FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Silver, M Oakes, P AF Silver, M Oakes, P TI Evaluation of a new computer intervention to teach people with autism or Asperger syndrome to recognize and predict emotions in others SO AUTISM LA English DT Article DE Asperger syndrome; autism; computer; emotion; intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; NORMAL-CHILDREN; MIND; ABILITY; EXPRESSIONS; BELIEF; SKILLS AB This randomized controlled trial looked at the effect of a new computer program designed to teach people with autistic spectrum disorders to better recognize and predict emotional responses in others. Two groups of 11 children (age 12-18) with autism or Asperger syndrome at two special schools participated: one group used the computer program for 10 half-hour sessions over 2 weeks. Within-program data showed a significant reduction in errors made from first to last use. Students were assessed pre- and post-intervention using facial expression photographs, cartoons depicting emotion-laden situations, and non-literal stories. Scores were not related to age or verbal ability. The experimental group made gains relative to the control group on all three measures. Gains correlated significantly with the number of times the computer program was used and results suggest positive effects. Further research could assess whether these gains generalized into real life or improved performance on theory of mind measures. C1 St Jamess Univ Hosp, Child & Family Unit, Leeds LS9 7TF, W Yorkshire, England. Univ Hull, Kingston Upon Hull HU6 7RX, N Humberside, England. RP Silver, M (reprint author), St Jamess Univ Hosp, Child & Family Unit, Beckett St, Leeds LS9 7TF, W Yorkshire, England. 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The present study explored the effects of repeated sessions of imitation. Twenty children were recruited from a school for children with autism to attend three sessions during which an adult either imitated all of the children's behaviors or simply played with the child. During the second session the children in the imitation group spent a greater proportion of time showing distal social behaviors toward the adult including: (1) looking; (2) vocalizing; (3) smiling; and (4) engaging in reciprocal play. During the third session, the children in the imitation group spent a greater proportion of time showing proximal social behaviors toward the adult including: (1) being close to the adult; (2) sitting next to the adult; and (3) touching the adult. These data suggest the potential usefulness of adult imitative behavior as an early intervention. C1 Univ Miami, Sch Med, Dept Pediat, Touch Res Inst, Miami, FL 33101 USA. Inst Psychobiol, CNRS, Paris, France. RP Field, T (reprint author), Univ Miami, Sch Med, Dept Pediat, Touch Res Inst, POB 016820, Miami, FL 33101 USA. 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This paper answers that question by suggesting that integration will be pivotal to the successful treatment of autism in the future. Five main levels of integration are proposed: (a) integration of disciplines (e.g., applied behavior analysis with education, developmental psychology, neuroscience); (b) integration of treatment types (e.g., structured and naturalistic behavior therapy, speech therapy, medicine) (c) integration of the domains of behavior (e.g., language, play, attention); (d) integration of treatment programs (e.g., behavior therapy with school programming, occupational therapy); and, (e) integration of treatment providers (e.g., therapists, teachers and professionals with parents, siblings and peers). 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Therapy PD FAL PY 2001 VL 32 IS 4 BP 619 EP 632 DI 10.1016/S0005-7894(01)80012-5 PG 14 WC Psychology, Clinical SC Psychology GA 542YE UT WOS:000175072600002 ER PT J AU Scheeringa, MS AF Scheeringa, MS TI The differential diagnosis of impaired reciprocal social interaction in children: A review of disorders SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE reciprocal social interaction; developmental disorders; children ID DEVELOPMENTAL LANGUAGE DISORDERS; SEMANTIC-PRAGMATIC DISORDER; HIGH-LEVEL AUTISM; DSM-IV; PERSONALITY SUBTYPES; FIELD TRIAL; CHILDHOOD; PERFORMANCE; ATTACHMENT; ABILITIES AB Impairment in reciprocal social interaction in children that is less severe than autism can be difficult to diagnose due to the variety of developmental pathways that may lead to this problem. Seven childhood disorders are reviewed that include impaired reciprocal interaction: multisystem developmental disorder, nonverbal learning disability syndrome, semantic-pragmatic disorder, attachment disorders (including a developmental theory of limbic system damage), multiplex developmental disorder, schizoid personality disorder, and pervasive developmental disorder not otherwise specified. Clarification is needed for most of the disorders in the areas of operationalized criteria, assessment tools, and documenting causal relationships. C1 Tulane Univ, Sch Med, New Orleans, LA 70118 USA. RP Scheeringa, MS (reprint author), 1440 Canal St,TB52, New Orleans, LA 70112 USA. 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H., 2000, HDB INFANT MENTAL HL, P353 Zeanah CH, 2000, J DEV BEHAV PEDIATR, V21, P230 NR 56 TC 13 Z9 13 PU KLUWER ACADEMIC-HUMAN SCIENCES PRESS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA SN 0009-398X J9 CHILD PSYCHIAT HUM D JI Child Psychiat. Hum. Dev. PD FAL PY 2001 VL 32 IS 1 BP 71 EP 89 DI 10.1023/A:1017511714145 PG 19 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 489XV UT WOS:000172018900005 PM 11579660 ER PT J AU Vanhala, R Turpeinen, U Riikonen, R AF Vanhala, R Turpeinen, U Riikonen, R TI Low levels of insulin-like growth factor-I in cerebrospinal fluid in children with autism SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CEREBELLAR DEGENERATION; INFANTILE-AUTISM; DISORDERS; BRAIN; SYSTEM; ADULTS; SERUM; STAGE; GENE; SIZE AB Autism is a behaviourally defined syndrome characterized by disturbances of social interaction and communication and restrictions of behaviour patterns and imagination. The pathogenesis of autism is unknown but it is suspected that a number of genetic factors may be involved. Neurotrophic factors such as insulin-like growth factor-I (IGF-I) play a role in early brain development. The aim of this study was to determine whether IGF-I levels might be associated with the development of autism. IGF-I levels were measured in the CSF of 11 children with autism (4 females, 7 males; mean age 3.8 years, SD 1.1) using a sensitive radioimmunoassay method and compared with levels in 11 control participants (6 females, 5 males; mean age 3.8 years). Levels of IGF-I in the CSF were statistically significantly lower in the children with autism than in the control children (p=0.03). IGF-I may play a role in pathogenetic mechanisms of autism and the role of neurotrophic factors in autism and other neurodevelopmental diseases should be studied further. C1 Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. Univ Helsinki, Cent Hosp Lab, Helsinki, Finland. Univ Kuopio, Childrens Hosp, Dept Child Neurol, FIN-70211 Kuopio, Finland. RP Vanhala, R (reprint author), Childrens Castle Hosp, Hosp Children & Adolescents, Lastenlinnantie 2, SF-00250 Helsinki, Finland. 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Med. Child Neurol. PD SEP PY 2001 VL 43 IS 9 BP 614 EP 616 DI 10.1017/S0012162201001116 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 490MU UT WOS:000172056300006 PM 11570630 ER PT J AU Adrien, JL Rossignol-Deletang, N Martineau, J Couturier, G Barthelemy, C AF Adrien, JL Rossignol-Deletang, N Martineau, J Couturier, G Barthelemy, C TI Regulation of cognitive activity and early communication development in young autistic, mentally retarded, and young normal children SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article DE disorders of regulation; communication development; social interaction; autism; mental retardation; child ID EXECUTIVE FUNCTION; INFANTILE-AUTISM; JOINT ATTENTION; LANGUAGE; PLAY; DEFICITS; MIND AB Based on the Piagetian framework, this study examined regulation of Cognitive profiles and their interrelationship in groups of autistic, activity and developmental communication pro mentally retarded, and normal children of comparable overall, verbal, and oculo-manual developmental ages (from 6 to 24 months). Regulation of activity was assessed with both an object permanence test and an original behavior grid, and development of communication skills with the Guidetti-Tourrette scales (French adaptation of the Seibert-Hogan scales). The results showed evidence of certain types of dysregulation of cognitive activity and a general delay in communication ability In autistic children compared to the other two groups. Moreover although the intensity of some of these disorders decreased in relation to the developmental levels of social interaction and joint attention in normal children, they were related to both high and low levels of development of social interaction only in autistic children. These findings raise the hypothesis of a relationship between a disorder of disengaging from an activity and developmental levels of social interaction noted at two transitory periods of early development (12 and 24 months) only in children with autism. Developmental and neuropsychological interpretations of this particular pattern are proposed. (C) 2001 John Wiley & Sons, Inc. C1 CHU Bretonneau, INSERM, U316, F-37044 Tours, France. RP Adrien, JL (reprint author), CHU Bretonneau, INSERM, U316, 2 Bd Tonnelle, F-37044 Tours, France. CR ADRIEN JL, 1994, DEV ENFANT APPROCHES, P175 ADRIEN JL, 1987, J AUTISM DEV DISORD, V17, P407, DOI 10.1007/BF01487069 ADRIEN JL, 1988, NEUROPSYCHIAT ENFAN, V36, P9 ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 ADRIEN JL, 1993, EVALUATION COMMUNICA, P67 ADRIEN JL, 1996, AUTISME ENFANT DEV P ADRIEN JL, 1986, NEUROPSYCHIAT ENFAN, V34, P123 ADRIEN JL, 1995, J AUTISM DEV DISORD, V25, P247 American Psychiatric Association, 1987, DIAGN STAT MAN MENT BARONCOHEN S, 1992, J CHILD PSYCHOL PSYC, V33, P623, DOI 10.1111/j.1469-7610.1992.tb00896.x BARTHELEMY C, 1998, INFANTILE AUTISM EXC Barthélémy C, 1994, Acta Paedopsychiatr, V56, P261 Bruneau N, 1987, Electroencephalogr Clin Neurophysiol Suppl, V40, P584 BRUNER JS, 1990, DEV PSYCHOL PREMIERE CASATI I, 1969, MANUEL APPL Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 COURCHESNE E, 1994, ATYPICAL COGNITIVE D FERMANIAN J, 1984, REV EPIDEMIOL SANTE, V32, P408 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Gesell A., 1947, DEV DIAGNOSIS NORMAL GUIDETTI M, 1993, EVALUATION COMMUNICA 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 JARROLD C, 1994, J CHILD PSYCHOL PSYC, V35, P1473, DOI 10.1111/j.1469-7610.1994.tb01288.x Kasari C., 1993, ENHANCING CHILDRENS, P201 LELORD G, 1990, AUTISME ENFANT Lelord G, 1990, NEUROPSYCHIAT ENFAN, V38, P43 LOVELAND KA, 1986, J AUTISM DEV DISORD, V16, P335, DOI 10.1007/BF01531663 Martineau J, 1998, J PSYCHOPHYSIOL, V12, P275 MARTINEAU J, 1992, ELECTROEN CLIN NEURO, V82, P60, DOI 10.1016/0013-4694(92)90183-I MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x Mundy P., 1989, DEV PSYCHOPATHOL, V1, P173, DOI 10.1017/S0954579400000365 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x MUNDY P, 1987, J AUTISM DEV DISORD, V17, P349, DOI 10.1007/BF01487065 OZONOFF S, 1994, DEV PSYCHOPATHOL, V6, P415, DOI 10.1017/S0954579400006027 Piaget J., 1977, NAISSANCE INTELLIGEN PIAGET J., 1973, CONSTRUCTION REEL CH Rogers S. J., 1991, DEV PSYCHOPATHOL, V3, P137, DOI DOI 10.1017/S0954579400000043 Sauvage D, 1988, AUTISME NOURRISSON J Seibert J. M., 1982, INFANT MENT HEALTH J, V3, P244, DOI DOI 10.1002/1097-0355(198224)3:4<244::AID-IMHJ2280030406>3.0.CO;2-R SIGMAN M, 1989, J AM ACAD CHILD PSY, V28, P74, DOI 10.1097/00004583-198901000-00014 SIGMAN M, 1981, J ABNORM CHILD PSYCH, V9, P149, DOI 10.1007/BF00919111 Tardif C, 1995, INT J BEHAV DEV, V18, P727 Trevarthen C., 1996, CHILDREN AUTISM DIAG UZGIRIS JC, 1975, ASSESSMENT INFANCY ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 NR 46 TC 13 Z9 14 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0012-1630 J9 DEV PSYCHOBIOL JI Dev. Psychobiol. PD SEP PY 2001 VL 39 IS 2 BP 124 EP 136 DI 10.1002/dev.1036 PG 13 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA 470GX UT WOS:000170863500007 PM 11568882 ER PT J AU Dyches, TT Prater, MA Cramer, SF AF Dyches, TT Prater, MA Cramer, SF TI Characterization of mental retardation and autism in children's books SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article AB Although many authors have identified guidelines in the evaluation and subsequent selection of contemporary, children's literature, few have studied how individuals with mental retardation and autism (MR/A) are depicted in children's literature. Dyches and Prater (2000) took a unique approach in creating evaluation guidelines based not only upon general literary standards, but also with regard for the portrayal of individuals with disabilities (Turnbull, Turnbull, Shank, & Leal, 1999). Based on the Dyches and Prater guidelines, characterizations and plots in eligible children's books published during 1997 and 1998 were evaluated. Twelve books are discussed in detail, in terms of each guideline. The results showed that there was inconsistency in the books, in terms of the themes that emerged: (a) characterization and positive portrayal, (b) relationships, (c) changes in characters without MR/A, and (d) changes in characters with MR/A. Special topics that were Present in the books are also discussed: schooling, recreation, and residence. The characters in the books were portrayed as making more choices in their lives, and were educated in more inclusive setting, than characters in books in an earlier study by Prater (1998). The conclusion highlights the use of this study as the basis of an international award for children's literature that includes characters with mental retardation and/or autism. C1 Brigham Young Univ, Provo, UT 84602 USA. Univ Hawaii Manoa, Honolulu, HI 96822 USA. SUNY Buffalo, Buffalo, NY USA. RP Dyches, TT (reprint author), Brigham Young Univ, 328 MCKB,POB 25093, Provo, UT 84602 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAER J, 1997, HEARTLESS HERO BANKS SH, 1997, UNDER SHADOW WINGS Blaska J.K., 1996, USING CHILDRENS LIT BUTLER G, 1998, HANGASHORE CARTER AL, 1997, BIG BROTHER DUSTIN CRAMER SF, 1998, TEACHING EXCEPTIONAL, V34, P46 Dyches T. T., 2000, DEV DISABILITY CHILD EICHELBERGER D, 1998, BOY WHO SWAM STARS ELLIOTT TR, 1982, REHABIL LIT, V43, P348 FOX P, 1997, RADIANCE DESCENDING GOLDMANRUBIN S, 1997, EMILY LOVE Heim Annette B., 1994, SCH LIB J, V40, P139 Leal Dorothy, 1999, EXCEPTIONAL LIVES SP LEARS L, 1998, IANS WALK MAZER H, 1998, WILD KID MOORE CA, 1984, READING HORIZONS, V24, P274 MYLES BS, 1992, INTERV SCH CLIN, V27, P215 PRATER MA, 1998, LIT HAWAIIS CHILDREN, P126 Prater MA, 1999, EDUC TRAIN MENT RET, V34, P418 STUVEBODEEN S, 1998, WELL PAINT OCTOPUS R TASHJIAN J, 1997, TRU CONFESSIONS THURER S, 1980, REHABIL LIT, V41, P12 TWACHTMANCULLEN D, 1998, TREVOR TREVOR U.S. Department of Education, 2000, 22 ANN REP C IMPL IN 1999, CHILDRENS BOOKS PRIN NR 26 TC 7 Z9 7 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 0013-1237 J9 EDUC TRAIN MENT RET JI Educ. Train. Mental Retard. Dev. Disabil. PD SEP PY 2001 VL 36 IS 3 BP 230 EP 243 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 464AV UT WOS:000170511000002 ER PT J AU Myles, BS Barnhill, GP Hagiwara, T Griswold, DE Simpson, RL AF Myles, BS Barnhill, GP Hagiwara, T Griswold, DE Simpson, RL TI A synthesis of studies on the intellectual, academic, social/emotional and sensory characteristics of children and youth with Asperger syndrome SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article ID AUTISM AB A synthesis of studies designed to better understand characteristics of children and youth identified as having Asperger syndrome is Provided. Based on work associated with The Asperger Syndrome Research Project, summarized information on the unique intellectual, academic, social/emotional, and sensory characteristics of children and youth with Asperger syndrome is presented. Implications and practitioner information related to these findings is also included. C1 Univ Kansas, Med Ctr, Dept Special Educ, Kansas City, KS 66160 USA. RP Myles, BS (reprint author), Univ Kansas, Med Ctr, Dept Special Educ, 3901 Rainbow Blvd,HC Miller Bldg,4th Floor, Kansas City, KS 66160 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 Attwood T., 1998, ASPERGERS SYNDROME G Barnhill G., 2000, FOCUS AUTISM OTHER D, V15, P146, DOI [10.1177/108835760001500303, DOI 10.1177/108835760001500303] Barnhill G., 2000, DIAGNOSTIQUE, V25, P147 Barnhill G. P., 2001, FOCUS AUTISM OTHER D, V16, P46, DOI 10.1177/108835760101600112 BARNHILL GP, IN PRESS J POSITIVE BERTHIER ML, 1992, J AM ACAD CHILD PSY, V31, P735, DOI 10.1097/00004583-199207000-00023 BOWLER DM, 1992, J AUTISM OTHER DEV D, V21, P303 CESARONI L, 1991, J AUTISM DEV DISORD, V21, P303, DOI 10.1007/BF02207327 Church C., 2000, FOCUS AUTISM OTHER D, V15, P12, DOI DOI 10.1177/108835760001500102 Dennis M, 1999, J AUTISM DEV DISORD, V29, P5, DOI 10.1023/A:1025962431132 Dunn W., 1999, SENSORY PROFILE DUNN W, IN PRESS AM J OCCUPA Ehlers S, 1997, J CHILD PSYCHOL PSYC, V38, P207, DOI 10.1111/j.1469-7610.1997.tb01855.x Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279 GRISWOLD DE, 2000, UNPUB ASPERGER SYNDR Gross J, 1994, ED PSYCHOL PRACTICE, V10, P104, DOI 10.1080/0266736940100206 KERBESHIAN J, 1990, BRIT J PSYCHIAT, V156, P721, DOI 10.1192/bjp.156.5.721 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Kovacs M., 1992, CHILDRENS DEPRESSION Myles B. 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M., 1988, ASSESSMENT CHILDREN SELIGMAN MEP, 1984, J ABNORM PSYCHOL, V93, P235, DOI 10.1037//0021-843X.93.2.235 SILVAROLI N, 1993, CLASSROOM READING IN Smith Myles B., 2000, ASPERGER SYNDROME SE SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Tantam D., 1991, AUTISM ASPERGER SYND, P147, DOI 10.1017/CBO9780511526770.005 Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 WOLFF S, 1995, LIFE PATH UNUSUAL CH World Health Organization, 1993, INT CLASS DIS REL HL Zachman L., 1991, TEST PROBLEM SOLVING Zachman L., 1994, TEST PROBLEM SOLVING NR 40 TC 22 Z9 22 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 SEP PY 2001 VL 36 IS 3 BP 304 EP 311 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 464AV UT WOS:000170511000008 ER PT J AU Brown, J Murray, D AF Brown, J Murray, D TI Strategies for enhancing play skills for children with autism spectrum disorder SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article AB Children with autism spectrum disorder (ASD) do not develop play in the same way that children with typical development do (Libby, Powell, Messer, & Jordan, 1997; Murray-Slutsky & Paris, 2000; Wolfberg, 1999). This article describes play differences in children with ASD. It also suggests strategies for developing an intervention plan including assessment, goal setting, and teaching play skills. C1 Univ Cincinnati, Cincinnati, OH 45221 USA. Kelly OLeary Ctr PDD, Cincinnati, OH USA. RP Brown, J (reprint author), Childrens Hosp, Med Ctr, Kelly OLeary Ctr PDD, 3333 Burnet Ave,PAV 2nd Floor, Cincinnati, OH 45229 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bruner J. S., 1976, PLAY ITS ROLE DEV EV, P28 BURGHARDT C, 1984, PLAY ANIMALS HUMANS, P5 Garvey C., 1990, PLAY Grandin T., 1995, THINKING PICTURES GRAY C, 1994, SOCIAL STORY KIT HANNA S, 1990, FLOOR TIME Howlin P., 1999, TEACHING CHILDREN AU Janzen J., 1996, UNDERSTANDING NATURE Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 Lovaas O. I., 1981, TEACHING DEV DISABLE MacDonald J. D., 1989, BECOMING PARTNERS CH MURRAY D, 2000, M DIV MENT RET DEV D MURRAYSLUTSKY C, 2000, EXPLORING SPECTRUM A Peeters T., 1997, AUTISM THEORETICAL U Quill K. 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PD SEP PY 2001 VL 36 IS 3 BP 312 EP 317 PG 6 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 464AV UT WOS:000170511000009 ER PT J AU Raja, M Azzoni, A AF Raja, M Azzoni, A TI Asperger's disorder in the emergency psychiatric setting SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article DE Asperger's disorder; autism; psychotic disorders; diagnosis; psychiatric emergency ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISTIC-CHILDREN; OPEN-LABEL; CHILDHOOD SCHIZOPHRENIA; ONSET SCHIZOPHRENIA; PHENOMENOLOGY; HANDEDNESS; ADULTHOOD; PSYCHOSES; EPILEPSY AB Asperger's syndrome (AS) is a pervasive developmental disorder that may be unrecognized, especially if signs of other psychiatric disorders coexist. The objectives of this paper are: 1) to ascertain the prevalence of AS in the emergency psychiatric setting; and 2) to describe features of AS which may help to differentiate these patients from patients with psychotic disorders. Among 2500 patients admitted to a psychiatric intensive care unit, 5 (0.2%) received a diagnosis of AS, for the first time. Besides impairment of social interaction, common features were the following: male gender, left handedness, obsessive-compulsive symptoms, cognitive hyper-abilities, violent behavior, sense of humor, low WAIS total score, high WAIS verbal/performance score ratio, unusual, restricted interest and clumsiness. Comorbid schizophrenia is difficult to rule out in these patients. Psychotic symptoms should not be overvalued in making the diagnosis when specific features of AS are present. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Osped Santo Spirito, Dipartimento Salute Mentale, Rome, Italy. RP Raja, M (reprint author), Osped Santo Spirito, Dipartimento Salute Mentale, Rome, Italy. 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Hosp. Psych. PD SEP-OCT PY 2001 VL 23 IS 5 BP 285 EP 293 DI 10.1016/S0163-8343(01)00155-4 PG 9 WC Psychiatry SC Psychiatry GA 483CL UT WOS:000171616100007 PM 11600171 ER PT J AU Nurmi, EL Bradford, Y Chen, YH Hall, J Arnone, B Gardiner, MB Hutcheson, HB Gilbert, JR Pericak-Vance, MA Copeland-Yates, SA Michaelis, RC Wassink, TH Santangelo, SL Sheffield, VC Piven, J Folstein, SE Haines, JL Sutcliffe, JS AF Nurmi, EL Bradford, Y Chen, YH Hall, J Arnone, B Gardiner, MB Hutcheson, HB Gilbert, JR Pericak-Vance, MA Copeland-Yates, SA Michaelis, RC Wassink, TH Santangelo, SL Sheffield, VC Piven, J Folstein, SE Haines, JL Sutcliffe, JS TI Linkage disequilibrium at the Angelman syndrome gene UBE3A in autism families SO GENOMICS LA English DT Article DE autism; 15q11-q13; UBE3A; linkage disequilibrium; deletion ID RECEPTOR SUBUNIT BETA-3; CHROMOSOME 15Q11-Q13; CANDIDATE GENE; PROXIMAL 15Q; DISORDER; GABRB3; DUPLICATION; ASSOCIATION; UBE3A/E6-AP; PHENOTYPE AB Autistic disorder is a neuro developmental disorder with a complex genetic etiology. Observations of maternal duplications affecting chromosome 15q11-q13 in patients with autism and evidence for linkage and linkage disequilibrium to markers in this region in chromosomally normal autism families indicate the existence of a susceptibility locus. We have screened the families of the Collaborative Linkage Study of Autism for several markers spanning a candidate region covering similar to 2 Mb and including the Angelman syndrome gene (UMA) and a cluster of gamma -aminobutyric acid (GABAA) receptor subunit genes (GABRB3, GABRA5, and GABRG3). We found significant evidence for linkage disequilibrium at marker D15S122, located at the 5 ' end of UMA. This is the first report, to our knowledge, of linkage disequilibrium at UBE3A in autism families. Characterization of null alleles detected at D15S822 in the course of genetic studies of this region showed a small (similar to 5-kb) genomic deletion, which was present at somewhat higher frequencies in autism families than in controls. C1 Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. Univ Iowa, Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Howard Hughes Med Inst, Iowa City, IA 52242 USA. Univ N Carolina, Chapel Hill, NC 27599 USA. Tufts Univ, Boston, MA 02111 USA. Tufts Univ New England Med Ctr, Boston, MA 02111 USA. RP Sutcliffe, JS (reprint author), Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. RI Haines, Jonathan/C-3374-2012; Sutcliffe, James/C-1348-2012; Nurmi, Erika/P-4627-2014 OI Sutcliffe, James/0000-0001-5200-6007; Nurmi, Erika/0000-0003-4893-8957 CR Albrecht U, 1997, NAT GENET, V17, P75, DOI 10.1038/ng0997-75 ASHLEYKOCH A, 2000, AM J HUM GENET S, V67, pA46 Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 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 Bradford Y, 2001, AM J MED GENET, V105, P539, DOI 10.1002/ajmg.1497 Browne CE, 1997, AM J HUM GENET, V61, P1342, DOI 10.1086/301624 CLAYTONSMITH J, 1993, J MED GENET, V30, P529, DOI 10.1136/jmg.30.6.529 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 1997, AM J HUM GENET, V60, P928 Dhar M, 2000, PHYSIOL GENOMICS, V4, P93 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Feinstein C, 1998, J AUTISM DEV DISORD, V28, P393, DOI 10.1023/A:1026000404855 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Glatt K, 1997, GENOMICS, V41, P63, DOI 10.1006/geno.1997.4639 GLATT K, 1994, GENOMICS, V19, P157, DOI 10.1006/geno.1994.1027 Glatt Karen A., 1992, Human Molecular Genetics, V1, P348, DOI 10.1093/hmg/1.5.348 Gudbjartsson DF, 2000, NAT GENET, V25, P12, DOI 10.1038/75514 Herzing LBK, 2001, AM J HUM GENET, V68, P1501, DOI 10.1086/320616 Bailey A, 1998, HUM MOL GENET, V7, P571 KIRKNESS EF, 1993, J BIOL CHEM, V268, P4420 LEDBETTER DH, 1995, METABOLIC MOL BASES, P811 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Maddox LO, 1999, GENOMICS, V62, P325, DOI 10.1006/geno.1999.6017 Maestrini E, 1999, AM J MED GENET, V88, P492, DOI 10.1002/(SICI)1096-8628(19991015)88:5<492::AID-AJMG11>3.0.CO;2-X Mao R, 2000, GENET MED, V2, P131, DOI 10.1097/00125817-200003000-00003 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 Martin ER, 2000, AM J HUM GENET, V67, P146, DOI 10.1086/302957 Martin ER, 1997, AM J HUM GENET, V61, P439, DOI 10.1086/514860 Meguro M, 2001, NAT GENET, V28, P19, DOI 10.1038/88209 Nicholls RD, 1998, TRENDS GENET, V14, P194, DOI 10.1016/S0168-9525(98)01432-2 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 PICKLES A, 1995, AM J HUM GENET, V57, P717 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 ROBINSON CJ, 1993, IEEE T REHABIL ENG, V1, P1 Rougeulle C, 1998, NAT GENET, V19, P15, DOI 10.1038/ng0598-15 Rougeulle C, 1997, NAT GENET, V17, P14, DOI 10.1038/ng0997-14 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P19 Salmon B, 1999, AM J MED GENET, V88, P551, DOI 10.1002/(SICI)1096-8628(19991015)88:5<551::AID-AJMG21>3.0.CO;2-# Sambrook J., 1989, MOL CLONING LAB MANU 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 Smalley SL, 1998, J AUTISM DEV DISORD, V28, P407, DOI 10.1023/A:1026052421693 Veenstra-VanderWeele J, 1999, MOL PSYCHIATR, V4, P64, DOI 10.1038/sj.mp.4000472 Vu TH, 1997, NAT GENET, V17, P12, DOI 10.1038/ng0997-12 WILLIAMS CA, 1995, AM J MED GENET, V56, P237, DOI 10.1002/ajmg.1320560224 NR 47 TC 92 Z9 95 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD SEP PY 2001 VL 77 IS 1-2 BP 105 EP 113 DI 10.1006/geno.2001.6617 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 469GU UT WOS:000170806800016 PM 11543639 ER PT J AU McGregor, E AF McGregor, E TI Teaching children with autism to mind-read: A practical guide. SO INFANT AND CHILD DEVELOPMENT LA English DT Book Review C1 Univ Dundee, Dundee DD1 4HN, Scotland. RP McGregor, E (reprint author), Univ Dundee, Dundee DD1 4HN, Scotland. CR Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 Howlin P., 1999, TEACHING CHILDREN AU NR 2 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD SEP PY 2001 VL 10 IS 3 BP 151 EP 152 DI 10.1002/icd.237 PG 2 WC Psychology, Developmental SC Psychology GA 476CY UT WOS:000171209700006 ER PT J AU Dozier, CL Carr, JE Enloe, K Landaburu, H Eastridge, D Kellum, KK AF Dozier, CL Carr, JE Enloe, K Landaburu, H Eastridge, D Kellum, KK TI Using fixed-time schedules to maintain behavior: A preliminary investigation SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE fixed-time schedules; schedule density; maintenance; noncontingent reinforcement AB The purpose of this study was to evaluate the potential of fixed-time (FT) schedules to maintain behavior. Two children who had been diagnosed with autism were taught a functional task. Subsequently, three different FT schedules (i.e., yoked, thin, dense) were compared to determine their capacity to maintain task responding. Results suggested that FT schedules may be used to maintain previously acquired behavior. C1 Univ Nevada, Reno, NV 89557 USA. RP Dozier, CL (reprint author), Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. CR Carr JE, 2000, J APPL BEHAV ANAL, V33, P353, DOI 10.1901/jaba.2000.33-353 Carr JE, 1998, J APPL BEHAV ANAL, V31, P313, DOI 10.1901/jaba.1998.31-313 Ringdahl JE, 2001, J APPL BEHAV ANAL, V34, P1, DOI 10.1901/jaba.2001.34-1 VOLLMER TR, 1997, J APPL BEHAV ANAL, V32, P119 NR 4 TC 7 Z9 7 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD FAL PY 2001 VL 34 IS 3 BP 337 EP 340 DI 10.1901/jaba.2001.34-337 PG 4 WC Psychology, Clinical SC Psychology GA 481DB UT WOS:000171503700006 PM 11678529 ER PT J AU Hellings, JA Zarcone, JR Crandall, K Wallace, D Schroeder, SR AF Hellings, JA Zarcone, JR Crandall, K Wallace, D Schroeder, SR TI Weight gain in a controlled study of risperidone in children, adolescents and adults with mental retardation and autism SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PRADER-WILLI-SYNDROME; DOUBLE-BLIND; BODY-WEIGHT; SEROTONIN; STEATOHEPATITIS; DISORDER AB As part of an ongoing, prospective, ABA design, double-blind crossover study of risperidone versus placebo for the treatment of aggressive, destructive and self-injurious behavior in persons aged 6-65 years with mental retardation (MR) and autism, we measured the weight of 19 subjects at each study visit. We compared mean weight gain during the 16-week acute phase and 24-week open maintenance phase with that during the initial and middle placebo phases statistically, using a linear mixed model procedure. Results of the linear mixed model analysis showed that relative weight gain observed during the acute and maintenance drug phases was significantly greater than that observed during the initial and middle placebo phases respectively (p = .0001 and p = .0001). Over approximately a year, children aged 8-12 (n = 5) gained a mean of 8.2 kg (range = 2.7-17.7 kg); adolescents (n = 6) aged 13-16 gained a mean of 8.4 kg (range 3.6-15.5 kg); adults aged 21-51 (n = 8) gained a mean of 5.4 kg (range 0-9.5 kg). Weight gain observed in this controlled study of risperidone treatment in children, adolescents, and adults with MR and autism was significant. It may be greater in this population than in others reported and in this study was not limited to an acute effect only. Rate of weight gain diminished rapidly on tapering and stopping the drug. Further studies are urgently needed, including those incorporating diet and exercise programming. C1 Univ Kansas, Med Ctr, Dept Psychiat & Behav Sci, Kansas City, KS 66160 USA. Univ Kansas, Schiefelbusch Inst Life Span Studies, Lawrence, KS USA. RP Hellings, JA (reprint author), Univ Kansas, Med Ctr, Dept Psychiat & Behav Sci, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR Allison DB, 1999, AM J PSYCHIAT, V156, P1686 Aman M. G., 1999, 46 ANN M AM AC CHILD American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson G. 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Child Adolesc. Psychopharmacol. PD FAL PY 2001 VL 11 IS 3 BP 229 EP 238 DI 10.1089/10445460152595559 PG 10 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 478NF UT WOS:000171351700003 PM 11642473 ER PT J AU Posey, DJ Guenin, KD Kohn, AE Swiezy, NB McDougle, CJ AF Posey, DJ Guenin, KD Kohn, AE Swiezy, NB McDougle, CJ TI A naturalistic open-label study of mirtazapine in autistic and other pervasive developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DOUBLE-BLIND; FLUOXETINE TREATMENT; BEHAVIORAL SYMPTOMS; MAJOR DEPRESSION; ADULTS; CHILDREN; HALOPERIDOL; PLACEBO; RISPERIDONE; FENFLURAMINE AB Objective: The aim of this study was to conduct a naturalistic, open-label examination of the efficacy and tolerability of mirtazapine (a medication with both serotonergic and noradrenergic properties) in the treatment of associated symptoms of autism and other pervasive developmental disorders (PDDs). Methods: Twenty-six subjects (5 females, 21 males; ages 3.8 to 23.5 years; mean age 10.1 +/- 4.8 years) with PDDs (20 with autistic disorder, 1 with Asperger's disorder, 1 with Rett's disorder, and 4 with PDDs not otherwise specified were treated with open-label mirtazapine (dose range, 7.5-45 mg daily; mean 30.3 +/- 12.6 mg daily). Twenty had comorbid mental retardation, and 17 were taking concomitant psychotropic medications. At endpoint, subjects' primary caregivers were interviewed using the Clinical Global Impressions (CGI) scale, the Aberrant Behavior Checklist, and a side-effect checklist. Results: Twenty-five of 26 subjects completed at least 4 weeks of treatment (mean 150 +/- 103 days). Nine of 26 subjects (34.6%) were judged responders ("much improved" or "very much improved" on the CGI) based on improvement in a variety of symptoms including aggression, self-injury, irritability, hyperactivity, anxiety, depression, and insomnia. Mirtazapine did not improve core symptoms of social or communication impairment. Adverse effects were minimal and included increased appetite, irritability, and transient sedation. Conclusions: Mirtazapine was well tolerated but showed only modest effectiveness for treating the associated symptoms of autistic disorder and other PDDs. C1 Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, Indianapolis, IN USA. RP McDougle, CJ (reprint author), James Whitcomb Riley Hosp Children, 702 Barnhill Dr,Room 3701, Indianapolis, IN 46202 USA. 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Child Psychol. Psychiatry PD SEP PY 2001 VL 42 IS 6 BP 705 EP 717 DI 10.1111/1469-7610.00767 PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 473RH UT WOS:000171061500002 PM 11583243 ER PT J AU Farran, EK Jarrold, C Gathercole, SE AF Farran, EK Jarrold, C Gathercole, SE TI Block design performance in the Williams syndrome phenotype: A problem with mental imagery? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE visuospatial functioning; Williams syndrome ID INFANTILE HYPERCALCEMIA; ORGANIZATION; INDIVIDUALS; ABILITIES; CHILDREN; AUTISM AB Williams syndrome (WS) is a rare genetic disorder which, among other characteristics, has a distinctive cognitive profile. Nonverbal abilities are generally poor in relation to verbal abilities, but also show varying levels of ability in relation to each other. Performance on block construction tasks represents arguably the weakest nonverbal ability in WS. In this study we examined two requirements of block construction tasks in 21 individuals with WS and 21 typically developing (TD) control individuals. The Squares tasks, a novel two-dimensional block construction task, manipulated patterns by segmentation and perceptual cohesiveness to investigate the first factor, processing preference (local or global), and by obliqueness to examine the second factor, the ability to use mental imagery. These two factors were investigated directly by the Children's Embeded Figures Test (CEFT; Witkin, Oltman, Raskin, & Karp, 1971) and a mental rotation task respectively. Results showed that individuals with WS did not differ from the TD group in their processing style. However, the ability to use mental imagery was significantly poorer in the WS group than the TD group. This suggests that weak performance on the block construction tasks in WS may relate to an inability to use mental imagery. 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F., 1971, CHILDRENS EMBEDDED F NR 31 TC 60 Z9 61 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-9863 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD SEP PY 2001 VL 42 IS 6 BP 719 EP 728 DI 10.1111/1469-7610.00768 PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 473RH UT WOS:000171061500003 PM 11583244 ER PT J AU Kerbeshian, J Burd, L Avery, K AF Kerbeshian, J Burd, L Avery, K TI Pharmacotherapy of autism: A review and clinical approach SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Review DE autism; treatment; psychopharmacology; children; comorbidity; pervasive developmental disorders ID PERVASIVE DEVELOPMENTAL DISORDER; GROUP HOME RESIDENTS; MENTAL-RETARDATION; DOUBLE-BLIND; TOURETTES-SYNDROME; YOUNG-CHILDREN; DRUG-USE; TRICYCLIC ANTIDEPRESSANTS; FLUOXETINE TREATMENT; BEHAVIORAL SYMPTOMS AB Although there is a proliferating literature on the pharmacotherapy of autism, the results of these studies are often conflicting. A definitive medical intervention for the cove symptoms of autism 12 continues to elude us. In the absence of a definitive research-based pathway for the pharmacotherapeutic treatment of autism, our approach is necessarily clinically based and research informed. Common medication side effects also may confound the clinical picture. A major factor in the application of our approach is an awareness of conditions comorbid with autism in an individual patient. These comorbid conditions then serve as a guide in choice of specific drug therapies. Use of medication must be guided by an awareness of habilitative, behavioral, social, administrative, and ethical issues. C1 Univ N Dakota, Dept Neurosci, Sch Med & Hlth Sci, Grand Forks, ND 58201 USA. Univ N Dakota, Dept Pediat, Sch Med & Hlth Sci, Grand Forks, ND 58201 USA. RP Burd, L (reprint author), CETP, 1300 S Columbia Rd, Grand Forks, ND 58201 USA. 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RP Matthews, B (reprint author), Flinders Univ S Australia, Sch Special Educ & Disabil Studies, Adelaide, SA 5001, Australia. CR Lawson W., 1998, LIFE GLASS PERSONAL NR 1 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD SEP PY 2001 VL 26 IS 3 BP 275 EP 275 PG 1 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 463XL UT WOS:000170502500007 ER PT J AU Chauhan, VPS Chauhan, A Cohen, I Brown, WT AF Chauhan, VPS Chauhan, A Cohen, I Brown, WT TI Altered membrane fluidity in autism SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 New York State Inst Basic Res Dev Disabil, Staten Isl, NY 10314 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD SEP PY 2001 VL 78 SU 1 BP 19 EP 19 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 469AF UT WOS:000170789800063 ER PT J AU Bolton, PF Roobol, M Allsopp, L Pickles, A AF Bolton, PF Roobol, M Allsopp, L Pickles, A TI Association between idiopathic infantile macrocephaly and autism spectrum disorders SO LANCET LA English DT Article AB We conducted a case-controlled, catch-up study of a cohort of boys born with macrocephaly in order to determine whether infantile macrocephaly is a risk marker for the later development of autism spectrum disorders, Our results show that Infantile macrocephaly was associated with an increased risk of developing autism spectrum disorders (odds ratio 5.44, 95% CI 1.11-52.15; p=0.03). These findings suggest that neurobiological differences during infancy may predict behavioural manifestations of autism spectrum disorders. C1 Univ Cambridge, Autism Res Ctr, Cambridge CB2 2AH, England. Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ Manchester, Sch Epidemiol & Hlth Sci, Manchester, Lancs, England. Univ Manchester, Ctr Census & Survey Res, Manchester, Lancs, England. RP Bolton, PF (reprint author), Univ Cambridge, Autism Res Ctr, Cambridge CB2 2AH, England. RI Pickles, Andrew/A-9625-2011; Bolton, Patrick/E-8501-2010 OI Pickles, Andrew/0000-0003-1283-0346; Bolton, Patrick/0000-0002-5270-6262 CR Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 MORGAN M, 1983, J EPIDEMIOL COMMUN H, V37, P196, DOI 10.1136/jech.37.3.196 NR 5 TC 30 Z9 31 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD SEP 1 PY 2001 VL 358 IS 9283 BP 726 EP 727 DI 10.1016/S0140-6736(01)05903-7 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 467XR UT WOS:000170729500015 PM 11551582 ER PT J AU DeStefano, F AF DeStefano, F TI Vaccines and autism SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Editorial Material ID INFLAMMATORY-BOWEL-DISEASE; MEASLES-VIRUS; CHILDREN C1 Ctr Dis Control & Prevent, Atlanta, GA 30333 USA. 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Infect. Dis. J. PD SEP PY 2001 VL 20 IS 9 BP 887 EP 888 DI 10.1097/00006454-200109000-00013 PG 2 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA 472CW UT WOS:000170966500012 PM 11734770 ER PT J AU Di Martino, A Tuchman, RF AF Di Martino, A Tuchman, RF TI Antiepileptic drugs: Affective use in autism spectrum disorders SO PEDIATRIC NEUROLOGY LA English DT Review ID GAMMA-AMINOBUTYRIC-ACID; PERVASIVE DEVELOPMENTAL DISORDER; FOCAL INTERICTAL SPIKES; EPILEPSY-PRONE RATS; INFANTILE-AUTISM; VALPROIC ACID; PLASMA GABA; ANTICONVULSANT DRUGS; NEUROPSYCHIATRIC DISORDERS; SEROTONIN CONCENTRATION AB Antiepileptic drugs are widely administered to individuals with autistic spectrum disorders. There are several reasons for the use of antiepileptic drugs in autistic spectrum disorders, including the high incidence of epilepsy in these individuals, the anecdotal reports suggesting an improvement of communication and behavior in autistic subjects with epileptic discharges, and the increased awareness that some disruptive behaviors may be manifestations of an associated affective disorder. In this study, data on the current use of antiepileptic drugs in the treatment of autism, and on the association of affective disorders with epilepsy and autism, are reviewed. The evidence supporting the hypothesis that there may be a subgroup of autistic children with epilepsy and affective disorders that preferentially respond to antiepileptic drugs is still very preliminary, and further investigations with double-blind controlled studies are needed. 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Neurol. PD SEP PY 2001 VL 25 IS 3 BP 199 EP 207 DI 10.1016/S0887-8994(01)00276-4 PG 9 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 482VU UT WOS:000171598600002 PM 11587873 ER PT J AU Schneider, T Labuz, D Przewlocki, R AF Schneider, T Labuz, D Przewlocki, R TI Nociceptive changes in rats after prenatal exposure to valproic acid SO POLISH JOURNAL OF PHARMACOLOGY LA English DT Article DE animal model; autism; nociception; valproic acid ID INFANTILE-AUTISM; BRAIN-STEM; RECEPTORS; NEURONS; BEHAVIOR AB Abnormalities in anatomy and function of the cranial nerve, motor nuclei and brain stem structures have been demonstrated in some people with autism and can be modeled in rats by exposure to valproic acid (VPA) during very early nervous system developmental stages (neural tube closure). The aim of this study was to investigate if VPA will have an impact on nociception in rats because of reported hypoalgesia in a subgroup of autistic patients. Pregnant females were treated ip with 600 mg/kg of sodium valproate on day 12.5 of gestation. Nociception was measured in offsprings by tail-flick and thermal paw withdrawal tests in two developmental stages: prepubertal (80-90 g) and adulthood (360-440 g). Results showed significant differences in pain sensitivity with hypoalgesia in male rats treated with VPA compared to male control in both developmental stages. The outcome of our study suggests that rats exposed prenatally to VPA show abnormalities in nociception similar to those observed in human autistic patients. Interestingly, naloxone (1 mg/kg) had no impact on nociception in offsprings of VPA-treated rats. C1 Jagiellonian Univ, Inst Appl Psychol, PL-31056 Krakow, Poland. Polish Acad Sci, Inst Pharmacol, Dept Mol Neuropharmacol, PL-31343 Krakow, Poland. 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PD SEP-OCT PY 2001 VL 53 IS 5 BP 531 EP 534 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 506CB UT WOS:000172951400015 PM 11990073 ER PT J AU Bodier, C Lenoir, P Malvy, J Barthelemy, C Wiss, M Sauvage, D AF Bodier, C Lenoir, P Malvy, J Barthelemy, C Wiss, M Sauvage, D TI Autism-related diseases: clinical analysis of 295 children with major development disorders SO PRESSE MEDICALE LA French DT Article ID INFANTILE-AUTISM; MEDICAL CONDITIONS; EPIDEMIOLOGY AB OBJECTIVE: Known since the first descriptions in 1943, diseases related to autism and associated disorders have incited a growing body of work. Both theoretical interrogations (what is the pathogenic role of autism?) and practical measures (management, screening) are implied. Nevertheless the frequency of autism-related disease has varied from 10 to 37% depending on the series reported. We studied the frequency of these factors in a population of children with major development disorders cared for at the Tours university hospital over a 39-month period. PATIENTS AND METHODS: We reviewed retrospectively the medial features of 295 children examined in our psychiatrics and neurophysiology unit for children at the Tours center for major development disorders (based on the DSM IV diagnostic criteria) between September 1995 and December 1998. We divided these factors into 4 categories: hereditary diseases, serious medical conditions, minimal physical disorders and ante-or perinatal antecedents. RESULTS: Among these 295 children, 26.5% had a proven or probable hereditary disease, 19% had a serious medical condition and 21.7% had minimal physical disorders. Among the children with a serious medical condition, 34.4% also had ante- or perinatal antecedents. Among the 33% without any medical factor, 77% also had ante- or perinatal antecedents. CONCLUSION: Our data point out the quantitative importance of medical factors associated with major development disorders. They imply a close pluridisciplinary collaboration between child psychiatrists, pediatricians and geneticians in order to identify these disorders and develop an integrated management scheme. On a more theoretical level, it appears possible to identify subgroups of children among such a population based on associated diseases and neuropsychological patterns. This dimension would be useful for research into the pathogenic mechanisms involved. C1 CHRU, Serv Univ Pedopsychiat, Tours, France. CHRU, Ctr Ressources Autisme, Tours, France. CHRU, Serv Univ Explorat Fonct & Neurophysiol Pedopsych, Unite INSERM 316, Tours, France. RP Bodier, C (reprint author), Hop Bretonneau, Serv Univ Pedopsychiat, F-37044 Tours 1, France. 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PD SEP 1 PY 2001 VL 30 IS 24 BP 1199 EP 1203 PN 1 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 472MY UT WOS:000170989000003 PM 11577595 ER PT J AU Arnold, OR Butoya, EL AF Arnold, OR Butoya, EL TI Psychological effects of delphinine therapy SO PSIKHOLOGICHESKII ZHURNAL LA Russian DT Article DE delphinine therapy; psychotherapy; Luscher Farbwahl Test AB The delphinine therapy is a relatively new approach in alternative medicine and psychotherapy which is mostly effective in children suffered from cerebral palsy, Down syndrome and autism. The review of foreign researches on delphinine therapy is made and results of the authors work in the "Utrishsky dolphinarium" (Moscow) are presented. C1 Inst Personal Dev, Moscow, Russia. Small Enterprise Utrishsky Dolphinarium, Moscow, Russia. RP Arnold, OR (reprint author), Inst Personal Dev, Moscow, Russia. NR 0 TC 0 Z9 0 PU MEZHDUNARODNAYA KNIGA PI MOSCOW PA 39 DIMITROVA UL., 113095 MOSCOW, RUSSIA SN 0205-9592 J9 PSIKHOL ZH JI Psikhologicheskii Zhurnal PD SEP-OCT PY 2001 VL 22 IS 5 BP 98 EP 102 PG 5 WC Psychology, Multidisciplinary SC Psychology GA 496KE UT WOS:000172394100010 ER PT J AU Geller, JL AF Geller, JL TI Exiting Nirvana: A daughter's life with autism SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Univ Massachusetts, Sch Med, Worcester, MA USA. RP Geller, JL (reprint author), Univ Massachusetts, Sch Med, Worcester, MA USA. CR Park C.C., 2001, EXITING NIRVANA DAUG NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD SEP PY 2001 VL 52 IS 9 BP 1259 EP 1260 DI 10.1176/appi.ps.52.9.1259 PG 2 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 468XF UT WOS:000170782900031 ER PT J AU Kauffmann, C Vance, H Pumariega, AJ Miller, B AF Kauffmann, C Vance, H Pumariega, AJ Miller, B TI Fluvoxamine treatment of a child with severe PDD: A single case study SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISTIC DISORDER; MENTAL-RETARDATION; ADULTS; SERTRALINE AB Recent reports suggest that selective serotonin reuptake inhibitors (SSRIs) are useful in the treatment of individuals with autism and other pervasive developmental disorders. We report on a single case study of the use of fluvoxamine with a 7-year-old Caucasian girl with severe pervasive developmental disorder. Our findings indicate that fluvoxamine was significantly effective in reducing stereotypical, repetitive behaviors, anxiety, and aggression and in improving prelinguistic and social behaviors. Our results indicate that the use of the SSRIs as a platform for the longterm habilitation of these children should be considered, but further studies are required to establish the efficiency of fluvoxamine for the treatment of children with autism. C1 E Tennessee State Univ, James H Quillen Coll Med, Dept Psychiat & Behav Sci, Johnson City, TN 37614 USA. E Tennessee State Univ, James H Quillen Coll Med, Psychiat Res Lab, Johnson City, TN 37614 USA. RP Vance, H (reprint author), E Tennessee State Univ, James H Quillen Coll Med, Dept Psychiat & Behav Sci, 107 Hillrise Hall,POB 70567, Johnson City, TN 37614 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barlow D. H., 1984, SCI PRACTITIONER RES BORDENS KS, 1991, RES DESIGN METHODS P Cook Edwin H. 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Biol. Process. PD FAL PY 2001 VL 64 IS 3 BP 268 EP 277 DI 10.1521/psyc.64.3.268.18456 PG 10 WC Psychiatry SC Psychiatry GA 489RW UT WOS:000172006300013 PM 11708052 ER PT J AU Hogg, J Cavet, J Lambe, L Smeddle, M AF Hogg, J Cavet, J Lambe, L Smeddle, M TI The use of 'Snoezelen' as multisensory stimulation with people with intellectual disabilities: a review of the research SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article AB The past 15 years have seen a marked increase in the use of Snoezelen with a wide range of groups including people with intellectual disabilities. Research has been undertaken with respect to a variety of behaviors, notably changes in affect, challenging behavior, relaxation and interactions with both other persons and objects. Typically studies have adopted an applied behavior analysis approach, with a small number employing physiological measures. Research designs vary markedly in their technical adequacy and the participants have a wide range of intellectual disability, age, and additional characteristics such as autism. Much of the literature reviewed demonstrates a wide range of positive outcomes when Snoezelen Vs non-Snoezelen environments are contrasted, though there is little evidence of generalisation even to the immediate post-Snoezelen environment. Several studies, however, do yield entirely negative outcomes. It is difficult to attribute these differing outcomes to either participant characteristics or contrasted designs, given the diversity of approaches to evaluation and the relatively small number of studies. The review also addresses the issue of staff and carer attitudes and the place of Snoezelen in facilitating positive interactions, incidental to any specific sensory effects. 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Dev. Disabil. PD SEP-OCT PY 2001 VL 22 IS 5 BP 353 EP 372 DI 10.1016/S0891-4222(01)00077-4 PG 20 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 475GD UT WOS:000171153200002 PM 11580163 ER PT J AU Luiselli, JK Campbell, S Cannon, B DiPietro, E Ellis, JT Taras, M Lifter, K AF Luiselli, JK Campbell, S Cannon, B DiPietro, E Ellis, JT Taras, M Lifter, K TI Assessment instruments used in the education and treatment of persons with autism: brief report of a survey of national service centers SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article AB Although assessment is a critical component in the education and treatment of persons who have autism, there is insufficient information about the types of assessment instruments that are used routinely by practitioners. This brief report describes a survey of national service centers to determine their use of standardized instruments and the purposes of their assessment practices. Data from centers representing 30 states revealed that (a) the number of assessment instruments endorsed by centers increased as centers adopted a "multidisciplinary" approach to education and treatment, (b) the largest proportion of instruments fell within intellectual, motor, and language/communication domains, and (c) instruments were used most frequently for diagnostic and curriculum design purposes. Agreement among practitioners on the selection of instruments occurred most frequently in the domains of projective, adaptive behavior, and family assessment. The implications from these findings for assessment practices in autism are discussed. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 May Inst, Norwood, MA 02062 USA. May Ctr Appl Res, Norwood, MA 02062 USA. Northeastern Univ, Boston, MA 02116 USA. RP Luiselli, JK (reprint author), May Inst, Norwood, MA 02062 USA. CR ESTEBAN SE, 1998, UNPUB DIAGNOSTIC ASS MARCUS LM, 1993, HDB CHILD ADOLESCENT, P346 Ollendick T. H., 1993, HDB CHILD ADOLESCENT, P3 RUTTER M, 1988, ASSESSMENT DIAGNOSIS, P408 NR 4 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 SEP-OCT PY 2001 VL 22 IS 5 BP 389 EP 398 DI 10.1016/S0891-4222(01)00079-8 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 475GD UT WOS:000171153200004 PM 11580165 ER PT J AU Jahr, E AF Jahr, E TI Teaching children with autism to answer novel wh-questions by utilizing a multiple exemplar strategy SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article ID BEHAVIORAL TREATMENT; MAINTENANCE; SKILLS AB This study investigated the transfer and maintenance of question-answering skills in five children diagnosed with autism. A multiple baseline design across classes of questions (i.e., what, where, who and why) was applied for each child. Question-answer exemplars were selected within each class, and each class was trained separately in consecutive order. The dependent variable was the proportion of appropriate answers (i.e., complete sentences) to novel questions within each class, on first trial. The results showed that all children became able to answer novel questions with complete sentences within each of the classes that were trained, and they showed transfer of these skills across persons, settings and time. The findings support the use of analogous question-answer exemplars in order to facilitate response-transfer to novel questions. It is also suggested that this type of transfer is more likely to occur if the answers trained are in full sentence and there is a structural correspondence between the question and the answer in each single exemplar and across exemplars within a class of questions. (C) 2001 Elsevier Science Ltd. All ri-hts reserved. C1 Akershus Cent Hosp, Nordbyhagen, Norway. RP Jahr, E (reprint author), Akershus Cent Hosp, Nordbyhagen, Norway. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BALTAXE CA, 1981, SPEECH EVALUATION PS, P285 BLOM L, 1978, LANGUAGE DEV LANGUAG BOE R, 1978, J EXP ANAL BEHAV, V30, P213, DOI 10.1901/jeab.1978.30-213 BOE R, 1978, J GEN PSYCHOL, V99, P299 BROWN R, 1968, J VERB LEARN VERB BE, V7, P279, DOI 10.1016/S0022-5371(68)80002-7 BROWN WH, 1994, RES DEV DISABIL, V15, P99, DOI 10.1016/0891-4222(94)90016-7 Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 CURCIO F, 1987, J AUTISM DEV DISORD, V17, P81, DOI 10.1007/BF01487261 DUCHARME JM, 1992, J APPL BEHAV ANAL, V25, P166 Horner R. 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PD SEP-OCT PY 2001 VL 22 IS 5 BP 407 EP 423 DI 10.1016/S0891-4222(01)00081-6 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 475GD UT WOS:000171153200006 PM 11580167 ER PT J AU Zavala, M Castejon, HV Ortega, PA Castejon, OJ de Hidalgo, AM Montiel, N AF Zavala, M Castejon, HV Ortega, PA Castejon, OJ de Hidalgo, AM Montiel, N TI Imbalance of plasma amino acids inpatients with autism and subjects with attention deficit/hyperactivity disorder SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE attention-deficit/hyperactivity disorder; autism; plasma amino acids ID DEFICIT HYPERACTIVITY DISORDER; BLOOD-BRAIN-BARRIER; LIQUID-CHROMATOGRAPHY; HYPERKINETIC DISORDER; TRYPTOPHAN; OXIDATION; REQUIREMENTS; TRANSPORT; LIVER; SERUM AB Introduction. Plasma and brain amino acids are influenced by dietary intake. Alterations of plasma amino acid concentrations have been reported in neuropsychiatric disorders. Objective. To analyse the plasma amino acid values in subject diagnosed with autism, with attention-deficit/hyperactivity disorder (ADHD), and healthy subjects as controls. Patients and methods. Forty subjects affected by autism, 11 with ADHD and 41 healthy subjects (age range 3-18 years old) were included in this study. Peripheral venous blood was obtained in fasting condition, collected in EDTA tubes and centrifuged. Plasma was de-proteinised with sulfosalicylic acid. Amino acids were analysed by ion exchange liquid chromatography with an LKB amino acid analyser with sodium citrate elution system and ninhydrin reaction. Results were expressed as mu mol/L. Results and conclusions. In both disorders a diminution of phenylalanine and glutamine plasma concentrations was observed beside an increase of glycine. Lysine appeared increased only in autistic subjects. These alterations produce an imbalance with the rest of plasma amino acids competing at the brain-blood barrier by the same transport system thus causing alterations in the metabolism and/or transport of amino acids to the brain, altering CNS functions. The phenylalanine decreasing, beside glycine increasing appear to support the hypothesis of a disorder in the inhibitory neurotransmission system, especially in ADHD. The diminution of phenylalanine and the increasing of lysine in autism are suggestive that these two amino acids are metabolically related. C1 Univ Zulia, Inst Invest Biol, Lab Psiquiatria Biol, Fac Med, Maracaibo 4011, Venezuela. Univ Zulia, Fac Ciencias Expt, Lab Metodos Inmunol, Maracaibo 4011, Venezuela. 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PD FAL PY 2001 VL 65 IS 3 BP 278 EP 281 PG 4 WC Social Sciences, Interdisciplinary SC Social Sciences - Other Topics GA 476TL UT WOS:000171244800002 ER PT J AU [Anonymous] AF [Anonymous] TI Editorial perspectives - Of people, curves, and autism SO SCIENCE & SOCIETY LA English DT Editorial Material NR 0 TC 0 Z9 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 USA SN 0036-8237 J9 SCI SOC JI Sci. Soc. PD FAL PY 2001 VL 65 IS 3 BP 284 EP 285 PG 2 WC Social Sciences, Interdisciplinary SC Social Sciences - Other Topics GA 476TL UT WOS:000171244800003 ER PT J AU Mahoney, G AF Mahoney, G TI Autism spectrum disorders: A transactional developmental perspective SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Book Review C1 Case Western Reserve Univ, Mendel Sch Appl Social Sci, Cleveland, OH 44106 USA. RP Mahoney, G (reprint author), Case Western Reserve Univ, Mendel Sch Appl Social Sci, Cleveland, OH 44106 USA. 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Med. J. PD SEP PY 2001 VL 50 IS 3 BP 251 EP 253 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 500DG UT WOS:000172610200023 ER PT J AU Grice, SJ Spratling, MW Karmiloff-Smith, A Halit, H Csibra, G de Haan, M Johnson, MH AF Grice, SJ Spratling, MW Karmiloff-Smith, A Halit, H Csibra, G de Haan, M Johnson, MH TI Disordered visual processing and oscillatory brain activity in autism and Williams Syndrome SO NEUROREPORT LA English DT Article DE autism; binding; EEG; ERP; face processing; gamma; visual perception; Williams Syndrome ID RESPONSES; FACES AB Two developmental disorders, autism and Williams syndrome, are both commonly described as having difficulties in integrating perceptual features, i.e. binding spatially separate elements into a whole. It is already known that healthy adults and infants display electroencephalographic (EEG) gamma -band bursts (around 40 Hz) when the brain is required to achieve such binding. Here we explore gamma -band EEG in autism and Williams Syndrome and demonstrate differential abnormalities in the two phenotypes. We show that despite putative processing similarities at the cognitive level, binding in Williams syndrome and autism can be dissociated at the neurophysiological level by different abnormalities in underlying brain oscillatory activity. Our study is the first to identify that binding-related gamma EEG can be disordered in humans. NeuroReport 12:2697-2700 (C) 2001 Lippincott Williams & Wilkins. C1 Univ London Birkbeck Coll, Sch Psychol, Ctr Brain & Cognit Dev, London WC1E 7HX, England. Inst Child Hlth, Neurocogn Dev Unit, London WC1N 1EH, England. Inst Child Hlth, Dev Cognit Neurosci Unit, London WC1N 1EH, England. RP Johnson, MH (reprint author), Univ London Birkbeck Coll, Sch Psychol, Ctr Brain & Cognit Dev, London WC1E 7HX, England. RI Spratling, Michael/G-7689-2011; Csibra, Gergely/C-4345-2008 OI Spratling, Michael/0000-0001-9531-2813; Csibra, Gergely/0000-0002-7044-3056 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 Csibra G, 2000, SCIENCE, V290, P1582, DOI 10.1126/science.290.5496.1582 Deruelle C, 1999, BRAIN COGNITION, V41, P276, DOI 10.1006/brcg.1999.1127 Farah M.J, 2000, COGNITIVE NEUROSCIEN Frith U., 1989, AUTISM EXPLAINING EN GALABURDA AM, 2000, J COGNITIVE NEUROSCI, V12, P47 Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Herrmann CS, 1999, CLIN NEUROPHYSIOL, V110, P636, DOI 10.1016/S1388-2457(99)00002-4 HOBSON RP, 1988, BRIT J PSYCHOL, V79, P441 Karmiloff-Smith A, 1998, TRENDS COGN SCI, V2, P389, DOI 10.1016/S1364-6613(98)01230-3 Muller MM, 1996, EXP BRAIN RES, V112, P96 Rae C, 1998, NEUROLOGY, V51, P33 RODRIGUEZ E, 1999, NATURE, V397, P429 SINGER W, 1995, ANNU REV NEUROSCI, V18, P555, DOI 10.1146/annurev.neuro.18.1.555 TallonBaudry C, 1996, J NEUROSCI, V16, P4240 TANTAM D, 1989, J CHILD PSYCHOL PSYC, V30, P623, DOI 10.1111/j.1469-7610.1989.tb00274.x VALENTINE T, 1988, BRIT J PSYCHOL, V79, P471 NR 17 TC 167 Z9 169 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD AUG 28 PY 2001 VL 12 IS 12 BP 2697 EP 2700 DI 10.1097/00001756-200108280-00021 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 465QB UT WOS:000170600500021 PM 11522950 ER PT J AU Gross, M AF Gross, M TI Balancing interests in autism study SO CURRENT BIOLOGY LA English DT Editorial Material C1 Oxford Ctr Mol Sci, Oxford, England. RP Gross, M (reprint author), Oxford Ctr Mol Sci, Oxford, England. NR 0 TC 0 Z9 0 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTES AVE,, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD AUG 21 PY 2001 VL 11 IS 16 BP R630 EP R630 DI 10.1016/S0960-9822(01)00375-X PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 466GE UT WOS:000170636100002 PM 11525749 ER PT J AU Goffin, A Hoefsloot, LH Bosgoed, E Swillen, A Fryns, JP AF Goffin, A Hoefsloot, LH Bosgoed, E Swillen, A Fryns, JP TI PTEN mutation in a family with Cowden syndrome and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE PTEN mutation; Cowden syndrome; autism; multiple hamartoma syndrome ID RILEY-RUVALCABA-SYNDROME; GERMLINE MUTATIONS; DISEASE; DISORDERS; GENE; DUPLICATION; PHENOTYPE; PATIENT; ENTITY AB We report on a mother and son with Cowden syndrome and a PTEN mutation. The boy also exhibits autistic behavior and mental retardation, while his mother has a normal intelligence and social interaction pattern. We review the scanty literature data on the association of Cowden syndrome and autism and emphasize that the association of progressive macrocephaly and pervasive developmental disorder seems to be an indication for screening for PTEN mutations. (C) 2001 Wiley-Liss, Inc. C1 Catholic Univ Louvain, Ctr Human Genet, B-3000 Louvain, Belgium. Univ Nijmegen, Med Ctr, Dept Human Genet, Nijmegen, Netherlands. RP Fryns, JP (reprint author), Catholic Univ Louvain, Ctr Human Genet, Herestr 49, B-3000 Louvain, Belgium. 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PD AUG 8 PY 2001 VL 105 IS 6 BP 521 EP 524 DI 10.1002/ajmg.1477 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 459HG UT WOS:000170244500007 PM 11496368 ER PT J AU Bradford, Y Haines, J Hutcheson, H Gardiner, M Braun, T Sheffield, V Cassavant, T Huang, W Wang, K Vieland, V Folstein, S Santangelo, S Piven, J AF Bradford, Y Haines, J Hutcheson, H Gardiner, M Braun, T Sheffield, V Cassavant, T Huang, W Wang, K Vieland, V Folstein, S Santangelo, S Piven, J TI Incorporating language phenotypes strengthens evidence of linkage to autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article 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. C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA. Univ Iowa, Dept Elect & Comp Engn, Iowa City, IA 52242 USA. Univ Iowa, Dept Biostat, Div Stat Genet, Iowa City, IA 52242 USA. Univ Iowa, Dept Biostat & Psychiat, Div Stat Genet, Iowa City, IA 52242 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. RP Folstein, S (reprint author), Tufts Univ, New England Med Ctr, Dept Psychiat, 750 Washington St, Boston, MA 02111 USA. 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PD AUG 8 PY 2001 VL 286 IS 6 BP 671 EP 671 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 459VE UT WOS:000170271500016 ER PT J AU Farrow, TFD Zheng, Y Wilkinson, ID Spence, SA Deakin, JFW Tarrier, N Griffiths, PD Woodruff, PWR AF Farrow, TFD Zheng, Y Wilkinson, ID Spence, SA Deakin, JFW Tarrier, N Griffiths, PD Woodruff, PWR TI Investigating the functional anatomy of empathy and forgiveness SO NEUROREPORT LA English DT Article DE empathy; forgiveness; functional magnetic resonance imaging; medial prefrontal cortex; middle temporal gyrus ID CINGULATE CORTEX; MIND; AUTISM; PSYCHOLOGY; ADULTS; BRAIN AB Previous functional brain imaging studies suggest that the ability to infer the intentions and mental states of others (social cognition) is mediated by medial prefrontal cortex. Little is known about the anatomy of empathy and forgiveness. We used functional MRI to detect brain regions engaged by judging others' emotional states and the forgivability of their crimes. Ten volunteers read and made judgements based an social scenarios and a high level baseline task (social reasoning). Both empathic and forgivability judgements activated left superior frontal gyrus, orbitofrontal gyrus and precuneus. Empathic judgements also activated left anterior middle temporal and left inferior frontal gyri, while forgivability judgements activated posterior cingulate gyrus. Empathic and forgivability judgements activate specific regions of the human brain, which we propose contribute to social cohesion. NeuroReport 12:2433-2438 (C) 2001 Lippincott Williams & Wilkins. C1 Univ Sheffield, No Gen Hosp, Longley Ctr, Dept Psychiat,SCANLab, Sheffield S5 7JT, S Yorkshire, England. Univ Sheffield, No Gen Hosp, Longley Ctr, Dept Radiol, Sheffield S5 7JT, S Yorkshire, England. 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PD AUG 6 PY 2001 VL 175 IS 3 BP 127 EP 128 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 483XR UT WOS:000171661600004 PM 11548076 ER PT J AU McLellan, F AF McLellan, F TI IOM reviews evidence on thimerosal link to autism (vol 358, pg 214, 2001) SO LANCET LA English DT Correction CR McLellan F, 2001, LANCET, V358, P214, DOI 10.1016/S0140-6736(01)05451-4 NR 1 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 AUG 4 PY 2001 VL 358 IS 9279 BP 424 EP 424 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 459DE UT WOS:000170235100057 ER PT J AU Liu, JJ Nyholt, DR Magnussen, P Parano, E Pavone, P Geschwind, D Lord, C Iversen, P Hoh, J Ott, J Gilliam, TC AF Liu, JJ Nyholt, DR Magnussen, P Parano, E Pavone, P Geschwind, D Lord, C Iversen, P Hoh, J Ott, J Gilliam, TC CA Autism Genetic Resource Exchange C TI A genomewide screen for autism susceptibility loci SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SIB-PAIR LINKAGE; PERVASIVE DEVELOPMENTAL DISORDERS; GENETICALLY COMPLEX TRAITS; AFFECTED RELATIVE PAIRS; SEROTONIN TRANSPORTER; GENOMIC SCREEN; CHROMOSOME; STRATEGIES; CHILDREN; MARKERS AB We report the analysis of 335 microsatellite markers genotyped in 110 multiplex families with autism. All families include at least two "affected" siblings, at least one of whom has autism; the remaining affected sibs carry diagnoses of either Asperger syndrome or pervasive developmental disorder. Affected sib-pair analysis yielded multipoint maximum LOD scores (MLS) that reach the accepted threshold for suggestive linkage on chromosomes 5, X, and 19. Nominal evidence for linkage (point-wise) was obtained on chromosomes 2, 3, 4, 8, 10, 11, 12, 15, 16, 18, and 20, and secondary loci were found on chromosomes 5 and 19. Analysis of families sharing alleles at the putative X chromosomal linked locus and one or more other putative linked loci produced an MLS of 3.56 for the DXS470-D19S174 marker combination. In an effort to increase power to detect linkage, scan statistics were used to evaluate the significance of peak LOD scores based on statistical evidence at adjacent marker loci. 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PD AUG PY 2001 VL 69 IS 2 BP 470 EP 470 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 456XN UT WOS:000170108200024 ER PT J AU Pearce, CB Martin, H Duncan, HD Goggin, PM Poller, DN AF Pearce, CB Martin, H Duncan, HD Goggin, PM Poller, DN TI Colonic lymphoid hyperplasia in melanosis coli SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID RETT-SYNDROME AB We describe the case of a patient with Rett syndrome, a syndrome characterized by progressive infant encephalopathy, developmental delay, dementia, autism, ataxia, microcephaly, spastic paraparesis, and autonomic neuropathy with constipation. At colonoscopy, multiple foci of tiny white, sessile, polypoid lesions were seen throughout the colon and rectum, mimicking the appearances of small hyperplastic or adenomatous polyps, associated with generalized melanosis coli. This is the first case to our knowledge describing melanosis coli in a patient with Rett syndrome. 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Med. Child Neurol. PD AUG PY 2001 VL 43 IS 8 BP 529 EP 533 DI 10.1017/S0012162201000962 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 463RA UT WOS:000170490000004 PM 11508918 ER PT J AU Hook, DJ Palfreyman, MG AF Hook, DJ Palfreyman, MG TI The influence of genetics on psychiatric disease SO DRUG DISCOVERY TODAY LA English DT Review ID AUTISM SUSCEPTIBILITY GENES; CHROMOSOME 22Q12-Q13.1; POTENTIAL LINKAGE; SCHIZOPHRENIA; TWIN; EXPRESSION; DISORDERS; HISTORY AB The balance of evidence from numerous studies on psychiatric diseases and disorders suggests that for (at the least) schizophrenia, bipolar disorder, autism and unipolar depression, a significant component of these disorders can be linked to a genetic component. This article will give a broad overview of the influence of genetics on psychiatric disease, and attempt to bring in recent molecular approaches to the understanding of the effects of genetic and environmental influences on these disorders. C1 Psychiat Genom, Gaithersburg, MD 20878 USA. RP Hook, DJ (reprint author), Psychiat Genom, 19 Firstfield Rd, Gaithersburg, MD 20878 USA. 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Today PD AUG 1 PY 2001 VL 6 IS 15 SU S BP S86 EP S90 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 462LR UT WOS:000170422000006 ER PT J AU Boddaert, N Belin, P Chabanne, N Mouren-Simeoni, MC Barthelemy, C Ribeiro, MJ Samson, Y Zilbovicius, M AF Boddaert, N Belin, P Chabanne, N Mouren-Simeoni, MC Barthelemy, C Ribeiro, MJ Samson, Y Zilbovicius, M TI Temporal lobe dysfunction in autism: A PET auditory activation study SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 CEA, Serv Hosp Frederic Joliot, DSV, F-91406 Orsay, France. Hop Robert Debre, F-75019 Paris, France. CHU Bretonneau, INSERM, U316, F-37044 Tours, France. Hop La Pitie Salpetriere, Paris, France. NR 0 TC 0 Z9 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD AUG PY 2001 VL 28 IS 8 SU S MA OS285 BP 1035 EP 1035 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 464HZ UT WOS:000170528300285 ER PT J AU Torres, AR Maciulis, A Odell, D AF Torres, AR Maciulis, A Odell, D TI The association of MHC genes with autism SO FRONTIERS IN BIOSCIENCE LA English DT Review DE autism; HLA; complement; TNF; review ID TUMOR-NECROSIS-FACTOR; MAJOR HISTOCOMPATIBILITY COMPLEX; SYSTEMIC LUPUS-ERYTHEMATOSUS; C4B GENES; CLASS-II; ENDOGENOUS RETROVIRUSES; FACTOR MICROSATELLITES; RHEUMATOID-ARTHRITIS; INCREASED FREQUENCY; FACTOR TNF AB Several immune abnormalities have been noted in autistic subjects. These associations have been extended to the Major Histocompatibility Complex (MHC), a section of DNA remarkable for the number of encoded proteins with immunological functions. The strongest MHC association identified thus far is for the null allele of C4B in the class III region. The complex allelic composition of C4 as determined by immunoelectrophoresis is discussed. Low levels of C4 resulting from the null allele may be important in disease pathogenesis especially since C4 has been identified in developing brain neurons. The DNA region just telomeric to C4 has several genes including tumor necrosis factor which encode proteins with immunological functions. These proteins may act in concert with C4 in disease contribution and the genes should be more closely examined. C1 Utah State Univ, CPD, Logan, UT 84322 USA. Utah State Univ, Dept Biol, Logan, UT 84322 USA. RP Torres, AR (reprint author), Utah State Univ, CPD, 6895 Old Main Hill, Logan, UT 84322 USA. 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Biosci. PD AUG PY 2001 VL 6 BP D936 EP D943 DI 10.2741/Torres PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 460PU UT WOS:000170318400011 PM 11487481 ER PT J AU Loveland, KA Pearson, DA Tunali-Kotoski, B Ortegon, J Gibbs, MC AF Loveland, KA Pearson, DA Tunali-Kotoski, B Ortegon, J Gibbs, MC TI Judgments of social appropriateness by children and adolescents with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; social appropriateness ID PERVASIVE DEVELOPMENTAL DISORDERS; EMOTION-RECOGNITION; FACIAL EXPRESSION; DOWN-SYNDROME; MIND; COMPREHENSION; BEHAVIOR; NEUROPSYCHOLOGY; SENSITIVITY; INDIVIDUALS AB Children and adolescents with autism (autism group, n = 19) and those without autism (Nonautism group, n = 19) of similar age and IQ were asked to make judgments of the social appropriateness of 24 videotaped, staged scenes with adult actors. Each scene depicted an appropriate or an inappropriate interaction. Half contained verbalizations, and half did not. After each scene, the participant was asked: (1) Was that o.k. or was something wrong with it? If the participant judged the scene was wrong, she or he was asked: (2) What was wrong with it?; and (3) Why was that wrong? Both groups correctly identified inappropriate behaviors most of the time, and correct behaviors almost all of the time. However, the Nonautism group detected inappropriate behaviors significantly more often than the Autism group, for verbal but not nonverbal scenes. It was also significantly easier for both groups to identify inappropriate behaviors in the nonverbal than in the verbal scenes. Ratings of the explanations given for Question 3 differed significantly between the groups for verbal but not for nonverbal scenes, with Nonautism participants more likely to give explanations involving social norms and principles, and the Autism group more likely to give explanations that were irrelevant or idiosyncratic. C1 Univ Texas, Sch Med, Ctr Human Dev Res, Dept Psychiat & Behav Sci, Houston, TX 77030 USA. Texas A&M Univ, Dept Educ Psychol, College Stn, TX 77843 USA. RP Loveland, KA (reprint author), Univ Texas, Sch Med, Ctr Human Dev Res, Dept Psychiat & Behav Sci, 1300 Moursund, Houston, TX 77030 USA. 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Autism Dev. Disord. PD AUG PY 2001 VL 31 IS 4 BP 367 EP 376 DI 10.1023/A:1010608518060 PG 10 WC Psychology, Developmental SC Psychology GA 470QZ UT WOS:000170883800002 PM 11569583 ER PT J AU Bernard-Opitz, V Sriram, N Nakhoda-Sapuan, S AF Bernard-Opitz, V Sriram, N Nakhoda-Sapuan, S TI Enhancing social problem solving in children with autism and normal children through computer-assisted instruction SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; social problem solving; computer-assisted instruction ID SKILLS; MIND AB Children with autism have difficulty in solving social problems and in generating multiple solutions to problems. They are, however, relatively skilled in responding to visual cues such as pictures and animations. Eight distinct social problems were presented on a computer, along with a choice of possible solutions, and an option to produce alternative solutions. Eight preschool children with autism and eight matched normal children went through 10 training sessions interleaved with 6 probe sessions. Children were asked to provide solutions to animated problem scenes in all the sessions. Unlike the probe sessions, in the training sessions problem solutions were first explained thoroughly by the trainer. Subsequently these explanations were illustrated using dynamic animations of the solutions. Although children with autism produced significantly fewer alternative solutions compared to their normal peers, a steady increase across probe sessions was observed for the autistic group. The frequency of new ideas was directly predicted by the diagnostic category of autism. Results suggest young children with autism and their normal peers can be taught problem-solving strategies with the aid of computer interfaces. More research is required to establish whether such computer-assisted instruction will generalize to nontrained problem situations in real-life contexts. C1 Natl Univ Singapore, Dept Social Work & Psychol, Singapore 117570, Singapore. RP Bernard-Opitz, V (reprint author), Natl Univ Singapore, Dept Social Work & Psychol, 11 Law Link, Singapore 117570, Singapore. CR BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BERRY J, 1995, LETS TALK SAYING NO Camp B. W., 1985, THINK ALOUD INCREASI *CITY NAT CTR CLIN, 1992, EM FDN SCH READ DUNN LM, 1981, BRIT PICTURE VOCABUL ELIAS MJ, 1992, SOCIAL DECISION MAKI GOLEMAN D, 1998, WORKING EMOTIONAL IN Goleman D, 1997, EMOTIONAL INTELLIGEN HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 HEIMANN M, 1995, J AUTISM DEV DISORD, V25, P459, DOI 10.1007/BF02178294 HOBSON RP, 1989, BRIT J DEV PSYCHOL, V7, P237 Howlin P., 1999, TEACHING CHILDREN AU Kaufman A. 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PD AUG PY 2001 VL 31 IS 4 BP 377 EP 384 DI 10.1023/A:1010660502130 PG 8 WC Psychology, Developmental SC Psychology GA 470QZ UT WOS:000170883800003 PM 11569584 ER PT J AU Keen, D Sigafoos, J Woodyatt, G AF Keen, D Sigafoos, J Woodyatt, G TI Replacing prelinguistic behaviors with functional communication SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE prelinguistic behaviors; functional communication training; autism ID SEVERE DISABILITIES; CHILDREN; SETTINGS AB This study evaluated the effectiveness of a teacher-implemented intervention package designed to replace prelinguistic behaviors with functional communication. Four young children with autism participated in a multiple-probe design across three communicative functions. Initially, three existing communication functions were selected for each child. Next, the existing prelinguistic behaviors that the children used to achieve these functions were identified. Replacement forms that were considered more recognizable and symbolic were defined to achieve these same functions. After a baseline phase, teachers received inservice training, consultation, and feedback on how to encourage, acknowledge, and respond to the replacement forms. During intervention, the replacement forms increased and prelinguistic behaviors decreased in most cases. The results suggested that the teacher-implemented intervention was effective in replacing prelinguistic behaviors with alternative forms of functional communication. C1 Univ Queensland, Grad Sch Educ, Brisbane, Qld, Australia. Caroline Chisholm Ctr, Brisbane, Qld, Australia. Univ Sydney, Fac Educ, Sydney, NSW, Australia. CHERI, Sydney, NSW, Australia. Univ Queensland, Dept Speech Pathol & Audiol, Brisbane, Qld, Australia. RP Sigafoos, J (reprint author), Univ Texas, Dept Special Educ, George I Sanchez Bldg, Austin, TX 78712 USA. 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M., 1993, AUGMENTATIVE ALTERNA, V9, P168 DURAND VM, 1991, J APPL BEHAV ANAL, V24, P251, DOI 10.1901/jaba.1991.24-251 EINFELD S, 1994, DEV BEHAV CHECKLIST HAYNES W, 1998, COMMUNICATION DEV FD, P73 HORNER RD, 1978, J APPL BEHAV ANAL, V11, P189, DOI 10.1901/jaba.1978.11-189 HORNER RH, 1991, J APPL BEHAV ANAL, V24, P719, DOI 10.1901/jaba.1991.24-719 HOUGHTON J, 1987, J ASSOC PERS SEVERE, V12, P18 KASARI C, 1988, J ABNORM CHILD PSYCH, V16, P45, DOI 10.1007/BF00910499 LIM L, 1998, J BEHAV ED, V8, P81 Mirenda P., 1997, AUGMENTATIVE ALTERNA, V13, P207, DOI 10.1080/07434619712331278048 Reichle J, 1997, J SPEC EDUC, V31, P110 Reichle J., 1993, ENHANCING CHILDRENS, P105 Risley T. R., 1995, MEANINGFUL DIFFERENC Sailor W., 1975, TOPEKA ASS RETARDED SCHULER A, 1987, HDB AUTISM PERVASIVE Siegel-Causey E., 1989, ENHANCING NONSYMBOLI Sigafoos J, 2000, COMMUNICATION DISORD, V21, P77, DOI 10.1177/152574010002100202 Watson LR, 1998, J AUTISM DEV DISORD, V28, P51, DOI 10.1023/A:1026063003289 Wetherby A. M., 1992, COMMUNICATION LANGUA, V1, P217 Wetherby A.M., 1992, AUTISM IDENTIFICATIO, P107 Windmiller M., 1981, AAMD ADAPTIVE BEHAV NR 30 TC 35 Z9 36 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2001 VL 31 IS 4 BP 385 EP 398 DI 10.1023/A:1010612618969 PG 14 WC Psychology, Developmental SC Psychology GA 470QZ UT WOS:000170883800004 PM 11569585 ER PT J AU Kaminsky, L Dewey, D AF Kaminsky, L Dewey, D TI Siblings relationships of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS 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 DE autism; sibling relationships; Down syndrome ID CHILDHOOD; PERCEPTIONS; LINKS AB This study investigated sibling relationships of children with autism compared to children with Down syndrome and siblings of normally developing children. Ninety siblings (30 per group) between the ages of 8 and 18 participated in this study. Results indicated that sibling relationships in families of children with autism were characterized by less intimacy, prosocial behavior, and nurturance than those of the two comparison groups. Both siblings of children with autism and siblings of children with Down syndrome reported greater admiration of their sibling and less quarreling and competition in their relationships relative to normally developing comparison children. C1 Alberta Childrens Prov Gen Hosp, Behav Res Unit, Calgary, AB T2T 5C7, Canada. Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Paediat, 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. CR ABRAMOVITCH R, 1987, J CHILD PSYCHOL PSYC, V28, P865, DOI 10.1111/j.1469-7610.1987.tb00675.x American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 BLISHEN BR, 1987, CAN REV SOC ANTHROP, V24, P465 DUNN J, 1986, J CHILD PSYCHOL PSYC, V27, P583, DOI 10.1111/j.1469-7610.1986.tb00184.x DUNN J, 1988, J CHILD PSYCHOL PSYC, V29, P119, DOI 10.1111/j.1469-7610.1988.tb00697.x BUHRMESTER D, 1990, CHILD DEV, V61, P1387, DOI 10.1111/j.1467-8624.1990.tb02869.x Gilliam J. E., 1995, GILLIAM AUTISM RATIN HOWLIN P, 1988, CHILD CARE HLTH DEV, V14, P395, DOI 10.1111/j.1365-2214.1988.tb00591.x JENKINS JM, 1990, J AM ACAD CHILD PSY, V29, P60, DOI 10.1097/00004583-199001000-00011 KNOTT F, 1995, J CHILD PSYCHOL PSYC, V36, P965, DOI 10.1111/j.1469-7610.1995.tb01343.x LOBATO D, 1985, J AUTISM DEV DISORD, V15, P345, DOI 10.1007/BF01531505 MCHALE SM, 1986, J AUTISM DEV DISORD, V16, P399, DOI 10.1007/BF01531707 RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 Sparrow S, 1984, VINELAND ADAPTIVE BE STOCKER C, 1990, BRIT J DEV PSYCHOL, V8, P227 STOCKER CM, 1994, J CHILD PSYCHOL PSYC, V35, P1447, DOI 10.1111/j.1469-7610.1994.tb01286.x STONEMAN Z, 1987, AM J MENT RETARD, V92, P290 NR 18 TC 60 Z9 61 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2001 VL 31 IS 4 BP 399 EP 410 DI 10.1023/A:1010664603039 PG 12 WC Psychology, Developmental SC Psychology GA 470QZ UT WOS:000170883800005 PM 11569586 ER PT J AU Beglinger, LJ Smith, TH AF Beglinger, LJ Smith, TH TI A review of subtyping in autism and proposed dimensional classification model SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; subtyping; symptom heterogeneity ID PERVASIVE DEVELOPMENTAL DISORDER; CLUSTER-ANALYSIS; MEDICAL CONDITIONS; SOCIAL-BEHAVIOR; CHILDREN; SUBGROUPS; SUBCLASSIFICATION; IDENTIFICATION; QUESTIONNAIRE; ABNORMALITIES AB Autism has been divided into subtypes based on social interaction/communication, developmental level, or both. The validity of subtyping systems and the extent to which they overlap were examined. According to this review, a single subtyping system capable of accounting for the symptom heterogeneity in autism has not yet been proposed; however, evidence supports the presence of a three-factor continuum containing at least four subgroups. Foremost among directions for future research is the need for comprehensive studies in which medical screening, careful selection of measures, and longitudinal data collection are included. C1 Washington State Univ, Pullman, WA 99164 USA. RP Beglinger, LJ (reprint author), Indiana Univ, Riley Hosp,Sch Med, Sect Neuropsychol, Dept Neurol, 702 Barnhill Dr, Indianapolis, IN 46202 USA. CR Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 1987, DIAGN STAT MAN MENT 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 Bimbrauer J. 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PD AUG PY 2001 VL 31 IS 4 BP 411 EP 422 DI 10.1023/A:1010616719877 PG 12 WC Psychology, Developmental SC Psychology GA 470QZ UT WOS:000170883800006 PM 11569587 ER PT J AU Goldstein, G Johnson, CR Minshew, NJ AF Goldstein, G Johnson, CR Minshew, NJ TI Attentional processes in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; attentional processes ID EXECUTIVE FUNCTION; DIAGNOSTIC INTERVIEW; CHILDREN; DEFICITS; INDIVIDUALS AB Attentional processes in individuals with high-functioning autism were compared with a matched control group. Participants for the study were 103 children and adults with autism and 103 control subjects. Measures administered corresponded to Mirsky et al.'s (1991) factor analysis of tests of attention. Diminished performance was noted on measures that loaded on the Focus-Execute and Shift factors, but not on the Sustain and Encode factors. For tests in which psychomotor speed was used as the score, and the difference between groups was significant, covariance analyses were performed, using tests of basic motor functions as covariates. This procedure led to attenuation to the point of nonsignificant differences in the case of some of the attention tests. Thus, this comprehensive analysis of attention in individuals with high-functioning autism only found differences on measures in which the task placed demands on cognitive flexibility or psychomotor speed. Thus, purported attention deficits in autism may actually be primary deficits in complex decision making or psychomotor abilities. C1 Vet Adm Pittsburgh Healthcare Syst, Pittsburgh, PA 15206 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. RP Goldstein, G (reprint author), Vet Adm Pittsburgh Healthcare Syst, 7180 Highland Dr 151R, Pittsburgh, PA 15206 USA. CR BARRY RJ, 1988, INT J PSYCHOPHYSIOL, V6, P139, DOI 10.1016/0167-8760(88)90045-1 Bauman M. 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A., 1965, DERANGED MEMORY TOWNSEND J, 1994, J COGNITIVE NEUROSCI, V6, P220, DOI 10.1162/jocn.1994.6.3.220 Wainwright JA, 1996, J AUTISM DEV DISORD, V26, P423, DOI 10.1007/BF02172827 WAINWRIGHTSHARP JW, 1993, J AUTISM DEV DISORD, V26, P423 Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D., 1981, WAIS R MANUAL YEATES KO, 1998, NEUROPSYCHOLOGY, P35 Zubin J, 1975, EXPT APPROACHES PSYC, P139 NR 53 TC 69 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 AUG PY 2001 VL 31 IS 4 BP 433 EP 440 DI 10.1023/A:1010620820786 PG 8 WC Psychology, Developmental SC Psychology GA 470QZ UT WOS:000170883800008 PM 11569589 ER PT J AU Remington, G Sloman, L Konstantareas, M Parker, K Gow, R AF Remington, G Sloman, L Konstantareas, M Parker, K Gow, R TI Clomipramine versus haloperidol in the treatment of autistic disorder: A double-blind, placebo-controlled, crossover study SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; OBSESSIVE-COMPULSIVE DISORDER; RATING-SCALE; BEHAVIORAL SYMPTOMS; MENTAL-RETARDATION; ADULTS; CHILDREN; DESIPRAMINE AB Clomipramine, haloperidol, and placebo were compared with baseline in the treatment of autism, and overall outcome, specific symptoms, and side effects were examined. It was hypothesized that clomipramine would be better tolerated than haloperidol and prove superior on a measure of stereotypy. Individuals with a DSM-TV diagnosis of autistic disorder (mean age, 16.3 years; range, 10-36 years) were randomly assigned, by using a Latin square design, to the following 7-week trials: placebo, clomipramine (mean daily dose, 128.4 mg; range, 100-150 mg), or haloperidol (mean daily dose, 1.3 mg; range, 1-1.5 mg). Data on 36 subjects were analyzed and taken together; the results favored haloperidol. In those patients who were able to complete a full therapeutic trial, clomipramine proved comparable to haloperidol in terms of improvement compared with baseline. However, significantly fewer individuals receiving clomipramine versus haloperidol were able to complete the trial(37.5% vs. 69.7%,respectively) for reasons related to both side effects and efficacy or behavior problems. In the intent-to-treat sample, which is perhaps more clinically relevant, only haloperidol proved superior to baseline on a global measure of autistic symptom severity, as well as specific measures for irritability and hyperactivity. Clomipramine did not seem more effective on a measure of stereotypy, nor was it better tolerated. C1 Univ Toronto, Clarke Div, Ctr Addict & Mental Hlth, Toronto, ON M5T 1R8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Pediat, Toronto, ON, Canada. RP Remington, G (reprint author), Univ Toronto, Clarke Div, Ctr Addict & Mental Hlth, 250 Coll St, Toronto, ON M5T 1R8, Canada. CR AMAN MG, 1985, AM J MENT DEF, V89, P485 ANDERSON LT, 1984, AM J PSYCHIAT, V141, P1195 ANDERSON LT, 1989, J AUTISM DEV DISORD, V19, P227, DOI 10.1007/BF02211843 BARR LC, 1992, J CLIN PSYCHIAT, V53, P17 BRASIC JR, 1994, NEUROLOGY, V44, P1309 Brasic JR, 1997, J AM ACAD CHILD PSY, V36, P1165, DOI 10.1097/00004583-199709000-00006 Brodkin ES, 1997, J CHILD ADOL PSYCHOP, V7, P109, DOI 10.1089/cap.1997.7.109 CAMPBELL M, 1982, J AUTISM DEV DISORD, V12, P167, DOI 10.1007/BF01531306 CHOUINARD G, 1980, CAN J NEUROL SCI, V7, P233 Fatemi SH, 1998, J AUTISM DEV DISORD, V28, P303, DOI 10.1023/A:1026008602540 GORDON CT, 1993, ARCH GEN PSYCHIAT, V50, P441 GORDON CT, 1992, AM J PSYCHIAT, V149, P363 Hellings JA, 1996, J CLIN PSYCHIAT, V57, P333 MCDOUGLE CJ, 1990, J AUTISM DEV DISORD, V20, P537, DOI 10.1007/BF02216058 McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 MCDOUGLE CJ, 1995, AM J PSYCHIAT, V152, P772 MCDOUGLE CJ, 1997, HDB AUTISM PERVASIVE, P707 MCDOUGLE CJ, 1992, J AM ACAD CHILD PSY, V31, P746, DOI 10.1097/00004583-199207000-00025 CAMPBELL M, 1985, PSYCHOPHARMACOL BULL, V21, P1063 Potenza MN, 1999, J CLIN PSYCHOPHARM, V19, P37, DOI 10.1097/00004714-199902000-00008 Sanchez LE, 1996, J AM ACAD CHILD PSY, V35, P537, DOI 10.1097/00004583-199604000-00021 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SNEAD RW, 1994, J AM ACAD CHILD PSY, V33, P909, DOI 10.1097/00004583-199407000-00022 NR 23 TC 58 Z9 58 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD AUG PY 2001 VL 21 IS 4 BP 440 EP 444 DI 10.1097/00004714-200108000-00012 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 454QF UT WOS:000169982700012 PM 11476129 ER PT J AU Nguyen, M Murphy, T AF Nguyen, M Murphy, T TI Mirtazapine for excessive masturbation in an adolescent with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 Univ Florida, Div Child & Adolescent Psychiat, Gainesville, FL USA. RP Nguyen, M (reprint author), Univ Florida, Div Child & Adolescent Psychiat, Gainesville, FL USA. RI Murphy, Tanya/J-7079-2013 CR BRASIC JR, 1998, CNS SPECTRUMS, V3, P39 Coleman E., 1990, AM J PREVENTATIVE PS, V2, P9 Kehoe WA, 1996, FORMULARY, V31, P455 Levitsky AM, 1999, J AM GERIATR SOC, V47, P231 RICHER M, 1993, ANN PHARMACOTHER, V27, P316 NR 5 TC 8 Z9 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD AUG PY 2001 VL 40 IS 8 BP 868 EP 869 DI 10.1097/00004583-200108000-00004 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 454RP UT WOS:000169985800005 PM 11501682 ER PT J AU Malone, RP Cater, J Sheikh, RM Choudhury, MS Delaney, MA AF Malone, RP Cater, J Sheikh, RM Choudhury, MS Delaney, MA TI Olanzapine versus haloperidol in children with autistic disorder: An open pilot study SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autistic disorder; neuroleptic drug treatment ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; BEHAVIORAL SYMPTOMS; INFANTILE-AUTISM; TARDIVE-DYSKINESIA; YOUNG-CHILDREN; LONG-TERM; RISPERIDONE; TRIAL; ADOLESCENTS AB Objectives: Conventional neuroleptics ameliorate symptoms in children with autistic disorder; however, they are known to cause dyskinesias. Atypical neuroleptics, including olanzapine, may have less risk for dyskinesia, but their efficacy in autistic disorder is not established. This study was designed to investigate the safety and effectiveness of open-label olanzapine as a treatment for children with autistic disorder by using haloperidol as a standard comparator treatment. Method: In a parallel groups design, 12 children with DSM-I autistic disorder (mean age 7.8 +/- 2.1 years) were randomized to 6 weeks of open treatment with olanzapine or haloperidol. Mean final dosages were 7.9 +/- 2.5 mg/day for olanzapine and 1.4 +/- 0.7 mg/day for haloperidol. Outcome measures included the Clinical Global Impressions (CGI) and the Children's Psychiatric Rating Scale (CPRS). Results: Both groups had symptom reduction. Five of six in the olanzapine group and three of six in the haloperidol group were rated as responders according to the CGI Improvement item. Subjects showed improvement on the CPRS Autism Factor (F-1,F-9 = 24.4, p = .0008). Side effects included drowsiness and weight gain. Conclusions: The findings suggest that olanzapine is a promising treatment for children with autistic disorder. Further placebo-controlled and long-term studies of olanzapine in autistic disorder are required. C1 Med Coll Penn & Hahnemann Univ, Eastern Penn Psychiat Inst, Dept Psychiat, Philadelphia, PA 19129 USA. Biomet Stat Consulting, Wynnewood, PA USA. Temple Univ, Philadelphia, PA 19122 USA. RP Malone, RP (reprint author), Med Coll Penn & Hahnemann Univ, Eastern Penn Psychiat Inst, Dept Psychiat, 3200 Henry Ave, Philadelphia, PA 19129 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD AUG PY 2001 VL 40 IS 8 BP 887 EP 894 DI 10.1097/00004583-200108000-00009 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 454RP UT WOS:000169985800010 PM 11501687 ER PT J AU Brudnak, MA AF Brudnak, MA TI Application of genomeceuticals to the molecular and immunological aspects of autism SO MEDICAL HYPOTHESES LA English DT Article ID DIPEPTIDYL-PEPTIDASE-IV; EXPRESSION; PURIFICATION; CLONING; GLUCAN; ENZYME; CELLS AB Autism is a developmental disease affecting as many as 1 in 300 children and is often characterized as a mental disorder originating in infancy that is associated with self-absorption, inability to interact socially, behavior, and language dysfunction (e.g. echolalia). Current theories indicate an important role of diet in the development of disease. It is thought that, as a result of maldigestion of casein and gluten, opioid-type peptides, or exorphins, are produced. Additionally, because of the time-frame of development of the disease, there has been an association with childhood vaccination. Consequently, prevailing therapies attempt to address these causes in one, or a combination, of three ways: diet restriction (removing casein and gluten); supplementation with exogenous enzymes; and probiotic bacteria. Until recently, none of the therapies addressed the molecular mechanisms that may be at work in the development and progression of autism. This paper presents potential molecular and cellular mechanism related to autism as well as discusses their application to the treatment of the disease through the application of genomeceuticals. Additionally, a link between developmentally associated aberrant immune and inflammatory responses, and autism is suggested and explored. (C) 2001 Harcourt Publishers Ltd. C1 MAK Wood Inc, Thiensville, WI USA. RP Brudnak, MA (reprint author), MAK Wood Inc, 1235 Dakota Dr, Grayton, WI 53024 USA. 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Hypotheses PD AUG PY 2001 VL 57 IS 2 BP 186 EP 191 DI 10.1054/mehy.2001.1331 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 456UJ UT WOS:000170100400013 PM 11461171 ER PT J AU Fuentes, J Gallano, I AF Fuentes, J Gallano, I TI Medical treatment of pervasive developmental disorders SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autism; child neurology; early identification; genetic counselling; pervasive developmental disorders; psychopharmacological treatment ID SPECTRUM DISORDERS; AUTISM AB Objective. Pervasive developmental disorders, exemplified by autism, constitute clinical entities which require the attention of child neurologists. Development. The increasing frequency with which these disorders are diagnosed supports the need to review and bring up to date the available data, so as to achieve good practice. Conclusions. There are many studies and initiatives to orient the child neurologist as to the steps to be taken regarding aspects such as early identification, association with known syndromes, genetic counselling and medical advice in general, neuroimaging techniques, treatment of possible associated epilepsy and use of psychotropic drugs. All these elements have to be incorporated into an overall individualized program which, at the present time, has to be basically educational and rehabilitation, so as to attain maximum self-sufficiency and social participation. C1 Policlin Gipozkoa, Serv Psiquiatria Infanto Juvenil, E-20011 San Sebastian, Spain. GAUTENA, San Sebastian, Gipuzkoa, Spain. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Arnold LE, 2000, J AUTISM DEV DISORD, V30, P99, DOI 10.1023/A:1005451304303 BARTHELEMY C, 2000, DESCRIPTION AUTISM FERNANDEZMATAMO.I, 1992, ESCALA HAIZEALLEVANT Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 FUENTES J, 2001, PHARMAUTISME SISTEMA Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 RUTTER M, 1997, HDB AUTISM PERVASIVE Tuchman R, 2000, J AUTISM DEV DISORD, V30, P485, DOI 10.1023/A:1005572128200 Volkmar Fred, 1999, Journal of the American Academy of Child and Adolescent Psychiatry, V38, p32S WHO, 1993, ICD 10 CLASS MENT BE NR 12 TC 1 Z9 1 PU REVISTA DE NEUROLOGIA PI BARCELONA PA C/O CESAR VIGUERA, EDITOR, APDO 94121, 08080 BARCELONA, SPAIN SN 0210-0010 J9 REV NEUROLOGIA JI Rev. Neurologia PD AUG 1 PY 2001 VL 33 IS 3 BP 208 EP 210 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 480QN UT WOS:000171473600002 PM 11588711 ER PT J AU Tuchman, RF AF Tuchman, RF TI How to construct a social brain: Lessons from autism SO REVISTA DE NEUROLOGIA LA English DT Article DE autism; children; social communication ID DEVELOPMENTAL LANGUAGE DISORDER; POSITRON-EMISSION-TOMOGRAPHY; INFANTILE-AUTISM; DIAGNOSTIC INTERVIEW; CHILDHOOD AUTISM; SEROTONIN SYNTHESIS; GLUCOSE-METABOLISM; DYSPHASIC CHILDREN; CEREBELLAR VERMIS; SPECTRUM DISORDER AB Autism is the prototype disorder of social and cognitive development and provides an important opportunity to observe and delineate the regions of the brain that are responsible for the behaviors that define our social relationships. Our present understanding of autism suggests that deficits in social communication can be identified by the assessment of joint attention, affective reciprocity, and theory of mind. Present evidence suggests that deficits in social communication in children with autism may be related to dysfunction in the amygadala, hippocampus and related limbic and cortical structures. Other neuroanatomic structures such as the cerebellum may also form part of this distributed neuronal social network. At a neurochemical level the principal neurotransmitter implicated in autism is serotonin suggesting that this neurotransmitter may play a crucial role in the social brain network. An understanding of the neuronal networks responsible for social behavior will allow for rational implementation of social communication interventions which will have benefits not only for children with autism and related disorders but to our whole society. C1 Dan Marino Ctr, Weston, FL 33331 USA. Miami Childrens Hosp, Dept Neurol, Miami, FL USA. 