FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Parker, SW Nelson, CA AF Parker, SW Nelson, CA CA Bucharest Early Intervention Proj TI An event-related potential study of the impact of institutional rearing on face recognition SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID 6-MONTH-OLD INFANTS; FACIAL EXPRESSIONS; BRAIN; CHILDREN; DEPRIVATION; CHILDHOOD; RESPONSES; DISORDER; EMOTION; AUTISM AB Event-related potentials (ERPs) were recorded to brief images of caregivers' and strangers' faces for 72 institutionalized children (IG), ages 7-32 months, and compared with ERPs from 33 children, ages 8-32 months, who had never been institutionalized. All children resided in Bucharest, Romania. Prominent differences in four ERP components were observed: early negative (N170), early positive (P250), midlatency negative (Nc), and positive slow wave (PSW). For all but the P250, the amplitude of these components was larger in the never instituionalized group than the institutionalized group; this pattern was reversed for the P250. Typical effects of the Nc (amplitude greater to stranger vs. caregiver) were observed in both groups; in contrast, the IG group showed an atypical pattern in the PSW. These findings are discussed in the context of the role of experience in influencing the neural circuitry putatively involved in recognizing familiar and novel faces. C1 Randolph Macon Coll, Dept Psychol, Ashland, VA 23005 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. RP Parker, SW (reprint author), Randolph Macon Coll, Dept Psychol, POB 5005, Ashland, VA 23005 USA. 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Psychopathol. PD SUM PY 2005 VL 17 IS 3 BP 621 EP 639 DI 10.1017/S0954579405050303 PG 19 WC Psychology, Developmental SC Psychology GA 990VT UT WOS:000233772000004 PM 16262985 ER PT J AU Dawson, G Webb, SJ Wijsman, E Schellenberg, G Estes, A Munson, J Faja, S AF Dawson, G Webb, SJ Wijsman, E Schellenberg, G Estes, A Munson, J Faja, S TI Neurocognitive and electrophysiological evidence of altered face processing in parents of children with autism: Implications for a model of abnormal development of social brain circuitry in autism SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Review ID HUMAN EXTRASTRIATE CORTEX; SPECTRUM DISORDER; FAMILY HISTORY; JOINT ATTENTION; YOUNG-CHILDREN; DIAGNOSTIC INTERVIEW; COGNITIVE PHENOTYPE; ASPERGERS-SYNDROME; FUSIFORM GYRUS; PRAIRIE VOLES AB Neuroimaging and behavioral studies have shown that children and adults with autism have impaired face recognition. Individuals with autism also exhibit atypical event-related brain potentials to faces, characterized by a failure to show a negative component (N170) latency advantage to face compared to nonface stimuli and a bilateral, rather than right lateralized, pattern of N170 distribution. In this report, performance by 143 parents of children with autism on standardized verbal, visual-spatial, and face recognition tasks was examined. It was found that parents of children with autism exhibited a significant decrement in face recognition ability relative to their verbal and visual spatial abilities. Event-related brain potentials to face and nonface stimuli were examined in 21 parents of children with autism and 21 control adults. Parents of children with autism showed an atypical event-related potential response to faces, which mirrored the pattern shown by children and adults with autism. These results raise the possibility that face processing might be a functional trait marker of genetic susceptibility to autism. Discussion focuses on hypotheses regarding the neurodevelopmental and genetic basis of altered face processing in autism. A general model of the normal emergence of social brain circuitry in the first year of life is proposed, followed by a discussion of how the trajectory of normal development of social brain circuitry, including cortical specialization for face processing, is altered in individuals with autism. The hypothesis that genetic-mediated dysfunction of the dopamine reward system, especially its functioning in social contexts, might account for altered face processing in individuals with autism and their relatives is discussed. C1 Univ Washington, Autism Ctr, Seattle, WA 98195 USA. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Vet Affairs Med Ctr, Seattle, WA 98108 USA. RP Dawson, G (reprint author), Univ Washington, Autism Ctr, Box 357920, Seattle, WA 98195 USA. 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PD SUM PY 2005 VL 17 IS 3 BP 679 EP 697 DI 10.1017/S0954579405050327 PG 19 WC Psychology, Developmental SC Psychology GA 990VT UT WOS:000233772000006 PM 16262987 ER PT J AU Simon, TJ Bish, JP Bearden, CE Ding, LJ Ferrante, S Nguyen, V Gee, JC McDonald-McGinn, DM Zackai, EH Emanuel, BS AF Simon, TJ Bish, JP Bearden, CE Ding, LJ Ferrante, S Nguyen, V Gee, JC McDonald-McGinn, DM Zackai, EH Emanuel, BS TI A multilevel analysis of cognitive dysfunction and psychopathology associated with chromosome 22q 11.2 deletion syndrome in children SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Review ID CARDIO-FACIAL SYNDROME; FUNCTIONAL MAGNETIC-RESONANCE; OBSESSIVE-COMPULSIVE DISORDER; ANTERIOR CINGULATE CORTEX; O-METHYLTRANSFERASE GENE; 22Q11.2 DELETION; VELOCARDIOFACIAL-SYNDROME; SPATIAL ATTENTION; WHITE-MATTER; NEUROPSYCHIATRIC DISORDERS AB We present a multilevel approach to developing potential explanations of cognitive impairments and psychopathologies common to individuals with chromosome 22q11.2 deletion syndrome. Results presented support our hypothesis of posterior parietal dysfunction as a central determinant of characteristic visuospatial and numerical cognitive impairments. Converging data suggest that brain development anomalies, primarily tissue reductions in the posterior brain and changes to the corpus callosum, may affect parietal connectivity. Further findings indicate that dysfunction in "frontal" attention systems may explain some executive cognition impairments observed in affected children, and that there may be links between these domains of cognitive function and some of the serious psychiatric conditions, such as attention-deficit/hyperactivity disorder, autism, and schizophrenia, that have elevated incidence rates in the syndrome. Linking the neural structure and the cognitive processing levels in this way enabled us to develop an elaborate structure/function mapping hypothesis for the impairments that are observed. 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PD SUM PY 2005 VL 17 IS 3 BP 753 EP 784 DI 10.1017/S0954579405050364 PG 32 WC Psychology, Developmental SC Psychology GA 990VT UT WOS:000233772000010 PM 16262991 ER PT J AU Waltz, M AF Waltz, M TI Reading case studies of people with autistic spectrum disorders: a cultural studies approach to issues of disability representation SO DISABILITY & SOCIETY LA English DT Article AB Autistic spectrum disorders have been described, defined and differentiated from other neurological conditions primarily on the basis of case studies. A small group of highly influential case studies forms a core narrative of autism, which is challenged by other narratives. In this research, analytical techniques from cultural studies are used to uncover the social construction of autism through the production and interpretation of these narratives. 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Soc. PD JUN PY 2005 VL 20 IS 4 BP 421 EP 435 DI 10.1080/09687590500086575 PG 15 WC Rehabilitation; Social Sciences, Interdisciplinary SC Rehabilitation; Social Sciences - Other Topics GA 930UC UT WOS:000229441600005 ER PT J AU Yilmaz, I Birkan, B Konukman, F Erkan, M AF Yilmaz, I Birkan, B Konukman, F Erkan, M TI Using a constant time delay procedure to teach aquatic play skills to children with autism SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article; Proceedings Paper CT Annual Convention for American Alliance of Health Physical Education Recreation and Dance CY APR, 2002 CL Philadelphia, PA ID INTELLECTUAL DISABILITIES; LEISURE SKILLS; ADOLESCENTS; MODERATE; PERFORMANCE; RESPONSES; STUDENT; PROGRAM; ADULTS AB Effects of a constant time delay procedure on aquatic play skills of children with autism was investigated. A single subject multiple probe model across behaviors with probe conditions was used. Participants were four boys, 7-9 years old. 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PD JUN PY 2005 VL 40 IS 2 BP 171 EP 182 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 931ZM UT WOS:000229524000007 ER PT J AU Ayres, KM Langone, J AF Ayres, KM Langone, J TI Intervention and instruction with video for students with autism: A review of the literature SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID PURCHASING SKILLS; CHILDREN; SELF; SETTINGS AB Efficacy research on video based instruction for children with autism is a promising area for practitioners and researchers. Researchers are successfully using video to teach a variety of social and functional skills. This literature review synthesizes these findings and examines critical features of each of the studies that contribute most to the ways of educators, care givers and others can best employ video to teach young people with autism. 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PD JUN PY 2005 VL 40 IS 2 BP 183 EP 196 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 931ZM UT WOS:000229524000008 ER PT J AU Danielsson, S Gillberg, IC Billstedt, E Gillberg, C Olsson, I AF Danielsson, S Gillberg, IC Billstedt, E Gillberg, C Olsson, I TI Epilepsy in young adults with autism: A prospective population-based follow-up study of 120 individuals diagnosed in childhood SO EPILEPSIA LA English DT Article DE epilepsy; seizures; autism; outcome ID MENTALLY-RETARDED CHILDREN; SPECTRUM DISORDERS; ACTIVE EPILEPSY; SEIZURE DISORDERS; INFANTILE-AUTISM; CLASSIFICATION; EPIDEMIOLOGY; PREVALENCE; ABNORMALITIES; RETARDATION AB Purpose: Little is known about the long-term outcome of epilepsy in autism and the epilepsy characteristics of adults with autism. This prospective population-based study was conducted in an attempt to point out differences on a group basis between adults with autism with or without epilepsy, and to describe the occurrence, the seizure characteristics, and the outcome of epilepsy in autism. Methods: One hundred eight of 120 individuals with autism diagnosed in childhood and followed up prospectively for a period of 13-22 years were reevaluated at ages 17-40 years. As adults, the majority had mental retardation and autistic disorder or autistic-like condition. Interviews were performed with the caretakers of 42 of 43 individuals with a history of epilepsy, and their medical records were reviewed. Results: Adults with autism and mental retardation constituted a severely disabled group. On a group basis, both the cognitive level and the adaptive behavior level were lower in the epilepsy group than in the nonepilepsy group (p<0.05). In all, 38% had epilepsy. One third had epilepsy onset before age 2 years. Remission of epilepsy was seen in 16%. Partial seizures with or without secondarily generalized seizures were the dominating seizure type. Conclusions: In a community sample of individuals with autism followed up from childhood through to adult age, one of three had epilepsy since childhood/adolescence. Severe mental retardation and autism are significantly associated with epilepsy, especially in female patients. Seizure frequency has a great impact on the individuals' lives. Specialist medical care is needed in this severely communication-disabled population. C1 Queen Silvia Childrens Hosp, Child Neuropsychiat BNK, Dept Pediat, S-41118 Gothenburg, Sweden. Queen Silvia Childrens Hosp, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RP Danielsson, S (reprint author), Queen Silvia Childrens Hosp, Child Neuropsychiat BNK, Dept Pediat, Otterhallegatan 12A, S-41118 Gothenburg, Sweden. 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Sixty four autistic patients (mean age 9.4 +/- 5.6 years) were entered into a cluster analysis. The clustering analysis was based on MRI data. The clusters obtained did not differ significantly in the overall severity of autistic symptomatology as measured by the total score on the Childhood Autism Rating Scale (CARS). The clusters could be characterized as showing significant differences: Cluster 1: showed the largest sizes of the genu and splenium of the corpus callosum (CC), the lowest pregnancy order and the lowest frequency of facial dysmorphic features. Cluster 2: showed the largest sizes of the amygdala and hippocampus (HPC), the least abnormal visual response on the CARS, the lowest frequency of epilepsy and the least frequent abnormal psychomotor development during the first year of life. Cluster 3: showed the largest sizes of the caput of the nucleus caudatus (NC), the smallest sizes of the HPC and facial dysmorphic features were always present. Cluster 4: showed the smallest sizes of the genu and splenium of the CC, as well as the amygdala, and caput of the NC, the most abnormal visual response on the CARS, the highest frequency of epilepsy, the highest pregnancy order, abnormal psychomotor development during the first year of life was always present and facial dysmorphic features were always present. This multidisciplinary approach seems to be a promising method for subtyping autism. C1 Charles Univ, Sch Med 2, Dept Child Psychiat, Prague 15006, Czech Republic. Charles Univ, Sch Med 2, Dept Imaging Methods, Prague 15006, Czech Republic. Charles Univ, Sch Med 2, Dept Child Neurol, Prague 15006, Czech Republic. Charles Univ, Sch Med 2, Inst Biol & Med Genet, Prague 15006, Czech Republic. Acad Sci Czech Republ, Inst Psychol, Brno 60200, Czech Republic. RP Hrdlicka, M (reprint author), Charles Univ, Sch Med 2, Dept Child Psychiat, V Uvalu 84, Prague 15006, Czech Republic. 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Three distinct clusters have been identified within the OCD spectrum, i.e. disorders concerning preoccupations with bodily sensations or appearance, impulsive disorders, and neurologically based disorders, and these share phenotypic features. Using one example from each of these clusters, body dysmorphic disorder (BDD), pathological gambling ( PG) and autism, respectively, the phenomenology, neurobiology and pharmacotherapy indicates that specific biological factors are shared by OCD and by these disorders and correlate with the severity of repetitive behaviours. Thus, in common with OCDs, in BDD there is increased activity in the limbic regions; in PG there is evidence of deficiencies in 5-HT function and receptors; and in autism there are restricted interests and repetitive behaviours which may be influenced by serotonergic mechanisms. Our findings support the notion that targeted treatments, for example using SSRIs, for the behaviours associated with these disorders are effective. Our review considers one SSRI treatment in particular, fluvoxamine, and conclusions should be drawn in light of this. Further testing of our hypothesis would be prudent to confirm its validity. C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. RP Hollander, E (reprint author), CUNY Mt Sinai Sch Med, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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A., 1999, J GAMBL STUD, V15, P289, DOI 10.1023/A:1023005115932 KOZAK MJ, 1994, BEHAV RES THER, V32, P343, DOI 10.1016/0005-7967(94)90132-5 Mundo E, 2001, HUM PSYCHOPHARM CLIN, V16, P461 Phillips KA, 1996, J CLIN PSYCHIAT, V57, P61 PHILLIPS KA, 1994, PSYCHOPHARMACOL BULL, V30, P179 Phillips KA, 1998, J CLIN PSYCHIAT, V59, P165, DOI 10.4088/JCP.v59n0404 PHILLIPS KA, 1995, J CLIN PSYCHIAT, V56, P41 Shaffer H J, 1996, J Gambl Stud, V12, P193, DOI 10.1007/BF01539174 Shaffer HJ, 1999, AM J PUBLIC HEALTH, V89, P1369, DOI 10.2105/AJPH.89.9.1369 Simansky KJ, 2004, PHYSIOL BEHAV, V82, P97, DOI 10.1016/j.physbeh.2004.04.028 Winstanley CA, 2004, NEUROPSYCHOPHARMACOL, V29, P1331, DOI 10.1038/sj.npp.1300434 Winstanley CA, 2004, PSYCHOPHARMACOLOGY, V176, P376, DOI 10.1007/s00213-004-1884-9 NR 33 TC 14 Z9 14 PU TAYLOR & FRANCIS AS PI OSLO PA PO BOX 12 POSTHUSET, NO-0051 OSLO, NORWAY SN 1365-1501 J9 INT J PSYCHIAT CLIN JI Int. J. Psychiat. Clin. PD JUN PY 2005 VL 9 IS 2 BP 79 EP 86 DI 10.1080/13651500510018347 PG 8 WC Psychiatry SC Psychiatry GA 934AQ UT WOS:000229679300002 PM 24930787 ER PT J AU De Cesarei, AO AF De Cesarei, AO TI Early trauma and narcissism-autism bipolarity SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Article; Proceedings Paper CT IJP Rio Conference CY JUN, 2004 CL Rio de Janeiro, BRAZIL DE early trauma; narcissism-autism; hard core; fear of breakdown; regression ID OBJECT AB The analyst makes a series of considerations taken-a posteriori-from the analysis of a small number of patients. These patients have saved themselves from an early narcissistic catastrophe by developing precocious mental processes, while affective relationships rudimentarily repeat the impact with the original trauma. Primitive defences, essentially denial and vertical splitting, dissociate the tear in the psyche and structure a 'narcissism-autism bipolarity, revealed in aspects of the character which oblige the patient to automatically repeat a single matrix of experience. In therapy, it is necessary to construct a first time of the trauma, by finding and linking threads of the primary relationship and strengthening them in the analytic relationship. This reconstruction of the background, a screen to project what had originally been rejected, is the prerequisite for coming out, in deferred action, from the hold of the pathological identifications. The author dedicates particular attention to the undifferentiated background, the nature-environment torn by the trauma, and to the need to reconstruct this fabric of experience in the analytical relationship, as a fundamental element to the recomposition of the dissociated nuclei. In the clinical case, the analyst describes in particular how the analyst words encounter an unbridgeable gap, a failure in the capacity for representation when opening the autistic nucleus. Through a regression lasting for about a year a patient was able to live the experience of primitive agonies' and that of an unbearable helplessness and, at the same time, was able to feel how the analyst supported her sense of existence. Subsequently, the patient was able to give shape, through visual images, to deep states of being and start the process of metabolising and symbolising the trauma. RP De Cesarei, AO (reprint author), Via B Varisco 33-A, I-25123 Brescia, Italy. EM anna.oliva@tin.it CR Alvarez A, 1992, LIVE CO PSYCHOANALYT BICK E, 1968, INT J PSYCHOANAL, V49, P484 BOSCHAN PJ, 1987, INT J PSYCHOANAL, V68, P109 Cohen D, 1996, INT J PSYCHOANAL, V77, P913 CONROTTO F, 1987, NARCISSIMO RELAZIONE, P13 CORREALE A, 2001, BORDERLINE SFONDO PS FERRARO F, 1995, FANTASIA REALTA RELA, P33 Ferro A., 1996, ANAL CONSULTING ROOM Freud S., 1941, SE, V23, P299 Freud S., 1923, STANDARD EDITION, V19, P12 Freud S., 1937, STANDARD EDITION, V23, P216 FREUD S., 1921, STANDARD EDITION, V18, P69 GADDINI E, 1969, INT J PSYCHOANAL, V50, P475 GENOVESE C, 1991, PROSPETTIVE PSICHOAN, V9, P265 GOMBEROFF MJ, 1990, INT J PSYCHOANAL, V71, P249 Green A, 2001, LIFE NARCISSISM DEAT Greenacre P, 1952, TRAUMA GROWTH PERSON INNESSMITH J, 1987, INT J PSYCHOANAL, V68, P405 KLEIN S, 1980, INT J PSYCHOANAL, V61, P395 Kohut H., 1971, ANAL SELF MALDONADO JL, 1987, INT J PSYCHOANAL, V68, P379 Mitrani J, 1998, INT J PSYCHOANAL, V79, P301 NEGRINI SM, 1991, UNPUB CTR MIL PSIC NICOLAIDIS N, 1984, REPRESENTATION ESSAI Ogden T. H., 1986, MATRIX MIND OBJECT R PONTALIS JB, 1981, FRONTIERS PSYHCOANAL Racamier PC, 1992, GENIE ORIGINES PSYCH Rosenfeld HA, 1987, IMPASSE INTERPRETATI Tustin F, 1986, AUTISTIC BARRIERS NE Tustin F., 1981, AUTISTIC STATES CHIL Winnicott D. W., 1971, PLAYING REALITY, P111 Winnicott D. W., 1971, PLAYING REALITY, P65 WINNICOTT DW, 1974, BRIT SCH PSYCHOANALY, P173 WINNICOTT DW, 1958, PAEDIAT PSYHCOANALYS Winnicotts D. W., 1965, MATURATIONAL PROCESS, P179 NR 35 TC 2 Z9 2 PU INST PSYCHO-ANALYSIS PI LONDON PA BYRON HOUSE, 112A-114 SHIRLAND RD, LONDON W9 2EQD, ENGLAND SN 0020-7578 J9 INT J PSYCHOANAL JI Int. J. Psychoanal. PD JUN PY 2005 VL 86 BP 657 EP 675 PN 3 PG 19 WC Psychology, Psychoanalysis SC Psychology GA 936OQ UT WOS:000229865700006 PM 16096069 ER PT J AU De Ahumada, LCB Ahumada, JL AF De Ahumada, LCB Ahumada, JL TI From mimesis to agency: Clinical steps in the work of psychic two-ness SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Article; Proceedings Paper CT IJP Rio Conference CY JUN, 2004 CL Rio de Janeiro, BRAZIL DE autism; childhood autism; mimetic autism; pseudostupidity; trauma; cumulative trauma; precursor object; mind-blindness; crisis of twoness; symbol formation AB In this paper through the study of the clinical process of a girl starting treatment at the age of 3 years 10 months, who was thought of as a 'dummy' by her family and who came for consultation when the assumed genetic aetiology was questioned, the authors build upon Tustin's contributions on the context of togetherness and the crisis of two-ness, and upon Eugenio and Renata Gaddini's on the precursor object. The mimetic phenomena enacted with an older brother and at the kindergarten are found to result from cumulative trauma at her contacting a loving but mind-blind mother After an initial stage of transference autism, enactment in the session of the traumatic situation was the first step in surmounting her autistic pseudo-stupidity. Mimetic transference dynamics took place principally at the level of the gaze, leading to the unfolding of the work of two-ness to a differentiation from the analyst as psychic breast, on the road to symbol formation and personal agency. RP Ahumada, JL (reprint author), Av Heras 3898 Tercer Piso H, Buenos Aires, DF, Argentina. EM jahumada@elsitio.net CR AHUMADA JL, 1990, INT REV PSYCHO-ANAL, V17, P177 AHUMANDA JL, 1980, LOGICS MIND CLIN VIE AHUMANDA JL, 2001, LOGICS MIND CLIN VIE ALVAREZ A, 1995, ENCOUNTERS AUTISTIC Balint Michael, 1968, BASIC FAULT THERAPEU Bion W., 1962, LEARNING EXPERIENCE Bion WR, 1965, TRANSFORMATIONS Bleger J., 1967, SIMBIOSIS AMBIGUEDAD COWLEY G, 2000, NEWSWEEK 0731, P44 De Ahumada LCB, 2003, INT J PSYCHOANAL, V84, P291 ETCHEGOYEN RH, 2002, PENSER LIMITES ESSAI FERENCZI S, 1932, FINAL CONTRIBUTIONS FERENCZI S, 1909, 1 CONTRIBUTIONS PSYC Freud Anna, 1936, EGO MECH DEFENCE Freud S., 1920, SE Freud S, 1923, STANDARD EDITION, V18, P235 Freud Sigmund, 1957, STANDARD EDITION, V11, P63 GADDINI E, 1995, ENCOUNTERS AUTISTIC GADDINI E, 1984, IPA MONOGRAPH, V4 KLEIN S, 1980, INT J PSYCHOANAL, V61, P395 Kohut H, 1971, ANAL SELF SYSTEMATIC MAHELR M, 1975, PSYCHOL BIRTH HUMAN MAHLER MS, 1958, INT J PSYCHOANAL, V39, P77 MATTELBANCO I, 1988, THIKING FEELING BEIN MATTELBANCO I, 1975, UNCONSCIOUS INFINITE MONEYKYRLE R, 1968, COLLECTED PAPERS R M Searles H, 1965, COLLECTED PAPERS SCH Symington N., 1993, NARCISSISM NEW THEOR Tustin F, 1986, AUTISTIC BARRIERS NE Tustin F., 1981, AUTISTIC STATES CHIL TUSTIN F, 1988, INT REV PSYCHO-ANAL, V15, P93 NR 31 TC 3 Z9 3 PU INST PSYCHO-ANALYSIS PI LONDON PA BYRON HOUSE, 112A-114 SHIRLAND RD, LONDON W9 2EQD, ENGLAND SN 0020-7578 J9 INT J PSYCHOANAL JI Int. J. Psychoanal. PD JUN PY 2005 VL 86 BP 721 EP 736 PN 3 PG 16 WC Psychology, Psychoanalysis SC Psychology GA 936OQ UT WOS:000229865700009 ER PT J AU Lee, L Harkness, KL Sabbagh, MA Jacobson, JA AF Lee, L Harkness, KL Sabbagh, MA Jacobson, JA TI Mental state decoding abilities in clinical depression SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE major depression; theory of mind; mental state decoding ID HIGH-FUNCTIONING AUTISM; RATING-SCALE; ASPERGERS-SYNDROME; FACIAL EXPRESSION; NORMAL ADULTS; MIND; SCHIZOPHRENIA; RECOGNITION; PEOPLE; INVENTORY AB Background: Depression is associated with profound impairments in social functioning. Past research and theory suggests that these impairments may be related to a difficulty in the ability of depressed individuals to identify and decode others' social cues. However, the nature of this difficulty is equivocal. This investigation is the first to adopt a theory-of-mind framework to examine unipolar depressed individuals' ability to identify complex mental states from eye expressions. Methods: Women with unipolar clinical depression (N = 52) and nondepressed controls (N = 30) completed the "Reading the Mind in the Eyes Task" (Baron-Cohen, S., Wheelwright, S., Hill, J., Raste, Y., Plumb, I., 200 1. The "Reading the Mind in the Eyes" test revised version: a study with normal adults, and adults with Asperger syndrome or high-functioning autism. J. Child Psychol. Psychiatry, 42, 241-251.). All participants also completed self-report measures assessing depressive and anxious symptoms. Results: Depressed women were significantly impaired in their ability to identify mental states in the Eyes task compared to nondepressed participants. This difference remained after controlling for anxiety and was stronger for the affective than the somatic symptoms of depression. Limitations: The present study was limited by its sample size, resulting in low power for some comparisons. In addition, the study is limited by its use of a heterogeneous depressed sample, including outpatients and volunteers from the community, as well as its use of only female participants. Conclusions: Our results demonstrate that severely depressed individuals are significantly impaired in their ability to decode others' mental states. We suggest that strategies based on improving basic theory-of-mind reasoning could be incorporated into current therapeutic interventions for depressed individuals to ameliorate their understanding and interpretation of social information. (c) 2005 Elsevier B.V All rights reserved. C1 Queens Univ, Dept Psychol, Kingston, ON K7L 3N6, Canada. RP Lee, L (reprint author), Queens Univ, Dept Psychol, Kingston, ON K7L 3N6, Canada. 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Affect. Disord. PD JUN PY 2005 VL 86 IS 2-3 BP 247 EP 258 DI 10.1016/j.jad.2005.02.007 PG 12 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 936TX UT WOS:000229879400015 PM 15935244 ER PT J AU Volkert, VM Lerman, DC Vorndran, C AF Volkert, VM Lerman, DC Vorndran, C TI The effects of reinforcement magnitude on functional analysis outcomes SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; developmental disabilities; functional analysis; reinforcement magnitude ID SELF-INJURIOUS-BEHAVIOR; DISRUPTIVE CLASSROOM-BEHAVIOR; WITHIN-SESSION PATTERNS; OPERANT RESPONSE RATES; DEVELOPMENTAL-DISABILITIES; ESTABLISHING OPERATIONS; DESTRUCTIVE BEHAVIOR; ABERRANT BEHAVIOR; SCHEDULES; CHILDREN AB The duration or magnitude of reinforcement has varied and often appears to have been selected arbitrarily in functional analysis research. Few studies have evaluated the effects of reinforcement magnitude on problem behavior, even though basic findings indicate that this parameter may affect response rates during functional analyses. In the current Study, 6 children with autism or developmental disabilities who engaged in severe problem behavior were exposed to three separate functional analyses, each of which varied in reinforcement magnitude. Results of these functional analyses were compared to determine if a particular reinforcement magnitude was associated with the most conclusive outcomes. In most cases, the same conclusion about the functions of problem behavior was drawn regardless of the reinforcement magnitude. C1 Louisiana State Univ, Baton Rouge, LA 70803 USA. RP Volkert, VM (reprint author), 82 Colleen Court, Baton Rouge, LA 70808 USA. 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Appl. Behav. Anal. PD SUM PY 2005 VL 38 IS 2 BP 147 EP 162 DI 10.1901/jaba.2005.111-04 PG 16 WC Psychology, Clinical SC Psychology GA 932IE UT WOS:000229546600002 PM 16033163 ER PT J AU Ahearn, WH Clark, KM DeBar, R Florentino, C AF Ahearn, WH Clark, KM DeBar, R Florentino, C TI On the role of preference in response competition SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; automatic reinforcement; preference assessment; response competition ID BEHAVIOR AB A duration-based preference assessment identified items that matched and did not match the sensory consequences hypothesized to maintain stereotypy. When evaluated in treatment, these items effectively competed with the occurrence of stereotypy, regardless of their sensory properties. It is suggested that relative preference, as measured in duration-based assessment, can be as significant as type of stimulation produced in interventions that reduce automatically reinforced problem behavior. C1 New England Ctr Children, Southborough, MA 01772 USA. RP Ahearn, WH (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. EM Bahearn@necc.org CR IWATA BA, 1994, J APPL BEHAV ANAL, V27, P215, DOI 10.1901/jaba.1994.27-215 Piazza CC, 2000, J APPL BEHAV ANAL, V33, P13, DOI 10.1901/jaba.2000.33-13 Piazza CC, 1998, J APPL BEHAV ANAL, V31, P165, DOI 10.1901/jaba.1998.31-165 Ringdahl JE, 1997, J APPL BEHAV ANAL, V30, P203, DOI 10.1901/jaba.1997.30-203 VOLLMER TR, 1994, J APPL BEHAV ANAL, V27, P331, DOI 10.1901/jaba.1994.27-331 Vollmer TR, 1995, J APPL BEHAV ANAL, V28, P561, DOI 10.1901/jaba.1995.28-561 NR 6 TC 25 Z9 25 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 2005 VL 38 IS 2 BP 247 EP 250 DI 10.1901/jaba.2005.36-04 PG 4 WC Psychology, Clinical SC Psychology GA 932IE UT WOS:000229546600011 PM 16033172 ER PT J AU Peyton, RT Lindauer, SE Richman, DM AF Peyton, RT Lindauer, SE Richman, DM TI The effects of directive and nondirective prompts on noncompliant vocal behavior exhibited by a child with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE vocal behavior; instructions; nondirective prompts; functional analysis; autism; developmental disabilities AB Results of an analogue functional analysis indicated that noncompliant vocal behavior exhibited by a young girl with autism was maintained by negative reinforcement. Follow-up analyses suggested that the immediate escape contingency assessed in the demand condition did not appear to maintain the behavior. Instead, noncompliant vocal behavior occurred in response to directive prompts. Nondirective prompts reduced noncompliant vocal behavior to near zero. C1 Kennedy Krieger Inst, Baltimore, MD 21205 USA. Univ Kansas, Lawrence, KS 66045 USA. Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA. RP Peyton, RT (reprint author), Kennedy Krieger Inst, 707 M Broadway, Baltimore, MD 21205 USA. EM peyton@kennedykrieger.org CR IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Piazza CC, 1997, J APPL BEHAV ANAL, V30, P705, DOI 10.1901/jaba.1997.30-705 Richman DM, 2001, J APPL BEHAV ANAL, V34, P289, DOI 10.1901/jaba.2001.34-289 Shirley MJ, 1999, J APPL BEHAV ANAL, V32, P201, DOI 10.1901/jaba.1999.32-201 NR 4 TC 4 Z9 4 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 2005 VL 38 IS 2 BP 251 EP 255 DI 10.1901/jaba.2005.125-04 PG 5 WC Psychology, Clinical SC Psychology GA 932IE UT WOS:000229546600012 PM 16033173 ER PT J AU Vlamings, PHJM Stauder, JEA van Son, IAM Mottron, L AF Vlamings, PHJM Stauder, JEA van Son, IAM Mottron, L TI Atypical visual orienting to gaze- and arrow-cues in adults with high functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Eye Direction Detector; autism; visual orienting; reaction times; asymmetry ID FACE PERCEPTION; JOINT ATTENTION; DIRECTION CUES; EYE-DIRECTION; CHILDREN; INFANTS; HUMANS; INDIVIDUALS; MECHANISMS; HYPOTHESIS AB The present study investigates visual orienting to directional cues ( arrow or eyes) in adults with high functioning autism (n = 19) and age matched controls ( n = 19). A choice reaction time paradigm is used in which eye- or arrow direction correctly ( congruent) or incorrectly ( incongruent) cues target location. In typically developing participants, the visual orienting re. ex is longer for eyes than for arrows. Right side cueing, but not left side cueing, induced a congruence effect for eyes, while this effect was evident for right as well as for left side arrow cues. In participants with autism the overall visual orienting reflex was not different between arrows and eyes and no laterality effect was found for eyes cueing. These findings suggest that, instead of a specific Eye Direction Detector persons with autism might have a general 'Symbol Direction Detector'. C1 Univ Maastricht, Fac Psychol, Biol Dev Psychol Sect, NL-6200 MD Maastricht, Netherlands. Hop Rivieres Prairies, Clin Specialisee Autisme, Montreal, PQ H1E 1A4, Canada. RP Stauder, JEA (reprint author), Univ Maastricht, Fac Psychol, Biol Dev Psychol Sect, POB 616, NL-6200 MD Maastricht, Netherlands. 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PD JUN PY 2005 VL 35 IS 3 BP 267 EP 277 DI 10.1007/s10803-005-3289-y PG 11 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200002 PM 16119468 ER PT J AU Goldberg, MC Mostofsky, SH Cutting, LE Mahone, EM Astor, BC Denckla, MB Landa, RJ AF Goldberg, MC Mostofsky, SH Cutting, LE Mahone, EM Astor, BC Denckla, MB Landa, RJ TI Subtle executive impairment in children with autism and children with ADHD SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE CANTAB((R)); high functioning autism; HFA; ADHD; executive function; working memory ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; FRONTAL-LOBE; OCULOMOTOR ABNORMALITIES; NONRETARDED-CHILDREN; COGNITIVE DEFICITS; READING-DISABILITY; INHIBITORY CONTROL; TOURETTE-SYNDROME; PERFORMANCE AB Background: The executive functions of inhibition, planning, flexible shifting of actions, and working memory are commonly reported to be impaired in neurodevelopmental disorders. Method: We compared these abilities in children (8-12 years) with high functioning autism (HFA, n = 17), attention deficit-hyperactivity disorder (ADHD, n = 21) and healthy controls ( n = 32). Response inhibition was assessed using the Stroop Color and Word Test ( Golden, 1978). Problem solving, set- shifting, and nonverbal memory were assessed using three tasks, respectively, from the CANTAB (R) ( Cambridge Cognition, 1996): the Stockings of Cambridge task; the Intra-Dimensional/Extra-Dimensional set- shifting task; and the Spatial Working Memory task (SWM) with tokens hidden behind 3, 4, 6, and 8 boxes. Results: There were no group differences on the response inhibition, planning, or set- shifting tasks. On the SWM task, children with HFA made significantly more between-search errors compared with controls on both the most difficult problems (8-box) and on the mid-difficulty problems (6-box); however, children with ADHD made significantly more errors compared to controls on the most difficult (8-box) problems only. Conclusion: Our findings suggest that spatial working memory is impaired in both ADHD and HFA, and more severely in the latter. More detailed investigation is needed to examine the mechanisms that differentially impair spatial working memory, but on this set of tasks there appears to be sparing of other executive functions in these neuropsychiatric developmental disorders. C1 Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21218 USA. RP Goldberg, MC (reprint author), Kennedy Krieger Inst, 707 N Broadway,Suite 232, Baltimore, MD USA. 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PD JUN PY 2005 VL 35 IS 3 BP 279 EP 293 DI 10.1007/s10803-005-3291-4 PG 15 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200003 PM 16119469 ER PT J AU Beglinger, L Smith, T AF Beglinger, L Smith, T TI Concurrent validity of social subtype and IQ after early intensive behavioral intervention in children with autism: A preliminary investigation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; treatment; IQ; social; subtype ID PERVASIVE DEVELOPMENTAL DISORDER; SEVERE MENTAL-RETARDATION; CLASSIFICATION; QUESTIONNAIRE; IMPAIRMENTS; SUBGROUPS; AGE AB Three subtypes of autism based on social style have been proposed by Wing: active-but-odd, passive, or aloof. Previous research has shown evidence of an association between IQ and Wing subtype in untreated children and adults. Because IQ changes can accompany behavioral treatment, but often only for a subset of children, social subtype may be related to treatment responsiveness. We administered a social subtyping measure, the Wing Subgroups Questionnaire ( WSQ), at various points in treatment to younger children than previously studied with autism in early, intensive behavioral intervention ( EIBI). Thirty-seven children in EIBI (aged 39-71 months, amount of EIBI 0-44 months) were assessed to determine whether Wing's three proposed subtypes were found in this sample and whether subtypes were associated with current IQ and change in IQ after a period of EIBI. Results confirmed that all three subtypes were present and correlated with IQ after a period of intervention, as well as with change in IQ. Participants classified as aloof had significantly lower IQ scores and changes in IQ after EIBI than other children. Future studies should extend these findings by examining whether social subtype at pretreatment predicts EIBI outcome. C1 Washington State Univ, Pullman, WA 99164 USA. Univ Rochester, Med Ctr, Rochester, NY 14642 USA. 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Autism Dev. Disord. PD JUN PY 2005 VL 35 IS 3 BP 295 EP 303 DI 10.1007/s10803-005-3292-3 PG 9 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200004 PM 16119470 ER PT J AU O'Reilly, M Sigafoos, J Lancioni, G Edrisinha, C Andrews, A AF O'Reilly, M Sigafoos, J Lancioni, G Edrisinha, C Andrews, A TI An examination of the effects of a classroom activity schedule on levels of self-injury and engagement for a child with severe autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; challenging behavior; self-injury; functional analysis; individualized schedules; curriculum ID BEHAVIOR AB We examined the effects of an individualized schedule on levels of engagement and self-injury for a student with severe autism. We first conducted a series of functional analyses to identify contexts in which self-injury occurred in his classroom. Results of the functional analyses suggested that self-injury was associated with academic demands. Self-injury rarely occurred during the play and no interaction conditions (i.e., when the teacher was present but did not attend to him) of the functional analysis. Furthermore, when the functional analysis conditions were organized according to a specific schedule ( no interaction-play-demand) self-injury did not occur. This schedule of activities was then evaluated within the context of his regular curriculum and produced substantial reductions in self-injury and increases in engagement. Positive results maintained for up to five months following the assessment. These findings seem to indicate that functional analysis methodologies might provide helpful information when developing individualized schedules for students who may not have the skills to comprehend and follow a schedule. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. Univ Bari, Dept Psychol, I-70100 Bari, Italy. Autist Treatment Ctr, San Antonio, TX 78247 USA. RP O'Reilly, M (reprint author), Univ Texas, Dept Special Educ, 1 Univ Stn D5300, Austin, TX 78712 USA. EM markoreilly@mail.utexas.edu CR BROWN F, 1991, J ASSOC PERS SEVERE, V16, P75 CARR EG, 1976, J ABNORM CHILD PSYCH, V4, P139, DOI 10.1007/BF00916518 Heflin L.J., 1998, FOCUS AUTISM OTHER D, V13, P194, DOI DOI 10.1177/108835769801300401 Horner RH, 2002, J AUTISM DEV DISORD, V32, P423, DOI 10.1023/A:1020593922901 IWATA B, 1994, ANAL INTERVENTION DE, V2, P1 Iwata B. A., 1990, PERSPECTIVES USE NON, P301 Knoster TP, 2000, J ASSOC PERS SEVERE, V25, P201, DOI 10.2511/rpsd.25.4.201 Mesibov GB, 2002, J POSIT BEHAV INTERV, V4, P73, DOI 10.1177/109830070200400202 Schopler E., 1988, CHILDHOOD AUTISM RAT SIGAFOOS J, 2003, CHALLENGING BEHAV DE Sparrow S, 1984, VINELAND ADAPTIVE BE STURMEY P, 1995, RES DEV DISABIL, V16, P269, DOI 10.1016/0891-4222(95)00014-E NR 12 TC 26 Z9 26 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 2005 VL 35 IS 3 BP 305 EP 311 DI 10.1007/s10803-005-3294-1 PG 7 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200005 PM 16119471 ER PT J AU Mandell, DS Walrath, CM Manteuffel, B Sgro, G Pinto-Martin, J AF Mandell, DS Walrath, CM Manteuffel, B Sgro, G Pinto-Martin, J TI Characteristics of children with autistic spectrum disorders served in comprehensive community-based mental health settings SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; asperger's disorder; child abuse; community mental health services; behavioral disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSIS; ABUSE; ADOLESCENTS; PREVALENCE; ACCURACY; SERVICES; IMPACT AB This study describes the characteristics of children with autistic spectrum disorders (ASD) receiving treatment in community mental health settings. Data from a national community mental health initiative was used to identify children who had received a primary diagnosis of ASD. These children were compared with children with other diagnoses on socio-demographic and psychosocial characteristics, presenting problems and service histories. Regardless of diagnosis, children were most often referred to service because of disruptive behaviors. Children with ASD were less likely to be referred for drug use, truancy or running away, but were more likely to be referred for social interaction difficulties and strange behavior. Many children had family histories of mental illness, substance abuse and domestic violence. Implications of these findings are discussed in detail. C1 Univ Penn, Sch Med, Ctr Mental Hlth Policy & Serv Res, Philadelphia, PA 19104 USA. Univ Penn Med, ORC Macro, Philadelphia, PA USA. Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. RP Mandell, DS (reprint author), Univ Penn, Sch Med, Ctr Mental Hlth Policy & Serv Res, 3535 Mkt St,3rd Floor, Philadelphia, PA 19104 USA. EM mandelld@mail.med.upenn.edu RI Mandelld, David/A-1044-2007; Mandell, David/H-2730-2012 OI Mandell, David/0000-0001-8240-820X CR Aman MG, 2000, J AUTISM DEV DISORD, V30, P451, DOI 10.1023/A:1005559725475 American Psychiatric Association, 1994, DIAGN STAT MAN METN AMMERMAN RT, 1989, CHILD ABUSE NEGLECT, V13, P335, DOI 10.1016/0145-2134(89)90073-2 AMMERMAN RT, 1994, J AM ACAD CHILD PSY, V33, P567, DOI 10.1097/00004583-199405000-00015 Angold A, 1998, AM J PUBLIC HEALTH, V88, P75, DOI 10.2105/AJPH.88.1.75 BIRENBAUM A, 1990, MONOGRAPHS AM ASS ME, V14, P1 Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Center for Mental Health Services, 1999, ANN REP C EV COMPR C COOK EH, 1993, J AM ACAD CHILD PSY, V32, P1292, DOI 10.1097/00004583-199311000-00025 Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 Fendrich M, 1999, J AM ACAD CHILD PSY, V38, P147, DOI 10.1097/00004583-199902000-00013 Filipek PA, 2000, NEUROLOGY, V55, P468 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Hill A, 2001, PSYCHOPATHOLOGY, V34, P187, DOI 10.1159/000049305 Holden EW, 2001, J EMOT BEHAV DISORD, V9, P4, DOI 10.1177/106342660100900102 HOWLIN P, 1995, J AUTISM DEV DISORD, V25, P337, DOI 10.1007/BF02179372 Jacobson JW, 2000, J AUTISM DEV DISORD, V30, P585, DOI 10.1023/A:1005691411255 Jarbrink K, 2001, AUTISM, V5, P7, DOI 10.1177/1362361301005001002 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Mandell DS, 2002, J AM ACAD CHILD PSY, V41, P1447, DOI 10.1097/01.CHI.0000024863.60748.53 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 Mouridsen SE, 1999, PSYCHOPATHOLOGY, V32, P177, DOI 10.1159/000029087 PALFREY JS, 1987, J PEDIATR-US, V111, P651, DOI 10.1016/S0022-3476(87)80238-X PERKINS M, 1991, ARCH DIS CHILD, V66, P693 Roberts S, 2001, J AM ACAD CHILD PSY, V40, P1366, DOI 10.1097/00004583-200112000-00005 Stroul BA, 1986, SYSTEM CARE SEVERELY THARINGER D, 1990, CHILD ABUSE NEGLECT, V14, P301, DOI 10.1016/0145-2134(90)90002-B *US DEP ED, 2001, 23 ANN REP C IMPL IN Volkmar Fred, 1999, Journal of the American Academy of Child and Adolescent Psychiatry, V38, p32S Walrath C, 2003, J BEHAV HEALTH SER R, V30, P452, DOI 10.1007/BF02287432 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 Wu P, 1999, J AM ACAD CHILD PSY, V38, P1081, DOI 10.1097/00004583-199909000-00010 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 33 TC 26 Z9 26 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 2005 VL 35 IS 3 BP 313 EP 321 DI 10.1007/s10803-005-3296-z PG 9 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200006 PM 16119472 ER PT J AU Heidgerken, AD Geffken, G Modi, A Frakey, L AF Heidgerken, AD Geffken, G Modi, A Frakey, L TI A survey of autism knowledge in a health care setting SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; health care; survey; diagnosis; knowledge ID SCHIZOPHRENIA; EPIDEMIOLOGY AB The current study extends research by Stone [Cross-disciplinary perspectives on autism? Journal of Pediatric Psychology, 12, ( 1988) 615; A comparison of teacher and parent views of autism. Journal of Autism and Development Disorders, 18, ( 1988) 403] exploring the knowledge and beliefs about autism across multiple health care professions. One hundred and eleven CARD personnel (i.e., professional with the Center for Autism Related Disabilities, CARD), specialists (i.e., psychiatry, speech and language pathology, and clinical psychology), and primary health care providers (i.e., family practice, pediatrics, and neurology) completed a measure assessing knowledge of diagnostic criteria, course, treatment, and prognosis of autism. Results indicated that all three groups reflected accurate endorsement of the DSM-IV criteria. Primary health care providers and specialists were found to differentially endorse a variety of statements regarding prognosis, course, and treatment in comparison with CARD. Overall, primary providers demonstrated the greatest number of differences. Clinical implications and future recommendations are discussed. C1 Univ Florida, Dept Psychiat, Gainesville, FL 32610 USA. RP Heidgerken, AD (reprint author), Univ Florida, Dept Psychiat, Box 100234, Gainesville, FL 32610 USA. EM Amanda@psychiatry.ufl.edu CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BURKE JC, 1991, AM J MENT RETARD, V96, P37 Clark AF, 1998, J CHILD PSYCHOL PSYC, V39, P1071, DOI 10.1017/S0021963098003242 Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 FARBER JM, 1984, CLIN PEDIATR, V23, P199, DOI 10.1177/000992288402300401 Farrell PM, 2001, PEDIATRICS, V107, P1, DOI 10.1542/peds.107.1.1 Helps S, 1999, AUTISM, V3, P287, DOI 10.1177/1362361399003003006 KANER L, 1943, NERV CHILD, V2, P217 Konstantareas MM, 2001, J AUTISM DEV DISORD, V31, P19, DOI 10.1023/A:1005605528309 Lord C., 1997, HDB AUTISM PERVASIVE, P460 *NAT I CHILD HLTH, 2003, AUT FACTS Newsom C., 1998, TREATMENT CHILDHOOD, P416 RAPIN I, 1997, HDB AUTISM PERVASIVE, P847 Schopler E., 1988, CHILDHOOD AUTISM RAT Shah K, 2001, AUTISM, V5, P127, DOI 10.1177/1362361301005002003 STONE WK, 1987, J PEDIATR PSYCHOL, V21, P615 STONE WL, 1988, J AUTISM DEV DISORD, V18, P403, DOI 10.1007/BF02212195 Volkmar F. R., 1997, HDB AUTISM PERVASIVE, P5 Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 NR 21 TC 36 Z9 39 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 2005 VL 35 IS 3 BP 323 EP 330 DI 10.1007/s10803-005-3298-x PG 8 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200007 PM 16119473 ER PT J AU Woodbury-Smith, MR Robinson, J Wheelwright, S Baron-Cohen, S AF Woodbury-Smith, MR Robinson, J Wheelwright, S Baron-Cohen, S TI Screening adults for asperger syndrome using the AQ: A preliminary study of its diagnostic validity in clinical practice SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger Syndrome; Autism Quotient; high-functioning autism; screening; diagnosis; validity ID AUTISM-SPECTRUM QUOTIENT; FUNCTIONING AUTISM; DISORDERS; CHILDREN AB The Autism Spectrum Quotient (AQ) has been developed to measure the degree to which an adult with normal intelligence has autistic traits. In this paper it is evaluated for its potential as a screening questionnaire in clinical practice on one hundred consecutive referrals to a diagnostic clinic for adults suspected of having Asperger Syndrome or high functioning autism (AS/HFA). The results indicate that it has good discriminative validity and good screening properties at a threshold score of 26. The implications of these results are discussed. C1 Univ Cambridge, Dept Psychiat, Cambridge CB2 1TN, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Cambridge Lifespan Asperger Syndrome Serv, Cambridge, England. Autism Res Ctr, Cambridge, England. RP Woodbury-Smith, MR (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd POB 207900, New Haven, CT 06520 USA. EM marc.woodbury-smith@yale.edu CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th BARNARD J, 2001, IGNORED OR INELIGIBL Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Bishop DVM, 2004, J CHILD PSYCHOL PSYC, V45, P1431, DOI 10.1111/j.1469-7610.2004.00325.x Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x GARNETT M, 1995, 1995 AUSTR NAT AUT C Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MAYES SD, 2001, J ABNORM CHILD PSYCH, V3, P263 Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 Powell A., 2002, TAKING RESPONSIBILIT *STAT CORP, 2001, STAT VERS 7 Wing L., 1997, AUTISTIC SPECTRUM World Health Organization, 1992, 10 REV INT CLASS DIS NR 17 TC 187 Z9 188 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 2005 VL 35 IS 3 BP 331 EP 335 DI 10.1007/s10803-005-3300-7 PG 5 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200008 PM 16119474 ER PT J AU Werner, E Dawson, G Munson, J Osterling, J AF Werner, E Dawson, G Munson, J Osterling, J TI Variation in early developmental course in autism and its relation with behavioral outcome at 3-4 years of age SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; regression; early course; outcome; prognosis ID SPECTRUM DISORDER; EARLY RECOGNITION; INFANTILE-AUTISM; HOME VIDEOTAPES; ONSET; REGRESSION; CHILDREN; INFANCY AB The aims of the present study were to describe variations in the early course of development in autism by utilizing an in-depth parent interview that incorporated techniques to improve accuracy of parent recall, and to examine the relation between variations in early developmental course in autism and behavioral outcome at 3-4 years of age. The Early Development Interview, which consisted of questions about child's behavior in several domains from birth through 2 years of age, was created and administered to parents of 72 3-4-year- old children with autism spectrum disorder and 34 3-4-year- old children with developmental delay, who were matched on mental and chronological age, and 39 1-4-year-old typically developing children, who were matched to the clinical groups on mental age. At 3-4 years of age, children were administered standardized measures ( some clinician administered and some parent report); these included verbal and nonverbal IQ, autism symptom severity, and adaptive and aberrant behavior. Based on the Early Development Interview, children with autism spectrum disorder (ASD) were reported to have elevated symptoms in the social and regulatory domains by 3-6 months. By 12-15 months, parents of children with ASD reported significantly higher levels of social symptoms than parents of children with developmental delay. At 3-4 years of age, children with autism with early vs. late onset of symptoms, and with vs. without a history of loss of skills (regression) were not found to di. er on standardized tests of verbal and nonverbal IQ and observational measures of autism symptom severity. C1 Univ Washington, UW Autism Ctr, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. RP Dawson, G (reprint author), Univ Washington, UW Autism Ctr, Box 357920, Seattle, WA 98195 USA. CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BROWN J, 1995, J AUTISM DEV DISORD, V25, P305, DOI 10.1007/BF02179291 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 Dawson G, 2000, J APPL DEV PSYCHOL, V21, P299, DOI 10.1016/S0193-3973(99)00042-8 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 HARPER J, 1975, J AUTISM CHILD SCHIZ, V5, P25, DOI 10.1007/BF01537970 HOLLINGSHEAD, 1975, 4 FACTOR INDEX SOCIA HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 Kanner L, 1943, NERV CHILD, V2, P217 KELLER M, 1987, ARCH GEN PSYCHIAT, V44, P40 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x Maestro S, 1999, PSYCHOPATHOLOGY, V32, P292, DOI 10.1159/000029102 MULLEN EM, 1997, MANUAL MULLEN SCALES OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 Perneger TV, 1998, BRIT MED J, V316, P1236 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 SHROUT PE, 1979, PSYCHOL BULL, V86, P420, DOI 10.1037//0033-2909.86.2.420 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P717, DOI 10.1111/j.1469-7610.1989.tb00784.x VOLKMAR FR, 1985, AM J PSYCHIAT, V142, P1450 Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 NR 30 TC 97 Z9 101 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 2005 VL 35 IS 3 BP 337 EP 350 DI 10.1007/s10803-005-3301-6 PG 14 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200009 PM 16119475 ER PT J AU Billstedt, E Gillberg, C Gillberg, C AF Billstedt, E Gillberg, C Gillberg, C TI Autism after adolescence: Population-based 13- to 22-year follow-up study of 120 individuals with autism diagnosed in childhood SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; epidemiology; outcome; epilepsy; adolescence ID RECEPTIVE LANGUAGE DISORDER; EARLY ADULT LIFE; INFANTILE-AUTISM; SPECTRUM DISORDERS; ASPERGER-SYNDROME; CHILDREN; INTERVIEW; OUTCOMES; EPILEPSY AB Background: Prospective population-based follow-up study of 120 individuals with autism followed from childhood to adulthood. Methods: Individuals with autism, diagnosed in childhood, were followed prospectively for a period of 13-22 years and re-evaluated at ages 17-40 years. The instruments used at follow-up were the DISCO, WAIS-R, WISC-III, Vineland Adaptive Behavior Scales, psychiatric-medical examination and GAF-scale. A set of criteria was used for the classification of outcomes, taking into consideration employment, higher education/vocational training, independent living and peer relations. Results: Six of the 120 (5%) had died at the time of follow-up, and six declined participation. Overall outcome was poor in 78% of cases. Only four individuals were independent albeit leading fairly isolated lives. Childhood IQ-level was positively correlated with better adult outcome, as was the existence of some communicative phrase speech at age six years. Conclusions: Children with autism as diagnosed in the 1960s, 1970s, and 1980s may have an even worse psychosocial outcome than previously believed. C1 Queen Silvias Hosp Children & Adolescents, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RP Billstedt, E (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgatan 12, S-41119 Gothenburg, Sweden. 