FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Seshardri, K Alimokhtari, S Weisel, C Mars, A Moreno, R Buckley, B Lioy, P Lambert, G AF Seshardri, K Alimokhtari, S Weisel, C Mars, A Moreno, R Buckley, B Lioy, P Lambert, G TI Preliminary results of home environmental assessment and chemical exposure, and body burdens of children with autism spectrum disorder or PDD-NOS (ASD) SO EPIDEMIOLOGY LA English DT Meeting Abstract CT 16th Conference of the International-Society-for-Environmental-Epidemiology CY AUG 01-04, 2004 CL New York, NY SP NYU Sch Med, UMDNJ Robert Wood Johnson Med Sch C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pediat, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Environm & Community Med, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA. State Univ New Jersey, Piscataway, NJ USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JUL PY 2004 VL 15 IS 4 BP S219 EP S219 DI 10.1097/00001648-200407000-00582 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 834GO UT WOS:000222399800581 ER PT J AU Windham, G Gunier, R Zhang, LX Croen, L Grether, J AF Windham, G Gunier, R Zhang, LX Croen, L Grether, J TI Investigating hazardous air pollutants in relation to autism spectrum disorders SO EPIDEMIOLOGY LA English DT Meeting Abstract CT 16th Conference of the International-Society-for-Environmental-Epidemiology CY AUG 01-04, 2004 CL New York, NY SP NYU Sch Med, UMDNJ Robert Wood Johnson Med Sch C1 CA Dept Hlth Serv, Akland, CA USA. Kaiser Div Res, Oakland, CA USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JUL PY 2004 VL 15 IS 4 BP S217 EP S218 DI 10.1097/00001648-200407000-00577 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 834GO UT WOS:000222399800576 ER PT J AU Finucane, BM Haas-Givler, B Simon, EW AF Finucane, BM Haas-Givler, B Simon, EW TI Autism and chromosome 15: evidence for atypical progression of autistic symptoms among children with a supernumerary isodicentric 15 chromosome. SO GENETICS IN MEDICINE LA English DT Meeting Abstract CT Annual Clinical Meeting of the American-College-of-Medical-Genetics CY MAR 04, 2004 CL Orlando, FL SP Amer Coll Med Genet C1 Elwyn Training & Res Inst, Elwyn, PA USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD JUL-AUG PY 2004 VL 6 IS 4 MA 19 BP 255 EP 255 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 838WX UT WOS:000222745200031 ER PT J AU Martin, L Johnson, J Wells, W Meiser, L AF Martin, L Johnson, J Wells, W Meiser, L TI Autism and novel duplication in 15q11-13 GABRB3 region. SO GENETICS IN MEDICINE LA English DT Meeting Abstract CT Annual Clinical Meeting of the American-College-of-Medical-Genetics CY MAR 04, 2004 CL Orlando, FL SP Amer Coll Med Genet C1 Rockford Hlth Syst, NW Illinois Reg Perinatal Ctr, Rockford, IL USA. Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD JUL-AUG PY 2004 VL 6 IS 4 MA 116 BP 301 EP 301 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 838WX UT WOS:000222745200126 ER PT J AU Wolpert, C Grubber, J Donnelly, S Cope, H Abramson, R Wright, H Gilbert, J Cuccaro, M Pericak-Vance, MA AF Wolpert, C Grubber, J Donnelly, S Cope, H Abramson, R Wright, H Gilbert, J Cuccaro, M Pericak-Vance, MA TI Evidence supporting the multifactorial threshold model (MTM) in autism. SO GENETICS IN MEDICINE LA English DT Meeting Abstract CT Annual Clinical Meeting of the American-College-of-Medical-Genetics CY MAR 04, 2004 CL Orlando, FL SP Amer Coll Med Genet C1 DUMC, Duke Ctr Human Genet, Durham, NC USA. WS Hall Psychiat Ctr, Columbia, SC USA. NR 0 TC 1 Z9 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD JUL-AUG PY 2004 VL 6 IS 4 MA 144 BP 314 EP 314 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 838WX UT WOS:000222745200153 ER PT J AU Sommer, S Feng, J Shibayama, A Glanzmann, C Yan, J Cook, E Craddock, N Jones, I Goldman, D Heston, LL AF Sommer, S Feng, J Shibayama, A Glanzmann, C Yan, J Cook, E Craddock, N Jones, I Goldman, D Heston, LL TI MECP2 variants in psychiatric diseases: possible association with autism. SO GENETICS IN MEDICINE LA English DT Meeting Abstract CT Annual Clinical Meeting of the American-College-of-Medical-Genetics CY MAR 04, 2004 CL Orlando, FL SP Amer Coll Med Genet C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Birmingham, Div Neurosci, Queen Elizabeth Psychiat Hosp, Birmingham, W Midlands, England. NIAAA, Dept Psychiat, NIH, Bethesda, MD USA. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. RI Jones, Ian/B-4925-2009 NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD JUL-AUG PY 2004 VL 6 IS 4 MA 239 BP 361 EP 361 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 838WX UT WOS:000222745200246 ER PT J AU Mann, SM Wang, NJ Liu, DH Wang, L Schultz, RA Dorrani, N Sigman, M Schanen, NC AF Mann, SM Wang, NJ Liu, DH Wang, L Schultz, RA Dorrani, N Sigman, M Schanen, NC TI Supernumerary tricentric derivative chromosome 15 in two boys with intractable epilepsy: another mechanism for partial hexasomy SO HUMAN GENETICS LA English DT Article AB Rearrangements of chromosome 15q, including isodicentric 15 chromosomes and interstitial duplications and triplications, have been previously reported in association with autism spectrum disorders. We have identified two boys with exceptionally large der(15) chromosomes that are tricentric and contain four copies of the proximal long arm, including the Prader Willi/Angelman critical region, and leading to hexasomy of the involved segment. Biallelic inheritance of maternal alleles and methylation analysis indicate that the markers are maternally derived. Clinical assessment of the boys indicated severe cognitive impairment associated with marked delays in gross and fine motor skills. Social and language deficits were present in both, although the severity of the mental retardation precluded diagnosis of autism (both were considered to have pervasive developmental disorder-not otherwise specified). Neurologic manifestations included infantile spasms evolving into intractable early-onset myoclonic seizures, psychomotor regression, and profound diffuse hypotonia. These patients represent the most severe end of the spectrum of phenotypes associated with segmental aneuploidy for chromosome 15q11-q13. C1 Alfred I duPont Hosp Children, Nemours Childrens Clin, Nemours Biomed Res, Wilmington, DE 19899 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA USA. Univ Texas, SW Med Ctr, McDermott Ctr Human Growth & Dev, Dallas, TX USA. Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX USA. Univ Calif Los Angeles, David Geffen Sch Med, Inst Neuropsychiat, Los Angeles, CA USA. RP Schanen, NC (reprint author), Alfred I duPont Hosp Children, Nemours Childrens Clin, Nemours Biomed Res, POB 269,1600 Rockland Rd, Wilmington, DE 19899 USA. EM cschanen@nemours.org CR CAINE A, 1993, PRENATAL DIAG, V13, P1061, DOI 10.1002/pd.1970131111 Eggermann K, 2002, CLIN GENET, V62, P89, DOI 10.1034/j.1399-0004.2002.620113.x Glenn CC, 1996, AM J HUM GENET, V58, P335 Huang B, 2003, AM J MED GENET A, V121A, P277, DOI 10.1002/ajmg.a.20182 Maggouta F, 2003, J MED GENET, V40, DOI 10.1136/jmg.40.7.e84 Mullen PD, 1995, HEALTH EDUC QUART, V22, P329 Nietzel A, 2003, J Med Genet, V40, pe28, DOI 10.1136/jmg.40.3.e28 Qumsiyeh MB, 2003, AM J MED GENET A, V116A, P356, DOI 10.1002/ajmg.a.10050 SCHRECK RR, 1977, HUM GENET, V36, P1, DOI 10.1007/BF00390430 SCHWARTZ S, 1998, AM J HUM GENET, V63, pA40 Schwartz S., 1996, American Journal of Human Genetics, V59, pA14 Thomas NS, 2003, AM J MED GENET A, V120A, P596, DOI 10.1002/ajmg.a.20140 Ungaro P, 2001, J MED GENET, V38, P26, DOI 10.1136/jmg.38.1.26 NR 13 TC 18 Z9 19 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JUL PY 2004 VL 115 IS 2 BP 104 EP 111 DI 10.1007/s00439-004-1127-5 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 831RP UT WOS:000222214100003 PM 15141347 ER PT J AU Coonrod, EE Stone, WL AF Coonrod, EE Stone, WL TI Early concerns of parents of children with autistic and nonautistic disorders SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; early identification; parent report; social communication ID SPECTRUM DISORDER; EARLY RECOGNITION; PEDIATRICIANS ROLE; HOME VIDEOTAPES; FOLLOW-UP; DIAGNOSIS; AGE; SYMPTOMS; MANAGEMENT; POPULATION AB The purpose of this study was to extend previous research on the early concerns of parents of children with autism by (a) obtaining information from parents of very young children who have not yet received a diagnosis; (b) including a developmentally matched comparison sample; and (c) querying about first concerns as well as current concerns and behaviors. During their child's initial diagnostic evaluation, parents of 44 two-year-old children (22 with autism, 22 with developmental delay) responded to open-ended questions regarding their early concerns about their child's development as well as specific questions about social-communicative behaviors. The age of children when parents first became concerned and the specific nature of first concerns were similar for both groups, with the most frequent concerns related to children's language development. When asked specific questions about current social and communicative behaviors, parents of children with autism reported more deficits in both areas than did parents in the comparison group. These results suggest that specific questions about children's social-communicative behaviors may have more utility than open-ended questions in identifying young children who are at risk for an autism diagnosis. C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA. RP Stone, WL (reprint author), Vanderbilt Ctr Child Dev, 426 Med Ctr S,2100 Pierce Ave, Nashville, TN 37232 USA. EM wendy.stone@vanderbilt.edu CR Adrien J L, 1992, Acta Paedopsychiatr, V55, P71 ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 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 Bayley N, 1969, MANUAL BAYLEY SCALES Bayley N, 1993, BAYLEY SCALES INFANT Sandler AD, 2001, PEDIATRICS, V107 Sandler AD, 2001, PEDIATRICS, V107, P1221 Committee on Educational Interventions for Children with Autism, 2001, ED CHILDR AUT Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 DULCAN MK, 1990, J AM ACAD CHILD PSY, V29, P453, DOI 10.1097/00004583-199005000-00018 Fenson L, 1993, MACARTHUR COMMUNICAT FENSON L, 1991, UNPUB TECHNICAL MANU Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 GLASCOE FP, 1989, AJDC, V143, P855 GLASCOE FP, 1995, J PEDIATR-US, V127, P831, DOI 10.1016/S0022-3476(95)70184-2 HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P215, DOI 10.1111/j.1469-7610.1994.tb01159.x 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, 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 Mandell DS, 2002, J AM ACAD CHILD PSY, V41, P1447, DOI 10.1097/01.CHI.0000024863.60748.53 Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 OHTA M, 1987, J AUTISM DEV DISORD, V17, P549, DOI 10.1007/BF01486970 ORNITZ EM, 1977, J AUTISM CHILD SCHIZ, V7, P207, DOI 10.1007/BF01538999 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 Schopler E., 1988, CHILDHOOD AUTISM RAT SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 SIEGEL B, 1988, J DEV BEHAV PEDIATR, V9, P199 SMITH B, 1994, J AUTISM DEV DISORD, V24, P551, DOI 10.1007/BF02172137 STONE WL, 1992, UNPUB SOCIAL BEHAV C Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 STONE WL, 1990, PEDIATRICS, V86, P267 Stone WL, 2000, J AUTISM DEV DISORD, V30, P607, DOI 10.1023/A:1005647629002 STONE WL, 1994, ARCH PEDIAT ADOL MED, V148, P174 STONE WL, 1988, J AUTISM DEV DISORD, V18, P403, DOI 10.1007/BF02212195 STUTSMAN R, 1948, GUIDE ADM MERRILLPAL VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 VOLKMAR FR, 1985, AM J PSYCHIAT, V142, P1450 Vostanis P., 1998, AUTISM, V2, P229, DOI 10.1177/1362361398023002 Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 Wimpory DC, 2000, J AUTISM DEV DISORD, V30, P525, DOI 10.1023/A:1005683209438 NR 51 TC 38 Z9 39 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0896-3746 J9 INFANT YOUNG CHILD JI Infants Young Child. PD JUL-SEP PY 2004 VL 17 IS 3 BP 258 EP 268 PG 11 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 834XM UT WOS:000222444200007 ER PT J AU Paparella, T Kasari, C AF Paparella, T Kasari, C TI Joint attention skills and language development in special needs populations - Translating research to practice SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; deafness; Down syndrome; intervention; joint attention; language ID AUTISTIC-CHILDREN; NONVERBAL-COMMUNICATION; DEAF; PREDICT; MOTHERS; INFANT; PLAY AB Recent research has documented the importance of joint attention skills to language development in young typical children. A number of studies have also examined joint attention skills in children with different disabilities. This article reviews the literature concerning joint attention skills in children with specific language difficulties-children with Down syndrome, deafness, and autism. Our review focuses on joint attention that is conceptualized both as a state and as declarative gestures, and covers issues related to topic control in mother-child interactions, proportion of time spent in joint attention, caregiver strategies within episodes of joint attention, and child contributions to joint attention. Research findings are then discussed in terms of translating these findings to intervention practice. C1 Univ Calif Los Angeles, Grad Sch Educ & Informat Studies, Div Child Psychiat, Neuropsychiat Inst, Los Angeles, CA 90095 USA. RP Kasari, C (reprint author), Univ Calif Los Angeles, Grad Sch Educ & Informat Studies, Div Child Psychiat, Neuropsychiat Inst, 3132B Moore Hall,Box 951521, Los Angeles, CA 90095 USA. 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PD JUL-SEP PY 2004 VL 17 IS 3 BP 269 EP 280 PG 12 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 834XM UT WOS:000222444200008 ER PT J AU Norbury, CF Nash, M Baird, G Bishop, DVM AF Norbury, CF Nash, M Baird, G Bishop, DVM TI Using a parental checklist to identify diagnostic groups in children with communication impairment: a validation of the Children's Communication Checklist - 2 SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE specific language impairment; autism; diagnosis; pragmatic language impairment; assessment ID DEVELOPMENTAL LANGUAGE DISORDERS; HIGH-LEVEL AUTISM; EARLY ADULT LIFE; FOLLOW-UP; PSYCHOLINGUISTIC MARKERS; PRAGMATIC DIFFICULTIES; OUTCOMES; SPEECH; SUBGROUPS; SLI AB Background: The Children's Communication Checklist (CCC 1998) was revised in 2003 (CCC-2) to provide a general screen for communication disorder and to identify pragmatic/social interaction deficits. Two validation studies were conducted with different populations of children with language and communication impairments. Methods & Procedures: In Study 1, the questionnaire was given to families of 87 children attending full-time special education for specific language impairment, pragmatic language impairments or autistic spectrum disorders. In addition, the teachers of half the sample completed CCC-2 forms for the same children, providing evidence for interrater agreement. In Study 2, the sample was increased to include 24 children with similar diagnoses in educational contexts in Scotland and 27 children referred for clinical evaluation at a neurodevelopment centre. Outcomes & Results: The CCC-2 distinguished children with communication impairments from non-impaired peers. Furthermore, the social-interaction deviance composite (SIDC) of the CCC-2 identified children with disproportionate pragmatic and social difficulties in relation to their structural language impairments. This measure also had good interrater agreement (r = 0.79). Conclusions: CCC-2 provides a useful screening measure for communication impairment and can be helpful in identifying children who should be referred for more detailed assessment of possible autistic spectrum disorder. However, the present data highlight substantial overlap amongst groups with 'distinct' diagnoses. It is suggested that it is unrealistic to use the CCC-2 to make categorical distinctions on this continuum of disorder. C1 Univ Oxford, Dept Expt Psychol, Oxford Study Childrens Commun Impairments, Oxford OX1 3UD, England. Royal Hosp Sick Children, Speech & Language Therapy Dept, Edinburgh, Midlothian, Scotland. Guys Hosp, Newcomen Ctr, London, England. RP Norbury, CF (reprint author), Univ Oxford, Dept Expt Psychol, Oxford Study Childrens Commun Impairments, S Parks Rd, Oxford OX1 3UD, England. 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PD JUL-SEP PY 2004 VL 39 IS 3 BP 345 EP 364 DI 10.1080/13682820410001654883 PG 20 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 824FE UT WOS:000221670500004 PM 15204445 ER PT J AU Heaton, P Wallace, GL AF Heaton, P Wallace, GL TI Annotation: The savant syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE savant; autism; talent; intelligence ID UNUSUAL MECHANICAL ABILITY; IDIOT-SAVANT; CALENDRICAL CALCULATORS; FRONTOTEMPORAL DEMENTIA; SPECTRUM DISORDERS; FUNCTIONING AUTISM; MENTAL-RETARDATION; GRAPHIC ABILITIES; WILLIAMS-SYNDROME; READING-SKILLS AB Background: Whilst interest has focused on the origin and nature of the savant syndrome for over a century, it is only within the past two decades that empirical group studies have been carried out. Methods: The following annotation briefly reviews relevant research and also attempts to address outstanding issues in this research area. Traditionally, savants have been defined as intellectually impaired individuals who nevertheless display exceptional skills within specific domains. However, within the extant literature, cases of savants with developmental and other clinical disorders, but with average intellectual functioning, are increasingly reported. Results: We thus propose that focus should diverge away from IQ scores to encompass discrepancies between functional impairments and unexpected skills. It has long been observed that savant skills are more prevalent in individuals with autism than in those with other disorders. Therefore, in this annotation we seek to explore the parameters of the savant syndrome by considering these skills within the context of neuropsychological. accounts of autism. A striking finding amongst those with savant skills, but without the diagnosis of autism, is the presence of cognitive features and behavioural traits associated with the disorder. Conclusions: We thus conclude that autism (or autistic traits) and savant skills are inextricably linked and we should therefore look to autism in our quest to solve the puzzle of the savant syndrome. C1 Univ London, Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London, England. RP Heaton, P (reprint author), Univ London, Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. 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V., 1995, MIND SAVANT LANGUAGE Smith S. B., 1983, GREAT MENTAL CALCULA SNOWLING M, 1986, J EXP CHILD PSYCHOL, V42, P392, DOI 10.1016/0022-0965(86)90033-0 SOUTHALL G, 1983, CONTINUING ENSLAVEME SOUTHALL G, 1979, BLIND TOM POST CIVIL Spearman C., 1927, ABILITIES MAN SPITZ HH, 1973, AM J MENT DEF, V77, P757 SPITZ HH, 1995, NEW IDEAS PSYCHOL, V13, P167, DOI 10.1016/0732-118X(95)00003-Y STEEL JG, 1984, J AM ACAD CHILD PSY, V23, P704 Temple CM, 1996, CORTEX, V32, P335 Toichi M, 2001, J AUTISM DEV DISORD, V31, P483, DOI 10.1023/A:1012216925216 Tredgold A., 1952, MENTAL DEFICIENCY Treffert D. A., 1989, EXTRAORDINARY PEOPLE Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 UDWIN O, 1991, J CLIN EXP NEUROPSYC, V13, P232, DOI 10.1080/01688639108401040 VALENTINE ER, 1994, PSYCHOL, V7, P405 VOLKMAR FR, 1999, AUTISM PERVASIVE DEV WATERHOUSE L, 1988, EXCEPTIONAL BRAIN, P493 WELSH MC, 1987, BRAIN LANG, V32, P76, DOI 10.1016/0093-934X(87)90118-0 WING L, 2002, MENT RETARD, V99, P186 YOUNG R, 1995, THESIS U ADELAIDE S Young R., 1995, J AUTISM DEV DISORD, V25, P229 YOUNG RL, 1994, AM J MENT RETARD, V99, P186 NR 131 TC 55 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 JUL PY 2004 VL 45 IS 5 BP 899 EP 911 DI 10.1111/j.1469-7610.2004.t01-1-00284.x PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 832RK UT WOS:000222284400001 PM 15225334 ER PT J AU Lord, C Shulman, C DiLavore, P AF Lord, C Shulman, C DiLavore, P TI Regression and word loss in autistic spectrum disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; autistic spectrum disorders; language; regression; longitudinal ID PERVASIVE DEVELOPMENTAL DISORDERS; DISINTEGRATIVE DISORDER; DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; HOME VIDEOTAPES; SPEECH LOSS; AGE; LANGUAGE; CHILDHOOD; CHILDREN AB Background: For many years, researchers and clinicians have described parent reports of an unusual developmental phenomenon in a substantial minority of children with Autistic Spectrum Disorders (ASD), the acquisition and then loss of communication skills during the second year of life. Methods: As part of a longitudinal study of 110 children referred for assessments of possible autism at age 2 years or younger, 21 developmentally delayed children and 33 typically developing controls, 19 children were described by their parents at age 2 as having gained and lost spontaneous, meaningful words, and 12 children as having a history of less specific loss of imitated words or nonword vocalizations. A battery of diagnostic and cognitive tasks was administered to all children at study entrance, at ages 3 (for the referral children only) and 4 or 5 (for referral and developmentally delayed children). Results: Results indicated that the acquisition of a small number of spontaneous words used meaningfully and consistently followed by loss of all words, often associated with other social changes, was unique to children diagnosed at 5 years with ASD. Few differences, besides those that defined the pattern of word loss, emerged between children with ASD with and without word loss. Loss of less specific, nonword vocalizations was associated with cognitive delay, with or without autism. Conclusions: Word loss is a reliably identifiable phenomenon in early childhood that appears to be unique, but not universal to, ASD. Histories and outcome of children with word loss were not in keeping with a sudden change from normal to abnormal functioning, but did suggest that this type of loss in the second year of life may be a useful 'red flag' for ASD in a significant minority of cases. C1 Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Hebrew Univ Jerusalem, Jerusalem, Israel. Univ N Carolina, Chapel Hill, NC USA. RP Lord, C (reprint author), Univ Michigan, Autism & Commun Disorders Ctr, 1111 E Catherine St, Ann Arbor, MI 48109 USA. EM celord@umich.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BISHOP DVM, 1982, J CHILD PSYCHOL PSYC, V23, P1, DOI 10.1111/j.1469-7610.1982.tb00045.x Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Elliott C. D., 1990, DIFFERENTIAL ABILITI FENSON L, 1994, MONOGR SOC RES CHILD, V59, pR5 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 GOLDBERG WA, 2003, BIANN M SOC RES CHIL Goldberg WA, 2003, J AUTISM DEV DISORD, V33, P607, DOI 10.1023/B:JADD.0000005998.47370.ef Kanner L, 1943, NERV CHILD, V2, P217 Klein SK, 2000, J CHILD NEUROL, V15, P36, DOI 10.1177/088307380001500109 KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mullen E, 1995, MULLEN SCALES EARLY Nazzi T, 2003, DEVELOPMENTAL SCI, V6, P136, DOI 10.1111/1467-7687.00263 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 PARR J, 2002, WORLD C PSYCH GEN BR Rodier PM, 1998, MENT RETARD DEV D R, V4, P121, DOI 10.1002/(SICI)1098-2779(1998)4:2<121::AID-MRDD9>3.0.CO;2-S ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1169, DOI 10.1192/bjp.113.504.1169 Shinnar S, 2001, PEDIATR NEUROL, V24, P183 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 SWISHER L, 1976, HEARING DAVIS ESSAYS, P323 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P717, DOI 10.1111/j.1469-7610.1989.tb00784.x Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 WERNER E, 2001, INT M AUT RES SAN DI WERNER EB, 2001, SOC RES CHILD DEV BI WOODWARD AL, 1994, DEV PSYCHOL, V30, P553, DOI 10.1037//0012-1649.30.4.553 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 35 TC 126 Z9 133 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 JUL PY 2004 VL 45 IS 5 BP 936 EP 955 DI 10.1111/j.1469-7610.2004.t01-1-00287.x PG 20 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 832RK UT WOS:000222284400004 PM 15225337 ER PT J AU Gilmour, J Hill, B Place, M Skuse, DH AF Gilmour, J Hill, B Place, M Skuse, DH TI Social communication deficits in conduct disorder: a clinical and community survey SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE social communication; pragmatics assessment; language impairment; autism; conduct disorder ID AUTISM; CHILDREN; SKILLS; IMPAIRMENT; BEHAVIORS; CHECKLIST; BOYS AB Background: Increasing numbers of children are referred to Child and Adolescent Mental Health Services because of disruptive behaviour. Recent reviews on the origins of conduct problems indicate that the most severe and persistent forms are found predominantly among males with a range of neurodevelopmental vulnerabilities, which are likely to have biological substrates. In this study, we tested the hypothesis that many children who are identified with conduct disorder actually have a primary deficit in pragmatic language skills, of a quality and degree that is similar to children on the autistic spectrum. We hypothesised that pragmatic difficulties may underlie the antisocial behaviour in a proportion of children who are labelled as conduct disordered. Methods: Using the Children's Communication Checklist (Bishop, 1998), we surveyed 142 children who had been referred for clinical investigation, with a predominant diagnosis of either an autistic spectrum condition (n = 87) or conduct disorder (n = 55), and 60 typically developing comparison children. Among children with conduct disorders, males predominated 9:1. Results: On the basis of parent and teacher ratings, two-thirds of those with conduct disorders had pragmatic language impairments and other behavioural features similar in nature and degree to those of children with autism, independent of IQ. In a further study, we surveyed 54 children who had been excluded from elementary schools in a socio-economically disadvantaged inner-London borough and found over two-thirds to have comparable deficits. Conclusions: These findings have both theoretical and practical implications. First, they indicate the presence of communicative problems in a sub-group of children in whom conduct rather than language had been the major concern. Second, they indicate that severe deficits in pragmatic abilities and autistic-like behaviours can coexist with psychiatric conditions other than autism, especially in boys. 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Child Psychol. Psychiatry PD JUL PY 2004 VL 45 IS 5 BP 967 EP 978 DI 10.1111/j.1469-7610.2004.t01-1-00289.x PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 832RK UT WOS:000222284400006 PM 15225339 ER PT J AU Dyck, MJ Hay, D Anderson, M Smith, LM Piek, J Hallmayer, J AF Dyck, MJ Hay, D Anderson, M Smith, LM Piek, J Hallmayer, J TI Is the discrepancy criterion for defining developmental disorders valid? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE intelligence; motor coordination; language; empathy; attention; developmental disorders; normal development ID DEFICIT-HYPERACTIVITY DISORDER; EARLY INFANTILE-AUTISM; LEARNING-DISABILITIES; COORDINATION DISORDER; RESPONSE-INHIBITION; EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; CONTROL CHILDREN; FRONTAL-LOBE; BASE-RATES AB Background: Most developmental disorders are defined by an achievement discrepancy in which achievement on one or more specific abilities is substantially less than a person's measured intelligence. We evaluated the validity of this discrepancy criterion by assessing parameters that determine variability across abilities and by assessing relationships between achievement discrepancies and behavioral disturbances. Methods: Measures of intelligence, language, motor coordination, empathic ability, and attentional. control were administered to a representative sample of 390 children aged 3 to 12 years. Parent ratings of child behavior were obtained. Results: Results indicate that achievement discrepancies are a function of the correlation between ability measures, the shape of the ability distributions, and position on an index ability dimension. Discrepancies in achievement were not related to behavioral disturbance, but underachievement relative to age peers was invariably related to behavioral disturbance. Conclusions: We conclude that developmental disorders need to be redefined in ways that are consistent with how Mental Retardation is now defined, by (a) underachievements, (b) of defined magnitude, (c) using standardized measures, (d) with known relations to normal development, and (e) concurrent deficits on standardized measures of impaired function. C1 Curtin Univ Technol, Sch Psychol, Perth, WA 6845, Australia. Univ Western Australia, Sch Psychol, Nedlands, WA 6009, Australia. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA USA. RP Dyck, MJ (reprint author), Curtin Univ Technol, Sch Psychol, GPO Box U1987, Perth, WA 6845, Australia. 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Psychiatry PD JUL PY 2004 VL 45 IS 5 BP 979 EP 995 DI 10.1111/j.1469-7610.2004.t01-1-00290.x PG 17 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 832RK UT WOS:000222284400007 PM 15225340 ER PT J AU Hill, EL Sally, D Frith, U AF Hill, EL Sally, D Frith, U TI Does mentalising ability influence cooperative decision-making in a social dilemma? Introspective evidence from a study of adults with autism spectrum disorder SO JOURNAL OF CONSCIOUSNESS STUDIES LA English DT Article ID ASPERGER-SYNDROME; PRISONERS-DILEMMA; MIND; BELIEFS; CHILD AB The choice to cooperate or compete with others confronts us on a daily basis, and it is plausible that we use our mentalising skills to aid decision-making in such situations. We investigated the relationship between mentalising and decision-making in the prisoner's dilemma in adults with autism spectrum disorders (ASD), who show impaired mentalising, and normal adults. After completion of three versions of the prisoner's dilemma, we conducted a semi-structured interview. This interview attempted to elicit a participant's spontaneous strategy when playing each version of the game, as well as on their conception of the nature and strategy choice of their opponents (human vs. computer). Contrary to expectations, the behavioural choices of the adults with and without ASD were quantitatively similar, as were the qualitative responses to questions used in the interview. The consistency of the evidence from both measures suggests that mentalising ability was not involved in selecting the choices made in these prisoner's dilemma tasks. Instead they suggest the hypothesis that a purely logical strategy may have been adopted. The introspections of at least a subgroup of high-functioning individuals with ASD can on the whole be trusted and this use of mixed methods strengthens the validity of the conclusions drawn. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. UCL, Inst Cognit Neurosci, London, England. RP Hill, EL (reprint author), Univ London Goldsmiths Coll, Dept Psychol, New Cross, London SE14 6NW, England. 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Conscious. Stud. PD JUL-AUG PY 2004 VL 11 IS 7-8 BP 144 EP 161 PG 18 WC Philosophy; Social Sciences, Interdisciplinary SC Philosophy; Social Sciences - Other Topics GA 854IL UT WOS:000223896200010 ER PT J AU Stahlberg, O Soderstrom, H Rastam, M Gillberg, C AF Stahlberg, O Soderstrom, H Rastam, M Gillberg, C TI Bipolar disorder, schizophrenia, and other psychotic disorders in adults with childhood onset AD/HD and/or autism spectrum disorders SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE AD/HD; autism; bipolar; psychosis; comorbidity ID WEAK CENTRAL COHERENCE; ASPERGER-SYNDROME; COGNITIVE PHENOTYPE; 7-YEAR-OLD CHILDREN; TOTAL POPULATION; EPIDEMIOLOGY; SIBLINGS; PARENTS AB Individuals with attention-deficit/hyperactivity disorder (AD/HD) and autism spectrum disorders (ASD) often display symptoms from other diagnostic categories. Exclusion criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) and the International Statistical Classification of Diseases and Related Health Problems (ICD-10) impede the use of categorical diagnoses to describe the particular problem constellation in a patient. In this study, we describe the prevalence and patterns of comorbid bipolar and psychotic disorders in 241 consecutively referred adult patients with AD/HD and/or ASD. Thirty per cent of patients with AD/HD had comorbid ASD and 38% of patients with ASD had comorbid AD/HD. Of the subjects with ASD, 7% had bipolar disorder with psychotic features, and 7.8% had schizophrenia or another psychotic disorder. The corresponding figures for the patients with AD/HD were 5.0% and 5.0%, respectively. Current diagnostic criteria have to be revised to acknowledge the comorbidity of bipolar and/or psychotic disorders in AD/HD and ASD. C1 Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41124 Gothenburg, Sweden. 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PD JUL PY 2004 VL 111 IS 7 BP 891 EP 902 DI 10.1007/s00702-004-0115-1 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 835VU UT WOS:000222514400010 PM 15206005 ER PT J AU Palmen, SJMC van Engeland, H AF Palmen, SJMC van Engeland, H TI Review on structural neuroimaging findings in autism SO JOURNAL OF NEURAL TRANSMISSION LA English DT Review DE autism; MRI; neuroimaging; review ID PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT-HYPERACTIVITY DISORDER; POSTERIOR-FOSSA STRUCTURES; LEFT-RIGHT ASYMMETRIES; CORPUS-CALLOSUM; INFANTILE-AUTISM; HEAD CIRCUMFERENCE; CEREBELLAR HYPOPLASIA; WHITE-MATTER; BRAIN VOLUME AB Autism is now widely viewed as a neurodevelopmental disorder, although the underlying biological causes remain to be established. In this review, we examine the literature in magnetic resonance imaging (MRI) as applied to autism, discuss the findings that have emerged, and give directions for potential future research. To date, structural MRI results are inconsistent, partly due to the heterogeneity of the disorder itself, and partly due to the different composition and the varied degree of matching of the studied groups. However, recent studies have begun to elucidate the underlying neuroanatomical abnormalities and brain-behavior relationships in autism, with the most consistent finding being increased brain volume in autism. Future large-scale longitudinal structural imaging studies, starting at very young ages, investigating homogeneous groups of patients and extensively matched control groups, and making use of (combinations of) newer and more sophisticated techniques, hold a great promise to further elucidate the enigma of autism. C1 Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, NL-3584 CX Utrecht, Netherlands. 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Neural Transm. PD JUL PY 2004 VL 111 IS 7 BP 903 EP 929 DI 10.1007/s00702-003-0068-9 PG 27 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 835VU UT WOS:000222514400011 PM 15206006 ER PT J AU Kuntz, A Clement, HW Lehnert, W van Calker, D Hennighausen, K Gerlach, M Schulz, E AF Kuntz, A Clement, HW Lehnert, W van Calker, D Hennighausen, K Gerlach, M Schulz, E TI Effects of secretin on extracellular amino acid concentrations in rat hippocampus SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE secretin; autistic disorder; microdialysis; glutamate; GABA; rat; hippocampus ID VASOACTIVE-INTESTINAL-PEPTIDE; IN-VIVO MICRODIALYSIS; BLOOD-BRAIN-BARRIER; GLUTAMATE RELEASE; ADENYLATE-CYCLASE; BASAL GANGLIA; AUTISM; AMYGDALA; NEURONS; NEUROTRANSMITTER AB In 1998, Horvath et al. (1998) observed a marked improvement in speech, eye contact, and attention in autistic children five weeks after treatment with secretin, which ocurred in the course of an endoscopic investigation. Since autism is hypothesized to be a hypoglutamatergic disorder we investigated the in vivo effects of secretin on extracellular amino acids in the rat brain. Studies were carried out on freely moving rats with microdialysis probes in the hippocampus. Amino acids were examined using tandem mass spectroscopy and HPLC/fluorometric detection. Following secretin injection (8.7 mug/kg i.p.), considerable increases in microdialysate glutamate and gamma-aminobutyric acid (GABA) levels were observed; other amino acids were not affected. The observed increased microdialysate concentrations of glutamate and GABA following secretin application may explain the results of the Horvath study. C1 Univ Freiburg, Dept Child & Adolescent Psychiat, D-7800 Freiburg, Germany. Univ Freiburg, Metab Unit, Univ Childrens Hosp, D-7800 Freiburg, Germany. Univ Freiburg, Dept Psychiat, D-7800 Freiburg, Germany. Univ Wurzburg, Dept Child & Adolescent Psychiat, D-97070 Wurzburg, Germany. RP Clement, HW (reprint author), Univ Freiburg Klinikum, Abt Psychiat & Psychotherapie Kindes & Jugendalte, Hauptstr 8, D-79104 Freiburg, Germany. 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Neural Transm. PD JUL PY 2004 VL 111 IS 7 BP 931 EP 939 DI 10.1007/s00702-003-0082-y PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 835VU UT WOS:000222514400012 PM 15206007 ER PT J AU Silva, SC Correia, C Fesel, C Barreto, M Coutinho, AM Marques, C Miguel, TS Ataide, A Bento, C Borges, L Oliveira, G Vicente, AM AF Silva, SC Correia, C Fesel, C Barreto, M Coutinho, AM Marques, C Miguel, TS Ataide, A Bento, C Borges, L Oliveira, G Vicente, AM TI Autoantibody repertoires to brain tissue in autism nuclear families SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE autism; nuclear families; autoantibody reactivities; immunoblots; multiparametric analysis; heritability ID MYELIN BASIC-PROTEIN; ANTIBODY REPERTOIRES; IMMUNOLOGICAL TREATMENTS; GLOBAL ANALYSIS; T-CELLS; AUTOIMMUNITY; DISORDERS; CHILDREN; IMMUNE; ENTEROPATHY AB The hypothesis of an immune dysfunction in autism spectrum disorders has previously been put forward without, however, compelling evidence of a direct relation to its etiology or pathogenesis. To further understand if autoimmunity could play a significant role in autism, we analyzed autoantibody repertoires to brain tissue extract in the plasma of 171 autism children, their parents, and 54 controls, by quantitative immunoblotting. Multiparametric analysis revealed significant differences between patients and controls, and showed that one single reactivity in Section 32 of the blot had the most power to discriminate between these samples. Family correlation coefficients and heritability estimates did not provide any evidence that this reactivity was genetically determined. While the molecular weight of the target protein suggested that it might be an isoform of Myelin Basic Protein (MBP), inhibition assays with human MBP argued against this hypothesis. The study evidences the widespread occurrence of autoreactivities to brain tissue in autism patients, which may represent the immune system's neuroprotective response to a previous brain injury occurred during neurodevelopment. The molecular identification of the target protein in Section 32 will contribute to the understanding of the role of immune responses against brain antigens in autistic patients. (C) 2004 Elsevier B.V. All rights reserved. C1 Inst Gulbenkian Ciencias, P-2781196 Oeiras, Portugal. Hosp Pediat Coimbra, P-3000 Coimbra, Portugal. RP Vicente, AM (reprint author), Inst Gulbenkian Ciencias, Rua Quinta Grande 6, P-2781196 Oeiras, Portugal. 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Psychiatry PD JUL PY 2004 VL 75 IS 7 BP 945 EP 948 DI 10.1136/jnnp.2003.018713 PG 4 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 835XO UT WOS:000222519000001 PM 15201345 ER PT J AU Ohayon, EL Kalitzin, S Suffczynski, P Jin, FY Tsang, PW Borrett, DS Burnham, WM Kwan, HC AF Ohayon, EL Kalitzin, S Suffczynski, P Jin, FY Tsang, PW Borrett, DS Burnham, WM Kwan, HC TI Charting epilepsy by searching for intelligence in network space with the help of evolving autonomous agents SO JOURNAL OF PHYSIOLOGY-PARIS LA English DT Article; Proceedings Paper CT Ladislav Tauc Conference in Neurobiology CY DEC 04-05, 2003 CL Gif sur Yvette, FRANCE DE seizures; autism; synchrony; graph theory; close return; recurrent neural network; robot; artificial life; computer modeling; genetic algorithm; self-organization ID COMPLEX NETWORKS; ELECTRICAL STIMULATION; DYNAMICAL DISEASES; NEONATAL SEIZURES; KINDLED SEIZURES; NEURAL-NETWORKS; BRAIN SYSTEMS; MECHANISMS; SYNCHRONIZATION; NEUROSCIENCE AB The problem of demarcating neural network space is formidable. A simple fully connected recurrent network of five units (binary activations, synaptic weight resolution of 10) has 3.2 * 10(26) possible initial states. The problem increases drastically with scaling. Here we consider three complementary approaches to help direct the exploration to distinguish epileptic from healthy networks. {1} First, we perform a gross mapping of the space of five-unit continuous recurrent networks using randomized weights and initial activations. The majority of weight patterns (>70%) were found to result in neural assemblies exhibiting periodic limit-cycle oscillatory behavior. {2} Next we examine the activation space of non-periodic networks demonstrating that the emergence of paroxysmal activity does not require changes in connectivity. {3} The next challenge is to focus the search of network space to identify networks with more complex dynamics. Here we rely on a major available indicator critical to clinical assessment but largely ignored by epilepsy modelers, namely: behavioral states. To this end, we connected the above network layout to an external robot in which interactive states were evolved. The first random generation showed a distribution in line with approach {1}. That is, the predominate phenotypes were fixed-point or oscillatory with seizure-like motor output. As evolution progressed the profile changed markedly. Within 20 generations the entire population was able to navigate a simple environment with all individuals exhibiting multiply-stable behaviors with no cases of default locked limit-cycle oscillatory motor behavior. The resultant population may thus afford us a view of the architectural principles demarcating healthy biological networks from the pathological. 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Physiol.-Paris PD JUL-NOV PY 2004 VL 98 IS 4-6 BP 507 EP 529 DI 10.1016/j.jphysparis.2005.09.018 PG 23 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 996OX UT WOS:000234184700019 PM 16290117 ER PT J AU Girolametto, L Weitzman, E Greenberg, J AF Girolametto, L Weitzman, E Greenberg, J TI The effects of verbal support strategies on small-group peer interactions SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE peer interaction; preschoolers; inservice education; day care; adult-child interaction ID SOCIAL-INTERACTION; CHILD-CARE; INTEGRATED PRESCHOOLS; YOUNG-CHILDREN; LANGUAGE; INTERVENTION; DISABILITIES; SEQUENCES; AUTISM; PLAY AB Purpose: This study investigated whether child care providers could learn to facilitate peer interactions by using verbal support strategies (e.g., prompts, invitations, or suggestions to interact) during naturalistic play activities. Method: Seventeen caregivers were randomly assigned to experimental and control groups, stratified by center so that staff from one center could attend the training program together. The experimental group received inservice training on how to facilitate peer interaction; the control group received training on adult-child communication strategies. Caregivers in the experimental group were taught to facilitate children's interactions with their peers by using indirect referrals (e.g., alerting children to situational information, offering praise) and direct referrals (e.g., telling a child what to say to a peer, inviting children to play together). Results: At posttest, the caregivers in the experimental group used more verbal supports for peer interaction than the caregivers in the control group. Specifically, they used more utterances to promote communication between press and to invite children in the experimental group initiated interactions with peers more often and engaged in extended peer sequences more often than the children in the control group. Clinical Implications: The results support the viability of this training model in early childhood education settings and suggest that future research of its effects with children who have disabilities is warranted. C1 Univ Toronto, Grad Dept Speech Language Pathol, Toronto, ON M5G 1V7, Canada. Hanen Ctr, Toronto, ON, Canada. RP Girolametto, L (reprint author), Univ Toronto, Grad Dept Speech Language Pathol, 500 Univ Ave,Room 160, Toronto, ON M5G 1V7, Canada. 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PD JUL PY 2004 VL 9 IS 7 BP 644 EP 644 DI 10.1038/sj.mp.4001522 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 832HJ UT WOS:000222257800002 PM 15111982 ER PT J AU Deth, R AF Deth, R TI Thimerosal and autism - Reply SO MOLECULAR PSYCHIATRY LA English DT Letter C1 Northeastern Univ, Boston, MA 02115 USA. RP Deth, R (reprint author), Northeastern Univ, 360 Huntington Univ, Boston, MA 02115 USA. EM r.deth@neu.edu CR Baskin DS, 2003, TOXICOL SCI, V74, P361, DOI 10.1093/toxsci/kfg126 Bernard S, 2004, JAMA-J AM MED ASSOC, V291, P180, DOI 10.1001/jama.291.2.180-b Holmes AS, 2003, INT J TOXICOL, V22, P277, DOI 10.1080/10915810390220054 Hviid A, 2003, JAMA-J AM MED ASSOC, V290, P1763, DOI 10.1001/jama.290.13.1763 SAGER P, 2004, I MED PRESENTATION Verstraeten T, 2003, PEDIATRICS, V112, P1039 NR 6 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD JUL PY 2004 VL 9 IS 7 BP 645 EP 645 DI 10.1038/sj.mp.4001520 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 832HJ UT WOS:000222257800003 ER PT J AU Belmonte, MK Cook, EH Anderson, GM Rubenstein, JLR Greenough, WT Beckel-Mitchener, A Courchesne, E Boulanger, LM Powell, SB Levitt, PR Perry, EK Jiang, YH DeLorey, TM Tierney, E AF Belmonte, MK Cook, EH Anderson, GM Rubenstein, JLR Greenough, WT Beckel-Mitchener, A Courchesne, E Boulanger, LM Powell, SB Levitt, PR Perry, EK Jiang, YH DeLorey, TM Tierney, E TI Autism as a disorder of neural information processing: directions for research and targets for therapy SO MOLECULAR PSYCHIATRY LA English DT Review DE autism; development; neurochemistry; genetics; animal models ID FRAGILE-X-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION PROTEIN; SEROTONIN TRANSPORTER GENE; WEAK CENTRAL COHERENCE; LEMLI-OPITZ-SYNDROME; CLASS-I MHC; MICE LACKING; COGNITIVE PHENOTYPE; PREPULSE INHIBITION AB The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which they feed, is hampered by the large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging, and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 2AH, England. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Yale Univ, Child Study Ctr, New Haven, CT USA. Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA. Univ Illinois, Beckman Inst, Urbana, IL 61801 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA. Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA. Vanderbilt Univ, Kennedy Ctr Res Human Dev, Nashville, TN USA. Univ Newcastle Upon Tyne, Ctr Dev Clin Brain Ageing, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Mol Res Inst, Mountain View, CA USA. Kennedy Krieger Inst, Baltimore, MD USA. 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Results with special consideration of socially adaptive behavior SO NERVENARZT LA German DT Article DE Kanner's syndrome; developmental factors; social adaptation ID FUNCTIONING AUTISTIC-CHILDREN; FOLLOW-UP; ADULTS AB The course of development of 18 patients with Kanner autism (mean age 28 years) in their second and third decades was explored and recorded with respect to factors affecting social competence in adulthood. To validate the diagnosis, we used the Childhood Autism Rating Scale. A version of the Vineland Adaptive Behavior Scales was employed to assess social adaptation. On average, the individuals showed socially adaptive skills that are typical for healthy children at the age of 4 years and 3 months. Of the autistic persons, 72% showed a characteristic pattern: scoring highest in daily living skills and lowest in social skills, especially in interpersonal relationships, where they performed at an average age equivalent of only 2 years and 7 months. 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While the validity of autism (Kanner-syndrom) has been shown through multiple different levels of evidence, the validity of Asperger-Syndrom is still unestablished. The few literature is extremely difficult to summarize (Volkmar u. Klin 2000), given that a range of important methodological issues render comparability of findings across studies virtually impossible: these include differences in definition and circularity in definition relative to validating measures. In terms of causes of Asperger-Syndrom the following factors are discussed: genetic reasons, neurobiological disturbances and neuropsychological deficits. C1 Klin Kinder & Jugendpsychiat & Psychotherapie, D-35033 Marburg, Germany. RP Kamp-Becker, I (reprint author), Klin Kinder & Jugendpsychiat & Psychotherapie, Hans Sachs Str 4 & 6, D-35033 Marburg, Germany. 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PD JUL-AUG PY 2004 VL 53 IS 6 BP 371 EP 394 PG 24 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 848MG UT WOS:000223471200001 PM 15376613 ER PT J AU Nilsson, M Carlsson, A Markinhuhta, KR Sonesson, C Pettersson, F Gullme, M Carlsson, ML AF Nilsson, M Carlsson, A Markinhuhta, KR Sonesson, C Pettersson, F Gullme, M Carlsson, ML TI The dopaminergic stabiliser ACR16 counteracts the behavioural primitivization induced by the NMDA receptor antagonist MK-801 in mice: implications for cognition SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE autism; cognition; dopaminergic stabiliser; grooming; mice; MK-801; movement pattern; schizophrenia; video tracking ID WORKING-MEMORY; PREFRONTAL CORTEX; SCHIZOPHRENIA; STRIATUM; GLUTAMATE; RELEASE; TRANSMISSION; HUMANS; BRAIN; DOPA AB The Carlsson research group has developed a series of compounds capable of stabilising the dopamine system without inducing the deleterious hypodopaminergia that encumbers the currently used antipsychotic drugs. In the present study one of these dopaminergic stabilisers, ACR16, was tested in a mouse model for cognitive deficits of schizophrenia and autism. Since we believe that hypoglutamatergia is a key element in both schizophrenia and autism we used mice rendered hypoglutamatergic by treatment with the N-methyl-D-aspartate (NMDA) antagonist MK-801. MK-801 causes both hyperactivity and a behavioural primitivization. ACR16 attenuated the MK-801-induced hyperactivity and, in addition, caused a marked improvement of behavioural quality with a movement pattern approaching that of control animals. Since we believe that the impoverishment of the behavioural repertoire caused by MK-801 may correspond to the cognitive deficits seen in schizophrenia and autism, these results suggest that ACR16 may improve cognitive status in these disorders. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Gothenburg, Inst Clin Neurosci, Sect Expt Neurosci, Neuropsychiat Res Unit, SE-41346 Gothenburg, Sweden. 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Neuro-Psychopharmacol. Biol. Psychiatry PD JUL PY 2004 VL 28 IS 4 BP 677 EP 685 DI 10.1016/j.pnpbp.2004.05.004 PG 9 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 847KY UT WOS:000223392600009 PM 15276693 ER PT J AU Lawrence, EJ Shaw, P Baker, D Baron-Cohen, S David, AS AF Lawrence, EJ Shaw, P Baker, D Baron-Cohen, S David, AS TI Measuring empathy: reliability and validity of the Empathy Quotient SO PSYCHOLOGICAL MEDICINE LA English DT Article ID HIGH-FUNCTIONING AUTISM; DEPERSONALIZATION DISORDER; PSYCHOMETRIC PROPERTIES; EMOTIONAL EMPATHY; ASPERGER-SYNDROME; SCALE; INVENTORY; AMYGDALA; ADULTS; MIND AB Background. Empathy plays a key role in social understanding, but its empirical measurement has proved difficult. The Empathy Quotient (EQ) is a self-report scale designed to do just that. This series of four studies examined the reliability and validity of the EQ and determined its factor structure. Method. In Study 1, 53 people completed the EQ, Social Desirability Scale (SDS) and a non-verbal mental state inference test, the Eyes Task. In Study 2, a principal components analysis (PCA) was conducted on data from 110 healthy individuals and 62 people reporting depersonalisation (DPD). Approximately I year later, Study 3, involved the re-administration of the EQ (n = 24) along with the Interpersonal Reactivity Index (IRI; n = 28). In the last study, the EQ scores of those with DPD, a condition that includes a subjective lack of empathy, were examined in depth. Results. An association was found between the Eyes task and EQ, and only three EQ items correlated with the SDS. PCA revealed three factors: (1) 'cognitive empathy'; (2) 'emotional reactivity', and (3) 'social skills'. Test-retest reliability was good and moderate associations were found between the EQ and IRI subscales, suggesting concurrent validity. People with DPD did not show a global empathy deficit, but reported less social competence. Conclusions. The EQ is a valid, reliable scale and the different subscales may have clinical applications. C1 Inst Psychiat, Sect Cognit Neuropsychiat, Dept Psychol Med, London SE5 8AF, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 3EB, England. RP David, AS (reprint author), Inst Psychiat, Sect Cognit Neuropsychiat, Dept Psychol Med, De Crespigny Pk,Denmark Hill,Box 68, London SE5 8AF, England. 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PD JUL PY 2004 VL 34 IS 5 BP 911 EP 919 DI 10.1017/S0033291703001624 PG 9 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 844EF UT WOS:000223139500015 PM 15500311 ER PT J AU Campbell, JM Ferguson, JE Herzinger, CV Jackson, JN Marino, CA AF Campbell, JM Ferguson, JE Herzinger, CV Jackson, JN Marino, CA TI Combined descriptive and explanatory information improves peers' perceptions of autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE autism; attitudes; behavioral intentions; information; inclusion ID CHILDRENS ATTITUDES; BEHAVIORAL INTENTIONS; INTERVENTIONS; ADOLESCENTS; PARENTS AB Authors examined the combined effects of descriptive and explanatory information on peers' perceptions and behavioral intentions toward an unfamiliar child with autism. Children (N = 576; M age = 10.06 years) were randomly assigned to view two videotapes of a boy engaging in typical and autistic behaviors receiving either descriptive (AUT-D) or descriptive and explanatory information (AUT-D + E). Children responded to measures of attitudes (Adjective Checklist) and behavioral intentions (Shared Activities Questionnaire). Children rated the typical boy more favorably than the boy showing autistic symptoms. When compared to descriptive information alone, the combination of descriptive and explanatory information resulted in improved third- and fourth-graders' but not fifth-graders' attitudes toward the child with autism. Combined information improved behavioral intentions across grades; however, girls (vs. boys) were more responsive to information as evidenced by differences in academic intentions. The combination of descriptive and explanatory information about autism appears to have a positive effect on children's attitudes and behavioral intentions. 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PD JUL-AUG PY 2004 VL 25 IS 4 BP 321 EP 339 DI 10.1016/j.ridd.2004.01.005 PG 19 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 833NN UT WOS:000222344600002 PM 15193668 ER PT J AU Sigafoos, J O'Reilly, M Seely-York, S Edrisinha, C AF Sigafoos, J O'Reilly, M Seely-York, S Edrisinha, C TI Teaching students with developmental disabilities to locate their AAC device SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE voice output communication aids; AAC intervention; location training; least-to-most prompting autism; developmental disability ID COMMUNICATION; ACQUISITION AB Students with autism and related developmental disabilities who do not speak are often taught to use some type of augmentative and alternative communication (AAC) system, such as a voice output communication aid (VOCA). One problem with such devices is that the person may be unable to communicate when the device is not readily accessible. We first taught three nonverbal students with autism to use a VOCA to request access to preferred items. Following this initial acquisition phase, however, none of the students would locate their VOCA when it was not within reach. A least-to-most prompting procedure was implemented to teach the students to locate their AAC device. The effectiveness of this procedure for teaching VOCA location skills was evaluated in a delayed multiple-baseline across subjects design. The results showed that the intervention was effective in teaching the students to locate their AAC device when they needed it to request access to preferred objects. Teaching VOCA location skills may be a useful and necessary component in AAC interventions for some people with developmental disabilities. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. RP Sigafoos, J (reprint author), Univ Texas, Dept Special Educ, Austin, TX 78712 USA. 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PD JUL-AUG PY 2004 VL 25 IS 4 BP 371 EP 383 DI 10.1016/j.ridd.2003.07.002 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 833NN UT WOS:000222344600005 PM 15193671 ER PT J AU Cabanyes-Truffino, J Garcia-Villamisar, D AF Cabanyes-Truffino, J Garcia-Villamisar, D TI Identification and early diagnosis of the autistic spectrum disorders SO REVISTA DE NEUROLOGIA LA Spanish DT Review DE autism; autistic spectrum disorders; early diagnosis; joint attention ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X-SYNDROME; QUALITY-STANDARDS-SUBCOMMITTEE; CHILD-NEUROLOGY-SOCIETY; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; EARLY INTERVENTION; JOINT ATTENTION; FOLLOW-UP AB Aim. To review the empirical evidence and recommendations for early identification and diagnosis of autistic spectrum disorders (ASD). Development. ASD often remains unrecognized and undiagnosed until late preschool age. A significant delay of almost 3 years was reported between parents' initial concerns about their child and the age of diagnosis. Some research provides further evidence that signs of ASD are evident in the first 2 years of life. The importance of early diagnosis is that it opens the door to early intervention programs which are essentials for the future of these children. Earl), diagnosis can be facilitated most effectively if early detection is made possible. Progress has recently been made in the earlier identification of children with ASD. Recent researches have identified early behavioural difficulties in social reciprocity, joint attention, theory of mind, gaze engagement, social referencing and hypersensitivity to sound. Professionals need to be aware and sensitive to these behavioural patterns. Their identification would increase the likelihood of a reliable earl), diagnosis. Conclusions. At present, it is possible to make earlier diagnosis of ASD. 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PD JUN 30 PY 2004 VL 127 IS 1-2 BP 43 EP 53 DI 10.1016/j.psychres.2004.02.016 PG 11 WC Psychiatry SC Psychiatry GA 841SU UT WOS:000222952700006 PM 15261704 ER PT J AU Huang, CH Chen, ML Tsai, YL Tsai, MT Chen, CH AF Huang, CH Chen, ML Tsai, YL Tsai, MT Chen, CH TI Elevated adrenomedullin mRNA in lymphoblastoid cells from schizophrenic patients SO NEUROREPORT LA English DT Article DE adrenomedullin; association; biomarker; lymphoblastoid cells; pathophysiology; schizophrenia ID NITRIC-OXIDE; PATHOPHYSIOLOGICAL ROLE; BIOLOGICAL MARKERS; HUMAN BRAIN; EXPRESSION; PEPTIDE; SITES; GENE AB Adrenomedullin (ADM) is a 52 amino acid peptide with multiple physiological functions and wide tissue distributions including brain. Recently, elevated plasma levels of ADM were found in patients with schizophrenia, bipolar affective disorder and autism, suggesting the involvement of ADM in the pathophysiology of mental diseases. Using real-time quantitative PCR, we compared the ADM mRNA levels in lymphoblastoid cell lines between schizophrenic patients and controls. Male but not female schizophrenia patients had 2- to 3-fold higher ADM mRNA levels than controls (p<0.01). Our data support that ADM may be associated with the pathophysiology of schizophrenia, although the cause of the association needs further study. C1 Tzu Chi Gen Hosp, Dept Psychiat, Hualien 970, Taiwan. Tzu Chi Univ, Inst Human Genet, Hualien 970, Taiwan. RP Chen, CH (reprint author), Tzu Chi Gen Hosp, Dept Psychiat, Hualien 970, Taiwan. 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Normal children had the same neural networks for the MS and mentalizing as adults. Common activations were found in the superior temporal sulcus and the fusiform gyri, whereas mentalizing specific activation was found in the medial prefrontal, temporal pole and the inferior parietal cortices. We suggest that mentalizing might evolve from a capacity to detect the motion of agents and to infer intentions. Further, mentalizing might require self-perspectives. C1 Natl Ctr Hosp Mental Nervous & Muscular Disorders, Natl Ctr Neurol & Psychiat, Dept Radiol, Kodaira, Tokyo 1878551, Japan. NIMH, Dept Dev Disorders, Natl Ctr Neurol & Psychiat, Tokyo, Japan. RP Ohnishi, T (reprint author), Natl Ctr Hosp Mental Nervous & Muscular Disorders, Natl Ctr Neurol & Psychiat, Dept Radiol, 4-1-1 Ogawa, Kodaira, Tokyo 1878551, Japan. 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RP Jick, H (reprint author), Boston Univ, Sch Med, Lexington, MA 02421 USA. CR Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 MILLER E, 2004, IMM SAF REV COMM M 9 NR 4 TC 11 Z9 11 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUN 24 PY 2004 VL 350 IS 26 BP 2722 EP 2723 DI 10.1056/NEJM200406243502623 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 831MR UT WOS:000222199000033 PM 15215496 ER PT J AU [Anonymous] AF [Anonymous] TI Autism link? SO NEW SCIENTIST LA English DT News Item NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD JUN 19 PY 2004 VL 182 IS 2452 BP 5 EP 5 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 829ZT UT WOS:000222092100010 ER PT J AU [Anonymous] AF [Anonymous] TI "It is not clear if the brain damage really is comparable to autism" SO NEW SCIENTIST LA English DT News Item NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD JUN 19 PY 2004 VL 182 IS 2452 BP 5 EP 5 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 829ZT UT WOS:000222092100011 ER PT J AU Vastag, B AF Vastag, B TI Autism interventions come of age SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT News Item CR LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 NR 1 TC 1 Z9 1 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 16 PY 2004 VL 291 IS 23 BP 2807 EP 2808 DI 10.1001/jama.291.23.2807 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 828GT UT WOS:000221962500003 PM 15199014 ER PT J AU Seeman, C AF Seeman, C TI Supporting individuals with autism spectrum disorder in recreation. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Libs, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Libs, Toledo, OH USA. CR CUYNE P, 2004, SUPPORTING INDIVIDUA NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD JUN 15 PY 2004 VL 129 IS 11 BP 86 EP 87 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA 835YH UT WOS:000222521000179 ER PT J AU Srivastava, V AF Srivastava, V TI Reporting science correctly: Who is responsible? SO CURRENT SCIENCE LA English DT Letter ID AUTISM C1 Univ Delhi, Dept Genet, Delhi 110007, India. RP Srivastava, V (reprint author), Univ Delhi, Dept Genet, South Campus,Benito Juraez Marg,Dhaula Kuan, Delhi 110007, India. EM vibhutisrivastava@yahoo.com CR Balaram P, 2004, CURR SCI INDIA, V86, P887 Gharani N, 2004, MOL PSYCHIATR, V9, P540, DOI 10.1038/sj.mp.4001515 Gong XH, 2004, AM J MED GENET B, V127B, P113, DOI 10.1002/ajmg.b.20162 Muhle R., 2004, PEDIATRICS, V113, P472 Szatmari P, 2003, BRIT MED J, V326, P173, DOI 10.1136/bmj.326.7382.173 NR 5 TC 0 Z9 0 PU CURRENT SCIENCE ASSN PI BANGALORE PA C V RAMAN AVENUE, PO BOX 8005, BANGALORE 560 080, INDIA SN 0011-3891 J9 CURR SCI INDIA JI Curr. Sci. PD JUN 10 PY 2004 VL 86 IS 11 BP 1469 EP 1469 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 829SK UT WOS:000222069800002 ER PT J AU Mobbs, D Garrett, AS Menon, V Rose, FE Bellugi, U Reiss, AL AF Mobbs, D Garrett, AS Menon, V Rose, FE Bellugi, U Reiss, AL TI Anomalous brain activation during face and gaze processing in Williams syndrome SO NEUROLOGY LA English DT Article ID VISUAL-CORTEX; AUTISM; AREA; NEUROANATOMY; INDIVIDUALS; RECOGNITION; OBJECTS; FMRI; HYPERSOCIABILITY; REPRESENTATIONS AB Objective: To investigate the discrete neural systems that underlie relatively preserved face processing skills in Williams syndrome (WS). Methods: The authors compared face and eye-gaze direction processing abilities in 11 clinically and genetically diagnosed WS subjects with 11 healthy age- and sex-matched controls, using functional MRI ( fMRI). Results: Compared to controls, WS subjects showed a strong trend toward being less accurate in determining the direction of gaze and had significantly longer response latencies. Significant increases in activation were observed in the right fusiform gyrus (FuG) and several frontal and temporal regions for the WS group. By comparison, controls showed activation in the bilateral FuG, occipital, and temporal lobes. Between-group analysis showed WS subjects to have more extensive activation in the right inferior, superior, and medial frontal gyri, anterior cingulate, and several subcortical regions encompassing the anterior thalamus and caudate. Conversely, controls had greater activation in the primary and secondary visual cortices. Conclusion: The observed patterns of activation in WS subjects suggest a preservation of neural functioning within frontal and temporal regions, presumably resulting from task difficulty or compensatory mechanisms. 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SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract CT 37th Annual Meeting of the Society-for-Epidemiologic-Research CY JUN 15-18, 2004 CL Salt Lake City, UT SP Soc Epidemiol Res C1 Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD 21205 USA. NR 0 TC 0 Z9 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 2004 VL 159 IS 11 SU S BP S25 EP S25 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 826GH UT WOS:000221816800099 ER PT J AU Schaeffer, AJ Chung, J Heretis, K Wong, A Ledbetter, DH Martin, CL AF Schaeffer, AJ Chung, J Heretis, K Wong, A Ledbetter, DH Martin, CL TI Comparative genomic hybridization-array analysis enhances the detection of aneuploidies and submicroscopic imbalances in spontaneous miscarriages SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID HIGH-RESOLUTION ANALYSIS; SPONTANEOUS-ABORTIONS; CYTOGENETIC ANALYSIS; MICROARRAYS; CHROMOSOME; TUMORS; ABERRATION; PATIENT; CGH AB Miscarriage is a condition that affects 10%-15% of all clinically recognized pregnancies, most of which occur in the first trimester. Approximately 50% of first-trimester miscarriages result from fetal chromosome abnormalities. Currently, G-banded chromosome analysis is used to determine if large-scale genetic imbalances are the cause of these pregnancy losses. This technique relies on the culture of cells derived from the fetus, a technique that has many limitations, including a high rate of culture failure, maternal overgrowth of fetal cells, and poor chromosome morphology. Comparative genomic hybridization (CGH)-array analysis is a powerful new molecular cytogenetic technique that allows genomewide analysis of DNA copy number. By hybridizing patient DNA and normal reference DNA to arrays of genomic clones, unbalanced gains or losses of genetic material across the genome can be detected. In this study, 41 product-of-conception (POC) samples, which were previously analyzed by G-banding, were tested using CGH arrays to determine not only if the array could identify all reported abnormalities, but also whether any previously undetected genomic imbalances would be discovered. The array methodology detected all abnormalities as reported by G-banding analysis and revealed new abnormalities in 4/41 (9.8%) cases. Of those, one trisomy 21 POC was also mosaic for trisomy 20, one had a duplication of the 10q telomere region, one had an interstitial deletion of chromosome 9p, and the fourth had an interstitial duplication of the Prader-Willi/Angelman syndrome region on chromosome 15q, which, if maternally inherited, has been implicated in autism. This retrospective study demonstrates that the DNA-based CGH-array technology overcomes many of the limitations of routine cytogenetic analysis of POC samples while enhancing the detection of fetal chromosome aberrations. C1 Emory Univ, Dept Human Genet, Sch Med, Atlanta, GA 30322 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. RP Martin, CL (reprint author), Emory Univ, Dept Human Genet, Sch Med, 615 Michael St,Room 315, Atlanta, GA 30322 USA. EM clmartin@genetics.emory.edu CR ALBERTSON DG, 2003, HUM MOL GENET, pR145 Bell GJ, 1999, NAV RES LOG, V46, P341, DOI 10.1002/(SICI)1520-6750(199906)46:4<341::AID-NAV1>3.0.CO;2-A Bell KA, 2001, FERTIL STERIL, V75, P374, DOI 10.1016/S0015-0282(00)01703-9 Cai WW, 2002, NAT BIOTECHNOL, V20, P393, DOI 10.1038/nbt0402-393 Cook EH, 1997, AM J HUM GENET, V60, P928 Daniely M, 1998, HUM REPROD, V13, P805, DOI 10.1093/humrep/13.4.805 Fritz B, 2001, EUR J HUM GENET, V9, P539, DOI 10.1038/sj.ejhg.5200669 Goddijn M, 2000, BEST PRACT RES CL OB, V14, P855, DOI 10.1053/beog.2000.0124 Gunn SR, 2003, AM J MED GENET A, V120A, P127, DOI 10.1002/ajmg.a.20026 HASSOLD T, 1980, ANN HUM GENET, V44, P151, DOI 10.1111/j.1469-1809.1980.tb00955.x Hodgson G, 2001, NAT GENET, V29, P459, DOI 10.1038/ng771 KALLIONIEMI A, 1992, SCIENCE, V258, P818, DOI 10.1126/science.1359641 Ki A, 2003, AM J MED GENET A, V120A, P365, DOI 10.1002/ajmg.a.20236 Kirchhoff M, 2001, J MED GENET, V38, P740, DOI 10.1136/jmg.38.11.740 Lomax B, 2000, AM J HUM GENET, V66, P1516, DOI 10.1086/302878 Paris PL, 2003, AM J PATHOL, V162, P763, DOI 10.1016/S0002-9440(10)63873-4 Pinkel D, 1998, NAT GENET, V20, P207, DOI 10.1038/2524 Schwaenen C, 2003, ANN HEMATOL, V82, P323, DOI 10.1007/s00277-003-0649-6 Snijders AM, 2001, NAT GENET, V29, P263, DOI 10.1038/ng754 Tabet AC, 2001, PRENATAL DIAG, V21, P613, DOI 10.1002/pd.115 Veltman JA, 2002, AM J HUM GENET, V70, P1269, DOI 10.1086/340426 Vissers LELM, 2003, AM J HUM GENET, V73, P1261, DOI 10.1086/379977 NR 22 TC 119 Z9 128 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JUN PY 2004 VL 74 IS 6 BP 1168 EP 1174 DI 10.1086/421250 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 823ZB UT WOS:000221651900009 PM 15127362 ER PT J AU Martin, A Scahill, L Anderson, GM Aman, M Arnold, LE McCracken, J McDougle, CJ Tierney, E Chuang, S Vitiello, B AF Martin, A Scahill, L Anderson, GM Aman, M Arnold, LE McCracken, J McDougle, CJ Tierney, E Chuang, S Vitiello, B TI Weight and leptin changes among risperidone-treated youths with autism: 6-month prospective data SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 49th Annual Meeting of the American-Academy-of-Child-and-Adolescent-Psychiatry CY OCT 23-27, 2002 CL SAN FRANCISCO, CA SP Amer Acad Child & Adolescent Psychiat ID GAIN; OLANZAPINE; ADOLESCENTS; CHILDREN; ASSOCIATION; INCREASE AB Objective: The authors examined the developmental impact and temporal characteristics of risperidone-associated weight change. Method: Weight change was measured for 63 children and adolescents with autism treated with risperidone for 6 months. Change in serum leptin levels after 2 months was examined as a predictor of final weight gain in mixed regression models that controlled for site, gender, age, and risperidone dose. Results: Age- and gender-standardized weight increased after 6 months of treatment (gross: mean=5.6 kg [SD=3.9]; standardized: mean=0.6 z [SD=0.5]) and was positively correlated with weight gained after I month. Change in leptin levels after 2 months of treatment (mean=-0.3 ng/ml, SD=6.2) (N=48) did not predict final weight gain. Conclusions: Chronic risperidone exposure in children with autism causes weight gain in excess of developmentally expected norms that follows a curvilinear trajectory and decelerates over time. Serum leptin change does not reliably predict risperidone-associated weight gain. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Martin, A (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd,POB 107900, New Haven, CT 06520 USA. EM andres.martin@yale.edu CR Allison DB, 1999, AM J PSYCHIAT, V156, P1686 Bromel T, 1998, MOL PSYCHIATR, V3, P76, DOI 10.1038/sj.mp.4000352 Eder U, 2001, AM J PSYCHIAT, V158, P1719, DOI 10.1176/appi.ajp.158.10.1719 Gothelf D, 2002, AM J PSYCHIAT, V159, P1055, DOI 10.1176/appi.ajp.159.6.1055 Kelly DL, 1998, J CHILD ADOL PSYCHOP, V8, P151, DOI 10.1089/cap.1998.8.151 Martin A, 2000, J CHILD ADOL PSYCHOP, V10, P259, DOI 10.1089/cap.2000.10.259 Ratzoni G, 2002, J AM ACAD CHILD PSY, V41, P337, DOI 10.1097/00004583-200203000-00014 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Reynolds GP, 2002, LANCET, V359, P2086, DOI 10.1016/S0140-6736(02)08913-4 Scahill L, 2001, J CHILD ADOL PSYCHOP, V11, P377, DOI 10.1089/104454601317261555 Woods SW, 2002, J AM ACAD CHILD PSY, V41, P1439, DOI 10.1097/01.CHI.0000024871.60748.74 NR 11 TC 62 Z9 64 PU AMER PSYCHIATRIC PRESS, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JUN PY 2004 VL 161 IS 6 BP 1125 EP 1127 DI 10.1176/appi.ajp.161.6.1125 PG 3 WC Psychiatry SC Psychiatry GA 826NV UT WOS:000221836700028 PM 15169706 ER PT J AU Woo, EJ Ball, R Bostrom, A Shadomy, SV Ball, LK Evans, G Braun, M AF Woo, EJ Ball, R Bostrom, A Shadomy, SV Ball, LK Evans, G Braun, M TI Vaccine risk perception among reporters of autism after vaccination: Vaccine adverse event reporting system 1990-2001 SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID RUBELLA VACCINATION; MEASLES; MUMPS; POPULATION; ASSOCIATION; THIMEROSAL AB Objectives. We investigated vaccine risk perception among reporters of autism to the Vaccine Adverse Event Reporting System (VAERS). Methods. We conducted structured interviews with 124 parents who reported autism and related disorders to VAERS from 1990 to 2001 and compared results with those of a published survey of parents in the general population. Results. Respondents perceived vaccine-preventable diseases as less serious than did other parents. Only 15% of respondents deemed immunization extremely important for children's health; two thirds had withheld vaccines from their children. Conclusions. Views of parents who believe vaccines injured their children differ significantly from those of the general population regarding the benefits of immunization. Understanding the factors that shape this perspective can improve communication among vaccine providers, policymakers, and parents/patients. C1 US FDA, Vaccine Safety Branch, Div Epidemiol, Ctr Biol Evaluat & Res, Rockville, MD 20852 USA. Georgia Inst Technol, Sch Publ Policy, Atlanta, GA 30332 USA. Off Publ Hlth & Sci, Dept Hlth & Human Serv, Rockville, MD USA. US Hlth Resources & Serv Adm, Natl Vaccine Injury Compensat Program, Dept Hlth & Human Serv, Rockville, MD 20857 USA. RP Woo, EJ (reprint author), US FDA, Vaccine Safety Branch, Div Epidemiol, Ctr Biol Evaluat & Res, HFM-222,1401 Rockville Pike, Rockville, MD 20852 USA. EM wooj@cber.fda.gov CR Akobeng A K, 1999, J Pediatr Gastroenterol Nutr, V28, P351, DOI 10.1097/00005176-199903000-00032 Atkinson William L, 2002, MMWR Recomm Rep, V51, P1 BOSTROM A, 1994, RISK ANAL, V14, P789, DOI 10.1111/j.1539-6924.1994.tb00290.x CHEN RT, 1994, VACCINE, V12, P542, DOI 10.1016/0264-410X(94)90315-8 Ellenberg SS, 2002, DRUG SAFETY, V25, P145, DOI 10.2165/00002018-200225030-00001 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Gellin BG, 2000, PEDIATRICS, V106, P1097, DOI 10.1542/peds.106.5.1097 Hviid A, 2003, JAMA-J AM MED ASSOC, V290, P1763, DOI 10.1001/jama.290.13.1763 *I MED IMM SAF REV, 2001, MEASL MUMPS RUB VACC Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Lingam R, 2003, ARCH DIS CHILD, V88, P666, DOI 10.1136/adc.88.8.666 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Madsen KM, 2003, PEDIATRICS, V112, P604, DOI 10.1542/peds.112.3.604 Makela A, 2002, PEDIATRICS, V110, P957, DOI 10.1542/peds.110.5.957 PICKERING LK, 2000, 2000 RED BOOK REPORT Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 1999, MMWR MORB MORTAL WKL, V48, P563 NR 19 TC 23 Z9 23 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JUN PY 2004 VL 94 IS 6 BP 990 EP 995 DI 10.2105/AJPH.94.6.990 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 824WK UT WOS:000221717700025 PM 15249304 ER PT J AU Lotspeich AF Lotspeich TI Investigation of neuroanatomical differences between autism and Asperger syndrome (vol 61, pg 291, 2004) SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Correction CR LOTSPEICH, 2004, ARCH GEN PSYCHIAT, V61, P291 NR 1 TC 0 Z9 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 2004 VL 61 IS 6 BP 606 EP 606 PG 1 WC Psychiatry SC Psychiatry GA 826JG UT WOS:000221824800009 ER PT J AU Glasson, EJ Bower, C Petterson, B de Klerk, N Chaney, G Hallmayer, JF AF Glasson, EJ Bower, C Petterson, B de Klerk, N Chaney, G Hallmayer, JF TI Perinatal factors and the development of autism - A population study SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CONGENITAL CYTOMEGALOVIRUS-INFECTION; INFANTILE-AUTISM; ASPERGER SYNDROME; CESAREAN-SECTION; PARENTAL AGE; MATERNAL AGE; SPONTANEOUS MUTATION; EPIDURAL ANALGESIA; POSTNATAL FACTORS; NEONATAL FACTORS AB Background: Autism is considered to have a genetic basis, although exposure to certain stimuli in the prenatal period has been implicated to be causal in some cases. Some investigations have shown an association with obstetric complications but findings have been inconsistent owing to differences in sampling and methods. Objective: To examine the association of obstetric factors with autism spectrum disorders for a cohort of children, using obstetric data contained in a statutory database collected at the time of birth. Design: Subjects born in Western Australia between 1980 and 1995 and diagnosed with an autism spectrum disorder by 1999 were included as cases (n = 465). Siblings of the cases (n = 481) and a random population-based control group (n = 1313) were compared with the cases on obstetric information contained in the Maternal and Child Health Research Database of Western Australia. Results: Compared with control subjects, cases had significantly older parents and were more likely to be firstborn. Case mothers had greater frequencies of threatened abortion, epidural caudal anesthesia use, labor induction, and a labor duration of less than 1 hour. Cases were more likely to have experienced fetal distress, been delivered by an elective or emergency cesarean section, and had an Apgar score of less than 6 at 1 minute. Cases with a diagnosis of autism had more complications than those with pervasive developmental disorder not otherwise specified or Asperger syndrome. Nonaffected siblings of cases were more similar to cases than control subjects in their profile of complications. Conclusions: Autism is unlikely to be caused by a single obstetric factor. The increased prevalence of obstetric complications among autism cases is most likely due to the underlying genetic factors or an interaction of these factors with the environment. C1 Univ Western Australia, Sch Populat Hlth, Perth, WA 6009, Australia. Univ Western Australia, Sch Populat Hlth, Perth, WA 6009, Australia. Univ Western Australia, Sch Clin Neurosci, Perth, WA 6009, Australia. Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6009, Australia. Graylands Hosp, Ctr Clin Res Neuropsychiat, Perth, WA, Australia. Disabil Serv Commiss, Perth, WA, Australia. Princess Margaret Hosp, Perth, WA, Australia. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA USA. RP Glasson, EJ (reprint author), Univ Western Australia, Sch Populat Hlth, 35 Stirling Hwy, Crawley, WA 6009, Australia. 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CHILD PSY, V41, P572, DOI 10.1097/00004583-200205000-00015 NR 89 TC 196 Z9 201 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 2004 VL 61 IS 6 BP 618 EP 627 DI 10.1001/archpsyc.61.6.618 PG 10 WC Psychiatry SC Psychiatry GA 826JG UT WOS:000221824800011 PM 15184241 ER PT J AU Bardenheier, B Yusuf, H Schwartz, B Gust, D Barker, L Rodewald, L AF Bardenheier, B Yusuf, H Schwartz, B Gust, D Barker, L Rodewald, L TI Are parental vaccine safety concerns associated with receipt of measles-mumps-rubella, diphtheria and tetanus toxoids with acellular pertussis, or hepatitis B vaccines by children? SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID RISK-FACTORS; IMMUNIZATION; AUTISM AB objectives: To identify parental perceptions regarding vaccine safety and assess their relationship with the immunization status of children. Design, Setting, and Participants: Case-control study based on a survey of a sample of households participating in the 2000-2001 National Immunization Survey, a quarterly random-digit-dialing sample of US children aged 19 to 35 months. Three groups of case children not up-to-date for 3 vaccines were compared with control children who were up-to-date for each respective vaccine. Main Outcome Measure: Measles-containing or measles-mumps-rubella, diphtheria and tetanus toxoids and pertussis or diphtheria and tetanus toxoids with acellular pertussis, and hepatitis B vaccination coverage. Results: Among those sampled from the 2000-2001 National Immunization Survey, the household response rate was 2315 (52.1%) of 4440. Most respondents (>90%) in all groups believed vaccinations are important. In each case-control group, there was no significant difference between the percentage of case and control parents expressing general vaccine safety (range, 53.5%-64.1%). However, case parents were more likely to have asked that their child not be vaccinated for reasons other than illness (range, 10.2%-13.7% vs range, 2.9%-5.3%, respectively) and to believe their children received too many vaccinations (range, 3.4%-7.6% vs range, 0.8%-1.0%, respectively). Among the case-control group receiving a measles-containing or measles-mumps-rubella vaccination, only a small percentage of parents knew about the alleged association between autism and measles-mumps-rubella vaccinations (8.2%), and case parents were more likely to believe it than control parents (4.4% vs 1.5%, respectively; chi(2) P=.04). Conclusions: Despite belief in the importance of immunization by a vast majority of parents, the majority of parents had concerns regarding vaccine safety. Strategies to address important misperceptions about vaccine safety as well as additional research assessing vaccine safety are needed to ensure public confidence. 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Pediatr. Adolesc. Med. PD JUN PY 2004 VL 158 IS 6 BP 569 EP 575 DI 10.1001/archpedi.158.6.569 PG 7 WC Pediatrics SC Pediatrics GA 826KJ UT WOS:000221827700011 PM 15184221 ER PT J AU van Berckelaer-Onnes, I AF van Berckelaer-Onnes, I TI Special issue on autism and learning disability SO AUTISM LA English DT Editorial Material C1 Leiden Univ, NL-2300 RA Leiden, Netherlands. RP van Berckelaer-Onnes, I (reprint author), Leiden Univ, NL-2300 RA Leiden, Netherlands. NR 0 TC 0 Z9 0 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 JUN PY 2004 VL 8 IS 2 BP 123 EP 124 DI 10.1177/1362361304042717 PG 2 WC Psychology, Developmental SC Psychology GA 829MS UT WOS:000222053300001 ER PT J AU O'Brien, G Pearson, J AF O'Brien, G Pearson, J TI Autism and learning disability SO AUTISM LA English DT Article DE autism; learning disability ID PERVASIVE DEVELOPMENTAL DISORDERS; NONAUTISTIC RETARDED-CHILDREN; MENTAL-RETARDATION; FOLLOW-UP; BEHAVIORAL-CHARACTERISTICS; DIAGNOSTIC-ASSESSMENT; SPECTRUM DISORDERS; ADAPTIVE-BEHAVIOR; DOWN-SYNDROME; CLASSIFICATION AB In this article a short overview is given of the relationship between autism and learning disability. Autism exists with any level of intelligence, but many individuals with autism suffer also from learning disability. Although both disorders show overlap in some behaviours they are different in many aspects. 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Although identification of genes is usually straightforward in Mendelian disorders, it has proved to be much more difficult to establish in polygenic disorders like autism. Neither genome screens of affected siblings nor the large number of association studies using candidate genes have resulted in finding autism susceptibility genes. We focus on the alternative approach of 'positional cloning' through chromosomal aberrations in individuals with autism. In particular, balanced aberrations such as reciprocal translocations or inversions offer a unique opportunity, since only the genes in the breakpoint regions are candidate genes. This approach, in combination with others, is likely to produce results in the coming years. C1 Univ Louvain, B-3001 Louvain, Belgium. RP Devriendt, K (reprint author), Univ Louvain, B-3001 Louvain, Belgium. 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Identification of autism in children with Angelman syndrome presents a diagnostic challenge. In the present study, 16 children with Angelman syndrome, all with a 15q11-13 deletion, were examined for ASDs. Thirteen children with Angelman syndrome received an ADOS-G algorithm classification of ASD; the remaining three were outside the autistic spectrum. Ten fulfilled the criteria for autism, and three for PDD-NOS. The 10 children with Angelman syndrome and comorbid autism were compared with eight children with only autism regarding their social and communicative skills. The results indicated that Angelman syndrome is better understood in terms of developmental delay, and autism in terms of developmental deviance. It is concluded that autism might have been overdiagnosed due to the extremely low mental age of the children with Angelman syndrome. C1 Aarhus Univ Hosp, DK-8000 Aarhus, Denmark. RP Trillingsgaard, A (reprint author), Aarhus Univ Hosp, DK-8000 Aarhus, Denmark. 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The existing literature on catatonic-like states in people with autistic spectrum disorders is summarized, and it is suggested that such states are not directly comparable with the existing concepts of catatonia. A concept of 'autistic catatonia' is outlined in terms of both its phenomenology and its possible aetiological and maintaining factors. A case study is presented that examines this phenomenon from a cognitive neuropsychological perspective, together with implications for everyday management. The implications of this work for both research and clinical practice are discussed. C1 Univ Manchester, Manchester M13 9PL, Lancs, England. Univ Liverpool, Liverpool L69 3BX, Merseyside, England. RP Hare, DJ (reprint author), Univ Manchester, Manchester M13 9PL, Lancs, England. 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The problems are characterized by a lack of intentionality and symbol formation, which indicates that the deviant development of communication in autism is associated with a specific cognitive style. The central coherence theory can offer insight into the specific communication problems of people with autism, since a weaker drive for central coherence leads to problems in sense-making and, consequently, in communication. In the case of the comorbidity of autism and learning disability, the communication problems are aggravated. The crucial point is the determination of the level of sense-making, taking this comorbidity into account. Assessment and intervention have to be tuned to individual needs, in order to increase the communicative competence of people with autism and learning disability. C1 Leiden Univ, NL-2300 RA Leiden, Netherlands. RP Noens, I (reprint author), Leiden Univ, NL-2300 RA Leiden, Netherlands. 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SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID IMAGERY; MIND; ABNORMALITIES; MOVEMENTS; AUTISM; TASK AB The general applicability of forward models in brain function has previously been recognized. Grush's contribution centers largely on broadening the extent and scope of forward models. However, in his effort to expand and generalize, important distinctions may have been overlooked. A better grounding in the underlying physiology would have helped to illuminate such valuable differences and similarities. C1 Johns Hopkins Univ, Dept Biomed Engn, Baltimore, MD 21205 USA. Columbia Univ Coll Phys & Surg, Dept Psychiat, Div Child & Adolescent Psychiat, New York, NY 10032 USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. RP Donchin, O (reprint author), Johns Hopkins Univ, Dept Biomed Engn, Baltimore, MD 21205 USA. 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PD JUN PY 2004 VL 27 IS 3 BP 402 EP + PG 9 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 883NY UT WOS:000226021100044 ER PT J AU Bar-Haim, Y Henkin, Y Ari-Even-Roth, D Schneider, ST Hildesheimer, M Muchnik, C AF Bar-Haim, Y Henkin, Y Ari-Even-Roth, D Schneider, ST Hildesheimer, M Muchnik, C TI Reduced auditory efferent activity in childhood selective mutism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE auditory processing; middle ear acoustic reflex; otoacoustic emission; selective mutism; social anxiety; vocalization ID EVOKED OTOACOUSTIC EMISSIONS; MEDIAL OLIVOCOCHLEAR SYSTEM; ECHOLOCATING HORSESHOE BATS; ELECTIVE MUTISM; MIDDLE-EAR; NEURAL ATTENUATION; STAPEDIUS REFLEX; INFANTILE-AUTISM; SOCIAL PHOBIA; CHILDREN AB Background: Selective mutism is a psychiatric disorder of childhood characterized by consistent inability to speak in specific situations despite the ability to speak normally in others. The objective of this study was to test whether reduced auditory efferent activity, which may have direct hearings on speaking behavior, is compromised in selectively mute children. Methods: Participants were 16 children with selective mutism and 16 normally developing control children matched for age and gender. All children were tested for pure-tone audiometry, speech reception thresholds, speech discrimination, middle-ear acoustic reflex thresholds and decay function, transient evoked otoacoustic emission, suppression of transient evoked otoacoustic emission, and auditory brainstem response. Results: Compared with control children, selectively mute children displayed specific deficiencies in auditory efferent activity. These aberrations in efferent activity appear along with normal pure-tone and speech audiometry and normal brainstem transmission as indicated by auditory brainstem response latencies. Conclusions: The diminished auditory efferent activity detected in some children with SM may result in desensitization of their auditory pathways by self-vocalization and in reduced control of masking and distortion of incoming speech sounds. These children may gradually learn to restrict vocalization to the minimal amount possible in contexts that require complex auditory processing. C1 Tel Aviv Univ, Dept Psychol, Sackler Fac Med, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Dept Commun Disorders, Sackler Fac Med, IL-69978 Tel Aviv, Israel. Chaim Sheba Med Ctr, Speech & Hearing Ctr, Tel Aviv, Israel. RP Bar-Haim, Y (reprint author), Tel Aviv Univ, Dept Psychol, Sackler Fac Med, IL-69978 Tel Aviv, Israel. 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Psychiatry PD JUN 1 PY 2004 VL 55 IS 11 BP 1061 EP 1068 DI 10.1016/j.biopsych.2004.02.021 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 823IZ UT WOS:000221605800003 PM 15158424 ER PT J AU Font-Montgomery, E Weaver, DD Walsh, L Christensen, C Thurston, VC AF Font-Montgomery, E Weaver, DD Walsh, L Christensen, C Thurston, VC TI Clinical and cytogenetic manifestations of subtelomeric aberrations: Report of six cases SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Article DE subtelomeric FISH probes; idiopathic mental retardation; birth defects; chromosomes; autism ID CHROMOSOMAL REARRANGEMENTS; MENTAL-RETARDATION; REGIONS; CHILDREN; DELETION; PROBES AB BACKGROUND: Fluorescent subtelomeric probes for the 41 different subtelomeric regions (the p arms of the acrocentric chromosomes were excluded) have been developed over the last 10 years. These probes can detect deletions, duplications, and translocations in the gene-rich subtelomeric regions of human chromosomes, regions where crossing over frequently occurs and where a high number of abnormalities have been found. Recently, commercially produced probes have become available, which has led to the detection of subtelomeric abnormalities in 7.4% of patients with moderate to severe mental retardation (Knight et al., 1999). CASES: We evaluated 43 dysmorphic children with developmental delay and/or mental retardation of unknown etiology and/or autism who were previously assessed for chromosome abnormalities, metabolic disorders, or recognizable dysmorphic syndromes, all of which were ruled out. Of the 43 children tested, 6 (14%) were found to have subtelomeric aberrations. CONCLUSIONS: We recommend that patients with dysmorphic features and mental retardation of unknown etiology who also have a normal standard chromosome analysis should have subtelomeric FISH testing performed earlier in their clinical workup. (C) 2004 Wiley-Liss, Inc. C1 Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Neurol, Indianapolis, IN 46202 USA. RP Font-Montgomery, E (reprint author), Indiana Univ, Sch Med, Dept Med & Mol Genet, 975 W Walnut St,IB 130, Indianapolis, IN 46202 USA. 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PD JUN PY 2004 VL 70 IS 6 BP 417 EP 417 DI 10.1002/bdra.20015 PG 1 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA 834NZ UT WOS:000222419100009 ER PT J AU Sabbagh, MA AF Sabbagh, MA TI Understanding orbitofrontal contributions to theory-of-mind reasoning: Implications for autism SO BRAIN AND COGNITION LA English DT Article ID FACIAL EXPRESSIONS; ASPERGER-SYNDROME; BIOLOGICAL BASIS; NEURAL SYSTEMS; YOUNG-CHILDREN; NORMAL ADULTS; RECOGNITION; DISORDER; DAMAGE; AMYGDALA AB Autism is a lifelong developmental disorder that is associated with severe difficulties with "theory-of-mind"-the understanding that others' behaviors are motivated by internal mental states. Here, we raise the possibility that research examining the neural bases of theory-of-mind reasoning has the potential to inform researchers about the elusive functional neural impairments associated with autism. 