FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Stone, VE Baron-Cohen, S Calder, AJ Keane, J Young, A AF Stone, VE Baron-Cohen, S Calder, AJ Keane, J Young, A TI Acquired theory of mind impairments in individuals with bilateral amygdala lesions SO NEUROPSYCHOLOGIA LA English DT Article DE theory of mind impairment; amygdala; theory of mind; social intelligence ID FACE PROCESSING IMPAIRMENTS; HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; VOCAL EXPRESSIONS; FRONTAL-LOBE; RECOGNITION; CHILDREN; DAMAGE; FEAR AB Studies in humans suggest that the amygdala plays a role in processing social information. A key component of social information processing is what developmental psychologists call "theory of mind": the ability to infer others' mental states. Recent studies have raised the possibility that the amygdala is involved in theory of mind, showing amygdala activation during a theory of mind task, or showing impairment on theory of mind tasks in a patient with amygdala damage acquired in childhood. Here, we present the first evidence of theory of mind deficits following amygdala damage acquired in adulthood. Two participants, D.R. and S.E., with acquired bilateral amygdala damage showed difficulties with two theory of mind tasks, "Recognition of Faux Pas" (for D.R., z = -5.17; for S.E., z = -1.83) and "Reading the Mind in the Eyes" (for S.E., z = -1.91; for D.R., z = -1.4). The items on which D.R. and S.E. made errors on these tasks were uncorrelated with the items that control participants found most difficult, indicating that these deficits cannot be attributed solely to the cognitive difficulty of the tasks. These results indicate that the amygdala's critical role in theory of mind may not be just in development, but also in "on-line" theory of mind processing in the adult brain. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 3EB, England. MRC, Cognit & Brain Sci Unit, Cambridge CB2 2EF, England. Univ York, Dept Psychol, York YO1 5DD, N Yorkshire, England. RP Stone, VE (reprint author), Univ Denver, Dept Psychol, 2155 S Race St, Denver, CO 80208 USA. 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SO NEUROPSYCHOLOGIA LA English DT Article DE psychopathy; theory of mind; amygdala ID ASPERGER-SYNDROME; AUTISM; ADULTS AB There have been suggestions that Theory of Mind (ToM) impairment might lead to aggressive behaviour and psychopathy. Psychopathic and matched non-psychopathic individuals, as defined by the Hare Psychopathy Checklist [The Hare Psychopath Checklist-Revised, 1991] completed the 'Reading the Mind in the Eyes' ToM Test [Journal of Child Psychology and Psychiatry, 1997;38:813]. This test requires the self-paced identification of mental states from photographs of the eye region alone. Results indicated that the psychopathic individuals did not present with any generalised impairment in ToM. The data are discussed with reference to the putative neural system mediating performance on this task and models of psychopathy. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 NIMH, Unit Affect Cognit Neurosci, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA. UCL, Dept Psychol, Inst Cognit Sci, London, England. HMP Wormwood Scrubs, London, England. Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 3EB, England. RP Blair, RJR (reprint author), NIMH, Unit Affect Cognit Neurosci, Mood & Anxiety Disorders Program, 15K North Dr,Room 206,MSC 2670, Bethesda, MD 20892 USA. EM blairj@intra.nimh.nih.gov CR Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Blair J, 1996, J FORENSIC PSYCHIATR, V7, P15, DOI 10.1080/09585189608409914 Blair RJR, 1997, PSYCHOPHYSIOLOGY, V34, P192 Blair RJR, 2001, J NEUROL NEUROSUR PS, V71, P727, DOI 10.1136/jnnp.71.6.727 CRICK NR, 1994, PSYCHOL BULL, V115, P74, DOI 10.1037/0033-2909.115.1.74 Feshbach N. 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These poor visuo-spatial abilities have been ascribed to a local processing bias by some [R. Rossen, E.S. Klima, U. Bellugi, A. Bihrle, W. Jones, Interaction between language and cognition: evidence from Williams syndrome, in: J. Beitchman, N. Cohen, M. Konstantareas, R. Tannock (Eds.), Language, Learning and Behaviour disorders: Developmental, Behavioural and Clinical Perspectives, Cambridge University Press, New York, 1996, pp. 367-392] and conversely, to a global processing bias by others [Psychol. Sci. 10 (1999) 453]. In this study, two identification versions and one drawing version of the Navon hierarchical processing task, a non-verbal task, were employed to investigate this apparent contradiction. The two identification tasks were administered to 21 individuals with WS, 21 typically developing individuals, matched by non-verbal ability, and 21 adult participants matched to the WS group by mean chronological age (CA). The third, drawing task was administered to the WS group and the typically developing (TD) controls only. It was hypothesised that the WS group would show differential processing biases depending on the type of processing the task was measuring. Results from two identification versions of the Navon task measuring divided and selective attention showed that the WS group experienced equal interference from global to local as from local to global levels, and did not show an advantage of one level over another. This pattern of performance was broadly comparable to that of the control groups. The third task, a drawing version of the Navon task, revealed that individuals with WS were significantly better at drawing the local form in comparison to the global figure, whereas the typically developing control group did not show a bias towards either level. 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NEUROPSYCHOLOGIA JI Neuropsychologia PY 2003 VL 41 IS 8 BP 894 EP 905 DI 10.1016/S0028-3932(03)00002-2 PG 12 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 671HW UT WOS:000182460100004 PM 12667526 ER PT J AU Gottwald, B Mihajlovic, Z Wilde, B Mehdorn, HM AF Gottwald, B Mihajlovic, Z Wilde, B Mehdorn, HM TI Does the cerebellum contribute to specific aspects of attention? SO NEUROPSYCHOLOGIA LA English DT Article DE cognition; divided attention; selective attention; working memory; cerebellar lesion ID DEFICIT HYPERACTIVITY DISORDER; SELECTIVE ATTENTION; VERBAL FLUENCY; FRONTAL-LOBE; CHILDREN; AUTISM; MEMORY; TASKS AB We present data on attentional and neuropsychological functions of 16 patients with focal cerebellar lesions (13 tumours, 3 haematomas) compared to normative test data, and to I I control subjects matched for age, gender, and years of education. Patients showed distinct deficits in qualitative aspects of a divided attention task, and in a working memory task. Performance in selective attention was unimpaired. The results support the concept that the cerebellum plays a role not only in motor, but also in higher cognitive functions. They are discussed on the basis of the idea that prediction and preparation are fundamental functions of the cerebellum. Therefore, the results confirm the idea that cerebellar lesions lead to reduced performance in specific attention tasks. (C) 2003 Elsevier Science Ltd. All rights reserved. C1 Univ Kiel, Klinikum Schleswig Holstein, Neurochirurg Klin, Dept Neurosurg, D-24106 Kiel, Germany. RP Gottwald, B (reprint author), Univ Kiel, Klinikum Schleswig Holstein, Neurochirurg Klin, Dept Neurosurg, Weimarer Str 8, D-24106 Kiel, Germany. RI Mehdorn, Maximilian /D-2495-2010 CR Akshoomoff NA, 1997, INT REV NEUROBIOL, V41, P575 Allen G, 1997, SCIENCE, V275, P1940, DOI 10.1126/science.275.5308.1940 APPOLLONIO IM, 1993, NEUROLOGY, V43, P1536 Baumler G., 1985, FARBE WORT INTERFERE Berquin PC, 1998, NEUROLOGY, V50, P1087 Carpenter M. 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H., 1994, CLIN NEUROPSYCHOLOGY Wechsler D., 1981, WAIS R MANUAL WECHSLER D, 1987, MEMORY SCALE REVISED Zimmermann P, 1993, TESTBATTERIE AUFMERK NR 42 TC 76 Z9 79 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2003 VL 41 IS 11 BP 1452 EP 1460 DI 10.1016/S0028-3932(03)00090-3 PG 9 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 703XT UT WOS:000184308300003 PM 12849763 ER PT J AU Temple, CA Sanfilippo, PM AF Temple, CA Sanfilippo, PM TI Executive skills in Klinefelter's syndrome SO NEUROPSYCHOLOGIA LA English DT Article DE Klinefelter's syndrome; executive functions; additional X-chromosome ID DEFICIT HYPERACTIVITY DISORDER; TEMPORAL-LOBE LESIONS; FRONTAL-LOBE; TURNERS-SYNDROME; CHILDREN; CHILDHOOD; BOYS; CONSEQUENCES; PROFILES; FLUENCY AB Executive skills are those involved in concept formation, problem solving, switching tasks, inhibiting inappropriate responses, initiating rapid and fluent responses, planning and sustained attention. Different patterns of disorder amongst these skills have been found in several developmental abnormalities including autism, attention deficit hyperactivity disorder (ADHD) and Turner's syndrome (TS). This study explored, for the first time, executive skills in children with Klinefelter's syndrome (KS), a sex chromosome abnormality in which there is one or more additional X-chromosomes. Intelligence in KS is normal but there is academic underachievement. A battery of executive tasks was administered, in a series of case studies, to three 10-year-old boys with KS and to controls matched for age, sex and intelligence. The results demonstrate that children with KS have impairments in executive skills. However, the pattern of impairment is task-specific. There is evidence from multiple tasks of impairment in inhibitory skills, for each case of KS. In contrast, concept formation, problem solving, task switching and speeded responding are normal. These results support theories that argue for distinct sub-components of executive skills within development that may develop relatively independently. The results have relevance for modelling both child and adult executive systems. They also confirm that an additional X-chromosome has highly selective effects upon the consequent cognitive phenotype seen in development. (C) 2003 Elsevier Science Ltd. All rights reserved. C1 Univ Essex, Dept Psychol, Dev Neuropsychol Unit, Colchester CO4 3SQ, Essex, England. RP Temple, CA (reprint author), Univ Essex, Dept Psychol, Dev Neuropsychol Unit, Wivenhoe Pk, Colchester CO4 3SQ, Essex, England. 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There is evidence that abnormalities exist in peptide systems, particularly the oxytocin system, in autism spectrum patients. Furthermore, oxytocin and the closely related peptide vasopressin are known to play a role in social and repetitive behaviors. This study examined the impact of oxytocin on repetitive behaviors in 15 adults with autism or Asperger's disorder via randomized double-blind oxytocin and placebo challenges. The primary outcome measure was an instrument rating six repetitive behaviors: need to know, repeating, ordering, need to tell/ask, self-injury, and touching. Patients with autism spectrum disorders showed a significant reduction in repetitive behaviors following oxytocin infusion in comparison to placebo infusion. Repetitive behavior in autism spectrum disorders may be related to abnormalities in the oxytocin system, and may be partially ameliorated by synthetic oxytocin infusion. 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Recent observations that the deficits in social reciprocity skills seen in young (3-4-year-old) autistic children are improved after secretin infusions suggest an additional influence on neuronal activity. We show here that i.v. administration of secretin in rats induces Fos protein expression in the neurons of the central amygdala as well as the area postrema, bed nucleus of the stria terminalis, external lateral parabrachial nucleus and supraoptic nucleus. However, secretin infusion did not induce Fos expression in the solitary tract nucleus or para-ventricular nucleus, regions normally activated by related peptides such as cholecystokinin. The peak blood levels of secretin that induce Fos protein expression in rat brain are similar to the peak blood levels observed during i.v. treatment with secretin in humans. The amygdala is known to be critical for developing reciprocal social interaction skills and abnormalities in this brain region have been demonstrated in autistic children. (C) 2003 IBRO. Published by Elsevier Science Ltd. All rights reserved. C1 Repligen Corp, Waltham, MA 02453 USA. RP Rusche, JR (reprint author), Repligen Corp, Bldg 1,Suite 100,41 Seyon st, Waltham, MA 02453 USA. 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Both genetic, developmental and degenerative aberrations are to be encompassed within such an approach, as well as all deviations from the necessary components of behaviour that are generally understood to incorporate "normal" functioning. In the present treatise, both conditions of hyperactivity/hypoactivity, akinesia and bradykinesia together with a constellation of other symptoms and syndromes are considered in conjunction with the neuropharmacological and brain morphological alterations that may or may not accompany them, e.g. following neonatal denervation. As a case in point, the neuroanatomical and neurochemical points of interaction in Attention Deficit and Hyperactivity disorder (ADHD) are examined with reference to both the perinatal metallic and organic environment and genetic backgrounds. The role of apoptosis, as opposed to necrosis, in cell death during brain development necessitates careful considerations of the current explosion of evidence for brain nerve growth factors, neurotrophins and cytokines, and the processes regulating their appearance, release and fate. Some of these processes may possess putative inherited characteristics, like a-synudein, others may to greater or lesser extents be endogenous or semi-endogenous (in food), like the tetrahydroisoquinolines, others exogenous until inhaled or injested through environmental accident, like heavy metals, e.g. mercury. Another central concept of neurodevelopment is cellular plasticity, thereby underlining the essential involvement of glutamate systems and N-methyl-D-aspartate receptor configurations. Finally, an essential assimilation of brain development in disease must delineate the relative merits of inherited as opposed to environmental risks not only for the commonly regarded movement disorders, like Parkinson's disease, Huntington's disease and epilepsy, but also for afflictions bearing strong elements of psychosocial tragedy, like ADHD, autism and Savantism. C1 Univ Gothenburg, Dept Psychol, SE-40530 Gothenburg, Sweden. Hosp 12 Octubre, Serv Psiquiatria, E-28041 Madrid, Spain. Queens Univ, Dept Psychol & Psychiat, Kingston, ON K7L 3N6, Canada. E Tennessee State Univ, Dept Pharmacol, Quillen Coll Med, Johnson City, TN 37614 USA. RP Archer, T (reprint author), Univ Gothenburg, Dept Psychol, Box 500, SE-40530 Gothenburg, Sweden. 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Res. PY 2003 VL 5 IS 1-2 BP 1 EP 26 PG 26 WC Neurosciences SC Neurosciences & Neurology GA 691MQ UT WOS:000183610400001 PM 12832221 ER PT J AU Leonard, H Petterson, B Bower, C Sanders, R AF Leonard, H Petterson, B Bower, C Sanders, R TI Prevalence of intellectual disability in Western Australia SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY LA English DT Article ID MILD MENTAL-RETARDATION; FINNISH BIRTH COHORT; METROPOLITAN ATLANTA; RISK-FACTORS; FOLLOW-UP; CHILDREN; CHILDHOOD; MUNICIPALITY; EPIDEMIOLOGY; AUTISM AB Record linkage of multiple sources was used to ascertain children with intellectual disability born in Western Australia between 1983 and 1992. The prevalence was 14.3 per 1000, 10.6 per 1000 for children with mild or moderate and 1.4 per 1000 for those with a severe level of intellectual disability. Prevalence was greater in males (prevalence ratio 1.6) and in children of Aboriginal mothers (prevalence ratio 2.3). 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Perinat. Epidemiol. PD JAN PY 2003 VL 17 IS 1 BP 58 EP 67 DI 10.1046/j.1365-3016.2003.00469.x PG 10 WC Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics SC Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics GA 641JB UT WOS:000180740700009 PM 12562473 ER PT J AU Bonneh, YS Pei, F Iverson, P Merzenich, MM AF Bonneh, YS Pei, F Iverson, P Merzenich, MM TI Cross-modal extinction in autism: A case report SO PERCEPTION LA English DT Meeting Abstract C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Cure Autism Now, Los Angeles, CA 90036 USA. Smith Kettlewell Eye Res Inst, San Francisco, CA 94115 USA. Weizmann Inst Sci, IL-76100 Rehovot, Israel. NR 0 TC 1 Z9 1 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2003 VL 32 SU S BP 9 EP 10 PG 2 WC Psychology; Psychology, Experimental SC Psychology GA 720KH UT WOS:000185259600026 ER PT J AU Ferro, A AF Ferro, A TI Marcella: The transition from explosive sensoriality to the ability to think SO PSYCHOANALYTIC QUARTERLY LA English DT Article AB The author discusses an analytic case in which it was necessary to first address the patient's need for containment of her protoemotions-her sensoriality-before the analysis could proceed along more standard lines, with interpretation of the transference, work on displacement and aspects of her childhood history, and so forth. 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PY 2003 VL 72 IS 1 BP 183 EP 200 PG 18 WC Psychology, Psychoanalysis SC Psychology GA 640MF UT WOS:000180692000007 PM 12616872 ER PT J AU Davidson, RJ Schultz, RT Schmidt, LA Sutton, SK AF Davidson, RJ Schultz, RT Schmidt, LA Sutton, SK TI Neurobiological correlates of autism and autism spectrum disorders SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 43rd Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 29-NOV 02, 2003 CL CHICAGO, ILLINOIS SP Soc Psychophysiol Res NR 0 TC 8 Z9 8 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2003 VL 40 SU 1 BP S3 EP S3 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 715BV UT WOS:000184951400002 ER PT J AU Davidson, RJ Dalton, K AF Davidson, RJ Dalton, K TI Dysfunctions in the neural circuitry of emotional face processing in individuals with autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 43rd Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 29-NOV 02, 2003 CL CHICAGO, ILLINOIS SP Soc Psychophysiol Res C1 Univ Wisconsin, Madison, WI USA. NR 0 TC 8 Z9 8 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2003 VL 40 SU 1 BP S3 EP S3 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 715BV UT WOS:000184951400003 ER PT J AU Schmidt, LA AF Schmidt, LA TI Psychophysiology of social deficits in extreme childhood shyness: Implications for understanding socio-emotional processes in childhood autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 43rd Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 29-NOV 02, 2003 CL CHICAGO, ILLINOIS SP Soc Psychophysiol Res C1 McMaster Univ, Hamilton, ON L8S 4L8, Canada. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2003 VL 40 SU 1 BP S3 EP S3 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 715BV UT WOS:000184951400005 ER PT J AU Schultz, RT Klin, A Grelotti, DJ Herrington, J Volkmar, F AF Schultz, RT Klin, A Grelotti, DJ Herrington, J Volkmar, F TI FMRI studies of the fusiform face area in autism spectrum disorders SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 43rd Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 29-NOV 02, 2003 CL CHICAGO, ILLINOIS SP Soc Psychophysiol Res C1 Yale Univ, New Haven, CT 06520 USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2003 VL 40 SU 1 BP S3 EP S3 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 715BV UT WOS:000184951400004 ER PT J AU Sutton, SK Burnette, CP Mundy, PC AF Sutton, SK Burnette, CP Mundy, PC TI Resting frontal cortical activity in high-functioning children with autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 43rd Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 29-NOV 02, 2003 CL CHICAGO, ILLINOIS SP Soc Psychophysiol Res C1 Univ Miami, Coral Gables, FL 33124 USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2003 VL 40 SU 1 BP S4 EP S4 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 715BV UT WOS:000184951400006 ER PT J AU Ross, DE Greer, RD AF Ross, DE Greer, RD TI Generalized imitation and the mand: inducing first instances of speech in young children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE generalized imitation; mand; autism ID TIME-DELAY; LANGUAGE; BEHAVIOR AB It has been suggested that the use of a generalized motor imitation sequence before a vocal model may be an effective procedure for teaching nonvocal children with autism to speak. However, the tactic has rarely been empirically demonstrated. The purpose of this experiment was to test the effects of presenting a rapid generalized motor imitation sequence before an opportunity to imitate on the vocal speech of nonvocal children with autism. Participants emitted no vocal imitations during a mand training baseline. During the intervention, a rapid motor imitation sequence was presented before an opportunity to imitate a model's vocalizations. The teacher's presentation of the rapid motor imitation sequence was then faded by presenting an opportunity to vocally imitate without the sequence followed by an opportunity to independently mand. Results of the intervention phase indicated that all of the participants began to vocalize with the generalized motor imitation sequence and that mands were maintained during a follow-up phase and 3-month follow-up probes. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Columbia Univ, Teachers Coll, New York, NY 10027 USA. 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PY 2003 VL 1008 BP 91 EP 101 DI 10.1196/annals.1301.010 PG 11 WC Psychology, Developmental; Multidisciplinary Sciences; Pediatrics; Psychology SC Psychology; Science & Technology - Other Topics; Pediatrics GA BY70S UT WOS:000189443700009 PM 14998875 ER PT S AU Di Martino, A Castellanos, FX AF Di Martino, A Castellanos, FX BE King, JA Ferris, CF Lederhendler, II TI Functional neuroimaging of social cognition in pervasive developmental disorders - A brief review SO ROOTS OF MENTAL ILLNESS IN CHILDREN SE Annals of the New York Academy of Sciences LA English DT Review CT Conference on Roots of Mental Illness in Children CY MAR 15-17, 2003 CL New York, NY SP NY Acad Sci, NIMH, Janssen Pharmaceutica Inc DE social cognition; pervasive developmental disorders; functional neuroimaging ID ASPERGER-SYNDROME; AUTISM; BRAIN; FACE; MIND; AMYGDALA; INDIVIDUALS AB An emerging literature on the neuroanatomical correlates of social cognition in pervasive developmental disorders is reviewed. 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PY 2003 VL 1008 BP 256 EP 260 DI 10.1196/annals.1301.027 PG 5 WC Psychology, Developmental; Multidisciplinary Sciences; Pediatrics; Psychology SC Psychology; Science & Technology - Other Topics; Pediatrics GA BY70S UT WOS:000189443700025 PM 14998891 ER PT J AU Asmus, JM Franzese, JC Conroy, MA Dozier, CL AF Asmus, JM Franzese, JC Conroy, MA Dozier, CL TI Clarifying functional analysis outcomes for disruptive behaviors by controlling consequence delivery for stereotypy SO SCHOOL PSYCHOLOGY REVIEW LA English DT Article ID ABERRANT BEHAVIOR; DEVELOPMENTAL-DISABILITIES; PROTECTIVE EQUIPMENT; SELF-INJURY; TOPOGRAPHIES AB Although individuals may engage in several topographies of aberrant behavior, each with different functions, it is not uncommon for researchers to conduct one functional analysis. We conducted two functional analyses for a child with autism, one with and one without consequences for stereotypic vocalizations. 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PY 2003 VL 32 IS 4 BP 624 EP 630 PG 7 WC Psychology, Educational SC Psychology GA 762AA UT WOS:000187946600012 ER PT S AU Happe, F AF Happe, F BE LeDoux, J Debiec, J Moss, H TI Theory of mind and the self SO SELF: FROM SOUL TO BRAIN SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on the Self - From Soul to Brain CY SEP 26-28, 2002 CL NEW YORK, NY SP NY Acad Sci, Mushett Family Fdn Inc DE theory of mind; autism; self-awareness; development; neuroimaging; brain ID FALSE BELIEF; AUTISM; BRAIN; ATTRIBUTION; INTENTION; CHILDREN; REPRESENTATION; NEUROANATOMY; KNOWLEDGE; STATES AB This paper will discuss one aspect of the self, the ability to reflect on one's own inner states, in relation to recent work on the cognitive and neural basis of "theory of mind." Are the same representational resources required for "reading" one's own and other minds? Relevant literature from the study of normal development of theory of mind will be reviewed, along with research on a developmental disorder characterized by an apparent inability to think about thoughts: autism. Functional neuroimaging studies of theory of mind will be discussed as will studies that may tap the neural basis of self-reflection. From these different strands of evidence the speculative suggestion will be made that reflecting on one's own thoughts is not a privileged process, but rather relies on-and may have evolved from-the same cognitive and neural functions used for attributing thoughts to others. C1 Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London SE5 8AF, England. RP Happe, F (reprint author), Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, Box P0890,De Crespigny Pk, London SE5 8AF, England. 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PY 2003 VL 1001 BP 134 EP 144 DI 10.1196/annals.1279.008 PG 11 WC Multidisciplinary Sciences; Psychology; Psychology, Multidisciplinary SC Science & Technology - Other Topics; Psychology GA BY06H UT WOS:000187495900008 PM 14625359 ER PT J AU Malhi, P Singhi, P AF Malhi, P Singhi, P TI Recognition of autism in young children SO STUDIA PSYCHOLOGICA LA English DT Article DE autism; young children; early recognition; developmental disorders ID SYMPTOMS; 1ST AB The paper aims at describing the early clinical and developmental profile of autism in children less than five years of age. Twenty four consecutive children younger than 60 months (Mean = 40.8) with a clinical diagnosis of autism as per DSM IV criteria were recruited from the Department of Pediatrics, PGIMER, Chandigarh. In addition, all children obtained scores within the autistic range (Mean = 38.2) on the Childhood Autism Rating Scale (CARS). The developmental status of each child was assessed using the Developmental Profile II and the Indian adaptation of the Vineland Social Maturity Scale. Six behavioral characteristics including absence of imaginative play (100%), lack of emotional and social/emotional reciprocity (95.8%), impairment in use of non-verbal behavior (87.5%), impaired peer relationships (87.5%), no mode of communication (83.3%) and restricted range of interests (79.2%) were more salient than other behavioral characteristics such as insistence on routines (8.3%), impairment in ability to initiate conversation (12.5%), stereotyped use of language (16.7%) and pre-occupation with parts of objects (37.5%). Developmental testing revealed that children with autism have weaker socialization and communication skills. Some behavioral characteristics may be more important than others for the early diagnosis of autism. C1 Postgrad Inst Med Educ & Res, Dept Pediat, Chandigarh 160012, India. RP Malhi, P (reprint author), Postgrad Inst Med Educ & Res, Dept Pediat, Chandigarh 160012, India. 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PY 2003 VL 45 IS 1 BP 75 EP 80 PG 6 WC Psychology, Multidisciplinary SC Psychology GA 673BN UT WOS:000182559400008 ER PT J AU Krasnoperova, MG Bashina, VM Skvortsov, IA Simashkova, NV AF Krasnoperova, MG Bashina, VM Skvortsov, IA Simashkova, NV TI The effect of cerebrolysin on cognitive functions in childhood autism and in Asperger's syndrome SO ZHURNAL NEVROPATOLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE autism; Asperger's syndrome; cognitive functions; cerebrolysin AB Nineteen children with childhood autism and 8 with Asperger's syndrome aged 2-8 year, were treated with cerebrolysin (CL) in inpatient clinic. All the patients received 10 microinjections (intramuscularly and perinervously) of 0,1 ml CL daily during 5 days. Clinical study was combined with device estimation of cognitive functions and communicative skills. CL therapy resulted in improvement of cognitive functions (expressive and receptive speech, fine motoring, playing). Positive effects were revealed in all the patients with Asperger's syndrome and in 89% of the patients with childhood autism. Any negative effects were not found. With regard to cognitive functions development, therapeutic efficacy proved to be more pronounced in the patients with Asperger's syndrome as compared to childhood autistic group (p<0,005). C1 Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. Moscow Psychoneurol Disabil Treatment & Prevent S, Moscow, Russia. RP Krasnoperova, MG (reprint author), Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. CR BASHINA VM, 1999, AUTIZM DETSTVE, P233 *CDCP, 2000, PREV AUT BRICK TOWNS, V14, P2 SKVORTSOV IA, 2000, RAZVITIE NERVNOI SIS, P200 Skvortsov IA, 1998, ZH NEVROPATOL PSIKH, V98, P17 SKVORTSOV IA, 1989, ZH NEVROPATOL PSIKH, V89, P23 NR 5 TC 3 Z9 3 PU IZD VO MEDITSINA PI MOSCOW PA PETROVERIGSKII PER 6-8, K-142 MOSCOW, RUSSIA SN 0044-4588 J9 ZH NEVROPATOL PSIKH JI Zhurnal Nevropatol. Psikhiatrii Im. 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Am. Med. Assoc. PD DEC 25 PY 2002 VL 288 IS 24 BP 3155 EP 3158 DI 10.1001/jama.288.24.3155 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 628QQ UT WOS:000180008200026 PM 12495396 ER PT J AU Masuo, Y Ishido, M Morita, M Oka, S AF Masuo, Y Ishido, M Morita, M Oka, S TI Effects of neonatal 6-hydroxydopamine lesion on the gene expression profile in young adult rats SO NEUROSCIENCE LETTERS LA English DT Article DE hyperkinetic disorder; 6-hydroxydopamine; spontaneous motor activity; cDNA array; dopamine transporter; dopamine receptor; glutamate transporter ID DEFICIT HYPERACTIVITY DISORDER; DOPAMINE TRANSPORTER; MOTOR-ACTIVITY; ANIMAL-MODEL; ATTENTION; RECEPTORS; SYSTEM; LOCALIZATION; BRAIN; ADHD AB Patients with pervasive developmental disorders, including autism, and attention-deficit hyperactivity disorder show behavioral hyperactivity during childhood. We investigated the effects of a neonatal 6-hydroxydopamine lesion on multiple gene expression in the rat striatum and midbrain. Spontaneous motor activity was significantly increased at 4-5 weeks of age. The animals were sacrificed, and the striatum and midbrain were subjected to gene expression profiling using a membrane array with 1176 kinds of cDNAs. Alterations were found in several classes of gene expression, depending on the brain region. Enhanced expression of the glutamate transporter gene was found in the striatum. Expression of the dopamine receptor D4 gene and dopamine transporter gene was also increased in the midbrain. These results suggest that 6-hydroxydopamine-treated rats may partly mimic human hyperkinesia not only in behavior but also in gene expression. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Natl Inst Adv Ind Sci & Technol, Int Patent Organ Deposit, Tsukuba, Ibaraki 3058566, Japan. New Energy & Ind Technol Dev Organ, Toshima Ku, Tokyo 1706028, Japan. Natl Inst Environm Studies, Endocrine Disruptors & Dioxin Res Projects, Tsukuba, Ibaraki 3058506, Japan. RP Masuo, Y (reprint author), Natl Inst Adv Ind Sci & Technol, Int Patent Organ Deposit, Tsukuba Cent 6,1-1-1 Higashi, Tsukuba, Ibaraki 3058566, Japan. 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PD DEC 25 PY 2002 VL 335 IS 2 BP 124 EP 128 DI 10.1016/S0304-3940(02)01167-9 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 625MZ UT WOS:000179821400013 PM 12459514 ER PT J AU Verdoux, H Sutter, AL AF Verdoux, H Sutter, AL TI Perinatal risk factors for schizophrenia: Diagnostic specificity and relationships with maternal psychopathology SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article; Proceedings Paper CT Schizophrenia: From Prediction to Prevention-The Challenge of the 21st Century CY NOV 30-DEC 01, 2000 CL LYON, FRANCE DE obstetric complications; schizophrenia; diagnostic specificity; maternal depression ID LOW-BIRTH-WEIGHT; INDIVIDUAL PATIENT DATA; OBSTETRIC COMPLICATIONS; POSTNATAL DEPRESSION; PRENATAL EXPOSURE; DELIVERY COMPLICATIONS; CESAREAN-SECTION; PRETERM BIRTH; PREGNANCY; CHILDREN AB Although a growing body of evidence supports the hypothesis that exposure to obstetric complications (OCs) increases the vulnerability for schizophrenia, some questions remain unanswered regarding the diagnostic specificity and the etiological significance of this association. Associations with a history of OCs have been reported for other severe psychiatric disorders, such as autism, anorexia nervosa, or psychotic affective disorder. Thus, OCs may increase in a relatively non-specific way the vulnerability for a range of severe mental disorders, the expression of this vulnerability depending on the interaction between OCs and other risk factors, such as the genetic liability for specific psychiatric disorder, or exposure to later environmental risk factors. The causal pathway between OCs, maternal psychopathology, and psychotic outcome in the offspring is not fully elucidated. The directions of the associations are often bi-directional, and the mediating variables, if any, are not clearly identified. OCs may have a direct negative impact on fetal brain development, may be on the causal pathway between prepartum maternal depression/exposure to stress and increased risk of schizophrenia, or may indirectly increase the risk of child's later psychiatric disorder by acting as risk factors for maternal postpartum depression. The links and possible interactions between somatic perinatal risk factors and maternal psychopathology in the association with offspring's increased vulnerability for psychosis have to be further explored. (C) 2002 Wiley-Liss, Inc. C1 Univ Bordeaux 2, Dept Psychiat, F-33076 Bordeaux, France. RP Verdoux, H (reprint author), Univ Bordeaux, Dept Psychiat, Hop Charles Perrens, 121 Rue Bechade, F-33076 Bordeaux, France. 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J. Med. Genet. PD DEC 8 PY 2002 VL 114 IS 8 BP 898 EP 905 DI 10.1002/ajmg.10906 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 618EL UT WOS:000179405500003 PM 12457383 ER PT J AU Elgar, K Campbell, R Skuse, D AF Elgar, K Campbell, R Skuse, D TI Are you looking at me? Accuracy in processing line-of-sight in Turner syndrome SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Article DE gaze acuity; Turner syndrome; autism ID EYE GAZE; AUTISM; BRAIN; DISCRIMINATION; PERCEPTION; ATTENTION; DIRECTION; FACE; SCHIZOPHRENIA; STIMULI AB The behavioural phenotype of women with Turner syndrome (X-monosomy, 45,X) is poorly understood, but includes reports of some social development anomalies. With this in mind, accuracy of direction of gaze detection was investigated in women with Turner syndrome. Two simple experimental tasks were used to test the prediction that the ability to ascertain gaze direction from face photographs showing small lateral angular gaze deviations would be impaired in this syndrome, compared with a control population of men and women. The prediction was confirmed and was found to affect both the detection of egocentric gaze from the eyes ('is the face looking at me?') and the detection of allocentric gaze, where the eyes in a photographed face inspected one of a number of locations of attention ('where is she looking?'). We suggest that dosage-sensitive X-linked genes contribute to the development of gaze-monitoring abilities. C1 UCL, Dept Human Commun Sci, London WC1N 1PF, England. Inst Child Hlth, Dept Behav & Brain Sci, London WC1N 1EH, England. RP Campbell, R (reprint author), UCL, Dept Human Commun Sci, Chandler House,Wakefield St, London WC1N 1PF, England. EM r.campbell@ucl.ac.uk RI Campbell, Ruth/K-5934-2012 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 ANSTIS SM, 1969, AM J PSYCHOL, V82, P474, DOI 10.2307/1420441 Baron-Cohen S., 1995, MIND BLINDNESS ESSAY Baron-Cohen S, 2000, NEUROSCI BIOBEHAV R, V24, P355, DOI 10.1016/S0149-7634(00)00011-7 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 BARONCOHEN S, 1996, BR J DEV PSYCHOL, V31, P379 Brothers L., 1990, CONCEPTS NEUROSCIENC, V1, P27 Calder AJ, 2002, NEUROPSYCHOLOGIA, V40, P1129, DOI 10.1016/S0028-3932(02)00008-8 CAMPBELL R, 1990, NEUROPSYCHOLOGIA, V28, P1123, DOI 10.1016/0028-3932(90)90050-X Collaer ML, 2002, HORM BEHAV, V41, P139, DOI 10.1006/hbeh.2001.1751 CRESWELL C, 2000, NEUROCASE, V5, P511 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 ELGAR K, 2002, IN PRESS NEUROPSYCHO Franck N, 1998, PSYCHIAT RES, V81, P67, DOI 10.1016/S0165-1781(98)00082-1 Goldstein JM, 2001, CEREB CORTEX, V11, P490, DOI 10.1093/cercor/11.6.490 Good CD, 2001, NEUROIMAGE, V14, P685, DOI 10.1006/nimg.2001.0857 Good CD, 2001, NEUROIMAGE, V13, pS793 HEYWOOD CA, 1992, PHILOS T ROY SOC B, V335, P31, DOI 10.1098/rstb.1992.0004 Howard MA, 2000, NEUROREPORT, V11, P2931, DOI 10.1097/00001756-200009110-00020 HUTT C, 1966, BEHAV SCI, V11, P346, DOI 10.1002/bs.3830110504 Kawashima R, 1999, BRAIN, V122, P779, DOI 10.1093/brain/122.4.779 Langton SRH, 2000, TRENDS COGN SCI, V4, P50, DOI 10.1016/S1364-6613(99)01436-9 Leekam S, 1997, BRIT J DEV PSYCHOL, V15, P77 MCCAULEY E, 1987, CHILD DEV, V58, P464, DOI 10.1111/j.1467-8624.1987.tb01394.x MONACO AP, 2001, LANCET S3, V358 PERRETT DI, 1985, PROC R SOC SER B-BIO, V223, P293, DOI 10.1098/rspb.1985.0003 Ricciardelli P, 2000, COGNITION, V77, pB1, DOI 10.1016/S0010-0277(00)00092-5 ROSS JL, 1995, AM J MED GENET, V58, P74, DOI 10.1002/ajmg.1320580115 ROSS JL, 1999, NEURODEVELOPMENTAL D, P251 ROSSE RB, 1994, AM J PSYCHIAT, V151, P919 Ruffman T, 2001, J CHILD PSYCHOL PSYC, V42, P1083, DOI 10.1111/1469-7610.00807 Swettenham J, 1998, J CHILD PSYCHOL PSYC, V39, P747, DOI 10.1017/S0021963098002595 TEMPLE CM, 1995, CORTEX, V31, P109 Toran-Allerand CD, 1999, FRONT NEUROENDOCRIN, V20, P97, DOI 10.1006/frne.1999.0177 Turner HH, 1938, ENDOCRINOLOGY, V23, P566 Ward LC, 1996, PSYCHOL ASSESSMENT, V8, P69 WESCHLER D, 1981, ADULT INTELLIGENCE S NR 38 TC 23 Z9 23 PU ROYAL SOC PI LONDON PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND SN 0962-8452 J9 P ROY SOC B-BIOL SCI JI Proc. R. Soc. B-Biol. Sci. PD DEC 7 PY 2002 VL 269 IS 1508 BP 2415 EP 2422 DI 10.1098/rspb.2002.2173 PG 8 WC Biology; Ecology; Evolutionary Biology SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences & Ecology; Evolutionary Biology GA 630LM UT WOS:000180108400005 PM 12495483 ER PT J AU Brownstein, S AF Brownstein, S TI Autism (Comment) SO TLS-THE TIMES LITERARY SUPPLEMENT LA English DT Letter CR HUDSON L, 2002, TLS 1004 NR 1 TC 1 Z9 1 PU TIMES SUPPLEMENTS LIMITED PI MARKET HARBOROUGH PA TOWER HOUSE, SOVEREIGN PARK, MARKET HARBOROUGH LE87 4JJ, ENGLAND SN 0307-661X J9 TLS-TIMES LIT SUPPL JI TLS-Times Lit. Suppl. PD DEC 6 PY 2002 IS 5201 BP 17 EP 17 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 626BR UT WOS:000179851000012 ER PT J AU Sandler, L AF Sandler, L TI Risperidone in children with autism and serious behavioral problems SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP Sandler, L (reprint author), 5895 Friendship Dr, New Concord, OH 43762 USA. CR Carr E. G., 1994, COMMUNICATION BASED Koegel R. L., 1995, TEACHING CHILDREN AU O'Neill R. E., 1997, FUNCTIONAL ASSESSMEN, V2nd McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 NR 4 TC 3 Z9 3 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 DEC 5 PY 2002 VL 347 IS 23 BP 1890 EP 1890 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 621NW UT WOS:000179596900022 PM 12466518 ER PT J AU Valiquette, G AF Valiquette, G TI Risperidone in children with autism and serious behavioral problems SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 New York Med Coll, Valhalla, NY 10595 USA. RP Valiquette, G (reprint author), New York Med Coll, Valhalla, NY 10595 USA. CR Miller KK, 1999, J CLIN ENDOCR METAB, V84, P1775, DOI 10.1210/jc.84.6.1775 Yasui-Furukori N, 2002, PSYCHOPHARMACOLOGY, V162, P63, DOI 10.1007/s00213-002-1058-6 NR 2 TC 3 Z9 3 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 DEC 5 PY 2002 VL 347 IS 23 BP 1890 EP 1891 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 621NW UT WOS:000179596900023 PM 12472071 ER PT J AU Munarriz, R Bennett, L Goldstein, I AF Munarriz, R Bennett, L Goldstein, I TI Risperidone in children with autism and serious behavioral problems SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID PRIAPISM C1 Boston Univ, Sch Med, Boston, MA 02118 USA. RP Munarriz, R (reprint author), Boston Univ, Sch Med, Boston, MA 02118 USA. CR Berger R, 2001, INT J IMPOT RES, V13, pS39 EMES CE, 1994, CAN J PSYCHIAT, V39, P315 Maizel Shmuel, 1996, Harefuah, V130, P799 Nicolson R, 1997, J CLIN PSYCHOPHARM, V17, P133, DOI 10.1097/00004714-199704000-00022 TEKELL JL, 1995, AM J PSYCHIAT, V152, P1097 NR 5 TC 1 Z9 1 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 5 PY 2002 VL 347 IS 23 BP 1891 EP 1891 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 621NW UT WOS:000179596900024 ER PT J AU Scahill, L Vitiello, B AF Scahill, L Vitiello, B CA Res Units Pediat Psychopharmacolog TI Risperidone in children with autism and serious behavioral problems - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Yale Univ, New Haven, CT 06520 USA. NIMH, Bethesda, MD 20892 USA. RP Scahill, L (reprint author), Yale Univ, New Haven, CT 06520 USA. CR AMAN MG, IN PRESS J AUTISM DE Deirmenjian JM, 1998, J CLIN PSYCHOPHARM, V18, P351, DOI 10.1097/00004714-199808000-00023 Freudenreich O, 2002, J CLIN PSYCHIAT, V63, P249 Owley T, 2001, J CHILD ADOL PSYCHOP, V11, P441, DOI 10.1089/104454601317261627 Schreibman L, 2000, J AUTISM DEV DISORD, V30, P373, DOI 10.1023/A:1005535120023 NR 5 TC 0 Z9 0 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 5 PY 2002 VL 347 IS 23 BP 1891 EP 1891 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 621NW UT WOS:000179596900025 ER PT J AU Astrinidis, A Cash, TP Hunter, DS Walker, CL Chernoff, J Henske, EP AF Astrinidis, A Cash, TP Hunter, DS Walker, CL Chernoff, J Henske, EP TI Tuberin, the tuberous sclerosis complex 2 tumor suppressor gene product, regulates Rho activation, cell adhesion and migration SO ONCOGENE LA English DT Article DE tuberous sclerosis complex; TSC2; tuberin; RhoA; cell migration; cell attachment ID TSC1 GENE; EKER RAT; TYROSINE PHOSPHORYLATION; GROWTH-FACTOR; KINASE GENE; GTPASE-RHO; HAMARTIN; PROLIFERATION; EXPRESSION; CANCER AB Tuberous sclerosis complex (TSC) is a tumor suppressor gene syndrome characterized by seizures, mental retardation, autism, and tumors of the brain, kidney, heart, retina, and skin. TSC is caused by mutations in either TSC1 or TSC2, both of which are tumor suppressor genes. Hamartin, the protein product of TSC1, was found to interact with the ezrin-radixin-moesin family of cytoskeletal proteins and to activate the small GTPase Rho. To determine whether tuberin, the TSC2 product, can also activate Rho, we stably expressed full-length human tuberin in two cell types: MDCK cells and ELT3 cells. ELT3 cells lack endogenous tuberin expression. We found that expression of human tuberin in both MDCK and ELT3 cells was associated with an increase in the amount of Rho-GTP, but not in Rac1-GTP or cdc42-GTP. Tuberin expression increased cell adhesion in both cell types, and decreased chemotactic cell migration in ELT3 cells. In MDCK cells, there was a decrease in the amount of total Focal Adhesion Kinase (FAK) and an increase in the fraction of phosphorylated FAK. These findings demonstrate for the first time that tuberin activates Rho and regulates cell adhesion and migration. Pathways involving Rho activation may have relevance to the clinical manifestations of TSC, including pulmonary lymphangioleiomyomatosis. C1 Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ Texas, MD Anderson Canc Ctr, Smithville, TX 78957 USA. RP Henske, EP (reprint author), Fox Chase Canc Ctr, 7701 Burholme Ave, Philadelphia, PA 19111 USA. 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Material and methods: We conducted a retrospective cohort study of all children born in Denmark from January 1991 through December 1998. The cohort was established based on data from the Danish Civil Registration System. A unique person identifiable number given to all subjects enabled linkage with other national registries. MMR vaccination status was obtained from the Danish National Board of Health. Information on the children's autism status was obtained from the Danish Psychiatric Central Register which contains information on all diagnoses received from psychiatric hospitals, psychiatric wards, and outpatient clinics in Denmark. We obtained information on potential confounders from the Danish Medical Birth Registry, the National Hospital Registry, and Statistics Denmark. Results: In the cohort of 537,303 children (2,129,864 person-years), 440,655 children had been MMR vaccinated. We identified 316 children with a diagnosis of autistic disorder and 442 with a diagnosis of other spectrum disorders. After adjusting for potential confounders, the risk for autistic disorder and other spectrum disorders was not increased in vaccinated compared with unvaccinated children (relative risk 0.92; 95 percent confidence interval, 0.68 to 1.24 and relative risk 0.83; 95 percent confidence interval, 0.65 to 1.07). There was no association between age at vaccination, time since vaccination or calendar period at time of vaccination and development of autistic disorder. Discussion: This study provides strong evidence against the hypothesis that MMR vaccination causes autism. C1 Aarhus Univ, Inst Epidemiol & Socialmed, Ctr Epidemiol Grundforskning, DK-8000 Aarhus C, Denmark. State Serum Inst, Ctr Epidemiol Grundforskning, Copenhagen, Denmark. Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA USA. RP Madsen, KM (reprint author), Aarhus Univ, Inst Epidemiol & Socialmed, Ctr Epidemiol Grundforskning, DK-8000 Aarhus C, Denmark. 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Laeg. PD DEC 2 PY 2002 VL 164 IS 49 BP 5741 EP 5744 PG 4 GA 623WA UT WOS:000179724800001 PM 12523209 ER PT J AU Guerin, P AF Guerin, P TI Medicinal treatment of autism. SO A N A E-APPROCHE NEUROPSYCHOLOGIQUE DES APPRENTISSAGES CHEZ L ENFANT LA French DT Article DE autistic disorder; medicinal treatments; neuroleptics; serotonin reuptake inhibitors; naltrexone; secretin ID DOUBLE-BLIND; SPECTRUM DISORDERS; CHILDREN; HALOPERIDOL; RISPERIDONE; NALTREXONE; OLANZAPINE; TERM AB Autistic disorders cover some extremely wide clinical tableaux and probably a number of physiopathological mechanisms. No curative treatment has as yet been identified. Several types of medicine (neuroleptics, serotonin reuptake inhibitors, opiate antagonists, lithium, anticonvulsants, vitamins, neuropeptides) have been proposed, but in cases where clinical improvement is obtained, it remains symptomatic, limited and patchy. Properly conducted pharmacological studies are scarce. Medicinal treatment in autistic disorders is only conceived of as a follow up to a detailed analysis of functional behaviour. C1 Hop St Brice, Ctr Hosp Chartres, Serv Psychiat Infanto Juvenile, Unite Diagnost & Traitement Trouble Envahissants, F-28000 Chartres, France. 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Apprentiss. Enfant PD DEC PY 2002 VL 14 IS 5 BP 333 EP 338 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 666HV UT WOS:000182172600008 ER PT J AU Kimmel, SR AF Kimmel, SR TI Vaccine adverse events: Separating myth from reality SO AMERICAN FAMILY PHYSICIAN LA English DT Article ID MULTIPLE-SCLEROSIS; B VACCINATION; RISK; DETERMINANTS; IMMUNIZATION; CHILDHOOD; COMMUNITY; MEASLES AB Vaccines have turned many childhood diseases into distant memories in industrialized countries. However, questions have been raised about the safety of some vaccines because of rare but serious adverse effects that have beenattributed to them. Pain, swelling, and redness at the injection site are common local reactions to vaccines. Fever and irritability may occur after some immunizations. Currently, no substantial evidence links measles-mumps-rubelia vaccine to autism, or hepatitis B vaccine to multiple sclerosis. Thimerosal is being eliminated from routine childhood vaccines. because of concerns that multiple immunizations with vaccines containing this preservative could exceed recommended mercury exposures. Family physicians should be knowledgeable about vaccines so that they can inform their patients of the benefits of immunization. and any proven risks. If immunization rates fall, the incidence of vaccine-preventable illnesses may rise. Copyright(C) 2002 American Academy of Family Physicians. C1 Med Coll Ohio, Dept Family Med, Toledo, OH 43614 USA. RP Kimmel, SR (reprint author), Med Coll Ohio, Dept Family Med, 1015 Garden Lake Pkwy, Toledo, OH 43614 USA. 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Physician PD DEC 1 PY 2002 VL 66 IS 11 BP 2113 EP 2120 PG 8 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA 623WL UT WOS:000179725800009 PM 12484693 ER PT J AU Galanopoulou, AS Vidaurre, J McVicar, K Ballaban-Gil, K Shinnar, S Tuchman, R Moshe, SL AF Galanopoulou, AS Vidaurre, J McVicar, K Ballaban-Gil, K Shinnar, S Tuchman, R Moshe, SL TI Language and behavioral disturbances associated with epileptiform EEGs SO AMERICAN JOURNAL OF ELECTRONEURODIAGNOSTIC TECHNOLOGY LA English DT Review DE autism; autistic regression; centrotemporal spikes; electrical status epilepticus in sleep; epilepsy; Landau-Kleffner syndrome; Rett syndrome ID LANDAU-KLEFFNER-SYNDROME; ELECTRICAL STATUS EPILEPTICUS; BENIGN PARTIAL EPILEPSY; AUTISTIC-SPECTRUM DISORDERS; PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD DISINTEGRATIVE DISORDER; MULTIPLE SUBPIAL TRANSECTION; LONG-TERM PROGNOSIS; MYOCLONIC-ASTATIC EPILEPSY; PSEUDO-LENNOX-SYNDROME AB The appearance of language or behavioral regression in previously normal children is a devastating experience for both the family and the patients. In some cases, evaluation with prolonged sleep electroencephalograms (EEGs) reveals a dramatic activation of epileptiform activities. These may be continuous and diffusely appearing spike-wave discharges in slow-wave sleep, also known as "electrical status epilepticus in sleep" (ESES), or they may be more focal but very frequent temporal, centrotemporal, or multifocal spikes. The typical syndromes are the encephalopathy associated with ESES or continuous spike waves during slow-wave sleep (CSWS) and Landau-Kleffner syndrome (LKS). A significant minority of children with pre-existing impairments in sociability, communication, and behavior, typical of autistic spectrum disorders, may manifest epileptiform abnormalities, which perhaps further exacerbate the language or neuropsychiatric dysfunction. Patients with autistic regression with epileptiform EEGs (AREE) may have clinical and electrographic similarities with CSWS or LKS children. In this review, we will summarize the existing knowledge about these syndromes and the existing therapeutic strategies. Awareness about these syndromes is of paramount importance in order to implement early detection and treatment, which may ameliorate the outcome. C1 Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Montefiore Einstein Epilepsy Management Ctr, Bronx, NY 10461 USA. Miamia Childrens Hosp, Dept Neurol, Miami, FL USA. 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J. Electroneurodiagn. Technol. PD DEC PY 2002 VL 42 IS 4 BP 181 EP 209 PG 29 WC Medical Laboratory Technology; Neurosciences SC Medical Laboratory Technology; Neurosciences & Neurology GA 644AD UT WOS:000180895000001 ER PT J AU Lainhart, JE Ozonoff, S Coon, H Krasny, L Dinh, E Nice, J McMahon, W AF Lainhart, JE Ozonoff, S Coon, H Krasny, L Dinh, E Nice, J McMahon, W TI Autism, regression, and the broader autism phenotype SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; broader autism phenotype; regression; environment ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HISTORY; CHILDREN; DEFICITS; PARENTS; INDIVIDUALS; PERSONALITY; RELATIVES; SPECTRUM; SCHEDULE AB The broader autism phenotype (BAP) is a subclinical set of personality and other features that is thought to index familiality and/or genetic liability to autism. Eighteen parents of autistic probands with a history of language regression and 70 parents of autistic probands without regression were assessed for features of the BAP and compared with published rates in parents of nonautistic subjects. Parents of probands with regressive and nonregressive autism demonstrated similar rates of the BAP (27.8% vs. 32.9%; P = 0.33). The rate of the BAP was significantly higher in both groups of autism parents than in parents of nonautistic subjects (P less than or equal to 0.01). Thus, this measure of genetic liability is increased equally in families with both forms of autism when compared with controls. Environmental events are therefore unlikely to be the sole cause of regressive autism in our sample. Environmental events, however, may act in an additive or "second-hit" fashion in individuals with a genetic vulnerability to autism. (C) 2002 Wiley-Liss, Inc. C1 Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. Univ Calif Davis, Dept Psychiat, MIND Inst, Sacramento, CA 95817 USA. RP Lainhart, JE (reprint author), Utah Neurodev Genet Program, 546 Chipeta Way,Suite 441, Salt Lake City, UT 84108 USA. 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J. Med. Genet. PD DEC 1 PY 2002 VL 113 IS 3 BP 231 EP 237 DI 10.1002/ajmg.10615 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 614CV UT WOS:000179171500002 PM 12439889 ER PT J AU Toomim, H AF Toomim, H TI The use of HEG in the treatment of autism, Parkinson's disease, attention hyperactive disorder, epilepsy, stroke and depression SO APPLIED PSYCHOPHYSIOLOGY AND BIOFEEDBACK LA English DT Meeting Abstract DE autism; Parkinson's; ADD/ADHD; HEG C1 Biocomp Res Inst, Los Angeles, CA 90048 USA. NR 0 TC 0 Z9 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1090-0586 J9 APPL PSYCHOPHYS BIOF JI Appl. Psychophysiol. Biofeedback PD DEC PY 2002 VL 27 IS 4 BP 317 EP 317 PG 1 WC Psychology, Clinical SC Psychology GA 614QQ UT WOS:000179201200055 ER PT J AU Andrews, N Miller, E Taylor, B Lingam, R Simmons, A Stowe, J Waight, P AF Andrews, N Miller, E Taylor, B Lingam, R Simmons, A Stowe, J Waight, P TI Recall bias, MMR, and autism SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID VACCINE; CHILDREN; MEASLES; MUMPS AB Parents of autistic children with regressive symptoms who were diagnosed after the publicity alleging a link with measles, mumps, and rubella (MMR) vaccine tended to recall the onset as shortly after MMR more often than parents of similar children who were diagnosed prior to the publicity. This is consistent with the recall bias expected under such circumstances. C1 Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, London NW9 5EQ, England. Publ Hlth Lab Serv, Stat Univ, London NW9 5EQ, England. UCL Royal Free & Univ Coll, Sch Med, Ctr Community Child Hlth, London NW3 2PF, England. RP Miller, E (reprint author), Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, 61 Colindale Ave, London NW9 5EQ, England. EM emiller@phls.org.uk CR Elliman DAC, 2001, ARCH DIS CHILD, V85, P271, DOI 10.1136/adc.85.4.271 FARRINGTON CP, 1995, BIOMETRICS, V51, P228, DOI 10.2307/2533328 LINGAM R, UNPUB PREVALENCE AUT 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 NR 6 TC 13 Z9 14 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD DEC PY 2002 VL 87 IS 6 BP 493 EP 494 DI 10.1136/adc.87.6.493 PG 2 WC Pediatrics SC Pediatrics GA 622PJ UT WOS:000179655200010 PM 12456546 ER PT J AU Yonamine, SM da Silva, AA AF Yonamine, SM da Silva, AA TI Characteristics of the communication in individuals with fragile X syndrome SO ARQUIVOS DE NEURO-PSIQUIATRIA LA French DT Article DE fragile X syndrome; speech; language; communication ID LINKED MENTAL-RETARDATION; LANGUAGE CHARACTERISTICS; AUTISM; MALES AB The aim of this study was to make a characterization of the communication in a group with fragile X syndrome (FXS), based on normal development scale. The sample has 10 boys, between 6 and 13 years and with FXS. All of them were submitted to language evaluation. The most part of them had the communication in linguistic form (80%), until 3 years old. It was considered that the data confirmed the significant delay in the acquisition and development of the communication, being necessary an early and specialized intervention. C1 Univ Estadual Campinas, Dept Oftalmootorrinolaringol & Genet med, Fac Ciencias Med, BR-13081970 Campinas, SP, Brazil. 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Neuro-Psiquiatr. PD DEC PY 2002 VL 60 IS 4 BP 981 EP 985 DI 10.1590/S0004-282X2002000600018 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 628RQ UT WOS:000180010700018 PM 12563393 ER PT J AU Rinehart, NJ Bradshaw, JL Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Brereton, AV Tonge, BJ TI A clinical and neurobehavioural review of high-functioning autism and Asperger's disorder SO AUSTRALIAN AND NEW ZEALAND JOURNAL OF PSYCHIATRY LA English DT Article DE Asperger's disorder; autism; epidemiology; genetics; neuropsychology ID MOVEMENT-RELATED POTENTIALS; COGNITIVE PHENOTYPE; IDENTICAL TRIPLETS; CENTRAL COHERENCE; CHILDHOOD AUTISM; VISUAL ILLUSIONS; CHILDREN; MIND; ATTENTION; PATTERNS AB Objective: To compare, contrast and review clinical and neuropsychological studies of high-functioning autism and Asperger's disorder. Method: This paper reviews past and contemporary conceptualizations of autism and Asperger's disorder, together with epidemiological information, genetic and neurobehavioural findings. This paper focuses on neurobehavioural studies, in particular, executive functioning, lateralization, visual-perceptual and motor processing, which have provided an important source of information about the potential neurobiological dissociation that may exist between autism and Asperger's disorder. Results: The clinical profiles of autism and Asperger's disorder contain a mixture of psychiatric and neurological symptoms: for example, movement abnormalities (i.e. stereotyped behaviours, hand flapping, toe walking, whole-body movements), atypical processing of parts and wholes, verbal and non-verbal deficits, ritualistic/compulsive behaviour, disturbances in reciprocal social interaction and associated depression and anxiety. The considerable clinical overlap between autism and Asperger's disorder has led many to question whether Asperger's disorder is merely a mild form of autism, or whether it should be considered as a separate clinical entity. Conclusion: In light of the growing body of epidemiological information, genetic, and neurobehavioural evidence that distinguishes autism from Asperger's disorder, it is premature to rule out the possibility that these disorders may be clinically, and possibly neurobiologically separate. C1 Monash Univ, Sch Psychol Psychiat & Psychol Med, Caulfield, Vic 3145, Australia. Monash Univ, Neuropsychol Res Unit, Melbourne, Vic 3004, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Sch Psychol Psychiat & Psychol Med, POB 197, Caulfield, Vic 3145, Australia. 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PD DEC PY 2002 VL 36 IS 6 BP 762 EP 770 DI 10.1046/j.1440-1614.2002.01097.x PG 9 WC Psychiatry SC Psychiatry GA 624DX UT WOS:000179746000005 PM 12406118 ER PT J AU Brereton, AV AF Brereton, AV TI Exiting nirvana: a daughter's life with autism SO AUSTRALIAN AND NEW ZEALAND JOURNAL OF PSYCHIATRY LA English DT Book Review CR Park C.C., 2001, EXITING NIRVANA DAUG NR 1 TC 0 Z9 0 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 DEC PY 2002 VL 36 IS 6 BP 833 EP 833 DI 10.1046/j.1440-1614.2002.t01-3-01121f.x PG 1 WC Psychiatry SC Psychiatry GA 624DX UT WOS:000179746000024 ER PT J AU Wellman, HM Baron-Cohen, S Caswell, R Gomez, JC Swettenham, J Toye, E Lagattuta, K AF Wellman, HM Baron-Cohen, S Caswell, R Gomez, JC Swettenham, J Toye, E Lagattuta, K TI Thought-bubbles help children with autism acquire an alternative to a theory of mind SO AUTISM LA English DT Article DE false belief; mental states; pictures-in-the-head; theory of mind; thought-bubbles ID TEACHING THEORY; FALSE BELIEF; DEFICIT; INDIVIDUALS; DECEPTION AB Children with autism have specific difficulties understanding complex mental states like thought, belief, and false belief and their effects on behaviour. Such children benefit from focused teaching, where beliefs are likened to photographs-in-the-head. Here two studies, one with seven participants and one with 10, tested a picture-in-the-head strategy for dealing with thoughts and behaviour by teaching children with autism about cartoon thought-bubbles as a device for representing such mental states. This prosthetic device led children with autism to pass not only false belief tests, but also related theory of mind tests. These results confirm earlier findings of the efficacy of picture-in-the-head teaching about mental states, but go further in showing that thought-bubble training more easily extends to children's understanding of thoughts (not just behaviour) and to enhanced performance on several transfer tasks. Thought-bubbles provide a theoretically interesting as well as an especially easy and effective teaching technique. C1 Univ Michigan, Ctr Human Growth & Dev, Ann Arbor, MI 48109 USA. Univ Cambridge, Cambridge CB2 1TN, England. Univ St Andrews, St Andrews KY16 9AJ, Fife, Scotland. UCL, London WC1E 6BT, England. RP Wellman, HM (reprint author), Univ Michigan, Ctr Human Growth & Dev, 300 N Ingalls Bldg,10th Level, Ann Arbor, MI 48109 USA. 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Possible autism-specific impairments include an inability to engage in goal-directed behaviors and adjust behaviors given environmental demands. What has been described as executive functions is based largely on observations of performance in the laboratory rather than in natural settings. An ecological method first described by Barker and Wright and adapted by Scott was used to assess the patterns of goal-directed behaviors of eight children with autism and eight chronological and mental age comparable children with Down syndrome. Quantitative and qualitative features of naturalistic behaviors were collected, and coded using previously described categories of children's behavior. Results indicated that children with autism exhibited shorter and less overlapping goal-directed behaviors. These data suggest a cognitive difference rather than developmental delay, and lend support for impaired executive functions in autism. Practical implications for educators and caregivers are discussed. C1 Vanderbilt Univ, Nashville, TN 37240 USA. Indiana Univ, Bloomington, IN 47405 USA. RP Ruble, LA (reprint author), Univ Louisville, WeissKopf Ctr Evaluat Children, Dept Pediat, 571 So Floyd St,Suite 100, Louisville, KY 40202 USA. EM larubl01@gwise.louisville.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barker R. G., 1955, MIDWEST ITS CHILDREN Barkley RA, 2000, J AM ACAD CHILD PSY, V39, P1064, DOI 10.1097/00004583-200008000-00025 BRYSON S, 1997, CHILDHOOD ATTENTION, P232 DUMKE R, 1986, THESIS INDIANA U GUMP PV, 1974, SCHOOL REV, V82, P575, DOI 10.1086/443151 Gump P. 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The interpretation of executive function deficits is difficult because the concept itself is poorly defined (inhibition of prepotent responses, set-shifting, action planning etc.). Analyses have focused mainly on the attention participants pay to physical entities (object handling and problem solving) rather than social ones. The present study investigated whether these two types of attention are linked in autistic development. Fifteen children with autism (mean mental age = 24 months) were compared to 21 normally developing children (mean mental age = 25 months). A strong correlation was found between joint attention and set-shifting in the typically developing children but not those with autism. The results are discussed from a psychopathological perspective on development. C1 Univ Montpellier 3, EA 1977, F-34199 Montpellier 5, France. CHU Montpellier, Serv Medicopsychol Enfants & Adolescents, Montpellier, France. RP Stahl, L (reprint author), Univ Montpellier 3, EA 1977, Route Mende, F-34199 Montpellier 5, France. 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Thirty-seven families and 66 parents were involved in each case, and four psychological tests were used. It was found that lower levels of coping were associated with higher levels of strain on the family system, that the level of strain on the family system was greater in the families with a child with an ASD, and that the two groups differed in their pattern of coping behavior. It is argued that limited contact between the child with an ASD and its parents, claimed earlier to be a cause of autism, can be explained in terms of strain on the family system and the resulting pattern of coping. C1 Lund Univ, S-22100 Lund, Sweden. RP Sivberg, B (reprint author), Dept Nursing, Sect Caring Sci, POB 157, SE-22100 Lund, Sweden. CR Altman DG, 1999, PRACTICAL STAT MED R American Psychiatric Association, 2000, DIAGN STAT MAN MENT ANTONOVSKY A, 1993, SOC SCI MED, V36, P725, DOI 10.1016/0277-9536(93)90033-Z Antonovsky A, 1987, UNRAVELLING MYSTERY Antonovsky A, 1979, NEW PERSPECTIVES MEN Bristol M. M., 1984, EFFECTS AUTISM FAMIL, P289 Bristol M. M., 1983, AUTISM ADOLESCENTS A, P251 CANTWELL DP, 1984, EFFECTS AUTISM FAMIL, P41 Cohen D. J, 1997, HDB AUTISM PERVASIVE Crumbaugh J, 1988, INT FORUM LOGOTHERAP, V11, P76 FISMAN S, 1991, PSYCHIAT CLIN N AM, V14, P199 Frankl V., 1958, J PASTORAL CARE, V12, P82 Frankl V. E., 1962, MANS SEARCH MEANING GILLBERG C, 2001, INT J CIRCUMPOLAR S1, V60, P36 Gillberg C, 1995, EPIDEMIOLOGY CHILD A, P227 Hallum A, 1995, Curr Probl Pediatr, V25, P12, DOI 10.1016/S0045-9380(06)80013-7 HANSSON K, 1995, KANSLA SAMMANHANG HOLMES N, 1991, J AUTISM DEV DISORD, V21, P159, DOI 10.1007/BF02284757 HOOK B, 1992, FAMILJERELATIONSSKAL Lazarus R. S., 1984, STRESS APPRAISAL COP Mahler M., 1975, PSYCHOL BIRTH HUMAN Marcus L. M., 1997, HDB AUTISM PERVASIVE, P631 MORGAN SB, 1988, J AUTISM DEV DISORD, V18, P263, DOI 10.1007/BF02211952 Norusis M. J., 1993, SPSS WINDOWS SIVBERG B, 2001, UNPUB CULTURAL EXPLO SIVBERG B, 2001, UNPUB COPING STRATEG Spitz R. A., 1965, 1 YEAR LIFE TIDEMAN E, 1999, SWEDISH VERSION WECH Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D, 1981, WECHSLER ADULT INTEL NR 31 TC 54 Z9 57 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2002 VL 6 IS 4 BP 397 EP 409 DI 10.1177/1362361302006004006 PG 13 WC Psychology, Developmental SC Psychology GA 631DJ UT WOS:000180151900005 PM 12540130 ER PT J AU Whitaker, P AF Whitaker, P TI Supporting families of preschool children with autism - What parents want and what helps SO AUTISM LA English DT Article DE autism; early intervention; parent training ID MOTHERS AB This paper describes a local education authority project to provide support to the families of preschool children with autistic spectrum disorders. As part of an evaluation study, all parents were interviewed when their children entered full-time education and left the service's caseload. The report outlines key findings regarding levels of satisfaction with the service provided and describes parental responses to the different components of the support offered. All parents rated the input of the support worker as 'very useful'. Parents particularly valued the following: support to 'make sense' of their child's development and needs; practical strategies for facilitating language and engaging in interactive play; and support to the nurseries and playgroups attended by their children. The interviews also looked at parents' experience of diagnosis and their needs in the immediate aftermath. Key implications of these findings, and of this. model of service delivery, are also discussed. RP Whitaker, P (reprint author), Educ Psychol Serv, Cty Hall, Leicester LE3 8RF, Leics, England. CR BONDY AS, 1994, PRE SCH ED PROGRAMS Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 HOPPES K, 1990, J CLIN CHILD PSYCHOL, V19, P365, DOI 10.1207/s15374424jccp1904_8 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Kaufman Barry N., 1994, SON RISE MIRACLE CON KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P205, DOI 10.1007/BF01058151 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x Randall P., 1999, SUPPORTING FAMILIES Shields J, 2001, AUTISM, V5, P49, DOI 10.1177/1362361301005001005 WEITZMAN K, 1992, LEARNING LANGUAGE LO NR 10 TC 22 Z9 22 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2002 VL 6 IS 4 BP 411 EP 426 DI 10.1177/1362361302006004007 PG 16 WC Psychology, Developmental SC Psychology GA 631DJ UT WOS:000180151900006 PM 12540131 ER PT J AU McConachie, H AF McConachie, H TI Educating children with autism SO AUTISM LA English DT Book Review C1 Univ Newcastle Upon Tyne, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP McConachie, H (reprint author), Univ Newcastle Upon Tyne, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. CR McGee J. P., 2001, ED CHILDREN AUTISM NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2002 VL 6 IS 4 BP 437 EP 438 DI 10.1177/1362361302006004011 PG 2 WC Psychology, Developmental SC Psychology GA 631DJ UT WOS:000180151900010 ER PT J AU Dillenburger, K AF Dillenburger, K TI Raising a child with autism: A guide to applied behavior analysis for parents SO AUTISM LA English DT Book Review C1 Queens Univ Belfast, Sch Social Work, Belfast BT7 1NN, Antrim, North Ireland. RP Dillenburger, K (reprint author), Queens Univ Belfast, Sch Social Work, Belfast BT7 1NN, Antrim, North Ireland. CR Richman Shira, 2001, RAISING CHILD AUTISM NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2002 VL 6 IS 4 BP 438 EP 440 DI 10.1177/1362361302006004012 PG 3 WC Psychology, Developmental SC Psychology GA 631DJ UT WOS:000180151900012 ER PT J AU Dillenburger, K AF Dillenburger, K TI Caring for a child with autism: A practical guide for parents SO AUTISM LA English DT Book Review C1 Queens Univ Belfast, Sch Social Work, Belfast BT7 1NN, Antrim, North Ireland. RP Dillenburger, K (reprint author), Queens Univ Belfast, Sch Social Work, Belfast BT7 1NN, Antrim, North Ireland. CR IVES M, 2002, CARING CHILD AUTISM NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2002 VL 6 IS 4 BP 438 EP 440 DI 10.1177/1362361302006004012 PG 3 WC Psychology, Developmental SC Psychology GA 631DJ UT WOS:000180151900011 ER PT J AU Slonims, V AF Slonims, V TI A picture's worth: PECS and other visual communication strategies in autism SO AUTISM LA English DT Book Review C1 Guys Hosp, Newcomen Ctr, London SE1 9RT, England. RP Slonims, V (reprint author), Guys Hosp, Newcomen Ctr, London SE1 9RT, England. CR BONDY A, PICTURES WORTH PECS NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2002 VL 6 IS 4 BP 440 EP 441 DI 10.1177/1362361302006004013 PG 2 WC Psychology, Developmental SC Psychology GA 631DJ UT WOS:000180151900013 ER PT J AU Muller, RA AF Muller, RA TI Weak evidence for a strong case against modularity in developmental disorders SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID LANGUAGE DISORDER; ASPERGER-SYNDROME; INHERITED SPEECH; BRAIN; AUTISM; MIND; SEROTONIN; MECHANISMS; RECOVERY; APHASIA AB Thomas & Karmiloff-Smith (T&K-S) provide evidence from computational modeling against modular assumptions of "Residual Normality" (RN) in developmental disorders. Even though I agree with their criticism, I find their choice of empirical evidence disappointing. Cognitive neuroscience cannot as yet provide a complete understanding of most developmental disorders, but what is known is more than enough to debunk the idea of RN. C1 San Diego State Univ, Dept Psychol, San Diego, CA 92120 USA. RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, San Diego, CA 92120 USA. EM amueller@sciences.sdsu.edu CR Akshoomoff N, 2002, DEV PSYCHOPATHOL, V14, P613, DOI 10.1017/S0954579402003115 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Betancur C, 2002, MOL PSYCHIATR, V7, P67, DOI 10.1038/sj/mp/4000923 Buitelaar JK, 2000, EUR CHILD ADOLES PSY, V9, P85 Calder AJ, 2002, NEUROPSYCHOLOGIA, V40, P1129, DOI 10.1016/S0028-3932(02)00008-8 Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Chomsky N, 2002, NATURE LANGUAGE Chugani DC, 2002, MOL PSYCHIATR, V7, pS16, DOI 10.1038/sj.mp.4001167 Dawson G, 2002, DEV PSYCHOPATHOL, V14, P581, DOI 10.1017/S0954579402003103 Gottlieb G, 2002, DEV PSYCHOPATHOL, V14, P421, DOI 10.1017/S0954579402003021 Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 Lai CSL, 2001, NATURE, V413, P519, DOI 10.1038/35097076 Leslie A.M., 1992, CURRENT DIRECTIONS P, V1, P18, DOI 10.1111/1467-8721.ep10767818 Muller RA, 1999, NEUROPSYCHOLOGIA, V37, P545, DOI 10.1016/S0028-3932(98)00109-2 Pinker S., 1999, WORDS RULES Rosen HJ, 2000, NEUROLOGY, V55, P1883 Rumsey JM, 2000, MENT RETARD DEV D R, V6, P171, DOI 10.1002/1098-2779(2000)6:3<171::AID-MRDD4>3.0.CO;2-N Rutherford MD, 2002, J AUTISM DEV DISORD, V32, P189, DOI 10.1023/A:1015497629971 Scholl BJ, 2001, CHILD DEV, V72, P696, DOI 10.1111/1467-8624.00308 Stone VE, 1998, J COGNITIVE NEUROSCI, V10, P640, DOI 10.1162/089892998562942 Thulborn KR, 1999, STROKE, V30, P749 Vargha-Khadem F, 1997, CURR PROB E, V11, P774 Watkins KE, 2002, BRAIN, V125, P452, DOI 10.1093/brain/awf058 Watkins KE, 2002, BRAIN, V125, P465, DOI 10.1093/brain/awf057 Whitaker-Azmitia PM, 2001, BRAIN RES BULL, V56, P479, DOI 10.1016/S0361-9230(01)00615-3 NR 25 TC 0 Z9 0 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 DEC PY 2002 VL 25 IS 6 BP 764 EP + PG 10 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 834MV UT WOS:000222416100051 ER PT J AU Kushner, HI AF Kushner, HI TI Autism in history: The case of Hugh Blair of Borgue. SO BULLETIN OF THE HISTORY OF MEDICINE LA English DT Book Review C1 Emory Univ, Atlanta, GA 30322 USA. RP Kushner, HI (reprint author), Emory Univ, Atlanta, GA 30322 USA. CR Houston Rab, 2000, AUTISM HIST CASE HUG NR 1 TC 0 Z9 0 PU JOHNS HOPKINS UNIV PRESS PI BALTIMORE PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD 21218-4319 USA SN 0007-5140 J9 B HIST MED JI Bull. Hist. Med. PD WIN PY 2002 VL 76 IS 4 BP 821 EP 822 DI 10.1353/bhm.2002.0188 PG 2 WC Health Care Sciences & Services; History & Philosophy Of Science SC Health Care Sciences & Services; History & Philosophy of Science GA 618ND UT WOS:000179423400021 ER PT J AU Gilotty, L Kenworthy, L Sirian, L Black, DO Wagner, AE AF Gilotty, L Kenworthy, L Sirian, L Black, DO Wagner, AE TI Adaptive skills and executive function in autism spectrum disorders SO CHILD NEUROPSYCHOLOGY LA English DT Article ID BEHAVIOR SCALES; CHILDREN; PERFORMANCE; DEFICITS; MEMORY AB There is active debate regarding the nature of executive dysfunction in autism. Additionally, investigations have yet to show a relationship between deficits in executive function and the everyday behavioral difficulties that may originate from them. The present study examined the relationship between executive abilities and adaptive behavior in 35 children with Autism Spectrum Disorders, using two parent reports of everyday functioning, the Vineland Adaptive Behavior Scales (VABS) and the Behavior Rating Inventory of Executive Function (BRIEF). Results found several relationships: The Initiate and Working Memory domains were negatively correlated with most domains of adaptive behavior. Also, the Communication and Socialization domains of the VABS were negatively correlated with several areas of executive functioning, suggesting that impairments in executive abilities are strongly associated with the deficits in communication, play and social relationships found in children with autism. C1 Childrens Natl Med Ctr, Spring Valley Reg Outpatient Ctr, Dept Pediat, Div Psychol, Washington, DC 20009 USA. NIMH, Child & Adolescent Treatment Res Branch, Bethesda, MD 20892 USA. RP Gilotty, L (reprint author), Childrens Natl Med Ctr, Spring Valley Reg Outpatient Ctr, Dept Pediat, Div Psychol, 4900 Massachusetts Ave,Suite 320, Washington, DC 20009 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x Burgess P, 1997, METHODOLOGY FRONTAL, P81 Denckla MB, 1994, FRAMES REFERENCE ASS Gioia GA, 2000, BRIEF BEHAV RATING I Griffith EM, 1999, CHILD DEV, V70, P817, DOI 10.1111/1467-8624.00059 Hollingshead A. B., 1975, 4 FACTOR INDEX SOCIA JANUSZ J, 2002, ANN M INT NEUR SOC T Kanner L, 1943, NERV CHILD, V2, P217 Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 Klinger LG, 2000, J CLIN CHILD PSYCHOL, V29, P479, DOI 10.1207/S15374424JCCP2904_3 Liss M, 2001, J CHILD PSYCHOL PSYC, V42, P261, DOI 10.1017/S0021963001006679 Lord C., 1993, UNDERSTANDING OTHER, P292 Manly T., 1999, TEA CH TEST EVERYDAY McDonough L, 1997, DEV PSYCHOPATHOL, V9, P17 Ozonoff S., 1998, ASPERGER SYNDROME HI, P263 Ozonoff S, 2000, ASPERGER SYNDROME, P72 Ozonoff S, 1997, AUTISM EXECUTIVE DIS, P179 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x PERRY A, 1989, J AUTISM DEV DISORD, V19, P41, DOI 10.1007/BF02212717 RAVER CC, 1993, HUM DEV, V36, P350 RODRIGUE JR, 1991, J AUTISM DEV DISORD, V21, P187, DOI 10.1007/BF02284759 RUMSEY JM, 1985, J AUTISM DEV DISORD, V15, P23, DOI 10.1007/BF01837896 Schopler E, 1998, ASPERGER SYNDROME HI, P385 Sparrow S, 1984, VINELAND ADAPTIVE BE Szatmari P, 1998, ASPERGER SYNDROME HI, P61 Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 VOLKMAR FR, 1987, J AM ACAD CHILD PSY, V26, P156, DOI 10.1097/00004583-198703000-00005 NR 28 TC 83 Z9 84 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD DEC PY 2002 VL 8 IS 4 BP 241 EP 248 DI 10.1076/chin.8.4.241.13504 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 680QW UT WOS:000182989700003 PM 12759821 ER PT J AU Honomichl, RD Goodlin-Jones, BL Burnham, MM Hansen, RL Anders, TF AF Honomichl, RD Goodlin-Jones, BL Burnham, MM Hansen, RL Anders, TF TI Secretin and sleep in children with autism SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE autism; sleep; secretin ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; CONTROLLED TRIAL; BEHAVIOR; CAREGIVERS AB The objectives of this pilot study were 1) to examine possible effects of secretin infusions on sleep-wake state organization in children with autism, and 2) to assess the feasibility of home recordings using time-lapse videosomnography in children with autism. Participants were a subset of subjects from two double blind, placebo-control, multi-center clinical trials. One trial, the UC Irvine study, assessed the effects of porcine secretin vs. saline infusions on children's behavior, language and IQ. The UC Davis trial assessed the effects of synthetic human secretin vs. saline infusions on behavior, language and gastrointestinal function. The sleep study enrolled some of the children from each of the two trials to observe possible secretin effects on sleep. To examine sleep, the UC Irvine trial used the Children's Sleep Habits Questionnaire and daily sleep diaries, whereas the UC Davis study used home-recorded time-lapse video-sonmography. Because of the small sample size, the results from both trials are preliminary. They suggest that secretin, porcine or synthetic, does not improve sleep-wake state organization dramatically. C1 Univ Calif Davis, Sch Med, Davis, CA 95616 USA. Univ Nevada, Reno, NV 89557 USA. RP Anders, TF (reprint author), Univ Calif Davis, Sch Med, Davis, CA 95616 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERS T, 1985, SLEEP, V48, P173 ANDERS TF, 1976, PSYCHOPHYSIOLOGY, V13, P155, DOI 10.1111/j.1469-8986.1976.tb00092.x ANDERS TF, 1978, J AM ACAD CHILD PSY, V17, P421, DOI 10.1016/S0002-7138(09)62298-6 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 CHARLTON CG, 1982, PEPTIDES, V3, P565, DOI 10.1016/0196-9781(82)90127-9 Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 DeMeyer M. K., 1979, PARENTS CHILDREN AUT DILALLA DL, 1994, J AUTISM DEV DISORD, V24, P115, DOI 10.1007/BF02172092 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 Elia M, 2000, BRAIN DEV-JPN, V22, P88, DOI 10.1016/S0387-7604(99)00119-9 FREMEAU RT, 1947, J NEUROCHEM, V46, P198 Hering E, 1999, J AUTISM DEV DISORD, V29, P143, DOI 10.1023/A:1023092627223 HONOMICHL RD, IN PRESS J AUTISM DE Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Johnson CR, 1996, CHILD ADOL PSYCH CL, V5, P673 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 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Mullen E., 1997, MULLEN SCALES EARLY Owens JA, 2000, SLEEP, V23, P1043 OWLEY T, 1999, MEDSCAPE GEN MED Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 Roberts W, 2001, PEDIATRICS, V107, part. no., DOI 10.1542/peds.107.5.e71 ROGERS SJ, 1993, J AM ACAD CHILD PSY, V32, P1274, DOI 10.1097/00004583-199311000-00023 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Segawa Masaya, 1992, Brain Dysfunction, V5, P211 SIGMAN M, 1986, J CHILD PSYCHOL PSYC, V27, P647, DOI 10.1111/j.1469-7610.1986.tb00189.x *SW AUT RES CTR, 2001, OUR REACH 2000 ANN R Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 34 TC 15 Z9 15 PU KLUWER ACADEMIC-HUMAN SCIENCES PRESS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA SN 0009-398X J9 CHILD PSYCHIAT HUM D JI Child Psychiat. Hum. Dev. PD WIN PY 2002 VL 33 IS 2 BP 107 EP 123 DI 10.1023/A:1020778108068 PG 17 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 617UR UT WOS:000179379700002 PM 12462350 ER PT J AU Bolte, S Poustka, F AF Bolte, S Poustka, F TI The relation between general cognitive level and adaptive behavior domains in individuals with autism with and without co-morbid mental retardation SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE adaptive behaviour; mental retardation; intelligence; autism; PDD ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; CHILDREN; AGE; SCALE; IQ AB This study examined the association between adaptive behavior and general cognitive level in individuals with autism or PDD-NOS with and without comorbid mental retardation. Data from the screening version of the Vineland Adaptive Scales and the Wechsler Intelligence Scales were analysed in a sample of 67 subjects. While in the higher functioning individuals (IQ > 70, n = 34) IQ and adaptive behavior level differed significantly, performances were fairly comparable in subjects showing lower cognitive functioning (IQ < 70, n = 33). Regression models revealed a higher correlation between IQ and single adaptive behavior domains in the non-mentally retarded participants, with the domain Communication reaching the highest predictive power of the single adaptive behavior areas. Findings indicate, the relationship between adaptive and cognitive function in autistic disorders is mediated by the presence of a qualitative reduction of intelligence. Methodological limitations of the study are discussed. C1 Univ Frankfurt, D-6000 Frankfurt, Germany. RP Bolte, S (reprint author), Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. CR ANDO H, 1980, J AUTISM DEV DISORD, V10, P173, DOI 10.1007/BF02408468 Bolte S, 2000, Z KINDER JUG-PSYCH, V28, P151, DOI 10.1024//1422-4917.28.3.151 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 FOMBONNE E, 1993, J CHILD PSYCHOL PSYC, V34, P1051, DOI 10.1111/j.1469-7610.1993.tb01108.x Freeman BJ, 1999, J AUTISM DEV DISORD, V29, P379, DOI 10.1023/A:1023078827457 FREEMAN BJ, 1988, J AM ACAD CHILD PSY, V27, P428, DOI 10.1097/00004583-198807000-00008 KAMPHAUS RW, 1987, J SPEC EDUC, V21, P27 KLIN A, 1997, HDB AUTISM PERVASIVE, P418 Kraijer D, 2000, J AUTISM DEV DISORD, V30, P39, DOI 10.1023/A:1005460027636 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 PLATT LO, 1991, PSYCHOL REP, V68, P139 Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 RUHL D, 1995, UNPUB VINELAND BEURT SCHATZ J, 1995, J AUTISM DEV DISORD, V25, P51, DOI 10.1007/BF02178167 SPARROW SS, 1985, VINELAND ADAPTIVES B Tewes U., 1991, HAMBURG WECHSLER INT Tewes U., 1983, HAMBURG WECHSLER INT VanMeter L, 1997, J AUTISM DEV DISORD, V27, P557, DOI 10.1023/A:1025830110640 VOLKMAR FR, 1987, J AM ACAD CHILD ADOL, V26, P151 NR 23 TC 71 Z9 71 PU KLUWER ACADEMIC-HUMAN SCIENCES PRESS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA SN 0009-398X J9 CHILD PSYCHIAT HUM D JI Child Psychiat. Hum. Dev. PD WIN PY 2002 VL 33 IS 2 BP 165 EP 172 DI 10.1023/A:1020734325815 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 617UR UT WOS:000179379700005 PM 12462353 ER PT J AU Trevarthen, C AF Trevarthen, C TI Autism personality: Findings from the Tavistock Autism Workshop SO CONTEMPORARY PSYCHOLOGY-APA REVIEW OF BOOKS LA English DT Book Review ID INFANT C1 Tavistock Clin, London NW3 5BA, England. Univ Edinburgh, Dept Psychol, Edinburgh EH8 9JZ, Midlothian, Scotland. RP Trevarthen, C (reprint author), Tavistock Clin, London NW3 5BA, England. CR Aitken K. J., 1997, DEV PSYCHOPATHOL, V9, P651 ALVAREZ A, 1999, AUTISM PERSONALITY F Braten S., 1998, INTERSUBJECTIVE COMM, P105 CALASSO R, 1999, KA FRAIBERG SELMA, 1980, CLIN STUDIES INFANT Siegel D. J., 1999, DEV MIND NEUROBIOLOG Stern D. N., 2000, INTERPERSONAL WORLD Trevarthen C, 2001, INFANT MENT HEALTH J, V22, P95, DOI 10.1002/1097-0355(200101/04)22:1<95::AID-IMHJ4>3.0.CO;2-6 Trevarthen C, 2001, J CHILD PSYCHOL PSYC, V42, P3, DOI 10.1017/S0021963001006552 NR 9 TC 0 Z9 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD DEC PY 2002 VL 47 IS 6 BP 779 EP 782 PG 4 WC Psychology, Multidisciplinary SC Psychology GA 622XU UT WOS:000179673700052 ER PT J AU Newbury, DF Monaco, AP AF Newbury, DF Monaco, AP TI Molecular genetics of speech and language disorders SO CURRENT OPINION IN PEDIATRICS LA English DT Review ID INHERITED SPEECH; GENOMIC SCREEN; CHROMOSOME 7Q; AUTISM; IMPAIRMENT; LOCALIZATION; CHILDREN; LINKAGE; FAMILY; TWINS AB In 2001, scientists characterized the first gene to be implicated in the cause of a speech and language disorder (FOXP2). Although FOXP2 was discovered using a unique family in which a severe speech and language disorder segregates in a monogenic fashion, at the time this discovery was heralded as "a milestone in understanding this uniquely human characteristic." Approximately 1 year later, we discuss the impact of this gene discovery on the study of language and review the relevance of this gene to both specific language impairment and language aspects of the autistic phenotype. We also discuss recent molecular genetic advances made in the study of generalized specific language impairment. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. RP Monaco, AP (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. 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OPIN. PEDIATR. PD DEC PY 2002 VL 14 IS 6 BP 696 EP 701 DI 10.1097/00008480-200212000-00009 PG 6 WC Pediatrics SC Pediatrics GA 617PY UT WOS:000179371100009 PM 12436038 ER PT J AU Michelotti, J Charman, T Slonims, V Baird, G AF Michelotti, J Charman, T Slonims, V Baird, G TI Follow-up of children with language delay and features of autism from preschool years to middle childhood SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY ADULT LIFE; INFANTILE-AUTISM; COMMUNICATION CHECKLIST; SPECTRUM DISORDER; OUTCOMES; AGE AB Eighteen children (13 males, five females) who had severe developmental language delay/disorder and some features of autism (although insufficient in severity and combination to meet ICD-10 diagnostic criteria for childhood autism) at preschool age (Time 1; mean age 4 years 4 months) were followed up 4 years later (Time 2; mean age 8 years 7 months). At the initial assessment the diagnostic dilemma was how much the social communication impairments and behavioural problems were secondary to the language problem and how much they constituted a genuine case of a pervasive developmental disorder. It was anticipated that at follow-up some children would continue to show social impairments but that in others social impairments would have receded as language competence improved. Follow-up assessments included the Wechsler Intelligence Scale for Children, the Clinical Evaluation of Language Fundamentals, the Children's Communication Checklist, and the Social Communication Questionnaire. At follow-up, five children had continuing language disorder and were considered to fulfil diagnostic criteria for childhood autism, four children had continuing language disorder and met criteria for atypical autism, and nine met criteria for atypical autism but had somewhat recovered language skills. Thus, even in the subgroup of children whose language ability had improved the features of autism had not dissipated. Severity of social communication impairments and repetitive behaviours at Time 1, rated retrospectively from case notes, were associated with severity of autism symptoms and pragmatic competence at Time 2. The findings are discussed in relation to the unclear boundary between autism spectrum disorders and language delay/disorder. C1 UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. City & Hackney Community Serv NHS Trust, Donald Winnicott Ctr, London, England. Guys Hosp, Newcomen Ctr, London SE1 9RT, England. RP Charman, T (reprint author), UCL, Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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PD DEC PY 2002 VL 44 IS 12 BP 812 EP 819 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 619FH UT WOS:000179464800004 PM 12455857 ER PT J AU Okten, A Kalyoncu, M Yaris, N AF Okten, A Kalyoncu, M Yaris, N TI The ratio of second- and fourth-digit lengths and congenital adrenal hyperplasia due to 21-hydroxylase deficiency SO EARLY HUMAN DEVELOPMENT LA English DT Article DE second and fourth digits ratio; 21-hydroxylase deficiency; androgen excess ID CORONARY-ARTERY DISEASE; SEXUAL DIMORPHISM; 2ND; DIAGNOSIS; TESTOSTERONE; PERFORMANCE; ASSOCIATION; POPULATION; MANAGEMENT; ANDROGENS AB Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency results in excessive androgen exposure in the gestational period and various degrees of masculinization of the external genitalia in female foetuses. Intrauterine gonadal steroids are not only essential for the development of the genital organs but also affect some other extragenital organ development. The second to fourth digit (2D/4D) ratio shows a sexually dimorphic pattern with longer fourth digit from second digit in men compared to women. A low 2D/4D ratio is associated with high sperm count, testosterone levels and reproductive success in men. A high 2D/4D ratio is associated with high oestrogen levels in women. Second and fourth digit ratio has also found to be correlated with sexual orientation, left hand preference autism and some adult onset diseases such as breast cancer and myocardial infarction. We found lower 2D/4D ratio in female patients with 21-hydroxylase deficiency compared to healthy girls (p = 0.000) and equal 2D/4D ratio for female patients when compared to male controls. Male patients with 21-hydroxylase deficiency had significantly lower 2D/4D ratio than female and male controls in the right hand. Healthy boys had lower 2D/4D ratio than healthy girls. 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Dev. PD DEC PY 2002 VL 70 IS 1-2 BP 47 EP 54 DI 10.1016/S0378-3782(02)00073-7 PG 8 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA 623BX UT WOS:000179684300006 PM 12441204 ER PT J AU Ross, DE AF Ross, DE TI Replacing faulty conversational exchanges for children with autism by establishing a functionally equivalent alternative response SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article ID SCRIPT-FADING PROCEDURE; DEVELOPMENTAL-DISABILITIES; DESTRUCTIVE BEHAVIOR; SOCIAL SKILLS; SELF-INJURY; SPEECH; REINFORCEMENT; ADOLESCENTS AB This study used modified functional analysis procedures and functional communication training to assess and replace the faulty communication responses of three older children with autism during conversational exchanges. Participants exhibited frequent amounts of delayed echolalia and perseverative utterances when conversing with adults and peers. 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PD DEC PY 2002 VL 37 IS 4 BP 343 EP 362 PG 20 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 619MJ UT WOS:000179479500001 ER PT J AU Kanner, AM AF Kanner, AM TI Psychiatric comorbidity in patients with developmental disorders and epilepsy: a practical approach to its diagnosis and treatment SO EPILEPSY & BEHAVIOR LA English DT Article DE depression; anxiety; psychosis; aggression; intractable epilepsy; antidepressant drugs; antiepileptic drugs; autism; antipsychotic drugs ID MENTALLY-RETARDED PERSONS; POSTICTAL PSYCHOSIS; AGGRESSIVE-BEHAVIOR; SEIZURES; CHILDREN; SAFETY; ANTIDEPRESSANTS; PSYCHOPATHOLOGY; RETARDATION; LAMOTRIGINE AB Psychiatric comorbidity in patients with developmental disorders and epilepsy (PDDEs) is relatively frequent. The majority of its pharmacological treatment has consisted of the use of neuroleptic drugs in an attempt to control behavioral disturbances, despite the fact that these symptoms may often mask underlying psychiatric disorders such as anxiety and depression, which require other types of psychotropic drugs. In this article, we review the pathogenic mechanisms that mediate the clinical manifestations of psychiatric disorders in PDDEs, highlight diagnostic strategies that may help in elucidating the correct psychiatric diagnosis, and review the psychopharmacological treatments available. (C) 2002 Published by Elsevier Science (USA). C1 Rush Med Coll, Dept Neurol Sci, Chicago, IL 60612 USA. Rush Presbyterian St Lukes Med Ctr, Rush Epilepsy Ctr, Chicago, IL 60612 USA. RP Kanner, AM (reprint author), Rush Med Coll, Dept Neurol Sci, Chicago, IL 60612 USA. 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PD DEC PY 2002 VL 3 IS 6 SU S BP S7 EP S13 PN 2 PG 7 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 703XK UT WOS:000184307500003 ER PT J AU Charman, T AF Charman, T TI The prevalence of autism spectrum disorders - Recent evidence and future challenges SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Review DE autism spectrum disorders; Asperger syndrome; PDD; prevalence; epidemiology ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; ASPERGER DISORDER; RUBELLA VACCINE; FIELD TRIAL; DSM-IV; CHILDREN; POPULATION; EPIDEMIOLOGY; MEASLES AB Background: Until recently best estimate prevalence rates for autism spectrum disorders (ASD) were 0.5/1,000 for autism and 2.0/1,000 for the broader spectrum. Three recent studies have suggested a significantly higher prevalence rate for ASD of 6.0/1,000 (mean 95% CI = 4.8-8.0). Method Possible determinants of the apparent increase in the prevalence of ASD are outlined. Methodological aspects of the three recent studies are examined. Findings Increased recognition, the broadening of the diagnostic concept over time and methodological differences across studies may account for most or all of the apparent increase in prevalence, although this cannot be quantified. Conclusions Findings from ongoing studies should help confirm or disconfirm the putative rate of 6.0/1,000 for all ASD. The possibility that autism has been over-diagnosed in recent studies needs to be ruled out. Notwithstanding these outstanding questions, it appears likely that the current true prevalence of ASD is considerably greater than previously recognised. This has significant implications for our scientific understanding of ASD and for families and services. Future directions for epidemiological research are outlined. 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. RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 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 *CAL DEP DEV SERV, 1999, CHANG POP PERS AUT P Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 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 ELHERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Fombonne E, 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, 2002, MOL PSYCHIATR, V7, pS4, DOI 10.1038/sj.mp.4001162 Fombonne E, 2001, J AUTISM DEV DISORD, V31, P363 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Gillberg C., 2000, BIOL AUTISTIC SYNDRO GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Halsey N A, 2001, Pediatrics, V107, pE84, DOI 10.1542/peds.107.5.e84 Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Kanner L, 1943, NERV CHILD, V2, P217 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Kerr A, 2001, RETT DISORDER DEV BR Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 Lord C, 1998, MENT RETARD DEV D R, V4, P90, DOI 10.1002/(SICI)1098-2779(1998)4:2<90::AID-MRDD5>3.0.CO;2-0 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Medical Research Council, 2001, REV AUT RES EP CAUS Miller JN, 2000, J ABNORM PSYCHOL, V109, P227, DOI 10.1037/0021-843X.109.2.227 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Nylander L, 2001, ACTA PSYCHIAT SCAND, V103, P428, DOI 10.1034/j.1600-0447.2001.00175.x STRATTEN K, 2001, MEASLES MUMPS RUBELL 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 VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 World Health Organization, 1993, MENT DIS GLOSS GUID NR 48 TC 68 Z9 73 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD DEC PY 2002 VL 11 IS 6 BP 249 EP 256 DI 10.1007/s00787-002-0297-8 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 644VE UT WOS:000180939400001 PM 12541002 ER PT J AU Drew, A Baird, G Baron-Cohen, S Cox, A Slonims, V Wheelwright, S Swettenham, J Berry, B Charman, T AF Drew, A Baird, G Baron-Cohen, S Cox, A Slonims, V Wheelwright, S Swettenham, J Berry, B Charman, T TI A pilot randomised control trial of a parent training intervention for pre-school children with autism - Preliminary findings and methodological challenges SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; early intervention; parent training; language; randomised control trial (RCT) ID PERVASIVE DEVELOPMENTAL DISORDERS; LANGUAGE-IMPAIRED CHILDREN; JOINT ATTENTION; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; DIAGNOSIS; AGE AB Few attempts have been made to conduct randomised control trials (RCTs) of interventions for pre-school children with autism. We report findings of a pilot RCT for a parent training intervention with a focus on the development of joint attention skills and joint action routines. Twenty-four children meeting ICD-10 criteria for childhood autism (mean age = 23 months) were identified using the CHAT screen and randomised to the parent training group or to local services only. A follow-up was conducted 12 months later (mean age = 35 months). There was some evidence that the parent training group made more progress in language development than the local services group. However, the present pilot study was compromised by several factors: a reliance on parental report to measure language, non-matching of the groups on initial IQ, and a lack of systematic checking regarding the implementation of the parent training intervention. Furthermore, three parents in the local services group commenced intensive, home-based behavioural intervention during the course of the study. The difficulties encountered in the conduct of RCTs for pre-school children with autism are discussed. Methodological challenges and strategies for future well-designed RCTs for autism interventions are highlighted. C1 UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. Guys Hosp, Newcomen Ctr, London, England. Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge, England. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge, England. UCL, Dept Human Commun & Sci, London WC1N 1EH, England. RP Charman, T (reprint author), UCL, Inst Child Hlth, Behav & Brain Sci Unit, 30 Guildford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR Abidin R. 