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Neurologia PD AUG 1 PY 2001 VL 33 IS 3 BP 292 EP 299 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 480QN UT WOS:000171473600012 ER PT J AU Jones, S AF Jones, S TI Autism in history: The case of Hugh Blair of Borgue SO SOCIAL HISTORY OF MEDICINE LA English DT Book Review C1 Norfolk Mental Hlth Care NHS Trust, Norwich, Norfolk, England. RP Jones, S (reprint author), Norfolk Mental Hlth Care NHS Trust, Norwich, Norfolk, England. CR Houston Rab, 2000, AUTISM HIST CASE HUG NR 1 TC 0 Z9 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0951-631X J9 SOC HIST MED JI Soc. Hist. Med. PD AUG PY 2001 VL 14 IS 2 BP 362 EP 363 PG 2 WC History & Philosophy Of Science SC History & Philosophy of Science GA 467GR UT WOS:000170694500018 ER PT J AU McMahon, CL Braddock, SR AF McMahon, CL Braddock, SR TI Septo-optic dysplasia as a manifestation of valproic acid embryopathy SO TERATOLOGY LA English DT Article ID NEURAL-TUBE DEFECTS; SPINA-BIFIDA; INFANTS; NERVES; AUTISM AB Background: The use of valproic acid during pregnancy has been associated with adverse fetal outcomes, including major and minor congenital malformations, intrauterine growth retardation (IUGR), hyperbilirubinemia, hepatotoxicity, transient hyperglycemia, and fetal and neonatal distress. In addition, intrauterine exposure to valproic acid has been associated with an increased risk of central nervous system abnormalities, primarily neural tube defects. Optic nerve hypoplasia has been reported in association with other prenatal anticonvulsant exposures, but the occurrence of septo-optic dysplasia as a manifestation of valproic acid embryopathy has not been reported previously. Results: We report on a woman who received Depakote (valproic acid) throughout her pregnancy for the treatment of a seizure disorder. The patient presented with features typical of valproic acid embryopathy, including bitemporal narrowing, hypertelorism, short palpebral fissures, epicanthal folds, microphthalmia, a flat broad nasal bridge, small mouth, hypoplastic nails, mild clinodactyly, and camptoclactyly. MRI showed hypoplasia of the optic chiasm and absence of the septum pellucidum. Conclusions: We report the first case of septo-optic dysplasia associated with maternal exposure to valproic acid throughout pregnancy. This case expands the clinical phenotype of valproate embryopathy. (C) 2001 Wiley-Liss, Inc. C1 Univ Missouri, Div Med Genet, Dept Child Hlth, Columbia, MO 65212 USA. Northwestern Univ, Dept Obstet & Gynecol, Sect Reprod Genet, Chicago, IL 60611 USA. RP Braddock, SR (reprint author), Univ Missouri, Div Med Genet, Dept Child Hlth, 1 Hosp Dr, Columbia, MO 65212 USA. 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Methods: A principal component exploratory factor analysis routine with varimax-rotation and extraction of factors following the Scree criterion was run using data from the Autism Diagnostic Interview-Revised (ADI-R) of N = 262 individuals exhibiting autism or autistic features. Results: A three-factor solution consisting of two socio-communicative and one language dimension and accounting for 46.1% of the total variance was found to best describe the data. These factors yielded only vague correspondence with the idea of behavior domains described in ICD-10 and DSM-IV. In addition, factor loadings of items representing repetitive, stereotyped patterns were generally weak. Conclusions: The factor-analytic approach to autism indicates a conception of the disorder divergent from that defined in the contemporary psychiatric classification systems, especially regarding the area of repetitive, stereotyped behavior. C1 Klinikum JWG Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, D-60528 Frankfurt, Germany. RP Bolte, S (reprint author), Klinikum JWG Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. 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Kinder-und Jugendpsy. Psychother. PD AUG PY 2001 VL 29 IS 3 BP 221 EP 229 DI 10.1024//1422-4917.29.3.221 PG 9 WC Psychiatry SC Psychiatry GA 464MD UT WOS:000170535600006 PM 11524898 ER PT J AU Warnke, A AF Warnke, A TI Understanding, explaining and treating autism - A reader SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Book Review CR LELORD G, 2000, AUTISMUS SPUR VERSTE NR 1 TC 0 Z9 0 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD AUG PY 2001 VL 29 IS 3 BP 247 EP 248 DI 10.1024//1422-4917.29.3.247 PG 2 WC Psychiatry SC Psychiatry GA 464MD UT WOS:000170535600014 ER PT J AU Courchesne, E Karns, CM Davis, HR Ziccardi, R Carper, RA Tigue, ZD Chisum, HJ Moses, P Pierce, K Lord, C Lincoln, AJ Pizzo, S Schreibman, L Haas, RH Akshoomoff, NA Courchesne, RY AF Courchesne, E Karns, CM Davis, HR Ziccardi, R Carper, RA Tigue, ZD Chisum, HJ Moses, P Pierce, K Lord, C Lincoln, AJ Pizzo, S Schreibman, L Haas, RH Akshoomoff, NA Courchesne, RY TI Unusual brain growth patterns in early life in patients with autistic disorder - An MRI study SO NEUROLOGY LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; INFANTILE-AUTISM; MENTAL-RETARDATION; HEAD CIRCUMFERENCE; FRONTAL-LOBE; NEURAL BASIS; CEREBELLAR; CHILDREN; ABNORMALITY; HYPOPLASIA AB Objective: To quantify developmental abnormalities in cerebral and cerebellar volume in autism. Methods: The authors studied 60 autistic and 52 normal boys (age, 2 to 16 years) using MRI. Thirty autistic boys were diagnosed and scanned when 5 years or older. The other 30 were scanned when 2 through 4 years of age and then diagnosed with autism at least 2.5 years later, at an age when the diagnosis of autism is more reliable. Results: Neonatal head circumferences from clinical records were available for 14 of 15 autistic 2- to 5-year-olds and, on average, were normal (35.1 +/- 1.3 cm versus clinical norms: 34.6 +/- 1.6 cm), indicative of normal overall brain volume at birth; one measure was above the 95th percentile. By ages 2 to 4 years, 90% of autistic boys had a brain volume larger than normal average, and 37% met criteria for developmental macrencephaly. Autistic 2- to 3-year-olds had more cerebral (18%) and cerebellar (39%) white matter, and more cerebral cortical gray matter (12%) than normal, whereas older autistic children and adolescents did not have such enlarged gray and white matter volumes. In the cerebellum, autistic boys had less gray matter, smaller ratio of gray to white matter, and smaller vermis lobules VI-VII than normal controls. Conclusions: Abnormal regulation of brain growth in autism results in early overgrowth followed by abnormally slowed growth. Hyperplasia was present in cerebral gray matter and cerebral and cerebellar white matter in early life in patients with autism. C1 Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Psychol, La Jolla, CA 92093 USA. Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, San Diego, CA USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Calif Sch Profess Psychol, San Diego, CA 92121 USA. RP Courchesne, RY (reprint author), Lab Res Neurosci Autism, 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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P., 1961, ACTA ANAT, V47, P72 Schmahmann J. D., 2000, MRI ATLAS HUMAN CERE Schmahmann JD, 1998, BRAIN, V121, P561, DOI 10.1093/brain/121.4.561 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Stevenson RE, 1997, LANCET, V349, P1744, DOI 10.1016/S0140-6736(05)62956-X WILLIAMS RS, 1980, ARCH NEUROL-CHICAGO, V37, P749 Zilbovicius Monica, 1995, Neurology, V45, pA612 NR 67 TC 659 Z9 668 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL 24 PY 2001 VL 57 IS 2 BP 245 EP 254 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 454WG UT WOS:000169994300014 PM 11468308 ER PT J AU Edwardes, M Baltzan, M AF Edwardes, M Baltzan, M TI Measles, mumps, and rubella (MMR) vaccine and autism - Argument is too simplistic SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Royal Victoria Hosp, Div Clin Epidemiol, Montreal, PQ H3A 1A1, Canada. Mt Sinai Hosp, Montreal, PQ H4W 1S7, Canada. RP Edwardes, M (reprint author), Royal Victoria Hosp, Div Clin Epidemiol, Ross 4-06,687 Pine Ave W, Montreal, PQ H3A 1A1, Canada. CR Altmann D, 2000, LANCET, V355, P409, DOI 10.1016/S0140-6736(05)74033-2 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 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 NR 5 TC 1 Z9 1 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 JUL 21 PY 2001 VL 323 IS 7305 BP 163 EP 163 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 456WR UT WOS:000170106200027 PM 11484721 ER PT J AU Smeeth, L Hall, AJ Rodrigues, LC Huang, XN Smith, PG Fombonne, E AF Smeeth, L Hall, AJ Rodrigues, LC Huang, XN Smith, PG Fombonne, E TI Measles, mumps, and rubella (MMR) vaccine and autism - Ecological studies cannot answer main question SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, London WC1E 7HT, England. Univ London London Sch Hyg & Trop Med, Infect Dis Epidemiol Unit, London WC1E 7HT, England. Univ London London Sch Hyg & Trop Med, Dept Infect & Trop Med, London WC1E 7HT, England. Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, MRC,Child Psychiat Unit, London SE5 8AF, England. RP Smeeth, L (reprint author), Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, Keppel St, London WC1E 7HT, England. EM liam.smeeth@lshtm.ac.uk CR Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Smeeth L, 2001, BMC PUBLIC HEALTH, V1, DOI 10.1186/1471-2458-1-2 NR 3 TC 2 Z9 2 PU BMJ PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1756-1833 J9 BRIT MED J JI Br. Med. J. PD JUL 21 PY 2001 VL 323 IS 7305 BP 163 EP 163 DI 10.1136/bmj.323.7305.163 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 456WR UT WOS:000170106200026 PM 11463692 ER PT J AU Yazbak, FE AF Yazbak, FE TI Measles, mumps, and rubella (MMR) vaccine and autism - MMR cannot be exonerated without explaining increased incidence of autism SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 TL Autism Res, Falmouth, MA 02540 USA. RP Yazbak, FE (reprint author), TL Autism Res, 70 Viewcrest Dr, Falmouth, MA 02540 USA. CR Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 NR 1 TC 1 Z9 1 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 JUL 21 PY 2001 VL 323 IS 7305 BP 163 EP 164 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 456WR UT WOS:000170106200028 PM 11484720 ER PT J AU Kaye, JA Melero-Montes, MD Jick, H AF Kaye, JA Melero-Montes, MD Jick, H TI Measles, mumps, and rubella (MMR) vaccine and autism - MMR cannot be exonerated without explaining increased incidence of autism - Reply SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, Lexington, MA 02421 USA. RP Kaye, JA (reprint author), Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, 11 Muzzey St, Lexington, MA 02421 USA. CR Last JM, 2001, DICT EPIDEMIOLOGY NR 1 TC 0 Z9 0 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 JUL 21 PY 2001 VL 323 IS 7305 BP 164 EP 164 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 456WR UT WOS:000170106200029 ER PT J AU McLellan, F AF McLellan, F TI IOM reviews evidence on thimerosal link to autism SO LANCET LA English DT News Item NR 0 TC 1 Z9 1 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD JUL 21 PY 2001 VL 358 IS 9277 BP 214 EP 214 DI 10.1016/S0140-6736(01)05451-4 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 454HL UT WOS:000169967100021 ER PT J AU Beyer, KS Klauck, SM Wiemann, S Poustka, A AF Beyer, KS Klauck, SM Wiemann, S Poustka, A TI Construction of a physical map of an autism susceptibility region in 7q32.3-q33 SO GENE LA English DT Article DE bacterial artificial chromosome clones; end sequencing; sequence tag site; expressed sequence tag ID GENOMIC SCREEN; GENES; LOCI; SCAN; DNA AB The fast evolving progress of the human genome mapping and sequencing efforts facilitate the detection of genes also for complex traits. We focus on the detection of susceptibility loci for autism, a prototypical pervasive developmental disorder. Five genome screens worldwide have identified several putative locations of susceptibility genes thus far, with the most common region on chromosome 7q. In order to identify new candidate genes for infantile autism we constructed a physical map of bacterial artificial chromosome, Pl-derived artificial chromosome and yeast artificial chromosome clones of a 3 Mb region between D7S1575 and D7S500. including a complete contig of the similar to 1.2 Mb region around D7S2533, the marker with the most significant association result. We developed 16 novel sequence tag sites and mapped 23 genes/expressed sequence tags to the contigs. As this map contains a putative autistic disorder locus this integrated physical and transcript map provides a valuable resource for identification of candidate gene(s). (C) 2001 Published by Elsevier Science B.V. All rights reserved. C1 Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, D-69120 Heidelberg, Germany. RP Poustka, A (reprint author), Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, Neuenheimer Feld 280, D-69120 Heidelberg, Germany. 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We have found the novel GXAlu allele absent in 204 patients from the South Carolina Autism Project and 200 controls. The autism population studied includes a significant number of patients with hypotonia, stereotyped behaviors, or postural, gait, and motor abnormalities similar to those seen in the patients previously reported to possess the novel GXAlu allele, This suggests that the novel (AAAT)(6) GXAlu allele is not associated with autism. (C) 2001 Wiley-Liss. Inc. C1 Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. Presbyterian Coll, Clinton, SC USA. Clemson Univ, Clemson, SC USA. RP Michaelis, RC (reprint author), Greenwood Genet Ctr, JC Self Res Inst, 1 Gregor Mendel Circle, Greenwood, SC 29646 USA. 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PD JUL 8 PY 2001 VL 105 IS 5 BP 404 EP 405 DI 10.1002/ajmg.1432 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 447QD UT WOS:000169583200002 PM 11449390 ER PT J AU Wassink, TH Piven, J Vieland, VJ Huang, J Swiderski, RE Pietila, J Braun, T Beck, G Folstein, SE Haines, JL Sheffield, VC AF Wassink, TH Piven, J Vieland, VJ Huang, J Swiderski, RE Pietila, J Braun, T Beck, G Folstein, SE Haines, JL Sheffield, VC TI Evidence supporting WNT2 as an autism susceptibility gene SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; candidate gene; linkage disequilibrium; chromosome 7q ID LINKAGE ANALYSIS; EXPRESSION PATTERNS; LANGUAGE DISORDER; CHROMOSOME 7Q; LOD SCORES; MOUSE; LOCALIZATION; SEQUENCE; INHERITANCE; IMPAIRMENT AB We examined WNT2 as a candidate disease gene for autism for the following reasons. First, the WNT family of genes influences the development of numerous organs and systems, including the central nervous system. Second, WNT2 is located in the region of chromosome 7q31-33 linked to autism and is adjacent to a chromosomal breakpoint in an individual with autism. Third, a mouse knockout of Dvl1, a member of a gene family essential for the function of the WNT pathway, exhibits a behavioral phenotype characterized primarily by diminished social interaction. We screened the WNT2 coding sequence for mutations in a large number of autistic probands and found two families containing nonconservative coding sequence variants that segregated with autism in those families. We also identified linkage disequilibrium (LD) between a WNT2 3'UTR SNP and our sample of autism-affected sibling pair (ASP) families and trios. The LD arose almost exclusively from a subgroup of our ASP families defined by the presence of severe language abnormalities and was also found to be associated with the evidence for linkage to 7q from our previously published genomewide linkage screen. Furthermore, expression analysis demonstrated WNT2 expression in the human thalamus, Based on these findings, we hypothesize that rare mutations occur in the WNT2 gene that significantly increase susceptibility to autism even when present in single copies, while a more common WNT2 allele (or alleles) not yet identified may exist that contributes to the disorder to a lesser degree (C) 2001 Wiley-Liss, Inc. C1 Univ Iowa, Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27515 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27515 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, Dept Pediat, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Howard Hughes Med Inst, Iowa City, IA 52242 USA. Univ Iowa, Interdept Genet PhD Program, Iowa City, IA 52242 USA. Tufts Univ, Coll Med, Dept Psychiat, Medford, MA USA. Vanderbilt Med Ctr, Program Human Genet, Nashville, TN USA. RP Wassink, TH (reprint author), Univ Iowa, Coll Med, Dept Psychiat, Psychiat Res MEB, Iowa City, IA 52242 USA. 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J. Med. Genet. PD JUL 8 PY 2001 VL 105 IS 5 BP 406 EP 413 DI 10.1002/ajmg.1401 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 447QD UT WOS:000169583200003 PM 11449391 ER PT J AU Kroisel, PM Petek, E Emberger, W Windpassinger, C Wladika, W Wagner, K AF Kroisel, PM Petek, E Emberger, W Windpassinger, C Wladika, W Wagner, K TI Candidate region for Gilles de la Tourette Syndrome at 7q31 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE chromosome 7q; cytogenetic analysis; duplication; mental retardation; Tourette syndrome ID PREVALENCE; CHILDREN; AUTISM AB Gilles de la Tourette Syndrome (GTS) is a complex n europsychiatric disorder characterized by motor and vocal ties. The cause of this syndrome is unknown, although based on family studies there is evidence of a strong genetic component. We report on a 13-year-old boy with GTS, minor physical anomalies, and a de novo partial duplication of chromosome 7q [dup(7)(q22.1-q31.1)]. The distal breakpoint in our patient is similar to the breakpoint of an apparently balanced familial translocation t(7;18) segregating with G;TS, Together, these cases provide evidence that a gene located in the breakpoint region at 7q31 can be involved in the formation of GTS, (C) 2001 Wiley-Liss, Inc. C1 Graz Univ, Inst Med Biol & Human Genet, A-8010 Graz, Austria. Klagenfurt Hosp, Dept Pediat Neuropsychiat, Klagenfurt, Austria. RP Kroisel, PM (reprint author), Graz Univ, Inst Med Biol & Human Genet, Harrachgasse 21-8, A-8010 Graz, Austria. 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PD JUL 1 PY 2001 VL 101 IS 3 BP 259 EP 261 DI 10.1002/1096-8628(20010701)101:3<259::AID-AJMG1374>3.0.CO;2-# PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 445TX UT WOS:000169475600012 PM 11424142 ER PT J AU Watling, RL Deitz, J White, O AF Watling, RL Deitz, J White, O TI Comparison of sensory profile scores of young children with and without autism spectrum disorders SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE child development disorders, pervasive; pediatric occupational therapy; sensory integration ID BEHAVIORS; MOTOR AB Objectives. The purpose of this study was to describe the sensory-based behaviors of young children with autism as reported by their parents on the Sensory Profile. Factor scores of children with autism were compared with those of children without autism. Method. The Sensory Profile questionnaire was completed by parents of 40 children with autism 3 through 6 years of age and parents of 40 children without autism 3 through 6 years of age. Results. The performance of children with autism was significantly different from that of children without autism on 8 of 10 factors. Factors where differences were found included Sensory Seeking, Emotionally Reactive, Low Endurance/Tone, Oral Sensitivity, Inattention/Distractibility, Poor Registration, Fine Motor/Perceptual, and Other. Conclusion. Findings from the study suggest that young children with autism have deficits in a variety of sensory processing abilities as measured by the Sensory Profile. Further research is needed to replicate these findings, to examine the possibility of subgroups on the basis of sensory processing, and to contrast the sensory processing abilities of children with other disabilities to those of children with autism. C1 Univ Washington, Dept Rehabil Med, Div Occupat Therapy, Seattle, WA 98195 USA. Univ Washington, Coll Educ, Seattle, WA 98195 USA. RP Watling, RL (reprint author), Univ Washington, Dept Rehabil Med, Div Occupat Therapy, Box 356490, Seattle, WA 98195 USA. CR Ayres A. J., 1972, SENSORY INTEGRATION Ayres AJ, 1979, SENSORY INTEGRATION Baranek GT, 1997, AM J OCCUP THER, V51, P91 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 DAHLGREN SO, 1989, EUROPEAN ARCH PSCYHI, V238, P33 *DAT DESCR, 1997, DAT DESK 6 0 COMP SO Dawson G, 2000, J AUTISM DEV DISORD, V30, P415, DOI 10.1023/A:1005547422749 DeGangi G. 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J. Occup. Ther. PD JUL-AUG PY 2001 VL 55 IS 4 BP 416 EP 423 PG 8 WC Rehabilitation SC Rehabilitation GA 454BJ UT WOS:000169952300008 PM 11723986 ER PT J AU Perry, EK Lee, MLW Martin-Ruiz, CM Court, JA Volsen, SG Merrit, J Folly, E Iversen, PE Bauman, ML Perry, RH Wenk, GL AF Perry, EK Lee, MLW Martin-Ruiz, CM Court, JA Volsen, SG Merrit, J Folly, E Iversen, PE Bauman, ML Perry, RH Wenk, GL TI Cholinergic activity in autism: Abnormalities in the cerebral cortex and basal forebrain SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID NICOTINIC ACETYLCHOLINE-RECEPTORS; MESSENGER-RNA LEVELS; NERVE GROWTH-FACTOR; NEUROTROPHIC FACTOR; HUMAN BRAIN; NEUROCHEMICAL MARKERS; ENZYME-IMMUNOASSAY; BINDING; RATS; SCHIZOPHRENIA AB Objective: Measures of cholinergic transmitter activity were investigated in patients with autism because of reported neuropathological abnormalities in cholinergic nuclei in the basal forebrain. Method: Levels of cholinergic enzyme and receptor activity were measured in the frontal and parietal cerebral cortex of deceased autistic adults, similarly aged normal adults without mental retardation, and nonautistic mentally retarded adults. The immunoreactivity levels of brain-derived neurotrophic factor and nerve growth factor were,measured in the basal forebrain. Results: There were no differences between the autistic and comparison groups in choline acetyltransferase or acetylcholinesterase activity in the cerebral cortex and basal forebrain or in muscarinic Mt receptor or a-bungarotoxin binding within the cortex. Cortical M-1 receptor binding was up to 30% lower than normal in the autistic subjects, and the difference reached significance in the parietal cortex. In both the parietal and frontal cortices, differences in nicotinic receptors assessed by [H-3]epibatidine binding were significant and extensive (65%-73% lower in the autistic group than in the normal subjects); there were no differences in nicotine binding in the basal forebrain. Immunochemical analysis indicated lower levels of both the alpha (4) and beta (2) nicotinic receptor subunits in the parietal cortex. The M1 receptor-abnormality was not evident in the nonautistic group with mental retardation, although the lower [H-3]epibatidine binding was apparent. In the basal forebrain, the level of brain-derived neurotrophic factor in the autistic group was three times as high as the level of the normal group. Conclusions: These neurochemical abnormalities implicate the cholinergic system in developmental disorders such as autism and suggest the potential for intervention based on cholinergic receptor modulation. 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J. Psychiat. PD JUL PY 2001 VL 158 IS 7 BP 1058 EP 1066 DI 10.1176/appi.ajp.158.7.1058 PG 9 WC Psychiatry SC Psychiatry GA 450YT UT WOS:000169773000011 PM 11431227 ER PT J AU Thrasher, JD Kilburn, KH AF Thrasher, JD Kilburn, KH TI Embryo toxicity and teratogenicity of formaldehyde SO ARCHIVES OF ENVIRONMENTAL HEALTH LA English DT Article DE anomalies; chromosomes; embryo; formaldehyde; mitochondria; mutagenicity; neurogenesis; teratogenicity ID SISTER-CHROMATID EXCHANGES; MITOCHONDRIAL-DNA; DEVELOPMENTAL NEUROTOXICITY; GESTATIONAL EXPOSURE; INHALED FORMALDEHYDE; INHALATION EXPOSURE; RAT-LIVER; CHLORPYRIFOS; STUDENTS; INDUCTION AB C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. The following questions must be addressed: What adducts (e.g., N-methyl amino acids) are formed in the blood following formaldehyde inhalation? What role do N-methyl-amino adducts play in alkylation of nuclear and mitochondrial deoxyribonucleic acid, as well as mitochondrial peroxidation? The fact that the free formaldehyde pool in blood is not affected following exposure to the chemical does not mean that formaldehyde is not involved in altering cell and deoxyribonucleic acid characteristics beyond the nasal cavity. The teratogenic effect of formaldehyde in the English literature has been sought, beginning on the 6th day of pregnancy (i.e., rodents) (Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545-48; Martin WJ. Reprod Toxicol 1990, pp 237-39; Ulsamer AG, et al. Hazard Assessment of Chemicals; Academic Press, 1984, pp 337-400; and U.S. Department of Health and Human Services. Toxicological Profile of Formaldehyde; ATSDR, 1999 [references 1-4., respectively, herein]). The exposure regimen is critical and may account for the differences in outcomes. Pregnant rats were exposed (a) prior to mating, (b) during mating, (c) or during the entire gestation period. These regimens (a) increased embryo mortality; (b) increased fetal anomalies (i.e., cryptochordism and aberrant ossification centers); (c) decreased concentrations of ascorbic acid; and (d) caused abnormalities in enzymes of mitochondria, lysosomes, and the endoplasmic reticulum. The alterations in enzymatic activity persisted 4 mo following birth. In addition, formaldehyde caused metabolic acidosis, which was augmented by iron deficiency. Furthermore, newborns exposed to formaldehyde in utero had abnormal performances in open-field tests. Disparities in teratogenic effects of toxic chemicals are not unusual. For example, chlorpyrifos has not produced teratogenic effects in rats when mothers are exposed on days 6-15 (Katakura Y, et al. Br J Ind Med 1993, pp 176-82 [reference 5 herein]) of gestation (Breslin WJ, et al. Fund Appl Toxicol 1996, pp 119-30; and Hanley TR, et al. Toxicol Sci 2000, pp 100-08 [references 6 and 7, respectively, herein]). However, either changing the endpoints for measurement or exposing neonates during periods of neurogenesis (days 1-14 following birth) and during subsequent developmental periods produced adverse effects. These effects included neuroapoptosis, decreased deoxyribonucleic acid and ribonucleic acid synthesis, abnormalities in adenylyl cyclase cascade, and neurobehavioral effects (Johnson DE, et al. Brain Res Bull 1998, pp 143-47; Lassiter TL, et al. Toxicol Sci 1999, pp 92-100; Chakraborti TK, et al. Pharmacol Biochem Behav 1993, pp 219-24; Whitney KD, et al. Toxicol Appl Pharm 1995, pp 53-62; Chanda SM, et al. Pharmacol Biochem Behav 1996, pp 771-76; Dam K, et al. Devel Brain Res 1998, pp 39-45; Campbell CG, et al. Brain Res Bull 1997, pp 179-89; and Xong X, et al. Toxicol Appl Pharm 1997, pp 158-74 [references 8-15, respectively, herein]). Furthermore, the terata caused by thalidomide is a graphic human example in which the animal model and timing of exposure were key factors (Parman T, et al. Natl Med 1999, pp 582-85; and Brenner CA, et al. Mol Human Repro 1998, pp 887-92 [references 16 and 17, respectively, herein]). Thus, it appears that more sensitive endpoints (e.g., enzyme activity, generation of reactive oxygen species, timing of exposure) for the measurement of toxic effects of environmental agents on embryos, fetuses, and neonates are more coherent than are gross terata observations. The perinatal period from the end of organogenesis to the end of the neonatal period in humans approximates the 28th day of gestation to 4 wk postpartum. Therefore, researchers must investigate similar stages of development (e.g., neurogenesis occurs in the 3rd trimester in humans and neonatal days occur during days 1-14 in rats and mice, whereas guinea pigs behave more like humans). Finally, screening for teratogenic events should also include exposure of females before mating or shortly following mating. Such a regimen is fruitful inasmuch as environmental agents cause adverse effects on ovarian elements (e.g., thecal cells and ova [nuclear-deoxyribonucleic acid and mitochondrial deoxyribonucleic acid]), as well as on zygotes and embryos before implantation. Mitochondrial deoxyribonucleic acid mutations and deletions occur in human oocytes and embryos (Parman T, et al. Natl Med 1999, pp 582-85; and Brenner CA, et al. Mol Human Repro 1998, pp 887-92 [references 16 and 17, respectively, herein]). Thus, it is likely that xenobiotics directly affect n-deoxyribonucleic acid and/or mitochondrial deoxyribonucleic acid in either the ovum or the zygote/embryo or both (Thrasher JD. Arch Environ Health 2000, pp 292-94 [reference 18 herein]), and they could account for the increasing appearance of a variety of mitochondrial diseases, including autism (Lomard L. Med Hypotheses 1998, pp 497-99; Wallace EC. Proc Natl Acad Sci 1994, pp 8730-46; and Giles RE, et al. Proc Natl Acad Sci 1980, pp 6715-19 [references 19-21, respectively, herein]). Two cases of human birth defects were reported in formaldehyde-contaminated homes (Woodbury MA, et al. Formaldehyde Toxicity 1983; pp 203-11 [reference 22 herein]). One case was anencephalic at 2.76 ppm, and the other defect at 0.54 ppm was not characterized. Further observations on human birth defects are recommended. C1 Sam 1 Trust, Alto, NM 88312 USA. 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Health PD JUL-AUG PY 2001 VL 56 IS 4 BP 300 EP 311 PG 12 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA 473TQ UT WOS:000171064500004 PM 11572272 ER PT J AU Cimons, M AF Cimons, M TI IOM report discounts link between MMR vaccine use and autism SO ASM NEWS LA English DT Article NR 0 TC 0 Z9 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0044-7897 J9 ASM NEWS JI ASM News PD JUL PY 2001 VL 67 IS 7 BP 342 EP 343 PG 2 WC Microbiology SC Microbiology GA 451XR UT WOS:000169828300005 ER PT J AU Maurice, C Mannion, K Letso, S Perry, L AF Maurice, C Mannion, K Letso, S Perry, L TI Parent voices: Difficulty in accessing behavioral intervention for autism; Working toward solutions SO BEHAVIORAL INTERVENTIONS LA English DT Article AB The history of autism treatment has been dominated by a series of failed treatments, passing fads. and misinformed theories of etiology. With the advances in teaching methods derived from the science of Applied Behavior Analysis however, significant remediation of the disorder is now possible. Yet at present parents or caregivers still face serious challenges in identifying scientifically-validated treatment models, and in securing competent and well-trained therapists. Four parents report on these challenges, on the steps they have taken to mitigate these difficulties in their own families, and on the long-term solutions they are attempting to implement in the wider community. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 ASAT, Great Neck, NY 11021 USA. RP Maurice, C (reprint author), ASAT, 175 Great Neck Rd,Suite 406, Great Neck, NY 11021 USA. CR KAUFMAN B, 1974, SON RISE Maurice C., 1993, LET ME HEAR YOUR VOI SHOOK GL, 1993, BEHAV ANALYST, V16, P87 NR 3 TC 5 Z9 5 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD JUL-SEP PY 2001 VL 16 IS 3 BP 147 EP 165 DI 10.1002/bin.89 PG 19 WC Psychology, Clinical SC Psychology GA 462XY UT WOS:000170446300001 ER PT J AU Healey, JJ Ahearn, WH Graff, RB Libby, ME AF Healey, JJ Ahearn, WH Graff, RB Libby, ME TI Extended analysis and treatment of self-injurious behavior SO BEHAVIORAL INTERVENTIONS LA English DT Article ID FUNCTIONAL-ANALYSIS; ABERRANT BEHAVIOR; DISABILITIES; INDIVIDUALS AB In experiment 1, an extended functional analysis of self-injury was conducted with a 21-year-old male diagnosed with autism and profound mental retardation. The multielement phase yielded undifferentiated results. Subsequent blocking of conditions plus the addition of a component allowing access to multiple sensory stimuli suggested that self-injury was unrelated to programmed positive or negative reinforcement contingencies. The behavior appeared to be automatically reinforced; its occurrence decreased when access to alternative sensory stimuli was provided. Experiment 2 evaluated a treatment condition in which response-independent access to these sensory stimuli was provided within the participant's everyday environment. Baseline and treatment frequencies of self-injury were compared in a combined. multiple-baseline-across-settings and ABAB design. The level of self-injury decreased substantially during treatment. These results support the use of extended analog analyses of aberrant behavior in instances in which undifferentiated responding occurs in the initial analogue analysis. Additionally, a procedure is described for generalizing the intervention derived from the experimental analysis into the participant's everyday environment. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 New England Ctr Children, Southborough, MA 01772 USA. Northeastern Univ, Boston, MA 02115 USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Waltham, MA 02154 USA. 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PD JUL-SEP PY 2001 VL 16 IS 3 BP 181 EP 195 DI 10.1002/bin.91 PG 15 WC Psychology, Clinical SC Psychology GA 462XY UT WOS:000170446300003 ER PT J AU Saitoh, O Karns, CM Courchesne, E AF Saitoh, O Karns, CM Courchesne, E TI Development of the hippocampal formation from 2 to 42 years - MRI evidence of smaller area dentata in autism SO BRAIN LA English DT Article DE autism; MRI; neuroanatomy; development; hippocampus ID TEMPORAL-LOBE EPILEPSY; INFANTILE-AUTISM; ENTORHINAL CORTEX; NEUROGENESIS; BRAIN; RAT; ABNORMALITIES; ORGANIZATION; CEREBELLAR; DENSITIES AB Autism, a neuropsychiatric disorder that severely impairs social, language and cognitive development, has a clinical onset in the first years of life, Because components of the limbic system mediate memory, social and affective functions that are typically disturbed in autism, a developmental defect in the limbic system has been hypothesized to underlie different autistic symptoms, but no developmental study has been performed, To obtain neuroanatomical evidence of limbic system abnormality in autism, we measured the cross-sectional area of the area dentata (AD; dentate gyrus + CA4) and combined area of the subiculum and CA1-CA3 (CAS) using in vivo MRI, Autistic patients aged 29 months to 42 years (n = 59) and healthy normal controls (n = 51) participated, The cross-sectional area of the AD was significantly smaller than normal in autism, the largest deviation from normal size (-13.5%) being found in autistic children aged 29 months to 4 years, Strong age-related increases were seen in the cross-sectional area of GAS, but autistic and normal subjects were not Significantly different, This is the first direct evidence that anatomical abnormality within the limbic system exists from the earliest years of the disorder, and persists throughout development and to middle age. 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Hong Kong Polytech Univ, Dept Rehabil Sci, Hong Kong, Hong Kong, Peoples R China. RP Hong, WC (reprint author), Govt Off, Room 723,393 Canton Rd, Kowloon, Hong Kong, Peoples R China. 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PD JUL PY 2001 VL 47 IS 93 BP 73 EP 85 PN 2 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 454QE UT WOS:000169982600002 ER PT J AU Nelson, KB AF Nelson, KB TI Toward a biology of autism: possible role of certain neuropeptides and neurotrophins SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article DE autism; neuropeptides; neurotrophins ID VASOACTIVE-INTESTINAL-PEPTIDE; SPECTRUM DISORDERS; INFANTILE-AUTISM; VIP; NEURONS; BRAIN; CHILDREN; BDNF; EXPRESSION; GROWTH AB Autism is a behaviorally defined syndrome for which there is no known biologic marker. Although autism is thought to be a disorder of brain development, there have been few efforts to study early regulators of brain development in this disorder. This paper describes a recent study of neonatal blood of children with later-diagnosed of autistic spectrum disorders comparing them with two groups of affected children, those with mental retardation without autism, or with cerebral palsy. and unaffected control children, using recycling immunoaffinity chromatography. We measured concentrations of four neuropeptides and four neurotrophins, finding that neonatal concentrations of the neuropeptides vasoactive intestinal peptide. calcitonin gone-related peptide, and the neurotrophins brain derived neurotrophic factor and neurotrophin 415 were higher in children in the autistic spectrum. and in those with mental retardation without autism, than in children with cerebral palsy or healthy control children. In 99% of children with autism and 97% with mental retardation, levels of at least one of these substances exceeded those of all control children. Concentrations were similar in subgroups of the autistic spectrum (core syndrome with or without mental retardation, other autistic spectrum disorders with or without mental retardation), and in the presence or absence of a history of regression. Two other neuropeptides and two neurotrophins were present in similar concentrations in all groups examined. Thus overexpression of certain neuropeptides and neurotrophins was observed in neonatal blood of children with later diagnoses of autism or cognitive disability. (C) 2001 Association for Research in Nervous and Mental Disease. Published by Elsevier Science B.V. C1 NINCDS, Neuroepidemiol Branch, NIH, Bethesda, MD 20892 USA. RP Nelson, KB (reprint author), NINCDS, Neuroepidemiol Branch, NIH, Bldg 10,Room 5S221, Bethesda, MD 20892 USA. 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Neurosci. Res. PD JUL PY 2001 VL 1 IS 4 BP 300 EP 306 DI 10.1016/S1566-2772(01)00016-0 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 529FC UT WOS:000174288500007 ER PT J AU Russell, J Hill, EL Franco, F AF Russell, J Hill, EL Franco, F TI The role of belief veracity in understanding intentions-in-action - Preschool children's performance on the transparent intentions task SO COGNITIVE DEVELOPMENT LA English DT Article DE intention; the 3-4 transition; theory of mind; executive functioning; metarepresentation ID FALSE BELIEF; MIND; DECEPTION; ABILITY; AUTISM AB It is possible to have either true or false beliefs about what one is currently doing (an 'intention-in-action'; [Searle, J. R. (1983). Intentionality: an essay in the philosophy of mind. New York: Cambridge University Press.]). The theory-theory account of the development of 'mentalising' skills between 3 and 4 years of age predicts that younger children should find false intentions-in-action more difficult to report than true intentions-in-action, In contrast, an executive theory of development at 3 and 4 years of age would predict that the perceived outcome of the action at the time of questioning should determine the younger child's answer, with the truth-value of the past belief playing no role. We presented 3- and 4-year-old children with a novel drawing task- the transparent intentions task -in order to pit these two accounts against each other. The truth-value of the child's (or a puppet's) intention-in-action played no role in performance. Incorrect answers referred to the unexpected final outcome of the drawing. This result supports the executive theory. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 2EB, England. UCL, Inst Cognit Neurosci, London, England. Middlesex Univ, Dept Psychol, Enfield, Middx, England. RP Russell, J (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 2EB, England. 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PD JUL-SEP PY 2001 VL 16 IS 3 BP 775 EP 792 DI 10.1016/S0885-2014(01)00057-0 PG 18 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 510ET UT WOS:000173196300002 ER PT J AU Kugathasan, S AF Kugathasan, S TI Pediatric inflammatory bowel disease: clinical and therapeutic aspects SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article ID CEREVISIAE MANNAN ANTIBODIES; CROHNS-DISEASE; 6-MERCAPTOPURINE THERAPY; ULCERATIVE-COLITIS; CHILDREN; ADOLESCENTS; INFLIXIMAB; PREVALENCE; DURATION AB Epidemiologic data suggest that the incidences of pediatric ulcerative colitis and Crohn disease continue to evolve with geographic variations. One study suggests that children with autism have a unique inflammatory bowel disorder that is associated with gastrointestinal symptoms. The appropriate use of new diagnostic tests and novel treatments for inflammatory bowel disease (IBD) needs to be clarified in the pediatric population. Because of concerns regarding sensitivity and specificity, serologic markers measuring anti-Saccharomyces cerevisiae antibodies and perinuclear antineutrophil cytoplasmic antibodies cannot yet replace conventional diagnostic testing for screening or diagnosis of pediatric IBD. Large, prospective, pediatric population-based studies still need to be performed to ascertain their use as a noninvasive screening tool. Genetic studies using thiopurine methyl transferase and measurement of 6-mercaptopurine metabolites appear to be valuable for management of pediatric patients with IBD, in assisting clinicians in optimizing therapeutic response to 6-mercaptopurine, and in identifying individuals at increased risk for drug-induced toxicity. Newer immunomodulatory agents also are being explored in pediatric IBD. Open pilot trials of infliximab (Remicade; Centocor, Malvern, PA) for the treatment of children with Crohn disease that does not respond to conventional management have demonstrated short-term efficacy and safety. Trials of tacrolimus for treatment of fulminant colitis in children have been disappointing. C1 Med Coll Wisconsin, Childrens Hosp Wisconsin, Dept Pediat, Pediat Inflammatory Bowel Dis Ctr, Milwaukee, WI 53226 USA. RP Kugathasan, S (reprint author), Med Coll Wisconsin, Childrens Hosp Wisconsin, Dept Pediat, Pediat Inflammatory Bowel Dis Ctr, Milwaukee, WI 53226 USA. 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Med. Child Neurol. PD JUL PY 2001 VL 43 SU 87 BP 1 EP 70 PG 70 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 456KV UT WOS:000170082400001 ER PT J AU Vourc'h, P Bienvenu, T Beldjord, C Chelly, J Barthelemy, C Muh, JP Andres, C AF Vourc'h, P Bienvenu, T Beldjord, C Chelly, J Barthelemy, C Muh, JP Andres, C TI No mutations in the coding region of the Rett syndrome gene MECP2 in 59 autistic patients SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE autism; rett syndrome; MECP2 gene; DGGE analysis ID MENTAL-RETARDATION; X-CHROMOSOME; INSTABILITY; DIAGNOSIS AB Autistic disorder is a pervasive developmental disorder considered to have a multigenic origin. Mental retardation is present in 75% of autistic patients. Autistic features are found in Rett syndrome, a neurological disorder affecting girls and associated with severe mental retardation. Recently, the gene responsible for the Rett syndrome, methyl CpG-binding protein (MECP2) gene, was identified on the X chromosome by a candidate gene strategy. Mutations in this gene were also observed in some mentally retarded males. In this study we tested MECP2 as a candidate gene in autistic disorder by a DGGE analysis of its coding region and intron-exon boundaries. Among 59 autistic patients, 42 males and 17 females, mentally retarded or not, no mutations or polymorphisms were present in the MECP2 gene. Taking into account the size of our sample, we conclude that MECP2 coding sequence mutations are not an important factor (less than 5% of cases) in the aetiology of autistic disorder. C1 Fac Med Tours, INSERM U316, Lab Biochem & Biol Mol, F-37032 Tours, France. Fac Med Cochin, ICGM, Lab Genet Physiopathol Retards Mentaux, F-75014 Paris, France. Hop Bretonneau, Serv Univ Explorat Fonct & Neurophysiol Pedopsych, INSERM U316, F-37032 Tours, France. 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J. Hum. Genet. PD JUL PY 2001 VL 9 IS 7 BP 556 EP 558 DI 10.1038/sj.ejhg.5200660 PG 3 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 459PM UT WOS:000170259900012 PM 11464249 ER PT J AU Steinmetz, JE Tracy, JA Green, JT AF Steinmetz, JE Tracy, JA Green, JT TI Classical eyeblink conditioning: Clinical models and applications SO INTEGRATIVE PHYSIOLOGICAL AND BEHAVIORAL SCIENCE LA English DT Article ID BRAIN GROWTH SPURT; PURKINJE-CELL LOSS; NICTITATING-MEMBRANE RESPONSE; OBSESSIVE-COMPULSIVE DISORDER; NEONATAL ETHANOL EXPOSURE; FETAL ALCOHOL SYNDROME; INTERPOSITUS NUCLEUS; CEREBELLAR PURKINJE; PRENATAL EXPOSURE; EYELID RESPONSES AB In this paper, we argue that the main reason that classical eyeblink conditioning has proven so useful when applied to clinical situations, is that a great deal of information is known about the behavioral and neural correlates of this form of associative learning. 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PD JUL PY 2001 VL 41 IS 3 BP 217 EP 218 PG 2 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 451TL UT WOS:000169817300077 ER PT J AU Baron-Cohen, S AF Baron-Cohen, S TI Autism spectrum disorders, vol 9, A transactional developmental perspective. SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Book Review CR WETHERBY A, 2000, AUTISM SPECTRUM DISO, V9 NR 1 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-9863 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD JUL PY 2001 VL 42 IS 5 BP 702 EP 702 PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 456HR UT WOS:000170077500019 ER PT J AU Hollander, E Dolgoff-Kaspar, R Cartwright, C Rawitt, R Novotny, S AF Hollander, E Dolgoff-Kaspar, R Cartwright, C Rawitt, R Novotny, S TI An open trial of divalproex sodium in autism spectrum disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID BORDERLINE PERSONALITY-DISORDER; AGGRESSIVE-BEHAVIOR; INFANTILE-AUTISM AB Background: Autism spectrum disorders are characterized by core deficits in social interaction and speech/communication skills, repetitive behaviors, and restricted interests. Other abnormalities include seizures, electroencephalograph ic (EEG) abnormalities, affective instability, impulsivity, and aggression. Divalproex sodium is indicated as both an anticonvulsant in epilepsy and a mood stabilizer in bipolar illness and thus might be useful for these complicating symptoms in autism. Method: A retrospective pilot study was conducted to determine whether divalproex sodium was effective in treating core dimensions and associated features of autism. Fourteen patients who met DSM-IV criteria for autism, Asperger's disorder, or pervasive developmental disorder not otherwise specified, both with and without a history of seizure disorders or EEG abnormalities, were openly treated with divalproex sodium. Improvement was assessed via the Clinical Global Impressions-Improvement scale. Results: Of 14 patients who completed a trial of divalproex sodium, 10 (71%) were rated as having sustained response to treatment. The mean dose of divalproex sodium was 768 mg/day (range, 125-2500 mg/day), and it was generally well tolerated. Improvement was noted in core symptoms of autism and associated features of affective instability, impulsivity, and aggression. Conclusion: Divalproex sodium may be beneficial to patients with autism spectrum disorders, particularly those with associated features of affective instability, impulsivity, and aggression as well as those with a history of EEG abnormalities or seizures. Of note, all patients with an abnormal EEG and/or seizure history were rated as responders. However, these findings must be interpreted with caution, given the open retrospective nature of the study. Controlled trials are needed to replicate these preliminary findings. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. RP Hollander, E (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. 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Clin. Psychiatry PD JUL PY 2001 VL 62 IS 7 BP 530 EP 534 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 457KZ UT WOS:000170137400007 PM 11488363 ER PT J AU Schmitt, JE Eliez, S Warsofsky, IS Bellugi, U Reiss, AL AF Schmitt, JE Eliez, S Warsofsky, IS Bellugi, U Reiss, AL TI Enlarged cerebellar vermis in Williams syndrome SO JOURNAL OF PSYCHIATRIC RESEARCH LA English DT Article DE Williams syndrome; cerebellar vermis; neurogenetics; MRI; chromosome 7 ID FRAGILE-X-SYNDROME; JOUBERT-SYNDROME; DISORDER; BRAIN; COMMUNICATION; AUTISM; MRI; MORPHOLOGY; FEATURES; PROFILE AB Williams syndrome (WMS) is a rare genetic disorder characterized by relative preservations of language ability and facial processing despite deficits in overall intelligence, problem solving, and visuospatial processing, Subjects with WMS also display hypersocial behavior and excessive linguistic affect during conversations and when giving narratives. Neuroimaging studies have shown global reductions in the brain volumes of subjects with WMS compared with normal controls, but with preservations in cerebellar volume. This study examines the neuroanatomic structure of the cerebellar vermis in 20 subjects with WMS and 20 age- and gender-matched controls via high-resolution magnetic resonance imaging. The vermis was divided into lobules I-V, VI-VII, and VIII-X. Lobules VI-VII and VIII-X were both relatively enlarged in the WMS group, and after adjusting for the smaller size of the WMS brain, the posterior vermis was significantly larger in WMS (Mann-Whitney z-value = 4.27; P < 0.001). Given that reductions in posterior vermis size have been implicated in flattened affect and autistic features, increased vermis size in subjects with WMS may be related to the hypersociality and heightened affective expression characteristic of individuals with this genetic condition. (C) 2001 Published by Elsevier Science Ltd. All rights reserved. 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Am. Acad. Child Adolesc. Psychiatr. PD JUL PY 2001 VL 40 IS 7 BP 743 EP 748 DI 10.1097/00004583-200107000-00008 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 445XH UT WOS:000169483500008 PM 11437012 ER PT J AU Fombonne, E Simmons, H Ford, T Meltzer, H Goodman, R AF Fombonne, E Simmons, H Ford, T Meltzer, H Goodman, R TI Prevalence of pervasive developmental disorders in the British nationwide survey of child mental health SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE epidemiology; autism; Rett syndrome; pervasive developmental disorder; prevalence ID INFLAMMATORY-BOWEL-DISEASE; DIFFICULTIES QUESTIONNAIRE; AUTISM; MEASLES; PARENTS; EPIDEMIOLOGY; INFECTIONS; STRENGTHS; STRESS AB Objective: The prevalence of pervasive developmental disorders (PDD) is not well established and needs monitoring. The prevalence of PDD in the 1999 nationwide British survey of child and adolescent mental health was investigated. Method: A randomized, stratified sample of children (N = 12,529) aged 5 to 15 years was generated from the Child Benefit Register. Trained interviewers interviewed parents and youths aged 11 or older with a standardized diagnostic interview (Development and Well-Being Assessment). and questionnaire data (Strengths and Difficulties Questionnaire) were obtained from teachers and parents, who also completed self-report measures of psychological distress. Final diagnostic determination was achieved by a team of experienced clinicians using all data sources. Results: A total of 10,438 (83%) interviews were conducted. There were 2 girls with Rett syndrome (weighted prevalence: 3.8/10,000 girls) and 27 children with other PDD (weighted prevalence: 26.1/10,000). Compared with children with a psychiatric disorder other than PDD, social but not behavioral problems were more frequent in the PDD group. Parents of children with PDD had higher rates of psychological distress. than those from the two comparison groups. Conclusions: Consistent with other recent surveys, PDD rates are higher than those reported 30 years ago. The burden associated with PDD is very high. C1 Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, London SE5 8AF, England. Off Natl Stat, London, ON, Canada. RP Fombonne, E (reprint author), Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, De Crespigny Pk, Denmark Hill, London SE5 8AF, England. 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Am. Acad. Child Adolesc. Psychiatr. PD JUL PY 2001 VL 40 IS 7 BP 820 EP 827 DI 10.1097/00004583-200107000-00017 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 445XH UT WOS:000169483500017 PM 11437021 ER PT J AU Duchan, JF Calculator, S Sonnenmeier, R Diehl, S Cumley, GD AF Duchan, JF Calculator, S Sonnenmeier, R Diehl, S Cumley, GD TI A framework for managing controversial practices SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE augmentative and alternative communication; clinical practice guidelines; controversial practices; facilitated communication ID FACILITATED COMMUNICATION; SEXUAL ABUSE; AUTISM AB Every day, speech-language pathologists working in schools make difficult, life-impacting decisions regarding which assessment and intervention approaches to use with their clients. These decisions can become even more difficult when the approaches being considered for use are controversial. The risks involved in making choices about controversial practices are likely to have increased significance simply because the approach being considered is not widely accepted. The increased professional risk may cause decisions to be made based on risk avoidance rather than on a careful consideration of the pros and cons of the approach itself. This article offers a clinical practice framework for gathering information about controversial approaches and for implementing and monitoring their use. The frame-work will be illustrated using facilitated communication as an example of a controversial practice. C1 SUNY Buffalo, Buffalo, NY 14260 USA. Univ New Hampshire, Durham, NC USA. Univ S Florida, Tampa, FL USA. Univ Wisconsin, Stevens Point, WI 54481 USA. RP Duchan, JF (reprint author), 130 Jewett Pkwy, Buffalo, NY 14214 USA. 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Speech Hear. Serv. Sch. PD JUL PY 2001 VL 32 IS 3 BP 133 EP 141 DI 10.1044/0161-1461(2001/011) PG 9 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 453PZ UT WOS:000169926200003 ER PT J AU Bonvillian, JD Gershoff, ET Seal, BC Richards, HC AF Bonvillian, JD Gershoff, ET Seal, BC Richards, HC TI Hand preferences in sign-learning students with autistic disorder SO LATERALITY LA English DT Article ID PATHOLOGICAL LEFT-HANDEDNESS; INFANTILE-AUTISM; HEMISPHERIC-SPECIALIZATION; BRAIN LATERALIZATION; CHILDHOOD AUTISM; CHILDREN; LANGUAGE; IMITATION; ASYMMETRIES; DIAGNOSIS AB The purpose of the study was fourfold: (a) to document the hand preferences of nonspeaking individuals with autism as they produced signs and nonsign actions; (b) to find out if sign-language proficiency in such individuals is associated with directionality or consistency of signing hand preference; (c) to explore the link between hand preference for signing and standardised measures of cognitive and motor development; (d) to compare the hand preferences (sign and nonsign actions) of such individuals to sign-learning children with normal cognitive functioning. In this study, the hand preferences of 14 nonspeaking students with autistic disorder were determined from videotape records of their sign production and nonsign actions. In their sign production, four students strongly favoured their right hands, four had a distinct left-hand preference, and six did not significantly favour either hand. There was little evidence linking sign-language proficiency, cognitive maturity, or motor development to strongly lateralised signing or handedness in general in these students. Compared with the hand preferences of the children in the two comparison groups, the autistic students were markedly less lateralised with respect to signing, but not nonsign actions. C1 Univ Virginia, Dept Psychol, Charlottesville, VA 22904 USA. Columbia Univ, New York, NY 10027 USA. James Madison Univ, Harrisonburg, VA 22807 USA. RP Bonvillian, JD (reprint author), Univ Virginia, Dept Psychol, 102 Gilmer Hall,POB 400400, Charlottesville, VA 22904 USA. 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Parent-offspring transmission of the long (l) and short (s) alleles of the deletion/insertion polymorphism in the HTT promoter region was examined in families of 71 children with autism using the transmission test for linkage disequilibrium (TDT). Transmission of HTT promoter alleles did not differ between probands with autism and their unaffected siblings. However, allelic transmission in probands was dependent upon severity of impairments in the social and communication domains, with greater s allele transmission in severely impaired individuals and greater I transmission in mild/moderately impaired individuals. This relationship between HTT promoter alleles and severity of autistic impairment was also seen when ratings of social and communication behaviors were compared across genotypes. The data indicate that HTT promoter alleles by themselves do not convey risk for autism, but, rather, modify the severity of autistic behaviors in the social and communication domains. The results require replication and, given the size of the groups and subgroups examined, must be considered still preliminary. The results suggest that future research on the genetics of autism should carefully assess each of the major behavioral domains and seriously consider the possible role of modifying loci. C1 Univ Paris Sud, Fdn Vallee, F-94257 Gentilly, France. CNRS, FRE 2134, F-45071 Orleans 2, France. Yale Univ, Sch Med, Dept Child Psychiat, New Haven, CT USA. RP Tordjman, S (reprint author), Univ Paris Sud, Fdn Vallee, 7 Rue Benserade, F-94257 Gentilly, France. 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Psychiatr. PD JUL PY 2001 VL 6 IS 4 BP 434 EP 439 DI 10.1038/sj.mp.4000873 PG 6 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 439HG UT WOS:000169104900014 PM 11443529 ER PT J AU Ruhl, D Bolte, S Poustka, F AF Ruhl, D Bolte, S Poustka, F TI Language development and level of intelligence in autism: does Asperger's syndrome represent a different disorder? SO NERVENARZT LA German DT Article DE autism; Asperger's syndrome; diagnostic criteria ID HIGH-FUNCTIONING AUTISM; DIAGNOSTIC INTERVIEW; BEHAVIOR; CHILDREN AB Since the introduction of a separate diagnosis for Asperger's syndrome in the ICD-10 and DSM-IV classification systems, a controversial debate has continued on whether Asperger's syndrome is a specific, clearly distinguishable disorder within the autistic spectrum or whether it represents a milder phenotypical variation of autism. The effect on the amount of autistic symptoms of the variables language delay and level of intelligence was analyzed within a sample of individuals exhibiting autism diagnosed by standardized methods. Both variables showed a significant effect on the degree of autistic symptoms in that impairments in social interaction were less noticeable. In addition, a subsample of individuals exhibited symptoms assumed to be characteristic for Asperger's syndrome. The findings support the assumption that autism and Asperger's syndrome represent "extreme points" on a scale of severity, which leads to the suggestion that the classification of different subtypes of autism could be abandoned in favor of a dimensional (multiaxial) approach. C1 Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie Kindes & Jugensalt, D-60528 Frankfurt, Germany. RP Ruhl, D (reprint author), Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie Kindes & Jugensalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bolte S, 2000, DIAGNOSTICA, V46, P149, DOI 10.1026//0012-1924.46.3.149 Bonus B, 1997, FORTSCHR NEUROL PSYC, V65, P41, DOI 10.1055/s-2007-996308 Dilling H, 1991, INT KLASSIFIKATION P Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 FINE J, 1994, J AUTISM DEV DISORD, V24, P315, DOI 10.1007/BF02172230 Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 Howlin P, 2000, AUTISM, V4, P63, DOI DOI 10.1177/1362361300004001005 Bailey A, 1998, HUM MOL GENET, V7, P571 Kanner L, 1943, NERV CHILD, V2, P217 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x LORD C, 1995, AUTISM DIAGNOSTIC OB MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 MILLER NJ, 2000, J ABNORM PSYCHOL, V109, P227 Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 REMSCHMIDT H, 2000, MULTIAXIALES KLASSIF RUHL D, 1998, AUTISM DIAGNOSTIC OB SCHMOTZER G, 1995, AUTISMUS DIAGNOSTISC SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 NR 27 TC 4 Z9 4 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0028-2804 J9 NERVENARZT JI Nervenarzt PD JUL PY 2001 VL 72 IS 7 BP 535 EP 540 DI 10.1007/s001150170078 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 450KZ UT WOS:000169743200008 PM 11478225 ER PT J AU Cuerva, AG Sabe, L Kuzis, G Tiberti, C Dorrego, F Starkstein, SE AF Cuerva, AG Sabe, L Kuzis, G Tiberti, C Dorrego, F Starkstein, SE TI Theory of mind and pragmatic abilities in dementia SO NEUROPSYCHIATRY NEUROPSYCHOLOGY AND BEHAVIORAL NEUROLOGY LA English DT Article ID BRAIN-DAMAGED PATIENTS; ALZHEIMERS-DISEASE; MENTAL STATE; CHILDREN; RECOGNITION; ATTRIBUTION; REQUESTS; AUTISM; ADULTS; MEMORY AB Objective: "Theory of Mind" (Tom) is the capacity to attribute mental states to oneself and to others and to interpret behavior in terms of mental states. Deficits in both ToM and pragmatic abilities have been described in patients with neurologic disorders, such as frontal lobe lesions and right hemisphere strokes, but have not been assessed in demented patients. Methods: This study examined ToM and pragmatic abilities in a consecutive series of 34 patients with probable Alzheimer disease (AD) using a second-order false belief story, I I short stories assessing understanding of social situations, and a test of pragmatic abilities assessing both indirect requests and conversational implications. Results: Sixty-five percent of AD patients with mild dementia could not pass a second-order false belief task, whereas no failures were found in a group of 10 age-comparable healthy controls. AD patients who did not pass the second-order false belief task had more severe deficits on tests of verbal anterograde memory, verbal comprehension, abstract thinking, and naming, as compared with AD patients who passed the task. AD patients also showed significantly more severe pragmatic deficits than age-comparable healthy controls, and there was a significant association between ToM and pragmatic deficits. On the other hand, there were no significant associations between ToM or pragmatic deficits, and behavioral problems frequently reported in AD such as depression, delusions, apathy, and irritability. Conclusions: This initial exploratory investigation demonstrated significant deficits in both ToM and pragmatic abilities in a consecutive series of AD patients with mild dementia. C1 FLENI, Raul Carrea Inst Neurol Res, Dept Neuropsychiat, RA-1428 Buenos Aires, DF, Argentina. RP Cuerva, AG (reprint author), FLENI, Raul Carrea Inst Neurol Res, Dept Neuropsychiat, Montaneses 2325, RA-1428 Buenos Aires, DF, Argentina. CR BARONCOHEN S, 1994, BRIT J PSYCHIAT, V165, P640, DOI 10.1192/bjp.165.5.640 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Benton A. 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Neuropsychol. Behav. Neurol. PD JUL-SEP PY 2001 VL 14 IS 3 BP 153 EP 158 PG 6 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 462GN UT WOS:000170412500003 PM 11513098 ER PT J AU Van der Walt, JH Moran, C AF Van der Walt, JH Moran, C TI An audit of perioperative management of autistic children SO PAEDIATRIC ANAESTHESIA LA English DT Article DE anaesthesia : children, autism; premedication : ketamine, midazolam ID KETAMINE AB Background: Autistic children are very difficult to manage in the hospital setting because they react badly to any change in routine. Methods: We have developed a unique management program for autistic children admitted for medical and surgical procedures requiring a general anaesthetic. Details of each patient managed according to this program have been prospectively entered into an Autistic Register. Results: An audit of this database shows that we have administered anaesthesia on 87 occasions for 59 autistic children over 4 years. Conclusions: There is great variation in the severity of autism and hospital needs of these children. The focus is on early communication with the patient's families, flexibility to individualize the admission process and anaesthetic plan with admission and early discharge on the day of surgery whenever possible. Oral midazolam is an effective premedication for the milder cases and oral ketamine is the most reliable for moderate and severe cases. Comparison of oral midazolam and ketamine shows no significant different postoperative recovery and hospital discharge times. Routine intravenous fluids and antiemesis prophylaxis with removal of the i.v. cannula before return to the ward are also seen as important steps to decrease stress and smooth the postoperative phase. This program has also successfully been extended to the management of problem children due to other causes. C1 Womens & Childrens Hosp, Paediat Day Surg Unit, Adelaide, SA, Australia. Womens & Childrens Hosp, Dept Paediat Anaesthesia, Adelaide, SA, Australia. RP Van der Walt, JH (reprint author), Womens & Childrens Hosp, Dept Paediat Anaesthesia, 72 King William Rd, N Adelaide, SA 5006, Australia. CR CLEMENTS JA, 1982, J PHARM SCI, V71, P539, DOI 10.1002/jps.2600710516 ELLIOTT GR, 1996, RUDOLPHS PEDIAT, P168 GUTSTEIN HB, 1992, ANESTHESIOLOGY, V76, P28, DOI 10.1097/00000542-199201000-00004 GUTSTEIN HB, 1992, ANESTHESIOLOGY, V77, P605, DOI 10.1097/00000542-199209000-00037 Jensen AB, 2000, PAEDIATR ANAESTH, V10, P69, DOI 10.1046/j.1460-9592.2000.00401.x PARNIS SJ, 1992, ANAESTH INTENS CARE, V20, P9 Rainey L, 1998, ANAESTH INTENS CARE, V26, P682 Seid M, 1997, INT J PEDIATR OTORHI, V40, P107, DOI 10.1016/S0165-5876(97)01507-3 VANDERWALT JH, 2001, IN PRESS ANAESTH INT NR 9 TC 20 Z9 21 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 1155-5645 J9 PAEDIATR ANAESTH JI Paediatr. Anaesth. PD JUL PY 2001 VL 11 IS 4 BP 401 EP 408 DI 10.1046/j.1460-9592.2001.00688.x PG 8 WC Anesthesiology; Pediatrics SC Anesthesiology; Pediatrics GA 452ZV UT WOS:000169890500003 PM 11442855 ER PT J AU Kastner, JL Gellin, BG AF Kastner, JL Gellin, BG TI Measles-mumps-rubella vaccine and autism: The rise (and fall?) of a hypothesis SO PEDIATRIC ANNALS LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; POLYMERASE-CHAIN-REACTION; CROHNS-DISEASE; VIRUS INFECTION; IN-UTERO; EXPOSURE; CHILDREN; ABSENCE; DISORDER; TISSUES AB The authors provide an overview of the theory linking the measles-mumps-rubella vaccine with the subsequent development of autism and review evidence that disproves this theory. C1 Vanderbilt Univ, Sch Med, Dept Publ Hlth, Nashville, TN 37232 USA. RP Gellin, BG (reprint author), Vanderbilt Univ, Sch Med, Dept Publ Hlth, 221 Kirkland Hall, Nashville, TN 37232 USA. 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Annu. PD JUL PY 2001 VL 30 IS 7 BP 408 EP + PG 9 WC Pediatrics SC Pediatrics GA 477JN UT WOS:000171280600005 PM 11469172 ER PT J AU Vancassel, S Durand, G Barthelemy, C Lejeune, B Martineau, J Guilloteau, D Andres, C Chalon, S AF Vancassel, S Durand, G Barthelemy, C Lejeune, B Martineau, J Guilloteau, D Andres, C Chalon, S TI Plasma fatty acid levels in autistic children SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; BLOOD-CELL MEMBRANES; SCHIZOPHRENIC-PATIENTS; PHOSPHOLIPASE-A2 ACTIVITY; PSYCHIATRIC-DISORDERS; SEROTONIN TRANSPORTER; CHOLESTERYL ESTERS; DEPRESSED-PATIENTS; RETT-SYNDROME; METABOLISM AB Phospholipid fatty acids are major structural components of neuronal cell membranes, which modulate membrane fluidity and hence function. Evidence from clinical and biochemical sources have indicated changes in the metabolism of fatty acids in several psychiatric disorders. We examined the phospholipid fatty acids in the plasma of a population of autistic subjects compared to mentally retarded controls. Our results showed a marked reduction in the levels of 22: 6n-3 (23%) in the autistic subjects, resulting in significantly lower levels of total (n-3) polyunsaturated fatty acids (PUFA) (20%), without significant reduction in the (n-6) PUFA series, and consequently a significant increase in the (n-6)/(n-3) ratio (25%). These variations are discussed in terms of potential differences in PUFA dietary intake, metabolism, or incorporation into cellular membranes between the two groups of subjects. These results open up interesting perspectives for the investigation of new biological indices in autism. Moreover, this might have new therapeutic implications in terms of child nutrition. (C) 2001 Harcourt Publishers Ltd. C1 INRA, Lab Nutr & Secur Alimentaire, F-78352 Jouy En Josas, France. CHU Bretonneau, INSERM, U316, Serv Pedopsychiat, F-37044 Tours, France. Fac Pharm, INSERM, U316, Lab Biophys Med & Pharmaceut, Tours, France. Lab Biochim & Biol Mol, Tours, France. Fac Med, Tours, France. RP Vancassel, S (reprint author), INRA, Lab Nutr & Secur Alimentaire, F-78352 Jouy En Josas, France. 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Essent. Fatty Acids PD JUL PY 2001 VL 65 IS 1 BP 1 EP 7 DI 10.1054/plef.2001.0281 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 466CZ UT WOS:000170627900001 PM 11487301 ER PT J AU Hill, A Bolte, S Petrova, G Beltcheva, D Tacheva, S Poustka, F AF Hill, A Bolte, S Petrova, G Beltcheva, D Tacheva, S Poustka, F TI Stability and interpersonal agreement of the interview-based diagnosis of autism SO PSYCHOPATHOLOGY LA English DT Article DE autism; diagnostic stability; interpersonal agreement ID RELIABILITY; INSTRUMENTS; DISORDER AB Interpersonal agreement and stability of the Autism Diagnostic Interview-Revised (ADI-R) was examined in this study. Four raters judging 55 subjects agreed moderately to excellently on the items of the diagnostic algorithm, operationalizing the main autistic symptoms according to the classification guidelines of ICD-10 and DSM-IV. When retesting 33 individuals, some items revealed only weak stability. On the level of domains of autistic behavior and diagnosis, the interrater reliability and retest reliability were consistently convincing. Copyright (C) 2001 S. Karger AG, Basel. C1 Univ Sofia, Dept Child & Adolescent Psychiat, Sofia, Bulgaria. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. RP Poustka, F (reprint author), Klinikum JWG Univ Frankfurt AM, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. CR Angold A, 1996, J CHILD PSYCHOL PSYC, V37, P657, DOI 10.1111/j.1469-7610.1996.tb01457.x Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 BOLTE S, IN PRESS AUTISM CONGER AJ, 1980, PSYCHOL BULL, V88, P322, DOI 10.1037/0033-2909.88.2.322 Fleiss JL, 1981, STAT METHODS RATES P FOMBONNE E, 1992, J AUTISM DEV DISORD, V22, P563, DOI 10.1007/BF01046328 Gillberg C, 1996, EUR CHILD ADOLES PSY, V5, P67 Howlin P., 1998, AUTISM PERVASIVE DEV, P209 Kanner L, 1943, NERV CHILD, V2, P217 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 Maughan B, 1997, J PERS DISORD, V11, P19 Pilowsky T, 1998, J AUTISM DEV DISORD, V28, P143, DOI 10.1023/A:1026092632466 Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 RUTTER M, 1988, ASSESSMENT DIAGNOSIS, P408 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 YIRMIYA N, 1994, J AUTISM DEV DISORD, V24, P281, DOI 10.1007/BF02172227 NR 19 TC 41 Z9 41 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD JUL-AUG PY 2001 VL 34 IS 4 BP 187 EP 191 DI 10.1159/000049305 PG 5 WC Psychiatry SC Psychiatry GA 474UV UT WOS:000171126000004 PM 11549928 ER PT J AU Eikeseth, S Jahr, E AF Eikeseth, S Jahr, E TI The UCLA reading and writing program: an evaluation of the beginning stages SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article ID AUTISTIC-CHILDREN; CONDITIONAL DISCRIMINATION; STIMULUS-EQUIVALENCE; AUDITORY STIMULUS; COMPLEX STIMULI; INDIVIDUALS; RETARDATION; BEHAVIOR; LANGUAGE; SAMPLE AB Some individuals with developmental disabilities fail to acquire functional speech despite extensive teaching efforts. To help such individuals develop functional communication skills, a "reading and writing" program was developed, This study was designed to evaluate early parts of the program. Acquisition, transfer, and maintenance of "reading and writing" skills was examined and compared with the acquisition, transfer, and maintenance of sign language. Participants were four children with autism, who scored within the mentally retarded range on standardized tests of intellectual, adaptive, and language functioning, and three 3-year-old non-disabled children. A simultaneous-treatment design was employed to compare the rate of acquisition of "reading and writing" skills to the rate at which the participants acquired receptive and expressive signs. For the participants with autism, acquisition of "reading and writing" was more successful than receptive and expressive signing on all variables assessed. All non-disabled participants acquired all of the "reading and writing" and sign language skills, but participants with autism did not. However, "reading" was acquired slightly quicker by the participants with autism than the non-disabled participants, and the participants with autism also showed some evidence of better transfer and maintenance than the non-disabled participants did. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Akershus Coll, N-1302 Sandvika, Norway. Glenne Ctr, N-1302 Sandvika, Norway. RP Eikeseth, S (reprint author), Akershus Coll, POB 372, N-1302 Sandvika, Norway. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BALTAXE C, 1981, FRONTIER KNOWLEDGE M, P223 BALTAXE CAM, 1975, J SPEECH HEAR DISORD, V40, P439 BALTAXE CA, 1981, SPEECH EVALUATION PS, P285 BARLOW DH, 1988, SINGLE CASE EXPT DES Bondy Andrew S., 1998, Seminars in Speech and Language, V19, P373, DOI 10.1055/s-2008-1064055 Carr E. G., 1982, ED UNDERSTANDING AUT, P142 CARR EG, 1985, J APPL BEHAV ANAL, V18, P111, DOI 10.1901/jaba.1985.18-111 CARR EG, 1983, J APPL BEHAV ANAL, V16, P297, DOI 10.1901/jaba.1983.16-297 Catania A. C., 1998, LEARNING Charlop M. H., 1994, AUTISM CHILDREN ADUL, P213 DEVANY JM, 1986, J EXP ANAL BEHAV, V46, P243, DOI 10.1901/jeab.1986.46-243 DEVILLIE.JG, 1974, J CONSULT CLIN PSYCH, V42, P111, DOI 10.1037/h0036073 Duarte AM, 1998, PSYCHOL REC, V48, P631 DUBE WV, 1989, J EXP ANAL BEHAV, V51, P65, DOI 10.1901/jeab.1989.51-65 DUGDALE N, 1990, BEHAVIOUR ANALYSIS IN THEORY AND PRACTICE, P115 EIKESETH S, 1997, ENVIRON BEHAV, P138 EIKESETH S, 1992, J EXP ANAL BEHAV, V58, P123, DOI 10.1901/jeab.1992.58-123 Fay W. H., 1980, EMERGING LANGUAGE AU Hayes S. C., 1994, BEHAV ANAL LANGUAGE, P9 HERMELIN JB, 1970, PSYCHOL EXPT AUTISTI Kazdin A. E., 1982, SINGLE CASE RES DESI KIERNAN C, 1983, J CHILD PSYCHOL PSYC, V24, P339, DOI 10.1111/j.1469-7610.1983.tb00115.x KOEGEL LK, 1992, J APPL BEHAV ANAL, V25, P341, DOI 10.1901/jaba.1992.25-341 Koegel Lynn Kern, 1994, P165 Lovaas O. I., 1981, TEACHING DEV DISABLE Lovaas O. I., 1987, J APPL BEHAV ANAL, V20, P45 Lovaas O. I., 1977, AUTISTIC CHILD LANGU MCGEE GG, 1985, J APPL BEHAV ANAL, V18, P17, DOI 10.1901/jaba.1985.18-17 PRIZANT BM, 1983, J SPEECH HEAR DISORD, V48, P269 Rosales-Ruiz J, 2000, PSYCHOL REC, V50, P173 RUTTER M, 1978, J AUTISM CHILD SCHIZ, V8, P139, DOI 10.1007/BF01537863 Rutter M., 1994, CHILD ADOL PSYCH CL, P569 SAUNDERS RR, 1988, J EXP ANAL BEHAV, V49, P95, DOI 10.1901/jeab.1988.49-95 SCHENK JJ, 1993, Q J EXP PSYCHOL-B, V46, P345 SCHENK JJ, 1995, PSYCHOL REC, V45, P477 Schiefelbusch R. L., 1972, LANGUAGE MENTALLY RE SCHREIBMAN L, 1986, ANAL INTERVEN DEVEL, V6, P109, DOI 10.1016/0270-4684(86)90009-1 SIDMAN M, 1986, ANAL INTERVEN DEVEL, V6, P1, DOI 10.1016/0270-4684(86)90003-0 SIDMAN M, 1973, AM J MENT DEF, V77, P515 SIDMAN M, 1971, J SPEECH HEAR RES, V14, P5 SIDMAN M, 1982, J EXP ANAL BEHAV, V37, P5, DOI 10.1901/jeab.1982.37-5 Sidman M., 1986, ANAL INTEGRATION BEH, P213 SMEETS PM, IN PRESS EUROPEAN J SMEETS PM, 1995, Q J EXP PSYCHOL-B, V48, P311 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 STROMER R, 1992, J APPL BEHAV ANAL, V25, P893, DOI 10.1901/jaba.1992.25-893 Stromer R, 1996, J APPL BEHAV ANAL, V29, P25, DOI 10.1901/jaba.1996.29-25 WATTHENLOVAAS N, IN PRESS TEACHING IN WOLFF S, 1965, J CHILD PSYCHOL PSYC, V6, P29, DOI 10.1111/j.1469-7610.1965.tb02152.x NR 50 TC 12 Z9 12 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 JUL-AUG PY 2001 VL 22 IS 4 BP 289 EP 307 DI 10.1016/S0891-4222(01)00073-7 PG 19 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 463DB UT WOS:000170460600003 PM 11523953 ER PT J AU Chakrabarti, S Fombonne, E AF Chakrabarti, S Fombonne, E TI Pervasive developmental disorders in preschool children SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID AUTISM DIAGNOSTIC INTERVIEW; MEDICAL CONDITIONS; ABNORMALITIES; EPIDEMIOLOGY; INSTRUMENT; SPECTRUM AB Context Prevalence rates of autism-spectrum disorders are uncertain, and speculation that their incidence is increasing continues to cause concern. Objective To estimate the prevalence of pervasive developmental disorders (PDDs) in a geographically defined population of preschool children. Design, Setting, and Participants Survey conducted July 1998 to June 1999 in Staffordshire, England. The area's 15500 children aged 2.5 to 6.5 years were screened for developmental problems. Children with symptoms suggestive of a PDD were intensively assessed by a multidisciplinary team, which conducted standardized diagnostic interviews and administered psychometric tests. Main Outcome Measure Prevalence estimates for subtypes of PDDs. Results A total of 97 children (79.4% male) were confirmed to have a PDD. The prevalence of PDDs was estimated to be 62.6 (95% confidence interval, 50.8-76.3) per 10000 children. Prevalences were 16.8 per 10000 for autistic disorder and 45.8 per 10000 for other PDDs. The mean age at diagnosis was 41 months, and 81% were originally referred by health visitors (nurse specialists). Of the 97 children with a PDD, 25.8% had some degree of mental retardation and 9.3% had an associated medical condition. Conclusions Our results suggest that rates of PDD are higher than previously reported. Methodological limitations in existing epidemiological investigations preclude interpretation of recent high rates as indicative of increased incidence of these disorders although this hypothesis requires further rigorous testing. Attention is nevertheless drawn to the important needs of a substantial minority of preschool children. C1 Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, MRC,Child Psychiat Unit, London SE5 8AF, England. Cent Clin, Child Dev Ctr, Stafford, England. RP Fombonne, E (reprint author), Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, MRC,Child Psychiat Unit, Denmark Hill, London SE5 8AF, England. 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Am. Med. Assoc. PD JUN 27 PY 2001 VL 285 IS 24 BP 3093 EP 3099 DI 10.1001/jama.285.24.3093 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 444FF UT WOS:000169388900022 PM 11427137 ER PT J AU Hyman, SL Rodier, PM Davidson, P AF Hyman, SL Rodier, PM Davidson, P TI Pervasive developmental disorders in young children SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID AUTISM C1 Univ Rochester, Sch Med & Dent, Strong Ctr Dev Disabil, Dept Pediat, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. RP Hyman, SL (reprint author), Univ Rochester, Sch Med & Dent, Strong Ctr Dev Disabil, Dept Pediat, 601 Elmwood Ave,Box 671, Rochester, NY 14642 USA. 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Am. Med. Assoc. PD JUN 27 PY 2001 VL 285 IS 24 BP 3141 EP 3142 DI 10.1001/jama.285.24.3141 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 444FF UT WOS:000169388900030 PM 11427145 ER PT J AU [Anonymous] AF [Anonymous] TI MMR vaccination and autism: no temporal correlation? SO INPHARMA LA English DT News Item CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P2852 Edwardes M, 2001, JAMA-J AM MED ASSOC, V285, P2852, DOI 10.1001/jama.285.22.2852 NR 2 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 JUN 23 PY 2001 IS 1293 BP 17 EP 17 PG 1 GA 447HB UT WOS:000169564900031 ER PT J AU Wong, K AF Wong, K TI The search for autism's roots SO NATURE LA English DT News Item ID DISORDER; CHILDREN; PREVALENCE; 15Q CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 1995, PSYCHOL MED, V25, P63 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1999, NEURODEVELOPMENTAL D, P401 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 1997, AM J HUM GENET, V60, P928 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 Bailey A, 1998, HUM MOL GENET, V7, P571 Joseph RM, 1997, J AUTISM DEV DISORD, V27, P385, DOI 10.1023/A:1025853321118 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 KEMPER TL, 1993, NEUROL CLIN, V11, P175 Manning JT, 2001, DEV MED CHILD NEUROL, V43, P160, DOI 10.1017/S0012162201000317 Manning JT, 1998, HUM REPROD, V13, P3000, DOI 10.1093/humrep/13.11.3000 Patja A, 2000, PEDIATR INFECT DIS J, V19, P1127, DOI 10.1097/00006454-200012000-00002 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 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 SCHULTZ RT, 2000, J ARCH GEN PSYCHIAT, V57, P331 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 *US CDCP, 2000, PREV AUT BRICK TOWNS Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Webb EVJ, 1997, DEV MED CHILD NEUROL, V39, P150 WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 NR 24 TC 2 Z9 2 PU MACMILLAN PUBLISHERS LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD JUN 21 PY 2001 VL 411 IS 6840 BP 882 EP 884 DI 10.1038/35082228 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 444EN UT WOS:000169386200014 PM 11418823 ER PT J AU Vastag, B AF Vastag, B TI Brain gene for autism SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT News Item NR 0 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 JUN 20 PY 2001 VL 285 IS 23 BP 2966 EP 2966 DI 10.1001/jama.285.23.2966 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 442AR UT WOS:000169263200004 ER PT J AU Farrington, CP Miller, E Taylor, B AF Farrington, CP Miller, E Taylor, B TI MMR and autism: further evidence against a causal association SO VACCINE LA English DT Article DE autism; MMR; adverse events ID CASE SERIES; VACCINE AB The hypothesis that MMR vaccines cause autism was first raised by reports of cases in which developmental regression occurred soon after MMR vaccination. A previous study found no evidence to support this hypothesis. It has recently been suggested that MMR vaccine might cause autism, but that the induction interval need not be short. The data from the earlier study were reanalysed to test this second hypothesis. Our results do not support this hypothesis. and provide further evidence against a causal association between MMR vaccination and autism. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Open Univ, Dept Stat, Milton Keynes MK7 6AA, Bucks, England. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, London NW9 5EQ, England. UCL, Ctr Community Child Hlth, Royal Free & Univ Coll Med Sch, London NW3 2QG, England. RP Farrington, CP (reprint author), Open Univ, Dept Stat, Walton Hall, Milton Keynes MK7 6AA, Bucks, England. EM c.p.farrington@open.ac.uk CR Bozosky Zoltan, 1998, BRIT MED J, V316, P561 FARRINGTON CP, 1995, BIOMETRICS, V51, P228, DOI 10.2307/2533328 Farrington CP, 1996, AM J EPIDEMIOL, V143, P1165 Roger JH, 2000, LANCET, V356, P160, DOI 10.1016/S0140-6736(05)73169-X Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Taylor B, 2000, LANCET, V356, P1273, DOI 10.1016/S0140-6736(05)73875-7 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 WAKEFIELD AJ, 2000, 106 C US HOUS REPR C NR 8 TC 86 Z9 86 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0264-410X J9 VACCINE JI Vaccine PD JUN 14 PY 2001 VL 19 IS 27 BP 3632 EP 3635 DI 10.1016/S0264-410X(01)00097-4 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 443AQ UT WOS:000169317500006 PM 11395196 ER PT J AU Dales, L Hammer, SJ Smith, NJ AF Dales, L Hammer, SJ Smith, NJ TI MMR immunization and autism - Reply SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 Calif Dept Hlth, Immunizat Branch, Berkeley, CA USA. RP Dales, L (reprint author), Calif Dept Hlth, Immunizat Branch, Berkeley, CA USA. CR *IMM SAF REV COMM, 2001, MEASL MUMPS RUB VACC Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 NR 4 TC 3 Z9 3 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 JUN 13 PY 2001 VL 285 IS 22 BP 2852 EP 2853 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 440BP UT WOS:000169156300013 ER PT J AU Edwardes, M Baltzan, M AF Edwardes, M Baltzan, M TI MMR immunization and autism SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 Royal Victoria Hosp, Montreal, PQ H3A 1A1, Canada. RP Edwardes, M (reprint author), Royal Victoria Hosp, Montreal, PQ H3A 1A1, Canada. CR *CAL DEP DEV SERV, 1999, CHANG POP PERS AUT P Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 NR 3 TC 3 Z9 3 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 JUN 13 PY 2001 VL 285 IS 22 BP 2852 EP 2852 DI 10.1001/jama.285.22.2852 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 440BP UT WOS:000169156300012 PM 11401594 ER PT J AU Lauritsen, MB Ewald, H AF Lauritsen, MB Ewald, H TI The genetics of autism SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Review DE autism; review; genetics; co-morbidity; chromosome abnormalities ID FRAGILE-X-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER 5-HTT; TUBEROUS SCLEROSIS COMPLEX; DSM-III-R; INFANTILE-AUTISM; FAMILY HISTORY; LINKAGE-DISEQUILIBRIUM; MULTIPLEX FAMILIES; NEUROPSYCHIATRIC DISORDERS AB Objective: To review systematically the empirical evidence for the involvement of genetic risk factors in infantile autism. Method: We aimed at including all relevant papers written in English. We conducted a Medline search in September 2000. In addition we searched the reference lists of related papers. Results: A relatively small number of reports including family and twin studies, comorbidity, cytogenetic and molecular genetic studies were reviewed. Conclusion: As well family, twin, cytogenetic and molecular genetic studies supported the importance of genetic risk factors in infantile autism. In most individual cases probably at least a few gene variants simultaneously determine the genetic risk. Presently the most interesting chromosome regions concerning the aetiology of autism are chromosomes 7q31-35, 15q11-13 and 16p13.3 which have been suggested by different lines of genetic research. C1 Univ Aarhus, Psychiat Hosp Aarhus, Inst Basic Psychiat Res, Dept Psychiat Demog, DK-8240 Risskov, Denmark. RP Lauritsen, MB (reprint author), Univ Aarhus, Psychiat Hosp Aarhus, Inst Basic Psychiat Res, Dept Psychiat Demog, DK-8240 Risskov, Denmark. 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Scand. PD JUN PY 2001 VL 103 IS 6 BP 411 EP 427 DI 10.1034/j.1600-0447.2001.00086.x PG 17 WC Psychiatry SC Psychiatry GA 435WX UT WOS:000168906100002 PM 11401655 ER PT J AU Nylander, L Gillberg, C AF Nylander, L Gillberg, C TI Screening for autism spectrum disorders in adult psychiatric out-patients: a preliminary report SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE autism; Asperger syndrome; prevalence; adults; psychiatry; screening ID ASPERGER-SYNDROME; TOTAL POPULATION; CHILDREN AB Objective: To estimate the prevalence of autism spectrum disorders (ASD) among adult psychiatric out-patients; to evaluate the efficacy of a new brief screening questionnaire (ASDASQ). Method: 1323 adult psychiatric out-patients were screened by staff. Analysis of psychiatric records of patients (n = 66) scoring high on the ASDASQ yielded 31 patients with a suspected ASD. Twenty-two of these patients were clinically examined. Three psychometric aspects of the questionnaire were studied. Results: Seventeen patients were found by clinical examination to have an ASD. Since two patients scoring low on the ASDASQ were known to have an ASD, at least 19 patients in this population (1.4%) had a definite ASD. Seventeen of the ASD patients had been previously diagnosed with other psychiatric disorders, most frequently schizophrenia (n = 5). Of patients attending a treatment centre for severe psychiatric disabilities (n = 499), 3.2% had an ASD. The ASDASQ showed good reliability across and within raters. Internal consistency was excellent. Conclusion: Adult psychiatric patients sometimes have undiagnosed autism spectrum disorders. The ASDASQ can be useful for screening. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. Univ Lund, Dept Psychiat, S-22101 Lund, Sweden. RP Nylander, L (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgaten 12, SE-41119 Gothenburg, Sweden. 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Scand. PD JUN PY 2001 VL 103 IS 6 BP 428 EP 434 DI 10.1034/j.1600-0447.2001.00175.x PG 7 WC Psychiatry SC Psychiatry GA 435WX UT WOS:000168906100003 PM 11401656 ER PT J AU Herzing, LBK Kim, SJ Cook, EH Ledbetter, DH AF Herzing, LBK Kim, SJ Cook, EH Ledbetter, DH TI The human aminophospholipid-transporting ATPase gene ATP10C maps adjacent to UBE3A and exhibits similar imprinted expression SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID ANGELMAN-SYNDROME; AUTISTIC DISORDER; CANDIDATE GENE; PROXIMAL 15Q; UBE3A/E6-AP; CHROMOSOME-15; MUTATIONS AB Maternal duplications of the imprinted 15q11-13 domain result in an estimated 1%-2% of autism-spectrum disorders, and linkage to autism has been identified within 15q12-13. UBE3A, the Angelman syndrome gene, has, to date, been the only maternally expressed, imprinted gene identified within this region, but mutations have not been found in autistic patients. Here we describe the characterization of ATP10C, a new human imprinted gene, which encodes a putative protein homologous to the mouse aminophospholipid-transporting ATPase Atp10c. ATP10C maps within 200 kb distal to UBE3A and, like UBE3A, also demonstrates imprinted, preferential maternal expression in human brain. The location and imprinted expression of ATP10C thus make it a candidate for chromosome 15-associated autism and suggest that it may contribute to the Angelman syndrome phenotype. C1 Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Lab Dev Neurosci, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. RP Ledbetter, DH (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St, Chicago, IL 60637 USA. 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Because decreasing sample heterogeneity would increase the power to identify genes, the effect on evidence for linkage of restricting a sample of autism-affected relative pairs to those with delayed onset (at age >36 mo) of phrase speech (PSD, for phrase speech delay) was studied. In the second stage of a two-stage genome screen for susceptibility loci involving 95 families with two or more individuals with autism or related disorders, a maximal multipoint heterogeneity LOD score (HLOD) of 1.96 and a maximal multipoint nonparametric linkage (NPL) score of 2.39 was seen on chromosome 2q. Restricting the analysis to the subset of families (n = 49) with two or more individuals having a narrow diagnosis of autism and PSD generated a maximal multipoint HLOD score of 2.99 and an NPL score of 3.32. The increased scores in the restricted sample, together with evidence for heterogeneity in the entire sample, indicate that the restricted sample comprises a population that is more genetically homogeneous, which could therefore increase the likelihood of positional cloning of susceptibility loci. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Neurobiol, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. St James Hosp, Dept Psychiat Elderly, Dublin 8, Ireland. Trinity Coll, Dept Psychiat, Dublin, Ireland. St Patricks Hosp, Dublin, Ireland. RP Buxbaum, JD (reprint author), CUNY 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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J. Hum. Genet. PD JUN PY 2001 VL 68 IS 6 BP 1514 EP 1520 DI 10.1086/320588 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 439DB UT WOS:000169094600023 PM 11353400 ER PT J AU Williams, CA Lossie, A Driscoll, D AF Williams, CA Lossie, A Driscoll, D CA RC Philips Unit TI Angelman syndrome: Mimicking conditions and phenotypes SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Angelman syndrome; mimicking conditions; phenotype; diagnosis ID MILD MENTAL-RETARDATION; LENNOX-GASTAUT-SYNDROME; RETT-SYNDROME; MOLECULAR CHARACTERIZATION; INTERSTITIAL DELETION; CLINICAL-FEATURES; PRADER-WILLI; ATR-X; MUTATION; AUTISM AB The diagnosis of Angelman syndrome (AS) can be confirmed by genetic laboratory in about 80% of cases. In 20%, the diagnosis remains clinical, but often there is uncertainty about the correctness of the clinical diagnosis and alternative diagnosis may be investigated. In evaluating individuals for AS in our center since 1989, we have encountered several mimicking conditions, and additional ones have been reported in the literature. Mimicking conditions can be grouped into the areas of chromosome, single gene, and symptom complex anomalies. Microdeletions or microduplications include chromosome regions 2,4,17, 22, and 15, Single gene conditions include methylene tetrahydrofolate reductase deficiency (MTHFR), Rett syndrome, alpha-thalassemia retardation syndrome (ATR-X), and Gurrieri syndrome. Symptom complexes include cerebral palsy, static encephalopathy, Lennox-Gastaut syndrome, autism spectrum disorder, pervasive developmental delay (PDD), and mitochondrial disorders. We present a review of these mimicking disorders to increase the awareness about conditions that can lead to an incorrect clinical diagnosis of AS. (C) 2001 Wiley-Liss, Inc. C1 Univ Florida, Div Genet, Gainesville, FL 32610 USA. RP Williams, CA (reprint author), Univ Florida, Div Genet, Gainesville, FL 32610 USA. 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J. Med. Genet. PD JUN 1 PY 2001 VL 101 IS 1 BP 59 EP 64 DI 10.1002/ajmg.1316 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 428EV UT WOS:000168449300014 PM 11343340 ER PT J AU Lazartigues, A Lemonnier, E Le Roy, F Moalic, K Moalic, K Baghdadli, A Fermanian, J Aussilloux, C AF Lazartigues, A Lemonnier, E Le Roy, F Moalic, K Moalic, K Baghdadli, A Fermanian, J Aussilloux, C TI From the first signs of autism to the initial acceptance of care. SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE autism; early signs; initial acceptance of care; initial paedopsychiatric consultation ID AGE; DISORDER; CHILDREN; RECOGNITION; INFANCY; ONSET AB Currently the diagnostis of autism takes place towards the 3rd year, however, when parents are questioned concerning the first signs, they had become concerned very much earlier, Paediatricians and general practitioners, who saw these children after the parents had observed problems, tended to reassure them, due to the fact that they lacked the necessary elements enabling them to give greater depth to their diagnostic questioning (decision tree lacked branches). The objective of this work is to specify age of the observation of the first signs by parents, age at initial paedopsychiatric consultation, age at the initial acceptance of care and the analyse factor wich influence those ages. (C) 2001 Editions scientifiques et medicales Elsevier SAS. C1 CHU Brest, Hop Bohars, F-29820 Bohars, France. CHU Montpellier, F-34295 Montpellier 1, France. CHU Necker, F-75015 Paris, France. RP Lazartigues, A (reprint author), CHU Brest, Hop Bohars, F-29820 Bohars, France. 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Med.-Psychol. PD JUN PY 2001 VL 159 IS 5 BP 403 EP 410 DI 10.1016/S0003-4487(01)00065-8 PG 8 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 462GG UT WOS:000170411900009 ER PT J AU Baird, G Charman, T Cox, A Baron-Cohen, S Swettenham, J Wheelwright, S Drew, A AF Baird, G Charman, T Cox, A Baron-Cohen, S Swettenham, J Wheelwright, S Drew, A TI Screening and surveillance for autism and pervasive developmental disorders SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID YOUNG-CHILDREN; SPECTRUM DISORDERS; DIAGNOSTIC INTERVIEW; BEHAVIORAL TREATMENT; FUNCTIONING AUTISM; ASPERGER-SYNDROME; PARENTS CONCERNS; RATING-SCALE; FOLLOW-UP; ADI-R C1 Guys Kings Coll & St Thomas Med Sch, Newcomen Ctr, London, England. Guys Kings Coll & St Thomas Med Sch, Bloomfield Clin, London, England. UCL, Inst Child Hlth, London, England. UCL, Dept Human Commun & Sci, London, England. 