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Data were obtained on 108 such children living within one geographical area in Northern Ireland and who spent 90 days or more in a 12-month period living away from the family home. However, this figure may under-estimate the numbers, given the difficulties in tracking children aged over 14 years who were admitted to hospitals on a short- or long-term basis. The median age of the children was 14 years; most had learning disabilities allied with challenging behaviours, communication difficulties, autism and some were technologically dependent. Many of their families experienced a range of problems. One-third of the children were accommodated in various residential settings but half of these placements were in hospital or adult residential accommodation. However, there were marked differences in the services provided to this client group by the four provider agencies. Future service needs included increased respite breaks for families and the provision of both more residential placements and more appropriate accommodation, especially for teenagers. The dilemmas in reconciling the need for local, but specialized, service provision are discussed. C1 Univ Ulster, Sch Nursing, Newtownabbey BT37 0QB, North Ireland. N & W Belfast Hlth & Social Serv Trust, Belfast, Antrim, North Ireland. RP McConkey, R (reprint author), Univ Ulster, Sch Nursing, Newtownabbey BT37 0QB, North Ireland. EM r.mcconkey@ulster.ac.uk CR ABBOTT D, 2002, DISABLED CHILDREN RE BLACHER J, 1993, RES DEV DISABIL, V14, P145, DOI 10.1016/0891-4222(93)90017-E *DEP HLTH SOC SERV, 2001, CHILDR MATT PHAS 2 Department of Health, 2001, VAL PEOPL NEW STRAT Foundation for People with Learning Disabilities, 2001, LEARN DIS FUND FACTS Lawton D., 1998, NUMBER CHARACTERISTI LLEWELLYN G, 1997, J INTELL DISABIL RES, V43, P219 MCCONKEY R, 2004, IN PRESS J SOCIAL WO McConkey R, 2000, CHILD CARE HLTH DEV, V26, P429, DOI 10.1046/j.1365-2214.2000.00163.x MONTEITH M, 1999, CIRCUMSTANCES EXPE 2 Morris J, 1997, DISABIL SOC, V12, P241, DOI 10.1080/09687599727353 MORRIS J, 1998, STILL MISSING, V2 PREWETT B, 2000, COMMITTED CARING VIE Robinson C, 2001, CHILD FAMILY SOCIAL, V6, P67, DOI 10.1046/j.1365-2206.2001.00185.x Treneman M, 1997, DEV MED CHILD NEUROL, V39, P548 TRUESDALE M, 2001, CHILD CARE PRACTICE, V7, P143 NR 16 TC 2 Z9 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0045-3102 J9 BRIT J SOC WORK JI Br. J. Soc. Work PD JUN PY 2004 VL 34 IS 4 BP 561 EP 576 DI 10.1093/bjsw/bch066 PG 16 WC Social Work SC Social Work GA 830IX UT WOS:000222116700007 ER PT J AU Harpaz-Rotem, I Rosenheck, RA AF Harpaz-Rotem, I Rosenheck, RA TI Changes in outpatient psychiatric diagnosis in privately insured children and adolescents from 1995 to 2000 SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE child; adolescent; diagnosis; prevalence; change; bipolar; autism ID SEROTONIN REUPTAKE INHIBITORS; DISORDER; CHILDHOOD; AUTISM AB This study examined changes in the diagnostic patterns among children and adolescents treated for mental health problems between the years 1995 and 2000. Using a large database (MarketScan(R)) which compiles claims information from private health insurance plans nationwide, our sample consisted of 100,716 children (under the age of 18) who submitted claims for outpatient mental health services, out of a total of 1,723,681 covered children. Over the five years period, there was a dramatic increase in the proportion of children diagnosed with both Autism and Bipolar disorders. An increase was also observed in Anxiety, ADHD and Depressive disorders. A decrease was observed in diagnostic prevalence of Oppositional, Adjustment and Substance Abuse disorders. C1 Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06519 USA. RP Harpaz-Rotem, I (reprint author), Yale Univ, Sch Med, Dept Psychiat, 25 Pk St, New Haven, CT 06519 USA. 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PD SUM PY 2004 VL 34 IS 4 BP 329 EP 340 PG 12 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 815EG UT WOS:000221025000005 PM 15039605 ER PT J AU Daoust, AM Limoges, T Bolduc, C Mottron, L Godbout, R AF Daoust, AM Limoges, T Bolduc, C Mottron, L Godbout, R TI EEG spectral analysis of wakefulness and REM sleep in high functioning autistic spectrum disorders SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE autism; electroencephalography; pervasive developmental disorder; rapid eye movement sleep; visual cortex ID MAGNETIC-RESONANCE SPECTROSCOPY; ASPERGERS-SYNDROME; CHILDHOOD AUTISM; QUANTITATIVE-ANALYSIS; SUBJECTIVE ALERTNESS; BRAIN; CHILDREN; INDIVIDUALS; DEFICITS; LOBE AB Objective: The aim of this study was to investigate the involvement of temporo-occipital regions in the pathophysiology of autistic spectrum disorders (ASD) by using REM sleep and waking EEG. Methods: The EEG recordings of 9 persons with ASD and 8 control participants were recorded using a 12-electrode montage. Spectral analysis (0.75-19.75 Hz) was performed on EEG activity recorded upon two activated states: REM sleep and wakefulness. Results: During REM sleep, persons with ASD showed a selective, significantly lower absolute beta (13.0-19.75 Hz) spectral amplitude over the primary (O-1, O-2) and associative (T-5, T-6) cortical visual areas compared to controls. Persons with ASD showed significantly higher absolute theta (4.0-7.75 Hz) spectral amplitude over the left frontal pole region (Fp1) compared to controls during evening wakefulness, but not during morning wakefulness. Significance: The results of waking EEG are consistent with previously reported observations of neuropsychological signs of frontal atypicalities in ASD; results from REM sleep are the first EEG evidence to support the hypothesis of abnormal visuoperceptual functioning in ASD. Altogether, these results point toward atypical thalamo-cortical mechanisms subserving the neural processing of information in ASD. (C) 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. C1 Hop Riviere des Prairies, Ctr Rech Fernand Seguin, Lab Sommeil, Neurodev Disorders Program, Montreal, PQ H1E 1A4, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. RP Godbout, R (reprint author), Hop Riviere des Prairies, Ctr Rech Fernand Seguin, Lab Sommeil, Neurodev Disorders Program, 7070 Boul Perras, Montreal, PQ H1E 1A4, Canada. 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PD JUN PY 2004 VL 7 IS 3 BP 313 EP 314 PG 2 WC Communication; Psychology, Applied SC Communication; Psychology GA 835RQ UT WOS:000222503600054 ER PT J AU Hill, EL AF Hill, EL TI Evaluating the theory of executive dysfunction in autism SO DEVELOPMENTAL REVIEW LA English DT Review DE autism spectrum disorder; executive function; frontal lobes ID CARD SORTING TEST; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; HUMAN CEREBRAL-CORTEX; FRONTAL-LOBE DAMAGE; COGNITIVE PHENOTYPE; MAGNETIC-RESONANCE; DEVELOPMENTAL DISORDERS; INDIVIDUAL-DIFFERENCES; PRESCHOOL-CHILDREN; PREFRONTAL CORTEX AB In this paper studies of executive function in autism spectrum disorder are reviewed. Executive function is an umbrella term for functions such as planning, working memory, impulse control, inhibition, and shifting set, as well as for the initiation and monitoring of action. In this review, the focus will be on planning, inhibition, shifting set, generativity, and action monitoring. While it is known that these functions depend upon the frontal lobes, and particularly on prefrontal cortex, very little is known about neuroanatomical correlates of executive function in autism. The review acknowledges the complexity of investigating executive functions in autism, the possible influence of IQ on executive performance in these groups and the possibility of overlap between performance on tests of executive function in other neurodevelopmental disorders that are likely to involve congenital deficits in the frontal lobes, such as attention deficit hyperactivity disorder and Tourette's syndrome. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. RP Hill, EL (reprint author), Univ London Goldsmiths Coll, Dept Psychol, Whitehead Bldg, London SE14 6NW, England. 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PD JUN PY 2004 VL 24 IS 2 BP 189 EP 233 DI 10.1016/j.dr.2004.01.001 PG 45 WC Psychology, Developmental SC Psychology GA 820EJ UT WOS:000221369700002 ER PT J AU Dawson, G Webb, SJ Carver, L Panagiotides, H McPartland, J AF Dawson, G Webb, SJ Carver, L Panagiotides, H McPartland, J TI Young children with autism show atypical brain responses to fearful versus neutral facial expressions of emotion SO DEVELOPMENTAL SCIENCE LA English DT Review ID FUSIFORM FACE AREA; HUMAN AMYGDALA; 6-MONTH-OLD INFANTS; RECOGNITION MEMORY; SPECTRUM DISORDER; DEVELOPMENTAL-CHANGES; MENTAL-RETARDATION; NEURAL SUBSTRATE; SOCIAL-BEHAVIOR; TEMPORAL CORTEX AB Evidence suggests that autism is associated with impaired emotion perception, but it is unknown how early such impairments are evident. Furthermore, most studies that have assessed emotion perception in children with autism have required verbal responses, making results difficult to interpret. This study utilized high-density event-related potentials (ERPs) to investigate whether 3-4-year-old children with autism spectrum disorder (ASD) show differential brain activity to fear versus neutral facial expressions. It has been shown that normal infants as young as 7 months of age show differential brain responses to faces expressing different emotions. ERPs were recorded while children passively viewed photos of an unfamiliar woman posing a neutral and a prototypic fear expression. The sample consisted of 29 3-4-year-old children with ASD and 22 chronological age-matched children with typical development. Typically developing children exhibited a larger early negative component (N300) to the difference in amplitude of this early ERP component fear than to the neutral face. In contrast, children with ASD did not show the to the fear versus neutral face. For a later component, typically developing children exhibited a larger negative slow wave (NSW) to the fear than to the neutral face, whereas children with autism did not show a differential NS W to the two stimuli. In children with ASD, faster speed of early processing (i.e. N300 latency) of the fear face was associated with better performance on tasks assessing social attention (social orienting, joint attention and attention to distress). These data suggest that children with ASD, as young as 3 years of age, show a disordered pattern of neural responses to emotional stimuli. C1 Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Washington, DC USA. Univ Calif San Diego, Dept Psychol, San Diego, CA 92103 USA. RP Dawson, G (reprint author), Univ Washington, Ctr Human Dev & Disabil, Box 357920, Seattle, WA 98195 USA. 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Today PD JUN 1 PY 2004 VL 9 IS 11 BP 473 EP 473 DI 10.1016/S1359-6446(04)03088-0 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 822VI UT WOS:000221568100006 PM 15149620 ER PT J AU Acosta, MT AF Acosta, MT TI Pharmacotherapy in autism: where to start? SO DRUG DISCOVERY TODAY LA English DT Editorial Material C1 Childrens Natl Med Ctr, Dept Neurol, Ctr Neurosci & Behav Med, Washington, DC 20010 USA. RP Acosta, MT (reprint author), Childrens Natl Med Ctr, Dept Neurol, Ctr Neurosci & Behav Med, 111 Michigan Ave NW, Washington, DC 20010 USA. 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Today PD JUN 1 PY 2004 VL 9 IS 11 BP 474 EP 474 DI 10.1016/S1359-6446(04)03089-2 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 822VI UT WOS:000221568100007 PM 15149621 ER PT J AU Carothers, DE Taylor, RL AF Carothers, DE Taylor, RL TI Social cognitive processing in elementary school children with Asperger syndrome SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID ADJUSTMENT; ADOLESCENT; PATTERNS; AUTISM AB Twenty students with Asperger syndrome were compared to 20 typically developing peers to determine their relative effectiveness in interpreting social intentions of others and to examine whether with a given interpretation of social intention there were differences in the social interaction strategies chosen by these two groups of students. An independent samples Nest indicates that the typically developing group performed significantly better on encoding conflicts and benign intention cues. 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PD JUN PY 2004 VL 39 IS 2 BP 177 EP 187 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 825ID UT WOS:000221748900008 ER PT J AU Colborn, T AF Colborn, T TI Neurodevelopment and endocrine disruption SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review DE ADHD; autism; behavior; endocrine disruptor; environmental contaminants; neurologic effects; prenatal exposure; thyroid ID DEFICIT-HYPERACTIVITY DISORDER; THYROID-HORMONE STATUS; PRENATAL PCB EXPOSURE; POLYCHLORINATED-BIPHENYLS; DEVELOPMENTAL EXPOSURE; POSTNATAL EXPOSURE; GREAT-LAKES; BRAIN; INFANTS; SYSTEM AB In this article I explore the possibility that contaminants contribute to the increasing prevalence of attention deficit hyperactivity disorder, autism, and associated neurodevelopmental and behavioral problems in developed countries. I discuss the exquisite sensitivity of the embryo and fetus to thyroid disturbance and provide evidence of human in utero exposure to contaminants that can interfere with the thyroid. Because it may never be possible to link prenatal exposure to a specific chemical with neurodevelopmental damage in humans, I also present alternate models where associations have been made between exposure to specific chemicals or chemical classes and developmental difficulties in laboratory animals, wildlife, and humans. C1 Endocrine Disrupt Exchange, Paonia, CO USA. Univ Florida, Dept Zool, Gainesville, FL 32611 USA. RP Colborn, T (reprint author), POB 1253, Paonia, CO 81428 USA. EM colborn@tds.net CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAYER SA, 1993, NEUROTOXICOLOGY, V14, P83 BERKOW R, 1987, MECK MANUAL DIAGNOSI Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Blount B. 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PD JUN PY 2004 VL 112 IS 9 BP 944 EP 949 DI 10.1289/ehp.6601 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 833DE UT WOS:000222315800002 PM 15198913 ER PT J AU Zoroglu, SS Armutcu, F Ozen, S Gurel, A Sivasli, E Yetkin, O Meram, I AF Zoroglu, SS Armutcu, F Ozen, S Gurel, A Sivasli, E Yetkin, O Meram, I TI Increased oxidative stress and altered activities of erythrocyte free radical scavenging enzymes in autism SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Article DE autism; thiobarbituric acid-reactive substances (TBARS); superoxide dismutase (SOD); catalase (CAT); xanthine oxidase (XO); adenosine deaminase (ADA); free radicals ID SUPEROXIDE-DISMUTASE; LIPID-PEROXIDATION; ANTIOXIDANT DEFENSE; XANTHINE-OXIDASE; SCHIZOPHRENIA; ASSOCIATION; DISORDER; PRODUCTS; DISEASE; ASSAY AB There is great evidence in recent years that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. The present study was performed to assess the changes in red blood cells thiobarbituric acid-reactive substances (TBARS) levels, and superoxide dismutase (SOD), catalase (CAT), adenosine deaminase (ADA) and xanthine oxidase (XO) activities in patients with autism (n = 27) compared to age- and sex-matched normal controls (n = 26). In the autistic group, increased TBARS levels (p < 0.001) and XO (p < 0.001) and SOD (p < 0.001) activity, decreased CAT (p < 0.001) activity and unchanged ADA activity were detected. It is proposed that antioxidant status may be changed in autism and this new situation may induce lipid peroxidation. These findings indicated a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism. C1 Gaziantep Typ Fak, TR-27200 Gaziantep, Turkey. Zonguldak Karaelmas Univ, Fac Med, Dept Biochem, Zonguldak, Turkey. Dicle Univ, Fac Med, Dept Psychiat, Diyarbakyr, Turkey. Gaziantep Univ, Fac Med, Dept Pediat, Gaziantep, Turkey. Zonguldak Karaelmas Univ, Fac Med, Dept Biochem, Zonguldak, Turkey. RP Zoroglu, SS (reprint author), Gaziantep Typ Fak, TR-27200 Gaziantep, Turkey. 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Arch. Psych. Clin. Neurosci. PD JUN PY 2004 VL 254 IS 3 BP 143 EP 147 DI 10.1007/s00406-004-0456-7 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 833EN UT WOS:000222319300001 PM 15205966 ER PT J AU Casanova, MF AF Casanova, MF TI Intracortical circuitry: One of psychiatry's missing assumptions SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Article DE psychiatry; neurology; neuropathology; minicolumns; macrocolumns ID MINICOLUMNAR ORGANIZATION; VISUAL-CORTEX; RHESUS-MONKEY; SCHIZOPHRENIA; AUTISM; BRAIN; NEUROSCIENCE; HYPOTHESIS; NEURONS; AXONS AB The brain operates as a constellation of modular functions focused on processing information. Neurons are arranged into repetitive circuits called minicolumns which themselves are assembled into macrocolumns. Most of the attention in neuroscience has focused on the experiences of organization-neuronal cellular function at one end and signal cascades and macrocolumns at the other. However, the search for pathological substrates of varied mental conditions are leading to a reassessment of the role of minicolumns in mental disorders. An appreciation of the modular framework of the brain provides a better insight as to how minicolumns contribute to the larger scope of information processing in the normal and pathological state. C1 Med Coll Georgia, Dept Psychiat, Augusta, GA 30910 USA. RP Casanova, MF (reprint author), Med Coll Georgia, Dept Psychiat, 1515 Pope St, Augusta, GA 30910 USA. 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Arch. Psych. Clin. Neurosci. PD JUN PY 2004 VL 254 IS 3 BP 148 EP 151 DI 10.1007/s00406-004-0457-6 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 833EN UT WOS:000222319300002 PM 15205967 ER PT J AU Santosh, PJ Mijovic, A AF Santosh, PJ Mijovic, A TI Social impairment in Hyperkinetic Disorder - Relationship to psychopathology and environmental stressors SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE ADHD; HKD; PDD; social impairment; child; adolescent ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PEER INTERACTION; CHILDREN; BOYS; COMORBIDITY; ADOLESCENTS; EMOTION; AUTISM; ADHD AB Background:. There is paucity of information concerning social impairment in children and adolescents referred to mental health services. Aims:. The aim of this study was to assess the association of social impairment, psychopathology and environmental stressors in Hyperkinetic Disorder (HKD) and to determine the frequency of pervasive developmental disorder (PDD) symptoms in HKD. Method:. 'Item sheets' about children and adolescents seen in child and adolescent mental health between 1992 and 2001 (n = 3644) were used to extract nine psychopathology domains, two social impairment subtypes and nine environmental stressors. The two social impairment subtypes were relationship difficulty (RD) and social communication difficulty (SCD) (i. e. autistic-like social impairment). The association of SCD/RD, psychopathology domains and environmental stressors was investigated in HKD cases and compared to a psychiatric control group. Results:. In children and adolescents with HKD, SCD was associated with speech and language difficulties, repetitive behaviour, developmental difficulties (all symptoms of PDD), affective symptoms, conduct problems and ADHD symptoms. Relationship difficulty was linked to conduct problems, affective symptoms and environmental stressors. Unlike SCD, RD was associated with all of the environmental stressors studied. There were significantly more children with PDD symptoms in the HKD group than in the control group. Conclusion:. This study highlights the importance of subtyping social impairment in HKD and its association with psychopathology and environmental stressors. In HKD, SCD reflecting autistic social impairment is associated with other autistic symptoms, such as speech and language problems and repetitive behaviour. A small subgroup of HKD cases may have a milder form of autistic spectrum disorder. C1 Inst Psychiat, Acad Dept Child & Adolescent Psychiat, London SE5 8AF, England. 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PD JUN PY 2004 VL 13 IS 3 BP 141 EP 150 DI 10.1007/s00787-004-0372-4 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 837OJ UT WOS:000222644500002 PM 15254841 ER PT J AU Humphrey, A Williams, J Pinto, E Bolton, PF AF Humphrey, A Williams, J Pinto, E Bolton, PF TI A prospective longitudinal study of early cognitive development in tuberous sclerosis - A clinic based study SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE tuberous sclerosis; mental retardation; epilepsy ID EARLY INTERVENTION; EPILEPSY; COMPLEX; INFANTS; AUTISM; DISORDERS; SEIZURES; CHILDREN; PROGRAM AB We report a prospective longitudinal study of cognitive development in a series of 20 clinic-referred infants with Tuberous Sclerosis. The infants were seen between the ages of 11 and 37 months and were assessed regularly at 6-month periods using a within-subjects repeated measures design. Assessment using the Mullen Scales of Early Learning, a measure of cognitive and motor showed that with the exception of one child, all children had composite developmental quotients that fell into the mentally retarded range of intellectual functioning. In general, the infants' developmental quotients changed little between 12 and 36 months of age. Developmental progress was evident; however, with small incremental changes in raw scores for subjects over the course of the study. In three children, the developmental quotient changed by more than 20 points during the course of the study. The findings are considered in relation to the neurobiological risk factors for cognitive development in Tuberous Sclerosis. C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ E Anglia, Dept Clin Physiol, Norwich NR4 7TJ, Norfolk, England. Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Appl Med Stat, Cambridge CB2 1TN, England. 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Child Adolesc. Psych. PD JUN PY 2004 VL 13 IS 3 BP 159 EP 165 DI 10.1007/s00787-004-0383-1 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 837OJ UT WOS:000222644500004 PM 15254843 ER PT J AU Martin, LA Escher, T Goldowitz, D Mittleman, G AF Martin, LA Escher, T Goldowitz, D Mittleman, G TI A relationship between cerebellar Purkinje cells and spatial working memory demonstrated in a lurcher/chimera mouse model system SO GENES BRAIN AND BEHAVIOR LA English DT Article DE ataxia; cerebellum; cognition; delayed matching; DMTP; motor ID SHORT-TERM-MEMORY; INFANTILE-AUTISM; AGED RATS; MICE; LANGUAGE; LESIONS; CORTEX; BRAIN AB New emphasis has been placed upon cerebellar research because of recent reports demonstrating involvement of the cerebellum in non-motor cognitive behaviors. Included in the growing list of cognitive functions associated with cerebellar activation is working memory. In this study, we explore the potential role of the cerebellum in spatial working memory using a mouse model of Purkinje cell loss. Specifically, we make aggregation chimeras between heterozygous lurcher (Lc/+) mutant embryos and +/+ (wildtype) embryos and tested them in the delayed matching-to-position (DMTP) task. Lc/+ mice lose 100% of their Purkinje cells postnatally due to a cell-intrinsic gain-of-function mutation. Lc/+<->+/+ chimeras therefore have Purkinje cells ranging from 0 to normal numbers. Through histological examination of chimeric mice and observations of motor ability, we showed that ataxia is dependent upon both the number and distribution of Purkinje cells in the cerebellum. In addition, we found that Lc/+ mice, with a complete loss of Purkinje cells, have a generalized deficit in DIVITP performance that is probably associated with their motor impairment. Finally, we found that Lc/+<->+/+ chimeric mice, as a group, did not differ from control mice in this task. Rather, surprisingly, analysis of their total Purkinje cells and performance in the DIVITP task revealed a significant negative relationship between these two variables. Together, these findings indicate that the cerebellum plays a minor or indirect role in spatial working memory. C1 Univ Calif Davis, MIND Inst, Dept Psychiat & Behav Sci, Davis, CA 95616 USA. Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. Univ Tennessee, Hlth Sci Ctr, Dept Anat & Neurobiol, Memphis, TN USA. RP Martin, LA (reprint author), Univ Calif Davis, MIND Inst, Dept Psychiat & Behav Sci, 1 Shields Ave, Davis, CA 95616 USA. 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PD JUN PY 2004 VL 3 IS 3 BP 158 EP 166 DI 10.1111/j.1601-183x.2004.00067.x PG 9 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 827IQ UT WOS:000221893300004 PM 15140011 ER PT J AU Bonnet-Brilhault, E Gomot, M Blanc, R Raynaud, M Lemonnier, E Andres, C Barthelemy, C Moraine, C Briault, S AF Bonnet-Brilhault, E Gomot, M Blanc, R Raynaud, M Lemonnier, E Andres, C Barthelemy, C Moraine, C Briault, S TI A mutation in the NLGN4 gene, implicated in the glutamatergic transmission, is associated with X-linked mental retardation and autism SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Univ Hosp, INSERM, U619, Tours, France. Univ Brest, Brest, France. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S475 EP S475 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663002578 ER PT J AU Corbett, B Medoza, SP Levine, S AF Corbett, B Medoza, SP Levine, S TI Cortisol dysregulation in children with autism SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Univ Calif Davis, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S298 EP S299 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663001529 ER PT J AU Dhossche, D AF Dhossche, D TI A GABA hypothesis of autism SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Univ Mississippi, Ctr Med, University, MS 38677 USA. CR Blatt GJ, 2001, J AUTISM DEV DISORD, V31, P537, DOI 10.1023/A:1013238809666 DHOSSCHE D, 2002, ELEVATED PLASMA GABA, P6 Fatemi SH, 2002, BIOL PSYCHIAT, V52, P805, DOI 10.1016/S0006-3223(02)01430-0 ROLF LH, 1993, ACTA PSYCHIAT SCAND, V87, P312, DOI 10.1111/j.1600-0447.1993.tb03378.x NR 4 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S218 EP S219 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663001234 ER PT J AU Hendry, JD DeVito, T Gelman, N Rajakumar, N Williamson, P Pavlosky, W Drost, DJ Nicolson, R AF Hendry, JD DeVito, T Gelman, N Rajakumar, N Williamson, P Pavlosky, W Drost, DJ Nicolson, R TI The limbic system in autism: Tissue abnormalities detected through transverse relaxation time imaging SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Univ Western Ontario, London, ON N6A 3K7, Canada. RI Nicolson, Robert/E-4797-2011 NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S472 EP S472 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663002567 ER PT J AU Lazarev, VV Genofre, MA Pontes, A deAzevedo, L AF Lazarev, VV Genofre, MA Pontes, A deAzevedo, L TI Electroencephalographic photic driving and functional alterations in partial epilepsy and autism in children SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Oswaldo Cruz Fdn, Rio De Janeiro, Brazil. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S447 EP S448 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663002477 ER PT J AU McDougle, CJ AF McDougle, CJ TI Pharmacotherapy of autism SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Indiana Univ, Sch Med, Dept Psychiat, Bloomington, IN 47405 USA. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S42 EP S42 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663000159 ER PT J AU Nicolson, R Smith, J AF Nicolson, R Smith, J TI An open label trial of galantamine in the treatment of children and adolescents with autism SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 Univ Western Ontario, London, ON N6A 3K7, Canada. RI Nicolson, Robert/E-4797-2011 NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S274 EP S275 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663001441 ER PT J AU Wicker, B Hubert, B Gepner, B Tardif, C Deruelle, C AF Wicker, B Hubert, B Gepner, B Tardif, C Deruelle, C TI The emotional brain in autism: Effective connectivity analysis of brain regions involved in explicit facial emotion processing SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 24th CINP Congress CY JUN 20-24, 2004 CL Paris, FRANCE SP CINP C1 CNRS, Inst Neurosci Physiol & Cognit, Marseille, France. Hop Montperrin, Aix En Provence, France. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUN PY 2004 VL 7 SU 1 BP S21 EP S21 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 864WF UT WOS:000224663000076 ER PT J AU Bourret, J Vollmer, TR Rapp, JT AF Bourret, J Vollmer, TR Rapp, JT TI Evaluation of a vocal mand assessment and vocal mand training procedures SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE developmental disabilities; language; mands; response class ID BEHAVIORAL CUSPS; REINFORCEMENT; CHILDREN AB A common deficiency in the verbal repertoires of individuals with autism and related disorders is the absence of socially appropriate vocal mands. The vocal mand repertoires of these individuals may be lacking in several respects: (a) The individual might engage in no mands whatsoever, (b) the mand might be topographically dissimilar to an appropriate response, (c) the mand might be only partially topographically similar to an appropriate response, and (d) the mand might occur only after prompting. Depending on specific deficiencies in an individuals repertoire, different procedures for establishing appropriate mands may be needed. The purpose of Study 1was to evaluate an assessment prior to teaching vocal mands for 3 individuals with developmental disabilities. The assessment showed that I individual displayed partial utterances of mands, I displayed vocal mands after mands had been reinforced, and I displayed vocal mands when prompted. Thus, in Study 2, a different teaching strategy was tested for each individual. Results showed that the assessment information could be linked directly to mand training for all 3 participants. 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PD SUM PY 2004 VL 37 IS 2 BP 129 EP 144 DI 10.1901/jaba.2004.37-129 PG 16 WC Psychology, Clinical SC Psychology GA 836TW UT WOS:000222579700001 PM 15293633 ER PT J AU Harding, JW Wacker, DP Berg, WK Rick, G Lee, JF AF Harding, JW Wacker, DP Berg, WK Rick, G Lee, JF TI Promoting response variability and stimulus generalization in martial arts training SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE extinction; martial arts; response variability; stimulus generalization ID SKILLS; REINFORCEMENT; PERFORMANCE; INDIVIDUALS; FOOTBALL; PLAYERS; TENNIS; AUTISM AB The effects of reinforcement and extinction on response variability and stimulus generalization in the punching and kicking techniques of 2 martial arts students were evaluated across drill and sparring conditions. During both conditions, the students were asked to demonstrate different techniques in response to an instructor's punching attack. During baseline, the students received no feedback on their responses in either condition. During the intervention phase, the students received differential reinforcement in the form of instructor feedback for each different punching or kicking technique they performed during a session of the drill condition, but no reinforcement was provided for techniques in the sparring condition. Results showed that both students increased the number of different techniques they performed when reinforcement and extinction procedures were conducted during the drill condition, and that this increase in response variability generalized to the sparring condition. C1 Univ Iowa, Iowa City, IA 52242 USA. RP Harding, JW (reprint author), 197 Glenn Dr, Iowa City, IA 52245 USA. 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Appl. Behav. Anal. PD SUM PY 2004 VL 37 IS 2 BP 185 EP 195 DI 10.1901/jaba.2004.37-185 PG 11 WC Psychology, Clinical SC Psychology GA 836TW UT WOS:000222579700005 PM 15293637 ER PT J AU Roane, HS Fisher, WW Sgro, GM Falcomata, TS Pabico, RR AF Roane, HS Fisher, WW Sgro, GM Falcomata, TS Pabico, RR TI An alternative method of thinning reinforcer delivery during differential reinforcement SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; differential reinforcement; reinforcement thinning ID TOLERANCE AB Differential reinforcement of alternative behavior (DRA) may result in rates of reinforcement that are impractical for caregivers to implement; therefore, recent research has examined methods for thinning reinforcer delivery during DRA. In this study, reinforcer delivery was thinned during DRA by restricting access to the participant's alternative response materials. C1 Marcus Inst, Atlanta, GA 30329 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Emory Univ, Sch Med, Atlanta, GA 30322 USA. RP Roane, HS (reprint author), Marcus Inst, 1920 Briarcliff Rd, Atlanta, GA 30329 USA. EM Henry.Roane@Marcus.org CR Dixon MR, 2003, J APPL BEHAV ANAL, V36, P263, DOI 10.1901/jaba.2003.36-263 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Fisher WW, 2000, BEHAV MODIF, V24, P3, DOI 10.1177/0145445500241001 Hanley GP, 2001, J APPL BEHAV ANAL, V34, P17, DOI 10.1901/jaba.2001.34-17 Shirley MJ, 1997, J APPL BEHAV ANAL, V30, P93, DOI 10.1901/jaba.1997.30-93 NR 5 TC 17 Z9 17 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2004 VL 37 IS 2 BP 213 EP 218 DI 10.1901/jaba.2004.37-213 PG 6 WC Psychology, Clinical SC Psychology GA 836TW UT WOS:000222579700008 PM 15293640 ER PT J AU Conyers, C Miltenberger, RG Peterson, B Gubin, A Jurgens, M Selders, A Dickinson, J Barenz, R AF Conyers, C Miltenberger, RG Peterson, B Gubin, A Jurgens, M Selders, A Dickinson, J Barenz, R TI An evaluation of in vivo desensitization and video modeling to increase compliance with dental procedures in persons with mental retardation SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE compliance; medical procedures; mental retardation; video modeling ID CHILDREN; AUTISM AB Fear of dental procedures deters many individuals with mental retardation from accepting dental treatment. This study was conducted to assess the effectiveness of two procedures, in vivo desensitization and video modeling, for increasing compliance with dental procedures in participants with severe or profound mental retardation. Desensitization increased compliance for all 5 participants, whereas video modeling increased compliance for only 1 of 3 participants. C1 N Dakota State Univ, Dept Psychol, Fargo, ND 58105 USA. RP Miltenberger, RG (reprint author), N Dakota State Univ, Dept Psychol, Fargo, ND 58105 USA. CR ALLEN KD, 1987, J APPL BEHAV ANAL, V20, P381, DOI 10.1901/jaba.1987.20-381 DAVILA JM, 1990, SPECIAL CARE DENT, V6, P210 Kohlenberg R., 1972, J DENT CHILD, V39, P61 LeBlanc LA, 2003, J APPL BEHAV ANAL, V36, P253, DOI 10.1901/jaba.2003.36-253 Luscre DM, 1996, J AUTISM DEV DISORD, V26, P547, DOI 10.1007/BF02172275 MELAMED BG, 1975, J DENT RES, V54, P797, DOI 10.1177/00220345750540041701 Neumann J. K., 2000, MENT HLTH ASPECTS DE, V3, P98 NR 7 TC 17 Z9 17 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2004 VL 37 IS 2 BP 233 EP 238 DI 10.1901/jaba.2004.37-233 PG 6 WC Psychology, Clinical SC Psychology GA 836TW UT WOS:000222579700012 PM 15293644 ER PT J AU Johnson, L McComas, J Thompson, A Symons, FJ AF Johnson, L McComas, J Thompson, A Symons, FJ TI Obtained versus programmed reinforcement practical considerations in the treatment of escape-reinforced aggression SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE concurrent schedules; functional communication training; obtained reinforcement; response allocation ID BEHAVIOR; QUALITY AB This investigation provides a preliminary examination of the difference between programmed and obtained reinforcement rates and its potential influence during treatment of aggression in a natural setting. Following a functional analysis that suggested that the aggression of a boy with autism was negatively reinforced, intervention was implemented by the boy's mother. Concurrent fixed-ratio (FR) 1 FR 1 schedules of escape were arranged for manding and aggression. When mands failed to compete effectively with aggression, obtained reinforcement ratios were calculated; these indicated that obtained reinforcement varied from the programmed schedule for aggression but not for mands. Increasing the rate of prompts for mands resulted in an increase in mands and a decrease in aggression to near-zero levels. C1 Univ Minnesota, Minneapolis, MN 55455 USA. RP McComas, J (reprint author), Univ Minnesota, 224 Burton Hall,178 Pillsbury Dr SE, Minneapolis, MN 55455 USA. EM jmccomas@umn.edu CR DeLeon IG, 2000, J APPL BEHAV ANAL, V33, P73, DOI 10.1901/jaba.2000.33-73 Hanley GP, 2001, J APPL BEHAV ANAL, V34, P17, DOI 10.1901/jaba.2001.34-17 Hoch H, 2002, J APPL BEHAV ANAL, V35, P171, DOI 10.1901/jaba.2002.35-171 NEEF NA, 1992, J APPL BEHAV ANAL, V25, P691, DOI 10.1901/jaba.1992.25-691 Shirley MJ, 1997, J APPL BEHAV ANAL, V30, P93, DOI 10.1901/jaba.1997.30-93 Worsdell AS, 2000, J APPL BEHAV ANAL, V33, P167, DOI 10.1901/jaba.2000.33-167 NR 6 TC 6 Z9 6 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 2004 VL 37 IS 2 BP 239 EP 242 DI 10.1901/jaba.2004.37-239 PG 4 WC Psychology, Clinical SC Psychology GA 836TW UT WOS:000222579700013 PM 15293645 ER PT J AU Orsmond, GI Krauss, MW Seltzer, MM AF Orsmond, GI Krauss, MW Seltzer, MM TI Peer relationships and social and recreational activities among adolescents and adults with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; social activities; adolescence; adulthood ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; CHILDREN; BEHAVIOR; INITIATIONS; SUPPORT; SKILLS; LIFE AB In this study, we investigate peer relationships and participation in social and recreational activities among 235 adolescents and adults with autism who live at home. The prevalence of having friendships, peer relationships, and participating in social and recreational activities were all low and comparable to previous research. Both individual and environmental factors were investigated as predictors of having peer relationships and participation in social and recreational activities. Having peer relationships was predicted by individual characteristics (younger age, and less impairment in social interaction skills), but not by characteristics of the environment. Greater participation in social and recreational activities was predicted by characteristics of the individual with autism (greater functional independence, less impairment in social interaction skills, higher levels of internalizing behaviors) and characteristics of the environment (greater maternal participation in social and recreational activities, greater number of services received, and inclusion in integrated settings while in school). C1 Boston Univ, Sargent Coll Hlth & Rehabil Sci, Boston, MA 02215 USA. Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02254 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Orsmond, GI (reprint author), Boston Univ, Sargent Coll Hlth & Rehabil Sci, Boston, MA 02215 USA. EM gorsmond@bu.edut CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ATTWOOD A, 1988, J AUTISM DEV DISORD, V18, P241, DOI 10.1007/BF02211950 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Bruininks R. H., 1986, INVENTORY CLIENT AGE Church C., 2000, FOCUS AUTISM OTHER D, V15, P12, DOI DOI 10.1177/108835760001500102 DEMYER MK, 1981, SCHIZOPHRENIA BULL, V7, P388 Duncan D, 1999, RES DEV DISABIL, V20, P441, DOI 10.1016/S0891-4222(99)00024-4 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 KONGING C, 2001, AUTISM, V5, P23 KRAUSS MW, 1992, AM J MENT RETARD, V96, P432 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lee S, 1996, J ASSOC PERS SEVERE, V21, P88 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 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x LORD C, 1990, BEHAVIOR DISORDERS OF ADOLESCENCE, P155 LORD C, 1995, DEV PSYCHOPATHOL, V7, P611 LORD C, 1986, J AUTISM DEV DISORD, V16, P249, DOI 10.1007/BF01531658 Marks SU, 2000, J ASSOC PERS SEVERE, V25, P3, DOI 10.2511/rpsd.25.1.3 Mesibov G. B., 1983, AUTISM ADOLESCENTS A, P37 Mesibov GB, 1997, HDB AUTISM PERVASIVE, P309 OKE NJ, 1990, J AUTISM DEV DISORD, V20, P479, DOI 10.1007/BF02216054 Persson B, 2000, J AUTISM DEV DISORD, V30, P61, DOI 10.1023/A:1005464128544 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 Ruble L. A., 1996, FOCUS AUTISM OTHER D, V11, P3 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 Seltzer MM, 2001, INT REV RES MENT RET, V23, P267 Seltzer MM, 2003, J AUTISM DEV DISORD, V33, P565, DOI 10.1023/B:JADD.0000005995.02453.0b SELTZER MM, 1989, AM J MENT RETARD, V94, P303 Seltzer MM, 1999, IMPROVING THE COMMUNICATION OF PEOPLE WITH DOWN SYNDROME, P217 Sigman M., 1999, MONOGRAPHS SOC RES C, V64 SNELL ME, 1997, QUALITY LIFE, V2, P43 STONE WL, 1990, J AUTISM DEV DISORD, V20, P437, DOI 10.1007/BF02216051 Sweet J. A., 1987, NATL SURVEY FAMILIES Travis LL, 1998, MENT RETARD DEV D R, V4, P65, DOI 10.1002/(SICI)1098-2779(1998)4:2<65::AID-MRDD2>3.0.CO;2-W Volkmar F., 1997, HDB AUTISM PERVASIVE, P173 Volkmar F. R., 1995, UNDERSTANDING OTHER, P40 VOLKMAR FR, 1987, J CHILD PSYCHOL PSYC, V28, P365, DOI 10.1111/j.1469-7610.1987.tb01758.x VOLKMAR FR, 1993, J AM ACAD CHILD PSY, V32, P627, DOI 10.1097/00004583-199305000-00020 *WHO, 1992, ICD 10 CLASSMENT BEH WILLIAMS TI, 1989, J AUTISM DEV DISORD, V19, P143, DOI 10.1007/BF02212726 NR 43 TC 127 Z9 129 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 2004 VL 34 IS 3 BP 245 EP 256 DI 10.1023/B:JADD.0000029547.96610.df PG 12 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500002 PM 15264493 ER PT J AU Iarocci, G Burack, JA AF Iarocci, G Burack, JA TI Intact covert orienting to peripheral cues among children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE selective attention; visual orienting; filtering; autism ID SPATIAL ATTENTION; CONFIDENCE-INTERVALS; SELECTIVE ATTENTION; DEFICITS; ABNORMALITY; CEREBELLAR AB The focus of the present study was to examine covert orienting responses to peripheral. ash cues among children with autism in a situation where attentional processes were taxed by the presence of distractors in the visual field. Fourteen children with autism (MA=6-7 years) were compared to their MA-matched peers without autism on a forced choice RT covert orienting paradigm. The task conditions varied with regard to the target location, the validity of the cue, and the presence or absence of distractors. The results showed no group differences as both children with autism and their MA-matched peers showed similar effects of cue validity and distractors. These findings are inconsistent with the view that orienting is generally impaired in children with autism. C1 Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada. McGill Univ, Dept Educ Psychol, Montreal, PQ H3A 2T5, Canada. RP Iarocci, G (reprint author), Simon Fraser Univ, Dept Psychol, 8888 Univ Dr, Burnaby, BC V5A 1S6, Canada. EM giarocci@sfu.ca CR AKHTAR N, 1989, J EXP CHILD PSYCHOL, V48, P315, DOI 10.1016/0022-0965(89)90008-8 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Brodeur D., 1997, ATTENTION DEV PSYCHO, P74 Brodeur DA, 1997, CAN J EXP PSYCHOL, V51, P20, DOI 10.1037/1196-1961.51.1.20 Brodeur DA, 2000, COGNITIVE DEV, V15, P367, DOI 10.1016/S0885-2014(00)00025-3 BRODEUR DA, 1990, DEV ATTENTION RES TH BURACK JA, 1994, J ABNORM PSYCHOL, V103, P535, DOI 10.1037/0021-843X.103.3.535 BURACK JA, 2001, RES BASIS AUTISM IMP Burack JA, 2002, DEV PSYCHOPATHOL, V14, P225 BURACK JA, 1997, AUTISM PERVASIVE DEV COURSCHENE E, 1994, ATYPICAL COGNITIVE D Cumming G, 2001, EDUC PSYCHOL MEAS, V61, P532, DOI 10.1177/00131640121971374 Enns J. 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I., 1975, ATTENTION PERFORM, V5, P669 POSNER MI, 1980, Q J EXP PSYCHOL, V32, P3, DOI 10.1080/00335558008248231 Randolph B, 2000, INT J BEHAV DEV, V24, P167 Smithson M., 2000, STAT CONFIDENCE Townsend J, 1999, J NEUROSCI, V19, P5632 Townsend J, 2001, COGNITIVE BRAIN RES, V11, P127, DOI 10.1016/S0926-6410(00)00072-0 Townsend J, 1996, DEV PSYCHOPATHOL, V8, P563 Wainwright JA, 1996, J AUTISM DEV DISORD, V26, P423, DOI 10.1007/BF02172827 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 NR 33 TC 29 Z9 30 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2004 VL 34 IS 3 BP 257 EP 264 DI 10.1023/B:JADD.0000029548.84041.69 PG 8 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500003 PM 15264494 ER PT J AU Noland, RM Gabriels, RL AF Noland, RM Gabriels, RL TI Screening and identifying children with autism spectrum disorders in the public school system: The development of a model process SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; public school; screening; identification; legal issues; clinical issues ID DIAGNOSTIC INTERVIEW; QUESTIONNAIRE; POPULATION; VALIDITY AB Heightened public awareness of autism and increased prevalence estimates of autism spectrum disorders (ASDs) has generated a sense of urgency within the public school system to identify children with these disorders for targeted intervention. Two multidisciplinary groups of professionals, one each from two separate school districts, were identified and trained to provide diagnostic and consultative services. This paper outlines a model process for school personnel to develop a basic level of training and competence in recognizing and serving students who have an ASD by (1) providing an overview of the legal and clinical issues involved in screening for children with ASD within the school system, (2) defining a school-based professional training process and (3) outlining a school-based ASD screening process. C1 Sam Houston State Univ, Huntsville, TX 77341 USA. Univ Colorado, Hlth Sci Ctr, Boulder, CO 80309 USA. RP Noland, RM (reprint author), Sam Houston State Univ, Campus Box 2447, Huntsville, TX 77341 USA. EM psy_rmn@shsu.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 *CO DEP ED, 2000, COL RES GUID AUT SPE *CO DEP ED, 2002, ED ID AUT DRAFT POS Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 GILLBERG C, 2000, BIIOL AUTISTIC SYNDR 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 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C., 2001, AUTISM DIAGNOSTIC OB 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 MCCONAUGHY SH, 1990, HDB SCH PSYCHOL, P244 *NAT ASS SCH PSYCH, 1992, INT ASS TEAMS MOD BU Sattler J. M., 2001, ASSESSMENT CHILDREN Schopler E., 1988, CHILDHOOD AUTISM RAT SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SHATTUCK PT, 2002, 35 ANN GATL C RES TH SHATTUCK PT, 2002, 126 ANN M AM ASS MEN Shea KM, 1996, AM J PUBLIC HEALTH, V86, P1168 SIEGEL B, 1996, UNPUB PERVASIVE DEV Smith C. R., 1983, IOWA MONOGRAPH TEAL MB, 1986, J AUTISM DEV DISORD, V16, P485, DOI 10.1007/BF01531713 Willard HF, 1999, NAT GENET, V23, P127, DOI 10.1038/13751 World Health Organisation, 1992, INT CLASS DIS 10 ED Yell ML, 2000, J SPEC EDUC, V33, P205, DOI 10.1177/002246690003300403 ZIRKEL PA, 2000, NAT SAT C NAT ASS ST 2000, SPECIAL ED BONUS REP, V1, P4 NR 33 TC 11 Z9 12 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 2004 VL 34 IS 3 BP 265 EP 277 DI 10.1023/B:JADD.0000029549.84385.44 PG 13 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500004 PM 15264495 ER PT J AU Ghaziuddin, M Mountain-Kimchi, K AF Ghaziuddin, M Mountain-Kimchi, K TI Defining the intellectual profile of Asperger syndrome: Comparison with high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; neuropsychology; validity studies ID INFANTILE-AUTISM; DISORDER; VALIDITY AB Asperger syndrome (AS) is a disorder of early childhood characterized by autistic social deficits, subtle communication impairment, and excessive isolated interests. There is no history of language delay or of mental retardation. Despite its increasing popularity as a distinct condition, its diagnostic validity remains uncertain. It is still unclear to what extent AS differs from autism with normal intelligence sometimes referred to as high-functioning autism (HFA). However, some reports have suggested that persons with AS possess a distinct pro. le on tests of intelligence characterized by a high verbal IQ and a low performance IQ, whereas in most cases with HFA, the pattern is reversed. Since few studies have directly compared AS subjects with HFA controls using unmodified diagnostic criteria and standardized measures of assessment, in this report we compared 22 AS subjects with 12 HFA controls, matched on age, sex and level of intelligence. As a group, subjects with AS showed a higher verbal IQ and higher scores on information and vocabulary subtests than those with HFA. However, scores of several AS and HFA subjects showed a mixed pattern. Implications of these findings are discussed in the context of the validity of Asperger Syndrome. C1 Univ Michigan, Div Child & Adolescent Psychiat, Med Ctr, Ann Arbor, MI 48109 USA. RP Ghaziuddin, M (reprint author), Univ Michigan, Div Child & Adolescent Psychiat, Med Ctr, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. EM mghaziud@umich.edu 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 DEMYER MK, 1981, SCHIZOPHRENIA BULL, V7, P388 FEIN D, 1986, J AM ACAD CHILD PSY, V25, P198, DOI 10.1016/S0002-7138(09)60227-2 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 GHAZIUDDIN M, 1995, J AUTISM DEV DISORD, V25, P311, DOI 10.1007/BF02179292 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lincoln A. 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P, 1989, NONVERBAL LEARNING D Rutter M., 1978, AUTISM REAPPRAISAL C, P85 Sattler J.M., 1992, ASSESSMENT CHILDREN SCHOPLER E, 1998, ASPERGER SYNDROME HI, P3 Siegel DJ, 1996, J AUTISM DEV DISORD, V26, P389, DOI 10.1007/BF02172825 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D, 1997, WECHSLER ADULT INTEL, V3rd WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1993, INT CLASS DIS 10 ED NR 27 TC 79 Z9 82 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 2004 VL 34 IS 3 BP 279 EP 284 DI 10.1023/B:JADD.0000029550.19098.77 PG 6 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500005 PM 15264496 ER PT J AU Williams, JHG Whiten, A Singh, T AF Williams, JHG Whiten, A Singh, T TI A systematic review of action imitation in autistic spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE imitation; gesture; action; autism; emulation; 'mirror neurons' ID YOUNG-CHILDREN; INFANTILE-AUTISM; MOTOR IMITATION; JOINT ATTENTION; MIRROR NEURONS; PRETEND PLAY; ABILITIES; MEMORY; ACTS; MIND AB Imitative deficits have been associated with autistic spectrum disorder (ASD) for many years, most recently through more robust methodologies. A fresh, systematic review of the significance, characteristics, and underlying mechanism of the association is therefore warranted. From 121 candidates, we focused on 21 well-controlled studies involving 281 cases of ASD. Overall, children with ASD performed worse on imitative tasks (Combined Logit p value<.00005). The emerging picture is of delayed development in imitation, implicating a deficit in mapping neural codings for actions between sensory and motor modalities, rather than in motivation or executive function. We hypothesise that ASD is characterised by abnormal development of these mappings, such that they are biased towards object-oriented tasks at the expense of those required for action imitation per se. C1 Univ Aberdeen, Dept Child Hlth, Sch Med, Aberdeen AB25 2ZD, Scotland. Univ St Andrews, Sch Psychol, St Andrews, Fife, Scotland. Torbay Hosp, Torquay, England. RP Williams, JHG (reprint author), Univ Aberdeen, Dept Child Hlth, Sch Med, Aberdeen AB25 2ZD, Scotland. 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PD JUN PY 2004 VL 34 IS 3 BP 285 EP 299 DI 10.1023/B:JADD.0000029551.56735.3a PG 15 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500006 PM 15264497 ER PT J AU Lawson, J Baron-Cohen, S Wheelwright, S AF Lawson, J Baron-Cohen, S Wheelwright, S TI Empathising and systemising in adults with and without Asperger Syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE empathising; systemising; autism; Asperger Syndrome; theory of mind ID HIGH-FUNCTIONING AUTISM; SEX-DIFFERENCES; CENTRAL COHERENCE; MIND; CHILDREN; METAANALYSIS AB An experiment was devised to test the empathising-systemising (E-S) theory of autism. Three groups of participants took part in the study: males with Asperger Syndrome ( AS) (n=18), males without AS, (n=44) and females from the general population (n=45). Each participant completed two tasks: one that involved empathising and another that involved systemising. On the empathising task, females scored significantly higher than control males who in turn scored higher than males with AS. Conversely, females scored significantly lower than both male groups on the systemising task, who did not differ significantly from each other. These results are in line with both the E-S theory of autism and the 'extreme male brain' theory of autism. Alternative explanations of the results are also explored, including an interpretation through the idea of open and closed systems. C1 Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge CB2 2AH, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 2AH, England. RP Lawson, J (reprint author), Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Autism Dev. Disord. PD JUN PY 2004 VL 34 IS 3 BP 301 EP 310 DI 10.1023/B:JADD.0000029552.42724.1b PG 10 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500007 PM 15264498 ER PT J AU Martin, I McDonald, S AF Martin, I McDonald, S TI An exploration of causes of non-literal language problems in individuals with Asperger Syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger Syndrome; Theory of Mind; central coherence; irony ID HIGH-FUNCTIONING AUTISM; WEAK CENTRAL COHERENCE; WILLIAMS-SYNDROME; EXECUTIVE FUNCTION; MIND; CHILDREN; ABILITIES; PERFORMANCE; COMPETENCE; PRECEDENCE AB Individuals with Asperger Syndrome (AS), a high functioning variant of Autism, are often noted to possess intact language ability, yet fail to use this language capacity to engage in interactive communication. This difficulty using language in a social context has been referred to as a deficit in pragmatic language. In particular, difficulty understanding non-literal language devices, such as irony has been observed. This paper examines the veracity of two theories that have attempted to explain the causes of pragmatic language difficulties in individuals with Asperger Syndrome; the theory of Weak Central Coherence (WCC) and Social Inference theory. Fourteen young adults with AS and 24 age-matched controls were assessed on cognitive tasks measuring WCC processes, social inference or Theory of Mind ability, and the ability to interpret ironic remarks. Results indicated that the ability to understand the belief states of others is critical to understanding ironic language in AS. C1 Univ New S Wales, Sch Psychol, Sydney, NSW 2052, Australia. Univ New S Wales, Sydney, NSW, Australia. RP McDonald, S (reprint author), Univ New S Wales, Sch Psychol, Sydney, NSW 2052, Australia. 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Autism Dev. Disord. PD JUN PY 2004 VL 34 IS 3 BP 311 EP 328 DI 10.1023/B:JADD.0000029553.52889.15 PG 18 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500008 PM 15264499 ER PT J AU Goldstein, S Schwebach, AJ AF Goldstein, S Schwebach, AJ TI The comorbidity of pervasive developmental disorder and attention deficit hyperactivity disorder: Results of a retrospective chart review SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE PDD; ADHD; inattentiveness; comorbidity ID AUTISTIC-CHILDREN; NALTREXONE; ADHD AB Objective: To determine if a sample of children meeting diagnostic criteria for a Pervasive Developmental Disorder (PDD) display symptoms and impairment related to Attention Deficit Hyperactivity Disorder (ADHD) sufficient to warrant a comorbid diagnosis of ADHD. Further, do children with PDD displaying such symptoms demonstrate more impairment in daily life activities than those children only having PDD? Method: A retrospective chart review was conducted on children (N=57) diagnosed with the PDD's of Autism or PDD-Not Otherwise Specified (PDD-NOS), or ADHD. Comparative analysis of questionnaire and neuropsychological test data was completed to determine the severity of ADHD-like symptoms presenting among children with PDD. Results: From the pool of subjects having PDD with sufficient data (N=27), 7 or 26% met DSM-IV criteria for the combined type of ADHD. Nine or 33% met diagnostic criteria for the Inattentive Type of ADHD and 11 or 41% did not demonstrate a significant number of ADHD symptoms to warrant a comorbid diagnosis of ADHD. Results indicate that a subgroup of children with PDD displaying significant ADHD-like symptoms may in fact have ADHD thus warranting a comorbid diagnosis of ADHD. Current data did not suggest children with PDD and the combined type of ADHD demonstrated significantly more impairment in daily life functioning than those children only having PDD. However, this appeared likely the result of small sample size. The data, however, does indicate such children experience more difficulties in daily situations as rated by parents and teachers. Conclusion: These findings reinforce clinical observations indicating that some children with PDD may also experience an independent comorbid condition of ADHD, suggesting that a comorbid diagnosis of ADHD with PDD be considered in such cases. If further findings are replicated, the current exclusionary DSM-IV-TR criteria of making such a comorbid diagnosis should be re-considered. C1 Univ Utah, Salt Lake City, UT 84112 USA. RP Goldstein, S (reprint author), Neurol Learning & Behav Ctr, 230 South 500 East,Suite 100, Salt Lake City, UT 84102 USA. EM info@samgoldstein.com CR Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barkley R. 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PD JUN PY 2004 VL 34 IS 3 BP 329 EP 339 DI 10.1023/B:JADD.0000029554.46570.68 PG 11 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500009 PM 15264500 ER PT J AU Kurita, H Osada, H Miyake, Y AF Kurita, H Osada, H Miyake, Y TI External validity of childhood disintegrative disorder in comparison with autistic disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; childhood disintegrative disorder; disintegrative psychosis; pervasive developmental disorder; regression ID FOLLOW-UP; RATING-SCALE; DSM-IV; PSYCHOSIS; CHILDREN; ABILITY; CARS AB To examine the external validity of DSM-IV childhood disintegrative disorder (CDD), 10 children (M=8.2 yrs) with CDD and 152 gender- and age-matched children with autistic disorder (AD) were compared on 24 variables. The CDD children had a significantly higher rate of epilepsy, significantly less uneven intellectual functioning, and a tendency of greater abnormality in auditory responsiveness than AD children, to validate CDD externally. Their short-term outcome, as shown in the degree of retardation, was not worse than the AD children, which is in disagreement with previous studies reporting worse outcomes in CDD than autism. These results need to be verified by a long-term prospective study that compares CDD and AD patients from infancy. C1 Univ Tokyo, Dept Mental Hlth, Fac Med, Bunkyo Ku, Tokyo 1130033, Japan. Natl Inst Mental Hlth, Div Stat Anal, Natl Ctr Neurol & Psychiat, Ichikawa, Japan. RP Kurita, H (reprint author), Univ Tokyo, Dept Mental Hlth, Fac Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. EM hkurita@m.u-tokyo.ac.jp CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DIAGN STAT MAN MENT BAILEY A, 1995, PSYCHOL MED, V25, P63 BARTAK L, 1976, J AUTISM CHILD SCHIZ, V6, P109, DOI 10.1007/BF01538054 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 Burd L, 1998, DEV MED CHILD NEUROL, V40, P702 CANTWELL DP, 1994, CHILD ADOL PSYCH CL, P3 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 EVANSJONES LG, 1978, DEV MED CHILD NEUROL, V20, P462 Heller Theodore, 1908, Z ERFORSCH BEHANDL J, V2, P17 HILL AE, 1986, DEV MED CHILD NEUROL, V28, P34 KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 KURITA H, 1988, JPN J PSYCHIAT NEUR, V42, P785 KURITA H, 1989, J AUTISM DEV DISORD, V19, P389, DOI 10.1007/BF02212937 KURITA H, 2003, PSYCHIAT CLIN NEUROS, V57, P233 LOCKYER L, 1970, BRIT J SOC CLIN PSYC, V9, P152 Malhotra S, 2002, EUR CHILD ADOLES PSY, V11, P108, DOI 10.1007/s00787-002-0270-6 Malhotra S, 1993, Acta Paedopsychiatr, V56, P37 Mouridsen SE, 1998, BRIT J PSYCHIAT, V172, P263, DOI 10.1192/bjp.172.3.263 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x TSUMORI M, 1961, NYUYOJI SEISHINHATTA TSUMORI M, 1965, NYUYOJI SEISHINHATTA VOLKMAR FR, 1992, J AUTISM DEV DISORD, V22, P625, DOI 10.1007/BF01046331 VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P717, DOI 10.1111/j.1469-7610.1989.tb00784.x *WHO, 1977, INT CLASS DIS 1975 R, V1 *WHO, 1989, ICD 10 CHAP 5 MENT B WHO, 1993, ICD 10 CLASS MENT BE NR 29 TC 13 Z9 13 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 2004 VL 34 IS 3 BP 355 EP 362 DI 10.1023/B:JADD.0000029556.25869.71 PG 8 WC Psychology, Developmental SC Psychology GA 825GQ UT WOS:000221744500011 PM 15264502 ER PT J AU Di Martino, A Melis, G Cianchetti, C Zuddas, A AF Di Martino, A Melis, G Cianchetti, C Zuddas, A TI Methylphenidate for pervasive developmental disorders: Safety and efficacy of acute single dose test and ongoing therapy: An open-pilot study SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; AUTISM RATING-SCALE; STIMULANT MEDICATION; SCHIZOPHRENIC CHILDREN; CHILDHOOD DISORDERS; INFANTILE-AUTISM; PHARMACOTHERAPY; PATTERNS; ADHD; PREVALENCE AB Objective: The aim of this study was to investigate the effects of ongoing methylphenidate (MPH) on ADHD-related and autistic symptoms in Pervasive Developmental Disorders (PDD) in children who did not present any adverse effects to an initial acute dose administered at the clinic. Methods: Participants included 13 subjects (12 males, with a mean age of 7.9 years) with PDD and moderate to severe hyperactivity/impulsivity. The severity of the symptoms assessment was based on Clinical Global Impression (CGI), Childhood Autism, Child Psychiatric and Conners Parent and Teacher Rating Scales (CPRS). Scores at baseline, and after 1 and 3 months of treatment, were compared to intent-to-treat analyses. Results: One (1) hour after a single MPH dose (0.4 mg/kg), 5 subjects exhibited increased hyperactivity, stereotypes, dysphoria, or motor tics and were rated as minimally or much worse on the CGI Global Improvement Scale. They received no further treatment with MPH. Four (4) of the remaining subjects were rated as improved, and four as unchanged; they proceeded to a 12-week open trial of MPH. Two children remained unchanged: they discontinued treatment after 1 week on maximally tolerated doses. However, in group analyses, behavioral measures of hyperactivity and impulsivity improved significantly, while autism core symptom measures were unaffected. No significant adverse effects were observed in any of the 8 subjects. Conclusions: Administering a single MPH test dose may be useful in identifying children with PDD who may benefit from prolonged therapy. C1 Univ Cagliari, Dept Neurosci, I-09124 Cagliari, Italy. NYU, Ctr Child Study, Inst Pediat Neurosci, New York, NY USA. RP Zuddas, A (reprint author), Univ Cagliari, Dept Neurosci, Via Osped 119, I-09124 Cagliari, Italy. EM azuddas@unica.it RI Di Martino, Adriana/L-2497-2014 CR AMAN M, 1988, J AM ACAD CHILD PSY, V27, P821, DOI 10.1097/00004583-198811000-00037 AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 Aman MG, 1996, RES DEV DISABIL, V17, P417, DOI 10.1016/S0891-4222(96)00023-6 Aman MG, 2000, J AUTISM DEV DISORD, V30, P451, DOI 10.1023/A:1005559725475 American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th BIRMAHER B, 1988, J AM ACAD CHILD PSY, V27, P248, DOI 10.1097/00004583-198803000-00020 CAMPBELL M, 1972, J AUTISM CHILD SCHIZ, V2, P343, DOI 10.1007/BF01538168 CAMPBELL M, 1976, CURR THER RES CLIN E, V19, P70 CAMPBELL M, 1985, PSYCHOPHARMACOL BULL, V21, P1047 Castellanos FX, 1997, J AM ACAD CHILD PSY, V36, P589, DOI 10.1097/00004583-199705000-00008 Conners C. K., 1997, CONNERS RATING SCALE DILALLA DL, 1994, J AUTISM DEV DISORD, V24, P115, DOI 10.1007/BF02172092 GELLER B, 1981, AM J PSYCHIAT, V138, P388 HANDEN BL, 1991, J AM ACAD CHILD PSY, V30, P241, DOI 10.1097/00004583-199103000-00012 Handen BL, 2000, J AUTISM DEV DISORD, V30, P245, DOI 10.1023/A:1005548619694 Langworthy-Lam KS, 2002, J CHILD ADOL PSYCHOP, V12, P311, DOI 10.1089/104454602762599853 LOVAAS OI, 1979, PSYCHOL BULL, V86, P1236, DOI 10.1037//0033-2909.86.6.1236 Martin A, 1999, J AM ACAD CHILD PSY, V38, P923, DOI 10.1097/00004583-199907000-00024 McDougle CJ, 2002, J AM ACAD CHILD PSY, V41, P1380, DOI 10.1097/01.CHI.0000024860.60748.88 Jensen PS, 1999, ARCH GEN PSYCHIAT, V56, P1073 Mundry R, 1998, ANIM BEHAV, V56, P256, DOI 10.1006/anbe.1998.0756 National Institute of Mental Health (NIMH), 1985, PSYCHOPHARMACOL BULL, V21, P1077 Nicolson R, 2000, J AUTISM DEV DISORD, V30, P461, DOI 10.1023/A:1005511809545 NIMH, 1985, PSYCHOPHARMACOL BULL, V21, P839 OVERALL JE, 1988, J CLIN PSYCHOL, V44, P708, DOI 10.1002/1097-4679(198809)44:5<708::AID-JCLP2270440507>3.0.CO;2-T QUINTANA H, 1995, J AUTISM DEV DISORD, V25, P283, DOI 10.1007/BF02179289 REALMUTO GM, 1989, J CLIN PSYCHOPHARM, V9, P122, DOI 10.1097/00004714-198904000-00009 Roid G, 1996, LEITER INT PERFORMAN Santosh PJ, 2000, EUR CHILD ADOLES PSY, V9, P27 SCHMIDT K, 1982, J DEV BEHAV PEDIATR, V3, P244, DOI 10.1097/00004703-198212000-00014 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SHAFFER D, 1983, ARCH GEN PSYCHIAT, V40, P1228 Spencer T, 1996, J AM ACAD CHILD PSY, V35, P409, DOI 10.1097/00004583-199604000-00008 SPORN A, 1981, AM J PSYCHIAT, V138, P997 STRAYHORN J, 1989, J AM ACAD CHILD PSY, V28, P299, DOI 10.1097/00004583-198903000-00031 VITRIOL C, 1981, AM J PSYCHIAT, V138, P1517 VOLKMAR FR, 1985, CLIN PEDIATR, V24, P127, DOI 10.1177/000992288502400301 Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D., 1967, MANUAL WECHSLER PRES NR 39 TC 34 Z9 36 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD SUM PY 2004 VL 14 IS 2 BP 207 EP 218 DI 10.1089/1044546041649011 PG 12 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 843MK UT WOS:000223087800007 PM 15319018 ER PT J AU Findling, RL McNamara, NK Gracious, BL O'Riordan, MA Reed, MD Demeter, C Blumer, JL AF Findling, RL McNamara, NK Gracious, BL O'Riordan, MA Reed, MD Demeter, C Blumer, JL TI Quetiapine in nine youths with autistic disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; RATING-SCALE; OPEN-LABEL; RISPERIDONE TREATMENT; INFANTILE-AUTISM; CHILDREN; HALOPERIDOL; ADOLESCENTS; TRIAL; PLACEBO AB Objective: The aim of this study was to examine the effectiveness of quetiapine in adolescents suffering from autistic disorder (AD). Methods: This was a 12-week, open-label study, for which medically healthy patients with AD between the ages of 10 and 17 years were eligible. Quetiapine treatment was gradually increased over the first 6 weeks of the study, to a total daily dose of 300 mg/day. Doses could then be increased to a maximum daily dose of 750 mg/day. Outcome measures included the Children's Psychiatric Rating Scale (CPRS) and the Clinical Global Impressions (CGI) scale. Results: Nine (9) males were enrolled. Six (6) patients had previously been treated with other psychotropic agents. Although improvements in several symptom domains were observed on quetiapine, only 2 patients met a priori criteria for response ("much" or "very much improved" on the Clinical Global Impressions-Improvement Scale). In addition, only these same 2 patients' parents/guardians chose to continue quetiapine pharmacotherapy after study participation. Conclusions: These data suggest that quetiapine may not be a particularly effective agent in the treatment of adolescent patients with AD. However, should future studies be performed, it seems reasonable that they be conducted with more rigor, less treatment-resistant cohorts, and, possibly, a different dosing strategy. C1 Case Western Reserve Univ, Univ Hosp Cleveland, Dept Psychiat, Cleveland, OH 44106 USA. Case Western Reserve Univ, Univ Hosp Cleveland, Dept Pediat, Cleveland, OH 44106 USA. Case Western Reserve Univ, Univ Hosp Cleveland, Dept Pharmacol, Cleveland, OH 44106 USA. RP Findling, RL (reprint author), Case Western Reserve Univ, Univ Hosp Cleveland, Dept Psychiat, 11100 Euclid Ave, Cleveland, OH 44106 USA. 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Child Adolesc. Psychopharmacol. PD SUM PY 2004 VL 14 IS 2 BP 287 EP 294 DI 10.1089/1044546041649129 PG 8 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 843MK UT WOS:000223087800014 PM 15319025 ER PT J AU Bate, JF AF Bate, JF TI Neurologic complications of immunization SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID GUILLAIN-BARRE-SYNDROME; HEPATITIS-B VACCINATION; MULTIPLE-SCLEROSIS; PERTUSSIS IMMUNIZATION; INFLUENZA VACCINATION; MEASLES ENCEPHALITIS; RABIES VACCINE; UNITED-STATES; AUTISM; RISK AB In the United States and many other developed countries, active immunization of children has virtually eliminated poliomyelitis, measles, rubella, tetanus, and other diseases, such as disease due to Haemophilus influenzae type b. Individual vaccines can produce systemic or neurologic reactions ranging from minor events, such as pain and erythema at the injection site, to major complications, such as seizures, shock, encephalopathy, or death. Immunization programs have also generated considerable controversy, as witnessed by recent concerns regarding the relationship between vaccines or their constituents and autism or multiple sclerosis. This review summarizes current information regarding vaccines, the diseases that they prevent, and the potential relationships between vaccines and neurologic disease. C1 Univ Utah, Div Pediat Neurol, Dept Pediat, Primary Childrens Med Ctr,Sch Med, Salt Lake City, UT 84113 USA. Univ Utah, Div Pediat Neurol, Dept Neurol, Sch Med, Salt Lake City, UT 84113 USA. RP Bate, JF (reprint author), Univ Utah, Div Pediat Neurol, Dept Pediat, Primary Childrens Med Ctr,Sch Med, Suite 2700,100 N Med Dr, Salt Lake City, UT 84113 USA. 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Child Neurol. PD JUN PY 2004 VL 19 IS 6 BP 405 EP 412 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 850RX UT WOS:000223631200002 ER PT J AU Serajee, FJ Nabi, R Zhong, HL Mahbubul, AHM AF Serajee, FJ Nabi, R Zhong, HL Mahbubul, AHM TI Polymorphisms in xenobiotic metabolism genes and autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID GENOMIC SCREEN; LINKAGE DISEQUILIBRIUM; POPULATION; DISORDER; ASSOCIATION; METALLOTHIONEIN; IDENTIFICATION; MEASLES; TESTS; POWER AB Autism is a neurodevelopmental syndrome defined by deficits in social reciprocity and communication and by unusual repetitive behaviors. Although there is an underlying genetic predisposition, the etiology of autism is currently unknown. A recent increase in prevalence suggests that genetically determined vulnerability to environmental exposure might contribute to the causation of autism. We performed family-based association studies of polymorphisms in metal-regulatory transcription factor 1(MTF1), a multispecific organic anion transporter (ABCC1), proton-coupled divalent metal ion transporters (SLC11A3 and SLC11A2), paraoxonase 1 (PON1), and glutathione S-transferase (GSTP1) genes in 196 autistic disorder families. There was deviation from the expected pattern of transmission for polymorphisms in MTF1 (Single nucleotide polyinorphism database reference identification number, dbSNP rs3790625, P = .02) and divalent metal ion transporter SLC11A3 (dbSNP rs2304704, P = .07) genes. Although these results might represent chance finding, further investigations of genetic variations of metal metabolism in autism are warranted. C1 Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA. Wayne State Univ, Dept Neurol, Detroit, MI 48202 USA. RP Mahbubul, AHM (reprint author), Childrens Hosp Michigan, Div Neurol, 3901 Beaubien Blvd, Detroit, MI 48201 USA. EM ahuq@med.wayne.edu CR Abecasis GR, 2002, NAT GENET, V30, P97, DOI 10.1038/ng786 Abecasis GR, 2000, BIOINFORMATICS, V16, P182, DOI 10.1093/bioinformatics/16.2.182 Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett S, 1999, AM J MED GENET, V88, P609 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Blatter Garin Marie-Claude, 1994, Biochemical Journal, V304, P549 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Chen WM, 2001, GENET EPIDEMIOL, V21, P53, DOI 10.1002/gepi.1018 Edelson SB, 1998, TOXICOL IND HEALTH, V14, P553, DOI 10.1177/074823379801400406 Ek U, 1998, DEV MED CHILD NEUROL, V40, P297 Geschwind DH, 2001, AM J HUM GENET, V69, P463, DOI 10.1086/321292 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Gillberg IC, 1996, J INTELL DISABIL RES, V40, P24, DOI 10.1111/j.1365-2788.1996.tb00599.x Gunshin H, 1997, NATURE, V388, P482, DOI 10.1038/41343 Bailey A, 1998, HUM MOL GENET, V7, P571 Kelly EJ, 1996, NAT GENET, V13, P219, DOI 10.1038/ng0696-219 Knapp M, 1999, AM J HUM GENET, V64, P1177, DOI 10.1086/302334 Latif A, 2002, AUTISM, V6, P103, DOI 10.1177/1362361302006001008 Liu JJ, 2001, AM J HUM GENET, V69, P327, DOI 10.1086/321980 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Madsen KM, 2003, PEDIATRICS, V112, P604, DOI 10.1542/peds.112.3.604 Martin ER, 1997, AM J HUM GENET, V61, P439, DOI 10.1086/514860 O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 PICKLES A, 1995, AM J HUM GENET, V57, P717 Rice D, 2000, ENVIRON HEALTH PERSP, V108, P511, DOI 10.2307/3454543 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 Saydam N, 2002, J BIOL CHEM, V277, P20438, DOI 10.1074/jbc.M110631200 Shao YJ, 2002, AM J MED GENET, V114, P99, DOI 10.1002/ajmg.10153 Sobel E, 1996, AM J HUM GENET, V58, P1323 Spielman RS, 1996, AM J HUM GENET, V59, P983 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Weiss B, 2000, ENVIRON HEALTH PERSP, V108, P373 NR 34 TC 36 Z9 37 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 2004 VL 19 IS 6 BP 413 EP 417 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 850RX UT WOS:000223631200003 PM 15446388 ER PT J AU Ip, P Wong, V Ho, M Lee, J Wong, W AF Ip, P Wong, V Ho, M Lee, J Wong, W TI Mercury exposure in children with autistic spectrum disorder: Case-control study SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 9th International Child Neurology Congress/7th Asian Oceanian Congress of the Child Neurology CY SEP 19-22, 2002 CL Beijing, PEOPLES R CHINA ID METHYLMERCURY EXPOSURE; NEURODEVELOPMENT; VACCINATION; DEFICIT; FISH AB Although mercury has been proven to be a neurotoxicant, there is a lack of data to evaluate the causal relationship between mercury and autism. We aim to see if there is increased mercury exposure in children with autistic spectrum disorder. We performed a cross-sectional cohort study over a 5-month period in 2000 to compare the hair and blood mercury levels of children with autistic spectrum disorder (n = 82; mean age 7.2 years) and a control group of normal children (11 = 55; mean age 7.8 years). There was no difference in the mean mercury levels. The mean blood mercury levels of the autistic and control groups were 19.53 and 17.68 nmol/L, respectively (P = .15), and the mean hair mercury levels of the autistic and control groups were 2.26 and 2.07 ppm, respectively (P = .79). Thus, the results from our cohort study with similar environmental mercury exposure indicate that there is no causal relationship between mercury as an environmental neurotoxin and autism. C1 Univ Hong Kong, Div Neurodev Paediat, Hong Kong, Hong Kong, Peoples R China. Queen Mary Hosp, Div Clin Biochem, Hong Kong, Hong Kong, Peoples R China. RP Ip, P (reprint author), Univ Hong Kong, Dept Paediat & Adolescent Med, Div Neurodev Paediat, Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China. EM vcnwong@hkucc.hku.hk CR Cranmer M, 1996, NEUROTOXICOLOGY, V17, P9 Davidson PW, 1998, JAMA-J AM MED ASSOC, V280, P701, DOI 10.1001/jama.280.8.701 Department of Developmental Services, 1999, CHANG POP PERS AUT P Filipek P. A., 1999, J AUTISM DEV DISORD, V29, P437 Filipek PA, 2000, NEUROLOGY, V55, P468 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 FOMBONNE E, 2001, ED CHILDREN AUTISM Grandjean P, 1997, NEUROTOXICOL TERATOL, V19, P417, DOI 10.1016/S0892-0362(97)00097-4 HATZAKIS PG, 1985, 5 INT C HEAV MET ENV, P47 Palferman S, 2001, AM J HUM GENET, V69, P570 Kaiser J, 2000, SCIENCE, V289, P371 LAIDLER JR, MERCURY DETOXIFICATI Lauritsen MB, 2001, ACTA PSYCHIAT SCAND, V103, P411, DOI 10.1034/j.1600-0447.2001.00086.x OSHEA T, 2000, AUT MERC SAN DIEG C Ozuah P O, 2000, Curr Probl Pediatr, V30, P91, DOI 10.1067/mps.2000.104054 Pless R, 2000, J PEDIATR-US, V136, P571, DOI 10.1067/mpd.2000.106797 SALONEN JT, 1995, CIRCULATION, V91, P645 Stajich GV, 2000, J PEDIATR-US, V136, P679, DOI 10.1067/mpd.2000.105133 Steuerwald U, 2000, J PEDIATR-US, V136, P599, DOI 10.1067/mpd.2000.102774 STODGELL CJ, 2000, INT REV RES MENT RET, V23, P57 Tuthill RW, 1996, ARCH ENVIRON HEALTH, V51, P214 US EPA (United States Environmental Protection Agency), 1997, MERC STUD REP C WHO (World Health Organization), 1990, ENV HLTH CRIT 101 ME NR 25 TC 45 Z9 49 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 2004 VL 19 IS 6 BP 431 EP 434 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 850RX UT WOS:000223631200006 PM 15446391 ER PT J AU Stein, MT Klin, A Miller, K Goulden, K Coolman, R Snyder, DM AF Stein, MT Klin, A Miller, K Goulden, K Coolman, R Snyder, DM TI When Asperger's syndrome and a nonverbal learning disability look alike SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material DE Asperger's syndrome; nonverbal learning disability; pragmatic learning disorder ID AUTISM; CHILD C1 Univ Calif San Diego, San Diego, CA 92103 USA. Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT USA. Tufts Univ, Sch Med, Floating Hosp Children, New England Med Ctr,Ctr Children Special Needs, Boston, MA 02111 USA. RP Stein, MT (reprint author), Univ Calif San Diego, San Diego, CA 92103 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 2000, DIAGN STAT MAN MENT, V4 GILLIAM J, 2003, GILLIAM ASPERGERS DI JESSOP DJ, 1994, PEDIATRICS, V93, P602 Klin A., 1997, HDB AUTISM PERVASIVE, P94 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Klin A, 2003, PHILOS T ROY SOC B, V358, P345, DOI 10.1098/rstb.2002.1202 KLIN A, 1997, HDB AUTISM PERVASIVE, P411 Lord C., 1999, ADOS G AUTISM DIAGNO LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 National Research Council, 2001, ED CHILDR AUT COMM E PERRN JM, 1993, HOME COMMUNITY CARE Rourke B. P, 1989, NONVERBAL LEARNING D Rourke BP, 2002, ANNU REV PSYCHOL, V53, P309, DOI 10.1146/annurev.psych.53.100901.135204 ROURKE BP, 2000, ASPERGERS SYNDROME Stein MT, 2001, J DEV BEHAV PEDIATR, V22, P188 TANGUAY PB, 2002, NONVERBAL LEARING DI Volkmar F. R., 2000, ASPERGER SYNDROME, P340 Wolraich M, 1996, CLASSIFICATION CHILD NR 19 TC 7 Z9 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD JUN PY 2004 VL 25 IS 3 BP 190 EP 195 DI 10.1097/00004703-200406000-00008 PG 6 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 830LJ UT WOS:000222123300008 PM 15194904 ER PT J AU Christopher, JA Sears, LL Williams, PG Oliver, J Hersh, J AF Christopher, JA Sears, LL Williams, PG Oliver, J Hersh, J TI Familial, medical and developmental patterns of children with autism and a history of language regression SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; pervasive developmental disorders; regression; developmental history; medical issues AB Autism is a developmental disorder characterized by impairments in social and communication skills, as well as repetitive and stereotypical patterns of behavior. A common feature of children with autism is regression or loss of spoken words. The aim of this study was to systematically review medical and familial conditions in children with autism with regression and those without regression in order to determine relevant factors, in regard to regression, that might lead to identifying factors in etiology. Eighty-two children with autism were evaluated by a multidisciplinary team. In addition, medical and familial information was collected on each child in order to determine any differences between the children with regression and those without. Results confirmed previous findings of minimal differences in child characteristics, family history, prenatal and perinatal factors, developmental concerns, behavioral concerns, and medical findings in children who regress. C1 Univ Louisville, Weisskopf Ctr Evaluat Children, Louisville, KY 40202 USA. RP Sears, LL (reprint author), Univ Louisville, Weisskopf Ctr Evaluat Children, 571 S Floyd St,Suite 100, Louisville, KY 40202 USA. EM lonnie.sears@louisville.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 NR 6 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 JUN PY 2004 VL 16 IS 2 BP 163 EP 170 DI 10.1023/B:JODD.0000026613.92643.60 PG 8 WC Rehabilitation SC Rehabilitation GA 818EQ UT WOS:000221228800003 ER PT J AU Bauminger, N Shulman, C Agam, G AF Bauminger, N Shulman, C Agam, G TI The link between perceptions of self and of social relationships in high-functioning children with autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE high-functioning children with autism; friendship; self perception; loneliness ID FRIENDSHIP; LONELINESS; COMPETENCE; ADOLESCENTS; SCALE AB This study examined the perception of friendship in high-functioning children with autism (8-17 years old) and the link between perceptions of self and of social relationships in these children. Sixteen typically developing children were matched to sixteen high-functioning children with autism, on chronological age, IQ, gender, and mother's education. Study measures included a friendship picture recognition task and three self-report questionnaires: qualities of friendship, loneliness, and self-perception profile. Main results indicated that even if children with autism more frequently related to the intersubjective qualities of friendship such as affective sharing or intimacy, they perceived their friendship to be as close as did typically developing children. Also, for the group with autism, friendship correlated positively with cognitive competencies and general self-worth and negatively with loneliness. In addition, children with autism perceived their social and athletic competencies as lower compared with typically developing children. Implications of the associations between self-perceptions and perceptions of friendship are discussed. C1 Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. Hebrew Univ Jerusalem, Sch Social Work, Jerusalem, Israel. RP Bauminger, N (reprint author), Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. EM bauminn@mail.biu.ac.il CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASHER SR, 1984, CHILD DEV, V55, P1456, DOI 10.2307/1130015 ASHER SR, 1985, J CONSULT CLIN PSYCH, V53, P500, DOI 10.1037/0022-006X.53.4.500 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Bauminger N, 2003, AUTISM, V7, P81, DOI 10.1177/1362361303007001007 BUHRMESTER D, 1990, CHILD DEV, V61, P1101, DOI 10.1111/j.1467-8624.1990.tb02844.x BUKOWSKI WM, 1994, J SOC PERS RELAT, V11, P471, DOI 10.1177/0265407594113011 CAPPS L, 1995, DEV PSYCHOPATHOL, V7, P137 CASSIDY J, 1992, CHILD DEV, V63, P350, DOI 10.1111/j.1467-8624.1992.tb01632.x Chamberlain B., 2001, DEV AUTISM PERSPECTI ERIKSON E, 1968, YOUTH SOC Evans D. 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J., 1991, DEV PSYCHOPATHOL, V3, P137, DOI DOI 10.1017/S0954579400000043 SCHOPLER E, 1985, J AUTISM DEV DISORD, V15, P359, DOI 10.1007/BF01531780 Sullivan H., 1953, INTERPERSONAL THEORY Wechsler D, 1974, WISC R MANUAL WECHSL Bauminger N, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P151 YIRMIYA N, 1991, CLIN PSYCHOL REV, V11, P669, DOI 10.1016/0272-7358(91)90125-E NR 34 TC 29 Z9 29 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1056-263X J9 J DEV PHYS DISABIL JI J. Dev. Phys. Disabil. PD JUN PY 2004 VL 16 IS 2 BP 193 EP 214 DI 10.1023/B:JODD.0000026616.24896.c8 PG 22 WC Rehabilitation SC Rehabilitation GA 818EQ UT WOS:000221228800006 ER PT J AU Celani, G AF Celani, G TI Comorbidity between autistic syndrome and biological pathologies: Which implications for the understanding of the etiology? SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Review DE autism; theoretical model; comorbidity; etiology; emotional communication ID INFANTILE-AUTISM; NORMAL-CHILDREN; CONGENITAL CYTOMEGALOVIRUS; FACIAL EXPRESSIONS; REDUCED OPTIMALITY; RETARDED-CHILDREN; MOTOR IMITATION; CASE-HISTORIES; DOWN-SYNDROME; RETT-SYNDROME AB It is estimated that at least 24% of cases of autism are potentially associated with other syndromes; with infective, metabolic, or genetic pathologies; and with anatomical or functional alterations. Problems connected with the interpretation of the association between biological damage and autistic behavioral phenotype in causal terms are briefly exposed. Three critical periods for the beginning of an anomalous behavioral development in the child with autism are identified: prenatal, prior to 9 months from birth, after 1 year of age. Psychopathological consequences potentially deriving from biological damages on every critical period are described, and their compatibility with the characteristic behavioral features observed in individuals affected by autism is discussed. On this basis, a theoretical model that represents infantile autism as a species-specific human psychopathology of early emotional communication during the primary intersubjectivity stage is proposed. C1 Univ Bologna, Dept Psychol, I-40127 Bologna, Italy. RP Celani, G (reprint author), Univ Bologna, Dept Psychol, Viale Berti Pichat 5, I-40127 Bologna, Italy. 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Dev. Phys. Disabil. PD JUN PY 2004 VL 16 IS 2 BP 215 EP 228 DI 10.1023/B:JODD.0000026617.62533.44 PG 14 WC Rehabilitation SC Rehabilitation GA 818EQ UT WOS:000221228800007 ER PT J AU Beadle-Brown, JD Whiten, A AF Beadle-Brown, JD Whiten, A TI Elicited imitation in children and adults with autism: is there a deficit? SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article ID YOUNG-CHILDREN; IMMEDIATE; ABILITIES; INFANTS; SKILLS AB Rogers and Pennington (1991) proposed that an early deficit in imitation, together with a cascade of developmental disorders in emotion sharing and theory of mind, could be important in understanding autism, but the research on deficits in imitation is not conclusive. Using a Do-As-I-Do procedure, the present study tested the existence of a deficit in elicited imitation in a group of individuals with autism aged from 4 to 34 years and compared their performance to that of typically developing children and to children with mild to moderate intellectual disabilities. On a large battery of tasks, the majority of children and adults with autism had few problems relative to controls, although certain actions did seem more difficult, especially for the youngest children. Taking into consideration the reasonably small sample sizes, which advise cautious interpretation, implications for both theory and practice are discussed. C1 Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England. Univ St Andrews, Sch Psychol, St Andrews, Fife, Scotland. RP Beadle-Brown, JD (reprint author), Univ Kent, Tizard Ctr, Beverley Farm, Canterbury CT2 7LZ, Kent, England. 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PD JUN PY 2004 VL 29 IS 2 BP 147 EP 163 DI 10.1080/13668250410001709494 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 834BD UT WOS:000222385700004 ER PT J AU Fombonne, E AF Fombonne, E TI The changing epidemiology of autism spectrum disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3H 1P3, Canada. EM eric.fombonne@mcgill.ca NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 283 EP 283 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300002 ER PT J AU Howlin, P AF Howlin, P TI Interventions and outcome in autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ London St Georges Hosp, Sch Med, Dept Community Hlth Sci, London SW17 0RE, England. EM phowlin@sghms.ac.uk NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 283 EP 283 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300004 ER PT J AU Rutter, M AF Rutter, M TI Aetiology of autism: Findings and questions SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Kings Coll London, Inst Psychiat, London WC2R 2LS, England. EM j.wickham@iop.kcl.ac.uk NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 284 EP 284 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300008 ER PT J AU Brown, W Nolin, S Dobkin, C Houck, G Glicksman, A Ding, X Gargano, A Crawford, L Gitcho, N Spence, S Geschwind, D AF Brown, W Nolin, S Dobkin, C Houck, G Glicksman, A Ding, X Gargano, A Crawford, L Gitcho, N Spence, S Geschwind, D TI Frequency of fragile X in multiplex autism: Testing the AGRE families SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Inst Basic Res Dev Disabil, Staten Isl, NY USA. EM WTBIR@aol.com NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 287 EP 287 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300029 ER PT J AU Lepisto, T Kujala, T Vanhala, R Naatanen, R AF Lepisto, T Kujala, T Vanhala, R Naatanen, R TI Speech perception in autism: Evidence from the auditory event-related potentials SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Helsinki, Cognit Brain Res Unit, FIN-00014 Helsinki, Finland. EM Tuulia.Lepisto@Helsinki.fi NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 287 EP 287 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300028 ER PT J AU Ylisaukko-oja, T Rehnstrom, K Auranen, M Varilo, T Vanhala, R Alen, R Nieminen-von Wendt, T Sarenius, S von Wendt, L Peltonen, L Jarvela, I AF Ylisaukko-oja, T Rehnstrom, K Auranen, M Varilo, T Vanhala, R Alen, R Nieminen-von Wendt, T Sarenius, S von Wendt, L Peltonen, L Jarvela, I TI Present concepts in the genetics of autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Helsinki, Dept Med Genet, FIN-00014 Helsinki, Finland. EM tero.ylisaukko-oja@ktl.fi RI Jarvela, Irma/L-5836-2013 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 287 EP 287 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300027 ER PT J AU Trajkovski, V Ajdinski, L Spiroski, M AF Trajkovski, V Ajdinski, L Spiroski, M TI Plasma concentration of immunoglobulin classes and subclasses in children with autism in the Republic of Macedonia SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Inst Special Educ & Rehabil, Skopje, Macedonia. EM vladotra@freemail.com.mk RI Trajkovski, Vladimir/I-4948-2012 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 288 EP 288 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300035 ER PT J AU Pierantoni, R Di Gemma, V Schirripa, GM AF Pierantoni, R Di Gemma, V Schirripa, GM TI Integrated treatment for subjects with Asperger Syndrome, high functioning autism and non verbal learning disabilities SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Local Hlth Dept Viterbo, Unita Operat Complesso Neuropsichiat Infanzie &, Lazio, Italy. EM g.schirripa@asl.vt.it NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 291 EP 291 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300049 ER PT J AU Baghdadli, A Grisi, S Aussilloux, C AF Baghdadli, A Grisi, S Aussilloux, C TI Risk factors for persistent self-injurious behaviors (SIB) in children with infantile autism: A longitudinal study SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 CHU Montpellier, Ctr Ressources Autisme, Montpellier, France. EM a-baghdadli@chu-montpellier.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 292 EP 292 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300054 ER PT J AU Bodfish, J AF Bodfish, J TI Phenomenology of repetitive behaviour in autism: Comparison to non-specific intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. EM jim.bodfish@NCMail.net NR 0 TC 1 Z9 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 292 EP 292 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300051 ER PT J AU Charbonneau-Marzo, C Labayle, R Chatagneret, M AF Charbonneau-Marzo, C Labayle, R Chatagneret, M TI Autism, schooling and special health needs SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Psychiat Infanto Juvenile Esssone, Ste Genevieve Des Bois, France. EM marzoclaire4@yahoo.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 295 EP 295 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300069 ER PT J AU Chydenius, E Laine, T Nikkinen, M Kaski, M AF Chydenius, E Laine, T Nikkinen, M Kaski, M TI Crisis intervention for people with autism and Asperger syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Rinnekoti Fdn, Espoo, Finland. EM esa.chydenius@rinnekoti.fi NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 295 EP 295 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300068 ER PT J AU Bradley, E Bolton, PF Bryson, SE AF Bradley, E Bolton, PF Bryson, SE TI Psychiatric comorbidity in persons with intellectual disability (ID) with and without autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Toronto, Toronto, ON, Canada. Surrey Pl Ctr, Toronto, ON, Canada. EM e.bradley@utoronto.ca RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 NR 0 TC 1 Z9 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 296 EP 296 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300074 ER PT J AU Brereton, AV Tonge, BJ King, NK AF Brereton, AV Tonge, BJ King, NK TI Autism: A parent-based early intervention SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Ctr Dev Psychiat & Psychol, Clayton, Vic 3168, Australia. EM Avril.Brereton@med.monash.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 296 EP 296 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300072 ER PT J AU Gray, KM Tonge, BJ Einfeld, S AF Gray, KM Tonge, BJ Einfeld, S TI Screening for autism in young children with developmental delay SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Ctr Dev Psychiat & Psychol, Clayton, Vic 3168, Australia. EM Kylie.Gray@med.monash.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 296 EP 296 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300071 ER PT J AU Tonge, B Brereton, A Einfeld, S Moseley, D AF Tonge, B Brereton, A Einfeld, S Moseley, D TI Autism: Change in behavioural and emotional disturbance over time SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Ctr Dev Psychiat & Psychol, Clayton, Vic 3168, Australia. EM Bruce.Tonge@med.monash.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 296 EP 296 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300073 ER PT J AU Willaye, E AF Willaye, E TI Escape: A holistic management of severe problem behaviours presented by people with intellectual disabilities and/or autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Mons, Escape, B-7000 Mons, Belgium. EM susa@umh.ac.be NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 298 EP 298 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300088 ER PT J AU Urwand, S Frydman, D AF Urwand, S Frydman, D TI Integration of the body self image: Two techniques used for children with intellectual disabilities (ID) and autism or psychotic symptoms SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 IMP Marie Auxiliatrice, Assoc Villipinte, Draveil, France. EM d.m.frydman@free.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 313 EP 313 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300170 ER PT J AU Singer, G Singer, J AF Singer, G Singer, J TI Planned Activity Training (PAT) with a sibling triad: Reducing severe problem behaviour in a young child with autism with collateral increases in sibling appropriate play behaviour SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. EM singer@education.ucsb.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 319 EP 319 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300203 ER PT J AU Reynolds, J AF Reynolds, J TI Investigating abilities in communication, cognition and play in children with both autism and severe intellectual disabilities (ID) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Northumbria Univ, Sch Hlth Community & Educ Studies, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England. EM joanna2.reynolds@unn.ac.uk NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 321 EP 321 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300211 ER PT J AU Trembath, D Balandin, S AF Trembath, D Balandin, S TI Speech generation devices and naturalistic teaching for preschool children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Sydney, Sch Commun Sci & Disorders, Sydney, NSW 2006, Australia. EM david.trembath@student.usyd.