates of mental disorders in hearing-impaired children and adolescents found in the literature vary from 15 % to 60 %. If autism and deafness may both confound each others' diagnosis, several studies also point out the high comorbidity observed between these 2 conditions. The significance of this association remains unclear. Many of the authors conclude that hearing impairment is unlikely to be an etiological factor in autism. However, auditory impairment may be a marker for brain damage in autism. Although some studies showed high rates of depression and anxiety disorders, particularly social phobias, in deaf and hard-of-hearing children and adolescents, most of the studies conclude that the prevalence of affective disorders in hearing-impaired children and adolescents is comparable with estimates of prevalence for hearing young people. A number of studies have suggested that deaf children show greater degrees of impulsivity than hearing children. However, it seems that this background of greater impulsivity does not lead to higher rates of attention-deficit/hyperactivily disorder (ADHD) among deaf children. Using standardized instruments to estimate the prevalence of ADHD in this population, recent studies conclude that deaf children with hereditary deafness are not at greater risk of developing ADHD but that children with acquired deafness are, and that this difference is probably related to the medical conditions and family climates distinguishing these two groups. Psychotic disorders are no more common among hearing-impaired young people than among young people with normal hearing. However, some recent studies showed that the presentation of schizophrenia can differ in deaf people because of the high frequency of visual hallucinations observed in them. Lastly, if "primitive personality" has been described as being more prevalent among hearing-impaired children and adolescents, most of the studies found a normal range of emotional-behavioral functioning in them. In summary, if varying incidences of emotional disturbances and behavioral problems have been reported for hearing-impaired children and adolescents, except autism, it seems that children with hearing impairment experience the same range of mental health problems as hearing children. A variety of demographic, medical and educational factors were investigated as possible etiological factors for the psychiatric disorders observed in hearing-impaired children. Factors such as medical conditions, degree of deafness, communication ability and social deprivation may play a role, However, many studies also emphasize that a number of other variables, including educational methods, parental adaptation and parental support, may have an impact, positive or negative, on the development of the hearing-impaired child. By this way, numerous investigations have shown that deaf children of deaf parents attain better emotional and cognitive development than do deaf children of hearing parents. Conclusion - A number of questions remain about the neuropsychiatric and psychosocial aspects of hearing-impairment in children. For instance, few studies have been conducted to examine the impact of the different methods of communication and education on the psychosocial adjustment of deaf children. However, this review clearly show that appropriate and effective management can occur only when the mental health professionals are knowledgeable and sensitive to the unique characteristics and experiences of hearing-impaired children and adolescents. C1 Hop St Marguerite, Federat Psychiat Enfant & Adolescent, Fac Med, F-13009 Marseille, France. Ctr Hosp Reg Univ, Serv Psychiat Enfant & Adolescent, Clin Fonton, F-59037 Lille, France. EPSM Val Lys Artois, Serv Psychiat Enfant & Adolescent, F-62350 St Venant, France. RP Bailly, D (reprint author), Hop St Marguerite, Federat Psychiat Enfant & Adolescent, Fac Med, 270 Blvd St Marguerite, F-13009 Marseille, France. 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PD JUL-AUG PY 2003 VL 29 IS 4 BP 329 EP 337 PN 1 PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 734RY UT WOS:000186072400006 PM 14615703 ER PT J AU Navelet, C AF Navelet, C TI From imitation to creation - Artistic activities in the treatment of psychoses and autism SO EVOLUTION PSYCHIATRIQUE LA French DT Book Review CR GAETNER R, 2000, IMITATION CREATION NR 1 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JUL-SEP PY 2003 VL 68 IS 3 BP 475 EP 475 DI 10.1016/S0014-3855(03)00089-6 PG 1 WC Psychiatry SC Psychiatry GA 733HL UT WOS:000185994000014 ER PT J AU Chang, HL Juang, YY Wang, WT Huang, CI Chen, CY Hwang, YS AF Chang, HL Juang, YY Wang, WT Huang, CI Chen, CY Hwang, YS TI Screening for autism spectrum disorder in adult psychiatric outpatients in a clinic in Taiwan SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article DE autism spectrum disorder; adult screening questionnaire ID PERVASIVE DEVELOPMENTAL DISORDERS; SCHIZOPHRENIA; LOCUS AB Patients with adult autism spectrum disorder (ASD) continue to suffer from impairment in socialization and communication skills, and a proportion of them may develop psychiatric symptoms. It is thus likely that physicians in adult psychiatric departments may see a number of patients with ASD. Identification of patients with ASD is helpful and important for rehabilitation. This study estimated the prevalence of ASD among adult psychiatric outpatients in a Taiwanese medical center. A total of 660 patients were screened with Nylander and Gillberg's "Autism Spectrum Disorder in Adult Screening Questionnaire." Patients with high scores then under-went a diagnostic clinical interview conducted by child psychiatrists. Four patients (0.6%) were found to have ASD. (C) 2003 Elsevier Inc. All rights reserved. C1 Chang Gung Children Hosp, Dept Child Psychiat, Kewi Shan, Taiwan. Chang Gung Mem Hosp, Dept Psychiat, Kewi Shan, Taiwan. RP Chang, HL (reprint author), Chang Gung Children Hosp, Dept Child Psychiat, Kewi Shan, Taiwan. CR Alarcon M, 2002, AM J HUM GENET, V70, P60, DOI 10.1086/338241 American Psychiatric Association, 1994, DIAGN STAT MAN MENT Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 CLARKE DJ, 1989, BRIT J PSYCHIAT, V155, P692 FERITER M, 2001, J AUTISM DEV DISORD, V31, P351 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 GILLBERG C, 1990, J CHILD PSYCHOL PSYC, V31, P99, DOI 10.1111/j.1469-7610.1990.tb02275.x Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x KANNER L, 1943, AMJ ORTHOPSYCHIATRY, V19, P416 Konstantareas MM, 2001, J AUTISM DEV DISORD, V31, P19, DOI 10.1023/A:1005605528309 LOTTER V, 1974, J AUTISM CHILDHOOD S, V4, P264 Nordin V, 1998, ACTA PSYCHIAT SCAND, V97, P99, DOI 10.1111/j.1600-0447.1998.tb09970.x Nylander L, 2001, ACTA PSYCHIAT SCAND, V103, P428, DOI 10.1034/j.1600-0447.2001.00175.x VOLKMAR FR, 1991, AM J PSYCHIAT, V148, P1705 Yu CE, 2002, AM J HUM GENET, V71, P100, DOI 10.1086/341291 NR 17 TC 8 Z9 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD JUL-AUG PY 2003 VL 25 IS 4 BP 284 EP 288 DI 10.1016/S0163-8343(03)00053-7 PG 5 WC Psychiatry SC Psychiatry GA 702AH UT WOS:000184201800010 PM 12850661 ER PT J AU Ng, B Au, M Verhoeven, M Johnston, L Perkins, C AF Ng, B Au, M Verhoeven, M Johnston, L Perkins, C TI The diagnosis of Asperger's Syndrome in an adult presenting with an index episode of mania SO GENERAL HOSPITAL PSYCHIATRY LA English DT Letter ID INDIVIDUALS; DISORDER; AUTISM C1 Middlemore Hosp, Dept Psychiat, Auckland 6, New Zealand. Dual Disabil Serv, Auckland, New Zealand. RP Ng, B (reprint author), Middlemore Hosp, Dept Psychiat, Auckland 6, New Zealand. CR BARENCOHEN S, 1995, MINDBLINDNESS ESSAY DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 Dewey M, 1991, AUTISM ASPERGER SYND, P184, DOI 10.1017/CBO9780511526770.006 Ehlers S, 1997, J CHILD PSYCHOL PSYC, V38, P207, DOI 10.1111/j.1469-7610.1997.tb01855.x Fombonne E, 2003, CHILD ADOL PSYCH CL, V12, P15, DOI 10.1016/S1056-4993(02)00050-0 KERBESHIAN J, 1990, BRIT J PSYCHIAT, V156, P721, DOI 10.1192/bjp.156.5.721 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Raja M, 2001, GEN HOSP PSYCHIAT, V23, P285, DOI 10.1016/S0163-8343(01)00155-4 STEINGARD R, 1987, J AM ACAD CHILD PSY, V26, P932, DOI 10.1097/00004583-198726060-00021 TANGAM DJH, 1991, AUTISM ASPERGER SYND, P147 Tantam D., 2000, ASPERGER SYNDROME, P367 WING L, 1981, PSYCHOL MED, V11, P115 NR 12 TC 2 Z9 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD JUL-AUG PY 2003 VL 25 IS 4 BP 295 EP 297 DI 10.1016/S0164-8343(03)00041-0 PG 3 WC Psychiatry SC Psychiatry GA 702AH UT WOS:000184201800013 PM 12850664 ER PT J AU Niederhofer, H Staffen, W Mair, A AF Niederhofer, H Staffen, W Mair, A TI Tianeptine: a novel strategy of psychopharmacological treatment of children with autistic disorder SO HUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL LA English DT Article DE autism; tianeptine; behaviour ID FLUOXETINE AB Objectives Many autistic children have problems of eye contact and expressive language that limit the effectiveness of educational and behavioural interventions. Few controlled psychopharmacological trials have been conducted in autistic children to determine which agents may be effective for these associated features. Methods Twelve male children (7.3 +/- 3.3 years) with autistic disorder, diagnosed by ICD-10 criteria, completed a placebo-controlled, double-blind crossover trial of tianeptine, which lasted for 12 weeks. Subjects were included in the study if their eye contact and expressive language was inadaequate for their developmental level. Subjects had not tolerated or responded to other psychopharmacological treatments (neuroleptics, methylphenidate, clonidine or desipramine). Results Teacher ratings on the aberrant behaviour checklist irritability, stereotypy and inappropriate speech factors were lower during treatment with tianeptine than during treatment with placebo. Clinician ratings (children's psychiatric rating scale autism, anger and speech deviance factors; children's global assessment scale; clinical global impressions efficacy) of videotaped sessions were not significantly different between tianeptine and placebo. Discussion Tianeptine were modestly effective in the short-term treatment of irritability in some children with autistic disorder. Copyright (C) 2003 John Wiley Sons, Ltd. C1 Reg Hosp Bolzano, Dept Pediat, I-39100 Bolzano, Italy. Christian Doppler Klin, Dept Neurol, A-5020 Salzburg, Austria. RP Niederhofer, H (reprint author), Reg Hosp Bolzano, Dept Pediat, I-39100 Bolzano, Italy. 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Psychopharmacol.-Clin. Exp. PD JUL PY 2003 VL 18 IS 5 BP 389 EP 393 DI 10.1002/hup.491 PG 5 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry; Psychology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry; Psychology GA 701ZX UT WOS:000184200500010 PM 12858327 ER PT J AU Vered, Y Golubchik, P Mozes, T Strous, R Nechmad, A Mester, R Weizman, A Spivak, B AF Vered, Y Golubchik, P Mozes, T Strous, R Nechmad, A Mester, R Weizman, A Spivak, B TI The platelet-poor plasma 5-HT response to carbohydrate rich meal administration in adult autistic patients compared with normal controls SO HUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL LA English DT Article DE autistic disorder; serotonin; carbohydrate-rich meal ID BLOOD SEROTONIN; 5-HYDROXYINDOLEACETIC ACID; HOMOVANILLIC-ACID; CHILDREN; TRYPTOPHAN; DISORDER AB There are cumulative data indicating involvement of the 5-HT system in autistic disorder. Most studies examining 5-HT function have focused on whole blood 5-HT content. The carbohydrate-rich meal test (CRMT) is a dietary manipulation that could significantly influence platelet-poor plasma (PPP) 5-HT levels and reflect the responsiveness of the serotonergic system in 'free' plasma. In this study, CRMT was used as an indicator of 5-HT responsivity in drug-free adults with autistic disorder (n = 7), compared with normal controls (n = 10). The PPP 5-HT levels were measured at baseline and during 3 h after administration of the CRMT. A significant elevation in PPP 5-HT levels in adult autistic patients was reached 60 min after meal administration (p < 0.03 vs control and p = 0.05 vs baseline) and a significant decrease was noted after 120 min (p < 0.01 vs baseline). In contrast to the biphasic response of the autistic patients, normal controls exhibited a gradual linear increase of PPP 5-HT levels. 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Psychopharmacol.-Clin. Exp. PD JUL PY 2003 VL 18 IS 5 BP 395 EP 399 DI 10.1002/hup.489 PG 5 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry; Psychology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry; Psychology GA 701ZX UT WOS:000184200500011 PM 12858328 ER PT J AU Cesari, A Maestro, S Cavallaro, C Chilosi, A Pecini, C Pfanner, L Muratori, F AF Cesari, A Maestro, S Cavallaro, C Chilosi, A Pecini, C Pfanner, L Muratori, F TI Diagnostic boundaries between regulatory and multisystem developmental disorders: A clinical study SO INFANT MENTAL HEALTH JOURNAL LA English DT Article ID YOUNG-CHILDREN; FOLLOW-UP; INFANTS; AUTISM AB The objective of the study was to define diagnostic boundaries between Regulatory Disorders (RD) and Multisystem Developmental Disorders (MSDD). Two groups of 15 subjects, between 20 and 36 months of age, diagnosed as RD or MSDD, according to DC: 0-3 (1994) criteria, were compared in relationship, linguistic, and behavioral profiles using specific instruments. The results showed that both RD and MSDD children were impaired on all linguistic measures with a higher significant impairment of MSDD for communicative gestures, spontaneous speech, and verbal comprehension. The Child Behavior Checklist (CBCL) showed significant differences for withdrawn, and somatic problems. Only the MSDD group reached the clinical cutoff score in total problems, internalizing and withdrawn behaviors. A discriminate analysis showed that the number of communicative gestures and the scores on withdrawn and somatic problems correctly predicted in 86% of cases. It was concluded that RD and MSDD children show quantitative and qualitative differences in many of the linguistic, behavioral, and relational dimensions that were explored. 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Health J. PD JUL-AUG PY 2003 VL 24 IS 4 BP 365 EP 377 DI 10.1002/imhj.10062 PG 13 WC Psychology, Developmental SC Psychology GA 703XQ UT WOS:000184308100006 ER PT J AU Watson, LR Baranek, GT DiLavore, PC AF Watson, LR Baranek, GT DiLavore, PC TI Toddlers with autism - Developmental perspectives SO INFANTS AND YOUNG CHILDREN LA English DT Article DE affect; assessment; autism; communication; play; sensory processing; toddlers ID JOINT ATTENTION; YOUNG-CHILDREN; SPECTRUM DISORDERS; SOCIAL BEHAVIORS; INFANTILE-AUTISM; MOTOR IMITATION; EARLY SYMPTOMS; DIAGNOSIS; INFANCY; PLAY AB Recent research has greatly expanded our knowledge about the early development of children with autism and related disorders. Familiarity with this literature will improve the ability of professionals to appropriately diagnose and intervene with young children with autism. This article reviews the literature pertaining to the development of children with autism under the age of 3 years. We examine findings on affective development, sensory processing and attention, praxis and imitation, communication, play, and motor features and stereotyped behaviors, and discuss the interrelationships among these different aspects of development. Screening and diagnostic tools with specific applicability to young children with autism are reviewed as well. C1 Univ N Carolina, Dept Allied Hlth Sci, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, Div Speech & Hearing Sci, Chapel Hill, NC USA. Univ N Carolina, Sch Med, Div Occupat Sci, Chapel Hill, NC USA. RP Watson, LR (reprint author), Univ N Carolina, Dept Allied Hlth Sci, Sch Med, CB 7190,Wing D, Chapel Hill, NC 27599 USA. 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PD JUL-SEP PY 2003 VL 16 IS 3 BP 201 EP 214 PG 14 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 689RW UT WOS:000183507600002 ER PT J AU Tomblin, JB Hafeman, LL O'Brien, M AF Tomblin, JB Hafeman, LL O'Brien, M TI Autism and autism risk in siblings of children with specific language impairment SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE autistic disorder; specific language impairment; siblings; developmental psychopathology ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; CONVERSATIONAL CHARACTERISTICS; KINDERGARTEN-CHILDREN; PRAGMATIC DISORDER; FAMILY HISTORY; INDIVIDUALS; PREVALENCE; PARENTS; TWINS AB Background: Several studies have shown that family members of children with autism have elevated rates of spoken and written speech and language problems. Aims: This study asked whether there was also a greater rate of siblings with autism among probands with specific language impairment. Methods & Procedures: The probands in this study were 158 children with specific language impairment and 132 children with normal language status. These probands had 522 siblings who were examined for risk of autism using the Autism Behavior Checklist. Siblings found to be at risk were then examined using the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule-G. Outcomes & Results: A concentration of siblings with risk for a diagnosis of autism was found in association with probands who had poor spoken language skills. Four siblings of the 522 (0.8%) met the diagnostic standards for autism. All the probands of these siblings had spoken language scores below -1 SD and three had diagnoses of spoken language impairment. Conclusions: These data provide additional support for a familial association between autism and spoken language impairment. C1 Univ Iowa, Dept Speech Pathol & Audiol, Iowa City, IA 52242 USA. RP Tomblin, JB (reprint author), Univ Iowa, Dept Speech Pathol & Audiol, 7 WJSCH, Iowa City, IA 52242 USA. 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PD JUL-SEP PY 2003 VL 38 IS 3 BP 235 EP 250 DI 10.1080/1368282031000086363 PG 16 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 692RF UT WOS:000183673500002 PM 12851077 ER PT J AU Charman, T Baron-Cohen, S Swettenham, J Baird, G Drew, A Cox, A AF Charman, T Baron-Cohen, S Swettenham, J Baird, G Drew, A Cox, A TI Predicting language outcome in infants with autism and pervasive developmental disorder SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE autism; pervasive developmental disorder (PDD); language; joint attention; play; imitation ID JOINT ATTENTION; YOUNG-CHILDREN; SPECTRUM DISORDERS; PRETEND PLAY; PRESCHOOL-CHILDREN; SYMBOLIC PLAY; 2ND YEAR; IMITATION; COMMUNICATION; AGE AB Background: To examine longitudinal associations between diagnosis, joint attention, play and imitation abilities and language outcome in infants with autism and pervasive developmental disorder. Methods and Procedures: Experimental measures of joint attention, play and imitation were conducted with a sample of infants with autism spectrum disorder at age 20 months. Language outcome was assessed at age 42 months. A within-group longitudinal correlational design was adopted. Outcomes and Results: Language at 42 months was higher for children with a diagnosis of pervasive developmental disorder than for children with a diagnosis of autism. Language at follow-up was also positively associated with performance on experimental measures of joint attention and imitation, but not with performance on experimental measures of play and 'goal detection' at 20 months, nor with a non-verbal intelligence quotient, although these associations were not examined independent of diagnosis. However, floor effects on the measure of play at 20 months and the small sample size limit the conclusions that can be drawn. Conclusions: Individual differences in infant social-communication abilities as well as diagnosis may predict language outcome in preschoolers with autism spectrum disorders. Attention should be directed at assessing these skills in 2- and 3-year-old children referred for a diagnosis of autism spectrum disorder. Imitation and joint attention abilities may be important targets for early intervention. C1 UCL, Behav & Brain Sci Unit, Inst Child Hlth, London WC1N 1EH, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 3EB, England. UCL, Dept Human Commun & Sci, London, England. Guys Hosp, Newcomen Ctr, London SE1 9RT, England. RP Charman, T (reprint author), UCL, Behav & Brain Sci Unit, Inst Child Hlth, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR 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 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P158, DOI DOI 10.1192/BJP.168.2.158 Baron-Cohen S, 2000, J ROY SOC MED, V93, P521 Bates E., 1979, EMERGENCE SYMBOLS CO BATES E, 1989, DEV PSYCHOL, V25, P1004, DOI 10.1037//0012-1649.25.6.1004 BATES E, 1980, MERRILL PALMER QUART, V26, P407 BUTTERWORTH GE, 1987, ANN C DEV PSYCH SECT Carpenter M., 1998, MONOGR SOC RES CHILD, V63, P1, DOI DOI 10.2307/1166214 Carpenter M, 2002, J AUTISM DEV DISORD, V32, P91, DOI 10.1023/A:1014836521114 Charman T, 2000, COGNITIVE DEV, V15, P481, DOI 10.1016/S0885-2014(01)00037-5 Charman T, 2000, UNDERSTANDING OTHER, P422 Charman T, 1998, AUTISM INT J RES PRA, V2, P61, DOI 10.1177/1362361398021006 Charman T, 2003, J CHILD LANG, V30, P213, DOI 10.1017/S0305000902005482 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 Charman T, 1997, J AUTISM DEV DISORD, V27, P325, DOI 10.1023/A:1025806616149 CHARMAN T, 1994, DEV PSYCHOPATHOL, V6, P403, DOI 10.1017/S0954579400006015 Charman T, 1998, INF MENTAL HLTH J, V19, P260, DOI 10.1002/(SICI)1097-0355(199822)19:2<260::AID-IMHJ12>3.0.CO;2-W 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 CURCIO F, 1978, J AUTISM CHILD SCHIZ, V8, P281, DOI 10.1007/BF01539631 DAWSON G, 1984, J ABNORM CHILD PSYCH, V12, P209, DOI 10.1007/BF00910664 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 DEMYER MK, 1967, PSYCHOL REP, V21, P973 Drew A, 2002, EUR CHILD ADOLES PSY, V11, P266, DOI 10.1007/s00787-002-0299-6 TOMASELLO M, 1986, CHILD DEV, V57, P1454, DOI 10.1111/j.1467-8624.1986.tb00470.x Griffiths R, 1986, ABILITIES BABIES HAMMES JGW, 1981, J AUTISM DEV DISORD, V11, P331, DOI 10.1007/BF01531515 Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 KASARI C, 1990, J AUTISM DEV DISORD, V20, P87, DOI 10.1007/BF02206859 KNOTT F, 1995, J CHILD PSYCHOL PSYC, V36, P965, DOI 10.1111/j.1469-7610.1995.tb01343.x LEWIS V, 1995, J AUTISM DEV DISORD, V25, P105, DOI 10.1007/BF02178499 LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 LEWY AL, 1992, J ABNORM CHILD PSYCH, V20, P555, DOI 10.1007/BF00911240 Lord C., 1999, AUTISM DIAGNOSTIC OB Lord C, 2002, CHILD ADOL PSYCH CL, P636 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 LOVELAND KA, 1994, DEV PSYCHOPATHOL, V6, P433, DOI 10.1017/S0954579400006039 MELTZOFF AN, 1988, CHILD DEV, V59, P217, DOI 10.2307/1130404 MUNDY P, 1994, DEV PSYCHOPATHOL, V6, P389, DOI 10.1017/S0954579400006003 Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 Mundy P, 1998, INFANT BEHAV DEV, V21, P469, DOI 10.1016/S0163-6383(98)90020-0 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x Mundy P, 2001, INT REV RES MENT RET, V23, P139 MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 Phillips W, 1995, J CHILD PSYCHOL PSYC, V36, P1383, DOI 10.1111/j.1469-7610.1995.tb01670.x PHILLIPS W, 1992, DEV PSYCHOPATHOL, V4, P375, DOI 10.1017/S0954579400000845 Reynell J., 1985, REYNELL DEV LANGUAGE RICKS DM, 1975, J AUTISM CHILD SCHIZ, V5, P191, DOI 10.1007/BF01538152 RIGUET CB, 1981, J AUTISM DEV DISORD, V11, P439 Rogers S. 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PD JUL-SEP PY 2003 VL 38 IS 3 BP 265 EP 285 DI 10.1080/136820310000104830 PG 21 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 692RF UT WOS:000183673500004 PM 12851079 ER PT J AU Norbury, CF Bishop, DVM AF Norbury, CF Bishop, DVM TI Narrative skills of children with communication impairments SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE narrative; autism; specific language impairment; pragmatics; mental state terms ID LANGUAGE-IMPAIRED CHILDREN; DISCOURSE; ABILITY; STORY; COMPREHENSION; AUTISM; INDIVIDUALS; DISORDERS; SLI AB Background: Narrative assessment is sensitive to the communication impairments of children with specific language impairment and those with autistic spectrum disorders. Although both groups of children tend to show deficits in narrative, it is unclear whether these deficits are qualitatively different and how language and pragmatic ability may impact on narrative competence. Comparing these two groups of children with children who exhibit pragmatic language impairment without autism may help to clarify these issues. Aims: This study explored the relationship between structural language ability and pragmatic competence in narrative in children with communication impairments and typically developing children. Methods and Procedures: Diagnostic status was determined using the Children's Communication Checklist. All children were asked to generate a narrative to the wordless picture book Frog, Where are You? (Mayer 1969). Narratives were analysed according to their global structure, local linguistic structure and the child's ability to provide evaluative comments, especially about mental or emotional states. Outcomes and Results: No group differences were seen in global structure or evaluation. Children with specific language impairment and autistic disorder made more syntactic errors, and children with autism were significantly more likely to provide ambiguous references in the story. No significant relationships were evident between the Children's Communication Checklist and narrative measures. The complexity of language used was related to evaluation in the clinical groups. Conclusions: Narrative is a good way of assessing linguistic ability in older children with communication impairments. Core language abilities rather than pragmatic skill or diagnostic status are likely to influence narrative development. C1 Oxford Study Childrens Commun Impairments, Oxford, England. RP Norbury, CF (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. 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J. Lang. Commun. Disord. PD JUL-SEP PY 2003 VL 38 IS 3 BP 287 EP 313 DI 10.1080/136820310000108133 PG 27 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 692RF UT WOS:000183673500005 PM 12851080 ER PT J AU Soderstrom, H Nilsson, A AF Soderstrom, H Nilsson, A TI Childhood-onset neuropsychiatric disorders among adult patients in a Swedish special hospital SO INTERNATIONAL JOURNAL OF LAW AND PSYCHIATRY LA English DT Article ID ASPERGER-SYNDROME; 7-YEAR-OLD CHILDREN; TOTAL POPULATION; EPIDEMIOLOGY; AUTISM C1 Dept Forens Psychiat, S-42204 Gothenburg, Sweden. Gothenburg Univ, Dept Psychiat, Inst Clin Neurosci, Gothenburg, Sweden. RP Soderstrom, H (reprint author), Dept Forens Psychiat, Box 4024, S-42204 Gothenburg, Sweden. RI Anckarsater, Henrik/C-2244-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CONNERS CK, 1969, AM J PSYCHIAT, V126, P884 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Kadesjo B, 1998, DEV MED CHILD NEUROL, V40, P796 Kadesjo B, 2000, J AM ACAD CHILD PSY, V39, P548, DOI 10.1097/00004583-200005000-00007 Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 SCRAGG P, 1994, BRIT J PSYCHIAT, V165, P679, DOI 10.1192/bjp.165.5.679 Siponmaa L, 2001, J AM ACAD PSYCHIATRY, V29, P420 SODERSTROM H, 2002, NEUROPSYCHIATRIC BAC SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 Wechsler D, 1992, WECHSLER ADULT INTEL NR 13 TC 5 Z9 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0160-2527 J9 INT J LAW PSYCHIAT JI Int. J. Law Psychiatr. PD JUL-AUG PY 2003 VL 26 IS 4 BP 333 EP 338 DI 10.1016/S0160-2527(03)00048-7 PG 6 WC Law; Psychiatry SC Government & Law; Psychiatry GA 678XE UT WOS:000182891300001 PM 12726808 ER PT J AU Holmes, AS Blaxill, MF Haley, BE AF Holmes, AS Blaxill, MF Haley, BE TI Reduced levels of mercury in first baby haircuts of autistic children SO INTERNATIONAL JOURNAL OF TOXICOLOGY LA English DT Article DE amalgam; autism; hair; mercury; thimerosal ID INFANTILE-AUTISM; RUBELLA VACCINE; POPULATION; METHYLMERCURY; EPIDEMIOLOGY; PREVALENCE; METABOLISM; EXPOSURE; ABSORPTION; DISORDERS AB Reported rates of autism have increased sharply in the United States and the United Kingdom. One possible factor underlying these increases is increased exposure to mercury through thimerosal-containing vaccines, but vaccine exposures need to be evaluated in the context of cumulative exposures during gestation and early infancy. Differential rates of postnatal mercury elimination may explain why similar gestational and infant exposures produce variable neurological effects. First baby haircut samples were obtained from 94 children diagnosed with autism using Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV) criteria and 45 age- and gender-matched controls. Information on diet, dental amalgam fillings, vaccine history, Rho D immunoglobulin administration, and autism symptom severity was collected through a maternal survey questionnaire and clinical observation. Hair mercury levels in the autistic group were 0.47 ppm versus 3.63 ppm in controls, a significant difference. The mothers in the autistic group had significantly higher levels of mercury exposure through Rho D immunoglobulin injections and amalgam fillings than control mothers. Within the autistic group, hair mercury levels varied significantly across mildly, moderately, and severely autistic children, with mean group levels of 0.79, 0.46, and 0.21 ppm, respectively. Hair mercury levels among controls were significantly correlated with the number of the mothers' amalgam fillings and their fish consumption as well as exposure to mercury through childhood vaccines, correlations that were absent in the autistic group. Hair excretion patterns among autistic infants were significantly reduced relative to control. These data cast doubt on the efficacy of traditional hair analysis as a measure of total mercury exposure in a subset of the population. In light of the biological plausibility of mercury's role in neurodevelopmental disorders, the present study provides further insight into one possible mechanism by which early mercury exposures could increase the risk of autism. C1 SafeMinds, Cambridge, MA USA. Univ Kentucky, Dept Chem, Lexington, KY 40506 USA. 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The subjects, ranging in age from 3 to 9 years, included 16 boys with Down syndrome + autism and 11 boys with Down syndrome only; 13 boys with fragile X syndrome + autism and 9 boys with fragile X syndrome only; 10 boys with idiopathic autism; and 22 controls. Diagnosis of autism was based on DSM-IV criteria, confirmed primarily by the Autism Diagnostic Interview. T-1-weighted midsagittal MRIs were used to measure midline structures. Intracranial area, reflecting brain size, was significantly smaller in subjects with Down syndrome. Therefore, all vermian measures were expressed as ratios to intracranial area. Analysis of covariance (covarying for age and IQ) demonstrated that posterior vermi (lobules VI-VII and VIII-X) were markedly smaller in both Down syndrome groups and those with fragile X syndrome only, whereas only lobules VI-VII were reduced in idiopathic autism. Factorial analyses of variance tested interactions between autism factor and the diagnosis of Down syndrome or fragile X syndrome. The size of lobules VI-VII/intracranial area was dependent on autism status only in fragile X syndrome, with ratios significantly larger in fragile X syndrome with autism with respect to fragile X syndrome only We conclude that selective posterior vermis hypoplasia is seen not only in idiopathic autism but also in Down syndrome and some individuals with fragile X syndrome. However, reductions in vermian lobules VI and VII appear to be specific to idiopathic autism, whereas increased size of lobules VI and VII is associated with autism in fragile X syndrome. The latter results are consistent with MRI studies showing lobules VI-VII hyperplasia in a subset of subjects with idiopathic autism and cerebral and hippocampal enlargements in fragile X syndrome. C1 Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA. Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. RP Kaufmann, WE (reprint author), Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, 707 N Broadway,Room 500, Baltimore, MD 21205 USA. 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There has been recent interest in applying computerized technology to pediatric neuropsychological assessment, which poses unique demands based on the need to interpret performance relative to the child's developmental level. Findings: However, pediatric neuropsychologists have tended to implement computers in the scoring, but not administration, of tests. This trend is changing based on the work of experimental neuropsychologists who frequently combine data obtained from test batteries with lesion or neuroimaging data allowing descriptions of brain-behavior relations to be made with increasing confidence. One such battery is the Cambridge Neuropsychological Testing Automated Battery (CANTAB), and current studies in which the CANTAB has been used to measure executive functions in children are reviewed. 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PD JUL PY 2003 VL 44 IS 5 BP 649 EP 663 DI 10.1111/1469-7610.00152 PG 15 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 691RR UT WOS:000183619700002 PM 12831110 ER PT J AU Rogers, SJ Hepburn, SL Stackhouse, T Wehner, E AF Rogers, SJ Hepburn, SL Stackhouse, T Wehner, E TI Imitation performance in toddlers with autism and those with other developmental disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; developmental delay; motor skills; imitation; fragile X syndrome; dyspraxia ID DIAGNOSTIC OBSERVATION SCHEDULE; FRAGILE-X-SYNDROME; YOUNG-CHILDREN; JOINT ATTENTION; COMMUNICATION DEFICITS; VERBAL IMITATION; INFANTILE-AUTISM; MOTOR IMITATION; MIRROR NEURONS; DOWN-SYNDROME AB Background: The present study sought to examine the specificity, developmental correlates, nature and pervasiveness of imitation deficits very early in the development of autism. Methods: Subjects were 24 children with autism (mean age 34 months), 18 children with fragile X syndrome, 20 children with other developmental disorders, and 15 typically-developing children. Tasks included manual, oral-facial, and object oriented imitations, developmental measures, joint attention ability, and motor abilities. Results: Children with autism were found to be significantly more impaired in overall imitation abilities, oral-facial imitation, and imitations of actions on objects than children in all of the other groups. Imitation skills of young children with fragile X syndrome were strongly influenced by the absence or presence of symptoms of autism. For children with autism, imitation skills were strongly correlated with autistic symptoms and joint attention, even when controlling for developmental level. For comparison groups, imitation was related to other developmental abilities including play, language, and visual spatial skills. Neither motor functioning nor social responsivity accounted for a significant amount of variance in imitation scores, when controlling for overall developmental level, which accounted for much of the variation in imitation ability. Conclusions: Simple imitation skills were differentially impaired in young children with autism, and lack of social cooperation did not account for their poor performance. In autism, imitation skills clustered with dyadic and triadic social interactions and overall developmental level, but were not related to play or language development. For comparison children, all these areas were inter-related. Hypotheses about a specific dyspraxic deficit underlying the imitation performance in autism were not supported. C1 Univ Colorado, Ctr Hlth Sci, Boulder, CO 80309 USA. RP Rogers, SJ (reprint author), Univ Colorado, Ctr Hlth Sci, Boulder, CO 80309 USA. 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Child Psychol. Psychiatry Allied Discip. PD JUL PY 2003 VL 44 IS 5 BP 763 EP 781 DI 10.1111/1469-7610.00162 PG 19 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 691RR UT WOS:000183619700012 PM 12831120 ER PT J AU Johnson, SM Hollander, E AF Johnson, SM Hollander, E TI Evidence that eicosapentaenoic acid is effective in treating autism SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Letter ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; OMEGA-3-FATTY-ACIDS; DISORDER C1 Autism Soc Amer, Manhattan Chapter, Bethesda, MD 20814 USA. Mt Sinai Sch Med, New York, NY USA. RP Johnson, SM (reprint author), Autism Soc Amer, Manhattan Chapter, Bethesda, MD 20814 USA. CR Fenton WS, 2001, AM J PSYCHIAT, V158, P2071, DOI 10.1176/appi.ajp.158.12.2071 Nemets B, 2002, AM J PSYCHIAT, V159, P477, DOI 10.1176/appi.ajp.159.3.477 Peet M, 2001, SCHIZOPHR RES, V49, P243, DOI 10.1016/S0920-9964(00)00083-9 Stoll AL, 1999, ARCH GEN PSYCHIAT, V56, P407, DOI 10.1001/archpsyc.56.5.407 Su KP, 2001, EUR NEUROPSYCHOPHARM, V11, P295, DOI 10.1016/S0924-977X(01)00098-0 Vancassel S, 2001, PROSTAG LEUKOTR ESS, V65, P1, DOI 10.1054/plef.2001.0281 NR 6 TC 21 Z9 21 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JUL PY 2003 VL 64 IS 7 BP 848 EP 849 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 702QB UT WOS:000184233600019 PM 12934990 ER PT J AU Kita, T Wagner, GC Nakashima, T AF Kita, T Wagner, GC Nakashima, T TI Current research on methamphetamine-induced neurotoxicity: Animal models of monoamine disruption SO JOURNAL OF PHARMACOLOGICAL SCIENCES LA English DT Review DE methamphetamine; neurotoxicity; free-radical; dopamine; apoptosis ID TYROSINE-HYDROXYLASE ACTIVITY; SELF-INJURIOUS-BEHAVIOR; DISMUTASE TRANSGENIC MICE; INDUCED DOPAMINERGIC NEUROTOXICITY; CONDITIONED AVOIDANCE-RESPONSE; ZINC SUPEROXIDE-DISMUTASE; AMPHETAMINE-TREATED RATS; INDUCED NEURONAL DAMAGE; LESCH-NYHAN-SYNDROME; STRIATAL DOPAMINE AB Methamphetamine (METH)-induced neurotoxicity is characterized by a long-lasting depletion of striatal dopamine (DA) and serotonin as well as damage to striatal dopaminergic and serotonergic nerve terminals. Several hypotheses regarding the mechanism underlying METH-induced neurotoxicity have been proposed. In particular, it is thought that endogenous DA in the striatum may play an important role in mediating METH-induced neuronal damage. This hypothesis is based on the observation of free radical formation and oxidative stress produced by autooxidation of DA consequent to its displacement from synaptic vesicles to cytoplasm. In addition, METH-induced neurotoxicity may be linked to the glutamate and nitric oxide systems within the striatum. Moreover, using knockout mice lacking the DA transporter, the vesicular monoamine transporter 2, c-fos, or nitric oxide synthetase, it was determined that these factors may be connected in some way to METH-induced neurotoxicity. Finally a role for apoptosis in METH-induced neurotoxicity has also been established including evidence of protection of bcl-2, expression of p53 protein, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), activity of caspase-3. The neuronal damage induced by METH may reflect neurological disorders such as autism and Parkinson's disease. C1 Nara Med Univ, Dept Pharmacol, Kashihara, Nara 6348521, Japan. Daiichi Coll Pharmaceut Sci, Dept Pharmacol, Minami Ku, Fukuoka 8158511, Japan. Rutgers State Univ, Dept Psychol, New Brunswick, NJ 08903 USA. RP Nakashima, T (reprint author), Nara Med Univ, Dept Pharmacol, 840 Shijo Cho, Kashihara, Nara 6348521, Japan. 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Pharmacol. Sci. PD JUL PY 2003 VL 92 IS 3 BP 178 EP 195 PG 18 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 704QX UT WOS:000184352300002 PM 12890883 ER PT J AU Robertson, MM AF Robertson, MM TI Diagnosing Tourette syndrome - Is it a common disorder? SO JOURNAL OF PSYCHOSOMATIC RESEARCH LA English DT Article; Proceedings Paper CT International Conference of the Tourette-Syndrome-Foundation-of-Canada CY MAY 31-JUN 02, 2002 CL MISSISSAUGA, CANADA SP Tourette Syndrome Fdn Canada ID SPECIAL-EDUCATION; STREPTOCOCCAL INFECTIONS; TIC DISORDERS; PREVALENCE; POPULATION; CHILDREN; ADOLESCENTS; CRITERIA; SCHOOLS; AUTISM AB Objectives: The evaluate the prevalence of Tourette syndrome (TS). Methods: A review of the literature on TS was undertaken to examine the prevalence of TS in mainstream children as well as those in special education. Results: Recent studies have indicated that TS occurs in around 1% of youngsters in mainstream schools between the ages of 5 and 16 years. 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Psychosomat. Res. PD JUL PY 2003 VL 55 IS 1 BP 3 EP 6 DI 10.1016/S0022-3999(02)00580-9 PG 4 WC Psychiatry SC Psychiatry GA 699WE UT WOS:000184078300002 PM 12842225 ER PT J AU Nurmi, EL Dowd, M Tadevosyan-Leyfer, O Haines, JL Folstein, SE Sutcliffe, JS AF Nurmi, EL Dowd, M Tadevosyan-Leyfer, O Haines, JL Folstein, SE Sutcliffe, JS TI Exploratory subsetting of autism families based on savant skills improves evidence of genetic linkage to 15q11-q13 SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; linkage; savant; gamma-aminobutyric acid receptor ID PRADER-WILLI; GENOMIC SCREEN; DIAGNOSTIC INTERVIEW; ANGELMAN-SYNDROMES; IDIOTS-SAVANTS; PROXIMAL 15Q; DISORDER; DISEQUILIBRIUM; CHROMOSOME-15; IMPAIRMENT AB Objective: Autism displays a remarkably high heritability but A complex genetic etiology. One approach to identifying susceptibility loci under these conditions is to define more homogeneous subsets of families on the basis of genetically relevant phenotypic or biological characteristics that vary from case to case. Method: The authors' performed a principal components analysis, using items from the Autism Diagnostic Interview, which resulted in six clusters of variables, five of which showed significant sib-sib correlation. the utility of these phenotypic subsets was tested in an exploratory genetic analysis of the autism candidate region on chromosome 15q11-q13. Results: When the Collaborative Linkage Study of Autism sample was divided, on the basis of mean proband score for the "savant skills" cluster, the heterogeneity logarithm of the odds under a recessive model at D15S511, within the GABRB3 gene, increased from 0.6 to 2.6 in the subset of families in which probands had greater savant skills. Conclusions: These data are consistent with the genetic contribution of a 15q locus to autism susceptibility in a subset of affected individuals exhibiting savant skills. Similar types of skills have been noted in individuals with Prader-Willi syndrome, which results from deletions of this chromosomal region. C1 Vanderbilt Univ, Dept Physiol & Mol Biophys, Program Human Genet, Nashville, TN 37232 USA. Vanderbilt Univ, Med Scientist Training Program, Nashville, TN 37232 USA. Tufts New England Med Ctr, Boston, MA USA. Vanderbilt Univ, Program Human Genet, Nashville, TN 37240 USA. RP Sutcliffe, JS (reprint author), Vanderbilt Univ, Dept Physiol & Mol Biophys, Program Human Genet, 702 Light Hall, Nashville, TN 37232 USA. RI Sutcliffe, James/C-1348-2012; Haines, Jonathan/C-3374-2012; Nurmi, Erika/P-4627-2014 OI Sutcliffe, James/0000-0001-5200-6007; Nurmi, Erika/0000-0003-4893-8957 CR Baron-Cohen Simon, 1997, AUTISM, V1, P101, DOI 10.1177/1362361397011010 Barrett S, 1999, AM J MED GENET, V88, P609 Bartlett CW, 2002, AM J HUM GENET, V71, P45, DOI 10.1086/341095 Bass MP, 2000, NEUROGENETICS, V2, P219, DOI 10.1007/s100480050067 Borgatti R, 2001, PEDIATR NEUROL, V24, P111, DOI 10.1016/S0887-8994(00)00244-7 Brown WA, 2003, J AUTISM DEV DISORD, V33, P163, DOI 10.1023/A:1022987309913 Browne CE, 1997, AM J HUM GENET, V61, P1342, DOI 10.1086/301624 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Buxbaum JD, 2002, MOL PSYCHIATR, V7, P311, DOI 10.1038/sj/mp/4001011 Cassidy SB, 2000, AM J MED GENET, V97, P136, DOI 10.1002/1096-8628(200022)97:2<136::AID-AJMG5>3.0.CO;2-V Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 1997, AM J HUM GENET, V60, P928 Dykens EM, 2002, J CHILD PSYCHOL PSYC, V43, P343, DOI 10.1111/1469-7610.00025 HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P1461, DOI 10.1111/j.1469-7610.1994.tb01287.x HILL AL, 1977, PERCEPT MOTOR SKILL, V44, P161 Jiang YH, 1998, CURR OPIN GENET DEV, V8, P334, DOI 10.1016/S0959-437X(98)80091-9 Kanner L, 1943, NERV CHILD, V2, P217 Kong A, 1997, AM J HUM GENET, V61, P1179, DOI 10.1086/301592 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Maestrini E, 1999, AM J MED GENET, V88, P492, DOI 10.1002/(SICI)1096-8628(19991015)88:5<492::AID-AJMG11>3.0.CO;2-X Martin ER, 2000, AM J MED GENET, V96, P43, DOI 10.1002/(SICI)1096-8628(20000207)96:1<43::AID-AJMG9>3.0.CO;2-3 Miller LK, 1999, PSYCHOL BULL, V125, P31, DOI 10.1037/0033-2909.125.1.31 Nicholls RD, 1998, TRENDS GENET, V14, P194, DOI 10.1016/S0168-9525(98)01432-2 Nurmi EL, 2001, GENOMICS, V77, P105, DOI 10.1006/geno.2001.6617 NURMI EL, IN PRESS MOL PSYCHIA OCONNOR N, 1991, PSYCHOL MED, V21, P959 OCONNOR N, 1988, J CHILD PSYCHOL PSYC, V29, P391, DOI 10.1111/j.1469-7610.1988.tb00732.x PICKLES A, 1995, AM J HUM GENET, V57, P717 PRING L, 1995, J CHILD PSYCHOL PSYC, V36, P1065, DOI 10.1111/j.1469-7610.1995.tb01351.x Rimland B., 1984, MENTAL RETARDATION D, V13, P155 Rimland B., 1978, COGNITIVE DEFECTS DE, P43 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 Robinson Wendy P., 1993, European Journal of Human Genetics, V1, P37 Rumsey J., 1992, CLIN NEUROPSYCHOL, V6, P320 Salmon B, 1999, AM J MED GENET, V88, P551, DOI 10.1002/(SICI)1096-8628(19991015)88:5<551::AID-AJMG21>3.0.CO;2-# SCHEERER M, 1945, PSYCHOL MONOGR, V58 Shao YJ, 2002, AM J MED GENET, V114, P99, DOI 10.1002/ajmg.10153 Shao YJ, 2002, AM J HUM GENET, V70, P1058, DOI 10.1086/339765 SPITZ HH, 1973, AM J MENT DEF, V77, P757 TREFFERT DA, 1988, AM J PSYCHIAT, V145, P563 Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D, 1981, WECHSLER ADULT INTEL Wolpert C, 2000, AM J MED GENET, V96, P128, DOI 10.1002/(SICI)1096-8628(20000207)96:1<128::AID-AJMG25>3.0.CO;2-5 YOUNG RL, 1995, J AUTISM DEV DISORD, V25, P231, DOI 10.1007/BF02179286 NR 46 TC 75 Z9 77 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 JUL PY 2003 VL 42 IS 7 BP 856 EP 863 DI 10.1097/01.CHI.0000046868.56865.0F PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 694AP UT WOS:000183750800017 PM 12819446 ER PT J AU Tadevosyan-Leyfer, O Dowd, M Mankoski, R Winklosky, B Putnam, S McGrath, L Tager-Flusberg, H Folstein, SE AF Tadevosyan-Leyfer, O Dowd, M Mankoski, R Winklosky, B Putnam, S McGrath, L Tager-Flusberg, H Folstein, SE TI A principal components analysis of the autism diagnostic interview-revised SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; Autism Diagnostic Interview-Revised; principal components analysis ID LANGUAGE IMPAIRMENT; INDIVIDUALS; DISORDERS; GENE; CHILDREN; FAMILIES; SCHEDULE; VERSION; DOMAINS; PARENTS AB Objective: To develop factors based on the Autism Diagnostic Interview-Revised (ADI-R) that index separate components of the autism phenotype that are genetically relevant and validated against standard measures of the constructs. Method: ADIs and ADI-Rs of 292 individuals with autism were subjected to a principal components analysis using VAR-CLUS. The resulting variable clusters were validated against standard measures. Results: Six clusters of variables emerged: spoken language, social intent, compulsions, developmental milestones, savant skills and sensory aversions. Five of the factors were significantly correlated with the validating measures and had good internal consistency, face validity, and discriminant and construct validity. Most intraclass correlations between siblings were adequate for use in genetic studies. Conclusion: The ADI-R contains correlated clusters of variables that are valid, genetically relevant, and that can be used in a variety of studies. C1 Tufts Univ, Sch Med, Dept Psychiat, Boston, MA 02111 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Folstein, SE (reprint author), Tufts Univ, Sch Med, Dept Psychiat, 750 Washington St,NEMC 1007, Boston, MA 02111 USA. RI Tager-Flusberg, Helen/D-5265-2009 CR Alarcon M, 2002, AM J HUM GENET, V70, P60, DOI 10.1086/338241 Barrett S, 1999, AM J MED GENET, V88, P609 Bartlett CW, 2002, AM J HUM GENET, V71, P45, DOI 10.1086/341095 Bradford Y, 2001, AM J MED GENET, V105, P539, DOI 10.1002/ajmg.1497 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 COX A, 1975, BRIT J PSYCHIAT, V126, P146, DOI 10.1192/bjp.126.2.146 CUCCARO M, IN PRESS CHILD PSYCH Dunn L. 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A., 1989, EXTRAORDINARY PEOPLE Williams K. T., 1997, EXPRESSIVE VOCABULAR NR 31 TC 90 Z9 90 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 JUL PY 2003 VL 42 IS 7 BP 864 EP 872 DI 10.1097/01.CHI.0000046870.56865.90 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 694AP UT WOS:000183750800018 PM 12819447 ER PT J AU Diehl, SF AF Diehl, SF TI Prologue - Autism spectrum disorder: The context of speech-language pathologist intervention SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Editorial Material ID PREVALENCE; CHILDREN; MIND C1 Univ S Florida, Dept Commun Sci & Disorders, Tampa, FL 33620 USA. RP Diehl, SF (reprint author), Univ S Florida, Dept Commun Sci & Disorders, 4202 E Fowler Ave,PCD 1017, Tampa, FL 33620 USA. EM diehl@chuma1.cas.usf.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT BARONCOHEN S, 1991, PSYCHIAT CLIN N AM, V14, P33 Buschbacher PW, 2003, LANG SPEECH HEAR SER, V34, P217, DOI 10.1044/0161-1461(2003/018) Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Hyman SL, 2001, JAMA-J AM MED ASSOC, V285, P3141, DOI 10.1001/jama.285.24.3141 Koegel LK, 2003, LANG SPEECH HEAR SER, V34, P228, DOI 10.1044/0161-1461(2003/019) LESLIE AM, 1987, COGNITION, V27, P291, DOI 10.1016/S0010-0277(87)80014-8 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Mirenda P, 2003, LANG SPEECH HEAR SER, V34, P203, DOI 10.1044/0161-1461(2003/017) National Research Council, 2001, ED CHILDR AUT Prelock PA, 2003, LANG SPEECH HEAR SER, V34, P194, DOI 10.1044/0161-1461(2003/016) Prizant BM, 1999, J ASSOC PERS SEVERE, V24, P199, DOI 10.2511/rpsd.24.3.199 Silliman ER, 2003, LANG SPEECH HEAR SER, V34, P236, DOI 10.1044/0161-1461(2003/020) Woods JJ, 2003, LANG SPEECH HEAR SER, V34, P180, DOI 10.1044/0161-1461(2003/015) Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 16 TC 0 Z9 2 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 JUL PY 2003 VL 34 IS 3 BP 177 EP 179 DI 10.1044/0161-1461(2003/014) PG 3 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 771ZW UT WOS:000188816800002 ER PT J AU Woods, JJ Wetherby, AM AF Woods, JJ Wetherby, AM TI Early identification of and intervention for infants and toddlers who are at risk for autism spectrum disorder SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Review DE early identification; early intervention; young children; autism; communication disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; SOCIAL-COMMUNICATIVE SKILLS; 6-YEAR FOLLOW-UP; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; NONVERBAL-COMMUNICATION; BEHAVIORAL TREATMENT; LANGUAGE-DEVELOPMENT; JOINT ATTENTION; AGE AB Providing intensive early intervention is critical to maximizing outcomes for children with autism spectrum disorder (ASD), and evidence suggests that the earlier intervention can begin, the better the outcome. The first purpose of this article is to review the earliest indicators of ASD in very young children-social and communication impairments-which have important implications for early identification. The second purpose is to review evidence-based intervention practices for children with ASD and to develop a set of guiding principles for providing intervention for infants and toddlers who are at risk for ASD. Issues that are delineated include providing intervention in natural environments, supporting families in early intervention, and embedding intervention in daily routines. C1 Florida State Univ, Dept Commun Disorders, Tallahassee, FL 32306 USA. RP Woods, JJ (reprint author), Florida State Univ, Dept Commun Disorders, RRC 107, Tallahassee, FL 32306 USA. EM jwoods@garnet.acns.fsu.edu CR Allen R. 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PD JUL PY 2003 VL 34 IS 3 BP 180 EP 193 DI 10.1044/0161-1461(2003/015) PG 14 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 771ZW UT WOS:000188816800003 ER PT J AU Prelock, PA Beatson, J Bitner, B Broder, C Ducker, A AF Prelock, PA Beatson, J Bitner, B Broder, C Ducker, A TI Interdisciplinary assessment of young children with autism spectrum disorder SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE interdisciplinary assessment; autism spectrum disorder; children; family-centered; collaboration AB This paper describes an interdisciplinary model for the assessment of children with autism spectrum disorder (ASD) that includes families as active participants and collaborators in the process. Family-centered care, cultural competence, and a strengths perspective provide the theoretical foundation for the assessment model. Steps in the assessment process include assignment of an assessment coordinator, intake, preassessment planning, community-based assessment, postassessment planning, report writing, community follow-up, and resource notebook development. Preliminary research examining the effectiveness of the assessment model reveals the positive impact of family-centered, culturally competent, and strengths-based service provision (Beatson & Prelock, 2002). The model has implications for school-based practitioners in increasing the role of families in the assessment of children with ASD. C1 Univ Vermont, Dept Commun Sci, Burlington, VT 05405 USA. Cooke Ctr Learning & Dev, New York, NY USA. Baird Ctr Children & Families, Burlington, VT USA. RP Prelock, PA (reprint author), Univ Vermont, Dept Commun Sci, 407 Pomeroy Hall,489 Main St, Burlington, VT 05405 USA. 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PD JUL PY 2003 VL 34 IS 3 BP 194 EP 202 DI 10.1044/0161-1461(2003/016) PG 9 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 771ZW UT WOS:000188816800004 ER PT J AU Mirenda, P AF Mirenda, P TI Toward functional augmentative and alternative communication for students with autism: Manual signs, graphic symbols, and voice output communication aids SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Review DE autism; manual signing; aided communication; augmentative and alternative communication ID YOUNG-CHILDREN; RESPONSE EFFICIENCY; TRAINING-PROGRAMS; LANGUAGE; SPEECH; DISABILITIES; SYSTEM; INTERVENTION; ACQUISITION; BEHAVIORS AB Many individuals with autism are candidates for augmentative and alternative communication (AAC) systems, either to supplement (i.e., augment) their existing speech or to act as their primary (i.e., alternative) method of expressive communication. The purpose of this article is to summarize research and directions for future research with regard to two questions related to the delivery of AAC supports to these individuals: (a) What AAC modality is preferable to use? and (b) What do we know about the use of voice output communication aids with people with autism?. C1 Univ British Columbia, Dept Educ & Counseling Psychol & Special Educ, Vancouver, BC V6T 1Z4, Canada. RP Mirenda, P (reprint author), Univ British Columbia, Dept Educ & Counseling Psychol & Special Educ, 2125 Main Mall, Vancouver, BC V6T 1Z4, Canada. EM pat.mirenda@ubc.ca CR Adkins T., 2001, BEHAV ANAL TODAY, V2, P259 American Speech-Language-Hearing Association, 1989, ASHA, V31, P107 BAILEY DN, 1986, J ANAL TOXICOL, V10, P156 BARRERA RD, 1980, J AUTISM DEV DISORD, V10, P21, DOI 10.1007/BF02408430 BARRERA RD, 1983, J APPL BEHAV ANAL, V16, P379, DOI 10.1901/jaba.1983.16-379 Berk L. E., 2002, INFANTS CHILDREN PRE Beukelman D. 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F., 1957, VERBAL BEHAV Smith R, 1996, Anal Verbal Behav, V13, P39 Stiebel D., 1999, J POSIT BEHAV INTERV, V1, P159, DOI 10.1177/109830079900100304 Sundberg C T, 1990, Anal Verbal Behav, V8, P31 Sundberg M. L., 1998, TEACHING LANGUAGE CH Sundberg M L, 1996, Anal Verbal Behav, V13, P21 Sundberg M L, 1993, Anal Verbal Behav, V11, P99 Sundberg ML, 2001, BEHAV MODIF, V25, P698, DOI 10.1177/0145445501255003 Wraikat R, 1991, Anal Verbal Behav, V9, P1 YODER PJ, 1988, J AUTISM DEV DISORD, V18, P217, DOI 10.1007/BF02211948 Yoon S Y, 2000, Anal Verbal Behav, V17, P75 NR 108 TC 81 Z9 81 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 JUL PY 2003 VL 34 IS 3 BP 203 EP 216 DI 10.1044/0161-1461(2003/017) PG 14 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 771ZW UT WOS:000188816800005 ER PT J AU Buschbacher, PW Fox, L AF Buschbacher, PW Fox, L TI Understanding and intervening with the challenging behavior of young children with autism spectrum disorder SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE positive behavior support; functional assessment; person-centered planning; functional communication training ID COMPETING BEHAVIORS; SEVERE DISABILITIES; FUNCTIONAL-ANALYSIS; MAINTENANCE; STUDENTS; SUPPORT AB Young children with autism and behavioral challenges are at great risk for lives that are characterized by social isolation and segregated placements. These restrictive placements often occur when the child's challenging behavior interferes with successful adaptation in educational, therapeutic, and community environments. In this article, positive behavior support is described as a process that may be used to understand and intervene effectively with the challenging behavior of young children with autism. The article describes the history, empirical support, and implementation steps of positive behavior support. A case study is provided to illustrate successful application of the process. C1 Univ S Florida, Louis de la Parte Florida Mental Hlth Inst, Dept Child & Family Studies, Tampa, FL 33612 USA. RP Buschbacher, PW (reprint author), Univ S Florida, Louis de la Parte Florida Mental Hlth Inst, Dept Child & Family Studies, MHC 2113A,13301 Bruce B Downs Blvd, Tampa, FL 33612 USA. EM buschbac@fmhi.usf.edu CR Albin R. W., 1996, POSITIVE BEHAV SUPPO, P81 ARNDORFER RE, 1994, TOP EARLY CHILD SPEC, V14, P64 BAER DM, 1987, J APPL BEHAV ANAL, V20, P313, DOI 10.1901/jaba.1987.20-313 Bambara L. 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J., 1997, INTEGRATED SERVICES, P75, DOI 10.1037/10236-004 DURAND VM, 1992, J APPL BEHAV ANAL, V25, P777, DOI 10.1901/jaba.1992.25-777 DURAND VM, 1991, J APPL BEHAV ANAL, V24, P251, DOI 10.1901/jaba.1991.24-251 DURAND VM, 1990, FUNCTIONAL COMMUNICA Field S, 1999, FOCUS AUTISM OTHER D, V14, P36, DOI DOI 10.1177/108835769901400105 FOREST M, 1987, MORE ED INTEGRATION, P1 FOSTER B, 1993, AM LAB, V25, P44 Fox L, 2000, COMM LANG INTERVEN, V9, P307 Fox L, 1997, J EARLY INTERVENTION, V21, P1 FOX L, 2000, UNPUB INDIVIDUALIZED Harrower J. K., 2000, EXCEPTIONALITY, V8, P189, DOI 10.1207/S15327035EX0803_5 HART C, 1995, TEACHING CHILDREN AU, P53 HEINEMAN M, 1999, BEHAV INTERVENT, P366 Holburn S, 1997, BEHAV ANALYST, V20, P61 HORNER RH, 1991, J APPL BEHAV ANAL, V24, P719, DOI 10.1901/jaba.1991.24-719 Horner RH, 1997, J SPEC EDUC, V31, P84 HORNER RH, 1993, SYSTEMATIC INSTRUCTI, P184 IWATA BA, 1982, ANAL INTERVEN DEVEL, V2, P3, DOI 10.1016/0270-4684(82)90003-9 KENNEDY CH, 1993, J APPL BEHAV ANAL, V26, P321, DOI 10.1901/jaba.1993.26-321 Kern L, 1998, ANTECEDENT CONTROL, P289 Kincaid D., 1996, POSITIVE BEHAV SUPPO, P439 Koegel LK, 1999, J ASSOC PERS SEVERE, V24, P174, DOI 10.2511/rpsd.24.3.174 Koegel LK, 1998, J ASSOC PERS SEVERE, V23, P111, DOI 10.2511/rpsd.23.2.111 KRUG DA, 1980, AUTISM BEHAV CHECKLI LALLI JS, 1995, J APPL BEHAV ANAL, V28, P261, DOI 10.1901/jaba.1995.28-261 Meyer L. H., 1989, NONAVERSIVE INTERVEN National Research Council, 2001, ED CHILDR AUT Newborg J., 1984, BATTELLE DEV INVENTO NORTHUP J, 1991, J APPL BEHAV ANAL, V24, P509, DOI 10.1901/jaba.1991.24-509 O'Neill R. E., 1997, FUNCTIONAL ASSESSMEN, V2nd ONEILL RE, 1998, TRANSITIONS PRELINGU, P313 Pearpoint J., 1998, PATH WORKBOOK PLANNI REEVE CE, 1996, THESIS STATE U NEW Y SLENTZ KL, 1992, J EARLY INTERVENTION, V16, P11 TILLY WD, 1998, FUNCTIONAL BEHAV ASS TOUCHETTE PE, 1985, J APPL BEHAV ANAL, V18, P343, DOI 10.1901/jaba.1985.18-343 Turnbull A. P., 1996, POSITIVE BEHAV SUPPO, P99 Turnbull A. P., 1997, FAMILIES PROFESSIONA Turnbull AP, 1996, MENT RETARD, V34, P280 WACKER DP, 1990, J APPL BEHAV ANAL, V23, P417, DOI 10.1901/jaba.1990.23-417 Walker H. M., 1998, TEACHING EXCEPTIONAL, V30, P16 WALKER HM, 1993, ANTISOCIAL BEHAV SCH Wetherby A.M., 1992, AUTISM IDENTIFICATIO, P107 Zwernick K., 1988, ITS NEVER TOO EARLY NR 62 TC 14 Z9 14 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 JUL PY 2003 VL 34 IS 3 BP 217 EP 227 DI 10.1044/0161-1461(2003/018) PG 11 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 771ZW UT WOS:000188816800006 ER PT J AU Koegel, LK Koegel, RL Frea, W Green-Hopkins, I AF Koegel, LK Koegel, RL Frea, W Green-Hopkins, I TI Priming as a method of coordinating educational services for students with autism SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE autism; homework; disruptive behavior; academic responding; listening comprehension ID LEARNING-DISABILITIES; HOMEWORK; BEHAVIOR; CHILDREN; INTERVENTION; PERFORMANCE; STRATEGIES AB Purpose: The importance of coordination of educational services has been well documented in the literature. For students with disabilities, coordinated programs result in more rapid acquisition of targeted behaviors and the increased likelihood of long-term maintenance of gains. The purpose of this study was to assess whether "priming" or exposing students with autism and disruptive behaviors to school assignments before their presentation in class would affect academic performance and problem behaviors. Method: Two students diagnosed with autism who attended general education classrooms, both of whom exhibited numerous disruptive behaviors and low academic performance, participated in this study. A repeated reversals design was used to monitor student progress. Results: The results demonstrated decreases in problem behavior and increases in academic responding when priming sessions occurred. Clinical Implications: Application is discussed in terms of a mechanism for speech-language pathologists to assist classroom teachers with a systematic educational coordination plan that can quickly produce improved school performance. C1 Univ Calif Santa Barbara, Autism Res & Training Ctr, CCS Psychol Program, Santa Barbara, CA 93106 USA. RP Koegel, LK (reprint author), Univ Calif Santa Barbara, Autism Res & Training Ctr, CCS Psychol Program, Santa Barbara, CA 93106 USA. EM koegel@education.ucsb.edu CR BARLOW DH, 1984, SINGLE CASE EXPT DES Bryan T, 2001, EDUC PSYCHOL, V36, P167, DOI 10.1207/S15326985EP3603_3 Callahan K., 1999, J POSIT BEHAV INTERV, V1, P117, DOI 10.1177/109830079900100206 Callahan K, 1998, REM SPEC EDUC, V19, P131 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd COHEN J, 1992, PSYCHOL BULL, V112, P155, DOI 10.1037/0033-2909.112.1.155 DERBY KM, 1992, J APPL BEHAV ANAL, V25, P713, DOI 10.1901/jaba.1992.25-713 DUNLAP G, 1993, COMMUNICATIVE ALTERN, V3, P177 Dunlap G, 1995, J ASSOC PERS SEVERE, V20, P248 Dunlap G., 1996, J BEHAV ED, V6, P481, DOI 10.1007/BF02110518 Dunn L. 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K, 1998, ANTECEDENT CONTROL I Moes DR, 1998, J ASSOC PERS SEVERE, V23, P319, DOI 10.2511/rpsd.23.4.319 SALEND SJ, 1995, REM SPEC EDUC, V16, P271 Sawyer V, 1996, LEARN DISABILITY Q, V19, P70, DOI 10.2307/1511249 Sparrow S, 1984, VINELAND ADAPTIVE BE Wilde L. D., 1992, INCREASING SUCCESS S Zanolli K, 1996, J AUTISM DEV DISORD, V26, P407, DOI 10.1007/BF02172826 NR 32 TC 12 Z9 12 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 JUL PY 2003 VL 34 IS 3 BP 228 EP 235 DI 10.1044/0161-1461(2003/019) PG 8 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 771ZW UT WOS:000188816800007 ER PT J AU Silliman, ER Diehl, SF Bahr, RH Hnath-Chisolm, T Zenko, CB Friedman, SA AF Silliman, ER Diehl, SF Bahr, RH Hnath-Chisolm, T Zenko, CB Friedman, SA TI A new look at performance on theory-of-mind tasks by adolescents with autism spectrum disorder SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE autism spectrum disorder; theory of mind; false belief tasks; logical inferencing; social inferencing ID NORMALLY DEVELOPING-CHILDREN; ASPERGER-SYNDROME; INDIVIDUAL-DIFFERENCES; 2ND-ORDER BELIEFS; VERBAL-ABILITY; FALSE BELIEF; LANGUAGE; EMOTION; KNOWLEDGE; ADULTS AB Purpose: A hallmark of autistic spectrum disorder (ASD) is disruption in theory-of-mind development, including the understanding of false beliefs. Previous studies have typically assessed the development of first- and second-order false belief concepts in, ASO, with tasks primarily emphasizing physical causality and logical inferencing. The present study investigated how preadolescents and adolescents with ASO performed on false belief tasks that,included social inferencing of psychological states as well as logical inferencing of physical states. Method: Two categories of tasks were administered: four traditional logical inferencing tasks and four social inferencing tasks specifically developed for this study. in addition, a prompt hierarchy was included to ascertain if performance on both task types improved. Participants were 45 children and adolescents primarily selected from three urban school districts: 15 adolescents with a previous diagnosis of ASO (ASO group); 15 typically developing children matched for age, gender, and ethnicity (CA group); and 15 typically developing children matched for language age, gender, and ethnicity (LA group). Results: Three findings were pertinent. First, the CA group performed at higher levels than did the LA group and the ASO group on both task sets. Second, although the CA and the LA groups performed equally well on both the logical and the social inferencing tasks, the ASO group performed better on the social inferencing tasks. Finally, the prompt hierarchy significantly improved overall task performance for the ASO and LA groups. Clinical Implications: These findings indicate that task type, variations in vocabulary ability, and the provision of support influenced performance on the false belief tasks. C1 Univ S Florida, Tampa, FL 33620 USA. Univ Florida, Ctr Autism & Related Disabilities, Gainesville, FL USA. Childrens Choice Therapy, Tampa, FL USA. RP Silliman, ER (reprint author), Univ S Florida, 4202 E Fowler Ave,PCD1017, Tampa, FL 33620 USA. 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PD JUL PY 2003 VL 9 IS 7 BP 823 EP 825 DI 10.1038/nm0703-823 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 698CD UT WOS:000183979300016 PM 12835694 ER PT J AU Manjaly, ZM Marshall, JC Stephan, KE Gurd, JM Zilles, K Fink, GR AF Manjaly, ZM Marshall, JC Stephan, KE Gurd, JM Zilles, K Fink, GR TI In search of the hidden: an fMRI study with implications for the study of patients with autism and with acquired brain injury SO NEUROIMAGE LA English DT Article DE Embedded Figures Task; local/global processing; visual search; parietal cortex; Asperger's syndrome ID VISUAL-ATTENTION; GLOBAL PRECEDENCE; ASPERGER-SYNDROME; FIGURES-TEST; CHILDREN; PERFORMANCE; MECHANISMS; ACTIVATION; LESIONS; STIMULI AB The Embedded Figures Task involves a search for a target hidden in a more complex visual pattern. The task has been used to study local perception and visual search in a range of normal and pathological populations. After acquired brain damage, impairment on embedded figures is strongly associated with aphasia; in the context of developmental disorder, people with autism or with Asperger's syndrome are reliably found to be better than normal controls on the task. The current study employed functional MRI with healthy volunteers to elucidate the brain regions that are specifically involved in the local search aspects of the Embedded Figures Task. We did so by analyzing the neural activations that are implicated in the task over and above those involved in an easier visual search task and in a straightforward shape recognition task. Significant activations (P < 0.05, corrected) specific in the above sense to the Embedded Figures Task were found in left inferior and left superior parietal cortex and in left ventral premotor cortex (inferior frontal gyrus). 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An outbreak of measles occurred in Ireland between December 1999 and July 2000. The majority of cases were in north Dublin, the catchment area of The Children's University Hospital (TCUH). Methods. Details of all of the 111 children attending the hospital with a diagnosis of measles be. tween December 1999 and July 2000 were prospectively entered into a database. Charts were subsequently reviewed to extract epidemiologic and clinical details. National figures were obtained from the National Disease Surveillance Centre. Results. In the study period 355 attended TCUH with a serologic or clinical diagnosis of measles, and 111 were admitted (47% female, 53% male). The main indications for admission were dehydration in 79%, pneumonia or pneumonitis in 47% and tracheitis in 32%. Thirteen children (11.7% of those admitted) required treatment in the intensive care unit, and in 7 of these mechanical ventilation was necessary. There were 3 deaths as a result of measles. 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CR 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 NR 2 TC 0 Z9 0 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 JUL PY 2003 VL 112 IS 1 BP 206 EP 206 DI 10.1542/peds.112.1.206 PG 1 WC Pediatrics SC Pediatrics GA 696WR UT WOS:000183911000053 PM 12837894 ER PT J AU Sergienko, EA Lebedeva, EI AF Sergienko, EA Lebedeva, EI TI Understanding of deception by healthy and autistic preschool children SO PSIKHOLOGICHESKII ZHURNAL LA Russian DT Article DE understanding of mind; "the theory of mind"; understanding of deception; healthy vs. autistic preschool children ID YOUNG-CHILDREN; MIND; COMMUNICATION; KNOWLEDGE AB There are presented the results of comparative research of children's understanding of deception as phenomenon of cognitive representation of mental organization in healthy children and in children suffered from autism. The Ss were 48 healthy children (3-6 years old) and 9 autists (5-7 years old). It was shown that children suffered from autism couldn't understand others mind. In healthy children "the theory of mind" development (since 4 years old) allows them to understand deception and its markers that is impossible if the theory is undeveloped. The use of symbolic tools - prompts of deception situations - didn't influence the understanding of deception in younger children. Thus neither child's activity in condition of deception nor mediation (markers) doesn't facilitate "the theory of mind" development in children of 3 years old and autists. C1 RAS, IP, Lab Cognit Proc, Moscow 117901, Russia. State Univ Humanities, Ctr Psychol Med Social Assistance Children & Adol, Moscow, Russia. RP Sergienko, EA (reprint author), RAS, IP, Lab Cognit Proc, Moscow 117901, Russia. CR BARONCOHEN S, 1985, COGNITION, V21 BARONCOHEN S, 1992, J CHILD PSYCHOL PSYC, V33, P1141, DOI 10.1111/j.1469-7610.1992.tb00934.x BARONCOHEN S, 2000, PERSPECTIVE DEV COGN Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Bartsch K., 1995, CHILDREN TALK MIND BASHINA VM, 1999, AUTIZM DETSTVE BASHINA VM, 1997, DETSKII AUTIZM CHANDLER M, 1989, CHILD DEV, V60 Flavell JH, 1999, ANNU REV PSYCHOL, V50, P21, DOI 10.1146/annurev.psych.50.1.21 Flavell JH, 2000, INT J BEHAV DEV, V24, P15 FODOR JA, 1992, COGNITION, V44, P283, DOI 10.1016/0010-0277(92)90004-2 GILBERG K, 1998, AUTIZM MED PEDAGOGIC GOPNIK A, 1988, CHILD DEV, V59, P26, DOI 10.2307/1130386 HOBSON PR, 1993, AUTISMM DEV MIND Jeannerod M, 1999, Q J EXP PSYCHOL-A, V52, P1, DOI 10.1080/027249899391205 KOVALEV VV, 1995, PSIKHIATRIYA DETSKOG LEBEDINSKII VV, 1990, EMOTSIONALNYE NARUSH Leslie A.M., 1994, MAPPING MIND DOMAIN, P119, DOI DOI 10.1017/CBO9780511752902.006 Meltzoff AN, 1999, J COMMUN DISORD, V32, P251, DOI 10.1016/S0021-9924(99)00009-X Moore C, 1996, BRIT J DEV PSYCHOL, V14, P19 Mundy P, 1997, MENT RETARD DEV D R, V3, P343 NIKOLSKAYA OS, 2000, AUTIZHNYI REBENOK PU Perner Josef, 1991, UNDERSTANDING REPRES RUFFMAN T, 1993, DEV PSYCHOL, V29, P74, DOI 10.1037//0012-1649.29.1.74 SERGIENKO EA, 2000, PROBLEMA SUBEKTA PSI SODIAN B, 1991, BRIT J DEV PSYCHOL, V9, P173 Wellman HM, 1998, PSYCHOL BULL, V123, P33, DOI 10.1037//0033-2909.123.1.33 NR 27 TC 4 Z9 4 PU MEZHDUNARODNAYA KNIGA PI MOSCOW PA 39 DIMITROVA UL., 113095 MOSCOW, RUSSIA SN 0205-9592 J9 PSIKHOL ZH JI Psikhologicheskii Zhurnal PD JUL-AUG PY 2003 VL 24 IS 4 BP 54 EP 65 PG 12 WC Psychology, Multidisciplinary SC Psychology GA 722ZG UT WOS:000185407500007 ER PT J AU Bolte, S Poustka, F AF Bolte, S Poustka, F TI The recognition of facial affect in autistic and schizophrenic subjects and their first-degree relatives SO PSYCHOLOGICAL MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; WEAK CENTRAL COHERENCE; ASPERGER-SYNDROME; DIAGNOSTIC INTERVIEW; COGNITIVE PHENOTYPE; NONPSYCHOTIC RELATIVES; CHILDREN; DEFICITS; PARENTS; FACE AB Background. Autism and schizophrenia are considered to be substantially influenced by genetic factors. The endophenotype of both disorders probably also includes deficits in affect perception. The objective of this study was to examine the capacity to detect facially expressed emotion in autistic and schizophrenic subjects, their parents and siblings. Method. Thirty-five subjects with autism and 102 of their relatives, 21 schizophrenic subjects and 46 relatives from simplex (one child affected) and multiplex (more than one child affected) families, as well as an unaffected control sample consisting of 22 probands completed a 50-item computer-based test to assess the ability to recognize basic emotions. Results. The autistic subjects showed a poorer performance on the facial recognition test than did the schizophrenic and the unaffected individuals. In addition, there was a tendency for subjects from multiplex families with autistic loading to score lower on the test than individuals from simplex families with autistic loading. Schizophrenic subjects and their relatives as well as siblings and parents of autistic subjects did not differ from the sample of unaffected subjects in their ability to judge facial affect. Conclusions. Findings corroborate the assumption that emotion detection deficits are part of the endophenotype of autism. In families with autistic children, the extent of facial recognition deficits probably indexes an elevation in familial burden. It seems unlikely that problems in emotion perception form a consistent part of the endophenotype of schizophrenia or the broader phenotype in relatives of patients with psychosis or autism. C1 Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jungendal, Dept Child & Adoelscent Psychiat, D-60528 Frankfurt, Germany. 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According to this hypothesis, an implicit, prereflexive form of understanding of other individuals is based on the strong sense of identity binding us to them. We share with our conspecifics a multiplicity of states that include actions, sensations and emotions. A new conceptual tool able to capture the richness of the experiences we share with others will be introduced: the shared manifold of intersubjectivity. I will posit that it is through this shared manifold that it is possible for us to recognize other human beings as similar to us. It is just because of this shared manifold that intersubjective communication and ascription of intentionality become possible. It will be argued that the same neural structures that are involved in processing and controlling executed actions, felt sensations and emotions are also active when the same actions, sensations and emotions are to be detected in others. 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RP Bargerhuff, ME (reprint author), Wright State Univ, Dayton, OH 45435 USA. CR MURRAYSLUTSKY C, 2000, EXPLORING SPECTRUM A NR 1 TC 1 Z9 1 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0741-9325 J9 REM SPEC EDUC JI Remedial Spec. Educ. PD JUL-AUG PY 2003 VL 24 IS 4 BP 255 EP 256 DI 10.1177/07419325030240040802 PG 2 WC Education, Special SC Education & Educational Research GA 703BY UT WOS:000184261200009 ER PT J AU Dautenhahn, K AF Dautenhahn, K TI Roles and functions of robots in human society: implications from research in autism therapy SO ROBOTICA LA English DT Article DE autism therapy; human society; robots ID SOCIAL INTERACTIONS; TECHNOLOGY; CHILDREN; USERS; WANT AB This paper discusses robots that are operational within a human-inhabited environment. Specifically, we identify different roles that such robots can adopt, reflecting different human-robot relationships. 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PD JUN 21 PY 2003 VL 178 IS 2400 BP 3 EP 3 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 692ZB UT WOS:000183689200001 ER PT J AU Lathe, R Le Page, M AF Lathe, R Le Page, M TI Toxic metal clue to autism - A study has revealed startling differences in mercury levels in the hair of autistic and normal children 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 JUN 21 PY 2003 VL 178 IS 2400 BP 4 EP 5 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 692ZB UT WOS:000183689200003 ER PT J AU Valdizan, JR Zarazaga-Andia, I Abril-Villalba, B Sans-Capdevila, O Mendez-Garcia, M AF Valdizan, JR Zarazaga-Andia, I Abril-Villalba, B Sans-Capdevila, O Mendez-Garcia, M TI Face recognition in autism SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autism; face recognition; visual development ID INVERSION; PERCEPTION; CHILDREN; DEFICIT; MEMORY; WHOLES; PARTS; AREA AB Introduction. We conducted a survey of the literature on face recognition (FR), an activity that is essential for social relations and their dynamics. Unlike the recognition of non-facial objects, this type of recognition is a special process since it is based on the detection of individual features. The most characteristic clinical parameter of autistic subjects is their inability to relate socially, possibly due to the difficulty they have in processing faces, although they are more skilled at recognising objects. Development We describe the two mechanisms involved in FR, one based on features and the other referring to the whole. The latter can be further divided into overall processing that allows a whole image to be compared with another previously assimilated image, and the processing of the arrangement of a face that is recognised as a whole. These may correspond to two different neuronal pathways. During the first days of life, the newborn baby has a predilection for faces in their feature and overall aspects, and processing of the arrangement is slower. Visual development in autistic children is erratic, similar to the level of a newborn infant, and their lack of interest for human faces is apparent during the first year of life, as they look at everything as if they were objects, that is, by features. Conclusions. The analysis of the literature enabled us to determine how FR mechanisms develop in the earliest days of the infant's life. It also high lighted the importance of the integrity of the pathway that facilitates stimulation for the recognition of facial arrangement, which is altered in autistic children perhaps from the peripheral area to the cortex. Further work on peripheral pathways and the fundamental cortical connections that are affected in autistic subjects will help us kto understand the inefficiency of their facial arrangement recognition system. [REV NEUROL 2003; 36: 1186-9]. C1 Hosp Univ Miguel Servet, Serv Neurofisiol Clin, Zaragoza, Spain. Ctr Especialidades Inocencio Jimenez, Serv Oftalmol, Zaragoza, Spain. 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Neurologia PD JUN 16 PY 2003 VL 36 IS 12 BP 1186 EP 1189 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 699MX UT WOS:000184061500017 PM 12833241 ER PT J AU Kampe, KKW Frith, CD Frith, U AF Kampe, KKW Frith, CD Frith, U TI "Hey John": Signals conveying communicative intention toward the self activate brain regions associated with "mentalizing," regardless of modality SO JOURNAL OF NEUROSCIENCE LA English DT Article DE Theory of Mind; mentalizing; eye gaze; faces; names; medial prefrontal cortex; paracingulate cortex; temporal poles; fMRI; autism ID ASPERGER-SYNDROME; MIND; AUTISM; FMRI; ATTRIBUTION; MECHANISMS; DISORDER; AROUSAL AB Successful communication between two people depends first on the recognition of the intention to communicate. Such intentions maybe conveyed by signals directed at the self, such as calling a person's name or making eye contact. In this study we use functional magnetic resonance imaging to show that the perception of these two signals, which differ in modality and sensory channel, activate common brain regions: the paracingulate cortex and temporal poles bilaterally. These regions are part of a network that has been consistently activated when people are asked to think about the mental states of others. Activation of this network is independent of arousal as measured by changes in pupil diameter. C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. Univ Hamburg, Klinikum Eppendorf, Dept Neurol, D-20246 Hamburg, Germany. UCL, Wellcome Dept Imaging Neurosci, Neurol Inst, London WC1N 3BG, England. RP Kampe, KKW (reprint author), Neurol Clin, Haus S10,Martinistr 52, D-20246 Hamburg, Germany. 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Neurosci. PD JUN 15 PY 2003 VL 23 IS 12 BP 5258 EP 5263 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 696MY UT WOS:000183891700053 PM 12832550 ER PT J AU Lahuis, B Kemner, C Van Engeland, H AF Lahuis, B Kemner, C Van Engeland, H TI Magnetic resonance imaging studies on autism and childhood-onset schizophrenia in children and adolescents - a review SO ACTA NEUROPSYCHIATRICA LA English DT Review DE autism; childhood-onset schizophrenia; magnetic resonance imaging ID DEFICIT-HYPERACTIVITY DISORDER; CORPUS-CALLOSUM MORPHOLOGY; BRAIN-STEM INVOLVEMENT; EARLY INFANTILE-AUTISM; QUANTITATIVE MORPHOLOGY; DEVELOPMENTAL DYSLEXIA; CAUDATE-NUCLEUS; POSTERIOR-FOSSA; 4TH VENTRICLE; WHITE-MATTER AB Objective: To find out whether the neurodevelopmental disorders autism and childhood-onset schizophrenia have a common developmental pathway and whether the abnormalities detected are 'disorder-specific', by reviewing magnetic resonance imaging (MRI) studies. Methods: As a result of a Medline search, we were able to access 28 studies on autism and 12 studies on childhood-onset schizophrenia, which focused on children and adolescents. Results: Larger lateral ventricles were found to be a common abnormality in both disorders. 'Disorder-specific' abnormalities in patients with autism were larger brains, a larger thalamic area, and a smaller right cingulate gyrus. Subjects with childhood-onset schizophrenia were found to have smaller brains, a smaller amygdalum and thalamus, and a larger nucleus caudatus. In subjects with childhood-onset schizophrenia, abnormalities appeared to progress over a limited period of time. Conclusions: Because the study designs varied so much, the results should be interpreted cautiously. Before abnormalities found in the disorders can be designated as equal or 'disorder-specific', it will be essential to perform large longitudinal and cross-sectional follow-up studies. 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PD JUN PY 2003 VL 15 IS 3 BP 140 EP 147 DI 10.1034/j.1601-5215.2003.00021.x PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 688FL UT WOS:000183423500008 ER PT J AU Ewing, KM Jones, TW AF Ewing, KM Jones, TW TI An educational rationale for deaf students with multiple disabilities SO AMERICAN ANNALS OF THE DEAF LA English DT Article ID STRATEGY AB DEAF STUDENTS WITH with multiple disabilities have a long history of limited opportunity, including limited access to educational opportunities available to their deaf peers. This article places the individual needs of deaf students with multiple disabilities in the context that guides much of deaf education-the importance of language acquisition. That emphasis provides a basis for placement and curriculum options for deaf students with multiple disabilities. The authors review the evolution of placement options, describe assumptions that should guide placement and curriculum decisions, and recommend practices for optimizing these students' education. Descriptions of three service delivery models-multidisciplinary, interdisciplinary, and transdisciplinary-are provided, as well as an overview of the effectiveness of person-centered planning for deaf students with multiple disabilities. Disability-specific resources are highlighted that relate to mental retardation, autism, visual impairments, learning disabilities, attention deficit hyperactivity disorder, emotional disorders, medical issues, and general resources. C1 Gallaudet Univ, Washington, DC 20002 USA. Council Educ Deaf, Washington, DC USA. RP Ewing, KM (reprint author), Gallaudet Univ, Washington, DC 20002 USA. 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Deaf PD SUM PY 2003 VL 148 IS 3 BP 267 EP 271 DI 10.1353/aad.2003.0019 PG 5 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 726AH UT WOS:000185574700008 PM 14574799 ER PT J AU O'Brien, EK Zhang, XY Nishimura, C Tomblin, JB Murray, JC AF O'Brien, EK Zhang, XY Nishimura, C Tomblin, JB Murray, JC TI Association of specific language impairment (SLI) to the region of 7q31 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MAJOR SUSCEPTIBILITY LOCUS; TRANSLOCATION BREAKPOINT; KINDERGARTEN-CHILDREN; AUTISTIC DISORDER; TOURETTE-SYNDROME; FAMILY HISTORY; SEVERE SPEECH; GENE; LINKAGE; CHROMOSOME-7 AB FOXP2 (forkhead box P2) was the first gene characterized in which a mutation affects human speech and language abilities. A common developmental language disorder, specific language impairment (SLI), affects 6%-7% of children with normal nonverbal intelligence and has evidence of a genetic basis in familial and twin studies. FOXP2 is located on chromosome 7q31, and studies of other disorders with speech and language impairment, including autism, have found linkage to this region. In the present study, samples from children with SLI and their family members were used to study linkage and association of SLI to markers within and around FOXP2, and samples from 96 probands with SLI were directly sequenced for the mutation in exon 14 of FOXP2. No mutations were found in exon 14 of FOXP2, but strong association was found to a marker within the CFTR gene and another marker on 7q31, D7S3052, both adjacent to FOXP2, suggesting that genetic factors for regulation of common language impairment reside in the vicinity of FOXP2. C1 Univ Iowa, Dept Otolaryngol, Iowa City, IA USA. Univ Iowa, Dept Speech Pathol & Audiol, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Dept Pediat, Iowa City, IA 52242 USA. RP Murray, JC (reprint author), Med Labs 2182, Iowa City, IA 52242 USA. 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J. Hum. Genet. PD JUN PY 2003 VL 72 IS 6 BP 1536 EP 1543 DI 10.1086/375403 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 685QV UT WOS:000183275500016 PM 12721956 ER PT J AU Thomas, JA Johnson, J Kraai, TLP Wilson, R Tartaglia, N LeRoux, J Beischel, L McGavran, L Hagerman, RJ AF Thomas, JA Johnson, J Kraai, TLP Wilson, R Tartaglia, N LeRoux, J Beischel, L McGavran, L Hagerman, RJ TI Genetic and clinical characterization of patients with an interstitial duplication 15q11-q13, emphasizing behavioral phenotype and response to treatment SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE chromosomal duplication; autism; attention deficit hyperactivity disorder; developmental delay ID PRADER-WILLI-SYNDROME; PROXIMAL 15Q; DEVELOPMENTAL DELAY; CHROMOSOME 15Q; REGION; AUTISM; METHYLATION; DIAGNOSIS; EPILEPSY; VARIANT AB The clinical significance of an interstitial duplication of (15)(q11-q13) remains unclear and controversial. The reported phenotypes vary widely and appear to be influenced by the parent of origin of the duplication. Aside from cases of dup(15) reported with autism, the behavioral phenotype of individuals with dup(15) has not been described. We present three families, two with intrachromosomal duplication (15)(q11-q13) ascertained because of developmental delay in a relative. Two families show clear evidence of multigenerational maternal inheritance. The individuals discussed in this paper have minor anomalies and developmental delays. In addition, we describe a behavioral phenotype which often includes attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder. Responses to medications used to manage these behaviors are also described, including a positive response to methylphenidate and a poor response to fluoxetine. The duplication in each presenting individual, and available family members, was investigated utilizing cytogenetic and molecular techniques including high resolution cytogenetics, fluorescence in situ hybridization (FISH), DNA methylation studies, and quantitative fluorescence PCR. High resolution cytogenetic techniques alone missed some cases, demonstrating the need to confirm results with other methods. (C) 2003 Wiley-Liss, Inc. C1 Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. Univ Colorado, Hlth Sci Ctr, Dept Pathol, Denver, CO USA. Shodair Hosp, Helena, MT USA. Childrens Hosp, IMD Clin, Child Dev Unit, Denver, CO 80218 USA. RP Thomas, JA (reprint author), Childrens Hosp, IMD Clin, Child Dev Unit, Box B-153,1056 E 19th Ave, Denver, CO 80218 USA. 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J. Med. Genet. A PD JUN 1 PY 2003 VL 119A IS 2 BP 111 EP 120 DI 10.1002/ajmg.a.10176 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 679PF UT WOS:000182930600003 PM 12749048 ER PT J AU Frenkel, LD Nielsen, K AF Frenkel, LD Nielsen, K TI Immunization issues for the 21st century SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY LA English DT Article; Proceedings Paper CT 1st Brazilian International Conference of Allergy and Immunology CY DEC 05-09, 2002 CL RIO DE JANEIRO, BRAZIL ID VACCINE; INFANTS; INTUSSUSCEPTION; IMMUNOGENICITY; EFFICACY; SAFETY; RISK AB Objective: Review and discuss major issues of vaccination and immunization. The development and application of vaccination and immunization is one of the most remarkable successes of the 20th century. This is true both in the United States and worldwide. In the United States, a number of vaccine-preventable diseases have been all but eliminated through the development of a recommended childhood immunization schedule by governmental and nongovernmental organizations, education of providers about these recommendations, and enforcement of these recommendations by school and day care entry mandates. Despite these successes, vaccine-preventable diseases continue to occur, in part because of missed opportunities by health care providers, antivaccine forces empowered by misguided mass media, and parental ignorance. Important aspects of the 2002 recommended childhood immunization schedule are reviewed, including: birth dose hepatitis B, diphtheria underimmunization and tetanus overimmunization, increasing pertussis disease, the success of conjugate vaccines, the change in poliovirus vaccines, measles vaccine and autism, the safety of varicella vaccine, and adult vaccination recommendations. Finally, future prospects for vaccination and immunization are discussed, including: combination vaccines, vaccines against new diseases such as rotavirus, new routes of delivery of immunizing agents, the use of computerized vaccine registries to prevent missed opportunities, and vaccines against bioterrorism agents. Conclusions: A careful analysis of risk and benefit suggests that the benefit of vaccination far outweighs the risks from the utilization of immunizing agents. Vaccination delayed may be protection denied. The bottom line is that vaccines are good and disease is bad. C1 Univ Illinois, Coll Med, Dept Pediat, Rockford, IL 61107 USA. RP Frenkel, LD (reprint author), Univ Illinois, Coll Med, Dept Pediat, 1601 Parkview Ave, Rockford, IL 61107 USA. CR Advisory Committee on Immunization Practices, 2000, MMWR RECOMM REP, V49, P1 [Anonymous], 2001, MMWR MORB MORTAL WKL, V50, P637 Ascherio A, 2001, JAMA-J AM MED ASSOC, V286, P3083, DOI 10.1001/jama.286.24.3083 BELLANTI JA, 1993, VACCINE, V11, P587, DOI 10.1016/0264-410X(93)90238-S Belshe RB, 2000, J PEDIATR-US, V136, P168, DOI 10.1016/S0022-3476(00)70097-7 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DECKER MD, 1999, VACCINES, P508 DeStefano F, 2001, PEDIATRICS, V108, DOI 10.1542/peds.108.6.e112 Dollenmaier G, 2001, VIROLOGY, V281, P216, DOI 10.1006/viro.2000.0796 Feikin DR, 2000, JAMA-J AM MED ASSOC, V284, P3145, DOI 10.1001/jama.284.24.3145 Gellin BG, 2000, PEDIATRICS, V106, P1097, DOI 10.1542/peds.106.5.1097 Horn M I, 1999, J Pediatr Health Care, V13, P18, DOI 10.1016/S0891-5245(99)90096-2 Murphy TV, 2001, NEW ENGL J MED, V344, P564, DOI 10.1056/NEJM200102223440804 Nathanson N, 2002, SCIENCE, V296, P269, DOI 10.1126/science.1071207 Offit PA, 2002, PEDIATRICS, V109, P124, DOI 10.1542/peds.109.1.124 Pichichero ME, 2000, PEDIATR CLIN N AM, V47, P407, DOI 10.1016/S0031-3955(05)70214-5 Reef SE, 2002, JAMA-J AM MED ASSOC, V287, P464, DOI 10.1001/jama.287.4.464 Rennels MB, 1998, PEDIATR INFECT DIS J, V17, P924, DOI 10.1097/00006454-199810000-00018 RODEWALD LE, 2001, AAP NEWS, V18, P89 Santoli JM, 1998, PEDIATR ANN, V27, P366 Seward JF, 2002, JAMA-J AM MED ASSOC, V287, P606, DOI 10.1001/jama.287.5.606 Shinefield H, 2002, PEDIATR INFECT DIS J, V21, P182, DOI 10.1097/00006454-200203000-00003 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Yeh SH, 2001, PEDIATR INFECT DIS J, V20, pS5, DOI 10.1097/00006454-200111001-00001 2002, MMWR MORB MORTAL WKL, V51, P394 2001, MMWR MORB MORTAL WKL, V50, P1058 2002, MMWR MORB MORTAL WKL, V51, P31 NR 27 TC 12 Z9 12 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 USA SN 1081-1206 J9 ANN ALLERG ASTHMA IM JI Ann. Allergy Asthma Immunol. PD JUN PY 2003 VL 90 IS 6 SU 3 BP 45 EP 52 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA 693FP UT WOS:000183706700010 PM 12839113 ER PT J AU Filipek, PA Juranek, J Smith, M Mays, LZ Ramos, ER Bocian, M Masser-Frye, D Laulhere, TM Modahl, C Spence, MA Gargus, JJ AF Filipek, PA Juranek, J Smith, M Mays, LZ Ramos, ER Bocian, M Masser-Frye, D Laulhere, TM Modahl, C Spence, MA Gargus, JJ TI Mitochondrial dysfunction in autistic patients with 15q inverted duplication SO ANNALS OF NEUROLOGY LA English DT Article ID DISORDER; GENE; INDIVIDUALS; EXPRESSION; 15Q11-13; PROTEIN; REGION; MUSCLE AB Two autistic children with a chromosome 15q11-q13 inverted duplication are presented. Both had uneventful perinatal courses, normal electroencephalogram and magnetic resonance imaging scans, moderate motor delay, lethargy, severe hypotonia, and modest lactic acidosis. Both had muscle mitochondrial enzyme assays that showed a pronounced mitochondrial hyperproliferation and a partial respiratory chain block most parsimoniously placed at the level of complex III, suggesting candidate gene loci for autism within the critical region may affect pathways influencing mitochondrial function. 