FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Ennis, S Wanjing, JN Kearney, G Fitzgerald, M Stallings, R Barton, DE Green, AJ Gallagher, L Gill, M AF Ennis, S Wanjing, JN Kearney, G Fitzgerald, M Stallings, R Barton, DE Green, AJ Gallagher, L Gill, M TI Mapping of a candidate region for autism on chromosome 2q32. SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT European-Society-of-Human-Genetics European Human Genetics Conference in Conjuction With European Meeting on Psychosocial Aspects of Genetics CY MAY 25-28, 2002 CL STRASBOURG, FRANCE SP European Soc Human Genet C1 Univ Coll Dublin, Dept Med Genet, Dublin 2, Ireland. Our Ladys Hosp Sick Children, Natl Ctr Med Genet, Dublin, Ireland. St James Hosp, Trinity Ctr Hlth Sci, Dept Psychiat, Dublin 8, Ireland. RI Barton, David/B-9460-2008 CR Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Palferman S, 2001, AM J HUM GENET, V69, P570 NR 2 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PD MAY PY 2002 VL 10 SU 1 BP 240 EP 240 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 752MW UT WOS:000187166100873 ER PT J AU Rutter, M AF Rutter, M TI Genetic influences on autism SO EUROPEAN PSYCHIATRY LA English DT Meeting Abstract C1 Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London, England. NR 0 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0924-9338 J9 EUR PSYCHIAT JI Eur. Psychiat. PD MAY PY 2002 VL 17 SU 1 BP 30S EP 30S PG 1 WC Psychiatry SC Psychiatry GA 581CM UT WOS:000177273600111 ER PT J AU Gousse, V Plumet, MH Chabane, N Mouren-Simeoni, MC Ferradian, N Leboyer, M AF Gousse, V Plumet, MH Chabane, N Mouren-Simeoni, MC Ferradian, N Leboyer, M TI Fringe phenotypes in autism: a review of clinical, biochemical and cognitive studies SO EUROPEAN PSYCHIATRY LA English DT Review DE autism; psychiatric genetics; phenotypes; cognitive, clinical and biochemical assessments ID WHOLE-BLOOD SEROTONIN; WEAK CENTRAL COHERENCE; FIRST-DEGREE RELATIVES; FAMILY HISTORY; INFANTILE-AUTISM; 1ST-DEGREE RELATIVES; PERSONALITY-CHARACTERISTICS; PSYCHIATRIC-DISORDERS; BETA-ENDORPHIN; CHILDREN AB Progress in identifying the genetic vulnerability factors in autism requires correct identification of the inherited phenotype(s). This can be achieved not only by the accurate description of the affected subject but also by the identification of vulnerability traits in non-affected relatives of autistic probands. This review will focus on this last strategy and principally on clinical, biochemical and cognitive traits. (C) 2002 Editions scientifiques et medicales Elsevier SAS. C1 Hop Paris, Assistance Publ, Hop Robert Debre,Consultat Autisme, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. Hop Paris, Assistance Publ, Hosp Albert Chenevier & Henri Mondor, Psychiat Serv, F-94000 Creteil, France. Hop Henri Mondor, INSERM U513, F-94000 Creteil, France. RP Leboyer, M (reprint author), Hop Paris, Assistance Publ, Hop Robert Debre,Consultat Autisme, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. 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Psychiat. PD MAY PY 2002 VL 17 IS 3 BP 120 EP 128 DI 10.1016/S0924-9338(02)00640-5 PG 9 WC Psychiatry SC Psychiatry GA 579VH UT WOS:000177198200002 PM 12052572 ER PT J AU Brendel, DH Bodkin, JA Hauptman, B Ornstein, A AF Brendel, DH Bodkin, JA Hauptman, B Ornstein, A TI "I see dead people": Overcoming psychic numbness SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article ID REUPTAKE INHIBITORS; DEPRESSION; SEROTONIN; DISORDERS; AUGMENTATION; PRAMIPEXOLE; SELEGILINE; AUTISM C1 McLean Hosp, Belmont, MA 02478 USA. Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Community Therapeut Day Sch, Lexington, MA USA. RP Brendel, DH (reprint author), McLean Hosp, 115 Mill St, Belmont, MA 02478 USA. 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PD MAY-JUN PY 2002 VL 10 IS 3 BP 166 EP 178 DI 10.1080/713854297 PG 13 WC Psychiatry SC Psychiatry GA 555VV UT WOS:000175814700004 PM 12023931 ER PT J AU Safran, JS AF Safran, JS TI A practitioner's guide to resources on Asperger syndrome SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Article ID HIGH-FUNCTIONING AUTISM; CHILDREN AB The purpose of this article is to identify and describe a selection of print and electronic resources that can help educators understand and support students with Asperger syndrome (AS). The most marked characteristic of this disorder is significant impairment in social interaction and relationships. Although children and youth with AS generally do not manifest noteworthy cognitive or language delays, their disability is significant. AS is beginning to affect special education practices in most of the United States, and increasing awareness in both the psychological and educational communities will undoubtedly result in greater numbers of children and youth being recognized. It is therefore critical that educators are provided with resources to help them acquire skills for working effectively with these students. C1 Ohio Univ, Coll Educ, Athens, OH 45701 USA. RP Safran, JS (reprint author), Ohio Univ, Coll Educ, Athens, OH 45701 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barnhill G., 2000, FOCUS AUTISM OTHER D, V15, P146, DOI [10.1177/108835760001500303, DOI 10.1177/108835760001500303] Bock SJ, 1999, EDUC TRAIN MENT RET, V34, P511 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 Frith U, 1999, MIND LANG, V14, P1 Frith U., 1991, AUTISM ASPERGER SYND, P1, DOI 10.1017/CBO9780511526770.001 GAGNON E, 2000, THIS IS ASPERGER SYN GAGNON E, 2001, POWER CARD STRATEGY Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 GILLBERG C, 1991, J AUTISM DEV DISORD, V21, P61, DOI 10.1007/BF02206998 Gray C. 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PD MAY PY 2002 VL 37 IS 5 BP 283 EP 291 DI 10.1177/105345120203700504 PG 9 WC Education, Special SC Education & Educational Research GA 543GY UT WOS:000175094100004 ER PT J AU Kaland, N Moller-Nielsen, A Callesen, K Mortensen, EL Gottlieb, D Smith, L AF Kaland, N Moller-Nielsen, A Callesen, K Mortensen, EL Gottlieb, D Smith, L TI A new 'advanced' test of theory of mind: evidence from children and adolescents with Asperger syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Asperger syndrome; cognitive tests; theory of mind; 'naturalistic' test battery; mental vs. physical inference; reaction time ID HIGH-FUNCTIONING ADULTS; EXECUTIVE FUNCTION; AUTISM; ATTRIBUTION; INDIVIDUALS; BELIEF; DISORDERS; MEMORY AB Background: The aim of the present study was to assess the ability of children and adolescents with Asperger syndrome (AS) (N=21) to infer physical versus mental states on a new `advanced' test of theory-of-mind - Stories from Everyday Life. The participants in the AS group were of normal intelligence and were compared with an age-matched control group (N= 20) of normally developing children and adolescents. Method: The test materials comprised 26 short stories or 13 pairs of different types of stories. This contextually complex theory-of-mind battery aimed to record the participants' ability to make inferences about physical as well as mental states. The first part of each story described a physical or mechanical event, and a test question then tested the participants' ability to make an inference about a physical state. The last part of the stories contained two questions, testing the ability to infer a mental state from the story context, e.g., understanding social communication such as a lie, white lie, figure of speech, misunderstanding, double bluff, irony, persuasion, contrary emotions, forgetting, jealousy, intentions, empathy and social blunders. The participants' reaction time and number of prompt questions were also recorded. Results: The participants in the AS group showed significantly more problems attributing mental state inferences relative to the control group. They performed considerably better on tasks involving a physical state, but still did less well than the controls. They had a tendency to interpret behaviour and utterances literally, without regard to context, and to choose a physical explanation when a mental state answer was more appropriate. They also needed significantly more prompt questions and used significantly more time than the controls to solve the tasks, especially those involving mental state inference. Conclusions: This study supports earlier findings that individuals with AS/HFA have difficulties attributing mental states in context, but seem to have significantly fewer difficulties inferring physical states. The fact that the clinical group also used significant longer reaction time and needed significantly more prompt questions to solve the tasks relative to the control group may also be related to their problems in understanding mental states. However, the possibility remains that these difficulties could represent a separate factor - or a distinct `cognitive style'- suggesting that at least some individuals with AS may be generally slow in solving cognitive tasks. C1 Lillehammer Coll, Lillehammer, Norway. Univ Copenhagen, Copenhagen, Denmark. Psychol Unit Copenhagen, Copenhagen, Denmark. Univ Oslo, Oslo, Norway. RP Kaland, N (reprint author), Hogskolen Lillehammer, N-2626 Lillehammer, Norway. 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Child Psychol. Psychiatry Allied Discip. PD MAY PY 2002 VL 43 IS 4 BP 517 EP 528 DI 10.1111/1469-7610.00042 PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 545JH UT WOS:000175213400010 PM 12030597 ER PT J AU Howlin, P AF Howlin, P TI The development of autism: Perspectives from theory and research. SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Book Review CR Burack J. A., 2001, DEV AUTISM PERSPECTI NR 1 TC 0 Z9 0 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 2002 VL 43 IS 4 BP 549 EP 549 DI 10.1111/1469-7610.t01-9-00044 PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 545JH UT WOS:000175213400021 ER PT J AU Howlin, P AF Howlin, P TI The research basis for autism intervention. SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Book Review CR Schopler E., 2001, RES BASIS AUTISM INT NR 1 TC 0 Z9 0 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 2002 VL 43 IS 4 BP 549 EP 549 DI 10.1111/1469-7610.t01-9-00044 PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 545JH UT WOS:000175213400022 ER PT J AU O'Brien, G AF O'Brien, G TI Dual diagnosis in offenders with intellectual disability: setting research priorities: a review of research findings concerning psychiatric disorder (excluding personality disorder) among offenders with intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Review DE autism; dual diagnosis; psychopathology ID MENTALLY-RETARDED ADULTS; ASPERGERS SYNDROME; LEARNING-DISABILITIES; BEHAVIOR; RETARDATION; VIOLENCE; HANDICAP; AUTISM; PSYCHOPATHOLOGY; SCHIZOPHRENIA AB Studies of so-called 'dual diagnosis', i.e. intellectual disability (ID) with an additional psychiatric disorder, are reviewed with particular reference to offending behaviour. Because of the paucity of studies of psychopathology in offenders with ID, the present paper opens with studies of broader issues of psychopathology among people with ID, notably those with depression, schizophrenia, mild depressive disorder, other major psychotic disorders, anxiety/neurotic disorder, autistic spectrum disorders and attention deficit hyperactivity disorder. There follows a review of the most established and commonly used measurement scales for dual diagnosis in ID. The review then focuses directly on those studies which have looked at the issues of dual diagnosis among offenders with ID. In keeping with other reviews in this series, the latter studies are classified according to the same criteria. Based on this review, it is apparent that there are high-priority research questions which concern the extent and nature of psychopathology among offenders with ID, most notably those with autistic spectrum disorders. C1 Northumbria Univ, Northgate Hosp, Morpeth NE61 3BP, England. RP O'Brien, G (reprint author), Northumbria Univ, Northgate Hosp, Morpeth NE61 3BP, England. CR Aman M. 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Intell. Disabil. Res. PD MAY PY 2002 VL 46 SU 1 BP 21 EP 30 DI 10.1046/j.1365-2788.2002.00002.x PG 10 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 556FA UT WOS:000175837600005 PM 12031015 ER PT J AU Panerai, S Ferrante, L Zingale, M AF Panerai, S Ferrante, L Zingale, M TI Benefits of the Treatment and Education of Autistic and Communication Handicapped Children (TEACCH) programme as compared with a non-specific approach SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; educational treatments; TEACCH AB Background Two educational treatments were compared, the Treatment and Education of Autistic and Communication Handicapped Children (TEACCH) programme and the integration programme for individuals with disabilities. Methods Two groups of eight subjects were matched by gender, chronological and mental age, and nosographic diagnosis (i.e. autism associated with severe intellectual disability, DSM-IV criteria and Childhood Autism Rating Scale scored. The TEACCH programme was applied to the experimental group, while the control group was integrated in regular schools with a support teacher. The Psycho-Educational Profile - Revised and the Vineland Adaptive Behaviour Scale were administered twice with a one-year interval between assessments. Results The scores of the experimental group increased more than the control group scores. Statistically significant differences were obtained in both groups because of the differences in the two approaches. C1 IRCCS Oasi Maris SS, Sci Res Inst Mental Retardat & Brain Ageing, I-94018 Troina, EN, Italy. RP Panerai, S (reprint author), IRCCS Oasi Maris SS, Sci Res Inst Mental Retardat & Brain Ageing, Via Conte Ruggero 73, I-94018 Troina, EN, Italy. 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Intell. Disabil. Res. PD MAY PY 2002 VL 46 BP 318 EP 327 DI 10.1046/j.1365-2788.2002.00388.x PN 4 PG 10 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 550XZ UT WOS:000175531500004 PM 12000583 ER PT J AU Wimpory, D Nicholas, B Nash, S AF Wimpory, D Nicholas, B Nash, S TI Social timing, clock genes and autism: a new hypothesis SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Editorial Material ID CHROMOSOMAL-ABNORMALITIES; INTERSTITIAL DELETION; GENOMIC SCREEN; CEREBELLAR; ATTENTION; INTERSUBJECTIVITY; DEFICITS; MUTATION; INFANCY; MARKERS AB Background Timing and social timing deficits are fundamental in autism and may play a developmental role in its manifestation. Sleep problems are associated with this disorder, as is a reduction or loss of Purkinje cells associated with regions of the brain which co-ordinate fine motor movements. Genetic studies suggest that a number of genes of limited effect lead to autism and that the genes are epistatic. Conclusions We suggest that anomalies in clock genes operating as timing genes in high frequency oscillator systems may underlie the timing deficits of autism. We outline how anomalies in methylation-related genes may also be implicated. C1 Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. RP Wimpory, D (reprint author), Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. 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Intell. Disabil. Res. PD MAY PY 2002 VL 46 BP 352 EP 358 DI 10.1046/j.1365-2788.2002.00423.x PN 4 PG 7 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 550XZ UT WOS:000175531500008 PM 12000587 ER PT J AU Badmaev, E Kuchna, I Nowicki, K Wegiel, J Brown, TW Kozlowski, PB Wegiel, J AF Badmaev, E Kuchna, I Nowicki, K Wegiel, J Brown, TW Kozlowski, PB Wegiel, J TI Developmental pathology in memory, cholinergic, and motor systems in autism. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 New York State Inst Basic Res Dev Disabil, Dept Pathol Neurobiol, Staten Isl, NY 10314 USA. New York State Inst Basic Res Dev Disabil, Dept Human Genet, Staten Isl, NY 10314 USA. NR 0 TC 0 Z9 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 USA SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 2002 VL 61 IS 5 MA 96 BP 466 EP 466 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 554FR UT WOS:000175724500104 ER PT J AU Bhattacharjee, MB Lopez-Alberola, R Lee, DA AF Bhattacharjee, MB Lopez-Alberola, R Lee, DA TI Growth factor expression in autism. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 Tulane Univ, Ctr Hlth Sci, Dept Pathol & Lab Med, New Orleans, LA 70118 USA. Tulane Univ, Ctr Hlth Sci, Dept Psychiat & Neurol, New Orleans, LA 70118 USA. NR 0 TC 0 Z9 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 USA SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 2002 VL 61 IS 5 MA 107 BP 469 EP 469 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 554FR UT WOS:000175724500114 ER PT J AU Yeung, DW Wong, V Sun, JG Chan, MS Ho, CL AF Yeung, DW Wong, V Sun, JG Chan, MS Ho, CL TI FDG PET brain scan in monitoring the effect of Tongue Acupuncture (TAC) in treatment of autism. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 Univ Calif San Diego, Dept Radiol, San Diego, CA 92103 USA. Hong Kong Sanat & Hosp, Dept Nucl Med & PET, Hong Kong, Hong Kong, Peoples R China. Univ Hong Kong, Dept Pediat, Hong Kong, Hong Kong, Peoples R China. Univ Hong Kong, Jocky Club MRI Engn Ctr, Hong Kong, Hong Kong, Peoples R China. NR 0 TC 0 Z9 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 2002 VL 43 IS 5 SU S MA 304 BP 84P EP 84P PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 551KL UT WOS:000175560800305 ER PT J AU Ryu, YH Shin, YJ Yune, MJ Shim, YW Yoon, CS Lee, JD AF Ryu, YH Shin, YJ Yune, MJ Shim, YW Yoon, CS Lee, JD TI Correlation of childhood autism rating scale and cerebral perfusion impairments on 99-Tc ECD brain SPECT and brain MRI in patients with autism spectrum disorders. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 Yonsei Univ, Seoul 120749, South Korea. NR 0 TC 0 Z9 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 2002 VL 43 IS 5 SU S MA 1391 BP 346P EP 346P PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 551KL UT WOS:000175560801302 ER PT J AU Zwaigenbaum, L Szatmari, P Jones, MB Bryson, SE MacLean, JE Mahoney, WJ Bartolucci, G Tuff, L AF Zwaigenbaum, L Szatmari, P Jones, MB Bryson, SE MacLean, JE Mahoney, WJ Bartolucci, G Tuff, L TI Pregnancy and birth complications in autism and liability to the broader autism phenotype SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; genetics; pregnancy complications; birth complications ID INFANTILE-AUTISM; FAMILY HISTORY; CHILDREN; TWIN; POPULATION; RELATIVES; DISORDER; ETIOLOGY; GENETICS; PAIRS AB Objective: To understand better the relationship between pregnancy and birth complications and genetic factors in autism. Method: The sample included 78 children with an autism spectrum disorder and 88 unaffected siblings. A standardized interview was used to ask mothers about the pregnancy and birth of each child, and an overall index reflecting freedom from complications (termed "optimality") was determined. The presence of autism-like traits (termed the "broader autism phenotype") in second- and third-degree relatives was ascertained by reports from multiple informants. The proportion of relatives with the broader autism phenotype, corrected for degree of relation, was used as an index of family loading. Results: Children with autism spectrum disorders have lower optimality (higher rates of complications) than unaffected siblings. High family loading for the broader autism phenotype is associated with higher rates of complications in unaffected siblings. Family loading was not significantly associated with complications in affected siblings in this sample. Overall, these findings argue against complications being a direct cause of autism, as one would expect to find the most complications in sporadic cases (i.e., in children without a positive family history). Conclusion: Increased rates of birth and pregnancy complications are likely secondary to familial factors associated with autism. C1 McMaster Univ, Chedoke Child & Family Ctr, Dept Paediat, Hamilton, ON L8N 3Z5, Canada. McMaster Univ, Dept Psychiat, Hamilton, ON, Canada. Dalhousie Univ, Dept Paediat, Halifax, NS, Canada. Penn State Univ, Milton S Hershey Med Ctr, Dept Behav Sci, Hershey, PA 17033 USA. RP Zwaigenbaum, L (reprint author), McMaster Univ, Chedoke Child & Family Ctr, Dept Paediat, 565 Sanatorium Rd, Hamilton, ON L8N 3Z5, Canada. 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Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 2002 VL 41 IS 5 BP 572 EP 579 DI 10.1097/00004583-200205000-00015 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 544YF UT WOS:000175188900015 PM 12014790 ER PT J AU Brudnak, MA AF Brudnak, MA TI Probiotics as an adjuvant to detoxification protocols SO MEDICAL HYPOTHESES LA English DT Article ID ENTEROCOCCUS-FAECIUM; MERCURY; RESISTANT; BACTERIA; CELLS; ORGANOMERCURIALS; FAECALIS; LACTOSE AB Autism is a developmental disease characterized by a spectrum of symptoms ranging from decreased verbal skills and social withdrawal, to repetitive behavior and violent outbursts. Genetic analysis has yielded a few potentially interesting genes, however no clear linkage has been established. For this reason, it has been suggested that the etiology of autism may involve multiple loci. This, in large part, explains why so many different theories abound. One such theory is that of mercury poisoning. Environmentally acquired mercury, either through some causal contact or through vaccination, has been postulated as the culprit. Mercury is thought to be exerting its neurological effect on the brain. The standard treatment has been to apply chelating agents in an attempt to extricate the mercury. One missing component in the treatment is the utilization of the body's own detoxification mechanisms. Arguably the largest detoxification component of the body, the endogenous enteric bacteria are an enormous reservoir, which can be constantly and safely replenished. This paper discusses the use of high-dose probiotics as an adjuvant for detoxification protocols with an emphasis on use in autistics. (C) 2002 Published by Elsevier Science Ltd. C1 MAK Wood Inc, Grafton, WI 53024 USA. RP Brudnak, MA (reprint author), MAK Wood Inc, 1235 Dakota Dr,Units E-F, Grafton, WI 53024 USA. 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Hypotheses PD MAY PY 2002 VL 58 IS 5 BP 382 EP 385 DI 10.1054/mehy.2001.1442 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 579FT UT WOS:000177168500007 PM 12056873 ER PT J AU Brudnak, MA Rimland, B Kerry, RE Dailey, M Taylor, R Stayton, B Waickman, F Waickman, M Pangborn, J Buchholz, I AF Brudnak, MA Rimland, B Kerry, RE Dailey, M Taylor, R Stayton, B Waickman, F Waickman, M Pangborn, J Buchholz, I TI Enzyme-based therapy for autism spectrum disorders - Is it worth another look? SO MEDICAL HYPOTHESES LA English DT Article ID LACTIC-ACID BACTERIA; CHAIN FATTY-ACIDS; LACTATE AB Autism is a developmental disease usually manifesting within the first three years of life. To date, no causative agent has been found. Similarly, treatment options have been limited. Of the treatment options available, a number of them have been nutritionally based in an attempt to address one or more of the theories regarding the etiology of the disease. An example would be enzyme therapy for the digestion of purported offending neuroactive peptides collectively known as exorphins. This paper discusses the exorphin theory of autism and subsequent treatment with dietary enzyme therapy. Novel data are presented in support of the theory that enzymes play a critical role in autism. Forty-six patients between the ages of 5 and 31 were selected for inclusion in the study based on a diagnosis placing them in the category of the autism spectrum disorders (ASD). The diets were supplemented with a novel dietary enzyme formulation, ENZYMAID, for a period of 12 weeks. Progress was tracked according to the Symptom Outcome Survey (SOS) (1) form method of symptom charting and presented in a table for further analysis. The novel enzyme formula, ENZYMAID, beneficially and safely affected all 13 of the parameters measured. Improvements ranged from 50-90%, depending on the parameter measured, Enzyme therapy to treat ASD may indeed a viable option in treatment protocols. These results indicate that further controlled studies are warranted. (C) 2002 Published by Elsevier Science Ltd. C1 MAK Wood Inc, Grafton, WI 53024 USA. Autism Res Inst, San Diego, CA USA. Triangle ENT Serv, Durham, NC 27704 USA. Bionost Inc, St Charles, IL 60175 USA. RP Brudnak, MA (reprint author), MAK Wood Inc, 1235 Dakota Dr,Units E-F, Grafton, WI 53024 USA. 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Hypotheses PD MAY PY 2002 VL 58 IS 5 BP 422 EP 428 DI 10.1054/mehy.2001.1513 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 579FT UT WOS:000177168500015 PM 12056881 ER PT J AU Deuel, RK AF Deuel, RK TI Autism: A cognitive developmental riddle SO PEDIATRIC NEUROLOGY LA English DT Review ID HIGH-FUNCTIONING ADULTS; LANDAU-KLEFFNER-SYNDROME; ASPERGER-SYNDROME; CORTICAL MECHANISMS; MENTAL SIMULATION; CHILDHOOD AUTISM; WORKING-MEMORY; YOUNG-CHILDREN; RETT-SYNDROME; DISORDERS AB It has been 60 years since the definitive descriptions of autism, yet it is only in the past decade that related advances in cognitive and basic neuroscience have begun to be incorporated in clinical practice. Some of the resultant clinical advances, which include a trend toward international standardization of diagnosis on the basis of behavioral criteria and which, in turn, seem to allow for earlier, more secure diagnosis and the application of behavioral therapy in early childhood, as well as more thorough genetic studies, are briefly reviewed. The three major defects in thought processing that are postulated by cognitive neuropsychologists to result in aberrant autistic behaviors are also reviewed and linked to recent functional imaging studies in autistic patients and some animal and bench research suggestive of both cortical and subcortical developmental vulnerabilities in autism. Overall it seems at least possible that neuroscientific research may yield results applicable to prevention or remediation of autism, a condition heretofore considered irremediable. (C) 2002 by Elsevier Science Inc. All rights reserved. C1 St Louis Univ, Dept Neurol, St Louis, MO 63104 USA. 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Neurol. PD MAY PY 2002 VL 26 IS 5 BP 349 EP 357 DI 10.1016/S0887-8994(02)00390-9 PG 9 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 563NQ UT WOS:000176262800001 PM 12057794 ER PT J AU Peele, PB Lave, JR Kelleher, KJ AF Peele, PB Lave, JR Kelleher, KJ TI Exclusions and limitations in children's behavioral health care coverage SO PSYCHIATRIC SERVICES LA English DT Article AB Objective: The objective of this study was to identify benefit limits, diagnostic exclusions, and service exclusions of private behavioral health care plans that can influence the delivery of care to children. Methods: A total of 128 commercial, employment-based behavioral health plans were examined for types of benefit limits, service exclusions, and diagnostic exclusions applicable to children. Results: Almost half of the plans had restrictions on the number of outpatient visits, with limits ranging from 12 to 60 clinic visits a year. More than half of the plans had limitations on the number of inpatient days, ranging from 20 to 60 days a year. Diagnoses excluded from coverage included autism, mental retardation, problems related to child abuse, and impulse control disorders, such as kleptomania and pyromania. Half of the services excluded could be categorized as either social and human services or complementary medicine rather than as mental health care. Conclusions: Plans commonly had service and diagnostic exclusions that could disrupt children's health care. The results of the study emphasize a need to address the types of treatment covered by mental health insurance. C1 Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15261 USA. Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA. RP Peele, PB (reprint author), Univ Pittsburgh, Grad Sch Publ Hlth, A649,130 DeSoto St, Pittsburgh, PA 15261 USA. 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PD MAY PY 2002 VL 53 IS 5 BP 591 EP 594 DI 10.1176/appi.ps.53.5.591 PG 4 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 546RB UT WOS:000175286300013 PM 11986509 ER PT J AU O'Callaghan, FJ AF O'Callaghan, FJ TI Autism - what is it and where does it come from? SO QJM-AN INTERNATIONAL JOURNAL OF MEDICINE LA English DT Editorial Material ID DISORDER; CHILDREN C1 Univ Oxford, Natl Perinatal Epidemiol Unit, Oxford OX1 2JD, England. RP O'Callaghan, FJ (reprint author), Univ Oxford, Natl Perinatal Epidemiol Unit, Oxford OX1 2JD, England. CR Arvidsson T., 1997, AUTISM, V1, P163, DOI 10.1177/1362361397012004 BAILEY A, 1995, PSYCHOL MED, V25, P63 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BURD L, 1987, J AM ACAD CHILD ADOL, V26, P704 DEBAENE S, 1997, NUMBER SENSE MIND CR DELONG GR, 1981, ARCH NEUROL-CHICAGO, V38, P191 FRITH U, 1989, DIAGNOSIS AND TREATMENT OF AUTISM, P33 GILLBERG C, 2000, BIOL AUTISTIC SYNDRO, P89 Kanner L, 1943, NERV CHILD, V2, P217 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P537, DOI 10.1017/S0021963099003935 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 11 TC 1 Z9 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1460-2725 J9 QJM-INT J MED JI QJM-An Int. J. Med. PD MAY PY 2002 VL 95 IS 5 BP 263 EP 265 DI 10.1093/qjmed/95.5.263 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 548QQ UT WOS:000175400700001 PM 11978896 ER PT J AU Tobing, LE Glenwick, DS AF Tobing, LE Glenwick, DS TI Relation of the Childhood Autism Rating Scale-Parent version to diagnosis, stress, and age SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE CARS-P; pervasive developmental disorder; Parenting Stress Index ID DISORDERS; CHILDREN; BEHAVIOR; CARS AB This study explored the relation of severity of functional impairment on the Childhood Autism Rating Scale-Parent version (CARS-P) to diagnosis, parenting stress. and child age. Twenty-two mothers of children with autism and 19 mothers of children with pervasive developmental disorder-not otherwise specified (PDD-NOS) completed the CARS-P and the Parenting Stress Index. The autism group received significantly higher (i.e., more severe impairment) CARS-P ratings that did the PDD-NOS group. For the total sample, severity of impairment was a significant predictor of child-related parenting stress. The CARS-P was inconsistently associated with age-significantly positive for the PDD-NOS group but nonsignificantly for the autism group. Implications for the use of the CARS-P in assessment of children and the evaluation of interventions are discussed. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Fordham Univ, Dept Psychol, Bronx, NY 10458 USA. RP Glenwick, DS (reprint author), Fordham Univ, Dept Psychol, Bronx, NY 10458 USA. CR Abidin RR, 1995, PARENTING STRESS IND American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 Dumas J. 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Dev. Disabil. PD MAY-JUN PY 2002 VL 23 IS 3 BP 211 EP 223 DI 10.1016/S0891-4222(02)00099-9 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 568YX UT WOS:000176573500004 PM 12102589 ER PT J AU Readinger, W AF Readinger, W TI Looking into autism SO TRENDS IN COGNITIVE SCIENCES LA English DT Editorial Material CR Milne E, 2002, J CHILD PSYCHOL PSYC, V43, P255, DOI 10.1111/1469-7610.00018 NR 1 TC 0 Z9 0 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1364-6613 J9 TRENDS COGN SCI JI TRENDS COGN. SCI. PD MAY PY 2002 VL 6 IS 5 BP 198 EP 198 DI 10.1016/S1364-6613(02)01917-4 PG 1 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 545TX UT WOS:000175234600008 ER PT J AU Schutz, CK Polley, D Robinson, PD Chalifoux, M Macciardi, F White, BN Holden, JJA AF Schutz, CK Polley, D Robinson, PD Chalifoux, M Macciardi, F White, BN Holden, JJA TI Autism and the X chromosome: No linkage to microsatellite loci detected using the affected sibling pair method SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; autism spectrum disorders; genetics; X chromosome ID DINUCLEOTIDE REPEAT POLYMORPHISM; PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X; MULTIPLEX FAMILIES; INFANTILE-AUTISM; GENE; RELATIVES; BEHAVIOR; HISTORY; REGION AB The etiology of autism spectrum disorders (ASDs) is poorly understood, although it is clear that genetic factors play a major role. ASDs appear to be a heterogeneous group of disorders, making genetic analysis difficult in the absence of etiologically definable subgroups. The excess of males in the affected population has led to suggestions that an X-linked locus could play a role in the causation of autism or a related pervasive developmental disorder. To examine this, we have investigated the genotypes of 31 families with two or more affected boys, at a series of 16 highly polymorphic loci distributed along the X chromosome with an average interlocus distance of 12 cM, in order to identify regions of significantly increased concordance among pairs of affected brothers. No locus tested showed a significant increase in concordance, supporting findings by others that there are no genes of major effect located on the X chromosome that contribute to increased susceptibility to ASD. (C) 2002 Wiley-Liss, Inc. C1 Ongwanada Resource Ctr, Dept Cytogenet, Kingston, ON K7M 8A6, Canada. 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J. Med. Genet. PD APR 15 PY 2002 VL 109 IS 1 BP 36 EP 41 DI 10.1002/ajmg.10138 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 536MB UT WOS:000174702900005 PM 11932990 ER PT J AU McDougle, C Scahill, L McCracken, JT Aman, MG Tierney, E Arnold, E Vitiello, B AF McDougle, C Scahill, L McCracken, JT Aman, MG Tierney, E Arnold, E Vitiello, B TI Therapeutic use of atypical antipsychotic in children with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. Yale Univ, Dept Psychiat, New Haven, CT 06520 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90024 USA. Kennedy Krieger Inst, Dept Psychiat, Baltimore, MD USA. Ohio State Univ, Dept Psychiat, Sunbury, OH USA. NIMH, Div Serv & Intervent Res, Bethesda, MD 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 2002 VL 51 IS 8 SU S MA 9 BP 3S EP 3S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 541JA UT WOS:000174980400006 ER PT J AU Hardan, AY Handen, BL AF Hardan, AY Handen, BL TI Case study: Donepezil treatment of children and adolescents with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Univ Pittsburgh, Pittsburgh, PA 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 2002 VL 51 IS 8 SU S MA 389 BP 132S EP 132S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 541JA UT WOS:000174980400377 ER PT J AU Davis, RA Wilt, MAB Murphy, RR Hetrick, WP O'Donnell, BF AF Davis, RA Wilt, MAB Murphy, RR Hetrick, WP O'Donnell, BF TI Subjective perceptual distortions and visual system dysfunction in children with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Indiana Univ, Dept Psychol, Bloomington, IN USA. RI Bockbrader, Marcia/J-6203-2013 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 2002 VL 51 IS 8 SU S MA 529 BP 181S EP 182S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 541JA UT WOS:000174980400512 ER PT J AU Hetrick, WP Kieffaber, PD Barron, JL White, MH Sandman, CA AF Hetrick, WP Kieffaber, PD Barron, JL White, MH Sandman, CA TI Sensory gating in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Indiana Univ, Dept Psychol, Bloomington, IN USA. Fairview Dev Ctr, Costa Mesa, CA USA. Calif State Univ Fullerton, Dept Psychol, Fullerton, CA 92634 USA. Univ Calif Irvine, Dept Psychiat & Human Behav, Irvine, CA 92717 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 2002 VL 51 IS 8 SU S MA 551 BP 189S EP 189S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 541JA UT WOS:000174980400533 ER PT J AU Hardan, AY Minshew, NJ Kilpatrick, M Keshavan, MS AF Hardan, AY Minshew, NJ Kilpatrick, M Keshavan, MS TI Motor test performances and anatomical MRI of the basal ganglia in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 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 2002 VL 51 IS 8 SU S MA 560 BP 192S EP 193S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 541JA UT WOS:000174980400542 ER PT J AU Marquardt, RK Levitt, JG Blanton, RE McCracken, JT Toga, A AF Marquardt, RK Levitt, JG Blanton, RE McCracken, JT Toga, A TI Abnormal morphometric characteristics of the anterior cingulate gyrus in children with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Div Child & Adolescent Psychiat, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Lab NeuroImaging, Los Angeles, CA 90024 USA. NR 0 TC 4 Z9 4 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 2002 VL 51 IS 8 SU S MA 561 BP 193S EP 193S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 541JA UT WOS:000174980400543 ER PT J AU Brosvic, GM Taylor, JN Dihoff, RE AF Brosvic, GM Taylor, JN Dihoff, RE TI Influences of early thyroid hormone manipulations: Delays in pup motor and exploratory behavior are evident in adult operant performance SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE thyroid; comparative; reversal learning; schedules of reinforcement; teratogen; visual search; PTU ID TREATED CONGENITAL HYPOTHYROIDISM; RAT PUPS; CHILDREN; DEFICIENCY; AUTISM; MICE AB The effects of thyroid hormone depletion and enhancement on litter size, survival, body mass, ambulation, quadrant crossing, home orientation, day of eye opening, and free serum T-3 and T-4 levels were examined in Study 1. In Study 2, the effects of the timing of prenatal insult and the level of thyroid hormone depletion on litter size, survival, body mass, and free serum T3 and T4 levels were examined. Upon the completion of Study 1, randomly selected pups were maintained on ad-libitum water and food for 2 years, and performance was evaluated on fixed and variable ratio schedules, fixed and variable interval schedules, and probability and reversal learning tasks (Study 3). In Study 4, human subjects diagnosed with and treated for either congenital hypothyroidism or congenital hyperthyroidism were tested on the operant procedures used in Study 3, as well as on a series of simple reaction time, serial timing, and conjunctive and disjunctive search tasks. Dose-dependent decreases in survival and delays in the presentation of early motor and exploratory skills were observed following thyroid hormone depletion; dose-dependent accelerations in the presentation of early motor and exploratory skills were observed following thyroid hormone enhancement. Pups that had been prenatally exposed to propylthiouracil (PTU) 1-2 years after the return of thyroid hormones to baseline levels were significantly less accurate at timing on fixed and variable interval schedules, demonstrated an inability to allocate responding on probability tasks, and committed more errors during original learning (OL) and on each reversal problem. Similar deficits were observed in follow-up tests with humans diagnosed with congenital hypothyroidism, as were deficits in serial timing and visual searching. Collectively, the present results demonstrate that the pervasive and negative effects of prenatal thyroid deficiency on early behavior are also expressed during adult operant performance. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Rider Univ, Dept Psychol, Lawrenceville, NJ 08648 USA. Rowan Univ, Dept Psychol, Glassboro, NJ 08028 USA. RP Brosvic, GM (reprint author), Rider Univ, Dept Psychol, Lawrenceville, NJ 08648 USA. 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Behav. PD APR 15 PY 2002 VL 75 IS 5 BP 697 EP 715 DI 10.1016/S0031-9384(02)00668-6 PG 19 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 564XE UT WOS:000176338200011 PM 12020735 ER PT J AU Giannotti, F Cortesi, F Cerquiglini, A Volzone, A Bernabei, P AF Giannotti, F Cortesi, F Cerquiglini, A Volzone, A Bernabei, P TI A questionnaire-based study of sleep problems in children with autism spectrum disorders. SO SLEEP LA English DT Meeting Abstract C1 Univ Roma La Sapienza, Dept Dev Neurol & Psychiat, Ctr Pediat Sleep Disorders, Rome, Italy. CR Owens JA, 2000, SLEEP, V23, P1043 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 NR 2 TC 0 Z9 0 PU AMER ACAD SLEEP MEDICINE PI ROCHESTER PA 6301 BANDEL RD, STE 101, ROCHESTER, MN 55901 USA SN 0161-8105 J9 SLEEP JI Sleep PD APR 15 PY 2002 VL 25 SU S MA 369 BP A269 EP A270 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 540KB UT WOS:000174927200371 ER PT J AU Nylander, L Holmqvist, M Zettervall, K AF Nylander, L Holmqvist, M Zettervall, K TI Workup for child neuropsychiatric disorders in adults often desirable - Functional disabilities can give rise to social maladjustment SO LAKARTIDNINGEN LA Swedish DT Article ID EPIDEMIOLOGY; ADHD AB So-called child neuropsychiatric disorders (ADHD/DAMP, autism spectrum disorders, Tourette's syndrome) are being recognized with increasing frequency in child and adolescent psychiatry. Through follow-up studies, case reports and autobiographical accounts it has become evident that these disorders often persist into adulthood, and the need for diagnostic evaluation of adults is increasing. The Neuropsychiatric Diagnostic Team for Adults in Lund, Sweden, was established in 1998 to meet this need. 228 adults, mostly 18 - 30 years old, have completed the diagnostic process, resulting in one of the above-mentioned diagnoses in 64%. 80 patients had ADHD/DAMP, 59 had autism spectrum disorders and 7 had Tourette's syndrome. The diagnostic process involves clinical interviews and observation, neuropsychological evaluation and, if possible, a parent interview. So far, the impact on quality of life of a child neuropsychiatric diagnosis received in adulthood is not known. Follow-up studies are needed. C1 Barnneuropsykiatriska Kliniken, BNK, Vuxenprojektet, Gothenburg, Sweden. Univ Sjukhuset Lund, Verksamhetsomrade Psykiatri Lund, Lund, Sweden. RP Nylander, L (reprint author), Lund Univ, Dept Psychiat, Neuropsychiat Diagnost Team, Annedalsvagen 9, SE-22764 Lund, Sweden. 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This well-replicated finding and subsequent studies of platelet serotonin receptors in autism indicate that the serotonin 2A receptor gene (HTR2A) on chromosome 13q is a primary candidate gene in autism. Converging data from recent genome screens also implicates the genomic region containing HTR2A. Based on these lines of evidence, the transmission/disequilibrium test (TDT) was used to assess transmission disequilibrium between autism and haplotypes of three polymorphisms, including the promoter -1438 G/A single nucleotide polymorphism (SNP) in perfect linkage disequilibrium with the 102 T/C SNP in previous studies, a newly identified SNP in intron I near exon 2, and the SNP responsible for the His452Tyr amino acid change in exon 3. Because expression studies have shown HTR2A to be polymorphically imprinted in the brain, secondary analyses were split into maternal and paternal transmissions. No evidence was found for unequal transmission of haplotypes; however, power analysis reveals low power to detect a parent-of-origin effect in this sample size. (C) 2002 Wiley-Liss, Inc. C1 Univ Chicago, Dept Psychiat, Lab Dev Neurosci Child & Adolescent Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Dev Disorders Clin, Chicago, IL 60637 USA. Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, La Jolla, CA USA. Univ Calif San Diego, Sch Med, Dept Psychiat, La Jolla, CA 92093 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. RP Cook, EH (reprint author), Univ Chicago, Dept Psychiat, Lab Dev Neurosci Child & Adolescent Psychiat, MC3077,5841 S Maryland Ave, Chicago, IL 60637 USA. 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PD APR 8 PY 2002 VL 114 IS 3 BP 277 EP 283 DI 10.1002/ajmg.10192 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 534QB UT WOS:000174596600004 PM 11920848 ER PT J AU Yirmiya, N Pilowsky, T Tidhar, S Nemanov, L Altmark, L Ebstein, RP AF Yirmiya, N Pilowsky, T Tidhar, S Nemanov, L Altmark, L Ebstein, RP TI Family-based and population study of a functional promoter-region monoamine oxidase A polymorphism in autism: Possible association with IQ SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE monoamine oxidase A; promoter-region repeat polymorphism; autism; transmission disequilibrium test (TDT); family study; IQ; intelligence ID A GENE PROMOTER; REGULATORY POLYMORPHISM; ABNORMAL-BEHAVIOR; PANIC DISORDER; HISTORY; DISEQUILIBRIUM; INDIVIDUALS; MILLENNIUM; LINKAGE AB Although the etiology of autism remains to be elucidated, genetic elements significantly contribute to this disorder, and genes on the X chromosome are of special interest because there is a 4:1 predominance of male probands in autism. In the current study, we therefore examined, using the robust transmission disequilibrium test (TDT), possible preferential transmission of variants of a functional monoamine oxidase A (MAO A) promoter region polymorphism for linkage to autism. In the 49 families examined (33 families with one proband and 15 families with two affected siblings), we did not find preferential transmission of MAO A from 33 heterozygous mothers to affected child (TDT chi-square = 0.29, NS). Nor was any significant difference in MAO A allele frequency observed between 43 male autism subjects versus a group of 108 non-autism control subjects (chi-square = 1.23, P = 0.27, NS). However, a trend was observed for an association between IQ in the probands and the MAO A genotype that just attained significance (F = 3.5, P = 0.046, N = 28) in the small group of autism subjects recruited from families with two affected siblings. (C) 2002 Wiley-Liss, Inc. C1 S Herzog Mem Hosp, Res Lab, IL-91351 Jerusalem, Israel. 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We focused on molecules influencing the central nervous system (CNS) and consecutively responsible for typical autistic behavior. We highlighted the mutual relationship between the serotonergic, immunological and endocrinological system and the interaction of these three pivotal systems with predisposing (genetic)and external (pre-, peri- and postnatal) conditions and xenobiotics. We stressed the influence of age, pubertal stage, sex, race and IQ on biological data. There is growing evidence that the complexity and variability of those interactions might be responsible for the heterogeneity of behavioral phenotypes and biological findings in Autism. Genetic, neuroanatomical and neurophysiological data were mentioned according their relevance to neurochemical opinions. C1 Univ Antwerp, Ctr Child & Adolescent Psychiat, B-2020 Antwerp, Belgium. Clin Res Res Ctr Mental Hlth, Antwerp, Belgium. 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PD APR PY 2002 VL 14 IS 2 BP 93 EP 102 DI 10.1034/j.1601-5215.2002.140209.x PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 578KM UT WOS:000177116500009 ER PT J AU Wakefield, AJ Puleston, JM Montgomery, SM Anthony, A O'Leary, JJ Murch, SH AF Wakefield, AJ Puleston, JM Montgomery, SM Anthony, A O'Leary, JJ Murch, SH TI Review article: the concept of entero-colonic encephalopathy, autism and opioid receptor ligands SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Review ID INFLAMMATORY-BOWEL-DISEASE; PERVASIVE DEVELOPMENTAL DISORDER; LYMPHOID-NODULAR HYPERPLASIA; FULMINANT HEPATIC-FAILURE; BLOOD-BRAIN-BARRIER; CELIAC-DISEASE; INFANTILE-AUTISM; INTESTINAL INFLAMMATION; NONSPECIFIC COLITIS; PLASMA-LEVELS AB There is growing awareness that primary gastrointestinal pathology may play an important role in the inception and clinical expression of some childhood developmental disorders. including autism. In addition to frequent gastrointestinal symptoms. children with autism often manifest complex biochemical and immunological abnormalities. The gut-brain axis is central to certain encephalopathies of extra-cranial origin, hepatic encephalopathy being the best characterized. Commonalities in the clinical characteristics of hepatic encephalopathy and a form of autism associated with developmental regression in an apparently previously normal child, accompanied by immune-mediated gastrointestinal pathology, have led to the proposal that there may be analogous mechanisms of toxic encephalopathy in patients with liver failure and some children with autism. Aberrations in opioid biochemistry are common to these two conditions, and there is evidence that opioid peptides may mediate certain aspects of the respective syndromes. The generation of plausible and testable hypotheses in this area may help to identify new treatment options in encephalopathics of extra-cranial origin. Therapeutic targets for this autistic phenotype may include: modification of diet and entero-colonic microbial milieu in order to reduce toxin substrates, improve nutritional status and modify mucosal immunity ant anti-inflammatory/immunomodulatory therapy: and specific treatment of dysmotility, focusing. for example, on the pharmacology of local opioid activity in the gut. C1 UCL Royal Free & Univ Coll Med Sch, Dept Med, Ctr Gastroenterol, London NW3 2QG, England. UCL Royal Free & Univ Coll Med Sch, Inflammatory Bowel Dis Study Grp, London, England. UCL Royal Free & Univ Coll Med Sch, Ctr Paediat Gastroenterol, London, England. Coombe Womens Hosp, Dept Pathol, Dublin, Ireland. Trinity Coll Dublin, Dublin, Ireland. RP Wakefield, AJ (reprint author), UCL Royal Free & Univ Coll Med Sch, Dept Med, Ctr Gastroenterol, Royal Free Campus, London NW3 2QG, England. 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PD APR PY 2002 VL 16 IS 4 BP 663 EP 674 DI 10.1046/j.1365-2036.2002.01206.x PG 12 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA 543RQ UT WOS:000175115300002 PM 11929383 ER PT J AU Ames, BN Elson-Schwab, I Silver, EA AF Ames, BN Elson-Schwab, I Silver, EA TI High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K-m): relevance to genetic disease and polymorphisms SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Review DE genetic disease; therapeutic vitamin use; binding defect; favism; alcohol intolerance; autism; migraine headaches; single nucleotide polymorphisms; enzyme mutations; review ID METHYLENETETRAHYDROFOLATE REDUCTASE GENE; SYRUP-URINE-DISEASE; LINKED SIDEROBLASTIC ANEMIA; HOLOCARBOXYLASE SYNTHETASE DEFICIENCY; ELECTRON-TRANSFER FLAVOPROTEIN; DELTA-AMINOLEVULINATE SYNTHASE; PYRUVATE-DEHYDROGENASE DEFICIENCY; METHYLMALONYL-COA MUTASE; COMPLEX-I DEFICIENCY; MITOCHONDRIAL ALDEHYDE DEHYDROGENASE AB many as one-third of mutations in a gene result in the corresponding enzyme having an increased Michaelis constant, or K-m, (decreased binding affinity) for a coenzyme, resulting in a lower rate of reaction. About 50 human genetic diseases due to defective enzymes can be remedied or ameliorated by the administration of high doses of the vitamin component of the corresponding coenzyme, which at least partially restores enzymatic activity. Several single-nucleotide polymorphisms, in which the variant amino acid reduces coenzyme binding and thus enzymatic activity, are likely to be remediable by raising cellular concentrations of the cofactor through high-dose vitamin therapy. Some examples include the alanine-to-valine substitution at codon 222 (Ala222-->Val) [DNA: C-to-T substitution at nucleotide 677 (677C-->T)] in methylenetetrahydrofolate reductase (NADPH) and the cofactor FAD (in relation to cardiovascular disease, migraines, and rages), the Pro187-->Ser (DNA: 609C-->T) mutation in NAD(P):quinone oxidoreductase 1 [NAD(P)H dehydrogenase (quinone)] and FAD (in relation to cancer), the Ala44-->Gly (DNA: 131C-G) mutation in glucose-6-phosphate l-dehydrogenase and NADP (in relation to favism and hemolytic anemia), and the Glu487-->Lys mutation (present in one-half of Asians) in aldehyde dehydrogenase (NAD(+)) and NAD (in relation to alcohol intolerance, Alzheimer disease, and cancer). C1 Childrens Hosp Oakland Res Inst, Oakland, CA 94609 USA. Univ Calif Berkeley, Dept Mol & Cellular Biol, Berkeley, CA 94720 USA. RP Ames, BN (reprint author), Childrens Hosp Oakland Res Inst, 5700 Martin Luther King Jr Way, Oakland, CA 94609 USA. 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PD APR PY 2002 VL 54 IS 1 BP 64 EP 64 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 556GY UT WOS:000175842100095 ER PT J AU Mulick, JA Butter, EM AF Mulick, JA Butter, EM TI Educational advocacy for children with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID INTENSIVE BEHAVIORAL INTERVENTION; PERVASIVE DEVELOPMENTAL DISORDER; POPULATION; OUTCOMES; DELAYS; IEP AB There exists a great divide between parents' demands for intensive behavioral interventions for their children with autism and the public education system's reluctance to support early intensive behavioral intervention programs. More and more, professionals with expertise in applied behavior analysis are being asked to advocate for effective, early behavioral intervention for autism in education litigation brought about by frustrated parents. The progress made in recent years in the behavioral treatment of children with autism and the schools' lack of adherence to the requirements of IDEA have made it possible for educational policy change through effective advocacy by behavioral interventionists. This paper discusses preparing for educational advocacy on behalf of young children with autism. We explore the personal and emotional reasons why parents choose to engage in the financially risky endeavor of educational litigation. We then outline an approach to developing expert testimony based upon evaluation of the target child and his/her educational history. Issues related to assessment, training, and ethical practice are addressed. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Columbus Childrens Hosp, Dept Psychol, Columbus, OH 43205 USA. Ohio State Univ, Columbus, OH 43210 USA. RP Mulick, JA (reprint author), Columbus Childrens Hosp, Dept Psychol, 700 Childrens Dr, Columbus, OH 43205 USA. 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CR Maurice C., 1996, BEHAV INTERVENTIONS Maurice C, 2001, MAKING DIFFERENCE BE NR 2 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR-JUN PY 2002 VL 17 IS 2 BP 107 EP 109 DI 10.1002/bin.109 PG 3 WC Psychology, Clinical SC Psychology GA 545LH UT WOS:000175218500006 ER PT J AU Daenen, EWPM Wolterink, G Gerrits, MAFM Van Ree, JM AF Daenen, EWPM Wolterink, G Gerrits, MAFM Van Ree, JM TI Amygdala or ventral hippocampal lesions at two early stages of life differentially affect open field behaviour later in life; an animal model of neurodevelopmental psychopathological disorders SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE amygdala; hippocampus; neonatal lesions rat; locomotor activity; animal model; neurodevelopmental disorder; schizophrenia ID PREFRONTAL CORTEX; NUCLEUS-ACCUMBENS; INFANTILE-AUTISM; DOPAMINE RELEASE; IBOTENIC ACID; RAT; SCHIZOPHRENIA; DAMAGE; BRAIN; AMPHETAMINE AB Psychiatric disorders like schizophrenia or autism are thought to result from disruption of the normal pattern of brain development. Abnormalities in the amygdaloid complex and hippocampus have been reported in these disorders. In the present study rats were lesioned in the amygdala or ventral hippocampus on day 7 of life (immature brain) or day 21 of life (almost mature brain) and open field behaviour was determined later in life before and after puberty. Lesioning on day 7 resulted in behavioural changes, interpreted as locomotor stereotypy and decreased anxiety in case of amygdala or hippocampus, respectively. These effects were more profoundly present after puberty. Lesioning on day 21 did not result in these behavioural changes, which subscribes to the importance of the stage of brain maturation on functional development. The results suggest that the behavioural changes in rats lesioned on day 7 may due to a malfunctioning of structures connected to the amygdala or ventral hippocampus. Brain lesions made on day 7 of life may serve as a potential model of psychopathological neurodevelopmental disorders. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Med Ctr, Dept Pharmacol, Div Pharmacol & Anat,Rudolf Magnus Inst Neurosci, NL-3508 AB Utrecht, Netherlands. RP Van Ree, JM (reprint author), Univ Utrecht, Med Ctr, Dept Pharmacol, Div Pharmacol & Anat,Rudolf Magnus Inst Neurosci, POB 3508, NL-3508 AB Utrecht, Netherlands. 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Brain Res. PD APR 1 PY 2002 VL 131 IS 1-2 BP 67 EP 78 DI 10.1016/S0166-4328(01)00350-3 PG 12 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 537UD UT WOS:000174777200007 PM 11844573 ER PT J AU Gregory, C Lough, S Stone, V Erzinclioglu, S Martin, L Baron-Cohen, S Hodges, JR AF Gregory, C Lough, S Stone, V Erzinclioglu, S Martin, L Baron-Cohen, S Hodges, JR TI Theory of mind in patients with frontal variant frontotemporal dementia and Alzheimer's disease: theoretical and practical implications SO BRAIN LA English DT Article DE theory of mind; social cognition; frontotemporal dementia; Alzheimer's disease; neuropsychiatry ID ASPERGER-SYNDROME; MENTAL STATE; AUTISM; CHILDREN; FEATURES; RECOGNITION; IMPAIRMENT; CONSENSUS; DIAGNOSIS; CRITERIA AB A key aspect of social cognition is the ability to infer other people's mental states, thoughts and feelings; referred to as 'theory of mind' (ToM). We tested the hypothesis that the changes in personality and behaviour seen in frontal variant frontotemporal dementia (fvFTD) may reflect impairment in this cognitive domain. Tests of ToM, executive and general neuropsychological ability were given to 19 fvFTD patients, a comparison group of Alzheimer's disease patients (n=12) and matched healthy controls (n=16). Neuropsychiatric assessment was undertaken using the Neuropsychiatric Inventory (NPI). Patients with fvFTD were impaired on all tests of ToM (first-order false belief; second-order false belief; faux pas detection; and Reading the Mind in the Eyes), but had no difficulty with control questions designed to test general comprehension and memory. By contrast, the Alzheimer's disease group failed only one ToM task (second-order false belief), which places heavy demands on working memory. Performance on the faux pas test revealed a double dissociation, with the fvFTD group showing deficits on ToM-based questions and the Alzheimer's disease group failing memory-based questions only. Rank order of the fvFTD patients according to the magnitude of impairment on tests of ToM and their degree of frontal atrophy showed a striking concordance between ToM performances and ventromedial frontal damage. There was a significant correlation between the NPI score and more sophisticated tests of ToM in the fvFTD group. This study supports the hypothesis that patients with fvFTD, but not those with Alzheimer's disease, are impaired on tests of ToM, and may explain some of the abnormalities in interpersonal behaviour that characterize fvFTD. C1 Univ Cambridge, MRC, Cognit & Brain Sci Unit, Cambridge CB2 2EF, England. Fulbourne Hosp, Cambridge, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 2EF, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 2EF, England. 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Autism is a severe neurodevelopmental disorder with potential genetic and environmental etiologies. Recent genetic linkage reports and biochemical analysis of postmortem autistic cerebellum point to Reelin, an important secretory extracellular protein, as being involved in the pathology of autism. 2. We hypothesized that blood levels of Reelin and its isoforms would be altered in autistic twins, and their first degree relatives versus normal controls. 3. We measured blood levels of unprocessed Reelin (410 kDa) and its proteolytic cleavage products (Reelins 330 and 180 kDa) as well as albumin and ceruloplasmin in 28 autistic individuals, their parents (13 fathers, 13 mothers), 6 normal siblings, and 8 normal controls using SDS-PAGE and western blotting. 4. Results indicated significant reductions in 410 kDa Reelin species in autistic twins (-70%, p < 0.01), their fathers (-62%, p < 0.01), their mothers (-72%, p < 0.01), and their phenotypically normal siblings (-70%, p < 0.01) versus controls. Reelin 330 kDa values did not vary significantly from controls. Reelin 180 kDa values for parents (fathers -32% p < 0.05 vs. controls, mothers -34%) declined when compared to controls. In contrast autistic Reelin 180 kDa increased, albeit nonsignificantly versus controls. Albumin and ceruloplasmin values for autistics and their first degree relatives did not vary significantly from controls. There were no significant meaningful correlations between Reelin, albumin and ceruloplasmin levels, age, sex, ADI scores, or age of onset. 5. These results suggest that Reelin 410 deficiency may be a vulnerability factor in the pathology of autism. C1 Univ Minnesota, Sch Med, Div Neurosci Res, Dept Psychiat, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Dept Neurosci, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Div Child & Adolescent Psychiat, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Div Neurosci Res, Dept Psychiat, MMC 392,420 Delaware St SE, Minneapolis, MN 55455 USA. 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Mol. Neurobiol. PD APR PY 2002 VL 22 IS 2 BP 139 EP 152 DI 10.1023/A:1019857620251 PG 14 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 586AG UT WOS:000177559300003 PM 12363196 ER PT J AU Fatemi, SH Halt, AR Realmuto, G Earle, J Kist, DA Thuras, P Merz, A AF Fatemi, SH Halt, AR Realmuto, G Earle, J Kist, DA Thuras, P Merz, A TI Purkinje cell size is reduced in cerebellum of patients with autism SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE cerebellum; autism; Purkinje cell; atrophy AB 1. The authors' goal was to compare the size and density of Purkinje cells in the cerebellum of subjects with and without autism. Blocks of cerebellum were dissected at autopsy from the brains of age, sex- and postmortem-intervaled (PMI) groups of autistic and normal control individuals (N = 5 per group). Frozen, unfixed blocks were sectioned and stained with 1% cresyl violet. 2. The linear, molecular, granular densities and cross-sectional area of Purkinje cells were measured using computer-assisted image analysis. The average cross-sectional areas of Purkinje cells of the patients with autism were smaller by 24% when compared to the normal subjects. Two of the five autistic subjects had mean Purkinje cell sizes that corresponded to greater than 50% reduction in size. There was a substantial effect size difference in Purkinje cell size (eta(2) = 0.29) between control and autistic brains (F(1, 8) = 3.32, P = 0.106). No differences in Purkinje cell densities were observed between the two groups. 3. These data indicate the possibility of Purkinje cell atrophy in autism with significant neurohistological heterogeneity among individuals diagnosed with this disorder. C1 Univ Minnesota, Dept Psychiat, Div Neurosci Res, Sch Med, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Psychiat, Div Child Psychiat, Sch Med, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Dept Psychiat, Div Neurosci Res, Sch Med, MMC 392,420 Delaware St SE, Minneapolis, MN 55455 USA. CR Fatemi SH, 1999, MOL PSYCHIATR, V4, P145, DOI 10.1038/sj.mp.4000520 Kemper T. L., 1994, NEUROBIOLOGY AUTISM, P19 Palay SL, 1974, CEREBELLAR CORTEX CY REYES MG, 1981, LANCET, V2, P700 Tran KD, 1998, AM J PSYCHIAT, V155, P1288 NR 5 TC 113 Z9 118 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD APR PY 2002 VL 22 IS 2 BP 171 EP 175 DI 10.1023/A:1019861721160 PG 5 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 586AG UT WOS:000177559300005 PM 12363198 ER PT J AU Ferguson, AP McKinlay, IA Hunt, A AF Ferguson, AP McKinlay, IA Hunt, A TI Care of adolescents with severe learning disability from tuberous sclerosis SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID INFANTILE SPASMS; CHILDREN; POPULATION; PREVALENCE; DISORDERS; BEHAVIOR; SEIZURES; COMPLEX; AUTISM AB A postal study was completed by 138 members of the Tuberous Sclerosis Association for individuals with severe learning disabilities from tuberous sclerosis complex (TSC) (78 males, median 20 years of age; 60 females median 19 years 6 months of age) to investigate the abilities and care needs of these adolescents and young adults. Results were compared with a Salford community survey of young people with severe learning disability (SLD) from a variety of causes (42 males, median 17 years; 29 females, median 17 years 8 months of age). Those with SLD associated with TSC had a higher level of verbal disability and were more dependent for managing toileting and bathing. The young people with TSC were less able to interact socially, showing autistic behaviour. Sexually, they were less aware and less active. Only 20 were thought by their parents to have received sex education. C1 Cent Manchester Primary Care Trust, Newton Heath Hlth Ctr, Manchester M40 2JF, Lancs, England. Univ Manchester, Royal Manchester Childrens Hosp, Mackay Gordon Ctr, Manchester, Lancs, England. Univ Cambridge, Tuberous Sclerosis Res Grp, Tuberous Sclerosis Assoc, Cambridge, England. RP Ferguson, AP (reprint author), Cent Manchester Primary Care Trust, Newton Heath Hlth Ctr, 2 Old Church St,Newton Heath, Manchester M40 2JF, Lancs, England. 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Med. Child Neurol. PD APR PY 2002 VL 44 IS 4 BP 256 EP 262 DI 10.1017/S0012162201002031 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 542XV UT WOS:000175071700007 PM 11995894 ER PT J AU Kuriyama, S Kamiyama, M Watanabe, MD Tamahashi, S Muraguchi, I Watanabe, T Hozawa, A Ohkubo, T Nishino, Y Tsubono, Y Tsuji, I Hisamichi, S AF Kuriyama, S Kamiyama, M Watanabe, MD Tamahashi, S Muraguchi, I Watanabe, T Hozawa, A Ohkubo, T Nishino, Y Tsubono, Y Tsuji, I Hisamichi, S TI 'Pyridoxine treatment in a subgroup of children with pervasive developmental disorders' SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Letter ID DEPENDENT SEIZURES; AUTISM C1 Tohoku Univ, Sch Med, Dept Publ Hlth, Sendai, Miyagi 9808575, Japan. Saka Gen Hosp, Shiogama, Miyagi, Japan. Miyagi Univ Educ, Dept Special Educ, Sendai, Miyagi, Japan. RP Kuriyama, S (reprint author), Tohoku Univ, Sch Med, Dept Publ Hlth, Sendai, Miyagi 9808575, Japan. 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PD APR PY 2002 VL 44 IS 4 BP 284 EP 286 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 542XV UT WOS:000175071700013 PM 11995900 ER PT J AU Grelotti, DJ Gauthier, I Schultz, RT AF Grelotti, DJ Gauthier, I Schultz, RT TI Social interest and the development of cortical face specialization: What autism teaches us about face processing SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Review DE autism; Asperger syndrome; social interest; face processing; fusiform gyrus; fusiform face area; amygdala; functional magnetic resonance imaging; expertise; modularity ID HUMAN EXTRASTRIATE CORTEX; FACIAL EXPRESSIONS; OBJECT RECOGNITION; ASPERGER-SYNDROME; HOME VIDEOTAPES; INVERTED FACES; HUMAN AMYGDALA; VISUAL-CORTEX; PERCEPTION; CHILDREN AB Investigations of face processing in persons with can autism spectrum disorder (ASD) inform upon theories of the development of "normal" face processing, and the story that emerges challenges some models of the nature and origin of cortical face specialization. Individuals with an ASD possess deficits in face processing and a lack of a fusiform face area (FFA). Evidence from studies of ASD can be conceptualized best using an expertise framework of face processing rather than models that postulate a face module in the fusiform gyrus. Because persons with an ASD have reduced social interest, they may fail to develop cortical face specialization. Face specialization may develop in normal individuals because they are socially motivated to regard the face, and such motivation promotes expertise for faces. The amygdala is likely the key node in the system that marks objects as emotionally salient and could be crucial to the development of cortical face specialization. (C) 2002 Wiley Periodicals, Inc. C1 Vanderbilt Univ, Dept Psychol, Nashville, TN 37203 USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dev Neuroimaging Program, New Haven, CT 06520 USA. 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Psychobiol. PD APR PY 2002 VL 40 IS 3 BP 213 EP 225 DI 10.1002/dev.10028 PG 13 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA 538NZ UT WOS:000174823200003 PM 11891634 ER PT J AU Torres, AR Maciulis, A Stubbs, EG Cutler, A Odell, D AF Torres, AR Maciulis, A Stubbs, EG Cutler, A Odell, D TI The transmission disequilibrium test suggests that HLA-DR4 and DR13 are linked to autism spectrum disorder SO HUMAN IMMUNOLOGY LA English DT Article DE autism; HLA; DR4; TDT; autoimmunity ID COMPLEMENT C4B PROTEIN; INCREASED FREQUENCY; X-CHROMOSOME; ASSOCIATION; REGION; BRAIN; MHC; RESPONSIVENESS; INDIVIDUALS; HAPLOTYPES AB We have evaluated possible contributions of HLA-DRB1 alleles to autism spectrum disorder (ASD) in 103 families of Caucasian descent. The DR4 allele occurred more often in probands than controls (0.007), whereas the DR13,14 alleles occurred less often in probands than controls (P = 0.003). The transmission disequilibrium test (TDT) indicated that the ASD probands inherited the DR4 allele more frequently than expected (p = 0.026) from the fathers, The TDT also revealed that fewer DR 13 alleles than expected were inherited from the mother by ASD probands (p = 0.006). We conclude that the TDT results suggest that DR4 and DR13 are linked to ASD. Reasons for the parental inheritance of specific alleles are poorly understood but coincide with current genetic research noting possible parent-of-origin effects in autism. (C) American Society for Histocompatibility and Immunogenetics, 2002. Published by Elsevier Science Inc. C1 Utah State Univ, Ctr Persons Disabil, Logan, UT 84322 USA. Oregon Hlth Sci Univ, Child Dev & Rehabil Ctr, Portland, OR 97201 USA. Utah State Univ, Dept Math & Stat, Logan, UT 84322 USA. RP Torres, AR (reprint author), Utah State Univ, Ctr Persons Disabil, 6895 Old Main Hill, Logan, UT 84322 USA. 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PD APR PY 2002 VL 14 IS 4 BP 1 EP 5 PG 5 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 535WL UT WOS:000174669300002 ER PT J AU Jensen, VK Sinclair, LV AF Jensen, VK Sinclair, LV TI Treatment of autism in young children: Behavioral intervention and applied behavior analysis SO INFANTS AND YOUNG CHILDREN LA English DT Article DE applied behavior analysis; autism; early intervention; pervasive developmental disorder; treatment ID PERVASIVE DEVELOPMENTAL DISORDER; 6-YEAR FOLLOW-UP; DIAGNOSTIC INTERVIEW; DIRECTIONS; SCIENCE; AGE AB Autism is one of the most widely recognized and reliably diagnosed developmental disorders. There is general professional consensus that autism is biologically based, with a strong genetic component and likely involvement of various neural structures. Distinct deficits in social reciprocity and relatedness are often apparent early in development typically by 12 to 15 months, with reliable and valid diagnosis usually possible by 24 months. Early and intensive behaviorally based treatment, in particular the use of applied behavior analysis, is effective in systematically teaching skills and reducing problematic behaviors. Despite evidence of efficacy, however, the limited availability of quality behavioral services for children with autism is a significant harrier to effective treatment. C1 Cleveland Clin Childrens Hosp, Sect Pediat Psychol, Cleveland, OH USA. Cleveland Clin Ctr Autism, Cleveland, OH USA. RP Jensen, VK (reprint author), Cleveland Clin Childrens Hosp, Sect Pediat Psychol, Cleveland, OH USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Arnold LE, 2000, J AUTISM DEV DISORD, V30, P99, DOI 10.1023/A:1005451304303 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P1 Barrett S, 1999, AM J MED GENET, V88, P609 BLACK J, 2000, QUALITY QUANTITY EXP Bristol-Power MM, 1999, J AUTISM DEV DISORD, V29, P435, DOI 10.1023/A:1021991718423 Carper RA, 2000, BRAIN, V123, P836, DOI 10.1093/brain/123.4.836 Chudley AE, 1998, J DEV BEHAV PEDIATR, V19, P321, DOI 10.1097/00004703-199810000-00001 *COMM CHILDR DIS, 2001, AM ACAD PEDIAT, V107, P1221 Committee on Educational Interventions for Children with Autism, 2001, ED CHILDR AUT Dawson G, 2000, DEV PSYCHOPATHOL, V12, P695, DOI 10.1017/S0954579400004089 Dawson G., 1997, EFFECTIVENESS EARLY, P307 *DEP HLTH EARL INT, 1999, CLIN PRACT GUID REP Filipek PA, 2000, NEUROLOGY, V55, P468 Gillberg C., 1992, BIOL AUTISTIC SYNDRO GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P489, DOI 10.1097/00004583-199105000-00022 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 GILLBERG C, 1990, International Review of Psychiatry, V2, P61, DOI 10.3109/09540269009028272 GREEN G, 1996, BEHAV INTERVENTION Y HARRIS SL, 1998, RIGHT START BEHAV IN Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Haznedar MM, 2000, AM J PSYCHIAT, V157, P1994, DOI 10.1176/appi.ajp.157.12.1994 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 IWATA BA, 1991, J APPL BEHAV ANAL, V24, P421, DOI 10.1901/jaba.1991.24-421 Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X Jacobson JW, 2000, J AUTISM DEV DISORD, V30, P585, DOI 10.1023/A:1005691411255 Jacobson JW, 2000, BEHAV ANALYST, V23, P149 JENSEN VK, 2001, INTENSIVE BEHAV INTE Koegel R. 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PD APR PY 2002 VL 14 IS 4 BP 42 EP 52 PG 11 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 535WL UT WOS:000174669300006 ER PT J AU Bolte, S Ozkara, N Poustka, F AF Bolte, S Ozkara, N Poustka, F TI Autism spectrum disorders and low body weight: Is there really a systematic association? SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article DE autism; Asperger syndrome; anorexia nervosa; weight; BMI ID ANOREXIA-NERVOSA; ASPERGERS-DISORDER; MALE-CHILDREN; ADOLESCENTS AB Objective: To examine the relationship between autism spectrum disorders and low body weight. Method: The effect of maladaptive social and communicative behavior as well as stereotyped features on the normative body mass index (BMI) was analyzed in 103 subjects with autism or Asperger syndrome. Statistics were controlled for medication, neurological signs, overactivity, and general intelligence. Results: Twenty-eight percent of the male individuals had a BMI in the fifth percentile or below. Except for hyperactive behavior, none of the predictors showed a significant association with BMI. None of the subjects met diagnostic criteria for anorexia nervosa. Discussion: Although low body weight is often present in male subjects with autism or Asperger syndrome, results indicate that this link is inconsistent and partly mediated by hyperactivity. The co-occurrence of autism spectrum disorders and anorexia nervosa is probably due to chance. (C) 2002 by Wiley Periodicals, Inc. C1 Univ Frankfurt, Dept Child & Adolescent Psychiat, D-60590 Frankfurt, Germany. RP Poustka, F (reprint author), Univ Frankfurt, Dept Child & Adolescent Psychiat, Deutschordenstr 50, D-60590 Frankfurt, Germany. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Fisman S, 1996, J AM ACAD CHILD PSY, V35, P937, DOI 10.1097/00004583-199607000-00021 Gillberg IC, 1996, COMPR PSYCHIAT, V37, P23, DOI 10.1016/S0010-440X(96)90046-2 Hebebrand J, 1997, ACTA PSYCHIAT SCAND, V96, P64, DOI 10.1111/j.1600-0447.1997.tb09906.x Hebebrand J., 1994, AKTUELLE ERNAHRUNGSM, P259 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 Nilsson EW, 1999, J AM ACAD CHILD PSY, V38, P1389, DOI 10.1097/00004583-199911000-00013 Sobanski E, 1999, EUR CHILD ADOLES PSY, V8, P312 NR 9 TC 27 Z9 28 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD APR PY 2002 VL 31 IS 3 BP 349 EP 351 DI 10.1002/eat.10015 PG 3 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA 534GJ UT WOS:000174576500016 PM 11920999 ER PT J AU van der Geest, JN Kemner, C Camfferman, G Verbaten, MN van Engeland, H AF van der Geest, JN Kemner, C Camfferman, G Verbaten, MN van Engeland, H TI Looking at images with human figures: Comparison between autistic and normal children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; gaze behavior; eye movements; social information processing ID PERVASIVE DEVELOPMENTAL DISORDERS; EYE-MOVEMENTS; INDIVIDUALS; CAREGIVERS; STIMULI AB Based on clinical observations of abnormal gaze behavior of autistic children, it has been suggested that autistic children have a problem in processing social information. Several studies on eye movements have indeed found indications that children with autism show particularly abnormal gaze behavior in relation to social stimuli. However, the methodology used in such investigations did not allow for precise gaze analysis. In the present study, the looking behavior of autistic children toward cartoon-like scenes that included a human figure was measured quantitatively using an infrared eye-tracking device. Fixation behavior of autistic children was similar to that of their age- and IQ-matched normal peers. These results do not support the notion that autistic children have a specific problem in processing socially loaded visual stimuli. Also, there is no indication for an abnormality in gaze behavior in relation to neutral objects. It is suggested that the often-reported abnormal use of gaze in everyday life is not related to the nature of the visual stimuli but that other factors, like social interaction, may play a decisive role. C1 Erasmus Univ, Dept Physiol, NL-3000 DR Rotterdam, Netherlands. Utrecht Med Ctr, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. Univ Utrecht, Dept Psychopharmacol, Utrecht Inst Pharmaceut Sci, Utrecht, Netherlands. RP van der Geest, JN (reprint author), Erasmus Univ, Dept Physiol, POB 1738, NL-3000 DR Rotterdam, Netherlands. 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R., 1990, DEV PSYCHOPATHOL, V2, P61, DOI 10.1017/S0954579400000596 Willemsen-Swinkels SHN, 1998, J AUTISM DEV DISORD, V28, P199, DOI 10.1023/A:1026013304241 Yarbus A. L., 1967, EYE MOVEMENTS VISION NR 20 TC 50 Z9 50 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 2002 VL 32 IS 2 BP 69 EP 75 DI 10.1023/A:1014832420206 PG 7 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100002 PM 12058845 ER PT J AU Siller, M Sigman, M AF Siller, M Sigman, M TI The behaviors of parents of children with autism predict the subsequent development of their children's communication SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; attention; communication; parent; language ID SPECIAL EDUCATIONAL TREATMENT; JOINT ATTENTION; DIAGNOSTIC INTERVIEW; LANGUAGE; PRESCHOOLERS; INTERVENTION; DISORDERS; CAREGIVERS; PSYCHIATRY; SPECTRUM AB The present study focused on behaviors that caregivers of children with autism show during play interactions, particularly the extent to which the caregiver's behavior is synchronized with the child's focus of attention and ongoing activity. The study had two major findings. First, caregivers of children with autism synchronized their behaviors to their children's attention and activities as much as did caregivers of children with developmental delay and caregivers of typically developing children, matched on language capacities. Second, caregivers of children with autism who showed higher levels of synchronization during initial play interactions had children who developed superior joint attention and language over a period of 1, 10, and 16 years than did children of caregivers who showed lower levels of synchronization initially. These findings suggest a developmental link between parental sensitivity and the child's subsequent development of communication skills in children with autism. Implications for parent training interventions are discussed. C1 Univ Calif Los Angeles, Sch Med, Dept Psychiat, Los Angeles, CA 90024 USA. 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PD APR PY 2002 VL 32 IS 2 BP 77 EP 89 DI 10.1023/A:1014884404276 PG 13 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100003 PM 12058846 ER PT J AU Carpenter, M Pennington, BF Rogers, SJ AF Carpenter, M Pennington, BF Rogers, SJ TI Interrelations among social-cognitive skills in young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; joint attention; imitation; gestural communication; point and gaze following; language ID DEVELOPMENTAL LANGUAGE DELAY; JOINT ATTENTION; COMMUNICATION; IMITATION; DIRECTION; DEFICITS; PROFILES; INFANTS; PLAY AB Typically developing infants show a reliable developmental sequence of emergence of early social-cognitive skills, such as joint attention, communicative gestures, gaze and point following, imitation, and referential language, First infants share others' attention, then they follow others' attention and then behavior, and then they direct others' attention and then behavior. The current study used a series of tests from a study of typically developing infants (Carpenter, Nagell, & Tomasello, 1998) to investigate interrelations among these social-cognitive skills in young children with autism and children with other developmental delays. Tests of object permanence, spatial relations, facial and manual imitation, and executive function also were included. We found that for most children with autism, unlike other children, tests involving others' attention were more difficult than tests involving others' behavior. However, within the domains of attention and behavior, the typical pattern of sharing, then following, and then directing was evident. There were several positive intercorrelations among the social-cognitive skills (as there were for typically developing infants), but there also was some evidence of individual differences in patterns. Implications for theories of social-cognitive and language development are discussed. C1 Max Planck Inst Evolut Anthropol, D-04103 Leipzig, Germany. Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. RP Carpenter, M (reprint author), Max Planck Inst Evolut Anthropol, Inselstr 22, D-04103 Leipzig, Germany. 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PD APR PY 2002 VL 32 IS 2 BP 91 EP 106 DI 10.1023/A:1014836521114 PG 16 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100004 PM 12058847 ER PT J AU Fisch, GS Simensen, RJ Schroer, RJ AF Fisch, GS Simensen, RJ Schroer, RJ TI Longitudinal changes in cognitive and adaptive Behavior scores in children and adolescents with the fragile X mutation or autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; fragile X; cognitive ability; adaptive behavior; longitudinal studies ID PROSPECTIVE MULTICENTER ANALYSIS; MENTAL-RETARDATION; MALES; AGE; IQ; STABILITY; PARAMETERS; ADULTS AB Studies of the relationship between the fragile X (FRAXA) mutation and autism have been controversial. Although there are differences between the two populations, individuals with FRAXA and autism exhibit remarkably similar aberrant behavior patterns. We examined comparably aged children and adolescents with FRAXA or autism to determine whether longitudinal changes in cognitive ability and adaptive behavior were similar in the two groups. We found decreases in IQ scores in young children with FRAXA as well as in those with autism. Declines in IQ scores were steeper among children with FRAXA. Older children and adolescents with autism exhibit stable test-retest scores, whereas older children with FRAXA continue to show decreases. Comparable declines in adaptive behavior composite scores were observed in both groups, at all ages tested, and across all adaptive behavior domains. C1 Yale Univ, Sch Med, Gen Clin Res Ctr, New Haven, CT 06520 USA. Greenwood Genet Ctr, Greenwood, SC 29646 USA. RP Fisch, GS (reprint author), Yale Univ, Sch Med, Gen Clin Res Ctr, 333 Cedar St,POB 208019, New Haven, CT 06520 USA. 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Autism Dev. Disord. PD APR PY 2002 VL 32 IS 2 BP 107 EP 114 DI 10.1023/A:1014888505185 PG 8 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100005 PM 12058838 ER PT J AU Lauritsen, MB Mors, O Mortensen, PB Ewald, H AF Lauritsen, MB Mors, O Mortensen, PB Ewald, H TI Medical disorders among inpatients with autism in Denmark according to ICD-8: A nationwide register-based study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; autism, infantile; medical disorders; etiology; Denmark; incidence ID EPIDEMIOLOGIC SURVEY; TUBEROUS-SCLEROSIS; FAMILY HISTORY; BEHAVIOR; CHILDREN; RISKS; TWIN AB Possible associations between autism and specific medical disorders have been suggested, and this could be of relevance in the clinical examination and treatment of patients and may help to identify factors involved in the etiology or pathophysiology of autism. Two population-based Danish registers were used to investigate the occurrence of medical disorders in patients with autism according to ICD-8 and in a matched control sample. A total of 29 of the 244 patients (11.9%) diagnosed with autism had one or more medical disorders. In contrast to previous studies, we did not find an increased occurrence of almost any medical disorders. A highly significant increased frequency of congenital malformations was found, which may indicate abnormalities in embryogenesis in the etiology of autism. C1 Aarhus Univ Hosp, Dept Psychiat Demog, Inst Basic Psychiat Res, Psychiat Hosp Aarhus, DK-8240 Risskov, Denmark. Univ Aarhus, Natl Ctr Register Based Res, Aarhus, Denmark. RP Lauritsen, MB (reprint author), Aarhus Univ Hosp, Dept Psychiat Demog, Inst Basic Psychiat Res, Psychiat Hosp Aarhus, DK-8240 Risskov, Denmark. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 1995, PSYCHOL MED, V25, P63 Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Breslow NE, 1987, STAT METHODS CANC RE, VII Dykens E. 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Autism Dev. Disord. PD APR PY 2002 VL 32 IS 2 BP 115 EP 119 DI 10.1023/A:1014840622023 PG 5 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100006 PM 12058839 ER PT J AU Baker, HC AF Baker, HC TI A comparison study of autism spectrum disorder referrals 1997 and 1989 SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; prevalence; Australian Capital Territory (ACT) ID PREVALENCE AB A number of overseas studies have indicated an increase in the prevalence of Autism Spectrum Disorder (ASD). In the Australian Capital Territory, information (number, age, sex, final diagnosis) was gathered on all children referred for suspected ASD to Child and Adolescent Mental Health Service during 1997, and the findings were compared with those from a similar study in 1989. It was found that (1) there was a 200% increase in positive diagnoses of ASD in 1997 despite a 0.5% decrease in population, (2) there was a wider age range in the 1997 cohort, (3) there was a 26% increase in milder cases in 1997, and (4) the ratio of boys to girls decreased from 8:1 in 1989 to 3.5:1 in 1997. These findings are compared with those overseas, and questions are raised for further exploration. C1 Child & Adolescent Mental Hlth Serv, Belconnen, ACT 2616, Australia. RP Baker, HC (reprint author), Child & Adolescent Mental Hlth Serv, POB 46, Belconnen, ACT 2616, Australia. CR Achenbach T., 1991, CHILD BEHAV CHECKLIS *AM PSYCH ASS, 1987, DSM 111 R DIAGN STAT American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th BARENCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285 BARENCOHEN S, 1995, COGNITION, V21, P37 EINFELD SL, 1995, J AUTISM DEV DISORD, V25, P81, DOI 10.1007/BF02178498 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 1996, J AUTISM DEV DISORD, V26, P673, DOI 10.1007/BF02172357 GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Klin A., 1995, CHILD ADOL PSYCH CL, V4, P617 Schopler E., 1986, CHILDHOOD AUTISM RAT VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Webb EVJ, 1997, DEV MED CHILD NEUROL, V39, P150 Wing L., 1982, SCHEDULE HANDICAPS B Wing L., 1996, PRESCHOOL CHILDREN I, P247 WING L, 1981, PSYCHOL MED, V11, P115 NR 16 TC 17 Z9 18 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 2002 VL 32 IS 2 BP 121 EP 125 DI 10.1023/A:1014892606093 PG 5 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100007 PM 12058840 ER PT J AU Luckett, T Powell, SD Messer, DJ Thornton, ME Schulz, J AF Luckett, T Powell, SD Messer, DJ Thornton, ME Schulz, J TI Do children with autism who pass false belief tasks understand the mind as active interpreter? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; theory of mind; interpretive diversity ID MENTAL-RETARDATION; PERFORMANCE; INDIVIDUALS; COMPETENCE; KNOWLEDGE; ABILITIES; DEFICIT; AGE AB Interpretive diversity is the term used by Carpendale and Chandler (1996) to refer to the fact that two individuals exposed to precisely the same stimulus may interpret it in quite different, but equally plausible, ways. An appreciation of interpretive diversity is said by Carpendale and Chandler to represent a development in understanding that is qualitatively different from that necessary to succeed on false belief tasks. A study is reported in which children with autism and children with general delay were given a battery of tasks consisting of false belief tasks and tasks designed to test for an understanding of interpretive diversity. Findings from the present study offer limited support for Carpendale and Chandler's claim that tasks which test for an understanding of interpretive diversity may be more difficult than false belief tasks. Between-group differences in the consistency and quality of responses given by participants suggest that autistic and delayed children may have differed somewhat in their approach to the tasks given. C1 Univ Hertfordshire, Dept Educ, Aldenham WD2 8AT, Herts, England. Univ Hertfordshire, Dept Psychol, Hatfield AL10 9AB, Herts, England. RP Luckett, T (reprint author), Univ Hertfordshire, Dept Educ, Watford Campus,Wall Hall, Aldenham WD2 8AT, Herts, England. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASTINGTON JW, 1995, HUM DEV, V38, P179 Baron-Cohen S, 2001, INT REV RES MENT RET, V23, P169 BARONCOHEN S, 1992, J CHILD PSYCHOL PSYC, V33, P1141, DOI 10.1111/j.1469-7610.1992.tb00934.x BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1994, BRIT J DEV PSYCHOL, V12, P397 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bartsch K., 1995, CHILDREN TALK MIND Bishop D. V. M., 1989, TEST RECEPTION GRAMM BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P607 Carpendale JI, 1996, CHILD DEV, V67, P1686, DOI 10.1111/j.1467-8624.1996.tb01821.x Chandler M. J., 1982, HDB DEV PSYCHOL, P387 Charman T, 1997, J CHILD PSYCHOL PSYC, V38, P725, DOI 10.1111/j.1469-7610.1997.tb01699.x DARLEY JM, 1986, PSYCHOLOGY Dunn L M., 1982, BRIT PICTURE VOCABUL Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X FRITH U, 1991, TRENDS NEUROSCI, V14, P433, DOI 10.1016/0166-2236(91)90041-R Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 Happe F., 1994, AUTISM INTRO PSYCHOL HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R HURLBURT RT, 1994, PSYCHOL MED, V24, P385 Jastrow Joseph, 1900, FACT FABLE PSYCHOL Kazak S, 1997, J CHILD PSYCHOL PSYC, V38, P1001, DOI 10.1111/j.1469-7610.1997.tb01617.x LEEKAM SR, 1991, COGNITION, V40, P203, DOI 10.1016/0010-0277(91)90025-Y Leslie A. M., 1993, UNDERSTANDING OTHER, P83 LESLIE AM, 1992, COGNITION, V43, P225, DOI 10.1016/0010-0277(92)90013-8 LESLIE AM, 1994, COGNITION, V50, P211, DOI 10.1016/0010-0277(94)90029-9 LOVELAND KA, 1990, BRIT J DEV PSYCHOL, V8, P9 Nelson K, 1998, HUM DEV, V41, P7 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x PERNER J, 1991, COGNITION, V39, P51, DOI 10.1016/0010-0277(91)90059-D Peterson CC, 1998, BRIT J DEV PSYCHOL, V16, P301 REED T, 1990, J AUTISM DEV DISORD, V20, P555, DOI 10.1007/BF02216060 Roth D, 1998, COGNITION, V66, P1, DOI 10.1016/S0010-0277(98)00005-5 Sacks Oliver, 1995, ANTHR MARS Scholl BJ, 1999, MIND LANG, V14, P131, DOI 10.1111/1468-0017.00106 SEGAR M, 1997, UNPUB COPING SURVIVA Surian L, 1999, BRIT J DEV PSYCHOL, V17, P141, DOI 10.1348/026151099165203 TAGERFLUSBERG H, 1994, J CHILD PSYCHOL PSYC, V35, P1059, DOI 10.1111/j.1469-7610.1994.tb01809.x Tager-Flusberg H, 1999, INT REV PSYCHIATR, V11, P325, DOI 10.1080/09540269974203 TAYLOR M, 1991, CHILD DEV, V62, P1334, DOI 10.1111/j.1467-8624.1991.tb01609.x Williams D, 1994, SOMEBODY SOMEWHERE Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x ZAITCHIK D, 1990, COGNITION, V35, P41, DOI 10.1016/0010-0277(90)90036-J NR 48 TC 7 Z9 9 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 2002 VL 32 IS 2 BP 127 EP 140 DI 10.1023/A:1014844722931 PG 14 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100008 PM 12058841 ER PT J AU Escalona, A Field, T Nadel, J Lundy, B AF Escalona, A Field, T Nadel, J Lundy, B TI Brief report: Imitation effects on children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; imitation; distal social behavior; proximal social behavior ID TO-FACE INTERACTION AB Twenty children with autism (mean age, 5 years) were recruited for the study from a school for children with autism. The children were randomly assigned to an imitation (n=10) or contingently responsive (n=10) interaction group based on a stratification table for gender and developmental and chronological age. The sessions consisted of four phases, with each phase lasting 3 minutes. In the first phase, the child walked into a room that was furnished with a sofa, a table, chairs, and two sets of identical toys. An adult was in the room sitting very still like a statue (first still-face condition). In the second phase, the adult either imitated the child or was contingently responsive to the child. In the third phase, the adult sat still again (second still-face condition), and in the fourth phase, the adult engaged in a spontaneous interaction. During the third phase (the second still-face condition), the children in the imitation group spent less time in gross motor activity and more time touching the adult, as if attempting to initiate an interaction. The contingency condition appeared to be a more effective way to facilitate a distal social behavior (attention), whereas the imitative condition was a more effective way to facilitate a proximal social behavior (touching). C1 Univ Miami, Sch Med, Dept Pediat, Touch Res Inst, Miami, FL 33101 USA. Touch Res Inst, Lab Psychobiol Dev, Paris, France. Indiana Univ Purdue Univ, Dept Psychol, Ft Wayne, IN 46805 USA. RP Field, T (reprint author), Univ Miami, Sch Med, Dept Pediat, Touch Res Inst, POB 016820, Miami, FL 33101 USA. CR BARANEK GT, 1999, SRCD BAYLEY N, 1969, BARMY SCALES INFANT COHEN J, 1968, PSYCHOL BULL, V70, P213, DOI 10.1037/h0026256 DAWSON G, 1984, J ABNORM CHILD PSYCH, V12, P209, DOI 10.1007/BF00910664 Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 FIELD TM, 1977, CHILD DEV, V48, P763, DOI 10.1111/j.1467-8624.1977.tb01232.x Hobson P, 1993, AUTISM DEV MIND Hollingshead A. B., 1975, 4 FACTOR INDEX SOCIA KERVELLA C, 1999, ENFANCE, V51, P191 LUBIN L, 1981, INT J BEHAV DEV, V4, P443 NADEL J, 2000, AUTISM, P133 Nadel J., 1993, NEW PERSPECTIVES EAR Piaget J., 1951, PLAY DREAMS IMITATIO TIEGERMAN E, 1981, J AUTISM DEV DISORD, V11, P427 TIEGERMAN E, 1984, J AUTISM DEV DISORD, V14, P27, DOI 10.1007/BF02408553 TRONICK E, 1978, J AM ACAD CHILD PSY, V17, P1, DOI 10.1016/S0002-7138(09)62273-1 NR 16 TC 35 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 APR PY 2002 VL 32 IS 2 BP 141 EP 144 DI 10.1023/A:1014896707002 PG 4 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100009 PM 12058842 ER PT J AU Blanchon, YC Gay, C Gibert, G Lauras, B AF Blanchon, YC Gay, C Gibert, G Lauras, B TI A case of N-acetyl galactosaminidase deficiency (Schindler disease) associated with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID CHILDHOOD C1 CHU, Federat Pediatry Genet & Pedopsychiat, Leo Kanner Ctr, F-42055 St Etienne Du Rouvray 2, France. RP Blanchon, YC (reprint author), CHU, Federat Pediatry Genet & Pedopsychiat, Leo Kanner Ctr, F-42055 St Etienne Du Rouvray 2, France. CR DESNICK RJ, 1994, METABOLIC BASIS INHE, V1, P2509 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 RIMLAND B, 1971, J AUTISM CHILD SCHIZ, V1, P161, DOI 10.1007/BF01537955 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Simonoff E, 1998, J AUTISM DEV DISORD, V28, P447, DOI 10.1023/A:1026060623511 NR 6 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 2002 VL 32 IS 2 BP 145 EP 146 PG 2 WC Psychology, Developmental SC Psychology GA 556LW UT WOS:000175852100010 PM 12058843 ER PT J AU Sokol, DK Dunn, DW Edwards-Brown, M Feinberg, J AF Sokol, DK Dunn, DW Edwards-Brown, M Feinberg, J TI Hydrogen proton magnetic resonance Spectroscopy in autism: Preliminary evidence of elevated choline/creatine ratio SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PEDIATRIC BRAIN-TUMORS; MENTAL-RETARDATION; ALZHEIMERS-DISEASE; WHITE-MATTER; MRI; ADRENOLEUKODYSTROPHY; DISORDER; CHILDREN; SPECT; GRAY AB Hydrogen proton magnetic resonance spectroscopy is only beginning to be studied in autistic individuals. We report, an association between hydrogen proton magnetic resonance spectroscopy choline/creatine ratios and severity of autism as measured by the Children's Autistic Rating Scale (Pearson r =.657, P =.04) in 10 autistic children. Hydrogen proton magnetic resonance spectroscopy choline/creatine ratio measures the concentration of cytosolic choline including free choline used in the synthesis of acetylcholine. Elevation in this ratio has been interpreted as a result of membrane degradation such as caused by a tumor or, alternatively, as a result of choline synthesis associated with increased cellular proliferation. Recent neuropathologic evidence has implicated disruption of acetylcholine transmission in the brains of autistic adults. A case-controlled study of hydrogen proton magnetic resonance spectroscopy choline/creatine ratios is warranted. C1 Indiana Univ, Sch Med, Dept Neurol, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Radiol, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Orthoped Surg, Indianapolis, IN USA. RP Sokol, DK (reprint author), Indiana Univ, Med Ctr, James Whitcomb Riley Hosp Children, Sect Pediat Neurol, 702 Barnhill Dr, Indianapolis, IN 46202 USA. 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PD APR PY 2002 SU S MA B20 BP 48 EP 48 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 525LP UT WOS:000174072000149 ER PT J AU Ziegler, A Herbert, MR Adrien, KT Makris, N Kennedy, DN Bakardjiev, A Hodgson, J Takeoka, M Harris, GJ Caviness, VS AF Ziegler, A Herbert, MR Adrien, KT Makris, N Kennedy, DN Bakardjiev, A Hodgson, J Takeoka, M Harris, GJ Caviness, VS TI Cortical asymmetries and language ability in boys with autism or specific language impairment SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Charlestown, MA USA. Childrens Hosp Oakland, Oakland, CA 94609 USA. Keio Univ, Sch Med, Tokyo, Japan. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD APR PY 2002 SU S MA D26 BP 101 EP 101 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 525LP UT WOS:000174072000393 ER PT J AU Boser, K Smrcka, V Wheelan, M Fitzgerald, A Hamdy, R Gordon, B AF Boser, K Smrcka, V Wheelan, M Fitzgerald, A Hamdy, R Gordon, B TI Familiarity and interference in learning single word-to-picture discrimination in low functioning autism SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD APR PY 2002 SU S MA F57 BP 160 EP 160 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 525LP UT WOS:000174072000662 ER PT J AU Frith, C Gallagher, S AF Frith, C Gallagher, S TI Models of the pathological mind SO JOURNAL OF CONSCIOUSNESS STUDIES LA English DT Editorial Material ID AUDITORY HALLUCINATIONS; PREFRONTAL CORTEX; FRONTAL LOBES; SCHIZOPHRENIA; MOVEMENT; BELIEF; PET; SYMPTOMATOLOGY; BEHAVIOR; AUTISM C1 Inst Neurol, Wellcome Dept Cognit Neurol, London WC1N 3BG, England. Canisius Coll, Dept Philosophy, Buffalo, NY 14208 USA. RP Frith, C (reprint author), Inst Neurol, Wellcome Dept Cognit Neurol, Queen Sq, London WC1N 3BG, England. 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PD APR PY 2002 VL 9 IS 4 BP 57 EP 80 PG 24 WC Philosophy; Social Sciences, Interdisciplinary SC Philosophy; Social Sciences - Other Topics GA 554ZC UT WOS:000175766400004 ER PT J AU Bowers, L AF Bowers, L TI An audit of referrals of children with autistic spectrum disorder to the dietetic service SO JOURNAL OF HUMAN NUTRITION AND DIETETICS LA English DT Article DE autism; autistic spectrum disorder; children; diet AB Autistic spectrum disorder (ASD) is a developing area for dietetic referrals. There is little published data on current dietetic practice. Some children with ASD are referred for gluten/casein free diet. The theory is that abnormal metabolites in the urine may be a result of incomplete breakdown of gluten and casein in the gut. There are some published open studies that support the efficiency of such a diet [Knivsberg et al. (1995) Scand. J. Educ. Res. 39: 223; Lucarelli et al. (1995) Panminerva Med. 37: 137; Whiteley et al. (1999) Int. J. Res. Practice 3: 451 and also that there are many anecdotal reports that the diet helps some children. Aims and objectives This study aimed to audit the types of referral made to the dietetic service to identify key dietetic issues and to describe factors which may influence outcome/disease management. Methods Dietetic records were used to audit the referrals to the dietetic service over a 3-month period. Seven-day diet histories were assessed using computer food composition tables and topics of interest recorded against a draft protocol agreed within the profession. Results Requests for gluten-free and casein-free dietetic advice, and/ or the management of food selectivity and dysfunctional feeding behaviour constituted the majority of referrals. In many cases, child's environment was rarely simple. Conclusions Despite the limitations of this small study, the findings suggest that the management of these referrals is highly complex. 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Diet. PD APR PY 2002 VL 15 IS 2 BP 141 EP 144 DI 10.1046/j.1365-277X.2002.00345.x PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 549UZ UT WOS:000175466300006 PM 11972743 ER PT J AU Szatmari, P Merette, C Bryson, SE Thivierge, J Roy, MA Cayer, M Maziade, M AF Szatmari, P Merette, C Bryson, SE Thivierge, J Roy, MA Cayer, M Maziade, M TI Quantifying dimensions in autism: A factor-analytic study SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; phenotype; measurement ID PERVASIVE DEVELOPMENTAL DISORDER; BEHAVIOR CHECKLIST; SPECTRUM DISORDERS; CHILDREN; DIAGNOSIS; VALIDITY; DOMAINS; SCALES; CLASSIFICATION; INDIVIDUALS AB Objective: The objective of this study was to determine whether the phenotypic variation in autism and the related pervasive developmental disorders (PDDs) is a unitary construct or whether it is composed of distinct dimensions of autistic symptoms and measures of level of functioning. Method: One hundred twenty-nine children with autism and other forms of PDD from two samples with different inclusion criteria were assessed with the Vineland Adaptive Behavior Scales to measure level of functioning and the Autism Diagnostic Interview to measure severity of autistic behaviors. A factor analysis with varimax rotation was performed on each sample, separately and combined. Results: Two factors emerged; one representing autistic symptoms and another representing level of functioning. The factor structure was remarkably similar and robust to variations in ascertainment and inclusion criteria between the samples. The validity of the distinction was supported by differences between males and females on the symptom factor, but not on the level of functioning factor. IQ was modestly correlated with level of functioning, but not with symptoms. Conclusions: The phenotypic variation seen in autism/PDD is composed of at least two different dimensions of autistic symptoms and level of functioning. The implications of this dimensional heterogeneity for research, classification, and clinical practice are discussed. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. York Univ, Dept Psychol, N York, ON M3J 1P3, Canada. Univ Laval, Ctr Rech Robert Giffard, Beauport, PQ, Canada. RP Szatmari, P (reprint author), Canadian Ctr Studies Children Risk, HHS Chedoke Site,Patterson 207, Hamilton, ON L8N 3Z5, Canada. 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Am. Acad. Child Adolesc. Psychiatr. PD APR PY 2002 VL 41 IS 4 BP 467 EP 474 DI 10.1097/00004583-200204000-00020 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 533HM UT WOS:000174523600021 PM 11931604 ER PT J AU Seeman, C AF Seeman, C TI A picture's worth: PECS and other visual communication strategies in 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, Toledo, OH 43606 USA. CR Bondy Andy, 2002, PICTURES WORTH PECS 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 2002 VL 127 IS 6 BP 132 EP 132 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 534ZJ UT WOS:000174619400182 ER PT J AU Skoyles, JR AF Skoyles, JR TI Is autism due to cerebral-cerebellum disconnection? SO MEDICAL HYPOTHESES LA English DT Article ID HUMAN BRAIN; NEUROANATOMICAL ABNORMALITIES; NEURONS; ORIGIN; PROJECTIONS; TRACKING; TARGET; AXONS; MIND; RAT AB Autism has been linked to thalidomide exposure at 20-24 days gestation. At this stage, the embryo is roughly the size of this 'C', and has yet to develop its brain (except for brainstem cranial motor nerve nuclei). The neuropathology responsible for autism is presently unknown, but whatever it is, it must logically be one that can be induced by such an early occurring brainstem cranial motor nerve nuclei defect. Many mental faculties impaired in autism (such as theory of mind) depend upon the prefrontal cortex. The maturation of cerebral-cerebellar connections, due to oddities in axon development, is vulnerable to pre-existing brainstem nuclei integrity. Many higher cognitions (including prefrontal ones) are dependent upon these links raising the possibility that abnormalities in them might produce autism. I conjecture that impaired cerebral-cerebellar connections, whether caused early, as by thalidomide, or later (including postnatally) by other factors, is the missing neuropathological cause of autism. (C) 2002 Published by Elsevier Science Ltd. C1 Univ London London Sch Econ & Polit Sci, Ctr Philosophy Nat & Social Sci, London WC2A 2AE, England. RP Skoyles, JR (reprint author), Univ London London Sch Econ & Polit Sci, Ctr Philosophy Nat & Social Sci, Houghton St, London WC2A 2AE, England. 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Hypotheses PD APR PY 2002 VL 58 IS 4 BP 332 EP 336 DI 10.1054/mehy.2001.1537 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 576UD UT WOS:000177023300016 PM 12027528 ER PT J AU Ijichi, S Ijichi, N AF Ijichi, S Ijichi, N TI Minor form of trigonocephaly is an autistic skull shape? A suggestion based on homeobox gene variants and MECP2 mutations SO MEDICAL HYPOTHESES LA English DT Article ID DISORDERS; HOXA1; HOXB1 AB A possible role for Hoxa1 genotype in susceptibility to autism spectrum disorders was recently proposed. Furthermore, it has been demonstrated that Rett syndrome, which is categorized into pervasive developmental disorders the same as the autism spectrum disorders are, is associated with mutations in MECP2gene. These findings suggest that the genetic backgrounds of these behavioral conditions may involve genes which also have an important role in the development of skull, because Hoxa1 is a key gene for skull development as well as for brain development and one of the clinical characteristics of Rett syndrome is deceleration in head growth. Together with this evolving knowledge, a series of ethical arguments concerning the indication of surgical treatment in patients with minor forms of trigonocephaly with autistic behaviors and/or hyperactivity leads us to hypothesize the presence of an autism subtype which may frequently be accompanied by specific morphological skull characteristics (autistic skull shape). (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Inst EGT, Kagoshima 8961411, Japan. RP Ijichi, S (reprint author), Inst EGT, 8-3 Nagahama, Kagoshima 8961411, Japan. 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Hypotheses PD APR PY 2002 VL 58 IS 4 BP 337 EP 339 DI 10.1054/mehy.2001.1528 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 576UD UT WOS:000177023300017 PM 12027529 ER PT J AU Winslow, JT Insel, TR AF Winslow, JT Insel, TR TI The social deficits of the oxytocin knockout mouse SO NEUROPEPTIDES LA English DT Article ID MATERNAL-BEHAVIOR; ARGININE-VASOPRESSIN; OLFACTORY-BULB; FEMALE RATS; RECOGNITION RESPONSES; AGGRESSIVE-BEHAVIOR; ENDOGENOUS OXYTOCIN; MEDIAL AMYGDALA; PRAIRIE VOLES; MICE AB Numerous studies have implicated oxytocin (OT) and oxytocin receptors in the central mediation of social cognition and social behavior. Much of our understanding of OT's central effects depends on pharmacological studies with OT agonists and antagonists. Recently, our knowledge of OT's effects has been extended by the development of oxytocin knockout (OTKO) mice. Mice with a null mutation of the OT gene manifest several interesting cognitive and behavioral changes, only some of which were predicted by pharmacological studies. Contrary to studies in rats, mice do not appear to require OT for normal sexual or maternal behavior, though OT is necessary for the milk ejection reflex during lactation. OTKO pups thrive if raised by a lactating female, but OTKO pups emit fewer ultrasonic vocalizations with maternal separation and OTKO adults are more aggressive than WT mice. Remarkably, OTKO mice fail to recognize familiar conspecifics after repeated social encounters, though olfactory and non-social memory functions appear to be intact. Central OT administration into the amygdala restores social recognition. The development of transgenic mice with specific deficits in social memory represents a promising approach to examine the cellular and neural systems of social cognition. 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Floating Hosp Children, Div Pediat & Adolescent Med, Boston, MA USA. Floating Hosp Children, Ctr Children Special Needs, Boston, MA USA. Tufts Univ New England Med Ctr, Dept Psychiat, Boston, MA 02111 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 2002 VL 51 IS 4 SU S MA 138 BP 24A EP 24A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600139 ER PT J AU Barbaresi, WJ Katusic, SK Colligan, RC Pankratz, VS Weaver, AL Jacobsen, SJ AF Barbaresi, WJ Katusic, SK Colligan, RC Pankratz, VS Weaver, AL Jacobsen, SJ TI Apparent increase in the rate of diagnosis of autism and other pervasive developmental disorders (PDD) in Olmsted County, Minnesota from 1976 to 1997 SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Mayo Clin, Div Dev & Behav Pediat, Rochester, MN USA. Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA. Mayo Clin, Dept Psychiat & Psychol, Rochester, MN 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 2002 VL 51 IS 4 SU S MA 2666 BP 458A EP 458A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602664 ER PT J AU Zwaigenbaum, L Bryson, SE Rombough, V McDermott, C Szatmari, P Roberts, W Adams, B Brian, J AF Zwaigenbaum, L Bryson, SE Rombough, V McDermott, C Szatmari, P Roberts, W Adams, B Brian, J TI Behavioural risk markers in infant siblings of children with autism SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 McMaster Univ, Hamilton, ON L8S 4L8, Canada. Dalhousie Univ, Halifax, NS B3H 3J5, Canada. Univ Toronto, Toronto, ON, Canada. 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 2002 VL 51 IS 4 SU S MA 2667 BP 458A EP 458A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602665 ER PT J AU Charman, T AF Charman, T TI Autism and MMR SO PSYCHOLOGIST LA English DT News Item ID CHILDREN C1 UCL, Behav & Brain Sci Unit, Inst Child Hlth, London WC1E 6BT, England. RP Charman, T (reprint author), UCL, Behav & Brain Sci Unit, Inst Child Hlth, London WC1E 6BT, England. 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PD MAR 29 PY 2002 IS 5165 BP 17 EP 17 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 535NX UT WOS:000174651500025 ER PT J AU Jyonouchi, H Sun, SN Le, H Rusche, J AF Jyonouchi, H Sun, SN Le, H Rusche, J TI CTLA4-Ig down-regulates IFN-gamma produced by peripheral blood mononuclear cells from children with autism spectrum disorder (ASD) and dietary protein intolerance (DPI) SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN 55455 USA. Repligen Corp, Needham, MA USA. NR 0 TC 0 Z9 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A712 EP A712 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603956 ER PT J AU Sergeant, JA Geurts, H Oosterlaan, J AF Sergeant, JA Geurts, H Oosterlaan, J TI How specific is a deficit of executive functioning for Attention-Deficit/Hyperactivity Disorder? SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Dopamine Hypothesis of ADHD CY FEB 14-25, 2000 CL CASTILLA LA MANCHA, SPAIN HO UNIV CASTILLA LA MANCHA DE attention-deficit/hyperactivity disorder; working memory; inhibition; attention; planning; stroop; fluency; higher functioning autism; working memory; Tower of London; stop-signal task ID FRONTAL-LOBE TESTS; CARD SORTING TEST; HYPERACTIVITY DISORDER; INHIBITORY CONTROL; RESPONSE-INHIBITION; CONDUCT DISORDER; NORMAL-CHILDREN; TOURETTE-SYNDROME; NEUROPSYCHOLOGICAL CHARACTERISTICS; HYPERKINETIC DISORDER AB A selective review of research in the executive functioning (EF) is given for attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), conduct disorder (CD), higher functioning autism (HFA) and Tourette syndrome. The review is restricted due to changes in the classification of the disorder in recent years and secondly the heterogeneity of EF is restricted to five key areas of concern, inhibition, set shifting, working memory, planning, and fluency. The review makes clear that there are strong differences between child psychopathological groups and controls on these EFs. However, future research will be needed to identify an EF deficit or profile, which is specific for these disorders. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Vrije Univ Amsterdam, Klin Neuropsychol, NL-1081 BT Amsterdam, Netherlands. RP Sergeant, JA (reprint author), Vrije Univ Amsterdam, Klin Neuropsychol, Boechorststr 1, NL-1081 BT Amsterdam, Netherlands. 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Brain Res. PD MAR 10 PY 2002 VL 130 IS 1-2 SI SI BP 3 EP 28 DI 10.1016/S0166-4328(01)00430-2 PG 26 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 536VF UT WOS:000174722000002 PM 11864714 ER PT J AU Philippe, A Guilloud-Bataille, M Martinez, M Gillberg, C Rastam, M Sponheim, E Coleman, M Zappella, M Aschauer, H Penet, C Feingold, J Brice, A Leboyer, M AF Philippe, A Guilloud-Bataille, M Martinez, M Gillberg, C Rastam, M Sponheim, E Coleman, M Zappella, M Aschauer, H Penet, C Feingold, J Brice, A Leboyer, M CA Paris Autism Res Int Sibpair Study TI Analysis of ten candidate genes in autism by association and linkage SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; linkage disequilibrium; linkage; sib-pair ID INFANTILE-AUTISM; DISORDERS; DISEQUILIBRIUM; MARKER AB We studied the possible involvement of ten candidate genes in autism: proenkephalin, prodynorphin, and proprotein convertase subtilisin/kexin type 2 (opioid metabolism); tyrosine hydroxylase, dopamine receptors D2 and D5, monoamine oxidases A and B (monoaminergic system); brain-derived neurotrophic factor, and neural cell adhesion molecule (involved in neurodevelopment). Thirty-eight families with two affected siblings and one family with two affected half-siblings, recruited by the Paris Autism Research International Sibpair Study (PARIS), were tested using the transmission disequilibrium test and two-point affected sib-pair linkage analysis. We found no evidence for association or linkage with intragenic or linked markers. Our family sample has good power for detecting a linkage disequilibrium of 0.80. Thus, these genes are unlikely to play a major role in the families studied, but further studies in a much larger sample would be needed to highlight weaker genetic effects. (C) 2002 Wiley-Liss, Inc. C1 Hop Henri Mondor, INSERM, U513, F-94010 Creteil, France. Hop La Pitie Salpetriere, INSERM, U289, Paris, France. Hop St Louis, INSERM, U358, Paris, France. Lab Anthropol Biol, Unite Rech Genet Epidemiol, Paris, France. AP HP, Hop Albert Chenevier & Henri Mondor, Psychiat Serv, Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ Oslo, Ctr Child & Adolescent Psychiat, Oslo, Norway. Georgetown Univ, Sch Med, Dept Pediat, Washington, DC 20007 USA. Azienda Osped Senese, Div Neuropsichiatria Infantile, Siena, Italy. Univ Hosp, Dept Gen Psychiat, Vienna, Austria. RP Leboyer, M (reprint author), Hop Henri Mondor, INSERM, U513, 8 Rue Gen Sarrail, F-94010 Creteil, France. RI Martinez, Maria/B-3111-2013 OI Martinez, Maria/0000-0003-2180-4537 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th COMINGS DE, 1991, JAMA-J AM MED ASSOC, V266, P1793, DOI 10.1001/jama.266.13.1793 COMINGS DE, 1995, BIOL PSYCHIAT, V37, P484, DOI 10.1016/0006-3223(94)00311-P HERAULT J, 1993, PSYCHIAT RES, V46, P261, DOI 10.1016/0165-1781(93)90094-W LATHROP GM, 1984, AM J HUM GENET, V36, P460 LEBOYER M, 1994, AM J PSYCHIAT, V151, P1797 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MARTINEAU J, 1992, DEV MED CHILD NEUROL, V34, P593 PANKSEPP J, 1979, TRENDS NEUROSCI, V2, P174, DOI 10.1016/0166-2236(79)90071-7 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Plioplys A V, 1990, J Neuropsychiatry Clin Neurosci, V2, P413 Smalley SL, 1997, AM J HUM GENET, V60, P1276, DOI 10.1086/515485 Spielman RS, 1996, AM J HUM GENET, V59, P983 TERWILLIGER J, 1996, PROGRAM SIBPAIR SIBP TERWILLIGER JD, 1995, AM J HUM GENET, V56, P777 NR 15 TC 21 Z9 22 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 8 PY 2002 VL 114 IS 2 BP 125 EP 128 DI 10.1002/ajmg.10041 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 523AU UT WOS:000173929800001 PM 11857571 ER PT J AU Spiker, D Lotspeich, LJ Dimiceli, S Myers, RM Risch, N AF Spiker, D Lotspeich, LJ Dimiceli, S Myers, RM Risch, N TI Behavioral phenotypic variation in autism multiplex families: Evidence for a continuous severity gradient SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; genetics studies; behavior ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; EXTENDED PEDIGREES; CHILDHOOD AUTISM; INFANTILE-AUTISM; SOCIAL-BEHAVIOR; GENOMIC SCREEN; CHILDREN; GENETICS; RELATIVES AB Recent genetic investigations of autism have studied multiplex families, typically including families with multiple siblings who meet criteria for a diagnosis of autism. However, little is known about the specific behavioral characteristics of siblings with autism in these multiplex families. We investigated the behavioral phenotypic variability and similarity of 351 siblings with autism in 171 multiplex families using cluster analysis and correlations. The results of cluster analyses showed that the individuals with autism could be characterized on a severity gradient: a continuum based on severity of symptoms and impairment as measured by Autism Diagnostic Interview-Revised (ADI-R) scores, verbal-nonverbal status, and nonverbal IQ scores. Clusters based on scores from the ADI-R for the autism diagnostic criteria of the DSM-IV and nonverbal IQ scores still represented a severity gradient when the effects of verbal-nonverbal status were removed. The severity gradient was shown to be heritable, with a sib correlation of 30% or a heritability of 60%. In summary, in a sample of 171 autism multiplex families, there was no evidence of discrete behaviorally defined subgroups of affected individuals or families characterized by distinct patterns of behavioral symptoms. Rather, the clusters could be characterized along a single, heritable, continuous severity dimension. (C) 2002 Wiley-Liss, Inc. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Div Child Psychiat & Child Dev, Stanford, CA USA. Stanford Univ, Sch Med, Dept Genet, Stanford, CA USA. RP Spiker, D (reprint author), SRI Int, Ctr Educ & Human Serv, 333 Ravenswood Ave, Menlo Pk, CA 94025 USA. 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J. Med. Genet. PD MAR 8 PY 2002 VL 114 IS 2 BP 129 EP 136 DI 10.1002/ajmg.10188 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 523AU UT WOS:000173929800002 PM 11857572 ER PT J AU Kim, SJ Herzing, LBK Veenstra-VanderWeele, J Lord, C Courchesne, R Leventhal, BL Ledbetter, DH Courchesne, E Cook, EH AF Kim, SJ Herzing, LBK Veenstra-VanderWeele, J Lord, C Courchesne, R Leventhal, BL Ledbetter, DH Courchesne, E Cook, EH TI Mutation screening and transmission disequilibrium study of ATP10C in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE ATP10C; polymorphism; association; autism; 15q11-q13 ID LINKAGE-DISEQUILIBRIUM; GENOMIC SCREEN; DISORDER; IDENTIFICATION; SPECTRUM; CONTIG; GENES AB Autism is a complex genetic disorder. Chromosome 15 is of particular interest in this disorder, because of previous reports of individuals with autism with chromosomal abnormalities in the 15q11-q13 region. Transmission disequilibrium between polymorphisms in this region and autism has been also been reported in some, but not all studies. Recently, a novel maternally expressed gene, ATP10C, was characterized and mapped to the chromosome 15q11-q13 region, 200 kb distal to UBE3A. It encodes a putative aminophospholipid translocase likely to be involved in the asymmetric distribution of proteins in the cell membrane. Preferential maternal expression has been demonstrated in fibroblasts and brain. Because of its physical location and imprinting pattern, ATP10C was considered to be a candidate gene for chromosome 15-associated autism. In an effort to find the genes responsible for autism in this chromosomal region, 1.5 kb of the 5' flanking region, as well as the coding and splicing regions of ATP10C, were screened for sequence variants. Several polymorphic markers including five nonsynonymous SNPs were identified. To investigate transmission disequilibrium between ATP10C and autism, a family-based association study was conducted for 14 markers in 115 autism trios. No significant transmission disequilibrium, was found, suggesting ATP10C is unlikely to contribute strongly to susceptibility to autism in these families. However, due to limited power to detect genes of modest effect, the possible functional role of the nonsynonymous SNPs and the functional implications of the SNPs identified from 5' flanking region and intron 2 splicing region may be evaluated in further studies. (C) 2002 Wiley-Liss, Inc. C1 Univ Chicago, Dept Psychiat MC3077, Lab Dev Neurosci Child & Adolescent Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat MC3077, Dev Disorders Clin, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. Childrens Hosp Res Ctr, Lab Res Neurosci Autism, La Jolla, CA USA. Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. RP Cook, EH (reprint author), Univ Chicago, Dept Psychiat MC3077, Lab Dev Neurosci Child & Adolescent Psychiat, 5841 S Maryland Ave, Chicago, IL 60637 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett S, 1999, AM J MED GENET, V88, P609 Bass MP, 2000, NEUROGENETICS, V2, P219, DOI 10.1007/s100480050067 Bolton PF, 2001, AM J MED GENET, V105, P675, DOI 10.1002/ajmg.1551 BUXBAUM J, UNPUB ASS GAMMA AMIN Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Chen XN, 1999, GENOME RES, V9, P492 Christian SL, 1998, GENOME RES, V8, P146 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 2001, CHILD ADOL PSYCH CL, V10, P333 Cook EH, 1997, AM J HUM GENET, V60, P928 Halleck MS, 1998, GENOME RES, V8, P354 Heinemeyer T, 1998, NUCLEIC ACIDS RES, V26, P362, DOI 10.1093/nar/26.1.362 Herzing LBK, 2001, AM J HUM GENET, V68, P1501, DOI 10.1086/320616 Bailey A, 1998, HUM MOL GENET, V7, P571 Palferman S, 2001, AM J HUM GENET, V69, P570 KIM SJ, UNPUB TRANSMISSION D Liu JJ, 2001, AM J HUM GENET, V69, P327, DOI 10.1086/321980 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X Maddox LO, 1999, GENOMICS, V62, P325, DOI 10.1006/geno.1999.6017 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 Meguro M, 2001, NAT GENET, V28, P19, DOI 10.1038/88209 Nurmi EL, 2001, GENOMICS, V77, P105, DOI 10.1006/geno.2001.6617 O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Pritchard JK, 2001, AM J HUM GENET, V69, P124, DOI 10.1086/321272 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 Spielman RS, 1996, AM J HUM GENET, V59, P983 Veenstra-VanderWeele J, 1999, MOL PSYCHIATR, V4, P64, DOI 10.1038/sj.mp.4000472 WANG CH, 2000, AM J HUM GENET, V67, P179 NR 35 TC 23 Z9 24 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 8 PY 2002 VL 114 IS 2 BP 137 EP 143 DI 10.1002/ajmg.10238 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 523AU UT WOS:000173929800003 PM 11857573 ER PT J AU Hellings, JA Hossain, S Martin, JK Baratang, RR AF Hellings, JA Hossain, S Martin, JK Baratang, RR TI Psychopathology, GABA, and the Rubinstein-Taybi syndrome: A review and case study SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Rubinstein-Taybi syndrome; manic-like; divalproex; aggression ID MENTAL-RETARDATION; DISORDERS; 16P13.3 AB An adult female with congenital Rubinstein-Taybi syndrome (RTS) and severe mental retardation is described, who presented with symptoms of severe over-activity, short attention span, mood lability, and aggressive outbursts in a cyclical pattern, suggestive of recurrent manic-like episodes. These symptoms improved significantly with divalproex (Depakote) monotherapy. Review of the existing studies showed that 10-76% of persons with RTS may be identified with similar behavioral symptoms. We postulate other persons with RTS may respond to divalproex, and there may be some relationship between the chromosome 16p13.3 deletion and gamma-aminobutyric acid (GABA) receptor or neurotransmitter abnormalities. Recent molecular genetic studies suggest a linkage of this region to bipolar mood disorder and autism, both of which were diagnosed in this patient. Further prospective study is needed of RTS persons regarding behavioral problems, comorbid psychiatric diagnoses, and treatment responses, correlated with genetic abnormalities. (C) 2002 Wiley-Liss, Inc. C1 Univ Kansas, Med Ctr, Dept Psychiat, Kansas City, KS 66160 USA. RP Hellings, JA (reprint author), Univ Kansas, Med Ctr, Dept Psychiat, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Stevens C A, 1990, Am J Med Genet Suppl, V6, P30 CHEN XN, 1995, CYTOGENET CELL GENET, V71, P56, DOI 10.1159/000134062 COFFIN GS, 1964, AM J DIS CHILD, V108, P351 Daniels RJ, 2001, HUM MOL GENET, V10, P339, DOI 10.1093/hmg/10.4.339 GOTTS EE, 1977, BIOL PSYCHIAT, V12, P413 Hagerman R. 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PD MAR 8 PY 2002 VL 114 IS 2 BP 190 EP 195 DI 10.1002/ajmg.10156 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 523AU UT WOS:000173929800011 PM 11857581 ER PT J AU Nagy, E Loveland, KA AF Nagy, E Loveland, KA TI Prolonged brainstem auditory evoked potentials: An autism-specific or autism-nonspecific marker SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter ID CHILDREN; DISABILITIES; RELATIVES; DISORDER C1 Univ Texas, Sch Med, Ctr Human Dev Res, Dept Psychiat & Behav Sci, Houston, TX 77030 USA. Univ Texas, Mental Sci Inst, Houston, TX 77030 USA. RP Nagy, E (reprint author), Univ Texas, Sch Med, Ctr Human Dev Res, Dept Psychiat & Behav Sci, 1300 Moursund St, Houston, TX 77030 USA. CR AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 Bachevalier J, 1996, J AUTISM DEV DISORD, V26, P217, DOI 10.1007/BF02172015 LAHAT E, 1995, DEV MED CHILD NEUROL, V37, P119 Maziade M, 2000, ARCH GEN PSYCHIAT, V57, P1077, DOI 10.1001/archpsyc.57.11.1077 Plumet MH, 1995, CORTEX, V31, P723 Purvis KL, 1997, J ABNORM CHILD PSYCH, V25, P133, DOI 10.1023/A:1025731529006 SKOFF BF, 1980, PSYCHIAT RES, V2, P157, DOI 10.1016/0165-1781(80)90072-4 THIVIERGE J, 1990, AM J PSYCHIAT, V147, P1609 Urasaki Eiichirou, 1995, Neurologia Medico-Chirurgica, V35, P353, DOI 10.2176/nmc.35.353 Zafeiriou DI, 2000, ACTA PAEDIATR, V89, P194, DOI 10.1080/080352500750028825 NR 10 TC 3 Z9 3 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 MAR PY 2002 VL 59 IS 3 BP 288 EP 289 DI 10.1001/archpsyc.59.3.288 PG 2 WC Psychiatry SC Psychiatry GA 529LK UT WOS:000174300800014 PM 11879171 ER PT J AU Thivierge, J Merette, C AF Thivierge, J Merette, C TI Prolonged brainstem auditory evoked potentials: An autism-specific or autism-nonspecific marker - In reply SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter C1 Univ Laval Robert Giffard, Ctr Rech, Beauport, PQ G1J 2G3, Canada. RP Thivierge, J (reprint author), Univ Laval Robert Giffard, Ctr Rech, 2601 Chemin Canardiere, Beauport, PQ G1J 2G3, Canada. CR Bachevalier J, 1996, J AUTISM DEV DISORD, V26, P217, DOI 10.1007/BF02172015 Maziade M, 2000, ARCH GEN PSYCHIAT, V57, P1077, DOI 10.1001/archpsyc.57.11.1077 Maziade M, 2001, MOL PSYCHIATR, V6, P684, DOI 10.1038/sj.mp.4000915 MAZIADE M, IN PRESS ENCY HUMAN Tsuang MT, 2000, AM J MED GENET, V97, P1, DOI 10.1002/(SICI)1096-8628(200021)97:1<1::AID-AJMG1>3.0.CO;2-P NR 5 TC 0 Z9 0 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 MAR PY 2002 VL 59 IS 3 BP 289 EP 290 PG 2 WC Psychiatry SC Psychiatry GA 529LK UT WOS:000174300800015 ER PT J AU Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ TI A deficit in shifting attention present in high-functioning autism but not Asperger's disorder (vol 5, pg 67, 2001) SO AUTISM LA English DT Correction CR Rinehart NJ, 2001, AUTISM, V5, P67, DOI 10.1177/1362361301005001007 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 2002 VL 6 IS 1 BP 4 EP + PG 2 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500001 ER PT J AU Scott, FJ Baron-Cohen, S Bolton, P Brayne, C AF Scott, FJ Baron-Cohen, S Bolton, P Brayne, C TI The CAST (Childhood Asperger Syndrome Test) - Preliminary development of a UK screen for mainstream primary-school-age children SO AUTISM LA English DT Article DE Asperger syndrome; autism spectrum; epidemiology; screening ID AUTISM; DISORDERS AB The article describes a pilot and follow-up study of the preliminary development of a new tool to screen for Asperger syndrome (AS) and related social and communication conditions (the Childhood Asperger Syndrome Test, CAST) in children aged 4-11 years, in a non-clinical setting. In the pilot study, parents of 13 children with AS and of 3 7 typically developing children completed the CAST. There were significant differences between the AS and typical sample means. The pilot was used to establish preliminary cut-off scores for the CAST. In the main study, parents of 115 0 primary-school-age children were sent the CAST, and 174 took part in the full data analysis. Results suggest that compared with other tools currently available, the CAST may be useful for identifying children at risk for AS and related conditions, in a mainstream non-clinical sample. Further research is ongoing. C1 Univ Cambridge, Dept Psychiat, Austism Res Ctr, Cambridge CB2 1TN, England. RP Scott, FJ (reprint author), Univ Cambridge, Dept Psychiat, Austism Res Ctr, 18B Trumpington Rd, Cambridge CB2 1TN, England. RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 2001, NIASA WORK GROUP M S 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 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x BREGMAN JD, 1997, HDB AUTISM PERVASIVE, P606 Cohen D. 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J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Volkmar FR, 1998, AUTISM, V2, P45, DOI DOI 10.1177/1362361398021005 WHO, 1993, ICD 10 CLASS MENT BE WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 25 TC 138 Z9 141 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 9 EP 31 DI 10.1177/1362361302006001003 PG 23 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500002 PM 11918111 ER PT J AU Salt, J Shemilt, J Sellars, V Boyd, S Coulson, T McCool, S AF Salt, J Shemilt, J Sellars, V Boyd, S Coulson, T McCool, S TI The Scottish Centre for Autism preschool treatment programme. II: The results of a controlled treatment outcome study SO AUTISM LA English DT Article DE autism; early intervention; evaluation; outcome; treatment ID YOUNG-CHILDREN; EARLY INTERVENTION; BEHAVIORAL TREATMENT; JOINT ATTENTION; DISORDERS; MODEL AB This article evaluates the effectiveness of a developmentally based early intervention programme. Two groups of children were compared, a treatment group and a no-treatment control group. Standardized assessments were administered before and after the intervention period by an independent clinician. Pre-treatment comparisons revealed that the control group had a significantly higher pre-treatment IQ; but the two groups were comparable for age, mental age, socioeconomic status and number of hours of non-experimental therapy. 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O., 1978, Journal of Statistical Computation and Simulation, V6, DOI 10.1080/00949657808810197 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 ROGERS SJ, 1991, TOP EARLY CHILD SPEC, V11, P29 ROGERS SJ, 1989, J AM ACAD CHILD PSY, V28, P207, DOI 10.1097/00004583-198903000-00010 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 SALT J, 1999, CLIN PSYCHOL FORUM, V132, P15 Salt J, 2001, AUTISM, V5, P362, DOI 10.1177/1362361301005004003 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 Smith T, 1999, CLIN PSYCHOL-SCI PR, V6, P33, DOI 10.1093/clipsy/6.1.33 Sparrow S, 1984, VINELAND ADAPTIVE BE Stone W. L., 1997, HDB AUTISM PERVASIVE WEITZMAN E, 1997, IMPRINT NEWSLETTER I, V18, P10 WETHERBY A, 1997, HDB AUTISM PERVASIVE World Health Organization, 1993, INT CLASS MENT BEH D NR 36 TC 28 Z9 28 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 33 EP 46 DI 10.1177/1362361302006001004 PG 14 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500003 PM 11918108 ER PT J AU Chandler, S Christie, P Newson, E Prevezer, W AF Chandler, S Christie, P Newson, E Prevezer, W TI Developing a diagnostic and intervention package for 2-to 3-year-olds with autism - Outcomes of the frameworks for communication approach SO AUTISM LA English DT Article DE autism; early intervention; language; pragmatics; social communication AB The aim of the research was to develop and evaluate a model of good practice which would make an explicit link between diagnosis and intervention, and so give parents a very clear rationale for the autism-specific yet individualized programme that they were carrying out. It employed an action research design, which essentially is responsive to participants, thus developing a user-friendly model. of service. The programme was based on the developmental perspective that the pragmatics of language are the precursors of speech itself and enable both communication and relationship between child and parents. Since these are impaired in autism they should therefore be prioritized in early intervention. Ten children aged 1: 10 to 2:9 at assessment, and with a diagnosis of autism, underwent an intervention based on home visits, modelling, workshops and written information, with parents as 'therapists' in naturally occurring situations. Within 18 months all children made substantial progress in social interaction and expressive communication, including gestural and verbal communication. C1 Early Years Diagnost Ctr, Nottingham NG15 9AH, England. RP Christie, P (reprint author), Early Years Diagnost Ctr, 272 Longdale Lane, Nottingham NG15 9AH, England. CR BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Bates E., 1979, EMERGENCE SYMBOLS CO CATTELL P, 1960, MEASUREMENT INTELLIG CHRISTIE P, 1992, HDB CHILD ADOLESCENT CHRISTIE P, 1986, COMMUNICATION, V20, P4 CHRISTIE P, 1998, PROJECT BOOKLETS INT Dewart H, 1988, PRAGMATICS PROFILE E Howlin P, 1998, CHILDREN AUTISM ASPE Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 JONES G, 1994, EVALUATIVE COMP STUD JONES O, 1977, STUDIES MOTHER INFAN LEWIS R, 1996, MUSICAL INTERACTION NEWSON E, 1976, EARLY MANAGEMENT HAN NEWSON E, 1982, GETTING YOUR HANDICA NEWSON E, 1998, PSYCHOBIOLOGY AUTISM NEWSON E, 2001, 2001 AUTISM ODYSSEY NEWSON E, 1992, CURRENT INTERVENTION NEWSON E, 1985, QUESTIONS PROBING PO NEWSON E, 2001, AUTISM SEARCH COHERE NEWSON E, 1985, DIAGNOSTIC ASSESSMEN NEWSON J, 1975, B BRIT PSYCHOL SOC, V28, P437 Newson J., 1974, B BRIT PSYCHOL SOC, V27, P251 PAWLBY SJ, 1977, STUDIES MOTHER INFAN *SUTH HOUS SCH REC, 1989, PREV COMM CHECKL Trevarthen C., 1994, DEV PSYCHOPATHOL, V6, P599, DOI [10.1017/S0954579400004703, DOI 10.1017/S0954579400004703] WALKER M, 1996, MAKATON CORE VOCABUL WIMPORY D, 1986, ENABLING COMMUNICATI NR 27 TC 9 Z9 9 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 47 EP 69 DI 10.1177/1362361302006001005 PG 23 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500004 PM 11918109 ER PT J AU Williams, C Wright, B Callaghan, G Coughlan, B AF Williams, C Wright, B Callaghan, G Coughlan, B TI Do children with autism learn to read more readily by computer assisted instruction or traditional book methods? A pilot study SO AUTISM LA English DT Article DE autism; children; computer assisted learning ID PERVASIVE DEVELOPMENTAL DISORDERS; OVERSELECTIVITY; COMMUNICATION; STUDENTS AB The study evaluates the progress of eight children aged 3-5 years with autism attending a specialist teaching unit in their development of reading skills in two conditions: computer instructed learning and book based learning. The authors developed a direct observation schedule to monitor autistic behaviours using computerized techniques. The children were matched by age, severity of autistic symptomatology and number of spoken words. They were initially randomly allocated to the computer or book condition and crossed over at 10 weeks. All of the children spent more time on task in the computer condition than in the book condition. By the end of the study after computer assisted learning, five of the eight children could reliably identify at least three words. It was found that children with autism spent more time on reading material when they accessed it through a computer and were less resistant to its use. C1 York NHS Trust, York, N Yorkshire, England. RP Williams, C (reprint author), Lime Trees Child & Family Unit, 31 Shipton Rd, York YO30 5RF, N Yorkshire, England. CR BARTAK L, 1973, J CHILD PSYCHOL PSYC, V14, P161, DOI 10.1111/j.1469-7610.1973.tb01185.x BERNARD-OPITZ V, 1990, Annals Academy of Medicine Singapore, V19, P611 CHEN SHA, 1993, MENT RETARD, V31, P368 COLBY KM, 1973, J AUTISM CHILD SCHIZ, V3, P254, DOI 10.1007/BF01538283 COLBY KM, 1971, CURRENT PSYCHIAT THE DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Dawson G., 1989, AUTISM NATURE DIAGNO, P49 FERRARA C, 1980, J AUTISM DEV DISORD, V10, P51, DOI 10.1007/BF02408432 FERSTER CB, 1961, J CHRON DIS, V13, P312, DOI 10.1016/0021-9681(61)90059-5 Frith U., 1989, AUTISM EXPLAINING EN HEDBRING C, 1985, J AUTISM DEV DISORD, V15, P9, DOI 10.1007/BF01837895 HEIMANN M, 1995, J AUTISM DEV DISORD, V25, P459, DOI 10.1007/BF02178294 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 JONES G, 2000, AUT EUR C GLASG JORDAN R, 1990, COMMUNICATION, V24, P20 JORDAN R, 1990, COMMUNICATION, V24, P23 Jordan R. R., 1995, UNDERSTANDING TEACHI Light JC, 1998, J COMMUN DISORD, V31, P153, DOI 10.1016/S0021-9924(97)00087-7 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 LOVAAS OI, 1971, BEHAV RES THER, V9, P305, DOI 10.1016/0005-7967(71)90042-8 MURRAY DKC, 1997, GUIDE GOOD PRACTICE Nelson K. E., 1997, COMMUNICATION LANGUA, P295 Nelson K. E., 1995, DELTA MESSAGES COMPU NELSON KE, 1991, ALPHA INTERACTIVE LA Nelson K.E., 1998, AUTISM, V2, P139, DOI 10.1177/1362361398022003 NELSON KE, 1991, LANGUAGE ACQUISITION, P399 PANYAN MV, 1984, J AUTISM DEV DISORD, V14, P375, DOI 10.1007/BF02409828 Powell S, 1996, AUTISM AGENDA, P128 Raven J. C., 1984, COLOURED PROGR MATRI REED T, 1994, J AUTISM DEV DISORD, V24, P53, DOI 10.1007/BF02172212 Romanczyk R. G., 1992, AUTISM IDENTIFICATIO, P21 RUSSO DC, 1978, J ABNORM CHILD PSYCH, V6, P189, DOI 10.1007/BF00919124 RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 Schopler E., 1988, CHILDHOOD AUTISM RAT SNOWLING M, 1986, J EXP CHILD PSYCHOL, V42, P392, DOI 10.1016/0022-0965(86)90033-0 Sperber D., 1986, RELEVANCE COMMUNICAT WHO, 1993, ICD 10 CLASS MENT BE Yamamoto J, 1999, RES DEV DISABIL, V20, P355, DOI 10.1016/S0891-4222(99)00017-7 NR 39 TC 42 Z9 43 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 71 EP 91 DI 10.1177/1362361302006001006 PG 21 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500005 PM 11918110 ER PT J AU Celani, G AF Celani, G TI Human beings, animals and inanimate objects - What do people with autism like? SO AUTISM LA English DT Article DE autism; categorization abilities; Down's syndrome; interpersonal relationships; sorting by preference ID CHILDREN; CATEGORIZATION; PREFERENCES AB An experimental strategy based on the 'sorting by preference' approach was used to obtain information about the nature of the autistic syndrome. Twelve participants with autism (mean age 11:9 years), 12 with Down's syndrome (mean age 11: 5 years) and 12 typically developing children (mean age 6:2 years) were matched on gender (M:F 9:3) and on verbal mental age. In a forced choice procedure they had to choose between: human beings or inanimate objects (relatedness condition); animals or inanimate objects (animate condition),drawings of a child handling a thing or of the same child in contact with another person (interpersonal relationship condition); pleasant or unpleasant situations without living beings (control condition). The performances of the groups differed only on the relatedness condition and on the interpersonal relationship condition. The results are discussed in the context of the social difficulties experienced by individuals with autism. C1 Univ Bologna, I-40126 Bologna, Italy. RP Celani, G (reprint author), Dept Psychol, Viale Berti Pichat 5, I-40127 Bologna, Italy. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1991, BRIT J DEV PSYCHOL, V9, P301 BARTHELEMY C, 1992, J AUTISM DEV DISORD, V22, P23, DOI 10.1007/BF01046400 Celani G, 1999, J AUTISM DEV DISORD, V29, P57, DOI 10.1023/A:1025970600181 Greenwald M.K., 1989, J PSYCHOPHYSIOL, V3, P51 HABERMAN SJ, 1973, BIOMETRICS, V29, P205, DOI 10.2307/2529686 Hobson R. Peter, 1993, AUTISM DEV MIND HOBSON RP, 1989, BRIT J DEV PSYCHOL, V7, P237 INOUE M, 1993, JAPANESE J BEHAV THE, V19, P37 KLIN A, 1991, J AUTISM DEV DISORD, V21, P29, DOI 10.1007/BF02206995 Lang P. J., 1988, INT AFFECTIVE PICTUR LELORD G, 1994, AUTISMO INFANTILE OCONNOR N, 1963, BRIT J SOC CLIN PSYC, V3, P29 TAGERFLUSBERG H, 1985, J EXP CHILD PSYCHOL, V40, P450, DOI 10.1016/0022-0965(85)90077-3 THAUT MH, 1987, J AUTISM DEV DISORD, V17, P425, DOI 10.1007/BF01487071 UNGERER JA, 1987, J AUTISM DEV DISORD, V17, P3, DOI 10.1007/BF01487256 WECHSLER D, 1973, WPPSI SCALA INTELLIG WECHSLER D, 1987, WISC R SCALA INTELLI Wing L., 1976, EARLY CHILDHOOD AUTI World Health Organization, 1992, INT STAT CLASS DIS I NR 20 TC 20 Z9 20 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 93 EP 102 DI 10.1177/1362361302006001007 PG 10 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500006 PM 11918112 ER PT J AU Latif, A Heinz, P Cook, R AF Latif, A Heinz, P Cook, R TI Iron deficiency in autism and Asperger syndrome SO AUTISM LA English DT Article DE Asperger syndrome; autistic spectrum disorder; iron deficiency; iron deficiency anaemia ID ANEMIC INFANTS; CHILDREN; SUPPLEMENTATION; CHILDHOOD; THERAPY; BRAIN AB This research considers the prevalence of iron deficiency in children with autism and Asperger syndrome and examines whether this will influence guidelines and treatment. Retrospective analysis of the full blood count and, as far as available, serum ferritin measurements of 9 6 children (5 2 with autism and 44 with Asperger syndrome) was undertaken. Six of the autistic group were shown to have iron deficiency anaemia and, of the 23 autistic children who had serum ferritin measured, 12 were iron deficient. Only two of the Asperger group had iron deficiency anaemia and, of the 22 children who had their serum ferritin measured, only three were iron deficient. Iron deficiency, with or without anaemia, can impair cognition and affect and is associated with developmental slowing in infants and mood changes and poor concentration in children. This study showed a very high prevalence of iron deficiency in children with autism, which could potentially compromise further their communication and behavioural impairments. C1 Royal Glamorgan Hosp, Children Ctr, Llantrisant CF72 8XR, Mid Glamorgan, Wales. Univ Glamorgan, Pontypridd CF37 1DL, M Glam, Wales. RP Latif, A (reprint author), Royal Glamorgan Hosp, Children Ctr, Llantrisant CF72 8XR, Mid Glamorgan, Wales. CR Abdullaev YG, 1997, NEUROSCI LETT, V234, P151, DOI 10.1016/S0304-3940(97)00680-0 AHMED S, 1995, CHEM-BIOL INTERACT, V96, P103 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S., 1993, AUTISM FACTS BEARD JL, 1993, NUTR REV, V51, P157 BENSHACHAR D, 1993, ISRAEL J MED SCI, V29, P587 Bruner AB, 1996, LANCET, V348, P992, DOI 10.1016/S0140-6736(96)02341-0 CONOR JR, 1996, GLIA, V17, P83 Cook James D., 1992, Nutrition Research Reviews, V5, P189, DOI 10.1079/NRR19920014 Cornish E, 1998, J HUM NUTR DIET, V11, P501, DOI 10.1046/j.1365-277X.1998.00132.x DALLMAN PR, 1986, ANNU REV NUTR, V6, P13 Dallman PR, 1996, IRON NUTR HLTH DIS, P65 DeMaeyer E, 1985, World Health Stat Q, V38, P302 Demaeyer EM, 1989, PREVENTING CONTROLLI Desforges JF, 1993, NEW ENGL J MED, V329, P190, DOI 10.1056/NEJM199307153290308 DUMAIS C, 1993, MED NUT, V29, P9 ENWONWU CO, 1989, ANN NUTR WORKSH SER, V3 GREGORY J.R., 1995, NATL DIET NUTR SURVE, V1 IDJRADINATA P, 1993, LANCET, V341, P1, DOI 10.1016/0140-6736(93)92477-B Lawson MS, 1998, ARCH DIS CHILD, V78, P420 LOZOFF B, 1992, NEW ENGL J MED, V326, P687 LOZOFF B, 1982, J PEDIATR-US, V100, P351, DOI 10.1016/S0022-3476(82)80428-9 Lozoff B, 1988, Adv Pediatr, V35, P331 MENDEZ MF, 1989, NEUROLOGY, V39, P349 MOFFATT MEK, 1994, J PEDIATR-US, V125, P527, DOI 10.1016/S0022-3476(94)70003-6 MRABET A, 1994, REV NEUROL, V150, P67 Nelson C, 1997, J NUTR, V127, P2282 NELSON M, 1993, BRIT J NUTR, V70, P147, DOI 10.1079/BJN19930112 OSKI FA, 1983, PEDIATRICS, V71, P677 OSKI FA, 1993, NEW ENGL J MED, V329, P190 OSKI FA, 1978, J PEDIATR-US, V92, P21, DOI 10.1016/S0022-3476(78)80063-8 Otero GA, 1999, INT J NEUROSCI, V99, P113 Oti-Boateng P, 1998, J PAEDIATR CHILD H, V34, P250, DOI 10.1046/j.1440-1754.1998.00205.x Pickett ER, 1998, NEUROPSYCHOLOGIA, V36, P173, DOI 10.1016/S0028-3932(97)00065-1 RAITEN DJ, 1986, J AUTISM DEV DISORD, V16, P133, DOI 10.1007/BF01531725 Requejo AM, 1999, INT J VITAM NUTR RES, V69, P127, DOI 10.1024/0300-9831.69.2.127 SCRIMSHAW NS, 1991, SCI AM, V265, P46 STEVENS D, 1991, ARCH DIS CHILD, V66, P886 Viteri FE, 1998, BIOMED ENVIRON SCI, V11, P46 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 WALTER T, 1989, PEDIATRICS, V84, P7 WALTER T, 1993, EUR J CLIN NUTR, V47, P307 WANG PY, 1991, CHUNG HUA I HSUEH TS, V47, P199 WING L, 1998, AUTISM, V2, P87, DOI 10.1177/1362361398021008 World Health Organization, 1993, ICD 10 INT STAT CLAS Worwood M, 1997, P NUTR SOC, V56, P409, DOI 10.1079/PNS19970042 YOUDIM MBH, 1983, ADV BIOCHEM PSYCHOPH, V37, P309 NR 47 TC 30 Z9 30 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 103 EP 114 DI 10.1177/1362361302006001008 PG 12 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500007 PM 11918106 ER PT J AU Weiss, MJ AF Weiss, MJ TI Hardiness and social support as predictors of stress in mothers of typical children, children with autism, and children with mental retardation SO AUTISM LA English DT Article DE autism; parental stress; social support ID FAMILY STRESS; HANDICAPPED-CHILDREN; LIFE STRESS; PROFILES; PARENTS; EVENTS AB This study assessed the effects of social support and hardiness on the level of stress in mothers of typical children and children with developmental disabilities. one hundred and twenty mothers participated (40 mothers of children with autism, 40 mothers of children with mental retardation, and 40 mothers of typically developing children). Results indicated significant group differences in ratings of depression, anxiety, somatic complaints and burnout. Regression analyses were conducted to determine the best predictors of the dependent measures. Both hardiness and social support were predictive of successful adaptation. The relationships among hardiness, support and coping are discussed. C1 Rutgers State Univ, Douglass Dev Disabil Ctr, New Brunswick, NJ 08901 USA. RP Weiss, MJ (reprint author), Rutgers State Univ, Douglass Dev Disabil Ctr, 25 Gibbons Circle, New Brunswick, NJ 08901 USA. CR AFFLECK G, 1993, COGNITIVE COPING FAM ALBANESE AL, 1996, TEACHING CHILDREN AU American Psychiatric Association, 1987, DIAGN STAT MAN MENT BARRERA M, 1981, AM J COMMUN PSYCHOL, V9, P435, DOI 10.1007/BF00918174 Beck A. 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R., 1983, STRESS FAMILY COPING, P3 FREEMAN NL, 1991, J CHILD PSYCHOL PSYC, V32, P1025, DOI 10.1111/j.1469-7610.1991.tb01927.x GALLAGHER JJ, 1981, J DIVISION EARLY CHI, V1, P3 GANELLEN RJ, 1984, J PERS SOC PSYCHOL, V47, P156, DOI 10.1037//0022-3514.47.1.156 GILL MJ, 1988, UNPUB FORMAL SUPPORT GILL MJ, 1991, J AUTISM DEV DISORD, V21, P407, DOI 10.1007/BF02206867 HARRIS SL, 1982, CHILD FAM BEHAV THER, V4, P21 HARRIS SL, 1984, FAM RELAT, V33, P127, DOI 10.2307/584597 Hill R., 1958, SOCIAL CASEWORK, V49, P139 Hill R., 1949, FAMILIES STRESS Holroyd J., 1974, J COMMUNITY PSYCHOL, V2, P92, DOI 10.1002/1520-6629(197401)2:1<92::AID-JCOP2290020133>3.0.CO;2-A HOLROYD J, 1976, AM J MENT DEF, V80, P431 HONIG AS, 1997, J PRIM PREVENT, V17, P285, DOI 10.1007/BF02248532 HOUSER RA, 1987, THESIS U PITTSBURGH JOHNSON JH, 1978, J PSYCHOSOM RES, V22, P205, DOI 10.1016/0022-3999(78)90025-9 KAZAK AE, 1984, AM J COMMUN PSYCHOL, V12, P645, DOI 10.1007/BF00922617 KAZANSKY VB, 1984, 8TH P INT C CAT, V3, P3 KIMMEL D, 1974, J MARRIAGE FAM, V36, P57, DOI 10.2307/350994 KOBASA SC, 1979, J PERS SOC PSYCHOL, V37, P1, DOI 10.1037/0022-3514.37.1.1 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P205, DOI 10.1007/BF01058151 Lazarus R. S., 1984, STRESS APPRAISAL COP LOCKE HJ, 1959, J MARRIAGE FAMILY LI, V21, P251 LYON S, 1983, FAMILY HANDICAPPED C, P203 MADDI SR, 1979, J HUMANIST PSYCHOL, V19, P73, DOI 10.1177/002216787901900407 MARCUS LM, 1977, AM J ORTHOPSYCHIAT, V47, P388 MARSH DT, 1993, FAMILIES MENTAL RETA Maslach C., 1981, MASLACH BURNOUT INVE, V2nd McCubbin H. I., 1983, MARRIAGE FAM REV, V6, P7, DOI DOI 10.1300/J002V06N01_02 MCCUBBIN HI, 1979, J MARRIAGE FAM, V41, P237, DOI 10.2307/351693 McCubbin H.I., 1983, SOCIAL STRESS FAMILY, P7 MOES D, 1996, TEACHING CHILDREN AU MOES D, 1992, PSYCHOL REP, V71, P1272, DOI 10.2466/PR0.71.8.1272-1274 Patterson J. M., 1982, FAMILY STRESS COPING, P26 RICHMAN N, 1977, BRIT J PSYCHIAT, V131, P525 RODRIGUE JR, 1990, J CLIN CHILD PSYCHOL, V19, P371, DOI 10.1207/s15374424jccp1904_9 Seligman M, 1997, ORDINARY FAMILIES SP Seligman MEP, 1991, LEARNED OPTIMISM SOBOTOR WJ, 1989, PREVENTIVE PSYCHIAT, P43 Turnbull A. P., 1990, FAMILIES PROFESSIONA VENTERS M, 1982, FAMILY STRESS COPING, P120 WIKLER LM, 1986, FAMILIES HANDICAPPED, P167 WOLF LC, 1989, J AUTISM DEV DISORD, V19, P157, DOI 10.1007/BF02212727 NR 65 TC 129 Z9 131 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2002 VL 6 IS 1 BP 115 EP 130 DI 10.1177/1362361302006001009 PG 16 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500008 PM 11918107 ER PT J AU Groden, J AF Groden, J TI Autism spectrum disorders: A transactional developmental perspective SO AUTISM LA English DT Book Review CR Wetherby A. M., 2000, AUTISM SPECTRUM DISO 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 2002 VL 6 IS 1 BP 136 EP 140 DI 10.1177/1362361302006001014 PG 5 WC Psychology, Developmental SC Psychology GA 525VJ UT WOS:000174094500013 ER PT J AU Rehfeldt, RA AF Rehfeldt, RA TI Activity schedules for children with autism: Teaching independent behavior: Toward the inclusion and integration of children with disabilities SO BEHAVIOR ANALYST LA English DT Book Review ID PHOTOGRAPHIC ACTIVITY SCHEDULES; MENTAL-RETARDATION; PICTURE; MAINTENANCE; ADOLESCENTS; STUDENTS; ADULTS; CHOICE 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 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson MD, 1997, RES DEV DISABIL, V18, P231, DOI 10.1016/S0891-4222(97)00006-1 Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 BONDY AS, 1993, BEHAV ANALYST, V16, P123 BONDY AS, 1995, LEARNING COGNITION A, P331 Carr E. G., 1994, COMMUNICATION BASED COOPER JO, 1987, APPL BEHAV ANAL, P315 Durand V. M., 1990, SEVERE BEHAV PROBLEM DYER K, 1990, J APPL BEHAV ANAL, V23, P515, DOI 10.1901/jaba.1990.23-515 Foxx R., 1982, DECREASING BEHAV SEV Green G., 1999, AUTISM BEHAV ANAL PE, P11 Green G., 1996, BEHAV INTERVENTION Y, P15 KENNEDY CH, 1993, J APPL BEHAV ANAL, V26, P63, DOI 10.1901/jaba.1993.26-63 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P137, DOI 10.1901/jaba.1993.26-137 LALLI JS, 1994, J APPL BEHAV ANAL, V27, P705, DOI 10.1901/jaba.1994.27-705 Lovaas O. I., 1981, TEACHING DEV DISABLE MACDUFF GS, 1993, J APPL BEHAV ANAL, V26, P89, DOI 10.1901/jaba.1993.26-89 McClannahan L. 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PD SPR PY 2002 VL 25 IS 1 BP 103 EP 108 PG 6 WC Psychology, Clinical SC Psychology GA 556UJ UT WOS:000175867100009 ER PT J AU Caron, MJ Mottron, L Rainville, C Sylvie, C AF Caron, MJ Mottron, L Rainville, C Sylvie, C TI Superior spatial orientation abilities in high functioning autism. SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 Univ Quebec, Montreal, PQ H3C 3P8, Canada. Inst Univ Geriatr Montreal, Ctr Rech, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0278-2626 J9 BRAIN COGNITION JI Brain Cogn. PD MAR-APR PY 2002 VL 48 IS 2-3 BP 247 EP 247 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 536ED UT WOS:000174687000034 ER PT J AU Kaya, M Karasalihoglu, S Ustun, F Gultekin, A Cermik, TF Fazlioglu, Y Ture, M Yigitbasi, ON Berkarda, S AF Kaya, M Karasalihoglu, S Ustun, F Gultekin, A Cermik, TF Fazlioglu, Y Ture, M Yigitbasi, ON Berkarda, S TI The relationship between Tc-99m-HMPAO brain SPECT and the scores of real life rating scale in autistic children SO BRAIN & DEVELOPMENT LA English DT Article DE autism; Tc-99m-hexamethylpropylene amine oxime brain SPECT; Ritvo-Freeman Real Life Rating Scale ID CEREBRAL BLOOD-FLOW; CHILDHOOD AUTISM; HMPAO SPECT; ADULTS; RECOGNITION; IQ AB Childhood autism is a developmental disability of unknown origin with probable multiple etiologies. The purpose of this study was to compare the changes of regional cerebral blood flow (rCBF) in autistic and non-autistic controls, and to determine the relationship between rCBF on Tc-99m-hexamethylpropylene amine oxime (HMPAO) brain SPECT and the scores of the Ritvo-Freeman Real Life Rating Scale (RLRS), IQ levels, and age of autistic children. Eighteen autistic children (four girls, 14 boys: mean age: 6.13 +/- 1.99 years) and I I non-autistic controls (five girls, six boys, mean age: 6.5 +/- 3.39 years) were examined using Tc-99m-HMPAO brain SPECT. All the children satisfying DSM-IV criteria for autistic disorder were taken into evaluation, and scored by the Ritvo-Freeman RLRS, IQ levels of these children were determined by Goodenough IQ test. Six cortical regions of interest (ROIs; frontal (F), parietal (P), frontotemporal (FT), temporal (T), temporo-occipital (TO), and occipital (0)) were obtained on transaxial slices for count data acquisition. The ratio of average counts in each ROI to whole-slice Counts for the autistic children was correlated with the scores of Ritvo-Freeman RLRS. Hypoperfusion in rCBF in autistic children compared with the control group were identified in bilateral F. FT, T, and TO regions. We found no relationship between rCBF on Tc-99m-HMPAO brain SPECT and the scores of the Ritvo-Freeman RLRS. There was a relationship between bilateral F regions perfusion on Tc-99m-HMPAO brain SPECT and the age of autistic children. There was also a negative correlation between IQ levels and the scores of sensory responses, social relationship to people, and sensory-motor responses. Our results suggest that Tc-99m-HMPAO brain SPECT is helpful to locate the perfusion abnormalities but no correlation is found between rCBF on Tc-99m-HMPAO brain SPECT and the scores of Ritvo-Freeman RLRS. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Trakya Univ, Fac Med, Dept Nucl Med, Nukl Tip ABD, TR-22030 Edirne, Turkey. Trakya Univ, Fac Med, Dept Pediat, Edirne, Turkey. Trakya Univ, Fac Med, Dept Biostat, Edirne, Turkey. RP Kaya, M (reprint author), Trakya Univ, Fac Med, Dept Nucl Med, Nukl Tip ABD, TR-22030 Edirne, Turkey. CR Aylward EH, 1999, NEUROLOGY, V53, P2145 BARONCOHEN S, 1994, BRIT J PSYCHIAT, V165, P640, DOI 10.1192/bjp.165.5.640 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x BUCHSBAUM MS, 1992, J AUTISM DEV DISROD, V180, P413 Buitelaar JK, 1999, J CHILD PSYCHOL PSYC, V40, P869, DOI 10.1017/S0021963099004321 CHIRON C, 1995, DEV MED CHILD NEUROL, V37, P849 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 FREEMAN BJ, 1986, J AM ACAD CHILD PSY, V25, P130, DOI 10.1016/S0002-7138(09)60610-5 GAFFNEY GR, 1987, BRIT J PSYCHIAT, V151, P831, DOI 10.1192/bjp.151.6.831 GARBER HJ, 1992, AM J PSYCHIAT, V149, P245 GEORGE MS, 1992, J NERV MENT DIS, V180, P413, DOI 10.1097/00005053-199207000-00002 Jambaque I, 1998, J NEUROL NEUROSUR PS, V65, P555, DOI 10.1136/jnnp.65.4.555 KJOS BO, 1990, AM J NEURORADIOL, V11, P1035 MOUNTZ JM, 1993, CLIN NUCL MED, V18, P1067, DOI 10.1097/00003072-199312000-00013 MOUNTZ JM, 1995, J NUCL MED, V36, P1156 MOUNTZ JM, 1994, SEMIN NUCL MED, V24, P256, DOI 10.1016/S0001-2998(05)80018-2 Ohnishi T, 2000, BRAIN, V123, P1838, DOI 10.1093/brain/123.9.1838 Sarikaya A, 1999, BRAIN DEV-JPN, V21, P179, DOI 10.1016/S0387-7604(99)00002-9 SCHATZ J, 1995, J AUTISM DEV DISORD, V25, P51, DOI 10.1007/BF02178167 SIEGEL BV, 1992, J NEUROPSYCH CLIN N, V4, P406 ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 ZILBOVICIUS M, 1992, AM J PSYCHIAT, V149, P924 NR 22 TC 14 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD MAR PY 2002 VL 24 IS 2 BP 77 EP 81 DI 10.1016/S0387-7604(02)00006-2 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 539ZQ UT WOS:000174903800004 PM 11891096 ER PT J AU Lang, B Perner, J AF Lang, B Perner, J TI Understanding of intention and false belief and the development of self-control SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT Biennial Meeting of the Society-for-Research-in-Child-Development CY APR 15-18, 1999 CL ALBUQUERQUE, NEW MEXICO SP Soc Res Child Dev ID EXECUTIVE CONTROL; MIND; DESIRES; PRESCHOOLERS; DECEPTION; AUTISM AB We tested the prediction that there is a direct developmental link between understanding false belief, understanding that reflex movements are not intentional actions and the ability to inhibit interfering action tendencies. The common ability consists of the understanding of mental states as representations with causal efficacy (Perner, 1991). One false belief task, the knee-jerk reflex task and two executive function tasks (Dimensional Change Card Sorting Test and hand game) were given to 69 children aged 3, 4 and 5 years old. The results showed that the relationship between false belief and executive control tasks also extends to children's understanding of reflex movements. C1 Salzburg Univ, Inst Educ, A-5020 Salzburg, Austria. RP Lang, B (reprint author), Salzburg Univ, Inst Educ, Akademiestr 26, A-5020 Salzburg, Austria. 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J. Dev. Psychol. PD MAR PY 2002 VL 20 BP 67 EP 76 DI 10.1348/026151002166325 PN 1 PG 10 WC Psychology, Developmental SC Psychology GA 538VT UT WOS:000174836300004 ER PT J AU Johnson, E Hastings, RP AF Johnson, E Hastings, RP TI Facilitating factors and barriers to the implementation of intensive home-based behavioural intervention for young children with autism SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism; applied behaviour analysis; early intervention; family experiences; behavioural intervention AB Background Although international interest in intensive home-based early behavioural intervention for children with autism is increasing, there is little or no published research on the experiences of families conducting these programmes. Methods One hundred and forty-one UK parents conducting Lovaas-style interventions with their young child with autism were asked to identify factors that acted as facilitative factors and barriers to the implementation of these programmes. Parents responded to written questions contained within a questionnaire survey, and their responses were subjected to a content analysis procedure. Results Several of the facilitative factors and barriers were found to be similar. For example, a supportive therapy team was the most frequently cited facilitative factor, and problems recruiting and maintaining a suitable team was the most frequently reported barrier. Other factors seemed to be more independent constructs. For example, an important barrier was the lack of time and personal energy, but plenty of time and energy was not cited as a facilitative factor. Conclusions The practical implications of these results for families and for services supporting families engaged in intensive early behavioural intervention are discussed. In addition, more general implications for the designers of behavioural intervention programmes are identified. C1 Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. RP Hastings, RP (reprint author), Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 CR CORRIGAN PW, 1995, AM PSYCHOL, V50, P514, DOI 10.1037//0003-066X.50.7.514 CORRIGAN PW, 1993, J BEHAV THER EXP PSY, V24, P219, DOI 10.1016/0005-7916(93)90024-Q Dey I, 1993, QUALITATIVE DATA ANA EMERSON E, 1987, MENT RETARD, V25, P101 FACTOR DC, 1990, J AUTISM DEV DISORD, V20, P139, DOI 10.1007/BF02206863 Hastings RP, 2001, J AUTISM DEV DISORD, V31, P327, DOI 10.1023/A:1010799320795 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 Remington B., 1993, CLIN PSYCHOL FORUM, V55, P9 NR 9 TC 25 Z9 25 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD MAR PY 2002 VL 28 IS 2 BP 123 EP 129 PG 7 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 536PC UT WOS:000174710300001 PM 11952647 ER PT J AU Dawson, G Munson, J Estes, A Osterling, J McPartland, J Toth, K Carver, L Abbott, R AF Dawson, G Munson, J Estes, A Osterling, J McPartland, J Toth, K Carver, L Abbott, R TI Neurocognitive function and joint attention ability in young children with autism spectrum disorder versus developmental delay SO CHILD DEVELOPMENT LA English DT Article ID PREFRONTAL CORTEX; EXECUTIVE FUNCTION; SOCIAL-STIMULI; RHESUS-MONKEYS; HUMAN INFANTS; TO-SAMPLE; PERFORMANCE; LESIONS; RECOGNITION; INDIVIDUALS AB Studies have shown that young children with autism are not impaired on prefrontal tasks relative to what would be expected for their mental age, raising questions about the executive dysfunction hypothesis of autism. These studies did not include ventromedial prefrontal tasks, however. The present study examined whether young children with autism spectrum disorder (ASD) are impaired on ventromedial prefrontal tasks, and whether performance on such tasks is correlated with a core autism symptom, joint attention ability. Seventy-two 3- to 4-year-old children with ASD, 34 3- to 4-year-old developmentally delayed children, and 39 12- to 46-month-old typically developing children, matched on mental age, were administered ventromedial and dorsolateral prefrontal tasks and joint attention tasks. Children with ASD performed similarly to comparison groups on all executive function tasks, indicating that at this early age, there is no autism-specific pattern of executive dysfunction. Ventromedial, but not dorsolateral, prefrontal task performance was strongly correlated with joint attention ability, however. The ventromedial prefrontal cortex is hypothesized to play a role in the development of joint attention and possibly some aspects of the autistic syndrome. C1 Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. RP Dawson, G (reprint author), Univ Washington, Ctr Human Dev & Disabil, Box 357920, Seattle, WA 98195 USA. 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PD MAR-APR PY 2002 VL 73 IS 2 BP 345 EP 358 DI 10.1111/1467-8624.00411 PG 14 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 537FA UT WOS:000174747000002 PM 11949896 ER PT J AU Nakamura, K AF Nakamura, K TI Aniracetam: Its novel therapeutic potential in cerebral dysfunctional disorders based on recent pharmacological discoveries SO CNS DRUG REVIEWS LA English DT Review DE aniracetam; cognition enhancers; nootropic drugs; aniracetam metabolites; cerebral dysfunction; new therapeutic indications ID DEFICIT-HYPERACTIVITY DISORDER; SPONTANEOUSLY HYPERTENSIVE RATS; NICOTINIC ACETYLCHOLINE-RECEPTORS; CEREBELLAR GRANULE CELLS; AGED RATS; ALZHEIMERS-DISEASE; PERFORMANCE IMPAIRMENT; HIPPOCAMPAL SLICES; NUCLEUS-ACCUMBENS; AMPA RECEPTORS AB Aniracetam is a pyrrolidinone-type cognition enhancer that has been clinically used in the treatment of behavioral and psychological symptoms of dementia following stroke and in Alzheimer's disease. New discoveries in the behavioral pharmacology, biochemistry and pharmacokinetics of aniracetam provided new indications for this drug in the treatment of various CNS disorders or disease states. This article reviews these new findings and describes the effects of aniracetain in various rodent models of mental function impairment or cerebral dysfunction. Also, several metabolites of aniracetam have been reported to affect learning and memory in animals. It is, therefore, conceivable that major metabolites of aniracetam contribute to its pharmacological effects. The animal models, used in pharmacological evaluation of aniracetam included models of hypoattention, hypovigilance-arousal, impulsiveness, hyperactivity, fear and anxiety, depression, impaired rapid-eye movement sleep, disturbed temporal regulation, behavioral performance, and bladder hyperactivity. These are models of clinical disorders or symptoms that may include personality disorders, anxiety, depression, posttraumatic stress disorder, attention-deficit/hyperactivity disorder, autism, negative symptoms of schizophrenia, and sleep disorders. At present, there is no convincing evidence that promising effects of aniracetam in the animal models will guarantee its clinical efficacy. It is conceivable, however, that clinical trials will demonstrate beneficial effects of aniracetam in the above listed disease states. New findings regarding the mechanism of action of aniracetam, its central target sites, and its effects on signal transduction are also discussed in this review article. C1 Nippon Roche Res Ctr, Dept Prod Res, Clin PK Lab, Kamakura, Kanagawa 247, Japan. RP Nakamura, K (reprint author), Nippon Roche Res Ctr, Dept Prod Res, Clin PK Lab, 200 Kajiwara, Kamakura, Kanagawa 247, Japan. 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This article briefly outlines primary developmental innovations in theory, methodology, and the interpretation of findings. Specifically, we discuss two sets of issues that arise from the general notion of developmental level. One set is relevant to the choice of persons that comprise the comparison group and the other to the various implications of the subjects' levels of functioning. In sum, we contend that researcher,, need to frame their empirical work within the context of developmental theory and methodology and interpret their findings accordingly. This will lead to scientifically compelling work and an increasingly heuristic approach to the study of persons with autism. C1 McGill Univ, Dept Educ Psychol, Montreal, PQ H3A 1Y2, Canada. Hop Riviere Prairies, Montreal, PQ, Canada. Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada. City Univ London, London EC1V 0HB, England. Univ Montreal, Montreal, PQ, Canada. 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PD SPR PY 2002 VL 14 IS 2 BP 225 EP 237 PG 13 WC Psychology, Developmental SC Psychology GA 551HG UT WOS:000175553800002 PM 12030689 ER PT J AU Osterling, JA Dawson, G Munson, JA AF Osterling, JA Dawson, G Munson, JA TI Early recognition of 1-year-old infants with autism spectrum disorder versus mental retardation SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID 1ST 2 YEARS; YOUNG-CHILDREN; HOME MOVIES; AGE; ONSET; LIFE AB Previous work based on observations of home videotapes indicates that differences can be detected between infants with autism spectrum disorder and infants with typical development at I year of age, The present study addresses the question of whether autism can be distinguished from mental retardation by I year of age. Home videotapes of first birthday parties from 20 infants later diagnosed with autism spectrum disorder, 14 infants later diagnosed with mental retardation (without autism), and 20 typically developing infants were coded by blind raters with respect to the frequencies of specific social and communicative behaviors and repetitive motor actions. Results indicated that 1-year-olds with autism spectrum disorder can be distinguished from 1-year-olds with typical development and those with mental retardation. The infants with autism spectrum disorder looked at others and oriented to their names less frequently than infants with mental retardation. 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Information is provided on the characteristics of three key components of schoolwide PBS-universal support, group support, and individual support For each component, information is presented on policy, assessment, and intervention in terms of an evolving approach to schoolwide PBS with descriptions of how the components were implemented at the middle school with a particular emphasis on the eighth-grade student. The authors conclude with implications for practice in terms of assessing current resources, providing professional development, and intensifying universal support within urban schools to address some of the complex issues associated with poverty. C1 Univ Kansas, Beach Ctr Disabil, Lawrence, KS 66045 USA. RP Turnbull, A (reprint author), Univ Kansas, Beach Ctr Disabil, Haworth Hall,Room 3136,1200 Sunnyside Ave, Lawrence, KS 66045 USA. CR ARMSTRONG T, 1994, 374104 ERIC ED Bruns E. 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PD SPR PY 2002 VL 68 IS 3 BP 377 EP 402 PG 26 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 531ME UT WOS:000174418500006 ER PT J AU Pletnikov, MV Moran, TH Carbone, KM AF Pletnikov, MV Moran, TH Carbone, KM TI Borna disease virus infection of the neonatal rat: Developmental brain injury model of autism spectrum disorders SO FRONTIERS IN BIOSCIENCE LA English DT Review DE animal model; autism; Borna; brain; development; environment; rat; review ID CENTRAL-NERVOUS-SYSTEM; INFANTILE-AUTISM; POSTNATAL-DEVELOPMENT; ETIOLOGIC FACTOR; GENE-EXPRESSION; IMMUNE-SYSTEM; BDV INFECTION; LEWIS RATS; CELLS; PERSISTENT AB Autism spectrum disorders (ASD) have been the focus of a great deal of research and clinical speculation. This intense interest relates to both the perplexing pathogenesis and devastating consequences of these disorders. 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PD MAR PY 2002 VL 40 IS 127 BP 119 EP 119 PN 1 PG 1 WC History & Philosophy Of Science SC History & Philosophy of Science GA 530WM UT WOS:000174382000024 ER PT J AU Shabani, DB Katz, RC Wilder, DA Beauchamp, K Taylor, CR Fischer, KJ AF Shabani, DB Katz, RC Wilder, DA Beauchamp, K Taylor, CR Fischer, KJ TI Increasing social initiations in children with autism: Effects of a tactile prompt SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT Annual Meeting of the Association-for-Behavior-Analysis CY MAY, 2001 CL NEW ORLEANS, LOUISIANA SP Assoc Behav Anal DE autism; social initiations; social interaction; tactile prompts AB An ABAB design was used to assess the effects of a tactile prompting device (i.e., a vibrating pager) as a prompt for the social initiations of 3 children with autism during free-play activities with typically developing peers. Results indicated that the tactile prompt was effective in increasing verbal initiations for all 3 children, and responses to peers' initiations were higher for 2 participants when the tactile prompt was used. Efforts to reduce the frequency of prompts while still maintaining rates of initiations were partially successful for I participant. C1 Univ Pacific, Stockton, CA 95211 USA. RP Shabani, DB (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. CR KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 McClannahan L. E., 1997, ENVIRON BEHAV, P271 Taylor BA, 1998, J APPL BEHAV ANAL, V31, P651, DOI 10.1901/jaba.1998.31-651 NR 3 TC 39 Z9 39 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 2002 VL 35 IS 1 BP 79 EP 83 DI 10.1901/jaba.2002.35-79 PG 5 WC Psychology, Clinical SC Psychology GA 533VH UT WOS:000174550600009 PM 11936550 ER PT J AU Lattimore, LP Parsons, MB Reid, DH AF Lattimore, LP Parsons, MB Reid, DH TI A prework assessment of task preferences among adults with autism beginning a supported job SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; supported employment; preferences; assessment ID IDENTIFYING WORK PREFERENCES; DISABILITIES AB A prework paired-task assessment was evaluated for identifying work preferences among 3 adults with autism beginning a supported job. When the workers began the job, choices were provided between more and less preferred tasks (determined by previous assessment). Results supported the assessment for identifying single task preferences, but did not reveal preferences of 2 workers for alternate tasks. Results are discussed in terms of evaluating other prework assessments that may reveal task-alternation preferences. C1 Carolina Behav Anal & Support Ctr, Morganton, NC 28680 USA. Louisiana State Univ, Hlth Sci Ctr, Baton Rouge, LA 70803 USA. RP Reid, DH (reprint author), Carolina Behav Anal & Support Ctr, POB 425, Morganton, NC 28680 USA. CR MITHAUG DE, 1978, J APPL BEHAV ANAL, V11, P153, DOI 10.1901/jaba.1978.11-153 Parsons MB, 1998, J ASSOC PERS SEVERE, V23, P329, DOI 10.2511/rpsd.23.4.329 Reid DH, 1998, J APPL BEHAV ANAL, V31, P281, DOI 10.1901/jaba.1998.31-281 NR 3 TC 12 Z9 13 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 2002 VL 35 IS 1 BP 85 EP 88 DI 10.1901/jaba.2002.35-85 PG 4 WC Psychology, Clinical SC Psychology GA 533VH UT WOS:000174550600010 PM 11936551 ER PT J AU Tang, JC Kennedy, CH Koppekin, A Caruso, M AF Tang, JC Kennedy, CH Koppekin, A Caruso, M TI Functional analysis of stereotypical ear covering in a child with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE stereotypy; descriptive analysis; analogue functional analysis; autism ID SELF-INJURY AB We studied stereotypical car covering in a child with autism. Results of a descriptive analysis were inconclusive but revealed a correlation between ear covering and another child's screaming. An analogue functional analysis showed that ear covering was emitted only when the screaming was present. C1 Vanderbilt Univ, Dept Special Educ, Nashville, TN 37203 USA. RP Kennedy, CH (reprint author), Vanderbilt Univ, Dept Special Educ, Box 328 Peabody, Nashville, TN 37203 USA. CR Carr EG, 1997, J APPL BEHAV ANAL, V30, P673, DOI 10.1901/jaba.1997.30-673 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 IWATA BA, 1982, ANAL INTERVEN DEVEL, V2, P3, DOI 10.1016/0270-4684(82)90003-9 Kennedy CH, 2000, J APPL BEHAV ANAL, V33, P559, DOI 10.1901/jaba.2000.33-559 Van Camp CM, 2000, J APPL BEHAV ANAL, V33, P207, DOI 10.1901/jaba.2000.33-207 NR 5 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 2002 VL 35 IS 1 BP 95 EP 98 DI 10.1901/jaba.2002.35-95 PG 4 WC Psychology, Clinical SC Psychology GA 533VH UT WOS:000174550600012 PM 11936553 ER PT J AU Durand, VM AF Durand, VM TI Raising a child with autism: a guide to applied behavior analysis for parents SO JOURNAL OF BEHAVIOR THERAPY AND EXPERIMENTAL PSYCHIATRY LA English DT Book Review C1 SUNY Albany, Coll Arts & Sci, Dept Psychol, Albany, NY 12222 USA. RP Durand, VM (reprint author), SUNY Albany, Coll Arts & Sci, Dept Psychol, Albany, NY 12222 USA. RI Durand, V Mark/G-6157-2010 CR Richman Shira, 2001, RAISING CHILD AUTISM NR 1 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0005-7916 J9 J BEHAV THER EXP PSY JI J. Behav. Ther. Exp. Psychiatry PD MAR PY 2002 VL 33 IS 1 BP 64 EP 66 DI 10.1016/S0005-7916(02)00009-5 PG 3 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 600UF UT WOS:000178409600006 ER PT J AU Thirumalai, SS Shubin, RA Robinson, R AF Thirumalai, SS Shubin, RA Robinson, R TI Rapid eye movement sleep behavior disorder in children with autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 51st Annual Meeting of the American-Academy-of-Neurology CY APR 17-24, 1999 CL TORONTO, CANADA SP Amer Acad Neurol ID DISEASE AB We performed nocturnal polysomnography on 11 children with autism who had symptoms of disrupted steep and nocturnal awakenings. We identified rapid eye movement (REM) sleep behavior disorder in 5 of these 11 patients. Since REM sleep behavior disorder typically affects elderly males with neurodegenerative diseases, the identification of this phenomenon in autistic children could have profound implications for our understanding of the neurochemical and neurophysiologic bases of autism. Further, accurate diagnosis of REM sleep behavior disorder would enable specific treatment,with clonazepam and help the family and the child consolidate sleep and improve daytime performance. C1 Childrens Hosp Los Angeles, Dept Neurol, Los Angeles, CA 90027 USA. Huntington Hosp, Sleep Disorders Ctr, Pasadena, CA USA. Descanso Ctr Dev & Learning, La Canada Flintridge, CA USA. RP Thirumalai, SS (reprint author), Childrens Hosp Los Angeles, Dept Neurol, Mail Stop 82,4650 Sunset Blvd, Los Angeles, CA 90027 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Sleep Disorders Association, 1997, INT CLASS SLEEP DIS Boeve BF, 1998, NEUROLOGY, V51, P363 Comella CL, 1998, NEUROLOGY, V51, P526 CULEBRAS A, 1989, NEUROLOGY, V39, P1519 Elia M, 2000, BRAIN DEV-JPN, V22, P88, DOI 10.1016/S0387-7604(99)00119-9 Hering E, 1999, J AUTISM DEV DISORD, V29, P143, DOI 10.1023/A:1023092627223 HOSHINO Y, 1984, FOLIA PSYCHIAT NEU J, V38, P45 Picchietti DL, 1998, J CHILD NEUROL, V13, P588 Rechtschaffen A, 1968, MANUAL STANDARDIZED Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 SCHENCK CH, 1987, JAMA-J AM MED ASSOC, V257, P1786, DOI 10.1001/jama.257.13.1786 Schreck KA, 2000, J AUTISM DEV DISORD, V30, P127, DOI 10.1023/A:1005407622050 Sheldon SH, 1998, J CHILD NEUROL, V13, P257 Taira M, 1998, PSYCHIAT CLIN NEUROS, V52, P182, DOI 10.1111/j.1440-1819.1998.tb01018.x Takase M, 1998, PSYCHIAT CLIN NEUROS, V52, P181, DOI 10.1111/j.1440-1819.1998.tb01017.x TANGUAY PE, 1976, J AUTISM CHILD SCHIZ, V6, P275, DOI 10.1007/BF01543468 NR 17 TC 56 Z9 56 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 MAR PY 2002 VL 17 IS 3 BP 173 EP 178 DI 10.1177/088307380201700304 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 549FR UT WOS:000175434300004 PM 12026231 ER PT J AU Charman, T Baird, G AF Charman, T Baird, G TI Practitioner review: Diagnosis of autism spectrum disorder in 2-and 3-year-old children SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE Asperger syndrome; assessment; autism; diagnosis; pervasive developmental disorder; pre-school children ID PERVASIVE DEVELOPMENTAL DISORDERS; RECEPTIVE LANGUAGE DISORDER; LANDAU-KLEFFNER-SYNDROME; JOINT ATTENTION; YOUNG-CHILDREN; FOLLOW-UP; INFANTILE-AUTISM; BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; CHILDHOOD AUTISM AB Background: Progress has recently been made in the earlier identification of children with autism spectrum disorder (ASD). Whilst being welcome, this progress to earlier referral and diagnosis presents new challenges to clinical practice, including the accuracy and stability of early diagnosis, the utility of standardised assessment instruments with young pre-schoolers and the ability to indicate prognosis. Method: A selective review of recent research literature on the characteristic features of ASD in preschool children. Results: Multidisciplinary diagnostic assessment should include detailed information on developmental history, parents' descriptions of the everyday behaviour and activities of the child, direct assessment of the child's social interaction style, including where possible with age peers, and formal assessment of communicative, intellectual and adaptive function. Clinical assessments need to concentrate on the identification of impairments in early non-verbal social communication behaviours that characterise children with ASD from the second year of life, including social orienting, joint attention, imitation, play and reciprocal affective behaviour. The particular pattern of symptoms that presents in a 2-year-old with ASD may differ from that seen at the more prototypic age of 4 or 5 years. In particular, overt repetitive and stereotyped behaviours may be less notable, although where these are seen alongside the social and communicative impairments they are highly indicative of ASD. The use of standardised assessment instruments and the strict application of the DSM and ICD diagnostic criteria need to be employed with caution, as an expert clinical view has been shown to be more accurate. An important aspect of early diagnostic consultation is an open and straightforward approach to the negotiation of the diagnostic view with parents over time. Conclusions: Earlier diagnosis and rising recognition of ASD have significant implications for primary healthcare and specialist diagnostic and therapeutic services. C1 Univ London, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. Guys Kings Coll & St Thomas Hosp Med Sch, London, England. RP Charman, T (reprint author), Univ London, Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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Child Psychol. Psychiatry PD MAR PY 2002 VL 43 IS 3 BP 289 EP 305 DI 10.1111/1469-7610.00022 PG 17 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 532JB UT WOS:000174469800003 PM 11944873 ER PT J AU Wing, L Leekam, SR Libby, SJ Gould, J Larcombe, M AF Wing, L Leekam, SR Libby, SJ Gould, J Larcombe, M TI The Diagnostic Interview for Social and Communication Disorders: background, inter-rater reliability and clinical use SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE diagnosis; diagnostic interview; autism spectrum; reliability ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM; EPIDEMIOLOGY; INDIVIDUALS; IMPAIRMENTS; CHILDREN AB Background: The Diagnostic Interview for Social and Communication Disorders (DISCO) is a schedule for the diagnosis of autistic spectrum and related disorders and assessment of individual needs. It enables information to be recorded systematically for a wide range of behaviours and developmental skills and is suitable for use with all ages and levels of ability. In addition to helping the clinician to obtain a profile of each individual's pattern of development and behaviour, the DISCO also enables identification of specific features found in autistic spectrum disorders that are relevant for use with established diagnostic systems. Method: This paper describes the historical background of the DISCO, outlines its structure and reports the results of an inter-rater reliability study with parents of 82 children aged 3 to 11 years with autistic spectrum disorder, learning disability, language disorder or typical development. Results: Inter-rater reliability for the items in the inter-view was high (kappa coefficient or intra-class correlation at .75 or higher). This level of agreement was achieved for over 80% of the interview items. C1 Ctr Social & Communicat Disorders, Bromley BR2 9HT, Kent, England. Univ Durham, Durham DH1 3HP, England. Univ E Anglia, Norwich NR4 7TJ, Norfolk, England. Univ Plymouth, Plymouth PL4 8AA, Devon, England. RP Wing, L (reprint author), Ctr Social & Communicat Disorders, Elliot House,113 Masons Hill, Bromley BR2 9HT, Kent, England. 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Child Psychol. Psychiatry Allied Discip. PD MAR PY 2002 VL 43 IS 3 BP 307 EP 325 DI 10.1111/1469-7610.00023 PG 19 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 532JB UT WOS:000174469800004 PM 11944874 ER PT J AU Leekam, SR Libby, SJ Wing, L Gould, J Taylor, C AF Leekam, SR Libby, SJ Wing, L Gould, J Taylor, C TI The Diagnostic Interview for Social and Communication Disorders: Algorithms for ICD-10 childhood autism and Wing and Gould autistic spectrum disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article ID OBSERVATION SCHEDULE; EPIDEMIOLOGY; INDIVIDUALS; CHILDREN; BEHAVIOR AB Background: The Diagnostic Interview for Social and Communication Disorders (DISCO) is an interviewer-based schedule for use with parents and carers. In addition to its primary clinical purpose of helping the clinician to obtain a developmental history and description of the child or adult concerned, it can also be used to assist in providing a formal diagnostic category. Method: In this study we compared two algorithms based on the ninth revision of the schedule (DISCO 9). The algorithm for ICD-10 childhood autism comprised 91 individual, operationally defined items covering the behaviour outlined in the ICD-10 research criteria. The algorithm for the autistic spectrum disorder, as defined by Wing and Gould (1979), was based on S DISCO items that represented overarching categories of behaviour crucial for the diagnosis of autistic disorders. The aim of the study was to examine the implications for clinical diagnosis of these two different approaches. Parents of 36 children with clinical diagnoses of autistic disorder, 17 children with learning disability and 14 children with language disorders were interviewed by two inter-viewers. Algorithm diagnoses were applied to interview items in order to analyse the relationship between clinical and algorithm diagnoses and the inter-rater reliability between interviewers. Results: Clinical diagnosis was significantly related to the diagnostic outputs for both algorithms. Inter-rater reliability was also high for both algorithms. The ICD childhood disorder algorithm produced more discrepant diagnoses than the Wing and Gould autistic spectrum algorithm. Analysis of the ICD-10 algorithm items and combination of items helped to explain the reason for these discrepancies. Conclusions: The results indicate that the DISCO is a reliable instrument for diagnosis when sources of information are used from the whole inter-view. It is particularly effective for diagnosing disorders of the broader autistic spectrum. C1 Univ Durham, Dept Psychol, Durham DH1 3LE, England. Univ E Anglia, Norwich NR4 7TJ, Norfolk, England. RP Leekam, SR (reprint author), Univ Durham, Dept Psychol, South Rd, Durham DH1 3LE, England. CR *AM PSYCH ASS, 1987, DIAGN STAT MAN MENT, P33 *AM PSYCH ASS, 1980, DIAGN STAT MAN MENT, P86 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, P65 American Psychiatric Association, 2000, DIAGN STAT MAN MENT, P69 Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Bayley N, 1993, BAYLEY SCALES INFANT Berument S. K., 1999, BRIT J PSYCHIAT, V175, P44 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Eisenmajer R, 1998, J AUTISM DEV DISORD, V28, P527, DOI 10.1023/A:1026004212375 Fenson L, 1993, MACARTHUR COMMUNICAT FREEMAN BJ, 1981, AUTISM DIAGNOSIS INS, P17 Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 HOWLIN P, 1995, DEV MED CHILD NEUROL, V37, P406 Kanner L, 1943, NERV CHILD, V2, P217 Kanner L. E. L., 1956, AM J ORTHOPSYCHIAT, V26, P55 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 Leiter R. G., 1979, LEITER INT PERFORMAN LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lord C., 1997, AUTISM PERVASIVE DEV, P460 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 *PSYCH CORP, 1996, WECHSL OBJ LANG DIM Reynell J, 1987, REYNELL DEV LANGUAGE Schopler E., 1986, CHILD AUTISM RATING *WHO, 1978, MENT DIS GLOSS GUID, P33 *WHO, 1967, MAN INT STAT CLASS D, V1, P145 *WHO, 1974, GLOSS MENT DIS GUID, P54 Wing L., 1996, AUTISTIC SPECTRUM Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing L, 1997, HDB AUTISM PERVASIVE, P148 WING L, 1969, J CHILD PSYCHOL PSYC, V10, P1, DOI 10.1111/j.1469-7610.1969.tb02066.x Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 World Health Organisation, 1992, MAN INT STAT CLASS D, V1, P375 World Health Organization, 1977, MAN INT STAT CLASS D, V1 World Health Organization, 1993, ICD 10 CLASS MENT BE, P147 NR 40 TC 56 Z9 56 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 MAR PY 2002 VL 43 IS 3 BP 327 EP 342 DI 10.1111/1469-7610.00024 PG 16 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 532JB UT WOS:000174469800005 PM 11944875 ER PT J AU Dykens, EM AF Dykens, EM TI Are jigsaw puzzle skills 'spared' in persons with Prader-Willi syndrome? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE behavioral phenotypes; mental retardation; Prader-Willi Syndrome; visuo-spatial functioning ID WORKING-MEMORY; ISODICENTRIC CHROMOSOME-15; MALADAPTIVE BEHAVIOR; AUTISTIC DISORDER; CHILDREN; COMPULSIONS; RELIABILITY; PERFORMANCE; OBSESSIONS; SYMPTOMS AB Background: This three-part study examines previous clinical impressions that people with Prader-Willi syndrome have unusual jigsaw puzzle and word search skills. Results: Children with Prader-Willi syndrome showed relative strengths on standardized visual-spatial tasks (Object Assembly, Triangles, VMI) in that their scores were significantly higher than age- and IQ-matched peers with mixed mental retardation, but below those of age-matched normal children with average IQs. In striking contrast, children with Prader-Willi syndrome scored on par with normal peers on word searches, and they far outperformed them on the jigsaw puzzles, placing more than twice as many pieces as the typically-developing group. Within Prader-Willi syndrome, puzzle proficiency was not predicted by age, IQ, gender, degree of obesity, or obsessive-compulsive symptoms, but by genetic subtypes of this disorder. Conclusions: Findings are discussed in relation to splinter skills in autism, and to cases with autism and chromosome 15 anomalies that include the Prader-Willi region. C1 Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA 90024 USA. RP Dykens, EM (reprint author), Univ Calif Los Angeles, Inst Neuropsychiat, 7600 Westwood Plaza, Los Angeles, CA 90024 USA. CR Beery KE, 1997, DEV TEST VISUAL MOTO 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 CURFS LMG, 1991, CLIN GENET, V40, P430 Dykens E. M., 2000, GENETICS MENTAL RETA DYKENS EM, 1992, J AM ACAD CHILD PSY, V31, P1125, DOI 10.1097/00004583-199211000-00022 DYKENS EM, 1999, NEURODEVELOPMENTAL D, P137 Dykens EM, 1996, J CHILD PSYCHOL PSYC, V37, P995, DOI 10.1111/j.1469-7610.1996.tb01496.x Dykens EM, 1999, AM J MENT RETARD, V104, P158, DOI 10.1352/0895-8017(1999)104<0158:RBPPIW>2.0.CO;2 Dykens EM, 2001, AM J MENT RETARD, V106, P94, DOI 10.1352/0895-8017(2001)106<0094:DBIWWS>2.0.CO;2 Dykens EM, 1997, AM J MENT RETARD, V102, P228, DOI 10.1352/0895-8017(1997)102<0228:MBICWP>2.0.CO;2 Dykens EM, 1999, AM J MENT RETARD, V104, P67, DOI 10.1352/0895-8017(1999)104<0067:MBDIPS>2.0.CO;2 Dykens EM, 2000, MENT RETARD, V38, P163, DOI 10.1352/0047-6765(2000)038<0163:CAUFCW>2.0.CO;2 GABEL S, 1986, APPL RES MENT RETARD, V7, P459, DOI 10.1016/S0270-3092(86)80018-2 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006 Hill A.L., 1978, INT REV RES MENT RET, P277 Hodapp R. M., 1990, DEV PSYCHOPATHOL, V2, P213, DOI 10.1017/S0954579400000730 HODAPP RM, 1994, AM J MENT RETARD, V98, P675 Hodapp RM, 2001, AM J MENT RETARD, V106, P4, DOI 10.1352/0895-8017(2001)106<0004:SBROGM>2.0.CO;2 HOLLAND AJ, 1995, J INTELL DISABIL RES, V39, P373 HOLM VA, 1993, PEDIATRICS, V91, P398 Jernigan T. L., 1994, ATYPICAL COGNITIVE D, P23 Jolliffe T, 1997, J CHILD PSYCHOL PSYC, V38, P527, DOI 10.1111/j.1469-7610.1997.tb01539.x Kaufman A. S., 1990, KAUFMAN BRIEF INTELL Kaufman AS, 1983, KAUFMAN ASSESSMENT B Logie RH, 1997, EUR J COGN PSYCHOL, V9, P241, DOI 10.1080/713752559 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 McCarthy D, 1972, MANUAL MCCARTHY SCAL MERVIS CB, 1999, NEURODEVELOPMENTAL D, P65 NETTELBECK T, 1999, DEV INTELLIGENCE, P247 Newborg J., 1984, BATTELLE DEV INVENTO Postle BR, 2000, BRAIN RES PROTOC, V5, P57, DOI 10.1016/S1385-299X(99)00053-7 Postle BR, 1999, J COGNITIVE NEUROSCI, V11, P585, DOI 10.1162/089892999563652 Prior M., 1979, J ABNORMAL CHILD PSY, V2, P357 Rineer S, 1998, AM J MED GENET, V81, P428, DOI 10.1002/(SICI)1096-8628(19980907)81:5<428::AID-AJMG12>3.0.CO;2-E Roof E, 2000, J INTELL DISABIL RES, V44, P25, DOI 10.1046/j.1365-2788.2000.00250.x ROOF E, 1999, 14 ANN PRAD WILL SYN 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 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 Sparrow S, 1984, VINELAND ADAPTIVE BE State MW, 2000, J AM ACAD CHILD PSY, V39, P797, DOI 10.1097/00004583-200006000-00021 State MW, 1999, J AM ACAD CHILD PSY, V38, P329, DOI 10.1097/00004583-199903000-00021 Tager-Flusberg H, 1998, J COGNITIVE NEUROSCI, V10, P631, DOI 10.1162/089892998563031 TAYLOR S, 1995, CLIN PSYCHOL REV, V15, P261, DOI 10.1016/0272-7358(95)00015-H WANG PP, 1995, BRAIN COGNITION, V29, P54, DOI 10.1006/brcg.1995.1267 Wechsler D., 1991, MANUAL WECHSLER INTE 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 47 TC 69 Z9 73 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 MAR PY 2002 VL 43 IS 3 BP 343 EP 352 DI 10.1111/1469-7610.00025 PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 532JB UT WOS:000174469800006 PM 11944876 ER PT J AU Kemner, C Oranje, B Verbaten, MN van Engeland, H AF Kemner, C Oranje, B Verbaten, MN van Engeland, H TI Normal P50 gating in children with autism SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID STARTLE; SUPPRESSION; INHIBITION AB Background: An important characteristic of children with autism is their unusual reaction to stimuli, which may be related to problems in the filtering of sensory input. For this reason, sensory filtering was measured in children with autism using the P50 gating paradigm. Method: Twelve non-mentally retarded children with autism (i.e., having a DSM-IV diagnosis or either autistic disorder or pervasive developmental disorder not otherwise specified) and I I healthy control children were tested for their ability to suppress P50, measured at the Cz electrode. Results: No differences were found between the children with autism and the control children with regard to absolute P50 amplitudes and P50 suppression. Conclusion: The excitability of the neuronal substrate that causes P50 is normal in children with autism, as are the early, inhibitory processes related to P50 gating. These results distinguish between subjects with autism and subjects with schizophrenia, in whom sensory gating is abnormal. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, NL-3514 CX Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Adult Psychiat, NL-3514 CX Utrecht, Netherlands. Univ Utrecht, Fac Pharm, Dept Psychopharmacol, NL-3584 CA Utrecht, Netherlands. RP Kemner, C (reprint author), Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, F05-126,Heidelberglaan 100, NL-3514 CX Utrecht, Netherlands. CR Clementz BA, 1998, AM J PSYCHIAT, V155, P1691 Freedman R, 1996, ARCH GEN PSYCHIAT, V53, P1114 KOOTZ JP, 1982, J AUTISM DEV DISORD, V12, P185, DOI 10.1007/BF01531308 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MylesWorsley M, 1996, BIOL PSYCHIAT, V39, P289, DOI 10.1016/0006-3223(95)00134-4 NAGAMOTO HT, 1989, BIOL PSYCHIAT, V25, P549, DOI 10.1016/0006-3223(89)90215-1 Oranje B, 1999, BIOL PSYCHIAT, V45, P883, DOI 10.1016/S0006-3223(98)00128-0 ORNITZ EM, 1993, J AUTISM DEV DISORD, V23, P619, DOI 10.1007/BF01046105 RUMSEY JM, 1986, ARCH GEN PSYCHIAT, V43, P771 SCHWARZKOPF SB, 1993, BIOL PSYCHIAT, V33, P815, DOI 10.1016/0006-3223(93)90023-7 NR 10 TC 26 Z9 26 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 MAR PY 2002 VL 63 IS 3 BP 214 EP 217 PG 4 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 534WU UT WOS:000174613400007 PM 11926720 ER PT J AU Reed, T AF Reed, T TI Visual perspective taking as a measure of working memory in participants with autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; working memory; perspective taking ID EXECUTIVE FUNCTION; COGNITIVE PERSPECTIVE; CHILDHOOD AUTISM; FRAGILE-X; DEFICITS; DISORDER; CHILDREN; PERFORMANCE; INTACT; MEN AB There is mounting evidence that people with autism have executive function deficits and that those deficits are linked to the social impairment characteristic of autism. Bennetto et al. Child Dev. (1996) 67.: 1817-1835 suggest that, more specifically, people with autism may have a deficit in working memory. This hypothesis was tested using a visual perspective-taking task whose working memory load could be systematically varied. The performance of participants with autism on this task was significantly worse than that of the control participants. C1 Univ Maine, Dept Psychol, Farmington, ME 04938 USA. RP Reed, T (reprint author), Univ Maine, Dept Psychol, Farmington, ME 04938 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x CASE R, 1992, BRAIN COGNITION, V20, P51, DOI 10.1016/0278-2626(92)90061-P CHELUNE GJ, 1986, CHILD PSYCHIAT HUM D, V16, P221, DOI 10.1007/BF00706479 CLARK P, 1979, J CHILD PSYCHOL PSYC, V20, P271, DOI 10.1111/j.1469-7610.1979.tb00514.x HUGHES M, 1979, EDUC REV, V31, P133, DOI 10.1080/0013191790310207 Dunn L. M., 1981, PEABODY PICTURE VOCA HOBSON RP, 1984, J AUTISM DEV DISORD, V14, P85, DOI 10.1007/BF02408558 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 LLAMAS C, 1991, DEV FRONTAL CORTEX A MAZZOCCO MMM, 1992, J AM ACAD CHILD PSY, V31, P1141, DOI 10.1097/00004583-199211000-00025 MAZZOCCO MMM, 1993, J DEV BEHAV PEDIATR, V14, P328 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 Moffitt T. E., 1989, DEV PSYCHOPATHOL, V1, P105, DOI DOI 10.1017/S0954579400000298 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x PENNINGTON BF, 1993, DEV PSYCHOL, V29, P511, DOI 10.1037/0012-1649.29.3.511 PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 REED T, 1990, J AUTISM DEV DISORD, V20, P555, DOI 10.1007/BF02216060 REED T, 1994, J AUTISM DEV DISORD, V24, P53, DOI 10.1007/BF02172212 RUMSEY JM, 1985, J AUTISM DEV DISORD, V15, P23, DOI 10.1007/BF01837896 RUMSEY JM, 1990, J AUTISM DEV DISORD, V20, P155, DOI 10.1007/BF02284715 RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 RUSSELL J, 1991, BRIT J DEV PSYCHOL, V9, P331 Russell J, 1999, J AUTISM DEV DISORD, V29, P103, DOI 10.1023/A:1023084425406 SCHOPLER E, 1990, CHILDHOOD AUTISM RAT Shallice T, 1991, FRONTAL LOBE FUNCTIO SOBESKY WE, 1994, AM J MED GENET, V51, P1 Stuss DT, 1986, FRONTAL LOBES NR 31 TC 13 Z9 13 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 MAR PY 2002 VL 14 IS 1 BP 63 EP 76 DI 10.1023/A:1013515829985 PG 14 WC Rehabilitation SC Rehabilitation GA 516TH UT WOS:000173572500005 ER PT J AU Murray, L AF Murray, L TI Children with autism: a parents' guide, 2nd edition. SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Book Review CR Powers Michael D., 2000, CHILDREN AUTISM PARE NR 1 TC 0 Z9 0 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 MAR PY 2002 VL 27 IS 1 BP 73 EP 74 DI 10.1080/13668250120119626 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 542RW UT WOS:000175059000006 ER PT J AU Carvill, S Marston, G AF Carvill, S Marston, G TI People with intellectual disability, sensory impairments and behaviour disorder: a case series SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE mental retardation; psychiatric disorders; sensory impairments ID CHILDREN; AUTISM; DEPRESSION; POPULATION AB Background Sensory impairments (SIs) are more prevalent in people with intellectual disability (ID). Both conditions lead to higher rates of emotional and behavioural problems than in the general population. The identification of psychiatric disorders in this group can be difficult, particularly in those with severe ID and limited communication skills. Method The present paper presents a series of 18 case reports of individuals with ID, SI and behavioural problems. Results The majority of cases were young male caucasians with congenital rubella syndrome and autistic spectrum disorder, referred because of self-injurious behaviour (SIB) or aggression. Nine cases were treated with autidepressants, five underwent environmental changes and two had medication reduced. All showed some improvement. Conclusions The benefits of comprehensive assessments, the use of standardized assessment tools and trials of treatments are discussed in the context of making psychiatric diagnoses. C1 Admirals Court, Rugby CV22 7LW, England. Gulson Rd Hosp, North Warwickshire NHS Trust, Coventry, W Midlands, England. RP Carvill, S (reprint author), Admirals Court, 37 Nelson Way, Rugby CV22 7LW, England. 