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 323 EP 323 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300225 ER PT J AU Carr, D Felce, J AF Carr, D Felce, J TI The early effects of PECS on the communicative interactions of children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wales Coll Med, Welsh Ctr Learning Disabil, Cardiff CF4 4XN, S Glam, Wales. EM felceja@cf.ac.uk RI turton, miranda/F-4682-2011 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 324 EP 324 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300228 ER PT J AU Bartak, L Cleary, M Portaro, M AF Bartak, L Cleary, M Portaro, M TI Pragmatic deficits in children with autism spectrum disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Fac Educ, Clayton, Vic 3168, Australia. EM lawrie.bartak@education.monash.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 326 EP 326 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300245 ER PT J AU Hastings, R Remington, R Kovshoff, H Espinosa, FD Jahr, E Brown, T Filby, P Lemaic, M Ward, N AF Hastings, R Remington, R Kovshoff, H Espinosa, FD Jahr, E Brown, T Filby, P Lemaic, M Ward, N TI Outcomes for families of children with autism in Early Intensive Behavioural Intervention SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wales Bangor, Sch Psychol, Bangor, Gwynedd, Wales. EM r.hastings@bangor.ac.uk RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 327 EP 327 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300252 ER PT J AU Remington, R Hastings, R Espinosa, FD Kovshoff, H Jahr, E Brown, T AF Remington, R Hastings, R Espinosa, FD Kovshoff, H Jahr, E Brown, T TI The Southampton Childhood Autism Programme (SCAmP): The pleasures and pitfalls of public sector programmes SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Southampton, Sch Psychol, Southampton SO9 5NH, Hants, England. EM rer1@soton.ac.uk RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 327 EP 327 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300250 ER PT J AU Riby, DM Doherty-Sneddon, G Bruce, V AF Riby, DM Doherty-Sneddon, G Bruce, V TI Communicative face processing abilities in autism and Williams syndrome: Focusing on emotions, gaze and facial speech SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Stirling, Dept Psychol, Stirling FK9 4LA, Scotland. EM deborah.riby@stir.ac.uk RI Doherty-Sneddon, Gwyneth/A-4646-2009 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 327 EP 327 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300248 ER PT J AU Beadle-Brown, J Murphy, G Dorey, H AF Beadle-Brown, J Murphy, G Dorey, H TI Evaluation of early intervention in autism: A pilot study SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Kent, Tizard Ctr, Canterbury CT2 7NZ, Kent, England. EM j.d.beadle-brown@kent.ac.uk NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 328 EP 328 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300253 ER PT J AU Livoir-Petersen, MF AF Livoir-Petersen, MF TI Early intervention in autism: A developmental perspective SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Hop La Colombiere, Serv Med Psychol Enfants & Adolescents, Montpellier, France. EM mf-petersen@chu-montpellier.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 328 EP 328 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300257 ER PT J AU Magerotte, G Roge, B AF Magerotte, G Roge, B TI Family quality of life and early intervention in autism (Auti-qol) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Mons, Serv Univ Specialise Personnes Autisme, B-7000 Mons, Belgium. EM ghislain.magerotte@umh.ac.be NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 328 EP 328 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300256 ER PT J AU Barnhill, J AF Barnhill, J TI Evolution, neuro-ethology and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ N Carolina, Sch Med, Chapel Hill, NC USA. EM Jarrett_Barnhill@med.unc.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 329 EP 329 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300259 ER PT J AU Haag, G Urwand, S AF Haag, G Urwand, S TI The concept of 'corporal-self' and related disorders in children with autism and in children with intellectual disabilities and autistic traits SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Assoc Villepinte, Draveil, France. EM gisele.jubin@wanadoo.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 329 EP 329 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300260 ER PT J AU Rocque, S Langevin, J Dionne, C Papazian, A AF Rocque, S Langevin, J Dionne, C Papazian, A TI Metamodel of educational and social interventions for autism and other pervasive developmental disorders (PDD) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Montreal, Grp DEFI Apprentissage, Montreal, PQ H3C 3J7, Canada. EM anyp26@yahoo.com NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 329 EP 329 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300258 ER PT J AU Adrien, J Gattegno, MP AF Adrien, J Gattegno, MP TI Effects of home and school coaching for young children with autism on their psychological development, cerebral maturation and on families life quality SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Paris 05, Inst Psychol, Paris, France. EM Jean-Louis.Adrien@univ-paris5.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 330 EP 330 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300261 ER PT J AU Fernandes, MJ AF Fernandes, MJ TI Development of communication profiles in children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Ctr Resources Autisme, Montpellier, France. EM cent-ress-autisme@chu-montpellier.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 331 EP 331 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300267 ER PT J AU Pernon, E AF Pernon, E TI Autism and the perception of emotion: 'Attraction or addiction' SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 CHU Montpellier, Ctr Ressources Autisme, Montpellier, France. EM cent-ress-autisme@chu-montpellier.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 331 EP 331 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300266 ER PT J AU Pry, R AF Pry, R TI Attention and perception: Recent models and theories in autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Montpellier 3, F-34032 Montpellier, France. EM rene.pry@univ-montp3.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 331 EP 331 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300264 ER PT J AU Pry, R AF Pry, R TI Relationship between the development of expressive language and non-verbal interactive skills in young children with autism. SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Montpellier 3, F-34032 Montpellier, France. EM rene.pry@univ-montp3.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 331 EP 331 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300269 ER PT J AU Stahl, L Pry, R AF Stahl, L Pry, R TI Attention and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Montpellier 3, F-34032 Montpellier, France. EM laurastahl@free.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 331 EP 331 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300265 ER PT J AU Craig, KD AF Craig, KD TI Fine-grained studies of language and nonverbal behaviour in children with autism and intellectual disabilities (ID) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ British Columbia, Dept Psychol, Vancouver, BC, Canada. EM kcraig@psych.ubc.ca NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 332 EP 332 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300273 ER PT J AU Hastings, RP Beck, A Hill, C AF Hastings, RP Beck, A Hill, C TI Behaviour problems and pro-social behaviour in autism, intellectual disability (ID), and Down syndrome (DS) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wales Bangor, Sch Psychol, Bangor, Gwynedd, Wales. EM r.hastings@bangor.ac.uk RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 332 EP 332 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300270 ER PT J AU Tasse, MJ Havercamp, SM Morin, IN AF Tasse, MJ Havercamp, SM Morin, IN TI Behavioural profile of children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ N Carolina, Ctr Dev & Learning, Chapel Hill, NC 27515 USA. EM marc.tasse@cdl.unc.edu RI Havercamp, Susan/E-3218-2011 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 332 EP 332 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300271 ER PT J AU Kontu, E AF Kontu, E TI Mind and music as windows to autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Helsinki, FIN-00014 Helsinki, Finland. EM elina.kontu@helsinki.fi NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 333 EP 333 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300276 ER PT J AU Rattaz, C AF Rattaz, C TI Perception of a tactile unpleasant stimulus in children with Down syndrome (DS) or autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 CHU Montpellier, Serv Med Psychol Enfants & Adolescents, Montpellier, France. EM c.rattaz@free.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 333 EP 333 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300277 ER PT J AU Gillott, A Standen, P AF Gillott, A Standen, P TI Anxiety and stress in adults with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Nottingham Healthcare NHS Trust, Nottingham, England. EM alinda.gillott@nhc-tr.trent.nhs.uk NR 0 TC 1 Z9 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 335 EP 335 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300293 ER PT J AU Lenoir, P Hameury, L Bodier, C Ledorze, G Malvy, J Damie, D Wissocq, M Sauvage, D AF Lenoir, P Hameury, L Bodier, C Ledorze, G Malvy, J Damie, D Wissocq, M Sauvage, D TI Autism and care deficiency (ID): A clinical report SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 CHRU Tours, Serv Univ Pedopsychiat, Tours, France. EM p.lenoir@chu-tours.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 336 EP 336 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300299 ER PT J AU Martin, F Hayes, S AF Martin, F Hayes, S TI Interpersonal self-efficacy and problematic behaviour in high-functioning autism (HFA) and Asperger disorder (AD) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Sydney, Ctr Behav Sci Med, Sydney, NSW 2006, Australia. EM fionab@bsim.usyd.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 337 EP 337 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300302 ER PT J AU Schlottmann, A Ray, ED AF Schlottmann, A Ray, ED TI Perceptual causality in young children with autism and intellectual disabilities (ID) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 UCL, Dept Psychol, London WC1E 6BT, England. EM a.schlottmann@ucl.ac.uk NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 337 EP 337 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300305 ER PT J AU Schmidhofer, K AF Schmidhofer, K TI The relationship between empathy and behavioural problems in adolescents with high-functioning autism and Asperger disorder SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Sydney, Ctr Behav Sci Med, Sydney, NSW 2006, Australia. EM katherin@bsimusyd.edu.au NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 338 EP 338 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300306 ER PT J AU Seynhaeve, I Nader, N Dionne, C AF Seynhaeve, I Nader, N Dionne, C TI Assessment Evaluation and Programming System (AEPS): Evaluation of children with autism and intellectual disabilities (ID) by different stakeholders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Louvain, Louvain, Belgium. EM Isabel.seynhaeve@psp.ucl.ac.be NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 338 EP 338 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300307 ER PT J AU Venuti, P Esposito, G Giusti, Z AF Venuti, P Esposito, G Giusti, Z TI A qualitative analysis of crying and vocal distress in children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Trent, Dipartimento Sci Cogniz & Formaz, Rovereto, Italy. EM venuti@form.unitn.it RI Esposito, Gianluca/B-1374-2012 OI Esposito, Gianluca/0000-0002-9442-0254 NR 0 TC 6 Z9 6 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 338 EP 338 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300309 ER PT J AU Wissocq, M Lenoir, P Malvy, J Ramage, I Bodier, C Viaux, S Damie, D Sauvage, D AF Wissocq, M Lenoir, P Malvy, J Ramage, I Bodier, C Viaux, S Damie, D Sauvage, D TI Roles of ante and perinatal factors in autism. Descriptive and comparative study of 133 patients SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 CHRU Tours, Serv Univ Pedopsychiat, Tours, France. EM p.lenoir@chu-tours.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 339 EP 339 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300313 ER PT J AU Martin, P AF Martin, P TI Autism and epilepsy in intellectual disability (ID) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Epilepsy Ctr Kork, Kehl, Germany. EM pmartin@epilepsiezentrum.de NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 352 EP 352 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300384 ER PT J AU Magana, S Smith, M AF Magana, S Smith, M TI Depressive symptoms and mood states of Latina and non-Latina White mothers of adolescents and adults with an autism spectrum disorder (ASD) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Univ Wisconsin, Sch Social Work, Madison, WI 53706 USA. EM magana@waisman.wisc.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 368 EP 368 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300472 ER PT J AU Willaye, E Magerotte, G AF Willaye, E Magerotte, G TI Training parents of children with autism: A Way to reach a better quality of life SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Mons, Serv Univ Specialise Personnes Autisme, B-7000 Mons, Belgium. EM susa@umh.ac.be NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 369 EP 369 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300482 ER PT J AU Lecavalier, L AF Lecavalier, L TI The impact of problem behaviour on caregiver stress in children and adolescents with autism spectrum disorders (ASD) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Ohio State Univ, Nisonger Ctr MR DD, Columbus, OH 43210 USA. EM lecavalier.l@osu.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 371 EP 371 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300489 ER PT J AU Stoneman, Z Rivers, JW AF Stoneman, Z Rivers, JW TI Temperaments of non-disabled siblings as a source of stress in families of children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Georgia, Inst Human Dev & Disabil, Athens, GA 30602 USA. EM zo@uga.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 375 EP 375 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300515 ER PT J AU Johnson, J Sperry, L Banks, S AF Johnson, J Sperry, L Banks, S TI Families with autism: Let them stand tall! SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Hawaii, Ctr Disabil Studies, Honolulu, HI 96822 USA. EM jeanj@hawaii.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 385 EP 385 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300573 ER PT J AU Rodger, S Braithwaite, M Keen, D AF Rodger, S Braithwaite, M Keen, D TI Early intervention priorities identified by parents of children with autism spectrum disorder (ASD) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Queensland, Brisbane, Qld, Australia. EM deb.keen@uq.edu.au RI Keen, Deb/B-8998-2008; Rodger, Sylvia/F-8738-2010 NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 392 EP 392 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300609 ER PT J AU Alonim, H AF Alonim, H TI The Mifne method in Israel: Infants at risk and early intervention in the treatment of autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Mifne Ctr, Rosh Pinna, Israel. EM info@mifne-autism.com NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 395 EP 395 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300630 ER PT J AU Verrecchia, B AF Verrecchia, B TI The place of architecture and poetry in the development of a project for the care of children with autism: The Saint Pol Roux project SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Brest Univ Hosp, Dept Child & Adolescent Psychiat, Brest, France. EM bruno.verrecchia@chu-brest.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 412 EP 412 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300712 ER PT J AU Niemeijer, M Baars, E AF Niemeijer, M Baars, E TI Autism care: Exploration of expertise based notions and development of an evaluation instrument SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Louis Bolk Inst, Driebergen, Netherlands. EM mhn@planet.nl NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 416 EP 416 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300733 ER PT J AU Carminati, GG Constantin, N Gerber, F Legay, Y Baud, O Blanco, P Forestie, N Sopranzi, F Guyot, S Van der Schuren, AM AF Carminati, GG Constantin, N Gerber, F Legay, Y Baud, O Blanco, P Forestie, N Sopranzi, F Guyot, S Van der Schuren, AM TI Evolution of autistic clients living in residences with an Autism Structured Method Program SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Dept Psychiat, Psychiat Unit Mental Dev, Geneva, Switzerland. EM fabienne.gerber@hcuge.ch NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 423 EP 423 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300769 ER PT J AU Renty, J Roeyers, H AF Renty, J Roeyers, H TI Quality of services and schools for persons with autism: The client's perspective SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 State Univ Ghent, B-9000 Ghent, Belgium. EM Jo.Renty@UGent.be NR 0 TC 1 Z9 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 423 EP 423 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300773 ER PT J AU Iarocci, G Wang, S Wang, M Brown, RI AF Iarocci, G Wang, S Wang, M Brown, RI TI Quality of life of Taiwanese families coping with a child with autism spectrum disorder (ASD) SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada. EM giarocci@sfu.ca NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 445 EP 445 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300892 ER PT J AU Magerotte, G Roge, B AF Magerotte, G Roge, B TI How to work together in early intervention in autism to improve the quality of life of the family SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Mons, Dept Orthopedag, B-7000 Mons, Belgium. EM Ghislain.Magerotte@umh.ac.be NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 450 EP 450 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695300921 ER PT J AU Lenotre, L Deb, S AF Lenotre, L Deb, S TI A systematic review of the evidence on the use of drugs for the management of behaviour disorders in adults who have intellectual disability (ID) and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Birmingham, Neurpsychiat & Intellectual Disabil Res Grp, Birmingham B15 2TT, W Midlands, England. EM l.lenotre@bham.ac.uk NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 487 EP 487 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695301135 ER PT J AU Azema, B AF Azema, B TI A geographical analysis of services in autism in a French region SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Ctr Reg Enfants & Adultes Inadaptes, Montpellier, France. EM azemab@club-internet.fr NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 504 EP 504 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695301231 ER PT J AU Fombonne, E AF Fombonne, E TI Investigating the risk factors and the efficacy of biological interventions in autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 McGill Univ, Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada. EM eric.fombonne@mcgill.ca NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 514 EP 514 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695301287 ER PT J AU Guralnick, M AF Guralnick, M TI Theory and data in early intervention: Effectiveness research for children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Washington, Seattle, WA 98195 USA. EM migural@u.washington.edu NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 514 EP 514 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695301288 ER PT J AU Rutter, M AF Rutter, M TI How can genetic findings improve interventions relevant to autism? SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Inst Psychiat, London, England. EM j.wickham@iop.kcl.ac.uk NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN PY 2004 VL 48 BP 514 EP 514 PN 4-5 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 824OG UT WOS:000221695301286 ER PT J AU Whipple, J AF Whipple, J TI Music in intervention for children and adolescents with autism: A meta-analysis SO JOURNAL OF MUSIC THERAPY LA English DT Article ID THERAPY; RESPONSES; BEHAVIORS AB This meta-analysis of 12 dependent variables from 9 quantitative studies comparing music to no-music conditions during treatment of children and adolescents with autism resulted in an overall effect size of d = .77 and a mean weighted correlation of r = .36 (p =.00). Since the confidence interval did not include 0, results were considered to be significant. All effects were in a positive direction, indicating benefits of the use of music in intervention. The homogeneity Q value was not significant (p = .83); therefore, results of included studies are considered to be homogeneous and explained by the overall effect size. The significant effect size, combined with the homogeneity of the studies, leads to the conclusion that all music intervention, regardless of purpose or implementation, has been effective for children and adolescents with autism. Included studies are described in terms of type of dependent variables measured; theoretical approach; number of subjects in treatment sessions; participation in and use, selection, and presentation of music; researcher discipline; published or unpublished source; and subject age. Clinical implications as well as recommendations for future research are discussed. C1 Florida State Univ, Tallahassee, FL 32306 USA. RP Whipple, J (reprint author), Florida State Univ, Tallahassee, FL 32306 USA. 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Music Ther. PD SUM PY 2004 VL 41 IS 2 BP 90 EP 106 PG 17 WC Music; Rehabilitation SC Music; Rehabilitation GA 845KR UT WOS:000223241900001 PM 15307805 ER PT J AU Bursch, B Ingman, K Vitti, L Hyman, P Zeltzer, LK AF Bursch, B Ingman, K Vitti, L Hyman, P Zeltzer, LK TI Chronic pain in individuals with previously undiagnosed autistic spectrum disorders SO JOURNAL OF PAIN LA English DT Article DE pain; pervasive developmental disorders; autistic spectrum disorders ID RESTRICTION; CHILDREN AB The aim of this article is to heighten clinician awareness by describing 2 patients with signs and symptoms of a possible autistic disorder. Autistic spectrum disorders are neurodevelopmental disorders characterized by impairment in reciprocal social interaction skills or communication skills and/or by the presence of stereotyped behavior, interests, and activities. Pain can be the initial presenting symptom for individuals with a previously undiagnosed autistic spectrum disorder. Two case presentations show indicators, such as reported sensory abnormalities, impaired social behaviors, and unusual interests, that should lead the physician to consider a referral for further evaluation. An accurate diagnosis of autism or related disorder can lead to a greater understanding of the nature of the patient's pain, as well as to more appropriate and effective treatment strategies. In addition, such patients might benefit from therapeutic interventions to improve overall functioning and decrease distress and, consequently, to decrease pain and other symptoms. Finally, autism research might inform pain researchers on topics such as neurobiology, development, and treatment of chronic pain disorders. Perspective: Pain experts might be underrecognizing signs and symptoms of autistic spectrum disorders (ASDs) in their patients. Clinical evaluation for ASDs should be considered in patients with specific unusual characteristics. Research on the topic of ASDs and pain is encouraged. (C) 2004 by the American Pain Society. C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Biobehav Sci, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, Los Angeles, CA USA. Univ Kansas, Med Ctr, Dept Pediat, Kansas City, KS 66103 USA. RP Bursch, B (reprint author), 760 Westwood Plaza,48-253C NPI, Los Angeles, CA 90024 USA. 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The authors classified the 68 pertinent hearing/ review officer and court decisions published in EHLR (Education for Handicapped Law Report) and IDELR (Individuals with Disabilities Education Law Report) into 2 groups representing the central issues of contention between parents and districts-program selection (e.g., instructional approach) and program implementation (e.g., its location, duration, or frequency). For both groups, the outcomes, in terms of who won, did not favor either parents or districts. The three factors predominantly associated with wins by either party for both groups of decisions were testimony of witnesses, documentation of progress, and Individualized Education Program elements. C1 Lehigh Univ, Bethlehem, PA 18015 USA. RP Choutka, CM (reprint author), 61 Eileen Lane, Limerick, PA 19468 USA. 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Two polymorphisms, an insertion/deletion in the promoter region and a 12 repeat allele in a variable nucleotide tandem repeat ( VNTR) in intron 2, drive higher expression of the 5-HTT gene. Four studies have shown nominally significant excess transmission of alleles of the 5-HTT gene in autism, while three studies have reported no excess transmission. This present study investigates the role of 5-HTT in the genetically homogenous Irish population. In all, 84 families were genotyped for five polymorphisms ( three SNPs, a VNTR and an in/del). The analysis of allele transmissions using the transmission disequilibrium test (TDT) was undertaken and indicated preferential transmission of the short promoter allele (TDT P-value = 0.0334). Linkage disequilibrium between markers was calculated and haplotypes were assessed for excess transmission and odds ratios (ORs) to affected children. A number of haplotypes, especially those involving and surrounding SNP10, showed evidence of association. 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Both global brain volume differences and differences in the size of specific neural structures have been reported. Here, we report a voxel-based morphometric whole brain analysis, using a group specific template, on 16 individuals of normal intelligence with autistic spectrum disorder (ASD), and a group of 16 age-, sex- and IQ-matched controls. Total grey matter volume was increased in the ASD group relative to the control group, with local volume increases in the right fusiform gyrus, the right temporo-occipital region and the left frontal pole extending to the medial frontal cortex. A local decrease in grey matter volume was found in the right thalamus. A decrease in global white matter volume in the ASD group did not reach significance. 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A previous hypothetical explanation, an unbalance between excitatory and inhibitory lateral feedback in the neocortex, has been found to be difficult to reconcile with the relatively high comorbidity of autism with epilepsy. Two alternative explanations are discussed, an early low capacity for producing serotonin, documented in autism, and insufficient production of nitric oxide. An early low level of serotonin has in animal experiments caused narrow neural columns. Insufficient nitric oxide is known from neural network theory to cause narrow neural columns. C1 Lulea Univ Technol, Dept Comp Sci & Elect Engn, S-97187 Lulea, Sweden. RP Gustafsson, L (reprint author), Lulea Univ Technol, Dept Comp Sci & Elect Engn, S-97187 Lulea, Sweden. 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SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR C1 Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. Univ Calif Davis, Dept Epidemiol & Prevent Med, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 668 EP 669 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900029 ER PT J AU Mars, A Seshadri, K Georgopoulos, P Shalat, S Moreno, R Carmody, D Weisel, C Johnson, W Lioy, P Lambert, G AF Mars, A Seshadri, K Georgopoulos, P Shalat, S Moreno, R Carmody, D Weisel, C Johnson, W Lioy, P Lambert, G TI Autism and the environment: Exposure Assessment, intervention and clinical expression. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR C1 Rutgers State Univ, Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch,EOHSI,Dept Neurol, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ USA. Rutgers State Univ, Univ Med & Dent New Jersey,EOHSI, Robert Wood Johnson Med Sch,Dept Environm & Commu, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ USA. Rutgers State Univ, Univ Med & Dent New Jersey,EOHSI, Robert Wood Johnson Med Sch,Dept Pediat, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 670 EP 670 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900033 ER PT J AU Cheh, MA Halladay, AK Reuhl, KR Wagner, GC AF Cheh, MA Halladay, AK Reuhl, KR Wagner, GC TI A new model of autism: Behavioral markers following pre-and post-natal sodium valproate to BALB/c mice. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR C1 Rutgers State Univ, Joint Grad Program Neurosci, Piscataway, NJ USA. Rutgers State Univ, Joint Grad Program Toxicol, Piscataway, NJ USA. Rutgers State Univ, Dept Psychol, Piscataway, NJ USA. Rutgers State Univ, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 671 EP 671 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900036 ER PT J AU Shalat, SL Black, K Freeman, NCG Lambert, G Lioy, PJ AF Shalat, SL Black, K Freeman, NCG Lambert, G Lioy, PJ TI NJ autism study: The role of behavior in ingestion of environmental toxins. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR C1 Robert Wood Johnson Med Sch, Environm & Occupat Hlth Sci Inst, Piscataway, NJ USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 683 EP 683 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900068 ER PT J AU Bernard, S Redwood, L Blaxill, M AF Bernard, S Redwood, L Blaxill, M TI Thimerosal, mercury, and autism: Case study in the failure of the risk assessment paradigm. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR DE thimerosal; autism; precautionary principal C1 Safe Minds, Cranford, NJ USA. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 710 EP 710 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900133 ER PT J AU Halladay, AK Wagner, GC Zhou, R Reuhl, KR AF Halladay, AK Wagner, GC Zhou, R Reuhl, KR TI Neurodevelopmental consequences of MeHg in an animal model of autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR C1 Rutgers State Univ, Joint Grad Program Toxicol, Dept Pharmacol, New Brunswick, NJ 08903 USA. Rutgers State Univ, Joint Grad Program Toxicol, Dept Toxicol, New Brunswick, NJ 08903 USA. Rutgers State Univ, Joint Grad Program Toxicol, Dept Psychol, New Brunswick, NJ 08903 USA. Rutgers State Univ, Joint Grad Program Toxicol, Dept Biol Chem, New Brunswick, NJ 08903 USA. Rutgers State Univ, Ctr Childhood & Neurotoxicol & Exposure Assessmen, New Brunswick, NJ 08903 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 711 EP 711 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900136 ER PT J AU Cheh, MA Halladay, AK Reuhl, KR Wagner, GC AF Cheh, MA Halladay, AK Reuhl, KR Wagner, GC TI A new model of autism: Behavioral markers following, pre-and post-natal sodium valproate to Balb/c mice. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 20th International Neurotoxicology Conference CY NOV 18-21, 2002 CL LITTLE ROCK, AR C1 Rutgers State Univ, Joint Grad Program Neurosci, Piscataway, NJ USA. Rutgers State Univ, Joint Grad Program Toxicol, Piscataway, NJ USA. Rutgers State Univ, Dept Psychol, Piscataway, NJ USA. Rutgers State Univ, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD JUN PY 2004 VL 25 IS 4 BP 727 EP 728 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 830KW UT WOS:000222121900180 ER PT J AU Vojdani, A O'Bryan, T Green, JA McCandless, J Woeller, KN Vojdani, E Nourian, AA Cooper, EL AF Vojdani, A O'Bryan, T Green, JA McCandless, J Woeller, KN Vojdani, E Nourian, AA Cooper, EL TI Immune response to dietary proteins, gliadin and cerebellar peptides in children with autism SO NUTRITIONAL NEUROSCIENCE LA English DT Article DE autism; autoantibodies; celiac disease; gliadin and cerebellar peptides; gluten ataxia ID CELIAC-DISEASE; SPECTRUM DISORDERS; GLUTEN SENSITIVITY; ATAXIA; ANTIBODIES; INFECTION; ABNORMALITIES; DEGENERATION; AUTOIMMUNITY; EPITOPES AB The mechanisms behind autoimmune reaction to nervous system antigens in autism are not understood. We assessed the reactivity of sera from 50 autism patients and 50 healthy controls to specific peptides from gliadin and the cerebellum. A significant percentage of autism patients showed elevations in antibodies against gliadin and cerebellar peptides simultaneously. For examining cross-reaction between dietary proteins and cerebellar antigens, antibodies were prepared in rabbits, and binding of rabbit anti-gliadin, anti-cerebellar peptides, anti-MBP, anti-milk, anti-egg, anti-soy and anti-corn to either gliadin- or cerebellar-antigen-coated wells was measured. In comparison to anti-gliadin peptide binding to gliadin peptide at 100%, the reaction of anti-cerebellar peptide to gliadin peptide was 22%, whereas the binding of anti-myelin basic protein (MBP), anti-milk, anti-egg and anti-soy to gliadin was less than 10%. Further examination of rabbit anti-gliadin (EQVPLVQQ) and anti-cerebellar (EDVPLLED) 8 amino acid (AA) peptides with human-serum albumin (HSA) and an unrelated peptide showed no binding, but the reaction of these antibodies with both the cerebellar and gliadin peptides was greater than 60%. This cross-reaction was further confirmed by DOT-immunoblot and inhibition studies. We conclude that a subgroup of patients with autism produce antibodies against Purkinje cells and gliadin peptides, which may be responsible for some of the neurological symptoms in autism. C1 Immunosci Lab Inc, Sect Neuroimmunol, Beverly Hills, CA 90211 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurobiol, Lab Comparat Neuroimmunol, Los Angeles, CA 90095 USA. Omnis Grp, Glenview, IL 60025 USA. Evergreen Ctr, Oregon City, OR 97045 USA. Biohlth Ctr, San Diego, CA 92121 USA. Univ Calif Berkeley, Berkeley, CA 94702 USA. RP Vojdani, A (reprint author), Immunosci Lab Inc, Sect Neuroimmunol, 8693 Wilshire Blvd,Ste 200, Beverly Hills, CA 90211 USA. 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PD JUN PY 2004 VL 22 IS 2 BP 85 EP 100 PG 16 WC Education & Educational Research SC Education & Educational Research GA 833CK UT WOS:000222313800007 ER PT J AU Blaxill, MF AF Blaxill, MF TI Study fails to establish diagnostic substitution as a factor in increased rate of autism SO PHARMACOTHERAPY LA English DT Editorial Material ID CHANGING PREVALENCE; CALIFORNIA C1 Safe Minds, Cambridge, MA 02138 USA. RP Blaxill, MF (reprint author), Safe Minds, 22 Fayerweather St, Cambridge, MA 02138 USA. EM Blaxill.mark@bcg.com CR Byrd R., 2002, REPORT LEGISLATURE P Croen LA, 2003, J AUTISM DEV DISORD, V33, P227, DOI 10.1023/A:1022964132203 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 Jick H, 2003, EPIDEMIOLOGY, V14, P630, DOI 10.1097/01.EDE.0000082044.88833.c4 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 NR 6 TC 4 Z9 4 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD JUN PY 2004 VL 24 IS 6 BP 812 EP 813 DI 10.1592/phco.24.8.812.36060 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 826OA UT WOS:000221837200016 PM 15222674 ER PT J AU Jick, H Kaye, JA AF Jick, H Kaye, JA TI Study fails to establish diagnostic substitution as a factor in increased rate of autism - Reply SO PHARMACOTHERAPY LA English DT Editorial Material ID UK CR Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 Jick H, 2003, EPIDEMIOLOGY, V14, P630, DOI 10.1097/01.EDE.0000082044.88833.c4 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Last JM, 2001, DICT EPIDEMIOLOGY NR 6 TC 1 Z9 1 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD JUN PY 2004 VL 24 IS 6 BP 813 EP 815 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 826OA UT WOS:000221837200017 ER PT J AU Persico, AM D'Agruma, L Zelante, L Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Elia, M Palermo, M Rabinowitz, D Pascucci, T Puglisi-Allegra, S Reichelt, KL Muscarella, L Guarnieri, V Melgari, JM Conciatori, M Keller, F AF Persico, AM D'Agruma, L Zelante, L Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Elia, M Palermo, M Rabinowitz, D Pascucci, T Puglisi-Allegra, S Reichelt, KL Muscarella, L Guarnieri, V Melgari, JM Conciatori, M Keller, F TI Enhanced APOE2 transmission rates in families with autistic probands SO PSYCHIATRIC GENETICS LA English DT Article DE APOE; APOE receptor 2; autism; pervasive developmental disorders; reelin; transmission/disequilibrium test; very-low-density; lipoprotein receptor ID CHOLESTEROL TRANSPORT PROTEIN; APOLIPOPROTEIN-E POLYMORPHISM; GENE PROMOTER VARIANTS; REELIN GENE; TRANSMISSION/DISEQUILIBRIUM TEST; NEUROANATOMICAL ABNORMALITIES; SUSCEPTIBILITY GENES; MENTAL-RETARDATION; ALZHEIMERS-DISEASE; LIPID TRANSPORT AB We have previously described linkage/association between reelin gene polymorphisms and autistic disorder. APOE also participates in the Reelin signaling pathway, by competitively antagonizing Reelin binding to APOE receptor 2 and to very-low-density lipoprotein receptors. The APOE2 protein variant displays the lowest receptor binding affinity compared with APOE3 and APOE4. In this study, we assess linkage/association between primary autism and APOE alleles in 223 complete trios, from 119 simplex Italian families and 44 simplex and 29 multiplex Caucasian-American families. Statistically significant disequilibrium favors the transmission of epsilon2 alleles to autistic offspring, over epsilon3 and epsilon4 (allele-wise transmission/disequilibrium test [TDT], chi(2) = 6.16, 2 degrees of freedom [d.f.], P < 0.05; genotype-wise TDT, chi(2) = 10.68, 3 d.f., P < 0.05). A novel epsilon3r allele was also discovered in an autistic child and his mother. Autistic patients do not differ significantly from unaffected siblings (allele-wise TDT comparing autistic patients versus unaffected sibs, chi(2) = 1.83, 2 d.f., P < 0.40, not significant). The major limitation of this study consists of our small sample size of trios including one unaffected sibling, currently not possessing the statistical power necessary to conclusively discriminate a specific association of epsilon2 with autism, from a distorted segregation pattern characterized by enhanced epsilon2 transmission rates both to affected and unaffected offspring. Our findings are thus compatible with either (a) pathogenetic contributions by epsilon2 alleles to autism spectrum vulnerability, requiring additional environmental and/or genetic factors to yield an autistic syndrome, and/or (b) a protective effect of epsilon2 alleles against the enhanced risk of miscarriage and infertility previously described among parents of autistic children. (C) 2004 Lippincott Williams Wilkins. C1 Lab Mol Psychiat & Neurogenet, I-00155 Rome, Italy. Lab Dev Neurosci & Neural Plast, I-00155 Rome, Italy. IRCCS Casa Sollievo Sofferenza, Med Genet Serv, San Giovanni Rotondo, FG, Italy. Univ Naples 2, Dept Child Neuropsychiat, Naples, Italy. SW Autism Res Ctr, Phoenix, AZ USA. Osped Bambino Gesu, IRCCS, Dept Child Neuropsychiat, Rome, Italy. IRCCS Oasi Maria SS, Autism Treatment Ctr, Troina, EN, Italy. Columbia Univ, Dept Stat, New York, NY USA. Univ Roma La Sapienza, Dept Psychol, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, N-0027 Oslo, Norway. RP Persico, AM (reprint author), Lab Mol Psychiat & Neurogenet, Univ Campus Biomed,Via Longoni 83, I-00155 Rome, Italy. 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Genet. PD JUN PY 2004 VL 14 IS 2 BP 73 EP 82 DI 10.1097/01.ypg.0000128768.37838.17 PG 10 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 831JI UT WOS:000222190300004 PM 15167692 ER PT J AU Keenan, M AF Keenan, M TI ABA and autism SO PSYCHOLOGIST LA English DT Letter C1 Univ Ulster, Coleraine BT52 1SA, Londonderry, North Ireland. RP Keenan, M (reprint author), Univ Ulster, Coleraine BT52 1SA, Londonderry, North Ireland. NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD JUN PY 2004 VL 17 IS 6 BP 321 EP 321 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 830YG UT WOS:000222159500009 ER PT J AU Nikopoulos, C AF Nikopoulos, C TI ABA and autism SO PSYCHOLOGIST LA English DT Letter RP Nikopoulos, C (reprint author), 84 Portglenone Rd, Randalstown, Antrim, North Ireland. NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD JUN PY 2004 VL 17 IS 6 BP 321 EP 321 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 830YG UT WOS:000222159500008 ER PT J AU Lucyshyn, JM Irvin, LK Blumberg, ER Laverty, R Horner, RH Sprague, JR AF Lucyshyn, JM Irvin, LK Blumberg, ER Laverty, R Horner, RH Sprague, JR TI Validating the construct of coercion in family routines: Expanding the unit of analysis in behavioral assessment with families of children with developmental disabilities SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE developmental disabilities; parent-child interaction; family routines; behavioral assessment ID SOCIAL CONSTRUCTION; SUPPORT; INTERVENTION; MANAGEMENT; SCIENCE; MOTHERS; SYSTEM; ADULTS; FILES AB We conducted an observational study of parent-child interaction in home activity settings (routines) of families raising young children with developmental disabilities and problem behavior. 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PD SUM PY 2004 VL 29 IS 2 BP 104 EP 121 DI 10.2511/rpsd.29.2.104 PG 18 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 866ZN UT WOS:000224812000007 ER PT J AU Koegel, RL Openden, D Koegel, LK AF Koegel, RL Openden, D Koegel, LK TI A systematic desensitization paradigm to treat hypersensitivity to auditory stimuli in children with autism in family contexts SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE desensitization; autism; hypersensitivity; auditory stimuli; families ID MOTOR INTEGRATION; INTERVENTIONS; CUES; FEAR AB Many children with autism display reactions to auditory stimuli that seem as if the stimuli were painful or otherwise extremely aversive. This article describes, within the contexts of three experimental designs, how procedures of systematic desensitization can be used to treat hypersensitivity to auditory stimuli in three young children with autism. Stimuli included the sounds from a vacuum cleaner, blender, hand-mixer, toilet flushing, and specific animal sounds from musical toys. A changing criterion design was used and data were collected on (a) the number of hierarchical steps completed as comfortable with the stimulus per week and (b) the mean level of anxiety per probe. A clinical replication was implemented using a replication of the desensitization procedures for three children. In addition, a systematic replication across three different stimuli is presented for one child in a multiple baseline. The data show that the children's responses could be modified to the point where they were comfortable with these noises. Furthermore, this level of comfort was maintained at follow-up. The discussion suggests that the extreme reactions to auditory stimuli many children with autism exhibit may be decreased with procedures that have been shown to be effective with reducing phobias, and the possibility that the reactions may be symptomatic of a phobia rather than actual pain. C1 Univ Calif Santa Barbara, Grad Sch Educ, Counseling Clin Sch Psychol Program, Santa Barbara, CA 93106 USA. RP Koegel, RL (reprint author), Univ Calif Santa Barbara, Grad Sch Educ, Counseling Clin Sch Psychol Program, Santa Barbara, CA 93106 USA. 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Thirteen healthy children for whom anatomic brain MRI scans were obtained every 2 years, for 8-10 years, were studied. By using models of the cortical surface and sulcal landmarks and a statistical model for gray matter density, human cortical development could be visualized across the age range in a spatiotemporally detailed time-lapse sequence. The resulting time-lapse "movies" reveal that (i) higher-order association cortices mature only after lower-order somatosensory and visual cortices, the functions of which they integrate, are developed, and (ii) phylogenetically older brain areas mature earlier than newer ones. Direct comparison with normal cortical development may help understanding of some neurodevelopmental disorders such as childhood-onset schizophrenia or autism. C1 NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Sch Med, Dept Neurol, Lab Neuro Imaging, Los Angeles, CA 90095 USA. 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Natl. Acad. Sci. U. S. A. PD MAY 25 PY 2004 VL 101 IS 21 BP 8174 EP 8179 DI 10.1073/pnas.0402680101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 823ZC UT WOS:000221652000060 PM 15148381 ER PT J AU Comoletti, D De Jaco, A Jennings, LL Flynn, RE Gaietta, G Tsigelny, I Ellisman, MH Taylor, P AF Comoletti, D De Jaco, A Jennings, LL Flynn, RE Gaietta, G Tsigelny, I Ellisman, MH Taylor, P TI The Arg451Cys-neuroligin-3 mutation associated with autism reveals a defect in protein processing SO JOURNAL OF NEUROSCIENCE LA English DT Article DE neuroligin; neurexin; autism; cell adhesion proteins; thiol-retention; trafficking ID ENDOPLASMIC-RETICULUM; NEUROLIGIN; BINDING; EXPRESSION; DISORDERS; SECRETION; NEUREXINS; RETENTION; GENETICS; NLGN4 AB The neuroligins are a family of postsynaptic transmembrane proteins that associate with presynaptic partners, the beta-neurexins. Neurexins and neuroligins play a critical role in initiating formation and differentiation of synaptic junctions. A recent study reported that a mutation of neuroligin-3 (NL3), an X-linked gene, was found in siblings with autistic spectrum disorder in which two affected brothers had a point mutation that substituted a Cys for Arg451. To characterize the mutation at the biochemical level, we analyzed expression and activity of the mutated protein. Mass spectrometry comparison of the disulfide bonding pattern between the native and the mutated proteins indicates the absence of aberrant disulfide bonding, suggesting that the secondary structure of the mutated protein is conserved. However, the mutation separately affects protein expression and activity. The Cys mutation causes defective neuroligin trafficking, leading to retention of the protein in the endoplasmic reticulum. This, in turn, decreases the delivery of NL3 to the cell surface. Also, the small fraction of protein that reaches the cell membrane lacks or has markedly diminished beta-neurexin-1 (NX1beta) binding activity. Other substitutions for Arg451 allow for normal cellular expression but diminished affinity for NX1beta. Our findings reveal a cellular phenotype and loss of function for a congenital mutation associated with autistic spectrum disorders. C1 Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA. RP Taylor, P (reprint author), Univ Calif San Diego, Dept Pharmacol, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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Linkage analysis in our dataset of 57 New England and 80 AGRE multiplex autism families reveals a multipoint heterogeneity LOD (HLOD) score of 2.74 at D17S1871 in 17q11.2. Analysis of phenotypic subsets shows an increased HLOD of 3.62 in families with compulsive behaviors and rigidity. The serotonin transporter locus (SLC6A4) maps nearby and is considered a functional candidate gene in autism and obsessive-compulsive disorder. We genotyped an insertion/deletion polymorphism in the promoter (5-HTTLPR), and seven single nucleotide polymorphisms (SNPs) across the 38-kb transcriptional unit. Transmission disequilibrium (TD) analysis reveals nominal association at a SNP in intron 5 (P = 0.02) as well as 5-HTTLPR (P = 0.01), corresponding to over-transmission of the short allele. TD analysis in the rigid-compulsive subset shows no evidence for association. Intermarker linkage disequilibrium. was determined. All SNPs define a single haplotype block, while 5-HTTLPR lies 5' to this block. 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RP Sutcliffe, JS (reprint author), Vanderbilt Univ, Dept Physiol & Mol Biophys, Program Human Genet, 221 Kirkland Hall, Nashville, TN 37232 USA. 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J. Med. Genet. B PD MAY 15 PY 2004 VL 127B IS 1 BP 104 EP 112 DI 10.1002/ajmg.b.20151 PG 9 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 816UZ UT WOS:000221136100021 PM 15108191 ER PT J AU Gong, XH Jia, MX Ruan, Y Shuang, M Liu, J Wu, SP Guo, YQ Yang, JZ Ling, YS Yang, XL Zhang, D AF Gong, XH Jia, MX Ruan, Y Shuang, M Liu, J Wu, SP Guo, YQ Yang, JZ Ling, YS Yang, XL Zhang, D TI Association between the FOXP2 gene and autistic disorder in Chinese population SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; FOXP2; single nucleotide polymorphism; transmission/disequilibrium test; haplotype analysis ID SUSCEPTIBILITY GENE; LANGUAGE DISORDER; GENOMIC SCREEN; ABNORMALITIES; TRANSMISSION; MUTATION; LINKAGE; REGION; SPEECH AB Several genomewide screens indicated that chromosome 7q was linked to autistic disorder. FOXP2, located on 7q31, is a putative transcription factor containing a polyglutamine tract and a forkhead DNA binding domain. It is one member of the forkhead family who are known to be key regulators of embryogenesis. A point mutation at a highly conserved residue within the forkhead domain co-segregated with affected status in the KE family who was a unique three generation pedigree with a severe speech and language disorder and FOXP2 was directly disrupted by a translocation in an individual who had similar deficits as those of the KE family. Several studies have investigated the role of FOXP2 polymorphisms in autism and none of them found positive association. We performed a family-based association study of three single nucleotide polymorphisms (SNPs) of FOXP2 in 181 Chinese Han trios using the analyses of transmission/disequilibrium test (TDT) and haplotype. We found a significant association between autistic disorder and one SNP, as well as with specific haplotypes formed by this SNP with two other SNPs we investigated. Our findings suggest that the FOXP2 gene may be involved in the pathogenesis of autism in Chinese population. (C) 2004 Wiley-Liss, Inc. C1 Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. RP Zhang, D (reprint author), Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. 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B PD MAY 15 PY 2004 VL 127B IS 1 BP 113 EP 116 DI 10.1002/ajmg.b.20162 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 816UZ UT WOS:000221136100022 PM 15108192 ER PT J AU Addington, AM Gornick, M Sporn, AL Gogtay, N Greenstein, D Lenane, M Gochman, P Baker, N Balkissoon, R Vakkalanka, RK Weinberger, DR Straub, RE Rapoport, JL AF Addington, AM Gornick, M Sporn, AL Gogtay, N Greenstein, D Lenane, M Gochman, P Baker, N Balkissoon, R Vakkalanka, RK Weinberger, DR Straub, RE Rapoport, JL TI Polymorphisms in the 13q33.2 gene G72/G30 are associated with childhood-onset schizophrenia and psychosis not otherwise specified SO BIOLOGICAL PSYCHIATRY LA English DT Article DE candidate gene; genetic association; transmission disequilibrium test; quantitative transmission disequilibrium test; schizophrenia; children ID AFFECTIVE-DISORDERS; BIPOLAR DISORDER; K-SADS; AGE; DISEQUILIBRIUM; CHILDREN; LINKAGE; TRANSMISSION; SCHEDULE; VALIDITY AB Background: Childhood-onset schizophrenia (COS), defined as onset of psychotic symptoms by age 12 years, is a rare and severe form of the disorder that seems to be clinically and neurobiologically continuous with the adult disorder. Methods. We studied a rare cohort consisting of 98 probands; 71 of these probands received a DSM-defined diagnosis of schizophrenia, and the remaining 27 were diagnosed as psychosis not otherwise specified (NOS) (upon 2-6 year follow-up, 13 have subsequently developed bipolar disorder), Two overlapping genes, G72 and G30 on 13q33.2, were identified through linkage-disequilibrium-based positional cloning. Single nucleotide polymorphisms (SNPs) at the G72/G30 locus were independently associated with both bipolar illness and schizophrenia. We analyzed SNPs at this locus with a family-based transmission disequilibrium test (TDT) and haplotype analyses for the discrete trait, as well as quantitative TDT for intermediate phenotypes, using the 88 probands (including COS and pychosis-NOS) with parental participation. Results: We observed significant pairwise and haplotype associations between SNPs at the G72/G30 locus and psychotic illness. Furthermore, these markers showed associations with scores on a premorbid phenotype measured by the Autism Screening Questionnaire, and with age of onset. Conclusions. these findings, although limited by potential referral bias, confirm and strengthen previous reports that G72/G30 is a susceptibility locus both for schizophrenia and bipolar disorder. C1 NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA. NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA. RP Addington, AM (reprint author), NIMH, Child Psychiat Branch, NIH, 10 Ctr Dr,Bldg 10,Room 3N202, Bethesda, MD 20892 USA. 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Psychiatry PD MAY 15 PY 2004 VL 55 IS 10 BP 976 EP 980 DI 10.1016/j.biopsych.2004.01.024 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 819UZ UT WOS:000221342700003 PM 15121480 ER PT J AU Sporn, AL Addington, AM Gogtay, N Ordonez, AE Gornick, M Clasen, L Greenstein, D Tossell, JW Gochman, P Lenane, M Sharp, WS Straub, RE Rapoport, JL AF Sporn, AL Addington, AM Gogtay, N Ordonez, AE Gornick, M Clasen, L Greenstein, D Tossell, JW Gochman, P Lenane, M Sharp, WS Straub, RE Rapoport, JL TI Pervasive developmental disorder and childhood-onset schizophrenia: Comorbid disorder or a phenotypic variant of a very early onset illness? SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; child-onset schizophrenia; pervasive developmental disorder ID AUTISTIC DISORDER; PREMORBID ADJUSTMENT; DIAGNOSTIC INTERVIEW; K-SADS; GENE; ASSOCIATION; CHILDREN; MRI; LIFE; RELIABILITY AB Background: Childhood-onset schizophrenia (COS) is a severe form of the adult-onset disorder with a high rate of premorbid developmental abnormalities. Early symptoms of pervasive developmental disorder (PDD) have been reported in five independent studies of COS. In this study, we compared evidence for premorbid PDD as a nonspecific manifestation of impaired neurodevelopment seen in schizophrenia, or as an independent risk factor for COS. Methods. Diagnosis of past or current autism or PDD was made according to the DSM-IV criteria. COS patients with and without PDD were compared with respect to neuropsychological, clinical, and neurobiological measures. Several candidate genes for autism were examined in the entire COS sample and the subgroup with PDD using the Transmission Disequilibrium Test (TDT) and Quantitative TO T (QTDT). Results: Nineteen (25%) of COS probands bad a lifetime diagnosis of PDD: one met criteria for autism, two for Aspergers disorder, and 16 for PDD not otherwise specified. Premorbid social impairment was most common feature for COS-PDD subjects. The PDD group did not differ from the rest of the COS sample with respect to age of onset, IQ, response to medications, and rate of familial schizotypy. Unexpectedly, two siblings of COS-PDD probands met criteria for nuclear autism. There was no difference between PDD and non-PDD groups with respect to initial bra in magnetic resonance imaging (MRI) measures. However, rate of gray matter loss was greater for PDD (n = 12) than for the non-PDD (n = 2 7) subgroup (-19.5 +/- 11.3 mL/year vs. -9.6 +/- 15.3 mL/year; p = .05). None of eight candidate genes for autism were associated with COS or COS-PDD. Conclusions: Premorbid PDD in COS is more likely to be a nonspecific marker of severe early abnormal neurodevelopment. However, the occurrence of two siblings of COS-PDD probands (17016) with nuclear autism remains to be understood. C1 NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA. RP Sporn, AL (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10,Room 3N202, Bethesda, MD 20892 USA. 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Psychiatry PD MAY 15 PY 2004 VL 55 IS 10 BP 989 EP 994 DI 10.1016/j.biopsych.2004.01.019 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 819UZ UT WOS:000221342700005 PM 15121482 ER PT J AU Sivendran, S Patterson, D Spiegel, E McGowan, I Cowley, D Colman, R AF Sivendran, S Patterson, D Spiegel, E McGowan, I Cowley, D Colman, R TI Identification of 2 novel mutant human adenylosuccinate lyases(ASL) associated with autism and characterization of the equivalent mutant B-subtilis ASL SO FASEB JOURNAL LA English DT Meeting Abstract CT Annual Meeting of the American-Society-for-Biochemistry-and-Molecular-Biology/8th Congress of the International-Union-for-Biochemistry-and-Molecular-Biology CY JUN 12-16, 2004 CL Boston, MA SP Amer Soc BioChem & Mol Biol, Int Union Biochem & Mol Biol C1 Univ Delaware, Newark, DE 19716 USA. U Denver, Eleanor Roosevelt Inst, Denver, CO USA. Mater Misericordiae Hosp, Brisbane, Qld, Australia. RI Cowley, David/M-9674-2013 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 MAY 14 PY 2004 VL 18 IS 8 SU S BP C241 EP C242 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 823UP UT WOS:000221639101119 ER PT J AU Meek, C AF Meek, C TI Link between MMR and autism dispelled SO CANADIAN MEDICAL ASSOCIATION JOURNAL LA English DT News Item NR 0 TC 0 Z9 0 PU CANADIAN MEDICAL ASSOCIATION PI OTTAWA PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 3Y6, CANADA SN 0820-3946 J9 CAN MED ASSOC J JI Can. Med. Assoc. J. PD MAY 11 PY 2004 VL 170 IS 10 BP 1525 EP 1525 DI 10.1503/cmaj.1040603 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 821JN UT WOS:000221456400016 ER PT J AU Kennedy, T Regehr, G Rosenfield, J Roberts, SW Lingard, L AF Kennedy, T Regehr, G Rosenfield, J Roberts, SW Lingard, L TI Exploring the gap between knowledge and behavior: A qualitative study of clinician action following an educational intervention SO ACADEMIC MEDICINE LA English DT Article ID PRACTICE GUIDELINES; PHYSICIANS; PRACTITIONERS; ATTITUDES; DECISION AB Purpose. Many medical education interventions improve clinicians' knowledge but fail to change behavior. The authors exposed this knowledge-behavior gap through standardized clinical interactions, thus allowing in-depth exploration of the contributing factors. Method. A typical evidence-based educational intervention in one clinical domain (early signs of autism) was administered to family medicine residents at the University of Toronto in 2001-02, and change in knowledge was assessed through a multiple-choice test. Six to eight weeks later, participants' relevant knowledge was documented, and their clinical behavior was observed during four interactions with standardized patients. Factors producing a knowledge-behavior discrepancy were then explored using semistructured interviews, which were audiotaped, transcribed, and analyzed using grounded theory methods. Results. Half of participants demonstrated varying degrees of knowledge-behavior gap. Eight main rationalizations (relationships, patient agenda, knowledge deficit, clinical style, means to an end, ideals, autism stigma, and systems barriers) were used to justify choices of clinical behavior, and the same rationalizations were used to justify opposite choices of behavior. Two conditions that promote clinical action based on knowledge (level of certainty and sense of urgency) were identified. Conclusion. The knowledge-behavior gap was exposed and factors reported to influence clinicians' decisions about whether to implement new knowledge were elicited. That identical rationalizations were used to justify opposite behaviors implies these factors may not be behavioral determinants. Sense of urgency and level of certainty promote clinical action based on knowledge; focusing on these may increase the impact of education on practice. C1 Univ Toronto, Dept Pediat, Bloorview MacMillan Childrens Ctr, Toronto, ON, Canada. Univ Toronto, Dept Surg, Wilson Crt Res Educ, Richard & Elizabeth Currie Chair Hlth Profess Edu, Toronto, ON, Canada. Univ Toronto, Hosp Sick Children, Dept Pediat, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. RP Kennedy, T (reprint author), Univ Hlth Network, Ctr Res Educ, 200 Elizabeth St,Eaton S I-565, Toronto, ON M5G 2C4, Canada. EM tara.kennedy@utoronto.ca CR BEDELL SE, 1984, NEW ENGL J MED, V310, P1089, DOI 10.1056/NEJM198404263101706 Bero LA, 1998, BRIT MED J, V317, P465 BROWN A, 1992, FAM PRACT, V9, P32, DOI 10.1093/fampra/9.1.32 Cabana MD, 1999, JAMA-J AM MED ASSOC, V282, P1458, DOI 10.1001/jama.282.15.1458 Coleman T, 1996, FAM PRACT, V13, P526, DOI 10.1093/fampra/13.6.526 Davis D, 1999, JAMA-J AM MED ASSOC, V282, P867, DOI 10.1001/jama.282.9.867 Dowrick C, 2000, PSYCHOL MED, V30, P413, DOI 10.1017/S0033291799001531 Filipek PA, 2000, NEUROLOGY, V55, P468 Glaser B., 1967, DISCOVERY GROUNDED T HALL KH, 2003, MED EDUC, V36, P216 Harries C, 1996, TRAV HUMAIN, V59, P87 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 KUSHNER RF, 1995, PREV MED, V24, P546, DOI 10.1006/pmed.1995.1087 McCracken G., 1988, LONG INTERVIEW McKinlay JB, 1996, SOC SCI MED, V42, P769, DOI 10.1016/0277-9536(95)00342-8 Meyers DG, 1997, AM J PREV MED, V13, P45 MORSE JM, 1995, QUAL HEALTH RES, V5, P147, DOI 10.1177/104973239500500201 Mowatt G, 2001, J Contin Educ Health Prof, V21, P55, DOI 10.1002/chp.1340210109 Odell Lee, 1985, WRITING NONACADEMIC Poses R M, 1999, Jt Comm J Qual Improv, V25, P486 Siegel RM, 1996, CLIN PEDIATR, V35, P79, DOI 10.1177/000992289603500205 NR 21 TC 38 Z9 39 PU ASSOC AMER MEDICAL COLLEGES PI WASHINGTON PA 2450 N ST N W, WASHINGTON, DC 20037-1126 USA SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAY PY 2004 VL 79 IS 5 BP 386 EP 393 DI 10.1097/00001888-200405000-00006 PG 8 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA 840BK UT WOS:000222831800005 PM 15107277 ER PT J AU Kodituwakku, PW Cassell, C McClain, C Osbourn, P Wilbourne, P AF Kodituwakku, PW Cassell, C McClain, C Osbourn, P Wilbourne, P TI A comparison of executive dysfunction in children with autism and fetal alcohol spectrum disorders SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Meeting Abstract CT 27th Annual Meeting of the Research-Society-on-Alcoholism CY JUN 26-30, 2004 CL Vancouver, CANADA SP Res Soc Alcoholism C1 Univ New Mexico, Ctr Dev & Disabil, Albuquerque, NM 87107 USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD MAY PY 2004 VL 28 IS 5 SU S BP 43A EP 43A PG 1 WC Substance Abuse SC Substance Abuse GA 822OK UT WOS:000221549300222 ER PT J AU Ahn, RR Miller, LJ Milberger, S McIntosh, DN AF Ahn, RR Miller, LJ Milberger, S McIntosh, DN TI Prevalence of parents' perceptions of sensory processing disorders among kindergarten children SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID ELECTRODERMAL RESPONSES; AUTISM; SYMPTOMS AB This study is the first to systematically examine estimated rates of sensory processing disorders using survey data. Parents of incoming kindergartners from one suburban U.S. public school district were surveyed using the Short Sensory Profile, a parent-report screening tool that evaluates parents' perceptions of functional correlates of sensory processing disorders (McIntosh, Miller, Shyu, & Dunn, 1999a). A total of 703 completed surveys were returned, which represents 39% of the kindergarten enrollment (n = 1,796) in the district for the 1999-2000 school year. Of the 703 children represented by the surveys, 96 children (13.7% of 703) met criteria for sensory processing disorders based upon parental perceptions. A more conservative prevalence estimate of children having sensory processing disorders based on parental perceptions was calculated by assuming that all non-respondents failed to meet screening criteria. This cautious estimate suggests that based on parents' perceptions, 5.3% (96 of 1796) of the kindergarten enrollment met screening criteria for sensory processing disorders. These percentages are consistent with hypothesized estimates published in the literature. Findings suggest a need for rigorous epidemiological studies of sensory processing disorders. C1 KID Fdn, Littleton, CO 80120 USA. Univ Colorado, Hlth Sci Ctr, Dept Rehabil Med, Denver, CO USA. Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO USA. Wayne State Univ, Dev Disabil Inst, Detroit, MI USA. Univ Denver, Dept Psychol, Denver, CO 80208 USA. RP Ahn, RR (reprint author), KID Fdn, 1901 W Littleton Blvd, Littleton, CO 80120 USA. EM lucymiller@frii.com CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 Ayres A. J., 1989, SENSORY INTEGRATION BLANCHE EI, 2001, UNDERSTANDING NATURE, P345 Blanche R. I., 2001, UNDERSTANDING NATURE, P89 BUNDY AC, 2002, SENSORY INTEGRATION, P309 Bundy AC, 2002, SENSORY INTEGRATION, P3 BUNDY AC, 2002, SENSORY INTEGRATION, P227 BURLEIGH JM, 2002, SENSORY INTEGRATION, P141 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 Dunn W., 1999, SENSORY PROFILE EXAM ERMER J, IN PRESS AM J OCCUPA Hennekens CH, 1987, EPIDEMIOLOGY MED HICKMAN L, 2001, UNDERSTANDING NATURE, P409 Kandel E. R., 2000, PRINCIPLES NEURAL SC Kientz MA, 1997, AM J OCCUP THER, V51, P530 KINNEALEY M, 1995, AM J OCCUP THER, V49, P444 Linehan M. M., 1993, COGNITIVE BEHAV TREA Mailloux Z., 2001, UNDERSTANDING NATURE, P365 Mangeot SD, 2001, DEV MED CHILD NEUROL, V43, P399, DOI 10.1017/S0012162201000743 Mausner JS, 1985, EPIDEMIOLOGY INTRO T, P173 McIntosh D. N., 1999, SENSORY PROFILE EXAM, P59 McIntosh DN, 1999, DEV MED CHILD NEUROL, V41, P608, DOI 10.1017/S0012162299001267 MILLER LJ, IN PRESS HDB INFANT Miller LJ, 1999, AM J MED GENET, V83, P268, DOI 10.1002/(SICI)1096-8628(19990402)83:4<268::AID-AJMG7>3.3.CO;2-B Miller LJM, 2001, UNDERSTANDING NATURE, P247 OGNIBENE TC, 2003, UNPUB SENSORY HABITU ORNITZ EM, 1977, J AUTISM CHILD SCHIZ, V7, P207, DOI 10.1007/BF01538999 Parham L, 2001, OCCUPATIONAL THERAPY, P329 Roid G., 1997, LEITER INT PERFORMAN Schaaf R. C., 2001, UNDERSTANDING NATURE, P275 Schaaf RC, 2003, AM J OCCUP THER, V57, P442 Schore A, 1994, AFFECT REGULATION Shepherd G. M., 1994, NEUROBIOLOGY, P272 Talay-Ongan A., 2000, INT J DISABIL DEV ED, V47, P201, DOI DOI 10.1080/713671112 *US CENS BUR, CENS 2000 DEM DAT US NR 35 TC 69 Z9 72 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 MAY-JUN PY 2004 VL 58 IS 3 BP 287 EP 293 PG 7 WC Rehabilitation SC Rehabilitation GA 822GU UT WOS:000221527900007 PM 15202626 ER PT J AU Yochman, A Parush, S Ornoy, A AF Yochman, A Parush, S Ornoy, A TI Responses of preschool children with and without ADHD to sensory events in daily life SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; BEHAVIOR; PROFILE; COMORBIDITY; AUTISM AB OBJECTIVE. The purpose of this study was to compare parents' perceptions of the responses of their preschool children, with and without attention deficit hyperactivity disorder (ADHD), to sensory events in daily life in Israel. In addition, the relationship between levels of hyperactivity and sensory deficits was examined. METHOD. The Sensory Profile Questionnaire (SP) was completed by mothers of forty-eight 4- to 6-year-old children with ADHD, and mothers of 46 children without disabilities. A matched group comparison design was used to identify possible differences in sensory processing. RESULTS. Based on the measure of mothers' perceptions, children with ADHD demonstrated statistically significant differences from children without AND in their sensory responsiveness as reflected in 6 out of 9 factor scores (p < .001-.05), and on their sensory processing, modulation, and behavioral and emotional responses, as reflected in 11 out of 14 section scores (p < .001-.05). Scores on the SP yielded statistically significant low to moderate correlations with scores on the hyperactive scale of the Preschool Behavior Questionnaire (r = .28-.66). CONCLUSION. The findings of the present study suggest that young children with AND may be at increased risk of deficits in various sensory processing abilities, over and above the core symptoms of AND. Early identification and treatment of sensory processing deficits from a young age may extend our ability to support the successful performance of children with AND in meaningful and productive occupations. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Sch Occupat Therapy, IL-91010 Jerusalem, Israel. Hebrew Univ Jerusalem, Hadassah Med Sch, Lab Teratol, IL-91010 Jerusalem, Israel. Israeli Minist Hlth, Dept Child Dev & Rehabil, Jerusalem, Israel. RP Yochman, A (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Sch Occupat Therapy, POB 24026,Mt Scopus, IL-91010 Jerusalem, Israel. EM msshulap@pluto.huji.ac.il CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anastasi A., 1988, PSYCHOL TESTING Angold A, 1999, J CHILD PSYCHOL PSYC, V40, P57, DOI 10.1017/S0021963098003448 AYRES A J, 1964, Am J Occup Ther, V18, P6 Barkley RA, 1990, ATTENTION DEFICIT HY, V2nd BAUER BA, 1977, AM J OCCUP THER, V31, P447 Behar L, 1974, PRESCHOOL BEHAV QUES BEHAR LB, 1977, J ABNORM CHILD PSYCH, V5, P265, DOI 10.1007/BF00913697 Blondis TA, 1999, PEDIATR CLIN N AM, V46, P899, DOI 10.1016/S0031-3955(05)70162-0 CAMPBELL SB, 1986, J ABNORM CHILD PSYCH, V14, P217, DOI 10.1007/BF00915442 CAMPBELL SB, 1982, J ABNORM CHILD PSYCH, V10, P569, DOI 10.1007/BF00920755 CAMPBELL SB, 1995, J CHILD PSYCHOL PSYC, V36, P113, DOI 10.1111/j.1469-7610.1995.tb01657.x Cermak S., 1988, SENSORY INTEGRATION, V11, P1 Doyle S., 1995, OCCUPATIONAL THERAPY, V2, P229 Dunn W, 2001, AM J OCCUP THER, V55, P608 DUNN W, 2001, UNPUB INITIAL DEV IN Dunn W, 2002, OTJR-OCCUP PARTICI H, V22, P4 Dunn W., 1999, SENSORY PROFILE EXAM DuPaul GJ, 2001, J AM ACAD CHILD PSY, V40, P508, DOI 10.1097/00004583-200105000-00009 Ermer J, 1998, AM J OCCUP THER, V52, P283 Jensen PS, 1997, J AM ACAD CHILD PSY, V36, P1065, DOI 10.1097/00004583-199708000-00014 Kadesjo B, 1998, DEV MED CHILD NEUROL, V40, P796 Kientz MA, 1997, AM J OCCUP THER, V51, P530 LANE SJ, 2000, SENSORY INTEGRATION, V23, P2 LIBLICH A, 1973, WPPSI HEBREW MANUAL LIGHTSEY R, 1993, SENSORY INTEGRATION, V21, P6 Mangeot SD, 2001, DEV MED CHILD NEUROL, V43, P399, DOI 10.1017/S0012162201000743 McIntosh D. 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PD MAY-JUN PY 2004 VL 58 IS 3 BP 294 EP 302 PG 9 WC Rehabilitation SC Rehabilitation GA 822GU UT WOS:000221527900008 PM 15202627 ER PT J AU Yang, B Goulet, M Boismenu, R Ferguson, AV AF Yang, B Goulet, M Boismenu, R Ferguson, AV TI Secretin depolarizes nucleus tractus solitarius neurons through activation of a nonselective cationic conductance SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE gut-brain peptide; central nervous system; electrophysiology; patch clamp ID VASOACTIVE-INTESTINAL-PEPTIDE; PROTEIN-COUPLED RECEPTORS; OREXIN-A; IN-VITRO; RAT-BRAIN; CELLS; GENE; PHOSPHORYLATION; SOMATOSTATIN; LOCALIZATION AB The recent suggestion that secretin may be useful in treating autism and schizophrenia has begun to focus attention on the mechanisms underlying this gut-brain peptide's actions in the central nervous system (CNS). In vitro autoradiographic localization of I-125-secretin binding sites in rat brain shows the highest binding density in the nucleus tractus solitarius (NTS). Recent evidence suggests that intravenous infusion of secretin causes fos activation in NTS, a relay station playing important roles in the central regulation of autonomic functions. In this study, whole cell patch-clamp recordings were obtained from 127 NTS neurons in rat medullary slices. The mean resting membrane potential of these neurons was -54.7 +/- 0.3 mV, the mean input resistance was 3.7 +/- 0.2 GOmega, and the action potential amplitude of these neurons was always >70 mV. Current-clamp studies showed that bath application of secretin depolarized the majority (80.8%; 42/52) of NTS neurons tested, whereas the remaining cells were either unaffected (17.3%; 9/52) or hyperpolarized (1.9%; 1/52). These depolarizing effects were maintained in the presence of 5 muM TTX and found to be concentration dependent from 10(-12) to 10(-7) M. Using voltage-clamp techniques, we also identified modulatory actions of secretin on specific ion channels. Our results demonstrate that while secretin is without effect on net whole cell potassium currents, it activates a nonselective cationic conductance (NSCC). These results show that NTS neurons are activated by secretin as a consequence of activation of a NSCC and support the emerging view that secretin can act as a neuropeptide within the CNS. C1 Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. Repligen, Waltham, MA 02453 USA. RP Ferguson, AV (reprint author), Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. 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PD MAY PY 2004 VL 161 IS 5 BP 933 EP 933 DI 10.1176/appi.ajp.161.5.933 PG 1 WC Psychiatry SC Psychiatry GA 820BP UT WOS:000221361700045 PM 15121684 ER PT J AU Volden, J AF Volden, J TI Nonverbal learning disability: A tutorial for speech-language pathologists SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Review DE nonverbal learning disability; child language disorder; learning disability ID CHILDRENS COMMUNICATION CHECKLIST; PERVASIVE DEVELOPMENTAL DISORDER; SEMANTIC PRAGMATIC DISORDER; HIGH-LEVEL AUTISM; ASPERGER-SYNDROME; PSYCHOSOCIAL DIMENSIONS; FACIAL EXPRESSIONS; EXTERNAL VALIDITY; CORPUS-CALLOSUM; WHITE-MATTER AB Nonverbal learning disability (NLD) is a diagnostic category that is unfamiliar to most speech-language pathologists. This brief tutorial describes NLD's characteristics, a theoretical model proposed to explain its source, and areas of overlap between NLD and similar diagnostic categories. The communicative profile, made up of difficulties in pragmatic and semantic language in the presence of relatively preserved syntactic skill, is also discussed. Empirical evidence relevant to NLD is also evaluated. Many questions remain unresolved, but until systematic research provides definitive answers, speech-language pathologists are encouraged to rely on careful description of the individual child's communicative strengths and weaknesses to identify appropriate targets and to focus intervention on improving the child's ability to communicate effectively in everyday contexts. C1 Univ Alberta, Edmonton, AB T6G 2G4, Canada. RP Volden, J (reprint author), Univ Alberta, 2-70 Corbett Hall, Edmonton, AB T6G 2G4, Canada. 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J. Speech-Lang. Pathol. PD MAY PY 2004 VL 13 IS 2 BP 128 EP 141 DI 10.1044/1058-0360(2004/014) PG 14 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 970CR UT WOS:000232283300004 PM 15198632 ER PT J AU Philofsky, A Hepburn, SL Hayes, A Hagerman, R Rogers, SJ AF Philofsky, A Hepburn, SL Hayes, A Hagerman, R Rogers, SJ TI Linguistic and cognitive functioning and autism symptoms in young children with fragile X syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; MENTAL-RETARDATION; DEVELOPMENTAL DISORDERS; LANGUAGE DISORDERS; MALES; COMMUNICATION; BOYS; BEHAVIOR; ADULTS AB Linguistic and cognitive profiles were examined in 18 children with autism and 18 children with fragile X syndrome (mean ages = 34 months). State-of-the-art diagnostic procedures for autism symptom identification were administered. Eight children with fragile X met criteria for autism. Comparison of linguistic and cognitive profiles (autism, fragile X without autism, fragile X with autism) revealed that children with fragile X (with autism) were more impaired in nonverbal cognition and expressive language. Receptive language was a relative strength for children with fragile X (without autism). There were no differences in receptive language in children with autism, regardless of fragile X status. Low receptive language may be a marker for autism symptoms in young children with fragile X. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Univ Calif Davis, MIND Inst, Davis, CA USA. RP Philofsky, A (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, 4200 E 9th Ave,Box C68-30, Denver, CO 80262 USA. 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J. Ment. Retard. PD MAY PY 2004 VL 109 IS 3 BP 208 EP 218 DI 10.1352/0895-8017(2004)109<208:LACFAA>2.0.CO;2 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 822OT UT WOS:000221550200003 PM 15072521 ER PT J AU Abbeduto, L Seltzer, MM Shattuck, P Krauss, MW Orsmond, G Murphy, MM AF Abbeduto, L Seltzer, MM Shattuck, P Krauss, MW Orsmond, G Murphy, MM TI Psychological well-being and coping in mothers of youths with autism, Down syndrome, or fragile X syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID MENTALLY-RETARDED CHILDREN; PRADER-WILLI-SYNDROME; FAMILY HISTORY; YOUNG-CHILDREN; AGING MOTHERS; STRESS; RETARDATION; DISORDERS; DIAGNOSIS; RESOURCES AB The psychological well-being of mothers raising a child with a developmental disability varies with the nature of the disability. Most research, however, has been focused on Down syndrome and autism. We added mothers whose adolescent or young adult son or daughter has fragile X syndrome. The sample was comprised of mothers of a child with fragile X syndrome (n = 22), Down syndrome (n = 39), or autism (n = 174). Mothers of individuals with fragile X syndrome displayed lower levels of well-being than those of individuals with Down syndrome, but higher levels than mothers of individuals with autism, although group differences varied somewhat across different dimensions of well-being. The most consistent predictor of maternal outcomes was the adolescent or young adult's behavioral symptoms. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Waltham, MA 02254 USA. Boston Univ, Boston, MA 02215 USA. RP Abbeduto, L (reprint author), Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. 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J. Ment. Retard. PD MAY PY 2004 VL 109 IS 3 BP 237 EP 254 DI 10.1352/0895-8017(2004)109<237:PWACIM>2.0.CO;2 PG 18 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 822OT UT WOS:000221550200006 PM 15072518 ER PT J AU Donaldson, AI Heavner, KS Zwolan, TA AF Donaldson, AI Heavner, KS Zwolan, TA TI Measuring progress in children with autism spectrum disorder who have cochlear implants SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article; Proceedings Paper CT 9th Symposium on Cochlear Implants in Children CY APR, 2003 CL Washington, DC SP Johns Hopkins Listening Ctyr, River Sch Washington, DC ID HANDICAPPED-CHILDREN; PREVALENCE AB Objective: To quantify progress after cochlear implantation for children with autism spectrum disorder (ASD). Study Design: Retrospective review of speech and language and speech perception test scores of children with autism who have received a cochlear implant at our center. Setting: University of Michigan Medical Center, Cochlear Implant Program. Patients: Six children, ages 3 to 16 years, who received cochlear implants at the our center. All children were diagnosed as having ASD by a neuropsychologist, either before or after receiving a cochlear implant. Main Outcome Measures: Children participated in preoperative and postoperative speech and language and speech perception testing. A survey was administered to parents to evaluate subjective impressions of cochlear implant benefit and quality of life before and after implantation. Results: Improved scores were recorded for children on whom standardized expressive and receptive vocabulary testing was possible. Children who could not complete standardized tests demonstrated improvement in raw scores. Improvement on the Meaningful Auditory Integration Scale was noted for the 4 of 7 children who completed the scale preoperatively and postoperatively. Survey results suggested changes in responsiveness to sound, interest in music, vocalization, and eye contact following implantation. Five of the 6 families indicated that they would recommend a cochlear implant to another family in a similar situation. Conclusions: Gains made by children in our study were small compared with the general implant population; however, when compared with themselves preoperatively, these children did demonstrate progress. Improvements in behaviors and interaction point to a quality of life benefit following implantation that is difficult to quantify. C1 Univ Michigan, Cochlear Implant Program, Ann Arbor, MI 48109 USA. RP Donaldson, AI (reprint author), 475 Marketpl,Bldg 1,Suite A, Ann Arbor, MI 48108 USA. EM aidonald@umich.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baker HC, 2002, J AUTISM DEV DISORD, V32, P121, DOI 10.1023/A:1014892606093 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Carvill S, 2001, J INTELL DISABIL RES, V45, P467, DOI 10.1046/j.1365-2788.2001.00366.x Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3141 Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd Erber N.P., 1982, AUDITORY TRAINING Fenson L, 1993, MACARTHUR COMMUNICAT Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Hamzavi J, 2000, INT J PEDIATR OTORHI, V56, P169, DOI 10.1016/S0165-5876(00)00420-1 JURE R, 1991, DEV MED CHILD NEUROL, V33, P1062 ROBBINS AM, 1991, AM J OTOL, V12, P144 Waltzman SB, 2000, AM J OTOL, V21, P329, DOI 10.1016/S0196-0709(00)80040-X Wetherby A. M., 2000, AUTISM SPECTRUM DISO Williams K. T., 1997, EXPRESSIVE VOCABULAR Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 16 TC 41 Z9 41 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD MAY PY 2004 VL 130 IS 5 BP 666 EP 671 DI 10.1001/archotol.130.5.666 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA 819TX UT WOS:000221339800029 PM 15148195 ER PT J AU Jablensky, A AF Jablensky, A TI Researching psychiatry in Western Australia SO AUSTRALIAN AND NEW ZEALAND JOURNAL OF PSYCHIATRY LA English DT Article DE autism; endophenotypes; epidemiology; record linkage; schizophrenia AB Objective: To provide an overview of the development, approaches and main research projects of the Centre for Clinical Research in Neuropsychiatry (CCRN) in Perth, Western Australia. Method: Discursive. Results: Underlying concepts, methods and selected findings of recent research into the neurobiology and epidemiology of schizophrenia, autism and other psychotic disorders are presented. Conclusion: CCRN, one of Australia's youngest centres of psychiatric research, has invested fruitfully in research areas such as molecular genetics, neuropsychology, neurophysiology, behavioural pharmacology, diagnostic assessment procedures and record linkage epidemiology. C1 Univ Western Australia, Sch Psychiat & Clin Neurosci, Ctr Clin Res Neuropsychiat, Mt Claremont, WA 6010, Australia. RP Jablensky, A (reprint author), Univ Western Australia, Sch Psychiat & Clin Neurosci, Ctr Clin Res Neuropsychiat, John XXIII Ave, Mt Claremont, WA 6010, Australia. EM assen@cyllene.uwa.edu.au RI Jablensky, Assen/H-5116-2014 CR Hallmayer JF, 2003, MOL PSYCHIATR, V8, P511, DOI 10.1038/sj.mp.4001273 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 NR 2 TC 9 Z9 9 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-8674 J9 AUST NZ J PSYCHIAT JI Aust. N. Z. J. Psych. PD MAY PY 2004 VL 38 IS 5 BP 306 EP 315 DI 10.1080/j.1440-1614.2004.01265.x PG 10 WC Psychiatry SC Psychiatry GA 825OF UT WOS:000221767100003 PM 15144506 ER PT J AU Jick, H Kaye, JA Black, C AF Jick, H Kaye, JA Black, C TI Incidence and prevalence of drug-treated attention deficit disorder among boys in the UK SO BRITISH JOURNAL OF GENERAL PRACTICE LA English DT Article DE attention deficit disorder; attention deficit and disruptive behaviour disorders; incidence; management; prevalence ID PRACTICE RESEARCH DATABASE; HYPERACTIVITY DISORDER; CHILDREN; AUTISM; MEASLES; MUMPS AB Background: Drug treatment for attention deficit disorder (ADD) was rare in the United Kingdom (UK) until in the mid-1990s. This contrasts with North America, where such treatment has been used to treat ADD for many decades. Since no quantitative data on the incidence and prevalence of drug-treated ADD are available in the UK, we used the general practice research database (GPRD) to obtain such information. Aims: To provide estimates of incidence and prevalence of treated ADD in the UK for the years 1996-2001. Design of study: Follow-up study of boys aged 5-14 years. Setting, Data from UK general practices. Methods: From the GPRD, we identified all boys aged 5-14 years who were prescribed methylphenidate for ADD. Based on the population in that age and sex category, we estimated incidence rates and the prevalence for treated ADD for the years 1996-2001. Results: The incidence of first-time diagnosis of treated ADD increased among boys from the age of 5 years to reach a peak in boys aged 9-10 years, after which the incidence rate decreased. No material change in incidence was noted during the years 1996-2001. The prevalence of treated ADD was estimated to be 5.3 per 1000 boys in 1999. Conclusion: Drug treatment for ADD for boys treated for this disorder in the UK is substantially lower than the proportion of boys treated in North America. 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We assessed this hypothesis in patients with autism and in those with mixed connective tissue diseases. Associated with antigliadin and anti-HSP antibodies, children with autism and patients with autoimmune disease developed anti-dipeptidylpeptidase I (DPP I), anti-dipeptidylpeptidase IV (DPP IV [or CD26]) and anti-aminopeptidase N (CD13) autoantibodies. A significant percentage of autoimmune and autistic sera were associated with elevated immunoglobulin G (IgG), IgM, or IgA antibodies against three peptidases, gliadin, and HSP-60. These antibodies are specific, since immune absorption demonstrated that only specific antigens (e.g., DPP IV absorption of anti-DPP IV), significantly reduced IgG, IgM, and IgA antibody levels. For direct demonstration of SK, HSP-60, and gliadin peptide binding to DPP IV, microtiter wells coated with DPP IV were reacted with SK, HSP-60, and gliadin. They were then reacted with anti-DPP IV or anti-SK, anti-HSP, and antighadin antibodies. 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Genet. PD MAY PY 2004 VL 65 IS 5 BP 352 EP 357 DI 10.1111/j.1399-0004.2004.00242.x PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 814FY UT WOS:000220961800003 PM 15099341 ER PT J AU Abdi, Z Sharma, T AF Abdi, Z Sharma, T TI Social cognition and its neural correlates in schizophrenia and autism SO CNS SPECTRUMS LA English DT Review ID FACIAL AFFECT RECOGNITION; PERVASIVE DEVELOPMENTAL DISORDERS; GENERALIZED POOR PERFORMANCE; EMOTION RECOGNITION; ASPERGERS SYNDROME; CHILDS APPRAISAL; FACE PERCEPTION; MIND; PEOPLE; COMPREHENSION AB The study of social cognition in psychiatric disorders has become increasingly popular in recent years. This is due to the its proposed link to social functioning and the inability of general neurocognitive skills to explain the spectrum of impairments observed in patients. This article reviews research into two of the processes thought to underlie social cognition (emotion perception and theory of mind) in schizophrenia and autism. 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PD MAY PY 2004 VL 9 IS 5 BP 335 EP 343 PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895VE UT WOS:000226891100008 PM 15115945 ER PT J AU Ullman, MT AF Ullman, MT TI Contributions of memory circuits to language: the declarative/procedural model SO COGNITION LA English DT Review DE language; lexicon; grammar; declarative memory; procedural memory; syntax; morphology; regular; irregular; basal ganglia; neostriatum; caudate nucleus; cerebellum; Broca's area; dorsal stream; ventral stream; working memory; sequence learning; specific language impairment; dyslexia; attention deficit hyperactivity disorder; autism; aphasia; Parkinson's disease; Alzheimer's disease; Huntington's disease; semantic dementia; functional magnetic resonance imaging; positron emission tomography; event-related potential ID POSITRON-EMISSION-TOMOGRAPHY; EVENT-RELATED FMRI; INFERIOR PREFRONTAL CORTEX; MEDIAL TEMPORAL-LOBE; CEREBRAL-BLOOD-FLOW; DEFICIT HYPERACTIVITY DISORDER; ESTROGEN REPLACEMENT THERAPY; NORMALLY DEVELOPING-CHILDREN; SURGICALLY MENOPAUSAL WOMEN; BASAL GANGLIA AB The structure of the brain and the nature of evolution suggest that, despite its uniqueness, language likely depends on brain systems that also subserve other functions. The declarative/procedural (DP) model claims that the mental lexicon of memorized word-specific knowledge depends on the largely temporal-lobe substrates of declarative memory, which underlies the storage and use of knowledge of facts and events. The mental grammar, which subserves the rule-governed combination of lexical items into complex representations, depends on a distinct neural system. This system, which is composed of a network of specific frontal, basal-ganglia, parietal and cerebellar structures, underlies procedural memory, which supports the learning and execution of motor and cognitive skills, especially those involving sequences. The functions of the two brain systems, together with their anatomical, physiological and biochemical substrates, lead to specific claims and predictions regarding their roles in language. These predictions are compared with those of other neurocognitive models of language. Empirical evidence is presented from neuroimaging studies of normal language processing, and from developmental and adult-onset disorders. It is argued that this evidence supports the DP model. It is additionally proposed that "language" disorders, such as specific language impairment and non-fluent and fluent aphasia, may be profitably viewed as impairments primarily affecting one or the other brain system. Overall, the data suggest a new neurocognitive framework for the study of lexicon and grammar. (C) 2004 Elsevier B.V. All rights reserved. C1 Georgetown Univ, Dept Neurosci, Brain & Language Lab, Washington, DC 20057 USA. Georgetown Univ, Dept Linguist, Brain & Language Lab, Washington, DC 20057 USA. Georgetown Univ, Dept Psychol, Brain & Language Lab, Washington, DC 20057 USA. Georgetown Univ, Dept Neurol, Brain & Language Lab, Washington, DC 20057 USA. RP Ullman, MT (reprint author), Georgetown Univ, Dept Neurosci, Brain & Language Lab, Box 571464, Washington, DC 20057 USA. 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PD MAY PY 2004 VL 6 IS 2 BP 139 EP 146 DI 10.1177/1461445604041763 PG 8 WC Communication SC Communication GA 828HB UT WOS:000221963300001 ER PT J AU Ochs, E Kremer-Sadlik, T Sirota, KG Solomon, O AF Ochs, E Kremer-Sadlik, T Sirota, KG Solomon, O TI Autism and the social world: an anthropological perspective SO DISCOURSE STUDIES LA English DT Article DE autism; conversational turn-taking; culture; indexicality; perspective-taking; situational scenario; social membership ID HIGH-FUNCTIONING ADULTS; NORMAL-CHILDREN; PRAGMATIC DEFICITS; MIND; DISCOURSE; PLAY; COMMUNICATION; COMPETENCE; EMOTIONS; STORIES AB This article offers an anthropological perspective on autism, a condition at once neurological and social, which complements existing psychological accounts of the disorder, expanding the scope of inquiry from the interpersonal domain, in which autism has been predominantly examined, to the socio-cultural one. Persons with autism need to be viewed not only as individuals in relation to other individuals, but as members of social groups and communities who act, displaying both social competencies and difficulties, in relation to socially and culturally ordered expectations of behavior. The article articulates a socio-cultural approach to perspective-taking in autism in three social domains: (1) participating in conversational turn-taking and sequences; (2) formulating situational scenarios; and (3) interpreting socio-cultural meanings of indexical forms and behavior. Providing ethnographic data on the everyday lives of high-functioning children with autism and Asperger syndrome, the article outlines a cline of competence across the three domains, from most success in conversational turn-taking to least in inferring indexical meanings. 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A., 1997, AUTISM EXECUTIVE DIS, P57 Tylor E, 1865, RES EARLY HIST MANKI UNGERER JA, 1987, J AUTISM DEV DISORD, V17, P3, DOI 10.1007/BF01487256 UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 Vinden P. G., 2000, UNDERSTANDING OTHER, P503 WALLACE A, 1965, CULTURE PERSONALITY Wechsler D., 1992, MANUAL WECHSLER INTE, V3rd WETHERBY AM, 1986, J AUTISM DEV DISORD, V16, P295, DOI 10.1007/BF01531661 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wittgenstein Ludwig, 1958, PHILOS INVESTIGATION WULFF SB, 1985, J AUTISM DEV DISORD, V15, P139, DOI 10.1007/BF01531600 Zelazo PD, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P195 NR 156 TC 35 Z9 35 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1461-4456 J9 DISCOURSE STUD JI Discourse Stud. PD MAY PY 2004 VL 6 IS 2 BP 147 EP 183 DI 10.1177/1461445604041766 PG 37 WC Communication SC Communication GA 828HB UT WOS:000221963300002 ER PT J AU Kremer-Sadlik, T AF Kremer-Sadlik, T TI How children with autism and Asperger Syndrome respond to questions: a 'naturalistic' theory of mind task SO DISCOURSE STUDIES LA English DT Article DE Asperger Syndrome; autism; ethnography; parents as trainers; question-answer sequences; scaffolding; theory of mind ID HIGH-FUNCTIONING ADULTS; PRAGMATIC DEFICITS; SYMBOLIC PLAY; LANGUAGE; COMMUNICATION; DISORDER; ADEQUACY AB In light of a well-documented deficit in theory of mind found in high-functioning individuals with autism (HFA) and Asperger Syndrome (AS), this article explores HFA and AS children's social-cognitive understanding of other people as reflected in their linguistic performance when answering mundane, everyday questions posed by their family members during dinnertime interaction. Ethnographic observations and video recordings of spontaneous interaction at home reveal that, contrary to findings in cognitive psychological research, the majority of the time the children were able to detect their interlocutors' communicative intentions and produce relevant responses that were marked by their conversational partners as acceptable. This article proposes that this success is due in part to parents who, through different strategies, facilitate their HFA and AS children's access to socio-cultural perspective-taking and their interlocutors' intentions, and better their children's communicative skills. C1 Univ Calif Los Angeles, CELF, Los Angeles, CA 90095 USA. RP Kremer-Sadlik, T (reprint author), Univ Calif Los Angeles, CELF, 341 Haines Hall, Los Angeles, CA 90095 USA. EM tksadlik@ucla.edu CR Attwood T., 1998, ASPERGERS SYNDROME G Austin J., 1962, DO THINGS WORDS Bar-On A, 1999, BRIT J SOC WORK, V29, P5 BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 Baron-Cohen S., 1996, MINDBLINDNESS ESSAY 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 BARTOLUCCI G, 1977, BRIT J DISORD COMMUN, V12, P137 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Capps L., 1997, CHILDREN AUTISM DEV Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 Cohen D. 