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Dis. Child. PD JUN PY 2001 VL 84 IS 6 BP 468 EP 475 DI 10.1136/adc.84.6.468 PG 8 WC Pediatrics SC Pediatrics GA 439KY UT WOS:000169117100006 PM 11369559 ER PT J AU Sprovieri, MHS Assumpcao, FB AF Sprovieri, MHS Assumpcao, FB TI Family dynamics of autist children SO ARQUIVOS DE NEURO-PSIQUIATRIA LA Portuguese DT Article DE familly; familiar relationship; autism AB We studied 15 families with autists, 15 with Down's syndrome and 15 asymptomatic children. Patients' age ranged from 5 to 15 years-old. The parents of these three families' groups were appraised in regard to their family dynamics, to relate those symptoms to the functioning of an autist family, in a comparative study. Details were provided of the families, the overall autistic features, the autist's family, the family and the mental health, their limitations and difficulties throughout the vital cycle. An attempt was made to locale the factors that aid the family in hindering the healthy emotional development of its members. The field research was achieved by use of the instruments of the Family Dynamics Evaluation, (Carneiro, 1983). The data gathered were statistically compared. Considering the family population studied (n = 45), we found that the autists' families and victims of Down's syndrome made it difficult to sustain the emotional health of group members. We conclude that the autist's family dynamics caused difficulties to the emotional health of the group's members. C1 Pontificia Univ Catolica Sao Paulo, Sao Paulo, Brazil. Univ Fed Sao Paulo, Dept Psiquiatria, Fac Med, Sao Paulo, Brazil. FMUSP, Inst Psiquiatria, Hosp Clin, Serv Psiquiatria Infancia & Adolscencia, Sao Paulo, Brazil. CR ASSUMPCAO FB, 1991, INTRO ESTUDO DEFICIE BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 CARNEIRO TF, 1983, FAMILIA DIAGNOSTICO CATWELL DP, 1979, AUTISM REAPPRAISAL C, P269 COHEN S, 1985, DESPITE CARE PRINCIP CRAVEN RF, 1972, NURS FORUM, V11, P187 GILBERG G, 1990, ACTA PSYCHIAT SCAND, V81, P209 GOFFMAN E, 1982, ESTIGMAS NOTAS MANIP HERZ F, 1980, ETHNICITY FAMILY THE, P223 KRYNSKI S, 1969, DEFICIENCIA MENTAL LOMBARDI C, 1988, REV SAUDE PUBL, V22, P253, DOI 10.1590/S0034-89101988000400001 MCGOLDRICK M, 1991, LIVING LOSS DEATH FA Minuchin S., 1981, FAMILY THERAPY TECHN *OMS, 1995, DSM IV PAUL NL, 1965, COMMUNITY MENT HLT J, V1, P339, DOI 10.1007/BF01434390 RICCI MB, 1989, THESIS PONTIFICIA U SAMPAIO D, 1985, TERAPIA FAMILIAR Saraceno C., 1992, SOCIOLOGIA FAMILIA SATIR V, 1969, TERAPIA GRUPO FAMILI SHAPIRO J, 1983, SOC SCI MED, V17, P913, DOI 10.1016/0277-9536(83)90218-6 STIERLING H, 1974, SEPARATING PARENTS A SUMMERS CJ, 1989, SUPPORT CAREGIVING F, P27 TAYLOR SC, 1980, PEDIAT NURS NOV, P9 TERKELSEN KG, 1980, FAMILY LIFE CYCLE FR, P21 VALMAN M, 1981, BRIT MED J, V283, P1166 VIEIRA AB, 1983, THESIS PONTIFICIA U Wright L., 1979, ENCY PEDIAT PSYCHOL YARROW MJ, 1985, J SOC ISSUES, V11, P12 1974, FAMILIAS FUNCIONAMEN NR 29 TC 4 Z9 10 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD JUN PY 2001 VL 59 IS 2A BP 230 EP 237 DI 10.1590/S0004-282X2001000200016 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 436XC UT WOS:000168960300016 PM 11400032 ER PT J AU Bruck, I Antoniuk, SA Halick, SMS Spessatto, A Bruyn, LR Rodrigues, M Koneski, J Facchim, D AF Bruck, I Antoniuk, SA Halick, SMS Spessatto, A Bruyn, LR Rodrigues, M Koneski, J Facchim, D TI Rett syndrome: retrospective and prospective study of 28 patients SO ARQUIVOS DE NEURO-PSIQUIATRIA LA Portuguese DT Article DE typical Rett syndrome; atypical Rett syndrome; epilepsy; autism; milestone disturbances; hand stereotypies ID GIRLS; PREVALENCE; CRITERIA AB From November 1982 to May 1999, 28 children with Rett syndrome were followed-up for a medium period of 6 years and 2 months. Regression of developmental milestones started at the age between 5 and 20 months. Nineteen cases of typical Rett syndrome had uneventful pre and perinatal periods, loss of previously acquired purposeful hand skills, mental and motor regression and developed hand stereotypies; sixteen had head growth deceleration and 12 gait apraxia. Nine patients were atypical cases, 2 formes frustres, 2 congenital, 3 with early seizure onset, 1 preserved speech and 1 male. Epilepsy was present in 21 patients, predominantly partial seizures and the drug of choise was carbamazepine (15 patients). In the initial evaluation most patients were distributed on Stages II and III and on follow-up on Stages III and IV. Three children died. C1 Univ Fed Parana, HC, Dept Pediat, CENEP, BR-80060000 Curitiba, Parana, Brazil. Univ Estadual Campinas, Fac Ciencias Med, Campinas, SP, Brazil. CR ALMATEEN M, 1986, AM J DIS CHILD, V140, P761 ARMSTRONG D, 1995, J NEUROPATH EXP NEUR, V54, P195, DOI 10.1097/00005072-199503000-00006 Bruck I, 1990, Arq Neuropsiquiatr, V48, P489 BRUCK I, 1991, AM J MED GENET, V39, P415, DOI 10.1002/ajmg.1320390411 BUDDEN S, 1997, EUR CHILD ADOLES PSY, V1, P103 Clarke A, 1996, J MED GENET, V33, P693, DOI 10.1136/jmg.33.8.693 HAGBERG B, 1985, ACTA PAEDIATR SCAND, V74, P405, DOI 10.1111/j.1651-2227.1985.tb10993.x HAGBERG B, 1983, ANN NEUROL, V14, P471, DOI 10.1002/ana.410140412 HAGBERG B, 1995, ACTA PAEDIATR, V84, P971, DOI 10.1111/j.1651-2227.1995.tb13809.x HAGBERG B, 1985, BRAIN DEV-JPN, V7, P277 HAGBERG BA, 1994, PEDIATR NEUROL, V11, P5, DOI 10.1016/0887-8994(94)90082-5 HAGNE I, 1989, ELECTROEN CLIN NEURO, V72, P1, DOI 10.1016/0013-4694(89)90025-4 HOLM VA, 1985, J DEV BEHAV PEDIATR, V6, P32 Huang T J, 1994, Orthop Rev, V23, P931 Iyama C M, 1993, Adv Pediatr, V40, P217 Jan MMS, 1999, PEDIATR NEUROL, V20, P238, DOI 10.1016/S0887-8994(98)00150-7 KERR AM, 1985, BRIT MED J, V291, P579 KITT CA, 1995, NEUROPEDIATRICS, V26, P114, DOI 10.1055/s-2007-979739 NAIDU S, 1986, AM J MED GENET, V24, P61 REISS AL, 1993, ANN NEUROL, V34, P227, DOI 10.1002/ana.410340220 Rosemberg S, 1987, Arq Neuropsiquiatr, V45, P143 Sirianni N, 1998, AM J HUM GENET, V63, P1552, DOI 10.1086/302105 SWAIMAN KF, 1999, PEDIAT NEUROLOGY PRI, V2, P836 Tang J, 1997, PEDIATR NEUROL, V17, P327, DOI 10.1016/S0887-8994(97)00151-3 TREVATHAN E, 1988, ANN NEUROL, V23, P425 Wan MM, 1999, AM J HUM GENET, V65, P1520, DOI 10.1086/302690 WIELAWSKI I, 1986, PROVIDENCE J B ZOGHBI HY, 1990, BRAIN DEV-JPN, V12, P131 NR 28 TC 2 Z9 2 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD JUN PY 2001 VL 59 IS 2B BP 407 EP 410 DI 10.1590/S0004-282X2001000300018 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 451AV UT WOS:000169779700018 PM 11460188 ER PT J AU Werth, A Perkins, M Boucher, J AF Werth, A Perkins, M Boucher, J TI 'Here's the weavery looming up': Verbal humour in a woman with high-functioning autism SO AUTISM LA English DT Article DE Asperger syndrome; autism; creativity; verbal humour; word play AB A case study of Grace, a 29-year-old woman with high-functioning autism, is presented. Grace is unusual for a person with autism in that she produces a great deal of humorous and creative word play. She is also unusual in that she writes and then audio-records letters' to her family, and produces copious cartoon-like drawings which she annotates, with the result that multiple examples of her humour are available in permanent form. We present examples of Graces use of puns, jokes, neologisms, portmanteau words, irreverent humour, irony, sarcasm and word play based on her obsessional interests. The examples are used to illustrate the forms and content of Grace's humour, and are discussed in relation to current theories of autism and of normal humour. C1 Univ Sheffield, Dept Human Commun Sci, Sheffield S10 2TN, S Yorkshire, England. Community Hlth S London NHS Trust, London, England. Univ Warwick, Coventry CV4 7AL, W Midlands, England. RP Perkins, M (reprint author), Univ Sheffield, Dept Human Commun Sci, Sheffield S10 2TN, S Yorkshire, England. CR ASPERGER H, 1992, AUTISM ASPERGER SYND, P37 Attardo Salvatore, 1994, LINGUISTIC THEORIES Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Crystal David, 1998, LANGUAGE PLAY Dowker A, 1996, PSYCHOL MED, V26, P913 Everard M. P., 1976, INT S AUT ST GALL SW FORABOSCO G, 1992, HUMOR, V5, P45, DOI 10.1515/humr.1992.5.1-2.45 Freud Sigmund, 1976, JOKES THEIR RELATION, VVI HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R Happe FGE, 1991, AUTISM ASPERGER SYND, P207, DOI 10.1017/CBO9780511526770.007 KANNER L, 1946, AM J PSYCHIAT, V103, P242 Klinger L. G., 1995, LEARNING COGNITION A, P119 Koestler A., 1964, ACT CREATION McGhee Paul E., 1979, HUMOR ITS ORIGIN DEV Mesibov G., 1992, HIGH FUNCTIONING IND, P143 Mindess H., 1971, LAUGHTER LIBERATION Reddy V., 1997, INFANT DEV RECENT AD, P247 REDDY V, IN PRESS BRIT J PSYC RICKS DM, 1975, J AUTISM CHILD SCHIZ, V5, P191, DOI 10.1007/BF01538152 SCHULTZ TR, 1976, HUMOUR LAUGHTER THEO STJAMES PJ, 1994, J AUTISM DEV DISORD, V24, P603 VANBOURGONDIEN ME, 1987, J AUTISM DEV DISORD, V17, P417 Wing L., 1996, AUTISTIC SPECTRUM GU NR 23 TC 13 Z9 13 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 111 EP 125 DI 10.1177/1362361301005002002 PG 15 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700001 PM 11706860 ER PT J AU Shah, K AF Shah, K TI What do medical students know about autism? SO AUTISM LA English DT Article DE autism; early diagnosis; medical training ID ASPERGER-SYNDROME; EPIDEMIOLOGY; INTERVENTION AB Although recent research indicates the importance of early recognition and intervention for children with autism, it is clear that many families remain very dissatisfied with the diagnostic process. In order to improve this situation, it is essential that primary care practitioners, such as GPs, are fully aware of the core symptoms of autism. The present study reports on autism awareness amongst 250 medical students at different stages of their training. Differences between first-year and fourth-year students were compared with respect to their knowledge of various aspects of autism, including diagnosis, cause, symptomatology, treatment and outcome. Fourth-year students were significantly more likely to respond correctly to questions related to diagnostic criteria and core symptoms. However no significant differences were found between first-year and fourth-year students for other aspects, such as possible causes, IQ profiles, prognosis and treatment. These findings suggest that more emphasis needs to be placed on teaching medical students about autism if diagnosis and access to intervention are to be improved. C1 Care Of Professor P Howlon, Univ London St Georges Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. RP Shah, K (reprint author), Care Of Professor P Howlon, Univ London St Georges Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. CR Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BOLTON P, 1999, PSYCHOL MED, V28, P385 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x *NAT AUT SOC, 1997, MAN PEOPL HAV AUT SP Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 WHO, 1993, ICD 10 CLASS MENT BE WING L, 1976, PSYCHOL MED, V6, P89 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 NR 13 TC 21 Z9 22 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 127 EP 133 DI 10.1177/1362361301005002003 PG 7 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700002 PM 11706861 ER PT J AU Grant, CM Grayson, A Boucher, J AF Grant, CM Grayson, A Boucher, J TI Using tests of false belief with children with autism: how valid and reliable are they? SO AUTISM LA English DT Article DE autism; false belief; reliability; theory of mind; validity ID TEST-RETEST RELIABILITY; MENTAL-RETARDATION; MIND ABILITIES; INDIVIDUALS; TASKS; KNOWLEDGE AB Twenty-two children with autism were given four tests of false belief understanding: the Sally-Anne task, two variants of the deceptive box task, and the three boxes task. The overall consistency of the children's performance was high, 77 percent of the participants either passing or failing all of the tasks. The convergent validity (across-task consistency) of the deceptive box and the three boxes paradigms was high, and the convergent validity of the three boxes and Sally-Anne tasks was also acceptable. However, a weaker level of convergent validity was found for the deceptive box and Sally-Anne tasks, suggesting that these paradigms test slightly different aspects of cognition. The reliability (within-child consistency) of the children's performances across two versions of the deceptive box task was high. These findings are discussed in terms of their practical implications for practitioners and researchers. C1 Univ Sheffield, Sheffield S10 2TN, S Yorkshire, England. Open Univ, Milton Keynes MK7 6AA, Bucks, England. Univ Warwick, Coventry CV4 7AL, W Midlands, England. RP Grant, CM (reprint author), Queens Med Ctr, South Block,Floor E, Nottingham NG7 2UG, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Charman T, 1997, J CHILD PSYCHOL PSYC, V38, P725, DOI 10.1111/j.1469-7610.1997.tb01699.x Dunn L M., 1982, BRIT PICTURE VOCABUL EISENMAJER R, 1991, BRIT J DEV PSYCHOL, V9, P351 FLEISS JL, 1969, PSYCHOL BULL, V72, P323, DOI 10.1037/h0028106 Happe F., 1994, AUTISM INTRO PSYCHOL Hughes C, 2000, J CHILD PSYCHOL PSYC, V41, P483, DOI 10.1017/S0021963099005533 LESLIE AM, 1988, BRIT J DEV PSYCHOL, V6, P315 MACGREGOR E, 1998, AUTISM, V2, P367 MAYES LC, 1994, BRIT J DEV PSYCHOL, V12, P555 Mayes LC, 1996, J CHILD PSYCHOL PSYC, V37, P313, DOI 10.1111/j.1469-7610.1996.tb01408.x Mitchell P., 1996, ACQUIRING CONCEPTION PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Peterson DM, 1999, MIND LANG, V14, P80, DOI 10.1111/1468-0017.00104 PRIOR M, 1990, J CHILD PSYCHOL PSYC, V31, P587, DOI 10.1111/j.1469-7610.1990.tb00799.x Riggs KJ, 1998, COGNITIVE DEV, V13, P73, DOI 10.1016/S0885-2014(98)90021-1 Russell J., 1996, AGENCY ITS ROLE MENT Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x Zelazo PD, 1996, J CHILD PSYCHOL PSYC, V37, P479, DOI 10.1111/j.1469-7610.1996.tb01429.x NR 23 TC 5 Z9 6 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 135 EP 145 DI 10.1177/1362361301005002004 PG 11 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700003 PM 11706862 ER PT J AU Blackshaw, AJ Kinderman, P Hare, DJ Hatton, C AF Blackshaw, AJ Kinderman, P Hare, DJ Hatton, C TI Theory of mind, causal attribution and paranoia in Asperger syndrome SO AUTISM LA English DT Article DE Asperger syndrome; causal attributions; paranoia; theory of mind ID SITUATIONAL ATTRIBUTIONS; PERSECUTORY DELUSIONS; SELF-CONSCIOUSNESS; DEPRESSION; MEMORY; SCHIZOPHRENIA; DISCREPANCIES; AUTISM; PEOPLE; MODEL AB Theory of mind (ToM) deficits are central to autistic spectrum disorders, including Asperger syndrome. Research in psychotic disorders has developed a cognitive model of paranoid delusions involving abnormal causal attributions for negative events. Possible aetiologies of these include deficits in social reasoning, specifically ToM. The present study investigated this attributional model of paranoia in Asperger syndrome. Participants diagnosed with Asperger syndrome scored significantly higher on a measure of paranoia and lower on a measure of ToM, compared with the control group. They did not differ in self-concept and causal attributions, contrary to the attributional model of paranoia. A regression analysis highlighted private self-consciousness as the only predictor of paranoia. The theoretical and clinical implications of these findings are discussed. C1 Univ Liverpool, Dept Clin Psychol, Liverpool L69 3GB, Merseyside, England. Univ Manchester, Manchester M13 9PL, Lancs, England. Univ Lancaster, Lancaster LA1 4YW, England. RP Kinderman, P (reprint author), Univ Liverpool, Dept Clin Psychol, Whelan Bldg,Quadrangle,Brownlow Hill, Liverpool L69 3GB, Merseyside, England. RI Hatton, Chris/C-1924-2013 OI Hatton, Chris/0000-0001-8781-8486 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x BENTALL RP, 1998, OUTCOME INNOVATION P BENTALL RP, 1994, BEHAV RES THER, V32, P331, DOI 10.1016/0005-7967(94)90131-7 Bowler DM, 1997, NEUROPSYCHOLOGIA, V35, P65, DOI 10.1016/S0028-3932(96)00054-1 BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x BREWIN CR, 1985, PSYCHOL BULL, V98, P297, DOI 10.1037/0033-2909.98.2.297 CORCORAN R, 1995, SCHIZOPHR RES, V17, P5, DOI 10.1016/0920-9964(95)00024-G DAVIS HL, 1995, AUST J PSYCHOL, V47, P25, DOI 10.1080/00049539508258765 FENIGSTEIN A, 1975, J CONSULT CLIN PSYCH, V43, P522, DOI 10.1037/h0076760 FENIGSTEIN A, 1992, J PERS SOC PSYCHOL, V62, P129, DOI 10.1037/0022-3514.62.1.129 FOMBONNE E, 1997, AUTISM, V1, P227, DOI 10.1177/1362361397012008 Frith CD, 1996, PSYCHOL MED, V26, P521 Frith C.D., 1994, NEUROPSYCHOLOGY SCHI HIGGINS ET, 1986, J PERS SOC PSYCHOL, V4, P1 Kinderman P, 1997, J ABNORM PSYCHOL, V106, P341, DOI 10.1037/0021-843X.106.2.341 Kinderman P, 1996, PERS INDIV DIFFER, V20, P261, DOI 10.1016/0191-8869(95)00186-7 KINDERMAN P, 1997, BEHAV COGN PSYCHOTH, V25, P269 Kinderman P, 1996, J ABNORM PSYCHOL, V105, P106, DOI 10.1037/0021-843X.105.1.106 Klin A., 2000, ASPERGER SYNDROME LEZAK MD, 1995, NEUROPSYCHOLOGICAL A Nelson H. E., 1982, NATL ADULT READING T REHM LP, 1988, BEHAV ASSESSMENT PRA SCOTT L, 1993, J ABNORM PSYCHOL, V102, P282, DOI 10.1037/0021-843X.102.2.282 Stroop JR, 1935, J EXP PSYCHOL, V18, P643, DOI 10.1037/h0054651 TANTAM D, 1989, AUTISM ASPERGER SYND WELLS A, 1997, COGNITIVE THERAPY AN Wing L., 1996, AUTISTIC SPECTRUM GU WING L, 1981, PSYCHOL MED, V11, P115 Young J. E., 1990, COGNITIVE THERAPY PE ZIGMOND AS, 1983, ACTA PSYCHIAT SCAND, V67, P361, DOI 10.1111/j.1600-0447.1983.tb09716.x NR 33 TC 50 Z9 51 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 147 EP 163 DI 10.1177/1362361301005002005 PG 17 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700004 PM 11706863 ER PT J AU Shu, BC Lung, FW Tien, AY Chen, BC AF Shu, BC Lung, FW Tien, AY Chen, BC TI Executive function deficits in non-retarded autistic children SO AUTISM LA English DT Article DE autism; executive function; Wisconsin Card Sorting Test (WCST) ID CARD SORTING TEST; FRONTAL-LOBE DAMAGE; DEVELOPMENTAL NORMS; INFANTILE-AUTISM; TEST-PERFORMANCE; INDIVIDUALS; PARENTS; MIND; MEN AB The purpose of this study was to examine differences between Taiwanese children with autism and their typically developing peers on the Wisconsin Card Sorting Test (WCST). Twenty-six children with autism of normal IQ were included, and matched for chronological age with 52 controls. The WCST scores of the typically developing children were significantly higher for categories completed and percent conceptual level than in the autism group. Scores on perseverative responses, perseverative errors, the number of trials to complete the first category and non-perseverative errors were significantly higher in the autism group. The implications of these findings are discussed. C1 Natl Cheng Kung Univ, Coll Med, Sch Nursing, Tainan 70101, Taiwan. Mil Kaohsiung Gen Hosp, Kaohsiung, Taiwan. Johns Hopkins Univ, Baltimore, MD 21218 USA. W Virginia Univ, Morgantown, WV 26506 USA. RP Shu, BC (reprint author), Natl Cheng Kung Univ, Coll Med, Sch Nursing, 1 Univ Rd, Tainan 70101, Taiwan. CR ANDERSON SW, 1991, J CLIN EXP NEUROPSYC, V13, P909, DOI 10.1080/01688639108405107 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Berg EA, 1948, J GEN PSYCHOL, V39, P15 CHELUNE GJ, 1986, J CLIN EXP NEUROPSYC, V8, P219, DOI 10.1080/01688638608401314 COURCHESNE E, 1985, J AUTISM DEV DISORD, V15, P55, DOI 10.1007/BF01837899 DAMASIO AR, 1991, FRONTAL LOBE FUNCTION AND DYSFUNCTION, P217 Dawson G, 1989, AUTISM NATURE DIAGNO DUNCAN J, 1986, COGNITIVE NEUROPSYCH, V3, P271, DOI 10.1080/02643298608253360 GRAFMAN J, 1990, PERCEPT MOTOR SKILL, V71, P1120, DOI 10.2466/PMS.71.8.1120-1122 GRANT DA, 1948, J EXP PSYCHOL, V38, P404, DOI 10.1037/h0059831 Harris P., 1993, UNDERSTANDING OTHER, P228 Heaton RK, 1993, WISCONSIN CARD SORTI Hobson R. P., 1989, AUTISM NATURE DIAGNO Hughes C, 1997, PSYCHOL MED, V27, P209, DOI 10.1017/S0033291796004308 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 LANDA R, 1992, PSYCHOL MED, V22, P245 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x ORNITZ EM, 1985, J AM ACAD CHILD PSY, V24, P251, DOI 10.1016/S0002-7138(09)61084-0 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x OZONOFF S, 1993, J AUTISM DEV DISORD, V23, P429, DOI 10.1007/BF01046049 OZONOFF S, IN PRESS LEARNING CO Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 ROSSELLI M, 1993, CLIN NEUROPSYCHOL, V7, P145, DOI 10.1080/13854049308401516 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 Rutter M., 1978, AUTISM REAPPRAISAL C Shallice T, 1991, FRONTAL LOBE FUNCTIO Shu BC, 2000, CLIN NEUROPSYCHOL, V14, P275, DOI 10.1076/1385-4046(200008)14:3;1-P;FT275 STEEL JG, 1984, J AM ACAD CHILD PSY, V23, P704 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Tien Allen Y., 1996, Kaohsiung Journal of Medical Sciences, V12, P479 WELSH MC, 1988, DEV NEUROPSYCHOL, V4, P199 WING L, 1979, J AUTISM DEV DISORD, V9, P157 NR 35 TC 28 Z9 30 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 165 EP 174 DI 10.1177/1362361301005002006 PG 10 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700005 PM 11706864 ER PT J AU Tjus, T Heimann, M Nelson, KE AF Tjus, T Heimann, M Nelson, KE TI Interaction patterns between children and their teachers when using a specific multimedia and communication strategy - Observations from children with autism and mixed intellectual disabilities SO AUTISM LA English DT Article DE autism; communication; intellectual disabilities; interaction; multimedia ID SKILLS; MICROCOMPUTER AB This study reports on observed interaction patterns between 20 children with autism and mixed intellectual disabilities (mean chronological age = 11:4 years; language age = 4:7 years) and their nine teachers working with a specially developed multimedia program aiming to increase literacy skills. An increase in verbal expression was found over time for the total group. Children with autism also showed increased enjoyment and willingness to seek help from their teachers. Teachers for both diagnostic groups reduced their instructions on how to handle the computer during the program but the decrease was greater in the teachers for children with autism. When the total group of children was subdivided according to language age (high versus low), it appears that those with a low language age showed an increase in verbal expressiveness from start to end of training. Those with a high language age showed increased enjoyment. It is concluded that more detailed studies of the interaction patterns between teachers and children are needed, and these should be related to children's language level as well as to diagnostic group. C1 Univ Gothenburg, Dept Psychol, SE-40530 Gothenburg, Sweden. Penn State Univ, University Pk, PA 16802 USA. RP Tjus, T (reprint author), Univ Gothenburg, Dept Psychol, Box 500, SE-40530 Gothenburg, Sweden. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT BERNARD-OPITZ V, 1990, Annals Academy of Medicine Singapore, V19, P611 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 COLBY KM, 1973, J AUTISM CHILD SCHIZ, V3, P254, DOI 10.1007/BF01538283 Conti-Ramsden G., 1994, INPUT INTERACTION LA, P183 HAGTVET B, 1984, REYNELLS SPRAKTES Heimann M., 1993, SCANDINAVIAN J LOGOP, V18, P3 HEIMANN M, 1995, J AUTISM DEV DISORD, V25, P459, DOI 10.1007/BF02178294 JORDAN R, 1994, COMMUNICATION, V24, P20 JORDAN R, 1990, COMMUNICATION, V24, P23 Nelson K. E., 1997, COMMUNICATION LANGUA, P295 NELSON KE, 1991, BIOL BEHAV ASPECTS L, P399 NELSON KE, 1991, ALPHA INTERACTIVE LA Nelson K.E., 1998, AUTISM, V2, P139, DOI 10.1177/1362361398022003 NELSON KE, 1993, PSYCHOL PERSPECTIVES, P123 PRINZ PM, 1985, AM ANN DEAF, V130, P444 PRINZ PM, 1985, APPL PSYCHOLINGUIST, V6, P283, DOI 10.1017/S0142716400006214 Raven J. C., 1984, COLOURED PROGR MATRI Reynell J., 1977, REYNELL DEV LANGUAGE Schopler E., 1988, CHILDHOOD AUTISM RAT Snow C. E., 1995, HDB CHILD LANGUAGE, P180 WING L, 1989, DIAGNOSIS AND TREATMENT OF AUTISM, P5 NR 22 TC 15 Z9 18 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 175 EP 187 DI 10.1177/1362361301005002007 PG 13 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700006 PM 11706865 ER PT J AU McGregor, E Campbell, E AF McGregor, E Campbell, E TI The attitudes of teachers in Scotland to the integration of children with autism into mainstream schools SO AUTISM LA English DT Article DE autism; integration; teachers' attitudes ID SOCIAL-INTERACTION; STUDENTS; STRATEGIES; PEERS AB Around 4600 school-age children in Scotland fall within the spectrum of autistic disorders, of whom 780 have been identified in schools. This study sought the views of 23 specialist and 49 mainstream teachers, 22 with experience of autism, 27 without. They were questioned about the advantages and disadvantages of integration into mainstream for autistic children, their own ability to cope and predictors of success. Questionnaires were issued to special units and to mainstream primary and secondary schools. A minority of mainstream respondents believed children with autism should be integrated where possible. Mainstream teachers with experience of autism showed more confidence to deal with the children than those without experience. Many expressed concerns about effects on mainstream pupils but most were willing to undertake more training. Specialist teachers were more positive, although they acknowledged possible disadvantages for both groups of children and stressed that the success of integration depends on the individual child. C1 Univ Dundee, Dundee DD1 4HN, Scotland. Univ Abertay, Dundee, Scotland. RP McGregor, E (reprint author), Children Scotland, 5 Shandwick Pl, Edinburgh EH2 4RG, Midlothian, Scotland. CR BARBER C, 1996, BRIT J SPECIAL ED, V23, P19, DOI 10.1111/j.1467-8578.1996.tb00938.x BURACK J, 1997, HDB AUTISM DEV DISOR Farrell P, 1997, J APPL RES INTELLECT, V10, P1 FARRELL P, 1995, BRIT J LEARNING DISA, V23, P156 Hall J., 1996, WHOSE CHOICE CONTENT Helps S, 1999, AUTISM, V3, P287, DOI 10.1177/1362361399003003006 Hoyson M., 1985, J DIVISION EARLY CHI, V8, P157 JORDAN R, 1997, 46 RES INT UN SCOTT Kamps DM, 1995, BEHAV DISORDERS, V21, P89 LUSTHAUS E, 1992, MCGILL J ED, V27, P293 Mesibov GB, 1996, J AUTISM DEV DISORD, V26, P337, DOI 10.1007/BF02172478 MYLES BS, 1989, J SPEC EDUC, V22, P479 ODOM S, 1985, J APPL BEHAV ANAL, V19, P59 ODOM SL, 1986, J APPL BEHAV ANAL, V19, P59, DOI 10.1901/jaba.1986.19-59 ODOM SL, 1984, AM J ORTHOPSYCHIAT, V54, P544 Pierce K., 1997, FOCUS AUTISM OTHER D, V12, P207 Roeyers H, 1996, J AUTISM DEV DISORD, V26, P303, DOI 10.1007/BF02172476 SAINATO DM, 1992, J APPL BEHAV ANAL, V25, P127, DOI 10.1901/jaba.1992.25-127 Schwartz IS, 1998, TOP EARLY CHILD SPEC, V18, P132 *SCOTT EX STAT, 1999, SUMM RES SEPT 1998 S STAINBACK S, 1992, CONTROVERSIAL ISSUES WHINNERY KW, 1991, REM SPEC EDUC, V12, P6 NR 22 TC 14 Z9 14 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 189 EP 207 PG 19 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700007 PM 11706866 ER PT J AU Weiskop, S Matthews, J Richdale, A AF Weiskop, S Matthews, J Richdale, A TI Treatment of sleep problems in a 5-year-old boy with autism using behavioural principles SO AUTISM LA English DT Article DE autism; behavioural; intervention; parent training; sleep problems ID YOUNG-CHILDREN; DISABILITIES; DISTURBANCE; EXTINCTION; BEDTIME; INFANTS; WAKING AB This article presents a case study which is part of a larger project on sleep problems in children with autism. The successful treatment of sleep problems (night settling, night waking, and co-sleeping) in a boy of 5 years 4 months with autism is described. The intervention was based on behavioural principles and involved the parents attending an individually-run parent training programme. The programme consisted of an interview, three weekly training sessions and a review session. The parents learned how to use a bedtime routine, reinforcement, effective instructions, partner support strategies and extinction procedures. Once the techniques were implemented, the child learned how to settle himself to bed and how to sleep alone for the entire night. For this child, the results of the sleep programme were clinically significant as measured by a scale of goal achievement, and were maintained at a 3 month and a 12 month follow-up. C1 RMIT Univ, Dept Psychol & Disabil Studies, Bundoora, Vic 3083, Australia. RP Richdale, A (reprint author), RMIT Univ, Dept Psychol & Disabil Studies, POB 71, Bundoora, Vic 3083, Australia. CR ADAMS LA, 1989, PEDIATRICS, V84, P756 ANDERS TF, 1979, PEDIATRICS, V63, P860 Bramble D, 1997, DEV MED CHILD NEUROL, V39, P543 CLEMENTS J, 1986, J CHILD PSYCHOL PSYC, V27, P399, DOI 10.1111/j.1469-7610.1986.tb01841.x Didden R, 1998, J BEHAV THER EXP PSY, V29, P85, DOI 10.1016/S0005-7916(97)00038-4 DURAND VM, 1990, BEHAV MODIF, V14, P37, DOI 10.1177/01454455900141003 DURAND VM, 1996, J ASSOC PERS SEVERE, V21, P114 EDWARDS KJ, 1994, J DEV BEHAV PEDIATR, V15, P207 FERBER R, 1986, SOLVE YOUR CHILDS SL France KG, 1996, CHILD ADOL PSYCH CL, V5, P581 FRANCE KG, 1991, J DEV BEHAV PEDIATR, V12, P308 GRIFFIN MW, 1978, PARENTS THERAPISTS B Hewitt K., 1985, MENTAL HANDICAP, V13, P112 HOWLIN P, 1984, BEHAV PSYCHOTHER, V12, P257 HUDSON A, 1995, BEHAV CHANGE, V12, P207 Johns T, 1996, J CLIN NURS, V5, P3, DOI 10.1111/j.1365-2702.1996.tb00220.x JONES DPH, 1983, ARCH DIS CHILD, V58, P442 KERR S, 1994, CHILD CARE HLTH DEV, V20, P379, DOI 10.1111/j.1365-2214.1994.tb00400.x MCDONALD J, 1995, BETTER BEDTIME BEHAV MESSER DJ, 1994, CHILD CARE HLTH DEV, V20, P267, DOI 10.1111/j.1365-2214.1994.tb00389.x MILAN MA, 1981, CHILD BEHAV THERAPY, V3, P13 MURPHY GC, 1985, BEHAV CHANGE, V2, P6 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Piazza CC, 1997, DEV MED CHILD NEUROL, V39, P414 RICHDALE AL, 1995, EUR CHILD ADOLES PSY, V4, P175 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 RICHMAN N, 1981, J AM ACAD CHILD PSY, V20, P281, DOI 10.1016/S0002-7138(09)60989-4 RICHMAN N, 1985, J CHILD PSYCHOL PSYC, V26, P591, DOI 10.1111/j.1469-7610.1985.tb01643.x SADEH A, 1994, J CONSULT CLIN PSYCH, V62, P63, DOI 10.1037//0022-006X.62.1.63 Sanders MR, 1993, BEHAV FAMILY INTERVE SHREIBMAN L, 1984, PROGRAMMING EFFECTIV, P295 Sparrow S, 1984, VINELAND ADAPTIVE BE Wiggs L, 1996, J INTELL DISABIL RES, V40, P518, DOI 10.1046/j.1365-2788.1996.799799.x WILLIAMS CR, 1958, J SOC PSYCHOL, V59, P269 WOLF M, 1964, BEHAV RES THER, V1, P305 Zimmerman I.L., 1992, PRESCHOOL LANGUAGE S ZUCKERMAN B, 1987, PEDIATRICS, V80, P664 NR 37 TC 21 Z9 21 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 209 EP 221 DI 10.1177/1362361301005002009 PG 13 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700008 PM 11706867 ER PT J AU Wheelwright, S Baron-Cohen, S AF Wheelwright, S Baron-Cohen, S TI The link between autism and skills such as engineering, maths, physics and computing - A reply to Jarrold and Routh, Autism, 1998, 2 (3): 281-9 SO AUTISM LA English DT Article DE domain specificity; folk physics; folk psychology; genetics; parental occupation; phenotype AB In the first edition of this journal, we published a paper reporting that fathers and grandfathers of children with autism were over-represented in the field of engineering (Baron-Cohen et al., 1997). This result was interpreted as providing supporting evidence for the folk-psychology/folk-physics theory of autism. After carrying out further analyses on the same data, Jarrold and Routh (1998) found that fathers of children with autism were also over-represented in accountancy and science. They suggested that these results could either provide additional support for the folk-psychology/folk-physics theory or be accounted for by an over-representation of professionals amongst the fathers of children with autism. Here we present evidence that engineers are still over-represented among fathers of children with autism, even taking into account the professional bias. C1 Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. RP Wheelwright, S (reprint author), Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Downing St, Cambridge CB2 3EB, England. CR Baron-Cohen S, 1999, NEUROCASE, V5, P475, DOI 10.1080/13554799908402743 BARONCOHEN S, IN PRESS J DEV LEARN Baron-Cohen S, 2000, DEV PSYCHOPATHOL, V12, P489, DOI 10.1017/S0954579400003126 Baron-Cohen S., 1998, AUTISM, V2, P296, DOI 10.1177/1362361398023008 BARONCOHEN S, 1997, CHILDRENS THEORIES Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Baron-Cohen Simon, 1997, AUTISM, V1, P101, DOI 10.1177/1362361397011010 FOLSTEIN SE, 1988, J AUTISM DEV DISORD, V18, P3, DOI 10.1007/BF02211815 Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 JARROLD C, 1997, AUTISM, V1, P101 NR 10 TC 17 Z9 18 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2001 VL 5 IS 2 BP 223 EP 227 DI 10.1177/1362361301005002010 PG 5 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700009 PM 11706868 ER PT J AU Jones, R AF Jones, R TI Autism facts and strategies for parents SO AUTISM LA English DT Book Review C1 Univ Coll N Wales, Bangor LL57 2UW, Gwynedd, Wales. RP Jones, R (reprint author), Univ Coll N Wales, Bangor LL57 2UW, Gwynedd, Wales. CR JANZEN JE, 1999, AUTISM FACTS STRATEG 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 JUN PY 2001 VL 5 IS 2 BP 232 EP 232 DI 10.1177/1362361301005002014 PG 1 WC Psychology, Developmental SC Psychology GA 486GH UT WOS:000171809700013 ER PT J AU Van Camp, CM Vollmer, TR Daniel, D AF Van Camp, CM Vollmer, TR Daniel, D TI A systematic evaluation of stimulus preference, response effort, and stimulus control in the treatment of automatically reinforced self-injury SO BEHAVIOR THERAPY LA English DT Article ID DEVELOPMENTAL-DISABILITIES; ENVIRONMENTAL ENRICHMENT; BEHAVIOR AB Environmental enrichment (EE) was evaluated as treatment for the automatically reinforced self-injurious behavior (SIB) of a 13-year-old male diagnosed with autism. First, a functional analysis determined that the participant's SIB persisted in the absence of social consequences. Next, EE was implemented as treatment and various components of the intervention were manipulated. The results suggested that three factors were correlated with increased EE efficacy. stimulus preference, response effort, and inhibitory stimulus control. C1 Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. RP Vollmer, TR (reprint author), Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. 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Therapy PD SUM PY 2001 VL 32 IS 3 BP 603 EP 613 DI 10.1016/S0005-7894(01)80037-X PG 11 WC Psychology, Clinical SC Psychology GA 473VF UT WOS:000171068500010 ER PT J AU Bachevalier, J Malkova, L Mishkin, M AF Bachevalier, J Malkova, L Mishkin, M TI Effects of selective neonatal temporal lobe lesions on socioemotional behavior in infant rhesus monkeys (Macaca mulatta) SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID KLUVER-BUCY SYNDROME; HIPPOCAMPAL DAMAGE; RECOGNITION MEMORY; VISUAL RECOGNITION; SOCIAL-BEHAVIOR; LIMBIC LESIONS; AUTISM; AMYGDALA; CHILDREN; CORTEX AB Normal infant monkeys and infant monkeys with neonatal damage to either the medial temporal lobe or the inferior temporal visual area were assessed in dyadic social interactions at 2 and 6 months of age, Unlike the normal infant monkeys, which developed strong affiliative bonds and little or no behavioral disturbances, the lesioned monkeys (each of which was observed with an unoperated control) exhibited socioemotional abnormalities and aberrant behaviors. 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Neurosci. PD JUN PY 2001 VL 115 IS 3 BP 545 EP 559 DI 10.1037//0735-7044.115.3.545 PG 15 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 471DC UT WOS:000170911500002 PM 11439445 ER PT J AU Gergely, G AF Gergely, G TI The obscure object of desire: 'Nearly, but clearly not, like me': Contingency preference in normal children versus children with autism SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article ID MIND; PERCEPTION; INFANCY AB The author describes the central role of contingency detection in early socioemotional development. It has been proposed (Gergely & Watson, 1999) that infants are innately equipped with a complex perceptual mechanism, the "contingency detection module," which functions to establish the primary representation of the bodily self as well as the later orientation toward reactive social objects. According to the "contingency switch" model, the target value of the module that is initially genetically set to preferentially explore perfectly response-contingent stimulation is "switched" at around 3 months toward a preference for less-than-perfect social contingencies. It is hypothesized that the primary cause of childhood autism is a genetic defect, due to which the normal process of switching contingency preference at around 3 months does not take place. Preliminary results front an experimental study to test this model are reported. The study contrasts the preferential reactions of normal children and children with autism to perfect versus imitative (high-but-imperfect) contingencies. The results provide support for the contingency switch hypothesis of the etiology of childhood autism. C1 Hungarian Acad Sci, Inst Psychol, H-1394 Budapest, Hungary. Hungarian Acad Sci, Inst Psychol, Dept Dev Res, H-1394 Budapest, Hungary. Menninger Clin, Child & Family Ctr, Topeka, KS USA. RP Gergely, G (reprint author), Hungarian Acad Sci, Inst Psychol, POB 398, H-1394 Budapest, Hungary. 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PD SUM PY 2001 VL 65 IS 3 BP 411 EP 426 DI 10.1521/bumc.65.3.411.19853 PG 16 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA 465HN UT WOS:000170583700010 PM 11531136 ER PT J AU Corbett, B Khan, K Czapansky-Beilman, D Brady, N Dropik, P Goldman, DZ Delaney, K Sharp, H Mueller, I Shapiro, E Ziegler, R AF Corbett, B Khan, K Czapansky-Beilman, D Brady, N Dropik, P Goldman, DZ Delaney, K Sharp, H Mueller, I Shapiro, E Ziegler, R TI A double-blind, placebo-controlled crossover study investigating the effect of porcine secretin in children with autism SO CLINICAL PEDIATRICS LA English DT Article ID DISORDER AB Objectives: A recent patient series reported the incidental findings of improved social and language skills in 3 children with autistic spectrum disorders after the administration of secretin, a peptide hormone. However, a subsequent study did not find evidence for a drug effect, Parents are seeking treatment with secretin despite the absence of empirical investigations demonstrating amelioration in autism symptomology. In order to more precisely measure the effects of secretin, this study investigated the effect of a single intravenous dose of porcine secretin on 12 autistic children through a randomized, double-blind, placebo-controlled, crossover study. Children were assessed on objective language and on social, neuropsychological, and gastrointestinal measures to evaluate drug effects. The study was conducted over a 16-week trial. The results: indicated that significant differences were not observed on the majority of the dependent variables. Statistically significant differences were observed on measures of positive affect and activity level following secretin infusion. In general, the autistic children did not demonstrate the improvements described in the initial retrospective report. C1 Univ Minnesota, Sch Med, Div Pediat Neurol, Dept Pediat, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Div Pediat Gastroenterol, Dept Pediat, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Dept Commun Disorders, Minneapolis, MN 55455 USA. RP Corbett, B (reprint author), Univ Minnesota, Sch Med, Div Pediat Neurol, Dept Pediat, Mayo Mail Code 486,420 Delaware St,SE, Minneapolis, MN 55455 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th GORDON CT, 1993, ARCH GEN PSYCHIAT, V50, P441 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 McDougle CJ, 1996, ARCH GEN PSYCHIAT, V53, P1001 MILLER JF, 1985, SYSTEMTIC ANAL LANGU REALMUTO GM, 1989, J CLIN PSYCHOPHARM, V9, P122, DOI 10.1097/00004714-198904000-00009 ROETHLISBERGER FJ, MANAGEMENT WORKER Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 SHAPIRO E, 1997, MINNESOTA PRESCHOOL SHAPIRO EG, 1994, J PEDIATR PSYCHOL, V19, P325, DOI 10.1093/jpepsy/19.3.325 Sparrow S, 1984, VINELAND ADAPTIVE BE Thorndike R. L., 1986, STANFORDBINET INTELL Wetherby A. M., 1990, COMMUNICATION SYMBOL NR 15 TC 22 Z9 23 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 USA SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD JUN PY 2001 VL 40 IS 6 BP 327 EP 331 DI 10.1177/000992280104000604 PG 5 WC Pediatrics SC Pediatrics GA 445QJ UT WOS:000169468500004 PM 11824175 ER PT J AU Dyck, MJ Ferguson, K Shochet, IM AF Dyck, MJ Ferguson, K Shochet, IM TI Do autism spectrum disorders differ from each other and from non-spectrum disorders on emotion recognition tests? SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism spectrum; empathic ability; emotion recognition; theory of mind; developmental disorder ID MENTAL-RETARDATION; ASPERGER-SYNDROME; SOCIAL COMMUNICATION; STORY CHARACTERS; MIND DEVELOPMENT; NORMAL-CHILDREN; INDIVIDUALS; ABILITIES; BELIEFS; IMPAIRMENT AB We tested whether dimensional measures of empathic ability, theory of mind, and intelligence would differentiate autism spectrum disorders from each other and from non-spectrum disorders. Tests were administered to children with a diagnosis of Autistic Disorder (AutD; n = 20), Asperger's Disorder (AspD; n = 28), Attention Deficit/Hyperactivity Disorder (Inattentive Type) (ADHD; n = 35), Mental Retardation (Mild) (MR; n = 34), Anxiety Disorder (AnxD; n = 14), or No Psychological Disorder (NPD; n = 36). Results showed that empathic ability discriminated among groups on the autism spectrum (AutD < AspD < NPD). Because empathic ability is not independent of intelligence (AutD < AspD < NPD on intelligence; MR < ADHD < NPD on empathic ability), both dimensions are necessary to discriminate autism spectrum from non-spectrum disorders. When intelligence is covaried, empathic ability discriminated Auto, but not AspD, from other disorders (AutD < MR < ADHD < NPD = AnxD = AspD). C1 Curtin Univ Technol, Sch Psychol, Perth, WA 6845, Australia. Griffith Univ, Sch Appl Psychol, Mt Gravatt, Qld 4111, Australia. RP Dyck, MJ (reprint author), Curtin Univ Technol, Sch Psychol, GPO Box U1987, Perth, WA 6845, Australia. CR Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th BACHARA GH, 1980, AM ANN DEAF, V125, P38 BARONCOHEN S, 1995, DEV PSYCHOPATHOL, V1, P343 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x Buitelaar JK, 1999, DEV PSYCHOPATHOL, V11, P39, DOI 10.1017/S0954579499001947 Buitelaar JK, 1997, J AUTISM DEV DISORD, V27, P539, DOI 10.1023/A:1025878026569 Dahlgren SO, 1996, J CHILD PSYCHOL PSYC, V37, P759, DOI 10.1111/j.1469-7610.1996.tb01469.x DUNN J, 1995, COGNITION EMOTION, V9, P187, DOI 10.1080/02699939508409008 Eisenberg N., 1996, EMPATHIC ACCURACY, P73 Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 FLAVELL JH, 1992, J PIAGET SY, P107 FOMBONNE E, 1994, EUR CHILD ADOLES PSY, V3, P176 Frith U, 1996, J PSYCHOPHARMACOL, V10, P48, DOI 10.1177/026988119601000108 GILLBERG C, 1993, J INTELL DISABIL RES, V37, P343 GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x Greene RW, 1997, J CONSULT CLIN PSYCH, V65, P758, DOI 10.1037/0022-006X.65.5.758 HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P1461, DOI 10.1111/j.1469-7610.1994.tb01287.x HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 HOBSON RP, 1988, PSYCHOL MED, V18, P911 HOBSON RP, 1989, BRIT J DEV PSYCHOL, V7, P237 HOLROYD S, 1993, J AUTISM DEV DISORD, V23, P379, DOI 10.1007/BF01046226 Loveland KA, 1997, DEV PSYCHOPATHOL, V9, P579 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Matsumoto D., 1995, JAPANESE CAUCASIAN F McGregor E, 1998, BRIT J DEV PSYCHOL, V16, P281 Minter M, 1998, BRIT J DEV PSYCHOL, V16, P183 MYRH G, 1998, CANADIAN J PSYCHIAT, V43, P589 OZONOFF S, 1994, DEV PSYCHOPATHOL, V6, P415, DOI 10.1017/S0954579400006027 Peterson CC, 1998, BRIT J DEV PSYCHOL, V16, P301 PETERSON CC, 1995, J CHILD PSYCHOL PSYC, V36, P459, DOI 10.1111/j.1469-7610.1995.tb01303.x Phillips W, 1998, BRIT J DEV PSYCHOL, V16, P337 PRIOR M, 1990, J CHILD PSYCHOL PSYC, V31, P587, DOI 10.1111/j.1469-7610.1990.tb00799.x Sattler JM, 1974, ASSESSMENT CHILDRENS Scott FJ, 1996, DEV PSYCHOPATHOL, V8, P235 Seidman LJ, 1997, J AM ACAD CHILD PSY, V36, P366, DOI 10.1097/00004583-199703000-00015 SMALLEY SL, 1990, J AUTISM DEV DISORD, V20, P271, DOI 10.1007/BF02284724 SPARREVOHN R, 1995, J CHILD PSYCHOL PSYC, V36, P249, DOI 10.1111/j.1469-7610.1995.tb01823.x SPENCE S, 1988, BEHAV RES THER, V36, P545 STEFFENBURG S, 1991, DEV MED CHILD NEUROL, V33, P495 Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 WALTER B, 1958, TIJDSCRIFT OPVOEDKUN, V3, P224 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Yirmiya N, 1996, CHILD DEV, V67, P2045, DOI 10.1111/j.1467-8624.1996.tb01842.x Yirmiya N, 1996, DEV PSYCHOL, V32, P62 Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x ZALAZO P, 1996, J CHILD PSYCHOL PSYC, V37, P479 Ziatas K, 1998, J CHILD PSYCHOL PSYC, V39, P755, DOI 10.1017/S0021963098002510 NR 54 TC 75 Z9 74 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 JUN PY 2001 VL 10 IS 2 BP 105 EP 116 PG 12 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 447LK UT WOS:000169574700002 PM 11469282 ER PT J AU Buchsbaum, MS Hollander, E Haznedar, MM Tang, C Spiegel-Cohen, J Wei, TC Solimando, A Buchsbaum, BR Robins, D Bienstock, C Cartwright, C Mosovich, S AF Buchsbaum, MS Hollander, E Haznedar, MM Tang, C Spiegel-Cohen, J Wei, TC Solimando, A Buchsbaum, BR Robins, D Bienstock, C Cartwright, C Mosovich, S TI Effect of fluoxetine on regional cerebral metabolism in autistic spectrum disorders: a pilot study SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Article DE positron emission tomography; magnetic resonance imaging; selective serotonin reuptake inhibitor; cingulate gyrus; orbitofrontal cortex; autism; Asperger's syndrome ID POSITRON-EMISSION-TOMOGRAPHY; ANTERIOR CINGULATE; GLUCOSE-METABOLISM; PREFRONTAL CORTEX; DOUBLE-BLIND; SCHIZOPHRENIA; SERTRALINE; PLACEBO; BRAIN AB The regional metabolic effects of fluoxetine were examined in patients with autism spectrum disorders. Six adult patients with DSM-IV and Autism Diagnostic Interview (ADI) diagnoses of autism (n = 5) and Asperge's syndrome (n = 1), entered a 16-wk placebo-controlled cross-over trial of fluoxetine. The patients received F-18-deoxyglucose positron emission tomography with co-registered magnetic resonance imaging at baseline and at the end of the period of fluoxetine administration. After treatment, the patients showed significant improvement on the scores of the Yale-Brown Obsessive-Compulsive Scale - Obsessions subscale and the Hamilton Anxiety Scale; Clinical Global Impressions - Autism scores showed 3 of the patients much improved and 3 unchanged. Relative metabolic rates were significantly higher in the right frontal lobe following fluoxetine, especially in the anterior cingulate gyrus and the orbitofrontal cortex. Patients with higher metabolic rates in the medial frontal region and anterior cingulate when unmedicated were more likely to respond favourably to fluoxetine. These results are consistent with those in depression indicating that higher cingulate gyrus metabolic rates at baseline predict SRI response. C1 CUNY Mt Sinai Sch Med, Neurosci PET Lab, New York, NY 10029 USA. RP Buchsbaum, MS (reprint author), CUNY Mt Sinai Sch Med, Neurosci PET Lab, Box 1505,4 Gustave L Levy Pl, New York, NY 10029 USA. RI Robins, Diana/D-9959-2011 CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Buchsbaum MS, 1997, BIOL PSYCHIAT, V41, P15, DOI 10.1016/S0006-3223(96)00097-2 BUCHSBAUM MS, 1992, J AUTISM DEV DISORD, V22, P115, DOI 10.1007/BF01046407 Chugani DC, 1997, ANN NEUROL, V42, P666, DOI 10.1002/ana.410420420 DEVINSKY O, 1995, BRAIN, V118, P279, DOI 10.1093/brain/118.1.279 FRISTON KJ, 1991, J CEREBR BLOOD F MET, V11, P690 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006 GORDON CT, 1993, ARCH GEN PSYCHIAT, V50, P441 HAMILTON M, 1967, BRIT J SOC CLIN PSYC, V6, P278 HAMILTON M, 1959, BRIT J MED PSYCHOL, V32, P50 HAMILTON M, 1960, J NEUROL NEUROSUR PS, V23, P56, DOI 10.1136/jnnp.23.1.56 Hazlett EA, 1998, PSYCHOPHYSIOLOGY, V35, P186, DOI 10.1017/S0048577298001863 Haznedar MM, 2000, AM J PSYCHIAT, V157, P1994, DOI 10.1176/appi.ajp.157.12.1994 Haznedar MM, 1997, AM J PSYCHIAT, V154, P682 Haznedar MM, 1997, AM J PSYCHIAT, V154, P1047 Hollander E, 2000, NEUROPSYCHOPHARMACOL, V22, P163, DOI 10.1016/S0893-133X(99)00121-9 Hollander E, 1998, CNS SPECTRUMS, V3, P22 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mayberg HS, 1997, NEUROREPORT, V8, P1057, DOI 10.1097/00001756-199703030-00048 McDougle CJ, 1996, ARCH GEN PSYCHIAT, V53, P1001 MEHLINGER R, 1990, J AM ACAD CHILD PSY, V29, P985, DOI 10.1097/00004583-199011000-00032 Pascual J, 1996, CEPHALALGIA, V16, P317, DOI 10.1046/j.1468-2982.1996.1605317.x POLINE JB, 1993, J CEREBR BLOOD F MET, V13, P425 Shihabuddin L, 1998, ARCH GEN PSYCHIAT, V55, P235, DOI 10.1001/archpsyc.55.3.235 Siever LJ, 1999, NEUROPSYCHOPHARMACOL, V20, P413, DOI 10.1016/S0893-133X(98)00111-0 Steingard RJ, 1997, J CHILD ADOL PSYCHOP, V7, P9, DOI 10.1089/cap.1997.7.9 Talairach J., 1988, COPLANAR STEREOTAXIC Wu J, 1999, AM J PSYCHIAT, V156, P1149 NR 28 TC 50 Z9 51 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-9863 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2001 VL 4 IS 2 BP 119 EP 125 PG 7 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 452HU UT WOS:000169852900003 PM 11466160 ER PT J AU Mayes, SD Calhoun, SL Crites, DL AF Mayes, SD Calhoun, SL Crites, DL TI Does DSM-IV Asperger's disorder exist? SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE Asperger's disorder or syndrome; autism; DSM-IV ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM; CHILDREN; DISABILITIES; CONVERGENCE; SYMPTOMS; VALIDITY AB DSM-IV criteria for autistic and Asperger's disorders were applied to 157 children with clinical diagnoses of autism or Asperger's disorder. All children met the DSM-IV criteria for autistic disorder and none met criteria for Asperger's disorder, including those with normal intelligence and absence of early speech delay. The reason for this was that all children had social impairment and restricted and repetitive behavior and interests (required DSM-IV symptoms for both autistic and Asperger's disorders) and all had a DSM-IV-communication impairment (which then qualified them for a diagnosis of autistic disorder and not Asperger's disorder). Communication problems exhibited by all children were impaired conversational speech or repetitive, stereotyped, or idiosyncratic speech (or both), which are DSM-IV criteria for autism. These findings are consistent with those of 5 other studies and indicate that a DSM-IV diagnosis of Asperger's disorder is unlikely or impossible. C1 Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Dept Psychiat, Hershey, PA 17033 USA. RP Mayes, SD (reprint author), Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Dept Psychiat, POB 850, Hershey, PA 17033 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Attwood T., 1998, ASPERGERS SYNDROME G Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 Frith U, 1991, AUTISM ASPERGER SYND, P37 Frith U., 1991, AUTISM ASPERGER SYND, P1, DOI 10.1017/CBO9780511526770.001 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P643, DOI 10.1007/BF01046332 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 GILLBERG C, 1985, J AUTISM DEV DISORD, V15, P389, DOI 10.1007/BF01531783 Gillberg C., 1991, AUTISM ASPERGER SYND, P122, DOI 10.1017/CBO9780511526770.004 Gillberg C., 1998, ASPERGER SYNDROME HI, P79 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x HOOPER SR, 1998, ASPERGER SYNDROME HI, P317 Kanner L, 1943, NERV CHILD, V2, P217 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x KLIN A, 1994, CHILD ADOL PSYCH CL, V3, P131 Klin A., 1995, CHILD ADOL PSYCH CL, V4, P617 MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 MAYES SD, 1999, UNPUB INFLUENCE IQ A MAYES SD, IN PRESS AUTISM Mayes SD, 1999, INFANT YOUNG CHILD, V12, P90 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Myhr G, 1998, CAN J PSYCHIAT, V43, P589 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 Sattler J. M., 1988, ASSESSMENT CHILDREN Schopler E, 1996, J AUTISM DEV DISORD, V26, P109, DOI 10.1007/BF02276238 Schopler E, 1998, ASPERGER SYNDROME HI, P385 SCHOPLER E, 1985, J AUTISM DEV DISORD, V15, P359, DOI 10.1007/BF01531780 Siegel B., 1996, WORLD AUTISTIC CHILD SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 SZATMARI P, 1992, J AUTISM DEV DISORD, V22, P583, DOI 10.1007/BF01046329 SZATMARI P, 1991, PSYCHIAT CLIN N AM, V14, P81 Szatmari P, 1998, ASPERGER SYNDROME HI, P61 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x Twachtman-Cullen D., 1998, ASPERGER SYNDROME HI, P199 Volkmar F. R., 1998, ASPERGER SYNDROME HI, P107 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 Wing L, 1976, EARLY CHILDHOOD AUTI, V2nd, P15 WING L, 1981, PSYCHOL MED, V11, P115 Wing L, 1998, ASPERGER SYNDROME HI, P11 World Health Organization, 1992, INT CLASS DIS NR 48 TC 94 Z9 96 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0091-0627 J9 J ABNORM CHILD PSYCH JI J. Abnorm. Child Psychol. PD JUN PY 2001 VL 29 IS 3 BP 263 EP 271 DI 10.1023/A:1010337916636 PG 9 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 440ZQ UT WOS:000169206900008 PM 11411788 ER PT J AU Graham, G AF Graham, G TI Music and autism SO JOURNAL OF AESTHETIC EDUCATION LA English DT Article C1 Univ Aberdeen, Aberdeen AB9 1FX, Scotland. RP Graham, G (reprint author), Univ Aberdeen, Aberdeen AB9 1FX, Scotland. CR Evans K., 1998, INSCAPE, V3, P17, DOI 10.1080/17454839808413055 Grandin T., 1996, EMERGENCE LABELED AU Sacks O., 1995, ANTHROPOLOGIST MARS Sacks Oliver, 1985, MAN WHO MISTOOK HIS NR 4 TC 0 Z9 0 PU UNIV ILLINOIS PRESS PI CHAMPAIGN PA 1325 S OAK ST, CHAMPAIGN, IL 61820 USA SN 0021-8510 J9 J AESTHET EDUC JI J. Aesthet. Educ. PD SUM PY 2001 VL 35 IS 2 BP 39 EP 47 DI 10.2307/3333671 PG 9 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 462HT UT WOS:000170415200004 ER PT J AU Hagopian, LP Wilson, DM Wilder, DA AF Hagopian, LP Wilson, DM Wilder, DA TI Assessment and treatment of problem behavior maintained by escape from attention and access to tangible items SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE functional analysis; negative reinforcement; autism ID FUNCTIONAL-ANALYSIS AB The results obtained from two consecutive functional analyses conducted with a 6-year-old child wit h autism are described. In the initial functional analysis, the highest rates of problem behavior occurred in the play condition. In that condition, the delivery of attention appeared to occasion problem behaviors. A second functional analysis was conducted wherein an escape from attention condition and a tangible condition were added. In the second functional analysis, higher rates of responding were observed in the escape from attention and tangible conditions. The results suggested that problem behavior was maintained by negative reinforcement in the form of escape from attention and positive reinforcement in the form of gaining access to preferred tangible items. Problem behavior was treated using functional communication training combined with noncontingent reinforcement. C1 Kennedy Krieger Inst, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. RP Hagopian, LP (reprint author), Kennedy Krieger Inst, 707 N Broadway, Baltimore, MD 21205 USA. CR CARR EG, 1994, J APPL BEHAV ANAL, V27, P393, DOI 10.1901/jaba.1994.27-393 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 TAYLOR JC, 1992, BEHAV MODIF, V16, P305, DOI 10.1177/01454455920163002 NR 3 TC 32 Z9 32 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2001 VL 34 IS 2 BP 229 EP 232 DI 10.1901/jaba.2001.34-229 PG 4 WC Psychology, Clinical SC Psychology GA 441ZB UT WOS:000169258500011 PM 11421317 ER PT J AU Mueller, MM Wilczynski, SM Moore, JW Fusilier, I Trahant, D AF Mueller, MM Wilczynski, SM Moore, JW Fusilier, I Trahant, D TI Antecedent manipulations in a tangible condition effects of stimulus preference on aggression SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE aggression; antecedent manipulations; functional analysis; positive reinforcement ID SELF-INJURY AB After a functional analysis indicated that aggression of an 8-year-old boy with autism was maintained by access to preferred items, antecedent manipulations involving the relative preference of restrict-ed and noncontingently available stimuli were conducted. Restricting highly preferred items evoked the highest rates of aggression regardless of the preference level of the noncontingently available alternative items. Restricting less preferred stimuli was associated with moderate rates of aggression even when the alternative items were more preferred. C1 Univ So Mississippi, Dept Psychol, Hattiesburg, MS 39406 USA. RP Wilczynski, SM (reprint author), Univ So Mississippi, Dept Psychol, Box 5025, Hattiesburg, MS 39406 USA. CR AZRIN NH, 1966, J EXP ANAL BEHAV, V9, P191, DOI 10.1901/jeab.1966.9-191 Fischer SM, 1997, J APPL BEHAV ANAL, V30, P239, DOI 10.1901/jaba.1997.30-239 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Smith RG, 1995, J APPL BEHAV ANAL, V28, P515, DOI 10.1901/jaba.1995.28-515 NR 4 TC 15 Z9 15 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2001 VL 34 IS 2 BP 237 EP 240 DI 10.1901/jaba.2001.34-237 PG 4 WC Psychology, Clinical SC Psychology GA 441ZB UT WOS:000169258500013 PM 11421319 ER PT J AU Ozonoff, S Strayer, DL AF Ozonoff, S Strayer, DL TI Further evidence of intact working memory in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE executive functions; high-functioning autism; working memory ID EXECUTIVE FUNCTION; TOURETTE-SYNDROME; CHILDREN; DEFICITS; INDIVIDUALS; DISORDERS; MIND AB Earlier investigations have found mixed evidence of working memory impairment in autism. The present study examined working memory in a high-functioning autistic sample, relative to both a clinical control group diagnosed with Tourette Syndrome and a typically developing control group. No group differences were found across three tasks and five dependent measures of working memory. Performance was significantly correlated with both age and IQ. It is concluded that working memory is not one of the executive functions that is seriously impaired in autism. We also suggest that the format of administration of working memory tasks may be important in determining whether or not performance falls in the impaired range. C1 Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. RP Ozonoff, S (reprint author), Univ Utah, Dept Psychol, 390 South,1530 East,Room 502, Salt Lake City, UT 84112 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON JR, 1982, PSYCHOL REV, V89, P369, DOI 10.1037//0033-295X.89.4.369 Baddeley A. D., 1986, WORKING MEMORY BADDELEY A, 1992, Q J EXP PSYCHOL-A, V44, P1 Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x GOEL V, 1995, NEUROPSYCHOLOGIA, V33, P623, DOI 10.1016/0028-3932(95)90866-P Griffith EM, 1999, CHILD DEV, V70, P817, DOI 10.1111/1467-8624.00059 HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 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 Mottron L, 1999, NEUROCASE, V5, P485, DOI 10.1080/13554799908402744 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 Ozonoff S, 1997, AUTISM EXECUTIVE DIS, P179 OZONOFF S, 1995, NEUROPSYCHOLOGY, V9, P491, DOI 10.1037//0894-4105.9.4.491 OZONOFF S, 1994, DEV PSYCHOPATHOL, V6, P415, DOI 10.1017/S0954579400006027 Ozonoff S, 1998, J CHILD PSYCHOL PSYC, V39, P1109, DOI 10.1017/S0021963098003230 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Pascualvaca DM, 1998, J AUTISM DEV DISORD, V28, P467, DOI 10.1023/A:1026091809650 Pennington B.F, 1994, FUTURE ORIENTED PROC, P243 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x Russell J, 1996, J CHILD PSYCHOL PSYC, V37, P673, DOI 10.1111/j.1469-7610.1996.tb01459.x Shallice T., 1982, NEUROPSYCHOLOGY COGN, P199 NR 24 TC 111 Z9 115 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 257 EP 263 DI 10.1023/A:1010794902139 PG 7 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000002 PM 11518480 ER PT J AU Hauck, JA Dewey, D AF Hauck, JA Dewey, D TI Hand preference and motor functioning in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; hand preference; motor functioning ID INFANTILE-AUTISM; PRESCHOOL-CHILDREN; HANDEDNESS; SUBTYPES; LANGUAGE; ABILITY; SKILL AB This study examined three theories that have been proposed to explain the hi, gh rates of ambiguous hand preference in young children with autism. Twenty children wa autism were matched with 20 children with developmental delays and 20 normally developing children. The groups were compared on measures of hand preference and motor skills. Results indicated that the lack of development of a hand preference in children with autism was not a direct function of their cognitive delay, as the children with developmental delays showed a dissimilar pattern of hand preference. The lack of a definite hand preference in the children with autism was also not due to a lack of motor skill development, as the children with developmental delays displayed similar levels of gross and fine motor skills without the accompanying lack of a definite hand preference. The finding that children with autism with a definite hand preference displayed better performance on motor, language, and cognitive tasks than children with autism who did not display a definite hand preference. however, provided support for the bilateral brain dysfunction hypothesis. C1 Univ Calgary, Calgary, AB T2N 1N4, Canada. Alberta Childrens Prov Gen Hosp, Behav Res Unit, Calgary, AB T2T 5C7, Canada. RP Dewey, D (reprint author), Alberta Childrens Prov Gen Hosp, Behav Res Unit, 1820 Richmond Rd SW, Calgary, AB T2T 5C7, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANNETT M, 1970, BRIT J PSYCHOL, V61, P545 ARNOLD P, 1993, J CHILD PSYCHOL PSYC, V34, P255, DOI 10.1111/j.1469-7610.1993.tb00983.x BARRY RJ, 1978, J AUTISM CHILD SCHIZ, V8, P315, DOI 10.1007/BF01539634 Bayley N, 1993, BAYLEY SCALES INFANT Bishop D., 1990, HANDEDNESS DEV DISOR BLISHEN BR, 1987, CAN REV SOC ANTHROP, V24, P465 BRYSON SE, 1990, LEFT HANDEDNESS BEHA, P441 CALNAN M, 1976, ANN HUM BIOL, V3, P329, DOI 10.1080/03014467600001551 COLBY KM, 1977, J AUTISM CHILD SCHIZ, V7, P3, DOI 10.1007/BF01531110 Cornish KM, 1996, J AUTISM DEV DISORD, V26, P597, DOI 10.1007/BF02172349 Doll E. A., 1965, VINELAND SOCIAL MATU DUBOSE RF, 1977, DEV ACTIVITIES SCREE Dunn L. 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Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 265 EP 277 DI 10.1023/A:1010791118978 PG 13 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000003 PM 11518481 ER PT J AU Eaton, WW Mortensen, PB Thomsen, PH Frydenberg, M AF Eaton, WW Mortensen, PB Thomsen, PH Frydenberg, M TI Obstetric complications and risk for severe psychopathology in childhood SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's Syndrome; obstetric complications; psychiatric case register ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME AB The purpose of the study was to assess the association of obstetric complications with risk for mental disorders resulting in hospitalization before the age of 15. Records from all births in Denmark from 1973 through 1993 were linked to records of all psychiatric hospitalizations, Diagnoses were grouped into seven broad categories. A reference population of 10% of births in Denmark from 1973 to 1990 was used for comparison. Obstetric complications were associated with the range of mental disorders occurring in childhood. The strongest predictors were a variable indicating the interaction of birth weight with speed of growth and the 5-minute Apgar score. There was no diagnostic group that stood out as different with respect to obstetric complications. These results are consistent with the hypothesis of the continuum of reproductive casualty. C1 Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Mental Hyg, Baltimore, MD 21205 USA. Aarhus Univ, Natl Ctr Register Based Res, Aarhus, Denmark. Aarhus Univ, Detp Child Psychiat, Aarhus, Denmark. Aarhus Univ, Dept Biostat, Aarhus, Denmark. RP Eaton, WW (reprint author), Johns Hopkins Univ, Sch Publ Hlth, 624 N Broadway,880 Hampton House, Baltimore, MD 21205 USA. 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G., 1982, EPIDEMIOLOGIC RES PR KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x KNUDSEN LB, 1986, COMMUNITY MED, V8, P29 Munk-Jørgensen P, 1993, Acta Psychiatr Scand Suppl, V370, P27 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x PASAMANICK B, 1961, PREVENTION MENTAL DI TANTAM D, 1993, J AUTISM DEV DISORD, V23, P111, DOI 10.1007/BF01066422 TANTAM D, 1988, BRIT J PSYCHIAT, V153, P783, DOI 10.1192/bjp.153.6.783 Volkmar FR, 1998, J AUTISM DEV DISORD, V28, P457, DOI 10.1023/A:1026012707581 NR 13 TC 78 Z9 81 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 279 EP 285 DI 10.1023/A:1010743203048 PG 7 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000004 PM 11518482 ER PT J AU Mostert, MP AF Mostert, MP TI Facilitated Communication since 1995: A review of published studies SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE facilitated communication; autism; literature review ID MENTAL-RETARDATION; AUTISM; CHILDREN; SCIENCE; WORDS; INDIVIDUALS; PERSPECTIVE; AUTHORSHIP; STUDENTS; VALIDITY AB Previous reviews of Facilitated Communication (FC) studies have clearly established that proponents' claims are largely unsubstantiated and that using FC as an intervention for communicatively impaired or noncommunicative individuals is not recommended. However, while FC is less prominent than in the recent past, investigations of the technique's efficacy continue. This review examines published FC studies since the previous major reviews by Jacobson, Mulick, and Schwartz (1995) and Simpson and Myles (1995a). Findings support the conclusions of previous reviews. Furthermore, this review critiques and discounts the claims of two studies purporting to offer empirical evidence of FC efficacy using control procedures. C1 Old Dominion Univ, Darden Coll Educ, Dept Early Childhood Speech Language Pathol & Spe, Norfolk, VA 23529 USA. RP Mostert, MP (reprint author), Old Dominion Univ, Darden Coll Educ, Dept Early Childhood Speech Language Pathol & Spe, Norfolk, VA 23529 USA. CR Ackerson S, 1994, BEHAV, V5, P13 BANGERTDROWNS RL, 1986, PSYCHOL BULL, V99, P388, DOI 10.1037/0033-2909.99.3.388 Bebko JM, 1996, J AUTISM DEV DISORD, V26, P19, DOI 10.1007/BF02276233 Beck AR, 1996, J AUTISM DEV DISORD, V26, P497, DOI 10.1007/BF02172272 BEUKELMAN DR, 1993, AAC AUGMENTATIVE ALT, V9, P63, DOI 10.1080/07434619312331276431 Biklen D, 1995, J ASSOC PERS SEVERE, V20, P45 BIKLEN D, 1994, J ASSOC PERS SEVERE, V19, P173 Biklen D., 1993, COMMUNICATION UNBOUN BIKLEN D, 1992, TOP LANG DISORD, V12, P1 BIKLEN D, 1990, HARVARD EDUC REV, V60, P291 Biklen D., 1997, CONTESTED WORDS CONT BIKLEN D, 1991, REM SPEC EDUC, V12, P46 BIKLEN D, 1992, HARVARD EDUC REV, V62, P242 Bomba C, 1996, J AUTISM DEV DISORD, V26, P43, DOI 10.1007/BF02276234 Braman BJ, 1995, BEHAV DISORDERS, V21, P110 Calculator S. N., 1995, AM J SPEECH-LANG PAT, V4, P49 Campbell D. T., 1963, EXPT QUASIEXPERIMENT Cardinal DN, 1996, MENT RETARD, V34, P231 Clarkson G, 1994, PREVENTING SCH FAILU, V28, P31 COOPER HM, 1982, REV EDUC RES, V52, P291, DOI 10.3102/00346543052002291 CREWS WD, 1995, J AUTISM DEV DISORD, V25, P205, DOI 10.1007/BF02178505 CROSSLEY R, 1992, TOP LANG DISORD, V12, P29 CROSSLEY R, 1992, TOP LANG DISORD, V12, P46 CUMMINS RA, 1992, HARVARD EDUC REV, V62, P228 Danforth S, 1997, MENT RETARD, V35, P93, DOI 10.1352/0047-6765(1997)035<0093:OWBHMP>2.0.CO;2 DONNELLAN AM, 1992, TOP LANG DISORD, V12, P69 Donnellan M., 1993, EMOTIONAL MATURITY W Edelson SM, 1998, J AUTISM DEV DISORD, V28, P153, DOI 10.1023/A:1026044716536 FERGUSON DL, 1994, MENT RETARD, V32, P305 FRANKAEL JR, 1999, DESIGN EVALUATE RES Gall J., 1999, APPL ED RES PRACTICA Glass Gene V., 1981, META ANAL SOCIAL RES GOODE D, 1994, MENT RETARD, V32, P307 GORMAN B. J., 1998, SKEPTIC, V6, P64 Gorman BJ, 1999, BEHAV SCI LAW, V17, P517, DOI 10.1002/(SICI)1099-0798(199910/12)17:4<517::AID-BSL362>3.3.CO;2-U GREEN G, 1992, FACILITATED COMMUNIC Green G., 1994, FACILITATED COMMUNIC, P157 GREEN G, 1994, J ASSOC PERS SEVERE, V19, P151 HALLE JW, 1994, MENT RETARD, V32, P311 HARRIS SL, 1995, LEARNING COGNITION A, P293 HECKLER S, 1994, CHILD ABUSE NEGLECT, V18, P495, DOI 10.1016/0145-2134(94)90003-5 HIRSHOREN A, 1995, PSYCHOL SCHOOLS, V32, P109, DOI 10.1002/1520-6807(199504)32:2<109::AID-PITS2310320206>3.0.CO;2-0 HITZING W, 1994, MENT RETARD, V32, P314 HORNER RH, 1994, J ASSOC PERS SEVERE, V19, P185 Hudson A., 1995, ADV CLIN PSYCHOL, V17, P59 JACOBSON JW, 1994, J BEHAV ED, V4, P93, DOI 10.1007/BF01560511 JACOBSON JW, 1994, AUTISM CHILDREN ADUL, P59 JACOBSON JW, 1995, AM PSYCHOL, V50, P750, DOI 10.1037//0003-066X.50.9.750 JANZENWILDE ML, 1995, J SPEECH HEAR RES, V38, P658 Kerrin R. G., 1998, FOCUS AUTISM OTHER D, V13, P73 Kezuka E, 1997, J AUTISM DEV DISORD, V27, P571, DOI 10.1023/A:1025882127478 LEVINE K, 1998, MENT RETARD, V32, P317 Margolin K. N., 1994, FACILITATED COMMUNIC, P227 MONTEE BB, 1995, J APPL BEHAV ANAL, V28, P189, DOI 10.1901/jaba.1995.28-189 MOSTERT MP, 1994, BEHAV, V5, P17 Mullen B., 1989, ADV BASIC META ANAL Myles B., 1996, FOCUS AUTISM OTHER D, V11, p[163, 190] MYLES BS, 1994, PSYCHOL SCHOOLS, V31, P208, DOI 10.1002/1520-6807(199407)31:3<208::AID-PITS2310310306>3.0.CO;2-Z Myles B. S., 1996, FOCUS AUTISM OTHER D, V11, P37 MYLES BS, 1996, FOCUS AUTISM OTHER D, V11, P190 Olney M, 1995, J ASSOC PERS SEVERE, V20, P57 Oswald D. P., 1994, J BEHAV ED, V4, P191, DOI 10.1007/BF01544112 Perry A, 1998, J AUTISM DEV DISORD, V28, P87, DOI 10.1023/A:1026023321945 REGAL RA, 1994, J AUTISM DEV DISORD, V24, P345, DOI 10.1007/BF02172232 Shane H. C., 1994, AM J SPEECH-LANG PAT, V3, P48 Shane Howard C., 1994, FACILITATED COMMUNIC Sheehan CM, 1996, MENT RETARD, V34, P94 SILLIMAN ER, 1992, TOP LANG DISORD, V12, P60 Simon EW, 1996, J AUTISM DEV DISORD, V26, P9, DOI 10.1007/BF02276232 SIMPSON RL, 1995, FOCUS EXCEPT CHILD, V27, P1 SIMPSON RL, 1995, J SPEC EDUC, V28, P424 SMITH MD, 1994, J AUTISM DEV DISORD, V24, P357, DOI 10.1007/BF02172233 Spitz H. H., 1997, NONCONSCIOUS MOVEMEN Vazquez CA, 1995, J AUTISM DEV DISORD, V25, P597, DOI 10.1007/BF02178190 Waterhouse L, 1996, J AUTISM DEV DISORD, V26, P59, DOI 10.1007/BF02276235 Weiss MJS, 1996, MENT RETARD, V34, P220 WILLIAMS D, 1994, J ASSOC PERS SEVERE, V19, P196 WOLFENSBERGER W, 1994, FACILITED COMMUNICAT, P57 WOLFENSBERGER W, 1992, TRAINING I HUMAN SER, V12, P39 ZIRKEL PA, 1995, PHI DELTA KAPPAN, V75, P815 NR 80 TC 64 Z9 64 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 287 EP 313 DI 10.1023/A:1010795219886 PG 27 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000005 PM 11518483 ER PT J AU Delprato, DJ AF Delprato, DJ TI Comparisons of discrete-trial and normalized behavioral language intervention for young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; children; behavioral interventions; discrete-trial treatment; normalized treatment; language intervention ID RESPONSE-REINFORCER RELATIONSHIPS; PRESCHOOL-CHILDREN; SPEECH; ACQUISITION; PARADIGM; PARENTS AB This critical review examined a series of 10 controlled studies in which traditional operant behavioral procedures were compared with more recently developed normalized interventions for teaching language to young children with autism. Main characteristics of the older treatments include highly structured direct teaching sessions of discrete trials, teacher initiation, artificial reinforcers, and response shaping. Normalized interventions consist of loosely structured sessions of indirect teaching with everyday situations, child initiation, natural reinforcers, and liberal criteria for presentation of reinforcers. The main conclusion was that in all eight studies with language criterion responses, normalized language training was more effective than discrete-trial training. Furthermore, in both studies that assessed parental affect, normalized treatment yielded more positive affect than discrete-trial training. C1 Eastern Michigan Univ, Dept Psychol, Ypsilanti, MI 48197 USA. RP Delprato, DJ (reprint author), Eastern Michigan Univ, Dept Psychol, Ypsilanti, MI 48197 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson S. 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PD JUN PY 2001 VL 31 IS 3 BP 315 EP 325 DI 10.1023/A:1010747303957 PG 11 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000006 PM 11518484 ER PT J AU Hastings, RP Johnson, E AF Hastings, RP Johnson, E TI Stress in UK families conducting intensive home-based behavioral intervention for their young child with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE applied behavior analysis; early intervention; parental stress; parental beliefs ID SOCIAL SUPPORT; DEVELOPMENTAL-DISABILITIES; PARENTS; CHECKLIST; DISORDER; MOTHERS; CARE; PREDICTORS; DEPRESSION; RESOURCES AB There is increasing international interest in intensive home-based behavioral intervention for children with autism. In the present study, 141 UK parents conducting such interventions completed a questionnaire addressing issues of stress, coping, and support. Regression analyses showed that parents' stress levels were predicted mainly by psychological rather than demographic variables. In particular, adaptive coping strategies, informal social support sources, and beliefs about the efficacy of the intervention were associated with lower reported stress and higher levels of autism symptomatology were associated with higher reported stress. There was also evidence that the use of Passive Appraisal coping and beliefs about the efficacy of the interventions moderated the effects of autism symptomatology on parents' pessimism. Implications of these findings for future research and for the support of families engaged in intensive home-based behavioral intervention are discussed. C1 Univ Southampton, Dept Psychol, Southampton SO17 1BJ, Hants, England. RP Hastings, RP (reprint author), Univ Southampton, Dept Psychol, Southampton SO17 1BJ, Hants, England. 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Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 327 EP 336 DI 10.1023/A:1010799320795 PG 10 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000007 PM 11518485 ER PT J AU Dawson, G Osterling, J Rinaldi, J Carver, L McPartland, J AF Dawson, G Osterling, J Rinaldi, J Carver, L McPartland, J TI Brief report: Recognition memory and stimulus-reward associations: Indirect support for the role of ventromedial prefrontal dysfunction in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID RHESUS-MONKEYS; LESIONS; PERFORMANCE C1 Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. RP Dawson, G (reprint author), Univ Washington, Ctr Human Dev & Disabil, Box 357920, Seattle, WA 98195 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT BACHEVALIER J, 1994, NEUROPSYCHOLOGIA, V32, P627, DOI 10.1016/0028-3932(94)90025-6 BACHEVALIER J, 1986, BEHAV BRAIN RES, V20, P249, DOI 10.1016/0166-4328(86)90225-1 BARBAS H, 1995, NEUROSCI BIOBEHAV R, V19, P499, DOI 10.1016/0149-7634(94)00053-4 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Brothers L., 1990, CONCEPTS NEUROSCIENC, V1, P27 Damasio A., 1994, DESCARTES ERROR EMOT DAWSON G, 2000, ROLE VENTROMEDIAL PR DAWSON G, 1998, CHILD DEV, V69, P1247 Dawson G, 1996, J AUTISM DEV DISORD, V26, P179, DOI 10.1007/BF02172008 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 DIAMOND A, 1995, J EXP CHILD PSYCHOL, V59, P419, DOI 10.1006/jecp.1995.1020 DIAMOND A, 1994, BEHAV NEUROSCI, V108, P1 JONES B, 1972, EXP NEUROL, V36, P362, DOI 10.1016/0014-4886(72)90030-1 KOWALSKA DM, 1991, NEUROPSYCHOLOGIA, V29, P583, DOI 10.1016/0028-3932(91)90012-W LEDOUX JE, 1994, SCI AM, V270, P50 Meunier M, 1997, NEUROPSYCHOLOGIA, V35, P999, DOI 10.1016/S0028-3932(97)00027-4 Meunier M, 1996, J NEUROPHYSIOL, V75, P1190 MISHKIN M, 1978, NATURE, V273, P297, DOI 10.1038/273297a0 NELSON CA, 1995, DEV PSYCHOL, V31, P723, DOI 10.1037/0012-1649.31.5.723 Schopler E., 1986, CHILDHOOD AUTISM RAT Sparrow S, 1984, VINELAND ADAPTIVE BE SQUIRE LR, 1988, BEHAV NEUROSCI, V102, P210, DOI 10.1037//0735-7044.102.2.210 ZIMMERMAN S, 1991, PRESCHOOL LANGUAGE S ZOLAMORGAN S, 1989, J NEUROSCI, V9, P897 NR 25 TC 42 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 JUN PY 2001 VL 31 IS 3 BP 337 EP 341 DI 10.1023/A:1010751404865 PG 5 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000008 PM 11518486 ER PT J AU Stein, D Ring, A Shulman, C Meir, D Holan, A Weizman, A Barak, Y AF Stein, D Ring, A Shulman, C Meir, D Holan, A Weizman, A Barak, Y TI Brief report: Children with autism as they grow up - Description of adult inpatients with severe autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID CHILDHOOD AUTISM; RATING-SCALE; CLASSIFICATION C1 Abarbanel Mental Hlth Ctr, IL-59100 Bat Yam, Israel. Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel. Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. Eitanim Psychiat Hosp, Jerusalem, Israel. Geha Psychiat Hosp, Petah Tiqwa, Israel. Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. Hebrew Univ Jerusalem, Hadassah Med Sch, IL-91010 Jerusalem, Israel. RP Barak, Y (reprint author), Abarbanel Mental Hlth Ctr, 15 Keren Kayemet Blvd, IL-59100 Bat Yam, Israel. CR *AM PSYCH ASS, 1960, CLASS MENT DIS American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CAMPBELL M, 1995, COMPREHENSIVE TXB PS, P2277 Erba HW, 2000, AM J ORTHOPSYCHIAT, V70, P82, DOI 10.1037/h0087826 First MB, 1995, STRUCTURED CLIN INTE GILLBERG C, 1986, BRIT J PSYCHIAT, V149, P68, DOI 10.1192/bjp.149.1.68 GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P375, DOI 10.1097/00004583-199105000-00004 KLEIN DF, 1980, DIAGNOSIS TREATMENT LORD C, 1991, PSYCHIAT CLIN N AM, V14, P69 Lotter V., 1978, AUTISM REAPPRAISAL C, P475 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 Njardvik U, 1999, J AUTISM DEV DISORD, V29, P287, DOI 10.1023/A:1022107318500 PARKS SL, 1983, J AUTISM DEV DISORD, V13, P255, DOI 10.1007/BF01531565 PERCK CL, 1970, 832638 NIH, V1 Raven J. C., 1976, COLORED PROGRESSIVE RUMSEY JM, 1985, J AM ACAD CHILD PSY, V24, P465, DOI 10.1016/S0002-7138(09)60566-5 SCHOPLER E, 1983, AUTISM ADOLESCENTS A, P3 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 Van Kammen D., 1995, COMPREHENSIVE TXB PS, P1987 Volavka J., 1995, NEUROBIOLOGY VIOLENC Wing L., 1987, HDB AUTISM PERVASIVE, P3 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 23 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 JUN PY 2001 VL 31 IS 3 BP 355 EP 360 DI 10.1023/A:1010707622612 PG 6 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000011 PM 11518489 ER PT J AU Roseman, B Schneider, E Crimmins, D Bostwick, H Visintainer, P Jaskow, PA Accardo, P AF Roseman, B Schneider, E Crimmins, D Bostwick, H Visintainer, P Jaskow, PA Accardo, P TI What to measure in autism drug trials. SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID SECRETIN C1 New York Med Coll, Valhalla, NY 10595 USA. RP Roseman, B (reprint author), New York Med Coll, Valhalla, NY 10595 USA. CR Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Lightdale JR, 2000, PEDIATR RES, V47, p29A Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 NR 4 TC 3 Z9 3 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 361 EP 362 PG 2 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000012 PM 11518490 ER PT J AU Fombonne, E AF Fombonne, E TI What is the prevalence of Asperger disorder? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID TOTAL POPULATION; AUTISM; CHILDREN; ACCOUNT CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 CHAKRABARTI S, JAMA EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x FOMBONNE E, 2001, IN PRESS MOL PSYCHIA Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Powell JE, 2000, DEV MED CHILD NEUROL, V42, P624, DOI 10.1017/S001216220000116X Sponheim E, 1998, J AUTISM DEV DISORD, V28, P217, DOI 10.1023/A:1026017405150 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 WING L, 1981, PSYCHOL MED, V11, P115 Wolff S, 1996, EUR CHILD ADOLES PSY, V5, P119 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 12 TC 25 Z9 25 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2001 VL 31 IS 3 BP 363 EP 364 PG 2 WC Psychology, Developmental SC Psychology GA 461TF UT WOS:000170379000013 PM 11518491 ER PT J AU Masi, G Cosenza, A Mucci, M De Vito, G AF Masi, G Cosenza, A Mucci, M De Vito, G TI Risperidone monotherapy in preschool children with pervasive developmental disorders SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID AUTISTIC-CHILDREN; INFANTILE-AUTISM; YOUNG-CHILDREN; RATING-SCALE; DOUBLE-BLIND; ADOLESCENTS; HALOPERIDOL; TRIAL; CLASSIFICATION; BEHAVIOR AB The aim of this preliminary study was to examine the short-term efficacy and safety of the atypical antipsychotic risperidone in preschool autistic children. The sample consisted of 10 subjects (7 males and 3 females) aged 3(9)/(12) to 6(6)/(12) years (mean age 4.7 years). A 16-week open-label trial with risperidone monotherapy was initiated at a starting dose of 0.25 mg daily and was increased to a maximum dose of 0.50 mg (0.027 mg/kg daily). Outcome measures were the Childhood Autism Rating Scale, the Children's Psychiatric Rating Scale, Clinical Global Impression (improvement score), and the Children's Global Assessment of Functioning. Two subjects did not complete the trial because of side effects (tachycardia and flushes, fever and hyporexia). After the 16-week treatment, data from the eight children who completed the trial indicated a modest improvement in the Childhood Autism Rating Scale total score, Children's Psychiatric Rating Scale total score, and Children's Global Assessment of Functioning. According to the Clinical Global Impression, the global improvement score for four subjects was much improved or very much improved; the score for the other four children was minimally improved. None of the children exhibited behavioral deterioration. The side effects in the eight children were not severe. C1 Univ Pisa, Div Child Neurol & Psychiat, I-56018 Pisa, Italy. Inst Ricovero & Cura Carattere Sci Stella Maris, Pisa, Italy. RP Masi, G (reprint author), Univ Pisa, Div Child Neurol & Psychiat, Via Giacinti 2, I-56018 Pisa, Italy. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CAMPBELL M, 1978, J AM ACAD CHILD PSY, V17, P640, DOI 10.1016/S0002-7138(09)61017-7 ANDERSON LT, 1984, AM J PSYCHIAT, V141, P1195 Armenteros JL, 1997, J AM ACAD CHILD PSY, V36, P694, DOI 10.1097/00004583-199705000-00021 CAMPBELL M, 1988, PSYCHOPHARMACOL BULL, V24, P251 CAMPBELL M, 1985, PSYCHOPHARMACOL BULL, V21, P1047 Casaer P, 1994, PEDIATR NEUROL, V11, P89, DOI 10.1016/0887-8994(94)90174-0 CHOUINARD G, 1993, J CLIN PSYCHOPHARM, V13, P25 CORBETT R, 1993, PHARMACOL BIOCHEM BE, V45, P9, DOI 10.1016/0091-3057(93)90079-9 Demb HB, 1996, J CHILD ADOL PSYCHOP, V6, P79, DOI 10.1089/cap.1996.6.79 Findling RL, 1997, PSYCHOPHARMACOL BULL, V33, P155 FISH B, 1985, PSYCHOPHARMACOL BULL, V21, P753 Fisman S, 1996, J CHILD ADOL PSYCHOP, V6, P177, DOI 10.1089/cap.1996.6.177 GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P375, DOI 10.1097/00004583-199105000-00004 Griffiths R, 1970, ABILITIES YOUNG CHIL Guy W., 1976, ECDEU ASSESSMENT MAN KANE J, 1988, ARCH GEN PSYCHIAT, V45, P789 Kumra S, 1996, ARCH GEN PSYCHIAT, V53, P1090 Leiter R. G., 1979, LEITER INT PERFORMAN LOMBROSO PJ, 1995, J AM ACAD CHILD PSY, V34, P1147, DOI 10.1097/00004583-199509000-00011 MANDOCKI MW, 1995, J CHILD ADOL PSYCHOP, V5, P69 MCDOUGLE CJ, 1994, CHILD ADOL PSYCH CL, V3, P71 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 MELTZER HY, 1989, J PHARMACOL EXP THER, V251, P238 MOLLER HJ, 1991, PHARMACOPSYCHIATRY, V24, P185, DOI 10.1055/s-2007-1014467 Nicolson R, 1998, J AM ACAD CHILD PSY, V37, P372, DOI 10.1097/00004583-199804000-00014 Perry R, 1997, J CHILD ADOL PSYCHOP, V7, P167, DOI 10.1089/cap.1997.7.167 PIVEN J, 1991, J AUTISM DEV DISORD, V21, P51, DOI 10.1007/BF02206997 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SHAFFER D, 1983, ARCH GEN PSYCHIAT, V40, P1228 Uzgiris I., 1975, ASSESSMENT INFANCY O Volkmar FR, 1996, CHILD ADOL PSYCH CL, V5, P963 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 WHITAKER A, 1992, PSYCHIAT CLIN N AM, V15, P243 NR 35 TC 19 Z9 22 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 JUN PY 2001 VL 16 IS 6 BP 395 EP 400 DI 10.1177/088307380101600602 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 473DY UT WOS:000171025800002 PM 11417603 ER PT J AU Hardan, AY Minshew, NJ Mallikarjuhn, M Keshavan, MS AF Hardan, AY Minshew, NJ Mallikarjuhn, M Keshavan, MS TI Brain volume in autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PATHWAY; MRI AB Increased brain size has been observed in individuals with autism with a wide range of cognitive functioning. The purpose of this investigation was to obtain measurements of the brain volume in a sample of nonmentally retarded autistic individuals. Magnetic resonance imaging scans from 16 nonmentally retarded individuals with autism and 19 male volunteer comparison subjects were obtained and the following structures were measured: third, fourth, and lateral ventricles and intracranial and cerebral volumes. Mean cerebral and third ventricle volumes in the autistic subjects were significantly greater than in the controls when adjusted for intracranial volume. No other significant results were found. Our finding of increased brain volume in autism is consistent with previous reports in the literature. Additional longitudinal neuroimaging and, more importantly, neuropathologic studies are warranted to provide a better understanding of the complexities underlying increased brain size in autism. C1 Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, 3811 OHara St, Pittsburgh, PA 15213 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT ARNDT S, 1991, PSYCHIAT RES-NEUROIM, V40, P79 Aylward EH, 1999, NEUROLOGY, V53, P2145 Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAILEY A, 1993, LANCET, V341, P1225, DOI 10.1016/0140-6736(93)91065-T Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Caviness V. S., 1992, ANN NEUROL, V32, P475 Chugani DC, 1997, ANN NEUROL, V42, P666, DOI 10.1002/ana.410420420 COLEMAN PD, 1985, J AUTISM DEV DISORD, V15, P245, DOI 10.1007/BF01531496 HOROWITZ B, 1988, ARCH NEUROL-CHICAGO, V45, P749 JACOBSON R, 1988, PSYCHOL MED, V18, P39 Kanner L, 1943, NERV CHILD, V2, P217 Kemper TL, 1998, J NEUROPATH EXP NEUR, V57, P645, DOI 10.1097/00005072-199807000-00001 Keshavan M. 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PD JUN PY 2001 VL 16 IS 6 BP 421 EP 424 DI 10.1177/088307380101600607 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 473DY UT WOS:000171025800007 PM 11417608 ER PT J AU O'Riordan, MA Plaisted, KC Driver, J Baron-Cohen, S AF O'Riordan, MA Plaisted, KC Driver, J Baron-Cohen, S TI Superior visual search in autism SO JOURNAL OF EXPERIMENTAL PSYCHOLOGY-HUMAN PERCEPTION AND PERFORMANCE LA English DT Article ID GUIDED SEARCH; CONJUNCTION SEARCH; ATTENTION; DEFICITS; MODEL; CEREBELLAR; SIMILARITY; COHERENCE; CHILDREN; FEATURES AB Children with a diagnosis of autism and normally developing children, matched for age and general ability, were tested on a series of visual search tasks in 2 separate experiments. The children with autism performed better than the normally developing children on difficult visual search tasks. This result occurred regardless of whether the target was uniquely defined by a single feature or a conjunction of features, as long as ceiling effects did not mask the difference. Superior visual search performance in autism can be seen as analogous to other reports of enhanced unique item detection in autism. Unique item detection in autism is discussed in the light of mechanisms proposed to be involved in normal visual search performance. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. UCL, Dept Psychol, London, England. RP O'Riordan, MA (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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Exp. Psychol.-Hum. Percept. Perform. PD JUN PY 2001 VL 27 IS 3 BP 719 EP 730 DI 10.1037//0096-1523.27.3.719 PG 12 WC Psychology; Psychology, Experimental SC Psychology GA 471TW UT WOS:000170945600016 PM 11424657 ER PT J AU Matthews, B Shute, R Rees, R AF Matthews, B Shute, R Rees, R TI An analysis of stimulus overselectivity in adults with autism SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article ID OVER-SELECTIVITY; RETARDED-CHILDREN; MAINTENANCE; PARADIGM AB The studies reported in this paper examined the effect of varying background colour and relative location of the stimulus on stimulus control in adults with autism and a mental-age matched control group (all adults with intellectual disability). The focus was on extending the stimulus overselectivity literature. The participants were taught to button-press in the presence of the "correct" visual stimulus presented on a computer monitor but to withhold from pressing when the "incorrect" stimulus was presented. Once the discrimination task had been learned, testing was then conducted to identify which components of the stimulus (location or size) had acquired stimulus control. It was found that the participants produced stimulus generalisation gradients which are comparable with other populations. Operationally defined stimulus overselectivity was also evident in adults with autism and controls. This is one of the few demonstrations of this in an adult population. Varying background colour in a discrimination task containing two relevant cues (location and size) did not lead to more evidence of stimulus overselectivity in either adults with autism or mental-age matched controls (study 1). Also, varying the relative placement of the training stimuli on the monitor had no effect (study 2). However, study 2 indicated a difference in stimulus overselectivity between the groups. The difference appeared to be related to the number of stimuli presented and the difference was in the opposite direction to that predicted. That is, participants with autism were less overselective than the mental-age matched control group. The relevance of these findings for the instruction of people with autism and intellectual disability is discussed. C1 Flinders Univ S Australia, Sch Educ Humanities Law & Theol, Sch Special Educ & Disabil, Bedford Pk, SA 5042, Australia. RP Matthews, B (reprint author), Flinders Univ S Australia, Sch Educ Humanities Law & Theol, Sch Special Educ & Disabil, Bedford Pk, SA 5042, Australia. 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Intellect. Dev. Dis. PD JUN PY 2001 VL 26 IS 2 BP 161 EP 176 PG 16 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 462YW UT WOS:000170448800004 ER PT J AU Gray, KM Tonge, BJ AF Gray, KM Tonge, BJ TI Are there early features of autism in infants and preschool children? SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Review DE autistic disorder; behaviour; children; infants ID YOUNG-CHILDREN; CHILDHOOD AUTISM; DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; FOLLOW-UP; ADI-R; AGE; EPIDEMIOLOGY; RECOGNITION; DIAGNOSIS AB Autism is characterized by impairments in three areas: (i) reciprocal social interaction; (ii) communication; and (iii) repetitive and stereotyped patterns of interest and behaviour. Despite the finding that parents notice abnormalities and problems with their child's development at a very early age, research shows that diagnoses are often made at an age beyond that recommended for the commencement of early intervention. This paper reviews the range of studies that have sought to elucidate the early features of autism in young, preschool children. Impairments in the capacity for reciprocal social interaction involving preverbal, verbal and non-verbal communication, and play and symbolic behaviour are the key features indicative of autism in infants and preschool children. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Monash Med Ctr, Clayton, Vic 3168, Australia. RP Gray, KM (reprint author), Monash Univ, Ctr Dev Psychiat & Psychol, Monash Med Ctr, Clayton, Vic 3168, Australia. RI Gray, Kylie/H-3345-2014 OI Gray, Kylie/0000-0001-6518-4240 CR ADRIEN JL, 1992, J AUTISM DEV DISORD, V22, P375, DOI 10.1007/BF01048241 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson GM, 1997, HDB AUTISM PERVASIVE, P325 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 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 Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 Charman T, 1998, INF MENTAL HLTH J, V19, P260, DOI 10.1002/(SICI)1097-0355(199822)19:2<260::AID-IMHJ12>3.0.CO;2-W CHUNG M, 1995, ED CHILD PSYCHOL, V12, P31 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 FOMBONNE E, 1997, AUTISM, V1, P227, DOI 10.1177/1362361397012008 GILLBERG C, 1989, DIAGNOSIS AND TREATMENT OF AUTISM, P23 GILLBERG C, 1990, J CHILD PSYCHOL PSYC, V31, P921, DOI 10.1111/j.1469-7610.1990.tb00834.x Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 HOSHINO Y, 1982, FOLIA PSYCHIAT NEU J, V36, P367 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 JOHNSON MH, 1992, DEV MED CHILD NEUROL, V34, P316 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F MARCUS LM, 1993, PRESCHOOL ISSUES AUT, P149 Minshew N. 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Paediatr. Child Health PD JUN PY 2001 VL 37 IS 3 BP 221 EP 226 DI 10.1046/j.1440-1754.2001.00653.x PG 6 WC Pediatrics SC Pediatrics GA 561YK UT WOS:000176170500003 PM 11468034 ER PT J AU Holaday, M Moak, J Shipley, MA AF Holaday, M Moak, J Shipley, MA TI Rorschach protocols from children and adolescents with Asperger's Disorder SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article ID AUTISM AB Rorschach protocols from 24 boys with Asperger's Disorder matched by age to 24 boys with other emotional or behavioral disorders (the contrast group) were compared to each other and to Exner's (1995) normative data. Eight variables based on Diagnostic and Statistical Manual of Mental Disorders (4th ed. [DSM-IV]; American Psychiatric Association, 1994) criteria and a review of the literature for Asperger's Disorder were predicted to discriminate between groups with the Asperger's group having more extreme scores. Five variables (COP, CDI, H, M, and EA) were significantly different from the contrast group and T and WSumC were significantly different from the normative data in both the Asperger's group and the contrast group. C1 Univ So Mississippi, Dept Psychol, Hattiesburg, MS 39406 USA. RP Holaday, M (reprint author), 705 Martens Court 71-74, Laredo, TX 78041 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARCHER RP, 1991, PROF PSYCHOL-RES PR, V22, P247, DOI 10.1037//0735-7028.22.3.247 Attwood T., 1998, ASPERGERS SYNDROME G Bauminger N, 1999, J AUTISM DEV DISORD, V29, P81, DOI 10.1023/A:1025974701090 Bender L, 1938, AM ORTHOPSYCHIATRIC, V3 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 Exner J. E., 1993, RORSCHACH COMPREHENS, V1 Exner J. E., 1995, RORSCHACH WORKBOOK C Fombonne E, 1998, AUTISM PERVASIVE DEV, P32 Gacono C. B., 1994, RORSCHACH ASSESSMENT GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Happe F., 1995, LEARNING COGNITION A, P177 KERBESHIAN J, 1990, BRIT J PSYCHIAT, V156, P721, DOI 10.1192/bjp.156.5.721 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Murray H. A., 1943, THEMATIC APPERCEPTIO POMEROY JC, 1998, ASPERGER SYNDROME HI, P29 Prior M, 1998, AUTISM PERVASIVE DEV, P64 Schopler E., 1986, CHILDHOOD AUTISM RAT SCHOPLER E, 1998, ASPERGER SYNDROME HI SZATMARI P, 1991, PSYCHIAT CLIN N AM, V14, P81 Volkmar FR, 1998, J AUTISM DEV DISORD, V28, P457, DOI 10.1023/A:1026012707581 Volkmar FR, 1998, AUTISM PERVASIVE DEV, P1 NR 23 TC 5 Z9 5 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD JUN PY 2001 VL 76 IS 3 BP 482 EP 495 DI 10.1207/S15327752JPA7603_09 PG 14 WC Psychology, Clinical; Psychology, Social SC Psychology GA 456GV UT WOS:000170075500009 PM 11499460 ER PT J AU Boyer, L Lee, C AF Boyer, L Lee, C TI Converting challenge to success: Supporting a new teacher of students with autism SO JOURNAL OF SPECIAL EDUCATION LA English DT Article AB A new teacher in a self-contained classroom for six kindergarten students with autism and autistic-like behaviors describes the challenges of beginning a new program in her school, planning instruction with the new state instructional standards in mind, being scrutinized by parents and advocates, and coordinating documentation of progress and development of Individualized Education Programs (IEPs). Her challenges become successes through the support of an induction program that includes a mentor who also teaches young children with autism, insightful administrators, and school district resources. Components of an induction program that meets the needs of new special educators are included. C1 George Mason Univ, Fairfax, VA 22030 USA. Fairfax Cty Publ Sch, Fairfax, VA USA. RP Boyer, L (reprint author), 7400 Clifton Rd, Clifton, VA 20124 USA. CR BILLINGSLEY B, 1995, IMPROVING RETENTION BOYER L, 2000, FUTURE TEACHER, V7, P6 Boyer L., 1999, THESIS G MASON U FAI COLBERT JA, 1992, J TEACH EDUC, V43, P193, DOI 10.1177/0022487192043003005 *COUNC EXC CHILDR, 1998, WHAT EV SPEC ED MUST French NK, 1998, REM SPEC EDUC, V19, P357 Miller M. D., 1999, EXCEPT CHILDREN, V65, P201 *RECR NEW TEACH IN, 1999, LEARN ROP SURV IND P *RECR NEW TEACH IN, 1999, URB TEACH CHALL SMITHDAVIS J, 1989, PREVENTING ATTRITION STRONG M, 1999, NEW TEACHER CTR REFL, V3, P10 THIESSPRINTHAL L, 1986, J TEACHER ED NOV, P14 *US DEP ED, 1999, 21 US DEP ED White M., 1995, THESIS VANDERBILT U Wisniewski L, 1997, J SPEC EDUC, V31, P325 NR 15 TC 10 Z9 10 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 SUM PY 2001 VL 35 IS 2 BP 75 EP 83 DI 10.1177/002246690103500202 PG 9 WC Education, Special SC Education & Educational Research GA 455WT UT WOS:000170051300002 ER PT J AU Sturmey, P James, V AF Sturmey, P James, V TI Administrative prevalence of autism in the Texas school system SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 CUNY, Queens Coll, Dept Psychol, Grad Sch Psychol, Flushing, NY 11367 USA. Christus Santa Rosa Childrens Hosp, Texas Ctr Autism Res & Treatment, San Antonio, TX USA. RP Sturmey, P (reprint author), CUNY, Queens Coll, Dept Psychol, Grad Sch Psychol, Flushing, NY 11367 USA. CR Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 NR 2 TC 13 Z9 13 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JUN PY 2001 VL 40 IS 6 BP 621 EP 621 DI 10.1097/00004583-200106000-00005 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 433XR UT WOS:000168786400005 PM 11392338 ER PT J AU King, BH Wright, DM Handen, BL Sikich, I Zimmerman, AW McMahon, W Cantwell, E Davanzo, PA Dourish, CT Dykens, EM Hooper, SR Jaselskis, CA Leventhal, BL Levitt, J Lord, C Lubetsky, MJ Myers, SM Ozonoff, S Shah, BG Snape, M Shernoff, EW Williamson, K Cook, EH AF King, BH Wright, DM Handen, BL Sikich, I Zimmerman, AW McMahon, W Cantwell, E Davanzo, PA Dourish, CT Dykens, EM Hooper, SR Jaselskis, CA Leventhal, BL Levitt, J Lord, C Lubetsky, MJ Myers, SM Ozonoff, S Shah, BG Snape, M Shernoff, EW Williamson, K Cook, EH TI Double-blind, placebo-controlled study of amantadine hydrochloride in the treatment of children with autistic disorder SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE N-methyl-D-aspartate (NMDA); hyperactivity; irritability; placebo ID PERVASIVE DEVELOPMENTAL DISORDERS; ABERRANT BEHAVIOR CHECKLIST; EXCITATORY AMINO-ACIDS; RETT-SYNDROME; SCHIZOPHRENIC CHILDREN; ADULTS; RECEPTORS; GLUTAMATE; BRAIN AB Objective: To test the hypothesis that amantadine hydrochloride is a safe and effective treatment for behavioral disturbances-for example, hyperactivity and irritability-in children with autism. Method: Thirty-nine subjects (intent to treat; 5-19 years old; IQ > 35) had autism diagnosed according to DSM-IV and ICD-10 criteria using the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule-Generic. The Aberrant Behavior Checklist-Community Version (ABC-CV) and Clinical Global Impressions (CGI) scale were used as outcome variables. After a 1-week, single-blind placebo run-in, patients received a single daily dose of amantadine (2.5 mg/kg per day) or placebo for the next week, and then bid dosing (5.0 mg/kg per day) for the subsequent 3 weeks. Results: When assessed on the basis of parent-rated ABC-CV ratings of irritability and hyperactivity, the mean placebo response rate was 37% versus amantadine at 47% (not significant). However, in the amantadine-treated group there were statistically significant improvements in absolute changes in clinician-rated ABC-CVs for hyperactivity (amantadine -6.4 versus placebo -2.1; p =.046) and inappropriate speech (-1.9 versus 0.4; p =.008). CGI scale ratings were higher in the amantadine group: 53% improved versus 25% (p =.076). Amantadine was well tolerated. Conclusions: Parents did not report statistically significant behavioral change with amantadine. However, clinician-rated improvements in behavioral ratings following treatment with amantadine suggest that further studies with this or other drugs acting on the glutamatergic system are warranted. The design of these and similar drug trials in children with autistic disorder must take into account the possibility of a large placebo response. C1 Dartmouth Med Sch, Hanover, NH USA. Vernalis Grp PLC, Winnersh, England. Univ Calif Los Angeles, Neuropsychiat Inst, Los Angeles, CA 90024 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Kennedy Krieger Inst, Baltimore, MD USA. Univ Utah, Salt Lake City, UT USA. Univ Chicago, Chicago, IL 60637 USA. RP King, BH (reprint author), Dartmouth Coll, Hitchcock Med Ctr, Dept Psychiat, 1 Med Ctr Dr, Lebanon, NH 03756 USA. 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Method: Volume measurements of the cerebellum, vermis, and brainstem were obtained from coronal magnetic resonance imaging scans in 16 autistic subjects and 19 group-matched healthy controls. For the purpose of comparison with previous studies, area measurements of the midbrain, pens, medulla, total cerebellar vermis, and its three subregions were also obtained from a larger sample of 22 autistic males (mean age: 22.4 years; range: 12.2-51.8 years) and 22 individually matched controls (mean age 22.4 years; range: 12.9-52.2 years). Results: The total volume of the cerebellum and the cerebellar hemispheres were significantly larger in the autistic subjects with and without correcting for total brain volume. Volumes of the vermis and the brainstem and all area measurements did not differ significantly between groups. Conclusions: There is an increase in the volume of the cerebellum in people with autism consistent with the increase in regional and total brain size reported in this developmental disorder. This finding is also concordant with evidence of cerebellar abnormalities from neuropathological and neuropsychological studies that point to the role of this structure, as part of a complex neural system, in the pathophysiology of autism. C1 Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, 3811 OHara St, Pittsburgh, PA 15213 USA. 