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PD MAR PY 2002 VL 46 BP 264 EP 272 DI 10.1046/j.1365-2788.2002.00400.x PN 3 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 543TB UT WOS:000175116300009 PM 11896812 ER PT J AU Butler, MG Bittel, D Talebizadeh, Z AF Butler, MG Bittel, D Talebizadeh, Z TI Prader-Willi syndrome and a deletion/duplication within the 15q11-q13 region SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID ANGELMAN-SYNDROME; PROXIMAL 15Q; MOLECULAR CHARACTERIZATION; DUPLICATION; AUTISM; HYPOPIGMENTATION; BREAKPOINTS; DELETION; PATIENT; MAP C1 Univ Missouri, Sch Med, Childrens Mercy Hosp & Clin, Sect Med Genet & Mol Med, Kansas City, MO 64108 USA. RP Butler, MG (reprint author), 2401 Gillham Rd, Kansas City, MO 64108 USA. 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PD SPR PY 2002 VL 4 IS 2 BP 73 EP 79 DI 10.1177/109830070200400202 PG 7 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 637ZY UT WOS:000180544600002 ER PT J AU Nuzzolo-Gomez, R Leonard, MA Ortiz, E Rivera, CM Greer, RD AF Nuzzolo-Gomez, R Leonard, MA Ortiz, E Rivera, CM Greer, RD TI Teaching children with autism to prefer books or toys over stereotypy or passivity SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID SELF-STIMULATORY-BEHAVIOR; PLAY AB Two experiments were conducted with 4 students with autism to test the relationship between either toys or books as conditioned reinforcers for observing or playing and their effect on stereotypy and passivity Experiment I consisted of a single preschool student who emitted frequent intervals of passive behavior and infrequent intervals of looking at books in a free play setting. After systematic training sessions involving pairings of reinforcers with looking at books, he engaged in looking at books significantly more than in his baseline in free play and decreased intervals of passivity. Experiment 2 involved a multiple baseline across 3 students. Baseline data were followed by toy-play conditioning sessions run concurrently with free-play observations. The 2 students who emitted frequent rates of stereotypy in baseline had significantly fewer intervals of stereotypy after toys were conditioned as reinforcers and toy play increased for all 3 students. C1 Columbia Univ, Teachers Coll, New York, NY 10027 USA. 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Posit. Behav. Interv. PD SPR PY 2002 VL 4 IS 2 BP 80 EP 87 DI 10.1177/109830070200400203 PG 8 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 637ZY UT WOS:000180544600003 ER PT J AU Koegel, RL Symon, JB Koegel, LK AF Koegel, RL Symon, JB Koegel, LK TI Parent education for families of children with autism living in geographically distant areas SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID BEHAVIORAL TREATMENT; TRAINING PARENTS; INTERVENTION; REMOTE; DISABILITIES; DELIVERY; SERVICES; PARADIGM; SKILLS; SPEECH AB Many families who are geographically distant from a center that specializes in intervention for autism are unable to access specialized services for their children. This article describes an evaluation of an intensive, week-long, center-based parent education program that teaches procedures for improving social communication for children with autism. Five represntative families who participated in this program are described. Data were collected on parent implementation of target behaviors using specific motivational teaching procedures of Pivotal Response Training. Data suggest improvements in the parents' use of the procedures, parent affect, and child expressive language during a week-long parent education session. Furthermore, follow-up measures demonstrate that these positive changes generalized to the families' home communities and maintained over time. These findings suggest the feasibility of a short-term, intensive parent education program for families who live in areas that are geographically distant from an intervention center. C1 Univ Calif Santa Barbara, Grad Sch Educ, Autism Res & Training Ctr, Santa Barbara, CA 93106 USA. RP Koegel, RL (reprint author), Univ Calif Santa Barbara, Grad Sch Educ, Autism Res & Training Ctr, Santa Barbara, CA 93106 USA. CR Albin R. 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PD SPR PY 2002 VL 4 IS 2 BP 88 EP 103 DI 10.1177/109830070200400204 PG 16 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 637ZY UT WOS:000180544600004 ER PT J AU Barnard, L Young, AH Pearson, J Geddes, J O'Brien, G AF Barnard, L Young, AH Pearson, J Geddes, J O'Brien, G TI A systematic review of the use of atypical antipsychotics in autism SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Review DE atypical antipsychotics; autistic disorder; learning disability; review; risperidone ID PERVASIVE DEVELOPMENTAL DISORDERS; RISPERIDONE TREATMENT; BEHAVIORAL SYMPTOMS; OPEN-LABEL; INFANTILE-AUTISM; YOUNG-CHILDREN; DOUBLE-BLIND; HALOPERIDOL; ADOLESCENTS; ADULTS AB Conventional antipsychotic medication is commonly prescribed to patients with autistic spectrum disorder. However, a high incidence of severe adverse reactions highlights the need to find more favourable treatments. Atypical antipsychotics may combine efficacy in ameliorating some autistic symptoms with a lower incidence of some adverse reactions. This article reviews: the use of atypical antipsychotics in autistic disorder, with particular focus on behaviour, cognition and physical well-being. Thirteen studies using risperidone, three using olanzapine, one using clozapine, one using amisulpride and one using quetiapine were identified. Few firm conclusions can be drawn due to the limitations of the studies; however, there is an indication that risperidone may be effective in reducing hyperactivity, aggression and repetitive behaviours, often without inducing severe adverse reactions. Olanzapine and clozapine may also be effective; however, there is little evidence for using amisulpride or quetiapine in this population. Randomized trials are required to clarify the effectiveness of these agents. C1 Dev Psychiat Res Unit, Newcastle Upon Tyne, Tyne & Wear, England. 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PD MAR PY 2002 VL 41 IS 3 BP 235 EP 236 DI 10.1097/00004583-200203000-00001 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 526FD UT WOS:000174118400001 PM 11886016 ER PT J AU Duffy, K Al-Saleem, T Karbowniczek, M Ewalt, D Prowse, AH Henske, EP AF Duffy, K Al-Saleem, T Karbowniczek, M Ewalt, D Prowse, AH Henske, EP TI Mutational analysis of the von Hippel Lindau gene in clear cell renal carcinomas from tuberous sclerosis complex patients SO MODERN PATHOLOGY LA English DT Article DE angiomyolipoma; loss of heterozygosity; pair 3; renal cell carcinoma; tuberous sclerosis; von Hippel-Lindau disease ID TUMOR-SUPPRESSOR GENE; SOMATIC MUTATIONS; EPITHELIOID ANGIOMYOLIPOMA; TSC2 GENE; RAT MODEL; EKER RAT; VHL; DISEASE; KIDNEY; CANCER AB Tuberous sclerosis complex (TSC) is an autosomal-dominant disorder characterized by seizures, mental retardation, autism, and tumors of multiple organs. Renal disease in TSC includes angiomyolipomas, cysts, and renal cell carcinomas. It is known that somatic mutations in the von Hippel Lindau (VHL) tumor suppressor gene occur in most clear cell renal carcinomas. To determine whether TSC-associated clear cell carcinomas also contain VHL mutations, we analyzed six tumors for loss of heterozygosity in the VHL gene region of chromosome 3p and for mutations in the VHL gene. Four of the patients were women between the ages of 34 and 68 years, and two were males under the age of 21 years. The loss of heterozygosity analysis was performed using polymorphic microsatellite markers, and the mutational analysis was performed using direct sequencing. Chromosome 3p loss of heterozygosity was not detected, and no VHL mutations were identified. These findings suggest that mutations in the TSC1 and TSC2 genes lead to clear cell renal carcinogenesis via an alternate pathway not involving VHL mutations. 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Pathol. PD MAR PY 2002 VL 15 IS 3 BP 205 EP 210 DI 10.1038/modpathol.3880517 PG 6 WC Pathology SC Pathology GA 537CM UT WOS:000174740200004 PM 11904337 ER PT J AU Korvatska, E Van de Water, J Anders, TF Gershwin, ME AF Korvatska, E Van de Water, J Anders, TF Gershwin, ME TI Genetic and immunologic considerations in autism SO NEUROBIOLOGY OF DISEASE LA English DT Review DE autism; multigenic traits; viral infection; autoimmunity; neuroimmune pathology ID PERVASIVE DEVELOPMENTAL DISORDER; SEROTONIN TRANSPORTER 5-HTT; CPG-BINDING PROTEIN-2; T-LYMPHOCYTE FUNCTION; NERVE GROWTH-FACTOR; INFANTILE-AUTISM; RETT-SYNDROME; LINKAGE-DISEQUILIBRIUM; SPECTRUM DISORDERS; IMMUNE ABNORMALITIES AB According to recent epidemiological surveys, autistic spectrum disorders have become recognized as common childhood psychopathologies. These life-lasting conditions demonstrate a strong genetic determinant consistent with a polygenic mode of inheritance for which several autism susceptibility regions have been identified. Parallel evidence of immune abnormalities in autistic patients argues for an implication of the immune system in pathogenesis. This review summarizes advances in the molecular genetics of autism, as well as recently emerging concerns addressing the disease incidence and triggering factors. The neurochemical and immunologic findings are analyzed in the context of a neuroimmune hypothesis for autism. Studies of disorders with established neuroimmune nature indicate multiple pathways of the pathogenesis; herein, we discuss evidence of similar phenomena in autism. (C) 2002 Elsevier Science (USA). C1 Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA. Univ Calif Davis, Dept Psychiat, Davis, CA 95616 USA. 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Dis. PD MAR PY 2002 VL 9 IS 2 BP 107 EP 125 DI 10.1006/nbdi.2002.0479 PG 19 WC Neurosciences SC Neurosciences & Neurology GA 532PW UT WOS:000174485100001 PM 11895365 ER PT J AU Sweeten, TL Posey, DJ Shekhar, A McDougle, CJ AF Sweeten, TL Posey, DJ Shekhar, A McDougle, CJ TI The amygdala and related structures in the pathophysiology of autism SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Review DE autism; amygdala; neurodevelopment; social behaviors ID POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-FLOW; HERPES-SIMPLEX ENCEPHALITIS; RESONANCE-IMAGING EVIDENCE; MEDIAL TEMPORAL-LOBE; INFANTILE-AUTISM; BASOLATERAL AMYGDALA; CHILDHOOD AUTISM; POSTERIOR-FOSSA; CORPUS-CALLOSUM AB Autism is a neurodevelopmental disorder that is defined behaviorally by severe deficiencies in reciprocal social interaction, verbal and nonverbal communication, and restricted interests. The amygdala is involved in the regulation of social behaviors and may be an important site of pathology for the social dysfunction seen in autism. This review focuses on lesion, postmortem, and neuroimaging studies that investigate the amygdala and related structures in this disorder. Other brain regions potentially involved in the neuropathology of autism are also briefly discussed. Although supportive evidence exists for amygdala dysfunction in autism, the currently available data are inconsistent and additional research is needed. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, 541 Clin Dr,Room 298, Indianapolis, IN 46202 USA. 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Biochem. Behav. PD MAR PY 2002 VL 71 IS 3 BP 449 EP 455 DI 10.1016/S0091-3057(01)00697-9 PG 7 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA 524BT UT WOS:000173992600010 PM 11830179 ER PT J AU Kahne, D Tudorica, A Borella, A Shapiro, L Johnstone, F Huang, W Whitaker-Azmitia, PM AF Kahne, D Tudorica, A Borella, A Shapiro, L Johnstone, F Huang, W Whitaker-Azmitia, PM TI Behavioral and magnetic resonance spectroscopic studies in the rat hyperserotonemic model of autism SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE autism; serotonin; auditory; tactile; ultrasonic vocalization; negative geotaxis; spontaneous alternation; magnetic resonance spectroscopy ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONERGIC GROWTH-FACTOR; 5-HT1A RECEPTORS; SUMATRIPTAN CHALLENGE; HORMONE RESPONSE; CHILDREN; SYNAPTOGENESIS; STIMULATION; FEATURES; EPILEPSY AB Autism is classified as a pervasive developmental disorder, with several cardinal features including sensory disturbances, obsessive-compulsive-like behavior, lack of bonding to caregivers and motor disturbances, To date, there is a lack of an animal model of the disease. The current work is aimed at producing such a model by treating developing rat pups with a serotonergic agonist, 5-methoxytryptamine (5-MT; 1 mg/kg) during development (from gestational age 12 days to postnatal day 20), thus mimicking one of the hallmark neurochemical features of the illness-increases in the neuro transmitter, serotonin. Animals were then tested in behavioral paradigms that may resemble the human illness. Treated rat pups were found to be overreactive to auditory or tactile sensory stimuli, to display changes in the negative geotaxic test of motor development, to show lack of separation-induced vocalizations when their dam was removed and to show decreased alternation in the spontaneous alternation task. As well, the animals showed metabolic abnormalities in the brain using in vivo proton magnetic resonance spectroscopy, which are consistent with those observed in autistic children. In summary, the model we are proposing shows some of the behavioral and metabolic features of autism, as well as being produced through alteration of a neurochemical system known to be altered in autism. (C) 2002 Elsevier Science Inc. All rights reserved. C1 SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. SUNY Stony Brook, Dept Radiol & Chem, Stony Brook, NY 11794 USA. RP Whitaker-Azmitia, PM (reprint author), SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. 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Behav. PD MAR PY 2002 VL 75 IS 3 BP 403 EP 410 DI 10.1016/S0031-9384(01)00673-4 PG 8 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 539RE UT WOS:000174883600018 PM 11897268 ER PT J AU Kehrer, HE AF Kehrer, HE TI Parents' education as autism therapists. Applied Behavior analysis in context. SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Book Review CR Keenan M., 2000, PARENTS ED AUTISM TH NR 1 TC 0 Z9 0 PU VANDENHOECK & RUPRECHT PI GOTTINGEN PA THEATERSTRASSE 13,, D-37073 GOTTINGEN, GERMANY SN 0032-7034 J9 PRAX KINDERPSYCHOL K JI Prax. Kinderpsychol. Kinderpsychiatr. PD MAR PY 2002 VL 51 IS 3 BP 225 EP 226 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 539ZF UT WOS:000174902900007 ER PT J AU Cohen, S Angus, J AF Cohen, S Angus, J TI Reaching out, joining in: Teaching social skills to young children with autism. SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Book Review C1 CUNY Hunter Coll, New York, NY 10021 USA. RP Cohen, S (reprint author), CUNY Hunter Coll, New York, NY 10021 USA. CR Attwood T., 1998, ASPERGERS SYNDROME G Fling Echo R., 2000, EATING ARTICHOKE MOT Grandin T., 1995, THINKING PICTURES OT Koegel LK, 1999, J ASSOC PERS SEVERE, V24, P174, DOI 10.2511/rpsd.24.3.174 Quill K. A., 2000, DO WATCH LISTEN SAY Romanowski Bashe P., 2001, OASIS GUIDE ASPERGER WEISS MJ, 2001, REACHING JOINGING TE NR 7 TC 0 Z9 0 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SPR PY 2002 VL 27 IS 1 BP 93 EP 94 DI 10.2511/rpsd.27.1.93 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BK UT WOS:000222242000010 ER PT J AU Bridges, D Lira, P AF Bridges, D Lira, P TI The effects of choice making to promote behavior support for individuals with autism SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Calif State Univ Los Angeles, Los Angeles, CA 90032 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. Sport PD MAR PY 2002 VL 73 IS 1 SU S BP A102 EP A102 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 534VN UT WOS:000174610500267 ER PT J AU Bering, JM AF Bering, JM TI The existential theory of mind SO REVIEW OF GENERAL PSYCHOLOGY LA English DT Review ID CHIMPANZEES PAN-TROGLODYTES; EVOLUTIONARY PSYCHOLOGY; COGNITIVE-DEVELOPMENT; ASPERGER-SYNDROME; GREAT APES; CHILDREN; EXPLANATIONS; OBJECTS; REPRESENTATION; COMPREHENSION AB The primary causal explanatory model for interpreting behavior, theory of mind, may have expanded into corridors of human cognition that have little to do with the context in which it evolved, questioning the suitability of domain-specific accounts of mind reading. Namely, philosophical-religious reasoning is a uniquely derived explanatory system anchored in intentionality that does not clearly involve behavior. 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O., 1978, HUMAN NATURE Woolley JD, 1997, CHILD DEV, V68, P991, DOI 10.2307/1132282 Woolley JD, 2000, IMAGINING IMPOSSIBLE, P99, DOI 10.1017/CBO9780511571381.005 YALOM JF, 1980, EXISTENTIAL PSYCHOTH Zihlman Adrienne, 1996, P293, DOI 10.1017/CBO9780511752414.023 ZUK GH, 1961, CHILD DEV, V32, P525, DOI 10.1111/j.1467-8624.1961.tb05049.x NR 121 TC 56 Z9 57 PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA SN 1089-2680 J9 REV GEN PSYCHOL JI Rev. Gen. Psychol. PD MAR PY 2002 VL 6 IS 1 BP 3 EP 24 DI 10.1037//1089-2680.6.1.3 PG 22 WC Psychology, Multidisciplinary SC Psychology GA 553LZ UT WOS:000175677800001 ER PT J AU Garfinkle, AN Schwartz, IS AF Garfinkle, AN Schwartz, IS TI Peer imitation: Increasing social interactions in children with autism and other developmental disabilities in inclusive preschool classrooms SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID TIME-DELAY; INSTRUCTION; SKILLS; RESPONSIVENESS; ACQUISITION; RESPONSES; STUDENTS; MODELS AB A single subject research design was conducted across four participants to evaluate the effectiveness of a peer imitation intervention. Three of the participants were preschool children with autism, and one of the participants was a preschooler with developmental delays. The intervention was implemented as part of the integrated classroom regular small-group activity. Data were collected at small-group time to assess the implementation and effectiveness of the intervention. Data were collected at free play, the generalization setting, to assess any changes in peer imitation behaviors, nonimitative social behavior, and nonsocial engagement. Results of the intervention indicate that the participants increased peer imitation behaviors in small-group and in free-play settings. Increases were also seen in social behavior (both in proximity to peers and in number of interactions) as well as in levels of nonsocial engagement. The results are discussed in terms of the importance of how interventions are planned, the importance of measuring the effects of interventions broadly, and the importance of developing interventions that teachers are likely to use. C1 Vanderbilt Univ, Nashville, TN USA. Univ Washington, Seattle, WA 98195 USA. RP Garfinkle, AN (reprint author), Dept Special Educ, MRL 304,Magnolia Circle, Nashville, TN 37203 USA. CR APOLLONI T, 1977, PERCEPT MOTOR SKILL, V44, P231 Bandura A., 1977, SOCIAL LEARNING THEO Biederman GB, 1998, EXCEPT CHILDREN, V64, P503 Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 BRODY GH, 1978, J APPL BEHAV ANAL, V11, P87, DOI 10.1901/jaba.1978.11-87 CARR EG, 1990, J AUTISM DEV DISORD, V20, P45, DOI 10.1007/BF02206856 CHARLOP MH, 1986, J APPL BEHAV ANAL, V19, P307, DOI 10.1901/jaba.1986.19-307 Christensen A. M., 1996, ED TREATMENT CHILDRE, V19, P3 COOKE TP, 1977, EXCEPT CHILDREN, V43, P531 DAWSON G, 1984, J ABNORM CHILD PSYCH, V12, P209, DOI 10.1007/BF00910664 EGEL AL, 1981, J APPL BEHAV ANAL, V14, P3, DOI 10.1901/jaba.1981.14-3 Goldstein H., 1989, EDUC TREAT CHILD, V12, P5 GRESHAM FM, 1981, REV EDUC RES, V51, P139 GRESHAM FM, 1980, J CONSULT CLIN PSYCH, V48, P718, DOI 10.1037/0022-006X.48.6.718 GRIFFEN AK, 1992, J APPL BEHAV ANAL, V25, P193, DOI 10.1901/jaba.1992.25-193 Hwang B, 1995, EDUC TRAIN MENT RET, V30, P336 IHRIG K, 1988, J AUTISM DEV DISORD, V18, P67, DOI 10.1007/BF02211819 KEEL MC, 1992, EXCEPT CHILDREN, V58, P357 LOWENTHAL B, 1995, INFANT TODDLER INTER, V5, P15 MORRIS EK, 1979, GENET PSYCHOL MONOGR, V99, P291 PECK CA, 1978, J SPEC EDUC, V12, P195 PETERSON C, 1977, EXCEPT CHILDREN, V43, P223 Rogers S. J., 1999, IMITATION INFANCY, P254 Sandall S. R., 2000, DEC RECOMMENDED PRAC SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SCHUNK DH, 1987, REV EDUC RES, V57, P149 Smith T., 2001, FOCUS AUTISM OTHER D, V16, P86, DOI 10.1177/108835760101600204 STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 STRICHART SS, 1975, AM J MENT DEF, V79, P506 Taubman M, 2001, RES DEV DISABIL, V22, P205, DOI 10.1016/S0891-4222(01)00068-3 Tryon A. S., 1986, J ABNORMAL CHILD PSY, V14, P532 VARNI JW, 1979, J ABNORM CHILD PSYCH, V7, P31, DOI 10.1007/BF00924508 Venn M. L., 1993, EARLY CHILDHOOD RES, V8, P277, DOI DOI 10.1016/S0885-2006(05)80068-7 Werts M. G., 1995, J BEHAV ED, V5, P55, DOI 10.1007/BF02110214 Werts MG, 1996, J APPL BEHAV ANAL, V29, P53, DOI 10.1901/jaba.1996.29-53 WOLERY M, 1991, EXCEPT CHILDREN, V57, P462 NR 36 TC 50 Z9 50 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0271-1214 J9 TOP EARLY CHILD SPEC JI Top. Early Child. Spec. Educ. PD SPR PY 2002 VL 22 IS 1 BP 26 EP 38 DI 10.1177/027112140202200103 PG 13 WC Education, Special SC Education & Educational Research GA 539KX UT WOS:000174870200003 ER PT J AU Hancock, TB Kaiser, AP AF Hancock, TB Kaiser, AP TI The effects of trainer-implemented Enhanced Milieu Teaching on the social communication of children with autism SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID LANGUAGE INTERVENTION; BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; PARENTS; SPEECH; DISCOURSE; INCREASE; PARADIGM AB This study examined the effects of Enhanced Milieu Teaching on the social communication skills of preschool children with autism when delivered by trained interventionists. A modified single-subject design across four children was used to assess the children's acquisition, maintenance, and generalized use of language targets and social communication skills as a result of the intervention. Observational data indicated that all children showed positive increases for specific target language use at the end of 24 intervention sessions, and these results were maintained through the 6 month follow-up observations. There was also evidence of positive changes in the complexity and diversity of language for children on observational measures. Three of the four children also generalized these positive language effects to interactions with their mothers at home, with the greatest changes seen immediately after the intervention. Parent satisfaction with the intervention procedures and child outcomes were high. C1 Vanderbilt Univ, Peabody Coll, Dept Special Educ, Nashville, TN 37203 USA. RP Hancock, TB (reprint author), Vanderbilt Univ, Peabody Coll, Dept Special Educ, Box 328, Nashville, TN 37203 USA. CR ALPERT CL, 1992, COMBINED CODE MILIEU Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Bayley N, 1993, BAYLEY SCALES INFANT Dunn L. M., 1981, PEABODY PICTURE VOCA DURAND VM, 1992, J APPL BEHAV ANAL, V25, P777, DOI 10.1901/jaba.1992.25-777 EDWARDS DR, 1991, AM FAM PHYSICIAN, V44, P1755 GARDNER MF, 1990, EXPRESSIVE ONE WORD GARTNER D, 1990, Women and Therapy, V10, P159 HALLE JW, 1981, J APPL BEHAV ANAL, V14, P389, DOI 10.1901/jaba.1981.14-389 HART B, 1975, J APPL BEHAV ANAL, V8, P411, DOI 10.1901/jaba.1975.8-411 HEDRICK DL, 1983, SEQUENCED INVENTORY HEMMETER ML, 1994, J EARLY INTERVENTION, V18, P269 HUNT P, 1988, J ASSOC PERS SEVERE, V13, P20 Kaiser A. P., 2000, EARLY EDUC DEV, V11, P423, DOI 10.1207/s15566935eed1104_4 KAISER AP, 1998, 31 ANN GATL C RES TH KAISER AP, 1994, J SPEECH HEAR RES, V37, P1320 KOEGEL RL, 1987, J AUTISM DEV DISORD, V17, P187, DOI 10.1007/BF01495055 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P141, DOI 10.1007/BF01058147 KOEGEL RL, 1988, J AUTISM DEV DISORD, V18, P525, DOI 10.1007/BF02211871 LANDA R, 1991, J SPEECH HEAR RES, V34, P1339 LASKI KE, 1988, J APPL BEHAV ANAL, V21, P391, DOI 10.1901/jaba.1988.21-391 LEMANEK KL, 1993, J CLIN CHILD PSYCHOL, V22, P68, DOI 10.1207/s15374424jccp2201_7 LORD C, 1993, PRESCHOOL ISSUES AUT, P199 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MCGEE GG, 1985, J APPL BEHAV ANAL, V18, P17, DOI 10.1901/jaba.1985.18-17 MILLER J, 1984, SALT SYSTEMATIC ANAL NORTON P, 1994, AM J FAM THER, V22, P67, DOI 10.1080/01926189408251298 Ostrosky M. M, 1991, TEACHING EXCEPTIONAL, V23, P6 SCHERER NJ, 1989, J SPEECH HEAR DISORD, V54, P383 SCHREIBMAN L, 1991, BEHAV THER, V22, P479, DOI 10.1016/S0005-7894(05)80340-5 Tawney J. W., 1984, SINGLE SUBJECT RES S WARREN SF, 1984, J SPEECH HEAR DISORD, V49, P43 Wechsler D., 1989, WECHSLER PRESCHOOL P Weiss R. S., 1981, J DIVISION EARLY CHI, V4, P40 Wetherby A.M., 1992, AUTISM IDENTIFICATIO, P107 YODER PJ, 1993, J SPEECH HEAR RES, V36, P158 NR 37 TC 36 Z9 36 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0271-1214 J9 TOP EARLY CHILD SPEC JI Top. Early Child. Spec. Educ. PD SPR PY 2002 VL 22 IS 1 BP 39 EP 54 DI 10.1177/027112140202200104 PG 16 WC Education, Special SC Education & Educational Research GA 539KX UT WOS:000174870200004 ER PT J AU [Anonymous] AF [Anonymous] TI MMR vaccine: no evidence for new variant of autism SO INPHARMA LA English DT News Item CR Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 NR 1 TC 0 Z9 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1173-8324 J9 INPHARMA JI Inpharma PD FEB 23 PY 2002 IS 1326 BP 20 EP 20 PG 1 GA 528DB UT WOS:000174228200031 ER PT J AU [Anonymous] AF [Anonymous] TI Time to look beyond MMR in autism research SO LANCET LA English DT Editorial Material NR 0 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 FEB 23 PY 2002 VL 359 IS 9307 BP 637 EP 637 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 526AZ UT WOS:000174107400001 ER PT J AU Walker-Smith, J AF Walker-Smith, J TI Autism, bowel inflammation, and measles SO LANCET LA English DT Letter ID CHILDREN C1 UCL, Wellcome Trust Ctr Hist Med, London NW1 1AD, England. RP Walker-Smith, J (reprint author), UCL, Wellcome Trust Ctr Hist Med, London NW1 1AD, England. CR Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 MORRIS A, 2002, NEW EVIDENCE VIRAL P UHLMANN V, 2002, POTENTIAL VIRAL PATH Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 Walker-Smith JA, 1998, LANCET, V351, P1356, DOI 10.1016/S0140-6736(05)79084-X NR 6 TC 9 Z9 10 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD FEB 23 PY 2002 VL 359 IS 9307 BP 705 EP 706 DI 10.1016/S0140-6736(02)07783-8 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 526AZ UT WOS:000174107400033 PM 11879886 ER PT J AU Burke, M AF Burke, M TI Every parent's choice? Autism and vaccination - the jury's out SO CHEMISTRY & INDUSTRY LA English DT Article NR 0 TC 0 Z9 0 PU SOC CHEMICAL INDUSTRY PI LONDON PA 14 BELGRAVE SQUARE, LONDON SW1X 8PS, ENGLAND SN 0009-3068 J9 CHEM IND-LONDON JI Chem. Ind. PD FEB 18 PY 2002 IS 4 BP 10 EP 10 PG 1 WC Chemistry, Applied SC Chemistry GA 526QZ UT WOS:000174142300016 ER PT J AU Taylor, B Miller, E Lingam, R Andrews, N Simmons, A Stowe, J AF Taylor, B Miller, E Lingam, R Andrews, N Simmons, A Stowe, J TI Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: Population study SO BRITISH MEDICAL JOURNAL LA English DT Article ID CAUSAL ASSOCIATION; MMR; DISORDERS AB Objectives To investigate whether measles, mumps, and rubella (MMR) vaccination is associated with bowel problems and developmental regression in children with autism, looking for evidence of a "new variant" form of autism. Design Population study with case note review linked to independently recorded vaccine data. Setting Five health districts in north east London. Participants 278 children with core autism and 195 with atypical autism, mainly identified froth computerised disability registers and born between 1979 and 1998. Main outcome measures Recorded bowel problems lasting at least three months, age of reported regression of the child's development where it was a feature, and relation of these to MMR vaccination. Results The proportion of children with developmental regression (25% overall) or bowel symptoms (17%) did not change significantly (P value for trend 0.50 and 0.47, respectively) during the 20 years from 197 9, a period which included the introduction of MMR vaccination in October 1988. No significant difference was found in rates of bowel problems or regression in children who received the MMR vaccine before their parents became concerned about their development (where MMR might have caused or triggered the autism with regression or bowel problem), compared with those who received it only after such concern and those who had not received the MMR vaccine. A possible association between non-specific bowel problems and regression in children with autism was seen but this was unrelated to MMR vaccination. Conclusions These findings provide no support for an MMR associated "new variant" form of autism with developmental regression and bowel problems, and further evidence against involvement of MMR vaccine in the initiation of autism. C1 UCL, Royal Free & Univ Coll Med Sch, Ctr Community Child Hlth, London NW3 2PF, England. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, London NW9 5EQ, England. RP Taylor, B (reprint author), UCL, Royal Free & Univ Coll Med Sch, Ctr Community Child Hlth, Royal Free Campus, London NW3 2PF, England. EM b.taylor@rfc.ucl.ac.uk CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DeWilde S, 2001, BRIT J GEN PRACT, V51, P226 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 Halsey NA, 2001, PEDIATRICS, V107, P1 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 NR 12 TC 162 Z9 165 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD FEB 16 PY 2002 VL 324 IS 7334 BP 393 EP 396 DI 10.1136/bmj.324.7334.393 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 524HC UT WOS:000174006300016 PM 11850369 ER PT J AU Motluk, A AF Motluk, A TI A stab at the truth - There must be a way to find if MMR is linked to autism 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 FEB 16 PY 2002 VL 173 IS 2330 BP 13 EP 13 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 523ZB UT WOS:000173986500012 ER PT J AU Prasad, C Marles, S Prasad, AN Nikkel, S Longstaffe, S Peabody, D Eng, B Wright, S Waye, JS Nowaczyk, MJM AF Prasad, C Marles, S Prasad, AN Nikkel, S Longstaffe, S Peabody, D Eng, B Wright, S Waye, JS Nowaczyk, MJM TI Smith-Lemli-Opitz syndrome: New mutation with a mild phenotype SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Smith-Lemli-Opitz syndrome; 7-dehydrocholesterol; DHCR7 mutations; autism spectrum behaviors ID REDUCTASE GENE; METABOLISM AB Smith-Lemli-Opitz syndrome (SLOS) (Online Mendelian Inheritance in Man, OMIM(TM), 2001, http://www.ncbi.nlm.nih.gov/omim/ for SLOS, MIM 270400) is an autosomal recessive disorder of cholesterol biosynthesis caused by mutations of the 3beta-hydroxysterol Delta(7)-reductase gene, DHCR7. We report on a female infant with an exceptionally mild phenotype of SLOS, in whom molecular studies identified a new mutation in DHCR7. The proposita initially presented with feeding difficulties, failure to thrive, hypotonia, mild developmental delay, and oral tactile aversion. She had minor facial anomalies and 2-3 syndactyly of her toes in both feet. The plasma cholesterol was borderline low at 2.88 mmol/L (normal 2.97-4.40 mmol/L). Elevated plasma 7-dehydrocholesterol level of 200.0 mumol/L confirmed the clinical diagnosis of SLOS. Molecular analysis demonstrated compound heterozygosity for IVS8-1G -->C and Y280C, a new missense mutation in DHCR7. Since the other mutation in this patient is a known null mutation, this newly discovered mutation is presumably associated with significant residual enzyme activity and milder expression of clinical phenotype. (C) 2002 Wiley-Liss, Inc. C1 Univ Manitoba, Dept Biochem & Med Genet, Winnipeg, MB, Canada. Univ Manitoba, Sect Child Neurol, Winnipeg, MB, Canada. Univ Manitoba, Dept Pediat, Winnipeg, MB, Canada. Hamilton Reg Lab Med Program, Hamilton, ON, Canada. McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. RP Nowaczyk, MJM (reprint author), McMaster Univ, Med Ctr, 1200 Main St W,Rm 3N16, Hamilton, ON L8S 4J9, Canada. 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J. Med. Genet. PD FEB 15 PY 2002 VL 108 IS 1 BP 64 EP 68 DI 10.1002/ajmg.10211 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 515PB UT WOS:000173503500012 PM 11857552 ER PT J AU Casanova, MF Buxhoeveden, DP Switala, AE Roy, E AF Casanova, MF Buxhoeveden, DP Switala, AE Roy, E TI Minicolumnar pathology in autism SO NEUROLOGY LA English DT Article ID PARABELT AUDITORY-CORTEX; EARLY INFANTILE-AUTISM; MACAQUE MONKEYS; CYTOARCHITECTONIC DEFINITION; QUANTITATIVE-ANALYSIS; PREFRONTAL AREAS; CEREBRAL-CORTEX; RHESUS-MONKEY; VISUAL-CORTEX; ORGANIZATION AB Objective: To determine whether differences exist in the configuration of minicolumns between the brains of autistic and control patients. Background: Autism is a severe and pervasive developmental disturbance of childhood, characterized by disturbances in both social interactions and communication, as well as stereotyped patterns of interests, activities, and behaviors. Postmortem neuropathologic studies remain inconclusive. Methods: The authors used a computerized imaging program to measure details of cell column morphologic features in area 9 of the prefrontal cortex and areas 21 and posterior 22 (Tpt) within the temporal lobe of nine brains of autistic patients and controls. Results: The authors found significant differences between brains of autistic patients and controls in the number of minicolumns, in the horizontal spacing that separates cell columns; and in their internal structure, that is, relative dispersion of cells. Specifically, cell columns in brains of autistic patients were more numerous, smaller, and less compact in: their cellular configuration with reduced neuropil space in the periphery. Conclusions: In autism, there are minicolumnar abnormalities in the frontal and temporal lobes of the brain. C1 Downtown VA Med Ctr, Psychiat Serv 26, Augusta, GA 30910 USA. Univ S Carolina, Dept Anthropol, Columbia, SC 29208 USA. Med Coll Georgia, Augusta, GA 30912 USA. 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PD FEB 2 PY 2002 VL 324 IS 7332 BP 296 EP 296 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 519LT UT WOS:000173728300032 PM 11823369 ER PT J AU Cheney, CL Pechstein, S Lucas, B Trahms, C McBride, B Dawson, G AF Cheney, CL Pechstein, S Lucas, B Trahms, C McBride, B Dawson, G TI Nutritional status and restricted diets in children with autism spectrum disorder. SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract C1 Univ Washington, Seattle, WA 98195 USA. NR 0 TC 0 Z9 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD FEB PY 2002 VL 75 IS 2 SU S MA P181 BP 395S EP 396S PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 516FU UT WOS:000173542600179 ER PT J AU Newbury, DF Ishikawa-Brush, Y Marlow, AJ Fisher, SE Monaco, AP Stott, CM Merricks, MJ Goodyer, IM Bolton, PF Jannoun, L Slonims, V Baird, G Pickles, A Bishop, DVM Conti-Ramsden, G Helms, PJ AF Newbury, DF Ishikawa-Brush, Y Marlow, AJ Fisher, SE Monaco, AP Stott, CM Merricks, MJ Goodyer, IM Bolton, PF Jannoun, L Slonims, V Baird, G Pickles, A Bishop, DVM Conti-Ramsden, G Helms, PJ CA SLI Consortium TI A genomewide scan identifies two novel loci involved in specific language impairment SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID QUANTITATIVE-TRAIT LOCUS; DEVELOPMENTAL DYSLEXIA; VARIANCE-COMPONENTS; LINKAGE ANALYSIS; CHROMOSOME 6P; DISORDERS; SPEECH; AUTISM; CHILDREN; TWIN AB Approximately 4% of English-speaking children are affected by specific language impairment (SLI), a disorder in the development of language skills despite adequate opportunity and normal intelligence. Several studies have indicated the importance of genetic factors in SLI; a positive family history confers an increased risk of development, and concordance in monozygotic twins consistently exceeds that in dizygotic twins. However, like many behavioral traits, SLI is assumed to be genetically complex, with several loci contributing to the overall risk. We have compiled 98 families drawn from epidemiological and clinical populations, all with probands whose standard language scores fall greater than or equal to1.5 SD below the mean for their age. Systematic genomewide quantitative-trait-locus analysis of three language-related measures (i.e., the Clinical Evaluation of Language Fundamentals-Revised [CELF-R] receptive and expressive scales and the nonword repetition [NWR] test) yielded two regions, one on chromosome 16 and one on 19, that both had maximum LOD scores of 3.55. Simulations suggest that, of these two multipoint results, the NWR linkage to chromosome 16q is the most significant, with empirical P values reaching 10 5 5, under both Haseman-Elston (HE) analysis (LOD score 3.55; P = .00003) and variance-components (VC) analysis (LOD score 2.57; P = .00008). Single-point analyses provided further support for involvement of this locus, with three markers, under the peak of linkage, yielding LOD scores >1.9. The 19q locus was linked to the CELF-R expressive-language score and exceeds the threshold for suggestive linkage under all types of analysis performed-multipoint HE analysis (LOD score 3.55; empirical P = .00004) and VC (LOD score 2.84; empirical P = .00027) and single-point HE analysis (LOD score 2.49) and VC (LOD score 2.22). 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Pharmacother. PD FEB PY 2002 VL 36 IS 2 BP 305 EP 311 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 519LK UT WOS:000173727600021 PM 11847953 ER PT J AU Blair, RJR Perschardt, KS AF Blair, RJR Perschardt, KS TI Empathy: A unitary circuit or a set of dissociable neuro-cognitive systems? SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID FACIAL EXPRESSIONS AB We question whether empathy is mediated by a unitary circuit. We argue that recent neuroimaging data indicate dissociable neural responses for different facial expressions as well as for representing others' mental states (Theory of Mind, TOM). We also argue that the general empathy disorder considered characteristic of autism and psychopathy is not general but specific for each disorder. C1 NIMH, Mood & Anxiety Program, Bethesda, MD 20892 USA. UCL, Inst Cognit Neurosci, London WC1H 3AR, England. RP Blair, RJR (reprint author), NIMH, Mood & Anxiety Program, Bethesda, MD 20892 USA. 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PD FEB PY 2002 VL 25 IS 1 BP 27 EP + PG 15 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 692XQ UT WOS:000183685900009 ER PT J AU Charman, T AF Charman, T TI Understanding the imitation deficit in autism may lead to a more specific model of autism as an empathy disorder SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID CHILDS APPRAISAL; JOINT ATTENTION; NEUROPSYCHOLOGY; EXPRESSIONS; CEREBELLAR; RESPONSES; EMOTION; INFANTS; OTHERS; PLAY AB Preston & de Waal are understandably cautious in applying their model to autism. They emphasise multiple cognitive impairments in autism, including prefrontal-executive, cerebellar-attention, and amygdala-emotion recognition deficits. Further empirical examination of imitation ability in autism may reveal deficits in the neural and cognitive basis of perception-action mapping that have a specific relation to the empathic deficit. 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PD FEB PY 2002 VL 25 IS 1 BP 29 EP + PG 15 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 692XQ UT WOS:000183685900011 ER PT J AU Preston, SD de Waal, FBM AF Preston, SD de Waal, FBM TI Empathy: Each is in the right - hopefully, not all in the wrong - Response SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID PET EXPLORATION; AUTISM; RECOGNITION; SIMULATION; ANTICIPATION; CHIMPANZEES; CEREBELLUM; PERCEPTION; ATTENTION; IMITATION AB Only a broad theory that looks across levels of analysis can encompass the many perspectives on the phenomenon of empathy. We address the major points of our commentators by emphasizing that the basic perception-action process, while automatic, is subject to control and modulation, and is greatly affected by experience and context because of the role of representations. 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Brain Sci. PD FEB PY 2002 VL 25 IS 1 BP 49 EP 71 PG 23 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 692XQ UT WOS:000183685900033 ER PT J AU Fatemi, SH Earle, J Kanodia, R Kist, D Emamian, ES Patterson, PH Shi, LM Sidwell, R AF Fatemi, SH Earle, J Kanodia, R Kist, D Emamian, ES Patterson, PH Shi, LM Sidwell, R TI Prenatal viral infection leads to pyramidal cell atrophy and macrocephaly in adulthood: Implications for genesis of autism and schizophrenia SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE human influenza virus; prenatal exposure; pyramidal cell atrophy; macrocephaly; autism; schizophrenia ID NEONATAL MICE; REELIN IMMUNOREACTIVITY; MAJOR DEPRESSION; NNOS EXPRESSION; IN-UTERO; AUTOANTIBODIES; HIPPOCAMPUS; DISORDERS; REDUCTION; EXPOSURE AB We investigated the role of maternal exposure to human influenza virus (H1N1) in C57BL/6 mice on Day 9 of pregnancy on pyramidal and nonpyramidal cell density, pyramidal nuclear area, and overall brain size in Day 0 neonates and 14-week-old progeny and compared them to sham-infected cohorts. Pyramidal cell density increased significantly (p < 0.0038) by 170% in Day 0 infected mice vs. controls. Nonpyramidal cell density decreased by 33% in Day 0 infected progeny vs. controls albeit, nonsignificantly. Pyramidal cell nuclear size decreased significantly (p < 0.0465) by 29% in exposed newborn mice vs. controls. Fourteen-week-old exposed mice continued to show significant increases in both pyramidal and nonpyramidal cell density values vs. controls respectively (p < 0.0085 E1 (exposed group 1), p < 0.0279 E2 (exposed group 2) pyramidal cell density; p < 0.0092 E1, p < 0.0252 E2, nonpyramidal cell density). By the same token, pyramidal cell nuclear size exhibited 37-43% reductions when compared to control values; these were statistically significant vs. controls (p < 0.04 E1, p < 0.0259 E2). Brain and ventricular area measurements in adult exposed mice also showed significant increases and decreases respectively vs. controls. Ventricular brain ratios exhibited 38-50% decreases in exposed mice vs. controls. While the rate of pyramidal cell proliferation per unit area decreased from birth to adulthood in both control and exposed groups, nonpyramidal cell growth rate increased only in the exposed adult mice. These data show for the first time that prenatal exposure of pregnant mice on Day 9 of pregnancy to a sublethal intranasal administration of influenza virus has both short-term and long-lasting deleterious effects on developing brain structure in the progeny as evident by altered pyramidal and nonpyramidal cell density values; atrophy of pyramidal cells despite normal cell proliferation rate and final enlargement of brain. Moreover, abnormal corticogenesis is associated with development of abnormal behavior in the exposed adult mice. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Neurosci, Minneapolis, MN 55455 USA. CALTECH, Dept Biol, Pasadena, CA 91125 USA. Utah State Univ, Inst Antiviral Res, Logan, UT 84322 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Box 392 Mayo Bldg,420 Delaware St SE, Minneapolis, MN 55455 USA. 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RP Koenig, K (reprint author), Yale Univ, Yale Child Study Ctr, 230 S Frontage Rd,POW 207900, New Haven, CT 06520 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bettleheim B, 1967, EMPTY FORTRESS INFAN Kanner L, 1943, NERV CHILD, V2, P217 Powers M. D., 1989, CHILDREN AUTISM PARE Powers Michael D., 2000, CHILDREN AUTISM PARE Rimland B., 1964, INFANTILE AUTISM SYN NR 6 TC 0 Z9 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD FEB PY 2002 VL 47 IS 1 BP 63 EP 65 PG 3 WC Psychology, Multidisciplinary SC Psychology GA 517PK UT WOS:000173619000027 ER PT J AU Patterson, PH AF Patterson, PH TI Maternal infection: window on neuroimmune interactions in fetal brain development and mental illness SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID INFLAMMATORY RESPONSE SYNDROME; VIRUS INFECTION; NEONATAL MICE; INTERLEUKIN-6; SCHIZOPHRENIA; INFLUENZA; CYTOKINES; PREGNANCY; MODEL AB Direct viral infection of the developing brain can have disastrous consequences for the fetus. More subtle and perhaps more insidious are viral infections of the pregnant mother, which can have long-lasting effects such as an increased risk of schizophrenia in the offspring, A recent mouse model has shown that respiratory infection in the pregnant mother leads to marked behavioral and pharmacological abnormalities in the offspring, some of which are relevant for schizophrenia and autism. This effect on fetal brain development might be caused by the maternal antiviral immune response, possibly mediated by cytokines. C1 CALTECH, Div Biol, Pasadena, CA 91125 USA. RP Patterson, PH (reprint author), CALTECH, Div Biol, Pasadena, CA 91125 USA. 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Opin. Neurobiol. PD FEB PY 2002 VL 12 IS 1 BP 115 EP 118 DI 10.1016/S0959-4388(02)00299-4 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 520ZE UT WOS:000173813000016 PM 11861174 ER PT J AU Danielsson, S Rydenhag, B Uvebrant, P Nordborg, C Olsson, I AF Danielsson, S Rydenhag, B Uvebrant, P Nordborg, C Olsson, I TI Temporal lobe resections in children with epilepsy: Neuropsychiatric status in relation to neuropathology and seizure outcome SO EPILEPSY & BEHAVIOR LA English DT Article DE epilepsy surgery; children; neuropsychiatry; cognitive impairment; neuropathology; malformations of cortical development; outcome ID CORTICAL DEVELOPMENT; HISTOPATHOLOGICAL FINDINGS; SURGICAL-TREATMENT; SURGERY; MICRODYSGENESIS; DYSGENESIS; CHILDHOOD; DYSPLASIA; SCLEROSIS; FEATURES AB The purpose of this work was to relate clinical neuropsychiatric findings to histopathological diagnoses and seizure outcome in a retrospective study of 16 children undergoing temporal lobe resections due to medically intractable epilepsy. These children constitute a heterogeneous group in which neuropsychiatric symptoms were common. The results of this study indicate a correlation between malformations of cortical development, less chance of seizure freedom, and neuropsychiatric problems in children with pharmacoresistant temporal lobe epilepsy. It is important to include neuropsychiatric assessments pre- and postoperatively and to inform parents that symptoms of autism spectrum disorders may or may not be improved after epilepsy surgery. (C) 2002 Elsevier Science (USA). C1 Sahlgrens Univ Hosp, Inst Hlth Women & Children, Dept Pediat, S-41345 Gothenburg, Sweden. Sahlgrens Univ Hosp, Inst Clin Neurosci, Dept Neurosurg, S-41345 Gothenburg, Sweden. Sahlgrens Univ Hosp, Inst Lab Med, Dept Pathol, S-41345 Gothenburg, Sweden. RP Danielsson, S (reprint author), Sahlgrens Univ Hosp, Inst Hlth Women & Children, Dept Pediat, S-41345 Gothenburg, Sweden. EM susanna.danielsson@pediat.gu.se CR Adams CBT, 1990, J EPILEPSY S1, V3, P157 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asarnow RF, 1997, DEV MED CHILD NEUROL, V39, P430 Bourgeois M, 1999, J NEUROSURG, V90, P833, DOI 10.3171/jns.1999.90.5.0833 BROWN RT, 1982, J CLIN CHILD PSYCHOL, V11, P262, DOI 10.1207/s15374424jccp1103_12 CONNERS CK, 1969, AM J PSYCHIAT, V126, P884 Duchowny M, 1997, CURR PROB E, V11, P261 Edwards JC, 2000, NEUROLOGY, V55, P1110 Engel Jr J., 1987, SURG TREATMENT EPILE, P553 Eriksson S, 1999, ACTA NEUROL SCAND, V99, P8 HUMPHREYS P, 1990, ANN NEUROL, V28, P727, DOI 10.1002/ana.410280602 Kuzniecky RI, 1994, EPILIPSIA, V35S6, P44 Lendt M, 2000, J NEUROL NEUROSUR PS, V69, P739, DOI 10.1136/jnnp.69.6.739 LINDSAY J, 1979, DEV MED CHILD NEUROL, V21, P630 MEENCKE HJ, 1992, MOL NEUROBIOLOGY EPI, P31 MISCHEL PS, 1995, J NEUROPATH EXP NEUR, V54, P137, DOI 10.1097/00005072-199503000-00001 Mohamed A, 2001, NEUROLOGY, V56, P1643 Nordborg C, 1999, J NEUROL NEUROSUR PS, V67, P521, DOI 10.1136/jnnp.67.4.521 PIVEN J, 1990, AM J PSYCHIAT, V147, P734 Purpura D P, 1982, Brain Res, V281, P287 RAYMOND AA, 1995, BRAIN, V118, P629, DOI 10.1093/brain/118.3.629 SISODIYA SM, 1995, BRAIN, V118, P1039, DOI 10.1093/brain/118.4.1039 Sisodiya SM, 2000, BRAIN, V123, P1075, DOI 10.1093/brain/123.6.1075 SPERLING MR, 1995, NEUROLOGY, V45, P970 Sperling MR, 1999, ANN NEUROL, V46, P45, DOI 10.1002/1531-8249(199907)46:1<45::AID-ANA8>3.0.CO;2-I Szabo CA, 1999, PEDIATR NEUROL, V20, P349, DOI 10.1016/S0887-8994(99)00003-X Szabo CA, 1998, EPILEPSIA, V39, P814, DOI 10.1111/j.1528-1157.1998.tb01174.x Vinters Harry V., 1993, P593 Wyllie E, 1998, ANN NEUROL, V44, P740, DOI 10.1002/ana.410440507 ZENTNER J, 1995, J NEUROL NEUROSUR PS, V58, P666, DOI 10.1136/jnnp.58.6.666 NR 30 TC 19 Z9 19 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1525-5050 J9 EPILEPSY BEHAV JI Epilepsy Behav. PD FEB PY 2002 VL 3 IS 1 BP 76 EP 81 DI 10.1006/ebeh.2001.0297d PG 6 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 553ML UT WOS:000175679500012 ER PT J AU Hellzen, O Asplund, K AF Hellzen, O Asplund, K TI Being in a fragmented and isolated world: interviews with carers working with a person with a severe autistic disorder SO JOURNAL OF ADVANCED NURSING LA English DT Article DE autistic disorder; consolation; disturbing behaviour; narratives; nurse's reactions; self-injurious behaviour; violence ID LEARNING-DISABILITIES; CHILDREN; ADULTS; NARRATIVES; FAMILIES; NURSES AB Aim. To illuminate the meaning of being a carer for a person with a severe autistic disorder. Background. Carets working with people with severe autism are occasionally exposed to residents' self-injurious behaviours and violent actions and at time residents appear resistant to all forms of treatment. Design/method. A qualitative case study was conducted. Six Swedish carets enrolled nurses (ENs), working on a special ward in a nursing home were interviewed about their lived experiences when caring for an individual with a severe autistic disorder. Narrative interviews were conducted and interpreted using a phenomenological-hermeneutic method inspired by Paul Ricoeur. Findings. Two themes were formulated which describe the caters' reality and their dream of an ideal. This ideal described carers' experiences of being trapped in a segmented and isolated care reality and their longing to achieve a sense of wholeness. The findings were interpreted and reflected on in the light of a framework inspired by the German philosopher Karl Jaspers in order to achieve a deeper understanding of the text. Conclusions. In their desperation, the carets used their empirical knowledge based on scientific knowledge, which could be understood as a substitute for their vision of a consolating wholeness. This paper shows that searching for a substitute to consolation seems to be an important aspect of the meaning of being a carer for a person with a severe autistic disorder. C1 Mid Sweden Univ, Dept Nursing & Hlth Sci, S-85170 Sundsvall, Sweden. Umea Univ, Dept Nursing, Umea, Sweden. RP Hellzen, O (reprint author), Mid Sweden Univ, Dept Nursing & Hlth Sci, S-85170 Sundsvall, Sweden. CR ASTROM G, 1993, CANCER NURS, V16, P179 BARTAK L, 1973, J CHILD PSYCHOL PSYC, V14, P161, DOI 10.1111/j.1469-7610.1973.tb01185.x Bhaumik S, 1997, BRIT J PSYCHIAT, V170, P502, DOI 10.1192/bjp.170.6.502 BOLLNOW OF, 1984, PHILOS G MARCEL, V17, P177 Carson RC, 1998, ABNORMAL PSYCHOL MOD Charman T, 1998, J AUTISM DEV DISORD, V28, P33, DOI 10.1023/A:1026058802381 Collacott RA, 1998, BRIT J PSYCHIAT, V173, P428, DOI 10.1192/bjp.173.5.428 DONENBERG G, 1993, J ABNORM CHILD PSYCH, V21, P179, DOI 10.1007/BF00911315 EAVES LC, 1994, J AUTISM DEV DISORD, V24, P3, DOI 10.1007/BF02172209 Edberg A K, 1995, J Psychiatr Ment Health Nurs, V2, P159, DOI 10.1111/j.1365-2850.1995.tb00051.x Frith U, 1991, AUTISM ASPERGER SYND GILLBERG C, AUTISM AUTISM LIKE D, P94 Hellzen O, 1995, J Psychiatr Ment Health Nurs, V2, P279, DOI 10.1111/j.1365-2850.1995.tb00093.x HOLMES N, 1991, J AUTISM DEV DISORD, V21, P159, DOI 10.1007/BF02284757 JASPERS K, 1969, PHILSOPHY, V1 JASPERS K, 1970, PHILOSPHY, V2 KOSE G, 1983, DEV PSYCHOL, V19, P636, DOI 10.1037//0012-1649.19.4.636 LINDSETH A, 1994, J ADV NURS, V20, P245, DOI 10.1046/j.1365-2648.1994.20020245.x LOOVAS OI, 1977, AUTISTIC CHILD LANGU LOOVAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3 MESIBOV GB, 1992, HIGH FUNCTIONING IND Mishler E., 1986, RES INTERVIEWING CON Patton MQ., 1990, QUALITATIVE EVALUATI PETERS T, 1998, AUTISM THEORETICAL U POLKINGHORNE DE, 1988, NARRATIVE KNOWING HU, P31 Poustka F, 1993, Acta Paedopsychiatr, V56, P69 PRIZANT BM, 1981, J SPEECH HEAR DISORD, V46, P241 RASMUSSEN BH, 1999, AM J HOSPICE PALLIAT, V17, P31 Rasmussen BH, 1997, CANCER NURS, V20, P330, DOI 10.1097/00002820-199710000-00004 RICOEUR P, 1997, MAIN TRENDS PHILOS Ricoeur P., 1976, INTERPRETATION THEOR RICOEUR P, 1991, ESSAYS HERMENEUTICS ROBINSON SE, 1991, RES NURS HEALTH, V14, P223, DOI 10.1002/nur.4770140309 RUTTER M, 1985, J CHILD PSYCHOL PSYC, V26, P193, DOI 10.1111/j.1469-7610.1985.tb02260.x SCRAGG P, 1994, BRIT J PSYCHIAT, V165, P679, DOI 10.1192/bjp.165.5.679 Söderberg A, 1996, Intensive Crit Care Nurs, V12, P207, DOI 10.1016/S0964-3397(96)80064-4 Wetherby A.M., 1992, AUTISM IDENTIFICATIO, P107 Yin R. K., 1989, APPL SOCIAL RES METH, V5 NR 38 TC 2 Z9 2 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0309-2402 J9 J ADV NURS JI J. Adv. Nurs. PD FEB PY 2002 VL 37 IS 4 BP 346 EP 354 DI 10.1046/j.1365-2648.2002.02102.x PG 9 WC Nursing SC Nursing GA 521XC UT WOS:000173865800004 PM 11872104 ER PT J AU Grigorenko, EL Klin, A Pauls, DL Senft, R Hooper, C Volkmar, F AF Grigorenko, EL Klin, A Pauls, DL Senft, R Hooper, C Volkmar, F TI A descriptive study of hyperlexia in a clinically referred sample of children with developmental delays SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE hyperlexia; K-ABC; PDD; word recognition; precocious ability ID IMPROVEMENT; DISORDERS; AUTISM AB In this study, we evaluated the incidence of hyperlexia in a clinically referred sample of 80 children with developmental delays. Based on hypotheses previously formulated in the literature, the study investigated the frequency of hyperlexia among boys and girls, the incidence of hyperlexia in children with Pervasive Developmental Disorders (PDD)-spectrum compared with non-PDD diagnoses, the range of IQ and of various cognitive skills in children with and without hyperlexia, and the developmental outcomes of children with and without hyperlexia. The results revealed no significant differences in the frequency of hyperlexia in girls compared with boys. However, the frequency of hyperlexia was significantly elevated among children with PDD compared with children with non-PDD diagnoses. The range of IQ and other cognitive skills and the developmental outcomes of children with hyperlexia were comparable to those of children without hyperlexia. C1 Yale Univ, Dept Psychol, PACE Ctr, New Haven, CT 06520 USA. Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA. Moscow MV Lomonosov State Univ, Dept Psychol, Moscow 117234, Russia. RP Grigorenko, EL (reprint author), Yale Univ, Dept Psychol, PACE Ctr, Box 208205, New Haven, CT 06520 USA. CR ARAM DM, 1984, NATI ASI SERIES BASHINA VM, 1999, AUTISM DETSTVE Beery KE, 1997, DEV TEST VISUAL MOTO BURD L, 1985, PERCEPT MOTOR SKILL, V60, P940 BURD L, 1987, J AM ACAD CHILD PSY, V26, P407, DOI 10.1097/00004583-198705000-00022 BURD L, 1985, PSYCHOL REP, V57, P236 COBRINIK L, 1974, J AUTISM CHILD SCHIZ, V4, P163, DOI 10.1007/BF02105368 Dunn L. M., 1981, PEABODY PICTURE VOCA FISHER W, 1988, J MENT DEFIC RES, V32, P357 GARDNER MF, 1990, EXPRESSIVE ONE WORD GOLDBERG TE, 1987, J AUTISM DEV DISORD, V17, P29, DOI 10.1007/BF01487258 GOLDBERG TE, 1984, BRAIN, V107, P759, DOI 10.1093/brain/107.3.759 HEALY JM, 1982, READ RES QUART, V17, P319, DOI 10.2307/747522 HEALY JM, 1982, BRAIN LANG, V9, P1 Jackson N. 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PD FEB PY 2002 VL 32 IS 1 BP 3 EP 12 DI 10.1023/A:1017995805511 PG 10 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600002 PM 11916330 ER PT J AU Daley, TC Sigman, MD AF Daley, TC Sigman, MD TI Diagnostic conceptualization of autism among Indian psychiatrists, psychologists, and pediatricians SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Indian psychologist; autism; autism diagnostic; diagnostic conceptualization ID DISORDERS; CHILDREN AB Diagnostic criteria for autism and background characteristics used by 937 Indian psychiatrists, psychologists and pediatricians were examined. Participants were asked to rate 18 behaviors as necessary for a diagnosis of autism, helpful but not necessary, or not helpful in a diagnosis of autism, and were asked to provide other information about their experiences with autism. Professionals' experience with diagnosing cases did not vary by profession and, in general, the three professions agreed about the characteristics most necessary for a diagnosis. However, within-group differences were found on the agreement over the usefulness of individual characteristics and amount of experience diagnosing cases as autistic. Comparisons with DSM-III and DSM-IV criteria suggest that Indian professionals may adhere to these systems. Conclusions about diagnosis in a cultural context and areas for future research are suggested. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90095 USA. RP Daley, TC (reprint author), Univ Calif Los Angeles, Dept Psychol, Box 951563, Los Angeles, CA 90095 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DSM 3 Berry J. W., 1992, CROSS CULTURAL PSYCH Cohen D. J., 1997, HDB AUTISM PERVASIVE, P947 Cohen Stephen P., 2001, INDIA EMERGING POWER Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 GALLAGHER BJ, 1990, J CLIN PSYCHOL, V46, P934, DOI 10.1002/1097-4679(199011)46:6<934::AID-JCLP2270460640>3.0.CO;2-4 GAUTAM RP, 1974, INDIAN J PSYCHIAT, V16, P238 GILLBERG C, 1986, BRIT J PSYCHIAT, V149, P68, DOI 10.1192/bjp.149.1.68 GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Gilliam J., 1982, BEHAV DISORDERS, V7, P189 JOSHI MC, 1992, INT PSYCHOL VIEWS WO, P206 Klin A, 2000, J AUTISM DEV DISORD, V30, P163, DOI 10.1023/A:1005415823867 KUMAR R, 1988, CHILD DEV INDIA HLTH LANDIS JR, 1977, BIOMETRICS, V33, P159, DOI 10.2307/2529310 MCCONACHIE H, 1995, DISABLED CHILDREN DE, P110 Segall MH, 1998, AM PSYCHOL, V53, P1101, DOI 10.1037//0003-066X.53.10.1101 STONE WL, 1987, J PEDIATR PSYCHOL, V12, P615, DOI 10.1093/jpepsy/12.4.615 Sturmey P., 1994, AUTISM CHILDREN ADUL, P13 World Health Organization, 1992, INT CLASS DIS NR 20 TC 21 Z9 21 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 2002 VL 32 IS 1 BP 13 EP 23 DI 10.1023/A:1017947922349 PG 11 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600003 PM 11916328 ER PT J AU Tunali, B Power, TG AF Tunali, B Power, TG TI Coping by redefinition: Cognitive appraisals in mothers of children with autism and children without autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; cope; cognitive appraisals; stress ID SOCIAL SUPPORT; ADJUSTMENT; STRESS; FAMILIES; PARENTS; ILLNESS AB To test a model of how mothers cope with the stresses of raising a child with autism (Tunali & Power, 1993), mothers of children with and without autism were interviewed. As predicted, mothers of autistic children: (1) placed less emphasis on career success and were more likely to believe that mothers of young children should not work outside of the home; (2) spent more leisure time with their extended family; (3) placed less emphasis on others' opinions of their child's behavior; (4) placed more emphasis on spousal support and parental roles in their discussions of marriage; (5) had more difficulty understanding their child's behavior; and (6) showed a marginally significant difference in their tolerance of ambiguity. Moreover, mothers of children with autism who showed these characteristics had the greatest life satisfaction overall. C1 Washington State Univ, Dept Human Dev, Pullman, WA 99164 USA. Univ Houston, Houston, TX 77004 USA. RP Power, TG (reprint author), Washington State Univ, Dept Human Dev, POB 646236, Pullman, WA 99164 USA. CR Bristol M. M., 1984, EFFECTS AUTISM FAMIL, P289 CARVER CS, 1993, J PERS SOC PSYCHOL, V65, P375, DOI 10.1037/0022-3514.65.2.375 CUMMINGS ST, 1976, AM J ORTHOPSYCHIAT, V46, P246 CUTLER BC, 1987, HDB AUTISM PERVASIVE, P513 DAVIDSON B, 1982, FAM RELAT, V31, P295, DOI 10.2307/584409 Dyson LL, 1997, AM J MENT RETARD, V102, P267, DOI 10.1352/0895-8017(1997)102<0267:FAMOSC>2.0.CO;2 FARVER CA, 1982, J VOCAT BEHAV, V20, P67 Festinger L, 1957, THEORY COGNITIVE DIS FOLKMAN S, 1986, J PERS SOC PSYCHOL, V50, P571, DOI 10.1037//0022-3514.50.3.571 GILL MJ, 1991, J AUTISM DEV DISORD, V21, P407, DOI 10.1007/BF02206867 GUMP JP, 1972, J SOC ISSUES, V28, P79 Harmon-Jones E, 2001, HANDBOOK OF AFFECT AND SOCIAL COGNITION, P237 Holroyd J., 1974, J COMMUNITY PSYCHOL, V2, P92, DOI 10.1002/1520-6629(197401)2:1<92::AID-JCOP2290020133>3.0.CO;2-A HOWARD J, 1978, CHILD INFLUENCES MAR, P275 INTAGLIATA J, 1984, MENT RETARD, V22, P4 KAZAK AE, 1984, FAM RELAT, V33, P67, DOI 10.2307/584591 KOEGEL RL, 1983, J CONSULT CLIN PSYCH, V51, P683 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LAVIGNE JV, 1979, PEDIATRICS, V63, P616 LOCKE HJ, 1959, MARRIAGE FAMILY AUG, P251 Maslow A., 1954, MOTIVATION PERSONALI McCubbin H., 1982, FAMILY STRESS COPING MCDONALD AP, 1970, PSYCHOL REP, V26, P791 MILGRAM NA, 1988, J AUTISM DEV DISORD, V18, P415, DOI 10.1007/BF02212196 Rao C.R., 1973, LINEAR STAT INFERENC ROTHBAUM F, 1982, J PERS SOC PSYCHOL, V42, P5, DOI 10.1037/0022-3514.42.1.5 Rutter M., 1983, HDB CHILD PSYCHOL, V4, P775 RYDELL ST, 1966, PSYCHOL REP, V19, P139 SABBETH BF, 1984, PEDIATRICS, V73, P762 TAYLOR SE, 1983, AM PSYCHOL, V38, P1161, DOI 10.1037//0003-066X.38.11.1161 Terry DJ, 1998, J PERS SOC PSYCHOL, V74, P1078, DOI 10.1037/0022-3514.74.4.1078 TUNALI B, 1993, J CHILD PSYCHOL PSYC, V34, P945, DOI 10.1111/j.1469-7610.1993.tb01100.x WILTON K, 1986, J MENT DEFIC RES, V30, P163 ZUNG WWK, 1965, ARCH GEN PSYCHIAT, V12, P63 NR 34 TC 50 Z9 50 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 2002 VL 32 IS 1 BP 25 EP 34 DI 10.1023/A:1017999906420 PG 10 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600004 PM 11916329 ER PT J AU Estecio, MRH Fett-Conte, AC Varella-Garcia, M Fridman, C Silva, AE AF Estecio, MRH Fett-Conte, AC Varella-Garcia, M Fridman, C Silva, AE TI Molecular and cytogenetic analyses on Brazilian youths with pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE cytogenetic analysis; PDD; PDD-NOS; fragile X; genetic factors ID FRAGILE-X SYNDROME; CHROMOSOMAL-ABNORMALITIES; PSYCHIATRIC-DISORDERS; MENTAL-RETARDATION; GENETIC INFLUENCES; AUTISTIC DISORDER; INFANTILE-AUTISM; EXPRESSION; RECEPTOR; SUBUNIT AB The Pervasive Developmental Disorders (PDDs) constitute a group of behavioral and neurobiological impairment conditions whose main features are delayed communicative and cognitive development. Genetic factors are reportedly associated with PDDs and particular genetic abnormalities are frequently found in specific diagnostic subgroups such as the autism spectrum disorders. This study evaluated cytogenetic and molecular parameters in 30 youths with autism or other PDDs. The fragile X syndrome was the most common genetic abnormality detected, presented by I patient with autism and I patient with PPD not-otherwise specified (PPD-NOS). One girl with PDD-NOS was found to have tetrasomy for the 15q11-q13 region, and one patient with autism exhibited in 2/100 metaphases an inv(7)(p15q36), thus suggesting a mosaicism 46,XX/46,XX,inv(7)(p15q36) or representing a coincidental finding. The high frequency of chromosomopathies support the hypothesis that PDDs may develop as a consequence to chromosomal abnormalities and justify the cytogenetic and molecular assessment in all patients with PDDs for establishment of diagnosis. C1 UNESP, Dept Biol, Inst Biociencias Letras & Ciencias Exatas, Lab Citogenet & Biol Mol, BR-15054000 Sao Jose Do Rio Preto, SP, Brazil. FAMERP, Genet Lab, Dept Biol Mol, Sao Jose do Rio Preto, SP, Brazil. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. Univ Sao Paulo, Inst Biociencias, Sao Paulo, Brazil. RP Silva, AE (reprint author), UNESP, Dept Biol, Inst Biociencias Letras & Ciencias Exatas, Lab Citogenet & Biol Mol, Rua Cristovao Colombo 2265,Jardim Nazareth, BR-15054000 Sao Jose Do Rio Preto, SP, Brazil. 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Autism Dev. Disord. PD FEB PY 2002 VL 32 IS 1 BP 35 EP 41 PG 7 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600005 PM 11916331 ER PT J AU Williams, MA Moss, SA Bradshaw, JL Rinehart, NJ AF Williams, MA Moss, SA Bradshaw, JL Rinehart, NJ TI Random number generation in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; randomness; inhibition; executive function ID WORKING-MEMORY; EXECUTIVE FUNCTIONS; PERFORMANCE; TASK AB This study explored the ability of individuals with autism to generate a unique series of digits. Fourteen low-functioning individuals with autism, 14 intellectually disabled individuals, and 14 postgraduate university students generated a series of pseudo-random digits. Individuals with autism were more likely to repeat previous digits than were either of the control groups. The normal control group, however, was less likely to attempt cycling through all digits before repeating. 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Autism Dev. Disord. PD FEB PY 2002 VL 32 IS 1 BP 43 EP 47 DI 10.1023/A:1017904207328 PG 5 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600006 PM 11916332 ER PT J AU Rapin, I AF Rapin, I TI Diagnostic dilemmas in developmental disabilities: Fuzzy margins at the edges of normality. An essay prompted by Thomas Sowell's new book: The Einstein Syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE developmental disorders; classification; high-functioning autism; cognition; language delay; early intervention ID AUTISM; DISORDERS; CHILDREN; SPECTRUM; LANGUAGE; ADULTS; BRAIN AB Sowell's "Einstein children" are rare, extraordinarily gifted children, often the offspring of engineers or other highly educated musical families, in whom exceptional visual/spatial reasoning skills mature much earlier than language skills. Sowell states that speechless children with demonstrably superior nonverbal problem-solving skills and mathematical ability whose language comprehension is adequate have a favorable outlook with or without intervention, even if their social skills and behavior are suboptimal. He stresses that listening to parents' reports of their children's accomplishments at home provides more reliable information than questionnaires or formal one-time evaluations to distinguish between inability and unwillingness to speak or perform. He strongly objects to invasive and stressful tests for such children and questions the effectiveness of the many early interventions offered to children with developmental disorders. Certainly, providing a definite prognosis in very young children is hazardous because it is so subject to error, unless there is independent evidence for a serious neurologic problem with brain dysfunction or incontrovertible signs of truly exceptional cognitive ability. Early, individualized intervention is mandatory for children, no matter how bright, whose language comprehension is inadequate, and for those with troublesome behavioral traits bordering on or indicative of an autistic spectrum (pervasive developmental disorder/PDD) diagnosis. Children with isolated abilities who are functionally inept in every day life are not "Einstein children" and their deficits must be addressed promptly and specifically. Sowell's book raises important issues about behaviorally based diagnoses. Developmental disorders are not diseases that one does or does not have but are behaviorally defined dimensional traits along a continuum with fuzzy edges and a wide range of severity. Therefore, there is no crisp partition between normalcy and disorder, and between disorders with different names yet shared features, even when there is no controversy regarding the identification of prototypic exemplars. The utility for practical and research reasons of agreed upon standard diagnostic criteria is not in question, provided the statistical rather than biological nature of the criteria is kept in mind. Most subtypes of disorders like autism, dyslexia, or attention deficit are defined by arbitrary cuts in a bell-shaped spectrum of disability, which in no way invalidates their organic, neurologic basis. Developmental disorders are rarely the consequences of single gene defects or of definable postnatal insults; they have many causes that vary among individuals. Like many complex human traits, they are the expression of extremely complex multigenic influences on brain development. Because single gene defects are rare causes of these disorders, medical testing needs to be constrained by the history and examination. Intervention must address each child's particular needs and is, for the most part, educational. C1 Yeshiva Univ Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Rose F Kennedy Ctr Res Mental Retardat & Human De, Bronx, NY 10461 USA. RP Rapin, I (reprint author), Yeshiva Univ Albert Einstein Coll Med, Saul R Korey Dept Neurol, 1300 Morris Pk Ave, Bronx, NY 10461 USA. 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PD FEB PY 2002 VL 32 IS 1 BP 61 EP 62 PG 2 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600010 PM 11916335 ER PT J AU Volkmar, F AF Volkmar, F TI Predicting outcome in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter CR Howlin P., 1998, AUTISM PERVASIVE DEV, P209 NR 1 TC 5 Z9 5 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD FEB PY 2002 VL 32 IS 1 BP 63 EP 64 PG 2 WC Psychology, Developmental SC Psychology GA 531HU UT WOS:000174410600011 PM 11916336 ER PT J AU Casanova, MF Buxhoeveden, DP Switala, AE Roy, E AF Casanova, MF Buxhoeveden, DP Switala, AE Roy, E TI Asperger's syndrome and cortical neuropathology SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PARABELT AUDITORY-CORTEX; CYTOARCHITECTONIC DEFINITION; PREFRONTAL AREAS; MACAQUE MONKEYS; RHESUS-MONKEY; ORGANIZATION; CONNECTIONS; ASYMMETRIES; NEOCORTEX; REGION AB Asperger's disorder or syndrome is characterized by impaired social interaction, normal intelligence, and adequate language skills in the areas of grammar and vocabulary. The symptoms are pervasive in nature and usually manifested in childhood. Despite the gravity and chronicity of the condition. the medical literature remains sparse and offers no information about possible neuropathologic underpinnings. The present study is a case report on two patients with Asperger's syndrome. Neuropathologic examination revealed no degenerative changes or gliosis. A more detailed assessment with computerized image analysis indicated abnormalities in the minicolumnar organization of the three areas examined (9, 21, 22) (P =.032). Specifically, minicolumns were smaller, and their component cells were more dispersed than normal. A similar neuropathology has recently been reported for autism and disputes the uniqueness of these findings. The minicolumnar changes provide a possible link to receptive field abnormalities and a useful clinicopathologic correlate to Asperger's syndrome. C1 Downtown VA Med Ctr, Augusta, GA 30904 USA. Med Coll Georgia, Dept Psychiat, Augusta, GA 30912 USA. RP Casanova, MF (reprint author), Downtown VA Med Ctr, 3B-121,24,1 Freedom Way, Augusta, GA 30904 USA. 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Child Neurol. PD FEB PY 2002 VL 17 IS 2 BP 142 EP 145 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 536ZH UT WOS:000174731400011 PM 11952076 ER PT J AU Milne, E Swettenham, J Hansen, P Campbell, R Jeffries, H Plaisted, K AF Milne, E Swettenham, J Hansen, P Campbell, R Jeffries, H Plaisted, K TI High motion coherence thresholds in children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autistic disorder; motion perception; central coherence; magnocellular pathway; visual processing ID VISUAL AREA MT; MACAQUE MONKEY; COLOR; INDIVIDUALS; SENSITIVITY; PERFORMANCE; PRECEDENCE; PERCEPTION; ABILITIES; DYSLEXICS AB Background: We assessed motion processing in a group of high functioning children with autism and a group of typically developing children, using a coherent motion detection task. Method: Twenty-five children with autism (mean age I I years, 8 months) and 22 typically developing children matched for non-verbal mental ability and chronological age were required to detect the direction of moving dots in a random dot kinematogram. Results: The group of children with autism showed significantly higher motion coherence thresholds than the typically developing children (i.e., they showed an impaired ability to detect coherent motion). Conclusions: This finding suggests that some individuals with autism may show impairments in low-level visual processing - specifically in the magnocellular visual pathway. The findings are discussed in terms of implications for higher-level cognitive theories of autism, and the suggestion is made that more work needs to be carried out to further investigate low-level visual processing in autism. C1 UCL, Dept Human Commun Sci, London WC1N 1PF, England. Univ Oxford, Oxford OX1 2JD, England. Univ Cambridge, Cambridge, England. RP Milne, E (reprint author), UCL, Dept Human Commun Sci, 2 Wakefield St, London WC1N 1PF, England. 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C., 1992, STANDARD PROGR MATRI Ropar D, 1999, J CHILD PSYCHOL PSYC, V40, P1283, DOI 10.1017/S0021963099004667 Saitoh O, 1998, PSYCHIAT CLIN NEUROS, V52, P219 SCHILLER PH, 1990, VISUAL NEUROSCI, V5, P321 SERGENT J, 1982, J EXP PSYCHOL HUMAN, V8, P253, DOI 10.1037/0096-1523.8.2.253 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 SINGER W, 1973, BRAIN RES, V49, P291, DOI 10.1016/0006-8993(73)90424-1 Spencer J, 2000, NEUROREPORT, V11, P2765, DOI 10.1097/00001756-200008210-00031 SWETTENHAM J, 2000, J COGNITIVE NEURO D, V53 Talcott JB, 2000, NEUROPSYCHOLOGIA, V38, P935, DOI 10.1016/S0028-3932(00)00020-8 Talcott JB, 1998, NEURO-OPHTHALMOLOGY, V20, P187, DOI 10.1076/noph.20.4.187.3931 VanMeter L, 1997, J AUTISM DEV DISORD, V27, P557, DOI 10.1023/A:1025830110640 NR 49 TC 185 Z9 187 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD FEB PY 2002 VL 43 IS 2 BP 255 EP 263 DI 10.1111/1469-7610.00018 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 519ZR UT WOS:000173755800010 PM 11902604 ER PT J AU Kaminsky, L Dewey, D AF Kaminsky, L Dewey, D TI Psychosocial adjustment in siblings of children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; siblings; psychological adjustment ID MIDDLE CHILDHOOD; MATERNAL REPORTS; DOWNS-SYNDROME; LONELINESS; DISABILITIES; FAMILIES; ILLNESS; STRESS; SCHOOL; BOYS AB Background: This study investigated psychosocial adjustment in siblings of children with autism compared to siblings of children with Down syndrome and siblings of normally developing children. In addition, the relationships between feelings of loneliness, social support and psychosocial adjustment, and the influence of gender and family size on psychological adjustment were examined. Methods: Ninety siblings (30 per group) between the ages of 8 and 18 and one parent of each child participated in this study. Results: Results indicated that siblings of children with autism, as well as comparison siblings, were well adjusted and reported low levels of loneliness. Siblings of children with autism also reported that they received high levels of social support in their lives. Conclusions: Large family size appears to facilitate healthy adjustment in siblings of children with autism. C1 Alberta Childrens Prov Gen Hosp, Behav Res Unit, Calgary, AB T2T 5C7, Canada. Univ Calgary, Calgary, AB T2N 1N4, Canada. RP Dewey, D (reprint author), Alberta Childrens Prov Gen Hosp, Behav Res Unit, 1820 Richmond Rd SW, Calgary, AB T2T 5C7, Canada. 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Child Psychol. Psychiatry Allied Discip. PD FEB PY 2002 VL 43 IS 2 BP 225 EP 232 DI 10.1111/1469-7610.00015 PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 519ZR UT WOS:000173755800007 PM 11902601 ER PT J AU Hastings, RP Brown, T AF Hastings, RP Brown, T TI Behavioural knowledge, causal beliefs and self-efficacy as predictors of special educators' emotional reactions to challenging behaviours SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE behavioural knowledge; challenging behaviour; emotional reactions; self-efficacy; special education; staff ID CARE STAFF; INJURIOUS-BEHAVIOR; LEARNING-DISABILITIES; CHILDREN; RESPONSES; PEOPLE; ATTRIBUTIONS AB Background Theoretical models and emerging empirical data suggest that the emotional reactions of staff to challenging behaviours may affect their responses to challenging behaviours and their psychological well-being. However, there have been few studies focusing on factors related to staff emotional reactions. Methods Seventy staff working in educational environments with children with intellectual disability and/or autism. completed a self-report questionnaire that measured demographic factors, behavioural causal beliefs, behavioural knowledge, perceived self-efficacy, and emotional reactions to challenging behaviours. Results Regression analyses revealed that behavioural causal beliefs were a positive predictor, and self-efficacy and behavioural knowledge were negative predictors of negative emotional reactions to challenging behaviours. Staff with formal qualifications also reported more negative emotional reactions. No other demographic factors, emerged as significant predictors. Conclusions The results suggest that behavioural causal beliefs, low self-efficacy and low behavioural knowledge may make staff vulnerable to experiencing negative emotional reactions to challenging behaviours. Researchers and clinicians need to address these issues in staff who work with people with challenging behaviours. C1 Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. RP Hastings, RP (reprint author), Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 CR BERRYMAN J, 1994, J BEHAV THER EXP PSY, V25, P241, DOI 10.1016/0005-7916(94)90024-8 BROMLEY J, 1995, J INTELL DISABIL RES, V39, P341 Chavira V, 2000, J CHILD PSYCHOL PSYC, V41, P245, DOI 10.1017/S0021963099005144 Dagnan D, 1998, BRIT J CLIN PSYCHOL, V37, P59 FURTKAMP E, 1982, J BEHAV THER EXP PSY, V13, P131, DOI 10.1016/0005-7916(82)90054-4 HALL S, 1992, BEHAV PSYCHOTHER, V20, P355 Hastings R. 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PD FEB PY 2002 VL 46 BP 144 EP 150 DI 10.1046/j.1365-2788.2002.00378.x PN 2 PG 7 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 522XA UT WOS:000173921200006 PM 11869385 ER PT J AU Anderson, RJ Bendell, DJ Garnett, I Groundwater, PW Lough, WJ Mills, MJ Savery, D Shattock, PEG AF Anderson, RJ Bendell, DJ Garnett, I Groundwater, PW Lough, WJ Mills, MJ Savery, D Shattock, PEG TI Identification of indolyl-3-acryloylglycine in the urine of people with autism SO JOURNAL OF PHARMACY AND PHARMACOLOGY LA English DT Article AB Autism is a lifelong pervasive developmental disorder that manifests as problems with communication, social skills and imagination. It affects 80000 people in the UK (data from the National Autistic Society, London 1997) and, at present, can only be diagnosed by reference to behavioural and psychological characteristics. For many years there has been interest in the analysis of body fluids from people with autism in the search for unusual correlates which could be used as markers for the disorder, and which would provide evidence for a physiological dysfunction (Panksepp 1979; Gillberg 1988; Adrien et al 1989; Knivsberg et al 1990; Shattock et al 1990). As a result of an ongoing programme in this laboratory, screening the urine from people with autism by high-performance liquid chromatography (HPLC), it was noted that there was a particular peak present in all the chromatograms from the sample population (Mills et al 1998). This peak was often present in greatly increased concentrations, based on peak height and area by HPLC, compared with those found in controls. We have reported the isolation and structural elucidation of this compound. C1 Univ Sunderland, Inst Pharm Chem & Biomed Sci, Sunderland SR1 3SD, England. Univ Sunderland, Sch Sci, Autism Res Unit, Sunderland SR1 3SD, England. RP Anderson, RJ (reprint author), Univ Sunderland, Inst Pharm Chem & Biomed Sci, Sunderland SR1 3SD, England. 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Pharm. Pharmacol. PD FEB PY 2002 VL 54 IS 2 BP 295 EP 298 DI 10.1211/0022357021778349 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 521ME UT WOS:000173843100017 PM 11858215 ER PT J AU Malone, RP Maislin, G Choudhury, MS Gifford, C Delaney, MA AF Malone, RP Maislin, G Choudhury, MS Gifford, C Delaney, MA TI Risperidone treatment in children and adolescents with autism: Short- and long-term safety and effectiveness SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article; Proceedings Paper CT 152nd Annual Meeting of the American-Psychiatric-Association CY MAY 15-20, 1999 CL WASHINGTON, D.C. SP Amer Psychiat Assoc DE neuroleptics; dyskinesia; pervasive developmental disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL SYMPTOMS; INFANTILE-AUTISM; YOUNG-CHILDREN; DOUBLE-BLIND; WEIGHT-GAIN; OPEN-LABEL; HALOPERIDOL; TRIAL; EFFICACY AB Objective: Atypical neuroleptics, including risperidone, are used to treat children with autism, despite limited efficacy and safety data. Many clinicians believe that risperidone will not induce dyskineslas in children. The authors investigated open risperidone treatment in children with autism and included findings on dyskineslas. Method: The sample included 22 outpatients (mean age = 7.1 years) diagnosed with autism (DSM-IV). Treatment consisted of a 1-month short-term phase followed by a 6-month long-term phase. At the end of the long-term phase, drug was discontinued, and the need for further drug treatment and the occurrence of withdrawal dyskinesias were assessed. Measures included the Clinical Global Impressions (CGI), Children's Psychiatric Rating Scale (CPRS), and the Abnormal Involuntary Movement Scale, Results: The mean risperidone dosage was 1.2 mg/day. Overall, the children had significant clinical improvement as assessed by the CPRS and CGI. Untoward effects included sedation, increased appetite, and weight gain. Two of 13 (15.4%) children treated long-term developed mild, reversible withdrawal dyskinesias when risperidone was discontinued. No child developed dyskineslas on risperidone. Conclusions: Risperidone shows promise as a treatment in autism. However, withdrawal dyskinesas were noted. Further assessment of the risk of risperidone-related dyskinesias is indicated. C1 Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA. Temple Univ, Philadelphia, PA 19122 USA. Biomed Stat Consulting, Wynnewood, PA USA. RP Malone, RP (reprint author), Eastern Penn Psychiat Inst, Dept Psychiat, 3200 Henry Ave, Philadelphia, PA 19129 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD FEB PY 2002 VL 41 IS 2 BP 140 EP 147 DI 10.1097/00004583-200202000-00007 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 514PZ UT WOS:000173451400007 PM 11837403 ER PT J AU Noterdaeme, M Amorosa, H AF Noterdaeme, M Amorosa, H TI Early diagnosis of infantile autism SO MONATSSCHRIFT KINDERHEILKUNDE LA German DT Article DE autistic spectrum disorder; early recognition; diagnosis ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM; CHILDREN; ABNORMALITIES; RECOGNITION; AGE AB The diagnostic criteria of infantile autism define the age of onset of the disorder within the first three years of life. Although the symptom constellation around the age of 18 months is quite typical, the formal diagnosis is often delayed over several years. The difficulty of an early diagnosis is partly due to developmental processes in early childhood. The behavioural characteristics of autism can be recognised when typical language skills, play and social skills which are to be expected in normal children do not develop. over time, some autistic behaviours disappear (e.g. eating problems), whereas other characteristical behaviours (e.g. echolalia) emerge. The spectrum of behaviour in autism is extremely wide and partly determined by the cognitive and language development of each individual child. Deficits in processing and sending emotional and social signals belong to the typical problems of children with infantile autism. To make an early diagnosis in one and a half to three years old children, it is often necessary to observe the child carefully over a certain period of time. In addition, extensive parent information is required about the development of the child. An early diagnosis is required to provide these children with appropriate therapeutical interventions. C1 Heckscher Klin, Abt Teilleistungsstroungen & Verhaitensauffalligk, D-81479 Munich, Germany. RP Noterdaeme, M (reprint author), Heckscher Klin, Abt Teilleistungsstroungen & Verhaitensauffalligk, Wolfratshauser Str 350, D-81479 Munich, Germany. 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PD FEB PY 2002 VL 150 IS 2 BP 149 EP + DI 10.1007/s00112-001-0401-z PG 7 WC Pediatrics SC Pediatrics GA 535AL UT WOS:000174621900003 ER PT J AU Simeon, J Milin, R Walker, S AF Simeon, J Milin, R Walker, S TI A retrospective chart review of risperidone use in treatment-resistant children and adolescents with psychiatric disorders SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE children and adolescents; risperidone; treatment resistance ID CHRONIC-SCHIZOPHRENIC PATIENTS; TARDIVE-DYSKINESIA; BIPOLAR DISORDER; AGGRESSIVE-BEHAVIOR; ELDERLY PATIENTS; OPEN-LABEL; MULTICENTER; HALOPERIDOL; OLANZAPINE; EFFICACY AB Antipsychotic drugs are used to treat a wide variety of child psychiatric disorders characterized by psychotic symptoms, aggression, excitement, tics, stereotypies and hyperactivity nonresponsive to other therapies. Unfortunately, typical antipsychotics have many adverse effects limiting their long-term use. Novel antipsychotics with combined dopaminergic and serotonergic action, such as risperidone, appear to offer better safety and efficacy profiles in controlled studies of adult patients, and therefore appeared as promising pharmacotherapeutic agents in child psychiatry. The purpose of this retrospective chart review was to obtain data on the potential effectiveness and tolerability of risperidone in children and adolescents presenting with a variety of chronic and severe psychiatric disorders who had been unresponsive to previous pharmacological treatments. Charts for 106 children and adolescents (males n = 81 or 76.4%; females n = 25 or 23.6%), presenting with attention deficit and/or hyperactivity disorder (n = 49 or 46.2%), conduct disorder (n = 13 or 12.3%), oppositional-defiant disorder (n = 5 or 4.7%), behavioural problems not otherwise specified (n = 2 or 1.9%), autism (n = 8 or 7.5%), Asperger's syndrome (n = 8 or 7.5%), pervasive developmental disorder (PDD) not otherwise specified (n = 4 or 3.8%), anxiety (n = 6 or 5.7%), depression (n = 2 or 1.9%), dysthymia (n = 2 or 1.9%), schizophrenia (n = 4 or 3.8%), adjustment disorder (n = 1 or 0.9%) and obsessive-compulsive disorder (n = 2 or 1.9%) were reviewed retrospectively to determine the tolerability and potential efficacy of risperidone treatment for a variety of psychiatric disorders. Six subjects also presented with mental retardation. The average length of illness prior to risperidone treatment was 5 years and the average age of risperidone treatment onset was 11 years. The mean daily dose of risperidone was 1.2 mg (range = 0.25 to 8.0 mg). Very few adverse effects were reported. The average length of risperidone treatment was 11 months with the majority (n = 75 or 76%) of patients maintained on risperidone following study termination. Seven cases (6.6%) were missing follow-up data. The majority (n = 78 or 74%) of patients were taking concurrent psychiatric medications, most commonly stimulants for the treatment of ADHD. Clinical global improvements for children and adolescents at the final study visit were marked (n = .37 or 34.9%), moderate (n = .40 or 37.7%), mild (n = 13 or 12.4%), none (n = 12 or 11.3%), or worse (n = 1 or 1%). Three cases (2.9%) were missing clinical improvement data. Results suggest that risperidone may be useful for managing behavioural disturbances and psychotic symptoms associated with a wide variety of childhood psychiatric disorders. For most patients in the study, a combination of risperidone and adjunctive pharmacotherapy was beneficial. Controlled and discontinuation studies of risperidone treatment in children and adolescents with behavioural and psychotic disorders are recommended. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Royal Ottawa Hosp, Ottawa, ON K1Z 7K4, Canada. RP Simeon, J (reprint author), Royal Ottawa Hosp, Ottawa, ON K1Z 7K4, Canada. 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Neuro-Psychopharmacol. Biol. Psychiatry PD FEB PY 2002 VL 26 IS 2 BP 267 EP 275 DI 10.1016/S0278-5846(01)00264-0 PG 9 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 507BB UT WOS:000173005700008 PM 11817503 ER PT J AU Page, T Moseley, C AF Page, T Moseley, C TI Metabolic treatment of hyperuricosuric autism SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE autism; hyperuricosuria; metabolic disorders AB A single male subject with hyperuricosuric autism was treated for a period of 2 years with an oral dose of uridine, which increased from 50 to 500 mg/kg/day. This patient experienced dramatic social, cognitive, language, and motor improvements. These improvement decreased within 72 h of the discontinuation of uridine, but reappeared when uridine supplementation was resumed. Thus, it appears that patients with hyperuricosuric autism benefit from metabolic therapy with oral uridine therapy in a manner similar to that seen in other disorders of purine metabolism in which there is autistic symptomatology. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Clin Studies, Arlington, VA 22209 USA. RP Page, T (reprint author), Univ Calif San Diego, Dept Neurosci, 0624,9500 Gilman Dr, La Jolla, CA 92093 USA. 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Neuro-Psychopharmacol. Biol. Psychiatry PD FEB PY 2002 VL 26 IS 2 BP 397 EP 400 DI 10.1016/S0278-5846(01)00249-4 PG 4 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 507BB UT WOS:000173005700027 PM 11817520 ER PT J AU [Anonymous] AF [Anonymous] TI Defining review of autism SO PSYCHOLOGIST LA English DT News Item NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD FEB PY 2002 VL 15 IS 2 BP 52 EP 52 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 524QP UT WOS:000174024600002 ER PT J AU Pablo, MJ Valdizan, JR Carvajal, P Bernal, M Peralta, P de Cabezon, AS AF Pablo, MJ Valdizan, JR Carvajal, P Bernal, M Peralta, P de Cabezon, AS TI Landau-Kleffner syndrome SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autism; epilepsy with continuous spike-wave during slow sleep; Landau-Kleffner syndrome ID SLOW-WAVE SLEEP; ACQUIRED APHASIA; DISORDERS; CHILDREN AB Introduction. The Landau-Kleffner syndrome (SLK) is associated with paroxystic alterations of the electroencephalogram which are intensified during sleep, with acquired aphasia and epilepsy, in 75-83% of the cases, The syndrome is associated with other features, such as personality disorders presenting as autistic behaviour, cognitive regression and in some cases, motor dysfunction. The epileptic activity appears to be responsible for the disorder, Treatment with anti-epileptic drugs is ineffective in many cases, although there may be periods of spontaneous improvement, or there may be permanent sequelas of language. Design, A systematic revision of one case. Case report. A five year old boy with no previous clinical history had, at the age of four years, presented with behaviour changes and aphasia, accompanied by paroxystic changes on the EEG and nocturnal polysomnogram. On cranial CT there was a mid-line cyst. He had had no seizures. Treatment. Treatment with carbamazepine led to clinical improvement in behaviour, reduction in the paroxysms and appearance of sleep spindles, but little effect on the degree of aphasia. Conclusions. The case described is a variant of SLK, with no epileptic seizures, some improvement on carbamazepine and a mid-line cyst. C1 Hosp Miguel Servet, Serv Neurofisiol Clin, E-50009 Zaragoza, Spain. 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Neurologia PD FEB 1 PY 2002 VL 34 IS 3 BP 262 EP 264 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 553UP UT WOS:000175694100014 PM 12022077 ER PT J AU Kissgen, R Schleiffer, R AF Kissgen, R Schleiffer, R TI About the specificity of a theory of mind deficit in autism SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE autism; theory of mind; ADI-R; diagnosis; Down's syndrome ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; DIAGNOSTIC INTERVIEW; PSYCHIATRIC CONTROL; EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; NORMAL-CHILDREN; INDIVIDUALS; INSTRUMENT; BEHAVIOR AB Objectives: In order to test the hypothesis that a theory of mind deficit is specific for autism, the present study presents the first replication of the Sally-Anne test (Baron-Cohen, Leslie & Frith, 1985) in the German-speaking countries. Methods: The Sally-Anne test was administered to 16 autistic, 24 probands with Down's syndrome and 20 normal preschool prosands. The intelligence of the autistic group and that with Down's syndrome was measured by the CPM/SPM. In addition, the ADI-R was used with the principal caregivers of the autistic and Down's syndrome subjects. Results: With regard to the clinical diagnosis, theory of mind deficit turned out to be not specific for autism. Six of 16 (37.5%) autistic subjects passed the theory of mind tasks. Thus performance in the autistic group surpassed that of both control groups. Out of 16 autistic subjects, autism could be confirmed in only 8 on the basis of the ADI-R diagnostic criteria, only one of whom showed a theory of mind. The autistic individuals with a theory of mind differed significantly in their mean IQ from those without this ability. Conclusions: Spectrum and specificity of a theory of mind deficit in autism remain controversial, For further research it seems important to administer the ADI-R during the diagnostic process. 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Kinder-und Jugendpsy. Psychother. PD FEB PY 2002 VL 30 IS 1 BP 29 EP 40 DI 10.1024//1422-4917.30.1.29 PG 12 WC Psychiatry SC Psychiatry GA 519UB UT WOS:000173742900004 PM 11876079 ER PT J AU Niederhofer, H Kucan, S Hackenberg, B Huber, M Gasteiger, W AF Niederhofer, H Kucan, S Hackenberg, B Huber, M Gasteiger, W TI Childhood psychosis versus childhood autism? Differential diagnosis by means of a one week observation in a ward setting SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Editorial Material DE early childhood psychosis; autistic disorder; case report; differential diagnosis ID ONSET SCHIZOPHRENIA; FOLLOW-UP; CHILDREN AB We report on the case of a 4-year-old child suffering for the past six months from a lingering psychotic development. Several months of outpatient observation did not permit a clear differential diagnosis of either childhood autism or an early psychosis. During a one-week inpatient stay at our hospital recurring productive-psychotic episodes were observed that finally led to the exclusion of the diagnosis of "childhood autism" (ICD-10 F 84.0 (Dilling et al., 1993)) and to the diagnosis of "other disintegrative childhood disorder" (ICD-10: F 84.3 (Dilling et al., 1993)). C1 Univ Innsbruck, Psychiat Klin, Abt Kinder & Jugendpsychiat, A-6020 Innsbruck, Austria. RP Niederhofer, H (reprint author), Univ Innsbruck, Psychiat Klin, Abt Kinder & Jugendpsychiat, Anichstr 35, A-6020 Innsbruck, Austria. 