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Child Adolesc. Psych. PD DEC PY 2002 VL 11 IS 6 BP 266 EP 272 DI 10.1007/s00787-002-0299-6 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 644VE UT WOS:000180939400004 PM 12541005 ER PT J AU Kamps, D Royer, J Dugan, E Kravits, T Gonzalez-Lopez, A Garcia, J Carnazzo, K Morrison, L Kane, LG AF Kamps, D Royer, J Dugan, E Kravits, T Gonzalez-Lopez, A Garcia, J Carnazzo, K Morrison, L Kane, LG TI Peer training to facilitate social interaction for elementary students with autism and their peers SO EXCEPTIONAL CHILDREN LA English DT Article ID CHILDREN; SKILLS AB There is increasing evidence that peer-mediated interventions for students with autism are effective in increasing participation in natural settings. Still unknown are the contributions peers make to the generalization of social behaviors. Results from two investigations of this issue are reported In Study 1, social interaction with peers increased during interventions compared to controls, however students in cooperative learning control groups showed higher level of generalization than those in social groups. In Study 2, videotaped probes of 34 students indicated greater generalization of skills from groups with trained peers, and less from groups with untrained and stranger peers. Implications are discussed regarding the value of ongoing peer training and structured groups to establish relationships and generalization of skills over time. C1 Univ Kansas, Juniper Gardens Childrens Project, Kansas City, KS USA. Behav Milestones Inc, Kansas City, MO USA. Olathe Publ Sch, Olathe, KS USA. Melmark Sch, Berwyn, PA USA. Univ Kansas, Med Ctr, Qual Improvement Ctr Disabil, Kansas City, KS 66103 USA. Univ Louisville, Kentucky Autism Training Ctr, Louisville, KY 40292 USA. SW Missouri State Univ, Springfield, MO 65802 USA. RP Kamps, D (reprint author), Univ Kansas, Juniper Gardens Childrens Project, Kansas City, KS USA. CR American Psychiatric Association, DIAGN STAT MAN MENT *AUT SOC AM, 1999, ADV NEWSL AUT SOC AM, V32, P3 BACON P, 1991, STATES REGIONS BARLOW DH, 1984, SINGLE CASE EXPT DES DUGAN E, 1995, J APPL BEHAV ANAL, V28, P175, DOI 10.1901/jaba.1995.28-175 Gonzalez-Lopez A., 1997, FOCUS AUTISM OTHER D, V12, P2 GREENWOOD CR, 1997, TOGETHER CAN CLASS W HARING TG, 1987, J ASSOC PERS SEVERE, V12, P280 Harrell L. G., 1998, ED TREATMENT CHILDRE, V21, P107 HOPS H, 1997, SOCIAL SKILLS TUTORI JOHNSON D, 1986, LEARNING TOGETHER AL Kamps D., 1997, J BEHAV ED, V7, P335, DOI 10.1023/A:1022879607019 KAMPS D, 1995, BEHAV DISORDERS, V21, P88 KAMPS DM, 1994, J APPL BEHAV ANAL, V27, P49, DOI 10.1901/jaba.1994.27-49 KAMPS DM, 1992, J APPL BEHAV ANAL, V25, P281, DOI 10.1901/jaba.1992.25-281 Koegel L. K., 1996, POSITIVE BEHAV SUPPO Koegel L. 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S., 2001, FOCUS AUTISM OTHER D, V16, P120, DOI DOI 10.1177/108835760101600208 TAPP J, 1992, MULTIPLE OPTION OBSE TAYLOR BA, 1995, J APPL BEHAV ANAL, V28, P3, DOI 10.1901/jaba.1995.28-3 VERNON S, 1993, SCORE SKILLS SOCIAL WALKER H, 1988, SOCIAL SKILLS TUTORI Werts MG, 1996, J APPL BEHAV ANAL, V29, P53, DOI 10.1901/jaba.1996.29-53 NR 32 TC 27 Z9 27 PU COUNCIL EXCEPTIONAL CHILDREN PI RESTON PA 1920 ASSOCIATION DR, RESTON, VA 22091-1589 USA SN 0014-4029 J9 EXCEPT CHILDREN JI Except. Child. PD WIN PY 2002 VL 68 IS 2 BP 173 EP 187 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 531MD UT WOS:000174418400002 ER PT J AU [Anonymous] AF [Anonymous] TI Large-scale study finds no link between autism and MMR vaccine SO FORMULARY LA English DT Editorial Material NR 0 TC 0 Z9 0 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 USA SN 1082-801X J9 FORMULARY JI Formulary PD DEC PY 2002 VL 37 IS 12 BP 616 EP 616 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 626QJ UT WOS:000179884100006 ER PT J AU Thjodleifsson, B Davidsdottir, K Agnarsson, U Sigthorsson, G Kjeld, M Bjarnason, I AF Thjodleifsson, B Davidsdottir, K Agnarsson, U Sigthorsson, G Kjeld, M Bjarnason, I TI Effect of Pentavac and measles-mumps-rubella (MMR) vaccination on the intestine SO GUT LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; FECAL CALPROTECTIN; CROHNS-DISEASE; VIRUS INFECTION; CHILDREN; CHILDHOOD; PERMEABILITY; EXCRETION; DISORDERS; PROTEIN AB Background: The safety of infant vaccination has been questioned in recent years. In particular it has been suggested that the measles, mumps, and rubella (MMR) vaccination leads to brain damage manifesting as autism consequent to the development of an "enterocolitis" in the immediate post-vocci nation period. Aim: To assess if MMR vaccination is associated with subclinical intestinal inflammation, which is central to the autistic "enterocolitis" theory. Methods: We studied 109/58 infants, before and two and four weeks after immunisation with Pentavac and MMR vaccines, for the presence of intestinal inflammation (faecal calprotectin). Results: Neither vaccination was associated with any significant increase in faecal calprotectin concentrations. Conclusions: The failure of the MMR vaccination to cause an intestinal inflammatory response provides evidence against the proposed gut-brain interaction that is central to the autistic "enterocolitis" hypothesis. C1 Guys Kings St Thomas Med Sch, Dept Med, London SE5 9PJ, England. RP Bjarnason, I (reprint author), Guys Kings St Thomas Med Sch, Dept Med, Denmark Hill Campus,Bessemer Rd, London SE5 9PJ, England. CR Anthony A, 2000, GUT, V46, pA3 ASSAAD F, 1983, REV INFECT DIS, V5, P452 Ball LK, 2001, PEDIATRICS, V107, P1147, DOI 10.1542/peds.107.5.1147 BJARNASON I, 1995, GASTROENTEROLOGY, V108, P1566, DOI 10.1016/0016-5085(95)90708-4 Bunn SK, 2001, J PEDIATR GASTR NUTR, V32, P171, DOI 10.1097/00005176-200102000-00015 Bunn SK, 2001, J PEDIATR GASTR NUTR, V33, P14, DOI 10.1097/00005176-200107000-00003 DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x DOHAN FC, 1970, LANCET, V1, P897 FRIEDMAN DI, 1991, PHARMACEUT RES, V8, P93, DOI 10.1023/A:1015842609565 Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 GERSHON A, 1998, HARRISONS PRINCIPLES, P1123 Ghosh S, 2001, GUT, V48, P748, DOI 10.1136/gut.48.6.748 Halsey N A, 2001, Pediatrics, V107, pE84, DOI 10.1542/peds.107.5.e84 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Johne B, 2001, SCAND J GASTROENTERO, V36, P291, DOI 10.1080/003655201750074618 Montgomery SM, 1999, GASTROENTEROLOGY, V116, P796, DOI 10.1016/S0016-5085(99)70062-4 Reichelt WH, 1998, J PEDIATR GASTR NUTR, V26, P305, DOI 10.1097/00005176-199803000-00012 ROSETH AG, 1992, SCAND J GASTROENTERO, V27, P793, DOI 10.3109/00365529209011186 Roseth AG, 1999, SCAND J GASTROENTERO, V34, P50 Rugtveit J, 2002, J PEDIATR GASTR NUTR, V34, P323, DOI 10.1097/00005176-200203000-00022 SUMMERS BA, 1994, NEUROPATH APPL NEURO, V20, P525, DOI 10.1111/j.1365-2990.1994.tb01006.x Sun Z., 1999, AUTISM, V3, P85, DOI 10.1177/1362361399003001007 Tibble J, 2000, GUT, V47, P506, DOI 10.1136/gut.47.4.506 Tibble JA, 2000, GASTROENTEROLOGY, V119, P15, DOI 10.1053/gast.2000.8523 Ton H, 2000, CLIN CHIM ACTA, V292, P41, DOI 10.1016/S0009-8981(99)00206-5 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2002, ALIMENT PHARM THER, V16, P663, DOI 10.1046/j.1365-2036.2002.01206.x WAKEFIELD AJ, 1995, GASTROENTEROLOGY, V108, P911, DOI 10.1016/0016-5085(95)90467-0 WAKEFIELD AJ, 1993, J MED VIROL, V39, P345, DOI 10.1002/jmv.1890390415 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 WOOD NC, 1987, BRIT J PSYCHIAT, V150, P853, DOI 10.1192/bjp.150.6.853 NR 31 TC 4 Z9 4 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0017-5749 J9 GUT JI Gut PD DEC PY 2002 VL 51 IS 6 BP 816 EP 817 DI 10.1136/gut.51.6.816 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 617XH UT WOS:000179385900016 PM 12427783 ER PT J AU Boddaert, N Chabane, N Barthelemy, C Bourgeois, M Poline, JB Brunelle, F Samson, Y Zilbovicius, M AF Boddaert, N Chabane, N Barthelemy, C Bourgeois, M Poline, JB Brunelle, F Samson, Y Zilbovicius, M TI Temporal lobe dysfonction in childhood autism: a PET study SO JOURNAL DE RADIOLOGIE LA French DT Article DE positron emission tomography (TEP); functional imaging; cerebral blood flow (CBF); autism; temporal cortex ID CEREBRAL BLOOD-FLOW; HERPES-SIMPLEX ENCEPHALITIS; GLUCOSE-UTILIZATION; SCAN FINDINGS; BRAIN; TOMOGRAPHY; METABOLISM; CHILDREN; CORTEX; SPECT AB Purpose: Childhood autism is a severe developmental disorder that impairs the acquisition of some of the most important skills in human life. Progress in understanding the neural basis of childhood autism requires clear and reliable data indicating specific neuroanatomical or neurophysiological abnormalities. The purpose-of the present study was to research localized brain dysfunction in autistic children using functional brain imaging. Patients and methods: Regional cerebral blood flow (rCBF) was measured with positron emission tomography (PET) in 21 primary autistic children and 10 age-matched non autistic children. Results: A statistical parametric analysis of rCBF images revealed significant bilateral temporal hypoperfusion in the associative auditory cortex (superior temporal gyrus) and in the multimodal cortex (superior temporal sulcus) in the autistic group (p<0.001). In addition, temporal hypoperfusion was detected individually in 77% of autistic children. Conclusion: These findings provide robust evidence of well localized functional abnormalities in autistic children located in the superior temporal lobe. Such localized abnormalities were not detected with the low resolution PET camera (14-22). This study suggests that high resolution PET camera combined with statistical parametric mapping is useful to understand developmental disorders. C1 Hop Necker Enfants Malad, Serv Radiol Pediat, F-75015 Paris, France. CEA, DRM, DSV, ER M INSERM 0205, F-91406 Orsay, France. Hop Robert Debre, Serv Pedopsychiat, F-75019 Paris, France. CHU Bretonneau, INSERM, U316, F-37044 Tours, France. Dept Pediat, Paris, France. Hop La Pitie Salpetriere, Serv Urgences Cerebraux Vasc, Paris, France. RP Boddaert, N (reprint author), Hop Necker Enfants Malad, Serv Radiol Pediat, 149 Rue Sevres, F-75015 Paris, France. CR Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 *APA, 1994, APA DIAGN STAT MAN M, P70 BACHEVALIER J, 1994, CONTRIBUTION MEDIAL, P146 BACHEVALIER J, 1994, NEUROPSYCHOLOGIA, V32, P627, DOI 10.1016/0028-3932(94)90025-6 Boddaert N., 2001, NEUROIMAGE, V13, pS0128 BODDAERT N, 2000, TEMPORAL LOBE DYSFUN, V26, P2007 DEVOLDER A, 1987, BRAIN DEV-JPN, V9, P581 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 Bruneau N, 1999, CLIN NEUROPHYSIOL, V110, P1927, DOI 10.1016/S1388-2457(99)00149-2 CAMPBELL M, 1982, AM J PSYCHIAT, V139, P510 CHIRON C, 1995, DEV MED CHILD NEUROL, V37, P849 Chugani HT, 1996, ANN NEUROL, V39, P643, DOI 10.1002/ana.410390514 COURCHESNE E, 1988, NEW ENGL J MED, V318, P1349, DOI 10.1056/NEJM198805263182102 COURCHESNE E, 1994, NEUROLOGY, V44, P214 COYLE JT, 1986, BRAIN RES BULL, V16, P773, DOI 10.1016/0361-9230(86)90074-2 DAMASIO H, 1980, ARCH NEUROL-CHICAGO, V37, P504 Friston KJ, 1995, HUMAN BRAIN MAPPING, V2, P89 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P107, DOI 10.1007/BF01046406 GILLBERG C, 1983, J AUTISM DEV DISORD, V13, P19, DOI 10.1007/BF01531356 GILLBERG C, 1986, J AUTISM DEV DISORD, V16, P369, DOI 10.1007/BF01531665 GILLBERG C, 1992, BIOL AUTISTIC SYNDRO, P63 Gillberg IC, 1993, EUROPEAN CHILD ADOLE, V2, P50 GLOOR P, 1997, TEMPORAL LOBE LIMBIC, P3 Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 HEROLD S, 1988, PSYCHOL MED, V18, P823 HORWITZ B, 1988, ARCH NEUROL-CHICAGO, V45, P749 Kanner L, 1943, NERV CHILD, V2, P217 MOUNTZ JM, 1995, J NUCL MED, V36, P1156 MURAKAMI JW, 1992, AM J ROENTGENOL, V159, P177 Ohnishi T, 2000, BRAIN, V123, P1838, DOI 10.1093/brain/123.9.1838 Pandya D.N., 1985, CEREB CORTEX, V4, P3 PIVEN J, 1990, AM J PSYCHIAT, V147, P734 PIVEN J, 1992, BIOL PSYCHIAT, V31, P491, DOI 10.1016/0006-3223(92)90260-7 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 RUMSEY JM, 1985, ARCH GEN PSYCHIAT, V42, P448 SELTZER B, 1978, BRAIN RES, V149, P1, DOI 10.1016/0006-8993(78)90584-X SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 Zilbovicius M, 2000, AM J PSYCHIAT, V157, P1988, DOI 10.1176/appi.ajp.157.12.1988 ZILBOVICIUS M, 1992, AM J PSYCHIAT, V149, P924 NR 41 TC 6 Z9 8 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0221-0363 J9 J RADIOL JI J. Radiol. PD DEC PY 2002 VL 83 IS 12 BP 1829 EP 1833 PN 1 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 633TY UT WOS:000180299600005 PM 12511838 ER PT J AU Lee, R McComas, JJ Jawor, J AF Lee, R McComas, JJ Jawor, J TI The effects of differential and lag reinforcement schedules on varied verbal responding by individuals with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE behavioral variability; lag reinforcement schedules; verbal responding ID BEHAVIORAL VARIABILITY; OPERANT AB Variability has been shown to be a reinforceable dimension of behavior. One procedure that has been demonstrated to increase variability in basic research is the lag reinforcement schedule. On this type of schedule, a response is reinforced if it differs from a specified number of previous responses. Lag schedules are rarely used, however, for increasing response variability in applied settings. The purpose of the present study was to investigate the effects of a lag schedule of differential reinforcement on varied and appropriate verbal responding to social questions by 3 males with autism. A reversal design with a multiple baseline across subjects was used to evaluate the effects of the lag schedule. During baseline, differential reinforcement of appropriate responding (DRA) resulted in little or no varied responding. During the intervention, a Lag 1 requirement was added to the DRA (Lag 1/DRA) resulting in an increase in the percentage of trials with varied and appropriate verbal responding for 2 of the 3 participants. In addition, an increase in the cumulative number of novel verbal responses was also observed for the same 2 participants. These results are discussed in terms of reinforcement schedules that support variability, generalization, and potential stimulus control over varied responding. C1 CUNY Queens Coll, New York, NY USA. CUNY Grad Sch & Univ Ctr, New York, NY 10036 USA. RP Lee, R (reprint author), 67-72 152 St,296A, Flushing, NY 11367 USA. CR Denney J, 1998, ANIM LEARN BEHAV, V26, P154, DOI 10.3758/BF03199208 DUKER PC, 1991, J APPL BEHAV ANAL, V24, P379, DOI 10.1901/jaba.1991.24-379 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 GOETZ EM, 1973, J APPL BEHAV ANAL, V6, P209, DOI 10.1901/jaba.1973.6-209 LALLI JS, 1994, J APPL BEHAV ANAL, V27, P735, DOI 10.1901/jaba.1994.27-735 MACHADO A, 1989, J EXP ANAL BEHAV, V52, P155, DOI 10.1901/jeab.1989.52-155 Miller N, 2000, J APPL BEHAV ANAL, V33, P151, DOI 10.1901/jaba.2000.33-151 MORGAN L, 1990, ANIM LEARN BEHAV, V18, P257, DOI 10.3758/BF03205284 NEURINGER A, 1991, J EXP PSYCHOL ANIM B, V17, P3, DOI 10.1037/0097-7403.17.1.3 NEURINGER A, 1993, ANIM LEARN BEHAV, V21, P83, DOI 10.3758/BF03213386 PAGE S, 1985, J EXP PSYCHOL ANIM B, V11, P429, DOI 10.1037//0097-7403.11.3.429 PRYOR KW, 1969, J EXP ANAL BEHAV, V12, P653, DOI 10.1901/jeab.1969.12-653 SCHOENFE.WN, 1966, PSYCHOL REP, V19, P551 SCHWARTZ B, 1982, J EXP PSYCHOL GEN, V111, P23, DOI 10.1037//0096-3445.111.1.23 Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 Williams G, 2000, J APPL BEHAV ANAL, V33, P627, DOI 10.1901/jaba.2000.33-627 NR 16 TC 30 Z9 30 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2002 VL 35 IS 4 BP 391 EP 402 DI 10.1901/jaba.2002.35-391 PG 12 WC Psychology, Clinical SC Psychology GA 636TQ UT WOS:000180473400005 PM 12555910 ER PT J AU Koczat, DL Rogers, SJ Pennington, BF Ross, RG AF Koczat, DL Rogers, SJ Pennington, BF Ross, RG TI Eye movement abnormality suggestive of a spatial working memory deficit is present in parents of autistic probands SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE endophenotype; saccade; autism ID PERVASIVE DEVELOPMENTAL DISORDERS; SMOOTH-PURSUIT; EXECUTIVE FUNCTION; TRACKING; INDIVIDUALS; AGE; CHILDREN; ADULTS; TASK; SCHIZOPHRENIA AB Autistic probands exhibit impaired spatial accuracy and impaired response suppression errors during a delayed oculomotor response task. Family members of autistic probands, and thus the possible familial nature of these deficits, have not been assessed. Eleven parents of autistic probands and 17 adults from unaffected families, ages 25-50 years, completed oculomotor delayed-response tasks. Parents of autistic probands demonstrated poorer spatial accuracy than the comparison group (p = .002), with no significant differences between groups on percentage of premature saccades or latency of remembered saccades. Spatial working memory deficits, as measured by the delayed oculomotor response task, appear to be familial in families with an autistic proband. These deficits deserve further evaluation as a potential endophenotypic marker for genetic risk for autism. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Univ Denver, Dept Psychol, Denver, CO 80208 USA. Denver Vet Adm Med Ctr, Dept Psychiat, Denver, CO USA. RP Ross, RG (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Box C268-31,4200 E 9th Ave, Denver, CO 80262 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 1995, PSYCHOL MED, V25, P63 Bailey DB, 1998, J AUTISM DEV DISORD, V28, P499 Becker W, 1989, NEUROBIOLOGY SACCADI, P13 Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 FREEDMAN R, 1999, PSYCHOPHARMACOLOGY 4 FUNAHASHI S, 1993, J NEUROSCI, V13, P1479 Hughes C, 1997, PSYCHOL MED, V27, P209, DOI 10.1017/S0033291796004308 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 HUTTON JT, 1993, ELECTROENCEPHALOGR C, V56, P414 Kanayama R, 1994, Acta Otolaryngol Suppl, V511, P131 Kikuchi-Yorioka Y, 2000, NAT NEUROSCI, V3, P1075 KUECHENMEISTER CA, 1977, ARCH GEN PSYCHIAT, V34, P578 LALOUEL JM, 1985, AM J HUM GENET, V37, P700 LANDA R, 1992, PSYCHOL MED, V22, P245 LARSBY B, 1988, ACTA OTO-LARYNGOL, V105, P21, DOI 10.3109/00016488809119441 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 Minshew NJ, 1999, NEUROLOGY, V52, P917 Olincy A, 1997, NEUROBIOL AGING, V18, P483, DOI 10.1016/S0197-4580(97)00109-7 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x OZONOFF S, 1993, J AUTISM DEV DISORD, V23, P429, DOI 10.1007/BF01046049 PARK S, 1995, ARCH GEN PSYCHIAT, V52, P821 PIVEN J, 1991, J AM ACAD CHILD PSY, V30, P471, DOI 10.1097/00004583-199105000-00019 RADANT AD, 1992, SCHIZOPHR RES, V6, P225, DOI 10.1016/0920-9964(92)90005-P Rineer S, 1998, AM J MED GENET, V81, P428, DOI 10.1002/(SICI)1096-8628(19980907)81:5<428::AID-AJMG12>3.0.CO;2-E Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 Roberts RJ, 1996, DEV NEUROPSYCHOL, V12, P105 Ross RG, 1996, J AM ACAD CHILD PSY, V35, P941, DOI 10.1097/00004583-199607000-00022 Ross RG, 1999, BIOL PSYCHIAT, V46, P383, DOI 10.1016/S0006-3223(98)00369-2 Ross RG, 2000, PSYCHIAT RES, V95, P35, DOI 10.1016/S0165-1781(00)00153-0 RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 SHARPE JA, 1978, INVEST OPHTH VIS SCI, V17, P465 SPOONER JW, 1980, ARCH NEUROL-CHICAGO, V37, P575 NR 36 TC 23 Z9 23 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 513 EP 518 DI 10.1023/A:1021246712459 PG 6 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100002 PM 12553588 ER PT J AU Moes, DR Frea, WD AF Moes, DR Frea, WD TI Contextualized behavioral support in early intervention for children with autism and their families SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE behavioral assessment; ecocultural assessment; early intervention; functional communication ID FUNCTIONAL ASSESSMENT; DEVELOPMENTAL DELAYS; SOCIAL SUPPORT; YOUNG-CHILDREN; SETTINGS; ECOLOGY; LIFE; DISABILITIES; MAINTENANCE; ADAPTATION AB Parent education programs have become an effective mode of treatment delivery for teaching families effective behavioral strategies to manage challenging behavior in young children with autism. Functional assessment and functional communication training (FCT) are empirically validated procedures that have recently been introduced into parent education programming to help resolve challenging behaviors. The success of these procedures, however, is contingent on family members' ability to integrate them into the specific contexts in which challenging behaviors occur. Consequently, the application of these procedures in home settings necessitates consideration of the family context in the assessment and treatment planning process. A study is presented that investigated the use of information on family context (i.e., caregiving demands, family support, patterns of social interaction) to direct the assessment and intervention planning process. More specifically, information on family context was used to individualize behavioral support plans designed to support family use of functional communication training within important family routines. Through parent-investigator collaboration we individualized the manner in which functional communication training procedures were taught and implemented so they were contextually relevant. Utilizing a multiple baseline design, the challenging behaviors and functional communication of three children with autism were monitored across baseline, intervention (i.e., FCT, and contextulized FCT), and follow-up phases. Multiple routines for each participant were selected and monitored across all phases to evaluate changes in the dependent measures within training and generalization routines. A self-report questionnaire was administered intermittently to parents to determine if consideration of family context improved the "goodness of fit" of the functional communication training treatment packages across FCT and contextualized FCT intervention phases. Results from the study indicate that consideration of family context in the assessment and intervention planning process does not jeopardize and may contribute to the stability and durability of reductions in challenging behavior achieved with functional assessment and functional communication training procedures. C1 Calif State Univ Los Angeles, Div Special Educ, Los Angeles, CA 90032 USA. Univ Calif Los Angeles, Los Angeles, CA USA. RP Frea, WD (reprint author), Calif State Univ Los Angeles, Div Special Educ, Los Angeles 5151 State Univ Dr, Los Angeles, CA 90032 USA. RI Sandall, Jane/D-4146-2009 OI Sandall, Jane/0000-0003-2000-743X CR Albanese A. L., 1995, TEACHING CHILDREN AU, P95 Albin R. W., 1996, POSITIVE BEHAV SUPPO, P81 BAILEY DB, 1987, TOP EARLY CHILD SPEC, V7, P59 BAILEY DN, 1986, J ANAL TOXICOL, V10, P156 Bellack A. 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E., 1990, FUNCTIONAL ANAL PROB ODONNELL CR, 1993, AM J COMMUN PSYCHOL, V21, P501, DOI 10.1007/BF00942157 Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 PATTERSON JM, 1983, FAM RELAT, V32, P255, DOI 10.2307/584685 Peck C. A., 1993, Integrating young children with disabilities in community programs: Ecological perspectives on research and implementation, P3 Reichle J., 1993, COMMUNICATIVE ALTERN REPP AC, 1988, J APPL BEHAV ANAL, V21, P281, DOI 10.1901/jaba.1988.21-281 REPP AC, 1989, J SPECIAL ED TECHNOL, V9, P207 ROBBINS FR, 1991, J EARLY INTERVENTION, V15, P173 RODRIGUE JR, 1990, J CLIN CHILD PSYCHOL, V19, P371, DOI 10.1207/s15374424jccp1904_9 SALZINGER S, 1980, ECOSYSTEM SICK CHILD, P1 Schopler E., 1997, HDB AUTISM PERVASIVE, P767 SCHREIBMAN L, 1989, INNOVATIONS CHILD BE, P395 Schreibman L., 1984, EFFECTS AUTISM FAMIL, P187 Simeonsson R. J., 1986, INFANT MENT HEALTH J, V7, P81, DOI 10.1002/1097-0355(198621)7:1<81::AID-IMHJ2280070109>3.0.CO;2-3 SINGER GHS, 1989, SUPPORT CAREGIVING F, P85 TRACY EM, 1987, CHILD YOUTH SERV REV, V9, P249, DOI 10.1016/0190-7409(87)90020-X TRIVETTE C, 1986, DIAGNOSTIQUE, V11, P246 Turnbull A.P., 1993, COGNITIVE COPING FAM Turnbull AP, 1986, FAMILIES HANDICAPPED, P45 Vaughn BJ, 1997, J APPL BEHAV ANAL, V30, P713, DOI 10.1901/jaba.1997.30-713 Wehman T., 1998, FOCUS AUTISM OTHER D, V13, P80 Weisner T. S., 1997, ECOCULTURAL FAMILY I WILLEMS EP, 1974, J APPL BEHAV ANAL, V7, P151, DOI 10.1901/jaba.1974.7-151 NR 82 TC 53 Z9 54 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 519 EP 533 DI 10.1023/A:1021298729297 PG 15 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100003 PM 12553589 ER PT J AU Scattone, D Wilczynski, SM Edwards, RP Rabian, B AF Scattone, D Wilczynski, SM Edwards, RP Rabian, B TI Decreasing disruptive behaviors of children with autism using social stories SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; social stories; disruptive behavior ID ACCEPTABILITY; INTERVENTIONS; INFORMATION AB Few studies have been conducted in the area of social stories, and the limitations of these studies (i.e., improper story construction and methodological confounds) raise questions about effectiveness of social story interventions. This study examined the effectiveness of properly constructed social stories that have been introduced into the natural environment to target the disruptive behavior of three children with autism. A multiple baseline design across participants was employed, and a decrease in disruptive behavior was evidenced when the intervention was implemented for all participants. Based on the results of the present research, future areas of investigation outlining the limitations and potential benefits of social stories were discussed. C1 Univ Mississippi, Med Ctr, Dept Pediat, Div Child Dev & Behav Med, Jackson, MS 39216 USA. Univ Nebraska, Med Ctr, Lincoln, NE 68583 USA. Univ So Mississippi, Hattiesburg, MS 39406 USA. Penn State Univ, University Pk, PA 16802 USA. RP Scattone, D (reprint author), Univ Mississippi, Med Ctr, Dept Pediat, Div Child Dev & Behav Med, 2500 N State St, Jackson, MS 39216 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CUPERTINO CA, 1994, HYP COMP SOFTW GRAY C, 1998, MORNING NEWS, V10, P2 Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 HARRIS MJ, 1992, J PERS SOC PSYCHOL, V63, P41, DOI 10.1037//0022-3514.63.1.41 Hayes S. C., 1999, SCI PRACTITIONER RES Kaufman A. S., 1983, K ABC KAUFMAN ASSESS Kazdin A. E., 1982, SINGLE CASE RES DESI Kuttler S., 1998, FOCUS AUTISM OTHER D, V13, P176, DOI DOI 10.1177/108835769801300306 MARTENS BK, 1985, PROF PSYCHOL-RES PR, V16, P191, DOI 10.1037/0735-7028.16.2.191 Myles B. S., 1999, FOCUS AUTISM OTHER D, V14, P82, DOI 10.1177/108835769901400203 Norris C, 1999, FOCUS AUTISM OTHER D, V14, P180, DOI DOI 10.1177/108835769901400307 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Thorndike R. L., 1986, STANFORDBINET INTELL VONBROCK MB, 1987, J SCHOOL PSYCHOL, V25, P131, DOI 10.1016/0022-4405(87)90022-7 Williams K. T., 1997, EXPRESSIVE VOCABULAR NR 16 TC 60 Z9 60 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 535 EP 543 DI 10.1023/A:1021250813367 PG 9 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100004 PM 12553590 ER PT J AU Molloy, CA Manning-Courtney, P Swayne, S Bean, J Brown, JM Murray, DS Kinsman, AM Brasington, M Ulrich, CD AF Molloy, CA Manning-Courtney, P Swayne, S Bean, J Brown, JM Murray, DS Kinsman, AM Brasington, M Ulrich, CD TI Lack of benefit of intravenous synthetic human secretin in the treatment of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; human synthetic secretin; clinical trial ID CONTROLLED TRIAL; CHILDREN; DISORDER AB The objective of this study was to determine if an intravenous infusion of synthetic human secretin improves language and behavioral symptoms in children with autism. Forty-two children with the diagnosis of autism were randomized to one of two groups in this double-blind cross-over trial. One group received 2 IU/kg of intravenous synthetic human secretin at the first visit, followed by an equal volume of intravenous saline placebo at week 6. The other group received treatments in the reverse order. All children were evaluated at weeks 1, 3, 6, 9, and 12 with standardized assessments of language, behavior, and autism symptomatology. There were no significant differences in the mean scores on any measure of language, behavior, or autism symptom severity after treatment with secretin compared to treatment with placebo. The results of this study do not support secretin as a treatment for autism. C1 Univ Cincinnati, Coll Med, Dept Pediat, Div Dev Disabil, Cincinnati, OH 45221 USA. Univ Cincinnati, Coll Med, Dept Pediat, Ctr Biostat & Epidemiol, Cincinnati, OH 45221 USA. Univ Cincinnati, Coll Med, Dept Internal Med, Cincinnati, OH 45221 USA. Univ Cincinnati, Coll Allied Hlth Sci, Dept Commun Sci & Disorders, Cincinnati, OH 45221 USA. Childrens Hosp, Med Ctr, Kelly OLeary Ctr Pervas Dev Disorders, Cincinnati, OH 45229 USA. RP Molloy, CA (reprint author), Childrens Hosp, Med Ctr, Kelly OLeary Ctr Pervas Dev Disorders, Locat E2-58,3333 Burnet Ave, Cincinnati, OH 45229 USA. CR AMAN M, 1994, ABBERRANT BEHAV CHEC American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bristol-Power MM, 1999, J AUTISM DEV DISORD, V29, P435, DOI 10.1023/A:1021991718423 Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 Coniglio SJ, 2001, J PEDIATR-US, V138, P649, DOI 10.1067/mpd.2001.112474 Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 FREMEAU RT, 1986, J NEUROCHEM, V46, P1947 Gilliam J. E., 1995, GILLIAM AUTISM RATIN Hammill DD, 1993, DEV TEST VISUAL PERC Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 KRUG DA, 1980, AUTISM BEHAV CHECKLI Mullen E, 1995, MULLEN SCALES EARLY OWLEY T, 1999, MEDSCAPE GEN MED J 1 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Schopler E., 1988, CHILDHOOD AUTISM RAT SHIPLEY KG, 1992, ASSESSMENT SPEECH LA Somogyi L, 2000, PANCREAS, V21, P262, DOI 10.1097/00006676-200010000-00007 SOMOGYI L, 1999, PANCREAS, V19, P439 STUTSMAN R, 1981, MERRILLPALMER SCALE Ulrich CD, 1998, GASTROENTEROLOGY, V114, P382, DOI 10.1016/S0016-5085(98)70491-3 NR 23 TC 19 Z9 19 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 545 EP 551 DI 10.1023/A:1021202930206 PG 7 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100005 PM 12553591 ER PT J AU Honomichl, RD Goodlin-Jones, BL Burnham, M Gaylor, E Anders, TF AF Honomichl, RD Goodlin-Jones, BL Burnham, M Gaylor, E Anders, TF TI Sleep patterns of children with pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE sleep; autism; neurodevelopmental disorder; night waking; behavior ID AUTISTIC-CHILDREN; MENTAL HANDICAP; YOUNG-CHILDREN; BEHAVIOR AB Data on sleep behavior were gathered on 100 children with pervasive developmental disorders (PDD), ages 2-11 years, using sleep diaries, the Children's Sleep Habits Questionnaire (CSHQ), and the Parenting Events Questionnaire. Two time periods were sampled to assess short-term stability of sleep-wake patterns. Before data collection, slightly more than half of the parents, when queried, reported a sleep problem in their child. Subsequent diary and CSHQ reports confirmed more fragmented sleep in those children who were described by their parents as having a sleep problem compared to those without a designated problem. Interestingly, regardless of parental perception of problematic sleep, all children with PDD exhibited longer sleep onset times and greater fragmentation of sleep than that reported for age-matched community norms. The results demonstrate that sleep problems identified by the parent, as well as fragmentation of sleep patterns obtained from sleep diary and CSHQ data, exist in a significant proportion of children with PDD. C1 Univ Calif Davis, Sch Med, Deans Off, TFA,Dept Psychiat, Davis, CA 95616 USA. Univ Calif Davis, Dept Human & Comm Dev, Davis, CA 95616 USA. RP Anders, TF (reprint author), Univ Calif Davis, Sch Med, Deans Off, TFA,Dept Psychiat, Davis, CA 95616 USA. 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E., 1993, PRESCHOOL ISSUES AUT, P129 VELABUENO A, 1984, ARCH NEUROL-CHICAGO, V41, P294 WOLKE D, 1995, J CHILD PSYCHOL PSYC, V36, P203, DOI 10.1111/j.1469-7610.1995.tb01821.x NR 30 TC 75 Z9 75 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 553 EP 561 DI 10.1023/A:1021254914276 PG 9 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100006 PM 12553592 ER PT J AU Boser, K Higgins, S Fetherston, A Preissler, MA Gordon, B AF Boser, K Higgins, S Fetherston, A Preissler, MA Gordon, B TI Semantic fields in low-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE low-functioning autism; single word learning; semantic knowledge; assessment; categorization; overselectivity ID NORMAL-CHILDREN; STIMULUS; OVERSELECTIVITY; CATEGORIZATION; DISCRIMINATION; SAMPLE; WORD; SIMILARITY; PARADIGM; LANGUAGE AB Restricted semantic fields and resultant stimulus overselectivity are often thought to be typical of low-functioning autism, as is a strong visual processing preference. However, these conclusions may in part be an artifact of testing methodology. A 12-year-old, low-functioning and nonverbal autistic boy was tested on an auditory word-to-picture selection task. The picture foils were chosen to have visual features, semantic features, both, or neither in common with the correct answer. Errors were made more often to semantically than to visually related items, and he showed generalization to items that had not been explicitly trained. This is taken as evidence that his semantic fields are broader than otherwise apparent, and that he was capable of expanding his semantic representations independently of specific training. C1 Johns Hopkins Sch Med, Dept Neurol, Div Cognit Neurol, Baltimore, MD 21287 USA. NYU, Dept Psychol, New York, NY 10003 USA. Johns Hopkins Sch Med, Dept Cognit Sci, Baltimore, MD 21287 USA. RP Boser, K (reprint author), Johns Hopkins Sch Med, Dept Neurol, Div Cognit Neurol, 600 N Wolfe St,Meyer 222, Baltimore, MD 21287 USA. 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PD DEC PY 2002 VL 32 IS 6 BP 563 EP 582 DI 10.1023/A:1021207031114 PG 20 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100007 PM 12553593 ER PT J AU Hillier, A Allinson, L AF Hillier, A Allinson, L TI Understanding embarrassment among those with autism: Breaking down the complex emotion of embarrassment among those with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; embarrassment; empathy; theory of mind ID CHILDREN; OTHERS; ATTRIBUTIONS; EMPATHY; MIND AB Scenarios manipulating various factors within the emotion of embarrassment, such as whether or not an audience was present when an embarrassing act was committed, the type of audience present, empathic embarrassment, etc., were presented to high-functioning participants with autism and comparison groups of those with learning difficulties and typically developing participants matched for verbal and nonverbal mental age. Participants were required to rate the level of embarrassment of the protagonist and justify their responses. It was predicted that those with autism would differ significantly from the comparison groups in their ratings and also their ability to provide justifications. The results showed those with autism to have difficulty with such concepts as empathic embarrassment but showed a surprisingly good understanding of other variables manipulated such as the presence of an audience. C1 Univ Lincoln & Humberside, Lincoln, England. RP Hillier, A (reprint author), Ohio State Univ, Med Ctr, Dept Neurol, 408 Means Hall,1654 Upham Dr, Columbus, OH 43210 USA. 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Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 583 EP 592 DI 10.1023/A:1021259115185 PG 10 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100008 PM 12553594 ER PT J AU South, M Williams, BJ McMahon, WM Owley, T Filipek, PA Shernoff, E Corsello, C Lainhart, JE Landa, R Ozonoff, S AF South, M Williams, BJ McMahon, WM Owley, T Filipek, PA Shernoff, E Corsello, C Lainhart, JE Landa, R Ozonoff, S TI Utility of the Gilliam autism rating scale in research and clinical populations SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; diagnosis; assessment; psychometrics ID PERVASIVE DEVELOPMENTAL DISORDERS; SCREENING QUESTIONNAIRE; SPECTRUM DISORDERS; DIAGNOSIS; RELIABILITY; CHECKLIST; VALIDITY; CHILDREN; TRIAL; AGE AB The Gilliam Autism Rating Scale (GARS) was developed as a relatively easy, inexpensive aid in the surveillance and diagnosis of autism. This study examined the validity of the GARS when used with a sample of 119 children with strict DSM-IV diagnoses of autism, ascertained from both clinical and research settings. The GARS consistently underestimated the likelihood that autistic children in this sample would be classified as having autism. The sample mean for the Autism Quotient, a hypothesized index of the likelihood of having autism, was 90.10, significantly below the reference mean of 100. Diagnostic classification according to criteria specified by the GARS resulted in a sensitivity of only .48. Limitations of rating scales in general and of the GARS specifically are discussed. It is recommended that clinicians and researchers using or considering using the GARS for autism diagnosis or ratings of autism severity recognize the need for further research regarding its use. C1 Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Calif Irvine, Dept Pediat & Neurol, Irvine, CA 92717 USA. Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD USA. Johns Hopkins Sch Med, Kennedy Krieger Inst, Baltimore, MD 21205 USA. Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. RP Ozonoff, S (reprint author), Univ Calif Davis Hlth Syst, MIND Inst, 4860 Y St,Ste 3020, Sacramento, CA 95817 USA. RI South, Mikle/H-4978-2013 OI South, Mikle/0000-0003-0152-1257 CR PERRIN J, 1994, PEDIATRICS, V93, P863 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Bristol-Power MM, 1999, J AUTISM DEV DISORD, V29, P435, DOI 10.1023/A:1021991718423 *CA DEP ED DEV SER, 1997, BEST PRACT DES DEL E Dawson G., 1997, EFFECTIVENESS EARLY, P307 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 Gilliam J. E., 1995, GILLIAM AUTISM RATIN Klin A, 2000, J AUTISM DEV DISORD, V30, P163, DOI 10.1023/A:1005415823867 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 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Schreck KA, 2000, J AUTISM DEV DISORD, V30, P127, DOI 10.1023/A:1005407622050 Sparrow S., 1984, VINELAND SCALES ADAP STONE WL, 1999, J CHILD PSYCHOL PSYC, V40, P216 STREINER DL, 1993, CAN J PSYCHIAT, V38, P140 TEAL MB, 1986, J AUTISM DEV DISORD, V16, P485, DOI 10.1007/BF01531713 VOLKMAR F, 1997, HDB AUTISM PERVASIVE VOLKMAR FR, 1988, J AUTISM DEV DISORD, V18, P81, DOI 10.1007/BF02211820 NR 24 TC 50 Z9 50 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2002 VL 32 IS 6 BP 593 EP 599 DI 10.1023/A:1021211232023 PG 7 WC Psychology, Developmental SC Psychology GA 618VN UT WOS:000179438100009 PM 12553595 ER PT J AU Langworthy-Lam, KS Aman, MG Van Bourgondien, ME AF Langworthy-Lam, KS Aman, MG Van Bourgondien, ME TI Prevalence and patterns of use of psychoactive medicines in individuals with autism in the autism society of North Carolina SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DOUBLE-BLIND; DEVELOPMENTAL-DISABILITIES; ATYPICAL ANTIPSYCHOTICS; MENTAL-RETARDATION; CHILDREN; DISORDER; PLACEBO; ADULTS AB The aim of this study was to assess the prevalence and patterns of psychoactive and over-the-counter medicines in a large cohort of individuals with autism. We conducted a mail survey of 3,228 families that are members of the Autism Society of North Carolina. This is one of the largest chapters of the Autism Society of America. The survey form addressed current medicines used, side effects, demographic characteristics, and medical conditions. Some 1,538 member families within the society (48%) responded to the survey. In all, 703 (45.7%) individuals with autism were taking psychotropic drugs, 191 (12.4%) antiepileptic drugs (AEDs), and 86 (5.7%) supplements for autism. The total number taking psychotropic, antiepileptic, or vitamin treatments was 816 (53.1%). Antidepressants (taken by 21.7% of the sample), anti-psychotics (16.8%), and stimulants (13.9%) were the most commonly prescribed agents. Univariate and multivariate analyses were conducted to examine factors associated with treatment. Greater age, more severe autism and mental retardation, and more restricted housing were often associated with greater use of psychoactive agents. These findings suggest that individuals with autism are a frequently medicated group, although the empirical research support for most agents being used is still very limited. C1 Ohio State Univ, Nisonger Ctr Mental Retardat & Dev Disabil, Columbus, OH 43210 USA. Univ N Carolina, Div TEACCH, Chapel Hill, NC USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr Mental Retardat & Dev Disabil, 1581 Dodd Dr, Columbus, OH 43210 USA. CR Aman MG, 1999, MENT RETARD DEV D R, V5, P253, DOI 10.1002/(SICI)1098-2779(1999)5:4<253::AID-MRDD2>3.0.CO;2-R AMAN MG, 1991, J AM ACAD CHILD PSY, V30, P246, DOI 10.1097/00004583-199103000-00013 AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 Aman MG, 1999, MENT RETARD DEV D R, V5, P279, DOI 10.1002/(SICI)1098-2779(1999)5:4<279::AID-MRDD5>3.0.CO;2-6 AMAN MG, IN PRESS J AUTISM DE COOK EH, 1992, J AM ACAD CHILD PSY, V31, P739, DOI 10.1097/00004583-199207000-00024 Findling RL, 1997, J AUTISM DEV DISORD, V27, P467, DOI 10.1023/A:1025861522935 GORDON CT, 1993, ARCH GEN PSYCHIAT, V50, P441 Handen BL, 1997, J ABNORM CHILD PSYCH, V25, P287, DOI 10.1023/A:1025760302598 Institute of Medicine Food and Nutrition Board, 1998, DIET REF INT RISK AS Kapur S, 2001, AM J PSYCHIAT, V158, P360, DOI 10.1176/appi.ajp.158.3.360 KERLINGER FN, 2000, FDN BEHAV RES, P599 King BH, 2001, J AM ACAD CHILD PSY, V40, P658, DOI 10.1097/00004583-200106000-00010 Kozlowski B W, 1992, J Child Adolesc Psychopharmacol, V2, P307, DOI 10.1089/cap.1992.2.307 Martin A, 1999, J AM ACAD CHILD PSY, V38, P923, DOI 10.1097/00004583-199907000-00024 McDougle CJ, 1996, ARCH GEN PSYCHIAT, V53, P1001 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 SINGH NN, 1998, PSYCHOTROPIC MED DEV, P311 Tsai LY, 1999, PSYCHOSOM MED, V61, P651 TSAI LY, 1996, COMPREHENSIVE TXB CH, P219 WALTER SD, 1987, AM J EPIDEMIOL, V125, P319 NR 21 TC 58 Z9 59 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD WIN PY 2002 VL 12 IS 4 BP 311 EP 321 DI 10.1089/104454602762599853 PG 11 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 644KD UT WOS:000180915700028 PM 12625991 ER PT J AU Cesena, M Gonzalez-Heydrich, J Szigethy, E Kohlenberg, TM DeMaso, DR AF Cesena, M Gonzalez-Heydrich, J Szigethy, E Kohlenberg, TM DeMaso, DR TI A case series of eight aggressive young children treated with risperidone SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; PEDIATRIC PSYCHOPHARMACOLOGY; WEIGHT-GAIN; FOLLOW-UP; ADOLESCENTS; SCHIZOPHRENIA; MEDICATIONS; BEHAVIOR; EPILEPSY; AUTISM AB The aim of this study was to examine the use of risperidone in routine clinical care for very aggressive young children. This is a retrospective medical chart review of patients age less than 6 years 11 months who were treated with risperidone for 1 to 10 months during the 1-year study period. Treatment response, side effects, and Clinical Global Impression (CGI) scores were identified. One hundred and five such young children were identified; 8 had been treated with risperidone (6 boys, 2 girls: mean age 4.9 +/- 0.8 years). Risperidone was used in combination with other psychotropic medications in 7 of the 8 children. The mean daily dose of risperidone was 1.25 +/- 0.27 mg. Seventy-five percent of the children were on concomitant lithium, valproate, or carbamazepine; 63% were on stimulants or alpha adrenergics. This was a highly comorbid group, with 7 children presenting with attention deficit hyperactivity disorder and 5 children with bipolar disorder not otherwise specified. The average baseline CGI severity was 5.5 (SD = 0.5), and at last visit it was 3.5 (SD = 0.5), p < 0.0001. Mean CGI improvement score was 1.9 (SD = 0.6). Adverse effects included significant weight gain (mean 5.5 +/- 4.9 kg, p < 0.05) in 6 patients. One child had hyperprolactinemia. Given the potential development of atherosclerosis in obesity and endocrine response in hyperprolactinemia, risperidone should be reserved for those children with severe aggressive behavior who failed multiple trials with other agents. Further controlled trials are needed. C1 Harvard Univ, Childrens Hosp, Sch Med, Dept Psychiat, Boston, MA 02115 USA. RP Cesena, M (reprint author), Fegan 8,300 Longwood Ave, Boston, MA 02115 USA. RI Szigethy, Eva/I-7860-2013 CR Berlin CM, 1996, PEDIATRICS, V98, P143 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Armenteros JL, 1997, J AM ACAD CHILD PSY, V36, P694, DOI 10.1097/00004583-199705000-00021 Bouchard RH, 2000, J CLIN PSYCHOPHARM, V20, P295, DOI 10.1097/00004714-200006000-00002 Bruun RD, 1996, J CLIN PSYCHIAT, V57, P29 Buitelaar JK, 2000, J CHILD ADOL PSYCHOP, V10, P19, DOI 10.1089/cap.2000.10.19 CAESAR P, 1994, PEDIATR NEUROL, V11, P89 Campbell M, 1997, J AM ACAD CHILD PSY, V36, P835, DOI 10.1097/00004583-199706000-00022 Colao A, 1998, J CLIN ENDOCR METAB, V83, P2777, DOI 10.1210/jc.83.8.2777 CONVIT A, 1991, BIOL PSYCHIAT, V30, P363, DOI 10.1016/0006-3223(91)90292-T DEVINSKY O, 1993, NEUROL CLIN, V11, P127 DRAKE ME, 1992, NEUROPSYCHOBIOLOGY, V26, P125 DUFOUR DR, 1995, PRINCIPLES PRACTICE, P1992 Fenwick P, 1991, EPILEPSY BEHAV, P85 Findling RL, 2000, J AM ACAD CHILD PSY, V39, P509, DOI 10.1097/00004583-200004000-00021 Fitzgerald KD, 1999, J CHILD ADOL PSYCHOP, V9, P115, DOI 10.1089/cap.1999.9.115 Frazier JA, 1999, J AM ACAD CHILD PSY, V38, P960, DOI 10.1097/00004583-199908000-00011 Galli-Tsinopoulou A, 2000, J PEDIATR ENDOCR MET, V13, P439 Gerard ME, 1998, NEUROLOGY, V50, P384 Gonzalez-Heydrich J, 2000, INT J MED INFORM, V57, P109, DOI 10.1016/S1386-5056(00)00058-7 Gracious BL, 2001, PEDIATR ANN, V30, P138 Hellings JA, 2001, J CHILD ADOL PSYCHOP, V11, P229, DOI 10.1089/10445460152595559 Ho BC, 1999, J CLIN PSYCHIAT, V60, P658 KAPLAN SL, 1994, J AM ACAD CHILD PSY, V33, P35, DOI 10.1097/00004583-199401000-00006 Martin A, 2000, J CHILD ADOL PSYCHOP, V10, P259, DOI 10.1089/cap.2000.10.259 Masi G, 2001, J CHILD ADOL PSYCHOP, V11, P389, DOI 10.1089/104454601317261564 MASI G, 2001, J AM ACAD CHILD ADOL, V40, P14206 MASI G, 2000, J CHILD NEUROL, V16, P395 MCDOUGLE CJ, 2001, AM COLL NEUR ACNP DE McGill HC, 2000, AM J CLIN NUTR, V72, p1307S Nicolson R, 1998, J AM ACAD CHILD PSY, V37, P372, DOI 10.1097/00004583-199804000-00014 Perry R, 1997, J CHILD ADOL PSYCHOP, V7, P167, DOI 10.1089/cap.1997.7.167 Petty RG, 1999, SCHIZOPHR RES, V35, pS67, DOI 10.1016/S0920-9964(98)00158-3 Posey DJ, 1999, J CHILD ADOL PSYCHOP, V9, P273, DOI 10.1089/cap.1999.9.273 PUZANTIAN T, 2000, CNS NEWS SPECIAL EDI, V12, P77 RAPOPORT J, 1985, PSYCHOPHARMACOL B, V21, P809 Schreier HA, 1998, J CHILD ADOL PSYCHOP, V8, P49, DOI 10.1089/cap.1998.8.49 Schwam JS, 1998, J AM ACAD CHILD PSY, V37, P572, DOI 10.1097/00004583-199806000-00005 Shiwach RS, 1998, ACTA PSYCHIAT SCAND, V98, P81, DOI 10.1111/j.1600-0447.1998.tb10046.x Teicher M H, 1990, J Child Adolesc Psychopharmacol, V1, P33, DOI 10.1089/cap.1990.1.33 TURGAY A, 2001, NAT I MENT HLTH NEW van Elst LT, 2000, BRAIN, V123, P234, DOI 10.1093/brain/123.2.234 Vitiello B, 2001, PEDIATRICS, V108, P983, DOI 10.1542/peds.108.4.983 Vitiello B, 1998, CAN J PSYCHIAT, V43, P582 WONG MTH, 1994, ACTA PSYCHIAT SCAND, V90, P97, DOI 10.1111/j.1600-0447.1994.tb01562.x Wudarsky M, 1999, J CHILD ADOL PSYCHOP, V9, P239, DOI 10.1089/cap.1999.9.239 Zito JM, 2000, JAMA-J AM MED ASSOC, V283, P1025, DOI 10.1001/jama.283.8.1025 Zuddas A, 2000, J CHILD ADOL PSYCHOP, V10, P79, DOI 10.1089/cap.2000.10.79 NR 48 TC 23 Z9 24 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD WIN PY 2002 VL 12 IS 4 BP 337 EP 345 DI 10.1089/104454602762599880 PG 9 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 644KD UT WOS:000180915700031 PM 12625994 ER PT J AU Dunn, W Daniels, DB AF Dunn, W Daniels, DB TI Initial development of the infant/toddler sensory profile SO JOURNAL OF EARLY INTERVENTION LA English DT Article ID CHILDREN; DISABILITIES; PERFORMANCE; BEHAVIORS; PATTERNS; AUTISM AB We report on initial development of the Infant/Toddler Sensory Profile; a parent questionnaire assessing a child's sensory processing abilities. Parents of 401 typically developing infants and toddlers completed the 81-item questionnaire. Findings suggest that 48 of 81 items best characterized sensory processing for children 7 to 36 months of age, whereas 36 items appeared relevant for children birth to 6 months of age. Principal component analysis for 7 to 36 month olds produced an 8-component structure accounting for 47% of score variance. Reliability analyses were consistent with clusters previously identified in Dunn's model of sensory processing for older children (Dunn, 1997a). Implications for future work include replication with a large national sample and with specific disability groups. C1 Univ Kansas, Med Ctr, Dept Occupat Therapy Educ, Kansas City, KS 66160 USA. RP Dunn, W (reprint author), Univ Kansas, Med Ctr, Dept Occupat Therapy Educ, 3033 Robinson Hall,3901 Rainbow Blvd, Kansas City, KS 66160 USA. EM wdunn@kumc.edu CR ARVEDSON JC, 1992, INT J PEDIATR OTORHI, V23, P237, DOI 10.1016/0165-5876(92)90105-X Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARANEK GT, 1994, J AUTISM DEV DISORD, V24, P457, DOI 10.1007/BF02172128 Brown C, 2002, ADOLESCENT ADULT SEN Brown C, 2001, AM J OCCUP THER, V55, P75 Dunn W, 1997, AM J OCCUP THER, V51, P490 DeGangi G., 1996, BRIT J OCCUPATIONAL, V59, P457 DeGangi GA., 2000, PEDIAT DISORDERS REG DUNBAR S, 1998, AM J OCCUPATIONAL TH, V53, P231 Dunn J.T., 1997, THYROID TODAY, VXX, P1 Dunn W, 1997, INFANT YOUNG CHILD, V9, P23 Dunn W, 2002, OTJR-OCCUP PARTICI H, V22, P4 Dunn W., 1999, SENSORY PROFILE DUNN W, 1994, AM J OCCUP THER, V48, P967 Dunn W, 2002, INFANT TODDLER SENSO Dunn W, 1997, OCCUPATIONAL THERAPY, P182 Dunn WW, 2000, OCCUP THER J RES, V20, p6S Ermer J, 1998, AM J OCCUP THER, V52, P283 Greenspan S, 1993, HDB INFANT MENTAL HL, P280 Huebner R.A., 2001, AUTISM SENSORIMOTOR Kandel E. 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PD WIN-SPR PY 2002 VL 25 IS 1 BP 27 EP 41 DI 10.1177/105381510202500104 PG 15 WC Education, Special; Psychology, Educational; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 658DW UT WOS:000181707200004 ER PT J AU Morrison, RS Sainato, DM Benchaaban, D Endo, S AF Morrison, RS Sainato, DM Benchaaban, D Endo, S TI Increasing play skills of children with autism using activity schedules and correspondence training SO JOURNAL OF EARLY INTERVENTION LA English DT Article ID YOUNG-CHILDREN; TEACHERS; DISABILITIES; INCLUSION; CLASSROOM; TASK AB Play is a critical component of preschool children's development. For children with autism, restricted play skills eliminate common tools needed to build independent performance and peer relationships. The purpose of this study was to investigate a strategy to improve the independent performance of preschoolers with autism during playtime in an inclusive setting. A multiple-baseline design across subjects was employed to determine the effectiveness of correspondence training and activity schedules on the on-task and play correspondence behavior of 4 preschoolers with autism. Partial-interval recording was used to measure on-task behavior and experimenter prompts, whereas a frequency count was used for on-schedule behavior. Procedural integrity and social validity were also measured. Results of the study indicated that all 4 participants' on-task and play correspondence behavior increased, while experimenter prompts gradually decreased. C1 Ohio State Univ, Columbus, OH 43214 USA. RP Sainato, DM (reprint author), Ohio State Univ, 356 Arps Hall,1945 N High St, Columbus, OH 43214 USA. 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Early Interv. PD WIN-SPR PY 2002 VL 25 IS 1 BP 58 EP 72 DI 10.1177/105381510202500106 PG 15 WC Education, Special; Psychology, Educational; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 658DW UT WOS:000181707200006 ER PT J AU Matters, J AF Matters, J TI Reaching out, joining in: teaching social skills to young children with autism. SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Book Review C1 Univ Newcastle, Ctr Special Educ & Disabil Studies, Callaghan, NSW, Australia. RP Matters, J (reprint author), Univ Newcastle, Ctr Special Educ & Disabil Studies, Callaghan, NSW, Australia. CR Weiss M. J, 2001, REACHING OUT JOINING NR 1 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK,, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD DEC PY 2002 VL 27 IS 4 BP 346 EP 346 DI 10.1080/1366825021000055826 PG 1 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 622UB UT WOS:000179664500011 ER PT J AU Lorimer, PA Simpson, RL Myles, BS Ganz, JB AF Lorimer, PA Simpson, RL Myles, BS Ganz, JB TI The use of social stories as a preventative behavioral intervention in a home setting with a child with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID TEACHING THEORY; INITIATIONS; SKILLS; PEERS; MIND AB The purpose of this study was to determine the efficacy of a social story intervention implemented in a home setting to decrease precursors to tantrum behavior in a 5-year-old boy with autism. Using an ABAB design, two social stories were presented and withdrawn while using an event recording procedure in which interrupting verbalizations, determined to be precursors to tantrum behavior, were tallied. Data revealed a decrease in interrupting verbalizations and tantrums when the social stories were available and an increase in these behaviors when the social stories were withdrawn. C1 Univ Kansas, Med Ctr, Dept Special Educ, Kansas City, KS 66160 USA. RP Simpson, RL (reprint author), Univ Kansas, Med Ctr, Dept Special Educ, 3901 Rainbow Blvd,4th Floor,HC Miller Bldg, Kansas City, KS 66160 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Dettmer S., 2000, FOCUS AUTISM OTHER D, V15, P163, DOI DOI 10.1177/108835760001500307 Dunlap G., 1999, J POSIT BEHAV INTERV, V1, P2, DOI 10.1177/109830079900100101 Durand V. M., 1992, MOTIVATION ASSESSMEN FREEMAN S, 1996, TEACH ME LANGUAGE LA Gray C., 1995, TEACHING CHILDREN AU, P219 Gray C. 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PD WIN PY 2002 VL 4 IS 1 BP 53 EP 60 DI 10.1177/109830070200400109 PG 8 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 637ZW UT WOS:000180544400008 ER PT J AU Smith, SR Reddy, LA Wingenfeld, SA AF Smith, SR Reddy, LA Wingenfeld, SA TI Assessment of psychotic disorders in inpatient children and adolescents: Use of the Devereux Scales of Mental Disorders SO JOURNAL OF PSYCHOPATHOLOGY AND BEHAVIORAL ASSESSMENT LA English DT Article DE psychosis; assessment of children; Devereux Scales; Behavior Rating Scales AB The Devereux Scales of Mental Disorders (DSMD), with its 3-factor model of measurement (i.e., Internalizing, Externalizing, and Critical Pathology), may be useful in screening for psychotic disorders in children. This study assessed the ability of the DSMD to differentiate between inpatient children and adolescents with psychotic disorders (n = 18) and those with other clinical syndromes (n = 71). Results of ANCOVAs indicated that the psychotic group scored significantly higher on most DSMD scales and composites than the nonpsychotic clinical group. However estimates of effect size were particularly large for the Critical Pathology Composite and the Autism and Acute Problems Scales. Diagnostic efficiency statistics revealed that the DSMD's Critical Pathology Composite was highly accurate in differentiating between the 2 clinical groups. These findings support the utility of the DSMD in identifying children and adolescents with psychotic disorders. C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. Fairleigh Dickinson Univ, Dept Psychol, Teaneck, NJ USA. La Trobe Univ, Sch Psychol Sci, Bundoora, Vic 3083, Australia. Austin & Repatriat Med Ctr, Heidelberg, Vic, Australia. RP Smith, SR (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 55 Fruit St,WRN 605, Boston, MA 02114 USA. CR Achenbach T. 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PD DEC PY 2002 VL 24 IS 4 BP 269 EP 273 DI 10.1023/A:1020731117022 PG 5 WC Psychology, Clinical SC Psychology GA 606YQ UT WOS:000178764000007 ER PT J AU Mandell, DS Listerud, J Levy, SE Pinto-Martin, JA AF Mandell, DS Listerud, J Levy, SE Pinto-Martin, JA TI Race differences in the age at diagnosis among medicaid-eligible children with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autistic disorder; health disparities; children's mental health services; Medicaid ID PERVASIVE DEVELOPMENTAL DISORDERS; HEALTH-SERVICE UTILIZATION; ADOLESCENTS; SYMPTOMS; CARE AB Objective: To examine racial differences in the age at which Medicaid-eligible children first receive an autistic disorder (AD) diagnosis and to examine time in mental health treatment until an AD diagnosis was received. Method: Philadelphia Medicaid specialty mental health claims identified 406 children who received services in 1999 for AD. Claims from 1993-1999 were used to identify the date of first mental health visit, first receipt of AD diagnosis, and number of visits occurring between those dates. Linear regression was used to examine the relationship among race, age at first diagnosis of AD, time in mental health treatment, and number of visits until the diagnosis was made. Results: On average, white children received the AD diagnosis at 6.3 years of age, compared with 7.9 years for black children (p <.001). White children entered the mental health system at an earlier age (6.0 versus 7.1 years, p =.005); however, after adjusting for age, sex, and time eligible for Medicaid, black children required more time in treatment before receiving the diagnosis. Conclusions: Important disparities exist in the early detection and treatment of autism. These disparities may be the result of differences in help-seeking, advocacy and support, and clinician behaviors. J. Am. Acad. Child Addlesc. Psychiatry, 2002, 41(12):1447-1453. C1 Univ Penn, Ctr Mental Hlth Policy & Serv Res, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA. Univ Penn, Dept Pediat, Sch Med, Philadelphia, PA 19104 USA. Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. RP Mandell, DS (reprint author), Univ Penn, Ctr Mental Hlth Policy & Serv Res, Sch Med, Dept Psychiat, 3535 Market St,3rd Floor, Philadelphia, PA 19104 USA. 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SO LIBRARY JOURNAL LA English DT Book Review C1 Jewish Hosp Lib, Cincinnati, OH USA. RP Seeman, C (reprint author), Jewish Hosp Lib, Cincinnati, OH USA. CR MAROHN S, 2002, NATURAL MED GUIDE AU NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD DEC PY 2002 VL 127 IS 20 BP 163 EP 164 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA 624JT UT WOS:000179757100271 ER PT J AU Cohen, BI AF Cohen, BI TI The significance of ammonia/gamma-aminobutyric acid (GABA) ratio for normality and liver disorders SO MEDICAL HYPOTHESES LA English DT Article AB Cohen (1,2) has illustrated that extremely high Gamma-aminobutyric acid (GABA) levels in the urine and blood and high plasma ammonia were observed for an autistic male child diagnosed with infantile autism. GABA is a major inhibitory neurotransmitter of the mammalian brain and the enzyme responsible for catabolism is GABA-Transaminase (GABA-T). Elevated levels of ammonia in the plasma results in a decrease in the efficiency for the GABA-T enzyme and this results in higher GABA concentrations after regulation in the liver. It is postulated that a link between plasma ammonia and plasma GABA exists where the concentration of GABA in the plasma is directly related to the ammonia plasma concentration. A ratio of approximately 0.30 (plasma ammonia/GABA) is a consistent finding for normal subjects and for subjects with infantile autism and liver diseases such as hepatic encephalopathy. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 ED Labs, S Hackensack, NJ 07606 USA. RP Cohen, BI (reprint author), ED Labs, 89 Leuning St, S Hackensack, NJ 07606 USA. 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Hypotheses PD DEC PY 2002 VL 59 IS 6 BP 757 EP 758 DI 10.1016/S0306-9877(02)00325-0 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 625YM UT WOS:000179843200024 PM 12445521 ER PT J AU Onda, H Crino, PB Zhang, HB Murphey, RD Rastelli, L Rothberg, BEG Kwiatkowski, DJ AF Onda, H Crino, PB Zhang, HB Murphey, RD Rastelli, L Rothberg, BEG Kwiatkowski, DJ TI Tsc2 null murine neuroepithelial cells are a model for human tuber giant cells, and show activation of an mTOR pathway SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID P70 S6 KINASE; SCLEROSIS COMPLEX; DIAGNOSTIC-CRITERIA; CORTICAL TUBERS; GENETIC-ASPECTS; PHOSPHORYLATION; HAMARTOMAS; PROTEIN; GROWTH; IDENTIFICATION AB Cortical tubers are developmental brain malformations in the tuberous sclerosis complex (TSC) that cause epilepsy and autism in TSC patients whose pathogenesis is uncertain. Tsc2 null murine neuroepithelial progenitor (NEP) cells display persistent growth when growth factors are withdrawn, express GFAP at high levels, and have reduced expression of a set of early neuronal lineage markers. Tsc2 null NEP cells exhibit aberrant differentiation into giant cells that express both betaIII-tubulin and GFAP and that are morphologically similar to giant cells in human tubers. Tsc2 null giant cells and tuber giant cells have similar transcriptional profiles. Tsc2 null NEP cells express high levels of phosphorylated S6kinase, S6, Stat3, and 4E-BP-1, which is reversed by treatment with rapamycin, an inhibitor of mTOR. We conclude that giant cells in human tubers likely result from a complete loss of TSC2 expression and activation of an mTOR pathway during cortical development. C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA. Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA. Univ Penn, PENN Epilepsy Ctr, Philadelphia, PA 19104 USA. 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Cell. Neurosci. PD DEC PY 2002 VL 21 IS 4 BP 561 EP 574 DI 10.1006/mcne.2002.1184 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 628ZQ UT WOS:000180026300004 PM 12504590 ER PT J AU Backes, M von Gontard, A AF Backes, M von Gontard, A TI Behavioural phenotype of fragile X syndrome SO MONATSSCHRIFT KINDERHEILKUNDE LA German DT Article DE fragile X syndrome (FXS); Tuberous Sclerosis (TSC); Child Behavior Checklist (CBCL); Developmental Behavior Checklist (DBC); Fragebogen uber Verhalten und Soziale; Kommunikation" (VSK) ID TUBEROUS SCLEROSIS; MENTAL-RETARDATION; FMR-1 GENE; CGG REPEAT; DIAGNOSTIC INTERVIEW; DOWN-SYNDROME; YOUNG BOYS; AUTISM; MALES; QUESTIONNAIRE AB Aim of the study. As many phenotypic signs develop postpubertally, the aim of the study was to analyse the specific behavioural phenotype of the fragile X syndrome (FXS). In addition to that the practical relevance of the applied questionnaires was examined with respect to the pediatric practice. Methods. Parents of 49 boys with FXS and 16 boys with Tuberous Sclerosis filled out the "Child Behavior Checklist" (CBCL/4-18), the "Developmental Behavior Checklist" (DBC) and the "Fragebogen uberVerhalten und soziale Kommunikation"(VSK). Results. 90% of boys with FXS had clinically relevant behavioural problems, mainly attentional and hyperactive symptoms. Also social problems and autistic behaviour are common, which can lead to a misdiagnosis of infantile autism. This pattern of behaviour is specific for FXS, even compared to other types of mental retardation. Conclusions. Boys with FXS show a specific behavioural phenotype with a high psychiatric comorbidity - both in comparison to children with normal intelligence and mental retardation. Parental questionnaires, especially for mentally retarded children (DBC), are highly relevant in assessing the behavioural phenotype and planing therapeutical interventions. C1 Klin & Poliklin Psychiat & Psychotherapie Kindes, D-50931 Cologne, Germany. 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Kinderheilkd. PD DEC PY 2002 VL 150 IS 12 BP 1486 EP + DI 10.1007/s00112-002-0598-5 PG 9 WC Pediatrics SC Pediatrics GA 629HP UT WOS:000180044500007 ER PT J AU Puri, BK Singh, I AF Puri, BK Singh, I TI Normal phospholipid-related signal transduction in autism SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE arachidonic acid; autism; highly unsaturated fatty acids; phospholipid-related signal transduction ID FATTY-ACID METABOLISM; NIACIN SKIN FLUSH; SCHIZOPHRENIA; DISORDER; SPECTRUM AB The aim of this study was to test the hypothesis that autism (a neurodevelopmental disorder of unknown etiology) is associated with altered phospholipid-related signal transduction using the niacin skin flush test. This is the first reported use of this test in this disorder. The response to topical aqueous methyl nicotinate solution was recorded at 5-min intervals over 20 min in eight patients with autism and in 16 age- and sex-matched normal individuals with no history of this or any other major neuropsychiatric disorder. There was no significant difference between the mean volumetric macin response (VNR) (+/-S.E.M.) in the patients with autism, 27.0 (+/-2.2) mol s l(-1), and the mean VNR of 27.6 (+/-2.4) mol s l(-1) in the control group (P >.8). Therefore, there appears to be no evidence of altered phosopholipid-related signal transduction in autism as assessed by this test. Furthermore, since the VNR is reduced in a related disorder, schizophrenia, these results suggest fatty acid abnormalities in autism are likely to differ from those in schizophrenia. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Hammersmith Hosp, Imperial Coll, Sch Med, MRI Unit,MRC Clin Sci Ctr, London W12 0HS, England. 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Psychiatry PD DEC PY 2002 VL 26 IS 7-8 BP 1405 EP 1407 DI 10.1016/S0278-5846(02)00303-2 PG 3 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 619HH UT WOS:000179470200023 PM 12502030 ER PT J AU Willemsen-Swinkels, SHN Buitelaar, JK AF Willemsen-Swinkels, SHN Buitelaar, JK TI The autistic spectrum: subgroups, boundaries, and treatment SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD DISINTEGRATIVE DISORDER; ASPERGER-SYNDROME; DSM-IV; CLUSTER-ANALYSIS; FAMILY HISTORY; FIELD TRIAL; DIMENSIONAL CLASSIFICATION; PSYCHIATRIC-DISORDERS; BORDERLINE SYNDROME AB Consensus exists about the disorders that comprise the autistic spectrum with autistic disorder, Asperger's disorder, and pervasive developmental disorder-not otherwise specified as the most typical examples and Rett's disorder and disintegrative disorder as the other components. 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PD DEC PY 2002 VL 9 IS 4 BP 672 EP 705 DI 10.3758/BF03196324 PG 34 WC Psychology, Mathematical; Psychology, Experimental SC Psychology GA 647QE UT WOS:000181104600003 PM 12613672 ER PT J AU Hopkins, J AF Hopkins, J TI MMR vaccine is not linked with autism, says Danish study SO BRITISH MEDICAL JOURNAL LA English DT News Item CR CAMPION E, 2002, NEW ENGL J MED, V347, P1477 NR 1 TC 0 Z9 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD NOV 16 PY 2002 VL 325 IS 7373 BP 1134 EP 1134 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 618XN UT WOS:000179443100015 ER PT J AU Daenen, EWPM Wolterink, G Gerrits, MAFM Van Ree, JM AF Daenen, EWPM Wolterink, G Gerrits, MAFM Van Ree, JM TI The effects of neonatal lesions in the amygdala or ventral hippocampus on social behaviour later in life SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE neurodevelopment; social behaviour; amygdala; hippocampus; schizophrenia; autism ID JUVENILE RATS; PLAY-BEHAVIOR; PREFRONTAL CORTEX; INFANTILE-AUTISM; LABORATORY RAT; IBOTENIC ACID; BRAIN-STEM; SCHIZOPHRENIA; ABNORMALITIES; DAMAGE AB Disruption of normal social behaviour is seen in psychiatric neurodevelopmental disorders like schizophrenia or autism. In a rat model of neurodevelopmental disorders we investigated the social behavioural changes after damage of limbic brain areas, at two early stages of life. The effects of ibotenic acid lesions made on day 7 or 21 of life in the amygdala (AM) ((baso)lateral/medical) or ventral hippocampal area on social play behaviour, social behaviour unrelated to social play behaviour early in life, and social behaviour in adulthood were assessed. Lesions of the AM, but not lesions of the ventral hippocampal area, resulted in decreased social play behaviour, and no differences were found between lesions made on day 7 or 21 of life. Social behaviour unrelated to social play behaviour early in life and in adulthood was decreased in animals lesioned in the AM on day 7 but not in animals lesioned on day 21 of life. This effect was particularly present in animals with an additional lesion in the medial nuclei of the AM. Lesions in the ventral hippocampal area did not affect social behaviour. It is concluded that the AM is an important structure for social play behaviour. The effects on social behaviour that are dependent on the day of lesioning (day 7 vs. 21) are an indication of a neurodevelopmental deficit of structures connected to the (medial part) of the AM. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Med Ctr, Dept Pharmacol & Anat, Rudolf Magnus Inst Neurosci, NL-3508 AB Utrecht, Netherlands. RP Van Ree, JM (reprint author), Univ Utrecht, Med Ctr, Dept Pharmacol & Anat, Rudolf Magnus Inst Neurosci, POB 85060, NL-3508 AB Utrecht, Netherlands. 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Brain Res. PD NOV 15 PY 2002 VL 136 IS 2 BP 571 EP 582 DI 10.1016/S0166-4328(02)00223-1 PG 12 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 620GC UT WOS:000179524800026 PM 12429419 ER PT J AU Adolphs, R Baron-Cohen, S Tranel, D AF Adolphs, R Baron-Cohen, S Tranel, D TI Impaired recognition of social emotions following amygdala damage SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID FACIAL EXPRESSIONS; ASPERGER-SYNDROME; NEURAL RESPONSES; NORMAL ADULTS; AUTISM; FEAR; BRAIN; EYES AB Lesion, functional imaging, and single-unit studies in human and nonhuman animals have demonstrated a role for the amygdala in processing stimuli with emotional and social significance. We investigated the recognition of a wide variety of facial expressions, including basic emotions (e.g., happiness, anger) and social emotions (e.g., guilt, admiration, flirtatiousness). Prior findings with a standardized set of stimuli indicated that recognition of social emotions can be signaled by the eye region of the face and is disproportionately impaired in autism (Baron-Cohen, Wheelwright, & Jolliffe, 1997). To test the hypothesis that the recognition of social emotions depends on the amygdala, we administered the same stimuli to 30 subjects with unilateral amygdala damage (16 left, 14 right), 2 with bilateral amygdala damage, 47 brain-damaged controls, and 19 normal controls. Compared with controls, subjects with unilateral or bilateral amygdala damage were impaired when recognizing social emotions; moreover, they were more impaired in recognition of social emotions than in recognition of basic emotions, and, like previously described patients with autism, they were impaired also when asked to recognize social emotions from the eye region of the face alone. The findings suggest that the human amygdala is relatively specialized to process stimuli with complex social significance. The results also provide further support for the idea that some of the impairments in social cognition seen in patients with autism may result from dysfunction of the amygdala. C1 Univ Iowa, Coll Med, Dept Neurol, Div Cognit Neurosci, Iowa City, IA 52242 USA. Univ Cambridge, Cambridge CB2 1TN, England. RP Adolphs, R (reprint author), Univ Iowa, Coll Med, Dept Neurol, Div Cognit Neurosci, 200 Hawkins Dr, Iowa City, IA 52242 USA. CR Adolphs R., 2000, AMYGDALA FUNCTIONAL, P587 Adolphs R, 1999, NEUROPSYCHOLOGIA, V37, P1111, DOI 10.1016/S0028-3932(99)00039-1 ADOLPHS R, 1994, NATURE, V372, P669, DOI 10.1038/372669a0 Adolphs Ralph, 2002, Behav Cogn Neurosci Rev, V1, P21, DOI 10.1177/1534582302001001003 Adolphs R, 1998, NATURE, V393, P470, DOI 10.1038/30982 Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 Anderson AK, 2000, NEUROPSYCHOLOGY, V14, P526, DOI 10.1037//0894-4105.14.4.526 Baron-Cohen S, 2000, NEUROSCI BIOBEHAV R, V24, P355, DOI 10.1016/S0149-7634(00)00011-7 BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Beck A. T., 1987, BECK DEPRESSION INVE Benton A. L., 1983, CONTRIBUTIONS NEUROP Benton A. 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Cogn. Neurosci. PD NOV 15 PY 2002 VL 14 IS 8 BP 1264 EP 1274 DI 10.1162/089892902760807258 PG 11 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 613ZZ UT WOS:000179163500012 PM 12495531 ER PT J AU Seeman, C AF Seeman, C TI The ride together: A brother and sister's memoir of autism in the family. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Libs, Toledo, OH 43606 USA. RP Seeman, C (reprint author), Univ Toledo Libs, 2801 W Bancroft St, Toledo, OH 43606 USA. CR KARASIK J, 2003, RIDE TOGETHER BROTHE 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 NOV 15 PY 2002 VL 127 IS 19 BP 88 EP 88 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 615TU UT WOS:000179263500167 ER PT J AU Koves, K Kausz, M Reser, D Horvath, K AF Koves, K Kausz, M Reser, D Horvath, K TI What may be the anatomical basis that secretin can improve the mental functions in autism? SO REGULATORY PEPTIDES LA English DT Article DE immunohistochemistry; cerebellum; brain stem; primary sensory ganglia ID BRAIN; ABNORMALITIES; CHILDREN; DISORDERS; TRIAL; RAT AB Autism was first described and characterized as a behavioral disorder more than 50 years ago. The major abnormality in the central nervous system is a cerebellar atrophy. The characteristic histological sign is a striking loss or abnormal development in the Purkinje cell count. Abnormalities were also found in the limbic system, in the parietal and frontal cortex, and in the brain stem. The relation between secretin and autism was observed 3 years ago. Clinical observations by Horvath et al. [J. Assoc. Acad. Minor. Physicians 9 (1998) 9] supposed a defect in the role of secretin and its receptors in autism. The aim of the present work was to study the precise localization of secretin immunoreactivity, in the nervous system using an immunohistochemical approach. No secretin immunoreactivity was observed in the forebrain structures. In the brain stem, secretin immunoreactivity was observed in the mesencephalic nucleus of the trigeminal nerve, in the superior olivary nucleus, and in scattered cells of the reticular formation. The most intensive secretin immunoreactivity was observed in the Purkinje cells of the whole cerebellum and in some of the neurons of the central cerebellar nuclei. Secretin immunoreactivity was also observed in a subpopulation of neurons in the primary sensory ganglia. This work is the first immunohistochemical demonstration of secretin-immunoreactive elements in the brain stem and in primary sensory ganglia. (C) 2002 Elsevier Science B.V All rights reserved. C1 Semmelweis Univ, Fac Med, Dept Human Morphol & Dev Biol, H-1094 Budapest, Hungary. Univ Maryland, Sch Med, Div Pediat Gastroenterol & Nutr, Baltimore, MD 21201 USA. RP Koves, K (reprint author), Semmelweis Univ, Fac Med, Dept Human Morphol & Dev Biol, Tuzolto U 58, H-1094 Budapest, Hungary. 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Pept. PD NOV 15 PY 2002 VL 109 IS 1-3 BP 167 EP 172 DI 10.1016/S0167-0115(02)00200-8 PG 6 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 614WA UT WOS:000179213400023 PM 12409229 ER PT J AU Madsen, KM Hviid, A Vestergaard, M Schendel, D Wohlfahrt, J Thorsen, P Olsen, J Melbye, M AF Madsen, KM Hviid, A Vestergaard, M Schendel, D Wohlfahrt, J Thorsen, P Olsen, J Melbye, M TI A population-based study of measles, mumps, and rubella vaccination and autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID MMR IMMUNIZATION; FOLLOW-UP; DISORDERS; PREVALENCE; DIAGNOSIS; REGISTER AB Background: It has been suggested that vaccination against measles, mumps, and rubella (MMR) is a cause of autism. Methods: We conducted a retrospective cohort study of all children born in Denmark from January 1991 through December 1998. The cohort was selected on the basis of data from the Danish Civil Registration System, which assigns a unique identification number to every live-born infant and new resident in Denmark. MMR-vaccination status was obtained from the Danish National Board of Health. Information on the children's autism status was obtained from the Danish Psychiatric Central Register, which contains information on all diagnoses received by patients in psychiatric hospitals and outpatient clinics in Denmark. We obtained information on potential confounders from the Danish Medical Birth Registry, the National Hospital Registry, and Statistics Denmark. Results: Of the 537,303 children in the cohort (representing 2,129,864 person-years), 440,655 (82.0 percent) had received the MMR vaccine. We identified 316 children with a diagnosis of autistic disorder and 422 with a diagnosis of other autistic-spectrum disorders. After adjustment for potential confounders, the relative risk of autistic disorder in the group of vaccinated children, as compared with the unvaccinated group, was 0.92 (95 percent confidence interval, 0.68 to 1.24), and the relative risk of another autistic-spectrum disorder was 0.83 (95 percent confidence interval, 0.65 to 1.07). There was no association between the age at the time of vaccination, the time since vaccination, or the date of vaccination and the development of autistic disorder. Conclusions: This study provides strong evidence against the hypothesis that MMR vaccination causes autism. C1 Danish Epidemiol Sci Ctr, Dept Epidemiol & Social Med, DK-8000 Aarhus C, Denmark. Statens Serum Inst, Danish Epidemiol Sci Ctr, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark. Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabilities, Atlanta, GA USA. RP Madsen, KM (reprint author), Danish Epidemiol Sci Ctr, Dept Epidemiol & Social Med, Vennelyst Blvd 6, DK-8000 Aarhus C, Denmark. 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PD NOV 7 PY 2002 VL 347 IS 19 BP 1477 EP 1482 DI 10.1056/NEJMoa021134 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 611XG UT WOS:000179042700002 PM 12421889 ER PT J AU Kovac, I Gopnik, M Palmour, RM AF Kovac, I Gopnik, M Palmour, RM TI Sibling resemblance for specific components of linguistic competence in families of speech/language impaired children SO JOURNAL OF NEUROLINGUISTICS LA English DT Article DE verb tense; familial resemblance; specific phenotype ID DEVELOPMENTAL LANGUAGE IMPAIRMENT; QUANTITATIVE-TRAIT LOCUS; GRAMMATICAL MORPHOLOGY; GENETIC DYSPHASIA; CHROMOSOME 6P; PAST-TENSE; DISORDERS; DEFICITS; SLI; HISTORY AB We examined performance on specific linguistic tests in 23 English and French speaking fan-lilies, recruited from clinical and other sources, of children who met the following criteria for specific language impairment (SLI): clinically diagnosed language impairment without peripheral hearing loss, mental retardation (non-verbal IQ 70), neurological disorder, schizophrenia or autism. Subjects, at least 9 years old, completed a battery of French or English language tests, including derivational morphology, verb tense morphology, grammaticality judgement, syntactic comprehension, and pointing. listening comprehension and WUG pluralization test were analyzed only in the English group. The verb tense morphology (real words) and verb tense morphology (non-real words), respectively, showed non-parametric sibling correlations of 0.39 and 0.35 (p < 0.05, two-tailed) in 38 pairs (mixed gender) from ten French test pedigrees. In the English group, derivational morphology showed significant 0.52 correlation in 41 sibling pairs from the densely affected FE pedigree. After controlling for age, sibling correlation for verb tense morphology (real words) remained significant, and derivational morphology correlation in the FE pedigree was borderline (p = 0.05). Impaired grammatical morphology is a predominant aspect of SLI, and the present study, which requires independent replication, suggests that verb tense morphology and derivational morphology warrant particular attention in future familial and genetic studies. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 McGill Univ, Dept Biol, Montreal, PQ H3A 1B1, Canada. McGill Univ, Dept Linguist Ret, Montreal, PQ H3A 1B1, Canada. McGill Univ, Dept Human Genet & Psychiat, Montreal, PQ H3A 1B1, Canada. RP Palmour, RM (reprint author), McGill Univ, Dept Biol, 1205 Doctor Penfield Ave, Montreal, PQ H3A 1B1, Canada. 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Physician PD NOV 1 PY 2002 VL 66 IS 9 BP 1610 EP + PG 2 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA 615CP UT WOS:000179228500001 PM 12449259 ER PT J AU Prater, CD Zylstra, RG AF Prater, CD Zylstra, RG TI Autism: A medical primer SO AMERICAN FAMILY PHYSICIAN LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; SCREENING-TEST; CHILDREN; EPIDEMIOLOGY; DIAGNOSIS; MEASLES; DENVER AB Autistic disorder, a pervasive developmental disorder resulting in social, language, or sensorimotor deficits, occurs in approximately seven of 10,000 persons. Early detection and intervention significantly improve outcome, with about one third of autistic persons achieving some degree of independent living. indications for developmental evaluation include no babbling, pointing, or use of other gestures by 12 months of age, no single words by 16 months of age, no two-word spontaneous phrases by 24 months of age, and loss of previously learned language or social skills at any age. The differential diagnosis includes other psychiatric and pervasive developmental disorders, deafness, and profound hearing loss. Autism is frequently associated with fragile X syndrome and tuberous sclerosis, and may be caused by lead poisoning and metabolic disorders. Common comorbidities include mental retardation, seizure disorder, and psychiatric disorders such as depression and anxiety. Behavior modification programs are helpful and are usually administered by multidisciplinary teams; targeted medication is used to address behavior concerns. Many different treatment approaches can be used, some of which are unproven and have little scientific support. Parents may be encouraged to investigate national resources and local support networks. Copyright (C) 2002 American Academy of Family Physicians. C1 Univ Tennessee, Coll Med, Dept Family Med, Chattanooga Unit, Chattanooga, TN 37403 USA. RP Zylstra, RG (reprint author), Univ Tennessee, Coll Med, Dept Family Med, Chattanooga Unit, 1100 E 3rd St, Chattanooga, TN 37403 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, P65 Anderson GM, 1997, HDB AUTISM PERVASIVE, P325 ARNOLD LE, 1998, PSYCHOTROPIC MED DEV, P229 Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 Baker P, 1998, J AUTISM DEV DISORD, V28, P279, DOI 10.1023/A:1026004501631 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Bryson S. 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Fam. Physician PD NOV 1 PY 2002 VL 66 IS 9 BP 1667 EP 1674 PG 8 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA 615CP UT WOS:000179228500006 PM 12449265 ER PT J AU Turner, G Partington, M Kerr, B Mangelsdorf, M Gecz, J AF Turner, G Partington, M Kerr, B Mangelsdorf, M Gecz, J TI Variable expression of mental retardation, autism, seizures, and dystonic hand movements in two families with an identical ARX gene mutation SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE X-linked mental retardation (XLMR); nonspecific mental retardation (MRX); focal dystonia; the West syndrome; hypsarrhythmia; autism; Partington syndrome ID INFANTILE SPASMS; LINKAGE AB Two families, originally diagnosed as having nonsyndromic X-linked mental retardation (NSXLMR), were reviewed when it was shown that they had a 24-bp duplication (428-45 1dup(24bp)) in the ARX gene [Stromme et al., 2002: Nat Genet 30:441-445]. This same duplication had also been found in three other families: one with X-linked infantile spasms and hypsarrhythmia (X-linked West syndrome, MIM 308350) and two with XLMR and dystonic movements of the hands (Partington syndrome, MIM 309510). On review, manifestations of both West and Partington syndromes were found in some individuals from both families. In addition, it was found that one individual had autism and two had autistic behavior, one of whom had epilepsy. The degree of mental retardation ranged from mild to severe. A GCG trinucleotide expansion (GCG)10+7 and a deletion of 1,517 by in the ARX gene have also been found in association with the West syndrome, and a missense mutation (1058C >T) in a family with a newly recognized form of myoclonic epilepsy, severe mental retardation, and spastic paraplegia [Scheffer et al., 2002: Neurology, in press]. Evidently all these disorders are expressions of mutations in the same gene. It remains to be seen what proportions of patients with infantile spasms, focal dystonia, autism, epilepsy, and nonsyndromic mental retardation are accounted for by mutations in the ARX gene. (C) 2002 Wiley-Liss, Inc. C1 Hunter Genet, Waratah, NSW 2298, Australia. Univ Newcastle, Waratah, NSW 2298, Australia. Manchester Childrens Univ Hosp NHS Trust, Manchester, Lancs, England. Womens & Childrens Hosp, Dept Cytogenet & Mol Genet, Adelaide, SA, Australia. Univ Adelaide, Dept Paediat, Adelaide, SA, Australia. RP Turner, G (reprint author), Hunter Genet, POB 84, Waratah, NSW 2298, Australia. 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PD NOV 1 PY 2002 VL 112 IS 4 BP 405 EP 411 DI 10.1002/ajmg.10714 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 603PN UT WOS:000178568700017 PM 12376946 ER PT J AU Herbert, MR Harris, GJ Adrien, KT Ziegler, DA Makris, N Kennedy, DN Lange, NT Chabris, CF Bakardjiev, A Hodgson, J Takeoka, M Tager-Flusberg, H Caviness, VS AF Herbert, MR Harris, GJ Adrien, KT Ziegler, DA Makris, N Kennedy, DN Lange, NT Chabris, CF Bakardjiev, A Hodgson, J Takeoka, M Tager-Flusberg, H Caviness, VS TI Abnormal asymmetry in language association cortex in autism SO ANNALS OF NEUROLOGY LA English DT Article ID INFERIOR PREFRONTAL CORTEX; PLANUM TEMPORALE ASYMMETRY; FUSIFORM FACE AREA; DEVELOPMENTAL DYSLEXIA; PARS TRIANGULARIS; ANATOMICAL ASYMMETRY; CEREBRAL STRUCTURE; ASPERGER-SYNDROME; STROKE PATIENTS; FUNCTIONAL MRI AB Autism is a neurodevelopmental disorder affecting cognitive, language, and social functioning. Although language and social communication abnormalities are characteristic, prior structural imaging studies have not examined language-related cortex in autistic and control subjects. Subjects included 16 boys with autism (aged 7-11 years), with nonverbal IQ greater than 80, and 15 age- and handedness-matched controls. Magnetic resonance brain images were segmented into gray and white matter; cerebral cortex was parcellated into 48 gyral-based divisions per hemisphere. Asymmetry was assessed a priori in language-related inferior lateral frontal and posterior superior temporal regions and assessed post hoc in all regions to determine specificity of asymmetry abnormalities. Boys with autism had significant asymmetry reversal in frontal language-related cortex: 27% larger on the right in autism and 17% larger on the left in controls. Only one additional region had significant asymmetry differences on post hoc analysis: posterior temporal fusiform gyrus (more left-sided in autism), whereas adjacent fusiform gyrus and temporooccipital inferior temporal gyrus both approached significance (more right-sided in autism). These inferior temporal regions are involved in visual face processing. In boys with autism, language and social/face processing-related regions displayed abnormal asymmetry. These structural abnormalities may relate to language and social disturbances observed in autism. C1 Massachusetts Gen Hosp, Ctr Morphometr Anal, Boston, MA 02114 USA. Massachusetts Gen Hosp, Radiol Comp Aided Diagnost Lab, Boston, MA 02114 USA. McLean Hosp, Brain Imaging Ctr, Belmont, MA 02178 USA. Boston Univ, Sch Med, Boston, MA 02215 USA. Childrens Hosp, Oakland, CA 94609 USA. Pennington Sch, Pennington, NJ USA. Keio Univ, Sch Med, Tokyo, Japan. 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The challenges for the future are discussed in relation to finding and understanding the following: (1) susceptibility genes; (2) environmentally mediated causal risk processes; (3) nature-nurture interplay; (4) the effects of psychosocial adversity on the organism; (5) the causal processes responsible for group differences in rates of disorder; and (6) age-related changes in psychopathological characteristics. C1 Kings Coll London, Inst Psychiat, SGDP Res Ctr, London SE5 8AF, England. RP Rutter, M (reprint author), Kings Coll London, Inst Psychiat, SGDP Res Ctr, De Crespigny Pk,Box P080,Denmark Hill, London SE5 8AF, England. 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Data from standard magnetic resonance imaging (MRI) and two Tc-99m-ethyl cysteine dimer (ECD)-single photon emission computer tomography (SPECT) (in resting condition and performing a mental calculation task) studies were analyzed. Results. Main neurologic findings were brachycephalia, right-side neurologic soft signs, obsessive personality profile, low color-word interference effect in Stroop test, and diffuse increased cerebral blood flow during calculation task in Tc-99m-ECD SPECT. MRI showed anatomical temporal plane inverse asymmetry. Conclusions. Evidence appears to support the hypothesis that savant skill is related to excessive and erroneous use of cognitive processing resources instigated by probable failure in central executive control mechanisms. (C) 2002 IMSS. Published by Elsevier Science Inc. C1 Hosp Civil Guadalajara, Hosp 270, Serv Neurol & Neurocirugia, OPD,Unidad Neurociencias, Guadalajara 44280, Jalisco, Mexico. 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Genet. PD NOV PY 2002 VL 32 IS 6 BP 397 EP 412 DI 10.1023/A:1020876010236 PG 16 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 607XC UT WOS:000178815200002 PM 12467338 ER PT J AU Ramsay, ME Yarwood, J Lewis, D Campbell, H White, JM AF Ramsay, ME Yarwood, J Lewis, D Campbell, H White, JM TI Parental confidence in measles, mumps and rubella vaccine: evidence from vaccine coverage and attitudinal surveys SO BRITISH JOURNAL OF GENERAL PRACTICE LA English DT Article DE immunisation; measles, mumps and rubella vaccine; vaccine coverage; parental attitudes ID INFLAMMATORY BOWEL-DISEASE; IMMUNIZATION; CAUSAL; AUTISM AB Background: The measles, mumps and rubella (MMR) vaccine has been the focus of considerable adverse publicity in recent years. Aim: To describe recent trends in parental attitudes to, and coverage of, MMR vaccine. Design of study: Routine surveillance of vaccine coverage and cross-sectional surveys of parental attitudes. Setting: All health authorities in England (vaccine coverage) and 132 enumeration districts in England (attitude survey). Method: Quarterly MMR vaccine coverage for all resident children in England at two years of age was requested from computerised child health information systems Data was also obtained from 26 English health authorities/trusts on MMR coverage at 16 months of age. The proportion of mothers who believed that MMR vaccine was safe or carried only a slight risk, and the proportion who intended to fully vaccinate any future children, was obtained from biannual interviews with a nationally representative sample of over 1000 mothers of children under three years of age. Results: Vaccine coverage at two years of age fell 8.6% (95% confidence interval [CI] = 8.4 to 8.8) between April and June 1995 and between April and June 2001. In September 2001, 67966 of mothers reported that the MMR vaccine was safe or carried only a slight risk and 92% of mothers agreed with the statement: 'If I had another child in the future I would have them fully immunised against all childhood diseases'. Conclusions: Despite considerable adverse publicity the fall in MMR coverage has been relatively small, mothers' attitudes to MMR remain positive, and most continue to seek advice on immunisation from health professionals. As the vast majority of mothers are willing to have future children fully immunised, we believe that health professionals should be able to use the available scientific evidence to help to maintain MMR coverage. C1 Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, London NW9 5EQ, England. Hlth Promot England, Immunisat Programme, London, England. British Mkt Res Bur Int, London, England. Dept Hlth, Immunisat Team, London SE1 6TE, England. RP Ramsay, ME (reprint author), Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, 61 Colindale Ave, London NW9 5EQ, England. 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PD NOV PY 2002 VL 44 IS 11 BP 782 EP 791 PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 610MB UT WOS:000178962900012 PM 12418621 ER PT J AU Brooks, R Meltzoff, AN AF Brooks, R Meltzoff, AN TI The importance of eyes: How infants interpret adult looking behavior SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT International Conference on Infants Studies CY APR, 2002 CL TORONTO, CANADA ID JOINT VISUAL-ATTENTION; GAZE; DIRECTION; CHILDREN; AUTISM; ACTS; CUES AB Two studies assessed the gaze following of 12-, 14-, and 18-month-old infants, The experimental manipulation was whether an adult could see the targets, In Experiment 1, the adult turned to targets with either open or closed eyes. Infants at all ages looked at the adult's target more in the open- versus closed-eyes condition. In Experiment 2, an inanimate occluder, a blindfold, was compared with it headband control. Infants 14- and 18-months-old looked more at the adult's target in the headband condition. Infants Acre not simple responding to adult head turning, which was controlled, but ere sensitive to the status of the adult's eyes. In the 2nd year, infants interpreted adult looking Lis object-directed-an act connecting the gazer and the object. C1 Univ Washington, Ctr Mind Brain & Learning, Seattle, WA 98195 USA. RP Brooks, R (reprint author), Univ Washington, Ctr Mind Brain & Learning, Box 357920, Seattle, WA 98195 USA. RI Brooks, Rechele/A-3089-2008 OI Brooks, Rechele/0000-0002-3798-3448 CR ARGYLE LM, 1976, GAZE MUTUAL GAZE BAKEMAN R, 1986, INFANT BEHAV DEV, V9, P215, DOI 10.1016/0163-6383(86)90030-5 Bakeman R, 1997, OBSERVING INTERACTIO Baldwin D. A., 1995, JOINT ATTENTION ITS, p131 Baldwin D. 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PD NOV PY 2002 VL 38 IS 6 BP 958 EP 966 DI 10.1037//0012-1649.38.6.958 PG 9 WC Psychology, Developmental SC Psychology GA 611BV UT WOS:000178997300008 PM 12428707 ER PT J AU [Anonymous] AF [Anonymous] TI Autism, ileal-lymphoid-nodular hyperplasia and measles SO EUROPEAN JOURNAL OF PEDIATRICS LA English DT News Item CR HORVATH K, J PEDIAT, V1354, P559 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P1389 Morris A, 2002, J CLIN PATHOL-MOL PA, V55, P83 RODIER PM, 2000, SCI AM, V282, P38 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 UHLMANN V, 2002, J CLIN PATHOL, V55, P6 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 7 TC 0 Z9 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0340-6199 J9 EUR J PEDIATR JI Eur. J. Pediatr. PD NOV PY 2002 VL 161 IS 11 BP 636 EP 636 PG 1 WC Pediatrics SC Pediatrics GA 618UD UT WOS:000179434900019 ER PT J AU Walz, NC Byars, AW Egelhoff, JC Franz, DN AF Walz, NC Byars, AW Egelhoff, JC Franz, DN TI Supratentorial tuber location and autism in tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 29th Annual Meeting of the International-Neuropsychological-Society CY FEB 14-17, 2001 CL CHICAGO, ILLINOIS SP Int Neuropsychol Soc ID CLINICAL-FEATURES; PREVALENCE; ATTENTION; DEFICITS AB The high rate of autism in tuberous sclerosis complex provides an opportunity to study the pathogenesis of autism. This study investigated the relationship between a DSM-IV diagnosis of autism and tuber location in a sample of 50 individuals with tuberous sclerosis complex. Chi-square analyses revealed no differences between individuals with autism (n = 15) and those without autism (n = 35) on the occurrence of tubers in the right or left frontal, occipital, parietal, or temporal regions. There were no differences between the two groups in the occurrence of tubers in subcortical or cortical regions. In the largest sample to date, these results fail to support the hypothesis that supratentorial tuber location is a marker for autism. C1 Childrens Hosp, Med Ctr, Dept Pediat, Div Psychol, Cincinnati, OH 45229 USA. Childrens Hosp, Med Ctr, Dept Pediat, Div Neurol, Cincinnati, OH 45229 USA. Childrens Hosp, Med Ctr, Dept Radiol, Cincinnati, OH 45229 USA. RP Walz, NC (reprint author), Childrens Hosp, Med Ctr, Dept Pediat, Div Psychol, MLC D3015 Burnet Ave, Cincinnati, OH 45229 USA. 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Child Neurol. PD NOV PY 2002 VL 17 IS 11 BP 830 EP 832 DI 10.1177/08830738020170111401 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 639LE UT WOS:000180629600008 PM 12585723 ER PT J AU Chez, MG Buchanan, CP Aimonovitch, MC Becker, M Schaefer, K Black, C Komen, J AF Chez, MG Buchanan, CP Aimonovitch, MC Becker, M Schaefer, K Black, C Komen, J TI Double-blind, placebo-controlled study of L-carnosine supplementation in children with autistic spectrum disorders SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID ANTISENESCENCE DRUG; EPILEPSY; SEIZURES; ZINC; COMPLEX; MUSCLE; COPPER; ACID AB L-Camosine, a dipeptide, can enhance frontal lobe function or be neuroprotective. It can also correlate with gamma-aminobutyric acid (GABA)-homocamosine interaction, with possible anticonvulsive effects. We investigated 31 children with autistic spectrum disorders in an 8-week, double-blinded study to determine if 800 mg L-carnosine daily would result in observable changes versus placebo. Outcome measures were the Childhood Autism Rating Scale, the Gilliam Autism Rating Scale, the Expressive and Receptive One-Word Picture Vocabulary tests, and Clinical Global Impressions of Change. Children on placebo did not show statistically significant changes. After 8 weeks on L-carnosine, children showed statistically significant improvements on the Gilliam Autism Rating Scale (total score and the Behavior, Socialization, and Communication subscales) and the Receptive One-Word Picture Vocabulary test (all P < .05). Improved trends were noted on other outcome measures. Although the mechanism of action Of L-carnosine is not well understood, it may enhance neurologic function, perhaps in the enterorhinal or temporal cortex. C1 Specialty Serv Illinois Ltd, Autism & Epilepsy, Div Res, Lake Bluff, IL 60044 USA. RP Chez, MG (reprint author), Specialty Serv Illinois Ltd, Autism & Epilepsy, Div Res, 40 E Scranton,POB 280, Lake Bluff, IL 60044 USA. CR Abe H, 2000, BIOCHEMISTRY-MOSCOW+, V65, P757 American Psychiatric Association A. 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Child Neurol. PD NOV PY 2002 VL 17 IS 11 BP 833 EP 837 DI 10.1177/08830738020170111501 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 639LE UT WOS:000180629600009 PM 12585724 ER PT J AU Silva, JA Ferrari, MM Leong, GB AF Silva, JA Ferrari, MM Leong, GB TI The case of Jeffrey Dahmer: Sexual serial homicide from a neuropsychiatric developmental perspective SO JOURNAL OF FORENSIC SCIENCES LA English DT Review DE forensic science; Jeffrey Dahmer; forensic Psychiatry; serial killers; paraphilias; necrophilia; anthropophagia; necrophagia; cannibalism; fetishism; Asperger's disorder; pervasive developmental disorders; autism; murder; homicide; aggression; violence; theory of mind; psychopathy; antisocial personality disorder; schizoid personality disorder ID ASPERGERS-SYNDROME; SCHIZOID PERSONALITY; ADULT LIFE; FUNCTIONING AUTISM; INFANTILE-AUTISM; VIOLENCE; DISORDERS; BEHAVIOR; MIND; CLUMSINESS AB Sexual serial homicidal behavior has received considerable attention during the last three decades. Substantial progress has been made in the development of methods aimed at identifying and apprehending individuals who exhibit these behaviors. In spite of these advances, the origins of sexual serial killing behavior remain for the most part unknown. In this article we propose a biopsychosocial psychiatric model for understanding the origins of sexual serial homicidal behavior from both neuropsychiatric and developmental perspectives, using the case of convicted serial killer Jeffrey Dahmer as the focal point. We propose that his homicidal behavior was intrinsically associated with autistic spectrum psychopathology, specifically Asperger's disorder. The relationship of Asperger's disorder to other psychopathology and to his homicidal behavior is explored. We discuss potential implications of the proposed model for the future study of the causes of sexual serial homicidal crime. C1 Palo Alto Vet Hlth Care Syst, Palo Alto, CA USA. Kaiser Permanente, Med Grp, Div Child & Adolescent Psychiat, Santa Clara, CA USA. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA USA. Western State Hosp, Ctr Forens Sci, Tacoma, WA USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. RP Silva, JA (reprint author), POB 20928, San Jose, CA 95160 USA. 