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, Sch Social Ecol, Dept Psychol & Social Behav, Irvine, CA 92717 USA. Univ Calif Irvine, Coll Med, Dept Physiol & Biophys, Irvine, CA 92717 USA. RP Filipek, PA (reprint author), Univ Calif Irvine, Med Ctr, Route 81-4482,101 City Dr S, Orange, CA 92868 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey DB, 2001, J AUTISM DEV DISORD, V31, P165 BAKER P, 1994, J AUTISM DEV DISORD, V24, P529, DOI 10.1007/BF02172133 Boles RG, 1997, LANCET, V350, P1299, DOI 10.1016/S0140-6736(05)62477-4 BUNDEY S, 1994, DEV MED CHILD NEUROL, V36, P736 Cook EH, 1997, AM J HUM GENET, V60, P928 Heddi A, 1999, J BIOL CHEM, V274, P22968, DOI 10.1074/jbc.274.33.22968 Herzing LBK, 2001, AM J HUM GENET, V68, P1501, DOI 10.1086/320616 HOOD DA, 1994, CAN J APPL PHYSIOL, V19, P12 Kirby DM, 1999, NEUROLOGY, V52, P1255 Long FL, 1998, J MED GENET, V35, P425, DOI 10.1136/jmg.35.5.425 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 Murdock DG, 1999, J BIOL CHEM, V274, P14429, DOI 10.1074/jbc.274.20.14429 Nicholls RD, 2001, ANNU REV GENOM HUM G, V2, P153, DOI 10.1146/annurev.genom.2.1.153 Repetto GR, 1998, AM J MED GENET, V79, P82, DOI 10.1002/(SICI)1096-8628(19980901)79:2<82::AID-AJMG2>3.0.CO;2-P Rougeulle C, 1997, NAT GENET, V17, P14, DOI 10.1038/ng0997-14 Schenck A, 2001, P NATL ACAD SCI USA, V98, P8844, DOI 10.1073/pnas.151231598 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 Wolpert CM, 2000, AM J MED GENET, V96, P365, DOI 10.1002/1096-8628(20000612)96:3<365::AID-AJMG25>3.0.CO;2-X NR 20 TC 62 Z9 64 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JUN PY 2003 VL 53 IS 6 BP 801 EP 804 DI 10.1002/ana.10596 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 682MF UT WOS:000183095200016 PM 12783428 ER PT J AU Steiner, CE Guerreiro, MM Marques-de-Faria, AP AF Steiner, CE Guerreiro, MM Marques-de-Faria, AP TI Genetic and neurological evaluation in a sample of individuals with pervasive developmental disorders SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE autism; Asperger syndrome; pervasive developmental disorders; fragile X syndrome; SPECT; magnetic resonance imaging ID FRAXE MENTAL-RETARDATION; INFANTILE-AUTISM; CHILDHOOD AUTISM; X-CHROMOSOME; CHILDREN; REPEAT; POPULATION; EPILEPSY; FEATURES; SITE AB With the aim of analyzing which complementary tests are relevant in the diagnostic evaluation of individuals with pervasive developmental disorders, a protocol of clinical and laboratory evaluation was applied in 103 outpatients. The protocol included chromosomal analysis, screening for inborn errors of metabolism, cytogenetic and molecular study of the FRAXA, FRAXE, and FRAXF mutations, EEG, SPECT, and magnetic resonance imaging study. Eighty-four subjects concluded the complementary tests and were classified either as having autism, atypical autism or Asperger syndrome according to the DSM-IV criteria. Sixteen individuals, all bellonging to the two autistic groups, presented genetic or enviromental factors that may have lead to the behavioral disorders, showing the importance of diagnostic evaluation in this group of conditions. Neuroimaging and EEG findings were non-specific and occurred in similar proportion among the groups, being considered of relative low significance in the diagnostic evaluation of individuals with pervasive developmental disorders. C1 Univ Estadual Campinas, Dept Med Genet, Fac Ciencias Med, BR-13081970 Campinas, SP, Brazil. Univ Estadual Campinas, Dept Neurol, BR-13081970 Campinas, SP, Brazil. 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Neuro-Psiquiatr. PD JUN PY 2003 VL 61 IS 2A BP 176 EP 180 DI 10.1590/S0004-282X2003000200003 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 688QR UT WOS:000183447700003 PM 12806492 ER PT J AU Bandim, JM Ventura, LO Miller, MT Almeida, HC Costa, AES AF Bandim, JM Ventura, LO Miller, MT Almeida, HC Costa, AES TI Autism and Mobius sequence - An exploratory study of children in northeastern Brazil SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE autism; Mobius sequence ID MEDICAL CONDITIONS; EARLY-PREGNANCY; MISOPROSTOL; ANOMALIES AB The psychiatric examination was performed with diagnostic instruments for autism (DSM-IV and Childhood Autism Rating Scale-CARS) in 23 children with Mobius sequence. From the 23 patients studied with Mobius sequence, five (26.1%) met the diagnostic criteria for infantile autism according DSM-IV and two (8.6%), under two years old, showed autistic-like behavior. The scores for six children were compatible to severe autism symptoms according CARS and one child met the criteria for moderate autism symptoms. Among five children with autism, three (60%) had positive history of misoprostol exposure during the first trimester of pregnancy and from two cases autistic-like, one (50%) had positive history of misoprostol exposure during pregnancy. According to our data, this is the first report of Mobius sequence with autism and positive history of misoprostol use during pregnancy. C1 Univ Fed Pernambuco, Dept Neuropsiquiat, Recife, PE, Brazil. Inst Materno Infantil Pernambuco, Recife, PE, Brazil. Fdn Altino Ventura, Dept Oftalmol Pediat, Recife, PE, Brazil. Hosp Olhos Pernambuco, Recife, PE, Brazil. Univ Illinois, Dept Oftalmol, Chicago, IL USA. Univ Fed Minas Gerais, Dept Oftalmol, Belo Horizonte, MG, Brazil. AACD, Psicol Clin, Recife, PE, Brazil. 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Neuro-Psiquiatr. PD JUN PY 2003 VL 61 IS 2A BP 181 EP 185 DI 10.1590/S0004-282X2003000200004 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 688QR UT WOS:000183447700004 PM 12806493 ER PT J AU Young, RL Brewer, N Pattison, C AF Young, RL Brewer, N Pattison, C TI Parental identification of early behavioural abnormalities in children with autistic disorder SO AUTISM LA English DT Article DE autism; behavioural abnormalities; diagnosis; parent identification ID PERVASIVE DEVELOPMENTAL DISORDERS; FOLLOW-UP; INFANTILE-AUTISM; JOINT ATTENTION; PRESCHOOL-CHILDREN; ASPERGER-SYNDROME; HOME VIDEOTAPES; ADI-R; AGE; SYMPTOMS AB The aim of the study was to identify early behavioural abnormalities in children later diagnosed with autistic disorder. Accurate identification of such deficits has implications for early diagnosis, intervention and prognosis. The parents of 153 children with autistic disorder completed a questionnaire asking them to describe early childhood behaviours of concern and to recall the age of onset. Core deficit-linked behaviours were then identified and the ontogeny of their development was noted. Behaviour categories were: (1) gross motor difficulties, (2) social awareness and play deficits, (3) language and communication difficulties, and (4) unusual preoccupations. The findings supported the notion that the nature and prevalence of these deficits depend on age. Consistent with past research, there was a significant interval between parents first noticing abnormalities and the making of a definitive diagnosis. The implications for this delay are discussed. C1 Flinders Univ S Australia, Sch Psychol, Adelaide, SA 5001, Australia. RP Young, RL (reprint author), Flinders Univ S Australia, Sch Psychol, GPO Box 2100, Adelaide, SA 5001, Australia. 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R., 1997, HDB AUTISM PERVASIVE, P5 Volkmar FR, 1998, AUTISM, V2, P45, DOI DOI 10.1177/1362361398021005 VOLKMAR FR, 1985, AM J PSYCHIAT, V142, P1450 Vostanis P., 1998, AUTISM, V2, P229, DOI 10.1177/1362361398023002 Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 NR 71 TC 53 Z9 56 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2003 VL 7 IS 2 BP 125 EP 143 DI 10.1177/1362361303007002002 PG 19 WC Psychology, Developmental SC Psychology GA 692KC UT WOS:000183659400002 PM 12846383 ER PT J AU Reaven, J Hepburn, S AF Reaven, J Hepburn, S TI Cognitive-behavioral treatment of obsessive-compulsive disorder in a child with Asperger syndrome - A case report SO AUTISM LA English DT Article DE Asperger syndrome; case study; cognitive-behavioral treatment; obsessive-compulsive disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; REPETITIVE THOUGHTS; AUTISM; ADOLESCENTS AB This case report outlines the cognitive-behavioral treatment of obsessive-compulsive disorder in a 7-year-old female with Asperger syndrome. Interventions were based upon the work of March and Mulle and were adapted in light of the patient's cognitive, social, and linguistic characteristics. Obsessive-compulsive symptoms improved markedly after approximately 6 months of treatment. Issues regarding symptom presentation, assessment, and treatment of a dually diagnosed patient are discussed. C1 Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA. RP Reaven, J (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Pediat, 4200 E 9th Ave,Box C-234, Denver, CO 80262 USA. 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The study site was a clinic specializing in ASD in a large pediatric medical center serving a 10 county area in the midwestern USA. In a sample of 13 7 children, age 24-96 months, classified as having autism or ASD by the Autism Diagnostic Observation Schedule-Generic, 24 percent had a history of at least one chronic gastrointestinal symptom. The most common symptom was diarrhea, which occurred in 17 percent. There was no association between chronic gastrointestinal symptoms and a history of developmental regression. The potential phenotypic association between autism and gastrointestinal symptoms is discussed. C1 Cincinnati Childrens Hosp, Med Ctr, Ctr Biostat & Epidemiol, Cincinnati, OH 45229 USA. RP Molloy, CA (reprint author), Cincinnati Childrens Hosp, Med Ctr, Ctr Biostat & Epidemiol, MLC 5041,3333 Burnet Ave, Cincinnati, OH 45229 USA. CR BERTANI I, 2001, RRD MICROBIOL 1, V5, P1 Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419 Cade R, 2000, NUTR NEUROSCI, V3, P57, DOI 10.1080/1028415042000198807 DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x DONOVAN E, 2000, REPORT WELL BEING CH Fiorica-Howells E, 2000, J NEUROSCI, V20, P294 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Knivsberg AM, 2001, NUTR NEUROSCI, V4, P25 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Melmed R. D., 2000, JPGN, V31, pS31 Sandler RH, 2000, J CHILD NEUROL, V15, P429, DOI 10.1177/088307380001500701 TAYLOR B, 2001, INT M AUT RES SAN DI Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 YEARGINALLSOPP M, 2001, INT M AUT RES SAN DI NR 15 TC 78 Z9 79 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2003 VL 7 IS 2 BP 165 EP 171 DI 10.1177/1362361303007002004 PG 7 WC Psychology, Developmental SC Psychology GA 692KC UT WOS:000183659400004 PM 12846385 ER PT J AU Binnie, L Williams, J AF Binnie, L Williams, J TI Intuitive psychology and physics among children with autism and typically developing children SO AUTISM LA English DT Article DE autism; domain specificity; intuitive physics; intuitive psychology ID ASPERGER-SYNDROME; COGNITIVE-DEVELOPMENT; FALSE BELIEFS; CORE DOMAINS; MIND; PRESCHOOLERS; REPRESENTATION; KNOWLEDGE; ORIGINS; REALITY AB Many studies have documented poor understanding of intuitive psychology among children with autism; however, few have investigated claims of superior understanding of intuitive physics said to be evident in this group. This study aimed to investigate the reported differential preference of intuitive psychology and intuitive physics among children with autism by employing three tasks each with a psychological and a physical condition. In order to gain a detailed developmental picture the study compared children with autism, an age matched comparison group, and typically developing preschoolers, 7-year-olds and 10-year-olds. Results demonstrated that children with autism preferred to employ physical causality when reasoning about novel physical and psychological events. Furthermore, their performance on a multiple-choice task confirmed their impairment in intuitive psychology whilst highlighting a superior ability to reason about physical phenomena in relation to all other comparison groups. The theoretical implications of this potential cognitive strength are discussed. C1 Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland. RP Williams, J (reprint author), Fac Educ, St Johns Land,Holyrood Rd, Edinburgh EH8 8AQ, Midlothian, Scotland. 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Different variables were investigated such as breadth of vocabulary and number of vocabulary errors, type of paraphasias, and mechanisms used to name the meanings that children were not aware of or could not recall, and the particular meanings that were difficult for each group. Preliminary findings showed that vocabulary errors were similar in both groups, except under-extension, which was not used by the autism group. Children with autism tended to use all mechanisms in order to name something they did not know and to focus on parts of the object in order to name it, while unknown words were similar in both groups. C1 Hosp Psychiat, Thessaloniki, Greece. Univ Leicester, Leicester, Leics, England. RP Vogindroukas, I (reprint author), Med Psychopedag Ctr No Greece, 52 Giannitson Str, Thessaloniki, Greece. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Ball M. 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We expected both groups to show arousal as increased heart rate when watching the video of the crying baby, and the children with autism to attend less than the other children to both videos. However, the children with autism were as attentive to the videos as the other children, and both groups showed heart rate slowing compared with a baseline condition. There was no change in heart rate during interactions with a stranger or separation from mothers. The findings suggest that the lack of social attention often demonstrated by children with autism does not stem from increased arousal in social situations. An alternative explanation is considered. C1 Univ Calif Los Angeles, Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA. La Trobe Univ, Melbourne, Vic, Australia. RP Sigman, M (reprint author), Univ Calif Los Angeles, Sch Med, Dept Psychiat, Room 68-237, Los Angeles, CA 90095 USA. 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RP Loddo, S (reprint author), Neuropsichiatria Eta Evolut, Oristano, Italy. CR Malvy J., 1999, AUTISM, V3, P357, DOI 10.1177/1362361399003004004 Salt J, 2002, AUTISM, V6, P33, DOI 10.1177/1362361302006001004 Williams D, 1996, AUTISM INSIDE OUT AP NR 3 TC 1 Z9 1 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2003 VL 7 IS 2 BP 226 EP 227 DI 10.1177/1362361303007002009 PG 2 WC Psychology, Developmental SC Psychology GA 692KC UT WOS:000183659400009 PM 12846390 ER PT J AU Martin, I McDonald, S AF Martin, I McDonald, S TI Weak coherence, no theory of mind, or executive dysfunction? Solving the puzzle of pragmatic language disorders SO BRAIN AND LANGUAGE LA English DT Review DE pragmatic language; autism; right-hemisphere dam ge; traumatic brain injury; theory of mind; executive dysfunction; central coherence ID BRAIN-DAMAGED PATIENTS; CLOSED-HEAD-INJURY; HIGH-FUNCTIONING AUTISM; RIGHT-HEMISPHERE DAMAGE; ASPERGER-SYNDROME; FRONTAL-LOBE; CHILDRENS KNOWLEDGE; WILLIAMS-SYNDROME; LINGUISTIC HUMOR; NORMAL ADULTS AB Deficits in pragmatic language ability are common to a number of clinical populations, for example, right-hemisphere damage (RHD), Autism and traumatic brain injury (TBI). In these individuals the basic structural components of language may be intact, but the ability to use language to engage socially is impaired. Despite the nature of these difficulties being well documented, exactly what causes these difficulties is less clear. Furthermore, the current status of causal explanations for pragmatic difficulties across these populations is divergent and sometimes contradictory. This paper explores the empirical validity of three theories that attempt to explain pragmatic language impairment. It is recommended that a new, more convergent approach to investigating the causes of pragmatic language disability be adopted. (C) 2003 Elsevier Science (USA). All rights reserved. C1 Univ New S Wales, Sch Psychol, Sydney, NSW 2052, Australia. RP McDonald, S (reprint author), Univ New S Wales, Sch Psychol, Sydney, NSW 2052, Australia. 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PD JUN PY 2003 VL 85 IS 3 BP 451 EP 466 DI 10.1016/S0093-934X(03)00070-1 PG 16 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA 683RR UT WOS:000183163800012 PM 12744957 ER PT J AU Mouridsen, SE AF Mouridsen, SE TI Childhood disintegrative disorder SO BRAIN & DEVELOPMENT LA English DT Review DE differential diagnosis; epidemiology; treatment; outcome ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; DSM-IV; FIELD TRIAL; PSYCHOSIS; REGRESSION; PREVALENCE; CHILDREN AB In 1908 a Viennese remedial educator Theodor Heller described six children under the name of dementia infantilis who had insidiously developed a severe mental regression between the 3rd and 4th years of life after normal mental development. Neuropathological and other medical conditions are sometimes associated with this disorder, but contrary to earlier belief this is not typical. Interest in childhood disintegrative disorder has increased markedly in recent years and in this review attention is given to more recently published cases based on ICD-9, ICD-10 and DSM-IV diagnostic systems. Information is provided related to nosology, epidemiological data, differential diagnosis, aetiology, treatment and outcome. (C) 2003 Elsevier Science B.V. All rights reserved. C1 Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. RP Mouridsen, SE (reprint author), Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. 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PD JUN PY 2003 VL 25 IS 4 BP 225 EP 228 DI 10.1016/S0387-7604(02)00228-0 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 687UF UT WOS:000183394800001 PM 12767450 ER PT J AU Eriksson, K Kylliainen, A Hirvonen, K Nieminen, P Koivikko, M AF Eriksson, K Kylliainen, A Hirvonen, K Nieminen, P Koivikko, M TI Visual agnosia in a child with non-lesional occipito-temporal CSWS SO BRAIN & DEVELOPMENT LA English DT Article DE visual agnosia; continuous spike-wave discharges in slow sleep; neuropsychology; child ID ELECTRICAL STATUS EPILEPTICUS; LANDAU-KLEFFNER-SYNDROME; SLOW-WAVE SLEEP AB In this paper we describe a case of severe visual agnosia in a child with an electrophysiological pattern of continuous spike-wave discharges in slow sleep (CSWS) in the occipito-temporal regions. The neuropsychological spectrum related to this phenomenon is discussed. Published paediatric reports associate visual agnosia (i.e. an inability to recognize objects without impairment of visual acuity) mainly with symptomatic occipito-temporal aetiology (e.g. cortical dysplasia, vascular insults) and other neurological symptoms (e.g. autism). We describe a detailed 2 year electrophysiological and neuropsychological follow-up of an 8-year-old boy with sporadic seizures, occipito-temporal CSWS and visual agnosia. The growth and neurological development of the child had been considered as normal, neurological examination did not reveal any focal signs, visual acuity was intact and MRI was normal. First EEG and six consecutive 24 It video EEG recordings during the follow-up of 22 months showed continuous spike-and-wave activity covering over 85% of the non-REM sleep. According to structured neuropsychological tests (Wechsler Intelligence Scale for Children - Third Edition, A Developmental Neuropsychological Assessment (NEPSY), Test of Visual-Perceptual Skills, Corsi block, Hooper Visual Organization Test) the boy had normal verbal intelligence but major deficits in visual perception, especially in object recognition, impaired shape discrimination and detection, and poor copying skills. Attention and executive functions were intact. There were no difficulties in short- or long-term memory. Verbal cues and naming the objects improved visual memory. Tracing the objects with a finger or by moving the head improved object recognition. Currently the boy attends a special school with a rehabilitation plan including neuropsychological and occupational therapies. This case adds a new facet to the spectrum of neuropsychological deficits in children with CSWS. Sleep EEG should be included in the etiological studies of children with specific neuropsychological problems and detailed neuropsychological assessment is needed for diagnostic and rehabilitation purposes. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Tampere Univ Hosp, Pediat Neurol Unit, FIN-33521 Tampere, Finland. Tampere Univ, Sch Med, FIN-33101 Tampere, Finland. Tampere Univ, Dept Psychol, Human Informat Proc Lab, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Dept Clin Neurophysiol, Helsinki, Finland. Haaga Neurol Res Ctr, Helsinki, Finland. RP Eriksson, K (reprint author), Tampere Univ Hosp, Pediat Neurol Unit, POB 2000, FIN-33521 Tampere, Finland. 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PD JUN PY 2003 VL 25 IS 4 BP 262 EP 267 DI 10.1016/S0387-7604(02)00225-5 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 687UF UT WOS:000183394800008 PM 12767457 ER PT J AU Dobbinson, S Perkins, M Boucher, J AF Dobbinson, S Perkins, M Boucher, J TI The interactional significance of formulas in autistic language SO CLINICAL LINGUISTICS & PHONETICS LA English DT Article; Proceedings Paper CT 9th Meeting of the International-Clinical-Phonetics-and-Linguistic-Association CY MAY 04, 2002 CL HONG KONG, PEOPLES R CHINA SP Int Clin Phonet & Linguist Assoc DE autism; Conversation Analysis; formulaicity; discourse functions; echolalia; processing mechanisms ID IMMEDIATE ECHOLALIA; CHILDREN; DISORDERS AB The phenomenon of echolalia in autistic language is well documented. Whilst much early research dismissed echolalia as merely an indicator of cognitive limitation, later work identified particular discourse functions of echolalic utterances. The work reported here extends the study of the interactional significance of echolalia to formulaic utterances. Audio and video recordings of conversations between the first author and two research participants were transcribed and analysed according to a Conversation Analysis framework and a multi-layered linguistic framework. Formulaic language was found to have predictable interactional significance within the language of an individual with autism, and the generic phenomenon of formulaicity in company with predictable discourse function was seen to hold across the research participants, regardless of cognitive ability. The implications of formulaicity in autistic language for acquisition and processing mechanisms are discussed. C1 York St John Coll, York YO31 7X, N Yorkshire, England. Univ Sheffield, Sheffield S10 2TN, S Yorkshire, England. Univ Warwick, Coventry CV4 7AL, W Midlands, England. 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Linguist. Phon. PD JUN-AUG PY 2003 VL 17 IS 4-5 BP 299 EP 307 DI 10.1080/0269920031000080046 PG 9 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 709RU UT WOS:000184638800007 PM 12945605 ER PT J AU Martin, BL Nelson, MR Hershey, JN Engler, RJM AF Martin, BL Nelson, MR Hershey, JN Engler, RJM TI Adverse reactions to vaccines SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY LA English DT Review DE adverse reactions; adjuvants; gelatin; allergy; risk communication; temporal association ID IMMEDIATE-TYPE REACTIONS; PERTUSSIS VACCINATION; GELATIN; ANAPHYLAXIS; CHILDREN; MEASLES; IGE; DIPHTHERIA; ALLERGY; TETANUS AB (The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.) Immunization healthcare is becoming increasingly complex as the number and types of vaccines have continued to expand. Like all prescription drugs, vaccines may be associated with adverse events. The majority of these reactions are self-limited and not associated with prolonged disability. The media, Internet and public advocacy groups have focused on potentially serious vaccine-associated adverse events with questions raised about causal linkages to increasing frequencies of diseases such as autism and asthma. Despite a lack of evidence of a causal relationship to a variety of vaccine safety concerns, including extensive reviews by the Institute of Medicine, questions regarding vaccine safety continue to threaten the success of immunization programs. Risk communication and individual risk assessment is further challenged by the public health success of vaccine programs creating the perception that certain vaccines are no longer necessary or justified because of the rare reaction risk. There is a need for improved understanding of true vaccine contraindications and precautions as well as host factors and disease threat in order to develop a patient specific balanced risk communication intervention. When they occur, vaccine related adverse events must be treated, documented and reported through the VAERS system. The increasing complexity of vaccination health care has led the Center of Disease Control and Prevention (CDC) to identify Vaccine Safety Assessment and Evaluation as a potential new specialty. C1 Walter Reed Army Med Ctr, Allergy Immunol Dept, Washington, DC 20307 USA. RP Martin, BL (reprint author), Walter Reed Army Med Ctr, Allergy Immunol Dept, Washington, DC 20307 USA. 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PD JUN PY 2003 VL 48 IS 3 BP 395 EP 395 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 687PG UT WOS:000183385200048 ER PT J AU Kuddo, T Nelson, KB AF Kuddo, T Nelson, KB TI How common are gastrointestinal disorders in children with autism? SO CURRENT OPINION IN PEDIATRICS LA English DT Review ID RUBELLA VACCINATION; CONSTIPATION; DISEASE; MEASLES; MUMPS AB We could identify no report that describes the prevalence of gastrointestinal disorders in a representative group of children with a diagnosis of autism compared with appropriate controls. Thus, we found no evidence upon which to base a confident conclusion as to whether gastrointestinal symptoms are more common in children with than without autism. However, the frequency of gastrointestinal symptoms observed in population-based samples of autistic children indicate that gastrointestinal problems are not nearly as common in children with autism as reports from pediatric gastroenterology clinics suggest. 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PD SUM PY 2003 VL 15 IS 3 BP 501 EP 527 DI 10.1017/S0954579403000270 PG 27 WC Psychology, Developmental SC Psychology GA 721GU UT WOS:000185309300002 PM 14582930 ER PT J AU Webb, E Morey, J Thompsen, W Butler, C Barber, M Fraser, WI AF Webb, E Morey, J Thompsen, W Butler, C Barber, M Fraser, WI TI Prevalence of autistic spectrum disorder in children attending mainstream schools in a Welsh education authority SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; TOTAL POPULATION; EPIDEMIOLOGY; DIAGNOSIS AB All mainstream primary schools in Cardiff were invited in July 1998 to participate in a prevalence survey of autistic spectrum disorder. Teachers of each class filled in a questionnaire based on ICD-10 criteria for autistic disorders. The Autism Spectrum Screening Questionnaire (ASSQ) was completed on children identified with problems identified by the questionnaire. A total of 11692 children born between 1 September 1986 and 31 August 1990 were screened: 234 (2%) children were identified as requiring an ASSQ; 151 of 234 (65%) ASSQs were returned. Of the 151, 60 children (52 male, 8 female; 40%) scored 22 or more. Their notes and the involved professionals were consulted. Thirty-five children, unknown to specialist services or with complex features, required additional assessment. Seventeen children (all male) were found to be on the autistic spectrum. When the overall rubric was disentangled we found a diverse population of affected children including a handful who did not fit easily into ICD-10 classification. Correcting for incomplete ascertainment we found a minimum prevalence of 20.2 out of every 10 000 (SE=4.5) for autistic spectrum disorder in this population. C1 UHW, Childrens Ctr, Dept Child Hlth, Cardiff CF14 4XN, S Glam, Wales. Univ Wales Coll Cardiff, Coll Med, Dept Psychol Med, Cardiff, S Glam, Wales. St Davids Hosp, Carmarthen, Dyfed, Wales. Cardiff Cty Council, Sch Serv, Cardiff, S Glam, Wales. RP Webb, E (reprint author), UHW, Childrens Ctr, Dept Child Hlth, Cardiff CF14 4XN, S Glam, Wales. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT DEWEY M, 1991, AUSTISM ASPERGER SYN 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 ELLIS HD, 1994, EUR CHILD ADOLES PSY, V3, P255 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Gillberg C, 2000, ACTA PSYCHIAT SCAND, V102, P321, DOI 10.1034/j.1600-0447.2000.102005321.x Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Kugler B., 1998, AUTISM, V2, P11, DOI 10.1177/1362361398021003 Meltzer H, 1999, MENTAL HLTH CHILDREN Schopler E, 1996, J AUTISM DEV DISORD, V26, P109, DOI 10.1007/BF02276238 Spencer N., 2000, POVERTY CHILD HLTH SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 Waterhouse L, 1996, J AUTISM DEV DISORD, V26, P59, DOI 10.1007/BF02276235 Webb EVJ, 1997, DEV MED CHILD NEUROL, V39, P150 *WELSH OFF, 1997, HLTH CHILDR WAL WHO, 1993, ICD 10 CLASS MENT BE WING L, 1976, HDB AUTISM PERVASIVE, P199 NR 20 TC 22 Z9 22 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4221 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JUN PY 2003 VL 45 IS 6 BP 377 EP 384 DI 10.1017/S001216220300720 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 686JR UT WOS:000183318900004 PM 12785438 ER PT J AU Rosenhall, U Nordin, V Brantberg, K Gillberg, C AF Rosenhall, U Nordin, V Brantberg, K Gillberg, C TI Autism and auditory brain stem responses SO EAR AND HEARING LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; EVOKED-POTENTIALS; CENTRAL TINNITUS; CONDUCTION TIME; HEARING-LOSS; CHILDREN; LATENCIES; DIFFERENTIATION; TRANSMISSION; INDIVIDUALS AB Objective: To study a controversy that has been discussed for more than two decades: whether or not children with autism have abnormalities affecting the cochlear nerve or the auditory pathway in the brain stem and, if so, to describe these abnormalities. Design: A group of 153 children and adolescents with autistic disorder were included in an investigation of auditory brain stem responses (ABR). Two thirds of this group, 101 individuals (75 boys, 26 girls), had normal hearing and they were selected for an in-depth ABR study. The results from the study group were compared with those of an age-matched comparison group. Results: The III-V interpeak latency (IPL) was significantly prolonged in both boys and girls with autism, compared with the controls. The latencies of ABR waves I and V were also significantly lengthened in the study groups. The individual test results showed that more than half of this normal-hearing autistic disorder group (58%) had abnormalities of one or more of eight ABR parameters studied. The most common abnormalities were prolongation of wave V (38%), and of I-V IPL (28%). A lengthening of the IN IPL was also recorded in 27% of 49 children who were difficult to test or who had hearing loss. Abnormal left-right differences of ABR latencies were found in 18% of autism cases with normal hearing. Conclusions: Possible causes of the reported ABR abnormalities, observed here as well as in other studies, are discussed. Brain stem lesion, occult cochlear dysfunction, and involvement of the cochlear efferent system are probable factors that can explain the ABR findings. C1 Univ Lund Hosp, Dept Paediat, S-22185 Lund, Sweden. Univ Gothenburg, Sahlgrens Univ Hosp, Gothenburg, Sweden. RP Rosenhall, U (reprint author), Karolinska Hosp, Dept Audiol, Inst Clin Neurosci, SE-17176 Stockholm, Sweden. 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PD JUN PY 2003 VL 24 IS 3 BP 206 EP 214 DI 10.1097/01.AUD.0000069326.11466.7E PG 9 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA 747CE UT WOS:000186787000004 PM 12799542 ER PT J AU Park, YD AF Park, YD TI The effects of vagus nerve stimulation therapy on patients with intractable seizures and either Landau-Kleffner syndrome or autism SO EPILEPSY & BEHAVIOR LA English DT Article DE epilepsy; intractable seizures; language disorders; behavioral disorders; autism; Landau-Kleffner syndrome; vagus nerve stimulation therapy; pharmacoresistant epilepsy ID REFRACTORY EPILEPSY; LONG-TERM; SPECTRUM DISORDERS; CHILDREN; EEG AB Acquired and developmental comorbid conditions, including language and behavioral disorders, are often associated with epilepsy. Although the relationship between these disorders is not fully understood, their close association may indicate that they share common features, suggesting that these conditions may respond to the same therapies. Not only has vagus nerve stimulation (VNS) therapy been proven to reduce the frequency of pharmacoresistant seizures in epilepsy patients, but preliminary studies also indicate that VNS therapy may improve neurocognitive performance. On the basis of these findings, we hypothesized that VNS therapy would improve the quality of life of patients with either Landau-Kleffner syndrome (LKS) or autism, independent of its effects on seizures. Data were retrospectively queried from the VNS therapy patient outcome registry (Cyberonics, Inc; Houston, TX, USA). A constant cohort of 6 LKS patients and 59 autistic patients were identified. Among the LKS patients, 3 patients at 6 months experienced at least a 50% reduction in seizure frequency as compared with baseline. Physicians reported quality-of-life improvements in all areas assessed for at least 3 of the 6 children. More than half of the patients with autism (58%) experienced at least a 50% reduction in seizure frequency at 12 months. Improvements in all areas of quality of life monitored were reported for most patients, particularly for alertness (76% at 12 months). Although these preliminary findings are encouraging, a prospective study using standardized measurement tools specific to these disorders and a longer-term follow-up are necessary to better gauge the efficacy of VNS therapy among these patient populations. (C) 2003 Elsevier Science (USA). All rights reserved. C1 Med Coll Georgia, Dept Neurol Child, Augusta, GA 30912 USA. RP Park, YD (reprint author), Med Coll Georgia, Dept Neurol Child, 1120 15th St,Room BG 2000H, Augusta, GA 30912 USA. 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PD JUN PY 2003 VL 4 IS 3 BP 286 EP 290 DI 10.1016/S1525-5050(03)00080-5 PG 5 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 689PT UT WOS:000183502700011 PM 12791330 ER PT J AU Eisermann, MM DeLaRaillere, A Dellatolas, G Tozzi, E Nabbout, R Dulac, O Chiron, C AF Eisermann, MM DeLaRaillere, A Dellatolas, G Tozzi, E Nabbout, R Dulac, O Chiron, C TI Infantile spasms in Down syndrome - effects of delayed anticonvulsive treatment SO EPILEPSY RESEARCH LA English DT Article DE infantile spasms; Down syndrome; treatment lag; treatment efficacy; long-term outcome; autism; antiepileptogenesis ID LONG-TERM PROGNOSIS; FIRST-LINE TREATMENT; WEST-SYNDROME; TUBEROUS SCLEROSIS; NATURAL-HISTORY; VIGABATRIN; ACTH; EPILEPSY; CHILDREN; THERAPY AB To investigate the impact of treatment lag in infantile spasms (IS) on treatment response, occurrence of later epilepsy, and long-term cognition and behavior in patients with one single etiological entity, we examined 18 patients with Down syndrome (DS) and earlier IS retrospectively (follow-up period of 32-180 months with a mean of 85.1 months), and determined their history and present condition, in terms of previously mentioned items. There was a statistically significant correlation between treatment lag and lag to cessation of spasms (R = 0.55, P = 0.02), developmental quotient (DQ) (R = -0.75, P = 0.003), and score of autistic features (AF) (R = 0.57, P = 0.04). Moreover we found that the later the response to treatment of IS, the lower was the DQ (R = -0.86, P = 0.001) and the higher was the score of autistic features (R = 0.5, P = 0.06). A long duration of spasms also determined a low DQ (R = -0.93, P < 0.0001) and a high score of autistic features (R = 0.66, P < 0.01). All patients with persistent epilepsy (n = 5) had had a treatment lag of over 2 months. Conversely, for all children treated within 2 months (n = 8) spasms ceased within 3 months of treatment and none of them had later epilepsy. This group of patients with a treatment lag of less than 2 months had earlier treatment response (P = 0.002), higher DQ (P = 0.004) and lower score of autistic features (P = 0.006). The data stress the importance of a short treatment lag in view of mental development and prevention of later epilepsy and autistic features, and raise the question of antiepileptogenic effect in this specific condition. (C) 2003 Elsevier B.V. All rights reserved. C1 Hop St Vincent de Paul, Dept Neuropediat, F-75674 Paris 14, France. Ctr Med Jerome Lejeune, Paris, France. INSERM, U472, Villejuif, France. Pediat Clin, Laquila, Italy. RP Eisermann, MM (reprint author), Hop St Vincent de Paul, Dept Neuropediat, 82 Ave Denfert Rochereau, F-75674 Paris 14, France. 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PD JUN-JUL PY 2003 VL 55 IS 1-2 BP 21 EP 27 DI 10.1016/S0920-1211(30)00088-3 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 721PX UT WOS:000185325700003 PM 12948613 ER PT J AU Baghdadli, A Picot, MC Pascal, C Pry, R Aussilloux, C AF Baghdadli, A Picot, MC Pascal, C Pry, R Aussilloux, C TI Relationship between age of recognition of first disturbances and severity in young children with autism SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; early detection; medical condition; severity ID ADAPTIVE-BEHAVIOR SCALE; INFANCY; ONSET AB Autism is now thought to be present right from birth. Although usually not officially diagnosed until after the child's second birthday, parents often report disturbances before then. The age of detection of disturbances varies and may be linked to differences in the severity of the autism and its associated retardation. This study evaluates the developmental characteristics of 193 children with pervasive developmental disorder, using the same standard procedures for all subjects. Our goal was to determine the relationship between age of parental recognition of disturbances and disorder severity. The results indicated mainly a link between early abnormalities, associated medical condition and severity measured on cognitive tests. They suggest systematic screening for signs of autism in very young children. C1 CHU Montpellier, Clin Peyre Plantade, Child & Adolescent Psychiat Unit, F-34295 Montpellier 5, France. CHU Montpellier, Dept Med Informat, F-34295 Montpellier, France. RP Baghdadli, A (reprint author), CHU Montpellier, Clin Peyre Plantade, Child & Adolescent Psychiat Unit, 291 Ave Doyen Giraud, F-34295 Montpellier 5, France. 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PD JUN PY 2003 VL 12 IS 3 BP 122 EP 127 DI 10.1007/s00787-003-0314-6 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 691AL UT WOS:000183582600002 PM 12768459 ER PT J AU White, JF AF White, JF TI Intestinal pathophysiology in autism SO EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Review DE autism; intestine; casein; celiac disease; endoscopy; gluten; glycosaminoglycan; immunoglobulin; secretin; vaccine ID PERVASIVE DEVELOPMENTAL DISORDER; ADULT CELIAC-DISEASE; LYMPHOID-NODULAR HYPERPLASIA; INFLAMMATORY-BOWEL-DISEASE; INFANTILE-AUTISM; MEASLES-VIRUS; CROHNS-DISEASE; EPITHELIAL MONOLAYERS; PSYCHIC DISTURBANCES; NONSPECIFIC COLITIS AB Autism is a life-long developmental disorder affecting as many as 1 in 500 children. The causes for this profound disorder are largely unknown. Recent research has uncovered pathology in the gastrointestinal tract of autistic children. 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Biol. Med. PD JUN PY 2003 VL 228 IS 6 BP 639 EP 649 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 833ES UT WOS:000222319800001 PM 12773694 ER PT J AU Geier, MR Geier, DA AF Geier, MR Geier, DA TI Neurodevelopmental disorders after thimerosal-containing vaccines: A brief communication SO EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article DE autism; neurodevelopmental disorders; thimerosal; VAERS ID REPORTING SYSTEM VAERS; ADVERSE REACTIONS; VACCINATION; CHILDREN; AUTISM; SAFETY AB We were initially highly skeptical that differences in the concentrations of thimerosal in vaccines would have any effect on the incidence rate of neurodevelopmental disorders after childhood immunization. This study presents the first epidemiologic evidence, based upon tens of millions of doses of vaccine administered in the United States, that associates increasing thimerosal from vaccines with neurodevelopmental disorders. Specifically, an analysis of the Vaccine Adverse Events Reporting System (VAERS) database showed statistical increases in the incidence rate of autism (relative risk [RR] 6.0), mental retardation (RR = 6.1), and speech disorders (RR 2.2) after thimerosal-containing diphtheria, tetanus, and acellular pertussis (DTaP) vaccines in comparison with thimerosal-free DTaP vaccines. The male/female ratio indicated that autism (17) and speech disorders (2.3) were reported more in males than females after thimerosal-containing DTaP vaccines, whereas mental retardation (1.2) was more evenly reported among male and female vaccine recipients. Controls were employed to determine if biases were present in the data, but none were found. It was determined that overall adverse reactions were reported in similar-aged populations after thimerosal-containing DTaP (2.4 +/- 3.2 years old) and thimerosal-free DTaP (2.1 +/- 2.8 years old) vaccinations. Acute control adverse reactions such as deaths (RR = 1.0), vasculitis (RR = 1.2), seizures (RR = 1.6), ED visits (RR = 1.4), total adverse reactions (RR = 1.4), and gastroenteritis (RR = 1.1) were reported similarly after thimerosal-containing and thimorosal-free DTaP vaccines. An association between neurodevelopmental disorders and thimerosal-containing DTaP vaccines was found, but additional studies should be conducted to confirm and extend this study. C1 Genet Ctr Amer, Silver Spring, MD 20905 USA. RP Geier, MR (reprint author), Genet Ctr Amer, 14 Redgate Court, Silver Spring, MD 20905 USA. EM mgeier@erols.com CR Ball LK, 2001, PEDIATRICS, V107, P1147, DOI 10.1542/peds.107.5.1147 Bernard S, 2001, MED HYPOTHESES, V56, P462, DOI 10.1054/mehy.2000.1281 Geier DA, 2002, CLIN EXP RHEUMATOL, V20, P217 Geier DA, 2002, ANN PHARMACOTHER, V36, P776 Geier DA, 2002, TOXICOL MECH METHOD, V12, P71, DOI 10.1080/15376510209167937 Geier DA, 2001, CLIN EXP RHEUMATOL, V19, P724 Geier MR, 2002, ANN PHARMACOTHER, V36, P370, DOI 10.1345/aph.1A304 Krause I, 2002, J AUTISM DEV DISORD, V32, P337, DOI 10.1023/A:1016391121003 MAGOS L, 1985, ARCH TOXICOL, V57, P260, DOI 10.1007/BF00324789 Niu MT, 1998, J CLIN EPIDEMIOL, V51, P503, DOI 10.1016/S0895-4356(98)00014-6 Tan M, 2000, INT J PHARM, V208, P23, DOI 10.1016/S0378-5173(00)00514-7 Uhlmann V, 2002, J CLIN PATHOL-MOL PA, V55, P84 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 NR 13 TC 49 Z9 54 PU SOC EXPERIMENTAL BIOLOGY MEDICINE PI MAYWOOD PA 195 WEST SPRING VALLEY AVE, MAYWOOD, NJ 07607-1727 USA SN 1535-3702 J9 EXP BIOL MED JI Exp. Biol. Med. PD JUN PY 2003 VL 228 IS 6 BP 660 EP 664 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 833ES UT WOS:000222319800003 PM 12773696 ER PT J AU Neumarker, KJ AF Neumarker, KJ TI Leo Kanner: his years in Berlin, 1906-24. The roots of autistic disorder SO HISTORY OF PSYCHIATRY LA English DT Biographical-Item DE autism; child psychiatry; childhood psychosis; Germany; history; Kanner; psychiatry; 20th century ID ASPERGER-SYNDROME; RETT-SYNDROME AB By providing the first description of infantile autism Leo Kanner (1894-1981) has substantially influenced the field of child and adolescent psychiatry. The classification of the disorder seems to be evolving with progress in clinical and diagnostic research, epidemiologv and genetics. In the current classification systems of ICD-10 and DSM-IV, Kanner's name is merely mentioned, in contrast to other specified pervasive developmental disorders. This article draws attention to Kanner's early scientific career at Berlin's Charite University Hospital which ended in 1924 with Kanner's emigration to the United States. The study is based on original documents such as the files of Kanner's doctoral thesis on electrocardiography and cardiophonography found at the archives of Humboldt University of Berlin, and his unpublished autobiography, located at the library of the American Psychiatric Association in Washington, DC. C1 Humboldt Univ, Fak Med, Klinikum Charite, Klin & Poliklin Psychiat & Psychotherapie Kindes, D-10098 Berlin, Germany. RP Neumarker, KJ (reprint author), DRK Kliniken Westend, Kinder & Jugendpsychiat Klin, Spandauer Damm 130, D-14050 Berlin, Germany. EM k.-j.neumaerker@drk-kliniken-westend.de CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th [Anonymous], 1992, INT STAT CLASS DIS R APA, 1968, DIAGN STAT MAN MENT Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 ASPERGER H, 1968, ACTA PAEDOPSYCHIATR, V35, P136 BENDER L, 1982, J AM ACAD CHILD PSY, V21, P88, DOI 10.1097/00004583-198201000-00016 Berney TP, 2000, BRIT J PSYCHIAT, V176, P20, DOI 10.1192/bjp.176.1.20 Bonus B, 1997, FORTSCHR NEUROL PSYC, V65, P41, DOI 10.1055/s-2007-996308 BUSZKO J, 1984, INNEREN VERHALTNISSE, P282 Eisenberg L, 2001, J AM ACAD CHILD PSY, V40, P743, DOI 10.1097/00004583-200107000-00008 EISENBERG L, 1981, AM J PSYCHIAT, V138, P1122 EISENBERG L, 1994, AM J PSYCHIAT, V151, P751 EISENBERG L, 1981, J CHILD PSYCHOL PSYC, V22, P317 GILLBERG C, 1997, EUROPEAN CHILD AD S1, V6 Gillberg C, 2000, ACTA PSYCHIAT SCAND, V102, P321, DOI 10.1034/j.1600-0447.2000.102005321.x GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x GROSCHEL C, 2001, BRODY GESCHICHTE BED, P1 Holdorff Bernd, 2002, J Hist Neurosci, V11, P19, DOI 10.1076/jhin.11.1.19.9106 *INT MOL GEN STUD, 1998, HUM MOL GENET, V7, P571 KANNER L, PUBLICATION LIST Kerr AM, 2001, CURR OPIN PSYCHIATR, V14, P437, DOI 10.1097/00001504-200109000-00003 KURZ G, 1991, CHARITE ANN, V11, P239 LUTZ J, 1981, ACTA PAEDOPSYCHIATR, V47, P179 MAGNUS N, 1984, KATALOG NO LANDESMUS, P85 MIETKE H, 1960, Z ARZTL FORTBILD, V54, P465 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 NEUMARKER KJ, 2001, MMW-FORTSCH MEDIZIN, V143, P70 Rett A, 1966, Wien Med Wochenschr, V116, P723 ROHRSCHNEIDER W, 1965, Munch Med Wochenschr, V107, P1174 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P169, DOI 10.1017/S0021963098003461 SANUA VD, 1990, CHILD PSYCHIAT HUM D, V21, P3, DOI 10.1007/BF00709924 SCHOPLER E, 1981, J AUTISM DEV DISORD, V11, P257, DOI 10.1007/BF01531509 SCHWARTZ P, 1936, NOTGEMEINSCHAFT BERI SCHWARTZ P, 1975, FORTSCHRITTE MED, V93, P1139 SCHWARTZ P, 1961, BIRTH INJURIES NEWBO Shahbazian MD, 2001, CURR OPIN NEUROL, V14, P171, DOI 10.1097/00019052-200104000-00006 VANKREVELEN DA, 1975, ACTA PAEDOPSYCHIATR, V42, P49 WALDEYER A, 1939, DTSCH MED WOCHENSCHI, V65, P1098 1971, ENCY JUDAICA, V4, P1396 2000, CHARITE UNIVERSITATS, P16 NR 40 TC 8 Z9 8 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0957-154X J9 HIST PSYCHIATR JI Hist. Psychiatr. PD JUN PY 2003 VL 14 IS 54 BP 205 EP 218 DI 10.1177/0957154X030142005 PN 2 PG 14 WC History Of Social Sciences; Psychiatry SC Social Sciences - Other Topics; Psychiatry GA 768KV UT WOS:000188542900005 PM 14518490 ER PT J AU Psillas, G Daniilidis, J AF Psillas, G Daniilidis, J TI Low-frequency hearing assessment by middle latency responses in children with pervasive developmental disorder SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article DE MLR; pervasive developmental disorder; auditory responses; low-frequency hearing impairment; autistic disorder ID AUDITORY BRAIN-STEM; WAARDENBURGS-SYNDROME; AUTISM; MUTATIONS; DIAGNOSIS; GENE; WFS1 AB Objective: In this study, we assessed middle latency responses (MLR) in children diagnosed with pervasive developmental disorder (PDD) in order to detect low-frequency auditory thresholds. Methods: 35 children, 25 mates and 10 females, aged below 5, diagnosed with PDD were referred to rule out any possible hearing deficit. Audiologic evaluation included free-field testing, tympanometry, and both MLR and auditory brainstem responses. A control group of 15 normal children matched for sex and age were used. Results: In 9 out of 35 children (25%), low-frequency sensory hearing loss was revealed. The hearing loss was unilateral in seven children and bilateral in two, and varied from slight to severe. In four out of the nine cases (44%), parents had not suspected hearing loss, since these children always responded to sound. Conclusions: Among children diagnosed with PDD a significant proportion (25%) was affected by low-frequency sensory hearing loss, detected by MLR. In these children, when low-frequency hearing loss was found bilateral or severe unilateral, aural. rehabilitation was initiated in order to improve their responses to auditory stimuli and their impaired communication with the environment. PDD children, even if their reaction to sound is normal, must be referred to thorough audiometric evaluation white low-frequency hearing level should always be tested. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved. C1 Aristotle Univ Thessaloniki, AHEPA Hosp, ORL Clin, GR-54006 Thessaloniki, Greece. RP Psillas, G (reprint author), Aristotle Univ Thessaloniki, AHEPA Hosp, ORL Clin, 1 Stilponos Kyriakidi St, GR-54006 Thessaloniki, Greece. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bespalova IN, 2001, HUM MOL GENET, V10, P2501, DOI 10.1093/hmg/10.22.2501 Cryns K, 2002, HUM GENET, V110, P389, DOI 10.1007/s00439-002-0719-1 DAVIS H, 1976, ANN OTOL RHINOL LA S, V28, P1 Edwards BM, 2002, PEDIATRICS, V110, P119, DOI 10.1542/peds.110.1.119 Evereklioglu C, 2001, J LARYNGOL OTOL, V115, P704 Fernell E, 1999, DEV MED CHILD NEUROL, V41, P270, DOI 10.1017/S0012162299000572 Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 FRIA TJ, 1980, ANN OTO RHINOL LARYN, V89, P200 Hall J, 1992, HDB AUDITORY EVOKED Hausler R, 1991, Acta Otolaryngol Suppl, V482, P58 Ho PT, 1999, LARYNGOSCOPE, V109, P129, DOI 10.1097/00005537-199901000-00025 JAMAL MN, 1995, ANN OTO RHINOL LARYN, V104, P957 JERGER J, 1970, ARCHIV OTOLARYNGOL, V92, P311 JURE R, 1991, DEV MED CHILD NEUROL, V33, P1062 KLIN A, 1993, J AUTISM DEV DISORD, V23, P15, DOI 10.1007/BF01066416 LANDGREN M, 1992, DEV MED CHILD NEUROL, V34, P999 Liu XZ, 1997, ANN OTO RHINOL LARYN, V106, P220 KRAUS N, 1993, EAR HEARING, V14, P36, DOI 10.1097/00003446-199302000-00006 MENDELSON T, 1979, ARCH OTOLARYNGOL, V105, P17 Merchant SN, 2001, ANN OTO RHINOL LARYN, V110, P875 PHELPS PD, 1983, J LARYNGOL OTOL, V97, P995, DOI 10.1017/S0022215100095888 Rosenhall U, 1999, J AUTISM DEV DISORD, V29, P349, DOI 10.1023/A:1023022709710 Spence MA, 2001, CURR OPIN PEDIATR, V13, P561, DOI 10.1097/00008480-200112000-00012 WU CY, 1994, HEARING RES, V78, P169, DOI 10.1016/0378-5955(94)90022-1 NR 27 TC 0 Z9 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-5876 J9 INT J PEDIATR OTORHI JI Int. J. Pediatr. Otorhinolaryngol. PD JUN PY 2003 VL 67 IS 6 BP 613 EP 619 DI 10.1016/S0165-5876(03)00071-5 PG 7 WC Otorhinolaryngology; Pediatrics SC Otorhinolaryngology; Pediatrics GA 682VY UT WOS:000183114100006 PM 12745154 ER PT J AU Takahashi, H Suzumura, S Shirakizawa, F Wada, N Tanaka-Taya, K Arai, S Okabe, N Ichikawa, H Sato, T AF Takahashi, H Suzumura, S Shirakizawa, F Wada, N Tanaka-Taya, K Arai, S Okabe, N Ichikawa, H Sato, T TI An epidemiological study on Japanese autism concerning routine childhood immunization history SO JAPANESE JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID CHILDREN AB To assess the causal association of autism with measles, mumps, and rubella (MMR) vaccine versus that with monovalent measles, mumps, and rubella immunization, a 1:2 sex-adjusted logistic regression analysis was conducted using data on subjects who were growing up in the Tokyo area between 1988 and 1992. When MMR immunization was used as a reference, monovalent measles immunization (odds ratio [OR] = 5.33, 99% confidence interval [Cl]: 1.03-27.74), non-mumps immunization (OR = 8, 99% CI: 1.33 - 48.2), and non-rubella immunization (OR = 8.57, 99% Cl: 1.30 - 56.4) with development of autistic spectrum disorders (ASD) were significantly increased. These results suggest a decreased, risk of developing ASD with MMR compared to monovalent antigens. However, our findings may reflect potential selection bias due to requiring written consent, possible delayed vaccination in suspected autism cases, and small sample size (case = 2 1). For the case group and the control group, immunization completeness rate of each antigen, regardless of the timing of immunization, was 90.5% versus 100% in measles, 42.9% versus 78.6% in mumps (P < 0.01), 52.3% versus 83.3% in rubella (P < 0.01), 14.3% versus 45.2% in varicella (P < 0.01), 100% versus 90.5% in poliogreater than or equal to2, 100% versus 97.6% in Diphtheria (D), pertussis, and tetanus (T) greater than or equal to3, 85.7% versus 66.7% in DT, 95.2% versus 92.9% in BCG, and 52.4% versus 81.0% in Japanese encephalitis greater than or equal to3 (P<0.01). Only two case subjects and four control subjects received their measles, mumps, and rubella immunizations separately, suggesting that few Japanese parents might have had concerns about the safety of MMR vaccine. A nation-wide study would be a practical measure to scientifically judge the safety of MMR and other routine childhood immunizations. C1 Japan Int Cooperat Agcy, Inst Int Cooperat, Shinjuku Ku, Tokyo 1628433, Japan. Tokyo Metropolitan Umegaoka Hosp, Tokyo 1560043, Japan. Wada Pediat Clin, Tokyo 1210812, Japan. Natl Inst Infect Dis, Infect Dis Surveillance Ctr, Tokyo 1628640, Japan. RP Takahashi, H (reprint author), Japan Int Cooperat Agcy, Inst Int Cooperat, Shinjuku Ku, Ichigaya Honmura Cho 10-5, Tokyo 1628433, Japan. EM takahashi.hiroshi@jica.go.jp CR DESTEFANO F, 2001, CNS DRUGS, V15, P1 KURITA H, 2001, CURRENT STATUS AUTIS, V103, P64 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Rodier PM, 1998, MENT RETARD DEV D R, V4, P121, DOI 10.1002/(SICI)1098-2779(1998)4:2<121::AID-MRDD9>3.0.CO;2-S Takahashi H, 2001, JPN J INFECT DIS, V54, P78 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 2000, LANCET, V355, P1379 NR 8 TC 6 Z9 6 PU NATL INST INFECTIOUS DISEASES PI TOKYO PA JPN J INFECT DIS ED OFF NATL INST INFECTIOUS DISEASES TOYAMA 1-23-1, SHINJUKU-KU, TOKYO, 162-8640, JAPAN SN 1344-6304 EI 1884-2836 J9 JPN J INFECT DIS JI Jpn. J. Infect. Dis. PD JUN PY 2003 VL 56 IS 3 BP 114 EP 117 PG 4 WC Infectious Diseases SC Infectious Diseases GA 718BL UT WOS:000185125200008 PM 12944678 ER PT J AU Lawson, J AF Lawson, J TI Depth accessibility difficulties: An alternative conceptualisation of autism spectrum conditions SO JOURNAL FOR THE THEORY OF SOCIAL BEHAVIOUR LA English DT Article ID CHILDREN; MIND AB Autism and Asperger syndrome are psychiatric conditions diagnosed primarily on the basis of deficits and problems in social behaviour; interaction and communication. At present the explanation of these behavioural features is dominated by three cognitive models. However, it is a characteristic of each of these models that they only explain a sub-set of the overall features. The aim of this paper is to suggest an alternative conceptual theory of autism and Asperger syndrome that mites the current three models. Thus, the aim is to situate the existing models as special cases of the one being proposed here. This alternative conceptualisation draws heavily on distinctions and ideas present in the philosophy of science, most especially in the area of critical realism. Central to the theory is the idea that the core "problem" in autism and Asperger syndrome concerns ontological depth. More specifically, that people with these conditions find it difficult to cope with phenomena characterised by depth (underlying needs, motives beliefs etc.), open systems (rapidly changing, multiple causes) and high internal relationality (converging or changing roles and demands). C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. RP Lawson, J (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,Trumpington Rd, Cambridge, England. CR *APA, 1994, DSM IV DIAGN STAT MA Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S, 1999, NEUROCASE, V5, P475, DOI 10.1080/13554799908402743 BARONCOHEN S, 2002, HDB COGNITIVE DEV Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen S., 1997, CHILDRENS THEORIES N Bhaskar R., 1989, POSSIBILITY NATURALI, V3rd Bhaskar Roy, 1978, REALIST THEORY SCI DUNCAN J, 1986, COGNITIVE NEUROPSYCH, V3, P271, DOI 10.1080/02643298608253360 FLEETWOOD S, 1999, EC SOCIAL THEORY FRITH U, 2002, NAT AUT SOC 40 ANN I Frith U., 1989, AUTISM EXPLAINING EN FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Hume D., 1975, ENQUIRIES CONCERNING, V3rd Kanner L, 1943, NERV CHILD, V2, P217 LAWSON J, UNPUB J AUTISM DEV D Lawson T., 1997, EC REALITY Liss M, 2001, J CHILD PSYCHOL PSYC, V42, P261, DOI 10.1017/S0021963001006679 Mitchell RLC, 2001, TRENDS COGN SCI, V5, P71, DOI 10.1016/S1364-6613(00)01599-0 Nation K, 1999, PSYCHOL BULL, V125, P338, DOI 10.1037/0033-2909.125.3.338 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x PREMACK D, 1990, COGNITION, V36, P1, DOI 10.1016/0010-0277(90)90051-K Premack D., 1978, BEHAVIORAL BRAIN SCI, V4, P515, DOI [10.1017/S0140525X00076512, DOI 10.1017/S0140525X00076512] Russell J., 1997, AUTISM EXECUTIVE DIS Scott FJ, 2002, AUTISM, V6, P231, DOI 10.1177/1362361302006003002 THORPE V, 1999, GUARDIAN 0314 VONBRENTANO F, 1874, PSYCHOL EMPIRICAL ST WELLMAN HM, 1992, ANNU REV PSYCHOL, V43, P337, DOI 10.1146/annurev.ps.43.020192.002005 WELLMAN HM, 1997, EMERGENCE CARE DOMAI NR 32 TC 11 Z9 11 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-8308 J9 J THEOR SOC BEHAV JI J. Theory Soc. Behav. PD JUN PY 2003 VL 33 IS 2 BP 189 EP + DI 10.1111/1468-5914.00213 PG 15 WC Psychology, Social SC Psychology GA 693UJ UT WOS:000183736500004 ER PT J AU LeBlanc, LA Coates, AM Daneshvar, S Charlop-Christy, MH Morris, C Lancaster, BM AF LeBlanc, LA Coates, AM Daneshvar, S Charlop-Christy, MH Morris, C Lancaster, BM TI Using video modeling and reinforcement to teach perspective-taking skills to children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; perspective taking; video modeling; theory of mind ID MIND AB We evaluated video modeling and reinforcement for teaching perspective-taking skills to 3 children with autism using a multiple baseline design. Video modeling and reinforcement were effective; however, only 2 children were able to pass an untrained task, indicating limited generalization. The findings suggest that video modeling may be an effective technology for teaching perspective taking if researchers can continue to develop strategies for enhancing the generalization of these new skills. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. Claremont Mckenna Coll, Claremont, CA 91711 USA. RP LeBlanc, LA (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. CR BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Capps L., 1997, CHILDREN AUTISM DEV CHANDLER M, 1989, CHILD DEV, V60, P263 Charlop-Christy MH, 2000, J AUTISM DEV DISORD, V30, P537, DOI 10.1023/A:1005635326276 Knoll M., 2000, CHILD STUDY J, V30, P273 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 SPRADLIN JE, 1999, AUTISM BEHAV ANAL PE, P49 NR 8 TC 72 Z9 73 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 SUM PY 2003 VL 36 IS 2 BP 253 EP 257 DI 10.1901/jaba.2003.36-253 PG 5 WC Psychology, Clinical SC Psychology GA 694FR UT WOS:000183763900008 PM 12858990 ER PT J AU Rehfeldt, RA Chambers, MR AF Rehfeldt, RA Chambers, MR TI Functional analysis and treatment of verbal perseverations displayed by an adult with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE verbal perseverations; functional analysis; autisml ID BIZARRE; SPEECH AB The function of perseverative speech for an adult man who had been diagnosed with autism and mental retardation was examined. Results showed that verbal perseverations were maintained by social attention. An intervention consisting of differential reinforcement of appropriate verbal responses and extinction of perseverative verbal responding was effective in decreasing verbal perseverations. C1 So Illinois Univ, Inst Rehabil, Rehabil Serv Program, Carbondale, IL 62901 USA. RP Rehfeldt, RA (reprint author), So Illinois Univ, Inst Rehabil, Rehabil Serv Program, Mailcode 4609, Carbondale, IL 62901 USA. CR DeLeon IG, 2003, J APPL BEHAV ANAL, V36, P101, DOI 10.1901/jaba.2003.36-101 Dixon MR, 2001, J APPL BEHAV ANAL, V34, P361, DOI 10.1901/jaba.2001.34-361 DURAND VM, 1987, J AUTISM DEV DISORD, V17, P17, DOI 10.1007/BF01487257 SCHREIBMAN L, 1978, J APPL BEHAV ANAL, V11, P453, DOI 10.1901/jaba.1978.11-453 Wilder DA, 2001, J APPL BEHAV ANAL, V34, P65, DOI 10.1901/jaba.2001.34-65 NR 5 TC 17 Z9 17 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 SUM PY 2003 VL 36 IS 2 BP 259 EP 261 DI 10.1901/jaba.2003.36-259 PG 3 WC Psychology, Clinical SC Psychology GA 694FR UT WOS:000183763900009 PM 12858991 ER PT J AU Heather, D AF Heather, D TI A user guide to the GF/CF diet for autism, Asperger syndrome and ADHD SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Book Review RP Heather, D (reprint author), Merchant House,Commercial Rd, Penryn TR10 8AE, Cornwall, England. CR Crossley N, 1996, INTERSUBJECTIVITY Grandin T., 1995, THINKING PICTURES JACKSON L, 2002, USER GUIDE GF CF DIE SHATTOCK P, 1997, AUTISM METABOLIC DIS NR 4 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD JUN PY 2003 VL 16 IS 2 BP 169 EP 170 DI 10.1046/j.1468-3148.2003.00137.x PG 2 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 679XT UT WOS:000182947800009 ER PT J AU Losh, M Capps, L AF Losh, M Capps, L TI Narrative ability in high-functioning children with autism or Asperger's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's syndrome; narrative; emotional understanding ID STORY CHARACTERS; MIND; INDIVIDUALS; DISCOURSE; ADULTS; STATES AB This study examines the narrative abilities of 28 high-functioning children with autism or Asperger's Syndrome and 22 typically developing children across two different discourse contexts. As compared with the typically developing children, the high-functioning group performed relatively well in the storybook context but exhibited difficulty imbuing their narratives of personal experience with the more sophisticated characteristics typically employed by the comparison group. Furthermore, children with autism or Asperger's Syndrome demonstrated impairments inferring and building on the underlying causal relationships both within and across story episodes in both narrative contexts. Findings further revealed that the narrative abilities of children with autism or Asperger's Syndrome were associated with performance on measures of emotional understanding, but not theory of mind or verbal IQ. Findings are discussed in relation to the social and emotional underpinnings of narrative discourse. C1 Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. RP Losh, M (reprint author), Univ Calif Berkeley, Dept Psychol, 3210 Tolman Hall,1650, Berkeley, CA 94720 USA. EM losh@socrates.berkeley.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th APPELBEE AN, 1978, CHILDS CONCEPT STORY ASTINGTON JW, 1990, NARRATIVE THOUGHT AND NARRATIVE LANGUAGE, P151 BAMBERG M, 1991, DISCOURSE PROCESS, V14, P277 BAMBERG M, 1991, J CHILD LANG, V18, P689 BAMBERG M, 1991, J COGNITIVE PSYCHOTH, V5, P275 Bamberg MGW, 1997, J NARRAT LIFE HIST, V7, P335 Baron-Cohen S., 1993, UNDERSTANDING OTHER BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bellugi U., 1990, DEV PSYCHOPATHOL, V2, P367, DOI DOI 10.1017/S0954579400005782 Berman R. A., 1994, RELATING EVENTS NARR Bloom L., 1991, LANGUAGE DEV 2 3 Bruner J, 1986, ACTUAL MINDS POSSIBL Bruner J. 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R., 1989, ENTERING CIRCLE HERM, P185 Shweder R., 1993, HDB EMOTIONS, P417 SOBEL D, 2000, INT C INF STUD BRIGH Stein NR, 1979, NEW DIRECTIONS DISCO, P53 TAGERFLUSBERG H, 1992, CHILD DEV, V63, P161, DOI 10.1111/j.1467-8624.1992.tb03604.x TAGERFLUSBERG H, 1995, BRIT J DEV PSYCHOL, V13, P45 TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 World Health Organisation (WHO), 1993, INT CLASS DIS NR 62 TC 104 Z9 106 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 239 EP 251 DI 10.1023/A:1024446215446 PG 13 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500002 PM 12908827 ER PT J AU Emerich, DM Creaghead, NA Grether, SM Murray, D Grasha, C AF Emerich, DM Creaghead, NA Grether, SM Murray, D Grasha, C TI The comprehension of humorous materials by adolescents with high-functioning autism and Asperger's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's syndrome; humor; cartoons; jokes ID APPRECIATION; COMPETENCE; CHILDREN; LANGUAGE; JOKES AB This study investigated the ability of adolescents with Asperger's syndrome or high-functioning autism and an age-matched group of typical adolescents to comprehend humorous materials. The analysis of humor focused on picking funny endings for cartoons and jokes. As expected, the adolescents with autism had significantly poorer comprehension of cartoons and jokes. Both groups had more difficulty with the joke than the cartoon task, but when compared with the typical group, the adolescents with autism performed significantly poorer. Examination of the error patterns revealed that subjects with autism had difficulty handling surprise and coherence within humorous narratives. C1 Kenton Cty Publ Sch, Erlanger, KY USA. Univ Cincinnati, Dept Commun Sci & Disorders, Cincinnati, OH USA. Cincinnati Childrens Hosp, Med Ctr, Kelly Oleary Ctr Autism Spectrum Disorders, Cincinnati, OH USA. Cincinnati Childrens Hosp, Med Ctr, Div Dev Disabilities, Cincinnati, OH USA. RP Emerich, DM (reprint author), 357 Marble Cliff Dr, Lakeside Pk, KY 41017 USA. CR Attwood T., 1998, ASPERGERS SYNDROME G BIHRLE AM, 1986, BRAIN COGNITION, V5, P399, DOI 10.1016/0278-2626(86)90042-4 Brodzinsky D. M., 1980, CHILDRENS HUMOUR, P181 BROWNELL HH, 1983, BRAIN LANG, V18, P20, DOI 10.1016/0093-934X(83)90002-0 de Villiers J. G., 1978, LANGUAGE ACQUISITION DUNN L, 1997, EXAMIENRS MANUAL PEA FOWLES B, 1977, J CHILD LANG, V4, P433 HORGAN D, 1981, J CHILD LANG, V8, P217 MASTEN AS, 1986, CHILD DEV, V57, P461, DOI 10.1111/j.1467-8624.1986.tb00045.x McGhee Paul E., 1979, HUMOR ITS ORIGIN DEV MOULTON P, 1942, 2500 JOKES ALL OCCAS OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x Ozonoff S, 1996, BRAIN LANG, V52, P411, DOI 10.1006/brln.1996.0022 RICKS DM, 1975, J AUTISM CHILD SCHIZ, V5, P191, DOI 10.1007/BF01538152 SCHOPLER E, 1992, HIGH FUNCTIONING IND SHULTZ TR, 1974, DEV PSYCHOL, V10, P13 SOTTO CD, 1994, COMPREHENSION RIDDLE SPECTOR CC, 1990, J SPEECH HEAR DISORD, V55, P533 Suls J. M., 1972, PSYCHOL HUMOR, P81 Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 Van Kleeck A, 1984, LANGUAGE LEARNING DI, P128 VANBOURGONDIEN ME, 1987, J AUTISM DEV DISORD, V17, P417 ZIGLER E, 1967, J PERS SOC PSYCHOL, V6, P332, DOI 10.1037/h0024729 NR 23 TC 34 Z9 35 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 253 EP 257 DI 10.1023/A:1024498232284 PG 5 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500003 PM 12908828 ER PT J AU Crosland, KA Zarcone, JR Lindauer, SE Valdovinos, MG Zarcone, TJ Hellings, JA Schroeder, SR AF Crosland, KA Zarcone, JR Lindauer, SE Valdovinos, MG Zarcone, TJ Hellings, JA Schroeder, SR TI Use of functional analysis methodology in the evaluation of medication effects SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; functional analysis; risperidone; self-injurious behavior; aggression ID COMMON CLASSROOM CONTINGENCIES; SELF-INJURIOUS-BEHAVIOR; DEVELOPMENTAL-DISABILITIES; DOUBLE-BLIND; MENTAL-RETARDATION; RISPERIDONE; METHYLPHENIDATE; DISORDERS; ADULTS AB The atypical antipsychotic medication risperidone was evaluated using a double-blind, placebo-controlled design in the treatment of destructive behavior in two individuals with autism. Premedication functional analyses indicated that destructive behavior was maintained by escape from demands, attention, or access to tangible items. For both individuals, destructive behavior during the demand condition was significantly reduced during the medication phases, whereas destructive behavior continued to occur to obtain tangible items ( Reggie) and attention (Sean). In addition, there appeared to be a differential effect of the medication on self-injurious behavior (SIB) versus aggression for Sean. Results of the study demonstrate how functional analysis may provide information on those conditions and behaviors that are most likely to be affected by a specific medication. C1 Univ Kansas, Schiefelbusch Inst Life Span Studies, Lawrence, KS 66045 USA. Univ Kansas, Med Ctr, Kansas City, KS 66103 USA. RP Zarcone, JR (reprint author), Univ Kansas, Schiefelbusch Inst Life Span Studies, 1000 Sunnyside Ave,Room 1052, Lawrence, KS 66045 USA. RI Valdovinos, Maria/F-5721-2014 CR Aman MG, 1999, MENT RETARD DEV D R, V5, P253, DOI 10.1002/(SICI)1098-2779(1999)5:4<253::AID-MRDD2>3.0.CO;2-R FISHER W, 1989, J BEHAV THER EXP PSY, V20, P241, DOI 10.1016/0005-7916(89)90029-3 Fisman S, 1998, J AM ACAD CHILD PSY, V37, P15, DOI 10.1097/00004583-199801000-00011 Garcia D, 1999, RES DEV DISABIL, V20, P1, DOI 10.1016/S0891-4222(98)00028-6 GARDNER WI, 1996, MANUAL DIAGNOSIS PRO, P355, DOI 10.1037/10203-027 Gillberg C., 1992, BIOL AUTISTIC SYNDRO Hardan A, 1996, J AM ACAD CHILD PSY, V35, P1551, DOI 10.1097/00004583-199611000-00025 Horrigan JP, 1997, J AUTISM DEV DISORD, V27, P313, DOI 10.1023/A:1025854532079 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Khan BU, 1997, J AUTISM DEV DISORD, V27, P479, DOI 10.1023/A:1025813607005 LINDAUER SL, 2002, J APPL BEHAV ANAL, V35, P209 LUISELLI JK, 1986, J BEHAV THER EXP PSY, V1, P275 Mace FC, 1995, MENT RETARD DEV D R, V1, P104, DOI 10.1002/mrdd.1410010206 McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 Napolitano DA, 1999, MENT RETARD DEV D R, V5, P322, DOI 10.1002/(SICI)1098-2779(1999)5:4<322::AID-MRDD10>3.0.CO;2-F NICHOLSON R, 1998, J AM ACAD CHILD ADOL, V37, P372 NORTHUP J, 1997, J APPL BEHAV ANAL, V30, P614 Northup J, 1997, J APPL BEHAV ANAL, V30, P121, DOI 10.1901/jaba.1997.30-121 Northup J, 1999, J APPL BEHAV ANAL, V32, P35, DOI 10.1901/jaba.1999.32-35 REESE RM, 1999, PSYCHIAT BEHAV DISOR SCHAAL DW, 1994, AM J MENT RETARD, V99, P123 Schroeder SR, 2001, MENT RETARD DEV D R, V7, P3, DOI 10.1002/1098-2779(200102)7:1<3::AID-MRDD1002>3.0.CO;2-# SCHROEDER SR, 1990, ADV DEV BEHAV PEDIAT, P181 SPRAGUE RL, 1971, INT REV RES MENTAL R Thompson T, 1999, CHALLENGING BEHAVIOR OF PERSONS WITH MENTAL HEALTH DISORDERS AND SEVERE DEVELOPMENTAL DISABILITIES, P125 Thompson T., 1994, DESTRUCTIVE BEHAV DE, P133 VANDENBORRE R, 1993, ACTA PSYCHIAT SCAND, V87, P167 Zarcone JR, 2001, AM J MENT RETARD, V106, P525, DOI 10.1352/0895-8017(2001)106<0525:EOROAB>2.0.CO;2 NR 28 TC 21 Z9 22 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 271 EP 279 DI 10.1023/A:1024402500425 PG 9 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500005 PM 12908830 ER PT J AU Sperry, LA Symons, FJ AF Sperry, LA Symons, FJ TI Maternal judgments of intentionality in young children with autism: the effects of diagnostic information and stereotyped behavior SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE diagnosis; autism; intentionality; maternal judgments; stereotypes; family functioning ID ATTRIBUTION; DISORDER; STRESS AB This study examined the relation among maternal judgment of intentionality and variables relevant to families of children with autism. Thirty-six mothers of children with autism rated segments of home videotape of behavior from very young children later diagnosed with autism. Mothers were randomly assigned to either a diagnostic or a no diagnostic information group. No significant difference was found on overall ratings of intentionality. Maternal stress was not correlated with overall ratings of intentionality for either group. Mothers in the diagnostic information group rated stereotyped behavior as less intentional. Post hoc analyses showed no differences on maternal ratings of intentionality when the child was in a social setting or interacting with an object, but there were significant differences between ratings when the child was alone. The results are discussed in relation to early development and identification issues in autism. C1 Univ Minnesota, Dept Educ Psychol, Minneapolis, MN 55455 USA. Univ N Carolina, Chapel Hill, NC USA. RP Symons, FJ (reprint author), Univ Minnesota, Dept Educ Psychol, 227 Burton Hall,178 Pillsbury Dr, Minneapolis, MN 55455 USA. CR Abidin RR, 1995, PARENTING STRESS IND American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAKER BL, 1991, AM J MENT RETARD, V96, P127 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BEAUMONT SL, 1991, 1 LANGUAGE, V5, P235 Bell R. Q., 1977, CHILD EFFECTS ADULTS BELSKY J, 1984, CHILD DEV, V55, P83, DOI 10.1111/j.1467-8624.1984.tb00275.x BENDELL RD, 1986, J CLIN CHILD PSYCHOL, V15, P304, DOI 10.1207/s15374424jccp1504_3 BREEN MJ, 1988, J PEDIATR PSYCHOL, V13, P265, DOI 10.1093/jpepsy/13.2.265 Bristol M. M., 1983, AUTISM ADOLESCENTS A, P251 Bristol MM, 1996, J AUTISM DEV DISORD, V26, P121, DOI 10.1007/BF02172002 BUGENTAL DB, 1989, DEV PSYCHOL, V25, P532, DOI 10.1037/0012-1649.25.4.532 COHEN DJ, 1997, HDB AUTISM PERVGASIV CRONBACH LJ, 1951, PSYCHOMETRIKA, V16, P297 DIX T, 1993, PERS SOC PSYCHOL B, V19, P633, DOI 10.1177/0146167293195014 DIX T, 1989, CHILD DEV, V60, P1373, DOI 10.1111/j.1467-8624.1989.tb04010.x Dumas J. 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H., 1992, AUTISM IDENTIFICATIO, P187 REZNICK JS, 1999, THEORIES MIND ACTION, P243 Schopler E., 1988, CHILDHOOD AUTISM RAT SIGMAN M, 1986, J CHILD PSYCHOL PSYC, V27, P647, DOI 10.1111/j.1469-7610.1986.tb00189.x Sperry LA, 1999, INFANT YOUNG CHILD, V11, P17 SPERRY LA, 2000, THESIS U N CAROLINA Stone WL, 1997, J AUTISM DEV DISORD, V27, P677, DOI 10.1023/A:1025854816091 THELEN E, 1979, ANIM BEHAV, V27, P699, DOI 10.1016/0003-3472(79)90006-X WALDEN TA, 1988, CHILD DEV, V59, P1230, DOI 10.1111/j.1467-8624.1988.tb01492.x Walden TA, 1997, AM J MENT RETARD, V102, P292, DOI 10.1352/0895-8017(1997)102<0292:DISSPB>2.0.CO;2 ZEEDYK MS, 1994, THESIS YALE U NR 39 TC 4 Z9 6 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 281 EP 287 DI 10.1023/A:1024454517263 PG 7 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500006 PM 12908831 ER PT J AU Rutherford, MD Rogers, SJ AF Rutherford, MD Rogers, SJ TI Cognitive underpinnings of pretend play in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pretend play; theory of mind; executive function ID DIAGNOSTIC OBSERVATION SCHEDULE; EXECUTIVE FUNCTION DEFICITS; SYMBOLIC PLAY; JOINT ATTENTION; YOUNG-CHILDREN; COMMUNICATION DEFICITS; STRATEGIC DECEPTION; MIND; LANGUAGE; REPRESENTATION AB This article examines the cognitive underpinnings of spontaneous and prompted pretend play in 28 young children with autism, 24 children with other developmental disorders, and 26 typical children. The article compares theories that consider either theory of mind (ToM) or executive function (EF) to be causally important deficits in the development of pretend play in autism and important factors in pretend play. Each of these two theories posits a cognitive precursor to pretense, which would need to be present in typical development, and the absence of which could explain pretend play deficits in children with developmental disabilities such as autism. We tested which of these theories better predicts a child's production of pretend play. Children with autism were significantly delayed on pretend play scores. They also had significant deficits in our ToM measure, but not our EF measures. Regression analyses suggested a role for our measure of generativity, one of the EF measures. C1 Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Colorado, Hlth Sci Ctr, JFK Partners, Denver, CO USA. RP Rutherford, MD (reprint author), McMaster Univ, Dept Psychol, 1280 Main St W, Hamilton, ON L8S 4K1, Canada. 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Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 289 EP 302 DI 10.1023/A:1024406601334 PG 14 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500007 PM 12908832 ER PT J AU Saemundsen, E Magnusson, P Smari, J Sigurdardottir, S AF Saemundsen, E Magnusson, P Smari, J Sigurdardottir, S TI Autism Diagnostic Interview-Revised and the Childhood Autism Rating Scale: Convergence and discrepancy in diagnosing autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; diagnosis; Autism Diagnostic Interview-Revised; Childhood Autism Rating Scale ID DSM-III-R; SPECTRUM DISORDERS; ADI-R; VALIDITY; CLASSIFICATION; BEHAVIOR; VERSION; DOMAINS; SYSTEMS; ICD-10 AB The agreement between the Autism Diagnostic Interview - Revised (ADI-R) and the Childhood Autism Rating Scale ( CARS) was investigated in the diagnostic assessment of 54 children aged 22 - 114 months referred for possible autism. The observed agreement between the two systems was 66.7% (Cohen's kappa =.40) when the ADI-R definition for autism was applied (i.e., scores reaching cutoff in three domains on the ADI-R), but increased considerably with less stringent criteria; that is, scores reaching cutoffs in two domains and in one domain on the ADI-R. As predicted, the CARS identified more cases of autism than the ADI-R. Children classified as autistic according to both instruments had significantly lower IQ/DQ and more severe autistic symptomatology than those classified with the CARS only. C1 State Diagnost & Counseling Ctr, IS-200 Kopavogur, Iceland. Natl Univ Hosp Reykjavik, Dept Child & Adolescent Psychiat, Reykjavik, Iceland. Univ Iceland, Dept Social Sci, Reykjavik, Iceland. RP Saemundsen, E (reprint author), State Diagnost & Counseling Ctr, Digranesvegur 5, IS-200 Kopavogur, Iceland. 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Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 319 EP 328 DI 10.1023/A:1024410702242 PG 10 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500009 PM 12908834 ER PT J AU Mayes, SD Calhoun, SL AF Mayes, SD Calhoun, SL TI Analysis of WISC-III, Stanford-Binet : IV, and academic achievement test scores in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's syndrome; IQ; cognitive profiles; academic achievement ID PERVASIVE DEVELOPMENTAL DISORDERS; LEARNING-DISABLED STUDENTS; DEFICIT-HYPERACTIVITY DISORDER; HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; METHYLPHENIDATE; SYMPTOMS; DISABILITIES; INDIVIDUALS; DIAGNOSIS AB Nonverbal IQs were greater than verbal IQs for young children ( 3 - 7 years of age) on the Stanford-Binet: IV (n = 53). However, WISC-III verbal and nonverbal IQs were similar for older children, 6 - 15 years of age ( n = 63). Stanford-Binet: IV profiles were generally consistent for the low-IQ (< 80) and high-IQ (&GE; 80) groups, with high scores on visual matching tests ( Bead Memory and Quantitative Reasoning). The low- and high-WISC-III IQ groups both performed well relative to IQ on tests of lexical knowledge ( Similarities, Information, and Vocabulary), but not on language comprehension and social reasoning ( Comprehension). The low- IQ group did best on visuo-motor subtests ( Object Assembly and Block Design), but the high-IQ group did not. The high-IQ group had significantly low scores on the Digit Span, Arithmetic, Coding, VMI, and WIAT Written Expression tests, suggesting attention and writing weaknesses. C1 Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Dept Psychiat, Hershey, PA 17033 USA. RP Mayes, SD (reprint author), Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Dept Psychiat, POB 850, Hershey, PA 17033 USA. 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PD JUN PY 2003 VL 33 IS 3 BP 329 EP 341 DI 10.1023/A:1024462719081 PG 13 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500010 PM 12908835 ER PT J AU Collins, JS Schroer, RJ Bird, J Michaelis, RC AF Collins, JS Schroer, RJ Bird, J Michaelis, RC TI The HOXA1 A218G polymorphism and autism: Lack of association in white and black patients from the South Carolina Autism Project SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE neurobehavioral disorders; single nucleotide polymorphism; homeobox genes ID FETAL VALPROATE SYNDROME; GENOMIC SCREEN; SUSCEPTIBILITY; DISORDERS; HINDBRAIN; ETIOLOGY; GENETICS; HOX-1.6 AB A recent study has suggested that the A218G polymorphism in the homeobox A1 (HOXA1) gene may influence susceptibility to autism. We have determined the frequencies of the A and G alleles of the HOXA1 A218G polymorphism in both white and black patients from the South Carolina Autism Project ( SCAP) and controls. Marked differences were found in allele frequencies between the races, but no deviations from Hardy-Weinberg equilibrium were seen in either white or black SCAP family members. More direct tests, comparing genotype frequencies between probands and controls and tracking transmission of the A versus G alleles to affected offspring, did not support the contention that allele status for the HOXA1 A218G polymorphism influences one's susceptibility to autism. C1 Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. RP Michaelis, RC (reprint author), Greenwood Genet Ctr, JC Self Res Inst, 1 Gregor Mendel Circle, Greenwood, SC 29646 USA. 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Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 343 EP 348 DI 10.1023/A:1024414803151 PG 6 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500011 PM 12908836 ER PT J AU Kalachnik, JE Hanzel, TE Sevenich, R Harder, SR AF Kalachnik, JE Hanzel, TE Sevenich, R Harder, SR TI Brief report: Clonazepam behavioral side effects with an individual with mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE benzodiazepines; clonazepam; mental retardation; side effects; behavioral side effects; aggression ID ANXIETY DISORDERS; PANIC-DISORDER; EPILEPSY; MEDICATIONS; CHILDREN; ADULTS; DRUGS; AGGRESSION; SEIZURES; AUTISM AB Behavioral side effects associated with clonazepam may include agitation, aggression, hyperactivity, irritability, property destruction, and temper tantrums. These side effects may be inadvertently confused with other behavioral or psychiatric conditions, especially if exacerbation of existing challenging behavior occurs. This report describes an individual with mental retardation who experienced behavioral exacerbation associated with clonazepam prescribed at 2 mg/day (0.02 mg/kg/day) to treat aggression, self-injurious behavior, property destruction, and screaming, which was measured with a 15-minute partial interval recording measurement method. When clonazepam was reduced and discontinued, these behaviors significantly decreased from 3.1% of intervals (95% confidence band = 1.6% to 4.6%) to 0.1% of intervals ( 95% confidence band = 0% to 0.1%). Indicators suggesting review by appropriate medical personnel for possible clonazepam behavioral side effects are provided. C1 Univ S Carolina, Sch Med, Dept Pediat, Ctr Disabil Resources, Columbia, SC USA. Hanzel Consulting, New Prague, MN USA. St Josephs Hosp, Dept Psychiat, HealthEast Care Syst, St Paul, MN USA. St Croix River Educ Dist, Rush City, MN USA. RP Kalachnik, JE (reprint author), Iowa Dept Human Serv, Woodward Resource Ctr, 1251 334th St, Woodward, IA 50276 USA. 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Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 349 EP 354 DI 10.1023/A:1024466819989 PG 6 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500012 PM 12908837 ER PT J AU Benaron, LD AF Benaron, LD TI Inclusion to the point of dilution SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID AUTISM; CLASSIFICATION C1 Far No Reg Ctr, Chico, CA 95973 USA. RP Benaron, LD (reprint author), Far No Reg Ctr, 1377 E Lassen Ave, Chico, CA 95973 USA. CR BALE J, 1999, PEDIAT NEUROLOGY PRI, P1003 Beglinger LJ, 2001, J AUTISM DEV DISORD, V31, P411, DOI 10.1023/A:1010616719877 Brasic J. 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Autism Dev. Disord. PD JUN PY 2003 VL 33 IS 3 BP 355 EP 359 DI 10.1023/A:1024418904060 PG 5 WC Psychology, Developmental SC Psychology GA 693EM UT WOS:000183703500013 PM 12908838 ER PT J AU Berger, HJC Aerts, FHTM van Spaendonck, KPM Cools, AR Teunisse, JP AF Berger, HJC Aerts, FHTM van Spaendonck, KPM Cools, AR Teunisse, JP TI Central coherence and cognitive shifting in relation to social improvement in high-functioning young adults with autism SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article ID FOLLOW-UP; CHILDREN; MIND; DYSFUNCTION; ADOLESCENTS; DISORDERS; ABILITIES; AGE; IQ AB The objective of this prospective study was to evaluate the possible role of two cognitive styles-weak central coherence and poor cognitive shifting-in predicting social improvement in patients with autistic disorder. Thirty patients, largely similar in age (young adults), intelligence (high-functioning) and living conditions (residential treatment in the same unit) were assessed at two separate time points with a 3-year interval between pretest and posttest. At pretest central coherence, cognitive shifting and several aspects of social functioning-symptom severity, social intelligence and social competence-were measured. At posttest social functioning was reassessed. Unlike central coherence, cognitive shifting was identified as a significant prognostic marker. This differential outcome might be an indication that patients with poor cognitive shifting and patients with weak central coherence have different prognoses with the current, highly structured treatment milieu; it is unknown whether patients with poor cognitive flexibility might benefit more from treatments specifically designed to address this problem. C1 Univ Nijmegen, Dept Psychol Med, Med Ctr, NL-6500 HB Nijmegen, Netherlands. Dr Leo Kannerhuis, Oosterbeek, Netherlands. RP Berger, HJC (reprint author), Univ Nijmegen, Dept Psychol Med, Med Ctr, 118 MP,POB 9101, NL-6500 HB Nijmegen, Netherlands. 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Clin. Exp. Neuropsychol. PD JUN PY 2003 VL 25 IS 4 BP 502 EP 511 DI 10.1076/jcen.25.4.502.13870 PG 10 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 683GY UT WOS:000183141300006 PM 12911104 ER PT J AU Celani, G AF Celani, G TI Comorbidity between autistic syndrome and biological pathologies: Which implications for the understanding of the etiology? SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Review DE autism; comorbidity; etiology; biological pathologies ID INFANTILE-AUTISM; NORMAL-CHILDREN; CONGENITAL CYTOMEGALOVIRUS; FACIAL EXPRESSIONS; RETARDED-CHILDREN; MOTOR IMITATION; CASE-HISTORIES; DOWN-SYNDROME; DISORDERS; DEFICITS AB It is estimated that at least 24% of cases of autism are potentially associated with other syndromes, to infective, metabolic or genetic pathologies, and to anatomical or functional alterations. Problems connected with interpretation of the association between biological damage and autistic behavioral phenotype in causal terms are briefly exposed. Three critical periods for the beginning of an anomalous behavioral development in the child with autism are identified: prenatal, prior to 9 months from birth, after 1 year of age. Psychopathological consequences potentially deriving from biological damages on every critical period are described, and their compatibility with the characteristic behavioral features observed in individuals affected by autism is discussed. On this basis, a theoretical model that represents infantile autism as a specie-specific human psychopathology of early emotional communication during the primary intersubjectivity stage is proposed. C1 Univ Bologna, Dept Psychol, I-40127 Bologna, Italy. RP Celani, G (reprint author), Univ Bologna, Dept Psychol, Viale Berti Pichat 5, I-40127 Bologna, Italy. 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Dev. Phys. Disabil. PD JUN PY 2003 VL 15 IS 2 BP 141 EP 154 DI 10.1023/A:1022875300575 PG 14 WC Rehabilitation SC Rehabilitation GA 654PL UT WOS:000181505200004 ER PT J AU Engstrom, HA Ohlson, S Stubbs, EG Maciulis, A Caldwell, V Odell, JD Torres, AR AF Engstrom, HA Ohlson, S Stubbs, EG Maciulis, A Caldwell, V Odell, JD Torres, AR TI Decreased expression of CD95 (FAS/APO-1) on CD4(+) T-lymphocytes from participants with autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; apoptosis; FAS; CD95; APO-1 ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ASSOCIATION; COMPLEMENT; CELL; CHILDREN; DISEASES; SUGGESTS; BLOOD AB Although autism remains an enigmatic disease, there is mounting evidence that the immune system plays an important role in the pathogenesis. Immune system involvement is apparently widespread as numerous humoral and cellular abnormalities have been reported in both the innate and adaptive responses. Fas (CD95/APO-1) is a type I cell-surface protein from the TNF/NGF-R superfamily present on the surface of many immune related cells. Fas activation is instrumental in starting a complicated chain of events that results in programmed cell death (apoptosis) by DNA fragmentation. Preliminary data is presented, which indicate that subjects with austism have lower levels of Fas on their CD4(+) helper T cells (p=.048) than have normal subjects. Data also indicates subjects with autism have significantly higher levels of soluble Fas (p=.01) than have normal subjects. A maturing individual must eliminate cells for proper morphogenesis to occur. Preliminary data suggest that faulty apoptosis may be involved in the pathogenesis of autism. C1 Utah State Univ, Dept Biol, Ctr Persons Disabil, Logan, UT 84322 USA. Univ Kalmar, Dept Chem & Biomed Sci, Kalmar, Sweden. Univ Oregon, Child Dev & Rehabil Ctr, Portland, OR USA. RP Torres, AR (reprint author), Utah State Univ, Dept Biol, Ctr Persons Disabil, 6895 Old Main Hill, Logan, UT 84322 USA. CR Becher B, 1998, NEUROSCIENCE, V84, P627, DOI 10.1016/S0306-4522(97)00455-7 COHEN PL, 1991, ANNU REV IMMUNOL, V9, P243, DOI 10.1146/annurev.iy.09.040191.001331 Connolly AM, 1999, J PEDIATR-US, V134, P607, DOI 10.1016/S0022-3476(99)70248-9 Dorsam G, 2000, ANN NY ACAD SCI, V921, P79 Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 GIORDANO C, 1995, DIABETOLOGIA, V38, P449 Gupta S, 2000, J AUTISM DEV DISORD, V30, P475, DOI 10.1023/A:1005568027292 HEARD R, 1994, HLA DIS, pCH7 Janeway Jr CA, 1997, IMMUNOBIOLOGY IMMUNE Jodo S, 1997, CLIN EXP IMMUNOL, V107, P89, DOI 10.1046/j.1365-2249.1997.d01-901.x Messahel S, 1998, NEUROSCI LETT, V241, P17, DOI 10.1016/S0304-3940(97)00976-2 Musette P, 1998, DERMATOLOGY, V196, P281, DOI 10.1159/000017920 Nawa H, 2000, MOL PSYCHIATR, V5, P594, DOI 10.1038/sj.mp.4000730 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Nozawa K, 1997, ARTHRITIS RHEUM, V40, P1126, DOI 10.1002/art.1780400617 PLIOPLYS AV, 1994, DEV BRAIN DYSFUNCT, V7, P12 Potestio M, 1999, EXP GERONTOL, V34, P659, DOI 10.1016/S0531-5565(99)00041-8 Prodeus AP, 1998, IMMUNITY, V9, P721, DOI 10.1016/S1074-7613(00)80669-X Stassi G, 1997, HUM IMMUNOL, V55, P39, DOI 10.1016/S0198-8859(97)00072-4 Tokarnia Carlos Hubinger, 1996, Pesquisa Veterinaria Brasileira, V16, P5 Torres AR, 2002, HUM IMMUNOL, V63, P311, DOI 10.1016/S0198-8859(02)00374-9 Torres AR, 2001, FRONT BIOSCI, V6, pD936, DOI 10.2741/Torres WARREN RP, 1987, J AM ACAD CHILD PSY, V26, P333, DOI 10.1097/00004583-198705000-00008 WARREN RP, 1992, IMMUNOGENETICS, V36, P203, DOI 10.1007/BF00215048 Warren RP, 1997, J AUTISM DEV DISORD, V27, P187, DOI 10.1023/A:1025895925178 WARREN RP, 1995, NEUROPSYCHOBIOLOGY, V31, P53, DOI 10.1159/000119172 WARREN RP, 1991, CLIN EXP IMMUNOL, V83, P438 NR 27 TC 11 Z9 11 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1056-263X J9 J DEV PHYS DISABIL JI J. Dev. Phys. Disabil. PD JUN PY 2003 VL 15 IS 2 BP 155 EP 163 DI 10.1023/A:1022827417414 PG 9 WC Rehabilitation SC Rehabilitation GA 654PL UT WOS:000181505200005 ER PT J AU Jones, RSP Quigney, C Huws, JC AF Jones, RSP Quigney, C Huws, JC TI First-hand accounts of sensory perceptual experiences in autism: a qualitative analysis SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article ID INFANTILE-AUTISM; SCHIZOPHRENIA; CHILDREN; LIFE AB Five first-hand web page accounts of unusual sensory perceptual experiences written by persons who claimed to have high-functioning autism were selected,for qualitative analysis. Four core categories emerged, turbulent sensory perceptual experiences, coping mechanisms, enjoyable sensory perceptual experiences, and awareness of being different, suggesting that people with autism experience both distress and enjoyment from their sensory perceptual experiences. The use of specific coping mechanisms enabled the person to deal with the distress or difficulties experienced and helped the person derive some enjoyment from the experience. Some of these people were aware that their sensory perceptual experiences were different from non-autistic individuals, but this did not decrease the enjoyment derived from some of their sensory perceptual experiences. These sensory perceptual experiences form an integral part of the individual's biographical embodied sense of self, and probably of autism. C1 Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. RP Jones, RSP (reprint author), Univ Wales, Sch Psychol, Brigantia Bldg,Penrallt Rd, Bangor LL57 2AS, Gwynedd, Wales. RI Huws, Jaci/C-3289-2009 CR ATTWOOD F, 1998, ASPERGERS SYNDROME G Boutros NN, 1999, PSYCHIAT RES, V88, P119, DOI 10.1016/S0165-1781(99)00074-8 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 DeMeyer M. 