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Kinder-und Jugendpsy. Psychother. PD FEB PY 2002 VL 30 IS 1 BP 59 EP 63 DI 10.1024//1422-4917.30.1.59 PG 5 WC Psychiatry SC Psychiatry GA 519UB UT WOS:000173742900007 PM 11876084 ER PT J AU Parker, RA Hartman, EE AF Parker, RA Hartman, EE TI An 8-year-old boy with autism, 1 year later SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article CR Rapin I, 2001, JAMA-J AM MED ASSOC, V285, P1749, DOI 10.1001/jama.285.13.1749 NR 1 TC 0 Z9 0 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 23 PY 2002 VL 287 IS 4 BP 504 EP 504 DI 10.1001/jama.287.4.504 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 513VX UT WOS:000173401900028 PM 11798373 ER PT J AU Gross, M AF Gross, M TI Battling through autism confusion SO CURRENT BIOLOGY LA English DT Editorial Material C1 Univ London, Birkbeck Coll, Sch Crystallog, London, England. RP Gross, M (reprint author), Univ London, Birkbeck Coll, Sch Crystallog, London, England. NR 0 TC 0 Z9 0 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD JAN 22 PY 2002 VL 12 IS 2 BP R42 EP R42 DI 10.1016/S0960-9822(01)00666-2 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 515FV UT WOS:000173485500002 PM 11818072 ER PT J AU Li, J Tabor, HK Nguyen, L Gleason, C Lotspeich, LJ Spiker, D Myers, RM AF Li, J Tabor, HK Nguyen, L Gleason, C Lotspeich, LJ Spiker, D Myers, RM TI Lack of association between HoxA1 and HoxB1 gene variants and autism in 110 multiplex families SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; lack of association; Hox A1 and Hox B1 ID SEROTONIN TRANSPORTER 5-HTT; LINKAGE-DISEQUILIBRIUM; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; MARKERS; SUSCEPTIBILITY; HINDBRAIN; TWIN AB A recent report suggested that the HoxA1 and/or HoxB1 genes play a role in susceptibility to autism. To determine whether these findings could be confirmed, we screened these genes for DNA polymorphisms by sequencing all exons in 24 individuals with autism. We identified the same sequence variants in the genes that appeared in this report, which include one single-base substitution variant in HoxA1 and a common haplotype in HoxB1. We performed an association study by applying the transmission disequilibrium. test to detect possible association of these variants to autism in 110 multiplex families. Our results demonstrated no deviation from the null hypothesis of no association. We have also separately examined transmissions within individual mating types, for paternal versus maternal alleles, to affected versus unaffected children, and for transmission to affected boys versus girls. None of these subsets revealed significant deviation from the null expectation. Our interpretation of these findings is that it is unlikely that HoxA1 and HoxB1 play a significant role in the genetic predisposition to autism. (C) 2001 Wiley-Liss, Inc. C1 Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Myers, RM (reprint author), Stanford Univ, Sch Med, Dept Genet, M344, Stanford, CA 94305 USA. 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J. Med. Genet. PD JAN 8 PY 2002 VL 114 IS 1 SI SI BP 24 EP 30 DI 10.1002/ajmg.1618 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 509EP UT WOS:000173133600004 PM 11840501 ER PT J AU Silverman, JM Smith, CJ Schmeidler, J Hollander, E Lawlor, BA Fitzgerald, M Buxbaum, JD Delaney, K Galvin, P AF Silverman, JM Smith, CJ Schmeidler, J Hollander, E Lawlor, BA Fitzgerald, M Buxbaum, JD Delaney, K Galvin, P CA Autism Genetic Res Excange Consort TI Symptom domains in autism and related conditions: Evidence for familiality SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism spectrum; heterogeneity; genetics; affected sibling pairs; multiplex siblingships; broader affected phenotype; asperger disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HISTORY; INDIVIDUALS; PHENOTYPE; TWIN; PARENTS AB Heterogeneity in autism impairs efforts to localize and identify the genes underlying this disorder. As autism comprises severe but variable deficits and traits in three symptom domains (social interaction, communication, and repetitive behaviors) and shows variability in the presence and emergence of useful phrase speech, different genetic factors may be associated with each. The affected cases (n = 457) in multiply affected siblingships (n = 212), including a proband with autism and one or more siblings with either autism or marked deficits in autism symptom domains, were assessed using the Autism Diagnostic Interview, Revised. Symptom domain scores and language features were examined to determine their similarity within siblingships. The variance within siblingships was reduced for the repetitive behavior domain and for delays in and the presence of useful phrase speech. These features and the nonverbal communication subdomain provided evidence of familiality when we considered only the diagnosis of autism to define multiply affected siblingships (cases: n = 289; siblingships: n = 136). In addition, the same familial features identified also appeared familial for those with autism-related conditions. Finally, the level of severity of almost all of the familial features varied within multiplex siblingships independently. The features identified as familial replicate the combined set suggested in earlier, smaller studies. Furthermore, the familiality of these features extend to related conditions of milder severity than autism and appear to be independent. Making distinctions among families by the severity of these features may be useful for identifying more genetically homogeneous subgroups in studies targeted at genes for specific autism-related symptom domains. (C) 2001 Wiley-Liss, Inc. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Bronx Vet Adm Med Ctr, Psychiat Serv, Bronx, NY USA. St Jamess & St Patricks Hosp, Dept Psychiat Elderly, Dublin, Ireland. Univ Dublin Trinity Coll, Dept Psychiat, Dublin 2, Ireland. RP Silverman, JM (reprint author), Mt Sinai Sch Med, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. CR ABELSON RP, 1985, PSYCHOL BULL, V97, P129, DOI 10.1037/0033-2909.97.1.129 Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAILEY A, 1993, J CHILD PSYCHOL PSYC, V34, P673, DOI 10.1111/j.1469-7610.1993.tb01064.x BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x 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 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Bailey A, 1998, HUM MOL GENET, V7, P571 LANDA R, 1992, PSYCHOL MED, V22, P245 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MacLean JE, 1999, J AM ACAD CHILD PSY, V38, P746, DOI 10.1097/00004583-199906000-00023 PIVEN J, 1994, PSYCHOL MED, V24, P783 Piven J, 1997, AM J PSYCHIAT, V154, P185 RITVO ER, 1989, AM J PSYCHIAT, V146, P1032 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x 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, 1996, AM J MED GENET, V67, P354, DOI 10.1002/(SICI)1096-8628(19960726)67:4<354::AID-AJMG7>3.0.CO;2-M NR 25 TC 80 Z9 82 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 8 PY 2002 VL 114 IS 1 SI SI BP 64 EP 73 DI 10.1002/ajmg.10048 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 509EP UT WOS:000173133600011 PM 11840508 ER PT J AU Beyer, KS Klauck, SM Benner, A Poustka, F Poustkal, A AF Beyer, KS Klauck, SM Benner, A Poustka, F Poustkal, A TI Association studies of the HOPA dodecamer duplication variant in different subtypes of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE infantile autism; TRAP230; TNRC11; splice variant ID MENTAL-RETARDATION; REPETITIVE ELEMENT; GENOMIC SCREEN; X-CHROMOSOME; GENE HOPA; TWIN; OPA; DROSOPHILA; PAIRS; XQ13 AB The HOPA gene in Xq13 is coding for a protein involved in a nuclear thyroid receptor complex. Previous studies suggested association of the dodecamer duplication in the OPA-repeat region in exon 43 (according to the genomic database sequence) with autism, mental retardation, and schizophrenia/hypothyroidism. We determined the frequency of this 12 bp duplication variant in a sample of 155 patients divided in different subtypes of autism, 278 parents of those patients, and 157 control individuals. The allele frequency of the duplication variant was not significantly different between autistic patients, their parents, and the control group. Therefore, it is unlikely that this 12 bp duplication variant of the HOPA gene has major relevance to the susceptibility to different subtypes of autism at least in this German patient sample. In addition, we identified a third variant with a 15 bp deletion in the OPA-repeat region, recently described by another group, in one autistic patient. This third allele was also present in the patient's nonautistic mother and sister, who are heterozygous for this variant, but could not be detected in any other individual genotyped in this study. Expression analysis revealed transcription of all three allelic variants in lymphoblastoid cell lines. Furthermore, we identified a new splice variant that utilizes an additional 9 bp of the 3' intron subsequent to exon 39. Both alternative transcripts are coexpressed in all fetal and adult tissues examined. (C) 2001 Wiley-Liss, Inc. C1 Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, D-69120 Heidelberg, Germany. Deutsch Krebsforschungszentrum, Dept Biostat, D-6900 Heidelberg, Germany. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. RP Poustkal, A (reprint author), Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, Neuenheimer Feld 280, D-69120 Heidelberg, Germany. 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J. Med. Genet. PD JAN 8 PY 2002 VL 114 IS 1 SI SI BP 110 EP 115 DI 10.1002/ajmg.1613 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 509EP UT WOS:000173133600018 PM 11840515 ER PT J AU Sponheim, E Oftedal, G Helverschou, SB AF Sponheim, E Oftedal, G Helverschou, SB TI Multiple doses of secretin in the treatment of autism: a controlled study SO ACTA PAEDIATRICA LA English DT Article DE autism; placebo-controlled; secretin; treatment ID SOCIAL ATTACHMENT; PERSPECTIVES; BEHAVIOR AB Dramatic effects on autistic behaviour after repeated injections of the gastrointestinal hormone secretin have been referred in a number of case reports. In the absence of curative and effective treatments for this disabling condition, this information has created new hope among parents. Although controlled studies on the effect of mainly one single dose have not documented any effect, many children still continue to receive secretin. Six children enrolled in a double-blind, placebo-controlled crossover study in which each child was its own control. Human synthetic secretin, mean dose 3.4 clinical units, and placebo were administered intravenously in randomized order every 4th wk, on three occasions each. The measurement instruments were the visual analogue scale (VAS) and the aberrant behaviour checklist (ABC). Statistically significant differences were found for placebo in 3 out of 6 children and for secretin in one child, using parental ratings only (VAS scores). Differences were small and lacked clinical significance, which was in accordance with the overall impression of the parents and teachers and visual inspection of graphs. Conclusion: In this placebo-controlled study, multiple doses of secretin did not produce any symptomatic improvement. C1 Univ Hosp, Ctr Child & Adolescent Psychiat, Oslo, Norway. Humana Med Ctr, Sandvika, Norway. Haug Sch & Resource Ctr Children Special Needs, Bekkestua, Norway. 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PY 2002 VL 91 IS 5 BP 540 EP 545 DI 10.1080/080352502753711669 PG 6 WC Pediatrics SC Pediatrics GA 556TU UT WOS:000175865700013 PM 12113323 ER PT J AU Johansson, M Billstedt, E Danielsson, S Rastam, M Gillberg, C AF Johansson, M Billstedt, E Danielsson, S Rastam, M Gillberg, C TI Autism spectrum disorder in CHARGE association and Goldenhar syndrome SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Meeting Abstract C1 Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. NR 0 TC 0 Z9 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 2002 VL 105 SU 411 MA 102 BP 36 EP 37 PG 2 WC Psychiatry SC Psychiatry GA 550BX UT WOS:000175484700098 ER PT J AU Alarcon, M Cantor, RM Liu, JJ Gilliam, TC Geschwind, DH AF Alarcon, M Cantor, RM Liu, JJ Gilliam, TC Geschwind, DH CA Autism Genetic Resource Exchange C TI Evidence for a language quantitative trait locus on chromosome 7q in multiplex autism families SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SUSCEPTIBILITY GENES; LINKAGE ANALYSIS; GENOMIC SCREEN; DISORDER; INDIVIDUALS; HISTORY; PARENTS; LOCALIZATION; PHENOTYPE; GENETICS AB Autism is a syndrome characterized by deficits in language and social skills and by repetitive behaviors. We hypothesized that potential quantitative trait loci (QTLs) related to component autism endophenotypes might underlie putative or significant regions of autism linkage. We performed nonparametric multipoint linkage analyses, in 152 families from the Autism Genetic Resource Exchange, focusing on three traits derived from the Autism Diagnostic Interview: "age at first word," "age at first phrase," and a composite measure of "repetitive and stereotyped behavior." Families were genotyped for 335 markers, and multipoint sib pair linkage analyses were conducted. Using nonparametric multipoint linkage analysis, we found the strongest QTL evidence for age at first word on chromosome 7q (nonparametric test statistic [Z] 2.98; P = .001), and subsequent linkage analyses of additional markers and association analyses in the same region supported the initial result (Z = 2.85 P = .002 chi (2) = 18.84, df 8, P = .016). Moreover, the peak fine- mapping result for repetitive behavior (Z = 2.48; P = .007) localized to a region overlapping this language QTL. The putative autism-susceptibility locus on chromosome 7 may be the result of separate QTLs for the language and repetitive or stereotyped behavior deficits that are associated with the disorder. C1 Univ Calif Los Angeles, Dept Neurol, Reed Neurol Res Ctr, Sch Med, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Ctr Neurobehav Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Neuropsychiat Res Inst, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Dept Pediat, Los Angeles, CA 90095 USA. Columbia Univ, Columbia Genome Ctr, New York, NY USA. Columbia Univ, Dept Psychiat, New York, NY USA. Columbia Univ, Dept Genet & Dev, New York, NY USA. RP Geschwind, DH (reprint author), Univ Calif Los Angeles, Dept Neurol, Reed Neurol Res Ctr, Sch Med, 710 Westwood Plaza,1-145, Los Angeles, CA 90095 USA. CR Aita VM, 1999, EXP DERMATOL, V8, P439, DOI 10.1111/j.1600-0625.1999.tb00302.x Alarcon M, 2001, GENET EPIDEMIOL, V21, pS224 ANDERSON MA, 1984, IN VITRO CELL DEV B, V20, P856 Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett S, 1999, AM J MED GENET, V88, P609 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Bradford Y, 2001, AM J MED GENET, V105, P539, DOI 10.1002/ajmg.1497 Bryson SE, 1998, MENT RETARD DEV D R, V4, P97, DOI 10.1002/(SICI)1098-2779(1998)4:2<97::AID-MRDD6>3.0.CO;2-U Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Conover WJ, 1980, PRACTICAL NONPARAMET, V2 Cook EH, 2001, CHILD ADOL PSYCH CL, V10, P333 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 Folstein SE, 2000, AM J HUM GENET, V67, P278, DOI 10.1086/303034 Folstein SE, 1998, J AUTISM DEV DISORD, V28, P439, DOI 10.1023/A:1026008606672 Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 Geschwind DH, 2001, AM J HUM GENET, V69, P463, DOI 10.1086/321292 HASEMAN JK, 1972, BEHAV GENET, V2, P3, DOI 10.1007/BF01066731 Horvath S, 2001, EUR J HUM GENET, V9, P301, DOI 10.1038/sj.ejhg.5200625 Bailey A, 1998, HUM MOL GENET, V7, P571 Palferman S, 2001, AM J HUM GENET, V69, P570 Kruglyak L, 1996, AM J HUM GENET, V58, P1347 KRUGLYAK L, 1995, AM J HUM GENET, V57, P439 Lai CSL, 2000, AM J HUM GENET, V67, P357, DOI 10.1086/303011 Lake SL, 2000, AM J HUM GENET, V67, P1515, DOI 10.1086/316895 Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 LANDA R, 1991, J SPEECH HEAR RES, V34, P1339 LANDA R, 1992, PSYCHOL MED, V22, P245 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Liu JJ, 2001, AM J HUM GENET, V69, P327, DOI 10.1086/321980 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2001, AM J MED GENET, V105, P36, DOI 10.1002/1096-8628(20010108)105:1<36::AID-AJMG1053>3.0.CO;2-4 Maestrini E, 2000, NEURON, V28, P19, DOI 10.1016/S0896-6273(00)00081-7 O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 PICKLES A, 1995, AM J HUM GENET, V57, P717 PIVEN J, 1994, PSYCHOL MED, V24, P783 Piven J, 1997, AM J PSYCHIAT, V154, P185 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 SMALLEY SL, 1995, AM J MED GENET, V60, P19, DOI 10.1002/ajmg.1320600105 Stoltenberg SF, 2000, HUM MOL GENET, V9, P927, DOI 10.1093/hmg/9.6.927 Warburton P, 2000, AM J MED GENET, V96, P228, DOI 10.1002/(SICI)1096-8628(20000403)96:2<228::AID-AJMG20>3.0.CO;2-G NR 43 TC 180 Z9 185 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JAN PY 2002 VL 70 IS 1 BP 60 EP 71 DI 10.1086/338241 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 499LD UT WOS:000172571900007 PM 11741194 ER PT J AU Dunn, W Myles, BS Orr, S AF Dunn, W Myles, BS Orr, S TI Sensory processing issues associated with Asperger syndrome: a preliminary investigation SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE low thresholds; sensory seeking; sensory sensitivity ID YOUNG-CHILDREN; OCCUPATIONAL-THERAPY; AUTISM; DISORDERS AB OBJECTIVE. The purpose of this study was to identify the sensory processing patterns of children with Asperger syndrome. METHOD. Researchers compared the performance of 42 children with Asperger syndrome and 42 children without disabilities on section and factor scores of the Sensory Profile. RESULTS. As reported by parents on the Sensory Profile, the children with Asperger syndrome were significantly different from children without disabilities on 22 of 23 items. This result was obtained with good power estimates (.997-1.00) and large effect sizes (O2 =.267-.732). Both groups of children performed the same on modulation of visual input affecting emotional responses and activity level. CONCLUSION. This study provides initial evidence that clear differences exist in the sensory processing patterns of children with Asperger syndrome when compared with peers without disabilities. C1 Univ Kansas, Dept Occupat Therapy Educ, Kansas City, KS 66160 USA. Univ Kansas, Dept Special Educ, Kansas City, KS USA. United Methodist Church Resurrect, Leawood, KS USA. RP Dunn, W (reprint author), Univ Kansas, Dept Occupat Therapy Educ, 3033 Robinson,3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON E, 1996, UNLOCKING MYSTERIES Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Attwood T, 1998, ASPERGERS SYNDROME Ayres A. 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During the past 15 years considerable effort has been expended in trying to establish the genetic loci associated with susceptibility to these and other mental disorders using principally linkage analysis. Despite this, only a handful of specific genes have been identified, and it is now generally recognized that further advances along these lines will require the analysis of literally hundreds of affected individuals and their families. Fortunately, the emergence in the past three years of a number of new approaches and more effective tools has given new hope to those engaged in the search for the underlying genetic and environmental factors involved in causing these illnesses, which collectively are among the most serious in all societies. Chief among these new tools is the availability of the entire human genome sequence and the prospect that within the next several years the entire complement of human genes will be known and the functions of most of their protein products elucidated. In the meantime the search for susceptibility loci is being facilitated by the availability of single nucleotide polymorphisms (SNPs) and by the beginning of haplotype mapping, which tracks the distribution of clusters of SNPs that segregate as a group. Together with high throughput DNA sequencing, microarrays for whole genome scanning, advances in proteomics, and the development of more sophisticated computer programs for analyzing sequence and association data, these advances hold promise of greatly accelerating the search for the genetic basis of most mental illnesses while, at the same time, providing molecular targets for the development of new and more effective therapies. C1 NIMH, Bethesda, MD 20892 USA. 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Rev. Neurosci. PY 2002 VL 25 BP 1 EP 50 DI 10.1146/annurev.neuro.25.112701.142853 PG 50 WC Neurosciences SC Neurosciences & Neurology GA 582MK UT WOS:000177354800001 PM 12052903 ER PT J AU Rourke, BP Ahmad, SA Collins, DW Hayman-Abello, BA Hayman-Abello, SE Warriner, EM AF Rourke, BP Ahmad, SA Collins, DW Hayman-Abello, BA Hayman-Abello, SE Warriner, EM TI Child clinical/pediatric neuropsychology: Some recent advances SO ANNUAL REVIEW OF PSYCHOLOGY LA English DT Review DE pediatric neurology; childhood disorders; nonverbal learning disabilities; developmental disabilities ID HIGH-FUNCTIONING AUTISM; NONVERBAL LEARNING-DISABILITIES; SEX-CHROMOSOME ABNORMALITIES; ULLRICH-TURNER-SYNDROME; TRAUMATIC BRAIN INJURY; SCHOOL-AGE-CHILDREN; ASPERGER-SYNDROME; TOURETTES-SYNDROME; WILLIAMS-SYNDROME; HEAD-INJURY AB The neuropsychological assets and deficits of several types of pediatric neurological disease, disorder, and dysfunction are described. These are examined from the perspective of the syndrome of nonverbal learning disabilities (NLD) and the "white matter model" designed to explain its complex manifestations. It is concluded that children with some of these diseases exhibit the NLD phenotype, whereas others do not. For the most part, the diseases in which the NLD phenotype is particularly evident are those wherein it has been demonstrated that perturbations of white matter (long myelinated fibers) are particularly prominent. C1 Univ Windsor, Dept Psychol, Windsor, ON N9B 3P4, Canada. Yale Univ, Ctr Child Study, New Haven, CT 06510 USA. RP Rourke, BP (reprint author), Univ Windsor, Dept Psychol, Windsor, ON N9B 3P4, Canada. 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RP Rosenwasser, B (reprint author), Temple Univ, Philadelphia, PA 19122 USA. CR Bondy A, 2001, BEHAV MODIF, V25, P725, DOI 10.1177/0145445501255004 Department of Health & Human Services Office of the Surgeon General, 1999, MENT HLTH REP SURG G HARROWER JK, 2001, BEHAV MODIF, V25, P725 JACOBSON JW, 2000, BEHAV ANAL TODAY, V1, P6 Koegel LK, 2001, BEHAV MODIF, V25, P745, DOI 10.1177/0145445501255005 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 Pelios LV, 2001, BEHAV MODIF, V25, P678, DOI 10.1177/0145445501255002 Skinner B. F., 1957, VERBAL BEHAV Sundberg ML, 2001, BEHAV MODIF, V25, P698, DOI 10.1177/0145445501255003 WEHMAN P, 1992, EDUC TRAIN MENT RET, V27, P112 Weiss MJ, 2001, BEHAV MODIF, V25, P785, DOI 10.1177/0145445501255007 NR 12 TC 5 Z9 5 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD JAN PY 2002 VL 26 IS 1 BP 3 EP 8 DI 10.1177/0145445502026001001 PG 6 WC Psychology, Clinical SC Psychology GA 500QQ UT WOS:000172638600001 PM 11799653 ER PT J AU McClannahan, LE MacDuff, GS Krantz, PJ AF McClannahan, LE MacDuff, GS Krantz, PJ TI Behavior analysis and intervention for adults with autism SO BEHAVIOR MODIFICATION LA English DT Article ID SCRIPT-FADING PROCEDURE; SOCIAL-INTERACTION SKILLS; TEACHING-CHILDREN; PICTURE PROMPTS; ADOLESCENTS; TASKS AB This article describes a behavioral intervention program for adults with autism, suggests that preparation for adulthood should begin in early childhood, asserts that the curriculum should be just as comprehensive and evaluation criteria just as rigorous in programs for adults as in programs for children, and proposes that close examination of adults' repertoires may lead to key modifications of services; delivered to children. Along the way, the authors provide some data on the progress of 15 people who are now adults and whom they have known for 15 to 25 years. Finally, the authors argue that, because of the diversity of skills and skill deficits displayed by adults with autism, a program model that prevents "falling through the cracks" must provide an array of options-from training center to supported employment. C1 Princeton Child Dev Inst, Princeton, NJ USA. RP McClannahan, LE (reprint author), Princeton Child Dev Inst, Princeton, NJ USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bell G., 1988, P1 COOPER JO, 1987, APPL BEHAV ANAL, P298 Dunn L. 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B., 1983, AUTISM ADOLESCENTS A, P37 Smith M, 1995, GUIDE SUCCESSFUL EMP SPARROWS S, 1984, VINELAND ADAPTIVE BE Stevenson CL, 2000, BEHAV INTERVENT, V15, P1, DOI 10.1002/(SICI)1099-078X(200001/03)15:1<1::AID-BIN41>3.0.CO;2-V STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 TAYLOR WA, 1995, TOTAL QUAL MANAGE, V6, P3 WACKER DP, 1984, ANAL INTERVEN DEVEL, V4, P353, DOI 10.1016/0270-4684(84)90024-7 WACKER DP, 1983, J APPL BEHAV ANAL, V16, P417, DOI 10.1901/jaba.1983.16-417 NR 22 TC 16 Z9 16 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD JAN PY 2002 VL 26 IS 1 BP 9 EP 26 DI 10.1177/0145445502026001002 PG 18 WC Psychology, Clinical SC Psychology GA 500QQ UT WOS:000172638600002 PM 11799656 ER PT J AU Shook, GL Ala'i-Rosales, S Glenn, SS AF Shook, GL Ala'i-Rosales, S Glenn, SS TI Training and certifying behavior analysts SO BEHAVIOR MODIFICATION LA English DT Article ID AUTISTIC-CHILDREN; EARLY INTERVENTION; LANGUAGE; CONSULTATION; EDUCATION; COMMUNITY; PARENTS AB Proper professional certification and training of behavior analysts who work with individuals with autism is critical in ensuring that those individuals receive the highest quality behavior analytic services. This article discusses the current issues surrounding certification of behavior analysts and describes the important features of the Behavior Analyst Certification Board and its credentials. 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PD JAN PY 2002 VL 26 IS 1 BP 27 EP 48 DI 10.1177/0145445502026001003 PG 22 WC Psychology, Clinical SC Psychology GA 500QQ UT WOS:000172638600003 PM 11799652 ER PT J AU Eikeseth, S Smith, T Jahr, E Eldevik, S AF Eikeseth, S Smith, T Jahr, E Eldevik, S TI Intensive behavioral treatment at school for 4-to 7-year-old children with autism - A 1-year comparison controlled study SO BEHAVIOR MODIFICATION LA English DT Article ID YOUNG-CHILDREN; INTERVENTION; AGE AB This study was designed to evaluate I year of intensive treatment for 4- to 7-year-old children with autism. An independent clinician assigned children to either behavioral treatment (n = 13) or eclectic treatment (n = 12). Assignment was based on availability of personnel to supervise treatment and was not influenced by child characteristics or family preference. The two treatment groups received similar amounts of treatment (M = 28.52 hours per week at the child's school). Children in the behavioral treatment group made significantly larger gains on standardized tests than did children in the eclectic treatment group. Results suggest that some 4- to 7-year-olds may make large gains with intensive behavioral treatment, that such treatment can be successfully implemented in school settings, and that specific aspects of behavioral treatment (not just its intensity) may account for favorable outcomes. C1 Univ Rochester, Sch Med & Dent, Rochester, NY 14627 USA. CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Ayres A. J., 1972, SENSORY INTEGRATION Bayley N, 1993, BAYLEY SCALES INFANT Bimbrauer J. 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Modificat. PD JAN PY 2002 VL 26 IS 1 BP 49 EP 68 DI 10.1177/0145445502026001004 PG 20 WC Psychology, Clinical SC Psychology GA 500QQ UT WOS:000172638600004 PM 11799654 ER PT J AU Green, G Brennan, LC Fein, D AF Green, G Brennan, LC Fein, D TI Intensive behavioral treatment for a toddler at high risk for autism SO BEHAVIOR MODIFICATION LA English DT Article ID EARLY INTERVENTION; YOUNG-CHILDREN; JOINT ATTENTION; DISORDERS AB Intensive, comprehensive treatment using a variety of applied behavior analysis methods was provided to a toddler who was determined to be at high risk for autism at the age of about I year. Initially, treatment was delivered in a one-to-one adult-child format in the child's home and other settings, with gradual transitions to group instruction in early intervention and preschool classrooms. Intensive treatment continued for 3 years; by the 4th year, the child was spending most of her time in a regular preschool classroom, with minimal ongoing one-to-one instruction. Direct observational data and results of norm-referenced tests documented large increases in language, social, cognitive, and daily living skills over the course of treatment. After 4 years, the child demonstrated no behavioral or developmental abnormalities, performed above her chronological age level on norm-referenced tests of cognitive and language skills, and was functioning as a typical child in a regular public school kindergarten classroom. C1 Univ Massachusetts, Amherst, MA 01003 USA. Univ Connecticut, Storrs, CT 06269 USA. RP Green, G (reprint author), Inst Effect Educ, 2255 Camino Rio S, San Diego, CA 92108 USA. CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Anderson SR, 1999, J ASSOC PERS SEVERE, V24, P162, DOI 10.2511/rpsd.24.3.162 Bimbrauer J. 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PD JAN PY 2002 VL 26 IS 1 BP 69 EP 102 DI 10.1177/0145445502026001005 PG 34 WC Psychology, Clinical SC Psychology GA 500QQ UT WOS:000172638600005 PM 11799655 ER PT J AU Dudley, LL Johnson, C Barnes, RS AF Dudley, LL Johnson, C Barnes, RS TI Decreasing rumination using a starchy food satiation procedure SO BEHAVIORAL INTERVENTIONS LA English DT Article ID QUANTITY; BEHAVIOR AB A starchy food satiation procedure was evaluated in an ABAB withdrawal design on the post-meal rumination of a nine-year-old girt with autism. During treatment unlimited quantities of starchy foods were provided following each meal. High rates of rumination occurred during baseline conditions, followed by an immediate decrease in rumination during treatment. Rumination decreased to 82 and 97% of baseline during the first and second treatment conditions, respectively. In addition, follow-up probes were conducted at irregular intervals for 4 years following treatment, during which zero or near-zero rates of rumination were sustained. This study extends the literature on the functional relation between increased starchy food quantity and rumination in adults to rumination With a young child, and demonstrates maintenance of the treatment effect for 4 years. Copyright (C) 2002 John Wiley Sons, Ltd. C1 New England Ctr Children, Southborough, MA 01772 USA. Northeastern Univ, Boston, MA 02115 USA. RP Dudley, LL (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. CR Barton L. 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In one condition, teachers chose the reinforcers to be used and the order in which programs were conducted. In a second condition, students chose the order of programs and the reinforcers to be used. Speed of skill acquisition and the presence of competing behavior such as tantrums, aggression, escape attempts or idiosyncratic noncompliance responses were measured. Speed of skill acquisition did not differ between the two conditions, but competing behavior was markedly reduced during student choice conditions. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Assoc Manhattan Autist Children, New York, NY 10011 USA. CUNY Grad Sch & Univ Ctr, New York, NY 10036 USA. RP Newman, B (reprint author), Assoc Manhattan Autist Children, 25 W 17th St, New York, NY 10011 USA. 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PD JAN-MAR PY 2002 VL 17 IS 1 BP 31 EP 41 DI 10.1002/bin.99 PG 11 WC Psychology, Clinical SC Psychology GA 526VD UT WOS:000174149600004 ER PT J AU Gal, E Dyck, M Passmore, A AF Gal, E Dyck, M Passmore, A TI Sensory differences and stereotyped movements in children with autism SO BEHAVIOUR CHANGE LA English DT Article ID RHYTHMICAL STEREOTYPIES; INFANTILE-AUTISM; STIMULATION; BEHAVIOR AB This study was designed to test whether there is a functional relationship between sensory stimulation and stereotyped movements (SM). Four children with autism and intellectual disability (according to DSM-IV criteria) who showed stereotyped movements were studied. The Short Sensory Profile was used to define whether a child perceived stimulation within each sensory modality as aversive, attractive, or neutral. The Stereotyped and Self-Injurious Movements Interview was used to identify each child's repetitive movements. Children were then exposed to sensory stimuli that were neutral, aversive or attractive. Results indicate that children: (a) initiate or increase stereotyped movements immediately following the onset of an aversive stimulus, (b) terminate or decrease stereotyped movements following the onset of an attractive stimulus and (c) initiate or increase stereotyped movements during periods of neutral stimulation. We conclude that stereotyped movements are functionally related to sensory stimulation; individuals who frequently engage in stereotyped movements may do so in order to cope with under-stimulation and aversive over-stimulation. C1 Curtin Univ Technol, Sch Psychol, Perth, WA 6845, Australia. RP Dyck, M (reprint author), Curtin Univ Technol, Sch Psychol, GPO Box U11987, Perth, WA 6845, Australia. 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W., 1958, COLLECTED PAPERS PAE Young LJ, 1997, HORM BEHAV, V31, P221, DOI 10.1006/hbeh.1997.1377 NR 96 TC 75 Z9 82 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 JAN 1 PY 2002 VL 51 IS 1 BP 27 EP 43 DI 10.1016/S0006-3223(01)01277-X PG 17 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 512NG UT WOS:000173330000005 PM 11801229 ER PT J AU Andres, C AF Andres, C TI Molecular genetics and animal models in autistic disorder SO BRAIN RESEARCH BULLETIN LA English DT Review DE autistic disorder; developmental behavioural disorder; molecular genetics; linkage; association; animal models ID SEROTONIN TRANSPORTER GENE; PRADER-WILLI-SYNDROME; FRAGILE-X-SYNDROME; LINKAGE-DISEQUILIBRIUM; INFANTILE-AUTISM; ANGELMAN-SYNDROME; MOUSE MODEL; SUSCEPTIBILITY GENES; TUBEROUS SCLEROSIS; SPECTRUM DISORDERS AB Autistic disorder is a behavioural syndrome beginning before the age of 3 years and lasting over the whole lifetime. It is characterised by impaired communication, impaired social interactions, and repetitive interests and behaviour. The prevalence is about 7/10,000 taking a restrictive definition and more than 1/500 with a broader definition, including all the pervasive developmental disorders. The importance of genetic factors has been highlighted by epidemiological studies showing that autistic disorder is one of the most genetic neuropsychiatric diseases. The relative risk of first relatives is about 100-fold higher than the risk in the normal population and the concordance in monozygotic twin is about 60%. Different strategies have been applied on the track of susceptibility genes. The systematic search of linked loci led to contradictory results, in part due to the heterogeneity of the clinical definitions, to the differences in the DNA markers, and to the different methods of analysis used. An oversimplification of the inferred model is probably also cause of our disappointment. More work is necessary to give a clearer picture. One region emerges more frequently: the long arm of chromosome 7. Several candidate genes have been studied and some gave indications of association: the Reelin gene and the Wnt2 gene. Cytogenetical abnormalities are frequent at 15q11-13, the region of the Angelman and Prader-Willi syndrome. Imprinting plays an important role in this region, no candidate gene has been identified in autism. Biochemical abnormalities have been found in the serotonin system. Association and linkage studies gave no consistent results with some serotonin receptors and in the transporter, although it seems interesting to go further in the biochemical characterisation of the serotonin transporter activity, particularly in platelets, easily accessible. Two monogenic diseases have been associated with autistic disorder: tuberous sclerosis and fragile X. A better knowledge of the pathophysiology of these disorders can help to understand autism. Different other candidate genes have been tested, positive results await replications in other samples. Animal models have been developed, generally by knocking out the different candidate genes. Behaviour studies have mainly focused on anxiety and learning paradigms. Another group of models results from surgical or toxic lesions of candidate regions in the brain, in general during development. The tools to analyse these animals are not yet standardised, and an important effort needs to be undertaken. (C) 2002 Elsevier Science Inc. C1 INSERM, U316, F-37044 Tours, France. RP Andres, C (reprint author), INSERM, U316, 2 Bis Blvd Tonnelle, F-37044 Tours, France. 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Bull. PD JAN 1 PY 2002 VL 57 IS 1 BP 109 EP 119 DI 10.1016/S0361-9230(01)00642-6 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 520YM UT WOS:000173811400014 PM 11827743 ER PT J AU Raheja, S Libretto, SE Singh, I AF Raheja, S Libretto, SE Singh, I TI Successful use of risperidone in an adult with the pervasive developmental disorder, Asperger's syndrome: A case report SO BRITISH JOURNAL OF DEVELOPMENTAL DISABILITIES LA English DT Article ID 5-HYDROXYINDOLEACETIC ACID; HOMOVANILLIC-ACID; DOUBLE-BLIND; AUTISM; CHILDREN; TOLERABILITY; ADOLESCENTS; SEROTONIN; DOPAMINE C1 Janssen Cilag Ltd, High Wycombe HP14 4HJ, Bucks, England. Eric Shepherd Unit, Abbots Langley WD5 0HT, Herts, England. Hillingdon Hosp, Mental Hlth Unit, Uxbridge UB8 3NN, Middx, England. RP Libretto, SE (reprint author), Janssen Cilag Ltd, POB 79, High Wycombe HP14 4HJ, Bucks, England. CR ANDERSON GM, 1987, MED BIOL, V65, P67 ANDERSON GM, 1987, J CHILD PSYCHOL PSYC, V28, P885, DOI 10.1111/j.1469-7610.1987.tb00677.x BARTHELEMY C, 1988, J AUTISM DEV DISORD, V18, P583, DOI 10.1007/BF02211876 CHOUINARD G, 1993, J CLIN PSYCHOPHARM, V13, P25 COHEN DJ, 1977, ARCH GEN PSYCHIAT, V34, P545 COHEN DJ, 1974, ARCH GEN PSYCHIAT, V3, P845 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Fisman S, 1996, J CHILD ADOL PSYCHOP, V6, P177, DOI 10.1089/cap.1996.6.177 Hardan A, 1996, J AM ACAD CHILD PSY, V35, P1551, DOI 10.1097/00004583-199611000-00025 JANSSEN PAJ, 1988, J PHARMACOL EXP THER, V244, P685 McCartney KN, 1999, ADV THER, V16, P158 McDougle CJ, 1995, J CHILD ADOL PSYCHOP, V5, P273, DOI 10.1089/cap.1995.5.273 MCDOUGLE CJ, 1995, AM J PSYCHIAT, V152, P722 McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 McDougle CJ, 1997, J AM ACAD CHILD PSY, V36, P685, DOI 10.1097/00004583-199705000-00020 MINDERAA RB, 1989, J AM ACAD CHILD PSY, V28, P190, DOI 10.1097/00004583-198903000-00007 MOLLER HJ, 1991, PHARMACOPSYCHIATRY, V24, P185, DOI 10.1055/s-2007-1014467 NARAYAN M, 1993, BIOL PSYCHIAT, V33, P630, DOI 10.1016/0006-3223(93)90102-J OWENS DGC, 1994, J CLIN PSYCHIAT, V55, P29 PURDON SE, 1994, CAN J PSYCHIAT, V39, P400 SABARATNAM M, 1995, J DRUG DEV CLIN P CH, V2, P7 VANDENBORRE R, 1993, ACTA PSYCHIAT SCAND, V87, P167 *WHO, 1992, ICD 10 CLASS MENT BE, P252 YOUNG JG, 1982, J AUTISM DEV DISORD, V12, P147, DOI 10.1007/BF01531305 NR 24 TC 6 Z9 6 PU BRITISH SOC DEVELOPMENTAL DISABILITIES PI STRATFORD-UPON-AVON PA C/O SEFA PUBL LTD, 4 GREAT WILLIAM ST, STRATFORD-UPON-AVON CV37 6RY, WARWICK, ENGLAND SN 0969-7950 J9 BRIT J DEV DISABIL JI Br. J. Dev. Disabil. PD JAN PY 2002 VL 48 IS 94 BP 61 EP 66 PN 1 PG 6 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 518JM UT WOS:000173664300006 ER PT J AU Hogenboom, M AF Hogenboom, M TI Diet intervention and autism - Implementing the gluten free diet and casein free diet for autistic children and adults: A practical guide for parents SO BRITISH JOURNAL OF DEVELOPMENTAL DISABILITIES LA English DT Book Review CR LEBRETON M, 2001, DIET INTERVENTION AU NR 1 TC 0 Z9 0 PU BRITISH SOC DEVELOPMENTAL DISABILITIES PI STRATFORD-UPON-AVON PA C/O SEFA PUBL LTD, 4 GREAT WILLIAM ST, STRATFORD-UPON-AVON CV37 6RY, WARWICK, ENGLAND SN 0969-7950 J9 BRIT J DEV DISABIL JI Br. J. Dev. Disabil. PD JAN PY 2002 VL 48 IS 94 BP 71 EP 72 PN 1 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 518JM UT WOS:000173664300009 ER PT J AU Hrdlicka, M Kulisek, R Propper, L Lisy, J Belsan, T Neuwirth, J Komarek, V Blatny, M Urbanek, T AF Hrdlicka, M Kulisek, R Propper, L Lisy, J Belsan, T Neuwirth, J Komarek, V Blatny, M Urbanek, T TI Child autism and other pervasive disorders: The relation of autistic psychopathology to selected brain structures SO CESKOSLOVENSKA PSYCHOLOGIE LA Czech DT Article DE child autism; pervasive developmental disorders; magnetic brain resonance; CARS observation scale; ADI-R questionnaire ID CORPUS-CALLOSUM; DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS; MRI; INDIVIDUALS; HIPPOCAMPUS AB The goal of the study was to examine the relation of basic symptoms of autism to selected brain structures. The studied sample consisted of 77 autistic patients (61 boys, 16 girls) aged 9.1 +/- 5.3 years. The children were investigated by CARS observation scale, ADI-R structured interview, intelligence test, and structural MRI (1.5 Tesla). In MRI depict, both qualitative part (raw pathology), and quantitative part (planimetric measurement of brain-cortex width, the size of corpus callosum, amygdala, hippocampus, and nucleus caudatus) were assessed. 55 patients of the sample (79.7%) were mentally retarded. The sum CARS score was 37.3 +/- 6.7 and did not correlate significantly with any dimension in MRI pictures. Some subtests of ADI-R questionnaire correlated significantly with size of corpus callosum, amygdala, hippocampus, and nucleus caudatus. The results support the considerations about the participation of nucleus caudatus, hippocampus, corpus callosum, and amygdala in the pathogenesis of child autism. C1 UK, Detska Psychiat Klin, LF FN Motol 2, Prague 15006 5, Czech Republic. UK, Klin Zobrazovacich Metod, LF FN Motol 2, Prague 15006 5, Czech Republic. UK, Klin Detske Neurol, LF FN Motol 2, Prague 15006 5, Czech Republic. AV CR, Psychol Ustav, Brno, Czech Republic. RP Hrdlicka, M (reprint author), UK, Detska Psychiat Klin, LF FN Motol 2, V Uvalu 84, Prague 15006 5, Czech Republic. RI Urbanek, Tomas/G-9427-2014; Blatny, Marek/H-4293-2014 OI Urbanek, Tomas/0000-0002-8807-4869; Blatny, Marek/0000-0001-9831-0637 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 Aylward EH, 1999, NEUROLOGY, V53, P2145 Eliez S, 2000, J CHILD PSYCHOL PSYC, V41, P679, DOI 10.1017/S0021963099006095 GAFFNEY GR, 1987, BRIT J PSYCHIAT, V151, P831, DOI 10.1192/bjp.151.6.831 Hardan AY, 2000, NEUROLOGY, V55, P1033 Hendren RL, 2000, J AM ACAD CHILD PSY, V39, P815, DOI 10.1097/00004583-200007000-00010 HRDLICKA M, 2001, TRENDY MED, V3, P31 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Manes F, 1999, J NEUROPSYCH CLIN N, V11, P470 Pierce K, 2001, BIOL PSYCHIAT, V49, P655, DOI 10.1016/S0006-3223(00)01008-8 Piven J, 1997, AM J PSYCHIAT, V154, P1051 Piven J, 1998, J AUTISM DEV DISORD, V28, P105, DOI 10.1023/A:1026084430649 PROPPER L, 2001, CESK SLOV PSYCHIAT, V97, P269 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Sears LL, 1999, PROG NEURO-PSYCHOPH, V23, P613, DOI 10.1016/S0278-5846(99)00020-2 Shevell MI, 2001, J CHILD NEUROL, V16, P509, DOI 10.1177/088307380101600710 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 Volkmar F. R., 1998, AUTISM PERVASIVE DEV 1992, MEZINARODNI KLASIFIK NR 19 TC 4 Z9 4 PU ACADEMIA PI PRAGUE 1 PA PUBL HOUSE CZECH ACAD SCI VODICKOVA 40, PRAGUE 1 112 29, CZECH REPUBLIC SN 0009-062X J9 CESK PSYCHOL JI Cesk. Psychol. PY 2002 VL 46 IS 4 BP 289 EP 298 PG 10 WC Psychology, Multidisciplinary SC Psychology GA 607ZH UT WOS:000178820300001 ER PT J AU Solnit, AJ AF Solnit, AJ TI A child psychiatry chairman's view SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article AB The Yale Child Study Center at Yale University School of Medicine is a model of how the responsibilities and opportunities of an independent department of child psychiatry can be meshed. An independent academic department can sustain the momentum of multidisciplinary research, clinical services, and training associated with advances in the field of child psychiatry. These advances include the systematic description and evaluation of healthy child development; model clinical services in the community, schools, and hospital; and in-depth understanding of autism, Tourette's syndrome, and obsessive-compulsive disorders. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. RP Solnit, AJ (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06510 USA. CR GESELL A, 1952, HIST PSYCHOL AUTOBIO, P123, DOI 10.1037/11154-006 *GOV BLUE RIBB COM, 2000, EX SUMM, P5 Joint Commission on the Mental Health of Children, 1970, CRIS CHILD MENT HLTH KANDEL ER, 1979, NEW ENGL J MED, V301, P1028, DOI 10.1056/NEJM197911083011904 Kandel ER, 1998, AM J PSYCHIAT, V155, P457 PROVENCE S, 1963, MODERN PERSPECTIVES, pR18 SOLNIT AJ, 1966, J AMER ACAD CHILD PS, V5, P1, DOI 10.1016/S0002-7138(09)62032-X SOLNIT AJ, 1988, J AM ACAD CHILD PSY, V27, P658, DOI 10.1097/00004583-198809000-00026 SWIFT WJ, 2001, AACAP NEWS, V32, P116 NR 9 TC 0 Z9 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD JAN PY 2002 VL 11 IS 1 BP 91 EP + DI 10.1016/S1056-4993(03)00062-2 PG 13 WC Psychiatry SC Psychiatry GA 510MW UT WOS:000173212700007 PM 11793574 ER PT J AU Bartolo, PA AF Bartolo, PA TI Communicating a diagnosis of developmental disability to parents: multiprofessional negotiation frameworks SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE diagnosis; labelling; developmental delay; autism; communication; professionals; parents ID CHILDREN; AUTISM AB It is a hard task for professionals to give and parents to receive the bad news about a child's developmental disability. This study describes how findings about four preschool children, with difficulties suspected to lie within the autistic spectrum, were negotiated with parents by two multiprofessional groups, one in a Medical (Site M) and one in an Education setting (Site E). Each assessment was undertaken over half a day, the professionals jointly interacting with the child and family. All assessment discussions were audiotaped and each participant was interviewed after the assessment. Conversation analysis showed the activation of three major social-interaction frameworks: professionals at both sites applied a parent-friendly frame, but this was complemented by a hopeful-diagnostic-formulation frame at Site M, and a defocusing-of-bad-news frame at Site E. C1 Univ Malta, Dept Psychol, Msida, Malta. RP Bartolo, PA (reprint author), Univ Malta, Dept Psychol, Msida, Malta. CR Abrams EZ, 1998, J PEDIATR PSYCHOL, V23, P87, DOI 10.1093/jpepsy/23.2.87 ARONSSON K, 1995, REPRESENTATIONS HLTH, P131 Bartolo PA, 2001, J SCHOOL PSYCHOL, V39, P499, DOI 10.1016/S0022-4405(01)00086-3 BRYANS T, 1993, ASSESSING SPECIAL ED, P17 Buckman R, 1992, BREAK BAD NEWS GUIDE Cohen D. J, 1997, HDB AUTISM PERVASIVE COTTRELL DJ, 1990, CHILD CARE HLTH DEV, V16, P211, DOI 10.1111/j.1365-2214.1990.tb00655.x CUNNINGHAM CC, 1984, DEV MED CHILD NEUROL, V26, P33 DALE M, 1996, WORKING FAMILIES CHI Freeman BJ, 1997, J AUTISM DEV DISORD, V27, P641, DOI 10.1023/A:1025850715183 GILL VT, 1995, SOC PROBL, V42, P11, DOI 10.1525/sp.1995.42.1.03x0453k Hutchby I., 1998, CONVERSATION ANAL Johnson D. W, 1997, JOINING TOGETHER GRO Marcus L. M., 1997, HDB AUTISM PERVASIVE, P631 Maynard D. W., 1991, TALK SOCIAL STRUCTUR, P164 QUINE L, 1994, J CHILD PSYCHOL PSYC, V35, P1273, DOI 10.1111/j.1469-7610.1994.tb01234.x Shea V, 1993, PRESCHOOL ISSUES AUT, P185 Siegel B., 1997, HDB AUTISM PERVASIVE, P745 SMITH B, 1994, J AUTISM DEV DISORD, V24, P551, DOI 10.1007/BF02172137 TANNEN D, 1987, SOC PSYCHOL QUART, V50, P205, DOI 10.2307/2786752 Wakschlag LS, 1996, J AM ACAD CHILD PSY, V35, P963 NR 21 TC 14 Z9 14 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD JAN PY 2002 VL 28 IS 1 BP 65 EP 71 DI 10.1046/j.1365-2214.2002.00243.x PG 7 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 520QZ UT WOS:000173793700009 PM 11856189 ER PT J AU Morton, R Sharma, V Nicholson, J Broderick, M Poyser, J AF Morton, R Sharma, V Nicholson, J Broderick, M Poyser, J TI Disability in children from different ethnic populations SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE disability; children; ethnic; genetics; consanguinous ID CEREBRAL-PALSY; PREVALENCE; HEALTH AB We report on the prevalence of severe neurodisability in children in the Southern Derbyshire Health Authority from different ethnic groups. Information was obtained from the health records of children at the Child Development Centre (CDC), and analysed according to ethnic group. There were 53 in the Pakistani group, 20 in the Indian group and 764 in a mixed group, of which 95% were of European origin. It was estimated that all children with severe disability in the area of the Health Authority had notes at the CDC, except for 10% of the mixed group living on the periphery. The numbers of children with different disabling conditions were recorded, together with a measure of the level of individual disability; the 'Disability Scores'. We also noted if the condition was genetic or chromosomal in origin. Pakistani children showed a higher prevalence than the other groups of severe learning disorder, severe and profound hearing loss and severe visual problems. They also had a slightly increased prevalence of autism and cerebral palsy. Conversely, they showed a lower prevalence of language disorder. Disability scores for Pakistani children attending the CDC were higher than for other groups. Genetic disease causing disability was 10 times more common in the Pakistani children than other ethnic groups. Disability is more common in Pakistani children probably as a result of the cultural practice of consanguineous marriages. This community needs special help for disabled children, and their families, for general support and appropriate genetic counselling. C1 City Hosp, Derbyshire Childrens Hosp, Ronnie Mackeith Child Dev Ctr, Derby DE22 3NE, England. S Derbyshire Community Trust, Community Paediat Dept, Derby, England. RP Morton, R (reprint author), City Hosp, Derbyshire Childrens Hosp, Ronnie Mackeith Child Dev Ctr, Uttoxeter Rd, Derby DE22 3NE, England. CR BALLERINA R, 1995, HLTH TRENDS, V27, P14 Bundey Sarah, 1993, European Journal of Human Genetics, V1, P206 FISHER NL, 1992, PEDIATR CLIN N AM, V39, P55 FOSTER A, 1988, EYE S, V2, P527 Guy R, 2001, CHILD CARE HLTH DEV, V27, P173, DOI 10.1046/j.1365-2214.2001.00165.x Hutchesson ACJ, 1998, J MED GENET, V35, P366, DOI 10.1136/jmg.35.5.366 MCCORMICK B, 1995, MED PRACTITIONERS GU MURPHY CC, 1995, AM J PUBLIC HEALTH, V85, P319, DOI 10.2105/AJPH.85.3.319 Roberts A, 1996, J MED GENET, V33, P56, DOI 10.1136/jmg.33.1.56 Sinha G, 1997, DEV MED CHILD NEUROL, V39, P259 Webb EVJ, 1997, DEV MED CHILD NEUROL, V39, P150 Williams K, 1998, DEV MED CHILD NEUROL, V40, P182 NR 12 TC 15 Z9 16 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD JAN PY 2002 VL 28 IS 1 BP 87 EP 93 DI 10.1046/j.1365-2214.2002.00245.x PG 7 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 520QZ UT WOS:000173793700011 PM 11856191 ER PT J AU Lewis, MES AF Lewis, MES TI Genomic convergence of the divergent spectrum of autism disorder SO CLINICAL GENETICS LA English DT Editorial Material C1 Childrens & Womens Hosp, Dept Med Genet, Vancouver, BC V6H 3N1, Canada. RP Lewis, MES (reprint author), Childrens & Womens Hosp, Dept Med Genet, Rm 234,4500 Oak St, Vancouver, BC V6H 3N1, Canada. NR 0 TC 0 Z9 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2002 VL 61 IS 1 BP 7 EP 9 DI 10.1034/j.1399-0004.2002.610102.x PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 538RK UT WOS:000174828700003 PM 11903348 ER PT J AU Lewis, MES AF Lewis, MES TI Refining the spectrum of genes in autism spectrum disorder SO CLINICAL GENETICS LA English DT Editorial Material C1 Childrens & Womens Hosp, Dept Med Genet, Vancouver, BC V6H 3N1, Canada. RP Lewis, MES (reprint author), Childrens & Womens Hosp, Dept Med Genet, Rm 234,4500 Oak St, Vancouver, BC V6H 3N1, Canada. NR 0 TC 0 Z9 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2002 VL 61 IS 1 BP 7 EP 7 DI 10.1034/j.1399-0004.2002.610102.x PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 538RK UT WOS:000174828700002 PM 11903348 ER PT J AU Lewis, MES AF Lewis, MES TI Queuing up clues to the origins of autism on chromosome 7q SO CLINICAL GENETICS LA English DT Editorial Material C1 Children & Womens Hosp, Dept Med Genet, Vancouver, BC V6H 3N1, Canada. RP Lewis, MES (reprint author), Children & Womens Hosp, Dept Med Genet, Rm 234,4500 Oak St, Vancouver, BC V6H 3N1, Canada. NR 0 TC 0 Z9 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2002 VL 61 IS 1 BP 10 EP 11 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 538RK UT WOS:000174828700004 ER PT J AU Bellivier, F Roy, I Leboyer, M AF Bellivier, F Roy, I Leboyer, M TI Serotonin transporter gene polymorphisms and affective disorder-related phenotypes SO CURRENT OPINION IN PSYCHIATRY LA English DT Article ID BIPOLAR AFFECTIVE-DISORDER; TRIDIMENSIONAL PERSONALITY QUESTIONNAIRE; SEASONAL AFFECTIVE-DISORDER; REPEAT LENGTH POLYMORPHISM; ANXIETY-RELATED TRAITS; FUNCTIONAL POLYMORPHISM; PROMOTER POLYMORPHISM; POSSIBLE ASSOCIATION; SUICIDAL-BEHAVIOR; REGULATORY REGION AB Serotonin (5-hydroxytryptamine) is implicated in several psychiatric disorders such as anxiety, mood disorders, obsessive compulsive disorders and autism. The serotonin transporter, which ends the activity of serotonin in the brain after its release from serotonergic neurons, is a key protein in the serotonergic pathway as it regulates the concentration of serotonin in the synaptic cleft. Tricyclic antidepressants and serotonin reuptake inhibitors bind to sites that overlap with the serotonin binding site, thus reducing 5-hydroxytryptamine reuptake. Genetic factors have long been implicated in the etiology of bipolar disorder and unipolar depression, therefore the serotonin transporter gene is a strong candidate gene for affective disorders and in mood disorder-related phenotypes. Two polymorphisms of the transporter gene have been extensively studied in association with affective disorders (unipolar, bipolar, depressive symptoms, seasonal affective disorder) and more recently in response to antidepressants. Associations have also been reported between the serotonin transporter gene polymorphisms and transnosographical entities such as anxiety-related traits and suicidal behaviors. Both approaches obtained conflicting results. This review attempts to clarify the phenotypic uncertainties and the conflicting association results obtained with the serotonin transporter gene polymorphisms in psychiatry. (C) 2002 Lippincott Williams Wilkins. C1 Hop Henri Mondor, Assistance Publ Hop Paris, Adult Psychiat Serv, F-94010 Creteil, France. Albert Chenevier Hosp, Assistance Publ Hop Paris, Adult Psychiat Serv, F-94010 Creteil, France. Creteil Fac Med, INSERM U513, Neurobiol & Psychiat Unit, Creteil, France. RP Bellivier, F (reprint author), Hop Henri Mondor, Serv Psychiat Adulte, 51 Ave Mal Lattre Tassigny, F-94010 Creteil, France. 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PD JAN PY 2002 VL 15 IS 1 BP 49 EP 58 DI 10.1097/00001504-200201000-00009 PG 10 WC Psychiatry SC Psychiatry GA 512ML UT WOS:000173328100009 ER PT J AU Diler, RS Firat, S Avci, A AF Diler, RS Firat, S Avci, A TI An open-label trial of risperidone in children with autism SO CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL LA English DT Article DE child; autism; pervasive developmental disorders; risperidone ID PERVASIVE DEVELOPMENTAL DISORDER; ATYPICAL NEUROLEPTICS; YOUNG-CHILDREN; ADOLESCENTS; SCHIZOPHRENIA AB Background: Risperidone has potent effects on serotonin and dopamine neuronal systems, both of which have been implicated in the pathophysiology of autism .Risperidone is increasingly being used to treat specific symptoms in children with autism. Objective: The purpose of this study was to investigate the efficacy and tolerability of risperidone in young children with autism. Methods: In this single-site, 6-month, open-label study, young autistic children aged 3 to 7.5 years were administered risperidone 0.5 mg/d for 15 days and then 1 mg/d until 3 months; doses were thereafter individually adjusted to a maximum of 2 mg/d between the third and sixth month. The Clinical Global Impression-Severity of Illness (CGI-SI) scale, Childhood Autism Rating Scale (CARS), and Abnormal Involuntary Movement Scale (AIMS) were used to assess efficacy. The CGI-Adverse Effect scale and the Adverse Effect Checklist were used to assess the incidence and severity of adverse events. Results: A total of 20 children (mean age, 4.95 +/- 1.18; range, 3-7.5 years) were enrolled; 16 completed the 6-month study. Two children were withdrawn due to noncompliance with the treatment protocol during the first month, and 2 children were withdrawn from the study during the first month because of marked agitation, anger, and aggression thought to be related to treatment. The mean dose of risperidone was 1.53 mg/d (range, 0.04-0.11 mg/kg per day). Thirteen of the 16 children (81%) demonstrated at least 1 grade improvement on CGI-SI scores. Mean total CARS score significantly decreased from 39.06 +/- 6.23 to 32.03 +/- 8.73 after 6 months (P = 0.001). Scores on 11 of the 15 subscales of the CARS showed significant improvement (P < 0.05). Four subjects experienced mild sedation, and 2 experienced weight gain of < 10%. One child with mild sedation also experienced slight akathisia. Conclusion: In this population of young autistic children, risperidone had positive effects on most symptoms of autistic disorder. Additional double-blind, placebo-controlled studies are needed to determine the effectiveness of risperidone in the management of autism. C1 Cukurova Univ, Fac Med, Dept Child & Adolescent Psychiat, TR-01330 Adana, Turkey. RP Diler, RS (reprint author), Cukurova Univ, Fac Med, Dept Child & Adolescent Psychiat, Balcali, TR-01330 Adana, Turkey. 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Ther. Res.-Clin. Exp. PD JAN PY 2002 VL 63 IS 1 BP 91 EP 102 DI 10.1016/S0011-393X(02)80009-1 PG 12 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 514TW UT WOS:000173458000008 ER PT J AU Smith, M Woodroffe, A Smith, R Holguin, S Martinez, J Filipek, PA Modahl, C Moore, B Bocian, ME Mays, L Laulhere, T Flodman, P Spence, MA AF Smith, M Woodroffe, A Smith, R Holguin, S Martinez, J Filipek, PA Modahl, C Moore, B Bocian, ME Mays, L Laulhere, T Flodman, P Spence, MA TI Molecular genetic delineation of a deletion of chromosome 13q12 -> q13 in a patient with autism and auditory processing deficits SO CYTOGENETIC AND GENOME RESEARCH LA English DT Article ID DOUBLECORTIN; PROTEIN; MIND; EXPRESSION; LINKAGE; KINASE AB In a sporadic case of autism and language deficit due to auditory processing defects, molecular genetic studies revealed that a chromosomal deletion occurred in the 13q12-->q13 region. 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These rearrangements involve deletions found in approximately 70% of Prader-Willi or Angelman's syndrome patients (PWS, AS), duplications detected in some cases of autism, triplications and inverted duplications. HERC2-containing (HEct domain and RCc1 domain protein 2) segmental duplications or duplicons are present at two of these breakpoints (13132 and BP3) mainly associated with deletions. We show here that clusters containing several copies of the human chromosome 15 low-copy repeat (LCR15) duplicon are located at each of the six described 15q11-q14 BPS. In addition, our results suggest the existence of breakpoints for large 15q11-q13 deletions in a proximal duplicon-containing clone. The study reveals that HERC2-containing duplicons (estimated on 50-400 kb) and LCR15 duplicons (similar to 15 kb on 15q11-q14) share the golgin-like protein (GLP) genomic sequence. Through the analysis of a human BAC library and public databases we have identified 36 LCR15 related sequences in the human genome, most (27) mapping to chromosome 15q and being transcribed. LCR15 analysis in non-human primates and age-sequence divergences support a recent origin of this family of segmental duplications through human speciation. C1 Hosp Duran & Reynals, IRO, Ctr Genet Med & Mol, Barcelona 08907, Spain. Corp Parc Tauli, Genet Lab, Sabadell, Spain. RP Estivill, X (reprint author), Hosp Duran & Reynals, IRO, Ctr Genet Med & Mol, Gran Via Km 2-7, Barcelona 08907, Spain. 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J. Hum. Genet. PD JAN PY 2002 VL 10 IS 1 BP 26 EP 35 DI 10.1038/sj/ejhg/5200760 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 535QP UT WOS:000174655700005 PM 11896453 ER PT J AU Martinot, JL Zilbovicius, M Paillere, ML Boddaert, N Artiges, E Berthoz, S AF Martinot, JL Zilbovicius, M Paillere, ML Boddaert, N Artiges, E Berthoz, S TI Cerebral development in childhood and adolescence psychiatry. Neuroimaging approach SO EVOLUTION PSYCHIATRIQUE LA French DT Article DE psychiatry; childhood; adolescence; cerebral development; cerebral imaging; MRI; PET; schizophrenia; autism; mental retardation; obsessive-compulsive disorder; tourette; dyslexia; hyperactivity; anorexia; alexithymia; emotion; dependence ID OBSESSIVE-COMPULSIVE DISORDER; DEFICIT HYPERACTIVITY DISORDER; POSITRON EMISSION TOMOGRAPHY; ANTERIOR CINGULATE CORTEX; EARLY-ONSET SCHIZOPHRENIA; GLUCOSE METABOLIC RATES; MAGNETIC-RESONANCE; BLOOD-FLOW; ANOREXIA-NERVOSA; FUNCTIONAL NEUROANATOMY AB Modifications in cerebral development have either been demonstrated or their presence is probable in a number of psychiatric disorders which arise during childhood or adolescence. Their detection depends on new methods of image analysis examples are presented in this article. 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Psychiatr. PD JAN-MAR PY 2002 VL 67 IS 1 BP 122 EP 154 PG 33 WC Psychiatry SC Psychiatry GA 559RX UT WOS:000176040100007 ER PT J AU Wolff, DJ Clifton, K Karr, C Charles, J AF Wolff, DJ Clifton, K Karr, C Charles, J TI Pilot assessment of the subtelomeric regions of children with autism: Detection of a 2q deletion SO GENETICS IN MEDICINE LA English DT Article DE chromosome deletion; 2q; autism; subtelomere ID PERVASIVE DEVELOPMENTAL DISORDERS; IDIOPATHIC MENTAL-RETARDATION; CHROMOSOMAL REARRANGEMENTS; GENOMIC SCREEN; TELOMERE; GENE AB Purpose: Autism is a chronic neurodevelopmental disorder characterized by deficits in reciprocal social interaction, language and communication, and by the presence of stereotypical behaviors. The disorder is a complex genetic trait with no known predisposing genes. We report the results of a pilot project to screen for aberrations in the gene-rich subtelomeric chromosomal regions of a cohort of children with autism. Methods: For our pilot project, we used a multiprobe system that includes probes for the subtelomeric regions of all human chromosomes. We assessed the subtelomeric regions of chromosomes from 10 children with a diagnosis of autism. Results: The screen identified one child with an apparent deletion of the subtelomeric region of chromosome 2q; nine children and pooled control samples yielded normal results. The deletion in our patient was confirmed with two other subtelomeric probes and a targeted cytogenetic study revealed a subtle difference in appearance for one chromosome 2 homologue. Conclusion: There have been several reports of children with dysmorphic features, autistic behaviors, and 2q deletions detectable with standard cytogenetic techniques. It may be that the distal region of chromosome 2q harbors a gene or genes that may predispose to autism. C1 Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Clin Serv, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Pediat, Div Genet & Child Dev, Charleston, SC 29425 USA. RP Wolff, DJ (reprint author), Med Univ S Carolina, Dept Pathol & Lab Med, 165 Ashley Ave,suite 309, Charleston, SC 29425 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Ballif BC, 2000, AM J HUM GENET, V67, P1356 Barrett S, 1999, AM J MED GENET, V88, P609 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 CONRAD B, 1995, CLIN GENET, V48, P134 DILAVORE P, 1995, J AUTISM DEV DISORD, V24, P355 FLINT J, 1995, NAT GENET, V9, P132, DOI 10.1038/ng0295-132 Ghaffari SR, 1998, J MED GENET, V35, P225, DOI 10.1136/jmg.35.3.225 Ghaziuddin M, 1999, J AUTISM DEV DISORD, V29, P259, DOI 10.1023/A:1023088207468 Bailey A, 1998, HUM MOL GENET, V7, P571 KLIN A, 1999, HDB NEURODEVELOPMENT, P257 Knight SJL, 1999, LANCET, V354, P1676, DOI 10.1016/S0140-6736(99)03070-6 Knight SJL, 1997, EUR J HUM GENET, V5, P1 Kumar A, 1998, HUM GENET, V103, P173 Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C., 1998, AUTISM DIAGNOSTIC OB MACINA RA, 1994, HUM MOL GENET, V3, P1847, DOI 10.1093/hmg/3.10.1847 MAUK JE, 1993, PEDIATR CLIN N AM, V40, P567 Ning Y, 1996, NAT GENET, V14, P86, DOI 10.1038/ng0996-86 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x Schopler E., 1998, CHILDHOOD AUTISM RAT 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 Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 Trask BJ, 1998, HUM MOL GENET, V7, P13, DOI 10.1093/hmg/7.1.13 VOIT G, 1998, AM J HUM GENET S, V63, pA44 VORSANOVA SG, 1998, AM J HUM GENET S, V63, pA873 Weidmer-Mikhail E, 1998, J INTELL DISABIL RES, V42, P8, DOI 10.1046/j.1365-2788.1998.00091.x 2001, AM HUM GENET, V69, P570 NR 32 TC 33 Z9 34 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD JAN-FEB PY 2002 VL 4 IS 1 BP 10 EP 14 DI 10.1097/00125817-200201000-00002 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 549XW UT WOS:000175473400002 PM 11839952 ER PT J AU Schuntermann, P AF Schuntermann, P TI Pervasive developmental disorder and parental adaptation: Previewing and reviewing atypical development with parents in child psychiatric consultation SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article; Proceedings Paper CT Congress of the International-Association-for-Child-and-Adolescent-Psychiatry-and-Allied -Professions CY AUG 02-07, 1998 CL STOCKHOLM, SWEDEN SP Int Assoc Child & Adolescent Psychiat & Allied Profess ID HOME VIDEOTAPES; AUTISM; STRESS; RECOGNITION; FAMILIES; SUPPORT; BURDEN; AGE AB Parenting young children with pervasive developmental disorder engenders unique sustained stresses, which have been termed "burden of care." One specific source of stress for parents is the children's uneven developmental progress, in which delays and accelerations of adaptive functioning may exist side by side. This paper proposes a clinical method that may be incorporated into periodic child psychiatric consultations with parents of young children who have high-functioning autism or Asperger's disorder. Using a semistructured technique, the clinician reviews with the parents the details of the child's recent developmental course and attempts to identify emergent skills that may serve to preview upcoming developmental issues and gains. This method is aimed at enhancing parental abilities to track and anticipate developmental progress and the resultant shifts in the parent-child relationship, in order to reduce one source of sustained parental stress. Case illustrations of children ages 2-8 years old are discussed in light of recent literature on adaptive issues in families of individuals with a chronic medical or psychiatric condition and, specifically, families of children with pervasive developmental disorder. C1 Harvard Vanguard Med Associates, Dev Consultat Serv, Somerville, MA 02144 USA. Harvard Univ, Sch Med, Dept Psychiat, Childrens Hosp, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. RP Schuntermann, P (reprint author), Harvard Vanguard Med Associates, Dev Consultat Serv, Somerville Off,40 Holland St, Somerville, MA 02144 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson C, 1986, SCHIZOPHRENIA FAMILY Angold A, 1998, AM J PUBLIC HEALTH, V88, P75, DOI 10.2105/AJPH.88.1.75 ANGOLD A, 1999, CHILD ADOLESCENT IMP Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BECKMAN PJ, 1991, AM J MENT RETARD, V95, P585 BECKMAN PJ, 1983, AM J MENT DEF, V88, P150 Bristol M. 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Rev. Psychiatr. PD JAN-FEB PY 2002 VL 10 IS 1 BP 16 EP 27 DI 10.1093/hrp/10.1.16 PG 12 WC Psychiatry SC Psychiatry GA 510WQ UT WOS:000173230600002 PM 11751642 ER PT J AU Lutchmaya, S Baron-Cohen, S AF Lutchmaya, S Baron-Cohen, S TI Human sex differences in social and non-social looking preferences, at 12 months of age SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article ID ASPERGER-SYNDROME; AUTISM; MIND AB Twelve-month-old infants (n = 60) were presented with a video of cars moving, or a face moving, in a looking preference experimental design. This tested the prediction from our earlier work that attention in males is drawn more to mechanical motion, whilst attention in females is drawn more to biological motion. Results supported this prediction. These findings are discussed in relation to social and biological determinism. (C) 2002 Published by Elsevier Science Inc. C1 Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 3EB, England. RP Lutchmaya, S (reprint author), Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Downing Site, Cambridge CB2 3EB, England. CR Baron-Cohen S., 1999, NEURODEVELOPMENTAL D 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 CONNELLAN J, 2001, INFANT BEHAV DEV, V23, P113 FANTZ RL, 1963, SCIENCE, V140, P296, DOI 10.1126/science.140.3564.296 Geary David, 1998, MALE FEMALE EVOLUTIO HALL JA, 1978, PSYCHOL BULL, V85, P845, DOI 10.1037//0033-2909.85.4.845 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Lutchmaya S, 2002, INFANT BEHAV DEV, V25, P327, DOI 10.1016/S0163-6383(02)00094-2 Maccoby E, 1966, DEV SEX DIFFERENCES Rosenthal R., 1979, SENSITIVITY NONVERBA Servin A, 1999, SCAND J PSYCHOL, V40, P43, DOI 10.1111/1467-9450.00096 Skuse DH, 1997, NATURE, V387, P705, DOI 10.1038/42706 Swettenham J, 1998, J CHILD PSYCHOL PSYC, V39, P747, DOI 10.1017/S0021963098002595 NR 15 TC 46 Z9 47 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-6383 J9 INFANT BEHAV DEV JI Infant Behav. Dev. PY 2002 VL 25 IS 3 BP 319 EP 325 DI 10.1016/S0163-6383(02)00095-4 PG 7 WC Psychology, Developmental SC Psychology GA 623HL UT WOS:000179697200006 ER PT J AU Freeman, BJ Cronin, P AF Freeman, BJ Cronin, P TI Diagnosing autism spectrum disorder in young children: An update SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; childhood early intervention; communication delays; developmental disabilities; diagnosis; pervasive development disorder; social delays and deficits ID DEVELOPMENTAL DISORDERS; FOLLOW-UP; AGE; RELIABILITY; INDIVIDUALS; BEHAVIOR; INFANCY AB The article reviews studies of early diagnosis of Autistic Spectrum Disorder. Currently, there are no objective measures that can be used for accurate diagnosis, and the diagnosis remains clinical. The article provides guidelines for evaluation. C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Autism Evaluat Clin, Dept Child & Adolescent Psychiat, Inst Neuropsychiat, Los Angeles, CA 90024 USA. RP Freeman, BJ (reprint author), Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA. 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PD JAN PY 2002 VL 14 IS 3 BP 1 EP 10 PG 10 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 540EF UT WOS:000174916000003 ER PT J AU Harris, SL Delmolino, L AF Harris, SL Delmolino, L TI Applied Behavior analysis: Its application in the treatment of autism and related disorders in young children SO INFANTS AND YOUNG CHILDREN LA English DT Article DE ABA; autism; early intervention ID PRESCHOOL-CHILDREN; PARADIGM AB The techniques of applied behavior analysis (ABA) are effective in altering the developmental trajectory of some very young children with autism. This research suggests that early, intensive treatment using the methods of ABA enables a significant number of children to enter the educational mainstream and achieve normal intellectual functioning. Both home-based and center- or school-based models have been used to deliver these services. 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PD JAN PY 2002 VL 14 IS 3 BP 11 EP 17 PG 7 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 540EF UT WOS:000174916000004 ER PT J AU Levy, SE Hyman, SL AF Levy, SE Hyman, SL TI Alternative/complementary approaches to treatment of children with autistic spectrum disorders SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; autistic spectrum disorders; complementary and alternative medicine treatments ID PERVASIVE DEVELOPMENTAL DISORDER; YOUNG-CHILDREN; INTRAVENOUS IMMUNOGLOBULIN; SECRETIN; TRIAL; METHYLMERCURY; MAGNESIUM; EXPOSURE AB Early diagnosis of autistic spectrum disorders (ASD) allows for early referral for treatment and remediation of core deficits in communication, socialization, and behavior. The cornerstone of treatment is a comprehensive, intensive program of educational, developmental, and behavioral strategies. Since the etiology for most cases is not well defined, progress may be slow, and treatment may be intense, interest in alternative theories of causation and novel treatments is high. Families may pursue complementary and alternative medicine (CAM) therapies in addition to the standard treatments. There are two types of CAM: biologic and nonbiologic. Some of the treatments have been examined using standard research techniques, while others have not yet undergone such scrutiny. Families should be supported in their quest for effective treatments and assisted in learning about potential benefits and harm of each CAM. C1 Childrens Hosp Philadelphia, Div Child Dev & Rehabil, Childrens Seashore House, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. RP Levy, SE (reprint author), Childrens Hosp Philadelphia, Div Child Dev & Rehabil, Childrens Seashore House, Philadelphia, PA 19104 USA. 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PD JAN PY 2002 VL 14 IS 3 BP 33 EP 42 PG 10 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 540EF UT WOS:000174916000007 ER PT S AU Young, R Brewer, N AF Young, R Brewer, N BE Glidden, LM TI Diagnosis of autistic disorder: Problems and new directions SO INTERNATIONAL REVIEW OF RESEARCH IN MENTAL RETARDATION, VOL 25 SE International Review of Research in Mental Retardation LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; III-R CRITERIA; ASPERGERS SYNDROME; INFANTILE-AUTISM; DSM-III; SPECTRUM DISORDERS; CHILDHOOD AUTISM; CLUSTER-ANALYSIS; YOUNG-CHILDREN; FIELD TRIAL C1 Flinders Univ S Australia, Sch Psychol, Adelaide, SA 5001, Australia. RP Young, R (reprint author), Flinders Univ S Australia, Sch Psychol, Adelaide, SA 5001, Australia. 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Rev. Res. Ment. Retard. PY 2002 VL 25 BP 107 EP 134 DI 10.1016/S0074-7750(02)80007-6 PG 28 WC Education, Special; Psychology, Multidisciplinary; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA BT76M UT WOS:000173974200004 ER PT J AU Jyonouchi, H Sun, SN Le, HT Itokazu, N AF Jyonouchi, H Sun, SN Le, HT Itokazu, N TI Cytokine production against common dietary proteins in patients with autism spectrum disorder and developmental regression in comparison with patients with dietary protein intolerance SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN 55455 USA. NR 0 TC 1 Z9 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 2002 VL 109 IS 1 SU S MA 665 BP S221 EP S221 DI 10.1016/S0091-6749(02)81802-4 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 519UX UT WOS:000173744800664 ER PT J AU Sun, SN Itokazu, N Le, HT Jyonouchi, H AF Sun, SN Itokazu, N Le, HT Jyonouchi, H TI Innate immune responses and cytokine production against dietary proteins in children with autism spectrum disorder (ASD) and those with dietary protein intolerance (DPI) SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN 55455 USA. NR 0 TC 0 Z9 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 2002 VL 109 IS 1 SU S MA 668 BP S222 EP S223 DI 10.1016/S0091-6749(02)81805-X PG 2 WC Allergy; Immunology SC Allergy; Immunology GA 519UX UT WOS:000173744800667 ER PT J AU Magiati, I Dockrell, JE Logotheti, AE AF Magiati, I Dockrell, JE Logotheti, AE TI Young children's understanding of disabilities: the influence of development, context, and cognition SO JOURNAL OF APPLIED DEVELOPMENTAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 6th European Congress of Psychology CY JUL 04-09, 1999 CL ROME, ITALY DE disabilities; dyslexia; hyperactivity ID PERCEPTIONS; ATTITUDES; NEEDS; PEERS; AIDS AB Throughout Europe, educational support for children with disabilities has moved towards a model of inclusive education. Such policy changes mean that, for all children, there will be an increased likelihood of working with and encountering children with differing disabilities and difficulties. Previous research had indicated that children had poorly differentiated views of developmental differences. The present study investigated children's representations of different disabilities. Seventy-nine 8-9- and 10-11-year-old Greek children from an urban school and a rural school completed a rating scale of attitudes toward school inclusion and a semistructured interview. Responses to the attitude scale provided generally positive views of educational inclusion. However, children were less positive about activities that might directly reflect upon themselves. Children's responses in the interviews indicated that they were developing rich representations of differences and diversities. Children had the greatest understanding of sensory and physical disabilities, followed by learning disabilities. There was limited knowledge of dyslexia and hyperactivity and no child was familiar with the term autism. Both groups of children identified a range of developmental difficulties, with older children being more aware of specific learning disabilities, their origin and impact. Results are discussed in terms of children's developing knowledge systems and the implications for educational practices. (C) 2002 Published by Elsevier Science Inc. C1 Inst Educ, Dept Psychol & Human Dev, London WC1H 0AA, England. RP Magiati, I (reprint author), St George Hosp, Sch Med, Dept Psychol, Cranmer Terrace Tooting Broadway, London SW17 0RE, England. 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B., 1997, DISCOURSE TOOLS REAS SAFRAN SP, 1995, J EMOT BEHAV DISORD, V3, P66 SAKADAMIANGELOPOULOU N, 1994, PERCEPT MOTOR SKILL, V79, P19 Shapiro A., 1988, J READING WRITING LE, V4, P133 Sigelman CK, 1997, HEALTH EDUC BEHAV, V24, P191, DOI 10.1177/109019819702400207 Turner SA, 1997, INT J SCI EDUC, V19, P491, DOI 10.1080/0950069970190501 WADE B, 1995, EUROPEAN J SPECIAL N, V10, P17 Wood D, 1996, OXFORD REV EDUC, V22, P5, DOI 10.1080/0305498960220101 Zimmerman BJ, 2000, CURR PSYCHOL, V19, P175, DOI 10.1007/s12144-000-1014-8 NR 34 TC 29 Z9 29 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0193-3973 J9 J APPL DEV PSYCHOL JI J. Appl. Dev. Psychol. PY 2002 VL 23 IS 4 BP 409 EP 430 DI 10.1016/S0193-3973(02)00126-0 PG 22 WC Psychology, Developmental SC Psychology GA 638QL UT WOS:000180581700003 ER PT J AU Stephenson, J AF Stephenson, J TI Characterization of multisensory environments: Why do teachers use them? SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article ID SPECIAL-EDUCATION; FACILITATED COMMUNICATION; SEVERE DISABILITIES; TRANSLATE RESEARCH; CLASSROOM PRACTICE; CHILDREN; STUDENTS; AUTISM; YOUTH; GAP AB Background Special educators are increasingly using multisensory environments even though there is a lack of evidence for their effectiveness as an educational intervention. This paper explores the way multisensory rooms are presented on the World Wide Web in an attempt to understand why they are being used by teachers. Methods Searches of the World Wide Web were carried out to locate 48 relevant sites. The contents of the sites were analyzed in terms of aims or purposes, purported benefits and outcomes, use of research, confidence of claims, emphasis on student behaviour and building interpersonal relationships. Results The aims included sensory stimulation and relaxation. A wide range of purported outcomes were identified that were confidently claimed with little reference to the existing research base. Many sites did claim benefits for student behaviour and building up of relationships. Conclusions There is an uncritical presentation of the purported benefits of multisensory environments with a belief that sensory stimulation is, in itself, a good thing. It seems that a teacher's desire to build positive relationships and provide pleasant experiences may be an important factor in the use of these environments. C1 Univ Technol, Fac Educ, Lindfield, NSW 2070, Australia. RP Stephenson, J (reprint author), Univ Technol, Fac Educ, POB 222, Lindfield, NSW 2070, Australia. 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Appl. Res. Intellect. Disabil. PY 2002 VL 15 IS 1 BP 73 EP 90 DI 10.1046/j.1360 2322.2002.00102.x PG 18 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 532QF UT WOS:000174486000008 ER PT J AU Lerner, V Miodownik, C Kaptsan, A Cohen, H Loewenthal, U Kotler, M AF Lerner, V Miodownik, C Kaptsan, A Cohen, H Loewenthal, U Kotler, M TI Vitamin B-6 as add-on treatment in chronic schizophrenic and schizoaffective patients: A double-blind, placebo-controlled study SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID PYRIDOXINE; DISORDERS; THIAMINE AB Background: Vitamin B-6, or pyridoxine, plays an intrinsic role in the synthesis of certain neuro-transmitters that take part in development of psychotic states. Several reports indicate that vitamin B-6 may be a factor in a number of psychiatric disorders and related conditions, such as autism, Alzheimer's disease, hyperactivity, learning disability, anxiety disorder, and depression. Moreover, there are anecdotal reports of a reduction in psychotic symptoms after vitamin B-6 supplementation of psychopharmacologic treatment of patients suffering from schizophrenia or organic mental disorder. The aim of this study was to examine whether vitamin B-6 therapy influences psychotic symptoms in patients suffering from schizophrenia and schizoaffective disorder. Method: The effects of the supplementation of vitamin B-6 to antipsychotic treatment on positive and negative symptoms in 15 schizophrenic and schizoaffective patients (DSM-IV criteria) were examined in a double-blind, placebo-controlled, crossover study spanning 9 weeks. All patients had stable psychopathology for at least I month before entry into the study and were maintained on treatment with their prestudy psychoactive and antiparkinsonian medications throughout the study. All patients were assessed using the Positive and Negative Syndrome Scale (PANSS) for schizophrenia on a weekly basis. Patients randomly received placebo or vitamin B-6 starting at 100 mg/day in the first week and increasing to 400 mg/day in the fourth week by 100-mg increments each week. Results: PANSS scores revealed no differences between vitamin B-6- and placebo-treated patients in amelioration of their mental state. Conclusion: Further studies with larger populations and shorter duration of illness are needed to clarify the question of the possible efficacy of vitamin B-6 in treatment of psychotic symptoms in schizophrenia. C1 Ben Gurion Univ Negev, Fac Hlth Sci, Minist Hlth, Mental Hlth Ctr, Beer Sheva, Israel. RP Lerner, V (reprint author), Beer Sheva Mental Hlth Ctr, POB 4600, IL-84170 Beer Sheva, Israel. 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Clin. Psychiatry PD JAN PY 2002 VL 63 IS 1 BP 54 EP 58 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 516UW UT WOS:000173576000011 PM 11838627 ER PT J AU Hong, L Yamagata, T Mori, M Momoi, MY AF Hong, L Yamagata, T Mori, M Momoi, MY TI Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 SO JOURNAL OF HUMAN GENETICS LA English DT Article DE hereditary multiple exostoses; mental retardation; autism; EXT1; EXT2 ID GENE AB Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation. Their fathers both expressed a clinical phenotype of hereditary multiple exostoses milder than those of the patients and without the associated mental disorder. The EXT1 and EXT2 genes from lymphocytes of the affected individuals were analyzed by using, denaturing high-performance liquid chromatography and direct sequencing. A novel deletion mutation, 1742delTGT-G in exon 9 of EXT1, causing a frameshift was detected in one boy and his father. Another novel deletion mutation, 2093delTT in exon 11 of EXT1, causing, transcription termination was detected in the other affected boy and his father. EXTI is expressed in the brain, and both EXTI and EXT2 proteins are associated with glycosyltransferase activities required for the biosynthesis of heparan sulfate, which also has activity in the brain. The coincidental association of mental disorders in the boys was not completely excluded. However, these results suggest the involvement of EXTI in the development of mental disorders, including mental retardation and autism. C1 Jichi Med Sch, Dept Pediat, Minami Kawachi, Tochigi 3290498, Japan. RP Hong, L (reprint author), Jichi Med Sch, Dept Pediat, 3311-1 Yakushiji, Minami Kawachi, Tochigi 3290498, Japan. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bandtlow CE, 2000, PHYSIOL REV, V80, P1267 Bellaiche Y, 1998, NATURE, V394, P85 Cheung PK, 2001, AM J HUM GENET, V69, P55, DOI 10.1086/321278 Dobson-Stone C, 2000, EUR J HUM GENET, V8, P24, DOI 10.1038/sj.ejhg.5200409 Francannet C, 2001, J MED GENET, V38, P430, DOI 10.1136/jmg.38.7.430 IshikawaBrush Y, 1997, HUM MOL GENET, V6, P1241, DOI 10.1093/hmg/6.8.1241 Ludecke HJ, 2001, AM J HUM GENET, V68, P81, DOI 10.1086/316926 McCormick C, 2000, P NATL ACAD SCI USA, V97, P668, DOI 10.1073/pnas.97.2.668 Philippe C, 1997, AM J HUM GENET, V61, P520, DOI 10.1086/515505 Seki H, 2001, AM J MED GENET, V99, P59, DOI 10.1002/1096-8628(20010215)99:1<59::AID-AJMG1115>3.0.CO;2-Z Wells DE, 1997, HUM GENET, V99, P612, DOI 10.1007/s004390050415 Wuyts W, 1998, AM J HUM GENET, V62, P346, DOI 10.1086/301726 NR 13 TC 1 Z9 1 PU SPRINGER-VERLAG TOKYO PI TOKYO PA 3-3-13, HONGO, BUNKYO-KU, TOKYO, 113-0033, JAPAN SN 1434-5161 J9 J HUM GENET JI J. Hum. Genet. PY 2002 VL 47 IS 5 BP 262 EP 265 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 555EV UT WOS:000175781900009 ER PT J AU Miller, E AF Miller, E TI MMR vaccine: Review of benefits and risks SO JOURNAL OF INFECTION LA English DT Review ID INFLAMMATORY-BOWEL-DISEASE; CAUSAL ASSOCIATION; RUBELLA VACCINE; MEASLES-VIRUS; AUTISM; MUMPS; SURVEILLANCE; CHILDREN; EPIDEMIOLOGY; ENGLAND C1 Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Div Immunisat, London NW9 5EQ, England. RP Miller, E (reprint author), Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Div Immunisat, 61 Colindale Ave, London NW9 5EQ, England. CR Afzal MA, 2001, DIGEST DIS SCI, V46, P658, DOI 10.1023/A:1005632106643 BELLINI WJ, 1997, AM SOC VIR MONT STAT Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DeWilde S, 2001, BRIT J GEN PRACT, V51, P226 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 FARRINGTON P, 1995, LANCET, V345, P567, DOI 10.1016/S0140-6736(95)90471-9 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 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 GALBRAITH NS, 1984, LANCET, V1, P91 Gillberg C., 1998, AUTISM, V2, P423, DOI 10.1177/1362361398024007 GINDLER JS, 1992, EPIDEMIOL REV, V14, P270 Halsey NA, 2001, PEDIATRICS, V107, P1 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 KAYE JA, 2001, BRIT MED J, V322, P1 KOPLAN JP, 1982, AM J DIS CHILD, V136, P362 MCCLEAN ME, 1990, CANADA DIS WEEKLY RE, V16, P213 Metcalf J, 1998, BRIT MED J, V316, P166 MILLER C, 1992, INT J EPIDEMIOL, V21, P998, DOI 10.1093/ije/21.5.998 MILLER C, 1989, PRACTITIONER, V233, P69 Miller D, 1997, LANCET, V349, P730, DOI 10.1016/S0140-6736(05)60171-7 MILLER E, 1990, ARCH DIS CHILD, V65, P820 MILLER E, 1982, LANCET, V2, P781 MILLER E, 1986, PUBLIC HLTH VIROLOGY, P36 MILLER E, 1993, LANCET, V341, P979, DOI 10.1016/0140-6736(93)91069-X Morgan-Capner P, 1991, CDR (Lond Engl Rev), V1, pR57 PELTOLA H, 1986, LANCET, V1, P939 Slater PE, 1997, JAMA-J AM MED ASSOC, V278, P594, DOI 10.1001/jama.278.7.594 Stratton K, 2001, IMMUNIZATION SAFETY TAYLOR B, UNPUB POPULATION STU Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 Wakefield Andrew J., 2000, Adverse Drug Reactions and Toxicological Reviews, V19, P265 Weibel RE, 1998, PEDIATRICS, V101, P383, DOI 10.1542/peds.101.3.383 World Health Organization Expanded Programme on immunization, 1998, WER, V73, P33 1997, 1 MMR NR 37 TC 16 Z9 16 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0163-4453 J9 J INFECTION JI J. Infect. PD JAN PY 2002 VL 44 IS 1 BP 1 EP 6 DI 10.1053/jinf.2001.0930 PG 6 WC Infectious Diseases SC Infectious Diseases GA 554ZH UT WOS:000175766900001 PM 11972410 ER PT J AU Iqbal, Z AF Iqbal, Z TI Ethical issues involved in the implementation of a differential reinforcement of inappropriate behaviour programme for the treatment of social isolation and ritualistic behaviour in an individual with intellectual disabilities SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; differential reinforcement; ethics; ritualistic behaviour; social isolation AB The present case study describes an adult male with a 28-year history of institutional care underpinned by a moderate intellectual disability (ID), and ritualistic behaviour congruent with features of autism or obsessive-compulsive disorder. The subject's ID was recognized early in life and he was provided with a special educational placement at 6 years of age, although his increasingly disturbed behaviour had resulted in several psychiatric admissions by early adolescence, and by the age of 20, his presentation necessitated long-term secure psychiatric care. The present report describes the application and ethical issues pertaining to a differential reinforcement of inappropriate behaviour (DRI) programme for the reduction of ritualistic behaviour and social isolation, the latter being a direct consequence of the former, one year after the subject was admitted to a medium-secure assessment and treatment residential facility. The results suggest that, although the treatment was successful in targeting ritualization and reducing social isolation, ethical concerns extended to care staff concerns about the reinforcer adopted for the programme and the lack of informed consent from the subject. The former resulted in inconsistent application of the programme and its eventual termination. A follow-up assessment of the subject's extent of social isolation and ritualistic behaviour suggested a return to a pre-DRI level of morbidity. Limitations and suggestions for the future treatment of such cases are outlined. C1 Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. RP Iqbal, Z (reprint author), Community Management Unit, 28A Oxford Rd, Dewsbury WF12 4LL, W Yorkshire, England. 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PD JAN PY 2002 VL 46 BP 82 EP 93 DI 10.1046/j.1365-2788.2002.00357.x PN 1 PG 12 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 518UG UT WOS:000173685800009 PM 11851859 ER PT J AU Borchers, AT Keen, CL Schoenfeld, Y Silva, J Gershwin, ME AF Borchers, AT Keen, CL Schoenfeld, Y Silva, J Gershwin, ME TI Vaccines, viruses, and voodoo SO JOURNAL OF INVESTIGATIONAL ALLERGOLOGY AND CLINICAL IMMUNOLOGY LA English DT Review DE measles vaccine; autoimmunity; allergic reactions; vaccination; hepatitis B ID HEPATITIS-B VACCINATION; INFLAMMATORY-BOWEL-DISEASE; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CENTRAL-NERVOUS-SYSTEM; MYELIN BASIC-PROTEIN; T-CELL CLONES; JUVENILE RHEUMATOID-ARTHRITIS; INSTITUTE-OF-MEDICINE; BATTAFARANO ET-AL; THROMBOCYTOPENIC PURPURA AB Vaccinations are invaluable in protection from a wide variety of diseases that can cause substantial morbidity and mortality. Although a rare complication of vaccination, autoimmune disorders represent one of these morbidities. Recently, widespread public concern has arisen from case reports suggesting that-similar to what has been observed after natural vital infections-there might be an association between specific immunizations and autoimmune diseases. Herein we address the biological plausibility of such a connection, focusing particularly on the examples of hepatitis B, rubella, and measles-mumps-rubella (MMR) vaccinations, and the autoimmune diseases they are potentially associated with. Our review of the available data suggests that, for the general population, the risk:benefit ratio is overwhelmingly in favor of vaccinations. However, the possibility cannot be ruled out that, in genetically susceptible individuals, vaccination can result in the unmasking of an autoimmune disease triggered by the immunization. We also critically examine the existing data suggesting a link between immunization against MMR and autism, and briefly discuss the controversial evidence pointing to a possible relationship between mercury exposure from vaccines and autistic disorders. There is a continued urgent need for-rigorously designed and executed studies addressing these potential associations, although the use of vaccinations remains a critical public health tool for protection against infectious disease. C1 Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Sch Med, Davis, CA 95616 USA. Univ Calif Davis, Dept Nutr, Davis, CA 95616 USA. Chaim Sheba Med Ctr, Dept Med B, IL-52621 Tel Hashomer, Israel. RP Gershwin, ME (reprint author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Sch Med, TB 192,1 Shields Ave, Davis, CA 95616 USA. 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Philos. Sport PY 2002 VL 29 IS 2 BP 121 EP 135 PG 15 WC Ethics; Sport Sciences SC Social Sciences - Other Topics; Sport Sciences GA 603LE UT WOS:000178560300003 ER PT J AU Grimaldi, BL AF Grimaldi, BL TI The central role of magnesium deficiency in Tourette's syndrome: causal relationships between magnesium deficiency, altered biochemical pathways and symptoms relating to Tourette's syndrome and several reported comorbid conditions SO MEDICAL HYPOTHESES LA English DT Review ID OBSESSIVE-COMPULSIVE-DISORDER; RESTLESS LEGS SYNDROME; VITAMIN-E TREATMENT; RED-BLOOD-CELL; SUBSTANCE-P; HYPERACTIVITY DISORDER; MAST-CELLS; NEUROPSYCHIATRIC DISORDERS; RECEPTOR INHIBITION; STIMULANT TREATMENT AB Prior studies have suggested a common etiology involved in Tourette's syndrome and several comorbid conditions and symptomatology. Reportedly, current medications used in Tourette's syndrome have intolerable side-effects or are ineffective for many patients. After thoroughly researching the literature, I hypothesize that magnesium deficiency may be the central precipitating event and common pathway for the subsequent biochemical effects on substance P, kynurenine, NMDA receptors, and vitamin B6 that may result in the symptomatology of Tourette's syndrome and several reported comorbid conditions. These comorbid conditions and symptomatology include allergy, asthma, autism, attention deficit hyperactivity disorder, obsessive compulsive disorder, coprolalia, copropraxia, anxiety, depression, restless leg syndrome, migraine, self-injurious behavior, autoimmunity, rage, bruxism, seizure, heart arrhythmia, heightened sensitivity to sensory stimuli, and an exaggerated startle response. Common possible environmental and genetic factors are discussed, as well as biochemical mechanisms. Clinical studies to determine the medical efficacy for a comprehensive magnesium treatment option for Tourette's syndrome need to be conducted to make this relatively safe, low side-effect treatment option available to doctors and their patients. (C) 2002 Harcourt Publishers Ltd. RP Grimaldi, BL (reprint author), 11283 Meadowcroft St, Pickerington, OH 43147 USA. 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Hypotheses PD JAN PY 2002 VL 58 IS 1 BP 47 EP 60 DI 10.1054/mehy.2001.1447 PG 14 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 520DC UT WOS:000173764300010 PM 11863398 ER PT J AU Hagberg, B AF Hagberg, B TI Clinical manifestations and stages of Rett syndrome SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE Rett syndrome; clinical manifestations; stages of disease ID CRITERIA; COMMUNICATION; INCLUSION; AUTISM AB The presentation and clinical diagnosis of Rett syndrome at various ages and stages are reviewed. In addition to the classical form, variability in phenotype between different atypical Rett forms is given. Obligatory, supportive, and differential diagnostic criteria are summarized. Long-term follow-up findings in ageing Rett women are addressed. (C) 2002 Wiley-Liss, Inc. C1 Univ Gothenburg, Queen Silvia Childrens Hosp, Dept Neurol, SE-41685 Gothenburg, Sweden. RP Hagberg, B (reprint author), Univ Gothenburg, Queen Silvia Childrens Hosp, Dept Neurol, SE-41685 Gothenburg, Sweden. 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Retard. Dev. Disabil. Res. Rev. PY 2002 VL 8 IS 2 BP 61 EP 65 DI 10.1002/mrdd.10020 PG 5 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 560LK UT WOS:000176083400002 PM 12112728 ER PT J AU Hammer, S Dorrani, N Dragich, J Kudo, S Schanen, C AF Hammer, S Dorrani, N Dragich, J Kudo, S Schanen, C TI The phenotypic consequences of MECP2 mutations extend beyond Rett syndrome SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE Rett syndrome; MECP2; Angelman; X-linked mental retardation ID LINKED MENTAL-RETARDATION; CPG-BINDING DOMAIN; TRANSCRIPTIONAL REPRESSOR MECP2; X-CHROMOSOME INACTIVATION; METHYLATED DNA; SYNDROME FAMILY; EXCLUSION MAP; MALES; ENCEPHALOPATHY; INHERITANCE AB Although MECP2 was initially identified as the causative gene in classic Rett syndrome (RTT), the gene has now been implicated in several phenotypes that extend well beyond the clinically defined disorder. MECP2 mutations have been found in people with various disorders, including neonatal onset encephalopathy, X-linked recessive mental retardation (MRX), classic and atypical RTT, autism, and Angelman syndrome, as well as mildly affected females and normal carrier females, To make matters more complex, in approximately 20% of classic sporadic RTT cases and more than 50% of affected sister pairs, no mutation in MECP2 has been found. X-chromosome inactivation patterns can clearly affect the phenotypic expression in females, while the effect of the type and position of the mutation is more apparent in the broader phenotype than in RTT. Both males and females are at risk, although an excess of paternally derived mutations are found in most cases of classic RTT. Thus, because of the range of disparate phenotypes, the gene may account for a relatively large portion of mental retardation in the population. (C) 2002 Wiley-Liss, Inc. C1 Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Mental Retardat Res Ctr, Los Angeles, CA 90024 USA. Hokkaido Inst Publ Hlth, Kita Ku, Sapporo, Hokkaido, Japan. RP Schanen, C (reprint author), Alfred I duPont Hosp Children, Nemours Res Program, 1600 Rockland Rd,POB 269,Room H3B-337, Wilmington, DE 19899 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2002 VL 8 IS 2 BP 94 EP 98 DI 10.1002/mrdd.10023 PG 5 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 560LK UT WOS:000176083400008 PM 12112734 ER PT J AU Wing, L Potter, D AF Wing, L Potter, D TI The epidemiology of autistic spectrum disorders: Is the prevalence rising? SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; autistic spectrum disorder; Asperger's syndrome; prevalence; diagnostic criteria; MMR vaccination ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; ASPERGER-SYNDROME; CHILDHOOD AUTISM; TOTAL POPULATION; DIAGNOSTIC INTERVIEW; PRESCHOOL-CHILDREN; MEDICAL DISORDERS; RUBELLA VACCINE; AGE AB For decades after Kanner's original paper on the subject was published in 1943, autism was generally considered to be a rare condition with a prevalence of around 2-4 per 10,000 children. Then, studies carried out in the late 1990s and the present century reported annual rises in incidence of autism in pre-school children, based on age of diagnosis, and increases in the age-specific prevalence rates in children. Prevalence rates of up to 60 per 10,000 for autism and even more for the whole autistic spectrum were reported. Reasons for these increases are discussed. They include changes in diagnostic criteria, development of the concept of the wide autistic spectrum, different methods used in studies, growing awareness and knowledge among parents and professional workers and the development of specialist services, as well as the possibility of a true increase in numbers. Various environmental causes for a genuine rise in incidence have been suggested, including the triple vaccine for measles, mumps and rubella (MMR]. Not one of the possible environmental causes, including MMR, has been confirmed by independent scientific investigation, whereas there is strong evidence that complex genetic factors play a major role in etiology. The evidence suggests that the majority, if not all, of the reported rise in incidence and prevalence is due to changes in diagnostic criteria and increasing awareness and recognition of autistic spectrum disorders. Whether there is also a genuine rise in incidence remains an open question. (C) 2002 Wiley-Liss, Inc. C1 Ctr Social & Commun Disorders, Bromley BR2 9HT, Kent, England. Natl Autist Soc, Informat Serv, London, England. RP Wing, L (reprint author), Ctr Social & Commun Disorders, 113 Masons Hill, Bromley BR2 9HT, Kent, England. 