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A., 1994, VIOLENCE MENTAL DISO, P203 WILLEY LH, 1999, PRETENDING NORMAL LI Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 WING L, 1981, PSYCHOL MED, V11, P115 Wolff S., 2000, ASPERGER SYNDROME, P278 WOLFF S, 1986, PSYCHOL MED, V16, P677 Wolff S., 1995, LONERS LIFE PATH UNU WOLFF S, 1991, BRIT J PSYCHIAT, V159, P620, DOI 10.1192/bjp.159.5.620 WOLFF S, 1991, BRIT J PSYCHIAT, V159, P629, DOI 10.1192/bjp.159.5.629 WOLFF S, 1991, BRIT J PSYCHIAT, V159, P615, DOI 10.1192/bjp.159.5.615 YOUNG AW, 1998, FACE MIND, P2 NR 151 TC 20 Z9 20 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 USA SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD NOV PY 2002 VL 47 IS 6 BP 1347 EP 1359 PG 13 WC Medicine, Legal SC Legal Medicine GA 613BM UT WOS:000179111100025 PM 12455663 ER PT J AU Smith, C Felce, D Jones, E Lowe, K AF Smith, C Felce, D Jones, E Lowe, K TI Responsiveness to staff support: evaluating the impact of individual characteristics on the effectiveness of active support training using a conditional probability approach SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE conditional probability; direct observation; resident activity; residential services; staff support; staff training ID SEVERE INTELLECTUAL DISABILITY; COMMUNITY RESIDENCES; PEOPLE; DISSEMINATION; BEHAVIORS; OUTCOMES; SERVICES; ADULTS; WALES AB Background Active support training was fully conducted in 38 community houses accommodating 106 adults with intellectual disabilities (ID; group I), but not in a further 36 accommodating 82 adults with ID (group 2). The aims of the present study were to analyse whether staff became more effective in supporting resident activity after the implementation of active support, and whether there was evidence of differential responsiveness by people with differing status in relation to adaptive behaviour, psychiatric diagnosis, challenging behaviour or autism. Methods Observations of staff:resident interaction and resident engagement in activity were taken before and after active support training. Changes in Yule's Q statistics, indicating the likelihood that resident engagement in activity followed staff giving residents verbal instruction or non-verbal assistance, were compared for the two groups. In addition, changes in similar statistics were compared for residents within group I: (I) with Adaptive Behaviour Scale (ABS) scores above and below 180; and (2) with and without severe challenging behaviour, the triad of social impairments and mental illness. Results Yule's Q for engagement given non-verbal assistance significantly increased post-training among group I, but not among group 2. Similar significant increases were found among group I residents with ABS scores below 180 without challenging behaviour, with and without the triad of social impairments, and without mental illness, but not with an ABS score above 180, with challenging behaviour and with mental illness. Conclusion The present analysis reinforces previous studies on the effectiveness of active support training for adults with more severe ID (i.e. with ABS scores below 180). Active support was as effective for people with the triad of social impairments as for those without it. However, the effectiveness of support offered to people with challenging behaviour or mental illness did not significantly increase. C1 Univ Wales Coll Med, Welsh Ctr Learning Disabil Appl Res Unit, Cardiff CF14 3BG, S Glam, Wales. RP Felce, D (reprint author), Univ Wales Coll Med, Welsh Ctr Learning Disabil Appl Res Unit, Meridian Court,North Rd, Cardiff CF14 3BG, S Glam, Wales. CR Aman M., 1986, ABERRANT BEHAV CHECK Bakeman R., 2000, HDB RES METHODS SOCI, P138 Bakeman R, 1996, BEHAV RES METH INSTR, V28, P446, DOI 10.3758/BF03200524 Emerson E, 2000, BEHAVIORAL OBSERVATION, P47 EMERSON E, 1994, MOVING IMPACT RELOCA Emerson E, 2000, J INTELLECT DEV DIS, V25, P263, DOI 10.1080/13668250020019575 Felce D, 1998, J INTELL DISABIL RES, V42, P390, DOI 10.1046/j.1365-2788.1998.00153.x FELCE D, IN PRESS J APPL RES FELCE D, 1995, SOC SCI MED, V40, P799, DOI 10.1016/0277-9536(94)00152-J Felce D, 2000, RES DEV DISABIL, V21, P243, DOI 10.1016/S0891-4222(00)00040-8 Felce D., 2000, QUALITY LIFE SUPPORT Felce D., 1996, DEINSTITUTIONALIZATI, P117 Felce D, 1999, J APPL RES INTELLECT, V12, P273 Felce D, 2000, J INTELLECT DEV DIS, V25, P307, DOI 10.1080/13668250020019593 Hatton C, 1996, J INTELL DISABIL RES, V40, P466 Hewson S., 1992, MENT HANDICAP RES, V5, P188, DOI 10.1111/j.1468-3148.1992.tb00044.x HOLMES N, 1982, PSYCHOL MED, V12, P879 Jones E, 1999, J INTELL DISABIL RES, V43, P164, DOI 10.1046/j.1365-2788.1999.00177.x Jones E, 2001, J APPL RES INTELLECT, V14, P79, DOI 10.1046/j.1468-3148.2001.00064.x Jones E, 2001, AM J MENT RETARD, V106, P344, DOI 10.1352/0895-8017(2001)106<0344:EOTDOA>2.0.CO;2 Lowe K, 1998, J INTELL DISABIL RES, V42, P375, DOI 10.1046/j.1365-2788.1998.00154.x MANSELL J, 1998, TIZARD LEARNING DISA, V3, P17 Matson J. L, 1988, PSYCHOPATHOLOGY INST MCGILL P, 1993, SEVERE LEARNING DISA, P323 Nihira K, 1993, AAMR ADAPTIVE BEHAV PERRY J, 2000, SUBJECTIVE OBJECTIVE Reeves D., 1994, CALCULATING INTEROBS Siegel S., 1956, NONPARAMETRIC STAT B Stancliffe RJ, 1998, AM J MENT RETARD, V102, P552 Suen H. K., 1989, ANAL QUANTITATIVE BE Thompson T, 1996, AM J MENT RETARD, V101, P315 WING L, 1978, J AUTISM CHILD SCHIZ, V8, P79, DOI 10.1007/BF01550280 NR 32 TC 18 Z9 18 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 NOV PY 2002 VL 46 BP 594 EP 604 DI 10.1046/j.1365-2788.2002.00433.x PN 8 PG 11 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 621QA UT WOS:000179599900002 PM 12427166 ER PT J AU Unis, AS Munson, JA Rogers, SJ Goldson, E Osterling, J Gabriels, R Abbott, RD Dawson, G AF Unis, AS Munson, JA Rogers, SJ Goldson, E Osterling, J Gabriels, R Abbott, RD Dawson, G TI A randomized, double-blind, placebo-controlled trial of porcine versus synthetic secretin for reducing symptoms of autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; psychopharmacology; secretin ID PERVASIVE DEVELOPMENTAL DISORDER; CHILDREN AB Objective: To compare the effects of a single dose of biologic and synthetic porcine secretin to placebo on a variety of autism symptoms. Method: Eighty-five children with autism without other medical conditions and not taking other psychotropic medications participated (ages between 3 and 12 years, mean IQ = 55). Children were grouped into trios matched by age and communication level and then randomly assigned to one of three treatment groups: biologic secretin (2 CU/kg), synthetic secretin (0.4 mug/kg), and placebo. Measures collected 1 week before and 4 weeks after infusion included autism symptoms, language skills, and problem behaviors, gathered from parents, teachers, and investigators, who were all blind to treatment. Two-factor, repeated-measures analyses of variance (3 treatment levels by 2 repeated measures, pre- and postinfusion) were used to examine efficacy. Results: Direct observation measures did not show change over time related to secretin. Parent reports showed an overall reduction of symptom severity for all treatment groups, including the placebo group. One teacher-report measure showed decreases in autism symptoms in the placebo and synthetic secretin groups. Conclusions: No evidence that either biologic or synthetic secretin provided amelioration of symptoms beyond placebo was observed. This held true when children with and without gastrointestinal problems were examined separately. C1 Univ Washington, CHDD, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Educ Psychol, Seattle, WA 98195 USA. Univ Colorado, Hlth Sci Ctr, Denver, CO 80202 USA. RP Dawson, G (reprint author), Univ Washington, CHDD, Dept Psychiat & Behav Sci, Box 357920, Seattle, WA 98195 USA. 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PD NOV PY 2002 VL 41 IS 11 BP 1315 EP 1321 DI 10.1097/01.CHI.0000024858.60748.4C PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 607MW UT WOS:000178796200012 PM 12410073 ER PT J AU Brereton, AV Tonge, BJ MacKinnon, AJ Einfeld, SL AF Brereton, AV Tonge, BJ MacKinnon, AJ Einfeld, SL TI Screening young people for autism with the developmental behavior checklist SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; intellectual disability; screening instrument ID EMOTIONAL DISTURBANCE; INTELLECTUAL DISABILITY; CHILDHOOD AUTISM; CHILDREN; PSYCHOPATHOLOGY; QUESTIONNAIRE; ADOLESCENTS; INSTRUMENT; POPULATION; AGE AB Objective: To determine whether a subset of items from the Developmental Behavior Checklist (DBC) could be selected to construct a reliable autism screening tool. Method: A 29-item scale-the Developmental Behavior Checklist-Autism Screening Algorithm (DBC-ASA)-was developed by using items from the DBC and evaluated in a sample comprising 180 children who met criteria for DSM-IV autism and 180 controls matched for age, sex, and IQ range. Results: This study found that the DBC-ASA has good validity in discriminating young people (4-18 years) with autism and 10 ranging from normal to severe intellectual disability from others using a cutoff score of 17. Conclusion: The DBC-ASA is an effective autism screening questionnaire for at-risk young people, including those with intellectual disability. C1 Monash Univ, Ctr Dev Psychiat, Monash Med Ctr, Clayton, Vic 3168, Australia. Monash Univ, Dept Psychol Med, Clayton, Vic 3168, Australia. Univ New S Wales, Sch Psychiat, Kensington, NSW 2033, Australia. RP Tonge, BJ (reprint author), Monash Univ, Ctr Dev Psychiat, Monash Med Ctr, 246 Clayton Rd, Clayton, Vic 3168, Australia. CR Achenbach T. 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D., 1998, PSYCHOTROPIC MEDICAT, P85 Joreskog K, 1993, LISREL 8 STRUCTURAL KRAMER MS, 1988, CLIN EPIDEMIOLOGY BI, P204 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1994, J AUTISM DEV DISORD, V24, P551 Lord C., 1997, HDB AUTISM PERVASIVE, P460 Nunnally J.C., 1967, PSYCHOMETRIC THEORY OSWALD DP, 1991, J AUTISM DEV DISORD, V21, P543, DOI 10.1007/BF02206876 PFEIFFER SI, 1992, J AUTISM DEV DISORD, V22, P95, DOI 10.1007/BF01046405 PRIOR M, 1992, J CHILD PSYCHOL PSYC, V33, P249, DOI 10.1111/j.1469-7610.1992.tb00863.x Rimland B., 1964, INFANTILE AUTISM SYN Rutter M., 1970, ED HLTH BEHAV SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SIEGEL B, 1989, J AM ACAD CHILD PSY, V28, P542, DOI 10.1097/00004583-198907000-00013 SMITH B, 1994, J AUTISM DEV DISORD, V24, P551, DOI 10.1007/BF02172137 Tabachnick B.G., 1996, USING MULTIVARIATE S, V2nd Tonge B. J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 TONGE BJ, 1994, J PAEDIATR CHILD H, V30, P102, DOI 10.1111/j.1440-1754.1994.tb00590.x Tonge BJ, 1996, J INTELL DISABIL RES, V40, P198, DOI 10.1046/j.1365-2788.1996.771771.x VOSTANIS P, 1994, CHILD CARE HLTH DEV, V20, P165, DOI 10.1111/j.1365-2214.1994.tb00378.x World Health Organization, 1992, INT CLASS DIS NR 44 TC 32 Z9 32 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 2002 VL 41 IS 11 BP 1369 EP 1375 DI 10.1097/01.CHI.0000024838.94814.A5 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 607MW UT WOS:000178796200019 PM 12410080 ER PT J AU McDougle, CJ Posey, D AF McDougle, CJ Posey, D TI Genetics of childhood disorders: XLIV. Autism, Part 3: Psychopharmacology of autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; ADULTS C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46204 USA. RP McDougle, CJ (reprint author), Yale Univ, Sch Med, Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06520 USA. CR Krystal JH, 1999, HARVARD REV PSYCHIAT, V7, P125, DOI 10.1093/hrp/7.3.125 Marek GJ, 2000, CNS DRUG REV, V6, P206 MCCRACKEN JT, 2002, NEW ENGL J MED, V347, P302 McDougle CJ, 1996, ARCH GEN PSYCHIAT, V53, P1001 McDougle CJ, 2000, J AUTISM DEV DISORD, V30, P427, DOI 10.1023/A:1005551523657 McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 Posey DJ, 2000, HARVARD REV PSYCHIAT, V8, P45, DOI 10.1093/hrp/8.2.45 NR 7 TC 17 Z9 18 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 2002 VL 41 IS 11 BP 1380 EP 1383 DI 10.1097/01.CHI.0000024860.60748.88 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 607MW UT WOS:000178796200021 PM 12410082 ER PT J AU Dove, A AF Dove, A TI Big bucks for autism research SO NATURE MEDICINE LA English DT News Item NR 0 TC 0 Z9 0 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 2002 VL 8 IS 11 BP 1190 EP 1190 DI 10.1038/nm1102-1190a PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 614ZK UT WOS:000179221200005 PM 12411928 ER PT J AU Nevo, Y Kramer, U Shinnar, S Leitner, Y Fattal-Valevski, A Villa, Y Harel, S AF Nevo, Y Kramer, U Shinnar, S Leitner, Y Fattal-Valevski, A Villa, Y Harel, S TI Macrocephaly in children with developmental disabilities SO PEDIATRIC NEUROLOGY LA English DT Article; Proceedings Paper CT 4th International Congress of the European-Paediatric-Neurology-Society CY SEP 12-16, 2001 CL BADEN BADEN, GERMANY SP European Paediatric Neurol Soc ID EXTERNAL HYDROCEPHALUS; HEAD CIRCUMFERENCE; CLINICAL CHARACTERISTICS; NATURAL-HISTORY; BENIGN; AUTISM; INTELLIGENCE; DIAGNOSIS; DISORDERS; PROGNOSIS AB In a community-based study of 4,309 children with neurodevelopmental disabilities who were referred to the Institute for Child Development, Tel Aviv, Israel, 62 (1.4%) had macrocephaly (head circumference above the ninety-eighth percentile for age), of whom 42 (1%) had macrocephaly not associated with hydrocephalus. With the exception of neonatal respiratory distress the incidence of perinatal complications was not different from that in other children referred to the Institute for Child Development. In children with developmental disabilities, macrocephaly was a significant risk factor for febrile seizures (odds ratio = 3.1, P < 0.001) and epilepsy (odds ratio = 7.7, P < 0.001), but not for mental retardation (odds ratio = 1.1, P = 0.78) or cerebral palsy (odds ratio = 1.3, P = 0.67). Children with macrocephaly had a high rate of comorbid diagnosis. We conclude that in children with developmental disabilities the presence of macrocephaly even when not associated with hydrocephalus is associated with an increased risk of seizures. (C) 2002 by Elsevier Science Inc. All rights reserved. C1 Tel Aviv Univ, Inst Child Dev, IL-65211 Tel Aviv, Israel. Tel Aviv Univ, Sackler Sch Med, Tel Aviv Sourasky Med Ctr,Dana Childrens Hosp, Div Pediat,Pediat Neurol Unit, IL-65211 Tel Aviv, Israel. Montefiore Med Ctr, Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA. Montefiore Med Ctr, Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA. Montefiore Med Ctr, Albert Einstein Coll Med, Comprehens Epilepsy Management Ctr, Bronx, NY 10467 USA. RP Nevo, Y (reprint author), Tel Aviv Univ, Inst Child Dev, 14 Balfour St, IL-65211 Tel Aviv, Israel. 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Neurol. PD NOV PY 2002 VL 27 IS 5 BP 363 EP 368 DI 10.1016/S0887-8994(02)00454-X PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 631ML UT WOS:000180171500005 PM 12504204 ER PT J AU Felix, JF Badawi, N Dixon, G Keogh, JM Petterson, B Valentine, J Kurinczuk, JJ AF Felix, JF Badawi, N Dixon, G Keogh, JM Petterson, B Valentine, J Kurinczuk, JJ TI Autism following a history of newborn encephalopathy SO PEDIATRIC RESEARCH LA English DT Meeting Abstract CT Meeting of the European-Society-for-Paediatric-Research CY SEP 04-07, 2002 CL UTRECHT, NETHERLANDS SP European Soc Paediatric Res C1 TVW Telethon Inst Child Hlth Res, Perth, WA, Australia. Childrens Hosp, Westmead, NSW, Australia. Hornsby Hosp, Hornsby, Australia. Univ Leicester, Leicester LE1 7RH, Leics, England. 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 NOV PY 2002 VL 52 IS 5 MA 272 BP 824 EP 824 PG 1 WC Pediatrics SC Pediatrics GA 610TP UT WOS:000178977200299 ER PT J AU Makela, A Nuorti, JP Peltola, H AF Makela, A Nuorti, JP Peltola, H TI Neurologic disorders after measles-mumps-rubella vaccination SO PEDIATRICS LA English DT Article DE measles; mumps; rubella; MMR vaccine; immunization; adverse effects; encephalitis; aseptic meningitis; autism; autistic disorders ID INCLUSION-BODY ENCEPHALITIS; ASEPTIC-MENINGITIS; AUTISM; CHILDREN; IMMUNIZATION; FINLAND; DISEASE; PROGRAM; VIRUS; RISK AB Objective. The possibility of adverse neurologic events has fueled much concern about the safety of measles-mumps-rubella (MMR) vaccinations. The available evidence concerning several of the postulated complications is controversial. The aim of this study was to assess whether an association prevails between MMR vaccination and encephalitis, aseptic meningitis, and autism. Methods. A retrospective study based on linkage of individual MMR vaccination data with a hospital discharge register was conducted among 535 544 1- to 7-year-old children who were vaccinated between November 1982 and June 1986 in Finland. For encephalitis and aseptic meningitis, the numbers of events observed within a 3-month risk interval after vaccination were compared with the expected numbers estimated on the basis of occurrence of encephalitis and aseptic meningitis during the subsequent 3-month intervals. Changes in the overall number of hospitalizations for autism after vaccination throughout the study period were searched for. In addition, hospitalizations because of inflammatory bowel diseases were checked for the children with autism. Results. Of the 535 544 children who were vaccinated, 199 were hospitalized for encephalitis, 161 for aseptic meningitis, and 352 for autistic disorders. In 9 children with encephalitis and 10 with meningitis, the disease developed within 3 months of vaccination, revealing no increased occurrence within this designated risk period. We detected no clustering of hospitalizations for autism after vaccination. None of the autistic children made hospital visits for inflammatory bowel diseases. Conclusions. We did not identify any association between MMR vaccination and encephalitis, aseptic meningitis, or autism. C1 Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Hus 00029, Finland. Natl Publ Hlth Inst, Dept Infect Dis & Epidemiol, Helsinki, Finland. RP Makela, A (reprint author), Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Stenbackinkatu 11,PL 281, Hus 00029, Finland. CR Altman D. 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Research on the biological pathophysiology of autism has found some evidence that immune alterations may play a role in the pathophysiology of that illness. As a consequence we expected to find that autism is accompanied by abnormalities in the pattern obtained in serum protein electrophoresis and in the serum immunoglobulin (Ig) and IgG subclass profile. Method. We examined whether subjects with autism showed changes in total serum protein (TSP) and the serum concentrations of albumin, a I globulin, alpha2 globulin, beta globulin and gamma globulins, IgA, IgM and IgG and the IgG subclasses IgG1, IgG2, IgG3 and IgG4, compared with normal controls. Results. We found significantly increased concentrations of TSP in autistic subjects, which were attributable to increased serum concentrations of albumin and gamma globulin. Serum IgG, IgG2 and IgG4 were also significantly raised. In autism there were significant and positive correlations between social problems and TSP and serum 7 globulin and between withdrawal symptoms and TSP and serum albumin and IgG. Conclusions. The results suggest that autism is characterized by increased TSP, a unique pattern obtained in serum protein electrophoresis, i.e. increased serum albumin and IgG, and by a specific IgG subclass profile, i.e. increased serum IgG2 and IgG4. The increased serum concentrations of IgGs in autism may point towards an underlying autoimmune disorder and/or an enhanced susceptibility to infections resulting in chronic viral infections, whereas the IgG subclass skewing may reflect different cytokine-dependent influences on autoimmune B cells and their products. C1 Univ Antwerp, Ctr Child & Adolescent Psychiat, AZM, B-2020 Antwerp, Belgium. Univ Antwerp, Dept Med Biochem, Wilrijk, Belgium. AZ Middelheim, Clin Lab, Antwerp, Belgium. CRC MH, Limburg, Belgium. Eurogenet, Tessenderlo, Belgium. Univ Hosp Maastricht, Dept Psychiat, Maastricht, Netherlands. RP Croonenberghs, J (reprint author), Univ Antwerp, Ctr Child & Adolescent Psychiat, AZM, Lindendreef 1, B-2020 Antwerp, Belgium. CR Achenbach TM, 1991, MANUAL YOUTH SELF RE ACHENBANCH TM, 1983, MANUAL CHILD BEHAV C AMAN MG, 1994, ASSESSMENT REHABILIT, V1, P1 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANNEREN G, 1992, ARCH DIS CHILD, V67, P628 CHESS S, 1971, J AUTISM CHILD SCHIZ, V1, P33, DOI 10.1007/BF01537741 Connolly AM, 1999, J PEDIATR-US, V134, P607, DOI 10.1016/S0022-3476(99)70248-9 Croonenberghs J, 2002, NEUROPSYCHOBIOLOGY, V45, P1, DOI 10.1159/000048665 Denney DR, 1996, J AUTISM DEV DISORD, V26, P87, DOI 10.1007/BF02276236 Harrison KL, 1995, BIOCHEM SOC T, V23, pS603 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 KAWAUCHI M, 1994, REPORT NATL I BIOSCI, V2, P1 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Maes M, 1996, NEUROPSYCHOPHARMACOL, V15, P243, DOI 10.1016/0893-133X(95)00181-C MAES M, 1995, J AFFECT DISORDERS, V34, P61, DOI 10.1016/0165-0327(94)00106-J Messahel S, 1998, NEUROSCI LETT, V241, P17, DOI 10.1016/S0304-3940(97)00976-2 OUTSCHOORN I, 1993, CLIN IMMUNOL IMMUNOP, V66, P59, DOI 10.1006/clin.1993.1008 PHILIPSEN EK, 1995, SCAND J GASTROENTERO, V30, P50, DOI 10.3109/00365529509093235 PLIOPLYS AV, 1994, NEUROPSYCHOBIOLOGY, V29, P12, DOI 10.1159/000119056 PLIOPLYS AV, 1989, NEUROPEDIATRICS, V20, P93, DOI 10.1055/s-2008-1071273 PUTNAM FW, 1984, PLASMA PROTEINS STRU, P2 PUTNAM FW, 1984, PLASMA PROTEINS STRU, P46 RITZMANN SE, 1976, SERUM PROTEIN ABNORM, P3 SHATTOCK P, 1988, ASPECTS AUTISM, P1 SHAW W, 1998, BIOL TREATMENTS AUTI SINGH VK, 1993, BRAIN BEHAV IMMUN, V7, P97, DOI 10.1006/brbi.1993.1010 Singh VK, 1996, J NEUROIMMUNOL, V64, P135, DOI 10.1016/0165-5728(95)00161-1 Singh VK, 1997, PEDIATR NEUROL, V17, P88, DOI 10.1016/S0887-8994(97)00045-3 Singh VK, 1998, CLIN IMMUNOL IMMUNOP, V89, P105, DOI 10.1006/clin.1998.4588 SINGH VK, 1991, CLIN IMMUNOL IMMUNOP, V61, P448, DOI 10.1016/S0090-1229(05)80015-7 STUBBS EG, 1976, J AUTISM CHILD SCHIZ, V6, P269, DOI 10.1007/BF01543467 STUBBS EG, 1977, J AUTISM CHILD SCHIZ, V7, P49, DOI 10.1007/BF01531114 STUBBS EG, 1987, ASPECTS AUTISM BIOL, P91 STUBBS G, 1995, J AUTISM DEV DISORD, V25, P71, DOI 10.1007/BF02178169 Thomas L., 1998, CLIN LAB DIAGNOSTICS Van Hunsel F, 1998, PSYCHOL MED, V28, P301, DOI 10.1017/S0033291797006351 WARREN RP, 1987, J AM ACAD CHILD PSY, V26, P333, DOI 10.1097/00004583-198705000-00008 WARREN RP, 1990, IMMUNOL INVEST, V19, P245, DOI 10.3109/08820139009041839 WARREN RP, 1986, J AUTISM DEV DISORD, V16, P189, DOI 10.1007/BF01531729 WARREN RP, 1995, NEUROPSYCHOBIOLOGY, V31, P53, DOI 10.1159/000119172 ZIMMERMAN AW, 1993, INT C AUT 1993 TOR C NR 41 TC 69 Z9 70 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4221 USA SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD NOV PY 2002 VL 32 IS 8 BP 1457 EP 1463 DI 10.1017/S0033291702006037 PG 7 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 621AD UT WOS:000179565600014 PM 12455944 ER PT J AU Williams, TO Eaves, RC AF Williams, TO Eaves, RC TI The reliability of test scores for the pervasive developmental disorders rating scale SO PSYCHOLOGY IN THE SCHOOLS LA English DT Article ID INSTRUMENTS; VALIDITY; AUTISM AB The Pervasive Developmental Disorders Rating Scale (PDDRS; Eaves, 1993) is a screening instrument used in the assessment of autistic disorder. In this study, the reliability of test scores for the PDDRS was examined with three samples. The first sample consisted of 456 participants ranging in age from 1 to 12 years old and the second sample consisted of 111 participants in the 13 to 24 year-old range. Additionally, the test-retest reliability of scores for the PDDRS was examined with a sample of 40 participants. The results indicated that coefficient alpha for the PDDRS Total Score was adequate for screening purposes (r = .89) for both age groups. The results of the test-retest study also suggested that PDDRS had adequate test-retest reliability (r = .92) for the PDDRS Total Score. (C) 2002 Wiley Periodicals, Inc. C1 Virginia Polytech Inst & State Univ, Blacksburg, VA 24061 USA. Auburn Univ, Auburn, AL 36849 USA. RP Williams, TO (reprint author), Virginia Tech, Dept Teaching & Learning, 311 War Mem Hall, Blacksburg, VA 24061 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th EAVES EC, 1990, ANN AL C AUT BIRM AL Eaves R. C., 1993, PERVASIVE DEV DISORD Eaves RC, 2000, PSYCHOL SCHOOLS, V37, P311, DOI 10.1002/1520-6807(200007)37:4<323::AID-PITS2>3.0.CO;2-S EAVES RC, 1987, J SPEC EDUC, V21, P130 Gilliam J. 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Schools PD NOV PY 2002 VL 39 IS 6 BP 605 EP 611 DI 10.1002/pits.10059 PG 7 WC Psychology, Educational SC Psychology GA 614MA UT WOS:000179192700001 ER PT J AU Gray, DE AF Gray, DE TI 'Everybody just freezes. Everybody is just embarrassed': felt and enacted stigma among parents of children with high functioning autism SO SOCIOLOGY OF HEALTH & ILLNESS LA English DT Article DE autism; stigma; family; disability ID PEOPLE; WOMEN AB This paper reports the results of a study of felt and enacted stigma among a sample of parents of children with high functioning autism. The results indicate that a majority of the parents experienced both types of stigma, but that mothers were more likely to do so than fathers. This was especially true in the case of enacted stigma. where a majority of mothers, but only a minority of fathers, encountered avoidance, hostile staring and rude comments from others. The child's type of autistic symptoms was also related to the stigmatisation of their parents, with parents of aggressive children more likely to experience stigma than the parents of passive children. The study also found that the distinction between felt and enacted stigma was more distinct analytically than it was in practice, as many parents tended to conflate the different types of stigma. The results of the study are considered in the context of the changing conceptualisations of, and treatments for, high functioning autism and their implications for the stigmatisation of parents. C1 Univ New England, Sch Social Sci, Armidale, NSW 2351, Australia. RP Gray, DE (reprint author), Univ New England, Sch Social Sci, Armidale, NSW 2351, Australia. 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Health Ill. PD NOV PY 2002 VL 24 IS 6 BP 734 EP 749 DI 10.1111/1467-9566.00316 PG 16 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical; Sociology SC Public, Environmental & Occupational Health; Biomedical Social Sciences; Sociology GA 618ZB UT WOS:000179447100003 ER PT J AU Gepner, B Mestre, D AF Gepner, B Mestre, D TI Rapid visual-motion integration deficit in autism SO TRENDS IN COGNITIVE SCIENCES LA English DT Letter ID CHILDREN C1 Univ Aix Marseille 1, Montperrin Hosp, Child Psychiat Dept, Aix En Provence, France. CNRS, UMR 6057, Aix En Provence, France. RP Gepner, B (reprint author), Univ Aix Marseille 1, Montperrin Hosp, Child Psychiat Dept, Aix En Provence, France. 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PD NOV PY 2002 VL 6 IS 11 BP 455 EP 455 DI 10.1016/S1364-6613(02)02004-1 PG 1 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 614CD UT WOS:000179170000007 ER PT J AU Bolte, S Poustka, F AF Bolte, S Poustka, F TI Interventions for autism: Status quo, evidence-based, questionable and dubious techniques SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Review DE autism; diagnostics; therapy; intervention; review; evidence-based medicine ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; DIAGNOSTIC INTERVIEW; SOCIAL SKILLS; DOUBLE-BLIND; INTERRATER RELIABILITY; PRESCHOOL-CHILDREN; COMMUNICATION; PSYCHIATRY C1 Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie & Jugendalters, D-60528 Frankfurt, Germany. RP Bolte, S (reprint author), Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie & Jugendalters, Deutschodenstr 50, D-60528 Frankfurt, Germany. 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Autistic disorder is characterized by a qualitative impairment in verbal and non verbal communication, in imaginative activity, and in reciprocal social interactions. Communication in autism is so strikingly impaired that the function of the hearing system has been under study over the past 30 years, namely after the advent of physiological assessment of hearing with the auditory brainstem response (ABR). Many research studies were developed to study ABR in autism as they constitute a direct test of both hearing status and integrity of brainstem pathways, but the results obtained are contradictory. The authors present case reports of two children with autistic disorder, 2 and 4 years of age, in which the ABR findings document a prevalent Peak I in the four ears tested. This characteristic configuration in ABR has not been previously reported and future work is needed to establish the importance of this finding and its implications in the awareness of the auditory status in these children. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Hosp Criancas Maria Pia, Dept Otolaryngol, P-4050111 Oporto, Portugal. Hosp Criancas Maria Pia, Dept Child & Adolescent Psychiat, P-4050111 Oporto, Portugal. RP Coutinho, MB (reprint author), Hosp Criancas Maria Pia, Dept Otolaryngol, Rua Boavista 827, P-4050111 Oporto, Portugal. 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J. Pediatr. Otorhinolaryngol. PD OCT 21 PY 2002 VL 66 IS 1 BP 81 EP 85 DI 10.1016/S0165-5876(02)00211-2 PG 5 WC Otorhinolaryngology; Pediatrics SC Otorhinolaryngology; Pediatrics GA 610HE UT WOS:000178954000012 PM 12363427 ER PT J AU Garner, JP Mason, GJ AF Garner, JP Mason, GJ TI Evidence for a relationship between cage stereotypies and behavioural disinhibition in laboratory rodents SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE stereotypy; abnormal behaviour; schizophrenia; autism; animal welfare; basal ganglia; bar mouthing; executive functioning; striatal dysfunction ID VOLES CLETHRIONOMYS-GLAREOLUS; INDUCED JUMPING STEREOTYPY; MONKEYS MACACA-MULATTA; BANK VOLES; ENVIRONMENTAL ENRICHMENT; NUCLEUS-ACCUMBENS; MICE; RAT; MOVEMENT; PERSEVERATION AB Cage stereotypies-abnormal, repetitive, unvarying and apparently functionless behaviours-are common in many captive animals, sometimes resulting in self-injury or decreased reproductive success. However, a general mechanistic or neurophysiological understanding of cage stereotypies has proved elusive. In contrast, stereotypies in human mental disorder, or those induced by drugs or brain lesions, are well understood, and are thought to result from the disinhibition of behavioural selection by the basal ganglia. In this study, we found that the cage stereotypies of captive bank voles also correlate with signs of altered response selection by the basal ganglia. Stereotypic bar-mouthing in the caged voles correlated with inappropriate responding in extinction learning, impairments of response timing, evidence of a knowledge-action dissociation, increased rates of behavioural activation, and hyperactivity. Furthermore, all these signs intercorrelated, implicating a single underlying deficit consistent with striatal disinhibition of response selection. Bar-mouthing thus appears fundamentally similar to the stereotypies of autists, schizophrenics, and subjects treated with amphetamine or basal ganglial lesions. These results represent the first evidence for a neural substrate of cage stereotypy. They also suggest that stereotypic animals may experience novel forms of psychological distress, and that stereotypy might well represent a potential confound in many behavioural experiments. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA. Univ Oxford, Dept Zool, Oxford OX1 3PS, England. RP Garner, JP (reprint author), Univ Calif Davis, Dept Anim Sci, 1 Shields Ave, Davis, CA 95616 USA. 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PD OCT 17 PY 2002 VL 136 IS 1 BP 83 EP 92 DI 10.1016/S0166-4328(02)00111-0 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 607DM UT WOS:000178776300009 PM 12385793 ER PT J AU Fatemi, SH Halt, AR Stary, JM Kanodia, R Schulz, SC Realmuto, GR AF Fatemi, SH Halt, AR Stary, JM Kanodia, R Schulz, SC Realmuto, GR TI Glutamic acid decarboxylase 65 and 67 kDa proteins are reduced in autistic parietal and cerebellar cortices SO BIOLOGICAL PSYCHIATRY LA English DT Article DE glutamic acid decarboxylase; gamma amino butyric acid; autism; schizophrenia; parietal cortex; cerebellum; western blotting ID BIPOLAR DISORDER; INFANTILE-AUTISM; POSTMORTEM BRAIN; MESSENGER-RNAS; ALTERED LEVELS; DOUBLE-BLIND; REELIN; SCHIZOPHRENIA; ABNORMALITIES; ISOFORMS AB Background: A limited number of reports have demonstrated abnormalities involving the glutamate and gamma amino butyric acid systems in blood and platelets of subjects with autism. To further investigate these studies, brain levels of rate limiting enzyme, glutamic acid decarboxylase, which is responsible for normal conversion of glutamate to gamma amino butyric acid in the brain, were investigated. Methods: Postmortem cerebellar and parietal cortices of age (mean +/- SD for controls 23 +/- 4.2, autistic 25.2 +/- 5.2 cerebellum; controls 23.5 +/- 4.8, autistic 21.6 +/- 3.8 parietal cortex), gender and postmortem interval-matched autistic and control subjects (n = 8 control, n = 5 autism, cerebellum; n = 4 control, n = 5 autism, parietal cortex) were subjected to SDS-PAGE and western blotting. Brain levels of glutamic acid decarboxylase proteins of 65 and 67 kDa and beta-actin were determined. Results: Glutamic acid decarboxylase protein of 65 kDa was reduced by 48% and 50% in parietal and cerebellar (p < .02) areas of autistic brains versus controls respectively. By the same token, glutamic acid decarboxylase protein of 67 kDa was reduced by 61% and 51% in parietal (p < .03) and cerebellar areas of autistic brains versus controls respectively. Brain levels of beta-actin were essentially similar in both groups. Conclusions: The observed reductions in glutamic acid decarboxylase 65 and 67 kDa levels may account for reported increases of glutamate in blood and platelets of autistic subjects. Glutamic acid decarboxylase deficiency may be due to or associated with abnormalities in levels of glutamate/gamma amino butyric acid, or transporter/ receptor density in autistic brain. (C) 2002 Society of Biological Psychiatry. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, 420 Delaware St,SE,Mayo Bldg,Box 392, Minneapolis, MN 55455 USA. 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PD OCT 15 PY 2002 VL 12 IS 20 BP R679 EP R679 DI 10.1016/S0960-9822(02)01201-0 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 609KJ UT WOS:000178902100002 PM 12401179 ER PT J AU Sandman, CA Touchette, P Marion, S Lenjavi, M Chicz-Demet, A AF Sandman, CA Touchette, P Marion, S Lenjavi, M Chicz-Demet, A TI Disregulation of proopiomelanocortin and contagious maladaptive behavior SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT 23rd Winter Neuropeptide Conference CY FEB 02-05, 2002 CL BRECKENRIDGE, COLORADO DE beta-endorphin; ACTH; self-injury; autism; mental retardation ID SELF-INJURIOUS-BEHAVIOR; PLASMA BETA-ENDORPHIN; NALTREXONE TREATMENT; AUTISTIC-CHILDREN; INFANTILE-AUTISM; OPIATE BLOCKERS; DOUBLE-BLIND; POMC; PEPTIDES; FURIN AB Self-injurious behavior (SIB) is an untreatable and often life-threatening problem among individuals with developmental disorders, especially those diagnosed with autism. Functioning, relationships and processing of the proopiomelanocortin (POMC) system are "uncoupled" in subgroups of self-injuring individuals resulting in different ratios of ACTH and opioids in the bloodstream, particularly under conditions of stress. In this study, relations between SIB and POMC were evaluated in a multi-year study of the largest prospective sample studied to date, Observations were collected on palmtop computers for 45 treatment-resistant patients who exhibited chronic SIB. Behavior of each subject was observed in natural settings without disruption or intrusion, for continuous, 2.5-h periods, two times a day (morning and afternoon), 4 days a week for two consecutive weeks, for a total of 40 h/subject. Blood was collected in the morning, late afternoon and immediately after an SIB episode on two separate occasions separated by at least 6 months. Levels of beta-endorphin (RE) and ACTH were assayed by RIA. We discovered that the SIB was the best predictor of subsequent SIB. Moreover, the majority of subjects exhibited this contagious pattern of SIB. Levels of POMC fragments were reliable over a 6- to 9-month period. Subjects exhibiting POMC disregulation characterized by high morning levels of betaE had the highest transitional probabilities of SIB (i.e. contagious patterns; F=8.17, P<0.01). These findings suggest that subjects with "contagious" SIB may represent a behavioral phenotype associated with disregulated expression of the POMC gene. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Fairview Dev Ctr, Appl Neurodev Res Inst, Costa Mesa, CA 92626 USA. Univ Calif Irvine, Dept Psychiat, Irvine, CA 92717 USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. RP Sandman, CA (reprint author), Fairview Dev Ctr, Appl Neurodev Res Inst, Box 7, Costa Mesa, CA 92626 USA. 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PD OCT 8 PY 2002 VL 114 IS 7 MA O31 BP 723 EP 724 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400074 ER PT J AU Castermans, D Devriendt, K Wilquet, V Steyaert, J Fryns, JP van de Ven, W AF Castermans, D Devriendt, K Wilquet, V Steyaert, J Fryns, JP van de Ven, W TI Chromosomal anomalies in 4 children with autism: Breakpoints and 1 gene SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Katholieke Univ Leuven Hosp, Ctr Human Genet, Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O32 BP 724 EP 724 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400075 ER PT J AU Auranen, M Varilo, T Alen, R Vanhala, R Ayers, K Kempas, E Ylisaukko-oja, T Sinsheimer, JS Peltonen, L Jarvela, I AF Auranen, M Varilo, T Alen, R Vanhala, R Ayers, K Kempas, E Ylisaukko-oja, T Sinsheimer, JS Peltonen, L Jarvela, I TI Evidence for allelic association on chromosome 3q25-27 in families with autism spectrum disorders originating from a subisolate of Finland SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Helsinki, Dept Med Genet, FIN-00014 Helsinki, Finland. Kuopio Univ Hosp, Unit Child Neurol, SF-70210 Kuopio, Finland. Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. Univ Calif Los Angeles, Sch Med, Dept Biomath, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA USA. Univ Helsinki, Genet Mol Lab, Cent Hosp, FIN-00014 Helsinki, Finland. RI Jarvela, Irma/L-5836-2013 NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O43 BP 728 EP 728 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400086 ER PT J AU Barnby, GH AF Barnby, GH CA IMGSAC TI Candidate gene analysis, association studies and genotyping at the autism susceptibility locus on chromosome 16p SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX1 2JD, England. RI Bailey, Anthony/J-2860-2014; Bolton, Patrick/E-8501-2010 OI Bailey, Anthony/0000-0003-4257-972X; Bolton, Patrick/0000-0002-5270-6262 NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O44 BP 728 EP 729 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400087 ER PT J AU Gallagher, L Ennis, S Kearney, G Fitzgerald, M Stallings, R Barton, D Green, AJ Gill, M AF Gallagher, L Ennis, S Kearney, G Fitzgerald, M Stallings, R Barton, D Green, AJ Gill, M TI Fine mapping of a susceptibility region and candidate gene studies on chromosome 2q in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Trinity Coll Dublin, Dept Psychiat Genet, Dublin, Ireland. Univ Coll Dublin, Conway Inst, Dublin 2, Ireland. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O45 BP 729 EP 729 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400088 ER PT J AU Jamain, S Betancur, C Quach, H Gillberg, C Leboyer, M Bourgeron, T AF Jamain, S Betancur, C Quach, H Gillberg, C Leboyer, M Bourgeron, T TI Linkage and association of the GRIK2 (or GLUR6) gene with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Inst Pasteur, INSERM, E021, F-75724 Paris, France. Hop Henri Mondor, INSERM, U513, F-94010 Creteil, France. Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41124 Gothenburg, Sweden. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. Assistance Publ Hop Paris, Hop Albert Chenevier & Henri Mondor, Creteil, France. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O46 BP 729 EP 729 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400089 ER PT J AU Nurmi, EL Olson, LM Amin, T Jacobs, MM McCauley, JL Dowd, M Folstein, SE Haines, JL Sutcliffe, JS AF Nurmi, EL Olson, LM Amin, T Jacobs, MM McCauley, JL Dowd, M Folstein, SE Haines, JL Sutcliffe, JS TI Genetic analysis of the 15q11-q13 autism candidate region provides continued support for a susceptibility locus SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Vanderbilt Univ, Program Human Genet, Nashville, TN USA. Tufts Univ New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O47 BP 730 EP 730 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400090 ER PT J AU Betancur, C AF Betancur, C TI Linkage and association studies of the alpha 7 nicotinic acetylcholine receptor locus and three GABA (A) receptor subunit genes on chromosome 15q11-qi3 in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Hop Henri Mondor, INSERM, U513, F-94010 Creteil, France. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P157 BP 811 EP 811 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400308 ER PT J AU Cuccaro, ML Donnelly, S Ravan, SA Abramson, RA Wolpert, C Elston, L Wright, HH Pericak-Vance, MA AF Cuccaro, ML Donnelly, S Ravan, SA Abramson, RA Wolpert, C Elston, L Wright, HH Pericak-Vance, MA TI Clinical characterization ofa chromosome 15 phenotype for autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC USA. Univ S Carolina, William S Hall Psychiat Inst, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P161 BP 812 EP 813 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400312 ER PT J AU Klauck, SM Beyer, KS Blasi, F Bacchelli, E Benner, A Epp, S Poustka, F Maestrini, E Poustka, A AF Klauck, SM Beyer, KS Blasi, F Bacchelli, E Benner, A Epp, S Poustka, F Maestrini, E Poustka, A CA IMGSAC TI Candidate gene screening in susceptibility regions for autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany. Univ Bologna, Dept Biol, I-40126 Bologna, Italy. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. RI Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P171 BP 816 EP 816 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400322 ER PT J AU Lauritsen, MB Nyegaard, M Betancur, C Colineaux, C Kruse, T Leboyer, M Ewald, H AF Lauritsen, MB Nyegaard, M Betancur, C Colineaux, C Kruse, T Leboyer, M Ewald, H TI Test for linkage between autism and twelve single nucleotide polymorphisms in the somatostatin receptor 5 gene SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Psychiat Hosp Aarhus, Dept Psychiat Demog, Inst Basic Psychiat Res, Risskov, Denmark. Odense Univ Hosp, Dept Clin Biochem & Genet, DK-5000 Odense, Denmark. Hop Henri Mondor, INSERM, U513, F-94010 Creteil, France. Hop Robert Debre, Dept Child & Adolescent Psychiat, F-75019 Paris, France. Assistance Publ Hop Paris, Dept Psychiat, Hop Albert Chenevier & Henri Mondor, Creteil, France. Psychiat Hosp Aarhus, Dept Biol Psychiat, Inst Basic Psychiat Res, Risskov, Denmark. RI Nyegaard, Mette/G-4443-2012 NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P174 BP 817 EP 817 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400325 ER PT J AU Simons, A Croonenberghs, J Van Bever, Y Deboutte, D AF Simons, A Croonenberghs, J Van Bever, Y Deboutte, D TI Autism and translocation chromosome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Univ Antwerp, UCKJA, B-2020 Antwerp, Belgium. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P186 BP 821 EP 821 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400337 ER PT J AU Vincent, JB Kolozsvari, D Cheung, J Haddad, M Roberts, W Scherer, SW AF Vincent, JB Kolozsvari, D Cheung, J Haddad, M Roberts, W Scherer, SW TI An autism patient with a T (5;7) (q14; q31) translocation: Localization, identification and mutation-screening of candidate genes at the breakpoints SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P194 BP 824 EP 824 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400345 ER PT J AU Wolpert, CM Rosen-Sheidley, B Donnelly, SL Elston, L Soper, E Turner, C Cuccaro, ML Folstein, S Pericak-Vance, MA AF Wolpert, CM Rosen-Sheidley, B Donnelly, SL Elston, L Soper, E Turner, C Cuccaro, ML Folstein, S Pericak-Vance, MA TI Web-based genetic education for autism and related disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Duke Univ, Med Ctr, Durham, NC USA. Tufts Univ New England Med Ctr, Boston, MA 02111 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P197 BP 825 EP 825 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400348 ER PT J AU Frith, U AF Frith, U TI Autism - the quest continues: Reflections on the Novartis symposium on Autism, June 2002 SO NEUROREPORT LA English DT Editorial Material C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. UCL, Dept Psychol, London WC1N 3AR, England. RP Frith, U (reprint author), UCL, Inst Cognit Neurosci, Alexandra House,17 Queen Sq, London WC1N 3AR, England. EM u.frith@ucl.ac.uk RI Frith, Uta/C-1757-2008 OI Frith, Uta/0000-0002-9063-4466 NR 0 TC 1 Z9 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD OCT 7 PY 2002 VL 13 IS 14 BP 1703 EP 1705 DI 10.1097/00001756-200210070-00002 PG 3 WC Neurosciences SC Neurosciences & Neurology GA 613XK UT WOS:000179156600002 PM 12395107 ER PT J AU Casaer, P Croonenberghs, JAN Lagae, L Deboutte, D AF Casaer, P Croonenberghs, JAN Lagae, L Deboutte, D TI Risperidone in the treatment of childhood autistic disorder: an open pilot study SO ACTA NEUROPSYCHIATRICA LA English DT Article DE autism; behavioral disturbances; extrapyramidal symptoms; mental retardation; risperidone ID PERVASIVE DEVELOPMENTAL DISORDERS; ABERRANT BEHAVIOR CHECKLIST; DOUBLE-BLIND; INFANTILE-AUTISM; CHILDREN; PLACEBO; SCHIZOPHRENIA; HALOPERIDOL; ADOLESCENTS; ADULTS AB Objective: To evaluate the tolerability and efficacy of risperidone in childhood autistic disorder. Methods: A multicenter, open-label, dose-titration study involving seven autistic children (mean age 7.6years) receiving risperidone for 4 weeks. Results: Mean dose was 0.01 mg/kg/day on day 1, 0.019 mg/kg/day on day 7 (range 0.01-0.041 mg/kg/day) and 0.035 mg/kg/day on day 28 (range 0.014-0.064mg/kg/day). Over the 4-week period, the Ritvo-Freeman Real Life Rating Scale total score measuring autistic behavior was significantly decreased (P = 0.019), as was the affectual reactions subscale (P = 0.029). Aberrant Behavior Checklist total score was significantly improved (P < 0.001), as were all subscales except inappropriate speech. Visual Analog Scale for individual target symptoms was significantly decreased (P = 0.001), and Clinical Global Impression severity of illness score was significantly improved (P = 0.006). The incidence of adverse effects was low, and no extrapyramidal symptoms were observed. No significant changes or clinically relevant abnormalities occurred in laboratory tests, vital signs or electrocardiograms. Plasma concentrations of the drug were similar to those in adult patients. Conclusions: These favorable results suggest that larger controlled trials of risperidone should be performed in autistic or mentally retarded patients with behavioral disturbances. C1 Univ Antwerp, Ctr Child & Adolescent Psychiat, AZ Middelheim, B-2020 Antwerp, Belgium. Univ Hosp Gasthuisberg, Dept Pediat, B-3000 Louvain, Belgium. RP Croonenberghs, JAN (reprint author), Univ Antwerp, Ctr Child & Adolescent Psychiat, AZ Middelheim, Lindendreef 1, B-2020 Antwerp, Belgium. 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PD OCT PY 2002 VL 14 IS 5 BP 242 EP 249 DI 10.1034/j.1601-5215.2002.140508.x PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 624PT UT WOS:000179769100008 ER PT J AU Cantor-Chiu, RM Alarcon, M Yuan, JY Consortium, AGRE Geschwind, DH AF Cantor-Chiu, RM Alarcon, M Yuan, JY Consortium, AGRE Geschwind, DH TI Autism age-of onset quantitative trait loci (qtl). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 113 BP 186 EP 186 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800115 ER PT J AU Miles, JH Yarnal, R Takahashi, TN Stoelb, M McCathren, R AF Miles, JH Yarnal, R Takahashi, TN Stoelb, M McCathren, R TI Autism: Physical features can predict which children respond to intensive ABA therapy. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Missouri, Div Gen Med, Dept Child Hlth, Columbia, MO USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 112 BP 186 EP 186 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800113 ER PT J AU Vincent, JB Kolozsvari, D Cheung, J Haddad, M Roberts, W Scherer, SW AF Vincent, JB Kolozsvari, D Cheung, J Haddad, M Roberts, W Scherer, SW TI An autism patient with a t(5;7)(q14;q31)translocation: localization, identification and mutation-screening of candidate genes at the breakpoints. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. Hosp Sick Children, Child Dev Ctr, Toronto, ON, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 114 BP 186 EP 186 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800114 ER PT J AU Szatmari, P Merrette, C Jones, M Palmour, R Zwaigenbaum, L Roy, M Maziade, M AF Szatmari, P Merrette, C Jones, M Palmour, R Zwaigenbaum, L Roy, M Maziade, M TI Identifying genetically informative phenotypes in autism spectrum disorders (ASD). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 McMaster Univ, Dept Psychiat, Hamilton, ON, Canada. Univ Laval, Dept Psychiat, Quebec City, PQ, Canada. Penn State Univ, Coll Med, Hershey, PA 17033 USA. McGill Univ, Dept Psychiat, Montreal, PQ, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 510 BP 259 EP 259 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800509 ER PT J AU Yu, PT Takahashi, TN Miles, JH Sahota, PK AF Yu, PT Takahashi, TN Miles, JH Sahota, PK TI Autism: Characterization of sleep disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Missouri, Childrens Hosp, Columbia, MO USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 516 BP 260 EP 260 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800515 ER PT J AU Stodgell, CJ Hyman, SL Bryson, SE AF Stodgell, CJ Hyman, SL Bryson, SE TI Correlation of genotype with the Autism Diagnostic Intervine to stratifying cases of autism spectrum disorder. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Rochester, Dept OB GYN, Rochester, NY USA. Univ Rochester, Dept Pediat, Rochester, NY USA. Dalhousie Univ, IWK Hlth Ctr, Halifax, NS, Canada. RI Stodgell, Christopher/A-1161-2007 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 519 BP 261 EP 261 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800522 ER PT J AU Harris, SW Goodlin-Jones, BL Bacalman, S Jardini, T Rao, S Hagermann, RJ AF Harris, SW Goodlin-Jones, BL Bacalman, S Jardini, T Rao, S Hagermann, RJ TI Fragile X and autism diagnosis by two standard methodologies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Calif Davis, Ctr Med, MIND Inst, Sacramento, CA 95817 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 680 BP 288 EP 288 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800681 ER PT J AU Wolpert, CM Rosen-Sheidly, B Donelly, SL Elston, LA Tumer, CS Folstein, SE Pericak-Vance, MA AF Wolpert, CM Rosen-Sheidly, B Donelly, SL Elston, LA Tumer, CS Folstein, SE Pericak-Vance, MA TI Web-based survey of families with autism: Reassessing the need for genetic education. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Duke Univ, Med Ctr, Durham, NC 27706 USA. Tufts Univ New England Med Ctr, Boston, MA 02111 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1008 BP 344 EP 344 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801004 ER PT J AU Brown, WT Nolin, SL Dobkin, CS Houck, GS Glicksman, A Ding, XD Gargano, AD Crawford, L Gitcho, N Spence, SJ Geschwind, DH Agre AF Brown, WT Nolin, SL Dobkin, CS Houck, GS Glicksman, A Ding, XD Gargano, AD Crawford, L Gitcho, N Spence, SJ Geschwind, DH Agre TI Frequency of fragile X in multiplex autism: Testing the AGRE families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NYS Inst Basic Res, Dept Human Genet, Staten Isl, NY USA. Univ Calif Los Angeles, Sch Med, Program Behav Genet, Inst Neuropsychiat, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Neurol, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1025 BP 347 EP 347 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801021 ER PT J AU McInnes, LA Hallmayer, J Manghi, E Pritchard, J Wills, K Hervas, A Sanz, S Benitez, JL Guijarro, T Gay, E Sanchez, V Llanes, D Ruiz-Rubio, M AF McInnes, LA Hallmayer, J Manghi, E Pritchard, J Wills, K Hervas, A Sanz, S Benitez, JL Guijarro, T Gay, E Sanchez, V Llanes, D Ruiz-Rubio, M TI A population genetic study of autism in Andalucia, Spain. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Mt Sinai Sch Med, Dept Psychiat Human Gen, New York, NY USA. Stanford Univ, Sch Med, Dept Psychiat, Palo Alto, CA 94304 USA. Univ Chicago, Dept Disabil & Human Dev, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Childrens Hosp & Clin Minneapolis, Dept Psychol, Minneapolis, MN 55404 USA. Hosp Mutua Terrassa, Dept Child & Adolescent Psychiat, Barcelona 08022, Spain. Unidad Salud Mental Infantil, Cordoba 14071, Spain. Univ Cordoba, Dept Genet, E-14071 Cordoba, Spain. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1119 BP 363 EP 363 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801116 ER PT J AU Haefele, AL Figlewicz, DA Stodgell, CJ AF Haefele, AL Figlewicz, DA Stodgell, CJ TI Apparent uniparental disomy in a familial case of autism spectrum disorder. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Rochester, Rochester, NY USA. RI Stodgell, Christopher/A-1161-2007 NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1553 BP 436 EP 436 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801547 ER PT J AU Hutcheson, HB Olson, LM Bradford, Y Folstein, SE Santangelo, SL Sutcliffe, J Haines, JL AF Hutcheson, HB Olson, LM Bradford, Y Folstein, SE Santangelo, SL Sutcliffe, J Haines, JL TI Examination of candidate genes on chromosome 7 in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN USA. Tufts Univ, New England Med Ctr Hosp, Sch Med, Dept Psychiat, Boston, MA 02111 USA. Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1613 BP 446 EP 446 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801607 ER PT J AU Alarcon, M Geschwind, DH Gilliam, TC Cantor-Chiu, RM AF Alarcon, M Geschwind, DH Gilliam, TC Cantor-Chiu, RM CA A G R E Consortium TI Evidence supporting a language QTL on 7q in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. Columbia Univ, Columbia Genome Ctr, New York, NY USA. Cure Autism Now, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1689 BP 459 EP 459 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801690 ER PT J AU Bonora, E Beyer, KS Lamb, JA Klauck, SM Poltstka, A Bailey, AJ Monaco, AP AF Bonora, E Beyer, KS Lamb, JA Klauck, SM Poltstka, A Bailey, AJ Monaco, AP TI Analysis of Reelin in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Oxford, WTCHG, Oxford, England. Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, D-6900 Heidelberg, Germany. Inst Psychiat, Ctr Social Genet & Dev Psychiat, London, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London, England. RI Bailey, Anthony/J-2860-2014 OI Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1741 BP 468 EP 468 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801742 ER PT J AU Jones, MB Palmour, R Zwaigenbaum, L Szatman, P AF Jones, MB Palmour, R Zwaigenbaum, L Szatman, P TI Modifier effects in autism at the DHB and MAO-A loci. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Penn State Univ, Coll Med, Dept Behav Sci, Hershey, PA USA. McGill Univ, Dept Psychiat, Montreal, PQ, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. McMaster Univ, Dept Psychiat, Hamilton, ON, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1753 BP 470 EP 470 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801754 ER PT J AU Liu, X Mundo, E Zhang, C Holden, JJA AF Liu, X Mundo, E Zhang, C Holden, JJA TI The 5HT1D beta receptor gene in autism: Case-control study and genotype-phenotype correlation analysis in multiplex families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Queens Univ, Ongwanada Resource Ctr, Dept Psychiat & Psychol, Cytogenet & DNA Res Lab, Kingston, ON, Canada. Univ Toronto, Ctr Addict & Mental Hlth, Toronto, ON, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1759 BP 471 EP 471 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801760 ER PT J AU Woodroffe, A Flodman, P Mays, L Lord, J Holguin, S Modahl, C Osann, K Spence, MA Fein, D Smith, M AF Woodroffe, A Flodman, P Mays, L Lord, J Holguin, S Modahl, C Osann, K Spence, MA Fein, D Smith, M TI DNA polymorphisms in Oxytocin and 7B2 (SGNE1): evidence for association between polymorphisms and autism spectrum disorder. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Calif Irvine, Irvine, CA USA. Univ Connecticut, Storrs, CT USA. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1767 BP 472 EP 472 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801767 ER PT J AU Silva, SC Fesel, C Coutinho, AM Barreto, M Marques, C Miguel, T Ataide, A Bento, C Oliveira, G Vicente, AM AF Silva, SC Fesel, C Coutinho, AM Barreto, M Marques, C Miguel, T Ataide, A Bento, C Oliveira, G Vicente, AM TI Autoantibody repertoires against brain tissue in autism nuclear families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Gulbenkian Inst Sci, Oeiras, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. RI Barreto, Marta/F-5591-2012 OI Barreto, Marta/0000-0001-6464-548X NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1773 BP 473 EP 473 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801773 ER PT J AU Zhang, H Liu, X Zhang, C Mundo, E Macciardi, F Schwartz, CE Michaelis, R Holden, JJA AF Zhang, H Liu, X Zhang, C Mundo, E Macciardi, F Schwartz, CE Michaelis, R Holden, JJA TI The high-activity catechol-0-methyltransferase val allele is a risk factor for autism spectrum disorder SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Queens Univ, Kingston, ON, Canada. Univ Toronto, CAMH, Toronto, ON, Canada. Greenwood Genet Ctr, JC Self Res Inst, Ctr Mol Studies, Greenwood, SC 29646 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1772 BP 473 EP 473 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801775 ER PT J AU Shinya, M Yamamoto, A Oka, A Uchida, M Tokubo, E Sato, R Inoko, H AF Shinya, M Yamamoto, A Oka, A Uchida, M Tokubo, E Sato, R Inoko, H TI Mutation screening and association study of LIMK1 in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Tokai Univ, Sch Med, Isehara, Kanagawa 25911, Japan. JBIRC, Tokyo, Japan. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1777 BP 474 EP 474 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801778 ER PT J AU Kashork, CD Stockton, DW Sahoo, T Bercovich, D Shaffer, LG Beaudet, AL AF Kashork, CD Stockton, DW Sahoo, T Bercovich, D Shaffer, LG Beaudet, AL TI Genetics of autism: Identification of chromosomal abnormalities and susceptibility loci on chromosome 15q in autism families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Baylor Coll Med, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1793 BP 476 EP 476 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801792 ER PT J AU Persico, AM Stodgell, C D'Agruma, L Zelante, L Militerni, R Bravaccio, C Trillo, S Montecchi, F Schneider, C Melmed, R Elia, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Muscarella, LA Guarnieri, V Conciatori, M Rodier, P AF Persico, AM Stodgell, C D'Agruma, L Zelante, L Militerni, R Bravaccio, C Trillo, S Montecchi, F Schneider, C Melmed, R Elia, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Muscarella, LA Guarnieri, V Conciatori, M Rodier, P TI The HOXA1 G allele may be associated with dysmorphism in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 UCBM, Rome, Italy. Univ Rochester, Sch Med, Rochester, NY USA. IRCCS Casa Sollievo Sofferenza, Med Genet Serv, San Giovanni Rotondo, FG, Italy. Univ Naples 2, Naples, Italy. Osp Bambino Gesu, IRCCS, Rome, Italy. SARC, Phoenix, AZ USA. IRCCS Oasi Maria SS, Neurol Serv, Troina, EN, Italy. Univ Roma La Sapienza, Dept Psychol, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, N-0027 Oslo, Norway. RI Stodgell, Christopher/A-1161-2007 NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1801 BP 478 EP 478 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801802 ER PT J AU Coutinho, AM Silva, S Fesel, C Morgadinho, T Macedo, TR Bento, C Marques, C Ataide, A Miguel, T Oliveira, G Vicente, AM AF Coutinho, AM Silva, S Fesel, C Morgadinho, T Macedo, TR Bento, C Marques, C Ataide, A Miguel, T Oliveira, G Vicente, AM TI Role of serotonin transporter variants in the determination of platelet serotonin levels in autism spectrum disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Gulbenkian Inst Sci, Oeiras, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. Univ Coimbra, Fac Med, Coimbra, Portugal. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1836 BP 483 EP 483 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801837 ER PT J AU Robitaille, S Liu, X Currie, M Holden, JJA AF Robitaille, S Liu, X Currie, M Holden, JJA TI BDNF and susceptibility to autism spectrum disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. Queens Univ, Dept Psychiat, Kingston, ON K7L 3N6, Canada. Cytogenet & DNA Res Lab, Kingston, ON, Canada. CR Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Philippe A, 2002, AM J MED GENET, V114, P125, DOI 10.1002/ajmg.10041 NR 2 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1871 BP 489 EP 489 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801870 ER PT J AU Vander Molen, JE Kim, SJ Cooks, EH Cox, N AF Vander Molen, JE Kim, SJ Cooks, EH Cox, N TI Linkage disequilibrium mapping of the seratonin transporter gene (SLC6A4) region in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Chicago, Dept Psychiat, Lab Dev Neurosci Child & Adolescent Psychiat, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1876 BP 490 EP 490 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801878 ER PT J AU Huq, AHMM Zhong, H Nabi, R Serajee, F AF Huq, AHMM Zhong, H Nabi, R Serajee, F TI Analysis of six candidate genes for autism on 7q. . SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA. Wayne State Univ, Dept Neurol, Detroit, MI 48202 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1898 BP 494 EP 494 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801901 ER PT J AU Nabi, R Zhong, H Chugani, DC Serajee, FJ AF Nabi, R Zhong, H Chugani, DC Serajee, FJ TI Analysis of five serotonin system genes in autism by association and linkage. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA. Wayne State Univ, Dept Neurol, Detroit, MI 48202 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1899 BP 494 EP 494 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801899 ER PT J AU Zhong, H Serajee, FJ Nabi, R Huq, AHMM AF Zhong, H Serajee, FJ Nabi, R Huq, AHMM TI Association of the metabotropic glutamate receptor 8 gene at 7q31 with quantitative traits in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA. Wayne State Univ, Dept Neurol, Detroit, MI 48202 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1900 BP 494 EP 494 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801902 ER PT J AU Beyer, KS Klauck, SM Blasi, F Bacchelli, E Benner, A Epp, S Poustka, F Maestrini, E Poustka, A AF Beyer, KS Klauck, SM Blasi, F Bacchelli, E Benner, A Epp, S Poustka, F Maestrini, E Poustka, A TI Candidate gene analysis in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany. Univ Bologna, Dept Biol, I-40126 Bologna, Italy. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1906 BP 495 EP 495 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801908 ER PT J AU McCauley, JL Dowd, M Olson, LM Amin, T Blakely, RD Folstein, SE Haines, JL Sutcliffe, JS AF McCauley, JL Dowd, M Olson, LM Amin, T Blakely, RD Folstein, SE Haines, JL Sutcliffe, JS TI Genetic linkage and association of haplotypes at the serotonin transporter locus in a rigid-compulsions subphenotype of autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Tufts Univ New England Med Ctr, Boston, MA 02111 USA. Tufts Univ, Dept Psychiat, Medford, MA 02155 USA. Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA. Vanderbilt Univ, Dept Physiol & Mol Biophys, Program Human Genet, Nashville, TN USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1913 BP 496 EP 496 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801912 ER PT J AU Nurmi, EL Olson, LM Jacobs, MM Amin, T McCauley, JL Lam, AY Folstein, SE Haines, JL Sutcliffe, JS AF Nurmi, EL Olson, LM Jacobs, MM Amin, T McCauley, JL Lam, AY Folstein, SE Haines, JL Sutcliffe, JS TI Dense linkage disequilibrium mapping in the 15q11-q13 maternal expression domain yields evidence for association in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Tufts Univ New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. Vanderbilt Univ, Dept Physiol & Mol Biophys, Program Human Genet, Nashville, TN USA. Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1914 BP 496 EP 496 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801915 ER PT J AU Maestrini, E Bacchelli, E Blasi, F Biondolillo, M Bailey, AJ Monaco, AP AF Maestrini, E Bacchelli, E Blasi, F Biondolillo, M Bailey, AJ Monaco, AP CA Int Molecular Genetic Study TI Analysis of nine candidate genes for autism on chromosome 2q. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Oxford, WTCHG, Oxford, England. Inst Psychiat, CSGDP, London, England. Univ Bologna, Dept Biol, I-40126 Bologna, Italy. RI Bailey, Anthony/J-2860-2014 OI Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1915 BP 497 EP 497 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801916 ER PT J AU Copeland-Yates, SA Schroer, RJ Skinner, C Michaelis, RC AF Copeland-Yates, SA Schroer, RJ Skinner, C Michaelis, RC TI Normal methylation pattern at the 5 ' SNRPN locus in patients from the South Carolina autism project. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1931 BP 499 EP 499 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801929 ER PT J AU Michaelis, RC Lobo-Menendez, F Sossey-Alaoui, K Copeland-Yates, S Bell, JM Plank, SM Sanford, SO Skinner, C Simensen, RJ Schroer, RJ AF Michaelis, RC Lobo-Menendez, F Sossey-Alaoui, K Copeland-Yates, S Bell, JM Plank, SM Sanford, SO Skinner, C Simensen, RJ Schroer, RJ TI Absence of MECP2 mutations in patients from the South Carolina autism project. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Presbyterian Coll, Clinton, SC USA. Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1945 BP 502 EP 502 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801945 ER PT J AU Cuccaro, M Donnelly, S Ravan, SA Abramson, RK Elston, L Decena, K Wright, HH Pericak-Vance, MA AF Cuccaro, M Donnelly, S Ravan, SA Abramson, RK Elston, L Decena, K Wright, HH Pericak-Vance, MA TI Chromosome 15 and autism: Clinical characterization of phenotype. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1957 BP 504 EP 504 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801957 ER PT J AU Walker, SJ Xu, ASL Vrana, KE AF Walker, SJ Xu, ASL Vrana, KE TI SELDI-TOF mass spectrometry as a tool for biomarker discovery in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Wake Forest Univ, Sch Med, Dept Physiol Pharmacol, Winston Salem, NC 27109 USA. Ciphergen Biosyst Inc, Fremont, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1958 BP 504 EP 504 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801960 ER PT J AU Auranen, M Vanhala, R Varilo, T Ayers, K Kempas, E Ylisaukko-oja, T Sinsheimer, JS Peltonen, L Jarvela, I AF Auranen, M Vanhala, R Varilo, T Ayers, K Kempas, E Ylisaukko-oja, T Sinsheimer, JS Peltonen, L Jarvela, I TI A genomewide screen for autism-spectrum disorders: Evidence for a major susceptibility locus on chromosome 3q25-27 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID RECEPTIVE LANGUAGE DISORDER; FINNISH MULTIPLEX FAMILIES; EARLY ADULT LIFE; LINKAGE ANALYSIS; WIDE SCAN; PEDIGREE ANALYSIS; FOLLOW-UP; POPULATION; GENE; SCHIZOPHRENIA AB To identify genetic loci for autism-spectrum disorders, we have performed a two-stage genomewide scan in 38 Finnish families. The detailed clinical examination of all family members revealed infantile autism, but also Asperger syndrome (AS) and developmental dysphasia, in the same set of families. The most significant evidence for linkage was found on chromosome 3q25-27, with a maximum two-point LOD score of 4.31 (Z(max) (dom)) for D3S3037, using infantile autism and AS as an affection status. Six markers flanking over a 5-cM region on 3q gave Z(max) (dom) >3, and a maximum parametric multipoint LOD score (MLS) of 4.81 was obtained in the vicinity of D3S3715 and D3S3037. Association, linkage disequilibrium, and haplotype analyses provided some evidence for shared ancestor alleles on this chromosomal region among affected individuals, especially in the regional subisolate. Additional potential susceptibility loci with two-point LOD scores >2 were observed on chromosomes 1q21-22 and 7q. The region on 1q21-22 overlaps with the previously reported candidate region for infantile autism and schizophrenia, whereas the region on chromosome 7q provided evidence for linkage 58 cM distally from the previously described autism susceptibility locus (AUTS1). C1 Univ Helsinki, Dept Med Genet, Biomedicum, Helsinki 00290, Finland. Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Helsinki, Cent Hosp, Mol Genet Lab, Helsinki, Finland. Univ Calif Los Angeles, Sch Med, Dept Biomath, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA 90024 USA. Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. RP Peltonen, L (reprint author), Univ Helsinki, Dept Med Genet, Biomedicum, Haartmanink 8, Helsinki 00290, Finland. 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If true, this would have major consequences for the interpretation of twin studies. Both studies compared the number of affected twin pairs among affected sib pairs to expected values in two separate samples of multiplex families and reported a substantial and significant excess of twin pairs. Using data from our epidemiological study in Western Australia, we investigated the possibility of an increased rate of autism in twins. All children born between 1980 and 1995 with autism, Asperger syndrome, or pervasive developmental disorder not otherwise specified (PDD-NOS) were ascertained. Of the 465 children with a diagnosis, 14 were twin births (rate 30.0/1,000) compared to 9,640 children of multiple births out of a total of 386,637 births in Western Australia between 1980 and 1995 (twin rate weighted to number of children with autism or PDD per year 26.3/1,000). These data clearly do not support twinning as a substantial risk factor in the etiology of autism. 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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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J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 BP 941 EP 946 DI 10.1086/342990 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 604HT UT WOS:000178613800020 PM 12297988 ER PT J AU Smalley, SL Kustanovich, V Minassian, SL Stone, JL Ogdie, MN McGough, JJ McCracken, JT MacPhie, IL Francks, C Fisher, SE Cantor, RM Monaco, AP Nelson, SF AF Smalley, SL Kustanovich, V Minassian, SL Stone, JL Ogdie, MN McGough, JJ McCracken, JT MacPhie, IL Francks, C Fisher, SE Cantor, RM Monaco, AP Nelson, SF TI Genetic linkage of attention-deficit/hyperactivity disorder on chromosome 16p13, in a region implicated in autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; COMPLEX TRAITS; TUBEROUS SCLEROSIS; GENOMEWIDE SCREEN; STRATEGIES; SYMPTOMS; FAMILIES; CHILDREN; SCAN; LOCI AB Attention-deficit/hyperactivity disorder (ADHD) is the most commonly diagnosed behavioral disorder in childhood and likely represents an extreme of normal behavior. ADHD significantly impacts learning in school-age children and leads to impaired functioning throughout the life span. There is strong evidence for a genetic etiology of the disorder, although putative alleles, principally in dopamine-related pathways suggested by candidate-gene studies, have very small effect sizes. We use affected-sib-pair analysis in 203 families to localize the first major susceptibility locus for ADHD to a 12-cM region on chromosome 16p13 (maximum LOD score 4.2; P =.000005), building upon an earlier genomewide scan of this disorder. The region overlaps that highlighted in three genome scans for autism, a disorder in which inattention and hyperactivity are common, and physically maps to a 7-Mb region on 16p13. These findings suggest that variations in a gene on 16p13 may contribute to common deficits found in both ADHD and autism. C1 Univ Calif Los Angeles, Ctr Neurobehav Genet, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA 90024 USA. Wellcome Trust Ctr Human Genet, Oxford, England. RP Smalley, SL (reprint author), Univ Calif Los Angeles, Ctr Neurobehav Genet, 760 Westwood Plaza, Los Angeles, CA 90024 USA. EM ssmalley@mednet.ucla.edu RI Nelson, Stanley/D-4771-2009; Monaco, Anthony/A-4495-2010; Fisher, Simon/E-9130-2012; Francks, Clyde/E-1384-2012 OI Monaco, Anthony/0000-0001-7480-3197; Fisher, Simon/0000-0002-3132-1996; CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Brown RT, 2001, PEDIATRICS, V107, DOI 10.1542/peds.107.3.e43 Cantwell DP, 1996, J AM ACAD CHILD PSY, V35, P978, DOI 10.1097/00004583-199608000-00008 Faraone SV, 2001, AM J PSYCHIAT, V158, P1052, DOI 10.1176/appi.ajp.158.7.1052 Fisher SE, 2002, AM J HUM GENET, V70, P1183, DOI 10.1086/340112 Greene RW, 1996, J AM ACAD CHILD PSY, V35, P571, DOI 10.1097/00004583-199605000-00011 Handen BL, 2000, J AUTISM DEV DISORD, V30, P245, DOI 10.1023/A:1005548619694 Hirschhorn JN, 2000, P NATL ACAD SCI USA, V97, P12164, DOI 10.1073/pnas.210394597 Bailey A, 1998, HUM MOL GENET, V7, P571 Palferman S, 2001, AM J HUM GENET, V69, P570 Khare L, 2001, J MED GENET, V38, P347, DOI 10.1136/jmg.38.5.347 KRUGLYAK L, 1995, AM J HUM GENET, V57, P439 LANDER E, 1995, NAT GENET, V11, P241, DOI 10.1038/ng1195-241 Lander ES, 2001, NATURE, V409, P860, DOI 10.1038/35057062 Levy F, 1997, J AM ACAD CHILD PSY, V36, P737, DOI 10.1097/00004583-199706000-00009 Liu JJ, 2001, AM J HUM GENET, V69, P327, DOI 10.1086/321980 Nyholt DR, 2000, AM J HUM GENET, V67, P282, DOI 10.1086/303029 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 RISCH N, 1990, AM J HUM GENET, V46, P222 RISCH N, 1990, AM J HUM GENET, V46, P229 Sergeant JA, 2002, BEHAV BRAIN RES, V130, P3, DOI 10.1016/S0166-4328(01)00430-2 Smalley SL, 1997, AM J HUM GENET, V60, P1276, DOI 10.1086/515485 Smalley SL, 2000, J AM ACAD CHILD PSY, V39, P1135, DOI 10.1097/00004583-200009000-00013 Smalley SL, 1998, J AUTISM DEV DISORD, V28, P407, DOI 10.1023/A:1026052421693 Swanson J, 2001, Curr Psychiatry Rep, V3, P92, DOI 10.1007/s11920-001-0005-2 Venter JC, 2001, SCIENCE, V291, P1304, DOI 10.1126/science.1058040 NR 27 TC 132 Z9 138 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 BP 959 EP 963 DI 10.1086/342732 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 604HT UT WOS:000178613800023 PM 12187510 ER PT J AU Visscher, PM AF Visscher, PM TI Increased rate of twins among affected sib pairs SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Letter ID AUTISM; GENETICS; ETIOLOGY C1 Univ Edinburgh, Inst Cell Anim & Populat Biol, Edinburgh EH9 3JT, Midlothian, Scotland. RP Visscher, PM (reprint author), Univ Edinburgh, Inst Cell Anim & Populat Biol, W Mains Rd, Edinburgh EH9 3JT, Midlothian, Scotland. CR Betancur C, 2002, AM J HUM GENET, V70, P1381, DOI 10.1086/340364 Field LL, 2002, DIABETOLOGIA, V45, P21, DOI 10.1007/s125-002-8241-7 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Greenberg DA, 2001, AM J HUM GENET, V69, P1062, DOI 10.1086/324191 KYVIK KO, 1995, BRIT MED J, V311, P913 Lauritsen MB, 2001, ACTA PSYCHIAT SCAND, V103, P411, DOI 10.1034/j.1600-0447.2001.00086.x SMITH C, 1970, ANN HUM GENET, V34, P85, DOI 10.1111/j.1469-1809.1970.tb00223.x NR 7 TC 7 Z9 7 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 BP 995 EP 996 DI 10.1086/342991 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 604HT UT WOS:000178613800030 PM 12387274 ER PT J AU Hodge, SE Greenberg, DA Betancur, C Gillberg, C AF Hodge, SE Greenberg, DA Betancur, C Gillberg, C TI Increased rate of twins among affected sib pairs - Response to Visscher SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Letter ID DEPENDENT DIABETES-MELLITUS; FAMILY HISTORY; AUTISM; CONCORDANCE; SIBLINGS; DISORDER; GENETICS; ETIOLOGY; FINLAND C1 New York State Psychiat Inst & Hosp, Unit 24, New York, NY 10032 USA. Columbia Univ, Div Stat Genet, Dept Biostat, New York, NY USA. Fac Med, INSERM, U513, Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RP Hodge, SE (reprint author), New York State Psychiat Inst & Hosp, Unit 24, 1051 Riverside Dr, New York, NY 10032 USA. CR AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 BAILEY A, 1995, PSYCHOL MED, V25, P63 Betancur C, 2002, AM J HUM GENET, V70, P1381, DOI 10.1086/340364 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x CAHILL GF, 1979, GEETIC ANAL COMMON D, P113 Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 Dorman JS, 1995, DIABETES AM, P165 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Greenberg DA, 2001, AM J HUM GENET, V69, P1062, DOI 10.1086/324191 JAMES JW, 1971, ANN HUM GENET, V35, P47, DOI 10.1111/j.1469-1809.1956.tb01377.x KAPRIO J, 1992, DIABETOLOGIA, V35, P1060, DOI 10.1007/BF02221682 KYVIK KO, 1995, BRIT MED J, V311, P913 Lauritsen MB, 2001, ACTA PSYCHIAT SCAND, V103, P411, DOI 10.1034/j.1600-0447.2001.00086.x PIVEN J, 1990, J AM ACAD CHILD PSY, V29, P177, DOI 10.1097/00004583-199003000-00004 RISCH N, 1990, AM J HUM GENET, V46, P222 RITVO ER, 1989, AM J PSYCHIAT, V146, P1032 SMITH C, 1974, AM J HUM GENET, V26, P454 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x THOMSON G, 1988, AM J HUM GENET, V43, P799 Visscher PM, 2002, AM J HUM GENET, V71, P995, DOI 10.1086/342991 Wickramaratne PJ, 2001, AM J HUM GENET, V68, P807, DOI 10.1086/318784 NR 22 TC 2 Z9 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 BP 996 EP 999 DI 10.1086/342992 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 604HT UT WOS:000178613800031 ER PT J AU Planche, P Lemonnier, E Moalic, K Labous, C Lazartigues, A AF Planche, P Lemonnier, E Moalic, K Labous, C Lazartigues, A TI Modalities of information processing in autistic children SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE cognitive disorders; infantile autism; information processing AB (T)he objective of this study was to refine the understanding of cognitive disorders in autism and to clarify the modes of information processing mobilized by the subjects. Seven children were examined, aged 4,9-9,1 with a diagnosis of moderate autism. The Kaufman Assessment Battery for Children (K-ABC) was presented to each child. The results support an executive functioning deficit interpretation and a weak drive for central coherence in autism. Pratical implications of this study in terms of follow up are also discussed. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved. C1 Fac Lettres & Sci Sociales Victor Segalen, Dept Psychol, F-29285 Brest, France. CHU Brest, Hop Bohars, F-29820 Bohars, France. RP Planche, P (reprint author), Fac Lettres & Sci Sociales Victor Segalen, Dept Psychol, 20 Rue Duquesne,BP 814, F-29285 Brest, France. 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PD OCT PY 2002 VL 160 IS 8 BP 559 EP 564 DI 10.1016/S0003-4487(02)00231-7 PG 6 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 619VX UT WOS:000179499100003 ER PT J AU Murphy, DGM Critchley, HD Schmitz, N McAlonan, G van Amelsvoort, T Robertson, D Daly, E Rowe, A Russell, A Simmons, A Murphy, KC Howlin, P AF Murphy, DGM Critchley, HD Schmitz, N McAlonan, G van Amelsvoort, T Robertson, D Daly, E Rowe, A Russell, A Simmons, A Murphy, KC Howlin, P TI Asperger syndrome - A proton magnetic resonance spectroscopy study of brain SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; POSITRON EMISSION TOMOGRAPHY; AUTISTIC DISORDER; MR SPECTROSCOPY; CEREBROSPINAL-FLUID; INFANTILE-AUTISM; CHILDHOOD AUTISM; TURNERS-SYNDROME; CINGULATE GYRUS; NEURONAL LOSS AB Background: Asperger syndrome (AS; an autistic disorder) is associated with impaired social skills and obsessional/repetitive behavior. Patients with autism have significant abnormalities in the frontal lobe and frontoparietal connectivity. Nobody has examined the relationship between abnormalities in the frontal and parietal lobes and clinical symptoms in people with AS. Methods: We used in vivo proton magnetic resonance spectroscopy to examine neuronal integrity of the medial prefrontal and parietal lobes in 14 non-learning-disabled adults with AS and 18 control subjects (of similar sex, age, and IQ). We obtained measures of the prefrontal lobe in 11, the parietal lobe in 13, and both lobes in 10 subjects with AS. We measured concentrations and ratios of N-acetylaspartate (NAA), creatine and phosphocreatine (Cr+PCr), and choline (Cho). Levels of NAA, Cr + PCr, and Cho are indicators of neuronal density and mitochondrial metabolism, phosphate metabolism, and membrane turnover. Frontal metabolite levels were correlated with scores on the Yale-Brown Obsessive Compulsive Scale and the Autism Diagnostic Interview. Results: Subjects with AS had a significantly higher prefrontal lobe concentration of NAA (z=-3.1; P=.002), Cr+PCr,(z=-2.2;P=.03), and Cho (z=-2.9;P=.003). Increased prefrontal NAA concentration was significantly correlated with obsessional behavior (tau=0.67; P=.005); increased prefrontal concentration of Cho, with social function (tau=0.72; P=.02). We found no significant differences in parietal lobe metabolite concentrations. Conclusion: Subjects with AS have abnormalities in neuronal integrity of the prefrontal lobe, which is related to severity of clinical symptoms. C1 Inst Psychiat, Neuroimaging Res Grp, London SE5 8AF, England. Univ London St Georges Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. RP Murphy, DGM (reprint author), Inst Psychiat, Neuroimaging Res Grp, De Crespigny Pk, London SE5 8AF, England. 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Gen. Psychiatry PD OCT PY 2002 VL 59 IS 10 BP 885 EP 891 DI 10.1001/archpsyc.59.10.885 PG 7 WC Psychiatry SC Psychiatry GA 602EX UT WOS:000178493800003 PM 12365875 ER PT J AU Platek, SM Gallup, GG AF Platek, SM Gallup, GG TI A self frozen in time and space: Catatonia as a kinesthetic analog to mirrored self-misidentification SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID MIND; RECOGNITION; SCHIZOPHRENIA; AWARENESS; CHILDREN; AUTISM; PEOPLE; BRAIN AB Aspects of Northoffs argument lend themselves to the ongoing investigation of localizing the self in the brain. Recent data from the fields of neuropsychology and cognitive neuroscience provide evidence that the right hemisphere is a candidate for localization of self, The data on catatonia further that proposition and add insight into the continuing investigation of self in the brain across sensory and motor domains. C1 Drexel Univ, Dept Psychol, Philadelphia, PA 19102 USA. SUNY Albany, Dept Psychol, Albany, NY 12222 USA. RP Platek, SM (reprint author), Drexel Univ, Dept Psychol, Philadelphia, PA 19102 USA. EM steven.m.platek@drexel.edu; gallup@csc.albany.edu CR Baron-Cohen S, 2000, NEUROSCI BIOBEHAV R, V24, P355, DOI 10.1016/S0149-7634(00)00011-7 BARONCOHEN S, 1994, BRIT J PSYCHIAT, V165, P640, DOI 10.1192/bjp.165.5.640 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BINKOWSKI F, 1999, NEUROIMAGE, V9, pS769 Breen N, 2001, NEUROCASE, V7, P239, DOI 10.1093/neucas/7.3.239 Craik FIM, 1999, PSYCHOL SCI, V10, P26, DOI 10.1111/1467-9280.00102 DAWSON G, 1984, J AUTISM DEV DISORD, V14, P383, DOI 10.1007/BF02409829 Feinberg TE, 2001, ALTERED EGOS BRAIN C FLETCHER PC, 1995, COGNITION, V57, P109, DOI 10.1016/0010-0277(95)00692-R Frith CD, 1996, PSYCHOL MED, V26, P521 GALLUP GG, 1982, AM J PRIMATOL, V2, P237, DOI 10.1002/ajp.1350020302 Gallup GG, 2002, BEHAV BRAIN SCI, V25, P36 Keenan JP, 1999, NEUROPSYCHOLOGIA, V37, P1421, DOI 10.1016/S0028-3932(99)00025-1 Keenan JP, 2000, TRENDS COGN SCI, V4, P338, DOI 10.1016/S1364-6613(00)01521-7 KEENAN JP, 2001, NATURE, V409, P304 LANGDON R, 2000, COGNITION, V82, P1 Langdon R, 1999, COGNITION, V71, P43, DOI 10.1016/S0010-0277(99)00018-9 NORTHOFF G, IN PRESS BEHAV BRAIN Nyberg L, 1995, NEUROREPORT, V7, P249, DOI 10.1097/00001756-199512000-00060 ORBACH J, 1966, ARCH GEN PSYCHIAT, V14, P41 PFENNIG A, 2001, THESIS U MAGDEBURG PLATEK SM, UNPUB INTEGRATED INT PLATEK SM, IN PRESS SCHIZOPHREN Platek SM, 2002, SCHIZOPHR RES, V57, P311 Preilowski B, 1977, Act Nerv Super (Praha), V19 Suppl 2, P343 Sarfati Y, 1999, PSYCHOL MED, V29, P613, DOI 10.1017/S0033291799008326 SPERRY RW, 1979, NEUROPSYCHOLOGIA, V17, P153, DOI 10.1016/0028-3932(79)90006-X Stone VE, 1998, J COGNITIVE NEUROSCI, V10, P640, DOI 10.1162/089892998562942 STRIK WK, IN PRESS ELECTROPHEN Stuss DT, 2001, BRAIN, V124, P279, DOI 10.1093/brain/124.2.279 VOGEL K, 2001, NEUROIMAGE, V4, P170 NR 31 TC 1 Z9 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0140-525X J9 BEHAV BRAIN SCI JI Behav. Brain Sci. PD OCT PY 2002 VL 25 IS 5 BP 589 EP + PG 8 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 833XA UT WOS:000222373400014 ER PT J AU Thackeray, EJ Richdale, AL AF Thackeray, EJ Richdale, AL TI The behavioural treatment of sleep difficulties in children with an intellectual disability SO BEHAVIORAL INTERVENTIONS LA English DT Article ID SEVERE LEARNING-DISABILITIES; DAYTIME BEHAVIOR; CHALLENGING BEHAVIOR; MENTAL-RETARDATION; WRIST ACTIGRAPHY; DISORDERS; AUTISM; ADOLESCENTS; DEPRIVATION; PATTERNS AB Reinforcement, instruction giving, partner support strategies, bedtime routine, and standard extinction were taught to the parents of three boys (aged 5-10 years) with an intellectual disability and sleeping difficulties. Sleep was measured using sleep diaries and actigraphy, and daytime behaviour was monitored using diaries and direct observation. At referral, all children needed a parent present to fall asleep, two had co-sleeping difficulties, and two had night waking difficulties. At post-intervention, all children were falling asleep independently, co-sleeping was eliminated for two children, and night waking was reduced in one child. An extinction burst was experienced by two children, with one family putting their child back to bed 259 times on the first night. Though one child still had night waking difficulties following intervention, actigraph recording demonstrated an improvement in his sleep quality. In addition to the children's independence, improvements were seen for sleep length, sleep latency, and morning wake time. However, improvements in daytime behaviour showed inconsistency across behaviours and settings. Improvement in sleep was maintained at a three month follow-up. It was concluded that using extinction to address sleep problems in children with an intellectual disability is effective and approved of by parents, but any impact on daytime behaviour is equivocal. Copyright (C) 2002 John Wiley Sons, Ltd. C1 RMIT Univ, Dept Psychol & Disabil Studies, Bundoora, Vic, Australia. RP Richdale, AL (reprint author), RMIT Univ, Dept Psychol & Disabil Studies, Bundoora, Vic, Australia. CR Acebo C, 1999, SLEEP, V22, P95 ANDERS A, 1997, J AM ACAD CHILD ADOL, V36, P9 Blood ML, 1997, SLEEP, V20, P388 BRAMBLE D, 2000, DEV DISABILITY BEHAV, P106 Bramble D, 1997, DEV MED CHILD NEUROL, V39, P543 Bramble D, 1996, CHILD CARE HLTH DEV, V22, P355, DOI 10.1046/j.1365-2214.1996.810810.x *CAMBR NEUR, 1998, ACT ACT L ACT MON RE Curfs LMG, 1999, GENET COUNSEL, V10, P345 Durand V. M., 1998, SLEEP BETTER GUIDE I EINFELD SL, 1998, DEV BEH CHECKL TEACH Ferber R, 1996, NEUROL CLIN, V14, P493, DOI 10.1016/S0733-8619(05)70271-1 Hering E, 1999, J AUTISM DEV DISORD, V29, P143, DOI 10.1023/A:1023092627223 Hudson A, 1995, BEHAV CHANGE, V12, P209 Johnson CR, 1996, CHILD ADOL PSYCH CL, V5, P673 KRIPKE DF, 1978, ELECTROEN CLIN NEURO, V44, P674, DOI 10.1016/0013-4694(78)90133-5 Lancioni GE, 1999, AM J MENT RETARD, V104, P170, DOI 10.1352/0895-8017(1999)104<0170:ROSFTS>2.0.CO;2 MINDE K, 1994, J AM ACAD CHILD PSY, V33, P1114, DOI 10.1097/00004583-199410000-00007 Mindell JA, 1999, J PEDIATR PSYCHOL, V24, P465, DOI 10.1093/jpepsy/24.6.465 O'Reilly MF, 2000, RES DEV DISABIL, V21, P125, DOI 10.1016/S0891-4222(00)00029-9 OwensStively J, 1997, J DEV BEHAV PEDIATR, V18, P314, DOI 10.1097/00004703-199710000-00005 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Pilcher JJ, 1996, SLEEP, V19, P318 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, 1993, J INTELLECT DEV DIS, V25, P147 SADEH A, 1995, SLEEP, V18, P288 SADEH A, 1994, J CONSULT CLIN PSYCH, V62, P63, DOI 10.1037//0022-006X.62.1.63 Sanders MR, 1993, BEHAV FAMILY INTERVE Schreck KA, 2001, BEHAV INTERVENT, V16, P265, DOI 10.1002/bin.98 Shinkoda H, 1998, PSYCHIAT CLIN NEUROS, V52, P157, DOI 10.1111/j.1440-1819.1998.tb01004.x THORPY M, 1995, SLEEP, V18, P285 Stores G, 1996, J CHILD PSYCHOL PSYC, V37, P907, DOI 10.1111/j.1469-7610.1996.tb01489.x Stores R, 1996, J APPL RES INTELLECT, V9, P145 SUZLERAZAROFF B, 1991, BEHAV ANAL LASTING C Weiskop S, 2001, AUTISM, V5, P209, DOI 10.1177/1362361301005002009 Wiggs L, 1999, J CHILD PSYCHOL PSYC, V40, P627, DOI 10.1017/S0021963099003881 Wiggs L, 1996, J INTELL DISABIL RES, V40, P518, DOI 10.1046/j.1365-2788.1996.799799.x Wiggs L, 2000, SLEEP MED REV, V4, P299, DOI 10.1053/smrv.1999.0094 NR 38 TC 17 Z9 17 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD OCT-DEC PY 2002 VL 17 IS 4 BP 211 EP 231 DI 10.1002/bin.123 PG 21 WC Psychology, Clinical SC Psychology GA 620FF UT WOS:000179522800002 ER PT J AU Kubina, RM Morrison, R Lee, DL AF Kubina, RM Morrison, R Lee, DL TI Benefits of adding precision teaching to behavioral interventions for students with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID FLUENCY AB Students with autism have a variety of learning characteristics that can provide challenges to teachers. Precision Teaching, a method providing frequent assessment of performance, facilitation of curricular decisions, and techniques for developing fluency, can help teachers enhance educational outcomes for students with autism. Teachers can use the techniques found in Precision Teaching to augment their current instructional methods. This article purposes to examine the potential benefits of adding Precision Teaching to behavioral interventions for children with autism. This paper will define Precision Teaching, and review its guidelines within the context of a hypothetical case study. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Penn State Univ, Dept Special Educ, University Pk, PA 16802 USA. Ohio State Univ, Columbus, OH 43210 USA. Penn State Univ, Great Valley, PA USA. RP Kubina, RM (reprint author), Penn State Univ, Dept Special Educ, 227 Cedar Bldg, University Pk, PA 16802 USA. CR ALIROSALES S, 2000, PRECISE FREE OPERANT BECK R, 1991, J PRECISION TEACHING, V8, P8 BEDIENT G, 1999, PRECISION TEACHING B Bernard C., 1957, INTRO STUDY EXPT MED Binder C, 1993, EDUC TECHNOL, P8 Binder C., 1990, TEACHING EXCEPTIONAL, V22, P24 BINDER C, 1990, PERFORMANCE IMPROVEM, V3, P74 BINDER C, 1988, YOUTH POLICY, V10, P12 Binder C, 1996, BEHAV ANALYST, V19, P163 BLOOM BS, 1986, ED LEADERSHIP FEB, P70 CANCIO EJ, 1994, J PRECISION TEACHING, V12, P15 CARBONE V, 2000, PROGR PARTN NAT C AU COOPER JO, 2000, EXCEPT CHILDREN, P268 DESJARDINS A, 1993, J PRECISION TEACHING, V10, P25 EATON MD, 1978, 4 R RES CLASSROOM, P167 ERICSSON KA, 1993, PSYCHOL REV, V100, P363, DOI 10.1037/0033-295X.100.3.363 FUCHS LS, 1986, EXCEPT CHILDREN, V53, P199 GREEN G, 1996, BEHAV INTERVENTION Y, P181 Haughton E. 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S., 1972, HDB STANDARD BEHAV C POTTS L, 1993, BEHAV ANALYST, V16, P177 SAGAN C, 1993, BROCAS BRAIN REFLECT Scott J, 2000, STUDENTS AUTISM CHAR SIMMONS EK, 1998, J PRECISION TEACHING, V13, P50 SIMPSON RL, 2000, AUTISM INFORMATION R Skinner B. F, 1953, SCI HUMAN BEHAV Skinner B. F., 1938, BEHAV ORGANISMS SKINNER BF, 1956, AM PSYCHOL, V11, P221, DOI 10.1037/h0047662 Strain PS, 1998, YOUNG EXCEPTIONAL CH, V1, P8, DOI 10.1177/109625069800100202 WEST RP, 1992, DESIGNS EXCELLENCE E, P113 WEST RP, 1990, TEACHING EXCEPTIONAL, V22, P4 WHITE OR, 1986, EXCEPT CHILDREN, V52, P522 White O. R., 1980, EXCEPTIONAL TEACHING NR 58 TC 5 Z9 5 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD OCT-DEC PY 2002 VL 17 IS 4 BP 233 EP 246 DI 10.1002/bin.122 PG 14 WC Psychology, Clinical SC Psychology GA 620FF UT WOS:000179522800003 ER PT J AU Randall, P AF Randall, P TI Eating an artichoke: A mother's perspective on Asperger syndrome SO CONTEMPORARY PSYCHOLOGY-APA REVIEW OF BOOKS LA English DT Book Review ID DISORDER; AUTISM C1 Univ Hull, Sch Community & Hlth Studies, Kingston Upon Hull HU6 7RX, N Humberside, England. RP Randall, P (reprint author), Univ Hull, Sch Community & Hlth Studies, Cottingham Rd, Kingston Upon Hull HU6 7RX, N Humberside, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Department for Education, 1994, COD PRACT ID ASS SPE Department for Education and Science, 1981, ED ACT Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 Fling Echo R., 2000, EATING ARTICHOKE MOT HOCKEY V, 1991, SPECIAL CHILDREN MAR, P22 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Mayes SD, 2001, J ABNORM CHILD PSYCH, V29, P263, DOI 10.1023/A:1010337916636 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Randall P., 1999, SUPPORTING FAMILIES SCHOPLER E, 1985, J AUTISM DEV DISORD, V15, P359, DOI 10.1007/BF01531780 Wing L, 1998, ASPERGER SYNDROME HI, P11 Zwaigenbaum L, 2001, CAN FAM PHYSICIAN, V47, P2037 NR 13 TC 0 Z9 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD OCT PY 2002 VL 47 IS 5 BP 621 EP 623 PG 3 WC Psychology, Multidisciplinary SC Psychology GA 600MV UT WOS:000178395400054 ER PT J AU DeLong, GR Ritch, CR Burch, S AF DeLong, GR Ritch, CR Burch, S TI Fluoxetine response in children with autistic spectrum disorders: correlation with familial major affective disorder and intellectual achievement SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PSYCHIATRIC-DISORDERS; SEROTONIN SYNTHESIS; CLUSTER-ANALYSIS; HISTORY; INDIVIDUALS; DEPRESSION; SUBGROUPS; PHENOTYPE; PATTERNS; PARENTS AB One hundred and twenty-nine children, 2 to 8 years old, with idiopathic autistic spectrum disorder diagnosed by standard instruments (Childhood Austim Ratings Scale and Autism Diagnostic Observation Schedule) were treated with fluoxetine (0.15 to 0.5mg/kg) for 5 to 76 months (mean 32 to 36 months), with discontinuation trials. Response criteria are described. Family histories were obtained using the family history method in repeated interviews. Fluoxetine response, family history of major affective disorder, and unusual intellectual achievement, pretreatment language, and hyperlexia were used to define a coherent subgroup of autistic spectrum disorder. Statistical analyses were post hoc. Of the children, 22 (17%) had an excellent response, 67 (52%) good, and 40 (31%) fair/poor. Treatment age did not correlate with response. Fluoxetine response correlated robustly with familial major affective disorder and unusual intellectual achievement, and with hyperlexia in the child. Family history of bipolar disorder and of unusual intellectual achievement correlated strongly. Five children developed bipolar disorder during follow-up. Fluoxetine response, family history of major affective disorder (especially bipolar), unusual achievement, and hyperlexia in the children appear to define a homogeneous autistic subgroup. Bipolar disorder, unusual intellectual achievement, and autistic spectrum disorders cluster strongly in families and may share genetic determinants. C1 Duke Univ, Med Ctr, Div Pediat Neurol, Dept Pediat, Durham, NC 27710 USA. RP DeLong, GR (reprint author), Duke Univ, Med Ctr, Div Pediat Neurol, Dept Pediat, Box 3936, Durham, NC 27710 USA. 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Med. Child Neurol. PD OCT PY 2002 VL 44 IS 10 BP 652 EP 659 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 608YK UT WOS:000178875300002 PM 12418789 ER PT J AU Jones, W Hesslink, J Courchesne, E Duncan, T Matsuda, K Bellugi, U AF Jones, W Hesslink, J Courchesne, E Duncan, T Matsuda, K Bellugi, U TI Cerebellar abnormalities in infants and toddlers with Williams syndrome SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID BEUREN-SYNDROME; BRAIN; AUTISM; GENETICS; CHILDREN; SIZE; HYPERCALCEMIA; NEUROBIOLOGY; NEUROANATOMY; PERSPECTIVE AB One commonly observed neuroanatomical abnormality in adults with Williams syndrome is an enlarged cerebellum relative to a small cerebrum. Our study is the first to examine neuroanatomy in young children with Williams syndrome. Clinical brain MRI was examined in nine young children with Williams syndrome (mean age 21 months, range 7 to 43 months) relative to nine age- and sex-matched normally developing control children (mean age 29 months, range 20 to 42 months), and two children with undiagnosed developmental disorders (6 and 41 months). Two neuroradiologists who were blinded to participant classification, hypotheses, and regions of interest for the study, sorted the brain scans into two groups on the basis of six neuroanatomical criteria. The raters placed more of the MR scans from children with Williams syndrome into a separate group when they analyzed features of the cerebellum, but not when they analyzed other brain regions. Based on their written comments, the raters focused on the large size of the cerebellum in the children with Williams syndrome. The results lead us to suggest that abnormal cerebellar enlargement is evident in those with Williams syndrome at an early age. 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Child Adolesc. Psych. PD OCT PY 2002 VL 11 IS 5 BP 201 EP 209 DI 10.1007/s00787-002-0284-0 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 635FZ UT WOS:000180389500001 PM 12469237 ER PT J AU Militerni, R Bravaccio, C Falco, C Fico, C Palermo, MT AF Militerni, R Bravaccio, C Falco, C Fico, C Palermo, MT TI Repetitive behaviors in autistic disorder SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; stereotypies; repetitive behaviours; CARS ID OBSESSIVE-COMPULSIVE DISORDER; MENTAL-RETARDATION; STEREOTYPED BEHAVIORS; ASPERGER-SYNDROME; TOTAL POPULATION; FOLLOW-UP; PREVALENCE; CHILDREN; ADULTS; SCALE AB Introduction. Repetitive behaviors are common in autistic disorder, as in other developmental disabilities. Behaviors as diverse as stereotypies, cognitive inflexibility, and a need for sameness are grouped together under DSM IV classification, even though they are diverse in phenomenology, underlying neural circuitry, and possible clinical significance. In order to better define repetitive behaviors, we studied the relationship between such behaviors and chronological age, developmental level, estimated IQ, presumed mood state, severity of illness, as well as behavior reactivity to environmental stimuli, in a group of 121 consecutive autistic children, aged 2-4 and 7-11 years. Results. Younger autistic children displayed more motor and sensory repetitive behaviors. Older children had more complex behaviors. Children with higher IQ scores, likewise, demonstrated more complex repetitive behaviors. Most motor behaviors and self injury showed features of reactivity. Conclusions. 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Child Adolesc. Psych. PD OCT PY 2002 VL 11 IS 5 BP 210 EP 218 DI 10.1007/s00787-002-0279-x PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 635FZ UT WOS:000180389500002 PM 12469238 ER PT J AU Noterdaeme, M Mildenberger, K Minow, F Amorosa, H AF Noterdaeme, M Mildenberger, K Minow, F Amorosa, H TI Evaluation of neuromotor deficits in children with autism and children with a specific speech and language disorder SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE specific language disorder; autism; neuromotor problems; neurological evaluation ID ASPERGER-SYNDROME; CLUMSINESS; IMPAIRMENT; MOVEMENTS AB Several studies have described problems in motor functions in children with autism and children with a specific speech and language disorder. The purpose of this study was to identify neuromotor deficits in these neurodevelopmentally impaired children. A standardised neurological examination was performed in 11 children with childhood autism, 11 children with an expressive language disorder, 11 children with a receptive language disorder and 11 control children. The children were matched for age and non-verbal IQ, not for gender. All children had a non-verbal IQ above 85. The neurological examination procedure allowed for a qualitative and quantitative assessment of five specific neurological subsystems: fine and gross motor functions, balance, co-ordination and oral motor functions. The high-functioning children with autism and the children with a specific language disorder (expressive or receptive) had more motor problems than the control children on most neurological subsystems. There were few statistically significant differences between the three groups of developmentally impaired children. The frequent co-occurrence of verbal and non-verbal, in particular neuromotor, deficits in developmentally impaired children put an additional burden on the development of these children and should be diagnosed as early as possible. C1 Aussenstelle Munchen Solln, Heckscher Klin, D-81479 Munich, Germany. Univ Munich, Inst Kinder & Jugendpsychiat & Psychotherapie, D-80336 Munich, Germany. Univ Munich, Inst Soziale Padiat, D-81377 Munich, Germany. RP Noterdaeme, M (reprint author), Aussenstelle Munchen Solln, Heckscher Klin, Wolfratshauser Str 350, D-81479 Munich, Germany. 