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M., 1978, COGNITIVE DEFECTS DE, P24 ORNITZ EM, 1977, J AUTISM CHILD SCHIZ, V7, P207, DOI 10.1007/BF01538999 PRAGER S, 1993, SCHIZOPHRENIA BULL, V19, P755 Rabinowicz EF, 2000, ARCH GEN PSYCHIAT, V57, P1149, DOI 10.1001/archpsyc.57.12.1149 SILBERMAN EK, 1985, BRIT J PSYCHIAT, V146, P81, DOI 10.1192/bjp.146.1.81 Singer Judy, 1999, DISABILITY DISCOURSE, V1999, P59 Strauss A., 1990, BASICS QUALITATIVE R VOLKMAR FR, 1986, J AM ACAD CHILD PSY, V25, P190, DOI 10.1016/S0002-7138(09)60226-0 Williams D, 1996, AUTISM INSIDE OUT AP WING L, 1969, J CHILD PSYCHOL PSYC, V10, P1, DOI 10.1111/j.1469-7610.1969.tb02066.x NR 20 TC 35 Z9 35 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD JUN PY 2003 VL 28 IS 2 BP 112 EP 121 DI 10.1080/1366825031000147058 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 703FL UT WOS:000184269300002 ER PT J AU Richdale, AL AF Richdale, AL TI A descriptive analysis of sleep behaviour in children with Fragile X SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article; Proceedings Paper CT 36th Annual Conference of the Australian-Society-for-the-Study-of-Intellectual-Disability CY NOV, 2001 CL MELBOURNE, AUSTRALIA SP Australian Soc Study Intellectual Disabil ID SEVERE LEARNING-DISABILITIES; MENTAL-RETARDATION; YOUNG BOYS; DISTURBANCE; DISORDERS; PATTERNS; AUTISM AB The current paper reports on the sleep of 13 children aged 3-19 years with Fragile X (FraX). Their parents completed a sleep questionnaire, the Developmental Behaviour Checklist and the Parenting Hassles Scale. The parents of four children (31%) reported a current sleep problem, which held been present for more than 2 years in three cases. A further six children also exhibited various problematic sleep behaviours on the questionnaire. Parental reporting of a sleep problem was associated with more severe child psychopathology and parental stress. The findings suggest that sleep difficulties are relatively, common in FraX, are similar to those found in other children with an intellectual disability, may, be long term, and are related to clinically significant behavioural difficulties and parental stress. It is concluded that the parents' perceptions of problematic sleep and the impact on daytime behaviour and parental stress are important considerations for future research and clinical intervention. C1 RMIT Univ, Dept Psychol & Disabil Studies, Bundoora, Vic 3083, Australia. RP Richdale, AL (reprint author), RMIT Univ, Dept Psychol & Disabil Studies, POB 71, Bundoora, Vic 3083, Australia. CR ARMSTRONG KL, 1994, MED J AUSTRALIA, V161, P202 Bailey DB, 1998, J AUTISM DEV DISORD, V28, P499 BATSHAW ML, 1997, CHILDREN DISABILITIE, P377 Bramble D, 1996, CHILD CARE HLTH DEV, V22, P355, DOI 10.1046/j.1365-2214.1996.810810.x CRONISTER A, 1991, AM J MED GENET, V38, P503, DOI 10.1002/ajmg.1320380272 Didden R, 1998, J BEHAV THER EXP PSY, V29, P85, DOI 10.1016/S0005-7916(97)00038-4 Einfeld S. 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Intellect. Dev. Dis. PD JUN PY 2003 VL 28 IS 2 BP 135 EP 144 DI 10.1080/1366825031000147076 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 703FL UT WOS:000184269300004 ER PT J AU Alessi, NE AF Alessi, NE TI Ziprasidone in autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 Univ Michigan, Med Ctr, Dept Psychiat, Div Child & Adolescent Psychiat, Ann Arbor, MI 48109 USA. RP Alessi, NE (reprint author), Univ Michigan, Med Ctr, Dept Psychiat, Div Child & Adolescent Psychiat, Ann Arbor, MI 48109 USA. CR Citrome L, 2002, HARVARD REV PSYCHIAT, V10, P280, DOI 10.1093/hrp/10.5.280 KECK P, IN PRESS AM J PSYCHI Keck PE, 2001, J CLIN PSYCHOPHARM, V21, P27, DOI 10.1097/00004714-200102000-00007 McDougle CJ, 2002, J AM ACAD CHILD PSY, V41, P921, DOI 10.1097/00004583-200208000-00010 NR 4 TC 1 Z9 1 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 JUN PY 2003 VL 42 IS 6 BP 622 EP 623 DI 10.1097/01.CH1.0000046853.56865.10 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 681DQ UT WOS:000183022000003 PM 12921465 ER PT J AU Seeman, C AF Seeman, C TI Siblings of children with autism: A guide for families, 2d edition. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo, Lib, Toledo, OH 43606 USA. RP Seeman, C (reprint author), Univ Toledo, Lib, 2801 W Bancroft St, Toledo, OH 43606 USA. CR Harris S. L., 2003, SIBLINGS CHILDREN AU 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 JUN 1 PY 2003 VL 128 IS 10 BP 148 EP + PG 2 WC Information Science & Library Science SC Information Science & Library Science GA 685WX UT WOS:000183288100151 ER PT J AU Guerrero, APS Derauf, DC Nguyen, MAK AF Guerrero, APS Derauf, DC Nguyen, MAK TI Early detection and intervention for common causes of psychosocial morbidity and mortality in children and adolescents SO PEDIATRIC ANNALS LA English DT Article ID DEPRESSION; AUTISM; MANAGEMENT; PREVENTION; MANIA C1 Univ Hawaii Manoa, Dept Psychiat, Honolulu, HI 96813 USA. Univ Hawaii Manoa, Dept Pediat, Honolulu, HI 96813 USA. RP Guerrero, APS (reprint author), Univ Hawaii Manoa, Dept Psychiat, 1356 Lusitana St,4th Floor, Honolulu, HI 96813 USA. CR *AM AC CHILD AD PS, 1997, J AM ACAD CHILD PSY, V36, pS157 *AM AC CHILD AD PS, 2000, AACAP WORK FORC DAT Perrin JM, 2001, PEDIATRICS, V108, P1033 Homer CJ, 2000, PEDIATRICS, V105, P1158 Hagan JF, 2001, PEDIATRICS, V108, P1227 Spivak H, 1999, PEDIATRICS, V103, P173 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Barbaresi W, 2002, ARCH PEDIAT ADOL MED, V156, P217 Barkley RA, 1998, SCI AM, V279, P66 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Biederman J, 1999, PEDIATRICS, V104, part. no., DOI 10.1542/peds.104.2.e20 Biederman J, 1999, J AM ACAD CHILD PSY, V38, P468, DOI 10.1097/00004583-199904000-00021 *COMM PREV YOUTH V, 2000, YOUTH VIOL MED NURS Emslie GJ, 1997, ARCH GEN PSYCHIAT, V54, P1031 Filipek PA, 2000, NEUROLOGY, V55, P468 FRISTAD MA, 1992, J AM ACAD CHILD PSY, V31, P252, DOI 10.1097/00004583-199203000-00011 Galler JR, 1999, J DEV BEHAV PEDIATR, V20, P80, DOI 10.1097/00004703-199904000-00002 GISE LH, 1993, MED PSYCHIAT PRACTIC, V2, P246 Goodman SH, 1999, PSYCHOL REV, V106, P458, DOI 10.1037/0033-295X.106.3.458 HAGGERTY RJ, 1993, CHILD HLTH COMMUNITY, P94 HAMILTON JD, 2000, AACAP NEWS NOV, V31, P260 Jensen PS, 1999, J AM ACAD CHILD PSY, V38, P797, DOI 10.1097/00004583-199907000-00008 Kazdin AE, 1997, J AM ACAD CHILD PSY, V36, P1349, DOI 10.1097/00004583-199710000-00016 KOVACS M, 1985, PSYCHOPHARMACOL BULL, V21, P995 MacDorman MF, 2002, PEDIATRICS, V110, P1037, DOI 10.1542/peds.110.6.1037 McLennan JD, 2000, PEDIATRICS, V105, P1090, DOI 10.1542/peds.105.5.1090 Jensen PS, 1999, ARCH GEN PSYCHIAT, V56, P1073 *NICHD EARL CHILD, 1998, CHRON MAT DEPR SYMPT RADLOFF L S, 1977, Applied Psychological Measurement, V1, P385, DOI 10.1177/014662167700100306 Straus MA, 1997, ARCH PEDIAT ADOL MED, V151, P761 Weinberg MK, 1998, J CLIN PSYCHIAT, V59, P53 Zametkin AJ, 2001, JAMA-J AM MED ASSOC, V286, P3120, DOI 10.1001/jama.286.24.3120 NR 32 TC 0 Z9 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0090-4481 J9 PEDIATR ANN JI Pediatr. Annu. PD JUN PY 2003 VL 32 IS 6 BP 408 EP 412 PG 5 WC Pediatrics SC Pediatrics GA 687PH UT WOS:000183385300007 PM 12846019 ER PT J AU Bernabel, P Fenton, G Fabrizi, A Camaioni, L Perucchini, P AF Bernabel, P Fenton, G Fabrizi, A Camaioni, L Perucchini, P TI Profiles of sensorimotor development in children with autism and with developmental delay SO PERCEPTUAL AND MOTOR SKILLS LA English DT Article ID COMMUNICATION; LANGUAGE; INFANCY; IMPAIRMENTS; SCALES AB Aim of the study was (1) to evaluate sensorimotor development of children with autism in comparison with that of children with developmental delay, (2) to verify the possible unevenness of the developmental profiles through correlations amongst domains and between domains and chronological age. 46 children with autism were compared with 45 children with developmental delay. Mean chronological age was 3.7 yr. in children with autism and 3.6 yr. in children with mental retardation. Mean mental age was 1.3 yr. in children with autism and 1.1 yr. in children with developmental delay. Ordinal scales of Uzgiris-Hunt show that the two groups score significantly differently on the scales of Object Permanence, Means-Ends, Operational Causality, and Spatial Relations and that scores were higher for the children with autism. The comparison made between the developmental levels of each group indicate that the sensorimotor profile in children with developmental delay is fairly homogeneous, while it appears uneven in autistic children, for whom Object Permanence appears to be the most advanced skill, Verbal and Gestural Imitation and Schemes for Relating to Objects the lowest. The results are in keeping with the assumption that the pivotal defect of autism is a deficit in social interactive skills. C1 Univ Roma La Sapienza, Dept Childhood Neurol & Psychiat Sci, Rome, Italy. Univ Roma La Sapienza, Dept Dev & Social Psychol, Rome, Italy. 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Mot. Skills PD JUN PY 2003 VL 96 IS 3 BP 1107 EP 1116 DI 10.2466/PMS.96.4.1107-1116 PN 2 PG 10 WC Psychology, Experimental SC Psychology GA 701KY UT WOS:000184167800007 PM 12929762 ER PT J AU Etscheidt, S AF Etscheidt, S TI An analysis of legal hearings and cases related to individualized education programs for children with autism SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE autism; Individualized Education Programs (IEP); legal analysis ID SPECTRUM DISORDERS; EARLY INTERVENTION; YOUNG-CHILDREN; ISSUES AB Developing appropriate programs for students with autism has been an increasingly complex task for parents, schools, and other stakeholders. Parents of students with autism have challenged the appropriateness of proposed school district programs, and these disputes represent the fastest growing and most expensive area of litigation in special education. In this article, 68 hearings and cases were reviewed. The article discusses the outcomes of administrative and judicial decisions related to appropriate programs for children with autism. Three primary factors were identified: individualized education program (IEP) goals must be matched to evaluation data, IEP team members must be qualified to develop programs, and the methodology selected must be able to assist the students in achieving identified IEP goals. Implications for school teams are discussed. C1 Univ No Iowa, Cedar Falls, IA 50614 USA. RP Etscheidt, S (reprint author), Univ No Iowa, 655 Schindler Educ Ctr, Cedar Falls, IA 50614 USA. EM etscheidt@uni.edu CR Anderson SR, 1999, J ASSOC PERS SEVERE, V24, P162, DOI 10.2511/rpsd.24.3.162 Baird M. 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PD SUM PY 2003 VL 28 IS 2 BP 51 EP 69 DI 10.2511/rpsd.28.2.51 PG 19 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BP UT WOS:000222242500001 ER PT J AU Snell, ME Caves, K McLean, L Mollica, BM Mirenda, P Paul-Brown, D Romski, MA Rourk, J Sevcik, R Yoder, D AF Snell, ME Caves, K McLean, L Mollica, BM Mirenda, P Paul-Brown, D Romski, MA Rourk, J Sevcik, R Yoder, D TI Concerns regarding the application of restrictive "eligibility" policies to individuals who need communication services and supports: A response by the National Joint Committee for the Communication Needs of Persons with Severe Disabilities SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE communication; eligibility for services; legal issues; school policies; severe disabilities; autism ID CHILDREN; RETARDATION; SYSTEM; SPEECH AB Sometimes communication supports and services for school-aged children with extensive disabilities are reduced over time or removed on the basis of inappropriate reasons or eligibility criteria that are flawed. Family members may feel unequipped to argue against the decisions that schools or agencies make for their child, and professionals may be in a difficult position to disagree with their administrators. The National Joint Committee for the Communication Needs of Persons with Severe Disabilities has written a position statement on these restrictive eligibility practices. This position statement addresses concerns about inappropriate eligibility criteria and may be used to help individuals, family members, and providers gain access to necessary communication supports and services. C1 Univ Virginia, Curry Sch Educ, Charlottesville, VA 22904 USA. Duke Univ, Durham, NC 27706 USA. Univ N Carolina, Chapel Hill, NC USA. Univ Delaware, Newark, DE 19716 USA. Univ British Columbia, Vancouver, BC V5Z 1M9, Canada. Georgia State Univ, Atlanta, GA 30303 USA. RP Snell, ME (reprint author), Univ Virginia, Curry Sch Educ, 405 Emmet St S,POB 400273, Charlottesville, VA 22904 USA. 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PD SUM PY 2003 VL 28 IS 2 BP 70 EP 78 DI 10.2511/rpsd.28.2.70 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BP UT WOS:000222242500002 ER PT J AU Grasso, AC De Rinaldis, M Matricardi, M Brinciotti, M AF Grasso, AC De Rinaldis, M Matricardi, M Brinciotti, M TI Cortical and subtentorial dysfunction in tuberous sclerosis - The role of evoked potentials SO RIVISTA DI NEURORADIOLOGIA LA Italian DT Article; Proceedings Paper CT 6th National Congress of Pediatric Neuroradiology CY NOV 22-24, 2002 CL BOLOGNA, ITALY DE tuberous sclerosis; evoked potentials ID AUTISM AB Visual evoked potentials (VEP) and brain stem acoustic evoked potentials (BAEP) were studied in eight children with tuberous sclerosis (four boys and four girls, average age 4.5 years) comparing them with a control group of 21 healthy children (ten boys and 11 girls). The patients had an increased average latency of VEP (IV component or P2; p < .01694) and BAEP (right V wave = p < .001145; left V wave = p < 013792; right I-V interpeak = p < .000543; left I-V interpeak = p < .009854). Impaired responses were common in both VEP (80%) and BAEP (85%). In addition, altered BAEP were also present in patients without subtentorial structural abnormalities. Evoked potentials serve as a sensitive test for early diagnosis of tuberous sclerosis. C1 Univ Roma La Sapienza, Dipartimento Sci Neurol & Psichiat Eta Evolut, I-00185 Rome, Italy. RP Brinciotti, M (reprint author), Univ Roma La Sapienza, Dipartimento Sci Neurol & Psichiat Eta Evolut, Via DCI Sabelli 108, I-00185 Rome, Italy. CR *AM EL SOC, 1994, J CLIN NEUROPHYSIOL, V1, P3 Asano E, 2001, NEUROLOGY, V57, P1269 FERRI R, 1993, ITAL J NEUROL SCI, V14, P311, DOI 10.1007/BF02339297 Jay V, 1998, ULTRASTRUCT PATHOL, V22, P331 Marti-Bonmati L, 2000, AM J NEURORADIOL, V21, P557 Roach ES, 1999, J CHILD NEUROL, V14, P401, DOI 10.1177/088307389901400610 Sener RN, 1998, COMPUT MED IMAG GRAP, V22, P63, DOI 10.1016/S0895-6111(97)00042-6 Seri S, 1999, CLIN NEUROPHYSIOL, V110, P1825, DOI 10.1016/S1388-2457(99)00137-6 Stufflebeam Steven M., 2000, Journal of Basic and Clinical Physiology and Pharmacology, V11, P231 NR 9 TC 0 Z9 0 PU EDIZIONI CENTAURO PI BOLOGNA PA VIA DEL PRATELLO, 8, 40122 BOLOGNA, ITALY SN 1120-9976 J9 RIV NEURORADIOL JI Riv. Neuroradiol. PD JUN PY 2003 VL 16 IS 3 BP 489 EP 491 PG 3 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 736NT UT WOS:000186177400030 ER PT J AU Brinciotti, M AF Brinciotti, M TI The use of evoked potentials in tuberous sclerosis SO RIVISTA DI NEURORADIOLOGIA LA Italian DT Article; Proceedings Paper CT 6th National Congress of Pediatric Neuroradiology CY NOV 22-24, 2002 CL BOLOGNA, ITALY DE tuberous sclerosis; evolved potentials; visual evolved potentials brain stem auditory evolved potentials; somatosensory evolved potentials ID AUTISM; COMA AB Evoked potentials (EP) allow the assessment of the functional Integrity and degree of maturation of the main pathways of sensory afference (visual, acoustic and somaesthetic). For this reason, EP can be used in the study of patients with tuberous sclerosis. In clinical practice, EP serve to give information for early diagnosis and a better prognostic assessment of the individual patient. A recent analysis of visual evoked potentials (VEP) and brain stem acoustic evoked potentiials (BAEP) in children with tuberous sclerosis disclosed an increased average latency of sonic components of both VEP (component IV or P2) and BAEP (V wave and I-V interpeak). Impaired responses were present in 80% of VEP and 85% of BAEP In addition, impaired BAEP were also present in patients without subtentorial structural abnormalities. EP serve as a useful instrument for early diagnosis of tuberous sclerosis. Given the anatomofunctional differences of the systems stimulated and the preferential location of lesions in certain areas, the various different EP have varying degrees of sensitivity in disclosing abnormalities: visual and brain stem acoustic EP are more sensitive than somatosensory EP. C1 Univ Roma La Sapienza, Dipartimento Sci Neurol & Psichiat Eta Evolut, I-00185 Rome, Italy. RP Brinciotti, M (reprint author), Univ Roma La Sapienza, Dipartimento Sci Neurol & Psichiat Eta Evolut, Via Sabelli 108, I-00185 Rome, Italy. 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Neuroradiol. PD JUN PY 2003 VL 16 IS 3 BP 543 EP 545 PG 3 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 736NT UT WOS:000186177400042 ER PT J AU Finegold, SM Vaisanen, ML Molitoris, DR Tomzynski, TJ Song, Y Liu, C Collins, MD Lawson, PA AF Finegold, SM Vaisanen, ML Molitoris, DR Tomzynski, TJ Song, Y Liu, C Collins, MD Lawson, PA TI Cetobacterium somerae sp nov from human feces and emended description of the genus Cetobacterium SO SYSTEMATIC AND APPLIED MICROBIOLOGY LA English DT Article DE Cetobacterium somerae sp nov.; feces; autism; 16S rRNA; phylogeny; taxonomy AB Phenotypic and phylogenetic studies were performed on four isolates of an unidentified gram-negative, microaerotolerant, non-spore-forming, rod-shaped bacterium isolated from the feces of children. The unknown organism was bile resistant and produced acetic acid as the major end product of metabolism of peptides and carbohydrates. It possessed a low DNA G + C content of 31 mol %. Comparative 16S rRNA gene sequencing demonstrated that the four isolates were phylogenetically identical (100% 16S rRNA sequence similarity) and represent a hitherto unknown sub-line within the genus Cetobacterium. The novel bacterium displayed approximately 5% sequence divergence with Cetobacterium ceti, and can be readily distinguished from the latter by physiological and biochemical criteria. Based on phylogenetic and phenotypic evidence, it is proposed that the unknown fecal bacterium be classified in the genus Cetobacterium, as Cetobacterium somerae sp. nov. The proposed type strain of Cetobacterium somerae is WAL 14325(T) (ATCC BAA-474(T) = CCUG 46254T). C1 VA Med Ctr WLA, Infect Dis Sect, Los Angeles, CA 90073 USA. Vet Adm Med Ctr, Res Serv, Los Angeles, CA 91343 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. Univ Reading, Sch Food Biosci, Reading RG6 2AH, Berks, England. RP Finegold, SM (reprint author), VA Med Ctr WLA, Infect Dis Sect, 111 F,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. RI Lawson, Paul/E-3760-2012 CR Felsenstein J., 1989, CLADISTICS, V5, P164, DOI DOI 10.1111/J.1096-0031.1989.TB00562.X FOSTER G, 1995, LETT APPL MICROBIOL, V21, P202, DOI 10.1111/j.1472-765X.1995.tb01041.x LIPMAN DJ, 1985, SCIENCE, V227, P1435, DOI 10.1126/science.2983426 MESBAH M, 1989, INT J SYST BACTERIOL, V39, P159 MOORE LVH, 1994, INT J SYST BACTERIOL, V44, P338 Nicholas KB, 1997, EMBNEW NEWS, V4, P14 Page RDM, 1996, COMPUT APPL BIOSCI, V12, P357 Rasmussen S.W., 1995, DNATOOLS SOFTWARE PA Sandler RH, 2000, J CHILD NEUROL, V15, P429, DOI 10.1177/088307380001500701 Summanen P., 1993, WADSWORTH ANAEROBIC, Vfifth Wexler HM, 1996, INT J SYST BACTERIOL, V46, P252 NR 11 TC 13 Z9 14 PU URBAN & FISCHER VERLAG PI JENA PA BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY SN 0723-2020 J9 SYST APPL MICROBIOL JI Syst. Appl. Microbiol. PD JUN PY 2003 VL 26 IS 2 BP 177 EP 181 DI 10.1078/072320203322346010 PG 5 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA 701GV UT WOS:000184160600004 PM 12866843 ER PT J AU Mahoney, G Perales, F AF Mahoney, G Perales, F TI Using relationship-focused intervention to enhance the social-emotional functioning of young children with autism spectrum disorders SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID INFANT ATTACHMENT; IRRITABLE INFANTS; 2ND YEAR; RESPONSIVENESS; LANGUAGE; BEHAVIOR; MOTHERS; PLAY; SOCIALIZATION; SENSITIVITY AB This study investigates the effectiveness of relationship-focused intervention on the social and emotional well-being of children with autism spectrum disorders. Relationship-focused intervention is a general approach to developmental intervention that encourages and supports parents to enhance their use of responsive interactive strategies during routine interactions with their children. The sample for this study consisted of 20 young children diagnosed with autism or pervasive developmental disorder and their parents. Parents and children received weekly intervention sessions for 8 to 14 months. These sessions focused on encouraging parents to use a Responsive Teaching curriculum to promote children's socioemotional development. Comparisons of pre- and postassessments indicated that the intervention was successful at encouraging mothers to engage in more responsive interactions with their children. Increases in mothers' responsiveness were associated with significant improvements in children's social interaction, as well as in standardized measures of their social-emotional functioning. 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PD SUM PY 2003 VL 23 IS 2 BP 77 EP 89 PG 13 WC Education, Special SC Education & Educational Research GA 700RY UT WOS:000184126000003 ER PT J AU Nabi, R Zhong, H Serajee, FJ Huq, AM AF Nabi, R Zhong, H Serajee, FJ Huq, AM TI No association between single nucleotide polymorphisms in DLX6 and Piccolo genes at 7q21-q22 and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE forebrain development; homeobox; presynaptic matrix protein; quantitative traits ID LINKAGE ANALYSIS; TWIN; FAMILIES; DISORDER; ETIOLOGY; TRAITS; PAIRS AB Several independent genome scans have revealed excess allele sharing in an overlapping 40 cM region of 7q21-34 in autism. DLX6 and Piccolo (PCLO) at 7q21-q22 are two positional and functional candidate genes in autism. We have investigated a single nucleotide polymorphism (SNP) in exon 4 of the PCLO gene and a SNP in intron 1 of the DLX6 gene for linkage and association in autistic disorder using both qualitative and quantitative analyses. One hundred ninety-six multiplex autistic disorder families were tested using transmission disequilibrium. and two-point affected sib pair linkage analysis. We found no evidence of association or linkage with the two intragenic markers. In addition, there was also no linkage or association between language and stereotypic behavior quantitative traits in autism and the SNPs. In conclusion, our studies suggest that these two SNPs in DLX6 and PCLO genes are not in linkage disequilibrium with autism. (C) 2003 Wiley-Liss, Inc. C1 Childrens Hosp Michigan, Div Neurol, Detroit, MI 48201 USA. Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA. Wayne State Univ, Dept Neurol, Detroit, MI USA. RP Huq, AM (reprint author), Childrens Hosp Michigan, Div Neurol, 3901 Beaubien Blvd, Detroit, MI 48201 USA. 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J. Med. Genet. B PD MAY 15 PY 2003 VL 119B IS 1 BP 98 EP 101 DI 10.1002/ajmg.b.10012 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 672XF UT WOS:000182548100018 PM 12707945 ER PT J AU Zappella, M Meloni, I Longo, I Canitano, R Hayek, G Rosaia, L Mari, F Renieri, A AF Zappella, M Meloni, I Longo, I Canitano, R Hayek, G Rosaia, L Mari, F Renieri, A TI Study of MECP2 gene in Rett syndrome variants and autistic girls SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE RTT; PSV; preserved speech variant; mild mental retardation ID X-CHROMOSOME INACTIVATION; PRESERVED SPEECH VARIANT; HAND USE; MUTATIONS AB Mutations in MECP2 gene account for approximately 80% of cases of Rett syndrome (WIT), an X-linked severe developmental disorder affecting young girls, as well as for most cases of Preserved Speech Variant (PSV), a mild RTT variant in which autistic behavior is common. The aim of this study is to determine whether MECP2 mutations are responsible for PSV only or may cause other forms of autistic disorders. We screened for mutations by SSCP 19 girls with a clinical diagnosis of autism, two of them fulfilling the PSV criteria. A pathogenic mutation was found only in the latter two cases (R133C and R453X). A long follow-up of these two girls revealed a unique clinical course. They initially developed the first three stages of RTT, they were severely retarded and had autistic behavior. Over the years their abilities increased progressively and by early adolescence they lost autistic behavior, becoming adequately accustomed to people and reaching an IQ close to 45. These results confirm previous clinical studies suggesting that a wide spectrum of RTT exists including girls with mental abilities considerably higher than in classic RTT. We conclude that MECP2 mutations (missense or late truncating) can be found in girls with an IQ close to 45 and a clinical history of PSV of Rett syndrome. Furthermore, MECP2 mutations are not found in patients in which autism remains stable over the years. (C) 2003 Wiley-Liss, Inc. C1 Univ Siena, Dept Biol Mol, I-53100 Siena, Italy. Azienda Osped Senese, Dept Child Neuropsychiat, Siena, Italy. Ist Giannina Gaslini, I-16148 Genoa, Italy. RP Renieri, A (reprint author), Univ Siena, Dept Biol Mol, Viale Bracci 2, I-53100 Siena, Italy. 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PD MAY 3 PY 2003 VL 178 IS 2393 BP 10 EP 10 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 675VA UT WOS:000182715800008 ER PT J AU Scherer, SW Cheung, J MacDonald, JR Osborne, LR Nakabayashi, K Herbrick, JA Carson, AR Parker-Katiraee, L Skaug, J Khaja, R Zhang, JJ Hudek, AK Li, M Haddad, M Duggan, GE Fernandez, BA Kanematsu, E Gentles, S Christopoulos, CC Choufani, S Kwasnicka, D Zheng, XQH Lai, ZW Nusskern, D Zhang, Q Gu, ZP Lu, F Zeesman, S Nowaczyk, MJ Teshima, I Chitayat, D Shuman, C Weksberg, R Zackai, EH Grebe, TA Cox, SR Kirkpatrick, SJ Rahman, N Friedman, JM Heng, HHQ Pelicci, PG Lo-Coco, F Belloni, E Shaffer, LG Pober, B Morton, CC Gusella, JF Bruns, GAP Korf, BR Quade, BJ Ligon, AH Ferguson, H Higgins, AW Leach, NT Herrick, SR Lemyre, E Farra, CG Kim, HG Summers, AM Gripp, KW Roberts, W Szatmari, P Winsor, EJT Grzeschik, KH Teebi, A Minassian, BA Kere, J Armengol, L Pujana, MA Estivill, X Wilson, MD Koop, BF Tosi, S Moore, GE Boright, AP Zlotorynski, E Kerem, B Kroisel, PM Petek, E Oscier, DG Mould, SJ Dohner, H Dohner, K Rommens, JM Vincent, JB Venter, JC Li, PW Mural, RJ Adams, MD Tsui, LC AF Scherer, SW Cheung, J MacDonald, JR Osborne, LR Nakabayashi, K Herbrick, JA Carson, AR Parker-Katiraee, L Skaug, J Khaja, R Zhang, JJ Hudek, AK Li, M Haddad, M Duggan, GE Fernandez, BA Kanematsu, E Gentles, S Christopoulos, CC Choufani, S Kwasnicka, D Zheng, XQH Lai, ZW Nusskern, D Zhang, Q Gu, ZP Lu, F Zeesman, S Nowaczyk, MJ Teshima, I Chitayat, D Shuman, C Weksberg, R Zackai, EH Grebe, TA Cox, SR Kirkpatrick, SJ Rahman, N Friedman, JM Heng, HHQ Pelicci, PG Lo-Coco, F Belloni, E Shaffer, LG Pober, B Morton, CC Gusella, JF Bruns, GAP Korf, BR Quade, BJ Ligon, AH Ferguson, H Higgins, AW Leach, NT Herrick, SR Lemyre, E Farra, CG Kim, HG Summers, AM Gripp, KW Roberts, W Szatmari, P Winsor, EJT Grzeschik, KH Teebi, A Minassian, BA Kere, J Armengol, L Pujana, MA Estivill, X Wilson, MD Koop, BF Tosi, S Moore, GE Boright, AP Zlotorynski, E Kerem, B Kroisel, PM Petek, E Oscier, DG Mould, SJ Dohner, H Dohner, K Rommens, JM Vincent, JB Venter, JC Li, PW Mural, RJ Adams, MD Tsui, LC TI Human chromosome 7: DNA sequence and biology SO SCIENCE LA English DT Article ID HUMAN GENOME; SEGMENTAL DUPLICATIONS; LANGUAGE DISORDER; REGION; MAP; LOCALIZATION; SPEECH; GENES; MODEL AB DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. 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Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. RP McCormick, MC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Maternal & Child Hlth, 677 Huntington Ave, Boston, MA 02115 USA. 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Pediatr. PD MAY-JUN PY 2003 VL 3 IS 3 BP 119 EP 120 DI 10.1367/1539-4409(2003)003<0119:TAEIFT>2.0.CO;2 PG 2 WC Pediatrics SC Pediatrics GA 675GK UT WOS:000182685400004 PM 12708887 ER PT J AU Bakker, SC van der Meulen, EM Buitelaar, JK Sandkuijl, LA Pauls, DL Monsuur, AJ van't Slot, R Minderaa, RB Gunning, WB Pearson, PL Sinke, RJ AF Bakker, SC van der Meulen, EM Buitelaar, JK Sandkuijl, LA Pauls, DL Monsuur, AJ van't Slot, R Minderaa, RB Gunning, WB Pearson, PL Sinke, RJ TI A whole-genome scan in 164 Dutch sib pairs with attention-deficit/hyperactivity disorder: Suggestive evidence for linkage on chromosomes 7p and 15q SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; DOPAMINE TRANSPORTER GENE; AUTISTIC DISORDER; RECEPTOR GENE; SUSCEPTIBILITY LOCI; READING-DISABILITY; BETA-HYDROXYLASE; ASSOCIATION; CHILDREN; ADHD AB A genome scan was performed on 164 Dutch affected sib pairs (ASPs) with attention-deficit/hyperactivity disorder (ADHD). All subjects were white and of Dutch descent and were phenotyped according to criteria set out in the Diagnostic and Statistical Manual Of Mental Disorders, 4th edition. Initially, a narrow phenotype was defined, in which all the sib pairs met the full ADHD criteria (117 ASPs). In a broad phenotype, additional sib pairs were included, in which one child had an autistic-spectrum disorder but also met the full ADHD criteria (164 ASPs). A set of 402 polymorphic microsatellite markers with an average intermarker distance of 10 cM was genotyped and analyzed using the Mapmaker/sibs program. Regions with multipoint maximum likelihood scores (MLSs) >11.5 in both phenotypes were fine mapped with additional markers. This genome scan indicated several regions of interest, two of which showed suggestive evidence for linkage. The most promising chromosome region was located at 15q, with an MLS of 3.54 under the broad phenotype definition. This region was previously implicated in reading disability and autism. In addition, MLSs of 3.04 and 2.05 were found for chromosome regions 7p and 9q in the narrow phenotype. Except for a region on chromosome 5, no overlap was found with regions mentioned in the only other independent genome scan in ADHD reported to date. C1 Univ Med Ctr, Dept Med Genet, NL-3508 AB Utrecht, Netherlands. Univ Med Ctr, Dept Child & Adolescent Psychiat, NL-3508 AB Utrecht, Netherlands. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Psychiat & Neurodev Genet Unit, Boston, MA USA. Univ Groningen, Univ Med Ctr Groningen, Univ Ctr Child & Adolescent Psychiat, Groningen, Netherlands. Univ Amsterdam, Acad Med Ctr, Dept Child & Adolescent Psychiat, NL-1105 AZ Amsterdam, Netherlands. Leiden Univ, Dept Med Stat, Med Ctr, NL-2300 RA Leiden, Netherlands. Univ Med Ctr Nijmegen, Dept Psychiat, Nijmegen, Netherlands. RP Bakker, SC (reprint author), Univ Med Ctr, Dept Med Genet, KC 04-084-2,POB 85090, NL-3508 AB Utrecht, Netherlands. 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As part of an ongoing study of the genetic etiology of ADHD, we have performed a genomewide linkage scan in 204 nuclear families comprising 853 individuals and 270 affected sibling pairs (ASPs). Previously, we reported genomewide linkage analysis of a "first wave" of these families composed of 126 ASPs. A follow-up investigation of one region on 16p yielded significant linkage in an extended sample. The current study extends the original sample of 126 ASPs to 270 ASPs and provides linkage analyses of the entire sample, using polymorphic microsatellite markers that define an similar to10-cM map across the genome. Maximum LOD score (MLS) analysis identified suggestive linkage for 17p11 () and four nominal regions with MLS values >1.0, including 5p13, 6q14, 11q25, and 20q13. These MLS = 2.98 data, taken together with the fine mapping on 16p13, suggest two regions as highly likely to harbor risk genes for ADHD: 16p13 and 17p11. 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PD MAY PY 2003 VL 108 IS 3 BP 149 EP 160 DI 10.1352/0895-8017(2003)108<0149:RLSOAA>2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 671YC UT WOS:000182492000001 PM 12691594 ER PT J AU Bursztejn, C Baghdadli, A Lazartigues, A Philippe, A Sibertin-Blanc, D AF Bursztejn, C Baghdadli, A Lazartigues, A Philippe, A Sibertin-Blanc, D TI Towards an early screening of autism SO ARCHIVES DE PEDIATRIE LA French DT Article; Proceedings Paper CT National Congress of the Societe-Francaise-de-Pediatrie CY MAY 21-24, 2003 CL NANCY, FRANCE SP Soc Francaise Pediatrie C1 CHU Strasbourg, F-67091 Strasbourg, France. RP Bursztejn, C (reprint author), CHU Strasbourg, 1 Pl Hop, F-67091 Strasbourg, France. NR 0 TC 1 Z9 1 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0929-693X J9 ARCH PEDIATRIE JI Arch. Pediatr. PD MAY PY 2003 VL 10 SU 1 BP 129S EP 131S DI 10.1016/S0929-693X(03)90410-6 PG 3 WC Pediatrics SC Pediatrics GA 699AL UT WOS:000184033700053 PM 14509770 ER PT J AU Constantino, JN Todd, RD AF Constantino, JN Todd, RD TI Autistic traits in the general population - A twin study SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; RECIPROCAL SOCIAL-BEHAVIOR; FAMILY HISTORY; PHENOTYPE; SPECTRUM; CHILDREN; DOMAINS AB Background: Recent research has indicated that autism is not a discrete disorder and that family members of autistic probands have an increased likelihood of exhibiting autistic symptoms with a wide range of severity, often below the threshold for a diagnosis of an autism spectrum disorder. Objective: To examine the distribution and genetic structure of autistic traits in the general population using a newly established quantitative measure of autistic traits, the Social Responsiveness Scale (formerly known as the Social Reciprocity Scale). Methods: The sample consisted of 788 pairs of. twins aged 7 to 15 years, randomly selected from the pool of participants in a large epidemiologic study (the Missouri Twin Study). One parent of each pair of twins completed the Social Responsiveness Scale on each child. The data were subjected to structural equation modeling. Results: Autistic traits as measured by the Social Responsiveness Scale were continuously distributed and moderately to highly heritable. Levels of severity of autistic traits at or above the previously published mean for patients with pervasive developmental disorder not otherwise specified were found in 1.4% of boys and 0.3% of girls. Structural equation modeling revealed no evidence for the existence of sex-specific genetic influences, and suggested specific mechanisms by which females may be relatively protected from vulnerability to autistic traits. Conclusions: These data indicate that the social deficits characteristic of autism spectrum disorders are common. Given the continuous distribution of these traits, it may be arbitrary where cutoffs are made between research designations of being "affected" vs "unaffected" with a pervasive developmental disorder. The genes influencing autistic traits appear to be the same,for boys and girls. Lower prevalence (and severity) of autistic traits in girls may be the result of increased sensitivity to early environmental influences that operate to promote social competency. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, 660 S Euclid Ave,Campus Box 8134, St Louis, MO 63110 USA. CR Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 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 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 CONSTANTINO JN, IN PRESS J AUTISM DE Constantino JN, 2002, SOCIAL RESPONSIVENES CONSTANTINO JN, IN PRESS J AM ACAD C Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2000, J DEV BEHAV PEDIATR, V21, P2 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 Hudziak JJ, 2000, J AM ACAD CHILD PSY, V39, P469, DOI 10.1097/00004583-200004000-00016 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Neale M. C., 1992, METHODOLOGY GENETIC NEALE MC, 1999, MX STAT MODELING Piven J, 1997, AM J PSYCHIAT, V154, P185 Robertson JM, 1999, J AM ACAD CHILD PSY, V38, P738, DOI 10.1097/00004583-199906000-00022 Silverman JM, 2002, AM J MED GENET, V114, P64, DOI 10.1002/ajmg.10048 Skuse DH, 2000, PEDIATR RES, V47, P9, DOI 10.1203/00006450-200001000-00006 Spiker D, 2002, AM J MED GENET, V114, P129, DOI 10.1002/ajmg.10188 Volkmar FR, 1998, J AUTISM DEV DISORD, V28, P457, DOI 10.1023/A:1026012707581 Waterhouse L, 1996, J AUTISM DEV DISORD, V26, P59, DOI 10.1007/BF02276235 Wolff DJ, 1998, AM J MED GENET, V77, P401, DOI 10.1002/(SICI)1096-8628(19980605)77:5<401::AID-AJMG9>3.0.CO;2-P NR 24 TC 382 Z9 388 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAY PY 2003 VL 60 IS 5 BP 524 EP 530 DI 10.1001/archpsyc.60.5.524 PG 7 WC Psychiatry SC Psychiatry GA 676CU UT WOS:000182735000011 PM 12742874 ER PT J AU Herbert, MR Ziegler, DA Deutsch, CK O'Brien, LM Lange, N Bakardjiev, A Hodgson, J Adrien, KT Steele, S Makris, N Kennedy, D Harris, GJ Caviness, VS AF Herbert, MR Ziegler, DA Deutsch, CK O'Brien, LM Lange, N Bakardjiev, A Hodgson, J Adrien, KT Steele, S Makris, N Kennedy, D Harris, GJ Caviness, VS TI Dissociations of cerebral cortex, subcortical and cerebral white matter volumes in autistic boys SO BRAIN LA English DT Article DE autistic disorder; brain/growth and development; MRI; cerebral white matter; morphometry ID POSITRON-EMISSION-TOMOGRAPHY; NERVOUS-SYSTEM MYELINATION; BRAIN-DEVELOPMENT; INFANTILE-AUTISM; HEAD CIRCUMFERENCE; NEURODEVELOPMENTAL DAMAGE; POSTERIOR-FOSSA; HUMAN INFANCY; MRI; CHILDREN AB High-functioning autistic and normal school-age boys were compared using a whole-brain morphometric profile that includes both total brain volume and volumes of all major brain regions. We performed MRI-based morphometric analysis on the brains of 17 autistic and 15 control subjects, all male with normal intelligence, aged 7-11 years. Clinical neuroradiologists judged the brains of all subjects to be clinically normal. The entire brain was segmented into cerebrum, cerebellum, brainstem and ventricles. The cerebrum was subdivided into cerebral cortex, cerebral white matter, hippocampus-amygdala, caudate nucleus, globus pallidus plus putamen, and diencephalon (thalamus plus ventral diencephalon). Volumes were derived for each region and compared between groups both before and after adjustment for variation in total brain volume. Factor analysis was then used to group brain regions based on their intercorrelations. Volumes were significantly different between groups overall; and diencephalon, cerebral white matter, cerebellum and globus pallidus-putamen were significantly larger in the autistic group. Brain volumes were not significantly different overall after adjustment for total brain size, but this analysis approached significance and effect sizes and univariate comparisons remained notable for three regions, although not all in the same direction: cerebral white matter showed a trend towards being disproportionately larger in autistic boys, while cerebral cortex and hippocampus-amygdala showed trends toward being disproportionately smaller. Factor analysis of all brain region volumes yielded three factors, with central white matter grouping alone, and with cerebral cortex and hippocampus-amygdala grouping separately from other grey matter regions. This morphometric profile of the autistic brain suggests that there is an overall increase in brain volumes compared with controls. Additionally, results suggest that there may be differential effects driving white matter to be larger and cerebral cortex and hippocampus-amygdala to be relatively smaller in the autistic than in the typically developing brain. The cause of this apparent dissociation of cerebral cortical regions from subcortical regions and of cortical white from grey matter is unknown, and merits further investigation. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Waltham, MA USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. McLean Hosp, Dept Psychiat, Belmont, MA 02178 USA. Childrens Hosp Oakland, Dept Infect Dis, Oakland, CA 94609 USA. Pennington Sch, Pennington, NJ USA. Tufts Univ, Boston, MA 02111 USA. Univ Illinois, Chicago, IL USA. 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I., 1967, REGIONAL DEV BRAIN E, P3 Zhang K, 2000, P NATL ACAD SCI USA, V97, P5621, DOI 10.1073/pnas.090504197 NR 72 TC 218 Z9 223 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD MAY PY 2003 VL 126 BP 1182 EP 1192 DI 10.1093/brain/awg110 PN 5 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 668ZR UT WOS:000182327900017 PM 12690057 ER PT J AU Verte, S Roeyers, H Buysse, A AF Verte, S Roeyers, H Buysse, A TI Behavioural problems, social competence and self-concept in siblings of children with autism SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism spectrum disorder; high functioning; siblings; psychological adjustment ID DISABLED-CHILDREN; DIFFERENTIAL TREATMENT; LEARNING-DISABILITIES; MENTAL-RETARDATION; ADJUSTMENT; FAMILY; CHILDHOOD; STRESS; BROTHERS; SISTERS AB Introduction This study investigated the psychological adjustment of siblings of children with high-functioning autism (HFA) in comparison with siblings of normally developing children in the domain of behavioural problems, social competence and self-concept. Method Twenty-nine siblings of children with HFA and 29 siblings of children without a disorder participated in the study. Standardized, written questionnaires were used. Results Siblings of children with HFA, especially brothers and sisters between 6 and 11 years old, had more behavioural problems than siblings of the control group. Sisters of children with HFA ascribed higher social competence to themselves. Sisters of children with HFA between 12 and 16 years old had a more positive self-concept. In both groups siblings with a more negative self-concept had less social skills and siblings with a more positive self-concept scored better in the social domain. Finally, in accordance with the control group, the perception of the siblings' social competence of parents of children with HFA broadly matched the perception siblings had of themselves. Discussion Overall, siblings of children with HFA are not more susceptible to adaptation problems than siblings of children without a disorder. Implications for practice and further research are discussed. C1 State Univ Ghent, Res Grp Dev Disorders, B-9000 Ghent, Belgium. RP Verte, S (reprint author), State Univ Ghent, Res Grp Dev Disorders, H Dunantlaan 2, B-9000 Ghent, Belgium. 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PD MAY PY 2003 VL 29 IS 3 BP 193 EP 205 DI 10.1046/j.1365-2214.2003.00331.x PG 13 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 674RZ UT WOS:000182650900005 PM 12752610 ER PT J AU Sogut, S Zoroglu, SS Ozyurt, H Yilmaz, HR Ozugurlu, F Sivasli, E Yetkin, O Yanik, M Tutkun, H Savas, HA Tarakcioglu, M Akyol, O AF Sogut, S Zoroglu, SS Ozyurt, H Yilmaz, HR Ozugurlu, F Sivasli, E Yetkin, O Yanik, M Tutkun, H Savas, HA Tarakcioglu, M Akyol, O TI Changes in nitric oxide levels and antioxidant enzyme activities may have a role in the pathophysiological mechanisms involved in autism SO CLINICA CHIMICA ACTA LA English DT Article DE autism; thiobarbituric acid-reactive substances (TBARS); superoxide dismutase (SOD); glutathione peroxidase (GSH-Px); nitric oxide (NO) ID SCHIZOPHRENIA; DISORDER; SPECTRUM; BRAIN; MALONALDEHYDE; SYNTHASE; PRODUCTS; CHILDREN; NITRATE; SERUM AB Background: There is evidence that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. Although it has not been investigated yet, several recent studies proposed that nitric oxide (NO) and other parameters related to oxidative stress may have a pathophysiological role in autism. Methods: We assessed the changes in superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and thiobarbituric acid-reactive substances (TBARS) levels in plasma as well as NO levels in red blood cells (RBC) in patients with autism (n = 27) compared to age- and sex-matched normal controls (n = 30). Results: In the autistic group, increased RBC NO levels (p < 0.0001) and plasma GSH-Px activity (p < 0.0001) and unchanged plasma TBARS levels and SOD activity were detected. Conclusions: These findings indicate a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism. (C) 2003 Published by Elsevier Science B.V. C1 Inonu Univ, Fac Med, Dept Biochem, TR-44200 Malatya, Turkey. Gaziantep Univ, Dept Child & Adolescent Psychiat, Gaziantep, Turkey. Gaziosmanpasa Univ, Fac Med, Dept Biochem, Tokat, Turkey. Inonu Univ, Sci & Art Fac, Div Biol, Malatya, Turkey. Gaziantep Univ, Dept Pediat, Fac Med, Gaziantep, Turkey. Harran Univ, Fac Med, Dept Psychiat, Sanliurfa, Turkey. Gaziantep Univ, Fac Med, Dept Psychiat, Gaziantep, Turkey. Gaziantep Univ, Fac Med, Dept Biochem, Gaziantep, Turkey. RP Sogut, S (reprint author), Inonu Univ, Fac Med, Dept Biochem, Pasakosku Mahllesi 11,Sok Ozkaracalar Apt 42-4, TR-44200 Malatya, Turkey. RI zoroglu, suleyman /B-2077-2012 CR AKYOL O, 1995, REDOX REP, V1, P255 Bell JG, 2000, PROSTAG LEUKOTR ESS, V63, P21, DOI 10.1054/plef.2000.0186 Black MD, 1999, NEUROPHARMACOLOGY, V38, P1299, DOI 10.1016/S0028-3908(99)00041-6 CORTAS NK, 1990, CLIN CHEM, V36, P1440 DAWSON TM, 1992, ANN NEUROL, V32, P297, DOI 10.1002/ana.410320302 DAWSON VL, 1993, J NEUROSCI, V13, P2651 ESTERBAUER H, 1990, METHOD ENZYMOL, V186, P407 ESTERBAUER H, 1991, FREE RADICAL BIO MED, V11, P81, DOI 10.1016/0891-5849(91)90192-6 Fossier P, 1999, NEUROSCIENCE, V93, P597, DOI 10.1016/S0306-4522(99)00165-7 Giovannoni G, 1997, J NEUROL SCI, V145, P77, DOI 10.1016/S0022-510X(96)00246-8 GOLSE B, 1978, REV NEUROL, V134, P699 Herken H, 2001, MOL PSYCHIATR, V6, P66, DOI 10.1038/sj.mp.4000789 Herken H, 2001, SCHIZOPHR RES, V52, P289, DOI 10.1016/S0920-9964(00)00169-9 Johnson S, 2001, MED HYPOTHESES, V56, P641, DOI 10.1054/mehy.2000.1302 KANE PC, 1997, PROSTAGLANDINS LEUKO, V57, P265 KUO PC, 1995, ANN SURG, V221, P220, DOI 10.1097/00000658-199503000-00003 Lombard J, 1998, MED HYPOTHESES, V50, P497, DOI 10.1016/S0306-9877(98)90270-5 Nordin V, 1998, DEV MED CHILD NEUROL, V40, P587 PAGLIA DE, 1967, J LAB CLIN MED, V70, P158 Richardson AJ, 2000, PROSTAG LEUKOTR ESS, V63, P1, DOI 10.1054/plef.2000.0184 Savas HA, 2002, NEUROPSYCHOBIOLOGY, V45, P57, DOI 10.1159/000048677 SUN Y, 1988, CLIN CHEM, V34, P497 SZABO C, 1995, FEBS LETT, V363, P235, DOI 10.1016/0014-5793(95)00322-Z Totan Y, 2001, BRIT J OPHTHALMOL, V85, P1426, DOI 10.1136/bjo.85.12.1426 Vancassel S, 2001, PROSTAG LEUKOTR ESS, V65, P1, DOI 10.1054/plef.2001.0281 NR 25 TC 113 Z9 114 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD MAY PY 2003 VL 331 IS 1-2 BP 111 EP 117 DI 10.1016/S0009-8981(03)00119-0 PG 7 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 672EB UT WOS:000182507200015 PM 12691871 ER PT J AU Milana, V Crewther, SG Crewther, DP AF Milana, V Crewther, SG Crewther, DP TI Central or peripheral gaze: A psychophysical investigation of face recognition by typically developing children and children with autism SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract CT Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology CY MAY 04, 2003 CL FT LAUDERDALE, FLORIDA SP Assoc Res Vis & Ophthalmol C1 La Trobe Univ, Bundoora, Vic 3083, Australia. Swinburne Univ Technol, Brain Sci Inst, Hawthorn, Vic 3122, Australia. NR 0 TC 0 Z9 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAY PY 2003 VL 44 SU 2 MA 2795 BP U53 EP U53 PG 1 WC Ophthalmology SC Ophthalmology GA 709CK UT WOS:000184607000263 ER PT J AU Hardan, AY Kilpatrick, M Keshavan, MS Minshew, NJ AF Hardan, AY Kilpatrick, M Keshavan, MS Minshew, NJ TI Motor performance and anatomic magnetic resonance imaging (MRI) of the basal ganglia in autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 57th Annual Meeting of the Society-of-Biological-Psychiatry CY MAY 18, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Soc Biol Psychiat ID OBSESSIVE-COMPULSIVE DISORDER; INFANTILE-AUTISM; DIAGNOSTIC INTERVIEW; ASPERGER SYNDROME; CHILDHOOD AUTISM; GLUCOSE; ADULTS; BRAIN; BEHAVIOR; VOLUME AB This study was conducted to examine the volume of the basal ganglia in individuals with autism and to evaluate whether performance on specific motor tasks correlated with the volume of these structures. Volumetric measurements of the caudate nucleus and putamen were obtained from magnetic resonance images (MRI) of 40 non-mentally retarded individuals with autism and 41 healthy controls. Motor performance was assessed in these subjects by using the Finger Tapping Test, the Grooved Pegboard Test, and the measurement of Grip Strength. No volumetric differences of the basal ganglia were found between the two groups after adjusting for brain volume. The autistic subjects' performance was slower on the Grooved Pegboard Test and weaker on Grip Strength. Our findings suggest that the motor deficits observed in autism may not be related to structural abnormalities of the basal ganglia, and other brain regions, such as the cerebellum and the frontal lobe, may be involved in the pathophysiology of motor disturbances in autism. C1 Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, 3811 O Hara St, Pittsburgh, PA 15213 USA. 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Child Neurol. PD MAY PY 2003 VL 18 IS 5 BP 317 EP 324 DI 10.1177/08830738030180050801 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 687YY UT WOS:000183405600002 PM 12822815 ER PT J AU Szatmari, P Bryson, SE Boyle, MH Streiner, DL Duku, E AF Szatmari, P Bryson, SE Boyle, MH Streiner, DL Duku, E TI Predictors of outcome among high functioning children with autism and Asperger syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; Asperger syndrome; longitudinal studies; trajectory; outcome; prognosis ID BEHAVIOR CHECKLIST; DISORDER; INDIVIDUALS AB Background: The objective of this paper is to assess the extent to which measures of cognitive abilities taken in an inception cohort of young high functioning children with autism and Asperger syndrome predict outcome roughly two and six years later. Method: Children who received a diagnosis of autism or Asperger syndrome (AS) and who had a nonverbal IQ score in the 'non-retarded' range were included in the inception cohort. Measures of language and nonverbal skills were taken when the children were 4-6 years of age and outcome assessments were completed when the children were 6-8 and 10-13 years of age. The three outcome measures consisted of scales of adaptive behaviours in socialisation and communication and a composite measure of autistic symptoms (abnormal language, abnormal body and object use, difficulties relating to others, sensory issues and social and self-help difficulties). Results: The explanatory power of the predictor variables was greater for communication and social skills than for autistic symptoms. The power of prediction was stable over time but did differ by PDD subtype. In general, the association between language skills and outcome was stronger in the autism group than in the AS group. Conclusions: These results support the emphasis of early intervention programmes on language but more work needs to be done on understanding variables that influence outcome in social skills and autistic behaviours, particularly in those with AS. C1 McMaster Univ, Hamilton, ON L8S 4L8, Canada. Dalhousie Univ, IWK Hlth Ctr, Halifax, NS B3H 3J5, Canada. Baycrest Ctr Geriatr Care, Toronto, ON, Canada. Univ Toronto, Toronto, ON, Canada. RP Szatmari, P (reprint author), Chedoke Site, Patterson Bldg 207, Hamilton, ON L8N 3Z5, Canada. 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PD MAY PY 2003 VL 44 IS 4 BP 520 EP 528 DI 10.1111/1469-7610.00141 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 674BF UT WOS:000182615900005 PM 12751844 ER PT J AU Joseph, RM Tanaka, J AF Joseph, RM Tanaka, J TI Holistic and part-based face recognition in children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; face perception; social cognition ID HUMAN EXTRASTRIATE CORTEX; PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; FUNCTIONAL NEUROANATOMY; REVISED VERSION; YOUNG-CHILDREN; NORMAL ADULTS; PERCEPTION; MEMORY; EYES AB Background: There is substantial evidence that children with autism are impaired in face recognition. Although many researchers have suggested that this impairment derives from a failure of holistic face processing and a tendency to represent and encode faces on a part-by-part basis, this hypothesis has not been tested directly. Method: Holistic face processing was assessed by comparing children's ability to recognize a face part (eyes, nose, or mouth) in the context of the whole face in which it was learned with their ability to recognize the same face part in isolation. Results: In Study 1, as expected, typically developing 9-year-olds (n = 27) and 11-year-olds (n = 30) were significantly better at recognizing face parts presented in the whole than in the part test condition, and this effect was limited to upright faces and not found for inverted faces. Consistent with prior findings, typically developing children were most accurate when face recognition depended on the eyes. In Study 2, high-functioning children with autism (n = 22) evidenced a whole-test advantage for mouths only, and were markedly deficient when face recognition depended on the eyes. Their pattern of performance diverged from age- and IQ-matched comparison participants (n = 20), who performed similarly to the typically developing children in Study 1. Conclusions: These findings suggest that face recognition abnormalities in autism are not fully explained by an impairment of holistic face processing, and that there is an unusual significance accorded to the mouth region when children with autism process information from people's faces. 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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Child Psychol. Psychiatry Allied Discip. PD MAY PY 2003 VL 44 IS 4 BP 529 EP 542 DI 10.1111/1469-7610.00142 PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 674BF UT WOS:000182615900006 PM 12751845 ER PT J AU Heaton, P AF Heaton, P TI Pitch memory, labelling and disembedding in autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; absolute pitch; disembedding abilities; music ID ABSOLUTE PITCH; CENTRAL COHERENCE; INFANTILE-AUTISM; CHILDREN; INDIVIDUALS; ASYMMETRY; PERFORMANCE AB Background: Autistic musical savants invariably possess absolute pitch ability and are able to disembed individual musical tones from chords. Enhanced pitch discrimination and memory has been found in non-savant individuals with autism who also show superior performance on visual disembedding tasks. These experiments investigate the extent that enhanced disembedding ability will be found within the musical domain in autism. Method: High-functioning children with autism, together with age- and intelligence-matched controls, participated in three experiments testing pitch memory, labelling and chord disembedding. Results: The findings from experiment 1 showed enhanced pitch memory and labelling in the autism group. In experiment 2, when subjects were pre-exposed to labelled individual tones, superior chord segmentation was also found. However, in experiment 3, when disembedding performance was less reliant on pitch memory, no group differences emerged and the children with autism, like controls, perceived musical chords holistically. Conclusion: These findings indicate that pitch memory and labelling is superior in autism and can facilitate performance on musical disembedding tasks. However, when task performance does not rely on long-term pitch memory, autistic children, like controls, succumb to the Gestalt qualities of chords. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. RP Heaton, P (reprint author), Univ London Goldsmiths Coll, Dept Psychol, New Cross, London SE14 6NW, England. CR APPLEBAUM E, 1979, J AUTISM DEV DISORD, V9, P279, DOI 10.1007/BF01531742 BAGGALEY J., 1974, PSYCHOL MUSIC, V2, P11, DOI 10.1177/030573567422002 BAUMAN ML, 1999, NEURODEVELOPMENTAL D BHARUCHA JJ, 1991, MUSIC CONNECTIONISM BLACKSTOCK EG, 1978, J AUTISM CHILD SCHIZ, V8, P339, DOI 10.1007/BF01539636 CLANCY H, 1969, J CHILD PSYCHOL PSYC, V10, P233, DOI 10.1111/j.1469-7610.1969.tb02084.x CROSS I, 1997, PERCEPTION COGNITION DEUTSCH D, 1999, 138 M AC SOC AM COL EDWORTHY J, 1985, MUSIC PERCEPT, V2, P375 Frith U., 1989, AUTISM EXPLAINING EN HALPERN AR, 1989, MEM COGNITION, V17, P572, DOI 10.3758/BF03197080 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 HEATON P, 1998, THESIS U LONDON Heaton P, 1999, NEUROCASE, V5, P503, DOI 10.1080/13554799908402745 HEATON P, 2001, ANN NEW YORK ACAD SC, V930 Heaton P, 1998, MUSIC PERCEPT, V15, P291 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 Kanner L, 1943, NERV CHILD, V2, P217 Khalfa S, 2001, EUR J NEUROSCI, V13, P628, DOI 10.1046/j.1460-9568.2001.01423.x KLIN A, 1991, J AUTISM DEV DISORD, V21, P29, DOI 10.1007/BF02206995 KRUMHANSL CL, 1982, J EXP PSYCHOL HUMAN, V8, P24 LENHOFF HM, 2001, THEORY NEUROPLASTICI LEVITIN DJ, 1994, PERCEPT PSYCHOPHYS, V56, P414, DOI 10.3758/BF03206733 Miller L., 1989, MUSICAL SAVANTS EXCE Minshew NJ, 2001, J CHILD PSYCHOL PSYC, V42, P1095, DOI 10.1111/1469-7610.00808 Mottron L, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P131 Mottron L, 1999, NEUROCASE, V5, P485, DOI 10.1080/13554799908402744 Mottron L, 2000, J CHILD PSYCHOL PSYC, V41, P1057, DOI 10.1017/S0021963099006253 Muller RA, 1999, J AUTISM DEV DISORD, V29, P19, DOI 10.1023/A:1025914515203 OURA Y, 1981, C 16 INT MUS FEST BR OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Plaisted KC, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P149 PRING L, 1995, J CHILD PSYCHOL PSYC, V36, P1065, DOI 10.1111/j.1469-7610.1995.tb01351.x PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 PRIOR M, 1974, MED J AUSTR Raven JC, 1988, STANDARD PROGR MATRI Rimland B., 1984, MENTAL RETARDATION D, V13, P155 RUTTER M, 1968, J CHILD PSYCHOL PSYC, V9, P1, DOI 10.1111/j.1469-7610.1968.tb02204.x Saffran JR, 2001, DEV PSYCHOL, V37, P74, DOI 10.1037//0012-1649.37.1.74 SCHLAUG G, 1995, SCIENCE, V267, P699, DOI 10.1126/science.7839149 SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x SNODGRASS JG, 1980, J EXP PSYCHOL-HUM L, V6, P174, DOI 10.1037/0278-7393.6.2.174 SOUTHALL G, 1983, CONTINUING ENSLAVEME TAKEUCHI AH, 1993, PSYCHOL BULL, V113, P345, DOI 10.1037//0033-2909.113.2.345 TREHUB S, 1997, PERCEPTION COGNITION, P103 Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 YOUNG R, 1995, THESIS U ADELAIDE S Zatorre RJ, 1998, P NATL ACAD SCI USA, V95, P3172, DOI 10.1073/pnas.95.6.3172 NR 51 TC 87 Z9 88 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD MAY PY 2003 VL 44 IS 4 BP 543 EP 551 DI 10.1111/1469-7610.00143 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 674BF UT WOS:000182615900007 PM 12751846 ER PT J AU Brian, JA Tipper, SP Weaver, B Bryson, SE AF Brian, JA Tipper, SP Weaver, B Bryson, SE TI Inhibitory mechanisms in autism spectrum disorders: typical selective inhibition of location versus facilitated perceptual processing SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism spectrum disorders; selective attention; inhibition; executive function; perception; negative priming ID EXECUTIVE FUNCTION; VISUAL-SEARCH; CHILDREN; ATTENTION; DEFICITS; INDIVIDUALS; STIMULI; DISCRIMINATION; COMPREHENSION; PERFORMANCE AB Background: This study examined the inhibitory control mechanisms of selective attention in autism spectrum disorders. Two issues were engaged: First, we extend previous findings of normal inhibition of distractor identity in autism by examining whether inhibition of spatial location is also spared. The second issue concerns the selectivity of inhibition. in non-clinical participants inhibition is selectively directed to the properties of the distractor that compete for the control of action; we examined whether individuals with autism also show normal selectivity of inhibition. Method: A negative priming task was used to examine selective spatial inhibition in participants with autism relative to matched non-clinical controls. Results: We discovered that inhibition of distractor spatial location is within normal limits in autism, as is the ability to selectively direct inhibition to task-relevant stimulus features. In addition, we unexpectedly found that the irrelevant perceptual feature of colour produced a facilitation effect in autism, which has not been observed previously in typical controls. Conclusions: Evidence of colour facilitation implicates more fluent, but presumably less adaptive, perceptual processes in autism. C1 Hosp Sick Children, Autism Res Unit, Toronto, ON M5G 1X8, Canada. Univ Wales Coll Cardiff, Sch Psychol, Cardiff CF1 3NS, S Glam, Wales. McMaster Univ, Hamilton, ON L8S 4L8, Canada. Dalhousie Univ, Halifax, NS B3H 3J5, Canada. RP Brian, JA (reprint author), Hosp Sick Children, Autism Res Unit, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. RI Tipper, Steven/I-6884-2012 OI Tipper, Steven/0000-0002-1554-0531 CR AMELI R, 1988, J AUTISM DEV DISORD, V18, P601, DOI 10.1007/BF02211878 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Brian JA, 1996, J CHILD PSYCHOL PSYC, V37, P865, DOI 10.1111/j.1469-7610.1996.tb01482.x BRYSON SE, 1983, J ABNORM PSYCHOL, V92, P250, DOI 10.1037/0021-843X.92.2.250 BRYSON SE, 1997, ATTENTION DEV PSYCHO, P232 CASEY BJ, 1993, J CLIN EXP NEUROPSYC, V15, P933, DOI 10.1080/01688639308402609 COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Dunn L. M., 1981, PEABODY PICTURE VOCA ESKES GA, 1990, J AUTISM DEV DISORD, V20, P61, DOI 10.1007/BF02206857 FEIN D, 1990, J AUTISM DEV DISORD, V20, P263, DOI 10.1007/BF02284723 Harris NS, 1999, COGNITIVE BRAIN RES, V8, P61, DOI 10.1016/S0926-6410(99)00006-3 LANDRY JR, IN PRESS J CHILD PSY Logan Gordon D., 1994, P189 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x MILLIKEN B, 1994, J EXP PSYCHOL HUMAN, V20, P624, DOI 10.1037//0096-1523.20.3.624 O'Riordan M, 2000, COGNITION, V77, P81, DOI 10.1016/S0010-0277(00)00089-5 O'Riordan MA, 2001, J EXP PSYCHOL HUMAN, V27, P719, DOI 10.1037//0096-1523.27.3.719 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Ozonoff S, 1997, J AUTISM DEV DISORD, V27, P59, DOI 10.1023/A:1025821222046 OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P765, DOI 10.1017/S0021963098002601 Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P777, DOI 10.1017/S0021963098002613 PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 RAVEN JC, 1969, STANDARD PROGR MATRI Rosenblatt J., 1995, TEACHING CHILDREN AU, P33 RUMSEY JM, 1985, J AUTISM DEV DISORD, V15, P23, DOI 10.1007/BF01837896 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 Stroop JR, 1935, J EXP PSYCHOL, V18, P643, DOI 10.1037/h0054651 TIPPER SP, 1994, J EXP PSYCHOL HUMAN, V20, P478, DOI 10.1037//0096-1523.20.3.478 TIPPER SP, 1994, Q J EXP PSYCHOL-A, V47, P809 TIPPER SP, 1985, Q J EXP PSYCHOL-A, V37, P591 TIPPER SP, 1985, Q J EXP PSYCHOL-A, V37, P571 Townsend J, 1999, J NEUROSCI, V19, P5632 Wainwright JA, 1996, J AUTISM DEV DISORD, V26, P423, DOI 10.1007/BF02172827 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 NR 39 TC 31 Z9 31 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD MAY PY 2003 VL 44 IS 4 BP 552 EP 560 DI 10.1111/1469-7610.00144 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 674BF UT WOS:000182615900008 PM 12751847 ER PT J AU Hastings, RP AF Hastings, RP TI Child behaviour problems and partner mental health as correlates of stress in mothers and fathers of children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE fathers; behaviour problems; parents; mothers; mental health; stress; autism ID PSYCHOLOGICAL ADJUSTMENT; PARENTAL STRESS; FAMILY STRESS; DISABILITIES; RETARDATION; YOUNG; PERCEPTIONS; CARE; SATISFACTION; DEPRESSION AB Background Previous research has suggested that the mothers and fathers of children with disabilities experience stress differently. Although there has been a great deal of research exploring how children affect parents, there have been many fewer studies of the interrelationships between mothers' and fathers' psychological well-being. Methods Eighteen married couples who were the parents of children with autism reported on their stress and their general mental health (i.e. anxiety and depression). Teachers rated the behaviour problems of the children with autism. Results Mothers and fathers did not differ in their levels of stress and depression, but mothers reported more anxiety than fathers. Partial correlation analyses revealed that child behaviour problems and fathers' mental health were associated with mothers' stress. However, neither child behaviour problems or mothers' mental health was associated with fathers' stress. Conclusion Although requiring replication, the results suggest that stress in mothers of children with disabilities may be affected by the psychological health of other family members, whereas fathers' stress is affected more by other factors. Methodological and conceptual issues, and the practical implications of these results are discussed. C1 Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. RP Hastings, RP (reprint author), Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 CR Abidin RR, 1995, PARENTING STRESS IND BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 BECKMAN PJ, 1991, AM J MENT RETARD, V95, P585 BRISTOL MM, 1988, DEV PSYCHOL, V24, P441, DOI 10.1037/0012-1649.24.3.441 EINFELD SL, 1995, J AUTISM DEV DISORD, V25, P81, DOI 10.1007/BF02178498 Essex EL, 1999, AM J MENT RETARD, V104, P545, DOI 10.1352/0895-8017(1999)104<0545:DICEAW>2.0.CO;2 FLOYD FJ, 1991, CHILD DEV, V62, P1434, DOI 10.1111/j.1467-8624.1991.tb01616.x FRIEDRICH WN, 1983, AM J MENT DEF, V88, P41 Glidden LM, 1997, AM J MENT RETARD, V102, P250, DOI 10.1352/0895-8017(1997)102<0250:DPDAFS>2.0.CO;2 GOLDBERG S, 1986, AM J MENT RETARD, V90, P610 Hannah ME, 1999, AM J MENT RETARD, V104, P22, DOI 10.1352/0895-8017(1999)104<0022:CAAOSO>2.0.CO;2 Hastings R. 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K., 1994, FDIC BANKING REV, V7, P1 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P205, DOI 10.1007/BF01058151 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x KRAUSS MW, 1993, AM J MENT RETARD, V97, P393 QUINE L, 1985, BRIT J SOC WORK, V15, P501 Roach MA, 1999, AM J MENT RETARD, V104, P422, DOI 10.1352/0895-8017(1999)104<0422:MAFOCW>2.0.CO;2 ROUSEY AM, 1992, AM J MENT RETARD, V97, P99 Seligman M, 1997, ORDINARY FAMILIES SP SLOPER P, 1991, J CHILD PSYCHOL PSYC, V32, P655, DOI 10.1111/j.1469-7610.1991.tb00342.x STONEMAN Z, 1983, AM J MENT DEF, V87, P591 TRUTE B, 1988, J MARITAL FAM THER, V14, P185, DOI 10.1111/j.1752-0606.1988.tb00734.x TRUTE B, 1995, J CHILD PSYCHOL PSYC, V36, P1225, DOI 10.1111/j.1469-7610.1995.tb01367.x WEISS SJ, 1991, CHILD PSYCHIAT HUM D, V21, P203, DOI 10.1007/BF00705906 WILLOUGHBY JC, 1995, AM J MENT RETARD, V99, P399 ZIGMOND AS, 1983, ACTA PSYCHIAT SCAND, V67, P361, DOI 10.1111/j.1600-0447.1983.tb09716.x NR 31 TC 141 Z9 147 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD MAY-JUN PY 2003 VL 47 BP 231 EP 237 DI 10.1046/j.1365-2788.2003.00485.x PN 4-5 PG 7 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 682CT UT WOS:000183073900003 PM 12787155 ER PT J AU Williams, KR Wishart, JG AF Williams, KR Wishart, JG TI The Son-Rise Program intervention for autism: an investigation into family experiences SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; family; intervention; parent therapists; Son-Rise Program ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE EARLY INTERVENTION; CHILDREN AB Background Despite the increasing involvement of parents as therapists in interventions for their children with autism, research to date has focused almost exclusively on the outcome for the child, and little is known about the effects of involvement on the whole family. This is true even of highly intensive home-based approaches such as the Son-Rise Program (SRP), the focus of the present paper. A longitudinal questionnaire-based study is reported which investigated a number of potential positive and negative effects for the family, how these changed over time, and their relation to child characteristics and patterns of intervention implementation. Methods Questionnaires examining family demographics, patterns of intervention use and perceived family effects were distributed three times over the course of a year to families who had attended an initial training course in the use of the SRP. Results The results indicated that, although involvement led to more drawbacks than benefits for the families over time, family stress levels did not rise in all cases. Few relationships were found between family effects and patterns of intervention use, although there was a strong connection with parental perceptions of intervention efficacy. Conclusions The findings of the present study emphasize the need for those supporting families using home-based interventions to consider the needs of the whole family. This may be especially important if there are periods during which the family find the intervention to be less effective. Families embarking on such intensive approaches may also benefit from considering ways in which any disruption to family life can be minimized. C1 Univ Edinburgh, Moray House Sch Educ, Edinburgh EH8 8AQ, Midlothian, Scotland. RP Williams, KR (reprint author), Univ Edinburgh, Moray House Sch Educ, Simon Laurie House, Edinburgh EH8 8AQ, Midlothian, Scotland. CR Bimbrauer J. 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PD MAY-JUN PY 2003 VL 47 BP 291 EP 299 DI 10.1046/j.1365-2788.2003.00491.x PN 4-5 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 682CT UT WOS:000183073900009 PM 12787161 ER PT J AU Olsson, MB Hwang, PC AF Olsson, MB Hwang, PC TI Influence of macrostructure of society on the life situation of families with a child with intellectual disability: Sweden as an example SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE life situation; macrostructure; society; Sweden ID MENTAL-RETARDATION; YOUNG-CHILDREN; DISABLED-CHILDREN; DOWN-SYNDROME; MOTHERS; PARENTS; STRESS; PERCEPTIONS; ADJUSTMENT; DEPRESSION AB Background Most studies on families with children with intellectual disability (ID) have been carried out in the UK or the USA, and are influenced by the societal organization, and political and economic climate of those countries. In the USA and the UK, the care and well-being of children, with or without ID, are seen almost exclusively as the individual family's responsibility. In Sweden, the care and well-being of children are seen more as a joint responsibility. Swedish society has developed many privileges for all parents in order to help them care for their children, and the support for parents of children with disabilities is provided exclusively by the Government and the community. The overall question explored in this descriptive, quantitative and qualitative study was: Are families in Sweden experiencing the stressors and life situations described in the studies of parents in more individualistic societies? Methods Two hundred and twenty-six families with children with ID and 234 control families with children ranging from 0 to 16 years of age answered mail surveys. Results Taken together, parents in Sweden describe most of the stressors proposed in the international literature with the exception of financial strain. Restricted social life and time restrictions seem to be the two most evident and bothersome stressors for Swedish families with children who have ID. Conclusions As in previous research, the parents of children with ID and autism experienced more stressors and restrictions in their lives than the parents of children with DS and control families. C1 Univ Gothenburg, Dept Psychol, S-40530 Gothenburg, Sweden. RP Olsson, MB (reprint author), Univ Gothenburg, Dept Psychol, POB 500, S-40530 Gothenburg, Sweden. EM malin.olsson@psy.gu.se CR Axtell S. 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The genetic aetiology of dyslexia is heterogeneous and loci on chromosomes 2, 3, 6, 15, and 18 have been repeatedly linked to it. We have conducted a genome scan with 376 markers in 11 families with 38 dyslexic subjects ascertained in Finland. Linkage of dyslexia to the vicinity of DYX3 on 2p was confirmed with a nonparametric linkage (NPL) score of 2.55 and a lod score of 3.01 for a dominant model, and a novel locus on 7q32 close to the SPCH1 locus was suggested with an NPL score of 2.77. The SPCH1 locus has previously been linked with a severe speech and language disorder and autism, and a mutation in exon 14 of the FOXP2 gene on 7q32 has been identified in one large pedigree. Because the language disorder associated with the SPCH1 locus has some overlap with the language deficits observed in dyslexia, we sequenced the coding region of FOXP2 as a candidate gene for our observed linkage in six dyslexic subjects. No mutations were identified. 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Lipopolysaccharide (LPS) or saline was administered to rats to model maternal infection, and levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in maternal plasma, placenta, amniotic fluid, fetal liver/spleen, fetal brain, and cerebral cortex after birth were determined by ELISA or semiquantitative Western blot analysis. BDNF expression was significantly increased in the fetal brain (p = 0.039); NGF expression was significantly increased in neonatal cortex (p = 0.0009). Neurotrophic factor expression was also altered in other tissues of the maternal-fetal unit. Abnormal expression of neurotrophic factors represents a potential mechanism through which maternal infection increases risk for neurodevelopmental disorders. (C) 2003 Elsevier Science B.V. All rights reserved. C1 Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RP Gilmore, JH (reprint author), Univ N Carolina, Dept Psychiat, CB 7160, Chapel Hill, NC 27599 USA. 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Neuroimmunol. PD MAY PY 2003 VL 138 IS 1-2 BP 49 EP 55 DI 10.1016/S0165-5728(03)00095-X PG 7 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 687ZC UT WOS:000183406100008 PM 12742653 ER PT J AU Field, D Garland, M Williams, K AF Field, D Garland, M Williams, K TI Correlates of specific childhood feeding problems SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Article DE childhood feeding problems; paediatric feeding disorders ID DOWNS-SYNDROME CHILDREN; ANOREXIA-NERVOSA; GASTROESOPHAGEAL REFLUX; SENSORIMOTOR THERAPY; BULIMIA NERVOSA; CEREBRAL-PALSY; INFANTS; DISEASE; 4-YEAR-OLD; DISORDERS AB Objective: The correlates of specific childhood feeding problems are described to further examine possible predisposing factors for feeding problems. We report our experience with 349 participants evaluated by an interdisciplinary feeding team. Methods: A review of records was conducted and each participant was identified as having one or more of five functionally defined feeding problems: food refusal, food selectivity by type, food selectivity by texture, oral motor delays, or dysphagia. The prevalence of predisposing factors for these feeding problems was examined. Predisposing factors included developmental disabilities, gastrointestinal problems, cardiopulmonary problems, neurological problems, renal disease and anatomical anomalies. Results: The frequencies of predisposing factors varied by feeding problem. Differences were found in the prevalence of the five feeding problems among children with three different developmental disabilities: autism, Down syndrome and cerebral palsy. Gastro-oesophageal reflux was the most prevalent condition found among all children in the sample and was the factor most often associated with food refusal. Neurological conditions and anatomical anomalies were highly associated with skill deficits, such as oral motor delays and dysphagia. Conclusions: Specific medical conditions and developmental disabilities are often associated with certain feeding problems. Information concerning predisposing factors of feeding problems can help providers employ appropriate primary, secondary and tertiary prevention measures to decrease the frequency or severity of some feeding problems. C1 Penn State Univ, Milton S Hershey Med Ctr, Feeding Program H094, Hershey, PA 17033 USA. RP Williams, K (reprint author), Penn State Univ, Milton S Hershey Med Ctr, Feeding Program H094, Hershey, PA 17033 USA. 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Child Health PD MAY PY 2003 VL 39 IS 4 BP 299 EP 304 DI 10.1046/j.1440-1754.2003.00151.x PG 6 WC Pediatrics SC Pediatrics GA 683YQ UT WOS:000183179000013 PM 12755939 ER PT J AU Fogt, JB Miller, DN Zirkel, PA AF Fogt, JB Miller, DN Zirkel, PA TI Defining autism: professional best practices and published case law SO JOURNAL OF SCHOOL PSYCHOLOGY LA English DT Article DE autism; eligibility; case law; assessment IDEA (Individuals with Disabilities Education Act) ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; DSM-III-R; YOUNG-CHILDREN; INTERVIEW; BEHAVIOR AB There are clear indications that both the reported incidence of autism in children and litigation involving this developmental disorder are increasing. However, to date there has been a dearth of research analyzing court cases and legal decisions concerning students with autism. The purpose of this review was to examine published hearing/review and court decisions concerning autism eligibility in educational settings in relation to empirically supported best practices in the assessment of autism. A total of 13 cases were identified for inclusion in the review. In general, the results indicated that hearing/review officers and judges neither relied upon nor explicitly acknowledged empirically supported assessment methods in their published eligibility decisions. It appeared that many hearing/review officers and judges relied on expert witnesses, who may or may not have had particular expertise and knowledge regarding current best practices in autism eligibility assessment. Implications of the findings and areas for future research are discussed. (C) 2003 Society for the Study of School Psychology. Published by Elsevier Science Ltd. All rights reserved. C1 Lehigh Univ, Centennial Sch, Bethlehem, PA 18017 USA. Lehigh Univ, Bethlehem, PA 18015 USA. 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Sch. Psychol. PD MAY-JUN PY 2003 VL 41 IS 3 BP 201 EP 216 DI 10.1016/S0022-4405(03)00045-1 PG 16 WC Psychology, Educational SC Psychology GA 682HN UT WOS:000183085800004 ER PT J AU Mehta, BK Munir, KM AF Mehta, BK Munir, KM TI Does the MMR vaccine and secretin or its receptor share an antigenic epitope? SO MEDICAL HYPOTHESES LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; MEASLES-VIRUS INFECTION; PERVASIVE DEVELOPMENTAL DISORDER; CROHNS-DISEASE; RUBELLA VACCINE; AUTISM; CHILDREN; AUTOANTIBODIES; ASSOCIATION; ANTIBODY AB In a subgroup of children with autism-spectrum like conditions symptoms seem to appear as a 'regression' (in normal development). It has been postulated that the onset of such autistic symptoms may involve an autoimmune response against the central nervous system and that the antigenic determinant could possibly be gastrointestinal in origin. It has been suggested that the presence of the measles virus and 'autistic enterocolitis' demonstrates the possibility that the MMR triple vaccine may be mediating the inflammation with possible production of antibodies against the virus containing vaccine. Such an antibody may share antigenic determinant to molecules found in the gut. We propose that this may be secretin or its receptor, found in the gut as well as in the central nervous system. The antibody response to the gut may also conceivably occur in the brain at a critical time in development: The modulation of development by secretin may be a static event possibly occurring at a specific time in early childhood development and if it involves an autoimmune response then a disruption in development may result. These hypothesized events can only occur if the MMR vaccine shares antigenic determinants that resemble secretin or any of its receptor types and remains to be studied. (C) 2003 Elsevier Science Ltd. All rights reserved. C1 Mem Univ Newfoundland, St Johns, NF A1C 5S7, Canada. Fac Med, St Johns, NF, Canada. RP Munir, KM (reprint author), Childrens Hosp, Mental Hlth & Dev Disabil MH DD Program, Div Gen Pediat, JB-2,300 Longwood Ave, Boston, MA 02115 USA. 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Hypotheses PD MAY PY 2003 VL 60 IS 5 BP 650 EP 653 DI 10.1016/S0306-9877(02)00395-X PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 667FG UT WOS:000182220100006 PM 12710897 ER PT J AU Jamain, S Quach, H Betancur, C Rastam, M Colineaux, C Gillberg, IC Soderstrom, H Giros, B Leboyer, M Gillberg, C Bourgeron, T AF Jamain, S Quach, H Betancur, C Rastam, M Colineaux, C Gillberg, IC Soderstrom, H Giros, B Leboyer, M Gillberg, C Bourgeron, T CA Paris Autism Res Int Sibpair Study TI Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism SO NATURE GENETICS LA English DT Article ID BINDING; EXPRESSION; DISORDERS AB Many studies have supported a genetic etiology for autism. Here we report Mutations in two X-linked genes encoding neuroligins NLGN3 and NLGN4 in siblings with autism-spectrum disorders. These mutations affect cell-adhesion molecules localized at the synapse and suggest that a defect of synaptogenesis may predispose to autism. C1 Univ Paris 07, Lab Genet Humaine & Fonct Cognit, INSERM, E0021,Inst Pasteur, F-75015 Paris, France. Univ Paris 12, INSERM, U513, Fac Med, F-94000 Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. Hop Robert Debre, Dept Child & Adolescent Psychiat, F-75019 Paris, France. Hop Albert Chenevier & Henri Mondor, Dept Psychiat, F-94000 Creteil, France. Univ London St Georges Hosp, Sch Med, London 5W17 ORE, England. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. RP Bourgeron, T (reprint author), Univ Paris 07, Lab Genet Humaine & Fonct Cognit, INSERM, E0021,Inst Pasteur, F-75015 Paris, France. 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PD MAY PY 2003 VL 34 IS 1 BP 27 EP 29 DI 10.1038/ng1136 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 674ZK UT WOS:000182667900011 PM 12669065 ER PT J AU Schubert, C Lo, P AF Schubert, C Lo, P TI Attending to autism SO NATURE MEDICINE LA English DT News Item NR 0 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 MAY PY 2003 VL 9 IS 5 BP 515 EP 515 DI 10.1038/nm0503-515 PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 673ZD UT WOS:000182610600030 ER PT J AU Barton, JJS AF Barton, JJS TI Disorders of face perception and recognition SO NEUROLOGIC CLINICS LA English DT Review ID SUPERIOR TEMPORAL SULCUS; RIGHT-HEMISPHERE DAMAGE; HUMAN NEURAL SYSTEM; CAPGRAS-SYNDROME; UNFAMILIAR FACES; INFEROTEMPORAL CORTEX; FACIAL RECOGNITION; VISUAL AGNOSIA; DELUSIONAL MISIDENTIFICATION; DEVELOPMENTAL PROSOPAGNOSIA AB Face recognition is one of the most complex visual tasks performed by the human brain. In monkeys, area IT may play a key role in identifying faces, and functional imaging in humans suggests a homologue in the medial occipitotemporal cortex, named the fusiform face area (FFA). Damage to medial occipitotemporal structures can cause prosopagnosia, the failure to recognize familiar faces. Prosopagnosia is likely a family of dysfunctions affecting different perceptual and memory stages in face processing. Research on the nature of the encoding deficits and the functional-anatomic correlations in this syndrome are ongoing. Deficits in face perception may also contribute to Capgras syndrome and may be linked to the social dysfunction in autism or Asperger syndrome. More recently identified deficits in face processing include the false recognition of unfamiliar faces and the impaired extraction of social information from faces. Face perception deficits can be placed in the context of cognitive models of face processing, and continue to inform us about the nature of high-level vision and memory in humans. C1 Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA USA. Boston Univ, Boston, MA 02118 USA. 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Clin. PD MAY PY 2003 VL 21 IS 2 BP 521 EP + DI 10.1016/S0733-8619(02)00106-8 PN 1 PG 29 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 683BV UT WOS:000183127800008 PM 12916490 ER PT J AU Owens, JA Rosen, CL Mindell, JA AF Owens, JA Rosen, CL Mindell, JA TI Medication use in the treatment of pediatric insomnia: Results of a survey of community-based pediatricians SO PEDIATRICS LA English DT Article DE insomnia; sleep disturbances; medications; hypnotics; prescribing practices ID SLEEP DISORDERS; BEHAVIORAL INTERVENTIONS; CURRENT MANAGEMENT; MENTAL HANDICAP; YOUNG-CHILDREN; DISTURBANCES; ADOLESCENTS; DRUGS; PHARMACOTHERAPY; PRESCHOOLERS AB Objectives. To examine clinical practice patterns, beliefs, and attitudes regarding the use of both nonprescription and prescription medications by community-based pediatricians for children with significant difficulties in initiating and/or maintaining sleep. Methods. A survey was mailed to 3424 American Academy of Pediatrics members in 6 US cities. Results. The final sample (n = 671) consisted of practitioners who identified themselves as primary care pediatricians. Three percent +/- 7% of visits in the respondents' practices were for pediatric insomnia, although there was a wide range in the numbers of children identified during a typical 6-month practice period. More than 75% of practitioners had recommended nonprescription medications, and >50% had prescribed a sleep medication. Specific clinical circumstances in which medications were most commonly used were acute pain and travel, followed by children with special needs (mental retardation, autism, and attention-deficit/hyperactivity disorder). Antihistamines were the most commonly reported nonprescription medications for sleep. Melatonin or herbal remedies had been recommended by approximately 15% of the respondents. alpha-agonists were the most frequently prescribed sleep medications (31%). The likelihood of prescribing medication for sleep was 2- to 4-fold greater in respondents who treated children with attention-deficit/hyperactivity disorder for daytime behavioral problems or nocturnal sleep problems, respectively. Practitioners expressed a range of concerns about sleep medication appropriateness, safety, tolerance, and side effects in children. Conclusions. The practice of prescribing or recommending sedatives and hypnotics for pediatric insomnia is common among community-based pediatricians, especially among special needs patients. An empirically based approach to the use of these medications is needed. C1 Brown Univ, Sch Med, Dept Pediat, Providence, RI 02912 USA. Brown Univ, Sch Med, Div Ambulatory Pediat, Providence, RI 02912 USA. Case Western Reserve Univ, Dept Pediat, Cleveland, OH 44106 USA. Case Western Reserve Univ, Div Clin Epidemiol, Cleveland, OH 44106 USA. Case Western Reserve Univ, Div Pediat Neurol, Cleveland, OH 44106 USA. Case Western Reserve Univ, Div Pediat Pulmonol, Cleveland, OH 44106 USA. Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Pulm Med, Philadelphia, PA 19104 USA. St Josephs Univ, Dept Psychol, Philadelphia, PA 19131 USA. RP Owens, JA (reprint author), Rhode Isl Hosp, Div Ambulatory Pediat, Potter 200,593 Eddy St, Providence, RI 02903 USA. 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Many diseases with complex etiologies originate during childhood (e.g., asthma, autism, attention deficit/hyperactivity disorder, epilepsy and juvenile rheumatoid arthritis) and persist into adulthood. Attempts to better understand the genetic basis of age-specific disease processes requires an appreciation that the period of human development encompasses the prenatal period through adolescence, and is a rapidly changing, dynamic process. As a result, pharmacologic modulation of developing gene networks may have unintended and unanticipated consequences that do not become apparent or relevant until later in life. Thus, there is considerable potential for large-scale pharmacogenomic technologies to impact the development and utilization of new therapeutic strategies in children. C1 Childrens Mercy Hosp & Clin, Sect Dev Pharmacol & Expt Therapeut, Div Pediat Pharmacol & Med Toxicol, Kansas City, MO 64108 USA. 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RP Casanova, MF (reprint author), Downtown VA Med Ctr, Psychiat Serv, 3B-121, Augusta, GA 30910 USA. CR Casanova MF, 2002, J CHILD NEUROL, V17, P515, DOI 10.1177/088307380201700708 Casanova MF, 2002, NEUROLOGY, V58, P428 Casanova MF, 2002, ANN NEUROL, V52, P108, DOI 10.1002/ana.10226 Casanova MF, 2002, J CHILD NEUROL, V17, P142 Gustafsson L, 1997, BIOL PSYCHIAT, V42, P1138, DOI 10.1016/S0006-3223(97)00141-8 PEARSON RCA, 1985, P NATL ACAD SCI USA, V82, P4531, DOI 10.1073/pnas.82.13.4531 THOMSON AM, 1994, TRENDS NEUROSCI, V17, P119, DOI 10.1016/0166-2236(94)90121-X NR 7 TC 8 Z9 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD MAY 1 PY 2003 VL 118 IS 1 BP 101 EP 102 DI 10.1016/S0165-1781(03)00061-1 PG 2 WC Psychiatry SC Psychiatry GA 682EK UT WOS:000183078200012 PM 12759166 ER PT J AU [Anonymous] AF [Anonymous] TI Time for autism rethink? SO PSYCHOLOGIST LA English DT News Item NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD MAY PY 2003 VL 16 IS 5 BP 228 EP 228 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 682CZ UT WOS:000183074900002 ER PT J AU Sutcliffe, JS Han, MK Amin, T Kesterson, RA Nurmi, EL AF Sutcliffe, JS Han, MK Amin, T Kesterson, RA Nurmi, EL TI Partial duplication of the APBA2 gene in chromosome 15q13 corresponds to duplicon structures SO BMC GENOMICS LA English DT Article ID PRADER-WILLI/ANGELMAN-REGION; MOLECULAR CHARACTERIZATION; INTRACHROMOSOMAL TRIPLICATION; INTERSTITIAL DUPLICATIONS; ANGELMAN-SYNDROMES; AUTISTIC DISORDER; PROXIMAL 15Q; 15Q11-Q13; WILLI; ORGANIZATION AB Background: Chromosomal abnormalities affecting human chromosome 15q11-q13 underlie multiple genomic disorders caused by deletion, duplication and triplication of intervals in this region. These events are mediated by highly homologous segments of DNA, or duplicons, that facilitate mispairing and unequal cross-over in meiosis. The gene encoding an amyloid precursor protein-binding protein (APBA2) was previously mapped to the distal portion of the interval commonly deleted in Prader-Willi and Angelman syndromes and duplicated in cases of autism. Results: We show that this gene actually maps to a more telomeric location and is partially duplicated within the broader region. Two highly homologous copies of an interval containing a large 5' exon and downstream sequence are located similar to5 Mb distal to the intact locus. The duplicated copies, containing the first coding exon of APBA2, can be distinguished by single nucleotide sequence differences and are transcriptionally inactive. Adjacent to APBA2 maps a gene termed KIAA0574. The protein encoded by this gene is weakly homologous to a protein termed X123 that in turn maps adjacent to APBA1 on 9q21.12; APBA1 is highly homologous to APBA2 in the C-terminal region and is distinguished from APBA2 by the N-terminal region encoded by this duplicated exon. Conclusion: The duplication of APBA2 sequences in this region adds to a complex picture of different low copy repeats present across this region and elsewhere on the chromosome. C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. RP Sutcliffe, JS (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. 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Med. Assoc. J. PD APR 29 PY 2003 VL 168 IS 9 BP 1171 EP 1171 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 674JC UT WOS:000182632800035 ER PT J AU Ceponiene, R Lepisto, T Shestakova, A Vanhala, R Alku, P Naatanen, R Yaguchi, K AF Ceponiene, R Lepisto, T Shestakova, A Vanhala, R Alku, P Naatanen, R Yaguchi, K TI Speech-sound-selective auditory impairment in children with autism: They can perceive but do not attend SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID EVENT-RELATED POTENTIALS; DEVELOPMENTAL LANGUAGE DISORDER; INVOLUNTARY ATTENTION; EVOKED-POTENTIALS; SPATIAL ATTENTION; BRAIN POTENTIALS; N1 WAVE; RESPONSES; STIMULI; INFORMATION AB In autism, severe abnormalities in social behavior coexist with aberrant attention and deficient language. In the attentional domain, attention to people and socially relevant stimuli is impaired the most. 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Natl. Acad. Sci. U. S. A. PD APR 29 PY 2003 VL 100 IS 9 BP 5567 EP 5572 DI 10.1073/pnas.0835631100 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 673ZY UT WOS:000182612600107 PM 12702776 ER PT J AU Sinkkonen, ST Homanics, GE Korpi, ER AF Sinkkonen, ST Homanics, GE Korpi, ER TI Mouse models of Angelman syndrome, a neurodevelopmental disorder, display different brain regional GABA(A) receptor alterations SO NEUROSCIENCE LETTERS LA English DT Article DE Angelman syndrome; E6-P ubiquitin-protein ligase gene; gamma-aminobutyric acid type beta 3; gamma-aminobutyric acid type A receptor; knockout mice; ligand autoradiography ID AMINOBUTYRIC-ACID RECEPTOR; SUBUNIT MESSENGER-RNAS; BETA(3) SUBUNIT; A RECEPTOR; AUTISTIC DISORDER; MICE LACKING; RAT-BRAIN; GENES; CHROMOSOME-15; ASSOCIATION AB Angelman syndrome is a severe neurodevelopmental disorder with cognitive impairment and neurological deficits. It results from a maternal deletion of human chromosome 15q11-13 containing two candidate genes E6-P ubiquitin-protein ligase (UBE3A) and GABA(A) receptor beta3 subunit (GABRB(3)), the latter of which has been also linked to autism. To clarify the potential role of GABA(A) beta3 subunit-containing inhibitory receptors in these disorders. we applied ligand autoradiography on brain sections from mice with inactivated GABRB3 or maternal UBE3A genes. Binding of GABAA receptor channel ([S-35]t-butylbicyclophosphorothionate) and benzodiazepine ([H-3]Ro 1545 13) site ligands was reduced in selected brain regions of the beta3-deficient mice as compared to controls. while the UBE3A-deficient mice failed to show reduced GABAA receptors. The results, suggesting two different pathophysiological mechanisms, are in agreement with positron emission tomography results from Angelman syndrome patients of the corresponding genetic backgrounds. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved. 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Lett. PD APR 17 PY 2003 VL 340 IS 3 BP 205 EP 208 DI 10.1016/S0304-3940(03)00123-X PG 4 WC Neurosciences SC Neurosciences & Neurology GA 669JB UT WOS:000182347200012 PM 12672542 ER PT J AU Symons, FJ Clark, RD Hatton, DD Skinner, M Bailey, DB AF Symons, FJ Clark, RD Hatton, DD Skinner, M Bailey, DB TI Self-injurious behavior in young boys with fragile X syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE fragile X syndrome; self-injurious behavior; behavioral phenotype ID SMITH-MAGENIS-SYNDROME; PRADER-WILLI-SYNDROME; LESCH-NYHAN DISEASE; AUTISM RATING-SCALE; ADAPTIVE-BEHAVIOR; DEVELOPMENTAL TRAJECTORIES; MALADAPTIVE BEHAVIOR; MALES; ADOLESCENTS; PHENOTYPE AB In this study, we distributed surveys to 67 families of young boys with fragile X syndrome to determine the prevalence, onset, form, function, location, and correlates of self-injurious behavior. Fifty-five surveys were completed (82%). The mean age of the boys at the time of the survey was 80 months (range = 20-144). Self-injurious behavior (SIB) was reported for 58% of the participants with a mean age of onset of 31 months. The mean number of forms of self-injury was 2 per participant. Biting was the most commonly reported form of self-injury with the fingers and back of the hand disproportionately targeted as the most prevalent self-injury body site. There was no linear increase in risk of SIB with age past 25 months. SIB was reported as most likely to occur following the presentation of difficult task demands or changes in routine. Significant group differences were found between overall ratings of problem behavior for boys with self-injury compared to those without self-injury. Groups did not differ on measures of fragile X mental retardation protein (FMRP), autism status, adaptive behavior, or age first medicated. 