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Retard. Dev. Disabil. Res. Rev. PY 2002 VL 8 IS 3 BP 151 EP 161 DI 10.1002/mrdd.10029 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 588ZQ UT WOS:000177733100005 PM 12216059 ER PT J AU Barker, JA AF Barker, JA TI Computer modeling and the fate of folk psychology SO METAPHILOSOPHY LA English DT Article DE AI; autism; computer modeling; folk psychology; mental simulation; mindreading; ProtoThinker; simulation theory; theory-theory; ToMM ID REPRESENTATION; MIND AB Although Paul Churchland and Jerry Fodor both subscribe to the so-called theory-theory--the theory that folk psychology (FP) is an empirical theory of behavior--they disagree strongly about FP's fate. Churchland contends that FP is a fundamentally flawed view analogous to folk biology, and he argues that recent advances in computational neuroscience and connectionist AI point toward development of a scientifically respectable replacement theory that will give rise to a new common-sense psychology. Fodor, however, wagers that GP will be largely preserved and vindicated by scientific investigations of behavior. Recent findings by developmental psychologists, I argue, will push both Churchlandians and Fodorians toward the pessimistic view that FP is a misguided theory that will never be displaced, because it is, so to speak, built into our cognitive systems. I explore the possibility of preserving optimism by rejecting the theory-theory and adopting the simulation theory, a competing view developed by Robert Gordon, Alvin Goldman, and Jane Heal. According to simulationists, common-sense interpretation fo behavior is accomplished by means of pretense-like operations that deploy the cognitive system's own reasoning capabilities in a disengaged manner. Since on this view no theory-like set of principles would be needed, the simulation theory seems to enjoy a simplicity advantage over the theory-theory. Steven Stich and Shawn Nichols, however, contend that as the cognitive system would require special mechanisms for disengaged operation, the simplicity question cannot be resolved until suitable computational models are developed. I describe a set of models I have constructed to meet this need, and I discuss the contribution such models can make to determining GP's fate. C1 So Illinois Univ, Dept Philos Studies, Edwardsville, IL 62026 USA. RP Barker, JA (reprint author), So Illinois Univ, Dept Philos Studies, Edwardsville, IL 62026 USA. 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In complex inheritance common diseases, there are many instances where one or two studies meet genome-wide criteria for significant or suggestive linkage but several other studies do not show even nominally significant results with the same region. One possibility for resolving differences between study results would be to combine an available result parameter of several studies. We describe here a method of regional meta-analysis, the multiple-scan probability (MSP), which can be used on published results. It combines the reported P-values of individual studies, after correcting each value for the size of the region containing a minimum P-value. Analyses of the power of MSP and of its type I error rates are presented. The type I error rate is at least as low as that for a single genome scan and thus genome-wide significance criteria may be applied. We also demonstrate appropriate criteria for this type of meta-analysis when the most significant study is included, and when that study is used to define a region of interest and then excluded. In our simulations, meta-analysis is at least as powerful as pooling data. Finally, we apply this method of meta-analysis to the evidence for linkage of autism susceptibility loci and demonstrate evidence for a susceptibility locus at 7q. C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. RP Badner, JA (reprint author), Univ Chicago, Dept Psychiat, 5841 S Maryland Ave,MC3077, Chicago, IL 60637 USA. 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PY 2002 VL 7 IS 1 BP 56 EP 66 DI 10.1038/sj/mp/4000922 PG 11 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 509BB UT WOS:000173123500011 PM 11803446 ER PT J AU Betancur, C Corbex, M Spielewoy, C Philippe, A Laplanche, JL Launay, JM Gillberg, C Mouren-Simeoni, MC Hamon, M Giros, B Nosten-Bertrand, M Leboyer, M AF Betancur, C Corbex, M Spielewoy, C Philippe, A Laplanche, JL Launay, JM Gillberg, C Mouren-Simeoni, MC Hamon, M Giros, B Nosten-Bertrand, M Leboyer, M CA Paris Autism Res Int Sibpair Study TI Serotonin transporter gene polymorphisms and hyperserotonemia in autistic disorder SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorder; serotonin; serotonin transporter; endophenotype; association; linkage disequilibrium ID WHOLE-BLOOD SEROTONIN; DOUBLE-BLIND; RELATIVES; REGION; VARIANTS; LINKAGE; ASSOCIATION; PLATELETS; PROBANDS; FAMILIES AB Previous studies have provided conflicting evidence regarding the association of the serotonin transporter (5-HTT) gene with autism. Two polymorphisms have been identified in the human 5-HTT gene, a VNTR in intron 21 and a functional deletion/insertion in the promoter region (5-HTTLPR) with short and long variants.(2) Positive associations of the 5-HTTLPR polymorphism with autism have been reported by two family-based studies, but one found preferential transmission of the short allele(3) and the other of the long allele.(4) Two subsequent studies failed to find evidence of transmission disequilibrium at the 5-HTTLPR locus.(5,6) These conflicting results could be due to heterogeneity of clinical samples with regard to serotonin (5-HT) blood levels; which have been found to be elevated in some autistic subjects.(7-9) Thus, we examined the association of the 5-HTTLPR and VNTR polymorphisms of the 5-HTT gene with autism, and we investigated the relationship between 5-HTT variants and whole-blood 5-HT. The transmission/disequilibrium test (TDT) revealed no linkage disequilibrium at either loci in a sample of 96 families comprising 43 trios and 53 sib pairs. Furthermore, no significant relationship between 5-HT blood levels and 5-HTT gene polymorphisms was found. Our results suggest that the 5-HTT gene is unlikely to play a major role as a susceptibility factor in autism. C1 Fac Med, INSERM U513, F-94010 Creteil, France. Hop La Pitie Salpetriere, CNRS, UMR 9923, F-75013 Paris, France. Hop Albert Chenevier & Henri Mondor, Dept Psychiat, F-94000 Creteil, France. Hop Lariboisiere, Serv Biochim, F-75010 Paris, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. Hop Robert Debre, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. Univ Paris 06, INSERM U288, F-75013 Paris, France. RP Betancur, C (reprint author), Fac Med, INSERM U513, 8 Rue Gen Sarrail, F-94010 Creteil, France. 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PY 2002 VL 7 IS 1 BP 67 EP 71 DI 10.1038/sj/mp/4000923 PG 5 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 509BB UT WOS:000173123500012 PM 11803447 ER PT J AU Jamain, S Quach, H Quintana-Murci, L Betancur, C Philippe, A Gillberg, C Sponheim, E Skjeldal, OH Fellous, M Leboyer, M Bourgeron, T AF Jamain, S Quach, H Quintana-Murci, L Betancur, C Philippe, A Gillberg, C Sponheim, E Skjeldal, OH Fellous, M Leboyer, M Bourgeron, T TI Y chromosome haplogroups in autistic subjects SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; sex chromosomes; polymorphisms; haplotypes; gender difference ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; ABNORMALITIES; GENES; HAPLOTYPES; LANGUAGE; FEMALES; BRAIN; MALES AB The male to female ratio in autism is 4:1 in the global autistic population, but increases to 23:1 in autistic subjects without physical or brain abnormalities.(1) Despite this well-recognised gender difference, male predisposition to autistic disorder remains unexplained and the role of sex chromosomes is still debated. Numerical and structural abnormalities of the sex chromosomes are among the most frequently reported chromosomal disorders associated with autism. However, genome scans have failed to detect linkage on the X chromosome(2-4) and this approach cannot study the non-recombining region of the Y chromosome. In this study, we searched for a specific Y chromosome effect in autistic subjects. Using informative Y-polymorphic markers, the Y chromosome haplotypes of 111 autistic subjects from France, Sweden and Norway were defined and compared with relevant control populations. No significant difference in Y-haplotype distribution between the affected and control groups was observed. Although this study cannot exclude the presence of a Y susceptibility gene, our results are not suggestive of a Y chromosome effect in autism. C1 Inst Pasteur, Lab Immunogenet Humaine, INSERM E021, F-75015 Paris, France. Fac Med, INSERM U513, F-94000 Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. Univ Oslo, Rikshosp, Dept Pediat, N-0027 Oslo, Norway. Hop Albert Chenevier & Henri Mondor, Dept Psychiat, F-94000 Creteil, France. RP Bourgeron, T (reprint author), Inst Pasteur, Lab Immunogenet Humaine, INSERM E021, 25 Rue Dr Roux, F-75724 Paris 15, France. 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PY 2002 VL 7 IS 3 BP 229 EP 229 DI 10.1038/sj/mp/4001088 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 538MY UT WOS:000174820800001 PM 11920146 ER PT J AU Kim, SJ Cox, N Courchesne, R Lord, C Corsello, C Akshoomoff, N Guter, S Leventhal, BL Courchesne, E Cook, EH AF Kim, SJ Cox, N Courchesne, R Lord, C Corsello, C Akshoomoff, N Guter, S Leventhal, BL Courchesne, E Cook, EH TI Transmission disequilibrium mapping at the serotonin transporter gene (SLC6A4) region in autistic disorder SO MOLECULAR PSYCHIATRY LA English DT Article DE SLC6A4; SNP; FP-TDI; TDT; linkage disequilibrium; autism ID SINGLE-NUCLEOTIDE POLYMORPHISMS; BLEOMYCIN HYDROLASE; SPECTRUM DISORDERS; MOLECULAR-CLONING; CODING REGION; DOUBLE-BLIND; ASSOCIATION; EXPRESSION; VARIANTS; LINKAGE AB The serotonin transporter gene (SLC6A4, MIM 182138) is a candidate gene in autistic disorder based on neurochemical, neuroendocrine studies and the efficacy of potent serotonin transporter inhibitors in reducing ritualistic behaviors and related aggression. An Insertion/deletion polymorphism (5-HTTLPR) in the promoter region and a variable number of tandem repeat polymorphism (VNTR) in the second intron, were previously identified and suggested to modulate transcription. Six previous family-based association studies of SLC6A4 in autistic disorder have been conducted, with four studies showing nominally significant transmission disequilibrium and two studies with no evidence of nominally significant transmission disequilibrium. In the present study, TDT was conducted in 81 new trios. A previous finding of transmission disequilibrium between a haplotype consisting of the 5-HTTLPR and Intron 2 VNTR was replicated in this study, but not preferential transmission of 5-HTTLPR as an independent marker. Because of inconsistent transmission of 5-HTTLPR across studies, SLC6A4 and its flanking regions were sequenced in 10 probands, followed by typing of 20 single nucleotide polymorphisms (SNPs) and seven simple sequence repeat (SSR) polymorphisms in 115 autism trios. When individual markers were analyzed by TDT, seven SNP markers and four SSR markers (six SNPs, 5-HTTLPR and the second intron VNTR from promoter 1A through intron 2 of SLC6A4, one SSR from intron 7 of SLC6A4, one SNP from the bleomycin hydrolase gene (BLMH, MIM 602403) and one SSR telomeric to BLMH) showed nominally significant evidence of transmission disequilibrium. Four markers showed stronger evidence of transmission disequilibrium (TDTmax P = 0.0005) than 5-HTTLPR. C1 Univ Chicago, Dept Psychiat MC3077, Lab Dev Neurosci Child & Adolescent Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Childrens Hosp Res Ctr, Lab Res Neurosci Autism, La Jolla, CA USA. 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We have followed a positional candidate gene approach to identify the relevant gene and report the analysis of four adjacent genes localised to a 800 kb region in 7q32 that contains an Imprinted domain: PEG1/MEST, COPG2, CPA1 and CPA5-a previously uncharacterised member of the carboxypeptidase gene family. Screening these genes for DNA changes and association analysis using intragenic single nucleotide polymorphisms (SNPs) provided no evidence for an etiological role in IMGSAC families. We also searched for imprinting mutations potentially implicated in autism: analysis of both DNA methylation and replication timing indicated a normal imprinting regulation of the PEG1/COPG2 domain in blood lymphocytes of all patients tested. The analysis of these four genes strongly suggests that they do not play a major role In autism aetiology, and delineates our strategy to screen additional candidate genes in the AUTS1 locus. 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PY 2002 VL 7 IS 3 BP 289 EP 301 DI 10.1038/sj/mp/4001004 PG 13 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 538MY UT WOS:000174820800009 PM 11920156 ER PT J AU Jamain, S Betancur, C Quach, H Philippe, A Fellous, M Giros, B Gillberg, C Leboyer, M Bourgeron, T AF Jamain, S Betancur, C Quach, H Philippe, A Fellous, M Giros, B Gillberg, C Leboyer, M Bourgeron, T CA Paris Autism Res Int Sibpair PARIS TI Linkage and association of the glutamate receptor 6 gene with autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorder; GluR6; GRIK2; kainate; mutation screening; affected sib-pair method; TDT; linkage disequilibrium; single nucleotide polymorphism; editing; isoforms ID KAINATE RECEPTORS; SUSCEPTIBILITY LOCUS; DIABETES-MELLITUS; GENOMIC SCREEN; MESSENGER-RNAS; COMPLEX TRAITS; CHROMOSOME 6Q; Q/R SITE; GLUR6; DISORDER AB A genome scan was previously performed and pointed to chromosome 6q21 as a candidate region for autism. This region contains the glutamate receptor 6 (GluR6 or GRIK2) gene, a functional candidate for the syndrome. Glutamate is the principal excitatory neurotransmitter in the brain and is directly involved in cognitive functions such as memory and learning. We used two different approaches, the affected sib-pair (ASP) method and the transmission disequilibrium test (TDT), to investigate the linkage and association between GluR6 and autism. The ASP method, conducted with additional markers on the 51 original families and In eight new sibling pairs, showed a significant excess of allele sharing, generating an elevated multipoint maximum LOD score (ASPEX MLS = 3.28). TDT analysis, performed in the ASP families and in an independent data set of 107 parent-off spring trios, Indicated a significant maternal transmission disequilibrium (TDTall P = 0.0004). Furthermore, TDT analysis (with only one affected proband per family) showed significant association between GluR6 and autism (TDT association P = 0.008). In contrast to maternal transmission, paternal transmission of GluR6 alleles was as expected in the absence of linkage, suggesting a maternal effect such as imprinting. Mutation screening was performed in 33 affected individuals, revealing several nucleotide polymorphisms (SNPs), including one amino acid change (M8671) in a highly conserved domain of the intracytoplasmic C-terminal region of the protein. This change is found in 8% of the autistic subjects and in 4% of the control population and seems to be more maternally transmitted than expected to autistic males (P = 0.007). Taken together, these data suggest that GluR6 is in linkage disequilibrium with autism. C1 Inst Pasteur, INSERM E021, Lab Immunogenet Humaine, F-75015 Paris, France. Fac Med, INSERM U513, F-94000 Creteil, France. 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Psychiatr. PY 2002 VL 7 IS 3 BP 302 EP 310 DI 10.1038/sj/mp/4000979 PG 9 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 538MY UT WOS:000174820800010 PM 11920157 ER PT J AU Buxbaum, JD Silverman, JM Smith, CJ Greenberg, DA Kilifarski, M Reichert, J Cook, EH Fang, Y Song, CY Vitale, R AF Buxbaum, JD Silverman, JM Smith, CJ Greenberg, DA Kilifarski, M Reichert, J Cook, EH Fang, Y Song, CY Vitale, R TI Association between a GABRB3 polymorphism and autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; transmission disequilibrium test (TDT); linkage analysis; gamma-aminobutyric acid type-A receptor beta 3 subunit; epilepsy ID RECEPTOR SUBUNIT BETA-3; LINKAGE-DISEQUILIBRIUM; CHROMOSOME 15Q11-Q13; BETA(3) SUBUNIT; DISEASE; DISORDERS; EPILEPSY; FAMILIES; MICE; INDIVIDUALS AB Autistic disorder (OMIM 209850) is a disease with a significant genetic component of a complex nature(1). Cytogenetic abnormalities In the Prader-Willi/Angelman syndrome critical region (15q11-13) have been described in several individuals with autism.(1) For this reason, markers across this region have been screened for evidence of linkage and association, and a marker (155CA-2) in the gamma-aminobutyric acid type-A receptor beta3 subunit gene (GABRB3) has been associated in one study(2) but not others.(3-5) We completed an association analysis with 155CA-2 using the transmission disequilibrium test (TDT) in a set of 80 autism families (59 multiplex and 21 trios). We also used four additional markers (69CA, 155CA-1, 85CA, and A55CA-1) localized within 150 kb of 155CA-2. The use of multi-allelic TDT (MTDT) (P < 0.002), as well as the TDT (P < 0.004), demonstrated an association between autistic disorder and 155CA-2 in these families. Meiotic segregation distortion could be excluded as a possible cause for these results since no disequilibrium was observed in unaffected siblings. These findings support a role for genetic variants within the GABA receptor gene complex in 15q11-13 in autistic disorder. C1 Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Neurobiol, New York, NY 10029 USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. Univ Chicago, Dept Psychiat, Lab Dev Neurosci, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Lab Dev Neurosci, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Dev Disorders Clin, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Dev Disorders Clin, Chicago, IL 60637 USA. RP Buxbaum, JD (reprint author), Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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Psychiatr. PY 2002 VL 7 IS 3 BP 311 EP 316 DI 10.1038/sj/mp/4001011 PG 6 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 538MY UT WOS:000174820800011 PM 11920158 ER PT J AU Licinio, J Alvarado, I Wong, ML AF Licinio, J Alvarado, I Wong, ML TI Autoimmunity in autism SO MOLECULAR PSYCHIATRY LA English DT Editorial Material C1 Univ Calif Los Angeles, Los Angeles, CA 90024 USA. RP Licinio, J (reprint author), Univ Calif Los Angeles, Los Angeles, CA 90024 USA. RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013 CR Licinio J, 2002, MOL PSYCHIATR, V7, P229, DOI 10.1038/sj/mp/4001088 Licinio J, 1999, MOL PSYCHIATR, V4, P317, DOI 10.1038/sj.mp.4000586 NR 2 TC 18 Z9 20 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PY 2002 VL 7 IS 4 BP 329 EP 329 DI 10.1038/sj/mp/4001137 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 544VQ UT WOS:000175182700001 PM 11986972 ER PT J AU Torrente, F Ashwood, P Day, R Machado, N Furlano, RI Anthony, A Davies, SE Wakefield, AJ Thomson, MA Walker-Smith, JA Murch, SH AF Torrente, F Ashwood, P Day, R Machado, N Furlano, RI Anthony, A Davies, SE Wakefield, AJ Thomson, MA Walker-Smith, JA Murch, SH TI Small intestinal enteropathy with epithelial IgG and complement deposition in children with regressive autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; small intestine; inflammation; lymphocytes; immunoglobulins; autoimmunity; complement ID INFLAMMATORY-BOWEL-DISEASE; CPG-BINDING PROTEIN-2; RETT-SYNDROME; RUBELLA VACCINE; DISORDERS; AUTOANTIBODIES; ASSOCIATION; HYPERPLASIA; FREQUENCY; GENETICS AB We have reported lymphocytic colitis in children with regressive autism, with epithelial damage prominent. We now compare duodenal biopsies in 25 children with regressive autism to 11 with coeliac disease, five with cerebral palsy and mental retardation and 18 histologically normal controls. Immunohistochemistry was performed for lymphocyte and epithelial lineage and functional markers. We determined the density of intraepithelial and lamina propria lymphocyte populations, and studied mucosal immunoglobulin and complement C1q localisation. Standard histopathology showed increased enterocyte and Paneth cell numbers in the autistic children. Immunohistochemistry demonstrated increased lymphocyte infiltration in both epithelium and lamina propria with upregulated crypt cell proliferation, compared to normal and cerebral palsy controls. Intraepithelial lymphocytes and lamina propria plasma cells were lower than in coeliac disease, but lamina propria T cell populations were higher and crypt proliferation similar. Most strikingly, IgG deposition was seen on the basolateral epithelial surface in 23/25 autistic children, co-localising with complement C1q. This was not seen in the other conditions. These findings demonstrate a novel form of enteropathy in autistic children, in which increases in mucosal lymphocyte density and crypt cell proliferation occur with epithelial IgG deposition. The features are suggestive of an autoimmune lesion. C1 UCL Royal Free & Univ Coll Sch Med, Ctr Paediat Gastroenterol, London NW3 2PF, England. UCL Royal Free & Univ Coll Sch Med, Inflammatory Bowel Dis Study Grp, London NW3 2PF, England. St Marks Hosp, IBD Res Unit, London EC1V 2PS, England. UCL Royal Free & Univ Coll Med Sch, Dept Med, London, England. UCL Royal Free & Univ Coll Med Sch, Dept Histopathol, London, England. RP Murch, SH (reprint author), UCL Royal Free & Univ Coll Sch Med, Ctr Paediat Gastroenterol, Royal Free Campus,Rowland Hill St, London NW3 2PF, England. 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In preclinical studies, arginine vasopressin (AVP) has been shown to increase a range of social behaviors, including affiliation and attachment, via the V-1a receptor (AVPR1A) in the brain. Both the behavioral effects of AVID and the neural distribution of the V1a receptor vary greatly across mammalian species. This difference in regional receptor expression as well as differences in social behavior may result from a highly variable repetitive sequence in the 5' flanking region of the Via gene (AVPR1A). Given this comparative evidence for a role in inter-species variation in social behavior, we explored whether within our own species, variation in the human AVPR1A may contribute to individual variations in social behavior, with autism representing an extreme form of social impairment. We genotyped two microsatellite polymorphisms from the 5' flanking region of AVPR1A for 115 autism trios and found nominally significant transmission disequilibrium between autism and one of the microsatellite markers by Multiallelic Transmission/Disequilibrium test (MTDT) that was not significant after Bonferroni correction. We also screened approximately 2 kb of the 5' flanking region and the coding region and identified 10 single nucleotide polymorphisms. C1 Univ Chicago, Dept Psychiat, Dev Disorders Clin, Chicago, IL 60637 USA. Univ Chicago, Lab Dev Neurosci Child & Adolescent Psychiat, Dept Psychiat, Chicago, IL 60637 USA. Emory Univ, Ctr Behav Neurosci, Atlanta, GA USA. Childrens Hosp Res Ctr, Lab Res Neurosci Autism, La Jolla, CA USA. Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA USA. RP Cook, EH (reprint author), Univ Chicago, Dept Psychiat, Dev Disorders Clin, MC3077,5841 South Maryland Ave, Chicago, IL 60637 USA. 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PY 2002 VL 7 IS 5 BP 503 EP 507 DI 10.1038/sj.mp.4001125 PG 5 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 568HB UT WOS:000176535400014 PM 12082568 ER PT J AU Fatemi, SH Emamian, ES Sidwell, RW Kist, DA Stary, JM Earle, JA Thuras, P AF Fatemi, SH Emamian, ES Sidwell, RW Kist, DA Stary, JM Earle, JA Thuras, P TI Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice SO MOLECULAR PSYCHIATRY LA English DT Article DE prenatal; influenza; infection; GFAP; schizophrenia; autism; mice ID IN-UTERO; HIPPOCAMPAL ASTROCYTES; MOUSE-BRAIN; SCHIZOPHRENIA; EXPRESSION; VIRUS; NEUROPATHOLOGY; GLIOSIS; CORTEX; INJURY AB Epidemiological reports describe a strong association between prenatal human influenza viral infection and later development of schizophrenia: Postmodern human brain studies, however, indicate a lack of gliosis in schizophrenic brains presumably secondary to absence of glial cells during the second trimester viral infection in utero. We hypothesized that human influenza infection in day 9 pregnant mice would alter the expression of glial fibrillary acidic protein (GFAP, an important marker of gliosis, neuron migration, and reactive injury) in developing brains of postnatal days 0, 14 and 35 mice. Determination of cellular GFAP immunoreactivity (IR) expressed as cell density in cortex and hippocampus of control and experimental brains showed increases in GFAP-positive density in exposed cortical (P = 0.03 day 14 vs control) and hippocampal cells (P = 0.035 day 14, P = 0.034 day 35). Similarly, ependymal cell layer GFAP-IR cell counts showed increases with increasing brain age from day 0, to days 14 and 35 in infected groups (P = 0.037, day 14) vs controls. The GFAP-positive cells in prenatally exposed brains showed `hypertrophy' and more stellate morphology. These results implicate a significant role of prenatal human influenza viral infection on subsequent gliosis, which persists throughout brain development in mice from birth to adolescence. C1 Univ Minnesota, Sch Med, Div Neurosci Res, Dept Psychiat, Minneapolis, MN 55455 USA. Utah State Univ, Inst Antiviral Res, Logan, UT 84322 USA. Vet Adm Med Ctr, Minneapolis, MN 55417 USA. Univ Minnesota, Sch Med, Dept Neurosci, Div Neurosci Res, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Div Neurosci Res, Dept Psychiat, MMC 392,Mayo,420 Delaware St SE, Minneapolis, MN 55455 USA. 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PY 2002 VL 7 IS 6 BP 633 EP 640 DI 10.1038/sj.mp.4001046 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 577TT UT WOS:000177078500017 PM 12140787 ER PT J AU Persico, AM Pascucci, T Puglisi-Allegra, S Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, M Rabinowitz, D Reichelt, KL Conciatori, M Marino, R Keller, F AF Persico, AM Pascucci, T Puglisi-Allegra, S Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, M Rabinowitz, D Reichelt, KL Conciatori, M Marino, R Keller, F TI Serotonin transporter gene promoter variants do not explain the hyperserotoninemia in autistic children SO MOLECULAR PSYCHIATRY LA English DT Article DE allelic association; autism; haplotype relative risk; linkage disequilibrium; peptiduria; pervasive developmental disorders; platelets; serotoninemia; transmission disequilibrium test ID PLATELET SEROTONIN; DISORDER; ASSOCIATION; PLASMA; REGION; POLYMORPHISM; RELATIVES; LINKAGE; ALLELES; TRAITS AB Autism is a biologically-heterogeneous disease. Distinct subgroups of autistic patients may be marked by intermediate phenotypes, such as elevated serotonin (5-HT) blood levels, potentially associated with different underlying disease mechanisms. This could lead to inconsistent genetic association results, such as those of prior studies on serotonin transporter (5-HTT) gene promoter variants and autistic disorder. Contributions of 5-HTT gene promoter alleles to 5-HT blood levels were thus investigated in 134 autistic patients and 291 first-degree relatives. Mean 5-HT blood levels are 11% higher in autistic patients carrying the L/L genotype, compared to patients with the S/S or S/L genotype; this trend is not observed in first-degree relatives. The probability of inheriting L or S alleles is significantly enhanced in patients with 5-HT blood levels above or below the mean, respectively (P < 0.05), but quantitative TDT analyses yield a non-significant trend (P=0.10), as this polymorphism explains only 2.5% of the variance in 5-HT blood levels of autistic patients. In conclusion, 5-HTT gene promoter variants seemingly exert a small effect on 5-HT blood levels in autistic children, which largely does not account for hyperserotoninemia. Nonetheless, the inconsistent outcome of prior association studies could partly stem from a selection bias of hyper- or hypo-serotoninemic probands. C1 Interdisciplinary Ctr Biomed Res, Neurosci Lab, I-00155 Rome, Italy. Univ Roma La Sapienza, Dept Psychol, Rome, Italy. IRCCS Fdn Santa Lucia, Rome, Italy. Univ Naples 2, Dept Child Neuropsychiat, Naples, Italy. IRCCS Osped Bambino Gesu, Rome, Italy. Clin Autism & Dev Disabil, Rome, Italy. Columbia Univ, New York, NY USA. 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PY 2002 VL 7 IS 7 BP 795 EP 800 DI 10.1038/sj.mp.4001069 PG 6 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 585KY UT WOS:000177525000019 PM 12192626 ER PT J AU Krebs, MO Betancur, C Leroy, S Bourdel, MC Gillberg, C Leboyer, M AF Krebs, MO Betancur, C Leroy, S Bourdel, MC Gillberg, C Leboyer, M CA PARIS Study TI Absence of association between a polymorphic GGC repeat in the 5 ' untranslated region of the reelin gene and autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorder; association study; transmission disequilibrium test; neurodevelopment; reelin ID BIPOLAR DISORDER; CEREBRAL-CORTEX; GENOMIC SCREEN; SCHIZOPHRENIA; BRAIN; TWIN; CHROMOSOME-7; CEREBELLAR; EXPRESSION; MUTATIONS AB Autism is a complex neurodevelopmental disorder with severe cognitive and communication disabilities, that has a strong genetic predisposition.(1) Reelin, a protein involved in neuronal migration during development, is encoded by a gene located on 7q22,(2) within the candidate region on 7q showing increased allele sharing in previous genome scanS.(3-8) A case/control and family-based association study recently reported a positive association between a trinucleotide repeat polymorphism (GGC) located in the 5' untranslated region (UTR) of the reelin gene and autism.(9) We performed a transmission disequilibrium test (TDT) analysis of the 5, UTR polymorphism in 167 families including 218 affected subjects (117 trios and 50 affected sib pairs) and found no evidence of linkage/association. Our results do not support previous findings and suggest that this GGC polymorphism of the reelin gene is unlikely to be a major susceptibility factor in autism and/or genetic heterogeneity. C1 Univ Paris 05, Dept Mental Hlth & Therapeut, Hop St Anne, INSERM,E0117, F-75014 Paris, France. Fac Med Creteil, INSERM, U513, F-94000 Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. Hop Albert Chenevier & Henri Mondor, Dept Psychiat, F-94000 Creteil, France. RP Krebs, MO (reprint author), Hop St Anne, Serv Hospitalouniv, 7 Rue Cabanis, F-75014 Paris, France. 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Psychiatr. PY 2002 VL 7 IS 7 BP 801 EP 804 DI 10.1038/sj.mp.4001071 PG 4 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 585KY UT WOS:000177525000020 PM 12192627 ER PT J AU Anderson, GM Gutknecht, L Cohen, DJ Brailly-Tabard, S Cohen, JHM Ferrari, P Roubertoux, PL Tordjman, S AF Anderson, GM Gutknecht, L Cohen, DJ Brailly-Tabard, S Cohen, JHM Ferrari, P Roubertoux, PL Tordjman, S TI Serotonin transporter promoter variants in autism: functional effects and relationship to platelet hyperserotonemia SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT 28th Annual Meeting of the Society-for-Neuroscience CY NOV 07-12, 1998 CL LOS ANGELES, CALIFORNIA SP Soc Neurosci DE serotonin transporter; platelet 5-HT uptake; autism; platelet hyperserotonemia; 5-HTTLPR; SLC6A4 locus ID MENTAL-RETARDATION; BLOOD SEROTONIN; DOUBLE-BLIND; WHOLE-BLOOD; DISORDER; GENE; CHILDREN; GENOTYPE; BINDING; PLASMA AB The well-replicated platelet hyperserotonemia of autism has stimulated interest in serotonin (5-HT) in autism. We have examined the effects of the serotonin transporter gene (5-HTT, locus SLC6A4) promoter polymorphism (5-HTTLPR) on platelet 5-HT physiology in autism. Platelet 5-HT uptake rates and affinities (V-max and K-m), uptake site densities (B-max) and 5-HT levels were examined in 31 French individuals with autism genotyped with respect to the 5-HTTLPR. Platelet 5-HT uptake and 5-HT levels were measured using HPLC; uptake sites were determined by radioligand binding. A 1.5-fold increased rate (V-max) of platelet 5-HT uptake was observed in II genotype individuals compared to those with Is and ss genotypes (Mann-Whitney U-test, P = 0.022). However, no significant relationship was observed between genotype and uptake site density (U-test, P = 0.51). Although median levels of platelet 5-HT in platelet-rich plasma were higher in the group, only trend level significance was observed (U-test, P = 0.069); platelet 5-HT content measured in whole blood was similar across genotypes. Uptake rates were well correlated with B-max values (r = 0.66, P = 0.002); correlations between uptake and platelet 5-HT levels and between B-max values and 5-HT levels were somewhat lower. While 5-HTTLPR alleles had an appreciable effect on platelet 5-HT uptake rates, effects on 5-HT levels and uptake site density were smaller or absent. Based on these preliminary data and prior studies of allele frequencies, we conclude that the 5-HTTLPR is not a major determinant of the group mean platelet serotonin elevation seen in autism. However, a role for increased uptake in the hyperserotonemia of autism can not be ruled out. In addition, it appears that studies of platelet 5-HT measures in autism and other disorders should take account of the effects of 5-HTTLPR genotype on 5-HT uptake. C1 Yale Univ, Sch Med, Ctr Child Study, Dept Child Psychiat, New Haven, CT 06510 USA. FRE 2134 CNRS Genet, Orleans 2, France. 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Psychiatr. PY 2002 VL 7 IS 9 BP 919 EP 920 DI 10.1038/sj.mp.4001248 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 610GQ UT WOS:000178952700001 PM 12399938 ER PT J AU Zhang, H Liu, X Zhang, C Mundo, E Macciardi, F Grayson, DR Guidotti, AR Holden, JJA AF Zhang, H Liu, X Zhang, C Mundo, E Macciardi, F Grayson, DR Guidotti, AR Holden, JJA TI Reelin gene alleles and susceptibility to autism spectrum disorders SO MOLECULAR PSYCHIATRY LA English DT Article DE reelin; RELN; autism; autism spectrum disorders; allelic association; family-based association test; affected sib-pair method; phenotype-genotype correlation ID SCHIZOPHRENIA; EXPRESSION; MOUSE; REPEAT; VULNERABILITY; ASSOCIATIONS; MUTATIONS; PHENOTYPE; DECREASE; ETIOLOGY AB A polymorphic trinucleotide repeat (CGG/GCC) within the human Reelin gene (RELN) was examined as a candidate gene for autism spectrum disorders (ASDs). This gene encodes a large extracellular matrix protein that orchestrates neuronal positioning during corticogenesis. The CGG-repeat within the 5' untranslated region of RELN exon 1 was examined in 126 multiple-incidence families. The number of CGG repeats varied from three to 16 in affected individuals and controls, with no expansion or contraction observed during maternal (n = 291) or paternal (n = 287) transmissions in families with autistic probands. Although the frequencies of the RELN alleles and genotypes in affected children were not different from those in the comparison group, a family-based association test (FBAT) showed that the larger RELN alleles (greater than or equal to11 repeats) were transmitted more often than expected to affected children (S = 43, E(S) = 34.5, P = 0.035); this was particularly the case for the 13-repeat RELN allele (S = 22, E(S) = 16, P = 0.034). Affected sib-pair (ASP) analysis found no evidence of excess sharing of RELN alleles in affected siblings. The impact of genotypes with large alleles (greater than or equal to 11 repeats) on the phenotypes in individuals with ASD was analyzed by ANOVA in a subset of the families for which results of the Autism Diagnostic Interview-Revised were available. Children with large RELN alleles did not show any difference in scores for questions related to the core symptoms of autistic disorder, but there was a tendency for children with at least one large RELN allele to have an earlier age at first phrase (chi(2) = 3.538, P = 0.06). Thus, although the case-control and affected sib-pair findings did not support a role for RELN in susceptibility to ASD, the more powerful family-based association study demonstrated that RELN alleles with larger numbers of CGG repeats may play a role in the etiology of some cases of ASD, especially in children without delayed phrase speech. 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PY 2002 VL 7 SU 2 BP S1 EP S1 DI 10.1038/sj.mp.4001160 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400001 ER PT J AU Minshew, NJ Sweeney, J Luna, B AF Minshew, NJ Sweeney, J Luna, B TI Autism as a selective disorder of complex information processing and underdevelopment of neocortical systems SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting on Microbiology Immunology and Toxicology of Autism and Other Neurodevelopmental Disorders CY FEB 11-14, 2001 CL COLD SPRING HARBOR, NEW YORK C1 Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA. Univ Illinois, Dept Psychiat MC912, Chicago, IL USA. RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, 3811 O Hara St,Bellefield Suite,430 Bellefield To, Pittsburgh, PA 15213 USA. 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PY 2002 VL 7 SU 2 BP S14 EP S15 DI 10.1038/sj.mp.4001166 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400007 PM 12142935 ER PT J AU Susser, E Bresnahan, M AF Susser, E Bresnahan, M TI Epidemiologic approaches to neurodevelopmental disorders SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting on Microbiology Immunology and Toxicology of Autism and Other Neurodevelopmental Disorders CY FEB 11-14, 2001 CL COLD SPRING HARBOR, NEW YORK ID PRENATAL EXPOSURE; BIRTH COHORT; SCHIZOPHRENIA; PSYCHOSIS; RUBELLA; AUTISM; RISK C1 Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA. New York Psychiat Inst, Epidemiol Brain Disorders Dept, New York, NY USA. RP Susser, E (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, 622 W 168th St,PH18-121, New York, NY 10032 USA. CR Bower C, 2000, J PAEDIATR CHILD H, V36, P213, DOI 10.1046/j.1440-1754.2000.00480.x Brown AS, 2000, AM J PSYCHIAT, V157, P438, DOI 10.1176/appi.ajp.157.3.438 CANNON TD, 1993, ARCH GEN PSYCHIAT, V50, P551 CHESS S, 1977, J AUTISM CHILD SCHIZ, V7, P69, DOI 10.1007/BF01531116 Erlenmeyer-Kimling L, 2000, AM J MED GENET, V97, P65, DOI 10.1002/(SICI)1096-8628(200021)97:1<65::AID-AJMG9>3.0.CO;2-V JONES P, 1994, LANCET, V344, P1398, DOI 10.1016/S0140-6736(94)90569-X LANDA R, 2001, COMMUNICATION Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Schaefer CA, 2000, SCHIZOPHRENIA BULL, V26, P275 SUSSER ES, 1992, ARCH GEN PSYCHIAT, V49, P983 TORREY EF, 1975, J AUTISM CHILD SCHIZ, V5, P287, DOI 10.1007/BF01540676 Wadsworth M., 1991, IMPRINT TIME CHILDHO Wyatt RJ, 2000, SCHIZOPHRENIA BULL, V26, P255 NR 13 TC 5 Z9 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PY 2002 VL 7 SU 2 BP S2 EP S3 DI 10.1038/sj.mp.4001161 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400002 PM 12142930 ER PT J AU Taylor, B Lingam, R Simmons, A Stowe, J Miller, E Andrews, N AF Taylor, B Lingam, R Simmons, A Stowe, J Miller, E Andrews, N TI Autism and MMR vaccination in North London; no causal relationship SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting on Microbiology Immunology and Toxicology of Autism and Other Neurodevelopmental Disorders CY FEB 11-14, 2001 CL COLD SPRING HARBOR, NY ID INFLAMMATORY-BOWEL-DISEASE; MEASLES; CHILDREN; MUMPS; ASSOCIATION C1 UCL, Ctr Community Child Hlth, Royal Free & Univ Coll, Sch Med, London NW3 2PF, England. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, London NW9 5EQ, England. RP Taylor, B (reprint author), UCL, Ctr Community Child Hlth, Royal Free & Univ Coll, Sch Med, Royal Free Campus, London NW3 2PF, England. EM b.taylor@rfc.ucl.ac.uk CR Chadwick N, 1998, J MED VIROL, V55, P305 DeWilde S, 2001, BRIT J GEN PRACT, V51, P226 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 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 GERSHON M, 2001, C US HOUS REPR COMM Morrell JM, 1997, AM J PRIMATOL, V41, P37, DOI 10.1002/(SICI)1098-2345(1997)41:1<37::AID-AJP3>3.0.CO;2-0 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 THOMPSON NP, 1995, LANCET, V345, P1071, DOI 10.1016/S0140-6736(95)90816-1 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 WAKEFIELD AJ, 2001, C US HOUS REPR COMM NR 12 TC 12 Z9 12 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PY 2002 VL 7 SU 2 BP S7 EP S8 DI 10.1038/sj.mp.4001163 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400004 PM 12142932 ER PT J AU Wakefield, A AF Wakefield, A TI Enterocolitis, autism and measles virus SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting on Microbiology Immunology and Toxicology of Autism and Other Neurodevelopmental Disorders CY FEB 11-14, 2001 CL COLD SPRING HARBOR, NY ID CHILDREN; DISORDERS C1 UCL Royal Free & Univ Coll, Sch Med, Dept Med, Ctr Gastroenterol, London NW3 2PF, England. UCL Royal Free & Univ Coll, Sch Med, Ctr Paediat Gastroenterol, London NW3 2PF, England. RP Wakefield, A (reprint author), UCL Royal Free & Univ Coll, Sch Med, Dept Med, Ctr Gastroenterol, Rowland Hill St, London NW3 2PF, England. 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PY 2002 VL 7 SU 2 BP S44 EP S46 DI 10.1038/sj.mp.4001178 PG 3 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400020 PM 12142948 ER PT J AU Yeargin-Allsopp, M AF Yeargin-Allsopp, M TI Past and future perspectives in autism epidemiology SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting on Microbiology Immunology and Toxicology of Autism and Other Neurodevelopmental Disorders CY FEB 11-14, 2001 CL COLD SPRING HARBOR, NEW YORK ID PREVALENCE C1 Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabilities, Atlanta, GA 30341 USA. RP Yeargin-Allsopp, M (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabilities, Atlanta, GA 30341 USA. 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PY 2002 VL 7 SU 2 BP S9 EP S11 DI 10.1038/sj.mp.4001164 PG 3 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400005 PM 12142933 ER PT J AU Young, LJ Pitkow, L Ferguson, JN AF Young, LJ Pitkow, L Ferguson, JN TI Neuropeptides and social behavior: animal models relevant to autism SO MOLECULAR PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting on Microbiology Immunology and Toxicology of Autism and Other Neurodevelopmental Disorders CY FEB 11-14, 2001 CL COLD SPRING HARBOR, NEW YORK ID FACIAL EXPRESSIONS; MONOGAMOUS VOLE; OXYTOCIN; VASOPRESSIN; AMYGDALA; RECOGNITION; RECEPTOR; GENE C1 Emory Univ, Yerkes Res Ctr, Dept Psychiat, Atlanta, GA 30322 USA. Emory Univ, Ctr Behav Neurosci, Atlanta, GA 30322 USA. RP Young, LJ (reprint author), Emory Univ, Yerkes Res Ctr, Dept Psychiat, 954 Gatewood Dr, Atlanta, GA 30322 USA. CR ADOLPHS R, 1994, NATURE, V372, P669, DOI 10.1038/372669a0 Baron-Cohen S, 2000, NEUROSCI BIOBEHAV R, V24, P355, DOI 10.1016/S0149-7634(00)00011-7 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 Ferguson JN, 2000, NAT GENET, V25, P284, DOI 10.1038/77040 Ferguson JN, 2001, J NEUROSCI, V21, P8278 INSEL TR, 2001, NAT NEUROSCI, V3, P129 Modahl C, 1998, BIOL PSYCHIAT, V43, P270, DOI 10.1016/S0006-3223(97)00439-3 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 WILLIAMS JR, 1994, J NEUROENDOCRINOL, V6, P247, DOI 10.1111/j.1365-2826.1994.tb00579.x WINSLOW JT, 1993, NATURE, V365, P545, DOI 10.1038/365545a0 Young LJ, 2001, HORM BEHAV, V40, P133, DOI 10.1006/hbeh.2001.1691 Young LJ, 1999, NATURE, V400, P766 Pitkow LJ, 2001, J NEUROSCI, V21, P7392 NR 13 TC 46 Z9 48 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PY 2002 VL 7 SU 2 BP S38 EP S39 DI 10.1038/sj.mp.4001175 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 579AZ UT WOS:000177154400017 PM 12142945 ER PT J AU Lincoln, A Lai, Z Jones, W AF Lincoln, A Lai, Z Jones, W TI Shifting attention and joint attention dissociation in Williams syndrome: Implications for the cerebellum and social deficits in autism SO NEUROCASE LA English DT Article ID INFANTILE-AUTISM; BRAIN; ABNORMALITIES; VII AB An experimental paradigm that assesses one's capacity to perform intermodality attention shifting has proved to be sensitive for persons with cerebellar dysfunction. The basic experiment includes three conditions, auditory focus, visual focus and shift attention. In the auditory focus condition, the participant is instructed to press a joystick button when they hear the target tone and to ignore the other tone and the two visual stimuli. In the visual focus condition, the participant is instructed to press only the button to the target colored square and to ignore the other colored square and the two tones. In the shift attention condition, the participant is instructed to press the button to the first auditory target and then to press to the next visual target. They are instructed to continue to alternate their responses between auditory and visual targets until the trial is complete. Three individuals with Williams Syndrome (WMS), a genetic disorder due to the deletion of the elastin gene, were examined under these experimental conditions. Each participant with WMS had previously completed magnetic resonance imaging, and mid-sagittal area measurements had been made of the vermal lobules I-V and VI-VII. Cases were selected on the basis of cerebellar findings: one case was hypoplastic, one was hyperplastic and one had measurements in a range within one standard deviation of average for normal controls. Each of the WMS participants showed a pattern of being impaired in being able to shift their attention rapidly when cue-to-target intervals were less than 2.5 s. Their performance was very similar to previous reports of persons with cerebellar abnormalities and persons with autism. All three participants improved their target accuracy when given more time to shift their attention. The three participants did not experience performance deficits to either long or short cue-to-target intervals in the auditory focus or visual focus conditions. The results are consistent with the presence of cerebellar dysfunction, and are the first to suggest problems with shifting attention in persons with WMS. However, the three WMS participants demonstrated normal joint attention and had none of the social deficits observed in persons with autism. C1 Alliant Int Univ, Calif Sch Profess Psychol, San Diego, CA 92121 USA. Salk Inst Biol Studies, Cognit Neurosci Lab, La Jolla, CA 92037 USA. RP Lincoln, A (reprint author), Alliant Int Univ, Calif Sch Profess Psychol, 6160 Cornerstone Ct E, San Diego, CA 92121 USA. 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We present two cases of adolescents with Asperger syndrome who show extreme deficits on measures of both cognitive and affective empathy. Analysis of their performance on tasks assessing cognitive and affective processing did not reveal significant impairment in executive functions, nor in their ability to recognize emotions or the ability to create a mental representation of another person's knowledge. However, both patients were unable to integrate the emotional content with mental representations and deduce the other person's emotional state. These results suggest that impaired empathy in individuals with Asperger syndrome may be due to impaired integration of the cognitive and affective facets of the other person's mental state. C1 Univ Haifa, Dept Psychol, IL-31905 Haifa, Israel. Univ Haifa, Brain & Behav Res Ctr, IL-31905 Haifa, Israel. Rambam Med Ctr, Cognit Neurol Unit, Haifa, Israel. 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The savant's performance was compared with that of two control participants, one a departmental secretary and the other a professor of mathematics. The facility with which the savant could master the rules governing the relationships between the series of items suggests that he possessed a flexibility of mental processing transcending his ability of calendar calculation. Furthermore, he could recalibrate previous knowledge to solve new hitherto unpractised tasks. When presented with novel problems, the savant, unlike the mathematician, made no initial errors at all on any of the presented tasks, thereby indicating his fast and spontaneous recognition of new rules and of new relationships between items. It is concluded that a cognitive style of 'weak central coherence' as adopted by autistic savants may protect single representations from being retained in the form of stable enduring wholes, and that such a segmentation strategy may allow for the transformation, reorganization and reconstruction of the relationship between single items of information. C1 Univ London, Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. RP Pring, L (reprint author), Univ London, Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. 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V., 1995, MIND SAVANT SMITH NV, 1993, LINGUA, V91, P279, DOI 10.1016/0024-3841(93)90002-E Wechsler D, 1981, WECHSLER ADULT INTEL WILDING J, 1994, BRIT J PSYCHOL, V85, P231 Witkin HA, 1971, MANUAL EMBEDDED FIGU NR 28 TC 9 Z9 9 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1355-4794 J9 NEUROCASE JI Neurocase PY 2002 VL 8 IS 4 BP 330 EP 337 DI 10.1093/neucas/8.4.330 PG 8 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 604HW UT WOS:000178614100007 PM 12221146 ER PT J AU Lamb, JA Parr, JR Baile, AJ Monaco, AP AF Lamb, JA Parr, JR Baile, AJ Monaco, AP TI Autism - In search of susceptibility genes SO NEUROMOLECULAR MEDICINE LA English DT Review DE autism; pervasive developmental disorder; genetics; linkage; candidate gene; chromosomal abnormality; heterogeneity; language ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER 5-HTT; FRAGILE-X-SYNDROME; LINKAGE-DISEQUILIBRIUM; SPECTRUM DISORDERS; LANGUAGE DISORDER; INFANTILE-AUTISM; CHROMOSOME 7Q; MULTIPLEX FAMILIES; MEDICAL CONDITIONS AB Autism is a neurodevelopmental disorder of unknown etiology. There is convincing data for the involvement of genetic factors in the development of autism, and the absence of any consistent evidence for an environmental, neuroanatomical, or biochemical cause has led to an increasing number of genetic studies to determine the basis of this complex disorder. The results of recent genetic linkage and candidate gene studies are reviewed in relation to the challenge of clinical and genetic heterogeneity, and prospects for the future of genetic research in autism are considered. C1 Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Inst Psychiat, Ctr Social Genet & Dev Psychiat, London SE5 8AF, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London SE5 8AF, England. RP Monaco, AP (reprint author), Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. 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Med. PY 2002 VL 2 IS 1 BP 11 EP 28 PG 18 WC Neurosciences SC Neurosciences & Neurology GA 608VJ UT WOS:000178867600002 PM 12230302 ER PT J AU Wilcox, J Tsuang, MT Ledger, E Algeo, J Schnurr, T AF Wilcox, J Tsuang, MT Ledger, E Algeo, J Schnurr, T TI Brain perfusion in autism varies with age SO NEUROPSYCHOBIOLOGY LA English DT Article DE autism; perfusion; SPECT ID CHILDHOOD AUTISM; CHILDREN; CEREBELLAR; ADOLESCENTS; DISORDER; STEM AB Our subjects consisted of 14 autistic individuals and 14 controls ranging in age from 3 to 37 years. A Tc-99m HMPAO single photon emission computed tomogram (SPECT) was used to examine blood flow variations between autistic subjects, compared to an age- and gender-matched control group. We found significant hypoperfusion in the prefrontal areas of autistic individuals as compared to normals in every case (p < 0.01). 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Evidence suggests that ASD may be accompanied by aberrant (inflammatory) innate immune responses. This may predispose ASD children to sensitization to common dietary proteins (DP), leading to GI inflammation and aggravation of some behavioral symptoms. Methods: We measured IFN-gamma, IL-5, and TNF-alpha production against representative DPs [gliadin, cow's milk protein (CMP), and soy] by peripheral blood mononuclear cells (PBMCs) from ASD and control children [those with DP intolerance (DPI), ASD siblings, and healthy unrelated children]. We evaluated the results in association with proinflammatory and counter-regulatory cytokine production with endotoxin (LPS), a microbial product of intestinal flora and a surrogate stimulant for innate immune responses. Results: ASD PBMCs produced elevated IFN-gamma and TNF-alpha, but not IL-5 with common DPs at high frequency as observed in DPI PBMCs. ASD PBMCs revealed increased proinflammatory cytokine responses with LPS at high frequency with positive correlation between proinflammatory cytokine production with LPS and IFN-gamma and TNF-alpha production against DPs. Such correlation was less evident in DPI PBMCs. Conclusion: Immune reactivity to DPs may be associated with apparent DPI and GI inflammation in ASD children that may be partly associated with aberrant innate immune response against endotoxin, a product of the gut bacteria. Copyright (C) 2002 S. KargerAG, Basel. C1 Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA. RP Jyonouchi, H (reprint author), Univ Med & Dent New Jersey, Dept Pediat, Div Allergy Immunol Pulm ID, 185 S Orange Ave, Newark, NJ 07103 USA. 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Products of the IRS, such as proinflammatory cytokines, may induce some of the behavioral symptoms of autism, such as social withdrawal, resistance to novelty and sleep disturbances. The main aim of the present study was to examine whether autism is accompanied by an activation of the IRS. Methods: We measured the production of interleukin (IL)-6, IL-10, the IL-1 receptor antagonist (IL-1RA), interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha by whole blood and the serum concentrations of IL-6, the IL-2 receptor (IL-2R) and IL-1RA. Results: This study showed a significantly increased production of IFN-gamma and IL-1RA and a trend toward a significantly increased production of IL-6 and TNF-alpha by whole blood of autistic children. There were no significant differences in the serum concentrations of IL-6, IL-2R and IL-1RA between autistic and normal children. Conclusions: These results suggest that autism may be accompanied by an activation of the monocytic (increased IL-1RA) and Th-1-like (increased IFN-)gamma arm of the IRS. It is hypothesized that increased production of proinflammatory cytokines could play a role in the pathophysiology of autism. Copyright (C) 2002 S. Karger AG, Basel. C1 Univ Ctr Child & Adolescent Psychiat, Antwerp, Belgium. Eurogenetics, Tessenderlo, Belgium. Acad Hosp Maastricht, Dept Psychiat & Neuropsychol, Maastricht, Netherlands. Clin Res Ctr Mental Hlth, Antwerp, Belgium. Vanderbilt Univ, Dept Psychiat, Nashville, TN USA. Inst Fatebenefratelli, IRCCS, Brescia, Italy. RP Maes, M (reprint author), Univ Hosp Maastricht, Dept Psychiat & Neuropsychol, Postbus 5800, NL-6202 AZ Maastricht, Netherlands. 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In addition, there have been hints from studies with individuals with autism that these cognitive subsystems can fractionate developmentally. However, there has been a paucity of systematic investigations. The present study involves the analysis of visual memory of a population of individuals with autism and age- and VIQ-matched comparison individuals. The individuals with autism presented selective impairments in face recognition in comparison to both the age- and VIQ-matched comparison populations. In addition, they were impaired relative to the age-matched comparison group on recognition memory for potential agents (i.e. objects capable of self-propelled motion) whether they were living (cats and horses) or non-living (motorbikes). In contrast, they were selectively superior relative to the VIQ-matched comparison group on recognition memory for such objects as topographical stimuli (buildings) and leaves that clearly do not have agency. The data is interpreted in terms of reduced sensitivity to agency cues in individuals with autism and general information processing capacity. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 UCL, Inst Cognit Neurosci, London WC1H 3AR, England. UCL, Dept Psychol, London WC1H 6BT, England. Natl Hosp Neurol & Neurosurg, Dept Clin Neuropsychol, London WC1N 3BG, England. RP Blair, RJR (reprint author), UCL, Inst Cognit Neurosci, Alexandra House,17 Queen Sq, London WC1H 3AR, England. 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However, people with autism haw been found to perform worse than ability-matched controls when verbal materials to be remembered are semantically related. In normal subjects, semantic processing of verbal materials facilitates LTM better than 'shallow' (phonological or perceptual) processing, which is known as the levels-of-processing effect. In this study, the relationship between LTM and semantic processing was investigated using a levels-of-processing task. In Study 1, a levels-of-processing task was conducted on healthy volunteers, which confirmed the levels-of-processing effect with our task. In study 2, the same task was conducted on autistic subjects with mild or no mental retardation and ability-matched controls. The levels-of-processing effect was confirmed in the control group. Although overall performance in the two groups was comparable, the levels-of-processing effect was not found in the autistic group. LTM resulting from perceptual processing was better in the autistic group than in the control group, indicating superior `rote memory' in individuals with autism. Furthermore, the pattern of correlations between LTM performance and cognitive measures differed greatly between the two groups. The lack of the levels-of-processing effect, which has not been reported in other psychiatric or neurapathological conditions, suggests an abnormal relationship between semantic memory and episodic memory in individuals with autism. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Case Western Reserve Univ, Univ Hosp Cleveland, Div Child & Adolescent Psychiat, Cleveland, OH 44106 USA. Kyoto Grad Univ, Fac Med, Dept Psychiat, Kyoto, Japan. RP Toichi, M (reprint author), Case Western Reserve Univ, Univ Hosp Cleveland, Div Child & Adolescent Psychiat, Cleveland, OH 44106 USA. 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Cambridge, MA: MIT Press, 1997] has suggested that the interpretation of gaze plays an important role in a normal functioning theory of mind (ToM) system. Consistent with this suggestion, functional imaging research has shown that both ToM tasks and eye gaze processing engage a similar region of the posterior superior temporal sulcus (STS). However, a second brain region associated with ToM, the medial prefrontal (MPF) cortex, has not been identified by previous eye gaze studies. We discuss the methodological issues that may account for the absence of MPF activation in these experiments and present a PET study that controls for these factors. Our experiment included three conditions in which the proportions of faces gazing at. and away from, the participant, were as follows: 100% direct [0% averted]. 50% direct-50% averted, and 100,70 horizontally averted [0% direct]. Two control conditions were also included in which the faces' gaze were averted down, or their eyes were closed. Contrasts comparing the gaze conditions with each of the control conditions revealed medial frontal involvement. Parametric analyses showed a significant linear relationship between increasing proportions of horizontally averted gaze and increased rCBF in the MPF cortex. The opposite parametric analysis (increasing proportions of direct gaze) was associated with increased rCBF in a number of areas including the superior and medial temporal gyri. Additional subtraction contrasts largely confirmed these patterns. Our results demonstrate a considerable degree of overlap between the medial frontal areas involved in eye gaze processing and theory of mind tasks. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 MRC, Cognit & Brain Sci Unit, Cambridge CB2 2EF, England. UCL, Dept Psychol, London WC1E 6BT, England. Univ Amsterdam, Dept Psychol, NL-1018 WB Amsterdam, Netherlands. Univ York, Dept Psychol, York YO1 5DD, N Yorkshire, England. RP Calder, AJ (reprint author), MRC, Cognit & Brain Sci Unit, 15 Chaucer Rd, Cambridge CB2 2EF, England. EM andy.calder@mrc-cbu.cam.ac.uk RI Scott, Sophie/A-1843-2010; Lawrence, Andrew/A-1673-2010; Young, Andy/G-2189-2011; Owen, Adrian/B-4997-2015 OI Young, Andy/0000-0002-1202-6297; CR Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 Ashburner J, 1997, NEUROIMAGE, V6, P344, DOI 10.1006/nimg.1997.0299 BAN T, 1991, ARCH ITAL BIOL, V129, P259 Baron-Cohen Simon, 1997, MINDBLINDNESS ESSAY Brett M, 2001, NEUROIMAGE, V13, pS85 Brunet E, 2000, NEUROIMAGE, V11, P157, DOI 10.1006/nimg.1999.0525 Castelli F, 2000, NEUROIMAGE, V12, P314, DOI 10.1006/nimg.2000.0612 Driver J, 1999, VIS COGN, V6, P509 Emery NJ, 2000, NEUROSCI BIOBEHAV R, V24, P581, DOI 10.1016/S0149-7634(00)00025-7 FLETCHER PC, 1995, COGNITION, V57, P109, DOI 10.1016/0010-0277(95)00692-R Friesen CK, 1998, PSYCHON B REV, V5, P490, DOI 10.3758/BF03208827 Friston KJ, 1994, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402 Frith CD, 1999, SCIENCE, V286, P1692, DOI 10.1126/science.286.5445.1692 Gallagher HL, 2000, NEUROPSYCHOLOGIA, V38, P11, DOI 10.1016/S0028-3932(99)00053-6 George N, 2001, NEUROIMAGE, V13, P1102, DOI 10.1006/nimg.2001.0769 Gusnard DA, 2001, NAT REV NEUROSCI, V2, P685, DOI 10.1038/35094500 Haxby JV, 2000, TRENDS COGN SCI, V4, P223, DOI 10.1016/S1364-6613(00)01482-0 HIKOSAKA K, 1993, BIOMED RES-TOKYO, V14, P41 Hoffman EA, 2000, NAT NEUROSCI, V3, P80, DOI 10.1038/71152 Jellema T, 2000, BRAIN COGNITION, V44, P280, DOI 10.1006/brcg.2000.1231 Kampe KKW, 2001, NATURE, V413, P589, DOI 10.1038/35098149 Kawashima R, 1999, BRAIN, V122, P779, DOI 10.1093/brain/122.4.779 KINAHAN PE, 1989, IEEE T NUCL SCI, V35, P680 Langton SRH, 1999, VIS COGN, V6, P541 McGuire PK, 1996, BRAIN, V119, P907, DOI 10.1093/brain/119.3.907 McGuire PK, 1996, NEUROREPORT, V7, P2095 NICHOLS KA, 1971, J EXP SOC PSYCHOL, V7, P623, DOI 10.1016/0022-1031(71)90024-2 PERRETT DI, 1992, PHILOS T ROY SOC B, V335, P23, DOI 10.1098/rstb.1992.0003 PERRETT DI, 1989, J EXP BIOL, V146, P87 Puce A, 1998, J NEUROSCI, V18, P2188 Wicker B, 1998, NEUROIMAGE, V8, P221, DOI 10.1006/nimg.1998.0357 WICKER B, UNPUB FUNCTIONAL NEU Worsley KJ, 1996, HUM BRAIN MAPP, V4, P58, DOI 10.1002/(SICI)1097-0193(1996)4:1<58::AID-HBM4>3.0.CO;2-O NR 33 TC 153 Z9 158 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2002 VL 40 IS 8 BP 1129 EP 1138 DI 10.1016/S0028-3932(02)00008-8 PG 10 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 548DQ UT WOS:000175373700003 PM 11931917 ER PT J AU Wilding, J Cornish, K Munir, F AF Wilding, J Cornish, K Munir, F TI Further delineation of the executive deficit in males with fragile-X syndrome SO NEUROPSYCHOLOGIA LA English DT Article DE false alarms; inhibition; response switching; reponse repetition; Down's syndrome; fragile-X syndrome ID CGG REPEAT; DEVELOPMENTAL PSYCHOPATHOLOGY; FMR1 GENE; PHENOTYPE; INHIBITION; MUTATION; PROFILE; AUTISM; RETURN; WOMEN AB This paper presents a detailed analysis of one aspect of performance by young males with fragile-X syndrome (FMR-1 full mutation) who were assessed on a computerised visual search task as part of a larger study examining aspects of attention [Neuropsychologia 38 (2000) 1261]. They were matched on chronological and mental age to 25 boys with Down's syndrome (trisomy 2 1) and on mental age to 50 mainstream school boys (controls). The controls were further divided into those matched on "poor attention" to the fragile-X boys and a "good" attention group, as rated by the comprehensive teacher rating scale (ACTeRS) questionnaire. Both fragile-X and Down's syndrome boys made significantly more repeated responses on targets (but a lower proportion of errors based on confusion of shape) than the two control groups and these differences were stronger in the fragile-X group. In the single target condition, search was for a single type of target throughout. In the dual target condition, participants were required to alternate between two different targets. Fragile-X boys showed significantly greater inability than Down's syndrome and normal boys to switch attention between targets and both learning-disabled groups were inferior to the control groups. Thus, both learning-disabled groups displayed a weakness in inhibiting repetition and in switching attention from one type of target to another and the impairments were more acute in fragile-X boys. The results provide further support for an attention deficit in this population at higher levels of attention control/executive functioning that involve switching visual attention and inhibiting repetitious behaviour. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ London, Royal Holloway & Bedford New Coll, Dept Psychol, Egham TW20 0EX, Surrey, England. Univ Nottingham, Queens Med Ctr, Div Psychiat, Sect Dev Psychiat, Nottingham NG7 2RD, England. RP Wilding, J (reprint author), Univ London, Royal Holloway & Bedford New Coll, Dept Psychol, Egham TW20 0EX, Surrey, England. 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K., 1984, PSYCHOPHARMACOLOGY B, V21, P339 VERKERK AJMH, 1991, CELL, V65, P905, DOI 10.1016/0092-8674(91)90397-H NR 32 TC 63 Z9 65 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2002 VL 40 IS 8 BP 1343 EP 1349 DI 10.1016/S0028-3932(01)00212-3 PG 7 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 548DQ UT WOS:000175373700023 PM 11931937 ER PT J AU Goldberg, MC Lasker, AG Zee, DS Garth, E Tien, A Landa, RJ AF Goldberg, MC Lasker, AG Zee, DS Garth, E Tien, A Landa, RJ TI Deficits in the initiation of eye movements in the absence of a visual target in adolescents with high functioning autism SO NEUROPSYCHOLOGIA LA English DT Article DE high functioning autism (HFA); ocular motor; eye movements; saccades ID NIGRA PARS RETICULATA; MONKEY CAUDATE NEURONS; PERVASIVE DEVELOPMENTAL DISORDERS; OCULOMOTOR FUNCTIONS; SUBSTANTIA NIGRA; CORTICAL CONTROL; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; GUIDED SACCADES; PREDICTIVE SACCADES AB Background: We used ocular motor paradigms to examine whether or not saccades are impaired in individuals with high functioning autism (HFA). Methods: We recorded eye movements in patients with HFA (n = 11), and in normal adolescents (n = 11) on anti-saccade, memory-guided saccade (MGS), predictive saccade and gap/overlap tasks. Results: Compared with the normal subjects, patients with HFA had (1) a significantly higher percentage of directional errors on the anti-saccade task (63.2% versus 26.6%), (2) a significantly higher percentage of response suppression errors on a MGS task (60.3% versus 29.5%) and (3) a significantly lower percentage of predictive eye movements on a predictive saccade task. They also showed longer latencies on a MGS task and for all conditions tested on a gap/null/overlap task (fixation target extinguished before, simultaneously, or after the new peripheral target appeared). When the latencies during the gap condition were subtracted from the latencies in the overlap condition, there was no difference between patients and normals. Conclusions: Abnormalities in ocular motor function in patients with HFA provide preliminary evidence for involvement of a number of brain regions in HFA including the dorsolateral prefrontal cortex (dIPFC) and the frontal eye fields (FEFs) and possibly the basal ganglia and parietal lobes. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA. Kennedy Krieger Inst, Baltimore, MD 21205 USA. RP Goldberg, MC (reprint author), Johns Hopkins Univ, Sch Med, 707 N Broadway,Suite 522, Baltimore, MD 21205 USA. 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The present study extends these prior findings to a more naturalistic face perception task. Matching tasks required subjects to indicate when a target face matched one of two probe faces. Matches could be either across-field, requiring inter-hemi spheric interaction, or within-field, not requiring inter-hemispheric interaction. Subjects indicated when faces matched in emotional expression (Experiment 1; n = 32) or in character identity (Experiment 2; n = 32). In both experiments, across-field performance was significantly better than within-field performance, supporting the primary hypothesis. Further, this advantage was greater for the more difficult character identity task. Results offer qualified support for the hypothesis that inter-hemispheric interaction is especially advantageous as task demands increase. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Haverford Coll, Dept Psychol, Haverford, PA 19041 USA. RP Compton, RJ (reprint author), Haverford Coll, Dept Psychol, 370 Lancaster Ave, Haverford, PA 19041 USA. CR Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 ADOLPHS R, 1999, NEUROPSYCHOLOGIA, V37, P111 BANICH MT, 1990, CORTEX, V26, P77 BANICH MT, 1998, BRAIN COGNITION, V36, P138 BANICH MT, 1994, NEUROPSYCHOLOGY, V8, P263, DOI 10.1037/0894-4105.8.2.263 Belger A, 1998, NEUROPSYCHOLOGY, V12, P380, DOI 10.1037/0894-4105.12.3.380 BELGER A, 1992, NEUROPSYCHOLOGIA, V30, P923, DOI 10.1016/0028-3932(92)90036-L Bobes MA, 2000, COGNITIVE BRAIN RES, V9, P249, DOI 10.1016/S0926-6410(00)00003-3 Burgund ED, 1997, BRAIN COGNITION, V35, P239, DOI 10.1006/brcg.1997.0940 Calder AJ, 1996, VIS COGN, V3, P81, DOI 10.1080/713756735 Celani G, 1999, J AUTISM DEV DISORD, V29, P57, DOI 10.1023/A:1025970600181 Compton RJ, 2001, NEUROPSYCHOLOGY, V15, P427, DOI 10.1037/0894-4105.15.4.427 EKMAN P, 1987, J PERS SOC PSYCHOL, V53, P712, DOI 10.1037/0022-3514.53.4.712 Ekman P., 1976, PICTURES FACIAL AFFE EKMAN P, 1971, J PERS SOC PSYCHOL, V17, P124, DOI 10.1037/h0030377 EKMAN P, 1994, PSYCHOL BULL, V115, P268, DOI 10.1037//0033-2909.115.2.268 ETCOFF NL, 1992, COGNITION, V44, P227, DOI 10.1016/0010-0277(92)90002-Y Farah MJ, 1996, BEHAV BRAIN RES, V76, P181, DOI 10.1016/0166-4328(95)00198-0 Forster B, 2000, NEUROPSYCHOLOGIA, V38, P32, DOI 10.1016/S0028-3932(99)00050-0 GAUTHIER I, 2000, COGNITIVE NEUROPSYCH, V17, P117 Gilboa-Schechtman E, 1999, COGNITION EMOTION, V13, P305, DOI 10.1080/026999399379294 Hellige JB, 2000, BRAIN COGNITION, V42, P7, DOI 10.1006/brcg.1999.1146 HELLIGE JB, 1988, BRAIN COGNITION, V7, P39, DOI 10.1016/0278-2626(88)90020-6 HUMPHREYS GW, 1993, NEUROPSYCHOLOGIA, V31, P173, DOI 10.1016/0028-3932(93)90045-2 Ley R.G., 1986, NEUROPSYCHOLOGY FACE, P269 Liederman J, 1998, BRAIN COGNITION, V36, P193, DOI 10.1006/brcg.1997.0952 Lundqvist D, 1999, COGNITION EMOTION, V13, P691 Marsolek CJ, 1999, PSYCHOL SCI, V10, P111, DOI 10.1111/1467-9280.00117 McCarthy G., 2000, NEW COGNITIVE NEUROS, P393 MEROLA JL, 1990, INT J NEUROSCI, V51, P35, DOI 10.3109/00207459009000506 Mogg K, 1999, COGNITION EMOTION, V13, P713 Munte TF, 1998, NEUROSCI RES, V30, P25, DOI 10.1016/S0168-0102(97)00118-1 NORMAN WD, 1992, CORTEX, V28, P623 Reuter-Lorenz PA, 1999, PSYCHOL SCI, V10, P494, DOI 10.1111/1467-9280.00195 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 Sergent J., 1994, VIS COGN, V1, P349, DOI 10.1080/13506289408402305 Sergent Justine, 1995, P157 Tovee MJ, 1998, NEURON, V21, P1239, DOI 10.1016/S0896-6273(00)80644-3 Weissman DH, 2000, J INT NEUROPSYCH SOC, V6, P313, DOI 10.1017/S1355617700633064 Weissman DH, 1999, J EXP PSYCHOL GEN, V128, P283, DOI 10.1037/0096-3445.128.3.283 Weissman DH, 2000, NEUROPSYCHOLOGY, V14, P41, DOI 10.1037//0894-4105.14.1.41 Young AW, 1997, COGNITION, V63, P271, DOI 10.1016/S0010-0277(97)00003-6 NR 42 TC 19 Z9 19 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2002 VL 40 IS 13 BP 2409 EP 2419 DI 10.1016/S0028-3932(02)00078-7 PG 11 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 623RH UT WOS:000179716300019 PM 12417469 ER PT J AU Jepsen, RH VonThaden, K AF Jepsen, RH VonThaden, K TI The effect of cognitive education on the performance of students with neurological developmental disabilities SO NEUROREHABILITATION LA English DT Article ID CURRICULUM AB A cognitive education program was developed to facilitate acquisition of cognitive skills and address the learning deficits of adolescent students with neurological, developmental disabilities, and autism. This study examined the outcomes of incorporating mediated cognitive education into special education classrooms. Cognitive education provided cognitive training utilizing REHABlT materials through mediated teaching. Following a matched pair model, forty-six students were assigned to either a treatment or a control group. All students received weekly instruction in Individual Educational Program (IEP) goals. Curriculum areas included IEP objectives in reading, math, social skills, health, science and social studies. Students in the control group received regular classroom instruction. Students in the treatment group participated in cognitive educated one hour per week replacing thirty minutes of reading and thirty minutes of math. Pre and posttest comparisons on measures of intelligence, achievement and adaptive behavior showed those students in the treatment group attained higher scores across measures. C1 Bancroft NeuroHlth, Clin Serv, Haddonfield, NJ 08033 USA. 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W., 1989, WOODCOCK JOHNSON PSY NR 50 TC 4 Z9 4 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1053-8135 J9 NEUROREHABILITATION JI Neurorehabilitation PY 2002 VL 17 IS 3 BP 201 EP 209 PG 9 WC Clinical Neurology; Rehabilitation SC Neurosciences & Neurology; Rehabilitation GA 611AJ UT WOS:000178994000004 PM 12237500 ER PT J AU Boddaert, N Zilbovicius, M AF Boddaert, N Zilbovicius, M TI Functional neuroimaging and childhood autism SO PEDIATRIC RADIOLOGY LA English DT Article; Proceedings Paper CT 37th Annual Meeting of the European-Society-of-Pediatric-Radiology CY MAY, 2000 CL LISBON, PORTUGAL SP European Soc Pediat Radiol DE autism; functional imaging; temporal lobe ID CEREBRAL BLOOD-FLOW; POSITRON EMISSION TOMOGRAPHY; GLUCOSE-UTILIZATION; ASPERGER-SYNDROME; SCAN FINDINGS; BRAIN; METABOLISM; CHILDREN; SPECT; PET AB Childhood autism is now widely viewed as being of developmental neurobiological origin. Yet, localised structural and functional brain correlates of autism have to be established. Structural brain-imaging studies performed in autistic patients have reported abnormalities such as increased total brain volume and cerebellar abnormalities. However, none of these abnormalities fully account for the full range of autistic symptoms. Functional brain imaging, such as positron emission tomography (PET), single photon emission computed tomography (SPECT) and functional MRI (fMRI) have added a new perspective to the study of normal and pathological brain functions. In autism, functional studies have been performed at rest or during activation. However, first-generation functional imaging devices were not sensitive enough to detect any consistent dysfunction. Recently, with improved technology, two independent groups have reported bilateral hypoperfusion of the temporal lobes in autistic children. In addition, activation studies, using perceptive and cognitive paradigms, have shown an abnormal pattern of cortical activation in autistic patients. These results suggest that different connections between particular cortical regions could exist in autism. The purpose of this review is to present the main results of rest and activation studies performed in autism. C1 Hop Necker Enfants Malad, Serv Radiol Pediat, F-75015 Paris, France. CEA, DSV, DRM, Serv Hosp Frederic Joliot, Orsay, France. CHU Bretonneau, INSERM Unite 316, F-37044 Tours, France. RP Boddaert, N (reprint author), Hop Necker Enfants Malad, Serv Radiol Pediat, 149 Rue Sevres, F-75015 Paris, France. CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th BACHEVALIER J, 1994, NEUROPSYCHOLOGIA, V32, P627, DOI 10.1016/0028-3932(94)90025-6 Bachevalier J., 1994, NEUROBIOLOGY AUTISM, P146 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Boddaert N., 1999, Society for Neuroscience Abstracts, V25, P894 BODDAERT N, 2000, SOC NEUR ABSTR, V26, P2007 BODDAERT N, 2001, PEDIAT RADIOL S1, V31, pS3 DEVOLDER A, 1987, BRAIN DEV-JPN, V9, P581 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 CAMPBELL M, 1982, AM J PSYCHIAT, V139, P510 CHIRON C, 1995, DEV MED CHILD NEUROL, V37, P849 Chugani HT, 1996, ANN NEUROL, V39, P643, DOI 10.1002/ana.410390514 CHUGANI HT, 1987, ANN NEUROL, V22, P487, DOI 10.1002/ana.410220408 COURCHESNE E, 1988, NEW ENGL J MED, V318, P1349, DOI 10.1056/NEJM198805263182102 COURCHESNE E, 1994, NEUROLOGY, V44, P214 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 DAMASIO H, 1980, ARCH NEUROL-CHICAGO, V37, P504 FILIPEK PA, 1995, CURR OPIN NEUROL, V8, P134, DOI 10.1097/00019052-199504000-00009 Friston KJ, 1994, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402 GARREAU B, 1994, DEV BRAIN DYSFUNCT, V7, P119 GILBERG C, 1992, BIOL AUTISTIC SYNDRO GILLBERG C, 1983, J AUTISM DEV DISORD, V13, P19, DOI 10.1007/BF01531356 Gillberg IC, 1993, EUROPEAN CHILD ADOLE, V2, P50 Gloor P., 1997, TEMPORAL LOBE LIMBIC Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 HEROLD S, 1988, PSYCHOL MED, V18, P823 HIER DB, 1979, J AUTISM DEV DISORD, V9, P153, DOI 10.1007/BF01531531 HORWITZ B, 1988, ARCH NEUROL-CHICAGO, V45, P749 Kanner L, 1943, NERV CHILD, V2, P217 MOUNTZ JM, 1995, J NUCL MED, V36, P1156 Muller RA, 1999, J AUTISM DEV DISORD, V29, P19, DOI 10.1023/A:1025914515203 Ohnishi T, 2000, BRAIN, V123, P1838, DOI 10.1093/brain/123.9.1838 Pandya D.N., 1985, CEREB CORTEX, V4, P3 PIVEN J, 1990, AM J PSYCHIAT, V147, P734 PIVEN J, 1992, BIOL PSYCHIAT, V31, P491, DOI 10.1016/0006-3223(92)90260-7 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Ring HA, 1999, BRAIN, V122, P1305, DOI 10.1093/brain/122.7.1305 RUMSEY JM, 1985, ARCH GEN PSYCHIAT, V42, P448 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 SELTZER B, 1978, BRAIN RES, V149, P1, DOI 10.1016/0006-8993(78)90584-X SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x Talairach J., 1988, COPLANAR STEREOTAXIC ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 Zilbovicius M, 2000, AM J PSYCHIAT, V157, P1988, DOI 10.1176/appi.ajp.157.12.1988 ZILBOVICIUS M, 1995, NEUROLOGY, V45, P3 ZILBOVICIUS M, 1992, AM J PSYCHIAT, V149, P924 NR 47 TC 53 Z9 55 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD JAN PY 2002 VL 32 IS 1 BP 1 EP 7 PG 7 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA 516GR UT WOS:000173546000001 PM 11819054 ER PT J AU Gandhi, S Rubinstein, I Tsueshita, T Onyuksel, H AF Gandhi, S Rubinstein, I Tsueshita, T Onyuksel, H TI Secretin self-assembles and interacts spontaneously with phospholipids in vitro SO PEPTIDES LA English DT Article DE surface tension; monolayer; critical micellar concentration; micelle; circular dichroism; neuropeptide; vasopressin DSPE-PEG ID VASOACTIVE-INTESTINAL-PEPTIDE; LIPOSOMES; POLYPEPTIDE; FORMULATION; VIP AB Secretin, a 27-amino acid neuropeptide, is a member of the secretin/glucagon/vasoactive intestinal polypeptide (VIP) superfamily of amphipathic peptides. The peptide modulates gastrointestinal and neuronal function and is currently being evaluated for the treatment of autism. However, as most peptides, it has a short circulation half-life. Previously. we have shown that VIP self-assembles in aqueous environment and interacts with a biomimetic phospholipid membrane. These in vitro characteristics increase VIP half-life and bioactivity in vivo. The purpose of this study was to investigate whether secretin exhibits similar properties in vitro by forming micelles in aqueous solution and interacting with phospholipids. Results of this study demonstrated that secretin self-assembles to form micelles in HEPES buffer at 25degreesC above similar to0.4 muM. Additionally, secretin interacts with a biomimetic phospholipid membrane as indicated from a significant increase in membrane surface pressure (from 25.5 +/- 1.3 to 32.5 +/- 3.0, P < 0.05). Importantly. the peptide undergoes conformational transition from predominantly random coil in saline to alpha-helix in the presence of phospholipid. distetroyl-phosphatidylcholine-poly(ethylene) glycol (mol mass 2000) micelles. We suggest that these distinct biophysical attributes could modulate secretin bioactivity in vivo. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Univ Illinois, Dept Bioengn, Chicago, IL 60612 USA. Univ Illinois, Dept Pharmaceut & Pharmacodynam, Chicago, IL 60612 USA. Univ Illinois, Dept Med, Chicago, IL 60612 USA. Chicago VA Hlth Care Syst, W Side Div, Chicago, IL 60612 USA. RP Onyuksel, H (reprint author), Univ Illinois, Dept Bioengn, Chicago, IL 60612 USA. 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The case documents the progressive deterioration of cognitive and social competencies. Given the paucity of research and information with respect to CDD, further clinical investigation is suggested. (C) 2002 John Wiley Sons, Inc. C1 Univ Connecticut, Dept Educ Psychol, Storrs, CT 06269 USA. RP Bray, MA (reprint author), Univ Connecticut, Dept Educ Psychol, 249 Glenbrook Rd,U-64, Storrs, CT 06269 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BROWN L, 1990, TESTS NONVERBAL INTE BURD L, 1988, J CHILD PSYCHOL PSYC, V29, P155, DOI 10.1111/j.1469-7610.1988.tb00700.x CORBETT J, 1987, J MENT DEFIC RES, V31, P349 Dawson G., 1997, EFFECTIVENESS EARLY, P307 Dowrick PW, 1999, APPL PREV PSYCHOL, V8, P23, DOI 10.1016/S0962-1849(99)80009-2 Dunn L. 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Schools PD JAN PY 2002 VL 39 IS 1 BP 101 EP 109 DI 10.1002/pits.10003 PG 9 WC Psychology, Educational SC Psychology GA 509BG UT WOS:000173124000010 ER PT J AU Carr, JE Dozier, CL Patel, MR Adams, AN Martin, N AF Carr, JE Dozier, CL Patel, MR Adams, AN Martin, N TI Treatment of automatically reinforced object mouthing with noncontingent reinforcement and response blocking: experimental analysis and social validation SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE automatic reinforcement; object mouthing; noncontingent reinforcement; response blocking ID BEHAVIOR; EXTINCTION; PUNISHMENT AB A brief functional analysis indicated the object mouthing of a Young girl diagnosed with autism was maintained independent of social consequences. Separate and combined effects of response blocking and noncontingent reinforcement (with preferred stimuli) were then evaluated as treatments for object mouthing. Although both interventions were unsuccessful when implemented separately, combining them resulted in generalized reductions that were socially valid. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. Univ Florida, Gainesville, FL USA. Marcus Inst, Atlanta, GA USA. Univ Nevada, Reno, NV 89557 USA. RP Carr, JE (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. CR FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Lalli JS, 1997, J APPL BEHAV ANAL, V30, P127, DOI 10.1901/jaba.1997.30-127 Lerman DC, 1996, J APPL BEHAV ANAL, V29, P231, DOI 10.1901/jaba.1996.29-231 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P437, DOI 10.1901/jaba.1996.29-437 Roscoe EM, 1998, J APPL BEHAV ANAL, V31, P635, DOI 10.1901/jaba.1998.31-635 Thompson RH, 1998, J APPL BEHAV ANAL, V31, P103, DOI 10.1901/jaba.1998.31-103 Thompson RH, 1999, J APPL BEHAV ANAL, V32, P317, DOI 10.1901/jaba.1999.32-317 Vollmer TR, 1995, J APPL BEHAV ANAL, V28, P561, DOI 10.1901/jaba.1995.28-561 NR 8 TC 15 Z9 15 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD JAN-FEB PY 2002 VL 23 IS 1 BP 37 EP 44 DI 10.1016/S0891-4222(01)00090-7 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 561XB UT WOS:000176167400003 PM 12071394 ER PT J AU Higbee, TS Carr, JE Pate, MR AF Higbee, TS Carr, JE Pate, MR TI The effects of interpolated reinforcement on resistance to extinction in children diagnosed with autism: a preliminary investigation SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE interpolated reinforcement; continuous reinforcement; autism ID BEHAVIOR AB Studies on the "interpolation of reinforcement" effect (IRE) suggest that switching from an intermittent (INT) to a continuous (CRF) reinforcement schedule may result in less resistance to extinction than if extinction had followed INT alone. The finding has been examined with both human and animal participants using both free- and restricted-operant research preparations with equivocal results. In the present study, the IRE was examined in four young children diagnosed with autism using a free-operant preparation. Participants were matched into pairs and were exposed, in a counterbalanced order, to extinction following CRF "interpolated" between INT and extinction, and to extinction following INT alone. Resistance to extinction was examined by comparing the number of responses emitted during extinction and the number of sessions required to reach an extinction criterion. Responding may be less resistant to extinction following interpolated CRF reinforcement than following INT alone. Methodological refinements necessary for more conclusively demonstrating the IRE are discussed. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Nevada, Reno, NV 89557 USA. RP Higbee, TS (reprint author), Spectrum Ctr, 2855 Telegraph Ave,Suite 312, Berkeley, CA 94705 USA. 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Dev. Disabil. PD JAN-FEB PY 2002 VL 23 IS 1 BP 61 EP 78 DI 10.1016/S0891-4222(01)00092-0 PG 18 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 561XB UT WOS:000176167400005 PM 12071396 ER PT J AU Bibby, P Eikeseth, S Martin, NT Mudford, OC Reeves, D AF Bibby, P Eikeseth, S Martin, NT Mudford, OC Reeves, D TI Progress and outcomes for children with autism receiving parent-managed intensive interventions (vol 22, pg 425, 2001) SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Correction DE autism; intensive behavioral treatment; UCLA model ID PERVASIVE DEVELOPMENTAL DISORDER; BEHAVIORAL TREATMENT; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; LANGUAGE; AGE; INDIVIDUALS; PROJECT AB Parent-managed behavioral interventions for young children with autism are Under-researched. We analysed data from 66 children served by 25 different early intervention consultants. After a mean of 31.6 months of intervention, IQ scores had not changed (N = 22). Vineland adaptive behavior scores had increased significantly by 8.9 points (N = 21). No children aged >72 months attained normal functioning, i.e., IQ > 85 and unassisted mainstream school placement (N = 42). Progress for 60 children across 12 months was found for mental age (5.4 months), adaptive behavior (9.7 months), and language (5.1 months). The interventions did not reproduce results from clinic-based professionally directed programs. The effectiveness of the parent-managed intervention model as it has developed and the adequacy of professional services in that model are discussed. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 ADDER, London SE22 9AQ, England. Akershus Coll, Oslo, Norway. Keele Univ, Keele, Staffs, England. Univ Manchester, Manchester, Lancs, England. RP Bibby, P (reprint author), ADDER, 62 Oakhurst Grove, London SE22 9AQ, England. 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Dev. Disabil. PD JAN-FEB PY 2002 VL 23 IS 1 BP 79 EP + DI 10.1016/S0891-4222(02)00094-X PG 25 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 561XB UT WOS:000176167400006 ER PT J AU Charman, T Ruffman, T Clements, W AF Charman, T Ruffman, T Clements, W TI Is there a gender difference in false belief development? SO SOCIAL DEVELOPMENT LA English DT Article DE theory of mind; false belief; gender ID INDIVIDUAL-DIFFERENCES; MIND DEVELOPMENT; SEX-DIFFERENCES; YOUNG-CHILDREN; VERBAL-ABILITY; EMOTION; AUTISM; TALK; LANGUAGE; AGE AB The contribution of children's social environment to their acquisition of theory of mind skills, combined with the well documented advantage for girls in mental state talk with siblings, peers and mothers, might lead to a female advantage on false belief tasks. We present a post-hoc analysis of large datasets from two independent laboratories. A slight advantage for girls on false belief task performance was found in both datasets and was only apparent in younger but not older children. Language ability could be controlled for only in a smaller subsample of one dataset and cannot be ruled out as a potential mediator of this effect. However, if there is an age-specific advantage for girls in false belief acquisition it is a weak effect only. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. Univ Sussex, Brighton BN1 9RH, E Sussex, England. RP Charman, T (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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Dev. PY 2002 VL 11 IS 1 BP 1 EP 10 DI 10.1111/1467-9507.00183 PG 10 WC Psychology, Developmental SC Psychology GA 520FC UT WOS:000173769500001 ER PT J AU Torres, AR Nield, A Ward, D AF Torres, AR Nield, A Ward, D TI SSP and SSO typing of class I and class IIHLA alleles from amplified DNA from subjects with autism SO TISSUE ANTIGENS LA English DT Meeting Abstract C1 Utah State Univ, Ctr Person Disabil, Logan, UT 84322 USA. Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PY 2002 VL 59 SU 2 BP 61 EP 61 PG 1 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA 564JM UT WOS:000176311300193 ER PT J AU Fido, A Dashti, H Al-Saad, S AF Fido, A Dashti, H Al-Saad, S TI Biological correlates of childhood autism: "trace elements" SO TRACE ELEMENTS AND ELECTROLYTES LA English DT Article DE biological correlates; trace element concentrations in hair; childhood autism ID CHILDREN; ZINC AB Objectives: Our aim was to determine if concentrations of certain minerals in the hair of autistic children were significantly different from those in non-autistic children and whether there are direct correlations between trace elements and diagnosis of autism. Material and methods: Fourty male children from single-incidence autism family aged 3 - 7 years with diagnosis of autism were studied. The study samples were compared with age-matched sampler of 40 normal children. Results: The mean concentration of calcium, zinc, magnesium, copper, manganese and chromium in the hair of autistic children were significantly lower (p < 0.05) than the mean level of age- and sex-matched healthy controls. Discriminant function analysis correctly classified 36 (90%) of the normal children and all 40 autistic children. The 4 elements with discriminatory power were calcium, copper, zinc and chromium. Conclusions: The results of this study prevail the potential for further insight into possible biomechanism underlying autism phenomenon. Data suggest that trace element concentration pattern in hair can be used as an additional diagnostic tool for autism. C1 Kuwait Univ, Fac Med, Dept Psychiat, Safat 13110, Kuwait. Kuwait Autism Ctr, Kuwait, Kuwait. Trace Element Inc, Kuwait, Kuwait. RP Fido, A (reprint author), Kuwait Univ, Fac Med, Dept Psychiat, POB 24923, Safat 13110, Kuwait. 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Electrolytes PY 2002 VL 19 IS 4 BP 205 EP 208 PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 608UQ UT WOS:000178865400008 ER PT J AU Wiedebusch, S Petermann, F AF Wiedebusch, S Petermann, F TI Interventions for promoting emotional competence in children SO ZEITSCHRIFT FUR KLINISCHE PSYCHOLOGIE PSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article ID AUTISM AB Emotional understanding and emotional regulation in children can be improved by age appropriate emotional skills interventions. in this article preventive parenting programmes to support emotional development in infants and toddlers, preventive interventions to foster emotional competence in preschool and elementary school children and therapeutic interventions to enhance emotional understanding in children with special risks are discussed. These interventions differ in procedure and focus. 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PY 2002 VL 50 IS 4 BP 368 EP 386 PG 19 WC Psychology, Clinical SC Psychology GA 605XD UT WOS:000178701600002 ER PT J AU Bolte, S Uhlig, N Poustka, F AF Bolte, S Uhlig, N Poustka, F TI The savant syndrome: A review SO ZEITSCHRIFT FUR KLINISCHE PSYCHOLOGIE UND PSYCHOTHERAPIE LA German DT Review DE idiot savant; mentally retarded; review; autism; cognitive abilities ID IDIOT-SAVANT; CALENDRICAL CALCULATORS; AUTISTIC SAVANT; MEMORY; ABILITIES; ARTISTS AB Background: The term savant-syndrome describes a condition of general intellectual impairment, mental or sensory disorder, appearing with an extraordinary performance within a limited area of cognitive function. Objective: To give a contemporary view on the description, prevalence, neuropsychology, and theories of the syndrome. Methods: On the basis of historical reports and current empirical data, the state of the art regarding the phenomenon is summarized and discussed. Results: The savant phenomenon includes talents in the areas of memory, drawing, music, calculation and reading, and still lacks adequate definition. Cases showing truly spectacular islets of abilities are scarce. More often subjects exhibit splinter skills. These competencies are only outstanding because they emerge in parallel with a dominating psychopathology. It seems that the prevalence of savants is elevated in autism. In the past, various attempts were undertaken to explain the savant condition, mostly based on case-studies. Among others, rote memory, cognitive strategies, low-level information processing, extensive rehearsal, genetic factors and cerebral characteristics have been suggested to be involved in the development of the savant-syndrome. Conclusions: Due to the heterogeneity of the phenomenon a non-uniform etiology of the condition is likely. C1 Klinikum JWG Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, D-60528 Frankfurt, Germany. 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Univ British Columbia, Dept Pediat, Vancouver, BC V6T 1W5, Canada. RP Fraser, FC (reprint author), 81 Chute Rd, Bear River, NS B0S 1B0, Canada. CR Arbour L, 1996, CLIN GENET, V50, P57 Miles JH, 2000, AM J MED GENET, V95, P339, DOI 10.1002/1096-8628(20001211)95:4<339::AID-AJMG9>3.0.CO;2-B NR 2 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD DEC 15 PY 2001 VL 104 IS 4 BP 342 EP 342 DI 10.1002/ajmg.10072 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 498JP UT WOS:000172506600015 PM 11754072 ER PT J AU Fatemi, SH Halt, AR AF Fatemi, SH Halt, AR TI Altered levels of Bcl2 and p53 proteins in parietal cortex reflect deranged apoptotic regulation in autism SO SYNAPSE LA English DT Article ID GENE-EXPRESSION C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Dept Neurosci, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Box 392,Mayo Bldg,420 Delaware St SE, Minneapolis, MN 55455 USA. CR Araki N, 2000, ELECTROPHORESIS, V21, P1880, DOI 10.1002/(SICI)1522-2683(20000501)21:9<1880::AID-ELPS1880>3.3.CO;2-0 Fatemi SH, 2001, NEUROREPORT, V12, P929, DOI 10.1097/00001756-200104170-00013 Jarskog LF, 2000, BIOL PSYCHIAT, V48, P641, DOI 10.1016/S0006-3223(00)00988-4 MIYASHITA T, 1994, ONCOGENE, V9, P1799 Sharova L, 2000, TERATOLOGY, V62, P420, DOI 10.1002/1096-9926(200012)62:6<420::AID-TERA9>3.0.CO;2-8 NR 5 TC 48 Z9 48 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0887-4476 J9 SYNAPSE JI Synapse PD DEC 15 PY 2001 VL 42 IS 4 BP 281 EP 284 DI 10.1002/syn.10002 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 488UE UT WOS:000171953500010 PM 11746727 ER PT J AU Bolton, PF Dennis, NR Browne, CE Thomas, NS Veltman, MWM Thompson, RJ Jacobs, P AF Bolton, PF Dennis, NR Browne, CE Thomas, NS Veltman, MWM Thompson, RJ Jacobs, P TI The phenotypic manifestations of interstitial duplications of proximal 15q with special reference to the autistic spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; chromosome 15; duplication; PWACR; imprinting; 15q11-q13 ID DIAGNOSTIC OBSERVATION SCHEDULE; DEVELOPMENTAL DELAY; CHROMOSOME 15Q; REGION; PATIENT; 15Q11-13; AMPLIFICATION; SIMILARITIES; INDIVIDUALS; EPILEPSY AB This study investigated the phenotypic manifestations of interstitial duplications of chromosome 15 that involve the Prader-Willi/Angelman syndrome critical region (PWACR). Twenty-one affected individuals from six families were evaluated in detail, using standardized and semi-standardized measures of intelligence, psychopathology, and physical anomalies. Special attention was placed on determining the prevalence of autism spectrum disorders as well as the relationship between the parental origin of the duplication and the phenotypic effects. Assessments of the affected individuals were compared with evaluations of the unaffected relatives from the same families. Results indicated that duplications in the region were associated with variable degrees of intellectual impairments and motor coordination problems. Four of the subjects received a diagnosis of pervasive developmental disorder. Three of these cases were probands and only one met criteria for classic autism. There was very little evidence of the duplication cosegregating with autism spectrum disorder diagnosis. Paternally inherited duplications were significantly less likely to give rise to phenotypic effects. The findings indicate that duplications in the PWACR give rise to developmental delay but not necessarily autism spectrum disorders. They also suggest that phenotypic expression is dependent on the parental origin of the duplication and implicate maternally active genes in the pathogenesis of the developmental impairments. Further research will be required to clarify the range and basis of the phenotypic manifestations. (C) 2001 Wiley-Liss, Inc.