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Autism Dev. Disord. PD JUN PY 2005 VL 35 IS 3 BP 351 EP 360 DI 10.1007/s10803-005-3302-5 PG 10 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200010 PM 16119476 ER PT J AU Dunn, MA Bates, JC AF Dunn, MA Bates, JC TI Developmental change in neutral processing of words by children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE intelligence; shortforms; assessment ID EVENT-RELATED POTENTIALS; AUDITORY-EVOKED-POTENTIALS; HIGH-FUNCTIONING AUTISM; SENTENCE COMPREHENSION; BRAIN POTENTIALS; CATEGORIZATION SKILLS; TEMPORAL-LOBE; INFORMATION; DISORDERS; CLASSIFICATION AB This study examined the development of neural processing of auditorally presented words in high functioning children with autism. The purpose was to test the hypothesis that electrophysiological abnormalities associated with impairments in early cortical processing and in semantic processing persist into early adolescence in autistic individuals. Eighteen children with autism and 18 normally developing children participated in the study. Ten of the children in each group were 8-9 years old, and 8 in each group were 11-12 years old (n=36). Lists of words were presented auditorally; half were words belonging to a specified semantic category and half were words outside the category. Results revealed that while early cortical processing abnormalities appeared to resolve with development, children with autism in both age groups failed to exhibit differential semantic processing of in-versus out-of-category words. Further, while 8 year-olds with autism generated a large N4 ( a late cognitive ERP component, which is sensitive to semantic deviance from a context) to words in both stimulus classes the 11 year-olds showed attenuated N4 relative to normal controls in response to both stimulus types. An attempt is made to integrate findings with current cognitive theories toward a parsimonious explanation of semantic classification deficits in autism. C1 Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA. RP Dunn, MA (reprint author), Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA. 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PD JUN PY 2005 VL 35 IS 3 BP 361 EP 376 DI 10.1007/s10803-005-3304-3 PG 16 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200011 PM 16119477 ER PT J AU Sugie, Y Sugie, H Fukuda, T Ito, M Sasada, Y Nakabayashi, M Fukashiro, K Ohzeki, T AF Sugie, Y Sugie, H Fukuda, T Ito, M Sasada, Y Nakabayashi, M Fukashiro, K Ohzeki, T TI Clinical efficacy of fluvoxamine and functional polymorphism in a serotonin transporter gene on childhood autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; selective serotonin transporter inhibiter; serotonin transporter gene; 5-HTTLPR ID ANXIETY-RELATED TRAITS; WHOLE-BLOOD SEROTONIN; REGULATORY REGION; ALLELIC VARIATION; DOUBLE-BLIND; DISORDER; CHILDREN; ASSOCIATION; FLUOXETINE; JAPANESE AB We studied the correlation between response to fluvoxamine and serotonin transporter gene promoter region polymorphism (5-HTTLPR). Eighteen children with autistic disorder completed a 12-week double-blind, placebo-controlled, randomized crossover study of fluvoxamine. Behavioral assessments were obtained before and at 12 weeks of treatment. 5-HTTLPR (long (l) or short(s)), was analyzed by the PCR method. Ten out of 18 patients responded to fluvoxamine treatment; allele type analysis revealed that clinical global effectiveness was noted significantly more in the l allele than in the s allele. However, with respect to language use, a significant effectiveness was noted in the s allele. 5-HTTLPR may influence the individual responses to fluvoxamine administration. C1 Hamamatsu City Med Ctr Dev Med, Dept Pediat Neurol, Hamakita 4340023, Japan. Hamamatsu Univ Sch Med, Dept Pediat, Hamamatsu, Shizuoka 43131, Japan. Hamamatsu City Med Ctr Dev Med, Div Clin Psychol, Hamakita 4340023, Japan. RP Sugie, Y (reprint author), Hamamatsu City Med Ctr Dev Med, Dept Pediat Neurol, 775-1Takazono, Hamakita 4340023, Japan. 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Autism Dev. Disord. PD JUN PY 2005 VL 35 IS 3 BP 377 EP 385 DI 10.1007/s10803-005-3305-2 PG 9 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200012 PM 16119478 ER PT J AU Hardan, AY Jou, RJ Handen, BL AF Hardan, AY Jou, RJ Handen, BL TI Retrospective study of quetiapine in children and adolescents with pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE quetiapine; antipsychotic agents; autism; pervasive developmental disorder; children; adolescents ID PROLACTIN LEVELS; RISPERIDONE; SCHIZOPHRENIA; TOLERABILITY; HALOPERIDOL AB A retrospective study was conducted in a clinic specialized in treating individuals with developmental disabilities to examine the effectiveness and tolerability of quetiapine in children and adolescents with pervasive developmental disorders. Ten consecutive outpatients ( age = 12.0 +/- 5.1 years) treated with quetiapine ( dose = 477 +/- 212 mg, duration = 22.0 +/- 10.1 weeks) were identified and six were judged to be responders based on impressions from chart review and Conners Parent Scale (CPS). Improvements were observed in the conduct, inattention, and hyperactivity subscales of the CPS. Adverse events were mild with sedation being the most common, and no patient required treatment termination. Quetiapine may be beneficial in children and adolescents with pervasive developmental disorders, however open-label and double-blind, placebo-controlled studies are warranted. C1 Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, 3811 Ohara St, Pittsburgh, PA 15213 USA. EM hardanay@msx.upmc.edu CR ADITYANJEE A, 2002, J CLIN PSYCHIAT S13, V63, P32 Arvanitis LA, 1997, BIOL PSYCHIAT, V42, P233, DOI 10.1016/S0006-3223(97)00190-X David SR, 2000, CLIN THER, V22, P1085, DOI 10.1016/S0149-2918(00)80086-7 Findling RL, 2002, J CLIN PSYCHIAT, V63, P27 GOYETTE CH, 1978, J ABNORM CHILD PSYCH, V6, P221, DOI 10.1007/BF00919127 Guy W., 1976, ECDEU ASSESSMENT MAN Kleinberg DL, 1999, J CLIN PSYCHOPHARM, V19, P57, DOI 10.1097/00004714-199902000-00011 MALONE RP, 1991, PSYCHOPHARMACOL BULL, V27, P113 Martin A, 1999, J CHILD ADOL PSYCHOP, V9, P99, DOI 10.1089/cap.1999.9.99 McConville BJ, 2000, J CLIN PSYCHIAT, V61, P252 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Sadock BJ, 2001, KAPLAN SADOCKS POCKE Shaw JA, 2001, J CHILD ADOL PSYCHOP, V11, P415, DOI 10.1089/104454601317261591 Taylor DM, 2000, ACTA PSYCHIAT SCAND, V101, P416, DOI 10.1034/j.1600-0447.2000.101006416.x NR 14 TC 26 Z9 27 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 2005 VL 35 IS 3 BP 387 EP 391 DI 10.1007/s10803-005-3306-1 PG 5 WC Psychology, Developmental SC Psychology GA 946GA UT WOS:000230559200013 PM 16119479 ER PT J AU Towbin, KE Pradella, A Gorrindo, T Pine, DS Leibenluft, E AF Towbin, KE Pradella, A Gorrindo, T Pine, DS Leibenluft, E TI Autism spectrum traits in children with mood and anxiety disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRICALLY DISTURBED-CHILDREN; UNSUSPECTED LANGUAGE IMPAIRMENTS; DIAGNOSTIC OBSERVATION SCHEDULE; ADAPTIVE-BEHAVIOR SCALES; COMMUNICATION-CHECKLIST; SOCIAL-BEHAVIOR; INTERVIEW; PREVALENCE; INDIVIDUALS AB The autism spectrum disorders (ASDs) can present with symptoms commonly found in mood and anxiety disorders. The Social Communication Questionnaire (SCQ), Children's Communication Checklist (CCC-2), and the Social Reciprocity Scale (SRS) were used to screen children in a mood disorders research clinic setting for symptoms of ASD. Ninety-three patients (mean age, 12.7 +/- 2.8 years; percent male, 63%) completed at least one scale, and 50 children completed all three. The prevalence of those screening positive for a possible ASD on one instrument was 62% and on all three measures was 8%. Fifty-seven percent (n = 21/37; odds ratio, 4.59 [95% confidence interval (CI) = 1.40-15.111) of those scoring in the "ASD-likely" range on the SRS scored in that range on the CCC-2. Only 16% (n = 6/37; odds ratio, not significant (NS)) of those scoring in the ASD-likely range on the SRS, and 14% (n = 5/37; odds ratio, NS) of those scoring in the ASD-likely range on the CCC-2, scored similarly on the SCQ. These results demonstrate a need to develop valid and reliable instruments to screen for ASDs in children presenting outside of ASD clinics. C1 NIMH, Mood & Anxiety Disorders Program, Intramural Res Program, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Towbin, KE (reprint author), NIMH, Mood & Anxiety Disorders Program, Intramural Res Program, NIH,Dept Hlth & Human Serv, Bldg 10,Rm 3,South 228A,9000 Rockville Pike, Bethesda, MD 20892 USA. EM Kenneth.Towbin@nih.gov CR Allen DA, 2001, EUR CHILD ADOLES PSY, V10, P67 Arnold LE, 2003, J AM ACAD CHILD PSY, V42, P1443, DOI 10.1097/01.chi.0000091946.28938.54 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 BISHOP DV, 2000, J CHILD PSCHOL PSYCH, V43, P917 Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 Bishop DVM, 2001, DEV MED CHILD NEUROL, V43, P809, DOI 10.1017/S0012162201001475 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Bryson S. 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Child Adolesc. Psychopharmacol. PD JUN PY 2005 VL 15 IS 3 BP 452 EP 464 DI 10.1089/cap.2005.15.452 PG 13 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 957UN UT WOS:000231398900011 PM 16092910 ER PT J AU van der Gaag, RJ Caplan, R van Engeland, H Loman, E Buitelaar, J AF van der Gaag, RJ Caplan, R van Engeland, H Loman, E Buitelaar, J TI A cop-trolled study of formal thought disorder in children with autism and multiple complex developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID CHILDHOOD SCHIZOPHRENIA; CLINICAL-ASSESSMENT; COMMUNICATION; ATTENTION; LANGUAGE; PHENOMENOLOGY; RELIABILITY; PSYCHOSIS; DIAGNOSIS; RELATIVES AB Along with well-defined categories in classification systems (e.g., autistic disorders and attention-deficit/hyperactivity disorder (ADHD)), practitioners are confronted with many children showing mixed forms of developmental psychopathology. These clusters of symptoms are on the borderlines of more defined categories. The late, Donald Cohen proposed heuristic criteria to study a. group defined by impaired social sensitivity, impaired regulation of affect, and thinking disorders under the name multiple complex developmental disorders (MCDD). Although these children meet criteria for pervasive developmental disorder-not otherwise specified (PDD-NOS), they have additional important clinical features, such as thought disorder. After highlighting similarities and differences between MCDD and comparable groups (e.g., multidimensionally impaired children), this paper presents the findings of a study comparing formal thought disorder scores in children with MCDD to children with autism spectrum diagnoses, such as autistic disorder (AD), and to children with nonspectrum diagnoses, such as ADHD and anxiety disorders. Methods: Videotaped speech samples of four groups of high-functioning, latency-aged children with MCDD, AD, ADHD, and anxiety disorders were compared to a control group of normal children using the Kiddie Formal Thought Disorder Rating Scale (K-FTDS). Results: High formal thought disorder scores were found both in the AD and MCDD groups, low rates in the ADHD groups, and no thought disorder in the anxiety disorder and normal control groups. The severity of formal thought disorder was related to verbal IQ scores within the AD and MCDD groups. Conclusion: High formal thought scores in children with complex developmental disorders, such as AD and MCDD, appear to reflect impaired communication skills rather than early signs of psychosis. C1 UMCN St Radboud, ACKJON, Acad Ctr Child & Adolescent Psychiat, NL-6525 GC Nijmegen, Netherlands. Univ Calif Los Angeles, Dept Psychiat & Behav Sci, Los Angeles, CA 90024 USA. Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. GGZ Regio, Breda, Netherlands. RP van der Gaag, RJ (reprint author), UMCN St Radboud, ACKJON, Acad Ctr Child & Adolescent Psychiat, Reinier Postlaan 12, NL-6525 GC Nijmegen, Netherlands. EM R.vanderGaag@psy.umcn.nl RI Buitelaar, Jan/E-4584-2012; Gaag, R.J./H-8030-2014 OI Buitelaar, Jan/0000-0001-8288-7757; CR ANDREASE.NJ, 1974, COMPR PSYCHIAT, V15, P27, DOI 10.1016/0010-440X(74)90061-3 ANDREASEN NC, 1979, ARCH GEN PSYCHIAT, V36, P1315 ARBOLEDA C, 1985, ARCH GEN PSYCHIAT, V42, P1004 Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Bakker SC, 2003, AM J HUM GENET, V72, P1251, DOI 10.1086/375143 Ballmaier M, 2004, PSYCHIAT RES-NEUROIM, V130, P43, DOI 10.1016/j.pscychresns.2003.10.001 BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 BEMPORAD JR, 1982, AM J PSYCHIAT, V139, P596 Bleuler E, 1911, DEMENTIA PRAECOX GRO BLOTE AEW, 1986, TIJDSCHRIFT PSYCHOL, V5, P226 Buitelaar JK, 1998, J CHILD PSYCHOL PSYC, V39, P911, DOI 10.1017/S0021963098002820 CAPLAN R, 1992, J AM ACAD CHILD PSY, V31, P151, DOI 10.1097/00004583-199201000-00023 Caplan R, 2001, J AM ACAD CHILD PSY, V40, P965, DOI 10.1097/00004583-200108000-00019 CAPLAN R, 1989, J AM ACAD CHILD PSY, V28, P408, DOI 10.1097/00004583-198905000-00018 Caplan R, 2002, J CHILD PSYCHOL PSYC, V43, P245, DOI 10.1111/1469-7610.00017 Caplan R, 2000, J AM ACAD CHILD PSY, V39, P771, DOI 10.1097/00004583-200006000-00016 CAPLAN R, J AM ACAD CHILD ADOL COHEN DJ, 1986, J AM ACAD CHILD PSY, V25, P158, DOI 10.1016/S0002-7138(09)60221-1 COHEN DJ, 1991, DEV FOLLOW UP CONCEP COHEN J, 1968, PSYCHOL BULL, V70, P213, DOI 10.1037/h0026256 DAHL EK, 1986, J AM ACAD CHILD PSY, V25, P170, DOI 10.1016/S0002-7138(09)60223-5 Docherty NM, 1999, PSYCHOL MED, V29, P189, DOI 10.1017/S0033291798007843 DYKENS E, 1991, J AUTISM DEV DISORD, V21, P291, DOI 10.1007/BF02207326 Green J, 1998, PATIENT CHILD PSYCHI Grigorenko EL, 2003, METH MOLEC MED, V77, P23 HOLZMAN PS, 1986, SCHIZOPHRENIA BULL, V12, P360 Howlin P, 2004, J CHILD PSYCHOL PSYC, V45, P212, DOI 10.1111/j.1469-7610.2004.00215.x JAMPALA VC, 1989, AM J PSYCHIAT, V146, P459 Jansen LMC, 2003, NEUROPSYCHOPHARMACOL, V28, P582, DOI 10.1038/sj.npp.1300046 Kaufman A. 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Child Adolesc. Psychopharmacol. PD JUN PY 2005 VL 15 IS 3 BP 465 EP 476 PG 12 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 957UN UT WOS:000231398900012 PM 16092911 ER PT J AU Gadow, KD DeVincent, CJ AF Gadow, KD DeVincent, CJ TI Clinical significance of tics and attention-deficit hyperactivity disorder (ADHD) in children with pervasive developmental disorder SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID TOURETTE-SYNDROME; AUTISTIC DISORDER; PRESCHOOL-CHILDREN; INFANTILE-AUTISM; SYMPTOMS; BEHAVIOR; BOYS; PDD; PSYCHOPATHOLOGY; ADOLESCENTS AB The goal of this study was to examine the clinical significance of co-occurring tics and attention-deficit hyperactivity disorder (ADHD) as indicators of a more complex symptomatology in children with and without pervasive developmental disorder. Parents and teachers completed a Diagnostic and Statistical Manual of Mental Disorders-IV-referenced rating scale for 3- to 5- (n = 182/135) and 6- to 12- (n = 301/191) year-old children with pervasive developmental disorder and clinic controls, respectively. The percentage of children with tic behaviors varied with age: preschoolers (25%,44%) versus elementary schoolchildren (60%, 66%) (parent and teacher ratings, respectively). For many psychiatric symptoms, screening prevalence rates were highest for the ADHD + tics group and lowest for the group with symptoms of neither, but the pattern of group differences varied by age group and informant. In general, there were few differences between the ADHD only and tics only groups. The pattern of ADHD/tic group differences was similar for both children with and without pervasive developmental disorder. We concluded that these findings support the notion that the co-occurrence of ADHD and tics is an indicator of a more complex psychiatric symptomatology in children with pervasive developmental disorder. C1 SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA. SUNY Stony Brook, Dept Pediat, Stony Brook, NY 11794 USA. RP Gadow, KD (reprint author), SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA. 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Child Neurol. PD JUN PY 2005 VL 20 IS 6 BP 481 EP 488 DI 10.1177/08830738050200060301 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 940PM UT WOS:000230156400003 PM 15996396 ER PT J AU Honda, H Shimizu, Y Rutter, M AF Honda, H Shimizu, Y Rutter, M TI No effect of MMR withdrawal on the incidence of autism: a total population study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE MMR vaccine; autism; incidence; etiology; regression; total population study ID PERVASIVE DEVELOPMENTAL DISORDERS; PRESCHOOL-CHILDREN; CHILDHOOD AUTISM; CUMULATIVE INCIDENCE; CHANGING PREVALENCE; RUBELLA VACCINATION; SPECTRUM DISORDERS; MEASLES; MUMPS; CALIFORNIA AB Background: A causal relationship between the measles, mumps, and rubella (MMR) vaccine and occurrence of autism spectrum disorders (ASD) has been claimed, based on an increase in ASD in the USA and the UK after introduction of the MMR vaccine. However, the possibility that this increase is coincidental has not been eliminated. The unique circumstances of a Japanese MMR vaccination program provide an opportunity for comparison of ASD incidence before and after termination of the program. Methods: This study examined cumulative incidence of ASD up to age seven for children born from 1988 to 1996 in Kohoku Ward (population approximately 300,000), Yokohama, Japan. ASD cases included all cases of pervasive developmental disorders according to ICD-10 guidelines. Results: The MMR vaccination rate in the city of Yokohama declined significantly in the birth cohorts of years 1988 through 1992, and not a single vaccination was administered in 1993 or thereafter. In contrast, cumulative incidence of ASD up to age seven increased significantly in the birth cohorts of years 1988 through 1996 and most notably rose dramatically beginning with the birth cohort of 1993. Conclusions: The significance of this finding is that MMR vaccination is most unlikely to be a main cause of ASD, that it cannot explain the rise over time in the incidence of ASD, and that withdrawal of MMR in countries where it is still being used cannot be expected to lead to a reduction in the incidence of ASD. C1 Yokohama Rehabil Ctr, Kohoku Ku, Yokohama, Kanagawa 2220035, Japan. Inst Psychiat, London, England. RP Honda, H (reprint author), Yokohama Rehabil Ctr, Kohoku Ku, 1770 Toriyama Cho, Yokohama, Kanagawa 2220035, Japan. 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Child Psychol. Psychiatry PD JUN PY 2005 VL 46 IS 6 BP 572 EP 579 DI 10.1111/j.1469-7610.2005.01425.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 924KZ UT WOS:000228979000003 PM 15877763 ER PT J AU Molesworth, CJ Bowler, DM Hampton, JA AF Molesworth, CJ Bowler, DM Hampton, JA TI The prototype effect in recognition memory: intact in autism? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; Asperger syndrome; prototype; categorization; recognition; central coherence ID ASPERGERS-SYNDROME; NORMAL-CHILDREN; CATEGORY KNOWLEDGE; MENTAL-RETARDATION; CENTRAL COHERENCE; VISUAL ILLUSIONS; FACE RECOGNITION; CLASSIFICATION; CATEGORIZATION; INDIVIDUALS AB Background: There are two accounts of categorization performance in autism: that there is an impairment in prototype formation (Klinger & Dawson, 2001) and that there is an impairment in processing features held in common between stimuli (Plaisted, O'Riordan, & Baron-Cohen, 1998). These accounts, together with central coherence theory ( Frith, 1989; Frith & Happe, 1994), imply a reduced or absent prototype effect in autism. Method: Children with autism or Asperger syndrome ( n = 15) matched on age, gender, and verbal mental age with typically developing children ( n = 15) completed a picture recognition task ( Experiment 1). These participants also studied categories of cartoon animals possessing either an average prototype structure ( Experiment 2) based on Younger's ( 1985) stimuli or a modal structure ( Experiment 3) based on Hayes and Taplin's (1993b) stimuli. Following the study phases, participants completed recognition tests comprising prototypes and other exemplars with varying degrees of similarity to the prototypes. Results: For both participant groups, recognition memory appeared intact ( Experiment 1) and a full prototype effect in recognition memory was observed in both Experiment 2 and Experiment 3. Conclusions: The present studies fail to support predictions of impaired prototype effects in autism. The discussion focuses on key methodological differences between these studies and those that support claims that central coherence, prototype formation, and common feature processing are impaired in autism. C1 City Univ London, Dept Psychol, London EC1V 0HB, England. 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Child Psychol. Psychiatry PD JUN PY 2005 VL 46 IS 6 BP 661 EP 672 DI 10.1111/j.1469-7610.2004.00383.x PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 924KZ UT WOS:000228979000010 PM 15877770 ER PT J AU Dalton, KM Kalin, NH Grist, TM Davidson, RJ AF Dalton, KM Kalin, NH Grist, TM Davidson, RJ TI Neural-cardiac coupling in threat-evoked anxiety SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID INSULAR CORTEX; AFFECTIVE STYLE; HUMAN AMYGDALA; FEAR; HUMANS; ACTIVATION; MECHANISMS; AROUSAL; FMRI AB Anxiety is a debilitating symptom of many psychiatric disorders including generalized anxiety disorder, mood disorders, schizophrenia, and autism. Anxiety involves changes in both central and peripheral biology,, yet extant functional imaging studies have focused exclusively on the brain. Here we show, using functional brain and cardiac imaging in sequential brain and cardiac magnetic resonance imaging (MRI) sessions in response to cues that predict either threat (a possible shock) or safety (no possibility of shock), that MR signal change in the amygdala and the prefrontal and insula cortices predicts cardiac contractility to the threat of shock. Participants with greater MR signal change in these regions show increased cardiac contractility to the threat versus safety condition, a measure of the sympathetic nervous system contribution to the myocardium. These findings demonstrate robust neural-cardiac coupling during induced anxiety and indicate that individuals with greater activation in brain regions identified with aversive emotion show larger magnitude cardiac contractility increases to threat. C1 Univ Wisconsin, Waisman Ctr, WM Keck Lab Funct Brain Imaging & Behav, Madison, WI 53705 USA. RP Dalton, KM (reprint author), Univ Wisconsin, Waisman Ctr, WM Keck Lab Funct Brain Imaging & Behav, 1500 Highland Ave, Madison, WI 53705 USA. EM kmdalton@facstaff.wisc.edu; rjdavids@wisc.edu CR Augustine JR, 1996, BRAIN RES REV, V22, P229, DOI 10.1016/S0165-0173(96)00011-2 Brownley K. 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Cogn. Neurosci. PD JUN PY 2005 VL 17 IS 6 BP 969 EP 980 DI 10.1162/0898929054021094 PG 12 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 934AA UT WOS:000229677700012 PM 15969913 ER PT J AU Sherer, MR Schreibman, L AF Sherer, MR Schreibman, L TI Individual behavioral profiles and predictors of treatment effectiveness for children with autism SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Article DE autism; behavioral treatment; behavioral profiles; individualized treatment; pivotal response training ID DIAGNOSTIC OBSERVATION SCHEDULE; EARLY INTERVENTION; YOUNG-CHILDREN; CLASSIFICATION AB Differential responsiveness to intervention programs suggests the inadequacy of a single treatment approach for all children with autism. One method for reducing outcome variability is to identify participant characteristics associated with different outcomes for a specific intervention. In this investigation, an analysis of archival data yielded 2 distinct behavioral profiles for responders and nonresponders to a widely used behavioral intervention, pivotal response training (PRT). In a prospective study, these profiles were used to select 6 children (3 predicted responders and 3 predicted nonresponders) who received PRT. Children with pretreatment responder profiles evidenced positive changes on a range of outcome variables. Children with pretreatment nonresponder profiles did not exhibit improvements; These results offer promise for the development of individualized treatment protocols for children with autism. C1 Univ Calif San Diego, Dept Psychol, La Jolla, CA 92093 USA. RP Schreibman, L (reprint author), Univ Calif San Diego, Dept Psychol, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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Consult. Clin. Psychol. PD JUN PY 2005 VL 73 IS 3 BP 525 EP 538 DI 10.1037/0022-006X.73.3.525 PG 14 WC Psychology, Clinical SC Psychology GA 938XH UT WOS:000230036200015 PM 15982150 ER PT J AU Yatchmink, Y AF Yatchmink, Y TI Autism spectrum disorders: A research review for practitioners SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Brown Univ, Sch Med, Hasbro Childrens Hosp, Child Dev Ctr, Providence, RI 02912 USA. RP Yatchmink, Y (reprint author), Brown Univ, Sch Med, Hasbro Childrens Hosp, Child Dev Ctr, Providence, RI 02912 USA. CR Ozonoff S, 2003, AUTISM SPECTRUM DISO NR 1 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 JUN PY 2005 VL 26 IS 3 BP 246 EP 246 DI 10.1097/00004703-200506000-00014 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 936HA UT WOS:000229844900011 ER PT J AU Handen, BL Hofkosh, D AF Handen, BL Hofkosh, D TI Secretin in children with autistic disorder: A double-blind, placebo-controlled trial SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; pervasive developmental disorder; secretin; children ID PERVASIVE DEVELOPMENTAL DISORDER; SYNTHETIC HUMAN SECRETIN; PORCINE SECRETIN; SPECTRUM DISORDERS; BEHAVIOR; BENEFIT AB A number of recent studies have examined the efficacy of secretin (a polypeptide neurotransmitter) to treat symptoms associated with autism. Initial anecdotal reports indicated significant gains in social relatedness and language. However, recent double-blind studies have documented few significant differences between placebo and active medication. We report the results of a double-blind, placebo-controlled, crossover study of the efficacy of secretin in eight children with autism. No group differences between placebo and secretin were found on measures of behavior and core features of autism. Parents reported anecdotal improvement in communication and social relatedness, but such gains tended to occur during both placebo and active medication conditions. However, a single subject did experience improvement in the core features of autism and behavior for a 3-4-week period following the secretin infusion. The results add further research support of the lack of clinical efficacy of this medication in the treatment of autism. C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Sch Med,Dept Psychiat, Merck Program, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Childrens Hosp Pittsburgh, Sch Med, Dept Pediat, Pittsburgh, PA USA. 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PD JUN PY 2005 VL 17 IS 2 BP 95 EP 106 DI 10.1007/s10882-005-3682-7 PG 12 WC Rehabilitation SC Rehabilitation GA 927SH UT WOS:000229220300001 ER PT J AU Fukuda, T Itoh, M Ichikawa, T Washiyama, K Goto, Y AF Fukuda, T Itoh, M Ichikawa, T Washiyama, K Goto, Y TI Delayed maturation of neuronal architecture and synaptogenesis in cerebral cortex of Mecp2-deficient mice SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE cerebral cortex; development Mecp2; mouse; neuron; Rett syndrome; synapse ID LINKED MENTAL-RETARDATION; CPG-BINDING PROTEIN-2; RETT-SYNDROME; TRANSCRIPTIONAL REPRESSOR; CHROMOSOMAL PROTEIN; MECP2 MUTATION; BRAIN; DIFFERENTIATION; NEUROPATHOLOGY; NEUROANATOMY AB We detected morphologic abnormalities in the cerebral cortex of Mecp2-hemizygous (Mecp2(-/y)) mice. The cortical thickness of both somatosensory and motor cortices in mutants did not increase after 4 weeks of age, as compared with that in wild-type male mice. The density of neurons in those areas was significantly higher in layers II/III and V of MecP2(-/y) mice than in wild-type mice, particularly in layers II/III after 4 weeks of age. In layer II/III of the somatosensory cortex of Mecp2(-/y) mice, the diameter of the apical dendrite was thin and the number of dendritic spines was small. Electron microscopy revealed that two-week-old mutants already bad numerous premature postsynaptic densities. These results indicate that Mecp2(-/y) mice suffered delayed neuronal maturation of the cerebral cortex and that the initial neuronal changes were caused by premature synapto-genesis. Rett syndrome patients with a heterozygous mutation of Mecp2 display developmental disorders including cortical malfunctions such as mental retardation, autism, and epilepsy. Our results provide evidence of the similarity with Rett syndrome brains in some respects and suggest that MeCP2/Mecp2 plays some role in synaptogenesis. C1 Natl Ctr Neurol & Psychiat, Inst Neurosci, Dept Mental REtardat & Birth Defect Res, Kodaira, Tokyo 1878502, Japan. Niigata Univ, Brain Res Inst, Dept Mol Neuropathol, Niigata 951, Japan. RP Itoh, M (reprint author), Natl Ctr Neurol & Psychiat, Inst Neurosci, Dept Mental REtardat & Birth Defect Res, 4-1-1 Ogawahigashi, Kodaira, Tokyo 1878502, Japan. 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PD SUM PY 2005 VL 7 IS 3 BP 159 EP 173 DI 10.1177/10983007050070030501 PG 15 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 938ZS UT WOS:000230042500005 ER PT J AU Tani, P Lindberg, N Matto, V Appelberg, B Wendt, TNV von Wendt, L Porkka-Heiskanen, T AF Tani, P Lindberg, N Matto, V Appelberg, B Wendt, TNV von Wendt, L Porkka-Heiskanen, T TI Higher plasma ACTH levels in adults with Asperger syndrome SO JOURNAL OF PSYCHOSOMATIC RESEARCH LA English DT Article DE Asperger syndrome; ACTH; cortisol; stress ID PSYCHOLOGICAL STRESS; AUTISM; CORTISOL; NEUROENDOCRINE; RESPONSES; AMYGDALA; HORMONE AB Objective: The aim of this preliminary study was to characterize the levels of plasma adrenocorticotropic hormone (ACTH) and cortisol in adult patients with Asperger syndrome (AS). Methods: Twenty medication-free individuals with high-functioning AS were recruited from a clinic specialized in autism spectrum disorders. Ten age-matched healthy persons (hospital staff or students) with no neuropsychiatric disorders served as controls. Blood samples for the assessment were collected at 8:00 a.m. Results: The patients with AS had significantly higher plasma ACTH values than did the healthy controls. Plasma-cortisol levels were similar in both groups. Conclusion: Increased plasma-ACTH levels are associated with AS. Future studies are needed to clarify whether this finding is a biological consequence of chronic anxiety and elevated stress, or a sign of facilitated response to an acute novel stressor. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Helsinki, Dept Psychiat, Helsinki, Finland. Univ Helsinki, Dept Physiol, Inst Biomed, Helsinki, Finland. Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland. RP Tani, P (reprint author), Biomed Helsinki, Inst Biomed, Dept Physiol, POB 63, Helsinki 00014, Finland. 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PD JUN PY 2005 VL 58 IS 6 BP 533 EP 536 DI 10.1016/j.jpsychores.2004.12.004 PG 4 WC Psychiatry SC Psychiatry GA 969TU UT WOS:000232258500008 PM 16125520 ER PT J AU Okuhira, Y Adachi, A Sakamaki, M Hashizume, M Tsuboi, K AF Okuhira, Y Adachi, A Sakamaki, M Hashizume, M Tsuboi, K TI Examination of the relevance of eating disorders and high-functioning pervasive developmental disorders with autism-spectrum quotients SO JOURNAL OF PSYCHOSOMATIC RESEARCH LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0022-3999 J9 J PSYCHOSOM RES JI J. Psychosomat. Res. PD JUN PY 2005 VL 58 IS 6 SU S BP S96 EP S96 PG 1 WC Psychiatry SC Psychiatry GA 971HQ UT WOS:000232375200442 ER PT J AU Glazebrook, CM Elliott, D AF Glazebrook, CM Elliott, D TI Strategies used by people with and without autism to minimize movement time SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 McMaster Univ, Hamilton, ON L8S 4L8, Canada. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2005 VL 27 SU S BP S68 EP S69 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 938AU UT WOS:000229973100134 ER PT J AU Moskowitz, S AF Moskowitz, S TI Playing dead: An unconscious fantasy, bodily focused defenses, and their roots in infancy SO JOURNAL OF THE AMERICAN PSYCHOANALYTIC ASSOCIATION LA English DT Article ID CONTINGENCY; OBJECT; PSYCHOANALYSIS; DISTURBANCES; EXPERIENCE; AWARENESS; SYMBIOSIS; AUTISM AB A patient's unconscious fantasy of being her mother's dead baby emerged during the course of a long analysis, and was understood as her expression and explanation, constructed and elaborated throughout her development, of a fundamental and formative early infant state and experience. This patient's identification with a baby who had died before she was born was connected to her major complaint, a pervasive feeling that she could not act with intention, and to her obsessive ruminations, compulsive actions, and masochistic attacks on her body. The bodily based aspects and focus of these defenses were autistic-like, self-directed activities that can be understood as having their roots in what was experienced as catastrophic loss in the earliest weeks and months of life. Infant research, particularly on contingency detection, is especially useful in clarifying the ways in which these defenses may form, and in reconstructing and tracing the trajectories and intricate transformations of body ego, self- and other representations, and defenses from their earliest beginnings to their current manifestations in patients' fantasies and symptoms. C1 CUNY, Doctoral Program Clin Psychol, New York, NY 10021 USA. 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PD SUM PY 2005 VL 53 IS 3 BP 891 EP 916 DI 10.1177/00030651050530031701 PG 26 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA 957BJ UT WOS:000231344000012 PM 16187638 ER PT J AU Skaar, DA Shao, Y Haines, JL Stenger, JE Jaworski, J Martin, ER DeLong, GR Moore, JH McCauley, JL Sutcliffe, JS Ashley-Koch, AE Cuccaro, ML Folstein, SE Gilbert, JR Pericak-Vance, MA AF Skaar, DA Shao, Y Haines, JL Stenger, JE Jaworski, J Martin, ER DeLong, GR Moore, JH McCauley, JL Sutcliffe, JS Ashley-Koch, AE Cuccaro, ML Folstein, SE Gilbert, JR Pericak-Vance, MA TI Analysis of the RELN gene as a genetic risk factor for autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; candidate gene; chromosome 7q; RELN; association ID PEDIGREE DISEQUILIBRIUM TEST; REELIN GENE; DIAGNOSTIC INTERVIEW; VULNERABILITY FACTOR; GENOMEWIDE SCREEN; CORTICAL-NEURONS; CANDIDATE GENE; ASSOCIATION; LINKAGE; DISORDER AB Several genome-wide screens have indicated the presence of an autism susceptibility locus within the distal long arm of chromosome 7 (7q). Mapping at 7q22 within this region is the candidate gene reelin ( RELN). RELN encodes a signaling protein that plays a pivotal role in the migration of several neuronal cell types and in the development of neural connections. Given these neurodevelopmental functions, recent reports that RELN influences genetic risk for autism are of significant interest. The total data set consists of 218 Caucasian families collected by our group, 85 Caucasian families collected by AGRE, and 68 Caucasian families collected at Tufts University were tested for genetic association of RELN variants to autism. Markers included five single-nucleotide polymorphisms ( SNPs) and a repeat in the 5'-untranslated region ( 5'-UTR). Tests for association in Duke and AGRE families were also performed on four additional SNPs in the genes PSMC2 and ORC5L, which flank RELN. Family-based association analyses (PDT, Geno-PDT, and FBAT) were used to test for association of single-locus markers and multilocus haplotypes with autism. The most significant association identified from this combined data set was for the 5'-UTR repeat ( PDT P-value = 0.002). These analyses show the potential of RELN as an important contributor to genetic risk in autism. C1 Duke Univ, Med Ctr, Dept Med, Ctr Human Genet,IGSP, Durham, NC 27710 USA. Vanderbilt Univ, Med Ctr, Ctr Human Genet Res, Nashville, TN USA. Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, Nashville, TN USA. Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Dept Med, Ctr Human Genet,IGSP, 595 LaSalle St,Bldg 7540,Box 3445, Durham, NC 27710 USA. 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Psychiatr. PD JUN PY 2005 VL 10 IS 6 BP 563 EP 571 DI 10.1038/sj.mp.4001614 PG 9 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 929ZO UT WOS:000229385600009 PM 15558079 ER PT J AU Mendez, MF Shapira, JS Miller, BL AF Mendez, MF Shapira, JS Miller, BL TI Stereotypical movements and frontotemporal dementia SO MOVEMENT DISORDERS LA English DT Article DE stereotypical movements; stereotypies; frontotemporal dementia; compulsions ID OBSESSIVE-COMPULSIVE DISORDER; LOBAR DEGENERATION; BEHAVIOR; CONSENSUS; CIRCUITS; CRITERIA; DISEASE; SCALE; SPECT AB Stereotypical movements are characteristic of autism or mental retardation but can also occur in patients with dementia, particularly frontotemporal dementia (FTD). In this study, we administered the Abnormal Involuntary Movement Scale (AIMS) to 18 patients with FTD and to 18 patients with the most common form of dementia, Alzheimer's disease (AD). The AIMS scores were gathered at the initial presentation of patients who had not received antipsychotic medications. Compared to the AD patients, the FTD patients had significantly more stereotypical movements, including frequent rubbing behaviors and some selfinjurious acts. All the FTD patients with stereotypical movements had compulsive-like behaviors, suggesting a similar pathophysiologic cause, and most had a decrease in their stereotypical movements with the administration of sertraline, a serotonin selective reuptake inhibitor. (c) 2005 Movement Disorder Society. C1 VA Greater Los Angeles Healthcare Ctr, Neurobehav Unit 691 116AF, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. RP Mendez, MF (reprint author), VA Greater Los Angeles Healthcare Ctr, Neurobehav Unit 691 116AF, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. 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Disord. PD JUN PY 2005 VL 20 IS 6 BP 742 EP 745 DI 10.1002/mds.20465 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 934UJ UT WOS:000229733800013 PM 15786492 ER PT J AU Raefski, AS O'Neill, MJ AF Raefski, AS O'Neill, MJ TI Identification of a cluster of X-linked imprinted genes in mice SO NATURE GENETICS LA English DT Article ID TURNERS-SYNDROME; CHROMOSOME; MOUSE; ORIGIN; INACTIVATION; EXPRESSION; DISORDER; AUTISM AB Complete or partial monosomy with respect to the X chromosome is the genetic basis of Turner syndrome in human females. Individuals with Turner syndrome have a spectrum of anatomical, physiological and behavioral phenotypes with expressivity dependent on the extent of monosomy and the parental origin of the single X-1. Parent- of- origin influences on social cognition in Turner syndrome might be due to the presence of imprinted genes on the X-2. Imprinting of X-linked genes has also been implicated in the male prevalence of autistic spectrum disorders(3), in male sexual orientation(4,5) and in the developmental delay of XO mouse embryos(6-8). The only molecular evidence for X-chromosome imprinting, however, concerns X-chromosome inactivation in specific circumstances(9,10) and does not account for these phenotypes. Using a mouse model for Turner syndrome, we searched for locus-specific imprinting of X-linked genes in developing brain. We identified a cluster of X-linked genes containing at least three genes that show transcriptional repression of paternal alleles. Imprinting of these three genes, Xlr3b, Xlr4b and Xlr4c, is independent of X-chromosome inactivation and has a dynamic and complex pattern of tissue and stage specificity. C1 Univ Connecticut, Dept Mol & Cell Biol, Storrs, CT 06269 USA. RP O'Neill, MJ (reprint author), Univ Connecticut, Dept Mol & Cell Biol, 354 Mansfield Rd,U-2131, Storrs, CT 06269 USA. 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PD JUN PY 2005 VL 37 IS 6 BP 620 EP 624 DI 10.1038/ng1567 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 931OT UT WOS:000229495300016 PM 15908953 ER PT J AU Davies, W Isles, A Smith, R Karunadasa, D Burrmann, D Humby, T Ojarikre, O Biggin, C Skuse, D Burgoyne, P Wilkinson, L AF Davies, W Isles, A Smith, R Karunadasa, D Burrmann, D Humby, T Ojarikre, O Biggin, C Skuse, D Burgoyne, P Wilkinson, L TI Xlr3b is a new imprinted candidate for X-linked parent-of-origin effects on cognitive function in mice SO NATURE GENETICS LA English DT Article ID TURNERS-SYNDROME; CHROMOSOME; MOUSE; SEQUENCE; GENOME; AUTISM; GENES; BRAIN; SCHIZOPHRENIA; REGIONS AB Imprinted genes show differential expression between maternal and paternal alleles as a consequence of epigenetic modification that can result in 'parent-of-origin' effects on phenotypic traits(1). There is increasing evidence from mouse and human studies that imprinted genes may influence behavior and cognitive functioning(2). Previous work in girls with Turner syndrome (45,XO) has suggested that there are X-linked parent-of-origin effects on brain development(3) and cognitive functioning(4), although the interpretation of these data in terms of imprinted gene effects has been questioned(5). We used a 39,XO mouse model to examine the influence of the parental origin of the X chromosome on cognitive behaviors and expression of X-linked genes in brain. Our findings confirm the existence of X-linked imprinted effects on cognitive processes and identify a new maternally expressed imprinted gene candidate on the X chromosome, Xlr3b, which may be of importance in mediating the behavioral effects. C1 Babraham Inst, Lab Cognit & Behav Neurosci, Cambridge CB2 4AT, England. Babraham Inst, Lab Dev Genet & Imprinting, Cambridge CB2 4AT, England. Natl Inst Med Res, MRC, Div Dev Genet, London NW7 1AA, England. Inst Child Hlth, Behav Sci Unit, London WC1N 1EH, England. RP Wilkinson, L (reprint author), Babraham Inst, Lab Cognit & Behav Neurosci, Babraham Res Campus, Cambridge CB2 4AT, England. 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PD JUN PY 2005 VL 37 IS 6 BP 625 EP 629 DI 10.1038/ng1577 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 931OT UT WOS:000229495300017 PM 15908950 ER PT J AU Singer, E AF Singer, E TI 'Phenome' project set to pin down subgroups of autism SO NATURE MEDICINE LA English DT News Item AB The autism phenome project will classify the differences in autistic children,analyzing various symptoms and biomolecules present in biological fluids. NR 0 TC 8 Z9 8 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD JUN PY 2005 VL 11 IS 6 BP 583 EP 583 DI 10.1038/nm0605-583a PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 932YD UT WOS:000229589800006 PM 15937456 ER PT J AU Liu, WS Pappas, GD Carter, CS AF Liu, WS Pappas, GD Carter, CS TI Oxytocin receptors in brain cortical regions are reduced in haploinsufficient (+/-)reeler mice SO NEUROLOGICAL RESEARCH LA English DT Article DE autism; oxytocin; oxytocin receptor; reeler mouse; reelin; schizophrenia ID HETEROZYGOUS REELER MOUSE; DENDRITIC SPINE; DOWN-REGULATION; SCHIZOPHRENIA; EXPRESSION; DISORDERS; NEURONS; SYSTEM; AUTISM; CORTEX AB Objective: Both oxytocin (OT) and reelin are particularly significant during development and the absence of either may interfere with normal brain development. In addition, reelin is critical to the development of the GABAergic system and GABA modulates the release of OT. Availability of the reelin haploinsufficient (+/-) reeler mouse (HRM) provides a model for examining the role of reelin in the development of the OT system and especially in the expression of the OT receptor (OTR). Methods: in this study we used immunocytochemistry and in situ hybridization in HRM versus wild-type (+/+) mice (WTM) to quantify OTR abundance in regions of the brain cortex. Results: Our findings reveal that the oxytocin receptor (OTR), measured either by immunohistochemistry or in situ hybridization, is significantly lower in HRM. Areas showing significant deficits included the piriform cortex, neocortex, retrosplenial cortex and certain regions of the hippocampus. Conclusion: Both reelin and OT play a role in regulating affect and mood. Down-regulation of reelin has been strongly correlated with schizophrenia and it is proposed that HRM may serve as a model for neural deficits seen in both schizophrenia and autism. We report that HRM show regionally specific reductions in OTRs, especially in cortical areas, which previously have been implicated in social memory and cognitive functions. These findings offer support for the more general hypothesis that down-regulation of reelin, of either genetic or epigenetic origin, through associated reductions in the OTRs, contributes to the deficiencies in social behavior that are characteristic of both schizophrenia and autism. C1 Univ Illinois, Psychiat Inst, Chicago, IL 60612 USA. Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA. Univ Illinois, Dept Anat & Cell Biol, Chicago, IL 60612 USA. Univ Illinois, Brain Body Ctr, Chicago, IL 60612 USA. RP Pappas, GD (reprint author), Univ Illinois, Psychiat Inst, 1601 W Taylor St, Chicago, IL 60612 USA. 