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J. Med. Genet. A PD APR 15 PY 2003 VL 118A IS 2 BP 115 EP 121 DI 10.1002/ajmg.a.10078 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 670HL UT WOS:000182401400002 PM 12655491 ER PT J AU Gauthier, J Joober, R Mottron, L Laurent, S Fuchs, M De Kimpe, V Rouleau, GA AF Gauthier, J Joober, R Mottron, L Laurent, S Fuchs, M De Kimpe, V Rouleau, GA TI Mutation screening of FOXP2 in individuals diagnosed with autistic disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE autism disorder; family-based association study; 7q31; eTDT; FOXP2 ID PERVASIVE DEVELOPMENTAL DISORDERS; LANGUAGE DISORDER; CHROMOSOME 7Q; ETIOLOGY; GENE AB Although it is well established that genetic factors play an important role in the etiology of autistic disorder (AD), no specific genes have as yet been implicated. Genetic epidemiological data, particularly the sharp fall in concordance rates from monozygotic to dizygotic twins, indicate that the mode of transmission of this disorder is complex and may involve several genes. The 7q31 locus has been repeatedly linked to AD, suggesting that this chromosomal region is likely to harbor a susceptibility gene for AD. Recently, variations in the FOXP2 gene were reported to be responsible for a severe speech and language disorder. Because of the chromosomal location of FOXP2 (7q31) and the putative implication of the 7q31 region both in autistic and in language disorders (a feature of AD), it has been hypothesized that FOXP2 may be implicated in the pathophysiology of AD. To test this hypothesis, we screened the FOXP2 gene coding sequence for mutations in subjects diagnosed with AD and in normal controls. We identified four silent polymorphisms that were equally distributed between patients and controls. Using an intra-family association design, we identified no transmission disequilibrium in any of the four identified alleles, suggesting that the FOXP2 gene does not play a significant role in AD. (C) 2003 Wiley-Liss, Inc. C1 McGill Univ, Ctr Hlth, Res Inst, Montreal, PQ H3G 1A4, Canada. McGill Univ, Douglas Hosp, Res Ctr, Verdun, PQ, Canada. Univ Montreal, Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ, Canada. RP Rouleau, GA (reprint author), McGill Univ, Ctr Hlth, Res Inst, L7 224,1650 Cedar Ave, Montreal, PQ H3G 1A4, Canada. 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J. Med. Genet. A PD APR 15 PY 2003 VL 118A IS 2 BP 172 EP 175 DI 10.1002/ajmg.a.10105 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 670HL UT WOS:000182401400008 PM 12655497 ER PT J AU Suzuki, A Levitt, JG Blanton, R McCracken, JT Toga, A AF Suzuki, A Levitt, JG Blanton, R McCracken, JT Toga, A TI Pre-frontal cerebral mapping in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Univ Calif Los Angeles, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 213 BP 75S EP 75S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000210 ER PT J AU Levitt, JG Blanton, R Peterson, J McCracken, JT Toga, A AF Levitt, JG Blanton, R Peterson, J McCracken, JT Toga, A TI 3-dimensional brain mapping in high-functioning autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Univ Calif Los Angeles, Dept Psychiat, Lab Neuroimaging, Los Angeles, CA 90025 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 216 BP 76S EP 76S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000213 ER PT J AU Novotny, SL King, AF Allen, A DeCaria, CM Aronowitz, BR Hollander, E AF Novotny, SL King, AF Allen, A DeCaria, CM Aronowitz, BR Hollander, E TI Increased repetitive behaviors and prolactin responsivity to m-chlorophenyl-piperazine in adults with autism spectrum disorders SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 CUNY Mt Sinai Sch Med, Seaver Autism Res Ctr, Dept Psychiat, New York, NY 10029 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 237 BP 84S EP 84S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000234 ER PT J AU Hardan, A Jou, RJ Handen, BL AF Hardan, A Jou, RJ Handen, BL TI Case series: Topiramate open-label treatment of children and adolescents with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 356 BP 125S EP 125S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000348 ER PT J AU Hardan, AY Jou, RJ Minshew, NJ Keshavan, MS AF Hardan, AY Jou, RJ Minshew, NJ Keshavan, MS TI Cortical abnormalities in autism: An MRI application of the gyrification index SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Western Psychiat Inst & Clin, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 355 BP 125S EP 125S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000347 ER PT J AU Rojas, DC Smith, JA Camou, S Benkers, TL Reite, ML Rogers, SJ AF Rojas, DC Smith, JA Camou, S Benkers, TL Reite, ML Rogers, SJ TI Hippocampus and amygdala volumes in the adult parents of children with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Univ Colorado Hlth Sci, Denver, CO USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. RI Rojas, Don/F-4296-2012 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 483 BP 170S EP 170S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000470 ER PT J AU Rojas, DC Benkers, TL Camou, S Bawn, SD Reite, ML Rogers, SJ AF Rojas, DC Benkers, TL Camou, S Bawn, SD Reite, ML Rogers, SJ TI Left hemisphere volume reduction of the planum temporale in autism: A cross-sectional developmental study from 7 to 47 years SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Univ Colorado, Hlth Sci Ctr, Denver, CO USA. Univ Calif Davis, Psychiat MIND Inst, Sacramento, CA 95817 USA. RI Rojas, Don/F-4296-2012 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 564 BP 200S EP 200S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000551 ER PT J AU Page, LA Daly, E McAlanon, GM Schmitz, N Critchley, HD Murphy, DGM AF Page, LA Daly, E McAlanon, GM Schmitz, N Critchley, HD Murphy, DGM TI Asperger's Syndrome and high functioning autism: Differences in structural brain anatomy SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 58th Annual Convention and Scientific Program of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CALIFORNIA SP Soc Bio Psychiatry C1 Inst Psychiat, Dept Psychol Med, London SE5 8AF, England. Univ Hong Kong, Dept Psychiat, Hong Kong, Hong Kong, Peoples R China. Inst Neurol, Funct Imaging Lab, London WC1N 3BG, England. RI Schmitz, Nicole /F-9471-2011; daly, eileen/B-6716-2011; critchley, hugo/G-9267-2011 OI Schmitz, Nicole /0000-0003-4178-4756; NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2003 VL 53 IS 8 SU S MA 596 BP 211S EP 211S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 670XU UT WOS:000182436000582 ER PT J AU Roizen, NJ Patterson, D AF Roizen, NJ Patterson, D TI Down's syndrome SO LANCET LA English DT Review ID CELIAC-DISEASE; PRENATAL-DIAGNOSIS; ATLANTOAXIAL INSTABILITY; THYROID-FUNCTION; METABOLIC-RATE; HEARING-LOSS; TS65DN MICE; CHILDREN; PREVALENCE; DISORDERS AB The sequencing of chromosome 21 and the use of models of Down's syndrome in mice have allowed us to relate genes and sets of genes to the neuropathogenesis of this syndrome, and to better understand its phenotype. Research in prenatal screening and diagnosis aims to find methods to identify fetuses with Down's syndrome, and reduce or eliminate the need for amniocentesis. Other areas of active research and clinical interest include the association of Down's syndrome with coeliac disease and Alzheimer's disease, and improved median age of death. Medical management of the syndrome requires an organised approach of assessment, monitoring, prevention, and vigilance. Improvements in quality of life of individuals with Down's syndrome have resulted from improvements in medical care, identification and treatment of psychiatric disorders (such as depression, disruptive behaviour disorders, and autism), and early educational interventions with support in typical educational settings. Approaches and outcomes differ throughout the world. C1 SUNY Upstate Med Univ, Dept Pediat, Syracuse, NY 13210 USA. Eleanor Roosevelt Inst Denver, Denver, CO USA. 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In the USA large linked databases have provided helpful information regarding the safety of vaccines. Very little prospectively collected data on vaccine safety is available from resource poor countries, but safety concerns may be even more relevant in such settings. Vaccine manufacturers do not have to pass the same rigorous safety standards as vaccine manufacturers in rich countries. Vaccines, which protect against cholera, Japanese encephalitis, rabies or typhoid fever are predominantly used in resource poor, tropical countries and frequently do not undergo vigorous post marketing surveillance. New vaccines specifically suited for resource poor countries are sometimes marketed without the scrutiny of vigilant, independent regulatory authorities. We describe here the design and implementation of a large linked database for a semi-rural province in central Vietnam. The design overcomes several problems inherent in data bases of medical events and vaccinations in developing countries. Assigning a permanent identification (ID) number to each resident avoids the ambiguities of ID numbers based on the address. The distribution and use of medical identification cards with a permanent ID number assists in the unambiguous identification of vaccinces and patients. Medical records of all admissions are coded according to International Classification of Diseases (ICD-10) and transcribed into a computer system. Because these processes are novel the data collected by the study will be validated. Project staff will check records on vaccinations and hospital admissions through household visits at regular intervals. Data describing vaccinations and medical events are linked to the data collected by the project staff in a computer system. Based on the validation of the data we hope to optimize this model. Once we find the model working it is planned export this vaccine data safety link to other settings of similar economic status. (C) 2002 Published by Elsevier Science Ltd. C1 Int Vaccine Inst, Kwanak Ku, Seoul, South Korea. Natl Inst Hyg & Epidemiol, Hanoi, Vietnam. Prov Hlth Serv, Nha Trang, Khanh Hoa, Vietnam. RP von Seidlein, L (reprint author), Int Vaccine Inst, Kwanak Ku, SNU Campus,POB 14, Seoul, South Korea. 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Toward further elucidating the genetic structure of shyness, the authors examined four functional polymorphisms that make biological sense for contributing to the development of this phenotype: serotonin transporter promoter region 44 base pair insertion/deletion (5-HTTLPR), dopamine D-4 receptor exon III repeat (DRD4), catechol O-methyltransferase (COMT), and monoamine oxidase A promoter region repeat (MAO(A)). Method: The authors assessed shyness after recruitment of a nonclinical sample (N=118, unscreened second-grade children) using a composite scale derived from questionnaires administered to the children, parents, and teachers. DNA from buccal smears successfully obtained from 98 children was genotyped by polymerase chain reaction methods for the 5-HTTLPR, DRD4, COMT, and MAO(A) polymorphisms. Results: Significant correlations were observed for parents', teachers', and children's ratings of shyness, and Cronbach's alpha reliability was high for all three scales. 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J. Psychiat. PD APR PY 2003 VL 160 IS 4 BP 671 EP 676 DI 10.1176/appi.ajp.160.4.671 PG 6 WC Psychiatry SC Psychiatry GA 664ZZ UT WOS:000182096300013 PM 12668354 ER PT J AU Dalton, P Deacon, R Blamire, A Pike, M McKinlay, I Stein, J Styles, P Vincent, A AF Dalton, P Deacon, R Blamire, A Pike, M McKinlay, I Stein, J Styles, P Vincent, A TI Maternal neuronal antibodies associated with autism and a language disorder SO ANNALS OF NEUROLOGY LA English DT Article ID ARTHROGRYPOSIS MULTIPLEX CONGENITA; MYASTHENIA-GRAVIS; MICE; AUTOANTIBODIES; SPECTROSCOPY; CHILDREN AB Neurodevelopmental disorders could be caused by maternal antibodies or other serum factors. We detected serum antibodies binding to rodent Purkinje cells and other neurons in a mother of three children: the first normal, the second with autism, and the third with a severe specific language disorder. 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CR Adinolfi Matteo, 1993, P155 Amyes E, 2001, J NEUROIMMUNOL, V114, P259, DOI 10.1016/S0165-5728(00)00445-8 Blaes F, 2000, ANN NEUROL, V47, P504, DOI 10.1002/1531-8249(200004)47:4<504::AID-ANA14>3.0.CO;2-Q Brueton LA, 2000, AM J MED GENET, V92, P1, DOI 10.1002/(SICI)1096-8628(20000501)92:1<1::AID-AJMG1>3.0.CO;2-H Crawley J.N, 2000, WHATS WRONG MY MOUSE Deacon RMJ, 2002, BEHAV BRAIN RES, V133, P57, DOI 10.1016/S0166-4328(01)00451-X FRAHM J, 1989, MAGNET RESON MED, V9, P79, DOI 10.1002/mrm.1910090110 Guenther K, 2001, EUR J NEUROSCI, V14, P401, DOI 10.1046/j.0953-816x.2001.01645.x Jacobson L, 1999, J CLIN INVEST, V103, P1031, DOI 10.1172/JCI5943 Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X Lougee L, 2000, J AM ACAD CHILD PSY, V39, P1120, DOI 10.1097/00004583-200009000-00011 Nilsson M, 2001, J NEURAL TRANSM, V108, P1181, DOI 10.1007/s007020170008 Polizzi A, 2000, TERATOLOGY, V62, P332, DOI 10.1002/1096-9926(200011)62:5<332::AID-TERA7>3.0.CO;2-E POUSTKA F, 1998, CAMBRIDGE MONOGRAPHS, P130 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Vincent A, 2002, J NEUROIMMUNOL, V130, P243, DOI 10.1016/S0165-5728(02)00226-6 Vincent A, 1999, J NEUROIMMUNOL, V100, P169, DOI 10.1016/S0165-5728(99)00210-6 VINCENT A, 1995, LANCET, V346, P24, DOI 10.1016/S0140-6736(95)92652-6 WARREN RP, 1990, J AM ACAD CHILD PSY, V29, P873, DOI 10.1097/00004583-199011000-00005 NR 20 TC 90 Z9 93 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 2003 VL 53 IS 4 BP 533 EP 537 DI 10.1002/ana.10557 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 660PQ UT WOS:000181841900016 PM 12666123 ER PT J AU Rollins, PR AF Rollins, PR TI Caregivers' contingent comments to 9-month-old infants: Relationships with later language SO APPLIED PSYCHOLINGUISTICS LA English DT Article ID CHILDREN; VOCABULARY; ATTENTION; AUTISM; SYNTAX; ACTS AB This prospective longitudinal study examined the relationship between caregiver input to 9-month-old infants and their subsequent language. Mother-infant dyads were videotaped at ages 9, 12, and 30 months. Language comprehension (at 12 and 18 months) was measured by parent report and correlated with an independent language measure. Three maternal style variables were reduced from the 9-month data. Only caregivers' contingent comments (CCC) related to infants' later language. These findings held after infants' skill with coordinated joint attention (CJA) was taken into account. The total number of words the mothers used when their infants were 9 months predicted vocabulary; however, the predictive power was encapsulated in the words the mother used during CCC. Because studies have typically examined maternal input once infants' CJA has emerged, this work contributes to current efforts to understand variations in early language development. C1 Univ Texas, Callier Ctr Commun Disorders, Dallas, TX 75235 USA. RP Rollins, PR (reprint author), Univ Texas, Callier Ctr Commun Disorders, 1966 Inwood Rd, Dallas, TX 75235 USA. CR Afifi A. A., 1984, COMPUTER AIDED MULTI Austin J., 1962, DO THINGS WORDS BAKEMAN R, 1984, CHILD DEV, V55, P1278, DOI 10.2307/1129997 Baldwin DA, 1996, CHILD DEV, V67, P1915, DOI 10.1111/j.1467-8624.1996.tb01835.x BaronCohen S, 1997, CHILD DEV, V68, P48 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x Bates E., 1988, 1 WORDS GRAMMAR INDI Bates E, 1997, LANG COGNITIVE PROC, V12, P507 Bornstein MH, 1997, INFANT BEHAV DEV, V20, P283, DOI 10.1016/S0163-6383(97)90001-1 Bruner J. 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R., 1999, SOCIAL WORLD CHILDRE ROLLINS PR, 1999, AM J SPEECH-LANG PAT, V8, P85 Rollins PR, 1998, J CHILD LANG, V25, P653 SCARBOROUGH HS, 1990, APPL PSYCHOLINGUIST, V11, P1, DOI 10.1017/S0142716400008262 SEARLE JR, 1976, LANG SOC, V5, P1 SNOW CE, 1987, CHILDRENS LANGUAGE, V6 Snow CE, 1989, INTERACTION HUMAN DE, P83 STREECK J, 1980, DISCOURSE PROCESS, V3, P133 THAL D, 1991, J SPEECH HEAR RES, V34, P604 Thal DJ, 1999, J SPEECH LANG HEAR R, V42, P482 Tomasello M., 1983, 1ST LANGUAGE, V4, P197, DOI DOI 10.1177/014272378300401202 Tomasello M., 1999, CULTURAL ORIGINS HUM Wheeler P., 1984, WORKING PAPERS DEV P NR 39 TC 27 Z9 27 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4221 USA SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD APR PY 2003 VL 24 IS 2 BP 221 EP 234 DI 10.1017/S0142716403000110 PG 14 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 674WC UT WOS:000182659200003 ER PT J AU Nikopoulos, CK Keenan, M AF Nikopoulos, CK Keenan, M TI Promoting social initiation in children with autism using video modeling SO BEHAVIORAL INTERVENTIONS LA English DT Article; Proceedings Paper CT ABA International Convention CY NOV, 2001 CL VENICE, ITALY SP ABA ID PRESCHOOL-CHILDREN; PEER; SKILLS; SELF; PLAY; INTERVENTION; BEHAVIORS AB A large number of studies have shown that children and youths with autism can improve their social skills when provided with appropriate and well planned treatment strategies. Here, a video modeling procedure was implemented with seven developmentally delayed children, using a multiple-treatment design. Each child watched a videotape showing a model and the experimenter engaged in a simple social interactive play in an adapted play setting. Afterwards each child's behavior was assessed in this setting, while the experimenter's behavior remained the same as that shown in the videotape. The video modeling training enhanced the social initiation skills of four children. It also facilitated appropriate play engagement, which generalized across settings, peers, and toys. These changes maintained after a 1- and 2-month follow-up period. The intervention was evaluated as a time-efficient teaching tool as well as a means of enhancing appropriate play skills. Copyright (C) 2003 John Wiley Sons, Ltd. C1 Univ Ulster, Sch Psychol, Coleraine BT52 1SA, Londonderry, North Ireland. RP Keenan, M (reprint author), Univ Ulster, Sch Psychol, Cronmore Rd, Coleraine BT52 1SA, Londonderry, North Ireland. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BALLARD KD, 1984, J ABNORM CHILD PSYCH, V12, P95, DOI 10.1007/BF00913463 BRADY MP, 1987, J AUTISM DEV DISORD, V17, P375, DOI 10.1007/BF01487067 CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Charlop-Christy MH, 2000, J AUTISM DEV DISORD, V30, P537, DOI 10.1023/A:1005635326276 COOPER JO, 1987, APPL BEHAV ANAL, P365 Dowrick PW, 1999, APPL PREV PSYCHOL, V8, P23, DOI 10.1016/S0962-1849(99)80009-2 Grant L, 1994, PRINCIPLES BEHAV ANA HARING TG, 1989, J ASSOC PERS SEVERE, V14, P58 HARING TG, 1987, J APPL BEHAV ANAL, V20, P89, DOI 10.1901/jaba.1987.20-89 Hobson RP, 1999, J CHILD PSYCHOL PSYC, V40, P649, DOI 10.1111/1469-7610.00481 IHRIG K, 1988, J AUTISM DEV DISORD, V18, P67, DOI 10.1007/BF02211819 KAMPS DM, 1994, J APPL BEHAV ANAL, V27, P49, DOI 10.1901/jaba.1994.27-49 KEHLE TJ, 1990, SCHOOL PSYCHOL REV, V19, P115 KOEGEL LK, 1992, J APPL BEHAV ANAL, V25, P341, DOI 10.1901/jaba.1992.25-341 MARTIN G, 1999, BEHAV MODIFICATION W, P288 McClannahan L. E., 1999, ACTIVITY SCHEDULES C MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 McGee GG, 1999, J ASSOC PERS SEVERE, V24, P133, DOI 10.2511/rpsd.24.3.133 MORGAN RL, 1992, J APPL BEHAV ANAL, V25, P365, DOI 10.1901/jaba.1992.25-365 Pierce K, 1997, J APPL BEHAV ANAL, V30, P157, DOI 10.1901/jaba.1997.30-157 PIERCE K, 1995, J APPL BEHAV ANAL, V28, P285, DOI 10.1901/jaba.1995.28-285 Roeyers H., 1995, BRIT J SPECIAL ED, V22, P161, DOI 10.1111/j.1467-8578.1995.tb00927.x Schreibman L., 2000, J POSIT BEHAV INTERV, V2, P3, DOI 10.1177/109830070000200102 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 STRAIN PS, 1979, J AUTISM DEV DISORD, V9, P41, DOI 10.1007/BF01531291 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 ZANOLLI K, 1998, J APPL BEHAV ANAL, V31, P17 Zanolli K, 1996, J AUTISM DEV DISORD, V26, P407, DOI 10.1007/BF02172826 NR 30 TC 66 Z9 67 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR PY 2003 VL 18 IS 2 BP 87 EP 108 DI 10.1002/bin.129 PG 22 WC Psychology, Clinical SC Psychology GA 669QK UT WOS:000182361800001 ER PT J AU Galiatsatos, GT Graff, RB AF Galiatsatos, GT Graff, RB TI Combining descriptive and functional analyses to assess and treat screaming SO BEHAVIORAL INTERVENTIONS LA English DT Article; Proceedings Paper CT Annual Meeting of the Association-for-Behavior-Analysis CY MAY 26, 2001 CL NEW ORLEANS, LOUISIANA SP Assoc Behav Anal ID SELF-INJURIOUS-BEHAVIOR; DISABILITIES; REINFORCERS; SPEECH; ADULT AB This study systematically examined the functional relation between screaming and environmental events in a 13-year-old boy diagnosed with autism and PDD-NOS. A functional analysis of screaming was conducted in study 1, with six conditions (attention, demand, play, alone, tangible-toy, and tangible-edible). Highest rates of screaming were observed during the tangible-toy and tangible-edible conditions. The analog assessment was followed by a descriptive assessment, which revealed the participant was most likely to scream when teacher attention was diverted to other students. Additionally, items found to maintain screaming during the analog assessment were never delivered contingent upon screaming in the participant's natural environment. The results of the descriptive assessment suggested that the analog assessment might have produced a false-positive outcome. A treatment based upon the results of the combined assessments led to a 50% reduction in screaming within four weeks. Two-year follow-up data indicated that screaming occurred at near-zero rates. Copyright (C) 2003 John Wiley Sons, Ltd. C1 New England Ctr Children, Southborough, MA 01772 USA. Northwestern Univ, Evanston, IL 60208 USA. RP Galiatsatos, GT (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. CR BIJOU SW, 1968, J APPL BEHAV ANAL, V1, P175, DOI 10.1901/jaba.1968.1-175 Desrochers MN, 1997, AM J MENT RETARD, V101, P535 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 FOXX RM, 1988, J APPL BEHAV ANAL, V21, P411, DOI 10.1901/jaba.1988.21-411 Graff RB, 1999, BEHAV INTERVENT, V14, P233, DOI 10.1002/(SICI)1099-078X(199910/12)14:4<233::AID-BIN39>3.0.CO;2-P IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 LALLI JS, 1993, J APPL BEHAV ANAL, V26, P227, DOI 10.1901/jaba.1993.26-227 LERMAN DC, 1993, J APPL BEHAV ANAL, V26, P293, DOI 10.1901/jaba.1993.26-293 MACE FC, 1991, J APPL BEHAV ANAL, V24, P553, DOI 10.1901/jaba.1991.24-553 ONEILL RE, 1997, FUNCTIONAL ANAL PROB, P35 PACE GM, 1994, J APPL BEHAV ANAL, V27, P301, DOI 10.1901/jaba.1994.27-301 REPP AC, 1988, J APPL BEHAV ANAL, V21, P281, DOI 10.1901/jaba.1988.21-281 Shirley MJ, 1999, J APPL BEHAV ANAL, V32, P201, DOI 10.1901/jaba.1999.32-201 TOUCHETTE PE, 1985, J APPL BEHAV ANAL, V18, P343, DOI 10.1901/jaba.1985.18-343 Wilder DA, 2001, J APPL BEHAV ANAL, V34, P65, DOI 10.1901/jaba.2001.34-65 NR 15 TC 10 Z9 10 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR PY 2003 VL 18 IS 2 BP 123 EP 138 DI 10.1002/bin.133 PG 16 WC Psychology, Clinical SC Psychology GA 669QK UT WOS:000182361800003 ER PT J AU Rapin, I Dunn, M AF Rapin, I Dunn, M TI Update on the language disorders of individuals on the autistic spectrum SO BRAIN & DEVELOPMENT LA English DT Review DE autism; language disorders; subtypes; children; genetics; auditory processing; epilepsy ID VERBAL AUDITORY AGNOSIA; INFANTILE-AUTISM; SUSCEPTIBILITY GENE; TUBEROUS SCLEROSIS; BROADER PHENOTYPE; CHILDREN; DYSFUNCTION; BEHAVIOR; COMPLEX; SKILLS AB Inadequate language is a defining feature of the autism spectrum disorders (autism). Autism is a behaviorally and dimensionally defined developmental disorder of the immature brain that has a broad range of severity and many etiologies, with multiple genes involved. Early studies, which focused on the language of verbal children on the autistic spectrum, emphasized aberrant features of their speech such as unusual word choices, pronoun reversal, echolalia, incoherent discourse, unresponsiveness to questions, aberrant prosody, and lack of drive to communicate. Persistent lack of speech of some individuals was attributed to the severity-of their autism and attendant mental retardation rather than possible inability to decode auditory language. Clinical study of unselected children with autism indicated that the language deficits of preschoolers fall into two broad types, perhaps with subtypes, those that involve reception and production of phonology (sounds of speech) and syntax (grammar), and those that do not but involve semantics (meaning) and pragmatics (communicative use of language, processing, and production of discourse). Except for the preschoolers' universally deficient pragmatics and comprehension of speech, many of their language deficits parallel those of non-autistic preschoolers with developmental language disorders. There is now biological support for the clinical observation that young autistic children are language disordered as well as autistic. Recent electrophysiological studies disclose auditory input abnormalities-in lateral temporal cortex even in verbal individuals on the autistic spectrum. Severe receptive deficits for phonology enhance the risk for epilepsy. Genetic studies indicate that linkage to chromosome 7q31-33 is limited to families with evidence for phonologic impairment as well as autism. Clearly, social and cognitive disorders alone provide an inadequate explanation for the range of language deficits in autism. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10467 USA. Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA. Albert Einstein Coll Med, Rose F Kennedy Ctr Res Mental Retardat & Human De, Bronx, NY 10467 USA. RP Rapin, I (reprint author), Albert Einstein Coll Med, Saul R Korey Dept Neurol, 1300 Morris Pk Ave, Bronx, NY 10467 USA. 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PD APR PY 2003 VL 25 IS 3 BP 166 EP 172 DI 10.1016/S0387-7604(02)00191-2 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 671XL UT WOS:000182490500004 PM 12689694 ER PT J AU Kanemura, H Aihara, M Aoki, S Araki, T Nakazawa, S AF Kanemura, H Aihara, M Aoki, S Araki, T Nakazawa, S TI Development of the prefrontal lobe in infants and children: a three-dimensional magnetic resonance volumetric study SO BRAIN & DEVELOPMENT LA English DT Article DE three dimensional magnetic resonance imaging; brain volumetry; frontal lobe; prefrontal lobe ID HUMAN-BRAIN SCIENCE; FRONTAL-CORTEX; MRI; DISORDERS; DAMAGE; AUTISM AB Relatively little is known about normal prefrontal lobe development. We used three-dimensional magnetic resonance imaging (MRI)-based brain volumetry to characterize developmental changes in prefrontal lobe volumes in infants and children. Prefrontal volumes were determined in 30 subjects aged 5 months to 18 years (221 months) and 3 adults aged 28-39 years (324-468 months). Images were acquired on a 1.5-T MRI system using T1-weighted gradient-echo sequences. Volumes of the frontal and prefrontal lobes were determined using a workstation, and the prefrontal-to-frontal volume ratio was calculated. Prefrontal lobe volume increased slowly until 8 years (96 months) of age, contrasting sharply with rapid growth between 8 and 14 years (96 and 168 months). The prefrontal-to-frontal volume ratio increased with age as a sigmoid growth curve. A prefrontal growth spurt occurs in late childhood. Knowledge of prefrontal lobe development is essential for understanding cognitive development and dysfunction. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Yamanashi, Dept Pediat, Sch Med, Tamaho, Yamanashi 4093898, Japan. Univ Yamanashi, Dept Radiol, Sch Med, Yamanashi, Japan. RP Aihara, M (reprint author), Univ Yamanashi, Dept Pediat, Sch Med, 1110 Shimokato, Tamaho, Yamanashi 4093898, Japan. 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I., 1967, REGIONAL DEV BRAIN E, P3 NR 36 TC 48 Z9 52 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 APR PY 2003 VL 25 IS 3 BP 195 EP 199 DI 10.1016/S0387-7604(02)00214-0 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 671XL UT WOS:000182490500009 PM 12689699 ER PT J AU Greicius, MD AF Greicius, MD TI Neuroimaging in developmental disorders SO CURRENT OPINION IN NEUROLOGY LA English DT Article DE autism; fragile X syndrome; brain volume; MRI ID FRAGILE-X-SYNDROME; VISUOSPATIAL WORKING-MEMORY; FUSIFORM FACE AREA; AUTISTIC DISORDER; MRI; CHILDREN; GROWTH; ADULTS; AGE AB Purpose of review This review considers the role of neuroimaging in developmental disorders by highlighting recent studies in two distinct, but overlapping, developmental disorders: autism and fragile X syndrome. Recent findings After a decade of conflicting results in neuroimaging studies of autism, recent studies have provided some convergent data. One well-replicated finding is that autistic subjects have larger brains. Further, this enlargement, present as early as 3 years of age, appears to represent accelerated growth in infancy and may be followed by slowed growth in late childhood. Other findings are discussed but considered preliminary in the absence of converging evidence or replication studies. Recent work in fragile X syndrome suggests aberrant fronto-striatal and fronto-parietal networks and relates these abnormalities 'forward' to behavior and 'backward' to decreased protein expression. Summary As the field of neuroimaging has matured, it has revealed its promise as a safe, reliable, in-vivo tool in the study of developmental disorders. By insisting on larger, more homogeneous patient groups and longitudinal rather than cross-sectional studies, the field is poised to fulfill its ultimate role of linking defects in molecular biology to aberrant behavior. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA. RP Greicius, MD (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Dept Neurol & Neurol Sci, 401 Quarry Rd, Stanford, CA 94305 USA. CR Aylward EH, 2002, NEUROLOGY, V59, P175 BARNEAGORALY N, IN PRESS NEUROPSYCHI Cody H, 2002, INT J DEV NEUROSCI, V20, P421, DOI 10.1016/S0736-5748(02)00053-9 Courchesne E, 2001, NEUROLOGY, V57, P245 Eliez S, 2001, BRAIN, V124, P1610, DOI 10.1093/brain/124.8.1610 Eliez S, 2001, BIOL PSYCHIAT, V49, P540, DOI 10.1016/S0006-3223(00)01005-2 Feinstein C, 1998, J AUTISM DEV DISORD, V28, P393, DOI 10.1023/A:1026000404855 Gauthier I, 2000, J COGNITIVE NEUROSCI, V12, P495, DOI 10.1162/089892900562165 Giedd JN, 2000, AM J PSYCHIAT, V157, P281, DOI 10.1176/appi.ajp.157.2.281 Herbert MR, 2002, ANN NEUROL, V52, P588, DOI 10.1002/ana.10349 Kates WR, 2002, MICROSC RES TECHNIQ, V57, P159, DOI 10.1002/jemt.10068 Korvatska E, 2002, NEUROBIOL DIS, V9, P107, DOI 10.1006/nbdi.2002.0479 Krasuski JS, 2002, AM J PSYCHIAT, V159, P74, DOI 10.1176/appi.ajp.159.1.74 Kwon H, 2002, P NATL ACAD SCI USA, V99, P13336, DOI 10.1073/pnas.162486399 Kwon H, 2001, AM J PSYCHIAT, V158, P1040, DOI 10.1176/appi.ajp.158.7.1040 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 Rivera SM, 2002, HUM BRAIN MAPP, V16, P206, DOI 10.1002/hbm.10048 Rojas DC, 2002, NEUROSCI LETT, V328, P237, DOI 10.1016/S0304-3940(02)00521-9 Saitoh O, 2001, BRAIN, V124, P1317, DOI 10.1093/brain/124.7.1317 Sparks BF, 2002, NEUROLOGY, V59, P184 Turner G, 1996, AM J MED GENET, V64, P196, DOI 10.1002/(SICI)1096-8628(19960712)64:1<196::AID-AJMG35>3.0.CO;2-G NR 21 TC 7 Z9 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1350-7540 J9 CURR OPIN NEUROL JI Curr. Opin. Neurol. PD APR PY 2003 VL 16 IS 2 BP 143 EP 146 DI 10.1097/01.wco.0000063763.15877.d2 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 672UW UT WOS:000182542200004 PM 12644740 ER PT J AU Morey-Canellas, J Sivagamasundari, U Barton, H AF Morey-Canellas, J Sivagamasundari, U Barton, H TI A case of autism in a child with Apert's syndrome SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE acrocephalosyndactyly syndromes; Apert's syndrome; autistic spectrum disorders; pervasive developmental disorders; learning disabilities ID MEDICAL CONDITIONS AB We present the case of a 7-year-old child with Apert's syndrome who was diagnosed as suffering from childhood autism. As far as we are aware this is the first described association between autism and acrocephalosyndactyly syndromes. We discuss issues regarding the diagnosis and co-morbidity of the autistic spectrum disorders. C1 Univ Wales Coll Med, Div Psychol Med, Children & Adolescent Psychiat Sect, Cardiff CF14 4XN, S Glam, Wales. RP Morey-Canellas, J (reprint author), Univ Wales Coll Med, Div Psychol Med, Children & Adolescent Psychiat Sect, Heath Pk, Cardiff CF14 4XN, S Glam, Wales. CR Apert E., 1906, B SOC MED HOP PARIS, V23, P1310 Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561 BLANK CE, 1960, ANN HUM GENET, V24, P151 COHEN MM, 1979, PENETRANCE VARIABILI, P13 COHEN MM, 1990, AM J MED GENET, V35, P36, DOI 10.1002/ajmg.1320350108 DAVID JD, 1982, CRANIOSYNOSTOSES CAU, P205 Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 Gilmour J, 1996, ARCH DIS CHILD, V75, P25 LEFEBVRE A, 1986, BRIT J PLAST SURG, V39, P510, DOI 10.1016/0007-1226(86)90122-0 PATTON MA, 1988, J MED GENET, V25, P164, DOI 10.1136/jmg.25.3.164 RENIER D, 1986, CRAN C U VIRG CHARL RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x RUTTER MR, 1994, AUTISM DIAGNOSTIC IN Sarimski K, 1998, DEV MED CHILD NEUROL, V40, P44 SHEARER M, 1972, EXCEPT CHILDREN, V36, P210 WHEATON SW, 1894, T PATHOL SOC LOND, V45, P238 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 17 TC 3 Z9 3 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 APR PY 2003 VL 12 IS 2 BP 100 EP 102 DI 10.1007/s00787-003-0289-3 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 667AP UT WOS:000182208900007 PM 12664274 ER PT J AU Kerbeshian, J Burd, L AF Kerbeshian, J Burd, L TI Tourette syndrome and prognosis in autism SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Letter ID IMPROVEMENT; CHILDREN C1 Dept Pediat, Grand Forks, ND 58202 USA. RP Burd, L (reprint author), Dept Pediat, 501 N Colombia Rd,Box 9037, Grand Forks, ND 58202 USA. CR Baron-Cohen S, 1999, J CHILD PSYCHOL PSYC, V40, P213 FISHER W, 1988, J MENT DEFIC RES, V32, P357 KANO Y, 1987, J AM ACAD CHILD PSY, V26, P937, DOI 10.1016/S0890-8567(09)65955-4 KERBESHIAN J, 1994, J DEV PHYS DISABIL, V6, P203, DOI 10.1007/BF02578411 KERBESHIAN J, 1992, ADV NEUROL, P67 ZAPELLA M, 2002, EUROPEAN CHILD ADOLE, V11, P18 NR 6 TC 6 Z9 6 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 APR PY 2003 VL 12 IS 2 BP 103 EP 103 DI 10.1007/s00787-003-0325-3 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 667AP UT WOS:000182208900008 PM 12747386 ER PT J AU Gritti, A Bove, D Di Sarno, AM D'Addio, AA Chiapparo, S Bove, RM AF Gritti, A Bove, D Di Sarno, AM D'Addio, AA Chiapparo, S Bove, RM TI Stereotyped movements in a group of autistic children SO FUNCTIONAL NEUROLOGY LA English DT Article DE autism; child psychiatry; stereotyped movements ID BEHAVIOR AB The authors studied the stereotyped movements presented by a group of 20 autistic children, evaluating the patient observation protocols according to a psychodynamic model of autism. The stereotyped movements were analysed considering ten different parameters: type, site, morphology, frequency, association, complexity, active sensory channel, trigger event, affect during stereotyped movement, and function. The results indicate that each autistic child possesses highly idiosyncratic "stereotypical behavioural equipment", which includes behaviours ranging from simple, reflex-like actions, to much more complex movement patterns. Stereotyped movements were found to appear, in response to different stimuli, at moments when the subject's psychophysical state needed "re-setting". Eight possible functions of stereotyped movements were identified. These correspond to two main purposes: reinforcement or weakening of the autistic barrier. The need for rehabilitation is questioned, since not all stereotyped behaviours interfere with explorative and cognitive activities. C1 Univ Naples 2, Dept Psychiat Child Neuropsychiat Audiophonol & D, Naples, Italy. Fusis Assoc Res Child & Adolescent Neuropsychiat, Alvignano, Italy. RP Gritti, A (reprint author), Univ Naples 2, Cattedra Neuropsichiat Infantile, Via Pansini 5, I-80131 Naples, Italy. CR *AM PSYCH ASS, 1995, AM PSYCH ASS DIAGN S ARNAUD M, 1986, PSYCHIAT ENFANT, V29, P387 Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x BUITELAAR JK, 1991, J CHILD PSYCHOL PSYC, V32, P995, DOI 10.1111/j.1469-7610.1991.tb01925.x FREUD S, 1975, OPERE S FREUD, V7, P249 FRITH CD, 1995, NEUROBIOLOGY STEREOT, P232 Frith U., 1989, AUTISM EXPLAINING EN GIANNOTTI A, 1989, DISEGUALE Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 GOLSE B, 1993, PSYCHIAT ENFANT, V36, P413 Haag G, 1995, PSYCHIAT ENFANT, V38, P495 JONES RSP, 1995, STEREOTYPED MOVEMENT Kanner L, 1943, NERV CHILD, V2, P217 LELORD G, 1990, AUTISME ENFANT Lord C., 1995, CHILD ADOL PSYCH CL, P569 Marcelli D., 1986, POSITION AUTISTIQUE Meltzer D., 1975, EXPLORATIONS AUTISM PIAGET G, 1937, NAISSANCE INTELLIGEN Stern D., 1985, INTERPERSONAL WORLD Turner M, 1999, J CHILD PSYCHOL PSYC, V40, P839, DOI 10.1017/S0021963099004278 TUSTIN F, 1985, AUTISTIC STATES CHIL TUSTIN F, 1994, J AM PSYCHOANAL ASS, V42, P1307 Tustin F, 1994, J CHILD PSYCHOTHERAP, V20, P103, DOI 10.1080/00754179408256743 VIROLE B, 1994, NEUROPSYCHIAT ENFAN, V42, P203 NR 24 TC 9 Z9 9 PU C I C-EDIZIONI INTERNAZIONALI SRL PI ROME PA CORSO TRIESTE, 42, 00198 ROME, ITALY SN 0393-5264 J9 FUNCT NEUROL JI Funct. Neurol. PD APR-JUN PY 2003 VL 18 IS 2 BP 89 EP 94 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 707DP UT WOS:000184494400006 PM 12911139 ER PT J AU Beyer, KS Blasi, F Bacchelli, E Klauck, SM Maestrini, E Poustka, A AF Beyer, KS Blasi, F Bacchelli, E Klauck, SM Maestrini, E Poustka, A CA IMGSAC TI Mutation analysis of the coding sequence of the MECP2 gene in infantile autism (vol 111, pg 305, 2002) SO HUMAN GENETICS LA English DT Correction C1 Deutsch Krebsforschungszentrum, Dept Mol Genome Anal H0600, D-69120 Heidelberg, Germany. Univ Bologna, Dept Biol, I-40126 Bologna, Italy. RP Poustka, A (reprint author), Deutsch Krebsforschungszentrum, Dept Mol Genome Anal H0600, Neuenheimer Feld 280, D-69120 Heidelberg, Germany. RI Bailey, Anthony/J-2860-2014; Bolton, Patrick/E-8501-2010 OI Bailey, Anthony/0000-0003-4257-972X; Bolton, Patrick/0000-0002-5270-6262 CR Beyer KS, 2002, HUM GENET, V111, P305, DOI 10.1007/s00439-002-0786-3 NR 1 TC 0 Z9 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD APR PY 2003 VL 112 IS 4 BP 437 EP 437 DI 10.1007/s00439-003-0928-2 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 671KP UT WOS:000182464200019 ER PT J AU De Ahumada, LCB AF De Ahumada, LCB TI Clinical notes on a case of transvestism in a child SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Article DE transvestism; perversion; autism; oral trauma; black hole; primal scene AB This clinical presentation describes the therapeutic process,of a 5-year-old male child presenting as a main symptom quasi-delusional feminine enactments starting at an early age, which persisted for most of his five-year treatment. This symptom was understood in terms of an attempt at restitution, itself the result of being confronted with an autistic structure stemming from a series of traumatic incidents during the oral phase: his mother's pregnancy, abortion, depression and subsequent three-month absence at the end of his first year of life. The clinical material, drawings included, illustrates the interplay of oral, anal and phallic levels, with enactment predominant in sessions. The oral traumatic situation initially led. to anal-manic play, then to quasi-delusional female personifications in sessions, later surfacing as an annihilating 'black hole'. All the above issued into a broad enacted phallic-genital unfolding that dramatised an oral-genital primal scene, in the course of which he managed to structure his male identity. Near the end of the analytic process the analysand reworked the 'stages' of the link to the analyst. To end, based on the clinical material, the respective participation of the early and the late Oedipus complex is examined. RP De Ahumada, LCB (reprint author), Av Las Heras 3898,3 H, RA-1425 Buenos Aires, DF, Argentina. 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J. Psychoanal. PD APR PY 2003 VL 84 BP 291 EP 313 PN 2 PG 23 WC Psychology, Psychoanalysis SC Psychology GA 672MQ UT WOS:000182524900008 ER PT J AU Jackson, CT Fein, D Wolf, J Jones, G Hauck, M Waterhouse, L Feinstein, C AF Jackson, CT Fein, D Wolf, J Jones, G Hauck, M Waterhouse, L Feinstein, C TI Responses and sustained interactions in children with mental retardation and autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; mental retardation; play; conversation; sustained interactions ID PERVASIVE DEVELOPMENTAL DISORDERS; PLAY; COMPREHENSION; OTHERS AB Sustained interactions and responses to social bids made by children with autism and verbal-age-matched children with mental retardation were recorded in two naturalistic settings. Children with autism produced fewer positive responses and more "no responses" than children with mental retardation; both groups were more likely to make positive responses to adults and not to respond to other children. Furthermore, although the frequency of conversations was not different for the two groups, children with autism were significantly less likely to engage in sustained play compared to children with mental retardation. Results suggest that children with autism are able to master the more rote and need-oriented social skills, such as simple conversation, but may not develop other forms of social interactions, like play. C1 Univ Connecticut, Dept Psychol, Storrs, CT USA. Holland Community Hosp, Holland, MI USA. Coll New Jersey, Ewing, NJ USA. Stanford Univ, Sch Med, Div Child & Adolescent Psychiat, Palo Alto, CA 94304 USA. RP Jackson, CT (reprint author), Connecticut DMHAS Res Div, 410 Capitol Ave,MS 14RSD,POB 341431, Hartford, CT 06134 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bacon AL, 1998, J AUTISM DEV DISORD, V28, P129, DOI 10.1023/A:1026040615628 BRAVERMAN M, 1989, J AUTISM DEV DISORD, V19, P301, DOI 10.1007/BF02211848 BRUNER JS, 1994, UNDERSTANDING OTHER Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 Charman T, 1997, J AUTISM DEV DISORD, V27, P325, DOI 10.1023/A:1025806616149 DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Dunn L. 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PD APR PY 2003 VL 33 IS 2 BP 115 EP 121 DI 10.1023/A:1022927124025 PG 7 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600002 PM 12757350 ER PT J AU Robertson, K Chamberlain, B Kasari, C AF Robertson, K Chamberlain, B Kasari, C TI General education teachers' relationships with included students with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; inclusion; social relationships ID CHILD RELATIONSHIP AB In this study, we examine the relationship between general education teachers and second- and third-grade included students with autism. We also examine the effect of childrens' behavior problems on these relationships, as well as inclusion within the social environment of the classroom. Included students with autism form multidimensional relationships with their general education teachers. These relationships are associated with student's display of behavior problems and level of inclusion in the class. Specifically, when teachers perceived their relationships with included students with autism to be more positive, children's levels of behavioral problems were lower and they were more socially included in the class. C1 Univ Calif Los Angeles, Grad Sch Educ, Los Angeles, CA 90095 USA. RP Kasari, C (reprint author), Univ Calif Los Angeles, Grad Sch Educ, 3132 Moore Hall,POB 951521, Los Angeles, CA 90095 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S., 1994, UNDERSTANDING OTHER Birch SH, 1998, DEV PSYCHOL, V34, P934, DOI 10.1037//0012-1649.34.5.934 Cairns R. B., 1994, LIFELINES RISKS PATH CAIRNS RB, 1990, UNPUB IDENTIFYING SO Denham S. A., 1997, EARLY EDUC DEV, V8, P27, DOI DOI 10.1207/S15566935EED0801_3 Giangreco MF, 1997, EXCEPT CHILDREN, V64, P7 HOWES C, 1994, CHILD DEV, V65, P253, DOI 10.1111/j.1467-8624.1994.tb00748.x Kasari C, 1996, EMOTIONAL DEVELOPMENT IN ATYPICAL CHILDREN, P109 Marks SU, 1999, EXCEPT CHILDREN, V65, P315 Pianta R. C., 1992, NEW DIRECTIONS CHILD, V57, P61 Pianta R. C, 1997, EARLY EDUC DEV, V8, P11, DOI DOI 10.1207/S15566935EED0801_2 PIANTA RC, 1994, J SCHOOL PSYCHOL, V32, P15, DOI 10.1016/0022-4405(94)90026-4 Pianta R. C., 1992, PARENT ROLE OTHER AD PIANTA RC, 1992, STUDENT TEACHER REL PIANTA RC, 1995, DEV PSYCHOPATHOL, V7, P295 Plants R. C., 1991, J APPLIED DEV PSYCHO, V12, P379, DOI DOI 10.1016/0193-3973(91)90007-Q SCHOPLER E, 1995, LEARNING COGNITION A Swanson J, 1995, SNAP 4 SCALE NR 19 TC 40 Z9 42 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 123 EP 130 DI 10.1023/A:1022979108096 PG 8 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600003 PM 12757351 ER PT J AU Van Bourgondien, ME Reichle, NC Schopler, E AF Van Bourgondien, ME Reichle, NC Schopler, E TI Effects of a model treatment approach on adults with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; adults; residential; treatment outcome; longitudinal ID MENTAL-RETARDATION; BEHAVIORS; QUALITY; LIFE AB The study evaluated the effectiveness of a residential program, based on the TEACCH model, in improving the quality of the treatment program and the adaptation of individuals with autism with severe disabilities. The results indicated that participants in the Carolina Living and Learning Center experienced an increase in structure and individualized programming in the areas of communication, independence, socialization, developmental planning, and positive behavior management compared to participants in control settings. The experimental program was viewed as a more desirable place to live than the other settings, and the families were significantly more satisfied. Based on exploratory analyses, the use of the TEACCH methods over time were related to a decrease in behavior difficulties. There was no difference in the acquisition of skills. C1 Univ N Carolina, Div TEACCH, Chapel Hill, NC 27599 USA. RP Van Bourgondien, ME (reprint author), Univ N Carolina, Div TEACCH, CB 7180, Chapel Hill, NC 27599 USA. EM mvan2@email.unc.ed CR BROWN F, 1991, J ASSOC PERS SEVERE, V16, P75 BURCHINAL MR, 1994, J EARLY INTERVENTION, V18, P403 *COMM SERV AUT AD, 1995, AD RES PROGR AD VOC ELLIOTT RO, 1994, J AUTISM DEV DISORD, V24, P565, DOI 10.1007/BF02172138 Everard M. P., 1976, INT S AUT ST GALL SW HILTON A, 1987, ENCY SPECIAL ED, P1350 HOLMES DL, 1990, J AUTISM DEV DISORD, V20, P339, DOI 10.1007/BF02206546 KANNER L, 1972, J AUTISM CHILD SCHIZ, V2, P9, DOI 10.1007/BF01537624 Landesman S., 1987, LIVING ENV MENTAL RE, P79 LANDESMAN S, 1986, MENT RETARD, V24, P141 LAVIGNA GW, 1983, AUTISM ADOLESCENTS A, P381 LETTICK AL, 1983, AUTISM ADOLESCENTS A, P355 MEISBOV GB, 1980, M SE PSYCHOL ASS WAS MESIBOV G, 1988, INDIVIDUALIZED ASSES, V4 Reese RM, 1998, J AUTISM DEV DISORD, V28, P159, DOI 10.1023/A:1026096700607 SCHALOCK RL, 1989, MENT RETARD, V27, P25 SCHOPLER E, 1995, LEARNING COGNITION A SCHOPLER E, 1985, CHILDHOOD AUTISM RAT SCHOPLER E, 1990, J AUTISM DEV DISORD, V20, P291, DOI 10.1007/BF02206542 SHERMAN J, 1988, J CHILD PSYCHIAT HUM, V19, P109 SMITH MD, 1985, J AUTISM DEV DISORD, V15, P163, DOI 10.1007/BF01531602 Sparrow S, 1984, VINELAND ADAPTIVE BE STONE WL, 1987, J PEDIATR PSYCHOL, V12, P615, DOI 10.1093/jpepsy/12.4.615 VANBOURGONDIEN ME, 1989, AUTISM NATURE DIAGNO, P367 Van Bourgondien ME, 1998, RES DEV DISABIL, V19, P381 VANBOURGONDIEN ME, 1996, STATUS GARDEN, P155 VANBOURGONDIEN ME, 1993, AM ASS MENT RET WASH VANBOURGONDIEN ME, 1997, HDB AUTISM PERVASIVE, P691 VANBOURGONDIEN ME, 1990, J AUTISM DEV DISORD, V20, P299 WALL AJ, 1990, J AUTISM DEV DISORD, V20, P353 NR 30 TC 30 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 APR PY 2003 VL 33 IS 2 BP 131 EP 140 DI 10.1023/A:1022931224934 PG 10 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600004 PM 12757352 ER PT J AU Hastings, RP AF Hastings, RP TI Behavioral adjustment of siblings of children with autism engaged in applied behavior analysis early intervention programs: The moderating role of social support SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE applied behavior analysis; autism; siblings; social support ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE EARLY INTERVENTION; MENTAL-RETARDATION; DIFFICULTIES QUESTIONNAIRE; CHRONIC DISABILITIES; PROTECTIVE FACTORS; DISABLED-CHILD; YOUNG AUTISM; COMPETENCE; CHECKLIST AB There have been few studies of the impact of intensive home-based early applied behavior analysis (ABA) intervention for children with autism on family functioning. In the present study, behavioral adjustment was explored in 78 siblings of children with autism on ABA programs. First, mothers' ratings of sibling adjustment were compared to a normative sample. There were no reported increases in behavioral adjustment problems in the present sample. Second, regression analyses revealed that social support functioned as a moderator of the impact of autism severity on sibling adjustment rather than a mediator or compensatory variable. In particular, siblings in families with a less severely autistic child had fewer adjustment problems when more formal social support was also available to the family. The implications of these data for future research and for practice are discussed. C1 Univ Wales, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. RP Hastings, RP (reprint author), Univ Wales, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. EM r.hastings@bangor.ac.uk RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 CR Abidin R, 1990, PARENTING STRESS IND Aiken L, 1991, MULTIPLE REGRESSION BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 BARON RM, 1986, J PERS SOC PSYCHOL, V51, P1173, DOI 10.1037/0022-3514.51.6.1173 BERESFORD BA, 1994, J CHILD PSYCHOL PSYC, V35, P171, DOI 10.1111/j.1469-7610.1994.tb01136.x Bimbrauer J. 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 141 EP 150 DI 10.1023/A:1022983209004 PG 10 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600005 PM 12757353 ER PT J AU Toichi, M Kamio, Y AF Toichi, M Kamio, Y TI Long-term memory in high-functioning autism: Controversy on episodic memory in autism reconsidered SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; memory; concreteness; word association; serial position effect ID FREE-RECALL; SPECTRUM DISORDER; AMNESIC SYNDROME; NORMAL-CHILDREN; COMPREHENSION; CONCRETENESS; INDIVIDUALS; PERFORMANCE; SIMILARITY; CHILDHOOD AB Two studies were conducted to examine the nature of verbal long-term memory (LTM) in people with autism. In Study 1, undergraduate students showed better LTM and more verbal associations for concrete than abstract nouns. Probability of recall of the nouns strongly correlated with the number of associations with those nouns. In Study 2, unlike controls, autistic subjects did not show superior recall of concrete over abstract nouns despite overall comparable performance. A highly significant correlation between probability of recall and associative value was found only in the controls. Furthermore, there was an unusual correlation between LTM performance and a nonverbal measure in the autistic group. The results were discussed in terms of the relation between episodic memory and semantic memory. C1 Shiga Univ, Hlth & Med Serv Ctr, Otsu, Shiga 5200862, Japan. Case Western Reserve Univ, Univ Hosp Cleveland, Div Child & Adolescent Psychiat, Cleveland, OH 44106 USA. Kyoto Grad Univ, Fac Med, Dept Neuropsychiat, Kyoto, Japan. RP Toichi, M (reprint author), Shiga Univ, Hlth & Med Serv Ctr, 2-5-1 Hiratsu, Otsu, Shiga 5200862, Japan. EM motomi@mbj.sphere.ne.jp CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Baddeley A. D., 1988, COGNITIVE NEUROPSYCH, P169 Baddeley A. 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 151 EP 161 DI 10.1023/A:1022935325843 PG 11 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600006 PM 12757354 ER PT J AU Brown, WA Cammuso, K Sachs, H Winklosky, B Mullane, J Bernier, R Svenson, S Arin, D Rosen-Sheidley, B Folstein, SE AF Brown, WA Cammuso, K Sachs, H Winklosky, B Mullane, J Bernier, R Svenson, S Arin, D Rosen-Sheidley, B Folstein, SE TI Autism-related language, personality, and cognition in people with absolute pitch: Results of a preliminary study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE absolute pitch; autism; perception; information processing; central coherence; musician ID PARENTS; GENETICS AB Reports of a relatively high prevalence of absolute pitch (AP) in autistic disorder suggest that AP is associated with some of the distinctive cognitive and social characteristics seen in autism spectrum disorders. Accordingly we examined cognition, personality, social behavior, and language in 13 musicians with strictly defined AP (APS) and 33 musician controls (MC) without AP using standardized interviews and tests previously applied to identify the broad autism phenotype seen in the relatives of autistic probands. These included the Pragmatic Rating Scale (PRS) ( social aspects of language) the Personality Assessment Schedule (PAS) (rigidity, aloofness, anxiety/worry, hypersensitivity), and WAIS performance subtests (PIQ). On the basis of their behavior in the interviews, subjects were classified as socially eccentric, somewhat eccentric, or not eccentric. Forty-six percent of the APS, but only 15% of the MC, were classified as socially eccentric (p<.03). APS but not MC showed higher scores on block design than on the other PIQ tests ( p<.06), a PIQ pattern seen in autism spectrum disorders. Although APS and MC did not differ significantly on other measures it is of note that APS mean scores on the PRS and PAS (5.69, 4.92) were almost twice as high as those for the MC (3.03, 2.45). Thus, musicians with AP show some of the personality, language, and cognitive features associated with autism. Piecemeal information processing, of which AP is an extreme and rare example, is characteristic of autism and may be associated as well with subclinical variants in language and behavior. We speculate that the gene or genes that underlie AP may be among the genes that contribute to autism. C1 Brown Med Sch, Dept Psychiat, Providence, RI USA. Bradley Hosp, E Providence, RI USA. Tufts New England Med Ctr, Boston, MA USA. RP Brown, WA (reprint author), 108 Driftwood Dr, Tiverton, RI 02878 USA. EM brown@brown.edu CR Baharloo S, 1998, AM J HUM GENET, V62, P224, DOI 10.1086/301704 Baharloo S, 2000, AM J HUM GENET, V67, P755, DOI 10.1086/303057 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 FRITHU, 1989, AUTISM EXPLAINING EN Gregersen Peter K., 1996, American Journal of Human Genetics, V59, pA179 Gregersen PK, 1999, AM J HUM GENET, V65, P911, DOI 10.1086/302541 Gregersen PK, 1998, AM J HUM GENET, V62, P221, DOI 10.1086/301734 Happe F, 2001, J CHILD PSYCHOL PSYC, V42, P299, DOI 10.1111/1469-7610.00723 Heaton P, 1998, MUSIC PERCEPT, V15, P291 KLEIN M, 1984, SCIENCE, V223, P1306, DOI 10.1126/science.223.4642.1306 LANDA R, 1992, PSYCHOL MED, V22, P245 MILLER LK, 1989, MUSICAL SAVANTS Piven J, 1997, AM J MED GENET, V74, P398, DOI 10.1002/(SICI)1096-8628(19970725)74:4<398::AID-AJMG11>3.0.CO;2-D Rimland B., 1988, EXCEPTIONAL BRAIN Saffran JR, 2001, DEV PSYCHOL, V37, P74, DOI 10.1037//0012-1649.37.1.74 SCHLAUG G, 1995, SCIENCE, V267, P699, DOI 10.1126/science.7839149 Siegel DJ, 1996, J AUTISM DEV DISORD, V26, P389, DOI 10.1007/BF02172825 TAKEUCHI AH, 1993, PSYCHOL BULL, V113, P345, DOI 10.1037//0033-2909.113.2.345 Ward W.D., 1999, PSYCHOL MUSIC Zatorre RJ, 1998, P NATL ACAD SCI USA, V95, P3172, DOI 10.1073/pnas.95.6.3172 NR 21 TC 34 Z9 34 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 163 EP 167 DI 10.1023/A:1022987309913 PG 5 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600007 PM 12757355 ER PT J AU Rimland, BA AF Rimland, BA TI Commentary: Autism-related language, personality, and cognition in people with absolute pitch: Results of the preliminary study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material C1 Autism Res Inst, San Diego, CA 92116 USA. RP Rimland, BA (reprint author), Autism Res Inst, San Diego, CA 92116 USA. NR 0 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 APR PY 2003 VL 33 IS 2 BP 169 EP 169 DI 10.1023/A:1022939426751 PG 1 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600008 ER PT J AU Thompson, RJ Bolton, PF AF Thompson, RJ Bolton, PF TI Case report: Angelman syndrome in an individual with a small SMC(15) and paternal uniparental disomy: A case report with reference to the assessment of cognitive functioning and autistic symptomatology SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Angelman syndrome; chromosome 15; uniparental disomy; autism ID PRADER-WILLI-SYNDROME; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; MOLECULAR CHARACTERIZATION; LINKAGE-DISEQUILIBRIUM; MENTAL-RETARDATION; CLINICAL-FEATURES; SYNDROME GENE; PHENOTYPE; BEHAVIOR AB The case of a 15-year-old male with Angelman syndrome, paternal uniparental disomy of chromosome 15, and a small supernumerary marker chromosome is discussed. Assessment of cognitive functioning revealed an uneven profile of ability across different domains; in particular, receptive language ability was found to be superior to expressive language ability, whilst both gross and fine motor skills were found to be relatively well developed. Assessment using the Autism Diagnostic Observation Schedule showed very little evidence of autistic symptomatology. The patient showed an interest in social interaction and used a variety of methods to communicate, including some gestures and several single words. A clinical history revealed febrile convulsions during childhood but an absence of seizures in the previous 5 years. The patient was not hypopigmented, and height, weight, and head circumference were within the normal range for his age. The implications of these features are discussed in the context of previous work describing a milder phenotype in nondeletion cases of Angelman syndrome and work that has examined the prevalence of autism spectrum disorders amongst individuals with Angelman syndrome. C1 Univ Cambridge, Autism Res Ctr, Sect Dev Psychiat, Cambridge CB2 2AH, England. RP Thompson, RJ (reprint author), Chromosome 15 Project, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 171 EP 176 DI 10.1023/A:1022991410822 PG 6 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600009 PM 12757356 ER PT J AU Oliveira, G Matoso, E Vicente, A Ribeiro, P Marques, C Ataide, A Miguel, T Saraiva, J Carreira, I AF Oliveira, G Matoso, E Vicente, A Ribeiro, P Marques, C Ataide, A Miguel, T Saraiva, J Carreira, I TI Partial tetrasomy of chromosome 3q and mosaicism in a child with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; chromosome 3; partial tetrasomy 3q; mosaicism ID HUMAN HOMOLOG; LANGUAGE DISORDER; INFANTILE-AUTISM; BRAIN-STEM; GENE; LOCALIZATION; DELETION; PATIENT; CLONING; IDENTIFICATION AB In this report we describe the case of an 11-year-old male with autism and mental retardation, presenting a tetrasomy of chromosome 3q. Cytogenetic analysis showed a mosaic for an unbalanced karyotype consisting of mos46, XY, add(12)(p13.3)(56)/46, XY(45). FISH using WCP and subtelomeric probes identified the extra material on 12p to be an inverted duplication of the distal segment of chromosome 3q. Anomalies in chromosome 3q have not been previously described in association with autism, although association with psychomotor delays and behavior problems has been frequently reported and are here further discussed. This chromosomal 3q segment is therefore likely to include genes involved in specific neurodevelopment pathways, and further analysis of the region is warranted for the identification of the molecular alterations that lead to the autistic features described. C1 Hosp Pediat Coimbra, Ctr Desenvolvimento Crianca, Consulta Autismo, P-3000076 Coimbra, Portugal. Univ Coimbra, Fac Med, Unidade Citogenet, P-3000 Coimbra, Portugal. Gulbenkian Inst Sci, Oeiras, Portugal. Ctr Hosp Coimbra, Serv Genet, Coimbra, Portugal. 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 177 EP 185 DI 10.1023/A:1022943627660 PG 9 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600010 PM 12757357 ER PT J AU Challman, TD Barbaresi, WJ Katusic, SK Weaver, A AF Challman, TD Barbaresi, WJ Katusic, SK Weaver, A TI The yield of the medical evaluation of children with pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorder-not otherwise specified; medical conditions; chromosomal disorders ID AUTISTIC SPECTRUM DISORDERS; EPIDEMIOLOGIC SURVEY; INFANTILE-AUTISM; CHILDHOOD AUTISM; CLASSIFICATION; SUBGROUPS; FRENCH AB Little information is available regarding the yield of the medical evaluation of children diagnosed with pervasive developmental disorder-not otherwise specified (PDD-NOS) compared to children diagnosed with autistic disorder. Medical records were reviewed for 182 patients less than 18 years of age with either PDD-NOS or autistic disorder evaluated between 1994 and 1998 at Mayo Clinic. A condition likely to be etiologically relevant was identified in 6/117 (5.1%) patients diagnosed with PDD-NOS and 2/65 (3.1%) patients diagnosed with autistic disorder. Genetic disorders, both chromosomal and single-gene, were the most commonly identified conditions. Seizure disorders, electroencephalogram abnormalities, and anomalies on brain imaging were common in both groups. The likelihood of uncovering an etiologically relevant condition in children diagnosed with either PDD-NOS or autistic disorder may be equivalent. The scope of the etiological search in an individual patient with an autistic spectrum disorder should not be limited by the specific diagnostic category. C1 Mayo Clin, Dept Pediat & Adolescent Med, Div Dev & Behav Pediat, Rochester, MN USA. Mayo Clin, Dept Hlth Sci Res, Div Epidemiol, Rochester, MN USA. 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 187 EP 192 DI 10.1023/A:1022995611730 PG 6 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600011 PM 12757358 ER PT J AU Zwaigenbaum, L Tarnopolsky, M AF Zwaigenbaum, L Tarnopolsky, M TI Two children with muscular dystrophies ascertained due to referral for diagnosis of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Annual Meeting of the Canadian-Pediatric-Society CY JUN 17, 2001 CL VANCOUVER, CANADA SP Canadian Pediat Soc DE autism; pervasive developmental disorder; muscular dystrophy; hypotonia ID STEINERTS MYOTONIC-DYSTROPHY; ASPERGER-SYNDROME; COGNITIVE IMPAIRMENT; NATURAL-HISTORY; ATROPHY AB We report two children who were referred for diagnostic assessment for autism and were subsequently determined to have a muscular dystrophy (MD). 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 193 EP 199 DI 10.1023/A:1022947728569 PG 7 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600012 PM 12757359 ER PT J AU Baieli, S Pavone, L Meli, C Fiumara, A Coleman, M AF Baieli, S Pavone, L Meli, C Fiumara, A Coleman, M TI Autism and phenylketonuria SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE phenylketonuria; autism association ID INFANTILE-AUTISM AB Phenylketonuria (PKU) has been also reported in children with infantile autism (IA); however, the frequency of this association is variably reported. Patients with various forms of hyperphenylalaninemia (HPA) were evaluated applying two methods: the Autism Diagnostic Interview-Revised (ADI-R) and the Childhood Autism Rating Scale (CARS). A total of 243 patients were investigated, 97 with classical PKU, 62 identified by neonatal screening, and 35 late diagnosed. None out of 62 patients with classic PKU diagnosed early met criteria for autism. In the group of 35 patients diagnosed late, two boys (5.71%) ages 16 and 13 years fulfilled the diagnostic criteria for autism. The present study confirms that classical PKU is one of the causes of autism, but the prevalence seems to be very low. C1 Univ Catania, Dept Paediat, Div Paediat Neurol, I-95123 Catania, Italy. Univ Catania, Dept Paediat, Reg Ctr Inborn Errors Metab, I-95124 Catania, Italy. Georgetown Univ, Sch Med, Dept Paediat, Washington, DC USA. RP Baieli, S (reprint author), Univ Catania, Dept Paediat, Div Paediat Neurol, Via S Sofia 78, I-95123 Catania, Italy. 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PD APR PY 2003 VL 33 IS 2 BP 201 EP 204 DI 10.1023/A:1022999712639 PG 4 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600013 PM 12757360 ER PT J AU Gale, S Ozonoff, S Lainhart, J AF Gale, S Ozonoff, S Lainhart, J TI Brief report: Pitocin induction in autistic and nonautistic individuals SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pitocin; opioid system; etiology ID NEUROHYPOPHYSEAL HORMONES; OXYTOCIN; VASOPRESSIN; ATTACHMENT; MECHANISMS; DISORDERS; DEFICITS AB Oxytocin plays an important role in social-affiliative behaviors. It has been proposed that exposure to high levels of exogenous oxytocin at birth, via pitocin induction of delivery, might increase susceptibility to autism by causing a downregulation of oxytocin receptors in the developing brain. This study examined the rates of labor induction using pitocin in children with autism and matched controls with either typical development or mental retardation. Birth histories of 41 boys meeting the criteria for autistic disorder were compared to 25 age- and IQ-matched boys without autism (15 typically developing and 10 with mental retardation). There were no differences in pitocin induction rates as a function of either diagnostic group (autism vs. control) or IQ level (average vs. subaverage range), failing to support an association between exogenous exposure to oxytocin and neurodevelopmental abnormalities. C1 Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. Univ Utah, Sch Med, Dept Psychiat, Salt Lake City, UT 84112 USA. RP Ozonoff, S (reprint author), UC Davis Hlth Syst, 4860 Y St,Suite 3020, Sacramento, CA 95817 USA. EM sjozonoff@ucdavis.edu CR ARGIOLAS A, 1991, NEUROSCI BIOBEHAV R, V15, P217, DOI 10.1016/S0149-7634(05)80002-8 BAILEY A, 1995, PSYCHOL MED, V25, P63 Barberis C, 1996, CRIT REV NEUROBIOL, V10, P119 Fein D, 1997, AM J PSYCHIAT, V154, P438 FERRIS CF, 2000, EXP PHYSIOL, V85, P85 Goldberg J, 1999, CAN J PSYCHIAT, V44, P793 Green LA, 2001, BIOL PSYCHIAT, V50, P609, DOI 10.1016/S0006-3223(01)01139-8 GREIDANUS TBV, 1990, EUR J PHARMACOL, V187, P1 Hollander E, 1998, CNS SPECTRUMS, V3, P18 Insel TR, 1999, BIOL PSYCHIAT, V45, P145, DOI 10.1016/S0006-3223(98)00142-5 Insel TR, 2001, NAT REV NEUROSCI, V2, P129, DOI 10.1038/35053579 Insel TR, 1997, AM J PSYCHIAT, V154, P726 INSEL TR, 1992, PSYCHONEUROENDOCRINO, V17, P3, DOI 10.1016/0306-4530(92)90073-G Palferman S, 2001, AM J HUM GENET, V69, P570 LANDGRAF R, 1995, J NEUROENDOCRINOL, V7, P243, DOI 10.1111/j.1365-2826.1995.tb00754.x Leiter R. 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Autism Dev. Disord. PD APR PY 2003 VL 33 IS 2 BP 205 EP 208 DI 10.1023/A:1022951829477 PG 4 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600014 PM 12757361 ER PT J AU Deutsch, CK Joseph, RM AF Deutsch, CK Joseph, RM TI Brief report: Cognitive correlates of enlarged head circumference in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; head circumference; IQ; macrocephaly ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM AB This study examined the frequency and cognitive correlates of enlarged head circumference in a sample of 63 children with autism between the ages of 4 and 14. Consistent with prior evidence, macrocephaly occurred at a significantly higher frequency than in a normal reference sample. Head circumference was not associated with language or executive functioning, nor was it related to verbal or nonverbal IQ. Head circumference was, however, correlated with discrepancies between verbal and nonverbal IQ scores, independent of absolute level of verbal ability. Children with discrepantly high nonverbal abilities had a mean standardized head circumference that was more than 1 SD greater than in the reference sample, and that was significantly greater than in autistic children with a relative verbal advantage or no discrepancy in cognitive abilities, for whom mean head circumference was within normal limits. This convergence of physical and cognitive features suggests a possible etiologically significant subtype of autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Univ Massachusetts, Sch Med, Eunice Kennedy Shriver Ctr, Worcester, MA 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 APR PY 2003 VL 33 IS 2 BP 227 EP 229 DI 10.1023/A:1022964132203 PG 3 WC Psychology, Developmental SC Psychology GA 659EB UT WOS:000181763600020 ER PT J AU Shamay-Tsoory, SG Tomer, R Berger, BD Aharon-Peretz, J AF Shamay-Tsoory, SG Tomer, R Berger, BD Aharon-Peretz, J TI Characterization of empathy deficits following prefrontal brain damage: The role of the right ventromedial prefrontal cortex SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID FRONTAL-LOBE DAMAGE; RIGHT-HEMISPHERE; ASPERGER-SYNDROME; SOCIAL COGNITION; AMYGDALA DAMAGE; MIND; RECOGNITION; AUTISM; LANGUAGE; CHILDREN AB Impaired empathic response has been described in patients following brain injury, suggesting that empathy may be a fundamental aspect of the social behavior disturbed by brain damage. However, the neuroanatomical basis of impaired empathy has not been studied in detail. The empathic response of patients with localized lesions in the prefrontal cortex (n = 25) was compared to responses of patients with posterior (n = 17) and healthy control subjects (n = 19). To examine the cognitive processes that underlie the empathic ability. the relationships between empathy scores and the performance on tasks that assess processes of cognitive flexibility, affect recognition, and theory of mind (TOM) were also examined. Patients with prefrontal lesions, particularly when their damage included the ventromedial prefrontal cortex, were significantly impaired in empathy as compared to patients with posterior lesions and healthy controls. However, among Patients with posterior lesions, those with damage to the right hemisphere were impaired, whereas those with left posterior lesions displayed empathy levels similar to healthy controls. Seven of nine patients with the most profound empathy deficit had a right ventromedial lesion. A differential pattern regarding the relationships between empathy and cognitive performance was also found: Whereas among patients with dorsolateral prefrontal damage empathy was related to cognitive flexibility but not to TOM and affect recognition, empathy scores in patients with ventromedial lesions were related to TOM but not to cognitive flexibility. Our findings suggest that prefrontal structures play an important part in a network mediating the empathic response and specifically that the right ventromedial cortex has a unique role in integrating cognition and affect to produce the empathic response. C1 Univ Haifa, Dept Psychol, IL-31905 Haifa, Israel. Rambam Med Ctr, Haifa, Israel. RP Shamay-Tsoory, SG (reprint author), Univ Haifa, Dept Psychol, IL-31905 Haifa, Israel. 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The medical charts of 15 children and adolescents (aged 6-16 yr) with Asperger syndrome, autism, or PDD not otherwise specified treated with citalopram were retrospectively reviewed. The final dose of citalopram was 16.9 +/- 12.1 mg/day with a treatment duration of 218.8 +/- 167.2 days. Independent ratings of the Clinical Global Impression (CGI) Severity and Improvement scales allowed comparison between baseline and PDD symptoms at the last visit. Eleven adolescents (73%) exhibited significant improvement in PDD, anxiety, or mood CGI score (z = 2.95; p = .003). Anxiety symptoms associated with PDDs improved significantly in 66% of patients (z = 2.83, p = .005), and mood symptoms improved significantly in 47% of patients (z = 2.78, p = .005). Mild side effects were reported by five patients (33%). These data suggest citalopram may be effective, safe, and well tolerated as part of the treatment of PDDs. 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Dev. Behav. Pediatr. PD APR PY 2003 VL 24 IS 2 BP 104 EP 108 PG 5 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 669LB UT WOS:000182351800004 PM 12692455 ER PT J AU Serajee, FJ Zhong, H Nabi, R Huq, AHMM AF Serajee, FJ Zhong, H Nabi, R Huq, AHMM TI The metabotropic glutamate receptor 8 gene at 7q31: partial duplication and possible association with autism SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID QUANTITATIVE-TRAIT LOCI; LINKAGE DISEQUILIBRIUM; INFANTILE-AUTISM; FUNCTIONAL EXPRESSION; SUSCEPTIBILITY GENE; NUCLEAR FAMILIES; GENOMIC SCREEN; DISORDER; TESTS; BRAIN C1 Wayne State Univ, Dept Pediat, Detroit, MI 48201 USA. Wayne State Univ, Dept Neurol, Detroit, MI 48201 USA. RP Huq, AHMM (reprint author), Childrens Hosp Michigan, Div Neurol, 3901 Beaubien Blvd, Detroit, MI 48201 USA. 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Med. Genet. PD APR PY 2003 VL 40 IS 4 AR e42 DI 10.1136/jmg.40.4.e42 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 666BN UT WOS:000182155900024 PM 12676915 ER PT J AU Marshall, BL Napolitano, DA McAdam, DB Dunleavy, JJ Tessing, JL Varrell, J AF Marshall, BL Napolitano, DA McAdam, DB Dunleavy, JJ Tessing, JL Varrell, J TI Venlafaxine and increased aggression in a female with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 Bancroft NeuroHealth, Haddonfield, NJ USA. RP Marshall, BL (reprint author), Bancroft NeuroHealth, Haddonfield, NJ USA. NR 0 TC 4 Z9 4 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 APR PY 2003 VL 42 IS 4 BP 383 EP 384 DI 10.1097/01.CHI.0000052508.98293.DE PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 658DN UT WOS:000181706500003 PM 12649624 ER PT J AU Constantino, JN Hudziak, JJ Todd, RD AF Constantino, JN Hudziak, JJ Todd, RD TI Deficits in reciprocal social behavior in male twins: Evidence for a genetically independent domain of psychopathology SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; pervasive developmental disorders; Social Responsiveness Scale; twins; genetic epidemiology ID INCIDENCE AUTISM FAMILIES; PHENOTYPE; DISORDERS; CHILDREN AB Objective: Previous studies have demonstrated substantial genetic influences on many child psychiatric disorders, including autism. In this study the authors attempted to quantify the degree to which genetic influences on deficits in reciprocal social behavior (a defining feature of pervasive developmental disorders) are shared with genetic influences on other domains of behavior in children. Method: Child Behavior Checklists (CBCL) and Social Responsiveness Scales (SRS) were completed for an epidemiological sample of 219 pairs of male twins. The SRS (formerly known as the Social Reciprocity Scale) is a measure of social impairment that distinguishes children with autism spectrum disorders from those with other child psychiatric disorders. Results: Regression analysis indicated that CBCL syndromes account for 43% of the variance in SRS scores. Bivariate analyses revealed that SRS scores are affected, in part, by phenotypic influences from the CBCL Social Problem syndrome. Forty-four percent of the causal influences on SRS scores, however, are independent from those on CBCL syndromes and are genetic in nature (90% confidence interval: 0.38-0.49). Conclusion: These results support the existence of a continuous distribution of deficits in reciprocal social behavior in the population, which are substantially genetically independent from other domains of child psychopathology. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Univ Vermont, Coll Med, Burlington, VT USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, Campus Box 8134,660 S Euclid Ave, St Louis, MO 63110 USA. EM constanino@psychiatry.wustl.edu CR Achenbach T. 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PD APR PY 2003 VL 42 IS 4 BP 458 EP 467 DI 10.1097/01.CHI.0000046811.95464.21 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 658DN UT WOS:000181706500012 PM 12649633 ER PT J AU Seeman, C AF Seeman, C TI Conquering autism: Reclaiming your child through natural therapies. 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 EDELSON SB, 2003, CONQ AUT RECL YOUR C NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 1 PY 2003 VL 128 IS 6 BP 121 EP 121 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 673WP UT WOS:000182603500152 ER PT J AU Singh, VK Jensen, RL AF Singh, VK Jensen, RL TI Elevated levels of measles antibodies in children with autism SO PEDIATRIC NEUROLOGY LA English DT Article ID AUTOANTIBODIES; RUBELLA; VIRUS AB Virus-induced autoimmunity may play a causal role in autism. To examine the etiologic link of viruses in this brain disorder, we conducted a serologic study of measles virus, mumps virus, and rubella virus. Viral antibodies were measured by enzyme-linked immunosorbent assay in the serum of autistic children, normal children, and siblings of autistic children. The level of measles antibody, but not mumps or rubella antibodies, was significantly higher in autistic children as compared with normal children (P = 0.003) or siblings of autistic children (P less than or equal to 0.0001). Furthermore, immunoblotting of measles vaccine virus revealed that the antibody was directed against a protein of approximately 74 kd molecular weight. The antibody to this antigen was found in 83% of autistic children but not in normal children or siblings of autistic children. Thus autistic children have a hyperimmune response to measles virus, which in the absence of a wild type of measles infection might be a sign of an abnormal immune reaction to the vaccine strain or virus reactivation. (C) 2003 by Elsevier Inc. All rights reserved. C1 Utah State Univ, Ctr Biotechnol, Logan, UT 84322 USA. Utah State Univ, Dept Biol, Logan, UT 84322 USA. RP Singh, VK (reprint author), Utah State Univ, Ctr Biotechnol, 4700 Old Main Hall, Logan, UT 84322 USA. 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PD APR PY 2003 VL 28 IS 4 BP 292 EP 294 DI 10.1016/S0887-8994(02)00627-6 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 701AP UT WOS:000184143600007 PM 12849883 ER PT J AU Byrd, RS AF Byrd, RS TI County-specific increases in autism in California SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Univ Calif Davis, Med Ctr, Sacramento, CA 95817 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 393 BP 69A EP 70A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900394 ER PT J AU Sukumaran, M Rappaport, L Munir, K Ware, J Wypij, D Albert-Berman, A Teixeira-Pinta, A Wu, A AF Sukumaran, M Rappaport, L Munir, K Ware, J Wypij, D Albert-Berman, A Teixeira-Pinta, A Wu, A TI Case control study of parental fertility and autism SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Childrens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 392 BP 69A EP 69A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900393 ER PT J AU Zachor, DA Eithan, D Ben Izhak, E AF Zachor, DA Eithan, D Ben Izhak, E TI Early intensive behavioral intervention for young children with autism (1.5-3y) in a unique preschool setting-outcome after one year SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Tel Aviv Univ, IL-69978 Tel Aviv, Israel. Bar Ilan Univ, IL-52100 Ramat Gan, Israel. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 394 BP 70A EP 70A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900395 ER PT J AU Harrington, JW Brand, DA Edwards, KS Patrick, PA AF Harrington, JW Brand, DA Edwards, KS Patrick, PA TI Parents' perspectives on their children with autism: Etiology, diagnosis, and treatment SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA. New York Med Coll, Ctr Primary Care Educ & Res, Valhalla, NY 10595 USA. Westchester Cty Med Ctr, Westchester Inst Human Dev, Valhalla, NY 10595 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 434 BP 77A EP 77A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900435 ER PT J AU Hsu, BS Miles, JH Takahashi, NT Maria, BL AF Hsu, BS Miles, JH Takahashi, NT Maria, BL TI Family history in Joubert syndrome and autism: A comparative analysis SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Univ Missouri Hlth Care, Columbia, MO USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 435 BP 77A EP 77A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900436 ER PT J AU Solomon, R Necheles, J Ferch, C Crawford, K AF Solomon, R Necheles, J Ferch, C Crawford, K TI Program evaluation of a statewide autism training and early intervention project: The University of Michigan PLAY Project SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Univ Michigan, Ann Arbor, MI 48109 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 450 BP 79A EP 80A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900451 ER PT J AU Solomon, R Necheles, J Ferch, C Crawford, K AF Solomon, R Necheles, J Ferch, C Crawford, K TI The University of Michigan PLAY Project Home Consultation (PPHC) program for young children with autism: Initial program evaluation SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Univ Michigan, Ann Arbor, MI 48109 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 449 BP 79A EP 79A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897900450 ER PT J AU Liu, DT Miles, JH Yu, PT Takahashi, NT Sahota, PK Bernard, ML AF Liu, DT Miles, JH Yu, PT Takahashi, NT Sahota, PK Bernard, ML TI Sleep disorders in Joubert syndrome and autism: A comparative analysis SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Society CY MAY 03-06, 2003 CL SEATTLE, WASHINGTON SP Pediat Acad Soc, Amer Pediat Soc, Soc Pediat Res, Ambulatory Pediat Assoc, Tulane Univ Hlth Sci Ctr, Ctr Continuing Educ C1 Univ Missouri Hlth Care, Columbia, MO USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2003 VL 53 IS 4 SU S MA 3121 BP 551A EP 551A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 661PA UT WOS:000181897903118 ER PT J AU Takaoka, K Takata, T AF Takaoka, K Takata, T TI Catatonia in childhood and adolescence SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Review DE autism; adolescent; catatonia; child; informed consent; malignant catatonia; pervasive developmental disorders ID NEUROLEPTIC MALIGNANT SYNDROME; FATAL HYPERTHERMIA SYNDROME; ELECTROCONVULSIVE-THERAPY; MENTAL-RETARDATION; LETHAL CATATONIA; YOUNG-PEOPLE; ECT; SCHIZOPHRENIA; STUPOR; DISORDERS AB Child and adolescent catatonia has been poorly investigated. A literature review was undertaken to clarify phenomenology, diagnosis, etiology, and treatment as well as ethical problems of catatonia in childhood and adolescence. Although there are no accepted standardized criteria for catatonia in childhood and adolescence, catatonic features described by child psychiatrists are similar to Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV) criteria for catatonia. With respect to etiology, the motor and behavioral symptoms that are part of catatonia bear some similarities with those seen in autism. Several case reports suggest an association between catatonia and general medical conditions. Certain drugs abused by youngsters as well as prescribed medicine can induce catatonia. Regarding catatonic cases originally diagnosed as schizophrenia, it is unclear whether all of these cases should be identified as schizophrenia or whether some of them are pervasive developmental disorders that develop psychic features in adolescence. Environmental changes preceding the onset of catatonia in patients with mood disorder play a possibly important role. Examples that suggest stress-induced catatonia, although rare, also exist. A few patients exhibit features of malignant catatonia, some without taking neuroleptics and others having taken them. Benzodiazepines and electroconvulsive therapy are considered to be effective treatments for catatonic youngsters. C1 Gifu Univ, Fac Med, Dept Psychopathol, Gifu 5008705, Japan. RP Takaoka, K (reprint author), Gifu Univ, Fac Med, Dept Psychopathol, 40 Tsukasa Machi, Gifu 5008705, Japan. 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E., 1992, CRITICAL ISSUES SPEC Zager D., 1999, AUTISM IDENTIFICATIO Zionts P., 1997, INCLUSION STRATEGIES NR 92 TC 33 Z9 33 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 APR-JUN PY 2003 VL 23 IS 2 BP 116 EP 133 PG 18 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 683PM UT WOS:000183158000005 ER PT J AU Koegel, LK Carter, CM Koegel, RL AF Koegel, LK Carter, CM Koegel, RL TI Teaching children with autism self-initiations as a pivotal response SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE autism; grammatical acquisition; language interventions; morphology; pivotal behaviors; self-initiations ID GRAMMATICAL MORPHEME ACQUISITION; LANGUAGE; INTERVENTION; VERBS; TALK AB The purpose of this study was to assess whether children with autism could be taught a child-initiated query as a pivotal response to facilitate the use of grammatical morphemes. Data were collected within the context of a multiple baseline design across two children who lacked the use of temporal morphemes. Results of the study indicated that both children learned the self-initiated strategy and both acquired and generalized the targeted morpheme. Additionally, generalized use of the self-initiation into other question forms and concomitant increases in mean length of utterance, verb acquisition, and diversity of verb use occurred for both children. These generalized effects and the applications of this procedure across linguistic targets are discussed. C1 Univ Calif Santa Barbara, Grad Sch Educ, Counseling Clin Sch Psychol Clin, Santa Barbara, CA 93106 USA. RP Koegel, RL (reprint author), Univ Calif Santa Barbara, Grad Sch Educ, Counseling Clin Sch Psychol Clin, Santa Barbara, CA 93106 USA. 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Lang. Disord. PD APR-JUN PY 2003 VL 23 IS 2 BP 134 EP 145 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 683PM UT WOS:000183158000006 ER PT J AU Polirstok, SR Dana, L Buono, S Mongelli, V Trubia, G AF Polirstok, SR Dana, L Buono, S Mongelli, V Trubia, G TI Improving functional communication skills in adolescents and young adults with severe autism using gentle teaching and positive approaches SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE autism; functional communication; gentle teaching; humanistic applied behavior analysis; positive approaches; self-injury; stereotypy AB A therapeutic intervention program for young adults with severe autism at the Oasi Institute in Troina Sicily is examined. The program, which integrates gentle teaching, humanistic applied behavior analysis, and functional communication training, values human interactions and provides opportunities to acquire functional skills through errorless learning activities. Reported are the results of an 18-month study to determine whether significant improvements in functional communication skills and an accompanying reduction in maladaptive/stereotypic behaviors could be evidenced in the environment using gentle teaching and positive approaches. The guiding principles of the program, its design, and staff training components are described along with an analysis of program findings. C1 CUNY Herbert H Lehman Coll, Bronx, NY 10468 USA. IRCCS Oasi Maria SS, Psychol Unit, Troina, Sicily, Italy. RP Polirstok, SR (reprint author), CUNY Herbert H Lehman Coll, Hall B-33,250 Bedford Pk Blvd W, Bronx, NY 10468 USA. CR BAILEY JS, 1992, J APPL BEHAV ANAL, V25, P879, DOI 10.1901/jaba.1992.25-879 DURAND VM, 1992, FUNCTIONAL COMMUNICA HALL PS, 1992, J HUMANISTIC ED DEV, V31, P22 MAZZELLI AM, 2000, J HUMANISTIC COUNSEL, V38, P206 McGee J., 1991, GENTLE TEACHING NONA McGee J. J., 1987, GENTLE TEACHING NONA *NEW YORK STAT OFF, 1988, STRAT CRIS INT PREV Polirstok S. R., 1986, ED TREATMENT CHILDRE, V9, P101 Sparrow S, 1984, VINELAND ADAPTIVE BE Sulzer-Azaroff B., 1991, BEHAV ANAL LASTING C WARREN B, 1991, POSITIVE APPROACHES, V1 NR 11 TC 3 Z9 3 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 APR-JUN PY 2003 VL 23 IS 2 BP 146 EP 153 PG 8 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 683PM UT WOS:000183158000007 ER PT J AU Safran, SP Safran, JS Ellis, K AF Safran, SP Safran, JS Ellis, K TI Intervention ABCs for children with Asperger syndrome SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE Asperger syndrome; diagnosis; school-based intervention ID AUTISM DIAGNOSTIC INTERVIEW; TOTAL POPULATION; DISORDERS; EPIDEMIOLOGY AB The number of children identified with Asperger syndrome (AS) is rapidly rising throughout the world. The purpose of this article is to promote understanding of the characteristics and behaviors associated with AS and to introduce a range of school-based interventions. First, a description of the indicators of AS is provided, followed by an overview of screening and diagnostic procedures. Next, the Application ABCs section covers knowledge-based interventions addressing deficits in Academics, Behavior, and Communication. Implications for speech language pathologists and related professionals working with youngsters with this autistic spectrum disorder are addressed. C1 Ohio Univ, Athens, OH 45701 USA. RP Safran, SP (reprint author), Coll Educ, McCracken Hall 201-202, Athens, OH 45701 USA. 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L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Szatmari P., 2000, ASPERGER SYNDROME, P403 Szatmari P, 1998, ASPERGER SYNDROME HI, P61 Terpstra J. E., 2002, FOCUS AUTISM OTHER D, V17, P119, DOI 10.1177/10883576020170020701 Williams K., 1995, FOCUS AUTISTIC BEHAV, V10, P9 Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 NR 57 TC 17 Z9 17 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 APR-JUN PY 2003 VL 23 IS 2 BP 154 EP 165 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 683PM UT WOS:000183158000008 ER PT J AU Johnson, SC AF Johnson, SC TI Detecting agents SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Article DE agency; infancy; self-propelled motion; intentionality; theory of mind; autism ID JOINT VISUAL-ATTENTION; FACE RECOGNITION; INFANTS; OBJECTS; PEOPLE; IMITATION; DIFFERENTIATION; DISCRIMINATION; COMMUNICATION; PERCEPTION AB This paper reviews a recent set of behavioural studies that examine the scope and nature of the representational system underlying theory-of-mind development. Studies with typically developing infants, adults and children with autism all converge on the claim that there is a specialized input system that uses not only morphological cues, but also behavioural cues to categorize novel objects as agents. Evidence is reviewed in which 12- to 15-month-old infants treat certain non-human objects as if they have perceptual/attentional abilities, communicative abilities and goal-directed behaviour. They will follow the attentional orientation of an amorphously shaped novel object if it interacts contingently with them or with another person. They also seem to use a novel object's environmentally directed behaviour to determine its perceptual/attentional orientation and object-oriented goals. Results from adults and children with autism are strikingly similar, despite adults' contradictory beliefs about the objects in question and the failure of children with autism to ultimately develop more advanced theory-of-mind reasoning. The implications for a general theory-of-mind development are discussed. C1 Stanford Univ, Dept Psychol, Stanford, CA 94305 USA. RP Johnson, SC (reprint author), Stanford Univ, Dept Psychol, Jordan Hall,Bldg 420, Stanford, CA 94305 USA. 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Trans. R. Soc. B-Biol. Sci. PD MAR 29 PY 2003 VL 358 IS 1431 BP 549 EP 559 DI 10.1098/rstb.2002.1237 PG 11 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 662GY UT WOS:000181940000011 PM 12689380 ER PT J AU Blair, RJR AF Blair, RJR TI Facial expressions, their communicatory functions and neuro-cognitive substrates SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Review DE facial expressions; amygdala; communication; psychopath; autism ID BILATERAL AMYGDALA DAMAGE; TEMPORAL VISUAL-CORTEX; FUSIFORM FACE AREA; PREFRONTAL CORTEX; HUMAN-BRAIN; SELECTIVE IMPAIRMENT; SOCIAL INFORMATION; AUTISTIC-CHILDREN; SMILE PRODUCTION; EMOTIONAL FACES AB Human emotional expressions serve a crucial communicatory role allowing the rapid transmission of valence information from one individual to another. This paper will review the literature on the neural mechanisms necessary for this communication: both the mechanisms involved in the production of emotional expressions and those involved in the interpretation of the emotional expressions of others. Finally, reference to the neuro-psychiatric disorders of autism, psychopathy and acquired sociopathy will be made. In these conditions, the appropriate processing of emotional expressions is impaired. In autism, it is argued that the basic response to emotional expressions remains intact but that there is impaired ability to represent the referent of the individual displaying the emotion. In psychopathy, the response to fearful and sad expressions is attenuated and this interferes with socialization resulting in an individual who fails to learn to avoid actions that result in harm to others. In acquired sociopathy, the response to angry expressions in particular is attenuated resulting in reduced regulation of social behaviour. C1 NIMH, Unit Affect Cognit Neurosci, Mood & Anxiety Disorders Program, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA. RP Blair, RJR (reprint author), NIMH, Unit Affect Cognit Neurosci, Mood & Anxiety Disorders Program, Dept Hlth & Human Serv,NIH, Room 206,MSC 2670,15K N Dr, Bethesda, MD 20892 USA. 