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D., 1999, PSYCHOL MUSIC, P265, DOI 10.1016/B978-012213564-4/50009-3 WILLIAMS JC, 1961, CIRCULATION, V24, P1311 YOUNG RL, 1995, J AUTISM DEV DISORD, V25, P231, DOI 10.1007/BF02179286 NR 36 TC 38 Z9 38 PU UNIV CALIF PRESS PI BERKELEY PA C/O JOURNALS DIVISION, 2000 CENTER ST, STE 303, BERKELEY, CA 94704-1223 USA SN 0730-7829 J9 MUSIC PERCEPT JI Music Percept. PD SUM PY 2001 VL 18 IS 4 BP 491 EP 503 DI 10.1525/mp.2001.18.4.491 PG 13 WC Music; Psychology, Experimental SC Music; Psychology GA 453RJ UT WOS:000169930000004 ER PT J AU DeFrancesco, L AF DeFrancesco, L TI Scientists question rise in autism SO NATURE MEDICINE LA English DT News Item CR Sandler AD, 2001, PEDIATRICS, V107, P1221 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 RUTTER M, 1997, NATURE, V265, P726 1997, J AUTISM DEV DISORDE, V9, P11 NR 4 TC 0 Z9 0 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD JUN PY 2001 VL 7 IS 6 BP 645 EP 645 DI 10.1038/88985 PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 438YH UT WOS:000169081500011 PM 11385482 ER PT J AU Boddaert, N Belin, P Poline, JB Chabanne, N Mouren-Simeoni, MC Barthelemy, C Samson, Y Zilbovicius, M AF Boddaert, N Belin, P Poline, JB Chabanne, N Mouren-Simeoni, MC Barthelemy, C Samson, Y Zilbovicius, M TI Temporal lobe dysfunction in autism: a PET auditory activation study. SO NEUROIMAGE LA English DT Meeting Abstract C1 CEA, Serv Hosp Frederic Joliot, DSV, DRM, F-91406 Orsay, France. Hop Necker Enfants Malad, Serv Radiopediatrie, Paris, France. McGill Univ, Montreal Neurol Inst, Neuropsychol Cognit Neurosci Unit, Montreal, PQ, Canada. Hop Robert Debre, Serv Pedopsychiat, F-75019 Paris, France. INSERM, U316, Tours, France. Hop La Pitie Salpetriere, Serv Urgences Cerebrovasc, Paris, France. CR Thivard L, 2000, NEUROREPORT, V11, P2969, DOI 10.1097/00001756-200009110-00028 Zilbovicius M, 2000, AM J PSYCHIAT, V157, P1988, DOI 10.1176/appi.ajp.157.12.1988 NR 2 TC 2 Z9 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD JUN PY 2001 VL 13 IS 6 SU S BP S1028 EP S1028 PN 2 PG 1 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 439HQ UT WOS:000169106301027 ER PT J AU Castelli, F Frith, U Happe, F Frith, CD AF Castelli, F Frith, U Happe, F Frith, CD TI Autism and the perception of intentionality in moving geometrical shapes SO NEUROIMAGE LA English DT Meeting Abstract RI Frith, Uta/C-1757-2008; Happe, Francesca/D-5544-2012 OI Frith, Uta/0000-0002-9063-4466; NR 0 TC 1 Z9 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD JUN PY 2001 VL 13 IS 6 SU S BP S1035 EP S1035 PN 2 PG 1 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 439HQ UT WOS:000169106301034 ER PT J AU Dierks, T Bolte, S Hubl, D Lanfermann, H Poustka, F AF Dierks, T Bolte, S Hubl, D Lanfermann, H Poustka, F TI Alterations of face processing strategies in autism: A fMRI study. SO NEUROIMAGE LA English DT Meeting Abstract C1 Univ Bern, Hosp Clin Psychiat, Dept Psychiat Neurophysiol, Bern, Switzerland. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. Univ Frankfurt, Dept Neuroradiol, D-6000 Frankfurt, Germany. RI Dierks, Thomas/B-7092-2012 OI Dierks, Thomas/0000-0002-4173-5308 NR 0 TC 1 Z9 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD JUN PY 2001 VL 13 IS 6 SU S BP S1042 EP S1042 PN 2 PG 1 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 439HQ UT WOS:000169106301041 ER PT J AU Salmond, CH Ashburner, J Friston, KJ Gadian, DG Vargha-Khadem, F AF Salmond, CH Ashburner, J Friston, KJ Gadian, DG Vargha-Khadem, F TI Behavioural and neuropathological evidence for medial temporal lobe abnormality in children with autism SO NEUROIMAGE LA English DT Meeting Abstract RI Vargha-Khadem, Faraneh/C-2558-2008; Friston, Karl/D-9230-2011; Ashburner, John/I-3757-2013 OI Friston, Karl/0000-0001-7984-8909; NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD JUN PY 2001 VL 13 IS 6 SU S BP S1095 EP S1095 PN 2 PG 1 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 439HQ UT WOS:000169106301094 ER PT J AU Wang, A Dapretto, M Hariri, A Sigman, M Bookheimer, SY AF Wang, A Dapretto, M Hariri, A Sigman, M Bookheimer, SY TI Processing affective and linguistic prosody in autism: An fMRI study SO NEUROIMAGE LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Brain Mapping Ctr, Los Angeles, CA 90024 USA. NIMH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. NR 0 TC 4 Z9 4 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD JUN PY 2001 VL 13 IS 6 SU S BP S621 EP S621 PN 2 PG 1 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 439HQ UT WOS:000169106300622 ER PT J AU Hisaoka, S Harada, M Nishitani, H Mori, K AF Hisaoka, S Harada, M Nishitani, H Mori, K TI Regional magnetic resonance spectroscopy of the brain in autistic individuals SO NEURORADIOLOGY LA English DT Article DE proton magnetic resonance spectroscopy; autism; speech centres ID INFANTILE-AUTISM AB We studied the variations in the concentration of metabolites with brain region and age in autistic individuals and normal controls using multiple analysis of covariance. We examined 55 autistic individuals (2-21 years old, 47 male and eight female) and 51 normal children (3 months-15 years old, 26 boys and 25 girls). Single volumes of interest were placed in the frontal, parietal and temporal region on both sides, the brain stem and cingulate gyrus. The concentration of each metabolite was quantified by the water reference method. The concentration of N-acetylaspartate in the temporal regions (Brodmann's areas 41 and 42) in the autistic individuals were significantly lower than those in the controls (P < 0.05), but concentrations in other regions were not significantly different between the autistic individuals and controls. This suggests low density or dysfunction of neurones in Brodmann's areas 41 and 42 in autistic individual, which might be related to the disturbances of the sensory speech centre (Wernicke's area) in autism. C1 Univ Tokushima, Sch Med, Dept Radiol, Tokushima 7708503, Japan. Univ Tokushima, Sch Med, Dept Paediat, Tokushima 7708503, Japan. RP Harada, M (reprint author), Univ Tokushima, Sch Med, Dept Radiol, 3-18-15 Kuramoto Cho, Tokushima 7708503, Japan. 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We focus instead on an imitative disturbance involving difficulties both in copying actions and in inhibiting more stereotyped mimicking, such as echolalia. A candidate for the neural basis of this disturbance may be found in a recently discovered class of neurons in frontal cortex, 'mirror neurons' (MNs). These neurons show activity in relation both to specific actions performed by self and matching actions performed by others, providing a potential bridge between minds. MN systems exist in primates without imitative and 'theory of mind' abilities and we suggest that in order for them to have become utilized to perform social cognitive functions, sophisticated cortical neuronal systems have evolved in which MNs function as key elements. Early developmental failures of MN systems are likely to result in a consequent cascade of developmental impairments characterised by the clinical syndrome of autism. Crown Copyright (C) 2001 Published by Elsevier Science Ltd. All rights reserved. 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PD JUN PY 2001 VL 25 IS 4 BP 287 EP 295 DI 10.1016/S0149-7634(01)00014-8 PG 9 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 459ZL UT WOS:000170281300001 PM 11445135 ER PT J AU [Anonymous] AF [Anonymous] TI Functional neuroanatomy of social behavior in autism SO NEUROSCIENTIST LA English DT Editorial Material CR Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1073-8584 J9 NEUROSCIENTIST JI Neuroscientist PD JUN PY 2001 VL 7 IS 3 BP 190 EP 190 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 437UL UT WOS:000169011900009 ER PT J AU Wassink, TH Piven, J Patil, SR AF Wassink, TH Piven, J Patil, SR TI Chromosomal abnormalities in a clinic sample of individuals with autistic disorder SO PSYCHIATRIC GENETICS LA English DT Article DE autism; genetics; chromosomal abnormalities; karyotype; mental retardation ID FRAGILE-X-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; UTAH EPIDEMIOLOGIC SURVEY; INFANTILE-AUTISM; SEROTONIN TRANSPORTER; MENTAL-RETARDATION; ANGELMAN-SYNDROME; 15Q11-13 REGION; DOWN-SYNDROME; PREVALENCE AB We examined data from the largest reported sample of autistic individuals who have been karyotyped with the aim of providing additional information in the search for autism disease genes. Individuals seen in the University of Iowa's Child and Adolescent Psychiatry Clinic since 1980 who had been diagnosed with autism were cross-referenced with the University of Iowa's Cytogenetics Laboratory database. We determined the number of individuals referred for cytogenetic testing and, of these, the number found to have gross cytological abnormalities. Medical records were reviewed for all cases with such abnormalities. Between 1980 and 1998, 898 subjects seen in the clinic were diagnosed with autism. Of these, 278 (30.1%) were referred for cytological studies; 25 (9.0%) of these were found to have chromosomal abnormalities. The most common chromosomal abnormalities were Fragile X, other sex chromosome anomalies, and chromosome 15 abnormalities. These data support the contribution of chromosomal abnormalities to a small but significant number of cases of autism, and highlight the involvement of chromosome 15 and the sex chromosomes. 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PD JUN PY 2001 VL 11 IS 2 BP 57 EP 63 DI 10.1097/00041444-200106000-00001 PG 7 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 460HW UT WOS:000170303000001 PM 11525418 ER PT J AU Persico, AM Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Conciatori, M Keller, F AF Persico, AM Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Conciatori, M Keller, F TI No association between the 4G/5G polymorphism of the plasminogen activator inhibitor-1 gene promoter and autistic disorder SO PSYCHIATRIC GENETICS LA English DT Article DE autism; macrocephaly; plasminogen; protease; serotonin; serpin family; urokinase ID PAI-1 GENE; PLASMINOGEN-ACTIVATOR-INHIBITOR-1 GENE; NEUROANATOMICAL ABNORMALITIES; LINKAGE DISEQUILIBRIUM; FAMILY HISTORY; UROKINASE; SYSTEM; MICE; CEREBELLAR; DEFICIENCY AB Plasmin, a serine protease, is involved in many physiologically relevant processes, including haemostasis, cellular recruitment during immune response, tumour growth, and also neuronal migration and synaptic remodelling. Both tissue-type and urokinase-type plasminogen activators can be efficiently inhibited by plasminogen activator inhibitor-1 (PAI-1), a protease inhibitor of the serpin family. The human PAI-1 gene is located on chromosome 7q, within or close to a region that has been linked to autism in several linkage studies. Autism seems to be characterized by altered neuronal cytoarchitecture, synaptogenesis and possibly also cellular immune responses. We began addressing the potential involvement of the PAI-1 gene in autistic disorder with this linkage/association study, assessing transmission patterns of the 4G/5G polymorphism in the PAI-1 gene promoter that was previously shown to significantly affect PAI-1 plasma levels. No linkage/association was found in 167 trios with autistic probands, recruited in Italy and in the USA. We thus found no evidence that this polymorphism, or putative functionally relevant gene variants in linkage disequilibrium with it, confer vulnerability to autistic disorder. Psychiatr Genet 11:99-103 (C) 2001 Lippincott Williams & Wilkins. C1 Univ Campus Biomed, Dept Physiol & Neurosci, Neurosci Lab, Rome, Italy. Univ Naples 2, Dept Child Neuropsychiat, Naples, Italy. SW Autism Res Ctr, Phoenix, AZ USA. IRCCS, Osped Bambino Gesu, Div Child Neurospsychiat, Rome, Italy. Univ Campus Biomed, Clin Cognit Disabilities, Rome, Italy. Univ Roma La Sapienza, Dept Psychol, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, N-0027 Oslo, Norway. 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Genet. PD JUN PY 2001 VL 11 IS 2 BP 99 EP 103 DI 10.1097/00041444-200106000-00008 PG 5 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 460HW UT WOS:000170303000008 PM 11525425 ER PT J AU Hayashi, E AF Hayashi, E TI Seasonal changes in sleep and behavioral problems in a pubescent case with autism SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article; Proceedings Paper CT 25th Annual Meeting of the Japanese-Society-of-Sleep-Research (JSSR) CY JUN 08-09, 2000 CL YOKOHAMA, JAPAN SP Japanese Soc Sleep Res DE autism; behavioral problems; seasonal changes; sleep problems AB This study reports on the seasonal changes in sleep problems and behavioral problems in a pubescent case with autism. His care diary, kept for 1 year, showed seasonal changes of sleep and behavioral problems, and that his behavioral problems preceded his sleep problems. C1 Kaga Welf Inst, Itabashi Ku, Tokyo 1730003, Japan. RP Hayashi, E (reprint author), Kaga Welf Inst, Itabashi Ku, 1-7-2 Kaga, Tokyo 1730003, Japan. CR Hayashi E, 2000, PSYCHIAT CLIN NEUROS, V54, P383, DOI 10.1046/j.1440-1819.2000.00725.x Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 NR 2 TC 10 Z9 10 PU BLACKWELL SCIENCE ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1323-1316 J9 PSYCHIAT CLIN NEUROS JI Psychiatry Clin. Neurosci. PD JUN PY 2001 VL 55 IS 3 BP 223 EP 224 DI 10.1046/j.1440-1819.2001.00833.x PG 2 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 450QP UT WOS:000169754800024 PM 11422849 ER PT J AU Weidenheim, KM AF Weidenheim, KM TI Neurobiology of autism: An update SO SALUD MENTAL LA English DT Article DE autism; Asperger's syndrome; Rett disorder ID SEVERE MENTAL-RETARDATION; EARLY INFANTILE-AUTISM; CPG-BINDING PROTEIN-2; RETT-SYNDROME; CHILDHOOD AUTISM; POSTERIOR-FOSSA; CEREBELLAR ABNORMALITIES; MEDICAL CONDITIONS; CELL COUNTS; BRAIN AB Consideration of available studies suggest, that many cases of autism caused by a neurodevelopmental disorder. In other cases, a known disease entity is found, either during life or at autopsy. A common factor linking primary idiopathic autism with double syndrome cases having autistic behavior may be malfunction in specific neuroanatomic systems, defects in which give rise to the clinically defined autistic symptomatology. The available evidence suggests that the limbic system is abnormal in most cases of autism, and that the hippocampus, basal forebrain, cingulate and orbitofrontal cortices are specifically involved. Evidence for neocortical involvement is less strong; additional investigations will be necessary to define the role of neocortical pathology observed in some, but not all, individuals with autism. Similarly, the role of the thalamus and hypothalamus and their subdivisions needs to be better defined. The role of the cerebellum in the causation of autistic symptoms is controversial. However, the consistency of the findings; of the Boston group suggest that additional study, especially studies focused on the connections of the cerebellum to thc diencephalic and telencephalic structures, is warranted. The evidence, then, suggests that autism is a disorder of connectivity, often but not exclusively arising during the gestational period and ongoing degeneration of involved neural systems may occur in some individuals. Since different investigators, who study different populations Of autistic individuals, have found involvement of multiple neuroanatomic sites, neural network(s) may be involved in pathogenesis of this complex behavior. A defect at any point in the network could produce autistic behavior, and differences in the specific network defect between individuals might account for observed differences in clinical phenotype. The recent identification OF abnormalities in serotonin synthesis in autistic individuals suggests that serotonergic systems are likely involved (23). However, the complexity of the brain's circuitry, especially in the limbic system (56), and the presence Of multiple neurotransmitters in any given anatomic site in the brain, suggests that investigations of additional neurotransmitter systems might be useful as well. While autism is now accepted to be an intrinsic disorder of the brain, much additional work needs to be done to elucidate the precise biochemical and physiologic defects that lead to the observed pathologic changes, Application of basic neuroscience Methods to clinical material will hopefully elucidate the pathogenesis of this disorder anti lead to effective therapy. C1 Albert Einstein Coll Med, Dept Pathol & Neurol, Bronx, NY 10467 USA. Montefiore Med Ctr, Dept Pathol & Neurol, Bronx, NY 10467 USA. RP Weidenheim, KM (reprint author), Albert Einstein Coll Med, Dept Pathol & Neurol, Bronx, NY 10467 USA. 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PD JUN PY 2001 VL 24 IS 3 BP 3 EP 9 PG 7 WC Psychiatry SC Psychiatry GA 456FZ UT WOS:000170073600002 ER PT J AU Kohler, FW Anthony, LJ Steighner, SA Hoyson, M AF Kohler, FW Anthony, LJ Steighner, SA Hoyson, M TI Teaching social interaction skills in the integrated preschool: An examination of naturalistic tactics SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID AUTISTIC-CHILDREN; LANGUAGE; COMMUNICATION; INTERVENTION AB The purpose of this study was to increase the social interaction skills of four pre-school children with autism. Four teachers in integrated preschool classrooms participated. Experimental sessions occurred during daily 10-minute activities in which all children in the class were free to select from six to eight different activities. Prior to beginning the study, all four teachers were introduced to a variety of naturalistic teaching tactics designed to stimulate children's play and interaction with others. A multiple baseline design was employed to examine three different conditions. In base line, teachers used these tactics with no assistance from research staff. In a second phase, teachers received daily feedback and technical assistance. Assistance was provided on only one occasion and then withdrawn during a maintenance phase. Results indicated that all four children increased their social interactions during the technical assistance phase. Each boy exhibited his skills-in a range of different play activities, and two continued to display high levels of interaction during a maintenance phase. C1 Univ No Iowa, Dept Special Educ, Cedar Falls, IA 50614 USA. RP Kohler, FW (reprint author), Univ No Iowa, Dept Special Educ, 155 Schindler Educ Ctr, Cedar Falls, IA 50614 USA. CR ALPERT CL, 1992, J EARLY INTERVENTION, V16, P31 Bailey Jr D. 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PD SUM PY 2001 VL 21 IS 2 BP 93 EP + DI 10.1177/027112140102100203 PG 12 WC Education, Special SC Education & Educational Research GA 445NH UT WOS:000169463600003 ER PT J AU Heyes, C AF Heyes, C TI Causes and consequences of imitation SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID CHIMPANZEES PAN-TROGLODYTES; NEONATAL IMITATION; JOINT ATTENTION; JAPANESE-QUAIL; AUTISM; CHILDREN; BEHAVIOR; GESTURES; INFANTS; MODEL AB Recent behavioural and neuroscientific research concerning imitation has revealed evidence of experience-dependent imitation in chimpanzees and birds, wide ranging imitation deficits in autism, and unintentional imitation in adult humans. This review examines these findings and also evaluates evidence of neonatal imitation and intentional imitation in infancy, and evidence suggesting that the left inferior frontal gyrus is specialized for imitation. At the theoretical level, the empirical findings support the view that the perceptual-motor translation that is a unique and defining property of imitation depends primarily on direct links between sensory and motor representations established through correlated experience of observing movements and carrying them out. C1 UCL, Dept Psychol, London WC1E 6BT, England. RP Heyes, C (reprint author), UCL, Dept Psychol, Gower St, London WC1E 6BT, England. 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SCI. PD JUN PY 2001 VL 5 IS 6 BP 253 EP 261 DI 10.1016/S1364-6613(00)01661-2 PG 9 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 441FH UT WOS:000169220000011 ER PT J AU Kaye, JA Jick, H AF Kaye, JA Jick, H TI Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: a time-trend analysis SO WESTERN JOURNAL OF MEDICINE LA English DT Article AB Objectives To estimate changes in the risk of autism and assess the relation of autism to the mumps, measles, and rubella (MMR) vaccine. Design Time-trend analysis of data from the UK general practice research database. Setting General practices in the United Kingdom. Participants Children aged 12 years or younger diagnosed with autism between 1988 and 1999, with further analysis of boys aged 2 to 5 years born between 1988 and 1993. Main outcome measures Annual and age-specific incidence for first recorded diagnoses of autism (that is, when the diagnosis of autism was first recorded) in the children aged 12 years or younger; annual birth cohort-specific risk of autism diagnosed in the 2- to 5-year-old boys; and coverage (prevalence) of MMR vaccination in the same birth cohorts. Results The incidence of newly diagnosed autism increased 7-fold, from 0.3/10,000 person-years in 1988 to 2.1/10,000 person-years in 1993. The peak incidence was among 3- and 4-year-olds, and 83% (254/305) of cases were in boys. In an annual birth-cohort analysis of 114 boys born between 1988 and 1993, the risk of autism in 2- to 5-year-old boys increased nearly 4-fold over time, from 8/10,000 (95% confidence interval [CI], 4-14/10,000) for boys born in 1988 to 29/10,000 (95% CI, 20-43/10,000) for boys born in 1993. For the same annual birth cohorts, the prevalence of MMR vaccination was more than 95%. Conclusions Because the incidence of autism among 2- to 5-year-olds increased markedly among boys born in each year separately from 1988 to 1993 while MMR vaccine coverage was more than 95% for successive annual birth cohorts, the data provide evidence that no correlation exists between the prevalence of MMR vaccination and the rapid increase in the risk of autism over time. The explanation for the marked increase in risk of the diagnosis of autism in the past decade remains uncertain. C1 Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, Lexington, MA 02421 USA. RP Kaye, JA (reprint author), Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, 11 Muzzey St, Lexington, MA 02421 USA. RI Research Datalink, Clinical Practice/H-2477-2013 CR Jick H, 1997, LANCET, V350, P1045, DOI 10.1016/S0140-6736(05)70451-7 JICK H, 1995, BRIT J GEN PRACT, V45, P107 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 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 6 TC 2 Z9 2 PU B M J PUBLISHING INC PI SAN FRANCISCO PA 221 MAIN ST, PO BOX 7690, SAN FRANCISCO, CA 94120-7690 USA SN 0093-0415 J9 WESTERN J MED JI West. J. Med. PD JUN PY 2001 VL 174 IS 6 BP 387 EP 390 DI 10.1136/ewjm.174.6.387 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 438PM UT WOS:000169062300013 ER PT J AU Coghlan, A AF Coghlan, A TI Out of the shadows - We're finally beginning to uncover the roots of autism SO NEW SCIENTIST LA English DT News Item NR 0 TC 1 Z9 1 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 USA SN 0262-4079 J9 NEW SCI JI New Sci. PD MAY 26 PY 2001 VL 170 IS 2292 BP 14 EP 14 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 436QE UT WOS:000168945900012 PM 11885640 ER PT J AU Vastag, B AF Vastag, B TI Congressional autism hearings continue - No evidence MMR vaccine causes disorder SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT News Item CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 3 TC 8 Z9 10 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 MAY 23 PY 2001 VL 285 IS 20 BP 2567 EP 2569 DI 10.1001/jama.285.20.2567 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 433LY UT WOS:000168761900003 PM 11368715 ER PT J AU DeFrancesco, L AF DeFrancesco, L TI Autism on the rise SO SCIENTIST LA English DT Editorial Material CR BAILEY A, 1995, PSYCHOL MED, V25, P63 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X STROMLAND K, 1994, DEV MED CHILD NEUROL, V36, P351 2001, I MED 0423 NR 6 TC 2 Z9 2 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 USA SN 0890-3670 J9 SCIENTIST JI Scientist PD MAY 14 PY 2001 VL 15 IS 10 BP 16 EP + PG 0 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA 440BF UT WOS:000169152700013 ER PT J AU Feng, JN Yan, J Michaud, S Craddock, N Jones, IR Cook, EH Goldman, D Heston, LL Peltonen, L Delisi, LE Sommer, SS AF Feng, JN Yan, J Michaud, S Craddock, N Jones, IR Cook, EH Goldman, D Heston, LL Peltonen, L Delisi, LE Sommer, SS TI Scanning of estrogen receptor alpha (ER alpha) and thyroid hormone receptor alpha (TR alpha) genes in patients with psychiatric diseases: Four missense mutations identified in ER alpha gene SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE ER alpha; TR alpha; schizophrenia; psychiatric diseases; DOVAM-S; mutation detection ID DEFICIT HYPERACTIVITY DISORDER; BREAST-CANCER; GENERALIZED RESISTANCE; PUERPERAL PSYCHOSIS; DOVAM-S; SCHIZOPHRENIA; SEQUENCE; LINKAGE; WOMEN; ASSOCIATION AB Estrogen and thyroid hormones exert effects on growth, development, and differentiation of the nervous system. Hormone administration can lead to changes in behavior, suggesting that genetic variants of the estrogen receptor alpha (ER alpha) and the thyroid hormone receptor alpha (TR alpha) genes may predispose to psychiatric diseases. To investigate this possibility, regions of likely functional significance tall coding exons and flanking splice junctions) of the ERa and TR alpha. genes were scanned in patients with schizophrenia (113), along with pilot studies in patients with bipolar illness (BPI), puerperal psychosis, autism, attention-deficit hyperactivity disorder (ADHD), and alcoholism. A total of 1.18 megabases of the ER alpha. gene and 1.16 megabases of the TR alpha gene were scanned with Detection of Virtually All Mutations-SSCP (DOVAM-S), a method that detects virtually all mutations. Four missense mutations, seven silent mutations and one deletion were identified in the ER alpha gene, while only four silent mutations were present in the TRa gene. Two of the missense mutations in ER alpha. are conserved in the six available mammalian and bird species (H6Y, K299R) and a third sequence variant (P146Q) is conserved in mammals, birds, and Xenopus laevis, hinting that these sequence changes will be of functional significance. These changes were found in one patient each with BPI, puerperal psychosis, and alcoholism, respectively. Analysis of the ER alpha and TR alpha genes in 240 subjects reveals that missense changes and splice site variants are uncommon (1.7% and 0%, respectively). Further analyses are necessary to determine if the missense mutations identified in this study are associated with predisposition or outcome for either psychiatric or nonpsychiatric diseases. (C) 2001 Wiley-Liss, Inc. C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Univ Birmingham, Queen Elizabeth Hosp, Div Neurosci, Birmingham B15 2TH, W Midlands, England. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. 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PD MAY 8 PY 2001 VL 105 IS 4 BP 369 EP 374 DI 10.1002/ajmg.1364 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 439KN UT WOS:000169116200012 PM 11378852 ER PT J AU Yirmiya, N Pilowsky, T Nemanov, L Arbelle, S Feinsilver, T Fried, I Ebstein, RP AF Yirmiya, N Pilowsky, T Nemanov, L Arbelle, S Feinsilver, T Fried, I Ebstein, RP TI Evidence for an association with the serotonin transporter promoter region polymorphism and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; serotonin promoter region polymorphism; (5-HT-TLPR); catechol-O-methyl-transferase (COMT); dopamine D4 receptor (DRD4); association; linkage; polymorphism; transmission disequilibrium test ID OBSESSIVE-COMPULSIVE DISORDER; COMPLEX HUMAN-DISEASES; INFANTILE-AUTISM; LINKAGE DISEQUILIBRIUM; 1ST-DEGREE RELATIVES; DIAGNOSTIC INTERVIEW; GENE POLYMORPHISM; NOVELTY SEEKING; GENOMIC SCREEN; FAMILY HISTORY AB We have examined three functional polymorphisms, serotonin transporter promoter region polymorphism (5-HTTLPR), dopamine D4 exon III repeat region (DRD4), surd catechol-O-methyltransferase (COMT), in a small family-based design toward identifying candidate genes that confer risk for autism. A significant excess of the long/long 5-HTTLPR genotype was observed (likelihood ratio = 7.18; P = 0.027; 2 df; n = 33 families) as well as preferential transmission of the long allele of the 5-HTTLPR (TDT chi-square = 5.44; P < 0.025; 1 df). No association was observed between the COMT and DRD4 polymorphisms and autism in this sample. Some previous studies have observed linkage between autism and the 5-HTTLPR polymorphism and the current results are similar to those first reported by Klauck et al, [1997: Hum Genet 100:224-229; 1997: Hum Mol Genet 6:2233-2238]. Additionally, elevated serotonin levels have been consistently found in 30%-50% of autistic patients and may represent a marker for familial autism, Hyperserotonemia in autism appears to be due to enhanced 5-HT uptake, as free 5-HT levels are normal and the current report of an excess of the long/long 5-HTTLPR genotype in autism could provide a partial molecular explanation for high platelet serotonin content in autism. 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J. Med. Genet. PD MAY 8 PY 2001 VL 105 IS 4 BP 381 EP 386 DI 10.1002/ajmg.1365 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 439KN UT WOS:000169116200014 PM 11378854 ER PT J AU Marwick, C AF Marwick, C TI US report finds no link between MMR and autism SO BRITISH MEDICAL JOURNAL LA English DT News Item CR Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 1 TC 1 Z9 1 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 MAY 5 PY 2001 VL 322 IS 7294 BP 1083 EP 1083 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 431JP UT WOS:000168628300013 PM 11337432 ER PT J AU Young, E AF Young, E TI Head start - Could it be possible to diagnose and even treat autism in newborns? SO NEW SCIENTIST LA English DT News Item NR 0 TC 0 Z9 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 USA SN 0262-4079 J9 NEW SCI JI New Sci. PD MAY 5 PY 2001 VL 170 IS 2289 BP 16 EP 16 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 430AA UT WOS:000168549900014 ER PT J AU Roberts, JE Mirrett, P Burchinal, M AF Roberts, JE Mirrett, P Burchinal, M TI Receptive and expressive communication development of young males with fragile X syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID AUTISM RATING-SCALE; ADAPTIVE-BEHAVIOR; DOWN-SYNDROME; LANGUAGE CHARACTERISTICS; CHILDHOOD AUTISM; CHILDREN; TRAJECTORIES; ASSOCIATIONS; ADOLESCENTS; MULTICENTER AB We prospectively examined the developmental trajectories of receptive and expressive communication skills of 39 young males, 20 to 86 months of age, with fragile X syndrome. Eight showed features characteristic of autism. Children were tested one to three times using a standardized language test. They showed marked delays in language development, but substantial individual variability. Participants acquired expressive language skills more slowly than receptive language over time, gaining receptive language at about half the rate expected for typically developing children and expressive language at one third the rate. Both cognitive skills and autistic characteristics of the young males with fragile X syndrome related to receptive and expressive communication development, but neither predicted the discrepancies between expressive and receptive language acquisition over time. C1 Univ N Carolina, Chapel Hill, NC USA. RP Roberts, JE (reprint author), Univ N Carolina, Chapel Hill, NC USA. CR Abbeduto L, 1997, MENT RETARD DEV D R, V3, P313, DOI 10.1002/(SICI)1098-2779(1997)3:4<313::AID-MRDD6>3.0.CO;2-O Adamson L. 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J. Ment. Retard. PD MAY PY 2001 VL 106 IS 3 BP 216 EP 230 DI 10.1352/0895-8017(2001)106<0216:RAECDO>2.0.CO;2 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 435GC UT WOS:000168868200004 PM 11389664 ER PT J AU Nelson, KB Grether, JK Croen, LA Dambrosia, JM Dickens, BF Jelliffe, LL Hansen, RL Phillips, TM AF Nelson, KB Grether, JK Croen, LA Dambrosia, JM Dickens, BF Jelliffe, LL Hansen, RL Phillips, TM TI Neuropeptides and neurotrophins in neonatal blood of children with autism or mental retardation SO ANNALS OF NEUROLOGY LA English DT Article ID VASOACTIVE-INTESTINAL-PEPTIDE; LONG-TERM POTENTIATION; CULTURED MOUSE EMBRYOS; HIPPOCAMPAL-FORMATION; SPECTRUM DISORDERS; CORTICAL-NEURONS; POLYPEPTIDE VIP; RAT-BRAIN; GROWTH; BDNF AB There has been little exploration of major biologic regulators of cerebral development in autism. In archived neonatal blood of children with autistic spectrum disorders (n = 69), mental retardation without autism (n = 60), or cerebral palsy (CP, n = 63) and of control children (n = 54), we used recycling immunoaffinity chromatography to measure the neuropeptides substance P (SP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP), and the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4/5 (NT4/5), Neonatal concentrations of VIP, CGRP, BDNF, and NT4/5 were higher (ANOVA, all p values < 0.0001 by Scheffe test for pairwise differences) in children in the autistic spectrum and in those with mental retardation without autism than in control children. In 99% of children with autism and 97% with mental retardation, levels of at least one of these substances exceeded those of all control children. Concentrations were similar in subgroups of the autistic spectrum (core syndrome with or without mental retardation, other autistic spectrum disorders with or without mental retardation) and in the presence or absence of a history of regression. Among children with mental retardation, concentrations did not differ by severity or known cause (n = 11, including 4 with Down syndrome). Concentrations of measured substances were similar in children with CP as compared with control subjects. SP, PACAP, NGF, and NT3 were not different by diagnostic group. No measured analyte distinguished children with autism from children with mental retardation alone. In autism and in a heterogeneous group of disorders of cognitive function, overexpression of certain neuropeptides and neurotrophins was observed in peripheral blood drawn in the first days of life. C1 NINDS, NIH, Bethesda, MD 20892 USA. Calif Dept Hlth Serv, March Dimes Birth Defect Fdn, Calif Birth Defects Monitoring Program, Emeryville, CA USA. George Washington Univ, Sch Med, Washington, DC 20052 USA. Univ Calif Davis, Davis, CA 95616 USA. NIH, Off Res Serv, Bethesda, MD 20892 USA. RP Nelson, KB (reprint author), NINDS, NIH, Bldg 10,Room 5S221, Bethesda, MD 20892 USA. 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Neurol. PD MAY PY 2001 VL 49 IS 5 BP 597 EP 606 DI 10.1002/ana.1024 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 427YE UT WOS:000168433700008 PM 11357950 ER PT J AU Spears, R Tollefson, N Simpson, R AF Spears, R Tollefson, N Simpson, R TI Usefulness of different types of assessment data in diagnosing and planning for a student with high-functioning autism SO BEHAVIORAL DISORDERS LA English DT Article ID CHILDREN; DISORDERS AB The study examines urban and rural school psychologists' ability to use formal and informal assessment data to diagnose autism and to plan an effective educational program for a male elementary student with high-functioning autism. The study also presents findings related to school psychologists' perceptions of the utility of formal and informal assessment information. Respondents had difficulty recognizing autism and distinguishing it from other exceptionalities, although this finding was even more the case for rural than urban psychologists. Nevertheless, school psychologists were able to select appropriate individualized education program (IEP) goals for the described student and generally agreed with a panel of autism experts on placement decisions. Contrary to expectation, respondents did not favor informal assessment data over formal assessment data when selecting IEP goals. Training and future research implications are also discussed. C1 Shawnee Hts Sch Dist, Tecumsah, KS USA. Univ Kansas, Dept Psychol Res Educ, Lawrence, KS 66045 USA. RP Spears, R (reprint author), Shawnee Hts Sch Dist, Tecumsah, KS USA. 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PD MAY PY 2001 VL 77 IS 2 BP 216 EP 240 DI 10.1006/brln.2000.2429 PG 25 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA 421YX UT WOS:000168092100006 PM 11300705 ER PT J AU Scholl, BJ Leslie, AM AF Scholl, BJ Leslie, AM TI Minds, modules, and meta-analysis SO CHILD DEVELOPMENT LA English DT Article ID FALSE BELIEF; REPRESENTATION; 3-YEAR-OLD; DECEPTION; CHILDREN; AUTISM; TASK AB Wellman and colleagues' meta-analysis of performance on the false-belief task is methodologically useful, but it does not lead to any theoretical progress concerning the nature of the mechanisms that underlie the existence and development of "theory of mind." In particular, the results of this meta-analysis are perfectly compatible with "early competence" accounts that posit a specific, innate, and possibly modular basis for theory of mind. 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PD MAY-JUN PY 2001 VL 72 IS 3 BP 696 EP 701 DI 10.1111/1467-8624.00308 PG 6 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 438JA UT WOS:000169048800005 PM 11405575 ER PT J AU Beglinger, LB Smith, TH Fagan, J AF Beglinger, LB Smith, TH Fagan, J TI Information processing ability in children with autism receiving behavioral treatment SO CLINICAL NEUROPSYCHOLOGIST LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 0920-1637 J9 CLIN NEUROPSYCHOL JI Clin. Neuropsychol. PD MAY PY 2001 VL 15 IS 2 BP 254 EP 254 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 465AM UT WOS:000170565600014 ER PT J AU Saulnier, CA Fein, D Liss, M AF Saulnier, CA Fein, D Liss, M TI Sensory reactivity in typical children vs. children with autism SO CLINICAL NEUROPSYCHOLOGIST LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 0920-1637 J9 CLIN NEUROPSYCHOL JI Clin. Neuropsychol. PD MAY PY 2001 VL 15 IS 2 BP 258 EP 258 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 465AM UT WOS:000170565600034 ER PT J AU Johansson, M Wentz, E Fernell, E Stromland, K Miller, MT Gillberg, C AF Johansson, M Wentz, E Fernell, E Stromland, K Miller, MT Gillberg, C TI Autistic spectrum disorders in Mobius sequence: a comprehensive study of 25 individuals SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID BRAIN-STEM CALCIFICATION; MOEBIUS SYNDROME; CHILDHOOD PSYCHOSIS; INFANTILE-AUTISM; PREGNANCY; CHILDREN; MISOPROSTOL; POPULATION; BEHAVIOR AB The prevalence of autistic disorder was analysed in 25 individuals with Mobius sequence, a disorder with brain-stem dysfunction, The sample consisted of 18 males and seven females (20 participants were aged 2 to 22 years, and five were aged 1, 19 and 23 months, and 55 years old). Participants were recruited after a nationwide call and were part of a multidisciplinary study of individuals with Mobius sequence. They were given a meticulous neuropsychiatric examination including standardized autism diagnostic interviews. Ten individuals had an autistic spectrum disorder. Six of these met all diagnostic criteria for autism. In 23 individuals cognitive development could be assessed. Eight of those 23 patients had clear learning disability and six individuals were functioning in the normal but subaverage range. Autistic spectrum disorder and learning disability occurred in more than a third of the examined patients. Considering the hospital-based nature of the sample, these findings may be overestimates. Nevertheless, awareness of this coexistence is important in the diagnosis and habilitation care of children with Mobius sequence. Moreover, the results provide further support for the notion of a subgroup of autistic spectrum disorders being caused by first trimester brain-stem damage. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. Astrid Lindgren Childrens Hosp, Dept Pediat, Stockholm, Sweden. Sahlgrenska Univ Hosp, Dept Ophthalmol, Ostra, Sweden. Univ Illinois, Dept Ophthalmol & Visual Sci, Chicago, IL USA. RP Johansson, M (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgatan 12, SE-41119 Gothenburg, Sweden. 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Med. Child Neurol. PD MAY PY 2001 VL 43 IS 5 BP 338 EP 345 DI 10.1017/S0012162201000627 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 434EP UT WOS:000168802400008 PM 11368487 ER PT J AU Jones, RSP Zahl, A Huws, JC AF Jones, RSP Zahl, A Huws, JC TI First-hand accounts of emotional experiences in autism: a qualitative analysis SO DISABILITY & SOCIETY LA English DT Article ID CHILDREN AB Internet-based first-hand accounts of five people who describe themselves as 'high functioning autistic' were analysed using a thematic analytic approach. Four central themes were identified. These were a sense of alienation, a sense of frustration, depression as a central emotion, and a pervasive sense of fear or apprehension. The findings not only imply that emotional issues are important and relevant to people with autism, but there is an implication that the predominant experienced emotions are unpleasant ones. This is in contrast to much of the literature on autism that points to the absence or lack of emotion compared to non-autistic controls. Issues of generalisability to a wider population of people with autism are discussed. C1 Univ Wales, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. RP Jones, RSP (reprint author), Univ Wales, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. RI Huws, Jaci/C-3289-2009 CR American Psychological Association, 1997, SERV TEL TEL INT STA Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BEMPORAD JR, 1979, J AUTISM DEV DISORD, V9, P179, DOI 10.1007/BF01531533 CAPPS L, 1993, J CONSULT CLIN PSYCH, V61, P475, DOI 10.1037/0022-006X.61.3.475 CESARONI L, 1991, J AUTISM DEV DISORD, V21, P303, DOI 10.1007/BF02207327 Ghaziuddin M, 1998, J AUTISM DEV DISORD, V28, P111, DOI 10.1023/A:1026036514719 GRADIN T, 1992, HIGH FUNCTIONING IND GRANDIN T, 1986, EMERGENCE LABELLED A Hobson R. 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PD MAY PY 2001 VL 16 IS 3 BP 393 EP 401 PG 9 WC Rehabilitation; Social Sciences, Interdisciplinary SC Rehabilitation; Social Sciences - Other Topics GA 426VX UT WOS:000168370000004 ER PT J AU Rubin, S Biklen, D Kasa-Hendrickson, C Kluth, P Cardinal, DN Broderick, A AF Rubin, S Biklen, D Kasa-Hendrickson, C Kluth, P Cardinal, DN Broderick, A TI Independence, participation, and the meaning of intellectual ability SO DISABILITY & SOCIETY LA English DT Article AB This article presents a non-speaking person's perspectives on independence and the implications of newfound communication abilities for her participation in the world and upon the meaning of intellectual ability. The person with the communication disability also has autism and, early in her life, was classified by school officials as 'severely retarded'. The narrative focuses especially on the concepts of independence, participation, and intellectual competence or intellectual performance, and their relationship to the concepts of democracy, freedom, and identity, all from a non-essentialist perspective. In addition, the article addresses practical questions about how, from her perspective, the non-speaking person developed the ability to communicate without physical support. C1 Whittier Coll, Whittier, CA 90608 USA. Syracuse Univ, Syracuse, NY 13244 USA. Chapman Univ, Orange, CA 92866 USA. RP Biklen, D (reprint author), Whittier Coll, 13406 Philadelphia St, Whittier, CA 90608 USA. CR Appiah K. A., 1995, IDENTITIES Bernstein B., 1996, PEDAGOGY SYMBOLIC CO Beukelman D. R., 1998, AUGMENTATIVE ALTERNA BIKLEN D, 1999, SHARISA MY LIFE PION Biklen D., 1997, CONTESTED WORDS CONT BLACKMAN L, 1999, LUCYS STORY AUTISM O BOGDAN R, 1998, INTRO QUALITATIVE RE BORTHWICK C, 1999, PSYCHOLOQUY, V10 BROWN C, 1970, DOWN ALL DAYS CROSSLEY R, 1984, ANNIES COMING OUT CROSSLEY R, 1997, SPEECHLESS Crossley R., 1994, FACILITATED COMMUNIC Glaser B., 1967, DISCOVERY GROUNDED T Grandin T., 1986, EMERGENCE LABELED AU JACOBSON JW, 1995, AM PSYCHOL, V50, P750, DOI 10.1037//0003-066X.50.9.750 KOHLI W, 1998, LIGHT DARK TIMES MAX MARCUS E, 1997, CONTESTED WORDS CONT RUBIN S, 1997, ADDRESS CALIFONIA AU RUBIN S, 1999, EXPERIENCE AUTISM RUBIN S, 1998, KEYNOTE ADDRESS Smith P, 1999, REV EDUC RES, V69, P117, DOI 10.2307/1170672 Taylor S. J., 1999, In search of the promised land: The collected papers of Burton Blatt Taylor SJ, 1984, INTRO QUALITATIVE RE Thomson Rosemarie Garland, 1997, EXTRAORDINARY BODIES NR 24 TC 22 Z9 22 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0968-7599 J9 DISABIL SOC JI Disabil. Soc. PD MAY PY 2001 VL 16 IS 3 BP 415 EP 429 PG 15 WC Rehabilitation; Social Sciences, Interdisciplinary SC Rehabilitation; Social Sciences - Other Topics GA 426VX UT WOS:000168370000006 ER PT J AU Schonauer, K Klar, M Kehrer, HE Arlt, V AF Schonauer, K Klar, M Kehrer, HE Arlt, V TI Course of infantile-onset autism in adulthood: a survey of longitudinal follow-up-data SO FORTSCHRITTE DER NEUROLOGIE PSYCHIATRIE LA German DT Article ID RECEPTIVE LANGUAGE DISORDER; MENTAL-RETARDATION; ASPERGER-SYNDROME; DOWN-SYNDROME; CHILDREN; PROGNOSIS; ADOLESCENTS; POPULATION; PSYCHOSIS; PATTERNS AB The symptoms of infantile autism were first described almost 60 years ago. In contrast to its course in puberty and adolescence, follow-up-data on the late course in adulthood are decidedly sparse. As the outcome of research in the literature, we found 21 methodologically heterogeneous follow-up-studies, The arithmetic mean age of all subjects investigated was 24.0 years. The results are supplemented by various case reports and sporadic biographical reports by affected persons. On the basis of the available data, the discontinuous and dynamic changes of course verified in puberty and adolescence are not applicable to the third and fourth decades to the same extent. Gains in competence and autonomy appear to develop in the vocational rather than in the domestic sphere. The significantly more favorable courses of the form described by Asperger are continued in adulthood, The disorder-associated lack of empathy and social interaction is by no means experienced in terms of self-satisfaction by those concerned but rather as a loss. 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Psychiatr. PD MAY PY 2001 VL 69 IS 5 BP 221 EP + DI 10.1055/s-2001-13933 PG 15 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 436JJ UT WOS:000168932500005 PM 11417262 ER PT J AU Barnhill, GP AF Barnhill, GP TI What is Asperger syndrome? SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Article ID TOTAL POPULATION; AUTISM; CHILDREN; MIND AB The prevalence of Asperger Syndrome appears to be increasing, yet many individuals are still not being diagnosed during their school years. It is imperative to disseminate knowledge regarding the characteristics of Asperger Syndrome to parents and educational, mental health, and medical professionals so that this condition can be recognized early, and appropriate interventions can be provided to assist individuals with Asperger Syndrome in coping successfully. This article focuses on the characteristics of this developmental disability. C1 Univ Kansas, Med Ctr, Austism Asperger Syndrome Resource Ctr, Kansas City, KS 66160 USA. RP Barnhill, GP (reprint author), Univ Kansas, Med Ctr, Austism Asperger Syndrome Resource Ctr, 4001 HC Miller Bldg,3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th [Anonymous], 1992, INT STAT CLASS DIS R Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 Attwood T., 1998, ASPERGERS SYNDROME G Barnhill G., 2000, FOCUS AUTISM OTHER D, V15, P146, DOI [10.1177/108835760001500303, DOI 10.1177/108835760001500303] BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 CARRUTHERS A, 1989, Australia and New Zealand Journal of Developmental Disabilities, V15, P57 Church C., 2000, FOCUS AUTISM OTHER D, V15, P12, DOI DOI 10.1177/108835760001500102 Duke M. 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PD MAY PY 2001 VL 36 IS 5 BP 259 EP 265 DI 10.1177/105345120103600501 PG 9 WC Education, Special SC Education & Educational Research GA 425LX UT WOS:000168293000001 ER PT J AU Brownell, MT Walther-Thomas, C Shore, S AF Brownell, MT Walther-Thomas, C Shore, S TI Steven Shore: Understanding the autism spectrum - What teachers need to know SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Editorial Material CR Attwood T., 1998, ASPERGERS SYNDROME G KRANOWITZ C, 1998, OUT SYNC CHILD RECOG Shore S., 2001, WALL PERSONAL EXPERI SMITH B, 2000, ASPERGER SYNDROME SE NR 4 TC 2 Z9 2 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1053-4512 J9 INTERV SCH CLIN JI Interv. Sch. Clin. PD MAY PY 2001 VL 36 IS 5 BP 293 EP + DI 10.1177/105345120103600506 PG 8 WC Education, Special SC Education & Educational Research GA 425LX UT WOS:000168293000006 ER PT J AU Ormsbee, CK AF Ormsbee, CK TI Making visual supports work in the home and community: Strategies for individuals with autism and Asperger Syndrome SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Book Review C1 Univ Oklahoma, Dept Educ Psychol, Norman, OK 73019 USA. RP Ormsbee, CK (reprint author), Univ Oklahoma, Dept Educ Psychol, 820 Van Vleet Oval, Norman, OK 73019 USA. CR Savner J.L., 2000, MAKING VISUAL SUPPOR NR 1 TC 0 Z9 0 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1053-4512 J9 INTERV SCH CLIN JI Interv. Sch. Clin. PD MAY PY 2001 VL 36 IS 5 BP 314 EP 315 DI 10.1177/105345120103600511 PG 2 WC Education, Special SC Education & Educational Research GA 425LX UT WOS:000168293000013 ER PT J AU Van der Does, AJW AF Van der Does, AJW TI The effects of tryptophan depletion on mood and psychiatric symptoms SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Review DE tryptophan depiction; mood; psychiatric symptoms; depression; relapse; cognition ID SEASONAL AFFECTIVE-DISORDER; FREE DEPRESSED-PATIENTS; SEROTONIN REUPTAKE INHIBITORS; MAJOR AFFECTIVE-DISORDER; HEALTHY-HUMAN SUBJECTS; NEUTRAL AMINO-ACIDS; PLASMA TRYPTOPHAN; RAPID DEPLETION; ANTIDEPRESSANT ACTION; NORMAL VOLUNTEERS AB Background: The number of studies using tryptophan depletion (TD) challenge has increased markedly in the past few years. Recently, a number or negative results have been published, implicating that the effect of TD on mood may be less consistent than previously thought. Methods: The literature on the mood effects of TD in psychiatric patients and healthy volunteers was reviewed. Results: TD has a mood-lowering effect in subgroups of recovered depressed patients, patients with seasonal affective disorder and vulnerable healthy subjects. The mood effect in former patients is of a different quality, however, than the effect in healthy subjects. Some recent negative studies in depression might be explained by insufficient lowering of plasma tryptophan levels. Preliminary evidence exists for an effect of TD on bulimia nervosa, autism, aggression and substance dependence. Conclusions: The effects of TD on mood may be more consistent than suggested by a number of recent negative studies. Response to TD in recovered depressed patients is associated with prior treatment. However, even in SSRI-treated patients the relapse rates are not higher than 50-60%, which needs to be explained. The clinical usefulness of the response to TD in recovered patients (prediction of relapse after treatment discontinuation) and in symptomatic patients (prediction of treatment refactoriness) deserves more research attention. Further suggestions for future research include the cognitive effects of TD in recovered depressed patients and the effect of dietary habits on response to TD. (C) 2001 Elsevier Science B;V. All rights reserved. C1 Leiden Univ, Dept Psychol, NL-2333 AK Leiden, Netherlands. Leiden Univ, Dept Psychiat, NL-2333 AK Leiden, Netherlands. RP Van der Does, AJW (reprint author), Leiden Univ, Dept Psychol, Wassenaarseweg 52, NL-2333 AK Leiden, Netherlands. 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The possibility that individual differences may account for the failure to replicate Happe's (1996) findings is explored by presenting a battery of visuospatial tasks thought to measure weak central coherence (embedded figures, block design, Rey complex figure test). Participants with autism were distinguished by relatively good performance on visuospatial tasks, though there was no superiority effect in those with Asperger's syndrome. Performance on the visuospatial battery did not significantly predict susceptibility to illusions in various participant groups, including those with autism and Asperger's syndrome. This suggests that perception of illusions and performance on visuospatial tasks may rely on different mechanisms. The implications for the theory of weak central coherence are discussed. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Ropar, D (reprint author), Univ Nottingham, Sch Psychol, Univ Pk, Nottingham NG7 2RD, England. 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Child Psychol. Psychiatry Allied Discip. PD MAY PY 2001 VL 42 IS 4 BP 539 EP 549 DI 10.1111/1469-7610.00748 PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 436AB UT WOS:000168913400013 PM 11383970 ER PT J AU Gallagher, S AF Gallagher, S TI The practice of mind - Theory, simulation or primary interaction SO JOURNAL OF CONSCIOUSNESS STUDIES LA English DT Article ID FALSE BELIEF; GRASP REPRESENTATIONS; INTENTIONAL RELATIONS; MORAL SIGNIFICANCE; 2ND PERSON; CHILDREN; IMITATION; AUTISM; PERCEPTION; INFANTS AB Theory of mind explanations of how we know other minds are limited in several ways. First, they construe intersubjective relations too narrowly in terms of the specialized cognitive abilities of explaining and predicting another person's mental states and behaviours. Second, they sometimes draw conclusions about second-person interaction from experiments designed to test third-person observation of another's behaviour. As a result, the larger claims that are sometimes made for theory of mind, namely that theory of mind is our primary and pervasive means for understanding other persons, go beyond both the phenomenological and the scientific evidence. I argue that the interpretation of 'primary intersubjectivity' as merely precursory to theory of mind is inadequate. Rather; primary intersubjectivity, understood as a set of embodied practices and capabilities, is not only primary in a developmental sense, but is the primary way we continue to understand others in second-person interactions. C1 Canisius Coll, Dept Philosophy, Buffalo, NY 14208 USA. RP Gallagher, S (reprint author), Canisius Coll, Dept Philosophy, Buffalo, NY 14208 USA. 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PD MAY-JUL PY 2001 VL 8 IS 5-7 BP 83 EP 108 PG 26 WC Philosophy; Social Sciences, Interdisciplinary SC Philosophy; Social Sciences - Other Topics GA 450PX UT WOS:000169753300005 ER PT J AU McGeer, V AF McGeer, V TI Psyche-practice, psyche-theory and the contrastive case of autism - How practices of mind become second-nature SO JOURNAL OF CONSCIOUSNESS STUDIES LA English DT Article ID FALSE BELIEFS; CHILDREN; REPRESENTATION; IMITATION; GESTURES; DEAF C1 NYU, Dept Philosophy, New York, NY 10003 USA. RP McGeer, V (reprint author), NYU, Dept Philosophy, 503 Main Bldg,100 Washington Sq E, New York, NY 10003 USA. 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H., 1999, PRETENDING BE NORMAL WILLIAMS D, 1999, AUTISM SENSING UNLOS WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1978, J AUTISM CHILD SCHIZ, V8, P79, DOI 10.1007/BF01550280 ZAITCHIK D, 1990, COGNITION, V35, P41, DOI 10.1016/0010-0277(90)90036-J NR 77 TC 21 Z9 21 PU IMPRINT ACADEMIC PI THORVERTON PA PO BOX 1, THORVERTON EX5 5YX, ENGLAND SN 1355-8250 J9 J CONSCIOUSNESS STUD JI J. Conscious. Stud. PD MAY-JUL PY 2001 VL 8 IS 5-7 BP 109 EP 132 PG 24 WC Philosophy; Social Sciences, Interdisciplinary SC Philosophy; Social Sciences - Other Topics GA 450PX UT WOS:000169753300006 ER PT J AU Khare, L Strizheva, GD Bailey, JN Au, KS Northrup, H Smith, M Smalley, SL Henske, EP AF Khare, L Strizheva, GD Bailey, JN Au, KS Northrup, H Smith, M Smalley, SL Henske, EP TI A novel missense mutation in the GTPase activating protein homology region of TSC2 in two large families with tuberous sclerosis complex SO JOURNAL OF MEDICAL GENETICS LA English DT Letter ID AUTISM; IDENTIFICATION; PRODUCT C1 Fox Chase Canc Ctr, Dept Med Oncol, Philadelphia, PA 19111 USA. Russian State Med Univ, Dept Mol Biol, Moscow 117437, Russia. Univ Calif Los Angeles, Sch Med, Dept Psychiat, Los Angeles, CA USA. Univ Texas, Sch Med, Dept Pediat, Div Med Genet, Houston, TX USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. RP Henske, EP (reprint author), Fox Chase Canc Ctr, Dept Med Oncol, 7701 Burholme Ave, Philadelphia, PA 19111 USA. CR Au KS, 1998, AM J HUM GENET, V62, P286, DOI 10.1086/301705 Bjornsson J, 1996, AM J PATHOL, V149, P1201 NELLIST M, 1993, CELL, V75, P1305 Hunt A., 1999, TUBEROUS SCLEROSIS C, P47 Bailey A, 1998, HUM MOL GENET, V7, P571 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 SMALLEY SL, 1994, J MED GENET, V31, P761, DOI 10.1136/jmg.31.10.761 Smalley SL, 1997, AM J HUM GENET, V60, P1276, DOI 10.1086/515485 SMITH M, 1990, GENOMICS, V6, P105, DOI 10.1016/0888-7543(90)90454-3 vanSlegtenhorst M, 1997, SCIENCE, V277, P805 WIENECKE R, 1995, J BIOL CHEM, V270, P16409 Xiao GH, 1997, J BIOL CHEM, V272, P6097 NR 13 TC 22 Z9 22 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD MAY PY 2001 VL 38 IS 5 BP 347 EP 349 DI 10.1136/jmg.38.5.347 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 431KW UT WOS:000168631200017 PM 11403047 ER PT J AU Coniglio, SJ Lewis, JD Lang, C Burns, TG Subhani-Siddique, R Weintraub, A Schub, H Holden, EW AF Coniglio, SJ Lewis, JD Lang, C Burns, TG Subhani-Siddique, R Weintraub, A Schub, H Holden, EW TI A randomized, double-blind, placebo-controlled trial of single-dose intravenous secretin as treatment for children with autism SO JOURNAL OF PEDIATRICS LA English DT Article AB Objective: To determine whether a single injection of intravenous secretin results in measurable improvements in socialization and/or communication skills in children with autism. Study design: Sixty subjects with autism were randomly selected and assigned to either treatment or placebo group. Subjects in the treatment group received 2.0 clinical units of secretin per kilogram of body weight as a single intravenous dose. Subjects in the placebo group received normal saline solution. Neurodevelopmental and behavioral assessments were performed for all subjects before injection and at 3 and 6 weeks after injection. Results: Assessment of language skills and parents' behavioral assessments revealed no significant differences between the treatment and placebo groups. Raters' assessments of severity of autistic symptoms did not differ for the 2 groups at 6 weeks after injection. A marginal statistically significant Improvement in autistic behaviors was seen in the treatment group at 3 weeks after injection (P = .051). Conclusions: A single dose of intravenous secretin does not appear to have significant effects on either parents' perception of autistic behaviors or language skills at 6 weeks after injection. Transient, marginally significant improvements in autistic behaviors may occur in some children. C1 Emory Univ, Marcus Inst, Div Dev Pediat, Atlanta, GA 30324 USA. Childrens Ctr Digest Hlth Care, Atlanta, GA USA. Scottish Rite Child Neurobiol Associates, Childrens Healthcare Atlanta, Neuropsychol Dept, Atlanta, GA USA. Macro Int Inc, Atlanta, GA USA. RP Coniglio, SJ (reprint author), Emory Univ, Marcus Inst, Div Dev Pediat, 1605 Chantilly Dr,Ste 100, Atlanta, GA 30324 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN BABARCZY E, 1995, PHARMACOL BIOCHEM BE, V51, P469, DOI 10.1016/0091-3057(95)00009-L CHARLTON CG, 1983, PEPTIDES, V4, P739, DOI 10.1016/0196-9781(83)90029-3 Gilliam J. E., 1995, GILLIAM AUTISM RATIN Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 JACOBSON NS, 1991, J CONSULT CLIN PSYCH, V59, P12, DOI 10.1037//0022-006X.59.1.12 RIMLAND B, 1999, AUTISM RES REV INT, V13, P3 SANDLER A, 1999, NEW ENGL J MED, V34, P1801 Schopler E., 1998, CHILDHOOD AUTISM RAT ZIMMERMANN IL, 1992, PRESCHOOL LANGUAGE S NR 10 TC 44 Z9 44 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAY PY 2001 VL 138 IS 5 BP 649 EP 655 DI 10.1067/mpd.2001.112474 PG 7 WC Pediatrics SC Pediatrics GA 431LY UT WOS:000168633800009 PM 11343038 ER PT J AU Johnson, S AF Johnson, S TI Micronutrient accumulation and depletion in schizophrenia, epilepsy, autism and Parkinson's disease? SO MEDICAL HYPOTHESES LA English DT Article ID MONOAMINE-OXIDASE AB Zinc has several crucial functions in brain development and maintenance: it binds to p53, preventing it from binding to supercoiled DNA and ensuring that p53 cause the expression of several paramount genes, such as the one that encodes for the type I receptors to pituitary adenine cylase-activator peptide (PACAP), which directs embryonic development of the brain cortex, adrenal glands, etc.; it is required for the production of CuZnSOD and Zn-thionein, which are essential to prevent oxidative damage; it is required for many proteins, some of them with Zn fingers, many of them essential enzymes for growth and homeostasis. For example, the synthesis of serotonin involves Zn enzymes and since serotonin is necessary for melatonin synthesis, a Zn deficiency may result in low levels of both hormones. Unfortunately, Zn levels tend to be low when there is excess Cu and Cd. Moreover, high estrogen levels tend to cause increased absorption of Cu and Cd, and smoking and eating food contaminated with Cd result in high levels of the latter. Furthermore, ethanol ingestion increases the elimination of Zn and Mg (which acts as a cofactor for CuZnSOD). Increased Cu levels may also be found in people with Wilson's disease, which is a rather rare disease. However, the heterozygote form (only one faulty copy of the chromosome) is not so rare. Therefore, the developing fetus of a pregnant women who is low in Zn and high in Cu may experience major difficulties in the early development of the brain, which may later manifest themselves as schizophrenia, autism or epilepsy. Similarly, a person who gradually accumulates Cu, will tend to experience a gradual depletion of Zn, with a corresponding increase in oxidative damage, eventually leading to Parkinson's disease. Also discussed are the crucial roles of histidine, histamine, vitamin D, essential fatty acids, vitamin E, peroxynitrate, etc. in the possible oxidative damage involved in these mental diseases. (C) 2001 Harcourt Publishers Ltd. RP Johnson, S (reprint author), 3743 Thayer Rd, Moses Lake, WA 98837 USA. 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Hypotheses PD MAY PY 2001 VL 56 IS 5 BP 641 EP 645 DI 10.1054/mehy.2000.1302 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 459RD UT WOS:000170264000016 PM 11388783 ER PT J AU Knecht, T AF Knecht, T TI Pica as a harbinger of schizophrenia SO NERVENARZT LA German DT Article DE pica; schizophrenia; coprophagia ID DETOXIFICATION; GEOPHAGY; SYMPTOM; AUTISM AB The author reports the case of a youth who first became salient by self-neglect and finally was hospitalized for heavy drug abuse. In the closed ward, he suddenly displayed pica behavior but, in the further course,developed a typical schizophrenic syndrome. The diagnostic criteria are presented as well as all subtypes of pica. The author goes into the question of the aetiology of this enigmatic disorder. Finally, he points out the typical complications of pica and the therapeutical possibilities which are determined most of all by the underlying disease. C1 Kantonale Psychiat Klin, CH-8596 Munsterlingen, Switzerland. RP Knecht, T (reprint author), Kantonale Psychiat Klin, CH-8596 Munsterlingen, Switzerland. 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It affects approximately one in 15 000 females and is characterized by a loss of purposeful hand use, autism. ataxia and seizure. The disorder is usually sporadic, but rare familial cases have also been reported. Recently it has been shown that familial cases are an X-linked dominant disorder and the disease locus maps to Xq28. A candidate gene called methyl-CpG-binding protein 2 was identified from the Xq28 region and was shown to contain mutations in about 77% of Rett syndrome patients. Since the encoded protein was previously shown to be a global transcriptional repressor, undesired expression of yet unidentified genes that are normally repressed is considered to be pathogenic in Rett syndrome. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Oakland Univ, Dept Biol Sci, Rochester, MI 48309 USA. RP Shastry, BS (reprint author), Oakland Univ, Dept Biol Sci, Rochester, MI 48309 USA. 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Int. PD MAY PY 2001 VL 38 IS 6 BP 503 EP 508 DI 10.1016/S0197-0186(00)00118-2 PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 422KR UT WOS:000168117500003 PM 11248398 ER PT J AU Vorhees, CV Weisenburger, WP Minck, DR AF Vorhees, CV Weisenburger, WP Minck, DR TI Neurobehavioral teratogenic effects of thalidomide in rats SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE thalidomide; prenatal effects; rats; Sprague-Dawley rats; developmental neurotoxicity; Morris water maze; Cincinnati water maze ID COLLABORATIVE BEHAVIORAL TERATOLOGY; PRENATAL EXPOSURE; VALPROIC ACID; AUTISM; PHENYTOIN; HYPERPHENYLALANINEMIA; MALNUTRITION; INTEGRATION; PERIOD AB Thalidomide-induced embryopathy has been known for four decades, however, the drug has been reintroduced for human use in a number of countries, including the United States. In utero thalidomide exposure in humans is associated with central nervous system (CNS) effects in addition to the well-known limb, ear and other malformations. Despite knowledge of these CNS effects,, not a single experimental study could be found that examined thalidomide for possible developmental neurobehavioral effects. In the present experiment, gravid Sprague-Dawley rats were treated with either thalidomide (100 mg/kg by gavage) or vehicle (propylene glycol) on embryonic days E7-18 and allowed to deliver and raise their own offspring. The offspring were evaluated in a series of neurobehavioral tests (reflexes, locomotor activity, startle reactivity and learning in the Morris and Cincinnati water mazes). There was a small reduction in maternal weight among thalidomide-treated dams during midgestation. Thalidomide offspring showed increased preweaning mortality and male-specific, late onset reduction in growth that persisted until the end of the study. Male thalidomide offspring showed significant increases in errors and latency in the multiple-T Cincinnati water maze. Although rats are refractory to thalidomide-induced teratogenesis, the present results suggest that thalidomide selectively impairs offspring survival and growth and at least one type of learning among male offspring. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Childrens Hosp Res Fdn, Div Dev Biol, Cincinnati, OH 45229 USA. RP Vorhees, CV (reprint author), Childrens Hosp Res Fdn, Div Dev Biol, 3333 Burnet Ave, Cincinnati, OH 45229 USA. 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Teratol. PD MAY-JUN PY 2001 VL 23 IS 3 BP 255 EP 264 DI 10.1016/S0892-0362(01)00140-4 PG 10 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA 445NK UT WOS:000169463800004 PM 11418267 ER PT J AU Sandler, AD Brazdziunas, D Cooley, WC de Pijem, LC Hirsch, D Kastner, TA Kummer, ME Quint, RD Ruppert, ES AF Sandler, AD Brazdziunas, D Cooley, WC de Pijem, LC Hirsch, D Kastner, TA Kummer, ME Quint, RD Ruppert, ES CA Comm Children Diasabilities TI Technical report: The pediatrician's role in the diagnosis and management of autistic spectrum disorder in children SO PEDIATRICS LA English DT Review DE autism; autistic spectrum disorder; pervasive developmental disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; YOUNG-CHILDREN; FACILITATED COMMUNICATION; OBSERVATION SCHEDULE; MENTAL-RETARDATION; INFANTILE-AUTISM; CHILDHOOD AUTISM; PARENTS CONCERNS; INTRAVENOUS IMMUNOGLOBULIN AB Autism and its milder variants are not rare. Most pediatricians will have the opportunity to provide a medical home for a child with autism. This technical report serves to complement and expand on the information in the accompanying policy statement to increase the pediatrician's fund of knowledge and comfort level in caring for children with autism. In so doing, it is anticipated that earlier diagnosis and referral for appropriate intervention will be possible and that this will, in turn, have a positive effect on long-term outcomes for children with autism and their families. C1 Amer Acad Pediat, Comm Children Disabil, Elk Grove Village, IL 60007 USA. RP Sandler, AD (reprint author), Amer Acad Pediat, Comm Children Disabil, Elk Grove Village, IL 60007 USA. 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The goal of this policy statement is to help the pediatrician recognize the early symptoms of autism and participate in its diagnosis and management. This statement and the accompanying technical report will serve to familiarize the pediatrician with currently accepted criteria defining the spectrum of autism, strategies used in making a diagnosis, and conventional and alternative interventions. 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RP Kallen, RJ (reprint author), Pediat & Adolescent Med, Childrens Med Grp, Kenosha, WI 53142 USA. CR American Academy of Pediatrics, 1996, CLASS CHILD AD MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561 LANDAU WM, 1992, ARCH NEUROL-CHICAGO, V49, P353 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 NR 6 TC 4 Z9 4 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 MAY PY 2001 VL 107 IS 5 BP 1232 EP 1234 DI 10.1542/peds.107.5.1232 PG 3 WC Pediatrics SC Pediatrics GA 427NA UT WOS:000168411100070 PM 11388320 ER PT J AU Lewine, JD Davis, JT Funke, M Jones, G Chong, B Provencal, S Orrison, WW Andrews, RV Patil, AA Weisend, M Lee, RR AF Lewine, JD Davis, JT Funke, M Jones, G Chong, B Provencal, S Orrison, WW Andrews, RV Patil, AA Weisend, M Lee, RR TI A long letter and an even longer reply about autism magnetoencephalography and electroencephalography - Reply SO PEDIATRICS LA English DT Letter ID SURGICAL-TREATMENT; REGRESSION; CHILDREN; EPILEPSY C1 Univ Utah, Dept Radiol, Salt Lake City, UT 84132 USA. Ra Neurol, Omaha, NE USA. Univ Nebraska, Dept Neurosurg, Omaha, NE 68182 USA. Vet Adm Med Ctr, Neuroradiol Sect, Albuquerque, NM USA. RP Lewine, JD (reprint author), Univ Utah, Dept Radiol, Salt Lake City, UT 84132 USA. 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NYU Med Ctr, New York, NY USA. RP Kanner, AM (reprint author), Rush Presbyterian St Lukes Med Ctr, 1653 W Congress Pkwy, Chicago, IL 60612 USA. CR Nass R, 1999, PEDIATR NEUROL, V21, P464, DOI 10.1016/S0887-8994(99)00029-6 NR 1 TC 0 Z9 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 2001 VL 107 IS 5 BP 1236 EP 1236 PG 1 WC Pediatrics SC Pediatrics GA 427NA UT WOS:000168411100072 ER PT J AU Roberts, W Weaver, L Brian, J Bryson, S Emelianova, S Griffiths, AM MacKinnon, B Yim, C Wolpin, J Koren, G AF Roberts, W Weaver, L Brian, J Bryson, S Emelianova, S Griffiths, AM MacKinnon, B Yim, C Wolpin, J Koren, G TI Repeated doses of porcine secretin in the treatment of autism: A randomized, placebo-controlled trial SO PEDIATRICS LA English DT Article DE autism; secretin; language; behavior; cognitive functioning; gastrointestinal abnormalities ID DIAGNOSTIC INTERVIEW AB Background and Objectives. Anecdotal reports on the efficacy of secretin in autism raised great hopes for the treatment of children with this disorder. Initial single-dose, randomized, controlled trials failed to demonstrate any therapeutic effects of secretin. The present study is the first to test the outcome of repeated doses and to examine whether there is a subgroup of children who are more likely to achieve positive effects. Method. Sixty-four children with autism (ages 2-7 years; 55 boys and 9 girls) with a range of intelligence quotient and verbal ability were randomly assigned, in a double-blind manner, to secretin or placebo groups. Children received 2 doses of placebo or porcine secretin, 6 weeks apart. Assessments were performed at baseline and 3 weeks after each injection using several outcome measures. Results. There were no group differences on formal measures of language, cognition, or autistic symptomatology. Subgroupings based on cognitive level, the presence or absence of diarrhea, or a history of regression failed to show any significant therapeutic effects of secretin. Conclusion. No evidence is provided for the efficacy of repeated doses of porcine secretin in the treatment of children with autism. The possible relationship between relief of biological symptoms and enhanced skill performance is discussed. C1 Univ Toronto, Hosp Sick Children, Child Dev Ctr, Autism Res Unit, Toronto, ON M5G 1X8, Canada. Univ Toronto, Hosp Sick Children, Div Clin Pharmacol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Hosp Sick Children, Div Toxicol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Hosp Sick Children, Dept Paediat, Toronto, ON M5G 1X8, Canada. RP Roberts, W (reprint author), Univ Toronto, Hosp Sick Children, Child Dev Ctr, Autism Res Unit, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BRYSON SE, 1996, P ANN M NEUR TER SOC 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 BRYSON SE, 1998, P NAT I HLTH NAT I C Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 COHEN J, 1992, PSYCHOL BULL, V112, P155, DOI 10.1037/0033-2909.112.1.155 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Krug DA, 1993, AUTISM SCREENING INS LANDRY RJ, 1998, THESIS YORK U TORONT LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LEITER RG, 1948, INT PERFORMANCE SCAL Lord C., 1997, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lotter V., 1978, AUTISM REAPPRAISAL C, P475 OWLEY T, 1999, MEDGENMED 1006 Roid G. H., 1995, LEITER INT PERFORMAN ROMBOUGH V, 2000, THESIS YORK U TORONT Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Sattler JM, 1990, ASSESSMENT CHILDREN Sparrow S, 1984, VINELAND ADAPTIVE BE Wing L., 1987, HDB AUTISM PERVASIVE, P3 Zimmerman I.L., 1992, PRESCHOOL LANGUAGE S NR 22 TC 25 Z9 25 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 MAY PY 2001 VL 107 IS 5 BP art. no. EP e71 DI 10.1542/peds.107.5.e71 PG 5 WC Pediatrics SC Pediatrics GA 427NA UT WOS:000168411100008 PM 11331721 ER PT J AU Jenkins, SC AF Jenkins, SC TI Unraveling the mystery of autism and pervasive developmental disorder: A mother's story of research and recovery SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Associates 2000, Rochester, MN USA. RP Jenkins, SC (reprint author), Associates 2000, Rochester, MN USA. CR SEROUSSI K, 2000, UNRAVELING MYSTERY A NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD MAY PY 2001 VL 52 IS 5 BP 697 EP 698 DI 10.1176/appi.ps.52.5.697 PG 2 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 432GB UT WOS:000168682900037 ER PT J AU Maestro, S Muratori, F Barbieri, F Casella, C Cattaneo, V Cavallaro, MC Cesari, A Milone, A Rizzo, L Viglione, V Stern, DD Palacio-Espasa, F AF Maestro, S Muratori, F Barbieri, F Casella, C Cattaneo, V Cavallaro, MC Cesari, A Milone, A Rizzo, L Viglione, V Stern, DD Palacio-Espasa, F TI Early behavioral development in autistic children: The first 2 years of life through home movies SO PSYCHOPATHOLOGY LA English DT Article DE autism; home movies; infant psychiatry; theory of mind ID YOUNG-CHILDREN; MIND; 1ST AB Objective: The main aim of the research is to study the early behavioral development in autistic children through home movies. Methods: fifteen home movies, regarding the first 2 years of life of autistic children are compared with the home movies of 15 normal children. The films of the two groups were mixed and rated by blind ratings with the Grid for the Assessment of Normal Behavior in Infants and Toddlers. The grid is composed of 17 items grouped into three developmental areas: social competence, intersubjectivity and symbolic activity. For every area, we have identified specific children's behaviors. Results: Significant differences between the two groups are found both in the range of age 0-6 for intersubjectivity, and in the ranges of age 6-12 and 18-24 for symbolic activity. Conclusions: The authors pose some hypotheses about an early-appearing impairment of intersubjectivity, the ability to represent other's state of mind, in subjects with autistic disorder. Copyright (C) 2001 S. Karger AG, Basel. C1 IUPG, Geneva, Switzerland. NYU, Cornell Med Ctr, New York, NY USA. Univ Pisa, Div Child Neuropsychiat, Sci Inst Stella Maris, Pisa, Italy. RP Muratori, F (reprint author), IRCCS, Via Giacinti 2, I-56018 Pisa, Italy. CR ADRIEN JL, 1992, ACTA PAEDOPSYCHIATR, V55, P59 ADRIEN JL, 1987, J AUTISM DEV DISORD, V17, P407, DOI 10.1007/BF01487069 ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 ADRIEN JL, 1991, J AUTISM DEV DISORD, V21, P43, DOI 10.1007/BF02206996 Baron Cohen S, 1996, BRIT J PSYCHIAT, V168, P158 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BERNABEI P, 1997, PSICOL CLIN SVILUPPO, V1, P245 BRAZELTON TB, 1987, EFFECT INFANT ITS CA BRUNER J, 1983, FRONTIERS INFANT PSY Camaioni L, 1997, J AUTISM DEV DISORD, V27, P715, DOI 10.1023/A:1025858917000 Charman T, 1997, J CHILD PSYCHOL PSYC, V38, P725, DOI 10.1111/j.1469-7610.1997.tb01699.x COHEN SB, 1995, MINDBLINDNESS DAVIES S, 1994, J CHILD PSYCHOL PSYC, V35, P1033, DOI 10.1111/j.1469-7610.1994.tb01808.x Frith U., 1989, AUTISM EXPLAINING EN Hobson R. Peter, 1993, AUTISM DEV MIND Hollander E, 1998, CNS SPECTRUMS, V3, P22 Maestro S, 1999, PSYCHOPATHOLOGY, V32, P292, DOI 10.1159/000029102 MASSIE HN, 1975, J AM ACAD CHILD PSY, V14, P683, DOI 10.1016/S0002-7138(09)61466-7 MASSIE HN, 1978, AM J PSYCHIAT, V135, P1371 MASSIE HN, 1978, J AM ACAD CHILD PSY, V17, P29, DOI 10.1016/S0002-7138(09)62275-5 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 ROGERS SJ, 1989, J AM ACAD CHILD PSY, V28, P207, DOI 10.1097/00004583-198903000-00010 ROSENTHAL J, 1980, J AUTISM DEV DISORD, V10, P433, DOI 10.1007/BF02414819 SAUVAGE D, 1987, ANN PSYCHIAT, V2, P338 SAUVAGE D, 1984, AUTISME NOURISSON JE Schaffer H. R., 1984, CHILDS ENTRY SOCIAL Sigman M, 1998, J CHILD PSYCHOL PSYC, V39, P817 Stern D., 1985, INTERPERSONAL WORLD STERN DN, 1989, RELATIONSHIP DISTRUB THREVARTHEN C, 1998, INTERSUBJECTIVE COMM NR 34 TC 55 Z9 58 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD MAY-JUN PY 2001 VL 34 IS 3 BP 147 EP 152 DI 10.1159/000049298 PG 6 WC Psychiatry SC Psychiatry GA 430EQ UT WOS:000168561700007 PM 11316961 ER PT J AU Mudford, OC Martin, NT Eikeseth, S Bibby, P AF Mudford, OC Martin, NT Eikeseth, S Bibby, P TI Parent-managed behavioral treatment for preschool children with autism: some characteristics of UK programs SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article ID PROJECT; INTERVENTION; RECOVERY AB Early intensive behavioral intervention for autism has attracted controversy since Lovaas (1987) reported that 47% of his experimental group attained normal functioning. We summarize child and program data from 75 children receiving EIBI in the UK. The majority of children (57%) started treatment later than in Lovaas (1987), and 16% did not exceed his minimum IQ criterion. Children experienced fewer hours of treatment (mean of 32 hours vs. 40 hours per week), and their programs received relatively infrequent supervision. 21% of programs received supervision from individuals currently accredited as competent to provide Lovaas's treatment. No child started early enough, and received 40 hours per week, and had accredited supervision. Due to these variations from his model, Lovaas (1987) findings are unlikely to be replicated for this sample of children. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Univ Keele, Keele ST5 5BG, Staffs, England. RP Bibby, P (reprint author), Univ Keele, Keele ST5 5BG, Staffs, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DIAGN STAT MAN MENT BIBBY P, 1996, WORK CHILDR SEC PROV Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 EIKESETH S, 1999, PEACH C LOND FOXX RM, 1993, AM J MENT RETARD, V97, P375 Green G, 1996, BEHAV INTERVENTION Y, P29 Gresham FM, 1997, BEHAV DISORDERS, V22, P185 Lovaas O. I., 1996, BEHAV INTERVENTION Y, P241 Lovaas O. I., 1997, PREVENTION TREATMENT, P61 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lovaas O. I., 1988, ADV CLIN CHILD PSYCH, V11, P285 LOVAAS OI, 1978, AUTISM REAPPRAISAL C, P367 Maurice C., 1993, LET ME HEAR YOUR VOI MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 *PEACH, 1998, RESULTS TELEPHONE SU PERRY R, 1995, J AM ACAD CHILD PSY, V34, P232, DOI 10.1097/00004583-199502000-00019 SALLOWS GO, 1999, PEACH C LOND Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 Smith T, 1997, BEHAV DISORDERS, V22, P202 Smith T, 1998, INFANT YOUNG CHILD, V10, P67 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 Weisz JR, 1998, ADV CLIN CHILD PSYCH, V20, P49 World Health Organization, 1993, INT CLASS DIS REL HL NR 24 TC 36 Z9 36 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 MAY-JUN PY 2001 VL 22 IS 3 BP 173 EP 182 DI 10.1016/S0891-4222(01)00066-X PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 435GT UT WOS:000168869600001 PM 11380057 ER PT J AU Taubman, M Brierley, S Wishner, J Baker, D McEachin, J Leaf, RB AF Taubman, M Brierley, S Wishner, J Baker, D McEachin, J Leaf, RB TI The effectiveness of a group discrete trial instructional approach for preschoolers with developmental disabilities SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article ID BEHAVIORAL TREATMENT; AUTISM; CHILDREN; STUDENTS; COMMUNICATION; INTERVENTION; CLASSROOMS AB Group behavioral classroom instruction for children with developmental disabilities has been shown to allow for increased efficiency, approximation to naturalistic arrangements, and enhanced opportunity for interaction, social teaching and observational learning. This study examines the effectiveness of a group instructional extension of one to one discrete trial teaching, which involves the overlapping of trials between students along with the use of sequential and choral group teaching. A multiple baseline design across tasks was employed to examine the effectiveness of the group instructional approach in promoting acquisition of educational skills among preschoolers with autism and other developmental disabilities. A time sample interval assessment of components of the group instruction was also conducted. The approach was demonstrated to consistently increase correct responding across the task areas. Results are discussed in terms of the advantages of the group instructional approach as an adjunct to one to one discrete trial instruction. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Autism Partnership, Seal Beach, CA 90740 USA. RP Taubman, M (reprint author), Autism Partnership, 200 C Marina Dr, Seal Beach, CA 90740 USA. CR Alig-Cybriwsky C., 1990, J EARLY INTERVENTION, V14, P99 FARMER JA, 1991, EDUC TRAIN MENT RET, V26, P190 GOLDSTEIN H, 1991, RES DEV DISABIL, V12, P401, DOI 10.1016/0891-4222(91)90035-Q HALLENBECK BA, 1995, J SPEC EDUC, V29, P45 HANDLEMAN JS, 1983, BEHAV DISORDERS, V9, P22 HANDLEMAN JS, 1991, LANG SPEECH HEAR SER, V22, P107 Jahr E, 1998, RES DEV DISABIL, V19, P73, DOI 10.1016/S0891-4222(97)00030-9 KAMPS D, 1992, J AUTISM DEV DISORD, V22, P277, DOI 10.1007/BF01058156 Kamps D., 1990, ED TREATMENT CHILDRE, V13, P197 KAMPS DM, 1994, AM J MENT RETARD, V99, P60 KAMPS DM, 1991, FOCUS AUTISTIC BEHAV, V6, P1 KEEL MC, 1992, EXCEPT CHILDREN, V58, P357 KOEGEL RL, 1993, J APPL BEHAV ANAL, V26, P369, DOI 10.1901/jaba.1993.26-369 LEAF R, 1999, UNPUB BEHAV MANAGEME 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 OI, 1981, ANAL INTERVEN DEVEL, V1, P363 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 Polloway E. A., 1986, REM SPEC EDUC, V7, P22 QUILL K, 1989, J AUTISM DEV DISORD, V19, P625, DOI 10.1007/BF02212861 SCHOEN SF, 1995, J AUTISM DEV DISORD, V25, P503, DOI 10.1007/BF02178297 Shelton B. S., 1991, LANG SPEECH HEAR SER, V22, P123 SIGAFOOS J, 1994, J AUTISM DEV DISORD, V24, P259, DOI 10.1007/BF02172226 SIGMAN M, 1995, CANADIAN J PSYCHIAT, V30, P289 STAHMER AC, 1992, J APPL BEHAV ANAL, V25, P447, DOI 10.1901/jaba.1992.25-447 Werts MG, 1996, J APPL BEHAV ANAL, V29, P53, DOI 10.1901/jaba.1996.29-53 NR 29 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 MAY-JUN PY 2001 VL 22 IS 3 BP 205 EP 219 DI 10.1016/S0891-4222(01)00068-3 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 435GT UT WOS:000168869600003 PM 11380059 ER PT J AU Ashraf, H AF Ashraf, H TI LIS expert group rejects link between MMR and autism SO LANCET LA English DT News Item ID PERIPHERAL MONONUCLEAR-CELLS; CHILDREN CR Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 Kawashima H, 1996, ARCH VIROL, V141, P877, DOI 10.1007/BF01718162 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 3 TC 2 Z9 2 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD APR 28 PY 2001 VL 357 IS 9265 BP 1341 EP 1341 DI 10.1016/S0140-6736(00)04531-1 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 427ND UT WOS:000168411400018 PM 11343745 ER PT J AU Gillberg, C AF Gillberg, C TI Child neuropsychiatric perspectives contribute to understanding psychosocial disadvantage SO LAKARTIDNINGEN LA Swedish DT Article ID DEVELOPMENTAL COORDINATION DISORDER AB At least five per cent of the general population of children suffer from severe neuropsychiatric impairment. Autism spectrum disorders, ADHD/DAMP, Tourette's syndrome, and a variety of cognitive impairment/neurological syndromes with severe behavioral/emotional symptoms are included among the child neuropsychiatric disorders, the majority of which will lead to ongoing social and academic problems in adult life. Substantial numbers of those affected commit crimes in early adult life, and the incidence of the above-mentioned disorders is higher among young criminal offenders. Early diagnosis, educational, psychological, and, occasionally, medical therapies can affect outcome in a positive way. Child neuropsychiatric disorders should therefore be recognized at an early age so that attitudes can be changed from rejection to understanding, and a gloomy psychosocial outcome avoided. C1 Queen Silvia Childrens Hosp, Child Neuropsychiat Clin, SE-41119 Gothenburg, Sweden. Sahlgrens Univ Hosp, Gothenburg, Sweden. RP Gillberg, C (reprint author), Queen Silvia Childrens Hosp, Child Neuropsychiat Clin, Kungsgatan 12, SE-41119 Gothenburg, Sweden. CR Aronson M, 1997, DEV MED CHILD NEUROL, V39, P583 Barkley R. A., 1998, ATTENTION DEFICIT HY, V2nd COHEND J, 1997, HDB AUTISM PERVASIVE FRITH U, 1991, AUTISM ASPERGER SYND, P247 Giedd JN, 2000, AM J PSYCHIAT, V157, P281, DOI 10.1176/appi.ajp.157.2.281 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Gillberg C., 2000, BIOL AUTISTIC SYNDRO Harris J. C., 1995, DEV NEUROPSYCHIATRY Kadesjo B, 2000, J AM ACAD CHILD PSY, V39, P548, DOI 10.1097/00004583-200005000-00007 Kadesjo B, 1999, J AM ACAD CHILD PSY, V38, P820, DOI 10.1097/00004583-199907000-00011 Rasmussen P, 2000, J AM ACAD CHILD PSY, V39, P1424, DOI 10.1097/00004583-200011000-00017 Robertson MM, 2000, BRAIN, V123, P425, DOI 10.1093/brain/123.3.425 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P19 Whitaker AH, 1997, ARCH GEN PSYCHIAT, V54, P847 NR 14 TC 0 Z9 0 PU SVERIGES LAKARFORBUND PI STOCKHOLM PA POST BOX 5603, 114 86 STOCKHOLM, SWEDEN SN 0023-7205 J9 LAKARTIDNINGEN JI Lakartidningen PD APR 25 PY 2001 VL 98 IS 17 BP 2032 EP 2034 PG 3 GA 426CN UT WOS:000168332600003 PM 11374232 ER PT J AU Stoll, C AF Stoll, C TI Problems in the diagnosis of fragile X syndrome in young children are still present SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; mental retardation; X-linked mental retardation; Prader-Willi syndrome ID SOTOS SYNDROME; AUTISM AB Fragile X syndrome is common; its prevalence approaches 1 per 5,000, Fragile X syndrome is the most common inherited cause of mental retardation. Many professionals must deal with fragile X individuals on a daily basis. However, despite the diverse information on the epidemiology, clinical features, unique pattern of inheritance, cytogenetic, and molecular diagnosis and scales for the diagnosis of this syndrome, the diagnosis of fragile X syndrome is still not always made by the patients' specialists. Here we present the difficulties in the diagnosis of fragile X syndrome in 11 children under 8 years of age, 10 boys and one girl. We report data on initial symptoms, behavioral features, and physical and mental development before molecular studies were considered. The possible causes for the diagnosis delay were multiple: nonspecific features (e.g,, macrocephaly, overgrowth, obesity), unremarkable physical examination, family history apparently noncontributory, and lack of or delayed molecular testing, Careful clinical examination of young children and DNA screening in case of doubt, and education of professionals in medical specialty areas, behavioral sciences, education, and other fields are recommended. (C) 2001 Wiley-Liss,Inc. C1 Ctr Hosp Univ, Serv Genet Med, Strasbourg, France. RP Stoll, C (reprint author), Hop Hautepierre, Serv Genet Med, Ave Moliere, F-67098 Strasbourg, France. CR ALEMBIK Y, 1995, GENET COUNSEL, V6, P207 BEEMER FA, 1986, AM J MED GENET, V23, P221, DOI 10.1002/ajmg.1320230117 BROWN WT, 1986, AM J MED GENET, V23, P341, DOI 10.1002/ajmg.1320230126 Cassidy SB, 1997, J MED GENET, V34, P917, DOI 10.1136/jmg.34.11.917 COLE TRP, 1994, J MED GENET, V31, P20, DOI 10.1136/jmg.31.1.20 DEVRIES BBA, 1995, J MED GENET, V32, P764 FRYNS JP, 1984, CLIN GENET, V26, P497 FRYNS JP, 1987, CLIN GENET, V32, P388 Gillberg C., 1992, BIOL AUTISTIC SYNDRO Hagerman R. J, 1996, FRAGILE X SYNDROME D, P3 HAGERMAN RJ, 1991, AM J MED GENET, V38, P282 HULL C, 1993, AM J DIS CHILD, V147, P1236 Kivitie-Kallio S, 1999, CLIN GENET, V56, P41, DOI 10.1034/j.1399-0004.1999.560106.x SHERMAN S, 1991, FRAGILE X SYNDROME D, P69 STOLL C, 1990, MED HYG, V48, P479 Swillen A, 1996, AM J MED GENET, V67, P315, DOI 10.1002/(SICI)1096-8628(19960531)67:3<315::AID-AJMG9>3.0.CO;2-L Turner G, 1996, AM J MED GENET, V64, P196, DOI 10.1002/(SICI)1096-8628(19960712)64:1<196::AID-AJMG35>3.0.CO;2-G VERKERK AJMH, 1991, CELL, V65, P905, DOI 10.1016/0092-8674(91)90397-H NR 18 TC 11 Z9 12 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 APR 22 PY 2001 VL 100 IS 2 BP 110 EP 115 DI 10.1002/1096-8628(20010422)100:2<110::AID-AJMG1242>3.0.CO;2-I PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 417XZ UT WOS:000167861900005 PM 11298371 ER PT J AU Fatemi, SH Halt, AR Stary, JM Realmuto, GM Jalali-Mousavi, M AF Fatemi, SH Halt, AR Stary, JM Realmuto, GM Jalali-Mousavi, M TI Reduction in anti-apoptotic protein Bcl-2 in autistic cerebellum SO NEUROREPORT LA English DT Article; Proceedings Paper CT 39th Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC, 2000 CL SAN JUAN, PUERTO RICO SP Amer Coll Neuropsychopharmacol DE beta-actin; apoptosis; autism; bcl-2; cerebellum; neuron-specific beta-tubulin; schizophrenia; Western blotting ID EXPRESSION; BRAIN; MITOCHONDRIA; DISORDERS; DISEASE; FAMILY; CORTEX; DEATH; BAX AB Autism is a neurodevelopmental disorder with genetic and environmental etiologies. Neurohistologic findings have shown Purkinje cell depletion and atrophy in the cerebellum of autistic subjects. We hypothesized that apoptotic mechanisms might explain these Purkinje cell findings. Bcl-2 is a potent anti-apoptotic regulatory protein, which is reduced in schizophrenic brains. Autistic and normal control cerebellar cortices matched for age, sex and PMI were prepared for SDS-gel electrophoresis and Western blotting using specific anti-Bcl-2 antibodies. Quantification of Bcl-2 showed a significant 34-51% reduction in autistic cerebellum (mean (+/- s.d.) optical density/75 mug protein 0.290 +/- 0.08, n = 5) compared with controls (0.595 +/- 0.31, n = 8; p < 0.04); levels of neuronal-specific class III (-tubulin (controls 49.8 +/- 6.7; autistics 36.2 +/- 18.2), or (beta -actin (controls 7.3 +/- 12.7; autistics 6.77 +/- 0.66) in the same homogenates did not differ significantly between groups. These results indicate for the first time that autistic cerebellum may be vulnerable to pro-apoptotic stimuli and to neuronal atrophy as a consequence of decreased Bcl-2 levels. NeuroReport 12:929-933 (C) 2001 Lippincott Williams & Wilkins. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Box 392,Mayo Bldg,420 Delaware St SE, Minneapolis, MN 55455 USA. 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DBH alleles are defined by a polymorphic AC repeal and the presence/ absence (DBH+/DBH-) of a 19-bp sequence 118 bp downstream in the 5 ' flanking region of the gene. There was no increased concordance for DBH alleles in affected siblings, but the mothers had a higher frequency of alleles containing the 19-bp deletion (DBH-), compared to an ethnically similar Canadian comparison group (phi (2) = 4.20, df = 1, P = 0.02 for all multiplex mothers; (phi (2) = 4.71, df = 1, P < 0.02 for mothers with only affected sons). Although the odds ratios suggested only a moderate relevance for the DBH-allele as a risk allele, the attributable risk was high (42%), indicating that this allele is an important factor in determining the risk for having a child with autism. DBH genotypes also differed significantly among mothers and controls, with 37% of mothers with two affected sons having two alleles, compared to 19% of controls ((2) = 5.81, df = 2, P = 0.03). D betaH enzyme activity was lower in mothers of autistic children than in controls (mean was 23.20 +/- 15.35 iU/ liter for mothers vs. 33.14 +/- 21.39 iU/liter for controls; t = -1.749, df = 46, P = 0.044). The DBH-allele was associated with lower mean serum D betaH enzyme activity (nondeletion homozygotes: 41.02 +/- 24.34 iU/liter; heterozygotes: 32.07 +/- 18.10 iU/liter; and deletion homozygotes: 22.31 +/- 13.48 iU/liter; F = 5.217, df = 2, P = 0.007) ina pooled sample of mothers and controls. Taken together, these findings suggest that lowered maternal serum I)PH activity results in a suboptimal uterine environment (decreased norepinephrine relative to dopamine), which, in conjunction with genotypic susceptibility of the fetus, results in autism spectrum disorder in some families. (C) 2001 Wiley-Liss, Inc. C1 Ongwanada Rsource Ctr, Cytogenet & DNA Res Lab, Kingston, ON K7M 8A6, Canada. McMaster Univ, Dept Biol, Hamilton, ON L8S 4L8, Canada. Queens Univ, Dept Psychiat, Kingston, ON K7L 3N6, Canada. Univ Toronto, CAMH, Unit Genet Epidemiol, Toronto, ON, Canada. McMaster Univ, Dept Biochem, Hamilton, ON L8S 4L8, Canada. Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. RP Holden, JJA (reprint author), Ongwanada Rsource Ctr, Cytogenet & DNA Res Lab, 191 Portsmouth Ave, Kingston, ON K7M 8A6, Canada. 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J. Med. Genet. PD APR 15 PY 2001 VL 100 IS 1 BP 30 EP 36 DI 10.1002/ajmg.1187 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 415HU UT WOS:000167716100005 PM 11337745 ER PT J AU Rojas, DC Bawn, SD Benkers, TL Reite, ML Rogers, SJ AF Rojas, DC Bawn, SD Benkers, TL Reite, ML Rogers, SJ TI Absence of planum temporale asymmetry in adults with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. RI Rojas, Don/F-4296-2012 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2001 VL 49 IS 8 SU S MA 108 BP 31S EP 31S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 423ET UT WOS:000168163000107 ER PT J AU Silverman, JM Smith, CJ Schmeidler, J Hollander, E Lawlor, BA Fitzgerald, M Buxbaum, JD Delaney, K AF Silverman, JM Smith, CJ Schmeidler, J Hollander, E Lawlor, BA Fitzgerald, M Buxbaum, JD Delaney, K TI Symptom domains in autism and related conditions: Evidence for familiality SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. Vet Affairs Med Ctr, Psychiat Serv, Bronx, NY USA. St James Hosp, Dept Psychiat, Dublin 8, Ireland. St Patricks Hosp, Dublin, Ireland. Trinity Coll, Dept Psychiat, Dublin, Ireland. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2001 VL 49 IS 8 SU S MA 112 BP 32S EP 32S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 423ET UT WOS:000168163000110 ER PT J AU Wilcox, JA Tsuang, MT AF Wilcox, JA Tsuang, MT TI SPECT abnormalities in the developmental course of autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Texas Tech Univ, Ctr Hlth Sci, Dept Neuropsychiat, Div Psychiat, El Paso, TX 79905 USA. Harvard Univ, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2001 VL 49 IS 8 SU S MA 315 BP 91S EP 91S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 423ET UT WOS:000168163000310 ER PT J AU Wilcox, JA AF Wilcox, JA TI A novel chromosomal anomaly in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Texas Tech Univ, Hlth Sci Ctr, Dept Neuropsychiat, Div Psychiat, El Paso, TX 79905 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2001 VL 49 IS 8 SU S MA 562 BP 164S EP 164S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 423ET UT WOS:000168163000554 ER PT J AU Pierce, K Courchesne, E AF Pierce, K Courchesne, E TI Evidence for a cerebellar role in reduced exploration and stereotyped behavior in autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; cerebellum; exploration; stereotyped behavior; frontal lobes; repetitive behavior ID DEGENERATION MUTANT MICE; SPONTANEOUS-ALTERNATION; CHILDHOOD AUTISM; SOCIAL-BEHAVIOR; ATTENTION; PATTERNS; CHILDREN; DISCRIMINATION; INVOLVEMENT; ABNORMALITY AB Background: Although limited environmental exploration in autism is an obvious behavioral feature and may be a manifestation of "restricted interests" as described in DSM-IV criteria, there have been no behavioral or neurobiological studies of this important aspect of the disorder. Given consistent reports of cerebellar abnormality in autism, combined with animal research showing a relationship between exploration and the cerebellum, this study aimed to test the possible link between cerebellar abnormality and exploration in autism. Methods: The relationship between visuospatial exploration, stereotyped motor movements, and magnetic resonance imaging measures of the cerebellar vermis, whole brain volume, and frontal lobes in 14 autistic and 14 normal children was investigated. Children were exposed to a large room with several exploration containers and instructed to play. Exploration behavior was videotaped and scored for percentage of time engaged in exploration, number of containers explored, as well as stereotyped movements. Results: Children with autism spent significantly less rime in active exploration and explored fewer containers overall than normal children. Measures of decreased exploration were significantly correlated with the magnitude of cerebellar hypoplasia of vermal lobules VI-VII in the autistic children, but no relationship to vermis size was found with normal control children. Further measures of rates of stereotyped behavior were significantly negatively correlated with area measures of cerebellar vermis lobules VI-VII and positively correlated with frontal lobe volume in the autism sample. Conclusions: Reduced environmental exploration and repetitive behavior may have particularly important developmental consequences for children with autism be cause it may lead them to miss learning opportunities that fall outside their scope of interest. Our findings represent the first documented link between the restricted range of interests and stereotyped behaviors pathognomonic of autism and particular neuroanatomic sires. (C) 2001 Society of Biological Psychiatry. C1 Univ Calif, Dept Neurosci, Sch Med, La Jolla, CA 92037 USA. 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Psychiatry PD APR 15 PY 2001 VL 49 IS 8 BP 655 EP 664 DI 10.1016/S0006-3223(00)01008-8 PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 423BL UT WOS:000168155500001 PM 11313033 ER PT J AU Muller, RA Pierce, K Ambrose, JB Allen, G Courchesne, E AF Muller, RA Pierce, K Ambrose, JB Allen, G Courchesne, E TI Atypical patterns of cerebral motor activation in autism: A functional magnetic resonance study SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; motor; neuroimaging; fMRI; individual variability ID INFANTILE-AUTISM; ASPERGER-SYNDROME; BRAIN-STEM; MOVEMENT; PET; CEREBELLAR; CORTEX; MRI; ABNORMALITIES; CHILDREN AB Background: Early neurodevelopmental pathogenesis in autism potentially affects emerging functional maps, but little imaging evidence is available. Methods: We studied eight male autistic and eight marched normal subjects, using functional magnetic resonance imaging during visually paced finger movement, compared to a control condition (visual stimulation in the absence of motor response). Results: Groupwise analyses showed activation in contralateral perirolandic cortex, basal ganglia, and thalamus, bilateral supplementary motor area, and ipsilateral cerebellum for both groups. However, activations were less pronounced in the autism group. Direct group com parisons demonstrated greater activation in perirolandic and supplementary motor areas in the control group and greater activation (or reduced deactivation) in posterior and prefrontal cortices in the autism group, Intraindividual analyses further showed that strongest activations were consistently located along the contralateral central sulcus in control subjects bur occurred in locations differing from individual to individual in the autism group. Conclusions: Our findings, though based on a rather small sample, suggest abnormal individual variability of functional maps and less distinct regional activation/deactivation patterns in autism. The observations may relate to known motor impairments in autism and are compatible with the general hypothesis of disturbances of functional differentiation in the autistic cerebrum. (C) 2001 Society of Biological Psychiatry. C1 Childrens Hosp, Res Ctr, Lab Neurosci Autism, La Jolla, CA 92037 USA. Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92103 USA. Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. San Diego State Univ, Joint Doctoral Program Clin Psychol, San Diego, CA 92182 USA. RP Muller, RA (reprint author), Childrens Hosp, Res Ctr, Lab Neurosci Autism, 8110 Jolla Shores Dr 200, La Jolla, CA 92037 USA. 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The most significant susceptibility region in the first whole genome screen of multiplex families was on chromosome 7q, although this linkage was evident only in UK IMGSAC families. Subsequently all other genome screens of non-UK families have found some evidence of increased allele sharing in an overlapping 40 cM region of 7q. To further characterize this susceptibility locus, linkage analysis has now been completed on 170 multiplex IMGSAC families. Using a 5 cM marker grid, analysis of 125 sib pairs meeting stringent inclusion criteria resulted in a multipoint maximum LOD score (MLS) of 2.15 at F7S477, whereas analysis of all 153 sib pairs generated an MLS of 3.37. The 71 non-UK sib pairs now contribute to this linkage. Linkage disequilibrium mapping identified two regions of association-one lying under the peak of linkage, the other some 27 cM distal. These results are supported in part by findings in independent German and American singleton families. 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PD APR 4 PY 2001 VL 285 IS 13 BP 1749 EP 1757 DI 10.1001/jama.285.13.1749 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 415FR UT WOS:000167710600029 PM 11277830 ER PT J AU Petek, E Windpassinger, C Vincent, JB Cheung, J Boright, AP Scherer, SW Kroisel, PM Wagner, K AF Petek, E Windpassinger, C Vincent, JB Cheung, J Boright, AP Scherer, SW Kroisel, PM Wagner, K TI Disruption of a novel gene (IMMP2L) by a breakpoint in 7q31 associated with Tourette syndrome SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID TRANSLOCATION BREAKPOINT; IDENTIFICATION; SCHIZOPHRENIA; LOCALIZATION; EXPRESSION; DISORDERS; PROTEASE; LINKAGE; CLONING; AUTISM AB Gilles de la Tourette syndrome (GTS) is a complex neuropsychiatric disorder characterized by multiple motor and phonic tics. We identified a male patient with GTS and other anomalies. It was determined that he carried a de novo duplication of the long arm of chromosome 7 [46,XY,dup(7)(q22.1-q31.1)]. Further molecular analysis revealed that the duplication was inverted. The distal chromosomal breakpoint occurred between the two genetic markers D7S515 and D7S522, which define a region previously shown to be disrupted in a familiar case of GTS. Yeast and bacterial artificial chromosome clones spanning the breakpoints were identified by means of FISH analysis. To further characterize the distal breakpoint for a role in GTS, we performed Southern blot hybridization analysis and identified a 6.5-kb SacI junction fragment in the patient's genomic DNA. The DNA sequence of this fragment revealed two different breaks in 7q31 within a region of similar to 500 kb. IMMP2L, a novel gene coding for the apparent human homologue of the yeast mitochondrial inner membrane peptidase subunit 2, was found to be disrupted by both the breakpoint in the duplicated fragment and the insertion site in 7q31. The cDNA of the human IMMP2L gene was cloned, and analysis of the complete 1,522-bp transcript revealed that it encompassed six exons spanning 860 kb. The possible role of IMMP2L and several other candidate genes within the region of chromosomal rearrangement, including NRCAM, Leu-Rch Rep, and Reelin, is discussed. The 7q31 breakpoint interval has also been implicated in other neuropsychiatric diseases that demonstrate some clinical overlap with GTS, including autism and speech-language disorder. C1 Graz Univ, Inst Med Biol & Human Genet, A-8010 Graz, Austria. Univ Toronto, Hosp Sick Children, Dept Genet, Toronto, ON M5G 1X8, Canada. RP Petek, E (reprint author), Graz Univ, Inst Med Biol & Human Genet, Harrachgasse 21-8, A-8010 Graz, Austria. 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Psychiatr. N. Am. PD APR PY 2001 VL 10 IS 2 BP 333 EP + PG 20 WC Psychiatry SC Psychiatry GA 431RB UT WOS:000168643400010 PM 11351802 ER PT J AU Caviness, VS AF Caviness, VS TI Research strategies in autism: a story with two sides SO CURRENT OPINION IN NEUROLOGY LA English DT Editorial Material C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. RP Caviness, VS (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. CR Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Folstein SE, 1998, J AUTISM DEV DISORD, V28, P439, DOI 10.1023/A:1026008606672 Frith CD, 1999, SCIENCE, V286, P1692, DOI 10.1126/science.286.5445.1692 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 NR 5 TC 3 Z9 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1350-7540 J9 CURR OPIN NEUROL JI Curr. Opin. Neurol. PD APR PY 2001 VL 14 IS 2 BP 141 EP 143 DI 10.1097/00019052-200104000-00001 PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 430GA UT WOS:000168565100001 PM 11262726 ER PT J AU Nasr, JT Gabis, L Savatic, M Andriola, MR AF Nasr, John T. Gabis, Lidia Savatic, Mirjana Andriola, Mary R. TI The Electroencephalogram in Children with Developmental Dysphasia SO EPILEPSY & BEHAVIOR LA English DT Article DE autism; dysphasia; electroencephalogram; language AB Speech and language delay is a common developmental or acquired disorder. It can be a feature of the autistic spectrum, and if regression of language coincides with epilepsy, the diagnosis of Landau-Kleffner syndrome is considered. Slow acquisition of language without regression is called developmental dysphasia. A retrospective review of clinical and electroencephalographic (including video electroencephalographic) data on 138 children with speech/language delay, seen in a year's time, is presented. The electroencephalogram (EEG) was abnormal in 61% of children with a history of language regression. The EEG was abnormal in only 15% of children with developmental language disorder, most of whom also had clinical seizures. The difference between the two groups was highly significant (P = 0.004). Therefore obtaining an EEG in children with regression of language, especially if a history of clinical seizures is elicited, is indicated. (C) 2001 Academic Press C1 [Nasr, John T.; Gabis, Lidia; Savatic, Mirjana; Andriola, Mary R.] SUNY Stony Brook, Dept Neurol, Sch Med, Stony Brook, NY 11794 USA. RP Gabis, L (reprint author), SUNY Stony Brook, Dept Neurol, Sch Med, HSC T12-020, Stony Brook, NY 11794 USA. 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PD APR PY 2001 VL 2 IS 2 BP 115 EP 118 DI 10.1006/ebeh.2001.0159 PG 4 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA V21LE UT WOS:000208208300007 ER PT J AU Casavant, TL Braun, TA Kaliannan, S Scheetz, TE Munn, KJ Birkett, CL AF Casavant, TL Braun, TA Kaliannan, S Scheetz, TE Munn, KJ Birkett, CL TI A parallel/distributed architecture for hierarchically heterogeneous web-based cooperative applications SO FUTURE GENERATION COMPUTER SYSTEMS LA English DT Article DE distributed; GenoMap; genetic; linkage; socket server ID LINKAGE AB A new class of applications is described which requires cooperation among diverse users in multiple data and problem instance domains. The hierarchy of parallelism includes heterogeneity within a single instance of the problem, homogeneity among subsets of users within a problem domain, and multiple problem domains which share computational resources. The particular problem of genetic linkage analysis is used to illustrate and implement the architecture. GenoMap, the first implementation of this system is being deployed for several groups of cooperating users at multiple institutions in a study to isolate the,genomic locus of the controlling gene(s) in several diseases including autism. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Iowa, Dept Elect & Comp Engn, Parallel Proc Lab, Iowa City, IA 52242 USA. Univ Iowa, Genet Program, Iowa City, IA 52242 USA. RP Braun, TA (reprint author), Univ Iowa, Dept Elect & Comp Engn, Parallel Proc Lab, Iowa City, IA 52242 USA. CR CASAVANT TL, TRECE981213 U IOW CORNELL G, 1997, CORE JAVA COTTINGHAM RW, 1993, AM J HUM GENET, V53, P252 Galperin MY, 2000, NAT BIOTECHNOL, V18, P609, DOI 10.1038/76443 GUSELLA JF, 1983, NATURE, V306 LALONEL J, 1996, ANAL GENETIC LINKAGE, P111 OTT J, 1991, ANAL HUMAN GENETIC L, P108 Scheetz TE, 1998, PARALLEL COMPUT, V24, P1567, DOI 10.1016/S0167-8191(98)00072-6 TANENBAUM AS, 1996, MODERN OPERATING SYS, P181 1995, HUMAN GENOME NEWS, V7 NR 10 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-739X J9 FUTURE GENER COMP SY JI Futur. Gener. Comp. Syst. PD APR PY 2001 VL 17 IS 6 BP 783 EP 793 DI 10.1016/S0167-739X(00)00104-7 PG 11 WC Computer Science, Theory & Methods SC Computer Science GA 418TR UT WOS:000167907900013 ER PT J AU Anthony, A Waring, R Murch, SH Wakefield, AJ AF Anthony, A Waring, R Murch, SH Wakefield, AJ TI Glutamine and glutamate: Glutamine ratios in children with regressive autism and entero-colitis: Preliminary evidence for an entero-colonic encephalopathy? SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 Royal Free Hosp, Sch Med, London, England. UCL, Sch Med, London W1N 8AA, England. Univ Birmingham, Birmingham, W Midlands, England. NR 0 TC 3 Z9 3 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 2001 VL 120 IS 5 SU 1 MA 3907 BP A726 EP A726 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 429KA UT WOS:000168514703608 ER PT J AU Slager, SL Foroud, T Haghighi, F Spence, MA Hodge, SE AF Slager, SL Foroud, T Haghighi, F Spence, MA Hodge, SE TI Stoppage: An issue for segregation analysis SO GENETIC EPIDEMIOLOGY LA English DT Article DE sequential sampling; ascertainment models; segregation ratio; complex disease ID ASCERTAINMENT; AUTISM AB Segregation analysis assumes that the observed family-size distribution (FSD), i.e.. distribution of number of offspring among nuclear families, is independent of the segregation ratio p. However, for certain serious diseases with early onset and diagnosis (e.g., autism), parents may change their original desired family size, based on having one or more affected children, thus violating that assumption. Here we investigate "stoppage," the situation in which such parents have fewer children than originally planned. Following Brookfield et al. [J Med Genet 25:181-185, 1988], we define a stoppage probability d that after the birth of an affected child, parents will stop having children and thus not reach their original desired family size. We first derive the full correct likelihood for a simple segregation analysis as a function of p, d, and the ascertainment probability pi. We show that p can be estimated from this likelihood if the FSD is known. Then, we show that under "random" ascertainment, the presence of stoppage does not bias estimates of p. However, for other ascertanment schemes, we show that is not the case. We use a simulation study to assess the magnitude of bias, and we demonstrate that ignoring the effect of stoppage can seriously bias the estimates of p when the FSD is ignored. In conclusion, stoppage, a realistic scenario for some complex diseases, can represent a serious and potentially intractable problem for segregation analysis. (C) 2001 Wiley-Liss. Inc. C1 Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY USA. New York State Psychiat Inst, New York, NY 10032 USA. Indiana Univ, Sch Med, Dept Med & Mol Genet, Bloomington, IN 47405 USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. Columbia Univ, Joseph L Mailman Sch Publ Hlth, Dept Comp Sci, New York, NY USA. Columbia Univ, Joseph L Mailman Sch Publ Hlth, Columbia Genome Ctr, New York, NY USA. Columbia Univ, Joseph L Mailman Sch Publ Hlth, Div Biostat, New York, NY USA. RP Slager, SL (reprint author), Mayo Clin, Dept Hlth Sci Res, 200 1st St SW, Rochester, MN 55905 USA. RI Slager, Susan/B-6756-2009 CR BROOKFIELD JFY, 1988, J MED GENET, V25, P181, DOI 10.1136/jmg.25.3.181 CANNINGS C, 1977, CLIN GENET, V12, P208 Cavalli-Sforza L. L., 1971, GENETICS HUMAN POPUL Dahlberg G, 1930, HEREDITAS, V14, P73 EWENS WJ, 1986, THEOR POPUL BIOL, V30, P388, DOI 10.1016/0040-5809(86)90042-0 EWENS WJ, 1986, AM J HUM GENET, V38, P555 GREENBERG DA, 1986, AM J HUM GENET, V39, P329 HODGE SE, 1985, AM J HUM GENET, V37, P166 Hodge SE, 1996, GENETICS, V144, P1215 JONES MB, 1988, J AUTISM DEV DISORD, V18, P31, DOI 10.1007/BF02211816 JONES MB, 1957, PSYCHOL BULL, V54, P158 MORTON NE, 1959, AM J HUM GENET, V11, P1 RITVO ER, 1985, AM J PSYCHIAT, V142, P187 Weinberg W., 1928, Z INDUKTIVE ABSTAMMU, V48, P179 NR 14 TC 5 Z9 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PD APR PY 2001 VL 20 IS 3 BP 328 EP 339 DI 10.1002/gepi.4.abs PG 12 WC Genetics & Heredity; Public, Environmental & Occupational Health SC Genetics & Heredity; Public, Environmental & Occupational Health GA 417EB UT WOS:000167821500004 PM 11255242 ER PT J AU Fox, S AF Fox, S TI Continued doubts on link between MMR vaccine and autism SO INFECTIONS IN MEDICINE LA English DT News Item CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 NR 1 TC 0 Z9 0 PU SCP COMMUNICATIONS INC PI NEW YORK PA 134 W 29TH ST, NEW YORK, NY 10001-5304 USA SN 0749-6524 J9 INFECT MED JI Infect. Med. PD APR PY 2001 VL 18 IS 4 BP 182 EP 182 PG 1 WC Infectious Diseases SC Infectious Diseases GA 424ZM UT WOS:000168263900005 ER PT J AU Estrada, B AF Estrada, B TI MMR and autism: Suspect or superstition? SO INFECTIONS IN MEDICINE LA English DT Article DE autism; vaccines C1 Univ S Alabama, Div Pediat Infect Dis, Mobile, AL 36688 USA. RP Estrada, B (reprint author), Univ S Alabama, Div Pediat Infect Dis, Mobile, AL 36688 USA. NR 0 TC 0 Z9 0 PU SCP COMMUNICATIONS INC PI NEW YORK PA 134 W 29TH ST, NEW YORK, NY 10001-5304 USA SN 0749-6524 J9 INFECT MED JI Infect. Med. PD APR PY 2001 VL 18 IS 4 BP 183 EP 183 PG 1 WC Infectious Diseases SC Infectious Diseases GA 424ZM UT WOS:000168263900006 ER PT J AU Conti-Ramsden, G Betting, N Simkin, Z Knox, E AF Conti-Ramsden, G Betting, N Simkin, Z Knox, E TI Follow-up of children attending infant language units: outcomes at 11 years of age SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE children with SLI; follow-up; profiles ID IMPAIRMENT; MEMORY; SLI AB A large cohort of 242 children who had been attending infants language units at 7 years of age was followed up when the children were in their final year of primary school. Two hundred (83%) of the children were reassessed at 11 years of age on a wide battery of language and literacy measures, on a test of non-verbal ability, an autism checklist and a communication checklist. In total, 89% of children still scored <1 SD from the mean on at least one test of language and the majority (63%) scored poorly on three or more assessments demonstrating widespread difficulties. Compared with non-verbal abilities at 7 years of age, a large proportion of the cohort also performed poorly on performance IQ subtests (28%). A further 10 children scored highly on a checklist for autistic spectrum disorder. Thus, only 115 (58%) children could be said to meet criteria for specific language impairment. A small group of 16 children appeared to have entirely resolved their difficulties. These outcomes and their implications for education and long-term impact of the disorder are discussed. C1 Univ Manchester, Sch Educ, Manchester M13 9PL, Lancs, England. RP Conti-Ramsden, G (reprint author), Univ Manchester, Sch Educ, Oxford Rd, Manchester M13 9PL, Lancs, England. CR Adams AM, 2000, INT J LANG COMM DIS, V35, P95 *AM PSYCH ASS, 1994, DSM, V4 GATHERCOLE SE, 1990, J MEM LANG, V29, P336, DOI 10.1016/0749-596X(90)90004-J BEITCHMAN JH, 1994, J AM ACAD CHILD ADOL, V33, P1323 Beitchman JH, 1996, J AM ACAD CHILD PSY, V35, P804, DOI 10.1097/00004583-199606000-00021 Bishop D. V. M, 1982, TEST RECEPTION GRAMM Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 Bishop DVM, 1996, J CHILD PSYCHOL PSYC, V37, P391, DOI 10.1111/j.1469-7610.1996.tb01420.x Botting N, 2000, CHILD LANG TEACH THE, V16, P105, DOI 10.1191/026565900668565128 Conti-Ramsden G, 1999, INT J LANG COMM DIS, V34, P359 ContiRamsden G, 1997, J SPEECH LANG HEAR R, V40, P765 DUNN L, 1998, BRIT PICTURE VOCABUL, V2 Ellis Weismer S, 1999, J Speech Lang Hear Res, V42, P1249 Hohnen B, 1999, DEV PSYCHOL, V35, P590, DOI 10.1037/0012-1649.35.2.590 Johnson CJ, 1999, J SPEECH LANG HEAR R, V42, P744 Johnston J. R., 1994, SPECIFIC LANGUAGE IM, P107 Marchman VA, 1999, J SPEECH LANG HEAR R, V42, P206 RAVEN JC, 1986, COLOURED PROGR RICE ML, 1995, J SPEECH HEAR RES, V38, P850 Sattler JM, 1974, ASSESSMENT CHILDRENS SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Semel E., 1987, CLIN EVALUATION LANG SIMKIN Z, 2001, THESIS U MANCHESTER Stothard SE, 1998, J SPEECH LANG HEAR R, V41, P407 Tomblin JB, 1997, J SPEECH LANG HEAR R, V40, P1245 TOMBLIN JB, 1992, J SPEECH HEAR RES, V35, P832 Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D., 1993, WECHSLER OBJECTIVE R Williams K. T., 1997, EXPRESSIVE VOCABULAR NR 29 TC 78 Z9 80 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR-JUN PY 2001 VL 36 IS 2 BP 207 EP 219 DI 10.1080/13682820010019883 PG 13 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 427AA UT WOS:000168381500004 PM 11344595 ER PT J AU Dobson, S Upadhyaya, S McNeil, J Venkateswaran, S Gilderdale, D AF Dobson, S Upadhyaya, S McNeil, J Venkateswaran, S Gilderdale, D TI Developing an information pack for the Asian carers of people with autism spectrum disorders SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article; Proceedings Paper CT 3rd Conference of the Royal-College-of-Speech-and-Language-Therapists CY APR 17-19, 2001 CL BIRMINGHAM, ENGLAND SP Royal Coll Speech & Language Therapists AB An investigation is described which forms the basis for the development of an information package for the Asian carers of people with autism spectrum disorders (ASD) and learning disabilities. The results of semi-structured interviews and planning for questionnaires with three different linguistic Asian groups (Urdu, Gujarati and Bengali) are presented. The views, attitudes and awareness of autism, knowledge of support sen ices and perceived priority of needs are analysed for the three different communities. The investigation concludes with recommendations as to whether separate information is needed by each culture or whether a single information pack can be used and presented in each language format. The possible presentation format in which the information can be produced is also discussed. C1 Bradford Community NHS Trust, Listonshields Day Ctr, Bradford BD4 6DN, W Yorkshire, England. RP Dobson, S (reprint author), Bradford Community NHS Trust, Listonshields Day Ctr, Bierley Lane, Bradford BD4 6DN, W Yorkshire, England. CR CHUNG SY, 1990, J AUTISM DEV DISORD, V20, P221, DOI 10.1007/BF02284720 *DEP HLTH, 1998, MOV MAINSTR REP NAT *DEP HLTH, 1998, SIGN POSTS SUCC COMM Department of Health, 1998, 1 CLASS SERV QUAL NE HOLT G, 1997, MENTAL HLTH LEARNING KIERESUK T, 1968, COMMUNITY MENTAL HLT, V4, P443 WING L, 1999, AUT 99 C NOV NR 7 TC 2 Z9 2 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR PY 2001 VL 36 IS 2 SU S BP 216 EP 221 PG 6 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 430YX UT WOS:000168604000040 PM 11340785 ER PT J AU Forbes, J Welbon, H AF Forbes, J Welbon, H TI Teacher/therapist collaboration: A Scottish higher education institution development SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article; Proceedings Paper CT 3rd Conference of the Royal-College-of-Speech-and-Language-Therapists CY APR 17-19, 2001 CL BIRMINGHAM, ENGLAND SP Royal Coll Speech & Language Therapists AB The collaborative work is described of a principal speech and language therapist (SLT) and a lecturer in a college of education in Scotland in writing and evaluating a Post Graduate Award Scheme (PGAS) module. This was in response to Her Majesty's Inspectorate's (HMI) (1996) recommendation that teacher education institutions should 'consider the in-service and post-graduate training needs of those working with pupils with language and communication disorders and autism'. Official Scottish Executive Education Department (SEED) statements were examined by analysing HMI (1996) and subsequent official documents. Higher educational (HE) institution statements were read in the PGAS handbook and in the module descriptor (Northern College 1998). Accounts of change are described in the thinking and practice of course members as a result of the module and the implications for future module development are considered. C1 No Coll Educ, Sch Educ Studies, Aberdeen AB24 4FA, Scotland. RP Forbes, J (reprint author), No Coll Educ, Sch Educ Studies, Hilton Pl, Aberdeen AB24 4FA, Scotland. CR *NO COLL, 1998, POSTGR AW SCHEM HDB *NO COLL, 1999, COLL APPR EFF PROV P *ROYAL COLL SPEECH, 1996, COMM QUAL, V2 *SCOTT CONS COUNC, 1999, SUPP LEARN 3 *SCOTT ED DEP, 1991, NAT GUID *SCOTT EX ED DEP, 2000, IMPR SCH SPEC ED NEE *SCOTT OFF HLTH DE, 1997, DES CAR REV NAT HLTH Scottish Office Education and Industry Department, 1998, MAN GOOD PRACT SPEC 1996, ED PUPILS LANGUAGE C 1994, EFFECTIVE PROVISION NR 10 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR PY 2001 VL 36 IS 2 SU S BP 417 EP 422 PG 6 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 430YX UT WOS:000168604000075 PM 11340824 ER PT J AU Aldred, C Pollard, C Adams, C AF Aldred, C Pollard, C Adams, C TI Child'sTalk - For children with autism and pervasive developmental disorder SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article; Proceedings Paper CT 3rd Conference of the Royal-College-of-Speech-and-Language-Therapists CY APR 17-19, 2001 CL BIRMINGHAM, ENGLAND SP Royal Coll Speech & Language Therapists ID CONVERSATIONAL CHARACTERISTICS; PRAGMATIC DISORDER AB A research assessment protocol and early intervention approach designed for use by multi-disciplinary professionals with children who have the severe social communication deficits of early autism and pervasive developmental disorder (PDD) are described. The assessment analyses the specific pattern of social communication impairment in each child and defines the characteristics of the dyadic communication between parent and child. The intervention aims to identify facilitative strategies, using video feedback, which lead to close interpersonal interaction between the child and their parents. Parents can reflect on their own interaction and identify which strategies successfully engage their child. Child'sTalk aims to facilitate adaptations to the child's level of communication by sensitively and finely tuning the interaction and mutual sharing of intentions as a fundamental agent for the emergence of communication. C1 Royal Sch Deaf, Rycroft Assessment Ctr, Cheadle Hulme SK8 6RQ, Cheshire, England. Univ Manchester, Ctr Human Commun & Deafness, Manchester M13 9PL, Lancs, England. RP Aldred, C (reprint author), Royal Sch Deaf, Rycroft Assessment Ctr, Stanley Rd, Cheadle Hulme SK8 6RQ, Cheshire, England. CR Abidin RR, 1995, PARENTING STRESS IND ADAMS C, 1989, BRIT J DISORD COMMUN, V24, P211 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BISHOP DMV, 1993, J CHILD PSYCHOL PSYC, V30, P79 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P241 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 Fenson L, 1993, MACARTHUR COMMUNICAT Fey M. E., 1995, LANGUAGE INTERVENTIO FOMBONNE E, 1997, AUTISM DEV DISORDERS HORSBOROUGH K, 1985, P 2 NAT CHILD DEV C HOWLINP, 1998, AUTISM PERVASIVE DEV JOHNSON SL, 1979, CHILD CARE HLTH DEV, V6, P47 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lord C, 1994, CHILD ADOLESCENT PSY McCullouch K., 1996, BRIT ABILITY SCALES MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 PHILLIPS W, 1992, DEV PSYCHOPATHOL, V4, P375, DOI 10.1017/S0954579400000845 Sigman M., 1994, 9 INT C INF STUD PAR Sparrow S, 1984, VINELAND ADAPTIVE BE TAGERFLUSBERG H, 1993, UNDERSTANDING OTHERS TANNOCK R, 1992, CAUSES EFFECTS COMMU NR 22 TC 4 Z9 4 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR PY 2001 VL 36 IS 2 SU S BP 469 EP 474 PG 6 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 430YX UT WOS:000168604000084 PM 11340834 ER PT J AU Patterson, A Rafferty, A AF Patterson, A Rafferty, A TI Making it to work: Towards employment for the young adult with autism SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article; Proceedings Paper CT 3rd Conference of the Royal-College-of-Speech-and-Language-Therapists CY APR 17-19, 2001 CL BIRMINGHAM, ENGLAND SP Royal Coll Speech & Language Therapists AB In the last few decades there has been an increase in the reported prevalence of autism and its correlates within what is now termed autistic spectrum disorder (ASD): from 20 in every 10,000 children being estimated by Wing and Gould (1979) to 91 in every 10,000 by the National Autistic Society (NAS) (1999). While changes in criteria may account for some of this it is accepted that such children are increasingly being identified and knowledge of autism is growing. Semi-structured interviews were conducted with nine teaching staff from seven different schools for children with special needs to elicit information in relation to preparing young adults with ASD for the world of work. Results indicated educational practices are being modified for children with autism. Currently the most specifically tailored packages are offered in schools for children with severe learning difficulties. C1 Univ Ulster, Sch Psychol & Commun, Newtownabbey BT37 0QB, Antrim, North Ireland. RP Patterson, A (reprint author), Univ Ulster, Sch Psychol & Commun, Newtownabbey BT37 0QB, Antrim, North Ireland. CR Aarons M., 1992, HDB AUTISM GUIDE PAR Grandin T., 1995, TEACHING CHILDREN AU Howlin P., 1997, AUTISM PREPARING ADU JORDAN R, 1990, AUTISM PROFESSIONAL Jordan R. R., 1995, UNDERSTANDING TEACHI LAWSON W, 1999, REFLECTION AUTISM CO Luce SC, 1995, BEHAV DISORDERS, V21, P36 MESIBOV G, 1998, WHAT IS TEACCH *NAT AUT SOC, 1999, MAN PEOPL AUT SPECTR Peeters T, 1999, AUTISM MED ED ASPECT Siegel B., 1996, WORLD AUTISTIC CHILD TAYLOR G, 1990, AUTISM PROFESSIONAL WING L, 1992, HIGH FUNCTIONING IND WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 14 TC 2 Z9 2 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR PY 2001 VL 36 IS 2 SU S BP 475 EP 480 PG 6 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 430YX UT WOS:000168604000085 PM 11340835 ER PT J AU Takahashi, H Arai, S Tanaka-Taya, K Okabe, N AF Takahashi, H Arai, S Tanaka-Taya, K Okabe, N TI Autism and infection/immunization episodes in Japan SO JAPANESE JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID PREVALENCE; MEASLES; CHILDREN; MUMPS C1 Natl Inst Infect Dis, Infect Dis Surveillance Ctr, Shinjuku Ku, Tokyo 1628640, Japan. RP Takahashi, H (reprint author), Natl Inst Infect Dis, Infect Dis Surveillance Ctr, Shinjuku Ku, Toyama 1-23-1, Tokyo 1628640, Japan. EM hiroshit@nih.go.jp CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 HONDA H, 2000, J CLIN PSY MED, V29, P487 *JAP ASS BIOL MAN, 1998, DAT VACC PROD, P49 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 KIMURA M, 2000, MMR VACCINE, P177 Smeeth L, 2001, BMC PUBLIC HEALTH, V1, DOI 10.1186/1471-2458-1-2 SUGIYAMA T, 1989, J AUTISM DEV DISORD, V19, P87, DOI 10.1007/BF02212720 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 TANOUE Y, 1988, J AUTISM DEV DISORD, V18, P155, DOI 10.1007/BF02211943 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 12 TC 6 Z9 7 PU NATL INST INFECTIOUS DISEASES PI TOKYO PA JPN J INFECT DIS ED OFF NATL INST INFECTIOUS DISEASES TOYAMA 1-23-1, SHINJUKU-KU, TOKYO, 162-8640, JAPAN SN 1344-6304 EI 1884-2836 J9 JPN J INFECT DIS JI Jpn. J. Infect. Dis. PD APR PY 2001 VL 54 IS 2 BP 78 EP 79 PG 2 WC Infectious Diseases SC Infectious Diseases GA 447QA UT WOS:000169582900008 PM 11427748 ER PT J AU Travis, L Sigman, M Ruskin, E AF Travis, L Sigman, M Ruskin, E TI Links between social understanding and social behavior in verbally able children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE social understanding; social behavior; autism ID MENTAL-RETARDATION; EXECUTIVE FUNCTION; MIND ABILITIES; INDIVIDUALS; DEFICITS; ADULTS AB This study investigated the relations between various measures of social understanding and social interaction competence in verbally able children with autism. Measures of social understanding included measures of verbalizable knowledge (false belief understanding, affective perspective taking), as well as measures of more intuitive forms of social responsiveness (empathy, concern to distress, and initiating joint attention). Two measures of social interaction competence were employed: level of engagement with peers on the playground, and prosocial behavior in a structured laboratory task. For children with autism, initiating joint attention and empathy were strongly related to both measures of social interaction competence. No understanding-behavior links were identified for a language-age matched comparison sample of developmentally delayed children. Several accounts of these understanding-behavior links are considered, including the possibility that for children with autism, more impaired forms of understanding are more closely linked to behavior because they serve as limits on competence. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Travis, L (reprint author), Univ Calif Los Angeles, Dept Psychol, 1285 Franz Hall,405 Hilgard Ave, Los Angeles, CA 90095 USA. 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L., 1986, STANFORDBINET INTELL Yirmiya N, 1996, CHILD DEV, V67, P2045, DOI 10.1111/j.1467-8624.1996.tb01842.x Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x NR 29 TC 44 Z9 44 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 2001 VL 31 IS 2 BP 119 EP 130 DI 10.1023/A:1010705912731 PG 12 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100002 PM 11450811 ER PT J AU Robins, DL Fein, D Barton, ML Green, JA AF Robins, DL Fein, D Barton, ML Green, JA TI The Modified Checklist for Autism in Toddlers: An initial study investigating the early detection of autism and pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; modified checklist; toddlers ID EARLY RECOGNITION; INFANTILE-AUTISM; CHILDHOOD AUTISM; FOLLOW-UP; CHILDREN; INFANCY; INDIVIDUALS; POPULATION; DIAGNOSIS; BEHAVIOR AB Autism, a severe disorder of development, is difficult to detect in very young children. However, children who receive early intervention have improved long-term prognoses. The Modified Checklist for Autism in Toddlers (M-CHAT), consisting of 23 yes/no items, was used to screen 1,293 children. Of the 58 children given a diagnostic/developmental evaluation, 39 were diagnosed with a disorder on the autism spectrum. Six items pertaining to social relatedness and communication were found to have the best discriminability between children diagnosed with and without autism/PDD. Cutoff scores were created for the best items and the total checklist. Results indicate that the M-CHAT is a promising instrument for the early detection of autism. C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. RP Robins, DL (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd,U-1020, Storrs, CT 06269 USA. RI Robins, Diana/D-9959-2011 CR Adrien J. 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R., 1998, AUTISM PERVASIVE DEV VOSTANIS P, 1994, CHILD CARE HLTH DEV, V20, P165, DOI 10.1111/j.1365-2214.1994.tb00378.x Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 Wetherby A., 1988, FOCUS AUTISTIC BEHAV, V4, P1 Wetherby A., 1993, COMMUNICATION SYMBOL Wing L, 1988, DIAGNOSIS ASSESSMENT NR 47 TC 452 Z9 470 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 2001 VL 31 IS 2 BP 131 EP 144 DI 10.1023/A:1010738829569 PG 14 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100003 PM 11450812 ER PT J AU Charman, T Baron-Cohen, S Baird, G Cox, A Wheelwright, S Swettenham, J Drew, A AF Charman, T Baron-Cohen, S Baird, G Cox, A Wheelwright, S Swettenham, J Drew, A TI Commentary: The modified checklist for autism in toddlers SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID DISORDERS; CHAT; AGE C1 Univ London, Inst Child Hlth, Behav Sci Unit, London WC1N 1EH, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 1TN, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 1TN, England. Guys Kings Coll, Newcomen Ctr, London, England. Guys Kings Coll, Bloomfield Clin, London, England. St Thomas Hosp Med Sch, London, England. UCL, Dept Human Commun & Sci, London WC1E 6BT, England. RP Charman, T (reprint author), Univ London, Inst Child Hlth, Behav Sci Unit, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 BAIRD G, IN PRESS ARCH DIS CH BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P158, DOI DOI 10.1192/BJP.168.2.158 Baron-Cohen S, 2000, J ROY SOC MED, V93, P521 Charman T, 2000, UNDERSTANDING OTHER, P422 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Glascoe FP, 1999, AMBULATORY CHILD HLT, V5, P197 Glascoe FP, 1999, J PAEDIATR CHILD H, V35, P1, DOI 10.1046/j.1440-1754.1999.00342.x HALL DM, 1996, HLTH ALL CHILDREN RE Robins DL, 2001, J AUTISM DEV DISORD, V31, P131, DOI 10.1023/A:1010738829569 SIEGEL B, 1999, BIENN M SOC RES CHIL SIEGEL B, 1989, J AM ACAD CHILD PSY, V28, P542, DOI 10.1097/00004583-198907000-00013 STONE WL, 1997, UNPUB SCREENING TEST NR 14 TC 37 Z9 38 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 EI 1573-3432 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 145 EP 148 DI 10.1023/A:1010790813639 PG 4 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100004 PM 11450813 ER PT J AU Robins, DL Fein, D Barton, ML Green, JA AF Robins, DL Fein, D Barton, ML Green, JA TI Reply to Charman et al.'s commentary on the Modified Checklist for Autism in Toddlers SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID FOLLOW-UP C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. RP Robins, DL (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd,U-1020, Storrs, CT 06269 USA. RI Robins, Diana/D-9959-2011 CR Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Charman T, 2001, J AUTISM DEV DISORD, V31, P145, DOI 10.1023/A:1010790813639 GLASCOE FP, 1993, J DEV BEHAV PEDIATR, V14, P344 GLASCOE FP, 1991, CLIN PEDIATR, V30, P8, DOI 10.1177/000992289103000101 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x RAPIN I, 1996, CLIN DEV MED, V139, P98 NR 6 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 APR PY 2001 VL 31 IS 2 BP 149 EP 151 DI 10.1023/A:1010743030478 PG 3 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100005 ER PT J AU Magnusson, P Saemundsen, E AF Magnusson, P Saemundsen, E TI Prevalence of autism in Iceland SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; prevalence; epidemiology; Autism Diagnostic Interview-Revised; Childhood Autism Rating Scale ID PERVASIVE DEVELOPMENTAL DISORDERS; DSM-III-R; SPECTRUM DISORDERS; RETT-SYNDROME; PSYCHIATRIC-DISORDERS; DIAGNOSTIC INTERVIEW; MEDICAL DISORDERS; CHILDREN; ICD-10; CRITERIA AB This clinic-based study estimated the prevalence of autism in Iceland in two consecutive birth cohorts, subjects born in 1974-1983 and in 1984-1993. In the older cohort classification was based on the ICD-9 in 72% of cases while in the younger cohort 89% of cases were classified according to the ICD-10. Estimated prevalence rates for Infantile autism/Childhood autism were 3.8 per 10,000 in the older cohort and 8.6 per 10,000 in the younger cohort. The characteristics of the autistic groups are presented in terms of level of intelligence, male:female ratio, and age at diagnosis. For the younger cohort scores on the Autism Diagnostic Interview-Revised and the Childhood Autism Rating Scale are reported as well. Results are compared with a previous Icelandic study and recent population-based studies in other countries based on the ICD-10 classification system. Methodological issues are discussed as well as implications for future research and service delivery. C1 Natl Univ Hosp, Dept Chid & Adolescent Psychiat, Reykjavik, Iceland. State Diagnost & Counseling Ctr, Kopavogur, Iceland. RP Magnusson, P (reprint author), Dept Child & Adolescent Psychiat, Dalbraut 12, IS-105 Reykjavik, Iceland. 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Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 153 EP 163 DI 10.1023/A:1010795014548 PG 11 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100006 PM 11450814 ER PT J AU Bailey, DB Hatton, DD Skinner, M Mesibov, G AF Bailey, DB Hatton, DD Skinner, M Mesibov, G TI Autistic behavior, FMR1 protein, and developmental trajectories in young males with fragile X syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE FMR1 protein expression; fragile X; autistic behavior ID MENTAL-RETARDATION; GROWTH; EXPRESSION; CHILDREN AB In the context of a longitudinal study, we assessed the relationship between ratings of autistic behavior, FMR1 protein expression (FMRP), and the developmental trajectories of 55 young males with fragile X syndrome. Autistic behavior, as measured by the Childhood Autism Rating Scale, was not related to FMRP expression. However, autistic behavior was a significant predictor of both developmental status and developmental change. Boys with both autistic behavior and fragile X syndrome functioned at significantly lower levels of development and grew at significantly slower rates than those without autistic behavior. FMRP expression accounted for less variance in developmental level than did autistic behavior, and was not significantly related to slope (developmental change over time). No autistic behavior x FMRP interaction was found. C1 Univ N Carolina, Dept Psychiat, Div TEACCH, Frank Porter Graham Child Dev Ctr, Chapel Hill, NC 27599 USA. RP Bailey, DB (reprint author), Univ N Carolina, Dept Psychiat, Div TEACCH, Frank Porter Graham Child Dev Ctr, CB 8180, Chapel Hill, NC 27599 USA. 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PD APR PY 2001 VL 31 IS 2 BP 165 EP 174 PG 10 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100007 PM 11450815 ER PT J AU Belsito, KM Law, PA Kirk, KS Landa, RJ Zimmerman, AW AF Belsito, KM Law, PA Kirk, KS Landa, RJ Zimmerman, AW TI Lamotrigine therapy for autistic disorder: A randomized, double-blind, placebo-controlled trial SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; lamotrigine ID DIAGNOSTIC OBSERVATION SCHEDULE; CHILDHOOD; BEHAVIOR; EPILEPSY; BRAIN AB In autism, glutamate may be increased or its receptors up-regulated as part of an excitotoxic process that damages neural networks and subsequently contributes to behavioral and cognitive deficits seen in the disorder. This was a double-blind, placebo-controlled, parallel group study of lamotrigine, an agent that modulates glutamate release. Twenty-eight children (27 boys) ages 3 to 11 years (M = 5.8) with a primary diagnosis of autistic disorder received either placebo or lamotrigine twice daily. In children on lamotrigine, the drug was titrated upward over 8 weeks to reach a mean maintenance dose of 5.0 mg/kg per day. This dose was maintained for 4 weeks. Following maintenance evaluations, the drug was tapered down over 2 weeks. The trial ended with a 4-week drug-free period. Outcome measures included improvements in severity and behavioral features of autistic disorder (stereotypies, lethargy, irritability, hyperactivity, emotional reciprocity, sharing pleasures) and improvements in language and communication, socialization, and daily living skills noted after 12 weeks (the end of a 4-week maintenance phase). We did not find any significant differences in improvements between lamotrigine or placebo groups on the Autism Behavior Checklist, the Aberrant Behavior Checklist, the Vineland Adaptive Behavior scales, the PL-ADOS, or the CARS. Parent rating scales showed marked improvements, presumably due to expectations of benefits. C1 Kennedy Krieger Inst, Ctr Autism & Related Disorders, Baltimore, MD USA. Johns Hopkins Univ Hosp, Baltimore, MD 21205 USA. RP Belsito, KM (reprint author), Kennedy Krieger Inst, Ctr Autism & Related Disorders, Baltimore, MD USA. 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PD APR PY 2001 VL 31 IS 2 BP 175 EP 181 DI 10.1023/A:1010799115457 PG 7 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100008 PM 11450816 ER PT J AU Purcell, AE Rocco, MM Lenhart, JA Hyder, K Zimmerman, AW Pevsner, J AF Purcell, AE Rocco, MM Lenhart, JA Hyder, K Zimmerman, AW Pevsner, J TI Assessment of neural cell adhesion molecule (NCAM) in autistic serum and postmortem brain SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; neural cell adhesion molecule; brain ID SYNAPTIC PLASTICITY; IMMUNOGLOBULIN SUPERFAMILY; GENE-EXPRESSION; MODULATION; DOMAINS AB Studies have identified structural abnormalities in areas of the autistic brain, with a pattern suggesting that a neurodevelopmental anomaly took place. Neural cell adhesion molecule (NCAM), which is involved in development of the central nervous system, was previously shown to be decreased in the serum of autistic individuals. In the present study, we measured NCAM protein in the sera from controls, patients with autism, siblings of autistic patients, and individuals with other neurologic disorders, but found no significant differences. We also measured NCAM protein in autistic postmortem brain samples and found the longest isoform, NCAM-180, to be significantly decreased. In addition, we investigated the mRNA expression of NCAM in these brain samples using cDNA microarrays and RT-PCR. Results show that NCAM mRNA levels are not altered in autism. C1 Kennedy Krieger Inst, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. CLONTECH Labs Inc, Palo Alto, CA 94303 USA. RP Pevsner, J (reprint author), Kennedy Krieger Inst, Dept Neurol, 707 N Broadway, Baltimore, MD 21205 USA. 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Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 183 EP 194 DI 10.1023/A:1010751232295 PG 12 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100009 PM 11450817 ER PT J AU Swaim, KF Morgan, SB AF Swaim, KF Morgan, SB TI Children's attitudes and behavioral intentions toward a peer with autistic behaviors: Does a brief educational intervention have an effect? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; autistic disorder; attitudes; behavioral intentions ID HANDICAPPED PEERS; INCLUSION AB This study examined children's ratings of attitudes and behavioral intentions toward a peer presented with or without autistic behaviors. The impact of information about autism on these ratings was investigated as well as age and gender effects. Third- and sixth-grade children (N = 233) were randomly assigned to view a video of the same boy in one of three conditions: No Autism, Autism, or Autism/Information. Children at both grade levels showed less positive attitudes toward the child in the two autism conditions. In rating their own behavioral intentions, children showed no differences between conditions. However, in attributing intentions to their classmates, older children and girls gave lower ratings to the child in the autism conditions. Information about autism did not affect ratings of either attitudes or behavioral intentions as ascribed to self or others. C1 Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. RP Morgan, SB (reprint author), Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. CR AIELLO K, 1977, KIDS BLOCK PROGRAM A Bell SK, 2000, J PEDIATR PSYCHOL, V25, P137, DOI 10.1093/jpepsy/25.3.137 Edwards A. 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PD APR PY 2001 VL 31 IS 2 BP 195 EP 205 DI 10.1023/A:1010703316365 PG 11 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100010 PM 11450818 ER PT J AU Groden, J Diller, A Bausman, M Velicer, W Norman, G Cautela, J AF Groden, J Diller, A Bausman, M Velicer, W Norman, G Cautela, J TI The development of a stress survey schedule for persons with autism and other developmental disabilities SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; stress survey ID SAMPLE-SIZE; NUMBER; COMPONENTS AB The Stress Survey Schedule is an instrument for measuring stress in the lives of persons with autism and other developmental disabilities. Development of the survey and analysis of the underlying measurement structure of the instrument is reported in three studies. Through the use of exploratory and confirmatory analysis procedures, eight dimensions of stress were identified: Anticipation/Uncertainry, Changes and Threats, Unpleasant Events, Pleasant Events, Sensory/Personal Contact, Food Related Activity, Social/Environmental Interactions, and Ritual Related Stress. These stress dimensions are highly relevant to the problems of autism and have not been addressed by other stress surveys. The information obtained from the Stress Survey can be used to plan for strategies to reduce the stress before it occurs or results in maladaptive behavior. C1 Groden Ctr, Providence, RI 02906 USA. Univ Rhode Isl, Kingston, RI 02881 USA. Stanford Univ, Sch Med, Stanford Ctr Res Dis Prevent, Palo Alto, CA 94304 USA. Behav Therapy Inst, Sudbury, MA USA. RP Groden, J (reprint author), Groden Ctr, 86 Mt Hope Ave, Providence, RI 02906 USA. EM groden@grodencenter.org CR Bentler P.M., 1989, EQS STRUCTURAL EQUAT Bentler PM, 1990, PSYCHOL BULL, V107, P256 Bollen K. 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Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 207 EP 217 DI 10.1023/A:1010755300436 PG 11 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100011 PM 11450819 ER PT J AU Liss, M Harel, B Fein, D Allen, D Dunn, M Feinstein, C Morris, R Waterhouse, L Rapin, I AF Liss, M Harel, B Fein, D Allen, D Dunn, M Feinstein, C Morris, R Waterhouse, L Rapin, I TI Predictors and correlates of adaptive functioning in children with developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; adaptive functioning ID AUTISTIC-CHILDREN; DOWN-SYNDROME; BEHAVIOR; ADULTS AB Autism is a developmental disorder marked by impairments in socialization, communication, and perseverative behavior and is associated with cognitive impairment and deficits in adaptive functioning. Research has consistently demonstrated that children with autism have deficits in adaptive functioning more severe than their cognitive deficits. This study investigates the correlates and predictors of adaptive functioning as measured by the Vineland Adaptive Behavior Scales in high- and low-functioning children with autism and their age and nonverbal IQ matched controls. Thirty-five 9-year-old children with high-functioning autism (HAD) were compared with 31 age-matched children with developmental language disorder (DLD), and 40 9-year-old children with low-functioning autism (LAD) were compared with 17 age-matched children with low IQ on adaptive functioning, IQ, autistic symptomology, and tests of language and verbal memory. Results indicate that both groups with autism were significantly impaired compared to their matched controls on Socialization and Daily Living, but not Communication and that these impairments were more pronounced in the HAD group than in the LAD group. Adaptive behavior was strongly correlated with autistic symptomology only in the HAD group. Regression analyses indicated that IQ was strongly predictive of adaptive behavior in both low-functioning groups, but tests of language and verbal memory predicted adaptive behavior in the higher functioning groups. Results suggest that IQ may act as a limiting factor for lower functioning children but higher functioning children are impaired by specific deficits, including autistic symptomology and impaired language and verbal memory. C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. Albert Einstein Sch Med, Bronx, NY USA. Stanford Univ, Sch Med, Palo Alto, CA 94304 USA. Georgia State Univ, Atlanta, GA 30303 USA. Coll New Jersey, New Brunswick, NJ USA. RP Fein, D (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd U-1020, Storrs, CT 06269 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bacon AL, 1998, J AUTISM DEV DISORD, V28, P129, DOI 10.1023/A:1026040615628 Carpentieri S, 1996, J AUTISM DEV DISORD, V26, P611, DOI 10.1007/BF02172350 DELIS DC, 1987, CALIFORNIA VERBAL LE DISMONI F, 1978, TOKEN TEST CHILDREN Dunn L. M., 1981, PEABODY PICTURE VOCA FREEMAN BJ, 1991, J AM ACAD CHILD PSY, V30, P479, DOI 10.1097/00004583-199105000-00020 FREEMAN BJ, 1988, J AM ACAD CHILD PSY, V27, P428, DOI 10.1097/00004583-198807000-00008 GARDNER MF, 1983, EXPRESSIVE ONE WORD Hammill D., 1986, TEST WRITTEN SPELLIN Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hedrick D. L., 1984, SEQUENCED INVENTORY Hollingshead A. B., 1975, 4 FACTOR INDEX SOCIA Hresko W. 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Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 219 EP 230 DI 10.1023/A:1010707417274 PG 12 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100012 PM 11450820 ER PT J AU Steele, MM Al-Adeimi, M Siu, VM Fan, YS AF Steele, MM Al-Adeimi, M Siu, VM Fan, YS TI Brief report: A case of autism with interstitial deletion of chromosome 13 SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; chromosome 13 ID ABNORMALITIES; CHILDREN AB A case of an 18-year-old male who meets the DSM-IV criteria for autistic disorder and borderline intelligence is described. Cytogenetic evaluation revealed a karyotype of 46, XY, del (13)(q14q22). The relevance of this case to the etiology of autism is discussed. C1 Univ Western Ontario, London Hlth Sci Ctr, Dept Psychiat, Div Child Psychiat, London, ON N6A 4G5, Canada. Univ Aden, Genet Unit, Aden, Yemen. Univ Western Ontario, Dept Pediat, London, ON N6A 3K7, Canada. Univ Western Ontario, Dept Pathol, London, ON N6A 3K7, Canada. RP Steele, MM (reprint author), Univ Western Ontario, London Hlth Sci Ctr, Dept Psychiat, Div Child Psychiat, Victoria Campus,346 South St,Room 102D, London, ON N6A 4G5, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Assumpcao FB, 1998, J AUTISM DEV DISORD, V28, P253 BAILEY A, 1993, J CHILD PSYCHOL PSYC, V34, P673, DOI 10.1111/j.1469-7610.1993.tb01064.x 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 BRYSON SE, 1988, J CHILD PSYCHOL PSYC, V29, P433, DOI 10.1111/j.1469-7610.1988.tb00735.x Fattal-Valevski A, 1999, DEV MED CHILD NEUROL, V41, P21, DOI 10.1017/S0012162299000055 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 HOTOPF M, 1995, J AUTISM DEV DISORD, V25, P41, DOI 10.1007/BF02178166 Bailey A, 1998, HUM MOL GENET, V7, P571 Klauck SM, 1997, HUM GENET, V100, P224, DOI 10.1007/s004390050495 Lauritsen M, 1999, J CHILD PSYCHOL PSYC, V40, P335, DOI 10.1017/S0021963098003710 MARINER R, 1986, J AUTISM DEV DISORD, V16, P425, DOI 10.1007/BF01531709 RITVO ER, 1988, AM J PSYCHIAT, V145, P229 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P169, DOI 10.1017/S0021963098003461 STEFFENBURG S, 1991, DEV MED CHILD NEUROL, V33, P495 NR 16 TC 10 Z9 10 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 2001 VL 31 IS 2 BP 231 EP 234 DI 10.1023/A:1010759401344 PG 4 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100013 PM 11450821 ER PT J AU O'Neill, RE Sweetland-Baker, M AF O'Neill, RE Sweetland-Baker, M TI Brief report: An assessment of stimulus generalization and contingency effects in functional communication training with two students with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID BEHAVIOR; MAINTENANCE C1 Univ Utah, Salt Lake City, UT 84112 USA. RP O'Neill, RE (reprint author), Univ Utah, 1705 E Campus Ctr Dr,Room 221, Salt Lake City, UT 84112 USA. CR Carr E. G., 1994, COMMUNICATION BASED Durand V. M., 1990, SEVERE BEHAV PROBLEM DURAND VM, 1992, J APPL BEHAV ANAL, V25, P777, DOI 10.1901/jaba.1992.25-777 DURAND VM, 1991, J APPL BEHAV ANAL, V24, P251, DOI 10.1901/jaba.1991.24-251 Durant V. M., 1993, COMMUNICATIVE ALTERN, P317 Hagopian L. 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PD APR PY 2001 VL 31 IS 2 BP 235 EP 240 DI 10.1023/A:1010711518182 PG 6 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100014 PM 11450822 ER PT J AU Tolbert, L Brown, R Fowler, P Parsons, D AF Tolbert, L Brown, R Fowler, P Parsons, D TI Brief report: Lack of correlation between age of symptom onset and contemporaneous presentation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; age of symptom onset; contemporaneous presentation ID AUTISM; CHILDREN; RECOGNITION; SCALE AB The parents/guardians of 50 individuals were surveyed using a semistructured interview to determine the feasibility of this method and to establish ages of symptom onset. Thirty-eight informants were able to recall sufficient derail to allow categorization of the age of symptom onset. Chi-square analysis confirmed a significant association between investigators' categorization and informants' categorization. Contemporaneous presentation was indexed using Childhood Autism Rating Scale, the Autism Behavior Checklist, the Conners Hyperactivity Index, and the Ritvo-Freeman Real Life Rating Scale for Autism. No significant correlations were determined between any of these indices of symptom severity and age of symptom onset. C1 Univ Alabama, Birmingham, AL 35294 USA. Glenwood Inc, Birmingham, AL USA. RP Tolbert, L (reprint author), Univ Alabama, SC 1001,1530 3rd Ave S, Birmingham, AL 35294 USA. 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PD APR PY 2001 VL 31 IS 2 BP 247 EP 248 DI 10.1023/A:1010715619091 PG 2 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100016 PM 11450824 ER PT J AU Clark, CE AF Clark, CE TI Re: Secretin and autism: A two-part clinical investigation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter NR 0 TC 1 Z9 1 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 248 EP 249 DI 10.1023/A:1010767603161 PG 2 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100017 PM 11450825 ER PT J AU Fisch, GS AF Fisch, GS TI Adaptive behavior in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter C1 Yale Univ, Sch Med, New Haven, CT 06520 USA. RP Fisch, GS (reprint author), Yale Univ, Sch Med, New Haven, CT 06520 USA. CR FISCH GS, 2000, J AUTISM DEV DISORDE Freeman BJ, 1999, J AUTISM DEV DISORD, V29, P379, DOI 10.1023/A:1023078827457 SPARROW SS, 1984, VINELAND ADAPTIVE BE, P155 NR 3 TC 0 Z9 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 249 EP 249 DI 10.1023/A:1010719720000 PG 1 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100018 PM 11450826 ER PT J AU Freeman, BJ AF Freeman, BJ TI Adaptive behavior in children with autism - Reply from B. J. Freeman SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA. RP Freeman, BJ (reprint author), Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2001 VL 31 IS 2 BP 249 EP 250 DI 10.1023/A:1010771704070 PG 2 WC Psychology, Developmental SC Psychology GA 448BC UT WOS:000169606100019 ER PT J AU Ravizza, SM Ivry, RB AF Ravizza, SM Ivry, RB TI Comparison of the basal ganglia and cerebellum in shifting attention SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID FRONTAL-LOBE DAMAGE; PARKINSONS-DISEASE; COGNITIVE FUNCTION; INVOLVEMENT; ACTIVATION; MECHANISMS AB The basal ganglia anti cerebellum have traditionally been associated with motor performance. Recently, there has been considerable interest regarding the contributions of these subcortical structures to aspects of cognition. In particular, both the basal ganglia and cerebellum have been hypothesized to be involved in the control of attentional set. To date, no neuropsychological studies have directly compared the effects of basal ganglia and cerebellar dysfunction on the same attention shifting tasks. To this end, we employed an alternating attention task that has been used to demonstrate putative attentional control deficits in children with cerebellar pathology, either related to autism or neurological insult. When adult patients with either Parkinson's disease or cerebellar lesions were tested on this task, a similar pattern of deficits was observed for both groups. However, when the motor demands were reduced, cerebellar patients showed a significant improvement on the alternating attention task, whereas the Parkinson patients continued to exhibit an impairment. This dissociation suggests that attentional deficits: reported previously as being due to cerebellar dysfunction may be, at least in part, secondary to problems related to coordinating successive responses. In contrast, attention-shifting deficits associated with basal ganglia impairment cannot be explained by recourse to the motor demands of the task. C1 Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. RP Ravizza, SM (reprint author), Univ Calif Berkeley, Dept Psychol, 3210 Tolman Hall 1650, Berkeley, CA 94720 USA. 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PD APR 1 PY 2001 VL 13 IS 3 BP 285 EP 297 DI 10.1162/08989290151137340 PG 13 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 425DR UT WOS:000168273500001 PM 11371307 ER PT J AU Whitehead, C AF Whitehead, C TI Social mirrors and shared experiential worlds SO JOURNAL OF CONSCIOUSNESS STUDIES LA English DT Review ID INDIVIDUAL-DIFFERENCES; PRETEND PLAY; LANGUAGE; DISSOCIATION; HYPNOSIS; AUTISM; CORTEX AB We humans have a formidable armamentarium of social display behaviours, including song-and-dance, the visual arts, and role-play. Of these, role-play is probably the crucial adaptation which makes us most different from other apes. Human childhood, a sheltered period of 'extended irresponsibility', allows us to develop our powers of make-believe and role-play, prerequisites for human cooperation, culture, and reflective consciousness. 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PD APR PY 2001 VL 8 IS 4 BP 3 EP 36 PG 34 WC Philosophy; Social Sciences, Interdisciplinary SC Philosophy; Social Sciences - Other Topics GA 422DG UT WOS:000168102800001 ER PT J AU Procter, HG AF Procter, HG TI Personal construct psychology and autism SO JOURNAL OF CONSTRUCTIVIST PSYCHOLOGY LA English DT Article ID MIND; CHILDREN AB There has been no significant writing within personal construct psychology about autistic spectrum disorders, despite the fact that this approach provides promising models in a number of other specific areas of human difficulty. This article outlines a PCP model of autism, based on a wide variety of recent research findings and writings, including those of autism sufferers themselves. Autism is considered in the light of Kelly's fundamental postulate and 11 corollaries as well as Procter's (1978) group and family corollaries. 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Constr. Psychol. PD APR-JUN PY 2001 VL 14 IS 2 BP 107 EP 126 DI 10.1080/10720530125885 PG 20 WC Psychology, Clinical SC Psychology GA 416NM UT WOS:000167787100002 ER PT J AU Weimer, AK Schatz, AM Lincoln, A Ballantyne, AO Trauner, DA AF Weimer, AK Schatz, AM Lincoln, A Ballantyne, AO Trauner, DA TI "Motor" impairment in Asperger syndrome: Evidence for a deficit in proprioception SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE Asperger syndrome; proprioception ID HIGH-FUNCTIONING AUTISM; LEARNING-DISABILITIES; RIGHT-HEMISPHERE; CHILDREN; CLUMSINESS; APRAXIA AB Motor impairment has frequently been described in Asperger syndrome (AS), a pervasive developmental disorder included in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV). Previous research focusing on this motor dysfunction has yielded inconsistent results, and the "clumsiness" observed clinically remains poorly defined. To clarify further the issue of motor impairment, we compared a group of 10 children and young adults who met DSM-IV criteria for AS with a control group with no neurological impairment. Subjects were matched on age, sex, socioeconomic status, and Verbal IQ. A broad battery of motoric tests was administered. Subjects with AS were found to perform more poorly than controls on tests of apraxia, one-leg balance with eyes closed, tandem gait, and repetitive finger-thumb apposition. No significant differences were found on tests of finger tapping, grooved pegboard, trail making, or visual-motor integration. The pattern of impairments suggests that a proprioceptive deficit may underlie the incoordination observed in AS and that these individuals may be overreliant on visual input to maintain balance and position in space. C1 Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA. 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Dev. Behav. Pediatr. PD APR PY 2001 VL 22 IS 2 BP 92 EP 101 PG 10 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 420GB UT WOS:000167996300002 PM 11332785 ER PT J AU Stein, MT Dixon, S Cowan, C AF Stein, MT Dixon, S Cowan, C TI A two-year-old boy with language regression and unusual social interactions SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material DE language delay; developmental regression; autistic spectrum disorder; autism; pervasive developmental delay ID SPECTRUM DISORDERS; YOUNG-CHILDREN; AUTISM; DIAGNOSIS C1 Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. Behav Pediat Practice, Great Falls, MT USA. Univ Washington, Sch Med, Seattle, WA USA. RP Stein, MT (reprint author), Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. 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Dev. Behav. Pediatr. PD APR PY 2001 VL 22 IS 2 SU S BP S105 EP S110 PG 6 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 423NV UT WOS:000168183100021 PM 11332787 ER PT J AU Kjelgaard, MM Tager-Flusberg, H AF Kjelgaard, MM Tager-Flusberg, H TI An investigation of language impairment in autism: Implications for genetic subgroups SO LANGUAGE AND COGNITIVE PROCESSES LA English DT Article ID INFANTILE-AUTISM; FOLLOW-UP; CHILDREN; COMPREHENSION; COMMUNICATION; INDIVIDUALS; DISORDERS; PATTERNS; DEFICITS; PARENTS AB Autism involves primary impairments in both language and communication, yet in recent years the main focus of research has been on the communicative deficits that define the population. The study reported in this paper investigated language functioning in a group of 89 children diagnosed with autism using the ADI-R, and meeting DSM-IV criteria. The children, who were between 4 and 14 years old, were administered a battery of standardised language tests tapping phonological, lexical, and higher-order language abilities. The main findings were that among the children with autism there was significant heterogeneity in their language skills, although across all the children, articulation skills were spared. Different subgroups of children with autism were identified on the basis of their performance on the language measures. Some children with autism have normal language skills; for other children, their language skills are significantly below age expectations. The profile of performance across the standardised measures for the language-impaired children with autism was similar to the profile that defines the disorder specific language impairment (or SLI). The implications of this language impaired subgroup in autism for understanding the genetics and definition of both autism and SLI are discussed. C1 Eunice Kennedy Shriver Ctr Mental Retardat Inc, Ctr Res Dev Disorders, Waltham, MA 02454 USA. Univ Massachusetts, Sch Med, Waltham, MA USA. RP Tager-Flusberg, H (reprint author), Eunice Kennedy Shriver Ctr Mental Retardat Inc, Ctr Res Dev Disorders, 200 Trapelo Rd, Waltham, MA 02454 USA. 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PD APR PY 2001 VL 16 IS 2-3 BP 287 EP 308 PG 22 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 432TM UT WOS:000168711800007 ER PT J AU Bernard, S Enayati, A Redwood, L Roger, H Binstock, T AF Bernard, S Enayati, A Redwood, L Roger, H Binstock, T TI Autism: a novel form of mercury poisoning SO MEDICAL HYPOTHESES LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; COMMON VARIABLE IMMUNODEFICIENCY; METHYL MERCURY; T-CELLS; RAT-BRAIN; METHYLMERCURY EXPOSURE; INDUCED AUTOIMMUNITY; CHILDREN; ABNORMALITIES; LYMPHOCYTES AB Autism is a syndrome characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recent epidemiological studies suggest that autism may affect 1 in 150 US children. Exposure to mercury can cause immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with autism, and the similarities extend to neuroanatomy, neurotransmitters, and biochemistry. Thimerosal, a preservative added to many vaccines, has become a major source of mercury in children who, within their first two years, may have received a quantity of mercury that exceeds safety guidelines. A review of medical literature and US government data suggests that: (i) many cases of idiopathic autism are induced by early mercury exposure from thimerosal; (ii) this type of autism represents an unrecognized mercurial syndrome; and (iii) genetic and non-genetic factors establish a predisposition whereby thimerosal's adverse effects occur only in some children. (C) 2001 Harcourt Publishers Ltd. C1 ARC Res, Cranford, NJ 07901 USA. RP Bernard, S (reprint author), ARC Res, 14 Commerce Dr, Cranford, NJ 07901 USA. 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Hypotheses PD APR PY 2001 VL 56 IS 4 BP 462 EP 471 DI 10.1054/mehy.2000.1281 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 428LF UT WOS:000168462600010 PM 11339848 ER PT J AU Binstock, T AF Binstock, T TI Intra-monocyte pathogens delineate autism subgroups SO MEDICAL HYPOTHESES LA English DT Review ID EPSTEIN-BARR-VIRUS; COMMON VARIABLE IMMUNODEFICIENCY; HUMAN CYTOMEGALOVIRUS-INFECTION; HEMATOPOIETIC PROGENITOR CELLS; HUMAN HERPESVIRUS-6 INFECTION; BONE-MARROW TRANSPLANTATION; POLYMERASE-CHAIN-REACTION; BLOOD MONONUCLEAR-CELLS; HUMAN ENDOTHELIAL-CELLS; NECROSIS-FACTOR SYSTEM AB Immune panels of many autism-spectrum children reveal signs of atypical infections and shifted cell counts. In conjunction with trait-related cerebral hypometabolism and hypoperfusion, these findings suggest a hypothesis: Several autism-spectrum subgroups derive from intra-monocyte pathogens such as measles virus, cytomegalovirus, human herpesvirus 6, and Yersinia enterocolitica. Furthermore, with much inter-child variation, their effects manifest as diminished hematopoiesis, impaired peripheral immunity, and altered blood-brain barrier function often accompanied by demyelination. in some such children, one or more of these pathogens persists as a chronic-active, seemingly subclinical infection etiologically significant to the child's autistic traits. Within these subgroups, immune impairments and atypical infections may be treatable. (C) 2001 Harcourt Publishers Ltd. C1 Inst Mol Introspect, Estes Pk, CO 80517 USA. RP Binstock, T (reprint author), Box 1788, Estes Pk, CO 80517 USA. 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Hypotheses PD APR PY 2001 VL 56 IS 4 BP 523 EP 531 DI 10.1054/mehy.2000.1247 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 428LF UT WOS:000168462600022 PM 11339860 ER PT J AU Bushwick, NL AF Bushwick, NL TI Social learning and the etiology of autism SO NEW IDEAS IN PSYCHOLOGY LA English DT Article DE autism; cognition; development; learning; language; theory of mind ID CHILDREN; PEOPLE AB A developmental theory of autism is presented as an alternative to current nativist theories. The traits of autism are seen as results of failure of the process of social learning. The distinction between social learning and ontogenic discovery is discussed and a model of normal social learning is presented, showing its cyclical nature and significance. 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PD APR PY 2001 VL 19 IS 1 BP 49 EP 75 DI 10.1016/S0732-118X(00)00016-7 PG 27 WC Psychology, Multidisciplinary; Psychology, Experimental SC Psychology GA 408KA UT WOS:000167324300003 ER PT J AU Stein, MT Cowan, C Dixon, S AF Stein, MT Cowan, C Dixon, S TI A two-year-old boy with language regression and unusual social interactions SO PEDIATRICS LA English DT Article DE language delay; developmental regression; autistic spectrum disorder; autism; pervasive developmental delay ID SPECTRUM DISORDERS; YOUNG-CHILDREN; AUTISM; DIAGNOSIS C1 Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. Behav Pediat Practice, Great Falls, MT USA. Univ Washington, Sch Med, Seattle, WA USA. RP Stein, MT (reprint author), Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. CR ANDERSON SR, 1994, PRESCHOOL ED PROGRAM, P15 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Dawson G., 1997, EFFECTIVENESS EARLY, P307 DEB S, 1994, BRIT J PSYCHIAT, V165, P395, DOI 10.1192/bjp.165.3.395 Dixon SD, 2000, ENCOUNTERS CHILDREN, V3rd Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Jensen VK, 1997, CLIN PEDIATR, V36, P555, DOI 10.1177/000992289703601001 Kanner L, 1943, NERV CHILD, V2, P217 LANDAU WM, 1957, NEUROLOGY, V7, P523 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 SIEGAL B, 1996, WORLD AUTISTIC CHILD SIEGEL B, 1998, NIH STAT SCI AUT SCR Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 Wolraich M, 1996, CLASSIFICATION CHILD NR 18 TC 1 Z9 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD APR PY 2001 VL 107 IS 4 SU S BP 910 EP 915 PG 6 WC Pediatrics SC Pediatrics GA 422QD UT WOS:000168130000021 ER PT J AU Juul-Dam, N Townsend, J Courchesne, E AF Juul-Dam, N Townsend, J Courchesne, E TI Prenatal, perinatal, and neonatal factors in autism, pervasive developmental disorder-not otherwise specified, and the general population SO PEDIATRICS LA English DT Article DE autism; pervasive developmental disorder; pregnancy; delivery; risk factors; neonatal ID INFANTILE-AUTISM; MATERNAL AGE; COMPLICATIONS; EPIDEMIOLOGY; PREGNANCY AB Objectives. To examine various pre-, peri-, and neonatal factors in autistic participants and in pervasive developmental disorder-not otherwise specified (PDD-NOS) participants and to compare the incidence of each factor to that of the normal population. Methods. Seventy-four participants (66 males, 8 females) were diagnosed with autism at 2.5 through 4 years of age using the most accurate and up-to-date methods, including the Diagnostic and Statistical Manual of Mental Disorders and the Autism Diagnostic Interview-Revised. At age 5, all participants were reevaluated using the Diagnostic and Statistical Manual of Mental Disorders, the Autism Diagnostic Interview-Revised, the Childhood Autism Rating Scale, and the Autism Diagnostic Observation Schedule-Revised, resulting in 61 autistic and 13 PDD-NOS participants. Twenty-eight pre-, peri-, and neonatal factors were examined in these 2 groups using both medical records and parental interviews. Incidences were compared with those of the US population as reported in the Report of Final Natality Statistics, 1995. This grand scale population group was used to closely approximate comparison to a normal, unbiased population. Results were analyzed using the binomial probability test, with a P value of <.05, constituting a significant difference in incidence. A Bonferroni correction was applied to the data to adjust for the number of factors investigated. Results. Although most of the factors showed comparable incidences between the index and control groups, several factors showed statistically significant differences. Following the Bonferroni correction, the autism group was found to have a significantly higher incidence of uterine bleeding, a lower incidence of maternal vaginal infection, and less maternal use of contraceptives during conception when compared with the general population. Similarly, the PDD-NOS group showed a higher incidence of hyperbilirubinemia when compared with the general population. Conclusions. The results of this study support previous findings suggesting a consistent association of unfavorable events in pregnancy, delivery, and the neonatal phase and the pervasive developmental disorders. However, interpretation of the meaningfulness of these results is difficult, as the specific complications that carried the highest risk of autism and PDD-NOS represented various forms of pathologic processes with no presently apparent unifying feature. Additional studies are needed to corroborate and strengthen these associations, as well as to determine the possibility of an underlying unifying pathological process. This study's analysis of obstetric and neonatal complications in combination with the use of participants diagnosed at an early age provides some interesting concepts to consider. Perhaps future research will confirm certain pre-, peri-, and neonatal associations that could be used to generate a high-risk historical profile with which to use in conjunction with currently employed diagnostic tools. This may, in turn, help to determine the reliability of a diagnosis of autism in younger children, leading to earlier intervention and assistance for an improved outcome in long-term functionality and quality of life. C1 Univ Calif San Diego, Sch Med, San Diego, CA 92103 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 Courchesne, E (reprint author), Lab Res Neurosci Autism, 8110 La Jolla Shore Dr,Suite 201, La Jolla, CA 92037 USA. 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J., 1997, MONTHLY VITAL STAT R, V45, P1 NEWMAN TB, 1993, PEDIATRICS, V92, P651 PIVEN J, 1993, J AM ACAD CHILD PSY, V32, P1256, DOI 10.1097/00004583-199311000-00021 SAFTLAS AF, 1990, AM J OBSTET GYNECOL, V163, P460 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SPELLACY WN, 1966, AM J OBSTET GYNECOL, V94, P1136 Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 TSAI LY, 1983, J AUTISM DEV DISORD, V13, P57, DOI 10.1007/BF01531359 Ventura S. J., 1997, MONTHLY VITAL STAT R, V45, P1 Xu B, 1999, ALLERGY, V54, P829, DOI 10.1034/j.1398-9995.1999.00117.x Xu BZ, 1999, INT J EPIDEMIOL, V28, P723, DOI 10.1093/ije/28.4.723 NR 25 TC 87 Z9 91 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 APR PY 2001 VL 107 IS 4 BP art. no. EP e63 DI 10.1542/peds.107.4.e63 PG 6 WC Pediatrics SC Pediatrics GA 422KC UT WOS:000168116200020 PM 11335784 ER PT J AU Abril, B Mendez, M Sans, O Valdizan, JR AF Abril, B Mendez, M Sans, O Valdizan, JR TI Sleep in infantile autisim SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE Asperger disorder; infantile autism; Landau-Kleffner's disorder; Rett's syndrome; sleep ID ASPERGERS SYNDROME; RETTS SYNDROME; CHILDREN; PATTERNS; DISORDERS AB Introduction. Analysis of nocturnal sleep in infantile autism has been presented in various studies. However, there has been no systematization including the different structural and paroxystic alterations at the same time as permitting the development of a general theory of the effect of sleep on prognosis and treatment, particularly in a spectrum in which there is currently no definite solution. Development. A systematic review was made of the literature obtained from publications included ill MEDLINE and web pages of the East 25 years using the key words: autism, Asperger's disorder, sleep, childhood and Rett's syndrome. Altogether 21 papers fulfilled criteria for inclusion. Disorders of sleep in infantile autism were classified into three types: immaturity of sleep, showing a destructured polysomnographic recording and negative correlation with the level of development; functional alterations of sleep with early waking and difficulty in going to sleep being the disorders most frequently seen; and paroxystic alterations with epileptiform discharges being the commonest, without necessarily occurring together with seizures. The opinions stated on questionnaires and the data observed on the polysomnography were not in agreement. Conclusions. Analysis the literature has permitted la to make an initial classification of sleep disorders in autistic children, and has shown a marked presence of these disorders in the evolution of autistic children. It is necessary that further studies being done, polysomnographic rather than by means of questionnaires, for two reasons: clinical and in order to obtain more precise classification. C1 Hosp Univ Miguel Servet, Serv Neurofisiol Clin, E-50009 Zaragoza, Spain. CR American Psychiatric Association (DSM-IV), 1995, MAN DIAGN EST TRAST Artigas J, 1999, Rev Neurol, V28 Suppl 2, pS118 BERTHIER ML, 1992, J AM ACAD CHILD PSY, V31, P735, DOI 10.1097/00004583-199207000-00023 Brown DW, 1996, MED HYPOTHESES, V47, P399, DOI 10.1016/S0306-9877(96)90220-0 CABANYES J, PERSPECTIVA NEUROPSI CHILSHOLM T, 1996, SLEEP, V19, P343 GLAZE DG, 1987, ANN NEUROL, V21, P377, DOI 10.1002/ana.410210410 GLAZE DG, 1987, ARCH NEUROL-CHICAGO, V44, P1053 Hering E, 1999, J AUTISM DEV DISORD, V29, P143, DOI 10.1023/A:1023092627223 HO HH, 1988, CLIN INVEST MED, V11, P234 HOSHINO Y, 1984, FOLIA PSYCHIAT NEU J, V38, P45 Klein SK, 2000, J CHILD NEUROL, V15, P36, DOI 10.1177/088307380001500109 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 LUKE Y, 1998, SLEEP PROBLEMS EFFEC MAZET P, 2000, ENCY MED CHIR PSYCHI, V37, P201 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Rapin I, 1995, Semin Pediatr Neurol, V2, P278, DOI 10.1016/S1071-9091(95)80007-7 SEGAWA M, 1992, BRAIN DEV S, V14, P46 Seri S, 1999, CLIN NEUROPHYSIOL, V110, P1825, DOI 10.1016/S1388-2457(99)00137-6 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 Tuchman R F, 1996, Rev Neurol, V24, P1446 Verdot L, 1998, INT J MOL MED, V1, P185 NR 24 TC 3 Z9 7 PU REVISTA DE NEUROLOGIA PI BARCELONA PA C/O CESAR VIGUERA, EDITOR, APDO 94121, 08080 BARCELONA, SPAIN SN 0210-0010 J9 REV NEUROLOGIA JI Rev. Neurologia PD APR 1 PY 2001 VL 32 IS 7 BP 641 EP 644 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 435VB UT WOS:000168901900010 PM 11391493 ER PT J AU Happe, F AF Happe, F TI Autism in history: The case of Hugh Blair of Borgue SO TRENDS IN COGNITIVE SCIENCES LA English DT Book Review C1 Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London SE5 8AF, England. RP Happe, F (reprint author), Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, 111 Denmark Hill, London SE5 8AF, England. EM f.happe@iop.kcl.ac.uk CR Houston R. A., 2000, AUTISM HIST CASE H B 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 APR PY 2001 VL 5 IS 4 BP 179 EP 179 DI 10.1016/S1364-6613(00)01605-3 PG 1 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 420CJ UT WOS:000167986100012 ER PT J AU Zelan, K AF Zelan, K TI 'Exiting Nirvana' (Autism) SO NEW YORK TIMES BOOK REVIEW LA English DT Letter CR BICKERTON D, 2001, NY TIMES BOOK R 0311 PARK CC, EXITING NIRVANA DAUG NR 2 TC 0 Z9 0 PU NEW YORK TIMES PI NEW YORK PA 229 W 43RD ST, NEW YORK, NY 10036-3959 USA SN 0028-7806 J9 NY TIMES BK REV JI N. Y. Times Book Rev. PD APR 1 PY 2001 BP 4 EP 4 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 413TQ UT WOS:000167628400002 ER PT J AU Lawson, C AF Lawson, C TI Autism and MMR - the debate continues SO NEW SCIENTIST LA English DT Letter C1 Univ Melbourne, Parkville, Vic 3052, Australia. RP Lawson, C (reprint author), Univ Melbourne, Parkville, Vic 3052, Australia. NR 0 TC 0 Z9 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 USA SN 0262-4079 J9 NEW SCI JI New Sci. PD MAR 31 PY 2001 VL 169 IS 2284 BP 52 EP 52 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 418RP UT WOS:000167905400032 ER PT J AU Gilmore, JH van Tol, JJ Streicher, HL Williamson, K Cohen, SB Greenwood, RS Charles, HC Kliewer, MA Whitt, JK Silva, SG Hertzberg, BS Chescheir, NC AF Gilmore, JH van Tol, JJ Streicher, HL Williamson, K Cohen, SB Greenwood, RS Charles, HC Kliewer, MA Whitt, JK Silva, SG Hertzberg, BS Chescheir, NC TI Outcome in children with fetal mild ventriculomegaly: a case series SO SCHIZOPHRENIA RESEARCH LA English DT Article DE ultrasound; magnetic resonance imaging; schizophrenia; autism; learning disorder; fetal brain development ID DEFICIT HYPERACTIVITY DISORDER; CLINICAL COURSE; KNOCKOUT MICE; IN-UTERO; SCHIZOPHRENIA; BRAIN; ULTRASOUND; INFANTS; AUTISM; RISK AB Mild enlargement of the lateral ventricles is associated with schizophrenia and other neurodevelopmental disorders. While it has been hypothesized that ventricle abnormalities associated with neurodevelopmental disorders arise during fetal brain development, there is little direct evidence to support this hypothesis. Using ultrasound, it is possible to image the fetal ventricles in utero, Fetal mild ventriculomegaly (MVM) has been associated with developmental delays in early childhood, though longer-term neurodevelopmental outcome has not been studied. Follow-up of five children (aged 4-9 years) with mild enlargement of the lateral ventricles on prenatal ultrasound and two unaffected co-twins is reported: one child had attention deficit hyperactivity disorder (ADHD), one had autism, and two had evidence of learning disorders. These cases suggest that the mild enlargement of the lateral ventricles associated with these neurodevelopmental disorders arises during fetal brain development and can be detected with prenatal ultrasound. In addition, the presence of mildly enlarged, asymmetric ventricles in two children on prenatal ultrasound and on follow-up MRI at age 6 years indicates that ventricle structure present in utero can persist well into childhood brain development. The study of fetal ventricle development with ultrasound may provide important insights into neurodevelopmental disorders and allow the identification of children at high risk. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Neurol, Sch Med, Chapel Hill, NC 27599 USA. Duke Univ, Ctr Med, Dept Radiol, Durham, NC 27710 USA. Univ N Carolina, Sch Med, Dept Obstet & Gynecol, Chapel Hill, NC 27599 USA. RP Gilmore, JH (reprint author), Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA. RI van Tol-Geerdink, Julia/A-8690-2011 CR ACHRION R, 1997, OBSTET GYNECOL, V89, P233 Beery K.E., 1989, VMI DEV TEST VISUAL Bloom SL, 1997, OBSTET GYNECOL, V90, P93, DOI 10.1016/S0029-7844(97)00112-9 BROMLEY B, 1991, AM J OBSTET GYNECOL, V164, P863 Castellanos FX, 1996, ARCH GEN PSYCHIAT, V53, P607 Dawson G, 1996, J AUTISM DEV DISORD, V26, P179, DOI 10.1007/BF02172008 Demyanenko GP, 1999, J NEUROSCI, V19, P4907 Dommergues M, 1996, PRENATAL DIAG, V16, P883, DOI 10.1002/(SICI)1097-0223(199610)16:10<883::AID-PD959>3.3.CO;2-X FILLY RA, 1994, RADIOLOGY, V193, P315 FISH B, 1992, ARCH GEN PSYCHIAT, V49, P221 Gilmore JH, 1996, SCHIZOPHR RES, V19, P141, DOI 10.1016/0920-9964(95)00099-2 Gilmore JH, 2000, SCHIZOPHR RES, V44, P158, DOI 10.1016/S0920-9964(99)00199-1 Gilmore JH, 1998, SCHIZOPHR RES, V33, P133, DOI 10.1016/S0920-9964(98)00073-5 Gordon M, 1987, TECHNICAL GUIDE GORD KREMEN WS, 1994, SCHIZOPHRENIA BULL, V20, P103 Lyoo IK, 1996, BIOL PSYCHIAT, V40, P1060 Marx Christine E., 1999, American Journal of Obstetrics and Gynecology, V181, P1125 Ment LR, 1998, DEV BRAIN RES, V111, P197, DOI 10.1016/S0165-3806(98)00139-4 MONTEAGUDO A, 1996, ULTRASONOGRAPHY PREN, P89 Orvaschel H., 1987, SCHEDULE AFFECTIVE D PATEL MD, 1994, RADIOLOGY, V192, P759 PILU G, 1993, ULTRASOUND OBST GYN, V3, P85, DOI 10.1046/j.1469-0705.1993.03020085.x Pilu G, 1999, ULTRASOUND OBST GYN, V14, P320, DOI 10.1046/j.1469-0705.1999.14050320.x PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Prassopoulos P, 1996, J CHILD NEUROL, V11, P197 Pulsifer M B, 1996, J Int Neuropsychol Soc, V2, P159 REISS AL, 1995, NAT MED, V1, P159, DOI 10.1038/nm0295-159 Reitan RM, 1974, CLIN NEUROPSYCHOLOGY Sanderson TL, 1999, LANCET, V354, P1867, DOI 10.1016/S0140-6736(99)01049-1 Speltz ML, 1997, CLEFT PALATE-CRAN J, V34, P374, DOI 10.1597/1545-1569(1997)034<0374:PAPMAP>2.3.CO;2 Vergani P, 1998, AM J OBSTET GYNECOL, V178, P218, DOI 10.1016/S0002-9378(98)80003-3 Wechsler D., 1991, MANUAL WECHSLER INTE Wechsler D., 1989, MANUAL WECHSLER PRES Wood GK, 1998, NEUROREPORT, V9, P461, DOI 10.1097/00001756-199802160-00019 Wright IC, 2000, AM J PSYCHIAT, V157, P16 NR 35 TC 33 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD MAR 30 PY 2001 VL 48 IS 2-3 BP 219 EP 226 DI 10.1016/S0920-9964(00)00140-7 PG 8 WC Psychiatry SC Psychiatry GA 424EZ UT WOS:000168220300007 PM 11295375 ER PT J AU Sacks, O AF Sacks, O TI Leaving Nirvana (Living with a child's autism) SO NEW YORK REVIEW OF BOOKS LA English DT Article CR Grandin T., 1996, THINKING PICTURES PARK CC, 1967, SIEGE PARK CC, EXITING NIRVANA DAUG RAWLENCE C, 1996, MIND TRAVELLER Sacks O., 1995, ANTHROPOLOGIST MARS NR 5 TC 0 Z9 0 PU NEW YORK REVIEW PI NEW YORK PA 250 WEST 57TH ST, NEW YORK, NY 10107 USA SN 0028-7504 J9 NEW YORK REV BOOKS JI N. Y. Rev. Books PD MAR 29 PY 2001 VL 48 IS 5 BP 4 EP 5 PG 2 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 410PM UT WOS:000167448400001 ER PT J AU Bertone, A Mottron, L Jelenic, P Faubert, J AF Bertone, A Mottron, L Jelenic, P Faubert, J TI High-fluctuating individuals with autism are selectively less sensitive to second-order motion. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 Univ Montreal, Ecole Optometrie, Montreal, PQ H3C 3J7, Canada. Hop Riviere Des Prairies, Clin Specialisee Autisme, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 2001 VL 42 IS 4 SU S MA 1617 BP S300 EP S300 PG 1 WC Ophthalmology SC Ophthalmology GA 427EP UT WOS:000168392101607 ER PT J AU Bickerton, D AF Bickerton, D TI Exiting nirvana: A daughter's life with autism SO NEW YORK TIMES BOOK REVIEW LA English DT Book Review CR PARK CC, EXITING NIRVANA DAUG NR 1 TC 0 Z9 0 PU NEW YORK TIMES PI NEW YORK PA 229 W 43RD ST, NEW YORK, NY 10036-3959 USA SN 0028-7806 J9 NY TIMES BK REV JI N. Y. Times Book Rev. PD MAR 11 PY 2001 BP 17 EP 17 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 407DP UT WOS:000167256900013 ER PT J AU Aitken, K AF Aitken, K TI Autism increase SO NEW SCIENTIST LA English DT Letter CR EUROPEAN CHILD ADOLE, V9, P162 J AM ACAD CHILD ADOL, V39, P694 NR 2 TC 0 Z9 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 USA SN 0262-4079 J9 NEW SCI JI New Sci. PD MAR 10 PY 2001 VL 169 IS 2281 BP 56 EP 56 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 410ML UT WOS:000167443700040 ER PT J AU Wells, C AF Wells, C TI Autism increase SO NEW SCIENTIST LA English DT Letter NR 0 TC 0 Z9 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 USA SN 0262-4079 J9 NEW SCI JI New Sci. PD MAR 10 PY 2001 VL 169 IS 2281 BP 56 EP 56 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 410ML UT WOS:000167443700041 ER PT J AU Jyonouchi, H Sun, S Le, H AF Jyonouchi, H Sun, S Le, H TI Proinflammatory/regulatory cytokine production in children with autism spectrum disorders (ASD) SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN 55455 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 8 PY 2001 VL 15 IS 5 BP A939 EP A939 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 410TA UT WOS:000167454201300 ER PT J AU Dales, L Hammer, SJ Smith, NJ AF Dales, L Hammer, SJ Smith, NJ TI Time trends in autism and in MMR immunization coverage in California SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article AB Context Considerable concern has been generated in the lay and medical communities by a theory that increased measles-mumps-rubella (MMR) immunization among young children may be the cause of an apparent marked increase in autism occurrence. Objective To determine if a correlation exists in secular trends of MMR immunization coverage among young children and autism occurrence. Design, Setting, and Participants Retrospective analyses of MMR immunization coverage rates among children born in 1980-1994 who were enrolled in California kindergartens (survey samples of 600-1900 children each year) and whose school immunization records were reviewed to retrospectively determine the age at which they first received MMR immunization; and of autism caseloads among children born in these years who were diagnosed with autism and were enrolled in the California Department of Developmental Services regional service center system. Main Outcome Measures Measles-mumps-rubella immunization coverage rates as of ages 17 months and 24 months and numbers of Department of Developmental Services system enrollees diagnosed with autism, grouped by year of birth. Results Essentially no correlation was observed between the secular trend of early childhood MMR immunization rates in California and the secular trend in numbers of children with autism enrolled in California's regional service center system. For the 1980-1994 birth cohorts, a marked, sustained increase in autism case numbers was noted, from 44 cases per 100000 live births in the 1980 cohort to 208 cases per 100000 live births in the 1994 cohort (a 373% relative increase), but changes in early childhood MMR immunization coverage over the same time period were much smaller and of shorter duration. Immunization coverage by the age of 24 months increased from 72% to 82%, a relative increase of only 14%, over the same time period. Conclusions These data do not suggest an association between MMR immunization among young children and an increase in autism occurrence. C1 Calif Dept Hlth Serv, Immunizat Branch, Berkeley, CA 94704 USA. RP Dales, L (reprint author), Calif Dept Hlth Serv, Immunizat Branch, 2151 Berkeley Way,Room 712, Berkeley, CA 94704 USA. CR *CA DEP DEV SERV, 1999, CHAN POP PERS AUT PE Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 FRIEDMAN GD, 1987, PRIMER EPIDEMIOLOGY, P170 Gillberg C., 1998, AUTISM, V2, P423, DOI 10.1177/1362361398024007 MANNING A, 2001, VACCINE AUTISM LINK RIMLAND B, 2001, LOS ANGELES TIM 0429 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 NR 9 TC 163 Z9 164 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 MAR 7 PY 2001 VL 285 IS 9 BP 1183 EP 1185 DI 10.1001/jama.285.9.1183 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 406BH UT WOS:000167194700022 PM 11231748 ER PT J AU Shaffer, RJ Jacokes, LE Cassily, JF Greenspan, SI Tuchman, RF Stemmer, PJ AF Shaffer, RJ Jacokes, LE Cassily, JF Greenspan, SI Tuchman, RF Stemmer, PJ TI Effect of interactive Metronome (R) training on children with ADHD SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE attention deficit disorder with hyperactivity coordination training; motor control ID DEFICIT-HYPERACTIVITY DISORDER; SWEDISH 7-YEAR-OLD CHILDREN; MOTOR CONTROL; SUSTAINED ATTENTION; PERCEPTION DAMP; JOINT ATTENTION; AUTISM; COORDINATION AB Objective. The purpose of this study was to determine the effects of a specific intervention, the Interactive Metronome(R), on selected aspects of motor and cognitive skills in a group of children with attention deficit hyperactivity disorder (ADHD). Method. The study included 56 boys who were 6 years to 12 years of age and diagnosed before they entered the study nr having ADHD. The participants were pretested and randomly assigned to one of three matched groups. A group of 19 participants receiving Ij hr of Interactive Metronome training exercises were compared with a group receiving no intervention and a group receiving training on selected computer video games. Results. A significant pattern of improvement across 53 of 58 variables favoring the Interactive Metronome treatment was found Additionally, several significant differences were found among the treatment groups and between pretreatment and postreatment factors on performance in areas of attention, motor control, language processing, rending, and parental reports of improvements in regulation of aggressive behavior. Conclusion. 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B., 1993, DYNAMIC SYSTEMS APPR STEMMER PM, 1996, 1996 ANN M AM ED ASS Wechsler D., 1992, WECHSLER INTELLIGENC Wilkinson G.S., 1993, WIDE RANGE ACHIEVEME, V3 1998, STAT PACKAGE SOCIAL NR 37 TC 22 Z9 22 PU AMER OCCUPATIONAL THERAPY ASSOC, INC PI BETHESDA PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA SN 0272-9490 J9 AM J OCCUP THER JI Am. J. Occup. Ther. PD MAR-APR PY 2001 VL 55 IS 2 BP 155 EP 162 PG 8 WC Rehabilitation SC Rehabilitation GA 412UH UT WOS:000167572400005 PM 11761130 ER PT J AU Kroeger, TL Rojahn, J Naglieri, JA AF Kroeger, TL Rojahn, J Naglieri, JA TI Role of planning, attention, and simultaneous and successive cognitive processing in facial recognition in adults with mental retardation SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID DISCRIMINATION TASK; EMOTION; AUTISM; EXPRESSIONS; CHILDREN; FACES AB Fifty adults with mental retardation completed the Cognitive Assessment System and the Facial Discrimination Task. Performances on the Facial Discrimination Task Emotion and Age Tasks were significantly correlated to the Cognitive Assessment System total score. Hierarchical regression analyses showed that processing of emotional stimuli was related to simultaneous and successive processing; whereas attention and planning failed to add significantly. The Emotion and Age Tasks yielded similar results, suggesting that cognitive processes are involved in processing facial stimuli in a similar way regardless of the type of facial cues involved. The results are discussed vis-a-vis modular models of emotion, future research directions, and the Age Task as a control task. C1 Ohio State Univ, Nisonger Ctr UAP, Columbus, OH 43210 USA. RP Rojahn, J (reprint author), Ohio State Univ, Nisonger Ctr UAP, 1581 Dodd Dr, Columbus, OH 43210 USA. CR ANGLIERI JA, 1997, COGNITIVE ASSESSMENT BASSILI JN, 1979, J PERS SOC PSYCHOL, V37, P2049, DOI 10.1037//0022-3514.37.11.2049 Cicchetti D., 1978, DEV AFFECT, P309 Das J. 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PD MAR PY 2001 VL 106 IS 2 BP 151 EP 161 DI 10.1352/0895-8017(2001)106<0151:ROPAAS>2.0.CO;2 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 417XU UT WOS:000167861400005 PM 11321606 ER PT J AU Balboni, G Pedrabissi, L Molteni, M Villa, S AF Balboni, G Pedrabissi, L Molteni, M Villa, S TI Discriminant validity of the vineland scales: Score profiles of individuals with mental retardation and a specific disorder SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID ADAPTIVE-BEHAVIOR; DOWN-SYNDROME; CHILDREN; AUTISM; DISABILITIES AB Utility of the Vineland Adaptive Behavior Scales-Expanded Form to discriminate among areas of adaptive behavior was substantiated by comparing profiles of scores obtained by three groups of individuals with mental retardation and either a communication, social behavior, or motor abilities disorder with those of matched individuals with mental retardation but no other disorder. Individuals with social behavior disorders obtained lower scores only in the Socialization domain; those with motor disorders, in the Motor domain and in the Personal and Domestic subscales that require motor competencies; and those with communication disorders, lower scores in the Communication domain and in the Community and Interpersonal Relationships subscales requiring expressive competencies. The utility of the Vineland Scales in obtaining an ecological evaluation of individuals with mental retardation is discussed. C1 Univ Padua, Dept Dev Psychol & Socializat, I-35131 Padua, Italy. Sci Inst Eugenio Medea, Lecco, Italy. RP Balboni, G (reprint author), Univ Padua, Dept Dev Psychol & Socializat, Via Venezia 8, I-35131 Padua, Italy. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Carpenter JW, 1996, EXOT PET PRACT, V1, P1 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 CICCHETTI DV, 1990, PERGAMON GEN PSYCHOL, V163, P173 Freund LS, 1995, DEV BRAIN DYSFUNCT, V8, P242 Harrison P. L., 1988, J PSYCHOEDUCATIONAL, V6, P188 JACOBSON JW, 1996, MANUAL DIAGNOSIS PRO, P13 LEHR CA, 1987, PSYCHOL SCHOOLS, V24, P390, DOI 10.1002/1520-6807(198710)24:4<390::AID-PITS2310240415>3.0.CO;2-V Loveland K. 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J. Ment. Retard. PD MAR PY 2001 VL 106 IS 2 BP 162 EP 172 DI 10.1352/0895-8017(2001)106<0162:DVOTVS>2.0.CO;2 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 417XU UT WOS:000167861400006 PM 11321607 ER PT J AU Dessiex, V Haas, C Rodrigues, C Junier, L Muller-Nix, C Ansermet, F AF Dessiex, V Haas, C Rodrigues, C Junier, L Muller-Nix, C Ansermet, F TI A psychoanalytic approach of autism and evaluation scales SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE autism; CARS; evaluation; IBSE; Haag's instrument; observation scales; psychoanalytic theory ID BEHAVIORAL SUMMARIZED EVALUATION; DIAGNOSTIC OBSERVATION SCHEDULE; RATING-SCALE; CHILDHOOD-AUTISM; DEVELOPMENTAL DISORDERS; CHILDREN; RELIABILITY; INSTRUMENTS; INTERVIEW; VALIDITY AB This paper puts in balance, as contributions to the study of autism, observation scales and cognitive epistemology versus psychodynamic evaluation. To what extend is the articulation of opposite stances valuable? What do observation scales add to the psychodynamic approach of the child and what are their limits? Our material comes from one of the outpatient clinics of the Department of Child and Adolescent Psychiatry with a close link to Neuropediatric Unit and we are trying to formalise the first steps for care of very young children with autistic disturbances. These steps are, first, the use of child behaviour observation scales (CARS, IBSE) which contributes for a shared phenomenological diagnosis. Second, away from strict observation, we use a clinical evaluation chart (Haag's instrument) which does help to give the meaning of different behaviour. Third, afar from instrument, we try to stress a close encounter of practitioner and child, always unique. (C) 2001 Editions scientifiques et medicales Elsevier SAS. C1 CHU Vaudois, Hop Nestle, Serv Univ Psychiat Enfant, CCN P,Unite Pedopsychiat Liason, CH-1011 Lausanne, Switzerland. RP Dessiex, V (reprint author), CHU Vaudois, Hop Nestle, Serv Univ Psychiat Enfant, CCN P,Unite Pedopsychiat Liason, Ave Pierre Decker 5, CH-1011 Lausanne, Switzerland. CR ADRIEN JL, 1994, DEVENIR, V6, P71 ADRIEN JL, 1992, J AUTISM DEV DISORD, V22, P375, DOI 10.1007/BF01048241 ANSERMET F, 1999, CLIN ORIGINES BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 BARTHELEMY C, 1986, NEUROPSYCHIAT ENFAN, V34, P63 BERNARDDESORIA O, 1995, J PSYCHOL, V132, P52 DILALLA DL, 1994, J AUTISM DEV DISORD, V24, P115, DOI 10.1007/BF02172092 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 GOLSE B, 1995, INFORM PSYCHIAT, V1, P18 GUIDETTI M, 1993, EVALUATION COMMUNICA Haag G., 1990, THERAPIE PSYCHOMOTRI, V86, P50 HAAG G, 1995, J PSYCHOL, V132, P28 Haag G, 1995, PSYCHIAT ENFANT, V38, P495 HAMEURY L, 1991, AUTISME ENFANT, P189 LAZNIKPENOT MC, 1998, EFFETS PAROLE REGARD, P256 LAZNIKPENOT MC, 1996, CONTRASTE, V5, P69 LELORD G, 1990, AUTISME ENFANT 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 Lowe M., 1988, SYMBOLIC PLAY TEST NIX CM, 1999, CAHIERS PSYCHIAT, V27, P173 PARKS SL, 1983, J AUTISM DEV DISORD, V13, P255, DOI 10.1007/BF01531565 Pilowsky T, 1998, J AUTISM DEV DISORD, V28, P143, DOI 10.1023/A:1026092632466 PORTE R, 1997, PROJET CTR REGIONAL ROGE B, 1985, METHODS ECHELLES EVA RUTTER M, 1988, AUTISTIC DIAGNOSITC SAUVAGE D, 1987, ANN PSYCHIAT, V2, P338 SCHOPLER E, 1994, PROFIL PSYCHO EDUCAT SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SEVIN JA, 1991, J AUTISM DEV DISORD, V21, P417, DOI 10.1007/BF02206868 YIRMIYA N, 1994, J AUTISM DEV DISORD, V24, P281, DOI 10.1007/BF02172227 NR 32 TC 0 Z9 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0003-4487 J9 ANN MED-PSYCHOL JI Ann. Med.-Psychol. PD MAR PY 2001 VL 159 IS 2 BP 111 EP 120 DI 10.1016/S0003-4487(00)00002-0 PG 10 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 462GB UT WOS:000170411400002 ER PT J AU Jarbrink, K Knapp, M AF Jarbrink, K Knapp, M TI The economic impact of autism in Britain SO AUTISM LA English DT Article DE autistic disorder; cost of illness; early intervention; education; health services ID RECEPTIVE LANGUAGE DISORDER; EARLY ADULT LIFE; FOLLOW-UP; EARLY INTERVENTION; CHILDREN; OUTCOMES; PREVALENCE; PATTERNS; DRUGS AB Little is known about the economic impact of autism. This study estimated the economic consequences of autism in the United Kingdom, based on published evidence and on the reanalysis of data holdings at the Centre for the Economics of Mental Health (CEMH). With an assumed prevalence of 5 per 10,000, the annual societal cost for the UK was estimated to exceed pound1 billion. The lifetime cost for a person with autism exceeded pound2.4 million. The main costs were for living support and day activities. Family costs account for only 2.3 percent of the total cost, but a lack of relevant information limited our ability to estimate these costs. Minor improvements in life outcome for people with autism could substantially reduce costs over the lifetime. C1 Inst Psychiat, Ctr Econ Mental Hlth, London SE5 8AF, England. Univ London London Sch Econ & Polit Sci, London WC2A 2AE, England. RP Knapp, M (reprint author), Inst Psychiat, Ctr Econ Mental Hlth, De Crespigny Pk,Denmark Hill, London SE5 8AF, England. 