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P., 1975, SYNTAX SEMANTICS, P41, DOI DOI 10.1017/S0022226700005296 Happe F., 1994, AUTISM INTRO PSYCHOL HARRIS S, 1985, COMMUNICATION PROBLE, P207 Hewitt LE, 1998, J COMMUN DISORD, V31, P135, DOI 10.1016/S0021-9924(97)00086-5 HOWLIN P, 1981, BRIT J DISORD COMMUN, V16, P73 Jordan R., 1993, CRITICAL INFLUENCES, P229 Kasari C, 2001, INT REV RES MENT RET, V23, P207 Keenan Ochs E., 1978, QUESTIONS POLITENESS, P44 Kleinman J, 2001, J AUTISM DEV DISORD, V31, P29, DOI 10.1023/A:1005657512379 KREMERSADLIK T, 2001, THESIS U LOS ANGELES Lave J, 1991, SITUATED LEARNING LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 Loveland K. 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A., 1992, RETHINKING CONTEXT L, P191 Schegloff Emmanuel, 1973, SEMIOTICA, V7, P289, DOI DOI 10.1515/SEMI.1973.8.4.289 Schutz A, 1932, PHENOMENOLOGY SOCIAL Sperber D., 1995, RELEVANCE COMMUNICAT SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 TagerFlusberg H, 1996, J AUTISM DEV DISORD, V26, P169, DOI 10.1007/BF02172006 TAGERFLUSBERG H, 1985, CHILD DEV, V56, P1167, DOI 10.1111/j.1467-8624.1985.tb00185.x Tager-Flusberg H, 2001, INT REV RES MENT RET, V23, P185 Tager-Flusberg H., 1988, DEV LANGUAGE LANGUAG, P249 Tager-Flusberg H., 1993, UNDERSTANDING OTHER, P138 TAGERFLUSBERG H, 1981, J AUTISM DEV DISORD, V11, P45, DOI 10.1007/BF01531340 TAGERFLUSBERG H, 1995, BRIT J DEV PSYCHOL, V13, P45 Tager-Flusberg H, 1989, AUTISM NATURE DIAGNO, P92 TAYLOR CE, 1995, THESIS U SO CALIFORN UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 Volkmar FR, 2001, INT REV RES MENT RET, V23, P83 Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER Wellman H. M., 1990, CHILDS THEORY MIND Wellman H, 1993, UNDERSTANDING OTHER, P10 WETHERBY AM, 1986, J AUTISM DEV DISORD, V16, P295, DOI 10.1007/BF01531661 WOLCHIK SA, 1982, J AUTISM DEV DISORD, V12, P43, DOI 10.1007/BF01531673 NR 65 TC 14 Z9 14 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1461-4456 J9 DISCOURSE STUD JI Discourse Stud. PD MAY PY 2004 VL 6 IS 2 BP 185 EP 206 DI 10.1177/1461445604041767 PG 22 WC Communication SC Communication GA 828HB UT WOS:000221963300003 ER PT J AU Sterponi, L AF Sterponi, L TI Construction of rules, accountability and moral identity by high-functioning children with autism SO DISCOURSE STUDIES LA English DT Article DE accountability; autism; moral positioning; practices of morality; sequential understanding ID MIND; DEFICITS; REPRESENTATION; DISCOURSE; BELIEF AB This article explores how high-functioning children with autism navigate in the social world, specifically how they orient in the realm of norms and standards. In particular, this investigation focuses on rule violations episodes and sheds light on how these children account for their (mis)conduct and position themselves in the moral framework. This analysis shows that high-functioning children with autism can actively engage in discourse about norms and transgressions in an initiatory capacity, thereby displaying a mastery of social rules as a guide for appropriate conduct and interpretation of others' behavior. Furthermore, this article argues that these social skills are linked with the ability to operate with sequentially based understandings: Prior courses of action constitute for the autistic children the fundamental source for reaching an understanding of the normative mechanics of everyday life, and subsequently for constructing their own lines of conduct and themselves as moral agents. C1 Univ Calif Los Angeles, Dept Anthropol, Los Angeles, CA 90095 USA. RP Sterponi, L (reprint author), Univ Calif Los Angeles, Dept Anthropol, Haines Hall, Los Angeles, CA 90095 USA. EM sterponi@humnet.ucla.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Asperger H., 1944, AUTISM ASPERGER SYND, P37 BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1986, BRIT J DEV PSYCHOL, V4, P113 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bergmann JR, 1998, RES LANG SOC INTERAC, V31, P279, DOI 10.1207/s15327973rlsi3103&4_1 Buttny Richard, 1993, SOCIAL ACCOUNTABILIT Dersley I, 2000, RES LANG SOC INTERAC, V33, P375, DOI 10.1207/S15327973RLSI3304_02 Dewey J., 1922, HUMAN NATURE CONDUCT Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X Frith U., 1995, COGNITION COGNITION, P13 Frith U., 1989, AUTISM EXPLAINING EN Garfinkel H, 1967, STUDIES ETHNOMETHODO Goffman Ervin, 1967, INTERACTION RITUAL Goffman Erving, 1981, FORMS TALK Happe F, 1999, PSYCHOLOGIST, V12, P540 HAPPE F, 1994, AUTISM Happe F, 1996, BRIT J DEV PSYCHOL, V14, P385 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 Infield Louis, 1775, LECT ETHICS, P228 Kanner L, 1943, NERV CHILD, V2, P217 KOEGEL LK, 1992, J APPL BEHAV ANAL, V25, P341, DOI 10.1901/jaba.1992.25-341 Lave J, 1991, SITUATED LEARNING LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 LESLIE AM, 1988, BRIT J DEV PSYCHOL, V6, P315 LESLIE AM, 1994, COGNITION, V50, P211, DOI 10.1016/0010-0277(94)90029-9 Leslie AM, 1988, DEV THEORIES MIND, P19 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Mills CW, 1940, AM SOCIOL REV, V5, P904, DOI 10.2307/2084524 Ochs E, 2001, SOC DEV, V10, P399, DOI 10.1111/1467-9507.00172 Ochs E, 2004, DISCOURSE STUD, V6, P147, DOI 10.1177/1461445604041766 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Rogoff B., 1984, EVERYDAY COGNITION I Rogoff Barbara, 1990, APPRENTICESHIP THINK Russell J., 1997, AUTISM EXECUTIVE DIS Sacks H., 1992, LECT CONVERSATION SCHEGLOFF EA, 1977, LANGUAGE, V53, P361, DOI 10.2307/413107 SCHEGLOFF EA, 1995, UNPUB SEQUENCE ORG Schutz A, 1932, PHENOMENOLOGY SOCIAL SCOTT MB, 1968, AM SOCIOL REV, V33, P46, DOI 10.2307/2092239 Sterponi L, 2003, DISCOURSE STUD, V5, P79, DOI 10.1177/1461445603005001840 Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x Whiten Andrew, 1991, NATURAL THEORIES MIN WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Wittgenstein Ludwig, 1958, PHILOS INVESTIGATION Wootton A. J., 1997, INTERACTION DEV MIND NR 51 TC 9 Z9 9 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1461-4456 J9 DISCOURSE STUD JI Discourse Stud. PD MAY PY 2004 VL 6 IS 2 BP 207 EP 228 DI 10.1177/1461445604041768 PG 22 WC Communication SC Communication GA 828HB UT WOS:000221963300004 ER PT J AU Sirota, KG AF Sirota, KG TI Positive politeness as discourse process: politeness practices of high-functioning children with autism and Asperger Syndrome SO DISCOURSE STUDIES LA English DT Article DE autism spectrum disorders; children; discourse; politeness; practice; social reciprocity ID IMMEDIATE ECHOLALIA; VERBAL-ABILITY; MIND AB This study draws upon naturalistic ethnographic data to expand current understandings regarding the socio-communicative capabilities and challenges of children with autism spectrum disorders in mid-childhood. Affording a view of the children's spontaneous interactions within naturally occurring family and community settings, the study explores a range of discursive resources utilized by the children to accomplish socially reciprocal positive politeness practices in tandem with others. Emphasizing contextualized deployment of politeness forms in interaction, the practice-based conception developed here construes positive politeness as a discursive process encompassing both socio-cultural and interpersonal knowledge/skills; and contributes to a perspective in which social and communicative realms are conceptualized as integrated domains of functioning. C1 Univ Calif Los Angeles, Dept Anthropol, Los Angeles, CA 90095 USA. RP Sirota, KG (reprint author), Univ Calif Los Angeles, Dept Anthropol, 341 Haines Hall,Box 951553, Los Angeles, CA 90095 USA. EM ksirota@ucla.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT BALTAXE CAM, 1985, PROSODIC DEV NORMAL Baron D, 2002, WIREL NETW, V8, P5, DOI 10.1023/A:1012744023290 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BLEULER E, 1916, LB PSYCHIAT BROWN JW, 1995, J MUSICOL RES, V15, P3, DOI 10.1080/01411899508574711 Brown P., 1987, POLITENESS SOME UNIV Brown Penelope, 1998, J LINGUIST ANTHROPOL, V8, P197, DOI [10.1525/jlin.1998.8.2.197, DOI 10.1525/JLIN.1998.8.2.197] Brown Penelope, 1978, QUESTIONS POLITENESS, P56 Bruner J. S., 1990, ACTS MEANING Cohen D. 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PD MAY PY 2004 VL 6 IS 2 BP 229 EP 251 DI 10.1177/1461445604041769 PG 23 WC Communication SC Communication GA 828HB UT WOS:000221963300005 ER PT J AU Solomon, O AF Solomon, O TI Narrative introductions: discourse competence of children with autistic spectrum disorders SO DISCOURSE STUDIES LA English DT Article DE autism; discourse competence; fictional narrative narrative; narrative introduction practices; narrative of personal experience ID HIGH-FUNCTIONING ADULTS; CENTRAL COHERENCE; MIND AB This article examines the discourse competence of high-functioning children with autistic spectrum disorders (ASD) to participate in narrative introduction sequences with family members. The analysis illuminates the children's own efforts to launch narratives, as well as their ability to build upon the contributions of others. Ethnographic, discourse analytic methodology is integrated with the theory of discourse organization and the weak central coherence account of autism. Introductions of both personal experience narratives as well as fictional narratives (from television programs, computer games and other media) are examined. The children were especially competent in the use of stable introductory practices when launching fictional narratives, pre-organized by the media of expression. Their challenge was not in the introduction, but in the narrative co-telling, which often was not globally organized over an extended course of propositions. The heterogeneity of the ASD children's discourse competence and its implications for discourse analysis are discussed. C1 Univ Calif Los Angeles, Dept Anthropol, Los Angeles, CA 90095 USA. RP Solomon, O (reprint author), Univ Calif Los Angeles, Dept Anthropol, 341 Haines Hall,Box 951553, Los Angeles, CA 90095 USA. EM solomono@ucla.edu CR American Psychiatric Association, 1980, DIAGN STAT MAN MENT ANDERSEN R, 1999, 1 UCLA CROSSL RES PR Atkinson J. M., 1984, STRUCTURES SOCIAL AC Bakhtin M. 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PD MAY PY 2004 VL 6 IS 2 BP 253 EP 276 DI 10.1177/1461445604041770 PG 24 WC Communication SC Communication GA 828HB UT WOS:000221963300006 ER PT J AU Akyol, O Zoroglu, SS Armutcu, F Sahin, S Gurel, A AF Akyol, O Zoroglu, SS Armutcu, F Sahin, S Gurel, A TI Nitric oxide as a physiopathological factor in neuropsychiatric disorders SO IN VIVO LA English DT Review DE nitric oxide; nitric oxide synthases; schizophrenia; mood disorder; depression; autism; Parkinson's disease; Alzheimer's disease; review ID MESSENGER-RNA EXPRESSION; CENTRAL-NERVOUS-SYSTEM; ESSENTIAL FATTY-ACIDS; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; SCHIZOPHRENIC-PATIENTS; LIPID-PEROXIDATION; PATHOPHYSIOLOGICAL ROLE; SYNTHASE INHIBITORS; SUBSTANTIA-NIGRA AB The dominant research subject on schizophrenia, mood disorders, autism and other central nervous system diseases has been related to neurotransmitter system abnormalities. For example, the dopamine hypothesis states that schizophrenia is the result of dopaminergic hyperactivity. The therapeutic approach has also been directed towards finding agents which will modulate or regulate these neurotransmitter systems at any step. There is substantial and mounting evidence that subtle abnormalities of reactive oxygen species (ROS) and nitric oxide (NO) may underlie a wide range of neuropsychiatric disorders. NO has chemical properties that make it uniquely suitable as an intracellular and intercellular messenger. It is produced by the activity of nitric oxide synthases which are present in peripheral tissues and in neurons. On the other hand, NO is known to be an oxygen radical in the central and peripheral nervous systems. NO has been implicated in a number of physiological functions such as noradrenaline and dopamine releases, memory and learning and certain pathologies such as schizophrenia, bipolar disorder and major depression. Evidence has been considered here for the proposal that an abnormality of NO metabolism may be a contributory factor in some neuropsychiatric disorders. The direct evidence for NO abnormalities in schizophrenia and other psychiatric disorders remains relatively limited to date, although there are some clinical and experimental studies. The suggestion that NO and other ROS may play a role in some neuropsychiatric disorders clearly has important implications for new treatment possibilities. The primary objective of the present review was to summarize and critically evaluate the current knowledge regarding a potential contribution of NO to the neuropathophysiology of schizophrenia as well as other neuropsychiatric disorders. C1 Hacettepe Univ, Sch Med, Dept Biochem, Fac Med, TR-06100 Ankara, Turkey. Gaziantep Univ, Fac Med, Dept Biochem, Gaziantep, Turkey. Zonguldak Karaelmas Univ, Fac Med, Dept Biochem, Zonguldak, Turkey. Gaziosmanpasa Univ, Dept Biochem, Tokat, Turkey. RP Akyol, O (reprint author), Hacettepe Univ, Sch Med, Dept Biochem, Fac Med, TR-06100 Ankara, Turkey. 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A young child with autism exhibited excessively loud screaming, yelling, humming, and other distracting noises during class activities in a special education setting. These disruptive behaviors were a serious concern and also hampered the teacher's efforts to place the child in more inclusive environments. The partnership members first systematically assessed the target behaviors and then consulted existing research interventions addressing those behaviors. Basing their efforts on previous research, the partnership members developed social stories and implemented them through a single-subject research design. Ongoing observations and consultations, as well as input from all partnership members, formed the basis for any changes made to the intervention. At morning circle time, data on inappropriate behavior (yelling) and appropriate sitting were collected during baseline, Intervention Phase 1, Intervention Phase 2, and return-to-baseline conditions. 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PD MAY PY 2004 VL 39 IS 5 BP 276 EP 287 DI 10.1177/10534512040390050401 PG 12 WC Education, Special SC Education & Educational Research GA 817FW UT WOS:000221164400004 ER PT J AU Lerman-Sagie, T Leshinsky-Silver, E Watemberg, N Lev, D AF Lerman-Sagie, T Leshinsky-Silver, E Watemberg, N Lev, D TI Should autistic children be evaluated for mitochondrial disorders? SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID RETT-SYNDROME; DYSFUNCTION; DIAGNOSIS; HYPOTONIA; AGE AB Autism is etiologically heterogeneous; medical conditions are implicated in only a minority of cases, whereas metabolic disorders are even less common. Recently, there have been articles describing the association of autism with mitochondrial abnormalities. We critically review the current literature and conclude that mitochondrial disorders are probably a rare and insignificant cause of pure autism; however, evidence is accumulating that both autosomal recessive and maternally inherited mitochondrial disorders can present with autistic features. Most patients will present with multisystem abnormalities associated with autistic behavior. Finding biochemical or structural mitochondrial abnormalities in an autistic child does not necessarily imply a primary mitochondrial disorder but can also be secondary to technical inaccuracies or another genetic disorder. Clinicians should be careful in diagnosing a mitochondrial disorder in an autistic child because it has important implications for accurate genetic counseling, prognosis, and therapy. C1 Wolfson Med Ctr, Pediat Neurol Unit, IL-58100 Holon, Israel. Wolfson Med Ctr, Inst Med Genet, IL-58100 Holon, Israel. Wolfson Med Ctr, Metab Neurogenet Serv, Mitochondrial Dis Clin, IL-58100 Holon, Israel. Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. RP Lerman-Sagie, T (reprint author), Wolfson Med Ctr, Pediat Neurol Unit, POB 5, IL-58100 Holon, Israel. EM asagie@post.tau.ac.il CR Berger A, 2001, DIAGN MOL PATHOL, V10, P55, DOI 10.1097/00019606-200103000-00009 BOFFOLI D, 1994, BBA-MOL BASIS DIS, V1226, P73, DOI 10.1016/0925-4439(94)90061-2 COKER SB, 1991, J CHILD NEUROL, V6, P164 COLEMAN M, 1985, J AUTISM DEV DISORD, V15, P1, DOI 10.1007/BF01837894 DOTTI MT, 1993, BRAIN DEV-JPN, V15, P103, DOI 10.1016/0387-7604(93)90045-A Filiano JJ, 2002, J CHILD NEUROL, V17, P435, DOI 10.1177/088307380201700607 Filipek PA, 2000, NEUROLOGY, V55, P468 Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 GILLBERG C, 1992, CLIN DEV MED, V126, P203 GILLBERG C, 1992, J INTELL DISABIL RES, V36, P201 Graf WD, 2000, J CHILD NEUROL, V15, P357, DOI 10.1177/088307380001500601 Heilstedt HA, 2002, AM J MED GENET, V111, P238, DOI 10.1002/ajmg.10633 Kang PB, 2001, J CHILD NEUROL, V16, P657, DOI 10.1177/088307380101600906 Lauritsen MB, 2001, ACTA PSYCHIAT SCAND, V103, P411, DOI 10.1034/j.1600-0447.2001.00086.x LEE CP, 1995, BBA-MOL BASIS DIS, V1271, P21, DOI 10.1016/0925-4439(95)00005-O LEFAI E, 1995, BBA-BIOENERGETICS, V1228, P43, DOI 10.1016/0005-2728(94)00157-Z Lombard J, 1998, MED HYPOTHESES, V50, P497, DOI 10.1016/S0306-9877(98)90270-5 Maestrini E, 2000, NEURON, V28, P19, DOI 10.1016/S0896-6273(00)00081-7 Nissenkorn A, 1999, ARCH DIS CHILD, V81, P209 TRIJBELS JMF, 1993, EUR J PEDIATR, V152, P178, DOI 10.1007/BF01956139 ZHANG X, 1990, BIOCHIM BIOPHYS ACTA, V1019, P1 NR 21 TC 18 Z9 18 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 MAY PY 2004 VL 19 IS 5 BP 379 EP 381 DI 10.1177/088307380401900510 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 829BD UT WOS:000222017000011 PM 15224710 ER PT J AU Frith, U AF Frith, U TI Emanuel Miller lecture: Confusions and controversies about Asperger Syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article ID HIGH-FUNCTIONING AUTISM; CEREBRAL-BLOOD-FLOW; DEVELOPMENTAL DISORDER; LANGUAGE IMPAIRMENT; FACIAL EXPRESSIONS; FOLLOW-UP; MIND; CHILDREN; ADULTS; ADOLESCENTS AB Background: Hans Asperger drew attention to individuals who show the core symptoms of autism in the presence of high verbal intelligence. Methods: A review of the literature explores current issues concerning the diagnosis and nature of Asperger syndrome. Results: The behavioural and neurophysiological evidence to date suggests that Asperger syndrome is a variant of autism typically occurring in high-functioning individuals, and not a separate disorder. One of the problems of diagnosis is that the typical impairment of social communication may be difficult to identify in early childhood, and can be camouflaged in adulthood by compensatory learning. The range and nature of the social impairments in Asperger syndrome are still in need of investigation, but appear to be less severe than in autism. Experimental evidence suggests that individuals with Asperger syndrome may lack an intuitive theory of mind (mentalising), but may be able to acquire an explicit theory of mind. Brain imaging studies pinpoint a network that links medial prefrontal and temporal cortex as the neural substrate of intuitive mentalising. This network shows reduced activation and poor connectivity in Asperger syndrome. While some individuals with Aspergcr syndrome have written eloquently about their lives, their ability to talk about their own emotions appears to be impaired (alexithymia). This impairment may be linked to depression and anxiety, which is common in adulthood. Little is as yet known about the often considerable cognitive strengths in Asperger syndrome, or about the difficulties observed in higher-level executive skills. Conclusions: Studies arc needed that define the developmental course of the disorder and the nature of the strengths and weaknesses in both social and non-social domains. This requires more sensitive assessment instruments than are currently available. Questions about the prevalence of Asperger syndrome, about associated and secondary features, and about optimal education and management, urgently call for such studies. C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. RP Frith, U (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England. 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J PSYCHIAT, V159, P895, DOI 10.1176/appi.ajp.159.6.895 Klin A., 2000, ASPERGER SYNDROME LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Little L, 2001, J AM ACAD CHILD PSY, V40, P995, DOI 10.1097/00004583-200109000-00007 Mayes SD, 2001, AUTISM, V5, P81, DOI 10.1177/1362361301005001008 Mayes SD, 2001, J ABNORM CHILD PSYCH, V29, P263, DOI 10.1023/A:1010337916636 McAlonan GM, 2002, BRAIN, V125, P1594, DOI 10.1093/brain/awf150 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Mottron L, 2003, J CHILD PSYCHOL PSYC, V44, P904, DOI 10.1111/1469-7610.00174 Murphy DGM, 2002, ARCH GEN PSYCHIAT, V59, P885, DOI 10.1001/archpsyc.59.10.885 Nieminen-von Wendt T, 2003, EUR CHILD ADOLES PSY, V12, P178, DOI 10.1007/s00787-003-0337-z Plaisted K, 2003, PHILOS T ROY SOC B, V358, P375, DOI 10.1098/rstb.2002.1211 PRIOR M, 2003, ASPERGER SYNDROME BE REITZEL J, 2003, ASPERGER SYNDROME BE, P35 Rinehart NJ, 2002, AUST NZ J PSYCHIAT, V36, P762, DOI 10.1046/j.1440-1614.2002.01097.x Roeyers H, 2001, J CHILD 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PSYC, V39, P755, DOI 10.1017/S0021963098002510 Ziatas K, 2003, DEV PSYCHOPATHOL, V15, P73, DOI 10.1017/S0954579403000051 NR 89 TC 159 Z9 159 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0021-9630 EI 1469-7610 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAY PY 2004 VL 45 IS 4 BP 672 EP 686 DI 10.1111/j.1469-7610.2004.00262.x PG 15 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 826CB UT WOS:000221805400003 PM 15056300 ER PT J AU Constantino, JN Gruber, CP Davis, S Hayes, S Passanante, N Przybeck, T AF Constantino, JN Gruber, CP Davis, S Hayes, S Passanante, N Przybeck, T TI The factor structure of autistic traits SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; pervasive developmental disorders; Social Responsiveness Scale (SRS); psychometrics; genetic studies; broader autism phenotype ID RECIPROCAL SOCIAL-BEHAVIOR; PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; PHENOTYPE; FAMILIES; CHILDREN; DOMAINS AB Background: Although DSM-IV requires symptoms in three criterion domains for a diagnosis of autistic disorder, the extent to which those domains are phenotypically independent is an unanswered and important question. The identification of endophenotypes'of the autistic syndrome may be very useful for genetic and neurobiologic studies of autism, but only if they represent truly independent sub domains of the disorder. Methods: In this study we examined the factor structure of autistic traits using data from 226 child psychiatric patients with and without pervasive developmental disorders, employing cluster analysis of data from the Autism Diagnostic Interview-Revised (ADI-r) and principal components factor analysis of data from the Social Responsiveness Scale (SRS, a quantitative genetic measure of autistic traits formerly known as the Social Reciprocity Scale). Results: The results were consistent with the existence of a singular, continuously distributed underlying factor, resulting in disparate phenotypic manifestations across the three criterion domains for autistic disorder (social deficits, language deficits, and repetitive/ stereotypic behaviors). Conclusion: The analyses generally failed to support the existence of independent sub domains of dysfunction in autism spectrum conditions. Future studies of the association between genetic/ neurobiologic markers and autistic symptomatology may be enhanced by approaches which consider autistic symptoms as quantitative traits, and which are informed by ongoing research on the development and phenomenology of core deficiencies in reciprocal social behavior. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, Campus Box 8134,660 S Euclid Ave, St Louis, MO 63110 USA. EM constantino@wustl.edu CR Charman T, 2003, PHILOS T ROY SOC B, V358, P315, DOI 10.1098/rstb.2002.1199 Constantino JN, 2003, J AM ACAD CHILD PSY, V42, P458, DOI 10.1097/01.CHI.0000046811.95464.21 Constantino JN, 2003, J AUTISM DEV DISORD, V33, P427, DOI 10.1023/A:1025014929212 Constantino JN, 2002, SOCIAL RESPONSIVENES Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2000, J DEV BEHAV PEDIATR, V21, P2 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 KLIN A, 2003, PHILOS T ROY SOC LON, V358, P348 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Miles JH, 2000, AM J MED GENET, V95, P339, DOI 10.1002/1096-8628(20001211)95:4<339::AID-AJMG9>3.0.CO;2-B Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 Piven J, 1997, AM J PSYCHIAT, V154, P185 Robertson JM, 1999, J AM ACAD CHILD PSY, V38, P738, DOI 10.1097/00004583-199906000-00022 *SAS I INC, 2000, SAS MAN Silverman JM, 2002, AM J MED GENET, V114, P64, DOI 10.1002/ajmg.10048 Spiker D, 2002, AM J MED GENET, V114, P129, DOI 10.1002/ajmg.10188 Waterhouse L, 1996, J AUTISM DEV DISORD, V26, P59, DOI 10.1007/BF02276235 WOLFF S, 1988, J CHILD PSYCHOL PSYC, V29, P143, DOI 10.1111/j.1469-7610.1988.tb00699.x NR 19 TC 146 Z9 147 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAY PY 2004 VL 45 IS 4 BP 719 EP 726 DI 10.1111/j.1469-7610.2004.00266.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 826CB UT WOS:000221805400007 PM 15056304 ER PT J AU Krol, N Morton, J De Bruyn, E AF Krol, N Morton, J De Bruyn, E TI Theories of conduct disorder: a causal modelling analysis SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE causal modelling; causal theories; conduct disorder ID EXECUTIVE FUNCTION DEFICITS; LIFE-COURSE-PERSISTENT; ANTISOCIAL-BEHAVIOR; CHILDREN; PSYCHOPATHY; AGGRESSION; AUTISM AB Background: If a clinician has to make decisions on diagnosis and treatment, he or she is confronted with a variety of causal theories. In order to compare these theories a neutral terminology and notational system is needed. The Causal Modelling framework involving three levels of description - biological, cognitive and behavioural - has previously been used to compare causal accounts for dyslexia and autism. Method: In this article we present this framework and explore its application to four causal theories of conduct disorder. We discuss the problems we encountered in this application and evaluate both the framework and the theories of conduct disorder. Conclusions: It was possible to capture parts of the theories of conduct disorder in the Causal Modelling framework but a multi-model approach may be necessary for the alternative theories of conduct disorder we evaluate. The application of the framework helps to see the relationships among the various theories of aspects of conduct disorder and demonstrates the need for more explicitness in the causal theories. C1 Univ Nijmegen, Fac Social Sci, NL-6500 HE Nijmegen, Netherlands. UCL, Inst Cognit Neurosci, London, England. 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Q., 1985, CRIME HUMAN NATURE NR 52 TC 13 Z9 13 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 MAY PY 2004 VL 45 IS 4 BP 727 EP 742 DI 10.1111/j.1469-7610.2004.00267.x PG 16 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 826CB UT WOS:000221805400008 PM 15056305 ER PT J AU Dyck, MJ Farrugia, C Shochet, IM Holmes-Brown, M AF Dyck, MJ Farrugia, C Shochet, IM Holmes-Brown, M TI Emotion recognition/understanding ability in hearing or vision-impaired children: do sounds, sights, or words make the difference? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE emotion recognition; empathy; language; conversation; deaf; blind ID HIGH-FUNCTIONING AUTISM; DEAF-CHILDREN; NONVERBAL INTELLIGENCE; ASPERGER-SYNDROME; INDIVIDUAL-DIFFERENCES; BLIND-CHILDREN; NORMAL ADULTS; MIND; LANGUAGE; BELIEFS AB Background: This study was designed to assess whether children with a sensory disability have consistent delays in acquiring emotion recognition and emotion understanding abilities. Method: Younger (6-11 years) and older (12-18 years) hearing-impaired children (HI; n = 49), vision-impaired children (VI; n = 42), and children with no sensory impairment (NSI; n = 72) were assessed with the Emotion Recognition Scales (ERS), which include two tests of the ability to recognize vocal expressions of emotion, two tests of the ability to recognize facial expressions of emotion, and three tests of emotion understanding. Results: Results indicate that when compared with age-peers, HI children and adolescents have significant delays or deficits on all ERS, but VI children and adolescents are delayed only on emotion recognition tasks. When compared with children group-matched for verbal ability (Wechsler verbal scales), the achievement of HI children on ERS equals or exceeds that of controls; VI children underachieve on an emotion recognition task and overachieve on an emotion vocabulary task compared to verbal ability matched peers. Conclusions: We conclude that VI children have a specific emotion recognition deficit, but among HI children, performance on emotion recognition and emotion understanding tasks reflects delayed acquisition of a broad range of language-mediated abilities. C1 Curtin Univ Technol, Sch Psychol, Perth, WA 6001, Australia. Griffith Univ, Sch Appl Psychol, Nathan, Qld 4111, Australia. RP Dyck, MJ (reprint author), Curtin Univ Technol, Sch Psychol, GPO Box U1987, Perth, WA 6001, Australia. EM m.dyck@curtin.edu.au RI Lee, Hyunjoo/D-9122-2011 CR BACHARA GH, 1980, AM ANN DEAF, V125, P38 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 Baron-Cohen S, 2002, MIND READING INTERAC BARONCOHEN S, 1994, CAH PSYCHOL COGN, V13, P513 BIGELOW A, 1990, J VISUAL IMPAIR BLIN, V84, P414 BIGELOW AE, 1992, J VISUAL IMPAIR BLIN, V86, P181 BRETHERTON I, 1982, DEV PSYCHOL, V18, P906, DOI 10.1037//0012-1649.18.6.906 BRNICH P, 1981, J COMMUN DISORD, V14, P429 Brubaker RG, 2000, CHILD FAM BEHAV THER, V22, P13, DOI 10.1300/J019v22n04_02 Courtin C., 2000, J DEAF STUD DEAF EDU, V5, P266, DOI DOI 10.1093/DEAFED/5.3.266 Cutting AL, 1999, CHILD DEV, V70, P853, DOI 10.1111/1467-8624.00061 DIMCOVIC N, 1995, J VISUAL IMPAIR BLIN, V89, P448 DYCK M, 2003, UNPUB IS DISCREPANCY DYCK M, 2003, UNPUB CORRELATIONS L Dyck M.J., 2003, J DEAF STUD DEAF EDU, V8, P348, DOI DOI 10.1093/DEAFED/ENG019 Dyck MJ, 2001, EUR CHILD ADOLES PSY, V10, P105 Garfield JL, 2001, MIND LANG, V16, P494, DOI 10.1111/1468-0017.00180 GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x Gray C. 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Child Psychol. Psychiatry PD MAY PY 2004 VL 45 IS 4 BP 789 EP 800 DI 10.1111/j.1469-7610.2004.00272.x PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 826CB UT WOS:000221805400013 PM 15056310 ER PT J AU Geurts, HM Vertie, S Oosterlaan, J Roeyers, H Sergeant, JA AF Geurts, HM Vertie, S Oosterlaan, J Roeyers, H Sergeant, JA TI How specific are executive functioning deficits in attention deficit hyperactivity disorder and autism? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE ADHD; autism; executive functions ID CARD-SORTING-TEST; CHILDRENS COMMUNICATION CHECKLIST; DIAGNOSTIC INTERVIEW SCHEDULE; INHIBITORY MOTOR CONTROL; LATENT-VARIABLE ANALYSIS; DEFICIT/HYPERACTIVITY DISORDER; FRONTAL-LOBE; RESPONSE-INHIBITION; DISRUPTIVE BEHAVIOR; WORKING-MEMORY AB Background: The objective of this study is to identify intact and deficient cognitive processes in children with attention deficit hyperactivity disorder (ADHD) and children with high functioning autism (HFA). Method: Three rigorously diagnosed groups of children aged between 6 and 12 years (54 ADHD, 41 HFA, and 41 normal controls) were tested on a wide range of tasks related to five major domains of executive functioning (EF): inhibition, visual working memory, planning, cognitive flexibility, and verbal fluency. In addition, the role of comorbid oppositional defiant disorder (ODD) and comorbid conduct disorder (CD) in ADHD was investigated by directly comparing 20 children with ADHD and 34 children with comorbid ADHD + ODD/CD. Results: ADED was associated with EF deficits in inhibiting a prepotent response and verbal fluency. Children with HFA demonstrated deficits in all EF domains, except interference control and working memory. The HFA group showed more difficulties than the ADHD group with planning and cognitive flexibility. The comorbid ADHD + ODD/CD group did not show a distinctive pattern of performance on the EF tests compared to the ADHD group. Conclusion: The present study indicates that children with HFA exhibit more generalised and profound problems with EF tasks compared to children with ADHD. C1 Univ Amsterdam, Div Psychon, NL-1018 WB Amsterdam, Netherlands. Vrije Univ Amsterdam, Dept Clin Neuropsychol, Amsterdam, Netherlands. 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Psychiatry PD MAY PY 2004 VL 45 IS 4 BP 836 EP 854 DI 10.1111/j.1469-7610.2004.00276.x PG 19 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 826CB UT WOS:000221805400017 PM 15056314 ER PT J AU Pilowsky, T Yirmiya, N Doppelt, O Gross-Tsur, V Shalev, RS AF Pilowsky, T Yirmiya, N Doppelt, O Gross-Tsur, V Shalev, RS TI Social and emotional adjustment of siblings of children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autistic disorder; behavioral genetics; social emotional adjustment; siblings ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HISTORY; COGNITIVE DISABILITIES; PHENOTYPE; RELATIVES; BOYS; INDIVIDUALS; IMPAIRMENT; EXPRESSION; COMPETENCE AB Background: Social and emotional adjustment of siblings of children with autism was examined, to explore their risk or resilience to effects of genetic liability and environmental factors involved in having a sibling with autism. Method: Social-emotional adjustment, behavior problems, socialization skills, and siblings' relationships were compared among 30 siblings of children with autism, 28 siblings of children with mental retardation of unknown genetic etiology (MR), and 30 siblings of children with developmental language disorders (DLD). Groups were matched by probands' gender, siblings' chronological age, gender, IQ, and birth order, and by family size, ethnicity, and parental income, employment, and stress level. Results: Four siblings of children with autism, three siblings of children with MR, and seven siblings of children with DLD received DSM-IV diagnoses. Nevertheless, most of the siblings were well adjusted. Conclusions: The adjustment of siblings of children with autism is in sharp contrast to the severe social and emotional disabilities characteristic of autism, and is noteworthy considering the stress involved in having a sibling with autism. 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Child Psychol. Psychiatry PD MAY PY 2004 VL 45 IS 4 BP 855 EP 865 DI 10.1111/j.1469-7610.2004.00277.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 826CB UT WOS:000221805400018 PM 15056315 ER PT J AU Skuse, D Warrington, R Bishop, D Chowdhury, U Lau, J Mandy, W Place, M AF Skuse, D Warrington, R Bishop, D Chowdhury, U Lau, J Mandy, W Place, M TI The developmental, dimensional and diagnostic interview (3di): A novel computerized assessment for autism spectrum disorders SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; interview; computerized; validity; reliability ID CHILDRENS COMMUNICATION CHECKLIST; K-SADS; SCHEDULE; RELIABILITY; PREVALENCE; VERSION; SCHIZOPHRENIA; IMPAIRMENT; FUTURE AB Objective: Autism is a diagnostic spectrum of variable severity, with significant comorbidity. No existing standardized interview measures autistic features dimensionally. The authors aimed to develop a parental autism interview that could be administered to unselected clinical and general population samples that measures both symptom intensity and comorbidity across the full range of the autistic spectrum. Method: A computerized procedure was devised for administration by trained interviewers that generates symptom and diagnostic profiles for both autism and non-autistic conditions. Test-retest reliability and interrater reliability were assessed in unselected clinical (n = 50) and nonclinical (n = 30) populations. Concurrent validity (n = 120), discriminant validity (n = 120), and criterion validity (n = 29) were evaluated in autistic spectrum and non-autistic patients. Results: Test-retest and interrater reliabilities were excellent (most intraclass correlation coefficients > 0.9). Concurrent validity (agreement with independent clinician formulation) was very good (mean kappa = 0.74). Criterion validity, a comparison with the Autism Diagnostic Interview, was excellent. Discrimination between autistic spectrum versus non-autistic subjects was almost perfect (sensitivity 1.0; specificity > 0.97). Conclusions: The Developmental, Dimensional and Diagnostic Interview (3di) provides an efficient and accurate means of assessing, in dimensional terms, the presence of autistic symptoms in both clinical and normal populations. It offers novel opportunities for those engaged in research and clinical practice. C1 UCL, Inst Child Hlth, London WC1N 1EH, England. Northumbria Univ, Ctr Parenting, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England. Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Skuse, D (reprint author), UCL, Inst Child Hlth, 30 Guilford St, London WC1N 1EH, England. 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EM eileen_simon@alum.barnard.edu CR Brown R., 1973, 1 LANGUAGE EARLY STA Horton R, 2004, LANCET, V363, P747, DOI 10.1016/S0140-6736(04)15714-0 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Wilkerson DS, 2002, INT J NEUROSCI, V112, P1085, DOI 10.1080/00207450290026076 WINDLE W F, 1969, Scientific American, V221, P76 NR 5 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 MAY 1 PY 2004 VL 363 IS 9419 BP 1473 EP 1474 DI 10.1016/S0140-6736(04)16110-2 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 816ST UT WOS:000221130300024 PM 15121413 ER PT J AU Gharani, N Benayed, R Mancuso, V Brzustowicz, LM Millonig, JH AF Gharani, N Benayed, R Mancuso, V Brzustowicz, LM Millonig, JH TI Association of the homeobox transcription factor, ENGRAILED 2, 3, with autism spectrum disorder SO MOLECULAR PSYCHIATRY LA English DT Article DE ENGRAILED2; cerebellum; autism; chromosome 7 ID SINGLE NUCLEOTIDE POLYMORPHISMS; CEREBELLAR PURKINJE-CELLS; EARLY INFANTILE-AUTISM; GENOMEWIDE SCREEN; TRANSMISSION/DISEQUILIBRIUM TEST; LINKAGE-DISEQUILIBRIUM; SEROTONIN TRANSPORTER; SUSCEPTIBILITY LOCI; BRAIN-STEM; GENE AB Mouse mutants of the homeobox transcription factor Engrailed2 (En2) and autistic individuals display similar cerebellar morphological abnormalities, which include hypoplasia and a decrease in the number of Purkinje cells.(1-19) Human EN2 maps to 7q36, a chromosomal region that has demonstrated suggestive linkage to autism spectrum disorder (ASD).(20-22) To investigate EN2 for evidence of association with ASD, four single-nucleotide polymorphisms (SNPs) (rs3735653, rs1861972, rs1861973, rs2361689) that span the majority of the 8.0 kb gene were assessed by the transmission/disequilibrium test(23-26). Initially, 138 triads of autistic individuals and their parents were tested. Two intronic SNPs (rs1861972 and rs1861973) demonstrated significant association with autism (rs1861972, P = 0.0018; rs1861973, P = 0.0003; haplotype, P = 0.000005). Flanking exonic SNPs (rs3735653 and rs2361689) did not display association. This analysis was then extended to include 167 small nuclear ASD pedigrees and significant association was again only observed for rs1861972 and rs1861973 under both the narrow and broad diagnostic criteria (narrow: rs1861972 P = 0.0290, rs1861973 P = 0.0073, haplotype P = 0.0009; broad: rs1861972 P = 0.0175, rs1861973 P = 0.0107, haplotype P = 0.0024). These data demonstrate association between a cerebellar patterning gene and ASD, suggesting a role for EN2 as a susceptibility locus and supporting a neurodevelopmental defect hypothesis in the etiology of autism. C1 Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA. 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Neurosci. PD MAY PY 2004 VL 7 IS 5 BP 499 EP 500 DI 10.1038/nn1223 PG 2 WC Neurosciences SC Neurosciences & Neurology GA 816HP UT WOS:000221101300026 PM 15077111 ER PT J AU Muhle, R Trentacoste, SV Rapin, I AF Muhle, R Trentacoste, SV Rapin, I TI The genetics of autism SO PEDIATRICS LA English DT Review DE autism; genetic; chromosome; review ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER GENE; TUBEROUS SCLEROSIS COMPLEX; RECEPTOR SUBUNIT GENES; FRAGILE-X-SYNDROME; ANGELMAN-SYNDROME; SPECTRUM DISORDERS; INFANTILE-AUTISM; LINKAGE-DISEQUILIBRIUM; SUSCEPTIBILITY GENE AB Autism is a complex, behaviorally defined, static disorder of the immature brain that is of great concern to the practicing pediatrician because of an astonishing 556% reported increase in pediatric prevalence between 1991 and 1997, to a prevalence higher than that of spina bifida, cancer, or Down syndrome. This jump is probably attributable to heightened awareness and changing diagnostic criteria rather than to new environmental influences. Autism is not a disease but a syndrome with multiple nongenetic and genetic causes. By autism ( the autistic spectrum disorders [ASDs]), we mean the wide spectrum of developmental disorders characterized by impairments in 3 behavioral domains: 1) social interaction; 2) language, communication, and imaginative play; and 3) range of interests and activities. Autism corresponds in this article to pervasive developmental disorder (PDD) of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition and International Classification of Diseases, Tenth Revision. Except for Rett syndrome - attributable in most affected individuals to mutations of the methyl-CpG-binding protein 2 (MeCP2) gene - the other PDD subtypes ( autistic disorder, Asperger disorder, disintegrative disorder, and PDD Not Otherwise Specified [PDD-NOS]) are not linked to any particular genetic or nongenetic cause. Review of 2 major textbooks on autism and of papers published between 1961 and 2003 yields convincing evidence for multiple interacting genetic factors as the main causative determinants of autism. Epidemiologic studies indicate that environmental factors such as toxic exposures, teratogens, perinatal insults, and prenatal infections such as rubella and cytomegalovirus account for few cases. These studies fail to confirm that immunizations with the measles-mumps- rubella vaccine are responsible for the surge in autism. Epilepsy, the medical condition most highly associated with autism, has equally complex genetic/nongenetic ( but mostly unknown) causes. Autism is frequent in tuberous sclerosis complex and fragile X syndrome, but these 2 disorders account for but a small minority of cases. Currently, diagnosable medical conditions, cytogenetic abnormalities, and single-gene defects (eg, tuberous sclerosis complex, fragile X syndrome, and other rare diseases) together account for < 10% of cases. There is convincing evidence that "idiopathic" autism is a heritable disorder. Epidemiologic studies report an ASD prevalence of &SIM; 3 to 6/1000, with a male to female ratio of 3: 1. This skewed ratio remains unexplained: despite the contribution of a few well characterized X-linked disorders, male-to-male transmission in a number of families rules out X-linkage as the prevailing mode of inheritance. The recurrence rate in siblings of affected children is &SIM;2% to 8%, much higher than the prevalence rate in the general population but much lower than in single-gene diseases. Twin studies reported 60% concordance for classic autism in monozygotic (MZ) twins versus 0 in dizygotic (DZ) twins, the higher MZ concordance attesting to genetic inheritance as the predominant causative agent. Reevaluation for a broader autistic phenotype that included communication and social disorders increased concordance remarkably from 60% to 92% in MZ twins and from 0% to 10% in DZ pairs. This suggests that interactions between multiple genes cause "idiopathic" autism but that epigenetic factors and exposure to environmental modifiers may contribute to variable expression of autism-related traits. The identity and number of genes involved remain unknown. The wide phenotypic variability of the ASDs likely reflects the interaction of multiple genes within an individual's genome and the existence of distinct genes and gene combinations among those affected. There are 3 main approaches to identifying genetic loci, chromosomal regions likely to contain relevant genes: 1) whole genome screens, searching for linkage of autism to shared genetic markers in populations of multiplex families ( families with > 1 affected family member); 2) cytogenetic studies that may guide molecular studies by pointing to relevant inherited or de novo chromosomal abnormalities in affected individuals and their families; and 3) evaluation of candidate genes known to affect brain development in these significantly linked regions or, alternatively, linkage of candidate genes selected a priori because of their presumptive contribution to the pathogenesis of autism. Data from whole-genome screens in multiplex families suggest interactions of at least 10 genes in the causation of autism. Thus far, a putative speech and language region at 7q31-q33 seems most strongly linked to autism, with linkages to multiple other loci under investigation. Cytogenetic abnormalities at the 15q11-q13 locus are fairly frequent in people with autism, and a "chromosome 15 phenotype" was described in individuals with chromosome 15 duplications. Among other candidate genes are the FOXP2, RAY1/ST7, IMMP2L, and RELN genes at 7q22-q33 and the GABA(A) receptor subunit and UBE3A genes on chromosome 15q11-q13. Variant alleles of the serotonin transporter gene (5-HTT) on 17q11-q12 are more frequent in individuals with autism than in nonautistic populations. In addition, animal models and linkage data from genome screens implicate the oxytocin receptor at 3p25-p26. Most pediatricians will have 1 or more children with this disorder in their practices. They must diagnose ASD expeditiously because early intervention increases its effectiveness. Children with dysmorphic features, congenital anomalies, mental retardation, or family members with developmental disorders are those most likely to benefit from extensive medical testing and genetic consultation. The yield of testing is much less in high-functioning children with a normal appearance and IQ and moderate social and language impairments. Genetic counseling justifies testing, but until autism genes are identified and their functions are understood, prenatal diagnosis will exist only for the rare cases ascribable to single-gene defects or overt chromosomal abnormalities. Parents who wish to have more children must be told of their increased statistical risk. It is crucial for pediatricians to try to involve families with multiple affected members in formal research projects, as family studies are key to unraveling the causes and pathogenesis of autism. Parents need to understand that they and their affected children are the only available sources for identifying and studying the elusive genes responsible for autism. Future clinically useful insights and potential medications depend on identifying these genes and elucidating the influences of their products on brain development and physiology. C1 Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10461 USA. Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA. Albert Einstein Coll Med, Rose F Kennedy Ctr Res Mental Retardat & Human De, Bronx, NY 10461 USA. RP Rapin, I (reprint author), Albert Einstein Coll Med, Saul R Korey Dept Neurol, K 807,1300 Morris Pk Ave, Bronx, NY 10461 USA. 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PD MAY PY 2004 VL 34 IS 5 BP 342 EP 342 PG 1 WC Psychiatry SC Psychiatry GA 820UW UT WOS:000221416000008 ER PT J AU [Anonymous] AF [Anonymous] TI Autism report identifies research priorities SO PSYCHOLOGIST LA English DT News Item NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD MAY PY 2004 VL 17 IS 5 BP 244 EP 244 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 823NF UT WOS:000221619000003 ER PT J AU Pakenham, KI Sofronoff, K Samios, C AF Pakenham, KI Sofronoff, K Samios, C TI Finding meaning in parenting a child with Asperger syndrome: correlates of sense making and benefit finding SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE Asperger syndrome; parent adjustment; coping; making meaning; family stress ID SOCIAL SUPPORT QUESTIONNAIRE; DOUBLE ABCX MODEL; MENTAL-RETARDATION; AUTISM; STRESS; ADAPTATION; STRATEGIES; ADJUSTMENT; DISORDERS; ADVERSITY AB This study explored the nature of two construals of meaning, benefit finding and sense making, in parents of a child with Asperger syndrome, and examined relations between both meaning constructs and the Double ABCX family stress model variables (initial stressor and pile-up of demands, appraisal, social support, coping strategies and adjustment) [H.I. McCubbin, J.M. Patterson, Social Stress and the Family: Advances and Developments in Family Stress Theory and Research, Haworth, New York, 1983, pp. 7-37]. A total of 59 parents completed questionnaires. Content analyses of parents' responses to questions inquiring about gains and sense making explanations revealed 8 benefit and 12 sense making themes. Results of correlations indicated that one or more of the meaning variables were related to each of the Double ABCX model predictors of parental adjustment. The meaning variables were positively related to adaptive coping processes: social support, self-efficacy, and problem-focused and emotional approach coping strategies. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Queensland, Sch Psychol, Behav Res & Therapy Ctr, Brisbane, Qld 4072, Australia. RP Pakenham, KI (reprint author), Univ Queensland, Sch Psychol, Behav Res & Therapy Ctr, Brisbane, Qld 4072, Australia. 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Dev. Disabil. PD MAY-JUN PY 2004 VL 25 IS 3 BP 245 EP 264 DI 10.1016/j.ridd.2003.06.003 PG 20 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 822ZG UT WOS:000221578900002 PM 15134791 ER PT J AU Ivanenko, A Barnes, ME Crabtree, VM Gozal, D AF Ivanenko, A Barnes, ME Crabtree, VM Gozal, D TI Psychiatric symptoms in children with insomnia referred to a pediatric sleep medicine center SO SLEEP MEDICINE LA English DT Article DE insomnia; psychiatric symptoms; children ID SCHOOL-AGE-CHILDREN; BEHAVIOR PROBLEMS; RESTLESS LEGS; DISORDERS; CHILDHOOD; DISTURBANCES; HYPERACTIVITY; CLINICS; AUTISM AB Background and purpose: To assess the frequency and nature of clinical and psychiatric symptoms in children referred to a pediatric sleep center for evaluation of insomnia. Patients and methods: A retrospective chart review of all children referred to the pediatric sleep medicine was conducted. Children presenting exclusively with sleep initiation and/or maintenance problems underwent a structured clinical psychiatric interview and their parents completed the behavioral assessment system for children (BASC), pediatric symptom checklist, the clinical attention problem scale and a detailed sleep questionnaire. Results: Twenty-three of 46 children (50%) with persistent insomnia had a professional diagnosis of another psychiatric disorder. In the remaining 50%, although parents denied any previous psychiatric history, 40% displayed psychiatric symptoms as documented by psychometric measures and clinical interview. A significant positive correlation was observed between depressive BASC score and sleep onset latency and an inverse correlation was present with REM sleep latency. 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A review of etiology, somatic findings, developmental aspects and psychiatric disorders SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Review DE 22q11.2 deletion syndrome; attention deficit/hyperactivity disorder; autism; affective disorders; schizophrenia ID CARDIO-FACIAL SYNDROME; 22Q11.2 DELETION SYNDROME; CATECHOL-O-METHYLTRANSFERASE; BIPOLAR AFFECTIVE-DISORDER; LOW-COPY REPEATS; CHROMOSOME 22Q11; VELOCARDIOFACIAL-SYNDROME; DIGEORGE-SYNDROME; DIGEORGE/VELOCARDIOFACIAL SYNDROME; LEARNING-DISABILITY AB 22q11.2-deletionssyndrome and its relevance to child and adolescent psychiatry. A review of etiology, somatic findings, developmental aspects and psychiatric disorders. 22q11.2 deletion syndrome is the most common interstitial deletion syndrome in humans. Patients with this syndrome can show a variety of somatic symptoms, especially characteristic facial abnormalities, heart defects, thymic hypo- or aplasia and velopharyngeal dysfunction with or without cleft palate. Disturbancies in motor, language, cognitive and social development are typical, as well as psychiatric disorders. Psychiatric disorders in children and adolescents are mostly attention-deficit/hyperactivity disorder; affective disorders, and autism spectrum problems. Schizophrenia in adults seems to be caused by 22q 11.2 deletion in about 2% of all patients. We review current knowledge about etiology, physical features developmental aspects and psychiatric comorbidity in 22q 11.2 deletion syndrome as well as possible therapeutic interventions. Clinical criteria for genetic examinations on 22q 11.2 deletion in children and adolescents with psychiatric disorders are defined. Until now 22q 11.2 deletion is underdiagnosed in this population - despite of its clinical relevance. C1 Kinderzentrum Munchen, Arbeitskreis Med Genet, Munich, Germany. RP Briegel, W (reprint author), Inst Ambulanz, Rudolf Guby Str 3, D-94032 Passau, Germany. 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Kinder-und Jugendpsy. Psychother. PD MAY PY 2004 VL 32 IS 2 BP 107 EP 115 DI 10.1024/1422-4917.32.2.107 PG 9 WC Psychiatry SC Psychiatry GA 825YI UT WOS:000221794400005 PM 15181786 ER PT J AU Gourion, D Leroy, S Bourdel, MC Goldberger, C Poirier, MF Olie, JP Krebs, MO AF Gourion, D Leroy, S Bourdel, MC Goldberger, C Poirier, MF Olie, JP Krebs, MO TI Cerebellum development and schizophrenia: an association study of the human homeogene Engrailed 2 SO PSYCHIATRY RESEARCH LA English DT Article DE schizophrenia; Engrailed 2; association study; genetics ID CHROMOSOMAL LOCALIZATION; COGNITIVE DYSMETRIA; CONTAINING GENES; EN2; MORPHOMETRY; EXPRESSION; MECHANISMS; ALLELES; MARKERS; AUTISM AB Epidemiological data and family studies in schizophrenia show that genetic factors contribute to the vulnerability to this disorder. The homeogene Engrailed 2 (EN2) is specifically involved in patterning the region that gives rise to the cerebellum and controls the plasticity of midbrain dopaminergic neurons. We carried out an association study for a CA repeat polymorphism located in the 3' region of the homeogene EN2. The subjects consisted of 165 patients with schizophrenia and 97 controls matched for age and ethnicity from a French Caucasian population. We found no significant association of schizophrenia with this bi-nucleotide repeat polymorphism of the EN2 gene. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 INSERM, E117, SHU St Anne, Paris, France. RP Gourion, D (reprint author), INSERM, E117, SHU St Anne, 7 Rue Cabanis, Paris, France. 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PD APR 30 PY 2004 VL 126 IS 2 BP 93 EP 98 DI 10.1016/j.psychres.2004.02.008 PG 6 WC Psychiatry SC Psychiatry GA 823QV UT WOS:000221629000001 PM 15123388 ER PT J AU Bekkedal, MYV Arfsten, D Mattie, D AF Bekkedal, MYV Arfsten, D Mattie, D TI An evaluation of neurobehavioral tests used to assess the neurodevelopmental effects of early ammonium perchlorate exposure SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article; Proceedings Paper CT Annual Conference on Toxicology and Risk Assessment CY APR 28-MAY 01, 2003 CL Fairborn, OH ID THYROID-HORMONE ACTION; DRINKING-WATER; BRAIN-DEVELOPMENT; CONGENITAL HYPOTHYROIDISM; IODINE DEFICIENCY; NEVADA COUNTIES; RAT-BRAIN; MODEL; THYROXINE; PREGNANCY AB Perchlorate is an anion known to interfere with normal production of thyroid hormones that are integrally involved in the development of the central nervous system and neurobehavioral capacities. Given the identification of drinking water contamination with perchlorate, there are efforts to investigate the effects of exposure in developing fetuses and children in order to guide the establishment of regulatory standards. Systematic neurobehavioral investigations in animal models have been completed to evaluate neurodevelopmental consequences of exposures at different concentrations in drinking water. However, these investigations have not directly addressed the public concern for increased incidences of childhood attention deficit disorders, autism, and lowered IQs of children in areas with known contamination. Although epidemiological data suggest there is not a relationship between drinking-water perchlorate exposure and these childhood disorders, it may be prudent to use animal models to systematically assess the potential for such problems. Given the behavioral complexity of these problems, an appropriate evaluation will require the use of nontraditional neurobehavioral tests such as operant conditioning tasks of varying levels of complexity, and juvenile rat play. Such tests will provide a more direct evaluation of the potential for attention deficits, autism, and lowered IQ scores related to thyroid hormone disruption due to early perchlorate exposure. C1 Wisconsin Bur Environm Hlth, Madison, WI 53701 USA. USN, Hlth Res Ctr, Toxicol Detachment, Wright Patterson AFB, OH USA. AFRL, HEST, Wright Patterson AFB, OH USA. RP Bekkedal, MYV (reprint author), Wisconsin Bur Environm Hlth, 1 W Wilson St,POB 2659, Madison, WI 53701 USA. 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Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 163 BP 47S EP 47S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300165 ER PT J AU Buxbaum, JD Ramoz, N Smith, CJ Silverman, JM Bespalova, I AF Buxbaum, JD Ramoz, N Smith, CJ Silverman, JM Bespalova, I TI Linkage and association of an aspartate/glutamate carrier with autism: Genetic variants are associated with a several-fold increased risk SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 59th Annual Meeting of the Society-of-Biological-Psychiatry CY APR 29-MAY 01, 2004 CL NEW YORK, NY SP Soc Biol Psychiat C1 Mt Sinai Sch Med, New York, NY USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 181 BP 52S EP 52S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300183 ER PT J AU Barnea-Goraly, N Kwon, H Menon, V Eliez, S Lotspeich, L Reiss, AL AF Barnea-Goraly, N Kwon, H Menon, V Eliez, S Lotspeich, L Reiss, AL TI White matter structure in autism: Preliminary evidence from diffusion tensor imaging SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 59th Annual Meeting of the Society-of-Biological-Psychiatry CY APR 29-MAY 01, 2004 CL NEW YORK, NY SP Soc Biol Psychiat C1 Stanford Univ, Palo Alto, CA 94304 USA. Univ Geneva, Sch Med, Div Child Adolescent Psychiat, CH-1211 Geneva, Switzerland. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 187 BP 54S EP 54S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300189 ER PT J AU Ambery, FZ Russell, AJ Richardson, L Murphy, DGM AF Ambery, FZ Russell, AJ Richardson, L Murphy, DGM TI Differences in performance on neuropsychological tests between people with Asperger's syndrome and those with high functioning autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 59th Annual Meeting of the Society-of-Biological-Psychiatry CY APR 29-MAY 01, 2004 CL NEW YORK, NY SP Soc Biol Psychiat C1 Inst Psychiat, London, England. RI Russell, Ailsa/J-8268-2013 OI Russell, Ailsa/0000-0002-8443-9381 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 409 BP 114S EP 114S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300399 ER PT J AU Jamain, S Quach, H Betancur, C Rastam, M Collineaux, C Gillberg, C Soderstrom, H Giros, B Leboyer, M Gillberg, C Bourgeron, T AF Jamain, S Quach, H Betancur, C Rastam, M Collineaux, C Gillberg, C Soderstrom, H Giros, B Leboyer, M Gillberg, C Bourgeron, T TI A major role for glutamatergic synapses in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 59th Annual Meeting of the Society-of-Biological-Psychiatry CY APR 29-MAY 01, 2004 CL NEW YORK, NY SP Soc Biol Psychiat C1 Inst Pasteur, Paris, France. INSERM U513, Paris, France. Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41124 Gothenburg, Sweden. Univ Paris 07, F-75221 Paris 05, France. RI Anckarsater, Henrik/C-2244-2009 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 415 BP 115S EP 116S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300405 ER PT J AU Hardan, AY Keshavan, MS Sreedhar, S Vemulapalli, M Minshew, NJ AF Hardan, AY Keshavan, MS Sreedhar, S Vemulapalli, M Minshew, NJ TI An MRI study of minor physical abnormalities in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 59th Annual Meeting of the Society-of-Biological-Psychiatry CY APR 29-MAY 01, 2004 CL NEW YORK, NY SP Soc Biol Psychiat C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 482 BP 134S EP 135S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300471 ER PT J AU Hardan, AY Jou, RJ Keshavan, MS Harrison, L Minshew, NJ AF Hardan, AY Jou, RJ Keshavan, MS Harrison, L Minshew, NJ TI An MRI application of the gyrification index in autism and Asperger's disorder SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 59th Annual Meeting of the Society-of-Biological-Psychiatry CY APR 29-MAY 01, 2004 CL NEW YORK, NY SP Soc Biol Psychiat C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2004 VL 55 SU 8 MA 631 BP 176S EP 177S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 811EN UT WOS:000220755300617 ER PT J AU Gerlai, R Gerlai, J AF Gerlai, R Gerlai, J TI Autism: a target of pharmacotherapies? SO DRUG DISCOVERY TODAY LA English DT Article; Proceedings Paper CT 11th Annual Meeting of the International-Behavioral-Neuroscience-Society (IBNS) CY JUN 23, 2002 CL CAPRI, ITALY SP Int Behav Neurosci Soc ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; FRAGILE-X-SYNDROME; MENTAL-RETARDATION; LANGUAGE DISORDER; INFANTILE-AUTISM; MEASLES-VIRUS; GENE; MODEL; MICE AB Autism is reaching epidemic proportions. The diagnosis can be made as early as 2 years of age, and autistic patients are expected to have a normal life span. Thus, in terms of the number of 'patient years', autism spectrum disorder (ASD) represents a market that is as large as that of the biggest neurological indication, Alzheimer's disease. However, despite the clear unmet medical need no effective treatment is yet available. This could be because the biology of ASD is not clearly understood and thus proper drug treatment has not been possible. However, significant advances are being made toward understanding the mechanisms of the disease. Here, we review the most recent preclinical advances in the hope that they will lead to a breakthrough in the near future. C1 Univ Hawaii Manoa, Dept Psychol, Honolulu, HI 96822 USA. RP Gerlai, R (reprint author), Univ Hawaii Manoa, Dept Psychol, 2430 Campus Rd, Honolulu, HI 96822 USA. 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Today PD APR 15 PY 2004 VL 9 IS 8 BP 366 EP 374 DI 10.1016/S1359-6446(04)03039-9 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 812OJ UT WOS:000220848500009 PM 15081964 ER PT J AU Seeman, C AF Seeman, C TI Overcoming autism: Finding the answers, strategies, and hope that can transform a child's life. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Lib, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Lib, Toledo, OH USA. CR Koegel Lynn K., 2004, OVERCOMING AUTISM FI NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 15 PY 2004 VL 129 IS 7 BP 108 EP 108 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 837VK UT WOS:000222668900175 ER PT J AU Seeman, C AF Seeman, C TI A mind apart: Understanding children with autism and Asperger syndrome. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Lib, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Lib, Toledo, OH USA. CR Szatmari P., 2004, MIND APART UNDERSTAN NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 15 PY 2004 VL 129 IS 7 BP 108 EP 108 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 837VK UT WOS:000222668900176 ER PT J AU Anagnostou, E Esposito, K Haznedar, M Buchsbaum, M Licalzi, E Hollander, E AF Anagnostou, E Esposito, K Haznedar, M Buchsbaum, M Licalzi, E Hollander, E TI Basal ganglia volume and repetitive behaviors in adults with autism SO NEUROLOGY LA English DT Meeting Abstract CT 56th Annual Meeting of the American-Academy-of-Neurology CY APR 24-MAY 01, 2004 CL San Francisco, CA SP Amer Acad Neurol NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR 13 PY 2004 VL 62 IS 7 SU 5 BP A66 EP A67 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 811HB UT WOS:000220761900168 ER PT J AU Lindgren, KA Folstein, SE Tomblin, JB Tager-Flusberg, H AF Lindgren, KA Folstein, SE Tomblin, JB Tager-Flusberg, H TI Comparison of language skills in probands with autism and specific language impairment SO NEUROLOGY LA English DT Meeting Abstract CT 56th Annual Meeting of the American-Academy-of-Neurology CY APR 24-MAY 01, 2004 CL San Francisco, CA SP Amer Acad Neurol RI Tager-Flusberg, Helen/D-5265-2009 NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR 13 PY 2004 VL 62 IS 7 SU 5 BP A67 EP A67 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 811HB UT WOS:000220761900169 ER PT J AU Balaram, P AF Balaram, P TI Autism, vaccines and editors SO CURRENT SCIENCE LA English DT Editorial Material NR 0 TC 1 Z9 1 PU CURRENT SCIENCE ASSN PI BANGALORE PA C V RAMAN AVENUE, PO BOX 8005, BANGALORE 560 080, INDIA SN 0011-3891 J9 CURR SCI INDIA JI Curr. Sci. PD APR 10 PY 2004 VL 86 IS 7 BP 887 EP 888 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 814JI UT WOS:000220970600001 ER PT J AU Martin-Ruiz, CM Lee, M Perry, RH Baumann, M Court, JA Perry, EK AF Martin-Ruiz, CM Lee, M Perry, RH Baumann, M Court, JA Perry, EK TI Molecular analysis of nicotinic receptor expression in autism SO MOLECULAR BRAIN RESEARCH LA English DT Article DE autism; nicotinic receptors; mRNA expression; protein; radioligand binding ID ACETYLCHOLINE-RECEPTOR; CEREBRAL-CORTEX; GENE; SEROTONIN; DISORDER; ABNORMALITIES; CHILDREN; ASSOCIATION; PROTEINS; PARIETAL AB Autism is a developmental disorder of unknown aetiopathology and lacking any specific pharmacological therapeutic intervention. Neurotransmitters such as serotonin, gamma-aminobutyric acid (GABA) and acetylcholine have been implicated. Abnormalities in nicotinic acetylcholine receptors have been identified including cortical loss of binding to the alpha4/beta2 subtype and increase in cerebellar alpha7 binding. Receptor expression (mRNA) has not so far been systematically examined. This study aims to further explore the role of nicotinic receptors in autism by analysing nicotinic receptor subunit mRNA in conjunction with protein levels and receptor binding in different brain areas. Quantitative RT-PCR for alpha4, alpha7 and beta2 subunit mRNA expression levels; alpha3, alpha4, alpha7 and beta2 subunit protein expression immunochemistry and specific radioligand receptor binding were performed in adult autism and control brain samples from cerebral cortex and cerebellum. Alpha4 and beta2 protein expression and receptor binding density as well as alpha4 mRNA levels were lower in parietal cortex in autism, while alpha8 did not change for any of these parameters. In cerebellum, alpha4 mRNA expression was increased, whereas subunit protein and receptor levels were decreased. Alpha7 receptor binding in cerebellum was increased alongside non-significant elevations in mRNA and protein expression levels. No significant changes were found for beta2 in cerebellum. The data obtained, using complementary measures of receptor expression, indicate that reduced gene expression of the alpha4beta2 nicotinic receptor in the cerebral cortex is a major feature of the neurochemical pathology of autism, whilst post-transcriptional abnormalities of both this and the alpha7 subtype are apparent in the cerebellum. The findings point to dendritic and/or synaptic nicotinic receptor abnormalities that may relate to disruptions in cerebral circuitry development. (C) 2004 Elsevier B.V. All rights reserved. C1 Newcastle Gen Hosp, Dept Neuropathol, Ctr Dev Clin Brain Ageing, Joint MRC Univ Newcastle upon Tyne, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. Harvard Univ, Sch Med, Childrens Neurol Serv,Ctr Dev Clin Brain Ageing, Joint MRC Univ Newcastle upon Tyne, Boston, MA 02114 USA. RP Martin-Ruiz, CM (reprint author), Newcastle Gen Hosp, CDCBA, MRC Bldg, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. 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Brain Res. PD APR 7 PY 2004 VL 123 IS 1-2 BP 81 EP 90 DI 10.1016/j.molbrainres.2004.01.003 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 814BF UT WOS:000220949500010 ER PT J AU Torrente, F Anthony, A Heuschkel, RB Thomson, MA Ashwood, P Murch, SH AF Torrente, F Anthony, A Heuschkel, RB Thomson, MA Ashwood, P Murch, SH TI Focal-enhanced gastritis in regressive autism with features distinct from Crohn's and Helicobacter pylori gastritis SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID RETT-SYNDROME; ONSET AUTISM; CHILDREN; DISORDERS; DISEASE; PHENOTYPE AB BACKGROUND: Immunohistochemistry allowed recent recognition of a distinct focal gastritis in Crohn's disease. Following reports of lymphocytic colitis and small bowel enteropathy in children with regressive autism, we aimed to see whether similar changes were seen in the stomach. We thus studied gastric antral biopsies in 25 affected children, in comparison to 10 with Crohn's disease, 10 with Helicobacter pylori infection, and 10 histologically normal controls. All autistic, Crohn's, and normal patients were H. pylori negative. METHODS: Snap-frozen antral biopsies were stained for CD3, CD4, CD8, gammadelta T cells, HLA-DR, IgG, heparan sulphate proteoglycan, IgM, IgA, and C1q. Cell proliferation was assessed with Ki67. RESULTS: Distinct patterns of gastritis were seen in the disease states: diffuse, predominantly CD4+ infiltration in H. pylori, and focal-enhanced gastritis in Crohn's disease and autism, the latter distinguished by striking dominance of CD8+ cells, together with increased intraepithelial lymphocytes in surface, foveolar and glandular epithelium. Proliferation of foveolar epithelium was similarly increased in autism, Crohn's disease and H. pylori compared to controls. A striking finding, seen only in 20/25 autistic children, was colocalized deposition of IgG and C1q on the subepithelial basement membrane and the surface epithelium. CONCLUSIONS: These findings demonstrate a focal CD8-dominated gastritis in autistic children, with novel features. The lesion is distinct from the recently recognized focal gastritis of Crohn's disease, which is not CD8-dominated. As in the small intestine, there is epithelial deposition of IgG. C1 UCL Royal Free & Univ Coll Sch Med, Ctr Paediat Gastroenterol, Dept Histopathol, London NW3 2PF, England. RP Murch, SH (reprint author), UCL Royal Free & Univ Coll Sch Med, Ctr Paediat Gastroenterol, Dept Histopathol, Royal Free Campus,Rowland Hill St, London NW3 2PF, England. 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PD APR PY 2004 VL 99 IS 4 BP 598 EP 605 DI 10.1111/j.1572-0241.2004.04142.x PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 816KF UT WOS:000221108100006 PM 15089888 ER PT J AU Kau, ASM Tierney, E Bukelis, I Stump, MH Kates, WR Trescher, WH Kaufmann, WE AF Kau, ASM Tierney, E Bukelis, I Stump, MH Kates, WR Trescher, WH Kaufmann, WE TI Social behavior profile in young males with fragile X syndrome: Characteristics and specificity SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE fragile X; social behavior profile; autism; autism diagnostic interview; child behavior checklist; social withdrawal ID AUTISM SPECTRUM DISORDERS; MENTAL-RETARDATION; ADAPTIVE-BEHAVIOR; DEVELOPMENTAL DISORDERS; MOLECULAR PHENOTYPE; PROTEIN EXPRESSION; DOWN-SYNDROME; CHILDREN; MUTATION; BOYS AB The present study characterizes distinctive and specific features of social behavior impairment, termed social behavior profile (SBP), in young males with fragile X syndrome (FraX). Fourteen males with FraX and autism (FraX+Aut), ages 3-8 years, were compared with either 41 FraX boys without autism (Aut), 7 age-matched males with developmental language delay and autism (DLD+Aut), or with 11 boys with non-selected (for language delay) idiopathic autism (IA), on several standardized instruments assessing social behavior and autistic features (i.e., autism diagnostic interview-revised, ADI-R). We found that FraX+Aut subjects displayed more impairment in overall cognition, problem/aberrant behavior, and adaptive behavior than the rest of the FraX cohort, even when individuals with pervasive developmental disorder (PDD) were included in the latter. Compared to both DLD+Aut and IA, FraX+Aut males were less impaired in ADI-R reciprocal social interaction (RECS) domain. However, boys with FraX+Aut were in general comparable to DLD+Aut subjects in problem/aberrant and adaptive behaviors. Based on the contrast between FraX+Aut and non-autistic FraX and DLD+Aut, we were able to identify measures (e.g., child behavior checklist (CBCL) withdrawn subscale) that better define social interaction impairment in FraX. Comparisons with DLD+Aut and IA led to the conclusion that communication impairment (COMM) and stereotypic behavior contribute relatively more to the diagnosis of autism in FraX+Aut. In agreement with recent studies, our data suggest that FraX+Aut, and more generally SBP, is a distinctive subphenotype among boys with FraX, which may share some pathophysiological mechanisms with IA. (C) 2004 Wiley-Liss, Inc. C1 Kennedy Krieger Inst, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21218 USA. SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21218 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21218 USA. 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A PD APR 1 PY 2004 VL 126A IS 1 BP 9 EP 17 DI 10.1002/ajmg.a.20218 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 808OB UT WOS:000220577300002 PM 15039968 ER PT J AU Collinson, MN Roberts, SE Crolla, JA Dennis, NR AF Collinson, MN Roberts, SE Crolla, JA Dennis, NR TI A familial balanced inverted insertion ins(15)(q15q13q11.2) producing Prader-Willi syndrome, Angelman syndrome and duplication of 15q11.2-q13 in a single family: Importance of differentiation from a paracentric inversion SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE chromosome 15; duplication; insertion; PWACR ID INTERSTITIAL DUPLICATIONS; PROXIMAL 15Q; MOLECULAR CHARACTERIZATION; METHYLATION PATTERNS; CHROMOSOME 15Q11-13; REGION; PATIENT; AUTISM; ATAXIA AB We reascertained a family in which first cousins were affected by Angelman syndrome and Prader-Willi syndrome. A paracentric inversion of 15q11-q15 had previously been reported in this family but we show, using fluorescence in situ hybridization (FISH), that the rearrangement segregating in this family is not a paracentric inversion but an inverted intrachromosomal insertion, inv ins(15)(q15q13q11.2). We also describe a further recombinant resulting in a maternal duplication of the Prader-Willi/ Angelman critical region. This family illustrates the importance of distinguishing paracentric inversions from intrachromosomal insertions. (C) 2004 Wiley-Liss, Inc. C1 Salisburg Dist Hosp, Wessex Reg Genet Lab, Salisbury SP2 8BJ, Wilts, England. Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England. RP Collinson, MN (reprint author), Salisburg Dist Hosp, Wessex Reg Genet Lab, Salisbury SP2 8BJ, Wilts, England. 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A PD APR 1 PY 2004 VL 126A IS 1 BP 27 EP 32 DI 10.1002/ajmg.a.26565 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 808OB UT WOS:000220577300004 PM 15039970 ER PT J AU Devlin, B Bennett, P Dawson, G Figlewicz, DA Grigorenko, EL McMahon, W Minshew, N Pauls, D Smith, M Spence, MA Rodier, PM Stodgell, C Schellenberg, GD AF Devlin, B Bennett, P Dawson, G Figlewicz, DA Grigorenko, EL McMahon, W Minshew, N Pauls, D Smith, M Spence, MA Rodier, PM Stodgell, C Schellenberg, GD CA CPEA Genetics Network TI Alleles of a Reelin CGG repeat do not convey liability to autism in a sample from the CPEA network SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; Reelin; language development; genetic association; autistic disorder ID FAMILY-BASED ASSOCIATION; GENOMEWIDE SCREEN; SUSCEPTIBILITY LOCUS; VULNERABILITY FACTOR; SPECTRUM DISORDERS; GENOMIC SCREEN; CHROMOSOME 7Q; GENERAL-CLASS; LINKAGE; SCHIZOPHRENIA AB A recent study by Persico et al. [2001: Mol Psychiatry 6:150-159] suggests alleles of a CGG polymorphism, just 5' of the reelin gene (RELN) initiator codon, confer liability for autism, especially alleles bearing 11 or more CGG repeats (long alleles). The association is consistent across both a case-control and family-based sample. We attempted to replicate their finding using a larger, independent family-based sample from the NIH Collaborative Programs of Excellence in Autism (CPEA) Network. In our data, allele transmissions to individuals with autism versus unaffected individuals are unbiased, both when alleles are classified by repeat length and when they are classified into long/short categories. Because of the apparent linkage of autism to chromosome 7q, particularly related to the development of language, we also evaluate the relationship between Reelin alleles and the age at which autism subjects use their first word or first phrase. Neither is significantly associated with Reelin alleles. Our results are not consistent with a major role for Reelin alleles in liability to autism. C1 Vet Affairs Med Ctr, Seattle, WA 98108 USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA. Univ Utah, Dept Psychiat, Div Child & Adolescent Psychiat, Salt Lake City, UT 84112 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Univ Michigan, Dept Neurol Neurobiol & Anat, Ann Arbor, MI 48109 USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. Yale Univ, Sch Med, Dept Psychol, New Haven, CT 06510 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Unit Psychiat & Neurodev Genet, Boston, MA USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. Univ Rochester, Med Ctr, Dept Obstet Gynecol, Rochester, NY 14627 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA. Univ Chicago, Chicago, IL 60637 USA. RP Schellenberg, GD (reprint author), Vet Affairs Med Ctr, 182B,1660 S Columbian Rd, Seattle, WA 98108 USA. 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J. Med. Genet. B PD APR 1 PY 2004 VL 126B IS 1 BP 46 EP 50 DI 10.1002/ajmg.b.20125 PG 5 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 808ZP UT WOS:000220607300009 PM 15048647 ER PT J AU Li, J Nguyen, L Gleason, C Lotspeich, L Spiker, D Risch, N Myers, RM AF Li, J Nguyen, L Gleason, C Lotspeich, L Spiker, D Risch, N Myers, RM TI Lack of evidence for an association between WNT2 and RELN polymorphisms and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autistic disorder; allelic association; linkage disequilibrium; SNP; candidate genes ID DIAGNOSTIC INTERVIEW; GENOMEWIDE SCREEN; GENOMIC SCREEN; LINKAGE DISEQUILIBRIUM; SPECTRUM DISORDERS; MULTIPLEX FAMILIES; REELIN GENE; SUSCEPTIBILITY; REGION; VARIANTS AB Autism is a pervasive neurodevelopmental disorder characterized by deficits in language development and social interaction, as well as stereotypical, repetitive behaviors. The etiology of autism is largely unknown. Family and twin studies have provided compelling evidence for a strong genetic component in most idiopathic cases. Several recent candidate gene studies have suggested that alleles of WNT2 and the reelin gene (RELN), two genes involved in distinct aspects of neurodevelopment, confer greater susceptibility to autism. We screened WNT2 for DNA polymorphisms by sequencing all exons and adjacent intronic regions in 24 autistic patients, and identified not only the WNT2 variants reported previously (two common single-nucleotide polymorphisms (SNPs) in the 5' upstream region and the 3' untranslated region (UTR), respectively), but also two new SNPs in its 3' UTR. We genotyped all four WNT2 polymorphisms and a polymorphic trinucleotide repeat in the 5' UTR of RELN in 107 families with multiple autistic children, and evaluated evidence for association between these variants and autism by the transmission disequilibrium test (TDT). Our results revealed no deviation from the null hypothesis of no association. Our interpretation of these findings is that it is unlikely that DNA variations in RELN and WNT2 play a significant role in the genetic predisposition to autism. (C) 2003 Wiley-Liss, Inc. C1 Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Myers, RM (reprint author), Stanford Univ, Sch Med, Dept Genet, M344, Stanford, CA 94305 USA. 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J. Med. Genet. B PD APR 1 PY 2004 VL 126B IS 1 BP 51 EP 57 DI 10.1002/ajmg.b.20122 PG 7 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 808ZP UT WOS:000220607300010 PM 15048648 ER PT J AU Jones, MB Palmour, RM Zwaigenbaum, L Szatmari, P AF Jones, MB Palmour, RM Zwaigenbaum, L Szatmari, P TI Modifier effects in autism at the MAO-A and DBH loci SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; genetics; catecholamires; DBH; MAO-A ID DOPAMINE-BETA-HYDROXYLASE; PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; WHOLE-BLOOD SEROTONIN; MATERNAL RISK-FACTORS; LINKAGE DISEQUILIBRIUM; MONOAMINE-OXIDASE; FUNCTIONAL POLYMORPHISM; 1ST-DEGREE RELATIVES; FOLATE METABOLISM AB Autism is one of a group of pervasive developmental disorders (PDD) characterized by qualitative impairments in reciprocal social communication and by a preference for repetitive, stereotyped activities, interests, and behaviors. The disorder is caused in large part by genetic mechanisms, though no disease genes have yet been identified. The objective of this study was to investigate three markers, two in the DBH gene and one in the MAO-A gene, for maternal or fetal modifier effects on level of functioning (IQ). At the same time, the possibility of maternal or fetal susceptibility effects was also examined. We assembled 67 affected sibpairs and 45 singletons and determined allele frequencies at the three markers among the affected children and first degree relatives. Sizeable and significant modifier effects were found at the MAO locus and, to a lesser extent, at the DBH locus. Susceptibility effects were also found but not without qualification. We conclude that maternal genotypes at the MAO-A locus, and possibly at the DBH one, may modify IQ in children with autism through the intrauterine environment. (C) 2004 Wiley-Liss, Inc. 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J. Med. Genet. B PD APR 1 PY 2004 VL 126B IS 1 BP 58 EP 65 DI 10.1002/ajmg.b.20172 PG 8 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 808ZP UT WOS:000220607300011 PM 15048649 ER PT J AU Ramoz, N Reichert, JG Smith, CJ Silverman, JM Bespalova, IN Davis, KL Buxbaum, JD AF Ramoz, N Reichert, JG Smith, CJ Silverman, JM Bespalova, IN Davis, KL Buxbaum, JD TI Linkage and association of the mitochondrial aspartate/ glutamate carrier SLC25A12 gene with autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID SPECTRUM DISORDERS; CANDIDATE GENES; EXPRESSION; DISEASE; SUSCEPTIBILITY; HETEROGENEITY; TRANSMISSION; CHROMOSOME-2; VARIANTS; BRAIN AB Objective: Autism/autistic disorder (MIM number 209850) is a complex, largely genetic psychiatric disorder. The authors recently mapped a susceptibility locus for autism to chromosome region 2q24-q33 (MIM number 606053). In the present study, genes across the 2q24-q33 interval were analyzed to identify an autism susceptibility gene in this region. Method: Mutation screening of positional candidate genes was performed in two stages. The first stage involved identifying, in unrelated subjects showing linkage to 2q24-q33, genetic variants in exons and flanking sequence within candidate genes and comparing the frequency of the variants between autistic and unrelated nonautistic subjects. Two single nucleotide polymorphisms (SNPs) that showed evidence for divergent distribution between autistic and nonautistic subjects were identified, both within SLC25A12, a gene encoding the mitochondrial aspartate/glutamate carrier (AGC1). In the second stage, the two SNPs in SLC25A12 were further genotyped in 411 autistic families, and linkage and association tests were carried out in the 197 informative families. Results: Linkage and association were observed between autistic disorder and the two SNPs, rs2056202 and rs2292813, found in SLC25A12. Using either a single affected subject per family or all affected subjects, evidence for excess transmission was found by the Transmission Disequilibrium Test for rs2056202, rs2292813, and a two-locus G*G haplotype. Similar results were observed using TRANSMIT for the analyses. Evidence for linkage was supported by linkage analysis with the two SNPs, with a maximal multipoint nonparametric linkage score of 1.57 and a maximal multipoint heterogeneity lod score of 2.11. Genotype relative risk could be estimated to be between 2.4 and 4.8 for persons homozygous at these loci. Conclusions: A strong association of autism with SNPs within the SLC25A12 gene was demonstrated. Further studies are needed to confirm this association and to decipher any potential etiological role of AGC1 in autism. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Neurobiol, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver Autism Excellence Res Ctr, Greater New York Autism Res Ctr Excellence, New York, NY 10029 USA. RP Buxbaum, JD (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, 1 Gustave L Levy Pl,Box 1668, New York, NY 10029 USA. 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J. Psychiat. PD APR PY 2004 VL 161 IS 4 BP 662 EP 669 DI 10.1176/appi.ajp.161.4.662 PG 8 WC Psychiatry SC Psychiatry GA 818WW UT WOS:000221276200012 PM 15056512 ER PT J AU Findling, RL Aman, MG Eerdekens, M Derivan, A Lyons, B AF Findling, RL Aman, MG Eerdekens, M Derivan, A Lyons, B CA Risperidone Disruptive Behav Study TI Long-term, open-label study of risperidone in children with severe disruptive behaviors and below-average IQ SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 12th World Congress of Biological Psychiatry CY AUG 24-29, 2002 CL YOKOHAMA, JAPAN ID PERVASIVE DEVELOPMENTAL DISORDER; DOUBLE-BLIND; ATYPICAL ANTIPSYCHOTICS; MENTAL-RETARDATION; SUBAVERAGE IQS; RATING-SCALE; ADOLESCENTS; TRIAL; AUTISM; DISTURBANCES AB Objective: This study determined the long-term safety and effectiveness of risperidone in treating severe disruptive behavior in children with subaverage intelligence. Method: This 48-week, open-label extension included 107 children ages 5-12 years with severe disruptive behavior disorders (according to DSM-IV criteria and a score of greater than or equal to 24 on the conduct problem subscale of the Nisonger Child Behavior Rating Form) and subaverage intelligence (IQ 36-84) who completed at least 2 weeks of a randomized, double-blind, placebo-controlled study of risperidone. All patients received 0.02-0.06 mg/kg/day of oral risperidone; the purpose was to accumulate long-term safety data. Scores on the Nisonger Child Behavior Rating Form were also obtained. Results: The mean risperidone dose was 1.5 mg/day. The most common adverse events reported were somnolence (33%), headache (33%), rhinitis (28%), and weight gain (21%). Somnolence was usually mild and transient. The mean weight increase was 5.5 kg; half was attributable to developmentally expected growth. Transient and asymptomatic increases in prolactin levels were observed. There were no significant changes in Extrapyramidal Symptom Rating Scale scores and no cases of tardive dyskinesia. No clinically relevant changes in ECGs or vital signs were noted. Risperidone was associated with rapid, significant improvement on the conduct problem subscale score of the Nisonger Child Behavior Rating Form in patients previously treated with placebo; improvement was maintained during long-term treatment and in patients previously given risperidone. Conclusions: Long-term risperidone appears to be generally safe, well tolerated, and effective for treating severely disruptive behaviors in children with subaverage intelligence. C1 Johnson & Johnson Pharmaceut Res Dev, Beerse, Belgium. Johnson & Johnson Pharmaceut Res & Dev, Titusville, NJ USA. Ohio State Univ, Ctr Excellence Dev Disabil, Nisonger Ctr, Columbus, OH 43210 USA. Case Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA. RP Findling, RL (reprint author), Case Western Reserve Univ, Univ Hosp Cleveland, Dept Psychiat, 11100 Euclid Ave, Cleveland, OH 44106 USA. 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J. Psychiat. PD APR PY 2004 VL 161 IS 4 BP 677 EP 684 DI 10.1176/appi.ajp.161.4.677 PG 8 WC Psychiatry SC Psychiatry GA 818WW UT WOS:000221276200014 PM 15056514 ER PT J AU Herbert, MR Ziegler, DA Makris, N Filipek, PA Kemper, TL Normandin, JJ Sanders, HA Kennedy, DN Caviness, VS AF Herbert, MR Ziegler, DA Makris, N Filipek, PA Kemper, TL Normandin, JJ Sanders, HA Kennedy, DN Caviness, VS TI Localization of white matter volume increase in autism and developmental language disorder SO ANNALS OF NEUROLOGY LA English DT Article ID CORPUS-CALLOSUM SIZE; TOPOGRAPHIC PARCELLATION; HEAD CIRCUMFERENCE; CEREBRAL-CORTEX; GROWTH-PATTERNS; HUMAN BRAIN; CHILDREN; MRI; IMPAIRMENT; AGE AB Increased brain volume in autism appears to be driven mainly by an unexplained white matter enlargement, and we have reported a similar phenomenon in developmental language disorder (DLD). Localization of this enlargement would strongly guide research into its cause, tissue basis, and functional implications. We utilized a white matter parcellation technique that divides cerebral white matter into an outer zone containing the radiate compartment and an inner zone containing sagittal and bridging system compartments. In both high-functioning autism and DLD, enlargement localized to the radiate white matter (all lobes in autism, all but parietal in DLD), whereas inner zone white matter compartments showed no volume differences from controls. Furthermore, in both autism and DLD, later or longer-myelinating regions showed greater volume increases over controls. Neither group showed cerebral cortex, corpus callosum, or internal capsule volume differences from control. Radiate white matter myelinates later than deep white matter; this pattern of enlargement thus is consistent with striking postnatal head circumference percentile increases reported in autism. These findings suggest an ongoing postnatal process in both autism and DLD that is probably intrinsic to white matter, that primarily affects intrahemispheric and corticocortical connections, and that places these two disorders on the same spectrum. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Morphometr Anal, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Cambridge, MA 02138 USA. Univ Calif Irvine, Coll Med, Dept Pediat, Irvine, CA 92717 USA. Univ Calif Irvine, Coll Med, Dept Neurol, Irvine, CA 92717 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02215 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. RP Herbert, MR (reprint author), Ctr Morphometr Anal, 149 13th St,Room 6012, Charlestown, MA 02129 USA. 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I., 1967, REGIONAL DEV BRAIN E, P3 NR 48 TC 334 Z9 344 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 2004 VL 55 IS 4 BP 530 EP 540 DI 10.1002/ana.20032 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 806ME UT WOS:000220437200010 PM 15048892 ER PT J AU Nishitani, N Avikainen, S Hari, R AF Nishitani, N Avikainen, S Hari, R TI Abnormal imitation-related cortical activation sequences in Asperger's syndrome SO ANNALS OF NEUROLOGY LA English DT Article ID MIRROR NEURONS; AUTISM; CORTEX; MECHANISMS; MOTOR; MIND; PERCEPTION; DYNAMICS; HUMANS; BRAIN AB Subjects with Asperger's syndrome (AS) are impaired in social interaction and imitation, but the underlying brain mechanisms are poorly understood. Because the mirror-neuron system (MNS) that matches observed and executed actions has been suggested to play an important role in imitation and in reading of other people's intentions, we assessed MNS functions in 8 adult AS subjects and in 10 healthy control subjects during imitation of still pictures of lip forms. In the control subjects, cortical activation progressed in 30 to 80-millisecond steps from the occipital cortex to the superior temporal sulcus, to the inferior parietal lobe, and to the inferior frontal lobe, and finally, 75 to 90 milliseconds later, to the primary motor cortex of both hemispheres. Similar activation sites were found in AS subjects but with slightly larger scatter. Activation of the inferior frontal lobe was delayed by 45 to 60 milliseconds and activations in the inferior frontal lobe and in the primary motor cortex were weaker than in control subjects. The observed abnormal premotor and motor processing could account for a part of imitation and social impairments in subjects with AS. C1 Helsinki Univ Technol, Low Temp Lab, Brain Res Unit, FIN-02015 Espoo, Finland. Natl Rehabil Ctr Persons Disabil, Inst Res, Dept Sensory & Communicat Disorders, Cognit Sci Sect, Tokorozawa, Saitama, Japan. Univ Helsinki, Cent Hosp, Dept Clin Neurophysiol, Helsinki, Finland. RP Hari, R (reprint author), Helsinki Univ Technol, Low Temp Lab, Brain Res Unit, POB 2200, FIN-02015 Espoo, Finland. 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PD APR PY 2004 VL 55 IS 4 BP 558 EP 562 DI 10.1002/ana.20031 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 806ME UT WOS:000220437200013 PM 15048895 ER PT J AU Duker, PC Hendriks, C Schroen, J AF Duker, PC Hendriks, C Schroen, J TI Effect of wave frequency of clinical electric shock: Pain sensation and startle response SO BEHAVIORAL INTERVENTIONS LA English DT Article ID SELF-INJURIOUS-BEHAVIOR; FOLLOW-UP AB Contingent shock has been used in a number of studies to suppress health-threatening self-injurious behavior of individuals with mental retardation and autism. As sustained suppression is an issue of clinical concern, research into procedural variables of contingent shock is needed. As research on subjects who have mental retardation and who show self-injurious behavior is ethically impossible, we conducted research on healthy volunteers. In this study, we compared the effect of wave frequency (i.e. Hz) of electric shock on subjects' pain sensation and startle response. It was found that 60Hz revealed a significantly stronger pain sensation rating than 30 Hz and that 90 Hz revealed a significantly stronger rating than 60Hz. Also, the magnitude of subjects' startle response significantly increased as wave frequency increased from 30 Hz to 60 Hz and from 60 to 90 Hz. Copyright (C) 2004 John Wiley Sons, Ltd. C1 Univ Nijmegen, Psychol Lab, NL-6500 HE Nijmegen, Netherlands. Plurijn Fdn, Nijmegen, Netherlands. RP Duker, PC (reprint author), Univ Nijmegen, Psychol Lab, POB 9104, NL-6500 HE Nijmegen, Netherlands. 