(dagger). C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England. Univ Southampton, Dept Human Genet, Southampton, Hants, England. Salisbury District Hosp, Wessex Reg Genet Lab, Salisbury, Wilts, England. RP Bolton, PF (reprint author), Univ Cambridge, Dev Psychiat Sect, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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J. Med. Genet. PD DEC 8 PY 2001 VL 105 IS 8 BP 675 EP 685 DI 10.1002/ajmg.1551 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 497TE UT WOS:000172470900005 PM 11803514 ER PT J AU Tentler, D Brandberg, G Betancur, C Gillberg, C Anneren, G Orsmark, C Green, ED Carlsson, B Dahl, N AF Tentler, D Brandberg, G Betancur, C Gillberg, C Anneren, G Orsmark, C Green, ED Carlsson, B Dahl, N TI A balanced reciprocal translocation t(5;7)(q14;q32) associated with autistic disorder: Molecular analysis of the chromosome 7 breakpoint SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; balanced reciprocal translocation; 7q31-q32; breakpoint mapping ID IDENTIFICATION; HYBRIDIZATION; TWIN; 7Q31 AB Autism is a neuropsychiatric disorder characterized by impairments in social interaction, restricted and stereotypic pattern of interest with onset by 3 years of age. The results of genetic linkage studied for autistic disorder (AD) have suggested a susceptibility locus for the disease on the long arm of chromosome 7. We report a girl with AD and a balanced reciprocal translocation t(5;7)(q14;q32). The mother carries the translocation but do not express the disease. Fluorescent in situ hybridization (FISH) analysis with chromosome 7-specific YAC clones showed that the breakpoint coincides with the candidate region for AD. We identified a PAC clone that spans the translocation breakpoint and the breakpoint was mapped to a 2 kb region. Mutation screening of the genes SSBP and T2R3 located just centromeric to the breakpoint was performed in a set of 29 unrelated autistic sibling pairs who shared at least one chromosome 7 haplotype. We found no sequence variations, which predict amino acid alterations. Two single nucleotide polymorphisms were identified in the T2R3 gene, and associations between allele variants and AD in our population were not found. The methylation pattern of different chromosome 7 regions in the patient's genomic DNA appears normal. Here we report the clinical presentation of the patient with AD and the characterization of the genomic organization across the breakpoint at 7q32. The precise localization of the breakpoint on 7q32 may be relevant for further linkage studies and molecular analysis of AD in this region. Published 2001 Wiley-Liss, Inc.(dagger). C1 Univ Uppsala, Rudbeck Lab, Clin Genet Unit, Dept Genet & Pathol, S-75185 Uppsala, Sweden. Falun Cty Hosp, Falun, Sweden. Fac Med Creteil, INSERM, U513, Paris, France. Sahlgrens Univ Hosp, S-41345 Gothenburg, Sweden. NHGRI, NIH, Bethesda, MD 20892 USA. RP Tentler, D (reprint author), Univ Uppsala, Rudbeck Lab, Clin Genet Unit, Dept Genet & Pathol, S-75185 Uppsala, Sweden. 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PD DEC 8 PY 2001 VL 105 IS 8 BP 729 EP 736 DI 10.1002/ajmg.1607 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 497TE UT WOS:000172470900012 PM 11803521 ER PT J AU Barrett, S Beck, JC Bernier, R Bisson, E Braun, TA Casavant, TL Childress, D Folstein, SE Garcia, M Gardiner, MB Gilman, S Haines, JL Hopkins, K Landa, R Meyer, NH Mullane, JA Nishimura, DY Palmer, P Piven, J Purdy, J Santangelo, SL Searby, C Sheffield, V Singleton, J Slager, S Struchen, T Svenson, S Vieland, V Wang, K Winklosky, B AF Barrett, S Beck, JC Bernier, R Bisson, E Braun, TA Casavant, TL Childress, D Folstein, SE Garcia, M Gardiner, MB Gilman, S Haines, JL Hopkins, K Landa, R Meyer, NH Mullane, JA Nishimura, DY Palmer, P Piven, J Purdy, J Santangelo, SL Searby, C Sheffield, V Singleton, J Slager, S Struchen, T Svenson, S Vieland, V Wang, K Winklosky, B CA Collaborative Linkage Study Autism TI An autosomal genomic screen for autism (vol 88, pg 609, 1999) SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Correction DE affected sib-pair; linkage; autism ID MULTIPLE-SCLEROSIS; LINKAGE ANALYSIS; LOD SCORES; SEROTONIN TRANSPORTER; DISORDER; INDIVIDUALS; INHERITANCE; 15Q11-13; FAMILIES; BEHAVIOR AB Autism is a severe neurodevelopmental disorder defined by social and communication deficits and ritualistic-repetitive behaviors that are detectable in early childhood. The etiology of idiopathic autism is strongly genetic, and oligogenic transmission is likely. The first stage of a two-stage genomic screen for autism was carried out by the Collaborative Linkage Study of Autism on individuals affected with autism from 75 families ascertained through an affected sib-pair. The strongest multipoint results were for regions on chromosomes 13 and 7. The highest maximum multipoint heterogeneity LOD (MMLS/het) score is 3.0 at D13S800 (approximately 55 cM from the telomere) under the recessive model, with an estimated 35% of families linked to this locus. The next highest peak is an MMLS/het score of 2.3 at 19 cM, between D13S217 and D13S1229. Our third highest MMLS/het score of 2.2 is on chromosome 7 and is consistent with the International Molecular Genetic Study of Autism Consortium report of a possible susceptibility locus somewhere within 7q31-33. These regions and others will be followed up in the second stage of our study by typing additional markers in both the original and a second set of identically ascertained autism families, which are currently being collected. By comparing results across a number of studies, we expect to be able to narrow our search for autism susceptibility genes to a small number of genomic regions. (C) 1999 Wiley-Liss, Inc. RI Slager, Susan/B-6756-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON MA, 1984, IN VITRO CELL DEV B, V20, P856 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAKER P, 1994, J AUTISM DEV DISORD, V24, P529, DOI 10.1007/BF02172133 Barrett S, 1999, AM J MED GENET, V88, P609 BASSAM BJ, 1991, ANAL BIOCHEM, V196, P80, DOI 10.1016/0003-2697(91)90120-I BLACKWELDER W C, 1985, Genetic Epidemiology, V2, P85, DOI 10.1002/gepi.1370020109 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 1997, MOL PSYCHIATR, V2, P247 Durner M, 1999, AM J HUM GENET, V64, P281, DOI 10.1086/302181 Ebers GC, 1996, NAT GENET, V13, P472, DOI 10.1038/ng0896-472 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 GREENBERG DA, 1989, AM J MED GENET, V34, P480, DOI 10.1002/ajmg.1320340406 GREENBERG DA, 1994, AM J HUM GENET, V55, P834 Haines JL, 1996, NAT GENET, V13, P469, DOI 10.1038/ng0896-469 Hauser ER, 1996, GENET EPIDEMIOL, V13, P117, DOI 10.1002/(SICI)1098-2272(1996)13:2<117::AID-GEPI1>3.0.CO;2-5 Haynes C., 1995, American Journal of Human Genetics, V57, pA193 HODGE SE, 1994, GENET EPIDEMIOL, V11, P329, DOI 10.1002/gepi.1370110403 Hodge SE, 1997, AM J HUM GENET, V60, P217 *INT MOL GEN STUD, 1998, AM J HUM GENET S, V63, pA298 Bailey A, 1998, HUM MOL GENET, V7, P571 Klauck SM, 1997, HUM MOL GENET, V6, P2233, DOI 10.1093/hmg/6.13.2233 KNAPP M, 1994, HUM HERED, V44, P44, DOI 10.1159/000154188 Kruglyak L, 1996, AM J HUM GENET, V58, P1347 Kuokkanen S, 1997, AM J HUM GENET, V61, P1379, DOI 10.1086/301637 LATHROP GM, 1985, AM J HUM GENET, V37, P482 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lord C., 1997, HDB AUTISM PERVASIVE, P195 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 PERICEKVANCE M, 1997, AM J HUM GENET S, V61, pS40 Raven JC., 1956, COLOURED PROGR MATRI RITVO ER, 1989, AM J PSYCHIAT, V146, P1032 SANTANGELO SL, 1999, NEURODEVELOPMENTAL D, P431 Sawcer S, 1996, NAT GENET, V13, P464, DOI 10.1038/ng0896-464 SCHEETZ TE, 1998, GENOMAP DISTRIBUTED 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 SHEFFIELD VC, 1995, HUM MOL GENET, V4, P1837, DOI 10.1093/hmg/4.10.1837 SMITH CAB, 1963, ANN HUM GENET, V27, P175, DOI 10.1111/j.1469-1809.1963.tb00210.x SPARROW SS, 1985, J PEDIATR PSYCHOL, V10, P215, DOI 10.1093/jpepsy/10.2.215 Suarez BK, 1994, GENETIC APPROACHES M, P23 VIELAND VJ, 1992, GENET EPIDEMIOL, V9, P45, DOI 10.1002/gepi.1370090106 Vieland VJ, 1996, AM J HUM GENET, V58, P1072 WANG K, GEN AN WORKSH AN GEN, V11 NR 43 TC 3 Z9 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. 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PD DEC 8 PY 2001 VL 105 IS 8 BP 805 EP + PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 497TE UT WOS:000172470900026 ER PT J AU Bradford, Y Braun, T Cassavant, T Folstein, S Haines, J Hutcheson, H Gardiner, M Huang, W Piven, J Santangelo, S Sheffield, V Vieland, V Wang, K AF Bradford, Y Braun, T Cassavant, T Folstein, S Haines, J Hutcheson, H Gardiner, M Huang, W Piven, J Santangelo, S Sheffield, V Vieland, V Wang, K CA Collaborative Linkage Study Autism TI Incorporating language phenotypes strengthens evidence of linkage to autism (vol 105, pg 539, 2001) SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Correction DE autism; language; linkage; analysis; parental phenotypes ID SINGLE-LOCUS APPROXIMATIONS; FAMILY HISTORY; OLIGOGENIC TRAITS; DISORDER; INDIVIDUALS; PARENTS; HETEROGENEITY; PERSONALITY; STRATEGIES; 15Q11-13 AB We investigated the effect of incorporating information about proband and parental structural language phenotypes into linkage analyses in the two regions for which we found the highest signals in our first-stage affected sibling pair genome screen: chromosomes 13q and 7q. We were particularly interested in following up on our chromosome 7q finding in light of two prior reports of linkage of this region to developmental language disorder, since one of the diagnostic criteria for autism is absent or abnormal language development. We hypothesized that if the language phenotype were genetically relevant to linkage at the chromosome 7q locus, then incorporating parents phenotypes would increase the signal at that locus, and most of the signal would originate from the subset of families in which both probands had severe language delay. The results support these hypotheses. The linkage signals we obtained on chromosome 7q as well as at least one signal on chromosome 13q are mainly attributable to the subgroup of families in which both probands had language delay. This became apparent only when the parents' history of language-related difficulties was also incorporated into the analyses. Although based on our data, we were not able to distinguish between epistasis or heterogeneity models, we tentatively concluded that there may be more than one autism susceptibility locus related to language development. (C) 2001 Wiley-Liss, Inc. 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Child variables (play level, motor imitation ability and joint attention) and environmental variables (socioeconomic status and hours of speech/language therapy between ages 2 and 3) were used to predict an aggregate measure of language outcome at age 4, After controlling for age 2 language skills, the only significant predictors were motor imitation and number of hours of speech/language therapy. Implications of these results for understanding the early developmental course of autism spectrum disorders and the effects of intervention are discussed. C1 Vanderbilt Univ, Vanderbilt Child Dev Ctr, Nashville, TN 37232 USA. RP Stone, WL (reprint author), Vanderbilt Univ, Vanderbilt Child Dev Ctr, 426 Med Ctr S,2100 Pierce Ave, Nashville, TN 37232 USA. 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I: A developmental approach to early intervention SO AUTISM LA English DT Article DE autism; early intervention; parent training; treatment ID JOINT ATTENTION; CHILDREN AB Early intervention is an area of intense current interest for parents and professionals. This article describes a mainstream National Health Service (NHS) approach to early intervention, developed at the Scottish Centre for Autism. The aims of treatment are to improve the child's early social communication and social interaction skills, leading to the potential development of play and flexibility of behaviour This is achieved by 1:1 intensive treatment by trained therapists, and a schedule of parent training. The treatment protocol incorporates a child led approach; the use of imitation as a therapeutic strategy; using language contingent on activities; and the introduction of flexibility into play and social exchanges. C1 Scottish Ctr Autism, Yorkhill NHS Trust, Dept Child & Family Psychiat, Glasgow G3 8SJ, Lanark, Scotland. RP Salt, J (reprint author), Scottish Ctr Autism, Yorkhill NHS Trust, Dept Child & Family Psychiat, Glasgow G3 8SJ, Lanark, Scotland. CR DAWSON G, 1984, J ABNORM CHILD PSYCH, V12, P209, DOI 10.1007/BF00910664 Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 TOMASELLO M, 1986, CHILD DEV, V57, P1454, DOI 10.1111/j.1467-8624.1986.tb00470.x Freeman BJ, 1997, J AUTISM DEV DISORD, V27, P641, DOI 10.1023/A:1025850715183 Hoare P., 1996, CLIN CHILD PSYCHOL P, V1, P229, DOI 10.1177/1359104596012005 *INT ASS AUT EUR, 2000, DESCR AUT Kaufman B. N, 1976, SON RISE LEWY AL, 1992, J ABNORM CHILD PSYCH, V20, P555, DOI 10.1007/BF00911240 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MCDADE A, 1996, PARTNERSHIP PARENTS Nadel J., 1993, NEW PERSPECTIVES EAR *NAS, 2000, NAS EARL BIRD PROGR SALT J, 1999, CLIN PSYCHOL FORUM, V132, P15 SALT J, IN PRESS AUTISM, V6 SHIELDS J, 1999, BRIT J THERAPY REHAB, V6, P526 Smith T, 1999, CLIN PSYCHOL-SCI PR, V6, P33, DOI 10.1093/clipsy/6.1.33 TIEGERMAN E, 1984, J AUTISM DEV DISORD, V14, P27, DOI 10.1007/BF02408553 Watson LR, 1998, J AUTISM DEV DISORD, V28, P51, DOI 10.1023/A:1026063003289 WEITZMAN E, 1997, IMPRINT NEWSLETTER I, V18, P10 NR 19 TC 4 Z9 4 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2001 VL 5 IS 4 BP 362 EP 373 DI 10.1177/1362361301005004003 PG 12 WC Psychology, Developmental SC Psychology GA 503WA UT WOS:000172823500003 PM 11777254 ER PT J AU Zercher, C Hunt, P Schuler, A Webster, J AF Zercher, C Hunt, P Schuler, A Webster, J TI Increasing joint attention, play and language through peer supported play SO AUTISM LA English DT Article DE integration; play; play groups; twins ID AUTISTIC-CHILDREN; PRETEND PLAY AB The purpose of the present study was to examine the effects of participation in an integrated play group on the joint atten- tion, symbolic play and language behavior of two young boys with autism. Two 6-year-old twin brothers participated in this study, along with three typically developing girls, ages 5, 9 and 11. A multiple base-line design was used with three phases: no intervention, intervention with adult coaching, and intervention without adult coaching. After being trained, the three typically developing children implemented the integrated play group techniques in 30 minute weekly play group sessions for over 16 weeks. Results indicate that participation in the integrated play group produced dramatic increases in shared attention to objects, symbolic play acts, and verbal utterances on the part of the participants with autism. These increases were maintained when adult support was withdrawn. Implications of these findings for inclusion of children with autism are discussed. C1 San Francisco State Univ, San Francisco, CA 94132 USA. RP Zercher, C (reprint author), SRI Int, Mailstop 135104,333 Ravenswood Ave, Menlo Pk, CA 94025 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th AUWARTER M, 1986, CHILDRENS WORLDS CHI BOUCHER J, 1990, BRIT J DEV PSYCHOL, V8, P205 Bruner J. S., 1983, CHILDS TALK LEARNING Charman T, 1997, J AUTISM DEV DISORD, V27, P325, DOI 10.1023/A:1025806616149 CORSARO WA, 1986, CHILDRENS WORLDS CHI Guralnick M., 1992, SOCIAL COMPETENCE YO, P37 Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 JARROLD C, 1993, J AUTISM DEV DISORD, V23, P281, DOI 10.1007/BF01046221 Kazdin A. E., 1982, SINGLE CASE RES DESI LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MUNDY P, 1995, DEV PSYCHOPATHOL, V7, P63 ODOM SL, 1993, INTEGRATING YOUNG CH Piaget J, 1962, PLAY DREAMS IMITATIO RICKS DM, 1975, J AUTISM CHILD SCHIZ, V5, P191, DOI 10.1007/BF01538152 SHCULER AL, 2000, TRANSACTIONAL FDN LA SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 Vygotsky L. S., 1962, THOUGHT LANGUAGE Werner H., 1963, SYMBOL FORMATION ORG Wolfberg P. J., 1999, PLAY IMAGINATION CHI WOLFBERG PJ, 1993, CHILD LANGUAGE TEACH, V15, P41 WOLFBERG PJ, 1995, INT PLAY J, V3, P38 WOLFBERG PJ, 1993, J AUTISM DEV DISORD, V23, P467, DOI 10.1007/BF01046051 NR 24 TC 31 Z9 33 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2001 VL 5 IS 4 BP 374 EP 398 DI 10.1177/1362361301005004004 PG 25 WC Psychology, Developmental SC Psychology GA 503WA UT WOS:000172823500004 PM 11777255 ER PT J AU Magiati, I Howlin, P AF Magiati, I Howlin, P TI Monitoring the progress of preschool children with autism enrolled in early intervention programmes - Problems in cognitive assessment SO AUTISM LA English DT Article DE cognitive assessment; early intervention; progress ID BEHAVIORAL TREATMENT; YOUNG-CHILDREN; STABILITY; LANGUAGE; AGE; INTELLIGENCE; SCORES AB This report examines how conclusions about the progress of preschool children enrolled in early intervention programmes may be influenced by the use of different cognitive assessment tools. As part of a longitudinal treatment outcome study, 24 children with autism aged between 27 and 58 months were each tested on the Bayley, Merrill-Palmer and Vineland scales. Their performance on each of these tests was compared. Results showed that, while scores on the different tests were highly correlated, actual test scores varied considerably, With the Bayley Lending to produce the lowest IQ scores and the Merrill-Palmer the highest. These findings have important implications, as it is evident that judgements about the effects of therapy may be significantly influenced by the selection of the tests for pre- and post-treatment assessments. Possible ways of collecting, recording and reporting test data, so as to avoid spurious conclusions about treatment effects, are discussed. C1 St George Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. RP Magiati, I (reprint author), St George Hosp, Sch Med, Dept Psychol, Cranmer Terrace, London SW17 0RE, England. RI Howlin, Patricia/A-7622-2011 CR *AM GUID SERV, 1997, MULL SCAL EARL LEARN BallabanGil K, 1996, PEDIATR NEUROL, V15, P217, DOI 10.1016/S0887-8994(96)00219-6 Bayley N, 1993, BAYLEY SCALES INFANT CLARK P, 1981, J AUTISM DEV DISORD, V11, P201, DOI 10.1007/BF01531685 CLARK P, 1979, J CHILD PSYCHOL PSYC, V20, P271, DOI 10.1111/j.1469-7610.1979.tb00514.x FREEMAN BJ, 1985, J AM ACAD CHILD PSY, V24, P459, DOI 10.1016/S0002-7138(09)60565-3 GOODE S, UNPUB FOLLOW UP STUD Gresham FM, 1998, J AUTISM DEV DISORD, V28, P5, DOI 10.1023/A:1026002717402 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 HOWLIN P, 1994, EUR J DISORDER COMM, V29, P279 Howlin P, 1987, TREATMENT AUTISTIC C Koegel LK, 1997, J AUTISM DEV DISORD, V27, P233, DOI 10.1023/A:1025894213424 KOEGEL RL, 1985, J CHILD PSYCHOL PSYC, V26, P185, DOI 10.1111/j.1469-7610.1985.tb02259.x Lewis M, 1985, HDB INTELLIGENCE THE, P505 LOCKYER L, 1969, BRIT J PSYCHIAT, V115, P865, DOI 10.1192/bjp.115.525.865 LORD C, 1989, J AUTISM DEV DISORD, V19, P483, DOI 10.1007/BF02212853 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LORD C, 1989, J CHILD PSYCHOL PSYC, V30, P575, DOI 10.1111/j.1469-7610.1989.tb00269.x LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MAGIATI I, 2000, 1 MALT INT C AUT JUL Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 Sparrow S, 1984, VINELAND ADAPTIVE BE Stutsman R., 1948, MERRILL PALMER SCALE Wechsler D., 1990, WECHSLER PRESCHOOL P NR 24 TC 37 Z9 39 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2001 VL 5 IS 4 BP 399 EP 406 DI 10.1177/1362361301005004005 PG 8 WC Psychology, Developmental SC Psychology GA 503WA UT WOS:000172823500005 PM 11777256 ER PT J AU Gabriels, RL Hill, DE Pierce, RA Rogers, SJ Wehner, B AF Gabriels, RL Hill, DE Pierce, RA Rogers, SJ Wehner, B TI Predictors of treatment outcome in young children with autism - A retrospective study SO AUTISM LA English DT Article DE autism; children; outcome; treatment ID RECEPTIVE LANGUAGE DISORDER; EARLY ADULT LIFE; FOLLOW-UP; BEHAVIORAL TREATMENT; FAMILY STRESS; EARLY INTERVENTION; DOWN-SYNDROME; CONTINUITY; MOTHERS; PARENTS AB This study examined predictors of developmental outcomes in 17 children diagnosed with autism or PDD-NOS, who received generic treatment over a mean period of 37 months. Pre-treatment evaluations occurred at a mean age of 31 months with follow-up evaluations at a mean age of 69 months. Significantly different developmental trajectories were observed among the participants at follow-up, separating the participants into two distinct groups (high and low outcome). However, groups did not differ significantly in treatment intensity or other outcome prediction measures. Pre-treatment developmental intelligence levels between the two groups approached significance. The results raise questions regarding the effect of treatment intensity and type, family stress factors, and intelligence ability in very early childhood on, outcome. C1 Univ Colorado, Hlth Sci Ctr, Denver, CO 80262 USA. Univ New Mexico, Albuquerque, NM 87131 USA. RP Gabriels, RL (reprint author), Univ Colorado, Hlth Sci Ctr, 4200 E 9th Ave,C221, Denver, CO 80262 USA. CR Albanese A. L., 1995, TEACHING CHILDREN AU, P95 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAYLEY N, 1992, BAYLEY SCALES INFANT BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 BOUMA R, 1990, J CLIN PSYCHOL, V46, P722, DOI 10.1002/1097-4679(199011)46:6<722::AID-JCLP2270460605>3.0.CO;2-6 BRISTOL MM, 1987, J AUTISM DEV DISORD, V17, P469, DOI 10.1007/BF01486964 Bzoch K., 1991, RECEPTIVE EXPRESSIVE CASTO G, 1993, EARLY ED DEV, V4, P224, DOI 10.1207/s15566935eed0404_2 Cohen I., 1988, STAT POWER ANAL BEHA Gresham FM, 1998, J AUTISM DEV DISORD, V28, P5, DOI 10.1023/A:1026002717402 HARRIS S, 1988, DIAGNOSIS ASSESSMENT Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Hedrick D. L., 1984, SEQUENCED INVENTORY Hollingshead A., 1975, SOCIAL CLASS MENTAL Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P205, DOI 10.1007/BF01058151 KOEGEL RL, 1999, TEACHING CHILDREN AU KONSTANTAREAS MM, 1992, J AUTISM DEV DISORD, V22, P217, DOI 10.1007/BF01058152 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1989, J CHILD PSYCHOL PSYC, V30, P575, DOI 10.1111/j.1469-7610.1989.tb00269.x LORD C, 1988, DIAGNOSIS ASSESSMENT LOTTER V, 1978, AUTISM REAPPRAISAL C LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Luiselli J. 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M., 1973, STANFORD BINET INTEL Wechsler D., 1989, WECHSLER PRESCHOOL P WETHERBY AM, 1982, J SPEECH HEAR DISORD, V47, P63 Woodcock R. W., 1989, WOODCOCK JOHNSON PSY Zimmerman I.L., 1992, PRESCHOOL LANGUAGE S NR 46 TC 47 Z9 47 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2001 VL 5 IS 4 BP 407 EP 429 DI 10.1177/1362361301005004006 PG 23 WC Psychology, Developmental SC Psychology GA 503WA UT WOS:000172823500006 PM 11777257 ER PT J AU Boyd, RD Corley, MJ AF Boyd, RD Corley, MJ TI Outcome survey of early intensive behavioral intervention for young children with autism in a community setting SO AUTISM LA English DT Article DE autism; behavioral treatment; early intervention ID RECOVERY; DISORDER; PROJECT; LOVAAS AB This article presents findings from an outcome survey of the effects of early intensive behavioral intervention (EIBI) for young children with autism in a community setting. Results from both indi- vidual case reviews and parent questionnaires are presented, with the data failing to support any instances of 'recovery' while still yielding a high degree of parental satisfaction with the treatment. Moreover, a follow-up inquiry into the type of services each child was receiving in his or her post-EIBI setting documents continued dependence on extensive educational and related developmental services, suggesting that the promise of future treatment sparing did not materialize. Limitations of the survey in evaluating community-based EIBI services are discussed a-long with the need for further research designed to document the effectiveness of services provided to young children with ASD in the community. C1 Golden Gate Reg Ctr, San Francisco, CA USA. RP Boyd, RD (reprint author), 120 Howard St, San Francisco, CA 94105 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Boyd RD, 1998, J AUTISM DEV DISORD, V28, P211, DOI 10.1023/A:1026065321080 Cattell-Gordon D, 1998, INFANT YOUNG CHILD, V10, P79 Dawson G., 1997, EFFECTIVENESS EARLY Feinberg E, 1998, INFANT YOUNG CHILD, V10, P54 Green G., 1996, BEHAV INTERVENTION Y, P15 Gresham FM, 1997, BEHAV DISORDERS, V22, P185 Gresham FM, 1998, J AUTISM DEV DISORD, V28, P5, DOI 10.1023/A:1026002717402 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 LOVAAS OI, 1989, J BEHAV THER EXP PSY, V20, P17 Luiselli J. K., 2000, AUTISM, V4, P426, DOI 10.1177/1362361300004004007 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 Maurice C., 1993, LET ME HEAR YOUR VOI MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MESIBOV GB, 1993, AM J MENT RETARD, V97, P379 MUNDY P, 1993, AM J MENT RETARD, V97, P381 PERRY R, 1995, J AM ACAD CHILD PSY, V34, P232, DOI 10.1097/00004583-199502000-00019 SCHOPLER E, 1989, J CONSULT CLIN PSYCH, V57, P162 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 SMITH GE, 1910, ARCHAEOLOGICAL SURVE, V6, P9 Smith JR, 1999, IEEE ROBOT AUTOM MAG, V6, P49, DOI 10.1109/100.755814 SMITH T, 1995, AM J MENT RETARD, V100, P317 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 STONE RK, 1989, AM J MENT RETARD, V93, P627 NR 27 TC 28 Z9 29 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2001 VL 5 IS 4 BP 430 EP 441 DI 10.1177/1362361301005004007 PG 12 WC Psychology, Developmental SC Psychology GA 503WA UT WOS:000172823500007 PM 11777258 ER PT J AU Roubertie, A Semprino, M Chaze, AM Rivier, F Humbertclaude, V Cheminal, R Lefort, G Echenne, B AF Roubertie, A Semprino, M Chaze, AM Rivier, F Humbertclaude, V Cheminal, R Lefort, G Echenne, B TI Neurological presentation of three patients with 22q11 deletion (CATCH 22 syndrome) SO BRAIN & DEVELOPMENT LA English DT Article DE 22q11 deletion; DiGeorge sequence; autism; hypocalcaemic seizures; atypical absence epilepsy; jumping translocation ID VELOCARDIOFACIAL SYNDROME; DIGEORGE-SYNDROME; FEATURES AB Chromosome 22q11 deletion (CATCH 22 syndrome or velocardiofacial syndrome) is one of the most frequent chromosomal syndromes. Neurological features other than cognitive disorders are probably the least-described part of the expanding phenotype of the 22q11 deletion. We report the neurological features of three unrelated children with a de novo deletion: one patient with an autistic disorder, a second patient with hypocalcaemic neonatal seizures and unusual persistent epileptic focus at electroencephalographic follow-up, and a third patient with atypical absence epilepsy. These observations enlarge the clinical and neurological spectrum of the 22q11 deletion. Awareness of such cases is necessary, and a diagnosis of the 22q11 deletion should be suspected in children with common neurological features associated with severe or mild dysmorphism. Diagnosis of the 22q11 deletion should be confirmed by fluorescence in situ hybridization analysis associated with standard chromosomal analysis. (C) 2001 Elsevier Science B.V. All rights reserved. C1 St Eloi Hosp, F-34295 Montpellier 5, France. Univ Montpellier, Arnaud De Villeneuve Hosp, Dept Genet, F-34059 Montpellier, France. RP Roubertie, A (reprint author), St Eloi Hosp, 2 Ave Bertin Sans, F-34295 Montpellier 5, France. RI Humbertclaude, Veronique/A-8383-2008 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Breviere GM, 1999, ARCH PEDIATRIE, V6, p305S, DOI 10.1016/S0929-693X(99)80448-5 Carratala F, 1998, DEV MED CHILD NEUROL, V40, P492 Gerdes M, 1999, AM J MED GENET, V85, P127, DOI 10.1002/(SICI)1096-8628(19990716)85:2<127::AID-AJMG6>3.0.CO;2-F GREENBERG F, 1993, J MED GENET, V30, P803, DOI 10.1136/jmg.30.10.803 HALFORD S, 1993, HUM MOL GENET, V2, P2099, DOI 10.1093/hmg/2.12.2099 Kozma C, 1998, AM J MED GENET, V81, P269, DOI 10.1002/(SICI)1096-8628(19980508)81:3<269::AID-AJMG12>3.0.CO;2-D Ogilvie CM, 2000, AM J MED GENET, V96, P15 Ryan AK, 1997, J MED GENET, V34, P798, DOI 10.1136/jmg.34.10.798 Wang PP, 2000, DEV MED CHILD NEUROL, V42, P422, DOI 10.1017/S0012162200000785 WILSON DI, 1994, AM J HUM GENET S, V55, pA975 NR 11 TC 17 Z9 17 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 DEC PY 2001 VL 23 IS 8 BP 810 EP 814 DI 10.1016/S0387-7604(01)00258-3 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 507WY UT WOS:000173055300007 PM 11720799 ER PT J AU Azmitia, EC AF Azmitia, EC TI Neuronal instability: implications for Rett's syndrome SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT World Congress on Rett Syndrome CY JUL 24-27, 2000 CL KARUIZAWA, JAPAN DE serotonin; 5-HT1A; MAP-2; regression; BDNF; S-100; cytoskeleton; apoptosis; petal alcohol syndrome; cocaine; autism ID PERVASIVE DEVELOPMENTAL DISORDERS; MICROTUBULE-ASSOCIATED PROTEIN-2; 5-HT1A RECEPTOR AGONIST; CENTRAL-NERVOUS-SYSTEM; ADULT-RAT; MESSENGER-RNA; GLIAL-CELLS; SEROTONERGIC NEURONS; CEREBROSPINAL-FLUID; NEUROTROPHIC FACTOR AB The maturational changes in the brain and spinal cord do not linearly proceed from immature in infants to mature in adults. Dendrites dynamically extend or retract as neurotrophic factors fluctuate. In certain cases mature neurons can be seen soon after birth, and in other cases immature neurons can be identified in the aged brain. Monoamine 'neurotransmitter'; such as serotonin (5-HT), dopamine and norepinephrine appear to function as Maintenance Growth Factors since they must be present in order to produce their maturational actions. Serotonin neurons contain TRK-B receptors and are sensitive to availability of the trophic factor, BDNF. 5-HT also functions by promoting the release of the glial extension factor, S-100beta. 5-HT and S-100beta can provide maturational signals to a variety of neurons, in both cortical and subcortical areas, and appear to be involved in regulating the maturation and release of acetylcholine and dopamine. We have shown that activation of the 5-HT1A receptor is particularly effective in inducing growth of stunted neurons. The mechanism of action of the 5-HT1A receptor involves both a direct inhibition on c-AMP and pCREB formation in postsynaptic neurons and a release of S-100beta from glial cells. Both these events are capable of stabilization and elaboration of the cytoskeleton of the neuron and inhibition of apoptosis. 5-HT1A receptors have been shown to effectively reverse stunted neurons and microencephaly produced,in animal models of fetal alcohol syndrome and prenatal cocaine administration. I discuss the implications for regressive disorders such as Rett's syndrome and autism, and the feasibility of treatments with 5-HT1A agonists in children with developmental disorders. (C) 2001 Elsevier Science B.V. All rights reserved. C1 NYU, Dept Biol, New York, NY 10003 USA. NYU, Dept Psychiat, New York, NY 10003 USA. NYU, Ctr Neural Sci, New York, NY 10003 USA. RP Azmitia, EC (reprint author), NYU, Dept Biol, 100 Washington Sq E, New York, NY 10003 USA. 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AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD DEC PY 2001 VL 23 SU 1 BP S1 EP S10 DI 10.1016/S0387-7604(01)00368-0 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 512UL UT WOS:000173341900002 PM 11738834 ER PT J AU Gorbachevskaya, N Bashina, V Gratchev, V Iznak, A AF Gorbachevskaya, N Bashina, V Gratchev, V Iznak, A TI Cerebrolysin therapy in Rett syndrome: clinical and EEG mapping study SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT World Congress on Rett Syndrome CY JUL 24-27, 2000 CL KARUIZAWA, JAPAN DE Rett syndrome; quantitative electroencephalogram; cerebrolysin; treatment; preschool girls ID AUTISM AB Based on the suggestion that nerve growth factor plays a core role in the brain Maturation process, which is altered in Rett syndrome, we investigate the influence of Cerebrolysin - the brain-derived peptidergic drug - on motor and higher cortical functions in Rett syndrome girls. The open pilot study was performed on nine Rett syndrome girls ( aged from 2 years and 2 months to 7 years and 6 months) at stage 3 of the illness, and included both clinical and quantitative EEG evaluations before and after Cerebrolysin treatment. After Cerebrolysin treatment, increases in the behavioral activity, attention level, motor functions. and non-verbal social Communication have been shown in Rett syndrome patients. EEG parameters after Cerebrolysin treatment also changed towards normal values, indicating an improvement of the brain functional state. EEG changes included: decrease of theta activity over all Cortical regions, increase of beta activity in the frequency band 13-15 Hz, and some restoration of the occipital alpha rhythm (in the narrow 8-9 Hz band), The data Obtained suggested possible perspectives of Cerebrolysin in complex therapy of Rett syndrome. (C) 2001 Elsevier Science B. V. All rights reserved. C1 Mental Hlth Res Ctr, Dept Neurophysiol, Moscow 115522, Russia. RP Gorbachevskaya, N (reprint author), Mental Hlth Res Ctr, Dept Neurophysiol, Kashirskoe Shosse 34, Moscow 115522, Russia. EM gorbachevskaya@aport2000.ru CR ARMSTRONG DD, 1992, BRAIN DEV S, V14, P89 Bashina VM, 1997, EUR CHILD ADOLES PSY, V6, P18 Belichenko PV, 1997, ACTA NEUROPATHOL, V93, P50 GORBACHEVSKAYA NL, 1996, HUMAN PHYSL, V22, P49 Gorbachevskaya N, 1998, NEW DEVELOPMENTS IN CHILD NEUROLOGY, P203 Hutter-Paier B, 1998, J NEURAL TRANSM-SUPP, P351 ISHIZAKI A, 1989, BRAIN DEV-JPN, V11, P407 Levi-Montalcini R., 1990, PROG NEUROENDOCRINOL, V3, P1 Lopes da Silva F, 1991, Electroencephalogr Clin Neurophysiol, V79, P81, DOI 10.1016/0013-4694(91)90044-5 Niedermeyer E, 1997, CLIN ELECTROENCEPHAL, V28, P36 PANUISHKINA S, 2000, THESIS MOSCOW Riikonen R, 1999, DEV MED CHILD NEUROL, V41, P148, DOI 10.1017/S0012162299000328 RUTHER E, 1994, PHARMACOPSYCHIATRY, V27, P32, DOI 10.1055/s-2007-1014271 Segawa M, 1997, EUR CHILD ADOLES PSY, V6, P56 Wenk GL, 1999, NEUROPEDIATRICS, V30, P125, DOI 10.1055/s-2007-973476 Windisch M, 1998, J NEURAL TRANSM-SUPP, P289 NR 16 TC 4 Z9 4 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 DEC PY 2001 VL 23 SU 1 BP S90 EP S93 DI 10.1016/S0387-7604(01)00349-7 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 512UL UT WOS:000173341900017 PM 11738849 ER PT J AU Gotoh, H Suzuki, I Maruki, K Mitomo, M Hirasawa, K Sasaki, N AF Gotoh, H Suzuki, I Maruki, K Mitomo, M Hirasawa, K Sasaki, N TI Magnetic resonance imaging and clinical findings examined in adulthood-studies on three adults with Rett syndrome SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT World Congress on Rett Syndrome CY JUL 24-27, 2000 CL KARUIZAWA, JAPAN DE Rett syndrome; magnetic resonance imaging; cerebellar atrophy; brainstem atrophy ID CPG-BINDING PROTEIN-2; NEUROANATOMY; CEREBELLAR; MUTATIONS; BRAIN; MR AB Purpose: To clarify magnetic resonance imaging (MRI) findings in three adult patients with Rett syndrome who had been diagnosed with mental retardation and autism. Method: Clinical and MRI findings in three adult cases with Rett syndrome were studied. Ages (in years) in three adult cases with Rett Syndrome were 46 in Case 1, 35 in Case 2 and 20 in Case 3. They were able to walk and their convulsions were well controlled. Results: MRI findings in all patients showed mild cerebral atrophy, especially in the frontal and temporal lobes and two of the cases also had mild cerebellar atrophy. One case also showed a narrowing of the brainstem and thinning of the corpus callosum, Conclusions: These results indicate that abnormalities in MRI imaging, in cases where there is narrowing of the brainstem and thinning of the corpus callosum, may be due to congenital hypoplasia. It was also seen that cerebellar atrophy became more distinct in older cases. (C) 2001 Elsevier Science B.V. All rights reserved. CR Amir RE, 1999, NAT GENET, V23, P185 HAGBERG B, 1995, ACTA PAEDIATR, V84, P971, DOI 10.1111/j.1651-2227.1995.tb13809.x Hagberg B, 1993, RETT SYNDROME CLIN B HASHIMOTO T, 1993, J CHILD NEUROL, V8, P149 JELLINGER K, 1988, ACTA NEUROPATHOL, V76, P142 KRAGELOHMANN I, 1989, BRAIN DEV-JPN, V11, P175 Manes F, 1999, J NEUROPSYCH CLIN N, V11, P470 MURAKAMI JW, 1992, AM J ROENTGENOL, V159, P177 NIHEI K, 1990, BRAIN DEV-JPN, V12, P101 REISS AL, 1993, ANN NEUROL, V34, P227, DOI 10.1002/ana.410340220 Saitoh O, 1998, PSYCHIAT CLIN NEUROS, V52, pS219 Subramaniam B, 1997, NEUROLOGY, V48, P399 TREVATHAN E, 1988, ANN NEUROL, V23, P425 Van den Veyver IB, 2000, CURR OPIN GENET DEV, V10, P275, DOI 10.1016/S0959-437X(00)00083-6 Vanhala R, 1998, DEV MED CHILD NEUROL, V40, P836 VANHANEN SL, 1994, AM J NEURORADIOL, V15, P1443 YANO S, 1991, PEDIATR NEUROL, V7, P289, DOI 10.1016/0887-8994(91)90047-O NR 17 TC 8 Z9 8 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 DEC PY 2001 VL 23 SU 1 BP S118 EP S121 DI 10.1016/S0387-7604(01)00355-2 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 512UL UT WOS:000173341900024 PM 11738856 ER PT J AU Kohyama, J Ohinata, J Hasegawa, T AF Kohyama, J Ohinata, J Hasegawa, T TI Disturbance of phasic chin muscle activity during rapid-eye-movement sleep SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT World Congress on Rett Syndrome CY JUL 24-27, 2000 CL KARUIZAWA, JAPAN DE rapid-eye-movement sleep; phasic inhibition index; Rett syndromes; infantile spasms; nocturnal enuresis; severe myoclonic epilepsy in infancy; autistic tendency; Parkinson's disease; pontine tegmentum ID REM-SLEEP; BEHAVIOR DISORDER; NOCTURNAL ENURESIS; INFANTILE SPASMS; MOTOR INHIBITION; WEST SYNDROME; MATURATION; AUTISM; STARTLE AB In patients with Rett syndrome (RS), a peculiar type of disturbance in phasic chin muscle activity during rapid-eye-movement sleep (REMS) (e.g. an elevation of phasic inhibition index (PII) without an affection of tonic inhibition index (TII)) hits been reported. The similar disturbance in REMS was reported not only in child patients with infantile spasms, severe myoclonic epilepsy in infancy (SMEI), severe nocturnal enuresis, and autism but also in adult patients with Parkinson's disease (PD). Except for SMEI and PD patients with the other four clinical entities including RS could express autistic tendency. Since the responsible lesion for the occurrence of an elevation of PII with a normal TII value is likely to be in the pontine tegmentum. This subcortical structure is hypothesized to be involved ill the appearance of autistic tendency. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Tokyo Med & Dent Univ, Grad Sch, Div Human Ontogeny & Childhood Dev, Tokyo 1138519, Japan. Tokyo Med & Dent Univ, Fac Med, Dept Clin Lab, Tokyo 1138519, Japan. RP Kohyama, J (reprint author), Tokyo Med & Dent Univ, Grad Sch, Div Human Ontogeny & Childhood Dev, 1-5-45 Yushima, Tokyo 1138519, Japan. 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PD DEC PY 2001 VL 23 SU 1 BP S104 EP S107 DI 10.1016/S0387-7604(01)00357-6 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 512UL UT WOS:000173341900021 PM 11738853 ER PT J AU Okado, N Narita, M Narita, N AF Okado, N Narita, M Narita, N TI A biogenic amine-synapse mechanism for mental retardation and developmental disabilities SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT World Congress on Rett Syndrome CY JUL 24-27, 2000 CL KARUIZAWA, JAPAN DE plasticity; synapse; biogenic amines; mental retardation; stress; environmental factors; critical period ID GROWTH CONE MOTILITY; CHICK SPINAL-CORD; 5-HT2A RECEPTOR; CEREBRAL-CORTEX; SEROTONINERGIC FIBERS; REGIONAL DIFFERENCES; HUMAN BRAIN; SYSTEM; NEUROTRANSMITTERS; DENSITY AB Recent studies have demonstrated that biogenic amines have a function of facilitating formation and maintenance of synapses in diverse regions of the central nervous system in developing and adult animals. The normal number of synapses maintained by biogenic amines are crucial to acquire learning and memory. The level of biogenic amines was reported to decrease in the brain by several neurodevelopmental disorders associated with mental retardation and developmental disabilities such as Rett syndrome, autism and Down syndrome. Taken into consideration this fact together with the function of biogenic amines for synapses, the density of synapses appears to decrease considerably in the brains of patients suffered from the neurodevelopmental disorders. The synaptic overproduction during the critical period of development especially 1 year after birth has been considered as a background mechanism to provide plasticity for the developing brain. Synaptic overproduction does not appear to occur in the brains of patients suffered from the neurodevelopmental disorders, which they are observed mental retardation occurring in the first 1 year after birth. Along with the neurodevelopmental disorders, environmental factors (stress, drugs and nutrition) during pre- and post-natal critical developmental periods are known to change levels of biogenic amines in the brain. In fact, maternal stress has been shown to decrease the levels of serotonin and the density of synapses in the hippocampus of the offspring, and they showed developmental disabilities in the spatial learning and memory, A cascade appears to exist from either the child neurological disorders or the environmental factors to mental retardation and developmental disabilities by decreases in the levels of biogenic amines and synaptic density. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Neurobiol Lab, Inst Basic Med Sci, Tsukuba, Ibaraki 3058577, Japan. RP Okado, N (reprint author), Univ Tsukuba, Neurobiol Lab, Inst Basic Med Sci, Tsukuba, Ibaraki 3058577, Japan. 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PD DEC PY 2001 VL 23 SU 1 BP S11 EP S15 DI 10.1016/S0387-7604(01)00371-0 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 512UL UT WOS:000173341900003 PM 11738835 ER PT J AU Wood, J AF Wood, J TI Helping children with autism to learn. SO BRITISH JOURNAL OF EDUCATIONAL PSYCHOLOGY LA English DT Book Review C1 Univ Exeter, Sch Educ, Exeter EX4 4QJ, Devon, England. RP Wood, J (reprint author), Univ Exeter, Sch Educ, Exeter EX4 4QJ, Devon, England. CR Powell S., 2000, HELPING CHILDREN AUT 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 DEC PY 2001 VL 71 BP 682 EP 683 PN 4 PG 2 WC Psychology, Educational SC Psychology GA 504KJ UT WOS:000172855600021 ER PT J AU Powell, S AF Powell, S TI Helping children with autism to learn. Response SO BRITISH JOURNAL OF EDUCATIONAL PSYCHOLOGY LA English DT Editorial Material C1 Univ Hertfordshire, Ctr Autism Studies, Hatfield AL10 9AB, Herts, England. RP Powell, S (reprint author), Univ Hertfordshire, Ctr Autism Studies, Hatfield AL10 9AB, Herts, England. 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 0007-0998 J9 BRIT J EDUC PSYCHOL JI Br. J. Educ. Psychol. PD DEC PY 2001 VL 71 BP 683 EP 684 PN 4 PG 2 WC Psychology, Educational SC Psychology GA 504KJ UT WOS:000172855600022 ER PT J AU Boyar, FZ Whitney, MM Lossie, AC Gray, BA Keller, KL Stalker, HJ Zori, RT Geffken, G Mutch, J Edge, PJ Voeller, KS Williams, CA Driscoll, DJ AF Boyar, FZ Whitney, MM Lossie, AC Gray, BA Keller, KL Stalker, HJ Zori, RT Geffken, G Mutch, J Edge, PJ Voeller, KS Williams, CA Driscoll, DJ TI A family with a grand-maternally derived interstitial duplication of proximal 15q SO CLINICAL GENETICS LA English DT Article DE Angelman; apraxia of speech; autism; chromosome 15; dyslexia; imprinting; interstitial duplication; phonological awareness deficit ID SYNDROME CHROMOSOME REGION; PRADER-WILLI; ANGELMAN-SYNDROMES; AUTISTIC DISORDER; MOLECULAR CHARACTERIZATION; LINKAGE-DISEQUILIBRIUM; METHYLATION IMPRINT; DNA METHYLATION; GENOMIC SCREEN; INV DUP(15) AB About 1% of individuals with autism or types of pervasive developmental disorder have a duplication of the 15q11-q13 region. These abnormalities can be detected by routine G-banded chromosome study, showing an extra marker chromosome, or demonstrated by fluorescence in situ hybridization (FISH) analysis, revealing an interstitial duplication. We report here the molecular, cytogenetic, clinical and neuropsychiatric evaluations of a family in whom 3 of 4 siblings inherited an interstitial duplication of 15q11-q13. This duplication was inherited from their mother who also had a maternally derived duplication. Affected family members had apraxia of speech, phonological awareness deficits, developmental language disorder, dyslexia, as well as limb apraxia but did not have any dysmorphic clinical features. The observations in this family suggest that the phenotypic manifestations of proximal 15q duplications may also involve language-based learning disabilities. C1 Univ Florida, Coll Med, Raymond C Philips Unit, Div Pediat Genet,Dept Pediat, Gainesville, FL 32610 USA. 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Genet. PD DEC PY 2001 VL 60 IS 6 BP 421 EP 430 DI 10.1034/j.1399-0004.2001.600604.x PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 515HX UT WOS:000173490400004 PM 11846734 ER PT J AU Fiddick, L AF Fiddick, L TI The descent of mind: Psychological perspectives on hominid evolution SO CONTEMPORARY PSYCHOLOGY-APA REVIEW OF BOOKS LA English DT Book Review ID AUTISM C1 Max Planck Project Grp, Bonn, Germany. RP Fiddick, L (reprint author), UCL, Ctr Econ Learning & Social Evolut, Dept Econ, Gower St, London WC1E 6BT, England. 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PD DEC PY 2001 VL 46 IS 6 BP 567 EP 570 PG 4 WC Psychology, Multidisciplinary SC Psychology GA 503JB UT WOS:000172794400009 ER PT J AU Petersilia, JR AF Petersilia, JR TI Crime victims with developmental disabilities - A review essay SO CRIMINAL JUSTICE AND BEHAVIOR LA English DT Review ID MENTAL-RETARDATION; CHILDREN; ABUSE; YOUTH; DEAF AB Rates of violence and abuse perpetrated on people with developmental disabilities (e.g., mental retardation, autism) appear significantly higher than for people without these disabilities. Few of these crimes get reported to police, and even fewer are prosecuted because officials hesitate to pursue cases that rely on the testimony of a person with a developmental disability. The author offers several conceptual models to explain their differential victimization risk, including routine activities theory, dependency-stress model, cultural stereotyping, and victim-learned compliance. This article summarizes the research evidence on crimes against children and adults with developmental disabilities. It is divided into four sections. The first section describes the nature and extent of crimes against individuals with developmental disabilities. The second reviews the literature on risk factors associated with their victimization. The third discusses the manner in which justice agencies respond to these crimes. The final section enumerates what research and policy initiatives might address the problem. C1 Univ Calif Irvine, Dept Criminol Law & Soc, Irvine, CA 92697 USA. RP Petersilia, JR (reprint author), Univ Calif Irvine, Dept Criminol Law & Soc, 2317 Social Ecol II, Irvine, CA 92697 USA. 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E., 1997, ARCH PHYS MED REHAB, V78, P34 NR 75 TC 39 Z9 39 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0093-8548 J9 CRIM JUSTICE BEHAV JI Crim. Justice Behav. PD DEC PY 2001 VL 28 IS 6 BP 655 EP 694 PG 40 WC Psychology, Clinical; Criminology & Penology SC Psychology; Criminology & Penology GA 491PP UT WOS:000172117600001 ER PT J AU Spence, MA AF Spence, MA TI The genetics of autism SO CURRENT OPINION IN PEDIATRICS LA English DT Review ID TRANSLOCATION BREAKPOINT; SUSCEPTIBILITY GENES; ETIOLOGIC FACTOR; DISORDER; CHROMOSOME; IDENTIFICATION; ASSOCIATION; EXPRESSION; DELETION; VARIANTS AB Autism is a significant childhood disorder. Studies are underway to define more clearly the disorder and its various manifestations and to correlate this information with an etiology. Genes are known to play an important role in autism, and a vigorous search is underway to define those genes. The Human Genome Project provides the basis that allows us to move beyond single gene disorders and to contemplate progress for complex disorders, such as autism. Genome screens of affected siblings and detailed molecular analyses of chromosome abnormalities identified in autistic subjects has led in the past year to the identification of several candidate genes. However, the problem of determining which are the real genes remains. This is complicated because the presentation of the disorder is so variable, and milder manifestations in relatives are not yet understood. But the fact that we can now name possible genes for this disorder reflects how quickly our understanding is progressing. (C) 2001 Lippincott Williams & Wilkins, Inc. C1 Univ Calif Irvine, Med Ctr, Dept Pediat, Orange, CA 92868 USA. RP Spence, MA (reprint author), Univ Calif Irvine, Med Ctr, Dept Pediat, 101 City Dr S,Bldg 2,Rm 346, Orange, CA 92868 USA. CR Auranen M, 2000, MOL PSYCHIATR, V5, P320, DOI 10.1038/sj.mp.4000708 Berney TP, 2000, BRIT J PSYCHIAT, V176, P20, DOI 10.1192/bjp.176.1.20 Bonde E, 2000, EUR CHILD ADOLES PSY, V9, P7 Buitelaar J K, 2000, Paediatr Drugs, V2, P67 Sandler AD, 2001, PEDIATRICS, V107, P1221 Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Filipek PA, 2000, NEUROLOGY, V55, P468 Folstein SE, 2000, AM J HUM GENET, V67, P278, DOI 10.1086/303034 Ghaziuddin M, 2000, J INTELL DISABIL RES, V44, P562, DOI 10.1046/j.1365-2788.2000.00271.x Goizet C, 2000, AM J MED GENET, V96, P839, DOI 10.1002/1096-8628(20001204)96:6<839::AID-AJMG29>3.0.CO;2-R Hoh J, 2000, P NATL ACAD SCI USA, V97, P9615, DOI 10.1073/pnas.170179197 Hunsinger DM, 2000, LIFE SCI, V67, P1667, DOI 10.1016/S0024-3205(00)00763-3 Ingram JL, 2000, TERATOLOGY, V62, P393, DOI 10.1002/1096-9926(200012)62:6<393::AID-TERA6>3.0.CO;2-V Lam C W, 2000, J Med Genet, V37, pE41, DOI 10.1136/jmg.37.12.e41 Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 London E, 2000, ENVIRON HEALTH PERSP, V108, P401 MacLean JE, 2000, AM J MED GENET, V90, P382, DOI 10.1002/(SICI)1096-8628(20000228)90:5<382::AID-AJMG7>3.0.CO;2-T Maestrini E, 2000, NEURON, V28, P19, DOI 10.1016/S0896-6273(00)00081-7 Mas C, 2000, GENOMICS, V65, P70, DOI 10.1006/geno.2000.6126 Michaelis RC, 2000, J AUTISM DEV DISORD, V30, P355, DOI 10.1023/A:1005583517994 Miles JH, 2000, AM J MED GENET, V91, P245, DOI 10.1002/(SICI)1096-8628(20000410)91:4<245::AID-AJMG1>3.0.CO;2-2 Murphy M, 2000, PSYCHOL MED, V30, P1411, DOI 10.1017/S0033291799002949 Nasr A, 2000, J INTELL DISABIL RES, V44, P170, DOI 10.1046/j.1365-2788.2000.00239.x Partington M, 2000, AM J MED GENET, V92, P57, DOI 10.1002/(SICI)1096-8628(20000501)92:1<57::AID-AJMG10>3.0.CO;2-0 Persico AM, 2000, AM J MED GENET, V96, P123, DOI 10.1002/(SICI)1096-8628(20000207)96:1<123::AID-AJMG24>3.0.CO;2-N Persico AM, 2001, MOL PSYCHIATR, V6, P150, DOI 10.1038/sj.mp.4000850 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 SCHELLENBERG G, 2001, UNPUB FAILURE REPLIC Senior K, 2000, LANCET, V356, P490, DOI 10.1016/S0140-6736(05)74160-X Smith M, 2000, AM J MED GENET, V96, P765, DOI 10.1002/1096-8628(20001204)96:6<765::AID-AJMG13>3.0.CO;2-L SMITH M, 2001, IN PRESS J MED GENET Stoltenberg SF, 2000, HUM MOL GENET, V9, P927, DOI 10.1093/hmg/9.6.927 Turner M, 2000, MOL MED TODAY, V6, P238, DOI 10.1016/S1357-4310(00)01712-3 Vincent JB, 2000, AM J HUM GENET, V67, P510, DOI 10.1086/303005 Warburton P, 2000, AM J MED GENET, V96, P228, DOI 10.1002/(SICI)1096-8628(20000403)96:2<228::AID-AJMG20>3.0.CO;2-G Wassink T H, 2000, Curr Psychiatry Rep, V2, P170, DOI 10.1007/s11920-000-0063-x Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 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 Yan WL, 2000, AM J MED GENET, V96, P749, DOI 10.1002/1096-8628(20001204)96:6<749::AID-AJMG10>3.0.CO;2-K NR 40 TC 13 Z9 13 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-8703 J9 CURR OPIN PEDIATR JI CURR. OPIN. PEDIATR. PD DEC PY 2001 VL 13 IS 6 BP 561 EP 565 DI 10.1097/00008480-200112000-00012 PG 5 WC Pediatrics SC Pediatrics GA 505UP UT WOS:000172934200012 PM 11753107 ER PT J AU Biro, S Russell, J AF Biro, S Russell, J TI The execution of arbitrary procedures by children with autism SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID MIND; COMMUNICATION; PERFORMANCE; ABILITIES; DEFICITS; INFANTS AB Executive tasks typically contain a prepotent lure. In addition, they require individuals either to (a) follow arbitrary procedures or (b) update their model of the physical world. Recent research suggests that children with autism may be challenged only by executive tasks of the former kind (containing arbitrary rules). We asked whether this continues to be true when there is no prepotent lure, comparing performance on (a) a task with arbitrariness but without prepotency with (b) a task with both features and (c) a task with neither. The participants with autism performed at a lower level than comparison groups on the first and second task but not on the third task. This outcome is consistent with the view that autism is associated with difficulties in following arbitrary procedures per se. We try to locate difficulties with acting on the basis arbitrary rules in relation to more mainstream ideas about autistic executive dysfunction. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Russell, J (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. CR ABRAHAMSEN EP, 1990, J AUTISM DEV DISORD, V20, P75, DOI 10.1007/BF02206858 ADRIEN JL, 1995, J AUTISM DEV DISORD, V25, P249, DOI 10.1007/BF02179287 Ahmed A, 1998, DEV PSYCHOL, V34, P441, DOI 10.1037//0012-1649.34.3.441 American Psychiatric Association, 1987, DIAGN STAT MAN MENT Baillargeon R., 1993, VISUAL PERCEPTION CO, P265 BARONCOHEN S, 1997, EMERGENCE CORE DOMAI BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 DIAMOND A, 1988, CHILD DEV, V59, P523, DOI 10.1111/j.1467-8624.1988.tb01486.x DIAMOND A, 1985, CHILD DEV, V56, P868, DOI 10.1111/j.1467-8624.1985.tb00160.x Duncan J., 1995, COGNITIVE NEUROSCIEN Duncker K., 1945, PSYCHOL MONOGR, V58, P5 Dunn L M., 1982, BRIT PICTURE VOCABUL FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Gibson J. J., 1979, ECOLOGICAL APPROACH HOOD B, 1995, COGNITIVE DEV, V10, P375 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 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x OZONOFF S, 1997, EXECUTIVE FUNCTIONIN 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 B, 1997, EXECUTIVE FUNCTIONIN Piaget J., 1954, CHILDS CONSTRUCTION RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 RUMSEY JM, 1985, J CONSULT CLIN PSYCH, V48, P605 Russell J, 1999, J CHILD PSYCHOL PSYC, V40, P859, DOI 10.1017/S0021963099004229 Russell J., 1997, AUTISM EXECUTIVE DIS Russell J, 1999, J AUTISM DEV DISORD, V29, P103, DOI 10.1023/A:1023084425406 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 WEHNER E, 1994, BIM M DEV PSYCH RES NR 31 TC 33 Z9 34 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-4930 USA SN 0954-5794 J9 DEV PSYCHOPATHOL JI Dev. Psychopathol. PD WIN PY 2001 VL 13 IS 1 BP 97 EP 110 DI 10.1017/S0954579401001079 PG 14 WC Psychology, Developmental SC Psychology GA 411MX UT WOS:000167504800007 PM 11346055 ER PT J AU Klinger, LG Dawson, G AF Klinger, LG Dawson, G TI Prototype formation in autism SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID MENTAL-RETARDATION; CATEGORIZATION; CHILDREN; INDIVIDUALS; MEMORY; LEVEL AB Individuals with autism have difficulty integrating information and generalizing previously learned concepts to new situations. It was hypothesized that these problems result from an underlying impairment in category formation. Persons with autism may not abstract a summary representation (a prototype) during category learning and, instead. may form categories by memorizing a list of rules. Children with autism, Down syndrome, and normal development participated in one set of category learning tasks that could be solved using a rule-based approach and a second set of tasks in which there was no rule that defined category membership (prototype tasks). In the rule-based tasks, all groups were successful at using a rule to learn a new category. In the prototype tasks, only the typically developing children were able to learn a new category. Neither the persons with autism nor the persons with Down syndrome appeared to develop a prototype during category learning. These data suggest that persons with autism and Down syndrome have difficulty categorizing new information by forming prototypes and, instead, tend to rely on a rule-based approach to learning. C1 Univ Alabama, Dept Psychol, Tuscaloosa, AL 35487 USA. Univ Washington, Seattle, WA 98195 USA. RP Klinger, LG (reprint author), Univ Alabama, Dept Psychol, Box 870348, Tuscaloosa, AL 35487 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT BERGER HJC, 1993, J AUTISM DEV DISORD, V23, P341, DOI 10.1007/BF01046224 BOMBA PC, 1983, J EXP CHILD PSYCHOL, V35, P294, DOI 10.1016/0022-0965(83)90085-1 Bowler DM, 1997, NEUROPSYCHOLOGIA, V35, P65, DOI 10.1016/S0028-3932(96)00054-1 COHEN LB, 1981, PRETERM BIRTH PSYCHO, P242 Courchesne E., 1994, ATYPICAL COGNITIVE D, P101 Dunn L. M., 1981, PEABODY PICTURE VOCA Frith U., 1989, AUTISM EXPLAINING EN FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Ganiban J., 1990, CHILDREN DOWN SYNDRO, P147, DOI 10.1017/CBO9780511581786.006 Grandin T., 1995, LEARNING COGNITION A, P137 HAYES BK, 1993, AM J MENT RETARD, V98, P293 Hermelin B, 1970, PSYCHOL EXPT AUTISTI HERMELIN B, 1986, PSYCHOL MED, V16, P885 HUSAIM JS, 1981, MERRILL PALMER QUART, V27, P443 INN D, 1993, B PSYCHONOMIC SOC, V31, P197 POSNER MI, 1970, J EXP PSYCHOL, V83, P304, DOI 10.1037/h0028558 Klinger L. G., 1995, LEARNING COGNITION A, P119 Klinger LG, 1992, CAUSES EFFECTS COMMU, P157 KOSSAN NE, 1981, CHILD DEV, V52, P290 Markman Ellen M., 1989, CATEGORIZATION NAMIN Minshew N J, 1997, J Int Neuropsychol Soc, V3, P303 MINSHEW NJ, 1992, J CLIN EXP NEUROPSYC, V14, P749, DOI 10.1080/01688639208402860 POSNER MI, 1968, J EXP PSYCHOL, V77, P353, DOI 10.1037/h0025953 Rosch E, 1978, COGNITION CATEGORIZA, P27 SHULMAN C, 1995, J ABNORM PSYCHOL, V104, P601, DOI 10.1037//0021-843X.104.4.601 STRAUSS MS, 1979, J EXPT PSYCHOL HUMAN, V5, P616 TAGERFLUSBERG H, 1985, CHILD DEV, V56, P1167, DOI 10.1111/j.1467-8624.1985.tb00185.x TAGERFLUSBERG H, 1985, J EXP CHILD PSYCHOL, V40, P450, DOI 10.1016/0022-0965(85)90077-3 UNGERER JA, 1987, J AUTISM DEV DISORD, V17, P3, DOI 10.1007/BF01487256 WALTON GE, 1993, PSYCHOL SCI, V4, P203, DOI 10.1111/j.1467-9280.1993.tb00488.x YOUNGER B, 1990, J EXP CHILD PSYCHOL, V50, P131, DOI 10.1016/0022-0965(90)90036-8 YOUNGER BA, 1985, CHILD DEV, V56, P1574, DOI 10.1111/j.1467-8624.1985.tb00222.x NR 33 TC 82 Z9 84 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-4930 USA SN 0954-5794 J9 DEV PSYCHOPATHOL JI Dev. Psychopathol. PD WIN PY 2001 VL 13 IS 1 BP 111 EP 124 DI 10.1017/S0954579401001080 PG 14 WC Psychology, Developmental SC Psychology GA 411MX UT WOS:000167504800008 PM 11346046 ER PT J AU Bishop, DVM Baird, G AF Bishop, DVM Baird, G TI Parent and teacher report of pragmatic aspects of communication: use of the Children's Communication Checklist in a clinical setting SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID DISORDERS; AUTISM AB The Children's Communication Checklist (CCC) was developed to provide an objective assessment of pragmatic aspects of children's communication difficulties. We aimed to (1) see whether the checklist provided valid and reliable information when completed by parents, and (2) consider its usefulness in a clinical context. Checklists were completed by parents and a professional who knew the child well for all 5 to 17-year-old referrals to a tertiary developmental paediatrics centre over a 31-month period. Children who were not yet speaking in sentences were excluded. From a sample of 151 children (81% male; mean age 8.7 years) with pervasive or specific developmental disorders, valid checklists were completed by 119 parents and 93 professionals. Reliability, as measured by internal consistency, was 0.7 or higher for most scales. Correlations between ratings for parents and professionals were in the range of 0.30 to 0.58 for individual pragmatic scales, with a correlation of 0.46 (n=82) for the pragmatic composite. For both parents and professionals, the pragmatic composite was lowest for children with a diagnosis of autism; intermediate for those with a diagnosis of Asperger syndrome, pervasive developmental disorder not otherwise specified or attention-deficit-hyperactivity disorder (ADHD); and highest for those with a diagnosis of specific learning disability. The strongest relation between the pragmatic composite and diagnosis was seen when ratings from parents and professionals were combined. Differences between diagnostic groups were not explicable in terms of age or verbal IQ. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Guys Hosp, Newcomen Ctr, London SE1 9RT, England. RP Bishop, DVM (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. CR Bishop D., 2000, SPEECH LANGUAGE IMPA, P99 Bishop D. V. M., 1997, UNCOMMON UNDERSTANDI Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 CONNERS CK, 1969, AM J PSYCHIAT, V126, P884 GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x Goodman R, 1997, J CHILD PSYCHOL PSYC, V38, P581, DOI 10.1111/j.1469-7610.1997.tb01545.x Kaufman AS, 1983, KAUFMAN ASSESSMENT B LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Oram J, 1999, AM J SPEECH-LANG PAT, V8, P72 Rapin I, 1983, NEUROPSYCHOLOGY LANG, P155 ROSENBLOOM L, 1987, CLIN DEV MED, V101 Semel E, 1995, CLIN EVALUATION LANG, V3rd VERHULST FC, 1989, J CHILD PSYCHOL PSYC, V30, P123, DOI 10.1111/j.1469-7610.1989.tb00772.x Wechsler D., 1992, WECHSLER INTELLIGENC World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 15 TC 116 Z9 116 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 DEC PY 2001 VL 43 IS 12 BP 809 EP 818 DI 10.1017/S0012162201001475 PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 507CJ UT WOS:000173009000005 PM 11769267 ER PT J AU Bescoby-Chambers, N Forster, P Bates, G AF Bescoby-Chambers, N Forster, P Bates, G TI 'Foetal valproate syndrome and autism: additional evidence of an association' SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Letter C1 Gulson Clin, SHO Psychiat, Coventry, W Midlands, England. Blakesley Ctr, Birmingham, W Midlands, England. RP Bescoby-Chambers, N (reprint author), Gulson Clin, SHO Psychiat, Coventry, W Midlands, England. CR CHRISTIANSON AL, 1994, DEV MED CHILD NEUROL, V36, P361 DILIBERTI JH, 1984, AM J MED GENET, V19, P473, DOI 10.1002/ajmg.1320190308 WHO, 1993, ICD 10 CLASS MENT BE Williams G, 2001, DEV MED CHILD NEUROL, V43, P202, DOI 10.1017/S001216220100038X Williams PG, 1997, DEV MED CHILD NEUROL, V39, P632 NR 5 TC 10 Z9 11 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 DEC PY 2001 VL 43 IS 12 BP 847 EP 847 DI 10.1017/S0012162201211542 PG 1 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 507CJ UT WOS:000173009000012 PM 11769274 ER PT J AU Ruef, MB Turnbull, AP AF Ruef, MB Turnbull, AP TI Stakeholder opinions on accessible informational products helpful in building positive, practical solutions to behavioral challenges of individuals with mental retardation and/or autism SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article ID TO-PRACTICE GAP; PARTICIPATORY ACTION RESEARCH; SPECIAL-EDUCATION; FAMILY PERSPECTIVES; SEVERE HANDICAPS; CHILDREN; INTERVENTION; CONTEXT; PEOPLE; LIFE AB The purpose of the study was twofold: (a) to explore the perceptions of administrators and policy makers, families, friends, individuals with challenging behavior and mental retardation and/or autism, researchers, and teachers regarding current behavioral information and dissemination and (b) to elicit suggestions on the kinds of user-friendly, low-cost informational products that they thought would be most helpful in increasing quality of life while reducing or eliminating behavioral challenges in individuals with disabilities. A qualitative method of inquiry using telephone focus groups and individual interviews was used. The study points to the importance of receiving condensed positive behavioral support information on both awareness and skill levels and to the continued existence of a long-standing gap between research and practice, a gap that exists despite the extensive research base on effective dissemination strategies and techniques. C1 Calif Polytech State Univ San Luis Obispo, Ctr Teacher Educ, San Luis Obispo, CA 93407 USA. Univ Kansas, Lawrence, KS 66045 USA. RP Ruef, MB (reprint author), Calif Polytech State Univ San Luis Obispo, Ctr Teacher Educ, Bldg 2,Room 106, San Luis Obispo, CA 93407 USA. CR Abbott M, 1999, EXCEPT CHILDREN, V65, P339 ALBERTI PA, 1990, APPL BEHAV ANAL TEAC BASHINSKI S, 1999, ANN C ASS PERS SEV D Beutler L. 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P., 1997, FAMILIES PROFESSIONA Turnbull AP, 1997, EXCEPT CHILDREN, V63, P211 TURNBULL AP, 2000, J POSIT BEHAV INTERV, V2, P190, DOI 10.1177/109830070000200310 Turnbull AP, 1996, MENT RETARD, V34, P280 Turnbull AP, 1998, J ASSOC PERS SEVERE, V23, P178, DOI 10.2511/rpsd.23.3.178 WESTBROOK JD, 1997, DISSEMINATION UTILIZ Whyte W. F., 1991, PARTICIPATORY ACTION, P19 WOODWARD J, 1993, ED TREATMENT CHILDRE, V16, P345 Zarb G., 1992, DISABILITY HANDICAP, V7, P125, DOI [10.1080/02674649266780161, DOI 10.1080/02674649266780161] NR 73 TC 4 Z9 4 PU COUNCIL EXCEPTIONAL CHILDREN PI RESTON PA 1920 ASSOCIATION DR, RESTON, VA 22091-1589 USA SN 0013-1237 J9 EDUC TRAIN MENT RET JI Educ. Train. Mental Retard. Dev. Disabil. PD DEC PY 2001 VL 36 IS 4 BP 441 EP 456 PG 16 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 502DN UT WOS:000172728600010 ER PT J AU Mildenberger, K Sitter, S Noterdaeme, M Amorosa, H AF Mildenberger, K Sitter, S Noterdaeme, M Amorosa, H TI The use of the ADI-R as a diagnostic tool in the differential diagnosis of children with infantile autism and children with a receptive language disorder SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; specific language impairment; receptive language disorder; developmental language disorder; ADI-R ID PERVASIVE DEVELOPMENTAL DISORDERS; COMPARATIVE FOLLOW-UP; EARLY ADULT LIFE; PSYCHIATRIC-DISORDERS; INTERVIEW; OUTCOMES; SPEECH; ISSUES AB Children with infantile autism and children with a specific receptive language disorder often show similar behavioural problems, making the differentiation between these two diagnostic categories difficult. The purpose of this study is to evaluate the usefulness of parental information in the differential diagnosis of the two types of disorders mentioned above. Sixteen children with a receptive language disorder and 11 children with infantile autism participated in the study. All children had normal non-verbal IQs. The ADI-R (Autism Diagnostic Interview-Revised) was performed with all children. The results showed that the ADI-R items reflecting behavioural. features at pre-school age (age range 4-5 years) were better suited to differentiate the groups than the items reflecting behavioural features at the time of the investigation (mean age: 9 years). The items on the dimension "Reciprocal social interaction" and "Communication and language" discriminated the groups better than the items of the dimension "Restricted interests". According to the ICD-10 algorithm of the ADI-R one child with autism and one child with a receptive language disorder were falsely classified. These false classifications were mainly due to a distorted parental perception of the child's behaviour. The ADI-R is a useful tool in the differential diagnosis of developmental disorders. C1 Heckscher Klin Kinder & Jugendpsychiat, Abt Teilleistungs & Verhaltensgestorte Kinder, D-81479 Munich, Germany. Univ Munich, Inst Kinder & Jugendpsychiat, D-80336 Munich, Germany. RP Mildenberger, K (reprint author), Heckscher Klin Kinder & Jugendpsychiat, Abt Teilleistungs & Verhaltensgestorte Kinder, Wolfratshauser Str 350, D-81479 Munich, Germany. CR ALLEN DA, 1992, INT CONGR SER, V965, P157 ALLEN DA, 1988, J CHILD NEUROL, V35, P48 AMOROSA H, 1992, AKTUELLE ENTWICKLUNG, P61 BARTAK L, 1976, J AUTISM CHILD SCHIZ, V6, P109, DOI 10.1007/BF01538054 BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 BEITCHMAN JH, 1986, J AM ACAD CHILD PSY, V25, P528, DOI 10.1016/S0002-7138(10)60013-1 BERGER F, 1990, Z KINDER JUG-PSYCH, V18, P71 BOLTE S, 1999, EUROPEAN CHILD ADOLE, V8, P70 CANTWELL D, 1978, J CHILD PSYCHOL PSYC, V19, P351, DOI 10.1111/j.1469-7610.1978.tb00481.x CANTWELL DP, 1989, J AUTISM DEV DISORD, V19, P19, DOI 10.1007/BF02212715 GRIMM H, 1978, HEIDELBERGER SPRACHE Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 Kaufman AS, 1991, KAUFMAN ASSESSMENT B LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X McFall RM, 1999, ANNU REV PSYCHOL, V50, P215, DOI 10.1146/annurev.psych.50.1.215 PAUL R, 1984, J AUTISM DEV DISORD, V14, P405, DOI 10.1007/BF02409831 PAUL R, 1983, J AM ACAD CHILD PSY, V22, P525, DOI 10.1097/00004583-198311000-00002 Rapin I., 1996, PRESCHOOL CHILDREN I, P190 Rapin I, 1998, INT J LANG COMM DIS, V33, P82 RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 SIEGEL B, 1990, J PSYCHIAT RES, V24, P293, DOI 10.1016/0022-3956(90)90002-8 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 WATERHOUSE L, 1996, PRESCHOOL CHILDREN I, P21 *WHO, 1991, ICD 10 INT KLASSIFIK ZWEIG MH, 1993, CLIN CHEM, V39, P561 NR 28 TC 22 Z9 22 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD DEC PY 2001 VL 10 IS 4 BP 248 EP 255 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 503CP UT WOS:000172780200005 PM 11794550 ER PT J AU Wong, SKF Tam, SF AF Wong, SKF Tam, SF TI Effectiveness of a multimedia programme and therapist-instructed training for children with autism SO INTERNATIONAL JOURNAL OF REHABILITATION RESEARCH LA English DT Article DE autism; children; interactive; multimedia programme; therapist-instructed training ID LEARNING-DISABILITIES; STUDENTS AB The present study aimed to evaluate the effectiveness of an interactive multimedia training programme and a conventional therapist-instructed training in improving the learning behaviours of children with autism. A multiple-subject, single case-study time-series research design was adopted in the study. Six children with autism, aged 2 years 4 months to 2 years 10 months, were recruited by convenience sampling. They attended a 12-session training programme on basic concepts (e.g. colours, shapes) that was presented as an interactive multimedia training programme and also as a conventional, therapist-led training programme. The attending behaviours and appropriate responses of the subjects were videotaped for further analysis. Participants who attended the conventional therapist-instructed training programme generally showed improvement in attending behaviours and response rates; participants attending the multimedia programme also showed improvement in their attending behaviours and response rates. The results support the hypothesis that both training programmes are effective in improving the attending behaviours and appropriate responses of children with autism. The authors suggest that, because children with autism respond differently to different training approaches, customized training programmes should be considered for individual children. The implications of the methodology and the potential impact of the present study on the training of children with autism are discussed. C1 Hong Kong Polytech Univ, Dept Rehabil Sci, Kowloon, Hong Kong, Peoples R China. RP Tam, SF (reprint author), Hong Kong Polytech Univ, Dept Rehabil Sci, Kowloon, Hong Kong, Peoples R China. CR BARKER J, 1990, INTERACTIVE LEARNING, P11 BARON CS, 1995, MINDBLINDNESS ESSAY, P59 COHEN SB, 1993, AUTISM FACTS Ferretti RP, 1996, J LEARN DISABIL-US, V29, P450 HAWKRIDGE D, 1992, LEARING DIFFICULTIES HEIMANN M, 1995, J AUTISM DEV DISORD, V25, P459, DOI 10.1007/BF02178294 JORDAN RR, 1996, ADV ASSESSMENT MANAG, V13, P41 Kirsh D, 1997, INSTR SCI, V25, P79, DOI 10.1023/A:1002915430871 Koegel R. L., 1989, AUTISM NATURE DIAGNO, P310 KOEGEL RL, 1995, TEACHING CHILDREN AU, P33 Kommers P, 1996, HYPERMEDIA LEARNING Light P., 1999, SOCIAL PROCESSES CHI POWERS MD, 1989, CHILDREN AUTISM PARE, P1 RUTTER M, 1994, TREATMENT AUTISTIC C, P10 Schopler E., 1995, LEARNING COGNITION A, P243 SCHOPLER E, 1987, AM PSYCHOL, V42, P379 Schopler E., 1988, CHILDHOOD AUTISM RAT Schopler E, 1990, PSYCHOEDUCATIONAL PR Schopler E, 1995, LEARING COGNITION AU, P13 SMITH MD, 1990, AUTISM LIFE COMMUNIT Wilson R, 1996, J LEARN DISABIL, V29, P382 Wissick CA, 1996, J LEARN DISABIL, V29, P494 NR 22 TC 3 Z9 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0342-5282 J9 INT J REHABIL RES JI Int. J. Rehabil. Res. PD DEC PY 2001 VL 24 IS 4 BP 269 EP 278 DI 10.1097/00004356-200112000-00003 PG 10 WC Rehabilitation SC Rehabilitation GA 502DB UT WOS:000172727500003 PM 11775031 ER PT J AU Thiemann, KS Goldstein, H AF Thiemann, KS Goldstein, H TI Social stories, written text cues, and video feedback: Effects on social communication of children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; communication; visual cues; videotape feedback; peer interaction ID PEER INTERACTIONS; BEHAVIOR; SKILLS; INTERVENTION; DISABILITIES; HYPERLEXIA; DISCOURSE; ABILITIES; LANGUAGE AB This study investigated the effects of written text and pictorial cuing with supplemental video feedback on the social communication of 5 students with autism and social deficits. Two peers without disabilities participated as social partners with each child with autism to form five triads. Treatment was implemented twice per week and consisted of 10 min of systematic instruction using visual stimuli, 10 min of social interaction, and 10 min of self-evaluation using video feedback. Results showed increases in targeted social communication skills when the treatment was implemented. Some generalized treatment effects were observed across untrained social behaviors, and I participant generalized improvements within the classroom. In addition, naive judges reported perceived improvements in the quality of reciprocal interactions. These findings support recommendations for using visually cued instruction to guide the social language development of young children with autism as they interact with peers without disabilities. C1 Florida State Univ, Tallahassee, FL 32306 USA. RP Thiemann, KS (reprint author), Juniper Gardens Childrens Project, 650 Minnesota Ave,2nd Floor, Kansas City, KS 66101 USA. CR BRINTON B, 1984, J SPEECH HEAR RES, V27, P350 Brown L., 1997, TEST NONVERBAL INTEL CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Dunn L. M., 1981, PEABODY PICTURE VOCA Garrison-Harrell L., 1997, FOCUS AUTISM OTHER D, V12, P241, DOI DOI 10.1177/108835769701200406 Gray C., 1995, TEACHING CHILDREN AU, P219 Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 Gresham F. M., 1990, SOCIAL SKILLS RATING HARING TG, 1992, J APPL BEHAV ANAL, V25, P319, DOI 10.1901/jaba.1992.25-319 HEALY JM, 1982, READ RES QUART, V17, P319, DOI 10.2307/747522 Hepting NH, 1996, TOP EARLY CHILD SPEC, V16, P407 Hodgdon L. Q., 1995, TEACHING CHILDREN AU, P265 Kamps D., 1997, J BEHAV ED, V7, P335, DOI 10.1023/A:1022879607019 KAMPS DM, 1992, J APPL BEHAV ANAL, V25, P281, DOI 10.1901/jaba.1992.25-281 KERNDUNLAP L, 1992, J APPL BEHAV ANAL, V25, P355, DOI 10.1901/jaba.1992.25-355 KISTNER J, 1988, J AUTISM DEV DISORD, V18, P191, DOI 10.1007/BF02211946 KOEGEL RL, 1993, J APPL BEHAV ANAL, V26, P369, DOI 10.1901/jaba.1993.26-369 KRANTZ P, 1993, J APPL BEHAV ANAL, V31, P191 LINCOLN AJ, 1988, J AUTISM DEV DISORD, V18, P505, DOI 10.1007/BF02211870 LORD C, 1995, DEV PSYCHOPATHOL, V7, P611 LOVELAND KA, 1988, J SPEECH HEAR RES, V31, P593 MENTIS M, 1994, TOP LANG DISORD, V14, P29 Myles B. S., 1999, FOCUS AUTISM OTHER D, V14, P82, DOI 10.1177/108835769901400203 Newcomer PL, 1988, TEST LANGUAGE DEV Norris C, 1999, FOCUS AUTISM OTHER D, V14, P180, DOI DOI 10.1177/108835769901400307 OKE NJ, 1990, J AUTISM DEV DISORD, V20, P479, DOI 10.1007/BF02216054 PIERCE K, 1995, J APPL BEHAV ANAL, V28, P285, DOI 10.1901/jaba.1995.28-285 PRUTTING CA, 1987, J SPEECH HEAR DISORD, V52, P105 *PSYCH CORP, 1994, CLIN EV LANG FUND Quill KA, 1997, J AUTISM DEV DISORD, V27, P697, DOI 10.1023/A:1025806900162 Ramberg C, 1996, EUR J DISORDER COMM, V31, P387 Sasso GM, 1998, BEHAV DISORDERS, V24, P34 Schopler E., 1988, CHILDHOOD AUTISM RAT Schuler A, 1995, TEACHING CHILDREN AU, P11 STONE WL, 1990, J AUTISM DEV DISORD, V20, P437, DOI 10.1007/BF02216051 TSAI L, 1992, HIGH FUNCTIONING IND VanMeter L, 1997, J AUTISM DEV DISORD, V27, P557, DOI 10.1023/A:1025830110640 Volkmar F., 1997, HDB AUTISM PERVASIVE, P173 WETHERBY AM, 1984, J SPEECH HEAR RES, V27, P364 WHITEHOUSE D, 1984, J AUTISM DEV DISORD, V14, P281, DOI 10.1007/BF02409579 WOLFBERG PJ, 1993, J AUTISM DEV DISORD, V23, P467, DOI 10.1007/BF01046051 Woodcock R. W., 1998, WOODCOCK READING MAS NR 42 TC 94 Z9 94 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2001 VL 34 IS 4 BP 425 EP 446 DI 10.1901/jaba.2001.34-425 PG 22 WC Psychology, Clinical SC Psychology GA 510AD UT WOS:000173185800003 PM 11800183 ER PT J AU McCord, BE Iwata, BA Galensky, TL Ellingson, SA Thomson, RJ AF McCord, BE Iwata, BA Galensky, TL Ellingson, SA Thomson, RJ TI Functional analysis and treatment of problem behavior evoked by noise SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE escape behavior; establishing operations; functional analysis; noise ID INJURIOUS ESCAPE BEHAVIOR; SELF-INJURY; DEVELOPMENTAL-DISABILITIES; ESTABLISHING OPERATIONS; SLEEP-DEPRIVATION; EXTINCTION; REINFORCEMENT; CHILDREN; AUTISM AB We conducted a four-part investigation to develop methods for assessing and treating problem behavior evoked by noise. In Phase 1, 7 participants with developmental disabilities who were described as being hypersensitive to specific noises were exposed to a series of noises under controlled conditions. Results for 2 of the participants verified that noise was apparently an aversive event. In Phase 2, results of functional analyses indicated that these 2 participants' problem behaviors were maintained by escape from noise. In Phase 3, preference assessments were conducted to identify reinforcers that might be used during treatment. Finally, in Phase 4, the 2 participants' problem behaviors were successfully treated with extinction, stimulus fading, and a differential-reinforcement-of-other-behavior (DRO) contingency (only I participant required DRO). Treatment effects for both participants generalized to their home environments and were maintained during a follow-up assessment. Procedures and results were discussed in terms of their relevance to the systematic assessment of noise as an establishing operation (EO) and, more generally, to the identification of idiosyncratic EO influences on behavior. C1 Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. RP Iwata, BA (reprint author), Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. RI Iwata, Brian/A-7391-2009 OI Iwata, Brian/0000-0001-8217-2049 CR Bettison S, 1996, J AUTISM DEV DISORD, V26, P361, DOI 10.1007/BF02172480 CARR EG, 1985, J APPL BEHAV ANAL, V18, P111, DOI 10.1901/jaba.1985.18-111 CARR EG, 1980, J APPL BEHAV ANAL, V13, P101, DOI 10.1901/jaba.1980.13-101 DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 Ellingson SA, 2000, J APPL BEHAV ANAL, V33, P41, DOI 10.1901/jaba.2000.33-41 FELDMAN MA, 1997, PREVENTION TREATMENT, P23 Fischer SM, 1997, J APPL BEHAV ANAL, V30, P335, DOI 10.1901/jaba.1997.30-335 ZARCONE JR, 1994, J APPL BEHAV ANAL, V27, P307, DOI 10.1901/jaba.1994.27-307 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P215, DOI 10.1901/jaba.1994.27-215 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 IWATA BA, 1990, J APPL BEHAV ANAL, V23, P11, DOI 10.1901/jaba.1990.23-11 Iwata BA, 2000, J APPL BEHAV ANAL, V33, P411, DOI 10.1901/jaba.2000.33-411 Kennedy CH, 1996, J APPL BEHAV ANAL, V29, P133, DOI 10.1901/jaba.1996.29-133 LALLI JS, 1995, J APPL BEHAV ANAL, V28, P261, DOI 10.1901/jaba.1995.28-261 Marcus BA, 1996, J APPL BEHAV ANAL, V29, P43, DOI 10.1901/jaba.1996.29-43 McGill P, 1999, J APPL BEHAV ANAL, V32, P393, DOI 10.1901/jaba.1999.32-393 MICHAEL J, 1982, J EXP ANAL BEHAV, V37, P149, DOI 10.1901/jeab.1982.37-149 MICHAEL J, 1993, BEHAV ANALYST, V16, P191 NORTHERN JL, 1978, HEARING CHILDREN OREILLY MF, 1995, J APPL BEHAV ANAL, V28, P225, DOI 10.1901/jaba.1995.28-225 O'Reilly MF, 2000, J APPL BEHAV ANAL, V33, P511, DOI 10.1901/jaba.2000.33-511 OReilly MF, 1997, J APPL BEHAV ANAL, V30, P165, DOI 10.1901/jaba.1997.30-165 PACE GM, 1993, J APPL BEHAV ANAL, V26, P205, DOI 10.1901/jaba.1993.26-205 PACE GM, 1994, J APPL BEHAV ANAL, V27, P301, DOI 10.1901/jaba.1994.27-301 PACLAWSKYJ TR, 1995, J APPL BEHAV ANAL, V28, P219, DOI 10.1901/jaba.1995.28-219 Rapp JT, 1998, J APPL BEHAV ANAL, V31, P665, DOI 10.1901/jaba.1998.31-665 RIMLAND B, 1995, J AUTISM DEV DISORD, V25, P61, DOI 10.1007/BF02178168 Smith RG, 1997, J APPL BEHAV ANAL, V30, P343, DOI 10.1901/jaba.1997.30-343 Smith RG, 1995, J APPL BEHAV ANAL, V28, P515, DOI 10.1901/jaba.1995.28-515 VOLLMER TR, 1995, J APPL BEHAV ANAL, V28, P15, DOI 10.1901/jaba.1995.28-15 Wacker DP, 1996, J APPL BEHAV ANAL, V29, P79, DOI 10.1901/jaba.1996.29-79 ZARCONE JR, 1993, J APPL BEHAV ANAL, V26, P353, DOI 10.1901/jaba.1993.26-353 NR 32 TC 18 Z9 18 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2001 VL 34 IS 4 BP 447 EP 462 DI 10.1901/jaba.2001.34-447 PG 16 WC Psychology, Clinical SC Psychology GA 510AD UT WOS:000173185800004 PM 11800184 ER PT J AU Dixon, MR Cummings, A AF Dixon, MR Cummings, A TI Self-control in children with autism response allocation during delays to reinforcement SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE self-control; delayed reinforcement; choice; concurrent activities; autism AB This study examined the use of a progressive-delay schedule of reinforcement to increase self-control and decrease disruptive behavior in children with autism. When initially given the choice between an immediate smaller reinforcer and a larger delayed reinforcer, all participants chose the smaller reinforcer. When access to the larger reinforcer required either no activity or engaging in a concurrent task during the delay, all participants demonstrated both self-control and preference for a response requirement. Disruptive behavior decreased during delays that required a concurrent task compared to sessions without an activity requirement. C1 So Illinois Univ, Inst Rehabil, Behav Anal & Therapy Program, Carbondale, IL 62901 USA. Western Michigan Univ, Kalamazoo, MI 49008 USA. RP Dixon, MR (reprint author), So Illinois Univ, Inst Rehabil, Behav Anal & Therapy Program, Carbondale, IL 62901 USA. CR Dixon MR, 1998, J APPL BEHAV ANAL, V31, P203, DOI 10.1901/jaba.1998.31-203 Dixon MR, 2000, J APPL BEHAV ANAL, V33, P611, DOI 10.1901/jaba.2000.33-611 MISCHEL H. N., 1972, Journal of Personality and Social Psychology, V16, P204 SCHWEITZER JB, 1988, J EXP ANAL BEHAV, V50, P173, DOI 10.1901/jeab.1988.50-173 NR 4 TC 22 Z9 22 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2001 VL 34 IS 4 BP 491 EP 495 DI 10.1901/jaba.2001.34-491 PG 5 WC Psychology, Clinical SC Psychology GA 510AD UT WOS:000173185800008 PM 11800188 ER PT J AU DeLeon, IG Neidert, PL Anders, BM Rodriguez-Catter, V AF DeLeon, IG Neidert, PL Anders, BM Rodriguez-Catter, V TI Choices between positive and negative reinforcement during treatment for escape-maintained behavior SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE differential reinforcement; compliance; choice; escape-maintained behavior; behavioral economics AB Positive reinforcement was more effective than negative reinforcement in promoting compliance and reducing escape-maintained problem behavior for a child with autism. Escape extinction was then added while the child was given a choice between positive or negative reinforcement for compliance and the reinforcement schedule was thinned. When the reinforcement requirement reached 10 consecutive tasks, the treatment effects became inconsistent and reinforcer selection shifted from a strong preference for positive reinforcement to an unstable selection pattern. C1 Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. RP DeLeon, IG (reprint author), Kennedy Krieger Inst, Neurobehav Unit, 707 N Broadway, Baltimore, MD 21205 USA. CR IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Lalli JS, 1999, J APPL BEHAV ANAL, V32, P285, DOI 10.1901/jaba.1999.32-285 Piazza CC, 1997, J APPL BEHAV ANAL, V30, P279, DOI 10.1901/jaba.1997.30-279 TUSTIN RD, 1994, J APPL BEHAV ANAL, V27, P597, DOI 10.1901/jaba.1994.27-597 NR 4 TC 26 Z9 27 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2001 VL 34 IS 4 BP 521 EP 525 DI 10.1901/jaba.2001.34-521 PG 5 WC Psychology, Clinical SC Psychology GA 510AD UT WOS:000173185800014 PM 11800194 ER PT J AU Pickett, J AF Pickett, J TI Current investigations in autism brain tissue research SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism brain research; brain tissue; neuropathology; neurohistology; magnetic resonance imaging (MRI) ID COUNTING NEURONS AB Brain tissue research has developed into a high-tech, multifaceted approach to understanding neurological disorders. Directed. toward autism spectrum disorders, this investigative approach combines with other disciplines, such as imaging and genetics, to help explain the range and intensity of behaviors that characterize these disorders. This report is intended as an update on current autism brain research efforts and has a dual purpose: first, to disseminate information to the scientific community in the hope of stimulating more thinking about autism research and future collaborations; and second, to let the autism community know what is happening with this precious resource that was donated in the hope of determining the cause of autism and finding effective treatments. C1 Autism Tissue Program, Princeton, NJ 08540 USA. RP Pickett, J (reprint author), Autism Tissue Program, 99 Wall St, Princeton, NJ 08540 USA. 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Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 521 EP 527 DI 10.1023/A:1013282524687 PG 7 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300002 PM 11814261 ER PT J AU Fatemi, SH Stary, JM Halt, AR Realmuto, GR AF Fatemi, SH Stary, JM Halt, AR Realmuto, GR TI Dysregulation of Reelin and Bcl-2 proteins in autistic cerebellum SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE cerebellum; autism; Reelin; Bcl-2 ID BIPOLAR DISORDER; EXPRESSION; SCHIZOPHRENIA; BRAIN; IMMUNOREACTIVITY; HIPPOCAMPUS; REDUCTION; DECREASE; CORTEX AB Autism is a severe neurodevelopmental disorder with potential genetic and environmental causes. Cerebellar pathology including Purkinje cell atrophy has been demonstrated previously. We hypothesized that cell migration and apoptotic mechanisms may account for observed Purkinje cell abnormalities. Reelin is an important secretory glycoprotein responsible for normal layering of the brain. Bcl-2 is a regulatory protein responsible for control of programmed cell death in the brain. Autistic and normal control cerebellar corteces matched for age, sex, and post-mortem interval (PMI) were prepared for SDS-gel efectrophoresis and Western blotting using specific anti-Reelin and anti-Bcl-2 antibodies. Quantification of Reelin bands showed 43%, 44%, and 44% reductions in autistic cerebellum (mean optical density +/- SD per 30 Rg protein 4.05 +/- 4.0, 1.98 +/- 2.0, 13.88 +/- 11.9 for 410 kDa, 330 kDa, and 180 kDa bands, respectively; N = 5) compared with controls (mean optical density SD per 30 mug protein, 7.1 +/- 1.6, 3.5 +/- 1.0, 24.7 +/- 5.0; N = 8, p < 0.0402 for 180 kDa band). Quantification of Bcl-2 levels showed a 34% to 51% reduction in autistic cerebellum (M SD per 75 mug protein 0.29 +/- 0.08; N = 5) compared with controls (M +/- SD per 75 Rg protein 0.59 +/- 0.31; N = 8, p < 0.0451). Measurement of beta-actin (M SD for controls 7.3 +/- 2.9; for autistics 6.77 +/- 0.66) in the same homogenates did not differ significantly between groups. These results demonstrate for the first time that dysregulation of Reelin and Bcl-2 may be responsible for some of the brain structural and behavioral abnormalities observed in autism. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Dept Neurosci, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Div Child Psychiat, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Box 392 Mayo Bldg,420 Delaware St SE, Minneapolis, MN 55455 USA. 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PD DEC PY 2001 VL 31 IS 6 BP 529 EP 535 DI 10.1023/A:1013234708757 PG 7 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300003 PM 11814262 ER PT J AU Blatt, GJ Fitzgerald, CM Guptill, JT Booker, AB Kemper, TL Bauman, ML AF Blatt, GJ Fitzgerald, CM Guptill, JT Booker, AB Kemper, TL Bauman, ML TI Density and distribution of hippocampal neurotransmitter receptors in autism: An autoradiographic study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; GABA(A) receptors; benzodiazepine receptors; serotoninergic receptors; cholinergic receptors; hippocampus ID BENZODIAZEPINE-RECEPTORS; RAT-BRAIN; INFANTILE-AUTISM; GABA RECEPTORS; BINDING-SITES; FLUNITRAZEPAM; LOCALIZATION; MONKEY; NMDA AB Neuropathological studies in autistic brains have shown small neuronal size and increased cell packing density in a variety of limbic system structures: including the hippocampus, a change consistent with curtailment of normal development. Based on these observations in the hippocampus, a series of quantitative receptor autoradiographic studies were undertaken to determine the density and distribution of eight types of neurotransmitter receptors from four neurotransmitter systems (GABAergic, serotoninergic [5-HT], cholinergic, and glutamatergic). Data from these single concentration ligand binding studies indicate that the GABAergic receptor system ((3)[H]-flunitrazepam labeled benzodiazepine binding sites and (3)[H]-muscimol labeled GABA(A) receptors) is significantly reduced in high binding regions, marking for the first time an abnormality in the GABA system in autism. In contrast, the density and distribution of the other six receptors studied ((3)[H]-8OH-DPAT labeled 5-HT(1A) receptors, (3)[H] ketanserin labeled 5-HT. receptors, (3)[H]pirenzepine labled M1 receptors, (3)[H]-hemicholinium labeled high affinity choline uptake sites, (3)[H]-MK801 labeled NMDA receptors, and (3)[H]-kainate labeled kainate receptors) in the hippocampus did not demonstrate any statistically significant differences in binding. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Neurobiol Dev Disorders Lab, Boston, MA 02118 USA. RP Blatt, GJ (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, Neurobiol Dev Disorders Lab, 715 Albany St, Boston, MA 02118 USA. 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Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 537 EP 543 DI 10.1023/A:1013238809666 PG 7 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300004 PM 11814263 ER PT J AU Purcell, AE Jeon, OH Pevsner, J AF Purcell, AE Jeon, OH Pevsner, J TI The abnormal regulation of gene expression in autistic brain tissue SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE pervasive developmental disorder; cDNA microarray; subtractive hybridization; diagnostic test ID INFANTILE-AUTISM; RETT-SYNDROME; NEUROBIOLOGY AB Autism is a pervasive developmental disorder of unknown etiology. It is likely caused by mutations in one or more genes. One approach to understanding the molecular changes that occur in autism is to measure gene expression in post-mortem brain samples from individuals diagnosed with autism. This may be accomplished with techniques such as cDNA microarrays or subtractive hybridization. In general, gene expression is regulated as a function of body region, developmental time, and physiological state. A premise of the approaches we describe is that gene expression is regulated in cells from autistic individuals as a consequence of the disease process. It may be useful to detect such changes in order to identify selective biological markers for autism. Additionally, the abnormal regulation of gene expression may reveal cellular pathways that have been disrupted, suggesting strategies for therapeutic intervention. C1 Kennedy Krieger Res Inst, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. RP Pevsner, J (reprint author), Kennedy Krieger Res Inst, Dept Neurol, 707 N Broadway, Baltimore, MD 21205 USA. 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Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 545 EP 549 DI 10.1023/A:1013290826504 PG 5 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300005 PM 11814264 ER PT J AU Hemby, SE Sanchez, MM Winslow, JT AF Hemby, SE Sanchez, MM Winslow, JT TI Functional Genomics approaches to a primate model of autistic symptomology SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; gene expression; temporal lobe; rhesus monkey; functional genomics ID HUMAN BRAIN; INFANTILE-AUTISM; OVERDOSE VICTIMS; RHESUS-MONKEYS; I-125 RTI-55; COCAINE; BINDING; SITES; HIPPOCAMPUS; SCLEROSIS AB Several studies indicate a primary dysfunction of the temporal lobe in autism, specifically the hippocampal formation and entorhinal cortex (EC). Assessment of gene expression in the EC and hippocampus will provide insight into the subtle alterations in neuronal function associated with autism. To this end, evaluations in a primate model of social attachment, which produces behaviors associated with autism, in addition to the use of human post-mortem tissue from individuals diagnosed with autism will provide heretofore unattainable information of how the complex neural circuitry of this region is altered in autism. Identification of altered expression of multiple genes should provide a molecular: "fingerprint" of autism and may provide new targets for pharmacotherapeutie intervention. C1 Emory Univ, Sch Med, Yerkes Reg Primate Res Ctr, Dept Pharmacol, Atlanta, GA 30329 USA. Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA 30329 USA. Emory Univ, Yerkes Reg Primate Res Ctr, Div Neurosci, Atlanta, GA 30322 USA. Emory Univ, Yerkes Reg Primate Res Ctr, Div Psychobiol, Atlanta, GA 30322 USA. RP Hemby, SE (reprint author), Emory Univ, Sch Med, Yerkes Reg Primate Res Ctr, Dept Pharmacol, 954 Gatewood Rd NE, Atlanta, GA 30329 USA. 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In this approach, tissue or cellular proteins from control and affected subjects are separated on two-dimensional (2-D) polyacrylamide gel electrophoresis, and those proteins that show marked changes in the concentration between control and affected subjects are identified by mass spectroscopy. This method has been successfully, applied in the elucidation of the molecular biological defect in classic late-infantile neuronal ceroid lipofuscinosis (Sleat et al., 1997). Unlike the classical methods of genome-wide screening for chromosomal localization followed by positional cloning, the proteomic approach requires limited number of tissue samples and the study can be completed in a relatively short time. Currently, these methods are available for relatively abundant proteins and generally are not applicable for hydrophobic proteins because 2-D gel electrophoresis is not very effective in the analysis of hydrophobic proteins. The genetic defect results in either total loss of proteins or changes in molecular weight and/or isoelectric point will be detectable by the proteomic method. Because autism is a neurogenetic disorder, brain is the tissue of choice for proteomic study. For an oligogenic disorder such as autism, at least some of the aberrant (genes) proteins may tic identified by this technology. C1 New York State Inst Basic Res Dev Disabil, Dept Dev Biochem, Staten Isl, NY 10314 USA. RP Pullarkat, RK (reprint author), New York State Inst Basic Res Dev Disabil, Dept Dev Biochem, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA. 