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There were significant differences between groups on CASP scores, SSRS scores, number of friends, frequency of contact and social competence. There was also a significant difference on receptive language. The clinically and statistically significant differences between the groups on the measures of social skills help us understand the nature of the social deficits in Asperger syndrome and suggest the need to focus on specific deficits. These findings are discussed in relation to diagnostic criteria and intervention. C1 Univ Alberta, Dept Occupat Therapy, Edmonton, AB T6G 2G4, Canada. Glenrose Rehabil Hosp, Edmonton, AB, Canada. RP Magill-Evans, J (reprint author), Univ Alberta, Dept Occupat Therapy, Room 2-64 Corbett Hall, Edmonton, AB T6G 2G4, Canada. CR Achenbach T. 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The National Autistic Society has developed an autism-specific three-month parent package, the NAS EarlyBird Programme, that emphasizes partnership With parents. Six families participate in each three-month programme, which combines weekly group training sessions for parents with individualized home visits. During the programme parents learn to understand autism, to build social communication, and to analyse and use structure, so as to prevent inappropriate behaviours. The use of video and the group dynamic amongst families are important components of the programme. An efficacy study evaluated the pilot programme and further monitoring is in Progress. Training courses in the licensed use of the NAS EarlyBird Programme are now available for teams of professionals with prior experience of autism. Strengths and weaknesses of the programme are discussed. This short-term, affordable package, with supporting evidence of efficacy, offers a model of early intervention that is very popular with parents. C1 Natl Atlantic Soc, London, England. RP Shields, J (reprint author), NAS, Early Bird Ctr, 3 Victoria Crescent W, Barnsley S75 2AE, S Yorkshire, England. CR BRISTOL MM, 1987, J AUTISM DEV DISORD, V17, P469, DOI 10.1007/BF01486964 Bristol M. M., 1984, EFFECTS AUTISM FAMIL, P289 Clements J., 1994, PROBLEM BEHAV PEOPLE Guralnick MJ., 1997, EFFECTIVENESS EARLY Hardy S, 1999, THESIS U TEESSIDE Kasari C, 1997, J AUTISM DEV DISORD, V27, P39, DOI 10.1023/A:1025869105208 KAUFMAN BN, 1981, MIRACLE BELIEVE KAUFMAN BN, 1977, LOVE IS BE HAPPY Koegel RL, 1996, J AUTISM DEV DISORD, V26, P347, DOI 10.1007/BF02172479 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 Manolson A., 1992, IT TAKES 2 TALK Schopler E., 1995, PARENT SURVIVAL MANU SHIELDS J, 1999, NAS EARLYBIRD PROGRA WING L, 1979, J AUTISM DEV DISORD, V15, P149 NR 15 TC 32 Z9 32 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2001 VL 5 IS 1 BP 49 EP 56 DI 10.1177/1362361301005001005 PG 8 WC Psychology, Developmental SC Psychology GA 486GG UT WOS:000171809600004 PM 11708389 ER PT J AU Gillberg, C Gillberg, C Rastam, M Wentz, E AF Gillberg, C Gillberg, C Rastam, M Wentz, E TI The Asperger Syndrome (and high-functioning autism) - Diagnostic Interview (ASDI): a preliminary study of a new structured clinical interview SO AUTISM LA English DT Article DE Asperger syndrome; autism; interview; reliability; validity ID DISORDERS; VERSION AB The development of the Asperger Syndrome (and high-functioning autism) Diagnostic Interview (ASDI) is described. Preliminary data from a clinical study suggest that inter-rater reliability and test-retest stability may be excellent, with kappas exceeding 0.90 in both instances. The validity appears to be relatively good. No attempt was made in the present study to validate the instrument as regards the distinction between Asperger syndrome and high-functioning autism. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, Annedals Clin, SE-41345 Gothenburg, Sweden. RP Gillberg, C (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Annedals Clin, SE-41345 Gothenburg, Sweden. EM christopher.gillberg@pediat.gu.se CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Ehlers S, 1997, J CHILD PSYCHOL PSYC, V38, P207, DOI 10.1111/j.1469-7610.1997.tb01855.x Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Gillberg C., 1991, AUTISM ASPERGER SYND, P122, DOI 10.1017/CBO9780511526770.004 Gillberg C., 1998, ASPERGER SYNDROME HI, P79 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Manjiviona J., 1999, AUTISM, V3, P327, DOI DOI 10.1177/1362361399003004003 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Nordin V, 1998, J AUTISM DEV DISORD, V28, P69, DOI 10.1023/A:1026067104198 Schopler E., 1988, CHILDHOOD AUTISM RAT Siegel B., 1996, WORLD AUTISTIC CHILD SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 WHO, 1993, ICD 10 CLASS MENT BE WING L, 1981, PSYCHOL MED, V11, P115 NR 19 TC 113 Z9 116 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2001 VL 5 IS 1 BP 57 EP 66 DI 10.1177/1362361301005001006 PG 10 WC Psychology, Developmental SC Psychology GA 486GG UT WOS:000171809600005 PM 11708390 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 SO AUTISM LA English DT Article DE Asperger's disorder; attention; executive dysfunction; high-functioning autism; visual-perceptual processing ID CHILDHOOD AUTISM; CHILDREN; IMPAIRMENT; PRECEDENCE; ABILITIES AB The aim of this study was to examine executive functioning, in particular, attentional set-shifting deficits in high-functioning autism (n = 12) and Asperger's disorder (n = 12). A large or global digit composed of smaller or local digits was presented during each trial. The participants indicated the presence of 1s or 2s by pressing the appropriate button. These targets could appear globally or locally. Relative to IQ, sex and age matched controls, reaction time to global targets in individuals with autism was retarded when the previous target appeared locally. This deficiency in shifting from local to global processing, however, was not observed in individuals with Asperger's disorder. The theoretical and neurobiological significance of this dissociation in executive functioning in these clinically related disorders was explored. C1 Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. Monash Med Ctr, Clayton, Vic 3168, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. CR Achenbach T. M., 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BERGER HJC, 1993, J AUTISM DEV DISORD, V23, P341, DOI 10.1007/BF01046224 CASEY BJ, 1993, J CLIN EXP NEUROPSYC, V15, P933, DOI 10.1080/01688639308402609 COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 Courchesne E., 1994, ATYPICAL COGNITIVE D, P101 CUMMINGS JL, 1993, ARCH NEUROL-CHICAGO, V50, P873 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Frith U., 1989, AUTISM EXPLAINING EN Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MAURER RG, 1982, J AUTISM DEV DISORD, V12, P195, DOI 10.1007/BF01531309 MOTTRON L, 1993, BRAIN COGNITION, V23, P279, DOI 10.1006/brcg.1993.1060 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P203, DOI 10.1017/S0021963098003333 NAVON D, 1977, COGNITIVE PSYCHOL, V9, P353, DOI 10.1016/0010-0285(77)90012-3 Ozonoff S, 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 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Pascualvaca DM, 1998, J AUTISM DEV DISORD, V28, P467, DOI 10.1023/A:1026091809650 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x Plaisted K, 1999, J CHILD PSYCHOL PSYC, V40, P733, DOI 10.1111/1469-7610.00489 PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 RINEHART NJ, IN PRESS J CHILD PSY, V41, P769 RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 Russell J., 1997, AUTISM EXECUTIVE DIS Sattler J.M., 1992, ASSESSMENT CHILDREN Sheppard DM, 1999, CLIN PSYCHOL REV, V19, P531, DOI 10.1016/S0272-7358(98)00059-2 Tonge B. J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Townsend J, 1996, J Int Neuropsychol Soc, V2, P541 Wainwright JA, 1996, J AUTISM DEV DISORD, V26, P423, DOI 10.1007/BF02172827 Ziatas K, 1998, J CHILD PSYCHOL PSYC, V39, P755, DOI 10.1017/S0021963098002510 NR 33 TC 95 Z9 96 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2001 VL 5 IS 1 BP 67 EP 80 DI 10.1177/1362361301005001007 PG 14 WC Psychology, Developmental SC Psychology GA 486GG UT WOS:000171809600006 PM 11708391 ER PT J AU Mayes, SD Calhoun, SL AF Mayes, SD Calhoun, SL TI Non-significance of early speech delay in children with autism and normal intelligence and implications for DSM-IV Asperger's disorder SO AUTISM LA English DT Article DE Asperger syndrome; Asperger's disorder; autism; DSM-IV; speech delay ID SYMPTOMS AB According to the DSM-IV, children with Asperger's disorder do not have significant cognitive or speech delays, whereas children with autistic disorder may or may not. In our study, children with normal intelligence who had clinical diagnoses of autism or Asperger syndrome were divided into two groups: those with and without a significant speech delay. The purpose was to determine if clinically meaningful differences existed between the two groups that would support absence of speech delay as a DSM-IV criterion for Asperger's disorder. No significant differences were found between the 23 children with a speech delay and the 24 children without a speech delay on any of the 71 variables analyzed, including autistic symptoms and expressive language. Results suggest that early speech delay may be irrelevant to later functioning in children who have normal intelligence and clinical diagnoses of autism or Asperger syndrome and that speech delay as a DSM-IV distinction between Asperger's disorder and autism may not be justified. C1 Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Dept Psychiat, Hershey, PA 17033 USA. RP Mayes, SD (reprint author), Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Dept Psychiat, POB 850, Hershey, PA 17033 USA. EM SueDMayes@aol.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 ATTWOOD T, 1998, ASPERGERS SYNDROM GU Bayley N, 1969, MANUAL BAYLEY SCALES Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 FENSON L, 1994, MONOGR SOC RES CHILD, V59, pR5 Frith U., 1991, AUTISM ASPERGER SYND, P1, DOI 10.1017/CBO9780511526770.001 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P643, DOI 10.1007/BF01046332 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 GILLBERG C, 1985, J AUTISM DEV DISORD, V15, P389, DOI 10.1007/BF01531783 Gillberg C., 1991, AUTISM ASPERGER SYND, P122, DOI 10.1017/CBO9780511526770.004 Gillberg C., 1998, ASPERGER SYNDROME HI, P79 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x HOOPER SR, 1998, ASPERGER SYNDROME HI, P317 Kanner L, 1943, NERV CHILD, V2, P217 KLIN A, 1994, CHILD ADOL PSYCH CL, V3, P131 Klin A., 1995, CHILD ADOL PSYCH CL, V4, P617 Lindgren S.D., 1987, ADV BEHAVIORAL ASSES, V3, P57 MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 MAYES SD, 2000, UNPUB INFLUENCE IQ A Mayes SD, 1999, INFANT YOUNG CHILD, V12, P90 MAYES SD, IN PRESS J ABNORMAL, P29 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Myhr G, 1998, CAN J PSYCHIAT, V43, P589 Schopler E, 1996, J AUTISM DEV DISORD, V26, P109, DOI 10.1007/BF02276238 Schopler E, 1998, ASPERGER SYNDROME HI, P385 SCHOPLER E, 1985, J AUTISM DEV DISORD, V15, P359, DOI 10.1007/BF01531780 Siegel B., 1996, WORLD AUTISTIC CHILD SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 SZATMARI P, 1992, J AUTISM DEV DISORD, V22, P583, DOI 10.1007/BF01046329 SZATMARI P, 1991, PSYCHIAT CLIN N AM, V14, P81 Szatmari P, 1998, ASPERGER SYNDROME HI, P61 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x Twachtman-Cullen D., 1998, ASPERGER SYNDROME HI, P199 Volkmar F. R., 1998, ASPERGER SYNDROME HI, P107 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 Wing L, 1976, EARLY CHILDHOOD AUTI, V2nd, P15 WING L, 1981, PSYCHOL MED, V11, P115 Wing L, 1998, ASPERGER SYNDROME HI, P11 NR 43 TC 41 Z9 41 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2001 VL 5 IS 1 BP 81 EP 94 DI 10.1177/1362361301005001008 PG 14 WC Psychology, Developmental SC Psychology GA 486GG UT WOS:000171809600007 PM 11708393 ER PT J AU Wolfberg, PJ AF Wolfberg, PJ TI Autism and play SO AUTISM LA English DT Book Review C1 Integrated Play Grp, San Francisco, CA USA. RP Wolfberg, PJ (reprint author), Integrated Play Grp, San Francisco, CA USA. CR BEYER J, 1999, AUTISM PLAY 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 2001 VL 5 IS 1 BP 95 EP 96 DI 10.1177/1362361301005001009 PG 2 WC Psychology, Developmental SC Psychology GA 486GG UT WOS:000171809600008 ER PT J AU Chiesa, M AF Chiesa, M TI A voice on autism from Europe: A review of parents' education as autism therapists SO BEHAVIOR ANALYST LA English DT Book Review C1 Univ Paisley, Sch Social Sci, Paisley PA1 2BE, Renfrew, Scotland. RP Chiesa, M (reprint author), Univ Paisley, Sch Social Sci, Paisley PA1 2BE, Renfrew, Scotland. CR KEENAN M, VOICE AUTISM EUROPE Keenan M., 2000, PARENTS ED AUTISM TH MACRAE CD, 2000, SPEACH, V3, P5 NR 3 TC 1 Z9 1 PU SOC ADVANCEMENT BEHAVIOR ANALYSIS PI KALAMAZOO PA WESTERN MICHIGAN UNIV, 260 WOOD HALL, KALAMAZOO, MI 49008-5052 USA SN 0738-6729 J9 BEHAV ANALYST JI Behav. Anal. PD SPR PY 2001 VL 24 IS 1 BP 101 EP 105 PG 5 WC Psychology, Clinical SC Psychology GA 432RR UT WOS:000168709900007 ER PT J AU Rowe, AD Bullock, PR Polkey, CE Morris, RG AF Rowe, AD Bullock, PR Polkey, CE Morris, RG TI 'Theory of mind' impairments and their relationship to executive functioning following frontal lobe excisions SO BRAIN LA English DT Article DE theory of mind; executive functions; frontal lobe excisions ID BRAIN-DAMAGED PATIENTS; WORKING-MEMORY; ASPERGERS SYNDROME; AUTISM; CHILDREN; DEFICITS; REPRESENTATION; APPRECIATION; RECOGNITION; LESIONS AB It has been suggested that mental states play an important role in determining behaviour and that mental state attributions ('theory of mind') underlie the ability to understand and predict other peoples' behaviour. Theory of mind was investigated in 31 patients with unilateral frontal lobe lesions (15 right-sided and 16 left-sided) by comparing their performance with that of 31 matched control subjects. The ability to infer first- and second-order beliefs was tested by requiring subjects to listen to stories in which a protagonist acted upon a false belief. Both patient groups exhibited significantly impaired performance on the two theory of mind measures. Both frontal lobe groups also exhibited a range of deficits in tests of executive functions, but analyses revealed that these seemed to be independent of theory of mind impairments. These findings are discussed in terms of the hypothesis of a specialized, adaptive brain system underlying theory of mind reasoning ability, and are related to observed difficulties in social functioning among patients with frontal lobe damage. C1 Inst Psychiat, Dept Psychol, London SE5 8AF, England. Inst Psychiat, Neuropsychol Unit, London SE5 8AF, England. Kings Coll London, Ctr Neurosci, London WC2R 2LS, England. RP Rowe, AD (reprint author), Inst Psychiat, Dept Psychol, De Crespigny Pk, London SE5 8AF, England. 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SP Soc Res Child Dev ID FALSE BELIEF; MIND; PRESCHOOLERS; TASK; REPRESENTATION; COMPETENCE; DECEPTION; KNOWLEDGE; AUTISM; TOMM AB Three studies investigated children's ability to draw inferences from the properties of one mental state to the properties of another. Inferences from knowledge/ignorance to the possible contents of pretends and beliefs are crucial to developing a representational cheery of mental states. In Experiment 1, we replicated Lillard's (1993) finding that 4- and 6-year-olds fail to appreciate that a character who does nor know about an entity cannot pretend to be that entity. We show that these children also fail a similar task in which the inference to be made is from not knowing to thinking (false belief). Lillard's inference casks may be difficult because of their performance demands-specifically, children are not offered a plausible alternative content for the agent's pretence or belief state. In a second experiment, children were presented with know-pretend and know-think inference casks which offered two options for the content of a character's mental state. One option was consistent with chat character's knowledge stare, while the other was not. Under these conditions, 4- and 6-year-old children's performance improved significantly on both pretend and chink. A third experiment investigated the role of the salience of the character's ignorance and the possible use of an association strategy in producing successful performance in Experiment 2. When the salience of the character's ignorance was reduced, children still succeeded on know-pretend inferences but failed on know-think inferences. These results suggest that children do not really grasp the theory of mental representation. The results better support the ToMM-SP model of 'theory of mind' development. According to this model, concept possession is prior to, and therefore does not depend upon, knowledge of theories, and task success depends upon the control of salience. C1 Univ Essex, Dept Psychol, Colchester CO4 3SQ, Essex, England. Rutgers State Univ, Dept Psychol, Piscataway, NJ 08855 USA. Rutgers State Univ, Ctr Cognit Sci, Piscataway, NJ 08855 USA. RP German, TP (reprint author), Univ Essex, Dept Psychol, Wivenhoe Pk, Colchester CO4 3SQ, Essex, England. 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SO BRITISH JOURNAL OF GENERAL PRACTICE LA English DT Article DE autism; MMR vaccine; consultation behaviour AB A close temporal association has been reported between the measles, mumps, and rubella (MMR) vaccinated and dramatic behavioural decline in children subsequently diagnosed as autistic. We hypothesised that such a decline would be reflected in increased consultations with the child's general practitioner: The Doctor's Independent Network database was used to examine whether children subsequently diagnosed as autistic consulted more frequently than controls after MMR vaccination. No difference in consulting behaviour was seen in the six months post MMR. Any dramatic effect of MMR on behaviour seems unlikely. C1 St George Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 0RE, England. St George Hosp, Sch Med, Dept Gen Practice & Primary Care, London SW17 0RE, England. CompuFile Ltd, Woking, Surrey, England. 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PD MAR PY 2001 VL 51 IS 464 BP 226 EP 227 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 408DT UT WOS:000167311800013 PM 11255906 ER PT J AU Teunisse, JP de Gelder, B AF Teunisse, JP de Gelder, B TI Impaired categorical perception of facial expressions in high-functioning adolescents with autism SO CHILD NEUROPSYCHOLOGY LA English DT Article ID FACE RECOGNITION; CHILDS APPRAISAL; EMOTION; IDENTITY; NEURONS; CORTEX AB Categorical perception of facial expressions is studied in high-functioning adolescents with autism, using three continua of facial expressions obtained by morphing. In contrast to the results of normal adults, the performance on the identification task in autistic subjects did not predict performance on the discrimination task, an indication that autistic individuals do not perceive facial expressions categorically. 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PD MAR PY 2001 VL 7 IS 1 BP 1 EP 14 DI 10.1076/chin.7.1.1.3150 PG 14 WC Clinical Neurology SC Neurosciences & Neurology GA 509FV UT WOS:000173136400001 PM 11815876 ER PT J AU Carmody, DP Kaplan, M Gaydos, AM AF Carmody, DP Kaplan, M Gaydos, AM TI Spatial orientation adjustments in children with autism in Hong Kong SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE autism; prisms; optometry; perceptual dysfunctions; ambient vision; gaze avoidance; posture ID VISUAL STABILIZATION; BEHAVIOR; DISORDERS; POSTURE; VISION; LENSES AB Abnormal spatial orientation and body postures in children with autism often interfere with Visual abilities to attend tasks and social interactions. Twenty-four children diagnosed with autism from Kowloon, Hong Kong were assessed for spatial orientation and spatial management abilities. Positive changes in spatial orientation were evident when the children wore ambient prism lenses and included changes in posture from slanted to erect. 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Hum. Dev. PD SPR PY 2001 VL 31 IS 3 BP 233 EP 247 DI 10.1023/A:1026481422227 PG 15 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 390HB UT WOS:000166288700005 PM 11196013 ER PT J AU Townsend, J Westerfield, M Leaver, E Makeig, S Jung, TP Pierce, K Courchesne, E AF Townsend, J Westerfield, M Leaver, E Makeig, S Jung, TP Pierce, K Courchesne, E TI Event-related brain response abnormalities in autism: evidence for impaired cerebello-frontal spatial attention networks SO COGNITIVE BRAIN RESEARCH LA English DT Review DE spatial attention; autism; cerebellum; frontal cortex; ERP; P300 ID FUNCTIONALLY INDEPENDENT COMPONENTS; PERVASIVE DEVELOPMENTAL DISORDERS; POSTERIOR-FOSSA STRUCTURES; ORIENTING GAZE SHIFTS; INFANTILE-AUTISM; NEUROANATOMICAL ABNORMALITIES; ELECTROPHYSIOLOGIC INDICATION; CEREBROCEREBELLAR SYSTEM; AUDITORY INFORMATION; DIAGNOSTIC INTERVIEW AB Although under some conditions the attention-related late positive event-related potential (ERP) response (LPC) is apparently normal in autism during visual processing, the LPC elicited by visuospatial processing may be compromised. Results from this study provide evidence for abnormalities in autism in two components of the LPC generated during spatial processing. The early frontal distribution of the LPC which may reflect attention orienting was delayed or missing in autistic subjects during conditions in which attention was to peripheral visual fields. The later parietal distribution of the LPC which may be associated with context updating was smaller in amplitude in autistic subjects regardless of attention location. Both abnormalities suggest disruption of function in spatial attention networks in autism. Evidence that the cerebellar abnormalities in autism may underlie these deficits comes fr om: (I) similar results in ERP responses and spatial attention deficits in patients with cerebellar lesions; (2) brain-behavior correlations in normally functioning individuals associating the size of the posterior cerebellar vermis and the latency of the frontal LPC; and (3) a previously reported complementary correlation between the size of the posterior vermal lobules and spatial orienting speed. Although the scalp-recorded LPC is thought to be cortically generated, it may be modulated by subcortical neural activity. The cerebellum may serve as a modulating influence by affecting the task-related antecedent attentional process. The electrophysiological abnormalities reported here index spatial attention deficits in autism that may reflect cerebellar influence on both frontal and parietal spatial attention function. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Diego, Dept Neurosci 0217, La Jolla, CA 92093 USA. Childrens Hosp, San Diego, CA USA. Univ Illinois, Dept Psychol, Urbana, IL 61801 USA. Univ Calif San Diego, Inst Neural Computat, San Diego, CA 92103 USA. Salk Inst, La Jolla, CA USA. USN, Hlth Res Ctr, San Diego, CA 92152 USA. RP Townsend, J (reprint author), Univ Calif San Diego, Dept Neurosci 0217, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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Brain Res. PD MAR PY 2001 VL 11 IS 1 BP 127 EP 145 DI 10.1016/S0926-6410(00)00072-0 PG 19 WC Computer Science, Artificial Intelligence; Neurosciences; Neuroimaging SC Computer Science; Neurosciences & Neurology GA 409NM UT WOS:000167389800011 ER PT J AU Manning, JT Baron-Cohen, S Wheelwright, S Sanders, G AF Manning, JT Baron-Cohen, S Wheelwright, S Sanders, G TI The 2nd to 4th digit ratio and autism SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID MINOR PHYSICAL ANOMALIES; CEREBRAL LATERALIZATION; CHILDREN; PSYCHOSIS; ASYMMETRY; DISEASE; LENGTH; WOMEN AB It has been suggested that autism may arise as the result of exposure to high concentrations of prenatal testosterone. There is evidence that the ratio of the lengths of the and and 4th digit (2D:4D) may be negatively correlated with prenatal testosterone. We measured 2D:4D in 95 families recruited via the National Autistic Society, UK. The sample comprised a total 72 children with autism (62 males, 10 females; age range 2 to 14 years), including 23 children (20 males, three females) with Asperger syndrome(AS), 34 siblings, 88 fathers, 88 mothers and sex- and age-matched control participants. We found that the 2D:4D ratios of children with autism, their siblings, fathers and mothers were lower than population normative values. Children with AS, who share the social and communicative symptoms of autism but have normal or even high IQ, had higher 2D:4D ratios than children with autism but lower ratios than population normative values. There were positive associations between 2D:4D ratios of children with autism and the ratios of their relatives. Children with autism had lower than expected 2D:4D ratios and children with AS higher ratios than expected in relation to their fathers' 2D:4D ratio. 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W., 1989, WOODCOCKJOHNSON PSYC NR 30 TC 139 Z9 147 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-4930 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD MAR PY 2001 VL 43 IS 3 BP 202 EP 206 DI 10.1017/S001216220100038X PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 415DF UT WOS:000167705000011 PM 11263692 ER PT J AU Afzal, MA Minor, PD Ghosh, S Jin, L AF Afzal, MA Minor, PD Ghosh, S Jin, L TI Measles virus persistence in specimens of inflammatory bowel disease and autism cases SO DIGESTIVE DISEASES AND SCIENCES LA English DT Letter ID POLYMERASE-CHAIN-REACTION; CROHNS-DISEASE; GENOME SEQUENCE; ABSENCE; TISSUES C1 Natl Inst Biol Stand & Controls, Div Virol, Potters Bar EN6 3QG, Herts, England. Univ Edinburgh, Dept Med, Western Gen Hosp, Gastroenterol Unit, Edinburgh, Midlothian, Scotland. Cent Publ Hlth Lab, Enter & Resp Lab, London NW9 5HT, England. RP Afzal, MA (reprint author), Natl Inst Biol Stand & Controls, Div Virol, S Mimms, Potters Bar EN6 3QG, Herts, England. CR Afzal MA, 2000, J MED VIROL, V62, P377, DOI 10.1002/1096-9071(200011)62:3<377::AID-JMV10>3.0.CO;2-1 Afzal MA, 1998, J MED VIROL, V55, P243, DOI 10.1002/(SICI)1096-9071(199807)55:3<243::AID-JMV11>3.0.CO;2-H Chadwick N, 1998, J MED VIROL, V55, P305 Haga Y, 1996, GUT, V38, P211, DOI 10.1136/gut.38.2.211 IIZUKA M, 1995, LANCET, V345, P199 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 NR 6 TC 5 Z9 5 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD MAR PY 2001 VL 46 IS 3 BP 658 EP 660 DI 10.1023/A:1005632106643 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 421ZB UT WOS:000168092500035 PM 11318548 ER PT J AU Starr, EM Foy, JB Cramer, KM AF Starr, EM Foy, JB Cramer, KM TI Parental perceptions of the education of children with pervasive developmental disorders SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article ID PERSPECTIVES; STUDENTS; DISABILITIES; INCLUSION; AUTISM AB Parents of 69 children (59 male, 10 female, ranging in age from 4 to 19) with pervasive developmental disorders (PDD) were surveyed about their perceptions of and their satisfaction with the education their children were receiving. The survey examined parental perceptions related to their children's classroom environment and education team, and whether perceptions were affected depending on the children 's communication ability, class placement, age, and whether there was more than one child with PDD in the family. Kruskall-Wallis and Mann Whitney U statistics of the total scores found no significant differences across educational settings, but did find significant differences between verbal and nonverbal children, and number of children with PDD in the family on classroom environment and education team items, and for age on education team items only. Parents of nonverbal children rated the items more highly, as did parents of the youngest age group and parents of more than one child with PDD, indicating either a more positive perception or greater satisfaction with the educational system. Results were also examined in terms of how parents felt their children were progressing, their satisfaction with their child's current placement, and if they felt their children were learning useful life skills. Of 49 parents identifying needs for services or programs for their children, 14 (28.6%) identified more autism-specific education and training for school personnel working with their children as a key need. Implications for inservice training regarding the nature of PDD, home-school collaboration, and educational inclusion are discussed. C1 Univ Windsor, Fac Educ, Windsor, ON N9B 3P4, Canada. Windsor Advisory Comm Disabil Issues, Windsor, ON, Canada. RP Starr, EM (reprint author), Univ Windsor, Fac Educ, 401 Sunset Ave, Windsor, ON N9B 3P4, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARICK J, 1989, EDUC TRAIN MENT RET, V24, P371 Attwood T., 1998, ASPERGERS SYNDROME G BAILEY A, 1992, SCI PROGR EDINBURGH, V75, P389 BANG M, 1996, ANN C ASS PERS SEV H Bryson S. E., 1997, HDB AUTISM PERVASIVE, P41 Coots JJ, 1998, EDUC TRAIN MENT RET, V33, P317 de Vaus D. A., 1993, SURVEYS SOCIAL RES DONNELLAN AM, 1984, J SPEC EDUC, V18, P505 ECCLES JS, 1993, TEACH COLL REC, V94, P568 EPPS S, 1989, EDUC TRAIN MENT RET, V24, P157 FALVEY MA, 1995, INCLUSIVE HETEROGENE, P23 Folstein S., 1977, J CHILD PSYCHOL PSYC, V18, P291 FOY J, 1998, UNPUB PARENT TEACHER FRIEND M, 1998, INCLUDING EXCEPTIONA Gilliam J., 1982, BEHAV DISORDERS, V7, P189 Gray C., 1995, TEACHING CHILDREN AU, P219 Hodapp RM, 1998, EDUC TRAIN MENT RET, V33, P342 Hodgdon L., 1995, VISUAL STRATEGIES IM, V1 Jones R, 1997, FAM PRACT, V14, P3, DOI 10.1093/fampra/14.1.3 Kasari C, 1999, J AUTISM DEV DISORD, V29, P297, DOI 10.1023/A:1022159302571 Klin A., 1997, HDB AUTISM PERVASIVE, P94 Koegel R. L., 1995, TEACHING CHILDREN AU Leyser Yona, 1985, CONTEMP EDUC, V57, P38 MEYERS CE, 1987, EXCEPT CHILDREN, V53, P441 MICHAEL MG, 1992, REM SPEC EDUC, V13, P24 POWELL S, 1991, SCHOOL PSYCHOL INT, V12, P315, DOI 10.1177/0143034391124004 SALISBURY C, 1992, COLLABORATIVE TEAMS, P43 Smith T.E., 1998, TEACHING STUDENTS SP STARR E, 1998, PROFESSIONALLY SPEAK, P18 STONE WL, 1987, J PEDIATR PSYCHOL, V12, P615, DOI 10.1093/jpepsy/12.4.615 STONE WL, 1988, J AUTISM DEV DISORD, V18, P403, DOI 10.1007/BF02212195 Westling D. L., 1997, FOCUS AUTISM OTHER D, V12, P67 Westling DL, 1996, EDUC TRAIN MENT RET, V31, P86 WOLERY M, 1995, EDUC TRAIN MENT RET, V30, P15 Wolf G, 1994, Tierarztl Prax, V22, P35 NR 36 TC 10 Z9 10 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 MAR PY 2001 VL 36 IS 1 BP 55 EP 68 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 448TZ UT WOS:000169647200005 ER PT J AU Gourion, D Viot, G Goldberger, C Cartier, M Bourdel, MC Poirier, MF Olie, JP Loo, H Krebs, MO AF Gourion, D Viot, G Goldberger, C Cartier, M Bourdel, MC Poirier, MF Olie, JP Loo, H Krebs, MO TI Validation of the French version of a Minor Physical Anomalies scale in schizophrenic patients and their parents SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE development; Minor Physical Anomalies; schizophrenia ID DIAGNOSTIC INTERVIEW; SIBLINGS; FEATURES; ORIGINS AB Minor Physical Anomalies represent valuable indices of disturbance in early neurodevelopment. They are frequently observed in individuals with various brain disorders, including mental retardation, autism, epilepsy, hyperactivity, foetal alcohol syndrome and schizophrenia. The high prevalence of Minor Physical Anomalies in schizophrenia provides considerable support for a neurodevelopmental model in this disorder. However, studies in large sample using standardised scale are lacking. Such studies are needed in order to confirm their actual frequency and study the clinical correlates or morphological anomalies. Objective : The aim of this study was to revise and validate a French version of a scale designed for the evaluation of Minor Physical Anomalies in adult psychiatric patients and notably in patients with schizophrenia. Methodology : The scale was revised from the Waldrop scale. The choice of items was done on the basis of frequency, reliability in the adult, reliability of rating. Some new items, related to know syndroms with comportmental symptoms were added. Both raters had previously had a short initiation to the rating of the scale. Interrater reliability between two examiners, blind with regards to the diagnosis was evaluated. Results : The interrater reliability was good, with an intraclass correlation coefficient at 0.97. Patients had significantly more minor physical anomalies than comparison subjects, and also more Minor Physical Anomalies than their parents. Fathers and mothers of these schizophrenic patients had significantly more Minor Physical Anomalies than normal comparison subjects. Conclusion: Although the evaluation of physical anomalies relies on subjective appreciation of normal vs abnormal, the revised Version of minor physical anomalies scale (French version) was found to be a reliable tool, provided that a short initiation to the rating is performed. The scale differentia ted schizophrenic patients from their parents, and the latter from the normal controls. A lot of questions remains unanswered concerning the neurodevelopmental hypothesis of schizophrenia. This scale appeared as a useful complementary tool to help in the determination of the developmental phenotypic status of the patients enrolled in pathophysiological studies aiming the identification of developmental factors in schizophrenia. C1 Univ Paris, Lab Psychiat Biol, SHU, Hop St Anne, F-75014 Paris, France. Grp Hosp Cochin St Vincent Paul, Serv Prof D Cabrol, F-75014 Paris, France. 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Psychiatr. Clin. Biol. Ther. PD MAR-APR PY 2001 VL 27 IS 2 BP 143 EP 147 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 439DE UT WOS:000169094900005 PM 11407266 ER PT J AU Noterdaeme, M Amorosa, H Mildenberger, K Sitter, S Minow, F AF Noterdaeme, M Amorosa, H Mildenberger, K Sitter, S Minow, F TI Evaluation of attention problems in children with autism and children with a specific language disorder SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; language disorder; attention; neuropsychology ID LONG-TERM CONSISTENCY; EXECUTIVE FUNCTION; BEHAVIOR CHECKLIST; SPEECH/LANGUAGE PROFILES; IMPAIRED CHILDREN; DEFICITS; COMPREHENSION; INDIVIDUALS; ABILITIES; DYSPHASIA AB Children with autism and children with a specific language disorder show additional attention deficits. The literature on the neuropsychological investigation of attention in both groups of children suggests that the nature of their attention problems might be different. The purpose of this study is to examine the attention test profiles in these two groups of children with developmental disorders. Nineteen children and adolescents with autism, 17 subjects with a specific language disorder and 19 control subjects participated in the study. Non-verbal intelligence was normal for all subjects. The "Testbatterie zur Aufmerksamkeitsprufung" was administered to all subjects. This instrument provides the possibility to examine a wide range of attention functions and executive functions. The results showed that the autistic individuals had deficits in executive functions, whereas the language impaired children had deficits in auditory sustained attention, in auditory selective attention, and in the domain of executive functions. It is concluded that although both groups of developmentally impaired subjects showed attention problems, the deficits are not the same in both groups. The different neuropsychological profiles probably reflect different mechanisms in the pathogenesis of the attention deficits in both types of developmental disorders. C1 Heckscher Klin Kinder & Jugendpsychiat, Abt Teilleistungs & Verhaltensgestorte Kinder, D-81479 Munich, Germany. Univ Munich, Inst Kinder & Jugendpsychiat, Munich, Germany. Univ Munich, Inst Soziale Padiatrie, Munich, Germany. RP Noterdaeme, M (reprint author), Heckscher Klin Kinder & Jugendpsychiat, Abt Teilleistungs & Verhaltensgestorte Kinder, Wolfratshauser Str 350, D-81479 Munich, Germany. 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Child Adolesc. Psych. PD MAR PY 2001 VL 10 IS 1 BP 58 EP 66 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 417FX UT WOS:000167825700008 PM 11315537 ER PT J AU Allen, DA Steinberg, M Dunn, M Fein, D Feinstein, C Waterhouse, L Rapin, I AF Allen, DA Steinberg, M Dunn, M Fein, D Feinstein, C Waterhouse, L Rapin, I TI Autistic disorder versus other pervasive developmental disorders in young children: same or different? SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; subgroups; diagnosis; specificity; cognition ID CLUSTER-ANALYSIS; CLASSIFICATION; SUBGROUPS AB Eighteen preschool children diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders Third Edition Revised (DSM III-R) as having Pervasive Developmental Disorder-Not Otherwise Specified (PDD-NOS) were compared to 176 children with DSM III-R Autistic Disorder (AD), and to 311 non-autistic children with developmental language disorders (DLD) (N = 201) or low IQ (N = 110). All children were partitioned into "high" and "low" cognitive subgroups at a nonverbal IQ of 80. Within cognitive subgroups, the 18 PDD-NOS children did not differ significantly from either the DLD or the AD children in verbal and adaptive skills and obtained scores intermediate between those of these groups. The PDD-NOS did not differ from the AD children in maladaptive behaviors, Both the PDD-NOS and AD children had many more of these behaviors than the non-autistic comparison groups. Children in the "high" and "low" cognitive subgroups of AD, but not of PDD-NOS, differed substantially on most measures, with the children with lower cognitive scores significantly more impaired on all measures. Similarity of PDD-NOS children to AD children in maladaptive behaviors and an intermediate position between autistic and non-autistic groups on virtually all measures explains the difficulty clinicians encounter in classifying children with PDD and raises questions about the specificity of these diagnostic subtypes of the autistic spectrum. C1 Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, Rose F Kennedy Ctr Res Mental Retardat Human Dev, Bronx, NY 10461 USA. New Jersey Med Coll, Child Behav Study, Trenton, NJ USA. Stanford Univ, Sch Med, Dept Psychiat, Div Child Psychiat, Stanford, CA 94305 USA. Univ Connecticut, Dept Psychol, Storrs, CT USA. Marymount Coll, Dept Psychol, Tarrytown, NY USA. Albert Einstein Coll Med, Dept Psychiat, Div Child Psychiat, Bronx, NY 10467 USA. RP Rapin, I (reprint author), Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, Rose F Kennedy Ctr Res Mental Retardat Human Dev, 1300 Morris Pk Ave, Bronx, NY 10461 USA. CR ALLEN DA, 1988, J CHILD NEUROL, V3, pS48 American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association (APA), 1980, DIAGN STAT MAN MENT APA, 1987, DIAGN STAT MAN MENT BARTAK L, 1976, J AUTISM CHILD SCHIZ, V6, P109, DOI 10.1007/BF01538054 Bayley N., 1969, BAYLEY SCALES INFANT Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 BURACK JA, 1992, J CHILD PSYCHOL PSYC, V33, P607, DOI 10.1111/j.1469-7610.1992.tb00894.x Cohen D. 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Y., 1992, HIGH FUNCTIONING IND, P11 VOLKMAR FR, 1998, TXB PEDIAT NEUROPSYC, P429 VOLKMAR FR, 1988, PSYCHOL MED, V18, P191 VOLKMAR FR, 1997, HDB AUTISM PERVASIVE, P1 Waterhouse L, 1996, J AUTISM DEV DISORD, V26, P59, DOI 10.1007/BF02276235 Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 World Health Organization, 1993, MENT DIS GLOSS GUID NR 39 TC 18 Z9 18 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PLATZ DER DEUTSCHEN EINHEIT 25, D-64293 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD MAR PY 2001 VL 10 IS 1 BP 67 EP 78 PG 12 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 417FX UT WOS:000167825700009 PM 11315538 ER PT J AU Njiokiktjien, C Verschoor, A de Sonneville, L Huyser, C Veld, VOH Toorenaar, N AF Njiokiktjien, C Verschoor, A de Sonneville, L Huyser, C Veld, VOH Toorenaar, N TI Disordered recognition of facial identity and emotions in three Asperger type autists SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Asperger's syndrome; autism; facial emotion; right hemisphere deficit ID RIGHT-HEMISPHERE; CHILDS APPRAISAL; FUNCTIONAL MRI; EXPRESSIONS; PERCEPTION; DISGUST; PERFORMANCE; LANGUAGE; FACES AB In this report we aim to explore severe deficits in facial affect recognition in three boys all of whom meet the criteria of Asperger's syndrome (AS), as well as overt prosopagnosia in one (B) and covert prosopagnosia in the remaining two (C and D). Subject B, with a familially-based talent of being highly gifted in physics and mathematics, showed no interest in people, a quasi complete lack of comprehension of emotions, and very poor emotional reactivity. The marked neuropsychological deficits were a moderate prosopagnosia and severely disordered recognition of facial emotions, gender and age. Expressive facial emotion, whole body psychomotor expression and speech prosody were quasi absent as well. In all three boys these facial processing deficits were more or less isolated, and general visuospatial functions, attention, formal language and scholastic performances were normal or even highly developed with the exception of deficient gestalt perception in B. We consider the deficient facial emotion perception as an important pathogenetic symptom for the autistic behaviour in the three boys. Prosopagnosia, the absent facial and bodily expression, and speech prosody were important but varying co-morbid disorders. The total clinical picture of nonverbal disordered communication is a complex of predominantly bilateral and/or right hemisphere cortical deficits. Moreover, in B, insensitivity to pain, smells, noises and internal bodily feelings suggested a more general emotional anaesthesia and/or a deficient means of expression. It is possible that a limbic component might be involved, thus making affective appreciation also deficient. C1 Free Univ Amsterdam Hosp, Pediat Outpatients Clin, NL-1007 MB Amsterdam, Netherlands. Inst Child & Adolescent Psychiat, Triversum, NL-1817 EZ Alkmaar, Netherlands. RP Njiokiktjien, C (reprint author), Free Univ Amsterdam Hosp, Pediat Outpatients Clin, POB 7057, NL-1007 MB Amsterdam, Netherlands. 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Child Adolesc. Psych. PD MAR PY 2001 VL 10 IS 1 BP 79 EP 90 PG 12 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 417FX UT WOS:000167825700010 PM 11315539 ER PT J AU Lucas, P AF Lucas, P TI John Howard and Asperger's syndrome: psychopathology and philanthropy SO HISTORY OF PSYCHIATRY LA English DT Article AB John Howard's (1726-1790) motives as a prison reformer appear obscure and a sense of his personality remains elusive. Biographies and contemporary texts suggest this is not merely the effect of historical distance: John Howard was considered eccentric by many of his contemporaries. It is suggested that Howard suffered from Asperger's Syndrome (AS), a disorder allied to autism. Sufferers may have high intelligence but characteristically,manifest impairments in social, communicative and imaginative functioning with inflexible thinking and an often fanatical preoccupation with a narrow special interest. The hypothesis may help explain enigmatic aspects of Howard's career and personal life, as well as our difficulty forming a sense of his identity. The correspondence between Howard's idiosyncratic perspective, putatively related to AS, and the direction of the profound 'disciplinary' transformation of eighteenth-century society is highlighted. C1 N London Forens Serv, Enfield EN2 8JL, Middx, England. RP Lucas, P (reprint author), N London Forens Serv, Hadley Lodge,Chase Farm Hosp Site,Ridgeway, Enfield EN2 8JL, Middx, England. 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Psychiatr. PD MAR PY 2001 VL 12 IS 45 BP 73 EP 101 DI 10.1177/0957154X0101204504 PN 1 PG 29 WC History Of Social Sciences; Psychiatry SC Social Sciences - Other Topics; Psychiatry GA 449LN UT WOS:000169686200004 ER PT J AU Elgar, K Campbell, R AF Elgar, K Campbell, R TI The development of face-identification skills: What lies behind the face module? SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE autism; face recognition; Tuner syndrome; Williams syndrome ID WILLIAMS-SYNDROME; TURNERS-SYNDROME; AUTISM; CHILDREN; ACTIVATION; STIMULI; CORTEX; MIND; RECOGNITION; PATTERNS C1 UCL, Behav Sci Unit, Inst Child Hlth, London WC1N 1EH, England. UCL, Dept Human Commun Sci, London, England. RP Elgar, K (reprint author), UCL, Behav Sci Unit, Inst Child Hlth, 30 Guilford St, London WC1N 1EH, England. 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PD MAR-JUN PY 2001 VL 10 IS 1-2 BP 25 EP 30 DI 10.1002/icd.242 PG 6 WC Psychology, Developmental SC Psychology GA 427TU UT WOS:000168422200005 ER PT J AU Nicoll, A AF Nicoll, A TI Benefits, safety, and risks of immunisation programmes SO INTERDISCIPLINARY SCIENCE REVIEWS LA English DT Article ID INFLAMMATORY BOWEL-DISEASE; VACCINE SAFETY; MEASLES VACCINATION; ADVERSE REACTIONS; UNITED-STATES; IMMUNIZATION; PERTUSSIS; CHILDREN; AUTISM; DATALINK AB Immunisation is potentially the most effective and efficient of all preventive medical activities. It is also unique among interventions in that it protects both the individual and the community. The UK's immunisation programme has been highly successful in controlling a number of life threatening infectious diseases, and consequently public concern has shifted from the diseases to vaccine safety. In recent years a series of vaccine myths and vaccine safety scares have affected the UK and other industrialised countries. Although an effective vaccine without any risk is probably unachievable, the vaccines in use in the UK are very safe. Serious adverse outcomes truly attributable to vaccination are extremely rare, always far rarer than adverse outcomes among individuals acquiring the vaccines' target infections. Vaccine safety may be called into question, however, on the basis of spurious coincidental associations between vaccination and adverse events. An inadequate public health response in the 1970s to a scare over whooping cough vaccine allowed substantial losses of professional and public confidence to take place. Vaccine coverage halved and much preventable morbidity and mortality resulted. Plausible vaccine associations must be investigated thoroughly, and the UK has become a world leader in developing techniques for rapid investigations. The public health response to scares over MMR (measles, mumps, and rubella) vaccine safety has been faster and firmer than for whooping cough and no link has been found between MMR vaccine and inflammatory bowel disease or autism. Consequently the impact on immunisation coverage has been small, though the cumulative threat of measles, mumps, and rubella epidemics is growing. Recently an international investigation excluded a possible association of intussusception with oral polio vaccine before it could become a vaccine scare. A clearer chain of communication in responding to vaccine myths and scares is needed. This must provide rapid information and, if appropriate, reassurance to professionals and the public. Considerably more training is needed for professionals in providing information to the public and supporting parents in making difficult decisions over vaccination. 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Sci. Rev. PD SPR PY 2001 VL 26 IS 1 BP 20 EP 30 PG 11 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA 439ZL UT WOS:000169147700006 ER PT J AU Bernard-Opitz, V Kwook, KW Sapuan, S AF Bernard-Opitz, V Kwook, KW Sapuan, S TI Epidemiology of autism in Singapore: findings of the first autism survey SO INTERNATIONAL JOURNAL OF REHABILITATION RESEARCH LA English DT Article DE autism; epidemiology; Singapore ID INFANTILE-AUTISM; DISORDERS; DIAGNOSIS; LANGUAGE; CHILDREN; JAPAN AB The report describes the results of a survey conducted on 176 parents of children with autism in Singapore. The ages of the children ranged from 3 to 12 years. The survey focused on the child's background, behaviour problems and skill profile, the home and school situation as well as the linguistic and social background. It was noted that the Singapore population confirms the international distribution regarding a predominance of boys over girls and a low incidence of birth complications. A positive trend noted was the fact that 60% of the children were diagnosed before the age of 3 years. Discussion focuses on possible risk factors and psychosocial adversities for autism such as a high frequency of caregivers who are foreign maids, the use of multiple languages and the high level of punitive educational practices. The possible influence of psychosocial deprivation on child development is discussed. International Journal of Rehabilitation Research 24:1-6 (C) 2001 Lippincott Williams & Wilkins. C1 Natl Univ Singapore, Dept Social Work & Psychol, Singapore 119260, Singapore. RP Bernard-Opitz, V (reprint author), Natl Univ Singapore, Dept Social Work & Psychol, 10 Kent Ridge Crescent, Singapore 119260, Singapore. CR BERNARDOPITZ V, 1993, AUTISM NEWS SINGAPOR, V1, P9 BERNARDOPITZ V, 1996, 24 DEP SOC WORK PSYC BRYSON SE, 1988, J CHILD PSYCHOL PSYC, V29, P433, DOI 10.1111/j.1469-7610.1988.tb00735.x Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 BRYSON SE, 1988, J AM ACAD CHILD PSY, V27, P418, DOI 10.1097/00004583-198807000-00006 CHUNG SY, 1990, J AUTISM DEV DISORD, V20, P221, DOI 10.1007/BF02284720 CREAK M, 1960, J CHILD PSYCHOL PSYC, V1, P156, DOI 10.1111/j.1469-7610.1960.tb01990.x Cryan E, 1996, J AUTISM DEV DISORD, V26, P453, DOI 10.1007/BF02172829 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 1998, AUTISM PERVASIVE DEV, P32 FRASER A, 1987, INTELLECTUAL DISABIL, P350 GILLBERG C, 1982, J AUTISM DEV DISORD, V12, P223, DOI 10.1007/BF01531368 GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x GOH CW, 1980, ANN ACAD MED, V8, P252 HOWLIN P, 1998, AUTISM, V2, P205, DOI 10.1177/1362361398022008 Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 HOWLIN P, 1999, EV PROBL SEM TREATM Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Joel R.Arick, 1978, AUTISM SCREENING INS KASARI C, 1993, DEV PSYCHOPATHOL, V5, P403, DOI 10.1017/S0954579400004491 KOBAYASHI R, 1992, J AUTISM DEV DISORD, V22, P395, DOI 10.1007/BF01048242 Kong S G, 1986, J Singapore Paediatr Soc, V28, P94 Lotter V, 1967, SOCIAL PSYCHIATRY, V1, P163, DOI 10.1007/BF00578950 Prizant BM, 1996, J AUTISM DEV DISORD, V26, P173, DOI 10.1007/BF02172007 RITVO ER, 1983, J AM ACAD CHILD PSY, V22, P549, DOI 10.1097/00004583-198311000-00006 RUTTER M, 1978, J AUTISM CHILD SCHIZ, V8, P139, DOI 10.1007/BF01537863 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P537, DOI 10.1017/S0021963099003935 Siegel B., 1996, WORLD AUTISTIC CHILD Sponheim E, 1998, J AUTISM DEV DISORD, V28, P217, DOI 10.1023/A:1026017405150 TANOUE Y, 1988, J AUTISM DEV DISORD, V18, P155, DOI 10.1007/BF02211943 Tao K, 1982, J CHINESE NEUROPSYCH, V2, P104 TAO KT, 1987, J AUTISM DEV DISORD, V17, P289 Wing L., 1997, AUTISM, V1, P13, DOI 10.1177/1362361397011004 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 NR 34 TC 4 Z9 5 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 MAR PY 2001 VL 24 IS 1 BP 1 EP 6 DI 10.1097/00004356-200103000-00001 PG 6 WC Rehabilitation SC Rehabilitation GA 414XJ UT WOS:000167691200001 PM 11302459 ER PT J AU Ganz, J AF Ganz, J TI Teaching children with autism to mind-read: A practical guide SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Book Review C1 Univ Kansas, Lawrence, KS 66045 USA. RP Ganz, J (reprint author), Univ Kansas, Lawrence, KS 66045 USA. CR Howlin P., 1999, TEACHING CHILDREN AU NR 1 TC 0 Z9 0 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1053-4512 J9 INTERV SCH CLIN JI Interv. Sch. Clin. PD MAR PY 2001 VL 36 IS 4 BP 245 EP 246 PG 2 WC Education, Special SC Education & Educational Research GA 405LW UT WOS:000167162000013 ER PT J AU Davidovitch, M Holtzman, G Tirosh, E AF Davidovitch, M Holtzman, G Tirosh, E TI Autism in the Haifa area - An epidemiological perspective SO ISRAEL MEDICAL ASSOCIATION JOURNAL LA English DT Article DE autism; pervasive developmental disorder; incidence; epidemiology; Israel ID PREVALENCE; CHILDREN; DISORDER AB Background: Autism is a pervasive developmental disorder. The incidence rate and other related epidemiological characteristics of the Israeli population are not available. Objectives: To assess the incidence rate of autism in the Haifa area and to compare family characteristics with previous reports from other countries. Methods: We approached facilities in the Haifa area that are involved with the diagnosis and treatment of autism. The study group comprised children born between 1989 and 1993. Records of the children were scrutinized and 69% of the mothers were interviewed. Live-birth cohorts of the same years were employed for incidence computation. Results: An incidence rate of 1/1,000 was derived. Male to female ratio was 4.2:1. Pregnancy and perinatal periods were mostly uneventful. A low prevalence of developmental and emotional morbidity was reported for family members. Conclusions: The epidemiological characteristics found in the Haifa area are similar to those reported from non-Israeli communities. This finding supports an underlying biological mechanism for this disorder. These data can be used for future trend analyses in Israel. C1 Bnai Zion Med Ctr, Hannah Khousy Child Dev Ctr, IL-31048 Haifa, Israel. Technion Israel Inst Technol, Rappoport Fac Med, IL-31096 Haifa, Israel. RP Davidovitch, M (reprint author), Bnai Zion Med Ctr, Hannah Khousy Child Dev Ctr, 47 Golomb St,POB 4940, IL-31048 Haifa, Israel. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x GILLBERG C, 1992, DEV MED CHILD NEUROL, V34, P389 Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 Irie Norio, 1999, No To Hattatsu, V31, P32 NELSON KB, 1991, PEDIATRICS, V87, P761 Piven J, 1999, AM J PSYCHIAT, V156, P557 RITVO ER, 1989, AM J PSYCHIAT, V146, P194 Webb EVJ, 1997, DEV MED CHILD NEUROL, V39, P150 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 11 TC 22 Z9 22 PU ISRAEL MEDICAL ASSOC JOURNAL PI RAMAT GAN PA 2 TWIN TOWERS, 11TH FL, 35 JABOTINSKY ST, PO BOX 3604, RAMAT GAN 52136, ISRAEL SN 1565-1088 J9 ISRAEL MED ASSOC J JI Isr. Med. Assoc. J. PD MAR PY 2001 VL 3 IS 3 BP 188 EP 189 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 425XA UT WOS:000168315900007 PM 11303376 ER PT J AU Sarokoff, RA Taylor, BA Poulson, CL AF Sarokoff, RA Taylor, BA Poulson, CL TI Teaching children with autism to engage in conversational exchanges: Script fading with embedded textual stimuli SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; script fading; language acquisition; developmental disabilities; antecedent control AB A multiple baseline across three sets of stimuli was used to assess the effects of a script-fading procedure using embedded text to teach 2 children with autism to engage in conversation statements about the stimuli. Both students stated all the scripted statements, and unscripted statements also increased. Generalization was assessed with novel peers and with untrained stimuli. C1 Alpine Learning Grp, Paramus, NJ 07652 USA. CUNY Grad Sch & Univ Ctr, New York, NY 10036 USA. RP Taylor, BA (reprint author), Alpine Learning Grp, 777 Paramus Rd, Paramus, NJ 07652 USA. CR Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 NR 2 TC 37 Z9 37 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 2001 VL 34 IS 1 BP 81 EP 84 DI 10.1901/jaba.2001.34-81 PG 4 WC Psychology, Clinical SC Psychology GA 414CZ UT WOS:000167649500010 PM 11317993 ER PT J AU Kern, JK Miller, VS Cauller, L Kendall, R Mehta, J Dodd, M AF Kern, JK Miller, VS Cauller, L Kendall, R Mehta, J Dodd, M TI Effectiveness of N,N-dimethylglycine in autism and pervasive developmental disorder SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID DIMETHYLGLYCINE DEHYDROGENASE; IMMUNE-RESPONSE; T-CELLS; PROTEIN; ASSOCIATION; DEFICIENCY; METABOLISM; CHILDREN; BETAINE; SERUM AB N,N-dimethylglycine, a dietary supplement, has been reported to be beneficial in children with autism and pervasive developmental disorder. We examined the effectiveness of dimethylglycine in children with autism and pervasive developmental disorder in a double-blind, placebo-controlled study Thirty-seven children between 3 and 11 years of age with a diagnosis of autism and/or pervasive developmental disorder were gender and age matched and randomly assigned to receive either placebo or dimethylglycine for 4 weeks. All children were assessed before and after treatment on two behavioral measures, the Vineland Maladaptive Behavior Domain and the Aberrant Behavior Checklist. Standardized neurologic examinations before and after treatment on 33 children showed no change. An overall improvement on all behavioral measures was observed for both the placebo and the dimethylglycine groups. However, the improvement among the children who received dimethylglycine was not statistically different from the improvement observed among the children who received the placebo. The children who participated in this study were a heterogeneous group; and their apparent responses to the dimethylglycine varied. Some children appeared to respond positively to the dimethylglycine, and there was a smaller proportion of negative changes in the dimethylglycine group, but the quantitative changes in the dimethylglycine behavioral assessments were not significantly different from what was observed among children who received placebo. C1 Univ Texas, SW Med Ctr, Dept Human Dev, Dallas, TX 75235 USA. Univ Texas, SW Med Ctr, Dept Pediat Neurol, Dallas, TX 75235 USA. Univ Bridgeport, Dept Biochem, Bridgeport, CT USA. RP Kern, JK (reprint author), Univ Texas, SW Med Ctr, Dept Human Dev, 5323 Harry Hines Blvd,Suite 520,St Paul Profess B, Dallas, TX 75235 USA. 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Child Neurol. PD MAR PY 2001 VL 16 IS 3 BP 169 EP 173 DI 10.1177/088307380101600303 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 473DV UT WOS:000171025500003 PM 11305684 ER PT J AU Happe, F Briskman, J Frith, U AF Happe, F Briskman, J Frith, U TI Exploring the cognitive phenotype of autism: Weak "central coherence" in parents and siblings of children with autism: I. Experimental tests SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Asperger's disorder; autistic disorder; behavioural phenotypes; cognition; genetics; visuospatial functioning ID SEX-DIFFERENCES; SUBCLINICAL MARKERS; EMBEDDED FIGURES; WISC-R; PERFORMANCE; MIND; INDIVIDUALS; RELATIVES; PATTERNS; FAMILIES AB Previous twin and family studies have indicated that there are strong genetic influences in the etiology of autism, and provide support for the notion of a broader phenotype in first-degree relatives. The present study explored this phenotype in terms of one current cognitive theory of autism. Parents and brothers of boys with autism. boys with dyslexia, and normal boys were given tests of "central coherence", on which children with autism perform unusually well due to an information-processing bias favouring part/detail processing over processing of wholes/meaning. Results indicated that fathers of boys with autism, as a group, showed piecemeal processing across four tests of central coherence. This was not true for any other group. These findings raise the possibility that the broader autism phenotype may include a "cognitive style" (weak central coherence) that can confer information-processing advantages. C1 Kings Coll London, Inst Psychiat, London WC2R 2LS, England. UCL, Inst Cognit Neurosci, London WC1E 6BT, England. RP Happe, F (reprint author), SGDP Res Ctr, Inst Psychiat, 111 Denmark Hill, London SE5 8AF, England. 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F., 1965, WIDE RANGE ACHIEVEME JENSEN AR, 1983, PERS INDIV DIFFER, V4, P223, DOI 10.1016/0191-8869(83)90029-6 Kanner L, 1943, NERV CHILD, V2, P217 LANDA R, 1991, J SPEECH HEAR RES, V34, P1339 LYNN R, 1991, PERS INDIV DIFFER, V12, P1179, DOI 10.1016/0191-8869(91)90082-M MINTON J, 1982, J AM ACAD CHILD PSY, V21, P256, DOI 10.1016/S0002-7138(09)60880-3 OZONOFF S, 1993, J AUTISM DEV DISORD, V23, P429, DOI 10.1007/BF01046049 Piven J, 1997, AM J PSYCHIAT, V154, P185 Russel J., 1997, AUTISM EXECUTIVE DIS SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 SMALLEY SL, 1990, J AUTISM DEV DISORD, V20, P271, DOI 10.1007/BF02284724 Snowlings M., 1997, J RES READ, V20, P31, DOI DOI 10.1111/1467-9817.00018 SZATMARI P, 1993, J AM ACAD CHILD PSY, V32, P1264, DOI 10.1097/00004583-199311000-00022 VOGEL SA, 1987, ANN DYSLEXIA, V37, P142, DOI 10.1007/BF02648064 Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D, 1981, WECHSLER ADULT INTEL Witkin HA, 1971, MANUAL EMBEDDED FIGU YIRMIYA N, 2000, UNPUB COMPARISON SIB NR 46 TC 153 Z9 155 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 MAR PY 2001 VL 42 IS 3 BP 299 EP 307 DI 10.1111/1469-7610.00723 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 433QC UT WOS:000168770400003 PM 11321199 ER PT J AU Briskman, J Happe, F Frith, U AF Briskman, J Happe, F Frith, U TI Exploring the cognitive phenotype of autism: Weak "central coherence" in parents and siblings of children with autism: II. Real-life skills and SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Asperger's disorder; autistic disorder; behavioural phenotypes; cognition ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY-HISTORY; RELATIVES; MIND AB information on everyday life activities and preferences in both social and nonsocial domains was obtained From parents and children who had taken part in an experimental study of central coherence. Comparisons were made between parents who had a son with autism, parents with a dyslexic son, and families without a history of developmental disorder, as well as the male siblings in these families. Data on everyday preferences and abilities were elicited by means of an experimental questionnaire. Significant group differences in social and nonsocial preferences were found, suggesting that some parents showed similarities with their son with autism, in preference for nonsocial activities and ability in detail-focused processing. A similar experimental questionnaire, completed by parents on behalf of their sons. discriminated between autism group probands and controls. but did not differentiate sibling groups. The relevance of the nonsocial items to central coherence is discussed in the light of the findings in Part I: autism parents who reported more autism-related nonsocial (but not social) preferences. tended to show a piecemeal processing style on the experimental tasks. C1 Kings Coll London, Inst Psychiat, London WC2R 2LS, England. UCL, Inst Cognit Neurosci, London, England. RP Happe, F (reprint author), SGDP Res Ctr, Inst Psychiat, 111 Denmark Hill, London SE5 8AF, England. RI Frith, Uta/C-1757-2008; Happe, Francesca/D-5544-2012 OI Frith, Uta/0000-0002-9063-4466; CR Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 Baron-Cohen S, 1997, ADV INFANCY RES, V11, P193 BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 BARONCOHEN S, J AUTISM DEV DISORDE Baron-Cohen S., 1998, AUTISM, V2, P296, DOI 10.1177/1362361398023008 Baron-Cohen Simon, 1997, AUTISM, V1, P101, DOI 10.1177/1362361397011010 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Happe F, 2001, J CHILD PSYCHOL PSYC, V42, P299, DOI 10.1111/1469-7610.00723 Happe FGE, 1997, BRIT J DEV PSYCHOL, V15, P1 Jarrold C, 2000, DEV PSYCHOL, V36, P126, DOI 10.1037/0012-1649.36.1.126 Piven J, 1997, AM J MED GENET, V74, P398, DOI 10.1002/(SICI)1096-8628(19970725)74:4<398::AID-AJMG11>3.0.CO;2-D Piven J, 1997, AM J PSYCHIAT, V154, P185 SANTANGELO S, 1999, NEURODEVELOPMENTAL D SZATMARI P, 1993, J AM ACAD CHILD PSY, V32, P1264, DOI 10.1097/00004583-199311000-00022 SZATMARI P, 1995, AM J MED GENET, V60, P282, DOI 10.1002/ajmg.1320600405 YIRMIYA N, 2000, UNPUB COMPARISON SIB NR 19 TC 55 Z9 55 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 MAR PY 2001 VL 42 IS 3 BP 309 EP 316 DI 10.1111/1469-7610.00724 PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 433QC UT WOS:000168770400004 PM 11321200 ER PT J AU Russell, J Hill, EL AF Russell, J Hill, EL TI Action-monitoring and intention reporting in children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; cognition; executive functions; false belief task; intention; theory of mind ID MIND; REPRESENTATION; INDIVIDUALS; CONCEPTION; DISORDERS AB The "mindblindness" theory of core cognitive impairment in autism and at least one of the executive theories of the core cognitive deficit both predict that children with autism should find it difficult to report what their intention was when it diverged from an outcome. The former predicts this because it takes intention reporting to require a "theory of mind" and the latter predicts it because the theory posits an impairment in the monitoring of goal-directed actions. The latter also predicts impairments in the ability to monitor basic actions Our three studies failed to support either of these views. Experiment 1 demonstrated intact abilities in the monitoring of basic actions (detecting which stimulus of a number of stimuli one is controlling). Experiment 2 demonstrated intact abilities in reporting an intention. both for self and for another agent, when the outcome was unintended but desired. in Experiment 3, using the novel " transparent intentions task ", we found (with a minor qualification) intact ability in reporting on nonballistic intended actions when the result that the action achieved was unexpected. The implications of these results for views of the relation between theory of mind and executive difficulties in autism are discussed. 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 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASTINGTON JW, 1990, 20 ANN S J PIAG SOC BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BEAL CR, 1990, BRIT J DEV PSYCHOL, V8, P393 BIRO S, 2001, DEV PSYCHOPATHOL, V13, P95 Bishop D. V. 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Child Psychol. Psychiatry Allied Discip. PD MAR PY 2001 VL 42 IS 3 BP 317 EP 328 DI 10.1017/S0021963001006874 PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 433QC UT WOS:000168770400005 PM 11321201 ER PT J AU Jordan, R AF Jordan, R TI Parents' education as autism therapists: Applied behaviour analysis in context. SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Book Review CR KEENAN M, 2000, PARENTS EDUC AUTIMS NR 1 TC 4 Z9 4 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-9863 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD MAR PY 2001 VL 42 IS 3 BP 421 EP 421 DI 10.1017/S0021963001216795 PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 433QC UT WOS:000168770400015 ER PT J AU Rapport, MD AF Rapport, MD TI Bridging theory and practice: Conceptual understanding of treatments for children with attention deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), autism, and depression SO JOURNAL OF CLINICAL CHILD PSYCHOLOGY LA English DT Article AB Serves as an introduction to a special edition of the journal on bridging theory and clinical practice for childhood disorders. Issues concerning the current trend of developing and evaluating new treatments devoid of a theoretical perspective are discussed. A conceptual model of child psychopathology is presented to illustrate the relevance and interplay between theory and the design and evaluation of treatments with particular emphasis on the selection and measurement of target behaviors. The means by which theory and empirical evidence interact and their relevance to understanding particular childhood disorders are discussed and emphasize the need for theoretical and conceptual models that describe the linkages among hypothesized brain substrates, cognitive function, behavior. and the environment to augment the development of potent biological and psychological interventions. C1 Univ Cent Florida, Dept Psychol, Orlando, FL 32816 USA. RP Rapport, MD (reprint author), Univ Cent Florida, Dept Psychol, POB 161390, Orlando, FL 32816 USA. 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PD MAR PY 2001 VL 30 IS 1 BP 3 EP 7 DI 10.1207/S15374424JCCP3001_2 PG 5 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 418MF UT WOS:000167895400001 PM 11294075 ER PT J AU Koegel, RL Koegel, LK McNerney, EK AF Koegel, RL Koegel, LK McNerney, EK TI Pivotal areas in intervention for autism SO JOURNAL OF CLINICAL CHILD PSYCHOLOGY LA English DT Review ID INTENSIVE BEHAVIORAL TREATMENT; MANAGEMENT TREATMENT PACKAGE; MENTALLY-RETARDED CHILDREN; SELF-MANAGEMENT; YOUNG-CHILDREN; DISRUPTIVE BEHAVIOR; PRESCHOOL-CHILDREN; TEACHING-CHILDREN; SOCIAL-BEHAVIOR; STIMULUS OVERSELECTIVITY AB Discusses several core pivotal areas that appear to be influential in intervention for autism. Literature and outcome data are reviewed with respect to several core areas that appear to be particularly helpful in intervention for autism, including improving motivation, responsivity to multiple cues, self-management, and self-initiation of social interactions. 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Clin. Child Psychol. PD MAR PY 2001 VL 30 IS 1 BP 19 EP 32 DI 10.1207/S15374424JCCP3001_4 PG 14 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 418MF UT WOS:000167895400003 PM 11294074 ER PT J AU Volkmar, FR AF Volkmar, FR TI Pharmacological interventions in autism: Theoretical and practical issues SO JOURNAL OF CLINICAL CHILD PSYCHOLOGY LA English DT Article ID INFANTILE-AUTISM; BEHAVIORAL SYMPTOMS; CHILDREN; FENFLURAMINE; HALOPERIDOL; NALTREXONE; ADULTS; PLACEBO; TRIAL; HYDROCHLORIDE AB Focused on issues of drug treatment in relation to autism. Pharmacological treatment studies in autism are complicated by various factors including a tremendous range of syndrome expression, a lack of robust animal models of the disorder, and various methodological problems. Theories have tended to follow treatments, and various neurochemical systems have been the focus of study. Neurochemical systems potentially implicated include those involving dopamine, norepinephrine, serotonin, and neuropeptides. The dopaminergic system has been the most extensively studied. Treatments developed are effective relative to certain disabling symptoms but "core" problems (e.g., in social relatedness and communication) appear less responsive to medications. The development of new approaches to assessment, including integration of behavioral and pharmacological approaches, is an important research priority. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Volkmar, FR (reprint author), Yale Univ, Ctr Child Study, POB 207900, New Haven, CT 06520 USA. 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Child Psychol. PD MAR PY 2001 VL 30 IS 1 BP 110 EP 113 DI 10.1207/S15374424JCCP3001_12 PG 4 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 418MF UT WOS:000167895400011 PM 11294068 ER PT J AU Adolphs, R Sears, L Piven, J AF Adolphs, R Sears, L Piven, J TI Abnormal processing of social information from faces in autism SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID HUMAN AMYGDALA; FACIAL EXPRESSIONS; ASPERGER-SYNDROME; WILLIAMS-SYNDROME; RECOGNITION; BRAIN; CHILDREN; EMOTION; DAMAGE; NEUROANATOMY AB Autism has been thought to be characterized, in part, by dysfunction in emotional and social cognition, but the pathology of the underlying processes and their neural substrates remain poorly understood. Several studies have hypothesized that abnormal amygdala function may account for some of the impairments seen in autism, specifically, impaired recognition of socially relevant information from faces. We explored this issue in eight high-functioning subjects with autism in four experiments that assessed recognition of emotional and social information, primarily from faces. All tasks used were identical to those previously used in studies of subjects with bilateral amygdala damage, permitting direct comparisons. All subjects with autism made abnormal social judgments regarding the trustworthiness of faces; however, all were able to make normal social judgments from lexical stimuli, and all had a normal ability to perceptually discriminate the stimuli. Overall, these data from subjects with autism show some parallels to those from neurological subjects with focal amygdala damage. We suggest that amygdala dysfunction in autism might contribute to an impaired ability to link visual perception of socially relevant stimuli with retrieval of social knowledge and with elicitation of social behavior. C1 Univ Iowa, Iowa City, IA 52242 USA. RP Adolphs, R (reprint author), Univ Iowa Hosp & Clin, Dept Neurol, 200 Hawkins Dr, Iowa City, IA 52242 USA. 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PD MAR PY 2001 VL 13 IS 2 BP 232 EP 240 DI 10.1162/089892901564289 PG 9 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 409AR UT WOS:000167362800007 PM 11244548 ER PT J AU Tomasello, M AF Tomasello, M TI Cultural transmission - A view from chimpanzees and human infants SO JOURNAL OF CROSS-CULTURAL PSYCHOLOGY LA English DT Article ID 18-MONTH-OLD CHILDREN; LEARN WORDS; OBJECTS; IMITATION; BEHAVIOR; CONTEXTS; AUTISM; ACTS AB Human beings are biologically adapted for culture in ways that other primates are not, as evidenced most clearly by the fact that only human cultural traditions accumulate modifications over historical time (the ratchet effect). The key adaptation is one that enables individuals to understand other individuals as intentional agents like the self This species-unique form of social cognition emerges in human ontogeny at around 1 year of age as infants begin to engage with other persons in various kinds of joint attentional activities involving gaze following, social referencing, and gestural communication. Young children's joint attentional skills then engender some uniquely powerful forms of cultural learning, enabling the acquisition of language, discourse skills, tool use practices, and many other conventional activities. These novel forms of cultural learning allow human beings to pool their cognitive resources bath contemporaneously and over historical time in ways that are unique in the animal kingdom. C1 Max Planck Inst Eovlutionary Anthropol, Leipzig, Germany. RP Tomasello, M (reprint author), Max Planck Inst Eovlutionary Anthropol, Leipzig, Germany. CR Akhtar N, 1996, BRIT J DEV PSYCHOL, V14, P79 BAKEMAN R, 1984, CHILD DEV, V55, P1278, DOI 10.2307/1129997 BaronCohen S, 1997, CHILD DEV, V68, P48 BARONCOHEN S, 1993, UNDERSTANDING OTHER, P211 Basalla G., 1988, EVOLUTION TECHNOLOGY Boesch C, 1998, CURR ANTHROPOL, V39, P591, DOI 10.1086/204785 Boyd Robert, 1996, Proceedings of the British Academy, V88, P77 BROWN P, 2000, LANGUAGE ACQUISITION, P133 Call J., 1997, PRIMATE COGNITION Carpenter M., 1998, MONOGR SOC RES CHILD, V63, P1, DOI DOI 10.2307/1166214 Carpenter M, 1998, INFANT BEHAV DEV, V21, P315, DOI 10.1016/S0163-6383(98)90009-1 Galef B G, 1992, Hum Nat, V3, P157, DOI 10.1007/BF02692251 Hale G., 1979, ATTENTION COGNITIVE, P6 HAYES KJ, 1952, J COMP PHYSIOL PSYCH, V45, P450, DOI 10.1037/h0053609 Hobson P, 1993, AUTISM DEV MIND Kawai M, 1965, PRIMATES, V6, P1, DOI [10.1007/BF01794457, DOI 10.1007/BF01794457] Kruger A., 1996, HDB ED HUMAN DEV NEW, P169 KUMMER H, 1985, PHILOS T ROY SOC B, V308, P203, DOI 10.1098/rstb.1985.0020 MELTZOFF AN, 1988, DEV PSYCHOL, V24, P470, DOI 10.1037//0012-1649.24.4.470 MELTZOFF AN, 1995, DEV PSYCHOL, V31, P838, DOI 10.1037/0012-1649.31.5.838 Moore C., 1995, JOINT ATTENTION ITS SAVAGERUMBAUGH ES, 1990, PHILOS PSYCHOL, V3, P55, DOI 10.1080/09515089008572989 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 Tomasello Michael, 1996, P319, DOI 10.1016/B978-012273965-1/50016-9 Tomasello M, 1996, J CHILD LANG, V23, P157 Tomasello M., 1997, EVOLUTION COMMUNICAT, V1, P223, DOI [10.1075/eoc.1.2.04tom, DOI 10.1075/EOC.1.2.04TOM] Tomasello Michael, 1994, Yearbook of Physical Anthropology, V37, P273 TOMASELLO M, 1994, DEV PSYCHOL, V30, P639, DOI 10.1037/0012-1649.30.5.639 TOMASELLO M, 1993, CHILD DEV, V64, P1688, DOI 10.1111/j.1467-8624.1993.tb04207.x Tomasello M., 1999, CULTURAL ORIGINS HUM Tomasello M., 1995, JOINT ATTENTION ITS, P103 VISALBERGHI E, 1990, ANIM BEHAV, V40, P829, DOI 10.1016/S0003-3472(05)80983-2 Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER WHITEN A, 1996, SOCIAL LEARNING ANIM, P78 WHITEN A, 1992, ADV STUD BEHAV, V21, P239 Whiten A, 1999, NATURE, V399, P682, DOI 10.1038/21415 NR 36 TC 28 Z9 28 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0022-0221 J9 J CROSS CULT PSYCHOL JI J. Cross-Cult. Psychol. PD MAR PY 2001 VL 32 IS 2 BP 135 EP 146 DI 10.1177/0022022101032002002 PG 12 WC Psychology, Social SC Psychology GA 416NA UT WOS:000167786000002 ER PT J AU Gena, A Kymissis, E AF Gena, A Kymissis, E TI Assessing and setting goals for the attending and communicative behavior of three preschoolers with autism in inclusive kindergarten settings SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; inclusion; communicative behavior; normative data ID SOCIAL-SKILLS; SEVERE DISABILITIES; JOINT ATTENTION; PROFOUND DISABILITIES; PEER INTERACTIONS; CHILDREN; ADOLESCENTS; STUDENTS; INITIATIONS; SCHOOL AB Research findings of Helios II, a task plan for children with disabilities (1993-96) involving the nations of the European Economic Community, indicate that relevant and individualized inclusion plans, designed and used by well-trained specialists, is a key factor to successful inclusive education. The premise of this study was to set individualized goals that address the communicative difficulties of three preschoolers with autism in inclusive kindergarten settings. The findings of this study indicate that preschoolers with autism, compared with their typical peers in kindergarten, had low attending behavior; did not respond to their peer's comments, questions, and invitations; and did not initiate interactions with peers. Normative data were collected and analyzed in the domains for difficulty stated above, and inclusion goals for children with autism were set accordingly. Setting such goals was considered to be an important prerequisite for a systematic intervention addressing the needs of preschoolers with autism in inclusion settings. C1 Univ Athens, Dept Philosophy Educ Psychol, Athens, Greece. Effie Kymissis, Alpine Learning Grp, Alpine, NJ USA. RP Gena, A (reprint author), Aigaiou 50, Athens 17124, Greece. CR Baer D. M., 1970, CONTROL HUM BEHAV, V2, P319 Beckman P. J., 1983, J DIVISION EARLY CHI, V7, P69 BIERMAN KL, 1993, BEHAV MODIF, V17, P229, DOI 10.1177/01454455930173002 BRADLYN AS, 1983, BEHAV THER, V14, P314, DOI 10.1016/S0005-7894(83)80121-X BRADY MP, 1987, J AUTISM DEV DISORD, V17, P375, DOI 10.1007/BF01487067 DAHL EK, 1986, J AM ACAD CHILD PSY, V25, P170, DOI 10.1016/S0002-7138(09)60223-5 EAVES LC, 1977, J DEV PHYS DISAB, V9, P277 EVANS IM, 1992, J ASSOC PERS SEVERE, V17, P205 FOX JJ, 1993, BEHAV MODIF, V17, P339, DOI 10.1177/01454455930173006 GURALNICK MJ, 1990, TOP EARLY CHILD SPEC, V10, P1 GURALNICK MJ, 1980, J EXPT CHILD PSYCHOL, V31, P115 HAMRENIETUPSKI S, 1992, J ASSOC PERS SEVERE, V17, P53 HANLINE MF, 1993, J ASSOC PERS SEVERE, V18, P28 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hendrickson JM, 1996, EXCEPT CHILDREN, V63, P19 Joseph RM, 1997, J AUTISM DEV DISORD, V27, P385, DOI 10.1023/A:1025853321118 KAMPS DM, 1992, J APPL BEHAV ANAL, V25, P281, DOI 10.1901/jaba.1992.25-281 KASARI C, 1990, J AUTISM DEV DISORD, V20, P87, DOI 10.1007/BF02206859 KISHI GS, 1994, J ASSOC PERS SEVERE, V19, P277 KOEGEL LK, 1992, J APPL BEHAV ANAL, V25, P341, DOI 10.1901/jaba.1992.25-341 LEWY AL, 1992, J ABNORM CHILD PSYCH, V20, P555, DOI 10.1007/BF00911240 LOVELAND KA, 1986, J AUTISM DEV DISORD, V16, P335, DOI 10.1007/BF01531663 MCHALE SM, 1986, SOC BEHAV AUT, P191 MUELLER E, 1972, CHILD DEV, V43, P930, DOI 10.1111/j.1467-8624.1972.tb02046.x OKE NJ, 1990, J AUTISM DEV DISORD, V20, P479, DOI 10.1007/BF02216054 Peterson N.L., 1982, TOP EARLY CHILD SPEC, V2, P56 PRIZANT BM, 1987, J AM ACAD CHILD PSY, V26, P472, DOI 10.1097/00004583-198707000-00002 RUTTER M, 1978, J AUTISM CHILD SCHIZ, V8, P139, DOI 10.1007/BF01537863 SCHNORR RF, 1990, J ASSOC PERS SEVERE, V15, P231 SNYDER L, 1977, EXCEPT CHILDREN, V43, P262 STAINBACK W, 1981, EDUC TRAIN MENT RET, V16, P188 STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 STONE WL, 1990, J AUTISM DEV DISORD, V20, P437, DOI 10.1007/BF02216051 TREMBLAY A, 1981, BEHAV MODIF, V5, P237, DOI 10.1177/014544558152006 NR 34 TC 5 Z9 5 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 2001 VL 13 IS 1 BP 11 EP 26 DI 10.1023/A:1026553215508 PG 16 WC Rehabilitation SC Rehabilitation GA 413ZA UT WOS:000167640400002 ER PT J AU Furlano, RI Anthony, A Day, R Brown, A McGarvey, L Thomson, MA Davies, SE Berelowitz, M Forbes, A Wakefield, AJ Walker-Smith, JA Murch, SH AF Furlano, RI Anthony, A Day, R Brown, A McGarvey, L Thomson, MA Davies, SE Berelowitz, M Forbes, A Wakefield, AJ Walker-Smith, JA Murch, SH TI Colonic CD8 and gamma delta T-cell infiltration with epithelial damage in children with autism SO JOURNAL OF PEDIATRICS LA English DT Article ID ASSOCIATION; DISORDERS; AUTOANTIBODIES; COLITIS; MEASLES; DISEASE AB Objectives: We have reported colitis with ileal lymphoid nodular hyperplasia (LNH) in children with regressive autism. The aims of this study were to characterize this lesion and determine whether LNH is specific for autism. Methods: Ileo-colonoscopy was performed in 21 consecutively evaluated children with autistic spectrum disorders and bowel symptoms, Blinded comparison was made with 8 children with histologically normal ileum and colon, 10 developmentally normal children with ileal LNH, 15 with Crohn's disease, and 14 with ulcerative colitis. Immunohistochemistry was performed for cell lineage and functional markers, and histochemistry was performed for glycosaminoglycans and basement membrane thickness, Results: Histology demonstrated lymphocytic colitis in the autistic children, less severe than classical inflammatory bowel disease. However, basement membrane thickness and mucosal gamma delta cell density were significantly increased above those of all other groups including patients with inflammatory bowel disease. CD8(+) density and intraepithelial lymphocyte numbers were higher than those in the Crohn's disease, LNH, and normal control groups; and CD3 and plasma cell density and crypt proliferation were higher than those in normal and LNH control groups. Epithelial, but not lamina propria, glycosaminoglycans were disrupted. However, the epithelium was HLA-DR-, suggesting a predominantly T(H)2 response. Interpretation: Immunohistochemistry confirms a distinct lymphocytic colitis in autistic spectrum disorders in which the epithelium appears particularly affected. This is consistent with increasing evidence for gut epithelial dysfunction in autism. C1 UCL Royal Free & Univ Coll Med Sch, Univ Dept Paediat Gastroenterol, London NW3 2PF, England. UCL Royal Free & Univ Coll Med Sch, Inflammatory Bowel Dis Study Grp, London NW3 2PF, England. UCL Royal Free & Univ Coll Med Sch, Univ Dept Med, London NW3 2PF, England. UCL Royal Free & Univ Coll Med Sch, Univ Dept Histopathol, London NW3 2PF, England. UCL Royal Free & Univ Coll Med Sch, Dept Child & Adolescent Psychiat, London NW3 2PF, England. St Marks Hosp, IBD Res Unit, London EC1V 2PS, England. RP Murch, SH (reprint author), UCL Royal Free & Univ Coll Med Sch, Univ Dept Paediat Gastroenterol, Royal Free Campus,Rowland Hill St, London NW3 2PF, England. RI Day, Richard/C-5725-2009; Sherry, Angela/A-3293-2012 OI Sherry, Angela/0000-0003-2642-5376 CR Abuzakouk M, 1996, GUT, V39, P396, DOI 10.1136/gut.39.3.396 BEATTIE RM, 1995, ARCH DIS CHILD, V73, P354 Carroll MC, 1998, NAT GENET, V19, P3, DOI 10.1038/ng0598-3 Comi AM, 1999, J CHILD NEUROL, V14, P388, DOI 10.1177/088307389901400608 DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x Gupta S, 1998, J NEUROIMMUNOL, V85, P106, DOI 10.1016/S0165-5728(98)00021-6 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Iacono G, 1998, NEW ENGL J MED, V339, P1100, DOI 10.1056/NEJM199810153391602 Messahel S, 1998, NEUROSCI LETT, V241, P17, DOI 10.1016/S0304-3940(97)00976-2 Murch S, 1998, LANCET, V351, P908, DOI 10.1016/S0140-6736(05)70323-8 MURCH SH, 1993, LANCET, V341, P711, DOI 10.1016/0140-6736(93)90485-Y Ojuawo A, 1997, ARCH DIS CHILD, V76, P345 OMORAIN CA, 1986, J LAB CLIN MED, V108, P430 Reichelt K L, 1981, Adv Biochem Psychopharmacol, V28, P627 SHAETTOCK P, 1991, BRAIN DYSFUNCT, V3, P328 Shah N, 1999, NEW ENGL J MED, V340, P891 Singh VK, 1997, PEDIATR NEUROL, V17, P88, DOI 10.1016/S0887-8994(97)00045-3 Singh VK, 1998, CLIN IMMUNOL IMMUNOP, V89, P105, DOI 10.1006/clin.1998.4588 SMITH JW, 1999, DIS SMALL INTESTINE, P235 Sun Z, 1999, AUTISM, V3, P67, DOI 10.1177/1362361399003001006 Sun Z., 1999, AUTISM, V3, P85, DOI 10.1177/1362361399003001007 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 vanGent T, 1997, J CHILD PSYCHOL PSYC, V38, P337 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 WALKERSMITH JA, 1999, DIS SMALL INTESTINE, P299 WALKERSMITH JA, 1999, DIS SMALL INTESTINE, P29 WALKERSM.J, 1972, LANCET, V2, P883 Waring RH, 1997, DEV BRAIN DYSFUNCT, V10, P40 WARREN RP, 1995, NEUROPSYCHOBIOLOGY, V31, P53, DOI 10.1159/000119172 Warren RP, 1996, MOL CHEM NEUROPATHOL, V28, P77, DOI 10.1007/BF02815207 1998, CHANGES POPULATION P NR 33 TC 87 Z9 87 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAR PY 2001 VL 138 IS 3 BP 366 EP 372 DI 10.1067/mpd.2001.111323 PG 7 WC Pediatrics SC Pediatrics GA 413BZ UT WOS:000167591200014 PM 11241044 ER PT J AU Cede, M Tidwell, S AF Cede, M Tidwell, S TI Autism and the school nurse SO JOURNAL OF SCHOOL HEALTH LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; ADULTS; CHILDREN AB Until recently, treatment for children with autism involved housing them in hospitals for the developmentally disabled. Today, more states are returning children with autism to their home communities, and more parents are choosing or are brine required to keep their children with autism in their homes. Laws were developed to ensure that children with autism receive some form of education, often through the local school system. School nurses, who may not hav experience working with children with autism, may feel uncertain about how to provide support for the child with autism. 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Sch. Health PD MAR PY 2001 VL 71 IS 3 BP 96 EP 100 PG 5 WC Education & Educational Research; Education, Scientific Disciplines; Health Care Sciences & Services; Public, Environmental & Occupational Health SC Education & Educational Research; Health Care Sciences & Services; Public, Environmental & Occupational Health GA 420WB UT WOS:000168027300004 ER PT J AU Broderick, AA Kasa-Hendrickson, C AF Broderick, AA Kasa-Hendrickson, C TI "Say just one word at first": The emergence of reliable speech in a student labeled with autism SO JOURNAL OF THE ASSOCIATION FOR PERSONS WITH SEVERE HANDICAPS LA English DT Article DE qualitative research; interpretivist research; autism; speech development; language development; facilitated communication ID FACILITATED COMMUNICATION; MENTAL-RETARDATION; SCIENCE AB This article presents a qualitative, interpretivist research study that documents the emergence, in the context of typed expression, of increasingly useful and reliable speech for a young person labeled with autism. The authors construct a descriptive narrative of the process of this young man's emergent speech development and organize the data around four components of this complex, dynamic, and nonlinear process: (a) echolalia or "unreliable" speech, (b) reading out loud (c) using reliable speech, and (d) integrating speaking and typing. Additionally, the authors identify three categories of supports that this young man and his family experienced and interpreted as being supportive of his emergent speech. These categories include (a) the importance of taking risks, (b) the importance of seeing and hearing words together, and (c) the importance of an inclusive academic education including rich literacy experiences. Throughout, this inductive analysis constructs an understanding of how this young man and his family have experienced and interpreted his emergence as a reliable speaker. C1 Calif State Univ Long Beach, Dept Educ Psychol Adm & Counseling, Long Beach, CA 90840 USA. 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R., 1998, AUGMENTATIVE ALTERNA Biklen D, 2000, MENT RETARD, V38, P444, DOI 10.1352/0047-6765(2000)038<0444:LFTMNM>2.0.CO;2 Biklen D., 1999, Responding to the challenge: Current trends and international issues in developmental disabilities: Essays in honor of Gunnar Dybwad, P35 Biklen D, 1995, J ASSOC PERS SEVERE, V20, P45 BIKLEN D, 1999, SHARISA MY LIFE PION Biklen D., 1993, COMMUNICATION UNBOUN BIKLEN D, 1990, HARVARD EDUC REV, V60, P291 Biklen D., 1997, CONTESTED WORDS CONT BLACKMAN L, 1999, LUCYS STORY AUTISM O BOGDAN R, 1989, SOC PROBL, V36, P135, DOI 10.1525/sp.1989.36.2.03a00030 BOGDAN R, 1998, INTRO QUALITATIVE RE Borthwick C., 1999, PSYCOLOQUY, V10 BRODERICK A, 1999, FACILITATED COMMUNIC, V7, P2 CALCULATOR SN, 1992, TOP LANG DISORD, V12, pR9 Crossley R., 1994, FACILITATED COMMUNIC Crossley R., 1997, SPEECHLESS FACILITAT Denzin N. K., 2000, HDB QUALITATIVE RES DONNELLAN AM, 1995, MOVEMENT DIFFERENCES Ferguson P. M., 1992, INTERPRETING DISABIL Goode D. A., 1992, INTERPRETING DISABIL, P197 Goode David, 1994, WORLD WORDS SOCIAL C GREEN G, 1994, J ASSOC PERS SEVERE, V19, P151 JACOBSON JW, 1995, AM PSYCHOL, V50, P750, DOI 10.1037//0003-066X.50.9.750 Leary MR, 1996, MENT RETARD, V34, P39 MEYERS L, 1998, FACILITATED COMMUNIC, V6, P4 Richardson L., 2000, HDB QUALITATIVE RES Romski MA, 1999, AM J MENT RETARD, V104, P249, DOI 10.1352/0895-8017(1999)104<0249:CPOYWM>2.0.CO;2 Rubin S., 2001, Disability and Society, V16, P413 Smith P, 1999, REV EDUC RES, V69, P117, DOI 10.2307/1170672 Taylor SJ, 1998, INTRO QUALITATIVE RE THELEN E, 1995, AM PSYCHOL, V50, P79, DOI 10.1037//0003-066X.50.2.79 Thelen E., 1994, DYNAMIC SYSTEMS APPR WHEELER DL, 1993, MENT RETARD, V31, P49 NR 34 TC 21 Z9 21 PU ASSN PERS SEVERE HANDICAP PI BALTIMORE PA 29 W SUSQUEHANNA AVE STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 J ASSOC PERS SEVERE JI J. Assoc. Pers. Sev. Handicap PD SPR PY 2001 VL 26 IS 1 BP 13 EP 24 DI 10.2511/rpsd.26.1.13 PG 12 WC Rehabilitation SC Rehabilitation GA 439WQ UT WOS:000169140900002 ER PT J AU Koegel, LK AF Koegel, LK TI Autism spectrum disorders: A transactional developmental perspective. SO JOURNAL OF THE ASSOCIATION FOR PERSONS WITH SEVERE HANDICAPS LA English DT Book Review ID INTERVENTIONS C1 Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. RP Koegel, LK (reprint author), Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. CR Dawson G, 2000, J AUTISM DEV DISORD, V30, P415, DOI 10.1023/A:1005547422749 Koegel LK, 2000, J AUTISM DEV DISORD, V30, P383, DOI 10.1023/A:1005539220932 KOEGEL LK, 1995, AUTISM ASSESSMENT SU, P17 MCGEE GG, 1994, PRESCHOOL ED PROGRAM, P127 WETHERBY A, 2000, AUSTISM SPECTRUM DEV NR 5 TC 0 Z9 0 PU ASSN PERS SEVERE HANDICAP PI BALTIMORE PA 29 W SUSQUEHANNA AVE STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 J ASSOC PERS SEVERE JI J. Assoc. Pers. Sev. Handicap PD SPR PY 2001 VL 26 IS 1 BP 63 EP 65 DI 10.2511/rpsd.26.1.63 PG 3 WC Rehabilitation SC Rehabilitation GA 439WQ UT WOS:000169140900007 ER PT J AU Boone, LM AF Boone, LM TI Exiting nirvana: A daughter's life with autism. SO LIBRARY JOURNAL LA English DT Book Review C1 San Jose Publ Lib, San Jose, CA USA. RP Boone, LM (reprint author), San Jose Publ Lib, San Jose, CA USA. CR Park C.C., 2001, EXITING NIRVANA DAUG NR 1 TC 0 Z9 0 PU REED BUSINESS INFORMATION PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD MAR 1 PY 2001 VL 126 IS 4 BP 117 EP 117 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 405NB UT WOS:000167164900155 ER PT J AU Malek-Ahmadi, P AF Malek-Ahmadi, P TI Cytokines and etiopathogenesis of pervasive developmental disorders SO MEDICAL HYPOTHESES LA English DT Article ID TUMOR-NECROSIS-FACTOR; INTERLEUKIN-2 RECEPTORS; IMMUNE-SYSTEM; T-CELLS; AUTISM; PENTOXIFYLLINE; HALOPERIDOL; DEXAMETHASONE; DEFICIENCY; CHILDREN AB Autistic disorder, also known as early infantile autism, is a developmental disorder of unknown etiology. However, there is some evidence to suggest that abnormalities of the immune system mediate the pathophysiology of autistic disorder. Cytokines, which play a pivotal role in initiating and maintaining immune responses, have been implicated in the etiopathogenesis of major neuropsychiatric disorders including autism. Cytokines are synthesized in the periphery, as well as in the central nervous system, and exert their effects by binding to their receptors in the nervous tissues. It is suggested that, in genetically predisposed individuals, overproduction or decreased synthesis of certain cytokines may result in neurodevelopmental arrest and/or neurotoxicity. (C) 2001 Harcourt Publishers Ltd. C1 Texas Tech Univ, Hlth Sci Ctr, Sch Med, Dept Neuropsychiat, Lubbock, TX 79430 USA. RP Malek-Ahmadi, P (reprint author), Texas Tech Univ, Hlth Sci Ctr, Sch Med, Dept Neuropsychiat, Lubbock, TX 79430 USA. 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Psychiatr. PD MAR PY 2001 VL 6 IS 2 BP 129 EP 133 DI 10.1038/sj.mp.4000129 PG 5 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 402CH UT WOS:000166968100004 PM 11317213 ER PT J AU Persico, AM D'Agruma, L Maiorano, N Totaro, A Militerni, R Bravaccio, C Wassink, TH Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Conciatori, M Marino, R Quattrocchi, CC Baldi, A Zelante, L Gasparini, P Keller, F AF Persico, AM D'Agruma, L Maiorano, N Totaro, A Militerni, R Bravaccio, C Wassink, TH Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Conciatori, M Marino, R Quattrocchi, CC Baldi, A Zelante, L Gasparini, P Keller, F CA CLSA TI Reelin gene alleles and haplotypes as a factor predisposing to autistic disorder SO MOLECULAR PSYCHIATRY LA English DT Article DE allelic association; autism; cranial circumference; haplotype relative risk; linkage disequilibrium; reeler mouse; serotonin; splice junction; transmission/disequilibrium test; trinucleotide repeat ID TRANSMISSION/DISEQUILIBRIUM TEST; NEUROANATOMICAL ABNORMALITIES; LINKAGE DISEQUILIBRIUM; CORTICAL-NEURONS; MOUSE; MICE; ORGANIZATION; CEREBELLAR; MUTATION; BRAIN AB Autistic disorder (MIM 209850) is currently viewed as a neurodevelopmental disease. Reelin plays a pivotal role in the development of laminar structures Including the cerebral cortex, hippocampus, cerebellum and of several brainstem nuclei. Neuroanatomical evidence is consistent with Reelin involvement in autistic disorder. In this study, we describe several polymorphisms identified using RNA-SSCP and DNA sequencing. Association and linkage were assessed comparing 95 Italian patients to 186 ethnically-matched controls, and using the transmission/disequilibrium test and haplotype-based haplotype relative risk In 172 complete trios from 165 families collected in Italy and in the USA. Both case-control and family-based analyses yield a significant association between autistic disorder and a polymorphic GGC repeat located immediately 5' of the reelin gene (RELN) ATG initiator codon, as well as with specific haplotypes formed by this polymorphism with two single-base substitutions located in a splice junction in exon 6 and within exon 50. Triplet repeats located in 5' untranslated regions (5'UTRs) are indicative of strong transcriptional regulation. Our findings suggest that longer triplet repeats in the 5'UTR of the RELN gene center vulnerability to autistic disorder. C1 Libera Univ, Neurosci Lab, Dept Physiol & Neurosci, I-00155 Rome, Italy. IRCCS Casa Sollievo Sofferenza, Med Genet Serv, San Giovanni Rotondo, FG, Italy. Univ Naples 2, Dept Child Neuropsychiat, Naples, Italy. Univ Iowa, Coll Med, Dept Psychiat, Iowa City, IA USA. SW Autism Res Ctr, Phoenix, AZ USA. Osped Bambino Gesu, IRCCS, Div Child Neuropsychiat, Rome, Italy. Libera Univ, Clin Autism & Dev Disabilities, Rome, Italy. Univ La Sapienza, Dept Psychol, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, N-0316 Oslo, Norway. RP Keller, F (reprint author), Libera Univ, Neurosci Lab, Dept Physiol & Neurosci, Campus Bio Med,Via Longoni 83, I-00155 Rome, Italy. 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Psychiatr. PD MAR PY 2001 VL 6 IS 2 BP 150 EP 159 DI 10.1038/sj.mp.4000850 PG 10 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 402CH UT WOS:000166968100007 PM 11317216 ER PT J AU Feng, J Zheng, J Gelernter, J Kranzler, H Cook, E Goldman, D Jones, IR Craddock, N Heston, LL Delisi, L Peltonen, L Bennett, WP Sommer, SS AF Feng, J Zheng, J Gelernter, J Kranzler, H Cook, E Goldman, D Jones, IR Craddock, N Heston, LL Delisi, L Peltonen, L Bennett, WP Sommer, SS TI An in-frame deletion in the alpha(2C) adrenergic receptor is common in African-Americans SO MOLECULAR PSYCHIATRY LA English DT Article DE adrenergic receptor; schizophrenia; genetic polymorphism; case-control series; gene deletion; behavior disorder ID CLONIDINE TREATMENT; AUTISTIC DISORDER; MESSENGER-RNA; DOPAMINE; ASSOCIATION; MUTATIONS; GENE; POLYMORPHISMS; PHARMACOLOGY; POPULATION AB alpha (2) adrenergic receptors are activated by adrenaline and noradrenaline, and three subtypes (ie, A, B, C) have differential affinities for antagonists and medications. The alpha (2c) adrenergic receptor (ADRA2C), located on chromosome 4p16.3, is a candidate gene for schizophrenia because it binds clozapine, an atypical neuroleptic useful for treatment-resistant schizophrenia, In addition, ADRA2C binds clonidine which is prescribed for three psychiatric diseases. This report communicates the findings of the genetic scanning of this gene of very tough GC content. The complete coding sequences and splice junctions were scanned with [DOVAM]-S in 104 schizophrenics, and pilot probes of patients with alcoholism (41 patients), cocaine abuse (25 patients), puerperal psychosis (30 patients), attention deficient/hyperactivity disorder (25 patients) and autism (25 patients). Six sequence variants were found, including five silent polymorphisms (allele frequencies 0.6-25%) and an in-frame deletion of a homologous repeat at nucleotides 967-978 (ie, TIDRU1). Genotyping of the normal two repeat unit of the Third Intracytoplasmic Domain Repeat Unit (TIDRU2) and the deleted variant (TIDRU1) revealed that TIDRU1 had allelic frequencies of 39% (11/28) and 3.5% (6/172) in African-American and Caucasian schizophrenics, respectively, and it occurred with equal frequency in controls (44%, 31/70 and 3.0%, 6/198). TIDRU1 occurs at a location similar to the third intracytoptasmic 48-nucleotide repeat unit in the DRD4 that is associated with ADHD. Although these data do not suggest an association of TIDRU1 with schizophrenia, additional studies are needed to see whether TIDRU1 confers a clinical phenotype. C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Beckman Res Inst, Duarte, CA 91010 USA. VA CT Healthcare Syst, Dept Psychiat, W Haven, CT 06516 USA. Yale Univ, Sch Med, Dept Psychiat, W Haven, CT 06516 USA. Univ Connecticut, Sch Med, Dept Psychiat, Farmington, CT 06030 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60611 USA. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. Univ Birmingham, Div Neurosci, Birmingham B15 2QZ, W Midlands, England. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. SUNY Stony Brook, Dept Psychiat, Stony Brook, NY 11794 USA. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA. RP Sommer, SS (reprint author), City Hope Natl Med Ctr, Dept Mol Genet, Fox Plaza S,Room 2001,1500 E Duarte Rd, Duarte, CA 91010 USA. 