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Trans. R. Soc. B-Biol. Sci. PD MAR 29 PY 2003 VL 358 IS 1431 BP 561 EP 572 DI 10.1098/rstb.2002.1220 PG 12 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 662GY UT WOS:000181940000012 PM 12689381 ER PT J AU Gai, M Matsumoto, H Suzuki, K Ozawa, F Fukuda, R Uchiyama, I Suckling, J Isoda, H Mori, N Takei, N AF Gai, M Matsumoto, H Suzuki, K Ozawa, F Fukuda, R Uchiyama, I Suckling, J Isoda, H Mori, N Takei, N TI fMRl study of recognition of facial expressions in high-functioning autistic patients SO NEUROREPORT LA English DT Article DE autistic disorder; functional magnetic resonance imaging (fMRI); high-functioning; recognition of facial expressions; social dysfunction ID CEREBRAL BLOOD-FLOW; CHILDHOOD AUTISM; BRAIN; PERCEPTION; AMYGDALA; DISGUST; NEUROANATOMY; HIPPOCAMPUS; ADOLESCENTS; INDIVIDUALS AB Autistic disorder is associated with deficits in social function. The disorder may be related to dysfunction in the brain regions that are involved in the process of recognising facial expressions of other persons. Using fMRI, we investigated whether autistic patients with relatively high IQ would have different brain activation on the tasks of recognition of facial expressions (i.e. faces expressing disgust, fear, and happiness) compared with normal control subjects. In disgust and fear recognition tasks, there were different patterns of brain activation in the cortico-limbic neural circuits qbetween autistic and normal groups. Patients with autistic disorder may have difficulty in grasping facially expressed qemotions in others, and thereby cannot manipulate the interpersonally derived information. C1 Stanley Fdn Res Ctr Japan, Hamamatsu, Shizuoka 4313192, Japan. Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 4313192, Japan. Hamamatsu Univ Sch Med, Dept Radiol, Hamamatsu, Shizuoka 4313192, Japan. Tokai Univ, Sch Med, Dept Psychiat & Behav Sci, Isehara, Kanagawa 2591193, Japan. Univ Tokyo, Dept Psychiat, Bunkyo Ku, Tokyo 1138655, Japan. Doshisha Univ, Dept Psychol, Kyoto 6028580, Japan. Univ Cambridge, Addenbrookes Hosp, Dept Psychiat, Cambridge CB2 2QQ, England. Inst Psychiat, Dept Psychol Med, London SE5 8AF, England. RP Takei, N (reprint author), Stanley Fdn Res Ctr Japan, 1-20-1 Handayama, Hamamatsu, Shizuoka 4313192, Japan. 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NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD MAR 15 PY 2003 VL 60 IS 1 SU S BP 42 EP 42 DI 10.1016/S0920-9964(03)80122-6 PG 1 WC Psychiatry SC Psychiatry GA 658DE UT WOS:000181705700122 ER PT J AU Amaral, DG Schumann, CM AF Amaral, DG Schumann, CM TI MRI and postmortem stereological investigation of the amygdala in autism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2003 Meeting CY APR 11-15, 2003 CL SAN DIEGO, CALIFORNIA C1 Univ Calif Davis, Davis, CA 95616 USA. RI Frank, David/E-8213-2012 NR 0 TC 0 Z9 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 14 PY 2003 VL 17 IS 4 SU S BP A379 EP A379 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 658QZ UT WOS:000181733101802 ER PT J AU Jansson-Verkasalo, E Ceponiene, R Kielinen, M Suominen, K Jantti, V Linna, SL Moilanen, I Naatanen, R AF Jansson-Verkasalo, E Ceponiene, R Kielinen, M Suominen, K Jantti, V Linna, SL Moilanen, I Naatanen, R TI Deficient auditory processing in children with Asperger Syndrome, as indexed by event-related potentials SO NEUROSCIENCE LETTERS LA English DT Article DE Asperger syndrome; auditory event-related potentials; mismatch negativity ID DISCRIMINATION; AUTISM; SPEECH AB Asperger Syndrome (AS) is characterized by normal language development but deficient understanding and use of the intonation and prosody of speech. While individuals with AS report difficulties in auditory perception, there are no studies addressing auditory processing at the sensory level. In this study, event-related potentials (ERP) were recorded for syllables and tones in children with AS and in their control counterparts. Children with AS displayed abnormalities in transient sound-feature encoding, as indexed by the obligatory ERPs, and in sound discrimination, as indexed by the mismatch negativity. These deficits were more severe for the tone stimuli than for the syllables. These results indicate that auditory sensory processing is deficient in children with AS, and that these deficits might be implicated in the perceptual problems encountered by children with AS. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Oulu Univ, Dept Finnish Saami & Logoped, Oulu, Finland. Oulu Univ Hosp, Cognit Lab, FIN-90029 OYS, Finland. Univ Helsinki, Cognit Brain Res Unit, Dept Psychol, Helsinki, Finland. Univ Calif San Diego, Ctr Res Language, San Diego, CA 92103 USA. Oulu Univ Hosp, Dept Child Psychiat, Oulu, Finland. RP Jansson-Verkasalo, E (reprint author), Oulu Univ, Dept Finnish Saami & Logoped, Oulu, Finland. 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Lett. PD MAR 6 PY 2003 VL 338 IS 3 BP 197 EP 200 DI 10.1016/S0304-3940(02)01405-2 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 647CZ UT WOS:000181076000006 PM 12581830 ER PT J AU Spitzer, WO AF Spitzer, WO TI Measles, mumps, and rubella vaccination and autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 McGill Univ, Montreal, PQ H3G 1A4, Canada. RP Spitzer, WO (reprint author), McGill Univ, Montreal, PQ H3G 1A4, Canada. CR Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Spitzer Walter O., 2001, Adverse Drug Reactions and Toxicological Reviews, V20, P160 NR 2 TC 6 Z9 6 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. 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RP Noble, KK (reprint author), Childrens Natl Med Ctr, Tokyo 1578535, Japan. CR Campion EW, 2002, NEW ENGL J MED, V347, P1474, DOI 10.1056/NEJMp020125 Terada Kihei, 2002, Kansenshogaku Zasshi, V76, P180 2002, MMWR MORB MORTAL WKL, V51, P120 NR 3 TC 2 Z9 2 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 6 PY 2003 VL 348 IS 10 BP 952 EP 953 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 651UU UT WOS:000181341100017 ER PT J AU Wakefield, AJ AF Wakefield, AJ TI Measles, mumps, and rubella vaccination and autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Int Child Dev Resource Ctr, Boca Raton, FL 33431 USA. RP Wakefield, AJ (reprint author), Int Child Dev Resource Ctr, Boca Raton, FL 33431 USA. CR Bagenstose LM, 2001, PARASITE IMMUNOL, V23, P633, DOI 10.1046/j.1365-3024.2001.00427.x Uhlmann V., 2002, Molecular Pathology, V55, P84, DOI 10.1136/mp.55.2.84 Wakefield A, 2002, MOL PSYCHIATR, V7, pS44, DOI 10.1038/sj.mp.4001178 Wakefield AJ, 1999, ISR MED ASSOC J, V1, P183 NR 4 TC 1 Z9 1 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 6 PY 2003 VL 348 IS 10 BP 952 EP 952 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 651UU UT WOS:000181341100016 ER PT J AU Campion, EW AF Campion, EW TI Measles, mumps, and rubella vaccination and autism - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter NR 0 TC 0 Z9 0 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 6 PY 2003 VL 348 IS 10 BP 953 EP 954 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 651UU UT WOS:000181341100019 ER PT J AU Madsen, KM AF Madsen, KM TI Measles, mumps, and rubella vaccination and autism - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Danish Epidemiol Sci Ctr, DK-8000 Aarhus C, Denmark. RP Madsen, KM (reprint author), Danish Epidemiol Sci Ctr, DK-8000 Aarhus C, Denmark. NR 0 TC 2 Z9 2 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 6 PY 2003 VL 348 IS 10 BP 953 EP 953 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 651UU UT WOS:000181341100018 ER PT J AU Chiofalo, N David, P Breinbauer, C Ferreira, J AF Chiofalo, N David, P Breinbauer, C Ferreira, J TI Polysomnography in the spectrum of acquired epileptiform aphasia SO AMERICAN JOURNAL OF ELECTRONEURODIAGNOSTIC TECHNOLOGY LA English DT Article DE acquired epileptiform aphasia; autism; autistic spectrum disorders; electrical status during slow sleep; Landall-Kleffner syndrome; polysomnography ID SEIZURES; CHILDREN AB Full night polysomnography (PSG) is proving to be useful in evaluating children with language and developmental disorders. PSG evaluation sometimes demonstrates epileptiform activity in children with loss of language who have had no seizures. PSG is also helpful in diagnosing syndromes within the autistic spectrum, a step critical to early intervention and specific treatment. C1 Ctr Explorac Functional Del Cerebro, Santiago, Chile. CR DAVID P, 2000, 55 C NEUR OCT VIN MA DEONNA T, 1977, NEUROPADIATRIE, V8, P236 DEYKIN EY, 1979, AM J PSYCHIAT, V136, P1310 GASCON G, 1973, ARCH NEUROL-CHICAGO, V28, P156 *INT COUNC DEV LEA, 2000, CLIN PRACT GUID OV R KLEIN S, UNPUB INFLUENCE PREM LANDAU WM, 1992, ARCH NEUROL-CHICAGO, V49, P353 Perez ER, 1995, SEMIN PEDIAT NEUROL, V2, P269, DOI 10.1016/S1071-9091(95)80006-9 Rapin I, 1995, Semin Pediatr Neurol, V2, P278, DOI 10.1016/S1071-9091(95)80007-7 Tuchman R F, 1997, Semin Pediatr Neurol, V4, P93, DOI 10.1016/S1071-9091(97)80025-3 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 NR 11 TC 2 Z9 2 PU AMER SOC ELECTRONEURODIAGNOST TECHNOLOGISTS INC PI CARROLL PA 204 W. 7TH ST, CARROLL, IA 51401 USA SN 1086-508X J9 AM J ELECTRONEUROD T JI Am. J. Electroneurodiagn. Technol. PD MAR PY 2003 VL 43 IS 1 BP 13 EP 17 PG 5 WC Medical Laboratory Technology; Neurosciences SC Medical Laboratory Technology; Neurosciences & Neurology GA 684CM UT WOS:000183187900002 ER PT J AU Shao, YJ Cuccaro, ML Hauser, ER Raiford, KL Menold, MM Wolpert, CM Ravan, SA Elston, L Decena, K Donnelly, SL Abramson, RK Wright, HH Delong, GR Gilbert, JR Pericak-Vance, MA AF Shao, YJ Cuccaro, ML Hauser, ER Raiford, KL Menold, MM Wolpert, CM Ravan, SA Elston, L Decena, K Donnelly, SL Abramson, RK Wright, HH Delong, GR Gilbert, JR Pericak-Vance, MA TI Fine mapping of Autistic disorder to chromosome 15q11-q13 by use of phenotypic subtypes SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID PRADER-WILLI-SYNDROME; BLOOD-PRESSURE; GENOME SCAN; LINKAGE-DISEQUILIBRIUM; ISODICENTRIC CHROMOSOME-15; DIAGNOSTIC INTERVIEW; MULTIPLE-SCLEROSIS; ANGELMAN SYNDROME; GENETICS FUSION; COMPLEX TRAITS AB Autistic disorder (AutD) is a complex genetic disease. Available evidence suggests that several genes contribute to the underlying genetic risk for the development of AutD. However, both etiologic heterogeneity and genetic heterogeneity confound the discovery of AutD-susceptibility genes. Chromosome 15q11-q13 has been identified as a strong candidate region on the basis of both the frequent occurrence of chromosomal abnormalities in that region and numerous suggestive linkage and association findings. Ordered-subset analysis (OSA) is a novel statistical method to identify a homogeneous subset of families that contribute to overall linkage at a given chromosomal location and thus to potentially help in the fine mapping and localization of the susceptibility gene within a chromosomal area. For the present analysis, a factor that represents insistence on sameness (IS)-derived from a principal-component factor analysis using data on 221 patients with AutD from the repetitive behaviors/stereotyped patterns domain in the Autism Diagnostic Interview-Revised-was used as a covariate in OSA. Analysis of families sharing high scores on the IS factor increased linkage evidence for the 15q11-q13 region, at the GABRB3 locus, from a LOD score of 1.45 to a LOD score of 4.71. These results narrow our region of interest on chromosome 15 to an area surrounding the gamma-aminobutyric acid-receptor subunit genes, in AutD, and support the hypothesis that the analysis of phenotypic homogeneous subtypes may be a powerful tool for the mapping of disease-susceptibility genes in complex traits. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 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, Box 3445, Durham, NC 27710 USA. 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PD MAR PY 2003 VL 72 IS 3 BP 539 EP 548 DI 10.1086/367846 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 648LJ UT WOS:000181152600004 PM 12567325 ER PT J AU Keller, K Williams, C Wharton, P Paulk, M Bent-Williams, A Gray, B Ward, A Stalker, H Wallace, M Carter, R Zori, R AF Keller, K Williams, C Wharton, P Paulk, M Bent-Williams, A Gray, B Ward, A Stalker, H Wallace, M Carter, R Zori, R TI Routine cytogenetic and FISH studies for 17p11/15q11 duplications and subtelomeric rearrangement studies in children with autism spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE autism; autism spectrum disorder; telomere; cytogenetic analysis; dup (5)p; dup (15)(q11-13); dup (17)(p11.2) ID MENTAL-RETARDATION; COWDEN-SYNDROME; GENOMIC SCREEN; FAMILY HISTORY; PTEN MUTATION; DIAGNOSIS; GENETICS; DELETION; MARKERS; REGION AB To assess the frequency of cytogenetic abnormalities in children with autism spectrum disorders (ASDs), routine G-banded cytogenetic analyses and FISH studies to rule out 15q11.2 and 17p11.2 duplications were performed on 49 children with ASDs. Blood samples were further studied using a complete set of subtelomeric FISH probes. Routine chromosome study showed that one child had a small duplication of chromosome 5: 46,XY,dup(5)(p?14.2p?15.1). Another child had an interstitial duplication of the Prader-Willi and Angelman syndrome critical region of chromosome 15, detected by FISH analysis. The detection of these two cases underscores the importance of obtaining routine chromosome and 15q11-q13 FISH analyses in children with ASDs. No instance of 17p11.2 duplication was observed. Subtelomeric analysis did not reveal abnormalities in any of the subjects. (C) 2003 Wiley-Liss, Inc. C1 Univ Florida, Dept Pediat, Div Genet, Raymond C Philips Unit, Gainesville, FL 32610 USA. Univ Florida, Dept Mol Genet & Microbiol, Gainesville, FL USA. Univ Florida, Coll Med, Dept Stat, Gainesville, FL USA. Univ Florida, Jacksonville Ctr Autism & Related Disabil, Jacksonville, FL USA. RP Williams, C (reprint author), Univ Florida, Dept Pediat, Div Genet, Raymond C Philips Unit, POB 100296, Gainesville, FL 32610 USA. 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J. Med. Genet. A PD MAR 1 PY 2003 VL 117A IS 2 BP 105 EP 111 DI 10.1002/ajmg.a.10042 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 670HG UT WOS:000182401000001 PM 12567405 ER PT J AU Stone, WL Coonrod, EE Pozdol, SL Turner, LM AF Stone, WL Coonrod, EE Pozdol, SL Turner, LM TI The Parent Interview for Autism Clinical Version (PIA-CV) - A measure of behavioral change for young children with autism SO AUTISM LA English DT Article DE autism; change measure; early characteristic; parent interview; toddlers ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; NONVERBAL-COMMUNICATION; 3-YEAR-OLD CHILDREN; SPECTRUM DISORDERS; JOINT ATTENTION; RATING-SCALE; CHECKLIST; LANGUAGE; CLASSIFICATION AB The Parent Interview for Autism-Clinical Version (PIA-CV) was developed to measure autism symptom severity across a wide range of behavioral domains. Two studies were conducted to examine the psychometric properties of the PIA-CV for a sample of children under 3 years old. Results of study I revealed adequate internal consistency for nine of the 11 PIA-CV dimensions, as well as significant group differences on social-communication domains between 2-year-old children with autism and a developmentally matched sample. Study 2 examined the association between changes in PIA-CV scores and changes in autism symptomatology from age 2 to age 4. Results revealed that changes on PIA-CV dimensions assessing social and communication skills were associated with clinically significant behavioral and diagnostic improvements. These findings support the utility of the PIA-CV for obtaining ecologically valid information from parents and for measuring behavioral change in young children with autism. C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA. RP Stone, WL (reprint author), Vanderbilt Child Dev Ctr, 426 Med Ctr S,2100 Pierce Ave, Nashville, TN 37232 USA. 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On a rating of satisfaction, SS percent indicated that they were satisfied or very satisfied with the disclosure. Parents were more likely to be satisfied if they gave positive ratings to the manner of the professional and the quality of the information provided; if they had been given written information and the opportunity to ask questions; and if their early suspicions had been accepted by professionals. These factors were combined into a global index of satisfaction; those gaining higher scores were more likely to have been given the diagnosis of Asperger syndrome (as opposed to autism), to have had a definite diagnosis, and to have children who were not currently in an educational placement. These results underline the importance of the interaction between parent and professional during the disclosure interview. C1 Glasgow Caledonian Univ, Dept Psychol, Glasgow G4 0BA, Lanark, Scotland. RP Brogan, CA (reprint author), Glasgow Caledonian Univ, Dept Psychol, Cowcaddens Rd, Glasgow G4 0BA, Lanark, Scotland. 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Follow-up study of children assessed for autism at age 2 and development of an early diagnostic service SO AUTISM LA English DT Article DE assessment; autism; Autism Diagnostic Interview; early diagnosis; parent support ID YOUNG-CHILDREN; EARLY INTERVENTION; BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; HOME VIDEOTAPES; ADI-R; DISORDERS; INTERVIEW; 1ST; INDIVIDUALS AB Twenty children who presented with severe interactional and communication difficulties at age 2 underwent a comprehensive assessment for autism, and were reassessed at age 4-5. In common with other recent studies, diagnosis of autistic spectrum disorders at age 2 was found to be reliable and stable. The communication and social skills of the children showed little change overall by the second assessment. However, children whose scores deteriorated in the social domain tended to have presented initially with more significant behaviour problems. Few repetitive behaviours were observed at age 2, whereas these were more apparent by age 4-5. The finding that early diagnosis of autism is reliable and stable has led to the development of an early diagnostic service in Southampton, which is described. The importance of early diagnosis is that it opens the door to early intervention programmes, which in turn prevent many problems from occurring in later life. C1 Tremona Rd Childrens Ctr, Southampton SO16 6HU, Hants, England. RP Moore, V (reprint author), Tremona Rd Childrens Ctr, Wordsworth House,121-123 Tremona Rd, Southampton SO16 6HU, Hants, England. 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As age increased, so did IQ, which probably reflects both an actual increase in IQ over time and the likelihood that brighter children are diagnosed later. Early in life, 67 percent had normal motor and delayed speech milestones. Verbal IQ continued to lag behind non-verbal IQ during the preschool years. By school age, the gap between verbal and non-verbal IQs had closed. Visual reasoning exceeded graphomotor scores for all children, and surpassed IQ for most. Graphomotor scores were significantly below IQ for both high-IQ groups. For school-age children with low IQs, math, spelling, and writing scores were consistent with IQ and reading was above IQ. School-age children with high IQs had average reading, math, and spelling scores and a weakness in writing. RP Mayes, SD (reprint author), Milton S Hershey Med Ctr, Dept Psychiat, POB 850, Hershey, PA 17033 USA. 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R., 1998, ASPERGER SYNDROME HI, P107 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 YIRMIYA N, 1991, CLIN PSYCHOL REV, V11, P669, DOI 10.1016/0272-7358(91)90125-E NR 46 TC 50 Z9 52 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2003 VL 7 IS 1 BP 65 EP 80 DI 10.1177/1362361303007001006 PG 16 WC Psychology, Developmental SC Psychology GA 656RM UT WOS:000181622300004 PM 12638765 ER PT J AU Bauminger, N Shulman, C AF Bauminger, N Shulman, C TI The development and maintenance of friendship in high-functioning children with autism - Maternal perceptions SO AUTISM LA English DT Article DE friendship; high-functioning autism; maternal perception ID PARENTAL REPORT; DOWN-SYNDROME; PRESCHOOLERS; PERSPECTIVES; COMPETENCE AB The current study investigated mothers' perceptions of the development of friendship in high-functioning children with autism and in typically developing children. Fourteen mothers in each group (autism, typical) completed the Childhood Friendship Survey regarding their children's friendships. Main results indicated that both groups (autism and typical) tended to have same-gender and same-age friendships. However, friendships of children with autism differ compared with typical children's friendships on number of friends, friendship duration, frequency of meetings, and type of activities. Half of the friendships in the autism group were mixed (friendship with a typically developing child). Mixed differed from non-mixed friendships in that mixed pairs met and played mostly at home, whereas non-mixed pairs met and played at school. Factors contributing to the development and formation of friendship in each group are discussed. C1 Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. Hebrew Univ Jerusalem, IL-91905 Jerusalem, Israel. RP Bauminger, N (reprint author), Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asher S. R., 1996, CO THEY KEEP FRIENDS, P366 Bacon AL, 1998, J AUTISM DEV DISORD, V28, P129, DOI 10.1023/A:1026040615628 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 BUHRMESTER D, 1990, CHILD DEV, V61, P1101, DOI 10.1111/j.1467-8624.1990.tb02844.x Buhrmester D., 1996, CO THEY KEEP FRIENDS, P158 BUYSSE V, 1993, J EARLY INTERVENTION, V17, P380 Buysse V., 1991, EARLY CHILDHOOD FRIE CAPPS L, 1993, J CONSULT CLIN PSYCH, V61, P475, DOI 10.1037/0022-006X.61.3.475 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 Dunn J., 1993, YOUNG CHILDRENS CLOS GURALNICK MJ, 1995, AM J MENT RETARD, V99, P457 Hartley J, 2000, PSYCHOL CRIME LAW, V6, P1, DOI 10.1080/10683160008410828 Hartson H. R., 1992, Human-Computer Interaction, V7, DOI 10.1207/s15327051hci0701_1 Hartup W., 1996, CO THEY KEEP FRIENDS, P213 HOBSON RP, 1993, PHILOS PSYCHOL, V6, P227, DOI 10.1080/09515089308573090 Howes C., 1992, COLLABORATIVE CONSTR HOWES C, 1983, CHILD DEV, V54, P1041, DOI 10.1111/j.1467-8624.1983.tb00525.x Howes C., 1996, CO THEY KEEP FRIENDS, P66 Kanner L, 1943, NERV CHILD, V2, P217 Kasari C, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P309 Kasari C, 1999, J AUTISM DEV DISORD, V29, P297, DOI 10.1023/A:1022159302571 Lemerise EA, 2000, CHILD DEV, V71, P107, DOI 10.1111/1467-8624.00124 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 MEYER LH, 1998, MAKING FRIENDS INFLU, P31 Newcomb A. F., 1996, CO THEY KEEP FRIENDS, P289 PARKER JG, 1989, PEER RELATIONSHIPS C, P131 PARKER LG, 1995, DEV PSYCHOPATHOL, P161 ROOPNARINE JL, 1984, FRIENDSHIPS NORMAL H, P89 RUBENSTEIN J, 1976, CHILD DEV, V47, P597 Schreck KA, 2000, J AUTISM DEV DISORD, V30, P127, DOI 10.1023/A:1005407622050 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 STONE WL, 1990, J AUTISM DEV DISORD, V20, P437, DOI 10.1007/BF02216051 STONE WL, 1990, J AUTISM DEV DISORD, V20, P513, DOI 10.1007/BF02216056 WATERHOUSE L, 1997, HDB AUTISM PERVASIVE, P901 Wechsler D, 1974, WISC R MANUAL WECHSL Wimpory DC, 2000, J AUTISM DEV DISORD, V30, P525, DOI 10.1023/A:1005683209438 Bauminger N, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P151 NR 38 TC 31 Z9 32 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2003 VL 7 IS 1 BP 81 EP 97 DI 10.1177/1362361303007001007 PG 17 WC Psychology, Developmental SC Psychology GA 656RM UT WOS:000181622300005 PM 12638766 ER PT J AU Engstrom, I Ekstrom, L Emilsson, B AF Engstrom, I Ekstrom, L Emilsson, B TI Psychosocial functioning in a group of Swedish adults with Asperger syndrome or high-functioning autism SO AUTISM LA English DT Article DE Asperger syndrome; autism; long-term course; outcome ID FOLLOW-UP; CHILDREN; OUTCOMES AB This study reports on psychosocial functioning in Swedish adults with Asperger syndrome (AS) or high-functioning autism (HFA). A systematically selected sample of patients and relatives was interviewed concerning their psychosocial situation. The majority was living independently. All persons but one were unemployed. None was married and none had children. Only a few had some kind of partner. Most persons needed a high level of public and/or private support. The overall adjustment was rated good in 12 percent, fair in 7 5 percent and poor in 12 percent. Adult persons with AS/HFA have extensive need for support from their families and/or society. This information is important in order to provide adequate interventions that are in accordance with the expressed needs of the individuals themselves. C1 Psychiat Res Ctr, SE-70116 Orebro, Sweden. Orebro Cty Council, Orebro, Sweden. RP Engstrom, I (reprint author), Psychiat Res Ctr, POB 1613, SE-70116 Orebro, Sweden. CR Asperger H., 1991, AUTISM ASPERGER SYND DEMYER M, 1981, SCHIZOPHRENIA B, V7, P358 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Gillberg C, 1995, EPIDEMIOLOGY CHILD A, P227 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Goode S., 1999, AUTISM, V4, P63 Howlin P, 2000, AUTISM, V4, P63, DOI DOI 10.1177/1362361300004001005 KANNER L, 1971, J AUTISM CHILD SCHIZ, V1, P119, DOI 10.1007/BF01537953 Larsen FW, 1997, EUR CHILD ADOLES PSY, V6, P181 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x Lotter V, 1978, AUTISM REAPPRAISAL C, P187 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X Nordin V, 1998, ACTA PSYCHIAT SCAND, V97, P99, DOI 10.1111/j.1600-0447.1998.tb09970.x PHELAN M, 1995, BRIT J PSYCHIAT, V167, P589, DOI 10.1192/bjp.167.5.589 RUMSEY JM, 1985, J AM ACAD CHILD PSY, V24, P465, DOI 10.1016/S0002-7138(09)60566-5 SZATMARI P, 1989, J AUTISM DEV DISORD, V19, P213, DOI 10.1007/BF02211842 SZATMARI P, 1998, ASPERGER SYNDROME HI WING L, 1981, PSYCHOL MED, V11, P115 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 NR 20 TC 42 Z9 42 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2003 VL 7 IS 1 BP 99 EP 110 DI 10.1177/1362361303007001008 PG 12 WC Psychology, Developmental SC Psychology GA 656RM UT WOS:000181622300006 PM 12638767 ER PT J AU Leonard, A AF Leonard, A TI Autism and ICT: A guide for teachers and parents SO AUTISM LA English DT Book Review C1 Univ Nottingham, Nottingham NG7 2RD, England. RP Leonard, A (reprint author), Univ Nottingham, Nottingham NG7 2RD, England. CR Hardy C., 2002, AUTISM ICT GUIDE TEA NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2003 VL 7 IS 1 BP 112 EP 113 DI 10.1177/1362361303007001010 PG 2 WC Psychology, Developmental SC Psychology GA 656RM UT WOS:000181622300008 ER PT J AU Bovee, JP AF Bovee, JP TI Autism/Asperger's and sexuality: Puberty and beyond SO AUTISM LA English DT Book Review C1 Univ Missouri, Kansas City, MO 64110 USA. RP Bovee, JP (reprint author), Univ Missouri, Kansas City, MO 64110 USA. CR Newport Jerry, 2002, AUTISM ASPERGERS SEX NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2003 VL 7 IS 1 BP 115 EP 117 DI 10.1177/1362361303007001012 PG 3 WC Psychology, Developmental SC Psychology GA 656RM UT WOS:000181622300010 ER PT J AU Czapinski, P Bryson, SE AF Czapinski, P Bryson, SE TI Reduced facial muscle movements in Autism: Evidence for dysfunction in the neuromuscular pathway? SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 Hosp Sick Children, Child Dev Ctr, Autism Res Unit, Toronto, ON M5G 1X8, Canada. CR Izard C. E., 1979, MAXIMALLY DISCRIMINA KUMAR D, 1990, J MED GENET, V27, P122, DOI 10.1136/jmg.27.2.122 LOVELAND KA, 1994, DEV PSYCHOPATHOL, V6, P433, DOI 10.1017/S0954579400006039 Rodier PM, 1996, J COMP NEUROL, V370, P247, DOI 10.1002/(SICI)1096-9861(19960624)370:2<247::AID-CNE8>3.0.CO;2-2 YIRMIYA N, 1989, J CHILD PSYCHOL PSYC, V30, P725, DOI 10.1111/j.1469-7610.1989.tb00785.x NR 5 TC 6 Z9 6 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 MAR PY 2003 VL 51 IS 2 BP 177 EP 179 PG 3 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 669PX UT WOS:000182360600021 ER PT J AU Pellicano, E Rhodes, G AF Pellicano, E Rhodes, G TI The role of eye-gaze in understanding other minds SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID ASPERGER-SYNDROME; AUTISM; DIRECTION; ADULTS; ATTENTION; INFANTS; FACE AB From an early age, infants are sensitive to eye-gaze direction. This study examined Baron-Cohen's (1994, 1995) claim that the ability to use eye-gaze plays a crucial role in the child's developing understanding of other minds. Children aged 3 and 4 years participated in a face-reading task, which assessed their capacity to infer mental states from a character's direction of eye-gaze, and in a false-belief task. As predicted, no child passed the false-belief task without prior success on the face-reading task. However, contrary to a central claim within Baron-Cohen's model of mind-reading, presentation of an eye-gaze cue in the false-belief task did not enhance children's performance. Furthermore, children did not solely rely on eye-gaze as a cue, but used another directional cue (an arrow) in inferring a character's desire and intention. These results question the special role of eye-gaze in the child's developing ability to mind-read. C1 Univ Western Australia, Ctr Child Study, Sch Psychol, Crawley, WA 6009, Australia. RP Pellicano, E (reprint author), Univ Western Australia, Ctr Child Study, Sch Psychol, Crawley, WA 6009, Australia. CR ADAMSON LB, 1985, CHILD DEV, V56, P582, DOI 10.2307/1129748 Bakti A., 2000, INFANT BEHAV DEV, V23, P223 Baldwin D. A., 1995, JOINT ATTENTION ITS, p131 Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S., 1991, NATURAL THEORIES MIN, P233 BARONCOHEN S, 1989, BRIT J DEV PSYCHOL, V7, P113 BARONCOHEN S, 1995, BRIT J DEV PSYCHOL, V13, P379 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BARONCOHEN S, 1994, CAH PSYCHOL COGN, V13, P513 Baron-Cohen S, 1992, MIND LANG, V6, P173 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BRETHERTON I, 1991, CHILDRENS THEORIES OF MIND : MENTAL STATES AND SOCIAL UNDERSTANDING, P49 Butterworth G., 1991, NATURAL THEORIES MIN, P223 BUTTERWORTH G, 1990, ATTENTION PERFORM, V13, P605 Carlson SM, 1998, CHILD DEV, V69, P672, DOI 10.2307/1132197 Carlson SM, 2001, CHILD DEV, V72, P1032, DOI 10.1111/1467-8624.00333 Corkum V., 1995, JOINT ATTENTION ITS, P61 Doherty MJ, 1999, COGNITIVE DEV, V14, P549, DOI 10.1016/S0885-2014(99)00019-2 DohertySneddon G, 1997, J EXP PSYCHOL-APPL, V3, P105, DOI 10.1037//1076-898X.3.2.105 HAITH MM, 1977, SCIENCE, V198, P853, DOI 10.1126/science.918670 HOBSON RP, 1990, PSYCHOL REV, V97, P114, DOI 10.1037/0033-295X.97.1.114 Hood BM, 1998, PSYCHOL SCI, V9, P131, DOI 10.1111/1467-9280.00024 Johnson S, 1998, DEVELOPMENTAL SCI, V1, P233, DOI 10.1111/1467-7687.00036 Langton SRH, 2000, J EXP PSYCHOL HUMAN, V26, P747, DOI 10.1037//0096-1523.26.2.747 Lee K, 1998, DEV PSYCHOL, V34, P525, DOI 10.1037//0012-1649.34.3.525 Leslie AM, 1998, DEVELOPMENTAL SCI, V1, P247, DOI 10.1111/1467-7687.00038 MACBETH T, 1996, TUNING YOUNG VIEWERS MOORE C, 1994, DEV REV, V14, P349, DOI 10.1006/drev.1994.1014 Moore C, 1998, BRIT J DEV PSYCHOL, V16, P495 Perner Josef, 1991, UNDERSTANDING REPRES Symons LA, 1998, INFANT BEHAV DEV, V21, P531, DOI 10.1016/S0163-6383(98)90026-1 Tomasello M., 1995, JOINT ATTENTION ITS, P103 Vecera S. P., 1995, Visual Cognition, V2, DOI 10.1080/13506289508401722 NR 35 TC 10 Z9 10 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0261-510X J9 BRIT J DEV PSYCHOL JI Br. J. Dev. Psychol. PD MAR PY 2003 VL 21 BP 33 EP 43 DI 10.1348/026151003321164609 PN 1 PG 11 WC Psychology, Developmental SC Psychology GA 661VF UT WOS:000181910000003 ER PT J AU Richards, A AF Richards, A TI Incorporating social goals in the classroom - A guide for teachers and parents of children with high functioning autism and Asperger syndrome SO BRITISH JOURNAL OF EDUCATIONAL PSYCHOLOGY LA English DT Book Review C1 Univ Exeter, Exeter EX4 4QJ, Devon, England. RP Richards, A (reprint author), Univ Exeter, Exeter EX4 4QJ, Devon, England. CR MOYES RA, 2001, INCORPORATING SOCIAL 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 0007-0998 J9 BRIT J EDUC PSYCHOL JI Br. J. Educ. Psychol. PD MAR PY 2003 VL 73 BP 137 EP 139 PN 1 PG 3 WC Psychology, Educational SC Psychology GA 661VW UT WOS:000181911400014 ER PT J AU Ceccherini-Nelli, A Crow, TJ AF Ceccherini-Nelli, A Crow, TJ TI Disintegration of the components of language as the path to a revision of Bleuler's and Schneider's concepts of schizophrenia - Linguistic disturbances compared with first-rank symptoms in acute psychosis SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID HOMO-SAPIENS PAYS; COMMUNICATION DISORDERS; DIAGNOSTIC-SIGNIFICANCE; THOUGHT; DEFINITION; SPEECH; PRICE AB Background The 20th century ended without a resolution of the debate about the supremacy of Schneider's psychopathological conceptualisation of schizophrenia (the first-rank symptoms) over Bleuler's 'four As' (disorders of association and affect, ambivalence and autism). Aims To examine the relationships between linguistic deviations and symptoms in patients with acute psychosis. Method We assessed language disturbances and first-rank symptoms with the Clinical Language Disorder Rating Scale (CLANG) in 30 consecutive patients with acute psychosis, selected for the presence of at least one active first-rank symptom, and 15 control participants with depression but no psychotic symptoms. Results Strong positive correlations were found between the CLANG factor 'poverty' (of speech) and first-rank delusions of control and ('delusional perceptions') between semantic/ phonemic paraphasias and verbal auditory hallucinations. Language disturbances were superior to nuclear symptoms in discriminating ICD-10 schizophrenia from other psychoses. Conclusions Evaluating the features of psychosis as deviations in the cerebral organisation of language paves the way to a concept of psychosis that supersedes these traditional but competing categorical concepts. Declaration of interest None. C1 Univ Oxford, Prince Wales Int Ctr Res Schizophrenia & Depress, Oxford, England. RP Crow, TJ (reprint author), Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England. RI crow, timothy/M-8327-2014 OI crow, timothy/0000-0002-5482-6655 CR Altman DG, 2000, STAT CONFIDENCE CONF American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DIAGN STAT MAN MENT ANDREASEN NC, 1979, ARCH GEN PSYCHIAT, V36, P1325 ANDREASEN NC, 1986, SCHIZOPHRENIA BULL, V12, P348 ANDREASEN NC, 1979, ARCH GEN PSYCHIAT, V36, P1315 ANDREASEN NC, 1982, ARCH GEN PSYCHIAT, V39, P789 Bleuler E, 1911, DEMENTIA PRAECOX GRO Carpenter WT, 1996, BRIT J PSYCHIAT, V169, P541 Chen E.Y.H., 1996, HONG KONG J PSYCHIAT, V6, P4 CROW TJ, 1995, ARCH GEN PSYCHIAT, V52, P1011 Crow TJ, 1998, BRIT J PSYCHIAT, V173, P303, DOI 10.1192/bjp.173.4.303 CROW TJ, 1980, BRIT MED J, V280, P66 Crow TJ, 2000, BRAIN RES REV, V31, P118, DOI 10.1016/S0165-0173(99)00029-6 Crow TJ, 1997, SCHIZOPHR RES, V28, P127, DOI 10.1016/S0920-9964(97)00110-2 DeLisi LE, 2001, SCHIZOPHRENIA BULL, V27, P481 LIDDLE PF, 1987, BRIT J PSYCHIAT, V151, P145, DOI 10.1192/bjp.151.2.145 MELLOR CS, 1970, BRIT J PSYCHIAT, V117, P15 Peralta V, 1999, BRIT J PSYCHIAT, V174, P243, DOI 10.1192/bjp.174.3.243 Schneider K, 1957, THEMES VARIATIONS EU, P40 Sims A. C. P., 1995, SYMPTOMS MIND INTRO, V3rd Wing J.K., 1974, MEASUREMENT CLASSIFI World Health Organization, 1992, 10 REV INT CLASS DIS NR 23 TC 27 Z9 28 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON SW1X 8PG, ENGLAND SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD MAR PY 2003 VL 182 BP 233 EP 240 DI 10.1192/bjp.182.3.233 PG 8 WC Psychiatry SC Psychiatry GA 653NM UT WOS:000181431500013 PM 12611787 ER PT J AU Zoroglu, SS Yurekli, M Meram, I Sogut, S Tutkun, H Yetkin, O Sivasli, E Savas, HA Yanik, M Herken, H Akyol, O AF Zoroglu, SS Yurekli, M Meram, I Sogut, S Tutkun, H Yetkin, O Sivasli, E Savas, HA Yanik, M Herken, H Akyol, O TI Pathophysiological role of nitric oxide and adrenomedullin in autism SO CELL BIOCHEMISTRY AND FUNCTION LA English DT Article DE autism; pervasive developmental disorder; nitric oxide; adrenomedullin; total nitrite ID LIPID-PEROXIDATION; BRAIN INJURY; SYNTHASE; SCHIZOPHRENIA; PEROXYNITRITE; CELLS; BLOOD; RATS; HYPOTHALAMUS; EXPRESSION AB Several studies indicate that nitric oxide (NO) is involved in the aetiopathogenesis of many neuropsychiatric disorders such as schizophrenia, bipolar disorder, depression, Alzheimer's disease, Hungtington disease and stroke. Although it has not been investigated yet, several recent studies proposed that NO may have a pathophysiological role in autism. Adrenomedullin (AM), a recently discovered 52-amino acide peptide hormone, induces vasorelaxation by activating adenylate cyclase and also by stimulating NO release. AM immune reactivity is present in the brain consistent with a role as a neurotransmitter. It has been stated that NO and AM do function in the regulation of many neurodevelopmental processes. We hypothesized that NO and AM activities have been affected in autistic patients and aimed to examine these molecules. Twenty-six autistic patients and 22 healthy control subjects were included in this study. AM and total nitrite (a metabolite of NO) levels have been measured in plasma. The mean values of plasma total nitrite and AM levels in the autistic group were significantly higher than control values, respectively (p < 0.001, p = 0.028). There is no correlation between total nitrite and AM levels (r = 0.11, p = 0.31). Certainly, this subject needs much further research investigating autistic patients in earlier periods of life and with subtypes of the disorder. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Gaziantep Univ, Sch Med, Dept Child & Adolescent Psychiat, TR-27200 Gaziantep, Turkey. Gaziantep Univ, Sch Med, Dept Biochem, TR-27200 Gaziantep, Turkey. Gaziantep Univ, Sch Med, Dept Psychiat, TR-27200 Gaziantep, Turkey. Gaziantep Univ, Sch Med, Dept Pediat, TR-27200 Gaziantep, Turkey. Inonu Univ, Sch Med, Arts & Sci Fac, Dept Mol Biol, Malatya, Turkey. Inonu Univ, Sch Med, Dept Biochem, Malatya, Turkey. Harran Univ, Sch Med, Dept Psychiat, Sanliurfa, Turkey. RP Zoroglu, SS (reprint author), Gaziantep Univ, Sch Med, Dept Child & Adolescent Psychiat, TR-27200 Gaziantep, Turkey. 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Funct. PD MAR PY 2003 VL 21 IS 1 BP 55 EP 60 DI 10.1002/cbf.989 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 647MR UT WOS:000181097100008 PM 12579522 ER PT J AU Doussard-Roosevelt, JA Joe, CM Bazhenova, OV Porges, SW AF Doussard-Roosevelt, JA Joe, CM Bazhenova, OV Porges, SW TI Mother-child interaction in autistic and nonautistic children: Characteristics of maternal approach behaviors and child social responses SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID JOINT ATTENTION; YOUNG-CHILDREN; DOWN-SYNDROME; DEVELOPMENTAL DELAYS; POLYVAGAL THEORY; PLAY; COMMUNICATION; PARENT; DIRECTIVENESS; ATTACHMENT AB The nature of mother-child interaction in autism and the maternal approach characteristics that elicit social response in children with autism were examined in two studies. Mother-child play sessions of 24 preschool children with autism and 24 typically developing preschoolers were compared in Study 1, and play sessions of 9 mothers with their autistic child and with their nonautistic child were compared in Study 2. Mother-child interactions were coded using the Approach Withdrawal Interaction Coding System to quantify maternal approach behaviors and child responses. Results of Study 1 indicate that, although the quantity of approaches did not differ between mothers with their autistic children and mothers with their nonautistic children, there were qualitative differences. Mothers used more physical contact, more high-intensity behaviors, and fewer social verbal approaches with autistic children. Results of Study 2 replicated these findings with mothers showing a similar pattern of approach toward their autistic children but not their nonautistic children. 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Psychopathol. PD SPR PY 2003 VL 15 IS 2 BP 277 EP 295 DI 10.1017/S0954579403000154 PG 19 WC Psychology, Developmental SC Psychology GA 695NY UT WOS:000183838200003 PM 12931828 ER PT J AU Berthier, ML Kulisevsky, J Asenjo, B Aparicio, J Lara, D AF Berthier, ML Kulisevsky, J Asenjo, B Aparicio, J Lara, D TI Comorbid Asperger and Tourette syndromes with localized mesencephalic, infrathalamic, thalamic, and striatal damage SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; BASAL GANGLIA; AUTISTIC DISORDER; FUNCTIONAL NEUROANATOMY; MIDBRAIN INVOLVEMENT; MENTAL-RETARDATION; CHILDHOOD AUTISM; INFANTILE-AUTISM; BIPOLAR DISORDER AB We describe the coexistence of Asperger and Tourette syndromes (AS and TS) caused by discrete hypoxic-ischaemic necrosis of the midbrain, infrathalamic and thalamic nuclei, and striatum in an adolescent male with positive family history for ties and obsessive-compulsive disorder. Behavioural ratings, cognitive tests, and volumetric measurements of the basal ganglia were performed in the patient and five other individuals with AS-TS unassociated with MRI lesions. Cognitive deficits in attentional, executive, and visual-spatial domains were found both in the patient and control AS-TS group, though deficits were more severe in the former. MRI showed reduction of the left basal ganglia volume compared with the right in the patient, whereas the control group showed reduction of right basal ganglia volume compared with the left. It is suggested that individuals with a genetic predisposition to TS may develop AS and TS after involvement of midbrain and related components of basal ganglia-thalamocortical circuits normally implicated in the integration of emotional, cognitive, and motor functions. C1 Univ Malaga, Fac Med, Dept Med & Dermatol, Sch Med, E-29071 Malaga, Spain. Sant Pau Hosp, Dept Neurol, Movement Disorder Sect, Barcelona, Spain. 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Med. Child Neurol. PD MAR PY 2003 VL 45 IS 3 BP 207 EP 212 DI 10.1017/S0012162203000392 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 648RV UT WOS:000181165100012 PM 12613779 ER PT J AU Perez-Jimenez, A Villarejo, FJ del Castillo, MCF Garcia-Penas, JJ Carreno, M AF Perez-Jimenez, A Villarejo, FJ del Castillo, MCF Garcia-Penas, JJ Carreno, M TI Continuous giggling and autistic disorder associated with hypothalamic hamartoma SO EPILEPTIC DISORDERS LA English DT Article DE giggling; gelastic seizures; hypothalamic hamartoma; autism ID GELASTIC SEIZURES; ICTAL LAUGHTER; EPILEPSY; RESECTION; CHILDREN; SURGERY AB We present the case of a child affected since early infancy from recurring episodes of giggling mixed with stereotypical behaviours, mingled with head drops, and eventually with falls, in the context of an autistic disorder. Scalp video-EEG recordings revealed an epileptic encephalopathy with generalized slow spike-and-wave complexes alternating with electrodecremental periods, which generally corresponded to the onset of the aforementioned clinical sequences. A resection of a hypothalamic hamartoma was achieved at the age of two. Since then, after 22 months of follow-up, the child is totally free from the giggling and the drops, and the autistic behaviour significantly improved during the second year of follow-up. This case illustrates the difficulties to recognize some subtle ictal manifestations during infancy and childhood, and encourages the early surgical treatment of hypothalamic hamartomas when associated with epileptic encephalopathy and when technically possible. C1 Hosp Infantil Univ Nino Jesus, Unidad Epilepsia Video EEG, Clin Neurophysiol Sect, Madrid 28009, Spain. Hosp Infantil Univ Nino Jesus, Neurosurg Serv, Madrid 28009, Spain. 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PD MAR PY 2003 VL 5 IS 1 BP 31 EP 37 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 682KC UT WOS:000183089900005 PM 12773294 ER PT J AU Cisternas, FA Vincent, JB Scherer, SW Ray, PN AF Cisternas, FA Vincent, JB Scherer, SW Ray, PN TI Cloning and characterization of human CADPS and CADPS2, new members of the Ca2+-dependent activator for secretion protein family SO GENOMICS LA English DT Article ID CA2+-ACTIVATED EXOCYTOSIS; CAENORHABDITIS-ELEGANS; FUSION; SYNAPTOTAGMIN; CAPS; MEMBRANE; CALCIUM; AUTISM; VESICLES; RELEASE AB The recent identification of some of the components involved in regulated and constitutive exocytotic pathways has yielded important insights into the mechanisms of membrane trafficking and vesicle secretion. To understand precisely the molecular events taking place during vesicle exocytosis, we must identify all of the proteins implicated in these pathways. In this paper we describe the full-length cloning and characterization of human CADPS and CADPS2, two new homologs of the mouse Cadps protein involved in large dense-core vesicle (LDCV)-regulated exocytosis. We show that these two genes have disparate RNA expression patterns, with CADPS restricted to neural and endocrine tissues and CADPS2 expressed ubiquitously. We also identify a C2 domain, a known protein motif involved in calcium and phospholipid interactions, in both CADPS and CADPS2. We propose that CADPS functions as a calcium sensor in regulated exocytosis, whereas CADPS2 acts as a calcium sensor in constitutive vesicle trafficking and secretion. CADPS and CADPS2 were determined to span 475 kb and 561 kb on human chromosomes 3p21.1 and 7q31.3, respectively. The q31-q34 of human chromosome 7 has recently been identified to contain a putative susceptibility locus for autism (AUTSI). The function, expression profile, and location of CADPS2 make it a candidate gene for autism, and thus we conducted mutation screening for all 28 exons in 90 unrelated autistic individuals. We identified several nucleotide substitutions, including only one that would affect the amino acid sequence. No disease-specific variants were identified. (C) 2003 Elsevier Science (USA). All rights reserved. C1 Univ Toronto, Dept Mol & Med Genet, Toronto, ON, Canada. Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. RP Ray, PN (reprint author), Univ Toronto, Dept Mol & Med Genet, Toronto, ON, Canada. 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SO INFANT AND CHILD DEVELOPMENT LA English DT Book Review C1 Univ Lancaster, Lancaster LA1 4YW, England. RP Shimmon, K (reprint author), Univ Lancaster, Lancaster LA1 4YW, England. CR IVES M, 2002, CARING CHILD WITH AU NR 1 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD MAR PY 2003 VL 12 IS 1 BP 107 EP 108 DI 10.1002/ics.313 PG 2 WC Psychology, Developmental SC Psychology GA 655EP UT WOS:000181538600006 ER PT J AU Roane, HS Fisher, WW McDonough, EM AF Roane, HS Fisher, WW McDonough, EM TI Progressing from programmatic to discovery research: A case example with the overjustification effect SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; behavioral contrast; discovery research; overjustification; punishment ID RESPONSE DEPRIVATION; STIMULUS PREFERENCE; REINFORCEMENT; REWARDS; DISABILITIES; PUNISHMENT AB Scientific research progresses along planned (programmatic research) and unplanned (discovery research) paths. In the current investigation, we attempted to conduct a single-case evaluation of the overjustification effect (i.e., programmatic research). Results of the initial analysis were contrary to the overjusification hypothesis in that removal of the reward contingency produced an increase in responding. Based on this unexpected finding, we conducted subsequent analyses to further evaluate the mechanisms underlying these results (i.e., discovery research). Results of the additional analyses suggested that the reward contingency functioned as Punishment (because the participant preferred the task to the rewards) and that withdrawal of the contingency produced punishment contrast. C1 Marcus Inst, Atlanta, GA 30329 USA. Kennedy Krieger Inst, Atlanta, GA 30329 USA. Emory Univ, Sch Med, Atlanta, GA 30322 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. RP Roane, HS (reprint author), Marcus Inst, 1920 Briarcliff Rd, Atlanta, GA 30329 USA. CR Azrin N. H., 1966, OPERANT BEHAV AREAS, P380 AZRIN NH, 1960, J EXP ANAL BEHAV, V3, P123, DOI 10.1901/jeab.1960.3-123 BALSAM PD, 1983, J APPL BEHAV ANAL, V16, P283, DOI 10.1901/jaba.1983.16-283 BARMANN BC, 1980, J APPL BEHAV ANAL, V13, P693, DOI 10.1901/jaba.1980.13-693 BRADY JV, 1958, SCI AM, V199, P95 Catania A. C., 1992, LEARNING Crosbie J, 1997, J EXP ANAL BEHAV, V68, P161, DOI 10.1901/jeab.1997.68-161 DECI EL, 1971, J PERS SOC PSYCHOL, V18, P105, DOI 10.1037/h0030644 Eisenberger R, 1996, AM PSYCHOL, V51, P1153, DOI 10.1037/0003-066X.51.11.1153 Ferster C.B., 1957, SCHEDULES REINFORCEM FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Fisher WW, 1996, AM J MENT RETARD, V101, P15 GREENE D, 1974, CHILD DEV, V45, P1141, DOI 10.1111/j.1467-8624.1974.tb00720.x HERRNSTEIN RJ, 1975, J EXP ANAL BEHAV, V24, P107, DOI 10.1901/jeab.1975.24-107 KONARSKI EA, 1980, J APPL BEHAV ANAL, V13, P595, DOI 10.1901/jaba.1980.13-595 Lerman DC, 1996, J APPL BEHAV ANAL, V29, P231, DOI 10.1901/jaba.1996.29-231 MACE FC, 1994, J EXP ANAL BEHAV, V61, P529, DOI 10.1901/jeab.1994.61-529 Mackintosh N. J., 1974, PSYCHOL ANIMAL LEARN Nevin JA, 1996, J APPL BEHAV ANAL, V29, P535, DOI 10.1901/jaba.1996.29-535 PACLAWSKYJ TR, 1995, J APPL BEHAV ANAL, V28, P219, DOI 10.1901/jaba.1995.28-219 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P137, DOI 10.1901/jaba.1996.29-137 Premack D., 1971, NATURE REINFORCEMENT, P121 PREMACK D, 1959, PSYCHOL REV, V66, P219, DOI 10.1037/h0040891 Reitman D, 1998, J BEHAV THER EXP PSY, V29, P101, DOI 10.1016/S0005-7916(98)00011-1 REYNOLDS GS, 1961, J EXP ANAL BEHAV, V4, P57, DOI 10.1901/jeab.1961.4-57 Ringdahl JE, 1997, J APPL BEHAV ANAL, V30, P203, DOI 10.1901/jaba.1997.30-203 Roane HS, 1998, J APPL BEHAV ANAL, V31, P605, DOI 10.1901/jaba.1998.31-605 SIDMAN M, 1960, TACTIES SCI RES EVAL SKINNER BF, 1956, AM PSYCHOL, V11, P221, DOI 10.1037/h0047662 TIMBERLA.W, 1974, PSYCHOL REV, V81, P146, DOI 10.1037/h0036101 VASTA R, 1979, BEHAV MODIF, V3, P223, DOI 10.1177/014544557932006 NR 31 TC 8 Z9 8 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 SPR PY 2003 VL 36 IS 1 BP 35 EP 46 DI 10.1901/jaba.2003.36-35 PG 12 WC Psychology, Clinical SC Psychology GA 664XJ UT WOS:000182089700003 PM 12723865 ER PT J AU Lerman, DC Kelley, ME Vorndran, CM Van Camp, CM AF Lerman, DC Kelley, ME Vorndran, CM Van Camp, CM TI Collateral effects of response blocking during the treatment of stereotypic behavior SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE blocking; collateral effects; extinction; punishment; side effects; stereotypic behavior ID FUNCTIONAL-ANALYSIS; SELF-INJURY; PUNISHMENT; EXTINCTION AB The collateral effects of response blocking were evaluated while treating stereotypic behavior in a woman diagnosed with autism. Blocking stereotypic behavior (head and tooth tapping) was associated with decreases in leisure-item interaction and increases in another stereorypic response (hand wringing). Results suggested that the reduction in item interaction was due to adventitious punishment. Prompts to access an alternative source of reinforcement attenuated the side effects somewhat, but results suggested that the undesirable effects of response blocking may be fairly durable. C1 Louisiana State Univ, Baton Rouge, LA 70803 USA. RP Lerman, DC (reprint author), Louisiana State Univ, 236 Audobon Hall, Baton Rouge, LA 70803 USA. CR HAGOPIAN JP, 2001, J APPL BEHAV ANAL, V34, P527 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Lalli JS, 1996, J APPL BEHAV ANAL, V29, P129, DOI 10.1901/jaba.1996.29-129 Lerman DC, 1996, J APPL BEHAV ANAL, V29, P231, DOI 10.1901/jaba.1996.29-231 SINGH NN, 1982, J APPL BEHAV ANAL, V15, P309, DOI 10.1901/jaba.1982.15-309 Smith RG, 1999, J APPL BEHAV ANAL, V32, P367, DOI 10.1901/jaba.1999.32-367 SPRAGUE JR, 1992, J APPL BEHAV ANAL, V25, P735, DOI 10.1901/jaba.1992.25-735 Thompson RH, 1999, J APPL BEHAV ANAL, V32, P317, DOI 10.1901/jaba.1999.32-317 NR 8 TC 20 Z9 20 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 SPR PY 2003 VL 36 IS 1 BP 119 EP 123 DI 10.1901/jaba.2003.36-119 PG 5 WC Psychology, Clinical SC Psychology GA 664XJ UT WOS:000182089700013 PM 12723875 ER PT J AU Ritchie, D Kitty, W AF Ritchie, D Kitty, W TI Caring for a child with autism SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Book Review CR IVES M, 2002, CARING CHILD AUTISM NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD MAR PY 2003 VL 16 IS 1 BP 92 EP 93 DI 10.1046/j.1468-3148.2003.01253.x PG 2 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 646VA UT WOS:000181055200010 ER PT J AU Paavonen, EJ Nieminen-von Wendt, T Vanhala, R Aronen, ET von Wendt, L AF Paavonen, EJ Nieminen-von Wendt, T Vanhala, R Aronen, ET von Wendt, L TI Effectiveness of melatonin in the treatment of sleep disturbances in children with Asperger disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID SEVERE LEARNING-DISABILITIES; NOCTURNAL ASTHMA; AUTISM; PERFORMANCE; PATTERNS; BEHAVIOR AB Sleep disturbances are common in patients with Asperger disorder. Although these sleep problems are often persistent and may significantly impair the child's daytime well-being, no treatment studies have been reported. In this open clinical trial, the effectiveness of melatonin was studied in a sample of 15 children with Asperger disorder (13 boys, 2 girls) aged 6-17 years using several questionnaires and actigraph measurements. They included assessments of sleep quality, tiredness, and behavior. Melatonin (3 mg/day) was used for 14 days. All the measurements were made three times: before the treatment period, during the treatment (days 12-14), and 3 weeks after the discontinuation of the treatment. The sleep patterns of all the children improved, and half of them displayed excellent responses to melatonin. In particular, actigraphically measured sleep latency decreased from 40.02 +/- 24.09 minutes to 21.82 +/- 9.64 minutes (P = 0.002), whereas sleep duration remained steady at 477.40 +/- 55.56 minutes and 480.48 +/- 50.71 minutes. Despite the short duration of the treatment, behavioral measures also displayed a significant improvement, and most of the effect disappeared after the discontinuation of the melatonin (P = 0.001). In conclusion, melatonin may provide an interesting new and well-tolerated treatment option for children with Asperger disorder suffering from chronic insomnia. However, these results must be confirmed in a controlled study. C1 Univ Helsinki, Dept Child Psychiat, Helsinki, Finland. Univ Helsinki, Dept Child Neurol, Helsinki, Finland. RP Paavonen, EJ (reprint author), Lastenlinnantie 11 C 29,POB 280, Helsinki 00029, Finland. CR Achenbach T., 1991, CHILD BEHAV CHECKLIS Akaboshi S, 2000, PSYCHIAT CLIN NEUROS, V54, P379, DOI 10.1046/j.1440-1819.2000.00723.x American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Balentine J, 1997, J AM ACAD CHILD PSY, V36, P1013, DOI 10.1097/00004583-199708000-00001 Blader JC, 1997, ARCH PEDIAT ADOL MED, V151, P473 Bruni O, 1996, J SLEEP RES, V5, P251, DOI 10.1111/j.1365-2869.1996.00251.x Cagnacci A, 1996, J PINEAL RES, V21, P200, DOI 10.1111/j.1600-079X.1996.tb00287.x Chervin RD, 1997, SLEEP, V20, P1185 Corkum P, 1998, J AM ACAD CHILD PSY, V37, P637, DOI 10.1097/00004583-199806000-00014 DAHL RE, 1994, J AM ACAD CHILD PSY, V33, P834, DOI 10.1097/00004583-199407000-00009 Dahl R E, 1996, Semin Pediatr Neurol, V3, P44, DOI 10.1016/S1071-9091(96)80028-3 Diette GB, 2000, ARCH PEDIAT ADOL MED, V154, P923 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Etzioni A, 1996, NEUROLOGY, V46, P261 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 GILLBERG C, 1995, CLIN CHILD NEUROPSYC, P54, DOI 10.1017/CBO9780511570094.007 GILLBERG M, 1994, SLEEP, V17, P236 Godbout R, 2000, NEUROREPORT, V11, P127, DOI 10.1097/00001756-200001170-00025 Gould EL, 2000, AM J MED GENET, V95, P307 Hatonen T, 1999, MOL GENET METAB, V66, P401, DOI 10.1006/mgme.1999.2815 Horrigan JP, 1997, J AM ACAD CHILD PSY, V36, P1014, DOI 10.1097/00004583-199708000-00002 HOSHINO Y, 1984, FOLIA PSYCHIAT NEU J, V38, P45 Jan JE, 2000, J PINEAL RES, V29, P34, DOI 10.1034/j.1600-079X.2000.290105.x Jan JE, 1996, J PINEAL RES, V21, P193, DOI 10.1111/j.1600-079X.1996.tb00286.x Jan MMS, 2000, PEDIATR NEUROL, V23, P229, DOI 10.1016/S0887-8994(00)00188-0 Lord C, 1998, J AUTISM DEV DISORD, V28, P345, DOI 10.1023/A:1026072922104 Marcotte AC, 1998, J DEV BEHAV PEDIATR, V19, P178, DOI 10.1097/00004703-199806000-00005 Masters KJ, 1996, J AM ACAD CHILD PSY, V35, P704, DOI 10.1097/00004583-199606000-00009 Miyamoto A, 1999, BRAIN DEV-JPN, V21, P59, DOI 10.1016/S0387-7604(98)00072-2 Owens JA, 2000, J DEV BEHAV PEDIATR, V21, P27, DOI 10.1097/00004703-200002000-00004 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Pillar G, 2000, PEDIATR NEUROL, V23, P225, DOI 10.1016/S0887-8994(00)00161-2 Pillar G, 1998, ARCH DIS CHILD, V79, P63 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 Robertson JM, 1997, J AM ACAD CHILD PSY, V36, P822, DOI 10.1097/00004583-199706000-00020 Sadeh A, 1989, J AMBULATORY MONITOR, V2, P209 Smits MG, 2001, J CHILD NEUROL, V16, P86, DOI 10.1177/088307380101600204 THORPY M, 1995, SLEEP, V18, P285 Stores G, 1996, J CHILD PSYCHOL PSYC, V37, P907, DOI 10.1111/j.1469-7610.1996.tb01489.x Stores G, 1998, ARCH DIS CHILD, V78, P413 Taira M, 1998, PSYCHIAT CLIN NEUROS, V52, P182, DOI 10.1111/j.1440-1819.1998.tb01018.x Wiggs L, 1998, J SLEEP RES, V7, P119, DOI 10.1046/j.1365-2869.1998.00107.x Wiggs L, 1996, J INTELL DISABIL RES, V40, P518, DOI 10.1046/j.1365-2788.1996.799799.x Zhdanova IV, 1999, J PEDIATR ENDOCR MET, V12, P57 Zhdanova IV, 1997, SLEEP, V20, P899 NR 45 TC 59 Z9 59 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD SPR PY 2003 VL 13 IS 1 BP 83 EP 95 DI 10.1089/104454603321666225 PG 13 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 679QT UT WOS:000182934000009 PM 12804129 ER PT J AU Askalan, R Mackay, M Brian, J Otsubo, H McDermott, C Bryson, S Boyd, J Snead, C Roberts, W Weiss, S AF Askalan, R Mackay, M Brian, J Otsubo, H McDermott, C Bryson, S Boyd, J Snead, C Roberts, W Weiss, S TI Prospective preliminary analysis of the development of autism and epilepsy in children with infantile spasms SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID VISUAL-FIELD CONSTRICTION; PROGNOSTIC FACTORS; WEST-SYNDROME; VIGABATRIN; THERAPY; ACTH; EPIDEMIOLOGY; PREDNISONE; DISORDERS AB The objective of this study was to compare the efficacy of corticotropin (ACTH) versus vigabatrin in treating infantile spasms and to determine which medication has a more favorable long-term outcome in terms of cognitive function, evolution of epilepsy, and incidence of autism. Patients with infantile spasms were included in the study if they were 3 to 16 months old, had hypsarrhythmia, and had no previous treatment with vigabatrin or corticosteroids. Patient evaluation included electroencephalographic and psychometric measures before and after treatment. Patients were stratified based on etiology (idiopathic or symptomatic) and sex and then randomized between the ACTH and vigabatrin treatment groups. Each of the treatment groups received either ACTH or vigabatrin for 2 weeks. At the end of 2 weeks of treatment, patients were considered responders if spasms and hypsarrhythmia resolved. Nonresponders were crossed over and treated with the alternate drug. Nine patients were included in the study. Three patients received ACTH, one of whom was a responder. Six patients received vigabatrin, three of whom were responders. The five nonresponders received both therapies. All patients had some degree of developmental plateau or regression before the initiation of treatment. Four patients with idiopathic infantile spasms showed improved cognitive function following treatment. The remaining five patients remained significantly delayed. Five patients with symptomatic infantile spasms had epilepsy following treatment; three of them were in the autistic spectrum. The small number of infants in this pilot study is insufficient to determine which of the two drugs is more effective. However, the following trends were identified: vigabatrin may be more effective for patients with symptomatic infantile spasms; patients with idiopathic infantile spasms tend to have a better cognitive outcome; and patients with symptomatic infantile spasms tend to develop both epilepsy and autism. C1 Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Autism Res Unit, Child Dev Ctr, Toronto, ON, Canada. Royal Childrens Hosp, Dept Neurol, Parkville, Vic 3052, Australia. RP Weiss, S (reprint author), Hosp Sick Children, Div Neurol, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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Child Neurol. PD MAR PY 2003 VL 18 IS 3 BP 165 EP 170 DI 10.1177/08830738030180030801 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 669JY UT WOS:000182349200002 PM 12731640 ER PT J AU Whalen, C Schreibman, L AF Whalen, C Schreibman, L TI Joint attention training for children with autism using behavior modification procedures SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE joint attention; autism; intervention; behavior therapy; child development; social skills training ID LANGUAGE; INFANTS AB Background: Deficits in joint attention are considered by many researchers to be an early predictor of childhood autism (e.g., Osterling & Dawson, 1994) and are considered to be pivotal to deficits in language, play, and social development in this population (Mundy, 1995). Although many researchers have noted the importance of joint attention deficits in the development of children with autism (e.g., Mundy, Sigman, & Kasari, 1994) and have called for intervention strategies (e.g., Mundy & Crowson, 1997), few studies have attempted to target joint attention. In this study, joint attention behaviors were taught to children with autism using a behavior modification procedure. Methods: A multiple-baseline design was implemented to evaluate intervention effects. The following target behaviors were included in the intervention: 1) Responding to showing, pointing, and gaze shifting of adult; 2) Coordinated gaze shifting (i.e., coordinated joint attention); and 3) Pointing (with the purpose of sharing, not requesting). Generalization to setting and parent, follow-up sessions, and social validation measures were also analyzed. Results: Joint attention behaviors were effectively trained and targeted behaviors generalized to other settings. 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Child Psychol. Psychiatry Allied Discip. PD MAR PY 2003 VL 44 IS 3 BP 456 EP 468 DI 10.1111/1469-7610.00135 PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 654YG UT WOS:000181524100014 PM 12635974 ER PT J AU Fatemi, SH Merz, A Realmuto, GR AF Fatemi, SH Merz, A Realmuto, GR TI The roles of Reelin, Bcl2, and serotonin in cerebellar pathology in autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Review DE autism; cerebellum; Reelin; Bcl2; serotonin ID CONGENITAL CYTOMEGALOVIRUS-INFECTION; POSTERIOR-FOSSA STRUCTURES; EARLY INFANTILE-AUTISM; MENTAL-RETARDATION; TRINUCLEOTIDE REPEAT; CORTICAL DEVELOPMENT; APOPTOTIC REGULATION; EMISSION-TOMOGRAPHY; FRONTAL-LOBE; X-CHROMOSOME AB This review describes involvement of serotonin, Reelin, and Bcl2 in cerebellar pathology in autism. The literature regarding neurochemical, neuropathologic, and imaging aspects of autistic pathology as related to cerebellum is discussed. 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PD MAR PY 2003 VL 15 IS 1 BP 57 EP 65 DI 10.1023/A:1021404304361 PG 9 WC Rehabilitation SC Rehabilitation GA 623LQ UT WOS:000179704800004 ER PT J AU Coldren, JT Halloran, C AF Coldren, JT Halloran, C TI Spatial reversal as a measure of executive functioning in children with autism SO JOURNAL OF GENETIC PSYCHOLOGY LA English DT Article DE autism; executive processing; perseveration; spatial reversal ID IMPAIRMENT; DEFICITS AB The purpose of this experiment was to compare the executive functioning performance of children with autism with chronological- and verbal-matched controls in a spatial-reversal task. Three groups of children participated in this experiment. One group was identified as having autism (7 boys), the 2nd group contained 7 typically developing children (6 boys, 1 girl) who were matched to the 1st group based on their verbal performance, and the 3rd group contained 7 typically functioning children (6 boys, 1 girl) matched to the 1st group based on chronological age. Each group was given a spatial-reversal task containing 2 problems. In the 1st problem, children selected a toy on a particular side in a pair. In the 2nd problem, the contingencies were reversed such that children were to choose the toy on the opposite side. Children with autism generally performed worse than comparison groups as indicated by their overall higher rate of errors. However, these results must be qualified by considering the performance for each problem: Errors for the children with autism were infrequent during the 1st problem but increased in the 2nd, whereas errors for comparison children showed the opposite pattern. When these results from the spatial-reversal task were interpreted from the perspective of hypothesis-testing theory, the executive functioning deficiency of children with autism was found to involve the selection and testing of stereotypic response sets that were not likely to be revised or changed flexibly according to feedback from the environment or the demands of the task. C1 Youngstown State Univ, Dept Psychol, Youngstown, OH 44555 USA. RP Coldren, JT (reprint author), Youngstown State Univ, Dept Psychol, Youngstown, OH 44555 USA. 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Genet. Psychol. PD MAR PY 2003 VL 164 IS 1 BP 29 EP 41 PG 13 WC Psychology, Developmental; Psychology; Psychology, Multidisciplinary SC Psychology GA 664XD UT WOS:000182089100002 PM 12693742 ER PT J AU Prior, M AF Prior, M TI Is there an increase in the prevalence of autism spectrum disorders? SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Article DE autism spectrum disorders; diagnosis; prevalence ID CHILDREN; EPIDEMIOLOGY; POPULATION AB This report summarizes recent prevalence estimates for autism spectrum disorders and outlines possible reasons for an apparent increase in the numbers of children diagnosed with autism and Asperger syndrome. C1 Univ Melbourne, Dept Psychol, Parkville, Vic 3052, Australia. RP Prior, M (reprint author), Univ Melbourne, Dept Psychol, Parkville, Vic 3052, Australia. 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Posit. Behav. Interv. PD SPR PY 2003 VL 5 IS 2 BP 92 EP 100 DI 10.1177/10983007030050020401 PG 9 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 657QW UT WOS:000181678700004 ER PT J AU Manning, JT Callow, M Bundred, PE AF Manning, JT Callow, M Bundred, PE TI Finger and toe ratios in humans and mice: implications for the aetiology of diseases influenced by HOX genes SO MEDICAL HYPOTHESES LA English DT Article ID 4TH DIGIT LENGTH; 2ND; MUTATIONS; ESTROGEN; LEUKEMIA; FUSION AB The differentiation of gonads, fingers, and toes is influenced by HOXA and HOXD genes. Therefore variation in the development of the gonads, and their fetal products such as testosterone, may be reflected in the morphology of the fingers and toes. One trait, the relative length of the second and fourth digits (2D:4D), shows sex differences (lower values in males) which are determined early, and 2D:4D has been found to correlate with fetal growth, sperm counts, family size, autism, myocardial infarction, and breast cancer. HOX genes are highly conserved in mammals and they influence the differentiation of all the fingers and toes. We suggest that (a) 2D:4D and other ratios of finger and toe length show sex differences throughout the mammals including humans and mice, (b) finger and toe ratios correlate with sex determination, the fetal production of sex steroids, and fetal programming of disease, and (c) HOX gene influences on sex determination, the morphogenesis of the urinogenital system, fertility, haematopoiesis, and breast cancer suggests that finger and toe ratios in humans and mice may correlate with many sex dependent diseases. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Liverpool, Sch Biol Sci, Liverpool L69 3BX, Merseyside, England. Univ Liverpool, Dept Primary Care, Liverpool, Merseyside, England. RP Manning, JT (reprint author), Univ Liverpool, Sch Biol Sci, POB 147, Liverpool L69 3BX, Merseyside, England. CR Brown W. 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Hypotheses PD MAR PY 2003 VL 60 IS 3 BP 340 EP 343 DI 10.1016/S0306-9877(02)00400-0 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 648LD UT WOS:000181152100010 PM 12581609 ER PT J AU Abu-Akel, A AF Abu-Akel, A TI The neurochemical hypothesis of 'theory of mind' SO MEDICAL HYPOTHESES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; COGNITIVE FUNCTION; AUTISTIC DISORDER; SCHIZOPHRENIA; RISPERIDONE; DOPAMINE; CORTEX; SYMPTOMATOLOGY; NEUROLEPTICS; MODULATION AB This paper aims to explore the neurochemical basis of the ability to represent one's own or other's mental states such as intentions, beliefs, wants and knowledge, an ability often referred to as 'theory of mind'. Based on neurochemical and psychopharmacological investigations in autism and schizophrenia, pathologies in which this ability is impaired, it is hypothesized that 'theory of mind' abilities are contingent on the integrity of the serotonergic and dopaminergic system. 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Hypotheses PD MAR PY 2003 VL 60 IS 3 BP 382 EP 386 DI 10.1016/S0306-9877(02)00406-1 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 648LD UT WOS:000181152100016 PM 12581615 ER PT J AU Lee, DA Lopez-Alberola, R Bhattacharjee, M AF Lee, DA Lopez-Alberola, R Bhattacharjee, M TI Childhood autism: A circuit syndrome? SO NEUROLOGIST LA English DT Review DE autism; cerebellum; limbic system; serotonin ID PERVASIVE DEVELOPMENTAL DISORDERS; COGNITIVE-AFFECTIVE SYNDROME; POSTERIOR-FOSSA STRUCTURES; BORNA-DISEASE VIRUS; INFANTILE-AUTISM; DOUBLE-BLIND; MENTAL-RETARDATION; SEROTONIN RECEPTOR; CORPUS-CALLOSUM; TUBEROUS SCLEROSIS AB BACKGROUND- Autism is a disorder that can lead to life-long disability. Currently, the etiology of autism is unknown, and although there are treatments for some of the behavioral abnormalities, there is no cure. REVIEW SUMMARY- While this article will review the clinical, anatomic, and pathologic features seen in autism, the primary focus will be to present a new and provocative unifying theory regarding the underlying mechanisms causing this disorder. Current research advances, some controversial, will be discussed, and a novel definition of autism as a "circuit syndrome" will be presented. The work elaborated here will tie many of the disparate findings together, based on the idea that autism arises from abnormalities of the cerebellolimbic circuitry. Some of the more alternative theories of autism, such as mercury toxicity, linkage to the measles, mumps, and rubella vaccine, and the use of secretin will be discussed. Finally, pharmacologic treatment options will be reviewed. CONCLUSIONS- Autism is not single disorder but represents dysfunction of the cerebellolimbic circuitry that can arise from many different etiologies. 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stress; exercise; cortisol; autism; MCDD ID INFANTILE-AUTISM; CHILDREN; OXYTOCIN; BRAIN AB Multiple Complex Developmental Disorder (MCDD) represents a distinct group within the autistic spectrum based on symptomatology. Unlike autistic children, part of MCDD children develop schizophrenia in adult life. Despite the differences, patients of both disorders are mainly characterized by abnormal reactions to their social environment. At the biological level, we showed in a previous study that MCDD children have a reduced cortisol response to psychosocial stress. Given the fact that autistic children clinically show more social impairments, it was hypothesized that they may have even further decreased cortisol responses to psychosocial stress than MCDD patients. Therefore, 10 autistic children were compared to 10 MCDD children and 12 healthy control children in their response to a psychosocial stressor, consisting of a public speaking task. In order to test whether any impairments in the biological stress response are specific for psychosocial stress, the autistic children were compared with I I MCDD children and 15 control children in their response to a physical stressor, consisting of 10 min of bicycle exercise. Heart rate and salivary cortisol levels were used as indicators of response to the stress tests. Autistic children showed a relatively elevated cortisol response to psychosocial stress, in contrast to MCDD children who showed a reduced cortisol response. No differences in heart rate or cortisol responses to the physical stress test were found. The specific difference between autistic and MCDD children in their cortisol response to psychosocial stress indicates that the disturbed reactions to the social environment observed in these disorders may have different biological backgrounds. C1 Rudolf Magnus Inst Neurosci, NL-3508 TA Utrecht, Netherlands. RP Jansen, LMC (reprint author), Univ Utrecht, Ctr Med, Dept Child & Adolescent Psychiat, HP F05 126,POB 85500, NL-3508 GA Utrecht, Netherlands. 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Our purpose was to examine the contribution of medical impairments to functional disability and school activity limitations in 41 300 school-age children participating in the 1994-1995 National Health Interview Survey. Methods. The 1994 and 1995 National Health Interview Survey and Disability Interview Supplement samples provide International Classification of Diseases, Ninth Revision medical impairment codes for children with functional limitations or school activity limitations in a nationally representative US sample. Functional limitations were distributed as follows: mobility 12.4/1000 (95% confidence interval [CI]: 11.1-13.6), self-care 8.8/1000 (95% CI: 7.7-9.8), communication 52.9/1000 (95% CI: 50.2-55.5), and learning 104.6/1000 (95% CI: 100.7-108.4). Functional disability status was classified as 4.1% mild, 5.9% major, and 1.9% multiple. School activity limitations included 4.1% needing or receiving special education, 0.7% unable to attend, and 0.9% limited attendance. We categorized International Classification of Diseases, Ninth Revision impairment codes reported in conjunction with medical usage as physical disorders (n = 1251; eg, leukemia, diabetes), asthma (n = 916), neurodevelopmental disorders (n = 802; eg, cerebral palsy, epilepsy, mental retardation, autism, blindness, deafness), and learning-behavior disorders (n = 806; eg, attention-deficit/hyperactivity disorder, learning disability, anxiety) for children with functional or school activity limitations. Of children with multiple functional disabilities, 29.9% had neurodevelopmental disorders, 27.1% had learning-behavior disorders, 18.1% had physical disorders, 4.2% had asthma, and 20.8% did not have an identified medical impairment because they had not received medical services in the past year. Among children requiring special education, physical disorders accounted for 9.4%, neurodevelopmental disorders for 16.7%, learning and behavior disorders for 17%, asthma for 3.4%, and 53.4% did not have an identified medical impairment because they had not received medical services in the past year. Conclusions. Chronic health impairments, neurodevelopmental disorders, learning-behavior disorders, and functional limitations in essential activities are required to understand the complexity of disability in school-age children. A large number of children with functional disability or school activity limitations have not received ongoing medical services. C1 Rhode Isl Hosp, Child Dev Ctr, Providence, RI 02903 USA. Brown Univ, Populat Studies & Training Ctr, Providence, RI 02912 USA. RP Msall, ME (reprint author), Rhode Isl Hosp, Child Dev Ctr, APC-6,593 Eddy St, Providence, RI 02903 USA. 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Articles were selected from 15 journals. Participant, treatment, and experimental variables were evaluated. Three effect sizes were calculated for each article. Behavioral treatments are effective in reducing problematic behaviors in individuals with autism. Type of target behavior and type of treatment did not moderate the average effect of treatment. As measured by percentage of zero data (PZD), three variables were predictive of behavioral suppression beyond that accounted for by behavioral topography and treatment type. Reliability of observation and number of treatment data points were positively related to PZD scores. Treatments based on experimental functional analysis (EFA) produced higher average PZD scores than treatments that did not include an EFA. The implications of the findings, study limitations, and suggestions for future research are discussed. (C) 2003 Elsevier Science Ltd. All rights reserved. C1 Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. 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Sport PD MAR PY 2003 VL 74 IS 1 SU S BP A75 EP A75 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 657MH UT WOS:000181670600194 ER PT J AU Yilmaz, I Birkan, B Camursoy, I Erkan, M Konukman, F AF Yilmaz, I Birkan, B Camursoy, I Erkan, M Konukman, F TI Using constant time delay procedure to teach aquatic play skills for children with autism SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Cent Washington Univ, Ellensburg, WA USA. NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. 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Med. Virol. PD MAR-APR PY 2003 VL 13 IS 2 BP 69 EP 70 DI 10.1002/rmv.389 PG 2 WC Virology SC Virology GA 656CW UT WOS:000181592100001 PM 12627390 ER PT J AU Valdizan, JR Abril-Villalba, B Mendez-Garcia, M Sans-Capdevila, O Pablo, MJ Peralta, P Lasierra, Y Bernal-Lafuente, M AF Valdizan, JR Abril-Villalba, B Mendez-Garcia, M Sans-Capdevila, O Pablo, MJ Peralta, P Lasierra, Y Bernal-Lafuente, M TI Cognitive evoked potentials in autistic children SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE Asperger; autism; ERP; N400 ID EVENT-RELATED POTENTIALS; SCHIZOPHRENIA; N400 AB Aims. The aim of this study was to examine the latency, amplitude and distribution of N400 potential in order to evaluate the semantic processing capacity in autistic children and in children suffering from Asperger's syndrome (AS), and to compare them with a control group. Patients and methods. 24 autistic children, six boys with AS and 25 controls, aged between 6 and 14 years old. The cases were examined using the DSM IV diagnostic criteria. Auditory stimulation was performed with pairs of congruent and incongruent words: two lists of 20 pairs of semantically related words (congruent) and 20 pairs of words with no semantic relationship whatsoever (incongruent). Results. The most striking parameter is the increase in latency in N400 for the group of autistic children, which did not occur in the group of children with AS. Maximum N400 negativity for the children with autism was found in the left frontocentral region. No significant differences were observed for the amplitude of N400 between the three groups that were studied. Conclusion. Neurophysiologically, the autistic children and those affected by AS perhaps use different neuronal networks in semantic processing. The N400 wave can be a valid test for monitoring verbal processing in these children. C1 Hosp Univ Miguel Servet, Serv Neurofisiol Clin, E-50009 Zaragoza, Spain. 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Neurologia PD MAR 1 PY 2003 VL 36 IS 5 BP 425 EP 428 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 658QA UT WOS:000181730600006 PM 12640594 ER PT J AU Karellou, J AF Karellou, J TI Laypeople's attitudes towards the sexuality of people with learning disabilities in Greece SO SEXUALITY AND DISABILITY LA English DT Article DE attitudes; Greece; sexuality; learning disabilities ID MENTAL-RETARDATION; BEHAVIOR; ADULTS; STAFF; PERCEPTIONS; STUDENTS; HANDICAP; AUTISM AB The present study examines the attitudes of the Greek public towards the sexuality of people with learning disabilities (LD). Participants of three Greek towns completed a copy of the GSAQ-LD. Results indicated that age and level of education had a consistent effect on attitudes whereas other variables such as gender social class, marital status, and contact with a person with LD did not consistently influence participants' attitudes. 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RI Frith, Uta/C-1757-2008 OI Frith, Uta/0000-0002-9063-4466 CR Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 Booth R, 2003, PHILOS T ROY SOC B, V358, P387, DOI 10.1098/rstb.2002.1204 Charman T, 2003, PHILOS T ROY SOC B, V358, P315, DOI 10.1098/rstb.2002.1199 Hill EL, 2003, PHILOS T R SOC B, V358, P281, DOI 10.1098/rstb.2002.1209 Hippler K, 2003, PHILOS T ROY SOC B, V358, P291, DOI 10.1098/rstb.2002.1197 Hobson RP, 2003, PHILOS T R SOC B, V358, P335, DOI 10.1098/rstb.2002.1201 Klin A, 2003, PHILOS T ROY SOC B, V358, P345, DOI 10.1098/rstb.2002.1202 Plaisted K, 2003, PHILOS T ROY SOC B, V358, P375, DOI 10.1098/rstb.2002.1211 Salmond CH, 2003, PHILOS T ROY SOC B, V358, P405, DOI 10.1098/rstb.2002.1210 Schultz RT, 2003, PHILOS T ROY SOC B, V358, P415, DOI 10.1098/rstb.2002.1208 Swettenham J, 2003, PHILOS T R SOC B, V358, P325, DOI 10.1098/rstb.2002.1203 Tager-Flusberg H, 2003, PHILOS T ROY SOC B, V358, P303, DOI 10.1098/rstb.2002.1198 NR 12 TC 3 Z9 3 PU ROYAL SOC PI LONDON PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND SN 0962-8436 J9 PHILOS T R SOC B JI Philos. Trans. R. Soc. B-Biol. Sci. PD FEB 28 PY 2003 VL 358 IS 1430 BP 277 EP 280 DI 10.1098/rstb.2002.1212 PG 4 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200001 ER PT J AU Hill, EL Frith, U AF Hill, EL Frith, U TI Understanding autism: insights from mind and brain SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Article DE autism; Asperger syndrome; theory of mind; weak central coherence; executive dysfunction; phenotype ID CEREBRAL-BLOOD-FLOW; ASPERGER-SYNDROME; EXECUTIVE FUNCTION; CENTRAL COHERENCE; COGNITIVE PHENOTYPE; NEURAL MECHANISMS; SPECTRUM DISORDERS; CAUSAL ASSOCIATION; CHILDHOOD AUTISM; FUNCTIONAL MRI AB Autism is a developmental disorder characterized by impaired social interaction and communication as well as repetitive behaviours and restricted interests. The consequences of this disorder for everyday life adaptation are extremely variable. The general public is now more aware of the high prevalence of this lifelong disorder, with ca. 0.6% of the population being affected. However, the signs and symptoms of autism are still puzzling. Since a biological basis of autism was accepted, approaches from developmental cognitive neuroscience have been applied to further our understanding of the autism spectrum. The study of the behavioural and underlying cognitive deficits in autism has advanced ahead of the study of the underlying brain abnormalities and of the putative genetic mechanisms. However, advances in these fields are expected as methodological difficulties are overcome. In this paper, recent developments in the field of autism are outlined. In particular, we review the findings of the three main neuro-cognitive theories of autism: theory-of-mind deficit, weak central coherence and executive dysfunction. C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. RP Hill, EL (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 325 EP 334 DI 10.1098/rstb.2002.1203 PG 10 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200006 PM 12639330 ER PT J AU Hobson, RP Bishop, M AF Hobson, RP Bishop, M TI The pathogenesis of autism: insights from congenital blindness SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Article DE autism; blindness; social relations; intersubjectivity ID VISUAL IMPAIRMENT; INFANTILE-AUTISM; CHILDREN; PLAY; PRESCHOOLERS; BEHAVIORS; PATTERNS AB There is substantial heterogeneity in the aetiology and clinical presentation of autism. So how do we account for homogeneity in the syndrome? The answer to this question will be critical for any attempt to trace the links between brain pathology and the psychological disabilities that characterize autism. One possibility is that the source of homogeneity in autism is not to be found 'in the child', but rather in dysfunction of the system constituted by child-in-relation-to-other. We have been exploring this hypothesis through the study of congenitally blind children, among whom features of autism, and the syndrome of autism itself, are strikingly common. To justify such an approach, one needs to establish that the clinical features in blind children have qualities that are indeed 'autistic-like'. We conducted systematic observations of the social interactions of two matched groups of congenitally blind children who do not have autism, rating their social engagement, emotional tone, play and language during three sessions of free play in the school playground. The qualities of social impairment in the more disabled children were similar to those in sighted children with autism. Additional evidence came from independent ratings of the children in a different play setting: on the childhood autism rating scale (CARS), the socially impaired children had 'autistic-like' abnormalities in both social and non-social domains. If we can determine the way in which congenital blindness predisposes to features of autism, we shall be in a better position to trace the developmental pathways that lead to the syndrome in sighted children. C1 UCL, Tavistock Clin, Dev Psychopathol Res Unit, London NW3 5BA, England. UCL, Dept Psychiat & Behav Sci, London NW3 5BA, England. RP Hobson, RP (reprint author), UCL, Tavistock Clin, Dev Psychopathol Res Unit, 120 Belsize Lane, London NW3 5BA, England. 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Trans. R. Soc. B-Biol. Sci. PD FEB 28 PY 2003 VL 358 IS 1430 BP 335 EP 344 DI 10.1098/rstb.2002.1201 PG 10 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200007 PM 12639331 ER PT J AU Hippler, K Klicpera, C AF Hippler, K Klicpera, C TI A retrospective analysis of the clinical case records of 'autistic psychopaths' diagnosed by Hans Asperger and his team at the University Children's Hospital, Vienna SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE Asperger syndrome; 'autistic psychopathy'; high-functioning autism; diagnostic criteria ID HIGH-FUNCTIONING AUTISM; SCHIZOID PERSONALITY; ADULT LIFE; CHILDHOOD AB To date, it is questionable whether the diagnostic criteria for Asperger syndrome (AS) as stated by ICD-10 or DSM-IV still reflect Asperger's original account of 'autistic psychopathy' (AP) from the 1940s. The present study examined 74 clinical case records of children with AP diagnosed by Hans Asperger and his team at the Viennese Children's Clinic and Asperger's private practice between 1950 and 1986. The characteristic features of the children are outlined, including reasons for referral, parental background, behavioural problems, cognitive functioning, communication and interests. Results show that the patients of Asperger described in our study represent a subgroup of children with very high intellectual functioning, specific circumscribed interests and talents but impaired social, communication and motor skills. Sixty-eight percent of the sample met ICD-10 criteria for AS, while 25% fulfilled the diagnostic criteria for autism. Implications for the diagnosis of AS are discussed. C1 Neues Inst Gebaude, Abt Angew & Klin Psychol, A-1010 Vienna, Austria. RP Klicpera, C (reprint author), Neues Inst Gebaude, Abt Angew & Klin Psychol, Univ Str 7, A-1010 Vienna, Austria. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 291 EP 301 DI 10.1098/rstb.2002.1197 PG 11 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200003 PM 12639327 ER PT J AU Tager-Flusberg, H Joseph, RM AF Tager-Flusberg, H Joseph, RM TI Identifying neurocognitive phenotypes in autism SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Review DE autism; phenotype; cognitive profile; specific language impairment; language; macrocephaly ID PERVASIVE DEVELOPMENTAL DISORDERS; LANGUAGE IMPAIRMENT; COGNITIVE NEUROSCIENCE; SUSCEPTIBILITY GENE; HEAD CIRCUMFERENCE; NONWORD REPETITION; MEDICAL CONDITIONS; BROADER PHENOTYPE; INFANTILE-AUTISM; HUMAN NEOCORTEX AB Autism is a complex disorder that is heterogeneous both in its phenotypic expression and its etiology. The search for genes associated with autism and the neurobiological mechanisms that underlie its behavioural symptoms has been hampered by this heterogeneity. Recent studies indicate that within autism, there may be distinct subgroups that can be defined based on differences in neurocognitive profiles. This paper presents evidence for two kinds of subtypes in autism that are defined on, the basis of language profiles and on the basis of cognitive profiles. The implications for genetic and neurobiological studies of these subgroups are discussed, with special reference to evidence relating these cognitive phenotypes to volumetric studies of brain size and organization in autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Lab Dev Cognt Neurosci, Boston, MA 02118 USA. RP Tager-Flusberg, H (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, Lab Dev Cognt Neurosci, 715 Albany St L-814, Boston, MA 02118 USA. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 303 EP 314 DI 10.1098/rstb.2002.1198 PG 12 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200004 PM 12639328 ER PT J AU Charman, T AF Charman, T TI Why is joint attention a pivotal skill in autism? SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE autism; joint attention; play; imitation; language; symptom severity ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDER; YOUNG-CHILDREN; EARLY RECOGNITION; SOCIAL COMMUNICATION; HOME VIDEOTAPES; SYMBOLIC PLAY; AGE; LANGUAGE; INFANTS AB joint attention abilities play a crucial role in the development of autism. Impairments in joint attention are among the earliest signs of the disorder and joint attention skills relate to outcome, both in the 'natural course' of autism and through being targeted in early intervention programmes. In the current study, concurrent and longitudinal associations between joint attention and other social communication abilities measured in a sample of infants with autism and related pervasive developmental disorders at age 20 months, and language and symptom severity at age 42 months, were examined. Extending the findings from previous studies, joint attention ability was positively associated with language gains and (lower) social and communication symptoms, and imitation ability was also positively associated with later language. Some specificity in the association between different aspects of joint attention behaviours and outcome was found: declarative, triadic gaze switching predicted language and symptom severity but imperative, dyadic eye contact behaviours did not. Further, although joint attention was associated with later social and language symptoms it was unrelated to repetitive and stereotyped symptoms, suggesting the latter may have a separate developmental trajectory. Possible deficits in psychological and neurological processes that might underlie the impaired development of joint attention in autism are discussed. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. RP Charman, T (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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The magnitude of this discrepancy is now being documented through newer techniques such as eye tracking, which allows us to see and measure how individuals with autism search for meaning when presented with naturalistic social scenes. This paper offers an approach to social cognitive development intended to address the above discrepancy, which is considered a key element for any understanding of the pathophysiology of autism. This approach, called the enactive mind (EM), originates from the emerging work on 'embodied cognitive science', a neuroscience framework that views cognition as bodily experiences accrued as a result of an organism's adaptive actions upon salient aspects of the surrounding environment. The EM approach offers a developmental hypothesis of autism in which the process of acquisition of embodied social cognition is derailed early on, as a result of reduced salience of social stimuli and concomitant enactment of socially irrelevant aspects of the environment. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 345 EP 360 DI 10.1098/rstb.2002.1202 PG 16 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200008 PM 12639332 ER PT J AU Baron-Cohen, S Richler, J Bisarya, D Gurunathan, N Wheelwright, S AF Baron-Cohen, S Richler, J Bisarya, D Gurunathan, N Wheelwright, S TI The systemizing quotient: an investigation of adults with Asperger syndrome or high-functioning autism, and normal sex differences SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE Asperger syndrome; sex differences; systemizing; empathizing ID PSYCHOLOGY; ABILITIES; CHILDREN; EMPATHY; BRAIN; TWIN AB Systemizing is the drive to analyse systems or construct systems. A recent model of psychological sex differences suggests that this is a major dimension in which the sexes differ, with males being more drawn to systemize than females. Currently, there are no self-report measures to assess this important dimension. A second major dimension of sex differences is empathizing (the drive to identify mental states and respond to these with an appropriate emotion). Previous studies find females score higher on empathy measures. We report a new self-report questionnaire, the Systemizing Quotient (SQ), for use with adults of normal intelligence. It contains 40 systemizing items and 20 control items. On each systemizing item, a person can score 2, 1 or 0, so the SQ has a maximum score of 80 and a minimum of zero. In Study 1, we measured the SQ of n = 278 adults (114 males, 164 females) from a general population, to test for predicted sex differences (male superiority) in systemizing. All subjects were also given the Empathy Quotient (EQ) to test if previous reports of female superiority would be replicated. In Study 2 we employed the SQ and the EQ with n = 47 adults (33 males, 14 females) with Asperger syndrome (AS) or high-functioning autism (HFA), who are predicted to be either normal or superior at systemizing, but impaired at empathizing. Their scores were compared with n = 47 matched adults from the general population in Study 1. In Study 1, as predicted, normal adult males scored significantly higher than females on the SQ and significantly lower on the EQ. In Study 2, again as predicted, adults with AS/HFA scored. significantly higher on the SQ than matched controls, and significantly lower on the EQ than matched controls. The SQ reveals both a sex difference in systemizing in the general population and an unusually strong drive to systemize in AS/HFA. These results are discussed in relation to two linked theories: the 'empathizing-systemizing' (E-S) theory of sex differences and the extreme male brain (EMB) theory of autism. C1 Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Downing St, Cambridge CB2 3EB, England. 