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Child Adolesc. Psych. PD OCT PY 2002 VL 11 IS 5 BP 219 EP 225 DI 10.1007/s00787-002-0285-z PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 635FZ UT WOS:000180389500003 PM 12469239 ER PT J AU Hrdlicka, M Komarek, V Faladova, L Zumrova, A Kulisek, R Blatny, M Urbanek, T AF Hrdlicka, M Komarek, V Faladova, L Zumrova, A Kulisek, R Blatny, M Urbanek, T TI EEG abnormalities are not associated with symptom severity in child autism SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Charles Univ, Dept Child Psychiat, Prague, Czech Republic. Charles Univ, Dept Child Neurol, Prague, Czech Republic. Acad Sci Czech Republ, Inst Psychol, Brno, Czech Republic. RI Urbanek, Tomas/G-9427-2014; Blatny, Marek/H-4293-2014 OI Urbanek, Tomas/0000-0002-8807-4869; Blatny, Marek/0000-0001-9831-0637 CR Cohen D. J, 1997, HDB AUTISM PERVASIVE Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 NR 2 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S431 EP S431 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000745 ER PT J AU Beyer, KS Blasi, F Bacchelli, E Klauck, SM Maestrini, E Poustka, A AF Beyer, KS Blasi, F Bacchelli, E Klauck, SM Maestrini, E Poustka, A CA IMGSAC TI Mutation analysis of the coding sequence of the MECP2 gene in infantile autism SO HUMAN GENETICS LA English DT Article ID LINKED MENTAL-RETARDATION; PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; RETT-SYNDROME PATIENTS; X-CHROMOSOME; TWIN; INTERVIEW; REGION; PAIRS AB Mutations in the coding region of the methyl-CpG-binding protein 2 (MECP2) gene cause Rett syndrome and have also been reported in a number of X-linked mental retardation syndromes. Furthermore, such mutations have recently been described in a few autistic patients. In this study, a large sample of individuals with autism was screened in order to elucidate systematically whether specific mutations in MECP2 play a role in autism. The mutation analysis of the coding sequence of the gene was performed by denaturing high-pressure liquid chromatography and direct sequencing. Taken together, 14 sequence variants were identified in 152 autistic patients from 134 German families and 50 unrelated patients from the International Molecular Genetic Study of Autism Consortium affected relative-pair sample. Eleven of these variants were excluded for having an aetiological role as they were either silent mutations, did not cosegregate with autism in the pedigrees of the patients or represented known polymorphisms. The relevance of the three remaining mutations towards the aetiology of autism could not be ruled out, although they were not localised within functional domains of MeCP2 and may be rare polymorphisms. Taking into account the large size of our sample, we conclude that mutations in the coding region of MECP2 do not play a major role in autism susceptibility. Therefore, infantile autism and Rett syndrome probably represent two distinct entities at the molecular genetic level. C1 Deutsch Krebsforschungszentrum, Dept Mol Genome Anal H0600, D-69120 Heidelberg, Germany. Univ Bologna, Dept Biol, I-40126 Bologna, Italy. RP Beyer, KS (reprint author), Deutsch Krebsforschungszentrum, Dept Mol Genome Anal H0600, Neuenheimer Feld 280, D-69120 Heidelberg, Germany. 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Genet. PD OCT PY 2002 VL 111 IS 4-5 BP 305 EP 309 DI 10.1007/s00439-002-0786-3 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 611UC UT WOS:000179035300001 PM 12384770 ER PT J AU Downey, D Mraz, R Knott, J Knutson, C Holte, L Van Dyke, D AF Downey, D Mraz, R Knott, J Knutson, C Holte, L Van Dyke, D TI Diagnosis and evaluation of children who are not talking SO INFANTS AND YOUNG CHILDREN LA English DT Article DE articulation disorders; autism; communication disorders; hearing loss; mental retardation; speech and language delay ID LANGUAGE DISORDERS; HEARING-LOSS; SPEECH; BEHAVIOR; AUTISM AB "My child is not talking" is a concern voiced by many parents and families. Possible etiologies for developmental language disorders and articulation disorders are many: mental retardation, craniological disorders, cerebral palsy, autism, traumatic brain injury, hearing loss, sometimes there will be a single etiology: however, most times there are multiple etiologies, mild in nature, that come together to produce speeds and language delay. As health care providers, therapists, and educators it is essential that we assist the child's family in finding answers to their questions. We are wise to seek the advice of an interdisciplinary team of professionals to determine whether the child's communication abilities are developing normally or whether professional intervention is needed. It has been well documented that early diagnosis and treatment for speech and language problems greatly improve the child's overall prognosis, and can often prevent the development of additional disorders in the areas of behavior, learning, reading and social development. C1 Univ Iowa Hlth Care, Ctr Disabil & Dev, Div Dev Disabil, Iowa City, IA USA. RP Downey, D (reprint author), Univ Iowa Hlth Care, Ctr Disabil & Dev, Div Dev Disabil, Iowa City, IA USA. 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PD OCT PY 2002 VL 15 IS 2 BP 38 EP 48 PG 11 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 596QY UT WOS:000178177800005 ER PT J AU McConnell, SR AF McConnell, SR TI Interventions to facilitate social interaction for young children with autism: Review of available research and recommendations for educational intervention and future research SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE social interaction; autism; early intervention ID PRESCHOOL-CHILDREN; PEER INTERACTIONS; COMMUNICATIVE INTERACTION; SEVERE DISABILITIES; SOCIODRAMATIC PLAY; TEACHER PROMPTS; BEHAVIOR; SKILLS; INITIATIONS; MANAGEMENT AB The purpose of this paper is to review the knowledge available from aggregated research (primarily through 2000) on the characteristics of social interactions and social relationships among young children with autism, with special attention to strategies and tactics that promote competence or improved performance in this area. In its commissioning letter for the initial version of this paper, the Committee on Educational Interventions for Children with Autism of the National Research Council requested "a critical, scholarly review of the empirical research on interventions to facilitate the social interactions of children with autism, considering adult-child interactions (where information is available) as well as child-child interactions, and including treatment of [one specific question]: What is the empirical evidence that social irregularities of children with autism are amenable to remediation?" 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PD OCT PY 2002 VL 32 IS 5 BP 351 EP 372 DI 10.1023/A:1020537805154 PG 22 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700002 PM 12463515 ER PT J AU Goldstein, H AF Goldstein, H TI Communication intervention for children with autism: A review of treatment efficacy SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE autism; communication intervention; language development; social interaction ID HIGH-PROBABILITY REQUESTS; YOUNG-CHILDREN; LANGUAGE INTERVENTION; TIME-DELAY; DEVELOPMENTAL-DISABILITIES; RECIPROCAL INTERACTIONS; PRESCHOOL-CHILDREN; SPONTANEOUS SPEECH; TRAINING-PROGRAMS; BEHAVIOR PROBLEMS AB Empirical studies evaluating speech and language intervention procedures applied to children with autism are reviewed, and the documented benefits are summarized. In particular, interventions incorporating sign language, discrete-trial training, and milieu teaching procedures have been used successfully to expand the communication repertoires of children with autism. Other important developments in the field stem from interventions designed to replace challenging behaviors and to promote social and scripted interactions. The few studies of the parent and classroom training studies that included language measures also are analyzed. This article seeks to outline the extent to which previous research has helped identify a compendium of effective instructional practices that can guide clinical practice. It also seeks to highlight needs for further research to refine and extend current treatment approaches and to investigate more comprehensive treatment packages. C1 Florida State Univ, Tallahassee, FL 32306 USA. RP Goldstein, H (reprint author), Florida State Univ, Tallahassee, FL 32306 USA. 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Autism Dev. Disord. PD OCT PY 2002 VL 32 IS 5 BP 373 EP 396 DI 10.1023/A:1020589821992 PG 24 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700003 PM 12463516 ER PT J AU Baranek, GT AF Baranek, GT TI Efficacy of sensory and motor interventions for children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE sensorimotor therapies; evidence-based treatments; sensory integration ID LEARNING-DISABILITIES; YOUNG-CHILDREN; INFANTILE-AUTISM; STEREOTYPED BEHAVIORS; INTEGRATION TREATMENT; OCCUPATIONAL-THERAPY; PHYSICAL EXERCISE; PERFORMANCE; IMITATION; SYMPTOMS AB Idiosyncratic responses to sensory stimuli and unusual motor patterns have been reported clinically in young children with autism. The etiology of these behavioral features is the subject of much speculation. Myriad sensory- and motor-based interventions have evolved for use with children with autism to address such issues; however, much controversy exists about the efficacy of such therapies. This review paper summarizes the sensory and motor difficulties often manifested in autism, and evaluates the scientific basis of various sensory and motor interventions used with this population. Implications for education and further research are described. C1 Univ N Carolina, Clin Ctr Study Dev & Learning, Chapel Hill, NC 27599 USA. RP Baranek, GT (reprint author), Univ N Carolina, Clin Ctr Study Dev & Learning, Room 111 Med Sch Wing E,CB 7120, Chapel Hill, NC 27599 USA. 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Autism Dev. Disord. PD OCT PY 2002 VL 32 IS 5 BP 397 EP 422 DI 10.1023/A:1020541906063 PG 26 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700004 PM 12463517 ER PT J AU Horner, RH Carr, EG Strain, PS Todd, AW Reed, HK AF Horner, RH Carr, EG Strain, PS Todd, AW Reed, HK TI Problem behavior interventions for young children with autism: A research synthesis SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE autism; behavior support ID SELF-INJURIOUS-BEHAVIOR; FUNCTIONAL ASSESSMENT; FAMILY PERSPECTIVES; SUPPORT; REINFORCERS; DISABILITIES; STUDENTS; PEOPLE AB This paper provides a summary of research on behavioral interventions for children with autism 8 years of age or younger published between 1996 and 2000. The analysis is divided into four sections: (1) emerging themes in the technology of behavior support, (2) a review of existing research syntheses focusing on behavioral interventions, (3) a new literature review of current pertinent research, and (4) an evaluative discussion of the synthesis results and the field's future needs to develop effective behavioral interventions for young children with autism. The authors offer recommendations for strengthening the existing research base and advancing behavioral technology to meet the needs of the defined target population. C1 Univ Oregon, Eugene, OR 97403 USA. SUNY Stony Brook, Stony Brook, NY 11794 USA. Univ Colorado, Denver, CO 80204 USA. RP Horner, RH (reprint author), Univ Oregon, 1761 Alder,1235, Eugene, OR 97403 USA. 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PD OCT PY 2002 VL 32 IS 5 BP 423 EP 446 DI 10.1023/A:1020593922901 PG 24 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700005 PM 12463518 ER PT J AU Kasari, C AF Kasari, C TI Assessing change in early intervention programs for children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE autism; early intervention; measurement ID YOUNG-CHILDREN; BEHAVIORAL TREATMENT; JOINT ATTENTION; INDIVIDUAL-DIFFERENCES; LANGUAGE-DEVELOPMENT; SOCIODRAMATIC PLAY; PRESCHOOL-CHILDREN; SYMBOLIC PLAY; DISABILITIES; KNOWLEDGE AB Assessing the efficacy of any intervention can be a difficult task. In the case of children with autism who require comprehensive and long-lasting interventions, the task becomes even more difficult. In this paper, intervention studies based on comprehensive interventions for young children with autism are reviewed and examined in reference to elements that are essential to a well-designed treatment study, e. g., randomization/matching procedures, and outcome measures. Given the complexity of these comprehensive intervention programs, and the few data available on interventions with clear empirical validation, a plea is made for studies to consider the active ingredients or component parts of an intervention, e. g., number of hours, type of setting, and teaching approach. Suggestions are further made for improving future studies, including more rigorous designs, and measuring change. C1 Univ Calif Los Angeles, Los Angeles, CA 90095 USA. RP Kasari, C (reprint author), Univ Calif Los Angeles, Los Angeles, CA 90095 USA. CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Bimbrauer J. 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Autism Dev. Disord. PD OCT PY 2002 VL 32 IS 5 BP 447 EP 461 DI 10.1023/A:1020546006971 PG 15 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700006 PM 12463519 ER PT J AU Wolery, M Garfinkle, AN AF Wolery, M Garfinkle, AN TI Measures in intervention research with young children who have autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE outcome measures; measurement practices; treatment fidelity; risk factors; opportunity factors ID APPLIED BEHAVIOR ANALYSIS; SOCIAL-INTERACTION SKILLS; PARENT EDUCATION; TIME-DELAY; DISRUPTIVE BEHAVIOR; ABERRANT BEHAVIORS; PRESCHOOL-CHILDREN; PLAY SKILLS; HOME; COMMUNICATION AB In this paper, the outcome measures used in intervention research with young children with autism were analyzed. 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Autism Dev. Disord. PD OCT PY 2002 VL 32 IS 5 BP 463 EP 478 DI 10.1023/A:1020598023809 PG 16 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700007 PM 12463520 ER PT J AU Turnbull, HR Wilcox, BL Stowe, MJ AF Turnbull, HR Wilcox, BL Stowe, MJ TI A brief overview of special education law with focus on autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE autism; education; antidiscrimination; Individuals with Disabilities Education Act; Section 504 AB This article reviews the provisions of Individuals with Disabilities Education Act as they apply particularly to students with autism. It also refers to the antidiscrimination provisions of the Rehabilitation Act Amendments (Sec. 504) and to their relevance to students with autism. It attempts to answer specific questions posed by the National Academy of Science. C1 Univ Kansas, Beach Ctr Families & Disabil, Haworth, KS 66045 USA. RP Turnbull, HR (reprint author), Univ Kansas, Beach Ctr Families & Disabil, Haworth, KS 66045 USA. CR Sugai G., 1999, APPLYING POSITIVE BE Turnbull H. R., 2000, FREE APPROPRIATE PUB TURNBULL HR, IN PRESS J POSITIVE NR 3 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 OCT PY 2002 VL 32 IS 5 BP 479 EP 493 PG 15 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700008 PM 12463521 ER PT J AU Mandlawitz, MR AF Mandlawitz, MR TI The impact of the legal system on educational programming for young children with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Meeting of the Committee-on-Education-Interventions-for-Children-with-Autism CY APR, 2000 CL WASHINGTON, D.C. SP Committee Educ Intervent Children Autism DE autism; educational programming; due process; policy, law AB Since 1990, State Educational Agency (SEA) and Local Educational Agency (LEA) policies and practices of educational programming for young children with autism have evolved in response to the due process system and court decisions. This has become an issue because of an increase in the identification of children with autism, reclassification of children previously reported under other disability categories, publicity about the competition between methodologies, parent advocacy for specific methodologies, shortages of qualified personnel, and the demand for due process to ensure appropriate services. A review is made of substantive and procedural issues presented in due process and court cases, the legal standards used by hearing officers and judges, and a synthesis of the case law. It is recommended that school districts consider legal standards as programs are designed, that programs fit the unique needs of the child, that programs ensure appropriate progress educationally and socially, and that communication between parents and school districts be open and honest so that the due process system is used as the last resort. C1 MRM Associates, Washington, DC USA. RP Mandlawitz, MR (reprint author), MRM Associates, Washington, DC USA. NR 0 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 OCT PY 2002 VL 32 IS 5 BP 495 EP 508 DI 10.1023/A:1020502324718 PG 14 WC Psychology, Developmental SC Psychology GA 601EN UT WOS:000178433700009 PM 12463522 ER PT J AU Serra, M Loth, FL van Geert, PLC Hurkens, E Minderaa, RB AF Serra, M Loth, FL van Geert, PLC Hurkens, E Minderaa, RB TI Theory of mind in children with 'lesser variants' of autism: a longitudinal study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; child development; developmental delay; longitudinal studies; theory of mind; Pervasive Developmental Disorder; PDD-NOS ID PERVASIVE DEVELOPMENTAL DISORDER; HIGH-FUNCTIONING CHILDREN; ASPERGERS SYNDROME; BELIEF; ABILITIES; DEFICITS; EMOTIONS; PEOPLE; KNOWLEDGE; EMPATHY AB Background: The study investigated the development of theory-of-mind (ToM) knowledge in children with 'lesser variants' of autism (PDD-NOS) over a period thought to be critical for ToM development (i.e., 3 to 5 years of age). Method: The sample included 11 children with PDD-NOS; 23 normally developing children were included for cross-sectional comparison and 13 normally developing children for longitudinal comparison. The groups were comparable in verbal and non-verbal mental age. Two storybooks were used for repeated assessment of various aspects of the children's theory of mind: emotion recognition, the distinction between physical and mental entities, prediction of behaviour and emotions on the basis of desires and prediction of behaviour and emotions on the basis of beliefs. Results: The results showed that the children with PDD-NOS had specific difficulties in understanding and predicting other people's emotions on the basis of situational cues, desires and beliefs. However, their ability to predict actions from beliefs and desires were relatively intact. Compared to the normally developing children, these children achieved lower levels of theory-of-mind knowledge, both at time of initial assessment and approximately 6 months later. Conclusions: The data suggest that the theory-of-mind development of children with PDD-NOS is both delayed and deviant. The growth pattern of theory-of-mind skills in children with PDD-NOS seemed to be qualitatively different from the growth pattern found in the group of normally developing children. C1 Acad Ctr Child & Adolescent Psychiat, NL-9700 AR Groningen, Netherlands. Univ Groningen, Groningen, Netherlands. RP Serra, M (reprint author), Acad Ctr Child & Adolescent Psychiat, POB 660, NL-9700 AR Groningen, Netherlands. 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M., 1990, CHILDS THEORY MIND WELLMAN HM, 1990, COGNITION, V33, P321 WELLMAN HM, 1988, COGNITION, V30, P239, DOI 10.1016/0010-0277(88)90021-2 WELLMAN HM, 1986, CHILD DEV, V57, P910, DOI 10.2307/1130367 Wing L., 1996, AUTISTIC SPECTRUM GU Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 65 TC 22 Z9 23 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD OCT PY 2002 VL 43 IS 7 BP 885 EP 900 DI 10.1111/1469-7610.00104 PG 16 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 601UR UT WOS:000178467200007 PM 12405477 ER PT J AU Bishop, DVM Norbury, CF AF Bishop, DVM Norbury, CF TI Exploring the borderlands of autistic disorder and specific language impairment: a study using standardised diagnostic instruments SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; PDDNOS; pragmatics; language impairment; semantic-pragmatic disorder; diagnosis ID HIGH-LEVEL AUTISM; OBSERVATION SCHEDULE; CHILDREN AB Background: Two studies were conducted to test claims that pragmatic language impairment (PLI-previously referred to as semantic-pragmatic disorder) is simply another term for autistic disorder or pervasive developmental disorder not other-wise specified (PDDNOS). Method: In Study 1, 21 children aged from 6 to 9 years with language impairments were subdivided on the basis of the Children's Communication Checklist into 13 cases of pragmatic language impairment (PLI) and eight cases of typical specific language impairment (SLI-T). Parents completed the Autism Diagnostic Interview Revised (ADI-R) and the Social Communication Questionnaire (SCQ), and the children were given the Autism Diagnostic Observation Schedule - Generic (ADOS-G). In Study 2, a further 11 children with SLI-T and 18 with PLI were assessed using the SCQ and ADOS-G. In addition, six children diagnosed with high-functioning autism and 18 normally developing children were assessed. Results: There was good agreement between ADI-R and SCQ diagnoses, but poor agreement between diagnoses based on these parental report measures and those based on ADOS-G. In many children, symptom profiles changed with age. Four PLI children from Study I and one from Study 2 met criteria for autistic disorder on both parental report (ADI-R or SCQ) and ADOS-G. Many of the others showed some autistic features, but there was a subset of children with pragmatic difficulties who were not diagnosed as having autism or PDDNOS by either instrument. These children tended to use stereotyped language with abnormal intonation/ prosody, but they appeared sociable and communicative, had normal nonverbal communication, and showed few abnormalities outside the language/social communication domains. Conclusions: Presence of pragmatic difficulties in a child with communication problems should prompt the clinician to evaluate autistic symptomatology, but it is dangerous to assume that all children with pragmatic difficulties have autism or PDDNOS. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Bishop, DVM (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. CR Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Bishop D., 2000, SPEECH LANGUAGE IMPA, P99 BISHOP DVM, 1989, AGE COGNITIVE PERFOR Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 BISHOP DVM, 1987, CLIN DEV MED Bishop DVM, 2001, DEV MED CHILD NEUROL, V43, P809, DOI 10.1017/S0012162201001475 BROOK SL, 1992, J AUTISM DEV DISORD, V22, P61, DOI 10.1007/BF01046403 Conti-Ramsden G, 2001, J CHILD PSYCHOL PSYC, V42, P741, DOI 10.1111/1469-7610.00770 Conti-Ramsden G, 1999, J SPEECH LANG HEAR R, V42, P1195 Dunn L M., 1982, BRIT PICTURE VOCABUL Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 Joanette Y., 1997, AUTISM, V1, P37, DOI 10.1177/1362361397011006 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 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X Meyer M, 1969, FROG WHERE ARE YOU Noterdaeme M, 1999, Z KINDER JUG-PSYCH, V27, P251, DOI 10.1024//1422-4917.27.4.251 Rapin I, 1983, NEUROPSYCHOLOGY LANG, P155 RAPIN I, 1987, 1ST P INT S SPEC SPE, P20 RAVEN JC, 1986, RAVENS PROGRESSIVE M Semel E., 1987, CLIN EVALUATION LANG Shields J, 1996, DEV MED CHILD NEUROL, V38, P473 Shields J, 1996, DEV MED CHILD NEUROL, V38, P487 NR 24 TC 192 Z9 193 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD OCT PY 2002 VL 43 IS 7 BP 917 EP 929 DI 10.1111/1469-7610.00114 PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 601UR UT WOS:000178467200009 PM 12405479 ER PT J AU Kemner, C Willemsen-Swinkels, SHN de Jonge, M Tuynman-Qua, H van Engeland, H AF Kemner, C Willemsen-Swinkels, SHN de Jonge, M Tuynman-Qua, H van Engeland, H TI Open-label study of olanzapine in children with pervasive developmental disorder SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID ADULTS; ADOLESCENTS; AUTISM AB The effects of olanzapine on the symptomatology of children with pervasive developmental disorder with emphasis on problems of communication and the safety of the drug were investigated in a 3-month open-label, open-dosage study. Participating in the study were 25 children age 6 to 16 years with a diagnosis of either autistic disorder or pervasive developmental disorder not otherwise specified. Psychometric measures included the Clinical Global Impression of Severity/Improvement, the Aberrant Behavior Checklist, and the TARGET (a checklist of five target symptoms). Communication skills were assessed during behavioral analysis of a playroom session. Safety measures included clinical, chemistry variables, electrocardiography, the Simpson-Angus Neurological Rating Scale, the Barnes Akathisia Scale, and vital signs. Twenty-three children completed the study and showed significant improvement on three subscales of the Aberrant Behavior Checklist, (Irritability, Hyperactivity, and Excessive Speech) and the TARGET. The final mean dose was 10.7 mg/day. Several aspects of communication were also improved after olanzapine treatment However, only three children were considered responders in terms of the Clinical Global impression of Severity/Improvement. scores. The most important adverse events were weight gain, increased appetite, and loss of strength. Three children showed extrapyramidal symptoms that disappeared after the dose was lowered. Thus, while olanzapine was a relatively safe medication in children, its clinical relevance in children with pervasive developmental disorder may be limited. C1 Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, NL-3514 CX Utrecht, Netherlands. Univ Utrecht, Rudolf Magnus Inst Neurosci, Utrecht, Netherlands. Eli Lilly & Co, Utrecht, Netherlands. RP Kemner, C (reprint author), Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, F05-126,Heidelberglaan 100, NL-3514 CX Utrecht, Netherlands. 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Clin. Psychopharmacol. PD OCT PY 2002 VL 22 IS 5 BP 455 EP 460 DI 10.1097/01.jcp.0000033400.43191.6f PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 597EW UT WOS:000178210100003 PM 12352267 ER PT J AU Barbaresi, WJ Katusic, SK Colligan, RC Pankratz, VS Weaver, AL Jacobsen, SJ AF Barbaresi, WJ Katusic, SK Colligan, RC Pankratz, VS Weaver, AL Jacobsen, SJ TI Explaining the apparent increase in the incidence of autism in Olmsted County, Minnesota, from 1976 to 1997 SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Meeting Abstract C1 Mayo Clin, Rochester, MN USA. NR 0 TC 1 Z9 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD OCT PY 2002 VL 23 IS 5 BP 398 EP 399 PG 2 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 604CL UT WOS:000178598000027 ER PT J AU Sonoda, S Kitahara, M Nakayama, T AF Sonoda, S Kitahara, M Nakayama, T TI Detection of measles virus genome in bone-marrow aspirates from adults SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID PERIPHERAL MONONUCLEAR-CELLS; INFLAMMATORY-BOWEL-DISEASE; SECONDARY IMMUNE-RESPONSES; POLYMERASE CHAIN-REACTION; CROHNS-DISEASE; CHILDREN; INFECTION; AUTISM; GENE; RNA AB We investigated the presence of the measles virus genome in order to identify asymptomatic infections in the adult population. Bone-marrow aspirates were obtained from 179 patients, 20-96 years of age, for the diagnosis of malignant diseases (29 with malignant lymphoma, 28 with acute leukaemia, 21 with myelodysplastic syndrome, five with multiple myeloma and 96 with other diseases). The measles virus genome was detected in 17 (9.5%) of 179 individuals by RT-PCR and 28 (15.6%) through hybridization. The genomes detected in bone marrow were all in the same cluster, D5, the strain circulating during the study period, and no evidence of persistent infection was obtained. We conclude that asymptomatic infections of measles virus are common in adults and the presence of the measles virus genome would not be related to the pathogenesis of illness. C1 Kitasato Inst Life Sci, Lab Viral Infect, Minato Ku, Tokyo 1088641, Japan. Keio Univ, Sch Med, Dept Pediat, Shinjyuku Ku, Tokyo 1608582, Japan. Saiseikai Cent Hosp, Dept Internal Med, Minato Ku, Tokyo 1080073, Japan. RP Nakayama, T (reprint author), Kitasato Inst Life Sci, Lab Viral Infect, Minato Ku, Shirokane 5-9-1, Tokyo 1088641, Japan. 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PD OCT PY 2002 VL 83 BP 2485 EP 2488 PN 10 PG 4 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA 597BX UT WOS:000178203200018 PM 12237431 ER PT J AU Olsson, MB Hwang, CP AF Olsson, MB Hwang, CP TI Sense of coherence in parents of children with different developmental disabilities SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE depression; parental adaptation; sense of coherence ID BECK DEPRESSION INVENTORY; DISABLED-CHILDREN; RHEUMATOID-ARTHRITIS; PHYSICAL-DISABILITY; MENTAL-RETARDATION; MOTHERS; STRESS; ADJUSTMENT; FAMILIES; SUPPORT AB Background The aim of the present study was to test if Antonovsky's theory of sense of coherence can facilitate understanding: (1) individual differences in psychological adaptation in parents of children with intellectual disability (ID); and (2) why parents of children with ID generally experience higher levels of stress and depression than parents of children who develop normally. Methods Sense of coherence (SoC) and depression were assessed using the short SoC scale (13 items) and the Beck Depression Inventory in 216 families of children with ID and/or autism, and in 213 control families. Results It is argued that: (1) parents of children with ID with low SoC are at increased risk for developing depression compared to control parents with low SoC not experiencing this stressor; and (2) the life situation of parenting a child with ID may have a negative impact on parents' SoC levels that, in turn, will make them more vulnerable to experiencing stress and depression. Conclusion The SoC theory is valuable in understanding individual differences in psychological adaptation in parents of children with ID. C1 Univ Trollhattan Uddevalla, S-46228 Vanersborg, Sweden. Gothenburg Univ, Dept Psychol, S-41124 Gothenburg, Sweden. RP Olsson, MB (reprint author), Univ Trollhattan Uddevalla, Box 1236, S-46228 Vanersborg, Sweden. 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To date, however, personality theorists seldom have considered neuropsychological case material (Klein & Kihlstrom, 1998). In this paper we show how neuropsychological evidence can afford new insights for personality theorists. In particular, we show how examination of persons suffering from amnesia and autism can shed light on the way in which knowledge about self is represented in memory. We first review the literature on clinical amnesia and then present evidence from a new case study exploring the relation between personal and nonpersonal knowledge in a patient with autism. We conclude that the mind may have learning systems that are specialized both for acquiring and retrieving information about one's own personality. (C) 2002 Elsevier Science (USA). All rights reserved. C1 Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. RP Klein, SB (reprint author), Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. 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Res. Pers. PD OCT PY 2002 VL 36 IS 5 BP 490 EP 506 DI 10.1016/S0092-6566(02)00001-6 PG 17 WC Psychology, Social SC Psychology GA 601YQ UT WOS:000178477300006 ER PT J AU Maestro, S Muratori, F Cavallaro, MC Pei, F Stern, D Golse, B Palacio-Espasa, F AF Maestro, S Muratori, F Cavallaro, MC Pei, F Stern, D Golse, B Palacio-Espasa, F TI Attentional skills during the first 6 months of age in autism spectrum disorder SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; attention; social behaviors; intersubjectivity ID HOME MOVIES; CHILDREN; INFANCY; DIAGNOSIS; CHILDHOOD; ONSET; LIFE; 1ST AB Objective: To study the quality of early attention in autism spectrum disorder (ASD) through home movies. Method: Fifteen home movies from the first 6 months of life of children who later received a diagnosis of ASD were compared with home movies of 15 normal children. The diagnosis was performed after the third year of life of children by two senior child and adolescent psychiatrists using a checklist of symptoms according to the DSM-IV. The films of the two groups were mixed and rated by blind observers through a Grid for the Assessment of Attentional Skills in Infants, composed of 13 items grouped into three developmental areas. Results: Using multivariate analysis of variance, the authors found significant differences between the two groups for the items in the social attention and the social behavior areas; on the contrary, there were no differences in nonsocial attention. Conclusions: The authors pose some hypotheses about a specific early-appearing impairment of attention in ASD in which children shift their spontaneous attention mainly toward nonsocial stimuli rather than toward social stimuli. The importance of this finding for early diagnosis and treatment is underlined. C1 Univ Pisa, Sci Inst Stella Maris, Div Child Neuropsychiat, Pisa, Italy. Cornell Univ, New York, NY USA. Univ Paris 05, Paris, France. Univ Geneva, Geneva, Switzerland. RP Muratori, F (reprint author), IRCCS Stella Maris, Via Giacinti 2, I-56018 Calambrone, Pisa, Italy. 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PD OCT PY 2002 VL 1 IS 6 BP 352 EP 358 DI 10.1016/S1474-4422(02)00160-6 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 599PB UT WOS:000178343200019 PM 12849396 ER PT J AU Niemi, J Karna-Lin, E AF Niemi, J Karna-Lin, E TI Grammar and lexicon in facilitated communication: A linguistic authorship analysis of a Finnish case SO MENTAL RETARDATION LA English DT Article ID AUTISM AB This case study adds a new dimension to the discourse on the authorship issue in facilitated communication. The linguistic structure produced by a young Finnish man with severe cerebral palsy was examined. Data are based on transcripts he produced from 1993 until 1996 after facilitated communication had been introduced to him. In the data analysis, as explicit criteria for his idiosyncrasies, we used patterns typical of children acquiring Finnish as their first language and those found in normal slips of the tongue, acquired aphasia, and specific language impairment. Based on the analysis (i.e. the idiosyncrasy and agrammaticality of word-forms and sentences), we strongly suggest that his output can hardly be a product of any other speaker of Finnish, including that of his facilitators. C1 Univ Joensuu, FIN-80101 Joensuu, Finland. RP Niemi, J (reprint author), Univ Joensuu, POB 111, FIN-80101 Joensuu, Finland. EM jussi.niemi@joensuu.fi CR ALATALO T, 1999, OLEN JA SAAN SANOA BIKLEN D, 1990, HARVARD EDUC REV, V60, P291 BRANCH M, 1987, WORLDS MAJOR LANGUAG, P593 Cardinal DN, 1996, MENT RETARD, V34, P231 CARDINAL DN, 1997, CONTESTED WORDS CONT, P199 CROSSLEY R, 1992, TOP LANG DISORD, V12, P29 Crossley R., 1980, ANNIES COMING OUT DUCHAN JF, 1993, J SPEECH HEAR RES, V36, P1108 EBERLIN M, 1993, J AUTISM DEV DISORD, V23, P507, DOI 10.1007/BF01046053 FERGUSON DL, 1994, MENT RETARD, V32, P305 HAKULINEN A., 1979, NYKYSUOMEN LAUSEOPPI HIRSHOREN A, 1995, PSYCHOL SCHOOLS, V32, P109, DOI 10.1002/1520-6807(199504)32:2<109::AID-PITS2310320206>3.0.CO;2-0 Holmberg Anders, 1993, CASE OTHER FUNCTIONA Karlsson F., 1983, FINNISH GRAMMAR KARLSSON F, 1985, FOLIA LINGUIST, V29, P207 KLEWE L, 1993, J AUTISM DEV DISORD, V23, P559, DOI 10.1007/BF01046057 MONTEE BB, 1995, J APPL BEHAV ANAL, V28, P189, DOI 10.1901/jaba.1995.28-189 MYLES BS, 1994, PSYCHOL SCH, V3, P208 NIEMI J, 2000, J LANGUAGE VERBAL CO, V3, P80 NIEMI J, 1990, SPR S NEUR, P95 Niemi J, 1997, FOLIA LINGUIST, V31, P161, DOI 10.1515/flin.1997.31.1-2.161 Niemi J., 1990, AGRAMMATIC APHASIA C, P1013 NIEMI J, IN PRESS FESTSCHRIFT OGLETREE BT, 1993, FOCUS AUTISTIC BEHAV, V8, P1 Schubert A, 1997, MENT RETARD, V35, P347, DOI 10.1352/0047-6765(1997)035<0347:IWTTLE>2.0.CO;2 SIMON EW, 1994, J AUTISM DEV DISORD, V24, P647, DOI 10.1007/BF02172144 Spencer A., 1991, MORPHOLOGICAL THEORY Sulkala Helena, 1992, FINNISH VAZQUEZ CA, 1994, J AUTISM DEV DISORD, V24, P369, DOI 10.1007/BF02172234 VILKUNA M., 1989, FREE WORD ORDER FINN WHEELER DL, 1993, MENT RETARD, V31, P49 1995, SUOMEN KIELEN PERUSS NR 32 TC 15 Z9 15 PU AMER ASSOC MENTAL RETARDATION PI WASHINGTON PA 444 N CAPITOL ST, NW, STE 846, WASHINGTON, DC 20001-1512 USA SN 0047-6765 J9 MENT RETARD JI Ment. Retard. PD OCT PY 2002 VL 40 IS 5 BP 347 EP 357 DI 10.1352/0047-6765(2002)040<0347:GALIFC>2.0.CO;2 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 596GT UT WOS:000178156900001 PM 12215070 ER PT J AU Inui, N Katsura, Y AF Inui, N Katsura, Y TI Development of force control and timing in a finger-tapping sequence with an attenuated-force tap SO MOTOR CONTROL LA English DT Article DE finger-tapping; force control; timing; child; adolescent ID ADAPTIVE-CONTROL; RELATIVE FORCE; RETENTION; PATTERN; ADOLESCENTS; AUTISM; AGE AB We conducted an experiment to examine age-related differences in the control of force and timing in a finger-tapping sequence with an attenuated-force tap. Participants between 7 and 20 years old tapped on a load cell with feedback on practice trials. They were required to recall the force pattern (300 g, 300 g, 300 g, 100 g) and the intertap interval (400 ms) without feedback on test trials. Analysis indicated that the last attenuated tap affected the first three taps of the tapping sequence in adults and adolescents but not in children. Adults and adolescents appeared to respond with four taps as a chunk, resulting in a contextual effect on the timing of force control, but younger children had difficulty with such chunking. Further, adults and adolescents were able to more accurately produce individual force magnitudes to match target magnitudes than younger children. For the ratio of force in serial positions 1:4, 2:4, and 3:4, consequently, 7- to 8-year-old children had lower ratios than the other age groups. Although there was no difference among age groups for timing control of peak force to press duration as a control strategy of force, 7- to 8-year-old children spent more time to produce force than the other age groups. Peak force with a decreased force was more variable in the attenuated force serial position (4) than in the other serial positions in all five age groups. Peak force variability was particularly robust in younger children. These findings suggest that younger children have difficulty with both temporal and spatial (i.e., magnitude) components of force control. C1 Naruto Univ Educ, Dept Human Motor Control, Naruto 7728502, Japan. RP Inui, N (reprint author), Naruto Univ Educ, Dept Human Motor Control, Naruto 7728502, Japan. CR Bard C., 1990, DEV EYE HAND COORDIN, P283 DESMEDT JE, 1983, MOTOR CONTROL MECH H, P227 Harbst KB, 2000, MOTOR CONTROL, V4, P232 HENNINGSEN H, 1995, EXP BRAIN RES, V105, P304 Inui N, 2001, PERCEPT MOTOR SKILL, V92, P301, DOI 10.2466/PMS.92.1.301-308 Inui N, 2000, PERCEPT MOTOR SKILL, V91, P476, DOI 10.2466/PMS.91.6.476-482 Inui N, 2000, PERCEPT MOTOR SKILL, V91, P925 Inui N, 1998, PERCEPT MOTOR SKILL, V86, P403 Inui N, 1995, PERCEPT MOTOR SKILL, V81, P739 Inui N, 1999, PERCEPT MOTOR SKILL, V88, P1245, DOI 10.2466/PMS.88.3.1245-1250 Inui N, 2001, MOTOR CONTROL, V5, P385 IVRY RB, 1986, J MOTOR BEHAV, V18, P449 LEMON E, 1934, RES QUART, V5, P82 MILLER GA, 1956, PSYCHOL REV, V63, P81, DOI 10.1037/0033-295X.101.2.343 PIEK JP, 1993, PSYCHOL RES-PSYCH FO, V55, P116, DOI 10.1007/BF00419642 ROSENBUS.MH, 1968, PERCEPT MOTOR SKILL, V26, P1271 Schmidt R, 1988, MOTOR CONTROL LEARNI SHEA C H, 1982, Journal of Human Movement Studies, V8, P73 Vallbo A, 1981, MUSCLE RECEPTORS MOV, P263 WILLIAMS HG, 1992, J MOTOR BEHAV, V24, P165 Williams HM, 1933, PEDAGOG SEMIN J GEN, V43, P377 WILLIAMS K, 1985, J MOTOR BEHAV, V17, P389 WING AM, 1973, PERCEPT PSYCHOPHYS, V14, P5, DOI 10.3758/BF03198607 NR 23 TC 8 Z9 8 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, CHAMPAIGN, IL 61820-2200 USA SN 1087-1640 J9 MOTOR CONTROL JI Motor Control PD OCT PY 2002 VL 6 IS 4 BP 333 EP 346 PG 14 WC Neurosciences; Sport Sciences SC Neurosciences & Neurology; Sport Sciences GA 603TT UT WOS:000178576900003 PM 12429889 ER PT J AU Narita, N Kato, M Tazoe, M Miyazaki, K Narita, M Okado, N AF Narita, N Kato, M Tazoe, M Miyazaki, K Narita, M Okado, N TI Increased monoamine concentration in the brain and blood of fetal thalidomide- and valproic acid-exposed rat: Putative animal models for autism SO PEDIATRIC RESEARCH LA English DT Article ID NEUROTROPHIC FACTOR; SEROTONIN NEURONS; POPULATION; DISORDERS; SPECTRUM; ONTOGENY AB Autism is defined as a congenital neurodevelopmental disorder in which serotonergic dysfunction may be involved in its pathogenesis. One of the characteristic laboratory findings in autistic patients is hyperserotonemia, although its mechanism has not been elucidated to date because of difficulties in studying human patients. Recent reports have demonstrated that thalidomide or valproic acid exposure during early embryonic days (first trimester) in humans causes higher incidence of autism. Morphologic abnormalities found in autism (e.g. cerebellar anomalies, reduced motor neuron numbers) have been reported in animals administered with these teratogens prenatally, suggesting the possibility of the use of these animals as an experimental autistic model. In this study, we evaluated monoamine levels in the brain and blood of rats exposed to teratogens prenatally. Of the groups exposed to thalidomide on embryonic day (E)2, E4, E7, E9, and El 1, a significant increase of hippocampal serotonin was only observed in the group exposed on E9. Furthermore, E9 thalidomide and valproic acid exposure both resulted in an increase of hippocampal serotonin. frontal cortex dopamine, and hyperserotonemia. These results thus indicate that two potentially autism-inducing teratogens, thalidomide and valproic acid. have the same effect on early monoamine system development in the brain and the blood, which may explain the pathogenesis of autism. C1 Univ Tsukuba, Inst Basic Med Sci, Neurobiol Lab, Tsukuba, Ibaraki 3058575, Japan. Dokkyo Univ, Koshigaya Hosp, Dept Pediat, Sch Med, Koshigaya, Saitama, Japan. RP Narita, N (reprint author), Univ Tsukuba, Inst Basic Med Sci, Neurobiol Lab, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR ALTAR CA, 1994, J NEUROCHEM, V63, P1021 ANDERSON GM, 1990, ANN NY ACAD SCI, V600, P331, DOI 10.1111/j.1749-6632.1990.tb16893.x BAILEY A, 1995, PSYCHOL MED, V25, P63 Betancur C, 2002, MOL PSYCHIATR, V7, P67, DOI 10.1038/sj/mp/4000923 Calabrese L, 2000, AM J MED, V108, P487, DOI 10.1016/S0002-9343(99)00408-8 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Galter D, 1999, EUR J NEUROSCI, V11, P2444, DOI 10.1046/j.1460-9568.1999.00667.x Hansson SR, 1999, NEUROSCIENCE, V89, P243, DOI 10.1016/S0306-4522(98)00281-4 Hendricks T, 1999, J NEUROSCI, V19, P10348 Ichiyama T, 2000, BRAIN RES, V857, P246, DOI 10.1016/S0006-8993(99)02439-7 Ingram JL, 2000, NEUROTOXICOL TERATOL, V22, P319, DOI 10.1016/S0892-0362(99)00083-5 LAUDER JM, 1974, J COMP NEUROL, V155, P469, DOI 10.1002/cne.901550407 LAUDER JM, 1990, ANN NY ACAD SCI, V600, P297, DOI 10.1111/j.1749-6632.1990.tb16891.x Lesch KP, 1998, BIOL PSYCHIAT, V44, P179, DOI 10.1016/S0006-3223(98)00121-8 LIU JP, 1992, J NEUROSCI RES, V33, P248, DOI 10.1002/jnr.490330208 Mamounas LA, 1995, J NEUROSCI, V15, P7929 NANSON JL, 1992, ALCOHOL CLIN EXP RES, V16, P558, DOI 10.1111/j.1530-0277.1992.tb01417.x Narita N, 2001, PEDIATRICS, V107, P690, DOI 10.1542/peds.107.4.690 OKADO N, 1989, DEV BRAIN RES, V50, P217, DOI 10.1016/0165-3806(89)90197-1 Rodier PM, 1997, REPROD TOXICOL, V11, P417, DOI 10.1016/S0890-6238(97)80001-U STROMLAND K, 1994, DEV MED CHILD NEUROL, V36, P351 Uphouse L, 2000, BRAIN RES REV, V33, P242, DOI 10.1016/S0165-0173(00)00032-1 Williams G, 2001, DEV MED CHILD NEUROL, V43, P202, DOI 10.1017/S001216220100038X Ye WL, 1998, CELL, V93, P755, DOI 10.1016/S0092-8674(00)81437-3 Zhou FC, 2001, DEV BRAIN RES, V126, P147, DOI 10.1016/S0165-3806(00)00144-9 NR 25 TC 82 Z9 84 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 OCT PY 2002 VL 52 IS 4 BP 576 EP 579 DI 10.1203/01.PDR.0000028406.01104.76 PG 4 WC Pediatrics SC Pediatrics GA 598TA UT WOS:000178291500018 PM 12357053 ER PT J AU Perez-Alvarez, F Timoneda-Gallart, C AF Perez-Alvarez, F Timoneda-Gallart, C TI Emotional behaviors as a neurological dysfunction SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE behavior; cognition; emotion; masquerade defensive behavior theory neurological processing of information; PASS theory ID MEDIAL GENICULATE-BODY; ACOUSTIC STIMULI; PASS THEORY; AMYGDALA; RESPONSES; AUTISM; PROJECTIONS; HYPOTHESIS; DYSLEXIA; NUCLEUS AB Introduction. The hypothesis of the emotional component of behaviors can be explained by a specific neurological mechanism was stated. Patients and methods. A sample of 749 cases, all between 5 and 14 year old, with different behavioral and cognitive problems was selected from attendance to the Neuropediatric/Neuropsychopedagogic Unit from 1994 to 2000. A sub-sample of 20 cases with PASS planning processing scoring less than 1SD was also selected. A design of mainly qualitative research according to case analysis was followed, behavioral data being provided by patients and their parents and analyzed with video recorder assistance. To avoid the study to be biased techniques as triangulation were applied. Quantitative cognitive data were obtained by using DN:CAS battery for diagnosis of PASS processing. A procedure for diagnosis and treatment of behaviors, previously reported, was followed. The cases of the sub-sample were tested before and after emotional treatment without cognitive remediation, the results being tested by Student-t. Results. The responders were 82% according to not only the criterion of solution of the behavioral problem, for example, anorexia, psychosomatism, non-neurological paroxysm an so on, but also, the sufficient amelioration assessed by the patients, their parents and the researchers. All cases, however, were required the disappearance of observable defensive behaviors in enough quantity to deduce an important maturation change. Significant difference was observed in planning. Discussion. Defensive behaviors as masquerade behaviors are explained in the light of neurological reasons. The neurological processing of the 'sensibility' of danger is emphasized according to the most recent knowledge. Conclusion. All behaviors can activate the neurological processing of danger feeling. C1 Hosp Univ Dr Josep Trueta, Unidad Neuropediat, Unidad Neuropsicopedag, Serv Pediat, E-17007 Girona, Spain. 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Neurologia PD OCT 1 PY 2002 VL 35 IS 7 BP 612 EP 624 PG 13 WC Clinical Neurology SC Neurosciences & Neurology GA 606KP UT WOS:000178733400004 PM 12389145 ER PT J AU Martin, F Farnum, J AF Martin, F Farnum, J TI Animal-assisted therapy for children with pervasive developmental disorders SO WESTERN JOURNAL OF NURSING RESEARCH LA English DT Article ID PSYCHOEDUCATIONAL PROFILE; SEVERE DISABILITIES; AUTISM; INTERVENTIONS; BEHAVIOR AB The present study quantitatively evaluated the, effects of interaction with dogs on children with pervasive developmental disorders (PDD), disorders characterized by lack of social communications and abilities, While interacting with a therapist, children were exposed to three different conditions: (a) a nonsocial toy (ball), (b) a stuffed dog, and (c) a live dog. Prosocial and nonsocial interactions were evaluated in terms of both behavioral and verbal dimensions. Results show that children exhibited a more playful mood, were more focused, and were more aware of their social environments when in the presence of a therapy dog. These findings indicate that interaction with dogs may have specific benefits for this population and suggest that animal-assisted therapy (AAT) may he an appropriate form of therapy. C1 Washington State Univ, Coll Vet Med, Pullman, WA 99164 USA. RP Martin, F (reprint author), Washington State Univ, Coll Vet Med, Pullman, WA 99164 USA. 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W., 1986, ESSENTIAL PAPERS OBJ, P254 NR 33 TC 66 Z9 68 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0193-9459 J9 WESTERN J NURS RES JI West. J. Nurs. Res. PD OCT PY 2002 VL 24 IS 6 BP 657 EP 670 DI 10.1177/019394502236639 PG 14 WC Nursing SC Nursing GA 595JT UT WOS:000178106100005 PM 12365766 ER PT J AU Luna, B Minshew, NJ Garver, KE Lazar, NA Thulborn, KR Eddy, WF Sweeney, JA AF Luna, B Minshew, NJ Garver, KE Lazar, NA Thulborn, KR Eddy, WF Sweeney, JA TI Neocortical system abnormalities in autism - An fMRI study of spatial working memory SO NEUROLOGY LA English DT Article ID SACCADIC EYE-MOVEMENTS; POSITRON-EMISSION-TOMOGRAPHY; GLUCOSE-UTILIZATION; PREFRONTAL CORTEX; CHILDHOOD AUTISM; CINGULATE CORTEX; CORTICAL CONTROL; FRONTAL LOBES; ACTIVATION; MATURATION AB Objective: To test the hypothesis that deficits in spatial working memory in autism are due to abnormalities in prefrontal circuitry. Methods: Functional MRI (fMRI) at 3 T was performed in 11 rigorously diagnosed non-mentally retarded autistic and six healthy volunteers while they performed an oculomotor spatial working memory task and a visually guided saccade task. Results: Autistic subjects demonstrated significantly less task-related activation in dorsolateral prefrontal cortex (Brodmann area [BA] 9/46) and posterior cingulate cortex (BA 23) in comparison with healthy subjects during a spatial working memory task. In contrast, activation of autistic individuals was not reduced in other regions comprising the neural circuitry for spatial working memory including the cortical eye fields, anterior cingulate cortex, insula, basal ganglia, thalamus, and lateral cerebellum. Autistic subjects also did not demonstrate reduced activation in any brain regions while performing visually guided saccades. Conclusion: Impairments in executive cognitive processes in autism may be subserved by abnormalities in neocortical circuitry as evidenced by decreased activation in prefrontal and posterior cingulate circuitry during a spatial working memory task. C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Dept Neurol, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Dept Stat, Pittsburgh, PA 15213 USA. Univ Illinois, Dept Radiol, Chicago, IL USA. Univ Illinois, Dept Physiol, Chicago, IL USA. Univ Illinois, Dept Biophys, Chicago, IL USA. Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA. Univ Illinois, Dept Neurol, Chicago, IL USA. Univ Illinois, Dept Psychol, Chicago, IL 60680 USA. RP Luna, B (reprint author), Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Psychiat, 3501 Forbes Ave,Oxford Bldg,Rm 743, Pittsburgh, PA 15213 USA. 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SO A N A E-APPROCHE NEUROPSYCHOLOGIQUE DES APPRENTISSAGES CHEZ L ENFANT LA French DT Article DE Psychopathology; neuropsychology; autism; epilepsy ID ASPERGER-SYNDROME; INFANTILE-AUTISM; MIND; PET AB Child psychopathology and neuropsychology constitute complementary theoretical and methodological approaches When investigating infantile disorders, suffering and methods of adaptation. It seems clear that clinicians should henceforth attempt to integrate these approaches into their evaluative and therapeutic practices. After briefly putting into perspective these contrasting epistemological positions, we attempt-to illustrate this integrative approach by evoking the clinical, developmental case history of a child suffering from epilepsy from an early age and displaying autistic type, deficiencies in their cognitive and social functioning. C1 Univ Paris 05, Lab Psychol Clin & Psychopathol, Inst Psychol, F-75270 Paris 06, France. 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Enfant PD SEP PY 2002 VL 14 IS 3 BP 181 EP 186 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 644MZ UT WOS:000180923100004 ER PT J AU Moeschler, JB Mohandas, TK Hawk, AB Noll, WW AF Moeschler, JB Mohandas, TK Hawk, AB Noll, WW TI Estimate of prevalence of proximal 15q duplication syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article ID REGION; AUTISM; PATIENT C1 Dartmouth Coll Sch Med, Dept Clin Genet & Pediat, Lebanon, NH USA. Dartmouth Coll Sch Med, Dept Pathol, Lebanon, NH USA. RP Moeschler, JB (reprint author), Dartmouth Hitchcock Med Ctr, Dept Pediat, Clin Genet Program, 1 Med Ctr Dr, Lebanon, NH 03756 USA. 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PD SEP 1 PY 2002 VL 111 IS 4 BP 440 EP 442 DI 10.1002/ajmg.10419 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 586AW UT WOS:000177560700017 PM 12210307 ER PT J AU Baranek, GT Chin, YKH Hess, LMG Yankee, JG Hatton, DD Hooper, SR AF Baranek, GT Chin, YKH Hess, LMG Yankee, JG Hatton, DD Hooper, SR TI Sensory processing correlates of occupational performance in children with fragile X syndrome: Preliminary findings SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE developmental disabilities; sensory integration; sensory modulation ID TACTILE DEFENSIVENESS; MOTOR DEVELOPMENT; YOUNG-CHILDREN; BEHAVIOR; MALES; TRAJECTORIES; PREVALENCE; ENGAGEMENT; INFANT; AUTISM AB OBJECTIVES This preliminary study examined sensory processing and its relationship to occupational performance in children with fragile X syndrome (FXS) to guide research and evidence-based practice METHOD, Fifteen school-aged boys with full-mutation FXS were assessed with three occupational performance measures (School Function Assessment, Vineland Adaptive Behavior Scales, play duration) and three sensory processing measures (Sensory Profile, Tactile Defensiveness and Discrimination Test-Revised, Sensory Approach Avoidance Rating) Data were analyzed using partial correlation procedures RESULTS Several significant correlations were found, independent of effects of age and 10 Avoidance of sensory experiences (internally controlled) was associated with lower levels of school participation, self-care, and play Aversion to touch from externally controlled sources was associated with a trend toward greater independence in self-care-opposite of expectations CONCLUSION This study links sensory processing vulnerabilities with individual differences in occupational performance and supports a dynamic view of self-organizing systems Children's uses of avoidant versus independent behaviors may reflect different self-regulatory or coping strategies that potentially mediate the relationship between sensory processing deficits and occupational behaviors and warrant further investigation. 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PD SEP PY 2002 VL 52 IS 3 SU 1 BP S125 EP S126 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 591VG UT WOS:000177900500365 ER PT J AU Huq, AHMM Zhong, HL Nabi, R Chugani, DC Serajee, FJ AF Huq, AHMM Zhong, HL Nabi, R Chugani, DC Serajee, FJ TI Evidence for an additional susceptibility region for autism on human chromosome 7q36 SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2002 VL 52 IS 3 SU 1 BP S116 EP S117 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 591VG UT WOS:000177900500333 ER PT J AU Huq, AHMM Nabi, R Zhong, HL Chugani, DC Serajee, FJ AF Huq, AHMM Nabi, R Zhong, HL Chugani, DC Serajee, FJ TI Serotonergic neurotransmission and autism: A genetic analysis SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2002 VL 52 IS 3 SU 1 BP S115 EP S115 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 591VG UT WOS:000177900500328 ER PT J AU Lucarelli, P Palminiello, S Bottini, N De Luca, D Saccucci, P Elia, M Fiumara, A Curatolo, P AF Lucarelli, P Palminiello, S Bottini, N De Luca, D Saccucci, P Elia, M Fiumara, A Curatolo, P TI Association study of autism and chromosome 16p13 SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract RI Fiumara, Agata/F-7200-2012 NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2002 VL 52 IS 3 SU 1 BP S123 EP S123 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 591VG UT WOS:000177900500356 ER PT J AU Stump, MH Cooper, KL Newschaffer, CJ Capone, GT Mostofsky, SH Kates, WK Jann, AE Lanham, DC Kaufmann, WE AF Stump, MH Cooper, KL Newschaffer, CJ Capone, GT Mostofsky, SH Kates, WK Jann, AE Lanham, DC Kaufmann, WE TI Specificity of cerebellar vermian abnormalities in autism: A quantitative magnetic resonance imaging study SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2002 VL 52 IS 3 SU 1 BP S135 EP S136 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 591VG UT WOS:000177900500401 ER PT J AU Klin, A Jones, W Schultz, R Volkmar, F Cohen, D AF Klin, A Jones, W Schultz, R Volkmar, F Cohen, D TI Visual fixation patterns during viewing of naturalistic social situations as predictors of social competence in individuals with autism SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Annual Meeting of the National-Institute-of-Child-Health-and-Human-Development CY MAY 02, 2001 CL NEW HAVEN, CT SP NICHHD ID FACE RECOGNITION; ASPERGER-SYNDROME; SPEECH-PERCEPTION; EYE-MOVEMENT; CHILDREN; EXPERTISE; MECHANISMS; EXPRESSION; ATTENTION; STIMULI AB Background: Manifestations of core social deficits in autism are more pronounced in everyday settings than in explicit experimental tasks. To bring experimental n Measures in line with clinical observation, we report a novel method of quantifying atypical strategies of social monitoring in a setting that simulates the demands of daily experience. Enhanced ecological validity, was intended to maximize between-group effect sizes and assess the predictive utility of experimental variables relative to outcome measures of social competence. Methods: While viewing social scenes, eye-tracking technology measured visual fixations in 15 cognitively able males with autism and 15 age-, sex-, and verbal IQ-matched control subjects. We reliably coded fixations on 4 regions: mouth, eyes, body, and objects. Statistical analyses compared fixation time on regions of interest between groups and correlation of fixation time with outcome measures of social competence (ie, standardized measures of daily social adjustment and degree of autistic social symptoms). Results: Significant between-group differences were obtained for all 4 regions. The best predictor of autism was reduced eye region fixation time. Fixation on mouths and objects was significantly correlated with social functioning: increased focus on mouths predicted improved social adjustment and less autistic social impairment, whereas more time on objects predicted the opposite relationship. Conclusions: When viewing naturalistic social situations, individuals with autism demonstrate abnormal patterns of social visual pursuit consistent with reduced salience of eyes and increased salience of mouths, bodies, and objects. Fixation times on mouths and objects but not on eyes are strong predictors of degree of social competence. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Klin, A (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA. 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L., 1967, EYE MOVEMENTS VISION Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 54 TC 660 Z9 677 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD SEP PY 2002 VL 59 IS 9 BP 809 EP 816 DI 10.1001/archpsyc.59.9.809 PG 8 WC Psychiatry SC Psychiatry GA 592JV UT WOS:000177935300005 PM 12215080 ER PT J AU Ribeiro, KMN Assumpcao, FB Valente, KDR AF Ribeiro, KMN Assumpcao, FB Valente, KDR TI Landau-Kleffner and autistic regression: the importance of differential diagnosis SO ARQUIVOS DE NEURO-PSIQUIATRIA LA Spanish DT Article DE Landau-Kleffner syndrome; autistic regression; behavior disorder; epilepsy; EEG ID CHILDREN; APHASIA AB Some neurological disorders may present psychiatric signs and symptoms, therefore the search for an etiological diagnosis is crucial. The aim of this study is to report the case of a patient with a neurological disorder, diagnosed during a psychiatric admission. A boy with normal neuropsychomotor development until the age of 3 years, started presenting epileptic seizures, followed by behavioral disorder and language deterioration. During neurologic follow-up, the patient was referred to the Psychiatry Department with a diagnosis of autism, in this case an autistic regression (AR). During his admission, diagnosis of Landau-Kleffner syndrome (LKS) was established on clinical and EEG grounds. LKS is characterized by acquired aphasia, epilepsy, EEG abnormalities and behavioral changes, including autistic traits. Language regression is observed LKS and AR. We stress the main differences between these two entities because misdiagnosis may postpone early intervention and consequent benefits, as observed in our case. C1 FMUSP, HC, Inst Psiquiatria, Serv Eletrencefalog, BR-05403010 Sao Paulo, Brazil. FMUSP, HC, Inst Psiquiatria, Serv Psiquiatria Infancia & Adolescencia,SEPIA, BR-05403010 Sao Paulo, Brazil. FMUSP, Dept Psiquiatria, BR-05403010 Sao Paulo, Brazil. RI Valente, Kette/D-5609-2012 CR Aicardi J, 1999, REV NEUROLOGIA, V29, P380 Aicardi J, 1994, EPILEPSY CHILDREN AICARDI J, EPILEPSY CHILDREN, V2, P207 BEAUMANIOR A, 1995, CONTINUOUS SPIKES WA Beaumanoir Anne, 1992, P231 BINNIE CD, 1995, CHILD ADOLESCENT PSY, V3 BISHOP DVM, 1985, DEV MED CHILD NEUROL, V27, P705 DEONNA TW, 1991, J CLIN NEUROPHYSIOL, V8, P288, DOI 10.1097/00004691-199107010-00005 Guerreiro MM, 1996, EPILEPSIA, V37, P60, DOI 10.1111/j.1528-1157.1996.tb00513.x HIRATA ES, 1995, PSIQUIATRIA BASICA, P67 KAPLAN HI, 1997, COMPENDIO PSIQUIATRI, P324 LERMAN P, 1991, DEV MED CHILD NEUROL, V33, P257 MARESCAUX C, 1990, EPILEPSIA, V31, P768, DOI 10.1111/j.1528-1157.1990.tb05518.x Morrell F., 1992, Epilepsia, V33, P100 MORRELL F, 1989, Epilepsia, V30, P693 Morrell F, 1995, BRAIN, V118, P1529, DOI 10.1093/brain/118.6.1529 NEVILLE B, 2000, DEV DISABILITY BEHAV, P56 Organizacao Mundial da Saude, 1993, CLASS TRANST MENT CO OTUAMA LA, 1992, J NUCL MED, V33, P1758 REISS AL, 1985, J PEDIATR-US, V106, P247, DOI 10.1016/S0022-3476(85)80296-1 Tuchman R, 2000, J AUTISM DEV DISORD, V30, P485, DOI 10.1023/A:1005572128200 WILLIAMS DT, 1995, TRATADO PSIQUIATRIA, P642 YASUHARA A, 1991, EPILEPSIA, V32, P59, DOI 10.1111/j.1528-1157.1991.tb05612.x NR 23 TC 5 Z9 6 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD SEP PY 2002 VL 60 IS 3B BP 835 EP 839 DI 10.1590/S0004-282X2002000500027 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 595JU UT WOS:000178106200027 PM 12364957 ER PT J AU Scott, FJ Baron-Cohen, S Bolton, P Brayne, C AF Scott, FJ Baron-Cohen, S Bolton, P Brayne, C TI Brief report - Prevalence of autism spectrum conditions in children aged 5-11 years in Cambridgeshire, UK SO AUTISM LA English DT Article DE autism; autism spectrum; epidemiology; prevalence ID ASPERGER-SYNDROME; EPIDEMIOLOGY; POPULATION AB The study aimed to establish prevalence of the broader autistic spectrum, including Asperger syndrome, in 5- to 11-year-olds in Cambridgeshire, UK. Cases of diagnosed autism spectrum condition (ASC) in children who were in Cambridgeshire schools and aged between 5 and I I years on 31 December 1999 were sought using public records, screening instruments, educational psychology and special educational needs coordinator (SENCO) records. We report a prevalence of ASC in the age group 5- 11 years of almost 0.6 percent (5 7 in 10, 0 0 0). This is I I times higher than the rate of classic autism but in line with other recent national and international rates for the broader spectrum. In the responding mainstream schools the prevalence was 0.33 percent. In the responding special school population it was 12.5 percent. The overall sex ratio of the children with ASC replicated findings for classical autism of 4:1 (M: F), but in those children being educated in mainstream schools the sex ratio was 8:1 (M:F). C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 2AH, England. RP Scott, FJ (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x *CDC, 2000, PREV AUT BRICK TOWNS EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 KAZAKBERUMENT S, 1999, BRIT J PSYCHIAT, V175, P444 Kielinen M, 2000, EUR CHILD ADOLES PSY, V9, P162 Magnusson P, 2001, J AUTISM DEV DISORD, V31, P153, DOI 10.1023/A:1010795014548 WING L, 1981, PSYCHIAT RES, V5, P129, DOI 10.1016/0165-1781(81)90043-3 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 13 TC 83 Z9 83 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 231 EP 237 DI 10.1177/1362361302006003002 PG 7 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300001 PM 12212915 ER PT J AU Honda, H Shimizu, Y AF Honda, H Shimizu, Y TI Early intervention system for preschool children with autism in the community - The DISCOVERY approach in Yokohama, Japan SO AUTISM LA English DT Article DE autism; community services; early detection; early diagnosis; early intervention ID SPECIAL EDUCATIONAL TREATMENT; BEHAVIORAL TREATMENT AB The article reports on DISCOVERY, a conceptual model for a clinical system of early detection and early intervention in cases of autism that has been implemented in Yokohama, Japan. The minimal requirements for this system are subsystems dealing with detection, diagnosis and intervention, Specific issues involving early diagnosis that complicate the design of the system are the seemingly contradictory considerations of early versus precise diagnosis, the undifferentiated recognition of a child's disorder on the part of the parents, and the difficulty of establishing cooperative working relationships among related facilities. To overcome these issues, an 'interface' linking consecutive subsystems is emphasized in the DISCOVERY model. A clinical system based on this model has been developed in Yokohama. This system not only benefits clinical performance, but will also add significantly to research on autism. C1 Yokohama Rehabil Ctr, Kohoku Ku, Yokohama, Kanagawa 2220035, Japan. RP Honda, H (reprint author), Yokohama Rehabil Ctr, Kohoku Ku, 1770 Toriyama Cho, Yokohama, Kanagawa 2220035, Japan. 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The intervention was compared across two formats, a I day workshop and six individual sessions, and also with a non-intervention control group. The results indicated that, compared with the control group, parents in both intervention groups reported fewer problem behaviours and increased self-efficacy following the interventions, at both 4 weeks and 3 months follow-up. The results also showed a difference in self-efficacy between mothers and fathers, with mothers reporting a significantly greater increase in self-efficacy following intervention than fathers. There was no significant difference between the workshop format and the individual sessions. C1 Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. RP Sofronoff, K (reprint author), Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. 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B., 1999, EARLY EDUC DEV, V10, P445, DOI 10.1207/s15566935eed1004_2 MOUTON PY, 1988, J CLIN CHILD PSYCHOL, V17, P217, DOI 10.1207/s15374424jccp1703_4 PERKINS M, 1991, ARCH DIS CHILD, V66, P693 PEVSNER R, 1982, J BEHAV THER EXP PSY, V13, P119, DOI 10.1016/0005-7916(82)90052-0 Pincus D., 1999, EYBERG CHILD BEHAV I PRIOR M, 2000, UNDERSTANDING ASPERG RODRIGUE JR, 1992, J AUTISM DEV DISORD, V22, P249, DOI 10.1007/BF01058154 Ruma PR, 1996, BEHAV THER, V27, P159, DOI 10.1016/S0005-7894(96)80012-8 Sanderson MA, 1996, P FORAG GR, V5, P9 Serketich WJ, 1996, BEHAV THER, V27, P171, DOI 10.1016/S0005-7894(96)80013-X Solomonov YA, 1996, PISMA ZH TEKH FIZ+, V22, P1 NR 29 TC 55 Z9 57 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 271 EP 286 DI 10.1177/1362361302006003005 PG 16 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300004 PM 12212918 ER PT J AU Soderstrom, H Rastam, M Gillberg, C AF Soderstrom, H Rastam, M Gillberg, C TI Temperament and character in adults with Asperger syndrome SO AUTISM LA English DT Article DE anxiety; autism spectrum disorder; personality; rarity; Temperament and Character Inventory ID TRIDIMENSIONAL PERSONALITY QUESTIONNAIRE; NORMATIVE DATA; MODEL AB To study the personality characteristics of adults with Asperger syndrome, and investigate the value of self-rating personality inventories, we administered the Temperament and Character Inventory (TCI) to 31 outpatients with Asperger syndrome. The TCI is a self-rating personality inventory that has been validated in the Swedish general population. The results were compared with age- and sex-matched norm groups. Participants with Asperger syndrome scored significantly higher on harm avoidance and lower on self-directedness and cooperativeness. Reward dependence and novelty seeking tended to be low. They also had significantly higher rarity scores, reflecting idiosyncratic perspectives. The most common temperament configurations were 'obsessional', 'passive-dependent' and 'explosive'. Character, reflecting conceptual maturity, was poorly developed in the majority of our subjects. The self-ratings of persons with Asperger syndrome thus indicated anxious personalities with coping difficulties in the areas of social interaction and self-directedness, a picture corresponding to the clinical descriptions of Asperger syndrome. C1 Gothenburg Univ, S-41124 Gothenburg, Sweden. Univ London, London WC1E 7HU, England. RP Soderstrom, H (reprint author), Dept Forens Psychiat, Box 4024, S-42204 Hislings Backa, Sweden. RI Anckarsater, Henrik/C-2244-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Brandstrom S, 1998, COMPR PSYCHIAT, V39, P122, DOI 10.1016/S0010-440X(98)90070-0 Cloninger C. R., 1994, TEMPERAMENT CHARACTE Cloninger C. 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Scenarios involving embarrassing and non-embarrassing situations were presented to a group with autism and three comparison groups. Participants were required to rate the level of embarrassment felt by the protagonist and to justify their choices. The results indicated that those with autism generally gave similar ratings of embarrassment as the comparison groups, but did show significant difficulty with non-embarrassing scenarios, and in providing appropriate justifications for embarrassment. In addition, a significant relationship between scores from false belief tasks and justification scores was found, supporting the proposed link between theory of mind skills and understanding embarrassment. Participants with autism did, however, show a higher than expected understanding of this complex emotion. C1 Lincoln Univ, Lincoln, England. Univ Lincolnshire & Humberside, Kingston Upon Hull, N Humberside, England. RP Hillier, A (reprint author), Ohio State Univ, Dept Neurol, 1654 Upham Dr,469 Means Hall, Columbus, OH 43210 USA. CR BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BARONCOHEN S, 1991, CHILD DEV, V62, P385, DOI 10.1111/j.1467-8624.1991.tb01539.x Bennett JM, 2000, J HIST SEXUALITY, V9, P1 BENNETT M, 1991, J GENET PSYCHOL, V152, P303 BENNETT M, 1989, BRIT J DEV PSYCHOL, V7, P207 Buitelaar JK, 1999, DEV PSYCHOPATHOL, V11, P39, DOI 10.1017/S0954579499001947 BUSS AH, 1979, J PSYCHOL, V103, P227 CAPPS L, 1992, J CHILD PSYCHOL PSYC, V33, P1069 Dunn L. M., 1997, BRIT PICTURE VOCABUL, V2nd GOFFMAN E, 1956, AM J SOCIOL, V62, P264, DOI 10.1086/222003 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Harris P., 1989, COGNITION EMOTION, V3, P379, DOI DOI 10.1080/02699938908412713 Harris P. 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S., 1992, EMOTION SOCIAL BEHAV, P202 MILLER RS, 1996, EMBARRASSMENT PERNER J, 1985, J EXP CHILD PSYCHOL, V39, P437, DOI 10.1016/0022-0965(85)90051-7 Raven J.C., 1956, COLOURED PROGRESSIVE NR 28 TC 12 Z9 12 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 299 EP 314 DI 10.1177/1362361302006003007 PG 16 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300006 PM 12212920 ER PT J AU Solaas, KM Skjeldal, O Gardner, MLG Kase, BF Reichelt, KL AF Solaas, KM Skjeldal, O Gardner, MLG Kase, BF Reichelt, KL TI Urinary peptides in Rett syndrome SO AUTISM LA English DT Article DE opioids; peptides; Rett syndrome; urine ID ENDOGENOUS OPIOID SYSTEMS; DEVELOPING RAT-BRAIN; BETA-ENDORPHIN; DENDRITIC GROWTH; SPINE FORMATION; EXCRETION; MECP2; MUTATIONS; INCLUSION; CRITERIA AB Rett syndrome is a neuro-developmental disorder related to autistic behavior. Persons with autism have previously been found to have hyperpeptiduria. We here report a significantly higher level of peptides in the first fasting morning urine from 53 girls with Rett syndrome (both classical and congenital) compared with 53 healthy girls. This elevation in urinary peptides was similar to that in 35 girls with infantile autism. As in persons with autism, the individual levels of urinary peptides in the Rett syndrome group varied, and about a fifth were within the normal range. Levels of peptides were lower in girls with classic Rett syndrome than in girls with congenital Rett syndrome. This may be due to different etiological causes or to active and stagnant phases of the disease. Urine from girls with Rett syndrome was found to have higher frequency and higher levels of some urinary peptides that may cause inhibition of brain maturation and epilepsy. C1 Univ Oslo, Natl Hosp, Pediat Res Inst, N-0027 Oslo, Norway. Univ Oslo, Natl Hosp, Child Neurol Sect, Pediat Clin, N-0027 Oslo, Norway. Univ Bradford, Sch Biomed Sci, Bradford BD7 1DP, W Yorkshire, England. RP Reichelt, KL (reprint author), Univ Oslo, Natl Hosp, Pediat Res Inst, N-0027 Oslo, Norway. CR ABASSI Z, 1992, METABOLISM, V41, P683, DOI 10.1016/0026-0495(92)90303-R Amir RE, 1999, NAT GENET, V23, P185 Banks WA, 1996, NEUROTOXICOL TERATOL, V18, P711, DOI 10.1016/S0892-0362(96)00128-6 Belichenko PV, 1997, ACTA NEUROPATHOL, V93, P50 Bienvenu T, 2000, HUM MOL GENET, V9, P1377, DOI 10.1093/hmg/9.9.1377 BOHLEN P, 1980, INT J PEPT PROT RES, V16, P306 Cade R, 2000, NUTR NEUROSCI, V3, P57, DOI 10.1080/1028415042000198807 EHRMISCH A, 1983, J NEUROCHEM, V41, P1229 Gschanes A, 1999, BEHAV BRAIN RES, V100, P161, DOI 10.1016/S0166-4328(98)00127-2 HAGBERG B, 1985, BRAIN DEV-JPN, V7, P372 HAGBERG B, 1995, ACTA PAEDIATR, V84, P971, DOI 10.1111/j.1651-2227.1995.tb13809.x HAGBERG BA, 1994, PEDIATR NEUROL, V11, P5, DOI 10.1016/0887-8994(94)90082-5 HAUSER KF, 1989, J COMP NEUROL, V281, P13, DOI 10.1002/cne.902810103 HAUSER KF, 1987, BRAIN RES, V416, P157, DOI 10.1016/0006-8993(87)91509-5 Huppke P, 2000, HUM MOL GENET, V9, P1369, DOI 10.1093/hmg/9.9.1369 JOHNSTON MV, 1995, NEUROPEDIATRICS, V26, P119, DOI 10.1055/s-2007-979740 KERR AM, 1985, BRIT MED J, V291, P579 KERR AM, 2002, OUTCOMES NEURODEVELO, P241, DOI 10.1017/CBO9780511543876.011 KITT CA, 1995, NEUROPEDIATRICS, V26, P114, DOI 10.1055/s-2007-979739 LEBOYER M, 1994, AM J PSYCHIAT, V151, P1797 LORBER BA, 1990, BRAIN RES, V531, P329, DOI 10.1016/0006-8993(90)90795-D LUNDE H, 1982, J NEUROCHEM, V38, P238 MURAKAMI JW, 1992, AM J ROENTGENOL, V159, P177 MYARA I, 1984, LIFE SCI, V34, P1985, DOI 10.1016/0024-3205(84)90363-1 PAIER B, 1992, BEHAV BRAIN RES, V51, P23, DOI 10.1016/S0166-4328(05)80308-0 REICHELT K-L, 1990, Journal of Applied Nutrition, V42, P1 Reichelt K L, 1981, Adv Biochem Psychopharmacol, V28, P627 Reichelt Karl L., 1991, Brain Dysfunction, V4, P308 Reichelt WH, 1997, DEV BRAIN DYSFUNCT, V10, P44 REICHELT WH, 1997, POSSIBLE ROLE PEPTID, P227 Reichelt WH, 1998, J PEDIATR GASTR NUTR, V26, P305, DOI 10.1097/00005176-199803000-00012 Rett A, 1966, Wien Med Wochenschr, V116, P723 SHANAHAN MR, 2000, Patent No. 0069015 SHATTOCK P, 1990, Brain Dysfunction, V3, P328 STORM H, 1995, PEDIATR RES, V38, P205, DOI 10.1203/00006450-199508000-00012 Wan MM, 1999, AM J HUM GENET, V65, P1520, DOI 10.1086/302690 WATANABE Y, 1993, RES COMMUN CHEM PATH, V81, P323 ENGERSTROM IW, 1992, BRAIN DEV-JPN, V14, pS11 ZAGON IS, 1987, BRAIN RES, V412, P68, DOI 10.1016/0006-8993(87)91440-5 ZAGON IS, 1984, LIFE SCI, V35, P2057, DOI 10.1016/0024-3205(84)90563-0 NR 40 TC 8 Z9 9 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 315 EP 328 DI 10.1177/1362361302006003008 PG 14 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300007 PM 12212921 ER PT J AU Carrington, S AF Carrington, S TI Challenging behaviour and autism: Making sense - Making progress SO AUTISM LA English DT Book Review C1 Queensland Univ Technol, Brisbane, Qld, Australia. RP Carrington, S (reprint author), Queensland Univ Technol, Brisbane, Qld, Australia. RI Carrington, Suzanne/I-9756-2012 CR WHITAKER P, 2001, CHALLENGING BEHAV AU NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 329 EP 330 DI 10.1177/1362361302006003009 PG 2 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300008 ER PT J AU Boucher, J AF Boucher, J TI The development of autism: Perspectives from theory and research SO AUTISM LA English DT Book Review C1 Univ Warwick, Coventry CV4 7AL, W Midlands, England. RP Boucher, J (reprint author), Univ Warwick, Coventry CV4 7AL, W Midlands, England. CR BURACK JA, DEV AUTISM PERSPECTI NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 330 EP 334 DI 10.1177/1362361302006003010 PG 5 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300009 ER PT J AU Zarkowska, E AF Zarkowska, E TI Autism with severe learning difficulties SO AUTISM LA English DT Book Review C1 Appl Psychol Serv, Surrey, England. RP Zarkowska, E (reprint author), Appl Psychol Serv, Surrey, England. CR Jordan R, 2001, AUTISM SEVERE LEARNI NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2002 VL 6 IS 3 BP 334 EP 335 DI 10.1177/1362361302006003011 PG 2 WC Psychology, Developmental SC Psychology GA 588CC UT WOS:000177682300010 ER PT J AU Davis, BJ Smith, T Donahoe, P AF Davis, BJ Smith, T Donahoe, P TI Evaluating supervisors in the UCLA treatment model for children with autism: Validation of an assessment procedure SO BEHAVIOR THERAPY LA English DT Article; Proceedings Paper CT Meeting of the Association-for-Applied-Behavior-Analysis CY MAY, 2001 CL NEW ORLEANS, LOUISIANA SP Assoc Appl Behav Anal ID BEHAVIORAL INTERVENTION AB We examined the validity of competency measures for supervisors of early, intensive behavioral intervention (EIBI) for children with autism by comparing 26 supervisors and 22 aides on a behavior observation of participants' therapy and written examinations on instructional programming, ability to critique others' therapy, and knowledge of EIBI and autism. A discriminant analysis based on these measures correctly classified 97% of participants into their respective groups. The correct classification rate for the programming examination (95%) exceeded that for the behavior observation (78%), critique (73%), and written examination (88%). The results indicated that the measures had validity and that the program examination was especially useful. C1 Univ Rochester, Med Ctr, Strong Ctr Dev Disabil, Rochester, NY 14642 USA. Washington State Univ, Pullman, WA 99164 USA. RP Smith, T (reprint author), Univ Rochester, Med Ctr, Strong Ctr Dev Disabil, 601 Elmwood Ave,Box 671, Rochester, NY 14642 USA. CR *AUT SPEC INT GROU, 1998, GUID CONS APPL BEH A *CAL BOARD ED, 1999, FULL BOARD SESS MIN Cronbach L. 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Therapy PD FAL PY 2002 VL 33 IS 4 BP 601 EP 614 DI 10.1016/S0005-7894(02)80019-3 PG 14 WC Psychology, Clinical SC Psychology GA 607CZ UT WOS:000178774900008 ER PT J AU Binnie, LM Williams, JM AF Binnie, LM Williams, JM TI Intuitive psychological, physical and biological knowledge in typically developing preschoolers, children with autism and children with Down's syndrome SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID FALSE-BELIEF TASKS; COGNITIVE-DEVELOPMENT; CONCEPTUAL CHANGE; CORE DOMAINS; MIND; INDIVIDUALS; SPECIFICITY; RELIABILITY; UNDERSTAND; ABILITIES AB This study investigated intuitive concepts of biology, physics and psychology in typical preschoolers (N = 23), children with autism (N = 20) and children with Down's syndrome (DS; N = 18). Three tasks from Peterson and Siegal (1997) (false belief (Baron-Cohen, Leslie, & Frith, 1985), Use photo (Zaitchik, 1990) and innate potential (Gelman & Wellman, 1991)) were employed. A further three tasks (perception (Slaughter & Gopnik, 1996), balance (Siegler, 1976) and illness (Kalish, 1998)) were included to gain insight into the similarities and differences in understanding across groups of children and within each domain. Preschoolers performed well on both the intuitive psychology tasks, children with autism performed poorly on these tasks, and children with DS performed well on the perception task but poorly on the false belief task. By contrast, performance on the physics and biology tasks was not significantly different across groups. These findings support the argument that cognitive development is domain-specific and highlight the need for further research in this area. C1 Univ Edinburgh, Fac Educ, Edinburgh EH8 8AQ, Midlothian, Scotland. RP Williams, JM (reprint author), Univ Edinburgh, Fac Educ, St Johns Land,Holyrood Rd, Edinburgh EH8 8AQ, Midlothian, Scotland. EM Jo.Williams@education.ed.ac.uk CR Atran S, 1999, FOLKBIOLOGY, P119 Baillargeon R., 2000, INFANT DEV ESSENTIAL, P195 BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 BARONCOHEN S, 1993, COGNITION EMOTION, V7, P507, DOI 10.1080/02699939308409202 BARONCOHEN S, 1989, BRIT J DEV PSYCHOL, V7, P113 Baron-Cohen S, 1999, BRIT J PSYCHIAT, V175, P484, DOI 10.1192/bjp.175.5.484 Baron-Cohen S., 1997, NEW DIR CHILD ADOLES, V75, P45 BARONCOHEN S, 2000, UNDERSTANDING OTHER, P73 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen S, 1997, AUTISM INT J RES PRA, V1, P153 BARONCOHEN S, 1991, CHILD DEV, V62, P385, DOI 10.1111/j.1467-8624.1991.tb01539.x CAREY S, 2001, CONCEPTUAL CHANGE 3 Carey S., 1994, MAPPING MIND DOMAIN, P169, DOI 10.1017/CBO9780511752902.008 Carey Susan, 1985, CONCEPTUAL CHANGE CH Charman T, 1997, J CHILD PSYCHOL PSYC, V38, P725, DOI 10.1111/j.1469-7610.1997.tb01699.x DIAMOND A, 1991, J PIAGET SY, P67 Dunn L. 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F., 1997, AUTISM EXECUTIVE DIS, P143 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Peters CD, 1997, BIOCHEM CELL BIOL, V75, P55, DOI 10.1139/bcb-75-1-55 Peterson CC, 1998, BRIT J DEV PSYCHOL, V16, P301 Russell J., 1998, AUTISM EXECUTIVE DIS RUSSELL J, 1991, BRIT J DEV PSYCHOL, V9, P331 Russell J, 1999, J CHILD PSYCHOL PSYC, V40, P859, DOI 10.1017/S0021963099004229 SIEGLER RS, 1976, COGNITIVE PSYCHOL, V8, P481, DOI 10.1016/0010-0285(76)90016-5 Slaughter V, 1996, CHILD DEV, V67, P2967, DOI 10.1111/j.1467-8624.1996.tb01898.x SPELKE ES, 1992, PSYCHOL REV, V99, P605, DOI 10.1037//0033-295X.99.4.605 Springer K., 1999, CHILDRENS UNDERSTAND, P45, DOI 10.1017/CBO9780511659881.004 TAGERFULSBERG H, 2000, COGNITION, V76, P58 Wellman H., 1997, NEW DIRECTIONS CHILD, V75 Wellman H. M., 1997, NEW DIR CHILD ADOLES, V75, P7 WELLMAN HM, 1992, ANNU REV PSYCHOL, V43, P337, DOI 10.1146/annurev.ps.43.020192.002005 WELLMAN HM, 2000, CHILDHOOD COGNITIVE, P267 Wellman HM, 2000, UNDERSTANDING OTHER, P21 Williams JM, 2002, BRIT J HEALTH PSYCH, V7, P129, DOI 10.1348/135910702169402 Williams JM, 2000, BRIT J DEV PSYCHOL, V18, P625, DOI 10.1348/026151000165896 Wishart J. G., 1996, DOWNS SYNDROME PSYCH, P81 Wishart J. G., 1999, BLACKWELL READER DEV, P493 Wishart JG., 1996, NEW APPROACHES DOWN, P173 Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x ZAITCHIK D, 1990, COGNITION, V35, P41, DOI 10.1016/0010-0277(90)90036-J Zelazo PD, 1996, J CHILD PSYCHOL PSYC, V37, P479, DOI 10.1111/j.1469-7610.1996.tb01429.x NR 70 TC 7 Z9 7 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 SEP PY 2002 VL 20 BP 343 EP 359 DI 10.1348/026151002320620361 PN 3 PG 17 WC Psychology, Developmental SC Psychology GA 594NY UT WOS:000178058100003 ER PT J AU Carpenter, M Call, J Tomasello, M AF Carpenter, M Call, J Tomasello, M TI Understanding "prior intentions" enables two-year-olds to imitatively learn a complex task SO CHILD DEVELOPMENT LA English DT Article ID CHIMPANZEES PAN-TROGLODYTES; CHILDREN HOMO-SAPIENS; MISTAKES; RECALL; AUTISM; TOOL AB This study investigated children's understanding of others' intentions in a social learning context. Specifically, it investigated whether knowing an adult's prior intention before the adult gives a demonstration influences what children learn from the demonstration. In the five main experimental conditions, ninety-six 2-year-old children watched as an experimenter (E) pulled out a pin and opened the door of a box. Children in two No Prior Intention conditions saw this demonstration alone or paired with an irrelevant action. Children in three Prior Intention conditions knew what E was trying to do before the demonstration: they first saw E either attempt unsuccessfully to open the door, or visit and open several other containers, or they first saw that the door opened. Children opened the box themselves more often in each of these three conditions than in the two No Prior Intention conditions, even though children in all five conditions saw the exact same demonstration of how to open the box. C1 Max Planck Inst Evolutionary Anthropol, D-04103 Leipzig, Germany. RP Carpenter, M (reprint author), Max Planck Inst Evolutionary Anthropol, Inselstr 22, D-04103 Leipzig, Germany. CR ASTINGTON JW, 1991, CHILDRENS THEORIES OF MIND : MENTAL STATES AND SOCIAL UNDERSTANDING, P157 BAUER PJ, 1992, COGNITIVE DEV, V7, P1, DOI 10.1016/0885-2014(92)90002-9 BAUER PJ, 1993, CHILD DEV, V64, P1204, DOI 10.1111/j.1467-8624.1993.tb04196.x Bekkering H, 2000, Q J EXP PSYCHOL-A, V53, P153, DOI 10.1080/027249800390718 Belles JM, 1999, MOL PLANT MICROBE IN, V12, P227, DOI 10.1094/MPMI.1999.12.3.227 Call J, 1998, J COMP PSYCHOL, V112, P192, DOI 10.1037/0735-7036.112.2.192 CALL J, 2002, UNPUB FOCUSING OUTCO CALL J, 2002, IMITATION ANIMALS AR Carpenter M, 1998, INFANT BEHAV DEV, V21, P315, DOI 10.1016/S0163-6383(98)90009-1 Hobson RP, 1999, J CHILD PSYCHOL PSYC, V40, P649, DOI 10.1111/1469-7610.00481 Meltzoff AN, 1995, DEV PSYCHOL, V31, P1, DOI DOI 10.1037/0012-1649.31.5.838 NAGELL K, 1993, J COMP PSYCHOL, V107, P174, DOI 10.1037/0735-7036.107.2.174 Phillips W, 1998, BRIT J DEV PSYCHOL, V16, P337 Searle J. R., 1983, INTENTIONALITY ESSAY SHULTZ TR, 1980, BRIT J SOC CLIN PSYC, V19, P301 Tomasello Michael, 1996, P319, DOI 10.1016/B978-012273965-1/50016-9 TOMASELLO M, 2000, LANGUAGE ACQUISTION Tomasello M., 1999, CULTURAL ORIGINS HUM Travis L. L, 1997, DEV SPANS EVENT COMP, P111 Want SC, 2002, DEVELOPMENTAL SCI, V5, P1, DOI 10.1111/1467-7687.00194 Want SC, 2001, CHILD DEV, V72, P431, DOI 10.1111/1467-8624.00288 Whiten A, 1996, J COMP PSYCHOL, V110, P3, DOI 10.1037//0735-7036.110.1.3 NR 22 TC 67 Z9 68 PU BLACKWELL PUBLISHERS PI MALDEN PA 350 MAIN STREET, STE 6, MALDEN, MA 02148 USA SN 0009-3920 J9 CHILD DEV JI Child Dev. PD SEP-OCT PY 2002 VL 73 IS 5 BP 1431 EP 1441 DI 10.1111/1467-8624.00481 PG 11 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 598RX UT WOS:000178291200008 PM 12361310 ER PT J AU Peterson, CC AF Peterson, CC TI Drawing insight from pictures: The development of concepts of false drawing and false belief in children with deafness, normal hearing, and autism SO CHILD DEVELOPMENT LA English DT Article ID MENTAL STATES; MIND; PERSPECTIVE; 3-YEAR-OLDS; PERFORMANCE; INDIVIDUALS; INTENTION; LANGUAGE AB Theory-of-mind concepts in children with deafness, autism, and normal development (N = 154) were examined in three experiments using a set of standard inferential false-belief tasks and matched sets of tasks involving false drawings. Results of all three experiments replicated previously published findings by showing that primary school children with deafness or autism, aged 6 to 13 years, scored significantly lower than normal-developing 4-year-old preschoolers on standard misleading-container and unseen-change tests of false-belief understanding. Furthermore, deaf and autistic children generally scored higher on drawing-based tests than on corresponding standard tests and, on the most challenging of the false-drawing tests in Experiment 2, they significantly outperformed the normal-developing preschoolers by clearly understanding their own false intentions and another person's false beliefs about an actively misleading drawing. In Experiment 3, preschoolers; outperformed older deaf and autistic children on standard tasks, but did less well on a task that required the drawing of a false belief. Methodological factors could not fully explain the findings, but early social and conversational experiences in the family were deemed likely contributors. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Peterson, CC (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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PD SEP-OCT PY 2002 VL 73 IS 5 BP 1442 EP 1459 DI 10.1111/1467-8624.00482 PG 18 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 598RX UT WOS:000178291200009 PM 12361311 ER PT J AU Finegold, SM Molitoris, D Song, YL Liu, CX Vaisanen, ML Bolte, E McTeague, M Sandler, R Wexler, H Marlowe, EM Collins, MD Lawson, PA Summanen, P Baysallar, M Tomzynski, TJ Read, E Johnson, E Rolfe, R Nasir, P Shah, H Haake, DA Manning, P Kaul, A AF Finegold, SM Molitoris, D Song, YL Liu, CX Vaisanen, ML Bolte, E McTeague, M Sandler, R Wexler, H Marlowe, EM Collins, MD Lawson, PA Summanen, P Baysallar, M Tomzynski, TJ Read, E Johnson, E Rolfe, R Nasir, P Shah, H Haake, DA Manning, P Kaul, A TI Gastrointestinal microflora studies in late-onset autism SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT Anaerobe Odyssey Symposium held in honor of Sydney M Finegolds 80th Birthday CY AUG 12, 2001 CL LOS ANGELES, CALIFORNIA HO UNIV CALIF LOS ANGELES, FAC CLUB ID MYELIN BASIC-PROTEIN; AMINO-ACIDS; CHILDREN; BACTERIA; DEGRADATION; ANTIBODIES; INTESTINE; PRODUCTS; DISORDER; STRAINS AB Some cases of late-onset (regressive) autism may involve abnormal flora because oral vancomycin, which is poorly absorbed, may lead to significant improvement in these children. Fecal flora of children with regressive autism was compared with that of control children, and clostridial counts were higher. The number of clostridial species found in the stools of children with autism was greater than in the stools of control children. Children with autism had 9 species of Clostridium not found in controls, whereas controls yielded only 3 species not found in children with autism. In all, there were 25 different clostridial species found. In gastric and duodenal specimens, the most striking finding was total absence of non-spore-forming anaerobes and microaerophilic bacteria from control children and significant numbers of such bacteria from children with autism. These studies demonstrate significant alterations in the upper and lower intestinal flora of children with late-onset autism and may provide insights into the nature of this disorder. C1 W Los Angeles Vet Affairs Med Ctr, Infect Dis Sect 111 F, Los Angeles, CA 90073 USA. W Los Angeles Vet Affairs Med Ctr, Res Serv, Los Angeles, CA 90073 USA. W Los Angeles Vet Affairs Med Ctr, Clin Microbiol Lab, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Sch Med, Dept Microbiol Mol Genet & Immunol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA. Rush Childrens Hosp, Chicago, IL USA. Univ Wisconsin, Dept Food Microbiol & Toxicol & Bacteriol, Madison, WI USA. Texas Tech Univ, Hlth Sci Ctr, Dept Microbiol & Immunol, Lubbock, TX 79430 USA. Childrens Hosp, Med Ctr, Div Pediat Gastroenterol & Nutr, Cincinnati, OH 45229 USA. Univ Reading, Sch Food Biosci, Dept Microbiol, Reading, Berks, England. Cent Publ Hlth Lab, Publ Hlth Lab Serv, Identificat Serv Unit, London NW9 5HT, England. RP Finegold, SM (reprint author), W Los Angeles Vet Affairs Med Ctr, Infect Dis Sect 111 F, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. 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PD SEP 1 PY 2002 VL 35 SU 1 BP S6 EP S16 DI 10.1086/341914 PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 585PH UT WOS:000177533400002 PM 12173102 ER PT J AU Bolte AF Bolte TI The cognitive structure of higher functioning autism and schizophrenia: A comparative study (vol 43, pg 325, 2002) SO COMPREHENSIVE PSYCHIATRY LA English DT Correction CR BOLTE, 2002, COMPR PSYCHIAT, V43, P325 NR 1 TC 0 Z9 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0010-440X J9 COMPR PSYCHIAT JI Compr. Psychiat. PD SEP-OCT PY 2002 VL 43 IS 5 BP 411 EP 411 PG 1 WC Psychiatry SC Psychiatry GA 592NW UT WOS:000177944600012 ER PT J AU Draganov, P Toskes, PP AF Draganov, P Toskes, PP TI Chronic pancreatitis SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article ID CELIAC PLEXUS BLOCK; INTEROBSERVER AGREEMENT; ENDOSCOPIC ULTRASOUND; DIAGNOSIS; PAIN; EUS; ULTRASONOGRAPHY; SECRETIN AB The pathogenesis of idiopathic chronic pancreatitis remains poorly understood despite the high expectations for ascribing the pancreatic damage in affected patients to genetic defects. Neither mutations in the cationic trypsinogen gene nor mutations of the cystic fibrosis conductance regulator gene account for the chronic pancreatitis noted in most patients with idiopathic chronic pancreatitis. Attempts to find an autoimmune basis for the pancreatitis in these patients have not been very successful. The diagnosis of small duct idiopathic chronic pancreatitis remains a great source of frustration for clinicians. Such patients with negative results of radiographic studies often cannot be diagnosed unless a hormone stimulation test such as a secretin test is performed, Although the porcine biologic form of secretin, which has been used to diagnose chronic pancreatitis, became unavailable because of widespread use in the treatment of children with autism, a synthetic form of porcine secretin has now been approved by the US Food and Drug Administration and is available. The true value of endoscopic ultrasonography in diagnosing small duct chronic pancreatitis remains to be fully defined, Endoscopic ultrasonography is becoming the test of choice in detecting radiographic abnormalities in both the parenchyma and ducts of the pancreas. Endoscopic ultrasonography-guided celiac plexus block can be performed relatively easily and very safely. It can provide excellent short-term pain relief in some patients, but reliable predictors of which patients will be successful with this therapy are not yet available. Because long-term follow-up data on the use of endoscopic ultrasonography in this respect are not available, and because the pain of chronic pancreatitis is, indeed, chronic, the role of endoscopic ultrasonography-guided celiac plexus block should be limited to treating those patients with chronic pancreatitis whose pain has not responded to other modalities. (C) 2002 Williams Wilkins, Inc. C1 Univ Florida, Div Gastroenterol Hepatol & Nutr, Dept Med, Gainesville, FL 32610 USA. RP Draganov, P (reprint author), Univ Florida, Div Gastroenterol Hepatol & Nutr, Dept Med, 1600 SW Archer Rd,Room HD602,POB 100214, Gainesville, FL 32610 USA. CR BANKS PA, 1998, GASTROINTESTINAL LIV, P809 Boeck W G, 2001, Curr Gastroenterol Rep, V3, P95, DOI 10.1007/s11894-001-0004-9 Catalano MF, 1998, GASTROINTEST ENDOSC, V48, P11, DOI 10.1016/S0016-5107(98)70122-1 Chowdhury RS, 2001, GASTROENTEROLOGY, V120, pA647, DOI 10.1016/S0016-5085(08)83216-7 Forsmark CE, 2000, GASTROINTEST ENDOSC, V52, P293, DOI 10.1067/mge.2000.106889 Freeman ML, 2001, GASTROINTEST ENDOSC, V54, P425, DOI 10.1067/mge.2001.117550 Gress F, 1999, AM J GASTROENTEROL, V94, P900 Gress F, 2001, AM J GASTROENTEROL, V96, P409 Gunaratnam NT, 2001, GASTROINTEST ENDOSC, V54, P316, DOI 10.1067/mge.2001.117515 HAYAKAWA T, 1992, AM J GASTROENTEROL, V87, P1170 Hollerbach S, 2001, ENDOSCOPY, V33, P824, DOI 10.1055/s-2001-17337 JOSEPHSON SA, 1997, GASTROINTEST ENDOS S, V45, pAB159 Lau JYW, 1997, GASTROINTEST ENDOSC, V46, P33, DOI 10.1016/S0016-5107(97)70206-2 Lok CE, 1998, CHEST, V114, P1283, DOI 10.1378/chest.114.5.1283 Okazaki K, 2001, J GASTROENTEROL, V36, P293, DOI 10.1007/s005350170094 Parada KS, 2002, GASTROINTEST ENDOSC, V55, P328, DOI 10.1067/mge.2002.118948 Somogyi L, 2000, PANCREAS, V21, P262, DOI 10.1097/00006676-200010000-00007 Wallace MB, 2001, PANCREAS, V23, P26, DOI 10.1097/00006676-200107000-00004 Wallace MB, 2001, GASTROINTEST ENDOSC, V53, P294, DOI 10.1067/mge.2001.112191 WALSH TN, 1992, GUT, V33, P1566, DOI 10.1136/gut.33.11.1566 WIERSEMA MJ, 1993, ENDOSCOPY, V25, P555, DOI 10.1055/s-2007-1010405 WILLIAMS DB, 1999, INTERVENTIONAL ENDOS, V1, P151 NR 22 TC 5 Z9 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD SEP PY 2002 VL 18 IS 5 BP 558 EP 562 DI 10.1097/01.MOG.0000025263.17006.9D PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 584ZN UT WOS:000177498800006 PM 17033333 ER PT J AU Brereton, AV Tonge, BJ AF Brereton, AV Tonge, BJ TI Autism and related disorders in adults SO CURRENT OPINION IN PSYCHIATRY LA English DT Article DE adults; Asperger's syndrome; autism; high-functioning autism ID HIGH-FUNCTIONING ADULTS; SPECTRUM DISORDERS; ASPERGER-SYNDROME; MIND; AREA; MRI AB Purpose of review To review research published in 2001 in English language refereed journals that refer to autism and related disorders in adults. Recent findings Screening instruments for autism in general populations or psychiatric populations and measures of stress have been developed. Psychosis and other psychiatric co-morbidity are present in adults with autism, but should not overshadow the diagnosis. Genetic and neurobiological studies have provided evidence of complex multigene developmental and functional brain abnormalities, particularly involving the cerebral cortex, limbic system and cerebellum. Subtle deficits in mental state attributions have been discovered in attention to the eyes and voice in intelligent adults with autism. Attentional dysfunction in autistic adults is likely to be caused by deficits in cognitive flexibility and psychomotor speed, but memory deficits are less well understood. No robust randomized controlled trials of any psychological, educational or drug intervention for autism in adults have been published. A descriptive account of a behavioural intervention and an open trial of an anti-convulsant mood stabilizer are reported. Summary The developmental outcome, neurobiology, neuropsychology, psychopathology responses to treatment, and service needs are not well researched in adults with autism. Perhaps for reasons of convenience, research has mainly focused on intelligent adults with autism rather than the majority who have intellectual and other neurodevelopmental disabilities. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Sch Psychol Psychiat & Psychol Med, Monash Med Ctr, Clayton, Vic 3168, Australia. RP Brereton, AV (reprint author), Monash Univ, Ctr Dev Psychiat & Psychol, Sch Psychol Psychiat & Psychol Med, Monash Med Ctr, 246 Clayton Rd, Clayton, Vic 3168, Australia. CR Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Beversdorf DQ, 2001, J AUTISM DEV DISORD, V31, P97, DOI 10.1023/A:1005622031943 Frith U, 1991, AUTISM ASPERGER SYND Goldstein G, 2001, J AUTISM DEV DISORD, V31, P433, DOI 10.1023/A:1010620820786 GRICE SJ, 2001, BRAIN IMAG, V12, P2697 Groden J, 2001, J AUTISM DEV DISORD, V31, P207, DOI 10.1023/A:1010755300436 Hardan AY, 2001, J AM ACAD CHILD PSY, V40, P666, DOI 10.1097/00004583-200106000-00011 Hollander E, 2001, J CLIN PSYCHIAT, V62, P530 Kleinman J, 2001, J AUTISM DEV DISORD, V31, P29, DOI 10.1023/A:1005657512379 Konstantareas MM, 2001, J AUTISM DEV DISORD, V31, P19, DOI 10.1023/A:1005605528309 Lauritsen MB, 2001, ACTA PSYCHIAT SCAND, V103, P411, DOI 10.1034/j.1600-0447.2001.00086.x McClannahan LE, 2002, BEHAV MODIF, V26, P9, DOI 10.1177/0145445502026001002 MIRSKY A F, 1991, Neuropsychology Review, V2, P109, DOI 10.1007/BF01109051 Mottron L, 2001, J CHILD PSYCHOL PSYC, V42, P253, DOI 10.1017/S0021963001006722 Nylander L, 2001, ACTA PSYCHIAT SCAND, V103, P428, DOI 10.1034/j.1600-0447.2001.00175.x PHILLIPS JG, 1994, MOVEMENT DISORD, V9, P521, DOI 10.1002/mds.870090504 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 Purcell AE, 2001, NEUROLOGY, V57, P1618 Raja M, 2001, GEN HOSP PSYCHIAT, V23, P285, DOI 10.1016/S0163-8343(01)00155-4 Roeyers H, 2001, J CHILD PSYCHOL PSYC, V42, P271, DOI 10.1111/1469-7610.00718 Saitoh O, 2001, BRAIN, V124, P1317, DOI 10.1093/brain/124.7.1317 Stein D, 2001, J AUTISM DEV DISORD, V31, P355, DOI 10.1023/A:1010707622612 NR 24 TC 5 Z9 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0951-7367 J9 CURR OPIN PSYCHIATR JI Curr. Opin. Psychiatr. PD SEP PY 2002 VL 15 IS 5 BP 483 EP 487 DI 10.1097/00001504-200209000-00004 PG 5 WC Psychiatry SC Psychiatry GA 588WK UT WOS:000177725000004 ER PT J AU Dale, N Sonksen, P AF Dale, N Sonksen, P TI Developmental outcome, including setback, in young children with severe visual impairment SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID INFANTILE-AUTISM; BLIND-CHILDREN; LANGUAGE; DISORDERS; PATTERNS AB This study retrospectively investigated the developmental perspective of 69 children (40 males, 29 females) with 'potentially simple' congenital disorders of the peripheral visual system: development was examined in the context of degree of visual impairment. Developmental and visual assessments were carried out at 10 to 16 months (Time 1) and 27 to 54 months of age (Time 2). Participants were grouped according to (1) visual status: profound visual impairment (PVI), severe visual impairment (SVI); (2) developmental status on the Reynell-Zinkin scales. A majority of the sample showed normal development on all subscales (62% Time 1, 57% Time 2). Those with PVI were more developmentally vulnerable than SVI with a greater incidence of (1) uneven developmental profile at Time 1 (48% PVI, 16% SVI); (2) global learning difficulties at Time 2 (37% PVI, 0% SVI); (3) delay on individual subscales at Time 2 (p<0.02 PVI versus SVI); (4) deceleration (verbal comprehension 74% PVI, 24% SVI, sensorimotor understanding 70% PVI, 27% SVI); and (5) severe developmental setback (33% PVI, 7% SVI). Risk factors of visual level, age, and sex for poor developmental outcome in infants with visual impairment were established. C1 UCL, Great Ormond St Hosp Children NHS Trust, Inst Child Hlth, Wolfson Ctr, London WC1N 2AP, England. RP Dale, N (reprint author), UCL, Great Ormond St Hosp Children NHS Trust, Inst Child Hlth, Wolfson Ctr, Mecklenburgh Sq, London WC1N 2AP, England. 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Med. Child Neurol. PD SEP PY 2002 VL 44 IS 9 BP 613 EP 622 PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 593RT UT WOS:000178006600006 PM 12227616 ER PT J AU Huang, CT Heyes, C Charman, T AF Huang, CT Heyes, C Charman, T TI Infants' behavioral reenactment of "failed attempts": Exploring the roles of emulation learning, stimulus enhancement, and understanding of intentions SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID JOINT ATTENTION; INTENDED ACTS; IMITATION; CHILDREN; GESTURES; AUTISM; CHIMPANZEES; OBJECTS; MEMORY; PLAY AB Two studies were conducted to examine whether infants' reenactment of intended but unconsummated acts in A. N. Meltzoff's (1995) failed-attempt paradigm is due to reading the adult's underlying intention or to the effects of nonimitative social learning processes. Two novel conditions that emphasized the object affordances and the spatial contiguity of the object sets were devised. When infants' first actions only were counted, infants who observed the full-demonstration model produced more target acts. When all target acts produced within the 20-s response period were counted, infants in the emulation-learning and spatial contiguity conditions produced as many target acts as infants in the full-demonstration and failed-attempt conditions. This pattern of findings suggests that nonimitative social learning processes may influence infants' response in the behavioral reenactment paradigm. C1 UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. UCL, Dept Psychol, London WC1N 1EH, England. Tzu Chi Univ, Dept Human Dev, Hualien, Taiwan. RP Charman, T (reprint author), UCL, Inst Child Hlth, Behav & Brain Sci Unit, 30 Guildford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014; Heyes, Cecilia/F-8262-2014 OI Charman, Tony/0000-0003-1993-6549; CR ABRAVANEL E, 1985, DEV PSYCHOL, V21, P614, DOI 10.1037/0012-1649.21.4.614 Aldridge MA, 2000, DEVELOPMENTAL SCI, V3, P294, DOI 10.1111/1467-7687.00123 BAKEMAN R, 1984, CHILD DEV, V55, P1278, DOI 10.2307/1129997 Baron-Cohen S., 1991, NATURAL THEORIES MIN, P233 Barresi J, 1996, BEHAV BRAIN SCI, V19, P107 Bellagamba F, 1999, INFANT BEHAV DEV, V22, P277, DOI 10.1016/S0163-6383(99)00002-8 BRETHERTON I, 1991, CHILDRENS THEORIES OF MIND : MENTAL STATES AND SOCIAL UNDERSTANDING, P49 CALL J, IN PRESS IMITATION A Carpenter M., 1998, MONOGR SOC RES CHILD, V63, P1, DOI DOI 10.2307/1166214 Carpenter M, 1998, INFANT BEHAV DEV, V21, P315, DOI 10.1016/S0163-6383(98)90009-1 Carpenter M, 2002, DEVELOPMENTAL SCI, V5, P22, DOI 10.1111/1467-7687.00199 Charman T, 2002, DEVELOPMENTAL SCI, V5, P25, DOI 10.1111/1467-7687.00200 Charman T, 2000, COGNITIVE DEV, V15, P481, DOI 10.1016/S0885-2014(01)00037-5 Charman T, 2000, UNDERSTANDING OTHER, P422 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 CHARMAN T, 1994, DEV PSYCHOPATHOL, V6, P403, DOI 10.1017/S0954579400006015 Charman T, 1998, INF MENTAL HLTH J, V19, P260, DOI 10.1002/(SICI)1097-0355(199822)19:2<260::AID-IMHJ12>3.0.CO;2-W Custance D, 1999, J COMP PSYCHOL, V113, P13, DOI 10.1037/0735-7036.113.1.13 Devouche E, 1998, DEVELOPMENTAL SCI, V1, P65, DOI 10.1111/1467-7687.00014 Galef B.G. 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Psychol. PD SEP PY 2002 VL 38 IS 5 BP 840 EP 855 DI 10.1037//0012-1649.38.5.840 PG 16 WC Psychology, Developmental SC Psychology GA 588ZK UT WOS:000177732200017 PM 12220059 ER PT J AU Pons, F Harris, PL Doudin, PA AF Pons, F Harris, PL Doudin, PA TI Teaching emotion understanding SO EUROPEAN JOURNAL OF PSYCHOLOGY OF EDUCATION LA English DT Article DE development; emotion understanding; individual differences; teaching ID SOCIAL COMPETENCE; YOUNG-CHILDREN; MIND; AUTISM; BELIEF; EXPRESSIONS; FRIENDS; FAMILY; OTHERS; TALK AB The main goal of this research was to assess whether it is possible to help children develop their general understanding of emotions. Thirty-six nine-year-old children divided in two groups were examined using a pre-test/train/post-test design. The emotion understanding of the two groups was measured in the pre- and post-test phases using the Test of Emotion Comprehension (TEC). The experimental group received a teaching program about emotions during the training phase: School Matters In Lifeskills Education (SMILE). The control group received no special teaching about emotion during this phase. Results showed that the level of emotion understanding in the experimental group improved significantly between the pre- and post-test whereas no such change occurred in the control group. The theoretical and practical implications of the findings are discussed. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Univ Geneva, Fac Psychol & Educ Sci, CH-1205 Geneva, Switzerland. Harvard Univ, Grad Sch Educ, Cambridge, MA 02138 USA. Haute Ecol Pedag, Lausanne, Switzerland. RP Pons, F (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. CR Appleton M, 1996, SOC DEV, V5, P275, DOI 10.1111/j.1467-9507.1996.tb00086.x BARONCOHEN S, 1993, COGNITION EMOTION, V7, P507, DOI 10.1080/02699939308409202 Baron-Cohen S, 1995, MINDBLINDNESS BARONCOHEN S, 1991, CHILD DEV, V62, P385, DOI 10.1111/j.1467-8624.1991.tb01539.x BENNETT M, 1994, J GENET PSYCHOL, V154, P515 Bosacki S, 1999, SOC DEV, V8, P237, DOI 10.1111/1467-9507.00093 Brown JR, 1996, CHILD DEV, V67, P789, DOI 10.1111/j.1467-8624.1996.tb01764.x CASSIDY J, 1992, CHILD DEV, V63, P603, DOI 10.1111/j.1467-8624.1992.tb01649.x Clements WA, 2000, DEVELOPMENTAL SCI, V3, P81, DOI 10.1111/1467-7687.00102 DENHAM SA, 1990, CHILD DEV, V61, P1145, DOI 10.1111/j.1467-8624.1990.tb02848.x DOUDIN PA, 1999, REV FRANCAISE PEDAGO, V126, P121 DOUDIN PA, 2001, FORMATION CONTINUE R, P167 Doudin P.-A., 2000, VIOLENCE ECOLE FATAL DOUDIN PA, 2001, METACOGNITION ED DUNN J, 1991, DEV PSYCHOL, V27, P448, DOI 10.1037/0012-1649.27.3.448 Dunn J, 1997, AGGRESSIVE BEHAV, V23, P343, DOI 10.1002/(SICI)1098-2337(1997)23:5<343::AID-AB4>3.0.CO;2-J Dunn J, 1999, SOC DEV, V8, P201, DOI 10.1111/1467-9507.00091 EDWARDS R, 1984, EUR J SOC PSYCHOL, V14, P235, DOI 10.1002/ejsp.2420140212 Greenberg M. 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J. Psychol. Educ. PD SEP PY 2002 VL 17 IS 3 BP 293 EP 304 PG 12 WC Psychology, Educational SC Psychology GA 608AM UT WOS:000178823000006 ER PT J AU Vincent, JB Petek, E Thevarkunnel, S Kolozsvari, D Cheung, J Patel, M Scherer, SW AF Vincent, JB Petek, E Thevarkunnel, S Kolozsvari, D Cheung, J Patel, M Scherer, SW TI The RAY1/ST7 tumor-suppressor locus on chromosome 7q31 represents a complex multi-transcript system SO GENOMICS LA English DT Article DE autism; tumor suppressor; noncoding gene; antisense; alternative splicing ID GENOMIC SCREEN; AUTISM; GENE; TROPOMYOSIN; ST7; FIBROBLASTS AB We recently identified a novel gene, RAY1 (FAM4A1), which spans a translocation breakpoint at 7q31 in a patient with autism. This gene has more recently been reported to be a suppressor of tumorigenicity, ST7, although controversy surrounds this observation because subsequent reports have failed to corroborate these findings. Our further analysis of this locus reveals that it is composed of a multigene system that includes two noncoding sense-strand genes (ST7OT3 and ST7OT4) that overlap with many alternative forms of the coding RAY1/ST7 transcript, and two noncoding genes on the antisense strand (ST7OT1 and ST7OT2). RAY1/ST7 was determined to have at least three different 5' exons with alternative start codons, one of which seems to be used almost exclusively in the brain. We have also identified a third alternative 3' end of RAY1/ST7 that uses exons from ST7OT3. ST7OT3 spans from intron 10 to exon 14 of RAY1/ST7 and includes several exons. ST7OT4 has at least seven exons and is transcribed on the sense strand between RAY1/ST7 exon 1 and a tropomyosin-like sequence, TPM3L2. ST7OT1 overlaps with the RAY1/ST7 exon 1 and promoter. ST7OT2 spans from RAY1/ST7 intron 9 to intron 1, and has multiple isoforms. We screened the exons of RAY1/ST7 and ST7OT1-3 for sequence variants in 90 unrelated autism probands and identified several rare variants, including a Ile361Val substitution. Although these variants were not observed in a control population, it is unclear whether they contribute to the autistic phenotype. We postulate that the apparent noncoding genes at the RAY1/ST7 locus may be regulatory RNAs. The RAY1/ST7 may generate at least 18 possible isoforms, with many more arising if other sense-strand exons from ST7OT3 and ST7OT4 are used in a selective and possibly tissue-specific manner. C1 Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON M5T 1R8, Canada. Graz Univ, Inst Med Biol & Human Genet, A-8010 Graz, Austria. RP Vincent, JB (reprint author), Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. 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The biological mothers of 183 autistic children and 209 normals completed the Maternal Perinatal Scale (MPS), a maternal self-report that surveys complications of pregnancies and medical conditions of the mother. Previous research in this area has been limited, with no definitive conclusions. A discriminant analysis was performed to consider perinatal complications as predictors between the autistic and normal subjects. Using the MPS, 65% of the autistic cases were correctly grouped. The results further indicated significant differences on 3 of the 10 factors of the MPS, in particular, Gestational Age, Maternal Morphology, and Intrauterine Stress. When considered in an item by item fashion, 5 items were found to significantly predict group membership (prescriptions taken during pregnancy, length of labor, viral infection, abnormal presentation at delivery, and low birth weight). Finally, 3 maternal medical conditions were found to be highly significant and contribute to the separation between groups, including urinary infection, high temperatures, and depression. C1 Ball State Univ, Neuropsychol Lab, Muncie, IN 47306 USA. RP Dean, RS (reprint author), Ball State Univ, Neuropsychol Lab, 1407 Marsh St, Muncie, IN 47306 USA. 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J. Neurosci. PD SEP PY 2002 VL 112 IS 9 BP 1085 EP 1098 DI 10.1080/00207450290026076 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 600ZL UT WOS:000178421600007 PM 12487097 ER PT J AU Charlop-Christy, MH Carpenter, M Le, L LeBlanc, LA Kellet, K AF Charlop-Christy, MH Carpenter, M Le, L LeBlanc, LA Kellet, K TI Using the picture exchange communication system (PECS) with children with autism assessment of PECS acquisition, speech, social-communicative behavior, and problem behavior SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; communication; PECS ID TIME-DELAY; LANGUAGE; VERBALIZATIONS; DISORDERS AB The picture exchange communication system (PECS) is an augmentative communication system frequently used with children with autism (Bond), Frost, 1994; Siegel, 2000; Yamall, 2000). Despite its common clinical use, no well-controlled empirical investigations have been conducted to test the effectiveness of PECS. Using a multiple baseline design, the present study examined the acquisition of PECS with 3 children with autism. In addition, the study examined the effects of PECS training on the emergence of speech in play and academic settings. Ancillary measures of social-communicative behaviors and problem behaviors were recorded. Results indicated that all 3 children met the learning criterion for PECS and showed concomitant increases in verbal speech. Ancillary gains were associated with increases in social-communicative behaviors and decreases in problem behaviors. The results are discussed in terms of the provision of empirical support for PECS as well as the concomitant positive side effects of its use. C1 Claremont Mckenna Coll, Claremont, CA 91711 USA. Claremont Grad Univ, Claremont, CA USA. RP LeBlanc, LA (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. CR BAKER L, 1987, J AM ACAD CHILD PSY, V26, P546, DOI 10.1097/00004583-198707000-00015 BLACK B, 1995, CHILD DEV, V66, P255, DOI 10.1111/j.1467-8624.1995.tb00869.x Bondy A, 2001, BEHAV ANAL TODAY, V2, P127 Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 BONDY AS, 1993, BEHAV ANALYST, V16, P123 Bondy AS, 1995, LEARNING COGNITION A, P311 Carr E. G., 1982, ED UNDERSTANDING AUT, P142 CARR EG, 1985, J APPL BEHAV ANAL, V18, P111, DOI 10.1901/jaba.1985.18-111 CARR EG, 1983, J APPL BEHAV ANAL, V16, P297, DOI 10.1901/jaba.1983.16-297 Charlop M. 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PD FAL PY 2002 VL 35 IS 3 BP 213 EP 231 DI 10.1901/jaba.2002.35-213 PG 19 WC Psychology, Clinical SC Psychology GA 597CV UT WOS:000178205300001 PM 12365736 ER PT J AU Hardan, AY Handen, BL AF Hardan, AY Handen, BL TI A retrospective open trial of adjunctive donepezil in children and adolescents with autistic disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION; NICOTINE AB In light of the recently reported neuropathologic and neurochemical abnormalities of the cholinergic pathways in autism, donepezil, a tholinesterase inhibitori is a potentially useful agent in the treatment of cognitive and behavioral symptoms observed in this disorder. A ret-rospective pilot study was conducted to determine whether donepezil is effective in the treatment of children and adolescents with. autism. Eight patients (mean age = 11.0 +/- 4.1 years; range 7-19 years) who met Diagnostic and Statistical Manual of Mental Disorders (4th edition) criteria for autistic disorder were openly treated with donepezil. All patients were on I A. concomitant psychoactive medications. Four of these patients. (50%) demonstrated significant improvement as assessed by the Aberrant Behavior Checklist and the Clinical Global Impression Scale. Decreases in the Irritability and Hyperactivity subscales were observed, but no changes in the Inappropriate Speech, Lethargy, and Stereotypies subscales were noted. Limited and transient side effects were reported, with one patient experiencing gastrointestinal disturbances and another reporting mild irritability. Double-blind, placebo-controlled investigations are needed to provide further evidence of the potential benefits of donepezil to patients with autistic disorder. C1 Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, 3811 O Hara St, Pittsburgh, PA 15213 USA. CR AMAN MG, 1985, AM J MENT DEF, V89, P485 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Campbell M, 1997, J AM ACAD CHILD PSY, V36, P835, DOI 10.1097/00004583-199706000-00022 CHEZ MC, 2000, AM NEUR ASS ANN M ST Conners CK, 1996, PSYCHOPHARMACOL BULL, V32, P67 Handen BL, 2000, J AUTISM DEV DISORD, V30, P245, DOI 10.1023/A:1005548619694 Levin ED, 1996, NEUROPSYCHOPHARMACOL, V15, P429, DOI 10.1016/S0893-133X(96)00018-8 Minshew N J, 1997, J Int Neuropsychol Soc, V3, P303 MINSHEW NJ, 1992, J CLIN EXP NEUROPSYC, V14, P749, DOI 10.1080/01688639208402860 *NATL I MENT HLTH, 1985, PSYCHOPHARMACOL BULL, V21, P839 Perry EK, 2001, AM J PSYCHIAT, V158, P1058, DOI 10.1176/appi.ajp.158.7.1058 Posey D J, 2001, Expert Opin Pharmacother, V2, P587, DOI 10.1517/14656566.2.4.587 Rogers SL, 1998, ARCH INTERN MED, V158, P1021, DOI 10.1001/archinte.158.9.1021 Rojas-Fernandez C, 2000, J AM GERIATR SOC, V48, P597 Wilens TE, 2000, J CHILD ADOL PSYCHOP, V10, P217, DOI 10.1089/10445460050167322 NR 16 TC 44 Z9 44 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 FAL PY 2002 VL 12 IS 3 BP 237 EP 241 DI 10.1089/104454602760386923 PG 5 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 606LV UT WOS:000178736200007 PM 12427297 ER PT J AU Burd, L Kerbeshian, J Westerland, A Labine, J Barth, A Klug, MG Wagner, K AF Burd, L Kerbeshian, J Westerland, A Labine, J Barth, A Klug, MG Wagner, K TI Prospective long-term follow-up of patients with pervasive developmental disorders SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID FUNCTIONING AUTISTIC-CHILDREN; INFANTILE-AUTISM; DISINTEGRATIVE PSYCHOSIS; NORTH-DAKOTA; CHILDHOOD; PREVALENCE; JAPAN AB We conducted a 12-year prospective study of children with pervasive developmental disorders from North Dakota. In a prospective longitudinal follow-up study, of 59 patients, we found 52 patients with pervasive developmental disorders (88%). Ten (17%) declined to participate. We collected data on 42 (71%) of the original cohort. Of the 42 subjects, I died (1.7%). The other 41 were followed up for 492 person-years. Severity scores for the Diagnostic and Statistical Manual of Mental Disorders-III-Revised (DSM-III-R) declined 20% and for DSM-IV 23%. Global Assessment of Functioning improved 19%, and the average number of comorbidities decreased 45%. Thirty-seven percent of patients improved in all four measures, whereas only 5% improved in only one measure. Pervasive developmental disorders are developmental disorders with a long-term course of limited improvement for most patients. Male subjects demonstrated substantially more variability in improvement but, overall, demonstrated more improvement than female subjects. C1 Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, Grand Forks, ND 58201 USA. Univ N Dakota, Sch Med & Hlth Sci, Dept Neurosci, Grand Forks, ND 58201 USA. RP Burd, L (reprint author), 501 N Columbia Rd, Grand Forks, ND 58203 USA. 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Child Neurol. PD SEP PY 2002 VL 17 IS 9 BP 681 EP 688 DI 10.1177/088307380201700906 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 624VA UT WOS:000179781400006 PM 12503645 ER PT J AU Casanova, MF Buxhoeveden, DP Brown, C AF Casanova, MF Buxhoeveden, DP Brown, C TI Clinical and macroscopic correlates of minicolumnar pathology in autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID AREA-1 CELL COLUMNS; GAMMA-OSCILLATIONS; SPATIAL-ORGANIZATION; PERIPHERAL INPUT; CORTEX; BRAIN; PATTERNS; EPILEPSY; CAT; EEG AB All subcortical arrangements are primarily nuclear in type. The cortex has been the first part of the brain to evolve a radial and laminar arrangement of cells. The resultant modular arrangement is based on the cell minicolumn: a self-contained ecosystem of connectivity linking afferent, efferent, and inerneuronal connections. Recently, the cell minicolumn has been found to be abnormal in patients with autism. 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Child Neurol. PD SEP PY 2002 VL 17 IS 9 BP 692 EP 695 DI 10.1177/088307380201700908 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 624VA UT WOS:000179781400008 PM 12503647 ER PT J AU Joseph, RM Tager-Flusberg, H Lord, C AF Joseph, RM Tager-Flusberg, H Lord, C TI Cognitive profiles and social-communicative functioning in children with autism spectrum disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; behavioral phenotypes; cognition; individual differences; intelligence; symptomatology ID PERVASIVE DEVELOPMENTAL DISORDERS; INTELLECTUAL ABILITIES; HEAD CIRCUMFERENCE; FAMILY HISTORY; NEUROSCIENCE; PATTERNS; DEFICITS; PEOPLE; MIND AB Background: Whether there is an unusual degree of unevenness in the cognitive abilities of children with autism spectrum disorder (ASD) and whether different cognitive profiles among children with ASD might index etiologically significant subgroups are questions of continued debate in autism research. Method: The Differential Ability Scales (DAS) and the Autism Diagnostic Observation Schedule (ADOS) were used to examine profiles of verbal and nonverbal abilities and their relationship to autistic symptomatology in 120 relatively high-functioning children with ADI-confirmed diagnoses of autism. Results: Discrepancies between verbal and nonverbal ability scores occurred at a significantly higher rate than in the DAS normative sample (30%) in both a younger group of 73 children (56%) with a mean age of 5;5 and an older group of 47 children (62%) with a mean age of 8; 11. Discrepancies were mainly in favor of nonverbal ability in the younger group, but occurred equally in favor of verbal and nonverbal abilities in the older group. Comparison of the two age groups suggested a growing dissociation between verbal and nonverbal (and particularly visual processing) skills with age. In the older group, children with discrepantly higher nonverbal abilities demonstrated significantly greater impairment in social functioning, as measured on the ADOS, independent of absolute level of verbal and overall ability. Conclusions: These findings demonstrate a high rate of uneven cognitive development in children with ASD. Indications of a dissociation between verbal and visual-perceptual skills among the older children, and the specific association of discrepantly high nonverbal skills with increased social symptoms suggest that the nonverbal > verbal profile may index an etiologically significant subtype of autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Univ Chicago, Chicago, IL 60637 USA. RP Joseph, RM (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,L-814, Boston, MA 02118 USA. RI Tager-Flusberg, Helen/D-5265-2009; Joseph, Roy/D-8530-2015 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 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Carroll J. B., 1993, HUMAN COGNITIVE ABIL COHEN IL, 1994, BIOL PSYCHIAT, V36, P5, DOI 10.1016/0006-3223(94)90057-4 Courchesne E, 2001, NEUROLOGY, V57, P245 Davidovitch M, 1996, J CHILD NEUROL, V11, P389 DEUTSCH C, IN PRESS J AUTISM DE Elgar K, 2001, J CHILD PSYCHOL PSYC, V42, P705, DOI 10.1111/1469-7610.00767 Elliott C. D., 1979, BRIT ABILITY SCALES Elliott C. D., 1990, DIFFERENTIAL ABILITY Fein D, 1999, CHILD NEUROPSYCHOL, V5, P1, DOI 10.1076/chin.5.1.1.7075 Fidler DJ, 2000, DEV MED CHILD NEUROL, V42, P737, DOI 10.1017/S0012162200001365 Folstein SE, 1999, INT REV PSYCHIATR, V11, P269, DOI 10.1080/09540269974168 Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 FOMBONNE E, 1997, J CHILD PSYCHOL PSYC, V38, P67 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P1461, DOI 10.1111/j.1469-7610.1994.tb01287.x Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 KarmiloffSmith A, 1997, DEV NEUROPSYCHOL, V13, P513 Karmiloff-Smith A, 1998, TRENDS COGN SCI, V2, P389, DOI 10.1016/S1364-6613(98)01230-3 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 Lainhart JE, 1997, J AM ACAD CHILD PSY, V36, P282, DOI 10.1097/00004583-199702000-00019 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Lincoln A, 1998, ASPERGER SYNDROME HI, P145 Lincoln A. 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J., 1998, IQ HUMAN INTELLIGENC Manjiviona J., 1999, AUTISM, V3, P327, DOI DOI 10.1177/1362361399003004003 MERVIS CB, 1999, NEURODEVELOPMENTAL D, P65 Mottron L, 2000, J CHILD PSYCHOL PSYC, V41, P1057, DOI 10.1017/S0021963099006253 Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 Piven J, 1996, J AM ACAD CHILD PSY, V35, P530, DOI 10.1097/00004583-199604000-00020 Piven J, 1997, J CHILD PSYCHOL PSYC, V38, P1011, DOI 10.1111/j.1469-7610.1997.tb01618.x Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P765, DOI 10.1017/S0021963098002601 Plaisted KC, 2000, UNDERSTANDING OTHER, P222 Rumsey JM, 1992, HIGH FUNCTIONING IND, P41 Siegel DJ, 1996, J AUTISM DEV DISORD, V26, P389, DOI 10.1007/BF02172825 Szatmari P, 2000, J CHILD PSYCHOL PSYC, V41, P579, DOI 10.1017/S0021963099005831 VOLKMAR FR, 2001, ASPERGER SYNDROME, P25 WECHSLER D, 1991, WECHSLER INTELLIGEN Wechsler D, 1997, WECHSLER ADULT INTEL, V3rd Woodhouse W, 1996, J CHILD PSYCHOL PSYC, V37, P665, DOI 10.1111/j.1469-7610.1996.tb01458.x World Health Organization, 1993, INT CLASS DIS NR 49 TC 143 Z9 143 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD SEP PY 2002 VL 43 IS 6 BP 807 EP 821 DI 10.1111/1469-7610.00092 PG 15 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 584QG UT WOS:000177478700012 PM 12236615 ER PT J AU Cecil, KM Lin, A Ross, BD Egelhoff, JC AF Cecil, KM Lin, A Ross, BD Egelhoff, JC TI Methylsulfonylmethane observed by in vivo proton magnetic resonance spectroscopy in a 5-year-old child with developmental disorder: Effects of dietary supplementation SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE magnetic resonance spectroscopy methylsulfonylmethane, health food supplements; human brain metabolism ID HUMAN BRAIN; AUTISM AB Proton magnetic resonance spectroscopy (MRS) revealed a distinct resonance at 3.15 ppm in the brain of a 5-year-old male diagnosed with autism. The resonance assignment is attributable to ingestion of methylsulfonylmethane (MSM) as a dietary supplement. Glucosamine with MSM is marketed as a source of dietary sulfur and treatment of joint pain. Recognition of this chemical on brain proton MRS as an exogenous compound is necessary to avoid confusion as a pathologic metabolite of pediatric metabolic disease. C1 Univ Cincinnati, Childrens Hosp, Ctr Med, Dept Radiol, Cincinnati, OH 45229 USA. Huntington Med Res Inst, MR Spectroscopy Unit, Pasadena, CA USA. RP Cecil, KM (reprint author), Univ Cincinnati, Childrens Hosp, Ctr Med, Dept Radiol, MC 5031,3333 Burnet Ave, Cincinnati, OH 45229 USA. CR BRUDNAK MA, 2001, GUIDE INTESTINAL HLT Brudnak MA, 2001, MED HYPOTHESES, V57, P186, DOI 10.1054/mehy.2001.1331 DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x GOODFELLOW M, 1997, MYCOBACTERIA, V1, P1 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Knivsberg AM, 2001, NUTR NEUROSCI, V4, P25 LAWRENCE RM, 1998, INT J ANTIAGING MED, V1, P50 Lin A, 2001, TOXICOL LETT, V123, P169, DOI 10.1016/S0378-4274(01)00396-4 Rose SE, 2000, MAGN RESON IMAGING, V18, P95, DOI 10.1016/S0730-725X(99)00110-1 NR 9 TC 9 Z9 9 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD SEP-OCT PY 2002 VL 26 IS 5 BP 818 EP 820 DI 10.1097/00004728-200209000-00026 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 619LV UT WOS:000179478200026 PM 12439321 ER PT J AU Gray, DE AF Gray, DE TI Ten years on: a longitudinal study of families of children with autism SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article ID PARENTS AB This paper reports the results of a longitudinal, ethnographic study of the psychosocial adaptation of parents of children with autism. The results indicate that most parents have experienced improvements in terms of their own psychological well-being, the social experiences of their immediate family members and their relations with members of their extended family. They also reported changes to the stressful situations they experience and their strategies for coping with them. Stigmatizing reactions of non family members have also declined. The results were less favorable in the cases of families with aggressive and/or violent children. The parents in these families experienced high levels of stress and had few resources in terms of treatment or residential placement to deal with their situation. C1 Univ New England, Sch Social Sci, Armidale, NSW 2351, Australia. RP Gray, DE (reprint author), Univ New England, Sch Social Sci, Armidale, NSW 2351, Australia. CR Berry J. O., 1998, LIFESPAN PERSPECTIVE BRISTOL MM, 1987, J AUTISM DEV DISORD, V17, P469, DOI 10.1007/BF01486964 Bristol M. M., 1984, EFFECTS AUTISM FAMIL, P289 DeMeyer M. K., 1979, PARENTS CHILDREN AUT GRAY DE, 1993, SOC SCI MED, V36, P1037, DOI 10.1016/0277-9536(93)90121-J Gray David E., 1992, Australia and New Zealand Journal of Developmental Disabilities, V18, P83 GRAY DE, 1993, SOCIOL HEALTH ILL, V15, P102, DOI 10.1111/1467-9566.ep11343802 GRAY DE, 1994, SOCIOL HEALTH ILL, V16, P275, DOI 10.1111/1467-9566.ep11348729 GRAY DE, 1998, AUTISM FAMILY MARCUS L, 1977, AM J ORTHOPSYCHIAT, V47, P383 Marcus L. M., 1997, HDB AUTISM PERVASIVE, P631 Mesibov GB, 1997, HDB AUTISM PERVASIVE, P309 NR 12 TC 55 Z9 56 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 SEP PY 2002 VL 27 IS 3 BP 215 EP 222 DI 10.1080/1366825021000008639 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 590JP UT WOS:000177820000006 ER PT J AU Ennis, S Wanjing, JN Kearney, G Fitzgerald, M Stallings, R Barton, DE Green, AJ Gallagher, L Gill, M AF Ennis, S Wanjing, JN Kearney, G Fitzgerald, M Stallings, R Barton, DE Green, AJ Gallagher, L Gill, M TI Mapping of a candidate region for autism on chromosome 2q32. SO JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT British Human Genetics Conference 2002 CY SEP 23-25, 2002 CL YORK, ENGLAND HO UNIV YORK C1 Univ Coll Dublin, Natl Ctr Med Genet, Dept Med Genet, Dublin 2, Ireland. Our Ladys Hosp Sick Children, Natl Ctr Med Genet, Dublin, Ireland. St James Hosp, Trin Ctr Hlth Sci, Dept Psychiat, Dublin 8, Ireland. RI Barton, David/B-9460-2008 NR 0 TC 0 Z9 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD SEP PY 2002 VL 39 SU 1 MA 371 BP S81 EP S81 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594MX UT WOS:000178055300256 ER PT J AU Vojdani, A Campbell, A Anyanwu, E Kashanian, A Bock, K Vojdani, E AF Vojdani, A Campbell, A Anyanwu, E Kashanian, A Bock, K Vojdani, E TI Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus group A (vol 129, pg 168, 2002) SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Correction C1 Immunosci Lab Inc, Sect Neuroimmunol, Beverly Hills, CA 90211 USA. Ctr Immune Enviornm & Tox Disorders, Spring, TX 77386 USA. Rhinebeck Hlth Ctr, Rhinebeck, NY 12572 USA. RP Vojdani, A (reprint author), Immunosci Lab Inc, Sect Neuroimmunol, 8693 Wilshire Blvd,Suite 200, Beverly Hills, CA 90211 USA. CR Vojdani A, 2002, J NEUROIMMUNOL, V129, P168, DOI 10.1016/S0165-5728(02)00180-7 NR 1 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD SEP PY 2002 VL 130 IS 1-2 BP 248 EP 248 DI 10.1016/S0165-5728(02)00265-5 PG 1 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 599HX UT WOS:000178329200026 ER PT J AU Banks, WA Goulet, M Rusche, JR Niehoff, ML Boismenu, R AF Banks, WA Goulet, M Rusche, JR Niehoff, ML Boismenu, R TI Differential transport of a secretin analog across the blood-brain and blood-cerebrospinal fluid barriers of the mouse SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID ADENYLATE-CYCLASE; PIG BRAIN; AUTISM; RAT; HIPPOCAMPUS; POLYPEPTIDE; PEPTIDES AB Secretin is a gastrointestinal peptide belonging to the vasoactive intestinal peptide (VIP)/glucagon/pituitary adenylate cyclase-activating polypeptide (PACAP) family recently suggested to have therapeutic effects in autism. A direct effect on brain would require secretin to cross the blood-brain barrier (BBB), an ability other members of the VIP/PACAP family have. Herein, we examined whether a secretin analog (SA) radioactively labeled with I-131 (I-SA) could cross the BBB of 4-week-old mice. We found I-SA was rapidly cleared from serum with fragments not precipitating with acid appearing in brain and serum. Levels of radioactivity were corrected to reflect only intact I-SA as estimated by acid precipitation. After i.v. injection, I-SA was taken up by brain at a modest rate of 0.9 to 1.5 mul/g-mm. Capillary depletion, brain perfusion, and high-performance liquid chromatography were used to confirm the passage of intact I-SA across the BBB. I-SA entered every brain region, with the highest uptake into the hypothalamus and cerebrospinal fluid (CSF). Unlabeled SA (10 mug/mouse) did not inhibit uptake by brain but did inhibit clearance from blood and uptake by the CSF, colon, kidney, and liver. The decreased clearance of I-SA from blood increased the percentage of the i.v. injected dose taken up per brain (%Inj/g) from about 0.118 to 0.295% Inj/g. In conclusion, SA crosses the vascular barrier by a nonsaturable process and the choroid plexus by a saturable process in amounts that for other members of its family produce central nervous system (CNS) effects. This passage provides a pathway through which peripherally administered SA could affect the CNS. C1 St Louis Univ, Sch Med, Dept Internal Med, Div Geriatr, St Louis, MO 63106 USA. Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO USA. Repligen Corp, Needham, MA USA. RP Banks, WA (reprint author), St Louis Univ, Sch Med, Dept Internal Med, Div Geriatr, 915 N Grand Blvd, St Louis, MO 63106 USA. 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Pharmacol. Exp. Ther. PD SEP PY 2002 VL 302 IS 3 BP 1062 EP 1069 DI 10.1124/jpet.102.036129 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 584LB UT WOS:000177467100027 PM 12183664 ER PT J AU LaBelle, CA Charlop-Christy, MH AF LaBelle, CA Charlop-Christy, MH TI Individualizing functional analysis to assess multiple and changing functions of severe behavior problems in children with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID ANALYSIS METHODOLOGIES; SELF-INJURY; INTERVENTION; AGGRESSION AB Relatively few published studies have used functional analysis to assess severe behavior problems in children with autism, and virtually none have assessed behaviors maintained by multiple and changing functions. This study extended the use of a traditional functional analysis analogue by examining the functional relations between problem behaviors maintained by multiple and changing functions and specific environmental events. Three children with autism participated in this study. The target behaviors of disruptive behavior and inappropriate vocalizations were observed during periods of brief, repeated exposure to a series of analogue conditions (attention, tangible, escape, alone, and play) using a multielement experimental design. A new condition was added to assess changing functions of a single behavior. Results indicated that problem behaviors were maintained by multiple functions (attention, escape, tangibles, and automatic reinforcement). The new methodology for assessing changing functions of aberrant behavior revealed that contingencies initially applied to the target behavior were associated with changing functions of that behavior during the course of an experimental session. The implications of this study provide social significance in that a clear methodology for studying problem behaviors and what controls them can lead to a decrease in such behaviors and improved quality of life. 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Posit. Behav. Interv. PD FAL PY 2002 VL 4 IS 4 BP 231 EP 241 DI 10.1177/10983007020040040601 PG 11 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LX UT WOS:000180573400005 ER PT J AU Tookey, PA Cortina-Borja, M Peckham, CS AF Tookey, PA Cortina-Borja, M Peckham, CS TI Rubella susceptibility among pregnant women in North London, 1996-1999 SO JOURNAL OF PUBLIC HEALTH MEDICINE LA English DT Article DE rubella; routine data; pregnancy; inequality ID INFLAMMATORY BOWEL-DISEASE; MEASLES; VACCINE; MUMPS; AUTISM AB Background Rubella infection and congenital rubella are currently rare in the United Kingdom, although sporadic cases occur, often associated with travel abroad. Uptake of the combined measles, mumps and rubella (MMR) vaccine has declined in recent years, and there is a danger that rubella infection could start to circulate again, with serious implications for susceptible pregnant women. This could be a particular problem in communities where there are relatively high rubella susceptibility rates because of either poor vaccine uptake over several years or the presence of significant numbers of recent immigrants from countries without routine rubella vaccination programmes. Methods Routinely collected data on rubella susceptibility in pregnant women in the former North West Thames region were available for 1996-1999. Associations between year of delivery, maternal age, parity and ethnic group, and rubella susceptibility were explored. Results Overall rubella susceptibility declined significantly from 2.6 per cent to 2.4 per cent between 1996 and 1999. Whereas less than 2 per cent of British-born women were susceptible, overall susceptibility for other women was about 5 per cent. African and Asian women had particularly high susceptibility rates, and patterns of susceptibility by age and parity varied across ethnic groups. Conclusions If rubella were to re-establish itself in the United Kingdom, women who had come to Britain in later childhood or adult life would be at higher risk of acquiring infection in pregnancy than indigenous women. Appropriate local and national strategies should be devised to ensure that all such women are offered rubella vaccination at the earliest opportunity. C1 Inst Child Hlth, Ctr Paediat Epidemiol & Biostat, London WC1N 1EH, England. RP Tookey, PA (reprint author), Inst Child Hlth, Ctr Paediat Epidemiol & Biostat, 30 Guilford St, London WC1N 1EH, England. 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PD SEP PY 2002 VL 41 IS 9 BP 1137 EP 1137 DI 10.1097/01.CHI.0000020273.43550.17 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 586QY UT WOS:000177597000016 ER PT J AU Leung, AKC Lemay, JF AF Leung, AKC Lemay, JF TI Caring for a child with autism: a practical guide for parents SO JOURNAL OF THE ROYAL SOCIETY FOR THE PROMOTION OF HEALTH LA English DT Book Review CR IVES M, 2002, CARING CHILD AUTISM NR 1 TC 0 Z9 0 PU ROYAL SOC OF HEALTH PI LONDON PA 38A ST, GEORGES DR, LONDON SW1V 4BH, ENGLAND SN 1466-4240 J9 J R SOC PROMO HEALTH JI J. R. Soc. Promot. 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SO MEDICAL HYPOTHESES LA English DT Article ID POLYMORPHIC CAG REPEATS; BREAST-CANCER; ESTROGEN; MEN; TESTOSTERONE; PREDICTOR; CARCINOMA; DISEASE; RISK AB The androgen receptor gene (AR) contains a domain which includes a variable number of CAG sequences and alleles with low numbers of CAG repeats show high transactivation activity when complexed with testosterone. The ratio of 2nd and 4th digit length (2D:4D) is negatively correlated with phenotypic effects of testosterone. Low numbers of CAG repeats and low 2D:4D are both associated with high sperm numbers and protection against breast cancer. This suggests that CAG number and 2D:4D are correlated i.e. low CAG number and low 2D:4D indicate high activation of androgen-responsive genes. Findings from AR studies predict that low 2D:4D will be associated with prostate and hepatocellular cancer, urolithiasis, ADHD, ankylosing spondylitis, spontaneous abortion, and polycystic ovaries, while high 2D:4D will be associated with motor neuron diseases and endometrial cancer. Findings from 2D:4D studies predict that short CAG length will be common in autism and Asperger's syndrome, while high numbers of CAG repeats will be found in men who are prone to early myocardial infarction. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Liverpool, Sch Biol Sci, Populat Biol Res Grp, Liverpool L69 3BX, Merseyside, England. Univ Liverpool, Dept Primary Care, Liverpool L69 3BX, Merseyside, England. Univ Liverpool, Dept Immunol, Liverpool L69 3BX, Merseyside, England. RP Manning, JT (reprint author), Univ Liverpool, Sch Biol Sci, Populat Biol Res Grp, POB 147, Liverpool L69 3BX, Merseyside, England. CR Brown W. 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Hypotheses PD SEP PY 2002 VL 59 IS 3 BP 334 EP 336 DI 10.1016/S0306-9877(02)00181-0 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 598WK UT WOS:000178299300021 PM 12208164 ER PT J AU Pierson, R Corson, PW Sears, LL Alicata, D Magnotta, V O'Leary, D Andreasen, NC AF Pierson, R Corson, PW Sears, LL Alicata, D Magnotta, V O'Leary, D Andreasen, NC TI Manual and semiautomated measurement of cerebellar subregions on MR images SO NEUROIMAGE LA English DT Article ID POSTERIOR-FOSSA STRUCTURES; POSITRON-EMISSION-TOMOGRAPHY; COGNITIVE DYSMETRIA; INFANTILE-AUTISM; 4TH VENTRICLE; SCHIZOPHRENIC-PATIENTS; SAGITTAL PLANE; BRAIN; VERMIS; MORPHOLOGY AB Previous structural and functional imaging studies suggest that the corticocerebellar-thalamic-cortical circuit is dysfunctional in schizophrenia. Accurate identification and volumetric measurement of cerebellar subregions are essential to the assessment of the cerebellum's role in healthy and disease states. Manual parcellation of the cerebellum on MR images was performed with the use of guide traces. Guide traces identified relevant fissures and borders in several planes, and their intersections with the primary tracing plane were used to maintain consistency and accuracy during the parcellation. The cerebellum was parcellated into right and left anterior lobes, superior posterior lobes, inferior posterior lobes, and corpus medullare. A systematic review of the final traces ensured their accuracy. An artificial neural network was trained using a novel landmark-warped method to help account for wide variability in structure size and location. Overlaps of the manually traced lobes (intersection/union) ranged from 0.78 to 0.85 and intraclass correlations (r(2)) ranged from 0.82 to 0.94. In a comparison of the semiautomated method with the manual method overlaps ranged from 0.83 to 0.88 and intraclass correlations ranged from 0.92 to 0.97. 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In these syndromes urinary peptide abnormalities, derived from gluten, gliadin, and casein, are reported. They reflect processes with opioid effect. The aim of this single blind study was to evaluate effect of gluten and casein-free diet for children with autistic syndromes and urinary peptide abnormalities. A randomly selected diet and control group with 10 children in each group participated. Observations and tests were done before and after a period of 1 year. The development for the group of children on diet was significantly better than for the controls. C1 Stavanger Univ Coll, Ctr Reading Res, N-4068 Stavanger, Norway. Madlavoll Sch, N-4041 Hafrsfjord, Norway. Natl Hosp Norway, Pediat Res Inst, UiO, N-0027 Oslo, Norway. RP Knivsberg, AM (reprint author), Stavanger Univ Coll, Ctr Reading Res, POB 8002, N-4068 Stavanger, Norway. 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Neurosci. PD SEP PY 2002 VL 5 IS 4 BP 251 EP 261 DI 10.1080/10281450290028945 PG 11 WC Neurosciences; Nutrition & Dietetics SC Neurosciences & Neurology; Nutrition & Dietetics GA 579LZ UT WOS:000177180600005 PM 12168688 ER PT J AU Andrews, K AF Andrews, K TI Interpreting autism: a critique of Davidson on thought and language SO PHILOSOPHICAL PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING ADULTS; FALSE BELIEF; ASPERGER-SYNDROME; MENTAL REPRESENTATION; MIND; TASK; CHILDREN AB Donald Davidson's account of interpretation purports to be a priori, though I argue that the empirical facts about interpretation, theory of mind, and autism must be considered when examining the merits of Davidson's view. Developmental psychologists have made plausible claims about the existence of some people with autism who use language but who are unable to interpret the minds of others. This empirical claim undermines Davidson's theoretical claims that all speakers must be interpreters of other speakers and that one need not be a speaker in order to be a thinker. The falsity of these theses has consequences for other parts of Davidson's world-view; for example, it undermines his argument against animal thought. C1 York Univ, Dept Philosophy, N York, ON M3J 1P3, Canada. RP Andrews, K (reprint author), York Univ, Dept Philosophy, 4700 Keele St, N York, ON M3J 1P3, Canada. 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PD SEP PY 2002 VL 32 IS 3 BP 275 EP 309 PG 35 WC Ethics; Philosophy SC Social Sciences - Other Topics; Philosophy GA 582UZ UT WOS:000177370700001 ER PT J AU Kirillova, MG Kurek, NS AF Kirillova, MG Kurek, NS TI Emotions and motivations of patients suffered from schizophrenia in conditions of cooperation and competition SO PSIKHOLOGICHESKII ZHURNAL LA Russian DT Article DE interaction; cooperation; competition; emotions; motivation; autism; unhedonia; needs of social contacts; needs of self-rating; schizophrenia AB There were studied emotional states and emotional relations to the Partners before and after cooperation and competition along with perception of success and fail and desire to interact,again. The sample consisted of 40 dyads of patients suffered from schizophrenia, two control groups, of patients suffered from schizophrenia and 30 healthy Ss. Several methods were used including Nutten's experimental models, scales of emotional state and emotional relation to the partner, interview and observation. Comparative analysis revealed deficit of positive responce in cooperation and paradoxical positive response in competition, deficit. of communicational: skills and disturbance of probability laws of emotional impression. It Was shown, that deficit of motivation of self-rating is stronger than deficit of motivation of social contacts,. also. It was found that cooperation has phsychotherapeutic potential. C1 Ctr Psychol Med Social Assistance Children, Moscow, Russia. Moscow State Pedag Univ, Moscow 119435, Russia. RP Kirillova, MG (reprint author), Ctr Psychol Med Social Assistance Children, Moscow, Russia. CR ARGYL M, 1981, SOCIAL INTERACTION BLEILER E, 1981, KHRESTOMATIYA OBSHCH, P113 CHAPMAN LJ, 1976, J ABNORM PSYCHOL, V85, P374, DOI 10.1037//0021-843X.85.4.374 KUREK NS, 1978, SB T, V23, P71 KUREK NS, 1979, ZH NEVROPATOLOGII PS, P71 KUREK NS, 1988, 8 VSES SEZD NEVR PSI, V2 Laing RD, 1969, SELF OTHERS Maslow A., 1954, MOTIVATION PERSONALI Nuttin J., 1961, TACHE REUSSITE ECHEC NYUTTEN Z, 1985, PSIKHOLOGICHESKIE IS, P130 OLSHANNIKOVA AE, 1978, PROBLEMY OBSHCHEI VO, P93 POLYAKOV YF, 1974, PATOLOGIYA POZNAVATE RADO S, 1956, COLLECTED PAPERS REBER SA, 1985, PENGUIN DICT PSYCHOL SHIBUTANI T, 1969, SOTSIALNAYA PSIKHOLO Simonov P. V., 1987, MOTIVIROVANNYI MOZG SMIRNOV AA, 1948, PSIKHOLOGIYA ZAPOMIN WALLACE CJ, 1984, SCHIZOPHRENIA BULL, V10, P233 ZEIGARNIK B, 1927, BEHALTEN ERLEDIGTER, V9 Zinchenko P. I., 1961, NEPROIZVOLNOE ZAPOMI NR 20 TC 0 Z9 0 PU MEZHDUNARODNAYA KNIGA PI MOSCOW PA 39 DIMITROVA UL., 113095 MOSCOW, RUSSIA SN 0205-9592 J9 PSIKHOL ZH JI Psikhologicheskii Zhurnal PD SEP-OCT PY 2002 VL 23 IS 5 BP 80 EP 88 PG 9 WC Psychology, Multidisciplinary SC Psychology GA 603YY UT WOS:000178589900009 ER PT J AU Gomot, M Giard, MH Adrien, JL Barthelemy, C Bruneau, N AF Gomot, M Giard, MH Adrien, JL Barthelemy, C Bruneau, N TI Hypersensitivity to acoustic change in children with autism: Electrophysiological evidence of left frontal cortex dysfunctioning SO PSYCHOPHYSIOLOGY LA English DT Article ID DEVELOPMENTAL LANGUAGE DISORDER; EVENT-RELATED POTENTIALS; MISMATCH NEGATIVITY MMN; EVOKED-POTENTIALS; STIMULUS DEVIANCE; CHILDHOOD AUTISM; INVOLUNTARY ATTENTION; AUDITORY INFORMATION; FREQUENCY CHANGES; NOVELTY DETECTION AB Exaggerated reactions to even small changes in the environment and abnormal behaviors in response to auditory stimuli are frequently observed in children with autism (CWA). Brain mechanisms involved in the automatic detection of auditory frequency change were studied using scalp potential and scalp current density (SCD) mapping of mismatch negativity (MMN) in 15 CWA matched with 15 healthy children. Compared with the response in controls, MMN recorded at the Fz site in CWA showed significantly shorter latency and was followed by a P3a wave. Mapping of potentials indicated significant intergroup differences. Moreover, SCD mapping demonstrated the dynamics of the different MMN generators: Although temporal component was evidenced bilaterally in both groups, it occurred earlier on the left hemisphere in CWA, preceded by an abnormal early left frontal component. The electrophysiological pattern reported here emphasized a left frontal cortex dysfunctioning that might also be implicated in cognitive and behavioral impairment characteristic, of this complex neurodevelopmental disorder. C1 CHU Bretonneau, INSERM U316, Child Psychiat Unit, F-37044 Tours, France. Brain Signals & Proc Lab, INSERM U280, F-69003 Lyon, France. RP Gomot, M (reprint author), CHU Bretonneau, INSERM U316, Child Psychiat Unit, 2 Bd Tonnelle, F-37044 Tours, France. 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An alternating treatment design was used, and three 2-year-old boys with autism participated. In the teacher-selected condition, the teacher gave the child a toy; and in the child-choice condition, the teacher gave the child a choice between two toys. The toys were selected from a pool of toys based on each child's frequency of contact with the toys from measures taken before the study started. A 5-second momentary time sampling procedure was used during daily 10-min sessions to measure the child's engagement with toys, nonengagement, and problematic behaviors. The teacher's behaviors (physical prompt, modeling, talking, silent observation, and other) also were measured. The data suggest the child-choice condition resulted in more engaged time for each participant and fewer problematic behaviors for two of the three boys. The results are discussed in terms of clinical applications and future research. C1 Univ N Carolina, Ctr Study Dev & Learning, Chapel Hill, NC 27599 USA. Vanderbilt Univ, Nashville, TN 37240 USA. RP Reinhartsen, DB (reprint author), Univ N Carolina, Ctr Study Dev & Learning, CB 7255, Chapel Hill, NC 27599 USA. EM Debbie.reinhartsen@cdl.unc.edu CR Bailey Jr D. B., 1992, TEACHING INFANTS PRE BARLOW DH, 1979, J APPL BEHAV ANAL, V12, P199, DOI 10.1901/jaba.1979.12-199 Bricker D., 1998, ACTIVITY BASED APPRO Carter C. 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L, 2001, J POSIT BEHAV INTERV, V3, P194, DOI 10.1177/109830070100300401 Wehmeyer ML, 2001, J INTELL DISABIL RES, V45, P371, DOI 10.1046/j.1365-2788.2001.00342.x Wehmeyer ML, 1996, AM J MENT RETARD, V100, P632 WOLERY M, 1993, J SPEC EDUC, V27, P222 Wolery M., 2000, DEC RECOMMENDED PRAC, P29 NR 35 TC 16 Z9 16 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD FAL PY 2002 VL 27 IS 3 BP 175 EP 187 DI 10.2511/rpsd.27.3.175 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BM UT WOS:000222242200002 ER PT J AU Cicero, FR Pfadt, A AF Cicero, FR Pfadt, A TI Investigation of a reinforcement-based toilet training procedure for children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE reinforcement; home; environment; toilet training; autism; developmental disability AB Independent toileting is an important developmental skill which individuals with developmental disabilities often find a challenge to master. Effective toilet training interventions have been designed which rely on a combination of basic operant principles of positive reinforcement and punishment. In the present study, the effectiveness of a reinforcement-based toilet training intervention was investigated with three children with a diagnosis of autism. Procedures included a combination of positive reinforcement, graduated guidance, scheduled practice trials and forward prompting. Results indicated that all procedures were implemented in response to urination accidents. A three participants reduced urination accidents to zero and learned to spontaneously request use of the bathroom within 7-11 days of training. Gains were maintained over 6-month and 1-year follow-ups. Findings suggest that the proposed procedure is an effective and rapid method of toilet training, which can be implemented within a structured school setting with generalization to the home environment. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Eden II Programs, Staten Isl, NY 10303 USA. NYS Inst Basic Res Dev Disabil, Staten Isl, NY 10303 USA. RP Cicero, FR (reprint author), Eden II Programs, 150 Granite Ave, Staten Isl, NY 10303 USA. 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S., 1987, CONTINENCE INCONTINE SMITH PS, 1979, BEHAV RES THER, V17, P33, DOI 10.1016/0005-7967(79)90048-2 SMITH PS, 1975, BEHAV RES THER, V15, P301 TIERNEY AJ, 1973, NURS TIMES, V20, P1740 VANWAGENEN R, 1969, P ANN CONV AM PSYCH, V4, P781 NR 25 TC 26 Z9 26 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD SEP-OCT PY 2002 VL 23 IS 5 BP 319 EP 331 DI 10.1016/S0891-4222(02)00136-1 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 613JQ UT WOS:000179129500002 PM 12401483 ER PT J AU Hastings, RP Symes, MD AF Hastings, RP Symes, MD TI Early intensive behavioral intervention for children with autism: parental therapeutic self-efficacy SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE autism; self-efficacy; applied behavior analysis; early intervention ID PERVASIVE DEVELOPMENTAL DISORDER; YOUNG-CHILDREN; STRESS; CHECKLIST; DISABILITIES; FAMILIES; AGE AB Several authors have suggested that the quality of therapist performance accounts for some of the variability in outcomes observed in early intensive behavioral intervention for children with autism. However, there is a distinct lack of theoretical and empirical work addressing therapist performance in this context. In the present study, we explored predictors of one variable, beliefs about one's efficacy in the therapeutic role, that may be related to therapist performance. Eighty-five UK mothers who were acting as therapists for their child's program completed a questionnaire survey. Results showed that program variables (e.g., number of hours of therapy each week, time since program started) were unrelated to maternal therapeutic self-efficacy. However, support received from the program, the severity of the child's autism, and maternal stress were significant predictors. Regression analysis also showed that maternal stress mediated the impact of support from the program and autism severity on maternal therapeutic self-efficacy. Limitations of the study, suggestions for future research, and practical implications are briefly discussed. In particular, we advocate a role for supervisors in analyzing and developing interventions for therapist behavior. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabilities, Southampton, Hants, England. RP Hastings, RP (reprint author), Univ Coll N Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. 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Dev. Disabil. PD SEP-OCT PY 2002 VL 23 IS 5 BP 332 EP 341 DI 10.1016/S0891-4222(02)00137-3 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 613JQ UT WOS:000179129500003 PM 12401484 ER PT J AU Siegert, RJ Ward, T AF Siegert, RJ Ward, T TI Clinical psychology and evolutionary psychology: Toward a dialogue SO REVIEW OF GENERAL PSYCHOLOGY LA English DT Article ID MIND; PHOBIAS; PSYCHOPATHOLOGY; PREPAREDNESS; DEPRESSION; AUTISM; FEAR; CLASSIFICATION; SCHIZOPHRENIA; PERSPECTIVE AB The growth of evolutionary psychology as a theoretical framework for the study of human behavior has been spectacular, However, evolutionary psychology has been largely ignored by clinical psychology. This article is an attempt to encourage greater dialogue between the two. First, some of the major principles of evolutionary psychology are outlined, followed by consideration of some of the criticisms that have been made of this approach. 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O., 1975, SOCIOBIOLOGY Wolpe J., 1958, PSYCHOTHERAPY RECIPR Zeki S, 1993, VISION BRAIN NR 92 TC 4 Z9 7 PU EDUCATIONAL PUBLISHING FOUNDATION PI WASHINGTON PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA SN 1089-2680 J9 REV GEN PSYCHOL JI Rev. Gen. Psychol. PD SEP PY 2002 VL 6 IS 3 BP 235 EP 259 DI 10.1037//1089-2680.6.3.235 PG 25 WC Psychology, Multidisciplinary SC Psychology GA 592GP UT WOS:000177928800001 ER PT J AU Rufo-Campos, M AF Rufo-Campos, M TI Melatonin and epilepsy SO REVISTA DE NEUROLOGIA LA Spanish DT Article; Proceedings Paper CT 6th Refresher Course on Epilepsy CY FEB 21-22, 2002 CL SANTANDER, SPAIN DE epilepsy; infancy; mechanism of action; melatonin; physiology ID DOUBLE-BLIND; NEUROHORMONE MELATONIN; SLEEP DISORDERS; ORAL MELATONIN; PINEAL-GLAND; CHILDREN; SECRETION; SEIZURES; SUPPRESSION; RECEPTORS AB Objective. This review has been prepared in response to the increasing interest shown in understanding the part played by melatonin in the body, which has led to the search for new uses of it in cerebral disorders, such as sleep disorders including insomnia, irritability, depression, behaviour disorders and even the treatment of autism, since sleep disorders also occur in this condition. We pay particular attention to studies involving epilepsy. Development. We show that interest in melatonin is rapidly increasing and new discoveries are being made of the part it plays in the biological regulation of circadian rhythm, sleep, mood, ageing, tumour growth and reproduction. Perhaps these processes between them have led to its use in the treatment of many current problems such as neuroprotection, migraine and the control of epileptic seizures. Conclusions. It has been shown that in both children and adults melatonin is of low toxicity and may be used in high risk persons. In this paper we make a careful analysis of recent publications in the medical literature dealing with the use of melatonin in the control of epileptic seizures and discuss its advantages and disadvantages. However, as with other types of treatment, further study, both experimental and otherwise, is necessary for confirmation. C1 Hosp Infantil Univ Virgen Rocio, Secc Neurol Infantil, Seville, Spain. 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Neurologia PD SEP PY 2002 VL 35 SU 1 BP S51 EP S58 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 605WG UT WOS:000178699600008 PM 12373656 ER PT J AU Stromland, K Philipson, E Gronlund, MA AF Stromland, K Philipson, E Gronlund, MA TI Offspring of male and female parents with thalidomide embryopathy: Birth defects and functional anomalies SO TERATOLOGY LA English DT Article ID MUTAGEN; RADIATION; MECHANISM AB Background: The aim of the study was to evaluate congenital malformations and functional anomalies in the offspring of Swedish parents with thalidomide embryopathy (TE). Methods: Sixty-four children (29 girls, 35 boys) with ages ranging from 0-18 years, born to 34 Swedish parents (14 women, 20 men) with TE, were studied. Data on malformations and dysfunction were collected from medical records at maternity and child healthcare units, delivery units, hospitals, outpatient clinics and schools. Results: Five children had both a mother and father with TE, 23 had a mother suffering from TE, and in 36 children the father had TE. One girl had a major malformation consisting of pulmonary stenosis, and single cases of minor physical features and positional deformities were observed. One boy had autism. Four children were born preterm, all to a TE mother. One child died within 24 hr after birth. Seven spontaneous abortions were registered, five of them in TE mothers. The cesarian section rate was 39% among the TE mothers, compared to 14% among the non-TE mothers. Conclusions: Malformations or functional anomalies similar to those typical for TE were not found in this group of children born to Swedish parents with TE. Cesarian sections were more frequently performed in TE mothers, partly because of pelvic and uterine malformations. C1 Queen Silvia Childrens Hosp, Dept Pediat Ophthalmol, SE-41685 Gothenburg, Sweden. Univ Gothenburg, Inst Clin Neurosci, Ophthalmol Sect, Gothenburg, Sweden. RP Stromland, K (reprint author), Queen Silvia Childrens Hosp, Dept Pediat Ophthalmol, SE-41685 Gothenburg, Sweden. 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Design Nested case-control study. Setting UK General Practice Research Database. Subjects Children born after 1 January 1988 and registered with the General Practice Research Database within 6 months of birth. Outcome measures Chronic inflammation of the gastrointestinal tract, coeliac disease, food intolerance, and recurrent gastrointestinal symptoms recorded by the general practitioner. Results 9 of 96 (9%) children with a diagnosis of autism (cases) and 41 of 449 (9%) children without autism (matched controls) had a history of gastrointestinal disorders before the index date (the date of first recorded diagnosis of autism in the cases and the same date for controls). The estimated odds ratio for a history of gastrointestinal disorders among children with autism compared with children without autism was 1.0 (95% confidence interval 0.5 to 2.2). Conclusions No evidence was found that children with autism were more likely than children without autism to have had defined gastrointestinal disorders at any time before their diagnosis of autism. C1 Boston Univ, Boston Collaborat Drug Surveillance Program, Boston, MA 02421 USA. RP Black, C (reprint author), Boston Univ, Boston Collaborat Drug Surveillance Program, Boston, MA 02421 USA. 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Med. J. PD AUG 24 PY 2002 VL 325 IS 7361 BP 419 EP 421 DI 10.1136/bmj.325.7361.419 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 588RY UT WOS:000177715500020 PM 12193358 ER PT J AU Harrison, AF AF Harrison, AF TI Wittgenstein and autism (Comment) SO TLS-THE TIMES LITERARY SUPPLEMENT LA English DT Letter CR FITZGERALD M, 2002, TLS 0802 HARRISON AF, 2002, TLS 0809 RUSSELL J, 2002, TLS 0816 NR 3 TC 0 Z9 0 PU TIMES SUPPLEMENTS LIMITED PI MARKET HARBOROUGH PA TOWER HOUSE, SOVEREIGN PARK, MARKET HARBOROUGH LE87 4JJ, ENGLAND SN 0307-661X J9 TLS-TIMES LIT SUPPL JI TLS-Times Lit. Suppl. PD AUG 23 PY 2002 IS 5186 BP 15 EP 15 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 589XE UT WOS:000177786200015 ER PT J AU Rojas, DC Bawn, SD Benkers, TL Reite, ML Rogers, SJ AF Rojas, DC Bawn, SD Benkers, TL Reite, ML Rogers, SJ TI Smaller left hemisphere planum temporale in adults with autistic disorder SO NEUROSCIENCE LETTERS LA English DT Article DE magnetic resonance imaging; mental retardation; cerebral asymmetry; temporal lobe; language; developmental disorder ID ASYMMETRY; SCHIZOPHRENIA; DOMINANCE; MRI AB The structure of the planum temporale is often disturbed in disorders with associated communication problems, particularly in auditory and language processing areas in the brain. We hypothesized that people with autism would have reduced left hemisphere volumes in the planum temporale, a language related brain structure. We performed magnetic resonance imaging scans of 15 adults with autistic disorder and 15 comparison subjects, and measured the volume of gray matter in the planum temporale and Heschl's gyrus (HG) in both hemispheres. Planum temporale volume reduced in the left hemisphere of the autism group (P < 0.003). No differences in HG volumes were observed between the two groups. The volume reduction seen in the left hemisphere of the autism group may suggest an early neurodevelopmental disturbance in autism that impacts language development. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. RP Rojas, DC (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Box C268-68 CPH,4200 E 9th Ave, Denver, CO 80262 USA. 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Lett. PD AUG 16 PY 2002 VL 328 IS 3 BP 237 EP 240 DI 10.1016/S0304-3940(02)00521-9 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 589GK UT WOS:000177750300009 PM 12147315 ER PT J AU Russell, J AF Russell, J TI Wittgenstein and autism (Reader's response to letters of Michael Fitzgerald and Alexander Fiske Harrison) SO TLS-THE TIMES LITERARY SUPPLEMENT LA English DT Letter C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Russell, J (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. CR FITZGERALD M, 2002, TLS 0802 HARRISON AF, 2002, TLS 0809 NR 2 TC 0 Z9 0 PU TIMES SUPPLEMENTS LIMITED PI MARKET HARBOROUGH PA TOWER HOUSE, SOVEREIGN PARK, MARKET HARBOROUGH LE87 4JJ, ENGLAND SN 0307-661X J9 TLS-TIMES LIT SUPPL JI TLS-Times Lit. Suppl. PD AUG 16 PY 2002 IS 5185 BP 15 EP 15 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 585NT UT WOS:000177531400018 ER PT J AU Heilstedt, HA Shahbazian, MD Lee, B AF Heilstedt, HA Shahbazian, MD Lee, B TI Infantile hypotonia as a presentation of Rett syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Rett syndrome; hypotonia; MECP2 ID MECP2 GENE; MUTATIONAL ANALYSIS; GROWTH FAILURE; GIRLS; SEVERITY; ACCOUNT; DISEASE; DNA AB Rett syndrome (RTT) is classically defined by meeting certain clinical diagnostic criteria. It affects mostly females, and one possible pathogenic mechanism was considered to involve mitochondrial function. This was based on the finding of ultrastructural alterations in the mitochondria and decreased respiratory chain enzyme activity. However, the principal etiology of RTT has since been found to be mutations in the MECP2 gene, which is located on the X chromosome. Molecular analysis has allowed the phenotype of MECP2 mutations to be broadened beyond RTT to include girls who have mild mental retardation, autism, and an Angelman syndrome phenotype, as well as males with severe encephalopathy. We present a girl with a previously described mutation in the MECP2 gene whose phenotype is of atypical RTT. She presented with hypotonia and developmental delay in infancy without a clear period of normal development. As part of her evaluation for hypotonia, a muscle biopsy and respiratory chain enzyme analysis showed a slight decrease in respiratory chain enzyme activity consistent with previous reports. This report supports broadening the phenotype of patients who should be considered for MECP2 mutation analysis to include cases of developmental delay and hypotonia without evidence of an initial period of normal development. Furthermore, it supports the hypothesis of an underlying secondary defect in energy metabolism contributing to the pathogenesis of RTT. (C) 2002 Wiley-Liss, Inc. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. RP Heilstedt, HA (reprint author), 1 Baylor Plaza,Room T817, Houston, TX 77030 USA. 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J. Med. Genet. PD AUG 15 PY 2002 VL 111 IS 3 BP 238 EP 242 DI 10.1002/ajmg.10633 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 579PE UT WOS:000177186400002 PM 12210319 ER PT J AU [Anonymous] AF [Anonymous] TI Children with autism may benefit from risperidone SO PHARMACEUTICAL JOURNAL LA English DT News Item CR McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 NR 1 TC 0 Z9 0 PU ROYAL PHARMACEUTICAL SOC GREAT BRITAIN PI LONDON PA 1 LAMBETH HIGH ST, LONDON SE1 7JN, ENGLAND SN 0031-6873 J9 PHARM J JI Pharma. J. PD AUG 10 PY 2002 VL 269 IS 7210 BP 184 EP 184 PG 1 GA 593XY UT WOS:000178020800013 ER PT J AU Harrison, AF AF Harrison, AF TI Wittgenstein and autism (Comment) SO TLS-THE TIMES LITERARY SUPPLEMENT LA English DT Letter CR FITZGERALD M, 2002, TLS 0809 NR 1 TC 0 Z9 0 PU TIMES SUPPLEMENTS LIMITED PI MARKET HARBOROUGH PA TOWER HOUSE, SOVEREIGN PARK, MARKET HARBOROUGH LE87 4JJ, ENGLAND SN 0307-661X J9 TLS-TIMES LIT SUPPL JI TLS-Times Lit. Suppl. PD AUG 9 PY 2002 IS 5184 BP 15 EP 15 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 585NR UT WOS:000177531300017 ER PT J AU Devlin, B Bennett, P Cook, RH Dawson, G Gonen, D Grigorenko, EL McMahon, W Pauls, D Smith, M Spence, MA Schellenberg, GD AF Devlin, B Bennett, P Cook, RH Dawson, G Gonen, D Grigorenko, EL McMahon, W Pauls, D Smith, M Spence, MA Schellenberg, GD CA CPEA Genetics Network TI No evidence for linkage of liability to autism to HOXA1 in a sample from the CPEA network SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; HOXA1; Asperger syndrome; pervasive developmental disorder; genetic association; autistic disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; FETAL VALPROATE SYNDROME; FAMILY HISTORY; SPECTRUM DISORDERS; SUSCEPTIBILITY; DISEQUILIBRIUM; GENE; DUPLICATION; INDIVIDUALS; ASSOCIATION AB A recent study by Ingram et al. [2000b: Teratology 62:393-405] suggests a (His)73(Arg) polymorphism (A:G) in HOXA1 contributes substantially to a liability for autism. Using 68 individuals diagnosed with Autism Spectrum Disorders, they found a significant dearth of G homozygotes and biased transmission of G alleles from parents to affected offspring, especially from mothers. Because the connection between HOXA1 and liability to autism is compelling, we attempted to replicate their finding using a larger, independent sample from the Collaborative Programs of Excellence in Autism (CPEA) network. In our data, genotype frequencies conform to Hardy-Weinberg equilibrium; allele transmissions meet Mendelian expectations; and there is no obvious sex-biased allele transmission. Based on our sample size, calculations suggest that we would have at least 95% power to detect linkage and association even if the A:G polymorphism were to account for only 1% of the heritability of autism. Therefore, although we cannot exclude the possibility that the samples in the two studies are intrinsically different, our data from our sample argue against a major role for HOXA1 (His)73(Arg) in liability to autism. (C) 2002 Wiley-Liss, Inc. C1 Vet Affairs Med Ctr, Seattle, WA 98108 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Utah, Dept Psychiat, Div Child & Adolescent Psychiat, Salt Lake City, UT USA. Univ Chicago, Dept Obstet, Lab Dev Neurosci, Dept Psychiat, Chicago, IL 60637 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 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 Washington, Dept Med, Seattle, WA 98195 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Univ Washington, Dept Pharmacol, Seattle, WA 98195 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. PD AUG 8 PY 2002 VL 114 IS 6 BP 667 EP 672 DI 10.1002/ajmg.10603 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 579NU UT WOS:000177185400015 PM 12210285 ER PT J AU O'Brien, J Spencer, J Atkinson, J Braddick, O Wattam-Bell, J AF O'Brien, J Spencer, J Atkinson, J Braddick, O Wattam-Bell, J TI Form and motion coherence processing in dyspraxia: evidence of a global spatial processing deficit SO NEUROREPORT LA English DT Article DE developmental co-ordination disorder; dorsal; dyspraxia; form coherence; motion coherence; ventral; occipitoparietal; occipitotemporal; visual perception ID DEVELOPMENTAL COORDINATION DISORDER; CHILDREN AB Form and motion coherence was tested in children with dyspraxia and matched controls to assess their global spatial and global motion processing abilities. Thresholds for detecting form coherence patterns were significantly higher in the dyspraxic group than in the control group. No corresponding difference was found on the mocion coherence task. We tested eight children with dyspraxic disorder (mean age 8.2 years) and 50 verbal-mental-age matched controls (mean age 8.4 years) to test for a neural basis to the perceptual abnormalities observed in dyspraxia. The results provide evidence that children with dyspraxia have a specific impairment in the global processing of spatial information. This finding contrasts with other developmental disorders such as Williams syndrome, autism and dyslexia where deficits have been found in global motion processing and not global form processing. We conclude that children with dyspraxia may have a specific occipitotemporal deficit and we argue that testing form and motion coherence thresholds might be a useful diagnostic tool for the often coexistent disorders of dyspraxia and dyslexia. C1 Brunel Univ, Dept Human Sci, Uxbridge UB8 3PH, Middx, England. UCL, Dept Psychol, Visual Dev Unit, London WC1E 6BT, England. Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP O'Brien, J (reprint author), Brunel Univ, Dept Human Sci, Uxbridge UB8 3PH, Middx, England. 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Ind. PD AUG 5 PY 2002 IS 15 BP 5 EP 5 PG 1 WC Chemistry, Applied SC Chemistry GA 582FR UT WOS:000177339600003 ER PT J AU Fitzgerald, M AF Fitzgerald, M TI Wittgenstein and autism (Reader's response to Brian McGuinness's quotation of Michael Dummett) SO TLS-THE TIMES LITERARY SUPPLEMENT LA English DT Letter C1 Univ Dublin Trinity Coll, Dept Psychiat, Dublin 10, Ireland. RP Fitzgerald, M (reprint author), Univ Dublin Trinity Coll, Dept Psychiat, Dublin 10, Ireland. CR DUMMETT M, 2002, TLS 0614 MACGUINNESS B, 2002, TLS 0614 NR 2 TC 0 Z9 0 PU TIMES SUPPLEMENTS LIMITED PI MARKET HARBOROUGH PA TOWER HOUSE, SOVEREIGN PARK, MARKET HARBOROUGH LE87 4JJ, ENGLAND SN 0307-661X J9 TLS-TIMES LIT SUPPL JI TLS-Times Lit. Suppl. PD AUG 2 PY 2002 IS 5183 BP 15 EP 15 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 582ZD UT WOS:000177380300025 ER PT J AU Roberts, JE Mirrett, P Anderson, K Burchinal, M Neebe, E AF Roberts, JE Mirrett, P Anderson, K Burchinal, M Neebe, E TI Early communication, symbolic behavior, and social profiles of young males with fragile X syndrome SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE language assessment; mental retardation; fragile X syndrome; communication skills ID DOWN-SYNDROME; COGNITIVE PROFILES; JOINT ATTENTION; AUTISM; LANGUAGE; CHILDREN; LEVEL; BOYS; GAZE AB This study examined the communication and symbolic behavior profiles of 22 males with fragile X syndrome (FXS) developmentally younger than 28 months and the relationship of these profiles to the children's communication skills one year later. The boys, ranging in age from 21 to 77 months, were tested using the Communication and Symbolic Behavior Scales and the Reynell Developmental Language Scales. The children showed significant delays and substantial individual variability in their profiles. Overall, they showed relative strengths in verbal and vocal communication and relative weaknesses in gestures, reciprocity, and symbolic play skills. Children who scored higher in communicative functions, vocalizations, verbalizations, and reciprocity scored higher in verbal comprehension one year later. Children with higher scores in verbal communication also scored higher in expressive language development when tested one year later. C1 Univ N Carolina, Frank Porter Graham Child Dev Ctr, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Pediat, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Allied Hlth Sci, Div Speech & Hearing Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA. RP Roberts, JE (reprint author), Univ N Carolina, Frank Porter Graham Child Dev Inst, 105 Smith Level Rd,CB 8180, Chapel Hill, NC 27599 USA. EM joanne_roberts@unc.edu CR Abbeduto L, 1997, MENT RETARD DEV D R, V3, P313, DOI 10.1002/(SICI)1098-2779(1997)3:4<313::AID-MRDD6>3.0.CO;2-O Bailey DB, 1998, J AUTISM DEV DISORD, V28, P499 Bailey DB, 1998, AM J MENT RETARD, V103, P29, DOI 10.1352/0895-8017(1998)103<0029:EDTOMW>2.0.CO;2 Bates E., 1979, EMERGENCE SYMBOLS CO BAUMGARDNER TL, 1995, PEDIATRICS, V95, P744 Bennetto L, 1996, FRAGILE X SYNDROME D, P210 Bruner J. S., 1977, STUDIES MOTHER INFAN, P271 COHEN IL, 1989, J CHILD PSYCHOL PSYC, V30, P845, DOI 10.1111/j.1469-7610.1989.tb00286.x COHEN IL, 1991, AM J MED GENET, V38, P498, DOI 10.1002/ajmg.1320380271 COHEN IL, 1988, AM J MENT RETARD, V92, P436 DYKENS EM, 1994, BEHAV DEV FRAGILE 10 TOMASELLO M, 1986, CHILD DEV, V57, P1454, DOI 10.1111/j.1467-8624.1986.tb00470.x FERRIER LJ, 1991, DEV MED CHILD NEUROL, V33, P776 FREUND LS, 1991, AM J MED GENET, V38, P542, DOI 10.1002/ajmg.1320380409 HAGERMAN RJ, 1995, MENT RETARD DEV D R, V1, P276, DOI 10.1002/mrdd.1410010408 Hagerman RJ, 1996, DEV PSYCHOL, V32, P416 HANSON DM, 1986, AM J MED GENET, V23, P195, DOI 10.1002/ajmg.1320230114 HODAPP RM, 1992, AM J MENT RETARD, V97, P39 KEMPER MB, 1988, AM J MED GENET, V30, P191, DOI 10.1002/ajmg.1320300118 MCCATHREN RB, 1999, J SPEECH LANG HEAR R, V42, P924 MERVIS CB, 1999, CONTINTUITY CHANGE S MUNDY P, 1994, DEV PSYCHOPATHOL, V6, P389, DOI 10.1017/S0954579400006003 Newborg J., 1984, BATTELLE DEV INVENTO Newell K, 1983, FRAGILE X SYNDROME D, P175 PAUL R, 1984, J SPEECH HEAR DISORD, V49, P326 Reynell J., 1990, REYNELL DEV LANGUAGE Roberts JE, 2001, AM J MENT RETARD, V106, P216, DOI 10.1352/0895-8017(2001)106<0216:RAECDO>2.0.CO;2 ROBERTS JE, 1997, AM J SPEECH-LANG PAT, V6, P59 Rollins PR, 1998, J CHILD LANG, V25, P653 SCARBOROUGH HS, 1991, APPL PSYCHOLINGUIST, V12, P23, DOI 10.1017/S014271640000936X Schopler E., 1988, CHILDHOOD AUTISM RAT Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 SUDHALTER V, 1992, AM J MED GENET, V43, P65, DOI 10.1002/ajmg.1320430110 SUDHALTER V, 1990, AM J MENT RETARD, V94, P431 THAL DJ, 1992, J SPEECH HEAR RES, V35, P1281 Turner G, 1996, AM J MED GENET, V64, P196, DOI 10.1002/(SICI)1096-8628(19960712)64:1<196::AID-AJMG35>3.0.CO;2-G WETHERBY A, 1988, J SPEECH HEAR RES, V27, P364 Wetherby A., 1993, COMMUNICATION SYMBOL Wetherby A. M., 1998, TRANSITIONS PRELINGU, P135 Wetherby AM, 1998, AM J SPEECH-LANG PAT, V7, P79 Winer B.J., 1971, STAT PRINCIPLES EXPT WOLFF PH, 1989, AM J MENT RETARD, V93, P406 NR 42 TC 16 Z9 16 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1058-0360 EI 1558-9110 J9 AM J SPEECH-LANG PAT JI Am. J. Speech-Lang. Pathol. PD AUG PY 2002 VL 11 IS 3 BP 295 EP 304 DI 10.1044/1058-0360(2002/034) PG 10 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 714HC UT WOS:000184906400016 ER PT J AU Toichi, M Kamio, Y Okada, T Sakihama, M Youngstrom, EA Findling, RL Yamamoto, K AF Toichi, M Kamio, Y Okada, T Sakihama, M Youngstrom, EA Findling, RL Yamamoto, K TI A lack of self-consciousness in autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID MEMORY AB Objective: This study investigated self-consciousness in autism. Method: An incidental memory task was conducted on 18 adults with high-functioning autism and 18 normal comparison subjects. Three kinds of orienting questions (phonological, semantic, and self-referent, i.e., "Does the word describe you?") were asked about target words (adjectives for personality traits) in order to induce different types of processing. This was followed by an unexpected recognition test. Results: While semantic processing resulted in better memory than phonological processing in both groups, self-referent processing yielded better memory performance than semantic processing in the comparison group but not in the autistic group. Conclusions: The results suggest deficits in self-consciousness in individuals with autism. C1 Case Western Reserve Univ Hosp, Div Child & Adolescent Psychiat, Cleveland, OH 44106 USA. Shiga Univ, Hlth & Med Serv Ctr, Shiga, Japan. RP Toichi, M (reprint author), Case Western Reserve Univ Hosp, Div Child & Adolescent Psychiat, 11100 Euclid Ave, Cleveland, OH 44106 USA. CR Beversdorf DQ, 2000, P NATL ACAD SCI USA, V97, P8734, DOI 10.1073/pnas.97.15.8734 CRAIK FIM, 1975, J EXP PSYCHOL GEN, V104, P268, DOI 10.1037//0096-3445.104.3.268 DAWSON G, 1984, J AUTISM DEV DISORD, V14, P383, DOI 10.1007/BF02409829 Millward C, 2000, J AUTISM DEV DISORD, V30, P15, DOI 10.1023/A:1005455926727 Raven J. C., 1962, COLOURED PROGR MATRI ROGERS TB, 1977, J PERS SOC PSYCHOL, V35, P677, DOI 10.1037//0022-3514.35.9.677 Schopler E., 1986, CHILDHOOD AUTISM RAT Symons CS, 1997, PSYCHOL BULL, V121, P371, DOI 10.1037/0033-2909.121.3.371 NR 8 TC 49 Z9 50 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 2002 VL 159 IS 8 BP 1422 EP 1424 DI 10.1176/appi.ajp.159.8.1422 PG 3 WC Psychiatry SC Psychiatry GA 582AJ UT WOS:000177327300024 PM 12153838 ER PT J AU Castelli, F Frith, C Happe, F Frith, U AF Castelli, Fulvia Frith, Chris Happe, Francesca Frith, Uta TI Autism, Asperger syndrome and brain mechanisms for the attribution of mental states to animated shapes SO BRAIN LA English DT Article DE anterior cingulate; autism; extrastriate cortex; superior temporal sulcus; temporal poles; Theory of Mind ID FUSIFORM FACE AREA; CORTICAL CONNECTIONS; EXTRASTRIATE CORTEX; FUNCTIONING AUTISM; 2ND-ORDER BELIEFS; NORMAL-CHILDREN; VISUAL-CORTEX; MIND; PERCEPTION; AMYGDALA AB Ten able adults with autism or Asperger syndrome and 10 normal volunteers were PET scanned while watching animated sequences. The animations depicted two triangles moving about on a screen in three different conditions: moving randomly, moving in a goal-directed fashion (chasing, fighting), and moving interactively with implied intentions (coaxing, tricking). The, last condition frequently elicited descriptions in terms of mental states that viewers attributed to the triangles (mentalizing). The autism group gave fewer and less accurate descriptions of these latter animations, but equally accurate descriptions of the other animations compared with controls. While viewing animations that elicited mentalizing, in contrast to randomly moving shapes, the normal group showed increased activation in a previously identified mentalizing network (medial prefrontal cortex, superior temporal sulcus at the temporoparietal junction and temporal poles). The autism group showed less activation than the normal group in all these regions. However, one additional region, extrastriate cortex, which was highly active when watching animations that elicited mentalizing, showed the same amount of increased activation in both groups. In the autism group this extrastriate region showed reduced functional connectivity with the superior temporal sulcus at the temporo-parietal junction, an area associated with the processing of biological motion as well as with mentalizing. This finding suggests a physiological cause for the mentalizing dysfunction in autism: a bottleneck in the interaction between higher order and lower order perceptual processes. C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. UCL, Wellcome Dept Cognit Neurol, Inst Neurol, London WC1N 3AR, England. Kings Coll London, Inst Psychiat, London WC2R 2LS, England. RP Frith, U (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England. EM u.frith@ucl.ac.uk RI Frith, Uta/C-1757-2008; Frith, Chris/A-2171-2009; Happe, Francesca/D-5544-2012 OI Frith, Uta/0000-0002-9063-4466; Frith, Chris/0000-0002-8665-0690; CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 ABELL F, 2000, J COGNITIVE DEV, V15, P1 Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 AMARAL D G, 1992, P1 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Ammons RB, 1962, QUICK TEST Aylward EH, 1999, NEUROLOGY, V53, P2145 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Bauman M.L, 1994, NEUROBIOLOGY AUTISM Bauman ML, 1996, J AUTISM DEV DISORD, V26, P199, DOI 10.1007/BF02172012 Bonda E, 1996, J NEUROSCI, V16, P3737 BOUSSAOUD D, 1990, J COMP NEUROL, V296, P462, DOI 10.1002/cne.902960311 Bowler D, 2000, AUTISM, V4, P147, DOI 10.1177/1362361300004002004 Brunet E, 2000, NEUROIMAGE, V11, P157, DOI 10.1006/nimg.1999.0525 Carper RA, 2000, BRAIN, V123, P836, DOI 10.1093/brain/123.4.836 Castelli F, 2000, NEUROIMAGE, V12, P314, DOI 10.1006/nimg.2000.0612 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 EVANS AC, 1994, NATO ADV SCI INST SE, V264, P263 FELLEMAN DJ, 1987, J NEUROPHYSIOL, V57, P889 Felleman DJ, 1997, J COMP NEUROL, V379, P21, DOI 10.1002/(SICI)1096-9861(19970303)379:1<21::AID-CNE3>3.0.CO;2-K Fine C, 2001, BRAIN, V124, P287, DOI 10.1093/brain/124.2.287 FLETCHER PC, 1995, COGNITION, V57, P109, DOI 10.1016/0010-0277(95)00692-R FRISON L, 1992, STAT MED, V11, P1685, DOI 10.1002/sim.4780111304 Friston KJ, 1997, HUMAN BRAIN FUNCTION, P25 Friston KJ, 1994, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402 Friston KJ, 1995, HUM BRAIN MAPP, V3, P165, DOI 10.1002/hbm.460030303 Friston KJ, 2000, P NATL ACAD SCI USA, V97, P7591, DOI 10.1073/pnas.97.13.7591 Gallagher HL, 2000, NEUROPSYCHOLOGIA, V38, P11, DOI 10.1016/S0028-3932(99)00053-6 GOEL V, 1995, NEUROREPORT, V6, P1741, DOI 10.1097/00001756-199509000-00009 Happe F, 1996, BRAIN, V119, P1377, DOI 10.1093/brain/119.4.1377 Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Heider F, 1944, AM J PSYCHOL, V57, P243, DOI 10.2307/1416950 Howard MA, 2000, NEUROREPORT, V11, P2931, DOI 10.1097/00001756-200009110-00020 Kanwisher N, 1997, J NEUROSCI, V17, P4302 Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 LESLIE AM, 1992, COGNITION, V43, P225, DOI 10.1016/0010-0277(92)90013-8 MALACH R, 1995, P NATL ACAD SCI USA, V92, P8135, DOI 10.1073/pnas.92.18.8135 Olson IR, 2001, BRAIN, V124, P1417, DOI 10.1093/brain/124.7.1417 PERNER J, 1985, J EXP CHILD PSYCHOL, V39, P437, DOI 10.1016/0022-0965(85)90051-7 Perner J, 1989, Child Dev, V60, P688 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 PLANT GT, 1993, BRAIN, V116, P1337, DOI 10.1093/brain/116.6.1337 Puce A, 1998, J NEUROSCI, V18, P2188 Raven JC, 1958, STANDARD PROGR MATRI Roeyers H, 2001, J CHILD PSYCHOL PSYC, V42, P271, DOI 10.1111/1469-7610.00718 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 SODIAN B, 1992, J CHILD PSYCHOL PSYC, V33, P591, DOI 10.1111/j.1469-7610.1992.tb00893.x Sugase Y, 1999, NATURE, V400, P869, DOI 10.1038/23703 SULLIVAN K, 1994, DEV PSYCHOL, V30, P395, DOI 10.1037//0012-1649.30.3.395 Talairach J., 1988, COPLANAR STEREOTAXIC Vogeley K, 2001, NEUROIMAGE, V14, P170, DOI 10.1006/nimg.2001.0789 ZEKI SM, 1978, J PHYSIOL-LONDON, V277, P245 NR 58 TC 621 Z9 626 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD AUG PY 2002 VL 125 BP 1839 EP 1849 DI 10.1093/brain/awf189 PN 8 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA V42NS UT WOS:000202874800015 PM 12135974 ER PT J AU Stromme, P Mangelsdorf, ME Scheffer, IE Gecz, J AF Stromme, P Mangelsdorf, ME Scheffer, IE Gecz, J TI Infantile spasms, dystonia, and other X-linked phenotypes caused by mutations in Aristaless related homeobox gene, ARX SO BRAIN & DEVELOPMENT LA English DT Article DE aristaless related homeobox gene; ARX; dystonia; infantile spasms; seizures; X-linked mental retardation ID MENTAL-RETARDATION; LINKAGE AB Clinical data from 50 mentally retarded (MR) males in nine X-linked MR families, syndromic and non-specific, with mutations (duplication, expansion, missense, and deletion mutations) in the Aristaless related homeobox gene, ARX, were analysed. Seizures were observed with all mutations and occurred in 29 patients, including one family with a novel myoclonic epilepsy syndrome associated with the missense mutation. Seventeen patients had infantile spasms. Other phenotypes included mild to moderate MR alone, or with combinations of dystonia, ataxia or autism. These data suggest that mutations in the ARX gene are important causes of MR, often associated with diverse neurological manifestations. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Womens & Childrens Hosp, Dept Cytogenet & Mol Genet, Adelaide, SA 5006, Australia. Natl Hosp Norway, Dept Paediat, N-0027 Oslo, Norway. Univ Adelaide, Dept Paediat, Adelaide, SA, Australia. Royal Childrens Hosp, Dept Med Neurol, Melbourne, Vic, Australia. Univ Melbourne, Austin & Repatriat Med Ctr, Monash Med Ctr, Melbourne, Vic, Australia. RP Stromme, P (reprint author), Womens & Childrens Hosp, Dept Cytogenet & Mol Genet, Adelaide, SA 5006, Australia. EM petter.stromme@rikshospitalet.no RI Scheffer, Ingrid/G-1668-2013; Mangelsdorf, Marie/A-2318-2013 OI Scheffer, Ingrid/0000-0002-2311-2174; Mangelsdorf, Marie/0000-0002-7855-7701 CR Bienvenu T, 2002, HUM MOL GENET, V11, P981, DOI 10.1093/hmg/11.8.981 Bruyere H, 1999, CLIN GENET, V55, P173, DOI 10.1034/j.1399-0004.1999.550305.x Chelly J, 2001, NAT REV GENET, V2, P669, DOI 10.1038/35088558 Chiurazzi P, 2001, EUR J HUM GENET, V9, P71, DOI 10.1038/sj.ejhg.5200603 Claes S, 1997, ANN NEUROL, V42, P360, DOI 10.1002/ana.410420313 PARTINGTON MW, 1988, AM J MED GENET, V30, P251, DOI 10.1002/ajmg.1320300127 SCHEFFER IE, 2002, IN PRESS NEUROLOGY Stromme P, 2002, NAT GENET, V30, P441, DOI 10.1038/ng862 Stromme P, 1999, J MED GENET, V36, P374 Wong M, 2001, PEDIATR NEUROL, V24, P89, DOI 10.1016/S0887-8994(00)00238-1 NR 10 TC 103 Z9 105 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 EI 1872-7131 J9 BRAIN DEV-JPN JI Brain Dev. PD AUG PY 2002 VL 24 IS 5 BP 266 EP 268 DI 10.1016/S0387-7604(02)00079-7 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 586LQ UT WOS:000177585800002 PM 12142061 ER PT J AU Parmeggiani, A Posar, A Giovanardi-Rossi, P Andermann, F Zifkin, B AF Parmeggiani, A Posar, A Giovanardi-Rossi, P Andermann, F Zifkin, B TI Autism, macrocrania and epilepsy: How are they linked? SO BRAIN & DEVELOPMENT LA English DT Article DE autistic disorder; pervasive developmental disorders; epilepsy; macrocrania; macrocephaly; mental retardation AB To evaluate the possible association of autistic disorder (AD), macrocrania and epilepsy, we performed a retrospective study comparing epileptic and non-epileptic AD patients with macrocrania, and AD patients with macrocrania to age- and sex-matched AD controls without macrocrania. We found macrocrania in 17.3% of 121 patients with AD. Epilepsy was not significantly more frequent in AD patients with macrocrania than in those without macrocrania. There were no significant differences in the other clinical characteristics studied except for epileptiform EEG abnormalities which were more often found in AD patients with epilepsy. AD with macrocrania and epilepsy is not a syndrome but may be a marker for a group of subjects with AD. A role for familial macrocrania needs further assessment. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Bologna, Dept Neurol Sci, Child Neurol & Psychiat Unit, I-40123 Bologna, Italy. McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ, Canada. Montreal Neurol Hosp & Inst, Montreal, PQ H3A 2B4, Canada. Montreal Neurol Hosp, Epilepsy Clin, Montreal, PQ, Canada. Univ Montreal, Fac Med, Montreal, PQ H3C 3J7, Canada. RP Parmeggiani, A (reprint author), Univ Bologna, Dept Neurol Sci, Child Neurol & Psychiat Unit, Via Ugo Foscolo 7, I-40123 Bologna, Italy. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERMANN F, 1995, BRAIN DEV-JPN, V17, P362, DOI 10.1016/0387-7604(95)00092-P Andres C, 2002, BRAIN RES BULL, V57, P109, DOI 10.1016/S0361-9230(01)00642-6 Commission on Classification and Terminology of the International League Against Epilepsy, 1989, EPILEPSIA, V30, P389 DEKABAN AS, 1977, HDB CLIN NEUROLOGY C, P647 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 Rossi PG, 2000, BRAIN DEV-JPN, V22, P102 Lainhart JE, 1997, J AM ACAD CHILD PSY, V36, P282, DOI 10.1097/00004583-199702000-00019 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 ROSSI PG, 1995, BRAIN DEV-JPN, V17, P169, DOI 10.1016/0387-7604(95)00019-8 NR 11 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD AUG PY 2002 VL 24 IS 5 BP 296 EP 299 DI 10.1016/S0387-7604(02)00063-3 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 586LQ UT WOS:000177585800008 PM 12142067 ER PT J AU Sourander, A Ellila, H Valimaki, M Piha, J AF Sourander, A Ellila, H Valimaki, M Piha, J TI Use of holding, restraints, seclusion and time-out in child and adolescent psychiatric in-patient treatment SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE child and adolescent psychiatry; holding; in-patient; restraints; seclusion ID GLOBAL ASSESSMENT SCALE; INPATIENT TREATMENT; PHYSICAL RESTRAINT; BEHAVIOR; PREDICTORS; UNIT; CGAS AB The aim of the study was to analyse the use of holding, restraints, seclusion and time-out in child and adolescent psychiatric in-patient treatment in Finland. The study included 504 child and adolescent psychiatric in-patients in the year 2000. Time-out had been used for 28%, holding for 26%, seclusion for 8%, and mechanical restraints for 4% of the in-patients. In multivariate analysis, aggressive acts were the strongest factor associated with all kinds of restraint practices. Psychosis, suicidal acts and older age (13-18 years) were associated with seclusion and mechanical restraints. Younger age (< 13 years), attachment disorder and autism were associated with holding. The longer children had been in treatment, the more likely they were to have been restrained. The high prevalence of restraint techniques used indicates a need for guidelines of restraint and seclusion which take into account the child's need for protection from his/her own impulses and the legal rights of the child. C1 Turku Univ, Dept Child Psychiat, Turku 20520, Finland. Turku Univ, Dept Nursing Sci, Turku 20520, Finland. RP Sourander, A (reprint author), Turku Univ, Dept Child Psychiat, Turku 20520, Finland. 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Polymorphisms in promoter regions affecting expression of genes involved in regulating behaviour may play a role in generating individual variation in behaviour, including psychopathologies in humans, and probably are also important for the evolution of behaviour. Here we discuss the prairie vole vasopressin V1a receptor gene as a model that may be useful for understanding the evolution of promoter sequences and the relationship between gene sequence, expression and behavioural phenotype. C1 Emory Univ, Yerkes Reg Primate Res Ctr, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA. Emory Univ, Ctr Behav Neurosci, Atlanta, GA 30322 USA. RP Young, LJ (reprint author), Emory Univ, Yerkes Reg Primate Res Ctr, Dept Psychiat & Behav Sci, 954 Gatewood Rd, Atlanta, GA 30322 USA. 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J. Neurosci. PD AUG PY 2002 VL 16 IS 3 BP 399 EP 402 DI 10.1046/j.1460-9568.2002.02083.x PG 4 WC Neurosciences SC Neurosciences & Neurology GA 586QU UT WOS:000177596500008 PM 12193181 ER PT J AU Valdovinos, MG Napolitano, DA Zarcone, JR Hellings, JA Williams, DC Schroeder, SR AF Valdovinos, MG Napolitano, DA Zarcone, JR Hellings, JA Williams, DC Schroeder, SR TI Multimodal evaluation of risperidone for destructive behavior: Functional analysis, direct observations, rating scales, and psychiatric impressions SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; TARDIVE-DYSKINESIA; MENTAL-RETARDATION; DOUBLE-BLIND; ADULTS; ADOLESCENTS; CHILDREN; AUTISM; DISABILITIES; CHECKLIST AB Risperidone, an atypical neuroleptic, has become a popular option for treating destructive behaviors of persons with developmental disabilities. A few studies have been conducted that evaluate the effects of risperidone on destructive behavior; however, none of these studies have combined objective measures with rating scales to evaluate the effects of risperidone on destructive behavior across home and clinical settings. This study evaluated the wide range of effects of risperidone on destructive behavior of 2 persons with developmental disabilities using weekly functional analysis sessions, daily observations, hourly home data, weekly rating scales, and monthly psychiatric impressions. Results indicate that risperidone does decrease destructive behavior and that, for the most part, all of the various measures yielded similar results. C1 Univ Kansas, Schiefelbusch Inst Lifespan Studies, Lawrence, KS 66045 USA. RP Valdovinos, MG (reprint author), Vanderbilt Univ, Peabody Coll, Box 74, Nashville, TN 37203 USA. 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PD AUG PY 2002 VL 10 IS 3 BP 268 EP 275 DI 10.1037//1064-1297.10.3.268 PG 8 WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy; Psychiatry SC Psychology; Pharmacology & Pharmacy; Psychiatry GA 588QJ UT WOS:000177711900011 PM 12233987 ER PT J AU Sultana, R Yu, CE Yu, J Munson, J Chen, DH Hua, WH Estes, A Cortes, F de la Barra, F Yu, DM Haider, ST Trask, BJ Green, ED Raskind, WH Disteche, CM Wijsman, E Dawson, G Storm, DR Schellenberg, GD Villacres, EC AF Sultana, R Yu, CE Yu, J Munson, J Chen, DH Hua, WH Estes, A Cortes, F de la Barra, F Yu, DM Haider, ST Trask, BJ Green, ED Raskind, WH Disteche, CM Wijsman, E Dawson, G Storm, DR Schellenberg, GD Villacres, EC TI Identification of a novel gene on chromosome 7q11.2 interrupted by a translocation breakpoint in a pair of autistic twins SO GENOMICS LA English DT Article ID QUANTITATIVE TRAIT; GENOMIC SCREEN; DISORDER; LINKAGE; LOCUS; 7Q AB We report here the identification and characterization of a novel gene (AUTS2) that spans the 7q11.2 break-point in a monozygotic twin pair concordant for autism and a t(7;20) (q11.2; p11.2) translocation. AUTS2 is 1.2 Mb and has 19 exons. The predicted protein is 1295 amino acids and does not correspond to any known protein. DNA sequence analysis of autism subjects and controls revealed 22 biallelic polymorphic sites. For all sites, both alleles were observed in both cases and controls. Thus no autism-specific mutation was observed. Association analysis with two exonic polymorphic sites and linkage analysis of four dinucleotide repeat markers, two within and two flanking AUTS2, was negative. Thus, although it is unlikely that AUTS2 is an autism susceptibility gene for idiopathic autism, it may be the gene responsible for the disorder in the twins studied here. C1 Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. Univ Washington, Dept Mol Biotechnol, Seattle, WA 98195 USA. Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Univ Washington, Dept Pathol, Seattle, WA 98195 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Seattle Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Seattle, WA 98195 USA. Univ Chile, Genet & Met Dis Unit, INTA, Santiago 13811, Chile. Univ Chile, Psychiat & Mental Hlth Dept, Santiago 13811, Chile. NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. RP Villacres, EC (reprint author), Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. 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We characterized the human secretin locus to determine whether mutations in this gene might play a role in a fraction of autism patients. While the secretin gene (SCT) was not found to be mutated in the majority of autistic patients, rare heterozygous sequence variants were identified in three patients. We also investigated length variation in a variable number of tandem repeats (VNTR) immediately upstream of SCT and found no significant differences in length between patients with autism and normal controls. SCT is located on 11p15.5, adjacent to DRD4 and HRAS. This region has been reported to be associated with both autism and attention deficit hyperactivity disorder (ADHD). Although imprinting is a characteristic of some genes in the vicinity, we could find no evidence for methylation of SCT in lymphoblast cells from patients or control individuals. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Jichi Med Sch, Dept Pediat, Minami Kawachi, Tochigi, Japan. 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Analyses of the scanpath data revealed marked differences in the scanpaths of the two groups. The autistic participants viewed nonfeature areas of the faces significantly more often and core feature areas of the faces (i.e., eyes, nose, and mouth) significantly less often than did control participants. Across both groups of participants, scanpaths generally did not differ as a function of the instructions given to the participants (i.e., "Please look at the faces in any manner you wish." vs. "Please identify the emotions portrayed in these faces."). Autistic participants showed a deficit in emotion recognition, but this effect was driven primarily by deficits in the recognition of fear. Collectively, these results indicate disorganized processing of face stimuli in autistic individuals and suggest a mechanism that may subserve the social information processing deficits that characterize autism spectrum disorders. C1 Univ N Carolina, Dept Psychol, Chapel Hill, NC USA. 