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Res. PD JUN PY 2005 VL 27 IS 4 BP 339 EP 345 DI 10.1179/016164105X35602 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 933DS UT WOS:000229605200001 PM 15949229 ER PT J AU Lombardo, SA Leanza, G Meli, C Lombardo, ME Mazzone, L Vincenti, I Cioni, M AF Lombardo, SA Leanza, G Meli, C Lombardo, ME Mazzone, L Vincenti, I Cioni, M TI Maternal exposure to the antiepileptic drug vigabatrin affects postnatal development in the rat SO NEUROLOGICAL SCIENCES LA English DT Article DE vigabatrin; pregnancy; antiepileptic drugs; GABA; neuronal programming ID GAMMA-VINYL GABA; HIPPOCAMPAL-NEURONS; PLACENTAL-TRANSFER; BRAIN; ACID; EPILEPSY; THALIDOMIDE; GABAPENTIN; AUTISM; MICE AB The objective was to investigate, in the rat, the effects of maternal exposure to vigabatrin (VGB) on the postnatal motor-cognitive behaviour of the offspring. We used an experimental evaluator-blind, placebo-controlled study in the rat. Ten pregnant rats were divided into five groups and treated with different doses of VGB (250, 500, 750, 1000 mg/kg/day) or placebo from gestation day (GD) 6 to GD10. After delivery, 56 pups (40 pups prenatally exposed to VGB and 16 pups exposed to placebo) were evaluated for motor-cognitive behaviour throughout postpartum day 40. At the end of testing sessions the animals were sacrificed and brain tissues processed for biochemical analysis of GABA levels. Body weight of pups and young rats whose mothers were treated with a dose of 750 mg/kg/day were significantly lower both at birth and during the whole postnatal life with respect to the control groups. Young rats of this group exhibited impaired performance in both the open-field and water maze tasks. Brain GAGA contents were dramatically increased in this group of rats. No other significant nutritional, biochemical or behavioural changes were observed after treatments with doses of VGB lower than 750 mg/kg/day. The exposure to a dose of 1000 mg/kg caused abortion. Maternal exposure to VGB at relatively high doses (750 mg/kg/day) is likely to cause some important changes of the nutritional status during the pre- and postnatal life. Thus, the biochemical and cognitive abnormalities observed in this study could be related to some disturbances of brain development induced by malnutrition and/or to a disturbance of neuronal programming of the gabaergic system. C1 Univ Catania, Sch Med, Chaire Neuropharmacol, Dept Expt & Clin Pharmacol, I-95125 Catania, Italy. Univ Trieste, Sch Med, Dept Physiol & Pathol, I-34127 Trieste, Italy. IRCCS, Osai Inst Res Mental Retardat & Brain Ageing, OU Neuropsychopharmacol, Turin, Italy. Univ Catania, Sch Med, Dept Paediat, I-95124 Catania, Italy. Univ Catania, Dept Neuropsy Children, I-95124 Catania, Italy. Lab Toxicol F Gorgone, Catania, Italy. RP Cioni, M (reprint author), Univ Catania, Sch Med, Chaire Neuropharmacol, Dept Expt & Clin Pharmacol, Viale A Doria 6, I-95125 Catania, Italy. 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Sci. PD JUN PY 2005 VL 26 IS 2 BP 89 EP 94 DI 10.1007/s10072-005-0441-6 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 940TM UT WOS:000230167900005 PM 15995825 ER PT J AU Richell, RA Mitchell, DGV Peschardt, KS Winston, JS Leonard, A Dolan, RJ Blair, RJR AF Richell, RA Mitchell, DGV Peschardt, KS Winston, JS Leonard, A Dolan, RJ Blair, RJR TI Trust and distrust: the perception of trustworthiness of faces in psychopathic and non-psychopathic offenders SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE social cognition; trustworthiness; psychopathy; amygdala ID ANTISOCIAL PERSONALITY; IMPAIRED RECOGNITION; FEARFUL EXPRESSIONS; SOCIAL INFORMATION; ASPERGER-SYNDROME; HUMAN AMYGDALA; DISTRESS CUES; NORMAL ADULTS; AUTISM; CHILDREN AB Psychopathy is a disorder linked to impairments in social cognition. Individuals with psychopathy and comparison individuals, as defined by the Hare Psychopathy Checklist Revised (Hare, 1991), completed a task requiring complex social judgments. Participants viewed a series of male faces, and made judgments concerning how trustworthy they considered the person pictured to be and the degree to which each face was displaying specific emotions. Judgments of trustworthiness did not differ between the individuals with psychopathy and the comparison individuals. Trustworthiness judgments of the faces negatively correlated with, in particular, ratings of anger in the faces for both groups of participants. The data are discussed with reference to the neural systems, including the amygdala, considered to be involved in the mediation of task performance and also neuro-cognitive models of psychopathy. Published by Elsevier Ltd. C1 NIMH, Mood & Anxiety Disorders Program, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. UCL, Inst Cognit Neurosci, London, England. UCL, Dept Psychol, London, England. Wellcome Dept Imaging Neurosci, London WC1N 3BG, England. HMP Wormwood Scrubs, London W12 0AE, England. RP Blair, RJR (reprint author), NIMH, Mood & Anxiety Disorders Program, NIH, Dept Hlth & Human Serv, 15K N Dr,Room 206,MSC 2670, Bethesda, MD 20892 USA. EM blairj@intra.nimh.nih.gov RI Winston, Joel/F-6180-2010 OI Winston, Joel/0000-0002-3957-0612 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 Adolphs R, 2003, ANN NY ACAD SCI, V985, P326 Adolphs R, 1998, NATURE, V393, P470, DOI 10.1038/30982 Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 Adolphs R, 2002, J COGNITIVE NEUROSCI, V14, P1264, DOI 10.1162/089892902760807258 Amaral DG, 2003, NEUROPSYCHOLOGIA, V41, P516, DOI 10.1016/S0028-3932(03)00004-6 Ambrogi Lorenzini C. 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PD JUN PY 2005 VL 38 IS 8 BP 1735 EP 1744 DI 10.1016/j.paid.2004.11.017 PG 10 WC Psychology, Social SC Psychology GA 923WN UT WOS:000228940300001 ER PT J AU Vincent, JB Melmer, G Bolton, PF Hodgkinson, S Holmes, D Curtis, D Gurling, HMD AF Vincent, JB Melmer, G Bolton, PF Hodgkinson, S Holmes, D Curtis, D Gurling, HMD TI Genetic linkage analysis of the X chromosome in autism, with emphasis on the fragile X region SO PSYCHIATRIC GENETICS LA English DT Article DE autism; X chromosome; linkage analysis; fragile X ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; GENOMEWIDE SCREEN; GENOMIC SCREEN; SUSCEPTIBILITY LOCI; MULTIPLEX FAMILIES; MENTAL-RETARDATION; MUTATION ANALYSIS; MECP2 GENE; INDIVIDUALS AB The higher prevalence of autism in males than in females suggests the possible involvement of the X chromosome. To test the hypothesis that there are mutations increasing susceptibility to autism on the X chromosome, and in particular the distal portion of the long arm that encompasses the FMRI and MECP2 loci, a genetic linkage study was performed. Twenty-two fragile X-negative families multiplex for autism and related disorders were used for the study. Linkage analysis, for markers in the Xq27-q28 region, using model-free likelihood-based analysis, produced a maximum MLOD of 1.7 for the narrowest diagnostic category of the typical autism/severe autism spectrum, and nonparametric analysis produced a maximum non-parametric lod (NPL) score of 2.1 for a broad phenotype diagnostic model. Thus, this study offers modest support for a susceptibility locus for autism within the Xq27-q28 region. Further genetic investigations of this region are warranted. (c) 2005 Lippincott Williams & Wilkins. C1 Ctr Addict & Mental Hlth, Neurogenet Sect, Toronto, ON M5T 1R8, Canada. UCL, Windeyer Inst Med Sci, Dept Psychiat & Behav Sci, Mol Psychiat Lab, London, England. Univ Cambridge, Dept Dev Psychiat, Cambridge, England. Royal London Hosp, London E1 1BB, England. RP Vincent, JB (reprint author), Ctr Addict & Mental Hlth, Neurogenet Sect, 250 Coll St, Toronto, ON M5T 1R8, Canada. 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Genet. PD JUN PY 2005 VL 15 IS 2 BP 83 EP 90 DI 10.1097/00041444-200506000-00004 PG 8 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 937SA UT WOS:000229944600003 PM 15900222 ER PT J AU Romano, V Cali, F Seldita, G Mirisola, M D'Anna, RP Gambino, G Schinocca, P Romano, S Ayala, GF Canziani, F De Leo, G Elia, M AF Romano, V Cali, F Seldita, G Mirisola, M D'Anna, RP Gambino, G Schinocca, P Romano, S Ayala, GF Canziani, F De Leo, G Elia, M TI Suggestive evidence for association of D2S2188 marker (2q31.1) with autism in 143 Sicilian (Italian) TRIO families SO PSYCHIATRIC GENETICS LA English DT Article ID LINKAGE DISEQUILIBRIUM; CHROMOSOME-2; GENE AB We have screened 143 Sicilian (Italian) families with one autistic child to verify, by a linkage disequilibrium approach, the involvement of the 2q31.1 region in the cause of the disease in these families. Our study design includes the use of intrafamilial association to prevent a population stratification bias and ethnic homogeneity of the sample. The results of our analysis provided suggestive evidence of the occurrence of transmission disequilibrium between autism and the D2S2188 polymorphism in Sicilian TRIO families, a finding which provides further and independent support to the hypothesis of the existence of a susceptibility gene (or genes) for autism on chromosome 2q. (c) 2005 Lippincott Williams & Wilkins. C1 Univ Palermo, Fac Med & Chirurg, Dipartimento Biopatol & Metodol Biomed, I-90133 Palermo, Italy. Univ Palermo, Ctr Interdipartimentale Ric Clin & Sperimentale A, I-90133 Palermo, Italy. Univ Palermo, Dipartimento Neuropsichiatria Infantile, I-90133 Palermo, Italy. Univ Palermo, Dipartimento Psicol, I-90133 Palermo, Italy. Oasi Maria SS, IRCCS, Troina, EN, Italy. 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PD JUN PY 2005 VL 15 IS 2 BP 149 EP 150 DI 10.1097/00041444-200506000-00013 PG 2 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 937SA UT WOS:000229944600012 PM 15900231 ER PT J AU Bealke, JM Meighen, KG AF Bealke, JM Meighen, KG TI Risperidone treatment of three seriously medically ill children with secondary mood disorders SO PSYCHOSOMATICS LA English DT Article ID OPEN-LABEL; YOUNG-CHILDREN; ADOLESCENTS; AUTISM; BEHAVIOR; CONDUCT C1 Indiana Univ, Sch Med, James Whitcomb Riley Hosp Children, Dept Psychiat,Sect Child & Adolescent Psychiat, Indianapolis, IN 46202 USA. RP Meighen, KG (reprint author), Indiana Univ, Sch Med, James Whitcomb Riley Hosp Children, Dept Psychiat,Sect Child & Adolescent Psychiat, 702 Barnhill Dr ,Rm 4300, Indianapolis, IN 46202 USA. EM kmeighen@iupui.edu CR Brown Rebeccah L., 1996, Journal of Burn Care and Rehabilitation, V17, P34, DOI 10.1097/00004630-199601000-00009 Diler RS, 2002, CURR THER RES CLIN E, V63, P91, DOI 10.1016/S0011-393X(02)80009-1 Findling RL, 2000, J AM ACAD CHILD PSY, V39, P509, DOI 10.1097/00004583-200004000-00021 Gaffney GR, 2002, J AM ACAD CHILD PSY, V41, P330, DOI 10.1097/00004583-200203000-00013 Harrison AM, 2002, CLIN PEDIATR, V41, P51, DOI 10.1177/000992280204100111 Kafantaris V, 2001, J AM ACAD CHILD PSY, V40, P1448, DOI 10.1097/00004583-200112000-00016 Malone RP, 2002, J AM ACAD CHILD PSY, V41, P140, DOI 10.1097/00004583-200202000-00007 McDougle CJ, 1997, J AM ACAD CHILD PSY, V36, P685, DOI 10.1097/00004583-199705000-00020 Posey DJ, 1999, J CHILD ADOL PSYCHOP, V9, P273, DOI 10.1089/cap.1999.9.273 Schreier HA, 1998, J CHILD ADOL PSYCHOP, V8, P49, DOI 10.1089/cap.1998.8.49 Snyder R, 2002, J AM ACAD CHILD PSY, V41, P1026, DOI 10.1097/01.CHI.0000020270/43550.CC Stigler K A, 2001, Paediatr Drugs, V3, P927, DOI 10.2165/00128072-200103120-00005 Vercellino F, 2001, CAN J PSYCHIAT, V46, P559 NR 13 TC 3 Z9 3 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JUN PY 2005 VL 46 IS 3 BP 254 EP 258 DI 10.1176/appi.psy.46.3.254 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA 924QP UT WOS:000228994600008 PM 15883147 ER PT J AU Koegel, RL Werner, GA Vismara, LA Koegel, LK AF Koegel, RL Werner, GA Vismara, LA Koegel, LK TI The effectiveness of contextually supported play date interactions between children with autism and typically developing peers SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE autism; social development; play; inclusion ID SOCIAL-SKILLS; EXTERNALIZING BEHAVIOR; FRIENDSHIP; PARENTS; LONELINESS; CHILDHOOD; SCHOOL; HOME; VICTIMIZATION; INTERVENTION AB Difficulties with social interaction are characteristic of autism. This study presents data illustrating the use of motivational strategies in play dates to improve the quality of social interactions between children with autism and their typically developing peers. Specifically, a multiple baseline design across participants shows how a contextual support package implemented during play dates can promote reciprocal interactions and improve affect. These results support the use of intervention strategies that target the pivotal area of motivation and provide evidence for using play dates as a context for intervention. The findings are discussed in terms of promoting quality interactions and encouraging friendship development. C1 Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. RP Koegel, RL (reprint author), Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. CR Amado A. 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PD SUM PY 2005 VL 30 IS 2 BP 93 EP 102 DI 10.2511/rpsd.30.2.93 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 966MA UT WOS:000232022900004 ER PT J AU Handen, BL Lubetsky, M AF Handen, BL Lubetsky, M TI Pharmacotherapy in autism and related disorders SO SCHOOL PSYCHOLOGY QUARTERLY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; MENTALLY-RETARDED ADULTS; DOUBLE-BLIND; OPEN-LABEL; BEHAVIORAL SYMPTOMS; INFANTILE-AUTISM; PSYCHOACTIVE MEDICINES; FLUOXETINE TREATMENT; SPECTRUM DISORDERS AB Autistic disorder is characterized by qualitative impairment in the areas of social interaction and communication, as well as stereotypic, repetitive patterns of behavior. In addition to the core features of autism, many individuals display a range of behavioral concems including anxiety, aggression, agitation, overactivity, self-injury, and stereotypic behavior. Recent prevalence estimates indicate that over 45% of individuals with autism are prescribed psychotropic medications for management of associated behavioral disorders. Yet, there remain considerable gaps in our knowledge of medication efficacy and safety in this population. This article provides an overview of the research in this area, including efficacy and potential side effects of the most commonly prescribed psychotropic medications for children and adolescents with autism. C1 Univ Pittsburgh, Dept Psychiat, Western Psychiat Inst Clin, Sch Med, Pittsburgh, PA 15213 USA. RP Handen, BL (reprint author), Univ Pittsburgh, Dept Psychiat, Western Psychiat Inst Clin, Sch Med, Thomas Detre Hall,3811 OHara St, Pittsburgh, PA 15213 USA. 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Ironically, as advances in vaccination successfully limit disease outbreaks, the impact that these infectious agents once had on society becomes marginalized. Public confidence in vaccination may erode because of real or perceived risks associated with immunization, and this in turn may lead to lower vaccination coverage and loss of herd immunity. Here, we will discuss some of the elements associated with public perceptions and fear of vaccination and place these into the context of how deadly several vaccine-preventable childhood diseases can be if vaccination coverage is insufficient. C1 Oregon Hlth Sci Univ, Vaccine & Gene Therapy Inst, Beaverton, OR 97006 USA. RP Slifka, MK (reprint author), Oregon Hlth Sci Univ, Vaccine & Gene Therapy Inst, 505 NW 185th Ave, Beaverton, OR 97006 USA. 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PD SUM PY 2005 VL 18 IS 2 BP 307 EP 315 DI 10.1089/vim.2005.18.307 PG 9 WC Immunology; Virology SC Immunology; Virology GA 951RL UT WOS:000230948200005 PM 16035942 ER PT J AU Yan, J Feng, JN Craddock, N Jones, IR Cook, EH Goldman, D Heston, LL Chen, JS Burkhart, P Li, WY Shibayama, A Sommer, SS AF Yan, J Feng, JN Craddock, N Jones, IR Cook, EH Goldman, D Heston, LL Chen, JS Burkhart, P Li, WY Shibayama, A Sommer, SS TI Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases SO NEUROSCIENCE LETTERS LA English DT Article DE vitamin D receptor; schizophrenia; psychiatric diseases; DOVAM-S; mutation detection ID PREGNANT-WOMEN; DOVAM-S; GENE; DISORDER; ASSOCIATION; ASIANS AB Intriguing parallels have been noted previously between the biology of Vitamin D and the epidemiology of schizophrenia. We have scanned the Vitamin D receptor (VDR) gene by DOVAM-S (Detection of Virtually All Mutations-SSCP), a robotically enhanced multiplexed scanning method. In total, 100 patients with schizophrenia (86 Caucasians and 14 African-Americans) were scanned. In addition, pilot experiments were performed in patients with bipolar disorder (BPD) (24), autism (24), attention deficit hyperactivity disorder (ADHD) (24), and alcoholism (20). A total of 762 kb of the VDR genomic sequence was scanned. R208N and V339I were each found in one African-American patient, while absent in 35 African-American controls without schizophrenia (2/14 versus 0/35, P = 0.08). Within the power of the study (&GE; 1.6-fold relative risk), the common M1T variant is not associated with schizophrenia. In the 92 scanned patients with other psychiatric diseases, R173S was found in a single patient with bipolar disorder. In conclusion, we describe three novel structural variants of the Vitamin D receptor. Further study is required to clarify their role, if any, in psychiatric disease. © 2005 Elsevier Ireland Ltd. All rights reserved. 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Lett. PD MAY 20 PY 2005 VL 380 IS 1-2 BP 37 EP 41 DI 10.1016/j.neulet.2005.01.018 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 924DI UT WOS:000228958600008 PM 15854747 ER PT J AU Larsson, HJ Eaton, WW Madsen, KM Vestergaard, M Olesen, AV Agerbo, E Schendel, D Thorsen, P Mortensen, PB AF Larsson, HJ Eaton, WW Madsen, KM Vestergaard, M Olesen, AV Agerbo, E Schendel, D Thorsen, P Mortensen, PB TI Risk factors for autism: Perinatal factors, parental psychiatric history, and socioeconomic status SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE autistic disorder; fetal growth retardation; mental disorders; parturition; perinatology; pregnancy outcome ID NEONATAL FACTORS; OBSTETRIC COMPLICATIONS; PRESCHOOL-CHILDREN; INFANTILE-AUTISM; BIRTH-WEIGHT; POPULATION; PREVALENCE; PREGNANCY; SCHIZOPHRENIA; DISORDERS AB Research suggests that heredity and early fetal development play a causal role in autism. This case-control study explored the association between perinatal factors, parental psychiatric history, socioeconomic status, and risk of autism. The study was nested within a cohort of all children born in Denmark after 1972 and at risk of being diagnosed with autism until December 1999. Prospectively recorded data were obtained from nationwide registries in Denmark. Cases totaled 698 children with a diagnosis of autism; each case was individually matched by gender, birth year, and age to 25 controls. Analyses by conditional logistic regression produced risk ratios and 95% confidence intervals. Adjusted analyses showed that the risk of autism was associated with breech presentation (risk ratio (RR) = 1.63, 95% confidence interval (CI): 1.18, 2.26), low Apgar score at 5 minutes (RR = 1.89, 95% CI: 1.10, 3.27), gestational age at birth < 35 weeks (RR = 2.45, 95% CI: 1.55, 3.86), and parental psychiatric history (schizophrenia-like psychosis: RR = 3.44, 95% CI: 1.48, 7.95; affective disorder: RR = 2.91, 95% CI: 1.65, 5.14). Analyses showed no statistically significant association between risk of autism and weight for gestational age, parity, number of antenatal visits, parental age, or socioeconomic status. Results suggest that prenatal environmental factors and parental psychopathology are associated with the risk of autism. These factors seem to act independently. C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mental Hlth, Baltimore, MD 21205 USA. Univ Aarhus, Dept Epidemiol & Social Med, Aarhus, Denmark. Aarhus Univ Hosp, Dept Clin Epidemiol, DK-8000 Aarhus, Denmark. 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PD MAY 15 PY 2005 VL 161 IS 10 BP 916 EP 925 DI 10.1093/aje/kwi123 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 923SQ UT WOS:000228930000002 PM 15870155 ER PT J AU Newschaffer, CJ Cole, SR AF Newschaffer, CJ Cole, SR TI Invited commentary: Risk factors for autism - Perinatal factors, parental psychiatric history, and socioeconomic status SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Editorial Material ID COMPLICATIONS; PHENOTYPE C1 Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA. Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Autism & Dev Disabilities Epidemiol, Baltimore, MD 21205 USA. RP Newschaffer, CJ (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St,Room E6030, Baltimore, MD 21205 USA. EM cnewscha@jhsph.edu CR BOLTON A, 1998, J AUTISM DEV DISORD, V28, P369 Bolton PF, 1997, J AM ACAD CHILD PSY, V36, P272, DOI 10.1097/00004583-199702000-00018 Cole SR, 2002, INT J EPIDEMIOL, V31, P163, DOI 10.1093/ije/31.1.163 Glasson EJ, 2004, ARCH GEN PSYCHIAT, V61, P618, DOI 10.1001/archpsyc.61.6.618 Greenland S, 1999, EPIDEMIOLOGY, V10, P37, DOI 10.1097/00001648-199901000-00008 Hernan MA, 2002, AM J EPIDEMIOL, V155, P176, DOI 10.1093/aje/155.2.176 Hultman CM, 2002, EPIDEMIOLOGY, V13, P417, DOI 10.1097/01.EDE.0000016968.14007.E6 Larsson HJ, 2005, AM J EPIDEMIOL, V161, P916, DOI 10.1093/aje/kwi123 Micali N, 2004, AUTISM, V8, P21, DOI 10.1177/1362361304040636 Zwaigenbaum L, 2002, J AM ACAD CHILD PSY, V41, P572, DOI 10.1097/00004583-200205000-00015 NR 10 TC 6 Z9 6 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAY 15 PY 2005 VL 161 IS 10 BP 926 EP 928 DI 10.1093/aje/kwi124 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 923SQ UT WOS:000228930000003 ER PT J AU Seeman, C AF Seeman, C TI Diagnosis autism: Now what?; 10 steps to improve treatment outcomes SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Libs, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Libs, Toledo, OH USA. CR KAPLAN LP, 2005, DIAGNOSIS AUTISM 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 MAY 15 PY 2005 VL 130 IS 9 BP 132 EP 132 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 925ZE UT WOS:000229091500159 ER PT J AU Biever, C AF Biever, C TI Lots of clues, but still no answers SO NEW SCIENTIST LA English DT News Item AB Autism is a complicated combination of genetic and environmental factors. Workis ongoing to find the causes of this disease. A recent study has found the risk of autism in twins appears now to be related to the month they are born in. Is it the birth date that is important, or the date of conception? NR 0 TC 2 Z9 2 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 14 PY 2005 VL 186 IS 2499 BP 14 EP 15 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 925WU UT WOS:000229085000017 ER PT J AU [Anonymous] AF [Anonymous] TI lEarly test is on the way SO NEW SCIENTIST LA English DT News Item AB While the causes of autism are still unclear, we are closer than ever to a blood test that could detect the disease very early on perhaps even at birth. Differences in the levels of more than one hundred proteins and several small molecules, and higher levels of two types of immune cells were found in autistic children in comparison to non-autistic children. NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD MAY 14 PY 2005 VL 186 IS 2499 BP 15 EP 15 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 925WU UT WOS:000229085000018 ER PT J AU Dawkins, MS AF Dawkins, MS TI Animals in translation: Using the mysteries of autism to decode animal behaviour SO NATURE LA English DT Book Review C1 Univ Oxford, Dept Zool, Oxford OX1 3PS, England. RP Dawkins, MS (reprint author), Univ Oxford, Dept Zool, S Parks Rd, Oxford OX1 3PS, England. CR Grandin Temple, 2005, ANIMALS TRANSLATION NR 1 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD MAY 12 PY 2005 VL 435 IS 7039 BP 147 EP 148 DI 10.1038/435147b PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 924ZO UT WOS:000229021100018 ER PT J AU Cromwell, HC Anstrom, K Azarov, A Woodward, DJ AF Cromwell, HC Anstrom, K Azarov, A Woodward, DJ TI Auditory inhibitory gating in the amygdala: Single-unit analysis in the behaving rat SO BRAIN RESEARCH LA English DT Article DE auditory processing; gamma amino butyric acid; neural inhibition; aversion; in vivo electrophysiology; schizophrenia; autism ID POSTTRAUMATIC-STRESS-DISORDER; EVENT-RELATED POTENTIALS; PREPULSE INHIBITION; ANIMAL-MODEL; NICOTINIC RECEPTORS; TOURETTES-SYNDROME; PYRAMIDAL CELLS; P50 SUPPRESSION; BASAL GANGLIA; TEMPORAL-LOBE AB Inhibitory sensory gating has been proposed to be a fundamental physiological process that filters neural input. Its temporal properties could allow for a rapid influence on vigilance and attention processes. Inhibitory mechanisms are reflected by reductions in neural responsiveness to repeated and well-predicted stimuli; for auditory gating, this translates into an inhibition of the neural activation to subsequent tone stimuli embedded within sequential and identical tone presentations. Here we expand previous neurophysiological data on inhibitory gating by examining gating in the amygdala using single-unit recording in freely moving animals. Previous data have shown the amygdala to be important in mediating rapid auditory sensory processing involved in emotional conditioning. We measured inhibitory gating with two matching auditory tones presented in a repetitive fashion (10 ms tones, ISI = 500 ms and 10 s between pairs) for 1 h (360 pairs). The majority of the tone responsive units showed inhibitory gating (78/95 units) located in both the medial and lateral subnuclei of the ainygdala. Different types of tone responses were gated, including both shorter- and longer-duration excitatory tone responses as well as inhibitory tone responses. Different degrees of gating were found ranging from 100% inhibition (complete gating category) to 25% inhibition (graded gating category). The degree of gating varied over short-term and long-term time intervals. These findings demonstrate the existence of inhibitory gating in the amygdala and provide a detailed description of the basic properties of this rapid neural inhibition that could play an important role in filtering stimulus input. (c) 2005 Elsevier B.V. All rights reserved. C1 Wake Forest Univ, Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27157 USA. RP Cromwell, HC (reprint author), Bowling Green State Univ, Dept Psychol, Bowling Green, OH 43403 USA. 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Analysis of phenotypically homogeneous subtypes has been used to both confirm and narrow potential autism linkage regions such as the chromosomal region 15q11-q13. Increased evidence for linkage in this region had been found in a subgroup of 21 autism families (total families = 94) stratified based on a savant skill factor (SSF) from the Autism Diagnostic Interview, Revised (ADI-R). We examined the savant phenotypic finding in our sample of 91 multiplex autism families. Using two-point parametric analysis in stratification with a cutoff point of a savant skill score of 0.16, our families failed to demonstrate linkage to 15q11-q13. In addition, ordered subset analysis (OSA) using SSF as a covariate also failed to show evidence for linkage. Our findings do not support savant skills as an informative phenotypic subset for linkage in our sample. (c) 2005 Wiley-Liss, Inc. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Div Pediat Neurol, Durham, NC USA. 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The well-replicated involvement of the serotonin neurotransmitter system in autism has stimulated interest in many genes in the serotonin pathway as possible candidates for mutations leading to autism susceptibility. Serotonin synthesis is controlled by the rate-limiting enzyme tryptophan hydroxylase. A mouse study of the original tryptophan hydroxylase gene (TPH1) and the new isoform (TPH2) showed that while TPH1 is primarily expressed peripherally, TPH2 is found exclusively in brain tissue. We searched for human sequence variants in 6,467 nucleotides covering all 11 exons of TPH2, and also 248 nucleotides upstream of the start codon, and 935 nucleotides downstream of the stop codon. Eighteen variants were characterized in 88 subjects with autism studied at our two centers, and 95 unrelated control subjects. 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Atypical cerebral asymmetry (ACA), the absence of the left hemisphere dominance for language, may be a shared phenotype due to genes located in regions of overlap. A binomal test is used to evaluate whether linked regions overlap more than expected by chance for 15 genome-wide scans in autism, ADHD, and dyslexia. Significant evidence of linkage overlap (p=10(-7)) is seen for autism, ADHD, and dyslexia for seven chromosomal regions (2p11-12, 5p13, 7q22-33, 9q33-34, 13q22, 16p13, and 17p11-q11). Linkage analysis of ACA and molecular markers for 270 sibling pairs with ADHD is conducted using the Haseman-Elston statistic. Linkage analysis supports ACA as a shared phenotype with risk genes located on 9q33-34 or 16p13 (P < 0.004). Further support stems from the overlap of these regions in schizophrenia, bipolar illness, specific language impairment (SLI), and handedness, all traits associated with ACA. Autism, ADHD, and dyslexia share regions of linkage overlap and ACA may be a shared phenotype for such genes similar to HLA in autoimmune disease. Because ACA is associated with certain aspects of creativity, such risk genes may also be enhancer genes for creativity. (c) 2005 Wiley-Liss, Inc. C1 Univ Calif Los Angeles, David Geffen Sch Med, Inst Neuropsychiat, Ctr Neurobehav Genet, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, Los Angeles, CA USA. RP Smalley, SL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Inst Neuropsychiat, Ctr Neurobehav Genet, 760 Westwood Blvd, Los Angeles, CA 90024 USA. 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Selective serotonin reuptake inhibitor (SSRI) drugs are used to treat disorders such as depression, stress, eating disorders, autism, and schizophrenia. It is thought that these drugs act to prolong the action of 5-HT by blocking reuptake. This may lead to decreased 5-HT content in the nerve fibers themselves; however, this has not previously been directly demonstrated. We have studied the effects of administration of two drugs, imipramine and citalopram, on levels of 5-HT in nerve fibers in the murine brain. Quantitative analysis of the areal density of 5-HT fibers throughout the brain was performed using ImageJ software. While a high density of fibers was observed in mid- and hind-brain regions and areas such as thalamus and hypothalamus, densities were far lower in areas such as cortex, where SSRIs might be thought to exert their actions. As anticipated, imipramine and citalopram produced a decline in 5-HT levels in nerve fibers, but the result was not uniform. 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Radiol. PD MAY PY 2005 VL 12 IS 5 BP 533 EP 534 DI 10.1016/j.acra.2005.02.012 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 923ZV UT WOS:000228949100001 PM 15866124 ER PT J AU Fayed, N Modrego, PJ AF Fayed, N Modrego, PJ TI Comparative study of cerebral white matter in autism and attention-deficit/hyperactivity disorder by means of magnetic resonance spectroscopy SO ACADEMIC RADIOLOGY LA English DT Article DE autism; attention-deficit/hyperactivity disorder; brain magnetic resonance spectroscopy ID N-ACETYL ASPARTATE; BRAIN-METABOLITES; CHILDREN; MARKER AB Rationale and Objectives. Autism and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental disorders whose pathophysiology is mostly unknown. As far as the symptoms are different and, in some aspects, opposed, we hypothesize that there must be biochemical differences in the brain of the afflicted children. The aim of the study is to analyze comparatively the metabolite concentration of the cerebral white matter in autism, in ADHD, and in a control group of healthy children to test the hypothesis that N-acetyl aspartate (NAA) is decreased in autism and increased in ADHD. Patients and Methods. We included 21 autistic children according to DSM-IV criteria, 8 children with ADHD meeting the respective criteria of DSM-IV, and 12 healthy controls of similar age. Single-voxel proton magnetic resonance spectroscopy was performed on all of them with an echo time of 30 milliseconds and a repetition time of 2500 milliseconds. The voxel was placed in the left centrum semiovale. Metabolite ratios relative to creatine were reported for NAA, choline, and myoinositol. Results. Although we did not observe differences between autistic children and controls, we found a mean higher concentration of NAA in the left centrum semiovale of ADHD children (2.2; SD, 0.21) than that found in autistic children (1.88; SD, 0.18) and controls (1.91; SD, 0.01), which was significant (P =.01 in parametric and in nonparametric test). Conclusion. We conclude that white matter of autistic children does not present alterations on MRS. We hypothesize that the higher concentration of NAA in the white matter of ADHD points to mitochondrial hypermetabolism. This may constitute a new substrate in the pathophysiology and merits further research. © AUR, 2005. C1 Clin Quiron, Magnet Resonance Unit, Zaragoza 50009, Spain. RP Modrego, PJ (reprint author), Clin Quiron, Magnet Resonance Unit, Avda Juan Carlos 1,21, Zaragoza 50009, Spain. EM med009626@saludalia.com CR American Psychiatric Association (DSM-IV), 1995, MAN DIAGN EST TRAST Barker PB, 2001, ANN NEUROL, V49, P423, DOI 10.1002/ana.90 Bauman M.L., 2003, NOVART FDN SYMP, V251, P281, DOI DOI 10.1002/047086938.CH8 Brambilla P, 2003, BRAIN RES BULL, V61, P557, DOI 10.1016/j.brainresbull.2003.06.001 Carrey N, 2003, CLIN NEUROPHARMACOL, V26, P218, DOI 10.1097/00002826-200307000-00013 Castellanos FX, 2002, JAMA-J AM MED ASSOC, V288, P1740, DOI 10.1001/jama.288.14.1740 Chugani DC, 1999, PROG NEURO-PSYCHOPH, V23, P635, DOI 10.1016/S0278-5846(99)00022-6 Clark JB, 1998, DEV NEUROSCI-BASEL, V20, P271, DOI 10.1159/000017321 Frith C, 2003, NOVART FDN SYMP, V251, P149 Hashimoto T, 1997, J CHILD NEUROL, V12, P91 Kato T, 1997, BRAIN DEV-JPN, V19, P131, DOI 10.1016/S0387-7604(96)00496-2 MacMaster FP, 2003, BIOL PSYCHIAT, V53, P184, DOI 10.1016/S0006-3223(02)01401-4 Mostofsky SH, 2002, BIOL PSYCHIAT, V52, P785, DOI 10.1016/S0006-3223(02)01412-9 Murphy DGM, 2002, ARCH GEN PSYCHIAT, V59, P885, DOI 10.1001/archpsyc.59.10.885 Otsuka H, 1999, NEURORADIOLOGY, V41, P517 Sokol DK, 2002, J CHILD NEUROL, V17, P245, DOI 10.1177/088307380201700401 TOFT PB, 1994, JMRI-J MAGN RESON IM, V4, P674, DOI 10.1002/jmri.1880040510 VICTOR M, 2001, PRINCIPLES NEUROLOGY, P629 Yeo RA, 2003, J AM ACAD CHILD PSY, V42, P303, DOI 10.1097/01.CHI.0000037024.34553.1B NR 19 TC 33 Z9 35 PU ASSOC UNIV RADIOLOGISTS PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523-2251 USA SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD MAY PY 2005 VL 12 IS 5 BP 566 EP 569 DI 10.1016/j.acra.2005.01.016 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 923ZV UT WOS:000228949100005 PM 15866128 ER PT J AU Capone, GT Grados, MA Kaufmann, WE Bernad-Ripoll, S Jewell, A AF Capone, GT Grados, MA Kaufmann, WE Bernad-Ripoll, S Jewell, A TI Down syndrome and comorbid autism-spectrum disorder: Characterization using the aberrant behavior checklist SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE pervasive developmental disorder; stereotypic movements; childhood disintegrative disorder; dual-diagnosis; aberrant behavior checklist; trisomy 21 ID PSYCHIATRIC-DISORDERS; FAMILY-HISTORY; CHILDREN; DIAGNOSIS; CLASSIFICATION; VARIABILITY; ADOLESCENTS; PHENOTYPES; SCALE AB To report on the cognitive and behavioral attributes of 61 children with Down syndrome (DS) and autistic-spectrum disorder (ASD) according to DSM-IV criteria; to determine the utility of the aberrant behavior checklist (ABC) to characterize these subjects for research purposes; and to test the hypothesis that subjects with DS + ASD could be distinguished from their typical DS peers using the ABC. Cross-sectional design. Cases with DS + ASD (N = 61), comparison group of DS + stereotypymovement disorder (SMD) (N = 26) and typical DS controls without behavior problems (N = 44) were ascertained and enrolled sequentially upon presentation to a DS clinic at an academic medical center over a 10-year period from 1991 to 2001. All subjects underwent neurodevelopmental and medical evaluation, and standardized cognitive testing. The parents provided responses to standardized behavioral questionnaires. Cognitive function (IQ) differed markedly across the three groups. The Lethary and Stereotypy subscales of the ABC were highly significant (P < 0.001) in distinguishing the three groups from one another. Within the ASD group differences were apparent by DSM-IV type on the Lethargy subscale, which reached significance, ANOVA (F = 0.002) and t-test (Autism > PDD, P = 0.005; PDD < CDD, P 0.002). Using a multivariate regression model, the ABC scales alone explained 62% of variance of ASD outcome; addition of demographic variables explained up to 68% of the variance. There is good correlation between DSM-IV criteria for autism and subscales scores on the ABC in subjects with DS. This study demonstrates the feasibility of using the ABC to characterize the neurobehavioral phenotype of a cohort of children with trisomy 21 and ASD for ongoing research purposes. (c) 2005 Wiley-Liss, Inc. C1 Kennedy Krieger Inst, Dept Neurol & Dev Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD 21205 USA. Kennedy Krieger Inst, Ctr Genet Disorders Cognit & Behav, Baltimore, MD USA. RP Capone, GT (reprint author), Kennedy Krieger Inst, Dept Neurol & Dev Med, 707 N Broadway, Baltimore, MD 21205 USA. EM capone@kennedykrieger.org CR AMAN MG, 1985, AM J MENT DEF, V89, P485 AMAN MG, 1985, AM J MENT DEF, V89, P492 Aman MG, 2004, CNS SPECTRUMS, V9, P36 [Anonymous], 1994, DIAGNOSTIC STAT MANU *APA, 1987, DIAGNOSTIC STAT MANU BARTAK L, 1976, J AUTISM CHILD SCHIZ, V6, P109, DOI 10.1007/BF01538054 Bayley N., 1969, BAYLEY SCALES INFANT BIHM EM, 1991, AM J MENT RETARD, V96, P209 BREGMAN JD, 1988, J AM ACAD CHILD PSY, V27, P440, DOI 10.1097/00004583-198807000-00011 Capone GT, 2001, J DEV BEHAV PEDIATR, V22, P40 CLEMENTS PR, 1976, MENT RETARD, V14, P30 Coley WB, 1909, P ROY SOC MED, V3, P1 COLLACOTT RA, 1992, BRIT J PSYCHIAT, V161, P671, DOI 10.1192/bjp.161.5.671 GARDINER K, 2004, BRIEFINGS FUNCTIONAL, V3, P1 GATH A, 1986, BRIT J PSYCHIAT, V149, P156, DOI 10.1192/bjp.149.2.156 Ghaziuddin M, 2000, J INTELL DISABIL RES, V44, P562, DOI 10.1046/j.1365-2788.2000.00271.x Ghaziuddin M, 1997, J INTELL DISABIL RES, V41, P87, DOI 10.1111/j.1365-2788.1997.tb00681.x GHAZIUDDIN M, 1992, J INTELL DISABIL RES, V36, P449 GILLBERG C, 1986, BRIT J PSYCHIAT, V149, P68, DOI 10.1192/bjp.149.1.68 Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 GILLBERG C, 1992, J INTELL DISABIL RES, V36, P201 Gould J., 1995, DEV MED CHILD NEUROL, V37, P398 Gurney JG, 2003, ARCH PEDIAT ADOL MED, V157, P622, DOI 10.1001/archpedi.157.7.622 Hendry CN, 2000, CLIN PSYCHOL REV, V20, P77, DOI 10.1016/S0272-7358(98)00094-4 HOON AH, 1993, J PEDIATR-US, V123, pS1, DOI 10.1016/S0022-3476(05)81587-2 Kau ASM, 2004, AM J MED GENET A, V126A, P9, DOI 10.1002/ajmg.a.20218 Kent L., 1998, AUTISM INT J RES PRA, V2, P259, DOI 10.1177/1362361398023004 Kent L, 1999, DEV MED CHILD NEUROL, V41, P153, DOI 10.1017/S001216229900033X LEVINSON A, 1955, PEDIATRICS, V16, P43 LUND J, 1988, ACTA PSYCHIAT SCAND, V78, P369, DOI 10.1111/j.1600-0447.1988.tb06350.x Moldavsky M, 2001, J AM ACAD CHILD PSY, V40, P749, DOI 10.1097/00004583-200107000-00009 MOSER H, 1985, NATL I HLTH, V1149, P121 MYERS BA, 1991, J NERV MENT DIS, V179, P609, DOI 10.1097/00005053-199110000-00004 RASMUSSEN P, 2001, DEV MED CHILD NEUROL, V43, P70 RITVO ER, 1990, AM J PSYCHIAT, V147, P1614 ROGERS SJ, 2001, DEV BEHAV PEDIAT, V22, P409 ROJAHN J, 1991, J AUTISM DEV DISORD, V21, P17, DOI 10.1007/BF02206994 SEAHILL J, 2002, NEW ENGL J MED, V347, P314 Thorndike RL, 1986, STANFORD BINET INTEL WAKABAYASHI S, 1979, J AUTISM DEV DISORD, V9, P31, DOI 10.1007/BF01531289 Waterhouse L, 1996, J AUTISM DEV DISORD, V26, P59, DOI 10.1007/BF02276235 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 42 TC 49 Z9 49 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD MAY 1 PY 2005 VL 134A IS 4 BP 373 EP 380 DI 10.1002/ajmg.a.30622 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 921IT UT WOS:000228758400006 PM 15759262 ER PT J AU Pfeiffer, B Kinnealey, M Reed, C Herzberg, G AF Pfeiffer, B Kinnealey, M Reed, C Herzberg, G TI Sensory modulation and affective disorders in children and adolescents with Asperger's disorder SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID ADAPTIVE-BEHAVIOR; DOWN-SYNDROME; ANXIETY; DEPRESSION; SYMPTOMS; AUTISM; MODEL; DEFENSIVENESS; IMPACT AB OBJECTIVE. The purpose of the study was to determine if there were significant relationships between dysfunction in sensory modulation, symptoms of affective disorders, and adaptive behaviors in children and adolescents with Asperger's disorder between 6 and 17 years of age. METHOD. Parents of 50 children and adolescents between 6 and 17 years of age diagnosed with Asperger's disorder based on the Diagnostic and Statistical Manual of Mental Disorders-IV criteria, completed the (a) Sensory Profile for children 6 to 10 years of age or the Adolescent/Adult Sensory Profile for adolescents 11 to 17 years of age; (b) the Adaptive Behavior Assessment System: Parent Version; (c) Revised Children's Manifest Anxiety Scale Adapted Parent's Version; and (d) the Children's Depression Inventory Adapted Parent's Version. Descriptive statistics and the Pearson product-moment coefficient of correlation calculations were used for data analysis. RESULTS. The results indicated that there were significantly strong positive correlations between sensory defensiveness and anxiety (r=.476, p =.000) in children and adolescents with Asperger's disorder. There were also significant relationships between symptoms of depression and hyposensitivity in the total group (r=.214, p=.05) and the older group (r=.492, p=.027). There were no significant relationships between depression and overall adaptive behavior (r=-.243, p=.089) or anxiety and overall adaptive behavior (r=-.108, p=.455). Significantly strong inverse relationships were found between the specific adaptive behaviors of functional academics, leisure, social skills, and symptoms of depression. Functional academics were also significantly inversely related to anxiety. Specifically, sensory hyper- and hypersensitivity were significantly inversely related to community use and social skills. CONCLUSION. The data supports positive relationships between anxiety and sensory defensiveness in all age ranges and a relationship between depression and hyposensitivity in older children. Stronger inverse relationships were apparent between specific adaptive behaviors including: (a) symptoms of depression and functional academics, leisure, social skills; (b) anxiety and functional academics; and (c) both sensory hyper- and hyposensitivity and community use and social skills. In this study, as the symptoms of affective disorders increased in children and adolescents with Asperger's disorder, the functional performance in the adaptive behaviors of functional academics and social skills appeared to decrease. Performance in the adaptive behaviors of community use and socials skills appeared to decrease as symptoms of dysfunction in sensory modulation increase. Further research is necessary to determine the impact of treatment for dysfunction on sensory modulation on affective disorders and performance in specific adaptive behaviors. C1 Coll Misericordia, Dallas, PA 18612 USA. Pediat Therapy Associates Lehigh Valley, PC, Allentown, PA USA. Temple Univ, Philadelphia, PA 19122 USA. Nova SE Univ, Ft Lauderdale, FL 33314 USA. RP Pfeiffer, B (reprint author), Coll Misericordia, 301 Lake St, Dallas, PA 18612 USA. 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PD MAY-JUN PY 2005 VL 59 IS 3 BP 335 EP 345 PG 11 WC Rehabilitation SC Rehabilitation GA 930HM UT WOS:000229406500010 PM 15969281 ER PT J AU Goldman, KJ Flanagan, T Shulman, C Enns, JT Burack, JA AF Goldman, KJ Flanagan, T Shulman, C Enns, JT Burack, JA TI Voluntary orienting among children and adolescents with down syndrome and MA-matched typically developing children SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID SELECTIVE ATTENTION; YOUNG-CHILDREN; LIFE-SPAN; AUTISM AB A forced-choice reaction-time (RT) task was used to examine voluntary visual orienting among children and adolescents with trisomy 21 Down syndrome and typically developing children matched at an MA of approximately 5.6 years, an age when the development of orienting abilities reaches optimal adult-like efficiency. Both groups displayed faster reaction times (RTs) when the target location was cued correctly than when cued incorrectly under both short and long SOA conditions, indicating intact orienting among children with Down syndrome. This finding is further evidence that the efficiency of many of the primary components of attention among persons with Down syndrome is consistent with their developmental level. C1 David Yellin Coll Educ, Jerusalem, Israel. McGill Univ, Montreal, PQ, Canada. Hebrew Univ Jerusalem, Jerusalem, Israel. Univ British Columbia, Vancouver, BC V5Z 1M9, Canada. RP Burack, JA (reprint author), David Yellin Coll Educ, Jerusalem, Israel. EM jake.burack@mcgill.ca CR AKHTAR N, 1989, J EXP CHILD PSYCHOL, V48, P315, DOI 10.1016/0022-0965(89)90008-8 Brodeur DA, 1997, CAN J EXP PSYCHOL, V51, P20, DOI 10.1037/1196-1961.51.1.20 BURACK JA, 1994, J ABNORM PSYCHOL, V103, P535, DOI 10.1037/0021-843X.103.3.535 Burack J. 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PD MAY PY 2005 VL 110 IS 3 BP 157 EP 163 DI 10.1352/0895-8017(2005)110<157:VOACAA>2.0.CO;2 PG 7 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 919AJ UT WOS:000228590400001 PM 15804191 ER PT J AU Heikura, U Linna, SL Olsen, P Hartikainen, AL Taanila, A Jarvelin, MR AF Heikura, U Linna, SL Olsen, P Hartikainen, AL Taanila, A Jarvelin, MR TI Etiological survey on intellectual disability in the Northern Finland birth cohort 1986 SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID SEVERE MENTAL-RETARDATION; SWEDISH COUNTY; PATHOGENETIC ASPECTS; CHILDREN; MILD; PREVALENCE; AUTISM; AGE AB The etiology of intellectual disability was studied both in incident (n = 9,432) and prevalent (n = 9,351) populations in a one-year birth cohort born in Northern Finland in 1985-1986. Data from multiple sources were used to follow the children until the age of 11.5 years. Of the incident cases (n = 119) with intellectual disabilities, 66.4% had etiologically biomedical associative factor. Paranatal factors were relatively fewer and prenatal more common compared with earlier studies. We found nearly double the prevalence of genetic factors leading to intellectual disabilities compared with a contemporary study from Norway. The differences between the populations, despite random variation, some dissimilarities between etiological categorization and diagnostic accuracy, are in most part due to true differences between the study populations and genetic pool. C1 Univ Oulu, Oulu 90014, Finland. Univ Hosp Oulu, Oulu, Finland. Univ London Imperial Coll Sci Technol & Med, Sch Med, London SW7 2AZ, England. RP Heikura, U (reprint author), Univ Oulu, Oulu 90014, Finland. 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S., 1963, BIOL MENTAL DEFECT RANTAKALLIO P, 1985, ARCH DIS CHILD, V60, P946 RANTAKALLIO P, 1986, AM J MENT RETARD, V90, P380 ROELEVELD N, 1997, DEV MED CHILD NEUROL, V28, P544 RUTTER M, 2000, J ABNORMAL CHILD PSY, V1, P3 Simonoff E, 1996, J CHILD PSYCHOL PSYC, V37, P259, DOI 10.1111/j.1469-7610.1996.tb01404.x Stromme P, 2000, DEV MED CHILD NEUROL, V42, P76, DOI 10.1017/S0012162200000165 Szymanski Ludwik, 1999, Journal of the American Academy of Child and Adolescent Psychiatry, V38, p5S SZYMANSKI LS, 1996, PSYCHIATRY, P605 THAPAR A, 1994, BRIT J PSYCHIAT, V164, P747, DOI 10.1192/bjp.164.6.747 Wilson D, 1999, COMPUT CONTROL ENG J, V10, P242 YANNET H, 1956, Adv Pediatr, V8, P217 YearginAllsopp M, 1997, DEV MED CHILD NEUROL, V39, P142 NR 38 TC 3 Z9 4 PU AMER ASSOC MENTAL RETARDATION PI WASHINGTON PA 444 N CAPITOL ST, NW, STE 846, WASHINGTON, DC 20001-1512 USA SN 0895-8017 J9 AM J MENT RETARD JI Am. J. Ment. Retard. PD MAY PY 2005 VL 110 IS 3 BP 171 EP 180 DI 10.1352/0895-8017(2005)110<171:ESOIDI>2.0.CO;2 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 919AJ UT WOS:000228590400003 PM 15804193 ER PT J AU Crosland, KA Zarcone, JR Schroeder, S Zarcone, T Fowler, S AF Crosland, KA Zarcone, JR Schroeder, S Zarcone, T Fowler, S TI Use of an antecedent analysis and a force sensitive platform to compare stereotyped movements and motor tics SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID LA-TOURETTE-SYNDROME; TARDIVE-DYSKINESIA; REPETITIVE BEHAVIOR; MENTAL-RETARDATION; BODY-ROCKING; DISORDERS; DYNAMICS; CHILDREN; AUTISM AB Stereotyped movements displayed by 6 participants and tics displayed by 6 children were evaluated using an antecedent behavioral analysis and a force sensitive platform. We found that tics occurred more often in an alone condition when compared to high preference toy and play conditions, whereas stereotyped movements were more variable across conditions. Using temporal measures and spectral analysis data from the force sensitive platform, we found that stereotyped movements tended to be longer in duration and displayed more rhythmic qualities when compared to tics. Results indicate that stereotyped movements and tics differ both quantitatively and qualitatively and support the use of new technologies, such as force plate technology, to more accurately evaluate these differences. C1 Univ Rochester, Med Ctr, Strong Ctr Dev Disabil, Dept Pediat, Rochester, NY 14642 USA. Univ Kansas, Lawrence, KS 66045 USA. RP Zarcone, JR (reprint author), Univ Rochester, Med Ctr, Strong Ctr Dev Disabil, Dept Pediat, 601 Elmwood Ave,Box 671, Rochester, NY 14642 USA. EM jennifer_zarcone@urmc.rochester.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN DIS Baumeister A. A., 1973, INT REV RES MENT RET, P55, DOI 10.1016/S0074-7750(08)60037-3 Bodfish J. W., 1999, W CAROLINA CTR RES R Bodfish JW, 2001, AM J MENT RETARD, V106, P123, DOI 10.1352/0895-8017(2001)106<0123:SAMCDI>2.0.CO;2 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 BRUUN RD, 1984, J AM ACAD CHILD PSY, V23, P126, DOI 10.1097/00004583-198403000-00002 CAINE ED, 1988, NEUROLOGY, V38, P472 CAMPBELL M, 1990, PSYCHOPHARMACOL BULL, V26, P260 Cutson TM, 1997, J AM GERIATR SOC, V45, P435 Fowler SC, 2001, J NEUROSCI METH, V107, P107, DOI 10.1016/S0165-0270(01)00359-4 KALACHNIK JE, 1994, ANN PHARMACOTHER, V28, P185 LECKMAN JF, 1988, TOURETTES SYNDROME T, P3 LEWIS M, 1984, AM J MENT DEF, V89, P287 Lewis MH, 1998, MENT RETARD DEV D R, V4, P80, DOI 10.1002/(SICI)1098-2779(1998)4:2<80::AID-MRDD4>3.0.CO;2-0 Liu YJ, 1998, J AM GERIATR SOC, V46, P431 Newell KM, 1999, AM J MENT RETARD, V104, P279, DOI 10.1352/0895-8017(1999)104<0279:VOSBIA>2.0.CO;2 Peterson BS, 1998, BIOL PSYCHIAT, V44, P1337, DOI 10.1016/S0006-3223(98)00176-0 SINGER HS, 1991, MEDICINE, V70, P15 Sprague R. L., 1996, STEREOTYPED MOVEMENT SPRAGUE RL, 1993, J NERV MENT DIS, V181, P42, DOI 10.1097/00005053-199301000-00008 SPRAGUE RL, 1995, AM J MENT RETARD, V100, P345 NR 21 TC 8 Z9 8 PU AMER ASSOC MENTAL RETARDATION PI WASHINGTON PA 444 N CAPITOL ST, NW, STE 846, WASHINGTON, DC 20001-1512 USA SN 0895-8017 J9 AM J MENT RETARD JI Am. J. Ment. Retard. PD MAY PY 2005 VL 110 IS 3 BP 181 EP 192 DI 10.1352/0895-8017(2005)110<181:UOAAAA>2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 919AJ UT WOS:000228590400004 PM 15804194 ER PT J AU Gray, KM Tonge, BJ AF Gray, KM Tonge, BJ TI Screening for autism in infants and preschool children with developmental delay SO AUSTRALIAN AND NEW ZEALAND JOURNAL OF PSYCHIATRY LA English DT Article DE autism; children; infants; screening ID YOUNG-CHILDREN; SPECTRUM DISORDERS; BEHAVIOR CHECKLIST; MENTAL-RETARDATION; ADI-R; SYMPTOMS; AGE; RECOGNITION; POPULATION; INSTRUMENT AB Objective: This study aimed to identify emotional and behavioural problems specific to young children with autism using the Developmental Behaviour Checklist (DBC-P) and thus evaluate the efficacy of this checklist as a screening tool for autism in children with developmental delay aged 18-48 months. Method: Subjects were 60 children with autism and developmental delay and 60 children with developmental delay without autism. Results: Features were identified which differentiated the children with autism from those with developmental delay without autism. Analyses revealed that a 17-item version of the DBC-P performed well as a screening tool for autism, with an 'area under the curve' of 0.874, sensitivity of 0.8750, and specificity of 0.6909. Conclusions: The DBC-P offers a potential simple and inexpensive method of screening at risk populations of preschool children with developmental delay for autism, thus facilitating timely referral to scarce specialist autism diagnostic services. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Dept Child & Adolescent Psychiat, Monash Med Ctr, Clayton, Vic 3168, Australia. RP Gray, KM (reprint author), Monash Univ, Ctr Dev Psychiat & Psychol, Dept Child & Adolescent Psychiat, Monash Med Ctr, 246 Clayton Rd, Clayton, Vic 3168, Australia. EM kylie.gray@med.monash.edu.au RI Gray, Kylie/H-3345-2014 OI Gray, Kylie/0000-0001-6518-4240 CR ADRIEN JL, 1992, J AUTISM DEV DISORD, V22, P375, DOI 10.1007/BF01048241 ALTMAN DG, 1994, BRIT MED J, V308, P1552 ALTMAN DG, 1994, BRIT MED J, V309, P102 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th AMES LB, 1979, GESELL I CHILD 1 6 Arbuckle J. 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N. Z. J. Psych. PD MAY PY 2005 VL 39 IS 5 BP 378 EP 386 DI 10.1080/j.1440-1614.2005.01585.x PG 9 WC Psychiatry SC Psychiatry GA 920LH UT WOS:000228689900009 PM 15860026 ER PT J AU Higgins, DJ Bailey, SR Pearce, JC AF Higgins, DJ Bailey, SR Pearce, JC TI Factors associated with functioning style and coping strategies of families with a child with an autism spectrum disorder SO AUTISM LA English DT Article DE ASD; Asperger syndrome; autism; coping; family support; respite ID MENTAL-RETARDATION; DOWN-SYNDROME; STRESS; PARENTS; MOTHERS AB A survey of parents/caregivers of a child with an autism spectrum disorder (ASD) was conducted to examine the relationship between ASD characteristics, family functioning and coping strategies. Having a child with ASD places considerable stress on the family. Primary caregivers of a child with ASD from a regional and rural area in Victoria, Australia (N = 53) were surveyed concerning their child with ASD, family functioning (adaptability and cohesion) I marital satisfaction, self-esteem and coping strategies. Results suggest that these caregivers had healthy self-esteem, although they reported somewhat lower marital happiness, family cohesion and family adaptability than did norm groups. Coping strategies were not significant predictors of these outcome variables. Results highlight the need for support programmes to target family and relationship variables as well as ASD children and their behaviours, in order to sustain the family unit and improve quality of life for parents and caregivers as well as those children. C1 Deakin Univ, Geelong, Vic 3217, Australia. EM daryl.higgins@aifs.gov.au CR Bristol M, 1984, AUTISM ADOLESCENTS A, P251 Gray David E., 1992, Australia and New Zealand Journal of Developmental Disabilities, V18, P83 Hayes V E, 1997, Sch Inq Nurs Pract, V11, P259 HECIMOVIC A, 1999, AUTISM IDENTIFICATIO, P261 HOLROYD J, 1976, AM J MENT DEF, V80, P431 HOPPES K, 1990, J CLIN CHILD PSYCHOL, V19, P365, DOI 10.1207/s15374424jccp1904_8 JONES G, 1997, ED CHILD PSYCHOL, V14, P71 KLIN A, 1997, DEV PSYCHOPATHOL, P208 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P205, DOI 10.1007/BF01058151 KONSTANTAREAS M, 1995, J AUTISM DEV DISORD, V25, P443, DOI 10.1007/BF02179378 Kraijer D, 2000, J AUTISM DEV DISORD, V30, P39, DOI 10.1023/A:1005460027636 LILLY H, 1977, AUSTR AUTISM REV, V1, P27 MCCUBBIN HI, 1983, J MARRIAGE FAM, V45, P359, DOI 10.2307/351514 MILGRAM NA, 1988, J AUTISM DEV DISORD, V18, P415, DOI 10.1007/BF02212196 NORTON R, 1983, J MARRIAGE FAM, V45, P141, DOI 10.2307/351302 Olson D. H., 1982, FACES POWERS MD, 1989, CHILDREN AUSTISM PAR, P105 ROBBINS FR, 1991, J EARLY INTERVENTION, V15, P173 RODRIGUE JR, 1990, J CLIN CHILD PSYCHOL, V19, P371, DOI 10.1207/s15374424jccp1904_9 ROEYERS H, 1995, CHILD CARE HLTH DEV, V21, P305, DOI 10.1111/j.1365-2214.1995.tb00760.x Rosenberg M., 1965, SOC ADOLESCENT SELFI Sanders JL, 1997, CHILD FAM BEHAV THER, V19, P15, DOI 10.1300/J019v19n04_02 SCHREIBMAN L, 1988, AUSTIM, V17 Senel H., 1996, INT J ADV COUNS, V18, P61 Sharpley CF, 1997, J INTELLECT DEV DIS, V22, P19, DOI 10.1080/13668259700033261 TOMMASONE L, 1989, CHILDREN AUTISM PARE, P31 Tonge B. J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Williams K. E., 2002, PSYCHOL HEALTH MED, V7, P127, DOI [10.1080/13548500120116076, DOI 10.1080/13548500120116076] Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 29 TC 95 Z9 97 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 MAY PY 2005 VL 9 IS 2 BP 125 EP 137 DI 10.1177/1362361305051403 PG 13 WC Psychology, Developmental SC Psychology GA 926VZ UT WOS:000229153100002 PM 15857858 ER PT J AU Murray, D Lesser, M Lawson, W AF Murray, D Lesser, M Lawson, W TI Attention, monotropism and the diagnostic criteria for autism SO AUTISM LA English DT Article DE attention; strategies; interest; monotropism; motivation ID ASPERGERS SYNDROME; MIND; CHILDREN; ABILITIES; DISORDER; DEFICIT; ADULTS; TASK AB The authors conclude from a range of literature relevant to the autistic condition that atypical strategies for the allocation of attention are central to the condition. This assertion is examined in the context of recent research, the diagnostic criteria for autism in DSM-IV and ICD-10, and the personal experiences of individuals with autism including one of the authors of the article. The first two diagnostic criteria are shown to follow from the restricted range of interests referred to in the third criterion. Implications for practice are indicated. C1 Autism & Comp, London N19 3AZ, England. RP Murray, D (reprint author), Autism & Comp, 42 Cheverton Rd, London N19 3AZ, England. EM dinahmurray@beeb.net CR ALLEN PM, 1993, EVOLUTION COGNITIVE American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASPERGER H, 1992, AUTISM ASPERGER SYND, P37 ATTWOOD T, 1992, COMMUNICATION, V26 Bara BG, 2001, BRAIN LANG, V77, P216, DOI 10.1006/brln.2000.2429 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Blackburn R, 2000, GOOD AUTISM PRACTICE, V1, P2 BLACKMAN L, 2001, LUCYS STORY AUSTISM Bogdashina O, 2003, SENSORY PERCEPTUAL I BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Brock J, 2002, DEV PSYCHOPATHOL, V14, P209 BRYSON SE, 1997, ATTENTION DEV PSYCHO, P232 CESARONI L, 1991, J AUTISM DEV DISORD, V21, P303, DOI 10.1007/BF02207327 COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 Dahlgren SO, 1996, J CHILD PSYCHOL PSYC, V37, P759, DOI 10.1111/j.1469-7610.1996.tb01469.x Engel AK, 2001, NAT REV NEUROSCI, V2, P704, DOI 10.1038/35094565 Frith U, 1991, AUTISM ASPERGER SYND GARNER I, 2001, SEARCH COHERENCE, P75 Ghaziuddin M, 2002, J AUTISM DEV DISORD, V32, P299, DOI 10.1023/A:1016330802348 Goldstein G, 2001, J AUTISM DEV DISORD, V31, P433, DOI 10.1023/A:1010620820786 Grandin T., 1995, THINKING PICTURES GRANDIN T, 1986, EMERGENCE LABELLED A GREEN J, 2001, LANGUAGE Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Hermelin B., 2001, BRIGHT SPLINTERS MIN Hobson R. P., 1990, DEV PSYCHOPATHOL, V2, P163, DOI 10.1017/S0954579400000687 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 Jordan D., 1990, Endangered Species Technical Bulletin, V15, P6 JORDAN R, 1999, AUTISTIC SPECTRUM DI JORDAN RR, 1999, GOOD AUTISM PRAC APR, P27 Kanner L, 1943, NERV CHILD, V2, P217 Klin A, 2003, PHILOS T ROY SOC B, V358, P345, DOI 10.1098/rstb.2002.1202 Lawson W., 2001, UNDERSTANDING WORKIN Lawson W., 1998, LIFE GLASS PERSONAL Lee A, 1998, J CHILD PSYCHOL PSYC, V39, P1131, DOI 10.1111/1469-7610.00417 LOVAAS OI, 1971, J ABNORM PSYCHOL, V77, P211, DOI 10.1037/h0031015 LYONS J, 1968, INTRO THEORETICAL LI Mari M, 2003, PHILOS T ROY SOC B, V358, P393, DOI 10.1098/rstb.2002.1205 Mottron L, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P131 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P203, DOI 10.1017/S0021963098003333 MURRAY DKC, 1992, LIVING AUSTISM INDIV MURRAY DKC, 1996, THERAPEUTIC INTERVEN MURRAY DKC, 1986, THESIS U LONDON OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P765, DOI 10.1017/S0021963098002601 Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P777, DOI 10.1017/S0021963098002613 Plaisted K. C, 2001, The development of autism: perspectives from theory and research, P131 POLAISTED KC, 1999, J CHILD PSYCHOL PSYC, V40, P742 Roeyers H, 2001, J CHILD PSYCHOL PSYC, V42, P271, DOI 10.1111/1469-7610.00718 RUSSELL J, 2002, COGNITIVE DEFICITS B SEGAR M, 1997, COPING SURVIVAL GUID SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x WEBSTER A, 2002, ED CHILD PSYCHOL, V19, P54 *WHO, 1992, ITN CLASS MENT BEH D Willey L. H., 2003, ASPERGER SYNDROME AD Williams D, 1994, SOMEBODY SOMEWHERE Williams D., 1998, AUTISM SENSING UNLOS Wing L., 1996, AUTISTIC SPECTRUM GU NR 58 TC 21 Z9 21 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 MAY PY 2005 VL 9 IS 2 BP 139 EP 156 DI 10.1177/1362361305051398 PG 18 WC Psychology, Developmental SC Psychology GA 926VZ UT WOS:000229153100003 PM 15857859 ER PT J AU Hale, CM Tager-Flusberg, H AF Hale, CM Tager-Flusberg, H TI Social communication in children with autism - The relationship between theory of mind and discourse development SO AUTISM LA English DT Article DE discourse skills; social communication; theory of mind ID INDIVIDUAL-DIFFERENCES; ASPERGER-SYNDROME; JOINT ATTENTION; YOUNG-CHILDREN; ROLE-TAKING; LANGUAGE; DEFICITS; BELIEFS; KNOWLEDGE; DISORDERS AB This longitudinal study investigated the developmental trajectory of discourse skills and theory of mind in 57 children with autism. Children were tested at two time points spaced 1 year apart. Each year they provided a natural language sample while interacting with one parent, and were given standardized vocabulary measures and theory of mind a developmentally sequenced battery of tasks. The language samples were coded for conversational skills, specifically the child's use of topic-related contingent utterances. Children with autism made significant gains over 1 year in the ability to maintain a topic of discourse. Hierarchical regression analyses demonstrated that theory of mind skills contributed unique variance to individual differences in contingent discourse ability and vice versa, when measured concurrently; however, they did not predict longitudinal changes. The findings offer some empirical support for the hypothesis that theory of mind is linked to communicative competence in children with autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Harvard Univ, Sch Med, Childrens Hosp, Cambridge, MA 02138 USA. RP Tager-Flusberg, H (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,L-814, Boston, MA 02118 USA. 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Symptom intensity, overall language level, age of recognition of first disturbances and level of psychological development were examined in 222 children with pervasive developmental disorder with a mean age of 5 years. Results showed a positive correlation between language level and psychological development as well as between language level and intensity of symptoms. The central position of language in psychological development is discussed. C1 Univ Montpellier 3, F-34199 Montpellier, France. RP Pry, R (reprint author), Univ Montpellier 3, Route de Mende, F-34199 Montpellier, France. CR ALLEN DA, 1992, INT CONGR SER, V965, P157 AUSSILLOUX C, 1996, ETUDE FACTEURS EVOLU BAGHDADLI A, IN PRESS J INTELLECT BAGHDADLI A, IN PRESS EUROPEAN J Baron-Cohen S., 2000, UNDERSTANDING OTHER, P3 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P158, DOI DOI 10.1192/BJP.168.2.158 Di Giacomo A., 1998, EUROPEAN CHILD ADOLE, V7, P131 FECTEAU S, IN PRESS J CHILD PSY 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 Hosmer DW, 2000, APPL LOGISTIC REGRES, V2nd Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 Jarrold C., 1997, AUTISM, V1, P57, DOI [10.1177/1362361397011007, DOI 10.1177/1362361397011007] KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C., 1997, HDB AUTISM PERVASIVE, P195 Malvy J., 1999, AUTISM, V3, P357, DOI 10.1177/1362361399003004004 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X Petersen A F, 1983, Hist Philos Life Sci, V5, P69 PIVEN J, 1996, J AM ACAD CHILD ADOL, V37, P51 Pry R., 1996, ENFANCE, V3, P315 Pry R., 2000, PSYCHOL PSYCHOMETRIE, V21, P33 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 Schopler E., 1986, CHILDHOOD AUTISM RAT Sparrow S, 1984, VINELAND ADAPTIVE BE TAGERFLUSBERG H, 1997, HDB AUTISM PERVASIVE, P894 TAGERFLUSBERG H, 1981, J AUTISM DEV DISORD, V11, P45, DOI 10.1007/BF01531340 Tager-Flusberg H, 1989, AUTISM NATURE DIAGNO, P92 TUCHMAN RF, 1991, PEDIATRICS, V88, P1219 VOLKMAR FR, 1985, AM J PSYCHIAT, V142, P1450 WATTERHOUSE L, 1982, BRAIN LANG, V15, P307 WLALON H, 1925, ENFANT TURBULENT RET WLALON H, 1942, ACTE PENSEE ESSAI PS World Health Organziation, 1992, ICD10 CLASS MENT BEH NR 34 TC 10 Z9 10 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 EI 1461-7005 J9 AUTISM JI Autism PD MAY PY 2005 VL 9 IS 2 BP 179 EP 189 DI 10.1177/1362361305047222 PG 11 WC Psychology, Developmental SC Psychology GA 926VZ UT WOS:000229153100005 PM 15857861 ER PT J AU Pakenham, KI Samios, C Sofronoff, K AF Pakenham, KI Samios, C Sofronoff, K TI Adjustment in mothers of children with Asperger syndrome: An application of the double ABCX model of family adjustment SO AUTISM LA English DT Article DE Asperger syndrome; diagnosis; double ABCX model; maternal adjustment ID SOCIAL SUPPORT QUESTIONNAIRE; MENTALLY-RETARDED CHILDREN; AUTISTIC-CHILDREN; CHILDHOOD AUTISM; CHRONICALLY ILL; RATING SCALE; STRESS; PARENTS; ADAPTATION; IMPACT AB The present study examined the applicability of the double ABCX model of family adjustment in explaining maternal adjustment to caring for a child diagnosed with Asperger syndrome. Forty-seven mothers completed questionnaires at a university clinic while their children were participating in an anxiety intervention. The children were aged between 10 and 12 years. Results of correlations showed that each of the model components was related to one or more domains of maternal adjustment in the direction predicted, with the exception of problem-focused coping. Hierarchical regression analyses demonstrated that, after controlling for the effects of relevant demographics, stressor severity, pile-up of demands and coping were related to adjustment. Findings indicate the utility of the double ABCX model in guiding research into parental adjustment when caring for a child with Asperger syndrome. Limitations of the study and clinical implications are discussed. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Pakenham, KI (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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RP Harrison, J (reprint author), Univ Florida, Coll Nursing, Gainesville, FL 32611 USA. CR Wolfberg P. J., 2003, PEER PLAY AUTISM SPE NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2005 VL 9 IS 2 BP 217 EP 220 DI 10.1177/1362361305051407 PG 4 WC Psychology, Developmental SC Psychology GA 926VZ UT WOS:000229153100008 ER PT J AU Welchew, DE Ashwin, C Berkouk, K Salvador, R Suckling, J Baron-Cohen, S Bullmore, ET AF Welchew, DE Ashwin, C Berkouk, K Salvador, R Suckling, J Baron-Cohen, S Bullmore, ET TI Functional disconnectivity of the medial temporal lobe in Asperger's syndrome SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; functional connectivity; multivariate analysis; neuroimaging; systems; dysmodularity ID EMOTIONALLY INFLUENCED MEMORY; INDIVIDUAL-DIFFERENCES; CHILDHOOD AUTISM; SOCIAL COGNITION; BRAIN; SCHIZOPHRENIA; CONNECTIVITY; NEUROBIOLOGY; DISORDER; SYSTEM AB Background: Autistic spectrum disorders (ASD) are neurodevelopmental conditions that may be caused by abnormal connectivity between brain regions constituting neurocognitive networks for specific aspects of social cognition. Methods. We used three-way multidimensional scaling of regionally parcellated functional magnetic resonance imaging (fMRI) data to explore the hypothesis of abnormal functional connectivity in people with ASD. Thirteen high-functioning individuals with Asperger's syndrome and 13 healthy volunteers were scanned during incidental processing of fearful facial expressions. Results: Using permutation tests for inference, we found evidence,for significant abnormality of functional integration of amygdala and parabippocampal gyrus (p < .05, false discovery rate [FDR] corrected) in people with Asperger's syndrome. There were less salient abnormalities in functional connectivity of anterior cingulate, inferior occipital, and inferior frontal cortex, but there was no significant difference between groups in whole brain functional connectivity. Conclusions: We conclude there is evidence that functional connectivity of medial temporal lobe structures specifically is abnormal in people with Asperger's syndrome during fearful face processing. C1 Univ Cambridge, Brain Mapping Unit, Cambridge CB2 2QQ, England. Univ Cambridge, Autism Res Ctr, Cambridge CB2 2QQ, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 2QQ, England. Univ Cambridge, Dept Psychol, Cambridge CB2 2QQ, England. Univ Cambridge, Wolfson Brain Imaging Ctr, Cambridge CB2 2QQ, England. RP Bullmore, ET (reprint author), Univ Cambridge, Addenbrookes Hosp, Dept Psychiat, Brain Mapping Unit, Cambridge CB2 2QQ, England. EM etb23@cam.ac.uk RI Bullmore, Edward/C-1706-2012 OI Bullmore, Edward/0000-0002-8955-8283 CR Adolphs R, 2001, CURR OPIN NEUROBIOL, V11, P231, DOI 10.1016/S0959-4388(00)00202-6 Adolphs R, 2002, J COGNITIVE NEUROSCI, V14, P1264, DOI 10.1162/089892902760807258 Aggleton J. 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Psychiatry PD MAY 1 PY 2005 VL 57 IS 9 BP 991 EP 998 DI 10.1016/j.biopsych.2005.01.028 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 919IO UT WOS:000228611900006 PM 15860339 ER PT J AU Pelphrey, KA Morris, JP McCarthy, G AF Pelphrey, KA Morris, JP McCarthy, G TI Neural basis of eye gaze processing deficits in autism SO BRAIN LA English DT Article DE autism; eye gaze; functional MRI ID SUPERIOR TEMPORAL SULCUS; HIGH-FUNCTIONING AUTISM; CHILDHOOD AUTISM; CORTICAL ACTIVATION; SOCIAL-PERCEPTION; JOINT ATTENTION; REVISED VERSION; HUMAN BRAIN; FMRI; CHILDREN AB Impairments in using eye gaze to establish joint attention and to comprehend the mental states and intentions of other people are striking features of autism. Here, using event-related functional MRI (fMRI), we show that in autism, brain regions involved in gaze processing, including the superior temporal sulcus (STS) region, are not sensitive to intentions conveyed by observed gaze shifts. On congruent trials, subjects watched as a virtual actor looked towards a checkerboard that appeared in her visual field, confirming the subject's expectation regarding what the actor 'ought to do' in this context. On incongruent trials, she looked towards empty space, violating the subject's expectation. Consistent with a prior report from our laboratory that used this task in neurologically normal subjects, 'errors' (incongruent trials) evoked more activity in the STS and other brain regions linked to social cognition, indicating a strong effect of intention in typically developing subjects (n = 9). The same brain regions were activated during observation of gaze shifts in subjects with autism (n = 10), but did not differentiate congruent and incongruent trials, indicating that activity in these regions was not modulated by the context of the perceived gaze shift. These results demonstrate a difference in the response of brain regions underlying eye gaze processing in autism. We conclude that lack of modulation of the STS region by gaze shifts that convey different intentions contributes to the eye gaze processing deficits associated with autism. C1 Duke Univ, Med Ctr, Duke UNC Brain Imaging & Anal Ctr, Durham, NC 27710 USA. Vet Affairs Med Ctr, Dept Vet Affairs, Durham, NC USA. Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC USA. RP Pelphrey, KA (reprint author), Duke Univ, Med Ctr, Duke UNC Brain Imaging & Anal Ctr, Box 3918, Durham, NC 27710 USA. 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In order to establish whether sleep disorders truly belong to the autism spectrum disorder (ASD) phenotype, we conducted a subjective and objective study of sleep in a group of high-functioning adults with ASD but without sleep complaints, psychiatric disorders or neurological comorbidity. We compared the subjective data of 27 ASD participants with those of 78 healthy controls matched for chronological age and gender. Subjective measures of sleep in the clinical group were compatible with insomnia and/or a tolerable phase advance of the sleep-wake cycle. Subjective data were confirmed by objective laboratory sleep recordings in a subset of 16 patients and 16 controls. Persons with autism presented with a longer sleep latency (P < 0.04), more frequent nocturnal awakenings (P < 0.03), lower sleep efficiency (P < 0.03), increased duration of stage 1 sleep (P < 0.02), decreased non-REM sleep (stages 2 + 3 + 4, P < 0.04) and slow-wave sleep (stages 3 + 4, P < 0.05), fewer stage 2 EEG sleep spindles (P < 0.004), and a lower number of rapid eye movements during REM sleep (P < 0.006) than did control participants. On clinical scales, the scores of persons with ASD on the Beck Depression Inventory were similar to those of persons without, but their trait anxiety scores on the Spielberger Anxiety Scale were higher (P < 0.02). The state anxiety scores of the Spielberger scale and cortisol levels were the same in the two groups. Objective total sleep time correlated negatively with the Social (-0.52, P < 0.05) and Communication (-0.54, P < 0.02) scales of the Autism Diagnostic Interview-Revised. 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Neurosciences SC Neurosciences & Neurology GA 919RM UT WOS:000228635300015 PM 15705609 ER PT J AU van Harskamp, NJ Rudge, P Cipolotti, L AF van Harskamp, NJ Rudge, P Cipolotti, L TI Cognitive and social impairments in patients with superficial siderosis SO BRAIN LA English DT Article DE superficial siderosis; theory of mind; cerebellum; cognitive functioning; social cognition ID CENTRAL-NERVOUS-SYSTEM; POSTERIOR-FOSSA TUMORS; CEREBRAL-BLOOD-FLOW; CEREBELLAR CONTRIBUTION; STORY COMPREHENSION; ACQUIRED SOCIOPATHY; INFANTILE-AUTISM; MIND; BRAIN; ABNORMALITIES AB Superficial siderosis of the CNS is a rare condition, caused by deposition of haemosiderin in the superficial layers of the CNS due to repeated chronic subarachnoid or intraventricular haemorrhage. Typically, the hindbrain structures, especially the cerebellum, are most affected. There is a surprising lack of studies investigating in detail the behavioural functioning of patients with such a condition. In this study, we document for the first time the cognitive, social and emotional processing of six patients with a confirmed clinical diagnosis of superficial siderosis. They were aged between 40 and 62 years, with a mean age of 50.2 years; four were male. We administered a comprehensive battery of general cognitive ability and social cognitive tasks. A review of MRI was also undertaken. The findings indicate selective cognitive impairments affecting speech production, visual recall memory and executive functions. In addition, a selective pattern of social dysfunction, affecting the ability to represent other people's mental states, was found. These behavioural dysfunctions are reported in the context of MRI-documented lesions maximally involving the cerebellum, in particular the superior vermis, as well as the medial and inferior frontal cortex. These results suggest that superficial siderosis is associated with a distinct pattern of cognitive and social impairments. They are consistent with the recently proposed role of the cerebellum as a modulator of cognitive, social and emotional functions. C1 UCL Natl Hosp Neurol & Neurosurg, Dept Neuropsychol, London WC1N 3BG, England. RP Cipolotti, L (reprint author), UCL Natl Hosp Neurol & Neurosurg, Dept Neuropsychol, Queen Sq, London WC1N 3BG, England. 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In this paper we compared the outcome of a linear registration method for brain images of psychiatric and control, groups of different ages in order to assess the relative adequacy of normalization in such diverse groups. Methods: Magnetic Resonance images (MRI) of the brains of pediatric and adolescent subjects (mean ages 19 and 10.5 years) with a pervasive developmental disorder (PDD) and their healthy controls were included. A simple voxel-wise test of the group variances in image intensities was performed to evaluate regional differences in registration quality. Dipole analysis of visual P1 was performed to establish whether source locations were comparable across groups. Results: Significant differences between pediatric groups were found in white matter and thalamic regions of the brain. For all other group-wise comparisons, differences were confined to skull and neck regions. Dipole locations were found to be more anteriorly located in the adolescent groups. Conclusions: The normalization procedure used in this paper is based on a brain template of normal adult brains from a restricted age group, and the results show that the use of this method in pediatric groups is less adequate. The method seems suitable for use in psychiatric groups. Also, the generators of visual P1 in PDD patients were found to be comparable to controls. Significance: The results suggest that this existing normalization method can be used in diverse populations, but is less suitable for pediatric images. © 2005 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. C1 Univ Utrecht, Fac Pharmaceut Sci, Dept Psychopharmacol, NL-3584 CA Utrecht, Netherlands. Univ Utrecht, Fac Social Sci, Dept Psychonom, Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. RP Hoeksma, MR (reprint author), Univ Utrecht, Fac Pharmaceut Sci, Dept Psychopharmacol, Sorbonnelaan 16, NL-3584 CA Utrecht, Netherlands. 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Neurophysiol. PD MAY PY 2005 VL 116 IS 5 BP 1188 EP 1194 DI 10.1016/j.clinph.2004.12.021 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 923DL UT WOS:000228889200023 PM 15826861 ER PT J AU Teder-Salejarvi, WA Pierce, KL Courchesne, E Hillyard, SA AF Teder-Salejarvi, WA Pierce, KL Courchesne, E Hillyard, SA TI Auditory spatial localization and attention deficits in autistic adults SO COGNITIVE BRAIN RESEARCH LA English DT Article DE evoked potentials; autism; auditory ID EVENT-RELATED POTENTIALS; DEVELOPMENTAL LANGUAGE DISORDER; DIAGNOSTIC OBSERVATION SCHEDULE; SELECTIVE-ATTENTION; SOUND-LOCALIZATION; SHIFTING ATTENTION; EVOKED POTENTIALS; INFANTILE-AUTISM; CORPUS-CALLOSUM; FREE-FIELD AB The objective of this study was to compare autistic adults and matched control subjects in their ability to focus attention selectively on a sound source in a noisy environment. Event-related brain potentials (ERPs) were recorded while subjects attended to a fast paced sequence of brief noise bursts presented in free-field at a central or peripheral location. Competing sequences of noise bursts at adjacent locations were to be ignored. Both behavioral measures of target detection and auditory ERP amplitudes indicated that control subjects were able to focus their attention more sharply on the relevant sound source than autistic subjects. These findings point to a fundamental deficit in the spatial focusing of auditory attention in autism, which may be a factor that impedes social interactions and sensory-guided behavior, particularly in noisy environments. (c) 2004 Elsevier B.V. All rights reserved. C1 Univ Calif San Diego, Dept Neurosci 0608, Sch Med, La Jolla, CA 92093 USA. Childrens Hosp Res Ctr, Lab Res Neurosci Autism, La Jolla, CA 92037 USA. 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Brain Res. PD MAY PY 2005 VL 23 IS 2-3 BP 221 EP 234 DI 10.1016/j.cogbrainres.2004.10.021 PG 14 WC Computer Science, Artificial Intelligence; Neurosciences; Neuroimaging SC Computer Science; Neurosciences & Neurology GA 923BK UT WOS:000228883500007 ER PT J AU Sebanz, N Knoblich, G Stumpf, L Prinz, W AF Sebanz, N Knoblich, G Stumpf, L Prinz, W TI Far from action-blind: Representation of others' actions in individuals with autism SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; ASPERGER-SYNDROME; CHILDS THEORY; MAGNETIC STIMULATION; BIOLOGICAL BASIS; MIRROR NEURONS; MIND; PERCEPTION; IMITATION; COMMUNICATION AB It has been suggested that theory of mind may rely on several precursors including gaze processing, joint attention, the ability to distinguish between actions of oneself and others, and the ability to represent goal-directed actions. Some of these processes have been shown to be impaired in individuals with autism, who experience difficulties in theory of mind. However, little is known about action representation in autism. Using two variants of a spatial compatibility reaction time (RT) task, we addressed the question of whether high-functioning individuals with autism have difficulties in controlling their own actions and in representing those of others. Participants with autism showed automatic response activation and had no difficulties with response inhibition. When two action alternatives were distributed among pairs of participants, participants with autism represented a co-actor's task, showing the same pattern of results as the matched control group. We discuss the possibility that in high-functioning individuals with autism, the system matching observed actions onto representations of one's own actions is intact, whereas difficulties in higher-level processing of social information persist. C1 Max Planck Inst Psychol Res, D-80799 Munich, Germany. Integrat Ctr Individuals Autism, Munich, Germany. RP Sebanz, N (reprint author), Max Planck Inst Psychol Res, Amalienstr 33, D-80799 Munich, Germany. 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PD MAY-JUN PY 2005 VL 22 IS 3-4 BP 433 EP 454 DI 10.1080/02643290442000121 PG 22 WC Psychology; Psychology, Experimental SC Psychology GA 934YW UT WOS:000229746500013 PM 21038260 ER PT J AU Kelly, B AF Kelly, B TI 'Chocolate ... makes you autism': impairment, disability and childhood identities SO DISABILITY & SOCIETY LA English DT Article ID SOCIAL MODEL AB This paper discusses perceptions and experiences of impairment and disability from the perspectives of learning disabled children, their parents and their social workers. The author reports on findings from her doctoral study that adults often fail to take into account the views and experiences of learning disabled children. As a result, these children developed their own interpretations of impairment and disability based on their experiences and interactions with others. Whilst this indicates that they are active social interpreters, it also suggests that adults should make greater efforts to inform and consult learning disabled children. The author concludes by reflecting on the relevance of these findings to contemporary theories of disability and childhood. RP Kelly, B (reprint author), 44 Dundas St,POB 6189, Dunedin, New Zealand. 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PD MAY PY 2005 VL 20 IS 3 BP 345 EP 349 DI 10.1080/09687590500060810 PG 5 WC Rehabilitation; Social Sciences, Interdisciplinary SC Rehabilitation; Social Sciences - Other Topics GA 921ZX UT WOS:000228806000008 ER PT J AU Baghdadli, A Gonnier, V Valancogne, F Aussilloux, C AF Baghdadli, A Gonnier, V Valancogne, F Aussilloux, C TI Descriptive study of psychotropic use in the 20-35 age adults with autism in Languedoc-Roussillon SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE adaptative profile; adults; autism; descriptive study; pervasive developmental disorders; psycho-active treatment ID PERVASIVE DEVELOPMENTAL DISORDERS; ADAPTIVE-BEHAVIOR SCALES; INTELLECTUAL DISABILITY; MENTAL-RETARDATION; CHILDREN; PSYCHOPHARMACOLOGY; PHARMACOTHERAPY; MEDICATION; PATTERNS AB The Pervasive Developmental Disorders complications can lead to an important life long handicap. There is an important literature about autism, but in most cases, specifically concerning children and adolescents problems. We wished to focus our attention on adults, in order to describe, on one hand their socio-adaptive profile, and on the other hand, the necessity to resort to a psycho-active treatment. The geographic zone chosen in order to carry out this, was Languedoc-Roussillon, and the applied method was a descriptive study of psychotropic use in the 20-35 age adults with autism. The instruments used were standardized and validated. The diagnosis was confirmed using ICD 10 criteria checklist and individual characteristics including adaptive profile estimated on the Vineland scale, were collected. Moreover the prescriber's global impressions were collected on the CGI scale. Out of 165 case files collected, the sex-ratio was 3 men for 2 women, 45% showed associated somatic disorders (of which 24% epileptic), 66% benefited from a psycho-active treatment; 85% had been admitted in institutions during childhood or adolescence. The admittance framework being respectfully, MAS 21.8%, community homes 35.2%, CAT 17.6% and psychiatric services 20.6%. Mean equivalent age, in the three Vineland adaptive domains, were from 21 months in Communication to 43 months in Autonomy in daily life Skills and 17 months in Socialization. The development quotient showed adaptive retardation in 100% of cases. The 110 persons benefiting from a medicinal treatment, were treated for aggressiveness in 62.7% of cases, agitation in 43.6% of cases and anxiety in 48.2% of cases. The therapeutic categories used were, in majority, antipsychotics in 85% of cases, anxiolitics in 40.2% of cases; hypnotics as well as anti-depressants or mood-regulators, each representing 10% of prescriptions. Associations of several molecules representing 83% of cases. The therapeutic effect was considered interesting in more than two-thirds of cases. Undesirable side-effects were reported in 50% of the patients under treatment; 50% of the persons treated had been administered the same treatment for more than 5 years. The adaptive-profile significantly varied, depending on the accommodation structures and also the presence or absence of a psycho-active treatment. The results of this study portrayed the level of social adaptation and the types of psychoactive treatment in adults with autism, who are severely limited in their adaptive functioning due to their handicaps. C1 Praticien Hosp, Ctr Ressources Autisme Languedoc Roussillon, SMPEA Peyre Plantade, F-34295 Montpellier, France. Ctr Hosp Montpellier, Polyclin Psychiat Adulte, Montpellier, France. 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Magnetoencephalography (MEG) was used to study the neuronal responses associated with the processing of faces in 12 able adults with autism spectrum disorders (ASD), performing image categorization and image identification tasks. The neuromagnetic data were analysed using nonparametric time-series analysis and equivalent current dipole estimation. Comparison data were obtained from 22 normally developing adults. In individuals with ASD, the neural responses to images of faces, observed in right extrastriate cortices at approximate to 145 ms after stimulus onset, were significantly weaker, less lateralized and less affected by stimulus repetition than in control subjects. Early latency (30-60 ms) responses to face images, over right anterior temporal regions, differed significantly between the two subject groups in the image identification task. No such difference was observed for images of mugs or meaningless geometrical patterns. These findings suggest that, during the course of development in individuals with ASD, the cortical activity associated with the processing of human faces assumes a different-from-normal localization in extrastriate brain regions. This abnormal localization may be associated with unusual, but nevertheless face-specific, fast processing pathways. C1 Univ Oxford, Dept Psychiat, Univ Sect Child & Adolescent Psychiat, Oxford OX3 7LQ, England. Open Univ, Dept Phys & Astron, Milton Keynes MK7 6AA, Bucks, England. Helsinki Univ Technol, Brain Res Unit, Low Temp Lab, FIN-02015 Espoo, Finland. Univ London, Inst Psychiat, London WC1E 7HU, England. RP Bailey, AJ (reprint author), Univ Oxford, Dept Psychiat, Univ Sect Child & Adolescent Psychiat, Oxford OX3 7LQ, England. 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PD MAY PY 2005 VL 21 IS 9 BP 2575 EP 2585 DI 10.1111/j.1460-9568.2005.04061.x PG 11 WC Neurosciences SC Neurosciences & Neurology GA 928PN UT WOS:000229284100026 PM 15932615 ER PT J AU Strous, RD Golubchik, P Maayan, R Mozes, T Tuati-Werner, D Weizman, A Spivak, B AF Strous, RD Golubchik, P Maayan, R Mozes, T Tuati-Werner, D Weizman, A Spivak, B TI Lowered DHEA-S plasma levels in adult individuals with autistic disorder SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Article DE autistic disorder; autism; neurosteroid; dehydroepiandrosterone; DHEA; DHEA-S; aggression ID DEHYDROEPIANDROSTERONE-SULFATE; NEUROACTIVE STEROIDS; HIPPOCAMPAL-NEURONS; INFANTILE-AUTISM; SIGMA-RECEPTORS; NEUROSTEROIDS; BRAIN; RAT; SCALE; SCHIZOPHRENIA AB The aim of this study was to determine for the first time neurosteroid levels, dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S) in particular, in a group of adult patients with autistic disorder and compare these levels with normal healthy individuals. Levels of DHEA, DHEA-S and cortisol were compared between 15 adult drug-free patients with autistic disorder and 13 healthy controls. The Ritvo-Freeman Real-Life Rating Scale (RLRS) and the Overt Aggression Scale (OAS) were assessed as a measure of symptom severity. Significant lower DHEA-S levels were observed in the group with autistic disorder as compared to controls (p < 0.05). DHEA-S levels appear to be low in patients with autistic disorder and, while speculative, may play a role in the etiopathophysiology of the disorder. (c) 2005 Elsevier B.V. and ECNP. All rights reserved. C1 Geha Mental Hlth Ctr, IL-49100 Petah Tiqwa, Israel. Beer Yaakov Mental Hlth Ctr, Beer Yaagov, Israel. Tel Aviv Univ, Sackler Fac Med, Tel Aviv, Israel. RP Weizman, A (reprint author), Geha Mental Hlth Ctr, POB 102, IL-49100 Petah Tiqwa, Israel. 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Neuropsychopharmacol. PD MAY PY 2005 VL 15 IS 3 BP 305 EP 309 DI 10.1016/j.euroneuro.2004.12.004 PG 5 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 920QN UT WOS:000228705300009 PM 15820420 ER PT J AU Berthoz, S Hill, EL AF Berthoz, S Hill, EL TI The validity of using self-reports to assess emotion regulation abilities in adults with autism spectrum disorder SO EUROPEAN PSYCHIATRY LA English DT Article DE emotion regulation; alexithymia; autism spectrum disorder; TAS-20; BVAQ ID TORONTO-ALEXITHYMIA-SCALE; PSYCHOMETRIC PROPERTIES; FUNCTIONING AUTISM; GENERAL-POPULATION; RELIABILITY; DEPRESSION; PREVALENCE; QUOTIENT AB Purpose. - The current paper focused on the validity of using self-reports to assess emotion regulation abilities in autism spectrum disorders (ASD). To assess this we sought responses to two alexithymia self-teports and a depression self-report at two time points from adults with and without ASD. Materials and methods. - An initial sample of 27 adults with ASD and 35 normal adults completed the 20-item Toronto alexithymia scale (TAS-20), the Bermond and Vorst alexithymia questionnaire-form B (BVAQ-B), and the Beck depression inventory (BDI), at test time 1. Of these individuals. 19 ASD and 29 controls participated again after a period ranging from 4 to 12 months. Results. - ASD participants were able to report about their own emotions using self-reports. BVAQ-B showed reasonable convergent validity and test-retest reliability in both groups. Scores oil both alexithymia scales were stable across the two participant groups. However, results revealed that although the TAS-20 total score discriminated between the two groups at both time points, the BVAQ-B total score did not. 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Psychiat. PD MAY PY 2005 VL 20 IS 3 BP 291 EP 298 DI 10.1016/j.eurpsy.2004.06.013 PG 8 WC Psychiatry SC Psychiatry GA 935FR UT WOS:000229765600016 PM 15935431 ER PT J AU Colgrove, J Bayer, R AF Colgrove, J Bayer, R TI Could it happen here? Vaccine risk controversies and the specter of derailment SO HEALTH AFFAIRS LA English DT Article ID RISK/BENEFIT COMMUNICATION; MMR VACCINATION; RUBELLA VACCINE; OFFICE SETTINGS; SAFETY CONCERNS; PUBLIC-HEALTH; IMMUNIZATION; CHILDREN; MEASLES; PEDIATRICIANS AB Controversy over vaccine safety has achieved high visibility over the past decade. At the same time, however, levels of coverage for routinely recommended childhood vaccines in the United States are at their highest ever. We examine this apparent paradox. We consider the ways in which concerns over vaccine safety have emerged and diffused through the popular media, legislative hearings, and Internet-based activism. 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PD MAY-JUN PY 2005 VL 24 IS 3 BP 729 EP 739 DI 10.1377/hlthaff.24.3.729 PG 11 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 924YK UT WOS:000229017000021 PM 15886167 ER PT J AU Epstein, RA AF Epstein, RA TI It did happen here: Fear and loathing on the vaccine trail SO HEALTH AFFAIRS LA English DT Article AB Adverse publicity that placed undue emphasis on a possible connection between autism and the measles-mumps-rubella (MMR) vaccine and vaccines containing thimerosal made parents in the United Kingdom reluctant to allow their children to receive the vaccine. The same concerns have played themselves out in the U.S. Food and Drug Administration's decision to recommend removal of thimerosal from other vaccines, even as the individual autism claims have been rejected. That recommendation, based on unsubstantiated safety concerns, reveals a deep-seated institutional overreaction that is more likely to cost lives than to save them. C1 Univ Chicago, Sch Law, Chicago, IL 60637 USA. Stanford Univ, Hoover Inst, Stanford, CA 94305 USA. RP Epstein, RA (reprint author), Univ Chicago, Sch Law, Chicago, IL 60637 USA. EM repstein@uchicago.edu CR ABRAHAM KS, 1987, VA LAW REV, V73, P845, DOI 10.2307/1072968 Angell Marcia, 1996, SCI TRIAL CLASH MED Colgrove J, 2005, HEALTH AFFAIR, V24, P729, DOI 10.1377/hlthaff.24.3.729 *HLTH RES SERV ADM, 2005, POST 1998 MONTHL STA *I MED, 2004, IMM SAF REV CACC AUT *IOM, 2004, FIN VACC 21 CENT ASS, P39 MANNING RL, 1994, J LAW ECON, V37, P247 HUBER P, 1985, COLUMBIA LAW REV, V85, P277, DOI 10.2307/1122439 *US FDA, 2005, THIM VACC Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 10 TC 5 Z9 5 PU PROJECT HOPE PI BETHESDA PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA SN 0278-2715 J9 HEALTH AFFAIR JI Health Aff. PD MAY-JUN PY 2005 VL 24 IS 3 BP 740 EP 743 DI 10.1377/hlthaff.24.3.740 PG 4 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 924YK UT WOS:000229017000022 PM 15886168 ER PT J AU Juneja, M Mukherjee, SB Sharma, S AF Juneja, M Mukherjee, SB Sharma, S TI A descriptive, hospital based study of children with autism SO INDIAN PEDIATRICS LA English DT Article DE autism; comprehensive assessment; screening AB The clinical and neurodevelopmental profile of 51 children with Autistic disorder from a referral population was studied. A detailed history and examination was undertaken. The development/intelligence quotient and social quotient were assessed. Standard diagnostic tests were applied in children above 2 years of age. Younger children were evaluated with a screening test and re-evaluated at 2 years. It was observed that a correct diagnosis had been made in only 5.8% of children prior to referral. The mean age of presentation was 3.28 years. Ninety-six percent of the autistic children had developmental delay. Qualitative impairment in social interaction and communication was more commonly observed than restricted interests and activities. Forty-seven (92.15%) children were severely autistic and 4 (7.84%) mildly to moderately autistic. All children less than 2 years were confirmed to have Autistic disorder later. C1 Maulana Azad Med Coll, Dept Pediat, Child Dev & Early Intervent Clin, New Delhi 110002, India. Lok Nayak Hosp, New Delhi 110002, India. RP Juneja, M (reprint author), Maulana Azad Med Coll, Dept Pediat, Child Dev & Early Intervent Clin, New Delhi 110002, India. EM drmonicajuneja@rediffmail.com CR American Academy of Pediatrics, 2001, PEDIATRICS, V107, P85 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P1 Daley TC, 2004, SOC SCI MED, V58, P1323, DOI 10.1016/S0277-9536(03)00330-7 DALTON R, 2003, NELSON TXB PEDIAT, P93 Filipek P. A., 1999, J AUTISM DEV DISORD, V29, P437 FILIPEK PA, 1999, PEDIAT NEUROLOGY PRI, P606 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 KLEINTZ MA, 1997, AM J OCCUP THER, V51, P530 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x KULSHETSHTRA SK, 1971, STANFORD BINET HINDI MALIN AJ, 1971, INDIAN ADAPTATION VI MUNDKUR N, 1999, EARLY DEV PROFILE DI RAPIN I, 2000, RECENT ADV PEDIAT, P121 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 Schopler E., 1988, CHILDHOOD AUTISM RAT SEVIN JA, 1991, J AUTISM DEV DISORD, V21, P417, DOI 10.1007/BF02206868 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 NR 20 TC 8 Z9 9 PU INDIAN ACADEMY PEDIATRICS PI NEW DELHI PA MAULANA AZAD MEDICAL COLLEGE, DEPT PEDIATRICS, NEW DELHI, 110 002, INDIA SN 0019-6061 J9 INDIAN PEDIATR JI Indian Pediatrics PD MAY PY 2005 VL 42 IS 5 BP 453 EP 458 PG 6 WC Pediatrics SC Pediatrics GA 002QJ UT WOS:000234626000005 PM 15923691 ER PT J AU Goh, S Thiele, EA AF Goh, S Thiele, EA TI Anorexia nervosa in a child with tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID CEREBRAL BLOOD-FLOW; EATING-DISORDERS; BRAIN HYPOMETABOLISM; EMISSION-TOMOGRAPHY; AUTISM; GLUCOSE AB Psychiatric disorders pose a significant burden to the quality of life of individuals with tuberous sclerosis complex and their caregivers. The relationship between the location and distribution of brain abnormalities in tuberous sclerosis complex and specific neuropsychiatric disorders is largely unknown. We present the first case in the literature of a child with tuberous sclerosis complex and anorexia nervosa and discuss the relevance of electroencephalography, magnetic resonance imaging, and neuropsychologic testing. To understand psychiatric disturbances in tuberous sclerosis complex, we must consider each of the following factors: cerebral pathology, seizure history, cognitive impairment, psychosocial stressors, and medications. C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Thiele, EA (reprint author), Massachusetts Gen Hosp, Dept Neurol, 55 Fruit St,VBK 830, Boston, MA 02114 USA. 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Child Neurol. PD MAY PY 2005 VL 20 IS 5 BP 457 EP 460 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 932TI UT WOS:000229575900017 PM 15968936 ER PT J AU Taylor, E Rogers, JW AF Taylor, E Rogers, JW TI Practitioner review: Early adversity and developmental disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE environment; gene-environment interaction; ADHD; autism; learning disability ID DEFICIT HYPERACTIVITY DISORDER; FETAL ALCOHOL SYNDROME; LOW-BIRTH-WEIGHT; POSTNATALLY DEPRESSED MOTHERS; TRAUMATIC BRAIN-INJURY; COGNITIVE-DEVELOPMENT; AUTISTIC-CHILDREN; MATERNAL SMOKING; FATTY-ACIDS; POLYCHLORINATED-BIPHENYLS AB Background: Knowledge of genetic influences, on developmental disorders such as autism spectrum, attention deficit/hyperactivity disorder and learning disabilities, has increased the opportunities for understanding the influences of the early environment. Methods: This paper provides a selective, narrative review for clinicians of the effects of factors such as exposure to toxins and stresses in utero and in postnatal life; brain injuries and perinatal compromise; neglect, malnutrition and selective food deficiencies. It also considers what is known about the mechanisms through which early adversities operate. Results: Gaps in the research are identified and suggestions made about clinical investigations. Several types of environmental adversity have associations with later disorders that suggest a causal role. The effects are often on a broad range of psychological processes, and are not always quickly reversible. Several adversities often coexist, calling for skilled judgement about priorities in treatment. Conclusions: Individuals vary considerably in their exposure to adversity and their vulnerability to its effects, and genetic inheritance can influence both. 