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Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD FEB 28 PY 2003 VL 358 IS 1430 BP 361 EP 374 DI 10.1098/rstb.2002.1206 PG 14 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200009 PM 12639333 ER PT J AU Plaisted, K Saksida, L Alcantara, J Weisblatt, E AF Plaisted, K Saksida, L Alcantara, J Weisblatt, E TI Towards an understanding of the mechanisms of weak central coherence effects: experiments in visual configural learning and auditory perception SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE perception; configuration; local; global; integration ID FILTER SHAPES; ENHANCED DISCRIMINATION; CONNECTIONIST MODEL; AUTISM; CHILDREN; LESIONS; TASK; SELECTIVITY; PRECEDENCE; ABILITIES AB The weak central coherence hypothesis of Frith is one of the most prominent theories concerning the abnormal performance of individuals with autism on tasks that involve local and global processing. Individuals with autism often outperform matched nonautistic individuals on tasks in which success depends upon processing of local features, and underperform on tasks that require global processing. We review those studies that have been unable to identify the locus of the mechanisms that may be responsible for weak central coherence effects and those that show that local processing is enhanced in autism but not at the expense of global processing. In the light of these studies, we propose that the mechanisms which can give rise to 'weak central coherence' effects may be perceptual. More specifically, we propose that perception operates to enhance the representation of individual perceptual features but that this does not impact adversely on representations that involve integration of features. This proposal was supported in the two experiments we report on configural and feature discrimination learning in high-functioning children with autism. We also examined processes of perception directly, in an auditory filtering task which measured the width of auditory filters in individuals with autism and found that the width of auditory filters in autism were abnormally broad. We consider the implications of these findings for perceptual theories of the mechanisms underpinning weak central coherence effects. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Dev Psychiat Sect, Cambridge CB2 2AH, England. RP Plaisted, K (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 375 EP 386 DI 10.1098/rstb.2002.1211 PG 12 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200010 PM 12639334 ER PT J AU Booth, R Charlton, R Hughes, C Happe, F AF Booth, R Charlton, R Hughes, C Happe, F TI Disentangling weak coherence and executive dysfunction: planning drawing in autism and attention-deficit/hyperactivity disorder SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE autism; coherence; executive function; cognitive style; drawing; planning ID CHILDREN; DEFICITS; MIND; BIAS AB A tendency to focus on details at the expense of configural information, 'weak coherence', has been proposed as a cognitive style in autism. In the present study we tested whether weak coherence might be the result of executive dysfunction, by testing clinical groups known to show deficits on tests of executive control. Boys with autism spectrum disorders (ASD) were compared with age- and intelligence quotient (IQ)-matched boys with attention-deficit/hyperactivity disorder (ADHD), and typically developing (TD) boys, on a drawing task requiring planning for the inclusion of a new element. Weak coherence was measured through analysis of drawing style. In line with the predictions made, the ASD group was more detail-focused in their drawings than were either ADHD or TD boys. The ASD and ADHD groups both showed planning impairments, which were more severe in the former group. Poor planning did not, however, predict detail-focus, and scores on the two aspects of the task were unrelated in the clinical groups. These findings indicate that weak coherence may indeed be a cognitive style specific to autism and unrelated to cognitive deficits in frontal functions. C1 Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London SE5 8AF, England. 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Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD FEB 28 PY 2003 VL 358 IS 1430 BP 387 EP 392 DI 10.1098/rstb.2002.1204 PG 6 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200011 PM 12639335 ER PT J AU Mari, M Castiello, U Marks, D Marraffa, C Prior, M AF Mari, M Castiello, U Marks, D Marraffa, C Prior, M TI The reach-to-grasp movement in children with autism spectrum disorder SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE autism; reach-to-grasp; human; motor control; human development; movement disorders ID PREHENSION MOVEMENTS AB Autism is associated with a wide and complex array of neurobehavioural symptoms. Examination of the motor system offers a particularly appealing method for studying autism by providing information about this syndrome that is relatively immune to experimental influence. In this article, we considered the relationship between possible movement disturbance and symptoms of autism and introduced an experimental model that may be useful for rehabilitation and diagnostic purposes: the reach-to-grasp movement. Research is reviewed that characterizes kinematically the reach-to-grasp movement in children with autism compared with age-matched 'controls'. Unlike the age-matched children, autistic children showed differences in movement planning and execution, supporting the view that movement disturbances may play a part in the phenomenon of autism. C1 Univ London, Royal Holloway & Bedford New Coll, Dept Psychol, Egham TW20 0EX, Surrey, England. Royal Childrens Hosp, Parkville, Vic 3052, Australia. RP Castiello, U (reprint author), Univ London, Royal Holloway & Bedford New Coll, Dept Psychol, Egham TW20 0EX, Surrey, England. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 393 EP 403 DI 10.1098/rstb.2002.1205 PG 11 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200012 PM 12639336 ER PT J AU Salmond, CH de Haan, M Friston, KJ Gadian, DG Vargha-Khadem, F AF Salmond, CH de Haan, M Friston, KJ Gadian, DG Vargha-Khadem, F TI Investigating individual differences in brain abnormalities in autism SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE autism; neurobiological basis; magnetic resonance imaging; voxel-based morphometry; startle response; amygdala ID VOXEL-BASED MORPHOMETRY; CARD SORTING TEST; FACIAL EXPRESSIONS; RHESUS-MONKEY; AMYGDALA; STARTLE; HIPPOCAMPUS; CHILDREN; EMOTION; PROJECTIONS AB Autism is a psychiatric syndrome characterized by impairments in three domains: social interaction, communication, and restricted and repetitive behaviours and interests. 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PD FEB 28 PY 2003 VL 358 IS 1430 BP 405 EP 413 DI 10.1098/rstb.2002.1210 PG 9 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200013 PM 12639337 ER PT J AU Schultz, RT Grelotti, DJ Klin, A Kleinman, J Van der Gaag, C Marois, R Skudlarski, P AF Schultz, RT Grelotti, DJ Klin, A Kleinman, J Van der Gaag, C Marois, R Skudlarski, P TI The role of the fusiform face area in social cognition: implications for the pathobiology of autism SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article DE amygdala; autism; fusiform face area; medial prefrontal cortex; social cognition; superior temporal sulcus ID MEDIAL PREFRONTAL CORTEX; BIOLOGICAL MOTION; ASPERGER-SYNDROME; FUNCTIONAL MRI; HUMAN AMYGDALA; OCCIPITOTEMPORAL CORTEX; FACIAL EXPRESSIONS; TEMPORAL CORTEX; PERCEPTION; RECOGNITION AB A region in the lateral aspect of the fusiform gyrus (FG) is more engaged by human faces than any other category of image. It has come to be known as the 'fusiform face area' (FFA). The origin and extent of this specialization is currently a topic of great interest and debate. This is of special relevance to autism, because recent studies have shown that the FFA is hypoactive to faces in this disorder. In two linked functional magnetic resonance imaging (fMRI) studies of healthy young adults, we show here that the FFA is engaged by a social attribution task (SAT) involving perception of human-like interactions among three simple geometric shapes. The amygdala, temporal pole, medial prefrontal cortex, inferolateral frontal cortex and superior temporal sulci were also significantly engaged. Activation of the FFA to a task without faces challenges the received view that the FFA is restricted in its activities to the perception of faces. We speculate that abstract semantic information associated with faces is encoded in the FG region and retrieved for social computations. 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Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD FEB 28 PY 2003 VL 358 IS 1430 BP 415 EP 427 DI 10.1098/rstb.2002.1208 PG 13 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 650WK UT WOS:000181286200014 PM 12639338 ER PT J AU Hutcheson, HB Bradford, Y Folstein, SE Gardiner, MB Santangelo, SL Sutcliffe, JS Haines, JL AF Hutcheson, HB Bradford, Y Folstein, SE Gardiner, MB Santangelo, SL Sutcliffe, JS Haines, JL TI Defining the autism minimum candidate gene region on chromosome 7 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE recombination breakpoint mapping; microsatellite markers; haplotype sharing; association analysis ID SUSCEPTIBILITY GENE; LANGUAGE DISORDER; FAMILY HISTORY; LINKAGE; ASSOCIATION; TWIN; 7Q31; HETEROGENEITY; BREAKPOINT; ETIOLOGY AB Previous genetic and cytogenetic studies provide evidence that points to one or more autism susceptibility genes residing on chromosome 7q (AUTS1,115-149 cM on the Marshfield map). However, further localization using linkage analysis has proven difficult. To overcome this problem, we examined the Collaborative Linkage Study of Autism (CLSA) data-set to identify only the families potentially linked to chromosome 7. Out of 94, 47 families were identified and 17 markers were used to generate chromosomal haplotypes. We performed recombination breakpoint analysis to determine if any portion of the chromosome was predominately shared across families. The most commonly shared region spanned a 6 cM interval between D7S501 and D7S2847. Additional markers at 1 cM intervals within this region were genotyped and association and recombination breakpoint analysis was again performed. Although no significant allelic association was found, the recombination breakpoint data points to a shared region between D7S496-D7S2418 (120-123 cM) encompassing about 4.5 Mb of genomic DNA containing over 50 genes. (C) 2003 Wiley-Liss, Inc. C1 Vanderbilt Univ, Med Ctr, Program Human Genet, Dept Physiol & Mol Biophys, Nashville, TN 37232 USA. Tufts Univ, Sch Med, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. RP Hutcheson, HB (reprint author), Vanderbilt Univ, Med Ctr, Program Human Genet, Dept Physiol & Mol Biophys, 519 Light Hall, Nashville, TN 37232 USA. 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B PD FEB 15 PY 2003 VL 117B IS 1 BP 90 EP 96 DI 10.1002/ajmg.b.10033 PG 7 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 670HN UT WOS:000182401600016 PM 12555242 ER PT J AU Lobo-Menendez, F Sossey-Alaoui, K Bell, JM Copeland-Yates, SA Plank, SM Sanford, SO Skinner, C Simensen, RJ Schroer, RJ Michaelis, RC AF Lobo-Menendez, F Sossey-Alaoui, K Bell, JM Copeland-Yates, SA Plank, SM Sanford, SO Skinner, C Simensen, RJ Schroer, RJ Michaelis, RC TI Absence of MeCP2 mutations in patients from the South Carolina Autism Project SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE epigenetic mechanisms; methyl-binding proteins; pervasive developmental disorders; mutation analysis; Xq28 ID LINKED MENTAL-RETARDATION; X-CHROMOSOME INACTIVATION; RETT-SYNDROME PATIENTS; CPG-BINDING-PROTEIN; ANGELMAN-SYNDROME; DNA METHYLATION; TRANSCRIPTIONAL REPRESSOR; IMPRINTED GENES; HIGH-FREQUENCY; MALES AB The methyl-CpG binding protein 2 (MeCP2) gene has recently been identified as the gene responsible for Rett syndrome (RS), a pervasive developmental disorder considered by many to be one of the autism spectrum disorders. Most female patients with MeCP2 mutations exhibit the classic features of RS, including autistic behaviors. Most male patients with MeCP2 mutations exhibit moderate to severe developmental delay/mental retardation. Ninety nine patients from the South Carolina autism project (SCAP) were screened for MeCP2 mutations, including all 41 female patients from whom DNA samples were available plus the 58 male patients with the lowest scores on standard IQ tests and/or the Vineland Adaptive Behavior Scale. No pathogenic mutations were observed in these patients. One patient had the C582T variant, previously reported in the unaffected father of an RS patient. Two other patients had single nucleotide polymorphisms in the 3' UTR of the gene, G1470A and C1516G. These variants were seen in 12/82 and 1/178 phenotypically normal male controls, respectively. The findings from this and other studies suggest that mutations in the coding sequence of the MeCP2 gene are not a significant etiological factor in autism. (C) 2003 Wiley-Liss, Inc. C1 Greenwood Genet Ctr, Self Res Inst, Greenwood, SC 29646 USA. Presbyterian Coll, Clinton, SC USA. RP Michaelis, RC (reprint author), Greenwood Genet Ctr, Self Res Inst, 1 Gregor Mendel Circle, Greenwood, SC 29646 USA. 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B PD FEB 15 PY 2003 VL 117B IS 1 BP 97 EP 101 DI 10.1002/ajmg.b.10016 PG 5 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 670HN UT WOS:000182401600017 PM 12555243 ER PT J AU Cohen, MM AF Cohen, MM TI Mental deficiency, alterations in performance, and CNS abnormalities in overgrowth syndromes SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Review DE Sotos syndrome; Weaver syndrome; Proteus syndrome; neurofibromatosis type I; fragile X syndrome; neonatal hypoglycemia; infants of diabetic mothers; Beckwith-Wiedemann syndrome; Perlman syndrome; Simpson-Golabi-Behmel syndrome; hemihyperplasia; Sturge-Weber syndrome; Bannayan-Riley-Ruvalcaba/Cowden syndrome; macrocephaly-autism syndrome; PEHO syndrome; Pallister-Killian syndrome; Costello syndrome ID FRAGILE-X-SYNDROME; STURGE-WEBER-SYNDROME; PALLISTER-KILLIAN-SYNDROME; MARMORATA-TELANGIECTATICA-CONGENITA; AUTOSOMAL-DOMINANT INHERITANCE; BANNAYAN-ZONANA SYNDROME; MYHRE-SMITH SYNDROME; NEUROFIBROMATOSIS TYPE-1; PROTEUS SYNDROME; COWDEN-SYNDROME AB Mental deficiency, alterations in performance, and central nervous system (CNS) abnormalities are discussed in the following overgrowth syndromes: Sotos syndrome, Weaver syndrome, Proteus syndrome, neurofibromatosis type 1, fragile X syndrome, syndromes with neonatal hypoglycemia, Simpson-Golabi-Behmel syndrome, hemihyperplasia, Sturge-Weber syndrome, Bannayan-Riley-Ruvalcaba/Cowden syndrome, macrocephaly-autism syndrome, PEHO syndrome, chromosomal syndromes, and other miscellaneous syndromes. 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J. Med. Genet. C PD FEB 15 PY 2003 VL 117C IS 1 BP 49 EP 56 DI 10.1002/ajmg.c.10013 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 670GY UT WOS:000182400200007 PM 12561058 ER PT J AU Finucane, B Haas-Givler, B Simon, EW AF Finucane, B Haas-Givler, B Simon, EW TI Genetics, mental retardation, and the forging of new alliances SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE mental retardation; eugenics; special education; psychiatry ID SMITH-MAGENIS-SYNDROME; FRAGILE-X-SYNDROME; HUMAN-GENOME-PROJECT; ADULTS; CHILDREN; INDIVIDUALS; BEHAVIOR; EUGENICS; AUTISM AB The lives of people with intellectual disabilities are tightly intermeshed with the philosophies and practices of special educators, therapists, psychologists, social workers, and others who make up the mental retardation field. These nonmedical workers represent a kind of extended family, which can strongly influence the decisions made and services received by the people they serve. By contrast, most individuals with mental retardation do not have extraordinary medical needs, and healthcare professionals play only a minor role in their human services family. There are deeply rooted historical differences between the medical model of mental retardation with which genetics professionals are familiar and the philosophies embraced by nonmedical workers who dominate the mental retardation field. These contrasts have an important impact on the genetic diagnostic process, as well as a more global effect on mental retardation research. Without the full participation of teachers, therapists, psychologists, and others outside the medical setting, many practical applications of genetic research can neither be implemented nor expanded upon, and an important opportunity for cross-fertilization is lost. It is in the interest of the genetics community to take advantage of recent overtures by the mental retardation field to forge new alliances and broaden its perspectives on intellectual disability. (C) 2003 Wiley-Liss, Inc. C1 Elwyn Training & Res Inst, Genet Serv, Elwyn, PA 19063 USA. RP Finucane, B (reprint author), Elwyn Training & Res Inst, Genet Serv, 111 Elwyn Rd, Elwyn, PA 19063 USA. 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Methods: The authors compared mortality in persons with (n = 8,156) and without (n = 72,526) history of epilepsy in a 1988 to 1999 California population of persons with mild developmental disabilities. Subjects had traumatic brain injury, cerebral palsy, Down syndrome, autism, or no identifiable condition. There were 506,204 person-years of data, with 1,523 deaths. Excess death rates and standardized mortality ratios were computed for the persons in the study with epilepsy, relative to those in the study without epilepsy. Controlled comparisons were made using logistic regression on person-years. Results: Compared to subjects with no epilepsy, the excess mortality was six (deaths per 1,000 persons per year) for persons with a recent (<12 months) history of status epilepticus, five for a recent history of generalized tonic-clonic seizure, three for a recent history of nonconvulsive seizures, and less than one for a history of epilepsy but no recent events. Proportion in remission and excess mortality showed no change over the 12-year study period. Conclusions: Persistent seizures are associated with increased mortality in remote symptomatic epilepsy. Mortality is highest among individuals with status epilepticus or generalized convulsions. C1 Univ Calif San Francisco, Life Expectancy Project, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. RP Day, SM (reprint author), 1439 17th Ave, San Francisco, CA 94122 USA. 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J. Nurs. PD FEB PY 2003 VL 103 IS 2 BP 86 EP 86 PG 1 WC Nursing SC Nursing GA 643CZ UT WOS:000180845500046 ER PT J AU Allen, G Courchesne, E AF Allen, G Courchesne, E TI Differential effects of developmental cerebellar abnormality on cognitive and motor functions in the cerebellum: An fMRI study of autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ANATOMIC-MR CORRELATION; SHIFTING ATTENTION; MENTAL-RETARDATION; SPATIAL ATTENTION; INFANTILE-AUTISM; SAGITTAL PLANE; BRAIN; NEUROPATHOLOGY; SCHIZOPHRENIA; ACTIVATION AB Objective: Recent years have seen a revolution in views regarding cerebellar function. New findings suggest that the cerebellum plays a role in multiple functional domains: cognitive, affective, and sensory as well as motor. These findings imply that developmental cerebellar pathology could play a role in certain nonmotor functional deficits, thereby calling for a broader investigation of the functional consequences of cerebellar pathology. Autism provides a useful model, since over 90% of autistic cerebella examined at autopsy have shown well-defined cerebellar anatomic abnormalities. The aim of the present study was to examine how such pathology ultimately impacts cognitive and motor function within the cerebellum. Method: Patterns of functional magnetic resonance imaging (fMRI) activation within anatomically defined cerebellar regions of interest were examined in eight autistic patients (ages 14-38 years) and eight matched healthy comparison subjects performing motor and attention tasks. For the motor task, subjects pressed a button at a comfortable pace, and activation was compared with a rest condition. For the attention task, visual stimuli were presented one at a time at fixation, and subjects pressed a button to every target. Activation was compared with passive. visual stimulation. 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PD FEB PY 2003 VL 160 IS 2 BP 262 EP 273 DI 10.1176/appi.ajp.160.2.262 PG 12 WC Psychiatry SC Psychiatry GA 642DE UT WOS:000180788300010 PM 12562572 ER PT J AU Belkadi, Z Gierski, F Clerc, C Bertot, V Brasselet, C Motte, J AF Belkadi, Z Gierski, F Clerc, C Bertot, V Brasselet, C Motte, J TI Asperger Syndrome in childhood: Review of four cases SO ARCHIVES DE PEDIATRIE LA French DT Review DE Asperger syndrome; child; neuropsychology ID HIGH-FUNCTIONING AUTISM; CHILDREN; DISORDERS AB Introduction - Asperger syndrome is a pervasive developmental disorder included lately in the international classifications. Observations - We report the observations of four children presenting this syndrome. For every patient, we collected antecedents and psychomotor development; we made neuropsychological assessment and video recording. Three patients underwent an EEG and one a cerebral MRI. Results - These patients were between ten- and sixteen-year old. The neuropsychological assessment showed a heterogeneous intellectual functioning with three times out of four a dissociation between high verbal level and low non-verbal level. Their language appeared sophisticated, apragmatic, their comprehension was inflexible. The mean age at diagnosis was ten years. They showed a sociability and autonomy improvement but they were conscious of their difference and suffered from it. Conclusion - Our four cases allow to present Asperger syndrome, slightly known in France. Collaborative studies and genetic studies are necessary to improve the knowledge of this syndrome. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All rights reserved. C1 CHU Reims, Amer Mem Hosp, Serv Pediat A, Unite Neurol Pediat, F-51092 Reims, France. RP Motte, J (reprint author), CHU Reims, Amer Mem Hosp, Serv Pediat A, Unite Neurol Pediat, 47 Rue Cognacq Jay, F-51092 Reims, France. CR AHLSEN G, 1993, BIOL PSYCHIAT, V33, P734, DOI 10.1016/0006-3223(93)90124-V Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Berthier M L, 1990, J Neuropsychiatry Clin Neurosci, V2, P197 Bonnet K, 1996, J CHILD NEUROL, V11, P483 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Ehlers S, 1997, J CHILD PSYCHOL PSYC, V38, P207, DOI 10.1111/j.1469-7610.1997.tb01855.x GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P643, DOI 10.1007/BF01046332 Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P375, DOI 10.1097/00004583-199105000-00004 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 GORDON CT, 1993, ARCH GEN PSYCHIAT, V50, P441 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Larsen FW, 1997, EUR CHILD ADOLES PSY, V6, P181 MCKELVEY JR, 1995, J CHILD NEUROL, V10, P310 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Nordin V, 1998, ACTA PSYCHIAT SCAND, V97, P99, DOI 10.1111/j.1600-0447.1998.tb09970.x OZBAYRAK KR, 1991, BRAIN DEV-JPN, V13, P454 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x Ramberg C, 1996, EUR J DISORDER COMM, V31, P387 RICKARBY G, 1991, J AUTISM DEV DISORD, V21, P341, DOI 10.1007/BF02207330 STRAYHORN J, 1989, J AM ACAD CHILD PSY, V28, P299, DOI 10.1097/00004583-198903000-00031 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 WING L, 1981, PSYCHIAT RES, V5, P129, DOI 10.1016/0165-1781(81)90043-3 WING L, 1981, PSYCHOL MED, V11, P115 NR 25 TC 4 Z9 4 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0929-693X J9 ARCH PEDIATRIE JI Arch. Pediatr. PD FEB PY 2003 VL 10 IS 2 BP 110 EP 116 DI 10.1016/S0929-693X(03)00306-3 PG 7 WC Pediatrics SC Pediatrics GA 675NY UT WOS:000182702500004 PM 12829351 ER PT J AU Lauwerier, L de Lenclave, MBD Bailly, D AF Lauwerier, L de Lenclave, MBD Bailly, D TI Hearing impairment and cognitive development SO ARCHIVES DE PEDIATRIE LA French DT Review DE cognition; deafness; child; developmental disabilities ID COMMUNICATION; MIND; CHILDREN; AUTISM AB The study of the cognitive abilities of hearing-impaired children is important for both practical (e.g. to determine appropriate teaching strategies) and theoretical reasons (e.g. to examine the role of language in thought processes). The aim of this paper is to examine the cognitive function of hearing-impaired children from a review of the literature. If most studies show that deaf children are similar to normal children in virtually all aspects of cognitive function, many studies also emphasize pronounced differences in their academic achievement. Besides the degree of hearing loss and the age at onset of deafness, environmental factors (such as parental support and educational methods) seem to play an important role in the cognitive development and academic success of these children. This underlines the importance of the measures adopted for the deaf children as they may have a positive or negative impact on their development. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All fights reserved. C1 Hop St Marguerite, Federat Psychiat Enfant & Adolescent, F-13009 Marseille, France. CHU Lille, Clin Fontan, Serv Psychiat Enfant & Adolescent, F-59037 Lille, France. EPSM, Serv Psychiat Enfant & Adolescent, F-62350 St Venant, France. RP Bailly, D (reprint author), Hop St Marguerite, Federat Psychiat Enfant & Adolescent, 270 Blvd St Marguerite, F-13009 Marseille, France. CR BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BOUCHER J, 1989, BRIT J DISORD COMMUN, V24, P181 BOWE FG, 1973, J REHABIL DEAF, V6, P1 BRADEN JP, 1991, ADVANCES IN COGNITION, EDUCATION, AND DEAFNESS, P56 Bradley-Johnson S, 1991, PSYCHOEDUCATIONAL AS CASBY MW, 1985, J COMMUNICATION DEV, V72, P67 CLARKE BR, 1981, J SPEECH HEAR RES, V24, P48 CORNELIUS G, 1990, AM ANN DEAF, V135, P316 de Villiers J. G., 1994, CONSTRAINTS LANGUAGE, P9 de Villiers P. A, 1988, J ACAD REHABILITATIV, V21, P41 DEVILLIERS J, 1993, APPL PSYCHOLINGUIST, V14, P319 Duchan J. 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PD FEB PY 2003 VL 10 IS 2 BP 140 EP 146 DI 10.1016/S0929-693X(03)00312-9 PG 7 WC Pediatrics SC Pediatrics GA 675NY UT WOS:000182702500010 PM 12829357 ER PT J AU Cans, C Guillem, P Fauconnier, J Rambaud, P Jouk, PS AF Cans, C Guillem, P Fauconnier, J Rambaud, P Jouk, PS TI Disabilities and trends over time in a French county, 1980-91 SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID VISUAL IMPAIRMENT; CEREBRAL-PALSY; MENTAL-RETARDATION; CHANGING PANORAMA; PREVALENCE; CHILDREN; AUTISM; DISORDERS; BIRTH AB Aim: To describe trends over time and types of disability for children born in a French county from 1980 to 1991. Methods: Data were collected from medical records of a morbidity register; disabled children with at least one severe deficiency have been included. Prevalence rates are given per 1000 resident children, over four three-year periods. Results: Overall, 7.73 per 1000 children (that is, 1360 children), had a severe childhood disability, and the prevalence rate had increased significantly since 1980. This increase was mainly owing to an increase in cerebral palsy and psychiatric disorder prevalence rates. Conclusion: Future research aimed to explain these trends over time can be based on such data. The present knowledge is useful for planning purposes. C1 Registre Handicap Enfant & Observ Perinatale Iser, F-38000 Grenoble, France. CHU Grenoble, Dept Informat & Biostat, F-38043 Grenoble 09, France. CHU Grenoble, Dept Neonatol, F-38043 Grenoble 09, France. RP Cans, C (reprint author), Registre Handicap Enfant & Observ Perinatale Iser, 23 Av Albert 1er Belgique, F-38000 Grenoble, France. RI Cans, Christine/M-6153-2014; Fauconnier, Jerome/M-6720-2014; Jouk, Pierre-Simon/M-7367-2014 OI Cans, Christine/0000-0003-3071-9959; CR AMIELTISON C, 1997, INFIRMITE MOTRICE OR Armitage P, 1987, STAT METHODS MED RES Arnaud C, 1998, PAEDIATR PERINAT EP, V12, P228, DOI 10.1046/j.1365-3016.1998.00106.x BAILLE MF, 1996, ARCH PUBLIC HLTH S1, V53, P13 BURD L, 1987, J AM ACAD CHILD PSY, V26, P700, DOI 10.1097/00004583-198709000-00014 Cans C, 2000, DEV MED CHILD NEUROL, V42, P816 CIALDELLA P, 1989, J CHILD PSYCHOL PSYC, V30, P165, DOI 10.1111/j.1469-7610.1989.tb00775.x DOLK H, 1996, PAEDIATR PERINAT EP, V10, pA4 Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Guillem P, 2000, REV EPIDEMIOL SANTE, V48, P41 HAGBERG B, 1989, BRAIN DEV-JPN, V11, P368 Hagberg B, 2001, ACTA PAEDIATR, V90, P271, DOI 10.1080/080352501300067532 MANCIAUX M, 1981, ARCH FR PEDIATR, V38, P627 MURPHY CC, 1995, AM J PUBLIC HEALTH, V85, P319, DOI 10.2105/AJPH.85.3.319 NICOLOSI A, 1994, INT J EPIDEMIOL, V23, P359, DOI 10.1093/ije/23.2.359 PHARAOH PD, 1990, ARCH DIS CHILD, V62, P379 Pharoah P O, 1985, Int Rehabil Med, V7, P11 RIISE R, 1992, ACTA OPHTHALMOL, V70, P145 ROBERTSON CMT, 1992, PEDIATRICS, V90, P750 RumeauRouquette C, 1997, INT J EPIDEMIOL, V26, P137, DOI 10.1093/ije/26.1.137 RUMEAUROUQUETTE C, 1994, PREB HAND EV TROIS G SCHAEFER GB, 1992, PEDIATR CLIN N AM, V39, P929 STANLEY FJ, 1991, MED J AUSTRALIA, V154, P623 TAYLOR DJ, 1985, LANCET, V1, P713 1975, ORIENTATION FAVEUR P NR 27 TC 13 Z9 13 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD FEB PY 2003 VL 88 IS 2 BP 114 EP 117 DI 10.1136/adc.88.2.114 PG 4 WC Pediatrics SC Pediatrics GA 641LG UT WOS:000180745800015 PM 12538309 ER PT J AU Barton, JJS Cherkasova, MV Press, DZ Intriligator, JM O'Connor, M AF Barton, JJS Cherkasova, MV Press, DZ Intriligator, JM O'Connor, M TI Developmental prosopagnosia: A study of three patients SO BRAIN AND COGNITION LA English DT Article DE perception; prosopagnosia; developmental ID FACE RECOGNITION; VISUAL AGNOSIA; CONFIGURAL INFORMATION; ASPERGERS SYNDROME; SPATIAL RELATIONS; DISCRIMINATION; PERCEPTION; AUTISM; CHILDREN; DISORDER AB We studied perception in three patients with prosopagnosia of childhood onset. All had trouble with other 'within-category' judgments. All were deficient on face matching tests and severely impaired on tests of perception of the spatial relations of facial features and abstract designs, indicating a deficit in the encoding of coordinate relationships, similar to adult-onset prosopagnosia with lesions of the fusiform face area. Two had difficulty perceiving feature colour, which correlated with reduced luminance sensitivity. In contrast to adult-onset patients, saturation discrimination was spared in two and spatial resolution impaired in two. Curvature discrimination was relatively spared. Contrast sensitivity showed variable reductions at different spatial frequencies. We conclude that developmental prosopagnosia is similar to the adult-onset form in encoding deficits for the spatial arrangement of facial elements. Deficits in luminance perception and spatial resolution are more associated with defective encoding for basic object-level recognition, as shown on tests of object and spatial perception. (C) 2003 Elsevier Science (USA). All rights reserved. C1 Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Dept Ophthalmol, Boston, MA 02215 USA. Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA. RP Barton, JJS (reprint author), Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. EM jbarton@caregroup.harvard.edu RI Barton, Jason/A-6362-2012 CR ALBERT MS, 1979, ARCH NEUROL-CHICAGO, V36, P211 Ariel R, 1996, CORTEX, V32, P221 BARTON J, 2003, IN PRESS PERCEPTUAL Barton JJS, 2002, NEUROLOGY, V58, P71 Barton JJS, 2001, BRIT J PSYCHOL, V92, P527, DOI 10.1348/000712601162329 Barton JJS, 2001, NEUROLOGY, V57, P1161 BAUER RM, 1988, BRAIN COGNITION, V8, P240, DOI 10.1016/0278-2626(88)90052-8 Bentin S, 1999, NEUROREPORT, V10, P823, DOI 10.1097/00001756-199903170-00029 BENTON AL, 1972, J NEUROL SCI, V15, P167, DOI 10.1016/0022-510X(72)90004-4 Boucher J, 1998, J CHILD PSYCHOL PSYC, V39, P171, DOI 10.1017/S0021963097001820 Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x BRUYER R, 1983, BRAIN COGNITION, V2, P257, DOI 10.1016/0278-2626(83)90014-3 BRUYER R, 1991, BRAIN COGNITION, V15, P223, DOI 10.1016/0278-2626(91)90027-6 CAMPBELL R, 1992, MENTAL LIVES CASE ST, P216 CAREY S, 1992, PHILOS T ROY SOC B, V335, P95, DOI 10.1098/rstb.1992.0012 CASS HD, 1994, ARCH DIS CHILD, V70, P192 Cooper EE, 2000, J EXP PSYCHOL LEARN, V26, P470, DOI 10.1037//0278-7393.26.2.470 DAMASIO A, 1985, TRENDS NEUROSCI, P132 DAMASIO AR, 1990, ANNU REV NEUROSCI, V13, P89, DOI 10.1146/annurev.neuro.13.1.89 DAMASIO AR, 1982, NEUROLOGY, V32, P331 DAVIES S, 1994, J CHILD PSYCHOL PSYC, V35, P1033, DOI 10.1111/j.1469-7610.1994.tb01808.x DEHAAN EHF, 1991, CORTEX, V27, P489 DEHAAN EHF, 1987, CORTEX, V23, P309 DERENZI E, 1991, CORTEX, V27, P213 DERENZI E, 1986, NEUROPSYCHOLOGIA, V24, P385 DIAMOND R, 1986, J EXP PSYCHOL GEN, V115, P107, DOI 10.1037/0096-3445.115.2.107 Duchaine BC, 2000, NEUROREPORT, V11, P79, DOI 10.1097/00001756-200001170-00016 Farah M.J., 1990, VISUAL AGNOSIA DISOR FARAH MJ, 1995, NEUROPSYCHOLOGIA, V33, P661, DOI 10.1016/0028-3932(95)00002-K Freire A, 2000, PERCEPTION, V29, P159, DOI 10.1068/p3012 Gauthier I, 2000, NAT NEUROSCI, V3, P191, DOI 10.1038/72140 GOODMAN R, 1990, DEV MED CHILD NEUROL, V32, P808 Haxby JV, 2000, TRENDS COGN SCI, V4, P223, DOI 10.1016/S1364-6613(00)01482-0 HEYWOOD CA, 1991, EUR J NEUROSCI, V3, P802, DOI 10.1111/j.1460-9568.1991.tb01676.x HEYWOOD CA, 1987, J NEUROL NEUROSUR PS, V50, P22, DOI 10.1136/jnnp.50.1.22 Jambaque I, 1998, J NEUROL NEUROSUR PS, V65, P555, DOI 10.1136/jnnp.65.4.555 Kanwisher N, 1997, J NEUROSCI, V17, P4302 Klin A, 1999, J AUTISM DEV DISORD, V29, P499, DOI 10.1023/A:1022299920240 KOSSLYN SM, 1995, BRAIN COGNITION, V27, P36, DOI 10.1006/brcg.1995.1003 KRACKE I, 1994, DEV MED CHILD NEUROL, V36, P873 LANDIS T, 1986, CORTEX, V22, P243 Leder H, 2000, Q J EXP PSYCHOL-A, V53, P513, DOI 10.1080/027249800390583 MALONE D, 1982, J NEUROL NEUROSUR PS, V45, P802 MCCONACHIE HR, 1976, CORTEX, V12, P76 MCNEIL JE, 1993, Q J EXP PSYCHOL-A, V46, P1 MEADOWS JC, 1974, J NEUROL NEUROSUR PS, V37, P489, DOI 10.1136/jnnp.37.5.489 MILNER AD, 1989, CORTEX, V25, P489 Mottron L, 1997, DEV MED CHILD NEUROL, V39, P699 RIZZO M, 1987, ANN NEUROL, V22, P41, DOI 10.1002/ana.410220111 RIZZO M, 1993, NEUROLOGY, V43, P995 SIMPSON TL, 1995, OPTOMETRY VISION SCI, V72, P371, DOI 10.1097/00006324-199506000-00004 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 TAKAHASHI N, 1995, CORTEX, V31, P317 TANTAM D, 1989, J CHILD PSYCHOL PSYC, V30, P623, DOI 10.1111/j.1469-7610.1989.tb00274.x TEMPLE C, 1992, MENTAL LIVES CASE ST, P99 TEUNISSE JP, 1994, INT J NEUROSCI, V77, P1 VICTOR JD, 1989, CLIN VISION SCI, V4, P183 Warrington E., 1984, WARRINGTON RECOGNITI Warrington EK, 1991, VISUAL OBJECT SPACE Wechsler D, 1981, WECHSLER ADULT INTEL YOUNG A, 1994, NEUROPSYCHOLOGY HIGH YOUNG AW, 1989, BRAIN COGNITION, V9, P16, DOI 10.1016/0278-2626(89)90042-0 NR 62 TC 46 Z9 47 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 FEB PY 2003 VL 51 IS 1 BP 12 EP 30 DI 10.1016/S0278-2626(02)00516-X PG 19 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 659NK UT WOS:000181783000002 PM 12633587 ER PT J AU Mundy, P Burnette, CP Thorp, DM AF Mundy, P Burnette, CP Thorp, DM TI The development of autism: Perspectives from theory and research SO CONTEMPORARY PSYCHOLOGY-APA REVIEW OF BOOKS LA English DT Book Review C1 Univ Miami, Dept Psychol, Coral Gables, FL 33146 USA. RP Mundy, P (reprint author), Univ Miami, Dept Psychol, 5665 Ponce Leon Blvd, Coral Gables, FL 33146 USA. CR Burack J. A., 2001, DEV AUTISM PERSPECTI CICCHETTI D, 1984, CHILD DEV, V55, P1, DOI 10.2307/1129830 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 GLIDDEN LM, 2001, AUTISM INT REV RES M, V23 GREENOUGH WT, 1987, CHILD DEV, V58, P539, DOI 10.1111/j.1467-8624.1987.tb01400.x Jarbrink K, 2001, AUTISM, V5, P7, DOI 10.1177/1362361301005001002 Klin A., 2000, ASPERGER SYNDROME Mundy P, 2001, INT REV RES MENT RET, V23, P139 ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 NR 9 TC 1 Z9 2 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 FEB PY 2003 VL 48 IS 1 BP 96 EP 99 PG 4 WC Psychology, Multidisciplinary SC Psychology GA 646KN UT WOS:000181034300042 ER PT J AU Hunter, LC O'Hare, A Herron, WJ Fisher, LA Jones, GE AF Hunter, LC O'Hare, A Herron, WJ Fisher, LA Jones, GE TI Opioid peptides and dipeptidyl peptidase in autism SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PRESCHOOL-CHILDREN; VACCINE; MEASLES; IV AB It has been hypothesized that autism results from an 'opioid peptide excess'. The aims of this study were to (1) confirm the presence of opioid peptides in the urine of children with autism and (2) determine whether dipeptidyl. peptidase IV (DPPIV/CD26) is defective in children with autism. Opioid peptides were not detected in either the urine of children with autism (10 children; nine males, one female; age range 2 years 6 months to 10 years 1 month) or their siblings (10 children; seven males, three females; age range 2 years 3 months to 12 years 7 months) using liquid chromatography-ultraviolet-mass spectrometric analysis (LC-UV-MS). Plasma from 11 normally developing adults (25 years 5 months to 55 years 5 months) was also tested. The amount and activity of DPPIV in the plasma were quantified by an ELISA and DPPIV enzyme assay respectively; DPPIV was not found to be defective. The percentage of mononuclear cells expressing DPPIV (as CD26) was determined by flow cytometry. Children with autism had a significantly lower percentage of cells expressing CD3 and CD26, suggesting that they had lower T-cell numbers than their siblings. In conclusion, this study failed to replicate the findings of others and questions the validity of the opioid peptide excess theory for the cause of autism. C1 Royal Hosp Sick Children, Community Child Hlth Serv, Edinburgh EH9 1TS, Midlothian, Scotland. Quintiles Ltd, Drug Metab & Pharmacokinet, Edinburgh, Midlothian, Scotland. RP O'Hare, A (reprint author), Royal Hosp Sick Children, Community Child Hlth Serv, 10 Chalmers Crescent, Edinburgh EH9 1TS, Midlothian, Scotland. 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Med. Child Neurol. PD FEB PY 2003 VL 45 IS 2 BP 121 EP 128 DI 10.1017/S0012162203000227 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 666LD UT WOS:000182178000008 PM 12578238 ER PT J AU Teitelbaum, P AF Teitelbaum, P TI A proposed primate animal model of autism SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE thalidomide; primate animal model; autism AB Based on the fact that thalidomide, at a certain point in human pregnancy, produces autism, we propose administering thalidomide to pregnant monkeys at an appropriate point after conception. The infant monkeys born after thalidomide treatment of the pregnant mothers should manifest aberrations in social vocalization and in socialization behavior. Histological analysis of their brains should reveal areas whose damage will lead to autism. This can then be produced stereotaxically in infant monkeys to allow the better determination of the relation of degree of damage in these areas to the severity of autism. C1 Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. RP Teitelbaum, P (reprint author), Univ Florida, Dept Psychol, POB 112250, Gainesville, FL 32611 USA. 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PD FEB PY 2003 VL 12 IS 1 BP 48 EP 49 DI 10.1007/s00787-003-0306-6 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 658ZC UT WOS:000181750300008 PM 12601565 ER PT J AU Tentler, D Johannesson, T Johansson, M Rastam, M Gillberg, C Orsmark, C Carlsson, B Wahlstrom, J Dahl, N AF Tentler, D Johannesson, T Johansson, M Rastam, M Gillberg, C Orsmark, C Carlsson, B Wahlstrom, J Dahl, N TI A candidate region for Asperger syndrome defined by two 17p breakpoints SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE Asperger syndrome; autism; balanced translocation; candidate region ID DIAGNOSTIC INTERVIEW; AUTISM; CLONING; GENE; FAMILIES; CELLS; TRANSLOCATION; HYBRIDIZATION; DISORDERS; RECEPTOR AB Asperger syndrome (AS) is a mild form of autistic disorder characterised by impairment in social interaction as well as a restricted pattern of behaviour, interests, and activities. Two patients with AS and balanced translocations t(13; 17) and t(17; 19), respectively, were identified. Fluorescent in situ hybridisation (FISH) analysis with chromosome 17 specific clones to metaphase chromosomes from both patients showed that the chromosome 17 breakpoints are located within a 300 kb region at 17p13. The region spans 14 known genes. The expression of these genes was analysed in lymphoblastoid RNA derived from the patients and healthy control individuals. The CHRNE, DKFZP566H073, LOC90048, PFN1, SPAG7, KIAA0909, ZNF232 and KIF1C genes showed similar levels of expression in cell lines with the translocations when compared with cell lines with normal karyotype. No expression was detected for the MINK, GP1BA, SLC25A11, ENO3, FLJ10060 and USP6 genes in any of the cell lines. The close physical relation of the two 17p breakpoints suggest a common genetic aetiology for the phenotype in the patients. Structural and functional analysis of the genes located around the two 17p breakpoints in t(13; 17) and t(17; 19) patients may reveal candidate sequences for the AS phenotype. C1 Uppsala Univ, Rudbeck Lab, Unit Clin Genet, Dept Genet & Pathol,Sect Clin Genet, S-75185 Uppsala, Sweden. Gothenburg Univ, Dept Clin Genet, Gothenburg, Sweden. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. St George Hosp, Sch Med, London, England. RP Dahl, N (reprint author), Uppsala Univ, Rudbeck Lab, Unit Clin Genet, Dept Genet & Pathol,Sect Clin Genet, S-75185 Uppsala, Sweden. 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J. Hum. Genet. PD FEB PY 2003 VL 11 IS 2 BP 189 EP 195 DI 10.1038/sj.ejhg.5200939 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 655FE UT WOS:000181540000014 PM 12634868 ER PT J AU Camaioni, L Perucchini, P Muratori, F Parrini, B Cesari, A AF Camaioni, L Perucchini, P Muratori, F Parrini, B Cesari, A TI The communicative use of pointing in autism: developmental profile and factors related to change SO EUROPEAN PSYCHIATRY LA English DT Article DE autism; pointing; CARS ID YOUNG-CHILDREN; JOINT ATTENTION; RATING-SCALE; OPEN TRIAL; INTERVENTION; ADOLESCENTS; RISPERIDONE; DISORDERS; LANGUAGE AB Purpose. - To describe different longitudinal profiles in communicative abilities and symptoms severity in early autism. Methods. - Five children with autism, aged from 3;3 to 4; 10 years at baseline, were tested for production and comprehension of imperative and declarative pointing at about 4-nnonth intervals. Concurrently with these sessions, children were evaluated in terms of cognitive and communicative abilities, and symptoms severity. Results. - Four subjects showed a mild to severe retardation in communicative and linguistic abilities. For production, all children exhibited the imperative pointing and only one the declarative pointing. For comprehension, two subjects showed the same profile as in production ('only imperative' and 'first imperative-later declarative', respectively). One child did not show any clear comprehension of the pointing gestures produced by the experimenter, and one child was able to understand both pointing in the same session. Childhood autism rating scale (CARS) global scores tended to decrease across sessions for all subjects and different individual profiles were identified. Discussion. - Declarative or experience-sharing pointing emerged later in one child only; it remained absent in four children as production, and in two children as comprehension. 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PD FEB PY 2003 VL 47 IS 1 BP 47 EP 57 DI 10.1177/0306624X02239274 PG 11 WC Criminology & Penology; Psychology, Applied SC Criminology & Penology; Psychology GA 636GR UT WOS:000180446700004 PM 12613431 ER PT J AU Renz, K Lorch, EP Milich, R Lemberger, C Bodner, A Welsh, R AF Renz, K Lorch, EP Milich, R Lemberger, C Bodner, A Welsh, R TI On-line story representation in boys with attention deficit hyperactivity disorder SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE ADHD; on-line; story comprehension ID TELEVISION STORIES; CHILDREN; RECALL; EVENTS; ABILITIES; NARRATION; LANGUAGE; AUTISM; MEMORY; PEERS AB Children with attention deficit hyperactivity disorder (ADHD) face an increased risk of poor achievement in school. Thus, knowledge of the cognitive processing abilities of children with ADHD is critical to understanding and improving their academic performance. Although many studies have focused on the specific nature of the attention deficit experienced by children with ADHD, few have examined higher order cognitive processing such as comprehension of stories. The present study examined the processes of encoding story information, building a story representation, and modifying a story representation in boys with ADHD and nonreferred boys. Boys were asked to narrate a story from a picture book twice. Boys with ADHD showed deficits in representing goals and goal plans in their narrations, as compared to nonreferred boys. Boys with ADHD also committed more errors than nonreferred boys, but did correct certain types of errors on their second telling. Implications are discussed in terms of future research needed to identify the cognitive deficits that account for these narrative deficits. C1 Univ Kentucky, Dept Psychol, Lexington, KY 40506 USA. Univ Kentucky, Dept Psychiat, Lexington, KY USA. RP Lorch, EP (reprint author), Univ Kentucky, Dept Psychol, Lexington, KY 40506 USA. CR ABIKOFF H, 1977, J CONSULT CLIN PSYCH, V45, P772, DOI 10.1037//0022-006X.45.5.772 Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ATKINS MS, 1985, J ABNORM CHILD PSYCH, V13, P155, DOI 10.1007/BF00918379 Barkley R. A., 1997, ADHD NATURE SELF CON Barkley RA, 1990, ATTENTION DEFICIT HY, V2nd BERMAN RA, 1994, DIFFERENT WAYS RELAT, P39 Capps I, 2000, J ABNORM CHILD PSYCH, V28, P193 Douglas VI, 1999, HDB DISRUPTIVE BEHAV, P105 Gaub M, 1997, J AM ACAD CHILD PSY, V36, P1036, DOI 10.1097/00004583-199708000-00011 Gernsbacher MA, 1997, DISCOURSE PROCESS, V23, P265 GOLDMAN SR, 1986, J MEM LANG, V25, P401, DOI 10.1016/0749-596X(86)90034-3 Hinshaw S. 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PD FEB PY 2003 VL 31 IS 1 BP 93 EP 104 DI 10.1023/A:1021777417160 PG 12 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 629JM UT WOS:000180046600008 PM 12597702 ER PT J AU Howlin, P AF Howlin, P TI Outcome in high-functioning adults with autism with and without early language delays: Implications for the differentiation between autism and Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; Asperger syndrome; long-term outcome ID DISORDER; CLUMSINESS; CHILDREN; VALIDITY AB The question of whether Asperger syndrome and high-functioning autism should be considered as the same or different conditions has been a source of debate and controversy over recent years. In the present study, 34 adults with autism who had shown early delays in language were compared with 42 individuals who were reported to have had no such delays, either in their use of words or phrases. All participants were at least 18 years of age, had a nonverbal IQ of 70 or above and met ADI-R criteria for age of onset, communication and social impairments, and stereotyped behaviors. Those in the language delay group were diagnosed as having high-functioning autism. The remainder were designated as having Asperger syndrome. The groups were matched for age, nonverbal IQ and gender. No significant differences were found between the groups either in their total ADI-R algorithm scores, or in their algorithm scores on individual domains. Social outcome ratings and ADI-R scores based on current functioning also failed to differentiate between the groups. Scores on tests of language comprehension and expression were also similar, but in both groups language abilities were well below chronological age level. The implications of these results with respect to the differences between Asperger syndrome and high-functioning autism are discussed. The poor performance on language tests also challenges the assumption that early language development in Asperger syndrome is essentially normal. C1 St George Hosp, Sch Med, Dept Psychol, London SW17 ORE, England. RP Howlin, P (reprint author), St George Hosp, Sch Med, Dept Psychol, Cranmer Terrace, London SW17 ORE, England. RI Howlin, Patricia/A-7622-2011 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bryson S. E., 2000, AUTISM, V4, P117, DOI DOI 10.1177/1362361300004002002 Department of Health, 2001, VAL PEOPL NEW STRAT Dunn L M., 1982, BRIT PICTURE VOCABUL Dunn L. M., 1997, BRIT PICTURE VOCABUL, V2nd 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 GARDNER M, 1982, EXPRESSIVE ONE WORD Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 Ghaziuddin M, 1995, J INTELL DISABIL RES, V39, P538 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 GHAZIUDDIN M, 1995, J AUTISM DEV DISORD, V25, P311, DOI 10.1007/BF02179292 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P43, DOI 10.1046/j.1365-2788.1998.00065.x Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 HOWLIN P, IN PRESS J CHILD PSY IWANAGA R, 2000, J AUTISM DEV DISORD, V30, P16 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x KLIN A, 2002, ASPERGER SYNDROME Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 Kugler B., 1998, AUTISM, V2, P11, DOI 10.1177/1362361398021003 Kurita H, 1997, PSYCHIAT CLIN NEUROS, V51, P67, DOI 10.1111/j.1440-1819.1997.tb02909.x LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 Manjiviona J., 1999, AUTISM, V3, P327, DOI DOI 10.1177/1362361399003004003 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X Mayes SD, 2001, AUTISM, V5, P81, DOI 10.1177/1362361301005001008 Miller JN, 2000, J ABNORM PSYCHOL, V109, P227, DOI 10.1037/0021-843X.109.2.227 Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x Pomeroy JC, 1998, ASPERGER SYNDROME HI Raven J. C., 1956, STANDARD PROGR MATRI Rinehart NJ, 2001, AUTISM, V5, P67, DOI 10.1177/1362361301005001007 SCHOPLER E, 1998, ASPERGER SYNDROME HI Szatmari P., 2000, ASPERGER SYNDROME, P403 SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Tonge B. J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Volkmar F. R., 2000, ASPERGER SYNDROME, P25 Volkmar F. R., 2000, ASPERGER SYNDROME, P340 Wechsler D, 1981, WECHSLER ADULT INTEL Wechsler D, 1997, WECHSLER ADULT INTEL, V3rd Wechsler D, 1999, WECHSLER ABBREVIATED WING L, 1981, PSYCHOL MED, V11, P115 Wing Lorna, 2000, ASPERGER SYNDROME, P418 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 51 TC 217 Z9 222 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 FEB PY 2003 VL 33 IS 1 BP 3 EP 13 DI 10.1023/A:1022270118899 PG 11 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700002 PM 12708575 ER PT J AU Starr, E Szatmari, P Bryson, S Zwaigenbaum, L AF Starr, E Szatmari, P Bryson, S Zwaigenbaum, L TI Stability and change among high-functioning children with pervasive developmental disorders: A 2-year outcome study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; ADI-R; follow-up ID AUTISM DIAGNOSTIC INTERVIEW; ASPERGERS-SYNDROME; ADOLESCENTS; ADULTS AB This study prospectively compared the 2-year outcome of children diagnosed with autism or Asperger syndrome at age 6-8 years in terms of symptoms from the Autism Diagnostic Interview. Significant differences were seen in the three-domain summary scores of social interaction, communication, and repetitive activities, with the Asperger syndrome group demonstrating fewer and/or less severe symptoms at both times. There was a trend for the trajectories to come together over time on the socialization and communication domains, but not the repetitive activities domain. Differences were not attributable to IQ. Analysis of individual items indicated that the autism group improved over time on seven items and showed increased symptom severity on three items. On the other hand, the Asperger syndrome group improved on only two items and showed increased symptom severity on six items. Results suggest that the two PDD subtypes represent similar developmental trajectories, although the Asperger syndrome group maintains its advantage. Educational and clinical implications of the results are discussed. C1 Univ Windsor, Fac Educ, Windsor, ON N9B 3P4, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. Dalhousie Univ, IWK Hlth Ctr, Dept Pediat, Halifax, NS, Canada. Dalhousie Univ, IWK Hlth Ctr, Dept Psychol, Halifax, NS, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. RP Starr, E (reprint author), Univ Windsor, Fac Educ, 401 Sunset Ave, Windsor, ON N9B 3P4, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1998, ASPERGERS SYNDROME G Bruning J.L., 1977, COMPUTATIONAL HDB ST FRID PJ, 1998, EVIDENCE BASED MENTA, V1, P121 Haber A., 1977, GEN STAT Klin A., 1997, HDB AUTISM PERVASIVE, P94 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Leiter R. G., 1948, LEITER INT PERFORMAN LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 Myhr G, 1998, CAN J PSYCHIAT, V43, P589 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1183, DOI 10.1192/bjp.113.504.1183 Sparrow S, 1984, VINELAND ADAPTIVE BE Szatmari P., 2000, ASPERGER SYNDROME, P403 SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 Szatmari P, 2002, J AM ACAD CHILD PSY, V41, P467, DOI 10.1097/00004583-200204000-00020 Szatmari P, 2000, AM J PSYCHIAT, V157, P1980, DOI 10.1176/appi.ajp.157.12.1980 Thorndike RL, 1986, STANFORD BINET INTEL Volkmar F. R., 2000, ASPERGER SYNDROME, P25 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 21 TC 43 Z9 43 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 FEB PY 2003 VL 33 IS 1 BP 15 EP 22 DI 10.1023/A:1022222202970 PG 8 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700003 PM 12708576 ER PT J AU Tsatsanis, KD Dartnall, N Cicchetti, D Sparrow, SS Klin, A Volkmar, FR AF Tsatsanis, KD Dartnall, N Cicchetti, D Sparrow, SS Klin, A Volkmar, FR TI Concurrent validity and classification accuracy of the Leiter and Leiter-R in low-functioning children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Leiter International Performance Scale; Leiter-R; concurrent validity; nonverbal intelligence ID INTELLECTUAL ABILITIES; DISORDERS; CRITERIA; SCALE AB The concurrent validity of the Leiter International Performance Scale (Leiter) and Leiter International Performance Scale-Revised (Leiter-R) was examined in a sample of children with autism who could not be assessed with more traditional measures of intelligence (e. g., the Wechsler scales). The sample consisted of 26 children ranging in age from 4 to 16 years. The correlation between the Leiter scales was high (r = .87), and there was a difference of 3.7 points between the two mean scores, nonsignificant at both statistical and clinical levels. However, significant intraindividual discrepancies were present in 10 cases, 2 of which were both large (24 and 36 points) and clinically meaningful. The mean profile of performance on Leiter-R subtests is also presented for this sample of children with autism, to allow for comparison with other groups. Based on the results of this initial evaluation, together with the current normative data, good psychometric properties, and availability of global and subtest scores with the Leiter-R, the instrument is generally recommended for use with children with autism. However, because of changes in the design of the Leiter-R, there may be greater clinical success with the original Leiter for those children who are very low functioning and severely affected, particularly younger children. C1 Yale Univ, Yale Child Study Ctr, New Haven, CT 06520 USA. Connecticut Dept Mental Retardat, Hartford, CT USA. RP Tsatsanis, KD (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, 149 13th St,10th Floor, Charlestown, MA 02129 USA. CR ARAM DM, 1984, J SPEECH HEAR RES, V27, P232 BORENSTEIN M, 1997, POWER PRECISION COMP BORENSTEIN M, 1998, RES METHODS COMPREHE, V3, P313 Carroll J. B., 1993, HUMAN COGNITIVE ABIL CICCHETTI DV, 1981, AM J MENT DEF, V86, P127 Cicchetti DV, 1995, CHILD NEUROPSYCHOL, V1, P26, DOI 10.1080/09297049508401340 COHEN J, 1997, MASTER LECT SERIES Fleiss JL, 1981, STAT METHODS RATES P Flemmer DD, 1997, PSYCHOL REP, V80, P1115 FLYNN JR, 1984, PSYCHOL BULL, V95, P29, DOI 10.1037//0033-2909.95.1.29 GUSTAFSSON JE, 1984, INTELLIGENCE, V8, P179, DOI 10.1016/0160-2896(84)90008-4 Leiter R. G., 1979, INSTRUCTION MANUAL L Lincoln A. J., 1995, LEARNING COGNITION A, P89 LORD C, 1996, UNPUB AUTISM DIAGNOS LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MALTZ A, 1981, J AUTISM DEV DISORD, V11, P413 REEVE RR, 1983, J CONSULT CLIN PSYCH, V51, P458 Roid G., 1997, LEITER INT PERFORMAN Rust JO, 1996, PSYCHOL REP, V79, P618 Rust JO, 1997, PSYCHOL REP, V80, P89, DOI 10.2466/PR0.80.1.89-90 Salvia J., 1991, ASSESSMENT Sattler J.M., 1992, ASSESSMENT CHILDREN SHAH A, 1985, J AUTISM DEV DISORD, V15, P195, DOI 10.1007/BF01531605 SHARP HC, 1957, J CLIN PSYCHOL, V13, P372, DOI 10.1002/1097-4679(195710)13:4<372::AID-JCLP2270130413>3.0.CO;2-N SPARROW SS, 1984, SURVEY FORM MANUAL V TATE ME, 1952, J ABNORM SOC PSYCH, V47, P497, DOI 10.1037/h0053948 NR 26 TC 25 Z9 25 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD FEB PY 2003 VL 33 IS 1 BP 23 EP 30 DI 10.1023/A:1022274219808 PG 8 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700004 PM 12708577 ER PT J AU Cohen, IL Schmidt-Lackner, S Romanczyk, R Sudhalter, V AF Cohen, IL Schmidt-Lackner, S Romanczyk, R Sudhalter, V TI The PDD Behavior inventory: A rating scale for assessing response to intervention in children with pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorder; rating scale; psychometrics; treatment assessment ID JOINT ATTENTION; AUTISM; INDIVIDUALS; CAREGIVERS; VALIDITY AB The PDD Behavior Inventory (PDDBI) is a rating scale filled out by caregivers or teachers that was designed to assess children having a Pervasive Developmental Disorder (PDD; autism, Asperger disorder, PDD-NOS, or childhood disintegrative disorder). Both adaptive and maladaptive behaviors are assessed in the scale, making it useful for treatment studies in which decreases in maladaptive behaviors and improvements in adaptive social and language skills relevant to PDD are expected. The adaptive behaviors assessed include core features of the disorder such as joint attention skills, pretend play, and referential gesture. The maladaptive behaviors sample a wide variety of behaviors observed in both lower- and higher-functioning individuals and include stereotyped behaviors, fears, aggression, social interaction deficits, and aberrant language. The inventory was found to have a high degree of internal consistency. Inter-rater reliability was better for adaptive behaviors than for maladaptive behaviors. Factor analyses confirmed the structure of the PDDBI and indicated good construct validity. In a subsample of children between 3 and 6 years of age, raw scores for adaptive behaviors increased with age in the parent and teacher versions, as did measures of social pragmatic problems. It was concluded that the PDDBI is both reliable and valid and is useful in providing information not typically available in most instruments used to assess children with PDD. C1 New York State Inst Basic Res Dev Disabil, Dept Psychol, Staten Isl, NY 10314 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Child Psychiat Div, Inst Neuropsychiat, Los Angeles, CA 90024 USA. SUNY Binghamton, Dept Psychol, Binghamton, NY 13902 USA. RP Cohen, IL (reprint author), New York State Inst Basic Res Dev Disabil, Dept Psychol, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA. CR Aman MG, 1996, RES DEV DISABIL, V17, P41, DOI 10.1016/0891-4222(95)00039-9 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anastasi A., 1988, PSYCHOL TESTING Barkley R. A., 1981, HYPERACTIVE CHILDREN BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 Cohen IL, 2003, J AUTISM DEV DISORD, V33, P47, DOI 10.1023/A:1022278420716 COHEN IL, 1993, J AUTISM DEV DISORD, V23, P443, DOI 10.1007/BF01046050 Conners C.K., 1973, PSYCHOPHARMACOLOGY B, P24 FISCH GS, 1985, J AUTISM DEV DISORD, V15, P233, DOI 10.1007/BF01531609 Gilliam J. E., 1995, GILLIAM AUTISM RATIN KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 MUNDY P, 1987, J AUTISM DEV DISORD, V17, P344 MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 PARKS SL, 1983, J AUTISM DEV DISORD, V13, P255, DOI 10.1007/BF01531565 Schopler E., 1988, CHILDHOOD AUTISM RAT SIGMAN M, 1986, J CHILD PSYCHOL PSYC, V27, P647, DOI 10.1111/j.1469-7610.1986.tb00189.x Sparrow S, 1984, VINELAND ADAPTIVE BE *STATS, 1995, STAT NR 24 TC 67 Z9 67 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 FEB PY 2003 VL 33 IS 1 BP 31 EP 45 DI 10.1023/A:1022226403878 PG 15 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700005 PM 12708578 ER PT J AU Cohen, IL AF Cohen, IL TI Criterion-related validity of the PDD behavior inventory SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorder; rating scale; treatment assessment; validity ID AUTISM AB The PDD Behavior Inventory (PDDBI) is a rating scale filled out by parents and teachers that is designed to assess response to intervention in children with PDD. It consists of subscales that measure both maladaptive and adaptive behaviors and also provides a summary "Autism Score" reflective of the severity of the condition. The scale has been shown to have very good internal consistency as well as developmental and construct validity. In this study, the PDDBI's criterion-related validity was assessed. Correlations with the Childhood Autism Rating Scale and the Autism Diagnostic Interview-Revised were good. Selected maladaptive scales from the PDDBI correlated well with comparable factors of the Nisonger Child Behavior Rating Form. The adaptive sections of the PDDBI correlated highly with the Griffiths Mental Development Scales and with the Vineland Adaptive Behavior Scales. These results confirm the validity of the PDDBI and suggest that the scale will have value in assessing treatment-related changes in maladaptive and adaptive behaviors associated with PDD. C1 New York State Inst Basic Res Dev Disabil, Dept Psychol, Staten Isl, NY 10314 USA. RP Cohen, IL (reprint author), New York State Inst Basic Res Dev Disabil, Dept Psychol, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA. CR Aman MG, 1996, RES DEV DISABIL, V17, P41, DOI 10.1016/0891-4222(95)00039-9 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 Griffiths R., 1984, ABILITIES YOUNG CHIL Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Schopler E., 1988, CHILDHOOD AUTISM RAT Sparrow S, 1984, VINELAND ADAPTIVE BE NR 8 TC 38 Z9 38 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 FEB PY 2003 VL 33 IS 1 BP 47 EP 53 DI 10.1023/A:1022278420716 PG 7 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700006 PM 12708579 ER PT J AU Martin, A Koenig, K Anderson, GM Scahill, L AF Martin, A Koenig, K Anderson, GM Scahill, L TI Low-dose fluvoxamine treatment of children and adolescents with pervasive developmental disorders: A prospective, open-label study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE fluvoxamine; PDD; Asperger; autism; serotonin ID OBSESSIVE-COMPULSIVE DISORDER; POSTTRAUMATIC-STRESS-DISORDER; RANDOMIZED CONTROLLED TRIAL; AUTISTIC DISORDER; DOUBLE-BLIND; SERTRALINE TREATMENT; FLUOXETINE TREATMENT; MENTAL-RETARDATION; PLATELET SEROTONIN; GENDER DIFFERENCES AB The objective of this study was to assess the efficacy and tolerability of low-dose fluvoxamine (1.5 mg/kg/day) in youngsters with pervasive developmental disorders (PDDs). This was a prospective, open-label trial that included 18 subjects with a mean age of 11.3 +/- 3.6 years. Fourteen children (78%) completed the 10-week study. Premature discontinuation due to behavioral activation occurred in three participants. Although there was no response for the group as a whole, eight subjects (including all four females) were considered at least partial responders in intent-to-treat analyses. Neither pubertal status nor serotonin levels predicted clinical response. Fluvoxamine can be beneficial in the treatment of select children and adolescents with PDDs. Gender differences in selective serotonin reuptake inhibitor (SSRI) response warrant further investigation. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. Yale New Haven Med Ctr, Childrens Psychiat Inpatient Serv, New Haven, CT 06504 USA. Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06510 USA. Yale Univ, Sch Nursing, New Haven, CT 06536 USA. RP Martin, A (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. 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Autism Dev. Disord. PD FEB PY 2003 VL 33 IS 1 BP 77 EP 85 DI 10.1023/A:1022234605695 PG 9 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700009 PM 12708582 ER PT J AU Cuccaro, ML Shao, YJ Bass, MP Abramson, RK Ravan, SA Wright, HH Wolpert, CM Donnelly, SL Pericak-Vance, MA AF Cuccaro, ML Shao, YJ Bass, MP Abramson, RK Ravan, SA Wright, HH Wolpert, CM Donnelly, SL Pericak-Vance, MA TI Behavioral comparisons in autistic individuals from multiplex and singleton families SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; MANCOVA; behavior heterogeneity ID DIAGNOSTIC OBSERVATION SCHEDULE; ALZHEIMERS-DISEASE; SPECTRUM DISORDER; INFANTILE-AUTISM; GENETICS; TWIN; CLASSIFICATION; PHENOTYPE; INTERVIEW; CHILDREN AB Autistic disorder (AD) is a complex neurodevelopmental disorder. The role of genetics in AD etiology is well established, and it is postulated that anywhere from 2 to 10 genes could be involved. As part of a larger study to identify these genetic effects we have ascertained a series of AD families: Sporadic (SP, 1 known AD case per family and no known history of AD) and multiplex (MP, greater than or equal to2 cases per family). The underlying etiology of both family types is unknown. It is possible that MP families may constitute a unique subset of families in which the disease phenotype is more likely due to genetic factors. Clinical differences between the two family types could represent underlying genetic heterogeneity. We examined ADI-R data for 69 probands from MP families and 88 from SP families in order to compare and contrast the clinical phenotypes for each group as a function of verbal versus nonverbal status. Multivariate analysis controlling for covariates of age at examination, gender, and race (MANCOVA) revealed no differences between either the verbal or nonverbal MP and SP groups for the three ADI-R area scores: social interaction, communication, and restricted/repetitive interests or behaviors. These data failed to find clinical heterogeneity between MP and SP family types. This supports previous work that indicated that autism features are not useful as tools to index genetic heterogeneity. Thus, although there may be different underlying etiologic mechanisms in the SP and MP probands, there are no distinct behavioral patterns associated with probands from MP families versus SP families. These results suggests the possibility that common etiologic mechanisms, either genetic and/or environmental, could underlie all of AD. C1 Univ S Carolina, Dept Neuropsychiat, WS Hall Psychiat Inst, Columbia, SC 29208 USA. Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. RP Cuccaro, ML (reprint author), Univ S Carolina, Dept Neuropsychiat, WS Hall Psychiat Inst, Columbia, SC 29208 USA. CR BAILEY A, 1995, PSYCHOL MED, V25, P63 CORDER EH, 1993, SCIENCE, V261, P921, DOI 10.1126/science.8346443 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x FOLSTEIN SE, 1991, PEDIATRICS, V87, P767 HANSON DR, 1976, J AUTISM CHILD SCHIZ, V6, P209, DOI 10.1007/BF01543463 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LOTSPEICH LJ, 1997, AM J MED GENET, V32, P570 LOTSPEICH LJ, 1993, INT REV NEUROBIOL, V35, P87 MacLean JE, 1999, J AM ACAD CHILD PSY, V38, P746, DOI 10.1097/00004583-199906000-00023 PICKLES A, 1995, AM J HUM GENET, V57, P717 Piven J, 1997, AM J MED GENET, V74, P398, DOI 10.1002/(SICI)1096-8628(19970725)74:4<398::AID-AJMG11>3.0.CO;2-D Piven J, 1997, AM J PSYCHIAT, V154, P185 Robertson JM, 1999, J AM ACAD CHILD PSY, V38, P738, DOI 10.1097/00004583-199906000-00022 RUTTER M, 1990, J CHILD PSYCHOL PSYC, V31, P3, DOI 10.1111/j.1469-7610.1990.tb02272.x SAUNDERS AM, 1993, NEUROLOGY, V43, P1467 SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 SPIKER D, 1994, AM J MED GENET, V54, P27, DOI 10.1002/ajmg.1320540107 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Szatmari P, 1999, J PSYCHIATR NEUROSCI, V24, P159 SZATMARI PB, 1994, AM J MED GENET, V67, P354 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 26 TC 17 Z9 17 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 FEB PY 2003 VL 33 IS 1 BP 87 EP 91 DI 10.1023/A:1022286622534 PG 5 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700010 PM 12708583 ER PT J AU Aldred, S Moore, KM Fitzgerald, M Waring, RH AF Aldred, S Moore, KM Fitzgerald, M Waring, RH TI Plasma amino acid levels in children with autism and their families SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; plasma; amino acids; glutamate/glutamine ratio ID GLUTAMATE TRANSPORTER; DOPAMINE AB Plasma amino acid levels were measured in autistic and Asperger syndrome patients, their siblings, and parents. The results were compared with values from age-matched controls. Patients with autism or Asperger syndrome and their siblings and parents all had raised glutamic acid, phenylalanine, asparagine, tyrosine, alanine, and lysine (p<.05) than controls, with reduced plasma glutamine. Other amino acids were at normal levels. These results show that children with autistic spectrum disorders come from a family background of dysregulated amino acid metabolism and provide further evidence for an underlying biochemical basis for the condition. C1 Aston Univ, Inst Pharmaceut Sci, Birmingham B4 7ET, W Midlands, England. Lucena Clin, Child & Adolescent Mental Hlth Serv, Dublin 24, Ireland. Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England. RP Waring, RH (reprint author), Aston Univ, Inst Pharmaceut Sci, Birmingham B4 7ET, W Midlands, England. CR Alam Z, 1998, J NEUROL SCI, V156, P102, DOI 10.1016/S0022-510X(98)00023-9 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARTHELEMY C, 1988, J AUTISM DEV DISORD, V18, P583, DOI 10.1007/BF02211876 COOK EH, 1990, SYNAPSE, V6, P292, DOI 10.1002/syn.890060309 Fray AE, 1998, EUR J NEUROSCI, V10, P2481, DOI 10.1046/j.1460-9568.1998.00273.x GARNIER C, 1986, J AUTISM DEV DISORD, V16, P23, DOI 10.1007/BF01531575 GARREAU B, 1988, DEV MED CHILD NEUROL, V30, P93 HIRSCHBERGER LL, 1985, J CHROMATOGR, V343, P303, DOI 10.1016/S0378-4347(00)84599-5 Kanner L, 1943, NERV CHILD, V2, P217 Kojima S, 1999, J NEUROSCI, V19, P2580 MATHERN GW, 1999, NEUROLOGY, V52, P441 Mennini T, 1998, J NEUROL SCI, V157, P31, DOI 10.1016/S0022-510X(98)00072-0 ROLF LH, 1993, ACTA PSYCHIAT SCAND, V87, P312, DOI 10.1111/j.1600-0447.1993.tb03378.x RUTTER M, 1978, J AUTISM CHILD SCHIZ, V8, P139, DOI 10.1007/BF01537863 RUTTER M, 1993, NATURE NURTURE Semba J, 1998, GEN PHARMACOL, V31, P399, DOI 10.1016/S0306-3623(98)00047-0 NR 16 TC 70 Z9 71 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 FEB PY 2003 VL 33 IS 1 BP 93 EP 97 DI 10.1023/A:1022238706604 PG 5 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700011 PM 12708584 ER PT J AU Hastings, RP AF Hastings, RP TI Brief report: Behavioral adjustment of siblings of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE siblings; maternal stress; behavioral adjustment ID MENTAL-RETARDATION; DIFFICULTIES QUESTIONNAIRE; CHRONIC DISABILITIES; DOWNS-SYNDROME; COMPETENCE; CHECKLIST; STRENGTHS; FAMILY; HOME AB Existing research studies have shown mixed results relating to the impact upon children of having a sibling with a disability. However, siblings of children with autism may be more at risk than siblings of children with other disabilities. In the present study, data were gathered on 22 siblings of children with autism. These children were rated by their mothers as having more behavior problems and fewer prosocial behaviors than a normative sample. Analysis of variables predicting sibling behavioral adjustment revealed that boys with siblings who have autism, and also those younger than their sibling with autism, engaged in fewer prosocial behaviors. Psychological adjustment of mothers (stress) and the child with autism (behavior problems) were not predictive of sibling behavioral adjustment. 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. RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 CR BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 Boyce G., 1993, EFFECTS MENTAL RETAR Damiani VB, 1999, FAM SOC-J CONTEMP H, V80, P34 EINFELD SL, 1995, J AUTISM DEV DISORD, V25, P81, DOI 10.1007/BF02178498 Eisenberg L, 1998, J CHILD PSYCHOL PSYC, V39, P355, DOI 10.1017/S0021963097002084 Fisman S, 1996, J AM ACAD CHILD PSY, V35, P1532, DOI 10.1097/00004583-199611000-00023 Fisman S, 2000, CAN J PSYCHIAT, V45, P369 Fombonne E, 1997, J CHILD PSYCHOL PSYC, V38, P667, DOI 10.1111/j.1469-7610.1997.tb01694.x FRIEDRICH WN, 1983, AM J MENT DEF, V88, P41 GATH A, 1986, BRIT J PSYCHIAT, V149, P161, DOI 10.1192/bjp.149.2.161 Glasberg BA, 2000, J AUTISM DEV DISORD, V30, P143, DOI 10.1023/A:1005411722958 GOLD N, 1993, J AUTISM DEV DISORD, V23, P147, DOI 10.1007/BF01066424 Goodman R, 1999, J ABNORM CHILD PSYCH, V27, P17, DOI 10.1023/A:1022658222914 Goodman R, 1997, J CHILD PSYCHOL PSYC, V38, P581, DOI 10.1111/j.1469-7610.1997.tb01545.x Hannah ME, 1999, AM J MENT RETARD, V104, P22, DOI 10.1352/0895-8017(1999)104<0022:CAAOSO>2.0.CO;2 Hastings RP, 2002, AM J MENT RETARD, V107, P222, DOI 10.1352/0895-8017(2002)107<0222:BPOCWA>2.0.CO;2 Hastings RP, 2001, J AUTISM DEV DISORD, V31, P423, DOI 10.1023/A:1010668703948 Helff CM, 1998, MENT RETARD, V36, P457, DOI 10.1352/0047-6765(1998)036<0457:MPOLNT>2.0.CO;2 HOWLIN P, 1988, CHILD CARE HLTH DEV, V14, P395, DOI 10.1111/j.1365-2214.1988.tb00591.x Hughes C, 1999, J CHILD PSYCHOL PSYC, V40, P705, DOI 10.1017/S0021963099004023 KNOTT F, 1995, J CHILD PSYCHOL PSYC, V36, P965, DOI 10.1111/j.1469-7610.1995.tb01343.x MATES TE, 1990, J AUTISM DEV DISORD, V20, P545, DOI 10.1007/BF02216059 MCHALE SM, 1986, J AUTISM DEV DISORD, V16, P399, DOI 10.1007/BF01531707 Meltzer H, 2000, MENTAL HLTH CHILDREN RODRIGUE JR, 1993, J AUTISM DEV DISORD, V23, P665, DOI 10.1007/BF01046108 ROEYERS H, 1995, CHILD CARE HLTH DEV, V21, P305, DOI 10.1111/j.1365-2214.1995.tb00760.x Rossiter L., 2001, J CHILD FAM STUD, V10, P65, DOI DOI 10.1023/A:1016629500708 Rutter M, 1970, HLTH ED BEHAV SUMMERS CR, 1994, J SOC BEHAV PERS, V9, P169 WILSON CJ, 1992, J INTELL DISABIL RES, V36, P325 NR 30 TC 57 Z9 59 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD FEB PY 2003 VL 33 IS 1 BP 99 EP 104 DI 10.1023/A:1022290723442 PG 6 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700012 PM 12708585 ER PT J AU Gallagher, L Becker, K Kearney, G Dunlop, A Stallings, R Green, A Fitzgerald, M Gill, M AF Gallagher, L Becker, K Kearney, G Dunlop, A Stallings, R Green, A Fitzgerald, M Gill, M TI Brief report: A case of autism associated with del(2)(q32.1q32.2) or (q32.2q32.3) SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; genetics; cytogenetics; chromosome 2q ID INTERSTITIAL DELETION; LONG ARM; MENTAL-RETARDATION; CHROMOSOME-2; ANOMALIES; TWIN AB Autism is a neurodevelopmental disorder presenting in the first 3 years of life. Deficits occur in the three core areas of communication, social interaction, and behavior. The causes of autism are unknown, but clinical genetic studies show strong evidence in favor of a genetic etiology. Molecular genetic studies report some association with candidate genes, and candidate regions have emerged from several genome-wide linkage studies. Here we report a clinical case of autism with a deletion on chromosome 2 in a young male with high-functioning autism. The deletion seems to correspond with regions emerging from linkage studies. We propose this as a possible candidate region in the search for autism genes. C1 Trinity Coll Dublin, Dept Psychiat, Dublin, Ireland. Univ Dublin Trinity Coll, Dept Genet, Smurfit Inst, Dublin 2, Ireland. Our Ladys Hosp, Natl Ctr Med Genet, Dublin 12, Ireland. Univ Coll, Conway Inst, Dept Med Genet, Dublin, Ireland. Univ Dublin Trinity Coll, Autism Res Grp, Dublin 2, Ireland. RP Gallagher, L (reprint author), Trinity Coll Dublin, Dept Psychiat, Dublin, Ireland. 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Autism Dev. Disord. PD FEB PY 2003 VL 33 IS 1 BP 105 EP 108 DI 10.1023/A:1022242807513 PG 4 WC Psychology, Developmental SC Psychology GA 642LK UT WOS:000180805700013 PM 12708586 ER PT J AU Charman, T Drew, A Baird, C Baird, G AF Charman, T Drew, A Baird, C Baird, G TI Measuring early language development in preschool children with autism spectrum disorder using the MacArthur Communicative Development Inventory (Infant Form) SO JOURNAL OF CHILD LANGUAGE LA English DT Article ID DOWN-SYNDROME; VOCABULARY DEVELOPMENT; LEXICAL DEVELOPMENT; JOINT ATTENTION; VARIABILITY; DIAGNOSIS; GESTURE AB Parent report data on early language development measured using the MacArthur Communicative Development Inventory (CDI-Infant Form) was collected on 134 preschool children with autism spectrum disorder. The pattern of development of understanding of phrases, word comprehension and expression, and production of gestures, was compared to the typical pattern. In common with typical development there was considerable variability in language acquisition, although for the group as a whole this was significantly delayed compared to the normal course. In addition, atypical patterns were identified in the emergence of language skills in the sample. Comprehension of words was delayed in comparison to word production, and production of early gestures (involving sharing reference) was delayed relative to production of later gestures (involving use of objects). However, other aspects of language development were similar to that found in typically developing infants, including word comprehension being in advance of word production in absolute terms, gesture production acting as a 'bridge' between word comprehension and word production and the broad pattern of acquisition across word categories and word forms. The implications for assessment and intervention with preschool children with autism spectrum disorder are discussed. C1 UCL, Behav & Brain Sci Unit, Inst Child Hlth, London WC1N 1EH, England. Guys Hosp, Newcomen Ctr, London SE1 9RT, England. Univ Bristol, Sch Med, Bristol BS8 1TH, Avon, England. RP Charman, T (reprint author), UCL, Behav & Brain Sci Unit, Inst Child Hlth, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bates E., 1988, 1 WORDS GRAMMAR INDI BATES E, 1994, J CHILD LANG, V21, P85 Bates E., 1979, EMERGENCE SYMBOLS CO BATES E, 1989, DEV PSYCHOL, V25, P1004, DOI 10.1037//0012-1649.25.6.1004 BATES E, 1975, MERRILL PALMER QUART, V21, P205 BONDY AS, 1995, LEARNING COGNITION A Bzoch K, 1971, RECEPTIVE EXPRESSIVE Caselli MC, 1998, J SPEECH LANG HEAR R, V41, P1125 Charman T, 2000, COGNITIVE DEV, V15, P481, DOI 10.1016/S0885-2014(01)00037-5 Charman T, 1998, INF MENTAL HLTH J, V19, P260, DOI 10.1002/(SICI)1097-0355(199822)19:2<260::AID-IMHJ12>3.0.CO;2-W Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Crais E. R., 1995, AM J SPEECH-LANG PAT, V4, P47 Dale PS, 1996, BEHAV RES METH INS C, V28, P125, DOI 10.3758/BF03203646 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Dunn L. 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H., 1992, CLIN EVALUATION LANG World Health Organization, 1993, MENT DIS GLOSS GUID NR 46 TC 92 Z9 94 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0305-0009 J9 J CHILD LANG JI J. Child Lang. PD FEB PY 2003 VL 30 IS 1 BP 213 EP 236 DI 10.1017/S0305000902005482 PG 24 WC Psychology, Developmental; Linguistics; Psychology, Experimental SC Psychology; Linguistics GA 667CL UT WOS:000182213200009 PM 12718299 ER PT J AU Evangeliou, A Vlachonikolis, I Mihailidou, H Spilioti, M Skarpalezou, A Makaronas, N Prokopiou, A Christodoulou, P Liapi-Adamidou, G Helidonis, E Sbyrakis, S Smeitink, J AF Evangeliou, A Vlachonikolis, I Mihailidou, H Spilioti, M Skarpalezou, A Makaronas, N Prokopiou, A Christodoulou, P Liapi-Adamidou, G Helidonis, E Sbyrakis, S Smeitink, J TI Application of a ketogenic diet in children with autistic behavior: Pilot study SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID KETONE-BODIES; DOUBLE-BLIND; METABOLISM; DISORDER; GLUTAMATE; MAGNESIUM AB A pilot prospective follow-up study of the role of the ketogenic diet was carried out on 30 children, aged between 4 and 10 years, with autistic behavior. The diet was applied for 6 months, with continuous administration for 4 weeks, interrupted by 2-week diet-free intervals. Seven patients could not tolerate the diet, whereas five other patients adhered to the diet for I to 2 months and then discontinued it. Of the remaining group who adhered to the diet, 18 of 30 children (60%), improvement was recorded in several parameters and in accordance with the Childhood Autism Rating Scale. Significant improvement (> 12 units of the Childhood Autism Rating Scale) was recorded in two patients (pre-Scale: 35.00 +/- 1.41 [mean +/- SD]), average improvement (> 8-12 units) in eight patients (pre-Scale: 41.88 +/- 3.14[mean SD]), and minor improvement (2-8 units) in eight patients (pre-Scale: 45.25 +/- 2.76 [mean +/- SD]). Although these data are very preliminary, there is some evidence that the ketogenic diet may be used in autistic behavior as an additional or alternative therapy. C1 Univ Crete, Sch Med, Dept Paediat, Iraklion, Greece. Univ Crete, Sch Med, Dept Neurol, Iraklion, Greece. Univ Crete, Biostat Lab, Iraklion, Crete, Greece. Childrens Hosp Agia Sofia, Inst Child Hlth, Athens, Greece. Ctr Mental Hlth, Iraklion, Crete, Greece. Ctr Mental Hlth, Khania, Crete, Greece. Univ Crete, Sch Med, Dept Ear Nose & Throat, Iraklion, Greece. Univ Athens, Dept Pediat 2, Athens, Greece. Univ Nijmegen Hosp, Dept Pediat, NL-6500 HB Nijmegen, Netherlands. RP Evangeliou, A (reprint author), Univ Hosp Heraklin, Dept Paediat, POB 1352, Iraklion 71110, Crete, Greece. RI Smeitink, Jan/C-1351-2013 CR ARMITAGE P., 1994, STAT METHODS MED RES BAILEY A, 1995, PSYCHOL MED, V25, P63 Bujas-Petković Z, 1989, Lijec Vjesn, V111, P458 Daikhin Y, 1998, DEV NEUROSCI-BASEL, V20, P358, DOI 10.1159/000017331 EATON I, 1988, MANUAL DIETETIC PRAC, P489 EATON J, 1994, CLIN DIETETICS, P168 Erecinska M, 1996, J NEUROCHEM, V67, P2325 Evangeliou A, 2001, J INHERIT METAB DIS, V24, P877, DOI 10.1023/A:1013904627537 Findling RL, 1997, J AUTISM DEV DISORD, V27, P467, DOI 10.1023/A:1025861522935 Haas R H, 1986, Am J Med Genet Suppl, V1, P225 Haznedar MM, 2000, AM J PSYCHIAT, V157, P1994, DOI 10.1176/appi.ajp.157.12.1994 Hori A, 1997, EPILEPSIA, V38, P750, DOI 10.1111/j.1528-1157.1997.tb01461.x MUNNICH A, 1996, INBORN METABOLIC DIS, P124 NEBELING LC, 1995, J AM DIET ASSOC, V95, P693, DOI 10.1016/S0002-8223(95)00189-1 NEBELING LC, 1995, J AM COLL NUTR, V14, P202 Nordli DR, 1997, EPILEPSIA, V38, P743, DOI 10.1111/j.1528-1157.1997.tb01460.x Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 PAPE T, 2000, J AUTISM DEV DISORD, V30, P471 PoggiTravert F, 1996, J INHERIT METAB DIS, V19, P478, DOI 10.1007/BF01799109 Reichelt K L, 1991, Tidsskr Nor Laegeforen, V111, P1286 Rimland B, 1998, J AUTISM DEV DISORD, V28, P581 RIMLAND B, 1997, J AUTISM DEV DISORD, V27, P467 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SHAW V, 1994, CLIN PAEDIAT DIETETI, P168 SIEGEL BV, 1995, SCHIZOPHR RES, V17, P85, DOI 10.1016/0920-9964(95)00033-I Vining EPG, 1998, ARCH NEUROL-CHICAGO, V55, P1433, DOI 10.1001/archneur.55.11.1433 Wassink TH, 2001, PSYCHIATR GENET, V11, P57, DOI 10.1097/00041444-200106000-00001 Wexler ID, 1997, NEUROLOGY, V49, P1655 WHELESS JW, 1995, J CHILD NEUROL, V10, P419 Wilder R, 1921, MAYO CLINIC B, V2, P307 WING RR, 1995, INT J OBESITY, V19, P811 ZSCHOCKE J, 1999, VADEMECUM METABOLICU, P25 NR 32 TC 45 Z9 48 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD FEB PY 2003 VL 18 IS 2 BP 113 EP 118 DI 10.1177/08830738030180020501 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 662AE UT WOS:000181922500006 PM 12693778 ER PT J AU Mann, TA Walker, P AF Mann, TA Walker, P TI Autism and a deficit in broadening the spread of visual attention SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; learning disability; visual attention; attentional spread ID HIGH-FUNCTIONING AUTISM; SPATIAL ATTENTION; ASPERGERS-DISORDER; CHILDREN; ABNORMALITY; PRECEDENCE; CEREBELLAR; ABILITIES; PEOPLE; TASK AB Background: This study examines if visual attention in autism is spatially overfocused (Townsend & Courchesne, 1994) and if there is an associated deficit in broadening the spatial spread of attention. Method: Two crosshairs were presented on each trial separated by a brief (500 ms) interval. There was a modest difference in the lengths of the two hairs in each crosshair and participants had to decide which one was longest. Previous research (Mack & Rock, 1998) has revealed that in making this judgement people spread their visual attention to embrace the whole crosshair. Varying the overall size of each crosshair was intended to control participants' spread of attention. The impact of the size of the first crosshair gave an indication of participants' default setting for the spread of attention. The impact of the size transition between the first and second crosshair gave an indication of the fluency with which participants could change the spatial spread of visual attention. Results: Based on the first proposal it was predicted that individuals with autism (N = 13), relative to ability-matched moderately. learning disabled (N = 15) and typically developing individuals (N = 15), would be more accurate and quicker to respond when the first crosshair was small rather than large. However, the results revealed no effects of the size of the first crosshair and no group differences. Based on the second proposal it was predicted that individuals with autism, relative to both control groups, would be less accurate and slower to respond to the second crosshair when the size transition from the first crosshair involved a change from small to large (in comparison with large to large), but would not differ when the change was from large to small (in comparison with small to small). This prediction was confirmed. Conclusion: Autism is associated with a deficit in broadening the spatial spread of visual attention. The implications of this for other visual and attentional. anomalies observed in autism are discussed. C1 Univ Lancaster, Dept Psychol, Lancaster LA1 4YF, England. RP Walker, P (reprint author), Univ Lancaster, Dept Psychol, Lancaster LA1 4YF, England. CR ALLEN C, 2001, FRONT BIOSCI, V6, P105 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CASEY BJ, 1993, J CLIN EXP NEUROPSYC, V15, P933, DOI 10.1080/01688639308402609 Dunn L. 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C., 1983, MANUAL RAVENS PROGR Rinehart NJ, 2001, AUTISM, V5, P67, DOI 10.1177/1362361301005001007 Rinehart NJ, 2000, J CHILD PSYCHOL PSYC, V41, P769, DOI 10.1017/S002196309900596X SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x TOWNSEND J, 1994, J COGNITIVE NEUROSCI, V6, P220, DOI 10.1162/jocn.1994.6.3.220 Townsend J, 1999, J NEUROSCI, V19, P5632 Townsend J, 1996, J Int Neuropsychol Soc, V2, P541 Townsend J, 1996, DEV PSYCHOPATHOL, V8, P563 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 NR 27 TC 46 Z9 47 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD FEB PY 2003 VL 44 IS 2 BP 274 EP 284 DI 10.1111/1469-7610.00120 PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 637ZV UT WOS:000180544300012 PM 12587863 ER PT J AU Lopez, B Leekam, SR AF Lopez, B Leekam, SR TI Do children with autism fail to process information in context? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; cognition; context; central coherence ID CENTRAL COHERENCE; VISUAL ILLUSIONS; MEMORY; IDENTIFICATION; COMPREHENSION; OBJECTS; SCENES; WORDS; INDIVIDUALS; RECOGNITION AB Background: This research investigated the proposal that children with autism are impaired in processing information in its context. To date, this proposal rests almost exclusively on evidence from verbal tasks. Given evidence of visuo-spatial proficiency in autism in other areas of functioning, it is possible that the ability to use context is spared in the visual domain but impaired in the verbal domain. Method: Fifteen children with autism and 16 age and IQ-matched typically developing children were tested on their ability to take account of visual context information (Experiment 1) and verbal context information (Experiment 2) using an adaptation of Palmer's (1975) visual context task. They were also given an adaptation of Tager-Flusberg's (1991) visual and verbal semantic memory task (Experiment 3) and Frith and Snowling's (1983) homograph task (Experiment 4). Results: Experiment 1 showed that children with autism were facilitated by the provision of visual context information. Experiments 2 and 3 showed that the same children were also able to use both verbal context information when identifying words and semantic category information in a verbal task when naming and recalling words. However, in Experiment 4 these children had difficulties with a sentence-processing task when using sentence context to disambiguate homographs. Conclusions: These findings demonstrate that children with autism do not have a general difficulty in connecting context information and item information as predicted by weak central coherence theory. Instead the results suggest that there is specific difficulty with complex verbal stimuli and in particular with using sentence context to disambiguate meaning. C1 York St John Coll, Sch Sports Sci & Psychol, York YO31 7EX, N Yorkshire, England. Univ Durham, Durham DH1 3HP, England. RP Lopez, B (reprint author), York St John Coll, Sch Sports Sci & Psychol, Lord Mayors Walk, York YO31 7EX, N Yorkshire, England. CR AMELI R, 1988, J AUTISM DEV DISORD, V18, P601, DOI 10.1007/BF02211878 American Psychiatric Association, 1987, DIAGN STAT MAN MENT Baayen R. 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Child Psychol. Psychiatry Allied Discip. PD FEB PY 2003 VL 44 IS 2 BP 285 EP 300 DI 10.1111/1469-7610.00121 PG 16 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 637ZV UT WOS:000180544300013 PM 12587864 ER PT J AU Bertone, A Mottron, L Jelenic, P Faubert, J AF Bertone, A Mottron, L Jelenic, P Faubert, J TI Motion perception in autism: a "complex'' issue SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID 2ND-ORDER MOTION; FIRST-ORDER; ASPERGER-SYNDROME; SOCIAL-BEHAVIOR; WORKING-MEMORY; CHILDREN; INDIVIDUALS; PERFORMANCE; MECHANISMS; DISORDER AB We present the first assessment of motion sensitivity for persons with autism and normal intelligence using motion patterns that require neural processing mechanisms of varying complexity. Compared to matched controls, our results demonstrate that the motion sensitivity of observers with autism is similar to that of nonautistic observers for different types of first-order (luminance-defined) motion stimuli, but significantly decreased for the same types of second-order (texture-defined) stimuli. The latter class of motion stimuli has been demonstrated to require additional neural computation to be processed adequately. This finding may reflect less efficient integrative functioning of the neural mechanisms that mediate visuoperceptual processing in autism. The contribution of this finding with regards to abnormal perceptual integration in autism, its effect on cognitive operations, and possible behavioral implications are discussed. C1 Univ Montreal, Ecole Optometrie, Visual Psychophys & Percept Lab, Montreal, PQ H3C 3J7, Canada. Hop Riviere des Prairies, Montreal, PQ, Canada. RP Bertone, A (reprint author), Univ Montreal, Ecole Optometrie, Visual Psychophys & Percept Lab, CP 6128,Succursale Ctr Ville, Montreal, PQ H3C 3J7, Canada. 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PD FEB PY 2003 VL 15 IS 2 BP 218 EP 225 DI 10.1162/089892903321208150 PG 8 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 653TJ UT WOS:000181452900006 PM 12676059 ER PT J AU Bonnel, A Mottron, L Peretz, I Trudel, M Gallun, E Bonnel, AM AF Bonnel, A Mottron, L Peretz, I Trudel, M Gallun, E Bonnel, AM TI Enhanced pitch sensitivity in individuals with autism: A signal detection analysis SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID DIVIDED ATTENTION; CHILDREN; SAVANT; DISCRIMINATION; COHERENCE; DEFICIT; STIMULI; CORTEX; TASK AB Past research has shown a superiority of participants with high-functioning autism over comparison groups in memorizing picture-pitch associations and in detecting pitch changes in melodies. A subset of individuals with autism, known as "musical savants,'' is also known to possess absolute pitch. This superiority might be due to an abnormally high sensitivity to fine-grained pitch differences in sounds. To test this hypothesis, psychoacoustic tasks were devised so as to use a signal detection methodology. Participants were all musically untrained and were divided into a group of 12 high-functioning individuals with autism and a group of 12 normally developing individuals. Their task was to judge the pitch of pure tones in a "same-different'' discrimination task and in a "high-low'' categorization task. In both tasks, the obtained psychometric functions revealed higher pitch sensitivity for subjects with autism, with a more pronounced advantage over control participants in the categorization task. These findings confirm that pitch processing is enhanced in "high-functioning'' autism. Superior performance in pitch discrimination and categorization extends previous findings of enhanced visual performance to the auditory domain. Thus, and as predicted by the enhanced perceptual functioning model for peaks of ability in autism (Mottron & Burack, 2001), autistic individuals outperform typically developing population in a variety of low-level perceptual tasks. C1 Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. Univ Montreal, Montreal, PQ H3C 3J7, Canada. RP Mottron, L (reprint author), Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, 7070 Blvd Perras, Montreal, PQ H1E 1A4, Canada. 