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PD APR PY 2004 VL 19 IS 2 BP 103 EP 110 DI 10.1002/bin.152 PG 8 WC Psychology, Clinical SC Psychology GA 817EO UT WOS:000221161000004 ER PT J AU DeLeon, IG Fisher, WW Marhefka, JM AF DeLeon, IG Fisher, WW Marhefka, JM TI Decreasing self-injurious behavior associated with awakening in a child with autism and developmental delays SO BEHAVIORAL INTERVENTIONS LA English DT Article ID SLEEP PROBLEMS; MENTAL-RETARDATION; FUNCTIONAL-ANALYSIS; ADULTS; DEPRIVATION; DISABILITIES AB Direct observation data revealed that self-injurious behavior (SIB) emitted by a young boy with autism occurred primarily within one hour after waking versus all other times of the day. Experimentally manipulated scheduled awakenings supported the hypothesized relation between waking and SIB. A faded-bedtime procedure was then implemented to stabilize his sleep patterns, which reduced awakenings by 81% and post-waking SIB by 82%. Copyright (C) 2004 John Wiley Sons, Ltd. C1 Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD 21205 USA. Marcus Inst, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. RP DeLeon, IG (reprint author), Kennedy Krieger Inst, Neurobehav Unit, 707 N Broadway, Baltimore, MD 21205 USA. 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Intervent. PD APR PY 2004 VL 19 IS 2 BP 111 EP 119 DI 10.1002/bin.154 PG 9 WC Psychology, Clinical SC Psychology GA 817EO UT WOS:000221161000005 ER PT J AU Diergaarde, L Gerrits, MAFM Stuy, A Spruijt, BM van Ree, JM AF Diergaarde, L Gerrits, MAFM Stuy, A Spruijt, BM van Ree, JM TI Neonatal amygdala lesions and juvenile isolation in the rat: Differential effects on locomotor and social behavior later in life SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID NEURODEVELOPMENTAL PSYCHOPATHOLOGICAL DISORDERS; ADULT RATS; BASOLATERAL AMYGDALA; THALAMIC STRUCTURES; INFANTILE-AUTISM; OPEN-FIELD; PLAY; NEUROBIOLOGY; MONKEYS; DEPRIVATION AB Pervasive developmental disorders such as autism are characterized by deficits in social interaction and communication. Disturbed development of limbic structures such as the amygdala might underlie these deficits. The authors examined the effects of amygdala lesions on Postnatal Day 7 and juvenile isolation (2 weeks of individual housing during Weeks 4 and 5 of life) on rat locomotor and social activity later in life. Before puberty, but more pronounced after puberty, lesioned rats displayed enhanced locomotor activity. Adult social behavior was selectively disturbed by the lesion and the isolation procedure. In particular, the combination of neonatal lesions and juvenile isolation severely disrupted social interaction. These results suggest that a combination of neonatal amygdala damage and juvenile isolation may serve as an animal model of certain psychopathological neurodevelopmental disorders, such as autism. C1 Univ Utrecht, Med Ctr, Dept Pharmacol & Anat, Rudolf Magnus Inst Neurosci, NL-3508 TA Utrecht, Netherlands. Univ Utrecht, Dept Anim & Soc, Div Ethol & Welf, Fac Vet Med, Utrecht, Netherlands. RP van Ree, JM (reprint author), Univ Utrecht, Med Ctr, Dept Pharmacol & Anat, Rudolf Magnus Inst Neurosci, POB 80040, NL-3508 TA Utrecht, Netherlands. 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Neurosci. PD APR PY 2004 VL 118 IS 2 BP 298 EP 305 DI 10.1177/0735-7044.118.2.298 PG 8 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 808YD UT WOS:000220603500005 PM 15113254 ER PT J AU Welch, MG Keune, JD Welch-Horan, TB Anwar, N Anwar, M Ludwig, RJ Ruggiero, DA AF Welch, MG Keune, JD Welch-Horan, TB Anwar, N Anwar, M Ludwig, RJ Ruggiero, DA TI Secretin: Hypothalamic distribution and hypothesized neuroregulatory role in autism SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Review DE secretin; autism; HPA stress axis; secretinergic neurons; conditioned response; oxytocin; visceral; neuroregulatory ID PLACEBO-CONTROLLED TRIAL; ANGIOTENSIN-II AT(1); PERVASIVE DEVELOPMENTAL DISORDER; PORCINE SECRETIN; REPETITIVE BEHAVIORS; PANCREATIC-SECRETION; SPECTRUM DISORDERS; INFANTILE-AUTISM; CYSTIC-FIBROSIS; AT(2) RECEPTORS AB 1. This study aims ( 1) to determine whether secretin is synthesized centrally, specifically by the HPA axis and ( 2) to discuss, on the basis of the findings in this and previous studies, secretin's possible neuroregulatory role in autism. 2. An immunocytochemical technique with single-cell resolution was performed in 12 age/weight-matched male rats pretreated with stereotaxic microinjection of colchicine (0.6 mug/kg) or vehicle into the lateral ventricle. Following 2-day survival, rats were anesthetized and perfused for immunocytochemistry. Brain segments were blocked and alternate frozen 30-mum sections incubated in rabbit antibodies against secretin, vasoactive intestinal peptide, glucagon, or pituitary-adenylate-cyclase-activating peptide. Adjacent sections were processed for Nissl stain. Preadsorption studies were performed with members of the secretin peptide family to demonstrate primary antibody specificity. 3. Specificity of secretin immunoreactivity (ir) was verified by clear-cut preadsorption control data and relatively high concentrations and distinct topographic localization of secretin ir to paraventricular/supraoptic and intercalated hypothalamic nuclei. Secretin levels were upregulated by colchicine, an exemplar of homeostatic stressors, as compared with low constitutive expression in untreated rats. 4. This study provides the first directimmunocytochemical demonstration of secretinergic immunoreactivity in the forebrain and offers evidence that the hypothalamus, like the gut, is capable of synthesizing secretin. Secretin's dual expression by gut and brain secretin cells, as well as its overlapping central distribution with other stress-adaptation neurohormones, especially oxytocin, indicates that it is stress-sensitive. A neuroregulatory relationship between the peripheral and central stress response systems is suggested, as is a dual role for secretin in conditioning both of those stress-adaptation systems. Colchicine-induced upregulation of secretin indicates that secretin may be synthesized on demand in response to stress, a possible mechanism of action that may underlie secretin's role in autism. C1 Columbia Univ, Coll Phys & Surg, Dept Psychiat, Div Neurosci,NYSPI, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Lab Childhood Regulatory Disorders, Div Neurosci,NYSPI, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Lab Behav Neuroanat, Div Neurosci,NYSPI, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Dept Anat & Cell Biol, Div Neurosci,NYSPI, New York, NY 10032 USA. RP Welch, MG (reprint author), Columbia Univ, Coll Phys & Surg, Dept Psychiat, Div Neurosci,NYSPI, 1051 Riverside Dr, New York, NY 10032 USA. 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Mol. Neurobiol. PD APR PY 2004 VL 24 IS 2 BP 219 EP 241 DI 10.1023/B:CEMN.0000018618.59015.a2 PG 23 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 800UM UT WOS:000220053200004 PM 15176437 ER PT J AU Morlet, T Hamburger, A Kuint, J Roth, DAE Gartner, M Muchnik, C Collet, L Hildesheimer, M AF Morlet, T Hamburger, A Kuint, J Roth, DAE Gartner, M Muchnik, C Collet, L Hildesheimer, M TI Assessment of medial olivocochlear system function in pre-term and full-term newborns using a rapid test of transient otoacoustic emissions SO CLINICAL OTOLARYNGOLOGY LA English DT Article DE MOCS; TEOAEs; newborn; maturation; outer hair cells ID COCHLEAR MICROMECHANICAL PROPERTIES; CONTRALATERAL SUPPRESSION; INFANTILE-AUTISM; ACOUSTIC TRAUMA; EFFERENT SYSTEM; HEARING; NOISE; MATURATION; ASYMMETRY; HUMANS AB This study was conducted to investigate maturation of the medial olivocochlear efferent system (MOCS) in pre- and full-term neonates using Quickscreen (Otodynamics Ltd) and to confirm previous findings on transient otoacoustic emission (TEOAE) suppression in neonates. MOCS maturation was investigated in 46 neonates born at the Chaim Sheba Medical Center, Tel Hashomer, Israel, using Quickscreen. All neonates were normal with no family history of general or auditory disease and no risk factors for hearing impairment. MOCS function appears gradually in human pre-term neonates and is considered to reach maturity shortly after term birth. The clinical value of MOCS testing in specific populations of newborns at risk for hearing and/or brainstem function can be legitimately raised as activation of the MOCS clearly alters cochlear output. The present results can be interpreted to support the testing of infants at risk of developing abnormal MOCS function using a commercially available rapid TEOAE measurement system. C1 Louisiana State Univ, Hlth Sci Ctr, Kresge Hearing Res Lab S, New Orleans, LA 70112 USA. Tel Aviv Univ, Sackler Sch Med, Chaim Sheba Med Ctr, Speech & Hearing Ctr, Tel Hashomer, Israel. Tel Aviv Univ, Sackler Sch Med, Chaim Sheba Med Ctr, Dept Neonatol, Tel Hashomer, Israel. UMR Neurosci & Syst Sensoriels 5020, Lyon, France. RP Morlet, T (reprint author), Louisiana State Univ, Hlth Sci Ctr, Kresge Hearing Res Lab S, New Orleans, LA 70112 USA. 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B., 1986, NEUROBIOLOGY HEARING, P333 WEN H, 1993, ABSTR ASS RES OT, V102 Zheng XY, 1997, HEARING RES, V107, P147, DOI 10.1016/S0378-5955(97)00031-2 NR 37 TC 6 Z9 11 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0307-7772 J9 CLIN OTOLARYNGOL JI Clin. Otolaryngol. PD APR PY 2004 VL 29 IS 2 BP 183 EP 190 DI 10.1111/j.0307-7772.2004.00786.x PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA 817HY UT WOS:000221169800019 PM 15113308 ER PT J AU Lutchmaya, S Baron-Cohen, S Raggatt, P Knickmeyer, R Manning, JT AF Lutchmaya, S Baron-Cohen, S Raggatt, P Knickmeyer, R Manning, JT TI 2nd to 4th digit ratios, fetal testosterone and estradiol SO EARLY HUMAN DEVELOPMENT LA English DT Article DE digit ratio; fetal testosterone; fetal estradiol ID LENGTH; ESTROGEN; CHILDREN AB Background: The ratio of 2nd to 4th digit length (2D:4D) is sexually dimorphic (mean 2D:4D is lower in males than females) and is thought to be fixed early in development. 2D:4D has been reported to be related to fetal growth, hand preference, autism, Asperger's syndrome, sperm counts, family size, age at myocardial infarction in men and breast cancer in women. There is indirect evidence that 2D:4D is established in utero and is negatively related to prenatal testosterone and positively with prenatal estradiol. However, there are no studies which show direct relationships between fetal testosterone (FT), fetal estradiol (FE) and 2D:4D. Aims: To investigate the relationships between 2D:4D ratios and FT and FE from amniotic fluid. Study design: Cohort study. Subjects: 33 children. Outcome measures: Radio immunoassays of FT and FE obtained from routine amniocentesis; 2D:4D ratios calculated from 2nd and 4th digit length of the right and left hands at age 2 years. Results: A significant negative association between right 2D:4D ratio and FT/FE ratio, which was independent of sex. Conclusions: These preliminary findings lend support to an association between low MAD and high levels of FT relative to FE, and high 2D:4D with low FT relative to FE.. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Univ Cent Lancashire, Dept Psychol, Preston PR1 2HE, Lancs, England. Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 3EB, England. Addenbrookes Hosp, Dept Clin Chem, Cambridge CB2 2QQ, England. RP Manning, JT (reprint author), Univ Cent Lancashire, Dept Psychol, Preston PR1 2HE, Lancs, England. 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The population included 74 infants between six and 35 months, evaluated with the Infant Behavioural Summarised Evaluation (IBSE) scale. Thirteen of the 33 items of the IBSE scale were selected according to previous studies on older patients with autistic disorder. Correspondence analysis was applied to these 13 items, followed by a classical cluster analysis. This procedure permitted the identification of four different profiles which were distinguished on the basis of five main behaviours: activity, auditory perception, sensorimotility, eye contact and use of objects. These profiles are similar to those identified in older children with autism. This study provides an objective description of early clinical markers of the heterogeneity in autism and thus contributes to the description of the onset of autistic disorder. It identified more precise clinical subtyping which will be valuable for future bioclinical studies. C1 CHU Bretonneau, Serv Univ Pedopsychiat, F-37044 Tours, France. 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Child Adolesc. Psych. PD APR PY 2004 VL 13 IS 2 BP 115 EP 122 DI 10.1007/s00787-004-0374-2 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 814HR UT WOS:000220966300008 PM 15103537 ER PT J AU Carter, C Meckes, L Pritchard, L Swensen, S Wittman, PP Velde, B AF Carter, C Meckes, L Pritchard, L Swensen, S Wittman, PP Velde, B TI The Friendship Club - An after-school program for children with Asperger syndrome SO FAMILY & COMMUNITY HEALTH LA English DT Article DE Asperger syndrome; hyperlexia; Lifestyle Performance Model; occupational therapy; pervasive developmental disorder; social skills ID YOUNG-CHILDREN; AUTISM AB The Friendship Club is a program designed and implemented by occupational therapy students and faculty to help teach children, ages 8-15, activities related to friendship and skills necessary to maintain friends. 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Community Health PD APR-JUN PY 2004 VL 27 IS 2 BP 143 EP 150 PG 8 WC Family Studies; Public, Environmental & Occupational Health SC Family Studies; Public, Environmental & Occupational Health GA 805FH UT WOS:000220351700007 PM 15596981 ER PT J AU D'Adamo, P Bacchelli, E Blasi, F Lipp, HP Toniolo, D Maestrini, E AF D'Adamo, P Bacchelli, E Blasi, F Lipp, HP Toniolo, D Maestrini, E CA Int Molecular Genetic Study Austis TI DNA variants in the human RAB3A gene are not associated with autism SO GENES BRAIN AND BEHAVIOR LA English DT Article DE ADHD; autism; human; mouse; mutation; Rab3a ID GENOMEWIDE SCREEN; LINKAGE; 7Q AB Mutation screening of the RAB3A gene in 47 individuals with autism provided no evidence that DNA variants in this gene are associated with autism. 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PD APR PY 2004 VL 3 IS 2 BP 123 EP 124 DI 10.1111/j.1601-183X.2003.00058.x PG 2 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 807AR UT WOS:000220474900008 PM 15005721 ER PT J AU Ess, KC Uhlmann, EJ Li, W Li, HZ Declue, JE Crino, PB Gutmann, DH AF Ess, KC Uhlmann, EJ Li, W Li, HZ Declue, JE Crino, PB Gutmann, DH TI Expression profiling in tuberous sclerosis complex (TSC) knockout mouse astrocytes to characterize human TSC brain pathology SO GLIA LA English DT Article DE tuber; hamartoma; hamartin; tuberin ID GIANT-CELL ASTROCYTOMA; BINDING PROTEIN; GENE-PRODUCTS; GLIAL-CELLS; HAMARTIN; NEURONS; MICE; IDENTIFICATION; TUMORIGENESIS; INHIBITORS AB Individuals with tuberous sclerosis complex (TSC) exhibit a variety of neurologic abnormalities, including mental retardation, epilepsy, and autism. Examination of human TSC brains demonstrate dysplastic astrocytes and neurons, areas of abnormal neuronal migration (tubers), and hamartomatous growths, termed subependymal nodules, which can progress to subependymal giant cell astrocytomas (SEGA). Previous studies have suggested that these neuropathologic features may result from abnormal neuroglial cell differentiation. In an effort to provide support for this hypothesis and to identify specific markers of aberrant neuroglial cell differentiation in TSC, we employed gene expression profiling on Tsc1 conditional knockout (Tsc1(GFAP) CKO) mouse astrocytes. We identified several transcripts implicated in central nervous system development that are differentially expressed in Tsc1(-/-) astrocytes compared to wild-type astrocytes. We validated the differential expression of select transcripts on the protein level both in primary cultures of Tsc1(-/-) astrocytes and in Tsc1(GFAP) CKO mouse brains. Moreover, we show that these markers are also differentially expressed within cortical tubers, but not in adjacent normal tissue from TSC patient brains. This study provides supportive evidence for a developmental defect in neuroglial cell differentiation relevant to the genesis of TSC nervous system pathology and underscores the utility of mouse modeling for understanding the molecular pathogenesis of human disease. (C) 2004 Wiley-Liss, Inc. C1 Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA. Univ Penn, Dept Neurol, PENN Epilepsy Ctr, Philadelphia, PA 19104 USA. NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA. RP Gutmann, DH (reprint author), Washington Univ, Sch Med, Dept Neurol, Box 8111,660 S Euclid Ave, St Louis, MO 63110 USA. 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Med. PD APR PY 2004 VL 21 IS 4 BP 148 EP 148 PG 1 WC Infectious Diseases SC Infectious Diseases GA 814QT UT WOS:000220989900001 ER PT J AU Volden, J AF Volden, J TI Conversational repair in speakers with autism spectrum disorder SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE autism spectrum disorder; conversational repair; pragmatics; theory of mind ID PERVASIVE DEVELOPMENTAL DISORDERS; RECEPTIVE LANGUAGE DISORDER; IMPAIRED CHILDREN; MIND; COMMUNICATION; RESPONSES; DISCOURSE; CLARIFICATION; REQUESTS; DEFICITS AB Background: The ability to repair communicative breakdown is an important pragmatic language skill, yet very little is known about it in the population of children with autism spectrum disorder (ASD). Previous investigations have shown that people with ASD, across a variety of ages and language levels, recognized communicative breakdown and responded to requests for clarification (RQCLs) with a wide variety of repair strategies. No previous work has assessed the repair abilities of speakers with ASD when faced with a persistent communicative breakdown indicated by a stacked series of RQCLs. Aims: The present paper aimed to determine whether school-aged, high-functioning children with ASD responded to a stacked series of RQCLs in a way similar to children matched for language age. Methods & Procedures: Nine school-aged, high-functioning children with ASD were recruited and matched to nine control group children based on language level. During conversation, an unfamiliar examiner engineered 10 episodes of communicative breakdown. Each consisted of a stacked series of three RQCLs ('What?', 'I don't understand', 'Tell me another way'). Verbal and non-verbal responses to each RQCL were coded. Reponses were analysed by a series of repeated measures analyses of variance with diagnostic group and RQCL type/ position as independent variables and type of repair as the dependent variable. Outcomes & Results: Children with ASD were similar to language age-matched control children in responding to RQCLs and employing a variety of repair strategies. In addition, their pattern of responding over the series of RQCLs was very similar to the controls in varying the repair strategy by adding increasingly more information as the breakdown persisted, i.e. as the sequence of RQCLs progressed. Children with ASD, however, were significantly more likely than language age-matched controls to respond to an RQCL with an inappropriate response. Conclusions: The ability to repair communicative breakdown successfully raises questions about some of the currently popular theories about the source and nature of social and communicative deficits in autism. In addition, the presence of significantly more inappropriate utterances in the group with ASD poses both theoretical and clinical challenges. In theoretical terms, several possible explanations are proposed, but future work will need to test these hypotheses. Clinically, it is important to focus on utterances that disrupt the conversational flow and that generate severe social penalties for the speaker with ASD. C1 Univ Alberta, Edmonton, AB T6G 2G4, Canada. RP Volden, J (reprint author), Univ Alberta, 3-10 Corbett Hall, Edmonton, AB T6G 2G4, Canada. EM joanne.volden@ualberta.ca CR Alexander Dianne, 1997, Seminars in Speech and Language, V18, P197, DOI 10.1055/s-2008-1064073 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Baltaxe CA, 1977, J PEDIATR PSYCHOL, V2, P176, DOI DOI 10.1093/JPEPSY/2.4.176 BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 Baron-Cohen S, 2001, INT REV RES MENT RET, V23, P169 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 BOUCHER J, 1989, BRIT J DISORD COMMUN, V24, P181 BRINTON B, 1988, J SPEECH HEAR DISORD, V53, P383 BRINTON B, 1985, CONVERSATIONAL MANAG BRINTON B, 1986, J SPEECH HEAR DISORD, V51, P370 Brown L., 1990, TEST NONVERBAL INTEL CANTWELL D, 1978, J CHILD PSYCHOL PSYC, V19, P351, DOI 10.1111/j.1469-7610.1978.tb00481.x Donahue ML, 1997, TOP LANG DISORD, V17, P41 EALES MJ, 1993, J AUTISM DEV DISORD, V23, P593, DOI 10.1007/BF01046104 Ellis-Weismer S., 2002, TOP LANG DISORD, V22, P15 FINE J, 1994, J AUTISM DEV DISORD, V24, P315, DOI 10.1007/BF02172230 Frith U., 1989, AUTISM EXPLAINING EN GALLAGHER TM, 1981, J CHILD LANG, V8, P51 GALLAGHER TM, 1977, J SPEECH HEAR RES, V20, P303 Geller E, 1998, BRIT J DEV DISABIL, V44, P71 Green SB, 2003, USING SPSS WINDOWS M HAMILL D, 1988, TEST LANGUAGE DEV IN Happe F, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P237 Happe F., 1994, AUTISM INTRO PSYCHOL KANNER L, 1946, AM J PSYCHIAT, V103, P242 Lord C., 1997, HDB AUTISM PERVASIVE, P195 *NAT RES COUNC, 2001, COMM ED INT CHILDR A Newcomer P., 1988, TEST LANGUAGE DEV PR OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Ozonoff S., 1995, LEARNING COGNITION A, P199 PAUL R, 1984, APPL PSYCHOLINGUIST, V5, P349, DOI 10.1017/S0142716400005221 Pennington B. F., 1997, AUTISM EXECUTIVE DIS, P143 Russell J., 1997, AUTISM EXECUTIVE DIS RUTTER M, 1965, CHILDREN COMMUNICATI, P39 TagerFlusberg H, 1996, J AUTISM DEV DISORD, V26, P169, DOI 10.1007/BF02172006 TAGERFLUSBERG H, 1991, J CHILD PSYCHOL PSYC, V32, P1123, DOI 10.1111/j.1469-7610.1991.tb00353.x Twatchtman-Cullen D., 1998, ASPERGER SYNDROME HI, P199 Volden J, 1999, J AUTISM DEV DISORD, V29, P203, DOI 10.1023/A:1023028021580 VOLDEN J, 2002, J SPEECH LANGUAGE PA, V26, P183 Wetherby Amy M., 2000, AUTISM SPECTRUM DISO, P109 NR 41 TC 19 Z9 19 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR-JUN PY 2004 VL 39 IS 2 BP 171 EP 189 DI 10.1080/13682820410001663252 PG 19 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 802ES UT WOS:000220147400002 PM 15204450 ER PT J AU Miller, CA AF Miller, CA TI False belief and sentence complement performance in children with specific language impairment SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE specific language impairment; theory of mind; sentence complements; preschool children ID OF-MIND DEVELOPMENT; SOCIAL COGNITION; SYMBOLIC PLAY; KNOWLEDGE; REPRESENTATION; PRETENSE; AUTISM; TASK AB Background: Children with specific language impairment (SLI) have language abilities not commensurate with other cognitive abilities. This pattern makes the SLI population of interest when investigating the relationship between language and theory of mind. One view regarding this relationship is that theory of mind develops independently of language, but certain language skills are required to meet the demands of tasks used to measure theory of mind, such as false belief. Another view is that language development facilitates theory of mind development, and specifically, that mastery of sentence complement structures is necessary for false belief. Aims: The study asked ( 1) if children with SLI can succeed on false belief, despite their language deficits, when the linguistic demands of the false belief task are low, and ( 2) if performance on sentence complement structures predicts false belief performance. Methods & Procedures: Fifteen children with SLI, 15 children matched for age and 15 children matched for language comprehension level participated in a false belief task with four conditions of differing linguistic complexity, and a test of sentence complementation understanding. Spontaneous production of sentence complements was also measured. Group differences for false belief and sentence complementation, and condition differences for false belief, were tested non-parametrically. Partial correlation analysis, log - linear analysis, and Wilcoxon - Mann - Whitney tests were used to explore relationships among the complementation and false belief measures for all children and for each group. Outcomes & Results: Children with SLI performed similarly to age-matched peers on false belief when linguistic complexity of the task was low, and performed more poorly than age-matched peers on understanding of sentence complements. For all children, sentence complement performance was correlated with false belief ( controlling for age), and those who performed well on sentence complements had higher mean rates of false belief success. Log linear analysis showed the sentence complement - false belief relationship to hold for a condition with relatively low linguistic demands. Conclusions: The study provides evidence that children with SLI can perform at age-appropriate levels when false belief tasks are less demanding, and that mastery of sentence complementation is a predictor of false belief ability. C1 Penn State Univ, Dept Commun Sci & Disorders, University Pk, PA 16802 USA. RP Miller, CA (reprint author), Penn State Univ, Dept Commun Sci & Disorders, 110 Moore Bldg, University Pk, PA 16802 USA. EM cam47@psu.edu CR ARTHUR G, 1952, ARTHUR ADAPTATION LE ASTINGTON J, 2002, WHY LANG MATT THEOR Astington J. W., 1993, CHILDS DISCOVERY MIN Astington JW, 1999, DEV PSYCHOL, V35, P1311, DOI 10.1037//0012-1649.35.5.1311 Bishop D. V. 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L., 1956, LANGUAGE THOUGHT REA, P207 WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Zelazo PD, 2001, J EXP CHILD PSYCHOL, V78, P107, DOI 10.1006/jecp.2000.2562 Ziatas K, 1998, J CHILD PSYCHOL PSYC, V39, P755, DOI 10.1017/S0021963098002510 NR 52 TC 20 Z9 20 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR-JUN PY 2004 VL 39 IS 2 BP 191 EP 213 DI 10.1080/13682820310001616994 PG 23 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 802ES UT WOS:000220147400003 PM 15204451 ER PT J AU Botting, N AF Botting, N TI Children's Communication Checklist (CCC) scores in 11-year-old children with communication impairments SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE Children's Communication Checklist (CCC); specific language impairment (SLI); pragmatic language impairment (PLI); autistic spectrum disorder (ASD) ID LANGUAGE IMPAIRMENT; AUTISM; SLI; PRAGMATICS; BEHAVIORS; DISORDER AB Background: The pragmatic skills of children with communication disorders and their assessment are currently an issue for speech and language therapy and educational placement. Aims: To explore whether different subgroups of children with communication disorders score differently on the Children's Communication Checklist (CCC) and to study how they compare with published normative data. Methods & Procedures: A sample of 161 eleven-year-old children with a history of communication disorders was assessed using the CCC. The main use of this questionnaire was to establish whether pragmatic impairments were part of a child's communication difficulty. Although the checklist was originally designed for research purposes, normative data for this scale have been recently published as well as group data from a number of different clinical groups. Whilst the present CCC data have been previously reported descriptively for a wider sample, they have not been examined in terms of subgroups or compared directly with normative information and similarly diagnosed individuals from other studies. Outcomes & Results: Of the children assessed, 52 (33%) scored in the normal range (within 1 SD) on the pragmatic scale, 40 (26%) fell between 1 and 2 SD below the normative mean, and 64 (41%) scored below 2 SD of the mean of typically developing children ( aged 6 - 16 years). Thus, the majority (67%) scored out of the normal range for pragmatic skill at 11 years of age. The cohort was separated into four diagnostic subcategories: those with a definite diagnosis of autistic spectrum disorder (n = 15); those with typical specific language impairment (n = 82); generally impaired (n = 37); and those with a clinical history of primary pragmatic language impairment ( independent of CCC score, n = 27). Conclusions: Findings show that those generally impaired and with specific language impairment were less impaired than the other groups on the CCC pragmatic scale. 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E., 1994, SPECIFIC LANGUAGE IM, V4, P161 Joanette Y., 1997, AUTISM, V1, P37, DOI 10.1177/1362361397011006 Nathan L., 2002, CHILD LANG TEACH THE, V18, P213, DOI 10.1191/0265659002ct236oa Rapin I., 1987, P 1 INT S SPEC SPEEC, P20 Rapin I, 1996, J CHILD PSYCHOL PSYC, V37, P643, DOI 10.1111/j.1469-7610.1996.tb01456.x Redmond SM, 1998, J SPEECH LANG HEAR R, V41, P688 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Tomblin JB, 1997, J SPEECH LANG HEAR R, V40, P1245 Wechsler D., 1992, WECHSLER INTELLIGENC Williams K. T., 1997, EXPRESSIVE VOCABULAR NR 30 TC 14 Z9 14 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD APR-JUN PY 2004 VL 39 IS 2 BP 215 EP 227 DI 10.1080/13682820310001617001 PG 13 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 802ES UT WOS:000220147400004 PM 15204452 ER PT J AU Hetzroni, OE Tannous, J AF Hetzroni, OE Tannous, J TI Effects of a computer-based intervention program on the communicative functions of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; functional communication; computers; echolalia ID ACQUISITION; ECHOLALIA; STUDENTS; DEFICITS; SKILLS; MIND AB This study investigated the use of computer-based intervention for enhancing communication functions of children with autism. The software program was developed based on daily life activities in the areas of play, food, and hygiene. The following variables were investigated: delayed echolalia, immediate echolalia, irrelevant speech, relevant speech, and communicative initiations. Multiple-baseline design across settings was used to examine the effects of the exposure of five children with autism to activities in a structured and controlled simulated environment on the communication manifested in their natural environment. Results indicated that after exposure to the simulations, all children produced fewer sentences with delayed and irrelevant speech. Most of the children engaged in fewer sentences involving immediate echolalia and increased the number of communication intentions and the amount of relevant speech they produced. Results indicated that after practicing in a controlled and structured setting that provided the children with opportunities to interact in play, food, and hygiene activities, the children were able to transfer their knowledge to the natural classroom environment. Implications and future research directions are discussed. C1 Univ Haifa, Fac Educ, IL-31905 Haifa, Israel. RP Hetzroni, OE (reprint author), Univ Haifa, Fac Educ, IL-31905 Haifa, Israel. EM hetzroni@construct.haifa.ac.il CR ALCANTARA PR, 1994, EXCEPT CHILDREN, V61, P40 BALTAXE CAM, 1977, J SPEECH HEAR DISORD, V42, P376 BARLOW DH, 1984, SINGLE CASE EXPT DES BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BATES E., 1976, LANGUAGE CONTEXT Bernard-Opitz V., 1989, J CHILD ADOL PSYCHOP, V17, P125 BERNARD-OPITZ V, 1990, Annals Academy of Medicine Singapore, V19, P611 Beukelman D. 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L., 1995, TEACHING CHILDREN AU KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P1, DOI 10.1901/jaba.1977.10-1 Lloyd LL, 1997, AUGMENTATIVE ALTERNA MESIBOV GB, 1994, BEHAV ISSUES AUTISM, P193 Mirenda P., 1997, AUGMENTATIVE ALTERNA, V13, P207, DOI 10.1080/07434619712331278048 PANYAN MV, 1984, J AUTISM DEV DISORD, V14, P375, DOI 10.1007/BF02409828 PRIZANT BM, 1981, J SPEECH HEAR DISORD, V46, P241 PRIZANT BM, 1983, J SPEECH HEAR DISORD, V48, P296 PRIZANT BM, 1984, J SPEECH HEAR RES, V27, P183 RYDELL PJ, 1995, TEACHING CHILDREN AU SCHREIBMAN L, 1978, J APPL BEHAV ANAL, V11, P453, DOI 10.1901/jaba.1978.11-453 TAGERFLUSBERG H, 1992, CHILD DEV, V63, P161, DOI 10.1111/j.1467-8624.1992.tb03604.x Tager-Flusberg H., 1993, UNDERSTANDING OTHER, P138 TAGERFLUSBERG H, 1997, COMMUNICATION LANGUA, P135 Wetherby A. M., 2000, AUTISM SPECTRUM DISO Yamamoto J, 1999, RES DEV DISABIL, V20, P355, DOI 10.1016/S0891-4222(99)00017-7 NR 36 TC 32 Z9 34 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2004 VL 34 IS 2 BP 95 EP 113 DI 10.1023/B:JADD.0000022602.40506.bf PG 19 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700002 PM 15162930 ER PT J AU O'Connor, IM Klein, PD AF O'Connor, IM Klein, PD TI Exploration of strategies for facilitating the reading comprehension of high-functioning students with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's syndrome; reading comprehension; strategy ID PRIOR KNOWLEDGE; ACADEMIC-ACHIEVEMENT; INFANTILE-AUTISM; WORKING-MEMORY; CHILDREN; READERS; TEXT; INDIVIDUALS; HYPERLEXIA; ACQUISITION AB Many students with autism spectrum disorders show good decoding combined with poor comprehension. Twenty adolescent students with autism spectrum disorders participated in a study concerning the effects of three kinds of facilitation on reading comprehension. In a within-subjects design, each students read passages under four conditions: answering prereading questions, completing cloze sentences embedded in the text, resolving anaphora by identifying relevant antecedents, and control (reading only). A repeated measures analysis of variance indicated that conditions differed significantly in their effects on reading comprehension. Post hoc contrasts showed that the effects of anaphoric cuing were statistically significant and medium in size; the effects of prereading questions and cloze completion were small and not statistically significant. Instructional implications for text preparation, remedial instruction, and the design of educational software are discussed. C1 Univ Western Ontario, Fac Educ, London, ON, Canada. RP Klein, PD (reprint author), 137 Western Rd, London, ON N6G 1G7, Canada. EM pklein@uwo.ca CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baddeley A. D., 1999, MODELS WORKING MEMOR, P28 Bereiter C., 1987, PSYCHOL WRITTEN COMP BOSSERT TS, 1995, READ RES INSTRUCT, V35, P109 Bryan LC, 2000, J AUTISM DEV DISORD, V30, P553, DOI 10.1023/A:1005687310346 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 Burack J. A., 1997, HDB AUTISM PERVASIVE, P796 Carr SC, 1996, LEARN DISABILITY Q, V19, P48, DOI 10.2307/1511053 Chafe W., 1994, DISCOURSE CONSCIOUSN Chan C, 1997, COGNITION INSTRUCT, V15, P1, DOI 10.1207/s1532690xci1501_1 COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 DEWITZ P, 1987, READ RES QUART, V22, P99, DOI 10.2307/747723 ERICSSON KA, 1995, PSYCHOL REV, V102, P211, DOI 10.1037//0033-295X.102.2.211 ESKES GA, 1990, J AUTISM DEV DISORD, V20, P61, DOI 10.1007/BF02206857 FINE J, 1994, J AUTISM DEV DISORD, V24, P315, DOI 10.1007/BF02172230 Frith U., 1983, BRIT J DEV PSYCHOL, V1, P329, DOI 10.1111/j.2044-835X.1983.tb00906.x GARNER R, 1990, REV EDUC RES, V60, P517, DOI 10.3102/00346543060004517 GARNER R, 1984, J EDUC PSYCHOL, V76, P300, DOI 10.1037//0022-0663.76.2.300 GERHARDT PF, 1997, HDB AUTISM PERVASIVE, P650 Givon T., 1995, FUNCTIONALISM GRAMMA Glass G. V., 1981, METAANALYSIS SOCIAL GOLDBERG TE, 1987, J AUTISM DEV DISORD, V17, P29, DOI 10.1007/BF01487258 GOLDSTEIN G, 1994, J CLIN EXP NEUROPSYC, V16, P671, DOI 10.1080/01688639408402680 Happe FGE, 1997, BRIT J DEV PSYCHOL, V15, P1 HEALY JM, 1982, READ RES QUART, V17, P319, DOI 10.2307/747522 JONGSMA EA, 1980, CLOZE INSTRUCTION RE Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Kintsch W., 1998, COMPREHENSION PARADI LEE A, 1994, J AUTISM DEV DISORD, V24, P155, DOI 10.1007/BF02172094 LIPSON MY, 1982, J READING BEHAV, V14, P243 Lovett MW, 1996, BRAIN LANG, V54, P447, DOI 10.1006/brln.1996.0085 MINSHEW NJ, 1994, J CLIN EXP NEUROPSYC, V16, P261, DOI 10.1080/01688639408402637 Montague M., 1991, LEARNING DISABILITIE, V6, P219 OAKHILL J, 1986, LANG SPEECH, V29, P25 OCONNOR N, 1994, J AUTISM DEV DISORD, V24, P501, DOI 10.1007/BF02172131 PATTI PJ, 1993, J AUTISM DEV DISORD, V23, P397, DOI 10.1007/BF01046228 PLAISTED J, 1999, J AUTISM DEV DISORD, V29, P29 Pressley M., 1995, VERBAL PROTOCOLS REA Quill KA, 1997, J AUTISM DEV DISORD, V27, P697, DOI 10.1023/A:1025806900162 Sadoski M., 2001, IMAGERY TEXT DUAL CO SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x SINATRA RC, 1977, READING IMPROVEMENT, V14, P86 SNOWLING M, 1986, J EXP CHILD PSYCHOL, V42, P392, DOI 10.1016/0022-0965(86)90033-0 Spires HA, 1998, J EDUC PSYCHOL, V90, P249, DOI 10.1037//0022-0663.90.2.249 SUMMERS JA, 1997, J AUTISM DEV DISORD, V27, P773 TAGERFLUSBERG H, 1990, J AUTISM DEV DISORD, V20, P1, DOI 10.1007/BF02206853 TAGERFLUSBERG H, 1981, J AUTISM DEV DISORD, V11, P45, DOI 10.1007/BF01531340 WHITEHOUSE D, 1984, J AUTISM DEV DISORD, V14, P281, DOI 10.1007/BF02409579 Whitney P, 1996, DISCOURSE PROCESS, V21, P341 Wing L, 1996, BRIT MED J, V312, P327 WISHER RA, 1986, ADV READING LANGUAGE, V4, P97 YUILL N, 1989, BRIT J PSYCHOL, V80, P351 Zellermayer M, 1996, INSTR SCI, V24, P177, DOI 10.1007/BF00119976 NR 53 TC 47 Z9 47 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 2004 VL 34 IS 2 BP 115 EP 127 DI 10.1023/B:JADD.0000022603.44077.6b PG 13 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700003 PM 15162931 ER PT J AU de Bildt, A Sytema, S Ketelaars, C Kraijer, D Mulder, E Volkmar, F Minderaa, R AF de Bildt, A Sytema, S Ketelaars, C Kraijer, D Mulder, E Volkmar, F Minderaa, R TI Interrelationship between autism diagnostic observation schedule-generic (ADOS-G), autism diagnostic interview-revised (ADI-R), and the diagnostic and statistical manual of mental disorders (DSM-IV-TR) classification in children and adolescents with mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE ADI-R; ADOS-G; PDD; MR ID PERVASIVE DEVELOPMENTAL DISORDERS; INTERRATER RELIABILITY; SPECTRUM DISORDERS; CHILDHOOD-AUTISM; RATING-SCALE; CRITERIA; SAMPLE AB The interrelationship between the Autism Diagnostic Interview-Revised (ADI-R), Autism Diagnostic Observation Schedule-Generic (ADOS-G) and clinical classification was studied in 184 children and adolescents with Mental Retardation (MR). The agreement between the ADI-R and ADOS-G was fair, with a substantial difference between younger and older children (5-8 vs. 8+ years). Compared with the Diagnostic and Statistical Manual of Mental Disorders-IV-TR (DSM-IV-TR) classification of Autistic Disorder (AD) and Pervasive Developmental Disorder (PDD), both instruments measure AD or PDD validly and reliably. Even in low-functioning children the interrelationship between the instruments and the clinical classification was satisfactory. The combination of ADI-R and ADOS-G identifies AD or PDD, as described in the DSM-IV-TR, most appropriately. Both instruments seem to be of great value in the diagnostic process of PDD in children and adolescents with MR. C1 Univ Groningen, Dept Psychiat Child & Adolrscent Psychiat, NL-9713 GZ Groningen, Netherlands. Stichtung Hendrik Van Boeijen, Assen, Netherlands. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP de Bildt, A (reprint author), Univ Groningen, Dept Psychiat Child & Adolrscent Psychiat, Hanzeplein 1, NL-9713 GZ Groningen, Netherlands. EM a.de.bilt@accare.nl RI Sytema, Sjoerd/B-2058-2010 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bayley N., 1969, BAYLEY SCALES INFANT BILDT AD, IN PRESS J AUTISM DE Bos A, 1997, WECHSLER PRESCHOOL P Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 CICCHETTI DV, 1981, AM J MENT DEF, V86, P127 Cicchetti DV, 2001, J CLIN EXP NEUROPSYC, V23, P695, DOI 10.1076/jcen.23.5.695.1249 Cicchetti DV, 1995, CHILD NEUROPSYCHOL, V1, P26, DOI 10.1080/09297049508401340 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 de Bildt A, 2003, J AUTISM DEV DISORD, V33, P595, DOI 10.1023/B:JADD.0000005997.92287.a3 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 FOMBONNE E, 1992, J AUTISM DEV DISORD, V22, P563, DOI 10.1007/BF01046328 KRAIJER D, 1972, SRZ SOCIALE REDZAAMH KRAIJER D, 1994, SRZ SOCIALE REDZAAMH Kraijer D. W., 1997, AUTISM AUTISTIC LIKE LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Levine S., 1963, CAIN LEVINE SOCIAL C Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1989, J AUTISM DEV DISORD, V19, P195 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C., 1997, HDB AUTISM PERVASIVE, P460 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 Luteijn EF, 2000, EUR CHILD ADOLES PSY, V9, P168 MEULEN VF, 1983, BAYLEY ONTWIKKELINGS Pilowsky T, 1998, J AUTISM DEV DISORD, V28, P143, DOI 10.1023/A:1026092632466 Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 Robertson JM, 1999, J AM ACAD CHILD PSY, V38, P738, DOI 10.1097/00004583-199906000-00022 Schopler E., 1988, CHILDHOOD AUTISM RAT SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SNIJDERS JT, 1996, SNIJDERS OOMEN NIET Sparrow S, 1984, VINELAND ADAPTIVE BE Vander Steene G., 1986, WECHSLER INTELLIGENC Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D, 1974, WECHSLER INTELLIGENC WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing L, 1997, HDB AUTISM PERVASIVE, P148 World Health Organization, 1992, 10 REV INT CLASS DIS NR 40 TC 101 Z9 101 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 2004 VL 34 IS 2 BP 129 EP 137 PG 9 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700004 PM 15162932 ER PT J AU Ozonoff, S Cook, I Coon, H Dawson, G Joseph, RM Klin, A McMahon, WM Minshew, N Munson, JA Pennington, BF Rogers, SJ Spence, MA Tager-Flusberg, H Volkmar, FR Wrathall, D AF Ozonoff, S Cook, I Coon, H Dawson, G Joseph, RM Klin, A McMahon, WM Minshew, N Munson, JA Pennington, BF Rogers, SJ Spence, MA Tager-Flusberg, H Volkmar, FR Wrathall, D TI Performance on Cambridge Neuropsychological Test Automated Battery subtests sensitive to frontal lobe function in people with autistic disorder: Evidence from the Collaborative Programs of Excellence in Autism Network SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; executive function; planning; set shifting; frontal lobes; CANTAB ID SPATIAL WORKING-MEMORY; CARD SORTING TEST; EXECUTIVE FUNCTION; COMMUNICATION DEFICITS; YOUNG-CHILDREN; LARGE-SAMPLE; DYSFUNCTION; SYSTEMS; CANTAB; DAMAGE AB Recent structural and functional imaging work, as well as neuropathology and neuropsychology studies, provide strong empirical support for the involvement of frontal cortex in autism. The Cambridge Neuropsychological Test Automated Battery (CANTAB) is a computer-administered set of neuropsychological tests developed to examine specific components of cognition. Previous studies document the role of frontal cortex in performance of two CANTAB subtests: the Stockings of Cambridge, a planning task, and the Intradimensional/Extradimensional Shift task, a measure of cognitive set shifting. To examine the integrity of frontal functions, these subtests were administered to 79 participants with autism and 70 typical controls recruited from seven universities who are part of the Collaborative Programs of Excellence in Autism network. The two groups were matched on age, sex, and full-scale IQ. Significant group differences were found in performance on both subtests, with the autism group showing deficits in planning efficiency and extradimensional shifting relative to controls. Deficits were found in both lower- and higher-IQ individuals with autism across the age range of 6 to 47 years. Impairment on the CANTAB executive function subtests did not predict autism severity or specific autism symptoms (as measured by the ADI-R and ADOS), but it was correlated with adaptive behavior. If these CANTAB subtests do indeed measure prefrontal function, as suggested by previous research with animals and lesion patients, this adds to the accumulating evidence of frontal involvement in autism and indicates that this brain region should remain an active area of investigation. C1 Univ Calif Davis, MIND Inst, Sch Med, Sacramento, CA 95817 USA. Univ Utah, Sch Med, Dept Psychiat, Salt Lake City, UT 84112 USA. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. RP Ozonoff, S (reprint author), Univ Calif Davis, MIND Inst, Sch Med, 2825 50th St, Sacramento, CA 95817 USA. EM sally.ozonoff@ucdmc.ucdavis.edu RI Tager-Flusberg, Helen/D-5265-2009; Joseph, Roy/D-8530-2015 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson CV, 1995, J CLIN EXP NEUROPSYC, V17, P900, DOI 10.1080/01688639508402438 Baker SC, 1996, NEUROPSYCHOLOGIA, V34, P515, DOI 10.1016/0028-3932(95)00133-6 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x Casanova MF, 2002, NEUROLOGY, V58, P428 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Dawson G, 2002, CHILD DEV, V73, P700, DOI 10.1111/1467-8624.00433 DENNIS M, 1991, DEV NEUROPSYCHOL, V7, P327 Dias R, 1996, NATURE, V380, P69, DOI 10.1038/380069a0 DUNCAN J, 1986, COGNITIVE NEUROPSYCH, V3, P271, DOI 10.1080/02643298608253360 Fray PJ, 1996, INT J GERIATR PSYCH, V11, P329 Grattan L., 1990, CLIN NEUROPSYCHOL, V4, P279 Griffith EM, 1999, CHILD DEV, V70, P817, DOI 10.1111/1467-8624.00059 HORWITZ B, 1988, ARCH NEUROL-CHICAGO, V45, P749 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 Luciana M, 1998, NEUROPSYCHOLOGIA, V36, P273, DOI 10.1016/S0028-3932(97)00109-7 Luna B, 2002, NEUROLOGY, V59, P834 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x Minshew NJ, 1999, NEUROLOGY, V52, P917 MOUNTAIN MA, 1993, CLIN NEUROPSYCHOL, V7, P108, DOI 10.1080/13854049308401893 OWEN AM, 1991, NEUROPSYCHOLOGIA, V29, P993, DOI 10.1016/0028-3932(91)90063-E Owen AM, 1996, EUR J NEUROSCI, V8, P353, DOI 10.1111/j.1460-9568.1996.tb01219.x Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x 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, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x PRICE BH, 1990, BRAIN, V113, P1383, DOI 10.1093/brain/113.5.1383 PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 Robbins TW, 1998, J INT NEUROPSYCH SOC, V4, P474 ROBBINS TW, 1994, DEMENTIA, V5, P266, DOI 10.1159/000106735 ROBERTS AC, 1988, Q J EXP PSYCHOL-B, V40, P321 RUMSEY JM, 1985, J AUTISM DEV DISORD, V15, P23, DOI 10.1007/BF01837896 RUMSEY JM, 1990, J AUTISM DEV DISORD, V20, P155, DOI 10.1007/BF02284715 RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 Russell J., 1997, AUTISM EXECUTIVE DIS STUSS DT, 1992, BRAIN COGNITION, V20, P8, DOI 10.1016/0278-2626(92)90059-U SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Turner M. A., 1997, AUTISM EXECUTIVE DIS, P57 NR 44 TC 151 Z9 151 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 2004 VL 34 IS 2 BP 139 EP 150 DI 10.1023/B:JADD.0000022605.81989.cc PG 12 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700005 PM 15162933 ER PT J AU Bradley, EA Summers, JA Wood, HL Bryson, SE AF Bradley, EA Summers, JA Wood, HL Bryson, SE TI Comparing rates of psychiatric and behavior disorders in adolescents and young adults with severe intellectual disability with and without autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; intellectual disability; adolescence; behavior and psychiatric disorders ID II DASH-II; PERVASIVE DEVELOPMENTAL DISORDERS; PROFOUND MENTAL-RETARDATION; DIAGNOSTIC-ASSESSMENT; HANDICAPPED-II; INFANTILE-AUTISM; FOLLOW-UP; CHILDREN; PSYCHOPATHOLOGY; EPIDEMIOLOGY AB Eight males and four females with an Autism Diagnostic Interview-Revised (ADI-R) diagnosis of autism ( mean age of 16.3 years) and severe intellectual disability (IQ < 40) were individually matched to controls on the basis of chronological age, gender, and nonverbal IQ. The dependent measure was the Diagnostic Assessment for the Severely Handicapped-II, which is used to screen for psychiatric and behavior disorders in lower-functioning individuals. Participants with autism showed significantly greater disturbances as measured by the Diagnostic Assessment for the Severely Handicapped-II total score and seven of 13 subscales. They also averaged 5.25 clinically significant disturbances compared with 1.25 disturbances for participants without autism. Specific vulnerabilities to anxiety, mood, sleep, organic syndromes, and stereotypies/tics were found in the participants with comorbid autism. C1 Surrey Pl Ctr, Biomed Sci & Res Div, Toronto, ON M5S 2C2, Canada. Univ Toronto, Toronto, ON, Canada. Hamilton Hlth Sci, Hamilton, ON, Canada. McMaster Univ, Hamilton, ON, Canada. Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Dalhousie Univ, Dept Pediat & Psychol, Halifax, NS, Canada. RP Bradley, EA (reprint author), Surrey Pl Ctr, Biomed Sci & Res Div, 2 Surrey Pl, Toronto, ON M5S 2C2, Canada. EM e.bradley@utoronto.ca CR American Academy of Child and Adolescent Psychiatry, 1999, J AM ACAD CHILD PSY, V38, p32S American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BORTHWICKDUFFY SA, 1994, J CONSULT CLIN PSYCH, V62, P17, DOI 10.1037//0022-006X.62.1.17 BRADLEY EA, 2002, CANADIAN J PSYCHIAT, V47, P427 BREGMAN JD, 1991, J AM ACAD CHILD PSY, V30, P861, DOI 10.1097/00004583-199111000-00001 BRERETON AV, 2001, AUSTR NAT AUT C AD A Bryson S. E., 2000, AUTISM, V4, P117, DOI DOI 10.1177/1362361300004002002 BRYSON SE, 2004, UNPUB PREVALENCE AUT Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Cherry KE, 1997, AM J MENT RETARD, V101, P445 Deb S., 2001, PRACTICE GUIDELINES Dunn L. M., 1981, MANUAL PEABODY PICTU Dykens E. 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Autism Dev. Disord. PD APR PY 2004 VL 34 IS 2 BP 151 EP 161 DI 10.1023/B:JADD.0000022606.97580.19 PG 11 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700006 PM 15162934 ER PT J AU Baron-Cohen, S Wheelwright, S AF Baron-Cohen, S Wheelwright, S TI The empathy quotient: An investigation of adults with Asperger syndrome or high functioning autism, and normal sex differences SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE empathy; sex differences; Asperger syndrome; social difficulties ID EMOTIONAL EMPATHY; MIND; CHILDREN; BEHAVIORS; CUES; TWIN AB Empathy is an essential part of normal social functioning, yet there are precious few instruments for measuring individual differences in this domain. In this article we review psychological theories of empathy and its measurement. Previous instruments that purport to measure this have not always focused purely on empathy. We report a new self-report questionnaire, the Empathy Quotient (EQ), for use with adults of normal intelligence. It contains 40 empathy items and 20 filler/control items. On each empathy item a person can score 2, 1, or 0, so the EQ has a maximum score of 80 and a minimum of zero. In Study 1 we employed the EQ with n = 90 adults (65 males, 25 females) with Asperger Syndrome (AS) or high-functioning autism (HFA), who are reported clinically to have difficulties in empathy. The adults with AS/HFA scored significantly lower on the EQ than n = 90 (65 males, 25 females) age-matched controls. Of the adults with AS/HFA, 81% scored equal to or fewer than 30 points out of 80, compared with only 12% of controls. In Study 2 we carried out a study of n = 197 adults from a general population, to test for previously reported sex differences (female superiority) in empathy. This confirmed that women scored significantly higher than men. The EQ reveals both a sex difference in empathy in the general population and an empathy deficit in AS/HFA. C1 Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 2AH, England. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Astington JW, 1988, DEV THEORIES MIND BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 1997, ADV INFANCY RES, V11, P193 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 1999, J AUTISM DEV DISORD, V29, P407, DOI 10.1023/A:1023035012436 Baron-Cohen S, 2003, J AUTISM DEV DISORD, V33, P509, DOI 10.1023/A:1025879411971 BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 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 Batson C. D., 1991, ALTRUISM QUESTION SO Blair RJR, 1997, PSYCHOPHYSIOLOGY, V34, P192 BLAIR RJR, 1995, COGNITION, V57, P1, DOI 10.1016/0010-0277(95)00676-P BOLTON P, 1990, International Review of Psychiatry, V2, P67, DOI 10.3109/09540269009028273 Chapin FS, 1942, AM SOCIOL REV, V7, P214, DOI 10.2307/2085176 CRONBACH LJ, 1955, PSYCHOL BULL, V52, P177, DOI 10.1037/h0044919 Davis M. H., 1980, JSAS CATALOG SELECTE, V10, P85 Davis M. H., 1994, EMPATHY SOCIAL PSYCH DAVIS MH, 1991, J RES PERS, V25, P70, DOI 10.1016/0092-6566(91)90006-C Dennett D, 1987, INTENTIONAL STANCE DYMOND RF, 1950, J CONSULT PSYCHOL, V14, P343 DYMOND RF, 1949, J CONSULTING PSYCHOL, V13, P127 EISENBERG N, 1987, PSYCHOL BULL, V101, P91, DOI 10.1037/0033-2909.101.1.91 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x FOLSTEIN SE, 1988, J AUTISM DEV DISORD, V18, P3, DOI 10.1007/BF02211815 FONAGY P, 1997, BONDING ATTACHMENT, V14, P31 Frith U, 1991, AUTISM ASPERGERS SYN Gillberg C., 1991, AUTISM ASPERGER SYND GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x HALL JA, 1978, PSYCHOL BULL, V85, P845, DOI 10.1037//0033-2909.85.4.845 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Hoffman M., 1984, EMOTIONS COGNITION B, P103 HOFFMAN ML, 1977, PSYCHOL BULL, V84, P712, DOI 10.1037//0033-2909.84.4.712 HOGAN R, 1969, J CONSULT CLIN PSYCH, V33, P307, DOI 10.1037/h0027580 JOHNSON JA, 1983, J PERS SOC PSYCHOL, V45, P1299, DOI 10.1037/0022-3514.45.6.1299 KERR W. A., 1954, J GEN PSYCHOL, V50, P369 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Kohler W., 1929, GESTALT PSYCHOL LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 Mead G.H., 1934, MIND SELF SOC MEHRABIA.A, 1972, J PERS, V40, P525, DOI 10.1111/j.1467-6494.1972.tb00078.x MEHRABIAN A, 1988, CURR PSYCHOL RES REV, V7, P221, DOI 10.1007/BF02686670 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Piaget J., 1932, MORAL JUDGMENT CHILD SMITH A., 1759, THEORY MORAL SENTIME Stotland E., 1969, ADV EXPT SOCIAL PSYC, V4, P271, DOI 10.1016/S0065-2601(08)60080-5 STOTLAND E, 1971, EMPATHY BIRTH ORDER, pS2205 Titchener E., 1909, ELEMENTARY PSYCHOL T WECHSLER D, 1958, SEX DIFFERENCES INTE Wellman H. M., 1990, CHILDRENS THEORIES M Whiten Andrew, 1991, NATURAL THEORIES MIN Wing L, 1988, ASPECTS AUTISM BIOL WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1994, INT CLASS DIS YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 61 TC 675 Z9 688 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 2004 VL 34 IS 2 BP 163 EP 175 DI 10.1023/B:JADD.0000022607.19833.00 PG 13 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700007 PM 15162935 ER PT J AU Grant, CM Riggs, KJ Boucher, J AF Grant, CM Riggs, KJ Boucher, J TI Counterfactual and mental state reasoning in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE counterfactual reasoning; belief reasoning; false belief task; autism ID COGNITIVE-COMPLEXITY; EXECUTIVE FUNCTION; MIND; BELIEF; UNDERSTAND; DISORDER AB The contributions of counterfactual conditional reasoning (CCR), belief understanding, and inferential reasoning to the performance of children with autism (CWA) on standard false belief tasks were investigated. To assess the roles of these three factors, we compared the performance of CWA on physical-state CCR tasks (which do not require either an understanding of belief or inferential reasoning); on Wellman and Bartsch's (1988) nonstandard tests of false belief (which require an understanding of belief, but not CCR or inferential reasoning), and on standard tests of false belief tasks. The CWA were impaired relative to controls on the physical-state CCR and standard false-belief tasks, but not on the nonstandard false-belief tasks, and the CWA's performance on the physical-state CCR and standard false-belief tasks correlated highly, even when the effects of verbal ability were partialled out. Finally, the CWA's performance on standard false-belief tasks was more impaired than their performance on the physical-state CCR tasks. We concluded that impaired performance on standard false-belief tasks in autism is associated with defective competence in CCR (or some of its component skills), plus defective competence in inferential reasoning and possibly generativity, but that impaired performance is not caused by an inadequate understanding of belief. The results are discussed in relation to other hypotheses concerning the cause or causes of impaired performance on standard false-belief tasks in children with autism. C1 Univ Sheffield, Dept Human Commun Sci, Sheffield, S Yorkshire, England. London Guildhall Univ, Sch Psychol, London, England. Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. RP Grant, CM (reprint author), Univ Birmingham, Birmingham B15 2TT, W Midlands, England. EM cmg242@bham.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BARONCOHEN S, 1991, CHILD DEV, V62, P385, DOI 10.1111/j.1467-8624.1991.tb01539.x Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Craig J, 1999, J AUTISM DEV DISORD, V29, P319, DOI 10.1023/A:1022163403479 DEVILLIERS JG, 1999, CHILDRENS REASONING Dunn L M., 1982, BRIT PICTURE VOCABUL Farrant A, 1999, CHILD DEV, V70, P107 Frith U., 1989, AUTISM EXPLAINING EN Frye D, 1998, CURR DIR PSYCHOL SCI, V7, P116, DOI 10.1111/1467-8721.ep10774754 Frye D, 1995, COGNITIVE DEV, V10, P483, DOI 10.1016/0885-2014(95)90024-1 Happe FGE, 1997, BRIT J DEV PSYCHOL, V15, P1 HARRIS PL, 2003, SOC RES CHILD DEV MO, V237 HARRIS PL, 1995, MENTAL SIMULATION EV HARRIS PL, 2000, CHILDRENS REASONING JARROLD C, 1994, J CHILD PSYCHOL PSYC, V35, P1473, DOI 10.1111/j.1469-7610.1994.tb01288.x LEEKAM SR, 1991, COGNITION, V40, P203, DOI 10.1016/0010-0277(91)90025-Y Leslie A., 1993, UNDERSTANDING OTHER LESLIE AM, 1992, COGNITION, V43, P225, DOI 10.1016/0010-0277(92)90013-8 LESLIE AM, 1995, MENTAL SIMULATION EV Minshew NJ, 1998, MENT RETARD DEV D R, V4, P129, DOI 10.1002/(SICI)1098-2779(1998)4:2<129::AID-MRDD10>3.0.CO;2-X Ozonoff S., 1997, AUTISM EXECUTIVE DIS PERNER J, 1989, COGNITION, V33, P315, DOI 10.1016/0010-0277(89)90032-2 PERNER J, 2000, UNPUB MISREPRESENTAT Perner Josef, 1991, UNDERSTANDING REPRES Peterson D., 2000, AUTISM, V4, P391, DOI 10.1177/1362361300004004005 Peterson DM, 1999, MIND LANG, V14, P80, DOI 10.1111/1468-0017.00104 PHILLIPS W, 1995, DEV PSYCHOPATHOL, V7, P151 Riggs KJ, 1998, COGNITIVE DEV, V13, P73, DOI 10.1016/S0885-2014(98)90021-1 RIGGS KJ, 2000, CHILDRENS REASONING Roth D, 1998, COGNITION, V66, P1, DOI 10.1016/S0010-0277(98)00005-5 Russell J, 2001, J CHILD PSYCHOL PSYC, V42, P317, DOI 10.1017/S0021963001006874 Scott FJ, 1999, BRIT J DEV PSYCHOL, V17, P349, DOI 10.1348/026151099165339 SMITH M, 2003, CHILD DEV, V76, P1709 SPARREVOHN R, 1995, J CHILD PSYCHOL PSYC, V36, P249, DOI 10.1111/j.1469-7610.1995.tb01823.x Tager-Flusberg H., 2000, UNDERSTANDING OTHER Tan J., 1991, DEV PSYCHOPATHOL, V3, P163, DOI 10.1017/S0954579400000055 Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 WELLMAN HM, 1988, COGNITION, V30, P239, DOI 10.1016/0010-0277(88)90021-2 Zelazo PD, 1998, CURR DIR PSYCHOL SCI, V7, P121, DOI 10.1111/1467-8721.ep10774761 NR 41 TC 15 Z9 16 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2004 VL 34 IS 2 BP 177 EP 188 DI 10.1023/B:JADD.0000022608.57470.29 PG 12 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700008 PM 15162936 ER PT J AU Gustafsson, L Paplinski, AP AF Gustafsson, L Paplinski, AP TI Self-organization of an artificial neural network subjected to attention shift impairments and familiarity preference, characteristics studied in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID CHILDREN AB Autism is a developmental disorder with possibly multiple pathophysiologies. It has been theorized that cortical feature maps in individuals with autism are inadequate for forming abstract codes and representations. Cortical feature maps make it possible to classify stimuli, such as phonemes of speech, disregarding incidental detail. Hierarchies of such maps are instrumental in creating abstract codes and representations of objects and events. Self-Organizing Maps (SOMs) are artificial neural networks that offer insights into the development of cortical feature maps. Attentional impairment is prevalent in autism, but whether it is caused by attention-shift impairment or strong familiarity preference or negative response to novelty is a matter of debate. We model attention shift during self-organization by presenting a SOM with stimuli from two sources in four different modes, namely, novelty seeking (regarded as normal learning), attention-shift impairment (shifts are made with a low probability), familiarity preference (shifts made with a lower probability to the source that is the less familiar to the SOM of the two sources), and familiarity preference in conjunction with attention-shift impairment. The resulting feature maps from learning with novelty seeking and with attention-shift impairment are much the same except that learning with attention-shift impairment often yields maps with a somewhat better discrimination capacity than learning with novelty seeking. In contrast, the resulting maps from learning with strong familiarity preference are adapted to one of the sources at the expense of the other, and if one of the sources has a set of stimuli with smaller variability, the resulting maps are adapted to stimuli from that source. When familiarity preference is less pronounced, the resulting maps may become normal or fully restricted to one of the sources, and in that case, always the source with smaller variability if such a source is present. Such learning, in a system with many different maps, will result in very uneven capacities. Learning with familiarity preference in conjunction with attention-shift impairment surprisingly has higher probability for the development of normal maps than learning with familiarity preference alone. C1 Monash Univ, Clayton, Vic 3800, Australia. Lulea Univ Technol, S-97187 Lulea, Sweden. RP Paplinski, AP (reprint author), Monash Univ, Clayton, Vic 3800, Australia. EM app@csse.monash.edu.au CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 COHEN I, 1978, NEURAL NETWORKS PSYC, P274 COHEN IL, 1994, BIOL PSYCHIAT, V36, P5, DOI 10.1016/0006-3223(94)90057-4 COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 Courchesne E., 1994, ATYPICAL COGNITIVE D, P101 Courchesne E, 1995, EEG CL N SU, P315 COURCHESNE E, 2002, IN WORLD AUT C MELB Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Frith U., 1989, AUTISM EXPLAINING EN Gillberg C., 2000, BIOL AUTISTIC SYNDRO Gustafsson L, 1997, BIOL PSYCHIAT, V42, P1138, DOI 10.1016/S0006-3223(97)00141-8 Happe FGE, 1991, AUTISM ASPERGER SYND, P207, DOI 10.1017/CBO9780511526770.007 Haykin S., 1999, NEURAL NETWORKS COMP, V2nd HERMELIN B, 1978, AUTISM REAPPRAISAL C, P141 Kandel E. R., 2000, PRINCIPLES NEURAL SC Kanner L, 1943, NERV CHILD, V2, P217 Kohonen T., 2001, SELF ORG MAPS KOOTZ JP, 1982, J AUTISM DEV DISORD, V12, P185, DOI 10.1007/BF01531308 McClelland JL, 2000, J AUTISM DEV DISORD, V30, P497, DOI 10.1023/A:1005576229109 Minshew NJ, 1999, NEUROLOGY, V52, P917 Oliver A, 2000, DEVELOPMENTAL SCI, V3, P1, DOI 10.1111/1467-7687.00094 Pascualvaca DM, 1998, J AUTISM DEV DISORD, V28, P467, DOI 10.1023/A:1026091809650 Price D. J., 2000, MECH CORTICAL DEV Ritter H, 1992, NEURAL COMPUTATION S SPITZER M, 1995, COMPR PSYCHIAT, V36, P83, DOI 10.1016/S0010-440X(95)90103-5 Townsend J, 1999, J NEUROSCI, V19, P5632 Townsend J, 1996, J Int Neuropsychol Soc, V2, P541 NR 28 TC 17 Z9 17 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 APR PY 2004 VL 34 IS 2 BP 189 EP 198 DI 10.1023/B:JADD.0000022609.31371.4d PG 10 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700009 PM 15162937 ER PT J AU Deruelle, C Rondan, C Gepner, B Tardif, C AF Deruelle, C Rondan, C Gepner, B Tardif, C TI Spatial frequency and face processing in children with autism and Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Asperger syndrome; face processing; high and low spatial frequency ID CENTRAL COHERENCE; CHILDHOOD AUTISM; RECOGNITION; PERCEPTION; INFORMATION; DEFICIT; PARTS; DISCRIMINATION; INDIVIDUALS; PERFORMANCE AB Two experiments were designed to investigate possible abnormal face processing strategies in children with autistic spectrum disorders. A group of 11 children with autism was compared to two groups of normally developing children matched on verbal mental age and on chronological age. In the first experiment, participants had to recognize faces on the basis of identity, emotion, gaze direction, gender, and lip reading. All aspects of face processing, except for identity matching, were deficient in the autistic population compared with controls. In the second study, children had to match faces on either high - (i.e., local facial features) or low - spatial frequency information (i.e., global configuration of faces). Contrary to the control subjects, children with autism showed better performance when using high rather than low spatial frequency, confirming face-processing peculiarities in this population. C1 CNRS, Ctr Res Cognit Neurosci, F-13402 Marseille 20, France. Montperrin Hosp, Dept Child Psychiat, Aix En Provence, France. Univ Aix Marseille 1, Aix En Provence, France. CNRS, Lab Psychol & Neurocognit, UMR 5105, Grenoble, France. RP Deruelle, C (reprint author), CNRS, Ctr Res Cognit Neurosci, 31 Chemin Joseph Aiguier, F-13402 Marseille 20, France. 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Autism Dev. Disord. PD APR PY 2004 VL 34 IS 2 BP 199 EP 210 DI 10.1023/B:JADD.0000022610.09668.4c PG 12 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700010 PM 15162938 ER PT J AU Dyches, TT Wilder, LK Sudweeks, RR Obiakor, FE Algozzine, B AF Dyches, TT Wilder, LK Sudweeks, RR Obiakor, FE Algozzine, B TI Multicultural issues in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; cross-cultural studies; etiology; incidence; genetics ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; AFRICAN-AMERICAN; CHILDHOOD AUTISM; CHILDREN; MOTHERS; SATISFACTION; DISABILITIES; PREVALENCE; FAMILIES AB The professional literature provides ample evidence that individuals with autism exhibit a myriad of unusual social, communication, and behavioral patterns of interactions that present challenges to their families and service providers. However, there is a dearth of quality works on multicultural issues regarding autistic spectrum disorders. In this article, we explore issues surrounding autism and multiculturalism, with the intent not to provide answers but to raise questions for further examination. We focus our discussions on two primary issues: autism within cultural groups and multicultural family adaptation based on the framework of pluralistic societies in which some cultural groups are a minority within the dominant culture. We found differences in prevalence rates across races for autism and little information regarding how multicultural families adapt to raising a child with autism. Further, students with multicultural backgrounds and autism are challenged on at least four dimensions: communication, social skills, behavioral repertoires, and culture. Future research in these areas is clearly warranted. C1 Brigham Young Univ, Provo, UT 84602 USA. Univ Wisconsin, Milwaukee, WI 53201 USA. 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A., 2001, SPECIAL ED MULTICULT Volkmar FR, 1998, AUTISM PERVASIVE DEV, P1 Wilder L. K. J., 2001, PREVENTING SCH FAILU, V45, P119 Wing L., 1987, HDB AUTISM PERVASIVE, P3 WING L, 1980, BRIT J PSYCHIAT, V137, P410, DOI 10.1192/bjp.137.5.410 Ysseldyke J.E., 2000, CRITICAL ISSUES SPEC NR 51 TC 47 Z9 47 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 2004 VL 34 IS 2 BP 211 EP 222 DI 10.1023/B:JADD.0000022611.80478.73 PG 12 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700011 PM 15162939 ER PT J AU Paul, R Miles, S Cicchetti, D Sparrow, S Klin, A Volkmar, F Coflin, M Booker, S AF Paul, R Miles, S Cicchetti, D Sparrow, S Klin, A Volkmar, F Coflin, M Booker, S TI Adaptive behavior in autism and Pervasive Developmental Disorder-Not Otherwise Specified: Microanalysis of scores on the Vineland Adaptive Behavior Scales SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Pervasive Developmental Disorders; adaptive behavior; communication; expressive language; socialization ID DOWN-SYNDROME; FIELD TRIAL; DSM-IV; CHILDREN; INDIVIDUALS; DEFICITS; CRITERIA AB The purpose of this study is to provide a microanalysis of differences in adaptive functioning seen between well-matched groups of school-aged children with autism and those diagnosed as having Pervasive Developmental Disorder-Not Otherwise Specified, all of whom functioned in the mild to moderate range of intellectual impairment. Findings indicate that the major area of difference between children with autism and those with Pervasive Developmental Disorder-Not Otherwise Specified, was expressive communication; specifically, the use of elaborations in syntax and morphology and in pragmatic use of language to convey and to seek information in discourse. Linear discriminant function analysis revealed that scores on just three of these expressive communication item sets correctly identified subjects in the two diagnostic categories with 80% overall accuracy. Implications of these findings for both diagnosis and intervention with children with Autism Spectrum Disorders will be discussed. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. So Connecticut State Univ, New Haven, CT 06515 USA. RP Paul, R (reprint author), Yale Univ, Ctr Child Study, POB 207900, New Haven, CT 06520 USA. EM rhea.paul@yale.edu CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Cicchetti DV, 1995, CHILD NEUROPSYCHOL, V1, P26, DOI 10.1080/09297049508401340 DEMYER MK, 1981, SCHIZOPHRENIA BULL, V7, P388 FLETCHER JM, 1978, CORTEX, V14, P564 Gillham JE, 2000, J AUTISM DEV DISORD, V30, P269, DOI 10.1023/A:1005571115268 Kanner L, 1943, NERV CHILD, V2, P217 Klin A, 2000, J AUTISM DEV DISORD, V30, P163, DOI 10.1023/A:1005415823867 KLIN A, 1992, J CHILD PSYCHOL PSYC, V33, P861, DOI 10.1111/j.1469-7610.1992.tb01961.x Liss M, 2001, J AUTISM DEV DISORD, V31, P219, DOI 10.1023/A:1010707417274 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 LOVELAND KA, 1991, AM J MENT RETARD, V96, P13 Prior M, 1998, AUTISM PERVASIVE DEV, P64 RODRIGUE JR, 1991, J AUTISM DEV DISORD, V21, P187, DOI 10.1007/BF02284759 SCHATZ J, 1995, J AUTISM DEV DISORD, V25, P51, DOI 10.1007/BF02178167 Sparrow S, 1984, VINELAND ADAPTIVE BE TAGERFLUSBERG H, 1995, CONSTRAINTS LANGUAGE, P175 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Volkmar FR, 1998, AUTISM PERVASIVE DEV, P1 VOLKMAR FR, 1987, J AM ACAD CHILD PSY, V26, P156, DOI 10.1097/00004583-198703000-00005 NR 22 TC 38 Z9 41 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2004 VL 34 IS 2 BP 223 EP 228 DI 10.1023/B:JADD.0000022612.18116.46 PG 6 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700012 PM 15162940 ER PT J AU Hill, E Berthoz, S Frith, U AF Hill, E Berthoz, S Frith, U TI Brief report: Cognitive processing of own emotions in individuals with autistic spectrum disorder and in their relatives SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID TORONTO-ALEXITHYMIA-SCALE; PSYCHOMETRIC PROPERTIES; CHILDREN; PARENTS; DEPRESSION AB Difficulties in the cognitive processing of emotions - including difficulties identifying and describing feelings - are assumed to be an integral part of autism. We studied such difficulties via self-report in 27 high-functioning adults with autistic spectrum disorders, their biological relatives (n = 49), and normal adult controls (n = 35), using the 20-item Toronto Alexithymia Scale and the Beck Depression Inventory. 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PD APR PY 2004 VL 34 IS 2 BP 229 EP 235 DI 10.1023/B:JADD.0000022613.41399.14 PG 7 WC Psychology, Developmental SC Psychology GA 808XB UT WOS:000220600700013 PM 15162941 ER PT J AU Asato, MR Hardan, AY AF Asato, MR Hardan, AY TI Neuropsychiatric problems in tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID POSITRON-EMISSION-TOMOGRAPHY; INFANTILE SPASMS; DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDER; AUTISTIC DISORDER; EPILEPSY SURGERY; DOUBLE-BLIND; CHILDREN; TSC1; NEUROTROPHINS AB Tuberous sclerosis complex is an autosomal dominant disorder characterized by abnormal cellular differentiation and proliferation, as well as abnormal neuronal migration. It is a disease affecting multiple organ systems and typically has brain involvement, causing severe disabilities. This article reviews the literature of the commonly associated neuropsychiatric complications, including mental retardation, autism-like features, and other behavior problems, which are discussed in the context of the neuropathology and epilepsy observed in tuberous sclerosis complex. The potential pathogenesis of neuropsychiatric problems is explored, including links to the genetics, neuropathology, neurotrophins, and epilepsy factors associated with tuberous sclerosis complex. Treatment of neuropsychiatric symptoms, including autism-like features, attention deficits, and sleep disorders, is also discussed. C1 Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Lab Neurocognit Dev, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Asato, MR (reprint author), Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Lab Neurocognit Dev, 3501 Forbes Ave,Oxford Bldg,Room 744, Pittsburgh, PA 15213 USA. 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Child Neurol. PD APR PY 2004 VL 19 IS 4 BP 241 EP 249 DI 10.1177/088307380401900401 PG 9 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 820VZ UT WOS:000221419000001 PM 15163088 ER PT J AU Casanova, MF Araque, J Giedd, J Rumsey, JM AF Casanova, MF Araque, J Giedd, J Rumsey, JM TI Reduced brain size and gyrification in the brains of dyslexic patients SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID ANATOMICAL RISK-FACTORS; DEVELOPMENTAL DYSLEXIA; PLANUM TEMPORALE; CEREBRAL-CORTEX; MINICOLUMNAR PATHOLOGY; AUTISM; MAMMALS; MEN AB Dyslexia is a specific learning disability that affects the way in which a person acquires reading skills. The pathologic substrate of the condition has been debated in the literature. Conclusions from postmortem studies remain controversial because series have been based on few and often ill-characterized cases. The present article expands on one of the reported neuropathologic findings in dyslexia, that is, wider minicolumns. Measurements were made of magnetic resonance images in a series of 16 dyslexic and 14 age- and sex-matched controls. Dyslexic patients had significantly smaller total cerebral volume (P = .014) and reduced gyrification index (P = .021). No changes were noted in cortical thickness, the ratio of gray to white matter, or the cross-sectional areas of the corpus callosum and medulla oblongata. The findings, although not conclusive, are in keeping with a minicolumnar defect in dyslexia. The decreased gyrification and preserved cortical thickness can alter the information processing capacity of the brain by providing a greater degree of cortical integration at the expense of a slower response time. The article also emphasizes the contrast between findings in dyslexia and in autism. C1 Univ Louisville, Dept Psychiat, Louisville, KY 40292 USA. Med Coll Georgia, Dept Anat, Augusta, GA 30912 USA. NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. NIMH, Clin Neurosci Branch, Bethesda, MD 20892 USA. RP Casanova, MF (reprint author), Univ Louisville, Dept Psychiat, 500 S Preston St,Bldg A,Rm 217, Louisville, KY 40292 USA. EM m0casa02@louisville.edu RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012 OI Giedd, Jay/0000-0003-0827-3460 CR AGGOUNAOUAOUI D, 1968, EUR J NEUROSCI, V6, P1132 ARMSTRONG E, 1995, CEREB CORTEX, V5, P56, DOI 10.1093/cercor/5.1.56 BROWN WE, 2001, NEUROLOGY, V56, P7812 Buxhoeveden DR, 2001, BRAIN BEHAV EVOLUT, V57, P349, DOI 10.1159/000047253 Casanova MF, 2002, J CHILD NEUROL, V17, P692, DOI 10.1177/088307380201700908 Casanova MF, 2002, ANN NEUROL, V52, P108, DOI 10.1002/ana.10226 Casanova MF, 2003, NEUROSCIENTIST, V9, P496, DOI 10.1177/1073858403253552 Compton D L, 2001, Dyslexia, V7, P125, DOI 10.1002/dys.198 DUARA R, 1991, ARCH NEUROL-CHICAGO, V48, P410 Eckert MA, 2000, MENT RETARD DEV D R, V6, P198, DOI 10.1002/1098-2779(2000)6:3<198::AID-MRDD7>3.0.CO;2-1 Eckert MA, 2003, BRAIN, V126, P482, DOI 10.1093/brain/awg026 Eden GF, 1996, NATURE, V382, P66, DOI 10.1038/382066a0 Eliez S, 2000, J CHILD PSYCHOL PSYC, V41, P637 GALABURDA AM, 1979, ANN NEUROL, V6, P94, DOI 10.1002/ana.410060203 GALABURDA AM, 1994, P NATL ACAD SCI USA, V91, P8010, DOI 10.1073/pnas.91.17.8010 GALABURDA AM, 1985, ANN NEUROL, V18, P222, DOI 10.1002/ana.410180210 Gibson KR, 2001, EVOLUTIONARY ANATOMY OF THE PRIMATE CEREBRAL CORTEX, P79 Giedd JN, 1996, CEREB CORTEX, V6, P551, DOI 10.1093/cercor/6.4.551 Gustafsson L, 1997, BIOL PSYCHIAT, V42, P1138, DOI 10.1016/S0006-3223(97)00141-8 Hofman MA, 2001, EVOLUTIONARY ANATOMY OF THE PRIMATE CEREBRAL CORTEX, P113 HOFMAN MA, 1982, BRAIN BEHAV EVOLUT, V20, P84, DOI 10.1159/000121583 Houzel JC, 1999, J PHYSIOLOGY-PARIS, V93, P271, DOI 10.1016/S0928-4257(00)80056-X HUMPHREYS P, 1990, ANN NEUROL, V28, P727, DOI 10.1002/ana.410280602 Kaas J.H., 1987, P347 Leonard CM, 2001, CEREB CORTEX, V11, P148, DOI 10.1093/cercor/11.2.148 Leonard CM, 2002, J COMMUN DISORD, V35, P501, DOI 10.1016/S0021-9924(02)00120-X MAUGHAN B, 1995, J CHILD PSYCHOL PSYC, V36, P357, DOI 10.1111/j.1469-7610.1995.tb01296.x OTSU N, 1979, IEEE T SYST MAN CYB, V9, P377 Parnavelas JG, 2000, TRENDS NEUROSCI, V23, P126, DOI 10.1016/S0166-2236(00)01553-8 PROTHERO JW, 1984, BRAIN BEHAV EVOLUT, V24, P152, DOI 10.1159/000121313 Rakic P, 2001, EVOLUTIONARY ANATOMY OF THE PRIMATE CEREBRAL CORTEX, P30 RUMSEY JM, 1990, J AUTISM DEV DISORD, V20, P155, DOI 10.1007/BF02284715 Rumsey JM, 1997, ARCH NEUROL-CHICAGO, V54, P562 Rumsey JM, 1997, ARCH NEUROL-CHICAGO, V54, P1481 SHAYWITZ SE, 1992, NEW ENGL J MED, V326, P145, DOI 10.1056/NEJM199201163260301 WAGNER RK, 1987, PSYCHOL BULL, V101, P192, DOI 10.1037//0033-2909.101.2.192 Wosinski M, 1996, Neurobiology (Bp), V4, P441 ZILLES K, 1989, BRAIN BEHAV EVOLUT, V34, P143, DOI 10.1159/000116500 NR 38 TC 44 Z9 44 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 APR PY 2004 VL 19 IS 4 BP 275 EP 281 DI 10.1177/088307380401900407 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 820VZ UT WOS:000221419000007 PM 15163094 ER PT J AU Akhondzadeh, S Erfani, S Mohammadi, MR Tehrani-Doost, M Amini, H Gudarzi, SS Yasamy, MT AF Akhondzadeh, S Erfani, S Mohammadi, MR Tehrani-Doost, M Amini, H Gudarzi, SS Yasamy, MT TI Cyproheptadine in the treatment of autistic disorder: a double-blind placebo-controlled trial SO JOURNAL OF CLINICAL PHARMACY AND THERAPEUTICS LA English DT Article DE autistic disorder; cyproheptadine; haloperidol; 5-HT ID NEUROLEPTIC INDUCED AKATHISIA; RATING-SCALE; CHRONIC-SCHIZOPHRENIA; RITANSERIN R-55667; SEROTONIN; CHILDREN; ANTAGONIST; PLATELETS; SYMPTOMS AB Objective: Autism is a childhood-onset disorder of unknown, possibly of multiple aetiologies. The core symptoms of autism are abnormalities in social interaction, communication and behaviour. The involvement of neurotransmitters such as 5-HT has been suggested in neuropsychiatric disorders and particularly in autistic disorder. Increased platelet 5-HT levels were found in 40% of the autistic population, suggesting that hyperserotonaemia may be a pathologic factor in infantile autism. Therefore, it is of interest to assess the efficacy of cyproheptadine, a 5-HT2 antagonist in the treatment of autistic disorder. In this 8-week double-blind, placebo-controlled trial, we assessed the effects of cyproheptadine plus haloperidol in the treatment of autistic disorder. Methods: Children between the ages 3 and 11 years (inclusive) with a DSM IV clinical diagnosis of autism and who were outpatients from a specialty clinic for children at Roozbeh Psychiatric Teaching Hospital were recruited. The children presented with a chief complaint of severely disruptive symptoms related to autistic disorder. Patients were randomly allocated to cyproheptadine + haloperidol (Group A) or haloperidol + placebo (Group B) for an 8-week, double-blind, placebo-controlled study. The dose of haloperidol and cyproheptadine was titrated up to 0.05 and 0.2 mg/kg/day respectively. Patients were assessed by a third-year resident of psychiatry at baseline and after 2, 4, 6 and 8 weeks of starting medication. The primary measure of the outcome was the Aberrant Behaviour Checklist-Community (ABC-C) and the secondary measure of the outcome was the Childhood Autism Rating Scale (relating to people and verbal communication). Side effects and extrapyramidal symptoms were systematically recorded throughout the study and were assessed using a checklist and the Extrapyramidal Symptoms Rating Scale, administered by a resident of psychiatry during weeks 1, 2, 4, 6 and 8. Results: The ABC-C and the Childhood Autism Rating Scale scores improved with cyproheptadine. The behaviour of the two treatments was not homogeneous across time (groups-by-time interaction, Greenhouse-Geisser correction; F = 7.30, d.f. = 1.68, P = 0.002; F = 8.21, d.f. = 1.19, P = 0.004 respectively). The difference between the two treatments was significant as indicated by the effect of group, and the between-subjects factor (F = 4.17, d.f. = 1, P = 0.048; F = 4.29, d.f. = 1, P = 0.045 respectively). No significant difference was observed between the two groups in terms of extrapyramidal symptoms (P = 0.23). The difference between the two groups in the frequency of side effects was not significant. Conclusion: The results suggest that the combination of cyproheptadine with a conventional antipsychotic may be superior to conventional antipsychotic alone for children with autistic disorder. However the results need confirmation by a larger randomized controlled trial. C1 Univ Tehran Med Sci, Psychiat Res Ctr, Roozbeh Hosp, Tehran, Iran. Inst Med Plants, Tehran, Iran. Shaheed Beheshti Univ Med Sci, Dept Psychiat, Tehran, Iran. RP Akhondzadeh, S (reprint author), No 29 39th St,Gisha St, Tehran 14479, Iran. 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Clin. Pharm. Ther. PD APR PY 2004 VL 29 IS 2 BP 145 EP 150 DI 10.1111/j.1365-2710.2004.00546.x PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 805RB UT WOS:000220382300006 PM 15068403 ER PT J AU Mehta, UC Patel, I Castello, FV AF Mehta, UC Patel, I Castello, FV TI EEG sedation for children with autism SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; EGG; sedation; clonidine ID SEIZURE DISORDERS; CHLORAL HYDRATE; CLONIDINE; EFFICACY; SLEEP AB Seizures are reported to occur more frequently among children with diagnoses of autism and pervasive developmental disorder (PDD), and some reports indicate a frequency as high as 30%. Sedation is often necessary to perform diagnostic electroencephalograms (EEGs) in these children, who are known to be difficult to sedate with current available pediatric sedating agents, including chloral hydrate. We used clonidine as a sedative agent in children with autism and PDD, and our findings are presented. In a prospective study, 27 children with autism and PDD diagnoses underwent conscious sedation for EEG recording. Informed consents were obtained, and clonidine was administered orally as a sedating agent in a dose ranging from 0.05 mg to 0.2 mg. Subjects were monitored for pulse rate, respiration rate, blood pressure, and oxygen saturation on a continuous basis by a registered nurse. Study parameters included time to induction, time to recovery, changes in vital signs, and technical quality of EEGs. Sedation was achieved in 23 of 27 patients (85%) per our sedation criteria, and this included five patients who had previously failed to be sedated with chloral hydrate. Two patients did not satisfy the sedation criteria but cooperated enough to allow acceptable EEG tracings, increasing the success rate to 93% (25/27). The mean time to achieve sedation was 58 minutes, and the mean time to recovery was 105 minutes. Two patients (0.07%) experienced an asymptomatic heart rate reduction up to 40%, which was not sustained and recovered promptly without any intervention. Two patients (0.07%) experienced systolic blood pressure reductions of 30% and 40%. They remained asymptomatic, had no changes in other cardiorespiratory parameters, and required no intervention. All EEGs were of good technical quality without any "drug effect." Clonidine is a viable alternative for sedation in children with autism and PDD. It is well tolerated without any significant side effects and is efficacious in children with autism and PDD. The advantages of clonidine include ease of administration, shorter duration of total sedation, lack of EEG drug effect, and high overall success rate. C1 Childrens Specialized Hosp, Mountainside, NJ 07092 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, New Brunswick, NJ USA. RP Mehta, UC (reprint author), Childrens Specialized Hosp, 150 New Providence Rd, Mountainside, NJ 07092 USA. 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Dev. Behav. Pediatr. PD APR PY 2004 VL 25 IS 2 BP 102 EP 104 DI 10.1097/00004703-200404000-00005 PG 3 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 812OY UT WOS:000220850000005 PM 15083132 ER PT J AU Van Heest, R Jones, S Giacomantonio, M AF Van Heest, R Jones, S Giacomantonio, M TI Rectal prolapse in autistic children SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE rectal prolapse; autism; mental retardation AB Rectal prolapse in children is not uncommon, but surgery is rarely indicated. In mentally challenged adults and children, rectal prolapse occurs more frequently than in the general population and often requires surgical intervention in the second to third decade of life. The authors describe 3 children with autism and mental retardation who presented with rectal prolapse at an earlier age than would be anticipated with mental retardation alone. All 3 children required surgical intervention. C1 Dalhousie Univ, IWK Hlth Ctr, Div Pediat Gen Surg, Halifax, NS B3J 3G9, Canada. Dalhousie Univ, Dept Gen Surg, Halifax, NS B3J 3G9, Canada. RP Jones, S (reprint author), Dalhousie Univ, IWK Hlth Ctr, Div Pediat Gen Surg, 5850 Univ Ave, Halifax, NS B3J 3G9, Canada. CR Cunniff C, 2001, PEDIATRICS, V107, P1192 Bishop PR, 1999, PEDIATR ANN, V28, P322 CORMAN ML, 1990, J PEDIATR SURG, V25, P992 DASELER EH, 1967, DIS COLON RECTUM, V10, P141, DOI 10.1007/BF02617362 DORMAN ML, 1985, DIS COLON RECTUM, V28, P535 FREDERICK W C, 1970, American Surgeon, V36, P533 QUST N, 1986, J PEDIATR SURG, V21, P887 1991, LANCET, V338, P605 NR 8 TC 5 Z9 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0022-3468 J9 J PEDIATR SURG JI J. Pediatr. Surg. PD APR PY 2004 VL 39 IS 4 BP 643 EP 644 DI 10.1016/j.jpedsurg.2003.12.028 PG 2 WC Pediatrics; Surgery SC Pediatrics; Surgery GA 811YP UT WOS:000220807500032 PM 15065049 ER PT J AU Piggot, J Kwon, H Mobbs, D Blasey, C Lotspeich, L Menon, V Bookheimer, S Reiss, AL AF Piggot, J Kwon, H Mobbs, D Blasey, C Lotspeich, L Menon, V Bookheimer, S Reiss, AL TI Emotional attribution in high-functioning individuals with autistic spectrum disorder: A functional imaging study SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism spectrum disorders; emotion; functional magnetic resonance imaging ID PERVASIVE DEVELOPMENTAL DISORDERS; HUMAN VISUAL-CORTEX; FUSIFORM FACE AREA; FACIAL EXPRESSIONS; ASPERGER-SYNDROME; SOCIAL INFORMATION; HUMAN AMYGDALA; NORMAL ADULTS; CHILDREN; RECOGNITION AB Objective: To determine whether expertise in the attribution of emotion from basic facial expressions in high-functioning individuals with autistic spectrum disorder (ASD) is supported by the amygdala, fusiform, and prefrontal regions of interest (ROI) and is comparable to that of typically developing individuals. Method: Functional magnetic resonance imaging scans were acquired from 14 males with ASD and 10 matched adolescent controls while performing emotion match (EM) (perceptual), emotion label (EL) (linguistic), and control tasks. Accuracy, response time, and average activation were measured for each ROI. Results: There was no significant difference in accuracy, response time, or ROI. activation between groups performing the EL task. The ASD group was as accurate as the control group performing the EM task but had a significantly longer response time and lower average fusiform activation. Conclusions: Expertise in the attribution of emotion from basic facial expressions was task-dependent in the high-functioning ASD group. The hypothesis that the high-functioning ASD group would be less expert and would have reduced fusiform activation was supported in the perceptual task but not the linguistic task. The reduced fusiform activation in the perceptual task was not explained by reduced expertise; it is therefore concluded that reduced fusiform activation is associated with the diagnosis of ASD. C1 Univ Glasgow, Dept Child & Adolescent Psychiat, Glasgow G12 8QQ, Lanark, Scotland. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. Univ Calif Los Angeles, Brain Mapping Ctr, Los Angeles, CA 90024 USA. RP Piggot, J (reprint author), Royal Hosp Sick Children, Caledonia House, Glasgow G3 8SJ, Lanark, Scotland. 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Am. Acad. Child Adolesc. Psychiatr. PD APR PY 2004 VL 43 IS 4 BP 473 EP 480 DI 10.1097/01.chi.0000111363.94169.37 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 805RV UT WOS:000220384300014 PM 15187808 ER PT J AU Wang, AT Dapretto, M Hariri, AR Sigman, M Bookheimer, SY AF Wang, AT Dapretto, M Hariri, AR Sigman, M Bookheimer, SY TI Neural correlates of facial affect processing in children and adolescents with autism spectrum disorder SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE amygdala; autism; facial expression; fusiform gyrus; functional magnetic resonance imaging ID FUSIFORM FACE AREA; ASPERGER-SYNDROME; HUMAN AMYGDALA; SOCIAL INFORMATION; EARLY RECOGNITION; BRAIN-AREAS; EXPRESSIONS; ACTIVATION; EXPLICIT; EMOTION AB Objective: To examine the neural basis of impairments in interpreting facial emotions in children and adolescents with autism spectrum disorders (ASD). Method: Twelve children and adolescents with ASD and 12 typically developing (TD) controls matched faces by emotion and assigned a label to facial expressions while undergoing functional magnetic resonance imaging. Results: Both groups engaged similar neural networks during facial emotion processing, including activity in the fusiform gyrus (FG) and prefrontal cortex. However, between-group analyses in regions of interest revealed that when matching facial expressions, the ASD group showed significantly less activity than the TD group in the FG, but reliably greater activity in the precuneus. During the labeling of facial emotions, no between-group differences were observed at the behavioral or neural level. Furthermore, activity in the amygdala was moderated by task demands in the TD group but not in the ASD group. Conclusions: These findings suggest that children and adolescents with ASD in part recruit different neural networks and rely on different strategies when processing facial emotions. High-functioning individuals with ASD may be relatively unimpaired in the cognitive assessment of basic emotions, yet still show differences in the automatic processing of facial expressions. C1 Univ Calif Los Angeles, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90095 USA. RP Dapretto, M (reprint author), Univ Calif Los Angeles, Ahmanson Lovelace Brain Mapping Ctr, 660 Charles Young Dr S, Los Angeles, CA 90095 USA. 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PD APR PY 2004 VL 43 IS 4 BP 481 EP 490 DI 10.1097/01.chi.0000111481.76722.66 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 805RV UT WOS:000220384300015 PM 15187809 ER PT J AU Mulder, EJ Anderson, GM Kema, IP de Bildt, A van Lang, NDJ den Boer, JA Minderaa, RB AF Mulder, EJ Anderson, GM Kema, IP de Bildt, A van Lang, NDJ den Boer, JA Minderaa, RB TI Platelet serotonin levels in pervasive developmental disorders and mental retardation: Diagnostic group differences, within-group distribution, and behavioral correlates SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE platelet serotonin; autism; pervasive developmental disorder-not otherwise specified; mental retardation; pervasive developmental disorders; hyperserotonemia; mixture-modeling ID WHOLE-BLOOD SEROTONIN; 1ST-DEGREE RELATIVES; AUTISTIC PROBANDS; RETARDED-CHILDREN; INDIVIDUALS; TRYPTOPHAN; MODEL AB Objective: To investigate group differences, the within-group distributions, and the clinical correlates of platelet serotonin (5-HT) levels in pervasive developmental disorders (PDD). Method: Platelet 5-HT levels were measured in Dutch children and young adults, recruited from 2001 through 2003, with PDD (autism, Asperger's, and PDD-not otherwise specified [PDD-NOS]; n = 81) or with mental retardation (MR; n = 54) but without PDD, and in normal controls (n = 60). The distribution of platelet 5-HT levels was assessed using mixture-modeling analyses. Relationships between platelet 5-HT levels and a full range of demographic, clinical, and behavioral variables were examined. Results: Group mean (+/- SD) platelet 5-HT levels (nmol/10(9) platelets) were significantly higher in the autistic (4.51 +/- 1.61, n = 33) and PDD-NOS (4.90 +/- 1.54, n = 43) groups compared to the MR (3.48 +/- 1.33, n = 54) or the normal control (3.58 +/- 1.08, n = 60) groups (F-4,F-190 = 9.35, p < .001). Platelet 5-HT values in the combined PDD group showed a bimodal distribution, and an empirical cutpoint for hyperserotonemia was determined. 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PD APR PY 2004 VL 43 IS 4 BP 491 EP 499 DI 10.1097/01.chi.0000111365.94169.b0 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 805RV UT WOS:000220384300016 PM 15187810 ER PT J AU Murphy, DL Lerner, A Rudnick, G Lesch, KP AF Murphy, DL Lerner, A Rudnick, G Lesch, KP TI Serotonin transporter: Gene, genetic disorders, and pharmacogenetics SO MOLECULAR INTERVENTIONS LA English DT Review ID OBSESSIVE-COMPULSIVE DISORDER; POSITRON-EMISSION-TOMOGRAPHY; HUMAN NOREPINEPHRINE TRANSPORTER; PRIMARY PULMONARY-HYPERTENSION/; DEFICIT HYPERACTIVITY DISORDER; ANTIDEPRESSANT-INDUCED MANIA; POLYMORPHIC REGION 5-HTTLPR; BIOGENIC-AMINE TRANSPORTERS; IRRITABLE-BOWEL-SYNDROME; CENTRAL-NERVOUS-SYSTEM AB The highly evolutionarily conserved serotonin transporter (SERT) regulates the entire serotoninergic system and its receptors via modulation of extracellular fluid serotonin concentrations. Differences in SERT expression and function produced by three SERT genes and their variants show associations with multiple human disorders. Screens of DNA from patients with autism, ADHD, bipolar disorder, and Tourette's syndrome have detected signals in the chromosome 17q region where SERT is located. Parallel investigations of SERT knockout mice have uncovered multiple phenotypes that identify SERT as a candidate gene for additional human disorders ranging from irritable bowel syndrome to obesity. Replicated studies have demonstrated that the SERT 5'-flanking region polymorphism SS genotype is associated with poorer therapeutic responses and more frequent serious side effects during treatment with antidepressant SERT antagonists, namely, the serotonin reuptake inhibitors (SRIs). C1 NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA. Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA. Univ Wurzburg, Dept Psychiat & Psychotherapy, D-97070 Wurzburg, Germany. RP Murphy, DL (reprint author), NIMH, Clin Sci Lab, NIH, Bldg 10,Room 3D41,10 Ctr Dr,MSC 1264, Bethesda, MD 20892 USA. 