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Child Psychol. Psychiatry PD MAY PY 2005 VL 46 IS 5 BP 451 EP 467 DI 10.1111/j.1469-7610.2004.00402.x PG 17 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 918PJ UT WOS:000228559800002 PM 15845126 ER PT J AU Charman, T Taylor, E Drew, A Cockerill, H Brown, JA Baird, G AF Charman, T Taylor, E Drew, A Cockerill, H Brown, JA Baird, G TI Outcome at 7 years of children diagnosed with autism at age 2: predictive validity of assessments conducted at 2 and 3 years of age and pattern of symptom change over time SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; outcome; predictors; IQ; language; communication; symptom severity ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY SCHOOL-AGE; PRESCHOOL-CHILDREN; SPECTRUM DISORDERS; FOLLOW-UP; METHODOLOGICAL CHALLENGES; LANGUAGE-DEVELOPMENT; COGNITIVE ASSESSMENT; JOINT ATTENTION; ADI-R AB Objective: To examine the predictive validity of symptom severity, cognitive and language measures taken at ages 2 and 3 years to outcome at age 7 in a sample of children diagnosed with autism at age 2. Method: Twenty-six children diagnosed with autism at age 2 were re-assessed at ages 3 and 7 years. At each age symptom severity, cognitive and language assessments were completed. Results: The pattern of autistic symptom severity varied over time by domain. Across time, children moved across diagnostic boundaries both in terms of clinical diagnosis and in terms of instrument diagnosis on the Autism Diagnostic Interview-Revised (ADI-R). On all measures group variability in scores increased with age. Although non-verbal IQ (NVIQ) for the group as a whole was stable across the 3 assessments, this masked considerable individual instability. Standard assessments at age 2 did not predict outcome at age 7 even within the same domain of functioning. In contrast, standard assessments at age 3 did predict outcome. However, a measure of rate of non-verbal communicative acts taken from an interactive play-based assessment at age 2 was significantly associated with language, communication and social outcomes at age 7. Conclusions: The trajectory of autism symptoms over time differed in different domains, suggesting that they may be, at least in part, separable. Variability in language, NVIQ and symptom severity increased over time. Caution is required when interpreting the findings from assessments of children with autism at age 2 years. At this age measures of rate of non-verbal communication might be more informative than scores on standard psychometric tests. Predictive validity of assessments at age 3 years was greater. C1 UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, 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. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 CHARMAN T, 2003, AUTISM NEURAL BASIS, V251, P10, DOI 10.1002/0470869380.ch2 Charman T, 2003, J CHILD LANG, V30, P213, DOI 10.1017/S0305000902005482 Charman T, 2003, PHILOS T ROY SOC B, V358, P315, DOI 10.1098/rstb.2002.1199 Charman T, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P325 Charman T, 2004, J AUTISM DEV DISORD, V34, P59, DOI 10.1023/B:JADD.0000018075.77941.60 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 DOLL EA, 1965, VINELAND SOC MATURIT Doyle LW, 2001, ARCH DIS CHILD, V85, pF159, DOI 10.1136/fn.85.3.F159 Drew A, 2002, EUR CHILD ADOLES PSY, V11, P266, DOI 10.1007/s00787-002-0299-6 Edwards S, 1997, REYNELL DEV LANGUAGE Fecteau S, 2003, AUTISM, V7, P255, DOI 10.1177/1362361303007003003 Fenson L, 1993, MACARTHUR COMMUNICAT Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 GILLBERG C, 1990, J CHILD PSYCHOL PSYC, V31, P921, DOI 10.1111/j.1469-7610.1990.tb00834.x Griffiths R, 1986, ABILITIES BABIES LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1989, J AUTISM DEV DISORD, V19, P483, DOI 10.1007/BF02212853 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 LORD C, 1989, J CHILD PSYCHOL PSYC, V30, P575, DOI 10.1111/j.1469-7610.1989.tb00269.x Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F Magiati I, 2001, AUTISM, V5, P399, DOI 10.1177/1362361301005004005 Moore V, 2003, AUTISM, V7, P47, DOI 10.1177/1362361303007001018 Mundy P, 1996, EARLY SOCIAL COMMUNI MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 Pickles A, 2003, DEV PSYCHOPATHOL, V15, P529, DOI 10.1017/S0954579403000282 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 Rapin I, 2003, BRAIN DEV-JPN, V25, P546, DOI 10.1016/S0387-7604(03)00127-X Reynell J., 1985, REYNELL DEV LANGUAGE Rogers SJ, 2001, INT REV RES MENT RET, V23, P1 Seibert J. 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Child Psychol. Psychiatry PD MAY PY 2005 VL 46 IS 5 BP 500 EP 513 DI 10.1111/j.1469-7610.2004.00377.x PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 918PJ UT WOS:000228559800006 PM 15845130 ER PT J AU Levitin, DJ Cole, K Lincoln, A Bellugi, U AF Levitin, DJ Cole, K Lincoln, A Bellugi, U TI Aversion, awareness, and attraction: investigating claims of hyperacusis in the Williams syndrome phenotype SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE hyperacusis; oxyacusis; allodynia; Williams syndrome; Williams-Beuren syndrome; loudness thresholds; odynacusis ID IDIOPATHIC INFANTILE HYPERCALCEMIA; BEUREN-SYNDROME; INDIVIDUALS; CHILDREN; QUESTIONNAIRE; ABILITIES; PROFILE; ADULTS; SKILLS; MUSIC AB Background: Williams syndrome (WS), a neurodevelopmental disorder, is characterized by pervasive cognitive deficits alongside a relative sparing of auditory perception and cognition. A frequent characteristic of the phenotype is adverse reactions to, and/or fascination with, certain sounds. Previously published reports indicate that people with WS experience hyperacusis, yet careful examination reveals that the term 'hyperacusis' has been used indiscriminately in the literature to describe quite different auditory abnormalities. Method: In an effort to clarify and document the incidence of auditory abnormalities in and among people with WS we collected data from parents of people with WS (n = 118) and comparison groups of people with Down syndrome, autism, and normal controls. Results: Our findings revealed four phenomenologically separate auditory abnormalities, all of which were significantly more prevalent in WS than the three comparison groups. Among people with WS, we found relatively few reports of true hyperacusis (lowered threshold for soft sounds) or auditory fascinations/fixations, whereas 80% reported fearfulness to idiosyncratically particular sounds, and 91% reported lowered uncomfortable loudness levels, or 'odynacusis.' Conclusions: Our results confirm anecdotal reports of an unusual auditory phenotype in WS, and provide an important foundation for understanding the nature of auditory experience and pathology in WS. We conclude by reviewing the ways in which the present findings extend and complement recent neuroanatomical and neurophysiological findings on auditory function in people with WS. C1 McGill Univ, Dept Psychol, Montreal, PQ H3A 1B1, Canada. Salk Inst Biol Studies, San Diego, CA 92138 USA. RP Levitin, DJ (reprint author), McGill Univ, Dept Psychol, 1205 Dr Penfield Ave, Montreal, PQ H3A 1B1, Canada. EM dlevitin@psych.mcgill.ca CR *AM AC PED COMM GE, 2001, HLTH CAR SUP CHILDR, P1192 Anari M, 1999, SCAND AUDIOL, V28, P219, DOI 10.1080/010503999424653 Baguley DM, 2003, J ROY SOC MED, V96, P582, DOI 10.1258/jrsm.96.12.582 BELLUGI U, 1999, ENCY NEUROSCIENCE, P2163 BELLUGI U, 1989, S INT NEUR SOC VANC BELLUGI U, 1996, LIF SPAN DEV IND SYN Bellugi U, 1990, Am J Med Genet Suppl, V6, P115 Bellugi U, 2000, J COGNITIVE NEUROSCI, V12, P7, DOI 10.1162/089892900561959 BROCHARD R, 2003, RHYTHM PERC PROD WOR Dirckx JH, 2001, STEDMANS CONCISE MED Don AJ, 1999, CHILD NEUROPSYCHOL, V5, P154, DOI 10.1076/chin.5.3.154.7337 DOYLE TF, 2003, AM J MED GENET A, V124, P263 Einfeld SL, 1997, AM J MENT RETARD, V102, P45, DOI 10.1352/0895-8017(1997)102<0045:BAEDII>2.0.CO;2 Francke U, 1999, HUM MOL GENET, V8, P1947, DOI 10.1093/hmg/8.10.1947 Galaburda AM, 2000, J COGNITIVE NEUROSCI, V12, P74, DOI 10.1162/089892900561995 GORDON A G, 1986, British Journal of Audiology, V20, P95, DOI 10.3109/03005368609079002 Hagerman R. 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B., 1999, NEURODEVELOPMENTAL D NIGAM A, 1994, J LARYNGOL OTOL, V108, P494 Pezzini G, 1999, DEV NEUROPSYCHOL, V15, P141 Phillips D P, 1998, J Am Acad Audiol, V9, P371 PRICE DD, 1977, PAIN, V3, P57, DOI 10.1016/0304-3959(77)90035-5 Rosenhall U, 1999, J AUTISM DEV DISORD, V29, P349, DOI 10.1023/A:1023022709710 STALLING C, 1990, C STALLING PROJECT M Stansfeld S A, 1992, Psychol Med, VSuppl 22, P1 TAGERFLUSBERG H, 1996, 7 INT PROF C WILL SY TAYLOR SM, 1984, J SOUND VIB, V96, P243, DOI 10.1016/0022-460X(84)90582-0 UDWIN O, 1991, J CLIN EXP NEUROPSYC, V13, P232, DOI 10.1080/01688639108401040 UDWIN O, 1990, DEV MED CHILD NEUROL, V32, P129 Venes D., 2001, TABERS CYCLOPEDIC ME NR 52 TC 60 Z9 61 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAY PY 2005 VL 46 IS 5 BP 514 EP 523 DI 10.1111/j.1469-7610.2004.00376.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 918PJ UT WOS:000228559800007 PM 15845131 ER PT J AU Pellicano, E Maybery, M Durkin, K AF Pellicano, E Maybery, M Durkin, K TI Central coherence in typically developing preschoolers: does it cohere and does it relate to mindreading and executive control? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE central coherence; theory of mind; visuospatial ability; executive functioning ID HIGH-FUNCTIONING AUTISM; WEAK CENTRAL COHERENCE; WORKING-MEMORY; ASPERGER-SYNDROME; VERBAL-ABILITY; MIND; CHILDREN; PERFORMANCE; DYSFUNCTION; DEFICITS AB Background: Frith and Happe (1994) describe central coherence (CC) as the normal tendency to integrate individual elements into a coherent whole, a cognitive style which varies in the general popu-lation. Individuals with autism are at the extreme (weak) end of the continuum of coherence. There has been debate over whether CC is independent from other psychological functions such as theory of mind and executive control. Methods: We examined the validity of the CC construct in 76 typically developing 4- and 5-year-old children using four visuospatial coherence tasks. We also investigated the extent to which individual differences in performance on CC measures were associated with individual differences on measures of mindreading and executive functioning (EF). Results: Unexpectedly, the CC variables were not highly intercorrelated and did not form a single coherence factor. Instead, the results revealed a two-factor structure, one of which corresponded to visuospatial constructional ability. Correlations between the emerging factors of coherence and mindreading ability were weak, even when developmental differences in age and verbal and nonverbal ability were taken into account. In contrast, visuospatial constructional ability was reliably related to measures of EF, whilst correlations between EF and the second CC factor were very weak. Conclusions: CC in typically developing preschoolers is not a unitary construct. Whilst there is little relationship between CC and mindreading abilities in these young children, executive control appears to be associated with one aspect of coherence: visuospatial construction. C1 Univ Western Australia, Sch Psychol, Nedlands, WA 6009, Australia. RP Pellicano, E (reprint author), Pk Hosp Children, Univ Sect, Old Rd, Oxford OX3 7LQ, England. EM liz.pellicano@psych.ox.ac.uk RI Maybery, Murray/H-5390-2014 CR Baddeley A. 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Psychiatry PD MAY PY 2005 VL 46 IS 5 BP 533 EP 547 DI 10.1111/j.1469-7610.2004.00380.x PG 15 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 918PJ UT WOS:000228559800009 PM 15845133 ER PT J AU Song, EY VanDunk, C Kuddo, T Nelson, PG AF Song, EY VanDunk, C Kuddo, T Nelson, PG TI Measurement of Vasoactive Intestinal Peptide using a Competitive Fluorescent Microsphere Immunoassay or ELISA in human blood samples SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE ELISA; fluorescent microsphere immunoassay; VIP ID NUCLEOTIDE POLYMORPHISM ANALYSIS; FLOWMETRIX(TM) SYSTEM; MULTIPLEXED ANALYSIS; HUMAN CYTOKINES; QUANTITATION; ASSAY; ANTIBODIES; SERUM; VIP AB The concentration of Vasoactive Intestinal Peptide (VIP) as measured by recycling immunoaffinity chromatography (RIC) has been reported to be elevated in the blood of patients with autism as compared with normal subjects. In this study, we have developed a "Competitive Fluorescent Microsphere Immunoassay" (cFMI) in which VIP competes with biotinylated VIP in binding to polyclonal antibodies on microspheres. The results were obtained using the Luminex too system. We measured VIP in serum, plasma, and material eluted from dried blood spots on filter paper with both the cFMI and an ELISA procedure. We found that a purification procedure was necessary for obtaining useful results from plasma and serum, however, a preincubation step was required with the blood eluates. This newly developed cFMI was more sensitive (2.5 vs. 20.0 pg/ml), and more reproducible than the ELISA. To get accurate measurements of VIP in eluted material high sensitivity is especially important. Thus, the cFMI using the Luminex system has definite advantages over a conventional ELISA including the possibility that samples can be assayed at higher dilutions. We have determined that the VIP concentrations of serum, plasma, and dried blood spot eluate specimens as measured with the cFMI assay system were similar to those measured with ELISA. Thus, the new cFMI using Luminex system may be useful for detection of VIP in human blood samples. Published by Elsevier B.V. C1 NICHHD, LDN, NIH, Bethesda, MD 20892 USA. RP Nelson, PG (reprint author), NICHHD, LDN, NIH, Bldg 31 Room 2A25, Bethesda, MD 20892 USA. 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Immunol. Methods PD MAY PY 2005 VL 300 IS 1-2 BP 63 EP 73 DI 10.1016/j.jim.2005.02.009 PG 11 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA 941MM UT WOS:000230218900006 PM 15894328 ER PT J AU de Bildt, A Serra, M Luteijn, E Kraijer, D Sytema, S Minderaa, R AF de Bildt, A Serra, M Luteijn, E Kraijer, D Sytema, S Minderaa, R TI Social skills in children with intellectual disabilities with and without autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; CSBQ; social skills; VABS ID PERVASIVE DEVELOPMENTAL DISORDER; ADAPTIVE-BEHAVIOR; MENTAL-RETARDATION; PSYCHIATRIC-DISORDERS; URBAN CHILDREN; YOUNG-ADULTS; ADOLESCENTS; QUESTIONNAIRE; EPIDEMIOLOGY; IMPAIRMENTS AB Background Social skills were studied in 363 children with mild intellectual disabilities (ID) and 147 with moderate ID with and without autism (age 4 through 18). The objective was to investigate the value of the Children's Social Behaviour Questionnaire (CSBQ), as a measure of subtle social skills, added to a measure of basic social skills with the Vineland Adaptive Behaviour Scales (VABS), in identifying children with ID with or without autism. Method Children with mild and moderate ID, with and without autistic symptomatology were compared on basic social skills, measured with the Communication and Socialization domains of the VABS, and subtle social skills, measured with the CSBQ. Results Measuring basic social skills is not sufficient in differentiating between levels of ID. Communicative skills and subtle social skills, that concern overlooking activities or situations and fear of changes in the existing situation, seem to play a far greater role. Additionally, with respect to identifying autistic symptomatology, basic social skills do not contribute, as opposed to communicative skills and the tendency to withdraw from others. Conclusions The results implicate that the CSBQ not only has specific value as a measure of subtle social skills to identify pervasive developmental disorders, but that the instrument also has a specific contribution to differentiating between the two levels of ID. Furthermore, our outcomes imply a slight difference between limitations in subtle social skills as mentioned by the AAMR (American Association on Mental Retardation 2002) and limitations in subtle social skills as seen in milder forms of pervasive developmental disorders. Clinical and theoretical implications will be discussed. C1 Univ Groningen, Dept Psychiat Child & Adolescent Psychiat, NL-9700 AR Groningen, Netherlands. De Enkschool, Zwolle, Netherlands. St Hendrik Boeijen, Assen, Netherlands. RP de Bildt, A (reprint author), Univ Groningen, Dept Psychiat Child & Adolescent Psychiat, POB 660, NL-9700 AR Groningen, Netherlands. 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Intell. Disabil. Res. PD MAY PY 2005 VL 49 BP 317 EP 328 DI 10.1111/j.1365-2788.2005.00655.x PN 5 PG 12 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 913ED UT WOS:000228133500002 PM 15817049 ER PT J AU Cornish, K Burack, JA Rahman, A Munir, F Russo, N Grant, C AF Cornish, K Burack, JA Rahman, A Munir, F Russo, N Grant, C TI Theory of mind deficits in children with fragile X syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; developmental psychopathology; Down syndrome; fragile X syndrome; social cognition; theory of mind ID MENTAL-RETARDATION; AUTISTIC BEHAVIOR; DOWN-SYNDROME; YOUNG MALES; ATTENTION; BOYS; INDIVIDUALS; PERFORMANCE; PHENOTYPE; PROFILES AB Background Given the consistent findings of theory of mind deficits in children with autism, it would be extremely beneficial to examine the profile of theory of mind abilities in other clinical groups such as fragile X syndrome (FXS) and Down syndrome (DS). Aim The aim of the present study was to assess whether boys with FXS are impaired in simple social situations that require them to understand their own and others' mental states - in essence: do they have a 'theory of mind'? Method Well-standardized tasks of theory of mind, the location change false belief task and the appearance-reality tasks were employed to examine whether any impairment might be specific to the FXS or part of a more generalized developmental deficit. Results The results suggest that children with FXS do have impairment in theory of mind that is comparable to the deficit reported in other groups with learning disabilities such as DS. However, closer inspection of the impairment between these groups revealed qualitative differences in error types (realist vs. phenomenist), suggestive of atypical development that goes beyond general cognitive delay. Conclusions The findings are discussed in terms of the teasing apart of different components of social cognition in order to identify syndrome-specific deficiencies and proficiencies. C1 McGill Univ, Dept Educ Psychol, Montreal, PQ, Canada. McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ, Canada. Canadian Ctr Cognit Res Neurodev Disorders, Montreal, PQ, Canada. Univ Nottingham, Inst Work Hlth & Org, Nottingham, England. Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. RP Cornish, K (reprint author), McGill Univ, Dept Educ Psychol, 3700 McTavish St, Montreal, PQ, Canada. EM kim.cornish@mcgill.ca CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bailey DB, 1998, J AUTISM DEV DISORD, V28, P499 Bailey DB, 2001, J AUTISM DEV DISORD, V31, P165 BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BAUMGARDNER TL, 1995, PEDIATRICS, V95, P744 Burack JA, 1999, INT J BEHAV DEV, V23, P519 COHEN IL, 1991, AM J MED GENET, V38, P498, DOI 10.1002/ajmg.1320380271 COHEN IL, 1988, AM J MENT RETARD, V92, P436 Cornish K, 2004, MENT RETARD DEV D R, V10, P11, DOI 10.1002/mrdd.20003 Cornish KM, 2004, J CHILD PSYCHOL PSYC, V45, P1042, DOI 10.1111/j.1469-7610.2004.t01-1-00297.x Cornish KM, 1999, CORTEX, V35, P263, DOI 10.1016/S0010-9452(08)70799-8 deVries BBA, 1997, AM J HUM GENET, V61, P660, DOI 10.1086/515496 Dunn L M., 1982, BRIT PICTURE VOCABUL Dykens E. M., 1997, HDB AUTISM PERVASIVE, P388 Feinstein C, 1998, J AUTISM DEV DISORD, V28, P393, DOI 10.1023/A:1026000404855 FISCH GS, 1992, AM J MED GENET, V43, P47, DOI 10.1002/ajmg.1320430107 FREUND LS, 1991, AM J MED GENET, V38, P542, DOI 10.1002/ajmg.1320380409 Frith U, 2003, PHILOS T R SOC B, V358, P459, DOI 10.1098/rstb.2002.1218 Garner C, 1999, J INTELL DISABIL RES, V43, P466, DOI 10.1046/j.1365-2788.1999.00207.x HAGERMAN RJ, 1986, AM J MED GENET, V23, P359, DOI 10.1002/ajmg.1320230128 HAGERMAN RJ, 1988, AM J MED GENET, V30, P377, DOI 10.1002/ajmg.1320300138 HODAPP RM, 1991, J AUTISM DEV DISORD, V21, P503, DOI 10.1007/BF02206873 HODAPP RM, 1992, AM J MENT RETARD, V97, P39 Jakala P, 1997, J CLIN INVEST, V100, P331, DOI 10.1172/JCI119538 LACHIEWICZ AM, 1992, AM J MED GENET, V43, P72, DOI 10.1002/ajmg.1320430111 Munir F, 2000, BRAIN COGNITION, V44, P387, DOI 10.1006/brcg.1999.1200 Munir F, 2000, NEUROPSYCHOLOGIA, V38, P1261, DOI 10.1016/S0028-3932(00)00036-1 REISS AL, 1990, BIOL PSYCHIAT, V27, P223, DOI 10.1016/0006-3223(90)90652-I Simon EW, 1996, AM J MED GENET, V67, P77, DOI 10.1002/(SICI)1096-8628(19960216)67:1<77::AID-AJMG13>3.0.CO;2-M SUDHALTER V, 1996, 5 INT FRAG 10 C PORT Turk J, 1998, J INTELL DISABIL RES, V42, P490, DOI 10.1046/j.1365-2788.1998.4260490.x Turk J., 1997, AUTISM, V1, P175, DOI 10.1177/1362361397012005 Turk J, 1998, J APPL RES INTELLECT, V11, P175 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 WILDING J, 2004, FOCUS DOWN SYNDROME Wilding J, 2002, NEUROPSYCHOLOGIA, V40, P1343, DOI 10.1016/S0028-3932(01)00212-3 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 Yirmiya N, 1996, DEV PSYCHOL, V32, P62 NR 40 TC 28 Z9 28 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD MAY PY 2005 VL 49 BP 372 EP 378 DI 10.1111/j.1365-2788.2005.00678.x PN 5 PG 7 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 913ED UT WOS:000228133500007 PM 15817054 ER PT J AU Jyonouchi, H Geng, L Ruby, A Reddy, C Zimmerman-Bier, B AF Jyonouchi, H Geng, L Ruby, A Reddy, C Zimmerman-Bier, B TI Evaluation of an association between gastrointestinal symptoms and cytokine production against common dietary proteins in children with autism spectrum disorders SO JOURNAL OF PEDIATRICS LA English DT Article ID TNF-ALPHA SECRETION; REGRESSIVE AUTISM; RESPONSES; ALLERGY; INNATE AB Objective To evaluate an association between cytokine production with common dietary proteins as a marker of non-allergic food hypersensitivity (NFH) and gastrointestinal (GI) symptoms in young children with autism spectrum disorders (ASD). Study design Peripheral blood mononuclear cells (PBMCs) were obtained from 109 ASD children with or without GI symptoms (GI [+] ASD. N = 75 and GI (-) ASD, N = 34], from children with NFH (N = 15), and control subjects (N = 19). Diarrhea and constipation were the major GI symptoms. We measured production of type 1 T-helper cells (Th1), type 2 T-helper cells (Th2). and regulatory cytokines by PBMCs stimulated with whole cow's milk protein (CMP), its major components (casein, beta-lactoglobulin, and alpha-lactoalbumin), gliadin, and soy. Results PBMCs obtained from GI (+) ASD children produced more tumor necrosis factor-alpha (TNF-alpha)/interleukin-12 (IL-12) than those obtained from control subjects with CMP, beta-lactoglobulin, and alpha-lactoalbumin, irrespective of objectivie GI symptoms. They also produced more TNF-alpha with gliadin, which was more frequently observed in the group with loose stools. PBMCs obtained front GI (-) ASD children produced more TNF-alpha/IL-12 with CMP than those front control subjects, but not with beta-lactoglobulin. alpha-lactoalbumin. or gliadin. Cytoldne production with casein and soy were unremarkable. Conclusion A high prevalence of elevated TNF-alpha/IL-12 production by GI (+) ASD PBMCs with CMP and its major components indicates a role of NFH in GI symptoms observed in children with ASD. C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Div Pulm Allergy Immunol & Infect Dis, Newark, NJ 07101 USA. RP Jyonouchi, H (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Div Pulm Allergy Immunol & Infect Dis, 185 S Orange Ave,POB 1709, Newark, NJ 07101 USA. EM jyanouha@umdnj.edu CR Agnello D, 2003, J CLIN IMMUNOL, V23, P147, DOI 10.1023/A:1023381027062 Ashwood P, 2003, J CLIN IMMUNOL, V23, P504, DOI 10.1023/B:JOCI.0000010427.05143.bb Benlounes N, 1999, J ALLERGY CLIN IMMUN, V104, P863 Fehervari Z, 2004, CURR OPIN IMMUNOL, V16, P203, DOI 10.1016/j.coi.2004.01.004 FURLANO R, 2001, J PEDIATR, V138, P3663 GLAVIN M, 2003, CURR OPIN IMMUNOL, V15, P690 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Jyonouchi H, 2002, NEUROPSYCHOBIOLOGY, V46, P76, DOI 10.1159/000065416 Jyonouchi H, 2001, J NEUROIMMUNOL, V120, P170, DOI 10.1016/S0165-5728(01)00421-0 LATCHAM F, 2003, J PEDIATR, V143, P193 Moore KW, 2001, ANNU REV IMMUNOL, V19, P683, DOI 10.1146/annurev.immunol.19.1.683 Motrich RD, 2003, CLIN IMMUNOL, V109, P203, DOI 10.1016/S1521-6616(03)00182-7 Ono SJ, 2000, ANNU REV IMMUNOL, V18, P347, DOI 10.1146/annurev.immunol.18.1.347 Sampson HA, 2004, J ALLERGY CLIN IMMUN, V113, P805, DOI 10.1016/j.jaci.2004.03.014 Sampson HA, 2000, J PEDIATR GASTR NUTR, V30, pS87, DOI 10.1097/00005176-200001001-00013 Sicherer SH., 2000, J PEDIAT GASTROENT S, V30, P45 Torrente F, 2002, MOL PSYCHIATR, V7, P375, DOI 10.1038/sj/mp/4001077 NR 17 TC 48 Z9 50 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAY PY 2005 VL 146 IS 5 BP 605 EP 610 DI 10.1016/j.peds.2005.01.027 PG 6 WC Pediatrics SC Pediatrics GA 926FQ UT WOS:000229109000008 PM 15870662 ER PT J AU Seeman, C AF Seeman, C TI A real boy: A true story of autism, early intervention, and recovery. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Lib, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Lib, Toledo, OH USA. CR Adams Christina, 2005, REAL BOY TRUE STORY 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 MAY 1 PY 2005 VL 130 IS 8 BP 105 EP 106 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA 921BD UT WOS:000228738300181 ER PT J AU Chung, MK Robbins, SM Dalton, KM Davidson, RJ Alexander, AL Evans, AC AF Chung, MK Robbins, SM Dalton, KM Davidson, RJ Alexander, AL Evans, AC TI Cortical thickness analysis in autism with heat kernel smoothing SO NEUROIMAGE LA English DT Article DE cortical thickness; autism; brain; heat kernel; diffusion smoothing ID VOXEL-BASED MORPHOMETRY; HUMAN CEREBRAL-CORTEX; CORPUS-CALLOSUM SIZE; SURFACE; BRAIN; REGISTRATION; IMAGES; MRI; ACTIVATION AB We present a novel data smoothing and analysis framework for cortical thickness data defined on the brain cortical manifold. Gaussian kernel smoothing, which weights neighboring observations according to their 3D Euclidean distance, has been widely used in 3D brain images to increase the signal-to-noise ratio. When the observations fie on a convoluted brain surface, however-, it is more natural to assign the weights based on the geodesic distance along the surface. We therefore develop a framework for geodesic distance-based kernel smoothing and statistical analysis on the cortical manifolds. As an illustration, we apply our methods in detecting the regions of abnormal cortical thickness in 16 high functioning autistic children via random field based multiple comparison correction that utilizes the new smoothing technique. © 2004 Elsevier Inc. All rights reserved. C1 Univ Wisconsin, Dept Stat, Madison, WI 53706 USA. Univ Wisconsin, WM Keck Lab Funct Brain Imaging & Behav, Madison, WI 53706 USA. Univ Wisconsin, Dept Psychiat & Psychol, Madison, WI 53706 USA. Univ Wisconsin, Dept Med Phys, Madison, WI 53706 USA. McGill Univ, Montreal Neurol Inst, Montreal, PQ H3A 2T5, Canada. RP Chung, MK (reprint author), Univ Wisconsin, Dept Stat, 1210 W Dayton St, Madison, WI 53706 USA. 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Normal central nervous system development is described, with particular emphasis on known vulnerable periods for toxic exposures. This article details three prevalent nervous system teratogens and the controversy regarding mercury exposure and the hypothesized link to autism. C1 Wilford Hall USAF Med Ctr, Dept Pediat, San Antonio Mil Pediat Consortium, Lackland AFB, TX 78236 USA. Wilford Hall USAF Med Ctr, Dept Neurol, San Antonio Mil Pediat Consortium, Lackland AFB, TX 78236 USA. RP Rotenberg, JS (reprint author), Wilford Hall USAF Med Ctr, Dept Pediat, San Antonio Mil Pediat Consortium, 2200 Bergquist Dr,Suite 1, Lackland AFB, TX 78236 USA. 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Clin. PD MAY PY 2005 VL 23 IS 2 BP 321 EP + DI 10.1016/j.ncl.2004.12.010 PG 17 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 911UY UT WOS:000228032600003 PM 15757787 ER PT J AU Shamay-Tsoory, SG Tomer, R Aharon-Peretz, J AF Shamay-Tsoory, SG Tomer, R Aharon-Peretz, J TI The neuroanatomical basis of understanding sarcasm and its relationship to social cognition SO NEUROPSYCHOLOGY LA English DT Article ID BRAIN-DAMAGED PATIENTS; FRONTAL-LOBE; RIGHT-HEMISPHERE; PREFRONTAL CORTEX; ASPERGER-SYNDROME; ORBITOFRONTAL CORTEX; EMPATHY DEFICITS; MIND; AUTISM; APPRECIATION AB The authors explored the neurobiology of sarcasm and the cognitive processes underlying it by examining the performance of participants with focal lesions on tasks that required understanding of sarcasm and social cognition. Participants with prefrontal damage (n = 25) showed impaired performance on the sarcasm task, whereas participants with posterior damage (n = 16) and healthy controls (n = 17) performed the same task without difficulty. Within the prefrontal group, right ventromedial lesions were associated with the most profound deficit in comprehending sarcasm. In addition, although the prefrontal damage was associated with deficits in theory of mind and right hemisphere damage was associated with deficits in identifying emotions, these 2 abilities were related to the ability to understand sarcasm. This suggests that the right frontal lobe mediates understanding of sarcasm by integrating affective processing with perspective taking. C1 Univ Haifa, Dept Psychol & Brain, IL-31905 Haifa, Israel. Rambam Med Ctr, Haifa, Israel. RP Shamay-Tsoory, SG (reprint author), Univ Haifa, Dept Psychol & Brain, IL-31905 Haifa, Israel. 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We additionally examined the behavioral effects of chronic pubertal treatment with the cannabinoid agonist WIN 55,212-2 (WIN) in order to test the hypothesis that early lesions render the brain vulnerable to cannabinoid intake in later life. Neonatal mPFC lesions and pubertal WIN treatment disrupted social play, social behavior, and self-grooming in juvenile and adult rats. Additionally, we observed more social play behaviors during light cycle in WIN-treated than in vehicle-treated rats. Notably, the combination of surgery and WIN treatment disrupted social behavior in lesioned and sham-lesioned rats. The present data indicate that the mPFC is important for adequate juvenile response selection in the context of social play and might be involved in the development of adult social and nonsocial behavior. Moreover, our data add further evidence for an involvement of the cannabinoid system in anxiety and social behavior. Additive effects of neonatal surgery-induced stress or cortical lesions in combination with pubertal cannabinoid administration are also shown, The disturbances of social and nonsocial behavior in rats are comparable to symptoms of early frontal cortex damage, as well as neurodevelopmental disorders in humans, such as schizophrenia and autism, Therefore, we propose the combination of neonatal cortical lesions with chronic cannabinoid administration during puberty as an animal model for studying neuronal mechanisms of impaired social functioning in neuropsychiatric disorders, C1 Univ Bremen, Brain Res Inst, Dept Neuropharmacol, D-28334 Bremen, Germany. RP Schneider, M (reprint author), Univ Bremen, Brain Res Inst, Dept Neuropharmacol, POB 33 04 40, D-28334 Bremen, Germany. 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10.1136/bmj.325.7374.1199 NR 99 TC 73 Z9 77 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD MAY PY 2005 VL 30 IS 5 BP 944 EP 957 DI 10.1038/sj.npp.1300634 PG 14 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 917HX UT WOS:000228452800011 PM 15592349 ER PT J AU Pisalchaiyong, T Trairatvorakul, C Jirakijja, J Yuktarnonda, W AF Pisalchaiyong, T Trairatvorakul, C Jirakijja, J Yuktarnonda, W TI Comparison of the effectiveness of oral diazepam and midazolam for the sedation of autistic patients during dental treatment SO PEDIATRIC DENTISTRY LA English DT Article DE sedation; midazolam; diazepam; autism ID CONSCIOUS SEDATION; CROSSOVER TRIAL; NITROUS-OXIDE; CHILDREN; PREMEDICATION; BENZODIAZEPINES; ANESTHESIA; TIME AB Purpose: This study was undertaken to compare the effectiveness of oral diazepam and midazolam in sedating autistic patients during dental treatment. Methods: The treatment regimen consisted of nitrous oxide/oxygen inhalation in conjunction with oral administration of either diazepam 0.3 mg/kg or midazolam 0.5 mg/kg in a cross-over design study of 13 subjects aged 5.8 to 14.7 years. A drug was classified as being effective when over 70% of the patients taking the drug were judged as "success" in all 3 behavioral criteria: (1) sleeping; (2) body movement; and (3) crying behaviors. The study was observed by an independent clinician with an intraexaminer reliability of 88%. Results: For sleeping behavior, midazolam was found to be significantly more effective than diazepam as the duration of stimulation increased (P <.05). For the movement and crying behaviors, midazolam also proved to be significantly more effective from the start of treatment through the 35- and 40-min markers, respectively (P <.05). For the remainder of treatment, however, there was no statistically significant difference in these behaviors between the trials (>.05). Diazepam and midazolam were rated as 77% and 100% successful, according to the overall behavior evaluation criteria (P=.02). Conclusions: Both diazepam and midazolam were shown to be effective sedative agents, successfully and safely used to sedate autistic patients for dental treatment. Midazolam was significantly more effective than diazepam in those portions of the procedure with increased stimulation. C1 Chulalongkorn Univ, Fac Dent, Dept Pediat Dent, Bangkok, Thailand. Chulalongkorn Univ, Fac Dent, Dept Oral & Maxillofacial Surg, Bangkok, Thailand. Yuwaprasart Waithayoprathum Child Psychit Hosp, Dept Dent, Sumutprakarn, Thailand. 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Dent. PD MAY-JUN PY 2005 VL 27 IS 3 BP 198 EP 206 PG 9 WC Dentistry, Oral Surgery & Medicine; Pediatrics SC Dentistry, Oral Surgery & Medicine; Pediatrics GA 001OQ UT WOS:000234546600007 PM 16173223 ER PT J AU Einspieler, C Kerr, AM Prechtl, HFR AF Einspieler, C Kerr, AM Prechtl, HFR TI Is the early development of girls with Rett disorder really normal? SO PEDIATRIC RESEARCH LA English DT Article ID CLINICAL-FEATURES; INFANTS; MECP2; MUTATIONS; MOVEMENTS; PRETERM; AUTISM AB An apparently normal early development was one of the initial criteria for classical Rett syndrome. However, several investigators considered Rett syndrome to be a developmental disorder manifesting very soon after birth. Videos of 22 Rett cases were assessed carefully for movements, posture, and behavior during the first 6 mo of life. All signs that deviated from the normal standard were recorded meticulously. Special attention was paid to the face, the hands, and body movements. A detailed analysis clearly demonstrated an abnormal quality of general movements (100%), tongue protrusion (62%), postural stiffness (58%), asymmetric eye opening and closing (56%), abnormal finger movements (52%), hand stereotypies (42%), bursts of abnormal facial expressions (42%), bizarre smile (32%), tremor (28%), and stereotyped body movements (15%). Our study is the first to apply specific standardized measures of early spontaneous movements to Rett infants, proving conclusively that the disorder is manifested within the first months of life. Although not necessarily specific, the signs that we have observed will be of value in alerting clinicians to the possibility of the diagnosis at an early stage, when intervention is likely to be most effective. C1 Med Univ Graz, Inst Physiol, Ctr Physiol Med, A-8010 Graz, Austria. Med Univ Graz, Sect Dev Physiol & Dev Neurol, A-8010 Graz, Austria. Gartnavel Royal Hosp, Acad Ctr, Dept Psychol Med, Glasgow G12 0XH, Lanark, Scotland. RP Einspieler, C (reprint author), Med Univ Graz, Inst Physiol, Ctr Physiol Med, Harrachgasse 21, A-8010 Graz, Austria. 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Res. PD MAY PY 2005 VL 57 IS 5 BP 696 EP 700 DI 10.1203/01.PDR.0000155945.94249.0A PN 1 PG 5 WC Pediatrics SC Pediatrics GA 919VM UT WOS:000228645700015 PM 15718369 ER PT J AU Perez-Gonzalez, LA Williams, G AF Perez-Gonzalez, LA Williams, G TI Comprehensive program to teach skills to children with autism SO PSICOTHEMA LA Spanish DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE BEHAVIORAL TREATMENT; CONDITIONAL DISCRIMINATIONS; FUNCTIONAL-ANALYSIS; STIMULUS-CONTROL; VERBAL-BEHAVIOR; INTERVENTION; SCHOOL AB Comprehensive program to teach skills to children with autism. The purpose of this research was to test a comprehensive system to teach skills to children diagnosed with autism. Three children received intensive teaching during three months, approximately. Each child received a daily set of programs tailored to his/her functional level. These programs had been demonstrated effective in previous studies to teach children with learning difficulties. 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DEL RIO, 4-1 B, 33001 OVIEDO, SPAIN SN 0214-9915 J9 PSICOTHEMA JI Psicothema PD MAY PY 2005 VL 17 IS 2 BP 233 EP 244 PG 12 WC Psychology, Multidisciplinary SC Psychology GA 919WA UT WOS:000228647100008 ER PT J AU Moss, T AF Moss, T TI Tutoring a child with autism (and the unexpected opportunities it can bring) SO PSYCHOLOGIST LA English DT Editorial Material C1 UCL, London WC1E 6BT, England. RP Moss, T (reprint author), UCL, London WC1E 6BT, England. EM tim@80ways.co.uk NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD MAY PY 2005 VL 18 IS 5 BP 299 EP 299 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 925VB UT WOS:000229080300045 ER PT J AU Bayliss, AP di Pellegrino, G Tipper, SP AF Bayliss, AP di Pellegrino, G Tipper, SP TI Sex differences in eye gaze and symbolic cueing of attention SO QUARTERLY JOURNAL OF EXPERIMENTAL PSYCHOLOGY SECTION A-HUMAN EXPERIMENTAL PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; VISUAL-ATTENTION; SPATIAL ATTENTION; DISCRIMINATION TASKS; LANGUAGE-DEVELOPMENT; GENDER-DIFFERENCES; SOCIAL-PERCEPTION; ASPERGER-SYNDROME; FACE RECOGNITION; JOINT ATTENTION AB Observing a face with averted eyes results in a reflexive shift of attention to the gazed-at location. Here we present results that show that this effect is weaker in males than in females (Experiment 1). This result is predicted by the 'extreme male brain' theory of autism (Baron-Cohen, 2003), which suggests that males in the normal population should display more autism-like traits than females (e.g., poor joint attention). Indeed, participants' scores on the Autism-Spectrum Quotient (Baron-Cohen, Wheelwright, Stott, Bolton, & Goodyear, 2001) negatively correlated with cueing magnitude. Furthermore, exogenous orienting did not differ between the sexes in two peripheral cueing experiments (Experiments 2a and 2b). However, a final experiment showed that using non-predictive arrows instead of eyes as a central cue also revealed a large gender difference. This demonstrates that reduced orienting from central cues in males generalizes beyond gaze cues. These results show that while peripheral cueing is equivalent in the male and female brains, the attention systems of the two sexes treat noninformative symbolic cues very differently. C1 Univ Coll N Wales, Sch Psychol, Ctr Cognit Neurosci, Bangor LL57 2AS, Gwynedd, Wales. RP Bayliss, AP (reprint author), Univ Coll N Wales, Sch Psychol, Ctr Cognit Neurosci, Bangor LL57 2AS, Gwynedd, Wales. EM a.bayliss@bangor.ac.uk RI Tipper, Steven/I-6884-2012 OI Tipper, Steven/0000-0002-1554-0531 CR Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 Argyle Michael, 1976, GAZE AND MUTUAL GAZE Baldwin D. 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J. Exp. Psychol. Sect A-Hum. Exp. Psychol. PD MAY PY 2005 VL 58 IS 4 BP 631 EP 650 DI 10.1080/02724980443000124 PG 20 WC Psychology; Psychology, Experimental SC Psychology GA 931IJ UT WOS:000229478700004 PM 16104099 ER PT J AU Keen, D AF Keen, D TI The use of non-verbal repair strategies by children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE non-verbal repairs; vocal prosidy; gestural prosidy ID SEVERE DISABILITIES; YOUNG-CHILDREN; COMMUNICATION AB This study examined possible links between the occurrence of prosodic changes to vocalizations and gestures and the use of problem behaviors by children with autism when attempting to repair communication breakdowns. The repair strategies of six children with autism aged 2-5 years and with fewer than 10 words or signs were analyzed. Mother-child dyads were videotaped at home interacting in naturally occurring contexts. Videotapes were analyzed and coded for communication breakdowns and repair attempts made by the child. Repairs were further analyzed according to the type of repair strategy used, changes in prosidy, and whether the repair mode involved problematic or non-problematic behavior. In most situations, this group of children attempted to repair breakdowns in communication that occurred while interacting with their mothers. Most children used both nonproblematic and problematic behaviors and were less likely to use augmentations as a repair strategy than repetitions and substitutions. Some repetitions and some augmentations involved the use of gestures or vocalizations with increased emphasis or prosidy. Possible links between repair strategies involving increased prosidy and the use of problem behaviors are discussed together with the implications and significance of these finding in relation to early intervention for children with significant communication impairments. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Queensland, Sch Educ, Brisbane, Qld 4072, Australia. RP Keen, D (reprint author), Univ Queensland, Sch Educ, Brisbane, Qld 4072, Australia. EM deb.keen@uq.edu.au RI Keen, Deb/B-8998-2008 CR Alexander Dianne, 1997, Seminars in Speech and Language, V18, P197, DOI 10.1055/s-2008-1064073 BRADY NC, 1995, J SPEECH HEAR RES, V38, P1334 BRUININKS RH, 1984, SCALES INDEPENDANT B Butterfield Nancy, 1991, Australia and New Zealand Journal of Developmental Disabilities, V17, P347 CARR EG, 1989, J AUTISM DEV DISORD, V19, P561, DOI 10.1007/BF02212858 DRASGOW E, 1995, TOP EARLY CHILD SPEC, V15, P164 DUNLAP G, 1994, MENT RETARD, V32, P206 Einfeld SL, 1996, J INTELL DISABIL RES, V40, P99, DOI 10.1111/j.1365-2788.1996.tb00611.x Goldbart J., 1994, ED CHILDREN PROFOUND, P15 GOLINKOFF RM, 1986, J CHILD LANG, V13, P455 HOUGHTON J, 1987, J ASSOC PERS SEVERE, V12, P18 KEEN D, 2003, UNPUB CODING INTERAC KEEN D, 2003, J DISABILITY DEV ED, V50, P53 Sigman M., 1995, JOINT ATTENTION ITS, P189 Stone WL, 1997, J AUTISM DEV DISORD, V27, P677, DOI 10.1023/A:1025854816091 Wetherby A., 1993, COMMUNICATION SYMBOL Wetherby A. M., 1998, TRANSITION PRELINGUI, V7, P197 Wetherby A.M., 1992, AUTISM IDENTIFICATIO, P107 YODER PJ, 1994, J SPEECH HEAR RES, V37, P841 NR 19 TC 13 Z9 13 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD MAY-JUN PY 2005 VL 26 IS 3 BP 243 EP 254 DI 10.1016/j.ridd.2004.07.002 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 897LP UT WOS:000227005900004 PM 15668075 ER PT J AU Smith, AJ Bihm, EM Tavkar, P Sturmey, P AF Smith, AJ Bihm, EM Tavkar, P Sturmey, P TI Approach-avoidance and happiness indicators in natural environments: a preliminary analysis of the Stimulus Preference Coding System SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE psychopathology; inter-observer agreement; stimulus preference ID PROFOUND MULTIPLE DISABILITIES; REINFORCER IDENTIFICATION; IDENTIFYING REINFORCERS; INCREASING INDEXES; PEOPLE; REPLICATION; HANDICAPS AB Two studies assessed the reliability and utility of the Stimulus Preference Coding System (SPCS) to measure approach, avoidance, and happy and unhappy behaviors in persons with developmental disorders. Study 1 took place in an institutional setting. The nine participants were all adults with mental retardation and multiple associated disabilities. Inter-observer reliability ranged from 72% to 100%. Study 2 took place in an after-school setting. The four participants were children diagnosed with autism and mental retardation. Inter-observer agreement ranged from 70% to 91%. Approach and avoidance behaviors were a function of staff person and task. The SPCS may be useful in identifying reinforcers, promoting happiness, analyzing task and staff effects, and clarifying the relationship of stimulus preference to psychopathology. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Cent Arkansas, Dept Psychol & Counseling, Conway, AR 72035 USA. Univ Nebraska, Dept Psychol, Lincoln, NE 68588 USA. CUNY, Queens Coll, New York, NY 10021 USA. CUNY, Grad Ctr, New York, NY 10021 USA. RP Bihm, EM (reprint author), Univ Cent Arkansas, Dept Psychol & Counseling, 201 S Donaghey, Conway, AR 72035 USA. EM elsonb@uca.edu CR BIHM EM, 1992, J AUTISM DEV DISORD, V22, P83, DOI 10.1007/BF01046404 Carver CS, 2000, AM J MENT RETARD, V105, P336, DOI 10.1352/0895-8017(2000)105<0336:OTCCOH>2.0.CO;2 DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 DeLeon IG, 1999, J APPL BEHAV ANAL, V32, P111, DOI 10.1901/jaba.1999.32-111 Dunlap G., 1982, ED UNDERSTANDING AUT, P106 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Green CW, 1997, J APPL BEHAV ANAL, V30, P217, DOI 10.1901/jaba.1997.30-217 Green CW, 1996, J APPL BEHAV ANAL, V29, P67, DOI 10.1901/jaba.1996.29-67 GREEN CW, 1988, J APPL BEHAV ANAL, V21, P31, DOI 10.1901/jaba.1988.21-31 GREEN CW, 1991, J APPL BEHAV ANAL, V24, P537, DOI 10.1901/jaba.1991.24-537 Helm DT, 2000, AM J MENT RETARD, V105, P326, DOI 10.1352/0895-8017(2000)105<0326:TMOH>2.0.CO;2 Higbee TS, 2000, RES DEV DISABIL, V21, P61, DOI 10.1016/S0891-4222(99)00030-X Ivancic MT, 1996, RES DEV DISABIL, V17, P77, DOI 10.1016/0891-4222(95)00038-0 Ivancic MT, 1997, RES DEV DISABIL, V18, P79, DOI 10.1016/S0891-4222(96)00039-X LOVAAS OI, 1966, J EXP CHILD PSYCHOL, V4, P109, DOI 10.1016/0022-0965(66)90011-7 PACE GM, 1985, J APPL BEHAV ANAL, V18, P249, DOI 10.1901/jaba.1985.18-249 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P137, DOI 10.1901/jaba.1996.29-137 Ringdahl JE, 1997, J APPL BEHAV ANAL, V30, P203, DOI 10.1901/jaba.1997.30-203 Roane HS, 1998, J APPL BEHAV ANAL, V31, P605, DOI 10.1901/jaba.1998.31-605 STURMEY P, 2003, BEHAV COGN PSYCHOTH, V31, P99 NR 20 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 MAY-JUN PY 2005 VL 26 IS 3 BP 297 EP 313 DI 10.1016/j.ridd.2004.06.001 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 897LP UT WOS:000227005900008 PM 15668079 ER PT J AU Flanders, S Engelhart, L AF Flanders, S Engelhart, L TI Direct cost of treatment for autism spectrum disorder in California Medicaid SO VALUE IN HEALTH LA English DT Meeting Abstract C1 Janssen Med Affairs, Grayslake, IL USA. Janssen Med Affairs, Titusville, NJ USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 1098-3015 J9 VALUE HEALTH JI Value Health PD MAY-JUN PY 2005 VL 8 IS 3 BP 298 EP 298 PG 1 WC Economics; Health Care Sciences & Services; Health Policy & Services SC Business & Economics; Health Care Sciences & Services GA 918PE UT WOS:000228559300201 ER PT J AU Schoumans, J Sanner, G Nordenskjold, M Anderlid, BM AF Schoumans, J Sanner, G Nordenskjold, M Anderlid, BM TI Detailed clinical description of four patients with 1.3 and 2.1 Mb chromosome imbalances derived from a familial t(12;17)(q24.33;q25.3) SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE duplication; deletion; 12q; 17q; subtelomeric; autism; mental retardation ID MENTAL-RETARDATION; TRISOMY; 12Q; DUPLICATION; FEATURES; REARRANGEMENTS; TRANSLOCATION; DELETION; COUSINS AB We describe a family carrying a submicroscopic reciprocal translocation involving 12qter and 17qter detected by subtelomeric FISH analysis. Four family members inherited unbalanced variants-two cases inherited the derivative chromosome 12 and the other two the derivative chromosome 17. The two individuals with the derivative chromosome 17 showed a distinct phenotype with mild mental retardation in combination with multiple minor malformations, while the phenotype in the cases with the derivative chromosome 12 was milder and only partly concordant. Detailed FISH analysis using 19 BAC clones covering the distal part of chromosome 12q and 17q estimated the imbalances to 2.1 and 1.3 Mb, respectively. The clinical and cytogenetic findings of the two different genotypes are reported and discussed. This family illustrates that small chromosome imbalances can be detected in individuals with mild phenotype and normal, or near-normal, cognitive functions. (c) 2005 Wiley-Liss, Inc. C1 Karolinska Inst, Dept Mol Med, Clin Genet Unit, Stockholm, Sweden. Cent Hosp Karlstad, Child Habilitat Ctr, Karlstad, Sweden. RP Schoumans, J (reprint author), Karolinska Inst, Dept Mol Med, Clin Genet Unit, Stockholm, Sweden. EM Jacqueline.Schoumans@cmm.ki.se CR Anderlid BM, 2002, AM J MED GENET, V107, P275, DOI 10.1002/ajmg.10029 Birney E, 2004, NUCLEIC ACIDS RES, V32, pD468, DOI 10.1093/nar/gkh038 CAINE A, 1989, J MED GENET, V26, P577, DOI 10.1136/jmg.26.9.577 de Vries BBA, 2003, J MED GENET, V40, P385, DOI 10.1136/jmg.40.6.385 DEMUELENAERE A, 1980, ANN GENET-PARIS, V23, P251 HARROD MJE, 1980, AM J MED GENET, V7, P123, DOI 10.1002/ajmg.1320070206 Kelly BD, 2002, AM J MED GENET, V112, P217, DOI 10.1002/ajmg.10626 Lagier-Tourenne C, 2004, AM J MED GENET A, V125A, P77, DOI 10.1002/ajmg.a.20450 MCCORQUODALE MM, 1986, AM J MED GENET, V24, P613, DOI 10.1002/ajmg.1320240405 Parmar RC, 2003, AM J MED GENET A, V117A, P275, DOI 10.1002/ajmg.a.10044 Rossi E, 2001, J MED GENET, V38, P417, DOI 10.1136/jmg.38.6.417 Sarri C, 1997, AM J MED GENET, V70, P87, DOI 10.1002/(SICI)1096-8628(19970502)70:1<87::AID-AJMG16>3.0.CO;2-T Sathya P, 1999, AM J MED GENET, V84, P116, DOI 10.1002/(SICI)1096-8628(19990521)84:2<116::AID-AJMG6>3.0.CO;2-3 Shashi V, 2003, CLIN GENET, V64, P361, DOI 10.1034/j.1399-0004.2003.00146.x TAJARA EH, 1985, J MED GENET, V22, P73, DOI 10.1136/jmg.22.1.73 TENGSTROM C, 1985, CLIN GENET, V28, P112 van Wijk E, 2003, J MED GENET, V40, P879, DOI 10.1136/jmg.40.12.879 NR 17 TC 4 Z9 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD APR 30 PY 2005 VL 134A IS 3 BP 254 EP 258 DI 10.1002/ajmg.a.30611 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 912MT UT WOS:000228083600006 PM 15704131 ER PT J AU Levinson, JN Chery, N Huang, K Wong, TP Gerrow, K Kang, R Prange, O Wang, YT El-Husseini, A AF Levinson, JN Chery, N Huang, K Wong, TP Gerrow, K Kang, R Prange, O Wang, YT El-Husseini, A TI Neuroligins mediate excitatory and inhibitory synapse formation - Involvement of PSD-95 and neurexin-1 beta in neuroligin-induced synaptic specificity SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-ADHESION; HIPPOCAMPAL-NEURONS; MENTAL-RETARDATION; BETA-NEUREXINS; AUTISM; PROTEINS; SYNAPTOGENESIS; PLASTICITY; MOLECULES; BINDING AB The balance between excitatory and inhibitory synapses is a tightly regulated process that requires differential recruitment of proteins that dictate the specificity of newly formed contacts. However, factors that control this process remain unidentified. Here we show that members of the neuroligin (NLG) family, including NLG1, NLG2, and NLG3, drive the formation of both excitatory and inhibitory presynaptic contacts. The enrichment of endogenous NLG1 at excitatory contacts and NLG2 at inhibitory synapses supports an important in vivo role for these proteins in the development of both types of contacts. Immunocytochemical and electrophysiological analysis showed that the effects on excitatory and inhibitory synapses can be blocked by treatment with a fusion protein containing the extracellular domain of neurexin-1 beta. We also found that overexpression of PSD-95, a postsynaptic binding partner of NLGs, resulted in a shift in the distribution of NLG2 from inhibitory to excitatory synapses. These findings reveal a critical role for NLGs and their synaptic partners in controlling the number of inhibitory and excitatory synapses. Furthermore, relative levels of PSD-95 alter the ratio of excitatory to inhibitory synaptic contacts by sequestering members of the NLG family to excitatory synapses. C1 Univ British Columbia, Dept Psychiat, Brain Res Ctr, Vancouver, BC V6T 1Z3, Canada. Univ British Columbia, Dept Med, Brain Res Ctr, Vancouver, BC V6T 1Z3, Canada. RP El-Husseini, A (reprint author), Univ British Columbia, Dept Psychiat, Brain Res Ctr, Vancouver, BC V6T 1Z3, Canada. 