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We prospectively identified 177 children with language regression at four major medical centers, and their clinical characteristics were recorded. Their mean age at regression was 22.8 months. The mean time-to-specialist referral was 38 months of age. Most children (88%) met criteria for autism or manifested autistic features, Males (P = 0.02) and children less than 3 years of age who regressed (P = 0.016) had a higher probability of developing autistic behaviors. Seizures were more common in children who regressed after they reached 3 years of age (P < 0.001), and children with seizures were less likely to have associated autistic regression (P < 0.001). Electroencephalogram abnormalities were reported in 37 % of patients and were more common in children with seizures (P < 0.001). At last follow-up, language function was impaired in 88% of the children, although some improvement was noted in 57%, We conclude that the loss of previously acquired language at any age, even if that language only includes a few words or communicative gestures, is often associated with a more global regression in cognition and/or behavior and has serious implications for future function. Early identification and referral of these children is necessary to allow for diagnosis and intervention. <(c)> 2001 by Elsevier Science Inc. All rights reserved. C1 Montefiore Med Ctr, Comprehens Epilepsy Management Ctr, Dept Neurol, Bronx, NY 10467 USA. Montefiore Med Ctr, Comprehens Epilepsy Management Ctr, Dept Pediat, Bronx, NY 10467 USA. Albert Einstein Coll Med, Rose F Kennedy ctr, Childrens Evaluat & Rehabil Ctr, Bronx, NY 10467 USA. Washington Univ, St Louis Childrens Hosp, Sch Med, Dept Neurol, St Louis, MO 63110 USA. Miami Childrens Hosp, Dept Neurol, Miami, FL USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. RP Shinnar, S (reprint author), Montefiore Med Ctr, Epilepsy Management Ctr, 111 E 210th St, Bronx, NY 10467 USA. 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Theory of mind or so-called Machiavellian intelligence, that is the capacity to infer mental states of other individuals and to manipulate them in order to maximise social success, probably emerged due to the need to cope with an increasingly complex social environment. Studies on social reasoning suggest disturbances of mental state attribution in psychiatric disorders. However, apart from autism spectrum disorders, the systematic evaluation of social cognition is still in its infancy, and the present data are ambiguous due to methodological difficulties. Based on the concept of the modular organisation of the mind, a stepwise investigation of social cognition in psychiatric disorders is proposed, including clinical description and available standardised methods, The specific characteristics of psychiatric disorders in respect of social cognition, therefore, may vary according to the hierarchical organisation of the social module. 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Children with autism typically fail tasks aimed at assessing their understanding of false beliefs. These features of autism are strikingly similar to some negative features of schizophrenia. Mental abilities were studied in 35 schizophrenics (DSM-IV) and 17 normal controls. Subjects heard four ToM stories and simultaneously were shown cartoons depicting the action occurring in the stories. All stories involved false beliefs or deception. As for the current symptomatology, schizophrenics were divided according to Liddle's three-dimensional model (reality distortion, psychomotor poverty, disorganisation). Our results show significant differences between schizophrenics and normal controls in all ToM stories, with schizophrenic people performing worse than controls. In first-order stories (a false belief about the state of the world) significant differences were found among symptom dimensions, with the psychomotor poverty group performing worse than disorganisation subjects and reality distortion ones. As for second-order stories (a false belief about the belief of another character), the psychomotor poverty group performed worse than the other groups only in one of the four ToM stories. More research in separating ToM deficits from attention disturbances is needed. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Aquila, Dept Psychiat, I-67100 Laquila, Italy. Univ Padua, Dept Dev Psychol, Padua, Italy. RP Mazza, M (reprint author), Via C Colombo 238, I-64020 S Nicolo Tordino, Teramo, Italy. 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Res. PD MAR 1 PY 2001 VL 47 IS 2-3 BP 299 EP 308 DI 10.1016/S0920-9964(00)00157-2 PG 10 WC Psychiatry SC Psychiatry GA 412CX UT WOS:000167537400022 PM 11278148 ER PT J AU Neysmith-Roy, JM AF Neysmith-Roy, JM TI The Tomatis Method with severely autistic boys: Individual case studies of behavioral changes SO SOUTH AFRICAN JOURNAL OF PSYCHOLOGY LA English DT Article ID MATERNAL SPEECH; PERCEPTION; PAIRS AB Six severely autistic males ranging in age from 4 years to 11 years received the Tomatis Method to assist in alleviating the severity of behaviours contributing to the diagnosis of autism. Ten minute video samples were taken of each boy, under two conditions of play, every time he completed one section of the treatment programme. As measured by the Children's Autism Rating Scale (CARS) all of the boys were severely autistic at the beginning of treatment. Three (50%) of the boys demonstrated positive behavioural changes by the end of the treatment. One boy was no longer considered to be autistic, two boys showed mild symptoms of autism and three boys remained within the severely autistic range. Of particular interest were the changes that occurred in pre-linguistic areas for five of the six boys. These included Adaptation to Change, Listening Response, Non Verbal Communication, Emotional Response and Activity Level. These behaviours are considered prerequisites for successful verbal communication. The children who demonstrated behavioural change were 6 years of age or younger at the beginning of treatment. The author suggests that the Tomatis Method may be helpful in making prelinguistic behaviours manageable and thus help prepare the child to learn basic skills necessary for the development of language and learning. C1 Univ Regina, Dept Psychol, Regina, SK S4S 0A2, Canada. RP Neysmith-Roy, JM (reprint author), Univ Regina, Dept Psychol, Regina, SK S4S 0A2, Canada. 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PD MAR PY 2001 VL 31 IS 1 BP 19 EP + PG 8 WC Psychology, Multidisciplinary SC Psychology GA 431LB UT WOS:000168631700005 ER PT J AU Hamilton, M AF Hamilton, M TI The MMR vaccination and autism: A lay person's contribution SO WEST INDIAN MEDICAL JOURNAL LA English DT Letter C1 Univ W Indies, Adm Initiat, Kingston 7, Jamaica. RP Hamilton, M (reprint author), Univ W Indies, Adm Initiat, Kingston 7, Jamaica. CR AFZAL M, 2000, B WORLD HEALTH ORGAN, V72, P199 Christie CDC, 2000, W INDIAN MED J, V49, P266 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 Kissoon N, 2000, W INDIAN MED J, V49, P257 Petrovic M, 2001, BRIT MED J, V322, P82, DOI 10.1136/bmj.322.7278.82 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 6 TC 1 Z9 1 PU UNIV WEST INDIES FACULTY MEDICAL SCIENCES PI KINGSTON PA MONA CAMPUS, KINGSTON 7, JAMAICA SN 0043-3144 J9 W INDIAN MED J JI West Ind. Med. J. PD MAR PY 2001 VL 50 IS 1 BP 87 EP 88 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 474MY UT WOS:000171112100025 PM 11398299 ER PT J AU Kissoon, N AF Kissoon, N TI The MMR vaccination and autism: A lay person's contribution - Comments SO WEST INDIAN MEDICAL JOURNAL LA English DT Letter C1 Univ Florida, HSC Jax, Jacksonville, FL 32207 USA. RP Kissoon, N (reprint author), Univ Florida, HSC Jax, 820 Prudential Dr,Suite 203,Howard Bldg, Jacksonville, FL 32207 USA. CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Feikin DR, 2000, JAMA-J AM MED ASSOC, V284, P3145, DOI 10.1001/jama.284.24.3145 Gillberg C., 1998, AUTISM, V2, P423, DOI 10.1177/1362361398024007 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 NR 4 TC 0 Z9 0 PU UNIV WEST INDIES FACULTY MEDICAL SCIENCES PI KINGSTON PA MONA CAMPUS, KINGSTON 7, JAMAICA SN 0043-3144 J9 W INDIAN MED J JI West Ind. Med. J. PD MAR PY 2001 VL 50 IS 1 BP 88 EP 89 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 474MY UT WOS:000171112100026 ER PT J AU Kaye, JA Melero-Montes, MD Jick, H AF Kaye, JA Melero-Montes, MD Jick, H TI Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: a time trend analysis SO BRITISH MEDICAL JOURNAL LA English DT Article AB Objective To estimate changes in the risk of autism and assess the relation of autism to the mumps, measles, and rubella (MMR) vaccine. Design Time trend analysis of data from the UK general practice research database (GPRD). Setting General practices in the United Kingdom. Subjects Children aged 12 years or younger diagnosed with autism 1988-99, with further analysis of boys aged 2 to 5 years born 1988-93. Main outcome measures Annual and age specific incidence for first recorded diagnoses of autism (that is, when the diagnosis of autism was first recorded) in the children aged 12 years or younger; annual, birth cohort specific risk of autism diagnosed in the 2 to 5 year old boys; coverage (prevalence) of MMR vaccination in the same birth cohorts. Results The incidence of newly diagnosed autism increased sevenfold, from 0.3 per 10 000 person years in 1988 to 2.1 per 10 000 person years in 1999, The peak incidence was among 3 and 4 year olds, and 83% (254/305) of cases were boys. In an annual birth cohort analysis of 114 boys born in 1988-93, the risk of autism in 2 to 5 year old boys increased nearly fourfold over time, from 8 (95% confidence interval 4 to 14) per 10 000 for boys born in 1988 to 29 (20 to 43) per 10 000 for boys born in 1993. For the same annual birth cohorts the prevalence of MMR vaccination was over 95%. Conclusions Because the incidence of autism among 2 to 5 year olds increased markedly among boys born in each year separately from 1988 to 1993 while MMR vaccine coverage was over 95% for successive annual birth cohorts, the data provide evidence that no correlation exists between the prevalence of MMR vaccination and the rapid increase in the risk of autism over time. The explanation for the marked increase in risk of the diagnosis of autism in the past decade remains uncertain. C1 Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, Lexington, MA 02421 USA. RP Kaye, JA (reprint author), Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, 11 Muzzey St, Lexington, MA 02421 USA. RI Research Datalink, Clinical Practice/H-2477-2013 CR Jick H, 1997, LANCET, V350, P1045, DOI 10.1016/S0140-6736(05)70451-7 JICK H, 1995, BRIT J GEN PRACT, V45, P107 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 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 6 TC 201 Z9 204 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-8138 J9 BRIT MED J JI Br. Med. J. PD FEB 24 PY 2001 VL 322 IS 7284 BP 460 EP 463 DI 10.1136/bmj.322.7284.460 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 406YD UT WOS:000167243000018 PM 11222420 ER PT J AU Skovgaard, AM Hoffmann, HM Moszkowicz, M Bjornholm, KI AF Skovgaard, AM Hoffmann, HM Moszkowicz, M Bjornholm, KI TI Child psychiatry in Denmark. SO UGESKRIFT FOR LAEGER LA Danish DT Article ID INFANCY AB Introduction: A descriptive epidemiological study of children aged 0-36 months. Methods: Diagnoses reported from the child psychiatric departments to The National Psychiatric Register were collected from a three-year period 1996, 1997, and 1998. The child psychiatric departments in Denmark filled in a questionnaire concerning referral, assessment, treatment, and consultant/liason functions. All the child psychiatric departments took part: in the study. Results: 529 children aged 0-3 years were reported to the National Psychiatric Register. In the perioded studied, there was a 30% increase in the number of children reported. Adjustment reactions were the commonest diagnosis in the youngest children, aged 0-12 months. Pervasive develop mental disorders, particularly infantile autism, were commonest used in the age group 2-3 years. Twentyfour per cent of the children reported, especially the youngest children, had, no specific psychiatric diagnosis. The increase in the number of children aged 0-1 year with adjustment reactions and non-specific diagnoses is discussed. Children aged 0-3 years are mainly treated as outpatients or by a consultant/liason child psychiatric service. The children referred to the child psychiatric departments in 1997 varied from fewer than 10 to about 100 children. Infant psychiatric units were established in two places in Denmark, in 1992 and 1997, Discussion: The increasing number of children aged 0-3 years reported to the National Psychiatric Register in the period 1996-1998 reflects an increase in the children aged 2-3 years diagnosed with pervasive developmental disorders, and in the case of the youngest children, aged 0-1 year, a more extensive child psychiatric intervention in relation to populations at risk, such as infants with mentally ill mothers. C1 Amtssygehuset Glostrup, Bornepsykiatrisk Afdeling, DK-2600 Glostrup, Denmark. HS Bispebjerg Hosp, Bornepsykiatrisk Afdeling, Copenhagen, Denmark. Roskilde Amtssygehus Fjorden, Bornepsykiatrisk Afdeling, Roskilde, Denmark. RP Skovgaard, AM (reprint author), Amtssygehuset Glostrup, Bornepsykiatrisk Afdeling, DK-2600 Glostrup, Denmark. CR Dunitz M, 1996, INF MENTAL HLTH J, V17, P12, DOI 10.1002/(SICI)1097-0355(199621)17:1<12::AID-IMHJ2>3.0.CO;2-3 EMDE RN, 1993, HDB INFANT MENTAL HL, P225 JANSEN H, 1999, BORNE UNGDOMSPSYKIAT, P219 JORGENSNE OS, 1999, BORNE UNGDONSPSYKIAT, P251 SKOVGAARD AM, 1988, ACTA PSYCHIAT SCAND, V77, P469, DOI 10.1111/j.1600-0447.1988.tb05153.x SKOVGAARD AM, 1999, BORNE UNGDOMSPSYKIAT, P17 SKUVGAARD AM, PSYKISKE FORSTYRRELS, V1, P59 Zeanah CH, 1997, J CHILD PSYCHOL PSYC, V38, P81, DOI 10.1111/j.1469-7610.1997.tb01506.x 1996, ARSRAPPORT FRA AFDEL 1998, MALSAETNINGER KVALIT NR 10 TC 5 Z9 5 PU LAEGEFORENINGENS FORLAG PI DK-1263 COPENHAGEN K PA ESPLANADEN 8A, DK-1263 COPENHAGEN K, DENMARK SN 0041-5782 J9 UGESKRIFT LAEGER JI Ugeskr. Laeg. PD FEB 19 PY 2001 VL 163 IS 8 BP 1112 EP 1115 PG 4 GA 403BR UT WOS:000167023100012 PM 11242673 ER PT J AU Le Page, M AF Le Page, M TI False alarm - Autism isn't really running riot. It's all in how you interpret the figures SO NEW SCIENTIST LA English DT News Item NR 0 TC 0 Z9 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 USA SN 0262-4079 J9 NEW SCI JI New Sci. PD FEB 17 PY 2001 VL 169 IS 2278 BP 17 EP 17 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 402MC UT WOS:000166991000014 ER PT J AU Humble, M Bejerot, S Bergqvist, PBF Bengtsson, F AF Humble, M Bejerot, S Bergqvist, PBF Bengtsson, F TI Reactivity of serotonin in whole blood: Relationship with drug response in obsessive-compulsive disorder SO BIOLOGICAL PSYCHIATRY LA English DT Article DE obsessive-compulsive disorder; serotonin kinetics; serotonin reuptake inhibitors; autism; prediction of response; randomized controlled trial ID CLOMIPRAMINE TREATMENT; TRANSPORTER GENE; LIQUID-CHROMATOGRAPHY; ANXIETY DISORDERS; SHORT-TERM; PLATELET; EFFICACY; SCALE; METAANALYSIS; POLYMORPHISM AB Background: Obsessive-compulsive disorder responds almost only to potent serotonin reuptake inhibitors. previous studies have suggested a relation between serotonergic function and clinical outcome in serotonin reuptake inhibitor treatment of obsessive - compulsive disorder. Methods: In a randomized, double-blind trial, comparing clomipramine, paroxetine, and a placebo in obsessive-compulsive disorder, serotonin levels in whole blood (WB-5-HT) were measured at baseline, after 1 week, and after 4 weeks of treatment and related to clinical outcome in 36 patients. Results: In patients treated with serotonin reuptake inhibitors there was a pronounced decrease of WB-5-HT, variable after 1 week and uniformly maximal after 4 weeks. The decrease of WB-5-HT after 1 week of serotonin reuptake inhibitor treatment correlated negatively with clinical outcome after 12 weeks (r = -.61, p = .0006); hence, patients with slower WB-5-HT reactivity eventually responded better to treatment. Baseline WB-5-HT, but not WB-5-Ht reactivity, was related to season. Depression, autistic traits, and previous serotonin reuptake inhibitor treatment predicted nonresponse. Conclusions: A fast decrease of WB-5-HT was associated with poor clinical outcome. This may be related to faster serotonin efflux from platelets, which has previously been linked to autism. Further studies are necessary to identify the underlying mechanism and discern whether serotonin reuptake inhibitor-induced WB-5-Ht decrease is clinically useful. C1 Mora Hosp, S-79285 Mora, Sweden. Danderyd Hosp, Div Psychiat, Karolinska Inst, Danderyd, Sweden. Univ Lund Hosp, Dept Clin Pharmacol, S-22185 Lund, Sweden. Uppsala Univ, Div Psychiat, Dept Neurosci, Uppsala, Sweden. Linkoping Univ Hosp, Dept Neurosci & Locomot, Div Psychiat, S-58185 Linkoping, Sweden. RP Humble, M (reprint author), Mora Hosp, S-79285 Mora, Sweden. 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Technical advances have improved methods for identifying brain regions involved during various types of cognitive activity, for tracing connections between parts of the brain, for visualizing individual neurons in living brain preparations, for recording the activities of neurons, and for studying the activity of single-ion channels and the receptors for various neurotransmitters, The most significant advances in the past 20 years have come from the application to the nervous system of molecular genetics and molecular cell biology, Discovery of the monogenic disorder responsible for Huntington disease and understanding its pathogenesis can serve as a paradigm for unraveling the much more complex, polygenic disorders responsible for such psychiatric diseases as schizophrenia, manic depressive illness, and borderline personality disorder. 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We conducted a series of experimental investigations to determine B,M,'s cognitive functioning, In line with his diagnoses, B,M, was found to be severely impaired in his ability to represent mental states. Following this, we conducted a second series of studies to determine B,M,'s executive functioning. In the literature, there have been frequent claims that theory of mind is mediated by general executive functioning. B,M, showed no indication of executive function impairment, passing 16 tests assessing his ability to inhibit dominant responses, create and maintain goal-related behaviours, and temporally sequence behaviour. The findings are discussed with reference to models regarding the role of the amygdala in the development of theory of mind and the degree of dissociation between theory of mind and executive functioning. 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PD FEB PY 2001 VL 37 IS 1 BP 39 EP 52 DI 10.1023/A:1026592305436 PG 14 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 414EF UT WOS:000167652400004 PM 11300666 ER PT J AU Ellaway, C Christodoulou, J AF Ellaway, C Christodoulou, J TI Rett syndrome: clinical characteristics and recent genetic advances SO DISABILITY AND REHABILITATION LA English DT Article ID X-CHROMOSOME INACTIVATION; DIFFERENTIAL-DIAGNOSIS; MITOCHONDRIAL ABNORMALITIES; OXIDATIVE-METABOLISM; MUTATIONAL ANALYSIS; GIRLS; INHERITANCE; DYSFUNCTION; AUTISM; MALES AB Purpose : Rett syndrome is a neurodevelopmental disorder that occurs almost exclusively in females. In recent years there has been increased knowledge concerning the multidisciplinary management of individuals with Rett syndrome. The aim of this paper is to provide an update of the clinical phenotype, natural history and current genetic understanding of the disorder. Results/Conclusion : Rett syndrome is thought to be the second most common cause of severe mental retardation in females after Down syndrome, it now appears that females with RS present with a much broader phenotype than originally described. Recently. mutations in the MECP2 gene encoding X-linked methyl-CpG-binding-protein 2 have been identified in some females with Rett syndrome. C1 Royal Alexandra Hosp Children, Western Sydney Genet Program, Parramatta, NSW 2124, Australia. Univ Sydney, Dept Paediat & Child Hlth, Sydney, NSW 2006, Australia. RP Christodoulou, J (reprint author), Royal Alexandra Hosp Children, Western Sydney Genet Program, POB 3515, Parramatta, NSW 2124, Australia. 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Rehabil. PD FEB-MAR PY 2001 VL 23 IS 3-4 BP 98 EP 106 PG 9 WC Rehabilitation SC Rehabilitation GA 414WC UT WOS:000167688300002 PM 11247014 ER PT J AU Mount, RH Hastings, RP Reilly, S Cass, H Charman, T AF Mount, RH Hastings, RP Reilly, S Cass, H Charman, T TI Behavioural and emotional features in Rett syndrome SO DISABILITY AND REHABILITATION LA English DT Article ID DIFFERENTIAL-DIAGNOSIS; AUTISM; PHENOTYPES; CHILDREN; SLEEP; DISABILITY; PATTERNS; SKILLS; GIRLS; BRAIN AB Purpose/Method: There is increasing agreement that many genetic disorders have characteristic behavioural phenotypes; that is genetic anomalies have specific effects on behaviour. In this paper the existing literature is reviewed with an aim to identify behavioural and emotional features that are candidates for Rett syndrome (RS) specific behaviours. Results/Conclusion: A number of behavioural and emotional features have been reported to be common in individuals with RS. These behaviours may constitute an RS-specific profile of behaviour or behavioural phenotype. Alternatively, these behaviours may simply reflect the multiple disabilities found in individuals with severe or profound cognitive impairment. The diagnostic criteria for Rett syndrome include a number of the behavioural features, such as hand stereotypies and breathing difficulties, although other behavioural features are not included. C1 Inst Child Hlth, London, England. Univ Southampton, Dept Psychol, Ctr Res Psychol Dev, Southampton SO9 5NH, Hants, England. La Trobe Univ, Sch Human Commun Sci, Melbourne, Vic, Australia. RP Mount, RH (reprint author), Inst Child Hlth, 30 Guilford St, London, England. 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Rehabil. PD FEB-MAR PY 2001 VL 23 IS 3-4 BP 129 EP 138 PG 10 WC Rehabilitation SC Rehabilitation GA 414WC UT WOS:000167688300005 PM 11247008 ER PT J AU Khalfa, S Bruneau, N Roge, B Georgieff, N Veuillet, E Adrien, JL Barthelemy, C Collet, L AF Khalfa, S Bruneau, N Roge, B Georgieff, N Veuillet, E Adrien, JL Barthelemy, C Collet, L TI Peripheral auditory asymmetry in infantile autism SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE lateralization; medial olivocochlear system; neurodevelopmental disorders; otoacoustic emission ID EVOKED OTOACOUSTIC EMISSIONS; HEARING-LOSS; LATERALIZATION; CHILDREN; NOISE; DYSFUNCTION; HANDEDNESS; COMPLEX; SYSTEM; HUMANS AB Difficulty in filtering relevant auditory information in background noise is one of the features of autism. Auditory filtering processes can be investigated at the peripheral level as they are hypothesized to involve active cochlear mechanisms which are regulated by the efferent activity of the medial olivocochlear (MOC) system. The aim of the present work was therefore to assess these peripheral auditory processes in 22 children and adolescents with autism compared with age- and gender-matched normal controls. Active cochlear mechanisms were evaluated with transiently evoked otoacoustic emissions (TEOAEs) and MOC system efficiency was assessed via TEOAEs which are decreased when stimulating the contralateral ear with noise. The MOC system evaluation was performed on 18 of the 22 children. In both studies, results were analysed according to age (from 4 to 10 years and from 11 to 20 years). The main result concerns the asymmetry of the efferent system which differs in individuals with autism. Several neural processes might be hypothesized as involved in the results obtained as the MOC system which originates in the brainstem received regulating controls from upper brain structures including auditory cortex. Lateralization abnormalities at the auditory periphery may reflect indirectly a problem at a higher level of auditory processing. A second important result shows a decrease in TEOAE amplitude with age, in patients, that may correspond to a decrease in hearing sensitivity. C1 Hop Edouard Herriot, CNRS, UPRESA 5020, F-69003 Lyon, France. CHU Bretonneau, INSERM, U316, Child Psychiat Unit, F-37044 Tours, France. Hop lagrave, Serv Psychiat & Psychol Med, F-31051 Toulouse, France. Hop Specialise Vinatier, F-69677 Bron, France. RP Khalfa, S (reprint author), Univ Montreal, Dept Psychol, CP 6128 Succursale Ctr Ville, Montreal, PQ H3C 3J7, Canada. 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J. Neurosci. PD FEB PY 2001 VL 13 IS 3 BP 628 EP 632 DI 10.1046/j.1460-9568.2001.01423.x PG 5 WC Neurosciences SC Neurosciences & Neurology GA 403PN UT WOS:000167051800023 PM 11168571 ER PT J AU Wolterink, G Daenen, LEWPM Dubbeldam, S Gerrits, MAFM van Rijn, R Kruse, CG Van Der Heijden, JAM Van Ree, JM AF Wolterink, G Daenen, LEWPM Dubbeldam, S Gerrits, MAFM van Rijn, R Kruse, CG Van Der Heijden, JAM Van Ree, JM TI Early amygdala damage in the rat as a model for neurodevelopmental psychopathological disorders SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Article DE neonatal lesions; amygdala; hippocampus; schizophrenia; autism; neurodevelopment ID PUTATIVE ANIMAL-MODEL; BRAIN ABNORMALITIES; HIPPOCAMPAL DAMAGE; SCHIZOPHRENIA; AUTISM; DYSFUNCTION; LESIONS; STRESS; CORTEX; LOBE AB Neurodevelopmental disorders in medial temporal lobe structures may underlie psychopathological diseases such as schizophrenia and autism. To construct an animal model for these developmental disorders, social and non-social behavioural responses were assessed in rats with ibotenic acid lesions of the (baso-)lateral and central amygdala or ventral hippocampus, induced early in life. Lesioning the amygdala on day 7 after birth resulted in a variety of behavioural disturbances later in life, whereas after similar lesions on day 21 after birth no disturbances developed, except for deficits in social behaviours. Lesioning the hippocampus led to much less disturbances. The results show that amygdala and hippocampus damage at a specific point early in life results in enduring behavioural disturbances that become more manifest after puberty. In particular, lesions of the amygdala on day 7 of life may serve as a rat model with face and construct validity for neurodevelopmental disorders in studying psychopathology. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Rudolf Magnus Inst Neurosci, Dept Med Pharmacol, NL-3584 CG Utrecht, Netherlands. Solvay Pharmaceut, NL-1381 CP Weesp, Netherlands. RP Van Ree, JM (reprint author), Univ Utrecht, Rudolf Magnus Inst Neurosci, Dept Med Pharmacol, Univ Weg 100, NL-3584 CG Utrecht, Netherlands. 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PD FEB PY 2001 VL 11 IS 1 BP 51 EP 59 DI 10.1016/S0924-977X(00)00138-3 PG 9 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 413KU UT WOS:000167612000007 PM 11226812 ER PT J AU Taieb, O Baleyte, JM Mazet, P Fillet, AM AF Taieb, O Baleyte, JM Mazet, P Fillet, AM TI Borna disease virus and psychiatry SO EUROPEAN PSYCHIATRY LA English DT Review DE autism; bipolar disorder; borna disease virus; neurodevelopmental hypothesis; schizophrenia ID BLOOD MONONUCLEAR-CELLS; NEUROPSYCHIATRIC DISORDERS; CEREBROSPINAL-FLUID; MOOD DISORDERS; BDV INFECTION; NUCLEIC-ACID; SCHIZOPHRENIA; BRAIN; SEQUENCE; RNA AB Borna disease virus (BDV), a noncytolytic neurotropic nonsegmented negative-stranded RNA virus with a wide geographic distribution, infects several vertebrate animal species and causes an immune-mediated central nervous system (CNS) disease with various manifestations, depending on both host and viral factors. 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Psychiat. PD FEB PY 2001 VL 16 IS 1 BP 3 EP 10 DI 10.1016/S0924-9338(00)00529-0 PG 8 WC Psychiatry SC Psychiatry GA 408HN UT WOS:000167320900001 PM 11246286 ER PT J AU Allen, G Courchesne, E AF Allen, G Courchesne, E TI Attention function and dysfunction in autism SO FRONTIERS IN BIOSCIENCE-LANDMARK LA English DT Article DE autism; selective attention; sustained attention; spatial attention; shifting attention; parietal lobe; cerebellum; review ID POSITRON-EMISSION-TOMOGRAPHY; VISUAL-SPATIAL ATTENTION; CEREBRAL GLUCOSE-METABOLISM; CONTINUOUS PERFORMANCE-TEST; INFANTILE-AUTISM; SUSTAINED ATTENTION; CHILDHOOD AUTISM; JOINT ATTENTION; HUMAN BRAIN; CEREBELLAR AB Impairments of attention are among the most consistently reported cognitive deficits in autism, and they continue to be a key focus of research. This is in no doubt due to the importance of normal attention function to the development of many so-called "higher level" cognitive operations, and to the likely involvement of attention dysfunction in certain clinical features of autism. Autistic individuals display a wide range of attentional abilities and deficits across the many domains of attention function, including selective, sustained, spatial, and shifting attention operations. This unique pattern of attention function and dysfunction has profound implications for the development and treatment of autistic children. The present review will explore this pattern of attentional strengths and weaknesses and the neural defects that underlie them. C1 Childrens Hosp Res Ctr, La Jolla, CA 92037 USA. Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Psychiat, La Jolla, CA 92093 USA. San Diego State Univ, Dept Psychol, San Diego, CA 92182 USA. 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PD FEB 1 PY 2001 VL 6 BP D105 EP D119 DI 10.2741/allen PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 397RU UT WOS:000166710000002 PM 11171544 ER PT J AU Jyonouchi, H Sun, SI Le, H AF Jyonouchi, H Sun, SI Le, H TI Innate and adaptive immune responses in children with regression autism: Evaluation of the effects of environmental factors including vaccination SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN USA. NR 0 TC 2 Z9 2 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 FEB PY 2001 VL 107 IS 2 SU S MA 897 BP S274 EP S274 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 405RE UT WOS:000167172300893 ER PT J AU Minshew, NJ AF Minshew, NJ TI Editorial preface SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID AUTISM CR Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 RUMSEY JM, 1986, ARCH GEN PSYCHIAT, V43, P771 VOLKMAR FR, 1991, AM J PSYCHIAT, V148, P1705 NR 3 TC 0 Z9 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 1 EP 3 DI 10.1023/A:1005642627400 PG 3 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700001 PM 11439747 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 SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism-Spectrum Quotient; Asperger syndrome; high-functioning autism; normal intelligence ID DIAGNOSTIC INTERVIEW; TWIN AB Currently there are no brief, self-administered instruments for measuring the degree to which an adult with normal intelligence has the traits associated with the autistic spectrum. In this paper, we report on a new instrument to assess this: the Autism-Spectrum Quotient (AQ). Individuals score in the range 0-50. Four groups of subjects were assessed: Group 1: 58 adults with Asperger syndrome (AS) or high-functioning autism (HFA); Group 2: 174 randomly selected controls. Group 3: 840 students in Cambridge University; and Group 4: 16 winners of the UK Mathematics Olympiad. The adults with AS/HFA had a mean AQ score of 35.8 (SD = 6.5), significantly higher than Group 2 controls (M = 16.4, SD = 6.3). 80% of the adults with AS/HFA scored 32+, versus 2% of controls. Among the controls, men scored slightly but significantly higher than women. No women scored extremely highly (AQ score 34+) whereas 4% of men did so. Twice as many men (40%) as women (21%) scored at intermediate levels (AQ score 20+). Among the AS/HFA group, male and female scores did not differ significantly. The students in Cambridge University did not differ from the randomly selected control group, but scientists (including mathematicians) scored significantly higher than both humanities and social sciences students, confirming an earlier study that autistic conditions are associated with scientific skills. Within the sciences, mathematicians scored highest. This was replicated in Group 4, the Mathematics Olympiad winners scoring significantly higher than the male Cambridge humanities students. 6% of the student sample scored 32+ on the AQ. On interview, 11 out of 11 of these met three or more DSM-IV criteria for AS/HFA, and all were studying sciences/mathematics, and 7 of the 11 met threshold on these criteria. Test-retest and interrater reliability of the AQ was good. The AQ is thus a valuable instrument for rapidly quantifying where any given individual is situated on the continuum from autism to normality. Its potential for screening for autism spectrum conditions in adults of normal intelligence remains to be fully explored. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 5 EP 17 DI 10.1023/A:1005653411471 PG 13 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700002 PM 11439754 ER PT J AU Konstantareas, MM Hewitt, T AF Konstantareas, MM Hewitt, T TI Autistic disorder and schizophrenia: Diagnostic overlaps SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; pervasive developmental disorder; schizophrenia; comorbidity ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD-ONSET SCHIZOPHRENIA; ASPERGERS SYNDROME; CHILDREN; PSYCHOSES AB Data on 14 males with autism and 14 with schizophrenia were collected to examine symptom overlap. The Structured Clinical Interview (SCID), the schedule for positive symptoms (SAPS) and the schedule for negative symptoms (SANS) of schizophrenia, the Childhood Autism Rating Scale (CARS), and the DSM-III-R were administered. On the SCID, none of the men with paranoid schizophrenia met criteria for autism while 7 of those with autism met criteria for schizophrenia, disorganized type, showing negative symptoms. In addition, 5 showed positive symptoms on the SAPS and 6 negative symptoms on the SANS. As the difference in measured nonverbal intelligence was not significant, the effects could not be attributed to it. Although the findings continue to support the differentiation of autism and schizophrenia, they are also consistent with a comorbidity of the two disorders, mainly in those diagnosed with autism. C1 Univ Guelph, Coll Social & Appl Human Sci, Dept Psychol, Guelph, ON N1G 2W1, Canada. Clarke Inst Psychiat, Toronto, ON M5T 1R8, Canada. Surrey Pl Ctr, Toronto, ON M5S 2C2, Canada. RP Konstantareas, MM (reprint author), Univ Guelph, Coll Social & Appl Human Sci, Dept Psychol, Guelph, ON N1G 2W1, Canada. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 19 EP 28 DI 10.1023/A:1005605528309 PG 10 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700003 PM 11439750 ER PT J AU Kleinman, J Marciano, PL Ault, RL AF Kleinman, J Marciano, PL Ault, RL TI Advanced theory of mind in high-functioning adults with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; theory of mind; adults ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; CHILDS APPRAISAL; VERBAL-ABILITY; EMOTION; INDIVIDUALS; SPEECH; EXPRESSIONS; KNOWLEDGE; LANGUAGE AB Twenty-four high-functioning adults with autism (16 men) who passed a first-order theory-of-mind task and 24 nonautistic adults (10 men) attributed mental states to recordings of various verbal intonations and to photos of people's eyes to assess advanced theory of mind. Participants with autism performed significantly worse than nonautistic participants on both tasks. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 29 EP 36 DI 10.1023/A:1005657512379 PG 8 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700004 PM 11439751 ER PT J AU Gepner, B Deruelle, C Grynfeltt, S AF Gepner, B Deruelle, C Grynfeltt, S TI Motion and emotion: A novel approach to the study of face processing by young autistic children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; motion perception; facial expression processing; reeducation ID STIMULUS OVERSELECTIVITY; INTERMODAL PERCEPTION; RECOGNITION; EXPRESSIONS; MECHANISMS; APPRAISAL; IDENTITY AB The specificity of facial processing impairment in autistic children, particularly in the domain of emotion, is still debated. The aim of our study was to assess the influence of motion on facial expression recognition in young autistic children. Thirteen autistic children (M age: 69.38 months) were matched for gender and developmental level with a control group of 13 normal children (M age: 40.53 months). They were compared on their ability to match videotaped ((Still,ll "dynamic," and "strobe" emotional and nonemotional facial expressions with photographs. Results indicate that children with autism do not perform significantly worse than their controls in any of our experimental conditions. Compared to previous studies showing lower performance in autistic than in control children when presented with static faces, our data suggest that slow dynamic presentations facilitate facial expression recognition by autistic children. This result could be of interest to parents and specialists involved in education and reeducation of these children. C1 Montperrin Hosp, Child Psychiat Dept, Aix En Provence, France. CNRS, Ctr Res Cognit Neurosci, Marseille, France. CH Valvert, Adult Psychiat Dept, Marseille, France. RP Gepner, B (reprint author), AFRTDET-137,Rue J Mermoz, F-13008 Marseille, France. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 37 EP 45 DI 10.1023/A:1005609629218 PG 9 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700005 PM 11439752 ER PT J AU Dennis, M Lazenby, AL Lockyer, L AF Dennis, M Lazenby, AL Lockyer, L TI Inferential language in high-function children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; high-function children; inferential language ID NORMALLY DEVELOPING-CHILDREN; STATE VERB KNOW; ASPERGER-SYNDROME; TEXT COMPREHENSION; ADULTS; MIND; RECOGNITION; PRESUPPOSITIONS; ACQUISITION; INDIVIDUALS AB Despite average verbal intelligence, high-function children with autism have social comprehension deficits that are expressed by how they use and understand language. In this paper, we explored the general hypothesis that high-function children with autism make some, but not all, of the pragmatic inferences necessary for successful communication, even when they have the ability to perform noninferential language tasks. We contrasted the ability of 8 high-function children with autism teach with Verbal IQ > 70) and typically developing children to use and understand: pragmatic inferences about given or presupposed knowledge in mental state words; pragmatic inferences about new or implied knowledge in mental state words; bridging inferences essential for coherence; elaborative inferences involved in enriching a communication by means of figurative language; and the intentional inferences involved in speech acts. High-function children with autism could define words and identify multiple meanings for ambiguous words. In understanding words for mental states, they made inferences from mental state verbs to given or presupposed knowledge. However, they failed to infer what mental state verbs implied in context; to make inferences about social scripts; to understand metaphor; and to produce speech acts, all of which are inferences that are the basis of successful social communication because they elaborate meaning or convey intentions. C1 Hosp Sick Children, Dept Psychol Res, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Surg, Toronto, ON, Canada. RP Dennis, M (reprint author), Hosp Sick Children, Dept Psychol Res, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 47 EP 54 DI 10.1023/A:1005661613288 PG 8 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700006 PM 11439753 ER PT J AU Teunisse, JP Cools, AR van Spaendonck, KPM Aerts, FHTM Berger, HJC AF Teunisse, JP Cools, AR van Spaendonck, KPM Aerts, FHTM Berger, HJC TI Cognitive styles in high-functioning adolescents with autistic disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; central coherence; cognitive shifting; social functioning ID PARKINSONS-DISEASE; EXECUTIVE FUNCTION; CENTRAL COHERENCE; VERBAL-ABILITY; CHILDREN; MIND; PERFORMANCE; INDIVIDUALS; RECOGNITION; DYSFUNCTION AB This study addressed the operationalization, the identification, and the prevalence of weak central coherence and poor cognitive shifting in 35 high-functioning adolescents with autism. Central coherence and cognitive shifting were represented by two factors in a factor analysis, each reflecting a constituent aspect of the domain in question. With regard to central coherence, these aspects were the ability of piecemeal processing and the ability to process meaning. The aspects related to cognitive shifting concerned internally and externally controlled shifting. Weak central coherence and poor cognitive shifting did not appear to be related to measures of symptom severity, social understanding, and social competence. Both these cognitive styles did not appear to be universal to autism. In our sample, weak central coherence and poor cognitive shifting were found to be significantly more common than in normative control subjects. C1 Univ Nijmegen, Nijmegen, Netherlands. RP Berger, HJC (reprint author), Univ Nijmegen Hosp, Dept Psychol Med, POB 9101, NL-6500 HB Nijmegen, Netherlands. CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S, 1997, HDB AUTISM PERVASIVE, P880 Bauminger N, 1999, J AUTISM DEV DISORD, V29, P81, DOI 10.1023/A:1025974701090 Berg EA, 1948, J GEN PSYCHOL, V39, P15 BERGER HJC, 1999, J CLIN EXPT NEUROPSY, V21, P676 BERGER HJC, 1989, NEUROPSYCHOLOGIA, V27, P629, DOI 10.1016/0028-3932(89)90109-7 BERGER HJC, 1993, J AUTISM DEV DISORD, V23, P341, DOI 10.1007/BF01046224 Brian JA, 1996, J CHILD PSYCHOL PSYC, V37, P865, DOI 10.1111/j.1469-7610.1996.tb01482.x BUYTENHUIJS EL, 1994, NEUROPSYCHOLOGIA, V32, P335, DOI 10.1016/0028-3932(94)90135-X Ciesielski KT, 1997, CHILD NEUROPSYCHOL, V3, P1, DOI 10.1080/09297049708401364 COOLS AR, 1993, MENTAL DYSFUNCTION P, P49 DELIS DC, 1987, CALIFORNIA VERBAL LE DOWNES JJ, 1989, NEUROPSYCHOLOGIA, V27, P1329, DOI 10.1016/0028-3932(89)90128-0 Ekstrom R. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 55 EP 66 DI 10.1023/A:1005613730126 PG 12 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700007 PM 11439755 ER PT J AU Williams, E Reddy, V Costall, A AF Williams, E Reddy, V Costall, A TI Taking a closer look at functional play in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; functional play ID DEVELOPMENTAL LANGUAGE DELAY; SYMBOLIC PLAY; PRETEND PLAY; JOINT ATTENTION; COMMUNICATION; DEFICITS; EXPERIENCE; IMITATION AB Research evidence indicates that children with autism may experience problems with functional play, in addition to their well-documented deficits in symbolic play. However, as a result of the tendency of previous studies to group all functional play into a single category, the precise nature and extent of this deficit remains unclear. The present study undertook a more refined analysis of such play, subtyping the functional acts into various categories, in terms of the developmental progression suggested by research with typical infants. The functional play of children with autism was compared to that of developmentally matched children with Down syndrome and typical infants. Although there were no group differences in overall measures of the proportion of total play time spent in functional play and in the number of functional acts performed, a closer analysis of the composition of this play did reveal striking, qualitative differences. The functional play of the autism group was less elaborated, less varied, and less integrated than that of the controls. The implications of these findings are explored in relation to current theoretical models of autism and in relation to the role of other people in mediating the appropriate use of objects. C1 Univ Portsmouth, Dept Psychol, Portsmouth PO1 2DY, Hants, England. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 67 EP 77 DI 10.1023/A:1005665714197 PG 11 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700008 PM 11439756 ER PT J AU Rinehart, NJ Bradshaw, JL Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Brereton, AV Tonge, BJ TI Movement preparation in high-functioning autism and Asperger disorder: A serial choice reaction time task involving motor reprogramming SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger disorder; autism; movement execution; movement preparation ID HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; CHILDHOOD AUTISM; CHILDREN; CLUMSINESS; ADULTS; IMPAIRMENT; ATTENTION; MIND AB Autism and Asperger disorder have long been associated with movement abnormalities, although the neurobehavioural details of these abnormalities remain poorly defined. Clumsiness has traditionally been associated with Asperger disorder but not autism, although this is controversial. Others have suggested that both groups demonstrate a similar global motor delay. In this study we aimed to determine whether movement preparation or movement execution was atypical in these disorders and to describe any differences between autism and Asperger disorder. A simple motor reprogramming task was employed. The results indicated that individuals with autism and Asperger disorder have atypical movement preparation with an intact ability to execute movement. An atypical deficit in motor preparation was found in Asperger disorder, whereas movement preparation was characterized by a "lack of anticipation" in autism. The differences in movement preparation profiles in these disorders were suggested to reflect differential involvement of the fronto-striatal region, in particular the supplementary motor area and anterior cingulate. C1 Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. Monash Univ, Monash Med Ctr, Ctr Dev Psychiat, Clayton, Vic 3168, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. CR ACHENBARCH TM, 1991, MANUAL CHILD BEHAV C ALLPORT A, 1989, FDN COGNITIVE SCI, P382 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BRADSHAW JL, 1992, J CLIN EXP NEUROPSYC, V14, P179, DOI 10.1080/01688639208402822 Bradshaw J.L., 2001, DEV DISORDERS FRONTO COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 Cunnington R, 1996, HUM MOVEMENT SCI, V15, P627, DOI 10.1016/0167-9457(96)00018-8 Dahlgren SO, 1996, J CHILD PSYCHOL PSYC, V37, P759, DOI 10.1111/j.1469-7610.1996.tb01469.x Damasio A. 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J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 VILENSKY JA, 1981, ARCH NEUROL-CHICAGO, V38, P646 Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 43 TC 109 Z9 112 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 2001 VL 31 IS 1 BP 79 EP 88 DI 10.1023/A:1005617831035 PG 10 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700009 PM 11439757 ER PT J AU Starr, E Berument, SK Pickles, A Tomlins, M Bailey, A Papanikolaou, K Rutter, M AF Starr, E Berument, SK Pickles, A Tomlins, M Bailey, A Papanikolaou, K Rutter, M TI A family genetic study of autism associated with profound mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; mental retardation; genetics ID DIAGNOSTIC OBSERVATION SCHEDULE; COGNITIVE DISABILITIES; RELATIVES; CHILDREN; PHENOTYPE; HISTORY; TWINS AB We sought to determine if the family loading for either the broader autism phenotype or for cognitive impairment differed according to whether or not autism was accompanied by severe mental retardation. The sample comprised 47 probands with autism meeting ICD-IO criteria, as assessed by the Autism Diagnostic Interview and the Autism Diagnostic Observation Schedule. Family history interview and findings were compared with those for the higher IQ autism and Down syndrome samples in the Bolton et al. (1994) study. The familial loading for autism and for the broader phenotype was closely comparable to that in the study of higher IQ autism, and different from that for Down syndrome. The family loading for scholastic achievement difficulties was slightly, but significantly, higher when autism was accompanied by severe retardation. C1 Inst Psychiat, MRC, Child Psychiat Unit, London, England. RP Starr, E (reprint author), Univ Windsor, Fac Educ, Windsor, ON N9B 3P4, Canada. RI Pickles, Andrew/A-9625-2011; Rutter, Michael/C-8570-2013; Bailey, Anthony/J-2860-2014 OI Pickles, Andrew/0000-0003-1283-0346; Bailey, Anthony/0000-0003-4257-972X CR AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 BAILEY A, 1992, SCI PROGR EDINBURGH, V75, P389 Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BAILEY A, 1993, J CHILD PSYCHOL PSYC, V34, P673, DOI 10.1111/j.1469-7610.1993.tb01064.x BAIRD TD, 1985, J AUTISM DEV DISORD, V15, P315, DOI 10.1007/BF01531501 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Bolton PF, 1997, J AM ACAD CHILD PSY, V36, P272, DOI 10.1097/00004583-199702000-00018 Boutin P, 1997, J AUTISM DEV DISORD, V27, P165, DOI 10.1023/A:1025891824269 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 FOLSTEIN S, 1987, NEUROBIOLOGICAL ISSU, P83 FOMBONNE E, 1997, J CHILD PSYCHOL PSYC, V38, P1 GILLBERG C, 1989, BIOL AUTISTIC SYNDRO Huber P, 1967, P 5 BERK S MATH STAT, P221 JONES MB, 1988, J AUTISM DEV DISORD, V18, P31, DOI 10.1007/BF02211816 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Leiter R. 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Autism Dev. Disord. PD FEB PY 2001 VL 31 IS 1 BP 89 EP 96 DI 10.1023/A:1005669915105 PG 8 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700010 PM 11439758 ER PT J AU Beversdorf, DQ Anderson, JM Manning, SE Anderson, SL Nordgren, RE Felopulos, GJ Bauman, ML AF Beversdorf, DQ Anderson, JM Manning, SE Anderson, SL Nordgren, RE Felopulos, GJ Bauman, ML TI Brief report: Macrographia in high-functioning adults with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; motor control; handwriting ID ASPERGER SYNDROME; MICROGRAPHIA; INFARCTION; DISEASE AB The initial description of Asperger syndrome commented on the poor handwriting and motor coordination difficulties of individuals with this condition. Early descriptions of autism do not remark upon such difficulties. Recent evidence, however, suggests that individuals with both conditions have a similar motor control impairment. Handwriting has not been formally assessed in this context. Our study compared handwriting size between individuals with autism spectrum disorder and age- and IQ-matched control subjects. Macrographia was observed among subjects with autism spectrum disorder which remained statistically significant when covaried with educational level. This finding may correlate with the anatomical abnormalities present in the cerebellum of individuals with autism spectrum disorder. C1 Ohio State Univ, Ctr Med, Dept Neurol, Columbus, OH 43210 USA. Massachusetts Gen Hosp, NMR Ctr, Boston, MA 02114 USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. Dartmouth Hitchcock Med Ctr, Dept Pediat, Lebanon, NH 03756 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pediat Neurol, Boston, MA 02114 USA. RP Beversdorf, DQ (reprint author), Ohio State Univ, Ctr Med, Dept Neurol, 1654 Upham Dr, Columbus, OH 43210 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 FRADIS A, 1985, ARCH PSYCHIAT NEUROL, V235, P82 Frith U, 1991, AUTISM ASPERGER SYND, P37 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 HAYMAKER W, 1956, BINGS LOCAL DIAGNOSI, P232 Kanner L, 1943, NERV CHILD, V2, P217 Kim JS, 1998, NEUROLOGY, V51, P625 Klatka LA, 1998, NEUROLOGY, V51, P620 LEWITT PA, 1983, J NEUROL NEUROSUR PS, V46, P1152, DOI 10.1136/jnnp.46.12.1152 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 MARGOLIN DI, 1983, ACTA PSYCHOL, V54, P263, DOI 10.1016/0001-6918(83)90039-2 MARTINEZVILA E, 1988, J NEUROL NEUROSUR PS, V51, P1353, DOI 10.1136/jnnp.51.10.1353 NODA S, 1994, NEUROLOGY, V44, P150 Parkinson J, 1817, ESSAY SHAKING PALSY PHILLIPS JG, 1994, MOVEMENT DISORD, V9, P521, DOI 10.1002/mds.870090504 Pick A, 1903, PRAG MED WOCHENSCHR, P1 PULLICINO P, 1994, MOVEMENT DISORD, V9, P371, DOI 10.1002/mds.870090323 RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 Schmahmann J. J., 1994, NEUROBIOLOGY AUTISM, P195 SCOLDING NJ, 1994, J NEUROL NEUROSUR PS, V57, P739, DOI 10.1136/jnnp.57.6.739 Yamamoto K, 1990, Rinsho Shinkeigaku, V30, P113 Yoshida T, 1989, Rinsho Shinkeigaku, V29, P1149 NR 26 TC 19 Z9 20 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 2001 VL 31 IS 1 BP 97 EP 101 DI 10.1023/A:1005622031943 PG 5 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700011 PM 11439759 ER PT J AU Williams, PG Allard, A Sears, L Dalrymple, N Bloom, AS AF Williams, PG Allard, A Sears, L Dalrymple, N Bloom, AS TI Brief report: Case reports on naltrexone use in children with autism: Controlled observations regarding benefits and practical issues of medication management SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID DOUBLE-BLIND; SYMPTOMS C1 Univ Louisville, Kosair Pediat Ctr 100, Louisville, KY 40202 USA. RP Williams, PG (reprint author), Univ Louisville, Kosair Pediat Ctr 100, 571 S Floyd St,Ped-CEC, Louisville, KY 40202 USA. CR Abidin RR, 1995, PARENTING STRESS IND Achenbach TM, 1991, MANUAL CHILD BEHAV C 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 BARRETT RP, 1989, AM J MENT RETARD, V93, P644 BORGHESE IF, 1991, SOC NEUR ABSTR 21 AN BOUVARD MP, 1995, PSYCHIAT RES, V58, P191, DOI 10.1016/0165-1781(95)02601-R Campbell M, 1996, J AM ACAD CHILD PSY, V35, P246, DOI 10.1097/00004583-199602000-00019 CAMPBELL M, 1993, J AM ACAD CHILD PSY, V32, P1283, DOI 10.1097/00004583-199311000-00024 CHAMBERLAIN RS, 1990, BIOL PSYCHIAT, V28, P773, DOI 10.1016/0006-3223(90)90513-2 GILLBERG C, 1995, DEV MED CHILD NEUROL, V37, P239 Gilliam J. 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PD FEB PY 2001 VL 31 IS 1 BP 103 EP 108 DI 10.1023/A:1005674016014 PG 6 WC Psychology, Developmental SC Psychology GA 445WC UT WOS:000169480700012 PM 11439748 ER PT J AU Roeyers, H Buysse, A Ponnet, K Pichal, B AF Roeyers, H Buysse, A Ponnet, K Pichal, B TI Advancing advanced mind-reading tests: Empathic accuracy in adults with a pervasive developmental disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; social cognition; empathic accuracy ID NATURALISTIC SOCIAL COGNITION; HIGH-FUNCTIONING ADULTS; ASPERGER-SYNDROME; STORY CHARACTERS; AUTISM; CHILDREN; INDIVIDUALS; SEX AB Research using advanced but static mind-reading tests with high-functioning adults with a pervasive developmental disorder (PDD) provided evidence for subtle social cognitive deficits. Tn the present study, adults with PDD were unimpaired on such tasks, relative to individually matched normal controls. Significant differences between the two groups were, however, found on a more naturalistic empathic accuracy task developed for this study. Participants viewed two videotaped interactions that both depicted a male and female stranger having an initial conversation and were asked to infer the unexpressed thoughts and feelings of the four targets. Subjects with PDD performed significantly worse on the second video. These findings suggest that the mind-reading deficit of a subgroup of able adults with PDD may only be apparent when a sufficiently complex naturalistic assessment method is being used. C1 Univ Ghent, Dept Psychol, B-9000 Ghent, Belgium. RP Roeyers, H (reprint author), Univ Ghent, Dept Psychol, H Dunantlaan 2, B-9000 Ghent, Belgium. EM Herbert.Roeyers@rug.ac.be CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Baumeister W, 1999, TRENDS CELL BIOL, V9, P81, DOI 10.1016/S0962-8924(98)01423-8 Blair RJR, 1999, PERS INDIV DIFFER, V26, P477, DOI 10.1016/S0191-8869(98)00154-8 BORKE H, 1971, DEV PSYCHOL, V18, P491 BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Buysse A, 1999, PSYCHOL HEALTH, V14, P351, DOI 10.1080/08870449908407333 Dahlgren SO, 1996, J CHILD PSYCHOL PSYC, V37, P759, DOI 10.1111/j.1469-7610.1996.tb01469.x Dawson G., 1989, AUTISM NATURE DIAGNO, P49 Eisenberg N., 1997, EMPATHIC ACCURACY, P73 EISENBERG N, 1991, HDB MORAL BEHAV DEV, V2, P93 FLAVELL JH, 1992, J PIAGET SY, P107 FOMBONNE E, 1994, EUR CHILD ADOLES PSY, V3, P176 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Howlin P., 1997, AUTISM PREPARING ADU Ickes W., 1997, EMPATHIC ACCURACY ICKES W, 1986, J PERS SOC PSYCHOL, V51, P66, DOI 10.1037//0022-3514.51.1.66 Ickes W., 1990, REV PERSONALITY SOCI, P16 ICKES W, 1990, J PERS SOC PSYCHOL, V59, P730, DOI 10.1037//0022-3514.59.4.730 Ickes W., 1988, HDB PERSONAL RELATIO, P79 Jolliffe T, 1999, J AUTISM DEV DISORD, V29, P395, DOI 10.1023/A:1023082928366 Kanner L, 1943, NERV CHILD, V2, P217 KLIN A, 1992, J CHILD PSYCHOL PSYC, V33, P861, DOI 10.1111/j.1469-7610.1992.tb01961.x KURTZ RR, 1972, J CONSULT CLIN PSYCH, V39, P106, DOI 10.1037/h0033190 LEVENSON RW, 1992, J PERS SOC PSYCHOL, V63, P234, DOI 10.1037/0022-3514.63.2.234 LEWY AL, 1992, J ABNORM CHILD PSYCH, V20, P555, DOI 10.1007/BF00911240 MARANGONI C, 1995, J PERS SOC PSYCHOL, V68, P854, DOI 10.1037//0022-3514.68.5.854 Nuyts J, 1997, EUR J DISORDER COMM, V32, P113 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PERNER J, 1985, J EXP CHILD PSYCHOL, V39, P437, DOI 10.1016/0022-0965(85)90051-7 Pierce K, 1997, J AUTISM DEV DISORD, V27, P265, DOI 10.1023/A:1025898314332 SIMPSON JA, 1995, J PERS SOC PSYCHOL, V69, P629, DOI 10.1037//0022-3514.69.4.629 STINSON L, 1992, J PERS SOC PSYCHOL, V62, P787, DOI 10.1037//0022-3514.62.5.787 TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 Wellman H, 1993, UNDERSTANDING OTHER, P10 WILSON FR, 1985, MEAS EVAL COUNS DEV, V18, P3 NR 38 TC 58 Z9 58 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 2001 VL 42 IS 2 BP 271 EP 278 DI 10.1111/1469-7610.00718 PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 428KP UT WOS:000168461100012 PM 11280423 ER PT J AU Gilchrist, A Green, J Cox, A Burton, D Rutter, M Le Couteur, A AF Gilchrist, A Green, J Cox, A Burton, D Rutter, M Le Couteur, A TI Development and current functioning in adolescents with Asperger syndrome: A comparative study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE adolescence; development; Asperger syndrome; autism ID AUTISM DIAGNOSTIC INTERVIEW; CONDUCT DISORDER; CLUSTER-ANALYSIS; CHILDREN; MIND; SPECTRUM; BEHAVIOR; HISTORY AB Adolescents with Asperger syndrome (AS: without delay in speech development, diagnosed according to ICD-10 clinical criteria) were compared with a group with high-functioning autism (HFA: all with delayed speech development), and a group with conduct disorder (CD). Family and genetic studies suggest that Asperger syndrome and autism form part of the same spectrum, whereas the social impairments in conduct disorder are assumed to have different origins. The aims were to explore the relationships between early speech development and other aspects of functioning in autistic disorders, and to compare autistic and nonautistic social impairments. Early and current behaviour and IQ profiles were investigated. The CD group were clearly different from both the AS and HFA groups. The AS group tended to have less severe early behavioural abnormalities than the HFA group, and were unlikely to have speech abnormalities, but other communicative, social, and restricted/stereotyped behavioural difficulties were largely of a similar pattern to the abnormalities in the HFA group. Eighty per cent of the AS group met criteria for autism on the diagnostic algorithm associated with the Autism Diagnostic Interview-Revised. By adolescence, the AS group were reported to be as abnormal as the HFA group but in structured 1:1 interaction their conversation was better. IQ profile in the AS group showed relative strength on verbal measures, unlike the WFA group, but relatively good performance on the Block Design subtest of the WLSC/WAIS was a feature of both the AS and HFA groups. The results indicate closely similar behavioural manifestations may arise by adolescence despite differences in speech development. Follow-up studies and further family investigations will be required to clarify the origins of these and other patterns of autistic development. C1 Royal Cornhill Hosp, Young Peoples Dept, Aberdeen AB25 2ZH, Scotland. Munro Ctr, London, England. Inst Psychiat, London, England. Booth Hall Childrens Hosp, Manchester, Lancs, England. Child & Adolescent Mental Hlth Serv, Macclesfield, Cheshire, England. Fleming Nuffield Unit, Newcastle Upon Tyne, Tyne & Wear, England. RP Gilchrist, A (reprint author), Royal Cornhill Hosp, Young Peoples Dept, Aberdeen AB25 2ZH, Scotland. 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Child Psychol. Psychiatry Allied Discip. PD FEB PY 2001 VL 42 IS 2 BP 227 EP 240 DI 10.1017/S0021963001006631 PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 428KP UT WOS:000168461100008 PM 11280419 ER PT J AU Baron-Cohen, S Wheelwright, S Hill, J Raste, Y Plumb, I AF Baron-Cohen, S Wheelwright, S Hill, J Raste, Y Plumb, I TI The "Reading the Mind in the Eyes" test revised version: A study with normal adults, and adults with Asperger syndrome or high-functioning autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE theory of mind; Asperger's Disorder; autistic disorder; social cognition ID PERCEPTION AB In 1997 in this Journal we published the "Reading the Mind in the Eyes" Test, as a measure of adult "mentalising''. Whilst that test succeeded in discriminating a group of adults with Asperger syndrome (AS) or high-functioning autism (HFA) from controls, it suffered from several psychometric problems. In this paper these limitations are rectified by revising the test. The Revised Eyes Test was administered to a group of adults with AS or HFA (N = 15) and again discriminated these from a large number of normal controls (N = 239) drawn from different samples. In both the clinical and control groups the Eyes Test was inversely correlated with the Autism Spectrum Quotient (the AQ), a measure of autistic traits in adults of normal intelligence. The Revised Eyes Test has improved power to detect subtle individual differences in social sensitivity. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S, 1999, NEUROCASE, V5, P475, DOI 10.1080/13554799908402743 BARONCOHEN S, IN PRESS J DEV LEARN BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 BARONCOHEN S, IN PRESS J AUTISM DE BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 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 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY EKMAN P, 1971, J PERS SOC PSYCHOL, V17, P124, DOI 10.1037/h0030377 FLAVELL JH, 1986, SOC RES CHILD DEV, V51 FLAVELL JH, 1978, CHILD DEV, V49, P1208, DOI 10.1111/j.1467-8624.1978.tb04090.x Morton J., 1991, TRENDS NEUROSCI, V14, P434 Premack D., 1978, BEHAVIORAL BRAIN SCI, V4, P515, DOI [10.1017/S0140525X00076512, DOI 10.1017/S0140525X00076512] Stone V, 1998, PATIENTS AMYGDALECTO STONE V, 1999, J COGNITIVE NEUROSCI, V10, P640 WALKER AS, 1982, J EXP CHILD PSYCHOL, V33, P514, DOI 10.1016/0022-0965(82)90063-7 WECHSLER D, 1939, MEASUREMENT ADULT IN Wellman H. M., 1990, CHILDRENS THEORIES M Whiten Andrew, 1991, NATURAL THEORIES MIN WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Wing L, 1988, ASPECTS AUTISM BIOL World Health Organization, 1994, INT CLASS DIS Young AW, 1996, NEUROPSYCHOLOGIA, V34, P31, DOI 10.1016/0028-3932(95)00062-3 NR 25 TC 1160 Z9 1175 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-4930 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD FEB PY 2001 VL 42 IS 2 BP 241 EP 251 DI 10.1017/S0021963001006643 PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 428KP UT WOS:000168461100009 PM 11280420 ER PT J AU Mottron, L Morasse, K Belleville, S AF Mottron, L Morasse, K Belleville, S TI A study of memory functioning in individuals with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; cognition; memory; neuropsychology; phonological processing ID FREE-RECALL; ASPERGER-SYNDROME; INFANTILE-AUTISM; AMNESIC SYNDROME; CHILDREN; DEFICIT; HIPPOCAMPUS; PERFORMANCE; SIMILARITY; AMYGDALA AB Memory tasks were administered to 14 high-functioning individuals with autism and 14 typically developing individuals matched on chronological age and verbal intelligence. The tasks consisted of free and cued recall of 15 semantically unrelated words in 3 encoding conditions: phonological encoding, semantic encoding, and a no encoding orientation. In both groups: semantic orientation led to better free recall than did orientation toward syllabic encoding or absence of orientation. In contrast, semantic cues at, retrieval led to better cued recall than phonological cues in typically developing individuals, whereas both types of cue had the same effect in prompting cued recall for individuals with autism. These findings are incompatible with the hypothesis of an amnesic deficit and do not support the notion of executive or semantic deficits in the memory problems of autistic individuals, at least for those with a high level of functioning. It is proposed that these findings can be accounted for by enhanced phonological processing in autism. This interpretation is consistent with other findings of enhanced processing of low-level perceptual information in the visual and auditory modality in autism. C1 Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ HE1 1A4, Canada. Univ Montreal, Ctr Rech, Inst Geriatrie, Montreal, PQ H3C 3J7, Canada. RP Mottron, L (reprint author), Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ HE1 1A4, Canada. 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PD FEB PY 2001 VL 42 IS 2 BP 253 EP 260 DI 10.1017/S0021963001006722 PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 428KP UT WOS:000168461100010 PM 11280421 ER PT J AU Liss, M Fein, D Allen, D Dunn, M Feinstein, C Morris, R Waterhouse, L Rapin, I AF Liss, M Fein, D Allen, D Dunn, M Feinstein, C Morris, R Waterhouse, L Rapin, I TI Executive functioning in high-functioning children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; executive function; language disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; FUNCTION DEFICITS; FOLLOW-UP; COMPREHENSION; INDIVIDUALS; CAPACITIES; INTACT; MEMORY; MIND AB Executive functioning was investigated in 34 children (24 boys and 10 girls) with developmental language disorder (DLD) and 21 children (18 boys and 3 girls) with high-functioning autistic disorder (HAD) matched on Full Scale IQ, Nonverbal IQ, age (mean age 9 year, 1 month), and SES. The DLD group had a Verbal IQ that was 10 points higher than the HAD group. These children were given the Wisconsin Card Sorting Test (WCST), the Mazes subtest from the WISC-R, the Underlining test, and the Rapid Automatized Naming test. In addition, these children were given the Vineland Scales of Adaptive Functioning and the Wing Diagnostic Symptom Checklist in order to assess severity of autistic symptomatology. Results indicated that the only significant difference between the two groups on the cognitive tasks was perseverative errors on the WCST; there was no significant difference on total number of categories achieved or total number of errors on the WCST or on the other executive function measures. There was also significant overlap in the scores between the two groups and the difference in perseverative errors was no longer significant when Verbal IQ was partialled out. Executive functioning was strongly related to all IQ variables in the DLD group and particularly related to Verbal IQ in the HAD group. Although there was a relationship in the HAD group between executive functioning and adaptive functioning, as well as between executive functioning and autistic symptomatology, these relationships were generally no longer significant in the HAD group after the variance due to Verbal IQ was accounted for. The results are interpreted to indicate that although impaired executive functioning is a commonly associated feature of autism, it is not universal in autism and is unlikely to cause autistic behaviors or deficits in adaptive function. C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. Stanford Univ, Sch Med, Palo Alto, CA 94304 USA. Coll New Jersey, Trenton, NJ USA. Albert Einstein Sch Med, New York, NY USA. Georgia State Univ, Atlanta, GA 30303 USA. 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A., 1997, AUTISM EXECUTIVE DIS, P57 Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 Wechsler D, 1974, WECHSLER INTELLIGENC Wetherby A., 1988, FOCUS AUTISTIC BEHAV, V4, P1 Wing L., 1985, CLIN DEV MED Yeates KO, 2000, PEDIAT NEUROPSYCHOLO, P92 NR 54 TC 115 Z9 117 PU CAMBRIDGE UNIV PRESS PI PORT CHESTER PA 110 MIDLAND AVE, PORT CHESTER, NY 10573-4930 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD FEB PY 2001 VL 42 IS 2 BP 261 EP 270 DI 10.1017/S0021963001006679 PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 428KP UT WOS:000168461100011 PM 11280422 ER PT J AU Salazar, L Wright, HH AF Salazar, L Wright, HH TI Infantile autism: Exchange and development therapy. SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Book Review C1 Univ S Carolina, Sch Med, Dept Neuropsychiat & Behav Sci, Columbia, SC 29208 USA. RP Salazar, L (reprint author), Univ S Carolina, Sch Med, Dept Neuropsychiat & Behav Sci, Columbia, SC 29208 USA. CR BARTHELEMY C, 1998, INFANTILE AUTISM EXC NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD FEB PY 2001 VL 40 IS 2 BP 258 EP 259 DI 10.1097/00004583-200102000-00024 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 397KL UT WOS:000166694800024 ER PT J AU Cunningham, E AF Cunningham, E TI Is there any research to support a gluten- and casein-free diet for a child that is diagnosed with autism? SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article NR 0 TC 1 Z9 1 PU AMER DIETETIC ASSOC PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 USA SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD FEB PY 2001 VL 101 IS 2 BP 222 EP 222 DI 10.1016/S0002-8223(01)00057-8 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 460MT UT WOS:000170311900020 ER PT J AU Woodward, G AF Woodward, G TI Autism and Parkinson's disease SO MEDICAL HYPOTHESES LA English DT Article ID EPIDEMIOLOGY; PESTICIDES; TOXINS; TWINS AB The pathogenesis of Parkinson's disease, a neurodegenerative disorder, is multifaceted, having a variety of genetic and environmental factors. There is considerable evidence to support the role of toxins, particularly pesticides and herbicides, in at least some of those affected (presumably, mostly the genetically vulnerable). The pathogenesis of autism is no less complex, but little is known about the potential role of toxins for autism, a neurodevelopmental disorder. The incidence of autism appears to be rising, and early exposure to synthetic chemicals is one suspect for this rise. Impaired detoxification of certain chemicals may be common to autism and Parkinson's disease. Further study of environmental influences for either disorder may lead to important insights regarding causation for both, and perhaps for other neurodegenerative and neurodevelopmental disorders as well. (C) 2001 Harcourt Publishers Ltd. C1 Univ Kansas, Dept Neurol, Kansas City, KS USA. RP Woodward, G (reprint author), 873 Harper Dr, Verona, WI 53593 USA. CR Alberti A, 1999, BIOL PSYCHIAT, V46, P420, DOI 10.1016/S0006-3223(98)00337-0 Bhatt MH, 1999, NEUROLOGY, V52, P1467 Caparros-Lefebvre D, 1999, LANCET, V354, P281, DOI 10.1016/S0140-6736(98)10166-6 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Hanna PA, 1999, ARCH NEUROL-CHICAGO, V56, P90, DOI 10.1001/archneur.56.1.90 JENNER P, 1993, PARKINSONS DIS MOVEM, P55 Kates WR, 1998, ANN NEUROL, V43, P782, DOI 10.1002/ana.410430613 Kruger R, 1999, ANN NEUROL, V45, P611, DOI 10.1002/1531-8249(199905)45:5<611::AID-ANA9>3.0.CO;2-X Kuopio AM, 1999, NEUROLOGY, V52, P302 McFadden SA, 1996, TOXICOLOGY, V111, P43, DOI 10.1016/0300-483X(96)03392-6 Mellick GD, 1999, NEUROLOGY, V53, P658 Menegon A, 1998, LANCET, V352, P1344, DOI 10.1016/S0140-6736(98)03453-9 Nakagawa R, 1999, J AOAC INT, V82, P716 *NIEHS, 1999, ENV HLTH PERSPECT, V107, P510 Rodier PM, 1997, REPROD TOXICOL, V11, P417, DOI 10.1016/S0890-6238(97)80001-U Schapira AHV, 1998, ARCH NEUROL-CHICAGO, V55, P1293, DOI 10.1001/archneur.55.10.1293 SILBERGELD EK, 1986, NEUROTOXICOLOGY, V7, P557 Vieregge P, 1999, NEUROLOGY, V53, P566 NR 18 TC 8 Z9 8 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 FEB PY 2001 VL 56 IS 2 BP 246 EP 249 DI 10.1054/mehy.2000.1189 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 406EM UT WOS:000167202000023 PM 11425297 ER PT J AU Borgatti, R Piccinelli, P Passoni, D Dalpra, L Miozzo, M Micheli, R Gagliardi, C Balottin, U AF Borgatti, R Piccinelli, P Passoni, D Dalpra, L Miozzo, M Micheli, R Gagliardi, C Balottin, U TI Relationship between clinical and genetic features in "inverted duplicated chromosome 15" patients SO PEDIATRIC NEUROLOGY LA English DT Article ID INV DUP(15) CHROMOSOMES; MOLECULAR CHARACTERIZATION; MENTAL-RETARDATION; AUTISTIC DISORDER; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; EPILEPSY; PSYCHOPATHOLOGY; PHENOTYPE; 15Q11-13 AB Inverted duplicated chromosome 15 (Inv dup [15]) syndrome is a genetic disorder characterized by psychologic or intellectual language delay; neurologic signs, such as hypotonia, ataxia, and epilepsy; mental retardation ranging from mild to severe; and facial dysmorphisms. All patients present with a psychopathologic impairment that is highly variable in severity but always classifiable as pervasive developmental disorder (PDD), Many genetic mechanisms have been hypothesized to explain the clinical variability. This article describes the neurologic and psychopathologic features of six Inv dup(15) patients, one male and five females, between 8 and 14 years of age, all with a maternal marker chromosome. Four patients were diagnosed with PDD not otherwise specified, whereas two patients received a diagnosis of autism. Epilepsy was present in three patients (two generalized symptomatic and one focal symptomatic), and a correlation between the severity of the disease and its outcome was not always observed. Nevertheless, the influence of gene content of the marker chromosome, particularly the three gamma -aminobutyric acid-A receptor subunit genes, may represent the link between epilepsy, mental retardation, and PDD. (C) 2001 by Elsevier Science Inc. All rights reserved. C1 Sci Inst Eugenio Medea, Dept Child Neurorehabil, Bosisio Parini, Lecco, Italy. Univ Insurbia, Dept Child Neuropsychiat, Varese, Italy. Univ Milan, Dept Biol & Genet Med Scim, Milan, Italy. Brescia Gen Hosp, Dept Child Neuropsychiat, Brescia, Italy. RP Borgatti, R (reprint author), IRCCS Eugenio Medea, Assoc La Nostra Famiglia, Via Don Luigi Monza 20, I-23842 Bosisio Parini, LC, Italy. CR *AM PSYCH ASS, 1994, AM PSYCH ASS DIAGN S, P65 Baker GA, 1996, EPILEPSY RES, V25, P29, DOI 10.1016/0920-1211(96)00017-4 BAKER P, 1994, J AUTISM DEV DISORD, V24, P529, DOI 10.1007/BF02172133 BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 Battaglia A, 1997, NEUROLOGY, V48, P1081 BLENNOW E, 1994, PRENATAL DIAG, V14, P1019, DOI 10.1002/pd.1970141103 Browne CE, 1997, AM J HUM GENET, V61, P1342, DOI 10.1086/301624 CHENG SD, 1994, AM J HUM GENET, V55, P753 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 1997, AM J HUM GENET, V60, P928 DeLong GR, 1999, NEUROLOGY, V52, P911 DODRILL CB, 1984, EPILEPSIA, V25, P168, DOI 10.1111/j.1528-1157.1984.tb04173.x Ferrarese C, 1998, EPILEPSY RES, V29, P129, DOI 10.1016/S0920-1211(97)00074-0 Flejter WL, 1996, AM J MED GENET, V61, P182, DOI 10.1002/(SICI)1096-8628(19960111)61:2<182::AID-AJMG17>3.0.CO;2-Q Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 GRAMMATICO P, 1994, CLIN GENET, V46, P233 GRIFFITHS R, 1984, COMP SYSTEM MENTAL M HERMANN BP, 1990, BRIT J PSYCHIAT, V156, P98, DOI 10.1192/bjp.156.1.98 Huang B, 1997, HUM GENET, V99, P11 International League Against Epilepsy, 1989, EPILEPSIA, V30, P389 Knight SJL, 1999, LANCET, V354, P1676, DOI 10.1016/S0140-6736(99)03070-6 Lauritsen M, 1999, J CHILD PSYCHOL PSYC, V40, P335, DOI 10.1017/S0021963098003710 LEANACOX J, 1994, AM J HUM GENET, V54, P748 Mignon C, 1996, EUR J HUM GENET, V4, P88 Miozzo M, 1996, CANCER RES, V56, P2285 Mohandas TK, 1999, AM J MED GENET, V82, P294, DOI 10.1002/(SICI)1096-8628(19990212)82:4<294::AID-AJMG4>3.0.CO;2-U Repetto GR, 1998, AM J MED GENET, V79, P82, DOI 10.1002/(SICI)1096-8628(19980901)79:2<82::AID-AJMG2>3.0.CO;2-P Robinson Wendy P., 1993, European Journal of Human Genetics, V1, P37 SCHRECK RR, 1977, HUM GENET, V36, P1, DOI 10.1007/BF00390430 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 WEBB T, 1994, J MED GENET, V31, P585, DOI 10.1136/jmg.31.8.585 Woods CG, 1997, AM J HUM GENET, V61, pA117 NR 32 TC 40 Z9 40 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD FEB PY 2001 VL 24 IS 2 BP 111 EP 116 DI 10.1016/S0887-8994(00)00244-7 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 418AV UT WOS:000167868400004 PM 11275459 ER PT J AU Fombonne, E AF Fombonne, E TI Is there an epidemic of autism? SO PEDIATRICS LA English DT Editorial Material C1 Inst Psychiat, MRC, Child Psychiat Unit, London SE5 8AF, England. RP Fombonne, E (reprint author), Inst Psychiat, MRC, Child Psychiat Unit, De Crespigny Pk, Denmark Hill, London SE5 8AF, England. CR Department of Developmental Services, 1999, CHANG POP PERS AUT P Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 FOMBONNE E, 2001, ED CHILDREN AUTISM Volkmar FR, 2000, J AUTISM DEV DISORD, V30, P74 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 NR 6 TC 119 Z9 127 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 FEB PY 2001 VL 107 IS 2 BP 411 EP 413 DI 10.1542/peds.107.2.411 PG 4 WC Pediatrics SC Pediatrics GA 397TT UT WOS:000166714000044 PM 11158478 ER PT J AU Pickup, GJ Frith, CD AF Pickup, GJ Frith, CD TI Theory of mind impairments in schizophrenia: symptomatology, severity and specificity SO PSYCHOLOGICAL MEDICINE LA English DT Article ID PEOPLE; BELIEFS; AUTISM; CLASSIFICATION; ATTRIBUTION; DEFICIT; OTHERS AB Background. Several studies have examined the ability of schizophrenic patients to represent mental states ("theory of mind"; ToM). There is consensus that some patients have impaired ToM, but there is disagreement about the relation between ToM and symptomatology, and about the severity and specificity of the deficit. Methods. Two first-order and one second-order false belief tests of ToM were given to groups of schizophrenic patients and psychiatric and normal controls. The relation between ToM and symptomatology was explored using regression and symptom subgroup analyses. Severity was investigated by using the same task methodology as in autism research, to enable direct comparison with that disorder. Specificity was investigated using matched control tasks which were as difficult as the ToM tasks, but did not require ToM. Results. Symptom subgroup analysis showed that schizophrenic patients with behavioural signs were impaired relative to controls on ToM, and that remitted patients and a single case with passivity symptoms performed as well as controls. Regression analysis showed that ratings of behavioural signs predicted impaired ToM in schizophrenia. There was weak evidence that a subgroup with paranoid symptoms had ToM impairments, although these were associated with low IQ. Schizophrenic patients only showed ToM deficits on the second-order task. No impairments appeared on the matched control tasks which did not require ToM. Conclusions. There is a clear association between ToM impairment and behavioural signs in schizophrenia. Deficits in paranoid patients are harder to detect with current tasks and may be compensated for by IQ-dependent problem-solving skills. ToM impairments in schizophrenia are less severe than in autism, but are specific and not a reflection of general cognitive deficits. C1 UCL, Sub Dept Clin Hlth Psychol, London, England. Neurol Inst, Dept Cognit Neurol, London, England. RP Pickup, GJ (reprint author), Hunter St Hlth Ctr, Dept Clin Psychol, 8 Hunter St, London WC1N 3BN, England. 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PD FEB PY 2001 VL 31 IS 2 BP 207 EP 220 PG 14 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 402TM UT WOS:000167004300003 PM 11232909 ER PT J AU Zarate, P Diaz, V AF Zarate, P Diaz, V TI Medical uses of musical therapy SO REVISTA MEDICA DE CHILE LA Spanish DT Article DE Alzheimer disease; music therapy; Parkinson disease; psychotherapy ID CARE AB Music therapy is a science that has been applied since many centuries ago, but it has been organized as a profession during the past century. This science studies the therapeutic effects of music in human beings. Professionals who practice this science are called "music therapists" and they must be trained not only in music theory and performance, but also in psychology, anatomy, research techniques, and other subjects. Today, we can find music therapy research in many areas such as the effects of music in children with autism, adults with psychiatric illnesses, elderly with Alzheimer and Parkinson disease, people with brain injuries, among others. Numerous studies demonstrate the functionality of music therapy in patients with neurological disorders. These studies show that music helps patients to gain control over their walking patterns after a brain injury, stimulates long and short term memory in patients with Alzheimer disease, and increase self esteem and social interaction in elders. C1 Univ Chile, Hosp Clin, Santiago, Chile. RP Diaz, V (reprint author), Hosp JJ Aguirre, 2 Piso E Santos Dumont 999, Santiago, Chile. 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Medica Chile PD FEB PY 2001 VL 129 IS 2 BP 219 EP 223 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 421JK UT WOS:000168061100015 PM 11351476 ER PT J AU Jolliffe, T Baron-Cohen, S AF Jolliffe, T Baron-Cohen, S TI A test of central coherence theory: Can adults with high-functioning autism or Asperger syndrome integrate objects in context? SO VISUAL COGNITION LA English DT Article ID CHILDS THEORY; MIND; PERFORMANCE; INDIVIDUALS; EXPLORATION; DISCOURSE; ABILITIES; TASK AB Weak central coherence was investigated by exploring the conceptual integration of objects. Normally intelligent adults with either autism or Asperger syndrome were given two novel experiments. Experiment 1, the Object Integration test, had sets of line drawings depicting objects and people. Each set had to be either visually integrated to make the most coherent scene, or compared for similarities. The clinical groups were significantly impaired in their ability to integrate objects, but they were not impaired in looking for similarities. Experiment 2, the Scenic test, presented black line drawings of scenes containing an item that was inappropriate for the context. Participants were required to describe the scenes, identify the type of scene and context-inappropriate object, and locate a name (incongruent) object as quickly as they could. The clinical groups' descriptions suggest that they did not spontaneously pay preferential treatment to local details, nor were they faster at locating a named incongruent object. Whereas only a few of their descriptions lacked coherence, there was a deficit in both their ability to spontaneously notice and identify incongruent objects, as well as to identify the scenes. These tests provide support for Frith's (1989) central coherence hypothesis. 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A genetic etiology is assumed in context with brain dysfunctions and neuropsychological deficits which are ail focused upon nonverbal learning, even though the general intellectual level is within the normal range. Treatment must take into account the individual aspects of each case and is based mainly on behavior therapy, group training of social skills, vocational training and adaptation, and if necessary, on medication, Medical treatment is indicated in the presence:of special symptoms such as hyperactivity, aggressive behavior, sleep disorders, or depression. C1 Univ Marburg, Klin Psychiat & Psychotherapie Kindes & Jugendalt, D-35033 Marburg, Germany. RP Remschmidt, H (reprint author), Univ Marburg, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Hans Sachs Str 6, D-35033 Marburg, Germany. 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PD FEB PY 2001 VL 29 IS 1 BP 59 EP 69 DI 10.1024//1422-4917.29.1.59 PG 11 WC Psychiatry SC Psychiatry GA 402BB UT WOS:000166965100007 PM 11234553 ER PT J AU Laakso, MP Vaurio, O Koivisto, E Savolainen, L Eronen, M Aronen, HJ Hakola, P Repo, E Soinien, H Tiihonen, J AF Laakso, MP Vaurio, O Koivisto, E Savolainen, L Eronen, M Aronen, HJ Hakola, P Repo, E Soinien, H Tiihonen, J TI Psychopathy and the posterior hippocampus SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE aggression; behavior; human; psychopathy; sociopathy; violence ID MEDIAL TEMPORAL-LOBE; DAMAGE; AUTISM; FEAR; IMPAIRMENT; ALCOHOLISM; VIOLENCE AB Neurobiology of psychopathy is of interest, not only because neural underpinnings of psychopathy remain obscure, but also because psychopaths may provide a model to study violent behavior, neurology of morals and impaired decision-making. Medial temporal lobe pathology has been suggested to be a part of the neural systems dysfunction which manifests as violent and psychopathic behavior. Yet, so far no sound evidence of neuroanatomical correlates for psychopathic behavior has been found. In this study regional hippocampal volumes were measured using magnetic resonance imaging in 18 habitually violent offenders with antisocial personality disorder and type 2 alcoholism (derived from forensic psychiatric evaluation). The regional volumes along the anteroposterior axis of the hippocampus were correlated with the subjects' degree of psychopathy as evaluated by the Psyhopathy Checklist-Revised. Strong negative correlations, up to - 0.79, were observed, among the study subjects, between the psychopathy scores and the posterior half of the hippocampi bilaterally. These data are in accordance with experimental studies proposing that lesions of the dorsal hippocampus impair acquisition of conditioned fear, and with theories on psychopathology according to which one of the central features in the birth of psychopathy is a deficit in acquisition of conditioned fear. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Kuopio Univ Hosp, Dept Neurol, Kuopio 70211, Finland. Kuopio Univ Hosp, Dept Clin Radiol, Kuopio 70211, Finland. Univ Kuopio, Niuvanniemi Hosp, Dept Forens Psychiat, Kuopio 70240, Finland. Vanha Vaasa Hosp, Vaasa 65381, Finland. Univ Kuopio, Dept Neurosci & Neurol, FIN-70211 Kuopio, Finland. Kuopio Univ Hosp, Dept Clin Physiol, Kuopio 70211, Finland. RP Laakso, MP (reprint author), Kuopio Univ Hosp, Dept Neurol, Bldg 5,POB 1777, Kuopio 70211, Finland. 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PD JAN 27 PY 2001 VL 322 IS 7280 BP 183 EP 184 DI 10.1136/bmj.322.7280.183 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 398BF UT WOS:000166733700001 PM 11159597 ER PT J AU Tierney, E Nwokoro, NA Porter, FD Freund, LS Ghuman, JK Kelley, RI AF Tierney, E Nwokoro, NA Porter, FD Freund, LS Ghuman, JK Kelley, RI TI Behavior phenotype in the RSH/Smith-Lemli-Opitz syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article; Proceedings Paper CT 46th Annual Meeting of the American-Academy-of-Child-and-Adolescent-Psychiatry CY OCT 19-24, 1999 CL CHICAGO, IL SP Amer Acad Child & Adolescent Psychiat DE Smith-Lemli-Opitz syndrome; behavior phenotype cholesterol; 7-dehyrocholesterol; metabolic disorder; autism; Autism Diagnostic Interview (ADI); Sensory Profile; Screen for Social Interaction; temperament dysregulation; multiple congenital disorder; opisthokinesis; Temperament and Atypical Behavior Scale (TABS) ID DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; SENSORY PROFILE; RSH SYNDROME; RATING FORM; CHILDREN; AUTISM; DISABILITIES; PERFORMANCE; DISORDERS AB The behavior phenotype of Smith-Lemli-Opitz syndrome (SLOS) was studied by assessing behavior, social, and communication abilities, sensory hyperreactivity, and the deficits associated with autistic disorder. Fifty-six SLOS subjects, age 0.3 to 32.3 years, were evaluated by multiple age-dependent questionnaires and telephone interviews. Of the 56 subjects, 50 (89%) had a history of repeated self-injury: 30 (54%) bit themselves; 27 (48%) head-banged; and 30 (54%) threw themselves backward in a highly characteristic upper body movement ("opisthokinesis"). Forty-seven of these subjects were also evaluated by direct observation and by direct interview of the parent or caregiver. Of 11 subjects 10 years or older, three (27%) had a stereotypic stretching motion of the upper body accompanied by hand flicking. Additional measures showed sensory hyperreactivity, temperament dysregulation, sleep disturbance, and social and communication deficits. Nine of 17 subjects (53%) met the diagnostic criteria for autistic disorder by the Autism Diagnostic Interview-Revised (ADI-R) algorithm questions [Lord et al,, 1993, 1994]. 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J. Med. Genet. PD JAN 15 PY 2001 VL 98 IS 2 BP 191 EP 200 DI 10.1002/1096-8628(20010115)98:2<191::AID-AJMG1030>3.0.CO;2-M PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 389BE UT WOS:000166217900013 PM 11223857 ER PT J AU Petrovic, M Roberts, R Ramsay, M AF Petrovic, M Roberts, R Ramsay, M TI Second dose of measles, mumps, and rubella vaccine: questionnaire survey of health professionals SO BRITISH MEDICAL JOURNAL LA English DT Article ID ADVERSE EVENTS; SURVEILLANCE; CAUSAL AB Objective To determine the knowledge, attitudes, and practices among health professionals regarding the measles, mumps, and rubella (MMR) vaccine, particularly the second dose. Design Self administered postal questionnaire survey. Setting North Wales Health Authority, 1998. Participants 148 health visitors, 239 practice nurses, and 206 general practitioners. Main outcome measures Respondents' views on MMR vaccination, including their views on the likelihood of an association with autism and Crohn's disease and on who is the best person to give advice to parents, whether they agree with the policy of a second dose of the vaccine, and how confident they are in explaining the rationale behind the second dose. Results Concerning the second dose of the vaccine, 48% of the professionals (220/460) had reservations and 3% (15) disagreed with the policy of giving it Over half the professionals nominated health visitors as the best initial source of advice on the second vaccine. 61% of health visitors (86/140), compared with 46% of general practitioners (73/158), reported feeling very confident about explaining the rationale of a two dose schedule to a well informed parent, but only 20% (28/138) would unequivocally recommend the second dose to a wavering parent 33% of the practice nurses (54/163) stated that the MMR vaccine was very likely or possibly associated with Crohn's disease and 27% (44/164) that it was associated with autism. Nearly a fifth of general practitioners (27/158) reported that they had not read the MMR section in the "green book," and 29% (44/152) reported that they had not received the Health Education Authority's factsheet on MMR immunisation. Conclusions Knowledge and practice among health professionals regarding the second dose of the MMR vaccine vary widely. Many professionals are not aware of or do not use the good written resources that exist, though local educational initiatives could remedy this. C1 N Wales Hlth Author, Dept Publ Hlth, Mold, Flint, Wales. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, London NW9 5EQ, England. RP Petrovic, M (reprint author), N Wales Hlth Author, Dept Publ Hlth, Mold, Flint, Wales. 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PD JAN 13 PY 2001 VL 322 IS 7278 BP 82 EP 85 DI 10.1136/bmj.322.7278.82 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 393XZ UT WOS:000166496100027 PM 11154622 ER PT J AU Leal, SM AF Leal, SM TI Phenotypes and genetic analysis of psychiatric and neuropsychiatric traits SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Editorial Material DE phenotype; complex traits; statistical genetics; workshop; psychiatric and neuropsychiatric traits ID INCIDENCE AUTISM FAMILIES; SCHIZOPHRENIA; DISORDER; CRITERIA; LINKAGE; PARENTS AB A workshop was held at Rockefeller University entitled "Phenotypes and Genetic Analysis of Complex Traits." The purpose of the workshop was to examine phenotype definition for complex traits, in particular, psychiatric and neuropsychiatric traits. An additional goal of the workshop was to examine statistical genetic approaches that specifically address the oligogenic nature of psychiatric traits. An overview of topics that were addressed and discussed at the workshop is presented in this article. Am, J. Med. Genet, (Neuropsychiatr. Genet,) 105:4-7, 2001, (C) 2001 Wiley-Liss, Inc. C1 Rockefeller Univ, Lab Stat Genet, New York, NY 10021 USA. RP Leal, SM (reprint author), Rockefeller Univ, Lab Stat Genet, 1230 York Ave,Box 192, New York, NY 10021 USA. CR BAILEY A, 1995, PSYCHOL MED, V25, P63 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x FARAONE SV, 1995, AM J PSYCHIAT, V152, P1286 Freedman R, 1997, P NATL ACAD SCI USA, V94, P587, DOI 10.1073/pnas.94.2.587 Gogos JA, 1999, NAT GENET, V21, P434 KENDELL RE, 1982, ARCH GEN PSYCHIAT, V39, P1334 Leckman JF, 1997, AM J PSYCHIAT, V154, P911 LEVY DL, 1994, SCHIZOPHRENIA BULL, V20, P47 MCGUFFIN P, 1991, ARCH GEN PSYCHIAT, V48, P764 MEEHL PE, 1962, AM PSYCHOL, V17, P827, DOI 10.1037/h0041029 Piven J, 1997, J CHILD PSYCHOL PSYC, V38, P1011, DOI 10.1111/j.1469-7610.1997.tb01618.x Piven J, 1997, AM J MED GENET, V74, P398, DOI 10.1002/(SICI)1096-8628(19970725)74:4<398::AID-AJMG11>3.0.CO;2-D Weissman MM, 1999, ARCH GEN PSYCHIAT, V56, P794, DOI 10.1001/archpsyc.56.9.794 Weissman MM, 2000, AM J MED GENET, V96, P24, DOI 10.1002/(SICI)1096-8628(20000207)96:1<24::AID-AJMG7>3.0.CO;2-E NR 14 TC 8 Z9 8 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 8 PY 2001 VL 105 IS 1 BP 4 EP 7 DI 10.1002/1096-8628(20010108)105:1<4::AID-AJMG1043>3.3.CO;2-M PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 390GA UT WOS:000166286300002 PM 11424993 ER PT J AU Piven, J AF Piven, J TI The broad autism phenotype: A complementary strategy for molecular genetic studies of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; phenotype; genetics; linkage ID TWIN; FAMILIES; PARENTS AB The genetic liability for autism appears to be expressed not only as the full syndrome of autism, but in milder, qualitatively similar characteristics that collectively have been referred to as constituting the broad autism phenotype, Identification of components of the broad autism phenotype that segregate independently in relatives of autistic individuals may provide an index of genes that, when present together, may interact to produce autism. Inclusion of information on the broad autism phenotype in relatives, in linkage studies of autism, may provide a potentially important, complementary approach for detecting the genes causing this condition. Am. J, Med, Genet, (Neuropsychiatr, Genet,) 105:34-35, 2001, (C) 2001 Wiley-Liss, Inc. C1 Univ N Carolina, N Carolina Mental Retardat & Dev Disabil Res Ctr, Chapel Hill, NC 27599 USA. Univ N Carolina, Div TEACCH, Chapel Hill, NC USA. RP Piven, J (reprint author), Univ N Carolina, N Carolina Mental Retardat & Dev Disabil Res Ctr, CB 7250, Chapel Hill, NC 27599 USA. CR BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett S, 1999, AM J MED GENET, V88, P609 Bolton P., 1994, J CHILD PSYCHOL PSYC, V35, P77 FISCHER S, 1998, NAT GENET, V18, P168 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Grigorenko EL, 1997, AM J HUM GENET, V60, P27 Bailey A, 1998, HUM MOL GENET, V7, P571 Maestrini E, 1998, J AUTISM DEV DISORD, V28, P427, DOI 10.1023/A:1026056522602 PICKLES A, 1995, AM J HUM GENET, V57, P717 Piven J, 1997, J CHILD PSYCHOL PSYC, V38, P1011, DOI 10.1111/j.1469-7610.1997.tb01618.x Piven J, 1997, AM J MED GENET, V74, P398, DOI 10.1002/(SICI)1096-8628(19970725)74:4<398::AID-AJMG11>3.0.CO;2-D Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 NR 12 TC 65 Z9 68 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 2001 VL 105 IS 1 BP 34 EP 35 DI 10.1002/1096-8628(20010108)105:1<34::AID-AJMG1052>3.0.CO;2-D PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 390GA UT WOS:000166286300011 PM 11424990 ER PT J AU Lord, C Leventhal, BL Cook, EH AF Lord, C Leventhal, BL Cook, EH TI Quantifying the phenotype in autism spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; PDD-NOS; ADI-R; ADOS; phenotype ID GENOMIC SCREEN; CHILDREN; DOMAINS AB Twin and family studies suggest that familial transmission in autism extends to a spectrum of social and behavioral deficits that characterize individuals who have significant impairments within the autism spectrum, but do not meet formal criteria for autistic disorder. Standardized diagnostic instruments, including the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS-WPS Edition), offer the opportunity to quantify deficits across the autism spectrum, controlling effects of language and cognitive delay, in individuals with significant impairments. It is suggested that quantitative measures of social reciprocity and repetitive behaviors and interests, with separate quantification of expressive language level and nonverbal intelligence, most accurately reflect the range of behavioral phenotypes in autism spectrum disorders. Am. J, Med, Genet, (Neuropsychiatr. Genet,) 105:36-38, 2001, (C) 2001 Wiley-Liss, Inc. C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. RP Lord, C (reprint author), Univ Chicago, Dept Psychiat, MC 3077,5841 S Maryland Ave, Chicago, IL 60637 USA. 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PD JAN 8 PY 2001 VL 105 IS 1 BP 36 EP 38 DI 10.1002/1096-8628(20010108)105:1<36::AID-AJMG1053>3.0.CO;2-4 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 390GA UT WOS:000166286300012 PM 11424991 ER PT J AU Young, LJ AF Young, LJ TI Oxytocin and vasopressin as candidate genes for psychiatric disorders: Lessons from animal models SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; neuropeptides; social behavior ID MATERNAL-BEHAVIOR AB Multiple approaches should be taken to investigate the genetic bases of psychiatric disorders, including the consideration of candidate genes. Studies in animal models suggest that the genes encoding oxytocin, vasopressin, and their respective receptors should be considered in a candidate gene approach for psychiatric disorders involving social deficits, such as autism or social phobias. These neuropeptide hormones may mediate the rewarding nature of social interactions and have been implicated in social attachment and social recognition in several animal models. Mutations in genes unrelated to oxytocin and vasopressin have been shown to have secondary effects on neuropeptide function and subsequent behavioral phenotypes, Genetic analysis of polymorphisms and expression analysis of candidate genes implicated in animal models may prove useful for determining the molecular mechanisms underlying psychiatric disorders, particularly in cases where other techniques proven difficult. Am. J, Med, Genet, (Neuropsychiatr. Genet,) 105: 53-54, 2001, (C) 2001 Wiley-Liss, Inc. C1 Emory Univ, Dept Psychiat, Yerkes Res Ctr, Atlanta, GA 30322 USA. Emory Univ, Ctr Behav Neurosci, Atlanta, GA 30322 USA. RP Young, LJ (reprint author), Emory Univ, Dept Psychiat, Yerkes Res Ctr, 954 Gatewood Rd, Atlanta, GA 30322 USA. 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PD JAN 8 PY 2001 VL 105 IS 1 BP 53 EP 54 DI 10.1002/1096-8628(20010108)105:1<53::AID-AJMG1059>3.0.CO;2-U PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 390GA UT WOS:000166286300018 PM 11424998 ER PT J AU Einfeld, SL Tonge, BJ Rees, VW AF Einfeld, SL Tonge, BJ Rees, VW TI Longitudinal course of behavioral and emotional problems in Williams syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID MENTAL-RETARDATION; CHILDREN; ADULTS; DISTURBANCE; ADOLESCENTS; ABILITIES; AUTISM AB A follow-up study of behavior and emotional problems in a cohort of young people with Williams syndrome 5 years after first assessment is described. Using a between-/within-subjects factorial layout, we compared scores on the Developmental Behaviour Checklist between young people with Williams syndrome and a large epidemiological control sample of young people with mental retardation due to other causes from Time 1 (1990/1991) to Time 2 (1995/1996) Results showed substantial persistence of the overall level of behavior and emotional problems. However, there were changes in certain types of behavior. Participants with Williams syndrome had significantly higher overall behavioral and emotional problems, communication disturbance, and anxiety over the 5-year period. Further, 10 or 13 checklist items maintained significantly higher levels among the Williams syndrome sample. C1 Univ New S Wales, Sydney, NSW, Australia. Monash Univ, Melbourne, Vic 3004, Australia. RP Einfeld, SL (reprint author), FRANZCP, 2 Short St, Kogarah, NSW 2217, Australia. 