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L., 1967, EYE MOVEMENTS VISION NR 73 TC 413 Z9 427 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2002 VL 32 IS 4 BP 249 EP 261 DI 10.1023/A:1016374617369 PG 13 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600002 PM 12199131 ER PT J AU Gunter, HL Ghaziuddin, M Ellis, HD AF Gunter, HL Ghaziuddin, M Ellis, HD TI Asperger syndrome: Tests of right hemisphere functioning and interhemispheric communication SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; nonverbal learning disabilities; right hemisphere dysfunction; interhemisphere communication; neuropsychological assessment ID LANGUAGE; AUTISM; INTELLIGENCE; DEFICITS; DISORDER; PEOPLE; DAMAGE; BRAIN; MIND AB The primary aim of this investigation was to assess to what extent Rourke's (1989, 1995) nonverbal learning disabilities syndrome (NLD) model resembles the pattern of assets and deficits seen in people with Asperger syndrome (AS). NLD can be characterized by a cluster of deficits primarily affecting nonverbal aspects of functioning, in the presence of proficiency in single word reading and a superior verbal memory. The neurological underpinnings of this syndrome may be dysfunction of white matter affecting right hemisphere functioning and interhemispheric communication. To explore this hypothesis, eight participants with AS (ages 10 to 41 years) were assessed in the following areas: the pragmatics of language and communication, verbal and visual memory, visual-spatial abilities, and bimanual motor skills. Results confirmed the close similarity in the neuropsychologic profiles of NLD and AS. C1 Cardiff Univ, Sch Psychol, Cardiff CF10 3YG, S Glam, Wales. Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA. RP Ellis, HD (reprint author), Cardiff Univ, Sch Psychol, Cardiff CF10 3YG, S Glam, Wales. 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PD AUG PY 2002 VL 32 IS 4 BP 263 EP 281 DI 10.1023/A:1016326701439 PG 19 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600003 PM 12199132 ER PT J AU Bauminger, N AF Bauminger, N TI The facilitation of social-emotional understanding and social interaction in high-functioning children with autism: Intervention outcomes SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; social-emotional understanding; social interaction; cognitive-behavioral intervention; social problem solving; affective education ID NONRETARDED-CHILDREN; TEACHING THEORY; MIND; RECOGNITION; INFORMATION; ADOLESCENTS; ATTRIBUTION; COMPETENCE; ABILITY; BELIEF AB This study evaluated the effectiveness of a 7-month cognitive behavioral intervention for the facilitation of the social-emotional understanding and social interaction of 15 high-functioning children (8 to 17 years old) with autism. Intervention focused on teaching interpersonal problem solving, affective knowledge, and social interaction. Preintervention and postintervention measures included observations of social interaction, measures of problem solving and of emotion understanding, and teacher-rated social skills. Results demonstrated progress in three areas of intervention. Children were more likely to initiate positive social interaction with peers after treatment; in particular, they improved eye contact and their ability to share experiences with peers and to show interest in peers. In problem solving after treatment, children provided more relevant solutions and fewer nonsocial solutions to different social situations. In emotional knowledge, after treatment, children provided more examples of complex emotions, supplied more specific rather then general examples, and included an audience more often in the different emotions. Children also obtained higher teacher-rated social skills scores in assertion and cooperation after treatment. The implications of these findings are discussed in terms of the effectiveness of the current model of intervention for high-functioning children with autism. C1 Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. RP Bauminger, N (reprint author), Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. 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PD AUG PY 2002 VL 32 IS 4 BP 283 EP 298 DI 10.1023/A:1016378718278 PG 16 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600004 PM 12199133 ER PT J AU Ghaziuddin, M Ghaziuddin, N Greden, J AF Ghaziuddin, M Ghaziuddin, N Greden, J TI Depression in persons with autism: Implications for research and clinical care SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; depression treatment; comorbidity; outcome ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGERS SYNDROME; MAJOR DEPRESSION; FLUOXETINE TREATMENT; SPECTRUM DISORDERS; FAMILY HISTORY; LIFE EVENTS; CHILDREN; CATATONIA; ADULTS AB Although several studies have investigated the occurrence of medical and neurological conditions in persons with autism, relatively few reports have focused on the phenomenology and treatment of psychiatric disorders in this population. 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Autism Dev. Disord. PD AUG PY 2002 VL 32 IS 4 BP 299 EP 306 DI 10.1023/A:1016330802348 PG 8 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600005 PM 12199134 ER PT J AU Geiger, DM Smith, DT Creaghead, NA AF Geiger, DM Smith, DT Creaghead, NA TI Parent and professional agreement on cognitive level of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE parent professional agreement; autism; cognition AB The aim of the study was to compare the extent of agreement between parents and professional evaluators regarding the cognitive level of children with autism. We sought to determine the degree of parent and standardized test agreement about the child's cognitive level for children at different levels of cognitive functioning. Information regarding parental view of cognitive levels was collected from the questionnaires used during the initial evaluation. These levels were compared with age equivalencies obtained by professionals from standardized intellectual measures. Significant difference between parental perception and professional assessment of the child's cognitive level was found. In addition, there was significant correlation between the level of agreement and cognitive functioning; agreement increased as the level of cognitive functioning increased. C1 Univ Affiliated Univ, Ctr Dev Disorders, Cincinnati, OH 45229 USA. Univ Cincinnati, Dept Speech & Hearing, Cincinnati, OH 45229 USA. Univ Cincinnati, Dept Psychol, Cincinnati, OH 45229 USA. RP Geiger, DM (reprint author), Cincinnati Childrens Hosp, Med Ctr, CCHMC Speech Pathol Dept, Pavil Bldg,3333 Burnet Ave, Cincinnati, OH 45229 USA. CR Abrams EZ, 1998, J PEDIATR PSYCHOL, V23, P87, DOI 10.1093/jpepsy/23.2.87 ACHENBACH TM, 1987, PSYCHOL BULL, V101, P213, DOI 10.1037/0033-2909.101.2.213 ALPEN GD, 1972, DEV PROFILE MANUAL American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychological Association, 1992, AM PSYCHOL, V47, P1597, DOI [10.1037/0003-066X.47.12.1597, DOI 10.1037/0003-066X.47.12.1597] BAILEY DB, 1996, ASSESSING INFANTS PR Bayley N, 1969, MANUAL BAYLEY SCALES GLASCOE FP, 1994, CLIN PEDIATR, V33, P292, DOI 10.1177/000992289403300507 Gray D E, 1995, Med Anthropol, V16, P99 Greenbaum P. E., 1994, PSYCHOL ASSESSMENT, V6, P141, DOI DOI 10.1037/1040-3590.6.2.141 Ho H H, 1994, Child Health Care, V23, P137, DOI 10.1207/s15326888chc2302_6 LeMay D. 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PD AUG PY 2002 VL 32 IS 4 BP 307 EP 312 DI 10.1023/A:1016382819186 PG 6 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600006 PM 12199135 ER PT J AU Vrancic, D Nanclares, V Soares, D Kulesz, A Mordzinski, C Plebst, C Starkstein, S AF Vrancic, D Nanclares, V Soares, D Kulesz, A Mordzinski, C Plebst, C Starkstein, S TI Sensitivity and specificity of the autism diagnostic inventory-telephone screening in Spanish SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; screening; assessment; pervasive developmental disorders ID INDIVIDUALS AB We report on the development in Argentina of a screening questionnaire for autism administered over the telephone. The Autism Diagnostic Inventory-Telephone Screening in Spanish (ADI-TSS) is based on the Autism Diagnostic Interview-Revised (ADI-R), keeping its structure but including fewer questions, which were rephrased to assess them over the telephone. The ADI-TSS went through different versions, with each modification gaining in reliability. The final version of the ADI-TSS could be assessed in 20 to 40 minutes and demonstrated a high validity (using the ADI-R as the diagnostic gold-standard), high intrarater and interrater reliability (as measured with intraclass correlations), and high internal consistency (as measured with Cronbach's alpha). The validity of the ADI-TSS remained high when used by a health-related professional without formal training in the assessment of autistic patients. We believe the ADI-TSS is useful in field research studies as a screening instrument for patients with a potential diagnosis of autism, although future validation studies should include larger samples. C1 Raul Carrea Inst Neurol Res FLENI, Dept Neuropsychiat, Div Child Psychiat, RA-1428 Buenos Aires, DF, Argentina. RP Vrancic, D (reprint author), Raul Carrea Inst Neurol Res FLENI, Dept Neuropsychiat, Div Child Psychiat, Montaneses 2325, RA-1428 Buenos Aires, DF, Argentina. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Leiter R. G., 1980, LEITER INT PERFORMAN LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 PIVEN J, 1994, NEUROBIOLOGY AUTISM, P18 Schopler E., 1986, CHILDHOOD AUTISM RAT Wechsler D, 1991, WECHSLER INTELLIGENC NR 11 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 AUG PY 2002 VL 32 IS 4 BP 313 EP 320 DI 10.1023/A:1016335003256 PG 8 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600007 PM 12199136 ER PT J AU Rinehart, NJ Bradshaw, JL Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Brereton, AV Tonge, BJ TI Lateralization in individuals with high-functioning autism and Asperger's disorder: A frontostriatal model SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; Asperger's disorder; executive function; laterality; frontostriatal ID RIGHT-HEMISPHERE DAMAGE; INFANTILE-AUTISM; CHILDHOOD AUTISM; EXECUTIVE FUNCTIONS; UNILATERAL NEGLECT; BRAIN; DYSFUNCTION; CHILDREN; ASYMMETRIES; ATTENTION AB Neurobiological and behavioural studies of possible left hemisphere dysfunction in autism have generated conflicting results. Left hemisphere dysfunction may manifest in autism only in tasks that invoke executive functions. Moreover, left hemisphere dysfunction may underpin autism but not Asperger's disorder. We thus aimed to systematically investigate reports of anomalous lateralization in individuals with high-functioning autism and Asperger's disorder. Two of the tasks were sensitive to executive dysfunction: a serial choice reaction-time task and a Posner-type paradigm; the remaining tasks instead investigated aspects of perceptual lateralisation. Compared with age- and IQ-matched controls, the autism group displayed deficiencies in right hemispace (and by implication, left hemisphere) performance on both executive function tasks; however, this group demonstrated normal lateralization effects on the nonexecutive, visual-perceptual tasks. In contrast, the Asperger's disorder group showed similar laterality effects to their age- and IQ-matched controls on both executive and nonexecutive function tasks. The etiological relevance of this neurobehavioral dissociation between high-functioning autism and Asperger's disorder was discussed; in particular, it was suggested that the period where dominance shifts from right to left hemisphere is important in whatever process might dictate the emergence of either autism or Asperger's disorder. C1 Monash Univ, Monash Med Ctr, Ctr Dev Psychiat, Clayton, Vic 3168, Australia. Monash Univ, Neuropsychol Res Unit, Clayton, Vic 3800, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Monash Med Ctr, Ctr Dev Psychiat, 246 Clayton Rd, Clayton, Vic 3168, Australia. 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PD AUG PY 2002 VL 32 IS 4 BP 333 EP 336 DI 10.1023/A:1016339104165 PG 4 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600009 PM 12199138 ER PT J AU Krause, I He, XS Gershwin, ME Shoenfeld, Y AF Krause, I He, XS Gershwin, ME Shoenfeld, Y TI Brief report: Immune factors in autism: A critical review SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; autoimmunity; autoantibodies; immune dysregulation; T cells; NK cells; vaccination; intravenous immunoglobulins ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; INFLAMMATORY-BOWEL-DISEASE; HEPATITIS-B VACCINATION; MEDIATED CYTO-TOXICITY; MYELIN BASIC-PROTEIN; INTRAVENOUS IMMUNOGLOBULIN; MEASLES-VIRUS; T-CELLS; INDUCED AUTOIMMUNITY; RUBELLA VACCINE AB Pervasive developmental disorders represent a group of neurodevelopmental disorders that affect children early in their development. Autistic disorder is the best described of these disorders, yet even this term covers a broad group of clinical presentations. Various immune system abnormalities, including autoimmunity and defects in different subsets of immune cells, have been reported in children with autistic disorder, suggesting that immune factors may play a role in the development of autism. Based on anecdotal observation, vaccination was proposed to cause autism in some children, but several controlled studies have failed to support this claim. Intravenous immunoglobulin infusions has been tested as immunotherapy for autism, although the preliminary results are inconclusive and there is a risk of potentially fatal transmission of blood-borne pathogens. To examine this issue, intensive well-controlled epidemiological and bench studies need to be carried out in defined and carefully controlled study subjects to establish the cellular and molecular basis of autism, against which the effects of each proposed immune factor can be examined. C1 Chaim Sheba Med Ctr, Dept Med B, Res Unit Autoimmune Dis, IL-52621 Tel Hashomer, Israel. Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA. RP Shoenfeld, Y (reprint author), Chaim Sheba Med Ctr, Dept Med B, Res Unit Autoimmune Dis, IL-52621 Tel Hashomer, Israel. 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Autism Dev. Disord. PD AUG PY 2002 VL 32 IS 4 BP 337 EP 345 DI 10.1023/A:1016391121003 PG 9 WC Psychology, Developmental SC Psychology GA 574AR UT WOS:000176866600010 PM 12199139 ER PT J AU Rugino, TA Samsock, TC AF Rugino, TA Samsock, TC TI Levetiracetam in autistic children: An open-label study SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE levetiracetam; autism; children ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; EPILEPSY; PIRACETAM; TRIAL AB The objectives of this study were to determine whether autistic children taking levetiracetam (1) showed improvement in the areas of aggression, impulsivity, hyperkinesis, and mood instability, and (2) showed a nootropic response. Ten white autistic boys ranging from 4 to 10 years were compared pretreatment and while taking levetiracetam for an average of 4.1 weeks. Inattention, hyperkinesis, and impulsivity were evaluated using the Achenbach Attention Problems scale, Conners DSM-IV Total scale, and the Conners Attention-Deficit Hyperactivity Disorder Index scale, all of which showed statistically significant improvements. Mood instability was measured with the Conners Global Index (CGI) Emotional Lability and CGI Total scales, both of which showed statistically significant improvements. Aggressive behavior, as measured with the Achenbach Aggression scale, showed statistically significant improvement only for subjects who were not recently weaned from medications that reduce aggression (e.g., risperidone, carbamazepine, desipramine). Levetiracetam may reduce hyperactivity, impulsivity, mood instability, and aggression in autistic children with these problems. No nootropic effect was observed. C1 Childrens Specialized Hosp, Toms River, NJ 08755 USA. Childrens Specialized Hosp, Mountainside, NJ 08755 USA. Marshall Univ, Joan C Edwards Sch Med, Dept Pediat, Huntington, WV USA. Univ Pediat, Helping Hands Dev Ctr, Huntington, WV USA. RP Rugino, TA (reprint author), Childrens Specialized Hosp, 94 Stevens Rd, Toms River, NJ 08755 USA. CR Achenbach T. 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Dev. Behav. Pediatr. PD AUG PY 2002 VL 23 IS 4 PG 6 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 584TB UT WOS:000177483700005 PM 12177568 ER PT J AU Soares, N Grossman, L AF Soares, N Grossman, L TI A picture's worth: PECS and other visual communication strategies in autism SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Univ Maryland, Div Behav & Dev Pediat, Baltimore, MD 21201 USA. RP Soares, N (reprint author), Univ Maryland, Div Behav & Dev Pediat, Baltimore, MD 21201 USA. CR Bondy Andy, 2002, PICTURES WORTH PECS NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD AUG PY 2002 VL 23 IS 4 BP 283 EP 283 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 584TB UT WOS:000177483700016 ER PT J AU Cornish, E AF Cornish, E TI Gluten and casein free diets in autism: a study of the effects on food choice and nutrition SO JOURNAL OF HUMAN NUTRITION AND DIETETICS LA English DT Article DE autism; casein; dietary assessment; food choice; gluten ID CHILDREN; DISORDER AB Background There is growing interest in possible dietary involvement in the aetiology and treatment of Autistic Spectrum Disorders (ASD). Research has focused on the physiological and behavioural effects of dietary change but has not examined the effect of exclusion diets on nutritional intake. Aims The aim of this study was to examine whether the removal of major dietary staples placed children with autism at risk of nutrient deficiency and compares their food choice with ASD children not following gluten and/or casein free diets. Methods A postal questionnaire was sent to parents of children aged 3-16 years, diagnosed with ASD belonging to the National Autistic Society in Leicestershire and southern Derbyshire. Detailed dietary information and a 3-day food diary were collected. The sample size was small: those using gluten/casein free diets (n = 8) and those not following diet (n = 29). Results Nutrient intakes fell below the Lower Reference Nutrient Intake (LRNI) in 12 children (32%) for zinc, calcium, iron, vitamin A, vitamin B12 and riboflavin in the nondiet group and four children (50%) for zinc and calcium in the diet group. Fruit and vegetable intakes were higher and cereal, bread and potato consumption were lower in those children using gluten and/or casein free diets. Conclusion No significant differences in the energy, protein and micronutrient intakes were found between the two groups of children. A longitudinal prospective study is suggested to examine whether differences in food choice are the result of dietary intervention or the prerequisite for the successful application of diet in this special group of children. C1 S Derbyshire Community Hlth NHS Trust, Community Nutr Serv, Dar Es Salaam, Tanzania. RP Cornish, E (reprint author), POB 60169, Dar Es Salaam, Tanzania. CR Cornish E, 1998, J HUM NUTR DIET, V11, P501, DOI 10.1046/j.1365-277X.1998.00132.x DeMeyer M. 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PD AUG PY 2002 VL 15 IS 4 BP 261 EP 269 DI 10.1046/j.1365-277X.2002.00372.x PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 580VB UT WOS:000177256000004 PM 12153499 ER PT J AU Vojdani, A Campbell, AW Anyanwu, E Kashanian, A Bock, K Vojdani, E AF Vojdani, A Campbell, AW Anyanwu, E Kashanian, A Bock, K Vojdani, E TI Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus group A SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE autoantibody; neuron-specific; antigen; autism; cross-reaction ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; MULTIPLE-SCLEROSIS; IMMUNE-RESPONSE; T-CELLS; BRAIN; AUTOANTIBODIES; NEUROPATHY; EXPOSURE; SERUM AB We measured autoantibodies against nine different neuron-specific antigens and three cross-reactive peptides in the sera of autistic subjects and healthy controls by means of enzyme-linked immunosorbent assay (ELISA) testing. The antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG), ganglioside (GM,), sulfatide (SULF), chondroitin sulfate (CONSO4), myelin oligodendrocyte glycoprotein (MOG), alpha,beta-crystallin (alpha,beta-CRYS), neurofilament proteins (NAFP), tubulin anti three cross-reactive peptides, Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin (BTN). Autistic children showed the highest levels of IgG, IgM and IgA antibodies against all neurologic antigens as well as the three cross-reactive peptides. These antibodies are specific because immune absorption demonstrated that only neuron-specific antigens or their cross-reactive epitopes could significantly reduce antibody levels. These antibodies may have been synthesized as a result of an alteration in the blood brain barrier. This harrier promotes access of preexisting T-cells and central nervous system antigens to immunocompetent cells, which may start a vicious cycle. 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Neuroimmunol. PD AUG PY 2002 VL 129 IS 1-2 BP 168 EP 177 DI 10.1016/S0165-5728(02)00180-7 PG 10 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 590BQ UT WOS:000177797700020 PM 12161033 ER PT J AU Cullen, LA Barlow, JH AF Cullen, LA Barlow, JH TI 'Kiss, cuddle, squeeze': exploring the experiences of attending a touch therapy intervention for parents of children with autism SO JOURNAL OF REPRODUCTIVE AND INFANT PSYCHOLOGY LA English DT Meeting Abstract C1 Coventry Univ, Interdisciplinary Res Ctr Hlth, Sch Hlth & Social Sci, Coventry, W Midlands, England. NR 0 TC 0 Z9 0 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0264-6838 J9 J REPROD INFANT PSYC JI J. Reprod. Infant Psychol. PD AUG PY 2002 VL 20 IS 3 BP 187 EP 187 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 591AV UT WOS:000177858300040 ER PT J AU McDougle, CJ Kem, DL Posey, DJ AF McDougle, CJ Kem, DL Posey, DJ TI Case series: Use of ziprasidone for maladaptive symptoms in youths with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; ziprasidone; psychopharmacology ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED TRIAL; OPEN-LABEL; SCHIZOAFFECTIVE DISORDER; ACUTE EXACERBATION; CHILDREN; RISPERIDONE; ADOLESCENTS; OLANZAPINE; CLOZAPINE AB Objective: To conduct a preliminary evaluation of the safety and effectiveness of ziprasidone in children, adolescents, and young adults with autism. Method: Twelve patients (mean age +/- SD, 11.62 +/- 4.38 years; range, 8-20 years) with DSM-IV-defined autism (n = 9) or pervasive developmental disorder not otherwise specified (n = 3) received open-label treatment with ziprasidone (mean daily dose, 59.23 +/- 34.76 mg; range, 20-120 mg) for at least 6 weeks (mean duration, 14,15 +/- 8.29 weeks; range, 6-30 weeks). Results: Six (50%) of the 12 patients were considered responders based on a Clinical Global Impression Scale rating of "much improved" or "very much improved." Transient sedation was the most common side effect. No cardiovascular side effects, including chest pain, tachycardia, palpitations, dizziness, or syncope, were observed or reported. The mean change in body weight for the group was -5.83 +/- 12.52 lb (range, -35 to +6 lb). Five patients lost weight, five had no change, one gained weight, and one had no follow-up weight obtained beyond the baseline measurement. Conclusions: Ziprasidone appears to have the potential for improving symptoms of aggression, agitation, and irritability in children, adolescents, and young adults with autism, Significant weight gain was not observed in this short-term trial, Double-blind, placebo-controlled studies are needed to substantiate these preliminary findings. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Krannert Bldg,Room A305,1111 W 10th St, Indianapolis, IN 46202 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD AUG PY 2002 VL 41 IS 8 BP 921 EP 927 DI 10.1097/00004583-200208000-00010 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 576FX UT WOS:000176993100009 PM 12164181 ER PT J AU Seeman, C AF Seeman, C TI A parent's guide to Asperger syndrome and high-functioning autism: How to meet the challenges and help your child thrive. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo, Lib, Toledo, OH 43606 USA. RP Seeman, C (reprint author), Univ Toledo, Lib, 2801 W Bancroft St, Toledo, OH 43606 USA. CR Ozonoff S, 2002, PARENTS GUIDE ASPERG NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD AUG PY 2002 VL 127 IS 13 BP 130 EP 130 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 584WF UT WOS:000177491200275 ER PT J AU Wank, R AF Wank, R TI Schizophrenia and other mental disorders require long-term adoptive immunotherapy SO MEDICAL HYPOTHESES LA English DT Article ID CSF LEVELS; INTERLEUKIN-2 AB Many different microbial factors seem to contribute to the pathogenesis of schizophrenic and other psychiatric disorders. Activation of all T lymphocytes reactivates those downregulated by low-grade chronic infections and restores equilibrium in immune cell subpopulations. Different immune cell subpopulations express different neurotrophin receptors and produce different cytokines, particularly brain-derived neurotrophin (BDNF) and neurotrophin 3 (NT3) [M. Besser, R. Wank, J. Immunol. 162 (1998) 6303-6306] that appear to play a key role in schizophrenic and bipolar disorders [E. Jonsson, S. Brene, X.R. Zhang, et al., Acta Psychiatr. 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Hypotheses PD AUG PY 2002 VL 59 IS 2 BP 154 EP 158 DI 10.1016/S0306-9877(02000163-9 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 596ZH UT WOS:000178196500006 PM 12208201 ER PT J AU Ng, SSM Yung, WH Chow, BKC AF Ng, SSM Yung, WH Chow, BKC TI Secretin as a neuropeptide SO MOLECULAR NEUROBIOLOGY LA English DT Article DE secretin; neuropeptide; autism; cerebellum; Purkinje cells; GABA; inhibitory postsynaptic currents ID CYCLASE-ACTIVATING POLYPEPTIDE; VASOACTIVE-INTESTINAL-PEPTIDE; PLACEBO-CONTROLLED TRIAL; ACID-INDUCED INHIBITION; PORCINE SECRETIN; DOUBLE-BLIND; CYCLIC-AMP; INTRAVENOUS SECRETIN; AUTISTIC DISORDER; MOLECULAR-CLONING AB The role of secretin as a classical hormone in the gastrointestinal system is well-established. The recent debate on the use of secretin as a potential therapeutic treatment for autistic patients urges a better understanding of the neuroactive functions of secretin. Indeed, there is an increasing body of evidence pointing to the direction that, in addition to other peptides in the secretin/glucagon superfamily, secretin is also a neuropeptide. The purpose of this review is to discuss the recent data for supporting the neurocrine roles of secretin in rodents. By in situ hybridization and immunostaining, secretin was found to be expressed in distinct neuronal populations within the cerebellum and cerebral cortex, whereas the receptor transcript was found throughout the brain. In the rat cerebellum, secretin functions as a retrograde messenger to facilitate GABA transmission, indicating that it can modulate motor and other functions. In summary, the recent data support strongly the neuropeptide role of secretin, although the secretin-autism link remains to be clarified in the future. C1 Univ Hong Kong, Dept Zool, Hong Kong, Hong Kong, Peoples R China. Chinese Univ Hong Kong, Dept Physiol, Shatin, Hong Kong, Peoples R China. RP Chow, BKC (reprint author), Univ Hong Kong, Dept Zool, Hong Kong, Hong Kong, Peoples R China. 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Neurobiol. PD AUG PY 2002 VL 26 IS 1 BP 97 EP 107 DI 10.1385/MN:26:1:097 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 602WM UT WOS:000178527500008 PM 12392059 ER PT J AU Lonsdale, D Shamberger, RJ Audhya, T AF Lonsdale, D Shamberger, RJ Audhya, T TI Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: A pilot study SO NEUROENDOCRINOLOGY LETTERS LA English DT Article DE autism; thiamine tetrahydrofurfuryl disulfide; urinary arsenic; sulfur metabolism ID LEAD; THIOSULFATE; EXCRETION; WATER; URINE AB OBJECTIVES: In a Pilot Study, the clinical and biochemical effects of thiamine tetrahydrofurfuryl disulfide (TTFD) on autistic spectrum children were investigated. SUBJECTS AND METHODS: Ten children were studied. Diagnosis was confirmed through the use of form E2, a computer assessed symptom score. For practical reasons, TTFD was administered twice daily for two months in the form of rectal suppositories, each containing 50 mg of TTFD. Symptomatic responses were determined through the use of the computer assessed Autism Treatment Evaluation Checklist (ATEC) forms *. The erythrocyte transketolase (TKA) and thiamine pyrophosphate effect (TPPE), were measured at outset and on completion of the study to document intracellular thiamine deficiency. Urines from patients were examined at outset, after 30 days and after 60 days of treatment and the concentrations of SH-reactive metals, total protein, sulfate, sulfite, thiosulfate and thiocyanate were determined. The concentrations of metals in hair were also determined. RESULTS: At the beginning of the study thiamine deficiency was observed in 3 out of the 10 patients. Out of 10 patients, 6 had initial urine samples containing arsenic in greater concentration than healthy controls. Traces of mercury were seen in urines from all of these autistic children. Following administration of TTFD an increase in cadmium was seen in 2 children and in lead in one child. Nickel was increased in the urine of one patient during treatment. Sulfur metabolites in urine did not differ from those measured in healthy children. CONCLUSIONS: Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically. We obtained evidence of an association of this increasingly occurring disease with presence of urinary SH-reactive metals, arsenic in particular. C1 Prevent Med Grp, Westlake, OH USA. King James Med Lab Inc, Westlake, OH 44145 USA. Vitamin Diagnost Inc, Cliffwood Bch, NJ 07735 USA. RP Lonsdale, D (reprint author), 24700 Ctr Ridge Rd, Westlake, OH 44145 USA. 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PD AUG PY 2002 VL 23 IS 4 BP 303 EP 308 PG 6 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 590CT UT WOS:000177800800009 PM 12195231 ER PT J AU Carper, RA Moses, P Tigue, ZD Courchesne, E AF Carper, RA Moses, P Tigue, ZD Courchesne, E TI Cerebral lobes in autism: Early hyperplasia and abnormal age effects SO NEUROIMAGE LA English DT Article DE MRI; magnetic resonance imaging; frontal lobe; autistic ID MAGNETIC-RESONANCE; INFANTILE-AUTISM; MENTAL-RETARDATION; BLOOD-FLOW; EMISSION-TOMOGRAPHY; CHILDHOOD AUTISM; FUNCTIONAL MRI; FRONTAL-LOBE; CELL COUNTS; BRAIN AB Metabolic, functional, behavioral, and histologic studies suggest that the structure of the cerebrum may be abnormal in autism. In a previous cross-sectional study we found abnormal enlargement of cerebral cortex and cerebral white matter volumes in autistic 2 and 3 year olds and abnormally slow rates of volume change across later ages. In the present study, we assessed whether these volume abnormalities are limited to particular cerebral regions or are pervasive throughout the: cerebrum. We used magnetic resonance imaging (MRI) to quantify volumes of cerebral lobes (frontal, temporal, parietal, and occipital regions), using Classic sulcal boundaries to define regions. We examined 38 boys with autism and 39 normal control boys between the ages of 2 and 11 years. Several regions, showed signs of gray matter and white matter hyperplasia in 2- and 3-year-old patients (as much as 20% enlargement), but there appeared to be an anterior to posterior gradient in the degree of hyperplasia. The frontal lobe showed the greatest enlargement while the occipital lobe was not significantly different from normal. Gray and white matter differences were not found in the older children. By examining the relationships between regional volumes and subject age, we found that frontal, temporal, and parietal white matter volumes, as well as frontal and temporal gray matter volumes, changed at significantly slower rates in autism patients than in controls across the 2- to 11-year-age range. For example, frontal lobe white matter volume increased by about 45% from 2-4 years of age to 9-11.5 years, but by only 13% in autistic patients. Mechanisms that might account for early hyperplasia are discussed as they might relate to the regional differences in degree of abnormality. For instance, possible influences of neurotrophic factors, or of abnormal afferent activity from other affected brain regions are considered. (C) 2002 Elsevier Science (USA). C1 Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, San Diego, CA USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92093 USA. RP Carper, RA (reprint author), Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, San Diego, CA USA. 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Similarly, music appreciation, like language comprehension, appears to be the product of a dedicated brain organization. Support for the existence of music-specific neural networks is found in various pathological conditions that isolate musical abilities from the rest of the cognitive system. Cerebrovascular accidents, traumatic brain damage, and congenital brain anomalies can lead to selective disorders of music processing. Conversely, autism and epilepsy can reveal the autonomous functioning and the selectivity, respectively, of the neural networks that subserve music. However, brain specialization for music should not be equated with the presence of a singular "musical center" in the brain. Rather, multiple interconnected neural networks are engaged, of which some may capture the essence of brain specialization for music. The encoding of pitch along musical scales is likely such an essential component. The implications of the existence of such special-purpose cortical processes are that the human brain might be hardwired for music. C1 Univ Montreal, Res Ctr, Inst Geriatr, Dept Psychol, Montreal, PQ H3C 3J7, Canada. 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L., 2000, ORIGINS MUSIC WARRIER CM, 1998, NEUROIMAGE, V7, pS383 Wieser HG, 1997, EPILEPSIA, V38, P200, DOI 10.1111/j.1528-1157.1997.tb01098.x ZATORRE RJ, 1994, J NEUROSCI, V14, P1908 NR 59 TC 26 Z9 28 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1073-8584 J9 NEUROSCIENTIST JI Neuroscientist PD AUG PY 2002 VL 8 IS 4 BP 372 EP 380 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 578PH UT WOS:000177126500019 PM 12194505 ER PT J AU McCracken, JT McGough, J Shah, B Cronin, P Hong, D Aman, MG Arnold, E Lindsay, R Nash, P Hollway, J McDougle, CJ Posey, D Swiezy, N Kohn, A Scahill, L Martin, A Koenig, K Volkmar, F Carroll, D Lancor, A Tierney, E Ghuman, J Gonzalez, NM Grados, M Vitiello, B Ritz, L Davies, M Robinson, J McMahon, D AF McCracken, JT McGough, J Shah, B Cronin, P Hong, D Aman, MG Arnold, E Lindsay, R Nash, P Hollway, J McDougle, CJ Posey, D Swiezy, N Kohn, A Scahill, L Martin, A Koenig, K Volkmar, F Carroll, D Lancor, A Tierney, E Ghuman, J Gonzalez, NM Grados, M Vitiello, B Ritz, L Davies, M Robinson, J McMahon, D CA Res Units Pediat Psychopharmacolog TI Risperidone in children with autism and serious behavioral problems SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; ATYPICAL ANTIPSYCHOTICS; INFANTILE-AUTISM; HALOPERIDOL; ADOLESCENTS; SYMPTOMS; NETWORK; NORMS AB Background Atypical antipsychotic agents, which block postsynaptic dopamine and serotonin receptors, have advantages over traditional antipsychotic medications in the treatment of adults with schizophrenia and may be beneficial in children with autistic disorder who have serious behavioral disturbances. However, data on the safety and efficacy of atypical antipsychotic agents in children are limited. Methods We conducted a multisite, randomized, double-blind trial of risperidone as compared with placebo for the treatment of autistic disorder accompanied by severe tantrums, aggression, or self-injurious behavior in children 5 to 17 years old. The primary outcome measures were the score on the Irritability subscale of the Aberrant Behavior Checklist and the rating on the Clinical Global Impressions - Improvement (CGI-I) scale at eight weeks. Results A total of 101 children (82 boys and 19 girls; mean [+/-SD] age, 8.8 +/- 2.7 years) were randomly assigned to receive risperidone (49 children) or placebo (52). Treatment with risperidone for eight weeks (dose range, 0.5 to 3.5 mg per day) resulted in a 56.9 percent reduction in the Irritability score, as compared with a 14.1 percent decrease in the placebo group (P < 0.001). The rate of a positive response, defined as at least a 25 percent decrease in the Irritability score and a rating of much improved or very much improved on the CGI-I scale, was 69 percent in the risperidone group (34 of 49 children had a positive response) and 12 percent in the placebo group (6 of 52, P < 0.001). Risperidone therapy was associated with an average weight gain of 2.7 +/- 2.9 kg, as compared with 0.8 +/- 2.2 kg with placebo (P < 0.001). Increased appetite, fatigue, drowsiness, dizziness, and drooling were more common in the risperidone group than in the placebo group (P < 0.05 for each comparison). In two thirds of the children with a positive response to risperidone at eight weeks (23 of 34), the benefit was maintained at six months. Conclusions Risperidone was effective and well tolerated for the treatment of tantrums, aggression, or self-injurious behavior in children with autistic disorder. The short period of this trial limits inferences about adverse effects such as tardive dyskinesia. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Ohio State Univ, Columbus, OH 43210 USA. Indiana Univ, Indianapolis, IN 46204 USA. Yale Univ, New Haven, CT USA. Kennedy Krieger Inst, Baltimore, MD USA. NIMH, Bethesda, MD 20892 USA. Columbia Univ, New York, NY USA. Nathan S Kline Inst Psychiat Res, Orangeburg, NY USA. RP Scahill, L (reprint author), Yale Univ, Ctr Child Study, POB 207900, New Haven, CT 06520 USA. 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PD AUG 1 PY 2002 VL 347 IS 5 BP 314 EP 321 DI 10.1056/NEJMoa013171 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 587WC UT WOS:000177665900003 PM 12151468 ER PT J AU Phillips, JO Backous, DD AF Phillips, JO Backous, DD TI Evaluation of vestibular function in young children SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID VESTIBULOOCULAR REFLEX; COCHLEAR IMPLANTATION; PERILYMPHATIC GUSHER; MOTOR PROFICIENCY; MIXED DEAFNESS; STAPES SURGERY; VISUAL-ACUITY; HUMAN INFANTS; HEARING; EAR AB Hearing loss poses a significant health problem for many infants and children. Hearing loss in these children results from a variety of factors, with inherited hearing loss accounting for 27% of permanent dysfunction. Other factors include fetal infections (3%), neonatal complications (6%), meningitis (4%), sequelae of middle ear infection (8%), otosclerosis (3%), unilateral deafness (7%), and outer ear malformation (4%). Of cases of permanent hearing loss, 25% result from unknown factors. Severe hearing impairment occurs in I of every 700 to 1100 neonates [1-4]. The prevalence of permanent hearing loss also increases with age, reaching 3 of 1000 children aged 5 to 9 years, and 5 of 1000 children aged 10 to 14 years [5]. The impact of this problem on normal development is so substantial that the National Institutes of Health consensus panel recommended that all infants be screened for hearing impairment within the first 3 months of life, in addition to regular monitoring of auditory function throughout childhood [6]. Infant screening and potential early intervention, such as surgical implantation of cochlear prostheses [7-9] or training in the use of other sensory modalities [10-11], is common in pediatric otolaryngology. This early testing and intervention program largely overlooks the possible loss of vestibular function. The end organ for balance and orientation lies close to the cochlea (the site of neural hearing transduction) in the inner ear. The nerve fibers that carry balance and orientation information to the brain lie adjacent to the fibers that carry auditory information to the brain. Hearing impairment is commonly accompanied by a disruption in balance and orientation function, but this latter function is only rarely assessed in children. Several studies have confirmed a strong correlation between hearing loss and impairment of vestibular function [12-18]. Hereditary disorders, which account for more than one fourth of all infant and childhood permanent hearing loss, are often associated with vestibular problems. Unilateral and bilateral vestibular hypofunction is found in more than 30% of patients with congenital autosomal-dominant (AD) hearing loss [19,20]. In addition, ipsilateral vestibular loss is found in 31% of patients with congenital AD unilateral hearing loss [21]. Severe congenital autosomal-recessive sensorineural hearing loss is associated with unilateral vestibular hypo- or hyperfunction [19,20,22-23]. Progressive mixed-hearing loss is often accompanied by bilateral or unilateral vestibular loss [24,25]. Waardenburg'syndrome shows a pattern of combined sensorineural hearing loss and vestibular loss [26]. Brachiootorenal dysplasia syndrome [27] produces hearing and vestibular loss. Recessive split hand-and-foot syndrome, Pendred syndrome, albinism deafness syndrome, congenital hearing loss with onychodystrophy, Klippel-Feil syndrome, Wildervanck syndrome, Albers-Schonberg disease, Usher syndrome, Wolfram syndrome, and related disorders show hearing and vestibular loss [13,28-31]. In addition, Alport syndrome, otosclerosis, osteogenesis imperfecta, AD progressive vestibulocochclear dysfunction with high-tone sensorineural hearing loss, progressive vestibulocochlear dysfunction, hereditary sensory radicular neuropathy with sensorineural hearing loss, and familial acoustic neuromas show combined hearing and vestibular loss, albeit typically later in life. Combined hearing and vestibular loss in a child poses potentially significant problems, even though this combined loss might only be expressed in subtle disturbances of normal development. One obvious problem is that the vestibular system is responsible for maintenance of visual acuity during movement [32]. Older children with combined hearing and vestibular loss are at risk for significant visual impairment during normal activity. Also, children and infants with vestibular problems are faced with motor incoordination and locomotor problems that could limit normal development [33]. Finally, the vestibular system is used to coordinate sensory information into a coherent percept by providing a head-centered reference to which other sensory signals can be aligned [34]. Vestibular loss can impair the process of integration of sensory stimuli critical to the development of a sense of self and delineation of external and internal sensations [35]. For example, there is a hypothesized link between autism and vestibular function [36]. These are issues especially critical to the development of deaf children. It is clearly important to integrate a thorough vestibular evaluation into the practice of pediatric otolaryngology. C1 Univ Washington, Sch Med 357923, HNS, Dept Otolaryngol, Seattle, WA 98195 USA. Virginia Mason Med Ctr, Listen Life Ctr Virginia Mason, Dept Otol Neurotol Skull Base Surg, Seattle, WA 98101 USA. RP Phillips, JO (reprint author), Univ Washington, Sch Med 357923, HNS, Dept Otolaryngol, Seattle, WA 98195 USA. 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Changes in frontal areas parallel those in postmortem N-methyl-D-aspartate receptor densities and could correlate with different clinical stages of the disease. This pattern differs from those described in Down syndrome, autism, and Alzheimer's disease. (C) 2002 by Elsevier Science Inc. All rights reserved. C1 Johns Hopkins Med Inst, Dept Radiol, Baltimore, MD 21287 USA. Johns Hopkins Med Inst, Kennedy Krieger Inst, Baltimore, MD 21287 USA. Johns Hopkins Med Inst, Dept Anesthesiol, Baltimore, MD 21287 USA. RP Wong, DF (reprint author), Johns Hopkins Med Inst, Dept Radiol, JOHC Res Room 3245,601 N Caroline St, Baltimore, MD 21287 USA. 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Neurol. PD AUG PY 2002 VL 27 IS 2 BP 117 EP 122 DI 10.1016/S0887-8994(02)00399-5 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 595BZ UT WOS:000178088100006 PM 12213612 ER PT J AU Herold, R Tenyi, T Lenard, K Trixler, M AF Herold, R Tenyi, T Lenard, K Trixler, M TI Theory of mind deficit in people with schizophrenia during remission SO PSYCHOLOGICAL MEDICINE LA English DT Article ID SCHIZOTYPY; PSYCHOSIS; AUTISM AB Background. The authors' goal was to investigate the presence or absence of theory of mind impairments among people with schizophrenia during remission. Recent research results interpret theory of mind deficits as state rather than trait characteristics, connecting these impairments mainly to the acute episode of psychosis. Methods. Twenty patients with schizophrenia in remission and 20 matched control subjects were evaluated. 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10.1016/0145-2134(94)00113-9 WILLIAMSON DE, 1995, BIOL PSYCHIAT, V37, P859, DOI 10.1016/0006-3223(94)00240-4 NR 127 TC 3 Z9 4 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD AUG PY 2002 VL 30 IS 3 BP 185 EP 198 DI 10.1024//1422-4917.30.3.185 PG 14 WC Psychiatry SC Psychiatry GA 585QH UT WOS:000177535700004 PM 12227221 ER PT J AU Amorosa, H Noterdaeme, M AF Amorosa, H Noterdaeme, M TI Early childhood autism: Age at onset and early regression SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE eearly infantile autism; age at onset; setback; regression ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; APHASIA AB Early Childhood Autism: Age at Onset and Early Regression Objectives: The age at onset of autistic symptoms and an early setback in the social or language development of children with early infantile autism has been discussed in the literature as a possible marker for a special subgroup. Information on the number of children with these symptoms varies widely in different reports. The purpose of this study is to analyse how often a late onset or a regression in social or language behaviour are reported in a clinical sample and how they are related to other abnormalities found in these children. Methods: The files on 101 children seen in a specialised outpatient department since 1993 and diagnosed with early infantile autism were analysed. Information on the six axes of the multiaxial classification, the age at onset of symptoms and at setback in social or language development was extracted. Results: Of these 101 children, 75% were described as being different from other children from the beginning. Fourteen showed a regression in social behaviour and 21 a regression in language development. These symptoms did not correlate with intelligence or the status of language development at the time of the assessment. Children with a setback more frequently had epileptic seizures than did children without a setback. Conclusions: The accumulated data permit the hypothesis that children with a late onset of autistic symptoms or a regression constitute a special subgroup within the group of children with early infantile autism. These symptoms should lead to an intensive diagnostic process in order to exclude epileptic abnormalities. C1 Heckscher Klin Munchen, Abt Solln, Munich, Germany. RP Amorosa, H (reprint author), Heckscher Klin, Abt Teilleistungs & Verhaltensgestorte Kinder, Wolfratshauserstr 350, D-80479 Munich, Germany. CR Adrien J. 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R., 1997, HDB AUTISM PERVASIVE, P5 NR 31 TC 2 Z9 3 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD AUG PY 2002 VL 30 IS 3 BP 211 EP 220 DI 10.1024//1422-4917.30.3.211 PG 10 WC Psychiatry SC Psychiatry GA 585QH UT WOS:000177535700006 PM 12227223 ER PT J AU Kamp-Becker, I AF Kamp-Becker, I TI Our journey through high functioning autism and Asperger-syndrome. A roadmap SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA English DT Book Review CR ANDRON L, 2001, JOURNEY HIGH FUNCTIO NR 1 TC 0 Z9 0 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD AUG PY 2002 VL 30 IS 3 BP 221 EP 221 PG 1 WC Psychiatry SC Psychiatry GA 585QH UT WOS:000177535700007 ER PT J AU Mink, JW McKinstry, RC AF Mink, JW McKinstry, RC TI Volumetric MRI in autism - Can high-tech craniometry provide neurobiological insights? SO NEUROLOGY LA English DT Editorial Material C1 Univ Rochester, Med Ctr, Sch Med & Dent, Rochester, NY 14642 USA. Washington Univ, Sch Med, St Louis, MO USA. RP Mink, JW (reprint author), Univ Rochester, Med Ctr, Sch Med & Dent, Box 631,601 Elmwood Ave, Rochester, NY 14642 USA. EM Jonathan_Mink@urmc.rochester.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Aylward EH, 2002, NEUROLOGY, V59, P175 Botteron KN, 2002, BIOL PSYCHIAT, V51, P342, DOI 10.1016/S0006-3223(01)01280-X Casey BJ, 1997, DEV PSYCHOBIOL, V30, P61, DOI 10.1002/(SICI)1098-2302(199701)30:1<61::AID-DEV6>3.0.CO;2-T Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J CHILD PSYCHOL PSYC, V40, P113, DOI 10.1017/S0021963098003308 Gould Stephen Jay, 1981, MISMEASURE MAN MINK JW, 1981, AM J PHYSIOL, V241, pR203 Sparks BF, 2002, NEUROLOGY, V59, P184 NR 9 TC 6 Z9 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL 23 PY 2002 VL 59 IS 2 BP 158 EP 159 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 574EL UT WOS:000176875400002 PM 12136049 ER PT J AU Aylward, EH Minshew, NJ Field, K Sparks, BF Singh, N AF Aylward, EH Minshew, NJ Field, K Sparks, BF Singh, N TI Effects of age on brain volume and head circumference in autism SO NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; CORPUS-CALLOSUM; POSTERIOR-FOSSA; MRI; CHILDREN; SIZE; CEREBELLUM; INDIVIDUALS; INTERVIEW AB Objective: To determine whether brain volume, as assessed on MRI scans, differs between individuals with autism and control subjects, and whether such differences are affected by age. Background: Previous studies have found increased brain weight, head circumference, and MRI brain volume in children with autism. However, studies of brain size in adults with autism have yielded conflicting results. The authors hypothesize that enlargement of the brain may be a feature of brain development during early childhood in autism that normalizes with maturational processes. Methods: The authors measured total brain volumes from 1.5-mm coronal MRI scans in 67 non-mentally retarded children and adults with autism and 83 healthy community volunteers, ranging in age from 8 to 46 years. Head circumference was also measured. Groups did not differ on age, sex, verbal IQ, or socioeconomic status. Results: Brain volumes were significantly larger for children with autism 12 years old and younger compared with normally developing children, when controlling for height. Brain volumes for individuals older than age 12 did not differ between the autism and control groups. Head circumference was increased in both younger and older groups of subjects with autism, suggesting that those subjects older than age 12 had increased brain volumes as children. Conclusions: Brain development in autism follows an abnormal pattern, with accelerated growth in early life that results in brain enlargement in childhood. Brain volume in adolescents and adults with autism is, however, normal, and appears to be due to a slight decrease in brain volume for these individuals at the same time that normal children are experiencing a slight increase. C1 Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98195 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Div Psychiat Neuroimaging, Baltimore, MD USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Aylward, EH (reprint author), Univ Washington, Sch Med, Dept Radiol, Box 357115, Seattle, WA 98195 USA. 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J., 1996, PRINCIPLES CHILD NEU, P1713 Minshew NJ, 1999, NEUROLOGY, V52, P917 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Pennington BF, 2000, J COGNITIVE NEUROSCI, V12, P223, DOI 10.1162/089892900561850 Piven J, 1996, J AM ACAD CHILD PSY, V35, P530, DOI 10.1097/00004583-199604000-00020 Piven J, 1999, NEUROLOGY, V52, P1106 PIVEN J, 1992, BIOL PSYCHIAT, V31, P491, DOI 10.1016/0006-3223(92)90260-7 Piven J, 1997, AM J PSYCHIAT, V154, P1051 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Reiss AL, 1996, BRAIN, V119, P1763, DOI 10.1093/brain/119.5.1763 Saitoh O, 1998, PSYCHIAT CLIN NEUROS, V52, pS219 Sears LL, 1999, PROG NEURO-PSYCHOPH, V23, P613, DOI 10.1016/S0278-5846(99)00020-2 Sparks BF, 2002, NEUROLOGY, V59, P184 STEG JP, 1975, J AUTISM CHILD SCHIZ, V5, P299, DOI 10.1007/BF01540677 Stevenson RE, 1997, LANCET, V349, P1744, DOI 10.1016/S0140-6736(05)62956-X NR 44 TC 260 Z9 269 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL 23 PY 2002 VL 59 IS 2 BP 175 EP 183 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA 574EL UT WOS:000176875400006 PM 12136053 ER PT J AU Sparks, BF Friedman, SD Shaw, DW Aylward, EH Echelard, D Artru, AA Maravilla, KR Giedd, JN Munson, J Dawson, G Dager, SR AF Sparks, BF Friedman, SD Shaw, DW Aylward, EH Echelard, D Artru, AA Maravilla, KR Giedd, JN Munson, J Dawson, G Dager, SR TI Brain structural abnormalities in young children with autism spectrum disorder SO NEUROLOGY LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; EARLY INFANTILE-AUTISM; CHILDHOOD AUTISM; MRI; HIPPOCAMPUS; AMYGDALA; VOLUME; AREA; INDIVIDUALS; CEREBELLAR AB Objective: To explore the specific gross neuroanatomic substrates of this brain developmental disorder, the authors examine brain morphometric features in a large sample of carefully diagnosed 3- to 4-year-old children with autism spectrum disorder (ASD) compared with age-matched control groups of typically developing (TD) children and developmentally delayed (DD) children. Methods: Volumes of the cerebrum, cerebellum, amygdala, and hippocampus were measured from three-dimensional coronal MR images acquired from 45 children with ASD, 26 TD children, and 14 DD children. The volumes were analyzed with respect to age, sex, volume of the cerebrum, and clinical status. Results: Children with ASD were found to have significantly increased cerebral volumes compared with TD and DD children. Cerebellar volume for the ASD group was increased in comparison with the TD group, but this increase was proportional to overall increases in cerebral volume. The DD group had smaller cerebellar volumes compared with both of the other groups. Measurements of amygdalae and hippocampi in this group of young children with ASD revealed enlargement bilaterally that was proportional to overall increases in total cerebral volume. There were similar findings of cerebral enlargement for both girls and boys with ASD. For subregion analyses, structural abnormalities were observed primarily in boys, although this may reflect low statistical power issues because of the small sample (seven girls with ASD) studied. Among the ASD group, structural findings were independent of nonverbal IQ. In a subgroup of children with ASD with strictly defined autism, amygdalar enlargement was in excess of increased cerebral volume. Conclusions: These structural findings suggest abnormal brain developmental processes early in the clinical course of autism. Research currently is underway to better elucidate mechanisms underlying these structural abnormalities and their longitudinal progression. C1 Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Psychiat, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Bioengn, Seattle, WA 98105 USA. NIMH, Bethesda, MD 20892 USA. Univ Washington, Sch Med, Ctr Human Dev & Disabil, Seattle, WA 98105 USA. RP Dager, SR (reprint author), Univ Washington, Sch Med, Dept Radiol, 4225 Roosevelt Way NE,Suite 306-C, Seattle, WA 98105 USA. 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PD JUL 20 PY 2002 VL 175 IS 2352 BP 19 EP 19 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 576JG UT WOS:000177000200013 ER PT J AU Pletnikov, MV Rubin, SA Vogel, MW Moran, TH Carbone, KM AF Pletnikov, MV Rubin, SA Vogel, MW Moran, TH Carbone, KM TI Effects of genetic background on neonatal Borna disease virus infection-induced neurodevelopmental damage I. Brain pathology and behavioral deficits SO BRAIN RESEARCH LA English DT Article DE Borna; hippocampus; cerebellum; startle; stereotypy; hyperactivity ID LEWIS RATS; PREPULSE INHIBITION; STRAIN DIFFERENCES; VIRAL-INFECTION; NERVOUS-SYSTEM; DENTATE GYRUS; BDV INFECTION; ADULT RATS; AUTISM; PERSISTENT AB The pathogenic mechanisms of gene-environment interactions determining variability of human neurodevelopmental disorders remain unclear. In the two consecutive papers, we used the neonatal Borna disease virus (BDV) infection rat model of neurodevelopmental damage to evaluate brain pathology, monoamine alterations, behavioral deficits, and responses to pharmacological treatments in two inbred rat strains, Lewis and Fisher344. The first paper reports that despite comparable virus replication and distribution in the brain of both rat strains, neonatal BDV infection produced significantly greater thinning of the neocortex in BDV-infected Fisher344 rats compared to BDV-infected Lewis rats, while no strain-related differences were found in BDV-induced granule cell loss in the dentate gyrus of the hippocampus and cerebellar hypoplasia. Unlike BDV-infected Lewis rats, more severe BDV-induced brain pathology in Fisher344 rats was associated with (1) greater locomotor activity to novelty and (2) impairment of habituation and prepulse inhibition of the acoustic startle response. The present data demonstrate that the same environmental insult can produce differential neuroanatomical and behavioral abnormalities in genetically different inbred rat strains. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. US FDA, Ctr Biol Evaluat & Res, Lab Pediat & Resp Viral Dis, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Univ Maryland, Maryland Psychiat Res Ctr, Dev Neurobiol Lab, Baltimore, MD 21228 USA. RP Pletnikov, MV (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, 720 Rutland Ave,Ross 618, Baltimore, MD 21205 USA. 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PD JUL 19 PY 2002 VL 944 IS 1-2 BP 97 EP 107 DI 10.1016/S0006-8993(02)02723-3 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 580FH UT WOS:000177224100011 PM 12106670 ER PT J AU Pletnikov, MV Rubin, SA Vogel, MW Moran, TH Carbone, KM AF Pletnikov, MV Rubin, SA Vogel, MW Moran, TH Carbone, KM TI Effects of genetic background on neonatal Borna disease virus infection-induced neurodevelopmental damage II. Neurochemical alterations and responses to pharmacological treatments SO BRAIN RESEARCH LA English DT Article DE Borna; monoamine; fluoxetine; 8-OH-DPAT; Lewis; Fisher344 ID VENTRAL TEGMENTAL AREA; LEWIS RATS; DOPAMINE RELEASE; SEROTONIN; RECEPTOR; AUTISM; PSYCHOSTIMULANTS; VULNERABILITY; SENSITIVITY; INHIBITION AB The gene-environment interplay is thought to determine variability in clinical conditions and responses to therapy in human neurodevelopmental disorders. Studying abnormal brain and behavior development in inbred strains of rodents can help in the identification of the complex pathogenic mechanisms of the host-environment interaction. This paper is the second one in a series of the two reports of the use of the Borna disease virus (BDV) infection model of neurodevelopmental damage to characterize effects of genetic background on virus-induced neurodevelopmental damage in inbred rat strains, Lewis and Fisher344. The present data demonstrate that neonatal BDV infection produced regional and strain-related alterations in levels of serotonin, norepinephrine and in levels of serotonin turnover at postnatal day 120. Neonatal BDV infection also induced upregulation of hippocampal 5-HT(1a) and cortical 5-HT(2a) receptors in Lewis rats and downregulation of cortical 5-HT(2a) receptors in Fisher344 rats. BDV-associated regional downregulation of D(2) receptors and dopamine transporter sites were noted in Fisher344 rats. In addition to the neurochemical disturbances, neonatal BDV infection induced differential responses to serotonin compounds. While 8-OH-DPAT suppressed virus-enhanced ambulation in BDV-infected Fisher344, fluoxetine inhibited virus-induced hyperactivity in BDV-infected Lewis rats only. The present data provide new insights into the pathogenic events that lead to differential responses to pharmacological treatments in genetically different animals following exposure to the same environmental challenge. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. US FDA, Ctr Biol Evaluat & Res, Lab Pediat & Resp Viral Dis, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Univ Maryland, Maryland Psychiat Res Ctr, Dev Neurobiol Lab, Baltimore, MD 21228 USA. RP Pletnikov, MV (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, 720 Rutland Ave,Ross 618, Baltimore, MD 21205 USA. 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Psychiatry PD JUL 15 PY 2002 VL 52 IS 2 BP 143 EP 143 DI 10.1016/S0006-3223(02)01406-3 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 572LY UT WOS:000176777200009 PM 12114006 ER PT J AU Pierce, K Courchesne, E AF Pierce, K Courchesne, E TI A further support to the hypothesis of a link between serotonin, autism, and the cerebellum - Reply SO BIOLOGICAL PSYCHIATRY LA English DT Letter C1 Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92037 USA. RP Pierce, K (reprint author), Univ Calif San Diego, Dept Neurosci, 8110 La Jolla Shores Dr, La Jolla, CA 92037 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 JUL 15 PY 2002 VL 52 IS 2 BP 143 EP 143 DI 10.1016/S0006-3223(02)01407-5 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 572LY UT WOS:000176777200010 ER PT J AU Herzing, LBK Cook, EH Ledbetter, DH AF Herzing, LBK Cook, EH Ledbetter, DH TI Allele-specific expression analysis by RNA-FISH demonstrates preferential maternal expression of UBE3A and imprint maintenance within 15q11-q13 duplications SO HUMAN MOLECULAR GENETICS LA English DT Article ID PRADER-WILLI-SYNDROME; SMALL NUCLEOLAR RNA; ANGELMAN-SYNDROME GENE; AUTISTIC DISORDER; PROXIMAL 15Q; NECDIN GENE; INTERSTITIAL DUPLICATIONS; GENOMIC ORGANIZATION; SPECTRUM DISORDERS; CHROMOSOMAL REGION AB 15q11-q13 contains many imprinted genes, and undergoes duplicon-mediated rearrangements, including deletions, duplications and triplications, and generation of marker chromosomes. Abnormal phenotypes, including language delays and autism spectrum disorders, are primarily observed with maternal 15q11-q13 duplication. To determine possible epigenetic effects on expression within duplicated 15q11-q13 regions, we utilized RNA-FISH to directly observe gene expression. RNA-FISH, unlike RT-PCR, is polymorphism-independent, and it also detects relative levels of expression at each allelle. Unamplified, gene-specific RNA signals were detected using cDNA probes. Subsequent DNA-FISH confirmed RNA signals and assigned parental origin by colocalization of genomic probes. SNRPN and NDN expression was detected primarily from paternal allelles. Control Dystrobrevin transcripts were detected equally from both alleles; however, maternal-UBE3A signals were consistently larger than paternal signals in normal fibroblasts and in neural-precursor cells. Larger UBE3A signals were also observed on one or both maternal alleles in a cell line carrying a maternal interstitial duplication, on both alleles of a maternally derived marker(15) chromosome, and occasionally on a paternal allele in a cell line carrying a paternal interstitial duplication. Expression of NDNL2, just distal to the duplicated region, was not markedly altered but paralleled changes in UBE3A expression. Excess total maternal-UBE3A RNA was confirmed by Northern blot analysis of cell lines carrying 15q11-q13 duplications or triplications. These results demonstrate that: (1) UBE3A is imprinted in fibroblasts, lymphoblasts and neural-precursor cells; (2) allelic imprint status is maintained in the majority of cells upon duplication both in c/s and in trans; and (3) alleles on specific types of duplications may exhibit an increase in expression levels/loss of expression constraints. C1 Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Lab Dev Neurosci, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. RP Ledbetter, DH (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St, Chicago, IL 60637 USA. 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Mol. Genet. PD JUL 15 PY 2002 VL 11 IS 15 BP 1707 EP 1718 DI 10.1093/hmg/11.15.1707 PG 12 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 575VU UT WOS:000176969800003 PM 12095913 ER PT J AU Farroni, T Csibra, G Simion, G Johnson, MH AF Farroni, T Csibra, G Simion, G Johnson, MH TI Eye contact detection in humans from birth SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID FACE PERCEPTION; JOINT ATTENTION; GAZE-DIRECTION; INFANTS; AUTISM; SENSITIVITY; RECOGNITION; MINDS; BRAIN; MECHANISMS AB Making eye contact is the most powerful mode of establishing a communicative link between humans. During their first year of life, infants learn rapidly that the looking behaviors of others conveys significant information. Two experiments were carried out to demonstrate special sensitivity to direct eye contact from birth. The first experiment tested the ability of 2- to 5-day-old newborns to discriminate between direct and averted gaze. In the second experiment, we measured 4-month-old infants' brain electric activity to assess neural processing of faces when accompanied by direct (as opposed to averted) eye gaze. The results show that, from birth, human infants prefer to look at faces that engage them in mutual gaze and that, from an early age, healthy babies show enhanced neural processing of direct gaze. The exceptionally early sensitivity to mutual gaze demonstrated in these studies is arguably the major foundation for the later development of social skills. C1 Univ London Birkbeck Coll, Sch Psychol, Ctr Brain & Cognit Dev, London WC1E 7HX, England. Univ Padua, Dipartimento Psicol Sviluppo & Socializzaz, I-35131 Padua, Italy. RP Farroni, T (reprint author), Univ London Birkbeck Coll, Sch Psychol, Ctr Brain & Cognit Dev, Malet St, London WC1E 7HX, England. 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Natl. Acad. Sci. U. S. A. PD JUL 9 PY 2002 VL 99 IS 14 BP 9602 EP 9605 DI 10.1073/pnas.152159999 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 572LE UT WOS:000176775400094 PM 12082186 ER PT J AU Jones, MB Szatmari, P AF Jones, MB Szatmari, P TI A risk-factor model of epistatic interaction, focusing on autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE multigenes; cumulative effects; threshold; associated conditions; male : female ratio ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HISTORY; PSYCHIATRIC-DISORDERS; THALIDOMIDE EMBRYOPATHY; SEROTONIN TRANSPORTER; MULTIPLEX FAMILIES; INFANTILE-AUTISM; COMPLEX DISEASES; X-CHROMOSOME; FRAGILE-X AB Research to date on the genetics of autism has not uncovered a major susceptibility locus and indications are that a number of genes, perhaps as many as 15-20, may play detectable but minor roles in the etiology of the condition. To cope with this situation, a risk-factor model based on standard epidemiologic designs is proposed. The model supposes that adding a factor to a fixed set of existing factors always increases the total risk. Thus, according to the model genetic contributions cumulate but are not necessarily additive. A threshold, hence, epistasis is required. The model is applied to several conditions in which the risk of autism is elevated, some genetic (fragile X, tuberous sclerosis) and some exogenous (rubella and thalidomide embryopathies). Male gender is discussed as a risk factor. This approach is contrasted primarily with Gillberg and Coleman's view of autism as "a syndrome or series of syndromes caused by many different separate individual diseases." The principal point of difference is whether the effects of different causes cumulate or do not cumulate. In the present approach they do, in Gillberg and Coleman's they do not. (C) 2002 Wiley-Liss, Inc. 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J. Med. Genet. PD JUL 8 PY 2002 VL 114 IS 5 BP 558 EP 565 DI 10.1002/ajmg.10513 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 562LU UT WOS:000176198900015 PM 12116194 ER PT J AU Wassink, TH Piven, J Vieland, VJ Pietila, J Goedken, RJ Folstein, SE Sheffield, VC AF Wassink, TH Piven, J Vieland, VJ Pietila, J Goedken, RJ Folstein, SE Sheffield, VC TI Evaluation of FOXP2 as an autism susceptibility gene SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE chromosome 7; specific language impairment; linkage; linkage disequilibrium; forkhead ID LANGUAGE DISORDER; LINKAGE ANALYSIS; SPEECH; DEFICITS; SPECTRUM AB A. mutation in the gene FOXP2 was recently identified as being responsible for a complicated speech and language phenotype in a single large extended pedigree. This gene is of interest to autism because it lies in one of the most consistently linked autism chromosomal regions of interest. We therefore tested this gene for its involvement in autism in a large sample of autism families. We completely sequenced the exon containing the mutation, screened the remaining coding sequence using SSCP technology, and identified and genotyped two novel intronic tetranucleotide repeat polymorphisms that were then analyzed for evidence of linkage and linkage disequilibrium (LD). We identified two families in which heterozygous deletions of a small number of glutamines in a long poly-glutamine stretch were found in one parent and the autistic probands; no other non-conservative coding sequence changes were identified. Linkage and LD analyses were performed in 75 affected sibling pair families and in two subgroups of this sample defined by the presence/absence of severe language impairment. One allele appeared to have an opposite pattern of transmission in the language based sub-groups, but otherwise the linkage and LD analyses were negative. 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PD JUL 8 PY 2002 VL 114 IS 5 BP 566 EP 569 DI 10.1002/ajmg.10415 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 562LU UT WOS:000176198900016 PM 12116195 ER PT J AU [Anonymous] AF [Anonymous] TI No evidence to link NWR vaccine with autism or bowel disease SO INPHARMA LA English DT News Item CR 2002, MEDIA RELEASE 0627 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 JUL 6 PY 2002 IS 1345 BP 16 EP 16 PG 1 GA 571CW UT WOS:000176698100029 ER PT J AU Marie, S Race, V Nassogne, MC Vincent, MF Van den Berghe, G AF Marie, S Race, V Nassogne, MC Vincent, MF Van den Berghe, G TI Mutation of a nuclear respiratory factor 2 binding site in the 5 ' untranslated region of the ADSL gene in three patients with adenylosuccinate lyase deficiency SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID PURINE NUCLEOTIDE SYNTHESIS; BIDIRECTIONAL PROMOTER; TRANSCRIPTION FACTOR; EXPRESSION; PROTEIN; NRF-1; IDENTIFICATION; ACTIVATION; SEQUENCE; SUBUNIT AB Adenylosuccinate lyase (ADSL; also called "adenylosuccinase") catalyzes two steps in the synthesis of purine nucleotides: (1) the conversion of succinylaminoimidazolecarboxamide ribotide into aminoimidazolecarboxamide ribotide and (2) the conversion of adenylosuccinate into adenosine monophosphate. ADSL deficiency, a recessively inherited disorder, causes variable-but most often severe-mental retardation, frequently accompanied by epilepsy and/or autism. It is characterized by the accumulation, in body fluids, of succinylaminoimidazolecarboxamide riboside and succinyladenosine, the dephosphorylated derivatives of the two substrates of the enzyme. Analysis of the ADSL gene of three unrelated patients with ADSL deficiency, in whom one of the ADSL alleles displayed a normal coding sequence, revealed a -49T-->C mutation in the 5 untranslated region of this allele. Measurements of the amount of mRNA transcribed from the latter allele showed that it was reduced to similar to33% of that transcribed from the alleles mutated in their coding sequence. Further investigations showed that the -49T-->C mutation provokes a reduction to 25% of wild-type control of promoter function, as evaluated by luciferase activity and mRNA level in transfection experiments. The mutation also affects the binding of nuclear respiratory factor 2 (NRF-2), a known activator of transcription, as assessed by gel-shift studies. Our findings indicate that a mutation of a regulatory region of the ADSL gene might be an unusually frequent cause of ADSL deficiency, and they suggest a role for NRF-2 in the gene regulation of the purine biosynthetic pathway. C1 Christian Duve Inst Cellular Pathol, Physiol Chem Lab, B-1200 Brussels, Belgium. Univ Catholique Louvain, B-1200 Brussels, Belgium. RP Van den Berghe, G (reprint author), Christian Duve Inst Cellular Pathol, Physiol Chem Lab, Ave Hippocrate 75-39, B-1200 Brussels, Belgium. 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To identify these inherited factors, linkage analysis of multiplex families is being performed on a sample of 105 families with two or more affected sibs. Segregation patterns of short tandem repeat polymorphic markers from four chromosomes revealed null alleles at four marker sites in 12 families that were the result of deletions ranging in size from 5 to >260 kb. In one family, a deletion at marker D7S630 was complex, with two segments deleted (37 kb and 18 kb) and two retained (2,836 bp and 38 bp). Three families had deletions at D7S517, with each family having a different deletion (96 kb, 183 kb, and 1 69 kb). Another three families had deletions at D8S264, again with each family having a different deletion, ranging in size from <5.9 kb to >260 kb. At a fourth marker, D8S272, a 192-kb deletion was found in five families. Unrelated subjects and additional families without autism were screened for deletions at these four sites. Families screened included 40 families from Centre d'Etude du Polymorphisme Humaine and 28 families affected with learning disabilities. Unrelated samples were 299 elderly control subjects, 121 younger control subjects, and 248 subjects with Alzheimer disease. The deletion allele at D8S272 was found in all populations screened. For the other three sites, no additional deletions were identified in any of the groups without autism. Thus, these deletions appear to be specific to autism kindreds and are potential autism-susceptibility alleles. An alternative hypothesis is that autism-susceptibility alleles elsewhere cause the deletions detected here, possibly by inducing errors during meiosis. C1 Puget Sound Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Seattle, WA USA. Univ Washington, Dept Med, Div Gerontol & Geriatr Med, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. 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J. Hum. Genet. PD JUL PY 2002 VL 71 IS 1 BP 100 EP 115 DI 10.1086/341291 PG 16 WC Genetics & Heredity SC Genetics & Heredity GA 564GY UT WOS:000176307700010 PM 12058345 ER PT J AU Perez-Gonzalez, LA Williams, G AF Perez-Gonzalez, LA Williams, G TI Multicomponent procedure to teach conditional discriminations to children with autism SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID MENTALLY-RETARDED ADULTS; LEARNING-SET AB Five children with autism with a history of failing to acquire conditional discriminations learned to discriminate objects in response to spoken names or to match amounts to numbers with a combined blocking procedure. The procedure for teaching object discriminations involved (a) presenting the same spoken word until 10 consecutive correct responses occurred and (b) keeping the left-right location of the objects on the table constant. After mastery, the requirement for changing the spoken word was gradually reduced. Finally, the spoken words were presented randomly. In the final stage, the objects were located randomly. The procedure to teach number matching was similar. All children learned these discriminations with few errors. This procedure may be beneficial in teaching conditional discriminations to children with learning difficulties. C1 Univ Oviedo, Oviedo, Spain. Appl Behav Consultant Serv Inc, New York, NY USA. RP Perez-Gonzalez, LA (reprint author), La Granja, Boal 33720, Asturias, Spain. 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J. Ment. Retard. PD JUL PY 2002 VL 107 IS 4 BP 293 EP 301 DI 10.1352/0895-8017(2002)107<0293:MPTTCD>2.0.CO;2 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 573GK UT WOS:000176820800006 PM 12069648 ER PT J AU Casanova, MF Buxhoeveden, DP Cohen, M Switala, AE Roy, EL AF Casanova, MF Buxhoeveden, DP Cohen, M Switala, AE Roy, EL TI Minicolumnar pathology in dyslexia SO ANNALS OF NEUROLOGY LA English DT Article ID NONHUMAN PRIMATE CORTEX; DEVELOPMENTAL DYSLEXIA; PLANUM TEMPORALE; VISUAL-CORTEX; CELL COLUMNS; ORGANIZATION; ABNORMALITIES AB The minicolumn is an anatomical and functional unit of the brain whose genesis accrues from germinal cell divisions in the ventricular zone of the brain. Disturbances in the morphometry of minicolumns have been demonstrated recently for both autism and Down's syndrome. We report minicolumnar abnormalities in the brain of a dyslexic patient. The corresponding developmental disturbance (ie, large minicolumns) could account for the perceptual errors observed in dyslexia. C1 Downtown Vet Affairs Med Ctr 24, Augusta, GA 30904 USA. Med Coll Georgia, Dept Psychiat & Neurol, Augusta, GA 30912 USA. Med Coll Georgia, Dept Neurol, Augusta, GA 30912 USA. RP Casanova, MF (reprint author), Downtown Vet Affairs Med Ctr 24, 3B-121,1 Freedom Way, Augusta, GA 30904 USA. 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Neurol. PD JUL PY 2002 VL 52 IS 1 BP 108 EP 110 DI 10.1002/ana.10226 PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 566WT UT WOS:000176451800019 PM 12112057 ER PT J AU Heisler, MA Guidry, JR AF Heisler, MA Guidry, JR TI Comment: secretin for autism: unproven treatment or ineffective treatment? SO ANNALS OF PHARMACOTHERAPY LA English DT Letter ID DOUBLE-BLIND; CHILDREN C1 Desert Samaritan Med Ctr, Clin Pharm Serv, Mesa, AZ 85202 USA. RP Heisler, MA (reprint author), Desert Samaritan Med Ctr, Clin Pharm Serv, 1400 S Dobson Rd, Mesa, AZ 85202 USA. 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RP McQueen, JM (reprint author), Ohio State Univ Hosp, Ambulatory Serv, Cincinnati, OH 45219 USA. NR 0 TC 0 Z9 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 USA SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD JUL-AUG PY 2002 VL 36 IS 7-8 BP 1295 EP 1295 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 570ZN UT WOS:000176690500033 ER PT J AU Goldstein, G Minshew, NJ Allen, DN Seaton, BE AF Goldstein, G Minshew, NJ Allen, DN Seaton, BE TI High-functioning autism and schizophrenia - A comparison of an early and late onset neurodevelopmental disorder SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Article DE autism; schizophrenia; cognition ID COGNITIVE HETEROGENEITY; PROFILES; DEFICITS; SUBTYPES; CHILDREN AB Autism and schizophrenia are separate neurodevelopmental disorders that share a number of interpersonal and cognitive deficits. The symptoms of autism first appear during early life while schizophrenic symptoms do not typically appear until adolescence at the earliest. Efforts have been made to characterize the pattern of cognitive function in both disorders, and certain resemblances have become apparent such as deficits in abstract reasoning and the more complex aspects of memory and language. The present study provided a comparison of cognitive function between the two disorders. The autistic sample consisted of well-diagnosed individuals with high-functioning autism (IQ greater than or equal to 70). The schizophrenic sample was divided into four subgroups using Ward's method of cluster analysis. Participants received the Wechsler Adult Intelligence Scale-Revised (WAIS-R), the Halstead Category Test, the Trail Making test, and the Wisconsin Card Sorting test (WCST). The profile of the autism sample was compared with the four schizophrenia cluster profiles. The autism group resembled only one of the schizophrenia clusters, with both showing elevations on the WAIS-R Information and Block Design subtests and depressions on Comprehension and Digit Symbol. It was concluded that individuals with high-functioning autism have a cognitive profile that resembles that of an empirically derived subgroup of schizophrenia patients but that does not resemble profiles found in other schizophrenia subgroups. The pattern itself, marked by a relatively depressed score on the Comprehension subtest among the Verbal subtests and a relatively elevated score on Block Design among the Performance subtests, has been characterized in the past as a prototypic profile for high-functioning autism. (C) 2002 National Academy of Neuropsychology. Published by Elsevier Science Ltd. C1 VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15206 USA. Univ Pittsburgh, Pittsburgh, PA USA. Univ Nevada, Las Vegas, NV 89154 USA. 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Clin. Neuropsychol. PD JUL PY 2002 VL 17 IS 5 BP 461 EP 475 DI 10.1016/S0887-6177(01)00129-9 PG 15 WC Psychology, Clinical; Psychology SC Psychology GA 567PL UT WOS:000176493100004 PM 14592000 ER PT J AU Smith, T Lovaas, NW Lovaas, OI AF Smith, T Lovaas, NW Lovaas, OI TI Behaviors of children with high-functioning autism when paired with typically developing versus delayed peers: A preliminary study SO BEHAVIORAL INTERVENTIONS LA English DT Article ID PLAY AB Children with high-functioning autistic disorder (HAD) in a comprehensive behavioral treatment program (n=9. age=5-7 years) alternated between pairings with a typically developing peer and pairings with a peer who had both autism and developmental delay. All pairings took place in a free play setting. The children with HAD displayed much more interactive play and speech (as well as much less self-stimulation) with typically developing peers than with delayed peers. They received frequent cues and consequences for interaction from typically developing peers, but not in sessions with delayed peers. These results suggest that placement with typically developing peers is critical for children with HAD in behavioral treatment. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Univ Rochester, Med Ctr, Dept Pediat, Strong Ctr Dev Disabil, Rochester, NY 14642 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. RP Smith, T (reprint author), Univ Rochester, Med Ctr, Dept Pediat, Strong Ctr Dev Disabil, 601 Elmwod Ave,Box 671, Rochester, NY 14642 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bayley N, 1993, BAYLEY SCALES INFANT Bierman K. L., 1997, ASSESSMENT CHILDHOOD, P328 CARR EG, 1990, J AUTISM DEV DISORD, V20, P45, DOI 10.1007/BF02206856 COE D, 1990, J AUTISM DEV DISORD, V20, P177, DOI 10.1007/BF02284717 Dunn L. 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The differential effectiveness of two different modeling conditions was compared, where in the first condition the children were trained to observe and imitate modeled cooperative play. In the second condition the children observed and described the modeled play prior to imitation. During training, modeled play episodes varied across play topics. The criterion for mastery in training was correct responding on first trial with new modeled play episodes. The results showed that the children became able to take turns in novel episodes of cooperative play and to show play variability only after including verbal description as part of the modeling procedure. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Akerhus Univ Hosp, Barneavdelingen, Seksjon Habilitering, N-1474 Nordbyhagen, Norway. RP Jahr, E (reprint author), Akerhus Univ Hosp, Barneavdelingen, Seksjon Habilitering, POB 48, N-1474 Nordbyhagen, Norway. 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Intervent. PD JUL-SEP PY 2002 VL 17 IS 3 BP 145 EP 157 DI 10.1002/bin.117 PG 13 WC Psychology, Clinical SC Psychology GA 583NW UT WOS:000177414800003 ER PT J AU Lee, M Martin-Ruiz, C Graham, A Court, J Jaros, E Perry, R Iversen, P Bauman, M Perry, E AF Lee, M Martin-Ruiz, C Graham, A Court, J Jaros, E Perry, R Iversen, P Bauman, M Perry, E TI Nicotinic receptor abnormalities in the cerebellar cortex in autism SO BRAIN LA English DT Article DE autism; cerebellum; cholinergic system; nicotinic receptors; muscarinic receptors ID POSTERIOR-FOSSA; BRAIN-STEM; ACETYLCHOLINE-RECEPTORS; INFANTILE-AUTISM; CHOLINE-ACETYLTRANSFERASE; MUSCARINIC RECEPTORS; PRENATAL DEVELOPMENT; COGNITIVE DEFICITS; CORPUS-CALLOSUM; BASAL FOREBRAIN AB Autism is a common developmental disorder associated with structural and inferred neurochemical abnormalities of the brain. Cerebellar abnormalities frequently have been identified, based on neuroimaging or neuropathology. Recently, the cholinergic neurotransmitter system has been implicated on the basis of nicotinic receptor loss in the cerebral cortex. Cerebellar cholinergic activities were therefore investigated in autopsy tissue from a series of autistic individuals. The presynaptic cholinergic enzyme, choline acetyltransferase, together with nicotinic and muscarinic receptor subtypes were compared in the cerebellum from age-matched mentally retarded autistic (eight), normal control (10) and non-autistic mentally retarded individuals (11). The nicotinic receptor binding the agonist epibatidine (the high affinity receptor subtype, consisting primarily of alpha3 and alpha4, together with beta2 receptor subunits) was significantly reduced by 40-50% in the granule cell, Purkinje and molecular layers in the autistic compared with the normal group (P < 0.05). There was an opposite increase (3-fold) in the nicotinic receptor binding α-bungarotoxin (to the α7 subunit) which reached significance in the granule cell layer (P < 0.05). These receptor changes were paralleled by a significant reduction (P < 0.05) and non-significant increase, respectively, of α4 and α7 receptor subunit immunoreactivity measured using western blotting. Immunohistochemically loss of α(4) reactivity was apparent from Purkinje and the other cell layers, with increased α7 reactivity in the granule cell layer. There were no significant changes in choline acetyltransferase activity, or in muscarinic M1 and M2 receptor subtypes in autism. In the non-autistic mentally retarded group, the only significant abnormality was a reduction in epibatidine binding in the granule cell and Purkinje layers. In two autistic cases examined histologically, Purkinje cell loss was observed in multiple lobules throughout the vermis and hemispheres. 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These symptoms lead to social exclusion and a significant healthcare burden; however, their neurobiological basis is poorly understood. There are few studies on brain anatomy of Asperger's syndrome, and no focal anatomical abnormality has been reliably reported from brain imaging studies of autism, although there is increasing evidence for differences in limbic circuits. These brain regions are important in sensorimotor gating, and impaired 'gating' may partly explain the failure of people with autistic disorders to inhibit repetitive thoughts and actions. Thus, we compared brain anatomy and sensorimotor gating in healthy people with Asperger's syndrome and controls. We included 21 adults with Asperger's syndrome and 24 controls. All had normal IQ and were aged 18-49 years. We studied brain anatomy using quantitative MRI, and sensorimotor gating using prepulse inhibition of startle in a subset of 12 individuals with Asperger's syndrome and 14 controls. We found significant age-related differences in volume of cerebral hemispheres and caudate nuclei (controls, but not people with Asperger's syndrome, had age-related reductions in volume). Also, people with Asperger's syndrome had significantly less grey matter in fronto-striatal and cerebellar regions than controls, and widespread differences in white matter. Moreover, sensorimotor gating was significantly impaired in Asperger's syndrome. People with Asperger's syndrome most likely have generalized alterations in brain development, but this is associated with significant differences from controls in the anatomy and function of specific brain regions implicated in behaviours characterizing the disorder. We hypothesize that Asperger's syndrome is associated with abnormalities in fronto-striatal pathways resulting in defective sensorimotor gating, and consequently characteristic difficulties inhibiting repetitive thoughts, speech and actions. C1 Inst Psychiat, Div Psychol Med, Dept Psychol Med, London SE5 8AF, England. Inst Psychiat, Dept Neuroimaging, London SE5 8AF, England. Univ London Kings Coll, Inst Psychiat, Social Genet Dev & Psychiat Ctr, London, England. Univ London St Georges Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. Univ Hong Kong, Dept Psychiat, Hong Kong, Hong Kong, Peoples R China. RP Murphy, DGM (reprint author), Inst Psychiat, Div Psychol Med, Dept Psychol Med, Room M216, London SE5 8AF, England. 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J. Dev. Disabil. PD JUL PY 2002 VL 48 IS 95 BP 113 EP 122 PN 2 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 581JB UT WOS:000177287400006 ER PT J AU Christensen, K Mortensen, PB AF Christensen, K Mortensen, PB TI Facial clefting and psychiatric diseases: A follow-up of the Danish 1936-1987 Facial Cleft Cohort SO CLEFT PALATE-CRANIOFACIAL JOURNAL LA English DT Article DE cleft lip; cleft palate; epidemiology; genetics; psychiatric diseases ID 22Q11 DELETION SYNDROME; PSYCHOSOCIAL ADJUSTMENT; PALATE; LIP; ADULTS; RECURRENCE; APPEARANCE; VARIABLES; CHILDREN AB Objective: This study assesses whether patients with facial cleft have an increased risk of psychiatric diseases. Design: Through the Danish Facial Cleft Database, patients with facial cleft born between 1936 and 1987 in Denmark were identified, and the admission pattern for these patients with facial cleft was available for the period 1969 through 1993 through the Danish Psychiatric Central Registry. Participants: A total of 6,462 patients with facial cleft followed up for a total of 127,068 person-years. Main Outcome Measure: Hospitalization for psychiatric diseases. The expected number of admissions for the cleft population was calculated by multiplication of the observed person-years with admission rates for Denmark stratified for sex, 1-year age group, and 1-year calendar period. Results: A total of 284 patients with facial cleft (4.4%) were hospitalized for psychiatric diseases. The relative risk of hospitalization was 1.65 (95% confidence interval 1.3 to 2.0) for patients with isolated cleft palate (CP) and 1.15 (95% confidence interval 0.99 to 1.29) for patients with cleft lip cleft palate (CL[P]). The overall risk estimates were above unity for both CP and CL(P) in all major diagnosis groups, neurosis and autism (for CL[P]) being the only exceptions. The excess risk was not accounted for by patients with known associated anomalies/syndromes. Conclusion: The risk of hospitalized mental disorders in general is increased in patients with CP but not to any substantial degree in patients with CL(P). Both groups had an increased risk of mental retardation and substance abuse, but the risk for schizophrenia or bipolar illness was not statistically significantly increased, compared with the background population. Further, our data provide no evidence that the psychosocial stressors associated with CL(P) and its treatment have any substantial impact on the risk for hospitalized mental illness. C1 Univ So Denmark, Inst Publ Hlth, Ctr Prevent Congenital Malformat, DK-5000 Odense C, Denmark. Inst Basic Psychiat Res, Dept Psychiat Demog, Risskov, Denmark. RP Christensen, K (reprint author), Univ So Denmark, Inst Publ Hlth, Ctr Prevent Congenital Malformat, Sdr Blvd 23A, DK-5000 Odense C, Denmark. 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Med. Imaging Graph. PD JUL-AUG PY 2002 VL 26 IS 4 BP 251 EP 264 DI 10.1016/S0895-6111(02)00011-3 PG 14 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 576UC UT WOS:000177023200006 PM 12074920 ER PT J AU Coghill, D AF Coghill, D TI Evidence-based psychopharmacology for children and adolescents SO CURRENT OPINION IN PSYCHIATRY LA English DT Review DE adolescence; antidepressive agents; antipsychotic agents; attention; central nervous system stimulants; child; child psychiatry; drug; mental disorders; preschool; psychiatric; research; safety ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; OBSESSIVE-COMPULSIVE DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; ONCE-A-DAY; AUTISTIC DISORDER; DOUBLE-BLIND; WORKING-MEMORY; BIPOLAR DISORDER; CONTROLLED TRIAL AB Purpose of review To provide an update of recent advances in child and adolescent psychopharmacology. Recent findings Changes in legislation in the United States and increased funding by the National Institute for Mental Health has led to a rapid increase in both the number and quality of clinical trials in child and adolescent psychiatry. Recent advances in the psychopharmacology of attention deficit hyperactivity disorder, depression, bipolar disorder, anxiety, obsessive compulsive disorder and autism are reviewed, and continuing gaps in knowledge are noted. Randomized controlled trials have been published supporting the use of modified release stimulant preparations and non-stimulant agents in attention deficit hyperactivity disorder and selective serotonin reuptake inhibitors in depression, anxiety disorders and obsessive compulsive disorders. Secondary analyses of the Multisite Multimodal Treatment Study of Children with Attention-Deficit Hyperactivity Disorder and evidence-based guidelines have given pointers towards more effective treatments for attention-deficit hyperactivity disorder. Pre-clinical studies that have made significant contributions to our theoretical understanding of both the pathophysiology and treatment of these child and adolescent psychiatric disorders are noted. Summary There is now significantly more evidence available to support the rational prescribing of psychoactive agents for several child and adolescent psychiatric disorders. However, there are still many gaps in our knowledge and further studies are required before it will be possible to practise in a truly evidence-based manner. C1 Univ Dundee, Ninewells Hosp & Med Sch, Dept Psychiat, Dundee DD1 9SY, Scotland. RP Coghill, D (reprint author), Univ Dundee, Ninewells Hosp & Med Sch, Dept Psychiat, Dundee DD1 9SY, Scotland. 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Opin. Psychiatr. PD JUL PY 2002 VL 15 IS 4 BP 361 EP 368 DI 10.1097/00001504-200207000-00004 PG 8 WC Psychiatry SC Psychiatry GA 575BT UT WOS:000176926500004 ER PT J AU Hultman, CM Sparen, P Cnattingius, S AF Hultman, CM Sparen, P Cnattingius, S TI Perinatal risk factors for infantile autism SO EPIDEMIOLOGY LA English DT Article DE infantile autism; perinatal; risk factors; maternal; intrauterine growth ID INTRAUTERINE-GROWTH; MATERNAL SMOKING; POPULATION; PREGNANCY; SCHIZOPHRENIA; DISORDER; DELIVERY; COMPLICATIONS; EPIDEMIOLOGY; CHILDHOOD AB Background. Etiologic hypotheses in infantile autism suggest a strong genetic component, as well as possible environmental risks linked to early fetal development. We evaluated the association of maternal, pregnancy, delivery, and infant characteristics and risk of infantile autism. Methods. We conducted a case-control study nested within a population-based cohort (all Swedish children born in 1974-1993). We used prospectively recorded data from the Swedish Birth Register, which were individually linked to the Swedish Inpatient Register. Cases were 408 children (321 boys and 87 girls) discharged with a main diagnosis ion infantile autism from any hospital in Sweden before 10 years of age in the period 1987-1994, plus 2,040 matched controls. Conditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Results. The risk of autism was associated with daily smoking in early pregnancy (OR = 1.4; CI = 1.1-1.8), maternal birth outside Europe and North America (OR - 3.0; CI = 1.7-5.2), cesarean delivery (OR = 1.6; CI = 1.1-2.3), being small for gestational age (SGA; OR = 2.1; CI = 1.1-3.0), a 5-minute Apgar score below 7 (OR = 3.2, CI = 1.2-8.2), and congenital malformations (OR = 1.8, CI = 1.1-3.1). No association was found between autism and head circumference, maternal diabetes, being a twin, or season of birth. Conclusions. 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Univ Tehran Med Sci, Dept Psychiat, Tehran, Iran. RP Gudarzi, SS (reprint author), Imam Hossein Hosp, Dept Psychiat, Sh Madani St, Tehran 16179, Iran. EM sh_gud@yahoo.com CR Akhondzadeh S, 1999, J CLIN PHARM THER, V24, P49, DOI 10.1046/j.1365-2710.1999.00197.x Akhondzadeh S, 2001, IDrugs, V4, P295 Goudie AJ, 1999, PHARMACOL BIOCHEM BE, V64, P193, DOI 10.1016/S0091-3057(99)00079-9 NR 3 TC 2 Z9 2 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0924-9338 J9 EUR PSYCHIAT JI Eur. Psychiat. PD JUL PY 2002 VL 17 IS 4 BP 230 EP 231 DI 10.1016/S0924-9338(02)00662-4 PG 2 WC Psychiatry SC Psychiatry GA 592LV UT WOS:000177939900009 PM 12231270 ER PT J AU Norbury, CF Bishop, DVM AF Norbury, CF Bishop, DVM TI Inferential processing and story recall in children with communication problems: a comparison of specific language impairment, pragmatic language impairment and high-functioning autism SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE autism; inferencing; semantic-pragmatic disorder; SLI; PLI; weak central coherence ID HIGH-LEVEL AUTISM; CENTRAL COHERENCE; ASPERGER-SYNDROME; COMPREHENSION; DISORDERS; ADULTS; MIND; INDIVIDUALS; SKILLS; SLI AB An investigation is reported into the story comprehension abilities of four groups of children: those with typical specific language impairment (SLI-T), those with pragmatic language impairments who were not autistic (PLI), those with high-functioning autism (HFA) and typically developing controls. The story comprehension task required children to answer questions about the literal content of the story, as well as questions involving two types of inferences: text-connecting and gap-filling. The control children outscored the three clinical groups on story comprehension, but the group means of the clinical groups did not differ. However, categorical examination of the data revealed that children with pragmatic difficulties related to HFA were more likely to have specific inferencing deficits. Error analysis suggested that all children could make inferences, but these were not always relevant to the story context. This supports the notion of weak central coherence underlying deficits in inferencing. There were no group differences on story recall. However, there was a strong relationship between story comprehension and recall, in that those who had better comprehension tended to have better recall. It is concluded that comprehension aids recall by enabling the listener to build a more stable mental representation of the story. The pragmatic deficits seen in autism compromise this process. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Norbury, CF (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. CR Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 BISHOP D, 2000, SPECIFIC LANGUAGE IM Bishop D. V. 