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These postulates, combined with the insight from the Trivers-Willard hypothesis regarding parental ability to vary offspring sex ratio, lead to the prediction that people who have strong male brains should have more sons than daughters, and people who have strong female brains should have more daughters than sons. The analysis of the 1994 US General Social Survey data provides support for this prediction. Our results suggest potentially fruitful extensions of both Baron-Cohen's theory and the Trivers-Willard hypothesis. (c) 2004 Elsevier Ltd. All rights reserved. C1 Univ London London Sch Econ & Polit Sci, Interdisciplinary Inst Management, London WC2A 2AE, England. Univ Ghent, Dept English, Ctr Gender Studies, B-9000 Ghent, Belgium. RP Kanazawa, S (reprint author), Univ London London Sch Econ & Polit Sci, Interdisciplinary Inst Management, Houghton St, London WC2A 2AE, England. 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PD APR 17 PY 2005 BP 20 EP 20 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 916CV UT WOS:000228363900022 ER PT J AU Amaral, DG AF Amaral, DG TI Neurobiological and immunological factors in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Univ Calif Davis, San Francisco, CA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 4 BP 1S EP 2S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338600006 ER PT J AU Hardan, AY Muddasani, S Vemulapalli, M Keshavan, MS Minshew, NJ AF Hardan, AY Muddasani, S Vemulapalli, M Keshavan, MS Minshew, NJ TI An MRI study of increased cortical thickness in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. Univ Texas, Hlth Sci Ctr, San Antonio, TX USA. Wayne State Univ, Detroit, MI USA. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 34 BP 10S EP 11S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338600036 ER PT J AU Piven, J AF Piven, J TI A longitudinal study of brain development in children with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 37 BP 11S EP 11S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338600039 ER PT J AU Casanova, MF Switala, A AF Casanova, MF Switala, A TI A negative study on the morphometric variability of minicolumns (pyramidal cell arrays) in the brains of patients with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Univ Louisville, Louisville, KY 40292 USA. RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012 OI Giedd, Jay/0000-0003-0827-3460 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 171 BP 49S EP 49S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338600173 ER PT J AU Patterson, PH AF Patterson, PH TI Respiratory infection in pregnant mice causes changes in the offspring resembling those in schizophrenia and autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 CALTECH, Pasadena, CA 91125 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 316 BP 86S EP 86S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338600308 ER PT J AU Hardan, AY Stanley, JA Keshavan, MS Vemulapalli, M Minshew, NJ AF Hardan, AY Stanley, JA Keshavan, MS Vemulapalli, M Minshew, NJ TI A proton magnetic resonance spectroscopy investigation of the frontal lobe in childhood autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. Wayne State Univ, Detroit, MI USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 367 BP 101S EP 102S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338600359 ER PT J AU Reichenberg, A AF Reichenberg, A TI Autism risk and advanced paternal age SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 525 BP 144S EP 144S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338601122 ER PT J AU LiCalzi, EM Haznedar, MH Anagnostou, E Wasserman, SL Hollander, E Buchsbaum, MS AF LiCalzi, EM Haznedar, MH Anagnostou, E Wasserman, SL Hollander, E Buchsbaum, MS TI Volume and anisotropy of the visual-temporal cortex and correlations to facial recognition in autism spectrum disorders SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 600 BP 165S EP 165S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338601197 ER PT J AU Wasserman, SL AF Wasserman, SL TI Divalproex sodium vs. placebo in the treatment of repetitive behaviors and the treatment of activation associated with fluoxetine in autism spectrum disorder SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Mt Sinai Sch Med, New York, NY USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 606 BP 166S EP 167S PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338601203 ER PT J AU McInnes, LA Richler, E Buxbaum, JD Reichert, J AF McInnes, LA Richler, E Buxbaum, JD Reichert, J TI Screening ultraconserved noncoding sequence in the FOXP2 gene for variants associated with autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 60th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 19-21, 2005 CL Atlanta, GA SP Soc Biol Psychiat C1 Mt Sinai Sch Med, New York, NY USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2005 VL 57 IS 8 SU S MA 686 BP 189S EP 189S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 915VE UT WOS:000228338601283 ER PT J AU Skuse, DH AF Skuse, DH TI X-linked genes and mental functioning SO HUMAN MOLECULAR GENETICS LA English DT Review ID HUMAN Y-CHROMOSOME; TURNER-SYNDROME; SEX-DIFFERENCES; NEURAL BASIS; HUMAN BRAIN; AUTISM; INACTIVATION; FEAR; RETARDATION; RECOGNITION AB The X-chromosome has played a crucial role in the development of sexually selected characteristics for over 300 million years. During that time it has accumulated a disproportionate number of genes concerned with mental functions. Evidence is emerging, from studies of both humans and mice, for a general influence upon intelligence (as indicated by the large number of X-linked mental retardation syndromes). In addition, there is evidence for relatively specific effects of X-linked genes on social-cognition and emotional regulation. Sexually dimorphic processes could be influenced by several mechanisms. First, a small number of X-linked genes are apparently expressed differently in male and female brains in mouse models. Secondly, many human X-linked genes outside the X-Y pairing pseudoautosomal regions escape X-inactivation. Dosage differences in the expression of such genes (which might comprise at least 20% of the total) are likely to play an important role in male-female neural differentiation. To date, little is known about the process but clues can be gleaned from the study of X-monosomic females who are haploinsufficient for expression of all non-inactivated genes relative to 46,XX females. Finally, from studies of both X-monosomic humans (45,X) and mice (39,X), we are learning more about the influences of X-linked imprinted genes upon brain structure and function. Surprising specificity of effects has been described in both species, and identification of candidate genes cannot now be far off. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. RP Skuse, DH (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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PD APR 15 PY 2005 VL 14 SI 1 BP R27 EP R32 DI 10.1093/hmg/ddi112 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 914PW UT WOS:000228241000005 PM 15809269 ER PT J AU Villalobos, ME Mizuno, A Dahl, BC Kemmotsu, N Muller, RA AF Villalobos, ME Mizuno, A Dahl, BC Kemmotsu, N Muller, RA TI Reduced functional connectivity between V1 and inferior frontal cortex associated with visuomotor performance in autism SO NEUROIMAGE LA English DT Article DE autism; functional connectivity; dorsal stream; mirror neurons ID RESTING-STATE; MAGNETIC-RESONANCE; CHILDHOOD AUTISM; INFANTILE-AUTISM; PREMOTOR CORTEX; BRAIN-STEM; DEVELOPMENTAL DISORDERS; SPECTRUM DISORDER; SPATIAL ATTENTION; EARLY RECOGNITION AB Some recent evidence has suggested abnormalities of the dorsal stream and possibly the mirror neuron system in autism, which may be responsible for impairments of joint attention, imitation, and secondarily for language delays. The current study investigates functional connectivity along the dorsal stream in autism, examining interregional blood oxygenation level dependent (BOLD) signal cross-correlation during visuomotor coordination. Eight high-functioning autistic men and eight handedness and age-matched controls were included. Visually prompted button presses were performed with the preferred hand. For each subject, functional connectivity was computed in terms of BOLD signal correlation with the mean time series in bilateral visual area 17. Our hypothesis of reduced dorsal stream connectivity in autism was only in part confirmed. Functional connectivity with superior parietal areas was not significantly reduced. However, the autism group showed significantly reduced connectivity with bilateral inferior frontal area 44, which is compatible with the hypothesis of mirror neuron defects in autism. More generally, our findings suggest that dorsal stream connectivity in autism may not be fully functional. (c) 2004 Elsevier Inc. All rights reserved. C1 San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA. Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92093 USA. RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, 6363 Alvarado Ct,225 E, San Diego, CA 92120 USA. 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Developmental surveillance of children to detect these disorders should be a routine part of medical practice. The persistence and pervasiveness of communication and socialising deficits differentiate children with autism from those with specific developmental language disorders. Hearing and vision assessment is essential in any communication disorder. Interventions, targeted to identified areas of need, should encompass communication enhancement, behavioural therapy, educational modification, parent education and family support. Pharmacological interventions have an important but discrete role in autism, but there are no magic bullets. It is important to remember that the normal childhood illnesses occur in children with developmental disorders. Parents should be directed to reliable websites on the Internet, and given information and books to read as well as phone numbers of relevant services (eg, autism associations). 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Using magnetoencephalography, we recorded evoked neural activity to 300-Hz and 700-Hz tones (and /u/ and /a/ vowels) presented in an oddball paradigm with deviant stimuli (15%) occurring within a train of standards (85%). The magnetic mismatch field was robustly observed in both groups, but children with autism spectrum disorder demonstrated a significantly delayed magnetic mismatch field compared with typically developing peers. Difficulty parsing transient differences in sounds may lead to impaired acoustic or phonological representations and subsequent language impairment in autism spectrum disorder. (c) 2005 Lippincott Williams T Wilkins. C1 Univ Toronto, Dept Med Imaging, Toronto, ON, Canada. Univ Toronto, Dept Paediat, Toronto, ON, Canada. Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. RP Cardy, JEO (reprint author), Univ Toronto, Dept Med Imaging, 100 Coll St, Toronto, ON, Canada. 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PD APR PY 2005 VL 94 IS 4 BP 386 EP 393 DI 10.1080/08035250410023304 PG 8 WC Pediatrics SC Pediatrics GA 917HJ UT WOS:000228451400001 PM 16092447 ER PT J AU Balzola, F Barbon, V Repici, A Rizzetto, M Clauser, D Gandione, M Sapino, A AF Balzola, F Barbon, V Repici, A Rizzetto, M Clauser, D Gandione, M Sapino, A TI Panenteric IBD-like disease in a patient with regressive autism shown for the first time by the wireless capsule enteroscopy: Another piece in the jigsaw of this gut-brain syndrome? SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Letter ID CHILDREN C1 Univ Turin, Molinette Hosp Turin, Dept Gastroenterol, I-10124 Turin, Italy. Univ Turin, Regina Margherita Pediat Hosp, Dept Neuropsychiat, Turin, Italy. Univ Turin, Molinette Hosp Turin, Dept Biomed Sci & Human Oncol, I-10124 Turin, Italy. RP Balzola, F (reprint author), Univ Turin, Molinette Hosp Turin, Dept Gastroenterol, I-10124 Turin, Italy. 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PD APR PY 2005 VL 100 IS 4 BP 979 EP 981 DI 10.1111/j.1572-0241.2005.41202_4.x PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 907LU UT WOS:000227720400039 PM 15784047 ER PT J AU Bartlett, CW Goedken, R Vieland, VJ AF Bartlett, CW Goedken, R Vieland, VJ TI Effects of updating linkage evidence across subsets of data: Reanalysis of the autism genetic resource exchange data set SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID GENOMEWIDE SCREEN; POSTERIOR PROBABILITY; LANGUAGE IMPAIRMENT; SUSCEPTIBILITY LOCI; SPECTRUM DISORDERS; GENOMIC SCREEN; CHROMOSOME 7Q; HETEROGENEITY; SCHIZOPHRENIA; DISEQUILIBRIUM AB Results of autism linkage studies have been difficult to interpret across research groups, prompting the use of ever-increasing sample sizes to increase power. However, increasing sample size by pooling disparate collections for a single analysis may, in fact, not increase power in the face of genetic heterogeneity. 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PD APR PY 2005 VL 28 IS 2 BP 146 EP + PG 11 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 956DX UT WOS:000231280500024 ER PT J AU Buckley, SD Strunck, PG Newchok, DK AF Buckley, SD Strunck, PG Newchok, DK TI A comparison of two multicomponent procedures to increase food consumption SO BEHAVIORAL INTERVENTIONS LA English DT Article ID ESCAPE EXTINCTION; REFUSAL; REINFORCEMENT AB We compared two procedural variations of response cost (RC) of preferred materials to increase mouth clean in a five-year-old boy diagnosed with autism. Noncontingent presentation of preferred materials (NCR) was compared to differential reinforcement of alternative behavior (DRA) when returning preferred materials once they have been removed for refusal or expulsion of food. Results indicated that both procedures increased swallowing and reduced problem behavior; however, NCR+ RC was superior to DRA + RC with respect to overall mean and initial treatment measures. Copyright (c) 2005 John Wiley & Sons, Ltd. C1 ALLEGRO Sch, Cedar Knolls, NJ USA. RP Buckley, SD (reprint author), Rockaway Township Publ Sch District, Rockaway, NJ USA. 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PD APR PY 2005 VL 20 IS 2 BP 139 EP 146 DI 10.1002/bin.188 PG 8 WC Psychology, Clinical SC Psychology GA 921UQ UT WOS:000228791200003 ER PT J AU Luiselli, JK Ricciardi, JN Gilligan, K AF Luiselli, JK Ricciardi, JN Gilligan, K TI Liquid fading to establish milk consumption by a child with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID FOOD REFUSAL; REINFORCEMENT; EXTINCTION AB Liquid avoidance by children with developmental disabilities is a common problem but has not been researched extensively. In this study, a 4-year-old girl who had autism and food selectivity was taught to drink milk through a liquid fading procedure. The feeding protocol consisted of gradually increasing the concentration of milk in a beverage she consumed 100% of the time. Intervention was implemented by educational staff in a school setting. Milk consumption was achieved rapidly without interruption to the fading sequence. Clinical and research issues related to liquid avoidance and fading treatments are discussed. Copyright (c) 2005 John Wiley & Sons, Ltd. C1 May Inst, Norwood, MA 02062 USA. May Ctr Appl Res, Norwood, MA 02062 USA. RP Luiselli, JK (reprint author), May Inst, 1 Commerce Way, Norwood, MA 02062 USA. 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PD APR PY 2005 VL 20 IS 2 BP 155 EP 163 DI 10.1002/bin.187 PG 9 WC Psychology, Clinical SC Psychology GA 921UQ UT WOS:000228791200005 ER PT J AU Fatemi, SH Snow, AV Stary, JM Araghi-Niknam, M Reutiman, TJ Lee, S Brooks, AI Pearce, DA AF Fatemi, SH Snow, AV Stary, JM Araghi-Niknam, M Reutiman, TJ Lee, S Brooks, AI Pearce, DA TI Reelin signaling is impaired in autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; beta-actin; bipolar disorder; cerebellum; Dab-1; GSK-3 beta; mRNA; Reelin; parietal cortex; superior frontal cortex; QPCR; schizophrenia; VLDLR; Western blotting ID DENSITY-LIPOPROTEIN RECEPTOR; FYN TYROSINE KINASE; BRAIN-DEVELOPMENT; MUTANT MICE; EXTRACELLULAR-MATRIX; NEURONAL MIGRATION; CORTICAL DEVELOPMENT; VULNERABILITY FACTOR; CEREBRAL-CORTEX; VLDL RECEPTOR AB Background: Autism is a severe neurodevelopmental disorder with genetic and environmental etiologies, Recent genetic linkage studies implicate Reelin glycoprotein in causation of autism. To further investigate these studies, brain levels of Reelin protein and mRNA and mRNAs for VLDLR, Dab-1, and GSK3 were investigated. Methods: Postmortem superior frontal, parietal, and cerebellar cortices of age, gender, and postmortem interval-matched autistic and control subjects were subjected to SDS-PAGE and Western blotting of Reelin protein. Quantitative reverse transcriptase polymerase chain reaction analysis of Reelin, VLDL-R, Dab-1, and GSK3 mRNA species in superior frontal and cerebellar cortices of autistic and control subjects were also performed. Results: Reelin 410, 330, and 180 kDa/beta-actin values were reduced significantly in frontal and cerebellar, and nonsignficantly in parietal, areas of autistic brains versus control subjects, respectively. The mRNAs for Reln and Dab-1 were reduced significantly whereas the mRNA for Reln receptor VLDLR was elevated significantly in superior-frontal and cerebellar areas Qf autistic brains versus control brains, respectively. Conclusions: Reductions in Reelin protein and mRNA and Dab 1 mRNA and elevations in Reln receptor VLDLR mRNA demonstrate impairments in the Reelin signaling system in autism, accounting for some of the brain structural and cognitive deficits observed in the disorder. C1 Univ Minnesota, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Univ Rochester, Sch Med & Dent, Ctr Funct Genom, Rochester, NY USA. Univ Rochester, Sch Med & Dent, Ctr Aging & Dev Biol, Rochester, NY USA. Univ Rochester, Sch Med & Dent, Dept Biochem, Rochester, NY USA. Univ Rochester, Sch Med & Dent, Dept Biophys, Rochester, NY USA. Univ Rochester, Sch Med & Dent, Dept Neurol, Rochester, NY USA. Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY USA. RP Fatemi, SH (reprint author), Univ Minnesota, Dept Psychiat, Div Neurosci Res, MMC 392,420 Delaware St SE, Minneapolis, MN 55455 USA. 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Psychiatry PD APR 1 PY 2005 VL 57 IS 7 BP 777 EP 787 DI 10.1016/j.biopsych.2004.12.018 PG 11 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 913BK UT WOS:000228125000012 PM 15820235 ER PT J AU Li, H Yamagata, T Mori, M Momoi, MY AF Li, H Yamagata, T Mori, M Momoi, MY TI Absence of causative mutations and presence of autism-related allele in FOXP2 in Japanese autistic patients SO BRAIN & DEVELOPMENT LA English DT Article DE dyslexia; FOXP2; DHPLC; 7q ID PERFORMANCE LIQUID-CHROMATOGRAPHY; LANGUAGE DISORDER; SUSCEPTIBILITY GENE; SEVERE SPEECH; 7Q AB We analyzed the FOXP2 gene, which encodes a putative transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain, for a possible causative mutation in autism. FOXP2 was reported to be mutated in patients with a severe speech and language disorder. FOXP2 was located on chromosome 7q31, which is one of the loci involved in autism. Autism and specific language impairment share some of their clinical phenotypes. In addition, FOXP2 was expressed abundantly in the brain. We screened all of the exons of FOXP2 for causative mutations in 53 Japanese autistic patients using denaturing high-performance liquid chromatography and direct sequencing. A delCAA in exon 5 causing one glutamine deletion in the first polyglutamine tract was detected in four patients and in 2 of 50 control individuals. The frequency of the TT allele with the G to T base change in intron 15 was significantly high in the autistic population. The other base changes included one silent base change (A569G) in exon 5 and three in introns. Our results may suggest a relationship between autism and the FOXP2 gene or a gene located nearby. (c) 2004 Elsevier B.V. All rights reserved. C1 Jichi Med Sch, Dept Pediat, Minami Kawachi, Tochigi 3290498, Japan. RP Momoi, MY (reprint author), Jichi Med Sch, Dept Pediat, 3311-1 Yakushiji, Minami Kawachi, Tochigi 3290498, Japan. EM mymomoi@jichi.ac.jp CR Balter M, 2001, SCIENCE, V294, P32 Bruce HA, 2002, HUM GENET, V111, P136, DOI 10.1007/s00439-002-0768-5 Cummings CJ, 2000, HUM MOL GENET, V9, P909, DOI 10.1093/hmg/9.6.909 Eng C, 2001, J MED GENET, V38, P824, DOI 10.1136/jmg.38.12.824 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 Folstein SE, 2000, AM J HUM GENET, V67, P278, DOI 10.1086/303034 Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 Palferman S, 2001, AM J HUM GENET, V69, P570 Jones AC, 2000, HUM GENET, V106, P663, DOI 10.1007/s004390050040 Kaufmann E, 1996, MECH DEVELOP, V57, P3, DOI 10.1016/0925-4773(96)00539-4 Lai CSL, 2001, NATURE, V413, P519, DOI 10.1038/35097076 Liu WG, 1998, NUCLEIC ACIDS RES, V26, P1396, DOI 10.1093/nar/26.6.1396 Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X Newbury DF, 2002, AM J HUM GENET, V70, P1318, DOI 10.1086/339931 O'Donovan MC, 1998, GENOMICS, V52, P44, DOI 10.1006/geno.1998.5411 Tager-Flusberg H, 2001, MENT RETARD DEV D R, V7, P21 Vincent JB, 2000, AM J HUM GENET, V67, P510, DOI 10.1086/303005 Wassink TH, 2002, AM J MED GENET, V114, P566, DOI 10.1002/ajmg.10415 NR 18 TC 22 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD APR PY 2005 VL 27 IS 3 BP 207 EP 210 DI 10.1016/j.braindev.2004.06.002 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 907TL UT WOS:000227740800008 PM 15737702 ER PT J AU Tsuchiya, E Oki, J Yahara, N Fujieda, K AF Tsuchiya, E Oki, J Yahara, N Fujieda, K TI Computerized version of the Wisconsin card sorting test in children with high-functioning autistic disorder or attention-deficit/hyperactivity disorder SO BRAIN & DEVELOPMENT LA English DT Article DE Wisconsin card sorting test; high-functioning autistic disorder; attention-deficit/hyperactivity disorder (ADHD); executive function; perseveration ID INDIVIDUALS; PERFORMANCE; ADOLESCENTS; DEFICIT; ADHD AB To determine executive dysfunctions in children with autistic disorder or attention-deficit/hyperactivity disorder (ADHD), we investigated high-functioning autistic (full scale IQ score;>=?:70), ADHD, and control children using the computerized version of the Wisconsin Card Sorting Test. Data were obtained from 17 autistic children (16 boys and 1 girl, mean age +/- SD: 12.5 +/- 4.3), 22 ADHD children (20 boys and 2 girls, mean age +/- SD 11.3 +/- 2.6), and 25 control children (13 boys and 12 girls, mean age +/- SD: 12.7 +/- 3.1). Performances, indicated by mean number of categories achieved (5.4 in autistic, 6.5 in ADHD, and 8.8 in control group), total errors (38.2, 38.4, and 25.6, respectively), perseverative errors (11.4, 13.5, and 5.7), nonperseverative errors (27.1, 25.0, and 19.9), and Nelson type perseverative errors (8.9, 8.4, and 2.3), were significantly poorer in both autistic and ADHD groups than control group (P < 0.01). Comparing the autistic group to the ADHD group, there were no significant differences in age, gender, scores of full-scale intelligent quotient (IQ), verbal or performance IQ, number of categories achieved or errors. The ADHD group, however, showed more frequent Milner type perseverative errors than the autistic group (P < 0.05). The present study suggests that some kinds of executive function are more impaired in children with ADHD than in those with high-functioning. autism, and that Milner type perseverative errors is useful parameter to differentiate the executive dysfunctions between autistic and ADHD children. (c) 2004 Elsevier B.V. All rights reserved. C1 Asahikawa Kosei Hosp, Dept Pediat, Asahikawa, Hokkaido 0788211, Japan. Asahikawa Med Coll, Asahikawa, Hokkaido 078, Japan. Asahikawa Med Coll, Dept Pediat, Asahikawa, Hokkaido 0788510, Japan. RP Oki, J (reprint author), Asahikawa Kosei Hosp, Dept Pediat, 1 Jo 24 Chome 111, Asahikawa, Hokkaido 0788211, Japan. 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PD APR PY 2005 VL 27 IS 3 BP 233 EP 236 DI 10.1016/j.braindev.2004.06.008 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 907TL UT WOS:000227740800013 PM 15737707 ER PT J AU Stahl, L Pry, R AF Stahl, L Pry, R TI Attentional flexibility and perseveration: Developmental aspects in young children SO CHILD NEUROPSYCHOLOGY LA English DT Article DE attentional flexibility; executive functions; perseveration; normal development ID FRONTAL-LOBE DAMAGE; CARD SORTING TEST; EXECUTIVE FUNCTION; RESPONSE CONTROL; CHILDHOOD; AUTISM; CORTEX; MEMORY AB Whereas a growing interest in the development of attentional flexibility ( AF) and in perseverative behavior, being one marker of this component, exists in neuropsychological studies and in the domain of developmental psychopathology ( e. g., PKU, infantile schizophrenia, autism and Parkinson's disease) ( Pennington & Ozonoff, 1996; Stahl & Pry, 2002), only a few studies have concerned themselves with this subject in normal children. It is thus of interest to add more empirical data to the existing literature in this domain. Therefore, the aim of our study was to explore the development of AF and of perseverative errors in young preschool children with normal development, aged 1.5 to 6 years. Using set- shifting tasks of increasing difficulty level, three age groups were compared with respect to their AF skills. Results show a developmental factor underlying AF, with different levels of this form becoming more and more complex with age, ranging from a rudimentary visual form to a complex representational form of flexibility. Overall, few perseverative errors occurred and they decreased with age. Results are discussed from a developmental and neuropsychological perspective. C1 Univ Montpellier 3, EA 1977, F-34199 Montpellier, France. CHU Montpellier, Serv Medicopsychol Enfants & Adolescents, Montpellier, France. RP Stahl, L (reprint author), Univ Montpellier 3, EA 1977, Route Mende, F-34199 Montpellier, France. 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PD APR PY 2005 VL 11 IS 2 BP 175 EP 189 DI 10.1080/092970490911315 PG 15 WC Clinical Neurology SC Neurosciences & Neurology GA 925FE UT WOS:000229036100004 PM 16036443 ER PT J AU Harvard, C Malenfant, P Koochek, M Creighton, S Mickelson, ECR Holden, JJA Lewis, MES Rajcan-Separovic, E AF Harvard, C Malenfant, P Koochek, M Creighton, S Mickelson, ECR Holden, JJA Lewis, MES Rajcan-Separovic, E TI A variant Cri du Chat phenotype and autism spectrum disorder in a subject with de novo cryptic microdeletions involving 5p15.2 and 3p24.3-25 detected using whole genomic array CGH SO CLINICAL GENETICS LA English DT Article DE array comparative genomic hybridization; autism spectrum disorder; Cri du Chat syndrome; cytogenetics; microarray; microdeletions in de novo rearrangements; microsatellite analysis; phenotype-genotype correlation; polymorphisms ID CRITICAL REGION; MOLECULAR CHARACTERIZATION; UNBALANCED TRANSLOCATION; CHROMOSOME 5P; DELETIONS; FEATURES; HYBRIDIZATION; PATIENT; ABNORMALITIES; RETARDATION AB Cri du Chat syndrome (CdCs) is a well-defined clinical entity, with an incidence of 1/15,000 to 1/50,000. The critical region for CdCs has been mapped to 5p15, with the hallmark cat-like cry sublocalized to 5p15.3 and the remaining clinical features to 5p15.2. We report findings in a subject with a de novo t(5;7)(p15.2;p12.2) and an inv(3)(p24q24), who was found to have a cryptic microdeletion in the critical region for CdCs detected using a 1-Mb genomic microarray. In addition to 5p deletion, the proband had a de novo single clone loss at the 3p breakpoint of inv(3)(p24q24) and a familial single clone deletion at 18q12. Deletions were confirmed using microsatellite analysis and fluorescence in situ hybridization. The 5p deletion encompasses approximately 3 Mb, mapping to the border between bands 5p15.2 and 5p15.31. The single clone deletion on chromosome 3 maps to 3p24.3-3p25, for which there is no known phenotype. The clinical features of our proband differ from the characteristic CdC phenotype, which may reflect the combined effect of the two de novo microdeletions and/or may further refine the critical region for CdCs. Typical features of CdCs that are present in the proband include moderate intellectual disability, speech, and motor delay as well as dysmorphic features (e.g. broad and high nasal root, hypertelorism, and coarse facies). Expected CdCs features that are not present are growth delay, microcephaly, round facies, micrognathia, epicanthal folds, and the signature high-pitched cry. Behavioral traits in this subject included autism spectrum disorder, attention-deficit hyperactivity disorder, and unmanageable behavior including aggression, tantrums, irritability, and self-destructive behavior. Several of these behaviors have been previously reported in patients with 5p deletion syndrome. Although most agree on the cat-cry critical region (5p15.3), there is discrepancy in the precise location and size of the region associated with the more severe manifestations of CdCs. The clinical description of this proband and the characterization of his 5p deletion may help to further refine the phenotype-genotype associations in CdCs and autism spectrum disorder. C1 Univ British Columbia, Dept Pathol, Vancouver, BC, Canada. Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada. Univ British Columbia, Dept Pediat, Vancouver, BC V6T 1W5, Canada. Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. Queens Univ, Dept Psychiat, Kingston, ON K7L 3N6, Canada. Autism Res Program, Kingston, ON, Canada. RP Rajcan-Separovic, E (reprint author), Univ British Columbia, Dept Pathol & Lab Med, Cytogenet Lab, Childrens & Womens Hlth Ctr BC, 4480 Oak St, Vancouver, BC V6H 3V4, Canada. 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Genet. PD APR PY 2005 VL 67 IS 4 BP 341 EP 351 DI 10.1111/j.1399-0004.2005.00406.x PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 901WW UT WOS:000227313900012 PM 15733271 ER PT J AU Bartlett, SC Armstrong, E Roberts, J AF Bartlett, SC Armstrong, E Roberts, J TI Linguistic resources of individuals with Asperger syndrome SO CLINICAL LINGUISTICS & PHONETICS LA English DT Article DE Asperger syndrome; autism; sociolinguistics; pragmatics ID HIGH-FUNCTIONING AUTISM; TRAUMATIC BRAIN-INJURY; DIFFERENT COMMUNICATION PARTNERS; NORMALLY DEVELOPING-CHILDREN; PRAGMATIC ASPECTS; DISCOURSE; LANGUAGE; DISORDER; MIND; CONVERSATION AB In this paper the available literature on the communication skills of individuals with Asperger Syndrome (AS) is reviewed. Current issues regarding diagnosing and understanding disorders with a core social deficit are examined as well as the potential application of sociolinguistic analyses to the study of Asperger Syndrome, such as that provided from within a Systemic Functional Linguistic framework. The need for investigations that address a broader view of "language'' and its use in social situations by individuals with AS as opposed to their mastery of syntactic aspects of language, will be discussed. C1 Macquarie Univ, Dept Linguist, N Ryde, NSW 2010, Australia. RP Bartlett, SC (reprint author), Macquarie Univ, Dept Linguist, N Ryde, NSW 2010, Australia. 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Linguist. Phon. PD APR-MAY PY 2005 VL 19 IS 3 BP 203 EP 213 DI 10.1080/02699200410001698634 PG 11 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 913VC UT WOS:000228182300006 PM 15823956 ER PT J AU Muller, U Zelazo, PD Imrisek, S AF Muller, U Zelazo, PD Imrisek, S TI Executive function and children's understanding of false belief: how specific is the relation? SO COGNITIVE DEVELOPMENT LA English DT Article DE false belief; performance; photograph ID OF-MIND DEVELOPMENT; INDIVIDUAL-DIFFERENCES; COGNITIVE-COMPLEXITY; VERBAL-ABILITY; SELF-CONTROL; AUTISM; TASK; PRESCHOOLERS; DECEPTION; LANGUAGE AB The present study examined developmental relations among understanding false belief, understanding "false" photographs, performance on the Dimensional Change Card Sort (DCCS), and performance on a picture-sentence verification task in 69 3-5-year-old children. 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PD APR-JUN PY 2005 VL 20 IS 2 BP 173 EP 189 DI 10.1016/j.cogdev.2004.12.004 PG 17 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 950OG UT WOS:000230866100002 ER PT J AU Gernsbacher, MA Dawson, M Goldsmith, HH AF Gernsbacher, MA Dawson, M Goldsmith, HH TI Three reasons not to believe in an autism epidemic SO CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE LA English DT Article DE autisrn; epidemiology; epidemic ID PERVASIVE DEVELOPMENTAL DISORDERS; PREVALENCE AB According to some lay groups, the nation is experiencing an autism epideatic - a rapid escalation in the prevalence of autism for unknown, reasons. However, no sound scientific evidence indicates that the increasing number of diagnosed cases of autism arises from anything other than purposely broadened diagnostic criteria, coupled with deliberately greater public awareness and intentionally improved case finding. Why is the public perception. so disconnected from the scientific evidence? In this article we review three primary sources of misunderstanding: lack of awareness about the changing diagnostic criteria, uncritical acceptance of a conclusion illogically drawn in a California-based study, and inattention to a crucial feature of the "child count" data reported annually by the U.S. Department of Education. C1 Univ Wisconsin, Dept Psychol, Madison, WI 53706 USA. Univ Montreal, Montreal, PQ H3C 3J7, Canada. RP Gernsbacher, MA (reprint author), Univ Wisconsin, Dept Psychol, 1202 W Johnson St, Madison, WI 53706 USA. 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L., 1956, AM J ORTHOPSYCHIAT, V26, P55 MIND Institute, 2002, REP LEG PRINC FIND E Rutter M., 1978, AUTISM REAPPRAISAL C, P1 *US DEP ED, 2002, 24 ANN REP C IMPL IN Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 NR 18 TC 54 Z9 54 PU BLACKWELL PUBLISHERS PI MALDEN PA 350 MAIN STREET, STE 6, MALDEN, MA 02148 USA SN 0963-7214 J9 CURR DIR PSYCHOL SCI JI Curr. Dir. Psychol. PD APR PY 2005 VL 14 IS 2 BP 55 EP 58 DI 10.1111/j.0963-7214.2005.00334.x PG 4 WC Psychology, Multidisciplinary SC Psychology GA 939LG UT WOS:000230073600001 ER PT J AU Harris, PL de Rosnay, M Pons, F AF Harris, PL de Rosnay, M Pons, F TI Language and children's understanding of mental states SO CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE LA English DT Article DE mind; emotion; language; conversation ID OF-MIND DEVELOPMENT; FALSE BELIEF; ABILITY; AUTISM; AGE AB Children progress through various landmarks in their understanding of mind and emotion. They eventually understand that people's actions, utterances, and emotions are determined by their beliefs. Although these insights emerge in all normal children, individual children vary in their rates of progress. Four lines of research indicate that language and conversation play a role in individual development: (a) Children with advanced language skills are better at mental-state understanding than those without advanced language skills, (b) deaf children born into nonsigning families lag in mental-state understanding, and (c) exposure to maternal conversation rich in references to mental states promotes mental-state understanding, as do (d) experimental language-based interventions. Debate centers on the mechanism by which language and conversation help children's understanding Of mental states. Three competing interpretations are evaluated here: lexical enrichment (the child gains from acquiring a rich mental-state vocabulary), syntactic enrichment (the child gains from acquiring syntactic tools for embedding one thought in another), and pragmatic enrichment (the child gains from conversations in which varying perspectives on a given topic are articulated). pragmatic enrichment emerges as the most promising candidate. C1 Harvard Univ, Cambridge, MA 02138 USA. Univ Cambridge, Cambridge CB2 1TN, England. Univ Aalborg, Aalborg, Denmark. RP Harris, PL (reprint author), Harvard Univ, 503A Larsen Hall,HGSE,Appian Way, Cambridge, MA 02138 USA. EM paul_harris@gsc.harvard.edu CR Astington J. 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PD APR PY 2005 VL 14 IS 2 BP 69 EP 73 DI 10.1111/j.0963-7214.2005.00337.x PG 5 WC Psychology, Multidisciplinary SC Psychology GA 939LG UT WOS:000230073600004 ER PT J AU Courchesne, E Pierce, K AF Courchesne, E Pierce, K TI Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; MATTER VOLUME INCREASE; SPECTRUM DISORDER; ASPERGER-SYNDROME; WORKING-MEMORY; YOUNG-CHILDREN; NEURAL BASIS; BRAIN; AGE; FMRI AB Although it has long been thought that frontal lobe abnormality must play an important part in generating the severe impairment in higher-order social, emotional and cognitive functions in autism, only recently have studies identified developmentally early frontal lobe defects. At the microscopic level, neuroinflammatory reactions involving glial activation, migration defects and excess cerebral neurogenesis and/or defective apoptosis might generate frontal neural pathology early in development. It is hypothesized that these abnormal processes cause malformation and thus malfunction of frontal minicolumn microcircuitry. It is suggested that connectivity within frontal lobe is excessive, disorganized and inadequately selective, whereas connectivity between frontal cortex and other systems is poorly synchronized, weakly responsive and information impoverished. Increased local but reduced long-distance cortical-cortical reciprocal activity and coupling would impair the fundamental frontal function of integrating information from widespread and diverse systems and providing complex context-rich feedback, guidance and control to lower-level systems. C1 Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. RP Courchesne, E (reprint author), Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. 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Opin. Neurobiol. PD APR PY 2005 VL 15 IS 2 BP 225 EP 230 DI 10.1016/j.conb.2005.03.001 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 925OT UT WOS:000229063100015 PM 15831407 ER PT J AU Segawa, M Nomura, Y AF Segawa, M Nomura, Y TI Rett syndrome SO CURRENT OPINION IN NEUROLOGY LA English DT Article DE clinical features; MeCP2; MECP2; methyl-CpG-binding protein 2; neurobiology; Rett syndrome ID BINDING PROTEIN MECP2; NEURODEVELOPMENTAL DISORDER; MENTAL-RETARDATION; MOUSE MODEL; EXPRESSION; MUTATIONS; AUTISM; BRAIN; DEFICIENCY; GIRLS AB Purpose of review Nearly 70 reports on Rett syndrome were published in 2004. We have selected 51 articles, including clinical reports, on pathophysiology, genotype-phenotype correlation, and clinical and basic molecular biology studies. These articles explain how mutation of the gene (MECP2) for methyl-CpG-binding protein 2 causes the particular disorders of Rett syndrome, and also induces other neurodevelopmental disorders, clarifying the situation for future studies. Recent findings The role of X-chromosome inactivation has been clarified in animal experiments. New isoforms of MeCP2 have been discovered and its functional characteristics are under research. Understanding of the influence of the MECP2 mutation on other neurodevelopmental disorders has increased. However, there is no apparent progress in neurophysiological studies. Summary Clinical studies included the pathophysiology of stereotyped movement, and cardiac and respiratory disturbances, and there were four therapeutic trials including one for epilepsy. For genotype-phenotype correlation the role of X-chromosome inactivation was looked at and its basic mechanisms were studied extensively in animals. Characteristics of mutations in the C-terminus and the biological function of the new isoform, exon 1, were introduced. In studies on related neurodevelopmental disorders, a relationship is suggested between the MECP2 gene and autism-related gene, with overlapping pathways, but this is not common to other neurodevelopmental disorders. Developmental studies 1 suggest an important role for MeCP2 in the formation and/ or maintenance of synapses, and clarify, the molecular biological aspects of Rett syndrome. However, early, involvement of the aminergic neurons, suggested as the basic, pathognomonic lesion of Rett syndrome, has unfortunately not been investigated with the MECP2 mutation. C1 Segawa Neurol Clin Children, Chiyoda Ku, Tokyo 1010062, Japan. RP Segawa, M (reprint author), Segawa Neurol Clin Children, Chiyoda Ku, 2-8 Surugadai Kanda, Tokyo 1010062, Japan. 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Opin. Neurol. PD APR PY 2005 VL 18 IS 2 BP 97 EP 104 DI 10.1097/01.wco.0000162848.99154.9a PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 912LG UT WOS:000228079100004 PM 15791137 ER PT J AU Freeman, SJ Roberts, W Daneman, D AF Freeman, SJ Roberts, W Daneman, D TI Type 1 diabetes and autism - Is there a link? SO DIABETES CARE LA English DT Article ID AUTOIMMUNE-DISEASE; PREVALENCE C1 Hosp Sick Children, Div Endocrinol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Toronto, ON, Canada. Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. RP Daneman, D (reprint author), Hosp Sick Children, Div Endocrinol, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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Vaccines PD APR PY 2005 VL 4 IS 2 BP 131 EP 132 DI 10.1586/14760584.4.2.131 PG 2 WC Immunology SC Immunology GA 982YZ UT WOS:000233199600004 ER PT J AU Bushara, KO AF Bushara, KO TI Neurologic presentation of celiac disease SO GASTROENTEROLOGY LA English DT Article; Proceedings Paper CT NIH Consensus Conference on Celiac Disease CY JUN 28-30, 2004 CL Bethesda, MD SP NIH, NIDDK ID VITAMIN-E-DEFICIENCY; CEREBRAL OCCIPITAL CALCIFICATIONS; PERVASIVE DEVELOPMENTAL DISORDER; IDIOPATHIC CEREBELLAR-ATAXIA; GLUTEN-FREE DIET; ANTIGLIADIN ANTIBODIES; SPINOCEREBELLAR DEGENERATION; INTESTINAL MALABSORPTION; PERIPHERAL NEUROPATHY; DIPEPTIDYL PEPTIDASE AB Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results, Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity. C1 Univ Minnesota, Minneapolis VA Med Ctr 127, Dept Neurol, Minneapolis, MN 55417 USA. RP Bushara, KO (reprint author), Univ Minnesota, Minneapolis VA Med Ctr 127, Dept Neurol, 1 Vet Dr, Minneapolis, MN 55417 USA. 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In situ hybridization analyses encompassing embryonic to 20-week postnatal age showed that transcripts are expressed in the central nervous system, with a progressive restriction during development culminating in localized strong expression in the cerebral cortex, olfactory bulb, hippocampal formation, and internal granule and Purkinje layer of the cerebellum. Real-time RT-PCR measurements of Mecp2 transcript levels showed variations with mouse age in two distinctive patterns that are unique to the central nervous system and the visceral organs, respectively. The 10-kb mRNA is the predominant form expressed in the brain in contrast to the shorter species expressed in the lung and liver. The developmental profile of Mecp2 mRNA highlights a potential tissue-specific function of the 3' UTR in the regulation of MeCP2 protein synthesis in response to the age-specific requirement of MeCP2 function during the life of the mouse. (c) 2004 Elsevier Inc. All rights reserved. C1 Childrens Med Res Inst, Embryol Unit, Sydney, NSW 2145, Australia. Univ Sydney, Dept Pediat & Child Hlth, Sydney, NSW 2006, Australia. Childrens Hosp Westmead, Western Sydney Genet Program, Sydney, NSW, Australia. RP Tam, PPL (reprint author), Childrens Med Res Inst, Embryol Unit, Sydney, NSW 2145, Australia. 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Georgia Inst Technol, GVU Ctr, Atlanta, GA 30332 USA. RP Hayes, GR (reprint author), Georgia Inst Technol, Coll Comp, Atlanta, GA 30332 USA. EM gillian@cc.gatech.edu; khai@cc.gatech.edu CR Hayes GR, 2004, LECT NOTES COMPUT SC, V3205, P161 KIRBY D, 2005, AUTISM TODAY WANG R, 2002, LNCS, V2498, P194 NR 3 TC 1 Z9 1 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1314 USA SN 1536-1268 J9 IEEE PERVAS COMPUT JI IEEE Pervasive Comput. PD APR-JUN PY 2005 VL 4 IS 2 BP 14 EP 17 DI 10.1109/MPRV.2005.27 PG 4 WC Computer Science, Information Systems; Engineering, Electrical & Electronic; Telecommunications SC Computer Science; Engineering; Telecommunications GA 918EQ UT WOS:000228525500004 ER PT J AU Corsello, CM AF Corsello, CM TI Early intervention in autism SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; early intervention; treatment ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; SOCIAL INITIATIONS; FOLLOW-UP; LANGUAGE; SKILLS; AGE AB We now know that professionals can diagnose children with autism when they are as young as 2 years of age (Lord, 1995). Screening and the role of the pediatrician have become even more critical as we have recognized the stability of early diagnosis over time and the importance of early intervention. At this point, experts working with children with autism agree that early intervention is critical. There is professional consensus about certain crucial aspects of treatment (intensity, family involvement, focus on generalization) and empirical evidence for certain intervention strategies. However, there are many programs developed for children with autism that differ in philosophy and a lack of research comparing the various intervention programs. Most of the programs for children with autism that exist are designed for children of preschool age, and not all are widely known or available. While outcome data are published for some of these programs, empirical studies comparing intervention programs are lacking. In this review, existing intervention programs and empirical studies on these programs will be reviewed, with a particular emphasis on the birth to 3 age group. C1 Univ Michigan, Ann Arbor, MI 48109 USA. RP Corsello, CM (reprint author), Univ Michigan, 1111 E Catherine St,2nd Floor, Ann Arbor, MI 48109 USA. 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PD APR-JUN PY 2005 VL 18 IS 2 BP 74 EP 85 PG 12 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 911AU UT WOS:000227974300001 ER PT J AU Noyes-Grosser, DM Holland, JP Lyons, D Holland, CL Romanczyk, RG Gillis, JM AF Noyes-Grosser, DM Holland, JP Lyons, D Holland, CL Romanczyk, RG Gillis, JM TI Rationale and methodology for developing guidelines for early intervention services for young children with developmental disabilities SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; clinical practice guidelines; communication disorders; developmental disabilities; Down syndrome; early intervention; hearing loss; motor disorders; vision impairment; young children AB Professionals providing early intervention services are increasingly asked to provide scientific evidence that the clinical methods they use will lead to positive functional outcomes for children with developmental disabilities. To address the need for such evidence, the New York State Department of Health sponsored the development of 6 science-based clinical practice guidelines for children younger than 3 years with those developmental conditions most often seen in the state's Early Intervention Program. Separate guidelines were developed for autism/pervasive developmental disorders, communication disorders, Down syndrome, hearing impairment, motor disorders, and vision impairment. Consensus panels were convened to develop the guidelines. Each panel helped define the scope of the guideline and specific clinical questions to be addressed to ensure that the guideline would be useful to the intended target audiences of parents, professionals providing early intervention services, local Early Intervention Program administrators, and primary healthcare professionals. Each of the guidelines provides evidence-based and consensus recommendations about assessment and intervention methods and explicitly states the strength of evidence for each recommendation. It is hoped that these clinical practice guidelines will contribute to improved functional outcomes for young children with developmental conditions, both directly through improved knowledge and better communication among parents and professionals and indirectly by fostering program improvements and research. C1 New York State Dept Hlth, Early Intervent Program, Albany, NY 12237 USA. SUNY Binghamton, Inst Child Dev, Binghamton, NY USA. RP Noyes-Grosser, DM (reprint author), New York State Dept Hlth, Early Intervent Program, Rm 287,Corning Tower Bldg,Empire State Plaza, Albany, NY 12237 USA. EM dmn02@health.state.ny.us CR Dawson G., 1997, EFFECTIVENESS EARLY, P307 *DIV EARL CHILDH C, 1993, DEC REC PRACT IND QU EDDY DM, 1995, CLIN PRACTICE GUIDEL, P41 Holland J. P., 1995, CURRENT OPINION ORTH, V6, P63 Institute of Medicine, 1992, GUID CLIN PRACT DEV National Research Council, 2001, ED CHILD AUT *NEW YORK STAT DEP, 1999, CLIN PRACT GUID COMM *NEW YORK STAT DEP, 1999, CLIN PRACT GUID AUT Sandall S. R., 2000, DEC RECOMMENDED PRAC SCHRIGER DL, 1995, CLIN PRACTICE GUIDEL, P115 Shekelle PG, 2001, JAMA-J AM MED ASSOC, V286, P1461, DOI 10.1001/jama.286.12.1461 Shonkoff Jack P., 2000, NEUR NEIGHB SCI EARL Smith BJ, 2002, J EARLY INTERVENTION, V25, P108, DOI 10.1177/105381510202500208 Woolf S. H., 1991, AHCPR PUBLICATION, V91-0018 Woolf S. H., 1995, AHCPR PUBLICATION, V95-0009, P105 NR 15 TC 4 Z9 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0896-3746 J9 INFANT YOUNG CHILD JI Infants Young Child. PD APR-JUN PY 2005 VL 18 IS 2 BP 119 EP 135 PG 17 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 911AU UT WOS:000227974300004 ER PT J AU DiCicco-Bloom, E AF DiCicco-Bloom, E TI Autism: Modeling human brain abnormalities in developing animal systems - Preface SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Editorial Material C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. RP DiCicco-Bloom, E (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, 675 Hoes Lane, Piscataway, NJ 08854 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 APR-MAY PY 2005 VL 23 IS 2-3 BP 117 EP 124 DI 10.1016/j.ijdevneu.2005.01.004 PG 8 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900001 ER PT J AU Schultz, RT AF Schultz, RT TI Developmental deficits in social perception in autism: the role of the amygdala and fusiform face area SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article; Proceedings Paper CT 3rd International Meeting for Autism Research CY MAY 07-08, 2004 CL Sacramento, CA DE autism; functional magnetic resonance imaging; amygdala ID HUMAN EXTRASTRIATE CORTEX; EXPERT OBJECT RECOGNITION; SPECTRUM DISORDER; FACIAL EXPRESSIONS; JOINT ATTENTION; SELECTIVE ATTENTION; SPATIAL-FREQUENCY; ASPERGER-SYNDROME; CONFIGURAL INFORMATION; EMOTION RECOGNITION AB Autism is a severe developmental disorder marked by a triad of deficits, including impairments in reciprocal social interaction, delays in early language and communication, and the presence of restrictive, repetitive and stereotyped behaviors. In this review, it is argued that the search for the neurobiological bases of the autism spectrum disorders should focus on the social deficits, as they alone are specific to autism and they are likely to be most informative with respect to modeling the pathophysiology of the disorder. Many recent studies have documented the difficulties persons with an autism spectrum disorder have accurately perceiving facial identity and facial expressions. This behavioral literature on face perception abnormalities in autism is reviewed and integrated with the functional magnetic resonance imaging (fMRI) literature in this area, and a heuristic model of the pathophysiology of autism is presented. This model posits an early developmental failure in autism involving the amygdala, with a cascading influence on the development of cortical areas that mediate social perception in the visual domain, specifically the fusiform "face area" of the ventral temporal lobe. Moreover, there are now some provocative data to suggest that visual perceptual areas of the ventral temporal pathway are also involved in important ways in representations of the semantic attributes of people, social knowledge and social cognition. Social perception and social cognition are postulated as normally linked during development such that growth in social perceptual skills during childhood provides important scaffolding for social skill development. It is argued that the development of face perception and social cognitive skills are supported by the amygdala-fusiform system, and that deficits in this network are instrumental in causing autism. (C) 2005 Published by Elsevier Ltd on behalf of ISDN. C1 Yale Child Study Ctr, New Haven, CT 06520 USA. RP Schultz, RT (reprint author), Yale Child Study Ctr, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. 