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Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 557 EP 560 DI 10.1023/A:1013242910574 PG 4 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300007 PM 11814266 ER PT J AU Schumann, CM Buonocore, MH Amaral, DG AF Schumann, CM Buonocore, MH Amaral, DG TI Magnetic resonance imaging of the post-mortem autistic brain SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; MRI; neuroimaging ID ALZHEIMERS-DISEASE; MRI AB Magnetic resonance imaging (MRI) is a valuable, noninvasive tool for understanding structural abnormalities in the brain. The M.I.N.D. Institute at UC Davis has developed a protocol utilizing MRI to investigate anatomical differences in the post-mortem brain by applying a proton density weighted imaging sequence for optimal differences in image intensity (contrast) between gray and white matter. Images of the brain obtained prior to distribution of tissue and further neuropathological examination provide a record of how the brain appeared prior to tissue processing. The virtual representation of the whole brain can also be subjected to additional analyses, such as measuring the volume of brain regions or area of the cortical surface. We describe our procedures for carrying out post-mortem MRI,of the human brain. C1 Univ Calif Davis, Ctr Neurosci, Davis, CA 95616 USA. Univ Calif Davis, MIND Inst, Dept Psychiat, Davis, CA 95616 USA. Univ Calif Davis, Sch Med, Dept Radiol, Davis, CA 95616 USA. RP Amaral, DG (reprint author), Univ Calif Davis, Ctr Neurosci, 1544 Newton Ct, Davis, CA 95616 USA. CR Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Blamire AM, 1999, ACTA RADIOL, V40, P593 Bobinski M, 2000, NEUROSCIENCE, V95, P721 JACK CR, 1992, NEUROLOGY, V42, P183 NAGARA H, 1987, J NEUROL SCI, V81, P67, DOI 10.1016/0022-510X(87)90184-5 NIXON JR, 1989, MAYO CLIN PROC, V64, P305 Piven J, 1996, J AM ACAD CHILD PSY, V35, P530, DOI 10.1097/00004583-199604000-00020 Saitoh O, 1998, PSYCHIAT CLIN NEUROS, V52, pS219 SCARPELLI M, 1994, NEURORADIOLOGY, V36, P393 SEAB JP, 1988, MAGNET RESON MED, V8, P200, DOI 10.1002/mrm.1910080210 TOVI M, 1992, ACTA RADIOL, V33, P400 NR 11 TC 21 Z9 21 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 561 EP 568 DI 10.1023/A:1013294927413 PG 8 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300008 PM 11814267 ER PT J AU Shavelle, RM Strauss, DJ Pickett, J AF Shavelle, RM Strauss, DJ Pickett, J TI Causes of death in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; PDD; cause of death; life expectancy; mental retardation level; mortality; standardized mortality ratio ID LONG QT SYNDROME; PHYSICAL-ACTIVITY; CEREBRAL-PALSY; MORTALITY; CHILDREN AB The objective of this study was to determine which causes of death are more frequent in persons with autism, and by how much, compared with the general population. Subjects were 13,111 ambulatory Californians with autism, followed between 1983 and 1997. The units of study were person-years, each linked to the subject's age, sex, and cause of death (if any) for the specific year. Observed numbers of cause-specific deaths were compared with numbers expected according to general population mortality rates. Standardized mortality rates (SMRs) were computed for each mental retardation level. Elevated death rates were observed for several causes, including seizures and accidents such as suffocation and drowning; elevated mortality due to respiratory disease was observed among persons with severe mental retardation. Overall, excess mortality was especially marked for persons with severe mental retardation, but life expectancy is reduced even for persons who are full, ambulatory and who have only mild mental retardation. C1 Autism Tissue Program, Princeton, NJ 08540 USA. Life Expectancy Project, San Francisco, CA USA. RP Pickett, J (reprint author), Autism Tissue Program, 99 Wall St,Res Pk, Princeton, NJ 08540 USA. CR Ackerman MJ, 2001, AM J FOREN MED PATH, V22, P105, DOI 10.1097/00000433-200106000-00001 Ackerman MJ, 1999, MAYO CLIN PROC, V74, P1088 Andreassen M D, 2000, Ugeskr Laeger, V162, P1366 Annegers JF, 1999, SEIZURE-EUR J EPILEP, V8, P347, DOI 10.1053/seiz.1999.0306 ARIAS M, 1983, PACIFIC STATE ARCH, V8, P28 *CAL DEP DEV SERV, 1978, CLIENT DEV EV REP Chiang CE, 2000, J AM COLL CARDIOL, V36, P1, DOI 10.1016/S0735-1097(00)00716-6 De Ponti F, 2001, EUR J CLIN PHARMACOL, V57, P185, DOI 10.1007/s002280100290 Ficker DM, 1998, NEUROLOGY, V51, P1270 GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P375, DOI 10.1097/00004583-199105000-00004 HARRIS C, 1982, INTERRATER RELIABILI International Classification of Diseases, 1995, INT CLASSIFICATION D Kahn HA, 1989, STAT METHODS EPIDEMI KAHN M, 2000, S DAK J MED, V53, P395 Lilienfeld AM, 1980, FDN EPIDEMIOLOGY MALTBY J, 2000, ADVOCATE NOV, P13 *OFF HLTH INF RES, 1983, STAT CAL 1983 1997 A PAFFENBARGER RS, 1986, NEW ENGL J MED, V314, P605, DOI 10.1056/NEJM198603063141003 PAFFENBARGER RS, 1993, NEW ENGL J MED, V328, P538, DOI 10.1056/NEJM199302253280804 SHAVELLE RM, 2001, LISTING CAUSES DEATH Shavelle R M, 1998, J Insur Med, V30, P220 *STAT CAL DEP FIN, 1988, RAC ETHN POP AG SEX Strauss D, 1999, DEV MED CHILD NEUROL, V41, P580, DOI 10.1017/S001216229900122X Strauss DJ, 1998, ARCH PHYS MED REHAB, V79, P1095, DOI 10.1016/S0003-9993(98)90177-0 Strauss DJ, 1998, PEDIATR NEUROL, V18, P143, DOI 10.1016/S0887-8994(97)00172-0 STRAUSS DJ, 1999, DEV MED CHILD NEUROL, V40, P369 Tuchman R, 2000, J AUTISM DEV DISORD, V30, P485, DOI 10.1023/A:1005572128200 Wang Q, 1998, MOL MED TODAY, V4, P382, DOI 10.1016/S1357-4310(98)01320-3 WIDAMAN KF, 1984, 92 ANN M AM PSYCH AS WIDAMAN KF, 1985, 109 ANN M AM ASS MEN NR 30 TC 56 Z9 58 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 569 EP 576 DI 10.1023/A:1013247011483 PG 8 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300009 PM 11814268 ER PT J AU Carpenter, M Pennington, BF Rogers, SJ AF Carpenter, M Pennington, BF Rogers, SJ TI Understanding of others' intentions in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE intention; imitation; theory of mind; joint attention ID ACCIDENTAL ACTIONS; IMITATION; INFANTS AB Many studies have shown that children with autism have difficulty understanding the thoughts and beliefs of other people. However, little research has been conducted on what these children understand about simpler mental states such as intentions. The current study tested the understanding of others' intentions in 2 1/2- to 5-year-old children with autism and a control group of children with other developmental delays. We used Meltzoff's (1995) test of understanding of others' unfulfilled intentions in an imitation context, with an additional "End State" condition. We found no significant between-group differences on any measure involving the understanding of others' intentions. Although within-group patterns suggested that children with autism may have a slightly less complex understanding of others' intentions than do other children, it was clear that any deficits these children showed in this area were not as marked as those they typically show on traditional theory of mind tasks. C1 Max Planck Inst Evolutionary Anthropol, D-04103 Leipzig, Germany. Univ Denver, Denver, CO 80208 USA. Univ Colorado, Hlth Sci Ctr, Boulder, CO 80309 USA. RP Carpenter, M (reprint author), Max Planck Inst Evolutionary Anthropol, Inselstr 22, D-04103 Leipzig, Germany. CR Aldridge MA, 2000, DEVELOPMENTAL SCI, V3, P294, DOI 10.1111/1467-7687.00123 Baron-Cohen S, 1993, UNDERSTANDING OTHER Baron-Cohen S., 2000, UNDERSTANDING OTHER, P3 BARONCOHEN S, 1995, BRIT J DEV PSYCHOL, V13, P379 BELLAGAMBA F, 1999, INFANT BEHAV DEV, V22 Call J, 1998, J COMP PSYCHOL, V112, P192, DOI 10.1037/0735-7036.112.2.192 CALL J, IN PRESS IMITATION A Carpenter M, 1998, INFANT BEHAV DEV, V21, P315, DOI 10.1016/S0163-6383(98)90009-1 CARPENTER M, IN PRESS J AUTISM DE Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 CHARMAN T, 1999, S IM AN ART SOC STUD FRITH U, 1989, BRIT J DISORD COMMUN, V24, P123 GERGELY G, 1995, COGNITION, V56, P165, DOI 10.1016/0010-0277(95)00661-H Happe F., 1994, AUTISM INTRO PSYCHOL Hobson R. Peter, 1993, AUTISM DEV MIND Hobson RP, 1999, J CHILD PSYCHOL PSYC, V40, P649, DOI 10.1111/1469-7610.00481 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Meltzoff AN, 1995, DEV PSYCHOL, V31, P1, DOI DOI 10.1037/0012-1649.31.5.838 Mundy P, 1993, UNDERSTANDING OTHER, P181 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Phillips W, 1998, BRIT J DEV PSYCHOL, V16, P337 PHILLIPS W, 1992, DEV PSYCHOPATHOL, V4, P375, DOI 10.1017/S0954579400000845 Rogers S. J., 1999, IMITATION INFANCY, P254 Rogers S. J., 1991, DEV PSYCHOPATHOL, V3, P137, DOI DOI 10.1017/S0954579400000043 Russell J., 1996, AGENCY ITS ROLE MENT Russell J, 2001, J CHILD PSYCHOL PSYC, V42, P317, DOI 10.1017/S0021963001006874 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 Tager-Flusberg H., 1993, UNDERSTANDING OTHER, P138 TOMASELLO M, 1993, BEHAV BRAIN SCI, V16, P495 WOODWARD AL, IN PRESS INFANT BEHA NR 30 TC 66 Z9 69 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 589 EP 599 DI 10.1023/A:1013251112392 PG 11 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300011 PM 11814270 ER PT J AU Baron-Cohen, S Wheelwright, S Skinner, R Martin, J Clubley, E AF Baron-Cohen, S Wheelwright, S Skinner, R Martin, J Clubley, E TI The autism-spectrum quotient (AQ): Evidence from Asperger Syndrome/high-functioning autism, males and females, scientists and mathematicians (vol 31, pg 5, 2001) SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Correction CR Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 NR 1 TC 9 Z9 9 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2001 VL 31 IS 6 BP 603 EP 603 PG 1 WC Psychology, Developmental SC Psychology GA 512MC UT WOS:000173327300012 ER PT J AU Scahill, L McCracken, J McDougle, CJ Aman, M Arnold, LE Tierney, E Cronin, P Davies, M Ghuman, J Gonzalez, N Koenig, K Lindsay, R Martin, A McGough, J Posey, DJ Swiezy, N Volkmar, F Ritz, L Vitiello, B AF Scahill, L McCracken, J McDougle, CJ Aman, M Arnold, LE Tierney, E Cronin, P Davies, M Ghuman, J Gonzalez, N Koenig, K Lindsay, R Martin, A McGough, J Posey, DJ Swiezy, N Volkmar, F Ritz, L Vitiello, B TI Methodological issues in designing a multisite trial of risperidone in children and adolescents with autism SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PEDIATRIC PSYCHOPHARMACOLOGY; DISORDER; NETWORK; DRUGS AB Objective: To describe the methodological challenges and decisions made in developing a multisite, controlled study of risperidone in children and adolescents with autism. Methods: Review the design considerations for clinical trials in children with autistic disorder accompanied by severe tantrums, aggressive and/or self-injurious behaviors. These design considerations include the definition of inclusion criteria that are relevant to clinical practice and matching study design to the goal of evaluating short- and long-term effects. Additional ethical and scientific issues concern the length of trial and sample size. Results: We undertook a short-term, placebo-controlled study to evaluate the efficacy and safety of risperidone in children and adolescents with autistic disorder. This trial design was followed by an extended open-label maintenance on risperidone to confirm durability of treatment effects and to monitor safety. Finally, a placebo-controlled discontinuation study tested the need for continuous treatment. Conclusions: In the absence of standard pharmacological treatment for children with autistic disorder, a placebo-controlled study remains the most appropriate method of testing efficacy and safety. The clinical relevance of this study is enhanced by the addition of an extended maintenance phase followed by a placebo discontinuation. C1 NIMH, Res Unit Pediat Psychopharmacol, Bethesda, MD 20892 USA. Columbia Univ, Res Unit Pediat Psychopharmacol, New York, NY USA. Kennedy Krieger Inst, Res Unit Pediat Psychopharmacol, Baltimore, MD USA. Ohio State Univ, Res Unit Pediat Psychopharmacol, Columbus, OH 43210 USA. Indiana Univ, Res Unit Pediat Psychopharmacol, Bloomington, IN USA. Univ Calif Los Angeles, Res Unit Pediat Psychopharmacol, Los Angeles, CA USA. Yale Univ, Res Unit Pediat Psychopharmacol, Autism Network, New Haven, CT USA. RP Scahill, L (reprint author), Yale Child Study Ctr, POB 207900, New Haven, CT 06520 USA. CR Aman M., 1986, ABERRANT BEHAV CHECK AMAN MG, 1985, AM J MENT DEF, V89, P485 AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 ANDERSON LT, 1989, J AUTISM DEV DISORD, V19, P277 Arnold LE, 2000, J AUTISM DEV DISORD, V30, P99, DOI 10.1023/A:1005451304303 Borenstein Michael, 1997, POWER PRECISION Campbell M, 1997, J AM ACAD CHILD PSY, V36, P835, DOI 10.1097/00004583-199706000-00022 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 COHEN DJ, 1997, HDB AUTISM PREVASIVE Fldiss JL, 1986, DESIGN ANAL CLIN EXP Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 GIBBONS RD, 1993, ARCH GEN PSYCHIAT, V50, P739 He N, 1999, EUR J CLIN PHARMACOL, V55, P457, DOI 10.1007/s002280050656 HEYKANTS J, 1994, J CLIN PSYCHIAT, V55, P13 Kumra S, 1997, J AM ACAD CHILD PSY, V36, P701, DOI 10.1097/00004583-199705000-00022 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Martin A, 2000, J CHILD ADOL PSYCHOP, V10, P259, DOI 10.1089/cap.2000.10.259 MASHBURN EC, 1992, J AUTISM DEV DISORD, V22, P357 McDougle CJ, 2000, CHILD ADOL PSYCH CL, V9, P201 Poolsup N, 2000, J CLIN PHARM THER, V25, P197 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Vitiello B, 1998, CAN J PSYCHIAT, V43, P582 Vitiello B, 1997, ARCH GEN PSYCHIAT, V54, P871 NR 23 TC 28 Z9 28 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD WIN PY 2001 VL 11 IS 4 BP 377 EP 388 DI 10.1089/104454601317261555 PG 12 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 518VU UT WOS:000173689200003 PM 11838820 ER PT J AU Masi, G Cosenza, A Mucci, M AF Masi, G Cosenza, A Mucci, M TI Prolactin levels in young children with pervasive developmental disorders during risperidone treatment SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID RECEPTOR OCCUPANCY; CLASSIFICATION; ADOLESCENTS; AUTISM; TRIAL; D-2 AB Although hyperprolactinemia is a common side effect during risperidone treatment in adult patients, no information is available on young children. The aim of this study is to report on serum prolactin levels in 25 young autistic children (22 males and 3 females, age range 3.9-7 years, mean age 4.10 years) during treatment with risperidone (dosage range 0.25-0.90 mg/day, mean dosage 0.52 mg/day). Prolactin levels were measured at baseline and after 10 weeks of treatment. The clinical outcome measure used was the Clinical Global Impression-Improvement. Serum prolactin was 9.77 +/- 3.94 ng/mL at baseline and 25.92 +/- 13.9 ng/mL during the 10th week of treatment (p < 0.001). Six children (24%) showed prolactin levels lower than 15 ng/mL, which is the upper normal level; eight children (28%) had prolactin levels higher than two times the upper limit (30 ng/mL). Hyperprolactinemia did not show significant correlations with age, weight, or risperidone dosage. There was no relation with clinical outcome. Dose reduction of risperidone resulted in a decrease of prolactin levels. None of the children showed clinical signs of hyperprolactinemia. Given the paucity of available data on potential effects of long-term hyperprolactinemia, a monitoring of prolactin during treatment with risperidone and other typical and atypical antipsychotics may be warranted. C1 Univ Pisa, Div Child Neurol & Psychiat, I-56018 Calambrone, PI, Italy. IRCCS Stella Maris, Pisa, Italy. RP Masi, G (reprint author), Univ Pisa, Div Child Neurol & Psychiat, Via Giacinti 2, I-56018 Calambrone, PI, Italy. 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Child Adolesc. Psychopharmacol. PD WIN PY 2001 VL 11 IS 4 BP 389 EP 394 DI 10.1089/104454601317261564 PG 6 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 518VU UT WOS:000173689200004 PM 11838821 ER PT J AU Rogers, SJ Wehner, EA Hagerman, R AF Rogers, SJ Wehner, EA Hagerman, R TI The behavioral phenotype in fragile X: Symptoms of autism in very young children with fragile X syndrome, idiopathic autism, and other developmental disorders SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE fragile X syndrome; autism; behavioral phenotype; development; mental retardation ID MALES; INDIVIDUALS; SPECTRUM; BOYS; AGE AB This study was designed to explore the behavioral phenotype of autism in a group of young children with fragile X syndrome (FXS).: Twenty-four children with FXS, ages 21 to 48 months, were compared with two well-matched groups: 27 children with autism (AD) and 23 children with other developmental delays (DD), on two standardized autism instruments, as well as on measures of development and adaptive behavior. Two FXS subgroups emerged. One subgroup (n = 16) did not meet study criteria for autism. Their profiles on the autism instruments and the developmental instruments were virtually, identical to the other DD group. The other FXS subgroup (n = 8, or 33% of the total FXS group) met study criteria for autism. Their profiles on the autism instruments were virtually identical to the group with autism. The finding of two FXS subgroups raises a hypothesis of additional genetic influences in the FXS autism group, warranting further genetic studies. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. Univ Calif Davis, Dept Pediat, Davis, CA 95616 USA. RP Rogers, SJ (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, 4200 E 9th Ave,Campus Box C234, Denver, CO 80262 USA. 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Dev. Behav. Pediatr. PD DEC PY 2001 VL 22 IS 6 BP 409 EP 417 PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 502LU UT WOS:000172745700007 PM 11773805 ER PT J AU Carvill, S AF Carvill, S TI Sensory impairments, intellectual disability and psychiatry SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Review DE autism; mental illness; sensory impairment ID VISUAL IMPAIRMENT; MEDICAL ASPECTS; AUTISM; POPULATION; CHILDREN; PEOPLE; DEAF AB The present review looks at: (1) prevalence studies of sensory impairments in people with intellectual disability (ID); (2) studies looking at psychological and psychiatric disorders in people with sensory impairments; and (3) studies that have examined the association of sensory impairments with autism. Research has indicated that sensory impairments are more common in people with ID. Psychiatric disorders are believed to be more common in children with visual impairment (VI) when associated with other handicaps. Some authors believe that hearing impairment (HI) can result in personality disorders. Studies have also shown a higher prevalence of psychiatric disorders in children with HI and a higher incidence of deaf people in psychiatric hospitals than in the general population. Psychiatric disorders in children with HI are particularly associated with low IQ and low communication ability especially in those with multiple handicaps. There is little evidence for a higher incidence of schizophrenia in people with HI. Blind people demonstrate many autistic-like features and there has been discussion in the literature as to their cause. Deaf people also demonstrate some similar features to those in autism, but an association with autism has not been conclusively made. Deaf-blind people commonly demonstrate problem behaviour (e.g. self-injury). Usher syndrome, which is the most common cause of deaf-blindness, is associated with psychiatric disorders, particularly psychosis. The need for assessment of sensory functioning in people with ID, the difficulties inherent in this and the need for specialist services is stressed. RP Carvill, S (reprint author), Admirals Court,37 Nelson Way, Rugby CV22 7LW, England. 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PD DEC PY 2001 VL 45 BP 467 EP 483 DI 10.1046/j.1365-2788.2001.00366.x PN 6 PG 17 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 497ZA UT WOS:000172484300001 PM 11737534 ER PT J AU Olsson, MB Hwang, CP AF Olsson, MB Hwang, CP TI Depression in mothers and fathers of children with intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE children; depression; fathers; mothers; intellectual disabilities (ID) ID DISABLED-CHILDREN; PARENTING STRESS; LATINA MOTHERS; DOWN-SYNDROME; FAMILIES; SUPPORT; RETARDATION; ADAPTATION; ADJUSTMENT; INVENTORY AB Parental depression was assessed using the Beck Depression Inventory (BDI) in 216 families with children with autism and/or intellectual disability (ID), and in 214 control families. Mothers with children with autism had higher depression scores (mean = 11.8) than mothers of children with ID without autism (mean = 9.2), who in turn, had higher depression scores than fathers of children with autism (mean = 6.2), fathers of children with ID without autism (mean = 5.0), and control mothers (mean = 5.0) and fathers (mean = 4.1). Forty-five per cent of mothers with children with ID without autism and 50% of mothers with children with autism had elevated depression scores (BDI > 9), compared to 15-21% in the other groups. Single mothers of children with disabilities were found to be more vulnerable to severe depression than mothers living with a partner. C1 Univ Trollhattan Uddevalla, SE-46228 Vanersborg, Sweden. Univ Gothenburg, Dept Psychol, S-40020 Gothenburg, Sweden. RP Olsson, MB (reprint author), Univ Trollhattan Uddevalla, Box 1240, SE-46228 Vanersborg, Sweden. CR Beck A. 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Intell. Disabil. Res. PD DEC PY 2001 VL 45 BP 535 EP 543 DI 10.1046/j.1365-2788.2001.00372.x PN 6 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 497ZA UT WOS:000172484300008 PM 11737541 ER PT J AU Symons, FJ Clark, RD Roberts, JP Bailey, DB AF Symons, FJ Clark, RD Roberts, JP Bailey, DB TI Classroom behavior of elementary school-age boys with fragile X syndrome SO JOURNAL OF SPECIAL EDUCATION LA English DT Article ID AUTISM RATING-SCALE; ADAPTIVE-BEHAVIOR; YOUNG BOYS; MALES; DISABILITIES; STUDENTS; TRAJECTORIES; TIME AB Despite reports suggesting numerous academic and social behavior deficits in boys with fragile X syndrome (FXS), little information is available concerning their actual classroom academic and social behavior. In this study, direct observational data were collected on the behavior of 26 elementary school-age boys with FXS during classroom academic activities in primarily self-contained special education classrooms. Results indicated moderate levels of academic engagement during periods of academic instruction, comparable to that of their classroom peers. Classroom engagement was not related to intrasubject variables such as severity of delay, autism status, or medication usage. A general measure of classroom quality and instruction was significantly correlated with engagement. Relatively low levels of stereotypic or self-injurious behavior were observed. These findings are discussed in relation to the existing engagement literature for school-age individuals with disabilities and issues concerning syndrome specific behaviors. C1 Univ N Carolina, Chapel Hill, NC 27515 USA. RP Symons, FJ (reprint author), Univ Minnesota, Coll Educ & Human Dev, Dept Educ Psychol, 224 Burton Hall,178 Pillsbury Dr SE, Minneapolis, MN 55455 USA. CR Aman M. 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W., 1984, SINGLE SUBJECT RES S VOLKMAR FR, 1987, J AM ACAD CHILD PSY, V26, P156, DOI 10.1097/00004583-198703000-00005 WOLFF PH, 1989, AM J MENT RETARD, V93, P406 NR 47 TC 6 Z9 7 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0022-4669 J9 J SPEC EDUC JI J. Spec. Educ. PD WIN PY 2001 VL 34 IS 4 BP 194 EP 202 DI 10.1177/002246690103400402 PG 9 WC Education, Special SC Education & Educational Research GA 397LJ UT WOS:000166696900002 ER PT J AU Scambler, D Rogers, SJ Wehner, EA AF Scambler, D Rogers, SJ Wehner, EA TI Can the Checklist for Autism in Toddlers differentiate young children with autism from those with developmental delays? SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE preschool screening; autism; other developmental delays ID SPECTRUM DISORDERS; DIAGNOSIS; INFANCY; AGE AB Objective: The Checklist for Autism in Toddlers (CHAT) has been demonstrated to be sensitive to the presence of autism in otherwise normally developing 18-month-old children. However, its ability to differentiate autism from other significant developmental delays is unknown. This study examined this question, Method: The CHAT was applied to a group of 44 children aged 2 and 3 years, rigorously diagnosed with autism or with other developmental problems. Results: By the original CHAT authors' criteria, the sensitivity and specificity of the CHAT were 65% and 100%, respectively. Slightly altering the criteria resulted in a sensitivity of 85% in the current group of children with developmental disabilities while maintaining specificity of 100%. Conclusions: The current study is the first to demonstrate that the CHAT successfully discriminates 2-year-old children with autism from those with other developmental disorders. In addition, the increased sensitivity of the Denver Criteria in children with developmental disabilities may improve its usefulness as a screening tool for community-based early-diagnostic teams and general practitioners. C1 Univ Colorado, Hlth Sci Ctr, Denver, CO 80262 USA. RP Scambler, D (reprint author), Univ Colorado, Hlth Sci Ctr, 4200 E 9th Ave Campus Box C234, Denver, CO 80262 USA. 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PD DEC PY 2001 VL 40 IS 12 BP 1457 EP 1463 DI 10.1097/00004583-200112000-00017 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 496HE UT WOS:000172389500017 PM 11765292 ER PT J AU Bambara, LM Gomez, O Koger, F Lohrmann-O'Rourke, S Xin, YP AF Bambara, LM Gomez, O Koger, F Lohrmann-O'Rourke, S Xin, YP TI More than techniques: Team members' perspectives on implementing positive supports for adults with severe challenging behaviors SO JOURNAL OF THE ASSOCIATION FOR PERSONS WITH SEVERE HANDICAPS LA English DT Article DE positive behavior support; team process; residential supports; adults with developmental disabilities; challenging behaviors ID AUTISM SPECTRUM DISORDERS; SEVERE DISABILITIES; COMMUNITY AB How teams implement and understand the process of positive behavior support provides an important source of information for improving supports for adults with developmental disabilities who engage in severe challenging behaviors in community settings. The purpose of the present study was to describe how positive behavior support was experienced and understood by team members from four residential, community-based teams who achieved positive outcomes for adults with severe challenging behaviors. In-depth, semistructured interviewing was the primary data source involving 19 participants. Data were analyzed within and across teams revealing team members' perceptions on their guiding values, struggles and barriers to implementing positive approaches, ways to support team members, the importance of staff relationships, and key elements of their direct support. Moving beyond techniques, the findings depict an overall culture of support consisting of interrelated layers of social context. Implications for practice and future research directions are discussed. C1 Lehigh Univ, Dept Educ & Human Serv, Bethlehem, PA 18015 USA. 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Assoc. Pers. Sev. Handicap PD WIN PY 2001 VL 26 IS 4 BP 213 EP 228 DI 10.2511/rpsd.26.4.213 PG 16 WC Rehabilitation SC Rehabilitation GA 530AU UT WOS:000174334100001 ER PT J AU Cohen, BI AF Cohen, BI TI GABA-transaminase, the liver and infantile autism SO MEDICAL HYPOTHESES LA English DT Article ID AMINOTRANSFERASE AB Gamma-aminobutyric acid (GABA) is a major inhibitory neurotransmitter of the mammalian brain and the enzyme responsible for catabolism (breakdown in the liver during regulation) is GABA-Transaminase (GABA-T). Recently, Cohen (1) has shown that extremely high GABA levels in the urine and blood were observed for an autistic child. The finding that elevated levels of GABA in the urine and blood are present for an autistic child could explain why autistic features (such as self-stimulatory behavior and language delays, etc.) are found. Increasing the GABA-T enzyme activity for this autistic patient could result in less plasma GABA (after liver regulation) entering into the bloodsteam and brain and it is postulated that this could result in a reduction of the autistic features (such as self-stimulatory behavior and language delays, etc.) due to abnormal development of the axon(s) in the corpus callosum. (C) 2001 Harcourt Publishers Ltd. C1 ED Labs, S Hackensack, NJ 07606 USA. RP Cohen, BI (reprint author), ED Labs, 89 Leuning St, S Hackensack, NJ 07606 USA. CR ARMIJO JA, 1989, INT J CLIN PHARM RES, V9, P283 COHEN BI, 1999, AUTISM, V3, P437, DOI 10.1177/1362361399003004010 Cohen BI, 2000, AUTISM, V4, P441, DOI 10.1177/1362361300004004010 Jayakumar AR, 1999, BRAIN RES, V837, P229, DOI 10.1016/S0006-8993(99)01692-3 WHITE HL, 1982, J NEUROCHEM, V39, P271, DOI 10.1111/j.1471-4159.1982.tb04733.x NR 5 TC 10 Z9 11 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD DEC PY 2001 VL 57 IS 6 BP 673 EP 674 DI 10.1054/mehy.2001.1350 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 505HV UT WOS:000172908100002 PM 11918424 ER PT J AU Binstock, T AF Binstock, T TI Anterior insular cortex: linking intestinal pathology and brain function in autism-spectrum subgroups SO MEDICAL HYPOTHESES LA English DT Article ID COORDINATING SPEECH ARTICULATION; IRRITABLE-BOWEL-SYNDROME; GUT AXIS; GASTROINTESTINAL-TRACT; EPILEPTIFORM ACTIVITY; ORAL INOCULATION; NERVOUS-SYSTEM; MESSENGER-RNA; CHILDREN; VIRUS AB Autism includes deficits in communications skills and is associated with intestinal pathology. Numerous parents and some physicians report that an autistic child's attention and language improve in response to treatments which eliminate certain dietary antigens and/or which improve intestinal health. For at least some autism-spectrum children, the link between intestinal pathology, attention, and language may derive from shared neuroanatomic pathways within the anterior insular cortex (alC); from a neurotrophic virus such as herpes simplex (HSV) migrating within afferents to the insular cortex; and/or from synaptic exhaustion in the alC as induced by chronically inappropriate neuronal activity in the enteric nervous system and/or its vagal efferents. (C) 2001 Harcourt Publishers Ltd. C1 Inst Mol Introspect, Estes Pk, CO 80517 USA. RP Binstock, T (reprint author), Inst Mol Introspect, Box 1788, Estes Pk, CO 80517 USA. 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PD DEC PY 2001 VL 24 IS 4 BP 661 EP + DI 10.1016/S0193-953X(05)70256-2 PG 16 WC Psychiatry SC Psychiatry GA 490ZU UT WOS:000172084200004 PM 11723626 ER PT J AU Whitaker-Azmitia, PM AF Whitaker-Azmitia, PM TI Serotonin and brain development: Role in human developmental diseases SO BRAIN RESEARCH BULLETIN LA English DT Review DE serotonin; S-100 beta; brain development; autism; Down syndrome ID GROWTH-HORMONE RESPONSE; DENTATE GRANULE CELLS; DOWNS-SYNDROME ADULT; PROTEIN KINASE-C; 5-HT1A RECEPTORS; POSTNATAL-DEVELOPMENT; SOMATOSENSORY CORTEX; S-100-BETA PROTEIN; MONOAMINE-OXIDASE; AUTISTIC DISORDER AB Serotonin is known to play a role in brain development prior to the time it assumes its role as a neurotransmitter In the mature brain. Serotonin regulates both the development of serotonergic neurons (termed autoregulation of development) and the development of target tissues. In both cases, the astroglial-derived protein, S-100 beta plays a role. 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Bull. PD NOV 15 PY 2001 VL 56 IS 5 BP 479 EP 485 DI 10.1016/S0361-9230(01)00615-3 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 505TE UT WOS:000172931000008 PM 11750793 ER PT J AU Purcell, AE Jeon, OH Zimmerman, AW Pevsner, J AF Purcell, AE Jeon, OH Zimmerman, AW Pevsner, J TI Postmortem brain abnormalities of the glutamate neurotransmitter system in autism SO NEUROLOGY LA English DT Article ID INFANTILE-AUTISM; CDNA MICROARRAYS; GENE-EXPRESSION; RECEPTORS; DISORDERS; PROTEIN; STEM AB Background: Studies examining the brains of individuals with autism have identified anatomic and pathologic changes in regions such as the cerebellum and hippocampus. Little, if anything, is known, however, about the molecules that are involved in the pathogenesis of this disorder. Objective: To identify genes with abnormal expression levels in the cerebella of subjects with autism. Methods: Brain samples from a total of 10 individuals with autism and 23 matched controls were collected, mainly from the cerebellum. Two cDNA microarray technologies were used to identify genes that were significantly up- or downregulated in autism. The abnormal mRNA or protein levels of several genes identified by microarray analysis were investigated using PCR with reverse transcription and Western blotting. alpha -Amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA)- and NMDA-type glutamate receptor densities were examined with receptor autoradiography in the cerebellum, caudate-putamen, and prefrontal cortex. Results: The mRNA levels of several genes were significantly increased in autism, including excitatory amino acid transporter I and glutamate receptor AMPA 1, two members of the glutamate system. Abnormalities in the protein or mRNA levels of several additional molecules in the glutamate system were identified on further analysis, including glutamate receptor binding proteins. AMPA-type glutamate receptor density was decreased in the cerebellum of individuals with autism (p < 0.05). Conclusions: Subjects with autism may have specific abnormalities in the AMPA-type glutamate receptors and glutamate transporters in the cerebellum. These abnormalities may be directly involved in the pathogenesis of the disorder. C1 Kennedy Krieger Inst, Dept Neurol, Baltimore, MD 21205 USA. Kennedy Krieger Inst, Dept Neurosci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. RP Pevsner, J (reprint author), Kennedy Krieger Inst, Dept Neurol, 707 N Broadway, Baltimore, MD 21205 USA. 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RP Cohen, H (reprint author), The Scientist, 3600 Market St,Suite 450, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 USA SN 0890-3670 J9 SCIENTIST JI Scientist PD NOV 12 PY 2001 VL 15 IS 22 BP 25 EP 25 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA 491ED UT WOS:000172094300015 ER PT J AU [Anonymous] AF [Anonymous] TI Biology of autism SO PHARMACEUTICAL JOURNAL LA English DT Editorial Material NR 0 TC 0 Z9 0 PU ROYAL PHARMACEUTICAL SOC GREAT BRITAIN PI LONDON PA 1 LAMBETH HIGH ST, LONDON SE1 7JN, ENGLAND SN 0031-6873 J9 PHARM J JI Pharma. J. PD NOV 10 PY 2001 VL 267 IS 7173 BP 696 EP 696 PG 1 GA 499KF UT WOS:000172569800053 ER PT J AU Greenberg, DA Hodge, SE Sowinski, J Nicoll, D AF Greenberg, DA Hodge, SE Sowinski, J Nicoll, D TI Excess of twins among affected sibling pairs with autism: Implications for the etiology of autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID GENOMIC SCREEN; PREGNANCIES; DISORDER; RISK AB It is widely accepted that genes play a role in the etiology of autism. Evidence for this derives, in part, from twin data. However, despite converging evidence from gene-mapping studies, aspects of the genetic contribution remain obscure. In a sample of families selected because each had exactly two affected sibs, we observed a remarkably high proportion of affected twin pairs, both MZ and DZ. Of 166 affected sib pairs, 30 (12 MZ, 17 DZ, and 1 of unknown zygosity) were twin pairs. Deviation from expected values was statistically significant (P<10(-6) for all twins); in a similarly ascertained sample of individuals with type I diabetes, there was no deviation from expected values. We demonstrate that to ascribe the excess of twins with autism solely to ascertainment bias would require very large ascertainment factors; for example, affected twin pairs would need to be, on average, 10 times more likely to be ascertained than affected nontwin sib pairs (or 7 times more likely if "stoppage" plays a role). Either risk factors (related to twinning or to fetal development) or other factors (genetic or nongenetic) in the parents may contribute to autism. C1 New York State Psychiat Inst & Hosp, Unit 24, New York, NY 10032 USA. Columbia Univ, Dept Biostat, Div State Genet, New York, NY USA. Human Biol Data Interchange, Philadelphia, PA USA. RP Greenberg, DA (reprint author), New York State Psychiat Inst & Hosp, Unit 24, 1051 Riverside Dr, New York, NY 10032 USA. 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J. Hum. Genet. PD NOV PY 2001 VL 69 IS 5 BP 1062 EP 1067 DI 10.1086/324191 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 479PU UT WOS:000171413400014 PM 11590546 ER PT J AU Dunn, W AF Dunn, W TI The sensations of everyday life: Empirical, theoretical, and pragmatic considerations SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE sensory processing; temperament; threshold ID TRAUMATIC BRAIN INJURY; SENSORY PROFILE; CHILDREN; SCHIZOPHRENIA; DEFENSIVENESS; DISABILITIES; INTEGRATION; BEHAVIORS; OUTCOMES; SEEKING AB The experience of being human is embedded in sensory events Of everyday life. This lecture reviews sensory processing literature, including neuroscience and social science perspectives. Introduced is Dunn's Model of Sensory Processing, and the evidence supporting this model is summarized Specifically, using Sensory Profile questionnaires (i.e., items describing responses to sensory events in daily life, persons mark the frequency of each behavior), persons birth to 90 years of age demonstrate four sensory processing patterns: sensory seeking, sensory avoiding, sensory sensitivity, and low registration. These patterns are based on a person's neurological thresholds and self-regulation strategies. Psychophysiology studies verify these sensory processing patterns; persons with strong preferences in each pattern also have unique patterns of habituation and responsivity in skin conductance. Studies also indicate that persons with disabilities respond differently than peers on these questionnaires, suggesting underlying poor sensory processing in certain disorders, including autism, attention deficit hyperactivity disorder, developmental delays, and schizophrenia. The author proposes relationships between sensory processing and temperament and personality traits. The four categories of temperament share some consistency with the four sensory processing patterns described in Dunn model. As with temperament, each person has some level of responsiveness within each sensory processing preference (i.e., a certain amount of seeking, avoiding, etc., not one or the other). The author suggests that ones sensory processing preferences simultaneously reflect his or her nervous system needs and form the basis for the manifestation of temperament and personality. The final section of this lecture outlines parameters for developing best practice that supports interventions based on this knowledge. C1 Univ Kansas, Dept Occupat Therapy Educ, Kansas City, KS 66160 USA. RP Dunn, W (reprint author), Univ Kansas, Dept Occupat Therapy Educ, 3901 Rainbow Blvd,3033 Robinson, Kansas City, KS 66160 USA. 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PD NOV-DEC PY 2001 VL 55 IS 6 BP 608 EP 620 PG 13 WC Rehabilitation SC Rehabilitation GA 493YX UT WOS:000172252000002 PM 12959225 ER PT J AU VandenBerg, NL AF VandenBerg, NL TI The use of a weighted vest to increase on-task behavior in children with attention difficulties SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE attention deficit disorder with hyperactivity; pressure; school based occupational therapy ID DEEP PRESSURE; OCCUPATIONAL-THERAPY; AUTISM AB Objective. Children described as having attention deficit hyperactivity disorder often demonstrate inability to sustain visual attention during classroom fine motor activities. This study investigated the effect of wearing a weighted vest (deep-pressure sensory input) on children on-task behavior in the classroom. Method. Four students with documented attention difficulties and hyperactivity were timed with a stopwatch to measure their on-task behavior during fine motor activities in the classroom. 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PD NOV-DEC PY 2001 VL 55 IS 6 BP 621 EP 628 PG 8 WC Rehabilitation SC Rehabilitation GA 493YX UT WOS:000172252000003 PM 12959226 ER PT J AU Strain, PS AF Strain, PS TI Empirically based social skill intervention: A case for quality-of-life improvement SO BEHAVIORAL DISORDERS LA English DT Article ID PRESCHOOL-CHILDREN; AUTISTIC-CHILDREN; POSTMODERN PERSPECTIVE; BEHAVIORAL-DISORDERS; INITIATIONS; PEERS AB This article offers a personalized review of research conducted over a 27-year period to enhance the peer-related social skills of young children with behavioral disorders or autism. The argument is made that a logical positivist approach has yielded significant quality-of-life benefits to research participants. Furthermore, it is suggested that the positivist approach has effectively challenged many outdated notions regarding assessment and intervention in the social skill domain. Finally, evidence is presented to suggest how the positivist approach has forced fundamental changes within our own line of inquiry and intervention. C1 Univ Colorado, Denver, CO 80202 USA. RP Strain, PS (reprint author), Univ Colorado, Denver, CO 80202 USA. 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PD NOV PY 2001 VL 27 IS 1 BP 30 EP 36 PG 7 WC Psychology, Clinical; Psychology, Educational SC Psychology GA 708ZP UT WOS:000184600500005 ER PT J AU Curatolo, P Seri, S Verdecchia, M Bombardieri, R AF Curatolo, P Seri, S Verdecchia, M Bombardieri, R TI Infantile spasms in tuberous sclerosis complex SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT International Symposium on the West Syndromme and Other Infantile Epileptic Encephalopathies (ISWS) CY FEB 09-11, 2001 CL TOKYO, JAPAN DE infantile spasms; tuberous sclerosis; partial seizures ID POSITRON-EMISSION-TOMOGRAPHY; CHILDREN; VIGABATRIN; EPILEPSY; PREVALENCE; SEIZURES; AUTISM AB The high incidence of infantile spasms (IS) and hypsarrhythmia in tuberous sclerosis complex (TSC) has long been emphasized but it is now, clear that infants with TSC show clinical and EEG differences from those with classical West syndrome. Seizures at onset are mainly characterized by partial motor seizures and IS. Subtle partial seizures may be present in the early neonatal period and may precede the onset of IS. Visual recording techniques have led to significant progress in the classification of seizures associated with TSC, demonstrating that they have a focal or multifocal origin in the vast majority of cases. In most cases, an awake interictal EEG shows focal or independent multifocal spike and slow-wave activity at onset and later a pseudo-hypsarrhythmic pattern. Ictal EEG starts with focal spikes originating from the posterotemporal, or occipital regions followed by a generalized irregular slow transient and an abrupt diffuse flattening. Although the pathophysiological mechanisms responsible for the coexistence of partial seizures and IS are still unclear, IS associated with TSC may be the result of a rapid secondary generalization. The presence of IS due to TSC is strongly predicted by the cortical tuber count, while the age of onset of seizures and the age of occurrence of EEG foci depend on the localization of cortical tubers with an earlier expression of the parietooccipital than of the frontal regions. Early recognition of these distinctive features appears worthwhile for therapeutic and prognostic implications. Despite the efficacy of vigabatrin the prognosis of IS is generally poor. Studies using combined topographic mapping of EEG, magnetic resonance imaging and positron emission tomography may provide new strategies for selecting candidates suitable for surgery. (C) 2001 Published by Elsevier Science B.V. C1 Univ Roma Tor Vergata, Rome, Italy. RP Curatolo, P (reprint author), Dept Neurosci, Via Tor Vergata 135, I-00133 Rome, Italy. CR Aicardi J, 1996, EPILEPSIA, V37, P638, DOI 10.1111/j.1528-1157.1996.tb00627.x BEBIN EM, 1993, EPILEPSIA, V34, P651, DOI 10.1111/j.1528-1157.1993.tb00442.x Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BRUNI O, 1995, BRAIN DEV-JPN, V17, P52, DOI 10.1016/0387-7604(94)00118-H CHIRON C, 1990, LANCET, V335, P363, DOI 10.1016/0140-6736(90)90660-W Chugani DC, 1998, ANN NEUROL, V44, P858, DOI 10.1002/ana.410440603 Crino PB, 1999, NEUROLOGY, V53, P1384 CURATOLO P, 1988, NEUROPHYSIOL CLIN, V18, P49 CURATOLO P, 1991, ANN NY ACAD SCI, V615, P8, DOI 10.1111/j.1749-6632.1991.tb37743.x CURATOLO P, 1994, NEUROPEDIATRICS, V25, P55, DOI 10.1055/s-2008-1071586 CURATOLO P, 1987, DEV MED CHILD NEUROL, V29, P550 CUSMAI R, 1990, EPILEPSIA, V31, P747, DOI 10.1111/j.1528-1157.1990.tb05516.x DEONNA T, 1993, DEV MED CHILD NEUROL, V35, P166 DULAC O, 1984, B LEGA IT EPIL, V45, P39 GILLBERG IC, 1994, DEV MED CHILD NEUROL, V36, P50 GOMEZ MR, 1988, TUBEROUS SCLEROSIS, P21 Goodman M, 1997, J CHILD NEUROL, V12, P85 HUNT A, 1993, J AUTISM DEV DISORD, V23, P323, DOI 10.1007/BF01046223 JAMBAQUE I, 1991, DEV MED CHILD NEUROL, V33, P698 Jones AC, 1999, AM J HUM GENET, V64, P1305, DOI 10.1086/302381 Jozwiak S, 1998, ARCH NEUROL-CHICAGO, V55, P379, DOI 10.1001/archneur.55.3.379 MAEDA M, 1995, J COMPUT ASSIST TOMO, V19, P660, DOI 10.1097/00004728-199507000-00033 MATSUMOTO A, 1981, EUR J PEDIATR, V135, P239, DOI 10.1007/BF00442097 Miller SP, 1998, J CHILD NEUROL, V13, P619 O'Callaghan FJK, 1998, LANCET, V351, P1490, DOI 10.1016/S0140-6736(05)78872-3 PAMPIGLIONE G, 1975, LANCET, V2, P1046 PLOUIN P, 1993, EPILEPSIA, V34, P686, DOI 10.1111/j.1528-1157.1993.tb00447.x POVEY S, 1994, ANN HUM GENET, V58, P107, DOI 10.1111/j.1469-1809.1994.tb01881.x Rintahaka PJ, 1997, J CHILD NEUROL, V12, P42 Roach ES, 1997, J CHILD NEUROL, V12, P75 SERI S, 1991, Neurophysiologie Clinique, V21, P161, DOI 10.1016/S0987-7053(05)80423-X Seri S, 1998, J CHILD NEUROL, V13, P34 SHEPHERD CW, 1995, AM J NEURORADIOL, V16, P149 STEPHENSONJPB, 1988, TUB SCLR S NOTT NR 34 TC 53 Z9 54 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 NOV PY 2001 VL 23 IS 7 BP 502 EP 507 DI 10.1016/S0387-7604(01)00300-X PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 500QT UT WOS:000172638800011 PM 11701245 ER PT J AU Kohyama, J AF Kohyama, J TI Polysomnographical assessment of the pathophysiology of West syndrome SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT International Symposium on the West Syndromme and Other Infantile Epileptic Encephalopathies (ISWS) CY FEB 09-11, 2001 CL TOKYO, JAPAN DE West syndrome; rapid eye movement sleep; pons; brainstem; phasic inhibition index; adrenocorticotropin ID RAPID EYE-MOVEMENTS; INFANTILE SPASMS; REM-SLEEP; PHASIC INHIBITION; BRAIN-STEM; ACTH; ACTIVATION; TEGMENTUM; NUCLEI; AUTISM AB In this brief review, the sleep studies on patients with West syndrome (WS) were summarized. In addition to the previously reported common finding for sleep in WS - reduction of the amount of rapid-eye-movement (REM) sleep - weakness of phasic suppression of chin muscle activity in WS patients has recently been found. The degree of this weakness is quantified by the phasic inhibition index (PII), which has been round to reflect a patient's prognosis as to convulsions. Pit is proposed to be a useful parameter for assessing the prognosis of WS. Since the pontine tegmentum is involved in the production of the REM-related phasic loss of muscle activity in REM sleep, WS patients are hypothesized to have a functional instability of the pontine tegmentum. After adrenocorticotropin (ACTH) treatment, Pll decreased significantly in all WS patients examined. Taken together with the effects of corticosteriods on PII, and the incidence of phasic chin muscle activity in patients with congenital adrenal hyperplasia and nephrotic syndrome, ACTH is hypothesized to suppress the spasms in WS patients not only through corticosteroids, but also through a direct action on the pontine tegmentum. Since Pll has been reported to be elevated in patients with an autistic tendency, the appearance of an autistic tendency is also hypothesized to be involved in the functional disturbance of the pontine tegmentum. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Tokyo Med & Dent Univ, Grad Sch, Div Human Ontogeny & Childhood Dev, Tokyo, Japan. RP Kohyama, J (reprint author), Tokyo Med & Dent Univ, Grad Sch, Div Human Ontogeny & Childhood Dev, Tokyo, Japan. CR APPLETON RE, 1993, ARCH DIS CHILD, V69, P614 BARAM TZ, 1993, ANN NEUROL, V33, P231, DOI 10.1002/ana.410330302 Braun AR, 1997, BRAIN, V120, P1173, DOI 10.1093/brain/120.7.1173 CHUGANI HT, 1992, ANN NEUROL, V31, P212, DOI 10.1002/ana.410310212 Diomedi M, 1999, BRAIN DEV-JPN, V21, P548, DOI 10.1016/S0387-7604(99)00077-7 FUKUYAMA Y, 1979, EUR NEUROL, V18, P302, DOI 10.1159/000115094 GARCIA RE, 1986, BRAIN RES, V396, P47 HASHIMOTO T, 1981, BRAIN DEV-JPN, V3, P51 HASHIMOTO T, 1978, ACTA PAEDIATR JAPON, V20, P1 HASHIMOTO T, 1995, J AUTISM DEV DISORD, V25, P1, DOI 10.1007/BF02178163 Hayashi M, 2000, NEUROPATHOLOGY, V20, P297, DOI 10.1046/j.1440-1789.2000.00353.x HENDRICKS JC, 1990, J APPL PHYSIOL, V68, P1435 HENDRICKS JC, 1991, J APPL PHYSIOL, V70, P1194 Hobson JA, 1998, NEUROREPORT, V9, pR1, DOI 10.1097/00001756-199802160-00033 HORITA H, 1979, NO TO HATTATSU, V11, P229 HRACHOVY RA, 1981, NEUROLOGY, V31, P688 JAMBAQUE I, 1993, EPILEPSIA, V34, P692, DOI 10.1111/j.1528-1157.1993.tb00448.x Kohyama J, 1999, ACTA NEUROL SCAND, V99, P368 Kohyama J, 1999, EPILEPSIA, V40, P992, DOI 10.1111/j.1528-1157.1999.tb00808.x Kohyama J, 2000, ACTA NEUROL SCAND, V101, P145, DOI 10.1034/j.1600-0404.2000.101003145.x KOHYAMA J, 1995, EXP BRAIN RES, V107, P137 Kohyama J, 1996, J NEUROL SCI, V143, P150, DOI 10.1016/S0022-510X(96)00209-2 Kohyama J, 2000, BRAIN DEV-JPN, V22, pS136 Kohyama J, 1998, CURR PROBL PEDIATR, V28, P73, DOI 10.1016/S0045-9380(98)80054-6 Kohyama J, 1996, J NEUROL SCI, V138, P82, DOI 10.1016/0022-510X(95)00342-Y KOHYAMA J, 2001, IN PRESS BRAIN DEV KONISHI Y, 1995, PEDIATR NEUROL, V13, P134, DOI 10.1016/0887-8994(95)00122-V Maquet P, 1996, NATURE, V383, P163, DOI 10.1038/383163a0 MATON B, 1992, NEUROSCI LETT, V134, P284, DOI 10.1016/0304-3940(92)90536-G MORI S, 1978, J NEUROPHYSIOL, V41, P1580 MORIMATSU Y, 1972, ADV NEUROL SCI TOKYO, V16, P465 NEVILLE BGR, 1972, DEV MED CHILD NEUROL, V14, P644 Okawa MSH, 1987, SLEEP ITS DISORDERS, P269 REKTOR I, 1990, BRAIN DEV-JPN, V12, P790 Rodier PM, 1996, J COMP NEUROL, V370, P247, DOI 10.1002/(SICI)1096-9861(19960624)370:2<247::AID-CNE8>3.0.CO;2-2 Rodier PM, 1997, REPROD TOXICOL, V11, P417, DOI 10.1016/S0890-6238(97)80001-U Rye DB, 1997, SLEEP, V20, P757 SATOH J, 1986, BRAIN DEV-JPN, V8, P443 SEGUIN JJ, 1973, ARCH ITAL BIOL, V111, P1 SHIONAGA A, 1976, CHOUNI GEKA NAIKA, V8, P1415 SNEAD OC, 1983, NEUROLOGY, V33, P966 TOMINAGA I, 1986, REV NEUROL PARIS, V5, P524 West W.J., 1841, LANCET, V1, P724 ZAPHIROPOULOS A, 1991, BRAIN RES BULL, V26, P99, DOI 10.1016/0361-9230(91)90194-O NR 44 TC 3 Z9 3 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 NOV PY 2001 VL 23 IS 7 BP 523 EP 527 DI 10.1016/S0387-7604(01)00309-6 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 500QT UT WOS:000172638800014 PM 11701248 ER PT J AU Riikonen, R AF Riikonen, R TI Long-term outcome of patients with West syndrome SO BRAIN & DEVELOPMENT LA English DT Article; Proceedings Paper CT International Symposium on the West Syndromme and Other Infantile Epileptic Encephalopathies (ISWS) CY FEB 09-11, 2001 CL TOKYO, JAPAN DE West syndrome; adrenocorticotropic hormone; infantile spasms ID INFANTILE SPASMS; DISORDERS; CHILDREN AB The long-term outcome of Finnish children with West syndrome was evaluated. Two hundred and fourteen patients were followed up for 20-35 years or until death. A third of the patients died before the age of 3 years. The most common cause of death was infection. Autopsy revealed brain anomalies in 25 of 38 (66%) autopsied patients. Intellectual outcome was normal or slightly impaired in a quarter of the patients. All of them completed their education at a normal school or in a school for the educationally impaired children. Another fourth were taught in special training schools. Specific cognitive deficits were seen in some patients with normal intelligence. Nine attended secondary schools and seven of them had a professional occupation. Ten were married and five had children. One third of the patients were seizure-free, another third had seizures daily or monthly, and the remaining patients had seizures less frequently. Factors associated with a good prognosis were cryptogenic etiology, normal development before the onset of the spasms, a short treatment lag, and a good response to adrenocorticotropic hormone; this was seen in both the symptomatic and the cryptogenic group, and there were no relapses. In this study, the late appearance of focal abnormalities in electroencephalography was not associated with an unfavorable outcome. Focal abnormalities in temporal region were often seen in patients with autism. The location of an abnormality may be of importance for the prognosis. In this study, all the patients (100%) could be followed, which may be due to the special circumstances characteristic of Finland. The outcome in children with West syndrome seems to be better than is generally believed. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Kuopio Univ Hosp, Dept Child Neurol, Kuopio 70211, Finland. RP Riikonen, R (reprint author), Kuopio Univ Hosp, Dept Child Neurol, POB 1777, Kuopio 70211, Finland. CR Chugani HT, 1996, ANN NEUROL, V39, P643, DOI 10.1002/ana.410390514 GLAZE DG, 1988, J PEDIATR-US, V112, P389, DOI 10.1016/S0022-3476(88)80318-4 KOO B, 1993, NEUROLOGY, V43, P2322 LOMBROSO CT, 1983, EPILEPSIA, V24, P135, DOI 10.1111/j.1528-1157.1983.tb04874.x RIIKONEN R, 1993, NEUROPEDIATRICS, V24, P274, DOI 10.1055/s-2008-1071556 RIIKONEN R, 1981, DEV MED CHILD NEUROL, V23, P747 RIIKONEN R, 1982, NEUROPEDIATRICS, V13, P14, DOI 10.1055/s-2008-1059590 RIIKONEN R, 1990, DEV MED CHILD NEUROL, V32, P203 Riikonen R, 1996, EPILEPSIA, V37, P367, DOI 10.1111/j.1528-1157.1996.tb00573.x NR 9 TC 63 Z9 71 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 NOV PY 2001 VL 23 IS 7 BP 683 EP 687 DI 10.1016/S0387-7604(01)00307-2 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 500QT UT WOS:000172638800043 PM 11701277 ER PT J AU Jewell, D AF Jewell, D TI MMR and the age of unreason SO BRITISH JOURNAL OF GENERAL PRACTICE LA English DT Editorial Material ID INFLAMMATORY BOWEL-DISEASE; RUBELLA VACCINE; MEASLES; AUTISM; MUMPS C1 Royal Coll Gen Practitioners, London SW7 1PU, England. RP Jewell, D (reprint author), Royal Coll Gen Practitioners, 14 Princess Gate,Hyde Pk, London SW7 1PU, England. CR Arlett P., 2001, Adverse Drug Reactions and Toxicological Reviews, V20, P37 *BAND, EV MOR MMR BARTLETT C, 2001, 4 INT C PEER REV BIO *DEP HLTH, 2000, NHS IMM STAT *DEP HLTH, MEASL MUMPS RUB VACC DeWilde S, 2001, BRIT J GEN PRACT, V51, P226 Elliman DAC, 2001, ARCH DIS CHILD, V85, P271, DOI 10.1136/adc.85.4.271 Evans M, 2001, BRIT J GEN PRACT, V51, P904 Fugelli P, 2001, BRIT J GEN PRACT, V51, P575 MAJEED A, 2001, BRIT MED J, V323, P163 Peltola H, 1998, LANCET, V351, P1327, DOI 10.1016/S0140-6736(98)24018-9 Sackett DL, 2000, BRIT MED J, V320, P1283, DOI 10.1136/bmj.320.7244.1283 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 THOMPSON NP, 1995, LANCET, V345, P1071, DOI 10.1016/S0140-6736(95)90816-1 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 15 TC 12 Z9 12 PU ROYAL COLL GENERAL PRACTITIONERS PI LONDON PA 14 PRINCES GATE, HYDE PARK, LONDON SW7 1PU, ENGLAND SN 0960-1643 J9 BRIT J GEN PRACT JI Br. J. Gen. Pract. PD NOV PY 2001 VL 51 IS 472 BP 875 EP 876 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 489AJ UT WOS:000171969400002 PM 11761198 ER PT J AU Evans, M Stoddart, H Condon, L Freeman, E Grizzell, M Mullen, R AF Evans, M Stoddart, H Condon, L Freeman, E Grizzell, M Mullen, R TI Parents' perspectives on the MMR immunisation: a focus group study SO BRITISH JOURNAL OF GENERAL PRACTICE LA English DT Article DE immunisation; measles, mumps and rubella vaccine; primary health care; attitude to health; decision making ID INFLAMMATORY BOWEL-DISEASE; QUALITATIVE-RESEARCH; IMMUNIZATION; VACCINATION; CHILDREN; MEASLES; AUTISM; HEALTH; MUMPS AB Background: The uptake of the combined measles, mumps and rubella immunisation (MMR) in Britain has fallen since 1998, when a link was hypothesised with the development of bowel disorders and childhood autism. Despite reassurances about the safely of MMR, uptake levels remain lower than optimal. we need to understand what influences parents' decisions on whether to accept MMR or not so that health professionals can provide a service responsive to their needs. Aim: To investigate what influences parents' decisions on whether to accept or refuse the primary MMR immunisation and the impact of the recent controversy over its safety. Design: Qualitative study using focus group discussions. Setting. Forty-eight parents, whose youngest child was between 14 months and three years old, attended groups at community halls in six localities in Avon and Gloucestershire. Methods Purposive sampling strategy was used to include parents from a variety of socioeconomic backgrounds. Three groups comprised parents who had accepted MMR and three groups comprised parents who had refused MMR. Data analysis used modified grounded theory techniques incorporating the constant comparative method. Results. All parents felt that the decision about MMR was difficult and stressful, and experienced unwelcome pressure from health professionals to comply, Parents were not convinced by Department of Health reassurances that MMR was the safest and best option for their children and many had accepted MMR unwillingly. Four key factors influenced parents' decisions: (a) beliefs about the risks and benefits of MMR compared with contracting the diseases, (b) information from the media and other sources about the safely of MMR, (c) confidence and trust in the advice of health professionals and attitudes towards compliance with this advice, and (d) views on the importance of individual choice within Government policy on immunisation. Conclusions. Parents wanted up-to-date information about the risks and benefits of MMR to be available in advance of their immunisation appointment. Many parents did not have confidence in the recommendations of health professionals because they were aware that GPs needed to reach immunisation targets. Most parents would, however, welcome more open discussion about immunisation with health professionals. C1 Univ Bristol, Div Primary Hlth Care, Bristol BS6 6JL, Avon, England. United Bristol Hlth Care Trust, Bristol, Avon, England. Gloucestershire Hlth Author, Gloucestershire Res & Dev Support Unit, Gloucester, England. Frenchay Hlth Trust, Bristol, Avon, England. RP Evans, M (reprint author), Univ Bristol, Div Primary Hlth Care, Cotham House,Cotham Hill, Bristol BS6 6JL, Avon, England. 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J. Gen. Pract. PD NOV PY 2001 VL 51 IS 472 BP 904 EP 910 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 489AJ UT WOS:000171969400008 PM 11761204 ER PT J AU Langdon, R Coltheart, M AF Langdon, R Coltheart, M TI Visual perspective-taking and schizotypy: evidence for a simulation-based account of mentalizing in normal adults SO COGNITION LA English DT Article DE perspective-taking; theory-of-mind; psychosis-proneness; schizotypy; schizophrenia ID MIND; SCHIZOPHRENIA; AUTISM; CHILDREN; TRANSFORMATION; ABILITIES; DEFICITS; PEOPLE; SPACE; AGE AB Modular theory-of-mind accounts attribute poor mentalizing to disruption of a cognitive module dedicated to computing higher-order representations of primary representations (metarepresentations). Since metarepresentational capacity is needed to mentalize about other people's beliefs but is not needed to judge visual perspectives (which can be done by mentally rotating primary representations of seen objects), this view predicts that visual perspective-taking will be intact in individuals with selective mentalizing impairments. Counter to that prediction, this study found evidence of disturbed visual perspective-taking in normal adults who score higher on the personality variable of schizotypy and who are known to be relatively poor mentalizers (despite intact ability to inhibit salient inappropriate information in order to reason consequentially on the basis of hypothetical states, other than mental states). Whereas high-schizotypal adults and low-schizotypal adults did not differ in their ability to judge item questions (asking the relative location of array features), high-schizotypal adults performed more poorly than low-schizotypal adults in judging appearance questions (asking how an array would appear from another perspective) under viewer-rotation instructions (asking subjects to imagine moving themselves relative to a fixed array) and performed better than low-schizotypal adults in judging appearance questions under array-rotation instructions (asking subjects to imagine rotating an array relative to their own fixed viewer position), Based on these and other findings we conclude that poor mentalizing in normal adults is better understood as an impairment of perspective-taking (visual and/or cognitive) and introduce the concept of allocentric simulation to explain the functional basis of this perspective-taking impairment. (C) 2001 Elsevier Science B.V. All rights reserved. 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Results suggest that the self-injury began in a different way from that of other young children with autism and/or developmental disabilities in that, from the start, self-injurious responses were sudden and violent, rather than emerging gradually over time. Drastic measures, such as removal of the teeth or provision of tooth guards, were often taken to prevent further tissue damage. Direct observations showed that the boys' self-injury occurred at lower rates, but their carers were highly concerned about the behaviour. Sequential analysis of the observational data indicated that on some occasions the children were more likely to self-injure during periods of low social interaction, suggesting that their self-injury may have been influenced by environmental factors. The theoretical and practical implications of these findings are discussed. C1 Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. Univ Kent, Tizard Ctr, Canterbury, Kent, England. 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Rev. Psych. PD NOV PY 2001 VL 13 IS 4 BP 295 EP 301 DI 10.1080/09540260127530 PG 7 WC Psychiatry SC Psychiatry GA 490UR UT WOS:000172071000008 ER PT J AU Schmahmann, JD AF Schmahmann, JD TI The cerebellar cognitive affective syndrome: clinical correlations of the dysmetria of thought hypothesis SO INTERNATIONAL REVIEW OF PSYCHIATRY LA English DT Article ID POSTERIOR-FOSSA TUMORS; DEFICIT HYPERACTIVITY DISORDER; POSITRON-EMISSION-TOMOGRAPHY; WHOLE-BRAIN RADIOTHERAPY; SUBSEQUENT DYSARTHRIA; MENTAL SKILLS; CHILDREN; MUTISM; CONTRIBUTES; ATTENTION AB The description of deficits in higher order behaviors in patients with focal cerebellar lesions has provided pivotal clinical corroboration of a cerebellar role in cognition and emotion. This paper reviews the principal observations of the cerebellar cognitive affective syndrome (CCAS) of Schmahmann & Sherman (1998) in both adults and children, namely deficits in executive, visual-spatial, linguistic and affective behaviors. 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PD NOV PY 2001 VL 16 IS 11 BP 809 EP 819 DI 10.1177/08830738010160110601 PG 11 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 493MZ UT WOS:000172228400005 PM 11732766 ER PT J AU Ruffman, T Garnham, W Rideout, P AF Ruffman, T Garnham, W Rideout, P TI Social understanding in autism: Eye gaze as a measure of core insights SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; eye gaze; explicit; implicit; language; theory of mind ID FALSE BELIEF TASKS; DEVELOPING-CHILDREN; YOUNG-CHILDREN; MIND; KNOWLEDGE; INDIVIDUALS; COMMUNICATION; PERFORMANCE; DISORDERS; ATTENTION AB Twenty-eight children with autism and 33 MLD children were given two tasks tapping social understanding and a control task tapping probability understanding. For each task there was a measure of eye gaze (where children looked when anticipating the return of a story character or an object) and a verbal measure (a direct question). We found that eye gaze was better than verbal performance at differentiating children with autism from children with MLD. Children with autism did not look to the correct location in anticipation of the story character's return in the social tasks, but they did look to the correct location in the nonsocial probability task. We also found that within the autistic group, children who looked least to the correct location were rated as having the most severe autistic characteristics. Further, we found that whereas verbal performance correlated with general language ability in the autistic group, eye gaze did not. We argue that: (a) eye gaze probably taps unconscious but core insights into social behavior and as such is better than verbal measures at differentiating children with autism from mentally handicapped controls, (b) eye gaze taps either spontaneous processes of simulation or rudimentary pattern recognition, both of which are less based in language, and (c) the social understanding of children with autism is probably based mostly on verbally mediated theories whereas control children also possess more spontaneous insights indexed by eye gaze. C1 Univ Sussex, Brighton BN1 9QG, E Sussex, England. RP Ruffman, T (reprint author), Univ Sussex, Brighton BN1 9QG, E Sussex, England. CR Baddeley A. 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Child Psychol. Psychiatry Allied Discip. PD NOV PY 2001 VL 42 IS 8 BP 1083 EP 1094 DI 10.1111/1469-7610.00807 PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 515FM UT WOS:000173484800012 PM 11806690 ER PT J AU Minshew, NJ Goldstein, G AF Minshew, NJ Goldstein, G TI The pattern of intact and impaired memory functions in autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Autistic Disorder; memory; learning; abstract reasoning; concept formation; information processing ID DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; CHILDREN; INDIVIDUALS; DISORDER AB A battery of tests of auditory and visual memory was used to investigate memory function in 52 high-functioning adolescents and young adults with autism and 40 group-matched normal controls. It was hypothesized that memory dysfunction is present in autism but is not modality specific and is produced by poor utilization of organizing strategies. It was therefore hypothesized that memory impairment in autism would become more prominent as task complexity was increased. The participants with autism performed as well as controls on short-term memory and paired-associate learning tasks, but performed significantly less well than controls on a list learning task. They also performed significantly more poorly on immediate and delayed recall of a story and of a complex geometric figure. On a maze learning task, their performance became progressively worse relative to controls as the complexity of the maze increased. On a series of span tasks, they did not differ from controls on letter span, but did significantly worse on word span and sentences of increasing complexity. These findings indicate a lack of modality specificity and a failure to initiate organizing strategies as evidenced by inefficiency in new learning, poor utilization of contextual cues in story and complex pattern recall, and greater impairment with increasing complexity of the material. C1 Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA. VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA. RP Minshew, NJ (reprint author), Western Psychiat Inst & Clin, Dept Psychiat, 3811 OHara St,Suite 430,Bellefield Towers Bldg, Pittsburgh, PA 15213 USA. CR AMELI R, 1988, J AUTISM DEV DISORD, V18, P601, DOI 10.1007/BF02211878 BARTH C, 1995, DEV NEUROPSYCHOL, V11, P53 Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x BOUCHER J, 1976, BRIT J PSYCHOL, V67, P73 BOUCHER J, 1981, J AUTISM DEV DISORD, V11, P293, DOI 10.1007/BF01531512 Boucher J., 1978, CHILD PSYCHOL PSYCHI, V19, P161 DELIS DC, 1987, CALIFORNIA VERBAL LE Fein D., 1996, PRESCHOOL CHILDREN I, P123 FRITH U, 1970, J EXP CHILD PSYCHOL, V10, P120, DOI 10.1016/0022-0965(70)90049-4 FRITH U, 1970, Journal of Abnormal Psychology, V76, P413, DOI 10.1037/h0020133 FYFFE C, 1978, BRIT J PSYCHOL, V69, P393 Griffith EM, 1999, CHILD DEV, V70, P817, DOI 10.1111/1467-8624.00059 HAMMILL DD, 1985, DTLA 2 DETROIT TESTS Hermelin B, 1970, PSYCHOL EXPT AUTISTI LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LEZAK MD, 1995, NEUROPSYCHOLOGICAL A, P475 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 MCCLELLAND J, 1996, PSYCHOL REV, V102, P419 Minshew N. 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F., 1997, AUTISM EXECUTIVE DIS, P143 PRIOR MR, 1976, J AUTISM CHILD SCHIZ, V6, P121, DOI 10.1007/BF01538055 RAPIN I, 1991, AM ACAD PEDIAT S, P751 RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 Russell J, 1999, J AUTISM DEV DISORD, V29, P103, DOI 10.1023/A:1023084425406 RYAN C, 1980, BIOL EFFECTS ALCOHOL, P701 TAGERFLUSBERG H, 1991, BRIT J DEV PSYCHOL, V9, P417 TAGERFLUSBERG H, 1985, CHILD DEV, V56, P1167, DOI 10.1111/j.1467-8624.1985.tb00185.x Wechsler D., 1987, WECHSLER MEMORY SCAL NR 36 TC 93 Z9 93 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 NOV PY 2001 VL 42 IS 8 BP 1095 EP 1101 DI 10.1111/1469-7610.00808 PG 7 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 515FM UT WOS:000173484800013 PM 11806691 ER PT J AU Jyonouchi, H Sun, SN Le, H AF Jyonouchi, H Sun, SN Le, H TI Proinflammatory and regulatory cytokine production associated with innate and adaptive immune responses in children with autism spectrum disorders and developmental regression SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE autism spectrum disorders; adaptive immune responses; innate immunity ID PITUITARY-ADRENOCORTICAL AXIS; BLOOD MONONUCLEAR-CELLS; COWS MILK ALLERGY; MOLECULAR MECHANISMS; INTERLEUKIN-6; ALPHA; DIFFERENTIATION; SEROTONIN; ANTIGEN; SYSTEM AB We determined innate and adaptive immune responses in children with developmental regression and autism spectrum disorders (ASD, N = 71), developmentally normal siblings (N = 23), and controls (N = 17). With lipopolysaccharide (LPS), a stimulant for innate immunity, peripheral blood mononuclear cells (PBMCs) from 59/71 (83.1%) ASD patients produced > 2 SD above the control mean (CM) values of TNF-alpha, IL-1 beta, and/or IL-6 produced by control PBMCs. ASD PBMCs produced higher levels of proinflammatory/counter-regulatory cytokines without stimuli than controls. With stimulants of phytohemagglutinin (PHA), tetanus, IL-12p70, and IL-18, PBMCs from 47.9% to 60% of ASD patients produced > 2 SD above the CM values of TNF-alpha depending on stimulants. Our results indicate excessive innate immune responses in a number of ASD children that may be most evident in TNF-alpha production. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA. RP Jyonouchi, H (reprint author), Univ Minnesota, Dept Pediat, MMC 610 FUMC,420 Delaware St SE, Minneapolis, MN 55455 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barkhudaryan N, 1999, NEUROCHEM RES, V24, P1169, DOI 10.1023/A:1020720722209 Benlounes N, 1999, J ALLERGY CLIN IMMUN, V104, P863 Benlounes N, 1997, CLIN EXP ALLERGY, V27, P942 Borish L, 1998, J ALLERGY CLIN IMMUN, V101, P293 Dunn AJ, 1999, ADV EXP MED BIOL, V461, P117 Flavell RA, 1999, IMMUNOL RES, V19, P159, DOI 10.1007/BF02786484 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Gupta S, 1998, J NEUROIMMUNOL, V85, P106, DOI 10.1016/S0165-5728(98)00021-6 Gupta S, 1996, J AUTISM DEV DISORD, V26, P439, DOI 10.1007/BF02172828 Jyonouchi H, 2000, ARCH OTOLARYNGOL, V126, P522 JYONOUCHI H, 1995, J NUTR, V125, P2483 Medzhitov R, 2000, NEW ENGL J MED, V343, P338 MohanKumar SMJ, 1998, BRAIN RES BULL, V47, P29, DOI 10.1016/S0361-9230(98)00037-9 Mossner R, 1998, NEUROCHEM INT, V33, P251, DOI 10.1016/S0197-0186(98)00026-6 Okamura H, 1998, CURR OPIN IMMUNOL, V10, P259, DOI 10.1016/S0952-7915(98)80163-5 Ono SJ, 2000, ANNU REV IMMUNOL, V18, P347, DOI 10.1146/annurev.immunol.18.1.347 Romagnani S, 1997, CURR OPIN IMMUNOL, V9, P773, DOI 10.1016/S0952-7915(97)80176-8 SINGH VK, 1993, BRAIN BEHAV IMMUN, V7, P97, DOI 10.1006/brbi.1993.1010 Singh VK, 1996, J NEUROIMMUNOL, V66, P143, DOI 10.1016/0165-5728(96)00014-8 Singh VK, 1997, BIOL PSYCHIAT, V41, P753, DOI 10.1016/S0006-3223(96)00522-7 Swain SL, 1999, CURR OPIN IMMUNOL, V11, P180, DOI 10.1016/S0952-7915(99)80030-2 Ulevitch RJ, 2000, IMMUNOL RES, V21, P49, DOI 10.1385/IR:21:2-3:49 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 Wang JP, 1999, BRAIN RES, V815, P337, DOI 10.1016/S0006-8993(98)01091-9 Wright SD, 1999, J EXP MED, V189, P605, DOI 10.1084/jem.189.4.605 NR 26 TC 163 Z9 164 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD NOV 1 PY 2001 VL 120 IS 1-2 BP 170 EP 179 DI 10.1016/S0165-5728(01)00421-0 PG 10 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 493LJ UT WOS:000172224100020 PM 11694332 ER PT J AU Owley, T McMahon, W Cook, EH Laulhere, T South, M Mays, LZ Shernoff, ES Lainhart, J Modahl, CB Corsello, C Ozonoff, S Risi, S Lord, C Leventhal, BL Filipek, PA AF Owley, T McMahon, W Cook, EH Laulhere, T South, M Mays, LZ Shernoff, ES Lainhart, J Modahl, CB Corsello, C Ozonoff, S Risi, S Lord, C Leventhal, BL Filipek, PA TI Multisite, double-blind, placebo-controlled trial of porcine secretin in autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autistic disorder; pervasive developmental disorder; secretin; psychopharmacology ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; CHILDREN; FENFLURAMINE; NALTREXONE; SYMPTOMS; ADULTS AB Objective: To examine the efficacy of intravenous porcine secretin for the treatment of autistic disorder. Method: Randomized, double-blind, placebo-controlled, crossover design. Fifty-six subjects with autistic disorder received either a secretin or placebo infusion at baseline and the other substance at week 4. Subjects were given the Autism Diagnostic Observation Schedule (ADOS) and other pertinent developmental measures at baseline and at weeks 4 and 8 to assess drug effects. Results, For the primary efficacy analysis, change of ADOS social-communication total score from week 0 to week 4, no statistically significant difference was obtained between placebo (-0.8 +/- 2.9) and secretin groups (-0.6 +/- 1.4; t(54) = 0.346, p < .73). The other measures showed no treatment effect for secretin compared with placebo. Conclusion: There was no evidence for efficacy of secretin in this randomized, placebo-controlled, double-blind trial. C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Utah, Salt Lake City, UT 84112 USA. Univ Calif Irvine, Irvine, CA 92717 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 2001 VL 40 IS 11 BP 1293 EP 1299 DI 10.1097/00004583-200111000-00009 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 485KE UT WOS:000171752900009 PM 11699803 ER PT J AU Garfield, JL Peterson, CC Perry, T AF Garfield, JL Peterson, CC Perry, T TI Social cognition, language acquisition and the development of the theory of mind SO MIND & LANGUAGE LA English DT Review ID WILLIAMS-SYNDROME; FALSE BELIEF; AUTISTIC-CHILD; DEAF-CHILDREN; MODULARITY; KNOWLEDGE; DEFICIT; COMMUNICATION; INDIVIDUALS; PERFORMANCE AB Theory of Mind (ToM) is the cognitive achievement that enables us to report our propositional attitudes, to attribute such attitudes to others, and to use such postulated or observed mental states in the prediction and explanation of behavior. Most normally developing children acquire ToM between the ages of 3 and 5 years, but serious delays beyond this chronological and mental age have been observed in children with autism, as well is in those with severe sensory impairments. We examine data from Studies of ToM in normally developing children and those with deafness, blindness, autism and Williams syndrome, as well as data from lower primates, in a search for answers to key theoretical questions concerning the origins, nature and representation of knowledge about the mind. In answer to these, we offer a framework according to which ToM is jointly dependent upon language and social experience, and is produced by a conjunction of language acquisition with children's growing social understanding, acquired through conversation and interaction with others. We argue that adequate language and adequate social skills are jointly causally sufficient, and individually causally necessary, for producing ToM. Thus our account supports a social developmental theory of the genesis of human cognition, inspired by the work of Sellars and Vygotsky. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. Smith Coll, Northampton, MA 01063 USA. Univ Tasmania, Hobart, Tas 7001, Australia. RP Peterson, CC (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. CR ASTINGTON J, 1996, WHAT THEORETICAL CHI Astington J. W., 1993, CHILDS DISCOVERY MIN Astington JW, 1999, DEV PSYCHOL, V35, P1311, DOI 10.1037//0012-1649.35.5.1311 Baier A. 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S., 1962, THOUGHT LANGUAGE Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER Wellman H. M., 1990, CHILDS THEORY MIND WHITEN A, 1996, DOES SMART BEHAV REA WHITEN A, 1994, GRADES MINDREADING WHITEN A, 1988, BEHAV BRAIN SCI, V11, P233 Wittgenstein L., 1956, PHILOS INVESTIGATION Wittgenstein L., 1969, CERTAINTY ZAJONC R, 1986, PSYCHOL TODAY, V2, P46 NR 120 TC 88 Z9 88 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0268-1064 J9 MIND LANG JI Mind Lang. PD NOV PY 2001 VL 16 IS 5 BP 494 EP 541 DI 10.1111/1468-0017.00180 PG 48 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 487YZ UT WOS:000171908400002 ER PT J AU Bertrand, J Mars, A Boyle, C Bove, F Yeargin-Allsopp, M Decoufle, P AF Bertrand, J Mars, A Boyle, C Bove, F Yeargin-Allsopp, M Decoufle, P TI Prevalence of autism in a United States population: The Brick Township, New Jersey, investigation SO PEDIATRICS LA English DT Article DE autism; prevalence; developmental disabilities; Brick Township ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; SURVEILLANCE; INDIVIDUALS; BEHAVIOR AB Objective. This study determined the prevalence of autism for a defined community, Brick Township, New Jersey, using current diagnostic and epidemiologic methods. Methods. The target population was children who were 3 to 10 years of age in 1998, who were residents of Brick Township at any point during that year, and who had an autism spectrum disorder. Autism spectrum disorder was defined as autistic disorder, pervasive developmental disorder-not otherwise specified (PDD-NOS), and Asperger disorder. The study used 4 sources for active case finding: special education records, records from local clinicians providing diagnosis or treatment for developmental or behavioral disabilities, lists of children from community parent groups, and families who volunteered for participation in the study in response to media attention. The autism diagnosis was verified (or ruled out) for 71% of the children through clinical assessment. The assessment included medical and developmental history, physical and neurologic evaluation, assessment of intellectual and behavioral functioning, and administration of the Autism Diagnostic Observation Schedule-Generic. Results. The prevalence of all autism spectrum disorders combined was 6.7 cases per 1000 children. The prevalence for children whose condition met full diagnostic criteria for autistic disorder was 4.0 cases per 1000 children, and the prevalence for PDD-NOS and Asperger disorder was 2.7 cases per 1000 children. Characteristics of children with autism in this study were similar to those in previous studies of autism. Conclusions. The prevalence of autism in Brick Township seems to be higher than that in other studies, particularly studies conducted in the United States, but within the range of a few recent studies in smaller populations that used more thorough case-finding methods. C1 Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30341 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Dev Disabil, New Brunswick, NJ USA. Agcy Tox Subst & Dis Registry, Atlanta, GA USA. RP Bertrand, J (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, 4770 Buford Hwy,MS-F49, Atlanta, GA 30341 USA. CR *AG TOX SUBST DIS, 2000, ATSDR PUBL HLTH ASS American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Arvidsson T., 1997, AUTISM, V1, P163, DOI 10.1177/1362361397012004 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAILEY A, 1993, LANCET, V341, P1225, DOI 10.1016/0140-6736(93)91065-T Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Boyle CA, 1999, INFANT YOUNG CHILD, V12, P75 BURD L, 1987, J AM ACAD CHILD PSY, V26, P700, DOI 10.1097/00004583-198709000-00014 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Davidovitch M, 1996, J CHILD NEUROL, V11, P389 Elliott C. D., 1990, DIFFERENTIAL ABILITY Filipek P. A., 1999, J AUTISM DEV DISORD, V29, P437 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 FROMBONNE E, 1999, J AUTISM DEV DISORD, V29, P113 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Hillman R E, 2000, Mo Med, V97, P159 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 KIRBY RS, 1995, J DEV BEHAV PEDIATR, V16, P318 Lainhart JE, 1997, J AM ACAD CHILD PSY, V36, P282, DOI 10.1097/00004583-199702000-00019 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lord C, 1998, MENT RETARD DEV D R, V4, P90, DOI 10.1002/(SICI)1098-2779(1998)4:2<90::AID-MRDD5>3.0.CO;2-0 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LORD C, 1998, NIH STAT SCI AUT SCR Miles JH, 2000, AM J MED GENET, V91, P245, DOI 10.1002/(SICI)1096-8628(20000410)91:4<245::AID-AJMG1>3.0.CO;2-2 NELSON KB, 2000, NEUROPEPTIDES NEUROT Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 RITVO ER, 1989, AM J PSYCHIAT, V146, P194 Rodier PM, 1997, TERATOLOGY, V55, P319, DOI 10.1002/(SICI)1096-9926(199705)55:5<319::AID-TERA4>3.0.CO;2-U Rogers SJ, 1998, MENT RETARD DEV D R, V4, P104 Schopler E., 1986, CHILDHOOD AUTISM RAT Sparrow S, 1984, VINELAND ADAPTIVE BE Stevenson RE, 1997, LANCET, V349, P1744, DOI 10.1016/S0140-6736(05)62956-X TUCHMAN RF, 1995, ANN NEUROL, V38, P526 *US BUR CENS, 1998, REP EC IND DAT WALKER HA, 1977, J AUTISM CHILD SCHIZ, V7, P165, DOI 10.1007/BF01537727 NR 37 TC 299 Z9 313 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD NOV PY 2001 VL 108 IS 5 BP 1155 EP 1161 DI 10.1542/peds.108.5.1155 PG 7 WC Pediatrics SC Pediatrics GA 488FH UT WOS:000171925200034 PM 11694696 ER PT J AU Lighdale, JR Hayer, C Duer, A Lind-White, C Jenkins, S Siegel, B Elliott, GR Heyman, MB AF Lighdale, JR Hayer, C Duer, A Lind-White, C Jenkins, S Siegel, B Elliott, GR Heyman, MB TI Effects of intravenous secretin on language and behavior of children with autism and gastrointestinal symptoms: A single-blinded, open-label pilot study SO PEDIATRICS LA English DT Article DE autism; intravenous secretin; gastrointestinal symptoms; children ID PERVASIVE DEVELOPMENTAL DISORDER AB Background. Autism is a severe developmental disorder with poorly understood etiology. A recently published case series describes 3 autistic children with gastrointestinal symptoms who underwent endoscopy and intravenous administration of secretin and were subsequently noted by their parents to demonstrate improved language skills over a 5-week period. This report sparked tremendous public interest, and investigators at several sites moved quickly to design controlled trials to test the efficacy of secretin as a therapy for autistic children. However, this is the first effort specifically designed to replicate the initial reported findings in terms of patient age, presenting symptoms, and drug administration. Objective. To rigorously apply the scientific method by assessing the reproducibility of the reported effects of intravenous secretin on the language of young children with autism and gastrointestinal symptoms. Methods. We performed a single-blinded, prospective, open-label trial by conducting formal language testing and blinded behavioral rating both before and repeatedly after a standardized infusion of secretin. We selected autistic children who were similar in age and profile to those described in the published retrospective case review. Inclusion criteria for study participation included age (3-6 years), confirmed diagnosis of autism, and reported gastrointestinal symptoms (16 had chronic diarrhea, 2 had gastroesophageal reflux, and 2 had chronic constipation). Twenty children (18 male) were admitted to the Pediatric Clinical Research Center at the University of California, San Francisco after administration of the Preschool Language Scale-3 (PLS-3). A 3 CU/kg dose of secretin (Secretin-Ferring) was administered intravenously (upper endoscopy was not performed). Behavioral ratings were derived using the Autism Observation Scale applied to a 30-minute time sample of the child's behavior consisting of a videotape of the PLS-3 (structured setting) and a second free play session with a standard set of developmentally appropriate toys. Participants then returned for follow-up evaluations, with readministrations of the PLS-3 at 1, 2, 3, and 5 weeks' postinfusion, and videotaping of each session for later blinded review by 2 independent observers using the Autism Observation Scale, uninformed about week of posttreatment. We also surveyed parents of our study children about their impressions of the effects of secretin using a 5-point Likert scale for parents to rate changes seen in their child. Results. With a total study completion rate across all participants of 96%, repeated measures analyses of variance revealed no significant increases in children's language skills from baseline across all 5 study time periods after a single infusion of secretin. Similarly, neither significant decreases in atypical behaviors nor increases in prosocial behaviors and developmentally appropriate play skills emerged. Furthermore, no relationship was found between parental reports of change and observable improvement in the sample. Despite the objective lack of drug effect, 70% of parents in our study reported moderate to high change in their child's language and behavior. Furthermore, 85% of parents reported that they felt that their child would obtain at least some additional benefits from another infusion of secretin. Conclusions. The results of our pilot study indicate that intravenous secretin had no effects in a 5-week period on the language and behavior of 20 children with autism and gastrointestinal symptoms. The open-label, prospective design of our study with blinded reviews of patients both before and after secretin administration follows the scientific method by seeking to reproduce an observed phenomenon using validating and reliable outcome measures. Pilot studies remain a mandatory step for the design of future randomized, clinical trials investigating potential treatments for children with autism. C1 Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. Harvard Univ, Sch Med, Combined Program Pediat Gastroenterol & Nutr, Boston, MA USA. Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA. RP Heyman, MB (reprint author), Univ Calif San Francisco, Dept Pediat, 500 Parnassus,MU 4 E,Rm 406, San Francisco, CA 94143 USA. 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EP e90 DI 10.1542/peds.108.5.e90 PG 5 WC Pediatrics SC Pediatrics GA 488FH UT WOS:000171925200013 PM 11694674 ER PT J AU Sarimski, K AF Sarimski, K TI Autism in children - Causes, forms and treatment SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Book Review CR SIGMAN M, 2000, AUTISMUS KINDERN URS NR 1 TC 0 Z9 0 PU VANDENHOECK & RUPRECHT PI GOTTINGEN PA THEATERSTRASSE 13,, D-37073 GOTTINGEN, GERMANY SN 0032-7034 J9 PRAX KINDERPSYCHOL K JI Prax. Kinderpsychol. Kinderpsychiatr. PD NOV-DEC PY 2001 VL 50 IS 9-10 BP 787 EP 788 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 509HK UT WOS:000173140800009 ER PT J AU O'Riordan, M Plaisted, K AF O'Riordan, M Plaisted, K TI Enhanced discrimination in autism SO QUARTERLY JOURNAL OF EXPERIMENTAL PSYCHOLOGY SECTION A-HUMAN EXPERIMENTAL PSYCHOLOGY LA English DT Article ID VISUAL-SEARCH; CHILDREN; TASK; MEMORY AB Children with autism are superior to typically developing children at visual search tasks (O'Riordan, Plaisted, Driver, & Baron-Cohen, in press; Plaisted, O'Riordan, & Baron-Cohen, l998b). This study investigates the reasons for this phenomenon. The performance of children with autism and of typically developing children was compared on a series of visual search tasks to investigate two related problems. The first issue was whether the critical determinant of search rate in children is the discriminability of the display items, as it is in normal adults. The second question investigated was whether the superior performance of individuals with autism on visual search tasks is due to an enhanced ability to discriminate between display items. The results demonstrated that discriminability is the rate-determining factor for children with and without autism, replicating earlier findings with normal adults, and that children with autism have an enhanced ability to discriminate between display items. Thus, it seems that an enhanced ability to discriminate between display items underlies superior visual search in autism. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP O'Riordan, M (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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J. Exp. Psychol. Sect A-Hum. Exp. Psychol. PD NOV PY 2001 VL 54 IS 4 BP 961 EP 979 DI 10.1080/02724980042000543 PG 19 WC Psychology; Psychology, Experimental SC Psychology GA 487BR UT WOS:000171854200001 PM 11765744 ER PT J AU Bibby, P Eikeseth, S Martin, NT Mudford, OC Reeves, D AF Bibby, P Eikeseth, S Martin, NT Mudford, OC Reeves, D TI Progress and outcomes for children with autism receiving parent-managed intensive interventions SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; BEHAVIORAL TREATMENT; YOUNG-CHILDREN; AGE; INDIVIDUALS; PRESCHOOL; LANGUAGE; PROJECT AB Parent-managed behavioral interventions for young children with autism are under-researched. We analyzed data from 66 children served by 25 different early intervention consultants. After a mean of 31.6 months of intervention IQ scores had not changed (N = 22). Vineland adaptive behavior scores had increased significantly by 8.9 points (N = 21). No children aged > 72 months attained normal functioning, i.e., IQ > 85 and unassisted mainstream school placement (N = 42). Progress for 60 children across 12 months was found for mental age (5.4 months), adaptive behavior (9.7 months), and language (5.1 months). The interventions did not reproduce results from clinic-based professionally directed programs. The effectiveness of the parent-managed intervention model as it has developed and the adequacy of professional services in that model are discussed. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Autism & Dev Disorders Educ Res, London SE22 9AQ, England. Univ Keele, Keele ST5 5BG, Staffs, England. Univ Manchester, Manchester, Lancs, England. RP Bibby, P (reprint author), Autism & Dev Disorders Educ Res, 62 Oakhurst Grove, London SE22 9AQ, England. 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 Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Bayley N, 1993, MANUAL BAYLEY SCALES Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 EDWARDS S, 1997, MANUAL REYNELL DEV L, V3 EIKESETH S, IN PRESS BEHAV MODIF Elliot C. D., 1997, BRIT ABILITY SCALES ELLIOT CD, 1977, BRIT ABILITY SCALES FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 FOXX RM, 2000, ASS BEH AN CONV WASH Griffiths R, 1970, ABILITIES YOUNG CHIL Harris H., 1991, GREAT LAKES WETLANDS, V2, P1 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 HART B, 1975, J APPL BEHAV ANAL, V8, P411, DOI 10.1901/jaba.1975.8-411 Jacobson JW, 2000, BEHAV ANALYST, V23, P149 JOHNSON E, 2000, UNPUB FACILITATING F Jordan R, 1998, ED INTERVENTIONS CHI Kazdin AE, 1998, RES DESIGNS CLIN PSY KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P197, DOI 10.1901/jaba.1977.10-197 Leaf R., 1999, WORK PROGR BEHAV MAN Leiter R. G., 1969, GEN INSTRUCTIONS LEI LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LORD C, 1989, J CHILD PSYCHOL PSYC, V30, P575, DOI 10.1111/j.1469-7610.1989.tb00269.x Lovaas O. I., 1996, BEHAV INTERVENTION Y, P241 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lovaas O. I., 1981, TEACHING DEV DISABLE Lovaas O. I., 1988, ADV CLIN CHILD PSYCH, V11, P285 LOVAAS OI, 1993, J APPL BEHAV ANAL, V26, P617, DOI 10.1901/jaba.1993.26-617 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 Maurice C., 1993, LET ME HEAR YOUR VOI McDonough K. A., 1996, BEHAV INTERVENTION Y, P63 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MUDFORD OC, IN PRESS RES DEV DIS Mudford OC, 2000, AM J MENT RETARD, V105, P118, DOI 10.1352/0895-8017(2000)105<0118:AITFCW>2.0.CO;2 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1169, DOI 10.1192/bjp.113.504.1169 Sattler J.M., 1992, ASSESSMENT CHILDREN Schreck KA, 2000, BEHAV INTERVENT, V15, P279, DOI 10.1002/1099-078X(200010/12)15:4<279::AID-BIN68>3.0.CO;2-B SHAH A, 1985, J AUTISM DEV DISORD, V15, P195, DOI 10.1007/BF01531605 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 SIEGEL B, 1986, J AUTISM DEV DISORD, V16, P275, DOI 10.1007/BF01531660 Smith T, 2000, BEHAV INTERVENT, V15, P83, DOI 10.1002/(SICI)1099-078X(200004/06)15:2<83::AID-BIN47>3.0.CO;2-W Smith T., 2000, PRESCHOOL PROGRAMS C, P23 Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 Smith T., 1996, BEHAV INTERVENTION Y, P45 Smith T, 1999, CLIN PSYCHOL-SCI PR, V6, P33, DOI 10.1093/clipsy/6.1.33 Smith T, 1998, INFANT YOUNG CHILD, V10, P67 Smith T, 2000, RES DEV DISABIL, V21, P297, DOI 10.1016/S0891-4222(00)00043-3 Sparrow S, 1984, VINELAND ADAPTIVE BE STUTSMAN R, 1948, MANUAL MERRILL PALME Wechsler D., 1992, MANUAL WECHSLER INTE, V3rd Wechsler D, 1990, MANUAL WECHSLER PRES Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F NR 54 TC 37 Z9 37 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD NOV-DEC PY 2001 VL 22 IS 6 BP 425 EP 447 DI 10.1016/S0891-4222(01)00082-8 PG 23 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 497PE UT WOS:000172464000001 PM 11768669 ER PT J AU Mullins, JL Christian, L AF Mullins, JL Christian, L TI The effects of progressive relaxation training on the disruptive behavior of a boy with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article ID SEVERE MENTAL-RETARDATION; ADULTS AB This study examined the effects of progressive relaxation training on the disruptive behaviors of a boy with autism. Moreover, his overt relaxed behaviors before and after relaxation training were measured using the Behavioral Relaxation Scale (Poppen, 1988, Poppen, 1998). After the participant received training in progressive relaxation procedures a multielement design with three conditions was utilized to determine the effects of the procedures on the duration of the boy's disruptive behaviors during leisure activity sessions. The conditions were: (a) relaxation prior to a leisure activity session; (b) cued relaxation; and (c) no relaxation prior to the session, which represented a baseline condition. Results indicated that the participant acquired progressive relaxation skills, displayed more relaxed behaviors after performing the procedures, and showed a decrease in the duration of his disruptive behaviors upon completing progressive relaxation training prior to a leisure activity session. Implications for future research are discussed. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Inst Appl Behav Anal, Los Angeles, CA 90045 USA. Univ Kansas, Lawrence, KS 66045 USA. RP Christian, L (reprint author), Inst Appl Behav Anal, 5777 W Century Blvd,Suite 675, Los Angeles, CA 90045 USA. EM lachristian@att.net CR ARMSTRONG FD, 1988, J CLIN CHILD PSYCHOL, V17, P310, DOI 10.1207/s15374424jccp1704_2 BORKOVEC T, 1978, BEHAV RES THER, V17, P119 CALAMARI JE, 1987, RES DEV DISABIL, V8, P55, DOI 10.1016/0891-4222(87)90040-0 Cautela JR, 1978, RELAXATION COMPREHEN FEJES K, 1987, CHILD FAMILY BEHAV T, V9, P55, DOI 10.1300/J019v09n01_05 GRODEN J, 1994, CURR I AUT, P177 HARVEY JR, 1978, J BEHAV THER EXP PSY, V9, P347, DOI 10.1016/0005-7916(78)90012-5 JACOBSON H, 1938, PROGR RELAXATION LAGRONE R, 1988, J CLIN PSYCHOL, V44, P271, DOI 10.1002/1097-4679(198803)44:2<271::AID-JCLP2270440230>3.0.CO;2-Q LINDSAY WR, 1994, RES DEV DISABIL, V15, P425, DOI 10.1016/0891-4222(94)90027-2 LINDSAY WR, 1989, RES DEV DISABIL, V10, P129, DOI 10.1016/0891-4222(89)90002-4 LUISELLI JK, 1979, BEHAV THER, V10, P663, DOI 10.1016/S0005-7894(79)80068-4 Luiselli JL, 1982, CHILD BEHAV THER, V3, P41 LUNDERVOLD D, 1986, REHABIL COUNS BULL, V30, P124 MCPHAIL CH, 1989, J MENT DEFIC RES, V33, P399 Norton M, 1997, J BEHAV THER EXP PSY, V28, P129, DOI 10.1016/S0005-7916(97)00004-9 POPPEN R, 1982, BIOFEEDBACK SELF-REG, V7, P491, DOI 10.1007/BF00998889 POPPEN R, 1998, BEHAV RELAXATION TRA Poppen R., 1988, BEHAV RELAXATION TRA RAYMER R, 1985, J BEHAV THER EXP PSY, V16, P309, DOI 10.1016/0005-7916(85)90005-9 To MYF, 2000, ARCH PSYCHIAT NURS, V14, P39, DOI 10.1016/S0883-9417(00)80007-2 NR 21 TC 9 Z9 9 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD NOV-DEC PY 2001 VL 22 IS 6 BP 449 EP 462 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 497PE UT WOS:000172464000002 PM 11768670 ER PT J AU Gray, DE AF Gray, DE TI Accommodation, resistance and transcendence: three narratives of autism SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE autism; narrative analysis; chronic illness ID CHRONIC ILLNESS; LIFE; CONSTRUCTION; EXPERIENCE; STORIES; CANCER; MODELS AB This paper presents a narrative analysis of autism. It follows much of the literature on illness and narrative by emphasising the moral quality of illness narratives and the role it plays in creating coherence out of the disordering effects of autism on family life. In particular, the significance of narratives as "moralizing antidotes" to the experience of marginality and their linkages to the cultural "master narratives" of science, politics and faith are stressed. The three narratives presented display both conformity and non-conformity with the official narrative of autism offered by the autistic treatment centre where the research was based. Accordingly, they are described as narratives of accommodation, resistance and transcendence. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Univ New England, Dept Sociol, Sch Social Sci, Armidale, NSW 2351, Australia. RP Gray, DE (reprint author), Univ New England, Dept Sociol, Sch Social Sci, Armidale, NSW 2351, Australia. 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K., 1993, NARRATIVE ANAL RIESSMAN CK, 2000, NARRATIVE CULTURAL C ROBINSON I, 1990, SOC SCI MED, V30, P1173, DOI 10.1016/0277-9536(90)90257-S SARIS AJ, 1995, CULT MED PSYCHIAT, V19, P39, DOI 10.1007/BF01388248 SCOTT RA, 1962, MAKING BLIND MEN WILLIAMS G, 1993, WOLRDS ILLNESS BIOGR WILLIAMS G, 1984, SOCIOL HEALTH ILL, V6, P175, DOI 10.1111/1467-9566.ep10778250 NR 27 TC 24 Z9 24 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD NOV PY 2001 VL 53 IS 9 BP 1247 EP 1257 DI 10.1016/S0277-9536(00)00424-X PG 11 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA 468MT UT WOS:000170762000012 PM 11556614 ER PT J AU Fatemi, SH Kroll, JL Stary, JM AF Fatemi, SH Kroll, JL Stary, JM TI Altered levels of Reelin and its isoforms in schizophrenia and mood disorders SO NEUROREPORT LA English DT Article DE bipolar disorder; blood; Caucasian; major depression; reelin; schizophrenia; Vietnamese; Western blotting ID CELL-ADHESION MOLECULE; MUTANT MICE; LIPOPROTEIN RECEPTORS; NEURONAL MIGRATION; CINGULATE CORTEX; CEREBRAL-CORTEX; VLDL RECEPTOR; GENE; PROTEINS; EXPRESSION AB Reelin is a secreted extracellular matrix protein similar to 410 kDa mol. wt that is reduced in brains of patients with schizophrenia, autism, bipolar disorder and major depression. Recent reports also indicate its near absence in sera of some patients with an autosomal recessive form of lissencephaly. Moreover, Reelin is involved not only in normal cortical lamination of the brain during mammalian embryogenesis but is also implicated in cell signaling systems subserving cognition in adult brain. Here, we show that blood levels of Reelin and its isoforms are altered in three psychiatric disorders, namely, schizophrenia, bipolar disorder and major depression. The changes include significant increases in 410kDa. Reelin moiety of 49% in schizophrenic patients (p<0.022) of four ethnic compositions (Caucasian, Vietnamese, Hmong and Laotian) and non-significant increases in depressed patients by 34% vs control blood. In contrast, 410 kDa Reelin levels decreased by 33% in bipolar blood, albeit non-significantly, vs controls. There was a significant increase of 90% (p<0.0061) in 330 kDa Reelin in Caucasian schizophrenics; the depressed value was elevated by 30% vs control but non-significantly. Again, in contrast, bipolar 330 kDa value decreased by 31% vs control (p<0.0480). Finally, all 180 kDa Reelin values varied minimally in schizophrenics vs controls. In contrast, the 180 kDa Reelin values dropped significantly by 49% (p<0.0117) and 29% (p<0.0424) in bipolar and depressed patients, respectively, compared with controls. The alterations in blood Reelin values appear to be specific since levels of two other blood proteins, ceruloplasmin and albumin did not vary significantly between all psychiatric subjects and controls. These findings suggest that blood Reelin levels and its isoforms may be used as potential peripheral markers to diagnose presence of several psychiatric disorders and may also serve as targets for future therapeutic interventions. NeuroReport 12:3209-3215 (C) 2001 Lippincott Williams & Wilkins. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Community Univ Hlth Care Clin, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Box 392,Mayo Bldg,420 Delaware St SE, Minneapolis, MN 55455 USA. 