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A., 1990, LANGUAGE COMPREHENSI HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Happe FGE, 1997, BRIT J DEV PSYCHOL, V15, P1 Jolliffe T, 1999, COGNITION, V71, P149, DOI 10.1016/S0010-0277(99)00022-0 Jolliffe T, 1999, J AUTISM DEV DISORD, V29, P395, DOI 10.1023/A:1023082928366 Leinonen E, 1999, INT J LANG COMM DIS, V34, P367 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 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 MINSHEW NJ, 1995, NEUROPSYCHOLOGY, V9, P255, DOI 10.1037//0894-4105.9.2.255 OAKHILL J, 1984, BRIT J EDUC PSYCHOL, V54, P31 OAKHILL J, 1996, MENTAL MODELS COGNIT, P77 Ozonoff S, 1996, BRAIN LANG, V52, P411, DOI 10.1006/brln.1996.0022 PAUL R, 1988, J AUTISM DEV DISORD, V18, P669, DOI 10.1007/BF02211884 Rapin I, 1996, J CHILD PSYCHOL PSYC, V37, P643, DOI 10.1111/j.1469-7610.1996.tb01456.x Raven J. C., 1986, RAVENS PROGR MATRICE Semel E., 1987, CLIN EVALUATION LANG Shields J, 1996, DEV MED CHILD NEUROL, V38, P473 Shields J, 1996, DEV MED CHILD NEUROL, V38, P487 SNOWLING M, 1983, BRIT J DEV PSYCHOL, V1, P329 Wechsler D., 1992, WECHSLER INTELLIGENC WEISMER SE, 1985, J SPEECH HEAR RES, V28, P175 Wiig E., 1985, TEST LANGUAGE COMPET YUILL N, 1988, APPL COGNITIVE PSYCH, V2, P33, DOI 10.1002/acp.2350020105 NR 38 TC 88 Z9 88 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 JUL PY 2002 VL 37 IS 3 BP 227 EP 251 DI 10.1080/13682820210136269 PG 25 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 583HL UT WOS:000177401200001 PM 12201976 ER PT J AU Bruneau, N Gomot, M Giard, MH Roux, S Barthelemy, C AF Bruneau, N Gomot, M Giard, MH Roux, S Barthelemy, C TI Brain processing of auditory stimulus deviance in children with autism: A topographic event-related potential study SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Hosp Tours, INSERM U 316, F-37044 Tours, France. Brain Signals & Proc Lab, INSERM U280, F-69003 Lyon, France. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD JUL PY 2002 VL 45 IS 1-2 BP 38 EP 39 PG 2 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 578AP UT WOS:000177095500087 ER PT J AU Lepisto, T Kujala, T AF Lepisto, T Kujala, T TI Auditory sensory processing in autism and Asperger's syndrome as reflected by event-related potentials SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, SF-00100 Helsinki, Finland. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD JUL PY 2002 VL 45 IS 1-2 BP 39 EP 40 PG 2 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 578AP UT WOS:000177095500090 ER PT J AU Stauder, JEA Mottron, L AF Stauder, JEA Mottron, L TI Visual gating, -attention and -context in autism: A cognitive ERP study SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Maastricht, Fac Psychol, Maastricht, Netherlands. Hop Riviere Des Prairies, Clin Specialisee Autisme, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD JUL PY 2002 VL 45 IS 1-2 BP 39 EP 39 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 578AP UT WOS:000177095500089 ER PT J AU Martineau, J Schmitz, C Assaiante, C Blanc, R Barthelemy, C AF Martineau, J Schmitz, C Assaiante, C Blanc, R Barthelemy, C TI Anticipatory postural adjustments during a bimanual load-lifting task: Electrophysiological study in autism using event-related desynchronisation SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Tours, Bretonneau Hosp, INSERM U 316, F-37044 Tours, France. CNRS UPR 9011, F-13402 Marseille 20, France. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD JUL PY 2002 VL 45 IS 1-2 BP 40 EP 40 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 578AP UT WOS:000177095500091 ER PT J AU Bolduc, C Daoust, AM Limoges, E Mottron, L Braun, CMJ Godbout, R AF Bolduc, C Daoust, AM Limoges, E Mottron, L Braun, CMJ Godbout, R TI EEG lateralization in high functioning autism SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Hop Louis H Lafontaine, Ctr Rech Fernand Seguin, Montreal, PQ, Canada. Hop Rivere Des Prairies, Montreal, PQ, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. UQAM, Dept Psychol, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD JUL PY 2002 VL 45 IS 1-2 BP 150 EP 150 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 578AP UT WOS:000177095500378 ER PT J AU Singh, VK Lin, SX Newell, E Nelson, C AF Singh, VK Lin, SX Newell, E Nelson, C TI Abnormal measles-mumps-rubella antibodies and CNS autoimmunity in children with autism SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Article DE autoantibodies; autism; autoimmunity; measles virus; measles-mumps-rubella antibodies; vaccines ID LYMPHOCYTE; VACCINATION; DISORDERS; SYSTEM AB Autoimmunity to the central nervous system (CNS), especially to myelin basic protein (MBP), may play a causal role in autism, a neurodevelopmental disorder. Because many autistic children harbor elevated levels of measles antibodies, we conducted a serological study of measles-mumps-rubella (MMR) and MBP autoantibodies. Using serum samples of 125 autistic children and 92 control children, antibodies were assayed by ELISA or immunoblotting methods. ELISA analysis showed a significant increase in the level of MMR antibodies in autistic children. Immunoblotting analysis revealed the presence of an unusual MMR antibody in 75 of 125 (60%) autistic sera but not in control sera. This antibody specifically detected a protein of 73-75 kD of MMR. This protein band, as analyzed with monoclonal antibodies, was immunopositive for measles hemagglutinin (HA) protein but not for measles nucleoprotein and rubella or mumps viral proteins. Thus the MMR antibody in autistic sera detected measles HA protein, which is unique to the measles subunit of the vaccine. Furthermore, over 90% of MMR antibody-positive autistic sera were also positive for MBP autoantibodies, suggesting a strong association between MMR and CNS autoimmunity in autism. Stemming from this evidence, we suggest that an inappropriate antibody response to MMR, specifically the measles component thereof, might be related to pathogenesis of autism. Copyright (C) 2002 National Science Council, ROC and S. Karger AG, Basel. C1 Utah State Univ, Ctr Biotechnol, Logan, UT 84322 USA. Utah State Univ, Dept Biol, Logan, UT 84322 USA. RP Singh, VK (reprint author), Utah State Univ, Ctr Biotechnol, 4700 Old Main Hill, Logan, UT 84322 USA. 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Biomed. Sci. PD JUL-AUG PY 2002 VL 9 IS 4 BP 359 EP 364 DI 10.1159/000065007 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 577MH UT WOS:000177064300010 PM 12145534 ER PT J AU Casanova, MF Buxhoeveden, DP Switala, AE Roy, E AF Casanova, MF Buxhoeveden, DP Switala, AE Roy, E TI Neuronal density and architecture (Gray Level Index) in the brains of autistic patients SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 154th Annual Meeting of the American-Psychiatric-Association CY MAY 05-10, 2001 CL NEW ORLEANS, LOUISIANA SP Amer Psychiat Assoc ID MONKEY CEREBRAL-CORTEX; AREA-1 CELL COLUMNS; QUANTITATIVE APPROACH; INFANTILE-AUTISM; STRUCTURAL INHOMOGENEITIES; MINICOLUMNAR ORGANIZATION; SPATIAL-ORGANIZATION; HEAD CIRCUMFERENCE; PERIPHERAL INPUT; CINGULATE CORTEX AB Although neuropathologic studies have centered on small samples, it is accepted that brains of autistic individuals tend to be large, on average. Knowledge regarding the cause of this macrocephaly is limited. Postmortem studies reveal little in terms of cortical dysplasia. Some of these studies suggest increased cell-packing density in subcortical structures. These neuronomorphometric studies have been subjective or based their conclusions on measures of neuronal density. Our study sought the possible presence of increased cell-packing density by using the Gray Level Index. The Gray Level Index is defined as the ratio of the area covered by Nissl-stained elements to unstained area in postmortem samples. Analyzed images included Brodmann's cortical areas 9, 21, and 22 of 9 autistic patients (7 males, 2 females; mean age of 12 years, with a range of 5 to 28 years) and 11 normal controls (7 males, 4 females; mean age of 14 years, with a range of 3 to 25 years). The overall multivariate test revealed significant differences both between autistic patients and controls (P =.001) and between hemispheres (P =.025). Follow-up univariate tests showed significant diagnosis-dependent effects in feature distance (P =.005), the standard deviation in distance (P =.0 16), and feature amplitude (P =.001). The overall mean Gray Level Index was 19.4% in controls and 18.7% in autism (P =.724). In autism, an increased number of minicolumns, combined with fewer cells per column (or their greater dispersion), results in no global difference in neuronal density. C1 Downtown VA Med Ctr, Dept Psychiat, Augusta, GA 30904 USA. Med Coll Georgia, Dept Psychiat, Augusta, GA 30912 USA. Med Coll Georgia, Dept Neurol, Augusta, GA 30912 USA. RP Casanova, MF (reprint author), Downtown VA Med Ctr, Dept Psychiat, 14,3B-121,1 Freedom Way, Augusta, GA 30904 USA. 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Child Neurol. PD JUL PY 2002 VL 17 IS 7 BP 515 EP 521 DI 10.1177/088307380201700708 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 594WM UT WOS:000178074800008 PM 12269731 ER PT J AU Ropar, D Mitchell, P AF Ropar, D Mitchell, P TI Shape constancy in autism: the role of prior knowledge and perspective cues SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; perception; prior knowledge; shape constancy; visuo-spatial functioning ID ASPERGERS-SYNDROME; VISUAL ILLUSIONS; SAVANT ARTISTS; INDIVIDUALS; PERFORMANCE; MEMORY; RECOGNITION; CHILDREN; STIMULI; ADULTS AB Background: Evidence suggests that individuals with autism may not attend to contextual information (conceptual or perceptual) when processing stimuli (Frith 1989; Shah &, Frith, 1983). Method: We investigated the role of prior knowledge and perspective cues when judging the shape of a slanted circle in individuals with and without autism. Individuals adjusted a shape on a computer screen to appear the same as a slanted circle. Results: Participants in all groups (autistic, moderate learning difficulties, children aged 9 years and adults) exaggerated circularity. Strikingly, however, individuals with autism were unique in exaggerating circularity significantly far less when perspective cues surrounding the slanted circle were eliminated. Prior knowledge that the shape was a slanted circle provoked a strong exaggeration effect in participants without autism, but not in those with autism. Conclusions: Perhaps classifying the stimulus as a 'circle' was sufficient to provoke a strong exaggeration effect in those without (but not with) autism. In this domain, we show that perception in autism may be less influenced by prior knowledge, and therefore less 'top-down'. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Ropar, D (reprint author), Univ Nottingham, Sch Psychol, Univ Pk, Nottingham NG7 2RD, England. 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Child Psychol. Psychiatry Allied Discip. PD JUL PY 2002 VL 43 IS 5 BP 647 EP 653 DI 10.1111/1469-7610.00053 PG 7 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 565FA UT WOS:000176357400009 PM 12120860 ER PT J AU Green, D Baird, G Barnett, AL Henderson, L Huber, J Henderson, SE AF Green, D Baird, G Barnett, AL Henderson, L Huber, J Henderson, SE TI The severity and nature of motor impairment in Asperger's syndrome: a comparison with Specific Developmental Disorder of Motor Function SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Asperger's syndrome; specific developmental disorder of motor function; developmental coordination disorder; motor coordination; gesture; classification ID MOVEMENT ASSESSMENT BATTERY; COORDINATION DISORDER; LANGUAGE IMPAIRMENT; AUTISTIC-CHILDREN; INFANTILE-AUTISM; IMITATION; CLUMSINESS; GESTURE; RELIABILITY; ADOLESCENTS AB Background: The aims of this study were to measure objectively the extent and severity of motor impairment in children with Asperger's syndrome and to determine whether the motor difficulties experienced by such children differed in any way from those classified as having a Specific Developmental Disorder of Motor Function (SDD-MF). Criteria derived from ICD 10-R were used to identify 11 children with Asperger's syndrome and a matched group of 9 children with a Specific Developmental Disorder of Motor Function. Children in both groups were required to have a verbal IQ of 80 or greater on the WISC IIIR. Method: The Autism Diagnostic Interview (Revised; Lord, Rutter, & LeCouteur, 1994) was used to identify features of AS in the first group and to exclude them in the latter. The Movement Assessment Battery for Children (Henderson &, Sugden, 1992) provided a standardised test of motor impairment. A Gesture Test based on that by Cermak, Coster, and Drake (1980) was used to assess the child's ability to mime the use of familiar tools and to imitate meaningless sequences of movements. Results: All the children with Asperger's syndrome turned out to meet our criterion for a diagnosis of motor impairment, five of the six most severely motor impaired children in the whole study being from this group. Performance of the Asperger group was also slightly poorer on the Gesture Test. The profile of performance on each test was examined in detail but no evidence of group differences in the pattern of impairment was found. Conclusions: This study is consistent with others suggesting a high prevalence of clumsiness in Asperger's syndrome. Our findings also attest to the widespread prevalence of motor impairment in developmental disorders and the problems such co-morbidity poses for attempts to posit discrete and functionally coherent impairments underlying distinct syndromes. C1 Guys Hosp, Newcomer Ctr, London SE1 9RT, England. Univ London, Inst Educ, London WC1N 1AZ, England. Univ London Imperial Coll Sci Technol & Med, Charing Cross Hosp, London SW7 2AZ, England. Univ Surrey, Guildford GU2 5XH, Surrey, England. RP Green, D (reprint author), Guys Hosp, Newcomer Ctr, St Thomas St, London SE1 9RT, England. 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H., 1978, BRUININKS OSERETSKY BURGOINE E, 1983, BRIT J PSYCHIAT, V143, P261, DOI 10.1192/bjp.143.3.261 CERMAK SA, 1980, AM J OCCUP THER, V34, P19 COX AD, 1991, ARCH DIS CHILD, V66, P259 Croce RV, 2001, PERCEPT MOTOR SKILL, V93, P275 DEMYER MK, 1972, J AUTISM CHILD SCHIZ, V2, P264, DOI 10.1007/BF01537618 DEWEY D, 1988, DEV MED CHILD NEUROL, V30, P743 DEWEY D, 1993, BRAIN COGNITION, V23, P203, DOI 10.1006/brcg.1993.1055 Frith U, 1991, AUTISM ASPERGERS SYN GEUZE RH, 2001, SPECIAL ISSUE HUMAN, V20, P7 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 GILLBERG C, 1991, AUTISM ASPERGERS SYN GILLBERG C, 2000, CLIN CHILD NEUROPSYC GILLBERG IC, 1989, DEV MED CHILD NEUROL, V31, P3 GREEN D, 1997, THESIS U SURREY GREEN J, 1990, DEV MED CHILD NEUROL, V32, P743 HANDERSON SE, 1992, MOVEMENT ASSESSMENT Harter S., 1985, SELF PERCEPTION PROF Henderson SE, 2002, ADAPT PHYS ACT Q, V19, P12 HENDERSON SE, 1998, PERSPECTIVES CLASSIF Hill EL, 1998, DEV MED CHILD NEUROL, V40, P388 Hill EL, 1998, HUM MOVEMENT SCI, V17, P655, DOI 10.1016/S0167-9457(98)00017-7 HOWLIN P, 2000, J CHILD PSYCHOL PSYC, V5, P120 Iverson JM, 1997, DEV PSYCHOL, V33, P453 JONES V, 1985, J AUTISM DEV DISORD, V15, P37, DOI 10.1007/BF01837897 Kadesjo B, 2001, J CHILD PSYCHOL PSYC, V42, P487, DOI 10.1017/S0021963001007090 Kaplan BJ, 1998, HUM MOVEMENT SCI, V17, P471, DOI 10.1016/S0167-9457(98)00010-4 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x 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 MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 MIYAHARA A, 1997, J AUTISM DEV DISORD, V27, P597 Miyahara M, 1998, HUM MOVEMENT SCI, V17, P679, DOI 10.1016/S0167-9457(98)00018-9 OHTA M, 1987, J AUTISM DEV DISORD, V17, P45, DOI 10.1007/BF01487259 OZONOFF S, 2000, ASPERGERS SYNDROME POWELL RP, 1992, DEV MED CHILD NEUROL, V34, P755 Rogers S. J., 1991, DEV PSYCHOPATHOL, V3, P137, DOI DOI 10.1017/S0954579400000043 Rogers SJ, 1996, CHILD DEV, V67, P2060, DOI 10.2307/1131609 RUTTER M, 1998, PERSPECTIVES CLASSIF Smith IM, 1998, COGNITIVE NEUROPSYCH, V15, P747, DOI 10.1080/026432998381087 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 SMITH IM, 2000, ASPERGERS SYNDROME Smyth MM, 1997, J CHILD PSYCHOL PSYC, V38, P1023, DOI 10.1111/j.1469-7610.1997.tb01619.x SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 TANTAM D, 1991, AUTISM ASPERGERS SYN TANTAM D, 1988, BRIT J PSYCHIAT, V153, P783, DOI 10.1192/bjp.153.6.783 VOLKMAR FR, 2000, ASPERGERS SYNDROME Wechsler D., 1992, WECHSLER INTELLIGENC WHO, 1993, ICD 10 CLASS MENT BE WING L, 2000, ASPERGERS SYNDROME WING L, 1981, PSYCHOL MED, V11, P115 WING L, 1969, J CHILD PSYCHOL PSYC, V10, P1, DOI 10.1111/j.1469-7610.1969.tb02066.x World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 64 TC 122 Z9 127 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD JUL PY 2002 VL 43 IS 5 BP 655 EP 668 DI 10.1111/1469-7610.00054 PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 565FA UT WOS:000176357400010 PM 12120861 ER PT J AU van der Geest, JN Kemner, C Verbaten, MN van Engeland, H AF van der Geest, JN Kemner, C Verbaten, MN van Engeland, H TI Gaze behavior of children with pervasive developmental disorder toward human faces: a fixation time study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; pervasive developmental disorder; face perception; eye movements; gaze behavior ID FAMILY HOME MOVIES; AUTISTIC-CHILDREN; RECOGNITION; PERCEPTION; CAREGIVERS; PEOPLE AB Background: The abnormal gaze behavior of autistic children toward human faces, as observed in daily-life situations, are investigated in two fixation time studies. It has been argued that faces are a special kind of stimuli for normal individuals and that this might not be the case for autistic children. Methods: A group of high-functioning autistic children (including a group of sub-threshold PDD-NOS children) was compared with a group of normal children, with respect to their fixation behavior for photographs of human faces. Using an infrared eye-tracking device, fixation times for the whole face and for the facial elements of faces were compared between the two groups. The first study dealt with faces having an emotional expression. The second study dealt with neutral faces presented either upright or upside-down. Results: Results of the two studies showed that autistic children have the same fixation behavior as normal children for upright faces, with or without an emotional expression. Furthermore, results of the second study showed that normal children spent less time looking at upside-down faces, but that the fixation times of autistic children were not influenced by the orientation of the faces. Conclusions: These results plead against the notion that the abnormal gaze behavior in everyday life is due to the presence of facial stimuli per se. Furthermore, the absence of a face orientation effect in autistic children might be a reflection of a lack of holistic processing of human faces in autism. C1 Erasmus Univ, Dept Physiol, NL-3000 DR Rotterdam, Netherlands. Utrecht Med Ctr, Utrecht, Netherlands. Univ Utrecht, NL-3584 CH Utrecht, Netherlands. RP van der Geest, JN (reprint author), Erasmus Univ, Dept Physiol, POB 1738, NL-3000 DR Rotterdam, Netherlands. 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PD JUL PY 2002 VL 43 IS 5 BP 669 EP 678 DI 10.1111/1469-7610.00055 PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 565FA UT WOS:000176357400011 PM 12120862 ER PT J AU Adams, C Green, J Gilchrist, A Cox, A AF Adams, C Green, J Gilchrist, A Cox, A TI Conversational behaviour of children with Asperger syndrome and conduct disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Asperger's disorder; communication; conduct disorder; conversation; emotion; pragmatics ID SEMANTIC PRAGMATIC DISORDER; HIGH-FUNCTIONING AUTISM; LANGUAGE; ADOLESCENTS; COGNITION AB Background: Social communication problems in individuals who have Asperger syndrome constitute one of the most significant problems in the syndrome. This study makes a systematic analysis of the difficulties demonstrated with the use of language (pragmatics) in adolescents who have Asperger syndrome. Method: Recent advances in discourse analysis were applied to conversational samples from a group of children with Asperger syndrome and a matched control group of children with severe conduct disorder. Two types of conversation were sampled from each group, differing in emotional content. Results: The results showed that in these contexts children with Asperger syndrome were no more verbose as a group than controls, though they showed a tendency to talk more in more emotion-based conversations. Children with Asperger syndrome, as a group, performed similarly to control subjects in ability to respond to questions and comments. However, they were more likely to show responses which were problematic in both types of conversation. In addition, individuals with Asperger syndrome showed more problems in general conversation than during more emotionally and socially loaded topics. The group with Asperger syndrome was found to contain a small number of individuals with extreme verbosity but this was not a reliable characteristic of the group as a whole. C1 Univ Manchester, Human Commun & Deafness Grp, Manchester M13 9PL, Lancs, England. Royal Cornhill Hosp, Aberdeen, Scotland. Guys Hosp, London SE1 9RT, England. RP Adams, C (reprint author), Univ Manchester, Human Commun & Deafness Grp, Oxford Rd, Manchester M13 9PL, Lancs, England. CR ADAMS C, 1989, BRIT J DISORD COMMUN, V24, P211 Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Asperger H., 1979, COMMUNICATION, V13, P45 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Bishop DVM, 1998, APPL PSYCHOLINGUIST, V19, P415, DOI 10.1017/S0142716400010249 Bishop DVM, 1983, TEST RECEPTION GRAMM Bishop DVM, 2000, DEV PSYCHOPATHOL, V12, P177, DOI 10.1017/S0954579400002042 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P241 Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 COULTHARD M, 1977, ITNRO DISCOURSE ANAL Dobbinson S, 1998, J COMMUN DISORD, V31, P113, DOI 10.1016/S0021-9924(97)00085-3 Dunn L M., 1982, BRIT PICTURE VOCABUL EALES MJ, 1993, J AUTISM DEV DISORD, V23, P593, DOI 10.1007/BF01046104 Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x GREEN J, 1990, DEV MED CHILD NEUROL, V32, P743 Green J, 2000, J AUTISM DEV DISORD, V30, P279, DOI 10.1023/A:1005523232106 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x KLIN A, 1997, HDB AUTISM DEV DISOR, P1092 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 McTear M. F., 1985, CHILDRENS CONVERSATI Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x *PSYCH CORP, 1986, WECHSL AD INT SCAL R *PSYCH CORP, 1974, WECHSL INT SC CHILDR Ramberg C, 1996, EUR J DISORDER COMM, V31, P387 Rapin I., 1987, P 1 INT S SPEC SPEEC Shields J, 1996, DEV MED CHILD NEUROL, V38, P487 SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x van KREVELEN D, 1962, Acta Paedopsychiatr, V29, P22 Volkmar FR, 2000, AM J PSYCHIAT, V157, P262, DOI 10.1176/appi.ajp.157.2.262 WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1992, INT CLASS MENT BEH D, V10th NR 37 TC 59 Z9 62 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD JUL PY 2002 VL 43 IS 5 BP 679 EP 690 DI 10.1111/1469-7610.00056 PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 565FA UT WOS:000176357400012 PM 12120863 ER PT J AU Kern, DL Posey, DJ McDougle, CJ AF Kern, DL Posey, DJ McDougle, CJ TI Priapism associated with trazodone in an adolescent with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, Indianapolis, IN 46202 USA. RP Kern, DL (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, Indianapolis, IN 46202 USA. CR DETRIADA IS, 1991, J UROLOGY, V145, P60 Patel AG, 1996, BRIT J HOSP MED, V55, P315 WARNER MD, 1987, J CLIN PSYCHIAT, V48, P244 NR 3 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0890-8567 EI 1527-5418 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JUL PY 2002 VL 41 IS 7 BP 758 EP 758 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 566JQ UT WOS:000176424500004 ER PT J AU Cohen, BI AF Cohen, BI TI Use of a GABA-transaminase agonist for treatment of infantile autism SO MEDICAL HYPOTHESES LA English DT Article AB This paper describes the use of a GABA-transaminase agonist for the treatment of infantile autism. An approximate one third reduction of GABA and ammonia levels for an autistic patient with noticeable improvement of verbal/language skills and a reduction of repetitious ritualistic self-stimulatory behavior (stimming) was observed. A reduction of the plasma GABA (by administrating a GABA-T agonist, Imipramine) probably results in more axon(s)-to-oligodendrocyte signaling in the corpus callosum and it is postulated that this could result in a reduction of the autistic features for the patient. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 ED Labs, Hackensack, NJ 07606 USA. RP Cohen, BI (reprint author), ED Labs, 89 Leuning St, Hackensack, NJ 07606 USA. CR Cohen BI, 2001, MED HYPOTHESES, V57, P673, DOI 10.1054/mehy.2001.1350 COHEN BI, 1999, AUTISM, V3, P437, DOI 10.1177/1362361399003004010 Cohen BI, 2000, AUTISM, V4, P441, DOI 10.1177/1362361300004004010 GULALTIERI CT, 1977, DIS NERV SYST, V38, P368 NR 4 TC 7 Z9 7 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD JUL PY 2002 VL 59 IS 1 BP 115 EP 116 DI 10.1016/S0306-9877(02)00157-3 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 598GM UT WOS:000178267700022 PM 12160695 ER PT J AU Minshew, NJ Meyer, J Goldstein, G AF Minshew, NJ Meyer, J Goldstein, G TI Abstract reasoning in autism: A dissociation between concept formation and concept identification SO NEUROPSYCHOLOGY LA English DT Article ID CARD SORTING TEST; CHILDREN; INDIVIDUALS; DIAGNOSIS AB The concept identification and concept formation aspects of abstract reasoning were examined in 90 nonmentally retarded individuals with autism and 107 normal controls. It was hypothesized that pronounced deficits would be found on concept formation tests, whereas performance on concept identification tests would be relatively intact. There was a significant difference between individuals with autism and individuals from a matched control group on all abstract reasoning tasks, but, with the exception of the Wisconsin Card Sorting Test (R. K. Heaton et al., 1993), differences on concept identification tests were not clinically significant. Factor analyses showed that concept formation and concept identification tasks loaded on separate factors in the autism group but not in the control group. Stepwise discriminant function analyses revealed that 2 tests of concept formation correctly classified 78.4% of cases, whereas concept identification tasks did not pass the tolerance test. C1 Vet Affairs Pittsburgh Healthcare Syst, Res Serv, Pittsburgh, PA 15206 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15260 USA. RP Goldstein, G (reprint author), Vet Affairs Pittsburgh Healthcare Syst, Res Serv, 7180 Highland Dr,151R, Pittsburgh, PA 15206 USA. CR Adams W. 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A., 1966, STUDIES COGNITIVE GR, P86 OZONOFF S, 1995, NEUROPSYCHOLOGY, V9, P491, DOI 10.1037//0894-4105.9.4.491 PERRINE K, 1993, J CLIN EXP NEUROPSYC, V15, P461, DOI 10.1080/01688639308402571 PRIOR M, 1990, J AUTISM DEV DISORD, V20, P4 Reitan RM, 1993, HALSTEAD REITAN NEUR RUMSEY JM, 1985, J AUTISM DEV DISORD, V15, P23, DOI 10.1007/BF01837896 RUTTER M, 1978, J AUTISM CHILD SCHIZ, V8, P139, DOI 10.1007/BF01537863 SCHNEIDER SG, 1987, J ABNORM CHILD PSYCH, V15, P29, DOI 10.1007/BF00916464 SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x Siegel DJ, 1996, J AUTISM DEV DISORD, V26, P389, DOI 10.1007/BF02172825 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 SPSS, 1999, SPSS WIND VERS 10 0 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Thorndike RL, 1986, STANFORD BINET INTEL Tsai L. Y., 1992, HIGH FUNCTIONING IND, P11 Wechsler D, 1981, WECHSLER ADULT INTEL NR 37 TC 85 Z9 85 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD JUL PY 2002 VL 16 IS 3 BP 327 EP 334 DI 10.1037//0894-4105.16.3.327 PG 8 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA 577RV UT WOS:000177076300004 PM 12146680 ER PT J AU Kennett, J AF Kennett, J TI Autism, empathy and moral agency SO PHILOSOPHICAL QUARTERLY LA English DT Article ID SIMULATION AB Psychopaths have long been of interest to moral philosophers, since a careful examination of their peculiar deficiencies may reveal what features are normally critical to the development of moral agency. What underlies the psychopath's amoralism? A common and plausible answer to this question is that the psychopath lacks empathy. Lack of empathy is also claimed to be a critical impairment in autism, yet it is not at all clear that autistic individuals share the psychopath's amoralism. How is empathy characterized in the literature, and how crucial is empathy, so described, to moral understanding and agency? I argue that an examination of moral thinking in high-functioning autistic people supports a Kantian rather than a Humean account of moral agency. C1 Monash Univ, Clayton, Vic 3168, Australia. RP Kennett, J (reprint author), Monash Univ, Clayton, Vic 3168, Australia. CR ADSHEAD G, 1996, PHILOS PSYCHIATRY PS, V3, P279, DOI 10.1353/ppp.1996.0038 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S, 1993, UNDERSTANDING OTHER BARONCOHEN S, 1999, PHILOS EXPLORATIONS, V11, P175 DEIGH J, 1995, ETHICS, V105, P743, DOI 10.1086/293751 DEWEY MA, 1992, HIGH FUNCTIONING IND, P281 ELLIOTT CA, 1992, J MED PHILOS, V17, P200 FESTINGER L, 1964, CONFLICT DECISION DI Fields L, 1996, PHILOS PSYCHIAT PSYC, V3, P261, DOI 10.1353/ppp.1996.0043 Frith U., 1989, AUTISM EXPLAINING EN FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 GOLDMAN AI, 1995, ETHICS, V105, P709, DOI 10.1086/293749 GORDON RM, 1995, ETHICS, V105, P727, DOI 10.1086/293750 HOBSON P, 1992, HIGH FUNCTIONING IND, P157 Hobson P, 1993, UNDERSTANDING OTHER, P204 Hume David, TREATISE HUMAN NATUR KANT I, GROUNDWORK METAPHYSI KANT I, DOCTRINE VIRTUE Motluk A., 2001, NEW SCI JAN, P22 Mundy P, 1993, UNDERSTANDING OTHER, P181 MURPHY JG, 1972, ETHICS, V82, P284, DOI 10.1086/291852 Sacks Oliver, 1995, ANTHR MARS Sinclair J., 1992, HIGH FUNCTIONING IND, P294 SULLIVAN RC, 1992, HIGH FUNCTIONING IND, P243 VELLEMAN D, 1999, P ARISTOTELIAN SOC, V99, P57 Velleman D., 1996, ETHICS, V106, P694 Wellman H, 1993, UNDERSTANDING OTHER, P10 Wing L., 1992, HIGH FUNCTIONING IND, P129 NR 28 TC 50 Z9 51 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0031-8094 J9 PHILOS QUART JI Philos. Q. PD JUL PY 2002 VL 52 IS 208 BP 340 EP 357 DI 10.1111/1467-9213.00272 PG 18 WC Philosophy SC Philosophy GA 565QX UT WOS:000176381900004 ER PT J AU Duker, PC Douwenga, H Joosten, S Franken, T AF Duker, PC Douwenga, H Joosten, S Franken, T TI Ffects of single and repeated shock on perceived pain and startle response in healthy volunteers SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE perceived pain; startle response; healthy volunteers; contingent shock ID SELF-INJURIOUS-BEHAVIOR; ELECTRICAL AVERSION TREATMENT AB Contingent shock (CS) 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 concern, research into procedural variables of CS is needed. In this study, clinical evidence was used to infer a variable that might be of relevance for the application of clinical contingent shock, that is, to assess the effect of single versus repeated shock at a specific location on the body. With pain intensity and startle response as dependent variables, shocks were administered to 48 healthy volunteers. Electric shocks were identical to those that used in clinical practice. The second shock in succession to the same location of the body produced higher pain intensity ratings than the first shock and that the third shock in succession to the same location of the body produced higher pain intensity ratings than the second shock in succession. Startle responses, however, failed to be affected in this direction. The latter result is consistent with a previous study. Our data suggest that repeated shock to the same location is likely to be more effective to establish suppression than repeated shock to different locations. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Nijmegen, Psychol Lab A5 04, NL-6500 HE Nijmegen, Netherlands. Plurijn Fdn, NL-6500 HE Nijmegen, Netherlands. RP Duker, PC (reprint author), Univ Nijmegen, Psychol Lab A5 04, POB 9104, NL-6500 HE Nijmegen, Netherlands. CR Cohen J., 1977, STAT POWER ANAL BEHA Didden R, 1997, AM J MENT RETARD, V101, P387 Duker PC, 2000, RES DEV DISABIL, V21, P235, DOI 10.1016/S0891-4222(00)00039-1 Duker PC, 1999, J BEHAV THER EXP PSY, V30, P199, DOI 10.1016/S0005-7916(99)00025-7 Duker PC, 1996, RES DEV DISABIL, V17, P293, DOI 10.1016/0891-4222(96)00014-5 DUKER PC, UNPUB PARAMETERIC ST ISRAEL ML, 2000, M EUR ASS BEH AN AM RICKETTS RW, 1993, J BEHAV THER EXP PSY, V24, P57, DOI 10.1016/0005-7916(93)90009-L Symons FJ, 1997, J INTELL DISABIL RES, V41, P456, DOI 10.1111/j.1365-2788.1997.tb00737.x VONHEYN RE, 1993, UNPUB COMP LONG TERM WILLIAMS DE, 1993, RES DEV DISABIL, V14, P207, DOI 10.1016/0891-4222(93)90031-E NR 11 TC 2 Z9 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD JUL-AUG PY 2002 VL 23 IS 4 BP 285 EP 292 DI 10.1016/S0891-4222(02)00119-1 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 596XH UT WOS:000178191400004 PM 12365852 ER PT J AU Casas-Fernandez, C AF Casas-Fernandez, C TI Communication disorders SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autism; communication; language; social interaction ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; PORCINE SECRETIN; AUTISM; CHILDREN AB Introduction, This is a round table presentation on disorders of communication. Diagnostic and therapeutic challenges are analyzed. Autism is considered to be an important clinical syndrome in which there may be different degrees of affectation of behaviour, alterations of language and deficit in social interaction. There is therefore a similar phenotype with slight differences probably due to different clinical genotypes in each clinical group. There is obviously genetic heterogeneity. Development. We consider the most useful diagnostic protocols to establish the differential diagnosis, but always based on essential prior clinical analysis of each case. Finally we study current therapeutic challenges. C1 Hosp Univ Virgen de la Arrixaca, Secc Neuropediat, Murcia, Spain. CR ALLEN DA, 1989, SCHOOL PSYCHOL REV, V18, P442 Artigas J, 1999, Rev Neurol, V28 Suppl 2, pS118 BADNER JA, 2002, MOL PSYCHIATR, V7, P56 BAUMAN ML, 1991, PEDIATRICS, V87, P791 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Betancur C, 2002, MOL PSYCHIATR, V7, P67, DOI 10.1038/sj/mp/4000923 CASASFERNANDEZ C, 2000, REV NEUROL CLIN, V1, P103 CASASFERNANDEZ C, 1999, PEDIAT INTEGRAL, V2, P42 CASASFERNANDEZ C, 1999, SE PEDIAT, V2, P5 Coniglio SJ, 2001, J PEDIATR-US, V138, P649, DOI 10.1067/mpd.2001.112474 Corbett B, 2001, CLIN PEDIATR, V40, P327, DOI 10.1177/000992280104000604 Dotti MT, 2002, NEUROLOGY, V58, P226 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 Garaizar C, 1997, REV NEUROLOGIA, V25, P187 Kanner L, 1943, NERV CHILD, V2, P217 LopezPison J, 1997, REV NEUROLOGIA, V25, P1535 Monaco A P, 2001, Lancet, V358 Suppl, pS3, DOI 10.1016/S0140-6736(01)07016-7 NARBONA J, 2000, TRASTORNOS LENGUAJE, P329 Narbona J., 1997, NEUROLOGIA PEDIAT, P683 Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 PERALTA F, 1997, LENGUAJE NINO DESARR, P195 Peralta MF, 1991, BORDON, V43, P285 RAPIN I, 1997, NEUROLOGIA PEDIAT, P693 Shahbazian MD, 2002, HUM MOL GENET, V11, P115, DOI 10.1093/hmg/11.2.115 Stone WL, 2001, AUTISM, V5, P341, DOI 10.1177/1362361301005004002 Sweeten TL, 2002, PHARMACOL BIOCHEM BE, V71, P449, DOI 10.1016/S0091-3057(01)00697-9 Tuchman RF, 2001, REV NEUROLOGIA, V33, P292 Tuchman R F, 1997, Semin Pediatr Neurol, V4, P93, DOI 10.1016/S1071-9091(97)80025-3 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 NR 29 TC 0 Z9 0 PU REVISTA DE NEUROLOGIA PI BARCELONA PA C/O CESAR VIGUERA, EDITOR, APDO 94121, 08080 BARCELONA, SPAIN SN 0210-0010 J9 REV NEUROLOGIA JI Rev. Neurologia PD JUL 1 PY 2002 VL 35 IS 1 BP 29 EP 32 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 578PK UT WOS:000177126700005 PM 12389189 ER PT J AU Narbona, J Patino, A AF Narbona, J Patino, A TI Genetic studies in communication disorders SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autistic spectrum; chromosome 7q; disphasia; language disorder; linkage; molecular genetics; neurogenetics; pervasive developmental disorder ID LANGUAGE IMPAIRMENT; BEHAVIORAL PHENOTYPES; FAMILIAL AGGREGATION; AUTISM FAMILIES; GENOMIC SCREEN; SEVERE SPEECH; CHROMOSOME; CHILDREN; ANGELMAN; HISTORY AB Objectives. To review current literature on population, cytogenetic and molecular studies of specific language disorders (SLD) and pervasive developmental disorders (PDD). Development. Clinical concordance studies in twins and in vertical familial groups suggest polygenic multifactorial modes of inheritance, but in some families an autosomal dominant model may be present. The data favour not a modular, but rather a molar model of the relationship between genes and neural abilities for communicative behaviors. Several extensive genome screenings have demonstrated linkage to specific markers on 7q for SLD, and on 7q and 2q for PDD. The strong evidence of linkage on 7q for both disorders has led to the hypothesis that this region contains several separate quantitative trait loci (QTL) related to different communicative abilities. Mutations in different QTL would facilitate the different disabilities and stereotyped behaviors associated with the phenotypic spectrum of PDD. There are other candidate regions for QTLs but the linkage is weaker and there is little agreement between studies; due, in part, to over-extensive inclusion criteria and small sizes of familial groups, Conclusions. To enhance linkage research in further molecular genetic studies, clinicians must refine behavioral target traits when selecting familial groups and enlarge the size of familial groups by including non-handicapped members with related behavioral traits. At present, a chromosome region in 7q shows the strongest evidence for communication-related QTL, but other QTL need to be identified elsewhere in the genome in order to explain the genetic contribution to the large spectrum of language and autistic disorders. C1 Univ Navarra, Fac Med, Navarra, Spain. Clin Univ, Dept Pediat, E-31080 Pamplona, Navarra, Spain. RI Patino-Garcia, Ana/I-4299-2012 CR AGUADO G., 1999, TRASTORNO ESPECIFICO Alarcon M, 2002, AM J HUM GENET, V70, P60, DOI 10.1086/338241 Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 Barrett S, 1999, AM J MED GENET, V88, P609 Bayley A, 1995, PSYCHOL MED, V25, P63 BELINCHON M, 1997, INSTRUCCION APRENDIZ, P231 Bellugi U, 1990, Am J Med Genet Suppl, V6, P115 BILLARD C, 1994, ANAE APPROCHE NEUROP, V6, P155 Bishop D., 2000, SPEECH LANGUAGE IMPA, P99 BISHOP DVM, 1995, DEV MED CHILD NEUROL, V37, P56 Bishop DVM, 2001, DEV MED CHILD NEUROL, V43, P809, DOI 10.1017/S0012162201001475 Bishop DVM, 2001, PHILOS T R SOC B, V356, P369, DOI 10.1098/rstb.2000.0770 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Borgatti R, 2001, PEDIATR NEUROL, V24, P111, DOI 10.1016/S0887-8994(00)00244-7 Brun-Gasca C, 2001, REV NEUROLOGIA, V33, pS29 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 BUXBAUM JD, 2001, AM J HUM GENET, V69, P470 CHEVRIEMULLER C, 2001, LENGUAJE NINO DESARR, P189 Finegan JA, 1998, AM J MED GENET, V81, P148, DOI 10.1002/(SICI)1096-8628(19980328)81:2<148::AID-AJMG5>3.0.CO;2-S Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 GOPNIK M, 1991, COGNITION, V39, P1, DOI 10.1016/0010-0277(91)90058-C Bailey A, 1998, HUM MOL GENET, V7, P571 Palferman S, 2001, HUM MOL GENET, V10, P973 KarmiloffSmith A, 1997, CHILD DEV, V68, P246, DOI 10.1111/j.1467-8624.1997.tb01938.x Klauck SM, 1997, HUM GENET, V100, P224, DOI 10.1007/s004390050495 Lai CSL, 2001, NATURE, V413, P519, DOI 10.1038/35097076 LEONARD CM, 1993, AM J MED GENET, V46, P26, DOI 10.1002/ajmg.1320460107 LINDAHL E, 1988, DEV MED CHILD NEUROL, V30, P571 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2001, AM J MED GENET, V105, P36, DOI 10.1002/1096-8628(20010108)105:1<36::AID-AJMG1053>3.0.CO;2-4 Moldavsky M, 2001, J AM ACAD CHILD PSY, V40, P749, DOI 10.1097/00004583-200107000-00009 PEMBREY M, 1992, SPECIFIC SPEECH AND LANGUAGE DISORDERS IN CHILDREN : CORRELATES, CHARACTERISTICS AND OUTCOMES, P51 PENNER KA, 1993, AM J MED GENET, V46, P34, DOI 10.1002/ajmg.1320460108 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Piven J, 1997, AM J PSYCHIAT, V154, P185 RAPIN I, 2001, LENGUAJE NINO DESARR, P357 Repetto GR, 1998, AM J MED GENET, V79, P82, DOI 10.1002/(SICI)1096-8628(19980901)79:2<82::AID-AJMG2>3.0.CO;2-P Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 RITVO ER, 1985, AM J PSYCHIAT, V142, P74 RIVIERE A, 1997, TRATAMIENTO AUTISMO, P61 Riviere A, 1997, TRATAMIENTO AUTISMO, P107 Salmon B, 1999, AM J MED GENET, V88, P551, DOI 10.1002/(SICI)1096-8628(19991015)88:5<551::AID-AJMG21>3.0.CO;2-# SCHIFF NB, 1979, J SPEECH HEAR RES, V22, P581 Sheldon L, 2000, DEV MED CHILD NEUROL, V42, P768, DOI 10.1017/S0012162200001420 SUDHALTER V, 1991, AM J MED GENET, V38, P493, DOI 10.1002/ajmg.1320380270 TALLAL P, 1989, J SPEECH HEAR DISORD, V54, P167 TEELE DW, 1984, PEDIATRICS, V74, P282 VanderLely HKJ, 1996, BRAIN LANG, V52, P484, DOI 10.1006/brln.1996.0026 VARGHAKHADEM F, 1995, P NATL ACAD SCI USA, V92, P930, DOI 10.1073/pnas.92.3.930 NR 49 TC 1 Z9 1 PU REVISTA DE NEUROLOGIA PI BARCELONA PA C/O CESAR VIGUERA, EDITOR, APDO 94121, 08080 BARCELONA, SPAIN SN 0210-0010 J9 REV NEUROLOGIA JI Rev. Neurologia PD JUL 1 PY 2002 VL 35 IS 1 BP 32 EP 36 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 578PK UT WOS:000177126700006 PM 12389190 ER PT J AU Campos-Castello, J Briceno-Cuadros, S AF Campos-Castello, J Briceno-Cuadros, S TI Communication disorders: Differential diagnosis SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE cognitive-affective cerebellar syndrome; disorders of neuronal migration and language EEG paroxysms and language POCSL spectrum epilepsy and language; metabolic disorders with neuropsychological expression ID LANDAU-KLEFFNER SYNDROME; ACQUIRED EPILEPTIC APHASIA; ELECTROENCEPHALOGRAPHIC ABNORMALITIES; CONVULSIVE DISORDER; CHILDREN; EEG; CHILDHOOD; AUTISM; SLEEP; MRI AB Objective. To evaluate components of clinical semiology in the differential diagnosis of communication disorders (TC) and their possible biological markers. We consider two groups, according to the communication disorders themselves and their effects on social interaction. In the first case both aspects are affected in parallel and in the second it is predominantly social interaction which is affected. Development. In the first groups we studied dyslalias, dyrhrythmias, acquired aphasias, TC relation to epilepsy, types of seizures and EEG discharges. The dysphasia of development and epilepsy may be associated by chance, as a result of the same cause or the epilepsy be responsible for the TC, either because of seizures or continuously (acquired epileptic-aphasia, SLK). Based on personal data and the literature we studied the semiology, possible biological markers and differential diagnosis. We consider disorders of neurone migration and metabolic alterations of initial neuropsychological semiology and cerebellar anomalies involved in cognitive functions. In the second group we assessed autism, generalized disorders of development and particular syndromes with semantic-pragmatic TC. Conclusions. The development of language cannot be separated from other aspects of neurological maturation. One cannot affirm that there is a direct relationship between epilepsy and TC, although this does occur in some cases, We accept the hypothesis that SLK, POCSL and atypical EPB are clinical forms of the same syndrome of epilepsy. Recognition of the cognitive-affective cerebellar syndrome by its involvement in social executive function, language and personality characterizes certain conditions (Williams, Asperger, fragile-X, autism). A progressive rational battery of complementary studies on clinical data is essential to determine biological markers in syndromes which still lack them. C1 Hosp Clin Univ San Carlos, Serv Neuropediat, E-28040 Madrid, Spain. 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Neurologia PD JUL 1 PY 2002 VL 35 IS 1 BP 36 EP 44 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA 578PK UT WOS:000177126700007 PM 12389191 ER PT J AU Wolfe, RM Sharp, LK Lipsky, MS AF Wolfe, RM Sharp, LK Lipsky, MS TI Content and design attributes of antivaccination Web sites SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PERTUSSIS VACCINATION; RUBELLA VACCINE; MEASLES; IMMUNIZATION; CHILDREN; AUTISM; ASTHMA; ASSOCIATION; EXEMPTIONS; CHILDHOOD AB Context Individuals searching the Internet for vaccine information may find anti-vaccination Web sites. Few published studies have systematically evaluated these sites. Objectives To examine antivaccination Web site attributes and to delineate the specific claims and concerns expressed by antivaccination groups. Design and Setting In late 2000, using a metasearch program that incorporates 10 other search engines, we reviewed and analyzed 772 links to find 12 Web sites that promulgated antivaccination information. Analyzing links from these 12 sites yielded another 10 sites, producing a total of 22 sites for study. Using a standardized form, 2 authors (R.M.W., L.K.S.) systematically evaluated these sites based on specific content and design attributes. Main Outcome Measures Presence or absence of 11 Web site content attributes (antivaccination claims) and 10 Web site design attributes. Results The most commonly found content claims were that vaccines cause idiopathic illness (100% of sites), vaccines erode immunity (95%), adverse vaccine reactions are underreported (95%), and vaccination policy is motivated by profit (91%). The most common design attributes were the presence of links to other antivaccination sites (100% of sites), information for legally avoiding immunizations (64%), and the use of emotionally charged stories of children who had allegedly been killed or harmed by vaccines (55%). Conclusion Antivaccination Web sites express a range of concerns related to vaccine safety and varying levels of distrust in medicine. The sites rely heavily on emotional appeal to convey their message. C1 Northwestern Univ, Feinberg Sch Med, Dept Family Med, Chicago, IL 60611 USA. Evanston NW Healthcare, Evanston, IL USA. RP Wolfe, RM (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Family Med, 710 N Lake Shore Dr,Room 1417, Chicago, IL 60611 USA. 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Am. Med. Assoc. PD JUN 26 PY 2002 VL 287 IS 24 BP 3245 EP 3248 DI 10.1001/jama.287.24.3245 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 566FF UT WOS:000176415800029 PM 12076221 ER PT J AU Valdizan-Uson, JR Abril-Villalba, B Mendez-Garcia, M Sans-Capdevila, O AF Valdizan-Uson, JR Abril-Villalba, B Mendez-Garcia, M Sans-Capdevila, O TI Nocturnal polysomnogram in childhood autism without epilepsy SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE autism; nocturnal polysomnogram ID ASPERGERS SYNDROME; RETTS SYNDROME; SLEEP; CHILDREN; PATTERNS; DISORDER AB Aims. To evaluate the presence of epileptiform discharges and the organisation of nocturnal sleep of autistic children without nocturnalpolysomnographic epileptic seizures. Subjects and methods. Cross-section analysis. Subjects: 21 boys and girls with autistic spectrum using DSH-IV criteria between the ages of 4 and 12, compared with a control group made up of normal children of the same ages. Methods: nocturnal polysomnogram with a minimum efficiency of 75%. Analysis: t-test to compare the cycles and phases of sleep with significance p < 0.05. Results. Subjects presented a maximum of four sleep cycles compared with five or six in the control subjects. From the first third of the night onwards there was an increase in the slowest phases. 66% presented epileptiform paroxysmal discharges, all of which originated in the anterior half of the brain. Conclusion. Sleep is not destructured, but it is reduced in length, with epileptiform paroxysms of predominantly frontal origin. This could indicate that these two parameters are intrinsic to the autistic spectrum, as well as indicating a more focused origin of the generalised picture which is possibly closely related with the qualitative alteration of the social experiences of these children. C1 Hosp Univ Miguel Servet, Serv Neurofisiol Clin, E-50009 Zaragoza, Spain. 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Neurologia PD JUN 16 PY 2002 VL 34 IS 12 BP 1101 EP 1105 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 576DY UT WOS:000176988600001 PM 12134270 ER PT J AU Barr, R AF Barr, R TI Autism, bowel inflammation, and measles SO LANCET LA English DT Letter C1 Alexander Harris, London E1N 2JT, England. RP Barr, R (reprint author), Alexander Harris, 1 Dyers Bldg, London E1N 2JT, England. CR Walker-Smith J, 2002, LANCET, V359, P705, DOI 10.1016/S0140-6736(02)07783-8 *WORK PART MMR VAC, 2002, REP WORK PART MMR VA 2002, MEASLES MUMPS RUBELL NR 3 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 JUN 15 PY 2002 VL 359 IS 9323 BP 2112 EP 2112 DI 10.1016/S0140-6736(02)08917-1 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 562JX UT WOS:000176194600030 PM 12086783 ER PT J AU Elphinstone, P AF Elphinstone, P TI Autism, bowel inflammation, and measles 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. CR Walker-Smith J, 2002, LANCET, V359, P705, DOI 10.1016/S0140-6736(02)07783-8 NR 1 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 JUN 15 PY 2002 VL 359 IS 9323 BP 2112 EP 2112 DI 10.1016/S0140-6736(02)08916-X PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 562JX UT WOS:000176194600029 PM 12086782 ER PT J AU Smeeth, L Hall, AJ Rodrigues, LC Cook, C Fombonne, E AF Smeeth, L Hall, AJ Rodrigues, LC Cook, C Fombonne, E TI Autism, bowel inflammation, and measles SO LANCET LA English DT Letter C1 Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, London WC1E 7HT, England. Univ London London Sch Hyg & Trop Med, Dept Infect & Trop Dis, London WC1E 7HT, England. McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3H 1P3, Canada. RP Smeeth, L (reprint author), Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, Keppel St, London WC1E 7HT, England. CR UHLMANN V, 2002, POTENTIAL VIRAL PATH Walker-Smith J, 2002, LANCET, V359, P705, DOI 10.1016/S0140-6736(02)07783-8 NR 2 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 JUN 15 PY 2002 VL 359 IS 9323 BP 2112 EP 2113 DI 10.1016/S0140-6736(02)08918-3 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 562JX UT WOS:000176194600031 PM 12086784 ER PT J AU Eden, OB AF Eden, OB TI Autism, bowel inflammation, and measles SO LANCET LA English DT Letter C1 Christie Hosp NHS Trust, Dept Paediat Oncol, Manchester M20 4BX, Lancs, England. RP Eden, OB (reprint author), Christie Hosp NHS Trust, Dept Paediat Oncol, Manchester M20 4BX, Lancs, England. CR Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 2002, LANCET, V359, P637 NR 2 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD JUN 15 PY 2002 VL 359 IS 9323 BP 2113 EP 2113 DI 10.1016/S0140-6736(02)08919-5 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 562JX UT WOS:000176194600032 PM 12086785 ER PT J AU Thrower, D AF Thrower, D TI Autism, bowel inflammation, and measles SO LANCET LA English DT Letter RP Thrower, D (reprint author), 49 Ackers Rd,Stockton Heath, Warrington WA4 2DZ, Cheshire, England. CR SINGH VK, 2002, J ALLERGY CLIN IMMUN, V109 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Walker-Smith J, 2002, LANCET, V359, P705, DOI 10.1016/S0140-6736(02)07783-8 NR 3 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 JUN 15 PY 2002 VL 359 IS 9323 BP 2113 EP 2113 DI 10.1016/S0140-6736(02)08920-1 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 562JX UT WOS:000176194600033 PM 12086786 ER PT J AU Uhlmann, EJ Apicelli, AJ Baldwin, RL Burke, SP Bajenaru, ML Onda, H Kwiatkowski, D Gutmann, DH AF Uhlmann, EJ Apicelli, AJ Baldwin, RL Burke, SP Bajenaru, ML Onda, H Kwiatkowski, D Gutmann, DH TI Heterozygosity for the tuberous sclerosis complex (TSC) gene products results in increased astrocyte numbers and decreased p27-Kip1 expression in TSC2 +/- cells SO ONCOGENE LA English DT Article DE tuberin; hamartin; glia; astrocytoma; tumor suppressor gene ID NF1 TUMOR-SUPPRESSOR; MISSENSE MUTATIONS; ALLELIC LOSS; HAMARTIN; MICE; PROLIFERATION; PROTEIN; GROWTH; LESIONS; IDENTIFICATION AB Tuberous sclerosis complex (TSC) is an autosomal dominant tumor predisposition syndrome characterized by benign proliferations (hamartomas). In the brain, individuals with TSC develop autism, mental retardation and seizures associated with focal cortical dysplasias, subependymal nodules, and subependymal giant cell astrocytomas (SEGAs). We hypothesize that dysregulated astrocyte function due to mutations in they tumor suppressor genes, TSC1 and TSC2, may contribute to the pathogenesis of these brain abnormalities. In this report, we demonstrate that mice heterozygous for a targeted defect in either the Tsc1 or Tsc2 genes (Tsc1+/- and Tsc2+/- mice) exhibit a 1.5-fold increase in the number of astrocytes in vivo. Whereas increased astrocyte numbers in vivo were suggestive of a proliferative advantage, Tsc2+/- primary astrocyte cultures did not show a cell-autonomous growth advantage, anchorage-independent growth, increased saturation density, or increased fluid-phase endocytosis compared to wild type astrocytes. Tsc2 null mouse embryonic fibroblasts (MEFs) however, did exhibit increased saturation density compared to Tsc2 wild type controls. In both Tsc2+/- astrocytes and Tsc2 null mouse embryonic fibroblasts, p27-Kip1 expression was decreased compared to wild type cells, and was reversed by tuberin re-expression in Tsc2-/- MEFs. In contrast, no change in endocytosis was observed upon tuberin re-expression in Tsc2-/- MEFs. Collectively, these results suggest Tsc heterozygosity may provide a non-cell-autonomous growth advantage for astrocytes that may involve p27-Kip1 expression. C1 Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA. Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 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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Genetic and neurofunctional research in autism has highlighted the need for improved characterization of the core social disorder defining the broad spectrum of syndrome manifestations. Method: This article reviews the advantages and limitations of current methods for the refinement and quantification of this highly heterogeneous social phenotype. Results. The study of social visual pursuit by use of eye-tracking technology is offered as a paradigm for novel tools incorporating these requirements and as a research effort that builds on the emerging synergy of different branches of social neuroscience. Conclusions: Advances in the area will require increased consideration of processes underlying experimental results and a closer approximation of experimental methods to the naturalistic demands inherent in real-life social situations. C1 Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT 06520 USA. 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Neuro-Psiquiatr. PD JUN PY 2002 VL 60 IS 2A BP 239 EP 241 PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 557CV UT WOS:000175890500011 ER PT J AU Silva, AE Vayego-Lourenco, SA Fett-Conte, AC Goloni-Bertollo, EM Varella-Garcia, M AF Silva, AE Vayego-Lourenco, SA Fett-Conte, AC Goloni-Bertollo, EM Varella-Garcia, M TI Tetrasomy 15q11-q13 identified by fluorescence in situ hybridization in a patient with autistic disorder SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE tetrasomy 15; 15q11-q13; autism; fluorescence in situ hybridization; GABA receptors ID PROXIMAL 15Q; DUPLICATION; CHROMOSOME; GENE; ANGELMAN; SUBUNIT; GABRA5; REGION AB We report a female child with tetrasomy of the 15q11-q13 chromosomal region, and autistic disorder associated with mental retardation, developmental problems and behavioral disorders. 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Neuro-Psiquiatr. PD JUN PY 2002 VL 60 IS 2A BP 290 EP 294 DI 10.1590/S0004-282X2002000200021 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 557CV UT WOS:000175890500022 PM 12068363 ER PT J AU Assumpcao, FB Kuczynski, E AF Assumpcao, FB Kuczynski, E TI Autism, bipolar disorder and mental retardation in a male adolescent with congenital rubella: case report SO ARQUIVOS DE NEURO-PSIQUIATRIA LA Portuguese DT Article DE infantile autism; congenital rubella; bipolar disorder ID INFANTILE-AUTISM AB We describe an autistic male adolescent with congenital rubella who has developed bipolar disorder, discussing possible diagnostic and therapeutic implications. C1 Univ Sao Paulo, Fac Med, Hosp Clin, Inst Psiquiatria Serv Psiquiatria, Sao Paulo, SP, Brazil. Catholic Univ, Doutor Psicol Clin Pontificia, Sao Paulo, Brazil. 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L., 1956, AM J ORTHOPSYCHIAT, V26, P55 KERBESHIAN J, 1990, J MENT DEFIC RES, V34, P205 KERBESHIAN J, 1987, J CLIN PSYCHOPHARM, V7, P401 Kerbeshian J, 1996, J AM ACAD CHILD PSY, V35, P681, DOI 10.1097/00004583-199605000-00024 LAINHART JE, 1994, J AUTISM DEV DISORD, V24, P587, DOI 10.1007/BF02172140 LEBOVICI S, 1991, AUTISMO PSICOSES CRI, P11 LELLORD G, 1991, AUTISME ENFANT MISES R, 1990, NEUROPSYCHIAT ENFAN, V38, P523 RITVO ER, 1976, AUTISM DIAGNOSIS CUR SPARROW SS, 1984, ADAPTATIVE BEHAV SCA Tsai LY, 1996, J AUTISM DEV DISORD, V26, P159, DOI 10.1007/BF02172004 *WHO, 1993, CLASS DOENC MENT CID NR 23 TC 2 Z9 2 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD JUN PY 2002 VL 60 IS 2A BP 324 EP 327 DI 10.1590/S0004-282X2002000200028 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 557CV UT WOS:000175890500029 PM 12068370 ER PT J AU Fombonne, E AF Fombonne, E TI Prevalence of childhood disintegrative disorder SO AUTISM LA English DT Article DE autism; childhood disintegrative disorder; epidemiology; pervasive developmental disorder; prevalence ID PERVASIVE DEVELOPMENTAL DISORDERS; PRESCHOOL-CHILDREN; DSM-IV; AUTISM; PSYCHOSIS; ONSET; AGE AB The prevalence of childhood disintegrative disorder (CDD) is unknown. In this study, 32 epidemiological surveys of autism and pervasive developmental disorders published in English language journals since 1966 were reviewed. Four surveys yielded estimates for CDD ranging from 1.1 to 6.4 per 100,000 subjects. A pooled estimate across these four surveys is 1.7 per 100,000 (95 percent Confidence Interval: 0.6-3.8 per 100,000). The conclusion is that CDD is very rare and its prevalence is 60 times less than that for autistic disorder, assuming a prevalence of 10 per 10,000 for autism. If a rate of 30 per 10 000 is taken for all PDDs, only one child out of 175 children with a DD diagnosis would, on average, meet criteria for CDD. C1 McGill Univ, Montreal Childrens Hosp, Canada Res Chair Child & Adolescent Psychiat, Dept Psychiat, Montreal, PQ H3Z 1P2, Canada. RP Fombonne, E (reprint author), McGill Univ, Montreal Childrens Hosp, Canada Res Chair Child & Adolescent Psychiat, Dept Psychiat, 4018 St Catherine St W, Montreal, PQ H3Z 1P2, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Amir RE, 1999, NAT GENET, V23, P185 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 BURD L, 1987, J AM ACAD CHILD PSY, V26, P700, DOI 10.1097/00004583-198709000-00014 *CAL DEP DEV SERV, 1999, CHANG POP PERS AUT P Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 FOMBONNE E, 2002, IN PRESS MOL PSYCHIA FOMBONNE E, 2001, ED CHILDREN AUTISM FOMBONNE E, 2001, PEDIATRICS, V108, P1 Heller T, 1908, Z ERFORSCHUNG BEHAND, V2, P141 Hillman R E, 2000, Mo Med, V97, P159 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Kielinen M, 2000, EUR CHILD ADOLES PSY, V9, P162 KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 Magnusson GT, 1977, LAEKNABLADID, V63, P237 Magnusson P, 2001, J AUTISM DEV DISORD, V31, P153, DOI 10.1023/A:1010795014548 Malhotra S, 1999, J AUTISM DEV DISORD, V29, P491, DOI 10.1023/A:1022247903401 Mouridsen SE, 1998, BRIT J PSYCHIAT, V172, P263, DOI 10.1192/bjp.172.3.263 Powell JE, 2000, DEV MED CHILD NEUROL, V42, P624, DOI 10.1017/S001216220000116X ROGERS JS, 1990, J AM ACAD CHILD ADOL, V29, P207 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 Sponheim E, 1998, J AUTISM DEV DISORD, V28, P217, DOI 10.1023/A:1026017405150 Tuchman R F, 1997, Semin Pediatr Neurol, V4, P93, DOI 10.1016/S1071-9091(97)80025-3 Volkmar F. R., 1997, HDB AUTISM PERVASIVE, P47 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 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 World Health Organisation, 1978, MENT DIS GLOSS GUID World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 35 TC 30 Z9 32 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 149 EP 157 DI 10.1177/1362361302006002002 PG 9 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400001 PM 12083281 ER PT J AU Noterdaeme, M Mildenberger, K Sitter, S Amorosa, H AF Noterdaeme, M Mildenberger, K Sitter, S Amorosa, H TI Parent information and direct observation in the diagnosis of pervasive and specific developmental disorders SO AUTISM LA English DT Article DE ADI-R; ADOS-G; diagnostic assessment; infantile autism; receptive language disorder ID RECEPTIVE LANGUAGE DISORDER; COMPARATIVE FOLLOW-UP; EARLY ADULT LIFE; OBSERVATION SCHEDULE; INFANTILE-AUTISM; OUTCOMES; CHILDREN; INTERVIEW; BEHAVIOR AB Children with autism and children with a severe specific receptive language disorder show clear deficits in communicative language skills and social relationships. In this study the usefulness of a standardized parent interview (ADI-R) and a standardized observation schedule (ADOS-G) for the differential diagnosis of these two groups was assessed. Eleven children with early infantile autism and 16 children with a specific receptive language disorder participated, The parent interview was conducted with all parents and the observation schedule was administered to all children. Ten out of I I children with autism were correctly classified as having autism on the ADI-R and the ADOS-G. One child with a receptive language disorder was falsely classified as having autism on the ADI-R, and none on the ADOS-G. Parent interview provides extensive information on the developmental course of the child. Direct observation gives an overview of actual relevant behavioural problems. The two instruments are complementary in the diagnosis of developmental disorders. C1 Heckscher Klin Kinder & Jugendpsychiat, Abt Teilleistungs & Verhaltensgestorte Kinder, D-81479 Munich, Germany. Univ Munich, D-80539 Munich, Germany. RP Noterdaeme, M (reprint author), Heckscher Klin Kinder & Jugendpsychiat, Abt Teilleistungs & Verhaltensgestorte Kinder, Wolfratshauser Str 350, D-81479 Munich, Germany. CR ALLEN DA, 1992, INT CONGR SER, V965, P157 ALLEN DA, 1988, J CHILD NEUROL, V35, P48 BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 Beitchman JH, 1996, J AM ACAD CHILD PSY, V35, P815, DOI 10.1097/00004583-199606000-00022 BEITCHMAN JH, 1986, J AM ACAD CHILD PSY, V25, P528, DOI 10.1016/S0002-7138(10)60013-1 CANTWELL DP, 1989, J AUTISM DEV DISORD, V19, P19, DOI 10.1007/BF02212715 GRIMM H, 1978, HEIDELBERGER SPRACHE Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 Kaufman AS, 1991, KAUFMAN ASSESSMENT B 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 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X Noterdaeme M, 1999, Z KINDER JUG-PSYCH, V27, P251, DOI 10.1024//1422-4917.27.4.251 Noterdaeme M, 1999, Z KINDER JUG-PSYCH, V27, P183, DOI 10.1024//1422-4917.27.3.183 Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 RUTTER M, 1992, SPECIFIC SPEECH AND LANGUAGE DISORDERS IN CHILDREN : CORRELATES, CHARACTERISTICS AND OUTCOMES, P63 *WHO, 1991, ICD 10 INT KLASS PSY NR 18 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 JUN PY 2002 VL 6 IS 2 BP 159 EP 168 DI 10.1177/1362361302006002003 PG 10 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400002 PM 12083282 ER PT J AU Sherratt, D AF Sherratt, D TI Developing pretend play in children with autism - A case study SO AUTISM LA English DT Article DE autism; play; pretence; symbolic ID MIND AB A classroom-based intervention study aimed to explore whether it was possible to teach children with autism and additional learning difficulties to use symbolic pretend play. Five children with autism were involved in a 4 month intervention that used structure, affect and repetition. The intervention progressively faded out the structuring over three phases. All the children were able to use some symbolic acts within play. The study suggests that some of the symbolic play was not the result of replicating previously modelled examples but was spontaneous and novel. CR BARONCOHEN S, 1989, BRIT J DISORD COMMUN, V24, P199 BEYER J, 2000, AUTISM PLAY Charman T, 1997, J AUTISM DEV DISORD, V27, P325, DOI 10.1023/A:1025806616149 Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 JARROLD C, 1993, J AUTISM DEV DISORDE, V23 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 LESLIE AM, 1994, COGNITION, V50, P211, DOI 10.1016/0010-0277(94)90029-9 Lewis V., 1998, TEST PRETEND PLAY LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 LOWE M, 1989, SYMBOLIC PLAY TEST Reynell J., 1977, REYNELL DEV LANGUAGE Schopler E., 1988, CHILDHOOD AUTISM RAT THORP DM, 1995, J AUTISM DEV DISORDE, V25 VANBERCKALAERON.IA, 1994, PLAY INTERVENTION WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wolfberg P. J., 1999, PLAY IMAGINATION CHI NR 18 TC 17 Z9 19 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 169 EP 179 DI 10.1177/1362361302006002004 PG 11 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400003 PM 12083283 ER PT J AU Kok, AJ Kong, TY Bernard-Opitz, V AF Kok, AJ Kong, TY Bernard-Opitz, V TI A comparison of the effects of structured play and facilitated play approaches on preschoolers with autism - A case study SO AUTISM LA English DT Article DE autism; communication; facilitated play; non-verbal; structured play ID SYMBOLIC PLAY; CHILDREN; SKILLS; BEHAVIOR AB This study compared the effect of structured play (SP) and facilitated play (FP) in promoting spontaneity and responsiveness in communication and play behaviors in children with autism. SP is characterized by the use of mass practice trials under the instruction of the experimenter while FP incorporated incidental teaching with multiple exemplars. Eight preschoolers participated in a crossover design of both play conditions. Gains in appropriate communication and play were observed across both treatments. Respondent communicative acts occurred more frequently across all participants during SP compared With FR The preliminary results indicate an interaction between the mental age of the child and the teaching paradigm used. The need to match treatment goals and specific methods of the play intervention to the skill profile of participants is discussed. C1 Natl Univ Singapore, Dept Social Work & Psychol, Singapore 119260, Singapore. RP Bernard-Opitz, V (reprint author), Natl Univ Singapore, Dept Social Work & Psychol, 10 Law Link, Singapore 119260, Singapore. CR BARLOW DH, 1984, SINGLE CASE EXPT DES BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 Bayley N., 1969, BAYLEY SCALES INFANT BELLMAN M, 1987, SCHEDULE GROWING SKI Bernard-Opitz V, 2000, PRAX KINDERPSYCHOL K, V49, P97 BEYER J, 1998, AUTISM PLAY CELIBERTI DA, 1993, BEHAV THER, V24, P573, DOI 10.1016/S0005-7894(05)80319-3 Cogher L., 1999, CHILD LANGUAGE TEACH, V15, P7, DOI 10.1191/026565999670736631 COLE KN, 1991, EXCEPT CHILDREN, V58, P36 DEWEY D, 1988, CAN J PSYCHOL, V42, P240 DUNLAP G, 1980, J APPL BEHAV ANAL, V13, P619, DOI 10.1901/jaba.1980.13-619 Dunlap G, 1994, J Appl Behav Anal, V27, P505, DOI 10.1901/jaba.1994.27-505 ELLIOTT RO, 1991, J AUTISM DEV DISORD, V21, P433, DOI 10.1007/BF02206869 GALLOWAY C, 1978, EARLY INTERVENTION I, P261 GOULD J, 1986, J AUTISM DEV DISORD, V16, P199, DOI 10.1007/BF01531730 Hart B. M., 1982, USE INCIDENTAL TEACH HENDERSON RW, 1989, EVENTLOG HORNER RH, 1985, ED LEARNERS SEVERE H, P289 HUNTER M, 1988, ENVIRON TECHNOL LETT, V9, P1 KOEGEL RL, 1987, J AUTISM DEV DISORD, V17, P187, DOI 10.1007/BF01495055 KOEGEL RL, 1987, J APPL BEHAV ANAL, V13, P91 KOK AJ, 1992, INFLUENCE SENSORY TO Krug D. A., 1979, AUTISM DIAGNOSIS INS Leiter R. G., 1979, LEITER INT PERFORMAN LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lovaas O. I., 1981, TEACHING DEV DISABLE LOVELAND KA, 1988, J SPEECH HEAR RES, V31, P593 MIRANDALINNE F, 1992, RES DEV DISABIL, V13, P191, DOI 10.1016/0891-4222(92)90025-2 POPLIN MS, 1992, CONTROVERSIAL ISSUES, P153 Prizant Barry, 1998, Seminars in Speech and Language, V19, P329, DOI 10.1055/s-2008-1064053 ROUX S, 1998, AUTISM, V2, P345, DOI 10.1177/1362361398024003 SCHREIBMAN L, 1994, BEHAV ISSUES AUTISM SCHULER A, 1980, EMERGING LANGUAGE AU SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 SIMPSON RL, 1993, FOCUS AUTISTIC BEHAV, V7, P1 SMITH PK, 1985, CHILD DEV, V56, P1042, DOI 10.1111/j.1467-8624.1985.tb00175.x STONE WL, 1990, PEDIATRICS, V86, P267 WETHERBY AM, 1984, J SPEECH HEAR RES, V27, P364 Wolfberg P., 1999, CHILD LANG TEACH THE, V15, P41, DOI 10.1191/026565999667036164 WOLFBERG PJ, 1993, J AUTISM DEV DISORD, V23, P467, DOI 10.1007/BF01046051 WULFF SB, 1985, J AUTISM DEV DISORD, V15, P139, DOI 10.1007/BF01531600 NR 43 TC 12 Z9 15 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 181 EP 196 DI 10.1177/1362361302006002005 PG 16 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400004 PM 12083284 ER PT J AU Mouridsen, SE Rich, B Isager, T AF Mouridsen, SE Rich, B Isager, T TI Body mass index in male and female children with infantile autism SO AUTISM LA English DT Article DE body mass index; infantile autism ID ASPERGERS-DISORDER; FAMILY HISTORY; ADOLESCENTS; GROWTH; CURVES; WEIGHT; BIRTH; AGE AB Morphometry, the measurement of forms, is an ancient practice. Recently, evidence has grown to support the notion that aberrant neurodevelopment may play a role in the pathophysiology of autism. Is the body, like the brain, affected by abnormal development in these patients? The aim of this study was to evaluate body mass index (BMI) of children with infantile autism, by comparing the BMI of 117 children with infantile autism with the corresponding BMI percentiles in an age- and sex-matched reference population. The BMI distribution of the male, but not female, children with infantile autism was significantly lower than that of the age-matched reference population. There was no evidence that BMI was associated with intelligence or socioeconomic status among children with infantile autism. C1 Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. Naestved Hosp, Naestved, Denmark. Glostrup Cty Hosp, DK-2600 Glostrup, Denmark. RP Mouridsen, SE (reprint author), Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. CR CAMPBELL M, 1978, AM J PSYCHIAT, V135, P573 CAMPBELL M, 1980, J AM ACAD CHILD PSY, V19, P193, DOI 10.1016/S0002-7138(09)60697-X CIOCCO ANTONIO, 1936, BULL INST HIST MED, V4, P23 COLE TJ, 1995, ARCH DIS CHILD, V73, P25 Creak M., 1964, DEV MED CHILD NEUROL, V6, P530 *CYT, 2000, STATX 4 WIND STAT SO DELONG R, 1994, DEV MED CHILD NEUROL, V36, P674 DELONG R, 1994, DEV MED CHILD NEUROL, V36, P441 Dowdney L, 1998, J CHILD PSYCHOL PSYC, V39, P1017, DOI 10.1017/S0021963098003060 DUTTON G, 1964, BRIT J PSYCHIAT, V110, P101, DOI 10.1192/bjp.110.464.101 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 Gillberg C, 2000, ACTA PSYCHIAT SCAND, V102, P321, DOI 10.1034/j.1600-0447.2000.102005321.x GRAY DS, 1989, MED CLIN N AM, V73, P1 HAMMER LD, 1991, AM J DIS CHILD, V145, P259 HANSEN EJ, 1982, PUBLICATION NATL I S, V110 HARPER JF, 1979, AUST PAEDIATR J, V15, P110 He Q, 2000, ACTA PAEDIATR, V89, P582, DOI 10.1080/080352500750027907 Hebebrand J, 1997, ACTA PSYCHIAT SCAND, V96, P64, DOI 10.1111/j.1600-0447.1997.tb09906.x Hennighausen K, 1999, ACTA PSYCHIAT SCAND, V99, P267, DOI 10.1111/j.1600-0447.1999.tb07224.x Kanner L, 1943, NERV CHILD, V2, P217 Montgomery SM, 1997, ARCH DIS CHILD, V77, P326 MOURIDSEN SE, 1993, J AUTISM DEV DISORD, V23, P387, DOI 10.1007/BF01046227 POWELL GF, 1967, NEW ENGL J MED, V276, P1271, DOI 10.1056/NEJM196706082762301 ROLLANDCACHERA MF, 1991, EUR J CLIN NUTR, V45, P13 RUDOLF MCJ, 1990, DEV MED CHILD NEUROL, V32, P1022 SIMON GB, 1964, BRIT J PSYCHIAT, V110, P104, DOI 10.1192/bjp.110.464.104 SKUSE D, 1998, GROWTH DISORDERS, P483 Skuse DH, 2000, PEDIATR RES, V47, P9, DOI 10.1203/00006450-200001000-00006 Sobanski E, 1999, EUR CHILD ADOLES PSY, V8, P312 Voss LD, 1998, CHILD CARE HLTH DEV, V24, P145 WALKER HA, 1977, J AUTISM CHILD SCHIZ, V7, P165, DOI 10.1007/BF01537727 World Health Organisation, 1992, ICD 10 CLASS MENT BE World Health Organization (WHO), 1978, INT CLASS DIS MENT D NR 33 TC 20 Z9 20 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 197 EP 205 DI 10.1177/1362361302006002006 PG 9 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400005 PM 12083285 ER PT J AU Powell, S AF Powell, S TI Children with autism: A parents' guide, 2nd edition SO AUTISM LA English DT Book Review C1 Univ Hertfordshire, Hatfield AL10 9AB, Herts, England. RP Powell, S (reprint author), Univ Hertfordshire, Hatfield AL10 9AB, Herts, England. CR Powers Michael D., 2000, CHILDREN AUTISM PARE NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 207 EP 208 DI 10.1177/1362361302006002007 PG 2 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400006 ER PT J AU Pennington, L AF Pennington, L TI More than words: Helping parents promote communication and social skills in children with autism spectrum disorder SO AUTISM LA English DT Book Review C1 Univ Manchester, Human & Commun & Deafness Grp, Manchester M13 9PL, Lancs, England. RP Pennington, L (reprint author), Univ Manchester, Human & Commun & Deafness Grp, Manchester M13 9PL, Lancs, England. CR SUSSMAN F, 2000, MORE WORDS HELPING P NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 211 EP 211 DI 10.1177/1362361302006002009 PG 1 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400008 ER PT J AU Van Berckelaer-Onnes, I AF Van Berckelaer-Onnes, I TI Helping children with autism to learn SO AUTISM LA English DT Book Review C1 Rijksuniv, Leiden, Netherlands. RP Van Berckelaer-Onnes, I (reprint author), Rijksuniv, Leiden, Netherlands. CR Powell S., 2000, HELPING CHILDREN AUT NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 211 EP 212 DI 10.1177/1362361302006002010 PG 2 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400009 ER PT J AU Norman, R AF Norman, R TI Someone I know/my brother/my sister has autism/I have autism SO AUTISM LA English DT Book Review CR CAMPBELL K, SOMEONE I KNOW MY BR NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 214 EP 215 DI 10.1177/1362361302006002012 PG 2 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400011 ER PT J AU Iarocci, G AF Iarocci, G TI Autism: Clinical and research issues SO AUTISM LA English DT Book Review C1 Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada. RP Iarocci, G (reprint author), Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada. CR ACCARDO PJ, 2000, AUTISM CLIN RES ISSU NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 215 EP 216 DI 10.1177/1362361302006002013 PG 2 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400012 ER PT J AU Luiselli, JK AF Luiselli, JK TI Autism in the early years: A practical guide SO AUTISM LA English DT Book Review CR Stevenson G., 2000, AUTISM EARLY YEARS P NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUN PY 2002 VL 6 IS 2 BP 220 EP 221 DI 10.1177/1362361302006002015 PG 2 WC Psychology, Developmental SC Psychology GA 562QX UT WOS:000176211400014 ER PT J AU Gerrans, P AF Gerrans, P TI The theory of mind module in evolutionary psychology SO BIOLOGY & PHILOSOPHY LA English DT Article DE Theory of Mind; Evolutionary Psychology; Autism; Modularity ID DEVELOPMENTAL DISORDERS; HUMAN AMYGDALA; FALSE BELIEFS; CHILDREN; AUTISM; REPRESENTATION AB Evolutionary Psychology is based on the idea that the mind is a set of special purpose thinking devices or modules whose domain-specific structure is an adaptation to ancestral environments. The modular view of the mind is an uncontroversial description of the periphery of the mind, the input-output sensorimotor and affective subsystems. The novelty of EP is the claim that higher order cognitive processes also exhibit a modular structure. Autism is a primary case study here, interpreted as a developmental failure of a module devoted to social intelligence or Theory of Mind. In this article I reappraise the arguments for innate modularity of TOM and argue that they fail. TOM ability is a consequence of domain general development scaffolded by early, innately specified, sensorimotor abilities. The alleged Modularity of TOM results from interpreting the outcome of developmental failures characteristic of autism at too high a level of cognitive abstraction. C1 Univ Adelaide, Dept Philosophy, Adelaide, SA 5005, Australia. RP Gerrans, P (reprint author), Univ Adelaide, Dept Philosophy, Adelaide, SA 5005, Australia. CR ADOLPHS R, 1994, NATURE, V372, P669, DOI 10.1038/372669a0 Adolphs R, 1998, NATURE, V393, P470, DOI 10.1038/30982 BARONCOHEN S, 1994, ORIGINS UNDERSTANDIN BARONCOHEN S, 1995, MINDBLINDNESS ESSAY, pR11 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Bloom P, 2000, COGNITION, V77, pB25, DOI 10.1016/S0010-0277(00)00096-2 Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x CARRUTHERS P, 1996, THEORIES THEORIES MI COLTHEART M, 2000, STEVENS HDB EXPT PSY, V4 Cosmides L., 1994, DOMAIN SPECIFICITY C Cosmides L., 1997, ORIGIN EVOLUTION INT, P71 Cosmides L., 1992, ADAPTED MIND EVOLUTI Cosmides L, 1992, COGNITIVE ADAPTATION DECETY J, 1994, NATURE, V371, P600, DOI 10.1038/371600a0 Fodor JA, 1987, ROBOTS DILEMMA FRAME Fodor Jerry A., 1983, MODULARITY MIND FRANK, 1988, PASSIONS REASON STRA Gallese V, 1996, BRAIN, V119, P593, DOI 10.1093/brain/119.2.593 Gerrans P, 1998, MIND LANG, V13, P56, DOI 10.1111/1468-0017.00065 GERRANS P, IN PRESS J LANGUAGE GOPNIK A, 1993, UNPUB MINDBLINDNESS GRIFFITHS PE, 1994, J PHILOS, V91, P277, DOI 10.2307/2940982 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Heberlein A. 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Philos. PD JUN PY 2002 VL 17 IS 3 BP 305 EP 321 DI 10.1023/A:1020183525825 PG 17 WC History & Philosophy Of Science SC History & Philosophy of Science GA 591HX UT WOS:000177874600002 ER PT J AU Bolton, PF Park, RJ Higgins, JNP Griffiths, PD Pickles, A AF Bolton, PF Park, RJ Higgins, JNP Griffiths, PD Pickles, A TI Neuro-epileptic determinants of autism spectrum disorders in tuberous sclerosis complex SO BRAIN LA English DT Article DE tuberous sclerosis; epilepsy; brain; neuroimaging; autism ID LANDAU-KLEFFNER-SYNDROME; INFANTILE SPASMS; WEST-SYNDROME; VIGABATRIN; PERCEPTION; PLASTICITY; DIRECTION; CHILDREN; CORTEX; ACTH AB Tuberous sclerosis is one of the few established medical causes of autism spectrum disorder and is a unique neurogenetic model for testing theories about the brain basis of the syndrome. We conducted a retrospective case study of the neuro-epileptic risk factors predisposing to autism spectrum disorder in individuals with tuberous sclerosis to test current neurobiological theories of autism spectrum disorder. We found that an autism spectrum disorder diagnosis was associated with the presence of cortical tubers in the temporal but not other lobes of the brain. Indeed, the presence of tubers in the temporal lobes appeared to be a necessary but not sufficient risk factor for the development of an autism spectrum disorder. However, contrary to the predictions of some theories, the location of tubers in specific regions of the temporal lobe, such as the superior temporal gyrus or the right temporal lobe, did not determine which individuals with temporal lobe tubers developed an autism spectrum disorder. Instead, outcome was associated with various indices of epileptic activity including evidence of temporal lobe epileptiform discharges on EEG, the age to onset of seizures in the first 3 years of life and a history of infantile spasms. The results indicated that individuals with tuberous sclerosis are at very high risk of developing an autism spectrum disorder when temporal lobe tubers are present and associated with temporal lobe epileptiform discharges and early-onset, persistent spasm-like seizures. These risk markers constitute useful clinical indicators of prognosis, but further research is required to identify the neurobiological mechanisms responsible for their association with outcome. Most especially, it will be important to test whether, as the findings suggest, there is a critical early stage of brain maturation during which temporal lobe epilepsy perturbs the development of brain systems that underpin 'social intelligence' and possibly other cognitive skills, thereby inducing an autism spectrum disorder. C1 Univ Cambridge, Autism Res Ctr, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ Cambridge, Addenbrookes Hosp, Dept Neuroradiol, Cambridge CB2 2AH, England. Univ Sheffield, Sect Acad Radiol, Sheffield S10 2TN, S Yorkshire, England. Univ Manchester, Sch Epidemiol & Hlth Sci, Manchester M13 9PL, Lancs, England. RP Bolton, PF (reprint author), Univ Cambridge, Autism Res Ctr, Dev Psychiat Sect, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. RI Pickles, Andrew/A-9625-2011; Bolton, Patrick/E-8501-2010 OI Pickles, Andrew/0000-0003-1283-0346; Bolton, Patrick/0000-0002-5270-6262 CR Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 Bachevalier J., 1994, NEUROBIOLOGY AUTISM, P146 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BROTHERS L, 1993, BEHAV BRAIN RES, V57, P53, DOI 10.1016/0166-4328(93)90061-T Cheadle JP, 2000, HUM GENET, V107, P97, DOI 10.1007/s004390000348 Chiron C, 1997, EPILEPSY RES, V26, P389, DOI 10.1016/S0920-1211(96)01006-6 Chugani HT, 1996, ANN NEUROL, V39, P643, DOI 10.1002/ana.410390514 CHUGANI HT, 1994, INFANTILE SPASMS W S, P156 Curatolo P, 2001, BRAIN DEV-JPN, V23, P502, DOI 10.1016/S0387-7604(01)00300-X Duvernoy H., 1999, HUMAN BRAIN Gutierrez GC, 1998, J AUTISM DEV DISORD, V28, P97, DOI 10.1023/A:1026032413811 Hancock E, 1999, J CHILD NEUROL, V14, P71, DOI 10.1177/088307389901400201 Hancock E, 2001, BRAIN DEV-JPN, V23, P624, DOI 10.1016/S0387-7604(01)00299-6 Hardus P, 2001, EPILEPSIA, V42, P262, DOI 10.1046/j.1528-1157.2001.15000.x Harrison JE, 1997, J CHILD PSYCHOL PSYC, V38, P603, DOI 10.1111/j.1469-7610.1997.tb01687.x Haxby JV, 2000, TRENDS COGN SCI, V4, P223, DOI 10.1016/S1364-6613(00)01482-0 HUNT A, 1987, DEV MED CHILD NEUROL, V29, P190 HUTTENLOCHER PR, 1994, MINN SYM CHILD PSYCH, V27, P35 Jambaque I, 2000, EPILEPSY RES, V38, P151, DOI 10.1016/S0920-1211(99)00082-0 Leekam S, 1997, BRIT J DEV PSYCHOL, V15, P77 Le Grand R, 2001, NATURE, V410, P890, DOI 10.1038/35073749 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Mantovani JF, 2000, DEV MED CHILD NEUROL, V42, P349, DOI 10.1017/S0012162200210621 MEHTA C, 2000, STATXACT LOGXACT WIN PERRETT DI, 1985, PROC R SOC SER B-BIO, V223, P293, DOI 10.1098/rspb.1985.0003 Ridler K, 2001, PSYCHOL MED, V31, P1437 Riikonen R, 2001, BRAIN DEV-JPN, V23, P642, DOI 10.1016/S0387-7604(01)00306-0 RIIKONEN R, 1981, DEV MED CHILD NEUROL, V23, P747 Roach ES, 1998, J CHILD NEUROL, V13, P624 Robinson RO, 2001, DEV MED CHILD NEUROL, V43, P243, DOI 10.1017/S0012162201000469 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P537, DOI 10.1017/S0021963099003935 Saitoh O, 2001, BRAIN, V124, P1317, DOI 10.1093/brain/124.7.1317 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 Seri S, 1999, CLIN NEUROPHYSIOL, V110, P1825, DOI 10.1016/S1388-2457(99)00137-6 SHEPHERD CW, 1995, AM J NEURORADIOL, V16, P149 SHEPHERD CW, 1999, TUBEROUS SCLEROSIS C, P24 Sur M, 2001, NAT REV NEUROSCI, V2, P251, DOI 10.1038/35067562 Taylor DC, 1999, EUR CHILD ADOLES PSY, V8, P189 Vigevano F, 1997, EPILEPSIA, V38, P1270 NR 44 TC 116 Z9 118 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD JUN PY 2002 VL 125 BP 1247 EP 1255 DI 10.1093/brain/awf124 PN 6 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 563XG UT WOS:000176282700006 PM 12023313 ER PT J AU Piyasirisilp, S Hemachudha, T AF Piyasirisilp, S Hemachudha, T TI Neurological adverse events associated with vaccination SO CURRENT OPINION IN NEUROLOGY LA English DT Article ID HEPATITIS-B VACCINATION; JAPANESE ENCEPHALITIS VACCINATION; WHOLE-CELL PERTUSSIS; MACROPHAGIC MYOFASCIITIS; RUBELLA VACCINE; MULTIPLE-SCLEROSIS; VARICELLA VACCINE; MEASLES-VIRUS; UNITED-STATES; AUTISM AB Public tolerance to adverse reactions is minimal. Several reporting systems have been established to monitor adverse events following immunization. The present review summarizes data on neurologic complications following vaccination, and provides evidence that indicates whether they were directly associated with the vaccines. These complications include autism (measles vaccine), multiple sclerosis (hepatitis B vaccine), meningoencephalitis (Japanese encephalitis vaccine), Guillain-Barre syndrome and giant cell arteritis (influenza vaccine), and reactions after exposure to animal rabies vaccine. Seizures and hypotonic/hyporesponsive episodes following pertussis vaccination and potential risks associated with varicella vaccination, as well as vaccine-associated paralytic poliomyelitis following oral poliovirus vaccination, are also described. In addition, claims that complications are caused by adjuvants, preservatives and contaminants [i.e. macrophagic myofasciitis (aluminium), neurotoxicity (thimerosal), and new variant Creutzfeldt-Jakob disease (bovine-derived materials)] are discussed. C1 Chiang Mai Univ, Fac Med, Dept Med, Div Neurol, Chiang Mai 50200, Thailand. Chulalongkorn Univ, Fac Med, Dept Med, Div Neurol, Bangkok 10330, Thailand. RP Piyasirisilp, S (reprint author), Chiang Mai Univ, Fac Med, Dept Med, Div Neurol, Chiang Mai 50200, Thailand. 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Opin. Neurol. PD JUN PY 2002 VL 15 IS 3 BP 333 EP 338 DI 10.1097/00019052-200206000-00018 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 560GT UT WOS:000176074900018 PM 12045734 ER PT J AU Trepagnier, C Sebrechts, MM Peterson, R AF Trepagnier, C Sebrechts, MM Peterson, R TI Atypical face gaze in autism SO CYBERPSYCHOLOGY & BEHAVIOR LA English DT Article; Proceedings Paper CT 10th Annual Medicine Meets Virtual Reality Conference CY JAN 23, 2002 CL NEWPORT BEACH, CALIFORNIA ID ASPERGER-SYNDROME; CHILDREN; INDIVIDUALS; DISORDERS; ADULTS; MIND AB An eye-tracking study of face and object recognition was conducted to clarify the character of face gaze in autistic spectrum disorders. Experimental participants were a group of individuals diagnosed with Asperger's disorder or high-functioning autistic disorder according to their medical records and confirmed by the Autism Diagnostic Interview-Revised (ADI-R). Controls were selected on the basis of age, gender, and educational level to be comparable to the experimental group. In order to maintain attentional focus, stereoscopic images were presented in a virtual reality (VR) headset in which the eye-tracking system was installed. Preliminary analyses show impairment in face recognition, in contrast with equivalent and even superior performance in object recognition among participants with autism-related diagnoses, relative to controls. Experimental participants displayed less fixation on the central face than did control-group participants. The findings, within the limitations of the small number of subjects and technical difficulties encountered in utilizing the helmet-mounted display, suggest an impairment in face processing on the part of the individuals in the experimental group. This is consistent with the hypothesis of disruption in the first months of life, a period that may be critical to typical social and cognitive development, and has important implications for selection of appropriate targets of intervention. C1 Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA. RP Trepagnier, C (reprint author), Natl Rehabil Hosp, Rehabil Engn Serv, 102 Irving St NW, Washington, DC 20010 USA. 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Behav. PD JUN PY 2002 VL 5 IS 3 BP 213 EP 217 DI 10.1089/109493102760147204 PG 5 WC Communication; Psychology, Applied SC Communication; Psychology GA 568QT UT WOS:000176554400007 PM 12123243 ER PT J AU Johnson, MH Halit, H Grice, SJ Karmiloff-Smith, A AF Johnson, MH Halit, H Grice, SJ Karmiloff-Smith, A TI Neuroimaging of typical and atypical development: A perspective from multiple levels of analysis SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID FUNCTIONAL BRAIN-DEVELOPMENT; WILLIAMS-SYNDROME; COGNITIVE-DEVELOPMENT; CORTICAL AREAS; DISORDERS; AUTISM; BEHAVIOR; INFANTS; SPECIALIZATION; SPECIFICATION AB To date, research involving functional neuroimaging of typical and atypical development has depended on several assumptions about the postnatal maturation of the brain. We consider evidence from multiple levels of analysis that brings into question these underlying assumptions and advance an alternative view. This alternative view, based on an "interactive specialization" approach to postnatal brain development, indicates that there is a need to: obtain data from early in development; focus more on differences in interregional interactions rather than searching for localized, discrete lesions; examine the temporal dynamics of neural processing; and move away from deficits to image tasks in which atypical participants perform as well as typically developing participants. C1 Univ London, Birkbeck Coll, Ctr Brain & Cognit Dev, Sch Psychol, London WC1E 7HX, England. Inst Child Hlth, London, England. RP Johnson, MH (reprint author), Univ London, Birkbeck Coll, Ctr Brain & Cognit Dev, Sch Psychol, Malet St, London WC1E 7HX, England. 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The need for such integration has been a fundamental tenet of the discipline of developmental psychopathology from its inception. It is likely that the discovery of autism susceptibility genes will depend on the development of dimensional measures of broader phenotype autism traits. It is argued that knowledge of the cognitive neuroscience of social and language behavior will provide a useful framework for defining such measures. In this article, the current state of knowledge of the cognitive neuroscience of social and language impairments in autism is reviewed. 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PD SUM PY 2002 VL 14 IS 3 BP 581 EP 611 DI 10.1017/S0954579402003103 PG 31 WC Psychology, Developmental SC Psychology GA 597GV UT WOS:000178214600010 PM 12349875 ER PT J AU Akshoomoff, N Pierce, K Courchesne, E AF Akshoomoff, N Pierce, K Courchesne, E TI The neurobiological basis of autism from a developmental perspective SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Review ID DIAGNOSTIC OBSERVATION SCHEDULE; POSTERIOR-FOSSA STRUCTURES; VISUAL-SPATIAL ATTENTION; FOCAL BRAIN INJURY; MAGNETIC-RESONANCE; INFANTILE-AUTISM; CORPUS-CALLOSUM; SPECTRUM DISORDERS; MENTAL-RETARDATION; NORMAL INDIVIDUALS AB Autism is a neurobiological disorder that is diagnosed through careful behavioral assessment in early childhood. In this paper, we review recent studies that have attempted to reveal the underlying causes of autism using a variety of techniques. Particular emphasis is placed on techniques that have been used by a number of different laboratories, including structural magnetic resonance imaging and postmortem studies of neuroanatomy. Neurobiological and neuropsychological data from individuals across a wide age range are examined from a neurodevelopmental perspective. We discuss how these recent advances have led us to develop a growth dysregulation hypothesis of autism. Finally, we discuss how this hypothesis may lead to new innovations in autism research. C1 Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, La Jolla, CA 92037 USA. RP Akshoomoff, N (reprint author), Childrens Hosp, Res Ctr, Lab Res Neurosci Autism, 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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Psychopathol. PD SUM PY 2002 VL 14 IS 3 BP 613 EP 634 DI 10.1017/S0954579402003115 PG 22 WC Psychology, Developmental SC Psychology GA 597GV UT WOS:000178214600011 PM 12349876 ER PT J AU Malhotra, S Gupta, N AF Malhotra, S Gupta, N TI Childhood disintegrative disorder - Re-examination of the current concept SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE childhood disintegrative disorder; autism; pervasive developmental disorder ID PERVASIVE DEVELOPMENTAL DISORDER; FOLLOW-UP; DSM-IV; PSYCHOSIS; AUTISM; ARGUMENT; DEBATE AB Childhood disintegrative disorder (CDD), which is classified as a sub-type of pervasive developmental disorder (PDD), has been recognised for many years. Research data on CDD, however, is sparse and it primarily describes the clinical parameters. In this research report clinical data on 12 cases of CDD and 21 cases of typical autism, seen during a specified period, are compared and critically evaluated in reference to the diagnostic criteria in ICD-10 for these disorders. While the findings support the clinical validity of CDD, these also highlight the limitations of the current criteria (ICD-10) particularly the age of onset in CDD and the conceptual confusion in labelling it as a 'PDD'. Need for more research in the areas of the biology, course and outcome of CDD is emphasised. C1 Postgrad Inst Med Educ & Res, Dept Psychiat, Chandigarh 160012, India. RP Malhotra, S (reprint author), Postgrad Inst Med Educ & Res, Dept Psychiat, Chandigarh 160012, India. 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PD JUN PY 2002 VL 11 IS 3 BP 108 EP 114 DI 10.1007/s00787-002-0270-6 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 596PX UT WOS:000178174200002 PM 12369769 ER PT J AU Ghaziuddin, M Al-Khouri, I Ghaziuddin, N AF Ghaziuddin, M Al-Khouri, I Ghaziuddin, N TI Autistic symptoms following herpes encephalitis SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE herpes encephalitis; autism ID SIMPLEX ENCEPHALITIS; CHILDHOOD AUTISM; FRONTAL-LOBE; DISORDERS; CHILDREN; BEHAVIOR; MODEL AB Autism is a childhood onset neurodevelopmental disorder characterized by reciprocal social deficits, communication impairment, and rigid ritualistic interests, with the onset almost always before three years of age. Although the etiology of the disorder is strongly influenced by genes, environmental factors are also important. In this context, several reports have described its association with known medical conditions, including infections affecting the central nervous system. In this report, we describe an 11-year-old Asian youngster who developed the symptoms of autism following an episode of herpes encephalitis. In contrast to previous similar reports, imaging studies suggested a predominant involvement of the frontal lobes. At follow-up after three years, he continued to show the core deficits of autism. This case further supports the role of environmental factors, such as infections, in the etiology of autism, and suggests that in a minority of cases, autistic symptoms can develop in later childhood. C1 Univ Michigan, Med Ctr, Div Child & Adolescent Psychiat, Ann Arbor, MI 48109 USA. RP Ghaziuddin, M (reprint author), Univ Michigan, Med Ctr, Div Child & Adolescent Psychiat, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. 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Child Adolesc. Psych. PD JUN PY 2002 VL 11 IS 3 BP 142 EP 146 DI 10.1007/s00787-002-0271-5 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 596PX UT WOS:000178174200008 PM 12369775 ER PT J AU Hill, EL Russell, J AF Hill, EL Russell, J TI Action memory and self-monitoring in children with autism: Self versus other SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE autism; action memory; executive function ID INTENTION AB One key component of executive function is self-monitoring. While a number of studies have implied that self-monitoring deficits may exist in autism (e.g. Russell and Jarrold, 1998), direct tests of this explanation have failed to reveal an autism-specific deficit (Russell and Hill, 2001). In order to assess further whether a self-monitoring deficit is present in autism, three groups of children (20 children with autism, 20 with moderate learning difficulties and 20 typically developing children, all matched for verbal mental age) participated in an action memory task. First, the participant and experimenter took turns to produce actions with pairs of objects. Second, participants were presented with an unexpected recall task in which they were required to (i) make a familiarity judgement, (ii) produce an event memory and (iii) produce a source attribution (self/other) concerning the actions performed on these pairs of objects. Broadly speaking, no performance differences were seen between the three participant groups, although there was a small but significant difference in source attributions for the accurately performing children with autism and the less accurately performing children with moderate learning difficulties. We discuss the findings in relation to the literature concerning self-monitoring in autism. Copyright (C) 2002 John Wiley Sons, Ltd. C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Hill, EL (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England. CR COHEN G, 1988, COGNITION ADULTHOOD CONWAY MA, 1995, Q J EXP PSYCHOL-A, V48, P125 Dunn L M., 1982, BRIT PICTURE VOCABUL Farrant A, 1998, J AUTISM DEV DISORD, V28, P43, DOI 10.1023/A:1026010919219 FRITH U, 1969, J CHILD PSYCHOL PSYC, V10, P153, DOI 10.1111/j.1469-7610.1969.tb02077.x HERMELIN B, 1975, Q J EXP PSYCHOL, V27, P295, DOI 10.1080/14640747508400488 Hsieh S, 1999, PERCEPT MOTOR SKILL, V89, P355, DOI 10.2466/PMS.89.6.355-367 HUGHES C, 1996, J AUTISM DEV DISORD, V26, P101 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Phillips W, 1998, BRIT J DEV PSYCHOL, V16, P337 Roberts A. 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PD JUN PY 2002 VL 11 IS 2 BP 159 EP 170 DI 10.1002/icd.303 PG 12 WC Psychology, Developmental SC Psychology GA 566RT UT WOS:000176442600007 ER PT J AU Zelazo, PD Jacques, S Burack, JA Frye, D AF Zelazo, PD Jacques, S Burack, JA Frye, D TI The relation between theory of mind and rule use: Evidence from persons with autism-spectrum disorders SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE executive function; rule use; theory of mind; autism ID APPEARANCE-REALITY DISTINCTION; EXECUTIVE FUNCTION; COGNITIVE-COMPLEXITY; MENTAL-RETARDATION; VERBAL-ABILITY; FALSE BELIEF; CHILDREN; INDIVIDUALS; TASK; SPECIFICITY AB Cognitive complexity and control (CCC) theory, which is a theory of executive function and its development, provides a metric for comparing task demands across domains. This metric allowed us to examine the relation between theory of mind (ToM) and one aspect of executive function, rule use, in 22 individuals with autism-spectrum disorders, including 12 severely impaired (VIQless than or equal to40; mean VMA=4.07 years; mean CA=17.47) and 10 mildly impaired (VIQ>40; mean VMA=6.15 years; mean CA=10.30) individuals. For severely impaired individuals, ToM performance was unrelated to rule use, r=-0.40, p>0.05). However, for mildly impaired individuals, the correlation between ToM and rule use was high, r=0.82, p<0.01). This latter finding challenges the hypothesis of a domain-specific, ToM module, and suggests instead that poor performance on ToM tasks may be attributed to a more general difficulty using higher order rules to integrate 2 incompatible perspectives into a single system of inferences. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Univ Toronto, Dept Psychol, Toronto, ON M5S 1A1, Canada. McGill Univ, Montreal, PQ, Canada. 