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PD APR-MAY PY 2005 VL 23 IS 2-3 BP 125 EP 141 DI 10.1016/j.ijdevneu.2004.12.012 PG 17 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900002 PM 15749240 ER PT J AU Zwaigenbaum, L Bryson, S Rogers, T Roberts, W Brian, J Szatmari, P AF Zwaigenbaum, L Bryson, S Rogers, T Roberts, W Brian, J Szatmari, P TI Behavioral manifestations of autism in the first year of life SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; visual attention; longitudinal study; early identification; temperament; language development; infant behavior ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY HOME MOVIES; EARLY RECOGNITION; YOUNG-CHILDREN; AGE; INFANCY; ONSET; TEMPERAMENT; SYMPTOMS; SPECTRUM AB In the interest of more systematically documenting the early signs of autism, and of testing specific hypotheses regarding their underlying neurodevelopmental substrates, we have initiated a longitudinal study of high-risk infants, all of whom have an older sibling diagnosed with an autistic spectrum disorder. Our sample currently includes 150 infant siblings, including 65 who have been followed to age 24 months, who are the focus of this paper. We have also followed a comparison group of low-risk infants. Our measures include a novel observational scale (the first, to our knowledge, that is designed to assess autism-specific behavior in infants), a computerized visual orienting task, and standardized measures of temperament, cognitive and language development. Our preliminary results indicate that by 12 months of age, siblings who are later diagnosed with autism may be distinguished from other siblings and low-risk controls on the basis of: (1) several specific behavioral markers, including atypicalities in eye contact, visual tracking, disengagement of visual attention, orienting to name, imitation, social smiling, reactivity, social interest and affect, and sensory-oriented behaviors; (2) prolonged latency to disengage visual attention; (3) a characteristic pattern of early temperament, with marked passivity and decreased activity level at 6 months, followed by extreme distress reactions, a tendency to fixate on particular objects in the environment, and decreased expression of positive affect by 12 months; and (4) delayed expressive and receptive language. We discuss these findings in the context of various neural networks thought to underlie neurodevelopmental abnormalities in autism, including poor visual orienting. Over time, as we are able to prospectively study larger numbers and to examine interrelationships among both early-developing behaviors and biological indices of interest, we hope this work will advance current understanding of the neurodevelopmental origins of autism. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 McMaster Univ, McMaster Childrens Hosp, Dept Paediat, Hamilton, ON L8N 3Z5, Canada. Dalhousie Univ, Dept Pediat, Halifax, NS B3H 4R2, Canada. Dalhousie Univ, Dept Psychol, Halifax, NS B3H 4R2, Canada. York Univ, Dept Psychol, N York, ON M3J 1P3, Canada. Univ Toronto, Hosp Sick Children, Dept Pediat, Toronto, ON M5E 1X8, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada. RP Zwaigenbaum, L (reprint author), McMaster Univ, McMaster Childrens Hosp, Dept Paediat, POB 2000, Hamilton, ON L8N 3Z5, Canada. 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PD APR-MAY PY 2005 VL 23 IS 2-3 BP 153 EP 170 DI 10.1016/j.ijdevneu.2005.01.003 PG 18 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900004 PM 15749242 ER PT J AU Chandana, SR Behen, ME Juhasz, C Muzik, O Rothermel, RD Mangner, TJ Chakraborty, PK Chugani, HT Chugani, DC AF Chandana, SR Behen, ME Juhasz, C Muzik, O Rothermel, RD Mangner, TJ Chakraborty, PK Chugani, HT Chugani, DC TI Signiticance of abnormalities in developmental trajectory and asymmetry of cortical serotonin synthesis in autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; serotonin; alpha[C-11]methyl-L-tryptophan; PET; cortical asymmetry; cortical development; language; handedness ID WHOLE-BLOOD SEROTONIN; HUMAN AUDITORY-CORTEX; POSITRON-EMISSION-TOMOGRAPHY; GENE PROMOTER VARIANTS; METHYL-L-TRYPTOPHAN; BRAIN-SEROTONIN; MONOAMINE-OXIDASE; IN-VIVO; MINICOLUMNAR PATHOLOGY; SOMATOSENSORY CORTEX AB The role of serotonin in prenatal and postnatal brain development is well documented in the animal literature. In earlier studies using positron en-fission tomography (PET) with the tracer alpha[C-11]methyl-L-tryptophan (AMT), we reported global and focal abnormalities of serotonin synthesis in children with autism. In the present study, we measured brain serotonin synthesis in a large group of autistic children (n = 117) with AMT PET and related these neuroimaging data to handedness and language function. Cortical AMT uptake abnormalities were objectively derived from small homotopic cortical regions using a predefined cutoff asymmetry threshold (>2 S.D. of normal asymmetry). Autistic children demonstrated several patterns of abnormal cortical involvement, including right cortical, left cortical, and absence of abnormal asymmetry. Global brain values for serotonin synthesis capacity (unidirectional uptake rate constant, K-complex) values were plotted as a function of age. K-complex values of autistic children with asymmetry or no asymmetry in cortical AMT uptake followed different developmental patterns, compared to that of a control group of non-autistic children. The autism groups, defined by presence or absence and side of cortical asymmetry, differed on a measure of language as well as handedness. Autistic children with left cortical AMT decreases showed a higher prevalence of severe language impairment, whereas those with right cortical decreases showed a higher prevalence of left and mixed handedness. Global as well as focal abnormally asymmetric development in the serotonergic system could lead to miswiring of the neural circuits specifying hemispheric specialization. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA. Wayne State Univ, Sch Med, Childrens Hosp Michigan, Carman & Ann Adams Dept Pediat, Detroit, MI 48201 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 171 EP 182 DI 10.1016/j.ijdevneu.2004.08.002 PG 12 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900005 PM 15749243 ER PT J AU Bauman, ML Kemper, TL AF Bauman, ML Kemper, TL TI Neuroanatomic observations of the brain in autism: a review and future directions SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE brain; neuroanatomy; limbic system; cerebellum; large brain; neurochemistry ID EARLY INFANTILE-AUTISM; STEM EVOKED-RESPONSES; CEREBELLAR CORTEX; CEREBRAL-CORTEX; CELL COUNTS; CHILDREN; ABNORMALITIES; NERVE; LIFE AB Infantile autism is a behaviorally defined disorder associated with characteristic cognitive, language and behavioral features. Several postmortem studies have highlighted areas of anatomic abnormality in the autistic brain. Consistent findings have been observed in the limbic system, cerebellum and related inferior olive. In the limbic system, the hippocampus, amygdala and entorhinal cortex have shown small cell size and increased cell packing density at all ages, suggesting a pattern consistent with development curtailment. Findings in the cerebellum have included significantly reduced numbers of Purkinje cells, primarily in the posterior inferior regions of the hemispheres. A different pattern of change has been noted in the vertical limb of the diagonal band of broca, cerebellar nuclei and inferior olive with plentiful and abnormally enlarged neurons in the brains of young autistic subjects, and in adult autistic brains, small, pale neurons that are reduced in number. These findings combined with reported age-related changes in brain weight and volume, have raised the possibility that the neuropathology of autism may represent an on-going process. (C) 2004 Published by Elsevier Ltd on behalf of ISDN. C1 Massachusetts Gen Hosp, Childrens Neurol Serv, Boston, MA 02114 USA. RP Bauman, ML (reprint author), Massachusetts Gen Hosp, Childrens Neurol Serv, 15 Parkman St, Boston, MA 02114 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 183 EP 187 DI 10.1016/j.ijdevneu.2004.09.006 PG 5 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900006 PM 15749244 ER PT J AU Arndt, TL Stodgell, CJ Rodier, PM AF Arndt, TL Stodgell, CJ Rodier, PM TI The teratology of autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE autism; autism spectrum disorders (ASDs); valproic acid; eyeblink conditioning; congenital malformations ID FETAL VALPROATE SYNDROME; LEMLI-OPITZ-SYNDROME; DE-LANGE-SYNDROME; SODIUM VALPROATE; JOUBERT-SYNDROME; MENTAL-RETARDATION; CONGENITAL-RUBELLA; PRENATAL EXPOSURE; INFANTILE-AUTISM; ALCOHOL SYNDROME AB Autism spectrum disorders affect behaviors that emerge at ages when typically developing children become increasingly social and communicative, but many lines of evidence suggest that the underlying alterations in the brain occur long before the period when symptoms become obvious. Studies of the behavior of children in the first year of life demonstrate that symptoms are often detectable in the first 6 months. The environmental factors known to increase the risk of autism have critical periods of action during embryogenesis. Minor malformations that occur frequently in people with autism are known to arise in the same stages of development. Anomalies reported from histological studies of the brain are consistent with an early alteration of development. Congenital syndromes with high rates of autism include somatic that originate early in the first trimester. In addition, it is possible to duplicate a number of anatomic and behavioral features characteristic of human cases by exposing rat embryos to a teratogenic dose of valproic acid at the time of neural tube closure. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Univ Rochester, Med Ctr, Dept Obstet & Gynecol, Rochester, NY 14642 USA. 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PD APR-MAY PY 2005 VL 23 IS 2-3 BP 189 EP 199 DI 10.1016/j.ijdevneu.2004.11.001 PG 11 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900007 PM 15749245 ER PT J AU Miller, MT Stromland, K Ventura, L Johansson, M Bandim, JM Gillberg, C AF Miller, MT Stromland, K Ventura, L Johansson, M Bandim, JM Gillberg, C TI Autism associated with conditions characterized by developmental errors in early embryogenesis: a mini review SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE autism; autism spectrum disorders (ASD); thalidomide embryopathy; Mobius sequence; misoprostol ID DUANES RETRACTION SYNDROME; CRANIAL NERVE ABNORMALITIES; SUPPLY DISRUPTION SEQUENCE; STEM TEGMENTAL NECROSIS; MOBIUS-LIKE SYNDROME; CHARGE-ASSOCIATION; MOEBIUS-SYNDROME; BRAIN-STEM; THALIDOMIDE EMBRYOPATHY; 1ST TRIMESTER AB Autism is a complex developmental disorder without an established single etiology but with significant contributions from genetic studies, functional research, and neuropsychiatric and neuroradiologic investigations. The purpose of this paper is to review the findings in five studies involving individuals manifesting the characteristic findings of autism spectrum disorder associated with malformations and dysfunctions known to result from early embryogenic defects. These investigations include two associated with teratogens (thalidomide embryopathy, Mobius sequence with misoprostol) and three (most Mobius sequence cases, CHARGE association, Goldenhar syndrome) with no known etiology. These studies suggest that early embryonic development errors often involving cranial nerve palsies, internal and external ear malformations. ophthalmologic anomalies, and a variety of systemic malformations may be associated with autism spectrum disorders statistically more frequently than expected in a normal population. Although the exact time of developmental insult for each condition cannot be identified, the evidence is that it may occur as early as week 4 to 6+ of embryogenesis. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Univ Illinois, Dept Ophthalmol & Visual Sci, Chicago, IL 60612 USA. Gothenburg Univ, Sahlgrenska Univ Hosp, Dept Ophthalmol, Gothenburg, Sweden. Altino Ventura Fdn, Dept Pediat Ophthalmol, Pernambuco, Brazil. Hosp Olhos Pernambuco, Pernambuco, Brazil. Gothenburg Univ, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ Fed Pernambuco, Maternal Infantile Inst Pernambuco, Dept Child & Adolescent Neuropsychiat, Recife, Brazil. Univ London, St Georges Hosp, Sch Med, London, England. RP Miller, MT (reprint author), Univ Illinois, Dept Ophthalmol & Visual Sci, 1855 W Taylor St,Rm 327, Chicago, IL 60612 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 201 EP 219 DI 10.1016/j.ijdevneu.2004.06.007 PG 19 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900008 PM 15749246 ER PT J AU Bartlett, CW Gharani, N Millonig, JH Brzustowicz, LM AF Bartlett, CW Gharani, N Millonig, JH Brzustowicz, LM TI Three autism candidate genes: a synthesis of human genetic analysis with other disciplines SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE autism; genetics; complex disease; linkage analysis; linkage disequilibrium ID PERVASIVE DEVELOPMENTAL DISORDERS; CEREBELLAR PURKINJE-CELLS; EARLY INFANTILE-AUTISM; WHOLE-BLOOD SEROTONIN; GENOMEWIDE SCREEN; LINKAGE DISEQUILIBRIUM; CHROMOSOME 7Q; REELIN GENE; SUSCEPTIBILITY LOCUS; ASSOCIATION ANALYSIS AB Autism is a particularly complex disorder when considered from virtually any methodological framework, including the perspective of human genetics. We first present a review of the genetic analysis principles relevant for discussing autism genetics research. From this body of work we highlight results from three candidate genes, REELIN (RELN), SEROTONIN TRANSPORTER (5HM, and ENGRAILED 2 (EN2) and discuss the relevant neuroscience, molecular genetics, and statistical results that suggest involvement of these genes in autism susceptibility. As will be shown, the statistical results from genetic analysis, when considered alone, are in apparent conflict across research groups. We use these three candidate genes to illustrate different problems in synthesizing results from non-overlapping research groups examining the same problem. However, when basic genetic principles and results from other scientific disciplines are incorporated into a unified theoretical framework, at least some of the difficulties with interpreting results can be understood and potentially overcome as more data becomes available to the field of autism research. Integrating results from several scientific frameworks provides new hypotheses and alternative data collection strategies for future work. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Rutgers State Univ, Dept Genet, Nelson Biol Labs, Piscataway, NJ 08854 USA. Univ Iowa, Ctr Stat Genet Res, Iowa City, IA USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Neurosci & Cell Biol, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, Piscataway, NJ 08854 USA. RP Brzustowicz, LM (reprint author), Rutgers State Univ, Dept Genet, Nelson Biol Labs, 604 Allison Rd, Piscataway, NJ 08854 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 221 EP 234 DI 10.1016/j.ijdevneu.2004.10.004 PG 14 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900009 PM 15749247 ER PT J AU Lim, MM Bielsky, IF Young, LJ AF Lim, MM Bielsky, IF Young, LJ TI Neuropeptides and the social brain: potential rodent models of autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE vasopressin VIa receptor; oxytocin receptor; social memory; knockout mice; pair bond; vole; oxytocin; vasopressin; neuropeptides ID VOLES MICROTUS-OCHROGASTER; MONOGAMOUS PRAIRIE VOLE; PAIR-BOND FORMATION; VASOPRESSIN RECEPTOR; MATERNAL-BEHAVIOR; FACE PERCEPTION; NEUROHYPOPHYSEAL PEPTIDES; CEREBROSPINAL-FLUID; PARTNER-PREFERENCE; PERSONALITY-TRAITS AB Conducting basic scientific research on a complex psychiatric disorder, such as autism, is a challenging prospect. It is difficult to dissociate the fundamental neurological and psychological processes that are disturbed in autism and, therefore, it is a challenge to discover accurate and reliable animal models of the disease. Because of their role in animal models of social processing and social bonding, the neuropeptides oxytocin and vasopressin are strong candidates for dysregulation in autism. In this review, we discuss the current animal models which have investigated oxytocin and vasopressin systems in the brain and their effects on social behavior. For example, mice lacking the oxytocin gene have profound deficits in social processing and social recognition, as do rats lacking vasopressin or mice lacking the vasopressin V I a receptor (V1aR). In another rodent model, monogamous prairie voles are highly social and form strong pair bonds with their mates. Pair bonds can be facilitated or disrupted by perturbing the oxytocin and vasopressin systems. Non-monogamous vole species that do not pair bond have different oxytocin and V1aR distribution patterns in the brain than monogamous vole species. Potential ties from these rodent models to the human autistic condition are then discussed. Given the hallmark disturbances in social function, the study of animal models of social behavior may provide novel therapeutic targets for the treatment of autism. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Emory Univ, Ctr Behav Neurosci, Atlanta, GA 30322 USA. Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA. RP Lim, MM (reprint author), Emory Univ, Yerkes Res Ctr, 954 Gatewood Rd, Atlanta, GA 30329 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 235 EP 243 DI 10.1016/j.ijdevneu.2004.05.006 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900010 PM 15749248 ER PT J AU Winslow, JT AF Winslow, JT TI Neuropeptides and non-human primate social deficits associated with pathogenic rearing experience SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; disorders; social deficits ID MONKEYS MACACA-MULATTA; CORTICOTROPIN-RELEASING-FACTOR; RHESUS-MONKEYS; CEREBROSPINAL-FLUID; OXYTOCIN RECEPTORS; MATERNAL-CARE; GLUCOCORTICOID-RECEPTORS; RECRUITMENT SCREAMS; PIGTAIL MACAQUES; PLASMA-CORTISOL AB There is a persuasive evidence that autism is highly heritable and likely to be substantially determined by polygenic mechanisms. Nevertheless, some intriguing findings in children raised in conditions of extreme social deprivation suggest that an autistic-like syndrome may occur as a consequence of environmental conditions. A particularly close model of this human syndrome has been studied in rhesus monkeys for almost half a century. Monkeys reared in pathogenic rearing conditions manifest considerable deficits in social interaction and increased self-directed behaviors. We have been interested in the possibility that disruptions in normal social development in non-human primates might be expressed in neuropeptide systems which have emerged in rodent studies as important candidates for a unique social biology. In recent studies, we have described persistently reduced CSF OT levels in male rhesus monkeys with significant social deficits. We also found that OT levels were positively related to the expression of affiliative social behaviors. Alterations were also detected in both CRH and AVP receptor binding patterns in limbic structures likely to influence social and emotional development. Taken together, these data suggest that abnormal rearing influences the development of brain systems critical to normal social and emotional competence in rhesus monkeys and may contribute to the development of autistic-like symptomatology associated with pathogenic rearing histories. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 NIMH, Nonhuman Primate Neurobiol Core, Intramural Res Program, Bethesda, MD 20892 USA. RP Winslow, JT (reprint author), NIMH, Nonhuman Primate Neurobiol Core, Intramural Res Program, Bldg NIHAC 110,Room 121,9000 Rockville Pike, Bethesda, MD 20892 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 245 EP 251 DI 10.1016/j.ijdevneu.2004.03.003 PG 7 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900011 PM 15749249 ER PT J AU Welsh, JP Ahn, ES Placantonakis, DG AF Welsh, JP Ahn, ES Placantonakis, DG TI Is autism due to brain desynchronization? SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; inferior olive; electrical synapses; neuronal oscillation; eyeblink conditioning; timing ID NICTITATING-MEMBRANE RESPONSE; INFANT-DEATH-SYNDROME; CONNEXIN 36-DEFICIENT MICE; INFERIOR OLIVARY NEURONS; CS-US INTERVAL; GAMMA OSCILLATIONS; PURKINJE-CELLS; MOTOR CONTROL; IN-VIVO; CEREBELLAR AB The hypothesis is presented that a disruption in brain synchronization contributes to autism by destroying the coherence of brain rhythms and slowing overall cognitive processing speed. Particular focus is on the inferior olive, a precerebellar structure that is reliably disrupted in autism and which normally generates a coherent 5-13 Hz rhythmic output. New electrophysiological data reveal that the continuity of the rhythmical oscillation in membrane potential generated by inferior olive neurons requires the formation of neuronal assemblies by the connexin36 protein that mediates electrical synapses and promotes neuronal synchrony. An experiment with classical eyeblink conditioning is presented to demonstrate that the inferior olive is necessary to learn about sequences of stimuli presented at intervals in the range of 250-500 ms, but not at 700 ms, revealing that a disruption of the inferior olive slows stimulus processing speed on the time scale that is lost in autistic children. A model is presented in which the voltage oscillation generated by populations of electrically synchronized inferior olivary neurons permits the utilization of sequences of stimuli given at, or faster than, 2 per second. It is expected that the disturbance in inferior olive structure in autism disrupts the ability of inferior olive neurons to become electrically synchronized and to generate coherent rhythmic output, thereby impairing the ability to use rapid sequences of cues for the development of normal language skill. Future directions to test the hypothesis are presented. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Oregon Hlth & Sci Univ, Inst Neurol Sci, Beaverton, OR 97006 USA. Univ Maryland, Sch Med, Dept Neurosurg, Baltimore, MD 21201 USA. Weill Cornell Med Ctr, Dept Neurol Surg, New York, NY 10021 USA. RP Welsh, JP (reprint author), Oregon Hlth & Sci Univ, Inst Neurol Sci, Beaverton, OR 97006 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 253 EP 263 DI 10.1016/j.ijdevneu.2004.09.002 PG 11 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900012 PM 15749250 ER PT J AU Murcia, CL Gulden, F Herrup, K AF Murcia, CL Gulden, F Herrup, K TI A question of balance: a proposal for new mouse models of autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE autism; PDDs; ASD ID NEURODEVELOPMENTAL PSYCHOPATHOLOGICAL DISORDERS; HOXA1 A218G POLYMORPHISM; FETAL VALPROATE SYNDROME; VIRUS BDV INFECTION; OPEN-FIELD BEHAVIOR; MICE LACKING; CEREBELLAR DEVELOPMENT; HEAD CIRCUMFERENCE; INFANTILE-AUTISM; ANIMAL-MODEL AB Autism spectrum disorder (ASD) represents a major mental health problem with estimates of prevalence ranging from 1/500 to 1/2000. While generally recognized as developmental in origin, little to nothing is certain about its etiology. Currently, diagnosis is made on the basis of a variety of early developmental delays and/or regressions in behavior. There are no universally agreed upon changes in brain structure or cell composition. No biomarkers of any type are available to aid or confirm the clinical diagnosis. In addition, while estimates of the heritability of the condition range from 60 to 90%, as of this writing no disease gene has been unequivocally identified. The prevalence of autism is three- to four-fold higher in males than in females, but the reason for this sexual dimorphism is unknown. In light of all of these ambiguities, a proposal to discuss potential animal models may seem the heart of madness. However, parsing autism into its individual genetic, behavioral. and neurobiological components has already facilitated a 'conversation' between the human disease and the neuropathology and biochemistry underlying the disorder. Building on these results, it should be possible to not just replicate one aspect of autism but to connect the developmental abnormalities underlying the ultimate behavioral phenotype. A reciprocal conversation such as this, wherein the human disease informs on how to make a better animal model and the animal model teaches of the biology causal to autism, would be highly beneficial. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Case Western Reserve Univ, Sch Med, Dept Neurosci, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Genet, Cleveland, OH 44106 USA. RP Herrup, K (reprint author), Case Western Reserve Univ, Sch Med, Dept Neurosci, E504 2109 Adelbert Rd, Cleveland, OH 44106 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 265 EP 275 DI 10.1016/j.ijdevneu.2004.07.001 PG 11 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900013 PM 15749251 ER PT J AU Scott, MM Deneris, ES AF Scott, MM Deneris, ES TI Making and breaking serotonin neurons and autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE austim; serotonin; hindbrain; genes ID DORSAL RAPHE NUCLEUS; VENTRAL CELL-TYPES; ETS DOMAIN FACTOR; SONIC HEDGEHOG; ISTHMIC ORGANIZER; MOTOR-NEURON; FLOOR PLATE; SPINAL-CORD; TRANSCRIPTIONAL CODES; SYNTHESIZING NEURONS AB Dysfunction of brain serotonin system development is hypothesized to contribute to autistic behaviors. The testing of this hypothesis will likely depend on a better understanding of the genes and mechanisms involved in serotonin neuron cell fate specification. In this review we summarize the main features of vertebrate serotonin neuroanatomical development and recent studies that have revealed critical steps in the molecular genetic program that controls serotonin neuron phenotype. We then discuss the potential relevance of these findings to advances in autism research and to new molecular genetic tools under development that will impact future testing of the hypothesis. (C) 2004 Published by Elsevier Ltd. on behalf of ISDN. C1 Case Western Reserve Univ, Sch Med, Dept Neurosci, Cleveland, OH 44106 USA. RP Deneris, ES (reprint author), Case Western Reserve Univ, Sch Med, Dept Neurosci, Rm E732,2109 Adelbert Rd, Cleveland, OH 44106 USA. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 277 EP 285 DI 10.1016/j.ijdevneu.2004.05.012 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900014 PM 15749252 ER PT J AU Miyazaki, K Narita, N Narita, M AF Miyazaki, K Narita, N Narita, M TI Maternal administration of thalidomide or valproic acid causes abnormal serotonergic neurons in the offspring: implication for pathogenesis of autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; animal model; differentiation; migration; raphe; serotonin ID EMBRYONIC STEM-CELLS; ANIMAL-MODELS; SODIUM VALPROATE; PLATELET COUNTS; BRAIN; RAT; CHILDREN; DIFFERENTIATION; PHENOTYPE; EXPOSURE AB Embryonic exposure to thalidomide (THAL) or valproic acid (VPA) before neural tube closure has been demonstrated as a useful model for human autism in rats. Abnormalities of the serotonergic system which are often observed in human autism have been shown in these rats. Thus, we examined whether early serotonergic neuronal development is perturbed by THAL/VPA. When pregnant rats were exposed to THAL or VPA on embryonic day 9, a dramatic shift of the distribution of serotonergic neurons in the dorsal raphe nucleus was observed on postnatal day 50. This alteration is thought to reflect abnormality of serotonergic neuronal differentiation and migration. In vitro studies revealed that VPA retards the maturation of serotonergic neuron from ES cell-derived neuronal progenitors, whereas exogenously added Sonic hedgehog, a morphogen that has been implicated in serotonergic cell fate, partially prevented this retardation. These results indicate that disruption of early serotonergic neuronal development might be involved in the etiology of autism. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. 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J. Dev. Neurosci. PD APR-MAY PY 2005 VL 23 IS 2-3 BP 287 EP 297 DI 10.1016/j.ijdevneu.2004.05.004 PG 11 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900015 PM 15749253 ER PT J AU Shi, LM Tu, N Patterson, PH AF Shi, LM Tu, N Patterson, PH TI Maternal influenza infection is likely to alter fetal brain development indirectly: the virus is not detected in the fetus SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE influenza; brain developmem; fetus ID PREGNANT MICE; SCHIZOPHRENIA; AUTISM; EPIDEMIC; FERRET; MOUSE; MODEL; LEADS; H3N2; RATS AB Epidemiological studies have shown that maternal infection can increase the risk for mental illness in the offspring. In a mouse model of maternal respiratory infection with influenza virus, the adult offspring display striking behavioral, pharmacological and histological abnormalities. Although influenza primarily infects the respiratory system, there are reports of viral mRNA and protein in the fetus of infected pregnant animals. To determine the extent of viral spread following maternal respiratory infection, we used RT-PCR to assay various maternal and fetal tissues for influenza A mRNAs coding for neuraminidase, non-structural protein 2, nuclear protein and matrix protein. While infected maternal lungs exhibit uniformly very strong signals, placentae are only rarely positive, and viral RNAs are not detectable in fetal brains from infected mothers. Thus, the effects of maternal infection on fetal brain development are likely to be indirect, probably involving the maternal inflammatory response. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 CALTECH, Div Biol, Pasadena, CA 91125 USA. RP Patterson, PH (reprint author), CALTECH, Div Biol, Pasadena, CA 91125 USA. 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PD APR-MAY PY 2005 VL 23 IS 2-3 BP 299 EP 305 DI 10.1016/j.ijdevneu.2004.05.005 PG 7 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 910PL UT WOS:000227943900016 PM 15749254 ER PT J AU Haag, G Tordjman, S Duprat, A Urwand, S Jardin, F Clement, MC Cukierman, A Druon, C Du Chatellier, AM Tricaud, J Dumont, AM AF Haag, G Tordjman, S Duprat, A Urwand, S Jardin, F Clement, MC Cukierman, A Druon, C Du Chatellier, AM Tricaud, J Dumont, AM TI Psychodynamic assessment of changes in children with autism under psychoanalytic treatment SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Article DE autistic children; cognitive/psychoanalytic converging viewpoints; body ego; skin formation; eye contact; vertical splitting; horizontal splitting; speech; spatial exploration; object exploration ID DIAGNOSTIC OBSERVATION SCHEDULE AB In this article the authors report insights into autism developed through their extensive experience of psychoanalytic therapy with children with autism. The first stages of body psychic development are seriously disrupted by this pathology, resulting in primitive anxieties of falling and of being liquefied These anxieties are connected to the fragile development of body ego and of its related spatiotemporal organisation. The changes in children observed by the authors during the therapeutic process lead them to offer a psychodynamic assessment tool, which revolves principally around the development of body ego. After the initial state of 'severe autism', the authors describe three stages: the stage of' 'recovery of the skin' (Bick); the established 'symbiotic phase, subdivided into 'vertical then horizontal splitting of the body ego'; and finally the stage of 'individuation'. First, the authors describe the principal psychoanalytic approaches to autism and reflect on the links possible with nonpsychoanalytic work. C1 Dept Child Psychiat, F-35000 Rennes, France. CMP, F-75005 Paris, France. 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A., 1965, 1 YEAR LIFE Tager-Flusberg H., 1993, UNDERSTANDING OTHER, P138 TORDJMAN S, 1996, PERSPECT PSYCHIAT, V35, P13 Tordjman S, 1997, J CHILD PSYCHOL PSYC, V38, P705, DOI 10.1111/j.1469-7610.1997.tb01697.x Trevarthen C., 1979, SPEECH BEGINNING INT, P321 TSAI LY, 1985, J AUTISM DEV DISORD, V15, P339, DOI 10.1007/BF01531504 Tustin F, 1986, AUTISTIC BARRIERS NE TUSTIN F, 1981, AUSTISTIC STATES CHI URWAND S, 2004, NEUROPSYCHIAT ENFAN, V52, P234 Volkmar F., 1987, HDB AUTISM PERVASIVE, P41 WATERHOUSE L, IN PRESS AUTISM PERV WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 49 TC 10 Z9 11 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0020-7578 J9 INT J PSYCHOANAL JI Int. J. Psychoanal. PD APR PY 2005 VL 86 BP 335 EP 352 DI 10.1516/WAB4-DW0R-8N9B-1UH8 PN 2 PG 18 WC Psychology, Psychoanalysis SC Psychology GA 926KG UT WOS:000229121500010 PM 16089194 ER PT J AU South, M Ozonoff, S McMahon, WM AF South, M Ozonoff, S McMahon, WM TI Repetitive behavior profiles in Asperger syndrome and high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; repetitive behavior; circumscribed interests ID DIAGNOSTIC INTERVIEW; HIGH-IQ; CHILDREN; DISORDERS; DISABILITIES; ADOLESCENTS; VALIDITY; ADULTS AB Although repetitive behaviors are a core diagnostic domain for autism spectrum disorders, research in this area has been neglected. This study had two major aims: (1) to provide a detailed characterization of repetitive behaviors in individuals with Asperger Syndrome (AS), high-functioning autism (HFA), and typically developing controls (TD); and (2) to examine whether differences in repetitive behavior profiles could provide evidence for the external validity of AS separate from HFA. Specifically, it was hypothesized that circumscribed interests would be more prevalent and cause more impairment in the AS group than the HFA group, while the reverse would be true for other categories of repetitive behavior. The parent(s) of 61 children and adolescents (19 with AS, 21 with HFA, and 21 TD) completed two interviews focused specifically on lifetime and current repetitive behavior symptoms. No reliable differences in repetitive behavior between AS and HFA children were found. Results suggested that circumscribed interests differ in developmental course from the three other DSM-IV-TR categories of repetitive behavior. Internal consistency among the four DSM-IV-TR categories of repetitive behavior was high, α=.84, providing evidence for a unitary repetitive behaviors factor. The importance of expanding research in the repetitive behavior domain is highlighted as part of the necessary integration of behavioral and neurobiological approaches to understanding the etiology of autism. C1 Univ Calif Davis, Hlth Syst, MIND Inst, Dept Psychiat & Behav Sci, Sacramento, CA 95817 USA. Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. RP Ozonoff, S (reprint author), Univ Calif Davis, Hlth Syst, MIND Inst, Dept Psychiat & Behav Sci, 2825 50th St, Sacramento, CA 95817 USA. 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PD APR PY 2005 VL 35 IS 2 BP 145 EP 158 DI 10.1007/s10803-005-1992-3 PG 14 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300002 PM 15909401 ER PT J AU Gillberg, C Cederlund, M AF Gillberg, C Cederlund, M TI Asperger syndrome: Familial and pre- and perinatal factors SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; familial; prenatal; perinatal ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; CHILDREN; POPULATION; CHILDHOOD; PHENOTYPE; SIBLINGS; PARENTS AB Objective: Study familial and pre- and perinatal factors in Asperger Syndrome (AS). Methods: One hundred boys with AS had their records reviewed. "Pathogenetic subgroups" were defined according to presence of medical syndromes/chromosomal abnormalities, indices of familiality, and pre- and perinatal risk factors predisposing to brain damage. Results: No major index of pathogenetic factors was found in 13%, a syndrome/chromosomal abnormality in 8%, pre- or perinatal risk 13%, combined pre- or perinatal risk and family history in 11%, and family history only in 55% Comment: About 50% of all boys with AS have a paternal family history of autism spectrum disorder. Pre- and perinatal risks appear to be important in about 25% of cases. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ Glasgow, Dept Med Psychol, Glasgow G12 8QQ, Lanark, Scotland. RP Gillberg, C (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. 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Autism Dev. Disord. PD APR PY 2005 VL 35 IS 2 BP 159 EP 166 DI 10.1007/s10803-005-1993-2 PG 8 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300003 PM 15909402 ER PT J AU McConachie, H Le Couteur, A Honey, E AF McConachie, H Le Couteur, A Honey, E TI Can a diagnosis of Asperger syndrome be made in very young children with suspected autism spectrum disorder? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE repetitive behaviours; Asperger syndrome; PDD-NOS; ADI-R; ADOS; first words ID PERVASIVE DEVELOPMENTAL DISORDERS; FOLLOW-UP; PRESCHOOL-CHILDREN; MIDDLE CHILDHOOD; AGE; LIFE AB Of a cohort of 104 children with Autism, PDD-NOS or specific language disorder, recruited at age 2-3 years of age, only three appeared to meet diagnostic assessment criteria for Asperger syndrome (AS). The children were followed up at 4-5 years, and assessments at both time points included the Autism Diagnostic Interview (ADI-R), the Autism Diagnostic Observation Schedule (ADOS) and the Mullen Scales of Early Learning. The paper explores the reasons why so few children with possible AS were identified early, including problems inherent in the assessment tools and the range of normal variation within characteristics required for a diagnosis. Only 10 children altogether had first words by 24 months, and abilities in the average range, and 9 were followed up. All of these able children had varied repetitive behaviours, and these increased in terms of ADI-R algorithm score over a 13 month interval. However, items concerning resistance to change and liking of routines tended to decrease in terms of reported impact on the child and family. Repetitive behaviours seem significant in the early referral of able children for a PDD diagnosis, but identification of children with AS is more likely to occur reliably once children are older and enter school. C1 Univ Newcastle Upon Tyne, Sch Clin Med Sci, Newcastle Upon Tyne NE2 4AE, Tyne & Wear, England. RP McConachie, H (reprint author), Univ Newcastle Upon Tyne, Sch Clin Med Sci, 1-2 Claremont Terrace, Newcastle Upon Tyne NE2 4AE, Tyne & Wear, England. EM h.r.mcconachie@ncl.ac.uk CR Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 CANTWELL DP, 1989, J AUTISM DEV DISORD, V19, P19, DOI 10.1007/BF02212715 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2004, J AUTISM DEV DISORD, V34, P59, DOI 10.1023/B:JADD.0000018075.77941.60 CHRMAN T, 2005, IN PRESS J CHILD PSY CHRMAN T, 2002, J CHILD PSYCHOL PSYC, V43, P289 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Eaves LC, 2004, J AUTISM DEV DISORD, V34, P367, DOI 10.1023/B:JADD.0000037414.33270.a8 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 HONEY E, 2004, EUR AC CHILDH DIS C Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 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 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x Lord C, 2004, J CHILD PSYCHOL PSYC, V45, P936, DOI 10.1111/j.1469-7610.2004.t01-1-00287.x Maestro S, 2001, PSYCHOPATHOLOGY, V34, P147, DOI 10.1159/000049298 Michelotti J, 2002, DEV MED CHILD NEUROL, V44, P812 Moore V, 2003, AUTISM, V7, P47, DOI 10.1177/1362361303007001018 Mullen E, 1995, MULLEN SCALES EARLY Noterdaeme M, 2002, AUTISM, V6, P159, DOI 10.1177/1362361302006002003 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Shao YJ, 2003, AM J HUM GENET, V72, P539, DOI 10.1086/367846 Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 Szatmari P, 2000, AM J PSYCHIAT, V157, P1980, DOI 10.1176/appi.ajp.157.12.1980 Szatmari P, 2003, J CHILD PSYCHOL PSYC, V44, P520, DOI 10.1111/1469-7610.00141 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 Volkmar F. R., 2000, ASPERGER SYNDROME, P25 NR 33 TC 32 Z9 33 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2005 VL 35 IS 2 BP 167 EP 176 DI 10.1007/s10803-005-1995-0 PG 10 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300004 PM 15909403 ER PT J AU Ghaziuddin, M AF Ghaziuddin, M TI A family history study of Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; autism; depression; schizophrenia; family history; genetics ID AUTISM DIAGNOSTIC INTERVIEW; HIGH-FUNCTIONING AUTISM; SCHIZOID PERSONALITY; THOUGHT-DISORDER; INDIVIDUALS; CHILDHOOD; SCHIZOPHRENIA; CRITERIA; CHILDREN; PARENTS AB Asperger syndrome (AS) is a childhood-onset disorder often described as a mild variant of autism. Although classified as a distinct disorder in the DSM-IV, its overlap with autism continues to be a matter of ongoing debate. While the family genetic origins of autism are well established, few studies have investigated this topic in AS using current operational criteria. In this report, we examined the family psychiatric history of 58 subjects with AS diagnosed according to DSM-IV criteria (48 males; mean age 13.34; mean full scale IQ 104.87). All subjects had a history of mild autistic social deficits; focused special interests; normal level of intelligence; and an odd and often pedantic manner of speaking. None had a previous diagnosis of autism. Of the 58 subjects with Asperger syndrome, three had first degree relatives with AS; nine (15%) had a family history of schizophrenia; and 35 (60%) had a family history of depression. Of the 64 siblings, four had a diagnosis of AS and none of autism. Compared with a group of 39 subjects with normal intelligence autism (high functioning autism, HFA; 33 males; mean age 15.34; mean full scale IQ 85.89) subjects with AS were more likely to have relatives with depression; schizophrenia; and the broader autistic phenotype. Possible reasons for and implications of these findings are discussed. C1 Univ Michigan, Med Ctr, Div Child Psychiat, Ann Arbor, MI 48109 USA. RP Ghaziuddin, M (reprint author), Univ Michigan, Med Ctr, Div Child Psychiat, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. 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Autism Dev. Disord. PD APR PY 2005 VL 35 IS 2 BP 177 EP 182 DI 10.1007/s10803-005-1996-z PG 6 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300005 PM 15909404 ER PT J AU Ashwin, C Wheelwright, S Baron-Cohen, S AF Ashwin, C Wheelwright, S Baron-Cohen, S TI Laterality biases to chimeric faces in Asperger syndrome: What is 'Right' about face-processing? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE Asperger syndrome; autism; face-processing; social cognition; brain laterality; emotional expression ID HIGH-FUNCTIONING AUTISM; PRECONSCIOUS SELECTIVE ATTENTION; PROSOPO-AFFECTIVE AGNOSIA; HUMAN NEURAL SYSTEMS; HUMAN FUSIFORM GYRUS; PERCEPTUAL ASYMMETRIES; FACIAL EXPRESSIONS; RIGHT-HANDERS; INFANTILE-AUTISM; CHILDREN AB People show a left visual field (LVF) bias for faces, i.e., involving the right hemisphere of the brain. Lesion and neuroimaging studies confirm the importance of the right-hemisphere and suggest separable neural pathways for processing facial identity vs. emotions. We investigated the hemispheric processing of faces in adults with and without Asperger syndrome (AS) using facial emotion and identity chimeric tasks. Controls showed an LVF bias in both tasks, but no perceptual bias in a non-social control task. The AS group showed an LVF bias during both tasks, however the bias was reduced in the identity condition. Further, the AS group showed an LVF bias in the non-social condition. These results show a differential pattern of hemispheric processing of faces in AS. C1 Univ Cambridge, Autism Res Ctr, Dept Psychol, Cambridge CB2 2AH, England. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 2AH, England. RP Ashwin, C (reprint author), Univ Cambridge, Autism Res Ctr, Dept Psychol, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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W., 1998, FACE MIND NR 106 TC 28 Z9 29 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2005 VL 35 IS 2 BP 183 EP 196 DI 10.1007/s10803-005-1997-y PG 14 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300006 PM 15909405 ER PT J AU Paul, R Augustyn, A Klin, A Volkmar, FR AF Paul, R Augustyn, A Klin, A Volkmar, FR TI Perception and production of prosody by speakers with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; prosody; language ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; ADAPTIVE-BEHAVIOR; MENTAL-RETARDATION; ASPERGER-SYNDROME; NORMAL-CHILDREN; DOWN-SYNDROME; FOLLOW-UP; LANGUAGE; SPEECH AB Speakers with autism spectrum disorders (ASD) show difficulties in suprasegmental aspects of speech production, or prosody, those aspects of speech that accompany words and sentences and create what is commonly called "tone of voice." However, little is known about the perception of prosody, or about the specific aspects of prosodic production that result in the perception of "oddness." The present study examined the perception and production of a range of specific prosodic elements in an experimental protocol involving natural speech among speakers with ASD between 14 and 21 years of age, in comparison with a typical control group. Results revealed ceiling effects limiting interpretation of findings for some aspects of prosody. However, there were significant between-group differences in aspects of stress perception and production. The implications of these findings for understanding prosodic deficits is speakers with autism spectrum disorders, and for future research in this area, are discussed. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. So Connecticut State Univ, New Haven, CT 06515 USA. RP Paul, R (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. EM rhea.paul@yale.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baltaxe C., 1984, J SPEECH HEAR RES, V24, P97 Baltaxe C., 1984, P 10 INT C PHON SCI, P713 Baltaxe C. A. M., 1985, COMMUNICATION PROBLE, P95, DOI 10.1007/978-1-4757-4806-2_7 BALTAXE CAM, 1987, J AUTISM DEV DISORD, V17, P255, DOI 10.1007/BF01495060 Bates Elizabeth, 1979, DEV PRAGMATICS, P167 Bolinger D., 1989, INTONATION ITS USES Boucher J, 1998, J CHILD PSYCHOL PSYC, V39, P171, DOI 10.1017/S0021963097001820 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Crystal D., 1986, LANG ACQUIS, P33 DEMYER MK, 1973, J AUTISM CHILD SCHIZ, V3, P199, DOI 10.1007/BF01538281 FAY WH, 1969, J COMMUN DISORD, V2, P38, DOI 10.1016/0021-9924(69)90053-7 FAY WH, 1980, EMERGING LANGAUGE AU FINE J, 1991, J CHILD PSYCHOL PSYC, V32, P771, DOI 10.1111/j.1469-7610.1991.tb01901.x Fosnot S. 