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These peptides are the bioactive amidated form (OT) and the C-terminal extended peptides, OT-Gly, OT-Gly-Lys and OT-Gly-Lys-Arg, which are designated together as OT-X. As an extension of our previous study finding decreased plasma OT in autism, studies were conducted to determine whether there were changes in OT peptide forms in autistic children. Methods: Twenty eight male subjects (97 +/- 20 months; range, 70 -139 months), diagnosed with DSM-IV autistic disorder through observation and semi-structured interview, were compared with 31 age-matched nonpsychiatric control subjects (106 +/- 22 months; range, 74-140 months). Using OT antisera with different specificity for the peptide forms, we measured plasma OT and OT-X in each group. Results: T tests showed that there was a decrease in plasma OT (t = 4.4, p < .0001), an increase in OT-X (t = 2.3, p < .03) and an increase in the ratio of OT-X/OT (t = 4.5, p < .0001) in the autistic sample, compared with control subjects. Conclusions: The results suggest that children with autistic disorder show alterations in the endocrine OT system. Deficits in OT peptide processing in children with autism may be important in the development of this syndrome. (C) 2001 Society of Biological Psychiatry. C1 Wright State Univ, Sch Med, Dept Pharmacol & Toxicol, Dayton, OH 45401 USA. Wayne State Univ, Sch Med, Detroit, MI USA. Univ Connecticut, Storrs, CT USA. Univ Calif Orange, Irvine Med Ctr, Orange, CA USA. Stanford Univ, Sch Med, Stanford, CA USA. Coll New Jersey, Trenton, NJ USA. RP Morris, M (reprint author), Wright State Univ, Sch Med, Dept Pharmacol & Toxicol, Box 927, Dayton, OH 45401 USA. CR ALTSTEIN M, 1988, J NEUROSCI, V8, P3967 AMICO JA, 1985, J CLIN ENDOCR METAB, V60, P5 BRAKS JAM, 1994, CELL, V78, P263, DOI 10.1016/0092-8674(94)90296-8 Cook EH, 1998, MENT RETARD DEV D R, V4, P113, DOI 10.1002/(SICI)1098-2779(1998)4:2<113::AID-MRDD8>3.0.CO;2-Q Dong WJ, 1997, J NEUROSCI, V17, P563 Dunn L. 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Psychiatry PD OCT 15 PY 2001 VL 50 IS 8 BP 609 EP 613 DI 10.1016/S0006-3223(01)01139-8 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 486HQ UT WOS:000171812700007 PM 11690596 ER PT J AU van der Geest, JN Kemner, C Camfferman, G Verbaten, MN van Engeland, H AF van der Geest, JN Kemner, C Camfferman, G Verbaten, MN van Engeland, H TI Eye movements, visual attention, and autism: A saccadic reaction time study using the gap and overlap paradigm SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; visual attention; saccadic eye movements; reaction time; gap effect ID PERVASIVE DEVELOPMENTAL DISORDER; FAMILY HOME MOVIES; INFANTILE-AUTISM; CHILDREN; FIELD; CORRELATE; SYSTEMS; MONKEY; MR AB Background: On the basis of the literature on autism, it was hypothesized that children with autism have deficits in attentional (dis-)engagement mechanisms. Methods: A saccadic gap- overlap task was used to study visual engagement and disengagement in 16 high-functioning autistic children of about 10 years of age and 15 age- and IQ-matched normal control children. Subjects were asked to make saccadic eye movements from a fixation point to a suddenly appearing target as fast as possible. The saccadic reaction time was compared in two conditions: 1) the overlap condition, in which the fixation point was continuously visible, and 2) the gap condition, in which the fixation point was turned off 200 msec before the target appeared. Results: Although no differences between the groups in either condition was observed, the gap effect (i.e., the difference in saccadic reaction time between the overlap condition and the gap condition) was smaller in the autistic group than in the control group. Conclusions: We concluded that autistic children show a lower level of attentional engagement. (C) 2001 Society of Biological Psychiatry. C1 Univ Utrecht, Dept Psychopharmacol, NL-3584 CA Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. RP van der Geest, JN (reprint author), Univ Utrecht, Dept Psychopharmacol, Sorbonnelaan 16, NL-3584 CA Utrecht, Netherlands. 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Psychiatry PD OCT 15 PY 2001 VL 50 IS 8 BP 614 EP 619 DI 10.1016/S0006-3223(01)01070-8 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 486HQ UT WOS:000171812700008 PM 11690597 ER PT J AU Plotkin, SA AF Plotkin, SA TI Lessons learned concerning vaccine safety SO VACCINE LA English DT Article; Proceedings Paper CT 5th European Conference on Vaccinology CY MAR 21-23, 2001 CL LUZERN, SWITZERLAND SP European Federat Pharmaceut Ind & Assoc, European Vaccine Mfg ID DEPENDENT DIABETES-MELLITUS; HEPATITIS-B VACCINATION; NO EVIDENCE; RUBELLA VACCINE; MEASLES; MUMPS; ASSOCIATION; AUTISM; SYSTEM AB The safety of vaccines is an issue that has been with us ever since Jenner, and it will not go away. The author argues that despite what may seem a waste of energy, most proposed relationships between vaccines and reactions must be thoroughly investigated, as some have been proved correct. Investigations that show the putative relationship to be incorrect serve as examples of scientific rigor, which are valuable for the public. The author draws eight lessons for the future from our recent experiences. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Univ Penn, Wistar Inst, Aventis Pasteur, Doylestown, PA 18901 USA. RP Plotkin, SA (reprint author), Univ Penn, Wistar Inst, Aventis Pasteur, 4650 Wismer Rd, Doylestown, PA 18901 USA. 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RP Heller, D (reprint author), Univ Manchester, Sch Med, Sch Epidemiol & Hlth Sci, Evidence Populat Hlth Unit, Manchester M13 9PT, Lancs, England. CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Gellin BG, 2001, NEW ENGL J MED, V344, P372, DOI 10.1056/NEJM200102013440509 HELLER RC, IN PRESS J EPIDEMIOL Institutes of Medicine, 2001, IMM SAF REV MEASL MU Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Nicoll A, 1998, BRIT MED J, V316, P715 Patja A, 2000, PEDIATR INFECT DIS J, V19, P1127, DOI 10.1097/00006454-200012000-00002 Roberts R, 1998, BRIT MED J, V316, P1824 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 WAKEFIELD AJ, 1998, LANCET, V351, P1327 Watson J C, 1998, MMWR Recomm Rep, V47, P1 WISE J, 2001, BRIT MED J, V322, P130 NR 12 TC 5 Z9 5 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD OCT 13 PY 2001 VL 323 IS 7317 BP 839 EP 840 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 483RW UT WOS:000171650500027 PM 11683152 ER PT J AU Asano, E Chugani, DC Muzik, O Behen, M Janisse, J Rothermel, R Mangner, TJ Chakraborty, PK Chugani, HT AF Asano, E Chugani, DC Muzik, O Behen, M Janisse, J Rothermel, R Mangner, TJ Chakraborty, PK Chugani, HT TI Autism in tuberous sclerosis complex is related to both cortical and subcortical dysfunction SO NEUROLOGY LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; SEROTONIN SYNTHESIS CAPACITY; HUMAN-BRAIN; FUNCTIONAL NEUROANATOMY; SURGICAL-TREATMENT; INFANTILE SPASMS; IN-VIVO; EPILEPSY; CHILDREN; GENE AB Objective: To examine the relationship between autism and epilepsy in relation to structural and functional brain abnormalities in children with tuberous sclerosis complex (TSC). Methods: Children with TSC and intractable epilepsy underwent MRI as well as PET scans with 2-deoxy-2-[F-18]fluoro-D-glucose (FDG) and alpha-[C-11]methyl-L-tryptophan (AMT). Based on the results of Autism Diagnostic Interview-Revised, Gilliam Autism Rating Scale, and overall adaptive behavioral composite (OABC) from Vineland Adaptive Behavior Scale, subjects were divided into three groups: autistic (OABC < 70; n = 9), mentally-retarded nonautistic (OABC < 70; n = 9), and relatively normal intelligence (OABC greater than or equal to 70; n = 8). Results: PET studies showed that the autistic group had decreased glucose metabolism in the lateral temporal gyri bilaterally, increased glucose metabolism in the deep cerebellar nuclei bilaterally, and increased AMT uptake in the caudate nuclei bilaterally, compared to the mentally-retarded nonautistic group. In addition, a history of infantile spasms and glucose hypometabolism in the lateral temporal gyri were both significantly associated with communication disturbance. Glucose hypermetabolism in the deep cerebellar nuclei and increased AMT uptake in the caudate nuclei were both related to stereotypical behaviors and impaired social interaction, as well as communication disturbance. Conclusions: These results suggest that generalized epilepsy in early life and functional deficits in the temporal neocortices may be associated with communication delays, and that functional imbalance in subcortical circuits may be associated with stereotypical behaviors and impaired social interaction in children with TSC. C1 Wayne State Univ, Childrens Hosp Michigan, Dept Pediat, PET Ctr, Detroit, MI 48201 USA. Wayne State Univ, Childrens Hosp Michigan, Dept Neurol, Detroit, MI 48201 USA. Wayne State Univ, Childrens Hosp Michigan, Dept Radiol, Detroit, MI 48201 USA. 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PD OCT 8 PY 2001 VL 105 IS 7 MA P119 BP 633 EP 633 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 478QZ UT WOS:000171358000228 ER PT J AU Wilcox, JA Tsuang, MT AF Wilcox, JA Tsuang, MT TI A case-control family study of pathology in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Texas Tech Univ, El Paso, TX 79905 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2001 VL 105 IS 7 MA P118 BP 633 EP 633 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 478QZ UT WOS:000171358000227 ER PT J AU Stokstad, E AF Stokstad, E TI New hints into the biological basis of autism SO SCIENCE LA English DT News Item NR 0 TC 31 Z9 33 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 5 PY 2001 VL 294 IS 5540 BP 34 EP 37 DI 10.1126/science.294.5540.34 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 480EJ UT WOS:000171448800012 PM 11588233 ER PT J AU Fourneret, P AF Fourneret, P TI Contribution of the cognitive approach to infant and juvenile psychopathology SO A N A E-APPROCHE NEUROPSYCHOLOGIQUE DES APPRENTISSAGES CHEZ L ENFANT LA French DT Article; Proceedings Paper CT Conference on Neuropsychological Assessment with a Teaching Step CY MAR 20-21, 2000 CL LYON, FRANCE DE cognitive neuropsychology; child psychopathology ID MIND ABILITIES; AUTISM; CHILDREN AB The cognitive neuropsychology has deeply renewed our comprehension of the cerebral processes underlying the mental operations. 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PD OCT PY 2001 VL 69 IS 4 SU 1 MA 87 BP 193 EP 193 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648900088 ER PT J AU Auranen, MP Kempas, E Vanhala, R Varilo, T Ylisaukko-oja, T Peltonen, L Jarvela, I AF Auranen, MP Kempas, E Vanhala, R Varilo, T Ylisaukko-oja, T Peltonen, L Jarvela, I TI A major susceptibility locus for autism spectrum disorders on chromosome 3q25-27 in the Finnish population. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Univ Helsinki, Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA. Univ Helsinki Hosp, Genet Mol Lab, Helsinki, Finland. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 124 BP 200 EP 200 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648900126 ER PT J AU Abramson, RK Cuccaro, ML Wieduwill, K Ravan, SA Decena, K Wright, HH AF Abramson, RK Cuccaro, ML Wieduwill, K Ravan, SA Decena, K Wright, HH TI Comparison of the autism diagnostic interview-revised (ADI) restrictive/repetitive behaviors and the aberrant behavior checklist (ABC) stereotopy scores. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 WS Hall Psychiat Ins, Columbia, SC USA. Univ S Carolina, Sch Med, Columbia, SC USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 592 BP 284 EP 284 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648900592 ER PT J AU Gordon, ES Minshew, NJ Gettig, E Devlin, BJ AF Gordon, ES Minshew, NJ Gettig, E Devlin, BJ TI The serotonin connection: a family history study of the possible association between autism and migraine headaches. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Pittsburgh, Pittsburgh, PA 15260 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 664 BP 296 EP 296 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648900664 ER PT J AU Wevrick, R Bischof, JM Chibuk, TK AF Wevrick, R Bischof, JM Chibuk, TK TI A necdin-like gene (NDNL2) in the chromosome 15 autism susceptibility region: expression, imprinting, and mapping of the human and mouse orthologues. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Alberta, Dept Med Genet, Edmonton, AB, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 996 BP 353 EP 353 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648900995 ER PT J AU Talebizadeh, Z Bittel, DC Miles, JH Butler, MG AF Talebizadeh, Z Bittel, DC Miles, JH Butler, MG TI Screening of the HOXA1 and HOXB1 genes in a group of autism subjects. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Missouri, Kansas City Sch Med, Kansas City, MO USA. Childrens Mercy Hosp, Kansas City, MO 64108 USA. Univ Missouri, Sch Med, Columbia, MO USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 1184 BP 385 EP 385 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648901185 ER PT J AU Thomas, AC Osann, K Modahl, C Laulhere, T Smith, M Escamilla, J Nguyen, V Flodman, P Spence, MA AF Thomas, AC Osann, K Modahl, C Laulhere, T Smith, M Escamilla, J Nguyen, V Flodman, P Spence, MA TI Twin zygosity and concordance for the autism phenotype. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Calif Irvine, Irvine, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 1209 BP 389 EP 389 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648901207 ER PT J AU Crawford, L Smalley, S Nelson, SF AF Crawford, L Smalley, S Nelson, SF TI Fine-scale SNP genotyping for autism using Single Base Extension and Tag Arrays. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 1912 BP 508 EP 508 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648901913 ER PT J AU Kim, S Herzing, LBK Veenstra-VanderWeele, J Lord, C Courchesne, R Leventhal, BL Ledbetter, DH Courchesne, E Cook, EH AF Kim, S Herzing, LBK Veenstra-VanderWeele, J Lord, C Courchesne, R Leventhal, BL Ledbetter, DH Courchesne, E Cook, EH TI Mutation screening and association study of ATP10C in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Chicago, Dept Psychiat, Dev Neurosci Lab, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL USA. Univ Chicago, Dept Psychiat, Dev Disorders Clin, Chicago, IL 60637 USA. Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, La Jolla, CA USA. Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 1992 BP 521 EP 521 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648901992 ER PT J AU Dowd, MF Mankoski, R Santangelo, S Folstein, S AF Dowd, MF Mankoski, R Santangelo, S Folstein, S TI Evidence of an epistatic interaction in a genetic linkage study of autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Tufts Univ New England Med Ctr, CLSA, Boston, MA 02111 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2006 BP 524 EP 524 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902008 ER PT J AU Ichikawa, S Liu, Y Miles, JH Hillman, RE Wang, CH AF Ichikawa, S Liu, Y Miles, JH Hillman, RE Wang, CH TI Identification of novel exons and analysis of autism-associated sequence variations within the chromosome 15q11-q13 region. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Missouri, Dept Biochem, Columbia, MO USA. Univ Missouri, Dept Child Hlth, Columbia, MO 65201 USA. Univ Missouri, Dept Psychiat, Columbia, MO 65201 USA. Univ Missouri, Dept Neurol, Columbia, MO USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2119 BP 543 EP 543 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902119 ER PT J AU Maestrini, E AF Maestrini, E CA IMGSAC TI Analysis of candidate genes for autism on chromosomes 7q, 2q and 16p. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract RI Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2151 BP 548 EP 548 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902150 ER PT J AU Jamain, S Betancur, C Quach, H Philippe, A Fellous, M Giros, B Gillberg, C Leboyer, M Bourgeron, T AF Jamain, S Betancur, C Quach, H Philippe, A Fellous, M Giros, B Gillberg, C Leboyer, M Bourgeron, T TI Linkage and association of the glutamate receptor 6 gene with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Inst Pasteur, Paris, France. INSERM U513, Fac Med, F-94000 Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2157 BP 549 EP 549 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902156 ER PT J AU Wassink, TH Piven, J Vieland, VJ Juang, J Swiderski, RE Pietila, J Searby, CC Braun, T Beck, G Folstein, SE Haines, JL Sheffield, VC AF Wassink, TH Piven, J Vieland, VJ Juang, J Swiderski, RE Pietila, J Searby, CC Braun, T Beck, G Folstein, SE Haines, JL Sheffield, VC TI WNT2 and autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Iowa, Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. Univ Iowa, Coll Publ Hlth, Dept Biostat, Iowa City, IA USA. Univ Iowa, Dept Stat & Actuarial Sci, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Howard Hughes Med Inst, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Dept Pediat, Iowa City, IA 52242 USA. Univ Iowa, Interdept Genet Program, Iowa City, IA USA. Tufts Univ, Coll Med, Dept Psychiat, Medford, MA 02155 USA. Vanderbilt Univ, Med Ctr, Program Human Genet, Nashville, TN USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2161 BP 550 EP 550 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902161 ER PT J AU Yamagata, T Li, H Mori, M Suwa, K Yasuhara, A Momoi, MY AF Yamagata, T Li, H Mori, M Suwa, K Yasuhara, A Momoi, MY TI Candidate gene screening on Japanese autism patients. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Jichi Med Sch, Dept Pediat, Minami Kawachi, Tochigi 32904, Japan. Kansai Med Univ, Kouri Hosp, Dept Pediat, Neyagawa, Osaka, Japan. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2168 BP 551 EP 551 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902170 ER PT J AU Copeland-Yates, SA Dupont, BR Skinner, CD Michaelis, RC AF Copeland-Yates, SA Dupont, BR Skinner, CD Michaelis, RC TI Characterization of a (9,15) translocation in a patient with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. Clemson Univ, Dept Biochem & Genet, Clemson, SC USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2196 BP 555 EP 555 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902196 ER PT J AU Smith, M Escamilla, JR Filipek, P Bocian, ME Modahl, C Flodman, P Spence, MA AF Smith, M Escamilla, JR Filipek, P Bocian, ME Modahl, C Flodman, P Spence, MA TI Deletion of chromosome 2q37.3: report of a case and of candidate genes for autism and osteodystrophy. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2201 BP 556 EP 556 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902199 ER PT J AU Johnson, RT Toji, LH Mars, A Beiswanger, CM Leonard, JC Bender, PK Beck, JC AF Johnson, RT Toji, LH Mars, A Beiswanger, CM Leonard, JC Bender, PK Beck, JC TI Coriell Autism Research Resource: multiplex families and their Hoxa1 polymorphism status. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Coriell Inst Med Res, Coriell Cell Repositories, Camden, NJ USA. Univ Med & Dent New Jersey, Dept Pediat, New Brunswick, NJ USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2208 BP 557 EP 557 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902208 ER PT J AU Wang, CH Liu, Y Yan, PS Huang, T Miles, JH Hillman, RE AF Wang, CH Liu, Y Yan, PS Huang, T Miles, JH Hillman, RE TI Autism DNA methylation profiling using CpG microarrays. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Missouri, Dept Psychiat & Neurol, Columbia, MO USA. Univ Missouri, Dept Biochem, Columbia, MO USA. Univ Missouri, Dept Pathol & Anatom Sci, Columbia, MO USA. Univ Missouri, Dept Child Hlth, Columbia, MO 65201 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2228 BP 561 EP 561 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902230 ER PT J AU Nurmi, EL Amin, T Bradford, Y Jacobs, MM Haines, JL Sutcliffe, JS AF Nurmi, EL Amin, T Bradford, Y Jacobs, MM Haines, JL Sutcliffe, JS CA Collaborative Linkage Study Autism TI Linkage disequilibrium mapping and haplotype analysis in the 11q11-q13 autism candidate region reveals suggestive association at ATP10C and OCA2 in the CLSA families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2300 BP 573 EP 573 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902302 ER PT J AU Hutcheson, HB Bradford, Y Folstein, SE Gardiner, MB Piven, J Santangelo, SL Sutcliffe, JS Vieland, V Wassink, TH Haines, JL AF Hutcheson, HB Bradford, Y Folstein, SE Gardiner, MB Piven, J Santangelo, SL Sutcliffe, JS Vieland, V Wassink, TH Haines, JL CA Collaborative Linkage Study Autism TI Testing autism candidate genes on chromosome 7. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Med Ctr, Program Human Genet, Nashville, TN USA. Tufts Univ New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. Tufts Univ, Sch Med, Boston, MA 02111 USA. Univ N Carolina, Neurosci Hosp, Chapel Hill, NC USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Univ Iowa, Div Stat Genet, Coll Publ Hlth, Iowa City, IA USA. Univ Iowa, Coll Med, Div Stat Genet, Iowa City, IA USA. Univ Iowa, Coll Med, Iowa City, IA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2314 BP 575 EP 575 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902315 ER PT J AU Jacobs, MM Nurmi, EL Bradford, Y Amin, T Haines, JL Sutcliffe, JS AF Jacobs, MM Nurmi, EL Bradford, Y Amin, T Haines, JL Sutcliffe, JS CA Collaborative Linkage Study Autism TI Genetic analysis of tryptophan hydroxylase gene polymorphisms in a chromosome 11p15 candidate region for autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Program Human Genet, Dept Mol Physiol & Biophys, Nashville, TN USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2315 BP 575 EP 575 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902313 ER PT J AU Li, J Tabor, HK Nguyen, L Gleason, C Lotspeich, LJ Spiker, D Risch, N Myers, RM AF Li, J Tabor, HK Nguyen, L Gleason, C Lotspeich, LJ Spiker, D Risch, N Myers, RM TI Lack of association between HoxA1, HoxB1, Reelin and WNT-2 gene variants and autism in 110 multiplex families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Stanford Univ, Dept Genet, Sch Med, Stanford, CA 94305 USA. Stanford Univ, Stanford, CA 94305 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2317 BP 576 EP 576 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902317 ER PT J AU Vincent, JB Petek, E Thevarkunnel, S Cheung, J Scherer, SW AF Vincent, JB Petek, E Thevarkunnel, S Cheung, J Scherer, SW TI Analysis of the gene RAY1(FAM4A1/ST7)at a translocation breakpoint region on 7q31.3 in an autism patient reveals a complex multigene system. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Hosp Sick Children, Dept Genet, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. Graz Univ, Inst Med Biol & Human Genet, Graz, Austria. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2323 BP 577 EP 577 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902323 ER PT J AU Stodgell, CJ Gnall, S Rodier, P AF Stodgell, CJ Gnall, S Rodier, P TI Valproic acid exposure alters gene expression in rat embryos: mechanism of teratogenicity and relationship to autism spectrum disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Rochester, Sch Med, Dept Obstet & Gynecol, Rochester, NY USA. NR 0 TC 0 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2001 VL 69 IS 4 SU 1 MA 2370 BP 584 EP 584 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 483RD UT WOS:000171648902370 ER PT J AU Titomanlio, L Marzano, MG Rossi, E D'Armiento, M De Brasi, D Vega, GR Andreucci, MV Orsini, AVM Santoro, L Sebastio, G AF Titomanlio, L Marzano, MG Rossi, E D'Armiento, M De Brasi, D Vega, GR Andreucci, MV Orsini, AVM Santoro, L Sebastio, G TI Case of Myhre syndrome with autism and peculiar skin histological findings SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Myhre syndrome; short stature; muscular build; autism ID GOMBO-SYNDROME AB Myhre syndrome (MS) (MIM 139210) is a rare disorder characterized by short stature, mental retardation, muscular build, blepharophimosis, and decreased joint mobility. We report on a 14-year-old boy with clinical findings consistent with a diagnosis of Myhre syndrome, associated with autism and peculiar skin histological findings. (C) 2001 Wiley-Liss, Inc. C1 Univ Naples Federico II, Dept Pediat, I-80131 Naples, Italy. Univ Pavia, I-27100 Pavia, Italy. Univ Naples Federico II, Dept Pathol, I-80131 Naples, Italy. Univ Naples Federico II, Dept Neurol Sci, I-80131 Naples, Italy. RP Sebastio, G (reprint author), Univ Naples Federico II, Dept Pediat, Via S Pansini 5, I-80131 Naples, Italy. CR BOTTANI A, 1995, AM J MED GENET, V59, P523, DOI 10.1002/ajmg.1320590423 GARCIACRUZ D, 1993, CLIN GENET, V44, P203 MYHRE SA, 1981, CLIN GENET, V20, P1 Ning Y, 1996, NAT GENET, V14, P86, DOI 10.1038/ng0996-86 SOLJAK MA, 1983, CLIN GENET, V23, P441 Verloes A, 2000, AM J MED GENET, V95, P185, DOI 10.1002/1096-8628(20001113)95:2<185::AID-AJMG19>3.0.CO;2-X NR 6 TC 19 Z9 19 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 1 PY 2001 VL 103 IS 2 BP 163 EP 165 DI 10.1002/ajmg.1517 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 473LK UT WOS:000171045300012 PM 11568925 ER PT J AU Elliman, DAC Bedford, HE AF Elliman, DAC Bedford, HE TI MMR vaccine-worries are not justified SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Editorial Material ID INFLAMMATORY BOWEL-DISEASE; POLYMERASE-CHAIN-REACTION; RUBELLA VACCINE; MEASLES VACCINATION; CROHNS-DISEASE; MUMPS; INFECTION; AUTISM; RISK C1 Univ London St Georges Hosp, Dept Child Hlth, London SW17 0QT, England. Inst Child Hlth, Ctr Paediat Epidemiol & Biostat, London WC1 1EH, England. RP Elliman, DAC (reprint author), Univ London St Georges Hosp, Dept Child Hlth, London SW17 0QT, England. 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Dis. Child. PD OCT PY 2001 VL 85 IS 4 BP 271 EP 273 DI 10.1136/adc.85.4.271 PG 3 WC Pediatrics SC Pediatrics GA 479GK UT WOS:000171396500001 PM 11567931 ER PT J AU Rosenwasser, B Axelrod, S AF Rosenwasser, B Axelrod, S TI The contributions of applied behavior analysis to the education of people with autism SO BEHAVIOR MODIFICATION LA English DT Article C1 Temple Univ, Philadelphia, PA 19122 USA. RP Rosenwasser, B (reprint author), Temple Univ, Philadelphia, PA 19122 USA. CR *COLL WORK GROUP A, 1997, BEST PRACT DES DEL E COWLEY G, 2000, NEWSWEEK 0731, P48 Department of Health, 1999, CLIN PRACT GUID GUID JACOBSON JW, 2000, BEHAV ANAL TODAY, V1, P6 KOPPEL T, 2001, NIGHTLINE 0309 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 *MADSEC AUT TASKF, 1999, EX SUMM PETESON I, 2000, NY TIMES 0506, pB2 Skinner B. F., 1957, VERBAL BEHAV U. S. Department of Health and Human Services, 1999, MENT HLTH REP SURG G NR 10 TC 7 Z9 7 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD OCT PY 2001 VL 25 IS 5 BP 671 EP 677 DI 10.1177/0145445501255001 PG 7 WC Psychology, Clinical SC Psychology GA 472CM UT WOS:000170965700001 PM 11642227 ER PT J AU Pelios, LV Lund, SK AF Pelios, LV Lund, SK TI A selective overview of issues on classification, causation, and early intensive behavioral intervention for autism SO BEHAVIOR MODIFICATION LA English DT Article ID DSM-III-R; CHILDREN; PARADIGM; CRITERIA; FLUENCY; SKILLS; MIND AB Autism is a behaviorally defined disorder that comprises a controversial diagnostic category due to heterogeneity in symptomatology, causation, and etiology and significant variance in response to intervention. 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PD OCT PY 2001 VL 25 IS 5 BP 678 EP 697 DI 10.1177/0145445501255002 PG 20 WC Psychology, Clinical SC Psychology GA 472CM UT WOS:000170965700002 PM 11573335 ER PT J AU Sundberg, ML Michael, J AF Sundberg, ML Michael, J TI The benefits of skinner's analysis of verbal behavior for children with autism SO BEHAVIOR MODIFICATION LA English DT Article ID STIMULUS-CONTROL PROCEDURES; ESTABLISHING OPERATIONS; AUTOMATIC REINFORCEMENT; INTRAVERBAL BEHAVIOR; LANGUAGE; INTERVENTION; RESPONSES; PRESCHOOL AB Behavior analysis has already contributed substantially to the treatment of children with autism, and further gains ran result from more use of Skinner's analysis of language in Verbal Behavior (1957) and in the resulting conceptual and experimental work. The approach emphasizes a unit of analysis consisting of the relations between behavior, motivative and discriminative variables, and consequences. 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PD OCT PY 2001 VL 25 IS 5 BP 698 EP 724 DI 10.1177/0145445501255003 PG 27 WC Psychology, Clinical SC Psychology GA 472CM UT WOS:000170965700003 PM 11573336 ER PT J AU Koegel, LK Koegel, RL Frea, WD AF Koegel, LK Koegel, RL Frea, WD TI Identifying early intervention targets for children with autism in inclusive school settings SO BEHAVIOR MODIFICATION LA English DT Article ID FOLLOW-UP; SOCIAL-BEHAVIOR; PEERS; CLASSROOMS; ISSUES AB This study assessed play and social behavior of young children with autism in inclusive school settings to identify important targets for intervention. Data were collected for five children with autism and for typically developing peers. All children with autism received intervention in one-on-one settings but did not have individual education plan goals that provided systematic intervention for developing play and social skills in their school settings. Results indicated the children with autism and their typically developing peers played with a comparable number of stimulus items (e.g., toys), but the children with autism engaged in these activities for shorter durations. Both children with autism and their typically developing peers engaged in similar levels of social interaction with adults. However, the children with autism rarely or never engaged in social interactions with their peers, whereas the typically developing peers frequently engaged in social interactions with other children. The results suggest important targets for intervention. C1 Univ Calif Santa Barbara, Autism Res & Training Ctr, Santa Barbara, CA 93106 USA. Calif State Univ Los Angeles, Los Angeles, CA 90032 USA. RP Koegel, LK (reprint author), Univ Calif Santa Barbara, Autism Res & Training Ctr, Santa Barbara, CA 93106 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baker M. 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S., 1986, CHILDRENS SOCIAL BEH STRAIN PS, 1983, ANAL INTERVEN DEVEL, V3, P23, DOI 10.1016/0270-4684(83)90024-1 Strain Phillip S., 1998, Seminars in Speech and Language, V19, P391, DOI 10.1055/s-2008-1064056 Strain PS, 2000, TOP EARLY CHILD SPEC, V20, P116, DOI 10.1177/027112140002000207 Zanolli K, 1996, J AUTISM DEV DISORD, V26, P407, DOI 10.1007/BF02172826 NR 31 TC 26 Z9 26 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD OCT PY 2001 VL 25 IS 5 BP 745 EP 761 DI 10.1177/0145445501255005 PG 17 WC Psychology, Clinical SC Psychology GA 472CM UT WOS:000170965700005 PM 11573338 ER PT J AU Harrower, JK Dunlap, G AF Harrower, JK Dunlap, G TI Including children with autism in general education classrooms - A review of effective strategies SO BEHAVIOR MODIFICATION LA English DT Article ID COOPERATIVE LEARNING GROUPS; HIGH-PROBABILITY REQUESTS; SEVERE DISABILITIES; SOCIAL INTERACTIONS; PEER INTERACTIONS; SELF-MANAGEMENT; YOUNG-CHILDREN; INTEGRATION STRATEGY; BEHAVIORAL MOMENTUM; SOCIODRAMATIC PLAY AB Children with autism can benefit from participation in inclusive classroom environments, and many experts assert that inclusion is a civil right and is responsible for nurturing appropriate social development. However, most children with autism require specialized supports to experience success in these educational contexts. This article provides a review of the empirical research that has addressed procedures for promoting successful inclusion of students with autism. Strategies reviewed include antecedent manipulations, delayed contingencies, self-management, peer-mediated interventions, and other approaches that have been demonstrated in the literature to be useful. The article concludes with a discussion of future research needs. C1 Univ S Florida, Florida Posit Behav Support Project, Tampa, FL 33620 USA. Univ S Florida, Louis Parte Florida Mental Hlth Inst, Dept Child & Family Studies, Div Appl Res & Educ Support, Tampa, FL 33620 USA. RP Harrower, JK (reprint author), Univ S Florida, Florida Posit Behav Support Project, Tampa, FL 33620 USA. 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D., 1992, INCREASING SUCCESS S Zanolli K, 1996, J AUTISM DEV DISORD, V26, P407, DOI 10.1007/BF02172826 NR 72 TC 55 Z9 55 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD OCT PY 2001 VL 25 IS 5 BP 762 EP 784 DI 10.1177/0145445501255006 PG 23 WC Psychology, Clinical SC Psychology GA 472CM UT WOS:000170965700006 PM 11573339 ER PT J AU Weiss, MJ Harris, SL AF Weiss, MJ Harris, SL TI Teaching social skills to people with autism SO BEHAVIOR MODIFICATION LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; SCRIPT-FADING PROCEDURE; NONHANDICAPPED PEERS; SEVERE DISABILITIES; SOCIODRAMATIC PLAY; SELF-MANAGEMENT; SYMBOLIC PLAY; DOWN-SYNDROME; CHILDREN; BEHAVIOR AB The treatment of social skills deficits remains one of the most challenging areas in meeting the needs of people with autism. Difficulties in understanding social stimuli, in initiating and responding to social bids, and in appreciating the affect that is intrinsic to social interactions can be baffling for people with autism. Researchers and practitioners of applied behavior analysis have tried a variety of strategies for teaching social skills. This article examines a range of useful procedures for teaching social skills to people with autism, including skills that are adult mediated, peer mediated, and child-with-autism mediated. The authors also consider the potential of classwide interventions in inclusive settings, pivotal response training, and the use of scripts to teach social initiations. C1 Rutgers State Univ, Piscataway, NJ 08855 USA. RP Weiss, MJ (reprint author), Rutgers State Univ, Piscataway, NJ 08855 USA. 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Modificat. PD OCT PY 2001 VL 25 IS 5 BP 785 EP 802 DI 10.1177/0145445501255007 PG 18 WC Psychology, Clinical SC Psychology GA 472CM UT WOS:000170965700007 PM 11573340 ER PT J AU Eikeseth, S AF Eikeseth, S TI Recent critiques of the UCLA young autism project SO BEHAVIORAL INTERVENTIONS LA English DT Article ID BEHAVIORAL TREATMENT; EARLY INTERVENTION; FOLLOW-UP; CHILDREN; AGE; REPLICATION; DISORDERS; PROGRAM; MODEL AB Lovaas and his associates at UCLA reported substantially better treatment outcomes for children with autism than had been reported previously. Many authors have closely scrutinized the UCLA research, and some have published major criticisms. Recently two critical reviews have appeared. Howlin (1997) evaluated the most common treatment approaches for children with autism, including the UCLA model. Additionally, the UK Department for Education and Employment commissioned a review of treatment research on autism written by Jordan, Jones, and Murray (1998). Although both reports contain useful information, they also contain inaccurate statements about the published results of the UCLA project. An aim of this paper is to illustrate the errors of fact and interpretation contained in the two papers and to clarify the existing data. A second aim is to identify points of agreement, which is also important when attempting to facilitate critical and accurate assessments of available scientific evidence. It is argued that Lovaas and colleagues made a convincing case for the efficacy of one model of early intensive behavioral treatment by presenting outcome data showing clinically meaningful, long-term gains in a population historically characterized by a severe and chronic disability, and an unfortunate history of treatment failures. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 Akersuhs Coll, N-1301 Sandvika, Norway. RP Eikeseth, S (reprint author), Akersuhs Coll, POB 372, N-1301 Sandvika, Norway. CR Anderson S. 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Intervent. PD OCT-DEC PY 2001 VL 16 IS 4 BP 249 EP 264 DI 10.1002/bin.95 PG 16 WC Psychology, Clinical SC Psychology GA 496ML UT WOS:000172399300001 ER PT J AU Schreck, KA AF Schreck, KA TI Behavioral treatments for sleep problems in autism: Empirically supported or just universally accepted? SO BEHAVIORAL INTERVENTIONS LA English DT Article ID CHILDREN; DISORDERS; ADOLESCENTS; BEDTIME AB With health maintenance organizations and insurance companies requiring proof of treatment efficacy, clinicians must determine whether research supports commonly used treatment methods. To determine the effectiveness of applied behavior analysis (ABA) for treating sleep problems in children with autism, a computer search of all relevant literature was conducted. The resulting articles revealed four basic themes of behavioral techniques for treating sleep disorders for children with autism: bedtime routines, extinction, stimulus fading, and faded bedtimes. Research on each technique was evaluated based on the Chambless criteria of treatment efficacy (Chambless and Hollon, 1998; Lonigan, Elbert, and Johnson, 1998). Of the ABA methods, only research on extinction provided sufficient evidence for a possibly efficacious intervention for sleep problems in children with autism. However, the lack of available research indicates significantly more research must be conducted before endorsing other ABA methods. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 Penn State Univ Harrisburg, Middletown, PA 17057 USA. RP Schreck, KA (reprint author), Penn State Univ Harrisburg, 777 W Harrisburg Pike, Middletown, PA 17057 USA. 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Intervent. PD OCT-DEC PY 2001 VL 16 IS 4 BP 265 EP 278 DI 10.1002/bin.98 PG 14 WC Psychology, Clinical SC Psychology GA 496ML UT WOS:000172399300002 ER PT J AU Shabani, DB Wilder, DA Flood, WA AF Shabani, DB Wilder, DA Flood, WA TI Reducing stereotypic behavior through discrimination training, differential reinforcement of other behavior, and self-monitoring SO BEHAVIORAL INTERVENTIONS LA English DT Article AB The effect of a treatment package designed to reduce stereotypic body rocking was examined in a child diagnosed with autism. After baseline, the participant was taught to discriminate between inappropriate (e.g. sitting in a chair and rocking) and appropriate (e.g. sitting in a chair without rocking) behavior. During intervention, both a therapist and the participant himself monitored the occurrence of rocking behavior. A non-resetting 5 min differential reinforcement of other behavior (DRO) schedule was also introduced. A multiple baseline across behaviors (sitting and standing) design was used to evaluate the effects of the intervention package. The results indicated that the intervention was effective in eliminating body rocking. In addition, the DRO schedule was successfully increased to 20 min for sitting and 17 min for standing and the treatment was successfully introduced at the child's school. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 Univ Pacific, Stockton, CA 95211 USA. RP Shabani, DB (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. CR BAUMEIST.AA, 1972, J CLIN PSYCHOL, V28, P586, DOI 10.1002/1097-4679(197210)28:4<586::AID-JCLP2270280442>3.0.CO;2-8 Baumeister A. 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PD OCT-DEC PY 2001 VL 16 IS 4 BP 279 EP 286 DI 10.1002/bin.96.abs PG 8 WC Psychology, Clinical SC Psychology GA 496ML UT WOS:000172399300003 ER PT J AU Crane, C AF Crane, Catherine TI Autism: Identification, Education and Treatment, 2nd edition SO BEHAVIOURAL AND COGNITIVE PSYCHOTHERAPY LA English DT Book Review C1 [Crane, Catherine] Univ Oxford, Dept Expt Psychol, Oxford OX1 2JD, England. RP Crane, C (reprint author), Univ Oxford, Dept Expt Psychol, Oxford OX1 2JD, England. CR Zager D., 1999, AUTISM IDENTIFICATIO NR 1 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1352-4658 J9 BEHAV COGN PSYCHOTH JI Behav. Cognit. Psychther. PD OCT PY 2001 VL 29 IS 4 BP 509 EP 510 DI 10.1017/S1352465801244117 PG 2 WC Psychology, Clinical SC Psychology GA V16RZ UT WOS:000207888000014 ER PT J AU Pierce, K Muller, RA Ambrose, J Allen, G Courchesne, E AF Pierce, K Muller, RA Ambrose, J Allen, G Courchesne, E TI Face processing occurs outside the fusiform 'face area' in autism: evidence from functional MRI SO BRAIN LA English DT Article DE autism; fMRI; amygdala; face perception; fusiform gyrus ID POSITRON-EMISSION-TOMOGRAPHY; HUMAN EXTRASTRIATE CORTEX; HUMAN VISUAL-CORTEX; FACIAL EXPRESSIONS; INFANTILE-AUTISM; HUMAN AMYGDALA; TEMPORAL-LOBE; HUMAN BRAIN; RECOGNITION; CHILDREN AB Processing the human face is at the focal point of most social interactions, yet this simple perceptual task is difficult for individuals with autism, a population that spends limited amounts of time engaged in face-to-face eye contact or social interactions in general. Thus, the study of face processing in autism is not only important because it may be integral to understanding the social deficits of this disorder, but also, because it provides a unique opportunity to study experiential factors related to the functional specialization of normal face processing. In short, autism may be one of the only disorders where affected individuals spend reduced amounts of time engaged in face processing from birth. Using functional MRI, haemodynamic responses during a face perception task were compared between adults with autism and normal control subjects. Four regions of interest (ROIs), the fusiform gyrus (FG), inferior temporal gyrus, middle temporal gyrus and amygdala were manually traced on non-spatially normalized images and the percentage ROI active was calculated for each subject. Analyses in Talairach space were also performed. Overall results revealed either abnormally weak or no activation in FG in autistic patients, as well as significantly reduced activation in the inferior occipital gyrus, superior temporal sulcus and amygdala. Anatomical abnormalities, in contrast, were present only in the amygdala in autistic patients, whose mean volume was significantly reduced as compared with normals. Reaction time and accuracy measures were not different between groups. Thus, while autistic subjects could perform the face perception task, none of the regions supporting face processing in normals were found to be significantly active in the autistic subjects. Instead, in every autistic patient, faces maximally activated aberrant and individual-specific neural sites (e.g. frontal cortex, primary visual cortex, etc.), which was in contrast to the 100% consistency of maximal activation within the traditional fusiform face area (FFA) for every normal subject. It appears that, as compared with normal individuals, autistic individuals 'see' faces utilizing different neural systems, with each patient doing so via a unique neural circuitry. Such a pattern of individual-specific, scattered activation seen in autistic patients in contrast to the highly consistent FG activation seen in normals, suggests that experiential factors do indeed play a role in the normal development of the FFA. C1 Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92103 USA. Childrens Hosp, Res Ctr, Lab Neurosci Autism, La Jolla, CA USA. Long Isl Jewish Med Ctr, Glen Oaks, NY USA. RP Pierce, K (reprint author), 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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PSYCHOL PSYC, V28, P137, DOI 10.1111/j.1469-7610.1987.tb00658.x NR 82 TC 446 Z9 452 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD OCT PY 2001 VL 124 BP 2059 EP 2073 DI 10.1093/brain/124.10.2059 PN 10 PG 15 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 481BX UT WOS:000171501000014 PM 11571222 ER PT J AU Howlin, P AF Howlin, P TI Autistic features in Cohen syndrome: a preliminary report SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID SYNDROME GENE; PRADER-WILLI; MENTAL-RETARDATION; DUPLICATION; DEFICIENCY; OBESITY AB Cohen syndrome is a rare, genetic, connective-tissue disorder, with the genetic abnormality linked to chromosome 8q22. Its physical features (particular facial characteristics; body, limb, and visual abnormalities; height and weight problems) have been well documented but little is known about the psychological and behavioural development of individuals with the condition. Suggestion of a dual diagnosis of autism in a small minority of individuals led to a more detailed survey of parents belonging to the Cohen Syndrome Support Group, based in the UK. Thirty-three individuals, 18 males and 15 females, aged from 2 to 45 years (mean age 15 years) were involved in the study. Over half of the participants (n = 19) showed a pattern of impairments in social and communication skills, together with rigid and stereotyped behaviours or interests that seemed to meet DSM-IV/ICD-10 criteria for autism. 'Autistic-type' problems were as common in females as in males. In almost all cases, parents had noted difficulties in their child before the child reached the age of I year. This study suffers from a number of methodological shortcomings including the fact that it was a postal survey, the sample size was small, and no standardized diagnostic or psychometric data were available. However, the incidence of social, communication, and behavioural problems would seem to warrant further research and a larger-scale study is planned in association with an independent investigation of physical and genetic characteristics in the same group of individuals. C1 St George Hosp, Sch Med, London SW17 0RE, England. RP Howlin, P (reprint author), St George Hosp, Sch Med, London SW17 0RE, England. 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Med. Child Neurol. PD OCT PY 2001 VL 43 IS 10 BP 692 EP 696 DI 10.1017/S0012162201001244 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 490MV UT WOS:000172056400007 PM 11665826 ER PT J AU Spiker, D Lotspeich, LJ Dimiceli, S Szatmari, P Myers, RM Risch, N AF Spiker, D Lotspeich, LJ Dimiceli, S Szatmari, P Myers, RM Risch, N TI Birth order effects on nonverbal IQ scores in autism multiplex families SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE multiplex families; birth order; IQ scores ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; GENOMIC SCREEN; GENETICS; PHENOTYPE; CHILDREN; LINKAGE; CHROMOSOME; RELATIVES; BEHAVIOR AB Lord (1992) published a brief report showing a trend for decreasing nonverbal IQ scores with increasing birth order in a sample of 16 autism multiplex families, and urged replication in a larger sample. In this report, analyses of nonverbal IQ scores for a sample of 144 autism multiplex families indicated that nonverbal IQ scores were significantly lower in secondborn compared with firstborn siblings with autism. This birth order effect was independent of gender as well as the age differences within sib pairs. No such birth order effects were found for social or communicative deficits as measured by the Autism Diagnostic Interview-Revised (ADI-R), but there was a modest tendency for increased scores for ritualistic behaviors for the firstborn sibs. Further, there were no gender differences on nonverbal IQ scores in this sample. Results are discussed in terms of implications for genetic studies of autism. C1 Stanford Univ, Sch Med, Div Child Psychiat & Child Dev, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. McMaster Univ, Dept Psychiat, Chedoke McMaster Hosp, Hamilton, ON L8N 3Z5, Canada. Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. RP Spiker, D (reprint author), SRI Int, Ctr Educ & Human Serv, 333 Ravenswood Ave, Menlo Pk, CA 94025 USA. 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Autism Dev. Disord. PD OCT PY 2001 VL 31 IS 5 BP 449 EP 460 DI 10.1023/A:1012217807469 PG 12 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000002 PM 11794410 ER PT J AU Channon, S Charman, T Heap, J Crawford, S Rios, P AF Channon, S Charman, T Heap, J Crawford, S Rios, P TI Real-life-type problem-solving in Asperger's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE executive functions; problem-solving; Asperger's syndrome; frontal lobes ID HIGH-FUNCTIONING ADULTS; LESIONS; AUTISM AB This study compared adolescents with Asperger's syndrome with typically developing adolescents on a novel problem-solving task that presented videotaped scenarios in real-life-type social contexts. The Asperger's group was impaired in several aspects of problem-solving, including recounting the pertinent facts, generating possible high-quality problem solutions, and selecting optimal and preferred solutions. 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PD OCT PY 2001 VL 31 IS 5 BP 461 EP 469 DI 10.1023/A:1012212824307 PG 9 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000003 PM 11794411 ER PT J AU Ruble, LA AF Ruble, LA TI Analysis of social interactions as goal-directed behaviors in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE naturalistic social interactions; autism; ecological psychology; executive function ID ADULTS; COMMUNICATION; INTERVENTION; ECHOLALIA; SKILLS AB An ecological psychology framework that considers the intentions of the child within the child's own social context was used to study the complexity of social interactions of 16 children with autism or Down syndrome. Children were observed in their homes and behaviors were recorded. Records were then analyzed by dividing behavior based on the children's own goals. Goal-directed behaviors were then categorized. 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F., 1967, RECORDING ANAL CHILD NR 53 TC 8 Z9 8 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD OCT PY 2001 VL 31 IS 5 BP 471 EP 482 DI 10.1023/A:1012264808377 PG 12 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000004 PM 11794412 ER PT J AU Toichi, M Kamio, Y AF Toichi, M Kamio, Y TI Verbal association for simple common words in high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; verbal association; semantic memory; priming ID SPREADING ACTIVATION; AMNESIC SYNDROME; FREE-RECALL; CHILDREN; MEMORY; SCHIZOPHRENIA; LANGUAGE; DISORDER; COMPREHENSION; SIMILARITY AB We investigated conceptual relationships in semantic memory using an indirect priming technique in high-functioning autistic adolescents and their controls who were matched for age, verbal IQ, performance IQ, and nonverbal reasoning ability. The prime was a single word and the target task was completing a word fragment that was semantically related or unrelated to the prime word. The autistic subjects and controls showed similar semantic priming effects, indicating intact conceptual relationships for simple common words in those with autism. Only in the autistic group was a significant correlation found between performance for the related items and two nonverbal cognitive measures, which suggests a possibility that semantic processing in individuals with autism might be qualitatively different from that in controls. C1 Case Western Reserve Univ, Div Child & Adolescent Psychiat, Cleveland, OH 44106 USA. Shiga Univ Med Sci, Hlth & Med Serv Ctr, Shiga, Japan. Kyoto Grad Univ, Fac Med, Dept Neuropsychiat, Kyoto, Japan. RP Toichi, M (reprint author), Case Western Reserve Univ, Univ Hosp Cleveland, Div Child & Adolescent Psychiat, 11100 Euclid Ave, Cleveland, OH 44106 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 ATKINSON RC, 1971, SCI AM, V225, P82 BADDELEY AD, 1966, Q J EXP PSYCHOL, V18, P302, DOI 10.1080/14640746608400047 BADDELEY AD, 1966, J VERB LEARN VERB BE, V5, P417, DOI 10.1016/S0022-5371(66)80054-3 Barch DM, 1996, J ABNORM PSYCHOL, V105, P592 Beversdorf DQ, 1998, J NEUROL NEUROSUR PS, V65, P685, DOI 10.1136/jnnp.65.5.685 BLUM NA, 1995, SCHIZOPHR RES, V16, P217, DOI 10.1016/0920-9964(94)00078-M BOUCHER J, 1978, J CHILD PSYCHOL PSYC, V19, P161, DOI 10.1111/j.1469-7610.1978.tb00457.x BOUCHER J, 1976, BRIT J PSYCHOL, V67, P73 BOUCHER J, 1988, J AUTISM DEV DISORD, V18, P637, DOI 10.1007/BF02211881 BOUCHER J, 1981, BRIT J PSYCHOL, V72, P211 Bowler DM, 1997, NEUROPSYCHOLOGIA, V35, P65, DOI 10.1016/S0028-3932(96)00054-1 BRYSON SE, 1983, J ABNORM PSYCHOL, V92, P250, DOI 10.1037/0021-843X.92.2.250 COLLINS AM, 1975, PSYCHOL REV, V82, P407, DOI 10.1037//0033-295X.82.6.407 CRAIK FIM, 1975, J EXP PSYCHOL GEN, V104, P268, DOI 10.1037//0096-3445.104.3.268 ESKES GA, 1990, J AUTISM DEV DISORD, V20, P61, DOI 10.1007/BF02206857 Fein D, 1996, CLIN DEV MED, P123 FRITH U, 1969, LANG SPEECH, V12, P29 FYFFE C, 1978, BRIT J PSYCHOL, V69, P393 GLANZER M, 1966, J VERB LEARN VERB BE, V5, P351, DOI 10.1016/S0022-5371(66)80044-0 HERMELIN B, 1967, BRIT J PSYCHOL, V58, P213 Kanner L, 1943, NERV CHILD, V2, P217 KANNER L, 1946, AM J PSYCHIAT, V103, P242 KWAPIL TR, 1990, J ABNORM PSYCHOL, V99, P215, DOI 10.1037/0021-843X.99.3.215 Minshew N. 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C., 1992, MANUAL RAVENS PROGR Raven J.C., 1960, STANDARD PROGR MATRI Renner P, 2000, J AUTISM DEV DISORD, V30, P3, DOI 10.1023/A:1005487009889 SPITZER M, 1993, BIOL PSYCHIAT, V34, P864, DOI 10.1016/0006-3223(93)90054-H SPITZER M, 1994, J ABNORM PSYCHOL, V103, P485, DOI 10.1037/0021-843X.103.3.485 TAGERFLUSBERG H, 1991, BRIT J DEV PSYCHOL, V9, P417 TAGERFLUSBERG H, 1985, CHILD DEV, V56, P1167, DOI 10.1111/j.1467-8624.1985.tb00185.x TOICHI M, IN PRESS NEUROPSYCHO TOICHI M, 1999, PSYCHIAT CLIN NEUROS, V54, pS97 NR 43 TC 27 Z9 27 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD OCT PY 2001 VL 31 IS 5 BP 483 EP 490 DI 10.1023/A:1012216925216 PG 8 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000005 PM 11794413 ER PT J AU Ahearn, WH Castine, T Nault, K Green, G AF Ahearn, WH Castine, T Nault, K Green, G TI An assessment of food acceptance in children with autism or pervasive developmental disorder-not otherwise specified SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE feeding assessment; selective eating; autism spectrum disorder ID FEEDING PROBLEMS AB Some children with autism and pervasive developmental disorder-not otherwise specified (PDD-NOS) have been reported to have atypical feeding behavior, such as sensitivity to food texture and selective preferences for particular foods. No systematic studies of feeding behavior in this population have been published. Munk and Repp (1994) developed methods for assessing feeding problems in individuals with cognitive and physical disabilities that allow categorization of individual feeding patterns based on responses to repeated presentations of food. In this study, we systematically replicated the Munk and Repp procedures with children with autism and PDD-NOS. Thirty children, ages 3 to 14 years, were exposed to 12 food items across 6 sessions. Food acceptance, food expulsion, and disruptive behavior were recorded on a trial-by-trial basis. Approximately half of the participants exhibited patterns of food acceptance, indicating selectivity by food category or food texture. Others consistently accepted or rejected items across food categories. Whether these patterns of food acceptance are atypical remains to be determined by comparison with the feeding patterns of typically developing children and other children with developmental delays. C1 New England Ctr Children, Southborough, MA 01772 USA. Northeastern Univ, Boston, MA 02115 USA. RP Ahearn, WH (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. CR AHEARN WH, 2000, ANN C INT ASS SCI ST AHEARN WH, IN PRESS MAKING DIFF BENTOVIM A, 1970, J PSYCHOSOM RES, V14, P267, DOI 10.1016/0022-3999(70)90053-X BIRCH LL, 1982, APPETITE, V3, P353 BURD D, 1995, ANN M ASS BEH AN WAS DEMEYER MK, 1979, PARENTS CHILDREN AUT, P171 FARRELL DA, 1996, ANN M ASS BEH AN SAN GOUGE AL, 1975, AM J MENT DEF, V80, P149 GREEN CW, 1991, J APPL BEHAV ANAL, V24, P537, DOI 10.1901/jaba.1991.24-537 MUNK DD, 1994, J APPL BEHAV ANAL, V27, P241, DOI 10.1901/jaba.1994.27-241 PALMER S, 1975, DEV MED CHILD NEUROL, V17, P333 PERSKE R, 1977, MEALTIMES SEVERELY P Powell T. H., 1992, AUTISM IDENTIFICATIO, P187 Ritvo E. M., 1978, J AUTISM CHILDHOOD S, V8, P162 NR 14 TC 92 Z9 95 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD OCT PY 2001 VL 31 IS 5 BP 505 EP 511 DI 10.1023/A:1012221026124 PG 7 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000007 PM 11794415 ER PT J AU Escalona, A Field, T Singer-Strunck, R Cullen, C Hartshorn, K AF Escalona, A Field, T Singer-Strunck, R Cullen, C Hartshorn, K TI Brief report: Improvements in the behavior of children with autism following massage therapy SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE massage therapy for autism AB Twenty children with autism, ages 3 to 6 years, were randomly assigned to massage therapy and reading attention control groups. Parents in the massage therapy group were trained by a massage therapist to massage their children for 15 minutes prior to bedtime every night for I month and the parents of the attention control group read Dr. Seuss stories to their children on the same time schedule. Conners Teacher and Parent scales, classroom and playground observations, and sleep diaries were used to assess the effects of therapy on various behaviors, including hyperactivity, stereotypical and off-task behavior, and sleep problems. Results suggested that the children in the massage group exhibited less stereotypic behavior and showed more on-task and social relatedness behavior during play observations at school, and they experienced fewer sleep problems at home. C1 Univ Miami, Sch Med, Touch Res Inst, Miami, FL 33101 USA. RP Field, T (reprint author), Univ Miami, Sch Med, Touch Res Inst, POB 016820,D-820, Miami, FL 33101 USA. CR Conners C. K., 1997, CONNERS RATING SCALE Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 EATON WO, 1988, INFANT BEHAV DEV, V11, P375, DOI 10.1016/0163-6383(88)90022-7 FIELD T, 1992, J AM ACAD CHILD PSY, V31, P125, DOI 10.1097/00004583-199201000-00019 FIELD T, 1996, EARLY CHILD DEV CARE, V120, P39, DOI 10.1080/0300443961200104 Field TM, 1998, AM PSYCHOL, V53, P1270 Field T, 1997, J AUTISM DEV DISORD, V27, P333, DOI 10.1023/A:1025858600220 Hollingshead A. B., 1975, 4 FACTOR INDEX SOCIA Klinger Laura Grofer, 1996, P311 Mesibov G. B., 1997, AUTISM UNDERSTANDING PORGES SW, 1997, INTEGRATIVE NEUROBIO, P62 ROGERS S, 1999, IMITATION INFANCY CA, P290 Schopler E., 1979, INDIVIDUALIZED ASSES, V1 TSAI L, 1996, AUTISM IDENTIFICATIO, P151 NR 14 TC 40 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 OCT PY 2001 VL 31 IS 5 BP 513 EP 516 DI 10.1023/A:1012273110194 PG 4 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000008 PM 11794416 ER PT J AU Minshew, N AF Minshew, N TI What are neuropeptides and neurotrophins and why are they important in autism? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material NR 0 TC 2 Z9 2 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD OCT PY 2001 VL 31 IS 5 BP 517 EP 517 PG 1 WC Psychology, Developmental SC Psychology GA 503MJ UT WOS:000172802000009 PM 11794417 ER PT J AU Ziter, J AF Ziter, J TI Children with autism: A parent's guide, 2nd edition SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Blackstone Valley Pediat & Adolescent Med, Cumberland, RI USA. RP Ziter, J (reprint author), Blackstone Valley Pediat & Adolescent Med, Cumberland, RI USA. CR Powers Michael D., 2000, CHILDREN AUTISM PARE NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD OCT PY 2001 VL 22 IS 5 BP 334 EP 335 PG 2 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 487YE UT WOS:000171906200009 ER PT J AU Hala, S Russell, J AF Hala, S Russell, J TI Executive control within strategic deception: A window on early cognitive development? SO JOURNAL OF EXPERIMENTAL CHILD PSYCHOLOGY LA English DT Article DE deception; executive function; theory of mind; preschool children; inhibitory control ID FALSE-BELIEF; YOUNG-CHILDREN; MIND; TASK; PRESCHOOLERS; 3-YEAR-OLDS; ABILITY; AUTISM; MARKER AB Recently it has been claimed that the difficulty young children have with tests of strategic deception may be due to limitations in executive control rather than lack of insight into mental concepts. In the studies reported here we asked how reducing the executive demands of one measure of strategic deception, the windows task (J. Russell, N. Mauthner, S. Sharpe, & T. Tidswell, 1991), would affect performance. Study I demonstrated that both providing an artificial response medium and having children play in partnership enabled 3-year-olds to adopt a successful strategy. Study 2 examined whether social or executive factors accounted for the good performance of children when they played in partnership. Study 3 ruled out the possibility that the effectiveness of the artificial media was a result of reducing social intimidation-the manipulations were effective even in the presence the opponent. These results argue for executive factors playing a substantial role in role development of strategic deception. (C) 2001 Academic Press. C1 Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Cambridge, Cambridge CB2 1TN, England. RP Hala, S (reprint author), Univ Calgary, Dept Psychol, 2500 Univ Dr NW, Calgary, AB T2N 1N4, Canada. EM hala@ucalgary.ca CR ASTINGTON JW, 1991, BRIT J DEV PSYCHOL, V9, P7 Baddeley A. 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PD OCT PY 2001 VL 80 IS 2 BP 112 EP 141 DI 10.1006/jecp.2000.2627 PG 30 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 471ZK UT WOS:000170958400002 PM 11529671 ER PT J AU Shriberg, LD Paul, R McSweeny, JL Klin, A Cohen, DJ Volkmar, FR AF Shriberg, LD Paul, R McSweeny, JL Klin, A Cohen, DJ Volkmar, FR TI Speech and prosody characteristics of adolescents and adults with high-functioning autism and Asperger Syndrome SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE articulation; Asperger syndrome; autism; phonology; prosody ID PERVASIVE DEVELOPMENTAL DISORDERS; NORMAL-CHILDREN; MENTAL-RETARDATION; FIELD TRIAL; DSM-IV; LANGUAGE; RECOGNITION; RELIABILITY; EXTENSIONS; EMOTION AB Speech and prosody-voice profiles for 15 male speakers with High-Functioning Autism (HFA) and 15 male speakers with Asperger syndrome (AS) were compared to one another and to profiles for 53 typically developing male speakers in the same 10- to 50-years age range. Compared to the typically developing speakers, significantly more participants in both the HFA and AS groups had residual articulation distortion errors, uncodable utterances due to discourse constraints, and utterances coded as inappropriate in the domains of phrasing, stress, and resonance. Speakers with AS were significantly more voluble than speakers with HFA, but otherwise there were few statistically significant differences between the two groups of speakers with pervasive developmental disorders. Discussion focuses on perceptual-motor and social sources of differences in the prosody-voice findings for individuals with Pervasive Developmental Disorders as compared with findings for typical speakers, including comment on the grammatical, pragmatic, and affective aspects of prosody. C1 Univ Wisconsin, Waisman Ctr Mental Retardat & Human Dev, Phonol Project, Madison, WI 53705 USA. Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT USA. 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PD OCT PY 2001 VL 44 IS 5 BP 1097 EP 1115 DI 10.1044/1092-4388(2001/087) PG 19 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 489YE UT WOS:000172019900014 PM 11708530 ER PT J AU Masi, G Cosenza, A Mucci, M Brovedani, P AF Masi, G Cosenza, A Mucci, M Brovedani, P TI Open trial of risperidone in 24 young children with pervasive developmental disorders SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autistic disorder; risperidone; children ID AUTISM RATING-SCALE; CHILDHOOD AUTISM; PEDIATRIC PSYCHOPHARMACOLOGY; INFANTILE-AUTISM; ADOLESCENTS; HALOPERIDOL; DIAGNOSIS; SYMPTOMS; EFFICACY; NETWORK AB Objective: To describe tolerability and efficacy of risperidone in very young children with pervasive developmental disorders, Method: Twenty-four children aged 3.6 to 6.6 years (mean 4.6 years +/- 8 months) enrolled during 1999 and 2000 participated in a 16-week open-label trial with risperidone monotherapy. Outcome measures included the Children's Psychiatric Rating Scale (CPRS), Childhood Autism Rating Scale (CARS), Clinical Global Impression-Improvement (CGI-I), and Children's Global Assessment Scale (C-GAS). Results: Two subjects did not complete the trial because of side effects. The optimal dose was 0.5 mg/day. After the treatment a 21 % improvement in CPRS and a 14% improvement in CARS total scores was found. Items related to behavioral control (hyperactivity, fidgetiness, rhythmic motions) and affect regulation (lability of affect, angry affect) improved more than 25%. Based on improvement of at least 25% on the CPRS and a score of 1 or 2 on the CGI-I, eight subjects were considered responders. Functional impairment (C-GAS) improved more than 25%. Thirteen subjects (54%) were free of any side effects; in the other participants risperidone was well tolerated, Only three subjects had a weight gain greater than 10%. 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Dis. PD OCT PY 2001 VL 8 IS 5 BP 784 EP 791 DI 10.1006/nbdi.2001.0420 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 486QH UT WOS:000171828100005 PM 11592848 ER PT J AU Chatterjie, N Alexander, G Wang, H AF Chatterjie, N Alexander, G Wang, H TI Synthesis of valproic acid amides of a melatonin derivative, a piracetam and amantadine for biological tests SO NEUROCHEMICAL RESEARCH LA English DT Article DE anticonvulsants; autism; neuroprotection; cognition; valproate; melatonin ID ANTICONVULSANT; EPILEPSY; AUTISM; RATS; METABOLITES; DISORDERS; POTENCIES; CHILDREN; ANALOGS; EMBRYO AB Three new amide derivatives of valproic acid have been synthesized and characterized by spectrophotometric studies. The rationale for the preparation of such agents has been based on the observation that chemical combination of the anticonvulsant pharmacophore, valproic acid with amine moieties produces more effective and less toxic amides. The amine components selected in this work also exhibit neuroactivity with the prospect of these agents being biologically active in controlling not just seizures and but also possessing neuroprotective properties. We report here the synthesis and properties of the valproylamides of 5-methoxytryptamine, related to melatonin ((1) under bar), of N-substituted 2-pyrrolidinone related to piracetam ((2) under bar), and of adamantylamine related to amantadine ((3) under bar). In preliminary tests these compounds showed low toxicity and a variety of anticonvulsive properties, including a delay in onset of activity. These compounds and their derivatives are now available to be tested additionally for control of subclinical seizures, enhancement of cognition, behavior modification and alleviation of symptoms and disorders due to neuronal damage. C1 New York State Inst Basic Res Dev Disabil, Dept Neurochem, Staten Isl, NY 10314 USA. CUNY Coll Staten Isl, Staten Isl, NY 10314 USA. 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Functional imaging supports the hypothesis that developmental dyslexia is frequently the result of deficits in phonologic processing and that normal reading requires a patent network organization of a number of anterior and posterior brain areas. In autism, anatomic imaging studies are conflicting. Functional imaging demonstrates temporal lobe abnormalities and abnormal interaction between frontal and parietal brain areas. In attention-deficit-hyperactivity disorder, imaging studies suggest an abnormality in the prefrontal and striatal regions. Neuroimaging studies are often contradictory, but trends, especially with functional imaging analysis, are evolving. Because neurobehavioral disorders seem to be a result of a dysfunction in brain circuits, no one region will be abnormal in all patients studied. Further studies with well-defined patient populations and appropriate activation paradigms will better elucidate the pathophysiology of these conditions. 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Neurol. PD OCT PY 2001 VL 25 IS 4 BP 278 EP 287 DI 10.1016/S0887-8994(01)00282-X PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 490EZ UT WOS:000172038600001 PM 11704396 ER PT J AU Vitiello, B AF Vitiello, B TI Psychopharmacology for young children: Clinical needs and research opportunities SO PEDIATRICS LA English DT Article DE children; preschoolers; psychopharmacology; research; mental ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PRESCHOOL-CHILDREN; DEVELOPMENTAL NEUROTOXICITY; PSYCHOTROPIC MEDICATIONS; BEHAVIOR PROBLEMS; METHYLPHENIDATE; DIAGNOSIS; AUTISM; ADHD; AGE AB In response to concerns about the increasing use of psychotropic medications in preschoolers, the National Institute of Mental Health and the Food and Drug Administration convened a workshop in October 2000 to examine the current state of knowledge regarding psychopharmacology for young children and discuss a variety of topics relevant to research in this age group, including safety, efficacy, investigational methods, and ethical aspects. The meeting gathered researchers, practitioners, ethicists, industry staff, and family and patient representatives. Efficacy and safety of psychotropics have not been systematically evaluated in preschoolers. The major limitation to this research is the diagnostic uncertainty surrounding most manifestations of psychopathology in early childhood. Research in developmental psychopathology is needed to clarify diagnosis and provide sensitive and specific methods for clinical trials. Possible approaches to expanding the research basis of this area of clinical practice, including a recently started study of methylphenidate in preschoolers, are reported here. C1 NIMH, Child & Adolescent Treatment & Prevent Intervent, Bethesda, MD 20892 USA. RP Vitiello, B (reprint author), NIMH, Child & Adolescent Treatment & Prevent Intervent, Room 7147,6001 Execut Blvd,MSC 9633, Bethesda, MD 20892 USA. 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A link has been postulated between measles-mumps-rubella (MMR) vaccine and a form of autism that is a combination of developmental regression and gastrointestinal symptoms that occur shortly after immunization. This hypothesis has involved 3 separate claims: 1) that there is new phenotype of autism involving regression and gastrointestinal symptoms, 2) that this new variant is responsible for the alleged rise of autism rates, and 3) that this phenotype is associated with biological findings suggestive of the persistence of measles infection. We tested the first of these claims. If this new "autistic enterocolitis" syndrome had some validity, then 1 or several of the following 6 predictions should be supported by empirical data: 1) childhood disintegrative disorder has become more frequent, 2) the mean age of first parental concern for autistic children who are exposed to MMR is closer to the mean immunization age than in children who are not exposed to MMR, 3) regression in the development of children with autism has become more common in MMR-vaccinated children, 4) the age of onset for autistic children with regression clusters around the MMR immunization date and is different from that of autistic children without regression, 5) children with regressive autism have distinct symptom and severity profiles, and 6) regressive autism is associated with gastrointestinal symptoms and/or inflammatory bowel disorder. Methods. Three samples were used. Epidemiologic data on 96 children (95 immunized with MMR at a median age of 13.5 months) who were born between 1992 and 1995 and had a pervasive developmental disorder diagnosis as reported in a recent UK survey (post-MMR sample) were compared with data from 2 previous clinical samples (1 pre-MMR [n = 98] and 1 post-MMR [n = 68]) of autistic patients. All patients were assessed with the standardized Autism Diagnostic Interview (ADI), allowing rigorous comparison of age at first parental concerns and rates of regression across samples. Reliability was excellent on ADI scores, age of parental concern, and developmental regression. Furthermore, data on bowel symptoms and disorders were available in the epidemiologic survey from both pediatric and parental sources, and immunization dates were obtained from computerized records. Results. The prevalence of childhood disintegrative disorder was 0.6/10000 (95% confidence interval: 0.02-3.6/10000); this very low rate is consistent with previous estimates and is not suggestive of an increased frequency of this form of pervasive developmental disorder in samples of children who are immunized with MMR. There was no difference in the mean age at first parental concern between the 2 samples exposed to MMR (19.3 and 19.2 months) and the pre-MMR sample (19.5 months). Thus, MMR immunization was not associated with a shift toward an earlier age for first parental concerns. Similarly, the rate of developmental regression reported in the post-MMR sample (15.6%) was not different from that in the pre-MMR sample (18.4%); therefore, there was no suggestion that regression in the developmental course of autism had increased in frequency since MMR was introduced. In the epidemiologic sample, the subset of autistic children with regression had no other developmental or clinical characteristics, which would have argued for a specific, etiologically distinct phenotype. Parents of autistic children with developmental regression detected the first symptoms at a very similar age (19.8 months) to those of autistic children without regression (19.3 months). Moreover, the mean intervals from MMR immunization to parental recognition of autistic symptoms were comparable in autistic children with or without regression (248 vs 272 days; not significant). In the epidemiologic sample, gastrointestinal symptoms were reported in 18.8% of children. Constipation was the most common symptom (9.4%), and no inflammatory bowel disorder was reported. Furthermore, there was no association between developmental regression and gastrointestinal symptoms (odds ratio: 0.63; 95% confidence interval: 0.06-3.2; not significant), and only 2.1% of the sample experienced both problems, a rate that did not exceed chance expectations. Conclusions. No evidence was found to support a distinct syndrome of MMR-induced autism or of "autistic enterocolitis." These results add to the recent accumulation of large-scale epidemiologic studies that all failed to support an association between MMR and autism at population level. When combined, the current findings do not argue for changes in current immunization programs and recommendations. C1 Univ London Kings Coll, Dept Child & Adolescent Psychiat, Inst Psychiat, London WC2R 2LS, England. Cent Clin, Child Dev Ctr, Stafford, England. RP Fombonne, E (reprint author), Montreal Childrens Hosp, Dept Child Psychiat, 4018 St Catherine W, Montreal, PQ H3Z 1P2, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 1995, PSYCHOL MED, V25, P63 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 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 CHESS S, 1971, J AUTISM CHILD SCHIZ, V1, P33, DOI 10.1007/BF01537741 CHESS S, 1977, J AUTISM CHILD SCHIZ, V7, P69, DOI 10.1007/BF01531116 CREAK EM, 1963, BRIT J PSYCHIAT, V109, P84, DOI 10.1192/bjp.109.458.84 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 Feinstein C, 1998, J AUTISM DEV DISORD, V28, P393, DOI 10.1023/A:1026000404855 FINE PEM, 1993, EPIDEMIOL REV, V15, P265 Fombonne E, 1998, LANCET, V351, P955 FOMBONNE E, IN PRESS ED CHILDREN Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 Hagerman RJ, 1996, FRAGILE X SYNDROME D, P3 HALSEY NA, 2001, PEDIATRICS, P107 *I MED, 2001, MEASL MUMPS RUB VACC Kanner L, 1943, NERV CHILD, V2, P217 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 Magnusson P, 2001, J AUTISM DEV DISORD, V31, P153, DOI 10.1023/A:1010795014548 ROGERS JS, 1990, J AM ACAD CHILD ADOL, V29, P207 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x Smalley SL, 1998, J AUTISM DEV DISORD, V28, P407, DOI 10.1023/A:1026052421693 Sponheim E, 1998, J AUTISM DEV DISORD, V28, P217, DOI 10.1023/A:1026017405150 STUTSMAN R, 1948, MERRILLPALMER SCAL 3 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 WAKABAYA.S, 1974, JPN J CHILD ADOL PSY, V15, P215 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 Wechsler D, 1990, MANUAL WECHSLER PRES WERNER E, 2001, REGRESSION AUTISM DE WHO, 1993, ICD 10 CLASS MENT BE WOLFF S, 1964, ACTA PSYCHIAT SCAND, V40, P438, DOI 10.1111/j.1600-0447.1964.tb07496.x NR 42 TC 133 Z9 133 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 OCT PY 2001 VL 108 IS 4 BP art. no. EP e58 DI 10.1542/peds.108.4.e58 PG 8 WC Pediatrics SC Pediatrics GA 478AC UT WOS:000171319600001 PM 11581466 ER PT J AU Mildenberger, K Noterdaeme, M Sitter, S Amorosa, H AF Mildenberger, K Noterdaeme, M Sitter, S Amorosa, H TI Behavioural problems in children with specific and pervasive developmental disorders, evaluated with the psychopathological documentation (AMDP) SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Article ID PSYCHIATRIC-DISORDERS; SPEECH; ADOLESCENTS; PREVALENCE; CHECKLIST AB Children with specific developmental disorders of speech and language have an increased rate of psychiatric disorder compared to children developing normally. Children with early infantile autism show psychopathological symptoms in addition to those that are required for the diagnosis. These are often important in daily dealings with the children. As part of a larger study 4 groups of school age children (21 with normal development, 18 with an expressive language disorder, 21 with a receptive language disorder and I I children with early infantile autism) were rated according to the psychopathological documentation for children (AMDP) within the assessment situation and according to reports of the behaviour outside. Several items were added to include symptoms that are not rated in the present documentation. Significant differences in the means were found between the group of children with autism and the control group. The children with language disorder showed a high variance which was interpreted as a sign for a heterogeneous group. Several of the added items improve the documentation of psychopathological findings in young school children. C1 Heckscher Klin Munchen, Abt Solln, D-81479 Munich, Germany. Univ Munich, Inst Kinder & Jugendpschiatrie, Munich, Germany. RP Mildenberger, K (reprint author), Heckscher Klin Munchen, Abt Solln, Wolfratshauser Str 350, D-81479 Munich, Germany. CR AMOROSA H, 1986, Z KINDER JUG-PSYCH, V14, P289 BAUER A, 1972, VERFAHREN MESSUNG BI BEITCHMAN JH, 1986, J AM ACAD CHILD PSY, V25, P528, DOI 10.1016/S0002-7138(10)60013-1 BERGER F, 1990, Z KINDER JUG-PSYCH, V18, P71 CANTWELL DP, 1987, J COMMUN DISORD, V20, P151, DOI 10.1016/0021-9924(87)90006-2 Dopfner M, 1997, PRAX KINDERPSYCHOL K, V46, P519 DOPFNER M, 1994, Z KINDER JUG-PSYCH, V22, P299 Dopfner M., 1999, PSYCHOPATHOLOGISCHES DOPFNER M, 1993, Z KINDER JUG-PSYCH, V21, P90 ENGLERT E, 1998, SPEKTRUM, V5, P129 Noterdaeme M, 1999, Z KINDER JUG-PSYCH, V27, P183, DOI 10.1024//1422-4917.27.3.183 Noterdaeme M, 1998, MONATSSCHR KINDERH, V146, P931, DOI 10.1007/s001120050345 *WHO, 1991, INT KLASS PSYCH STOR, V10 NR 13 TC 1 Z9 1 PU VANDENHOECK & RUPRECHT PI GOTTINGEN PA THEATERSTRASSE 13,, D-37073 GOTTINGEN, GERMANY SN 0032-7034 J9 PRAX KINDERPSYCHOL K JI Prax. Kinderpsychol. Kinderpsychiatr. PD OCT PY 2001 VL 50 IS 8 BP 649 EP 663 PG 15 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 493QY UT WOS:000172236000004 PM 11721613 ER PT J AU Sjogreen, L Andersson-Norinder, J Jacobsson, C AF Sjogreen, L Andersson-Norinder, J Jacobsson, C TI Development of speech, feeding, eating, and facial expression in Mobius sequence SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article DE Mobius sequence/syndrome; facial palsy; tongue palsy; feeding problems; dysphagia; dysarthria ID MOEBIUS SYNDROME; BRAIN-STEM; CHROMOSOME-TRANSLOCATION; VASCULAR ETIOLOGY; DUTCH FAMILY; MISOPROSTOL; PREGNANCY; CHILDREN; ABNORMALITIES; TRIMESTER AB Objective: Mobius sequence is a rare congenital disorder with the primary diagnostic criteria of congenital facial and abducens nerve palsy. Involvement from other cranial nerves is common. Orofacial anomalies and limb malformations may be associated with the disorder. Mental retardation and autism have been reported in some. The aim of this study was to describe orofacial dysfunction observed in a prospective, multidisciplinary study of individuals with Mobius sequence. Methods: Twenty-five patients with Mobius sequence, aged 2 months to 54 years, participated in the study. Clinical observations by different medical specialists were collected in an established database. Dentists and a speech pathologist made the orofacial examination. The parents or the patient described orofacial function and dysfunction th-rough interviews and a questionnaire. Results: Bilateral facial palsy was observed in 16 patients, unilateral palsy in 9. Observed orofacial anomalies were tongue dysfunction (16), micrognatia (8), microglossia (7), cleft palate (4), and cleft lip (1). Seventeen had speech problems, 16 reported feeding difficulties in infancy, 14 eating problems, and 8 drooling. Conclusions: Orofacial problems are common in Mobius sequence and have a significant impact on the quality of life for the patient and for the whole family. Early intervention by a speech pathologist and a paediatric dentist should be undertaken to improve orofacial function and symptoms. Plastic surgery, oral motor training, facial massage, speech therapy, and orthodontic treatment are some of the therapy methods that can be considered. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved. C1 Mun H Ctr Swedish Orofacial Resource Ctr, Dept Odontol, S-41390 Gothenburg, Sweden. RP Sjogreen, L (reprint author), Mun H Ctr Swedish Orofacial Resource Ctr, Dept Odontol, Medicinaregatan 12 A, S-41390 Gothenburg, Sweden. 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Unlike normals, the autistic children as a whole did not show a larger response to the person than to the cup. We also monitored sympathetic activity in autistic children as they engaged in a wide range of everyday behaviours. The children tended to use self-stimulation activities in order to calm hyper-responsive activity of the sympathetic ("fight or flight") branch of the autonomic nervous system. A small percentage of our autistic subjects had hyporesponsive sympathetic activity, with essentially no electrodermal responses except to self-injurious behaviour. We sketch a hypothesis about autism according to which autistic children use overt behaviour in order to control a malfunctioning autonomic nervous system and suggest that they have learned to avoid using certain processing areas in the temporal lobes. C1 Univ Calif San Diego, Ctr Brain & Cognit, La Jolla, CA 92093 USA. Cure Autism Now Fdn, Los Angeles, CA 90036 USA. 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We show here that in the rat cerebellar cortex, mRNAs encoding secretin are localized in the Purkinje cells, whereas those of its receptor are found in both Purkinje cells and GABAergic interneurons. Immunoreactivity for secretin is localized in the soma and dendrites of Purkinje cells. In addition, secretin facilitates evoked, spontaneous, and miniature IPSCs recorded from Purkinje cells. We propose that secretin is released from the somatodendritic region of Purkinje cells and serves as a retrograde messenger modulating GABAergic afferent activity. C1 Univ Hong Kong, Dept Zool, Hong Kong, Hong Kong, Peoples R China. Chinese Univ Hong Kong, Dept Physiol, Shatin, Hong Kong, Peoples R China. RP Chow, BKC (reprint author), Univ Hong Kong, Dept Zool, Kadoorie Biol Sci Bldg,Pokfulam Rd, Hong Kong, Hong Kong, Peoples R China. 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Evidence for a strong underlying genetic predisposition comes from twin and family studies, although susceptibility genes have not yet been identified. A whole-genome screen for linkage, using 83 sib pairs with autism, has been completed, and 119 markers have been genotyped in 13 candidate regions in a further 69 sib pairs. The addition of new families and markers provides further support for previous reports of linkages on chromosomes 7q and 16p. Two new regions of linkage have also been identified on chromosomes 2q and 17q. The most significant finding was a multipoint maximum LOD score (MLS) of 3.74 at marker D2S2188 on chromosome 2; this MLS increased to 4.80 when only sib pairs fulfilling strict diagnostic criteria were included. The susceptibility region on chromosome 7 was the next most significant, generating a multipoint MLS of 3.20 at marker D7S477. Chromosome 16 generated a multipoint MLS of 2.93 at D16S3102, whereas chromosome 17 generated a multipoint MLS of 2.34 at HTTINT2. With the addition of new families, there was no increased allele sharing at a number of other loci originally showing some evidence of linkage. These results support the continuing collection of multiplex sib-pair families to identify autism-susceptibility genes. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Inst Psychiat, Ctr Social Genet & Dev Psychiat, London, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London, England. Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX1 2JD, England. Guys Hosp, Newcomer Ctr, London SE1 9RT, England. Guys Hosp, Reg Genet Ctr, Div Med & Mol Genet, London SE1 9RT, England. Flemming Nuffield Unit, Newcastle Upon Tyne, Tyne & Wear, England. Newcastle Gen Hosp, Neuropsychol Dept, Newcastle Upon Tyne, Tyne & Wear, England. 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PD SEP PY 2001 VL 69 IS 3 BP 672 EP 672 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 459VD UT WOS:000170271400023 ER PT J AU Sudhalter, V Belser, RC AF Sudhalter, V Belser, RC TI Conversational characteristics of children with fragile x syndrome: Tangential language SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; SPREADING-ACTIVATION THEORY; AUTISM; MALES; ATTENTION; BEHAVIOR; PHENOTYPE; GAZE AB The production of tangential language during conversations was studied with people who have fragile X syndrome, autistic disorder, or mental retardation not caused by fragile X. Tangential language was found to be more prevalent among those with fragile X, compared to the control groups, especially within unsolicited comments. These results support our hypothesis that the tangential language seen in fragile X is not the result of either general developmental delay or undiagnosed autistic disorder. 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PD SEP PY 2001 VL 106 IS 5 BP 389 EP 400 DI 10.1352/0895-8017(2001)106<0389:CCOCWF>2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 490RE UT WOS:000172064200001 PM 11531459 ER PT J AU Boatman, D Alidoost, M Gordon, B Lipsky, F Zimmerman, AW AF Boatman, D Alidoost, M Gordon, B Lipsky, F Zimmerman, AW TI Tests of auditory processing differentiate Asperger's syndrome from high-functioning autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 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 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2001 VL 50 IS 3 SU 1 BP S95 EP S95 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 469FT UT WOS:000170804500278 ER PT J AU Connolly, AM Chez, M Streif, B Keeling, R Tempb, RJ Kwon, J Riviello, J Robinson, R Deuel, AMK AF Connolly, AM Chez, M Streif, B Keeling, R Tempb, RJ Kwon, J Riviello, J Robinson, R Deuel, AMK TI Antiendothelial autoantibodies: Characterization of antigenic targets of sera from children with Landau-Kleffner syndrome, Landau-Kleffner variant, autism, and epilepsy SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2001 VL 50 IS 3 SU 1 BP S123 EP S123 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 469FT UT WOS:000170804500374 ER PT J AU Lopez-Alberola, R Bhattacharjee, M Lee, DA AF Lopez-Alberola, R Bhattacharjee, M Lee, DA TI Reduced brain-derived neurotrophic factor in the cerebellum of autistic postmortem brain tissue: Implications for serotonergic pathways in the pathogenesis of autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2001 VL 50 IS 3 SU 1 BP S61 EP S61 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 469FT UT WOS:000170804500205 ER PT J AU Zimmerman, AW Tyler, JD Matteson, KJ AF Zimmerman, AW Tyler, JD Matteson, KJ TI Increased incidence of HLA-B60 and maternal DR4 in autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2001 VL 50 IS 3 SU 1 BP S122 EP S123 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 469FT UT WOS:000170804500373 ER PT J AU Park, RJ Bolton, PF AF Park, RJ Bolton, PF TI Pervasive developmental disorder and obstetric complications in children and adolescents with tuberous sclerosis SO AUTISM LA English DT Article DE cognitive development; obstetric complications; pervasive developmental disorder; tuberous sclerosis ID CARDIAC TUMORS; AUTISM; IDENTIFICATION; POPULATION; PREGNANCY; DIAGNOSIS; BEHAVIOR; FETAL; GENE; 9Q34 AB Children with autism have an increased risk for obstetric complications but it is not known whether these are of primary aetiological significance. It is also unclear whether obstetric complications play a secondary role in shaping phenotypic expression in individuals at genetic risk for autism. We investigated this question by studying the role of obstetric complications in determining phenotypic manifestations in tuberous sclerosis, a single gene disorder frequently associated with autism spectrum disorders. Obstetric histories of 43 children with non-familial TS and 40 unaffected siblings were obtained using a structured parent interview. ADI-R, ADOS-G and IQ evaluations were undertaken. Children with TS experienced more obstetric complications than their unaffected siblings, but these were related to mild rather than severe adversities. No differences in obstetric complications were found in children with and without autism spectrum disorders and there was no positive correlation between obstetric adversities and severity of autism spectrum disorders or intellectual impairments. C1 Univ Cambridge, Dept Psychiat, Dev Psychiat Sect, Autism & Related Condit Res Ctr, Cambridge CB3 9JE, England. RP Park, RJ (reprint author), Univ Cambridge, Dept Psychiat, Dev Psychiat Sect, Autism & Related Condit Res Ctr, 18B Trumpington Rd, Cambridge CB3 9JE, England. 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This article reports the reliability and validity study of this new scale. Factorial analysis computed on the 55 initial items identified six main dimensions which we characterized and labelled: interaction dysfunction, praxis dysfunction, auditory dysfunction, attention dysfunction, islet of ability and emotional dysfunction. Relationships between these six new variables and diagnostic subgroups, and chronological and developmental age, are discussed. The BFI offers precise information of the functional symptomatology of autism, showing clear evidence of some disordered areas of functioning. This new approach may provide valuable information in clinical research, especially for psychopathology and physiopathology studies. C1 Inserm U316, Tours, France. RP Adrien, JL (reprint author), Univ Tours, CHU Bretonneau, Serv Explorat Fonctionnelles & Neurophysiol Pedop, 2 Bd Tonnelle, F-37044 Tours, France. CR Adrien J. 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Peter, 1993, AUTISM DEV MIND HOBSON RP, 1989, BRIT J DEV PSYCHOL, V7, P237 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 Lelord G, 1991, AUTISME ENFANT Lewis MH, 1996, J AUTISM DEV DISORD, V26, P231, DOI 10.1007/BF02172018 MALVY J, 1997, NEUROPSYCHIAT ENFAN, V45, P749 MALVY J, 1994, ANAE, V26, P33 MARTINEAU J, 1992, ELECTROEN CLIN NEURO, V82, P60, DOI 10.1016/0013-4694(92)90183-I Mundy P., 1989, DEV PSYCHOPATHOL, V1, P173, DOI 10.1017/S0954579400000365 Ornitz E., 1988, BRAIN DYSFUNCT, V1, P309 ORNITZ EM, 1985, J AM ACAD CHILD PSY, V24, P251, DOI 10.1016/S0002-7138(09)61084-0 ORNITZ EM, 1983, INT J NEUROSCI, V19, P85, DOI 10.3109/00207458309148648 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 PERRONBORELLI M, 1978, ECHELLES DIFFERENTIE Rogers S. 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M., 1982, PROCEDURES MANUAL EA SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 TREVARTHEN C, 1996, CAHIERS CERFEE, V13, P9 WESCHSLER D, 1981, ECHELLE INTELLIGENCE WETHERBY AM, 1984, J SPEECH HEAR RES, V27, P364 NR 53 TC 11 Z9 11 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2001 VL 5 IS 3 BP 249 EP 264 DI 10.1177/1362361301005003003 PG 16 WC Psychology, Developmental SC Psychology GA 486GM UT WOS:000171810100002 PM 11708585 ER PT J AU Perry, DW Marston, GM Hinder, SAJ Munden, AC Roy, A AF Perry, DW Marston, GM Hinder, SAJ Munden, AC Roy, A TI The phenomenology of depressive illness in people with a learning disability and autism SO AUTISM LA English DT Article DE aggression; autism; behavioural disorder; depression; self-injurious behaviour ID MENTAL-RETARDATION; INTELLECTUAL DISABILITY; FLUOXETINE TREATMENT; SELF-INJURY; ADULTS; DISORDER; AGGRESSION; SEROTONIN; CHILDREN; EFFICACY AB People with autism may develop new behaviours in adolescence or early adult life, in addition to those associated with the primary disorder. Some of these behaviours have been postulated to be symptoms of depressive disorder. This article notes the methodological problems of investigating depression in people with autism. The authors also attempt to clarify the symptoms that may be significant in diagnosing depression in this group, by using treatment response methods. C1 Gulson Rd Hosp, Coventry CV1 2HR, W Midlands, England. Newtown Hosp, Newtown, Worcs, England. RP Perry, DW (reprint author), Gulson Rd Hosp, River House,Gulson Rd, Coventry CV1 2HR, W Midlands, England. CR Berney TP, 2000, BRIT J PSYCHIAT, V176, P20, DOI 10.1192/bjp.176.1.20 Clarke D, 1999, AUTISM, V3, P149, DOI DOI 10.1177/1362361399003002005 Clarke DJ, 1999, J INTELL DISABIL RES, V43, P413, DOI 10.1046/j.1365-2788.1999.043005413.x *CLIN PSYCH COMM, 1965, BRIT MED J, P881 Cooper Sally-Ann, 1996, Irish Journal of Psychological Medicine, V13, P105 COOPER SA, 1994, MENT HAND SECT ROYAL Department of Health, 1995, HLTH NAT STRAT PEOPL Fraser WI, 2000, BRIT J PSYCHIAT, V176, P10, DOI 10.1192/bjp.176.1.10 Ghaziuddin M, 1998, J AUTISM DEV DISORD, V28, P111, DOI 10.1023/A:1026036514719 GHAZIUDDIN M, 1991, BRIT J PSYCHIAT, V159, P721, DOI 10.1192/bjp.159.5.721 GHAZIUDDIN M, 1991, J AM ACAD CHILD PSY, V30, P508 GILLBERG C, 1989, DIAGNOSIS AND TREATMENT OF AUTISM, P375 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P36 Hellings JA, 1996, J CLIN PSYCHIAT, V57, P333 HOLMES N, 1982, PSYCHOL MED, V12, P879 HUMBLE M, 1992, INT CLIN PSYCHOPHARM, V6, P21, DOI 10.1097/00004850-199206005-00003 LAINHART JE, 1994, J AUTISM DEV DISORD, V24, P587, DOI 10.1007/BF02172140 LOWRY MA, 1992, J INTELL DISABIL RES, V36, P296 Marston GM, 1997, J INTELL DISABIL RES, V41, P476, DOI 10.1111/j.1365-2788.1997.tb00739.x MEINS W, 1995, J INTELL DISABIL RES, V39, P41 Meins W, 1996, J INTELL DISABIL RES, V40, P222, DOI 10.1046/j.1365-2788.1996.750750.x Perry DW, 1996, HUM PSYCHOPHARM CLIN, V11, P425, DOI 10.1002/(SICI)1099-1077(199609)11:5<425::AID-HUP822>3.0.CO;2-O REISS S, 1993, J INTELL DISABIL RES, V37, P287 RICKETTS RW, 1993, J AM ACAD CHILD PSY, V32, P865, DOI 10.1097/00004583-199307000-00024 SOVNER R, 1993, J INTELL DISABIL RES, V37, P301 SPREAT S, 1989, COMPR PSYCHIAT, V30, P505, DOI 10.1016/0010-440X(89)90080-1 World Health Organization, 1992, INT CLASS MENT BEH D, V10th NR 27 TC 19 Z9 20 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2001 VL 5 IS 3 BP 265 EP 275 DI 10.1177/1362361301005003004 PG 11 WC Psychology, Developmental SC Psychology GA 486GM UT WOS:000171810100003 PM 11708586 ER PT J AU Gillott, A Furniss, F Walter, A AF Gillott, A Furniss, F Walter, A TI Anxiety in high-functioning children with autism SO AUTISM LA English DT Article DE anxiety; autism; social worries; specific language impairment AB High-functioning children with autism were compared with two control groups on measures of anxiety and social worries. Comparison control groups consisted of children with specific language impairment (SLI) and normally developing children. Each group consisted of 15 children between the ages of 8 and 12 years and were matched for age and gender. Children with autism were found to be most anxious on both measures. High anxiety subscale scores for the autism group were separation anxiety and obsessive-compulsive disorder. These findings are discussed within the context of theories of autism and anxiety in the general population of children. Suggestions for future research-are made. C1 Highbury Hosp, Dept Learning Disabil, Nottingham NG6 9DR, England. Univ Leicester, Leicester LE1 7RH, Leics, England. Derbyshire Childrens Hosp, Derby, England. RP Gillott, A (reprint author), Highbury Hosp, Dept Learning Disabil, Nottingham NG6 9DR, England. CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1997, ASPERGERS SYNDROME G BARONCOHEN S, 1989, BRIT J CLIN PSYCHOL, V28, P193 BARONCOHEN S, 1985, COGNITION, V21, P385 CAPPS L, 1992, J CHILD PSYCHOL PSYC, V33, P1169, DOI 10.1111/j.1469-7610.1992.tb00936.x Despert JL, 1965, EMOTIONALLY DISTURBE Gillberg C., 1984, DEV MED CHILD NEUROL, V26, P122 Groden J., 1994, BEHAV ISSUES AUTISM HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Howlin P, 1998, CHILDREN AUTISM ASPE Howlin P., 1997, AUTISM PREPARING ADU JAMES EM, 1994, INT HDB PHOBIC ANXIE Kanner L, 1943, NERV CHILD, V2, P217 King NJ, 1997, J CHILD PSYCHOL PSYC, V38, P389, DOI 10.1111/j.1469-7610.1997.tb01524.x KOMOTO J, 1984, J AUTISM DEV DISORD, V14, P81, DOI 10.1007/BF02408557 LOVELAND KA, 1997, HDB AUTISM PERVASIVE Schopler E, 1994, BEHAV ISSUES AUTISM Sparrow S, 1984, VINELAND ADAPTIVE BE Spence S. H., 1995, SOCIAL SKILLS TRAINI Spence S. H., 1997, CHILD PSYCHOL PORTFO Spence SH, 1997, J ABNORM PSYCHOL, V106, P280, DOI 10.1037//0021-843X.106.2.280 SPENCE SH, 1994, M ASS ADV BEH THER S SZATMARI P, 1989, J AUTISM DEV DISORD, V19, P213, DOI 10.1007/BF02211842 TANTAM D, 1991, AUTISM ASPERGERS SYN THOMAS G, 1998, ASPERGER SYNDROME PR NR 25 TC 204 Z9 204 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2001 VL 5 IS 3 BP 277 EP 286 DI 10.1177/1362361301005003005 PG 10 WC Psychology, Developmental SC Psychology GA 486GM UT WOS:000171810100004 PM 11708587 ER PT J AU Bernabei, P Camaioni, L AF Bernabei, P Camaioni, L TI Developmental profile and regression in a child with autism - A single case study SO AUTISM LA English DT Article DE autism; cognitive development; communicative development; early diagnosis; home video; regression ID INFANTILE-AUTISM; YOUNG-CHILDREN; SPEECH LOSS; FOLLOW-UP; AGE; SENSORIMOTOR; INFANCY; COMMUNICATION; ONSET AB The developmental profile of a child with autism during the first 3 years of life is presented. Clinical material obtained from different sources is discussed: home videos from birth to 3 years, and cognitive and communicative evaluations at 24, 34 and 38 months. The videos show how the child appeared to make progress up to 12 months, but from 12 to 18 months some abilities that had been previously acquired were lost, and a decrease in social interaction, communication and language was observed. From 18 to 38 months communicative and linguistic abilities remained unchanged, but social interactive behaviours continued to decrease. The particular profile identified is discussed as one of the possible pathways through which autism may develop. C1 Univ Roma La Sapienza, Dept Childhood Neurol & Psychiat Sci, I-00147 Rome, Italy. RP Bernabei, P (reprint author), Univ Roma La Sapienza, Dept Childhood Neurol & Psychiat Sci, Via Giulio Adamoli 28, I-00147 Rome, Italy. 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