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D., 1997, LANGUAGE STRUCTURE D, P113 Zelazo PD, 1996, CHILD DEV, V67, P2478, DOI 10.1111/j.1467-8624.1996.tb01869.x Zelazo PD, 1996, COGNITIVE DEV, V11, P37, DOI 10.1016/S0885-2014(96)90027-1 ZELAZO PD, IN PRESS HDB CHILDHO Zelazo PD, 1998, DEV PSYCHOL, V34, P203, DOI 10.1037/0012-1649.34.2.203 Zelazo PD, 1996, J CHILD PSYCHOL PSYC, V37, P479, DOI 10.1111/j.1469-7610.1996.tb01429.x Zelazo PD, 1998, CURR DIR PSYCHOL SCI, V7, P121, DOI 10.1111/1467-8721.ep10774761 Zelazo PD, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P195 Zigler E, 1986, UNDERSTANDING MENTAL NR 90 TC 70 Z9 75 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD JUN PY 2002 VL 11 IS 2 BP 171 EP 195 DI 10.1002/icd.304 PG 25 WC Psychology, Developmental SC Psychology GA 566RT UT WOS:000176442600008 ER PT J AU Colvert, E Custance, D Swettenham, J AF Colvert, E Custance, D Swettenham, J TI Rule-based reasoning and theory of mind in autism: A commentary on the work of Zelazo, Jacques, Burack and Frye SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE cognitive complexity and control theory; rule-based reasoning; theory of mind; autism AB This commentary is concerned with the work of Zelazo, Jacques, Burack and Frye (2002) and highlights a number of aspects of the Zelazo et al. (2002) study that raise some concern, most notably the small sample size and lack of control groups. The commentary provides details of our own research (Colvert et al., The rule-based reasoning and theory of mind abilities of children with autism, poster presented at the biennial meeting, Society for Research in Child Development, Minneapolis, Minnesota, 2001, Rule-based reasoning and theory of mind in children with autism, submitted), which used a larger sample and a more carefully controlled design to provide a further examination of the possible links between rule-based reasoning and theory of mind (ToM) in autism. With these key modifications our study also found evidence of a significant link between these two aspects of development for high-functioning children with autism. It would seem that there is evidence that the ToM abilities of children with autism may not be a separate aspect of development, but may instead be linked to more general developments in embedded reasoning skills; as stated by the Cognitive Complexity and Control theory. However, the current commentary notes that caution is required when drawing such conclusions, as all evidence thus far is correlational in nature. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Kings Coll London, Inst Psychiat, London WC2R 2LS, England. Univ London Goldsmiths Coll, London SE14 6NW, England. UCL, Dept Human Commun Sci, London, England. RP Colvert, E (reprint author), Kings Coll London, Inst Psychiat, London WC2R 2LS, England. CR COLVERT E, 2001, BIENN M SOC RES CHIL COLVERT E, UNPUB RULE BASED REA COLVERT E, UNPUB QUESTIONING CO Dunn L M., 1982, BRIT PICTURE VOCABUL Frye D, 1995, COGNITIVE DEV, V10, P483, DOI 10.1016/0885-2014(95)90024-1 Happe F., 1994, AUTISM INTRO PSYCHOL Hughes C, 1998, DEV PSYCHOL, V34, P1326, DOI 10.1037/0012-1649.34.6.1326 Perner J, 1999, DEVELOPING THEORIES OF INTENTION, P133 Raven J. C., 1956, STANDARD PROGR MATRI Zelazo P. D., 1997, LANGUAGE STRUCTURE D Zelazo PD, 1996, J CHILD PSYCHOL PSYC, V37, P479, DOI 10.1111/j.1469-7610.1996.tb01429.x Zelazo PD, 2002, INFANT CHILD DEV, V11, P171, DOI 10.1002/icd.304 NR 12 TC 19 Z9 19 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD JUN PY 2002 VL 11 IS 2 BP 197 EP 200 DI 10.1002/icd.305 PG 4 WC Psychology, Developmental SC Psychology GA 566RT UT WOS:000176442600009 ER PT J AU Hughes, C AF Hughes, C TI Executive functions and development: Emerging themes SO INFANT AND CHILD DEVELOPMENT LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; TO-MANAGE PRESCHOOLERS; MIND; CHILDREN; AUTISM; DYSFUNCTION; COGNITION; INTENTION; BOYS AB Earlier in this special issue I outlined four themes that contribute to the growing research interest in studies of executive function in childhood populations. These were: (1) the importance of executive dysfunction in accounts of developmental disorders such as Autism and ADHD; (2) methodological insights arising from the development of new techniques for assessing children's emerging executive functions; (3) evidence for a fractionated or componential view of executive control; and (4) the relation between individual differences in young children's performance on tests of executive function and 'theory of mind'. In this paper, these four themes are used to integrate the findings from all the papers in this special issue on executive functions and development. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Univ Cambridge, Ctr Family Res, Cambridge CB2 3HF, England. RP Hughes, C (reprint author), Univ Cambridge, Ctr Family Res, Free Sch Lane, Cambridge CB2 3HF, England. 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Given that abnormalities in the formation of synaptic junctions are thought to contribute to cognitive dysfunction during brain development, we have analyzed and compared the gene structure of the Piccolo gene, PCLO, from humans and mice and determined their chromosomal localization. A comparison of the deduced amino acid sequence of cDNA clones encoding Piccolo from human, mouse, rat and chicken reveals the presence of distinct homology domains. Only subsets of these are also present in the structurally related active zone protein Bassoon indicating that Piccolo and Bassoon perform related but distinct functions at active zones. Characterization of the PCLO gene reveals the presence of 25 coding exons spread over 380 kb of genomic DNA. The human PCLO gene maps to 7q11.23-q21.3, a region of chromosome 7 implicated as a linkage site for autism and Williams Syndrome suggesting that alterations in the expression of Piccolo or the PCLO gene could contribute to developmental disabilities and mental retardation. (C) 2002 ISDN. Published by Elsevier Science Ltd. All rights reserved. C1 Univ Alabama, Dept Neurobiol, Birmingham, AL 35294 USA. RP Garner, CC (reprint author), Univ Alabama, Dept Neurobiol, 1719 6th Ave S,CIRC 589, Birmingham, AL 35294 USA. 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J. Dev. Neurosci. PD JUN-AUG PY 2002 VL 20 IS 3-5 BP 161 EP 171 DI 10.1016/S0736-5748(02)00046-1 PG 11 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 601AA UT WOS:000178422900004 PM 12175852 ER PT J AU Crnic, LS AF Crnic, LS TI The Colorado mental retardation and developmental disabilities research center SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE mental retardation; Down syndrome; dyslexia AB The Colorado MRRC was one of the original MRRCs funded and has maintained its focus on genetic and nutritional causes of mental retardation and developmental disabilities. Significant discoveries of the center have included a number of metabolic disorders, including glutaric academia types I and II, electron transport flavoprotein (ETF) deficiency, ETF dehydrogenase deficiency, glycerol kinase deficiency, sphingolipidoses, genetic linkages in dyslexia, phonological deficits in dyslexia, and the importance of the trace mineral Zn in early development. Current research at the center is supported by program of projects grants on inborn errors of metabolism, Down syndrome (DS), autism, and dyslexia. (C) 2002 ISDN. Published by Elsevier Science Ltd. All rights reserved. C1 Univ Colorado Hlth, BF Stolinsky Res Labs, Ctr Sci, Denver, CO 80262 USA. RP Crnic, LS (reprint author), Univ Colorado Hlth, BF Stolinsky Res Labs, Ctr Sci, 4200 E 9th Ave,POB C233, Denver, CO 80262 USA. NR 0 TC 1 Z9 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD JUN-AUG PY 2002 VL 20 IS 3-5 BP 297 EP 299 DI 10.1016/S0736-5748(02)00025-4 PG 3 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 601AA UT WOS:000178422900017 PM 12175865 ER PT J AU Cody, H Pelphrey, K Piven, J AF Cody, H Pelphrey, K Piven, J TI Structural and functional magnetic resonance imaging of autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE magnetic resonance imaging; autism; neuropsychology ID POSITRON-EMISSION-TOMOGRAPHY; BRAIN-STEM INVOLVEMENT; FUSIFORM FACE AREA; CORPUS-CALLOSUM; POSTERIOR-FOSSA; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; INFANTILE-AUTISM; EMOTION RECOGNITION; SOCIAL INFORMATION AB Magnetic resonance imaging (MRI) of brain structures and function is uniquely suited to characterize the range of neuroanatomical and physiological changes that characterize the autism phenotype as it develops over time. In this review, we examine the scientific literature in MRI as applied to autism and related areas, over approximately the last decade, discussing findings which have emerged, methodological stumbling blocks which have been identified, and potential future directions. Structural MRI studies have recently begun to elucidate the neurodevelopmental underpinnings and brain-behavior relationships in autism while fMRI studies, building on the wealth of data in normal individuals, are beginning to characterize the underlying neuropsychological deficits of the disorder. Together, these two methods combine to contribute to a better understanding of the neural basis and brain phenotype of this disorder. (C) 2002 ISDN. Published by Elsevier Science Ltd. All rights reserved. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. RP Cody, H (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, CB 3366, Chapel Hill, NC 27599 USA. 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Researchers have identified distinct behavioral phenotypes among developmental disabilities expressed as language development, cognitive profiles, adaptive behavior, and self-injury/aggression. In this article, we discuss evidence for the presence of polysomnographic phenotypes in developmental disabilities. Researchers using behavioral and/or electrophysiological measures have identified differences in sleep architecture among people with autism, Down syndrome, and fragile X syndrome. In general, the greater the level of mental retardation, the less time spent in rapid eye movement sleep. The presence of autism or Down syndrome is associated with fewer and briefer bouts of rapid eye movement sleep, and total sleep time. Autism is also associated with greater levels of undifferentiated sleep. These findings for autism and Down syndrome contrast with fragile X syndrome whose sleep architecture anomalies appear to be a function of mental retardation level. (C) 2002 ISDN. 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PD JUN-AUG PY 2002 VL 20 IS 3-5 BP 449 EP 458 DI 10.1016/S0736-5748(02)00038-2 PG 10 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 601AA UT WOS:000178422900038 PM 12175886 ER PT J AU Hoch, H McComas, JJ Thompson, AL Paone, D AF Hoch, H McComas, JJ Thompson, AL Paone, D TI Concurrent reinforcement schedules: Behavior change and maintenance without extinction SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE concurrent schedules; negative reinforcement; problem behavior; maintenance ID INJURIOUS ESCAPE BEHAVIOR; MAINTAINED DESTRUCTIVE BEHAVIOR; NEGATIVE REINFORCEMENT; ABERRANT BEHAVIOR; SELF-INJURY; QUALITY; CHOICE; TECHNOLOGY; PREVALENCE; SETTINGS AB We evaluated the effects of concurrent schedules of reinforcement on negatively reinforced problem behavior and task completion with 3 children with autism. Results indicated that problem behavior occurred at high levels and relatively few tasks were completed when problem behavior produced a break (from tasks) and task completion produced either no consequence or a break. By contrast, problem behavior was eliminated and tasks were completed when problem behavior produced a break and task completion produced a break with access to preferred activities. Treatment gains were maintained without the use of extinction when the response requirement was increased and the schedule of reinforcement was thinned. C1 CUNY, Grad Ctr, New York, NY USA. RP Hoch, H (reprint author), 137-13 72 Rd, Flushing, NY 11367 USA. CR DeLeon IG, 2001, J APPL BEHAV ANAL, V34, P521, DOI 10.1901/jaba.2001.34-521 DeLeon IG, 2001, J APPL BEHAV ANAL, V34, P463, DOI 10.1901/jaba.2001.34-463 DERBY KM, 1992, J APPL BEHAV ANAL, V25, P713, DOI 10.1901/jaba.1992.25-713 Dixon MR, 2001, J APPL BEHAV ANAL, V34, P491, DOI 10.1901/jaba.2001.34-491 Fisher WW, 1997, J APPL BEHAV ANAL, V30, P387, DOI 10.1901/jaba.1997.30-387 GOH HL, 1994, J APPL BEHAV ANAL, V27, P173, DOI 10.1901/jaba.1994.27-173 Golonka Z, 2000, J APPL BEHAV ANAL, V33, P243, DOI 10.1901/jaba.2000.33-243 Harding JW, 1999, J APPL BEHAV ANAL, V32, P63, DOI 10.1901/jaba.1999.32-63 HEIDORN SD, 1984, BEHAV RES THER, V22, P581, DOI 10.1016/0005-7967(84)90062-7 HERRSTEIN RJ, 1970, J EXP ANAL BEHAV, V13, P243, DOI 10.1901/jeab.1970.13-243 ZARCONE JR, 1994, J APPL BEHAV ANAL, V27, P307, DOI 10.1901/jaba.1994.27-307 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P215, DOI 10.1901/jaba.1994.27-215 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 IWATA BA, 1987, J APPL BEHAV ANAL, V20, P361, DOI 10.1901/jaba.1987.20-361 IWATA BA, 1990, J APPL BEHAV ANAL, V23, P11, DOI 10.1901/jaba.1990.23-11 KELLEHER RT, 1959, J EXP ANAL BEHAV, V2, P203, DOI 10.1901/jeab.1959.2-203 Lalli JS, 1996, J APPL BEHAV ANAL, V29, P391, DOI 10.1901/jaba.1996.29-391 Lerman DC, 1999, J APPL BEHAV ANAL, V32, P1, DOI 10.1901/jaba.1999.32-1 LERMAN DC, 1995, J APPL BEHAV ANAL, V28, P93, DOI 10.1901/jaba.1995.28-93 Lerman DC, 1996, J APPL BEHAV ANAL, V29, P345, DOI 10.1901/jaba.1996.29-345 LOGUE AW, 1978, J EXP ANAL BEHAV, V29, P61, DOI 10.1901/jeab.1978.29-61 Mace F. C., 1993, COMMUNICATIVE ALTERN, P113 MACE FC, 1994, J APPL BEHAV ANAL, V27, P585, DOI 10.1901/jaba.1994.27-585 Mace FC, 1996, J APPL BEHAV ANAL, V29, P11, DOI 10.1901/jaba.1996.29-11 Neef N A, 1994, J Appl Behav Anal, V27, P575, DOI 10.1901/jaba.1994.27-575 NEEF NA, 1993, J APPL BEHAV ANAL, V26, P37, DOI 10.1901/jaba.1993.26-37 NEEF NA, 1992, J APPL BEHAV ANAL, V25, P691, DOI 10.1901/jaba.1992.25-691 Neef NA, 2001, J APPL BEHAV ANAL, V34, P57, DOI 10.1901/jaba.2001.34-57 PACE GM, 1993, J APPL BEHAV ANAL, V26, P205, DOI 10.1901/jaba.1993.26-205 PACE GM, 1994, J APPL BEHAV ANAL, V27, P301, DOI 10.1901/jaba.1994.27-301 Piazza CC, 1997, J APPL BEHAV ANAL, V30, P279, DOI 10.1901/jaba.1997.30-279 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P569, DOI 10.1901/jaba.1996.29-569 NR 32 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 SUM PY 2002 VL 35 IS 2 BP 155 EP 169 DI 10.1901/jaba.2002.35-155 PG 15 WC Psychology, Clinical SC Psychology GA 566UG UT WOS:000176446200004 PM 12102135 ER PT J AU Hoch, H McComas, JJ Johnson, L Faranda, N Guenther, SL AF Hoch, H McComas, JJ Johnson, L Faranda, N Guenther, SL TI The effects of magnitude and quality of reinforcement on choice responding during play activities SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE reinforcer magnitude; quality; concurrent schedules; response allocation; choice responding; autism AB Three boys with autism participated in a study of the effects of magnitude and quality of reinforcement on choice responding. Two concurrent response alternatives were arranged: (a) to play in an area where a peer or sibling was located, or (b) to play in an area where there was no peer or sibling. During one condition, the magnitude (i.e., duration of access to toys) or quality (level of preference) of reinforcement provided for both responses was equal. During the other condition, the magnitude or quality of reinforcement was relatively greater for choosing the play area where the peer or sibling was located than the area where the peer or sibling was not located. Results showed that after repeated exposure to the unequal magnitude or quality condition, the participant increasingly allocated his responses to the play area where the peer or sibling was located. For 2 participants, this pattern of responding was maintained in the subsequent equal magnitude or quality condition. Overall, the analysis suggests that the dimensions of magnitude and quality of reinforcement can be arranged to influence choice responding in favor of playing near a peer or sibling rather than playing alone. C1 Univ Minnesota, Dept Educ Psychol, Minneapolis, MN 55455 USA. RP McComas, JJ (reprint author), Univ Minnesota, Dept Educ Psychol, 224 Burton Hall,178 Pillsbury Dr SE, Minneapolis, MN 55455 USA. CR BARLOW DH, 1984, SINGLE CASE EXPT DES Carr JE, 1998, J APPL BEHAV ANAL, V31, P313, DOI 10.1901/jaba.1998.31-313 CATANIA AC, 1963, J EXP ANAL BEHAV, V6, P299, DOI 10.1901/jeab.1963.6-299 DeLeon IG, 2001, J APPL BEHAV ANAL, V34, P463, DOI 10.1901/jaba.2001.34-463 Dixon MR, 2001, J APPL BEHAV ANAL, V34, P491, DOI 10.1901/jaba.2001.34-491 Fantino E., 1977, HDB OPERANT BEHAV, P313 FISHER WW, 1997, J APPL BEHAV ANAL, V27, P585 HERRSTEIN RJ, 1970, J EXP ANAL BEHAV, V13, P243, DOI 10.1901/jeab.1970.13-243 HOLLARD V, 1971, J EXP ANAL BEHAV, V16, P375, DOI 10.1901/jeab.1971.16-375 Lerman DC, 1999, J APPL BEHAV ANAL, V32, P197, DOI 10.1901/jaba.1999.32-197 Leslie J. C., 1996, PRINCIPLES BEHAV ANA Mace FC, 1996, J APPL BEHAV ANAL, V29, P11, DOI 10.1901/jaba.1996.29-11 Neef N A, 1994, J Appl Behav Anal, V27, P575, DOI 10.1901/jaba.1994.27-575 NEEF NA, 1993, J APPL BEHAV ANAL, V26, P37, DOI 10.1901/jaba.1993.26-37 NEEF NA, 1992, J APPL BEHAV ANAL, V25, P691, DOI 10.1901/jaba.1992.25-691 Neef NA, 2001, J APPL BEHAV ANAL, V34, P57, DOI 10.1901/jaba.2001.34-57 Peck SM, 1996, J APPL BEHAV ANAL, V29, P263, DOI 10.1901/jaba.1996.29-263 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P1, DOI 10.1901/jaba.1996.29-1 NR 18 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 2002 VL 35 IS 2 BP 171 EP 181 DI 10.1901/jaba.2002.35-171 PG 11 WC Psychology, Clinical SC Psychology GA 566UG UT WOS:000176446200005 PM 12102136 ER PT J AU Grindle, CF Remington, B AF Grindle, CF Remington, B TI Discrete-trial training for autistic children when reward is delayed: A comparison of conditioned cue value and response marking SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE conditioned reinforcement; cue value; response marking; discretetrial training; children with autism AB Three children with autism were taught to identify pictures of objects. Their speed of acquisition of receptive speech skills was compared across two conditions. In the cue-value condition, a compound audiovisual stimulus was presented after correct responses and again when a primary reinforcer was delivered after a 5-s delay; in the response-marking condition, a second stimulus was presented after both correct and incorrect responses, but not prior to the primary reinforcer. In both conditions primary reinforcement was delayed for 5 s. Although the children learned receptive speech skills in both conditions, acquisition was faster in the cue-value condition. C1 Univ Southampton, Southampton, Hants, England. RP Remington, B (reprint author), Univ Southampton, Southampton, Hants, England. CR Dixon MR, 2001, J APPL BEHAV ANAL, V34, P491, DOI 10.1901/jaba.2001.34-491 LIEBERMAN DA, 1979, J EXP PSYCHOL ANIM B, V5, P224, DOI 10.1037//0097-7403.5.3.224 Lovaas O. I., 1981, TEACHING DEV DISABLE LOVAAS OI, 1966, J EXP CHILD PSYCHOL, V4, P109, DOI 10.1016/0022-0965(66)90011-7 Neef NA, 2001, J APPL BEHAV ANAL, V34, P397, DOI 10.1901/jaba.2001.34-397 WILLIAMS BA, 1994, PSYCHON B REV, V1, P457, DOI 10.3758/BF03210950 NR 6 TC 8 Z9 8 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2002 VL 35 IS 2 BP 187 EP 190 DI 10.1901/jaba.2002.35-187 PG 4 WC Psychology, Clinical SC Psychology GA 566UG UT WOS:000176446200007 PM 12102138 ER PT J AU Lavie, T Sturmey, P AF Lavie, T Sturmey, P TI Training staff to conduct a paired-stimulus preference assessment SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE assessment; stimulus preference assessment; staff training AB Three staff members were trained to conduct stimulus preference assessments using a paired-stimulus format with 8 children with autism. Staff were trained to mastery level using brief instruction, a video model, and rehearsal with verbal feedback. Training took about 80 min per staff member. Results demonstrated that staff rapidly learned to correctly perform paired-stimulus preference assessments with children. C1 CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA. RP Sturmey, P (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissena Blvd, Flushing, NY 11367 USA. CR Carr JE, 2000, J APPL BEHAV ANAL, V33, P353, DOI 10.1901/jaba.2000.33-353 DeLeon IG, 2001, J APPL BEHAV ANAL, V34, P463, DOI 10.1901/jaba.2001.34-463 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Iwata BA, 2000, J APPL BEHAV ANAL, V33, P181, DOI 10.1901/jaba.2000.33-181 Reid D. H., 1995, MOTIVATING HUMAN SER NR 5 TC 40 Z9 40 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 2002 VL 35 IS 2 BP 209 EP 211 DI 10.1901/jaba.2002.35-209 PG 3 WC Psychology, Clinical SC Psychology GA 566UG UT WOS:000176446200012 PM 12102143 ER PT J AU Kern, JK Miller, VS Evans, PA Trivedi, MH AF Kern, JK Miller, VS Evans, PA Trivedi, MH TI Efficacy of porcine secretin in children with autism and pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; PDD; secretin; efficacy; gastrointestinal ID INFLAMMATORY BOWEL-DISEASE; WHITE-MATTER LESIONS; BRAIN AB Secretin, a gastrointestinal (GI) hormone, was reported in a preliminary study to improve language and behavior in children with autism/pervasive developmental disorder (PDD) and chronic diarrhea. To determine the efficacy of secretin, we completed a double-blind, placebo-controlled, crossover (3 weeks) study in children with autism/PDD and various GI conditions using a single dose of intravenous porcine secretin. Children with chronic, active diarrhea showed a reduction in aberrant behaviors when treated with the secretin but not when treated with the placebo. Children with no GI problems are unaffected by either secretin or placebo. The improvement seen with secretin in children with autism/PDD and chronic diarrhea suggests that there may be a subtype of children with autism/PDD who respond to secretin. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75390 USA. Univ Texas, SW Med Ctr, Dept Neurol, Dallas, TX 75390 USA. Childrens Dev Ctr, Dallas, TX 75230 USA. RP Kern, JK (reprint author), Univ Texas, SW Med Ctr, Dept Psychiat, St Paul Profess Bldg I,5959 Harry Hines Blvd,Suit, Dallas, TX 75390 USA. CR Aman M., 1986, ABERRANT BEHAV CHECK American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BRYSON SE, 1988, J CHILD PSYCHOL PSYC, V29, P433, DOI 10.1111/j.1469-7610.1988.tb00735.x Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 COHEN DJ, 1997, AUTISM PERVASIVE DEV DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x FENSON L, 1996, MACARTHUR COMMUNICAT Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 GEISSLER A, 1995, LANCET, V345, P897 Hadjivassiliou M, 1996, LANCET, V347, P369, DOI 10.1016/S0140-6736(96)90540-1 Hart PE, 1998, LANCET, V351, P1558, DOI 10.1016/S0140-6736(05)61123-3 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Kern JK, 2001, J CHILD NEUROL, V16, P169, DOI 10.1177/088307380101600303 KNICKELBEIN RG, 1990, AM J PHYSIOL, V259, pG807 LOSSOS A, 1995, NEUROLOGY, V45, P416 MITZNEGG P, 1977, GUT, V18, P468, DOI 10.1136/gut.18.6.468 MURCH SH, 1993, LANCET, V341, P711, DOI 10.1016/0140-6736(93)90485-Y OWLEY T, 1999, MEDSCAPE GEN MED Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Sasaki N, 1999, J VET MED SCI, V61, P167, DOI 10.1292/jvms.61.167 SUGIYAMA T, 1989, J AUTISM DEV DISORD, V19, P87, DOI 10.1007/BF02212720 VANTRAPPEN G, 1993, LANCET, V34, P730 VIADER F, 1995, PRESSE MED, V24, P222 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 25 TC 36 Z9 36 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 153 EP 160 DI 10.1023/A:1015441428154 PG 8 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800002 PM 12108616 ER PT J AU Carey, T Ratliff-Schaub, K Funk, J Weinle, C Myers, M Jenks, J AF Carey, T Ratliff-Schaub, K Funk, J Weinle, C Myers, M Jenks, J TI Double-blind placebo-controlled trial of secretin: Effects on aberrant behavior in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE secretin; autism; behavior; drug therapy AB Secretin has been proposed as a treatment alternative for autistic spectrum disorders, but empirical support is lacking. A double-blind placebo-controlled study examined the effect of a single dose of synthetic human secretin on aberrant behavior. Parent and teacher data from the Aberrant Behavior Checklist for eight male children were analyzed for reliable change in a clinical replication series. By parent and teacher report, the majority of change occurred either on the placebo trial or reflected deterioration subsequent to secretin infusion. Repeated-measures multivariate analysis of variance results were similar. Results are consistent with other studies, suggesting that secretin may not be an effective treatment option. C1 Med Coll Ohio, Dept Pediat, Div Dev & Behav Pediat, Toledo, OH 43608 USA. Univ Toledo, Dept Psychol, Toledo, OH 43606 USA. RP Carey, T (reprint author), Med Coll Ohio, Dept Pediat, Div Dev & Behav Pediat, 2222 Cherry St,Suite 2300, Toledo, OH 43608 USA. CR Aman M., 1986, ABERRANT BEHAV CHECK BARLOW DH, 1984, SINGLE CASE EXPT DES Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 HORVATH K, 2000, WORLD C PED GASTR BO JACOBSON NS, 1991, J CONSULT CLIN PSYCH, V59, P12, DOI 10.1037//0022-006X.59.1.12 OWLEY T, 1999, MEDSCAPE GEN MED, V1, P1 Richman D. M., 1999, FOCUS AUTISM OTHER D, V14, P204, DOI 10.1177/108835769901400402 Sandler AD, 2000, J DEV BEHAV PEDIATR, V21, P347 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 SCHOPLER E, 1988, MANUAL CHILDHOOD AUT SCHUTT CE, 1998, NAARRATIVE, V4 Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F NR 14 TC 17 Z9 17 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 161 EP 167 DI 10.1023/A:1015493412224 PG 7 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800003 PM 12108617 ER PT J AU Gross, TF AF Gross, TF TI Perception of human and nonhuman facial age by developmentally disabled children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE face perception; facial age; autism ID MACACA-FUSCATA; HOMO-SAPIENS; AUTISM; RECOGNITION; FACE; ATTRACTIVENESS; INFANTS; EXPRESSIONS; INFORMATION; MECHANISMS AB Human and nonhuman faces were shown to clinical controls, autistic, mentally retarded, and language-disordered children to assess their ability to detect and draw inferences about facial age. Children were asked to select from sets of three faces the one that appeared youthful or to select faces that would be associated with some age-related characteristic. In two studies, it was found that, relative to other children, autistic children had more difficulty perceiving youthfulness in nonhuman faces compared with human faces. These data are discussed with respect to differences in mechanisms and processes that may underlie facial information processing in autistic and nonautistic children. C1 Univ Redlands, Dept Psychol, Redlands, CA 92373 USA. RP Gross, TF (reprint author), Univ Redlands, Dept Psychol, 1200 E Colton Ave,POB 3080, Redlands, CA 92373 USA. 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Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 169 EP 179 DI 10.1023/A:1015445629062 PG 11 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800004 PM 12108618 ER PT J AU Miranda-Linne, FM Melin, L AF Miranda-Linne, FM Melin, L TI A factor analytic study of the Autism Behavior Checklist SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism Behavior Checklist; factor analysis; cut-off scores; autism spectrum disorders ID PSYCHOTIC CHILDREN; INSTRUMENTS; INDIVIDUALS; PREVALENCE; VALIDITY; SCALES AB The factor structure of the Autism Behavior Checklist (ABC) (Krug, Arick, & Almond, 1980a, 1980b), a 57-item screening instrument for autism, was examined on a sample of 383 individuals with autism spectrum disorders (i.e., autistic disorder, Asperger syndrome, and other autism-like conditions) aged 5-22 years. A five-factor model accounted for 80% of the total variance in the checklist. Thirty-nine of the 57 items had factor loadings of 0.4 or more, with 13 items loading on Factor 1, 11 items on Factor 2, 6 items on Factor 3, 5 items on Factor 4, and 4 items on Factor 5. No support was found for classifying the 57 items into the five subscales proposed by Krug et al. (1980a, 1980b) or for the three-factor solution suggested by Wadden, Bryson, and Rodger (1991). C1 Univ Uppsala, Dept Psychol, S-75142 Uppsala, Sweden. RP Miranda-Linne, FM (reprint author), Univ Uppsala, Dept Psychol, Box 1225, S-75142 Uppsala, Sweden. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CREAK EM, 1964, INFANTILE AUTISM, P221 GILLBERG C, 1986, DEV MED CHILD NEUROL, V28, P624 Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Krug D. A., 1980, AUTISM SCREENING INS KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LOTTER V, 1974, J AUTISM CHILD SCHIZ, V4, P263, DOI 10.1007/BF02115232 LOVAAS OI, 1965, J EXP CHILD PSYCHOL, V2, P108, DOI 10.1016/0022-0965(65)90036-6 LOVAAS OI, 1973, J APPL BEHAV ANAL, V6, P131, DOI 10.1901/jaba.1973.6-131 MirandaLinne FM, 1997, J AUTISM DEV DISORD, V27, P245, DOI 10.1023/A:1025846330262 Nunnally J. C., 1978, PSYCHOMETRIC THEORY PARKS SL, 1983, J AUTISM DEV DISORD, V13, P255, DOI 10.1007/BF01531565 Rendle-Short J., 1968, MED J AUSTRALIA, V1, P921 RIMLAND B, 1971, J AUTISM CHILD SCHIZ, V1, P161, DOI 10.1007/BF01537955 Ruttenberg B. A., 1977, BEHAV RATING INSTRUM RUTTENBE.BA, 1966, J AMER ACAD CHILD PS, V5, P453, DOI 10.1016/S0002-7138(09)62093-8 SCHOPLER E, 1972, J AUTISM CHILD SCHIZ, V2, P387, DOI 10.1007/BF01538171 SEVIN JA, 1991, J AUTISM DEV DISORD, V21, P417, DOI 10.1007/BF02206868 SMITH B, 1994, J AUTISM DEV DISORD, V24, P551, DOI 10.1007/BF02172137 STONE WL, 1993, J AUTISM DEV DISORD, V23, P639, DOI 10.1007/BF01046106 STURMEY P, 1992, J AUTISM DEV DISORD, V22, P321, DOI 10.1007/BF01058159 SZATMARI P, 1992, J AUTISM DEV DISORD, V22, P507, DOI 10.1007/BF01046325 TABACHNICK BARBARA G., 1989, USING MULTIVARIATE S, V2d TEAL MB, 1986, J AUTISM DEV DISORD, V16, P485, DOI 10.1007/BF01531713 VOLKMAR FR, 1988, J AUTISM DEV DISORD, V18, P81, DOI 10.1007/BF02211820 WADDEN NPK, 1991, J AUTISM DEV DISORD, V21, P529, DOI 10.1007/BF02206875 Wing L, 1996, BRIT MED J, V312, P327 WING L, 1976, PSYCHOL MED, V6, P89 WING L, 1980, BRIT J PSYCHIAT, V137, P410, DOI 10.1192/bjp.137.5.410 WING L, 1978, J AUTISM CHILD SCHIZ, V8, P79, DOI 10.1007/BF01550280 YIRMIYA N, 1994, J AUTISM DEV DISORD, V24, P281, DOI 10.1007/BF02172227 NR 32 TC 16 Z9 17 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 181 EP 188 DI 10.1023/A:1015519413133 PG 8 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800005 PM 12108619 ER PT J AU Rutherford, MD Baron-Cohen, S Wheelwright, S AF Rutherford, MD Baron-Cohen, S Wheelwright, S TI Reading the mind in the voice: A study with normal adults and adults with Asperger syndrome and high functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; theory of mind; Asperger syndrome; auditory ID CHILDS APPRAISAL; REVISED VERSION; EMOTION; RECOGNITION; EXPRESSIONS; INDIVIDUALS; DEFICITS AB People with high functioning autism (HFA) and Asperger syndrome (AS) have deficits in theory of mind (ToM). Traditional ToM tasks are not sensitive enough to measure ToM deficits in adults, so more subtle ToM tests are needed. One adult level test, the Reading the Mind in the Eyes test has shown that AS and HFA subjects have measurable deficits in the ability to make ToM inferences. Here we introduce a test that extends the above task into the auditory domain and that can be used with adults with IQ Scores in the normal range. We report the use of the test with an adult sample of people with AS/HFA and with two adult control groups. Results suggest that individuals with AS/HFA have difficulty extracting mental state information from vocalizations. These results are consistent with previous results suggesting that people with HFA and AS have difficulties drawing ToM inferences. C1 Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 3EB, England. RP Rutherford, MD (reprint author), Univ Denver, Dept Psychol, 2155 S Race St, Denver, CO 80208 USA. CR Adolphs R, 1998, NATURE, V393, P470, DOI 10.1038/30982 BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 Baron-Cohen S, 1999, J AUTISM DEV DISORD, V29, P407, DOI 10.1023/A:1023035012436 BARONCOHEN S, IN PRESS J AUTISM DE Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Corcoran R, 1997, SCHIZOPHR RES, V24, P319, DOI 10.1016/S0920-9964(96)00117-X Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 Happe F, 1999, COGNITION, V70, P211, DOI 10.1016/S0010-0277(99)00005-0 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 HOBSON RP, 1988, PSYCHOL MED, V18, P911 HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V27, P321, DOI 10.1111/j.1469-7610.1986.tb01836.x HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V27, P671, DOI 10.1111/j.1469-7610.1986.tb00191.x Kinderman P, 1998, BRIT J PSYCHOL, V89, P191 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 Loveland KA, 1997, DEV PSYCHOPATHOL, V9, P579 LOVELAND KA, 1995, DEV PSYCHOPATHOL, V7, P409 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x RUTHERFORD MD, 2001, BIANN M SOC RES CHIL STONE VE, 1999, UNDERSTANDING OTHER Stone VE, 1998, J COGNITIVE NEUROSCI, V10, P640, DOI 10.1162/089892998562942 *WHO, 1994, ICD10 CLASS MENT BEH Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 NR 32 TC 138 Z9 141 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 2002 VL 32 IS 3 BP 189 EP 194 DI 10.1023/A:1015497629971 PG 6 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800006 PM 12108620 ER PT J AU Beadle-Brown, J Murphy, G Wing, L Gould, J Shah, A Holmes, N AF Beadle-Brown, J Murphy, G Wing, L Gould, J Shah, A Holmes, N TI Changes in social impairment for people with intellectual disabilities: A follow-up of the Camberwell cohort SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; intellectual disabilities; changes in skills; social impairment; longitudinal ID BEHAVIORAL TREATMENT; AUTISTIC-CHILDREN; ADAPTIVE-BEHAVIOR; SKILLS AB The skills and social impairments of a total population of children with severe intellectual disabilities and/or autism from Camberwell, South London (Wing and Gould, 1978 and 1979), were assessed using the Handicaps, Behaviours and Skills schedule, and they were reassessed when they were adolescents and young adults (Shah, 1986). Changes in social impairment over time are presented here. As Shah (1986) had found with a smaller sample, social impairment remained relatively stable over time: on a simple "socially impaired" versus "sociable" dichotomous grouping, 93% did not change social group. Within the socially impaired group, there was a significant increase in impairment over time (i.e., people who were passive at Time 1, were aloof at Time 2). Implications of these results and predictions for a further follow-up study are discussed. C1 Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England. Nat Autist Soc, Bromley BR2 9HT, Kent, England. Kingston & Dist NHS Trust, Dept Clin Psychol, Thames Ditton KT7 OHY, Surrey, England. RP Beadle-Brown, J (reprint author), Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England. CR Bayley N., 1969, BAYLEY SCALES INFANT Beadle-Brown J, 2000, J INTELL DISABIL RES, V44, P12, DOI 10.1046/j.1365-2788.2000.00245.x GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 GOULD J, 1976, J MENTAL DEFICIENCY, V2, P129 GRAHAM P, 1968, BRIT J PSYCHIAT, V114, P581, DOI 10.1192/bjp.114.510.581 Howlin P, 1987, TREATMENT AUTISTIC C JACOBSON JW, 1990, J AUTISM DEV DISORD, V20, P205, DOI 10.1007/BF02284719 Kanner L, 1943, NERV CHILD, V2, P217 Leiter R. G., 1980, LEITER INT PERFORMAN LOTTER V, 1978, AUTISM REAPPRAISAL C LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 LOVELAND KA, 1988, AM J MENT RETARD, V93, P84 McCarthy J. J., 1961, ILLINOIS TEST PSYCHO MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 REYNELL JK, 1987, REYNELL LANGUAGE DEV Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 RUTTER M, 1994, CHILD ADOL PSYCH CL, P569 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1169, DOI 10.1192/bjp.113.504.1169 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1183, DOI 10.1192/bjp.113.504.1183 SCHATZ J, 1995, J AUTISM DEV DISORD, V25, P51, DOI 10.1007/BF02178167 SCHOPLER E, 1989, J CONSULT CLIN PSYCH, V57, P162 SHAH A, 1986, SCI SERVICE MENTAL R, P132 STUTSMAN R, 1931, MERRILLPALMER SCALE Wechsler D, 1949, WECHSLER INTELLIGENC Wing JK, 1972, EVALUATING COMMUNITY WING L, 1971, PSYCHOL MED, V1, P405 WING L, 1968, SOC PSYCHIATR, V3, P116, DOI 10.1007/BF00577835 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 WING L, 1978, J AUTISM CHILD SCHIZ, V8, P79, DOI 10.1007/BF01550280 Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 NR 32 TC 23 Z9 23 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 195 EP 206 DI 10.1023/A:1015401814041 PG 12 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800007 PM 12108621 ER PT J AU Croen, LA Grether, JK Hoogstrate, J Selvin, S AF Croen, LA Grether, JK Hoogstrate, J Selvin, S TI The changing prevalence of autism in California SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic spectrum disorders; epidemiology; prevalence; mental retardation ID INFANTILE-AUTISM; CHILDHOOD AUTISM; EPIDEMIOLOGIC SURVEY; TOTAL POPULATION; CHILDREN; JAPAN; DISORDERS; FRENCH; CLASSIFICATION; DISABILITY AB We conducted a population-based study of eight successive California births cohorts to examine the degree to which improvements in detection and changes in diagnosis contribute to the observed increase in autism prevalence. Children born in 1987-1994 who had autism were identified from the statewide agency responsible for coordinating services for individuals with developmental disabilities. To evaluate the role of diagnostic substitution, trends in prevalence of mental retardation without autism were also investigated. A total of 5038 children with full syndrome autism were identified from 4,590,333 California births, a prevalence of 11.0 per 10,000. During the study period, prevalence increased from 5.8 to 14.9 per 10,000, for an absolute change of 9.1 per 10,000. The pattern of increase was not influenced by maternal age, race/ethnicity, education, child gender, or plurality. During the same period, the prevalence of mental retardation without autism decreased from 28.8 to 19.5 per 10,000, for an absolute change of 9.3 per 10,000. These data suggest that improvements in detection and changes in diagnosis account for the observed increase in autism; whether there has also been a true increase in incidence is not known. C1 March Dimes Birth Defects Fdn, Calif Dept Hlth Serv, Calif Birth Defects Monitoring Program, Oakland, CA USA. Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94611 USA. 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Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 207 EP 215 DI 10.1023/A:1015453830880 PG 9 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800008 PM 12108622 ER PT J AU Croen, LA Grether, JK Selvin, S AF Croen, LA Grether, JK Selvin, S TI Descriptive epidemiology of autism in a California population: Who is at risk? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE maternal age; maternal education; SES; twins ID INFANTILE-AUTISM; CHILDHOOD AUTISM; OBSTETRIC COMPLICATIONS; SPECTRUM DISORDERS; PERINATAL FACTORS; NEONATAL FACTORS; MATERNAL AGE; SOCIAL-CLASS; URBAN AREAS; SEX-RATIOS AB We investigated the association between selected infant and maternal characteristics and autism risk. Children with autism born in California in 1989-1994 were identified through service agency records and compared with the total population of California live births for selected characteristics recorded on the birth certificate. Multivariate models were used to generate adjusted risk estimates. From a live birth population of more than 3.5 million, 4381 children with autism were identified. Increased risks were observed for males, multiple births, and children born to black mothers. Risk increased as maternal age and maternal education increased. Children born to immigrant mothers had similar or decreased risk compared with California-born mothers. Environmental factors associated with these demographic characteristics may interact with genetic vulnerability to increase the risk of autism. C1 March Dimes Birth Defects Fdn, Calif Dept Hlth Serv, Calif Birth Defects Monitoring Program, Oakland, CA 94606 USA. Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94612 USA. 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PD JUN PY 2002 VL 32 IS 3 BP 217 EP 224 DI 10.1023/A:1015405914950 PG 8 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800009 PM 12108623 ER PT J AU Kravits, TR Kamps, DM Kemmerer, K Potucek, J AF Kravits, TR Kamps, DM Kemmerer, K Potucek, J TI Brief report: Increasing communication skills for an elementary-aged student with autism using the picture exchange communication system SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Picture Exchange Communication System; augmentative communication; peer training ID CHILDREN AB The purpose of this study was to examine the effects of the Picture Exchange Communication System (PECS) on the spontaneous communication skills of a 6-year-old girl with autism across her home and school environments. The effects of the PECS were also examined for social interaction. Results indicated increases in spontaneous language (i.e., requests and comments) including use of the icons and verbalizations across those settings in which PECS was implemented. Intelligible verbalizations increased in two of three settings, and changes in peer social interaction were noted in one of the two school settings. C1 Univ Kansas, Juniper Gardens Childrens Project, Kansas City, KS 66101 USA. Univ Louisville, Autism Training Ctr, Louisville, KY 40292 USA. Project SAIL, Kansas City, MO 64131 USA. RP Kamps, DM (reprint author), Univ Kansas, Juniper Gardens Childrens Project, 650 Minnesota Ave,2nd Floor, Kansas City, KS 66101 USA. CR BAER DM, 1968, J APPL BEHAV ANAL, V1, P91, DOI 10.1901/jaba.1968.1-91 BONDY A, 1999, PICTURE EXCHANGE COM Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 Carta J. 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PD JUN PY 2002 VL 32 IS 3 BP 225 EP 230 DI 10.1023/A:1015457931788 PG 6 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800010 PM 12108624 ER PT J AU Gepner, B Mestre, DR AF Gepner, B Mestre, DR TI Brief report: Postural reactivity to fast visual motion differentiates autistic from children with asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger; visual motion; postural reactivity; visuopostural tuning ID CHILDHOOD AUTISM; BASAL GANGLIA; MOTOR; MOVEMENT; DISORDER; CLASSIFICATION; DISTURBANCES; CEREBELLUM; SPECTRUM; VISION AB The aim of the present study was to search for a sensorimotor marker (i.e., visuopostural tuning) that could be correlated with the severity of motor impairments in children with autistic spectrum disorders. Given that autistic children were previously reported to be posturally hypo-reactive to visually perceived environmental motion in comparison with normal control children (Gepner et al., 1995), we sought to determine whether children with Asperger syndrome (AS) would share the same postural hyporeactivity to visual motion. Three autistic children with mild to severe motor impairments, three AS children with soft motor signs, and nine normal control children were tested for overall postural instability and postural reactivity to environmental motion. Results indicate, first, that overall postural instability is significantly reduced in autistic children compared with both AS and normal children. Second, although postural oscillations in the fore-aft axis become more attuned to the oscillation frequency of an immersive dynamic visual display as visual speed is increased, in both control and AS subjects, this is not the case in autistic children. Despite the small number of subjects tested in this study, our data confirm the existence of a visuopostural detuning in autistic children. Third, they argue for a correlation between visuopostural tuning and severity of motor signs in children with autistic spectrum disorders. Finally, they suggest a differentiation between children with autism and children with AS with regard to postural reactivity to fast visual motion. Neurophysiological implications of these results are discussed. In particular, a visuocerebellar pathway deficit hypothesis in autism is proposed. C1 Montperrin Hosp, Ctr Psychiat Enfant, F-13617 Aix En Provence, France. CNRS, Ctr Rech Neurosci Cognit, F-13402 Marseille 20, France. RP Gepner, B (reprint author), AFRTDET, 137 Rue J Mermoz, F-13008 Marseille, France. EM bruno.gepner@wanadoo.fr CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4 Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Brunet O, 1951, DEV PSYCHOL PREMIERE BUTTERWORTH G, 1977, PERCEPTION, V6, P225 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Doya K, 2000, CURR OPIN NEUROBIOL, V10, P732, DOI 10.1016/S0959-4388(00)00153-7 Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 GEPNER B, 1995, NEUROREPORT, V6, P1211, DOI 10.1097/00001756-199505300-00034 Gepner B, 2001, PSYCHIAT ENFANT, V44, P77 Gepner B, 2001, J AUTISM DEV DISORD, V31, P37, DOI 10.1023/A:1005609629218 Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P43, DOI 10.1046/j.1365-2788.1998.00065.x GLICKSTEIN M, 1991, TRENDS NEUROSCI, V14, P480, DOI 10.1016/0166-2236(91)90055-Y Grandin T., 1995, THINKING PICTURES OT HALLETT M, 1993, ARCH NEUROL-CHICAGO, V50, P1304 Ito M, 1984, CEREBELLUM NEURAL CO Iwanaga R, 2000, J AUTISM DEV DISORD, V30, P169, DOI 10.1023/A:1005467807937 Johnson MTV, 2000, BRAIN RES REV, V33, P155, DOI 10.1016/S0165-0173(00)00027-8 JOUEN F, 1988, INT CONGR SER, V812, P13 Kanner L, 1943, NERV CHILD, V2, P217 KOHENRAZ R, 1992, J AUTISM DEV DISORD, V22, P419, DOI 10.1007/BF01048244 Leary MR, 1996, MENT RETARD, V34, P39 LISHMAN JR, 1973, PERCEPTION, V2, P287, DOI 10.1068/p020287 MASSON G, 1995, EXP BRAIN RES, V103, P137 Middleton FA, 2000, BRAIN RES REV, V31, P236, DOI 10.1016/S0165-0173(99)00040-5 Miller JN, 2000, J ABNORM PSYCHOL, V109, P227, DOI 10.1037/0021-843X.109.2.227 Minshew N J, 1997, J Int Neuropsychol Soc, V3, P303 ONeill M, 1997, J AUTISM DEV DISORD, V27, P283, DOI 10.1023/A:1025850431170 ORNITZ EM, 1974, J AUTISM CHILD SCHIZ, V4, P197, DOI 10.1007/BF02115226 ORNITZ EM, 1974, ARCH GEN PSYCHIAT, V31, P369 Prior M, 1998, J CHILD PSYCHOL PSYC, V39, P893, DOI 10.1111/1469-7610.00389 Schmuckler MA, 1997, J EXP PSYCHOL HUMAN, V23, P528, DOI 10.1037//0096-1523.23.2.528 Schopler E., 1979, INDIVIDUALIZED ASSES, V1 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 Spencer J, 2000, NEUROREPORT, V11, P2765, DOI 10.1097/00001756-200008210-00031 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 Teitelbaum P, 1998, P NATL ACAD SCI USA, V95, P13982, DOI 10.1073/pnas.95.23.13982 VILENSKY JA, 1981, ARCH NEUROL-CHICAGO, V38, P646 WECHSLER D, 1995, MANUAL INTELLIGENCE Williams D., 1992, NOBODY NOWHERE World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 43 TC 53 Z9 53 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUN PY 2002 VL 32 IS 3 BP 231 EP 238 DI 10.1023/A:1015410015859 PG 8 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800011 PM 12108625 ER PT J AU Fombonne, E AF Fombonne, E TI Is exposure to alcohol during pregnancy a risk factor for autism? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter CR Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 HARRIS SR, 1995, ALCOHOL CLIN EXP RES, V19, P660, DOI 10.1111/j.1530-0277.1995.tb01564.x NANSON JL, 1992, ALCOHOL CLIN EXP RES, V16, P558, DOI 10.1111/j.1530-0277.1992.tb01417.x NR 3 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 JUN PY 2002 VL 32 IS 3 BP 243 EP 243 DI 10.1023/A:1015466100838 PG 1 WC Psychology, Developmental SC Psychology GA 551ZL UT WOS:000175593800014 PM 12108626 ER PT J AU Filiano, JJ Goldenthal, MJ Rhodes, CH Marin-Garcia, J AF Filiano, JJ Goldenthal, MJ Rhodes, CH Marin-Garcia, J TI Mitochondrial dysfunction in patients with hypotonia, epilepsy, autism, and developmental delay: HEADD syndrome SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID KEARNS-SAYRE SYNDROME; DNA DELETIONS AB A group of 12 children clinically presenting with hypotonia, intractable epilepsy, autism, and developmental delay, who did not fall into previously described categories of mitochondrial encephalomyopathy, were evaluated for mitochondrial respiratory enzyme activity levels, mitochondrial DNA, and mitochondrial structural abnormalities. Reduced levels in specific respiratory activities were found solely in enzymes with subunits encoded by mitochondrial DNA in seven of eight biopsied skeletal muscle specimens evaluated. Five cases exhibited increased levels of large-scale mitochondrial DNA deletions, whereas pathogenic point mutations previously described in association with mitochondrial encephalomyopathies were not found. Mitochondrial structural abnormalities were present in three of four patients examined. Our findings suggest that mitochondrial dysfunction, including extensive abnormalities in specific enzyme activities, mitochondrial structure, and mitochondrial DNA integrity, may be present in children with a clinical constellation including hypotonia, epileptic seizures, autism, and developmental delay. The acronym HEADD is presented here to facilitate pursuit of mitochondrial defects in patients with this clinical constellation after other causes have been excluded. C1 Mol Cardiol & Neuromuscular Inst, HIghland Pk, NJ 08904 USA. Dartmouth Hitchcock Med Ctr, Dept Pediat, Lebanon, NH 03766 USA. Dartmouth Hitchcock Med Ctr, Dept Pathol, Lebanon, NH 03766 USA. RP Marin-Garcia, J (reprint author), Mol Cardiol & Neuromuscular Inst, 75 Raritan Ave, HIghland Pk, NJ 08904 USA. CR American Psychological Association, 1994, DIAGN STAT MAN 4 Buoni S, 2000, J CHILD NEUROL, V15, P380, DOI 10.1177/088307380001500605 DOTTI MT, 1993, BRAIN DEV-JPN, V15, P103, DOI 10.1016/0387-7604(93)90045-A Graf WD, 2000, J CHILD NEUROL, V15, P357, DOI 10.1177/088307380001500601 Marin-Garcia J, 1995, J Card Fail, V1, P285, DOI 10.1016/1071-9164(95)90003-9 MarinGarcia J, 1996, CARDIOVASC RES, V31, P306 Marin-Garcia J, 1999, PEDIATR NEUROL, V21, P538, DOI 10.1016/S0887-8994(99)00038-7 Mohandas TK, 1999, AM J MED GENET, V82, P294, DOI 10.1002/(SICI)1096-8628(19990212)82:4<294::AID-AJMG4>3.0.CO;2-U MORAES CT, 1989, NEW ENGL J MED, V320, P1293, DOI 10.1056/NEJM198905183202001 MORENO H, 1992, INVEST CLIN, V33, P13 Schon EA, 1997, J BIOENERG BIOMEMBR, V29, P131, DOI 10.1023/A:1022685929755 Vogel H, 2001, J NEUROPATH EXP NEUR, V60, P217 ZEVIANI M, 1988, NEUROLOGY, V38, P1339 NR 13 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 JUN PY 2002 VL 17 IS 6 BP 435 EP 439 DI 10.1177/088307380201700607 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 579XB UT WOS:000177202900007 ER PT J AU Levy, SE AF Levy, SE TI The development of autism: Perspectives from theory and research SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Univ Penn, Philadelphia, PA 19104 USA. RP Levy, SE (reprint author), Univ Penn, Childrens Seashore House, Philadelphia, PA 19104 USA. CR Burack J. A., 2001, DEV AUTISM PERSPECTI NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD JUN PY 2002 VL 23 IS 3 BP 183 EP 183 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 562LF UT WOS:000176197700014 ER PT J AU Ellis, JT Luiselli, JK Amirault, D Byrne, S O'Malley-Cannon, B Taras, M Wolongevicz, J Sisson, RW AF Ellis, JT Luiselli, JK Amirault, D Byrne, S O'Malley-Cannon, B Taras, M Wolongevicz, J Sisson, RW TI Families of children with developmental disabilities: Assessment and comparison of self-reported needs in relation to situational variables SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE developmental disabilities; children; families ID STRESS PROFILES; MOTHERS; FATHERS; AUTISM AB Parents of children with a developmental disability completed a survey that sampled self-reported needs (information, support, giving explanations to others, community services, finances, and family functioning) in relation to situational variables, such as age (child and parents), type of educational service received by the child, number of siblings, marital status of parents, family income, parents' level of education, and the family's participation in support services. Families of younger children were found to have the greatest overall needs. Increased number of hours per week of employment by fathers was associated with reduced needs. There also was less reported need by families who had a child enrolled in a residential-care setting. These findings extend the assessment of family needs to a population and age of children not addressed in previous research. Recommendations for the types of professional services that should be offered to families on the basis of an assessment of need are presented and discussed. C1 May Inst Inc, May Ctr Appl Res, Norwood, MA 02062 USA. RP Luiselli, JK (reprint author), May Inst Inc, May Ctr Appl Res, 1 Commerce Way, Norwood, MA 02062 USA. CR ALBANESE AL, 1996, TEACHING CHILDREN AU, P95 BAILEY DB, 1988, J SPEC EDUC, V22, P117 Bailey D. B., 1990, J EARLY INTERVENTION, V14, P196 BAILEY DB, 1992, AM J MENT RETARD, V97, P1 Baker B. L., 1989, PARENT TRAINING DEV Bristol M. M., 1984, SEVERELY HANDICAPPED, P91 DeMeyer M. 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PD JUN PY 2002 VL 14 IS 2 BP 191 EP 202 DI 10.1023/A:1015223615529 PG 12 WC Rehabilitation SC Rehabilitation GA 549PG UT WOS:000175452800007 ER PT J AU Parsons, S Mitchell, P AF Parsons, S Mitchell, P TI The potential of virtual reality in social skills training for people with autistic spectrum disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Review DE autism; executive function; mental simulation; social skills training; theory of mind; virtual reality ID HIGH-FUNCTIONING AUTISM; ASPERGERS-SYNDROME; FALSE BELIEF; JOINT ATTENTION; TEACHING THEORY; CHILDREN; REHABILITATION; MIND; ENVIRONMENTS; ADULTS AB Background People with autism experience profound and pervasive difficulties in the social domain. Attempts to teach social behaviours tend to adopt either a behavioural or a 'theory of mind' (ToM) approach. The beneficial aspects and limitations of both paradigms are summarized before an examination of how virtual reality technology may offer a way to combine the strengths from both approaches. Methods This is not an exhaustive review of the literature; rather, the papers are chosen as representative of the current understanding within each broad topic. Web of Science ISI, EMBASE and PsycInfo were searched for relevant articles. Results Behavioural and ToM approaches to social skills training achieve some success in improving specific skills or understanding. However, the failure to generalize learned behaviours to novel environments, and the unwieldy nature of some behavioural methodologies, means that there is a need for a training package that is easy to administer and successful in promoting learning across contexts. Conclusions Virtual reality technology may be an ideal tool for allowing participants to practise behaviours in role-play situations, whilst also providing a safe environment for rule learning and repetition of tasks. Role-play within virtual environments could promote the mental simulation of social events, potentially allowing a greater insight into minds. Practice of behaviours, both within and across contexts, could also encourage a more flexible approach to social problem solving. Virtual environments offer a new and exciting perspective on social skills training for people with autistic spectrum disorders. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Parsons, S (reprint author), Univ Nottingham, Sch Psychol, Univ Pk, Nottingham NG7 2RD, England. 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PD JUN PY 2002 VL 46 BP 430 EP 443 DI 10.1046/j.1365-2788.2002.00425.x PN 5 PG 14 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 556FC UT WOS:000175837800006 PM 12031025 ER PT J AU Borg, I Squire, M Menzel, C Stout, K Morgan, D Willatt, L O'Brien, PCM Ferguson-Smith, MA Ropers, HH Tommerup, N Kalscheuer, VM Sargan, DR AF Borg, I Squire, M Menzel, C Stout, K Morgan, D Willatt, L O'Brien, PCM Ferguson-Smith, MA Ropers, HH Tommerup, N Kalscheuer, VM Sargan, DR TI A cryptic deletion of 2q35 including part of the PAX3 gene detected by breakpoint mapping in a child with autism and a de novo 2;8 translocation SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID MENTAL-RETARDATION; GENOMIC SCREEN; REARRANGEMENTS; PHENOTYPE; OSTEODYSTROPHY; CHROMOSOMES; POPULATION; MUTATIONS; LINKAGE; PCR AB We report a de novo, apparently balanced (2;8)(q35;q21.2) translocation in a boy with developmental delay and autism. Cross species (colour) paint (Rx) and SKY FISH, forward and reverse chromosome painting, and FISH with subtelomeric probes were used to examine the patient's karyotype, but further rearrangements were not detected. FISH with region specific clones mapping near 2q35 and 8q21.2 breakpoints and STS mapping performed on the isolated derivative chromosomes were used to refine the location of the breakpoints further. A cryptic deletion of between 4.23 and 4.41 Mb in extent and involving at least 13 complete genes or transcription units was found at the breakpoint on 2q35. The deletion includes the promoter and 5' untranslated region of the paired box 3 (PAX3) gene. The child has very mild dystopia canthorum which may be associated with the PAX3 haploinsufficiency. The 8q21.2 breakpoint is within MMP16 which encodes matrix metalloproteinase 16. We postulate that the cryptic deletion and rearrangement are responsible for the patient's phenotype and that a gene (or genes) responsible for autism lies at 2q35 or 8q21.2. The results present a step towards identifying genes predisposing to autism. C1 Univ Cambridge, Dept Clin Vet Med, Ctr Vet & Biomed Sci, Mol Cytogenet Lab, Cambridge CB3 0ES, England. Max Planck Inst Mol Genet, Berlin, Germany. Addenbrookes NHS Trust, Clin Cytogenet Lab, Cambridge CB2 2QQ, England. Addenbrookes NHS Trust, Cytogenet Lab, Cambridge CB2 2QQ, England. Addenbrookes NHS Trust, Dept Med Genet, Cambridge CB2 2QQ, England. Univ Copenhagen, IMBG, Dept Med Genet, Wilhelm Johannsen Ctr Funct Genome Res, DK-1168 Copenhagen, Denmark. RP Borg, I (reprint author), Univ Cambridge, Dept Clin Vet Med, Ctr Vet & Biomed Sci, Mol Cytogenet Lab, Madingley Rd, Cambridge CB3 0ES, England. 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Med. Genet. PD JUN PY 2002 VL 39 IS 6 BP 391 EP 399 DI 10.1136/jmg.39.6.391 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 567YH UT WOS:000176514400004 PM 12070244 ER PT J AU Brownell, MD AF Brownell, MD TI Musically adapted social stories to modify behaviors in students with autism: Four case studies SO JOURNAL OF MUSIC THERAPY LA English DT Article ID CHILDREN; THERAPY AB The purpose of the present study was to investigate the effect of a musical presentation of social story information on the behaviors of students with autism. Social stories are a means of incorporating an individual with autism's propensity toward visual learning with educationally necessary behavior modifications. Participants in the study were four first- and second-grade students with a primary diagnosis of autism attending an elementary school in eastern Iowa. A unique social story was created for each student that addressed a current behavioral goal. Subsequently, original music was composed using the text of the social story as lyrics. The independent variable for this study was one of three treatment conditions: baseline (A); reading the story (B); and singing the story (C). The reading and singing versions of the social stories were alternately presented to the students using the counterbalanced treatment order ABAC/ACAB. The dependent variable was the frequency with which the target behavior occurred under each condition of the independent variable. Data were collected for a period of 1 hour following presentation of the social story. Results from all four cases indicated that both the reading condition (B) and the singing condition (Q) were significantly (p < .05) more effective in reducing the target behavior than the no-contact control condition (A). The singing condition was significantly more effective than the reading condition only in Case Study III. For the remaining case studies, the mean frequency of the target behavior was smaller during the singing condition, but not significantly so. These results suggested that the use of a musically adapted version of social stories is an effective and viable treatment option for modifying behaviors with this population. C1 Univ Kansas, Lawrence, KS 66045 USA. RP Brownell, MD (reprint author), Univ Kansas, Lawrence, KS 66045 USA. 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NR 0 TC 0 Z9 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD JUN PY 2002 VL 72 IS 6 BP 826 EP 826 PG 1 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 557DD UT WOS:000175891300050 ER PT J AU Howlin, P AF Howlin, P TI Autism and developmental receptive language disorder - A follow up comparison in early adult life. Social, behavioural, and psychiatric outcomes SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Meeting Abstract C1 St Georges Med Sch, London, England. NR 0 TC 0 Z9 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD JUN PY 2002 VL 72 IS 6 BP 826 EP 826 PG 1 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 557DD UT WOS:000175891300051 ER PT J AU Glasson, EJ AF Glasson, EJ TI The Western Australian Register for Autism Spectrum Disorders SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Letter ID PRESCHOOL-CHILDREN RI Glasson, Emma/H-5339-2013 OI Glasson, Emma/0000-0003-3996-9049 CR ALESSANDRI LM, 1996, DISABILITY COUNTS PR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bower C, 2000, J PAEDIATR CHILD H, V36, P213, DOI 10.1046/j.1440-1754.2000.00480.x Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Powell JE, 2000, DEV MED CHILD NEUROL, V42, P624, DOI 10.1017/S001216220000116X Tager-Flusberg H, 2001, MENT RETARD DEV D R, V7, P21 NR 6 TC 12 Z9 12 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1034-4810 J9 J PAEDIATR CHILD H JI J. Paediatr. Child Health PD JUN PY 2002 VL 38 IS 3 BP 321 EP 321 DI 10.1046/j.1440-1754.2002.00859.x PG 1 WC Pediatrics SC Pediatrics GA 557KH UT WOS:000175907400024 PM 12047707 ER PT J AU Shipley-Benamou, R Lutzker, JR Taubman, M AF Shipley-Benamou, R Lutzker, JR Taubman, M TI Teaching daily living skills to children with autism through instructional video modeling SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID MENTAL-RETARDATION; TIME-DELAY; SELF; INTERVENTIONS; RECOGNITION; STUDENTS; ADULT AB Research on video modeling has typically utilized either competent peer models or self-models engaging in criterion performances. Although both methods have demonstrated utility in achieving skill acquisition, each has potential disadvantages. The current research utilized a multiple probe design across tasks and replicated across participants in order to demonstrate the efficacy of an instructional video modeling technique to teach functional living skills to three children with autism. Five tasks were selected. Prior to the development of each training video, task analyses were created. Videotapes were developed from the participant's viewing perspective, that is, as the participant would be viewing the task. Instructional video modeling was effective in promoting skill acquisition across all three children and maintained during the postvideo phase and a 1-month follow up. C1 Ctr Dis Control & Prevent, Natl Ctr Injury Prevent & Control, Div Violence Prevent, Atlanta, GA 30341 USA. RP Shipley-Benamou, R (reprint author), Ctr Dis Control & Prevent, Natl Ctr Injury Prevent & Control, Div Violence Prevent, 4770 Buford Highway NE,Mail Stop K-60, Atlanta, GA 30341 USA. 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Posit. Behav. Interv. PD SUM PY 2002 VL 4 IS 3 BP 165 EP + PG 12 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LW UT WOS:000180573300005 ER PT J AU Murray, M Clarke, S Worcester, J AF Murray, M Clarke, S Worcester, J TI A teacher's perspective of using PBS in a classroom for a girl with multiple disabilities SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Editorial Material AB This article shares the perspective of a teacher involved in a collaborative team that utilized the process of positive behavior support in an effort to improve the behavior and quality of life of a 12-year-old girl with multiple disabilities. The teacher took the initiative and actively sought out the family, other school staff, and behavioral interventionists to join her in developing a behavioral support-plan that allowed a young girl identified with Autism Spectrum Disorder to remain in her classroom. The following is a description of her classroom, how the support plan evolved throughout the school year, and her perspectives and observations about the positive behavior support process. C1 Univ S Florida, Dept Child & Family Studies, Tampa, FL 33612 USA. Univ S Florida, Div Appl Res & Educ Support, Louis de la Parte Florida Mental Hlth Inst, Tampa, FL 33620 USA. RP Murray, M (reprint author), Univ S Florida, Dept Child & Family Studies, MHC2114 DARES,13301 Bruce B Downs Blvd, Tampa, FL 33612 USA. CR Fox L, 1997, J ASSOC PERS SEVERE, V22, P198 VAUGHN BJ, 1997, J ASSOC PERS SEVERE, V22, P185 NR 2 TC 0 Z9 0 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 SUM PY 2002 VL 4 IS 3 BP 189 EP 192 PG 4 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LW UT WOS:000180573300008 ER PT J AU Edwards, RJ Pople, IK AF Edwards, RJ Pople, IK TI Side-effects of risperidone therapy mimicking cerebrospinal fluid shunt malfunction: implications for clinical monitoring and management SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Article DE aggression; autism; hydrocephalus; mental retardation; risperidone; side-effects; shunt malfunction ID PERVASIVE DEVELOPMENTAL DISORDERS; OPEN-LABEL; AUTISTIC DISORDER; CHILDREN; HYDROCEPHALUS; ADOLESCENTS; ADULTS; TERM AB Risperidone is an atypical antipsychotic used in the treatment of several psychiatric disorders in both children and adults. We present two patients with hydrocephalus and learning difficulties who were admitted to the neurosurgical unit with a suspected cerebrospinal fluid shunt malfunction and raised intracranial pressure. They had both been commenced on risperidone for the treatment of aggressive outbursts. Twelve days after commencing risperidone, the first patient developed symptoms of headache, nausea, vomiting, drowsiness, lethargy and two episodes of collapse. The second patient presented with similar symptoms 4 days after his risperidone dose was increased. An unnecessary shunt exploration was averted in both cases when it was noted that the side-effect profile of risperidone mimicked exactly those of shunt malfunction. Discontinuation of the drug resulted in complete resolution of all symptoms within 72 h. Many patients with shunted hydrocephalus have associated developmental disorders that may warrant treatment with risperidone. Clinicians should be aware of the potential symptom overlap between shunt malfunction and risperidone side-effects in these patients. C1 Frenchay Hosp, Dept Neurosurg, Bristol BS16 1LE, Avon, England. RP Edwards, RJ (reprint author), Frenchay Hosp, Dept Neurosurg, Frenchay Pk Rd, Bristol BS16 1LE, Avon, England. 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Psychopharmacol. PD JUN PY 2002 VL 16 IS 2 BP 177 EP 179 PG 3 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 562NL UT WOS:000176204700009 PM 12095077 ER PT J AU Seeman, C AF Seeman, C TI A will of his own: Reflections on parenting a child with autism. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo, Lib, Toledo, OH 43606 USA. RP Seeman, C (reprint author), Univ Toledo, Lib, 2801 W Bancroft St, Toledo, OH 43606 USA. CR Harland Kelly, 2002, WILL HIS OWN REFLECT 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. 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The current piper criticizes, this because it falsely predicts that the same children will have a parallel problem with the False Photographs The fact that the content of representations make, a difference while the structure remains constant casts doubt upon their claim. C1 Smith Coll, Dept Psychol, Northampton, MA 01063 USA. Smith Coll, Dept Philosophy, Northampton, MA 01063 USA. RP Kamawar, D (reprint author), Smith Coll, Dept Psychol, Northampton, MA 01063 USA. 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SO NEUROSCIENTIST LA English DT Editorial Material CR Casanova MF, 2002, NEUROLOGY, V58, P428 NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1073-8584 J9 NEUROSCIENTIST JI Neuroscientist PD JUN PY 2002 VL 8 IS 3 BP 191 EP 191 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 555KY UT WOS:000175794300010 ER PT J AU Poole, J AF Poole, J TI Autism and MMR SO PSYCHOLOGIST LA English DT Letter RP Poole, J (reprint author), 48 Winchester Rd, Ramsey, Hants, England. NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD JUN PY 2002 VL 15 IS 6 BP 283 EP 283 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 561UH UT WOS:000176160800011 ER PT J AU Whiteley, P AF Whiteley, P TI Autism and MMR SO PSYCHOLOGIST LA English DT Letter C1 Univ Sunderland, Sch Sci, Autism Res Unit, Sunderland SR2 7EE, Durham, England. RP Whiteley, P (reprint author), Univ Sunderland, Sch Sci, Autism Res Unit, Sunderland SR2 7EE, Durham, England. NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD JUN PY 2002 VL 15 IS 6 BP 283 EP 283 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 561UH UT WOS:000176160800010 ER PT J AU Ruef, MB Turnbull, AP AF Ruef, MB Turnbull, AP TI The perspectives of individuals with cognitive disabilities and/or autism on their lives and their problem behavior SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE problem behavior; autism; cognitive disabilities; quality of life; participatory action research; focus groups ID TO-PRACTICE GAP; PARTICIPATORY ACTION RESEARCH; SPECIAL-EDUCATION; FAMILY PERSPECTIVES; MENTAL-RETARDATION; SELF-DETERMINATION; GENERAL-EDUCATION; PEOPLE; SUPPORT; FOCUS AB The purpose of the study was 2-fold: (a) to explore the perceptions of individuals with cognitive disabilities and/or autism regarding barriers and solutions they have experienced related to problem behavior, and (b) to elicit suggestions on areas viewed as most helpful in increasing quality of life while reducing or eliminating problem behavior. A qualitative method of inquiry using focus groups and individual interviews was used. Several themes emerged from the focus groups, including the difficulties participants experienced with communication; participants' need for personal decision making and privacy; and the importance of recreation, employment, selection of living situations, and relationships with friends and family members. The article indicates the importance of listening carefully to individuals with disabilities as a first step in improving the quality of their lives. C1 Calif Polytech State Univ San Luis Obispo, Univ Ctr Teacher Educ, San Luis Obispo, CA 93407 USA. Univ Kansas, Lawrence, KS 66045 USA. RP Ruef, MB (reprint author), Calif Polytech State Univ San Luis Obispo, Univ Ctr Teacher Educ, Bldg 2,Room 106, San Luis Obispo, CA 93407 USA. EM mruef@calpoly.edu CR Alberto P. 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P., 1996, POSITIVE BEHAV SUPPO, P99 TURNBULL AP, 2000, FAMILY QUALITY LIFE Turnbull AP, 1997, EXCEPT CHILDREN, V63, P211 TURNBULL AP, 2000, J POSIT BEHAV INTERV, V2, P190, DOI 10.1177/109830070000200310 Turnbull AP, 1999, TOP EARLY CHILD SPEC, V19, P164, DOI 10.1177/027112149901900308 Turnbull AP, 1998, J ASSOC PERS SEVERE, V23, P178, DOI 10.2511/rpsd.23.3.178 *US DOE, 1998, 20 ANN REP C IMPL IN Vaughn BJ, 1997, J APPL BEHAV ANAL, V30, P713, DOI 10.1901/jaba.1997.30-713 VAUGHN BJ, 1997, J ASSOC PERS SEVERE, V22, P185 WALKER ML, 1993, REHABIL COUNS BULL, V37, P2 Whyte W. F., 1991, PARTICIPATORY ACTION, P19 NR 87 TC 13 Z9 13 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2002 VL 27 IS 2 BP 125 EP 140 DI 10.2511/rpsd.27.2.125 PG 16 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BL UT WOS:000222242100003 ER PT J AU Small, KM AF Small, KM TI Topics in autism: A picture's worth (PECS and other visual communication strategies in autism). SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Book Review C1 Wings Learning Ctr, El Granada, CA USA. RP Small, KM (reprint author), Wings Learning Ctr, El Granada, CA USA. CR BONDY A, 2002, TOPICS AUTISM PICTUR NR 1 TC 0 Z9 0 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2002 VL 27 IS 2 BP 159 EP 161 PG 3 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BL UT WOS:000222242100007 ER PT J AU [Anonymous] AF [Anonymous] TI Reaching out, joining in: Teaching social skills to young children with autism (vol 27, pg 93, 2002) SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Correction CR 2002, RES PRACT PERS SEV D, V27, P93 NR 1 TC 0 Z9 0 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2002 VL 27 IS 2 BP 163 EP 163 PG 1 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BL UT WOS:000222242100008 ER PT J AU Baron-Cohen, S AF Baron-Cohen, S TI The extreme male brain theory of autism SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID ASPERGER-SYNDROME; SEX-DIFFERENCES; FUNCTIONING AUTISM; GENDER; CHILDREN; PERFORMANCE; TASK; COGNITION; ABILITIES; LANGUAGE AB The key mental domains in which sex differences have traditionally been studied are verbal and spatial abilities. In this article I suggest that two neglected dimensions for understanding human sex differences are 'empathising' and 'systemising'. The male brain is a defined psychometrically as those individuals in whom systemising is significantly better than empathising, and the female brain is defined as the opposite cognitive profile. Using these definitions, autism can be considered as an extreme of the normal male profile. There is increasing psychological evidence for the extreme male brain theory of autism. C1 Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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PD JUN PY 2002 VL 6 IS 6 BP 248 EP 254 DI 10.1016/S1364-6613(02)01904-6 PG 7 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 557VD UT WOS:000175928200009 ER PT J AU Megarbane, A Hersh, JH Chouery, E Fabre, M AF Megarbane, A Hersh, JH Chouery, E Fabre, M TI Craniosynostosis, telecanthus, scalp hair abnormalities, and sensorineural deafness in two sibs SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE craniosynostosis; deafness; mental retardation; scalp hair abnormalities; telecanthus AB A sister and a brother with anomalous skull configuration, facial abnormalities, abnormal scalp hair growth, sensorineural hearing loss and, in the boy, proven craniosynostosis, severe mental retardation, and autism were reported in 1986 in an abstract by Hersh et al. We reexamined this family and here review the literature focusing on the major clinical findings, and suggest that their clinical manifestations may represent a previously unreported syndrome. (C) 2002 Wiley-Liss, Inc. C1 St Josephs Univ, Fac Med, Unite Genet Med, Lab Biol Mol & Cytogenet, F-75007 Paris, France. Univ Louisville, Dept Pediat, Child Evaluat Ctr, Louisville, KY 40292 USA. Fac Med, Inst Histol, Strasbourg, France. RP Megarbane, A (reprint author), St Josephs Univ, Fac Med, Unite Genet Med, Lab Biol Mol & Cytogenet, 42 Rue Grenelle, F-75007 Paris, France. CR GORLIN RJ, 1995, OXFORD MONOGRAPHS ME, V28 HERSH JH, 1986, P GREENWOOD GENET CT, V5, P186 Sensenbrenner J A, 1975, Birth Defects Orig Artic Ser, V11, P372 YOUNG ID, 1989, J MED GENET, V26, P393, DOI 10.1136/jmg.26.6.393 NR 4 TC 2 Z9 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAY 15 PY 2002 VL 109 IS 4 BP 323 EP 327 DI 10.1002/ajmg.10370 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 546KH UT WOS:000175272900011 PM 11992488 ER PT J AU Lauritsen, MB Borglum, AD Betancur, C Philippe, A Kruse, TA Leboyer, M Ewald, H AF Lauritsen, MB Borglum, AD Betancur, C Philippe, A Kruse, TA Leboyer, M Ewald, H TI Investigation of two variants in the DOPA decarboxylase gene in patients with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE DDC; polymorphisms; association; autism; TDT ID SEROTONIN TRANSPORTER GENE; WHOLE-BLOOD SEROTONIN; TRANSMISSION/DISEQUILIBRIUM TEST; GENOMIC SCREEN; FAMILY HISTORY; DISORDER; ASSOCIATION; LINKAGE; RELATIVES; PROBANDS AB Though genetic risk factors are important for the development of autism, no specific risk alleles have yet been identified. DOPA decarboxylase (DDC) is involved in both the catecholaminergic and serotonergic pathways and may be considered a functional candidate gene for autism. The present study is the first to test if two new variants of possible functional significance in the DDC gene increase the susceptibility to autism. A total of 90 parent-offspring trios recruited in Denmark and France were investigated using the transmission disequilibrium. test (TDT). We found no evidence of linkage disequilibrium between autism and either of the two polymorphisms. Nor did we find linkage disequilibrium between autism and haplotypes of the two variants using a multiallelic TDT. These findings suggest that the DDC gene is unlikely to play a major role in the development of autism in our data set. (C) 2002 Wiley-Liss, Inc. C1 Aarhus Univ Hosp, Psychiat Hosp Aarhus, Inst Basic Psychiat Res, Dept Psychiat Demog, DK-8240 Risskov, Denmark. Aarhus Univ Hosp, Psychiat Hosp Aarhus, Inst Basic Psychiat Res, Dept Biol Psychiat, DK-8240 Risskov, Denmark. Univ Aarhus, Inst Human Genet, Aarhus C, Denmark. Fac Med, INSERM, U513, Creteil, France. 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CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1998, ASPERGERS SYNDROME G Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Constantino JN, 2000, J DEV BEHAV PEDIATR, V21, P2 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x *IMM SAF REV COMM, 2001, IMM SAF REV MEASL MU Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 MAYES SD, 2001, J ABNORM CHILD PSYCH, V3, P263 Rinehart NJ, 2001, AUTISM, V5, P67, DOI 10.1177/1362361301005001007 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 RUTTER M, 2001, RES INNOVATION ROAD, V1, P54 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 TONGE BJ, 1999, AUTISM, V2, P117 Wing L, 1997, HDB AUTISM PERVASIVE, P148 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 17 TC 9 Z9 9 PU AUSTRALASIAN MED PUBL CO LTD PI SYDNEY PA LEVEL 1, 76 BERRY ST, SYDNEY, NSW 2060, AUSTRALIA SN 0025-729X J9 MED J AUSTRALIA JI Med. J. Aust. PD MAY 6 PY 2002 VL 176 IS 9 BP 412 EP 413 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 549LM UT WOS:000175445400003 PM 12056990 ER PT J AU Phillips, H AF Phillips, H TI The key to autism - Does it really start with the body turning on itself? SO NEW SCIENTIST LA English DT News Item CR MOL PSYCHIAT, V7, P375 NR 1 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 MAY 4 PY 2002 VL 174 IS 2341 BP 14 EP 14 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 549YF UT WOS:000175474300012 ER PT J AU Newbury, DF Bonora, E Lamb, JA Fisher, SE Lai, CSL Baird, G Jannoun, L Slonims, V Stott, CM Merricks, MJ Bolton, PF Bailey, AJ Monaco, AP AF Newbury, DF Bonora, E Lamb, JA Fisher, SE Lai, CSL Baird, G Jannoun, L Slonims, V Stott, CM Merricks, MJ Bolton, PF Bailey, AJ Monaco, AP CA Int Molecular Genetic Study Autism TI FOXP2 is not a major susceptibility gene for autism or specific language impairment SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID FAMILY HISTORY; DISORDER; TWIN; SPEECH; CHILDREN; 7Q31; LOCALIZATION; DEFICITS; SYSTEM AB The FOXP2 gene, located on human 7q31 (at the SPCH1 locus), encodes a transcription factor containing a polyglutamine tract and a forkhead domain. FOXP2 is mutated in a severe monogenic form of speech and language impairment, segregating within a single large pedigree, and is also disrupted by a translocation in an isolated case. Several studies of autistic disorder have demonstrated linkage to a similar region of 7q (the AUTS1 locus), leading to the proposal that a single genetic factor on 7q31 contributes to both autism and language disorders. In the present study, we directly evaluate the impact of the FOXP2 gene with regard to both complex language impairments and autism, through use of association and mutation screening analyses. We conclude that coding-region variants in FOXP2 do not underlie the AUTS1 linkage and that the gene is unlikely to play a role in autism or more common forms of language impairment. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Guys Hosp, Newccomen Ctr, London SE1 9RT, England. Inst Psychiat, Ctr Social Genet & Dev Psychiat, London, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London, England. Univ Cambridge, Dev Psychiat Sect, Cambridge, England. RP Monaco, AP (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. RI Monaco, Anthony/A-4495-2010; Fisher, Simon/E-9130-2012; Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Monaco, Anthony/0000-0001-7480-3197; Fisher, Simon/0000-0002-3132-1996; Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X CR Abecasis GR, 2000, AM J HUM GENET, V66, P279, DOI 10.1086/302698 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th 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 Bishop D. V. 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J. Hum. Genet. PD MAY PY 2002 VL 70 IS 5 BP 1318 EP 1327 DI 10.1086/339931 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 541XT UT WOS:000175012400021 PM 11894222 ER PT J AU Betancur, C Leboyer, M Gillberg, C AF Betancur, C Leboyer, M Gillberg, C TI Increased rate of twins among affected sibling pairs with autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Letter C1 Fac Med, INSERM, U513, F-94010 Creteil, France. Assistance Publ Hop Paris, Hop Albert Chenevier & Henri Mondor, Dept Psychiat, Creteil, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RP Betancur, C (reprint author), Fac Med, INSERM, U513, 8 Rue Gen Sarrail, F-94010 Creteil, France. CR Greenberg DA, 2001, AM J HUM GENET, V69, P1062, DOI 10.1086/324191 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 NR 3 TC 30 Z9 31 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 MAY PY 2002 VL 70 IS 5 BP 1381 EP 1383 DI 10.1086/340364 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 541XT UT WOS:000175012400032 PM 11951183 ER PT J AU Hastings, RP Brown, T AF Hastings, RP Brown, T TI Behavior problems of children with autism, parental self-efficacy, and mental health SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID DIRECT-CARE STAFF; SEVERE INTELLECTUAL DISABILITY; CHALLENGING BEHAVIORS; LEARNING-DISABILITIES; HANDICAPPED-CHILDREN; STRESS; MOTHERS; DEPRESSION; COMPETENCE; PEOPLE AB Self-efficacy has been identified in the general parenting literature as an important variable affecting parent outcomes. In the present study, 26 mothers and 20 fathers of children with autism reported on their self-efficacy, anxiety, and depression. Teachers rated the behavior problems of the children. Regression analyses showed that self-efficacy mediated the effect of child behavior problems on mothers' anxiety and depression, but there was no evidence that it functioned as a mediator for fathers. However, there was evidence that self-efficacy moderated the effect of child behavior problems on fathers' anxiety. No evidence for the moderating effect of self-efficacy was apparent for mothers. Methodological issues and the theoretical and practical implications of these results are discussed. C1 Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. RP Hastings, RP (reprint author), Univ Southampton, Dept Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. 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PD MAY PY 2002 VL 107 IS 3 BP 222 EP 232 DI 10.1352/0895-8017(2002)107<0222:BPOCWA>2.0.CO;2 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 550TE UT WOS:000175518200007 PM 11966335 ER PT J AU Reddy, V Williams, E Vaughan, A AF Reddy, V Williams, E Vaughan, A TI Sharing humour and laughter in autism and Down's syndrome SO BRITISH JOURNAL OF PSYCHOLOGY LA English DT Article ID CHILDS APPRAISAL; JOINT ATTENTION; EXPRESSIONS; ATTRIBUTES; BEHAVIOR; EMOTION; OBJECTS; INFANTS; ADULTS; PEOPLE AB Everyday humour and laughter can tell us about children's ability to engage with and understand others. A group of 19 pre-school children with autism and 16 pre-school children with Down's syndrome, matched on non-verbal mental age, participated in a cross-sectional study. Parental reports revealed no group differences in overall frequencies of laughter or laughter at tickling, peekaboo or slapstick. However, in the autism group, reported laughter was rare in response to events such as funny faces or socially inappropriate acts, but was common in strange or inexplicable situations. Reported responses to others' laughter also differed: children with autism rarely attempted to join in others' laughter and rarely attempted to re-elicit it through acts of clowning or teasing. Analysis of videotaped interactions also showed no group differences in frequencies of child or adult laughter. However, the children with autism showed higher frequencies of unshared laughter in interactive situations and lower frequencies of attention or smiles in response to others' laughter. Humour is an affective and cultural phenomenon involving the sharing of affect, attention and convention; children with autism show problems in some simple affective and mutual as well as joint attentional and cultural aspects of humorous engagement. C1 Univ Portsmouth, Dept Psychol, Portsmouth PO1 2ER, Hants, England. 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J. Psychol. PD MAY PY 2002 VL 93 BP 219 EP 242 DI 10.1348/000712602162553 PN 2 PG 24 WC Psychology, Multidisciplinary SC Psychology GA 555ZU UT WOS:000175823600006 PM 12031149 ER PT J AU Stanley, JA AF Stanley, JA TI In vivo magnetic resonance spectroscopy and its application to neuropsychiatric disorders SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Review DE in vivo; proton; phosphorus; spectroscopy; schizophrenia; bipolar; depression; autism ID HUMAN-BRAIN INVIVO; N-ACETYL-ASPARTATE; NEUROLEPTIC-NAIVE PATIENTS; BIPOLAR AFFECTIVE-DISORDER; ANTERIOR CINGULATE CORTEX; GAMMA-AMINOBUTYRIC-ACID; HIGH-ENERGY PHOSPHATE; H-1 MR SPECTRA; IN-VIVO; SCHIZOPHRENIC-PATIENTS AB In vivo magnetic resonance spectroscopy (MRS) is the only noninvasive imaging technique that can directly assess the living biochemistry in localized brain regions. In the past decade, spectroscopy studies have shown biochemical alterations in various neuropsychiatric disorders. These first-generation studies have, in most cases, been exploratory but have provided insightful biochemical information that has furthered our understanding of different brain disorders. This review provides a brief description of spectroscopy, followed by a literature review of key spectroscopy findings in schizophrenia, affective disorders, and autism. In schizophrenia, phosphorus spectroscopy studies have shown altered metabolism of membrane phospholipids (MPL) during the early course of the illness, which is consistent with a neurodevelopmental abnormality around the critical period of adolescence when the illness typically begins. Children and adolescents who are at increased genetic risk for schizophrenia show similar MPL alterations, suggesting that schizophrenia subjects with a genetic predisposition may have a premorbid neurodevelopmental abnormality. Independent of medication status, bipolar subjects in the depressive state tended to have higher MPL precursor levels and a deficit of high-energy phosphate metabolites, which also is consistent with major depression, though these results varied. Further bipolar studies are needed to investigate alterations at the early stage. Lastly, associations between prefrontal metabolism of high-energy phosphate and MPL and neuropsychological performance and reduced N-acetylaspartate in the temporal and cerebellum regions have been reported in individuals with autism. These findings are consistent with developmental alterations in the temporal lobe and in the cerebellum of persons with autism. This paper discusses recent findings of new functions of N-acetylaspartate. C1 Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Stanley, JA (reprint author), Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Dept Psychiat, Room 721 Parran Hall,GSPH,130 DeSoto St, Pittsburgh, PA 15213 USA. 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A network of brain regions is proposed for social cognition that includes regions involved in processes relevant to social functioning (for example, self reference and emotion). We discuss the alterations of activity in these areas in patients with autism, depression, schizophrenia, and posttraumatic stress disorder in relation to deficits in social behaviour and symptoms. The evidence to date suggests that there may be some specificity of the brain regions involved in these 4 disorders, but all are associated with dysfunction in the amygdala and dorsal cingulate gyrus. Although there is much work remaining in this area, we are beginning to understand the complex interactions of brain function and behaviour that lead to disruptions of social abilities. C1 Rotman Res Inst, Baycrest Ctr Geriatr Care, Toronto, ON M6A 2E1, Canada. Univ Toronto, Dept Psychol, Toronto, ON M5S 1A1, Canada. Univ Toronto, Dept Psychiat, Toronto, ON M5S 1A1, Canada. RP Grady, CL (reprint author), Rotman Res Inst, Baycrest Ctr Geriatr Care, 3560 Bathurst St, Toronto, ON M6A 2E1, Canada. 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In Experiment I with fifty-six 3- to 6-year-old children, performance on the dimensional change card-sorting task as an executive function task was correlated with performance on the usual false-belief prediction task, r = .65, and the false-belief explanation task, r = .65, as measures of theory-of-mind development. Because the explanation version of the false-belief test is supposed to be free of the alleged executive demands inherent in the prediction version, the equally strong correlation with the executive function task suggests that this correlation cannot be due to common executive demands. In Experiment 2, the basic finding of Experiment I was replicated on another sample of 73 children, ages 3 to 5.5 years. The need for new theories to explain the developmental link between theory of mind and executive function development is discussed, and some existing candidates are evaluated. C1 Salzburg Univ, Dept Psychol, A-5020 Salzburg, Austria. RP Perner, J (reprint author), Salzburg Univ, Dept Psychol, Hellbrunnerstr 34, A-5020 Salzburg, Austria. 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PD MAY-JUN PY 2002 VL 73 IS 3 BP 752 EP 767 DI 10.1111/1467-8624.00436 PG 16 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 553TR UT WOS:000175692000006 PM 12038549 ER PT J AU Gillberg, C de Souza, L AF Gillberg, C de Souza, L TI Head circumference in autism, Asperger syndrome, and ADHD: a comparative study SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; CEREBROSPINAL-FLUID; SPECTRUM DISORDERS; CHILDREN AB This study was undertaken to test the hypothesis that children with autistic spectrum disorders often have macrocephalus, and that those without comorbid learning disability* are most frequently affected. Fifty consecutive children with Asperger syndrome (45 males, five females; mean age 9 years, range I year 6 months to 16 years) without indications of underlying medical disorders were matched for birth year and sex with 50 children (45 males, five females; mean age 6 years 4 months, range 1 year 4 months to 13 years 11 months) who met criteria for autistic disorder (a lower-functioning disorder within the autism spectrum) and with 50 children (45 males, five females; mean age 8 years 4 months, range 1 year 6 months to 15 years 5 months) who met criteria for attention-deficit-hyperactivity disorder. Birth and neuropsychiatric follow-up records were examined and data relating to occipitofrontal circumference, weight, and height were detailed. The group with Asperger syndrome included a subset of individuals with macrocephalus recorded both at birth and at follow-up after the first year of life. Another subgroup developed macrocephalus during early childhood. Autistic spectrum disorders include a subgroup with macrocephalus characterized by a relatively high level of functioning and a clinical presentation most often consistent with a diagnosis of Asperger syndrome. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. St George Hosp, Med Sch, Dept Psychiat, London, England. RP Gillberg, C (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgatan 12, SE-41119 Gothenburg, Sweden. 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Med. Child Neurol. PD MAY PY 2002 VL 44 IS 5 BP 296 EP 300 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 553TY UT WOS:000175692600003 PM 12033714 ER PT J AU Laing, E Butterworth, G Ansari, D Gsodl, M Longhi, E Panagiotaki, G Paterson, S Karmiloff-Smith, A AF Laing, E Butterworth, G Ansari, D Gsodl, M Longhi, E Panagiotaki, G Paterson, S Karmiloff-Smith, A TI Atypical development of language and social communication in toddlers with Williams syndrome SO DEVELOPMENTAL SCIENCE LA English DT Article ID JOINT VISUAL-ATTENTION; 2ND YEAR; CHILDREN; INFANTS; DISORDERS; AUTISM; MEMORY AB Williams syndrome (WS) is a genetic disorder which results in an uneven cognitive profile. Despite superior language compared to other syndromes in the phenotypic outcome, toddlers with WS are as delayed in their language onset and early linguistic development as are toddlers with other syndromes. The cause of this delay in WS is as yet unknown. In a series of experiments we examined whether atypical socio-interactive precursors to language could contribute to the explanation of the late language onset and atypical developmental pathways observed in WS. Experiment I showed that despite superficially good social skills, toddlers with WS were only proficient at dyadic interaction. They were impaired in triadic interaction, essential for the referential uses of language, and showed none of the correlations between socio-interactive markers and language seen in the typical controls. Experiment 2 focused on the comprehension and production of referential pointing. Again, the WS group was impaired, despite vocabulary levels higher than those of typically developing controls. Finally, Experiment 3 examined fine motor skills. The WS lack of pointing could not be explained in terms of motor impairments, since the WS toddlers were proficient at fine motor control, such as the pincer grip. 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PD MAY PY 2002 VL 5 IS 2 BP 233 EP 246 PG 14 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 558WT UT WOS:000175990800015 ER PT J AU Baghdadli, A Gonnier, V Aussilloux, C AF Baghdadli, A Gonnier, V Aussilloux, C TI Review of psychopharmacological treatments in adolescents and adults with autistic disorders SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE aggressive behaviour; autistic disorders; psychopharmacological treatment; psychotropic drugs; self-injury ID DOUBLE-BLIND; INFANTILE-AUTISM; BEHAVIORAL SYMPTOMS; BETA-ENDORPHIN; CHILDREN; HALOPERIDOL; NALTREXONE; MAGNESIUM; SEROTONIN; EFFICACY AB Autism is an early developmental disorder. It leads to severe and durable disturbances. Given this problem, no treatment can be excluded a priori. Thus, many approaches are used to deal with autistic disorders. In France, pharmacological treatments are, for instance, largely and mostly used in adults. In the USA, these treatments concern 50 % of persons with autism of any age. Nevertheless, they are rarely based on controlled studies. At the present, however, prescriptions and expected effects appear to be hard to localize. Furthermore, only few controlled studies validate their use. Aim-We offer a review of studies about medical treatments used in adolescents and adults with autism. They are classified in 3 categories : the first (category I) includes drugs used for their neurochemical effects focusing on autistic signs. The second (category II) covers drugs used for treatment of behavioural disorders frequently associated with autism. The third (category III) corresponds to a wide range of drugs or vitamins for wich only few case studies exist reporting irregular positive effects. The main hypothesis of this review is that autism involves a dysfunction of the neuromediation systems. This hypothesis opens new perspectives in the research of medical treatments in autism by focusing on molecules, which are supposed to have an effect on neuromediation systems. Method-Our review is based on studies, which have been published during the past twenty years. For many studies, data are limited to adolescents and adults. So we expanded our review to data available in children. The data bases that we have used are medline and psyclit. Keywords have been chosen according to : pharmacological considerations (psychotropic, psychoactive drugs, psychopharmacology) and clinical symptoms (autism, automutilations, aggressive behavior, and hyperactivity). Hypothesis of a dysfunction in the neuromediation systems in autism-Many studies exist about biochemical abnormalities in autism. As in schizophrenia and mental retardation, dysfunctions of the neuromediation systems are considered to be etiological factors. In 30 % of people with autism the most regular dysfunction is the increase of serotonine. This led to the serotoninergic hypothesis in autism and to the use of active drugs in the serotonine system. However, the presence of other neurometabolic abnormalities also motivates the use of drugs, supposed to be active in other neuromediation systems. Pharmacological treatments in autism-Category I 1 Active drugs in the dopamine system. Haloperidol (Dopamine antagonist) : The effects of this molecule have been broadly studied in autism. Results indicate high efficiency in some symptoms of autism (lack in social behaviour, stereotypical behaviour) and in behavioural impairments that may be associated with autism (aggressive behaviour, hyperactivity). Its side effects, particulary the risk of late dyskinesy, make atypical antiosychotics preferable because of their lower risks. Risperidone (Dopamine and serotonine antagonist) : Among several studies only few have been controlled. They indicate that Risperidone has positive effects on the behaviour and is quite well tolerated. 2 Active drugs in the serotonine system. Clomipramine : after promising results, the medium-term efficiency has decreased and severe side effects have limited its use. Fluvoxamine, Fluoxetine, Sertraline (Specific serotonine drugs) : Their efficiency has been mainly tested through open studies and their results are contrasted. In some cases, social behaviours have improved and aggressiveness and stereotyped behaviours have decreased. Fenfluramine : at present, this drug is removed from the market. Yet, some studies have suggested that it improves behavioural disturbances as well as performances in autism. 3 Active drugs in the opiate system. Naltrexone : Several controlled studies have indicated an improvement in social and aggressive behaviours. Neveltheless, these studies have used small size sample and have not been replicated. Category II. This category correspond to drugs supposed to be active on neurochemical disturbances found in autism but their target symptoms are not autism specific signs as defined by the ICD 10. Buspirone : This serotonine agonist may have a good impact on emotional disorders and sleeping confusions. Methylphenidate : Mostof the current studies about this noradrenergic drug concern children. The results are variable. Paradoxical effects may exist in children with severe mental retardation. Propanolol: Some isolated studies habe reported its efficiency on behavioural disturbances. Clonidine: This adrenergic drug treats efficiently some cases of aggressive behaviour and hyperactivity. Category III This category contains a wide range of drugs, vitamins or method used in autism after sporadic observations of their positive effects. Secretine: An important improvement has been reported in isolated cases. However, controlled studies in children do not confirm these results. Vitamines B6, B 12 and Magnesium: An improvement in socialization and in behavioural disorders have been reported in some cases, but these results are not yet confirmed. Lithium, Carbamazepine, Valproate : Results of some case studies have found it to be efficient in cyclic disorders. Gluten and casein free diet: An improvement of social behaviour have been reported by some parents after these diets. No controlled study has validated this observation. Conclusion-There is no consensus on the use of psychopharmacological treatments in autism. Although there exist many clinical observations, only few controlled studies have validated the efficiency and safely of these treatments. At the present time and until having sufficient studies, drugs are generally limited to severe disorders, for which usual psycho-educational approaches are insufficient. C1 CHU Montpellier, SMPEA Peyre Plantade, F-34295 Montpellier 5, France. 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