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PD APR PY 2004 VL 4 IS 2 BP 109 EP 123 DI 10.1124/mi.4.2.8 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 832DX UT WOS:000222248500008 PM 15087484 ER PT J AU Waly, M Olteanu, H Banerjee, R Choi, SW Mason, JB Parker, BS Sukumar, S Shim, S Sharma, A Benzecry, JM Power-Charnitsky, VA Deth, RC AF Waly, M Olteanu, H Banerjee, R Choi, SW Mason, JB Parker, BS Sukumar, S Shim, S Sharma, A Benzecry, JM Power-Charnitsky, VA Deth, RC TI Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; attention deficit hyperactivity disorder; P13-kinase; D4 dopamine receptor; DNA methylation; phospholipid methylation; lead; mercury ID DNA METHYLATION; GENE-EXPRESSION; NEURONAL DIFFERENTIATION; PHOSPHOLIPID METHYLATION; S-ADENOSYLHOMOCYSTEINE; COMBINED DEGENERATION; NEUROBLASTOMA-CELLS; PURINE METABOLISM; AUTISTIC DISORDER; INDUCED APOPTOSIS AB Methylation events play a critical role in the ability of growth factors to promote normal development. Neurodevelopmental toxins, such as ethanol and heavy metals, interrupt growth factor signaling, raising the possibility that they might exert adverse effects on methylation. We found that insulin-like growth factor-1 (IGF-1)- and dopamine-stimulated methionine synthase (MS) activity and folate-dependent methylation of phospholipids in SH-SY5Y human neuroblastoma cells, via a P13-kinase- and MAP-kinase-dependent mechanism. The stimulation of this pathway increased DNA methylation, while its inhibition increased methylation-sensitive gene expression. Ethanol potently interfered with IGF-1 activation of MS and blocked its effect on DNA methylation, whereas it did not inhibit the effects of dopamine. Metal ions potently affected IGF-1 and dopamine-stimulated MS activity, as well as folate-dependent phospholipid methylation: Cu2+ promoted enzyme activity and methylation, while Cu+, Pb2+, Hg2+ and Al3+ were inhibitory. The ethylmercury-containing preservative thimerosal inhibited both IGF-1- and dopamine-stimulated methylation with an IC50 of 1 nM and eliminated MS activity. Our findings outline a novel growth factor signaling pathway that regulates MS activity and thereby modulates methylation reactions, including DNA methylation. The potent inhibition of this pathway by ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target of neurodevelopmental toxins. C1 Northeastern Univ, Dept Pharmaceut Sci, Boston, MA 02115 USA. Univ Nebraska, Dept Biochem, Lincoln, NE 68588 USA. Tufts Univ, USDA, Human Nutr Res Ctr Aging, Vitamin Metab Lab, Boston, MA 02111 USA. Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA. RP Deth, RC (reprint author), Northeastern Univ, Dept Pharmaceut Sci, 312 Mugar Hall,360 Huntington Ave, Boston, MA 02115 USA. 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Psychiatr. PD APR PY 2004 VL 9 IS 4 BP 358 EP 370 DI 10.1038/sj.mp.4001476 PG 13 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 806QQ UT WOS:000220448800002 PM 14745455 ER PT J AU Frankland, PW Wang, Y Rosner, B Shimizu, T Balleine, BW Dykens, EM Ornitz, EM Silva, AJ AF Frankland, PW Wang, Y Rosner, B Shimizu, T Balleine, BW Dykens, EM Ornitz, EM Silva, AJ TI Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice SO MOLECULAR PSYCHIATRY LA English DT Article DE mouse model; FMRP; prepulse inhibition; startle ID ACOUSTIC STARTLE RESPONSE; FMR1 KNOCKOUT MICE; PREPULSE INHIBITION; MENTAL-RETARDATION; MOUSE MODEL; HALOPERIDOL; STIMULI; DECADE; MEMORY; REFLEX AB Fragile X syndrome (FXS) is the most common single gene (FMR1) disorder affecting cognitive and behavioral function in humans. 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CR FITZGERALD M, 2003, AUTISM CREATIVITY TH NR 1 TC 10 Z9 10 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD APR 1 PY 2004 VL 428 IS 6982 BP 470 EP 471 DI 10.1038/428470a PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 807ZT UT WOS:000220540100019 ER PT J AU Snyder, A AF Snyder, A TI Autism: Mind and brain SO NATURE LA English DT Book Review C1 Australian Natl Univ, Ctr Mind, Canberra, ACT 0200, Australia. Univ Sydney, Sydney, NSW 2006, Australia. RP Snyder, A (reprint author), Australian Natl Univ, Ctr Mind, Canberra, ACT 0200, Australia. CR Frith U., 2003, AUTISM MIND BRAIN NR 1 TC 10 Z9 10 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD APR 1 PY 2004 VL 428 IS 6982 BP 470 EP 471 DI 10.1038/428470a PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 807ZT UT WOS:000220540100020 ER PT J AU Spinney, L AF Spinney, L TI UK autism fracas fuels calls for peer review reform SO NATURE MEDICINE LA English DT News Item CR Giles J, 2004, NATURE, V428, P5, DOI 10.1038/428005a Ready T, 2003, NAT MED, V9, P1340, DOI 10.1038/nm1103-1340 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 3 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 2004 VL 10 IS 4 BP 321 EP 321 DI 10.1038/nm0404-321b PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 808RU UT WOS:000220587000007 PM 15057212 ER PT J AU Wagner, GC Avena, N Kita, T Nakashima, T Fisher, H Halladay, AK AF Wagner, GC Avena, N Kita, T Nakashima, T Fisher, H Halladay, AK TI Risperidone reduction of amphetamine-induced self-injurious behavior in mice SO NEUROPHARMACOLOGY LA English DT Article DE self-injurious behavior; risperidone; mice; dopamine; serotonin; autism ID LESCH-NYHAN-SYNDROME; GENETIC MOUSE MODEL; RECEPTOR ANTAGONIST; DOPAMINE-RECEPTORS; BRAIN DOPAMINE; RAT MODEL; IN-VIVO; D-1; SCH-23390; 6-HYDROXYDOPAMINE AB The behavioral and neurochemical effects of high doses of amphetamine administered to BALB/c mice were examined in the presence and absence of co-administered haloperidol (a D-2 antagonist), SCH 23390 (a D-1 antagonist) and risperidone (a mixed 5-HT2/D-2 antagonist). It was observed that mice displayed a dose-dependent increase in stereotypic behavior, oral dyskinesia, and self-injurious behavior (SIB) in response to amphetamine treatment. Furthermore, agents that blocked the SIB reversed the amphetamine-induced release of serotonin. This effect was unrelated to hyperthermia or non-specific sedation (as assessed by measurement of motor activity). These data are interpreted in the context of the underlying basis of murine SIB involving both dopaminergic and serotonergic activation and demonstrate the efficacy of risperidone in treating these behaviors. (C) 2004 Elsevier Ltd. All rights reserved. C1 Rutgers State Univ, Dept Psychol, New Brunswick, NJ 08903 USA. Rutgers State Univ, Ctr Childhood Neurotoxicol & Exposure Assessment, New Brunswick, NJ 08903 USA. Nara Med Univ, Dept Pharmacol, Nara 6348521, Japan. Rutgers State Univ, Dept Nutr Sci, New Brunswick, NJ 08903 USA. Rutgers State Univ, Dept Pharmacol & Toxicol, New Brunswick, NJ 08903 USA. RP Wagner, GC (reprint author), Rutgers State Univ, Dept Psychol, Busch Campus, New Brunswick, NJ 08903 USA. 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The majority of cases of sporadic Rett syndrome are caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2). MeCP2 binds methylated DNA and likely regulates gene expression and chromatin structure. Genotype/phenotype analysis revealed that the phenotypic spectrum of MECP2 mutations in humans is broader than initially suspected: Mutations have been discovered in Rett syndrome variants, mentally retarded males, and autistic children. A variety of in vivo and in vitro models has been developed that allow analysis of MeCP2 function and pathogenic studies of Rett syndrome. Because the neuropathology of Rett syndrome shares certain features with other neurodevelopmental disorders, a common pathogenic process may underlie these disorders. Thus, Rett syndrome is a prototype for the genetic, molecular, and neurobiological analysis of neurodevelopmental disorders. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. 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SO NORDISK PSYKOLOGI LA Danish DT Article ID HIGH-FUNCTIONING ADULTS; ASPERGER-SYNDROME; PRESCHOOL-CHILDREN; CENTRAL COHERENCE; AUTISM; MIND; BRAIN; COMMUNICATION; PATTERNS; DEFICITS AB This article is a literature review relevant for clinical practice with autism spectrum disorders in childhood and adolescence. The primary purpose is to describe current psychological theories on cognitive processes that mediate autistic behavior. The secondary purpose is to give a summary of other clinically relevant aspects of autism spectrum disorders; e.g. regarding prevalence and aetiology. The symptoms of autism spectrum disorders are manifold and divided into three categories: Social deficits, communicative dysfunctions, and restricted, repetitive interests and behaviors. Different psychological theories have been developed in order to understand the cognitive and emotional processes in these autistic behaviors. 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NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2004 VL 55 IS 4 SU S MA 438 BP 77A EP 77A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 808TJ UT WOS:000220591100455 ER PT J AU Solomon, R Necheles, JW Ferch, C David, B AF Solomon, R Necheles, JW Ferch, C David, B TI Evaluation of a training program for young children with autism: The Michigan PLAY project home consultation model SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Societies CY MAY 04, 2004 CL San Francisco, CA SP Pediatr Acad Soc C1 Univ Michigan, Ann Arbor, MI 48109 USA. Univ Calif Los Angeles, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. 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PD APR PY 2004 VL 55 IS 4 SU S MA 436 BP 77A EP 77A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 808TJ UT WOS:000220591100453 ER PT J AU Kim, SH Spence, SJ Geschwind, DH Alarcon, M AF Kim, SH Spence, SJ Geschwind, DH Alarcon, M TI Increased evidence for broad autism linkage on chromosome 2q using language delay endophenotype SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Societies CY MAY 04, 2004 CL San Francisco, CA SP Pediatr Acad Soc C1 George Washington Univ, Sch Med, Washington, DC USA. Univ Calif Los Angeles, Dept Neurol, Program Neurogenet, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2004 VL 55 IS 4 SU S MA 3291 BP 579A EP 580A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 808TJ UT WOS:000220591103368 ER PT J AU Roberts, SW Brian, JA McDermott, C Bryson, SE Szatmari, P Zwaigenbaum, L AF Roberts, SW Brian, JA McDermott, C Bryson, SE Szatmari, P Zwaigenbaum, L TI Understanding the emergence of autism in infancy SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Societies CY MAY 04, 2004 CL San Francisco, CA SP Pediatr Acad Soc C1 Hosp Sick Children, Pediat Child Dev Ctr, Toronto, ON M5G 1X8, Canada. Dalhouise IWK Hlth Ctr, Halifax, NS, Canada. McMaster Univ, Hamilton Hlth Sci, Hamilton, ON, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2004 VL 55 IS 4 SU S MA 3289 BP 579A EP 579A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 808TJ UT WOS:000220591103366 ER PT J AU Zahorodny, W Holmes, D van Driesen, D Brimacombe, M Rodriguez, V Vidal, J Goldfarb, M AF Zahorodny, W Holmes, D van Driesen, D Brimacombe, M Rodriguez, V Vidal, J Goldfarb, M TI Validity of the PDQ-1 and ABC as autism screeners SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Annual Meeting of the Pediatric-Academic-Societies CY MAY 04, 2004 CL San Francisco, CA SP Pediatr Acad Soc C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA. Eden Inst, Princeton, NJ USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2004 VL 55 IS 4 SU S MA 3290 BP 579A EP 579A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 808TJ UT WOS:000220591103367 ER PT J AU Msall, ME Phelps, DL Hardy, RJ Dobson, V Quinn, GE Summers, CG Tremont, MR AF Msall, ME Phelps, DL Hardy, RJ Dobson, V Quinn, GE Summers, CG Tremont, MR CA Cryotherapy Retinopathy Prematurit TI Educational and social competencies at 8 years in children with threshold retinopathy of prematurity in the CRYO-ROP multicenter study SO PEDIATRICS LA English DT Article ID LOW-BIRTH-WEIGHT; SCHOOL-AGE OUTCOMES; FUNCTIONAL INDEPENDENCE MEASURE; NEONATAL RESEARCH NETWORK; DEVELOPMENTAL-DISABILITIES; NATIONAL INSTITUTE; PRETERM INFANTS; CRYOTHERAPY; TRIAL; LESS AB Objective. To describe the educational status and special education services at 8 years among children who had threshold retinopathy of prematurity (ROP). Methods. A prospective study was conducted of a cohort of children who had birth weight of < 1251 g and threshold ROP in the Cryotherapy for Retinopathy of Prematurity multicenter study. At age 5.5 years, visual status, functional skills, and social information were obtained. At 8 years, special education classes, developmental disabilities, rehabilitation therapies, and academic and social competencies were determined by questionnaire. Visual status was considered favorable/ unfavorable on the basis of the better eye. Results. Of 255 survivors, 216 (85%) were evaluated at both 5.5 and 8 years. Major impairments were significantly more prevalent in children with unfavorable versus favorable visual status: cerebral palsy (39% vs 16%), developmental disability (57% vs 22%), autism (9% vs 1%), and epilepsy (23% vs 3%). Special education services (63% vs 27%), below-grade-level academic performance (84% vs 48%), and school-based rehabilitation services were significantly less common in children with favorable visual status. Favorable visual status, favorable functional ratings at 5.5 years, markers of higher socioeconomic status, and nonblack race were associated with significantly lower rates of both special education placement and below-grade-level academic performance at age 8. On multivariate logistic regression, only favorable visual status and functional status remained significant predictors for decreasing special education placement. Conclusion. Threshold ROP is associated with high rates of developmental, educational, and social challenges in middle childhood; preserved vision was associated with a clear advantage, with more than half of the children with favorable visual status performing at grade level. C1 Univ Chicago, Pritzker Sch Med, Comer Childrens Hosp, Chicago, IL 60637 USA. 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Practical considerations for the clinician SO PEDIATRICS LA English DT Article DE tics; obsessive-compulsive symptoms; streptococcal infection; autoimmunity; PANDAS ID GROUP-A; RHEUMATIC-FEVER; SYDENHAM CHOREA; CHILDREN; ANTIBODIES; IDENTIFICATION; DIAGNOSIS; PROTEINS; AUTISM; BRAIN AB Clinicians have been faced with much publicity and contradictory scientific evidence regarding a recently described condition termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection ( PANDAS). It has been proposed that children with PANDAS experience tics, obsessive-compulsive behavior, and perhaps other neuropsychiatric symptoms as an autoimmune response to streptococcal infection. We review current scientific information and conclude that PANDAS remains a yet-unproven hypothesis. Until more definitive scientific proof is forthcoming, there seems to be insufficient evidence to support 1) routine microbiologic or serologic testing for group A streptococcus in children who present with neuropsychiatric symptoms or 2) the clinical use of antibiotic or immune-modifying therapies in such patients. The optimum diagnostic and therapeutic approach awaits the results of additional research studies. C1 Univ Rochester, Sch Med, Dept Neurol, Cognit & Behav Neurol Unit, Rochester, NY 14642 USA. Univ Minnesota, Sch Med, Dept Pediat, WHO,Collaborating Ctr Reference & Res Streptococ, Minneapolis, MN 55455 USA. RP Kurlan, R (reprint author), Univ Rochester, Sch Med, Dept Neurol, Cognit & Behav Neurol Unit, Rochester, NY 14642 USA. 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First, exposure to environmental agents continues despite successes in reducing exposures to known toxicants such as lead, polychlorinated biphenyls (PCBs) and tobacco smoke. Second, there has been increasing concern about the cause of autism and other neurodevelopmental problems and hypotheses that environmental influences may play a role in the prevalence of these and other such childhood and adult conditions as asthma and obesity. Third, many other conditions are directly or indirectly related to environmental influences and are preventable, such as injuries, untoward consequences of alcohol, suicide, drug addiction, and gun-related deaths. There have been numerous publications since the 1970s of symposia, proceedings, monographs, and articles dealing with the increased susceptibility of the embryo, infant, and child to environmental toxicants,(1-17) reflecting a greater level of concern about embryonic and childhood exposures. Indeed, great deal of attention has been paid to the vulnerability of the embryo and the fetus to environmental chemicals, drugs, and physical agents. In fact, the publication edited by Miller(1) was primarily devoted to exposures to the embryo and the fetus. Because the embryo and the child are growing and their tissues and organs are differentiating, deleterious effects may occur at lower exposures to some chemicals, drugs, and physical agents and produce more severe effects than those seen in adults. In fact, some effects may not occur in adults. Thus, maximal permissible exposures (MPEs) for some environmental chemicals should be lower for the embryo and the child. It is important to note that children and adolescents have better recuperative capacities than adults for many toxic agents, and, similarly, appropriate drug dosages may be lower or higher on a mg/kg or surface area basis in children than in adults to attain effective therapeutic blood levels or to avoid toxicity. In addition, effects produced by drugs, chemicals, and physical agents are not always deleterious or always irreversible. This means that for some exposures, the young can recover from some effects more rapidly and completely than adults (table 1). If the exposure does result in irreversible effects by exceeding the threshold exposure, then the impact on a developing organism can be more severe than in the adult. Much of the discussion and publications that deal with the vulnerability of the developing embryo, infant, child, and adolescent to environmental agents have focused on particular environmental toxicants or agents, summarizing the spectrum of pathology that results from exposures to these agents. There is nothing wrong with this approach from the toxicologist's point of view, because it is obvious that the developing child and adolescent can be more severely or differently affected by some environmental toxicants. C1 Thomas Jefferson Univ, Alfred I duPont Hosp Children, Lab Clin & Environm Teratol, Wilmington, DE 19899 USA. Amer Acad Pediat, Ctr Child Hlth Res, Rochester, NY USA. Univ Rochester, Sch Med, Dept Pediat, Rochester, NY 14642 USA. RP Brent, RL (reprint author), Thomas Jefferson Univ, Alfred I duPont Hosp Children, Lab Clin & Environm Teratol, Rm 308,R-A,Box 269, Wilmington, DE 19899 USA. 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Some forms of mercury are especially neurotoxic, including clinical signs at high doses. However, typical human exposures occur at low to moderate doses. Only limited data about neurotoxicity at low doses are available, and scientists differ in their interpretation. Dose-response data on neurodevelopment are particularly limited. Despite or perhaps because of the lack of sufficient or consistent scientific data, public concern about a link between mercury exposure and developmental disabilities has been rising. After reviewing the data, the US Environmental Protection Agency proposed a reference dose (an estimate of a daily dose that is likely to be without a risk of adverse effects over a lifetime) for methyl mercury that is substantially lower than previous guidelines from the World Health Organization, the US Agency for Toxic Substances and Disease Registry, and the US Food and Drug Administration. Some questions have been raised about the Environmental Protection Agency's guidelines, but the issue remains unresolved. Meanwhile, consumer groups have raised questions about the potential link between mercury exposure and autism spectrum disorders as well as other adverse neurodevelopmental outcomes. This hypothesis has prompted some parents to seek regulatory, legal, or medical remedies in the absence of firm evidence. This article reviews what is known about mercury neurotoxicity and neurodevelopmental risk. Our intent is to focus the debate about mercury on 1) additional research that should be sought and 2) defining the principal issues that public policy makers face. C1 Univ Rochester, Sch Med & Dent, Rochester, NY USA. RP Davidson, PW (reprint author), Univ Rochester, Sch Med & Dent, Golisano Childrens Hosp Strong, Strong Ctr Dev Disabil, Box 671,URMC,601 Elmwood Ave, Rochester, NY 14642 USA. 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PD APR PY 2004 VL 53 IS 4 BP 295 EP 296 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 819OT UT WOS:000221325200009 ER PT J AU Kanai, C Koyama, T Kato, S Miyamoto, Y Osada, H Kurita, H AF Kanai, C Koyama, T Kato, S Miyamoto, Y Osada, H Kurita, H TI Comparison of high-functioning atypical autism and childhood autism by Childhood Autism Rating Scale-Tokyo version SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE atypical autism; autistic symptoms; childhood autism; high-functioning; pervasive developmental disorders (PDD) ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; EPIDEMIOLOGY; CARS AB To assess autistic symptom differences between high-functioning atypical autism (atypical symptomatology) (HAA; IQgreater than or equal to70) and childhood autism (HCA), 53 HAA children (mean:6.0+/-0.5 years) were compared with 21 HCA children (mean: 8.2+/-1.1 years) on the Childhood Autism Rating Scale-Tokyo version (CARS-TV). Because IQ on the Japanese version of the Stanford-Binet and CARS-TV total scores differed significantly between HAA and HCA, analysis of covariance was conducted with IQ and CARS-TV total scores controlled for. In two items of CARS-TV (relationship with people and general impressions) the HAA children were significantly less abnormal than the HCA children. Affect tended to be significantly milder in HAA than HCA. Anxiety reaction was significantly more abnormal in HAA than HCA. These findings may be useful to distinguish between HAA and HCA. C1 Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Bunkyo Ku, Tokyo 1130033, Japan. Univ Tokyo, Grad Sch Med, Dept Psychiat Nursing, Tokyo, Japan. Senshu Univ, Fac Law, Tokyo, Japan. RP Kanai, C (reprint author), Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. 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Med. PD APR PY 2004 VL 34 IS 3 BP 385 EP 389 DI 10.1017/S0033291703001326 PG 5 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 816ZD UT WOS:000221146900001 PM 15259823 ER PT J AU Lee, KH Farrow, TFD Spence, SA Woodruff, PWR AF Lee, KH Farrow, TFD Spence, SA Woodruff, PWR TI Social cognition, brain networks and schizophrenia SO PSYCHOLOGICAL MEDICINE LA English DT Review ID VARIANT FRONTOTEMPORAL DEMENTIA; MIND IMPAIRMENTS; NEUROCOGNITIVE DEFICITS; STORY COMPREHENSION; FALSE BELIEF; EMPATHY; AUTISM; PEOPLE; CHILDREN; RECOGNITION AB Background. A better understanding of the neural basis of social cognition including mindreading (or theory of mind) and empathy might help to explain some deficits in social functioning in people with schizophrenia. Our aim was to review neuroimaging and neuropsychological studies on social cognition, as they may shed light on the neural mechanisms of social cognition and its dysfunction in patients with schizophrenia. Method. A selective literature review was undertaken. Results. Neuroimaging and neuropsychological studies suggest convergence upon specific networks for mindreading and empathy (the temporal cortex, amygdala and the prefrontal cortex). The frontal lobe is likely to play a central role in enabling social cognition, but mindreading and empathic abilities may require relatively different weighting of subcomponents within the same frontal-temporal social cognition network. Conclusions. Disturbances in social cognition may represent an abnormal interaction between frontal lobe and its functionally connected cortical and subcortical areas. Future studies should seek to explore the heterogeneity of social dysfunction within schizophrenia. C1 Univ Sheffield, Acad Dept Clin Psychiat, SCAN Lab, Longley Ctr, Sheffield S5 7JT, S Yorkshire, England. RP Lee, KH (reprint author), Univ Sheffield, No Gen Hosp, Acad Dept Clin Psychiat, SCAN Lab,Longley Ctr, Sheffield S5 7JT, S Yorkshire, England. 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Med. PD APR PY 2004 VL 34 IS 3 BP 391 EP 400 DI 10.1017/S0033291703001284 PG 10 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 816ZD UT WOS:000221146900002 PM 15259824 ER PT J AU Chen, W Landau, S Sham, P Fombonne, E AF Chen, W Landau, S Sham, P Fombonne, E TI No evidence for links between autism, MMR and measles virus SO PSYCHOLOGICAL MEDICINE LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; RUBELLA VACCINE; ASEPTIC-MENINGITIS; FOLLOW-UP; MUMPS; CHILDREN; IMMUNIZATION; ASSOCIATION; POPULATION; EXPOSURE AB Background. We examined whether, in the UK, there is an increased risk of autism (AD) following exposures, in early life, to: (1) wild measles; (2) live attenuated measles, alone or in combination as MMR; and (3) the alteration of the mumps strain within MMR. Method. We conducted time trend analyses of 2407 AD subjects born between 1959-93; and for comparison, 4640 Down's syndrome (DS) subjects born between 1966-93. Between 1968-86, we correlated variations in AD and DS births with wild measles incidence. Between 1959-93, we tested for abrupt changes in the long-term AD birth trend for the effects of introducing: (1) monovalent measles vaccines in 1968; (2) MMR immunization in 1988; and (3) the 'overnight switch' from mixed use of Urabe MMR to exclusive use of Jeryl-Lynn MMR in 1992. Incidence rate ratios (IRRs) were used as measures of association. Results. We found no significant association between AD births and exposure (prenatal and postnatal up to 18 months age) to population rates of measles infections, and no 'step-up' increase in AD births associated with the introduction of monovalent measles and MMR vaccines, and changing mumps strain. An unexpected reduction in AD births of 21% (95% CI 6-9-33-3%; P=0.005) among the post-1987 birth cohorts was detected. Conclusion. No increased risk of AD following exposures to wild measles and vaccinations with monovalent measles, and Urabe or Jeryl-Lynn variants of MMR was detected. The precise meaning of the detected AD births reduction is unclear. Our study cannot exclude rare complications of MMR, given its correlational design. C1 McGill Univ, Dept Psychiat, Montreal Childrens Hosp, Div Psychiat, Montreal, PQ H3Z 1P2, Canada. Univ London Kings Coll, Inst Psychiat, London WC2R 2LS, England. Univ London, Guys Kings & St Thomas Sch Med, Dept Child & Adolescent Psychiat, London WC2R 2LS, England. RP Fombonne, E (reprint author), McGill Univ, Dept Psychiat, Montreal Childrens Hosp, Div Psychiat, 4018 Ste Catherine W, Montreal, PQ H3Z 1P2, Canada. 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Med. PD APR PY 2004 VL 34 IS 3 BP 543 EP 553 DI 10.1017/S0033291703001259 PG 11 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 816ZD UT WOS:000221146900017 PM 15259839 ER PT J AU Daley, TC AF Daley, TC TI From symptom recognition to diagnosis: children with autism in urban India SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE autism; India; diagnosis; symptom recognition; help-seeking; child health ID PSYCHIATRISTS; DISORDERS; AGE AB The period of time between initial recognition of a symptom and initial diagnosis warrants examination because it can serve as a window into broader cultural factors and allow for more immediate treatment. Research on this process among parents of autistic children to date has been useful, but has been limited to families in Western countries, whereas autism occurs all over the world. 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Are the media stirring up a fresh autism scare? SO BRITISH MEDICAL JOURNAL LA English DT Editorial Material CR 2002, BRIT MED J, V325, P603 NR 1 TC 1 Z9 1 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD MAR 27 PY 2004 VL 328 IS 7442 BP 773 EP 773 DI 10.1136/bmj.328.7442.773 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 809WH UT WOS:000220666300058 ER PT J AU Wallace, GL Treffert, DA AF Wallace, GL Treffert, DA TI Head size and autism SO LANCET LA English DT Editorial Material ID CIRCUMFERENCE; DISORDER; CHILDREN; GROWTH; LIFE; AGE C1 NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. St Agnes Hosp, Fond Du Lac, WI USA. Univ Wisconsin, Sch Med, Dept Psychiat, Madison, WI USA. RP Wallace, GL (reprint author), NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. 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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 EI 1530-6860 J9 FASEB J JI Faseb J. PD MAR 24 PY 2004 VL 18 IS 5 SU S BP A933 EP A933 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 806ZB UT WOS:000220470700832 ER PT J AU Jyonouchi, H Geng, L Ruby, A Zimmerman-Bier, B AF Jyonouchi, H Geng, L Ruby, A Zimmerman-Bier, B TI The effects of the elimination diet on cytokine production profile against common dietary proteins (DPs) in children with autism spectrum disorders (ASD) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2004 Annual Meeting CY APR 17-21, 2004 CL Washington, DC C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Div Pulm A1 & IDs, Newark, NJ 07101 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 EI 1530-6860 J9 FASEB J JI Faseb J. PD MAR 24 PY 2004 VL 18 IS 5 SU S BP A933 EP A934 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 806ZB UT WOS:000220470700833 ER PT J AU Grunwald, WC Morris, M Klykylo, WM Cool, DR AF Grunwald, WC Morris, M Klykylo, WM Cool, DR TI Oxytocin gene and protein analysis in children with autism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2004 Meeting CY APR 17-21, 2004 CL Washington, DC C1 Wright State Univ, Dayton, OH 45435 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 23 PY 2004 VL 18 IS 4 SU S BP A240 EP A241 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 806ZA UT WOS:000220470601156 ER PT J AU Hires, BB Forsythe, HW AF Hires, BB Forsythe, HW TI Nutrition implications to medications and supplements administered to children with autism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2004 Meeting CY APR 17-21, 2004 CL Washington, DC C1 Univ Kentucky, Grad Ctr Nutrit Sci, Lexington, KY 40506 USA. Univ Kentucky, Dept Nutr & Food Sci, Lexington, KY 40506 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 23 PY 2004 VL 18 IS 4 SU S BP A164 EP A164 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 806ZA UT WOS:000220470600793 ER PT J AU Jernigan, S Melnyk, SB Janak, L Cutler, P James, SJ AF Jernigan, S Melnyk, SB Janak, L Cutler, P James, SJ TI Impaired transsulfuration, oxidative stress, and genetic polymorphisms in children with autism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2004 Meeting CY APR 17-21, 2004 CL Washington, DC C1 Univ Arkansas Med Sci, Little Rock, AR 72202 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 23 PY 2004 VL 18 IS 4 SU S BP A105 EP A105 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 806ZA UT WOS:000220470600513 ER PT J AU Delorme, R Krebs, MO Chabane, N Roy, I Millet, B Mouren-Simeoni, MC Maier, W Bourgeron, T Leboyer, M AF Delorme, R Krebs, MO Chabane, N Roy, I Millet, B Mouren-Simeoni, MC Maier, W Bourgeron, T Leboyer, M TI Frequency and transmission of glutamate receptors GRIK2 and GRIK3 polymorphisms in patients with obsessive compulsive disorder SO NEUROREPORT LA English DT Article DE association studies; early onset; glutamate; obsessive-compulsive disorder; transmission disequilibrium test ID GENE; ASSOCIATION; SCHIZOPHRENIA; HIPPOCAMPUS; EPILEPSY; SEIZURES; KAINATE; LINKAGE; FAMILY; GLUR6 AB Several lines of evidence suggest that obsessive compulsive disorder (OCD) could be the consequence of glutamatergic dysfunction. We performed a case-control study in 156 patients and 141 controls and the transmission disequilibrium test in 124 parent-offspring trios to search for association between OCD and two kainate receptors, GRIK2 and GRIK3. Using three single nucleotide polymorphisms (SNP) in GRIK2 and one in GRIK3, we found no evidence for association in case-control or family-based analyses. Only the GRIK2 SNP 1867, recently associated with autism, was less transmitted than expected (p<0.03), supporting a functional role for this variant. These findings suggest the need for further investigation of the role of GRIK2 in OCD. C1 Fac Med, INSERM, U513, F-94010 Creteil, France. Hop Robert Debre, Assistance Publ Hop Paris, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. Hop St Anne, INSERM, E0117, F-75674 Paris, France. Univ Bonn, Dept Psychiat, D-5300 Bonn, Germany. Hop Henri Mondor & Albert Chenevier, Assistance Publ Hop Paris, Psychiat Serv, Creteil, France. Inst Pasteur, Paris, France. RP Delorme, R (reprint author), Fac Med, INSERM, U513, 8 Rue Gen Sarrail, F-94010 Creteil, France. 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Y. Times Book Rev. PD MAR 21 PY 2004 BP 12 EP 12 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 803BR UT WOS:000220207100010 ER PT J AU Samaco, RC Nagarajan, RP Braunschweig, D LaSalle, JM AF Samaco, RC Nagarajan, RP Braunschweig, D LaSalle, JM TI Multiple pathways regulate MeCP2 expression in normal brain development and exhibit defects in autism-spectrum disorders SO HUMAN MOLECULAR GENETICS LA English DT Article ID CPG-BINDING PROTEIN-2; LINKED MENTAL-RETARDATION; RETT-SYNDROME PATIENTS; SYNDROME GENE MECP2; ALTERNATIVE POLYADENYLATION; SEQUENCE-ANALYSIS; METHYLATED DNA; MUTATION TYPE; LOCALIZATION; IDENTIFICATION AB Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in MECP2, encoding methyl-CpG-binding protein 2 (MeCP2). Although MECP2 is ubiquitously transcribed, MeCP2 expression is developmentally regulated and heterogeneous in neuronal subpopulations, defined as MeCP2(lo) and MeCP2(hi). To test the hypothesis that pathways affecting MeCP2 expression changes may be defective in RTT, autism and other neurodevelopmental disorders without MECP2 mutations, a high-throughput quantitation of MeCP2 expression was performed on a tissue microarray containing frontal cortex samples from 28 different patients with neurodevelopmental disorders and age-matched controls. Combined quantitative analyses of MeCP2 protein and alternatively polyadenylated transcript levels were performed by laser scanning cytometry and tested for significant differences from age-matched controls. Normal cerebral samples showed an increase in total MeCP2 expression and the percentage of MeCP2(hi) cells with age that could be explained by increased MECP2 transcription within the MeCP2(hi) population. A significant decrease in the relative usage of the long transcript in the MeCP2(lo) population was observed in postnatal compared to fetal brain, but alternate polyadenylation did not correlate with MeCP2 expression changes at the single cell level. Brain samples from several related neurodevelopmental disorders, including autism, pervasive developmental disorder, Prader-Willi and Angelman syndromes showed significant differences in MeCP2 expression from age-matched controls by apparently different transcriptional and post-transcriptional mechanisms. These results suggest that multiple pathways regulate the complex developmental expression of MeCP2 and are defective in autism-spectrum disorders in addition to RTT. C1 Univ Calif Davis, Sch Med, Rowe Program Human Genet, Davis, CA 95616 USA. RP LaSalle, JM (reprint author), Univ Calif Davis, Sch Med, Rowe Program Human Genet, 1 Shields Ave, Davis, CA 95616 USA. EM jmlasalle@ucdavis.edu RI LaSalle, Janine/A-4643-2008 OI LaSalle, Janine/0000-0002-3480-2031 CR Akbarian S, 2001, NEUROBIOL DIS, V8, P784, DOI 10.1006/nbdi.2001.0420 Amir RE, 1999, NAT GENET, V23, P185 Amir RE, 2000, ANN NEUROL, V47, P670, DOI 10.1002/1531-8249(200005)47:5<670::AID-ANA20>3.0.CO;2-F Armstrong DD, 1997, J NEUROPATH EXP NEUR, V56, P843, DOI 10.1097/00005072-199708000-00001 Balmer D, 2003, J MOL MED-JMM, V81, P61, DOI 10.1007/s00109-002-0396-5 Beyer KS, 2002, HUM GENET, V111, P305, DOI 10.1007/s00439-002-0786-3 Bienvenu T, 2000, HUM MOL GENET, V9, P1377, DOI 10.1093/hmg/9.9.1377 Buyse IM, 2000, AM J HUM GENET, V67, P1428, DOI 10.1086/316913 Carney RM, 2003, PEDIATR NEUROL, V28, P205, DOI 10.1016/S0887-8994(02)00624-0 Cheadle JP, 2000, HUM MOL GENET, V9, P1119, DOI 10.1093/hmg/9.7.1119 Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Couvert P, 2001, HUM MOL GENET, V10, P941, DOI 10.1093/hmg/10.9.941 Coy JF, 1999, HUM MOL GENET, V8, P1253, DOI 10.1093/hmg/8.7.1253 DEsposito M, 1996, MAMM GENOME, V7, P533, DOI 10.1007/s003359900157 Girard M, 2001, EUR J HUM GENET, V9, P231, DOI 10.1038/sj.ejhg.5200618 Huppke P, 2000, HUM MOL GENET, V9, P1369, DOI 10.1093/hmg/9.9.1369 Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 Jung BP, 2003, J NEUROBIOL, V55, P86, DOI 10.1002/neu.10201 Lainhart JE, 2003, JAMA-J AM MED ASSOC, V290, P393, DOI 10.1001/jama.290.3.393 Lam C W, 2000, J Med Genet, V37, pE41, DOI 10.1136/jmg.37.12.e41 Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 LaSalle JM, 2001, HUM MOL GENET, V10, P1729, DOI 10.1093/hmg/10.17.1729 LEWIS JD, 1992, CELL, V69, P905, DOI 10.1016/0092-8674(92)90610-O Lobo-Menendez F, 2003, AM J MED GENET B, V117B, P97, DOI 10.1002/ajmg.b.10016 MEEHAN RR, 1992, NUCLEIC ACIDS RES, V20, P5085, DOI 10.1093/nar/20.19.5085 Orrico A, 2000, FEBS LETT, V481, P285, DOI 10.1016/S0014-5793(00)01994-3 Clayton-Smith J, 2000, LANCET, V356, P830, DOI 10.1016/S0140-6736(00)02661-1 Reichwald K, 2000, MAMM GENOME, V11, P182, DOI 10.1007/s003350010035 Shahbazian MD, 2002, AM J HUM GENET, V71, P1259, DOI 10.1086/345360 Shahbazian MD, 2002, HUM MOL GENET, V11, P115, DOI 10.1093/hmg/11.2.115 Sirianni N, 1998, AM J HUM GENET, V63, P1552, DOI 10.1086/302105 Trappe R, 2001, AM J HUM GENET, V68, P1093, DOI 10.1086/320109 Van den Veyver IB, 2000, CURR OPIN GENET DEV, V10, P275, DOI 10.1016/S0959-437X(00)00083-6 Villard L, 2000, NEUROLOGY, V55, P1188 Vourc'h P, 2001, EUR J HUM GENET, V9, P556, DOI 10.1038/sj.ejhg.5200660 Watson P, 2001, J MED GENET, V38, P224, DOI 10.1136/jmg.38.4.224 Xiang FQ, 2000, J MED GENET, V37, P250, DOI 10.1136/jmg.37.4.250 NR 37 TC 91 Z9 94 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. 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PD MAR 15 PY 2004 VL 13 IS 6 BP 629 EP 639 DI 10.1093/hmg/ddh063 PG 11 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 801CK UT WOS:000220073800006 PM 14734626 ER PT J AU Kawakubo, Y Maekawa, H Itoh, K Hashimoto, O Iwanami, A AF Kawakubo, Y Maekawa, H Itoh, K Hashimoto, O Iwanami, A TI Spatial attention in individuals with pervasive developmental disorders using the gap overlap task SO PSYCHIATRY RESEARCH LA English DT Article DE autism; attention process; saccadic eye movement ID MONKEY SUPERIOR COLLICULUS; EVENT-RELATED POTENTIALS; SACCADIC REACTION-TIMES; EXPRESS SACCADES; VISUAL-ATTENTION; EYE-MOVEMENTS; AUTISTIC-CHILDREN; FIXATION CELLS; DEFICITS; CEREBELLAR AB The present study examined spatial attention in individuals with pervasive developmental disorders (PDD) using the gap overlap task and analyzed the express saccade, which is defined by its extremely short reaction time, as a measure of the state of attention. Participants were required to move their eyes to the target stimulus, appearing on the left or right side of a fixation point. In this task, participants had to disengage their attention from the central fixation point and shift it to the peripheral target stimulus. In the gap condition, the fixation point disappeared 200 ms before the target stimulus was presented, and in the overlap condition, the fixation point remained while the target stimulus was presented. Saccade latencies were not different between the groups. However, the express saccade was more frequent in the PDD group than in the normal group in the overlap condition. We conclude that individuals with PDD have deficiencies in attentional engagement. Moreover, our study suggests that analysis of the express saccade will be useful in further examinations of attentional processes in PDD. (C) 2003 Elsevier Ireland Ltd. All rights reserved. C1 Univ Tsukuba, Doctoral Degree Program Disabil Sci, Tsukuba, Ibaraki 3058572, Japan. Univ Tsukuba, Inst Disabil Sci, Tsukuba, Ibaraki 3058572, Japan. Univ Tokyo, Grad Sch Med, Dept Cognit & Speech Sci, Tokyo 1138655, Japan. Univ Tokyo, Fac Med, Dept Neuropsychiat, Tokyo 1138655, Japan. RP Kawakubo, Y (reprint author), Univ Tsukuba, Doctoral Degree Program Disabil Sci, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058572, Japan. EM kawakubo@human.tsukuba.ac.jp CR Allport D. 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PD MAR 13 PY 2004 VL 181 IS 2438 BP 4 EP 4 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 802NY UT WOS:000220171400003 ER PT J AU Humphrey, A Higgins, JNP Yates, JRW Bolton, PF AF Humphrey, A Higgins, JNP Yates, JRW Bolton, PF TI Monozygotic twins with tuberous sclerosis discordant for the severity of developmental deficits SO NEUROLOGY LA English DT Article; Proceedings Paper CT 11th Annual Meeting of the Child Neurology Section CY SEP 28, 2001 CL Venice, ITALY ID AUTISM; DISORDERS; COMPLEX AB A pair of monozygotic male twins with tuberous sclerosis (TS) were followed between 18 months and 3 years of age. Twin A with 25 large cortical tubers and hence extensive brain involvement was moderately mentally retarded and met criteria for autism. The other twin had more (n = 31) but smaller tubers. He was not mentally retarded and did not meet criteria for autism. This study provides evidence that nongenetic factors such as extent of brain abnormality and not just number of cortical tubers are important in determining phenotypic variability in TS. The findings also raise questions about the mechanisms giving rise to autism in TS. C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ Cambridge, Dept Med Genet, Cambridge, England. Addenbrookes Hosp, Dept Neuroradiol, Cambridge, England. Inst Psychiat, Dept Child Psychiat, London, England. Inst Psychiat, MRC, Ctr Social Genet & Dev Psychiat, London, England. RP Humphrey, A (reprint author), Univ Cambridge, Dev Psychiat Sect, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. EM ah290@cam.ac.uk RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR Bolton PF, 2002, BRAIN, V125, P1247, DOI 10.1093/brain/awf124 BROTHERS L, 1993, BEHAV BRAIN RES, V57, P53, DOI 10.1016/0166-4328(93)90061-T GOMEZ MG, 1999, DEV PERSPECTIVES PSY GOMEZ MR, 1982, NEUROLOGY, V32, P604 Goodman M, 1997, J CHILD NEUROL, V12, P85 Klein B, 2000, NEUROLOGY, V55, P230 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Ridler K, 2001, PSYCHOL MED, V31, P1437 Sepp T, 1996, J MED GENET, V33, P962, DOI 10.1136/jmg.33.11.962 Weber AM, 2000, J AUTISM DEV DISORD, V30, P511, DOI 10.1023/A:1005679108529 NR 10 TC 27 Z9 27 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 9 PY 2004 VL 62 IS 5 BP 795 EP 798 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 801FY UT WOS:000220083000024 PM 15007135 ER PT J AU Pellock, JM AF Pellock, JM TI Understanding co-morbidities affecting children with epilepsy SO NEUROLOGY LA English DT Article; Proceedings Paper CT Symposium on Neurology of Special Population held at the 30th Annual Meeting of the Southern-Clinical-Neurological-Society CY JAN 20, 2003 CL Ixtapa, MEXICO SP SO Clin Neurol Soc ID ACID HEPATIC FATALITIES; RANDOMIZED CONTROLLED-TRIAL; ANTIEPILEPTIC DRUGS; PEDIATRIC EPILEPSY; BIPOLAR DISORDER; SODIUM VALPROATE; US EXPERIENCE; DOUBLE-BLIND; MIGRAINE; CARBAMAZEPINE AB Co-morbid conditions frequently occur in childhood epilepsy and may significantly affect epilepsy and its treatment. Similarly, epilepsy and antiepileptic drugs (AEDs) may affect these associated conditions. Co-morbidities that have a significant association with childhood epilepsy include attention-deficit/hyperactivity disorder, autism, developmental disabilities, accidental injury, migraine, and depression/anxiety. Understanding the interrelationships among co-morbidities, epilepsy, and their treatments is essential to optimal management of pediatric patients. Treatment should be individualized with consideration for specific co-morbidities and concomitant medications. Key treatment goals are to achieve seizure control and optimal physical and cognitive function using the simplest possible AED regimen. The clinician should consider whether an antiepileptic treatment can be chosen that also ameliorates the co-morbid condition. Newer AEDs, such as lamotrigine, topiramate, gabapentin, oxcarbazepine, and tiagabine, may benefit children with epilepsy and some co-morbid disorders. C1 Virginia Commonwealth Univ, Med Coll Virginia, Richmond, VA 23298 USA. RP Pellock, JM (reprint author), Virginia Commonwealth Univ, Med Coll Virginia, 1001 E Marshall St,Childrens Pavil,1st Floor, Richmond, VA 23298 USA. 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RP Horton, R (reprint author), The Lancet, London NW1 7BY, England. CR Calman KC, 2002, LANCET, V360, P166, DOI 10.1016/S0140-6736(02)09421-7 Davidoff F, 2001, LANCET, V358, P854, DOI 10.1016/S0140-6736(01)06035-4 DeFelice ML, 2003, AM J GASTROENTEROL, V98, P1777, DOI 10.1016/S0002-9270(03)00444-1 Farthing M, 2000, LANCET, V356, P2030, DOI 10.1016/S0140-6736(00)03398-5 GOODE E, 2004, NY TIMES 0126, pA1 Horton R, 2004, LANCET, V363, P820, DOI 10.1016/S0140-6736(04)15699-7 James A, 2004, LANCET, V363, P2, DOI 10.1016/S0140-6736(03)15229-4 James A, 2003, LANCET, V361, P8, DOI 10.1016/S0140-6736(03)12184-8 Jefferson T, 2004, LANCET INFECT DIS, V4, P135, DOI 10.1016/S1473-3099(04)00934-X Jefferson T, 2003, VACCINE, V21, P3954, DOI 10.1016/S0264-410X(03)00271-8 Kanner L, 1943, NERV CHILD, V2, P217 MCBRIDE WG, 1961, LANCET, V2, P1358 Medical Research Council, 2001, MRC REV AUT RES EP C Murch SH, 2004, LANCET, V363, P750, DOI 10.1016/S0140-6736(04)15715-2 Roberts KA, 2002, LANCET, V360, P1596, DOI 10.1016/S0140-6736(02)11560-1 Shapin S., 1995, SOCIAL HIST TRUTH TORRENTE F, IN PRESS AM J GASTRO VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P717, DOI 10.1111/j.1469-7610.1989.tb00784.x Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 2004, TIMES HIGHER ED 0227, P14 2004, INDEPENDENT 0224, P16 2003, DRUG THER B, V41, P1 NR 23 TC 30 Z9 30 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD MAR 6 PY 2004 VL 363 IS 9411 BP 747 EP 749 DI 10.1016/S0140-6736(04)15714-0 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 801JK UT WOS:000220092000003 PM 15016482 ER PT J AU Fombonne, E Heavey, L Smeeth, L Rodrigues, LC Cook, C Smith, PG Meng, LY Hall, AJ AF Fombonne, E Heavey, L Smeeth, L Rodrigues, LC Cook, C Smith, PG Meng, LY Hall, AJ TI Validation of the diagnosis of autism in general practitioner records SO BMC PUBLIC HEALTH LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PRACTICE RESEARCH DATABASE; RUBELLA VACCINATION; MMR VACCINATION; MEASLES; MUMPS; CHILDREN; POPULATION; PREVALENCE; CALIFORNIA AB Background: We report on the validity of the computerized diagnoses of autism in a large case-control study investigating the possible association between autism and the measles, mumps and rubella vaccine in the UK using the General Practitioner Research Database (GPRD). We examined anonymized copies of all relevant available clinical reports, including general practitioners' ( GP) notes, consultant, speech therapy and educational psychologists reports, on 318 subjects born between 1973 and 1997 with a diagnosis of autism or a related disorder recorded in their electronic general practice record. Methods: Data were abstracted to a case validation form allowing for the identification of developmental symptoms relevant to the diagnosis of pervasive developmental disorders (PDDs). Information on other background clinical and familial features was also abstracted. A subset of 50 notes was coded independently by 2 raters to derive reliability estimates for key clinical characteristics. Results: For 294 subjects (92.5%) the diagnosis of PDD was confirmed after review of the records. Of these, 180 subjects (61.2%) fulfilled criteria for autistic disorder. The mean age at first recording of a PDD diagnosis in the GPRD database was 6.3 years (SD = 4.6). Consistent with previous estimates, the proportion of subjects experiencing regression in the course of their development was 19%. Inter-rater reliability for the presence of a PDD diagnosis was good (kappa = .73), and agreement on clinical features such as regression, age of parental recognition of first symptoms, language delay and presence of epilepsy was also good (kappas ranging from .56 to 1.0). Conclusions: This study provides evidence that the positive predictive value of a diagnosis of autism recorded in the GPRD is high. C1 McGill Univ, Montreal Childrens Hosp, Montreal, PQ H3Z 1P2, Canada. Univ London London Sch Hyg & Trop Med, London WC1E 7HT, England. Inst Psychiat, London SE5 8AF, England. RP Fombonne, E (reprint author), McGill Univ, Montreal Childrens Hosp, 4018 St Catherine St W, Montreal, PQ H3Z 1P2, Canada. EM eric.fombonne@mcgill.ca; l.reidy@shu.ac.uk; liam.smeeth@lshtm.ac.uk; laura.rodrigues@lshtm.ac.uk; claire.cook@lshtm.ac.uk; peter.smith@lshtm.ac.uk; linyan.meng@muhc.mcgill.ca; andy.hall@lshtm.ac.uk CR BARTKO JJ, 1976, PSYCHOL BULL, V83, P762, DOI 10.1037//0033-2909.83.5.762 Bernard S, 2002, MOL PSYCHIATR, V7, pS42, DOI 10.1038/sj.mp.4001177 Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Chen W, 2004, PSYCHOL MED, V34, P543, DOI 10.1017/S0033291703001259 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 *DEP HLTH, 1990, NEW CLIN CLASS SYST DeWilde S, 2001, BRIT J GEN PRACT, V51, P226 Fombonne E., 2003, JAMA-J AM MED ASSOC, V289, P1 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Jick H, 1996, PHARMACOTHERAPY, V16, P321 KAYE JA, 2001, BMJ, V322 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Lingam R, 2003, ARCH DIS CHILD, V88, P666, DOI 10.1136/adc.88.8.666 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 LROD C, 2000, J AUTISM DEV DISORD, V30, P205 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Perry J, 1978, OXMIS PROBLEM CODES Ruigomez A, 2000, EPIDEMIOLOGY, V11, P620, DOI 10.1097/00001648-200011000-00002 Smeeth L, 2001, BMC PUBLIC HEALTH, V1, DOI 10.1186/1471-2458-1-2 SMEETH L, IN PRESS BMC MED Spitzer WO, 2003, NEW ENGL J MED, V348, P951 Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 Walley T, 1997, LANCET, V350, P1097, DOI 10.1016/S0140-6736(97)04248-7 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 34 TC 64 Z9 65 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2458 J9 BMC PUBLIC HEALTH JI BMC Public Health PD MAR 3 PY 2004 VL 4 AR 5 DI 10.1186/1471-2458-4-5 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 814NF UT WOS:000220980700001 PM 15113435 ER PT J AU Laumonnier, F Bonnet-Brilhault, F Gomot, M Blanc, R David, A Moizard, MP Raynaud, M Ronce, N Lemonnier, E Calvas, P Laudier, B Chelly, J Fryns, JP Ropers, HH Hamel, BCJ Andres, C Barthelemy, C Moraine, C Briault, S AF Laumonnier, F Bonnet-Brilhault, F Gomot, M Blanc, R David, A Moizard, MP Raynaud, M Ronce, N Lemonnier, E Calvas, P Laudier, B Chelly, J Fryns, JP Ropers, HH Hamel, BCJ Andres, C Barthelemy, C Moraine, C Briault, S TI X-linked mental retardation and autism are associated with a mutation in the NLGN4 gene, a member of the neuroligin family SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; SYNAPSES; UPDATE; SCREEN AB A large French family including members affected by nonspecific X-linked mental retardation, with or without autism or pervasive developmental disorder in affected male patients, has been found to have a 2-base-pair deletion in the Neuroligin 4 gene (NLGN4) located at Xp22.33. This mutation leads to a premature stop codon in the middle of the sequence of the normal protein and is thought to suppress the transmembrane domain and sequences important for the dimerization of neuroligins that are required for proper cell-cell interaction through binding to beta-neurexins. As the neuroligins are mostly enriched at excitatory synapses, these results suggest that a defect in synaptogenesis may lead to deficits in cognitive development and communication processes. The fact that the deletion was present in both autistic and nonautistic mentally retarded males suggests that the NLGN4 gene is not only involved in autism, as previously described, but also in mental retardation, indicating that some types of autistic disorder and mental retardation may have common genetic origins. C1 CHU Bretonneau, INSERM, U619, Serv Genet, F-37044 Tours, France. CHU Bretonneau, INSERM, U619, Serv Explorat Fonct & Neurophysiol Pedopsychiat, F-37044 Tours, France. CHU Hotel Dieu, Inst Biol, Serv Genet Med, Nantes, France. Ctr Inter Reg Etud & Ressource Autisme, Brest, France. CHU Hop Purpan, Serv Genet, Toulouse, France. CHU Cochin, ICGM, INSERM, U129, Paris, France. Ctr Human Genet, Louvain, Belgium. Max Planck Inst Mol Genet, Berlin, Germany. Univ Nijmegen Hosp, Dept Human Genet, NL-6500 HB Nijmegen, Netherlands. RP Briault, S (reprint author), CHU Bretonneau, INSERM, U619, Serv Genet, 2 Bd Tonnelle, F-37044 Tours, France. 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J. Hum. Genet. PD MAR PY 2004 VL 74 IS 3 BP 552 EP 557 DI 10.1086/382137 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 801TP UT WOS:000220118500021 PM 14963808 ER PT J AU Kates, WR Burnette, CP Eliez, S Strunge, LA Kaplan, D Landa, R Reiss, AL Pearlson, GD AF Kates, WR Burnette, CP Eliez, S Strunge, LA Kaplan, D Landa, R Reiss, AL Pearlson, GD TI Neuroanatomic variation in monozygotic twin pairs discordant for the narrow phenotype for autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PEDIATRIC BRAIN VOLUMES; SYNAPTIC PLASTICITY; CEREBELLAR CORTEX; INFANTILE-AUTISM; NEONATAL FACTORS; CEREBRAL LOBES; BROAD AUTISM; CHILDREN; INDIVIDUALS AB Objective: The broader autism phenotype includes relatives of individuals with autism who display social and language deficits that are qualitatively similar to those of autism but less severe. In previous studies of monozygotic twins discordant for autism, more than 75% of the twins without autism displayed the broader phenotype. Differences in neuroanatomy between discordant monozygotic twins might be associated with the narrow and broader behavioral phenotypes. The authors examined the relationship of twin pair differences in clinical phenotype to differences in neuroanatomic phenotype. Method: The subjects were 16 monozygotic twin pairs between the ages of 5 and 14 years and 16 matched singleton comparison subjects. Seven twin pairs were clinically concordant and nine twin pairs were clinically discordant for strictly defined autism. After magnetic resonance imaging, a semiautomated procedure was applied to images in which the brain tissue was subdivided into neurofunctional regions and segmented into gray, white, and ventricular compartments. Results: Both the concordant and discordant twin pairs exhibited concordance in cerebral gray and white matter volumes. However, only the clinically concordant pairs exhibited concordance in cerebellar gray and white matter volumes. within the discordant twin pairs, both the twins with autism and their co-twins exhibited frontal, temporal, and occipital white matter volumes that were lower than those of the comparison subjects. Conclusions: These findings support the role and the limits of genetic liability in autism. Continuing to clarify the neuroanatomic pathways in autistic spectrum disorders could illuminate the etiology of autism and, ultimately, contribute to treatments. C1 Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21218 USA. Kennedy Krieger Inst, Baltimore, MD USA. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Kates, WR (reprint author), SUNY Syracuse, Upstate Med Univ, Dept Psychiat, 750 E Adams St, Syracuse, NY 13210 USA. 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J. Psychiat. PD MAR PY 2004 VL 161 IS 3 BP 539 EP 546 DI 10.1176/appi.ajp.161.3.539 PG 8 WC Psychiatry SC Psychiatry GA 818WU UT WOS:000221276000021 PM 14992981 ER PT J AU Garrett, AS Menon, V MacKenzie, K Reiss, AL AF Garrett, AS Menon, V MacKenzie, K Reiss, AL TI Here's looking at you, kid - Neural systems underlying face and gaze processing in fragile X syndrome SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID HUMAN EXTRASTRIATE CORTEX; POSITRON-EMISSION-TOMOGRAPHY; HUMAN FUSIFORM GYRUS; EYE GAZE; CORTICAL ACTIVITY; TEMPORAL-LOBE; PERCEPTION; MALES; AREA; RECOGNITION AB Background: Children with fragile X syndrome (fraX) are at risk for manifesting abnormalities in social function that overlap with features of autism and social anxiety disorder. In this study, we analyzed brain activation in response to face and gaze stimuli to better understand neural functioning associated with social perception in fraX. Methods: Eleven female subjects with fraX, aged 10 to 22 years, were compared with age-matched female control subjects. Photographs of forward-facing and angled faces, each having direct and averted gaze (4 types of stimuli), were presented in an event-related design during functional magnetic resonance imaging. Subjects were instructed to determine the direction of gaze for each photograph. Activation in brain regions known to respond to face and gaze stimuli, the fusiform gyrus (FG) and superior temporal sulcus (STS), were compared between groups to isolate neural abnormalities in the perception of directed social stimuli. Results: The fraX subjects had decreased accuracy in determining the direction of gaze compared with controls. Region of interest analysis of the FG revealed a significant interaction between diagnostic group and face orientation. Specifically, control subjects had greater FG activation to forward than to angled faces, whereas fraX subjects had no difference in FG activation to forward and angled faces. Controls showed greater left STS activation to all stimuli compared with fraX subjects. Conclusions: Our results suggest that gaze aversion in fraX subjects is related to decreased specialization of the FG in the perception of face orientation. Decreased STS activation in fraX suggests aberrant processing of gaze. These data suggest that gaze aversion in fraX may be related to dysfunction of neural systems underlying both face and gaze processing. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford Psychiat Neuroimaging Lab, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Behav Neurogenet Res Ctr, Stanford, CA 94305 USA. RP Garrett, AS (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford Psychiat Neuroimaging Lab, 401 Quarry Rd, Stanford, CA 94305 USA. 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Gen. Psychiatry PD MAR PY 2004 VL 61 IS 3 BP 281 EP 288 DI 10.1001/archpsyc.61.3.281 PG 8 WC Psychiatry SC Psychiatry GA 800YY UT WOS:000220064800009 PM 14993116 ER PT J AU Lotspeich, L Kwon, H Schumann, CM Fryer, SL Goodlin-Jones, BL Buonocore, MH Lammers, CR Amaral, DG Reiss, AL AF Lotspeich, L Kwon, H Schumann, CM Fryer, SL Goodlin-Jones, BL Buonocore, MH Lammers, CR Amaral, DG Reiss, AL TI Investigation of neuroanatomical differences between autism and Asperger syndrome SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; CORPUS-CALLOSUM; HEAD CIRCUMFERENCE; POSTERIOR-FOSSA; INFANTILE-AUTISM; BRAIN VOLUME; CHILDREN; CEREBELLAR; SIZE AB Background: Autism and Asperger syndrome (ASP) are neurobiological conditions with overlapping behavioral symptoms and of unknown etiologies. Results from previous autism neuroimaging studies have been difficult to replicate, possibly owing to site differences in subject samples, scanning procedures, and image-processing methods. We sought (1) to determine whether low-functioning autism (LFA; IQ< 70), high-functioning autism (HFA; IQ greater than or equal to 70), and ASP constitute distinct biological entities as evidenced by neuroanatomical measures, and (2) to assess for intersite differences. Methods: Case-control study examining coronally oriented 124-section spoiled gradient echo images acquired on 3 magnetic resonance imaging (MRI) systems, and processed by BrainImage 5X Participants were recruited and underwent scanning at 2 academic medicine departments. Participants included 4 age-matched groups of volunteer boys aged 7.8 to 17.9 years (13 patients with LFA, 18 with HFA, 21 with ASP, and 21 control subjects), and 3 volunteer adults for neuroimaging reliability. Main outcome measures included volumetric measures of total, white, and gray matter for cerebral and cerebellar tissues. Results: Intersite differences were seen for subject age, IQ, and cerebellum measures. Cerebral gray matter volume was enlarged in both HFA and LFA compared with controls (P=.009 and P=.04, respectively). Cerebral gray matter volume in ASP was intermediate between that of HFA and controls, but nonsignificant. Exploratory analyses revealed a negative correlation between cerebral gray matter volume and performance IQ within HFA but not ASP. A positive correlation between cerebral white matter volume and performance IQ was observed within ASP but not HFA. Conclusions: Lack of replication between previous autism MRI studies could be due to intersite differences in MRI systems and subjects' age and IQ. Cerebral gray tissue findings suggest that ASP is on the mild end of the autism spectrum. 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Gen. Psychiatry PD MAR PY 2004 VL 61 IS 3 BP 291 EP 298 DI 10.1001/archpsyc.61.3.291 PG 8 WC Psychiatry SC Psychiatry GA 800YY UT WOS:000220064800010 PM 14993117 ER PT J AU Waltz, M Shattock, P AF Waltz, M Shattock, P TI Autistic disorder in nineteenth-century London - Three case reports SO AUTISM LA English DT Article DE autism; disability studies; Great Ormond Street Hospital for Children; medical history; social history; William Howship Dickinson ID CHILDREN AB This article examines the existence, description, perception, treatment, and outcome of symptoms consistent with autistic disorder in nineteenth-century London, England, based on case histories from the notes of Dr William Howship Dickinson at Great Ormond Street Hospital for Children. Three cases meeting the DSM-IV criteria for autistic disorder are described in detail. Other cases in which autistic traits are described are briefly summarized. The article explores the environment of contemporary medical practice, beliefs about childhood brain disorders, and social practice regarding children with brain disorders, and the impact of these factors on assessment and treatment. It correlates Dickinson's observations with current research on autism, providing information about children with autism before the condition was formally named in 1943. C1 Univ Sunderland, Medis Ctr St Peters, Sch Arts Design Media & Culture, Sunderland SR6 0DD, Durham, England. RP Waltz, M (reprint author), Univ Sunderland, Medis Ctr St Peters, Sch Arts Design Media & Culture, Sunderland SR6 0DD, Durham, England. EM mitzi.waltz@sunderland.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th [Anonymous], 1992, INT STAT CLASS DIS R Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BALDWIN N, 2001, WHOLE STORY HIST GRE Baron-Cohen S, 1999, PSYCHOL MED, V29, P1151, DOI 10.1017/S003329179900896X Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 *COMM LUN, 1847, 2 ANN REP COMM LUN L Dally A, 1997, SOC HIST MED, V10, P291, DOI 10.1093/shm/10.2.291 DICKINSON WH, 1869, NERVOUS DIS, V1 EDGAR CL, 1999, CARE FEEDING INFANTS ERDMANN R, 1995, PSYCHIAT PRAX, V22, P80 Fombonne E, 1998, AUTISM PERVASIVE DEV, P32 Frith U., 1989, AUTISM EXPLAINING EN GILLMAN MW, 1999, CIRCULATION, V99, P6 HOPKINS E, 1994, CHILDHOOD TRASFORMED Kanner L, 1943, NERV CHILD, V2, P217 KATZ I, 2000, WORLD HIST OWN AUTIS LOCOCK C, 1857, LANCET, V1, P528 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 MALMIVUO J, 1999, INT J BIOELECTROMAGN, V1, P2 *ROYAL COLL PHYS, 1955, MUNKS ROLL LIV FELL, V4 SCHARRE JE, 1992, OPTOMETRY VISION SCI, V69, P433, DOI 10.1097/00006324-199206000-00004 SHATTOCK P, 2001, P DURH AUT C SUND AU, P1 WING JK, 1976, EARLY CHILDHOOD AUTI, P4 Wing L., 1996, AUTISTIC SPECTRUM GU NR 25 TC 4 Z9 4 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 2004 VL 8 IS 1 BP 7 EP 20 DI 10.1177/1362361304040635 PG 14 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600002 PM 15070544 ER PT J AU Micali, N Chakrabarti, S Fombonne, E AF Micali, N Chakrabarti, S Fombonne, E TI The broad autism phenotype - Findings from an epidemiological survey SO AUTISM LA English DT Article DE autism; autoimmune disorders; family study; pervasive developmental disorders; psychiatric disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HISTORY; CHILDREN; PARENTS; TWIN; PERSONALITY; RELATIVES; GENETICS; PATTERNS AB This study aimed to determine if relatives of children with autism and less severe pervasive developmental disorders (PDDs) have higher rates of various components of the broad autistic phenotype. Psychiatric and medical disorders were investigated. Parents of children with PDDs were selected from an epidemiological survey and compared with parents of control children with non-autistic developmental problems. Rates of abnormalities and disorders were compared in relatives of 79 cases and 61 controls. Medical and autoimmune disorders in both groups were endorsed by few relatives. Specific developmental disorders were commoner in parents of controls. Depression and anxiety were significantly more prevalent in mothers of children with PDDs. Significantly more PDD children had at least one first-degree relative with anxiety and one second-degree relative with OCD. PDDs were commoner in first-degree relatives. The implications of the findings for the definition of the broad phenotype of autism are discussed. C1 Inst Psychiat, Dept Child & Adolescent Psychiat, London SE5 8AF, England. Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada. RP Micali, N (reprint author), Inst Psychiat, Dept Child & Adolescent Psychiat, De Crespigny Pk,POB 85, London SE5 8AF, England. EM N.Micali@iop.kcl.ac.uk RI Micali, nadia/E-6829-2010 OI Micali, nadia/0000-0001-5571-2273 CR Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 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 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 COMI A, 1991, J CHILD NEUROL, V14, P16 Denney DR, 1996, J AUTISM DEV DISORD, V26, P87, DOI 10.1007/BF02276236 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Fombonne E, 2002, MOL PSYCHIATR, V7, pS4, DOI 10.1038/sj.mp.4001162 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Fombonne E, 1997, J CHILD PSYCHOL PSYC, V38, P667, DOI 10.1111/j.1469-7610.1997.tb01694.x Gupta S, 1996, J AUTISM DEV DISORD, V26, P439, DOI 10.1007/BF02172828 Krause I, 2002, J AUTISM DEV DISORD, V32, P337, DOI 10.1023/A:1016391121003 LANDA R, 1992, PSYCHOL MED, V22, P245 Murphy M, 2000, PSYCHOL MED, V30, P1411, DOI 10.1017/S0033291799002949 Piven J, 1999, AM J PSYCHIAT, V156, P557 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 SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 NR 22 TC 85 Z9 87 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 2004 VL 8 IS 1 BP 21 EP 37 DI 10.1177/1362361304040636 PG 17 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600003 PM 15070545 ER PT J AU Kielinen, M Rantala, H Timonen, E Linna, SL Moilanen, I AF Kielinen, M Rantala, H Timonen, E Linna, SL Moilanen, I TI Associated medical disorders and disabilities in children with autistic disorder - A population-based study SO AUTISM LA English DT Article DE autistic disorder; comorbidity; Finland; medical disorders; population surveys ID TUBEROUS SCLEROSIS; NORTHERN FINLAND; INFANTILE-AUTISM; EPIDEMIOLOGIC SURVEY; SPECTRUM DISORDERS; CEREBRAL-PALSY; DOWN-SYNDROME; BIRTH COHORT; EPILEPSY; PREVALENCE AB A population-based survey was conducted among 152,732 Finnish children and adolescents aged under 16 years and living in northern Finland. Diagnoses and associated medical conditions were derived from the hospital and institutional records of this area. One hundred and eighty-seven children with DSM-IV autistic disorder were identified. Associated medical disorders or associated disorders of known or suspected genetic origin were found in 12.3 percent, including tuberous sclerosis, Down syndrome, fragile X syndrome, Klinefelter syndrome, XYY syndrome, chromosome 17 deletion, chromosome 46, XX, dup(8)(p) and mitochondriopathy. Other associated medical disorders identified were epilepsy, hydrocephalus, foetal alcohol syndrome and cerebral palsy. Hearing impairments were found in 8.6 percent and severe impairment of vision in 3.7 percent of the individuals with autistic disorder. Medical disorders seem to have a special impact on the genesis of autistic disorder and need to be thoroughly examined in each child with autistic disorder. C1 Univ Oulu, Clin Child Psychiat, Dept Paediat, FIN-90220 Oulu, Finland. RP Kielinen, M (reprint author), Univ Oulu, Clin Child Psychiat, Dept Paediat, Kajaanintie 52, FIN-90220 Oulu, Finland. CR AHLSEN G, 1994, ARCH NEUROL-CHICAGO, V51, P76 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Aronson M, 1997, DEV MED CHILD NEUROL, V39, P583 BAILEY A, 1993, J CHILD PSYCHOL PSYC, V34, P673, DOI 10.1111/j.1469-7610.1993.tb01064.x BREGMAN JD, 1988, J AM ACAD CHILD PSY, V27, P440, DOI 10.1097/00004583-198807000-00011 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Chess S, 1971, PSYCHIAT DISORDERS C CIALDELLA P, 1989, J CHILD PSYCHOL PSYC, V30, P165, DOI 10.1111/j.1469-7610.1989.tb00775.x Commission on Classification and Terminology of the International League Against Epilepsy, 1989, EPILEPSIA, V30, P389 Ek U, 1998, DEV MED CHILD NEUROL, V40, P297 FERNELL E, 1991, ACTA PAEDIATR SCAND, V80, P451, DOI 10.1111/j.1651-2227.1991.tb11881.x Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 Ghaziuddin M, 1997, J INTELL DISABIL RES, V41, P87, DOI 10.1111/j.1365-2788.1997.tb00681.x GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 GILLBERG C, 1984, APPL RES MENT RETARD, V5, P353, DOI 10.1016/S0270-3092(84)80056-9 GILLBERG C, 1984, J AUTISM DEV DISORD, V14, P1, DOI 10.1007/BF02408551 Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 GILLBERG C, 1987, DEV MED CHILD NEUROL, V29, P641 Gillberg C, 1995, EPIDEMIOLOGY CHILD A, P227 GILLBERG C, 2000, BIOL AUTISTIC SYNDRO, P4 GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 HEIKURA U, 2002, 126 AAMR ANN M EXH S Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 HOWLIN P, 1995, DEV MED CHILD NEUROL, V37, P406 Kent L, 1999, DEV MED CHILD NEUROL, V41, P153, DOI 10.1017/S001216229900033X Kielinen M, 2000, EUR CHILD ADOLES PSY, V9, P162 KOSKINIEMI M, 1989, LANCET, V1, P31 LEISTI J, 1982, KEHITYSVAMMAISUUDEN MATILAINEN R, 1995, ACTA PAEDIATR, V84, P261, DOI 10.1111/j.1651-2227.1995.tb13626.x Mouridsen S E, 1992, Acta Paedopsychiatr, V55, P15 Nordin V, 1998, ACTA PSYCHIAT SCAND, V97, P99, DOI 10.1111/j.1600-0447.1998.tb09970.x OLSSON I, 1988, ARCH NEUROL-CHICAGO, V45, P666 PAYTON JB, 1989, J AM ACAD CHILD PSY, V28, P417, DOI 10.1097/00004583-198905000-00019 Pharoah POD, 1998, ARCH DIS CHILD, V79, pF21 RANTAKALLIO P, 1979, SOC SCI MED-MED SOC, V13, P423, DOI 10.1016/0160-7979(79)90131-0 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 RASMUSSEN P, 2001, THESIS DEP CHILD ADO RITVO ER, 1990, AM J PSYCHIAT, V147, P1614 Rosenhall U, 1999, J AUTISM DEV DISORD, V29, P349, DOI 10.1023/A:1023022709710 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x SHEPHERD CW, 1991, ARCH NEUROL-CHICAGO, V48, P400 SIDENVALL R, 1993, ACTA PAEDIATR, V82, P60, DOI 10.1111/j.1651-2227.1993.tb12518.x Smalley SL, 1998, J AUTISM DEV DISORD, V28, P407, DOI 10.1023/A:1026052421693 *STAKES, 1996, REG CONG AN 1993 STEFFENBURG S, 1991, DEV MED CHILD NEUROL, V33, P495 TUCHMAN RF, 1991, PEDIATRICS, V88, P1219 VONWENDT L, 1985, ANN CLIN RES, V17, P156 VONWENDT L, 1985, EUR J PEDIATR, V144, P149 WING L, 1989, DIAGNOSIS AND TREATMENT OF AUTISM, P5 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 50 TC 84 Z9 86 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 2004 VL 8 IS 1 BP 49 EP 60 DI 10.1177/1362361304040638 PG 12 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600005 PM 15070547 ER PT J AU Barrett, S Prior, M Manjiviona, J AF Barrett, S Prior, M Manjiviona, J TI Children on the borderlands of autism - Differential characteristics in social, imaginative, communicative and repetitive behaviour domains SO AUTISM LA English DT Article DE autism; diagnostic discrimination; language disorders ID DEVELOPMENTAL LANGUAGE DISORDERS; HIGH-LEVEL AUTISM; INFANTILE-AUTISM; FOLLOW-UP; IMPAIRMENT; CLASSIFICATION; DIAGNOSIS; COGNITION; DEFICITS; PLAY AB A sample of 37 children aged 4-7 years who all showed some autistic features was investigated. Children with a primary diagnosis of autism were compared with those diagnosed with a language disorder, on behaviours within four domains; social behaviour, imaginative activities, repetitive behaviour and communication. The aim was to identify potentially differentiating features of the two groups using observational ratings and questionnaire measures provided by parents and teachers. Information on participants' intelligence and language skills was also collected. The children with autism showed greater deficits in joint attention, functional play and pragmatic language, and engaged in more repetitive behaviours, than the language disordered children. However, the groups did not differ significantly on formally assessed language skills. A cluster analysis produced three groups of children varying in level of functioning and parent-rated behaviours. The results are informative for clinicians dealing with the challenge of differential diagnosis. C1 Univ Melbourne, Dept Psychol, Parkville, Vic 3052, Australia. Royal Childrens Hosp, Melbourne, Vic, Australia. RP Prior, M (reprint author), Univ Melbourne, Dept Psychol, Parkville, Vic 3052, Australia. EM priorm@unimelb.edu.au CR ALLEN DA, 1992, INT CONGR SER, V965, P157 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1989, BRIT J DEV PSYCHOL, V7, P113 BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Bishop D., 2000, SPEECH LANGUAGE IMPA, P99 Bishop D. V. M., 1987, LANGUAGE DEV DISORDE, P16 Bishop D. V. 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M., 1997, HDB AUTISM PERVASIVE, P513 WETHERBY AM, 1984, J SPEECH HEAR RES, V27, P364 WillemsenSwinkels SHN, 1997, J CHILD PSYCHOL PSYC, V38, P327, DOI 10.1111/j.1469-7610.1997.tb01517.x Wing L., 1996, AUTISTIC SPECTRUM GU WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing L, 1997, HDB AUTISM PERVASIVE, P148 NR 57 TC 18 Z9 18 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 2004 VL 8 IS 1 BP 61 EP 87 DI 10.1177/1362361304040640 PG 27 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600006 PM 15070548 ER PT J AU Charman, T Howlin, P Berry, B Prince, E AF Charman, T Howlin, P Berry, B Prince, E TI Measuring developmental progress of children with autism spectrum disorder on school entry using parent report SO AUTISM LA English DT Article DE autism; developmental progress; monitoring; parent report; questionnaires ID ADAPTIVE-BEHAVIOR; YOUNG-CHILDREN; DOWN-SYNDROME; INTERVENTION; PERSPECTIVES; INDIVIDUALS; DIAGNOSIS; AGE AB Increasing numbers of children with autism spectrum disorder (ASD) are diagnosed in the preschool years, and their educational progress must be monitored. Parent questionnaire data can augment psychometric assessments and individual planning at low cost. One hundred and twenty-five parents of UK children who entered dedicated autism primary schools and units in two consecutive calendar years were asked to complete three questionnaires. Fifty-seven parents repeated the questionnaire measures one year later. Encouraging developmental progress was observed on the Vineland Adaptive Behavior Scales-Screener. Symptom severity as measured by the Social Communication Questionnaire did not change over time. The pattern of change scores on the Autism Treatment Evaluation Checklist was mixed, and confounding disadvantages this questionnaire. The study demonstrated that it is possible to collect useful information on the progress of children with ASD using parents as informants. Such data would assist in judging claims regarding developmental progress within particular programmes. C1 UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RP Charman, T (reprint author), UCL, Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Howlin, Patricia/A-7622-2011; Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 *DEP ED SKILLS, 2002, AUT SPECTR DIS GUID FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 Harris SL, 1995, SPECIAL SERVICES SCH, V10, P45, DOI 10.1300/J008v10n01_03 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Harrison JE, 1997, J CHILD PSYCHOL PSYC, V38, P603, DOI 10.1111/j.1469-7610.1997.tb01687.x HOWLIN P, 1995, DEV MED CHILD NEUROL, V37, P406 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1998, J CHILD PSYCHOL PSYC, V39, P307, DOI 10.1017/S0021963097002138 Jordan R, 1998, ED INTERVENTIONS CHI Kasari C, 1999, J AUTISM DEV DISORD, V29, P297, DOI 10.1023/A:1022159302571 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 McGregor E, 2001, AUTISM, V5, P189 *NAT AUT SOC, 1998, SCH UN CLASS CHILDR National Research Council, 2001, ED CHILDR AUT *NEW YORK STAT DEP, 1999, CLIN PRACT GUID AUT Rimland B, 1999, AUTISM TREATMENT EVA Rumsey JM, 2000, J AUTISM DEV DISORD, V30, P369, DOI 10.1023/A:1005595303185 SPARROW S, 2000, UNPUB VINELAND ADAPT Sparrow S, 1984, VINELAND ADAPTIVE BE Stone WL, 1999, AM J MENT RETARD, V104, P187, DOI 10.1352/0895-8017(1999)104<0187:POABIV>2.0.CO;2 NR 24 TC 26 Z9 30 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 2004 VL 8 IS 1 BP 89 EP 100 DI 10.1177/1362361304040641 PG 12 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600007 PM 15070549 ER PT J AU Mukaddes, NM Kaynak, FN Kinali, G Besikci, H Issever, H AF Mukaddes, NM Kaynak, FN Kinali, G Besikci, H Issever, H TI Psychoeducational treatment of children with autism and reactive attachment disorder SO AUTISM LA English DT Article DE autism; psychoeducation; reactive attachment disorder; Turkey AB The aim of the study was to evaluate and compare the efficacy of short-term psychoeducational treatment in children with autism and reactive attachment disorder (RAD). Ten boys with autism aged 24-66 months and 11 children with RAD (nine boys and two girls) aged 30-70 months were included in the study. The Ankara Developmental Screening Inventory was used to monitor progress following a 14-session psychoeducational programme. This focused on establishing a reciprocal-dyadic interaction between children and their caregivers and it also provided an educational programme for emotional, social, and language development. Although both groups showed significant changes on all scales of the ADSI, the children with RAD showed greater improvement than the autism group in their total development score, on the language-cognitive subscale, and in social/self-care abilities. C1 Istanbul Univ, Istanbul, Turkey. RP Mukaddes, NM (reprint author), Istanbul Tip Fak, PTT Si PK 53,Capa, TR-34272 Istanbul, Turkey. EM nmotavalli@yahoo.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bowlby J., 1969, ATTACHMENT LOSS, V1 CICCHETTI D, 1989, J CONSULT CLIN PSYCH, V57, P837 GAENSBAUER TJ, 1979, J AM ACAD CHILD PSY, V18, P236, DOI 10.1016/S0002-7138(09)61039-6 Hanson R F, 2000, Child Maltreat, V5, P137, DOI 10.1177/1077559500005002005 Keren M, 1998, ISRAEL J PSYCHIAT, V35, P262 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Mukaddes NM, 2000, CHILD PSYCHIAT HUM D, V30, P273 Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Provence S., 1962, INFANTS REARED I RICHTERS MM, 1994, J AM ACAD CHILD PSY, V33, P328, DOI 10.1097/00004583-199403000-00005 SAVASIR I, 1998, TURK PSIKOLOGLAR DER, V2 Scheeringa MS, 2001, CHILD PSYCHIAT HUM D, V32, P71, DOI 10.1023/A:1017511714145 Schopler E., 1995, LEARNING COGNITION A, P243 SCHOPLER E, 1987, AM PSYCHOL, V42, P376, DOI 10.1037/0003-066X.42.4.376 Schreibman L, 2000, J AUTISM DEV DISORD, V30, P373, DOI 10.1023/A:1005535120023 Shigley RH, 1984, EFFECTS AUTISM FAMIL, P65 Spitz RA, 1945, PSYCHOANAL STUD CHIL, V1, P53 NR 18 TC 5 Z9 5 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 2004 VL 8 IS 1 BP 101 EP 109 DI 10.1177/1362361304040642 PG 9 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600008 PM 15070550 ER PT J AU Ijichi, S Ijichi, N AF Ijichi, S Ijichi, N TI Beyond negative data in autism randomized trials SO AUTISM LA English DT Letter C1 Inst Externalizat Gifts & Talents, Kagoshima, Japan. RP Ijichi, S (reprint author), Inst Externalizat Gifts & Talents, Kagoshima, Japan. CR Diggle T., 2003, COCHRANE DB SYST REV, V1, DOI DOI 10.1002/14651858 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X NAKANE Y, 1995, KOREAN J PSYCHOPHARM, V6, P111 Shimoji T, 2002, CHILD NERV SYST, V18, P215, DOI 10.1007/s00381-002-0568-1 WHELAN J, 2000, DRUG DISCOV TODAY, V15, P487 NR 6 TC 2 Z9 2 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 2004 VL 8 IS 1 BP 111 EP 112 DI 10.1177/1362361304040644 PG 2 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600009 PM 15070551 ER PT J AU Bauminger, N AF Bauminger, N TI Relationship development intervention with young children: Social and emotional development activities for Asperger syndrome, autism, PDD, and NLD SO AUTISM LA English DT Book Review C1 Bar Ilan Univ, IL-52100 Ramat Gan, Israel. RP Bauminger, N (reprint author), Bar Ilan Univ, IL-52100 Ramat Gan, Israel. CR Gutstein S, 2002, RELATIONSHIP DEV INT NR 1 TC 0 Z9 0 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 2004 VL 8 IS 1 BP 114 EP 117 DI 10.1177/1362361304040645 PG 4 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600011 ER PT J AU Sofronoff, K AF Sofronoff, K TI A parents' guide to Asperger syndrome and high functioning autism SO AUTISM LA English DT Book Review C1 Univ Queensland, St Lucia, Qld 4067, Australia. RP Sofronoff, K (reprint author), Univ Queensland, St Lucia, Qld 4067, Australia. CR Ozonoff S, 2002, PARENTS GUIDE ASPERG NR 1 TC 0 Z9 0 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 2004 VL 8 IS 1 BP 117 EP 118 PG 2 WC Psychology, Developmental SC Psychology GA 776HY UT WOS:000189111600012 ER PT J AU Madden, GJ Klatt, KP Jewett, DC Morse, LA AF Madden, GJ Klatt, KP Jewett, DC Morse, LA TI A forgotten resource critical to the future of behavior analysis: Undergraduate psychology majors SO BEHAVIOR ANALYST LA English DT Article DE undergraduates; behavior analysis; teaching; certification ID PREVALENCE; AUTISM AB The demand for board-certified applied behavior analysts is not being met, and there is a perception that fewer students are exposed to systematic courses in basic and applied behavior analysis than was true a generation ago. This article outlines how we have successfully implemented an undergraduate curriculum in behavior analysis within a traditional department of psychology. Certification credentials offered by the Behavior Analysis Certification Board facilitated the approval of this curriculum, and the cultural practice selection contingencies that supported the creation of our curriculum in behavior analysis may be similar at other comprehensive universities. Advice for developing an undergraduate program in behavior analysis within a psychology department is outlined. We also summarize strategies we have used to attract talented students to the courses and the significant impact these strategies have had on the number of our graduates who pursue graduate training in basic and applied behavior analysis. Attracting the best and brightest students to behavior analysis is critical to the future of the field. C1 Univ Wisconsin, Dept Psychol, Eau Claire, WI 54702 USA. RP Madden, GJ (reprint author), Univ Wisconsin, Dept Psychol, 105 Garfield Ave, Eau Claire, WI 54702 USA. EM maddengj@uwec.edu RI Madden, Gregory/E-8524-2010 CR BETTAG T, 2001, ABC NEWS NIGHTLINE F Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 *LANG GRAND COLL N, 1999, RET OUR ROOTS ENG I LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Monks J., 1999, CHANGE, V31, P42 NR 6 TC 0 Z9 0 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 2004 VL 27 IS 1 BP 33 EP 41 PG 9 WC Psychology, Clinical SC Psychology GA 823IU UT WOS:000221605300004 PM 22478414 ER PT J AU Campbell, JM AF Campbell, JM TI Statistical comparison of four effect sizes for single-subject designs SO BEHAVIOR MODIFICATION LA English DT Article DE meta-analysis; quantitative synthesis; single-subject design ID QUANTITATIVE SYNTHESIS; PROBLEM BEHAVIOR; METAANALYSIS; ISSUES AB Controversy exists regarding appropriate methods for summarizing treatment outcomes for single-subject designs. Nonregression- and regression-based methods have been proposed to summarize the efficacy of single-subject interventions with proponents of both methods arguing for the superiority of their respective approaches. To compare findings for different single-subject effect sizes, 117 articles that targeted the reduction of problematic behaviors in 181 individuals diagnosed with autism were examined. Four effect sizes were calculated for each article: mean baseline reduction (MBLR), percentage of nonoverlapping data (PND), percentage of zero data (PZD), and one regression-based d statistic. Although each effect size indicated that behavioral treatment was effective, moderating variables were detected by the PZD effect size only. Pearson product-moment correlations indicated that effect sizes differed in statistical relationships to one another. In the present review, the regression-based d effect size did not improve the understanding of single-subject treatment outcomes when compared to nonregression effect sizes. C1 Univ Georgia, Dept Educ Psychol, Athens, GA 30602 USA. RP Campbell, JM (reprint author), Univ Georgia, Dept Educ Psychol, 325 Aderhold Hall, Athens, GA 30602 USA. EM jcampbel@coe.uga.edu CR ALLISON DB, 1995, CLIN PSYCHOL-SCI PR, V2, P279 ALLISON DB, 1994, BEHAV RES THER, V32, P885, DOI 10.1016/0005-7967(94)90170-8 ALLISON DB, 1993, BEHAV RES THER, V31, P621, DOI 10.1016/0005-7967(93)90115-B Campbell JM, 2003, RES DEV DISABIL, V24, P120, DOI 10.1016/S0891-4222(03)00014-3 Cohen J., 1983, APPL MULTIPLE REGRES, V2nd CROSBIE J, 1993, J CONSULT CLIN PSYCH, V61, P966, DOI 10.1037/0022-006X.61.6.966 Faith M. S., 1996, DESIGN ANAL SINGLE C, P245 GORMANSMITH D, 1985, J MENT DEFIC RES, V29, P295 Hedges L, 1985, STAT METHODS METAANA LUNDERVOLD D, 1988, BEHAV MODIF, V12, P590, DOI 10.1177/01454455880124006 OBRIEN S, 1990, J ASSOC PERS SEVERE, V15, P148 ROSENTHAL R, 1995, PSYCHOL BULL, V118, P183, DOI 10.1037//0033-2909.118.2.183 SCOTTI JR, 1991, AM J MENT RETARD, V96, P233 SCRUGGS TE, 1994, BEHAV RES THER, V32, P879, DOI 10.1016/0005-7967(94)90169-4 Scruggs TE, 1998, BEHAV MODIF, V22, P221, DOI 10.1177/01454455980223001 SCRUGGS TE, 1987, REM SPEC EDUC, V8, P24 SKIBA RJ, 1985, J SPEC EDUC, V19, P459 WEST SG, 1991, J PERS, V59, P609, DOI 10.1111/j.1467-6494.1991.tb00261.x WHITE DM, 1989, BEHAV ASSESS, V11, P281 WHITE OR, 1987, REM SPEC EDUC, V8, P34 NR 20 TC 63 Z9 63 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD MAR PY 2004 VL 28 IS 2 BP 234 EP 246 DI 10.1177/0145445503259264 PG 13 WC Psychology, Clinical SC Psychology GA 771PF UT WOS:000188794700005 PM 14997950 ER PT J AU Green, S Pring, L Swettenham, J AF Green, S Pring, L Swettenham, J TI An investigation of first-order false belief understanding of children with congenital profound visual impairment SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID BLIND-CHILDREN; VERBAL-ABILITY; MIND; AUTISM; COGNITION; DISORDER; AGE AB This study assessed theory of mind understanding in children with congenital profound visual impairment (CPVI): children who have had no access to visual information throughout development. Participants were 18 children with CPVI and no other impairments, aged between 5 and 11 years, and 18 children with normal vision, matched individually on chronological age, verbal IQ and verbal mental age. Three first-order false belief tasks were presented twice each; the three tasks varied in the extent of deception and involvement of the child. Six of the children with CPVI failed one or more of the false belief tasks; all sighted children passed all of the tasks. The manipulations of deception and involvement did not influence the performance of the children with CPVI. Participant characteristics of the children with CPVI were examined in relation to their performance on the false belief tasks: chronological age and type of school attended were not found to be related to performance; verbal IQ and verbal mental age were found to differ in children with good and poor performance on the false belief tasks. The results are consistent with either a general pattern of delay in theory of mind development for children with CPVI, or with a subset of children who have longer-term difficulties in this area. C1 Univ London, Univ London Goldsmiths Coll, Dept Psychol, London WC1E 7HU, England. Univ London, Univ Coll, London WC1E 7HU, England. RP Green, S (reprint author), Stepfamily Scotland, 5 Coates Pl, Edinburgh EH3 7AA, Midlothian, Scotland. EM sarah-green@O2.co.uk CR Baron-Cohen S, 1993, UNDERSTANDING OTHER BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x CARRUTHERS P, 1996, THEORIES THEORIES MI Chandler M., 1994, CHILDRENS EARLY UNDE DENNETT DC, 1978, BEHAV BRAIN SCI, V1, P568 Dunn J, 1994, CHILDRENS EARLY UNDE, P297 Fraiberg S., 1977, INSIGHTS BLIND FRITH U, 1991, TRENDS NEUROSCI, V14, P433, DOI 10.1016/0166-2236(91)90041-R GOOD WV, 1993, MANAGMENT VISUAL IMP, P30 GREEN S, 2003, UNPUB THEORY MIND DE HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Harris P. L, 1996, THEORIES THEORIES MI, P200 Hobson R. Peter, 1993, AUTISM DEV MIND HOBSON RP, 1994, CHILDRENS EARLY UNDE, P71 JAN JE, 1993, MANAGEMENT VISUAL IM, P49 Lewis C., 1994, CHILDRENS EARLY UNDE MCALPINE LM, 1995, J VISUAL IMPAIR BLIN, V89, P349 Meltzoff A. N., 1993, UNDERSTANDING OTHER, P335 Minter M, 1998, BRIT J DEV PSYCHOL, V16, P183 PERNER J, 1987, BRIT J DEV PSYCHOL, V5, P125 Peterson CC, 2000, BRIT J DEV PSYCHOL, V18, P431, DOI 10.1348/026151000165788 Sodian Beate, 1994, CHILDRENS EARLY UNDE, P385 SPARREVOHN R, 1995, J CHILD PSYCHOL PSYC, V36, P249, DOI 10.1111/j.1469-7610.1995.tb01823.x Warren D. H., 1994, BLINDNESS CHILDREN I Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D., 1976, WECHSLER INTELLIGENC Wechsler D, 1967, WECHSLER PRESCHOOL P Whitten A., 1991, NATURAL THEORIES MIN WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 34 TC 25 Z9 25 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0261-510X J9 BRIT J DEV PSYCHOL JI Br. J. Dev. Psychol. PD MAR PY 2004 VL 22 BP 1 EP 17 DI 10.1348/026151004772901087 PN 1 PG 17 WC Psychology, Developmental SC Psychology GA 807CZ UT WOS:000220480900001 ER PT J AU Butler, R AF Butler, R TI Paper linking MMR jab to autism questioned SO CHEMISTRY & INDUSTRY LA English DT News Item NR 0 TC 0 Z9 0 PU SOC CHEMICAL INDUSTRY PI LONDON PA 14 BELGRAVE SQUARE, LONDON SW1X 8PS, ENGLAND SN 0009-3068 J9 CHEM IND-LONDON JI Chem. Ind. PD MAR 1 PY 2004 IS 5 BP 5 EP 5 PG 1 WC Chemistry, Applied SC Chemistry GA 805YT UT WOS:000220402300004 ER PT J AU Robinson, AM Richdale, AL AF Robinson, AM Richdale, AL TI Sleep problems in children with an intellectual disability: parental perceptions of sleep problems, and views of treatment effectiveness SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE sleep problems; children; intellectual disability; treatment; parent perceptions ID BEHAVIORAL TREATMENTS; YOUNG-CHILDREN; DISORDERS; AUTISM; QUESTIONNAIRE; DIFFICULTIES; DISTURBANCE; ADOLESCENTS; CHILDHOOD; PATTERNS AB Background Sleep problems are common in children with an intellectual disability (ID), often lasting for many years. Many parents do not perceive their child to have a sleep problem, do not believe treatment is possible and do not seek treatment. This paper examined prevalence and duration of sleep problems in children with an ID and considered parental perceptions of sleep problems and views towards treatment. Method The paper reports on two studies (n = 149 and 243 respectively) of children between 3 and 18 years, with a range of disabilities. Parents in each study completed a questionnaire about their child's sleep problems, and the type and effectiveness of any treatment used to address their child's sleep problems. Results Prevalence rates ranged between 25.5% and 36.2% for sleep problems with an average duration of between 6 and 9 years. Around half of parents had sought treatment for their child's sleep problem in Study 1, while 76% had done so in Study 2. Parental ratings regarding treatment effectiveness were higher in Study 1 than in Study 2. Contrary to expectations, behavioural treatment was not rated as significantly more effective than other treatments in either study. Conclusions While sleep problems are common and chronic in children with an ID, parents may not recognize a sleep problem as present, often do not seek treatment for their child's sleep problems, and treatment advice and effectiveness is very variable. Thus, further research and parent and professional education regarding the identification and treatment of sleep problems in these children is required. C1 RMIT Univ, Dept Psychol & Disabil Studies, Bundoora, Vic 3083, Australia. RP Richdale, AL (reprint author), RMIT Univ, Dept Psychol & Disabil Studies, POB 71, Bundoora, Vic 3083, Australia. EM amanda.richdale@rmit.edu.au CR BARTLETT LB, 1985, BRIT J MENT SUBNORM, V31, P54 Bramble D, 1996, CHILD CARE HLTH DEV, V22, P355, DOI 10.1046/j.1365-2214.1996.810810.x Brylewski JE, 1998, J INTELL DISABIL RES, V42, P154, DOI 10.1046/j.1365-2788.1998.00111.x Chervin RD, 2001, PEDIATRICS, V107, P1375, DOI 10.1542/peds.107.6.1375 CLARKSON S, 1986, AUST PAEDIATR J, V22, P31 Didden R, 2001, RES DEV DISABIL, V22, P255, DOI 10.1016/S0891-4222(01)00071-3 Didden R, 2002, J INTELL DISABIL RES, V46, P537, DOI 10.1046/j.1365-2788.2002.00404.x DIDDEN R, 1998, J BEHAV THER EXP PSY, V29, P87 DURAND VM, 1996, J ASSOC PERS SEVERE, V21, P114 Ferber Richard, 1985, SOLVE YOUR CHILDS SL FRANCE KG, 1991, J DEV BEHAV PEDIATR, V12, P308 Honomichl RD, 2002, J AUTISM DEV DISORD, V32, P553, DOI 10.1023/A:1021254914276 Johnson CR, 1996, CHILD ADOL PSYCH CL, V5, P673 MINDELL J, 1997, EVALUATION TREATMENT, P427 MINDELL JA, 1993, J PEDIATR PSYCHOL, V18, P731, DOI 10.1093/jpepsy/18.6.731 Mindell JA, 1999, J PEDIATR PSYCHOL, V24, P465, DOI 10.1093/jpepsy/24.6.465 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 QUINE L, 1991, J MENT DEFIC RES, V35, P269 Quine L, 2001, CHILD CARE HLTH DEV, V27, P201, DOI 10.1046/j.1365-2214.2001.00213.x Richdale A, 2000, J INTELLECT DEV DIS, V25, P147 Richdale AL, 1999, J INTELL DISABIL RES, V43, P380, DOI 10.1046/j.1365-2788.1999.043005380.x 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 Schreck KA, 2001, BEHAV INTERVENT, V16, P265, DOI 10.1002/bin.98 SCOTT G, 1990, CHILD CARE HLTH DEV, V16, P283, DOI 10.1111/j.1365-2214.1990.tb00662.x Stores G, 2001, CLIN GUIDE SLEEP DIS Stores G, 1996, J CHILD PSYCHOL PSYC, V37, P907, DOI 10.1111/j.1469-7610.1996.tb01489.x Thackeray EJ, 2002, BEHAV INTERVENT, V17, P211, DOI 10.1002/bin.123 Weiskop S, 2001, AUTISM, V5, P209, DOI 10.1177/1362361301005002009 Wiggs L, 1998, BRIT J HEALTH PSYCH, V3, P345 Wiggs L, 1996, J APPL RES INTELLECT, V9, P159 Wiggs L, 2000, SLEEP MED REV, V4, P299, DOI 10.1053/smrv.1999.0094 NR 32 TC 51 Z9 51 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD MAR PY 2004 VL 30 IS 2 BP 139 EP 150 DI 10.1111/j.1365-2214.2004.00395.x PG 12 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 774NG UT WOS:000188988900006 PM 14961866 ER PT J AU Nader, R Oberlander, TF Chambers, CT Craig, KD AF Nader, R Oberlander, TF Chambers, CT Craig, KD TI Expression of pain in children with autism SO CLINICAL JOURNAL OF PAIN LA English DT Article; Proceedings Paper CT 21st Annual Meeting of the American-Pain-Society CY MAR 14-17, 2002 CL BALTIMORE, MD SP Amer Pain Soc DE autism; pain; facial expression; behavioral measures; parent report ID FACIAL CODING SYSTEM; INFANTILE-AUTISM; VENIPUNCTURE PAIN; DISABILITIES; VALIDATION; RESPONSES; RATINGS; RESPONSIVENESS; INDIVIDUALS; IMPAIRMENT AB Objectives: Reduced pain sensitivity is widely reported to be a common feature of children with autism, yet this conclusion frequently has been based on anecdotal observations and questionable measures of pain. The aims of the study were to (1) characterize the behavioral response of children with autism experiencing a venepuncture using objective observational measures of pain and distress, (2) examine parents' assessments of pain behavior in children with and without autism, including comparison of the relationship of parental reports with behavioral measures, and (3) compare the behavioral reactions and parental assessments of children with autism with children without autism undergoing venepuncture. Methods: Pain reactions to the invasive procedure of venepuncture were videotaped, systematically described and compared in 21 children with autism (3-7 years old) and 22 nonimpaired children, the latter providing a chronological age and gender equivalent comparison group. Parents provided observer reports of pain, and facial activity was used as an objective behavioral measure of pain. Results: The children with autism displayed a significant facial pain reaction in response to the venepuncture procedure. There was a lack of concordance between parental reports of pain and observed pain responses for the children with autism. Behavioral responses of the children with autism were generally similar to the comparison group, except the substantial facial pain reactivity instigated by the venepuncture in the children with autism exceeded that displayed by the nonimpaired comparison children. Parent reports of pain severity did not differ between the autism and comparison groups. The degree of concordance between parental report and observed pain responses was consistently better for the comparison group. Discussion: The findings demonstrate that children with autism display a significant behavioral reaction in response to a painful stimulus, and these findings are in sharp contrast to the prevailing beliefs of pain insensitivity described in the literature to date. The findings also raise questions about the appropriateness of parental global report as an assessment tool for pain in children with autism. C1 Univ British Columbia, Dept Psychol, Vancouver, BC V6T 1Z4, Canada. Univ British Columbia, Sunny Hill Hlth Ctr Children, Div Dev Pediat, Vancouver, BC V5Z 1M9, Canada. Univ British Columbia, Ctr Commun Child Hlth Res, Vancouver, BC V5Z 1M9, Canada. Univ British Columbia, Dept Pediat, Vancouver, BC V5Z 1M9, Canada. BC Res Inst CHildrens & Womens Hlth, Ctr Community Child Hlth Res, Vancouver, BC, Canada. RP Nader, R (reprint author), Univ British Columbia, Dept Psychol, 2136 W Mall, Vancouver, BC V6T 1Z4, Canada. 