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Cogn. Neurosci. PD FEB PY 2003 VL 15 IS 2 BP 226 EP 235 DI 10.1162/089892903321208169 PG 10 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 653TJ UT WOS:000181452900007 PM 12676060 ER PT J AU Sarimski, K AF Sarimski, K TI Early play behaviour in children with 5p-(Cri-du-Chat) syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE 5p-(Cri-du-Chat) syndrome; children; play behaviour ID DU-CHAT SYNDROME; YOUNG-CHILDREN; CRI; DELETION; AUTISM AB Background 5p- (Cri-du-Chat) syndrome (5p-S) is a well defined chromosomal condition. While the physical symptoms have frequently been documented, the developmental and behavioural aspects of the syndrome have not been explored adequately, especially in young children. Method Mental level, and complexity and style of play were analysed in 10 children who were homogeneously selected with respect to their chronological age (range = 2-7 years). Results A high rate of distractability and alow level of object-directed behaviours were observed in the play sessions. The findings were compared to two comparison groups (subjects with Down's syndrome or Cornelia-de-Lange syndrome) matched for mental age in order to analyse the specificity of these behavioural features for young children with 5p-S. Conclusions A low level of object-directed behaviours may be an early precursor of hyperactivity, distractability and stereotypy, which have been reported to be the characteristic features of the behavioural phenotype of older individuals with 5p-S. C1 Kinderzentrum, D-81377 Munich, Germany. RP Sarimski, K (reprint author), Kinderzentrum, Heiglhofstr 63, D-81377 Munich, Germany. CR Beeghly M., 1990, CHILDREN DOWN SYNDRO, P329, DOI 10.1017/CBO9780511581786.011 CARLIN M, 1990, ISSUES MENTAL RETARD, P64 Collins MSR, 2002, J INTELL DISABIL RES, V46, P133, DOI 10.1046/j.1365-2788.2002.00361.x Cornish KM, 1998, J COMMUN DISORD, V31, P73, DOI 10.1016/S0021-9924(97)00052-X Cornish KM, 1996, ARCH DIS CHILD, V75, P448 Cornish KM, 1999, DEV MED CHILD NEUROL, V41, P263, DOI 10.1017/S0012162299000559 Cornish KM, 1996, DEV MED CHILD NEUROL, V38, P941 Dykens E. 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SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Western Regional Meeting of the American-Federation-for-Medical-Research CY JAN 29-FEB 01, 2003 CL CARMEL, CALIFORNIA SP American Fed Med Res C1 Keck Sch Med, Los Angeles, CA USA. CALTECH, Div Biol, Pasadena, CA 91125 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 FEB PY 2003 VL 51 SU 1 MA 107 BP S110 EP S110 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 638KF UT WOS:000180569600113 ER PT J AU Hansen, RL Goodlin-Jones, B Bacalman, S Harris, S Jardini, T Herman, K Hagerman, RJ AF Hansen, RL Goodlin-Jones, B Bacalman, S Harris, S Jardini, T Herman, K Hagerman, RJ TI Discrepancies in the diagnosis of autism by ADOS-G and ADI-R criteria in fragile 3L SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Western Regional Meeting of the American-Federation-for-Medical-Research CY JAN 29-FEB 01, 2003 CL CARMEL, CALIFORNIA SP American Fed Med Res C1 Univ Calif Davis, Med Ctr, MIND Inst, 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 FEB PY 2003 VL 51 SU 1 MA 127 BP S113 EP S113 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 638KF UT WOS:000180569600133 ER PT J AU Peralta-Carcelen, AM Thomas, EL Harrington, L Bailey, K AF Peralta-Carcelen, AM Thomas, EL Harrington, L Bailey, K TI Perceived services for childen with autism. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Western Regional Meeting of the American-Federation-for-Medical-Research CY JAN 29-FEB 01, 2003 CL CARMEL, CALIFORNIA SP American Fed Med Res C1 Univ Alabama, Birmingham, AL 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 FEB PY 2003 VL 51 SU 1 MA 44 BP S263 EP S263 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 638KF UT WOS:000180569600572 ER PT J AU Jentsch, JD AF Jentsch, JD TI Genetic vasopressin deficiency facilitates performance of a lateralized reaction-time task: Altered attention and motor processes SO JOURNAL OF NEUROSCIENCE LA English DT Article DE attention; vasopressin; Brattleboro rat; cognition; autism; schizophrenia ID BRATTLEBORO RATS; SELECTIVE ATTENTION; AUTISM; NORADRENALINE; SCHIZOPHRENIA; AMPHETAMINE; OXYTOCIN; CHILDREN AB Brattleboro rats are a variety of the outbred Long-Evans strain that possess a single nucleotide deletion in the second exon of the arginine vasopressin gene, resulting in the synthesis of an altered protein that does not enter the normal secretory pathway. Rats heterozygous (di/+) for the deletion have a partial vasopressin deficiency and exhibit a variety of behavioral and neurochemical alterations compared with normal wild-type Long-Evans rats, which provide evidence for a CNS function for vasopressin. Here, we examined the acquisition and performance of a test of visuospatial attention by di/+ Brattleboro rats and their wild-type Long-Evans control counterparts. Surprisingly, di/+ rats exhibited superior performance of the task compared with wild-type controls; performance differences included greater accuracy of detection of visual target stimuli, faster overall reaction times, and fewer trial omissions. Di/+ rats also exhibited more approaches to the reinforcer receptacle at nonreinforcement times. These results indicate that alterations of vasopressin signaling result in a clear cognitive phenotype, including faster motor initiations and superior choice accuracy in a test of visual attention. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Jentsch, JD (reprint author), Univ Calif Los Angeles, Dept Psychol, POB 951563, Los Angeles, CA 90095 USA. 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PD FEB PY 2003 VL 42 IS 2 BP 253 EP 256 DI 10.1097/01.CHI.0000037006.34553.D2 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 637XP UT WOS:000180539300021 PM 12544187 ER PT J AU Gluer, K Pagin, P AF Gluer, K Pagin, P TI Meaning theory and autistic speakers SO MIND & LANGUAGE LA English DT Article; Proceedings Paper CT Workshop on Interpretation CY NOV, 2000 CL PRAGUE, CZECH REPUBLIC HO CZECH ACAD SCI ID CHILDREN; LANGUAGE; MIND; COMMUNICATION; CONSCIOUSNESS; IMPAIRMENTS; COMPETENCE; COGNITION AB Some theories of linguistic meaning, such as those of Paul Grice and David Lewis, make appeal to higher-order thoughts: thoughts about thoughts. Because of this, such theories run the risk of being empirically refuted by the existence of speakers who lack, completely or to a high degree, the capacity of thinking about thoughts. Research on autism during the past 15 years provides strong evidence for the existence of such speakers. 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PD FEB PY 2003 VL 18 IS 1 BP 23 EP 51 DI 10.1111/1468-0017.00213 PG 29 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 651EB UT WOS:000181306600002 ER PT J AU Chandler, KE Moffett, M Clayton-Smith, J Baker, GA AF Chandler, KE Moffett, M Clayton-Smith, J Baker, GA TI Neuropsychological assessment of a group of UK patients with Cohen syndrome SO NEUROPEDIATRICS LA English DT Article DE Cohen syndrome; mental retardation; maladaptive behaviour; autism; neuropsychology ID MENTAL-RETARDATION; SYNDROME GENE; FEATURES; DISABILITY; CHILDREN AB Cohen syndrome is a rare autosomal recessive syndrome with a distinctive clinical phenotype that includes mental retardation and a characteristic sociable disposition. Variability in the level of learning disability and the behavioural phenotype is seen in the published literature. In a cohort of Finnish Cohen syndrome patients, severe mental retardation and non-maladaptive behaviour were described. Outside of Finland, autistic-spectrum behaviour has been reported in a few isolated Cohen syndrome patients but in a recent UK study was found to be highly prevalent. We report the results of neuropsychological studies in a group of 16 genetically heterogeneous patients, all with the characteristic clinical features of Cohen syndrome. Of the 9 patients who underwent formal neuropsychological testing, all but one was functioning in the severely mentally impaired range. Of the remaining patients, 3 were below the age of formal testing and 4 had such profound learning and behavioural problems that they were deemed unable to participate in testing. Mild maladaptive behaviour was observed in 13 patients and 3 were documented as having significant maladaptive behaviour. In contrast to the Finnish group of Cohen syndrome patients, this UK study identifies significant neuropsychological impairment combined with maladaptive behaviour as a characteristic of Cohen syndrome. Although autistic-type behaviour was observed, an increased prevalence of autism in Cohen syndrome was not confirmed. C1 St Marys Hosp, Acad Unit Med Genet, Manchester M13 0JH, Lancs, England. St Marys Hosp, Reg Genet Serv, Manchester M13 0JH, Lancs, England. Walton Ctr Neurol & Neurosurg, Liverpool, Merseyside, England. RP Chandler, KE (reprint author), St Marys Hosp, Acad Unit Med Genet, Hathersage Rd, Manchester M13 0JH, Lancs, England. 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Nicotine can stimulate the release of several different neurotransmitters in many brain regions. In the present study, we found that stimulation of nAChRs by nicotine or the endogenous agonist, acetylcholine (ACh), induces a large spontaneous increase in glutamate release onto layer V pyramidal neurons of the prefrontal cortex. This release of glutamate, measured by spontaneous excitatory postsynaptic currents (sEPSCs) in the prefrontal cortical slice, depends on intact thalamocortical terminals. It can be suppressed by mu-opioids or eliminated by blocking action potentials. The increase in sEPSCs is sensitive to low concentrations of nicotine, suggesting the involvement of high-affinity (eg alpha(4)beta(2)) nAChRs. Recent work has shown alterations in prefrontal alpha(4)beta(2) nAChRs in autism and schizophrenia, two conditions that are distinguished by abnormal prefrontal cortical activation as well as difficulty in certain aspects of cognition and integrating social and emotional cues. We show that mice lacking the beta(2) nAChR subunit do not show increased sEPSCs with either nicotine or ACh, again implicating high-affinity nicotinic receptors. These findings give new insight into the mechanism by which nicotine affects excitatory neurotransmission to the output neurons of the cerebral cortex in a pathway that is critical for cognitive function and reward expectation. C1 Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA. Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA. RP Lambe, EK (reprint author), Connecticut Mental Hlth Ctr, Ribicoff Res Facil, Rm 307,34 Pk St, New Haven, CT 06508 USA. 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Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 649XM UT WOS:000181233300003 PM 12589374 ER PT J AU Marek, GJ Carpenter, LL McDougle, CJ Price, LH AF Marek, GJ Carpenter, LL McDougle, CJ Price, LH TI Synergistic action of 5-HT2A antagonists and selective serotonin reuptake inhibitors in neuropsychiatric disorders SO NEUROPSYCHOPHARMACOLOGY LA English DT Review DE risperidone; mirtazapine; olanzapine; 5-HT2A receptors; depression; obsessive-compulsive disorder ID OBSESSIVE-COMPULSIVE DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; RECENT-ONSET SCHIZOPHRENIA; BIPOLAR DEPRESSED-PATIENTS; MEDIAL PREFRONTAL CORTEX; RATE 72-SECOND SCHEDULE; HUMAN-BRAIN INVITRO; MAJOR DEPRESSION; DOUBLE-BLIND; RECEPTOR OCCUPANCY AB Recently, the addition of drugs with prominent 5-HT2 receptor antagonist properties (risperidone, olanzapine, mirtazapine, and mianserin) to selective serotonin reuptake inhibitors (SSRIs) has been shown to enhance therapeutic responses in patients with major depression and treatment-refractory obsessive-compulsive disorder (OCD). These 5-HT2 antagonists may also be effective in ameliorating some symptoms associated with autism and other pervasive developmental disorders (PDDs). At the doses used, these drugs would be expected to saturate 5-HT2A receptors. These findings suggest that the simultaneous blockade of 5-HT2A receptors and activation of an unknown constellation of other 5-HT receptors indirectly as a result of 5-HT uptake inhibition might have greater therapeutic efficacy than either action alone. Animal studies have suggested that activation of 5-HT1A and 5-HT2C receptors may counteract the effects of activating 5-HT2A receptors. Additional 5-HT receptors, such as the 5-HT1B/1D/5/7 receptors, may similarly counteract the effects of 5-HT2A receptor activation. 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SO NUTRITIONAL NEUROSCIENCE LA English DT Article DE autism; peptides; exorphins; urine; diet ID INFLAMMATORY BOWEL-DISEASE; ENDOGENOUS OPIOID SYSTEMS; WHITE-MATTER LESIONS; BLOOD-BRAIN-BARRIER; HUMAN-BREAST MILK; CELIAC-DISEASE; INFANTILE-AUTISM; CHILDREN; DISORDER; PLASMA AB Opioid peptides derived from food proteins (exorphins) have been found in urine of autistic patients. Based on the work of several groups, we try to show that exorphins and serotonin uptake stimulating factors may explain many of the signs and symptoms seen in autistic disorders. The individual symptoms ought to be explainable by the properties and behavioural effects of the found peptides. The data presented form the basis of an autism model, where we suggest that exorphins and serotonin uptake modulators are key mediators for the development of autism. 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Neurosci. PD FEB PY 2003 VL 6 IS 1 BP 19 EP 28 DI 10.1080/1028415021000042839 PG 10 WC Neurosciences; Nutrition & Dietetics SC Neurosciences & Neurology; Nutrition & Dietetics GA 644PD UT WOS:000180926400003 PM 12608733 ER PT J AU Thompson, L Kaufman, LM AF Thompson, L Kaufman, LM TI The visually impaired child SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID BLINDNESS; AUTISM AB With advanced perinatal health care in the United States and resultant survival of infants with eye and brain damage, evaluation of a child in the pediatrician's office who presents with apparent low vision has become more commonplace. This article discusses the causes of infantile and childhood blindness in the United States based on patient presentation, and defines the clinician's role in patient care. 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H., 1994, BLINDNESS CHILDREN I *WHO, 1997, GLOB IN EL AV BLINDN World Health Organization, 1977, MAN INT STAT CLASS D, V1 NR 17 TC 2 Z9 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD FEB PY 2003 VL 50 IS 1 BP 225 EP + DI 10.1016/S0031-3955(02)00112-8 PG 16 WC Pediatrics SC Pediatrics GA 668HT UT WOS:000182284800016 PM 12713115 ER PT J AU Ashwal, S Rust, R AF Ashwal, S Rust, R TI Child neurology in the 20th century SO PEDIATRIC RESEARCH LA English DT Article ID PERSPECTIVE AB Although considered a relatively new subspecialty, child neurology traces its origins to the Hippocratic descriptions of seizures and other neurologic conditions in children. Its true beginnings can be traced to the 1600s and 1700s with classical descriptions of chorea, hydrocephalus, spina bifida, and polio. It was, however, the remarkable clinical and scientific advances in neurology and pediatrics at the end of the 19th century that helped create its scientific foundation. Like other pediatric disciplines, child neurology evolved into a distinct clinical and scientific specialty early in the 20th century. Remarkable advances in the neurosciences, particularly in the fields of genetics, molecular biology, metabolism, immunology and nutrition, have greatly advanced our understanding of how the brain develops and responds to environmental influences. Advances in neuro-imaging, electroencephalography, electromyography, muscle histology, biochemistry, and neuropharmacology have considerably improved our ability to evaluate and treat children with neurological disorders. These advances have allowed new and expanding approaches, unique to children, in the fields of epilepsy, neurodegenerative and neurometabolic disorders, nervous system infections, demyelinating diseases and tumors, neonatal neurological conditions, and neuromuscular diseases. They have also led to a better understanding of the neurobiologic basis of common problems such as global developmental delay, cerebral palsy, and autism. As remarkable as the advances have been in the past century, the accelerating pace of our understanding of the fundamental mechanisms responsible for brain development will lead to even greater achievements in the clinical care of children with neurological disorders in the 21st century. C1 Loma Linda Univ, Sch Med, Dept Pediat, Div Child Neurol, Loma Linda, CA 92350 USA. Univ Virginia, Sch Med, Dept Neurol, Charlottesville, VA 22908 USA. Univ Virginia, Sch Med, Dept Pediat, Charlottesville, VA 22908 USA. 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PD FEB PY 2003 VL 53 IS 2 BP 345 EP 361 DI 10.1203/01.PDR.0000047655.66475.52 PG 17 WC Pediatrics SC Pediatrics GA 637KW UT WOS:000180511100023 PM 12538797 ER PT J AU Kabot, S Masi, W Segal, M AF Kabot, S Masi, W Segal, M TI Advances in the diagnosis and treatment of autism spectrum disorders SO PROFESSIONAL PSYCHOLOGY-RESEARCH AND PRACTICE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL TREATMENT; EARLY INTERVENTION; YOUNG-CHILDREN; PROGRAMS; HEALTH; LIFE; 1ST AB A dramatic increase in the number of children who are diagnosed with an autistic disorder has given rise to a deluge of articles on autism in the professional as well as the popular literature. This review of the current literature Summarizes and synthesizes recent information on the causes and manifestations of autism, the trends in screening, diagnosis, and assessment; and the salient features of different treatment progams. It provides an overview of the advances and controversial issues that are of special interest to practicing clinical psychologists. C1 Nova SE Univ, Mailman Segal Inst Early Childhood Studies, Ft Lauderdale, FL 33314 USA. RP Kabot, S (reprint author), Nova SE Univ, Mailman Segal Inst Early Childhood Studies, 3301 Coll Ave, Ft Lauderdale, FL 33314 USA. 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S., 1998, YOUNG EXCEPTIONA WIN, P8 Sundberg M. L., 1998, TEACHING LANGUAGE CH Sussman F., 1999, MORE WORDS HELPING P Tsai LY, 1998, PERVASIVE DEV DISORD Volkmar F, 1997, J AUTISM DEV DISORD, V27, P103, DOI 10.1023/A:1025877307025 Zero to Three, 1994, DIAGN CLASS MENT HLT NR 57 TC 25 Z9 25 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0735-7028 J9 PROF PSYCHOL-RES PR JI Prof. Psychol.-Res. Pract. PD FEB PY 2003 VL 34 IS 1 BP 26 EP 33 DI 10.1037/0735-7028.34.1.26 PG 8 WC Psychology, Multidisciplinary SC Psychology GA 639ZH UT WOS:000180660300004 ER PT J AU Tachimori, H Osada, H Kurita, H AF Tachimori, H Osada, H Kurita, H TI Childhood Autism Rating Scale - Tokyo Version for screening pervasive developmental disorders SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE autism; CARS; diagnosis; PDD; screening test ID DSM-III-R; EARLY INTERVENTION; VALIDITY; CHILDREN; CARS; RELIABILITY; ADOLESCENTS; DIAGNOSIS AB To assess the utility of the Childhood Autism Rating Scale - Tokyo Version (CARS-TV), its total score was compared among 430 children with DSM-IV per subgroup (i.e. autistic disorder (AD), childhood disintegrative disorder (CDD), Asperger's disorder, and pervasive developmental disorders (PDD) not otherwise specified (PDDNOS)). Values of Cronbach's alpha were 0.91 for the PDD group and 0.89 for the non-PDD mental retardation (MR) group, and 0.93 for both groups combined. The total score was significantly higher in PDD (mean = 30.1, SD = 4.5) than in non-PDD MR (mean = 22.9, SD = 3.3), t((503)) = 13.7, P < 0.0001. The cut-off to distinguish PDD from non-PDD MR was 25.5/26, with sensitivity, specificity, positive predictive value and negative predictive value of 0.86, 0.83, 0.97 and 0.50, respectively. The total score differed significantly among the four groups, with CDD and AD being significantly higher than both PDDNOS and Asperger's disorder, PDDNOS being significantly higher than Asperger's disorder and no significant difference between CDD and AD. The cut-off to distinguish AD from PDDNOS was 30/30.5, with sensitivity, specificity, positive predictive value and negative predictive value of 0.71, 0.75, 0.77 and 0.69, respectively. CARS-TV seems to be a useful instrument for differentiating between PDD and non-PDD MR and between AD and PDDNOS, although further replication is needed. C1 NIMH, Dept Mental Hlth Adm, Natl Ctr Neurol & Psychiat, Chiba 2720827, Japan. Univ Tokyo, Dept Mental Hlth, Grad Sch Med, Tokyo, Japan. RP Tachimori, H (reprint author), NIMH, Dept Mental Hlth Adm, Natl Ctr Neurol & Psychiat, 1-7-3 Konodai, Chiba 2720827, Japan. 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 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 DILALLA DL, 1994, J AUTISM DEV DISORD, V24, P115, DOI 10.1007/BF02172092 EAVES RC, 1993, J ABNORM CHILD PSYCH, V21, P481, DOI 10.1007/BF00916315 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x GARFIN DG, 1988, J AUTISM DEV DISORD, V18, P367, DOI 10.1007/BF02212193 Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 KURITA H, 1989, J AUTISM DEV DISORD, V19, P389, DOI 10.1007/BF02212937 MAYES L, 1993, J AUTISM DEV DISORD, V23, P79, DOI 10.1007/BF01066420 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 Nordin V, 1998, J AUTISM DEV DISORD, V28, P69, DOI 10.1023/A:1026067104198 Pilowsky T, 1998, J AUTISM DEV DISORD, V28, P143, DOI 10.1023/A:1026092632466 Ritvo E. 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Neurosci. PD FEB PY 2003 VL 57 IS 1 BP 113 EP 118 DI 10.1046/j.1440-1819.2003.01087.x PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 633GW UT WOS:000180275300016 PM 12519463 ER PT J AU Joinson, C O'Callaghan, FJ Osborne, JP Martyn, C Harris, T Bolton, PF AF Joinson, C O'Callaghan, FJ Osborne, JP Martyn, C Harris, T Bolton, PF TI Learning disability and epilepsy in an epidemiological sample of individuals with tuberous sclerosis complex SO PSYCHOLOGICAL MEDICINE LA English DT Article ID AUTISM; TSC1; POPULATION; PREVALENCE; FAMILIES; BEHAVIOR; DEFICITS; MUTATION; SCOTLAND; WEST AB Background. Intellectual impairments are a recognized feature of tuberous sclerosis complex (TSC), but the frequency and degree of intellectual impairments has not been systematically studied in large epidemiological samples using standardized measures. As such, the form of the IQ distribution (uni-or bi-modal) has not been established and the relationship between IQ and other features (e.g. epilepsy history) is poorly delineated. To address these shortcomings, we assessed the intellectual abilities of a large epidemiological sample of individuals with TSC, drawn from the 'Wessex' area of SW England and compared them with the abilities of their unaffected siblings. Method. Standardized tests were used to estimate the abilities of 108 (56 males, 52 females, median age = 25, range = 4-75) individuals with TSC and 29 unaffected siblings (14 males, 15 females, median age = 18, range = 6-55). Seizure history was obtained from informants and medical records. Results. Estimated IQ was bi-modally distributed: 55(.)5% had an IQ in the normal range; 14% had mild to severe impairments; and 30(.)5% had profound disability (IQ < 21). Forty-four per cent of the individuals with TSC had an IQ < 70. In the subset of normally intelligent individuals with TSC, IQ was normally distributed with a mean of 93(.)6. This mean was significantly lower than the mean IQ of unaffected siblings (IQ = 105(.)6). All individuals with learning disability had a history of seizures that usually commenced before 12 months of age and that often presented as infantile spasms. Multivariate analyses indicated that a history of seizures as well as a history of infantile spasms was predictive of the degree of intellectual impairment. Conclusions. Intellectual abilities were bi-modally distributed in a representative sample of individuals with TSC. The likelihood of impairment was associated with a history of seizures, particularly infantile spasms. The genetic and brain basis of these findings requires further investigation. C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 1TN, England. Royal United Hosp, Bath Unit Res Paediat, Childrens Ctr, Bath BA1 3NG, Avon, England. Univ Southampton, MRC, Environm Epidemiol Unit, Southampton, Hants, England. RP Bolton, PF (reprint author), Inst Psychiat, Dept Child Psychiat, De Crespigny Pk, London SE5 8AF, England. 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PD FEB PY 2003 VL 33 IS 2 BP 335 EP 344 DI 10.1017/S0033291702007092 PG 10 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 671RZ UT WOS:000182479000015 PM 12622312 ER PT J AU Gray, DE AF Gray, DE TI Gender and coping: the parents of children with high functioning autism SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE autism; coping; Asperger's syndrome; gender; family ID CHRONIC ILLNESS; SOCIAL SUPPORT; STRESS; WOMEN; STRATEGIES; FAMILY; HEALTH AB Gender is a concept that is frequently discussed in the literature on stress, coping and illness. Research has reported that women are more vulnerable than men are to stressful events and use different strategies to cope with them. Furthermore, it is often asserted that these gender-based differences in coping may partially explain the differential impact of stressful events on men and women. Unfortunately, much of this research has equated gender with sex and failed to contextualise the experience of illness and coping. This paper presents a qualitative analysis of the role of gender and coping among parents of children with high functioning autism or Asperger's syndrome in an Australian sample. It attempts to analyse the different meanings of the disability for mothers and fathers and describes the various strategies that parents use to cope with their child's disability. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ New England, Sch Social Sci, Discipline Sociol, Armidale, NSW 2351, Australia. RP Gray, DE (reprint author), Univ New England, Sch Social Sci, Discipline Sociol, Armidale, NSW 2351, Australia. 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PD FEB PY 2003 VL 56 IS 3 BP 631 EP 642 DI 10.1016/S0277-9536(02)00059-X PG 12 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA 639EJ UT WOS:000180614400015 PM 12570979 ER PT J AU Soldin, OP Lai, SH Lamm, SH Mosee, S AF Soldin, OP Lai, SH Lamm, SH Mosee, S TI Lack of a relation between human neonatal thyroxine and pediatric neurobehavioral disorders SO THYROID LA English DT Article; Proceedings Paper CT 73rd Annual Meeting of the American-Thyroid-Association CY SEP, 2001 CL WASHINGTON, D.C. SP Amer Thyroid Assoc ID DEFICIT HYPERACTIVITY DISORDER; TREATED CONGENITAL HYPOTHYROIDISM; THYROID-HORMONE ACTION; IODINE DEFICIENCY; MATERNAL HYPOTHYROXINEMIA; POTENTIAL REPERCUSSIONS; PSYCHOMOTOR DEVELOPMENT; BRAIN-DEVELOPMENT; ATTENTION; PREGNANCY AB The growth and differentiation of the central nervous system are closely related to the presence of iodine and thyroid hormones. It has been hypothesized that neurobehavioral disabilities of childhood, such as attention deficit hyperactivity disorder (ADHD), learning disorders, and autism can be attributed to fetal thyroidal endocrine disruption in utero. To determine whether there is an association between neonatal thyroid status and a subsequent diagnosis of a neurobehavioral disability, neonatal thyroxine (T-4) levels have been used as the indicator of the presence of intrauterine thyroidal dysfunction. Neonatal T-4 levels were obtained from the neonatal hypothyroidism screening program. All cases were diagnosed at medical school diagnostic clinics, the diagnostic categories being ADHD, autism spectrum disorder, behavioral disorder, cognitive disorder, developmental delay, emotional disorder, learning disability, and speech/language disorder. Conditional logistic regression analysis was performed for each clinical condition. Odds ratios for the conditions ranged from 0.92 to 1.13 with p values ranging between 0.19 and 0.84. No significant differences were detected between neonatal T-4 values of the cases and the controls for any of the neurobehavioral conditions. All neonatal T-4 values were within normal ranges. The data provide no evidence to suggest that intrauterine thyroid status as reflected by the neonatal T-4 values had an impact on the neurologic disorders diagnosed in childhood. C1 CEOH Inc, Washington, DC 20007 USA. Hosp Sick Children, Div Clin Pharmacol Toxicol, MotherRisk, Toronto, ON M5G 1X8, Canada. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD USA. Howard Univ, Coll Med, Washington, DC USA. RP Soldin, OP (reprint author), CEOH Inc, 2428 Wisconsin Ave NW, Washington, DC 20007 USA. 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RP Szatmari, P (reprint author), McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada. 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PD JAN 25 PY 2003 VL 326 IS 7382 BP 173 EP 174 DI 10.1136/bmj.326.7382.173 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 640LD UT WOS:000180689600001 PM 12543815 ER PT J AU Hollander, E King, A Delaney, K Smith, CJ Silverman, JM AF Hollander, E King, A Delaney, K Smith, CJ Silverman, JM TI Obsessive-compulsive behaviors in parents of multiplex autism families SO PSYCHIATRY RESEARCH LA English DT Article DE autism; obsessive-compulsive disorders; obsessions; compulsions; phenotype ID PERVASIVE DEVELOPMENTAL DISORDERS; REPETITIVE BEHAVIORS; INDIVIDUALS; PHENOTYPE; PATTERNS AB Parents of autistic probands with high and low rates of repetitive behaviors were compared for rates of obsessive-compulsive traits and disorder. The rate of repetitive behaviors was assessed using the Autism Diagnostic Interview-Revised (ADI-R) in 176 autistic probands from 57 multiplex families. Obsessive-compulsive disorder (OCD) in parents was determined by direct interview using a parental history questionnaire, with screening for obsessive-compulsive traits using the Yale-Brown Obsessive-Compulsive Scale checklist. Children who had high total scores on the repetitive behavior domain of the ADI-R were significantly more likely to have one or both parents with obsessive-compulsive traits or disorder compared with children who had low total scores on this domain. Children with high scores on D1/D2 of the ADI-R (narrow restricted interests and rituals) were significantly more likely to have one or both parents with OCD, especially fathers, than those with low D1/D2. The occurrence of obsessive-compulsive traits or disorder in parents of autistic children in multiplex families is significantly more likely if autistic children have a high occurrence of repetitive behaviors. Dichotomizing autistic probands by severity and type of repetitive behaviors (circumscribed interests and compulsive rituals) may yield more homogenous groups, which could be helpful in genetic linkage studies. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. RP Hollander, E (reprint author), Mt Sinai Sch Med, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. 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PD JAN 25 PY 2003 VL 117 IS 1 BP 11 EP 16 DI 10.1016/S0165-1781(02)00304-9 PG 6 WC Psychiatry SC Psychiatry GA 653NZ UT WOS:000181444000002 PM 12581816 ER PT J AU [Anonymous] AF [Anonymous] TI Autism funding dispute reaches Supreme Court SO CANADIAN MEDICAL ASSOCIATION JOURNAL LA English DT News Item NR 0 TC 0 Z9 0 PU CANADIAN MEDICAL ASSOCIATION PI OTTAWA PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 3Y6, CANADA SN 0820-3946 J9 CAN MED ASSOC J JI Can. Med. Assoc. J. PD JAN 21 PY 2003 VL 168 IS 2 BP 210 EP 210 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 639LB UT WOS:000180629200037 ER PT J AU Gadia, CA Tuchman, RF AF Gadia, CA Tuchman, RF TI Management of children with autism spectrum disorders SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autism; autistic spectrum disorder; pharmacology; psychophannacology; treatment ID PERVASIVE DEVELOPMENTAL DISORDERS; UTAH EPIDEMIOLOGIC SURVEY; INFANTILE-AUTISM; DOUBLE-BLIND; DIAGNOSTIC INTERVIEW; BEHAVIORAL SYMPTOMS; DYSPHASIC CHILDREN; CONTROLLED TRIAL; RETT-SYNDROME; FOLLOW-UP AB Introduction. Autistic spectrum disorders (ASD) are characterized by qualitative deficits in communication, social skills and a restrictive repertoire of interests and behaviors. Recent studies suggest that they may represent one of the most prevalent neurodevelopmental disorders. Method. Treatment of core deficits of ASD are primarily speech and language, behavioral and educational interventions. Clinical management of ASD requires a multidisciplinary approach to identify behaviors that could interfere with the individual's ability to benefit from those interventions. Medications, such as neuroleptics, antiepileptic drugs, SSRI's, neurostimulants and others have been used to target specific behaviors. Conclusions. Further research is much needed if medications are eventually to have a greater role in the treatment of core ASD symptoms. Recent attempts at neurosurgical interventions cannot be justified by our present level of knowledge. C1 Univ Miami, Miami Childrens Hosp, Dept Neurol, Weston, FL USA. 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Neurologia PD JAN 16 PY 2003 VL 36 IS 2 BP 166 EP 173 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 646BN UT WOS:000181015100014 PM 12589605 ER PT J AU Tsatsanis, KD Rourke, BP Klin, A Volkmar, FR Cicchetti, D Schultz, RT AF Tsatsanis, KD Rourke, BP Klin, A Volkmar, FR Cicchetti, D Schultz, RT TI Reduced thalamic volume in high-functioning individuals with autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE thalamus; autism; neuroimaging; brain; magnetic resonance imaging ID SHORT-TERM PLASTICITY; THALAMOCORTICAL INNERVATION; AUGMENTING RESPONSES; INFANTILE-AUTISM; CHILDHOOD AUTISM; BRAIN; CORTEX; ATTENTION; SYSTEMS; MEMORY AB Background: In this study,specific consideration is given to a role for the thalamus in autism. Methods: A volumetric analysis of the thalamus was conducted using magnetic resonance imaging, based on segmentation of continuous 1.2 mm(3) coronal images. The sample consisted of 12 high-functioning individuals with autism, mean age of 21.0 years (SD = 10.4) and mean IQ of 106.4 (SD = 18.3). Normal control subjects were selected to match this group; the mean age was 18.1 years (SD = 6.3); mean IQ was 108.8 (SD = 15.6). Results: Unadjusted mean thalamic volume was not significantly different; however, there were significant differences in the relationship between thalamic volume and total brain volume (TBV). The correlation was strong and positive in the control group but statistically nonsignificant in the autism group. Group differences were found when adjustments were made for TBV, achieved by grouping subjects' measurements on this variable using a split median procedure. Mean thalamic volume was significantly reduced in the autism group relative to normal control subjects, specifically within the high TBV group. 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Psychiatry PD JAN 15 PY 2003 VL 53 IS 2 BP 121 EP 129 DI 10.1016/S0006-3223(02)01530-5 PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 637NM UT WOS:000180518900003 PM 12547467 ER PT J AU Friedman, SD Shaw, DW Artru, AA Richards, TL Gardner, J Dawson, G Posse, S Dager, SR AF Friedman, SD Shaw, DW Artru, AA Richards, TL Gardner, J Dawson, G Posse, S Dager, SR TI Regional brain chemical alterations in young children with autism spectrum disorder SO NEUROLOGY LA English DT Article ID MAGNETIC-RESONANCE SPECTROSCOPY; IN-VIVO; EMISSION-TOMOGRAPHY; METABOLIC RESPONSE; INFANTILE-AUTISM; CHILDHOOD AUTISM; PROTON; MRS; INDIVIDUALS; ASPARTATE AB Objective: The authors evaluated regional brain chemistry for evidence of increased neuronal packing density in autism. Methods: Forty-five 3- to 4-year-old children with autism spectrum disorder (ASD), 13 children with typical development (TD), and 15 children with delayed development (DD) were studied using dual-echo proton echoplanar spectroscopic imaging (32 X 32 matrix-1 cm(3) voxels) to measure brain chemical concentrations and relaxation times. Chemical quantification was corrected for tissue partial volume and relative measures of chemical relaxation (T-2r) were calculated from the paired echoes. Measures from averaged and individual regions were compared using analysis of variance corrected for multiple comparisons. Results: ASD subjects demonstrated reduced N-acetylaspartate (NAA) (-10%), creatine (Cre) (-8%), and myo-inositol (-13%) concentrations compared to TD controls and prolonged NAA T-2r relative to TD (7%) and DD (9%) groups. Compared to DD subjects, children with ASD also demonstrated prolonged T-2r for choline (10%) and Cre (9%). Regional analyses demonstrated subtle patterns of chemical alterations in ASD compared to the TD and DD groups. Conclusions: Brain chemical abnormalities are present in ASD at 3 to 4 years of age. However, the direction and widespread distribution of these abnormalities do not support hypothesis of diffuse increased neuronal packing density in ASD. C1 Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Anesthesiol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Psychol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Psychiat, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Bioengn, Seattle, WA 98105 USA. Wayne State Univ, Dept Psychiat, Detroit, MI USA. RP Dager, SR (reprint author), Univ Washington, Sch Med, Dept Radiol, 4225 Roosevelt Way NE,Suite 306-C, Seattle, WA 98105 USA. 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This descriptive study profiles the children seen in one unit of this program. Setting.-A New England, university-affiliated Pediatric Environmental Health Center (PEHC). Methods.-Review and analysis of all children seen in the PEHC in calendar year 1999. Results.-Over the course of the year, 281 children made 863 visits to the PEHC. Presenting complaints fell into 4 major categories: new visit for management of lead intoxication (n = 248), return visit for management of lead intoxication (n = 569), new visit for evaluation of exposure to an environmental toxicant other than lead (n = 33), and return visit for the management of exposure to a non-lead toxicant (n = 13). Among those children with new visits for a non-lead toxicant, the most common chief complaints were exposure to solvent-contaminated water (n = 7), pesticide exposure (n = 6), illness associated with proximity to a hazardous waste site (n = 6), autism from suspected mercury intoxication (n = 4), and evaluation of school-induced, building-related illness ("sick school syndrome")(n = 4). Eleven children had autism or pervasive developmental delay. Families traveled distances as great as 450 kilometers for evaluation by a pediatric environmental health clinical specialist. Every child was evaluated by a pediatrician with subspecialty training in medical toxicology. Environmental investigation of air, water, paint, dust, or land was conducted for all except 4 children (all foreign-born adoptees). Therapeutic interventions included chelation therapy, relocation to a safe environment, removal from school, and termination of chelation therapy that had been initiated by another practitioner. Third-party payors provided full reimbursement for all visits. Conclusions.-The chief complaints of the children brought to pediatric environmental health specialty units are diverse, involving exposures to a wide range of toxicants from all environmental media (air, water, soil, and food). Parents desiring such an evaluation must often travel extensive distances, suggesting the need for a broader network of such centers. Third-party payors and health maintenance organizations are willing to provide full reimbursement for these services. C1 Childrens Hosp, Div Emergency Med, Boston, MA 02115 USA. Childrens Hosp, Program Clin Toxicol, Boston, MA 02115 USA. Cambridge Hosp, Div Occupat Environm Med, Cambridge, MA USA. Harvard Univ, Sch Med, Boston, MA USA. RP Shannon, M (reprint author), Childrens Hosp, Div Emergency Med, 300 Longwood Ave, Boston, MA 02115 USA. 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PD JAN-FEB PY 2003 VL 3 IS 1 BP 53 EP 56 DI 10.1367/1539-4409(2003)003<0053:CSEHOY>2.0.CO;2 PG 4 WC Pediatrics SC Pediatrics GA 638QK UT WOS:000180581600012 PM 12540255 ER PT J AU Spitzer, SL AF Spitzer, SL TI Using participant observation to study the meaning of occupations of young children with autism and other developmental disabilities SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE occupational science; qualitative method ID QUALITATIVE RESEARCH; THERAPY; LIVES AB Understanding the individual meaning of daily activities for children with developmental disabilities such as autism is both important and challenging for researchers and practitioners. Rigorous participant observation offers a method for developing this knowledge base by including the child's perspective. Through literature and examples from an ethnography of young children with autism, this article illustrates the application of participant observation to children with developmental disabilities. 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SO AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0002-9483 J9 AM J PHYS ANTHROPOL JI Am. J. Phys. Anthropol. 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SO AMYGDALA IN BRAIN FUNCTION: BACIC AND CLINICAL APPROACHES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on the Amygdala in Brain Function CY JUN 24-26, 2002 CL GALVESTON, TEXAS SP Univ Texas Med Branch, NY Acad Sci, NIH, RW Johnson Pharmaceut Inst, NIA, Natl Inst Neurol Dis & Stroke DE amygdala; emotion; social cognition; facial expression; reduction ID FACIAL EMOTION; IMPAIRED RECOGNITION; ASPERGER-SYNDROME; BILATERAL DAMAGE; NORMAL ADULTS; FEAR; EXPRESSIONS; NEURONS; STIMULI; AUTISM AB A number of studies in humans and other animals has confirmed the amygdala's role in modulating cognition and behavior on the basis of a stimulus' motivational, emotional, and social atttributes. This raises the question of how these attributes are related: is social information processing reducible to motivational processing? Some recent data suggest the possibility that the amygdala's primitive function may be motivational processing that is domain-general, but that its function in primates, and especially humans, may have evolved to process social information specifically. While the issue is unresolved, future experiments could provide additional support. C1 Univ Iowa, Coll Med, Dept Neurol, Div Cognit Neurosci, Iowa City, IA 52242 USA. RP Adolphs, R (reprint author), Univ Iowa Hosp & Clin, Dept Neurol, 200 Hawkins Dr, Iowa City, IA 52242 USA. 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RP Goulet, M (reprint author), Repligen Corp, Waltham, MA 02453 USA. CR Baron-Cohen S, 2000, NEUROSCI BIOBEHAV R, V24, P355, DOI 10.1016/S0149-7634(00)00011-7 BEYERMAN HC, 1981, LIFE SCI, V29, P885, DOI 10.1016/0024-3205(81)90389-1 Howard MA, 2000, NEUROREPORT, V11, P2931, DOI 10.1097/00001756-200009110-00020 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 SWEETEN RL, 2002, PHARM BIOCH BEHAV, V71, P449 NR 5 TC 0 Z9 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-404-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2003 VL 985 BP 522 EP 524 PG 3 WC Multidisciplinary Sciences; Neurosciences; Psychiatry SC Science & Technology - Other Topics; Neurosciences & Neurology; Psychiatry GA BW71H UT WOS:000182918800051 ER PT J AU Tonk, VS Wyandt, HE Huang, X Patel, N Morgan, DL Kukolich, M Lockhart, LH Velagaleti, GVN AF Tonk, VS Wyandt, HE Huang, X Patel, N Morgan, DL Kukolich, M Lockhart, LH Velagaleti, GVN TI Disease associated balanced chromosome rearrangements (DBCR): report of two new cases SO ANNALES DE GENETIQUE LA English DT Article DE DBCR; CCR; FISH; subtelomere; autism; deafness ID EPICANTHUS-INVERSUS SYNDROME; SYNDROME TYPE-III; HEARING-LOSS DFNA5; CAMPOMELIC DYSPLASIA; RECIPROCAL TRANSLOCATION; CANDIDATE GENES; SYNDROME BPES; BLEPHAROPHIMOSIS; PTOSIS; REGION AB Disease associated balanced chromosome rearrangements (DBCR) causing truncation, deletion, inactivation or over-expression of specific genes are instrumental in identifying and cloning several disease genes and are estimated to be much more common than anticipated. In one survey, the minimal frequency of combined balanced de novo reciprocal translocations and inversions causing abnormal phenotype is estimated to be 0.17%, a sixfold increase compared to the general population suggesting a causative linkage between the abnormality and the observed phenotypic traits. Here, we report two new cases of apparently balanced de novo translocations resulting in developmental delay and dysmorphic features. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All rights reserved. C1 Univ Texas, Childrens Hosp, Med Branch, Dept Pediat, Galveston, TX 77555 USA. Texas Tech Univ, Hlth Sci Ctr, Dept Pediat, Lubbock, TX 79430 USA. Texas Tech Univ, Hlth Sci Ctr, Dept Pathol, Lubbock, TX 79430 USA. Boston Univ, Sch Med, Ctr Human Genet, Boston, MA 02118 USA. Univ Texas, Med Branch, Dept Pathol, Galveston, TX 77550 USA. RP Velagaleti, GVN (reprint author), Univ Texas, Childrens Hosp, Med Branch, Dept Pediat, Suite 3350,301 Univ Blvd, Galveston, TX 77555 USA. 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Genet. PD JAN-MAR PY 2003 VL 46 IS 1 BP 37 EP 43 DI 10.1016/S0003-3995(03)00005-4 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 698AL UT WOS:000183975400007 PM 12818528 ER PT J AU Bespalova, IN Buxbaum, JD AF Bespalova, IN Buxbaum, JD TI Disease susceptibility genes for autism SO ANNALS OF MEDICINE LA English DT Review DE autism; linkage disequilibrium mapping; susceptibility loci; transmission disequilibrium test; whole genome scan ID SEROTONIN TRANSPORTER GENE; ANGELMAN-SYNDROME GENE; RECEPTOR SUBUNIT GENES; LINKAGE-DISEQUILIBRIUM; INFANTILE-AUTISM; CHROMOSOME 7Q; PSYCHIATRIC-DISORDERS; LANGUAGE IMPAIRMENT; MULTIPLEX FAMILIES; GENOMIC SCREEN AB Autism is a complex neurodevelopmental disorder characterized by impairment in social interaction accompanied by a delay or lack of language, restricted interests, stereotyped behavior, and repetitive movement. Genetic predisposition to autism is evident from family and twin studies, and heritability in idiopathic autism is estimated at over 90%. Frequency of the disorder is approximately 1:2000 with a male to female ratio of 4:1. Affected individuals look normal at birth, and the symptoms manifest at the first 2-3 years of life. The spectrum of clinical symptoms and the severity of the disorder are variable even among siblings. Family studies and several genome-wide linkage analyses support the hypothesis of complex inheritance with involvement of as many as 10-100 genes of moderate effect. Identification of genes responsible for the phenotype would help to understand the molecular mechanisms of the disorder. Several genes have been proposed to play a role in susceptibility to autism, and this paper will overview those genes and their potential role in the disorder. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, Seaver Autism Res Ctr, New York, NY 10029 USA. 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PY 2003 VL 54 SU 7 BP S129 EP S129 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 720KQ UT WOS:000185260300343 ER PT J AU Connolly, AM Streif, EM Chez, MG AF Connolly, AM Streif, EM Chez, MG TI Brain-derived neurotrophic factor and antibodies to brain-derived neurotrophic factor are elevated in children with autism, autism with regression, and epilepsy SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FLORIDA SP Child Neruol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2003 VL 54 SU 7 BP S146 EP S147 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 720KQ UT WOS:000185260300407 ER PT J AU Gropman, A AF Gropman, A TI Vigabatrin and newer interventions in succinic semialdehyde dehydrogenase deficiency SO ANNALS OF NEUROLOGY LA English DT Article; Proceedings Paper CT 1st International Symposium on Pediatric Neurotransmitter Diseases CY MAY 18-19, 2002 CL WASHINGTON, D.C. ID GAMMA-HYDROXYBUTYRIC ACID; 4-HYDROXYBUTYRIC ACIDURIA; MICE DEFICIENT; INBORN ERROR; PRENATAL-DIAGNOSIS; CLINICAL PHENOTYPE; GABA-METABOLISM; THERAPY; SEIZURES; PATIENT AB Succinic semialdehyde dehydrogenase (SSADH) deficiency is a rare disorder characterized by an inborn error of the catabolism of the inhibitory neurotransmitter GABA. Because of the deficiency of SSADH, the final enzyme of the GABA degradation pathway, the substrate, succinic semialdehyde, is shunted towards production of 4-hydroxybutyric acid (gamma-hydroxybutyric acid). Elevations of gamma-hydroxybutyric acid can be detected in the physiologic fluids of patients with SSADH deficiency, and forms the mainstay of diagnosis. The clinical features of SSADH deficiency include nonspecific neurologic manifestations such as mental retardation/developmental delay, absent speech, hypotonia, nonprogressive ataxia, features of autism or pervasive developmental delay, developmental language delay (dyspraxia, receptive, and expressive delays), and occasionally, seizures. Although the metabolic pathway has been established, it is not known whether insufficient GABA and/or excess gamma-hydroxybutyric acid contribute to the disease phenotype. Pharmacological therapy in patients with this disorder has been limited to vigabatrin, an anticonvulsant that blocks GABA transaminase. This review will discuss therapeutic options in SSADH deficiency, on the basis of patient experience, and preliminary work using a murine model. 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PY 2003 VL 54 SU 7 BP S119 EP S119 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 720KQ UT WOS:000185260300308 ER PT J AU Vargas, DL Zimmerman, AW Pardo, CA AF Vargas, DL Zimmerman, AW Pardo, CA TI Neuroglial activation in autism: A potential neuroinflammatory pathogenic mechanism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FLORIDA SP Child Neruol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2003 VL 54 SU 7 BP S147 EP S147 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 720KQ UT WOS:000185260300410 ER PT J AU Fisher, SE Lai, CSL Monaco, AP AF Fisher, SE Lai, CSL Monaco, AP TI Deciphering the genetic basis of speech and language disorders SO ANNUAL REVIEW OF NEUROSCIENCE LA English DT Review DE linkage analysis; quantitative trait locus; specific language impairment; SPCH1; FOXP2 ID QUANTITATIVE-TRAIT LOCUS; INHERITED SPEECH; FAMILY HISTORY; DEVELOPMENTAL DYSLEXIA; SUSCEPTIBILITY LOCUS; GENOMEWIDE SCAN; IMPAIRMENT; CHILDREN; AUTISM; LINKAGE AB A significant number of individuals have unexplained difficulties with acquiring normal speech and language, despite adequate intelligence and environmental stimulation. Although developmental disorders of speech and language are heritable, the genetic basis is likely to involve several, possibly many, different risk factors. Investigations of a unique three-generation family showing monogenic inheritance of speech and language deficits led to the isolation of the first such gene on chromosome 7, which encodes a transcription factor known as FOXP2. Disruption of this gene causes a rare severe speech and language disorder but does not appear to be involved in more common forms of language impairment. Recent genome-wide scans have identified at least four chromosomal regions that may harbor genes influencing the latter, on chromosomes 2, 13, 16, and 19. The molecular genetic approach has potential for dissecting neurological pathways underlying speech and language disorders, but such investigations are only just beginning. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. RP Fisher, SE (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. 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Rev. Neurosci. PY 2003 VL 26 BP 57 EP 80 DI 10.1146/annurev.neuro.26.041002.131144 PG 24 WC Neurosciences SC Neurosciences & Neurology GA 717MJ UT WOS:000185093200004 PM 12524432 ER PT J AU Goldenberg, A Chevy, F Bernard, C Wolf, C Cormier-Daire, V AF Goldenberg, A Chevy, F Bernard, C Wolf, C Cormier-Daire, V TI When should Smith-Lemli-Opitz syndrome be considered? A serie of 45 cases SO ARCHIVES DE PEDIATRIE LA French DT Article DE Smith-Lemli-Opitz syndrome; mutations; genetics; infant ID ABNORMAL CHOLESTEROL-METABOLISM; DELTA-7-STEROL REDUCTASE GENE; PHENOTYPE; MUTATIONS; SPECTRUM; PATIENT; DHCR7 AB Introduction. - SLO (Smith-Lemli-Opitz) syndrome is an autosomal recessive multiple congenital malformations syndrome, including mental retardation, failure to thrive, craniofacial abnormalities, incomplete development of male genitalia, limb anomalies and various internal organ abnormalities. This syndrome is caused by a deficiency of cholesterol biosynthesis at the distal step of 7-dehydrocholesterol reductase (7DHCR). Patients and methods. - We have reviewed 45 cases of SLO syndrome and showed the large clinical spectrum of this syndrome. Results. - The prenatal diagnosis should be considered when dealing with antenatal growth retardation and visceral malformations. At birth, a normal weight does not systematically exclude the diagnosis. Diagnosis was more difficult for older children especially for girls and should be suspected on the association of mental retardation, autism, short stature and microcephaly. We found a correlation between low plasmatic cholesterol measurement and clinical severity. Phenotype-genotype correlation was difficult to establish. However, homozygosity for IVS8-1G>C splice site mutation was associated With severe phenotype. Conclusion. - Better understanding of the 7DHCR gene regulation factors and of the compensatory mechanism of foeto-maternal cholesterol transfer are necessary to explain the wide clinical spectrum of the SLO syndrome. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All rights reserved. C1 Hop Necker Enfants Malad, Assistance Publ Hop Paris, Dept Med Genet, F-75743 Paris 15, France. Univ Paris 06, Lab Spectrometrie Masse, Paris, France. Hop St Antoine, Assistance Publ Hop Paris, Mol Biol Lab, F-75571 Paris, France. RP Cormier-Daire, V (reprint author), Hop Necker Enfants Malad, Assistance Publ Hop Paris, Dept Med Genet, 149 Rue Sevres, F-75743 Paris 15, France. 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Pediatr. PD JAN PY 2003 VL 10 IS 1 BP 4 EP 10 DI 10.1016/S0929-693X(03)00214-8 PG 7 WC Pediatrics SC Pediatrics GA 663WC UT WOS:000182028600003 PM 12818773 ER PT S AU Paplinski, AP Gustafsson, L AF Paplinski, AP Gustafsson, L BE Kaynak, O Alpaydin, E Oja, E Xu, L TI Detailed learning in narrow fields - Towards a neural network model of autism SO ARTIFICAIL NEURAL NETWORKS AND NEURAL INFORMATION PROCESSING - ICAN/ICONIP 2003 SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT Joint International Conference on Artificial Neural Networks (ICANN)/International on Neural Information Processing (ICONIP) CY JUN 26-29, 2002 CL ISTANBUL, TURKEY SP Bogazici Univ Fdn, USAF, European Off Aerosp Res & Dev, Turkish Sci & Tech Res Council ID CHILDREN AB Autism is a developmental disorder in which attention shifting is known to be restricted. Using an artificial neural network model of learning we show how detailed learning in narrow fields develops when attention shifting between different sources of stimuli is restricted by familiarity preference. Our model is based on modified Self-Organizing Maps (SOM) supported by the attention shift mechanism. The novelty seeking and the attention shifting restricted by familiarity preference learning modes are investigated for stimuli of low and high dimensionality which requires different techniques to visualise feature maps. To make learning more biologically plausible we project the stimuli onto a unity hyper-sphere. The distance between a stimulus and a weight vector can now be simply measured by the post-synaptic activities. The modified "dot-product" learning law that keeps evolving weights on the surface of the hyper-sphere has been employed. C1 Monash Univ, Clayton, Vic 3800, Australia. Lulea Univ Technol, S-97187 Lulea, Sweden. RP Paplinski, AP (reprint author), Monash Univ, Clayton, Vic 3800, Australia. 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SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 La Trobe Univ, Bundoora, Vic, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 7 EP 7 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200026 ER PT J AU Milana, V Crewther, SG Crewther, DP AF Milana, V Crewther, SG Crewther, DP TI Does noncentral gaze facilitate face recognition by typically developing children and children with autism? SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 La Trobe Univ, Bundoora, Vic, Australia. Swinburne Univ Technol, Hawthorn, Vic 3122, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 23 EP 24 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200091 ER PT J AU Sercombe, A Karayanidis, F Michie, P Passfield, T Johnston, P AF Sercombe, A Karayanidis, F Michie, P Passfield, T Johnston, P TI Face and facial emotion processing in children with autism SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Newcastle, Newcastle, NSW 2308, Australia. RI Johnston, Patrick/P-3158-2014 OI Johnston, Patrick/0000-0001-7703-1073 NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 109 EP 109 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200474 ER PT J AU Dudley, AL Rinehart, NJ Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG McGinley, J AF Dudley, AL Rinehart, NJ Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG McGinley, J TI Early motor features in children with autism SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 177 EP 178 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200767 ER PT J AU Kerr, S Durkin, K Maybery, M AF Kerr, S Durkin, K Maybery, M TI The screening of autism in 18-month-old infants: Implications for theories of autism SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Western Australia, Nedlands, WA 6009, Australia. NR 0 TC 0 Z9 2 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 189 EP 189 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200818 ER PT J AU Maley, A Maybery, M AF Maley, A Maybery, M TI The effectiveness of early intervention treatment for children with autism spectrum disorders SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Western Australia, Nedlands, WA 6009, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 194 EP 194 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200842 ER PT J AU Maybery, M Wong, D Maley, A Hallmayer, J Bishop, D Hill, W Dyck, M AF Maybery, M Wong, D Maley, A Hallmayer, J Bishop, D Hill, W Dyck, M TI Cognitive functioning in the parents of individuals with an autism spectrum disorder SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Western Australia, Nedlands, WA 6009, Australia. Stanford Univ, Stanford, CA 94305 USA. Univ Oxford, Oxford OX1 2JD, England. Curtin Univ Technol, Bentley, WA 6102, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 195 EP 195 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200849 ER PT J AU Pellicano, E Gibson, L Maybery, M Durkin, K AF Pellicano, E Gibson, L Maybery, M Durkin, K TI Elevated motion coherence thresholds in autism: Further evidence of 'weak' central coherence SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Western Australia, Nedlands, WA 6009, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 202 EP 202 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200879 ER PT J AU Rinehart, NJ Brereton, AV Tonge, BJ King, N AF Rinehart, NJ Brereton, AV Tonge, BJ King, N TI Autism: A parent-based early intervention SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 208 EP 208 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200903 ER PT J AU Rinehart, NJ Dudley, AL Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG McGinley, J AF Rinehart, NJ Dudley, AL Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG McGinley, J TI Movement-related potentials and gait function in high-functioning autism and Asperger's disorder SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 208 EP 208 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200904 ER PT J AU Wong, D Maybery, M Maley, A Hill, W Bishop, D Hallmayer, J AF Wong, D Maybery, M Maley, A Hill, W Bishop, D Hallmayer, J TI Theory of mind and executive function: Primacy and independence in autism SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Western Australia, Nedlands, WA 6009, Australia. Univ Oxford, Oxford OX1 2JD, England. Stanford Univ, Stanford, CA 94305 USA. NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2003 VL 55 SU S BP 221 EP 221 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 750GP UT WOS:000186983200965 ER PT S AU Rutter, M AF Rutter, Michael BE Bock, G Goode, J TI Introduction: autism - the challenges ahead SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; CAUSAL ASSOCIATION; CHILDREN; AGE; PHENOTYPES; PATTERNS; ETIOLOGY; SPECTRUM; RUBELLA C1 Inst Psychiat, Soc Genet & Dev Psychiat Res Ctr, London SE5 8AF, England. RP Rutter, M (reprint author), Inst Psychiat, Soc Genet & Dev Psychiat Res Ctr, De Crespigny Pk, Denmark Hill, London SE5 8AF, England. 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Increased recognition, the broadening of the diagnostic concept and methodological differences across studies may account for most or all of the apparent increase in prevalence, although this cannot be quantified. In addition to the implications for families and services, these conceptual changes will affect the scientific study of autism. At present, case definition is reliant on the behavioural and developmental picture alone. Because the behavioural phenotype of autism and the broader autism spectrum disorders includes individuals with different ultimate aetiologies, even when biological or genetic markers are found they will not be present in all individuals with the phenotype. The fact that autism is not a unitary, 'disorder' presents a significant challenge to genetic, biological, neurological and psychological research. Progress has recently been made in the earlier identification of autism both through screening programmes and by increased understanding and enhanced surveillance. This offers an opportunity to better understand the early developmental course of autism and may provide additional clues to the underlying pathology. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. RP Charman, T (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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Our understanding of the significance of milder phenotypes in other relatives has shifted from presumed environmental aetiological factors to variable manifestations of a complex disease process. In this paper we outline how the challenge of explaining the full range of phenotypic expression inevitably leads to more complex models of disease process than previously supposed. The implications of milder phenotypes for genetic, neurobiological and cognitive models of autism will be considered in relationship to several key features of complex diseases: complexity, hierarchy, emergence and coherence. C1 Univ Oxford, Dept Psychiat, Oxford OX3 7LQ, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London SE5 8AF, England. RP Bailey, A (reprint author), Univ Oxford, Dept Psychiat, Old Rd, Oxford OX3 7LQ, England. 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Symp. PY 2003 VL 251 BP 26 EP 47 PG 22 WC Medicine, General & Internal; Neurosciences; Psychiatry SC General & Internal Medicine; Neurosciences & Neurology; Psychiatry GA BGN65 UT WOS:000248830100003 PM 14521186 ER PT S AU Barnby, G Monaco, AP AF Barnby, G. Monaco, A. P. BE Bock, G Goode, J TI Strategies for autism candidate gene analysis SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID SINGLE-NUCLEOTIDE POLYMORPHISMS; AFFECTED SIBLING PAIRS; COMMON DISEASE GENES; LINKAGE DISEQUILIBRIUM; SUSCEPTIBILITY GENE; GENOMEWIDE SCREEN; COMPLEX DISEASES; CROHNS-DISEASE; GENOMIC SCREEN; DISORDER AB The identification of autism susceptibility genes has moved a step closer over the last four years with the completion of eight whole genome screens for linkage. Several overlapping areas of linkage have been reported, most notably on chromosomes 7q22-31 and 2q32. These regions of replicated linkage provide a focus to search for candidate genes whose normal functions in neurodevelopment are altered to increase the risk for autism. Strategies that aim to narrow further the rather broad size of these linkage regions, such as high density single nucleotide polymorphism (SNP)-based association studies, currently suffer from practical and statistical limitations. Alternatively, positional candidate genes can be screened for deleterious variants in autistic individuals selected from large samples such as those collected by the International Molecular Genetic Study of Autism Consortium (ENIGSAC). Targeted genotyping of candidate gene variants in this large multiplex family sample will then be performed to confirm association with autism. C1 Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. 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Dowd, Michael Mankoski, Raymond Tadevosyan, Ovsanna BE Bock, G Goode, J TI How might genetic mechanisms operate in autism? SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID FAMILY HISTORY; SEROTONIN TRANSPORTER; SUSCEPTIBILITY GENE; GENOMEWIDE SCREEN; INFANTILE-AUTISM; LINKAGE; DISORDER; INDIVIDUALS; CHILDREN; CHROMOSOME-2 AB Twin and family studies provide strong evidence that autism has a largely genetic aetiology. The pattern of familial aggregation suggests that in individual families, a small number of genes act together to cause the phenotype. However, it is unlikely that the same genes act in all families. Thus, the total number of genes involved could be large. One key to finding genes for disorders with considerable locus heterogeneity is to detect genetically more homogeneous subsamples. There exist several traits in families who have a child with autism-biochemical, physical, or behavioural-that are likely to reflect underlying genetic heterogeneity and can thus be used to divide families into more homogeneous subsets. These traits (1) show variation in autism samples; (2) are found in non-autistic family members more often than controls; (3) aggregate in particular autism families; and (4) result in increased signals when used in linkage analysis to define 'affected'. C1 Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. RP Folstein, SE (reprint author), Tufts Univ, New England Med Ctr, Dept Psychiat, 750 Washington St 1007, Boston, MA 02111 USA. 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Autism is the archetypal disorder of social cognitive skills, and increasing interest is being paid to the role played by efferent and afferent connectivity between the amygdala and neocortical brain regions, in predisposing to this condition. Such circuits are now known to be critical for the processing of social information. Recent research suggests a sub-cortical neural pathway, routed through the amygdala, may turn out to be a key player in the mystery of why humans are so prone to disorders of social adjustment. This pathway responds to certain simple classes of potential threat, including direct eve contact and, in humans, arousal evoked by this exquisitely social stimulus is modulated and controlled by a variety of specific (largely frontal) neocortical regions. 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Relatively few neuropathological studies have been performed on the brains of autistic subjects. Of those reported, abnormalities have been described in the cerebral cortex, the brainstem, the limbic system and the cerebellum. Although those with the disorder present with a specific set of core characteristics, each individual patient is somewhat different from another. Thus, it should not be surprising that the brains of these subjects should show a wide range of abnormalities. However, it is important to delineate the anatomic features, which are common to all cases, regardless of age, sex and IQ, in order to begin to understand the central neurobiological profile of this disorder. The results of our systematic studies indicate that the anatomic features that are consistently, abnormal in all cases include reduced numbers of Purkinje cells in the cerebellum, and small tightly packed neurons in the entothinal cortex and in the medially placed nuclei of the amygdala. It is known that the limbic system is important for learning and memory, and that the amygdala plays a role in emotion and behaviour. Research in the cerebellum indicates that this structure is important as a modulator of a variety of brain functions and impacts on language processing, anticipatory and motor planning, mental imagery and timed sequencing. Defining the differences and similarities in brain anatomy in autism and correlating these observations with detailed clinical descriptions of the patient may allow us greater insight into the underlying neurobiology of this disorder. C1 Massachusetts Gen Hosp, Childs Neurol Serv, Boston, MA 02114 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Bauman, ML (reprint author), Massachusetts Gen Hosp, Childs Neurol Serv, 55 Fruit St, Boston, MA 02114 USA. 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Investigation in animal models of the consequences of interactions between host response genes and microbes, toxins, and other environmental agents in a temporal context may elucidate the pathophisiology of a wide spectrum of chronic diseases. Here we review the evidence that infectious and immune factors may contribute to the pathogenesis of neurodevelopmental disorders, describe an animal model of neurodevelopmental disorders based upon viral infection, identify processes by which neural circuitry may be compromised, and outline plans for translational research in animal models and prospective human birth cohorts. C1 Columbia Univ, Mailman Sch Publ Hlth, Ctr Immunopathogenesis & Infect, New York, NY 10032 USA. RP Lipkin, WI (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Ctr Immunopathogenesis & Infect, 722 W 168th St, New York, NY 10032 USA. 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8SQ, WEST SUSSEX, ENGLAND SN 1528-2511 BN 978-0-470-85099-2 J9 NOVART FDN SYMP PY 2003 VL 251 BP 129 EP 148 PG 20 WC Medicine, General & Internal; Neurosciences; Psychiatry SC General & Internal Medicine; Neurosciences & Neurology; Psychiatry GA BGN65 UT WOS:000248830100008 PM 14521191 ER PT S AU Frith, C AF Frith, Chris BE Bock, G Goode, J TI What do imaging studies tell us about the neural basis of autism? SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID HUMAN CEREBRAL-CORTEX; HUMAN VISUAL-CORTEX; FUSIFORM FACE AREA; CHILDHOOD AUTISM; FACIAL EXPRESSIONS; ASPERGER-SYNDROME; INFANTILE-AUTISM; FUNCTIONAL MRI; TEMPORAL-LOBE; BLOOD-FLOW AB There is no clear evidence from imaging studies for specific structural abnormalities in the brains of people with autism. The most robust observation is of greater total brain volume. There is evidence that this greater volume is not present at birth, but appears during the first few years. This brain enlargement might be a marker of abnormal connectivity due to lack of pruning. While abnormalities have often been reported in the cerebellum and the amygdala, these are difficult to interpret since both increases and decreases in the size of these structures have been observed. Another way of identifying the neural basis of autism is to investigate brain systems underlying cognitive functions compromised in this disorder such as face perception and 'theory of mind'. Autistic people fail to activate the 'fusiform face area' during face perception tasks and show weak activation of medial frontal cortex and superior temporal gyrus when performing theory of mind tasks. These problems stem from a lack of integration of sensory processing with cognitive evaluation. I speculate that this problem reflects a failure of top-down modulation of early sensory processing. The problem could result from abnormal connectivity and lack of pruning. C1 Inst Neurol, Wellcome Dept Imaging Neurosci, London WC1N 3BG, England. 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Corbett, Blythe A. BE Bock, G Goode, J TI The amygdala, autism and anxiety SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID MEDIAL TEMPORAL-LOBE; BRAIN; CHILDREN; MONKEYS; IMPAIRMENT; DISORDERS; PRIMATES; BEHAVIOR; EMOTION; VOLUMES AB Brothers has proposed that the amygdala is an important component of the neural network that underlies social cognition. And Bauman and Kemper observed signs of neuropathology in the amygdala of the post-mortem autistic brain. These findings, in addition to recent functional neuroimaging data, have led Baron-Cohen and colleagues to propose that dysfunction of the amygdala may be responsible, in part, for the impairment of social functioning that is a hallmark feature of autism. Recent data from studies in our laboratory on the effects of amygdala lesions in the macaque monkey are at variance with a fundamental role for the amygdala in social behaviour. If the amygdala is not essential for normal social behaviour, as seems to be the case in both non-human primates and selected patients with bilateral amygdala damage, then it is unlikely to be the substrate for the abnormal social behaviour of autism. However, damage to the amygdala does have an effect on a monkey's response to normally fear-inducing stimuli, such as snakes, and removes a natural reluctance to engage novel conspecifics in social interactions. These findings lead to the conclusion that an important role for the amygdala is in the detection of threats and mobilizing an appropriate behavioural response, part of which is fear. If the amygdala is pathological in subjects with autism, it may contribute to their abnormal fears and increased anxiety rather than their abnormal social behaviour. 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SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEVELOPMENTAL DELAY; SPECTRUM DISORDER; CENTRAL COHERENCE; MIND IMPAIRMENTS; YOUNG-CHILDREN; ABILITY; LESIONS; MONKEY; SKILLS AB The aim of this paper is to provoke discussion concerning the nature of the cognitive impairments that characterize autism. Autism spectrum disorders appear to be heterogeneous at the biological and behavioural levels, but it is currently unclear whether one or more cognitive abnormalities may be universal to people with autism. In addition, it is unknown whether one cognitive deficit is primary and causal, or whether several complimentary accounts are needed to explain the full range of behavioural features. From research to date, it seems that the psychological abnormalities that characterize autism may be dissociable, and it is uncertain whether the degree of social and non-social impairments is related. Possible reasons for the co-occurrence of social and non-social cognitive abnormalities in autism are discussed. One implication is that searching for the biological bases of specific social and non-social deficits may be more profitable than searching for the aetiology of autism per se. C1 Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London SE5 8AF, England. RP Happe, F (reprint author), Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, De Crespigny Pk, Denmark Hill, London SE5 8AF, England. 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M. BE Bock, G Goode, J TI Autism and specific language impairment: categorical distinction or continuum? SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID FOLLOW-UP; INFANTILE-AUTISM; CONTROL CHILDREN; DISORDER; SPECTRUM AB Traditionally, autism and specific language impairment (SLI) are regarded as distinct disorders, with differential diagnosis hinging on two features. First, in SLI one sees isolated language impairments in the context of otherwise normal development, whereas in autism a triad of impairments is seen, affecting communication, social interaction and behavioural repertoire. Second, there are different communication problems in these two conditions. Children with SLI have particular difficulty with structural aspects of language (phonology and syntax). In contrast, abnormal use of language (pragmatics) is the most striking feature of autism. However, recently, this conventional view has been challenged on three counts. First, children with autism have structural language impairments similar to those in SLI. Second, some children have symptorns intermediate between autism and SLI. Third, there is a high rate of language impairments in relatives of people with autism, suggesting aetiological continuities between SLI and autism. One interpretation of these findings is to regard autism as 'SLI plus', i.e. to assume that the only factor differetiating the disorders is the n presence of additional impairments in autism. It is suggested that a more plausible interpretation is to regard structural and pragmatic language impairments as correlated but separable consequences of common underlying risk factors. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. 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BE Bock, G Goode, J TI Why have drug treatments been so disappointing? SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID WHOLE-BLOOD SEROTONIN; PERVASIVE DEVELOPMENTAL DISORDERS; ADRENOCORTICOTROPIC HORMONE 4-9; AUTISTIC-CHILDREN; INFANTILE-AUTISM; CEREBROSPINAL-FLUID; 5-HYDROXYINDOLEACETIC ACID; AMINE METABOLITES; ACTH-(4-9) ANALOG; HOMOVANILLIC-ACID AB The title of this contribution involves two consecutive questions: have the effects of medication in autism indeed been disappointing? And if so, why? The answer to the first question depends on whether one focuses on the core social and communicative deficits of autism, or on various complicating behaviour problems. Attempts over the past decades to develop drugs that specifically improve social and communicative functioning have failed. Among the most ambitious attempts were medical interventions in the endoenous opioid system that were motivated from 9 animal models on the involvement of this system in various aspects of social behaviour. By contrast, medications such as the newer antipsychotics, psychostimulants, presynaptic noradrenergic blocking agents (clonidine and guanfacine) and selective serotonin reuptake inhibitors were shown to reduce impairing complicating symptoms of affective instability, irritability, hyperactivity and inattentiveness, aggression, self-injury and stereotypies. The explanation for the medication-refractory status of social and communicative deficits should be sought in at least two related factors: (1) the as yet unidentified neurochemical basis of autism, and (2) the obvious lack of involvement of the main neurotransmitter systems (dopamine, noradrenaline and serotonin) in the pathophysiology of social and communicative behaviour. 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SO AUTISM: NEURAL BASIS AND TREATMENT POSSIBILITIES SE NOVARTIS FOUNDATION SYMPOSIUM LA English DT Article; Proceedings Paper CT Symposium on Autism - Neural Basis and Treatment Possibilities CY JUN 18-20, 2002 CL London, ENGLAND HO Novartis Fdn ID YOUNG-CHILDREN; SPECTRUM DISORDERS; FOLLOW-UP; BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; FUTURE-DIRECTIONS; ASPERGER-SYNDROME; COMMUNICATION; TRIAL; ADOLESCENTS AB Interventions for autism have come a long way since the condition was described by Kanner in the 1940s. At that time, autism was considered to be closely linked to schizophrenia, and inadequate parenting was viewed as the principal cause. Psychoanalysis was often the therapy of choice, but there was also widespread use of the drugs and even electroconvulsive treatments that had been developed for use in schizophrenia. Over the years, as autism has come to be recognized as a developmental disorder, interventions have focused instead on enhancing developmental skills and on ways of ameliorating behavioural difficulties. Recognition of the role that language deficits in particular play in causing behaviour problems has led to a focus on the teaching of more effective communication skills. The need for early support for families and appropriate education is also widely acknowledged. Nevertheless, follow-up studies indicate that the prognosis for the majority of individuals with autism remains poor. And despite claims to the contrary, there is little evidence that very early, intensive interventions can significantly alter the long-term course of the disorder. The paper discusses findings from follow-up studies over the years and assess the impact of different intervention procedures on outcome. C1 St George Hosp, Sch Med, Dept psychol, London SW17 0RE, England. 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One such system supports the development of face processing. Dawson and colleagues found that 3 year old children with autism failed to show differential eventrelated potentials (ERPs) to photographs of their mother's versus a stranger's face. Since differential ERP activity to familiar and unfamiliar faces is typically present by 6 months, this represents early brain dysfunction. McPartland and colleagues found that the face-specific ERP component ('N170') is atypical in older individuals with autism. N170 is typically larger to faces than non-faces, and prominent over the right hemisphere. In individuals with autism, N170 was larger for furniture than faces and bilaterally distributed. Biology and experience contribute to the development of face-processing systems. Newborns are capable of recognizing faces. Early face recognition abilities are thought to be served by a subcortical system, which is replaced by an experience-dependent cortical system. 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RP Hamilton, D (reprint author), Monash Univ, Clayton, Vic 3168, Australia. CR Lawson W., 2001, UNDERSTANDING WORKIN NR 1 TC 0 Z9 0 PU AUSTRALIAN ACAD PRESS PI BOWEN HILLS PA 32 JEAYS ST, BOWEN HILLS, QLD 4006, AUSTRALIA SN 0813-4839 J9 BEHAV CHANGE JI Behav. Change PY 2003 VL 20 IS 2 BP 124 EP 124 PG 1 WC Psychology, Clinical SC Psychology GA 767TX UT WOS:000188469700007 ER PT J AU Le Grice, B AF Le Grice, B TI Enabling communication in children with autism SO BEHAVIOUR CHANGE LA English DT Book Review C1 Christchurch Coll Educ, Ctr Special Educ, Christchurch, New Zealand. RP Le Grice, B (reprint author), Christchurch Coll Educ, Ctr Special Educ, Christchurch, New Zealand. CR Bondy Andrew S., 1998, Seminars in Speech and Language, V19, P373, DOI 10.1055/s-2008-1064055 Potter C., 2001, ENABLING COMMUNICATI Schwartz IS, 1998, TOP EARLY CHILD SPEC, V18, P144 NR 3 TC 0 Z9 0 PU AUSTRALIAN ACAD PRESS PI BOWEN HILLS PA 32 JEAYS ST, BOWEN HILLS, QLD 4006, AUSTRALIA SN 0813-4839 J9 BEHAV CHANGE JI Behav. Change PY 2003 VL 20 IS 4 BP 237 EP 238 PG 2 WC Psychology, Clinical SC Psychology GA 823IS UT WOS:000221605100011 ER PT J AU Tani, P Lindberg, N Nieminen-von Wendt, T von Wendt, L Alanko, L Appelberg, B Porkka-Heiskanen, T AF Tani, Pekka Lindberg, Nina Nieminen-von Wendt, Taina von Wendt, Lennart Alanko, Lauri Appelberg, Bjorn Porkka-Heiskanen, Tarja TI Insomnia is a frequent finding in adults with Asperger syndrome SO BMC PSYCHIATRY LA English DT Article AB Background: Asperger syndrome (AS) is a neurodevelopmental disorder belonging to autism spectrum disorders with prevalence rate of 0,35% in school-age children. It has been most extensively studied in childhood while there is scarcity of reports concerning adulthood of AS subjects despite the lifelong nature of this syndrome. In children with Asperger syndrome the initiation and continuity of sleep is disturbed because of the neuropsychiatric deficits inherent of AS. It is probable that sleep difficulties are present in adulthood as well. Our hypothesis was that adults with AS suffer from difficulty in initiating and maintaining sleep and nonrestorative sleep (insomnia). Methods: 20 AS without medication were compared with 10 healthy controls devoid of neuropsychiatric anamnesis. Clinical examination, blood test battery and head MRI excluded confounding somatic illnesses. Structured psychiatric interview for axis-I and axis-II disorders were given to both groups as well as Beck Depression Inventory and Wechsler adult intelligence scale, revised version. Sleep quality was assessed with sleep questionnaire, sleep diary during 6 consecutive days and description of possible sleep problems by the participants own words was requested. Results: compared with controls and with normative values of good sleep, AS adults had frequent insomnia. In sleep questionnaire 90% (18/20), in sleep diary 75% (15/20) and in free description 85% (17/20) displayed insomnia. There was a substantial psychiatric comorbidity with only 4 AS subject devoid of other axis-I or axis-II disorders besides AS. Also these persons displayed insomnia. It can be noted that the distribution of psychiatric diagnoses in AS subjects was virtually similar to that found among patient with chronic insomnia. Conclusions: the neuropsychiatric deficits inherent of AS predispose both to insomnia and to anxiety and mood disorders. Therefore a careful assessment of sleep quality should be an integral part of the treatment plan in these individuals. Conversely, when assessing adults with chronic insomnia the possibility of autism spectrum disorder as one of the potential causes of this condition should be kept in mind. C1 [Tani, Pekka; Lindberg, Nina; Appelberg, Bjorn] Univ Helsinki, Dept Psychiat, FIN-00014 Helsinki, Finland. [Nieminen-von Wendt, Taina; von Wendt, Lennart] Univ Helsinki, Hosp Children & Adolescents, Cent Hosp, FIN-00014 Helsinki, Finland. [Tani, Pekka; Alanko, Lauri; Porkka-Heiskanen, Tarja] Univ Helsinki, Inst Biomed, FIN-00014 Helsinki, Finland. RP Tani, P (reprint author), Univ Helsinki, Dept Psychiat, FIN-00014 Helsinki, Finland. EM pekka.tani@pp.inet.fi; nina.lindberg@pp3.inet.fi; taina.nieminen@sgic.fi; lennart.von.Wendt@hus.fi; lauri.alanko@helsinki.fi; bjorn.appelberg@hus.fi; porkka@cc.helsinki.fi FU Helsinki University Hospital [EVO: TYH 9233]; Yrjo Jahnsson Foundation; Finnish Psychiatric Association FX We wish to thank Miss Anna-Maarit Penttila for excellent technical assistance, Professor Dag Stenberg for useful advice in the course of the work, Tuula Kulomaki M.Sc, Anne Avellan M.Sc, and Jan-Henry Stenberg M.Sc for psychological assessment of the participants. The Research was funded by the Helsinki University Hospital (EVO: TYH 9233). Yrjo Jahnsson Foundation and The Finnish Psychiatric Association, provided additional funding. 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Med. Bull. PY 2003 VL 68 BP 209 EP 225 DI 10.1093/bmb/ldg029 PG 17 WC Medicine, General & Internal SC General & Internal Medicine GA 771NG UT WOS:000188791900013 PM 14757719 ER PT J AU Hessel, L AF Hessel, L TI Mercury in vaccines SO BULLETIN DE L ACADEMIE NATIONALE DE MEDECINE LA French DT Article DE vaccines; mercury; thimerosal; hypersensitivity; behavioral symptoms ID THIMEROSAL; AUTISM; THIOMERSAL AB Thiomersal, also called thimerosal, is an ethyl mercury derivative used as a preservative to prevent bacterial contamination of multidose vaccine vials after they have been opened Exposure to low doses of thiomersal has essentially been associated with hypersensitivity reactions. Nevertheless there is no evidence that allergy to thiomersal could be induced by thiomersal-containing vaccines. Allergy to thiomersal is usually of delayed-hypersensitivity type, but its detection through cutaneous tests is not very reliable. Hypersensitivity to thiomersal is not considered as a contraindication to the use of thiomersal-containing vaccines. In 1999 in the USA, thiomersal was present in approximately 30 different childhood vaccines, whereas there were only 2 in France. Although there were no evidence of neurological toxicity in infants related to the use of thiomersal-containing vaccines, the FDA considered that the cumulative dose of mercury received by young infants following vaccination was high enough (although lower than the FDA threshold for methyl mercury) to request vaccine manufacturers to remove thiomersal from vaccine formulations. Since 2002, all childhood vaccines used in Europe and the USA are thiomersal-free or contain only minute amounts of thiomersal. Recently published studies have shown that the mercury levels in the blood, faeces and urine of children who had received thiomersal-containing vaccines were much lower than those accepted by the American Environmental Protection Agency. It has also been demonstrated that the elimination of mercury in children was much faster than what was expected on the basis of studies conducted with methyl mercury originating from food. Recently, the hypothesis that mercury contained in vaccines could be the cause of autism and other neurological developmental disorders created a new debate in the medical community and the general public. To date, none of the epidemiological studies conducted in Europe and elsewhere support this assumption. Although any effort should be made to avoid useless exposure of vaccinees to a potentially toxic compound, it should be emphasised that 1) public communication on this issue has led to a decrease in the hepatitis B vaccination coverage of children born to HBs Ag positive mothers in the US; 2) this issue was not really relevant in France where until 2002, apart from two hepatitis B vaccines, all childhood vaccines were thiomersal-free, and 3) in developing countries using multidose vaccine vials, moving to thiomersal-free vaccines in unidose presentations would represent such an incremental cost that millions of children would no more have access to vaccination. Therefore the World Health Organisation still recommends the use of thiomersal-containing vaccines as part of the expanded programme of immunisation. C1 Aventis Pasteur, Affaires Med & Publ, Europe, F-69367 Lyon 07, France. RP Hessel, L (reprint author), Aventis Pasteur, Affaires Med & Publ, Europe, 8 Rue Jones Salk, F-69367 Lyon 07, France. 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Acad. Natl. Med. PY 2003 VL 187 IS 8 BP 1501 EP 1510 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 808DR UT WOS:000220550300022 PM 15146581 ER PT J AU Pletnikov, MV Rubin, SA Moran, TH Carbone, KM AF Pletnikov, MV Rubin, SA Moran, TH Carbone, KM TI Exploring the cerebellum with a new tool: neonatal Borna disease virus (BDV) infection of the rat's brain SO CEREBELLUM LA English DT Article DE Borna; cerebellum; developmental disorders; animal models ID CENTRAL-NERVOUS-SYSTEM; LYMPHOCYTIC CHORIOMENINGITIS VIRUS; PURKINJE-CELL DEGENERATION; HIPPOCAMPAL DENTATE GYRUS; RECEPTOR GENE-EXPRESSION; NEURODEVELOPMENTAL DAMAGE; POSTNATAL-DEVELOPMENT; PERSISTENT INFECTION; CHEMOKINE RECEPTOR; BIPOLAR DISORDER AB Cerebellar pathology has been associated with a number of developmental behavioral disorders, including autism spectrum disorders. Despite the fact that perinatal virus infections have been implicated in neurodevelopmental damage, few animal models have been developed to study the pathogenesis involved. One of the most interesting in vivo models of virus-induced cerebellar damage is the neonatal Borna disease virus (BDV) infection of the rat brain. The present review describes molecular, cellular, neuroanatomical, neurochemical and behavioral features of the BDV model and also provides a basis for a new understanding of the pathogenic mechanisms of cerebellar malformation and associated behavioral deficits. 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. US FDA, Ctr Biol Evaluat & Res, OD, Bethesda, MD USA. US FDA, Ctr Biol Evaluat & Res, LPRVD, DVP,OVRR, 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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The sample of 77 patients of autistic spectrum was examined (61 boys, 16 girls) with average age of 9.1 + 5.3 years. The observation scale CARS, semi-structured interview ADI-R, Stanford-Binet intelligence test, and Gessel's developmental scale were used in the examination. The clinical neurological examination included the EEG examination, too. 79.7 % of patients in the sample were mentally retarded. Epilepsy was found in 17 patients (22.1 %). The total mean score in CARS was 37.3 + 6.7 and it did not correlate significantly with the occurrence of epilepsy. The epilepsy was correlated significantly positively to CARS scale items number 2 ("imitation", p < 0.001) and 7 ("visual response", p < 0.001) and to subscales of ADI-R questionnaire "lack of shared enjoyment" (p = 0.02), "inability to compensate the missing speech by gestures" (p = 0.006), and "lack of spontaneous symbolic or social imitative play" (p = 0.012). 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A review of issues related to external validity is provided that points out the limitations of current research and lists several potentially beneficial areas of investigation into the nosologic status of the condition. It concludes with a discussion of the unequivocal need of individuals with severe social disabilities for comprehensive and adequate educational services and other treatments, regardless of the fact that the validity and usefulness of this specific diagnostic concept is far from resolved. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Klin, A (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA. 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PD JAN PY 2003 VL 12 IS 1 BP 1 EP + DI 10.1016/S1056-4993(02)00052-4 PG 14 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200003 PM 12512395 ER PT J AU Fombonne, E Tidmarsh, L AF Fombonne, E Tidmarsh, L TI Epidemiologic data on Asperger disorder SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID PRESCHOOL-CHILDREN; TOTAL POPULATION; AUTISM AB In 1944, Asperger described a syndrome that was subsequently given his name, although there is evidence from earlier European literature that clinical descriptions matching this disorder were available in the 1920s. Asperger's work was largely ignored until the seminal article by Wing, however, which led to a resurgence of interest in this diagnostic concept. Asperger disorder (AD) was only introduced as a separate diagnostic category in the latest revisions of ICD-10 and DSM-IV. Epidemiologic research on this disorder has only started in recent years and therefore data are still scarce on the prevalence of this syndrome. This article reviews available epidemiologic surveys that have shed light on the prevalence of AD. C1 McGill Univ, Dept Psychiat, Montreal Childrens Hosp, Montreal, PQ H3Z 1P2, Canada. RP Fombonne, E (reprint author), McGill Univ, Dept Psychiat, Montreal Childrens Hosp, 4018 St Catherine St W, Montreal, PQ H3Z 1P2, Canada. 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Psychiatr. N. Am. PD JAN PY 2003 VL 12 IS 1 BP 15 EP + DI 10.1016/S1056-4993(02)00050-0 PG 9 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200004 PM 12512396 ER PT J AU Towbin, KE AF Towbin, KE TI Strategies for phan-nacologic treatment of high functioning autism and Asperger syndrome SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN REUPTAKE INHIBITORS; POSITRON-EMISSION-TOMOGRAPHY; DOUBLE-BLIND; MENTAL-RETARDATION; OPEN-LABEL; SELF-INJURY; OPEN TRIAL; CHILDREN; ADULTS AB There are valuable strategies that can be applied when providing medication to individuals with Asperger syndrome (AS) and high functioning autism (HFA). The treatment of complex, polymorphous disorders like HFA/AS always brings particular challenges to pharmacotherapy. The specific characteristics presented by HFA/AS introduce unique complications and place unusual demands on a clinician's skill and experience. 