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J. Ment. Retard. PD JAN PY 2001 VL 106 IS 1 BP 82 EP 93 DI 10.1352/0895-8017(2001)106<0082:ABOTYO>2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 402DJ UT WOS:000166970500009 PM 11246716 ER PT J AU Williams, MA Bradshaw, JL Moss, SA Rinehart, NJ AF Williams, MA Bradshaw, JL Moss, SA Rinehart, NJ TI The possibility of temporal and spatial selectivity abnormalities in low-functioning individuals with autism SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. EM mark.williams@sci.monash.edu.au NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2001 VL 53 SU S BP 69 EP 69 PG 1 WC Psychology, Multidisciplinary SC Psychology GA V42OE UT WOS:000202876000317 ER PT J AU Rinehart, NJ Bradshaw, JL Brenton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Brenton, AV Tonge, BJ TI A neurobehavioural and clinical comparison of children with high-functioning autism and Asperger's disorder SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. EM nicole.rinehart@sci.monash.edu.au NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2001 VL 53 SU S BP 172 EP 172 PG 1 WC Psychology, Multidisciplinary SC Psychology GA V42OE UT WOS:000202876001293 ER PT J AU Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ TI An examination of left-hemisphere anomalies in high-functioning autism and Asperger's disorder using executive function and visual-perceptual paradigms SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. EM nicole.rinehart@med.monash.edu.au NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2001 VL 53 SU S BP 172 EP 172 PG 1 WC Psychology, Multidisciplinary SC Psychology GA V42OE UT WOS:000202876001294 ER PT J AU Wong, DK Maybery, M Hallmayer, J Maley, A Petterson, N Hill, W Bishop, D AF Wong, DK Maybery, M Hallmayer, J Maley, A Petterson, N Hill, W Bishop, D TI Executive functioning in children with autism and their first-degree relatives SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Western Australia, Nedlands, WA 6009, Australia. Stanford Univ, Stanford, CA 94305 USA. Ctr Clin Res Neuropsychiat, Claremont, Australia. Univ Oxford, Oxford OX1 2JD, England. EM dana@psy.uwa.edu.au NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2001 VL 53 SU S BP 203 EP 203 PG 1 WC Psychology, Multidisciplinary SC Psychology GA V42OE UT WOS:000202876001428 ER PT J AU Gutknecht, L AF Gutknecht, L TI Full-genome scans with autistic disorder: A review SO BEHAVIOR GENETICS LA English DT Article DE autistic disorder; affected sib pair; linkage; multipoint MLS; genetic heterogeneity ID GENETICALLY COMPLEX TRAITS; SEROTONIN TRANSPORTER 5-HTT; AFFECTED RELATIVE PAIRS; LINKAGE STRATEGIES; LANGUAGE DISORDER; PSYCHIATRIC-DISORDERS; FAMILY HISTORY; GENE; REGION; TWIN AB Autistic disorder is characterized by severe disturbances of social relatedness, impairments in language and communication, and restricted, repetitive, and stereotyped patterns of behaviors. Accumulated data strongly support the notion that genetic factors, as yet undetermined, play a significant role in the etiology of this syndrome. As genetic research in autism is still exploratory, full genomewide searches have been performed to localize susceptibility regions within the genome. Methods and results from the four first full-genome scans published to date (IMGSAC, 1998a; Philippe et al., 1999; Risch et al., 1999d; Barrett et al., 1999) are considered in this review. The four sets of multipoint linkage results are grouped in a single figure to facilitate comparisons among the four studies and with previous or future results. Although findings must be considered with caution because LOD score values do not reach the threshold for significant linkage, a region of approximately 50 cM on the long arm of chromosome 7 appears to play a role in the etiology of autistic disorder. C1 CNRS FRE 2134, F-45071 Orleans 02, France. RP Gutknecht, L (reprint author), CNRS FRE 2134, 3B Ferollerie, F-45071 Orleans 02, France. 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Genet. PD JAN PY 2001 VL 31 IS 1 BP 113 EP 123 DI 10.1023/A:1010218227600 PG 11 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 465HX UT WOS:000170584500011 PM 11529268 ER PT J AU Luiselli, JK Blew, P Thibadeau, S AF Luiselli, JK Blew, P Thibadeau, S TI Therapeutic effects and long-term efficacy of antidepressant medication for persons with developmental disabilities - Behavioral assessment in two cases of treatment-resistant aggression and self-injury SO BEHAVIOR MODIFICATION LA English DT Article ID MENTAL-RETARDATION; FLUOXETINE TREATMENT; ADULTS AB Recent advances in pharmacological treatment of severe behavior disorders in persons with developmental disabilities suggest the use of antidepressant medication for therapeutic management. This research evaluated two antidepressant medications for treatment-resistant aggression and self-injury exhibited by two persons with developmental disabilities. Behavioral assessment data documented that sertraline (a serotonin selective reuptake inhibitor) was effective in reducing self-injurious behaviors in a 20-year-old man with severe mental retardation and clomipramine (a tricyclic antidepressant) was associated with the elimination of aggressive behavior in a l l-year-old boy with autism. Clinical effects from the medications were measured in relation to and shown to be a function of dosage level. Extended follow-up assessments revealed maintenance of treatment gains with continued medication administration. C1 May Inst Inc, May Ctr Appl Res, Norwood, MA 02062 USA. RP Luiselli, JK (reprint author), May Inst Inc, May Ctr Appl Res, Norwood, MA 02062 USA. 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Modificat. PD JAN PY 2001 VL 25 IS 1 BP 62 EP 78 DI 10.1177/0145445501251004 PG 17 WC Psychology, Clinical SC Psychology GA 420KL UT WOS:000168004100004 PM 11151486 ER PT J AU Sherer, M Pierce, KL Paredes, S Kisacky, KL Ingersoll, B Schreibman, L AF Sherer, M Pierce, KL Paredes, S Kisacky, KL Ingersoll, B Schreibman, L TI Enhancing conversation skills in children with autism via video technology - Which is better, "self" or "other" as a model? SO BEHAVIOR MODIFICATION LA English DT Article ID RECOGNITION; SETTINGS AB The present study was designed to compare the efficacy of "self" versus "other" video-modeling interventions. Five children with autism ranging in age from 4 to 11 were taught to answer a series of conversation questions in both self and other video-modeled conditions. Results were evaluated using a combination of a multiple baseline and alternating treatments design. Three out of the five participants performed at levels of 100% accuracy at posttreatment. Results indicated no overall difference in rate of task acquisition between the two conditions, implying that children who were successful at learning from video in general, learned equally as well via both treatment approaches. Anecdotal evidence suggested that participants who were successful with video treatment had higher visual learning skills than children who were unsuccessful with this approach. Results are discussed in terms of a visual learning model for children with autism. C1 Univ Calif San Diego, San Diego, CA 92103 USA. RP Sherer, M (reprint author), Univ Calif San Diego, San Diego, CA 92103 USA. 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Modificat. PD JAN PY 2001 VL 25 IS 1 BP 140 EP 158 DI 10.1177/0145445501251008 PG 19 WC Psychology, Clinical SC Psychology GA 420KL UT WOS:000168004100008 PM 11151482 ER PT J AU McKerchar, TL Kahng, S Casioppo, E Wilson, D AF McKerchar, TL Kahng, S Casioppo, E Wilson, D TI Functional analysis of self-injury maintained by automatic reinforcement: Exposing masked social functions SO BEHAVIORAL INTERVENTIONS LA English DT Article ID EXTINCTION AB Two functional analyses for self-injurious behavior (SIB) exhibited by a child diagnosed with mental retardation and autism were conducted. Responding was high and undifferentiated in the first functional analysis, indicating that SIE was maintained by automatic reinforcement. During the second functional analysis, the client wore a padded helmet and all SIE was blocked. SIE decreased in all conditions except attention. suggesting that SIE was multiply controlled (social positive and automatic reinforcement). Copyright (C) 2001 John Wiley & Sons, Ltd. C1 Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. RP Kahng, S (reprint author), Kennedy Krieger Inst, Neurobehav Unit, 707 N Broadway, Baltimore, MD 21205 USA. RI Kahng, SungWoo/A-9994-2009 CR 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 Lerman DC, 1996, J APPL BEHAV ANAL, V29, P231, DOI 10.1901/jaba.1996.29-231 MAZALESKI JL, 1994, J APPL BEHAV ANAL, V27, P345, DOI 10.1901/jaba.1994.27-345 NR 4 TC 6 Z9 6 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 JAN-MAR PY 2001 VL 16 IS 1 BP 59 EP 63 DI 10.1002/bin.78 PG 5 WC Psychology, Clinical SC Psychology GA 411DP UT WOS:000167483100005 ER PT S AU Peretz, I AF Peretz, I BE Zatorre, RJ Peretz, I TI Brain specialization for music: New evidence from congenital amusia SO BIOLOGICAL FOUNDATIONS OF MUSIC SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on the Biological Foundations of Music CY MAY 20-22, 2000 CL NEW YORK, NEW YORK SP Charles A Dana Fdn, David & Lucile Packard Fdn HO ROCKEFELLER UNIV DE music agnosia; congenital amusia; music-specific neural networks; tone-deafness ID DEFICITS; AGNOSIA; DISCRIMINATION; INTERVALS; PATTERNS; AUTISM AB Brain specialization for music refers to the possibility that the human brain is equipped with neural networks that are dedicated to the processing of music. Finding support for the existence of such music-specific networks suggests that music may have biological roots. Conversely, the discovery that music may have systematic associations with other cognitive domains or variable brain organization across individuals supports the view that music is a cultural artifact. Currently, the evidence favors the biological perspective. There are numerous behavioral indications that music-specific networks are isolable in the brain. These neuropsychological observations are briefly reviewed here with special emphasis on a new condition, that of congenital amusia (also commonly referred to as tone deafness). C1 Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. RP Peretz, I (reprint author), Univ Montreal, Dept Psychol, CP 6128,Succ Ctr Ville, Montreal, PQ H3C 3J7, Canada. 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PY 2001 VL 930 BP 153 EP 165 PG 13 WC Multidisciplinary Sciences; Psychology SC Science & Technology - Other Topics; Psychology GA BT11G UT WOS:000172009400011 PM 11458826 ER PT S AU Heaton, P Pring, L Hermelin, B AF Heaton, P Pring, L Hermelin, B BE Zatorre, RJ Peretz, I TI Musical processing in high functioning children with autism SO BIOLOGICAL FOUNDATIONS OF MUSIC SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on the Biological Foundations of Music CY MAY 20-22, 2000 CL NEW YORK, NEW YORK SP Charles A Dana Fdn, David & Lucile Packard Fdn HO ROCKEFELLER UNIV DE autism; savant, musical; absolute pitch C1 Univ Greenwich, Sch Social Sci, London SE9 2BR, England. RP Heaton, P (reprint author), Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. CR Frith U., 1989, AUTISM EXPLAINING EN Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Heaton P, 1998, MUSIC PERCEPT, V15, P291 MILLER L, 1989, MUSICAL SAVANTES EXC SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x NR 6 TC 12 Z9 12 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-306-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2001 VL 930 BP 443 EP 444 PG 2 WC Multidisciplinary Sciences; Psychology SC Science & Technology - Other Topics; Psychology GA BT11G UT WOS:000172009400045 PM 11458863 ER PT J AU Chibuk, TK Bischof, JM Wevrick, R AF Chibuk, Thea K. Bischof, Jocelyn M. Wevrick, Rachel TI A necdin/MAGE-like gene in the chromosome 15 autism susceptibility region: expression, imprinting, and mapping of the human and mouse orthologues SO BMC GENETICS LA English DT Article AB Background: Proximal chromosome 15q is implicated in neurodevelopmental disorders including Prader-Willi and Angelman syndromes, autistic disorder and developmental abnormalities resulting from chromosomal deletions or duplications. A subset of genes in this region are subject to genomic imprinting, the expression of the gene from only one parental allele. Results: We have now identified the NDNL2 (also known as MAGE-G) gene within the 15q autistic disorder susceptibility region and have mapped its murine homolog to the region of conserved synteny near necdin (Ndn) on mouse Chr 7. NDNL2/MAGE-G is a member of a large gene family that includes the X-linked MAGE cluster, MAGED1 (NRAGE), MAGEL2 and NDN, where the latter two genes are implicated in Prader-Willi syndrome. We have now determined that NDNL2/Ndnl2 is widely expressed in mouse and human fetal and adult tissues, and that it is apparently not subject to genomic imprinting by the PWS/AS Imprinting Center. Conclusion: Although NDNL2/MAGE-G in the broadly defined chromosome 15 autistic disorder susceptibility region, it is not likely to be pathogenic based on its wide expression pattern and lack of imprinted expression. C1 [Chibuk, Thea K.; Bischof, Jocelyn M.; Wevrick, Rachel] Univ Alberta, Dept Med Genet, Edmonton, AB, Canada. RP Wevrick, R (reprint author), Univ Alberta, Dept Med Genet, Edmonton, AB, Canada. EM tchibuk@gpu.srv.ualberta.ca; jbischof@ualberta.ca; rachel.wevrick@ualberta.ca FU University of Miami Brain and Tissue Bank for Developmental Disorders through NICHD [NO1-HD-8-3284]; March of Dimes Birth Defects Foundation [6-FY00-196]; Alberta Heritage Foundation for Medical Research (AHFMR); Canadian Genetic Disease Network FX We thank Mary Barter from the Jackson Laboratories for the murine haplotype analysis, the MRC Genome Resource Facility and the RIKEN Genome Science Center for DNA clones, and Dr. A. Beaudet for the AS fibroblast cell line. Samples used in this study were provided by the University of Miami Brain and Tissue Bank for Developmental Disorders through NICHD contract # NO1-HD-8-3284. This work was supported in part by a Research Grant No. 6-FY00-196 from the March of Dimes Birth Defects Foundation, Summer Studentships to T. K. C. from the Alberta Heritage Foundation for Medical Research (AHFMR) and the Canadian Genetic Disease Network. R. W. is a Scholar of the AHFMR and the Canadian Institutes of Health Research. Research involving human subjects and animals has been performed in accordance with the Institutional policies of the University of Alberta. 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PY 2001 VL 2 AR 22 DI 10.1186/1471-2156-2-22 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA V31UU UT WOS:000208909300021 PM 11782285 ER PT J AU Manev, R Manev, H AF Manev, Radmila Manev, Hari TI Aminoglycoside antibiotics and autism: a speculative hypothesis SO BMC PSYCHIATRY LA English DT Article AB Background: Recently, it has been suspected that there is a relationship between therapy with some antibiotics and the onset of autism; but even more curious, some children benefited transiently from a subsequent treatment with a different antibiotic. Here, we speculate how aminoglycoside antibiotics might be associated with autism. Presentation: We hypothesize that aminoglycoside antibiotics could a) trigger the autism syndrome in susceptible infants by causing the stop codon readthrough, i.e., a misreading of the genetic code of a hypothetical critical gene, and/or b) improve autism symptoms by correcting the premature stop codon mutation in a hypothetical polymorphic gene linked to autism. Testing: Investigate, retrospectively, whether a link exists between aminoglycoside use (which is not extensive in children) and the onset of autism symptoms (hypothesis "a"), or between aminoglycoside use and improvement of these symptoms (hypothesis "b"). Whereas a prospective study to test hypothesis "a" is not ethically justifiable, a study could be designed to test hypothesis "b". Implications: It should be stressed that at this stage no direct evidence supports our speculative hypothesis and that its main purpose is to initiate development of new ideas that, eventually, would improve our understanding of the pathobiology of autism. C1 [Manev, Radmila; Manev, Hari] Univ Illinois, Inst Psychiat, Dept Psychiat, Chicago, IL 60612 USA. RP Manev, H (reprint author), Univ Illinois, Inst Psychiat, Dept Psychiat, Chicago, IL 60612 USA. 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This has led to considerable concern about the safety of the vaccine. Methods: A matched case-control study using data derived form the United Kingdom General Practice Research Database. Children with a possible diagnosis of autism will be identified from their electronic health records. All diagnoses will be validated by a detailed review of hospital letters and by using information derived from a parental questionnaire. Ten controls per case will be selected from the database. Conditional logistic regression will be used to assess the association between MMR vaccination and autism. In addition case series analyses will be undertaken to estimate the relative incidence of onset of autism in defined time intervals after vaccination. The study is funded by the United Kingdom Medical Research Council. Discussion: Electronic health databases offer tremendous opportunities for evaluating the adverse effects of vaccines. However there is much scope for bias and confounding. 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After reviewing the paediatric oncology literature addressing the use of general anaesthesia for short medical procedures, we have developed checklists of procedural guidelines and monitoring equipment for the safe use of daily anaesthesia in adult patients who require a fractionated course of radiation therapy. We illustrate this by describing the successful treatment of a woman with autism and Hodgkin's disease who required daily general anaesthesia for immobilization during a 4-week course of radiation therapy. Propofol was used as the primary drug and was not associated with any adverse side-effects. There was no development of tolerance. C1 Univ Toronto, Princess Margaret Hosp, Dept Radiat Oncol, Toronto, ON M5G 2M9, Canada. Markham Stouffville Hosp, Markham, ON, Canada. Univ Toronto, Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada. RP Tsang, RW (reprint author), Univ Toronto, Princess Margaret Hosp, Dept Radiat Oncol, 610 Univ Ave, Toronto, ON M5G 2M9, Canada. 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Oncol. PY 2001 VL 13 IS 6 BP 416 EP 421 DI 10.1007/s001740170004 PG 6 WC Oncology SC Oncology GA 517WG UT WOS:000173633000004 PM 11824877 ER PT J AU DeStefano, F Chen, RT AF DeStefano, F Chen, RT TI Autism and measles-mumps-rubella vaccination - Controversy laid to rest? SO CNS DRUGS LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; VIRUS; DISORDER; CHILDREN; ABSENCE; EVENTS; CAUSAL AB It has been suggested that vaccination, particularly with measles-mumps-rubella (MMR) vaccine, may be related to the development of autism. The main evidence for a possible association is that the prevalence of autism has been increasing at the same time that infant vaccination coverage has increased, and that in some cases there is an apparent temporal association in which autistic characteristics are first noted shortly after vaccination. Although the prevalence of autism and similar disorders appears to have increased recently, it is not clear if this is an actual increase or the result of increased recognition and changes in diagnostic criteria. The apparent onset of autism in close proximity to vaccination may be a coincidental temporal association. The clinical evidence in support of an association derives from a series of 12 patients with inflammatory bowel conditions and regressive developmental disorders, mostly autism. The possibility that measles vaccine may cause autism through a persistent bowel infection has generated much interest, since it provides a possible biological mechanism. Epidemiological studies, however, have not found an association between MMR vaccination and autism. The epidemiological findings are consistent with current understanding of the pathogenesis of autism, which has a strong genetic component and in which the neurological defects probably occur early in embryonic development. It seems unlikely that a vaccination that is given after birth could cause autism. A minority of cases of autism may have onset after I year of age (regressive autism), but the single epidemiological study that included such cases did not find an association with MMR vaccination. Currently, the weight of the available epidemiological and related evidence does not support a causal association between MMR vaccine, or any other vaccine or vaccine constituent, and autism. C1 Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30341 USA. Ctr Dis Control & Prevent, Natl Immunizat Program, Atlanta, GA USA. RP DeStefano, F (reprint author), Natl Ctr Birth Defects & Dev Disabil, 4770 Buford Highway NE,Mailstop F34, Atlanta, GA 30341 USA. 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The role of a robotic mediator in autism therapy SO COGNITIVE TECHNOLOGY: INSTRUMENTS OF MIND, PROCEEDINGS SE LECTURE NOTES IN ARTIFICIAL INTELLIGENCE LA English DT Article; Proceedings Paper CT 4th International Conference on Cognitive Technology - Instruments of Mind CY AUG 06-09, 2001 CL COVENTRY, ENGLAND HO UNIV WARWICK ID CHILDREN AB Increasingly socially intelligent agents (software or robotic) are used in education, rehabilitation and therapy. This paper discusses the role of interactive, mobile robots as social mediators in the particular domain of autism therapy. This research is part of the project AURORA that studies how mobile robots can be used to teach children with autism basic interaction skills that are important in social interactions among humans. Results from a particular series of trials involving pairs of two children and a mobile robot are described. The results show that the scenario with pairs of children and a robot creates a very interesting social context which gives rise to a variety of different social and non-social interaction patterns, demonstrating the specific problems but also abilities of children with autism in social interactions. Future work will include a closer analysis of interactional structure in human-human and robot-human interaction. We outline a particular framework that we are investigating. C1 Univ Reading, Dept Cybernet, Reading RG6 6AY, Berks, England. Univ Hertfordshire, Dept Comp Sci, Adapt Syst Res Grp, Hatfield AL10 9AB, Herts, England. RP Werry, I (reprint author), Univ Reading, Dept Cybernet, POB 225, Reading RG6 6AY, Berks, England. RI Harwin, William/N-1148-2014 OI Harwin, William/0000-0002-3928-3381 CR Abelson R., 1977, SCRIPTS PLANS GOALS Arkin R. C, 1998, BEHAV BASED ROBOTICS BILLARD A, 2000, P SOC INT AG HUM LOO, P9 Blocher K. 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The Narrative Intelligence Hypothesis suggests that the evolutionary origin of communicating in a narrative format co-evolved with increasingly complex social dynamics among our human ancestors. This article gives examples of social interactions in non-human primates and how these interactions can be interpreted in terms of nonverbal narratives. The particular format of preverbal narrative that infants learn through transactions with others is important for the development of communication and social skills. A possible impairment of the construction of narrative formats in children with autism is discussed. Implications of the Narrative Intelligence Hypothesis for research into communication and social interactions in animals and robots are outlined. The article concludes by discussing implications for humane technology development. C1 Univ Hertfordshire, Dept Comp Sci, Adapt Syst Res Grp, Hatfield AL10 9AB, Herts, England. 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Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Obstet Gynecol, New Brunswick, NJ 08901 USA. St Peters Coll, Dept Biol, Jersey City, NJ USA. RP Roginski, RS (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Anesthesiol, Clin Acad Bldg,Suite 3100,125 Paterson St, New Brunswick, NJ 08901 USA. CR Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 *IMGSAC, 1998, GENET, V7, P571 Korneev SA, 1999, J NEUROSCI, V19, P7711 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 Roginski RS, 2001, CYTOGENET CELL GENET, V93, P143, DOI 10.1159/000056971 NR 6 TC 0 Z9 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 2001 VL 95 IS 3-4 BP 238 EP 239 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 566CB UT WOS:000176408300020 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 Molecular genetic delineation of 2q37.3 deletion in autism and osteodystrophy: report of a case and of new markers for deletion screening by PCR SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID HEPARAN-SULFATE PROTEOGLYCAN; FRAGILE-X-SYNDROME; ALBRIGHT HEREDITARY OSTEODYSTROPHY; DEVELOPING NERVOUS-SYSTEM; MENTAL-RETARDATION; KH-DOMAIN; CHROMOSOME REARRANGEMENTS; RNA-BINDING; EXPRESSION; DISORDER AB We recently studied a patient who meets criteria for autistic disorder and has a 2q37 deletion. Molecular cytogenetic studies were carried out using DNA isolated from 22 different 2q37 mapped BACs to more precisely define the extent of the chromosome deletion. We also analyzed 2q37 mapped polymorphic markers. In addition DNA sequences of BACs in the deletion region were scanned to identify microsatellite repeats. We describe four new polymorphic microsatellite repeat markers in the 2q37.3 region. These markers enabled us to determine the parental origin of the deletion in our patient. DNA from 8-13 unrelated individuals was used to determine heterozygosity estimates for these markers. We review four genes deleted in our patient - genes whose known functions and sites of expression in the brain and/or bone make them candidates for involvement in autism and/or the osteodystrophy observed in patients with 2q37.3 deletions. Copyright (C) 2001 S. KargerAG, Basel. C1 Univ Calif Irvine, Dept Pediat, Irvine, CA 92697 USA. RP Smith, M (reprint author), Univ Calif Irvine, Dept Pediat, Med Sci 1 Room C237, Irvine, CA 92697 USA. 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Cell Genet. PY 2001 VL 94 IS 1-2 BP 15 EP 22 DI 10.1159/000048775 PG 8 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 496BU UT WOS:000172375600003 PM 11701947 ER PT J AU Roginski, RS Raj, BKM Finkernagel, SW Sciorra, LJ AF Roginski, RS Raj, BKM Finkernagel, SW Sciorra, LJ TI Assignment of an ionotropic glutamate receptor-like gene (GRINL1A) to human chromosome 15q22.1 by in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID AUTISM C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Anesthesiol, New Brunswick, NJ 08901 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Obstet Gynecol, New Brunswick, NJ USA. RP Roginski, RS (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Anesthesiol, Clin Acad Bldg,Suite 3100,125 Paterson St, New Brunswick, NJ 08901 USA. 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PD JAN-MAR PY 2001 VL 66 IS 1 BP 171 EP 171 PG 1 WC Psychiatry SC Psychiatry GA 421YZ UT WOS:000168092300042 ER PT J AU Agathon, M AF Agathon, M TI Teaching children with autism to mind-read: a practical guide. SO EVOLUTION PSYCHIATRIQUE LA French DT Book Review CR Howlin P., 1999, TEACHING CHILDREN AU NR 1 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JAN-MAR PY 2001 VL 66 IS 1 BP 171 EP 171 PG 1 WC Psychiatry SC Psychiatry GA 421YZ UT WOS:000168092300043 ER PT J AU Niklasson, L Rasmussen, P Oskarsdottir, S Gillberg, C AF Niklasson, L Rasmussen, P Oskarsdottir, S Gillberg, C TI Neuropsychiatric disorders in the 22q11 deletion syndrome SO GENETICS IN MEDICINE LA English DT Article DE 22q11 deletion syndrome; attention-deficit/hyperactivity disorder; deficits in attention; motor control; and perception (DAMP); autism; nonverbal learning disorder ID CARDIO-FACIAL SYNDROME; VELOCARDIOFACIAL-SYNDROME; ASPERGER-SYNDROME; LEARNING-DISABILITIES; CHILDREN; SCHIZOPHRENIA; SPECTRUM; ADULTS; VCFS AB Purpose: This study was undertaken with a view to establishing the occurrence of neuropsychiatric disorders in the 22q11 deletion syndrome. Methods: Thirty-two children and young adults with genetically confirmed 22q11 deletion were given comprehensive neuropsychiatric assessments. Results: Altogether, 56% had a neuropsychiatric disorder. Only 6% were of normal IQ and free of psychiatric disorder. Attention-deficit/hyperactivity disorder was diagnosed in 44% and 31% had an autism spectrum problem. In 16% criteria for both these diagnoses were met, fifty-three percent had mental retardation, often with a test-profile suggesting a nonverbal learning disorder. Conclusion: The findings imply that a majority of children and adolescents with 22q11 deletion syndrome are in need of neuropsychiatric assessment and intervention. C1 Univ Gothenburg, Queen Silvia Childrens Hosp, Sahlgrens Univ Hosp, Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. Univ Gothenburg, Queen Silvia Childrens Hosp, Sahlgrens Univ Hosp, Dept Pediat, SE-41119 Gothenburg, Sweden. RP Niklasson, L (reprint author), Univ Gothenburg, Queen Silvia Childrens Hosp, Sahlgrens Univ Hosp, Dept Child & Adolescent Psychiat, Kungsgatan 12, SE-41119 Gothenburg, Sweden. CR Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bassett AS, 1998, AM J MED GENET, V81, P328, DOI 10.1002/(SICI)1096-8628(19980710)81:4<328::AID-AJMG10>3.0.CO;2-N Conners C.K., 1990, CONNERS RATING SCALE Dallapiccola B, 1996, AM J HUM GENET, V59, P7 Devriendt K, 1998, J MED GENET, V35, P789, DOI 10.1136/jmg.35.9.789-a Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x 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 GOLDBERG R, 1993, AM J MED GENET, V45, P313, DOI 10.1002/ajmg.1320450307 GOLDINGKUSHNER KJ, 1985, J CRAN GENET DEV BIO, V5, P259 Griffiths R, 1970, ABILITIES YOUNG CHIL GROSSTSUR V, 1995, J LEARN DISABIL, V28, P80 Jönsson S, 1997, Lakartidningen, V94, P329 Kadesjo B, 1998, DEV MED CHILD NEUROL, V40, P796 Kaufman A. 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Med. PD JAN-FEB PY 2001 VL 3 IS 1 BP 79 EP 84 DI 10.1097/00125817-200101000-00017 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 409QB UT WOS:000167393400017 PM 11339385 ER PT J AU Huang, J Vieland, VJ AF Huang, J Vieland, VJ TI Comparison of 'model-free' and 'model-based' linkage statistics in the presence of locus heterogeneity: Single data set and multiple data set applications SO HUMAN HEREDITY LA English DT Article DE locus heterogeneity; model-free test; model-based test; multiple samples ID LOD SCORE ANALYSIS; GENOMIC SCREEN; AUTISM; INHERITANCE; TRAITS; PAIRS AB Earlier work [Knapp et al.: Hum Hered 1994;44:44-51] focusing on affected sib pair (ASP) data established the equivalence between the mean test and a test based on a simple recessive lod score, as well as equivalences between certain forms of the maximum likelihood score (MLS) statistic [Risch: Am J Hum Genet 1990;46:242-253] and particular forms of the lod score. Here we extend the results of Knapp et al, [1994] by reconsidering these equivalences for ASP data, but in the presence of locus heterogeneity. We show that Risch's MLS statistic under the possible triangle constraints [Holmans: Am J Hum Genet 1993;52:362-374] is locally equivalent to the ordinary heterogeneity rod score assuming a simple recessive model (HLOD/R); while the one-parameter MLS assuming no dominance variance is locally equivalent to the (homogeneity) recessive led. The companion paper (this issue, pp 199-208) showed that when considering multiple data sets in the presence of locus heterogeneity, the HLOD can suffer appreciable losses in power. We show here that in ASP data, these equivalences ensure that this same loss in power is incurred by both forms of the MLS statistic as well, The companion paper also introduced an adaptation of the led, the compound lod score (HLOD/C). We confirm that the HLOD/C maintains higher power than these 'model-free' methods when applied to multiple heterogeneous data sets, even when it is calculated assuming the wrong genetic model. Copyright (C) 2001 S. Karger AG, Basel. C1 Univ Iowa, Dept Stat & Actuarial Sci, Iowa City, IA 52242 USA. Univ Iowa, Dept Biostat, Iowa City, IA 52242 USA. Univ Iowa, Dept Psychiat, Iowa City, IA 52242 USA. RP Huang, J (reprint author), Univ Iowa, Dept Stat & Actuarial Sci, 241 Schaeffer Hall, Iowa City, IA 52242 USA. 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Hered. PY 2001 VL 51 IS 4 BP 217 EP 225 DI 10.1159/000053345 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 420EZ UT WOS:000167992700005 PM 11287743 ER PT J AU Astington, JW Barriault, T AF Astington, JW Barriault, T TI Children's theory of mind: How young children come to understand that people have thoughts and feelings SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; developmental delay; early identification; early intervention; individual differences; social cognition ID INDIVIDUAL-DIFFERENCES; FALSE BELIEF; AUTISM; KNOWLEDGE; EMOTION; PERFORMANCE; DECEPTION; LANGUAGE; TASK AB Children's theory of mind underlies their ability to explain and predict human behavior by taking into account a person's thoughts and feelings. It develops in the first 5 years of life, beginning with joint attention in infancy. The 3-year-old child understands that there is a difference between thoughts in the mind and things in the world and is aware of people's wants, feelings, and perceptions. The 5-year-old child understands false belief, and realizes that thoughts in the mind may not be true. Some recent work investigated individual differences in theory-of-mind development, showing antecedents of false-belief understanding in general language skills, pretend play, and style of family interaction. There is less work on the consequences of typical theory of mind development, but a large body of work demonstrating the consequences of its absence, particularly in autism. The article discusses the implications of this new area of developmental research for clinical practice and describes a screening tool and a teaching manual. C1 Univ Toronto, Dept Human Dev & Appl Psychol, Inst Child Study, Toronto, ON, Canada. 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This paper argues that to a certain extent, society has developed in a way that resembles autism, which is concerned with the manner people react and communicate. In particular, excessive use of IT and computers might cause Western societies to acquire characteristics of autism. Signs of this can be found in a variety of domains, such as telecommuting or Internet addiction. Cultural considerations must be put in place if we wish to keep a balance between private and public life. Implications for individuals, organizations and society are discussed. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ E Anglia, Sch Management, Norwich NR4 7TJ, Norfolk, England. RP Baruch, Y (reprint author), Univ E Anglia, Sch Management, Norwich NR4 7TJ, Norfolk, England. 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RP Cohen, DJ (reprint author), Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. NR 0 TC 5 Z9 6 PU GEFEN PUBLISHING HOUSE LTD PI JERUSALEM PA PO BOX 36004, JERUSALEM 91360, ISRAEL SN 0333-7308 J9 ISRAEL J PSYCHIAT JI Isr. J. Psychiatr. Relat. Sci. PY 2001 VL 38 IS 3-4 BP 226 EP 234 PG 9 WC Psychiatry SC Psychiatry GA 486TF UT WOS:000171832500008 PM 11725420 ER PT J AU Craig, J Baron-Cohen, S Scott, F AF Craig, J Baron-Cohen, S Scott, F TI Drawing ability in autism: A window into the imagination SO ISRAEL JOURNAL OF PSYCHIATRY AND RELATED SCIENCES LA English DT Article ID SYMBOLIC PLAY; CHILDREN AB This study investigated imagination via drawing tasks, in 15 children with autism and 15 children with Asperger Syndrome, compared to verbal mental age matched normal children and children with moderate learning difficulties (MLD). Experiment 1 used the Draw an Impossible Man Task. While children with autism were impaired relative to the normal group, they were not impaired relative to the children with MLD. In order to probe for an imagination deficit, Experiment 2 employed a more challenging measure of imaginative drawing, a task involving mixing categories to produce drawings of real or unreal entities (e.g., drawing half-fish/half-mouse). This revealed an autism-specific deficit. Experiment 3 confirmed this was not due to difficulties in combining elements per se. Experiment 4 required subjects to transform a picture (e.g., a cloud into a swan) and again found an autism-specific deficit. Children with Asperger Syndrome were only impaired when required to make such transformations spontaneously. C1 Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB3 3EB, England. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB3 3EB, England. RP Craig, J (reprint author), Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Downing St, Cambridge CB3 3EB, England. CR American Psychiatric Association [APA], 1994, DSM 4 DIAGN STAT MAN BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 Baron-Cohen S., 1996, J COGNITIVE NEUROSCI, V8, P400 Bishop DVM, 1983, TEST RECEPTION GRAMM FINKE RA, 1989, COGNITIVE SCI, V13, P51, DOI 10.1207/s15516709cog1301_2 HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 JARROLD C, 1993, J AUTISM DEV DISORD, V23, P281, DOI 10.1007/BF01046221 KARMILOFFSMITH A, 1990, COGNITION, V34, P57, DOI 10.1016/0010-0277(90)90031-E KEIL F, 1988, CONCEPTS KINDS COGNI Leevers HJ, 1998, J CHILD PSYCHOL PSYC, V39, P399, DOI 10.1017/S0021963097002096 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x SNODGRASS JG, 1980, J EXP PSYCHOL-HUM L, V6, P174, DOI 10.1037/0278-7393.6.2.174 Tager-Flusberg H., 1993, UNDERSTANDING OTHER UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 16 TC 9 Z9 9 PU GEFEN PUBLISHING HOUSE LTD PI JERUSALEM PA PO BOX 36004, JERUSALEM 91360, ISRAEL SN 0333-7308 J9 ISRAEL J PSYCHIAT JI Isr. J. Psychiatr. Relat. Sci. PY 2001 VL 38 IS 3-4 BP 242 EP 253 PG 12 WC Psychiatry SC Psychiatry GA 486TF UT WOS:000171832500012 PM 11725423 ER PT J AU Einat, H Belmaker, RH AF Einat, H Belmaker, RH TI The effects of inositol treatment in animal models of psychiatric disorders SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE inositol; animal models; depression; anxiety; second messengers ID ELEVATED PLUS-MAZE; CSF INOSITOL; DOUBLE-BLIND; LOCOMOTOR-ACTIVITY; CONTROLLED TRIAL; ANXIETY; DEPRESSION; BRAIN; RATS; SCHIZOPHRENIA AB Clinical trials indicate th;lt inositol may be effective in the treatment of patients with depression, panic disorder and obsessive compulsive disorder (OCD), but not in the treatment of patients with schizophrenia, Alzheimer's disease, ADHD or autism. This spectrum of clinical action parallels that of serotonin selective reuptake inhibitors (SSRIs), bur inositol is a precursor in the phosphatidylinositol cycle, a second messenger system distal to the receptor for 5HT-2. To study its mechanism of therapeutic action there is a need to test inositol's activity in animal models of psychopathology. In rats, chronic inositol was demonstrated to increase activity levels, reduce immobility time in the forced swim test and in the reserpine-induced hypoactivity models: of depression, and reduce anxiety-like behaviors in the elevated plus-maze. The reduction in anxiety-like behaviors appears to be related to baseline levels of activity. Inositol treatment was not observed to have any effect on amphetamine-induced hyperactivity, apomorphine-induced stereotypy, or on the performance of memory tasks by monkeys. Clinical controlled trials of inositol in patients with depression, panic disorder, and OCD were small, and positive psychoactive effects in animals clearly strengthen the case for further clinical trials and potential for general therapeutic use in humans. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Ben Gurion Univ Negev, Fac Hlth Sci, Minist Hlth, Mental Hlth Ctr, Beer Sheva, Israel. RP Belmaker, RH (reprint author), Ben Gurion Univ Negev, Fac Hlth Sci, Minist Hlth, Mental Hlth Ctr, Beer Sheva, Israel. EM belmaker@bgumail.bgu.ac.il RI Einat, Haim/A-7203-2009 CR Abramson LY, 1977, PSYCHOPATHOLOGY EXPT, P1 ADAMEC RE, 1993, PHYSIOL BEHAV, V54, P101, DOI 10.1016/0031-9384(93)90050-P Barak Y, 1996, PROG NEURO-PSYCHOPH, V20, P729, DOI 10.1016/0278-5846(96)00043-7 Barkai IA, 1978, BIOL PSYCHIAT, V13, P65 BENJAMIN J, 1995, AM J PSYCHIAT, V152, P1084 BORISINI F, 1988, PSYCHOPHARMACOLOGY B, V94, P147 Cohen H, 1997, J NEURAL TRANSM, V104, P299, DOI 10.1007/BF01273190 Cohen H, 1996, Depress Anxiety, V4, P144, DOI 10.1002/(SICI)1520-6394(1996)4:3<144::AID-DA8>3.0.CO;2-G Einat H, 1998, PROG NEURO-PSYCHOPH, V22, P999, DOI 10.1016/S0278-5846(98)00054-2 Einat H, 1998, INT J NEUROPSYCHOP, V1, P31, DOI 10.1017/S1461145798001035 Einat H, 1999, PSYCHOPHARMACOLOGY, V144, P158, DOI 10.1007/s002130050989 FILE SE, 1992, BIOL COUN S, P25 Fux M, 1996, AM J PSYCHIAT, V153, P1219 Gelfin Y, 1998, AM J PSYCHIAT, V155, P290 Hendrie CA, 1996, PHARMACOL BIOCHEM BE, V54, P13, DOI 10.1016/0091-3057(95)02176-0 Kaplan Z, 1996, ANXIETY, V2, P51 KELLY PH, 1976, EUR J PHARMACOL, V40, P45, DOI 10.1016/0014-2999(76)90352-6 KOFMAN O, 2000, ANXIOLYTIC EFFECT CH, V107, P241 KOFMAN O, 1993, ISRAEL J MED SCI, V29, P580 Kofman O, 1998, PSYCHOPHARMACOLOGY, V139, P239, DOI 10.1007/s002130050710 LEVINE J, 1993, BRAIN RES, V627, P168, DOI 10.1016/0006-8993(93)90761-B Levine J, 1997, EUR NEUROPSYCHOPHARM, V7, P147, DOI 10.1016/S0924-977X(97)00409-4 LEVINE J, 1995, AM J PSYCHIAT, V152, P792 LEVINE J, 1993, BIOL PSYCHIAT, V33, P673, DOI 10.1016/0006-3223(93)90112-Q LEVINE J, 1994, EUR NEUROPSYCHOPHARM, V4, P487, DOI 10.1016/0924-977X(94)90297-6 Levine J, 1997, J NEURAL TRANSM, V104, P307, DOI 10.1007/BF01273191 LEVINE J, 1993, HUM PSYCHOPHARM CLIN, V8, P49, DOI 10.1002/hup.470080109 Levine J, 1995, HUM PSYCHOPHARM CLIN, V10, P481, DOI 10.1002/hup.470100608 Levine J, 1996, J NEURAL TRANSM, V103, P1457, DOI 10.1007/BF01271260 LISTER RG, 1987, PSYCHOPHARMACOLOGY, V92, P180 LYON M, 1991, ANIMAL MODELS PSYCHI, V1, P25 OLTON DS, 1980, PHYSIOL PSYCHOL, V8, P239 Patishi Y, 1996, EUR NEUROPSYCHOPHARM, V6, P73, DOI 10.1016/0924-977X(95)00061-S PELLOW S, 1985, J NEUROSCI METH, V14, P149, DOI 10.1016/0165-0270(85)90031-7 PORSOLT RD, 1978, EUR J PHARMACOL, V47, P379, DOI 10.1016/0014-2999(78)90118-8 Raveh L, 1997, TOXICOL APPL PHARM, V145, P43, DOI 10.1006/taap.1997.8160 RODGERS RJ, 1994, ETHOLOGY AND PSYCHOPHARMACOLOGY, P9 Rodgers RJ, 1997, BEHAV PHARMACOL, V8, P477, DOI 10.1097/00008877-199711000-00003 Sanchez C, 1997, PSYCHOPHARMACOLOGY, V129, P197, DOI 10.1007/s002130050181 Shimon H, 1997, AM J PSYCHIAT, V154, P1148 SPECTOR R, 1988, NEUROCHEM RES, V13, P785, DOI 10.1007/BF00971603 TREIT D, 1993, PHARMACOL BIOCHEM BE, V44, P463, DOI 10.1016/0091-3057(93)90492-C Willner P, 1991, ANIMAL MODELS PSYCHI, P1 Willner P, 1991, BEHAV MODELS PSYCHOP, P3 NR 44 TC 27 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0327 J9 J AFFECT DISORDERS JI J. Affect. Disord. PD JAN PY 2001 VL 62 IS 1-2 BP 113 EP 121 DI 10.1016/S0165-0327(00)00355-4 PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 403NJ UT WOS:000167049100012 PM 11172878 ER PT J AU Adamson, LB McArthur, D Markov, Y Dunbar, B Bakeman, R AF Adamson, LB McArthur, D Markov, Y Dunbar, B Bakeman, R TI Autism and joint attention: Young children's responses to maternal bids SO JOURNAL OF APPLIED DEVELOPMENTAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT International Conference on Infant Studies CY APR, 1998 CL ATLANTA, GEORGIA DE joint attention; autism; mother-child interaction ID DEVELOPMENTAL LANGUAGE DELAY; PSYCHOPATHOLOGY; COMMUNICATION; EMOTIONS; BEHAVIOR; DISORDER; MOTHERS; INFANTS AB Problems with joint attention are an early manifestation of autism. Young boys with and without autism were observed communicating with their mothers in contexts that afforded commenting, requesting, and interacting. Mothers of autistic sons made as many attention-regulating bids as mothers of typically developing sons, and these bids did not differ significantly in duration. However, fewer occurred in commenting contexts, and they were less likely to rely on purely conventional means. Their sons accepted fewer bids, and they more often appeared unaware of a bid. These findings are discussed using a transactional view of communicative problems in autism in which a child's difficulty regulating shared attention prompts adults to augment conventional communication with literal, object-focused acts. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Georgia State Univ, Dept Psychol, Atlanta, GA 30303 USA. RP Adamson, LB (reprint author), Georgia State Univ, Dept Psychol, Univ Plaza, Atlanta, GA 30303 USA. CR Adamson L. B., 1998, TRANSITIONS PRELINGU, P15 Adamson LB, 1999, EARLY SOCIAL COGNITION, P281 ADAMSON LB, 1984, INFANT BEHAV DEV, V7, P467, DOI 10.1016/S0163-6383(84)80006-5 Adamson L.B., 1991, ANN CHILD DEV, V8, P1 ADAMSON LB, 1997, BIENN M SOC RES CHIL ADAMSON LB, 1999, COMMUNICATION PLAY P American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bakeman R, 1997, PSYCHOL METHODS, V2, P357, DOI 10.1037/1082-989X.2.4.357 Bakeman R, 1997, OBSERVING INTERACTIO Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 CICCHETTI D, 1993, DEV REV, V13, P471, DOI 10.1006/drev.1993.1021 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 Fenson L., 1992, MACARTHUR COMMUNICAT Fleiss JL, 1981, STAT METHODS RATES P HAPPE F, 1998, HDB NEUROLINGUISTICS, P525, DOI 10.1016/B978-012666055-5/50042-3 KASARI C, 1990, J AUTISM DEV DISORD, V20, P87, DOI 10.1007/BF02206859 KOPP CB, 1989, DEV PSYCHOL, V25, P343, DOI 10.1037//0012-1649.25.3.343 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LANDRY SH, 1988, J CHILD PSYCHOL PSYC, V29, P621, DOI 10.1111/j.1469-7610.1988.tb01884.x LOVELAND KA, 1986, J AUTISM DEV DISORD, V16, P335, DOI 10.1007/BF01531663 Maurice C., 1993, LET ME HEAR YOUR VOI McArthur D, 1996, J AUTISM DEV DISORD, V26, P481, DOI 10.1007/BF02172271 Moore C., 1995, JOINT ATTENTION ITS MUNDY P, 1995, DEV PSYCHOPATHOL, V7, P63 MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 Quera V., 1995, ANAL INTERACTION SEQ Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 SROUFE LA, 1984, CHILD DEV, V55, P17, DOI 10.2307/1129832 TRAD PV, 1993, J AUTISM DEV DISORD, V23, P361, DOI 10.1007/BF01046225 TRONICK EZ, 1989, AM PSYCHOL, V44, P112, DOI 10.1037//0003-066X.44.2.112 WETHERBY AM, 1984, J SPEECH HEAR RES, V27, P364 Williams E, 1999, J AUTISM DEV DISORD, V29, P367, DOI 10.1023/A:1023026810619 NR 33 TC 26 Z9 26 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0193-3973 J9 J APPL DEV PSYCHOL JI J. Appl. Dev. Psychol. PY 2001 VL 22 IS 4 BP 439 EP 453 DI 10.1016/S0193-3973(01)00089-2 PG 15 WC Psychology, Developmental SC Psychology GA 467FK UT WOS:000170691600006 ER PT J AU Baron-Cohen, S AF Baron-Cohen, S TI Autism and pervasive developmental disorders SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Book Review C1 Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge, England. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge, England. CR Baron-Cohen S., 1998, AUTISM, V2, P296, DOI 10.1177/1362361398023008 Baron-Cohen S, 1997, AUTISM INT J RES PRA, V1, P153 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P537, DOI 10.1017/S0021963099003935 VOLKMAR F, AUTISM PERVASIVE DEV WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 6 TC 0 Z9 0 PU BILD PUBLICATIONS PI CLEVEDON PA FRANKFURT LODGE, CLEVEDON HALL VICTORIA RD, CLEVEDON BS21 7SJ, AVON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PY 2001 VL 14 IS 1 BP 72 EP 74 DI 10.1046/j.1468-3148.2001.00043.x PG 3 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 423WA UT WOS:000168199700009 ER PT J AU Carr, D AF Carr, D TI Parents' education as autism therapists: Applied behaviour analysis in context SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Book Review C1 Welsh Ctr Learning Disabil, Appl Res Unit, Cardiff CF14 3BG, S Glam, Wales. RP Carr, D (reprint author), Welsh Ctr Learning Disabil, Appl Res Unit, North Rd, Cardiff CF14 3BG, S Glam, Wales. RI turton, miranda/F-4682-2011 CR Howlin P, 1998, J CHILD PSYCHOL PSYC, V39, P307, DOI 10.1017/S0021963097002138 Keenan M., 2000, PARENTS ED AUTISM TH Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 NR 4 TC 0 Z9 0 PU BILD PUBLICATIONS PI CLEVEDON PA FRANKFURT LODGE, CLEVEDON HALL VICTORIA RD, CLEVEDON BS21 7SJ, AVON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PY 2001 VL 14 IS 2 BP 157 EP 160 DI 10.1046/j.1468-3148.2001.0044b.x PG 4 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 450UN UT WOS:000169763300008 ER PT J AU Hastings, RP Mount, RH AF Hastings, RP Mount, RH TI Early correlates of behavioural and emotional problems in children and adolescents with severe intellectual disabilities: A preliminary study SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article ID SELF-INJURIOUS-BEHAVIOR; MENTAL-RETARDATION; CHALLENGING BEHAVIORS; POPULATION PREVALENCE; YOUNG-CHILDREN; PSYCHOPATHOLOGY; DIFFICULTIES; AUTISM AB Research and theory on behaviour problems in children with intellectual disabilities (IDS) have tended to focus on maintaining variables and present correlates of disorder. The present study focused on potential early correlates of behavioural problems. The parents of 188 children attending schools for those with 'severe learning difficulties' completed the Developmental Behaviour Checklist (DBC), and a questionnaire asking for demographic details and information about present and early correlates (i.e. epilepsy and physical ability, and early developmental progress, early feeding problems and obstetric complications). Hierarchical regression analyses were performed to explore whether potential early correlates from infancy could add to the prediction of behaviour problems from established correlates and diagnostic variables. Potential early correlates across all of the DBC domains did not add significantly to the prediction of behaviour problems. However, there were effects of sex, physical ability and diagnostic categories. A number of methodological factors (i.e. poor response rate, focus only on severe ID and retrospective data collection) are discussed in terms of how they impact on the results. However, analyses of large samples such as that reported in the present study may still provide a useful addition to research on the early development of behaviour problems. Such data may help in the identification of children at risk who may benefit from early intervention. C1 Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. UCL, Inst Child Hlth, Behav Sci Unit, London WC1N 1EH, England. RP Hastings, RP (reprint author), Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. 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PY 2001 VL 14 IS 4 BP 381 EP 391 DI 10.1046/j.13602322.2001.00079.x PG 11 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 502YP UT WOS:000172770600006 ER PT J AU Trevarthen, C Aitken, KJ AF Trevarthen, C Aitken, KJ TI Infant intersubjectivity: Research, theory, and clinical applications SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE infant intersubjectivity; parent-infant communication; developmental disorders; pathologies of empathy; therapies ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; TO-FACE INTERACTION; CEREBRO-CRANIOFACIAL DYSMORPHOGENESIS; BRAIN ELECTRICAL-ACTIVITY; 6-YEAR FOLLOW-UP; THEORY-OF-MIND; MOTHER-INFANT; DEPRESSED MOTHERS AB We review research evidence on the emergence and development of active "self-and-other" awareness in infancy, and examine the importance of its motives and emotions to mental health practice with children. This relates to how communication begins and develops in infancy, how it influences the individual subject's movement, perception, and learning, and how the infant's biologically grounded self-regulation of internal slate and self-conscious purposefulness is sustained through active engagement with sympathetic others. Mutual self-other-consciousness is found to play the lead role in developing a child's cooperative intelligence for cultural learning and language, A variety of preconceptions have animated rival research traditions investigating infant communication and cognition. We distinguish the concept of "intersubjectivity", and outline the history of its use in developmental research. The transforming body and brain of a human individual grows in active engagement with an environment of human factors-organic at first, then psychological or inter-mental. Adaptive, human-responsive processes are generated first by interneuronal activity within the developing brain as formation of the human embryo is regulated in a support-system of maternal tissues. Neural structures are further elaborated with the benefit of intra-uterine stimuli in the foetus, then supported in the rapidly growing forebrain and cerebellum of the young child by experience of the intuitive responses of parents and other human companions. We focus particularly on intrinsic patterns and processes in pre-natal and post-natal brain maturation that anticipate psychosocial support in infancy. The operation of an intrinsic motive formation (IMF) that developed in the core of the brain before birth is evident in the tightly integrated intermodal sensory-motor coordination of a newborn infant's orienting to stimuli and preferential learning of human signals, by the temporal coherence and intrinsic rhythms of infant behaviour, especially in communication, and neonates' extraordinary capacities for reactive and evocative imitation. The correct functioning of this integrated neural motivating system is found to be essential to the development of both the infant's purposeful consciousness and his or her ability to cooperate with other persons' actions and interests, and to learn from them. The relevance of infants' inherent intersubjectivity to major child mental health issues is highlighted by examining selected areas of clinical concern. 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Psychiatry PD JAN PY 2001 VL 42 IS 1 BP 3 EP 48 DI 10.1017/S0021963001006552 PG 46 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 428LB UT WOS:000168462200002 PM 11205623 ER PT J AU Coupland, NJ AF Coupland, NJ TI Social phobia: Etiology, neurobiology, and treatment SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Review ID FRAGILE-X-SYNDROME; BENZODIAZEPINE RECEPTOR SENSITIVITY; MAGNETIC-RESONANCE SPECTROSCOPY; DIRECT-INTERVIEW FAMILY; DSM-III-R; PANIC DISORDER; BEHAVIORAL-INHIBITION; ANXIETY DISORDER; HUMAN AMYGDALA; HEALTHY-VOLUNTEERS AB Social phobia is a common and often disabling condition, with an etiology that is not established. There is evidence at several levels for an interplay of biological and psychological processes in social phobia. Genetic studies show that both genetic and environmental factors are important, with evidence pointing to associations with 2 genetic conditions, autism and fragile X syndrome. Behavioral inhibition has emerged as an important precursor to social phobia and possibly to other anxiety disorders. Epidemiologic and clinical studies have suggested that factors within the family environment, such as overprotection, overcontrol, modeling of anxiety, criticism, and in some cases abuse, can play a role in the development of social phobia. During childhood, complex interactions between brain system disturbances that mediate responses to negative social cues and factors in the social setting may lead to the development of a distorted set of internal "blueprints" for social behavior. The impact of severe social anxiety on brain systems that mediate behavioral change may prevent patients from learning better "blueprints." These can be taught through cognitive-behavioral therapies. The effective control of social anxiety with medications enables patients to recover; whether recovery can last after discontinuation of medications may depend on whether a new "blueprint" has been developed and whether stable changes in affected brain systems have occurred. Neuroimaging techniques are at early stage of identifying abnormalities at the neurotransmitter and systems levels. C1 Univ Alberta, Dept Psychiat, Edmonton, AB T6G 2M7, Canada. RP Coupland, NJ (reprint author), Walter MacKenzie Ctr, Dept Psychiat, Room 1E713,8440 112th St, Edmonton, AB T6G 2B7, Canada. 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Clin. Psychiatry PY 2001 VL 62 SU 1 BP 25 EP 35 PG 11 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 397JD UT WOS:000166691800005 PM 11206031 ER PT J AU Rotheram-Borus, MJ Bickford, B Milburn, NG AF Rotheram-Borus, MJ Bickford, B Milburn, NG TI Implementing a classroom-based social skills training program in middle childhood SO JOURNAL OF EDUCATIONAL AND PSYCHOLOGICAL CONSULTATION LA English DT Article ID EXPRESSED EMOTION; CHILDREN; INTERVENTIONS; DISORDERS; AUTISM AB Although social skills training (SST) programs have been shown to improve children's long-term developmental outcomes, school personnel are not typically able to implement such programs. This article outlines the institutional and organizational supports, trainer selection criteria, and the training needed for school counselors to successfully implement and sustain a SST program for children. Social skills programs will only become routine in the classroom if the school setting provides administrative support for skills training, and structures to encourage implementation of SST programs (especially substantial and ongoing training based in the classroom setting). In addition to organizational level considerations, SST trainers need to be socially competent, be able to manage children in small groups, be familiar with the theoretical model underlying the SST program, have the opportunity to practice delivering the program, and have positive attitudes toward delivering the program. The procedures for selecting, training, monitoring, and evaluating school counselors who are SST trainers are described. C1 Univ Calif Los Angeles, Ctr Community Hlth, Los Angeles, CA 90024 USA. RP Rotheram-Borus, MJ (reprint author), Univ Calif Los Angeles, Ctr Community Hlth, 10920 Wilshire Blvd,Suite 350, Los Angeles, CA 90024 USA. 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PY 2001 VL 12 IS 2 BP 91 EP 111 DI 10.1207/S1532768XJEPC1202_02 PG 21 WC Psychology, Educational SC Psychology GA 455VN UT WOS:000170048600002 ER PT J AU Ungaro, P Christian, SL Fantes, JA Mutirangura, A Black, S Reynolds, J Malcolm, S Dobyns, WB Ledbetter, DH AF Ungaro, P Christian, SL Fantes, JA Mutirangura, A Black, S Reynolds, J Malcolm, S Dobyns, WB Ledbetter, DH TI Molecular characterisation of four cases of intrachromosomal triplication of chromosome 15q11-q14 SO JOURNAL OF MEDICAL GENETICS LA English DT Article DE chromosome 15 triplication; Prader-Willi syndrome; Angelman syndrome; autism ID PRADER-WILLI-SYNDROME; SYNDROME CRITICAL REGION; WILLI/ANGELMAN SYNDROME REGION; INV DUP(15) CHROMOSOMES; ANGELMAN-SYNDROME; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; DEVELOPMENTAL DELAY; DNA METHYLATION; EXPRESSED GENE AB Context-Chromosomal abnormalities that involve the proximal region of chromosome 15q occur relatively frequently in the human population. However, interstitial triplications involving one 15 homologue are very rare with three cases reported to date. Objective-To provide a detailed molecular characterisation of four additional patients with interstitial triplications of chromosome 15q11-q14. Design-Molecular analyses were performed using DNA markers and probes specific for the 15q11-q14 region. Setting-Molecular cytogenetics laboratory at the University of Chicago. Subjects-Four patients with mild to severe mental retardation and features of Prader-Willi syndrome (PWS) or Angelman syndrome (AS) were referred for molecular cytogenetic analysis following identification of a suspected duplication/triplication of chromosome 15q11-q14 by routine cytogenetic analysis. Main outcome measures fluorescence in situ hybridisation (FISH) was performed to determine the type of chromosomal abnormality present, the extent of the abnormal region, and the orientation of the extra chromosomal segments. Molecular polymorphism analysis was performed to determine the parental origin of the abnormality. Methylation and northern blot analyses of the SNRPN gene were performed to determine the effect of extra copies of the SNRPN gene on its methylation pattern and expression. Results-Fluorescence in situ hybridisation (FISH) using probes within and flanking the Prader-Willi/Angelman syndrome critical region indicated that all patients carried an intrachromosomal triplication of proximal 15q11-q14 in one of the two chromosome 15 homologues (trip(15)). In all patients the orientation of the triplicated segments was normal-inverted-normal, suggesting that a common mechanism of rearrangement may have been involved. Microsatellite analysis showed the parental origin of the trip(15) to be maternal in three cases and paternal in one case. The paternal triplication patient had features similar to PWS, one maternal triplication patient had features similar to AS, and the other two maternal triplication patients had non-specific findings including hypotonia and mental retardation. Methylation analysis at exon 1 of the SNRPN locus showed increased dosage of either the paternal or maternal bands in the paternal or maternal triplication patients, respectively, suggesting that the methylation pattern shows a dose dependent increase that correlates with the parental origin of the triplication. In addition, the expression of SNRPN was analysed by northern blotting and expression levels were consistent with dosage and parental origin of the triplication. Conclusions-These four additional cases of trip(15) will provide additional information towards understanding the phenotypic effects of this abnormality and aid in understanding the mechanism of formation of other chromosome 15 rearrangements. C1 Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Chulalongkorn Univ, Dept Anat, Genet Unit, Bangkok, Thailand. Genet & IVF Inst, Fairfax, VA 22039 USA. Shodair Hosp, Helena, MT USA. UCL, Inst Child Hlth, Clin & Mol Genet Unit, London, England. RP Ledbetter, DH (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St, Chicago, IL 60637 USA. 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Med. Genet. PD JAN PY 2001 VL 38 IS 1 BP 26 EP 34 DI 10.1136/jmg.38.1.26 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 389AN UT WOS:000166215500005 PM 11134237 ER PT J AU Linday, LA Tsiouris, JA Cohen, IL Shindledecker, R DeCresce, R AF Linday, LA Tsiouris, JA Cohen, IL Shindledecker, R DeCresce, R TI Famotidine treatment of children with autistic spectrum disorders: pilot research using single subject research design SO JOURNAL OF NEURAL TRANSMISSION 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 autism; pervasive developmental disorder; histamine-2 receptor antagonist ID ADJUNCTIVE PHARMACOTHERAPY; GASTROESOPHAGEAL REFLUX; CONTROLLED CROSSOVER; OPEN-LABEL; SCHIZOPHRENIA; NALTREXONE; HISTAMINE; DISEASE; BRAIN; ESOPHAGITIS AB Using single subject research design, we performed pilot research to evaluate the safety and efficacy of famotidine for the treatment of children with autistic spectrum disorders. We studied 9 Caucasian boys, 3.8-8.1 years old, with a DSM-IV diagnosis of a pervasive developmental disorder, living with their families, receiving no chronic medications, and without significant gastrointestinal symptoms. The dose of oral famotidine was 2mg/kg/day (given in two divided doses); the maximum total daily dose was 100mg. Using single-subject research analysis and medication given in a randomized, double-blind, placebo-controlled, cross-over design, 4 of 9 children randomized (44%) had evidence of behavioral improvement. Primary efficacy was based on data kept by primary caregivers, including a daily diary; daily visual analogue scales of affection, reciting, or aspects of social interaction; Aberrant Behavior Checklists (ABC, Aman); and Clinical Global Improvement scales. Children with marked stereotypy (meaningless, repetitive behaviors) did not respond. Our subjects did not have prominent gastrointestinal symptoms and endoscopy was not part of our protocol; thus, we cannot exclude the possibility that our subjects improved due to the effective treatment of asymptomatic esophagitis. The use of famotidine for the treatment of children with autistic spectrum disorders warrants further investigation. C1 Columbia Univ, St Lukes Roosevelt Hosp Ctr, Dept Pediat, New York, NY 10027 USA. Columbia Univ, Coll Phys & Surg, New York, NY 10032 USA. New York State Inst Basic Res Dev Disabil, IBR, Staten Isl, NY 10314 USA. Iona Coll, Grad Sch Arts & Sci, New Rochelle, NY 10801 USA. Rush Presbyterian St Lukes Hosp Med Ctr, Chicago, IL USA. RP Linday, LA (reprint author), 340 W 55th St,Suite 9A, New York, NY 10019 USA. 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PY 2001 VL 108 IS 7 BP 869 EP 878 DI 10.1007/s007020170036 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 456QR UT WOS:000170094200009 PM 11515752 ER PT J AU Nilsson, M Waters, S Waters, N Carlsson, A Carlsson, ML AF Nilsson, M Waters, S Waters, N Carlsson, A Carlsson, ML TI A behavioural pattern analysis of hypoglutamatergic mice - effects of four different antipsychotic agents SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE schizophrenia; autism; cognition; video tracking; MK-801; mice ID AUTISTIC-CHILDREN; INFANTILE-AUTISM; SCHIZOPHRENIA; RISPERIDONE; HYPOTHESIS; GLUTAMATE; MULTIVARIATE; HALOPERIDOL; DISORDER; DISEASE AB In a hypoglutamatergic rodent model, we have observed certain behaviours that might have relevance for the cognitive impairments seen in autism and schizophrenia. Thus, hypoglutamatergic mice show defective habituation, impaired attention, a meagre behavioural repertoire and a general behavioural primitivization. The aim of the present study was to characterise and quantify changes in movement pattern in mice rendered hypoglutamatergic by means of MK-801 treatment, using an automated video tracking system. Further, the effects of four different antipsychotic drugs, the classical neuroleptic haloperidol, the atypical antipsychotic clozapine, the DA D2/5HT2A antagonist risperidone and the selective 5-HT2A-receptor antagonist M100907, were compared with respect to effects on NMDA antagonist-induced movement pattern alterations. We found that each receptor antagonist had a unique effect on the MK-801-induced behavioural primitivization. Haloperidol was unable to affect the monotonous behaviour induced by MK-801, while risperidone, clozapine and M100907 produced movement patterns of high intricacy. C1 Univ Gothenburg, Dept Pharmacol, Inst Physiol & Pharmacol, SE-40530 Gothenburg, Sweden. Carlsson Res AB, Gothenburg, Sweden. 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PY 2001 VL 108 IS 10 BP 1181 EP 1196 DI 10.1007/s007020170008 PG 16 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 489LZ UT WOS:000171994000008 PM 11725821 ER PT J AU Menold, MM Shao, YJ Wolpert, CM Donnelly, SL Raiford, KL Martin, ER Ravan, SA Abramson, RK Wright, HH Delong, GR Cuccaro, L Pericak-Vance, MA Gilbert, JR AF Menold, MM Shao, YJ Wolpert, CM Donnelly, SL Raiford, KL Martin, ER Ravan, SA Abramson, RK Wright, HH Delong, GR Cuccaro, L Pericak-Vance, MA Gilbert, JR TI Association analysis of chromosome 15 GABA(A) receptor subunit genes in autistic disorder SO JOURNAL OF NEUROGENETICS LA English DT Article DE single nucleotide polymorphism; autistic disorder; gamma aminobutyric acids; oligonucleotide ligation assay; chromosome 15q11-q13 ID PRADER-WILLI-SYNDROME; AMINOBUTYRIC-ACID RECEPTOR; PERVASIVE DEVELOPMENTAL DISORDERS; PEDIGREE DISEQUILIBRIUM TEST; ANGELMAN-SYNDROME; LINKAGE-DISEQUILIBRIUM; MENTAL-RETARDATION; IMPRINTING CONTROL; INFANTILE-AUTISM; ALPHA-5 SUBUNIT AB Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain, acting via the GABA(A) receptors. The GABA(A) receptors are comprised of several different homologous subunits, forming a group of receptors that are both structurally and functionally diverse. Three of the GABA(A) receptor subunit genes (GABRB3. GABRA5 and GABRG3) form a cluster on chromosome 15q11-q13, in a region that has been genetically associated with autistic disorder (AutD). Based on these data. we examined 16 single nucleotide polymorphisms (SNPs) located within GABRB3, GABRA5 and GABRG3 for linkage disequilibrium (LD) in 226 AutD families (AutD patients and parents). Genotyping was performed using either OLA (oligonucleotide ligation assay), or SSCP (single strand conformation polymorphism) followed by DNA sequencing. We tested for LD using the Pedigree Disequilibrium Test (PDT). PDT results gave significant evidence that AutD is associated with two SNPs located within the GABRG3 gene (exon5_539T/C, p = 0.02 and intron5_687T/C, p = 0.03), suggesting that the GABRG3 gene or a gene nearby contributes to genetic risk in AutD. C1 Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, Durham, NC 27710 USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29202 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, CARL Bldg Box 3445, Durham, NC 27710 USA. 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PY 2001 VL 7 IS 1 BP 21 EP 29 PG 9 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 407TL UT WOS:000167286800004 PM 11241879 ER PT J AU Stoneman, Z AF Stoneman, Z TI Supporting positive sibling relationships during childhood SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE siblings; childhood; disability; families ID PARENTAL DIFFERENTIAL TREATMENT; PALSIED CHILDRENS INTERACTIONS; MENTALLY-RETARDED CHILDREN; HANDICAPPED-CHILDREN; PRESCHOOL SIBLINGS; MATERNAL-BEHAVIOR; OLDER SIBLINGS; DOWNS-SYNDROME; MOTHER-CHILD; AUTISM AB This paper reviews the research literature focusing on the interpersonal relationships between siblings when one child has a disability. Descriptive findings are presented that compare and contrast sibling warmth and positivity, engagement, and conflict in sibling pairs with and without a child with a disability. 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Retard. Dev. Disabil. Res. Rev. PY 2001 VL 7 IS 2 BP 134 EP 142 DI 10.1002/mrdd.1019 PG 9 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 437XY UT WOS:000169025700010 PM 11389569 ER PT J AU Kaiser, AP Hester, PP McDuffie, AS AF Kaiser, AP Hester, PP McDuffie, AS TI Supporting communication in young children with developmental disabilities SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE language development; children with disabilities ID LANGUAGE INTERVENTION; SOCIAL COMPETENCE; PRESCHOOL-CHILDREN; DOWN-SYNDROME; AUTISM; IMPAIRMENT; ATTENTION; DELAYS; SPEECH; PLAY AB The behavior of parents, adult caregivers, and peers comprises the critical features of community support for the development of communication in young children with developmental disabilities. In a bio-ecological model of development, communication development is the result of the interactions of individuals with specific characteristics, in particular contexts over time. From the perspective of this model, foundational findings of intervention research to current views of communication development in children with developmental disabilities are summarized. The contributions of individual child characteristics to child-caregiver interactions that support language development are illustrated based on research with children who have autism, Williams syndrome, Down syndrome, and children who use augmentative communication systems. Parent-child interaction and the quality and quantity of parent talk are discussed as factors in children's language development. 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PY 2001 VL 7 IS 2 BP 143 EP 150 DI 10.1002/mrdd.1020 PG 8 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 437XY UT WOS:000169025700011 PM 11389570 ER PT J AU Hornig, M Lipkin, WI AF Hornig, M Lipkin, WI TI Infectious and immune factors in the pathogenesis of neurodevelopmental disorders: Epidemiology, hypotheses, and animal models SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE neurodevelopmental disorders; autism; virus; immune; Borna disease virus; animal models ID BORNA-DISEASE-VIRUS; CENTRAL-NERVOUS-SYSTEM; IMMUNOGLOBULIN-A DEFICIENCY; CONGENITAL CYTOMEGALOVIRUS-INFECTION; ACTIVATED T-CELLS; INFANTILE-AUTISM; SERUM AUTOANTIBODIES; POSSIBLE ASSOCIATION; INCREASED FREQUENCY; AUTOIMMUNE-DISEASE AB Both genetic and environmental factors contribute to the pathogenesis of a wide variety of neurodevelopmental disorders, including autism, mental retardation, and schizophrenia. Some heritable disorders approach 100% penetrance; nonetheless, even in these disorders, subtle aspects of clinical disease expression may he influenced by the environment. In other disorders with genetic influences, exogenous factors, and the timepoint(s) during nervous system development at which they are introduced, modulate expression of disease. Elucidation of the mechanisms guiding this intricate interplay between host response genes, environmental agents, and the neurodevelopmental context within which these interactions occur, is necessary to understand the continuum of clinical outcomes. This chapter will review the evidence that infectious and immune factors may contribute to the pathogenesis of neurodevelopmental disorders, describe an animal model of neurodevelopmental disorders based upon viral infection, identify processes by which neural circuitry may be compromised, and outline areas for future research. (C) 2001 Wiley-Liss, Inc. C1 Univ Calif Irvine, Emerging Dis Lab, Irvine, CA 92697 USA. RP Lipkin, WI (reprint author), Univ Calif Irvine, Emerging Dis Lab, 3101 GNRF, Irvine, CA 92697 USA. 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PY 2001 VL 7 IS 3 BP 200 EP 210 DI 10.1002/mrdd.1028 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 470WH UT WOS:000170893900008 PM 11553936 ER PT J AU Lough, S Gregory, C Hodges, JR AF Lough, S Gregory, C Hodges, JR TI Dissociation of social cognition and executive function in frontal variant frontotemporal dementia SO NEUROCASE LA English DT Article ID MENTAL STATE; LOBE DAMAGE; MIND; CHILDREN; DEFICITS; AUTISM; PERFORMANCE; CRITERIA; BELIEFS; ADULTS AB In this paper, we adopt a neurodevelopmental stance to examining frontal variant frontotemporal dementia (fv-FTD) by using experimental procedures from the literature on the growth of social behaviour in children to examine the deficits in social reasoning which may underpin behavioural disturbance in fv-FTD, We present the case of a 47-year-old man with a diagnosis of fv-FTD and severe antisocial behaviour, Tests of general neuropsychology and of executive function were performed. In addition, the patient, JM, was assessed on tasks which test theory of mind. Theory of mind develops in distinct stages through childhood and is a core ability to represent the thoughts and feelings of others, independent of the level of intellectual ability. The results indicate relatively intact general neuropsychological and executive function, but extremely poor performance on tasks of theory of mind. This indicates a dissociation of social cognition and executive function suggesting that in psychiatric presentations of fv-FTD there may be a fundamental deficit in theory of mind independent of the level of executive function. The implications of this finding for diagnostic procedures and possible behavioural management are discussed. C1 Fulbourne Hosp, Dept Psychol, Addenbrookes NHS Trust, Cambridge CB1 5EF, England. Univ Cambridge, Cambridge, England. MRC, Cognit & Brain Sci Unit, Cambridge, England. RP Lough, S (reprint author), Fulbourne Hosp, Dept Psychol, Addenbrookes NHS Trust, Rowan House,Box 338, Cambridge CB1 5EF, England. 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US FDA, CBER, OVRR, DVP,LPRVD, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. RP Pletnikov, MV (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA. 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PY 2001 VL 939 BP 318 EP 319 PG 2 WC Multidisciplinary Sciences; Clinical Neurology SC Science & Technology - Other Topics; Neurosciences & Neurology GA BT12V UT WOS:000172028600036 PM 11462786 ER PT J AU Happe, F Malhi, GS Checkley, S AF Happe, F Malhi, GS Checkley, S TI Acquired mind-blindness following frontal lobe surgery? A single case study of impaired 'theory of mind' in a patient treated with stereotactic anterior capsulotomy SO NEUROPSYCHOLOGIA LA English DT Article DE social intelligence; 'theory of mind'; acquired lesion; affective disorder; autism ID OBSESSIVE-COMPULSIVE DISORDER; CHILDREN; DAMAGE; BRAIN; SCHIZOPHRENIA; ANATOMY; AUTISM; ADULTS; LESION; CORTEX AB Social insight, specifically the ability to represent thoughts and feelings ('theory of mind'), may have a circumscribed and dedicated neurological substrate. Evidence of deficits in 'theory of mind' following acquired lesions would support this idea. Previous studies of lesions resulting from stroke or head injury have been hampered by lack of detailed lesion information and pre-lesion documentation. We report the case of a 76-year-old man who, following a standard surgical procedure to treat bipolar affective disorder, showed evidence of impaired 'theory of mind'. This case, which is the first of its type, may contribute to the search for the brain basis of social insight. (C) 2000 Elsevier Science Ltd. All rights reserved. C1 Kings Coll London, SGDP, Res Ctr, Inst Psychiat, London SE5 8AF, England. RP Happe, F (reprint author), Kings Coll London, SGDP, Res Ctr, Inst Psychiat, 111 Denmark Hill, London SE5 8AF, England. EM f.happe@iop.kcl.ac.uk RI Happe, Francesca/D-5544-2012 CR Abbruzzese M, 1997, NEUROPSYCHOLOGIA, V35, P907, DOI 10.1016/S0028-3932(96)00095-4 ALEXANDER GE, 1990, PROG BRAIN RES, V85, P119 AVIS J, 1991, CHILD DEV, V62, P460, DOI 10.1111/j.1467-8624.1991.tb01544.x BARONCOHEN S, 1994, BRIT J PSYCHIAT, V165, P640, DOI 10.1192/bjp.165.5.640 Baron-Cohen S., 1999, UNDERSTANDING OTHER Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Brunet E, 2000, NEUROIMAGE, V11, P157, DOI 10.1006/nimg.1999.0525 Buchsbaum MS, 1998, NEUROREPORT, V9, P425, DOI 10.1097/00001756-199802160-00013 Byrne R. 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Humans with bilateral amygdala damage are impaired in judging negative emotion in facial expressions and making accurate judgements of trustworthiness (Adolphs et al., 1998, 1994). Amygdala dysfunction has also been implicated in human disorders ranging from social anxiety (Birbaumer et al., 1998) to depression (Drevets, 2000) to autism (Bachevalier, 1994; Baron-Cohen et al., 2000; Bauman and Kemper, 1993). We produced selective amygdala lesions in 2-week-old macaque monkeys who were returned to their mothers for rearing. At 6-8 months of age, the lesioned animals demonstrated less fear of novel objects such as rubber snakes than age-matched controls. However, they displayed substantially more fear behavior than controls during dyadic social interactions. These results suggest that neonatal amygdala lesions dissociate a system that mediates social fear from one that mediates fear of inanimate objects. 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It is usually caused by the transcriptional inactivation of the FMR-I gene. Although the cognitive defect is the most recognized symptom of fragile X syndrome, patients also show behavioral problems such as hyperarousal, hyperactivity, autism, aggression, anxiety and increased sensitivity to sensory stimuli. Here we investigated whether fragile X mice (fmr-1 gene knockout mice) exhibit abnormal sensitivity to sensory stimuli. First, hyperreactivity of fragile X mice to auditory stimulus was indicated in the prepulse inhibition paradigm. A moderately intense prepulse tone, that suppresses startle response to a strong auditory stimulus, elicited a significantly stronger effect in fragile X than in control mice. Second, sensory hyperreactivity of fragile X mice was demonstrated by a high seizure susceptibility to auditory stimulation. Selective induction of c-Fos, an early-immediate gene product, indicated that seizures involve auditory brainstem and thalamic nuclei. Audiogenic seizures were not due to a general increase in brain excitability because three different chemical convulsants (kainic acid, bicuculline and pentylenetetrazole) elicited similar effects in fragile X and wild-type mice. These data are consistent with the increased responsiveness of fragile X patients to auditory stimuli. The auditory hypersensitivity suggests an abnormal processing in the auditory system of fragile X mice, which could provide a useful model to study the molecular and cellular changes underlying fragile X syndrome. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved. C1 Cornell Univ, Weill Med Coll, Dept Pharmacol, New York, NY 10021 USA. RP Toth, M (reprint author), Cornell Univ, Weill Med Coll, Dept Pharmacol, 1300 York Ave,LC 522, New York, NY 10021 USA. 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We propose that OCD is often related to HFA and Asperger disorder. Self-report questionnaires may be useful in establishing the diagnosis. However, those with the most obvious autistic features seem to be less able to identify these traits in themselves. C1 Univ Uppsala Hosp, Dept Neurosci, SE-75185 Uppsala, Sweden. Univ Uppsala Hosp, Dept Psychiat, SE-75185 Uppsala, Sweden. RP Bejerot, S (reprint author), Univ Uppsala Hosp, Dept Neurosci, SE-75185 Uppsala, Sweden. 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J. Psychiatr. PY 2001 VL 55 IS 3 BP 169 EP 176 PG 8 WC Psychiatry SC Psychiatry GA 449GY UT WOS:000169677000004 PM 11827611 ER PT J AU Knivsberg, AM Reichelt, KL Nodland, M AF Knivsberg, AM Reichelt, KL Nodland, M TI Reports on dietary intervention in autistic disorders SO NUTRITIONAL NEUROSCIENCE LA English DT Article DE autism; casein; gluten; diet; peptides ID BLOOD-BRAIN-BARRIER; INFANTILE-AUTISM; OPIOID-PEPTIDES; BOVINE-MILK; CHILDREN; TRANSPORT; EXORPHINS; RELEASE; PASSAGE; HUMANS AB Autism is a developmental disorder for which no curt currently exists. Gluten and/or casein free diet has been implemented to reduce autistic behaviour, in addition to special education, since early in the eighties. Over the last twelve years various studies on this dietary intervention have been published in addition to anecdotal, parental reports. The scientific studies include both groups of participants as well as single cases, and beneficial results are reported in all, but one study. 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Neurosci. PY 2001 VL 4 IS 1 BP 25 EP 37 PG 13 WC Neurosciences; Nutrition & Dietetics SC Neurosciences & Neurology; Nutrition & Dietetics GA 416HP UT WOS:000167774500003 PM 11842874 ER PT J AU Wallace, S Bailey, A Coleman, M AF Wallace, S. Bailey, A. Coleman, M. TI Different strategies at detecting direction of eye gaze: comparing individuals with autism or Asperger's syndrome to IQ-matched controls SO PERCEPTION LA English DT Meeting Abstract C1 [Wallace, S.; Bailey, A.] Inst Psychiat, Dept Child & Adolescent Psychiat, London SE5 8AF, England. [Coleman, M.] UCL, Dept Human Commun Sci, London WC1N 1PG, England. EM spjwsbw@iop.kcl.ac.uk RI Bailey, Anthony/J-2860-2014 OI Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2001 VL 30 BP 56 EP 56 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA V05FY UT WOS:000207113100175 ER PT J AU Gepner, B AF Gepner, B TI What role is played by troubles of movement vision in infantile autism? A new neuropathological, developmental approach SO PSYCHIATRIE DE L ENFANT LA French DT Review ID SPATIOTEMPORAL CONTRAST SENSITIVITY; CHILDHOOD AUTISM; PARKINSONS-DISEASE; STIMULUS OVERSELECTIVITY; 5-MONTH-OLD INFANTS; KINETIC INFORMATION; CHILDREN; PERCEPTION; MOTION; FACE AB In this article, we present a new neuropathological developmental hypothesis in which early troubles with movement vision in their attentional, perceptive and/or visuo-motor integration aspects play a central role in certain forms of infantile autism by bringing about several cascades of developmental anomalies in such diverse and crucial domains as joint attention, perception, imitation, representation, comprehension and the expression of emotions and language, and finally, visuo-gestual and posturo-motor exchanges between the baby and his or her human environment. After a presentation of the principal experimental arguments and issues in the literature in favor of this hypothesis, we will try to show its advantages (diagnostic implications and reeducational applications) and its theoretico-clinical limits by confronting the theory with several contemporary neuro-physio and neuro-psychological approaches to infantile autism (notably, works on attention, visual perception and imitation). Also, we present some testimony from autistic adults about their visual world, and finally, several psychoanalytical works and concepts. We suggest that our model is, properly speaking, a neuro-psychodynamic one and that it can offer us several neuropsychological bases for thought in movement. C1 AFRTDET, F-13008 Marseille, France. RP Gepner, B (reprint author), AFRTDET, 137 Rue J Mermoz, F-13008 Marseille, France. 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Enfant PY 2001 VL 44 IS 1 BP 77 EP 126 PG 50 WC Psychiatry SC Psychiatry GA 487XG UT WOS:000171903900003 ER PT J AU Maheady, L Harper, GF Mallette, B AF Maheady, L Harper, GF Mallette, B TI Peer-mediated instruction and interventions and students with mild disabilities SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article ID ON-TASK BEHAVIOR; DISORDERS; INTEGRATION; STRATEGIES; CHILDREN; SKILLS; AUTISM AB Teaching is more difficult today than in the past. and most educators predict that it will become even more challenging in years to come. Exponential increases within the school curriculum, spectacular changes in student demographic characteristics, and dwindling instructional resources make it extremely difficult for even the most responsive teachers to provide a high-quality education for all pupils. These challenges become more formidable when teachers attempt to meet the needs of students with mild disabilities in less restrictive settings (e.g.. general education classrooms). In this article, we describe how a variety of peer-mediated instruction and interventions might assist classroom teachers in meeting such instructional challenges. We describe the extensive academic and behavioral needs of this population of students. provide an illustrative review of peer-teaching methods, and suggest future directions for research and practice. C1 SUNY Coll Fredonia, Sch Educ, Fredonia, NY 14063 USA. RP Maheady, L (reprint author), SUNY Coll Fredonia, Sch Educ, Fredonia, NY 14063 USA. CR AGRAN M, 1992, EDUC TRAIN MENT RET, V27, P230 ANTIA S, 1994, VOLTA REV, V96, P277 Armbruster B. B., 1984, COMPREHENSION INSTRU, P202 BAKER JM, 1990, EXCEPT CHILDREN, V56, P515 BECK IL, 1989, COGNITION INSTRUCT, V6, P99, DOI 10.1207/s1532690xci0602_1 BELL K, 1990, SCHOOL PSYCHOL REV, V19, P564 BENNETT WJ, 1986, TUTORINE WHAT WORKS Block M. 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PD JAN-FEB PY 2001 VL 22 IS 1 BP 4 EP 14 DI 10.1177/074193250102200102 PG 11 WC Education, Special SC Education & Educational Research GA 398YA UT WOS:000166783000002 ER PT J AU Covarrubias, AL Pina, M Flores, RD AF Covarrubias, AL Pina, M Flores, RD TI A guided workshop for mothers to promote social skills and self-care in children with autism and developmental retardation SO REVISTA MEXICANA DE PSICOLOGIA LA Spanish DT Meeting Abstract C1 Univ Nacl Autonoma Mexico, Fac Psicolog, Mexico City, DF, Mexico. NR 0 TC 0 Z9 0 PU SOC MEXICANA PSICOLOGIA PI TLALPAN PA APARTADO POSTAL 22-211, TLALPAN 14000, MEXICO SN 0185-6073 J9 REV MEX PSICOL JI Rev. Mex. Psicol. PD JAN PY 2001 VL 18 IS 1 BP 50 EP 51 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 449GV UT WOS:000169676700099 ER PT J AU Jalley, E AF Jalley, E TI On the threshold of the representable. Autism, infantile psychosis and body techniques SO REVUE PHILOSOPHIQUE DE LA FRANCE ET DE L ETRANGER LA French DT Book Review CR ALLOUCH E, 1999, SEUIL FIGURABLE AUTI NR 1 TC 0 Z9 0 PU PRESSES UNIV FRANCE PI EVRY CEDEX PA DEPT DES REVUES 14, AVENUE DU BOIS-DE-L EPINE B P 90, 91003 EVRY CEDEX, FRANCE SN 0035-3833 J9 REV PHILOS FR ETRANG JI Rev. Philos. Fr. Etrang. PD JAN-MAR PY 2001 VL 126 IS 1 BP 109 EP 109 PG 1 WC Philosophy SC Philosophy GA 412ZC UT WOS:000167584300050 ER PT J AU Ochs, E Kremer-Sadlik, T Solomon, O Sirota, KG AF Ochs, E Kremer-Sadlik, T Solomon, O Sirota, KG TI Inclusion as social practice: Views of children with autism SO SOCIAL DEVELOPMENT LA English DT Article DE high functioning autism; autism; confidentiality; inclusion ID COOPERATIVE LEARNING GROUPS; INTEGRATION STRATEGY; STUDENTS; PEERS; EXPRESSIONS; APPRAISAL; STORIES; EMOTION; MIND AB This study illuminates the social realities of inclusion of 16 high functioning children with autism (HFA) in public schools in the United States. The study suggests that the practice of inclusion rests primarily on unaffected schoolmates rather than teachers, it-ho typically are occupied monitoring academic progress and disciplinary transgressions across a range of children. Utilizing ethnographic observations and video recordings of quotidian classroom and playground activities, the analysis elucidates how classmates employ a range of positive and negative inclusion practices that either integrate or distance autistic children. Ethnographic observations of the study population indicate that the children whose diagnosis was fully disclosed enjoyed more consistent social support in the classroom and on the school playground. The study further suggests that high functioning children with autism exhibit a range of reactions to negative inclusion practices such as rejection and scorn. Such reactions include oblivion, immediate behavioral response, and emotionally charged accounts of disturbing school incidents shared after-the fact with family members. Significantly, these observations indicate that HFA children can be cognizant of and distressed by others' derisive stances and acts, despite symptomatic difficulties in interpreting others' intentions and feelings. C1 Univ Calif Los Angeles, Dept Anthropol, Los Angeles, CA 90095 USA. RP Ochs, E (reprint author), Univ Calif Los Angeles, Dept Anthropol, 3207 Hershey Hall,Box 951553, Los Angeles, CA 90095 USA. CR Attwood T., 1998, ASPERGERS SYNDROME G Baker E. 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W., 1997, FOCUS AUTISM OTHER D, V12, P196 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V16, P335 LISSER M, OUR JOURNEY HIGH FUN Nisbet J., 1994, ED REFORM SUMMARY RE PERNER J, 1993, UNDERSTANDING OTHER, P112 Siegel B., 1996, WORLD AUTISTIC CHILD Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 STRAIN PS, 1979, J AUTISM DEV DISORD, V9, P41, DOI 10.1007/BF01531291 TAGERFLUSBERG H, 1995, BRIT J DEV PSYCHOL, V13, P45 WAITE M, 1995, OXFORD DICT USAGE GU Wechsler D., 1992, MANUAL WECHSLER INTE, V3rd NR 42 TC 62 Z9 65 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0961-205X J9 SOC DEV JI Soc. Dev. PY 2001 VL 10 IS 3 BP 399 EP 419 DI 10.1111/1467-9507.00172 PG 21 WC Psychology, Developmental SC Psychology GA 470VD UT WOS:000170891100007 ER PT J AU Zapor, M Murphy, FT Enzenauer, R AF Zapor, M Murphy, FT Enzenauer, R TI Echolalia as a novel manifestation of neuropsychiatric systemic lupus erythematosus SO SOUTHERN MEDICAL JOURNAL LA English DT Article; Proceedings Paper CT 93rd Annual Scientific Session of the Southern-Medical-Association CY NOV 10-14, 1999 CL DALLAS, TEXAS SP SW med Assoc ID COGNITIVE IMPAIRMENT; ANTIBODIES; CRITERIA AB "That tongue of yours, by which I have been tricked, shall have its power curtailed and enjoy the briefest use of speech." With these words, Hera, of Creek mythology, deprived the nymph Echo of spontaneous speech, constraining her instead to merely repeating the words of others. Echolalia, which derives from the word "echo," is disordered speech in which an individual persistently repeats what is heard. Echolalia has been described in patients with a number of neuropsychiatric illnesses including autism and Tourette's syndrome. Neuropsychiatric systemic lupus erythematosus (NPSLE) is a heterogeneous disease with protean manifestations that may occur in approximately 25% to 50% of patients with systemic lupus erythematosus (SLE), Although the most common manifestations include cognitive dysfunction (50%) and seizures (20%), NPSLE may also present as peripheral neuropathy (15%), psychosis (10%), or other central nervous system abnormalities. We report the case of a 57-year-old woman with SLE and echolalia. C1 Brooke Army Med Ctr, Dept Med, Div Rheumatol, Ft Sam Houston, TX 78234 USA. RP Zapor, M (reprint author), Brooke Army Med Ctr, Dept Med, Div Rheumatol, 3851 Roger Brooke Dr, Ft Sam Houston, TX 78234 USA. 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PD JAN PY 2001 VL 94 IS 1 BP 70 EP 72 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 400CJ UT WOS:000166850800014 PM 11213948 ER PT J AU Bresnahan, M Susser, E AF Bresnahan, M Susser, E TI Advocacy movements in research and prevention: schizophrenia and autism SO SOZIAL-UND PRAVENTIVMEDIZIN LA English DT Editorial Material C1 Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10027 USA. RP Bresnahan, M (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10027 USA. CR Torrey E. F., 1994, SCHIZOPHRENIA MANIC NR 1 TC 0 Z9 0 PU BIRKHAUSER VERLAG AG PI BASEL PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND SN 0303-8408 J9 SOZ PRAVENTIV MED JI Sozial-und Pravent. PY 2001 VL 46 IS 3 BP 141 EP 142 DI 10.1007/BF01324244 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 463QL UT WOS:000170488700001 PM 11565437 ER PT J AU Gijswijt-Hofstra, M AF Gijswijt-Hofstra, M TI Autism in history: The case of Hugh Blair of Borgue SO TIJDSCHRIFT VOOR GESCHIEDENIS LA Dutch DT Book Review CR Houston R. A., 2000, AUTISM HIST CASE H B NR 1 TC 0 Z9 0 PU WOLTERS-NOORDHOFF B V PI GRONINGEN PA BOX 58, 9700 GRONINGEN, NETHERLANDS SN 0040-7518 J9 TIJDSCHR GESCHIEDEN JI Tijdschr. Geschied. PY 2001 VL 114 IS 4 BP 618 EP 620 PG 3 WC History SC History GA 492YU UT WOS:000172195800021 ER PT J AU Grachev, VV AF Grachev, VV TI Rett's syndrome: diagnostic aspects SO ZHURNAL NEVROPATOLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article ID NATURAL-HISTORY; CRITERIA; AUTISM; GIRLS AB Rett's syndrome (RS) is a severe disease of an early childhood, affecting girls mainly and manifesting in autistic symptoms, severe mental regression and motor dysfunction. The aim of the study was to analyze both early stages of clinical symptomatology and EEC correlates of RS. 65 patients aged 2,5-13 years with classic RS were examined. It was found that affective and autistic manifestations were the main symptoms during the 1-st stage of RS in approximately 50% of the cases. Two variants of classic RS were described according to the degree of motor dysfunction and behavioral disturbances: RS with motor disorders; RS with schizophrenoform disorders. 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S S Korsakova PY 2001 VL 101 IS 4 BP 55 EP 60 PG 6 WC Clinical Neurology; Pathology; Psychiatry SC Neurosciences & Neurology; Pathology; Psychiatry GA 471QN UT WOS:000170940200014 PM 11490439 ER PT J AU Veenstra-VanderWeele, J Anderson, GM Cook, EH AF Veenstra-VanderWeele, J Anderson, GM Cook, EH TI Pharmacogenetics and the serotonin system: initial studies and future directions SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Review DE pharmacogenetics; 5-HT (5-hydroxytryptamine, serotonin); tryptophan hydroxylase; 5-HT receptor; 5-HT (5-hydroxytryptamine, serotonin); transporter; monoamine oxidase; 5-HT (5-hydroxytryptamine, serotonin) reuptake inhibitor, selective; clozapine ID MONOAMINE-OXIDASE-A; FAMILY-BASED ASSOCIATION; INCREASED EXPLORATORY ACTIVITY; OBSESSIVE-COMPULSIVE DISORDER; TRYPTOPHAN-HYDROXYLASE GENE; SEASONAL AFFECTIVE-DISORDER; TRANSPORTER PROTEIN GENE; AMINO-ACID SUBSTITUTIONS; ANXIETY-RELATED TRAITS; HUMAN 5-HT1A RECEPTOR AB Serotonin (5-hydroxytryptamine, 5-HT) appears to play a role in the pathophysiology of a range of neuropsychiatric disorders, and serotonergic agents are of central importance in neuropharmacology. Genes encoding various components of the 5-HT system are being studied as risk factors in depression, schizophrenia, obsessive-compulsive disorder. aggression, alcoholism, and autism. Recently, pharmacogenetic research has begun to examine possible genetic influences on therapeutic response to drugs affecting the serotonin system. Genes regulating the synthesis (TPH), storage (VMAT2), membrane uptake (HTT), and metabolism (MAOA) of 5-HT, as well as a number of 5-HT receptors (HTR1A, HTR1B, HTR2A, HTR2C, and HTR5A), have been studied and this initial research is reviewed here. After a brief introduction to serotonin neurobiology and a general discussion of appropriate genetic methodology, each of the major 5-HT-related genes and their encoded proteins are reviewed in turn. For each gene, relevant polymorphisms and research on functional variants are discussed; following brief reviews of the disorder or trait association and linkage studies, pharmacogenetic studies performed to date are covered. The critical and manifold roles of the serotonin system, the great abundance of targets within the system, the wide range of serotonergic agents-available and in development-and the promising preliminary results suggest that the serotonin system offers a particularly rich area for pharmacogenetic research. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Chicago, Dept Psychiat, Lab Dev Neurosci Child & Adolescent Psychiat, Chicago, IL 60637 USA. Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06510 USA. Yale Univ, Sch Med, Dept Child Psychiat, New Haven, CT 06510 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. Univ Chicago, Comm Clin Pharmacol, Chicago, IL 60637 USA. 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J. Pharmacol. PD DEC 27 PY 2000 VL 410 IS 2-3 BP 165 EP 181 DI 10.1016/S0014-2999(00)00814-1 PG 17 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 391CW UT WOS:000166337400007 PM 11134668 ER PT J AU Miles, JH Hadden, LL Takahashi, TN Hillman, RE AF Miles, JH Hadden, LL Takahashi, TN Hillman, RE TI Head circumference is an independent clinical finding associated with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; head circumference; macrocephaly; clinical morphology ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HISTORY; INFANTILE-AUTISM; GENOMIC SCREEN; SIZE; CHILDREN; SCHIZOPHRENIA; RELIABILITY; INDIVIDUALS; PSYCHOSIS AB Occipitofrontal circumference (OFC) is one of the few physical findings in autism that varies significantly from the norm and is distinct and measurable. As part of a study of genetic heterogeneity of autism, we scrutinized data from a large sample of patients with idiopathic autism (N = 137), using OFC as the categorizing variable. The OFC standard deviation (OFCSD) values of the autistic propositi (0.61 +/- 1.6) varied significantly from that of the normal population (0.0 +/- 1.0), (P < 0.001), Comparison of the macrocephalic (OFCSD 2.0, N = 32) with the normocephalic individuals (-2 SD < OFCSD < +2 SD, N = 95) showed no significant differences in sex ratio, morphological status, IQ, seizure prevalence, or recurrence risks. The macrocephalic individuals were slightly less apt than those with normocephaly to have a family history of Attention Deficit Hyperactivity Disorder (ADHD) (P < 0.05), Each clinical subgroup of autism propositi, defined on the basis of phenotypic status, type of onset, seizure history, or IQ, had a higher than normal mean OFC indicating that macrocephaly is an independent clinical trait in autism. As in the non-autistic population, macrocephaly was highly familial with 45% of the macrocephalic and 37% of the normocephalic propositi having at least one macrocephalic parent. Microcephaly, however, was an independent significant variable that predicted the presence of other phenotypic or genetic traits and outcome. The microcephalic patients were more likely to have abnormal physical morphology, structural brain malformations, lower IQ, and seizures. Their sex ratio was closer to normal, and their relatives had a higher incidence of seizures. (C) 2000 Wiley-Liss, Inc. C1 Univ Missouri, Childrens Hosp, Div Med Genet, Columbia, MO 65212 USA. RP Miles, JH (reprint author), Univ Missouri, Childrens Hosp, Div Med Genet, 1 Hosp Dr, Columbia, MO 65212 USA. 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