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Three- to four-year-old children with autism spectrum disorder (ASD; n = 72), 3- to 4-year-old developmentally delayed children (n = 34), and 12- to 46-month-old typically developing children (n = 39), matched on mental age, were compared on measures of social orienting, joint attention, and attention to another's distress. Children with autism performed significantly worse than the comparison groups in all of these domains. Combined impairments in joint attention and social orienting were found to best distinguish young children with ASD from those without ASD. Structural equation modeling indicated that joint attention was the best predictor of concurrent language ability. Social orienting and attention to distress were indirectly related to language through their relations with joint attention. These results help to clarify the nature of social attention impairments in autism, offer clues to developmental mechanisms, and suggest targets for early intervention. 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However, few specific guidelines have been delineated for conducting these skills assessments or interpreting the results. In this study, we evaluated an efficient methodology for conducting skills assessments. Six children who had been diagnosed with autism participated. The relative efficacy of two assessment packages-one containing several reinforcement procedures and one containing several potentially effective prompts-was evaluated across two to three skills for each child using Multiple baseline and reversal designs. Results suggested that the methodology was useful for matching targeted skills to appropriate interventions. C1 Louisiana State Univ, Baton Rouge, LA 70803 USA. Louisiana Ctr Excellence Autism, Baton Rouge, LA 70803 USA. RP Lerman, DC (reprint author), Louisiana State Univ, 236 Audubon Hall, Baton Rouge, LA 70803 USA. 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S., 2001, MAKING DIFFERENCE BE, P37 MAURICE C, 1996, BEHAV INTERVENTION Y McComas JJ, 1996, J APPL BEHAV ANAL, V29, P397, DOI 10.1901/jaba.1996.29-397 McDonough K. A., 1996, BEHAV INTERVENTION Y, P63 NEEF NA, 1983, J APPL BEHAV ANAL, V16, P81, DOI 10.1901/jaba.1983.16-81 Noell GH, 2001, J SCHOOL PSYCHOL, V39, P335, DOI 10.1016/S0022-4405(01)00072-3 Notari A., 1990, J EARLY INTERVENTION, V14, P117 PARRISH JM, 1986, J APPL BEHAV ANAL, V19, P241, DOI 10.1901/jaba.1986.19-241 Richman DM, 2001, J APPL BEHAV ANAL, V34, P289, DOI 10.1901/jaba.2001.34-289 Roane HS, 2001, J APPL BEHAV ANAL, V34, P333, DOI 10.1901/jaba.2001.34-333 Romanczyk R. G., 2001, PRESCHOOL ED PROGRAM, P49 RUSSO DC, 1981, J APPL BEHAV ANAL, V14, P209, DOI 10.1901/jaba.1981.14-209 NR 25 TC 11 Z9 11 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 2004 VL 37 IS 1 BP 11 EP 26 DI 10.1901/jaba.2004.37-11 PG 16 WC Psychology, Clinical SC Psychology GA 808CG UT WOS:000220546600002 PM 15154212 ER PT J AU Moore, JW Fisher, WW Pennington, A AF Moore, JW Fisher, WW Pennington, A TI Systeamtic application and removal of protective equipment in the assessment of multiple topographies of self-injury SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE automatic reinforcement; functional analysis; protective equipment; self-injurious behavior ID FUNCTIONAL-ANALYSIS; BEHAVIOR AB We evaluated the effects of systematic application and removal of protective equipment on three topographies of self-injurious behavior (SIB) exhibited by a girl who had been diagnosed with autism. Results showed that when protective equipment was applied, SIB decreased to near-zero levels. In addition, withdrawal of protective equipment for specific topographies of SIB (by removing only the corresponding padding) increased rates of SIB only for that topography of SIB. Next, a functional analysis of hand SIB showed that protective equipment suppressed this behavior in all conditions and that the behavior was maintained by automatic reinforcement when padding was removed. Results are discussed in terms of sensory extinction as a possible mechanism responsible for response suppression. RP Moore, JW (reprint author), May S Inc, 1770 Exchange,Suite 140, Atlanta, GA 30339 USA. EM jmoore@mayinstitute.org CR Borrero JC, 2002, J APPL BEHAV ANAL, V35, P69, DOI 10.1901/jaba.2002.35-69 DORSEY MF, 1982, J APPL BEHAV ANAL, V15, P217, DOI 10.1901/jaba.1982.15-217 FISHER WW, 1994, J APPL BEHAV ANAL, V27, P447, DOI 10.1901/jaba.1994.27-447 Fisher WW, 1996, J APPL BEHAV ANAL, V29, P117, DOI 10.1901/jaba.1996.29-117 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Le DD, 2002, J DEV PHYS DISABIL, V14, P277, DOI 10.1023/A:1016028522569 RINCOVER A, 1978, J ABNORM CHILD PSYCH, V6, P299, DOI 10.1007/BF00924733 NR 7 TC 15 Z9 16 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 2004 VL 37 IS 1 BP 73 EP 77 DI 10.1901/jaba.2004.37-73 PG 5 WC Psychology, Clinical SC Psychology GA 808CG UT WOS:000220546600007 PM 15154217 ER PT J AU Taylor, BA Hughes, CE Richard, E Hoch, H Coello, AR AF Taylor, BA Hughes, CE Richard, E Hoch, H Coello, AR TI Teaching teenagers with autism to seek assistance when lost SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; safety skills; vibrating pager; getting lost; seeking assistance ID TACTILE PROMPT; INITIATIONS; CHILDREN AB Three teenagers with autism were taught to respond to a vibrating pager to seek assistance in community settings when physically separated from their parents or teachers. A multiple baseline probe design across participants demonstrated that, upon being paged, participants successfully handed a communication card to a community member indicating that they were lost. Generalization was assessed in nontraining community sites and on outings with the participants' parents. C1 Alpine Learning Grp, Paramus, NJ 07652 USA. CUNY, Grad Ctr, New York, NY USA. RP Taylor, BA (reprint author), Alpine Learning Grp, 777 Paramus Rd, Paramus, NJ 07652 USA. EM algbt@opcenter.net CR POCHE C, 1981, J APPL BEHAV ANAL, V14, P169, DOI 10.1901/jaba.1981.14-169 RISLEY R, 1980, BEHAV MODIF, V4, P513, DOI 10.1177/014544558044006 Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 Taylor BA, 1998, J APPL BEHAV ANAL, V31, P651, DOI 10.1901/jaba.1998.31-651 NR 4 TC 14 Z9 14 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 2004 VL 37 IS 1 BP 79 EP 82 DI 10.1901/jaba.2004.37-79 PG 4 WC Psychology, Clinical SC Psychology GA 808CG UT WOS:000220546600008 PM 15154218 ER PT J AU Falcomata, TS Roane, HS Hovanetz, AN Kettering, TL Keeney, KM AF Falcomata, TS Roane, HS Hovanetz, AN Kettering, TL Keeney, KM TI An evaluation of response cost in the treatment of inappropriate vocalizations maintained by automatic reinforcement SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; automatic reinforcement; inappropriate vocalizations; noncontingent reinforcement; response cost ID DEVELOPMENTAL-DISABILITIES; ABERRANT BEHAVIOR; SELF-INJURY AB In the current study, we examined the utility of a procedure consisting of noncontingent reinforcement with and without response cost in the treatment of inappropriate vocalizations maintained by automatic reinforcement. Results are discussed in terms of examining the variables that contribute to the effectiveness of response cost as treatment for problem behavior maintained by automatic reinforcement. C1 Marcus Inst, Atlanta, GA 30329 USA. Emory Univ, Sch Med, Atlanta, GA 30322 USA. RP Roane, HS (reprint author), Marcus Inst, 1920 Briarcliff Rd, Atlanta, GA 30329 USA. EM roane@marcus.org CR IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Keeney KM, 2000, J APPL BEHAV ANAL, V33, P255, DOI 10.1901/jaba.2000.33-255 MASON SA, 1990, J APPL BEHAV ANAL, V23, P361, DOI 10.1901/jaba.1990.23-361 Shore BA, 1997, J APPL BEHAV ANAL, V30, P21, DOI 10.1901/jaba.1997.30-21 VOLLMER TR, 1994, RES DEV DISABIL, V15, P187, DOI 10.1016/0891-4222(94)90011-6 Vollmer TR, 1995, J APPL BEHAV ANAL, V28, P561, DOI 10.1901/jaba.1995.28-561 NR 6 TC 33 Z9 33 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SPR PY 2004 VL 37 IS 1 BP 83 EP 87 DI 10.1901/jaba.2004.37-83 PG 5 WC Psychology, Clinical SC Psychology GA 808CG UT WOS:000220546600009 PM 15154219 ER PT J AU Nikopoulos, CK Keenan, M AF Nikopoulos, CK Keenan, M TI Effects of video modeling on social initiations by children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT Annual Meeting of the Experimental-Analysis-of-Behaviour-Group CY MAR, 2002 CL London, ENGLAND SP Exptl Anal Behav Grp DE autism; children; video modeling; social interaction; reciprocal play ID SKILLS AB We examined the effects of a video modeling intervention on social initiation and play behaviors with 3 children with autism using a multiple baseline across subjects design. Each child watched a videotape showing a typically developing peer, and the experimenter engaged in a simple social interactive play using one toy. For all children, social initiation and reciprocal play skills were enhanced, and these effects were maintained at 1- and 3-month follow-up periods. C1 Univ Ulster, Sch Psychol, Coleraine BT52 1SA, Londonderry, North Ireland. RP Nikopoulos, CK (reprint author), Univ Ulster, Sch Psychol, Cromore Rd, Coleraine BT52 1SA, Londonderry, North Ireland. CR KOEGEL LK, 2001, BEHAV MODIF, V25, P754 LeBlanc LA, 2003, J APPL BEHAV ANAL, V36, P253, DOI 10.1901/jaba.2003.36-253 Schopler E, 2002, CHILDHOOD AUTISM RAT Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 NR 5 TC 84 Z9 85 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 2004 VL 37 IS 1 BP 93 EP 96 DI 10.1901/jaba.2004.37-93 PG 4 WC Psychology, Clinical SC Psychology GA 808CG UT WOS:000220546600011 PM 15154221 ER PT J AU Rehfeldt, RA Kinney, EM Root, S Stromer, R AF Rehfeldt, RA Kinney, EM Root, S Stromer, R TI Creating activity schedules using microsoft (R) powerpoint (R) SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE activity schedules; autism; computers; PowerPoint (R) ID SCRIPT-FADING PROCEDURE; PHOTOGRAPHIC ACTIVITY SCHEDULES; SOCIAL-INTERACTION SKILLS; TEACHING-CHILDREN; AUTISM; BEHAVIOR; ADULTS AB We describe how PowerPoint(R) presentation software can be used to create computer activity schedules to teach individuals with special needs. Presented are the steps involved in creating activity schedules with close-ended and open-ended activities, and for preparing schedules that include photos, sounds, text, and videos that can be used to occasion an individual's engagement in a variety of learning activities. C1 So Illinois Univ, Inst Rehabil, Rehabil Serv Program, Carbondale, IL 62901 USA. Univ Massachusetts, Sch Med, Shriver Ctr, Waltham, MA 02254 USA. RP Rehfeldt, RA (reprint author), So Illinois Univ, Inst Rehabil, Rehabil Serv Program, Carbondale, IL 62901 USA. EM rehfeldt@siu.edu CR DAUPHIN M, IN PRESS J POSITIVE Dixon MR, 2003, J APPL BEHAV ANAL, V36, P271, DOI 10.1901/jaba.2003.36-271 Dowrick P. W., 1991, PRACTICAL GUIDE USIN Kimball J., 2003, TEACHING EXCEPTIONAL, V36, P40 KIMBALL JW, 2003, UNPUB VIDEO ENHANCED Kinney EM, 2003, J POSIT BEHAV INTERV, V5, P22, DOI 10.1177/10983007030050010301 Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P137, DOI 10.1901/jaba.1993.26-137 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 LALLI JS, 1994, J APPL BEHAV ANAL, V27, P705, DOI 10.1901/jaba.1994.27-705 MACDUFF GS, 1993, J APPL BEHAV ANAL, V26, P89, DOI 10.1901/jaba.1993.26-89 McClannahan L. E., 1999, ACTIVITY SCHEDULES C McClannahan LE, 2002, BEHAV MODIF, V26, P9, DOI 10.1177/0145445502026001002 NEUMANN L, 1999, VISUAL TEACHING METH Rehfeldt RA, 2003, RES DEV DISABIL, V24, P333, DOI 10.1016/S0891-4222(03)00059-3 Rehfeldt RA, 2003, BEHAV INTERVENT, V18, P209, DOI 10.1002/bin.139 Rehfeldt RA, 2002, BEHAV ANALYST, V25, P103 RUBIN M, 2002, LITTLE DIGITAL VIDEO Stevenson CL, 2000, BEHAV INTERVENT, V15, P1, DOI 10.1002/(SICI)1099-078X(200001/03)15:1<1::AID-BIN41>3.0.CO;2-V STROMER R, 2002, IN PRESS BEHAV MODIF Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 NR 21 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 SPR PY 2004 VL 37 IS 1 BP 115 EP 128 DI 10.1901/jaba.2004.37-115 PG 14 WC Psychology, Clinical SC Psychology GA 808CG UT WOS:000220546600016 PM 15154226 ER PT J AU Beadle-Brown, J AF Beadle-Brown, J TI Elicited imitation in children and adults with autism: the effect of different types of actions SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE autism; developmental perspective; imitation ID SYMBOLIC PLAY; MIND; REPRESENTATION; DISORDERS; DEFICITS AB Background It was proposed by Rogers & Pennington (1991) that an early deficit in imitation, together with a cascade of developmental disorders in emotion sharing and Theory of Mind, could be important in understanding autism. Having already found that imitation appeared not to be specifically or universally impaired in autism, the present study tested whether there were distinctions between different types of actions, such as symbolic versus non-symbolic, one-handed versus two-handed or symmetrical versus asymmetrical actions, on a test of elicited imitation. Methods A large battery of tasks was used to elicit imitation from three groups of autistic children and adults (aged 4-34 years of age), two groups of typically developing children and a group of children with mild-to-moderate intellectual disabilities. Results The majority of children and adults with autism had few impairments relative to the controls, although certain actions did seem more difficult, especially for the youngest children. For example, actions within the categories of 'symbolic actions' and 'asymmetrical actions' seemed to give some groups more problems. Certain types of errors such as hand reversals and using body parts as objects were found in both autistic and non-autistic groups, but, for the most part, in the youngest children in the whole sample. A final analysis compared the number of partial imitations for eight specific actions. Conclusions The overall picture was not one of an autism-specific deficit in imitation, but rather of a normal (i.e. age-related) developmental trend. These results are discussed in terms of Rogers & Pennington's theory and other leading theories. C1 Univ Kent, Tizard Ctr, Beverley Farm, Canterbury CT2 7LZ, Kent, England. RP Beadle-Brown, J (reprint author), Univ Kent, Tizard Ctr, Beverley Farm, Canterbury CT2 7LZ, Kent, England. EM j.d.beadle-brown@kent.ac.uk CR ABRAHAMSEN EP, 1990, J AUTISM DEV DISORD, V20, P75, DOI 10.1007/BF02206858 Bard K. A., 1995, BEHAVIOUR, V132, P839, DOI DOI 10.1163/156853995X00036 BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BEADLEBROWN J, 2004, IN PRESS J INTELLECT Bishop DVM, 1983, TEST RECEPTION GRAMM Braten S, 1999, INTERSUBJECTIVE COMM CHARMAN T, 1994, DEV PSYCHOPATHOL, V6, P403, DOI 10.1017/S0954579400006015 CURCIO F, 1978, J AUTISM CHILD SCHIZ, V8, P181, DOI 10.1007/BF01537867 DAWSON G, 1984, J ABNORM CHILD PSYCH, V12, P209, DOI 10.1007/BF00910664 Dawson G, 1989, AUTISM NATURE DIAGNO DAWSON G, 1991, ROCH S DEV PSYCH, V3 DEMYER MK, 1972, J AUTISM CHILD SCHIZ, V2, P264, DOI 10.1007/BF01537618 Dunn L M., 1982, BRIT PICTURE VOCABUL HAMMES JGW, 1981, J AUTISM DEV DISORD, V11, P331, DOI 10.1007/BF01531515 HEIMANN M, 1992, BEHAV NEUROL, V5, P219, DOI 10.3233/BEN-1992-5404 Heimann M., 1999, IMITATION INFANCY, P235 HERZIG ME, 1989, J AM ACAD CHILD ADOL, V28, P195 Hobson R. Peter, 1993, AUTISM DEV MIND HUGHES C, 1993, DEV PSYCHOL, V29, P496 JONES V, 1985, J AUTISM DEV DISORD, V15, P37, DOI 10.1007/BF01837897 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 LIBBY S, 1998, J AUTISM DEV DISORD, V27, P365 MELTZOFF AN, 1988, CHILD DEV, V59, P217, DOI 10.2307/1130404 MORGAN SB, 1989, J CHILD PSYCHOL PSYC, V30, P857, DOI 10.1111/j.1469-7610.1989.tb00287.x Nadel J., 1999, IMITATION INFANCY, P209 Nadel J, 1993, NEW PERSPECTIVES EAR, P139 OHTA M, 1987, J AUTISM DEV DISORD, V17, P45, DOI 10.1007/BF01487259 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Piaget J, 1962, PLAY DREAMS IMITATIO Rogers S. J., 1991, DEV PSYCHOPATHOL, V3, P137, DOI DOI 10.1017/S0954579400000043 ROGERS SJ, 1993, COMMUNICATION Rogers SJ, 1996, CHILD DEV, V67, P2060, DOI 10.2307/1131609 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 SMITH IM, 1995, SOC RES CHILD DEV IN Stern D., 1985, INTERPERSONAL WORLD STONE WL, 1990, PEDIATRICS, V86, P267 THATCHER M, 1977, THESIS CALIFORNIA I Whiten A., 2000, AUTISM, V4, P185, DOI 10.1177/1362361300004002006 WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 43 TC 5 Z9 5 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD MAR PY 2004 VL 17 IS 1 BP 37 EP 48 DI 10.1111/j.1468-3148.2004.00159.x PG 12 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 773HP UT WOS:000188892800007 ER PT J AU Jervis, N Baker, M AF Jervis, N Baker, M TI Clinical and research implications of an investigation into Theory of Mind (TOM) task performance in children and adults with non-specific intellectual disabilities SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE intellectual disabilities; Theory of Mind; social ID FALSE BELIEF; LEARNING-DISABILITIES; MENTAL-RETARDATION; AUTISM; INDIVIDUALS; ABILITY; PEOPLE AB Background Theory of Mind (TOM) has rarely been studied in people with intellectual disabilities. Wherever it has been studied, differing results have been found. These may be attributed to a variety of factors (e.g. the different chronological ages of samples). The validity of relating TOM performance to social behaviour has also been questioned in this population. The aim of this study was to compare TOM scores with chronological age and social ability in an attempt to contribute to current debate. Methods Twenty children were matched individually with 20 adults, all with non-specific intellectual disabilities. The British Picture Vocabulary Scale, Raven's Coloured Progressive Matrices and four TOM tasks were administered to the participants. Their carers were then given various sociability measures to complete. Results The children achieved significantly higher TOM scores than did the adults. TOM and social ability were significantly positively correlated for the children, but not for the adults. These results are discussed in terms of the different social experiences of adults and children with intellectual disabilities. Conclusions Longitudinal research in this area is needed to clarify the present findings. If confirmed, the suitability of some TOM tasks used may be questionable, and there are clear implications for staff and client training. C1 Manchester Learning Disabil Partnership, N Community Team Resource Ctr, Manchester M9 5XS, Lancs, England. Univ E London, London E15 4LZ, England. RP Jervis, N (reprint author), Manchester Learning Disabil Partnership, N Community Team Resource Ctr, Beech Manor, Manchester M9 5XS, Lancs, England. EM nicola.jervis@notes.manchester.gov.uk CR Ashcroft A, 1999, J APPL RES INTELLECT, V12, P58 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 2000, UNDERSTANDING OTHER BENSON G, 1993, AM J MENT RETARD, V98, P427 Bluma S., 1976, PORTAGE GUIDE EARLY Chappell A. L., 1992, DISABILITY HANDICAP, V7, P35, DOI 10.1080/02674649266780041 Charman T, 1998, J AUTISM DEV DISORD, V28, P33, DOI 10.1023/A:1026058802381 CHARMAN T, 1992, J CHILD PSYCHOL PSYC, V33, P1105, DOI 10.1111/j.1469-7610.1992.tb00929.x CHARMAN T, 1996, UNPUB DOES THEORY MI Charman T, 1998, COGNITIVE DEV, V13, P307, DOI 10.1016/S0885-2014(98)90013-2 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 DUNST CJ, 1990, CHILDREN DOWNS SYNDR FACON B, 1993, J INTELL DISABIL RES, V37, P373 Fonagy P, 1997, BRIT J DEV PSYCHOL, V15, P51 FRITH U, 1989, AUTISM EXPLAININ ENI Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X GOPNIK A, 1988, CHILD DEV, V59, P26, DOI 10.2307/1130386 Hadwin J, 1997, J AUTISM DEV DISORD, V27, P519, DOI 10.1023/A:1025826009731 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R Harris P., 1989, COGNITION EMOTION, V3, P379, DOI DOI 10.1080/02699938908412713 Kavale KA, 1996, J LEARN DISABIL, V29, P226 Kline P., 1993, HDB PSYCHOL TESTING LALONDE CE, 1995, COGNITION EMOTION, V9, P167, DOI 10.1080/02699939508409007 MCGEE JJ, 1985, GENTLE TEACHING NONA PRIOR M, 1990, J CHILD PSYCHOL PSYC, V31, P587, DOI 10.1111/j.1469-7610.1990.tb00799.x Raven J. C., 1984, COLOURED PROGR MATRI Siegel S., 1988, NON PARAMETRIC STAT Sparrow S, 1984, VINELAND ADAPTIVE BE WEISZ JR, 1981, PSYCHOL BULL, V90, P153, DOI 10.1037/0033-2909.90.1.153 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 33 TC 7 Z9 8 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD MAR PY 2004 VL 17 IS 1 BP 49 EP 57 DI 10.1111/j.1468-3148.2004.00172.x PG 9 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 773HP UT WOS:000188892800008 ER PT J AU Gagliano, A Germano, E Pustorino, G Impallomeni, C D'Arrigo, C Calamoneri, F Spina, E AF Gagliano, A Germano, E Pustorino, G Impallomeni, C D'Arrigo, C Calamoneri, F Spina, E TI Risperidone treatment of children with autistic disorder: Effectiveness, tolerability, and pharmacokinetic implications SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; NEUROLEPTIC-RELATED DYSKINESIAS; YOUNG-CHILDREN; BEHAVIORAL SYMPTOMS; INFANTILE-AUTISM; PROLACTIN LEVELS; RATING-SCALE; OPEN TRIAL; HALOPERIDOL; SCHIZOPHRENIA AB Background: Recent evidence indicates that atypical antipsychotics represent a promising option for the treatment of autistic disorder. In particular, risperidone appears to be effective in treating aggressiveness, hyperactivity, irritability, stereotypies, social withdrawal, and lack of interests. Objective: The aim of the present study was to evaluate the effectiveness and tolerability of risperidone in children with autistic disorder and to examine the correlation between plasma levels of risperidone and its active metabolite 9-hydroxyrisperidone (9-OH-risperidone) and the clinical response. Methods: The effect of treatment with risperidone (0.75-2 mg/day; mean +/-SD dose = 1.26 +/- 0.42 mg/day) was studied for 24 weeks in 20 children (14 boys, 6 girls) ages 3 to 10 years (mean age 6.0 +/- 2.4 years), diagnosed with autistic disorder. Fourteen items selected from the Children's Psychiatric Rating Scale (CPRS-14) and Clinical Global Impression (CGI) were used for behavioral evaluation. Patients were classified as responders if they showed a 25% or greater decrease on CPRS-14 total score at final evaluation compared with baseline and a final CGI rating of 1 or 2. Patients were rated for extrapyramidal side effects on the Abnormal Involuntary Movement Scale (AIMS). Other side effects, including the expected side effects of atypical antipsychotics drugs, were assessed by a checklist. Blood samples for determination of risperidone and its active metabolite 9-OH-risperidone were obtained after 12 weeks, and serum prolactin levels were measured on admission and at weeks 12 and 24. Results: The psychopathological state, as assessed by CPRS, improved significantly over the duration of treatment. The mean CPRS-14 scores decreased significantly from 63.7 +/- 10.0 at baseline to 52.9 +/- 14.3 at week 12 (p < 0.01). At the end of 12 weeks of treatment, 8 patients were considered responders, and 10 patients reached a minimal improvement. No further improvement was observed in the following 12 weeks. In all children, serum prolactin levels increased significantly (p < 0.001) from 166 88 UI/mL at baseline to 504 +/- 207 Ul/mL at week 12 of risperidone treatment. Weight gain and increased appetite were the most common unwanted effects. A mean increase of 3.7 +/- 1.7 kg in body weight was observed at final evaluation as compared with baseline. There was no significant correlation between percent improvement in total CPRS score and the plasma level of risperidone's active fractions (the sum of the risperidone and 9-OH-risperidone plasma concentration). Conclusions: This study provides further evidence of the beneficial effects of risperidone in children diagnosed with autistic disorder. However, the potential advantages of risperidone should be weighed against the risk of unwanted effects, such as an increase in serum prolactin levels and weight gain. No relation was observed between total plasma risperidone and 9-OH-risperidone concentrations and clinical response. C1 Univ Messina, Div Child Neurol & Psychiat, Messina, Italy. Univ Messina, Pharmacol Sect, Dept Clin & Expt Med & Pharmacol, Messina, Italy. RP Gagliano, A (reprint author), Policlin Univ, Div Child Neurol & Psychiat, Via Consolare Valeria, I-98125 Messina, Italy. 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Child Adolesc. Psychopharmacol. PD SPR PY 2004 VL 14 IS 1 BP 39 EP 47 DI 10.1089/104454604773840472 PG 9 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 815SK UT WOS:000221061800006 PM 15142390 ER PT J AU Stigler, KA Desmond, LA Posey, DJ Wiegand, RE McDougle, CJ AF Stigler, KA Desmond, LA Posey, DJ Wiegand, RE McDougle, CJ TI A naturalistic retrospective analysis of psychostimulants in pervasive developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; MENTALLY-RETARDED CHILDREN; EARLY INFANTILE-AUTISM; SCHIZOPHRENIC CHILDREN; METHYLPHENIDATE; ADHD; RETARDATION; EFFICACY; DRUG; PHARMACOTHERAPY AB Objective: We set out to examine the effectiveness and tolerability of psychostimulants in children and adolescents with pervasive developmental disorders (PDDs). Methods: Medical records of all patients with PDDs treated with a stimulant were retrospectively reviewed. Demographics, stimulant type, drug dosage, trial duration, and adverse effects were recorded. Global improvement, focused on symptoms of hyperactivity and inattention, was measured by the Clinical Global Impressions-Improvement scale, with positive response defined by a rating of much improved or very much improved. Results: Of 195 patients (174 males, 21 females; mean age +/-SD = 7.26 +/- 3.45 years, range 2-19 years), 61 had more than one trial, resulting in a total of 274 separate stimulant trials. It was discovered that 24.6%, 23.2%, and 11.1% of patients with a history of one, two, or three stimulant trials, respectively, responded to their first stimulant trial. Among first trial nonresponders, 6 (14.0%) of 43 patients responded to a second trial. Of those who did not respond to their first or second stimulant trial, 2 (14.3%) of 14 patients responded to a third trial. Patients with Asperger's disorder, in contrast to those with autistic disorder or PDD not otherwise specified, were significantly more likely to respond to a stimulant trial (p < 0.01). Use of concomitant medication (p < 0.007) positively affected response, whereas no association was found between stimulant type and IQ and response. Adverse effects, including agitation, dysphoria, and irritability, often occurred (154 [57.5%] of 268 trials, with 6 missing values). Conclusions: Overall, stimulants appeared ineffective and poorly tolerated for the majority of patients with PDDs. Response may differ with PDD subtype. Controlled studies are needed to further evaluate these preliminary findings in a systematic manner. C1 Indiana Univ, Sch Med, Dept Psychiat, James Whitcomb Riley Hosp Children, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, 1111 W 10th St,Psychiat Bldg,PB A305, Indianapolis, IN 46202 USA. 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PD SPR PY 2004 VL 14 IS 1 BP 49 EP 56 DI 10.1089/104454604773840481 PG 8 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 815SK UT WOS:000221061800007 PM 15142391 ER PT J AU Palermo, MT Curatolo, P AF Palermo, MT Curatolo, P TI Pharmacologic treatment of autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; OBSESSIVE-COMPULSIVE DISORDER; GENE PROMOTER VARIANTS; DOUBLE-BLIND; INFANTILE-AUTISM; SEROTONIN TRANSPORTER; SPECTRUM DISORDERS; OPEN-LABEL; BEHAVIORAL SYMPTOMS; ASPERGER-SYNDROME AB Autism is a chronic and lifelong pervasive developmental disorder for which there is yet no effective cure, and medical management remains a major challenge for clinicians. In spite of the possible similarities with conditions that have an established pharmacotherapy, and despite improvements in some associated "problematic behaviors" following the use of available medications, effective medical treatment for the core symptoms involving language and social cognition remains elusive. The purpose of the present article is to review current biologic knowledge about autism in an attempt to correlate clinical trials with known mechanisms of disease. In addition, the need for controlled studies and for the creation of homogeneous subgroups of patients based on clinical and genetic characteristics is emphasized. The application of molecular genetic investigations and pharmacogenetics in the diagnostic work-up of autistic patients can lead to more effective individualized medical care. C1 Assoc Anni Verdi, Res Ctr Autism, I-00148 Rome, Italy. Univ Roma Tor Vergata, Dept Child Neuropsychiat & Pediat Neurol, Rome, Italy. 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Child Neurol. PD MAR PY 2004 VL 19 IS 3 BP 155 EP 164 PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 813PD UT WOS:000220918100001 PM 15119475 ER PT J AU Chez, MG Aimonovitch, M Buchanan, T Mrazek, S Tremb, RJ AF Chez, MG Aimonovitch, M Buchanan, T Mrazek, S Tremb, RJ TI Treating autistic spectrum disorders in children: Utility of the cholinesterase inhibitor rivastigmine tartrate SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID EARLY INFANTILE-AUTISM; ALZHEIMERS-DISEASE; CEREBELLAR ABNORMALITIES; CONTROLLED TRIAL; US MULTICENTER; DOUBLE-BLIND; DONEPEZIL; EFFICACY; SAFETY AB Rivastigmine tartrate is a dual-action cholinesterase inhibitor shown to improve language, cognition, and global functioning in patients with Alzheimer's disease, likely via increased availability of cerebral acetylcholine. Because cholinergic receptor abnormalities can contribute to the neuropathology of autistic spectrum disorders, rivastigmine tartrate could prove to be an effective therapy for affected children. Observations of improved behavior and language output from prior open-label and double-blind treatment of autistic children with donepezil, another cholinesterase inhibitor, prompted this 12-week open-label study with rivastigmine tartrate of 32 autistic patients. Therapeutic indices were the Childhood Autistic Rating Scale, Gardner's Expressive and Receptive One-Word Picture Vocabulary tests, and the Conners' Parent Rating Scale. Testing administered at baseline, 6 weeks, and 12 weeks showed gains in both expressive speech and overall autistic behavior over baseline. These improvements were statistically significant and supported the hypothesis that treatment with cholinergic enhancing drugs in autistic spectrum disorders yields positive therapeutic effects. C1 Autism & Epilepsy Specialty Serv Illinois Ltd, Lake Bluff, IL USA. RP Chez, MG (reprint author), 1900 Hollister Dr,Suite 220, Libertyville, IL 60048 USA. 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PD MAR PY 2004 VL 19 IS 3 BP 165 EP 169 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 813PD UT WOS:000220918100002 PM 15119476 ER PT J AU Macintosh, KE Dissanayake, C AF Macintosh, KE Dissanayake, C TI Annotation: The similarities and differences between autistic disorder and Asperger's disorder: a review of the empirical evidence SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Asperger's disorder; autistic disorder; classification; diagnosis; pervasive developmental disorder; high-functioning autism ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; CLUSTER-ANALYSIS; CHILDREN; VALIDITY; LANGUAGE; SUBTYPES; MIND; CLUMSINESS AB Background: The ongoing controversy over the distinction between autistic disorder and Asperger's disorder is important to resolve because of the implications regarding an understanding of the aetiology and prognosis, and the diagnostic and clinical practices relating to these conditions. This paper provides a critical evaluation of current published research evidence. Method: Databases, such as PsychINFO and Medline, as well as book chapters, reference lists from relevant articles, and recent editions of key journals were searched for all relevant studies (until 2002) which incorporated participants diagnosed with high-functioning autism and Asperger's disorder using either cluster analysis or comparative approaches to examine similarities and differences between these groups. Keywords used in the searches included autistic disorder, Asperger's disorder, autism, high-functioning autism, and pervasive developmental disorder. Results: On the basis of the available evidence, there seem to be few qualitative differences between autistic disorder and Asperger's disorder. Conclusion: There is currently insufficient evidence to establish the validity of Asperger's disorder as a syndrome distinct from high-functioning autism. 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Psychiatry PD MAR PY 2004 VL 45 IS 3 BP 421 EP 434 DI 10.1111/j.1469-7610.2004.00234.x PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WD UT WOS:000221788500002 PM 15055363 ER PT J AU Kylliainen, A Hietanen, JK AF Kylliainen, A Hietanen, JK TI Attention orienting by another's gaze direction in children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE high-functioning autism; attention orienting; gaze direction; reaction time ID JOINT VISUAL-ATTENTION; FACE RECOGNITION; SOCIAL ATTENTION; EYE-DIRECTION; PERCEPTION; DEFICITS; INFANTS; CUES; ORIENTATION; INDIVIDUALS AB Background: The aim of this study was to investigate attention orienting triggered by another's gaze direction in autism. Method: Twelve high-functioning children with autism and gender- and age-matched normal control children were studied using two tasks. In the first task, children were asked to detect laterally presented target stimuli preceded by centrally presented facial cue stimuli in which gaze was either straight ahead or averted. The direction of the cue was either congruent, neutral, or incongruent with respect to the laterality of the target stimulus. In the second task, children were asked to discriminate the direction of eye gaze. Results: The results showed that another person's static gaze direction triggered an automatic shift of visual attention, both in children with autism and in normally developing children. The children in both groups were also able to overtly discriminate the direction of the gaze. Conclusion: These results seem to suggest that, in children with autism, the visual system processes information about another person's gaze direction and sends this information to those areas that subserve reflexive attention orienting. However, future studies are needed to investigate whether the processing of eyes and gaze direction relies on similar neural mechanisms in children with autism and in normally developing children. C1 Tampere Univ, Dept Psychol, FIN-33014 Tampere, Finland. RP Kylliainen, A (reprint author), Tampere Univ, Dept Psychol, FIN-33014 Tampere, Finland. 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Child Psychol. Psychiatry PD MAR PY 2004 VL 45 IS 3 BP 435 EP 444 DI 10.1111/j.1469-7610.2004.00235.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WD UT WOS:000221788500003 PM 15055364 ER PT J AU Senju, A Tojo, Y Dairoku, H Hasegawa, T AF Senju, A Tojo, Y Dairoku, H Hasegawa, T TI Reflexive orienting in response to eye gaze and an arrow in children with and without autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article; Proceedings Paper CT 13th Annual Meeting of the Human-Behavior-and-Evolution-Society CY JUN, 2001 CL LONDON, ENGLAND SP Human Behav & Evolut Soc DE autism; eye gaze; joint attention; reflexive orienting; arrow ID DEVELOPMENTAL LANGUAGE DELAY; JOINT ATTENTION SKILLS; VISUAL-ATTENTION; UNIQUE MORPHOLOGY; DIRECTION; DEFICITS; PERCEPTION; INFANT; INDIVIDUALS; MECHANISMS AB Background: This study investigated whether another person's social attention, specifically the direction of their eye gaze, and a non-social directional cue, an arrow, triggered reflexive orienting in children with and without autism in an experimental situation. Methods: Children with autism and typically developed children participated in one of two experiments. Both experiments involved the localization of a target that appeared to the left or right of the fixation point. Before the target appeared, the participant's attention was cued to the left or right by either an arrow or the direction of eye gaze on a computerized face. Results: Children with autism were slower to respond, which suggests a slight difference in the general cognitive ability of the groups. In Experiment 1, although the participants were instructed to disregard the cue and the target was correctly cued in only 50% of the trials, both groups of children responded significantly faster to cued targets than to uncued targets, regardless of the cue. In Experiment 2, children were instructed to attend to the direction opposite that of the cues and the target was correctly cued in only 20% of the trials. Typically developed children located targets cued by eye gaze more quickly, while the arrow cue did not trigger such reflexive orienting in these children. However, both social and non-social cues shifted attention to the cued location in children with autism. Conclusion: These results indicate that eye gaze attracted attention more effectively than the arrow in typically developed children, while children with autism shifted their attention equally in response to eye gaze and arrow direction, failing to show preferential sensitivity to the social cue. Difficulty in shifting controlled attention to the instructed side was also found in children with autism. C1 Univ Tokyo, Tokyo, Japan. Natl Inst Special Educ, Tokyo, Japan. Musashino Womens Univ, Tokyo, Japan. RP Senju, A (reprint author), Univ Tokyo, Tokyo, Japan. EM atsushi@darwin.c.u-tokyo.ac.jp RI Senju, Atsushi/C-4097-2008 OI Senju, Atsushi/0000-0002-8081-7170 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1995, BRIT J DEV PSYCHOL, V13, P379 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Batki A, 2000, INFANT BEHAV DEV, V23, P223, DOI 10.1016/S0163-6383(01)00037-6 Broks P, 1998, NEUROPSYCHOLOGIA, V36, P59, DOI 10.1016/S0028-3932(97)00105-X BUTTERWORTH G, 1991, BRIT J DEV PSYCHOL, V9, P55 Cameron EL, 2002, VISION RES, V42, P949, DOI 10.1016/S0042-6989(02)00039-1 Carrasco M, 2001, P NATL ACAD SCI USA, V98, P5363, DOI 10.1073/pnas.081074098 CASEY BJ, 1993, J CLIN EXP NEUROPSYC, V15, P933, DOI 10.1080/01688639308402609 Charman T, 2000, COGNITIVE DEV, V15, P481, DOI 10.1016/S0885-2014(01)00037-5 Corkum V., 1995, JOINT ATTENTION ITS, P61 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Driver J, 1999, VIS COGN, V6, P509 Eimer M, 1997, BIOL PSYCHOL, V46, P67, DOI 10.1016/S0301-0511(97)05254-X Farroni T, 2000, VIS COGN, V7, P705 Fodor Jerry A., 1983, MODULARITY MIND Friesen CK, 1998, PSYCHON B REV, V5, P490, DOI 10.3758/BF03208827 Goldstein G, 2001, J AUTISM DEV DISORD, V31, P433, DOI 10.1023/A:1010620820786 HALE S, 1990, CHILD DEV, V61, P653, DOI 10.1111/j.1467-8624.1990.tb02809.x Harris NS, 1999, COGNITIVE BRAIN RES, V8, P61, DOI 10.1016/S0926-6410(99)00006-3 Hietanen JK, 1999, NEUROREPORT, V10, P3443, DOI 10.1097/00001756-199911080-00033 Hobson P, 1993, UNDERSTANDING OTHER, P204 Hoffman EA, 2000, NAT NEUROSCI, V3, P80, DOI 10.1038/71152 Hommel B, 2001, PSYCHOL SCI, V12, P360, DOI 10.1111/1467-9280.00367 Hood BM, 1998, PSYCHOL SCI, V9, P131, DOI 10.1111/1467-9280.00024 Hughes C, 1996, J AUTISM DEV DISORD, V26, P99, DOI 10.1007/BF02276237 Jonides J., 1981, ATTENTION PERFORM, V9, P187 Kawashima R, 1999, BRAIN, V122, P779, DOI 10.1093/brain/122.4.779 Kingstone A, 2000, PSYCHOL SCI, V11, P159, DOI 10.1111/1467-9280.00232 Kobayashi H, 2001, J HUM EVOL, V40, P419, DOI 10.1006/jhev.2001.0468 Kobayashi H, 1997, NATURE, V387, P767, DOI 10.1038/42842 LANDRY SH, 1988, J CHILD PSYCHOL PSYC, V29, P621, DOI 10.1111/j.1469-7610.1988.tb01884.x Leekam S, 1997, BRIT J DEV PSYCHOL, V15, P77 Leekam SR, 1998, J CHILD PSYCHOL PSYC, V39, P951, DOI 10.1017/S0021963098003035 Leekam SR, 2000, DEV PSYCHOL, V36, P261, DOI 10.1037/0012-1649.36.2.261 Liss M, 2001, J CHILD PSYCHOL PSYC, V42, P261, DOI 10.1017/S0021963001006679 LOVELAND KA, 1986, J AUTISM DEV DISORD, V16, P335, DOI 10.1007/BF01531663 Minshew N J, 1997, J Int Neuropsychol Soc, V3, P303 Minshew NJ, 1999, NEUROLOGY, V52, P917 Moore C, 1998, BRIT J DEV PSYCHOL, V16, P495 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x Mundy P, 2000, DEV PSYCHOBIOL, V36, P325, DOI 10.1002/(SICI)1098-2302(200005)36:4<325::AID-DEV7>3.0.CO;2-F NEELY J, 2001, THESIS U DURHAM OGAWA T, 2002, KISOSHINRIGAKU KENKY, V21, P31 OKADA T, 2002, SEISHIN IGAKU, V44, P893 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Pascualvaca DM, 1998, J AUTISM DEV DISORD, V28, P467, DOI 10.1023/A:1026091809650 Perner Josef, 1991, UNDERSTANDING REPRES PERRETT DI, 1994, CAH PSYCHOL COGN, V13, P683 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 POSNER MI, 1980, Q J EXP PSYCHOL, V32, P3, DOI 10.1080/00335558008248231 Puce A, 1998, J NEUROSCI, V18, P2188 Ristic J, 2002, PSYCHON B REV, V9, P507, DOI 10.3758/BF03196306 SCAIFE M, 1975, NATURE, V253, P265, DOI 10.1038/253265a0 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 SENJU A, 2003, 10 ANN M COGN NEUR S SENJU A, IN PRESS COGNITION SENJU A, 2001, KISOSHINGIGAKU KENKY, V20, P33 SPENCE CJ, 1994, J EXP PSYCHOL HUMAN, V20, P555, DOI 10.1037//0096-1523.20.3.555 SWETTENHAM J, 2000, J COGNITIVE NEU D SS, V53 Swettenham J, 2003, PHILOS T R SOC B, V358, P325, DOI 10.1098/rstb.2002.1203 Tipples J, 2002, PSYCHON B REV, V9, P314, DOI 10.3758/BF03196287 Tomasello M, 1997, CHILD DEV, V68, P1067, DOI 10.2307/1132292 Tomasello M., 1995, JOINT ATTENTION ITS, P103 Townsend J, 1999, J NEUROSCI, V19, P5632 Townsend J, 1996, J Int Neuropsychol Soc, V2, P541 Vecera S. P., 1995, Visual Cognition, V2, DOI 10.1080/13506289508401722 Wainwright JA, 1996, J AUTISM DEV DISORD, V26, P423, DOI 10.1007/BF02172827 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 YOSHIKAWA S, 2000, SHINRIGAKU HYOURON, V43, P259 NR 71 TC 105 Z9 107 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 2004 VL 45 IS 3 BP 445 EP 458 DI 10.1111/j.1469-7610.2004.00236.x PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WD UT WOS:000221788500004 PM 15055365 ER PT J AU Brosnan, MJ Scott, FJ Fox, S Pye, J AF Brosnan, MJ Scott, FJ Fox, S Pye, J TI Gestalt processing in autism: failure to process perceptual relationships and the implications for contextual understanding SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autistic disorder; gestalt; visuo-spatial functioning ID HIGH-FUNCTIONING PERSONS; WEAK CENTRAL COHERENCE; HEMISPHERIC-DIFFERENCES; SELECTIVE ATTENTION; VISUAL-PERCEPTION; ORGANIZATION; CHILDREN; MIND; INFORMATION; DEFICIT AB Background: Deficits in autism have been characterised as a bias towards local over global processing. This paper examines whether there is a deficit in gestalt grouping in autism. Method: Twenty-five low-functioning children with autism and 25 controls who were matched for chronological age and verbal mental age took part in the study. Results: The autism group utilised gestalt grouping principles (proximity, similarity, closure) significantly less than the controls. Calculating an overall index of gestalt grouping, the autism group performed at chance level. There was also a deficit in identifying certain impossible figures. This pattern was not reflected in a drawing task, in which the autism sample conformed more to gestalt grouping principles than controls (non-significantly). Conclusions: The results are discussed in terms of a failure in autism to process inter-element relationships that would allow for the appreciation of larger perceptually coherent units that comprise of multiple elements and, consequently, context. The processes are argued to be preattentive. C1 Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England. Univ Cambridge, Autism Res Ctr, Cambridge CB2 1TN, England. RP Brosnan, MJ (reprint author), Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England. 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G., 1982, ANAL VISUAL BEHAV VANKLEECK MH, 1989, NEUROPSYCHOLOGIA, V27, P1179, DOI 10.1016/0028-3932(89)90100-0 VANKLEECK MH, 1989, NEUROPSYCHOLOGIA, V27, P1165, DOI 10.1016/0028-3932(89)90099-7 Westheimer G, 1999, PERCEPTION, V28, P5, DOI 10.1068/p2883 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 66 TC 72 Z9 73 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAR PY 2004 VL 45 IS 3 BP 459 EP 469 DI 10.1111/j.1469-7610.2004.00237.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WD UT WOS:000221788500005 PM 15055366 ER PT J AU Taber, KH Shaw, JB Loveland, KA Pearson, DA Lane, DM Hayman, LA AF Taber, KH Shaw, JB Loveland, KA Pearson, DA Lane, DM Hayman, LA TI Accentuated Virchow-Robin spaces in the centrum semiovale in children with autistic disorder SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE autism; development disorders; brain imaging; Virchow-Robin spaces ID MYOTONIC-DYSTROPHY; MR FINDINGS; PIA MATER; BRAIN; CHILDHOOD; SEROTONIN; MIGRAINE; SYSTEM; CT AB Objective: The purpose of this study was to assess the incidence of abnormal Virchow-Robin (VR) spaces in children and adolescents with an autistic disorder (AD). An increased incidence of enlarged VR spaces in children has been reported in several developmental disorders. Methods: Sixteen children and adolescents (13 male, 3 female; mean age = 143.5 months; mean IQ = 95.1) with an AD, verified by use of standardized procedures (Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule-Revised), received cranial magnetic resonance (MR) imaging. Sixteen children and adolescents (13 male, 3 female; mean age 160.7 months; mean IQ = 111.6) without AD, as determined using the same procedures, were scanned as a comparison group. The MR scans were performed using a 1.5-T scanner. Two T1-weighted spoiled GRASS sequences (0.7-mm coronal thin-slice, 0-mm gap; 1.5-mm sagittal, 0-mm gap) and a complementary T2-weighted fast spin echo sequence (1.5-mm, 0-mm gap) were obtained. A neuroradiologist and a neurobiologist without clinical information determined the incidence of normal, accentuated, and/or dilated VR spaces. Results: Seven of 16 subjects with AD (approximately 44%) had dilated VR spaces in the centrum semiovale. No grossly abnormal spaces were present in the control subjects. Conclusion: Unusually large VR spaces are seen in at most 22% to 27% of MR scans in children with tension headaches and other psychiatric disorders, suggesting that the incidence of spaces of this type is greater in AD than in other abnormal populations. The origin and significance of this phenomenon remain unknown. C1 Univ Texas, Sch Hlth Informat Sci, Hlth Sci Ctr, Houston, TX 77030 USA. Univ Texas, Sch Med, Hlth Sci Ctr, Ctr Human Dev Res,Dept Psychiat & Behav Sci, Houston, TX 77030 USA. Rice Univ, Dept Psychol, Houston, TX 77251 USA. RP Taber, KH (reprint author), Univ Texas, Sch Hlth Informat Sci, Hlth Sci Ctr, 7000 Fannin,UCT 880, Houston, TX 77030 USA. 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Comput. Assist. Tomogr. PD MAR-APR PY 2004 VL 28 IS 2 BP 263 EP 268 DI 10.1097/00004728-200403000-00017 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 803ZK UT WOS:000220268800017 PM 15091132 ER PT J AU Williams, G McChane, RH Schikler, K AF Williams, G McChane, RH Schikler, K TI Case report: 6-year-old male with autism and systemic onset juvenile rheumatoid arthritis SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; juvenile rheumatoid arthritis; autoimmune disorders ID RUBELLA VACCINE; IMMUNE-SYSTEM; ASSOCIATION; CHILDREN; DISORDERS; MEASLES; MUMPS AB Autism is a developmental disorder characterized by pervasive social and communication impairments and restricted range of interests and activities. Although the specific cause is unknown, proposed etiologies for autism have included autoimmune dysregulation of cellular or humoral components and maternal-fetal immunoregulation problems. Juvenile rheumatoid arthritis (JRA) constitutes several heterogeneous arthritides with onset in childhood. JRA is believed to be an autoimmune disorder whose pathogenesis is currently being elucidated. We present a case report of a 6-year-old male diagnosed with both autism and systemic onset JRA (SO-JRA). This co-occurrence has not previously been reported in the medical literature and raises the issue of a possible association between these 2 entities. Additional research to determine the frequency with which these 2 disorders coexist and to delineate potential immune mechanisms in autism could provide insights as to the etiology of both autism and SO-JRA and/or suggest a pathway to address treatment. C1 Univ Louisville, Weisskopf Ctr Evaluat Children, Sch Med, Dept Pediat,Sect Pediat Rheumatol, Louisville, KY 40204 USA. RP Williams, G (reprint author), Univ Louisville, Weisskopf Ctr Evaluat Children, Sch Med, Dept Pediat,Sect Pediat Rheumatol, 571 S Floyd,Suite 100, Louisville, KY 40204 USA. CR Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561 Comi AM, 1999, J CHILD NEUROL, V14, P388, DOI 10.1177/088307389901400608 DEYKIN EY, 1979, AM J EPIDEMIOL, V109, P628 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fishman D, 1998, J CLIN INVEST, V102, P1369, DOI 10.1172/JCI2629 Gallagher K T, 1999, Curr Opin Rheumatol, V11, P372, DOI 10.1097/00002281-199909000-00008 Gupta S, 1998, J NEUROIMMUNOL, V85, P106, DOI 10.1016/S0165-5728(98)00021-6 Gupta S, 1996, J AUTISM DEV DISORD, V26, P439, DOI 10.1007/BF02172828 Moore T L, 1999, Curr Opin Rheumatol, V11, P377, DOI 10.1097/00002281-199909000-00009 Onel KB, 2000, CURR OPIN PEDIATR, V12, P72, DOI 10.1097/00008480-200002000-00014 Peltola H, 1998, LANCET, V351, P1327, DOI 10.1016/S0140-6736(98)24018-9 Plioplys AV, 1998, J CHILD NEUROL, V13, P79 Shoenfeld Y, 2000, J AUTOIMMUN, V14, P1 SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 vanGent T, 1997, J CHILD PSYCHOL PSYC, V38, P337 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 WARREN RP, 1992, IMMUNOGENETICS, V36, P203, DOI 10.1007/BF00215048 Woo P, 1998, LANCET, V351, P969 Zimmerman AW, 2000, J AUTISM DEV DISORD, V30, P481, DOI 10.1023/A:1005520111362 NR 21 TC 0 Z9 0 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 2004 VL 16 IS 1 BP 117 EP 123 DI 10.1023/B:JODD.0000010043.89739.ca PG 7 WC Rehabilitation SC Rehabilitation GA 757EL UT WOS:000187535800008 ER PT J AU Barry-Walsh, JB Mullen, PE AF Barry-Walsh, JB Mullen, PE TI Forensic aspects of Asperger's Syndrome SO JOURNAL OF FORENSIC PSYCHIATRY & PSYCHOLOGY LA English DT Article DE Asperger's Syndrome; offending; insanity; disability; violence; autism ID DISORDERS; VIOLENCE AB Asperger's Syndrome is a pervasive developmental disorder on the Autistic spectrum. Antisocial behaviour is frequently described as an accompaniment of Asperger's Syndrome although the strength of any association between Asperger's Syndrome and offending remains uncertain. This paper presents five patients with Asperger's Syndrome with a history of offending. For each of them the offending is understandable in the context of the disorder. The specific and general issues raised by these cases in relation to Fitness to Plead and Legal Insanity are considered. Offenders with Asperger's Syndrome have deficits that raise the likelihood that their disorder will render them unfit or be of exculpatory value. C1 Monash Univ, Fairfield, Vic 3078, Australia. Thomas Embling Hosp, Victorian Inst Forens Mental Hlth, Fairfield, Vic 3078, Australia. Cent Reg Forens Mental Hlth Serv, Porirua, New Zealand. RP Mullen, PE (reprint author), Monash Univ, Locked Bag 10, Fairfield, Vic 3078, Australia. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 Attwood T., 1998, ASPERGERS SYNDROME G EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x EVERALL IP, 1990, BRIT J PSYCHIAT, V157, P284, DOI 10.1192/bjp.157.2.284 GHAZIUDDIN M, 1991, J AUTISM DEV DISORD, V21, P349, DOI 10.1007/BF02207331 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Kohn Y, 1998, ISRAEL J PSYCHIAT, V35, P293 MAWSON D, 1985, BRIT J PSYCHIAT, V147, P566, DOI 10.1192/bjp.147.5.566 MILLER RD, 1994, PRINCIPLES PRACTICE, P174 MURRIE D. C., 2002, INT J FORENSIC MENTA, V1, P59, DOI DOI 10.1080/14999013.2002.10471161 SCRAGG P, 1994, BRIT J PSYCHIAT, V165, P679, DOI 10.1192/bjp.165.5.679 SIMBLETT GJ, 1993, J INTELL DISABIL RES, V37, P85 Siponmaa L, 2001, J AM ACAD PSYCHIATRY, V29, P420 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WING L, 1981, PSYCHOL MED, V11, P115 WOLFF S, 1986, PSYCHOL MED, V16, P677 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 18 TC 28 Z9 28 PU ROUTLEDGE TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1478-9949 J9 J FORENSIC PSYCHI PS JI J. Forensic Psychiatry Psychol. PD MAR PY 2004 VL 15 IS 1 BP 96 EP 107 DI 10.1080/14789940310001638628 PG 12 WC Criminology & Penology; Psychiatry SC Criminology & Penology; Psychiatry GA 802RV UT WOS:000220181500007 ER PT J AU Coyle, C Cole, P AF Coyle, C Cole, P TI A videotaped self-modelling and self-monitoring treatment program to decrease off-task behaviour in children with autism SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article ID MANAGEMENT TREATMENT PACKAGE; TEACHING PRESCHOOLERS; SKILLS; ATTENTION; SETTINGS; STUDENTS; DISABILITIES; PERFORMANCE; TEENAGERS; PEOPLE AB The value of a videotaped self-modelling and self-monitoring treatment program teas investigated in the present study. The focus was the effect of the treatment program on the off-task classroom behaviour of 3 male children with autism. The participants were aged between 9 and 11 years. Two of the children were described as severely autistic and the other was described as moderately autistic. All 3 had deficient cognitive skills. Each of the studies in the research project employed a single-subject withdrawal design. The first two studies followed an A-B-A design and the third followed an A-B-A-C-A design. The results indicated considerable decreases in off-task behaviour during the period of intervention. Both short-term and long-term maintenance gains were in evidence. The intervention was then reimplemented daring follow-up and similar reductions in off-task behaviour Here demonstrated. Attention theory ribs used to support the outcomes of the research. C1 Edith Cowan Univ, Perth, WA, Australia. RP Coyle, C (reprint author), 15 Rowlands Court, Padbury, WA 6025, Australia. EM cathcoyle@bigpond.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BANDURA A, 1986, SOCIAL FDN THOUGHT A Buggey T, 1995, TOP EARLY CHILD SPEC, V15, P434 BURACK J., 1998, HDB MENTAL RETARDATI CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 CONNELL MC, 1993, J APPL BEHAV ANAL, V26, P345, DOI 10.1901/jaba.1993.26-345 Dowrick P. W., 1983, USING VIDEO PSYCHOL, P105 DOWRICK PW, 1980, J APPL BEHAV ANAL, V13, P51, DOI 10.1901/jaba.1980.13-51 DOWRICK PW, 1981, J APPL PSYCHOL, V66, P394, DOI 10.1037/0021-9010.66.3.394 Dunn L. M., 1959, PEABODY PICTURE VOCA GRAHAM P, 1999, CHILD PSYCHIAT DEV A HALLENBECK BA, 1995, J SPEC EDUC, V29, P45 HARCHIK AE, 1992, RES DEV DISABIL, V13, P211, DOI 10.1016/0891-4222(92)90026-3 HARING TG, 1987, J APPL BEHAV ANAL, V20, P89, DOI 10.1901/jaba.1987.20-89 Hulme C., 1992, WORKING MEMORY SEVER Johnston D. J., 1999, AQUACULTURE ASIA, V4, P6 Jordan R., 1999, M NEEDS CHILDREN AUT KERNDUNLAP L, 1992, J APPL BEHAV ANAL, V25, P355, DOI 10.1901/jaba.1992.25-355 KOEGEL LK, 1992, J APPL BEHAV ANAL, V25, P341, DOI 10.1901/jaba.1992.25-341 KOEGEL RL, 1990, J APPL BEHAV ANAL, V23, P119, DOI 10.1901/jaba.1990.23-119 MAAG JW, 1993, J APPL BEHAV ANAL, V26, P329, DOI 10.1901/jaba.1993.26-329 Miller N. E., 1941, SOCIAL LEARNING IMIT Newman B, 1996, EDUC TRAIN MENT RET, V31, P304 NEWMAN B, 1995, BEHAV DISORDERS, V20, P190 OAKE NJ, 1990, J AUTISM DEV DISORD, V20, P479 PIERCE KL, 1994, J APPL BEHAV ANAL, V27, P471, DOI 10.1901/jaba.1994.27-471 POWELL SD, 1992, J AUTISM DEV DISORD, V22, P413, DOI 10.1007/BF01048243 RAPPAPORT JL, 1996, DSM 4 TRAINING GUIDE REID R, 1993, EXCEPT CHILDREN, V60, P29 ROONEY KJ, 1984, J LEARN DISABIL, V17, P360 SAINATO DM, 1990, EXCEPT CHILDREN, V56, P540 Shearer D. D., 1996, EARLY EDUC DEV, V7, P205, DOI 10.1027/s15566935eed0703_1 STAHMER AC, 1992, J APPL BEHAV ANAL, V25, P447, DOI 10.1901/jaba.1992.25-447 STRAIN PS, 1994, J EMOT BEHAV DISORD, V2, P78 VARNI JW, 1979, J ABNORM CHILD PSYCH, V7, P31, DOI 10.1007/BF00924508 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 WEBBER J, 1993, REM SPEC EDUC, V14, P38 WITT JC, 1988, HDB BEHAV THERAPY ED WOLTERSDORF MA, 1992, CHILD FAM BEHAV THER, V14, P53, DOI 10.1300/J019v14n02_04 NR 39 TC 27 Z9 27 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD MAR PY 2004 VL 29 IS 1 BP 3 EP 15 DI 10.1080/08927020410001662642 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 818KD UT WOS:000221243100001 ER PT J AU Tomanik, S Harris, GE Hawkins, J AF Tomanik, S Harris, GE Hawkins, J TI The relationship between behaviours exhibited by children with autism and maternal stress SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article ID PARENTS; INTERVENTION; FAMILIES; IMPACT AB The present study investigated the relationship between behaviours exhibited by children with pervasive developmental disorders, particularly autism, and maternal stress levels. Participants consisted of 60 mothers who had et child diagnosed with a pervasive developmental disorder by an independent practitioner using DSM-IV criteria. Children were between 2 and 7 years of age. Mothers completed the,following self-report measures: the Parenting Stress Index (short-form), the Aberrant Behavior Checklist, AAMR Adaptive Behavior Scales and a demographic questionnaire. Two-thirds of the participants in the sample evidenced stress scores that were significantly elevated. Regression analyses revealed that child maladaptive behaviour and child adaptive behaviour accounted for a significant proportion of the variance in maternal stress. Methodological issues and considerations for,future research are discussed. C1 Univ Houston, Dept Psychol, Houston, TX 77204 USA. RP Harris, GE (reprint author), Univ Houston, Dept Psychol, 126 Heyne Bldg, Houston, TX 77204 USA. 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Intellect. Dev. Dis. PD MAR PY 2004 VL 29 IS 1 BP 16 EP 26 DI 10.1080/13668250410001662892 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 818KD UT WOS:000221243100002 ER PT J AU La Malfa, G Lassi, S Bertelli, M Salvini, R Placidi, GF AF La Malfa, G Lassi, S Bertelli, M Salvini, R Placidi, GF TI Autism and intellectual disability: a study of prevalence on a sample of the Italian population SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; intellectual disability; pervasive developmental disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; SEVERE MENTAL-RETARDATION; INFANTILE-AUTISM; CHILDREN; VALIDITY; ABNORMALITIES; EPIDEMIOLOGY; IMPAIRMENTS AB Background In 1994, the American Association on Mental Retardation with the DSM-IV has come to a final definition of pervasive developmental disorders (PDD), in agreement with the ICD-10. Prevalence of PDD in the general population is 0.1-0.15% according to the DSM-IV. PDD are more frequent in people with severe intellectual disability (ID). There is a strict relationship between ID and autism: 40% Of people with ID also present a PDD, on the other hand, nearly 70% of people with PDD also have ID. We believe that in Italy PDD are underestimated because there is no agreement about the classification system and diagnostic instruments. Method Our aim is to assess the prevalence of PDD in the Italian population with ID. The Scale of Pervasive Developmental Disorder in Mentally Retarded Persons (PDD-MRS) seems to be a very good instrument for classifying and diagnosing PDD. Results The application of the PDD-MRS and a clinical review of every individual case on a sample of 166 Italian people with ID raised the prevalence of PDD in this population from 7.8% to 39.2%. Conclusions The study confirms the relationship between ID and autism and suggests a new approach in the study of ID in order to elaborate a new integrated model for people with ID. C1 Univ Florence, Careggi Hosp, Dept Neurol & Psychiat Sci, Psychiat Unit, Florence, Italy. RP La Malfa, G (reprint author), Via Gordigiani 58, I-50127 Florence, Italy. EM gplamalfa@videosoft.it CR *AARM, 1994, MENT RET DEF CLASS S *AM PSYCH ASS, 1995, DSM IV MAN DIAGN STA American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASPERGER H, 1968, ACTA PAEDOPSYCHIATR, V35, P136 BAKER H, 1959, EXCEPTIONAL CHILDREN BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 BENASSI G, 1990, DEV MED CHILD NEUROL, V32, P895 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Bouras N., 1999, MENTAL HLTH MENTAL R BRYSON SE, 1988, J CHILD PSYCHOL PSYC, V29, P433, DOI 10.1111/j.1469-7610.1988.tb00735.x Cohen D. 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A., 1980, AUTISM SCREENING INS LAMALFA GP, 1996, 10 WORLD C INT ASS S Lauritsen M, 1999, J CHILD PSYCHOL PSYC, V40, P335, DOI 10.1017/S0021963098003710 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 MADSEN KM, 2002, NEW ENGL J MED, V347, P1474 Matson JL, 1998, J AUTISM DEV DISORD, V28, P77, DOI 10.1023/A:1026019221036 Morgan C. N., 2002, PSYCHIAT B, V26, P127, DOI 10.1192/pb.26.4.127 MORGAN S, 1988, J PSYCHOEDUCATIONAL, V6, P139, DOI 10.1177/073428298800600205 *NOT OSS AUT REG L, 1999, ANN REP Rimland B., 1964, INFANTILE AUTISM SYN Sarason S., 1953, PSYCHOL PROBLEMS MEN Schopler E., 1986, CHILDHOOD AUTISM RAT Singh VK, 2002, J BIOMED SCI, V9, P359, DOI 10.1159/000065007 STEFFENBURG S, 1986, BRIT J PSYCHIAT, V149, P81, DOI 10.1192/bjp.149.1.81 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 TSAI LY, 1983, BRIT J PSYCHIAT, V142, P373, DOI 10.1192/bjp.142.4.373 WAKEFIELD AJ, 1999, LANCET, V353, P2026 Wechsler D, 1981, WECHSLER ADULT INTEL Wechsler D., 1997, WESCHSLER ADULT INTE Wing L., 1987, HDB AUTISM PERVASIVE, P3 WING L, 1981, J AUTISM DEV DISORD, V11, P31, DOI 10.1007/BF01531339 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing L., 1976, EARLY CHILDHOOD AUTI World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 47 TC 49 Z9 49 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD MAR PY 2004 VL 48 BP 262 EP 267 DI 10.1111/j.1365-2788.2003.00567.x PN 3 PG 6 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 812OA UT WOS:000220847600007 PM 15025669 ER PT J AU Alcorn, A Berney, T Bretherton, K Mills, M Savery, D Shattock, P AF Alcorn, A Berney, T Bretherton, K Mills, M Savery, D Shattock, P TI Urinary compounds in autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; biochemistry; child; peptide; urine ID PEPTIDE COMPLEXES AB Background Although earlier claims to identify specific compounds in the urine of people with autism had been discredited, it was subsequently suggested that there might be biochemical characteristics that were specific to early childhood, particularly in those who also did not have a severe degree of intellectual disability This study was to establish whether autism might have a distinctive chromatographic profile on urinary analysis. Method Thirty-four prepubertal boys with autism were matched with two groups of boys without autism - one on ability and chronological age and the other on chronological age alone, being within the normal range of ability. Laboratory analysis of their urine samples was carried out blind as to the clinical diagnosis. Results The analysis correctly identified 53% Of the autism group as against misidentifying 33% and 18% of the other two groups. When children with a severe learning disability (both with and without autism) were excluded from the comparisons, the laboratory then identified 77% of the 13 boys left in the autism group and misidentified 8% and 18% of the other two groups. Conclusions The results would support the idea of a biological marker in prepubertal children and that it may be absent in, or obscured by the presence of severe LD. C1 Prudhoe Hosp, Dept Child & Adolescent Psychiat, Prudhoe NE42 5NT, Northd, England. Univ Sunderland, Autism Res Unit, Sunderland SR2 7EE, Durham, England. RP Berney, T (reprint author), Prudhoe Hosp, Dept Child & Adolescent Psychiat, Prudhoe NE42 5NT, Northd, England. EM t.p.berney@newcastle.ac.uk CR Anderson RJ, 2002, J PHARM PHARMACOL, V54, P295, DOI 10.1211/0022357021778349 DeLong GR, 1999, NEUROLOGY, V52, P911 GILLBERG C, 1982, J AUTISM DEV DISORD, V12, P229 LECOUTEUR A, 1988, J AUTISM DEV DISORD, V18, P181 PANKSEPP J, 1979, TRENDS NEUROSCI, V2, P174, DOI 10.1016/0166-2236(79)90071-7 Reichelt Karl L., 1991, Brain Dysfunction, V4, P308 REICHELT KL, 1986, BIOL PSYCHIAT, V21, P1279, DOI 10.1016/0006-3223(86)90310-0 Schopler E., 1988, CHILDHOOD AUTISM RAT SHATTOCK P, 1990, Brain Dysfunction, V3, P328 TRYGSTAD OE, 1980, BRIT J PSYCHIAT, V136, P59, DOI 10.1192/bjp.136.1.59 NR 10 TC 7 Z9 8 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD MAR PY 2004 VL 48 BP 274 EP 278 DI 10.1111/j.1365-2788.2003.00554.x PN 3 PG 5 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 812OA UT WOS:000220847600009 PM 15025671 ER PT J AU Lewis, JC Thomas, HV Murphy, KC Sampson, JR AF Lewis, JC Thomas, HV Murphy, KC Sampson, JR TI Genotype and psychological phenotype in tuberous sclerosis SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID TSC1 GENE; MUTATIONAL ANALYSIS; GROWTH SUPPRESSOR; CHROMOSOME 9Q34; COMPLEX; AUTISM; POPULATION; EPILEPSY; HAMARTIN; IDENTIFICATION C1 Univ Wales Coll Med, Inst Med Genet, Cardiff CF14 4N, S Glam, Wales. Univ Wales Coll Med, Dept Psychol Med, Cardiff CF4 4XN, S Glam, Wales. Beaumont Hosp, Royal Coll Surg Ireland, Dept Psychiat, Dublin 9, Ireland. RP Sampson, JR (reprint author), Univ Wales Coll Med, Inst Med Genet, Heath Pk, Cardiff CF14 4N, S Glam, Wales. 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Med. Genet. PD MAR 1 PY 2004 VL 41 IS 3 BP 203 EP 207 DI 10.1136/jmg.2003.012757 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 779ZR UT WOS:000189344300012 PM 14985384 ER PT J AU Dominey, PF Dodane, C AF Dominey, PF Dodane, C TI Indeterminacy in language acquisition: the role of child directed speech and joint attention SO JOURNAL OF NEUROLINGUISTICS LA English DT Review DE language acquisition; social interaction; native language ID MATERNAL SPEECH; YOUNG INFANTS; LEXICAL ACQUISITION; INTONATION CONTOURS; WORD SEGMENTATION; SOUND PATTERNS; CROSS-LANGUAGE; MOTHERS SPEECH; EYE GAZE; AUTISM AB Language acquisition represents one of the great learning achievements in human cognitive development. Perhaps, this process takes place in a relatively automatic manner in which, simply through exposure to language input, the child configures her language organ to coincide with the structure of the maternal language. In this context, the problem of the vast uncertainty between speech input and its external referent, related to the more general notion of the 'poverty of the stimulus' problem, takes on a significant importance, and motivates the nativist suggestion that language is already essentially preprogrammed, and acquisition consists of setting the parameters for the target language based on limited exposure. What if, however, the acquisition process was not so automatic, but rather was controlled by the operation of mechanisms that could direct the attention of the child to specific aspects of the sentence and its external referent? In this case, external and internal control of attention could significantly reduce the referential uncertainty, thus reducing the requirement for preprogrammed language. The current paper outlines evidence for this second scenario, in which child directed speech guides the child's attention to important aspects of the speech signal, and Joint Attention focuses his attention on the relevant aspects of the referential world, significantly reducing the poverty of the stimulus problem. Results from recent simulation studies are briefly reviewed that indicate how these mechanisms could then allow a relatively non-specific learning mechanism to acquire initial knowledge of grammatical constructions in the first steps of language acquisition. (C) 2003 Elsevier Ltd. All rights reserved. C1 Inst Cognit Sci, CNRS UMR 5015, F-69675 Bron, France. RP Dominey, PF (reprint author), Inst Cognit Sci, CNRS UMR 5015, 67 Blvd Pinel, F-69675 Bron, France. 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Neuropsychiatr. Clin. Neurosci. PD SPR PY 2004 VL 16 IS 2 BP 199 EP 213 DI 10.1176/appi.neuropsych.16.2.199 PG 15 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 817NF UT WOS:000221183500011 PM 15260372 ER PT J AU Stahmer, AC Ingersoll, B AF Stahmer, AC Ingersoll, B TI Inclusive programming for toddlers with autism spectrum disorders: Outcomes from the children's toddler school SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID EXCHANGE COMMUNICATION-SYSTEM; YOUNG-CHILDREN; EARLY INTERVENTION; BEHAVIORAL TREATMENT; ACQUISITION AB The passage of the Individuals with Disabilities Education Act of 1990 mandated the provision of interventions for young children with autism spectrum disorders (ASD) under the age of 3 years. Although Strain, McGee, and Kohler (2001) suggested that children with autism benefit from inclusive programming, inclusive early intervention programs are rare. In the current study, the authors used a quasi-experimental design to analyze the outcomes for 20 young children with ASD in an inclusive program for children under age 3. Both outcomes on standardized assessments and functional outcomes were compared at program entry and exit. Significant increases in standard scores were found for the standardized assessments from intake to exit, with 37% of the children functioning in the typical range at exit, compared to 11% at entry. Significant improvements in performance on functional measures were also seen. At intake, 50% of the study participants had no functional communication skills, whereas at exit, 90% used a functional communication system. Social and play behaviors also increased substantially. Use of augmentative communication systems and a combination of research-based programming are discussed. C1 Univ Calif San Diego, Childrens Hosp San Diego, Child & Adolescent Serv Res Ctr, San Diego, CA 92103 USA. 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S., 2001, EARLY CHILDHOOD INCL, P337 Strain PS, 1998, YOUNG EXCEPTIONAL CH, V1, P8, DOI 10.1177/109625069800100202 NR 50 TC 39 Z9 40 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD SPR PY 2004 VL 6 IS 2 BP 67 EP 82 DI 10.1177/10983007040060020201 PG 16 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 806UV UT WOS:000220459700001 ER PT J AU Durand, VM Christodulu, KV AF Durand, VM Christodulu, KV TI Description of a sleep-restriction program to reduce bedtime disturbances and night waking SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID DEVELOPMENTAL-DISABILITIES; YOUNG-CHILDREN; RESPONSE COST; FADED BEDTIME; DISORDERS; BEHAVIOR; INSOMNIA; TERRORS; FAMILY; ADULTS AB The authors describe a behavioral intervention designed to reduce sleep problems without increasing disruption at bedtime or throughout the evening. Sleep restriction was used to reduce the bedtime and nighttime sleep problems of two children, a 4-year-old girl with autism and a 4-year-old girl with developmental delay. Sleep restriction involved reducing the number of hours each child slept while maintaining a consistent bedtime and awake time. Once the program was successful, the amount of sleep was faded back to an age-appropriate level. The sleep-restriction programs appeared to result in the elimination of bedtime disturbances and the reduction of nighttime awakenings. The authors discuss the effectiveness of this behavioral intervention for the treatment of sleep disturbances in children with developmental disabilities. C1 SUNY Albany, Ctr Autism & Related Disabilities, Dept Psychol, Albany, NY 12222 USA. Univ S Florida, Coll Arts & Sci, St Petersburg, FL 33701 USA. RP Christodulu, KV (reprint author), SUNY Albany, Ctr Autism & Related Disabilities, Dept Psychol, 1400 Washington Ave, Albany, NY 12222 USA. 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Posit. Behav. Interv. PD SPR PY 2004 VL 6 IS 2 BP 83 EP 91 DI 10.1177/10983007040060020301 PG 9 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 806UV UT WOS:000220459700002 ER PT J AU Forest, EJ Horner, RH Lewis-Palmer, T Todd, AW AF Forest, EJ Horner, RH Lewis-Palmer, T Todd, AW TI Transitions for young children with autism from preschool to kindergarten SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID EARLY-CHILDHOOD; EARLY INTERVENTION; DISABILITIES; EDUCATION; TEACHERS; SKILLS AB The transition of young children with autism from preschool to kindergarten is an important event both for sustaining gains made during preschool and for establishing future social and academic development. This article provides a summary of 25 transition elements identified from the research literature as important for a successful transition. The elements were built into a survey instrument, and the instrument was used with the parents, preschool teachers, and kindergarten teachers for three children with autism who transitioned during 1999 to 2001. Results from the survey indicate that transition elements identified in the literature were perceived as important by families, preschool teachers, and kindergarten teachers. High variability, however, was reported in the perceived level of implementation for the transition elements. The report provides an index of transition elements that may be useful to guide future research and to facilitate effective transitions. C1 Univ Oregon, Eugene, OR 97403 USA. RP Horner, RH (reprint author), Univ Oregon, Eugene, OR 97403 USA. 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PD SPR PY 2004 VL 6 IS 2 BP 103 EP 112 DI 10.1177/10983007040060020501 PG 10 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 806UV UT WOS:000220459700004 ER PT J AU Akshoomoff, N Lord, C Lincoln, AJ Courchesne, RY Carper, RA Townsend, J Courchesne, E AF Akshoomoff, N Lord, C Lincoln, AJ Courchesne, RY Carper, RA Townsend, J Courchesne, E TI Outcome classification of preschool children with autism spectrum disorders using MRI brain measures SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism spectrum disorders; magnetic resonance imaging; neuroanatomy ID DIAGNOSTIC OBSERVATION SCHEDULE; INFANTILE-AUTISM; FOLLOW-UP; CEREBELLAR; ABNORMALITIES; ACTIVATION; INTERVIEW; AGE; VII AB Objective: To test the hypothesis that a combination of magnetic resonance imaging (MRI) brain measures obtained during early childhood distinguish children with autism spectrum disorders (ASD) from typically developing children and is associated with functional outcome. Method: Quantitative MRI technology was used to measure gray and white matter volumes (cerebrum and cerebellum), total brain volume, and the area of the cerebellar vermis in 52 boys with a provisional diagnosis of autism (aged 1.9-5.2 years) and 15 typically developing young children (aged 1.7-5.2 years). Diagnostic confirmation and cognitive outcome data were obtained after the children reached 5 years of age. Results: A discriminant function analysis of the MRI brain measures correctly classified 95.8% of the ASD cases and 92.3% of the control cases. This set of variables also correctly classified 85% of the ASD cases as lower functioning and 68% of the ASD cases as higher functioning. Conclusions: These results indicate that variability in cerebellar and cerebral size is correlated with diagnostic and functional outcome in very young children with ASD. C1 Childrens Hosp, Res Ctr, La Jolla, CA 92037 USA. Univ Calif San Diego, Sch Med, Dept Psychiat, San Diego, CA USA. Univ Calif San Diego, Sch Med, Dept Neurosci, San Diego, CA USA. Univ Michigan, Dept Psychol, Ann Arbor, MI USA. Univ Michigan, Ctr Autism & Commun Disorders, Ann Arbor, MI USA. Alliant Internatl Univ, San Diego, CA USA. RP Akshoomoff, N (reprint author), Childrens Hosp, Res Ctr, 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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PD MAR PY 2004 VL 43 IS 3 BP 349 EP 357 DI 10.1097/01.chi.0000103176.13414.67 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 776HJ UT WOS:000189110300016 PM 15076269 ER PT J AU Walsh, CM Suwattee, P Pope, E AF Walsh, CM Suwattee, P Pope, E TI Neurofibromatosis type 1, mastocytoma and autism SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Meeting Abstract CT 62nd Annual Meeting of the American-Academy-of-Dermatology CY FEB 06-11, 2004 CL WASHINGTON, DC SP Amer Acad Dermatol C1 Univ Toronto, Fac Med, Dept Pediat Med Dermatol, Toronto, ON, Canada. Univ Toronto, Fac Med, Dept Med, Div Dermatol, Toronto, ON, Canada. CR Gutmann DH, 1997, JAMA-J AM MED ASSOC, V278, P51, DOI 10.1001/jama.278.1.51 NURNBERGER M, 1994, DERMATOLOGY, V188, P296 RICCARDI VM, 1987, ARCH DERMATOL, V123, P1011, DOI 10.1001/archderm.123.8.1011 Young H, 2002, J CHILD NEUROL, V17, P613, DOI 10.1177/088307380201700812 NR 4 TC 0 Z9 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD MAR PY 2004 VL 50 IS 3 SU S MA P515 BP P133 EP P133 DI 10.1016/j.jaad.2003.10.457 PG 1 WC Dermatology SC Dermatology GA 802CC UT WOS:000220140600513 ER PT J AU Jefferson, T AF Jefferson, T TI Informed choice and balance are victims of the MMR-autism saga SO LANCET INFECTIOUS DISEASES LA English DT Letter ID MEASLES; RUBELLA; MUMPS; CHILDREN; VACCINE C1 Cochrane Vaccine Field, I-00061 Rome, Italy. RP Jefferson, T (reprint author), Cochrane Vaccine Field, Via Adige 28A, I-00061 Rome, Italy. EM toj1@aol.com CR Davis RL, 2001, ARCH PEDIAT ADOL MED, V155, P354 Jefferson T, 2003, VACCINE, V21, P3954, DOI 10.1016/S0264-410X(03)00271-8 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 2003, DRUG THER B, V41, P25 NR 7 TC 5 Z9 5 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1473-3099 J9 LANCET INFECT DIS JI Lancet Infect. Dis. PD MAR PY 2004 VL 4 IS 3 BP 135 EP 136 DI 10.1016/S1473-3099(04)00934-X PG 2 WC Infectious Diseases SC Infectious Diseases GA 780DN UT WOS:000189356700014 PM 14998496 ER PT J AU Geier, DA Geier, MR AF Geier, DA Geier, MR TI A comparative evaluation of the effects of MMR immunization and mercury doses from thimerosal-containing childhood vaccines on the population prevalence of autism SO MEDICAL SCIENCE MONITOR LA English DT Article DE autism; ethylmercury; MMR; neurodevelopmental disorders; thimerosal ID DEVELOPMENTAL DISORDERS; CHILDREN; MEASLES; MUMPS; DEATH AB Background: The purpose of the study was to evaluate the effects of MMR immunization and mercury from thimerosal-containing childhood vaccines on the prevalence of autism. Material/Methods: Evaluations of the Biological Surveillance Summaries of the Centers for Disease Control and Prevention (CDC), the U.S. Department of Education datasets, and the CDC's yearly live birth estimates were undertaken. Results: It was determined that there was a close correlation between mercury doses from thimerosal-containing childhood vaccines and the prevalence of autism from the late 1980s through the mid-1990s. In contrast, there was a potential correlation between the number of primary pediatric measles-containing vaccines administered and the prevalence of autism during the 1980s. In addition, it was found that there were statistically significant odds ratios for the development of autism following increasing doses of mercury from thimerosal-containing vaccines (birth cohorts: 1985 and 1990-1995) in comparison to a baseline measurement (birth cohort: 1984). The contribution of thimerosal from childhood vaccines (>50% effect) was greater than MMR vaccine on the prevalence of autism observed in this study. Conclusions: The results of this study agree with a number of previously published studies. These studies have shown that there is biological plausibility and epidemiological evidence showing a direct relationship between increasing doses of mercury from thimerosal-containing vaccines and neurodevelopmental disorders, and measles-containing vaccines and serious neurological disorders. It is recommended that thimerosal be removed from all vaccines, and additional research be undertaken to produce a MMR vaccine with an improved safety profile. C1 MedCon Inc, Silver Spring, MD USA. RP Geier, MR (reprint author), 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Monitor PD MAR PY 2004 VL 10 IS 3 BP PI33 EP PI39 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 867HC UT WOS:000224832100015 PM 14976450 ER PT J AU Dhossche, DM AF Dhossche, DM TI Autism as early expression of catatonia SO MEDICAL SCIENCE MONITOR LA English DT Review DE autism; pervasive developmental disorders; catatonia; psychotic disorders; children and adolescents; gamma-aminobutyric acid (GABA) ID PRADER-WILLI-SYNDROME; BENZODIAZEPINE-RECEPTOR-BINDING; PERIODIC CATATONIA; ANGELMAN-SYNDROME; INFANTILE-AUTISM; GENETIC-HETEROGENEITY; SPECTRUM DISORDERS; FAMILY HISTORY; CHILDREN; SCHIZOPHRENIA AB Background: Reports indicate that catatonia often occurs in autism. The association lacks a conceptual basis. Modern classificatory schemes define autism and catatonia separately and are not conducive to study areas of overlap. The exploration of the relation between autism and catatonia may be important because autism is increasingly recognized but effective treatments are lacking. Catatonia, on the other hand, is thought to be treatable, but is poorly recognized. Material/Methods: The literature on autism and catatonia are reviewed to identify areas of overlap. A hypothesis is formulated that, in some cases, autism may the early expression of catatonia. Results: Several areas of overlap between autism and catatonia are found. Catatonic symptoms are common in autism. Effects of anti-catatonic treatments on autistic symptoms are unknown. Abnormal gamma-aminobutyric acid (GABA) function has been implicated in both disorders. Neuroimaging studies show small cerebellar structures in both disorders. There is genetic evidence that susceptibility genes for autism and catatonia are located on the long arm of chromosome 15. Differences between autism and catatonia of age-of-onset, symptoms, and illness course, do not exclude a common genetic etiology. Conclusions: Focused research is needed to further evaluate the phenomenological, biological, and genetic overlap between autism and catatonia and to test the hypothesis that a subgroup of autism is early-onset catatonia. C1 Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. RP Dhossche, DM (reprint author), Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, 2500 N State St, Jackson, MS 39216 USA. 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Sci. Monitor PD MAR PY 2004 VL 10 IS 3 BP RA31 EP RA39 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 867HC UT WOS:000224832100020 PM 14976444 ER PT J AU Coutinho, AM Oliveira, G Morgadinho, T Fesel, C Macedo, TR Bento, C Marques, C Ataide, A Miguel, T Borges, L Vicente, AM AF Coutinho, AM Oliveira, G Morgadinho, T Fesel, C Macedo, TR Bento, C Marques, C Ataide, A Miguel, T Borges, L Vicente, AM TI Variants of the serotonin transporter gene (SLC6A4) significantly contribute to hyperserotonemia in autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; hyperserotonemia; serotonin transporter; SLC6A4 polymorphisms; quantitative trait; QTDT ID WHOLE-BLOOD SEROTONIN; PLATELET SEROTONIN; PROMOTER VARIANTS; 1ST-DEGREE RELATIVES; SUSCEPTIBILITY GENE; QUANTITATIVE TRAITS; FOUNDER POPULATION; DISORDER; REGION; ASSOCIATION AB The role of the serotonin system in the etiology and pathogenesis of autism spectrum disorders (ASD) is not clearly defined. High levels of platelet serotonin (5-HT) have been consistently found in a proportion of patients, and it is known that specific 5-HT transporter gene (SLC6A4) variants modulate transporter reuptake function, therefore possibly influencing the occurrence of hyperserotonemia in a subset of autistic patients. We have examined the association of platelet serotonin levels with two SLC6A4 polymorphisms, 5-HTT gene-linked polymorphic region (HTTLPR) in the promoter and intron 2 variable number of tandem repeats (VNTR), in a sample of 105 ASD patients, their parents, and 52 control children. Quantitative transmission disequilibrium test (QTDT) results showed a significant effect on 5-HT levels of each SLC6A4 marker (P=0.017 for HTTLPR; P=0.047 for intron 2 VNTR) and of haplotypes of the two markers (P=0.017), with a major contribution of the L. Stin2.10 haplotype (P=0.0013). A 5-HT mean value in the range of hyperserotonemia was associated with the homozygous L. Stin2.10 haplotype (H(1,N=97)=7.76, P=0.0054), which occurred in 33% of hyperserotonemic patients against 6% of patients with normal 5-HT levels (Fisher's exact test: P=0.013, OR=8). Allele interaction at the HTTLPR locus was found, with a significant dominance variance effect on 5-HT levels. We found no transmission disequilibrium of any of the SLC6A4 variants in ASD. Our results show that the SLC6A4 gene is a significant factor in the determination of 5-HT levels, and that specific SLC6A4 variants are associated with an increased risk for hyperserotonemia in our sample of autistic patients. The biological mechanism, however, is unlikely to involve the SLC6A4 gene solely. The associated SLC6A4 alleles likely interact with other genes or environmental factors to produce the abnormally high 5-HT levels observed in this subset of autistic patients, who possibly represent a separate etiological group. C1 Gulbenkian Inst Sci, P-2781196 Oeiras, Portugal. Hosp Pediat Coimbra, P-3000049 Coimbra, Portugal. Univ Coimbra, Fac Med, Dept Farmacol, P-3000 Coimbra, Portugal. Direccao Reg Educ Regiao Ctr, P-3030 Coimbra, Portugal. RP Vicente, AM (reprint author), Gulbenkian Inst Sci, Rua Quinta Grande 6, P-2781196 Oeiras, Portugal. 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By measuring the amount of protein using the Western blot technique, or by determining the percentage of immunoreactive cells, significant heterogeneity in MeCP2 distribution among various brain areas was observed. Highest expression was found in olfactory bulb and in frontal cortex. In contrast, little expression was detected in caudate-putamen, septum and hippocampus. Except in the olfactive nuclei, very few cells showed detectable MeCP2 protein at birth. The number increased during the first week of age, especially in cortex and nucleus accumbens. Rather than playing a global role in gene transcription, the heterogeneous distribution of MeCP2 transcription factor favors the idea that it has a specialized function in neurons. (C) 2004 Elsevier Inc. All rights reserved. C1 IFR 37 Neurosci, Lab Neurosci Comportementales & Cognit, CNRS, UMR 7521, F-67000 Strasbourg, France. Ctr Neurochim, INSERM, U575, F-67084 Strasbourg, France. RP Cassel, S (reprint author), IFR 37 Neurosci, Lab Neurosci Comportementales & Cognit, CNRS, UMR 7521, 12 Rue Goethe, F-67000 Strasbourg, France. 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Leukemia inhibitory factor (LIF) is induced by a variety of brain insults and known to have many influences on mature and immature nervous system. Here, we assessed the neurobehavioral and pathological consequences of peripheral administration of LIF in newborn rats. Subcutaneous LIF injection induced STAT3 phosphorylation in many brain regions and increased glial fibrillary acidic protein (GFAP) immunoreactivity in the neocortex, suggesting that LIF had direct effects in the central nervous system. The LIF-treated rats displayed decreased motor activity during juvenile stages, and developed abnormal prepulse inhibition in the acoustic startle test during and after adolescence. They displayed normal learning ability in active avoidance test, however. Brain neuronal structures and startle responses were grossly normal, except for the cortical astrogliosis during neonatal LIF administration. These results indicate that LIF induction in the periphery of the infant has a significant, but discrete impact on neurobehavioral development. (C) 2003 Elsevier Ireland Ltd and The Japan Neuroscience Society. All rights reserved. C1 Niigata Univ, Brain Res Inst, Div Mol Neurobiol, Niigata 9518585, Japan. CALTECH, Div Biol 216 76, Pasadena, CA 91125 USA. Niigata Univ, Brain Res Inst, Dept Pathol, Niigata 9518585, Japan. Niigata Univ, Brain Res Inst, Res Branch, Niigata 9518585, Japan. Niigata Univ, Grad Sch Med & Dent Sci, Dept Psychiat, Niigata 9518585, Japan. RP Nawa, H (reprint author), Niigata Univ, Brain Res Inst, Div Mol Neurobiol, Asahimachi Dori 1-757, Niigata 9518585, Japan. 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Schools PD MAR PY 2004 VL 41 IS 3 BP 405 EP 406 DI 10.1002/pits.10171 PG 2 WC Psychology, Educational SC Psychology GA 776GG UT WOS:000189107800013 ER PT J AU Carter, S AF Carter, S TI For just one day SO REHABILITATION COUNSELING BULLETIN LA English DT Editorial Material AB This essay explores the fantasy of a mother who wonders what her son would have been like if he were not severely disabled. For just one day, she confesses, she would like to know the anticipated son who disappeared from her life the day her disabled son was born, 21 years ago. The essay provides vivid examples of challenging experiences she has had with her son's autism and mental retardation, and it includes a list of recommended readings on parenting a child with a disability. C1 Univ Missouri, Coll Educ, Columbia, MO USA. Consortium Alternat Dispute Resolut Special Educ, Eugene, OR USA. RP Carter, S (reprint author), 911 Sunset Lane, Columbia, MO 65203 USA. 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PD SPR PY 2004 VL 29 IS 1 BP 25 EP 39 DI 10.2511/rpsd.29.1.25 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 844YQ UT WOS:000223200900005 ER PT J AU Gardenier, NC MacDonald, R Green, G AF Gardenier, NC MacDonald, R Green, G TI Comparison of direct observational methods for measuring stereotypic behavior in children with autism spectrum disorders SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article; Proceedings Paper CT 26th Annual Convention of the Association-for-Behavior-Analysis CY MAY, 2000 CL WASHINGTON, DC SP Assoc Behav Anal DE stereotypy; direct observational methods; measurement; autism ID MEASUREMENT ERROR; PARTIAL INTERVAL AB We compared partial-interval recording (PIR) and momentary time sampling (MTS) estimates against continuous measures of the actual durations of stereotypic behavior in young children with autism or pervasive developmental disorder-not otherwise specified. Twenty-two videotaped samples of stereotypy were scored using a low-tech duration recording method, and relative durations (i.e., proportions of observation periods consumed by stereotypy) were calculated. Then 10, 20, and 30 s MTS and 10 s PIR estimates of relative durations were derived from the raw duration data. Across all samples, PIR was found to grossly overestimate the relative duration of stereotypy. Momentary time sampling both over- and under-estimated the relative duration of stereotypy, but with much smaller errors than PIR (Experiment 1). These results were replicated across 27 samples of low, moderate and high levels of stereotypy (Experiment 2). (C) 2004 Elsevier Ltd. All rights reserved. C1 New England Ctr Children, Southborough, MA 01772 USA. Northeastern Univ, Boston, MA 02115 USA. Univ Massachusetts, Sch Med, Shriver Ctr, Waltham, MA USA. RP Gardenier, NC (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. 