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PD JAN PY 2003 VL 12 IS 1 BP 47 EP + DI 10.1016/S1056-4993(02)00056-1 PG 18 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200006 PM 12512398 ER PT J AU Attwood, T AF Attwood, T TI Frameworks for behavioral interventions SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID HIGH-FUNCTIONING CHILDREN; ASPERGER-SYNDROME; EXECUTIVE FUNCTIONS; FAMILY HISTORY; AUTISM; DISORDER; MIND; ADULTS; ATTRIBUTION; ADOLESCENTS AB This article examines two frameworks for behavioral interventions, namely the developmental stages in friendship skills with remedial strategies for each stage, and modifications to Cognitive Behavior Therapy to accommodate the unusual profile of cognitive skills of people with Asperger disorder. C1 Aspergers Syndrome Clin, Petrie, Qld 4502, Australia. RP Attwood, T (reprint author), Aspergers Syndrome Clin, POB 224, Petrie, Qld 4502, Australia. CR Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 American Psychiatric Association, 2000, DIAGN STAT MAN MENT ASTON M, 2001, OTHER HALF ASPERGERS Attwood T., 1998, ASPERGERS SYNDROME G Baron-Cohen S, 1999, J AUTISM DEV DISORD, V29, P407, DOI 10.1023/A:1023035012436 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 BERTHIER ML, 1995, NEUROPSY NEUROPSY BE, V8, P222 Blackshaw AJ, 2001, AUTISM, V5, P147, DOI 10.1177/1362361301005002005 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Bryson S. 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J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Werth A, 2001, AUTISM, V5, P111, DOI 10.1177/1362361301005002002 NR 57 TC 23 Z9 23 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD JAN PY 2003 VL 12 IS 1 BP 65 EP + DI 10.1016/S1056-4993(02)00054-8 PG 23 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200007 PM 12512399 ER PT J AU Paul, R AF Paul, R TI Promoting social communication in high functioning individuals with autistic spectrum disorders SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID SCRIPT-FADING PROCEDURE; YOUNG-CHILDREN; TEACHING-CHILDREN; FACILITATE SOCIALIZATION; PROSODY CHARACTERISTICS; SEVERE DISABILITIES; PRESCHOOL-CHILDREN; INTERACTION SKILLS; PEER-INITIATION; BEHAVIOR-CHANGE AB This article reviews a range of social communication interventions that have been developed for students with autism at the preschool, school age, and adolescent level. Adult-mediated and peer-mediated methods that use highly structured, child-centered, and hybrid methods are examined. Programs that provide information on generalization and maintenance are identified. A set of recommendations for programs that would seem to be most appropriate for students with Asperger syndrome is presented. C1 So Connecticut State Univ, Dept Commun Disorders, New Haven, CT 06520 USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Paul, R (reprint author), So Connecticut State Univ, Dept Commun Disorders, 501 Crescent St, New Haven, CT 06520 USA. 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L., 1993, INTEGRATING YOUNG CH, P39 ODOM SL, 1994, EXCEPT CHILDREN, V60, P226 ODOM SL, 1992, J APPL BEHAV ANAL, V25, P307, DOI 10.1901/jaba.1992.25-307 Odom SL, 1999, TOP EARLY CHILD SPEC, V19, P75, DOI 10.1177/027112149901900202 ODOM SL, 1986, J APPL BEHAV ANAL, V19, P59, DOI 10.1901/jaba.1986.19-59 OKE NJ, 1990, J AUTISM DEV DISORD, V20, P479, DOI 10.1007/BF02216054 Owens R. E, 1996, LANGUAGE DEV OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 PATTERSON J, 1994, COMMUNICATION DEV FD, P135 Pierce K, 1997, J APPL BEHAV ANAL, V30, P157, DOI 10.1901/jaba.1997.30-157 PIERCE K, 1995, J APPL BEHAV ANAL, V28, P285, DOI 10.1901/jaba.1995.28-285 Quill K. 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R., 2000, ASPERGER SYNDROME, P340 Whitaker P., 1998, BR J SPEC ED, V25, P60, DOI 10.1111/1467-8527.t01-1-00058 Wolfberg P., 1999, CHILD LANG TEACH THE, V15, P41, DOI 10.1191/026565999667036164 Wolfberg P. J., 1999, PLAY IMAGINATION CHI NR 82 TC 39 Z9 39 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD JAN PY 2003 VL 12 IS 1 BP 87 EP + DI 10.1016/S1056-4993(02)00047-0 PG 22 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200008 PM 12512400 ER PT J AU Krasny, L Williams, BJ Provencal, S Ozonoff, S AF Krasny, L Williams, BJ Provencal, S Ozonoff, S TI Social skills interventions for the autism spectrum: essential ingredients and a model curriculum SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID CHILDREN; ADOLESCENTS; ADULTS AB Despite the widespread recognition that social deficits are core features of autism spectrum disorders, few treatment programs for improving social adaptation have been developed. Curricula designed to practice social skills in a group setting are vital, but few are yet commercially available. This article outlines several elements the authors believe are important to successful group social skills intervention, provides specific examples translating these principles into actual practice, and includes illustrations from social skills groups conducted at the University of Utah. C1 Univ Utah, Dept Psychiat, Salt Lake City, UT 84108 USA. Univ Calif Davis, Hlth Syst, Dept Psychiat, MIND Inst, Sacramento, CA 95817 USA. RP Krasny, L (reprint author), Univ Utah, Dept Psychiat, 421 Wakava Way,Suite 143, Salt Lake City, UT 84108 USA. CR Gardner H., 1983, FRAMES MIND THEORY M Goldstein A.P, 1988, PREPARE CURRICULUM T Gray C., 1995, TEACHING CHILDREN AU, P219 Gray C.A., 1998, ASPERGER SYNDROME HI, P167 Gutstein S, 2002, RELATIONSHIP DEV INT HOWLIN P, 1993, AUTISM, V3, P299 Howlin P., 1998, AUTISM PERVASIVE DEV, P209 Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 KRASNY L, UNPUB MANUAL PROGR C MARRIAGE KJ, 1995, AUST NZ J PSYCHIAT, V29, P58, DOI 10.3109/00048679509075892 MCAFFEE J, 2001, NAVIGATING SOCIAL WO Mesibov G., 1992, HIGH FUNCTIONING IND, P143 MESIBOV GB, 1984, J AUTISM DEV DISORD, V14, P395, DOI 10.1007/BF02409830 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 PROVENCAL S, UNPUB U UTAH ADOLESC Quill K. A., 2000, DO WATCH LISTEN SAY Quill KA, 1997, J AUTISM DEV DISORD, V27, P697, DOI 10.1023/A:1025806900162 Schopler E., 1995, LEARNING COGNITION A, P243 Sheridan S., 1995, TOUGH KID SOCIAL SKI Strain PS, 2000, TOP EARLY CHILD SPEC, V20, P116, DOI 10.1177/027112140002000207 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Weiss MJ, 2001, BEHAV MODIF, V25, P785, DOI 10.1177/0145445501255007 Whitaker P., 1998, BR J SPEC ED, V25, P60, DOI 10.1111/1467-8527.t01-1-00058 WILLIAMS TI, 1989, J AUTISM DEV DISORD, V19, P143, DOI 10.1007/BF02212726 WINNER MG, 2000, INSIDE WHAT MAKES PE NR 26 TC 61 Z9 61 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD JAN PY 2003 VL 12 IS 1 BP 107 EP + DI 10.1016/S1056-4993(02)00051-2 PG 17 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200009 PM 12512401 ER PT J AU Tantam, D AF Tantam, D TI The challenge of adolescents and adults with Asperger syndrome SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID FUNCTIONING AUTISM; EPIDEMIOLOGY; SPECTRUM AB Despite the rapid growth of interest in Asperger disorder in children, there continues to be a lack of awareness of the diagnosis and its implications for adolescents and adults. The reasons for this lack of awareness lie in the history of the disorder and in the historical development of mental health services. Because, as Santayana wrote, "Those who cannot remember the past are condemned to repeat it," this article reprises some of the history given elsewhere in this issue, but in a highly partial way, to bring out what the author believes to be the historically grounded prejudices that are the first challenge to anyone wanting to help adolescents and adults with Asperger syndrome. C1 Univ Sheffield, Sch Hlth & Related Res, Ctr Study Conflict & Reconciliat, Sheffield S1 4DA, S Yorkshire, England. RP Tantam, D (reprint author), Univ Sheffield, Sch Hlth & Related Res, Ctr Study Conflict & Reconciliat, Regents Court,30 Regent St, Sheffield S1 4DA, S Yorkshire, England. CR Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Asperger H., 1979, COMMUNICATION, V13, P45 Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 BARNARD J, 2001, IGNORED INELIGIBLE Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 BURGOINE E, 1983, BRIT J PSYCHIAT, V143, P261, DOI 10.1192/bjp.143.3.261 DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 *DEP HLTH, 2002, NAT SERV FRAM MENT H *DEP MENT RET, 2001, ADV COMM SERV SUPP P Department of Health, 2001, VAL PEOPL NEW STRAT Fitzgerald M, 2001, J AM ACAD CHILD PSY, V40, P870, DOI 10.1097/00004583-200108000-00006 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Kanner L, 1943, NERV CHILD, V2, P217 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 MAWSON D, 1985, BRIT J PSYCHIAT, V147, P566, DOI 10.1192/bjp.147.5.566 Mayes SD, 2001, J ABNORM CHILD PSYCH, V29, P263, DOI 10.1023/A:1010337916636 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P537, DOI 10.1017/S0021963099003935 SCHOPLER E, 1998, ASPERGER SYNDROME HI, P3 TANTAM D, 1993, J AUTISM DEV DISORD, V23, P111, DOI 10.1007/BF01066422 TANTAM D, 1988, BRIT J PSYCHIAT, V153, P777, DOI 10.1192/bjp.153.6.777 TANTAM D, 1988, MIND THEIR OWN Tinbergen N., 1983, AUTISTIC CHILDREN NE Van Deurzen E., 2001, EXISTENTIAL COUNSELL van KREVELEN D, 1962, Acta Paedopsychiatr, V29, P22 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1981, PSYCHOL MED, V11, P115 NR 29 TC 47 Z9 47 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD JAN PY 2003 VL 12 IS 1 BP 143 EP + DI 10.1016/S1056-4993(02)00053-6 PG 23 WC Psychiatry SC Psychiatry GA 629CQ UT WOS:000180033200011 PM 12512403 ER PT J AU Ricciardi, JN Luiselli, JK AF Ricciardi, JN Luiselli, JK TI Behavioral intervention to eliminate socially mediated urinary incontinence in a child with autism SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE urinary incontinence; toilet training; developmental disabilities; functional behavioral assessment; child autism AB We report the case of an 11-year old boy with autism who demonstrated urinary incontinence that appeared to be maintained by social contingencies (adult attention and escape from activity "demands"). Although he wet himself frequently, he also used the bathroom appropriately and made many self-initiated toileting requests. Intervention was implemented at a day-school by (1) having the boy wear a disposable diaper so immediate clothes changing was not required (escape extinction), (2) limiting requests to Use the bathroom, (3) withholding attention contingent on incontinence, and (4) praising in-toilet urinating. Another element of intervention was the systematic fading of the diaper. Urinary incontinence was eliminated, the diaper withdrawn, and improvement maintained 6 months post-intervention. (C) 2003 by The Haworth Press, Inc. All rights reserved. C1 May Inst Inc, Internship Program Clin Psychol, Norwood, MA 02062 USA. RP Ricciardi, JN (reprint author), May Inst Inc, Internship Program Clin Psychol, 1 Commerce Way, Norwood, MA 02062 USA. 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PY 2003 VL 25 IS 4 BP 53 EP 63 DI 10.1300/J019v25n04_04 PG 11 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 750YH UT WOS:000187025700004 ER PT J AU Murphy, JV Patil, AA AF Murphy, JV Patil, AA TI Stimulation of the nervous system for the management of seizures - Current and future developments SO CNS DRUGS LA English DT Review ID CENTROMEDIAN THALAMIC NUCLEUS; LENNOX-GASTAUT-SYNDROME; PARTIAL-ONSET SEIZURES; LEFT VAGAL NERVE; MEDICALLY REFRACTORY EPILEPSY; ACTIVE-CONTROL TRIAL; VAGUS NERVE; ELECTRICAL-STIMULATION; LONG-TERM; BLOOD-FLOW AB Vagal nerve stimulation (VNS) for the treatment of refractory epilepsy appears to have started from the theory that since VNS can alter the EEG, it may influence epilepsy. It proved effective in several models of epilepsy and was then tried in short-term, open-label and double-blind trials, leading to approval in Canada, Europe and the US. Follow-up observations in these patients demonstrated continued improvement in seizure control for up to 2 years. Close to 50% of treated patients have achieved at least a 50% reduction in seizure frequency. This therapy was also useful as rescue therapy for ongoing seizures in some patients; many patients are more alert. The initial trials were completed in patients greater than or equal to12 years of age with refractory partial seizures. Subsequently, similar benefits were shown in patients with tuberous sclerosis complex, Lennox-Gastaut syndrome, hypothalamic hamartomas and primary generalised seizures. Implanting the generator and leads is technically easy, and complications are few. The method of action is largely unknown, although VNS appears to alter metabolic activity in specific brain nuclei. Considering that improvement in mood is frequently found in patients using VNS, it has undergone trials in patients with depression. Other illnesses deserving exploration with this unusual therapy are Alzheimer's disease and autism. Some aspects of VNS have proven disappointing. Although patients have fewer seizures, the number of antiepileptic drugs they take is not significantly reduced. In addition, there is no way to accurately predict the end of life of the generator. Optimal stimulation parameters, if they exist, are unknown. Deep brain stimulation is a new method for controlling medically refractory seizures. It is based on the observation that thalamic stimulation can influence the EEG over a wide area. Several thalamic nuclei have been the object of stimulation in different groups of patients. Intraoperative brain imaging is essential for electrode placement. The procedure is done under local anaesthesia. Experience with this therapy is currently limited, but growing. C1 Childrens Mercy Hosp, Pediat Epilepsy Res Ctr, Kansas City, MO 64108 USA. Univ Nebraska, Med Ctr, Omaha, NE USA. RP Murphy, JV (reprint author), Childrens Mercy Hosp, Pediat Epilepsy Res Ctr, 2401 Gilham Rd, Kansas City, MO 64108 USA. 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P1005, DOI 10.1111/j.1528-1157.1992.tb01751.x ZABARA J, 1972, SPACE LIFE SCI, V3, P282, DOI 10.1007/BF00928176 Zabara J., 1985, ELECTROENCEPHALOGR C, V61, P162 2000, CYBERONICS JAN NR 88 TC 16 Z9 18 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PY 2003 VL 17 IS 2 BP 101 EP 115 DI 10.2165/00023210-200317020-00003 PG 15 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 644LW UT WOS:000180920300003 PM 12521358 ER PT J AU Russell, J Hala, S Hill, E AF Russell, J Hala, S Hill, E TI The automated windows task: the performance of preschool children, children with autism, and children with moderate learning difficulties SO COGNITIVE DEVELOPMENT LA English DT Article DE autism; windows task; executive function; theory of mind; pre-school ID STRATEGIC DECEPTION; EXECUTIVE CONTROL; FALSE BELIEF AB The windows task (a hybrid executive/theory of mind task) requires participants to infer the utility of indicating a box in which a desired object is absent, adjacent to one where it is visible, in the presence of an experimenter in a completive role, and to maintain this response over a number of subsequent trials. We presented two pairs of groups (3 years vs. 4 years and autism vs. MLD) with an automated version of the task in order to find out whether the main locus of difficulty was executive or social. In two conditions the required response was to press a button beneath the chosen box, and in two conditions the deceptive or the merely competitive element was maintained. In the deceptive condition the participant had to tell the opponent which button to press. Automation removed group differences in performance on the first 'inferential' experimental trial, although group differences did remain in performance across all trials. We argue that it was the novel response mode used in the automated task that made it easier than the standard versions: button pressing (or indicating in the deceptive condition) rather than reference to a location. We discuss this possibility with regard to the kind of inhibitory requirements made by theory of mind tasks. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3AD, England. Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Inst Cognit Neurosci, London, England. RP Russell, J (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3AD, England. 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PD JAN PY 2003 VL 40 IS 1 BP 95 EP 96 DI 10.1016/S0360-1315(02)00096-9 PG 2 WC Computer Science, Interdisciplinary Applications; Education & Educational Research SC Computer Science; Education & Educational Research GA 638QY UT WOS:000180582800006 ER PT J AU Atkins, GJ Cosby, SL AF Atkins, GJ Cosby, SL TI Is an improved measles-mumps-rubella vaccine necessary or feasible? SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review DE virus; biosafety; vector; recombinant vaccine; autism; inflammatory bowel disease ID INFLAMMATORY-BOWEL-DISEASE; SEMLIKI-FOREST-VIRUS; T-CELL EPITOPES; PERIPHERAL-BLOOD LYMPHOCYTES; IMMUNOSUPPRESSION IN-VITRO; POLYMERASE-CHAIN-REACTION; LOUPING-ILL VIRUS; ATYPICAL MEASLES; E1 GLYCOPROTEIN; IMMUNE-RESPONSES AB The measles-mumps-rubella (MMR) vaccine has been very effective in the elimination of disease and has high biosafety. However, it has been associated with several adverse effects and has recently caused controversy with regard to its possible association with inflammatory bowel disease and autism. This has been postulated to be a property of the measles component of the vaccine, and a "new variant" autism has recently been described and suggested to be associated with vaccine virus. Although one study has reported the presence of measles RNA in inflammatory bowel disease associated with autism, this has not been independently confirmed. This and most of the other demonstrated or perceived adverse effects of the MMR vaccine could theoretically be ascribed to its composition as a mixture of three live replicating viruses, one of which (measles) can induce immunosuppression, although this hypothesis is speculative. It may nonetheless be desirable to improve the biosafety of the MMR vaccine by the development of a nonreplicating vaccine that will stimulate efficient immunity and protection. 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Although impairment in reciprocal social interaction in individuals with Asperger syndrome is closely correlated to their impaired perceptional abilities in non-verbal communication, especially facial expression, overt prosopagnosia, seems to be a rare neuropsychological symptom in persons with autistic disorders. C1 Univ Heidelberg, Childrens Hosp, Dept Paediat Neurol, D-6900 Heidelberg, Germany. RP Pietz, J (reprint author), Univ Heidelberg, Dept Paediat Neurol, Neuenheimer Feld 150, D-69120 Heidelberg, Germany. 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PD JAN PY 2003 VL 45 IS 1 BP 55 EP 57 DI 10.1017/S0012162203000100 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 640TR UT WOS:000180704500010 PM 12549756 ER PT J AU Farran, EK Jarrold, O AF Farran, EK Jarrold, O TI Visuospatial cognition in Williams syndrome: Reviewing and accounting for the strengths and weaknesses in performance SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID SYNDROME PHENOTYPE; BLOCK DESIGN; INFANTILE HYPERCALCEMIA; CONSTRUCTIVE COGNITION; NONVERBAL ABILITIES; CENTRAL COHERENCE; CHILDREN; AUTISM; PROFILE; NEUROPSYCHOLOGY AB Individuals with Williams syndrome typically show relatively poor visuospatial abilities in comparison to stronger verbal skills. However, individuals' level of performance is not consistent across all visuospatial tasks. The studies assessing visuospatial functioning in Williams syndrome are critically reviewed, to provide a clear pattern of the relative difficulty of these tasks. 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PY 2003 VL 23 IS 1-2 BP 173 EP 200 DI 10.1207/S15326942DN231&2_8 PG 28 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 664MP UT WOS:000182065100008 PM 12730024 ER PT J AU Wellington, K Goa, KL AF Wellington, K Goa, KL TI Measles, mumps, rubella vaccine (Priorix (TM); GSK-MMR) - A review of its use in the prevention of measles, mumps and rubella SO DRUGS LA English DT Review DE measles-mumps-rubella vaccine; measles; mumps; rubella; MMR; immunisation; children ID INFLAMMATORY-BOWEL-DISEASE; ASEPTIC-MENINGITIS; HEALTHY-CHILDREN; MASS VACCINATION; EPIDEMIOLOGIC EVIDENCE; CAUSAL ASSOCIATION; VARICELLA VACCINE; NO EVIDENCE; FOLLOW-UP; AUTISM AB GSK-MMR (Priorix((TM))) is a trivalent live attenuated measles, mumps and rubella (MMR) vaccine which contains the Schwarz measles, the RIT 4385 mumps (derived from the Jeryl Lynn mumps strain) and the Wistar RA 27/3 rubella strains. GSK-MMR as a primary vaccination demonstrated high immunogenicity in clinical trials in >7500 infants aged 9-27 months, and was as immunogenic as Merck-MMR (MMR(R) II). However, antimumps seroconversion rates and geometric mean titres (GMTs) were significantly higher in infants receiving GSK-MMR compared with Berna-MMR (Triviraten(TM)) recipients. Coadministration of GSK-MMR with a varicella vaccine (Varilrix(TM); GSK-M-MR/V) did not significantly affect the immunogenicity of GSK-MMR. A persistent immune response to GSK-MMR has been demonstrated in follow-up data from several randomised trials. GMTs for measles, mumps and rubella antibodies remained high in GSK-MMR recipients 1-2 years post-vaccination and were similar to those in Merck-MMR recipients. The immunogenicity of GSK-MMR was high, and similar to that of Merck-MMR, when used as a second dose in children aged 4-6 or 11-12 years who had received a primary vaccination with Merck-MMR in their second year of life. Although there are no protective efficacy data concerning the GSK-MMR vaccine to date, the rubella Wistar RA 27/3 rubella and Schwarz measles strains have well established protective efficacy; the new RIT 4385 mumps strain is expected to afford similar protection from mumps to that achieved with mumps vaccines that contain the Jeryl Lynn mumps strain (e.g. Merck-MMR). GSK-MMR was well tolerated as a primary or secondary vaccination, and in most clinical studies comparing GSK-MMR with Merck-MMR as a primary vaccination in infants, GSK-MMR was associated with significantly fewer local adverse events (e.g. pain, swelling and redness). The incidence of local adverse events with GSK-MMR, GSK-MMR/V or Berna-MMR was similar. GSK-MMR and Merck-MMR were associated with similar rates of fever, rash and parotid gland swelling, but Berna-MMR was associated with a lower incidence of fever. In conclusion, GSK-MMR is a highly immunogenic MMR vaccine with good tolerability. In clinical trials, the immunogenicity of GSK-MMR was similar to that of Merck-MMR, and the mumps component was more effective at eliciting seroprotection than that of Berna-MMR. Furthermore, GSK-MMR causes fewer injection-site adverse events than Merck-MMR. As such, GSK-MMR is an attractive alternative for immunisation against measles, mumps and rubella. C1 Adis Int Ltd, Auckland 1310, New Zealand. RP Wellington, K (reprint author), Adis Int Ltd, 41 Centorian Dr,Private Bag 65901, Auckland 1310, New Zealand. 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Toxicology SC Pharmacology & Pharmacy; Toxicology GA 728PW UT WOS:000185726400012 PM 12962524 ER PT S AU Keltner, D AF Keltner, D BE Ekman, P Campos, JJ Davidson, RJ DeWaal, FBM TI Expression and the course of life - Studies of emotion, personality, and psychopathology from a social-functional perspective SO EMOTIONS INSIDE OUT: 130 YEARS AFTER DARWIN'S THE EXPRESSION OF THE EMOTIONS IN MAN AND ANIMALS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Emotions Inside Out, 130 Years after Darwins the Expression of the Emotions in Man and Animals CY NOV 16-17, 2002 CL New York, NY SP New York Acad Sci, Mushett Family Fdn DE facial expression; personality; psychopathology; emotion; social interaction; course of life ID FACIAL EXPRESSIONS; FEAR; EMBARRASSMENT; PREPAREDNESS; BEREAVEMENT; APPEASEMENT; RECOGNITION; PERCEPTION; RESPONSES; BEHAVIOR AB In this paper I discuss how expressive behavior relates to personality and psychopathology, integrating recent findins from my laboratory and the insights of Charles Darwin on this topic. In the first part of the paper I challenge the view, in part espoused by Darwin, that humans are equipped to convey only a limited number of emotions with nonverbal behavior. Our lab has documented displays for several emotions, including embarrassment, love, desire, compassion, gratitude, and awe, to name just a few states that previously were thought not to possess a distinct display. I then present an argument for how individual differences in emotion, although fleeting, shape the social environment. This argument focuses on the functions of nonverbal display: to provide information to others, to evoke responses, and to serve as incentives of preceding or ensuing social behavior. This reasoning sets the stage for the study of the relationships between personality, psychopathology, and expressive behavior, to which I turn in the final part of the paper. Here I show that basic personality traits (e.g., extraversion, agreeableness) and psychological disorders (e.g., externalizing disorder in children, autism) have expressive signatures that shape social interactions and environments in profound ways that might perpetuate and transmit the trait or disorder. C1 Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. RP Keltner, D (reprint author), Univ Calif Berkeley, Dept Psychol, 3210 Tolman Hall, Berkeley, CA 94720 USA. EM keltner@socrates.berkeley.edu CR Anderson C, 2003, J PERS SOC PSYCHOL, V84, P1054, DOI 10.1037/0022-3514.84.5.1054 Axelrod R., 1984, EVOLUTION COOPERATIO Barrett K. 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PY 2003 VL 1000 BP 222 EP 243 DI 10.1196/annals.1280.011 PG 22 WC History & Philosophy Of Science; Multidisciplinary Sciences; Psychology; Psychology, Multidisciplinary SC History & Philosophy of Science; Science & Technology - Other Topics; Psychology GA BY70Q UT WOS:000189443500016 PM 14766634 ER PT J AU Nystad, R Benan, N Jaeger-Dahlen, K AF Nystad, R Benan, N Jaeger-Dahlen, K TI Epilepsy and autism spectrum disorders: A programme for quality improvement in the treatment of epilepsy SO EPILEPSIA LA English DT Meeting Abstract CT 25th International Epilepsy Congress CY OCT 12-16, 2003 CL LISBON, PORTUGAL SP Int League Against Epilepsy, Int Bureau Epilepsy NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2003 VL 44 SU 8 BP 138 EP 138 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 758LV UT WOS:000187636400539 ER PT J AU Dahlgren, S Sandberg, AD Hjelmquist, E AF Dahlgren, S Sandberg, AD Hjelmquist, E TI The non-specificity of theory of mind deficits: Evidence from children with communicative disabilities SO EUROPEAN JOURNAL OF COGNITIVE PSYCHOLOGY LA English DT Article ID ASPERGERS SYNDROME; ATTENTIONAL DEFICITS; AUTISTIC-CHILDREN; FALSE BELIEF; MEMORY; PRESCHOOLERS; DISORDERS; MOTOR; REPRESENTATION; DECEPTION AB The aim of the present paper was to investigate the performance on theory of mind tasks of four different clinical groups: children with deficits in attention, motor control and perception (DAMP), children with autism, children with Asperger syndrome, and non-vocal cerebral-palsied children. The children with DAMP performed on the same level as the comparison group on the first and second order theory of mind task. The children with autism and Asperger syndrome performed somewhat lower than the children with DAMP and the comparison group. However, in respect of the specificity issue, only 6 out of 14 of the non-vocal participants successfully solved the first order theory of mind task, while 13 out of 14 children in a comparison group did. The children were matched for chronological age and IQ. The findings suggest that deficits in theory of mind are not specific to the autistic continuum, but can be found in other groups with communicative disabilities, implying that linguistic and communicative skills are important precursors in the development of theory of mind. The study also shows that severe dysfunction in attention, motor control, and perception is not associated with any theory of mind difficulties. C1 Gothenburg Univ, Dept Psychol, SE-40530 Gothenburg, Sweden. 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PD JAN PY 2003 VL 15 IS 1 BP 129 EP 155 DI 10.1080/09541440244000030 PG 27 WC Psychology, Experimental SC Psychology GA 638TG UT WOS:000180586300006 ER PT J AU Geerts, M Steyaert, J Fryns, JP AF Geerts, M Steyaert, J Fryns, JP TI The XYY syndrome: A follow-up study on 38 boys SO GENETIC COUNSELING LA English DT Article DE XYY syndrome; Y chromosome; prenatal diagnosis; autism; extreme male brain ID SEX-CHROMOSOME ANEUPLOIDY; 4TH DIGIT LENGTH; PLASMA TESTOSTERONE; INTRAUTERINE DIAGNOSIS; 47,XYY KARYOTYPE; MENTAL STATUS; Y-CHROMOSOME; MALES; ABNORMALITIES; CHILDREN AB In the last decade there has been a significant increase in the proportion of XYY males detected prenatally, mostly as a fortuitous finding. It is of utmost importance to obtain a clear idea of the developmental profile of boys with karyotype 47,XYY and of possible problem areas during further development in order to inform the parents correctly during pregnancy and to provide an adequate surveillance later on. In this study we observed 38 XYY males, of which 12 were diagnosed prenatally. We found that these patients are at considerably increased risk for delayed language - and/or motor development. From birth on, weight, height and head circumference are above average values. The majority attends kindergarten in the normal education circuit although in 50% of the cases psychosocial problems are documented. From primary school age on, there is an increased risk for child psychiatric disorders such as autism. Moreover, although normally intelligent, many of these boys are referred to special education programmes. C1 Univ Hosp Leuven, Ctr Human Genet, Louvain, Belgium. Univ Hosp Leuven, Div Child Psychiat, Louvain, Belgium. Univ Hosp Maastricht, Dept Clin Genet, Maastricht, Netherlands. RP Geerts, M (reprint author), Ctr Human Genet, Herestr 49, B-3000 Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 CR ABRAMS N, 1971, J GENET PSYCHOL, V118, P13 Abramsky L, 1997, PRENATAL DIAG, V17, P363, DOI 10.1002/(SICI)1097-0223(199704)17:4<363::AID-PD79>3.0.CO;2-O Andersen SL, 2000, NEUROSCI BIOBEHAV R, V24, P137, DOI 10.1016/S0149-7634(99)00044-5 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 BLACKMAN JA, 1991, DEV MED CHILD NEUROL, V33, P162 BOSCHBANYERAS JM, 1985, ANN GENET-PARIS, V28, P125 COHEN FL, 1985, J SCHOOL HEALTH, V55, P99 First MB, 2000, DIAGNOSTIC STAT MANU Fryns JP, 1998, PRENATAL DIAG, V18, P303 FRYNS JP, 1995, GENET COUNSEL, V6, P197 GILLBERG C, 1984, APPL RES MENT RETARD, V5, P353, DOI 10.1016/S0270-3092(84)80056-9 Gillberg C., 1992, BIOL AUTISTIC SYNDRO HUDSON B, 1969, LANCET, V2, P699 Okten A, 2002, EARLY HUM DEV, V70, P47, DOI 10.1016/S0378-3782(02)00073-7 Kroes M, 2002, J AM ACAD CHILD PSY, V41, P955, DOI 10.1097/00004583-200208000-00014 Linden MG, 2002, AM J MED GENET, V110, P3, DOI 10.1002/ajmg.10391 Linden MG, 1996, OBSTET GYNECOL, V87, P468, DOI 10.1016/0029-7844(95)00419-X LINDENMANN WK, 1990, PUBLIC RELAT REV, V16, P3, DOI 10.1016/S0363-8111(05)80001-3 MALLIN SR, 1972, CLIN GENET, V3, P490 Manning JT, 2001, DEV MED CHILD NEUROL, V43, P160, DOI 10.1017/S0012162201000317 Manning JT, 2000, MED HYPOTHESES, V54, P855, DOI 10.1054/mehy.1999.1150 Manning JT, 2002, MED HYPOTHESES, V59, P334, DOI 10.1016/S0306-9877(02)00181-0 Nicolson R, 1998, CAN J PSYCHIAT, V43, P619 Nielsen J, 1990, Birth Defects Orig Artic Ser, V26, P209 NIELSEN J, 1973, J AUTISM CHILD SCHIZ, V3, P5, DOI 10.1007/BF01537551 Nielsen J, 1990, Birth Defects Orig Artic Ser, V26, P201 PELZMANN KS, 1976, LIFE SCI, V18, P1207, DOI 10.1016/0024-3205(76)90195-8 PLASSE JC, 1970, ANN GENET-PARIS, V13, P90 PRICE WH, 1970, J ENDOCRINOL, V47, P117, DOI 10.1677/joe.0.0470117 RATCLIFFE SG, 1994, HORM RES, V42, P106, DOI 10.1159/000184157 RATCLIFFE SG, 1994, DEV MED CHILD NEUROL, V36, P533 Ratcliffe S G, 1990, Birth Defects Orig Artic Ser, V26, P1 Rhee SH, 1999, J ABNORM PSYCHOL, V108, P24, DOI 10.1037//0021-843X.108.1.24 Robinson A, 1990, Birth Defects Orig Artic Ser, V26, P59 ROBINSON A, 1992, AM J MED GENET, V44, P365, DOI 10.1002/ajmg.1320440319 Robinson A, 1990, Birth Defects Orig Artic Ser, V26, P225 ROBINSON A, 1989, AM J MED GENET, V34, P552, DOI 10.1002/ajmg.1320340420 RUDD B T, 1968, Journal of Medical Genetics, V5, P286, DOI 10.1136/jmg.5.4.286 SANTEN RJ, 1970, LANCET, V2, P371 SCHIAVI RC, 1984, ARCH GEN PSYCHIAT, V41, P93 SHARMA M, 1975, STEROIDS, V26, P175, DOI 10.1016/S0039-128X(75)80018-3 TANSLEY P, 1981, CHILDREN SPECIFIC LE Theilgaard A, 1984, Acta Psychiatr Scand Suppl, V315, P1 Theilgaard A, 1986, Birth Defects Orig Artic Ser, V22, P277 WALZER S, 1991, BIRTH DEF, V26, P45 WEIDMERMIKHAIL E, 1997, CHROMOSOMES AUTISM C NR 46 TC 56 Z9 58 PU MEDECINE ET HYGIENE PI GENEVA 4 PA 78, AVE DE LA ROSERAIE, CASE POSTALE 456,, CH-1211 GENEVA 4, SWITZERLAND SN 1015-8146 J9 GENET COUNSEL JI Genet. Couns. PY 2003 VL 14 IS 3 BP 267 EP 279 PG 13 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Research & Experimental Medicine GA 730UP UT WOS:000185848800002 PM 14577671 ER PT J AU Sinsheimer, JS Palmer, CGS Woodward, JA AF Sinsheimer, JS Palmer, CGS Woodward, JA TI Detecting genotype combinations that increase risk for disease: The maternal-fetal genotype incompatibility test SO GENETIC EPIDEMIOLOGY LA English DT Article DE maternal-fetal interaction; case-parent triad; gene by environment; log-linear models; maternal-fetal genotype incompatibility ID CANDIDATE-GENE ASSOCIATION; CASE-PARENT TRIADS; OBSTETRIC COMPLICATIONS; LINKAGE DISEQUILIBRIUM; SCHIZOPHRENIA; TRAITS; AUTISM; HLA AB Biological mechanisms that involve gene-by-environment interactions have been hypothesized to explain susceptibility to complex familial disorders. Current research provides compelling evidence that one environmental factor, which acts prenatally to increase susceptibility arises from a maternal-fetal genotype incompatibility. Because it is genetic in origin, a maternal-fetal incompatibility is one possible source of an adverse environment that can be detected in genetic analyses and precisely studied, even years after the adverse environment was present. Existing statistical models and tests for gene detection are not optimal or even appropriate for identifying maternal-fetal genotype incompatibility loci that may increase the risk for complex disorders. We describe a new test, the maternal-fetal genotype incompatibility (MFG) test, that can be used with case-parent triad data (affected individuals and their parents) to identify loci for which a maternal-fetal genotype incompatibility increases the risk for disease. The MFG test adapts a log-linear approach for case-parent triads in order to detect maternal-fetal genotype incompatibility at a candidate locus, and allows the incompatibility effects to be estimated separately from direct effects of either the maternal or the child's genotype. Through simulations of two biologically plausible maternal-fetal genotype incompatibility scenarios, we show that the type-I error rate of the MFG test is appropriate, that the estimated parameters are accurate, and that the test is powerful enough to detect a maternal-fetal genotype incompatibility of moderate effect size. C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Biomath, Ctr Hlth Sci AV617, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. RP Sinsheimer, JS (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Biomath, Ctr Hlth Sci AV617, Los Angeles, CA 90095 USA. 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Epidemiol. PD JAN PY 2003 VL 24 IS 1 BP 1 EP 13 DI 10.1002/gepi.10211 PG 13 WC Genetics & Heredity; Public, Environmental & Occupational Health SC Genetics & Heredity; Public, Environmental & Occupational Health GA 632EJ UT WOS:000180210500001 PM 12508251 ER PT J AU Walker, DW AF Walker, DW TI Raising a child with autism: A guide to applied behavioral analysis for parents SO INFANT MENTAL HEALTH JOURNAL LA English DT Book Review CR Richman Shira, 2001, RAISING CHILD AUTISM NR 1 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD JAN-FEB PY 2003 VL 24 IS 1 BP 91 EP 92 DI 10.1002/imhj.10045 PG 2 WC Psychology, Developmental SC Psychology GA 637NR UT WOS:000180519300005 ER PT J AU Hepburn, SL AF Hepburn, SL TI Clinical implications of temperamental characteristics in young children with developmental disabilities SO INFANTS & YOUNG CHILDREN LA English DT Review DE child temperament; developmental disabilities; temperamental characteristics ID INFANT TEMPERAMENT; BEHAVIOR PROBLEMS; MOTHERS ATTRIBUTIONS; AUTISM; PRESCHOOLERS; CHILDHOOD; PARENTS; STRESS; SKILLS; PERCEPTIONS AB Temperament refers to the behavioral style of an individual, or the tendency to behave in a certain way in a certain situation. Although temperament has been studied extensively in typically developing children, relatively little research concerning individual differences in the behavioral styles of young children with developmental disabilities-has been conducted. The purposes of this article are: (1) to provide a brief review of the literature with regard to temperament and outcomes for children with developmental disabilities and, (2) to explore methods for integrating temperament information into early intervention practice. Consistent with the research on temperament and goodness of fit (Chess & Thomas, 1996), this article proposes that children with developmental disabilities who present with extreme scores in specific domains of temperament may benefit from specific early intervention practices. Ideas for linking practice with child temperament are presented, particularly for children who are resistant to change, non-persistent, or difficult to distract. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. RP Hepburn, SL (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. 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G., 1996, DOWNS SYNDROME PSYCH, P81 NR 102 TC 5 Z9 5 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 JAN-MAR PY 2003 VL 16 IS 1 BP 59 EP 76 PG 18 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 632RW UT WOS:000180237500007 ER PT J AU Hertzman, M AF Hertzman, M TI Galantamine in the treatment of adult autism: A report of three clinical cases SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE galantamine; autism; acetylcholinesterase inhibitors ID PLACEBO-CONTROLLED TRIAL; ALZHEIMERS-DISEASE; TREATMENT STRATEGY; RECEPTORS; EFFICACY; AD AB Objective: To study the usefulness of galantamine, a competitive, reversible acetylcholinesterase inhibitor (AChEI), in adults diagnosed with autism (in accordance with DSM-IV-TR Axis I clinical criteria) before age three years. Methods: To promote verbalization and meaningful speech sound production through biochemical enhancement of the serotonergic subsystem of the central nervous system (CNS), galantamine 4 mg qhs was administered, with indicated dose increases. Results: Verbal fluency increased in all patients, according to their caregivers. One patient developed a macular rash that abated when the medication was discontinued. After one month on donepezil 5 mg qhs, verbal and behavioral regression again led to discontinuation. Doses for the other patients have been escalated by 4 mg daily each month to a maximum of 12 mg, with improvement following each increase. Conclusions: Cholinergic stimulation of the CNS serotonergic subsystem with galantamine may enhance expressive language and communication in autistic adults. Clinical trials are needed to study adjuvant therapy with galantamine in such patients. RP Hertzman, M (reprint author), Suite 203,11404 Old Georgetown Rd, Rockville, MD 20852 USA. EM hertzman@attglobal.net CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Chugani DC, 2002, MOL PSYCHIATR, V7, pS16, DOI 10.1038/sj.mp.4001167 Croonenburghs J, 2002, ACTA NEUROPSYCHIATR, V14, P93, DOI 10.1034/j.1601-5215.2002.140209.x Erkinjuntti T, 2002, LANCET, V359, P1283, DOI 10.1016/S0140-6736(02)08267-3 Maelicke A, 2001, BIOL PSYCHIAT, V49, P279, DOI 10.1016/S0006-3223(00)01109-4 Maelicke A, 2000, EUR J PHARMACOL, V393, P165, DOI 10.1016/S0014-2999(00)00093-5 Posey D J, 2001, Expert Opin Pharmacother, V2, P587, DOI 10.1517/14656566.2.4.587 Raskind MA, 2000, NEUROLOGY, V54, P2261 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Rockwood K, 2001, J NEUROL NEUROSUR PS, V71, P589, DOI 10.1136/jnnp.71.5.589 Tariot PN, 2000, NEUROLOGY, V54, P2269 Wilcock GK, 2000, BRIT MED J, V321, P1445, DOI 10.1136/bmj.321.7274.1445 1995, COMPREHENSIVE TXB PS NR 13 TC 23 Z9 23 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 USA SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 2003 VL 33 IS 4 BP 395 EP 398 DI 10.2190/JE5Q-1NFT-FL40-7PMW PG 4 WC Psychiatry SC Psychiatry GA 819ZA UT WOS:000221353900007 PM 15152789 ER PT J AU Hertzman, M AF Hertzman, M TI Galantamine added to the treatment regimen for adult autism SO INTERNATIONAL PSYCHOGERIATRICS LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU SPRINGER PUBLISHING CO PI NEW YORK PA 536 BROADWAY, NEW YORK, NY 10012 USA SN 1041-6102 J9 INT PSYCHOGERIATR JI Int. Psychogeriatr. PY 2003 VL 15 SU 2 BP 265 EP 265 PG 1 WC Psychology, Clinical; Geriatrics & Gerontology; Gerontology; Psychiatry; Psychology SC Psychology; Geriatrics & Gerontology; Psychiatry GA 831QJ UT WOS:000222209400619 ER PT J AU Fombonne, E Simmons, H Ford, T Meltzer, H Goodman, R AF Fombonne, E Simmons, H Ford, T Meltzer, H Goodman, R TI Prevalence of pervasive developmental disorders in the British nationwide survey of child mental health (Reprinted from the Journal of the American Academy of Child and Adolescent Psychiatry, vol 40, pgs 820-827, 2001) SO INTERNATIONAL REVIEW OF PSYCHIATRY LA English DT Reprint ID INFLAMMATORY-BOWEL-DISEASE; DIFFICULTIES QUESTIONNAIRE; AUTISM; MEASLES; PARENTS; EPIDEMIOLOGY; INFECTIONS; STRENGTHS; STRESS AB The prevalence of pervasive developmental disorders (PDD) is not well established and needs monitoring. We investigated the prevalence of PDDs in the 1999 nationwide British survey of child and adolescent mental health. A randomized stratified sample of children (n = 12,529) aged 5-15 was generated from Child Benefit Records. Trained interviewers interviewed parents and youths aged 11 or older with a standardized diagnostic interview ( Development and Well-Being Assessment) and questionnaire data (Strengths and Difficulties Questionnaire) were obtained from teachers and parents who also completed self-report measures of psychological distress. A team of experienced clinicians using all data sources achieved final diagnostic determination. A total of 10,438 (83%) interviews were conducted. There were two girls with Rett syndrome (weighted prevalence: 3.8/10,000 girls) and 27 children with other PDDs (weighted prevalence: 26.1/10,000). Compared to children with a psychiatric disorder other than PDD, social but not behavioural problems were more frequent in the PDD group. Parents of children with PDDs had higher rates of psychological distress than those from the two comparison groups. Consistent with other recent surveys, PDD rates are higher than those reported 30 years ago. The burden associated with PDDs is very high. C1 Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, London SE5 8AF, England. Off Natl Stat, London, England. RP Fombonne, E (reprint author), Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, Denmark Hill, London SE5 8AF, England. EM e.fombonne@iop.kcl.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASTHANA JC, 1990, ARCH DIS CHILD, V65, P1133 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 DEYKIN EY, 1979, AM J PSYCHIAT, V136, P1310 Dunn L. M., 1997, BRIT PICTURE VOCABUL, V2nd Elliott C. D., 1996, BRIT ABILITY SCALES Fombonne E, 1999, J AUTISM DEV DISORD, V29, P349, DOI 10.1023/A:1022123822135 Fombonne E, 1998, LANCET, V351, P955 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 FOMBONNE E, 2001, ED CHILDREN AUTISM FOMBONNE E, 1994, BRIT J PSYCHIAT, V164, P69, DOI 10.1192/bjp.164.1.69 FOMBONNE E, 1996, J AUTISM DEV DISORD, V6, P673 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Goldberg D. P., 1988, USERS GUIDE GEN HLTH Goodman R, 2000, J CHILD PSYCHOL PSYC, V41, P645, DOI 10.1111/j.1469-7610.2000.tb02345.x Goodman R, 1997, J CHILD PSYCHOL PSYC, V38, P581, DOI 10.1111/j.1469-7610.1997.tb01545.x Goodman R, 1999, J CHILD PSYCHOL PSYC, V40, P791, DOI 10.1017/S0021963099004096 Hagberg B, 1997, EUR CHILD ADOLES PSY, V6, P5 HOLROYD J, 1976, AM J MENT DEF, V80, P431 Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 KONSTANTAREAS MM, 1987, J AUTISM DEV DISORD, V17, P585, DOI 10.1007/BF01486973 KONSTANTAREAS MM, 1991, PSYCHIAT CLIN N AM, V14, P183 LORD C, 1982, J AUTISM DEV DISORD, V12, P317, DOI 10.1007/BF01538320 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 Meltzer H, 2000, MENTAL HLTH CHILDREN RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x *STATA CORP, 1997, STAT DAT AN Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 WHITELEY P, 1909, AUTISM, V351, P637 WHO, 1993, ICD 10 CLASS MENT BE WOLF LC, 1989, J AUTISM DEV DISORD, V19, P157, DOI 10.1007/BF02212727 NR 36 TC 16 Z9 16 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0954-0261 J9 INT REV PSYCHIATR JI Int. Rev. Psych. PY 2003 VL 15 IS 1-2 BP 158 EP 165 DI 10.1080/0954026021000046119 PG 8 WC Psychiatry SC Psychiatry GA 660PV UT WOS:000181842300023 PM 12745327 ER PT J AU Yeargin-Allsopp, M Rice, C Karapurkar, T Doernberg, N Boyle, C Murphy, C AF Yeargin-Allsopp, M Rice, C Karapurkar, T Doernberg, N Boyle, C Murphy, C TI Prevalence of autism in a US metropolitan area SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; SURVEILLANCE; EPIDEMIOLOGY; POPULATION AB Context Concern has been raised about possible increases in the prevalence of autism. However, few population-based studies have been conducted in the United States. Objectives To determine the prevalence of autism among children in a major US metropolitan area and to describe characteristics of the study population. Design, Setting, and Population Study of the prevalence of autism among children aged 3 to 10 years in the 5 counties of metropolitan Atlanta, Ga, in 1996. Cases were identified through screening and abstracting records at multiple medical and educational sources, with case status determined by expert review. Main Outcome. Measures Autism prevalence by demographic factors, levels of cognitive functioning, previous autism diagnoses, special education eligibility categories, and sources of identification. Results A total of 987 children displayed behaviors consistent with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for autistic disorder, pervasive developmental disorder-not otherwise specified, or Asperger disorder. The prevalence for autism was 3.4 per 1000 (95% confidence interval [CI], 3.2-3.6) (male-female ratio,.4:1). Overall, the prevalence was comparable for black and white children (black, 3.4 per 1000 [95% CI, 3.0-3.7] and white, 3.4 per 1000 [95% CI, 3.2-3.7]). Sixty-eight percent of children with IQ or developmental test results (N = 880) had cognitive impairment. As severity of cognitive impairment increased from mild to profound, the male-female ratio decreased from 4.4 to 1.3. Forty percent of children with autism were identified only at educational sources. Schools were the most important source for information on black children, children of younger mothers, and children of mothers with less than 12 years of education. Conclusion The rate of autism found in this study was higher than the rates from studies conducted in the United States during the 1980s and early 1990s, but it was consistent with those of more recent studies. C1 Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30341 USA. Battelle Mem Inst, Ctr Publ Hlth Res & Evaluat, Atlanta, GA USA. RP Yeargin-Allsopp, M (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, 4770 Buford Hwy NE, Atlanta, GA 30341 USA. 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Am. Med. Assoc. PD JAN 1 PY 2003 VL 289 IS 1 BP 49 EP 55 DI 10.1001/jama.289.1.49 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 630XL UT WOS:000180136600025 PM 12503976 ER PT J AU Fombonne, E AF Fombonne, E TI The prevalence of autism SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID CHILDREN C1 Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada. McGill Univ, Montreal, PQ, Canada. RP Fombonne, E (reprint author), Montreal Childrens Hosp, 4018 St Catherine W, Montreal, PQ H3H 1P3, Canada. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DIAGN STAT MAN MENT Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 *CDCP, AUT DEV DIS MON NETW Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Department of Earthquake Disaster Prevention China Seismological Bureau, 1999, CAT CHIN MOD EARTHQ, P1 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2002, MOL PSYCHIATR, V7, pS4, DOI 10.1038/sj.mp.4001162 Kanner L, 1943, NERV CHILD, V2, P217 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Pichichero ME, 2002, LANCET, V360, P1737, DOI 10.1016/S0140-6736(02)11682-5 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Stratton K., 2001, IMMUNIZATION SAFETY Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 *U CA MIND I, 2002, COMPR PIL STUD WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 1977, FED REG 0823, V42, P42474 NR 22 TC 242 Z9 249 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JAN 1 PY 2003 VL 289 IS 1 BP 87 EP 89 DI 10.1001/jama.289.1.87 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 630XL UT WOS:000180136600031 PM 12503982 ER PT J AU Diler, RS Yolga, A Avci, A Scahill, L AF Diler, RS Yolga, A Avci, A Scahill, L TI Risperidone-induced obsessive-compulsive symptoms in two children SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; TOURETTE-SYNDROME; DISORDER; ADOLESCENTS; AUTISM AB Objective: To present two cases of rapid-onset obsessive-compulsive Symptoms in children treated with risperidone. Cases: "A" was an 8-year-old boy with attention deficit and chronic tic disorder who developed obsessive-compulsive symptoms within 2 weeks of starting risperidone. When the dose of 0.5 mg tid was discontinued, the obsessive-compulsive symptoms resolved with no return over 8 months of follow-up. "B" was an 11-year-old girl with mild mental retardation and aggression who was treated with risperidone 1 mg per day. Obsessive-compulsive symptoms suddenly emerged 10 days after starting risperidone and resolved within 3 days of discontinuation. In both cases, streptococcal pharyngitis was ruled out. Conclusion: Although the mechanism is not clear, these cases add to several other reports concerning the sudden emergence of obsessive-compulsive symptoms and anxiety symptoms in children treated with atypical antipsychotics. Clinicians should be alert to the possibility of these adverse effects in children treated with these drugs. C1 Cukurova Univ, Child & Adolescent Psychiat Dept, Fac Med, TR-01330 Adana, Turkey. Western Psychiat Inst & Clin, Div Child Psychiat, Pittsburgh, PA USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. RP Diler, RS (reprint author), Cukurova Univ, Child & Adolescent Psychiat Dept, Fac Med, TR-01330 Adana, Turkey. 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PY 2003 VL 13 SU 1 BP S89 EP S92 PG 4 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 704HZ UT WOS:000184335400010 PM 12880504 ER PT J AU Borgatti, R Piccinelli, P Passoni, D Romeo, A Viri, M Musumeci, SA Elia, M Cogliati, T Valseriati, D Grasso, R Raggi, ME Ferrarese, C AF Borgatti, R Piccinelli, P Passoni, D Romeo, A Viri, M Musumeci, SA Elia, M Cogliati, T Valseriati, D Grasso, R Raggi, ME Ferrarese, C TI Peripheral markers of the gamma-aminobutyric acid (GABA)ergic system in Angelman's syndrome SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID DIAZEPAM-BINDING INHIBITOR; PLASMA GABA; EPILEPSY; RECEPTOR; AUTISM; VIGABATRIN; SUBUNIT; SEIZURE; MICE AB It has recently been demonstrated that patients with Angelman's syndrome who exhibited a deletion on cytogenetic tests show more severe clinical pictures with drug-resistant epilepsy than patients with Angelman's syndrome not carrying the deletion. To verify if this difference in clinical severity can be attributed to genes for the threey-aminobutyric acid (GABA)(A) receptor subunits (GABRB3, GABRA5, GABRG3) located in the deleted region, a possible modification of peripheral markers of the GABAergic system was investigated in 12 subjects with Angelman's syndrome and 20 age-matched subjects (8 with idiopathic epilepsy and 12 not affected by neurologic diseases). The results confirmed a more severe clinical picture, and epilepsy syndrome in particular, in Angelman's syndrome patients with deletions versus patients without deletions. In contrast, biochemical study (based on dosage of plasma levels of GABA and diazepam binding inhibitor, an endogenous ligand of GABA(A) and peripheral benzodiazepine receptors, showed contradictory results: patients with Angelman's syndrome showed significantly higher levels of GABA and diazepam binding inhibitor than patients without neurologic impairment but significantly lower levels than epileptic controls. C1 IRCCS Eugenio Medea, I-23842 Bosisio Parnini, Italy. Univ Insubria, Neuropsychiat Unit, Varese, Italy. Fatebenefratelli & Oftalm Hosp, Reg Ctr Epilepsy, Milan, Italy. IRCCS, Oasi Inst Res Mental Retardat & Brain Aging, Enna, Italy. Univ Milano Bicocca, Dept Neurol, Monza, Italy. Spedali Civil Brescia, Dept Child Neuropsychiat, Brescia, Italy. RP Borgatti, R (reprint author), IRCCS Eugenio Medea, Via Don Luigi Monza 20, I-23842 Bosisio Parnini, Italy. 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PD JAN PY 2003 VL 18 IS 1 BP 21 EP 25 DI 10.1177/08830738030180010801 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 657BL UT WOS:000181645500005 PM 12661934 ER PT J AU Machado, CJ Bachevalier, J AF Machado, CJ Bachevalier, J TI Non-human primate models of childhood psychopathology: the promise and the limitations SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE amygdala; animal models; autism; Williams syndrome; critical periods ID INFANT RHESUS-MONKEYS; INFERIOR TEMPORAL CORTEX; ORBITAL PREFRONTAL CORTEX; MACAQUES MACACA-FUSCATA; SEX-DIFFERENCES; CEREBRAL-CORTEX; SOCIAL-DEVELOPMENT; ORBITOFRONTAL CORTEX; DEFENSIVE BEHAVIORS; STRIATAL DOPAMINE AB Although non-human primate models have been used previously to investigate the neurobiology of several sensory and cognitive developmental pathologies, they have been employed only sparingly to study the etiology of childhood psychopathologies for which deficits in social behavior and emotion regulation are major symptoms. Previous investigations of both adult human and non-human primates have indicated that primate social behavior and emotion are regulated by a complex neural network, in which the amygdala and orbital frontal cortex play major roles. Therefore, this review will provide information generated from the study of macaque monkeys regarding the timing of normal social and emotional behavior development, the normal pattern of anatomical and functional maturation of the amygdala and orbital frontal cortex, as well as information regarding the neural and behavioral effects of early perturbations of these two neural structures. We will also highlight 'critical periods' of macaque development, during which major refinements in the behavioral repertoire appear to coincide with significant neural maturation of the amygdala and/or orbital frontal cortex. The identification of these 'critical periods' may allow one to better predict the specific behavioral impairments likely to appear after neonatal damage to one or both of these neural areas at different time points during development. This experimental approach may provide a new and important way to inform and stimulate research on childhood psychopathologies, such as autism, schizophrenia and Williams syndrome, in which the development of normal social skills and emotional regulation is severely perturbed. Finally, the promise and limitations inherent to the use of non-human primate models of childhood psychopathology will be discussed. C1 Univ Texas, Hlth Sci Ctr, Sch Med, Dept Neurobiol & Anat, Houston, TX 77030 USA. RP Bachevalier, J (reprint author), Univ Texas, Hlth Sci Ctr, Sch Med, Dept Neurobiol & Anat, 6431 Fannin St, Houston, TX 77030 USA. 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Child Psychol. Psychiatry PD JAN PY 2003 VL 44 IS 1 BP 64 EP 87 DI 10.1111/1469-7610.00103 PG 24 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 636GG UT WOS:000180445800004 PM 12553413 ER PT J AU McDougle, CJ Stigler, KA Posey, DJ AF McDougle, CJ Stigler, KA Posey, DJ TI Treatment of aggression in children and adolescents with autism and conduct disorder SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Conference on Management of Aggression Across the Life Cycle CY JUN 04, 2002 CL ELECTR NETWORK ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED TRIAL; DISRUPTIVE BEHAVIOR DISORDERS; DOUBLE-BLIND; OPEN-LABEL; TRYPTOPHAN DEPLETION; SCHIZOAFFECTIVE DISORDER; DIVALPROEX TREATMENT; MENTAL-RETARDATION; ACUTE EXACERBATION AB The optimal clinical management of aggression in children and adolescents involves both behavioral and pharmacologic intervention strategies. This article reviews medication treatments for youngsters with autistic disorder and conduct disorder, conditions for which the pharmacologic management of aggression is often necessary. Efficacy results and associated adverse effects from selected clinical trials of most classes of psychotropic medications are discussed. While preliminary progress has been made in the development of medication treatments for these serious disorders of youth, additional controlled research and longitudinal studies are needed to better understand the efficacy and tolerability of currently available compounds within each diagnostic group. C1 Indiana Univ, Dept Psychiat, Sch Med, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Dept Psychiat, Sch Med, 1111 W 10th St,KI 2nd Floor, Indianapolis, IN 46202 USA. 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Clin. Psychiatry PY 2003 VL 64 SU 4 BP 16 EP 25 PG 10 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 667UL UT WOS:000182252100003 PM 12672261 ER PT J AU Nikolaenko, NN AF Nikolaenko, NN TI Study of metaphoric and associative thinking in children of different age groups and in patients with childhood autism SO JOURNAL OF EVOLUTIONARY BIOCHEMISTRY AND PHYSIOLOGY LA English DT Article ID ASYMMETRY; BRAIN AB The study was performed on 35 healthy children and 9 patients with childhood autism (Asperger's syndrome). It was shown that formation of metaphoric thinking in norm begins as early as at the age of 7-8 years, the ability to understand metaphors decreasing suddenly at the age of 13-15 years. In the patients with childhood autism the inability was revealed of understanding metaphors and idioms widely used in the verbal communication. It is suggested that the deficit of the metaphoric thinking is due to introduction of the logic, theoretical thinking and, hence, to the underlying increased activity of the left hemisphere, as well as to the deficit of the imaginative-metaphoric thinking and to the underlying decreased activity of the right hemisphere. The study of the associative process has shown that the healthy school children have a high degree of association between the words meaning the sensory world of objects. In the patients with autism there were revealed an attenuation of the object association and the predominance of the first names, which indicates the "left-hemispheric" type of the association process. C1 Russian Acad Sci, Sechenov Inst Evolutionary Biochem & Physiol, St Petersburg 196140, Russia. RP Nikolaenko, NN (reprint author), Russian Acad Sci, Sechenov Inst Evolutionary Biochem & Physiol, St Petersburg 196140, Russia. 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PD JAN-FEB PY 2003 VL 39 IS 1 BP 77 EP 83 DI 10.1023/A:1023931323471 PG 7 WC Biochemistry & Molecular Biology; Evolutionary Biology; Physiology SC Biochemistry & Molecular Biology; Evolutionary Biology; Physiology GA 689NP UT WOS:000183500100008 ER PT J AU Kashiwagi, A Meguro, M Hoshiya, H Haruta, M Ishino, F Shibahara, T Oshimura, M AF Kashiwagi, A Meguro, M Hoshiya, H Haruta, M Ishino, F Shibahara, T Oshimura, M TI Predominant maternal expression of the mouse Atp10c in hippocampus and olfactory bulb SO JOURNAL OF HUMAN GENETICS LA English DT Article DE Angelman syndrome; Atp10c/pfatp; tissue-specific imprinting; maternal expression; P-type ATPase ID ANGELMAN-SYNDROME GENE; IMPRINTED EXPRESSION; CANDIDATE GENE; ANTISENSE RNA; UBE3A; TRANSCRIPT; BRAIN; MUTATION; PROTEIN; AUTISM AB The human chromosome 15q11-q13 region is one of the most intriguing imprinted domains, and the abnormalities inherited are associated with neurological disorders including Prader-Willi syndrome (PWS), Angelman syndrome (AS) and autism. Recently we have identified a novel maternally expressed gene, ATP10C, that encodes a putative aminophospholipid translocase within this critical region, 200 kb distal to UBE3A in an imprinted domain on human chromosome 15. A TP10C, with UBE3A, displayed tissue-specific imprinting with predominant expression of the maternal allele in the brain. In this study, we demonstrated that the mouse homologue, Atp10c/pfatp, showed tissue-specific maternal expression in the hippocampus and olfactory bulb, which overlapped the region of imprinted Ube3a expression. These data suggest that the imprinted transcript of Atp10c in the specific region of CNS may be associated with neurological disorders including AS and autism. C1 Tottori Univ, Fac Med, Sch Life Sci, Dept Mol & Cellular Biol,Div Mol & Cell Genet, Yonago, Tottori 6838503, Japan. Tottori Univ, Fac Med, Lab Anim Res Ctr, Yonago, Tottori 683, Japan. Tokyo Inst Technol, Gene Res Ctr, Kanagawa, Japan. RP Oshimura, M (reprint author), Tottori Univ, Fac Med, Sch Life Sci, Dept Mol & Cellular Biol,Div Mol & Cell Genet, 86 Nishmachi, Yonago, Tottori 6838503, Japan. 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Hum. Genet. PY 2003 VL 48 IS 4 BP 194 EP 198 DI 10.1007/s10038-003-0009-3 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 674TP UT WOS:000182652300007 PM 12730723 ER PT J AU Inui, N Asama, K AF Inui, N Asama, K TI Timing of bimanual rhythmic finger tapping in adolescents with mental retardation or autism SO JOURNAL OF HUMAN MOVEMENT STUDIES LA English DT Article DE adolescents; autism; bimanual rhythmic finger tapping; mental retardation ID 2 HANDS; DOWN-SYNDROME; REACTION-TIME; COORDINATION; VARIABILITY; POLYRHYTHM; RESPONSES; PARALLEL; TASK; TAP AB An experiment was conducted to examine timing control of bimanual rhythmic finger-tapping sequences in adolescents with mental retardation or autism. Firstly, we examined the serial information processing of bimanual alternating finger-tapping sequences (required intertap intervals of 200, 400 and 800ms). At the shorter target intervals of 200 and 400ms, strong negative correlations between adjacent between-hand intervals were observed for adolescents with autism or mental retardation, suggesting that this might be accounted for by two coupled Wing-Kristofferson timing systems with left and right clock intervals kept in appropriate relative phase by corrections involving the previously preceding produced intervals. While the group with autism made faster tapping movements than the normal group over the three conditions, the group with mental retardation produced faster tapping movements than the other two groups only in the 800ms condition. This indicated that while adolescents with mental retardation or autism appeared to produce two taps with alternate hands as a chunk, they were unable to spontaneously reproduce the required target intertap intervals. Next, we examined the motor organisation strategy adopted by participants in a bimanual finger-tapping task of a 3:2 polyrhythm. Because strong negative correlations between between-hand taps were observed for participants with mental retardation, and further, their slow-hand movements were subordinate to the movements of the fast hand, they adopted a hierarchical integrated organisation. C1 Naruto Univ Educ, Fac Hlth & Living Sci, Dept Human Motor Control, Naruto 7728502, Japan. Mino Sch Handicapped Children, Mino, Japan. RP Inui, N (reprint author), Naruto Univ Educ, Fac Hlth & Living Sci, Dept Human Motor Control, Naruto 7728502, Japan. CR Anson J. G., 1992, APPROACHES STUDY MOT, P387 Baumeister A. 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Hum. Movement Stud. PY 2003 VL 45 IS 1 BP 59 EP 80 PG 22 WC Psychology, Experimental; Sport Sciences SC Psychology; Sport Sciences GA 708DW UT WOS:000184552700005 ER PT J AU Green, SE AF Green, SE TI They are beautiful and they are ours: Swapping tales of mothering children with disabilities through interactive interviews SO JOURNAL OF LOSS & TRAUMA LA English DT Editorial Material AB This article presents a layered account of an interactive interview in which the author and interviewee exchange stories of the joys and traumas surrounding the births, diagnoses, and early lives of their children with disabilities (cerebral palsy and autism). Woven into the narrative layers are also the author's reflections on this interview and those conducted with six other mothers of children with disabilities and/or chronic impairments. The power and therapeutic value, to researchers as well as interviewees, of narrative exchange through the vehicle of interactive interviews are highlighted in the author's emotional response to the interview process. C1 Univ S Florida, Dept Sociol, Tampa, FL 33755 USA. Univ S Florida, Inst Aging, Tampa, FL 33755 USA. RP Green, SE (reprint author), Univ S Florida, Dept Sociol, CPR 107,4202 E Fowler Ave, Tampa, FL 33755 USA. CR Bochner AP, 1996, J CONTEMP ETHNOGR, V25, P3, DOI 10.1177/089124196025001001 Denzin N.K., 1997, INTERPRETIVE ETHNOGR Ellis C, 1998, CONTEMP SOCIOL, V27, P422, DOI 10.2307/2655524 Ellis C., 1998, PERSPECTIVES LOSS SO, P49 Fleischer D., 2001, DISABILITY RIGHTS MO Green SE, 2002, J LOSS TRAUMA, V7, P21, DOI 10.1080/108114402753344463 Green SE, 2001, SOCIOL HEALTH ILL, V23, P798, DOI 10.1111/1467-9566.00276 Green SE, 2001, INT J AGING HUM DEV, V53, P11, DOI 10.2190/Q7M2-LE06-JLDL-GNWF HARVEY J, 2001, MEANING RECONSTRUCTI, P231, DOI 10.1037/10397-012 Harvey J. H., 1996, EMBRACING THEIR MEMO Orbuch TL, 1997, ANNU REV SOCIOL, V23, P455, DOI 10.1146/annurev.soc.23.1.455 Romanoff B. D., 2001, MEANING RECONSTRUCTI, P245, DOI 10.1037/10397-013 Ronai CR, 1997, MENT RETARD, V35, P417, DOI 10.1352/0047-6765(1997)035<0417:OLAHMM>2.0.CO;2 NR 13 TC 17 Z9 17 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1532-5024 J9 J LOSS TRAUMA JI J. Loss Trauma PD JAN-MAR PY 2003 VL 8 IS 1 BP 1 EP 13 DI 10.1080/15325020390168672 PG 13 WC Psychology, Social SC Psychology GA 616ZP UT WOS:000179334300001 ER PT J AU Shi, LM Fatemi, H Sidwell, RW Patterson, PH AF Shi, LM Fatemi, H Sidwell, RW Patterson, PH TI Maternal influenza infection causes marked behavioral and pharmacological changes in the offspring SO JOURNAL OF NEUROSCIENCE LA English DT Article DE schizophrenia; autism; mental retardation; prepulse inhibition; acoustic startle; open field; novel object; clozapine; chlorpromazine; ketamine; poly(I : C) ID VIRAL-INFECTION; NEONATAL MICE; CYTOKINE PRODUCTION; SPECTRUM DISORDERS; PRENATAL EXPOSURE; DENDRITIC CELLS; NNOS EXPRESSION; IN-UTERO; SCHIZOPHRENIA; AUTISM AB Maternal viral infection is known to increase the risk for schizophrenia and autism in the offspring. Using this observation in an animal model, we find that respiratory infection of pregnant mice (both BALB/c and C57BL/6 strains) with the human influenza virus yields offspring that display highly abnormal behavioral responses as adults. As in schizophrenia and autism, these offspring display deficits in prepulse inhibition (PPI) in the acoustic startle response. Compared with control mice, the infected mice also display striking responses to the acute administration of antipsychotic (clozapine and chlorpromazine) and psychomimetic (ketamine) drugs. Moreover, these mice are deficient in exploratory behavior in both open-field and novel-object tests, and they are deficient in social interaction. At least some of these behavioral changes likely are attributable to the maternal immune response itself That is, maternal injection of the synthetic double-stranded RNA polyinosinic-polycytidylic acid causes a PPI deficit in the offspring in the absence of virus. Therefore, maternal viral infection has a profound effect on the behavior of adult offspring, probably via an effect of the maternal immune response on the fetus. C1 CALTECH, Div Biol, Pasadena, CA 91125 USA. Univ Minnesota, Sch Med, Dept Psychiat, Minneapolis, MN 55455 USA. Utah State Univ, Inst Antiviral Res, Logan, UT 84322 USA. RP Patterson, PH (reprint author), CALTECH, Div Biol 216 76, Pasadena, CA 91125 USA. 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Neurosci. PD JAN 1 PY 2003 VL 23 IS 1 BP 297 EP 302 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 632BC UT WOS:000180202300036 PM 12514227 ER PT J AU Vannier, L Cochin, S Roux, S Bartheleu, C Martineau, J AF Vannier, L Cochin, S Roux, S Bartheleu, C Martineau, J TI A new paradigm to study emotional expressions recognition with qEEG in infantile autism SO JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Bretonneau Hosp, INSERM, U316, Tours, France. NR 0 TC 0 Z9 0 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 0269-8803 J9 J PSYCHOPHYSIOL JI J. Psychophysiol. PY 2003 VL 17 IS 1 BP 57 EP 57 PG 1 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA 693MD UT WOS:000183720600075 ER PT J AU Brown, C AF Brown, C TI Are 'normal' gamma components a function of learned inhibition? A study of autism in adolescence suggests that autistic processing may be a function of relatively unconstrained gamma activity SO JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Bristol, Bristol, Avon, England. NR 0 TC 0 Z9 0 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 0269-8803 J9 J PSYCHOPHYSIOL JI J. Psychophysiol. PY 2003 VL 17 IS 4 BP 230 EP 230 PG 1 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA 946XF UT WOS:000230605900024 ER PT J AU Veenstra-Vanderweele, J Cook, EH AF Veenstra-Vanderweele, J Cook, EH TI Genetics of childhood disorders: XLVI. Autism, part 5: Genetics of autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article ID LANGUAGE C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. RP Veenstra-Vanderweele, J (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA. CR Bradford Y, 2001, AM J MED GENET, V105, P539, DOI 10.1002/ajmg.1497 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Buxbaum JD, 2002, MOL PSYCHIATR, V7, P311, DOI 10.1038/sj/mp/4001011 Palferman S, 2001, AM J HUM GENET, V69, P570 Jamain S, 2002, MOL PSYCHIATR, V7, P302, DOI 10.1038/sj/mp/4000979 Kim SJ, 2002, MOL PSYCHIATR, V7, P278, DOI 10.1038/sj/mp/4001033 Lai CSL, 2001, NATURE, V413, P519, DOI 10.1038/35097076 LOMBROSO PJ, 2001, J AM ACAD CHILD ADOL, V39, P671 Newbury DF, 2002, AM J HUM GENET, V70, P1318, DOI 10.1086/339931 NR 9 TC 34 Z9 36 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 2003 VL 42 IS 1 BP 116 EP 118 DI 10.1097/01.CHI.0000024913.60748.41 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 629BF UT WOS:000180030000018 PM 12500084 ER PT S AU Gustafsson, L AF Gustafsson, L BE Palade, V Howlett, RJ Jain, L TI Neural network theory and recent neuroanatomical findings indicate that inadequate nitric oxide synthase will cause autism SO KNOWLEDGE-BASED INTELLIGNET INFORMATION AND ENGINEERING SYSTEMS, PT 2, PROCEEDINGS SE LECTURE NOTES IN ARTIFICIAL INTELLIGENCE LA English DT Article; Proceedings Paper CT 7th International Conference on Knowledge-Based Intelligent Information and Engineering Systems (KES 2003) CY SEP 03-05, 2003 CL OXFORD, ENGLAND HO UNIV OXFORD AB Neural network theory indicates that inadequate expression of nitric oxide will cause narrow cortical neural columns, predicted on theoretical grounds and recently observed in autism. Another recent neuroanatomical finding in autism, early rapid growth of the cerebrum, may also be explained by inadequate expression of nitric oxide. Another long known neuroanatomical abnormality in autism, a reduced number of Purkinje cells in the Cerebellum, may also be caused, or aggravated, by inadequate expression of nitric oxide synthase. Some characteristics, such as motor impairments, sleep problems, deficit in aggression control and reduced nociception, which are not uncommon in autism, have been found in animal studies when nitric oxide synthase has been suppressed. C1 Lulea Univ Technol, S-97187 Lulea, Sweden. RP Gustafsson, L (reprint author), Lulea Univ Technol, S-97187 Lulea, Sweden. 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Self-organization of neural networks, conditioned by different attention shifting characteristics is investigated for higher-dimensional stimuli presented to the network from different sources. The attention shifting modes axe 1) novelty seeking, 2) attention shift impairment (attention is shifted but with a low probability) and 3) attention is shifted with a preference for a source which has become familiar to the map. The feature maps resulting from self-organization axe much the same for modes 1 and 2 but distinctly different for mode 3, where the maps learn the stimuli from the source with the lowest variability in great detail, at the expense of the other source(s). Detailed learning in narrow fields is a known characteristic of autism. C1 Lulea Univ Technol, S-97187 Lulea, Sweden. Monash Univ, Ahmedabad 380009, Gujarat, India. RP Gustafsson, L (reprint author), Lulea Univ Technol, S-97187 Lulea, Sweden. 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All rights reserved. RP Bolte, ER (reprint author), 705 Misty Creek Dr, Lenox, IL 60451 USA. 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Hypotheses PD JAN PY 2003 VL 60 IS 1 BP 119 EP 122 DI 10.1016/S0306-9877(02)00345-6 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 633MU UT WOS:000180287700017 PM 12450778 ER PT S AU Sampath, Y Vetsa, K Styner, M Pizer, SM Lieberman, JA Gerig, G AF Sampath, Y Vetsa, K Styner, M Pizer, SM Lieberman, JA Gerig, G BE Ellis, RE Peters, TM TI Caudate shape discrimination in schizophrenia using template-free non-parametric tests SO MEDICAL IMAGE COMPUTING AND COMPUTER-ASSISTED INTERVENTION - MICCAI 2003, PT 2 SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 6th International Conference on Medical Imaging Computing and Computer-Assisted Intervention CY NOV 15-18, 2003 CL MONTREAL, CANADA SP Robarts Res Inst, No Digital Inc ID IMAGES; MODELS AB This paper describes shape analysis of the caudate nucleus structure in a large schizophrenia study (30 controls, 60 schizophrenics). Although analysis of the caudate has not drawn the same attention as the hippocampus, it is a key basal ganglia structure shown to present differences in early development (e.g. autism) and also to present changes due to drug treatment. Left and right caudate were segmented from high resolution MRI using a reliable, semi-automated technique. Shapes were parametrized by a surface description, aligned, and finally represented as medial mesh structures (m-reps). Since schizophrenia patients were categorized based on treatment, we could test size and shape differences between normals, atypically and typically treated subjects. Statistical shape analysis used permutation tests on objects represented by medial representations. This allowed us to bypass the common problems of feature reduction inherent to low sample size and high dimensional feature vectors. Moreover, this test is non-parametric and does not require the choice of a shape template. The choice of medial shape representations led to a separate testing of global and local growth versus deformation. Results show significant caudate size and shape differences, not only between treatment groups and controls, but also among the treatment groups. Shape differences were not found when both treatment groups were grouped into one patient group and compared to controls. There was a clear localization of width and deformation change in the caudate head. As with other clinical studies utilizing shape analysis, results need to be confirmed in new, independent studies to get full confidence in the interpretation of these findings. C1 Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RP Sampath, Y (reprint author), Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. 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RP Beals, KP (reprint author), Autism Language Therapies, 4630 Osage Ave, Philadelphia, PA 19143 USA. CR Bettelheim B., 1967, EMPTY FORTRESS INFAN Bloom P., 2000, CHILDREN LEARN MEANI Ehrenreich Barbara, 2001, HARPERS MAGAZINE NOV, P43 GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P375, DOI 10.1097/00004583-199105000-00004 Greenspan S. I., 1998, CHILD SPECIAL NEEDS GREENSPAN SI, 1995, CHALLENGING CHILD KEPHART B, 1998, SLANT SUN Park C.C., 1967, SIEGE 1 8 YEARS AUTI NR 8 TC 2 Z9 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1080-4013 J9 MENT RETARD DEV D R JI Ment. Retard. Dev. Disabil. Res. Rev. PY 2003 VL 9 IS 1 BP 32 EP 39 DI 10.1002/mrdd.10058 PG 8 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 652NV UT WOS:000181386000007 PM 12587136 ER PT J AU Chen, DT Miller, FG Rosenstein, DL AF Chen, DT Miller, FG Rosenstein, DL TI Ethical aspects of research into the etiology of autism SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; research ethics; pedigree; risk factor research; genetics; neuroimaging; research with healthy children; family members as research subjects ID METHODOLOGICAL ISSUES; PEDIGREE RESEARCH; DISORDERS; CHILDREN; CONSENT; PRIVACY AB Advances in understanding autism and other developmental neuropsychiatric disorders will come from an integration of various research strategies including phenomenologic, functional neuroimaging, and pharmacologic methods, as well as epidemiologic approaches aimed at identifying genetic and environmental risk factors. The highly heritable nature of autism makes it scientifically valuable to involve parents and siblings as research participants. However, many studies on autism pose ethical challenges because they do not offer the prospect of direct benefit to subjects. In this article, we present an in-depth ethical analysis of current nontherapeutic research strategies that are common in autism research. The ethical analysis applies a proposed ethical framework for evaluating clinical research focusing on seven ethical requirements: (1) social or scientific value, (2) scientific validity, (3) fair subject selection, (4) favorable risk-benefit ratio (5) independent review, (6) informed consent, and (7) respect for potentiai and enrolled research participants. (C) 2003 Wiley-Liss, Inc. C1 NIMH, Off Clin Director, Intramural Res Program, NIH, Bethesda, MD 20892 USA. NIH, Dept Clin Bioeth, Warren G Magnuson Clin Ctr, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Chen, DT (reprint author), NIMH, Off Clin Director, Intramural Res Program, NIH, Bldg 10,Room 3N242,10 Ctr Dr,MSC 1277, Bethesda, MD 20892 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2003 VL 9 IS 1 BP 48 EP 53 DI 10.1002/mrdd.10059 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 652NV UT WOS:000181386000009 PM 12587138 ER PT J AU Eigsti, IM Shapiro, T AF Eigsti, IM Shapiro, T TI A systems neuroscience approach to autism: Biological, cognitive, and clinical perspectives SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; functional and structural brain imaging; etiology; genetics; cognitive neuroscience; intervention ID RECEPTIVE LANGUAGE DISORDER; INFANTILE-AUTISM; SPECTRUM DISORDERS; POSTERIOR-FOSSA; FACILITATED COMMUNICATION; IMMUNOLOGICAL TREATMENTS; GRAMMATICAL MORPHEMES; AUTONOMIC RESPONSES; EMISSION-TOMOGRAPHY; CHILDHOOD AUTISM AB Autism is a behaviorally defined disorder characterized by a broad constellation of symptoms. Numerous studies directed to the biological substrate demonstrate clear effects of neurodevelopmental differences that will likely point to the etiology, course, and long-term outcomes of the disorder. Consistently replicated research on the neural underpinnings of autism is reviewed. In general, results suggest several main conclusions: First, autism is a heterogeneous disorder and is likely to have multiple possible etiologies; second, structural brain studies have indicated a variety of diffuse anatomical differences, reflective of an early developmental change in the growth or pruning of neural tissue, rather than localized lesions; similarly, neurochemical studies suggest early, neuromodulatory discrepancies rather than gross or localized abnormalities; and finally, there are a number of limitations on studies of brain activity that to date preclude definitive answers to questions of how the brain functions differently in autism. The large number of active research programs investigating the cognitive neuroscience of autism spectrum disorders, in combination with the exciting development of new methodologies and tools in this area, indicates the drama and excitement of work in this area. (C) 2003 Wiley-Liss, Inc. C1 Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA. Sackler Inst Dev Psychobiol Columbia, New York, NY 10032 USA. Cornell Univ, Weill Med Coll, New York, NY 10032 USA. RP Eigsti, IM (reprint author), Columbia Univ, Coll Phys & Surg, Dept Psychiat, 1051 Riverside Dr,Unit 40, New York, NY 10032 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2003 VL 9 IS 3 BP 205 EP 215 DI 10.1002/mrdd.10081 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 719HB UT WOS:000185196600010 PM 12953300 ER PT J AU Weiss, LA Escayg, A Kearney, JA Trudeau, M MacDonald, BT Mori, M Reichert, J Buxbaum, JD Meisler, MH AF Weiss, LA Escayg, A Kearney, JA Trudeau, M MacDonald, BT Mori, M Reichert, J Buxbaum, JD Meisler, MH TI Sodium channels SCN1A, SCN2A and SCN3A in familial autism SO MOLECULAR PSYCHIATRY LA English DT Article DE sodium channel; autism; genetic susceptibility; neurogenetics; Chr 2; calmodulin ID SUBUNIT MESSENGER-RNAS; FEBRILE SEIZURES PLUS; GENERALIZED EPILEPSY; SPECTRUM DISORDERS; ALPHA-SUBUNIT; GENE; MUTATIONS; SUSCEPTIBILITY; PATTERNS; MOUSE AB Autism is a psychiatric disorder with estimated heritability of 90%. One-third of autistic individuals experience seizures. A susceptibility locus for autism was mapped near a cluster of voltage-gated sodium channel genes on chromosome 2. Mutations in two of these genes, SCN1A and SCN2A, result in the seizure disorder GEFS +. To evaluate these sodium channel genes as candidates for the autism susceptibility locus, we screened for variation in coding exons and splice sites in 117 multiplex autism families. A total of 27 kb of coding sequence and 3 kb of intron sequence were screened. Only six families carried variants with potential effects on sodium channel function. Five coding variants and one lariat branchpoint mutation were each observed in a single family, but were not present in controls. The variant R1902C in SCN2A is located in the calmodulin binding site and was found to reduce binding affinity for calcium-bound calmodulin. R542Q in SCN1A was observed in one autism family and had previously been identified in a patient with juvenile myoclonic epilepsy. The effect of the lariat branchpoint mutation was tested in cultured lymphoblasts. Additional population studies and functional tests will be required to evaluate pathogenicity of the coding and lariat site variants. SNP density was 1/kb in the genomic sequence screened. We report 38 sodium channel SNPs that will be useful in future association and linkage studies. C1 Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA. Grad Univ Adv Studies, Natl Inst Physiol Sci, Dept Physiol Sci, Okazaki, Aichi, Japan. CUNY Mt Sinai Sch Med, Dept Psychiat, Seaver Autism Res Ctr, New York, NY 10029 USA. RP Meisler, MH (reprint author), Univ Michigan, Dept Human Genet, 4708 Med Sci 2, Ann Arbor, MI 48109 USA. 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Psychiatr. 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Chromosome 15q11-q13 has been proposed to harbor a gene for autism susceptibility based on (1) maternal-specific chromosomal duplications seen in autism and (2) positive evidence for linkage disequilibrium (LD) at 15q markers in chromosomally normal autism families. To investigate and localize a potential susceptibility variant, we developed a dense single nucleotide polymorphism (SNP) map of the maternal expression domain in proximal 15q. We analyzed 29 SNPs spanning the two known imprinted, maternally expressed genes in the interval (UBE3A and ATP10C) and putative imprinting control regions. With a marker coverage of 1/10 kb in coding regions and 1/15 kb in large 5' introns, this map was employed to thoroughly dissect LD in autism families. Two SNPs within ATP10C demonstrated evidence for preferential allelic transmission to affected offspring. The signal detected at these SNPs was stronger in singleton families, and an adjacent SNP demonstrated transmission distortion in this subset. All SNPs showing allelic association lie within islands of sequence homology between human and mouse genomes that may be part of an ancestral haplotype containing a functional susceptibility allele. The region was further explored for recombination hot spots and haplotype blocks to evaluate haplotype transmission. Five haplotype blocks were defined within this region. One haplotype within ATP10C displayed suggestive evidence for preferential transmission. Interpretation of these data will require replication across data sets, evaluation of potential functional effects of associated alleles, and a thorough assessment of haplotype transmission within ATP10C and neighboring genes. Nevertheless, these findings are consistent with the presence of an autism C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. 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Univ Palermo, Dept Quantitat Methods Human Sci, Palermo, Italy. Univ Palermo, Dept Psychol, Palermo, Italy. Univ Palermo, Res Ctr Autism & Other Pervas Dev Disorder, Palermo, Italy. RP Romano, V (reprint author), Univ Palermo, Fac Med & Chirurg, Dipartimento Biopatol & Metodol Biomed, Via Divisi 83, I-90133 Palermo, Italy. 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PY 2003 VL 8 IS 8 BP 716 EP 717 DI 10.1038/sj.mp.4001285 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 707XQ UT WOS:000184535600002 PM 12888798 ER PT J AU Auranen, M Varilo, T Alen, R Vanhala, R Ayers, K Kempas, E Ylisaukko-oja, T Peltonen, L Jarvela, I AF Auranen, M Varilo, T Alen, R Vanhala, R Ayers, K Kempas, E Ylisaukko-oja, T Peltonen, L Jarvela, I TI Evidence for allelic association on chromosome 3q25-27 in families with autism spectrum disorders originating from a subisolate of Finland SO MOLECULAR PSYCHIATRY LA English DT Article DE genetic isolate; genetics; infantile autism; asperger syndrome ID LINKAGE ANALYSIS; GENOMEWIDE SCREEN; GENOMIC SCREEN; SUSCEPTIBILITY LOCUS; PEDIGREE ANALYSIS; TWIN; 7Q; DISEQUILIBRIUM; POPULATION; ETIOLOGY AB Recent molecular studies on autism and related disorders have supported a multilocus etiology for the disease spectrum. To maximize genetic and cultural homogeneity, we have focused our molecular studies to families originating from a subisolate of Central Finland. Genealogical studies enabled the identification of a megapedigree comprising of 12 core families with autism and Asperger syndrome (AS). We analyzed two chromosomal regions on 1q and 3q showing highest lod scores in our genome-wide scan, as well as the AUTS1 locus on chromosome 7q. For markers on 3q25-27, more significant association was observed in families from subisolate compared to families from the rest of Finland. In contrast, no clear evidence for association on AUTS1 locus was obtained. The wide interval showing association, in particular, on chromosome 3q suggests a locus for autism spectrum of disorders on this chromosomal region. C1 Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Cent Hosp Cent Finland, Unit Child Neurol, Jyvaskyla, Finland. Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. Univ Calif Los Angeles, Sch Med, Dept Biomath, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA 90024 USA. Univ Helsinki, Cent Hosp, Mol Genet Lab, Helsinki, Finland. RP Auranen, M (reprint author), Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. 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Psychiatr. PY 2003 VL 8 IS 10 BP 879 EP 884 DI 10.1038/sj.mp.4001299 PG 6 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 730HM UT WOS:000185825200006 PM 14515138 ER PT J AU Bonora, E Beyer, KS Lamb, JA Parr, JR Klauck, SM Benner, A Paolucci, M Abbott, A Ragoussis, I Poustka, A Bailey, AJ Monaco, AP AF Bonora, E Beyer, KS Lamb, JA Parr, JR Klauck, SM Benner, A Paolucci, M Abbott, A Ragoussis, I Poustka, A Bailey, AJ Monaco, AP CA IMGSAC TI Analysis of reelin as a candidate gene for autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; candidate genes; brain development; reelin; mutation screening ID PERVASIVE DEVELOPMENTAL DISORDERS; LINKAGE DISEQUILIBRIUM; EXTRACELLULAR-MATRIX; FAMILY HISTORY; CHROMOSOME 7Q; SUSCEPTIBILITY; REGION; MOUSE; TWIN; CEREBELLUM AB Genetic studies indicate that chromosome 7q is likely to contain an autism susceptibility locus (AUTS1). We have followed a positional candidate gene approach to identify relevant gene(s) and report here the analysis of reelin ( RELN), a gene located under our peak of linkage. Screening RELN for DNA changes identified novel missense variants absent in a large control group; however, the low frequency of these mutations does not explain the relatively strong linkage results on 7q. Furthermore, analysis of a previously reported triplet repeat polymorphism and intragenic single nucleotide polymorphisms, using the transmission disequilibrium test, provided no evidence for association with autism in IMGSAC and German singleton families. The analysis of RELN suggests that it probably does not play a major role in autism aetiology, although further analysis of several missense mutations is warranted in additional affected individuals. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, D-6900 Heidelberg, Germany. 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PY 2003 VL 8 IS 10 BP 885 EP 892 DI 10.1038/sj.mp.4001310 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 730HM UT WOS:000185825200007 PM 14515139 ER PT J AU Bacchelli, E Blasi, F Biondolillo, M Lamb, JA Bonora, E Barnby, G Parr, J Beyer, KS Klauck, SM Poustka, A Bailey, AJ Monaco, AJ Maestrini, E AF Bacchelli, E Blasi, F Biondolillo, M Lamb, JA Bonora, E Barnby, G Parr, J Beyer, KS Klauck, SM Poustka, A Bailey, AJ Monaco, AJ Maestrini, E CA IMGSAC TI Screening of nine candidate genes for autism on chromosome 2q reveals rare nonsynonymous variants in the cAMP-GEFII gene SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorder; susceptibility gene; chromosome 2; mutation screening; association ID GLUTAMIC-ACID DECARBOXYLASE; GENOMEWIDE SCREEN; SUSCEPTIBILITY GENES; GENOMIC SCREEN; DLX GENES; DISORDER; LINKAGE; EXPRESSION; DISTINCT; FAMILY AB The results from several genome scans indicate that chromosome 2q21-q33 is likely to contain an autism susceptibility locus. We studied the potential contribution of nine positional and functional candidate genes: TBR-1; GAD1; DLX1; DLX2; cAMP-GEFII; CHN1; ATF2; HOXD1 and NEUROD1. Screening these genes for DNA variants and association analysis using intragenic single nucleotide polymorphisms did not provide evidence for a major role in the aetiology of autism. Four rare nonsynonymous variants were identified, however, in the cAMP-GEFII gene. These variants were present in five families, where they segregate with the autistic phenotype, and were not observed in control individuals. The significance of these variants is unclear, as their low frequency in IMGSAC families does not account for the relatively strong linkage signal at the 2q locus. Further studies are needed to clarify the contribution of cAMP-GEFII gene variants to autism susceptibility. C1 Univ Bologna, Dipartimento Biol Evoluzionist Sperimentale, I-40126 Bologna, Italy. Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. 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PY 2003 VL 8 IS 11 BP 916 EP 924 DI 10.1038/sj.mp.4001340 PG 9 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 741JA UT WOS:000186453900006 PM 14593429 ER PT J AU Ozaki, N Goldman, D Kaye, WH Plotnicov, K Greenberg, BD Lappalainen, J Rudnick, G Murphy, DL AF Ozaki, N Goldman, D Kaye, WH Plotnicov, K Greenberg, BD Lappalainen, J Rudnick, G Murphy, DL TI Serotonin transporter missense mutation associated with a complex neuropsychiatric phenotype SO MOLECULAR PSYCHIATRY LA English DT Article DE genetics; obsessive-compulsive disorder; autism; anorexia; constitutive activation ID OBSESSIVE-COMPULSIVE DISORDER; PROTEIN GENE SLC6A4; REGULATORY REGION; ANOREXIA-NERVOSA; SOCIAL PHOBIA; POLYMORPHISM; FAMILY; AUTISM; PREVALENCE; LOCALIZATION AB Two common serotonin transporter (SERT) untranslated region gene variants have been intensively studied, but remain inconclusively linked to depression and other neuropsychiatric disorders. We now report an uncommon coding region SERT mutation, Ile425Val, in two unrelated families with OCD and other serotonin-related disorders. Six of the seven family members with this mutation had OCD (n=5) or obsessive-compulsive personality disorder (n=1) and some also met diagnostic criteria for multiple other disorders (Asperger's syndrome, social phobia, anorexia nervosa, tic disorder and alcohol and other substance abuse/dependence). The four most clinically affected individuals-the two probands and their two slbs-had the I425V SERT gene gain-of-function mutation and were also homozygous for 50-UTR SERT gene variant with greater transcriptional efficacy. C1 NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA. Fujita Hlth Univ, Sch Med, Dept Psychiat, Aichi, Japan. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA USA. Butler Hosp, Providence, RI 02906 USA. 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