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R., 1990, HDB BEHAV MODIFICATI, P141 NR 23 TC 32 Z9 32 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 MAR-APR PY 2004 VL 25 IS 2 BP 99 EP 118 DI 10.1016/j.ridd.2003.05.004 PG 20 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 807YB UT WOS:000220535700001 PM 15026089 ER PT J AU Can, F Yilmaz, I Birkan, B Yanardag, M Konukman, F Bumin, G AF Can, F Yilmaz, I Birkan, B Yanardag, M Konukman, F Bumin, G TI Effects of Halliwick's swimming education program on water orientation skills of children with autism SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Hacettepe Univ, Ankara, Turkey. Anadolu Univ, Eskisehir, Turkey. EM ilkery@anadolu.edu.tr; bbirkan@anadolu.edu.tr; y_dag@hotmail.com; konukmaf@cwu.edu NR 0 TC 1 Z9 1 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2004 VL 75 IS 1 SU S BP A106 EP A107 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 806IT UT WOS:000220428300270 ER PT J AU Todd, T Reid, G AF Todd, T Reid, G TI Toward self-managing physical activity by individuals with autism spectrum disorder SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 McGill Univ, Montreal, PQ H3A 2T5, Canada. EM todd_teri@yahoo.ca; gregory.reid@mcgill.ca NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2004 VL 75 IS 1 SU S BP A113 EP A114 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 806IT UT WOS:000220428300288 ER PT J AU [Anonymous] AF [Anonymous] TI Age at MMR vaccination not different in children with autism SO INPHARMA LA English DT News Item CR DeStefano F, 2004, PEDIATRICS, V113, P259, DOI 10.1542/peds.113.2.259 NR 1 TC 0 Z9 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1173-8324 J9 INPHARMA JI Inpharma PD FEB 28 PY 2004 IS 1426 BP 20 EP 20 PG 1 GA 805EK UT WOS:000220349400034 ER PT J AU Hileman, B AF Hileman, B TI Vaccines and autism SO CHEMICAL & ENGINEERING NEWS LA English DT Article NR 0 TC 1 Z9 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0009-2347 J9 CHEM ENG NEWS JI Chem. Eng. News PD FEB 23 PY 2004 VL 82 IS 8 BP 18 EP + PG 3 WC Chemistry, Multidisciplinary; Engineering, Chemical SC Chemistry; Engineering GA 777BN UT WOS:000189154400035 ER PT J AU Gottlieb, S AF Gottlieb, S TI Study finds no connection between MMR vaccine and autism SO BRITISH MEDICAL JOURNAL LA English DT News Item CR DeStefano F, 2004, PEDIATRICS, V113, P259, DOI 10.1542/peds.113.2.259 NR 1 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD FEB 21 PY 2004 VL 328 IS 7437 BP 421 EP 421 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 777DV UT WOS:000189161000007 ER PT J AU Janusonis, S Gluncic, V Rakic, P AF Janusonis, S Gluncic, V Rakic, P TI Early serotonergic projections to Cajal-Retzius cells: Relevance for cortical development SO JOURNAL OF NEUROSCIENCE LA English DT Article DE serotonin (5-HT); Cajal-Retzius cells; reelin; autism; microcolumns; marginal zone ID HUMAN CEREBRAL-CORTEX; MINICOLUMNAR PATHOLOGY; REELIN IMMUNOREACTIVITY; NEURONAL MIGRATION; BRAIN-DEVELOPMENT; 5-HT1A RECEPTORS; VISUAL-CORTEX; RAT; SCHIZOPHRENIA; EXPRESSION AB Although the serotonergic system plays an important role in various neurological disorders, the role of early serotonergic projections to the developing cerebral cortex is not well understood. Because serotonergic fibers enter the marginal zone (MZ) before birth, it has been suggested that they may influence cortical development through synaptic contacts with Cajal-Retzius (CR) cells. We used immunohistochemistry combined with confocal and electron microscopy to show that the earliest serotonergic projections to the MZ form synaptic contacts with the somata and proximal dendrites of CR cells as early as embryonic day 17. To elucidate the functional significance of these early serotonergic contacts with CR cells, we perturbed their normal development by injecting pregnant mice with 5-methoxytryptamine. Lower reelin levels were detected in the brains of newborn pups from the exposed animals. Because reelin plays an important role in the cortical laminar and columnar organization during development, we killed some pups from the same litters on postnatal day 7 and analyzed their presubicular cortex. We found that the supragranular layers of the presubicular cortex (which normally display a visible columnar deployment of neurons) were altered in the treated animals. Our results suggest a mechanism of how serotonergic abnormalities during cortical development may disturb the normal cortical organization; and, therefore, may be relevant for understanding neurological disorders in which abnormalities of the serotonergic system are accompanied by cortical pathology ( such as autism). C1 Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA. RP Rakic, P (reprint author), Yale Univ, Sch Med, Dept Neurobiol, POB 208001, New Haven, CT 06520 USA. 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News PD FEB 16 PY 2004 VL 82 IS 7 BP 10 EP 10 PG 1 WC Chemistry, Multidisciplinary; Engineering, Chemical SC Chemistry; Engineering GA 774XD UT WOS:000189010900015 ER PT J AU Vincent, JB Thevarkunnel, S Kolozsvari, D Paterson, AD Roberts, W Scherer, SW AF Vincent, JB Thevarkunnel, S Kolozsvari, D Paterson, AD Roberts, W Scherer, SW TI Association and transmission analysis of the FMR1 IVS10+14C-T variant in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; FMR1; intronic variant; association; transmission ID FRAGILE-X-SYNDROME; POINT MUTATION; EXON 10; GENE; INTRON-10; DEMENTIA; RNA AB Evidence from the high male to female ratio of individuals with autism as well as suggestive linkage data have implicated the possible involvement of X chromosomal loci in the aetiology of autism. Studies of the FMR1 gene on Xq27 have shown that occasionally individuals, and particularly females, with the [CGG] repeat expansion and methylation mutation may present with autistic symptoms. However, molecular studies suggest that such mutations are not a major cause of autism. Previously, we have screened autism probands for mutations in regions of the FMR1 gene downstream of the [CGG] repeat and identified an intronic variant in the FMR1 gene, IVS10 + 14C-T, which was present at a significantly higher frequency in autistic individuals compared to controls individuals. We have now investigated this variant in a further 136 autism families and 186 control individuals. We have established that the variant is significantly more frequent among East Asian individuals within our affected and control groups (P < 0.0001) and although we observed a trend of higher transmission frequency of the rare allele to affected individuals, there was no significant evidence in either family-based or case/control association studies for this variant in autism (P > 0.05). (C) 2003 Wiley-Liss, Inc. C1 Ctr Addict Mental Hlth, Neurogenet Sect, Toronto, ON M5T 1R8, Canada. Hosp Sick Children, Program Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. RP Vincent, JB (reprint author), Ctr Addict Mental Hlth, Neurogenet Sect, 250 Coll St, Toronto, ON M5T 1R8, Canada. 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B PD FEB 15 PY 2004 VL 125B IS 1 BP 54 EP 56 DI 10.1002/ajmg.b.20088 PG 3 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 777PF UT WOS:000189186200009 PM 14755444 ER PT J AU Raiford, KL Shao, Y Allen, IC Martin, ER Menold, MM Wright, HH Abramson, RK Worley, G DeLong, GR Vance, JM Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Raiford, KL Shao, Y Allen, IC Martin, ER Menold, MM Wright, HH Abramson, RK Worley, G DeLong, GR Vance, JM Cuccaro, ML Gilbert, JR Pericak-Vance, MA TI No association between the APOE gene and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; association; APOE ID APOLIPOPROTEIN-E; CHROMOSOME 7Q; REELIN GENE; LINKAGE DISEQUILIBRIUM; ALZHEIMERS-DISEASE; PARKINSON-DISEASE; GENOMEWIDE SCREEN; INFANTILE-AUTISM; FAMILY HISTORY; DISORDER AB Autism is a neurodevelopmental disorder characterized by stereotypic and repetitive behavior and interests, together with social and communicative deficiencies. The results of several genomic screens suggest the presence of an autism susceptibility locus on chromosome 19p13.2-q13.4. The apolipoprotein E (APOE) gene on chromosome 19 encodes for a protein, apoE, whose different isoforms (E2, E3, E4) influence neuronal growth. APOE participates in lipid transport and metabolism, repair, growth, and maintenance of axons and myelin during neuronal development. The APOE protein competes with the Reelin protein for VLDL/APOER2 receptor binding. Several studies have reported evidence for an association between autism and the Reelin gene. Based on these data we tested for association between APOE and autism using family-based association methods in a data set of 322 autism families. Three promoter, one intronic, and one 3' UTR single nucleotide polymorphisms (SNPs) in the APOE gene (-491a/t, -427c/t, -219g/t, 113c/g, and 5361c/t) as well as the APOE functional polymorphism (E2, E3, E4) were examined and failed to reveal significant evidence that autism is associated with APOE. (C) 2003 Wiley-Liss, Inc. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Univ S Carolina, Sch Med, Columbia, SC USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Box 3445, Durham, NC 27710 USA. 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J. Med. Genet. B PD FEB 15 PY 2004 VL 125B IS 1 BP 61 EP 62 DI 10.1002/ajmg.b.20113 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 777PF UT WOS:000189186200011 PM 14755446 ER PT J AU Nabi, R Serajee, FJ Chugani, DC Zhong, HL Huq, AHMM AF Nabi, R Serajee, FJ Chugani, DC Zhong, HL Huq, AHMM TI Association of tryptophan 2,3 dioxygenase gene polymorphism with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; TDO2; serotonin ID PEDIGREE DISEQUILIBRIUM TEST; LINKAGE DISEQUILIBRIUM; SEROTONIN TRANSPORTER; TOURETTE-SYNDROME; RECEPTOR GENE; TRANSMISSION DISEQUILIBRIUM; SOMATOSENSORY CORTEX; DISORDER; DEPLETION; VARIANTS AB Although elevation of blood and platelet serotonin has been documented in autism, genetic analyses of serotonin transporter gene have given conflicting results. Tryptophan 2,3 dioxygenase (TDO2) is the rate-limiting enzyme in the catabolism of tryptophan, the precursor of serotonin. A mutation that results in decreased activity of the TDO2 can decrease catabolism of tryptophan and increase the level of whole body serotonin. As such it is a potential candidate gene for autism. We have investigated five single nucleotide polymorphisms in the TDO2 gene for association with autistic disorder. One hundred and ninety six multiplex autistic disorder families were tested using transmission disequilibrium test. There was a significant difference in the transmission of a promoter variant to autistic subjects (P = 0.0006). Haplotype analysis also demonstrated significant difference in the transmission of TDO2 haplotypes to autistic subjects (P = 0.0027). Our results suggest the presence of a susceptibility mutation in the TDO2 or a nearby gene, but may also represent a chance finding. (C) 2003 Wiley-Liss, Inc. C1 Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA. Wayne State Univ, Dept Radiol, Detroit, MI USA. Wayne State Univ, Dept Neurol, Detroit, MI USA. RP Huq, AHMM (reprint author), Childrens Hosp Michigan, Div Neurol, Detroit, MI 48201 USA. 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B PD FEB 15 PY 2004 VL 125B IS 1 BP 63 EP 68 DI 10.1002/ajmg.b.20147 PG 6 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 777PF UT WOS:000189186200012 PM 14755447 ER PT J AU Nair-Miranda, K Murch, A Petterson, B Hill, W Nikolova-Hill, A Bradley, L Jackson, S Hallmayer, J AF Nair-Miranda, K Murch, A Petterson, B Hill, W Nikolova-Hill, A Bradley, L Jackson, S Hallmayer, J TI An investigation into sub-telomeric deletions of chromosome 22 and pervasive developmental disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; ring 22; FISH; microdeletion ID DIAGNOSTIC OBSERVATION SCHEDULE; IDIOPATHIC MENTAL-RETARDATION; ADENYLOSUCCINATE LYASE ADSL; TERMINAL 22Q13 DELETION; AUTISTIC DISORDER; GENOMEWIDE SCREEN; MOLECULAR CHARACTERIZATION; RING CHROMOSOME-22; INFANTILE-AUTISM; PARTIAL MONOSOMY AB Deletions of the sub-telomeric region of chromosome 22 have been associated with mental retardation, developmental delay, and autistic behaviors. This study investigated sub-telomeric anomalies of chromosome 22 using fluorescent in situ hybridization (FISH) probes in 82 subjects diagnosed with autism and atypical autism. No microdeletions were detected in this group. Similar FISH analyses were undertaken on two children with developmental delay, who were ascertained to be ring 22 during routine cytogenetic investigations. One subject was shown to have a microdeletion in the sub-telomeric region tested. Both children met the social and communication cut off for autism on the ADI and but did not meet the cut off for restrictive and repetitive behaviors. Only one of the two children met the criteria for PDD on the ADOS. (C) 2003 Wiley-Liss, Inc. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA. Univ Western Australia, Sch Psychiat & Clin Neurosci, Perth, WA 6009, Australia. Graylands Hosp, Ctr Clin Res Neuropsychiat, Palo Alto, CA USA. Disabil Serv Commiss, Perth, WA, Australia. King Edward Mem Hosp, Dept Cytogenet, Subiaco, WA, Australia. RP Hallmayer, J (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, 1201 Welch Rd,Room P112, Palo Alto, CA 94304 USA. 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P., 1997, SMJ, V38, P85 ZWAIGENBAUM L, 1990, AM J HUM GENET, V47, pA45 NR 63 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 B JI Am. J. Med. Genet. B PD FEB 15 PY 2004 VL 125B IS 1 BP 99 EP 104 DI 10.1002/ajmg.b.20101 PG 6 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 777PF UT WOS:000189186200018 PM 14755453 ER PT J AU Rasmussen, SA Moore, CA AF Rasmussen, SA Moore, CA TI Public health approach to birth defects, developmental disabilities, and genetic conditions - Introduction SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Editorial Material ID NEURAL-TUBE DEFECTS; CONGENITAL-MALFORMATIONS; VITAMIN SUPPLEMENTATION; GENOMIC MEDICINE; FAMILY-HISTORY; PREVENTION; SURVEILLANCE; GUIDELINES; PREVALENCE; AUTISM C1 Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Div Birth Defects & Dev Disabil, Atlanta, GA 30333 USA. Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Pediat Genet Team, Atlanta, GA 30333 USA. RP Rasmussen, SA (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Div Birth Defects & Dev Disabil, 1600 Clifton Rd,MS E-86, Atlanta, GA 30333 USA. 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J. Med. Genet. C PD FEB 15 PY 2004 VL 125C IS 1 BP 1 EP 3 DI 10.1002/ajmg.c.30003 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 769LX UT WOS:000188652500001 PM 14755427 ER PT J AU Rice, C Schendel, D Cunniff, C Doernberg, N AF Rice, C Schendel, D Cunniff, C Doernberg, N TI Public health monitoring of developmental disabilities with a focus on the autism spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE developmental disabilities; autism spectrum disorders; surveillance; monitoring; tracking; public health ID CEREBRAL-PALSY; MOLECULAR-GENETICS; EASTERN DENMARK; PREVALENCE; CHILDREN; EPIDEMIOLOGY AB Developmental disabilities (DDs) are conditions characterized by physical, cognitive, psychological, sensory, adaptive, and/or communication impairments manifested during development. Approximately 17% of individuals in the United States 18 years and younger have a DID, and for most children the cause of their condition is unknown. Of particular interest are the autism spectrum disorders (ASDs), characterized by unusual social, communication, and behavioral development. Previously autism was thought to be a rare condition, but the number of children receiving services for an ASD has increased dramatically in the last decade. Concerns about increases in DDs, particularly ASDs, their causes, and the high costs of intervention have highlighted the need for systematic public health monitoring. Service provider data, such as annual reporting of special education services or of state DID programs, do not provide a complete estimate of the rates for DDs, including ASDs. Unlike genetic metabolic disorders or congenital hearing loss (HQ for which newborn screening programs can provide accurate prevalence rates, there are currently no genetic or biologic markers for the ASDs to enable consistent and early identification of affected children. Centers for Disease Control and Prevention's (CDC) Metropolitan Atlanta Developmental Disabilities Surveillance Program (MADDSP) is a model for population monitoring of ASDs/DDs that has been implemented in other states. This article discusses the role of ASD/DD tracking in public health, as well as the challenges of ASD/DD tracking, including case definition and identification, associated conditions, linkages, and data access. (C) 2004 Wiley-Liss, Inc. C1 Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30341 USA. Univ Arizona, Coll Med, Dept Pediat, Tucson, AZ 85721 USA. RP Rice, C (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, 4770 Buford Highway NE,Mailstop F-15, Atlanta, GA 30341 USA. 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C PD FEB 15 PY 2004 VL 125C IS 1 BP 22 EP 27 DI 10.1002/ajmg.c.30006 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 769LX UT WOS:000188652500004 PM 14755430 ER PT J AU Conciatori, M Stodgell, CJ Hyman, SL O'Bara, M Militerni, R Bravaccio, C Trillo, S Montecchi, F Schneider, C Melmed, R Elia, M Crawford, L Spence, SJ Muscarella, L Guarnieri, V D'Agruma, L Quattrone, A Zelante, L Rabinowitz, D Pascucci, T Puglisi-Allegra, S Reichelt, KL Rodier, PM Persico, AM AF Conciatori, M Stodgell, CJ Hyman, SL O'Bara, M Militerni, R Bravaccio, C Trillo, S Montecchi, F Schneider, C Melmed, R Elia, M Crawford, L Spence, SJ Muscarella, L Guarnieri, V D'Agruma, L Quattrone, A Zelante, L Rabinowitz, D Pascucci, T Puglisi-Allegra, S Reichelt, KL Rodier, PM Persico, AM TI Association between the HOXA1 A218G polymorphism and increased head circumference in patients with autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autistic disorder; cranial circumference; homeobox; macrocephaly; megalencephaly; pervasive developmental disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; NEUROANATOMICAL ABNORMALITIES; CRANIAL NERVES; GENE VARIANTS; MUTANT MICE; HOXB1; HINDBRAIN; MUTATIONS; CHILDREN; DEFECTS AB Background: The HOXA1 gene plays a major role in brainstem and cranial morphogenesis. The G allele of the HOXA1 A218G polymorphism has been previously found associated with autism. Methods. We performed case-control and family-based association analyses, contrasting 127 autistic patients with 174 ethnically matched controls, and assessing for allelic transmission disequilibrium in 189 complete trios. Results: A, and not G, alleles were associated with autism using both case-control (chi(2) = 8.96 and 5.71, 1 df, p < .005 and < .025 for genotypes and alleles, respectively), and family-based (transmission/disequilibrium test chi(2) = 8.80, 1 df, p < .005) association analyses. The bead circumference of 31 patients carrying one or two copies of the G allele displayed significantly larger median values (95.0th, vs. 82.5th percentile, p < .05) and dramatically reduced interindividual variability (p < .0001), compared with 166 patients carrying the A/A genotype. Conclusions. The HOXA1 A218G polymorphism explains approximately 5% of the variance in the bead circumference of autistic patients and represents to our knowledge the first known gene variant providing sizable contributions to cranial morphology. The disease specificity of this finding is currently being investigated. Nonreplications in genetic linkage/association studies could partly stem from the dyshomogeneous distribution of an endophenotype morphologically defined by cranial circumference. C1 Univ Campus Biomed, Lab Mol Psychiat & Neurogenet, I-00155 Rome, Italy. Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. Univ Naples 2, Dept Child Neuropsychiat, Naples, Italy. Osped Bambino Gesu, IRCCS, Div Child Neuropsychiat, Rome, Italy. SW Autism Res Ctr, Phoenix, AZ USA. IRCCS Oasi Maria SS, Neurol Serv, Troina, Italy. Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, Los Angeles, CA USA. Autism Genet Resource Exchange, Los Angeles, CA USA. IRCCS Casa Sollievo Sofferenza, Gen Med Serv, San Giovanni Rotondo, Italy. Columbia Univ, Dept Stat, New York, NY USA. Univ Roma La Sapienza, Dept Psychol, Rome, Italy. Fondaz Santa Lucia, Ist Ric Clin Carattere Sci, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, Oslo, Norway. RP Persico, AM (reprint author), Univ Campus Biomed, Lab Mol Psychiat & Neurogenet, Via Longoni 83, I-00155 Rome, Italy. 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Psychiatry PD FEB 15 PY 2004 VL 55 IS 4 BP 413 EP 419 DI 10.1016/j.biopsych.2003.10.005 PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 774DP UT WOS:000188964700012 PM 14960295 ER PT J AU Sweeten, TL Posey, DJ Shankar, S McDougle, CJ AF Sweeten, TL Posey, DJ Shankar, S McDougle, CJ TI High nitric oxide production in autistic disorder: A possible role for interferon-gamma SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; nitric oxide; interferon; cytokines; immunology; pathophysiology ID PERVASIVE DEVELOPMENTAL DISORDERS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; MULTIPLE-SCLEROSIS; FAMILIAL AUTOIMMUNITY; INCREASED PREVALENCE; GUANYLATE-CYCLASE; SYNTHASE; RELEASE; ACTIVATION; SPECTRUM AB Background: Neuroimmune regulation abnormalities have been implicated in the pathophysiology of autistic disorder. Nitric oxide (NO) is involved in immune reactivity and is known to affect brain neurodevelopmental processes. Recent evidence indicates that NO, and cytokines involved in NO production, may be high in children with autism. The purpose of this study was to verify that plasma NO is high in children with autism and determine whether this elevation is related to plasma levels of cytokines involved in NO production. Methods. The metabolites of NO, nitrite, and nitrate (NOx), along with the cytokines interferon-gamma (IFN-gamma), tumor necrosis factor-alpha, and interleukin-1beta, were measured in plasma of 29 children with autism (mean age +/- SD = 61 +/- 2.8 years) and 27 age- and gender-matcbed healthy comparison subjects using commercially available assay kits. Results: Plasma levels of NOx were significantly higher in the autistic subjects (p = .006); plasma levels of the cytokines did not differ between groups. NOx and IFN-gamma levels were positively correlated in the autistic subjects (r = .51; p = .005). 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Psychiatry PD FEB 15 PY 2004 VL 55 IS 4 BP 434 EP 437 DI 10.1016/j.biopsych.200309.001 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 774DP UT WOS:000188964700015 PM 14960298 ER PT J AU Katikireddi, V AF Katikireddi, V TI Increase in autism is due to changes in diagnosis, study claims SO BRITISH MEDICAL JOURNAL LA English DT News Item CR Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 NR 1 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD FEB 14 PY 2004 VL 328 IS 7436 BP 364 EP 364 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 775GA UT WOS:000189031300009 ER PT J AU Thrower, D AF Thrower, D TI MMR and autism: the debate continues SO LANCET LA English DT Letter RP Thrower, D (reprint author), 49 Ackers Rd,Stockton Heath, Warrington WA4 2DZ, Cheshire, England. EM David@ThrowerWarrington.freeserve.co.uk CR BUIE T, 2001, OAS 2001 C AUT PORTL Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Murch S, 2003, LANCET, V362, P1498, DOI 10.1016/S0140-6736(03)14699-5 *UK COMM SAF MED, 1999, REP WORK PART MMR VA NR 4 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 FEB 14 PY 2004 VL 363 IS 9408 BP 567 EP 568 DI 10.1016/S0140-6736(04)15549-9 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 774TA UT WOS:000188999900028 PM 14975622 ER PT J AU Harvey, P AF Harvey, P TI MMR and autism: the debate continues SO LANCET LA English DT Letter RP Harvey, P (reprint author), 134 Harley St, London W1G 7JY, England. 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 FEB 14 PY 2004 VL 363 IS 9408 BP 568 EP 568 DI 10.1016/S0140-6736(04)15550-5 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 774TA UT WOS:000188999900029 PM 14975624 ER PT J AU Murch, S AF Murch, S TI MMR and autism: the debate continues - Reply SO LANCET LA English DT Letter C1 Ctr Pediat Gastroenterol, London NW3 2PF, England. RP Murch, S (reprint author), Ctr Pediat Gastroenterol, Royal Free Campus,Rowland Hill St, London NW3 2PF, England. EM s.murch@rfc.ucl.ac.uk NR 0 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 FEB 14 PY 2004 VL 363 IS 9408 BP 568 EP 569 DI 10.1016/S0140-6736(04)15551-7 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 774TA UT WOS:000188999900030 ER PT J AU Elphinstone, P AF Elphinstone, P TI MMR and autism: the debate continues SO LANCET LA English DT Letter C1 Ampthill Sq Med Ctr, London NW1 1DR, England. RP Elphinstone, P (reprint author), Ampthill Sq Med Ctr, London NW1 1DR, England. EM Paula.Symons@gp-F83006.nhs.uk CR AMRSH B, 2003, DAILY MAIL 1004 Elphinstone P, 2002, LANCET, V359, P2112, DOI 10.1016/S0140-6736(02)08916-X *LEG SERV COMM, DEC REM FUND MMR LIT MURCH S, 2003, LANCET, V362, P9394 NR 4 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD FEB 14 PY 2004 VL 363 IS 9408 BP 569 EP 569 DI 10.1016/S0140-6736(04)15552-9 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 774TA UT WOS:000188999900031 PM 14975625 ER PT J AU Chauhan, V Chauhan, A Cohen, IL Brown, WT Sheikh, A AF Chauhan, V Chauhan, A Cohen, IL Brown, WT Sheikh, A TI Alteration in amino-glycerophospholipids levels in the plasma of children with autism: A potential biochemical diagnostic marker SO LIFE SCIENCES LA English DT Article DE autism; amino-glycerophospholipids; lipids; phosphatidylethanolamme; phosphatidylserine; plasma; membrane ID RED-BLOOD-CELLS; MEMBRANE BILAYER; GENOMIC SCREEN; IV CPLA2; PHOSPHATIDYLSERINE; PEROXIDATION; ERYTHROCYTES; DISORDERS; KINASE; ATPASE AB Currently, there is no biochemical test to assist in the behavioral diagnosis of autism. We observed that levels of phosphatidylethanolamine (PE) were decreased while phosphatidylserine (PS) were increased in the erythrocyte membranes of children with autism as compared to their non-autistic developmentally normal siblings. A new method using Trinitrobenezene sulfonic acid (TNBS) for the quantification of PE and PS (amino-glycerophospholipids, i.e., AGP) in the plasma of children was developed and standardized. Wavelength scans of TNBS-PE and TNBS-PS complexes gave two peaks at 320 nm and 410 nm. When varying concentrations of PS and PE were used, a linear regression line was observed at 410 nm with TNBS. Using this assay, the levels of AGP were found to be significantly increased in the plasma of children with autism as compared to their non-autistic normal siblings. It is proposed that plasma AGP levels may function as a potential diagnostic marker for autism. (C) 2003 Elsevier Inc. All rights reserved. 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These procedures attempt to accommodate a lack of informativity, nongenotyped loci, missing data, and related issues concerning the genetic markers used in a linkage study. However, such procedures often cannot overcome these phenomena in compelling ways and, as a result, assign relevant relative pairs allele-sharing values that are "expected" for those pairs. The practice of assigning expected allele-sharing values to relative pairs in the face of a lack of explicit allele-transmission information can bias traditional nonparametric linkage test statistics toward the null hypothesis of no locus effect. This bias is due to the use of expected values, rather than to a lack of information about actual allele sharing at relevant marker loci. The bias will vary from study to study on the basis of the DNA markers, sample size, relative-pair types, and pedigree structures used, but it can be extremely pronounced and could contribute to a lack of consistent success in the application of traditional nonparametric linkage analyses to complex human traits and diseases. There are several potential ways to overcome this problem, but their foundations deserve greater research. We expose many of the issues concerning allele sharing with data from a large affected-sibling-pair study investigating the genetic basis of autism. C1 Univ Calif San Diego, Dept Psychiat, Polymorphism Res Lab, La Jolla, CA 92093 USA. RP Schork, NJ (reprint author), Univ Calif San Diego, Dept Psychiat, Polymorphism Res Lab, 0603,9500 Gilman Dr, La Jolla, CA 92093 USA. 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PD FEB PY 2004 VL 13 IS 1 BP 3 EP 4 DI 10.1044/1058-0360(2004/002) PG 2 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 970CP UT WOS:000232283100002 PM 15101809 ER PT J AU Bopp, KD Brown, KE Mirenda, P AF Bopp, KD Brown, KE Mirenda, P TI Speech-language pathologists' roles in the delivery of positive behavior support for individuals with developmental disabilities SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE augmentative and alternative communication; autism; developmental disabilities; behavior problems; visual schedules ID PHOTOGRAPHIC ACTIVITY SCHEDULES; DESTRUCTIVE BEHAVIOR; CHALLENGING BEHAVIOR; RESPONSE EFFICIENCY; MULTIPLE FUNCTIONS; AUTISM; CHILDREN; REINFORCEMENT; MAINTENANCE; ACQUISITION AB Positive behavior support interventions such as functional communication training (FCT) and visual schedules are increasingly being used with individuals with autism and other severe developmental disabilities who engage in problem behavior and use augmentative and alternative communication (AAC). 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Distinct roles needed for language and communication SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID MIND; AUTISM AB Carpendale & Lewis's (C&L's) theory falls in with an existing set of theories that children's understanding of mind is collaboratively constructed in linguistically mediated social interaction. This social constructivist view needs to be clear about the complementary contributions of the child and of the social environment. I distinguish between the child's individual linguistic ability and the dyad's social communication, proposing that each makes a contribution to theory-of-mind development, differently balanced in different individuals. C1 Univ Toronto, Ontario Inst Studies Educ, Dept Human Dev & Appl Psychol, Toronto, ON M5S 1V6, Canada. RP Astington, JW (reprint author), Univ Toronto, Ontario Inst Studies Educ, Dept Human Dev & Appl Psychol, 100 Coll St, Toronto, ON M5S 1V6, Canada. EM iwastington@oise.utoronto.ca CR ASTINGTON J, 1996, THEORIES THEORIES MI ASTINGTON JW, 1995, HUM DEV, V38, P179 BOYES M, 1997, SOCIOGENETIC PERSPEC DUNN J, 1996, CHILDREN RES POLICY Fernyhough C, 1996, NEW IDEAS PSYCHOL, V14, P47, DOI 10.1016/0732-118X(95)00024-B Garfield JL, 2001, MIND LANG, V16, P494, DOI 10.1111/1468-0017.00180 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Harris P., 1999, DEV PSYCHOL ACHIEVEM HUGHES C, 2002, INT C WHY LANG MATT Jenkins JM, 1996, DEV PSYCHOL, V32, P70, DOI 10.1037/0012-1649.32.1.70 LOHMANN H, 2003, IN PRESS CHILD D JUL, V74 Montgomery DE, 2002, J COGN DEV, V3, P357, DOI 10.1207/S15327647JCD3,4-01 Nelson K., 1996, LANGUAGE COGNITIVE D Peterson CC, 2000, MIND LANG, V15, P123, DOI 10.1111/1468-0017.00126 ROGOFF B, 1993, BEHAV BRAIN SCI, V16, P533 SHATZ M, 1994, CHILDRENS EARLY UNDE TAGERFLUSBERG H, 2002, INT C WHY LANG MATT NR 17 TC 5 Z9 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0140-525X J9 BEHAV BRAIN SCI JI Behav. Brain Sci. PD FEB PY 2004 VL 27 IS 1 BP 96 EP + PG 13 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 858JM UT WOS:000224188100035 ER PT J AU Conroy, MA Asmus, JM Ladwig, CN Sellers, JA Valcante, G AF Conroy, MA Asmus, JM Ladwig, CN Sellers, JA Valcante, G TI The effects of proximity on the classroom behaviors of students with autism in general education settings SO BEHAVIORAL DISORDERS LA English DT Article; Proceedings Paper CT Council for Exceptional Children Conference CY 2002 CL New York, NY ID DISABILITIES; DISORDERS AB In this study the authors examined the descriptive effects of adult proximity on the behaviors of six elementary-aged students with autism spectrum disorders served in general education settings. A descriptive analysis was conducted to determine the effects of adult proximity on the rate of challenging behaviors and academic engagement. In addition, lag sequential analyses were conducted examining the effects of adult proximity on the relationship between adult directives and subsequent target child behaviors. The results indicated that adult proximity positively increased the rates of engagement and the likelihood that engagement followed an adult directive for most of the participants. However, idiosyncratic differences between adult proximity and problem behaviors were found across the participants. C1 Univ Florida, Dept Special Educ, Gainesville, FL 32611 USA. Univ Florida, Dept Educ Psychol, Gainesville, FL USA. Univ Florida, Ctr Autism & Related Disabil, Gainesville, FL USA. RP Conroy, MA (reprint author), Univ Florida, Dept Special Educ, Gainesville, FL 32611 USA. 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Disord. PD FEB PY 2004 VL 29 IS 2 BP 119 EP 129 PG 11 WC Psychology, Clinical; Psychology, Educational SC Psychology GA 939LI UT WOS:000230073900002 ER PT J AU Barnea-Goraly, N Kwon, H Menon, V Eliez, S Lotspeich, L Reiss, AL AF Barnea-Goraly, N Kwon, H Menon, V Eliez, S Lotspeich, L Reiss, AL TI White matter structure in autism: Preliminary evidence from diffusion tensor imaging SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; social cognition; DTI; white matter; brain; MRI ID FUSIFORM FACE AREA; SOCIAL COGNITION; ASPERGER-SYNDROME; BRAIN-DEVELOPMENT; CHILDREN; CORTEX; MIND; PERCEPTION; SEROTONIN; FEATURES AB Background: Individuals with autism have severe difficulties in social communication and relationships. Prior studies have suggested that abnormal connections between brain regions important for social cognition may contribute to the social deficits seen in autism. Methods. In this study, we used diffusion tensor imaging to investigate white matter structure in seven male children and adolescents with autism and nine age-, gender-, and IQ-matched control subjects. Results: Reduced fractional anisotropy (FA) values were observed in white matter adjacent to the ventromedial prefrontal cortices and in the anterior cingulate gyri as well as in the temporoparietal junctions. Additional clusters of reduced FA values were seen adjacent to the superior temporal sulcus bilaterally, in the temporal lobes approaching the amygdala bilaterally, in occipitotemporal tracts, and in the corpus callosum. Conclusions. Disruption of white matter tracts between regions implicated in social functioning may contribute to impaired social cognition in autism. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. Univ Geneva, Sch Med, Div Child & Adolescent Psychiat, CH-1211 Geneva, Switzerland. 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Psychiatry PD FEB 1 PY 2004 VL 55 IS 3 BP 323 EP 326 DI 10.1016/j.biopsych.2003.10.022 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 767HK UT WOS:000188434000019 PM 14744477 ER PT J AU Reilly, J Losh, M Bellugi, U Wulfeck, B AF Reilly, J Losh, M Bellugi, U Wulfeck, B TI "Frog, where are you?" - Narratives in children with specific language impairment, early focal brain injury, and Williams syndrome SO BRAIN AND LANGUAGE LA English DT Article DE specific language impairment; focal brain injury; Williams syndrome; morphology; plasticity; narratives; language development ID MOLECULAR-GENETICS; RIGHT-HEMISPHERE; EARLY-ONSET; DISCOURSE; HEMIDECORTICATION; HYPERSOCIABILITY; SUPERIORITY; AUTISM; AGE AB In this cross-population study, we use narratives as a context to investigate language development in children from 4 to 12 years of age from three experimental groups: children with early unilateral focal brain damage (FL; N = 52); children with specific language impairment (SLI; N = 44); children with Williams syndrome (WMS; N = 36), and typically developing controls. We compare the developmental trajectories of these groups in the following domains; morphological errors, use of complex syntax, complexity of narrative structure, and types and frequency of evaluative devices. For the children with early unilateral brain damage, there is initial delay. However, by age 10, they are generally within the normal range of performance for all narrative measures. Interestingly, there are few, if any, side specific differences. Children with SLI, who have no frank neurological damage and show no cognitive impairment demonstrate significantly more delay on all morphosyntactic measures than the FL group. Quantitatively, on morphosyntactic measures, the SLI group clusters with those children with WMS who are moderately retarded. Together these data help us to understand the extent and nature of brain plasticity for language development and those aspects of language and discourse that are dissociable. (C) 2003 Elsevier Science (USA). All rights reserved. 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For instance, the clinical phenotype of congenital nephrogenic diabetes insipidus has been linked to more than 155 loss-of-function putative mutations of the arginine vasopressin (AVP) V-2 receptor, which span each and every segment of this seven-transmembrane domain receptor. These mutant receptors, which are mostly trapped in the endoplasmic reticulum, can be rescued by membrane-permeant nonpeptidic AVIP receptor antagonists. An overexpression of V-1-vascular and V-3-pituitary AVP receptors has been observed in some endocrine tumors. The single nucleotide polymorphism of AVP receptors in the context of complex genetic traits is currently being investigated, and preliminary findings have been reported in arterial hypertension and autism. C1 Case Western Reserve Univ, Div Clin & Mol Endocrinol, Dept Med, Sch Med, Cleveland, OH 44106 USA. RP Thibonnier, M (reprint author), Case Western Reserve Univ, Div Clin & Mol Endocrinol, Dept Med, Sch Med, 10900 Euclid Ave, Cleveland, OH 44106 USA. 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Hypertens. Rep. PD FEB PY 2004 VL 6 IS 1 BP 21 EP 26 DI 10.1007/s11906-004-0006-8 PG 6 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 988ZX UT WOS:000233643800004 PM 14972085 ER PT J AU Sweeney, JA Takarae, Y Macmillan, C Luna, B Minshew, NJ AF Sweeney, JA Takarae, Y Macmillan, C Luna, B Minshew, NJ TI Eye movements in neurodevelopmental disorders SO CURRENT OPINION IN NEUROLOGY LA English DT Article DE autism; ADHD; Tourette's syndrome; neurodevelopmental disorders ID DEFICIT HYPERACTIVITY DISORDER; TOURETTES-SYNDROME; OCULOMOTOR ABNORMALITIES; REFLEXIVE SACCADES; VISUAL FIXATION; AUTISM; ATTENTION; CHILDREN; PERFORMANCE; ANTISACCADE AB Purpose of review The aim of this paper is to review the literature on eye-movement abnormalities associated with neurodevelopmental disorders. Eye-movement testing is a non-invasive quantitative approach for evaluating brain systems across the age spectrum. It thus provides a promising methodology for characterizing and documenting maturational abnormalities in brain systems associated with neurodevelopmental disorders. Recent findings Recent oculomotor studies have made significant contributions to the understanding of neurodevelopmental disorders, most notably in autism, attention-deficit/hyperactivity disorder, and Tourette's syndrome. Notably different patterns of deficits have been found in these disorders and have helped to clarify their pathophysiology. Summary Eye-movement studies have begun to serve as a useful approach for studying cognitive and neurophysiological aspects of neurodevelopmental disorders. They also have potential as a strategy for establishing quantitative endophenotypes for genetic research, and for monitoring beneficial and adverse effects of pharmacotherapies. Studies are needed that involve larger patient populations, longitudinal characterization of developmental failures, patients free from central nervous system-active medications, and that use functional imaging, as patients perform eye-movement tasks, for direct identification of clinically relevant abnormalities in brain systems. C1 Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA. Univ Illinois, Dept Neurol, Chicago, IL 60612 USA. Univ Illinois, Dept Psychol, Chicago, IL 60612 USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA. RP Sweeney, JA (reprint author), Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA. 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PD FEB PY 2004 VL 17 IS 1 BP 37 EP 42 DI 10.1097/01.wco.0000113936.12823.ad PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 780LY UT WOS:000189383200006 PM 15090875 ER PT J AU Flynn, E O'Malley, C Wood, D AF Flynn, E O'Malley, C Wood, D TI A longitudinal, microgenetic study of the emergence of false belief understanding and inhibition skills SO DEVELOPMENTAL SCIENCE LA English DT Article ID MIND DEVELOPMENT; AUTISM; PRESCHOOLERS; DECEPTION; BEHAVIOR AB Two theories that attempt to explain the relationship between false belief understanding and inhibition skills were investigated.(1) theory of mind development improves self-control, and (2) executive control is necessary for developing a theory of mind A microgenetic approach was adopted, with a group of 21 children completing a battery of inhibition and false belief understanding tasks every four weeks for six phases of testing The results showed that the majority of children were able to perform well on a test of executive inhibition before having a good understanding of false beliefs, thus supporting theory (2). 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PD FEB PY 2004 VL 7 IS 1 BP 103 EP 115 DI 10.1111/j.1467-7687.2004.00326.x PG 13 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 772LF UT WOS:000188842800012 PM 15323122 ER PT J AU Besag, FMC AF Besag, FMC TI Behavioral aspects of pediatric epilepsy syndromes SO EPILEPSY & BEHAVIOR LA English DT Article DE behavior; epilepsy syndrome; West; infantile spasms; Dravet; severe myoclonic; Lennox-Gastaut; Landau-Kleffner; rolandic; centrotemporal; janz; juvenile myoclonic epilepsy ID JUVENILE MYOCLONIC EPILEPSY; LANDAU-KLEFFNER-SYNDROME; LENNOX-GASTAUT-SYNDROME; VAGUS NERVE-STIMULATION; MULTIPLE SUBPIAL TRANSECTIONS; ACQUIRED APHASIA; CENTROTEMPORAL SPIKES; TUBEROUS SCLEROSIS; CHILDHOOD EPILEPSY; INFANTILE SPASMS AB Apart from control of the seizures, two of the most important factors in determining how well a child with epilepsy progresses toward independence are cognition and behavior. The diagnosis of the correct epilepsy syndrome often provides information with regard to probability of good seizure control and intellectual outcome. However, relatively little has been published on the behavioral aspects of the various epilepsy syndromes. In West syndrome there is emerging evidence that early effective treatment might improve outcome in terms of both cognition and behavior. The work on this syndrome in children with tuberous sclerosis has demonstrated an association between temporal lobe tubers and autism. In Dravet syndrome, a variety of psychiatric disorders have been reported, including hyperactivity and autistic features. This is another epilepsy syndrome that tends to be resistant to treatment, implying that the prognosis has to be guarded. The behavioral problems reported with Lennox-Gastaut syndrome also include autistic features, as well as generally sluggish behavior. It is very likely that these characteristics largely reflect the effect of ongoing seizure activity. Autistic features, aggression, and hyperkinesis have been described with Landau-Kleffner syndrome. The behavior may improve dramatically with appropriate medical treatment or after multiple subpial transection. Although the syndrome of benign partial seizures with centrotemporal or rolandic spikes is said to have a very good prognosis, it is becoming increasingly evident that behavioral problems such as concentration difficulties, tempers, hyperactivity, and impulsivity might occur. Juvenile myoclonic epilepsy has been associated with very variable behavioral traits, sometimes with immature personality features and poor social adjustment suggesting frontal lobe dysfunction. 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PD FEB PY 2004 VL 5 SU 1 BP S3 EP S13 DI 10.1016/j.yebeh.2003.11.002 PG 11 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 772ZY UT WOS:000188874300002 PM 14725841 ER PT J AU Veltman, MWM Thompson, RJ Roberts, SE Thomas, NS Whittington, J Bolton, PF AF Veltman, MWM Thompson, RJ Roberts, SE Thomas, NS Whittington, J Bolton, PF TI Prader-Willi syndrome - A study comparing deletion and uniparental disomy cases with reference to autism spectrum disorders SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Prader-Willi syndrome; autism spectrum disorders; autism; ASQ ID MALADAPTIVE BEHAVIOR; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; CHROMOSOME-15; INDIVIDUALS; PHENOTYPE; DIAGNOSIS; ANGELMAN; CHILDREN; DEFINE AB Prader Willi Syndrome (PWS) is a neuro-genetic disorder. It has been reported that cases due to paternal deletion 15q11-13 (Del) behave differently to cases due to uniparental disomy (UPD). Comparison of the two forms of PWS has, to date, not included the frequency of autistic behaviours, even though there are reports of an association between maternal duplications of 15q11-13 and autism spectrum disorders (ASD). It was predicted that maternal UPD PWS cases would be more prone to ASD than Del PWS cases due to their duplicated maternally expressed genes. A preliminary test of the hypothesis was conducted using postal and telephone surveys of matched, genetically verified, UPD and Del cases using the Autism Screening Questionnaire (ASQ) and the Vineland Adaptive Behaviour Scales (VABS). As predicted, UPD cases were reported as exhibiting significantly more autistic symptomatology. They also were born to older mothers and were reported on the VABS to have more deficits in motor control problems and fewer adaptive skills in the Daily Living Skills domain. Del cases were reportedly more skilled at jigsaw puzzles. The results lend further support to the notion that abnormality in the expression of maternal imprinted 15q11-13 genes may confer a susceptibility to ASD. They also suggest that there maybe cognitive differences between the groups in processing visuo-spatial information. C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ London, Inst Psychiat, MRC, Social Genet & Dev Psychiat Ctr, London WC1E 7HU, England. Wessex Reg Genet Lab, Salisbury, Wilts, England. Univ London, Inst Psychiat, Child & Adolescent Psychiat Dept, London WC1E 7HU, England. RP Veltman, MWM (reprint author), Univ Cambridge, Dev Psychiat Sect, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Child Adolesc. Psych. PD FEB PY 2004 VL 13 IS 1 BP 42 EP 50 DI 10.1007/s00787-004-0354-6 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 801ZG UT WOS:000220133200006 PM 14991431 ER PT J AU Kern, JK Espinoza, E Trivedi, MH AF Kern, JK Espinoza, E Trivedi, MH TI The effectiveness of secretin in the management of autism SO EXPERT OPINION ON PHARMACOTHERAPY LA English DT Review DE autism; efficacy; measures; secretin; subtypes; trials ID PLACEBO-CONTROLLED TRIAL; PERVASIVE DEVELOPMENTAL DISORDER; SYNTHETIC HUMAN SECRETIN; PORCINE SECRETIN; DOUBLE-BLIND; INTRAVENOUS SECRETIN; BRAIN-STEM; CHILDREN; ABNORMALITIES; CEREBELLUM AB Autism is a complex neurological disorder that severely impacts a child's ability to communicate and interact socially. Many treatments have attempted to alleviate the symptoms of autism, but with limited success. After reports of improvements in autistic children who received secretin, this hormone became popular as a possible treatment for autism. Since then, the interest in secretin has greatly increased, as well as the demand for secretin by parents of autistic children. However, there is still limited experimental evidence that supports its effectiveness. Many biological studies and clinical trials were conducted to test the effectiveness of secretin in treating autism. This review discusses the autistic disorder, instruments used in the trials, and reports the findings of some of these studies. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75235 USA. RP Kern, JK (reprint author), Univ Texas, SW Med Ctr, Dept Psychiat, 6363 Forest Pk Rd,Suite 1300, Dallas, TX 75235 USA. 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PD FEB PY 2004 VL 5 IS 2 BP 379 EP 387 DI 10.1517/eoph.5.2.379.26488 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 772HR UT WOS:000188837000016 PM 14996634 ER PT J AU Long, JM LaPorte, P Paylor, R Wynshaw-Boris, A AF Long, JM LaPorte, P Paylor, R Wynshaw-Boris, A TI Expanded characterization of the social interaction abnormalities in mice lacking Dcl1 SO GENES BRAIN AND BEHAVIOR LA English DT Article DE autism; behavior; genetics; mouse; sensorimotor gating; social dominance; social interaction ID HOUSE MICE; PSYCHIATRIC-DISORDERS; ANIMAL-MODELS; BEHAVIOR; MOUSE; OXYTOCIN; GENETICS; AUTISM; VASOPRESSIN; INHIBITION AB Dvl1 is one of three murine Dishevelled genes widely expressed in embryonic development and in the adult central nervous system. Dishevelled proteins are a necessary component of the Writ and planar cell polarity developmental signaling pathways. We reported previously that mice deficient in Dvl1 exhibited abnormal social interaction and sensorimotor gating. To assess the validity of our earlier findings, we replicated the previous behavioral tests and included several new assays. The behaviors assessed included: social interaction, sensorimotor reflexes, motor activity, nociception, prepulse inhibition of acoustic startle (PPI) and learning and memory. Assessments with an explicit social component included: social dominance test, whisker trimming, nest building, home-cage huddling and ultrasonic vocalization rate analysis in pups. In addition, separate cohorts of wildtype and Dvl1-null mice were assessed for social recognition of a conspecific. Replicating the original report, Dvl1-null mice were impaired in several tasks containing an explicit social component. However, no impairment was observed in the social memory task. A previously observed deficit in PPI did not replicate in two institutions. In conclusion, we provide evidence that the social interaction phenotype of Dvl1-deficient mice has a strong genetic influence, but the sensorimotor gating deficit was subject to environmental influences. The specificity of observed social interaction deficits also suggests that lack of Dvl1 is associated with deficits in the recognition of social hierarchy and dominance. C1 Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Med, La Jolla, CA 92093 USA. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. RP Wynshaw-Boris, A (reprint author), Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA. 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This article analyzes theoretically the relationship between complex developmental disorders and delinquency with the hypothesis that the delinquent behaviors reported in it resulted from comorbid psychopathology and not as a direct consequence of a developmental disorder A small series of patients diagnosed with a PDD and comorbid psychiatric illnesses whose admission to the hospital was precipitated by delinquent behavior is presented. C1 Ctr Sperimentale Lautismo Anni Verdi, I-00148 Rome, Italy. RP Palermo, MT (reprint author), Ctr Sperimentale Lautismo Anni Verdi, Via Silvio Sbricoli 8, I-00148 Rome, Italy. EM marktpalermo@virgilio.it CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1988, J CHILD PSYCHOL PSYC, V29, P351, DOI 10.1111/j.1469-7610.1988.tb00723.x Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Bryson S. 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J. Offender Ther. Comp. Criminol. PD FEB PY 2004 VL 48 IS 1 BP 40 EP 48 DI 10.1177/0306624X03257713 PG 9 WC Criminology & Penology; Psychology, Applied SC Criminology & Penology; Psychology GA 763NU UT WOS:000188093000004 PM 14969115 ER PT J AU Salomonsson, B AF Salomonsson, B TI Some psychoanalytic viewpoints on neuropsychiatric disorders in children SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Article DE child psychoanalysis; neuropsychiatry; ADHD; DAMP; aetiology; neurobiology ID ATTENTION; PERSPECTIVE; ATTACHMENT AB The author addresses issues interfacing neuropsychiatry and psychoanalysis. He recommends psychoanalysis for children with Attention Deficit, Hyperactivity Disorder (ADHD) and Dysfunction in Attention and activity control, Motility control and Perception (DAMP). He attributes its low status in neuropsychiatric treatment recommendations partly to the fact that psychoanalysts do not always declare their specific field of investigation. The scientific community then assumes that psychoanalysis aims to comment on issues outside its field of investigation, e.g. on neurobiological aetiology. The community therefore fails to discern the psychoanalyst's specific task, to help the child express and work through his conscious and unconscious experiences. Clarity on the analyst's part will improve relations with the scientific community and facilitate a relevant comparison of treatment methods. Another reason for neuropsychiatry's negative attitude towards analysis is its unwillingness to accept that unconscious conflict influences behaviour. With theoretical and clinical arguments, the author argues that unconscious factors must be taken in to understand and to treat the child. Countertransference, often cumbersome with neuropsychiatric children, becomes easier to handle if the analyst is clear about his field of investigation. If he sees through simplistic formulations on aetiology, countertransference gets even more manageable. Psychoanalysis can result in considerable intellectual and emotional development, as illustrated by work with a latency boy with DAMP, autism and slight mental retardation. In his psychoanalytic theoretical framework of the case, the author unites ego-psychological formulations with a Bionian conceptualisation of the thought disturbance. C1 Swedish Psychoanalyt Assoc, S-11641 Stockholm, Sweden. RP Salomonsson, B (reprint author), Swedish Psychoanalyt Assoc, Gaveliusgatan 11, S-11641 Stockholm, Sweden. EM bjorn.salomonsson@chello.se CR Balter L, 1980, PSYCHOANAL QUART, V49, P475 Barkley R. A., 1998, ATTENTION DEFICIT HY, V2nd Bion W., 1962, LEARNING EXPERIENCE Bion W. R., 1963, ELEMENTS PSYCHOANALY Bion W. 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PD FEB PY 2004 VL 85 BP 117 EP 135 PN 1 PG 19 WC Psychology, Psychoanalysis SC Psychology GA 779NA UT WOS:000189305600011 PM 15005897 ER PT J AU Burack, JA AF Burack, JA TI Research methodology - Matching - Preface SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID MENTAL-RETARDATION; DEVELOPMENTAL PSYCHOPATHOLOGY; AUTISM CR Burack JA, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P25 Burack J. A., 2001, INT REV RES MENT RET, V24, P300, DOI 10.1016/S0074-7750(01)80012-4 Burack JA, 2002, DEV PSYCHOPATHOL, V14, P225 CICCHETTI D, 1984, CHILD DEV, V55, P1, DOI 10.2307/1129830 Hermelin B, 1970, PSYCHOL EXPT AUTISTI Hodapp R. M., 1990, ISSUES DEV APPROACH, P3, DOI DOI 10.1017/CBO9780511582325.002 Iarocci G., 1998, HDB MENTAL RETARDATI, P349 Mervis CB, 1999, MONOGR SOC RES CHILD, V64, P115, DOI 10.1111/1540-5834.00011 Mervis CB, 2003, LANGUAGE COMPETENCE ACROSS POPULATIONS, P233 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 VOLKMAR FR, 1990, ISSUES DEV APPROACH, P246 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 YULE W, 1978, AUTISM REAPPRAISAL C ZIGLER E, 1967, SCIENCE, V155, P292, DOI 10.1126/science.155.3760.292 ZIGLER E, 1969, AM J MENT DEF, V73, P536 NR 15 TC 4 Z9 4 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 2004 VL 34 IS 1 BP 3 EP 5 DI 10.1023/B:JADD.0000018275.59897.10 PG 3 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300001 ER PT J AU Mervis, CB Klein-Tasman, BP AF Mervis, CB Klein-Tasman, BP TI Methodological issues in group-matching designs: alpha levels for control variable comparisons and measurement characteristics of control and target variables SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; developmental disability; matching; mental age; methodology; signal detection theory; spectrum ID WILLIAMS-SYNDROME; DOWN-SYNDROME; NULL HYPOTHESIS; AUTISM; TEMPERAMENT; BEHAVIOR; CHILDREN AB Group-matching designs are commonly used to identify the diagnosis-specific characteristics of children with developmental disabilities. In this paper, we address three issues central to the use of this design. The first concerns the a level to be used for considering groups to be matched on the control variable(s). The second involves the measurement characteristics of the control and target variables. We discuss the properties of standard scores, raw scores, and age equivalents and argue against the use of age equivalents. In addition, we consider the appropriateness of the commonly made prediction that groups that are matched for a control variable such as language ability or nonverbal reasoning ability but are not matched for chronological age should perform at equivalent levels on the target variable. Finally, we discuss issues related to the interpretation of significant between-group differences on the target variable, assuming groups are well-matched on the control variables, and describe the benefits of a method that focuses on characterizing a disorder on a case-by-case basis and then aggregating the cases, using the measures of sensitivity and specificity from signal detection theory. C1 Univ Louisville, Dept PSychol & Brain Sci, Louisville, KY 40292 USA. 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T., 1997, EXPRESSIVE VOCABULAR NR 31 TC 94 Z9 94 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD FEB PY 2004 VL 34 IS 1 BP 7 EP 17 DI 10.1023/B:JADD.0000018069.69562.b8 PG 11 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300002 PM 15098952 ER PT J AU Mottron, L AF Mottron, L TI Matching strategies in cognitive research with individuals with high-functioning autism: Current practices, instrument biases, and recommendations SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE British Picture Vocabulary Scale; high-functioning autism; IQ; matching strategy; methodology; peaks of ability; Raven Progressive Matrices; Wechsler Intelligence Scale ID RAVEN PROGRESSIVE MATRICES; WAIS-R; PPVT-R; DISORDER; STANDARD; VALIDITY; MIND; IQS AB A meta-analysis was performed on the 133 cognitive and behavioral papers in autism using comparison groups in the 1999-2002 period. High-functioning (average IQ: 84.7), adolescents (average, 14.4 years) are largely dominant. IQ is the most frequent matching variable in use (51.2%). The instruments that are most frequently used to determine IQ or general level are Wechsler scales (46.9%), British Picture Vocabulary Scale (BPVS; 22.3%), and Raven Progressive Matrices (RPM; 16.9%). In order to determine if these instruments were equivalent when applied to individuals with pervasive developmental disorders (PDDs), Wechsler IQ, EVIP (a French Canadian translation of the BPVS), and RPM were given to a group of 14 individuals with autism and 12 with Asperger syndrome. Comparison of Wechsler and RPM IQs values, expressed as percentiles, to percentile values of EVIP score revealed that EVIP (and to a lesser extent RPM) considerably overestimates the level of all PDD participants as compared to Wechsler Verbal IQ (VIQ), Performance IQ (PIQ), or Full-Scale IQ (FSIQ), whereas these instruments are reported to be strongly correlated in typically developing individuals. This study reveals that identification of objects from a verbal label - the BPVS-PPVT-EVIP task - is a peak of ability in high functioning individuals with PDDs. This peak of ability, even superior to that of block design, has a detrimental effect on matching based on this instrument. A recommendation to replace BPVS/PPVT/EVIP or RPM by Wechsler scale as a basis of IQ/level matching is provided. Accordingly, the former instruments are a potential source of type-1 (for cognitive deficits) or type-2 (for cognitive hyperfunctioning) errors. C1 Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Univ Montreal, Ctr Rech Fernand Seguin, Montreal, PQ, Canada. RP Mottron, L (reprint author), Hop Riviere Praires, Clin Specialisee Autisme, 7070 Blvd Perras, Montreal, PQ H1E 1A4, Canada. EM mottron1@istar.ca CR Burack JA, 2002, DEV PSYCHOPATHOL, V14, P225 BURKE HR, 1985, J CLIN PSYCHOL, V41, P231, DOI 10.1002/1097-4679(198503)41:2<231::AID-JCLP2270410216>3.0.CO;2-Z *DIG SYST, DAT 3 5 Dunn L. M., 1981, PEABODY PICTURE VOCA Dunn L. 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C., 1996, PROGR MATRICES PERCE RAVEN JC, 1947, COLORED PROGR MATRIC, V1 RAVEN JC, 1995, COLORED PROGR MATRIC, V2 Snitz BE, 2000, CLIN NEUROPSYCHOL, V14, P181, DOI 10.1076/1385-4046(200005)14:2;1-Z;FT181 Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D, 1981, WECHSLER ADULT INTEL Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 23 TC 85 Z9 85 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 2004 VL 34 IS 1 BP 19 EP 27 DI 10.1023/B:JADD.0000018070.88380.83 PG 9 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300003 PM 15098953 ER PT J AU Shaked, M Yirmiya, N AF Shaked, M Yirmiya, N TI Matching procedures in autism research: Evidence from meta-analytic studies SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; siblings; parents; theory of mind; broad phenotype; psychiatric status; cognition ID FAMILY-HISTORY; MIND ABILITIES; CHILDREN; PHENOTYPE; INDIVIDUALS; RELATIVES AB In this paper, we summarize some of our findings from a series of three meta-analyses and discuss their implications for autism research. In the first meta-analysis, we examined studies addressing the theory of mind hypothesis in autism. This analysis revealed that theory of mind disabilities are not unique to autism, although what may be unique is the severity of the dysfunction in this group. Variables such as the chronological and mental age of the participants, and the matching procedures that the researchers employed, were found to be significant moderator variables. In the next two meta-analyses, data regarding siblings and parents of individuals with autism were analyzed. Type of comparison group (e. g., siblings or parents of individuals with Down syndrome or learning disabilities) and type of outcome measure (cognitive, psychiatric, language) were found to be important moderator variables. Furthermore, method of assessing the psychiatric difficulties (e. g., self-report, clinical measures) was found to be a moderator variable in parents' meta-analysis. Suggestions for future research are discussed, highlighting variables such as type of comparison group, matching procedures, chronological and mental ages, gender, and birth order. C1 Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Sch Educ, IL-91905 Jerusalem, Israel. RP Yirmiya, N (reprint author), Hebrew Univ Jerusalem, Dept Psychol, Mt Scopus, IL-91905 Jerusalem, Israel. 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Autism Dev. Disord. PD FEB PY 2004 VL 34 IS 1 BP 35 EP 40 DI 10.1023/B:JADD.0000018072.42845.83 PG 6 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300005 PM 15098955 ER PT J AU Seltzer, MM Abbeduto, L Krauss, MW Greenberg, J Swe, A AF Seltzer, MM Abbeduto, L Krauss, MW Greenberg, J Swe, A TI Comparison groups in autism family research: Down syndrome, fragile X syndrome, and schizophrenia SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Down syndrome; families; fragile X; matching; schizophrenia ID FIRST-DEGREE RELATIVES; MENTAL-RETARDATION; INFANTILE-AUTISM; CHILDREN; SIBLINGS; PARENTS; STRESS; DISABILITIES; HISTORY; PERSONALITY AB This paper examines methodological challenges inherent in conducting research on families of children with autism and in comparing these families with others who are coping with different types of disabilities or who have nondisabled children. Although most comparative research has contrasted families whose child has autism with those whose child has Down syndrome, the range of comparison groups can be expanded to offer additional points of contrast and control. We discuss both matching and statistical control procedures and point to next steps in this line of comparative autism family research. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Heller Sch, Waltham, MA 02454 USA. RP Seltzer, MM (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave, Madison, WI 53705 USA. 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Autism Dev. Disord. PD FEB PY 2004 VL 34 IS 1 BP 41 EP 48 DI 10.1023/B:JADD.0000018073.92982.64 PG 8 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300006 PM 15098956 ER PT J AU Szatmari, P Zwaigenbaum, L Bryson, S AF Szatmari, P Zwaigenbaum, L Bryson, S TI Conducting genetic epidemiology studies of autism spectrum disorders: Issues in matching SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; genetics; matching; phenotype; siblings ID PERVASIVE DEVELOPMENTAL DISORDERS; WEAK CENTRAL COHERENCE; COGNITIVE PHENOTYPE; FAMILY-HISTORY; RISK-FACTORS; MENTAL-RETARDATION; RECURRENCE RISKS; HEALTH-PROBLEMS; LESSER VARIANT; DOWN-SYNDROME AB The objective of this review is to clarify the role of matching in family genetic studies of autism as a way of defining endophenotypes for linkage analysis. The concept of a confounding variable is reviewed and the importance of considering these in family studies of three endophenotypes in autism are considered: cognitive/language impairments, psychiatric disorders, and autistic-like traits. The importance of matching in infant sibling studies of autism is also addressed. Matching as a way of dealing with confounding variables has an important impact on understanding the extent to which these phenotypes are associated with the genes that confer susceptibility to autism and to the early detection of the disorder. Matching continues to be an important issue in the planning and conduct of family-genetic studies of the autism spectrum disorders, particularly as the search for autism susceptibility genes enters the next generation of studies. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. Dalhousie Univ, Dept Pediat, Halifax, NS, Canada. Dalhousie Univ, Dept Psychol, Halifax, NS, Canada. RP Szatmari, P (reprint author), HHS, Offord Ctr Child Studies, Chedoke Site,Patterson 207, Hamilton, ON L8N 3Z5, Canada. 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Autism Dev. Disord. PD FEB PY 2004 VL 34 IS 1 BP 49 EP 57 DI 10.1023/B:JADD.0000018074.74369.cd PG 9 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300007 PM 15098957 ER PT J AU Charman, T AF Charman, T TI Matching preschool children with autism spectrum disorders and comparison children for language ability: Methodological challenges SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE competency; instruments; language; matching; measurement; methodology ID DOWN-SYNDROME; COMMUNICATIVE DEVELOPMENT; INFANTS; LEVEL; INDIVIDUALS; WILLIAMS AB Earlier identification of children with autism spectrum disorders (ASDs) is welcome, but presents a number of challenges to the clinical and the research enterprises (see Charman & Baird [2002] for a review). In the research enterprise, one critical methodological challenge is the use of appropriate measures on which to match groups of preschoolers with ASDs to comparison groups with other neurodevelopmental conditions. Language and communication impairments are central to the diagnosis of ASD and, therefore, critical variables to consider in group-matched research designs. In the domain of language function the challenges include the very poor language competence of many preschoolers with ASDs, the fact that some early language competencies form part of the formal diagnostic criteria of ASD and diagnostic algorithms on research diagnostic instruments, the uneven profile of language competency in children with ASDs, and the difference between performance on measures of formal language competency in the testing situation and everyday language use. The current paper will review these challenges and suggest some possible approaches to overcome them, including using more than one measure of language ability and adopting a pragmatic approach to group composition and statistical analysis. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. RP Charman, T (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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PD FEB PY 2004 VL 34 IS 1 BP 59 EP 64 DI 10.1023/B:JADD.0000018075.77941.60 PG 6 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300008 PM 15098958 ER PT J AU Burack, JA Iarocci, G Flanagan, TD Bowler, DM AF Burack, JA Iarocci, G Flanagan, TD Bowler, DM TI On mosaics and melting pots: Conceptual considerations of comparison and matching strategies SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism research; comparison groups; matching strategies; methodology; mosaic ID HIGH-FUNCTIONING AUTISM; MENTAL-RETARDATION; INDIVIDUALS; CHILDREN; ISSUES; TASK; MIND AB Conceptual and pragmatic issues relevant to the study of persons with autism are addressed within the context of comparison groups and matching strategies. We argue that no choice of comparison group or matching strategy is perfect, but rather needs to be determined by specific research objectives and theoretical questions. 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Autism Dev. Disord. PD FEB PY 2004 VL 34 IS 1 BP 65 EP 73 DI 10.1023/B:JADD.0000018076.90715.00 PG 9 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300009 PM 15098959 ER PT J AU Tager-Flusberg, H AF Tager-Flusberg, H TI Strategies for conducting research on language in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; genetics; language; phenotype; subtypes ID INFANTILE-AUTISM; SCHIZOPHRENIC CHILDREN; IMPAIRMENT; DEFICITS; COMPREHENSION; INDIVIDUALS; PHENOTYPES; DISORDERS; BEHAVIOR; LOCUS AB Several different methodological approaches that have been used in studying language in children with autism are outlined. In classic studies, children with autism are compared to comparison groups typically matched on age, IQ, or mental age in order to identify which aspects of language are uniquely impaired in autism. Several methodological problems are noted with this approach including (a) heterogeneity of the autism population, (b) mental retardation, (c) developmental change with age, and (d) sample size and ascertainment. An alternative strategy is suggested which focuses on identifying the complex expression of the language phenotype in autism across the full range of the syndrome. This approach explores within-group individual differences in language functioning, and recently identified distinct language phenotypic subgroups within the autism population that are relevant to understanding the underlying genetic and neurobiological etiology of autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Tager-Flusberg, H (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St L-814, Boston, MA 02118 USA. 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Methodological issues in autism-related research SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE analysis of covariance; matching; methodology; normative regression; task control ID DEVELOPMENTAL-DISORDERS; WILLIAMS-SYNDROME; WORKING-MEMORY; DOWN-SYNDROME; COGNITIVE-ABILITIES; CHILDREN; PERFORMANCE; MIND; INTELLIGENCE; DISCIPLINES AB Studies of autism typically adopt a factorial matched-groups design aimed at eliminating nonspecific factors such as mental retardation as explanations of performance on experimental tasks. This paper reviews the issues involved in designing such studies and interpreting their results and suggests that the best approach to matching may be to equate performance on carefully designed control tasks. However, we also argue that the interpretation of such studies is often complicated by the fact that associations between background measures and experimental task performance are not clear. 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A., 1997, AUTISM EXECUTIVE DIS, P57 WEISS B, 1986, PSYCHOL BULL, V100, P157, DOI 10.1037//0033-2909.100.2.157 NR 39 TC 69 Z9 71 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD FEB PY 2004 VL 34 IS 1 BP 81 EP 86 DI 10.1023/B:JADD.0000018078.82542.ab PG 6 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300011 PM 15098961 ER PT J AU Eagle, RS AF Eagle, RS TI Commentary: Further commentary on the debate regarding increase in autism in California SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID ET-AL. 2002; CHANGING PREVALENCE; BLAXILL; SPITZER; BASKIN C1 Harbor Reg Ctr, Torrance, CA USA. RP Eagle, RS (reprint author), Harbor Reg Ctr, Torrance, CA USA. CR Blaxill MF, 2003, J AUTISM DEV DISORD, V33, P223, DOI 10.1023/A:1022912115365 California Department of Developmental Services, 2003, AUT SPECTR DIS CHANG California-Department-of-Developmental-Services, 2002, AUT SPECTR DIS BEST Croen LA, 2003, J AUTISM DEV DISORD, V33, P227, DOI 10.1023/A:1022964132203 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 *DEP DEV SERV, 2002, CAL ASD LEARN COLL P GILBERG C, 1999, INT COUNC DEV LEARN NR 7 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 FEB PY 2004 VL 34 IS 1 BP 87 EP 88 DI 10.1023/B:JADD.0000018079.62526.dd PG 2 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300012 PM 15098962 ER PT J AU Richdale, AL AF Richdale, AL TI A comment on Honomichl R. D. et al. (2002). Sleep patterns of children with pervasive developmental disorders. Journal of Autism and Developmental Disorders, 32(6), 553-561 SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID SEVERE LEARNING-DISABILITIES; RHYTHM C1 RMIT Univ, Dept Psychol & Disabil Studies, Bundoora, Vic 3083, Australia. RP Richdale, AL (reprint author), RMIT Univ, Dept Psychol & Disabil Studies, POB 71, Bundoora, Vic 3083, Australia. EM amanda.richdale@rmit.edu.au CR Didden R, 2001, RES DEV DISABIL, V22, P255, DOI 10.1016/S0891-4222(01)00071-3 Honomichl RD, 2002, J AUTISM DEV DISORD, V32, P553, DOI 10.1023/A:1021254914276 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Quine L, 2001, CHILD CARE HLTH DEV, V27, P201, DOI 10.1046/j.1365-2214.2001.00213.x Richdale A., 2001, SLEEP DISTURBANCE CH, P181 Richdale A, 2000, J INTELLECT DEV DIS, V25, P147 RICHDALE AL, 1995, EUR CHILD ADOLES PSY, V4, P175 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 RICHDALE AL, 1992, J AUTISM DEV DISORD, V22, P433, DOI 10.1007/BF01048245 Schreck KA, 2000, J AUTISM DEV DISORD, V30, P127, DOI 10.1023/A:1005407622050 Stores G, 1998, AUTISM, V2, P157, DOI 10.1177/1362361398022004 Wiggs L, 1998, BRIT J HEALTH PSYCH, V3, P345 Wiggs L, 1996, J INTELL DISABIL RES, V40, P518, DOI 10.1046/j.1365-2788.1996.799799.x NR 13 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 2004 VL 34 IS 1 BP 89 EP 90 DI 10.1023/B:JADD.0000018080.54353.57 PG 2 WC Psychology, Developmental SC Psychology GA 780FU UT WOS:000189362300013 PM 15098963 ER PT J AU Howlin, P Goode, S Hutton, J Rutter, M AF Howlin, P Goode, S Hutton, J Rutter, M TI Adult outcome for children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autistic disorder; prognosis; adulthood; follow-up studies ID RECEPTIVE LANGUAGE DISORDER; 15-YEAR FOLLOW-UP; INFANTILE PSYCHOSIS; DIAGNOSTIC INTERVIEW; BEHAVIORAL TREATMENT; LIFE AB Background: Information on long-term prognosis in autism is limited. Outcome is known to be poor for those with an IQ below 50, but there have been few systematic studies of individuals with an IQ above this. Method: Sixty-eight individuals meeting criteria for autism and with a performance IQ of 50 or above in childhood were followed up as adults. Their mean age when first seen was 7 years (range 3-15 years); at follow-up the average age was 29 years (range 21-48 years). Outcome measures included standardised cognitive, language and attainment tests. Information on social, communication and behavioural problems was obtained from the Autism Diagnostic Inter-view (ADI). Results: Although a minority of adults had achieved relatively high levels of independence, most remained very dependent on their families or other support services. Few lived alone, had close friends, or permanent employment. Communication generally was impaired, and reading and spelling abilities were poor. Stereotyped behaviours or interests frequently persisted into adulthood. Ten individuals had developed epilepsy. Overall, only 12% were rated as having a 'Very Good' outcome; 10% were rated as 'Good' and 19% as 'Fair'. The majority was rated as having a 'Poor' (46%) or 'Very Poor' (12%) outcome. Individuals with a childhood performance IQ of at least 70 had a significantly better outcome than those with an IQ below this. However, within the normal IQ range outcome was very variable and, on an individual level, neither verbal nor performance IQ proved to be consistent prognostic indicators. Conclusions: Although outcome for adults with autism has improved over recent years, many remain highly dependent on others for support. This study provides some information on prognostic indicators, but more fine-grained research is needed into the childhood variables that are associated with good or poor outcome. C1 St George Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. Croydon CAMHS S London & Maudsley Trust, London, England. Inst Psychiat, London, England. RP Howlin, P (reprint author), St George Hosp, Sch Med, Dept Psychol, Cranmer Terrace, London SW17 0RE, England. EM phowlin@sghms.ac.uk RI Howlin, Patricia/A-7622-2011; Rutter, Michael/C-8570-2013 CR BallabanGil K, 1996, PEDIATR NEUROL, V15, P217, DOI 10.1016/S0887-8994(96)00219-6 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x CLARK P, 1981, J AUTISM DEV DISORD, V11, P201, DOI 10.1007/BF01531685 CLARK P, 1979, J CHILD PSYCHOL PSYC, V20, P271, DOI 10.1111/j.1469-7610.1979.tb00514.x CREAK EM, 1963, BRIT J PSYCHIAT, V109, P84, DOI 10.1192/bjp.109.458.84 Dunn L M., 1982, BRIT PICTURE VOCABUL Dunn LM, 1965, PEABODY PICTURE VOCA EISENBERG L, 1956, AM J PSYCHIAT, V112, P607 Gillberg C., 1987, J AUTISM DEV DISORD, V17, P272 Howlin P, 1998, AUTISM DEV DISORDERS Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 HUTTON J, 1998, THESIS U LONDON KOBAYASHI R, 1992, J AUTISM DEV DISORD, V22, P395, DOI 10.1007/BF01048242 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Levine M. 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E., 1960, DIAGNOSTIC ATTAINMEN SPARROW S, 1984, VINELAND ADAPTIVE BA Stutsman R., 1948, MERRILL PALMER SCALE Szatmari P., 2000, ASPERGER SYNDROME, P403 SZATMARI P, 1989, J AUTISM DEV DISORD, V19, P213, DOI 10.1007/BF02211842 Tantam D., 1991, AUTISM ASPERGER SYND, P147, DOI 10.1017/CBO9780511526770.005 TERMAN LM, 1961, STANFORD BINET INTEL Venter A., 1992, HIGH FUNCTIONING IND, P187 Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D., 1990, WECHSLER PRESCHOOL P Wechsler D, 1981, WECHSLER ADULT INTEL NR 51 TC 435 Z9 440 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD FEB PY 2004 VL 45 IS 2 BP 212 EP 229 DI 10.1111/j.1469-7610.2004.00215.x PG 18 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WB UT WOS:000221788200004 PM 14982237 ER PT J AU Dorris, L Espie, CAE Knott, F Salt, J AF Dorris, L Espie, CAE Knott, F Salt, J TI Mind-reading difficulties in the siblings of people with Asperger's syndrome: evidence for a genetic influence in the abnormal development of a specific cognitive domain SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Asperger's syndrome; mind-reading; lesser variant deficits in siblings ID AUTISM; CHILDREN; PHENOTYPE; PARENTS; ADULTS; REPRESENTATION; TWIN AB Background: Previous research suggests that the phenotype associated with Asperger's syndrome (AS) includes difficulties in understanding the mental states of others, leading to difficulties in social communication and social relationships. It has also been suggested that the first-degree relatives of those with AS can demonstrate similar difficulties, albeit to a lesser extent. This study examined 'theory of mind' (ToM) abilities in the siblings of children with AS relative to a matched control group. Method: 2 7 children who had a sibling with AS were administered the children's version of the 'Eyes Test'(Baron-Cohen, Wheelwright, Stone, & Rutherford, 1999). The control group consisted of 27 children matched for age, sex, and a measure of verbal comprehension, and who did not have a family history of AS/autism. Results: A significant difference was found between the groups on the Eyes Test, the 'siblings' group showing a poorer performance on this measure of social cognition. The difference was more pronounced among female siblings. Discussion: These results are discussed in terms of the familial distribution of a neuro-cognitive profile associated with AS, which confers varying degrees of social handicap amongst first-degree relatives. The implication of this finding with regard to the autism/AS phenotype is explored, with some discussion of why this neuro-cognitive profile (in combination with corresponding strengths) may have an evolutionary imperative. C1 Univ Glasgow, Gartnavel Royal Hosp, Acad Ctr, Dept Psychol Med, Glasgow G12 OXH, Lanark, Scotland. RP Dorris, L (reprint author), Univ Glasgow, Gartnavel Royal Hosp, Acad Ctr, Dept Psychol Med, Glasgow G12 OXH, Lanark, Scotland. 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Child Psychol. Psychiatry PD FEB PY 2004 VL 45 IS 2 BP 412 EP 418 DI 10.1111/j.1469-7610.2004.00232.x PG 7 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WB UT WOS:000221788200021 PM 14982254 ER PT J AU Raymaekers, R van der Meere, J Roeyers, H AF Raymaekers, R van der Meere, J Roeyers, H TI Event-rate manipulation and its effect on arousal modulation and response inhibition in adults with high functioning autism SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTONOMIC RESPONSES; ASPERGER-SYNDROME; HUMAN-PERFORMANCE; INFANTILE-AUTISM; CHILDREN; ATTENTION; PEOPLE; MODEL; DEFICIT AB The aim of the current study was to evaluate arousal modulation and response inhibition in adults with high functioning autism (HFA). Using a go/no-go paradigm with varying presentation rate, it was found that performance efficiency (Mean RT, Standard Deviation of RT and Errors of Commission) in adults with HFA was the same as in the control group in the condition with a slow (6 s) and medium (2 s) Presentation rate, but that it decreased in the condition with a fast presentation rate (I s): many errors of commission were made in this condition. Findings were interpreted in terms of an arousal modulation deficiency that interfered with the capacity to inhibit responses in HFA. C1 State Univ Ghent, B-9000 Ghent, Belgium. Univ Groningen, NL-9700 AB Groningen, Netherlands. RP Raymaekers, R (reprint author), Res Grp Dev Disorders, Henri Dunantlaan 2, B-9000 Ghent, Belgium. EM Ruth.Raymaekers@ugent.be CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Belmonte M. 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Clin. Exp. Neuropsychol. PD FEB PY 2004 VL 26 IS 1 BP 74 EP 82 DI 10.1076/jcen.26.1.74.23927 PG 9 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 769TH UT WOS:000188665500007 PM 14972695 ER PT J AU Buescher, JJ AF Buescher, JJ TI Vaccinations containing thimerosal do not increase rates of autism SO JOURNAL OF FAMILY PRACTICE LA English DT Editorial Material C1 Univ Missouri, Dept Family & Community Med, Columbia, MO 65201 USA. RP Buescher, JJ (reprint author), Univ Missouri, Dept Family & Community Med, Columbia, MO 65201 USA. EM buescherjj@health.missouri.edu CR Pfeffer MA, 2003, NEW ENGL J MED, V349, P1893, DOI 10.1056/NEJMoa032292 NR 1 TC 2 Z9 2 PU DOWDEN PUBLISHING CORP PI MONTVALE PA 110 SUMMIT AVE, MONTVALE, NJ 07645-1712 USA SN 0094-3509 J9 J FAM PRACTICE JI J. Fam. Pract. PD FEB PY 2004 VL 53 IS 2 BP 94 EP + PG 2 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA 773AF UT WOS:000188875000003 PM 14764286 ER PT J AU Hatton, C Emerson, E Robertson, J Gregory, N Kessissoglou, S Walsh, RN AF Hatton, C Emerson, E Robertson, J Gregory, N Kessissoglou, S Walsh, RN TI The Resident Choice Scale: a measure to assess opportunities for self-determination in residential settings SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE choice; measurement; residential services; self-determination ID LIVING-UNIT SIZE; INTELLECTUAL DISABILITIES; MENTAL-RETARDATION; GROUP HOMES; COMMUNITY; ADULTS; QUALITY; STAFF; RELIABILITY; CHECKLIST AB Background A 26-item Resident Choice Scale was designed to assess service practices for promoting resident choice. Method The staff working with 560 UK/Irish adults with intellectual disability were interviewed. Specific examples of practices promoting resident choice were requested and independently rated by the interviewer. Results The interrater reliability of Resident Choice items was found to be acceptable (subsample n = 50). The psychometric properties of the Resident Choice Scale total score and scores on eight subscales were also acceptable. Consistently strong associations were found between greater resident choice and greater resident ability and, to a lesser extent, fewer resident challenging behaviours. Few associations were found between resident choice and autism or mental health problems. Even when controlling for resident ability and challenging behaviour, consistent associations were found between greater resident choice and the concurrent variables of greater community presence, fewer institutional practices, and greater user self-reported satisfaction (subsample n = 50). Conclusions Taken together, this pattern of results indicates that the Resident Choice Scale shows promise as a measure of the environmental opportunities available for adults with intellectual disability to exercise self-determination. Areas for future research testing the reliability and validity of the Resident Choice Scale are outlined. C1 Univ Lancaster, Inst Hlth Res, Lancaster LA1 4YT, England. Univ Coll Dublin, Dublin, Ireland. RP Hatton, C (reprint author), Univ Lancaster, Inst Hlth Res, Lancaster LA1 4YT, England. EM c.hatton@lancaster.ac.uk RI Hatton, Chris/C-1924-2013 OI Hatton, Chris/0000-0001-8781-8486 CR AMAN MG, 1995, AM J MENT RETARD, V100, P283 Azmi S, 1997, J APPL RES INTELLECT, V10, P250 Emerson E, 1996, J INTELLECT DEV DIS, V21, P17, DOI 10.1080/13668259600033021 Emerson E, 2000, AM J MENT RETARD, V105, P81, DOI 10.1352/0895-8017(2000)105<0081:QACOCR>2.0.CO;2 Emerson E., 1999, QUALITY COSTS RESIDE Emerson E, 2001, AM J MENT RETARD, V106, P401, DOI 10.1352/0895-8017(2001)106<0401:QACOSL>2.0.CO;2 Heal L. W., 1988, INTEGRATION DEV DISA Heller T, 1999, MENT RETARD, V37, P449, DOI 10.1352/0047-6765(1999)037<0449:AIRFAC>2.0.CO;2 Howlin P., 1996, AUTISM SCREENING QUE MANSELL J, 1996, DEINSTITUTIONALISM C MASON H, 1997, HARC CHALLENGING BEH Meyer L. H., 1991, CRITICAL ISSUES LIVE Moss S, 1998, J INTELL DISABIL RES, V42, P173, DOI 10.1046/j.1365-2788.1998.00116.x MOSS SC, 1996, PAS ADD CHECKLIST F Nihira K., 1993, ADAPTIVE BEHAV SCALE PERRY J, 2000, SUBJECTIVE OBJECTIVE PRATT MW, 1980, AM J MENT DEF, V85, P188 Rapley M, 1998, J INTELL DISABIL RES, V42, P37, DOI 10.1046/j.1365-2788.1998.00066.x Raynes N., 1994, COST QUALITY COMMUNI RAYNES NV, 1987, HOMES MENTALL HANDIC Robertson J, 2001, RES DEV DISABIL, V22, P487, DOI 10.1016/S0891-4222(01)00085-3 Stalker K, 1998, J APPL RES INTELLECT, V11, P60 Stancliffe RJ, 1997, MENT RETARD, V35, P1, DOI 10.1352/0047-6765(1997)035<0001:CLSSPA>2.0.CO;2 STANCLIFFE RJ, 1995, AM J MENT RETARD, V99, P418 Stancliffe RJ, 1997, MENT RETARD, V35, P159, DOI 10.1352/0047-6765(1997)035<0159:LSODAT>2.0.CO;2 Stancliffe RJ, 2000, AM J MENT RETARD, V105, P431, DOI 10.1352/0895-8017(2000)105<0431:PCATEO>2.0.CO;2 Stancliffe RJ, 1999, J INTELLECT DEV DIS, V24, P107, DOI 10.1080/13668259900033911 Tabachnick B., 2001, USING MULTIVARIATE S TAYLOR SJ, 1988, COMMUNITY INTEGRATIO TOSSEBRO J, 1995, AM J MENT RETARD, V100, P59 Wehmeyer ML, 1999, MENT RETARD, V37, P353, DOI 10.1352/0047-6765(1999)037<0353:SALAWE>2.0.CO;2 NR 31 TC 22 Z9 22 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD FEB PY 2004 VL 48 BP 103 EP 113 DI 10.1111/j.1365-2788.2004.00499.x PN 2 PG 11 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 775TA UT WOS:000189075700004 PM 14723653 ER PT J AU Abbeduto, L Short-Meyerson, K Benson, G Dolish, J AF Abbeduto, L Short-Meyerson, K Benson, G Dolish, J TI Relationship between theory of mind and language ability in children and adolescents with intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE language; narrative; social cognition; theory of mind ID MENTAL-RETARDATION; FRAGILE-X; INDIVIDUALS; AUTISM; PERFORMANCE AB Background The present study was designed to evaluate the validity of the false belief task as a measure of theory of mind development in individuals with intellectual disability (ID). In most if it variants, the false belief task is linguistically demanding. This raises the possibility that the finding that individuals with ID do poorly on it might reflect language difficulties rather than theory of mind difficulties. Complicating matters further, however, is the fact that there are theoretical reasons to suppose that there might be a relationship between some dimensions of language ability and theory of mind development in individuals with ID (as well as in other populations). Method In the present study, children and adolescents with ID and typically developing (non-verbal) mental age matches completed a standard false belief task and several tasks designed to measure language ability. Results We reasoned that a pattern in which false belief performance was correlated with all measures of language ability would reflect an artefactual relationship, whereas a more highly circumscribed, theoretically sensible pattern of correlations that was similar across both groups would support the validity of the false belief task. Conclusions The results indicated that for individuals with ID who have limited narrative language skills, those limitations contribute substantially to their failure on the false belief task. For individuals with ID who have more highly developed narrative language skills (about 40% of the sample tested), however, the false belief task may provide a valid measure of their progress towards acquiring an adequate theory of mind. This latter conclusion was suggested by the fact screening out individuals who failed to meet linguistic and cognitive prerequisites for dealing with the performance demands of the false belief task yielded non-significant correlations between false belief performance and the language measures for both the group with ID and the typically developing comparison group. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Univ Wisconsin, Oshkosh, WI 54901 USA. RP Abbeduto, L (reprint author), Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. EM abbeduto@waisman.wisc.edu CR ABBEDUTO L, 1998, J SPEECH LANG HEAR R, V41, P348 Abbeduto L, 1997, J SPEECH LANG HEAR R, V40, P20 Abbeduto L, 2001, Downs Syndr Res Pract, V7, P9, DOI 10.3104/reports.109 ABBEDUTO L, 1995, MENT RETARD, V33, P279 ASTINGTON JW, 1994, PRAGMATICS THEORY PR, P72 BENSON G, 1993, AM J MENT RETARD, V98, P427 BFYANT FB, 1995, READING UNDERSTANDIN, P99 Bishop D. V. M., 1989, TEST RECEPTION GRAMM DUNN J, 1995, COGNITION EMOTION, V9, P187, DOI 10.1080/02699939508409008 Elliot C. D., 1990, DIFFERENTIAL ABILITY Frith U, 1996, J PSYCHOPHARMACOL, V10, P48, DOI 10.1177/026988119601000108 Garner C, 1999, J INTELL DISABIL RES, V43, P466, DOI 10.1046/j.1365-2788.1999.00207.x HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x HEWITT LE, 1994, PRAGMATICS THEORY PR, P88 KARMILOFFSMITH A, 1994, J COGNITIVE NEUROSCI, V10, P197 Kasari C, 1998, HDB MENTAL RETARDATI, P411 Loban W., 1976, 18 NAT COUNC TEACH E MAZZOCCO MMM, 1993, J DEV BEHAV PEDIATR, V14, P328 MILLER J, 1992, SALT SYSTEMATIC ANAL MILLER JF, 1991, RESEARCH ON CHILD LANGUAGE DISORDERS : A DECADE OF PROGRESS, P211 Ninio A., 1996, PRAGMATIC DEV Odom S. L., 1996, SOCIAL POLICY REPORT, V10, P18 Perner Josef, 1991, UNDERSTANDING REPRES Rosenberg S, 1993, LANGUAGE COMMUNICATI Tager-Flusberg H, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P173 TAGERFLUSBERG H, 1994, J CHILD PSYCHOL PSYC, V35, P1059, DOI 10.1111/j.1469-7610.1994.tb01809.x TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 28 TC 13 Z9 14 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD FEB PY 2004 VL 48 BP 150 EP 159 DI 10.1111/j.1365-2788.2004.00524.x PN 2 PG 10 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 775TA UT WOS:000189075700008 PM 14723657 ER PT J AU Thiemann, KS Goldstein, H AF Thiemann, KS Goldstein, H TI Effects of peer training and written text cueing on social communication of school-age children with pervasive developmental disorder SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE autism/pervasive developmental disorder (PDD); social communication; written-text cues; peer training; treatment ID PRESCHOOL-CHILDREN; AUTISTIC-CHILDREN; YOUNG-CHILDREN; SKILLS; DISCOURSE; INTERVENTION; DISABILITIES; MANAGEMENT; BEHAVIORS; STUDENTS AB This study consecutively examined the effects of 2 social interventions-peer training and written text treatment-on the social communication of 5 elementary students with pervasive developmental disorder. Each child with autism was paired with 2 peers without disabilities to form 5 triads. In Intervention I (peer training), peers were taught to use 5 facilitative social skills over 5 days. After beer training, 4 children with autism increased or used more stable rates of initiations and contingent responses overall. However, all children continued to demonstrate deficits in specific social-communication skills. Once Intervention 2 (direct instruction using written text cues) was implemented, increased use of 3 different communication skills was observed across all 5 participants. In addition, social validity outcomes revealed improved quality of child-peer interactions, 2 teacher reports of improved social skill development, and improved acceptance and friendship ratings for the children with autism. 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W., 1998, WOODCOCK READING MAS NR 50 TC 36 Z9 36 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1092-4388 J9 J SPEECH LANG HEAR R JI J. Speech Lang. Hear. Res. PD FEB PY 2004 VL 47 IS 1 BP 126 EP 144 DI 10.1044/1092-4388(2004/012) PG 19 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 800QV UT WOS:000220043700012 PM 15072534 ER PT J AU Ducharme, JM Drain, TL AF Ducharme, JM Drain, TL TI Errorless academic compliance training: Improving generalized cooperation with parental requests in children with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; parent training; generalization; compliance training; errorless approaches ID BEHAVIOR PROBLEMS AB Objective: Children with autism often demonstrate distress and oppositionality when exposed to requests to complete academic or household tasks. Errorless academic compliance training is a success-focused, noncoercive intervention for improving child cooperation with such activities. In the present study, the authors evaluated treatment and generalization effects of this intervention on four children diagnosed with autism. Method: In a multiple baseline across-subjects design, parents delivered a range of academic and nonacademic requests to their children to determine the probability of compliance for each request. A hierarchy of academic requests ranging from those yielding high compliance (level 1) to those yielding low compliance (level 4) was then developed. Treatment began with the concentrated delivery of level 1 requests, with praise and reward for compliant responses. Over several weeks, children were gradually introduced to requests from subsequent probability levels with continued reward for compliance. Results: High compliance levels were demonstrated throughout and following treatment. Evidence of generalization to untrained academic requests and nonacademic requests emerged. Treatment gains were maintained up to 6 months after treatment. Conclusions: Errorless academic compliance training appears to be an effective intervention for enhancing generalized compliance in children with autism. C1 Univ Toronto, Dept Human Dev & Appl Psychol, OISE, Toronto, ON M5S 1V6, Canada. RP Ducharme, JM (reprint author), Univ Toronto, Dept Human Dev & Appl Psychol, OISE, 100 Coll St,252 Bloor St W, Toronto, ON M5S 1V6, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARBELLE S, 1994, J AUTISM DEV DISORD, V24, P693, DOI 10.1007/BF02172280 Barkley RA, 2000, J AM ACAD CHILD PSY, V39, P1004, DOI 10.1097/00004583-200008000-00015 BARLOW DH, 1984, SINGLE CASE EXPT DES Carr E. 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PD FEB PY 2004 VL 43 IS 2 BP 163 EP 171 DI 10.1097/01.chi.0000101370.03068.87 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 765NH UT WOS:000188289500011 PM 14726722 ER EF