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PD APR PY 2005 VL 35 IS 2 BP 205 EP 220 DI 10.1007/s10803-005-1999-9 PG 16 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300008 PM 15909407 ER PT J AU Klin, A Pauls, D Schultz, R Volkmar, F AF Klin, A Pauls, D Schultz, R Volkmar, F TI Three diagnostic approaches to Asperger syndrome: Implications for research SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; autism; diagnosis ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS; FAMILY HISTORY; DSM-IV; CHILDREN; PHENOTYPE; PSYCHOPATHY; INDIVIDUALS; ADOLESCENTS AB Objective: To examine the implications for research of the use of three alternative definitions for Asperger syndrome (AS). Differences across the three nosologic systems were examined in terms of diagnostic assignment, IQ profiles, comorbid symptoms, and familial aggregation of social and other psychiatric symptoms. Method: Standard data on diagnosis, intellectual functioning, comorbidity patterns, and family history were obtained on 65 individuals screened for a very high probability of having autism without mental retardation (or higher functioning autism, HFA) or AS. Diagnoses of AS were established based on three different approaches: DSM-IV, presence/absence of communicative phrase speech by 3 years, and a system designed to highlight prototypical features of AS. Results: Agreement between the three diagnostic systems was poor. AS could be differentiated from HFA (but not from PDD-NOS) on the basis of IQ profiles in two of the three systems. Differences in patterns of comorbid symptomatology were obtained in two of the three systems, although differences were primarily driven by the PDD-NOS category. Only one of the approaches yielded differences relative to aggregation of the "broader phenotype" in family members. Conclusions: Diagnostic assignments of AS based on three commonly used approaches have low agreement and lead to different results in comparisons of IQ profiles, patterns of comorbidity, and familial aggregation of psychiatric symptoms across the approach-specific resultant groups of HFA, AS, and PDD-NOS. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Klin, A (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA. 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PD APR PY 2005 VL 35 IS 2 BP 221 EP 234 DI 10.1007/s10803-005-2001-6 PG 14 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300009 PM 15909408 ER PT J AU Woodbury-Smith, M Klin, A Volkmar, F AF Woodbury-Smith, M Klin, A Volkmar, F TI Asperger's syndrome: A comparison of clinical diagnoses and those made according to the ICD-10 and DSM-IV SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; diagnosis; autism ID SCHIZOID PERSONALITY; DISORDER; CHILDHOOD; AUTISM AB The diagnostic criteria for Asperger Syndrome (AS) according to ICD-10 and DSM-IV have been criticized as being too narrow in view of the rules of onset and precedence, whereby autism takes precedence over AS in a diagnostic hierarchy. In order to investigate this further, cases from the DSM-IV multicenter study who had been diagnosed clinically with AS were assigned to appropriate DSM-IV/ICD-10 diagnostic categories. The analysis indicated that 11(23%) cases would be reassigned a diagnosis of autism by either ICD-10 or DSM-IV according to their onset and precedence rules, and 33(68%) would be diagnosed with AS. These results contrast with those of others who have stated that the diagnosis of AS using ICD-10/DSM-IV criteria is `virtually impossible'. It is suggested that this is due to limitations inherent in these criteria, and alternative conceptualizations are discussed. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. RP Woodbury-Smith, M (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. EM marc.woodbury-smith@yale.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Hippler K, 2003, PHILOS T ROY SOC B, V358, P291, DOI 10.1098/rstb.2002.1197 Kanner L, 1943, NERV CHILD, V2, P217 KLIN A, 1997, DEV PSYCHOPATHOL, P208 Klin A., 2000, ASPERGER SYNDROME Klin A., 2000, ASPERGER SYNDROME Lancia R., 2000, ASPERGER SYNDROME MAYES SD, 2001, J ABNORM CHILD PSYCH, V3, P263 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 OZONOFF S, 2000, ASPERGER SYNDROME, P73 Rourke B, 1987, CLIN NEUROPSYCHOL, V1, P209, DOI 10.1080/13854048708520056 Rourke B. 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PD APR PY 2005 VL 35 IS 2 BP 235 EP 240 DI 10.1007/s10803-005-2002-5 PG 6 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300010 PM 15909409 ER PT J AU Rutter, M AF Rutter, M TI Autism research: Lessons from the past and prospects for the future SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material DE experiments; epidemiology; matching groups; intervention studies; quantitative and molecular genetics; standardized measures; research-clinical interplay; collaboration; developmental regression; neural dysfunction; cognitive deficits; sex differences; Asperger syndrome; comorbidity; rising incidence ID RECEPTIVE LANGUAGE DISORDER; SPECIAL EDUCATIONAL TREATMENT; 15-YEAR FOLLOW-UP; EARLY ADULT LIFE; INFANTILE PSYCHOSIS; RESEARCH STRATEGIES; CLINICAL-PRACTICE; ASPERGER-SYNDROME; CHILD-PSYCHIATRY; BRAIN AB The paper uses both the author's experience of research training, and the empirical studies of autism in which he participated over the last 40-plus years, to derive research lessons and to consider the needs and prospects for future research. Attention is drawn to: the importance of mentors; the need to use technologies in a hypothesis-testing fashion; the important of possible creative/innovative leaps and of recognition of the unexpected; the need to ask challenging questions and to recognize when the original ideas were mistaken. There is great value in broadening the scientific strategies used to investigate a particular condition and much is to be gained by deliberately seeking parallels with other conditions. C1 Inst Psychiat, SGDP Ctr, London SE5 8AF, England. RP Rutter, M (reprint author), Inst Psychiat, SGDP Ctr, Box P080,De Crespigny Pk,Denmark Hill, London SE5 8AF, England. 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A., 1972, EARLY CHILDHOOD AUTI TINBERGEN EA, 1983, AUTISTIC CHILDREN NE VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 WHO, 1993, ICD 10 CLASS MENT BE NR 79 TC 35 Z9 39 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 2005 VL 35 IS 2 BP 241 EP 257 DI 10.1007/s10803-005-2003-4 PG 17 WC Psychology, Developmental SC Psychology GA 924YU UT WOS:000229018300011 PM 15909410 ER PT J AU Jou, RJ Handen, BL Hardan, AY AF Jou, RJ Handen, BL Hardan, AY TI Retrospective assessment of atomoxetine in children and adolescents with pervasive developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; SYMPTOMS; AUTISM AB A retrospective study was conducted to assess the effectiveness and tolerability of atomoxetine in children and adolescents with pervasive developmental disorders (PDD). An outpatient clinic registry of individuals with PDD was used to identify all children and adolescents who received atomoxetine over a period of 12 months. Patients were included if concomitant medications remained unchanged. Treatment response was assessed using the Global Improvement item of the Clinical Global Impressions scale (CGI-GI) based on the Conners Parent Rating Scale (CPRS) routinely completed by primary caretakers and other clinical information available in the registry. Twenty patients were identified, including 16 males and 4 females (age, 11.5 years; standard deviation, 3.5). Most patients (80%) were taking at least 1 concomitant medication. Treatment dose was 43.3 mg (standard deviation, 18.1) and duration was 19.5 weeks (standard deviation, 10.5). Twelve patients were judged to be responders, as defined by a score of 1 or 2 on the CGI-GI. Differences between baseline and the end of the trial period were observed in the following CPRS subscales: Conduct, hyperactivity, inattention, and learning. No differences were noted in the anxiety and psychosomatic subscales. One patient discontinued atomoxetine because of severe mood swings. Atomoxetine may be beneficial for treating secondary symptoms of PDD, and prospective open-label or double-blind, placebo-cont.rolled studies are needed to assess its efficacy and safety. C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Psychiat, Sch Med, Pittsburgh, PA 15213 USA. Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Psychiat, Sch Med, 3811 OHara St, Pittsburgh, PA 15213 USA. EM hardanay@upmc.edu CR AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 AMAN MG, 1996, J DEV PHYS DISABIL, V4, P1672 GOYETTE CH, 1978, J ABNORM CHILD PSYCH, V6, P221, DOI 10.1007/BF00919127 Guy W, 1976, NIMH PUBLICATION Handen BL, 2000, J AUTISM DEV DISORD, V30, P245, DOI 10.1023/A:1005548619694 Michelson D, 2002, AM J PSYCHIAT, V159, P1896, DOI 10.1176/appi.ajp.159.11.1896 Muris P, 1998, J ANXIETY DISORD, V12, P387, DOI 10.1016/S0887-6185(98)00022-X Wernicke JF, 2002, J CLIN PSYCHIAT, V63, P50 NR 8 TC 33 Z9 33 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD APR PY 2005 VL 15 IS 2 BP 325 EP 330 DI 10.1089/cap.2005.15.325 PG 6 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 935MS UT WOS:000229787000021 PM 15910217 ER PT J AU McGovern, CW Sigman, M AF McGovern, CW Sigman, M TI Continuity and change from early childhood to adolescence in autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; developmental continuity; diagnosis; adaptive behavior; emotional responsiveness ID ADAPTIVE-BEHAVIOR SCALES; DOWN-SYNDROME; CHILDREN; INDIVIDUALS; COMMUNICATION; ADULTS; AGE; IQ AB Background: This longitudinal study of 48 children diagnosed with autism at 2-5 years of age was designed to test the hypothesis that diagnosis would remain stable for most of the sample but that there would be improvements in symptom severity, adaptive behavior, and emotional responsiveness in adolescence. Methods: A sample of children with autism assessed in both early and middle childhood were observed in late adolescence with the Autism Diagnostic Observation Scale (ADOS) and their parents were administered the Autism Diagnostic Interview-Revised (ADI-R) and the Vineland Adaptive Behavior Scale. Results: All but 2 adolescents (46 of 48) met lifetime criteria for autism according to the ADI-R, and all but 4 adolescents (40 of 44) met criteria for autism spectrum disorder on the ADOS. In contrast to the continuity in diagnosis, parents described improvements in social interactions, repetitive/stereotyped behaviors, adaptive behaviors, and emotional responsiveness to others' distress in adolescence compared to middle childhood. High-functioning adolescents with autism showed more improvement in these domains than low-functioning adolescents with autism. The extent to which the adolescents were observed to be socially engaged with their peers in school in middle childhood predicted adaptive behavior skills even when intelligence level was statistically constrained. Conclusions: The developmental trajectory of children with autism appears to show both continuity and change. In this sample, most individuals continued to be diagnosed in the autism spectrum but parents reported improvements in adolescence. The results suggest that social involvement with peers improves adaptive behavior skills, and this argues for focusing intervention programs in this area. In addition, it is clear that high-functioning adolescents improve more than low-functioning individuals not only in cognitive abilities but also in social interaction skills. Thus, any early intervention that impacts the cognitive abilities of young children with autism is likely to have a parallel influence on their social skills as they mature into late adolescence and early adulthood. C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90095 USA. RP Sigman, M (reprint author), Univ Calif Los Angeles, Sch Med, 760 Westwood Plaza,Room 68-237C, Los Angeles, CA 90095 USA. EM msigman@ucla.edu CR American Psychiatric Association (APA), 1980, DIAGN STAT MAN MENT ANDO H, 1980, J AUTISM DEV DISORD, V10, P173, DOI 10.1007/BF02408468 APA, 1987, DIAGN STAT MAN MENT BONO M, IN PRESS J AUTISM DE Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Eaves LC, 1996, J AUTISM DEV DISORD, V26, P557, DOI 10.1007/BF02172276 Freeman BJ, 1999, J AUTISM DEV DISORD, V29, P379, DOI 10.1023/A:1023078827457 HOWES C, 1988, MONOGRAPHS SOC RES C, V53, P94 Kraijer D, 2000, J AUTISM DEV DISORD, V30, P39, DOI 10.1023/A:1005460027636 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x 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 Mesibov GB, 1997, HDB AUTISM PERVASIVE, P309 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 National Research Council, 2001, ED CHILDR AUT COMM E NIHIRA K, 1993, AAMR AD BEH SCAL RES PERRY A, 1989, J AUTISM DEV DISORD, V19, P41, DOI 10.1007/BF02212717 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 RODRIGUE JR, 1991, J AUTISM DEV DISORD, V21, P187, DOI 10.1007/BF02284759 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Schopler E., 1988, CHILDHOOD AUTISM RAT Schuler AL, 2000, COMM LANG INTERVEN, V9, P251 Semel E., 1987, CLIN EVALUATION LANG Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 SIGMAN MD, 1992, CHILD DEV, V63, P796, DOI 10.1111/j.1467-8624.1992.tb01662.x Siller M, 2002, J AUTISM DEV DISORD, V32, P77, DOI 10.1023/A:1014884404276 Sparrow S, 1984, VINELAND ADAPTIVE BE Thorndike RL, 1986, STANFORD BINET INTEL NR 28 TC 106 Z9 109 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD APR PY 2005 VL 46 IS 4 BP 401 EP 408 DI 10.1111/j.1469-7610.2004.00361.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 907HA UT WOS:000227705800008 PM 15819649 ER PT J AU Mahoney, G Perales, F AF Mahoney, G Perales, F TI Relationship-focused early intervention with children with pervasive developmental disorders and other disabilities: A comparative study SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE early intervention; pervasive developmental disorders; relationship focused intervention ID YOUNG-CHILDREN; 2ND YEAR; AUTISM; LANGUAGE; BEHAVIOR; INFANCY; PLAY AB This study compares the effects of relationship-focused early intervention on toddlers and preschool-age children who were classified as having either pervasive developmental disorders (PDDs) (N = 20) or developmental disabilities (DDs) (N = 30). The intervention was conducted over a 1-year period through weekly individual parent-child sessions. It focused on helping parents use responsive teaching strategies to encourage their children to acquire and use pivotal developmental behaviors that addressed their individualized developmental needs. Before and after comparisons indicated significant increases in parents' responsiveness and children's pivotal behavior. Both groups of children made significant improvements in their cognitive, communication, and socioemotional functioning. However, children with PDDs made statistically greater improvements on the developmental measures than children with DDs. On several developmental measures, children's improvements were related to increases in both their parents' responsiveness and their own pivotal behavior. C1 Case Western Reserve Univ, Mendel Sch Appl Social Sci, Cleveland, OH 44106 USA. RP Mahoney, G (reprint author), Case Western Reserve Univ, Mendel Sch Appl Social Sci, 10900 Euclid Ave, Cleveland, OH 44106 USA. EM gerald.mahoney@case.edu CR BACKERSMANSKRAN.MJ, 2003, PSYCHOL BULL, V129, P195 Bagnato S. J., 1999, TEMPERAMENT ATYPICAL Bagnato SJ, 1999, INFANT YOUNG CHILD, V12, P98 Beckwith L., 1989, NEW DIRECTIONS CHILD, P75 Bornstein MH, 1999, INFANT BEHAV DEV, V22, P65, DOI 10.1016/S0163-6383(99)80006-X Carter A. 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A., 1997, EFFECTIVENESS EARLY, P549 Myers CL, 1996, TOP EARLY CHILD SPEC, V16, P102 PRIZANT BM, 1989, AUTISM NATURE DIAGNO, P282 Rogers SJ, 2000, INT REV RES MENT RET, V23, P1 ROGERS SJ, 1991, TOP EARLY CHILD SPEC, V11, P29 Schopler E., 1986, CHILDHOOD AUTISM RAT Shadish W, 2002, EXPT QUASIEXPERIMENT Siller M, 2002, J AUTISM DEV DISORD, V32, P77, DOI 10.1023/A:1014884404276 TamisLeMonda CS, 1996, EARLY DEV PARENTING, V5, P173, DOI 10.1002/(SICI)1099-0917(199612)5:4<173::AID-EDP131>3.0.CO;2-V Trivette C., 2003, BRIDGES, V1, P1 WOLERY M, 1983, EXCEPT CHILDREN, V50, P167 ZEANAH CH, 2000, HDB INFANT MENTAL HL, P129 NR 40 TC 67 Z9 67 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 APR PY 2005 VL 26 IS 2 BP 77 EP 85 DI 10.1097/00004703-200504000-00002 PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 916KN UT WOS:000228383900001 PM 15827458 ER PT J AU Rutter, M AF Rutter, M TI Aetiology of autism: findings and questions SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Review DE autism spectrum disorders; epidemiology; genetic influences; incidence; measles-mumps-rubella vaccine ID PERVASIVE DEVELOPMENTAL DISORDERS; AFFECTED SIBLING PAIRS; TUBEROUS SCLEROSIS; LANGUAGE IMPAIRMENT; CHILD; TWINS; COMPLICATIONS; ENCEPHALITIS; POPULATION; COMPLEX AB Background Although there is good evidence that autism is a multifactorial disorder, an adequate understanding of the genetic and non-genetic causes has yet to be achieved. Methods Empirical research findings and conceptual reviews are reviewed with respect to evidence on possible causal influences. Results Much the strongest evidence concerns the importance of susceptibility genes, but such genes have yet to be identified. Specific somatic conditions (such as tuberous sclerosis and the fragile X anomaly) account for a small proportion of cases. Over recent decades there has been a major rise in the rate of diagnosed autism. The main explanation for this rise is to be found in better ascertainment and a broadening of the diagnostic concept. Nevertheless, some degree of true rise cannot be firmly excluded. However, the epidemiological evidence on the main hypothesized environmental explanation, namely the measles-mumps-rubella vaccine, is consistently negative. Conclusion Progress on the elucidation of the causes of autism will be crucially dependent on the combination of epidemiology with more basic science laboratory studies. C1 Inst Psychiat, SGDP Ctr, London SE5 8AF, England. RP Rutter, M (reprint author), Inst Psychiat, SGDP Ctr, De Crespigny Pk, Denmark Hill, London SE5 8AF, England. 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Intell. Disabil. Res. PD APR PY 2005 VL 49 BP 231 EP 238 DI 10.1111/j.1365-2788.2005.00676.x PN 4 PG 8 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 907MF UT WOS:000227721500001 PM 15816809 ER PT J AU Polimeni, MA Richdale, AL Francis, AJP AF Polimeni, MA Richdale, AL Francis, AJP TI A survey of sleep problems in autism, Asperger's disorder and typically developing children SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE Asperger's disorder; autism; behavioural treatment; children; medication; sleep problem AB Background Sleep problems are common in typically developing (TD) children and in children with autism, however, less is known about the sleep of children with Asperger's disorder (AD). The aim of this study was to compare sleep patterns of children with autism and AD to a TD group of children. Methods Sixty-six parents of TD children, 53 parents of children with autism, and.. parents of children with AD completed a survey on their child's sleep patterns, the nature and severity of any sleep problems and success of any treatment attempted. Results The results showed high prevalence of sleep problems with significantly more problems reported in the autism and AD groups (TD = .50%, autism = 73%, AD = 73%), with no significant differences between groups on severity or type of sleep problem. Children with AD were significantly more likely to be sluggish and disoriented after waking and had a higher Behavioral Evaluation of Disorders of Sleep (BEDS) total score compared to the other two groups. The autism and AD groups reported significantly better treatment success for medication compared to the TD group. The autism group reported significantly better success for behavioural treatment compared to the AD group. Conclusions In conclusion, children with AD may have more symptoms of sleep disturbance, and different types of sleep problems than children with autism. As this is the first study to compare autism and AD and to survey treatment outcomes, further research is needed to validate these findings. C1 RMIT Univ, Sch Hlth Sci, Bundoora, Vic 3083, Australia. RP Polimeni, MA (reprint author), RMIT Univ, Sch Hlth Sci, POB 71, Bundoora, Vic 3083, Australia. EM s9809728@student.rmit.edu.au CR [Anonymous], 2000, DIANG STAT MAN MENT BERGERON C, 1997, SLEEP RES, V26, P541 BERTHIER ML, 1992, J AM ACAD CHILD PSY, V31, P735, DOI 10.1097/00004583-199207000-00023 Didden R, 2001, RES DEV DISABIL, V22, P255, DOI 10.1016/S0891-4222(01)00071-3 Gillberg C., 2002, GUIDE ASPERGERS SYND Godbout R, 1998, DREAMING, V8, P75, DOI 10.1023/B:DREM.0000005898.95212.58 Godbout R, 2000, NEUROREPORT, V11, P127, DOI 10.1097/00001756-200001170-00025 Johnson CR, 1996, CHILD ADOL PSYCH CL, V5, P673 Kahn A, 1996, J CLIN NEUROPHYSIOL, V13, P184, DOI 10.1097/00004691-199605000-00002 Owens J. 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PD APR PY 2005 VL 49 BP 260 EP 268 DI 10.1111/j.1365-2788.2005.00642.x PN 4 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 907MF UT WOS:000227721500005 PM 15816813 ER PT J AU Butler, MG Dasouki, MJ Zhou, XP Talebizadeh, Z Brown, M Takahashi, TN Miles, JH Wang, CH Stratton, R Pilarski, R Eng, C AF Butler, MG Dasouki, MJ Zhou, XP Talebizadeh, Z Brown, M Takahashi, TN Miles, JH Wang, CH Stratton, R Pilarski, R Eng, C TI Subset of individuals with autism spectrum disorders and extreme macrocephaly associated with germline PTEN tumour suppressor gene mutations SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; RILEY-RUVALCABA-SYNDROME; COWDEN-SYNDROME; DISEASE; FAMILY; PHOSPHATASE; PREVALENCE; PATIENT AB The genetic aetiology of autism remains elusive. Occasionally, individuals with Cowden syndrome (a cancer syndrome) and other related hamartoma disorders such as Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Proteus-like conditions, are characterised by germline PTEN mutations, and may have neurobehavioural features resembling autism as well as overgrowth and macrocephaly. Therefore, we undertook PTEN gene mutation analysis in 18 subjects mainly prospectively ascertained with autism spectrum disorder and macrocephaly. Of these 18 autistic subjects (13 males and five females; ages 3.1-18.4 years) with a head circumference range from 2.5 to 8.0 standard deviations above the mean, three males (17%) carried germline PTEN mutations. These three probands had previously undescribed PTEN mutations: H93R (exon 4), D252G (exon 7), and F241S (exon 7). They had the larger head circumference measurements amongst all our study subjects. The three residues altered in our patients were highly evolutionarily conserved. We suggest that PTEN gene testing be considered for patients with autistic behaviour and extreme macrocephaly. The gene findings may impact on recurrence risks as well as medical management for the patient. C1 Childrens Mercy Hosp & Clin, Sect Med Genet & Mol Med, Kansas City, MO 64108 USA. Univ Missouri, Sch Med, Kansas City, MO 64108 USA. Ohio State Univ, Dept Internal Med, Div Human Genet,Clin Canc Genet Program, Comprehens Canc Ctr,Human Canc Genet Program, Columbus, OH 43210 USA. Univ Missouri, Dept Pediat, Columbia, MO USA. Stanford Univ, Med Ctr, Dept Neurol, Stanford, CA 94305 USA. SW Genet, San Antonio, TX USA. RP Butler, MG (reprint author), Childrens Mercy Hosp & Clin, Sect Med Genet & Mol Med, 2401 Gillham Rd, Kansas City, MO 64108 USA. EM mgbutler@cmh.edu CR *AM PSYCH ASS, 2000, DSM 4 TR 2000 DIAGN Arch EM, 1997, AM J MED GENET, V71, P489, DOI 10.1002/(SICI)1096-8628(19970905)71:4<489::AID-AJMG24>3.0.CO;2-B Bussaglia E, 2002, J INVEST DERMATOL, V118, P639, DOI 10.1046/j.1523-1747.2002.01728.x Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Eng C, 2003, HUM MUTAT, V22, P183, DOI 10.1002/humu.10257 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 Goffin A, 2001, AM J MED GENET, V105, P521, DOI 10.1002/ajmg.1477 HANSSEN AMN, 1995, J MED GENET, V32, P117, DOI 10.1136/jmg.32.2.117 Kohno T, 1998, JPN J CANCER RES, V89, P471 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Marsh DJ, 1998, HUM MOL GENET, V7, P507, DOI 10.1093/hmg/7.3.507 Myers MP, 1997, P NATL ACAD SCI USA, V94, P9052, DOI 10.1073/pnas.94.17.9052 Myers MP, 1998, P NATL ACAD SCI USA, V95, P13513, DOI 10.1073/pnas.95.23.13513 Reardon W, 2001, J MED GENET, V38, P820, DOI 10.1136/jmg.38.12.820 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P953 Talebizadeh Z, 2002, J Med Genet, V39, pe70, DOI 10.1136/jmg.39.11.e70 VOLKMAR FR, 1993, J AUTISM DEV DISORD, V23, P579, DOI 10.1007/BF01046103 Waite KA, 2002, AM J HUM GENET, V70, P829, DOI 10.1086/340026 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 Yonan AL, 2003, AM J HUM GENET, V73, P886, DOI 10.1086/378778 Zori RT, 1998, AM J MED GENET, V80, P399, DOI 10.1002/(SICI)1096-8628(19981204)80:4<399::AID-AJMG18>3.0.CO;2-O NR 25 TC 268 Z9 281 PU B M J PUBLISHING 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 APR PY 2005 VL 42 IS 4 BP 318 EP 321 DI 10.1136/jmg.2004.024646 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 912JV UT WOS:000228074900006 PM 15805158 ER PT J AU Zimmerman, RK Wolfe, RM Fox, DE Fox, JR Nowalk, MP Troy, JA Sharp, LK AF Zimmerman, RK Wolfe, RM Fox, DE Fox, JR Nowalk, MP Troy, JA Sharp, LK TI Vaccine criticism on the World Wide Web SO JOURNAL OF MEDICAL INTERNET RESEARCH LA English DT Article DE vaccines; Internet; immunization; vaccine safety; vaccine criticism; anti-vaccine ID SAFETY CONCERNS; IMMUNIZATION; PERTUSSIS; CHILDREN; SITES; INTERNET; PARENTS; RISK; NEWS AB Background: The incidence of vaccine-preventable diseases is directly related to the number of unvaccinated children. Parents who refuse vaccination of their children frequently express concerns about vaccine safety. The Internet can influence perceptions about vaccines because it is the fastest growing source of consumer health information. However, few studies have analyzed vaccine criticism on the Web. Objective: The purposes of this paper are to examine vaccine criticism on the Internet and to analyze the websites in order to identify common characteristics and ethical allegations. Methods: A structured Web search was conducted for the terms "vaccine," "vaccination," "vaccinate:" and "anti-vaccination" using a metasearch program that incorporated 8 search engines. This yielded 1138 Web pages representing 750 sites. Two researchers reviewed the sites for inclusion/exclusion criteria, resulting in 78 vaccine-critical sites, which were then abstracted for design, content, and allegations. Results: The most common characteristic of vaccine-critical websites was the inclusion of statements linking vaccinations with specific adverse reactions, especially idiopathic chronic diseases such as multiple sclerosis, autism, and diabetes. Other common attributes (>= 70% of websites) were links to other vaccine-critical websites; charges that vaccines contain contaminants, mercury, or "hot lots" that cause adverse events; claims that vaccines provide only temporary protection and that the diseases prevented are mild; appeals for responsible parenting through education and resisting the establishment; allegations of conspiracies and cover-ups to hide the truth about vaccine safety; and charges that civil liberties are violated through mandatory vaccination. Conclusions: Vaccine-critical websites frequently make serious allegations. With the burgeoning of the Internet as a health information source, an undiscerning or incompletely educated public may accept these claims and refuse vaccination of their children. As this occurs, the incidence of vaccine-preventable diseases can be expected to rise. C1 Univ Pittsburgh, Sch Med, Dept Family Med & Clin Epidemiol, Pittsburgh, PA 15261 USA. Univ Pittsburgh, Grad Sch Publ Hlth, Dept Behav Sci & Community Hlth, Pittsburgh, PA USA. Northwestern Univ, Feinberg Sch Med, Dept Family Med, Chicago, IL 60611 USA. RP Zimmerman, RK (reprint author), Univ Pittsburgh, Sch Med, Dept Family Med & Clin Epidemiol, 3518 5th Ave, Pittsburgh, PA 15261 USA. 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Med. Internet Res. PD APR-JUN PY 2005 VL 7 IS 2 AR e17 DI 10.2196/jimr.7.2.e17 PG 8 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA 953VV UT WOS:000231110400008 PM 15998608 ER PT J AU Kosinovsky, B Hermon, S Yoran-Hegesh, R Golomb, A Senecky, Y Goez, H Kramer, U AF Kosinovsky, B Hermon, S Yoran-Hegesh, R Golomb, A Senecky, Y Goez, H Kramer, U TI The yield of laboratory investigations in children with infantile autism SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE infantile; autism; investigation; EEG; Fragile-X ID PERVASIVE DEVELOPMENTAL DISORDERS; EPILEPTIFORM REGRESSION; TUBEROUS SCLEROSIS; SPECTRUM DISORDERS; DYSPHASIC CHILDREN; CHILDHOOD AUTISM; EPILEPSY; PATTERNS; SPIKES AB Purpose: To evaluate the yield of laboratory investigations in infantile autism. Methods: We retrieved and evaluated the results of investigative procedures recorded in the medical files of autistic infants in four child developmental centers and two pediatric psychiatric outpatient clinics. Results: One-hundred and thirty-two infants were included in the study of whom 47 (36%) underwent autistic regression at an average age of 20 months. The investigative procedures included electroencephalogram (n = 132), neuroimaging (n = 70), genetic studies to detect Fragile-X (n = 59) and a metabolic workup (n = 53). Except for the molecular diagnosis that revealed Fragile-X syndrome in two children (3%), all other tests were negative. The two infants with the Fragile-X syndrome belonged to the non-regressive group. Conclusions: The only investigative study that contributed to the diagnosis of autistic infants was the molecular diagnosis detecting Fragile-X. 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Neural Transm. PD APR PY 2005 VL 112 IS 4 BP 587 EP 596 DI 10.1007/s00702-004-0198-8 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 910BW UT WOS:000227905400011 PM 15503196 ER PT J AU Seeman, C AF Seeman, C TI The autism book: Answers to your most pressing questions. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Libs, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Libs, Toledo, OH USA. CR ROBLEDO SJ, 2005, AUTISM BOOK ANSWERS NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 1 PY 2005 VL 130 IS 6 BP 113 EP 113 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 913CK UT WOS:000228127800211 ER PT J AU Geier, DA Geier, MR AF Geier, DA Geier, MR TI A two-phased population epidemiological study of the safety of thimerosal-containing vaccines: a follow-up analysis SO MEDICAL SCIENCE MONITOR LA English DT Article DE mercury; merthiolate; thimerasol; thiomersal; VAERS; VSD ID EVENT REPORTING SYSTEM; WHOLE-CELL PERTUSSIS; DEVELOPMENTAL DISORDERS; CHILDHOOD VACCINES; CAUSAL ASSOCIATION; UNITED-KINGDOM; AUTISM; MERCURY; PREVALENCE; EXPOSURE AB Background: Thimerosal is an ethylmercury-containing preservative in vaccines. Toxicokinetic studies have shown children received doses of mercury front thimerosal-containing vaccines (TCVs) that were in excess of safety guidelines. Previously, an ecological study showing a significant association between TCVs and neurodevelopmental disorders (NDs) in the US was published in this journal. Material/Methods: A two phased population-based epidemiological study was undertaken. Phase one evaluated reported NDs to the Vaccine Adverse Event Reporting System (VAERS) following thimerosal-containing Diphtheria-Tetanus-acellular-Pertussis (DTaP) vaccines in comparison to thimerosal-free DTaP vaccines administered front 1997 through 2001. Phase two evaluated the automated Vaccine Safety Datalink (VSD) for cumulative exposures to mercury from TCVs at 1-, 2-, 3-, and 6-months-of-age for infants born from 1992 through 1997 and the eventual risk of developing NDs. Results: Phase one showed significantly increased risks for autism, speech disorders, mental retardation, personality disorders, and thinking abnomalities reported to VAERS following thimerosal-containing DTaP vaccines in comparison to thimerosal-free DTaP vaccines. Phase two showed significant associations between cumulative exposures to thimerosal and the following types of NDs: unspecified developmental delay, tics, attention deficit disorder (ADD), language delay, speech delay, and neurodevelopmental delays in general. Conclusions: This study showed that exposure to mercury from TCVs administered in the US was a consistent significant risk factor for the development of NDs. It is clear from these data and other recent publications linking TCVs with NDs that additional ND research should be undertaken in tire context of evaluating mercury-associated exposures and thimerosal-free vaccines should be made available. RP Geier, MR (reprint author), 14 Redgate Ct, Silver Spring, MD 20905 USA. 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RP Sommer, SS (reprint author), City Hope Natl Med Ctr, Dept Mol Genet, 1500 E Duarte Rd, Duarte, CA 91010 USA. 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We tested this hypothesis in two separate studies using eye tracking while measuring functional brain activity during facial discrimination tasks in individuals with autism and in typically developing individuals. Activation in the fusiform gyrus and amygdala was strongly and positively correlated with the time spent fixating the eyes in the autistic group in both studies, suggesting that diminished gaze fixation may account for the fusiform hypoactivation to faces commonly reported in autism. In addition, variation in eye fixation within autistic individuals was strongly and positively associated with amygdala activation across both studies, suggesting a heightened emotional response associated with gaze fixation in autism. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Univ Wisconsin, Waisman Lab Brain Imaging & Behav, Madison, WI 53705 USA. Univ Wisconsin, Dept Psychol, Madison, WI 53706 USA. Univ Wisconsin, Dept Psychiat, Madison, WI 53719 USA. 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METHODS: The influence of maternal testosterone on behaviour of 23 day old male and female offsprings was studied in a 20-minute open field test. A total of 9 behavioural events were compared between a control (male n=12, female n=8) and a testosterone group (male n=9, female n=9). Dynamics and patterns of association of these behavioural events were analyzed. The testosterone group was prenatally exposed to testosterone (a single intramuscular injection of 2.5 mg testosteroni isobutyras on gestation day 11). RESULTS: Male offsprings exposed prenatally to testosterone displayed significantly high levels of ambulation (P < 0.05), sniffing (P < 0.01), sniffing the air (P < 0.05), urination (P < 0.05) and significantly lower level of vocalization (P < 0.05) than control. Female offsprings exposed prenatally to testosterone displayed significantly higher level of sniffing the air (P < 0.05) than control. Significant differences in the dynamics of habituation process were registered only in the group of male. They were from 5 to 10 min in ambulation (P < 0.05), from 10 to 15 min in sniffing (P < 0.05) and vocalization (P < 0.05), from 10 to 15 min and from 15 to 20 min in sniffing the air (P < 0.05) and from 0 to 5 min in defecation (P < 0.05) and urination (P < 0.01). CONCLUSION: Our results suggest that maternal testosterone may influence especially male postnatal open field strategies. C1 Comenius Univ, Fac Nat Sci, Dept Anim Physiol & Ethol, Bratislava 84215, Slovakia. RP Krskova, L (reprint author), Comenius Univ, Fac Nat Sci, Dept Anim Physiol & Ethol, Mlynska Dolina B-2, Bratislava 84215, Slovakia. 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Lett. PD APR PY 2005 VL 26 IS 2 BP 121 EP 124 PG 4 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 928GZ UT WOS:000229260800006 PM 15855882 ER PT J AU Palfrey, JS Tonniges, TF Green, M Richmond, J AF Palfrey, JS Tonniges, TF Green, M Richmond, J TI Introduction: Addressing the millennial morbidity - The context of community pediatrics SO PEDIATRICS LA English DT Editorial Material ID HEALTH-CARE NEEDS; UNITED-STATES; PREVALENCE; CHILDREN; AUTISM C1 Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Amer Acad Pediat, Elk Grove Village, IL USA. Indiana Univ, Sch Med, Indianapolis, IN USA. RP Palfrey, JS (reprint author), Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA. 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PD APR PY 2005 VL 26 IS 4 BP 131 EP 140 DI 10.1542/pir.26-4-131 PG 10 WC Pediatrics SC Pediatrics GA 968IK UT WOS:000232155300003 PM 15805236 ER PT J AU Kurita, H Koyama, T Osada, H AF Kurita, H Koyama, T Osada, H TI Comparison of childhood disintegrative disorder and disintegrative psychosis not diagnosed as childhood disintegrative disorder SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE childhood disintegrative disorder; diagnosis; disintegrative psychosis; pervasive developmental disorder; regression ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM RATING-SCALE; FOLLOW-UP; INFANTILE-AUTISM; SPEECH LOSS; CHILDREN; VALIDITY; REGRESSION; ONSET; CARS AB To clarify the difference of Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV) childhood disintegrative disorder (CDD) from International Classification of Diseases (9th revision; ICD-9) disintegrative psychosis (DP), 10 CDD children (mean age, 7.7 years) and 18 DP children (mean, 6.5 years) not diagnosed as CDD divided into DSM-IV autistic disorder (DP-AD; n = 11) and pervasive developmental disorders not otherwise specified (DP-PDDNOS; n = 7) were compared on 31 variables not directly related to the normalcy before regression. The CDD, DP-AD, and DP-PDDNOS groups did not differ significantly in 28 variables. The DP-PDDNOS group met significantly a smaller number of items in criterion A of DSM-IV autistic disorder criteria than the CDD and DP-AD groups, both of which did not differ significantly in this respect. The CDD group tended to be more abnormal in auditory responsiveness and verbal communication than the DP-PDDNOS group. While CDD is distinct from DP-PDDNOS, its validity apart from AD with regression remains to be studied. C1 Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Bunkyo Ku, Tokyo 1130033, Japan. Senshu Univ, Fac Law, Tokyo, Japan. RP Kurita, H (reprint author), Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. 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Neurosci. PD APR PY 2005 VL 59 IS 2 BP 200 EP 205 DI 10.1111/j.1440-1819.2005.01358.x PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 909YJ UT WOS:000227896300015 PM 15823168 ER PT J AU Palmen, SJMC Pol, HEH Kemner, C Schnack, HG Durston, S Lahuis, BE Kahn, RS Van Engeland, H AF Palmen, SJMC Pol, HEH Kemner, C Schnack, HG Durston, S Lahuis, BE Kahn, RS Van Engeland, H TI Increased gray-matter volume in medication-naive high-functioning children with autism spectrum disorder SO PSYCHOLOGICAL MEDICINE LA English DT Article ID BRAIN VOLUME; SCHIZOPHRENIC-PATIENTS; DIAGNOSTIC INTERVIEW; HEAD CIRCUMFERENCE; INFANTILE-AUTISM; WHITE-MATTER; MR-IMAGES; INDIVIDUALS; ADOLESCENCE; CHILDHOOD AB Background. To establish whether high-functioning children with autism spectrum disorder (ASD) have enlarged brains in later childhood, and if so, whether this enlargement is confined to the gray and/or to the white matter and whether it is global or more prominent in specific brain regions. Method. Brain MRI scans were acquired from 21 medication-naive, high-functioning children with ASD between 7 and 15 years of age and 21 comparison subjects matched for gender, age, IQ, height, weight, handedness, and parental education, but not pubertal status. Results. Patients showed a significant increase of 6% in intracranium, total brain, cerebral gray matter, cerebellum, and of more than 40% in lateral and third ventricles compared to controls. The cortical gray-matter volume was evenly affected in all lobes. After correction for brain volume, ventricular volumes remained significantly larger in patients. Conclusions. High-functioning children with ASD showed a global increase in gray-matter, but not white-matter and cerebellar volume, proportional to the increase in brain volume, and a disproportional increase in ventricular volumes, still present after correction for brain volume. Advanced pubertal development in the patients compared to the age-matched controls may have contributed to the findings reported in the present study. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, NL-3584 CX Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Psychiat, Rudolf Magnus Inst Neurosci, NL-3584 CX Utrecht, Netherlands. RP Palmen, SJMC (reprint author), Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, HP-A01-468,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. 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PD APR PY 2005 VL 35 IS 4 BP 561 EP 570 DI 10.1017/S0033291704003496 PG 10 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 959EK UT WOS:000231499700010 PM 15856726 ER PT J AU [Anonymous] AF [Anonymous] TI Primates may hold clues to autism and unfairness SO PSYCHOLOGIST LA English DT News Item NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD APR PY 2005 VL 18 IS 4 BP 195 EP 195 PG 1 WC Psychology, Multidisciplinary SC Psychology GA V44DU UT WOS:000202984200012 ER PT J AU Calhoun, SL Mayes, SD AF Calhoun, SL Mayes, SD TI Processing speed in children with clinical disorders SO PSYCHOLOGY IN THE SCHOOLS LA English DT Article ID ATTENTION-DEFICIT DISORDER; SLUGGISH COGNITIVE TEMPO; TRAUMATIC HEAD-INJURY; WISC-III; LEARNING-DISABILITIES; ACADEMIC-ACHIEVEMENT; HYPERACTIVITY DISORDER; STRATEGY INSTRUCTION; READING DISABILITIES; SUBTEST PATTERNS AB The Processing Speed Index (PSI) was first introduced on the Wechsler Intelligence Scale, Third Edition (WISC-III; D. Wechsler, 1991), and little is known about its clinical significance. In a referred sample (N = 980), children with neurological disorders (ADHD, autism, bipolar disorder, and LD) had mean PSI and Freedom from Distractibility Index (FDI) scores that were below the group mean IQ and lower than Verbal Comprehension (VCI) and Perceptual Organization (POI). For these groups, Coding was lower than Symbol Search. The majority of these children had learning, attention, writing, and processing speed weaknesses. This pattern was not found in the other clinical groups. For children with depression, only PSI was low. Children with anxiety disorders, oppositional -defiant disorder, and mental retardation had no PSI weakness. PSI and POI were both low in children with traumatic brain injury and spina bifida. Implications for a revision of the WISC-III (WISC-IV; D. Wechsler, 2003) are discussed. (c) 2005 Wiley Periodicals, Inc. C1 Milton S Hershey Med Ctr, Dept Psychiat, Hershey, PA 17033 USA. Penn State Univ, Coll Med, University Pk, PA 16802 USA. RP Mayes, SD (reprint author), Milton S Hershey Med Ctr, Dept Psychiat, H073,POB 850, Hershey, PA 17033 USA. 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Schools PD APR PY 2005 VL 42 IS 4 BP 333 EP 343 DI 10.1002/pits.20067 PG 11 WC Psychology, Educational SC Psychology GA 912BT UT WOS:000228052800001 ER PT J AU Bruning, N Konrad, K Herpertz-Dahlmann, B AF Bruning, N Konrad, K Herpertz-Dahlmann, B TI Relevance and results of theory of mind research for autism and other psychiatric disorders SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Review DE autism; children and adolescents; Theory of Mind; false-belief task ID HIGH-FUNCTIONING CHILDREN; TEST-RETEST RELIABILITY; FUSIFORM FACE AREA; FALSE-BELIEF TASKS; ASPERGER-SYNDROME; INDIVIDUALS; SCHIZOPHRENIA; RECOGNITION; ABILITIES; COGNITION AB Relevance mid results of Theory of Mind research for autism and other psychiatric disorders Objectives: Disorders of the autistic spectrum are basically characterised by a triad of symptoms: dysfunction of social interaction, communication deficits, and stereotyped behaviour patterns and interests. One of the most prominent approaches to explaining these abnormalities is the "Theory of Mind" (Baron-Cohen et al, 1885). Methods: The present review discusses and critically examines the ongoing research and recapitulates the essential findings of the last tell years, focussing on their methodological quality and utility to explain other psychiatric disorders. Results: Despite considerable research efforts in this field, the existing concepts do not constitute a consistent framework for analysing the development of autism spectrum disorders. Conclusions: Future research should aim to verify the impact of the existing theoretical models and to emphasise the similarities of the different concepts in order to gain specific information about potential causal factors of autism. C1 Univ Klinikum Aachen, Klin Kinder & Jugendpsychiat & Psychotherapie, DE-52074 Aachen, Germany. RP Herpertz-Dahlmann, B (reprint author), Univ Klinikum Aachen, Klin Kinder & Jugendpsychiat & Psychotherapie, Neuenhofer Weg 21, DE-52074 Aachen, Germany. 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Kinder-und Jugendpsy. Psychother. PD APR PY 2005 VL 33 IS 2 BP 77 EP 88 DI 10.1024/1422-4917.33.2.77 PG 12 WC Psychiatry SC Psychiatry GA 921YM UT WOS:000228802100002 PM 15900802 ER PT J AU Cline, H AF Cline, H TI Synaptogenesis: A balancing act between excitation and inhibition SO CURRENT BIOLOGY LA English DT Editorial Material ID SYNAPSE FORMATION; AUTISM; POTENTIATION; NEUROLIGINS; PLASTICITY; GABA AB Recent studies have implicated a number of membrane-associated proteins, including the signaling pair neuroligin and beta-neurexin, in synapse formation, suggesting that they govern the ratio of inhibitory and excitatory synapses on CNS neurons. These findings, together with data indicating that the genes encoding neuroligin and PSD95 are altered in autism patients, suggest that a molecular understanding of complex neurological diseases is within reach. C1 Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. 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Biol. PD MAR 29 PY 2005 VL 15 IS 6 BP R203 EP R205 DI 10.1016/j.cub.2005.03.010 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 914EQ UT WOS:000228208400012 PM 15797012 ER PT J AU Moretti, P Sahoo, T Hyland, K Bottiglieri, T Peters, S del Gaudio, D Roa, B Curry, S Zhu, H Finnell, RH Neul, JL Ramaekers, VT Blau, N Bacino, CA Miller, G Scaglia, F AF Moretti, P Sahoo, T Hyland, K Bottiglieri, T Peters, S del Gaudio, D Roa, B Curry, S Zhu, H Finnell, RH Neul, JL Ramaekers, VT Blau, N Bacino, CA Miller, G Scaglia, F TI Cerebral folate deficiency with development delay, autism, and response to folinic acid SO NEUROLOGY LA English DT Article ID CEREBROSPINAL-FLUID AB The authors describe a 6-year-old girl with developmental delay, psychomotor regression, seizures, mental retardation, and autistic features associated with low CSF levels of 5-methyltetrahydrofolate, the biologically active form of folates in CSF and blood. Folate and B12 levels were normal in peripheral tissues, suggesting cerebral folate deficiency. Treatment with folinic acid corrected CSF abnormalities and improved motor skills. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Baylor Univ, Med Ctr, Inst Metab Dis, Dallas, TX USA. Texas A&M Univ, Hlth Sci Ctr, Inst Biosci & Technol, Houston, TX USA. Texas A&M Univ, Hlth Sci Ctr, Ctr Environm & Genet Med, Houston, TX USA. Univ Hosp Aachen, Dept Pediat Neurol, Aachen, Germany. Univ Hosp Aachen, Dept Pediat, Aachen, Germany. Sophia Childrens Univ Hosp, Div Clin Chem & Biochem, Zurich, Switzerland. RP Scaglia, F (reprint author), Baylor Coll Med, Dept Mol & Human Genet, 1 Baylor Pl, Houston, TX 77030 USA. EM fscaglia@bcm.tmc.edu CR American Psychiatric Association Task Force on DSM-IV, 2000, DIAGN STAT MAN MENT, V4th Blau N, 2003, NEUROLOGY, V61, P642 Hilton JE, 2003, HUM MUTAT, V22, P67, DOI 10.1002/humu.10236 HYLAND K, 1992, PTERIDINES, V3, P149 Luhby AL, 1965, J PEDIATR, V67, P1052, DOI 10.1016/S0022-3476(65)82179-5 Peters SU, 2004, AM J MED GENET A, V128A, P110, DOI 10.1002/ajmg.a.30065 Ramaekers VT, 2002, NEUROPEDIATRICS, V33, P301, DOI 10.1055/s-2002-37082 Ramaekers VT, 2003, NEUROLOGY, V61, P506 ROSENBLATT DS, 2000, INHERITED DISORDERS WEVERS RA, 1994, J NEUROL NEUROSUR PS, V57, P223, DOI 10.1136/jnnp.57.2.223 NR 10 TC 58 Z9 59 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 22 PY 2005 VL 64 IS 6 BP 1088 EP 1090 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 908RH UT WOS:000227806600037 PM 15781839 ER PT J AU Moretti, P Peters, S Hyland, K Bottiglieri, T Hopkin, R Peach, E Roa, B Bacino, C Scaglia, F AF Moretti, P Peters, S Hyland, K Bottiglieri, T Hopkin, R Peach, E Roa, B Bacino, C Scaglia, F TI Autism spectrum manifestations in cerebral folate deficiency SO NEUROLOGY LA English DT Meeting Abstract CT 57th Annual Meeting of the American-Academy-of-Neurology CY APR 09-19, 2005 CL Miami Beach, FL SP Amer Acad Neurol NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 22 PY 2005 VL 64 IS 6 SU 1 BP A434 EP A434 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 909DY UT WOS:000227841502484 ER PT J AU Zhang, H Zhou, M Zhou, P Chen, S AF Zhang, H Zhou, M Zhou, P Chen, S TI High levels of nitric oxide in both serum and cerebrospinal fluid in individuals with autism SO NEUROLOGY LA English DT Meeting Abstract CT 57th Annual Meeting of the American-Academy-of-Neurology CY APR 09-19, 2005 CL Miami Beach, FL SP Amer Acad Neurol NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 22 PY 2005 VL 64 IS 6 SU 1 BP A342 EP A342 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 909DY UT WOS:000227841502181 ER PT J AU Graham, JM Rosner, B Dykens, E Visootsak, J AF Graham, JM Rosner, B Dykens, E Visootsak, J TI Behavioral features of CHARGE syndrome (Hall-Hittner syndrome) comparison with Down syndrome, Prader-Willi syndrome, and Williams syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE coloboma; choanal atresia; ear anomalies; deafness; facial palsy; heart defect; CHARGE association; Hall-Hittner syndrome; behavior; autism; dual sensory impairment; deafness; blindness ID MULTIPLE ANOMALIES; MENTAL-RETARDATION; CHOANAL ATRESIA; HEART-DISEASE; ASSOCIATION; CHILDREN AB CHARGE syndrome, or Hall-Hitner syndrome (HHS), has been delineated as a common syndrome that includes coloboma, choanal atresia, cranial nerve dysfunction (particularly asymmetric facial palsy and neurogenic, swallowing problems), characteristic ear abnormalities, deafness with hypoplasia of the cochlea and semicircular canals, genital hypoplasia, and variable heart defects, orofacial clefting, tracheo-esophageal fistula, renal anomalies, thymic/parathyroid hypoplasia, spine anomalies, short broad neck with sloping shoulders, and characteristic facial features. We conducted behavioral and personality assessments in 14 boys with HHS syndrome aged 6-21 years, and compared their characteristics with similar data from 20 age-matched boys with Down syndrome (DS), 17 boys with Prader-Willi syndrome (PWS), and 16 boys with Williams syndrome (WS). We used the Reiss Profile of Fundamental Goals and Motivation Sensitivities, the Achenbach Child Behavior Checklist (CBCL), and the Aberrant Behavior Checklist (ABC). All 14 boys with HHS were legally deaf, and 10 of the 14 were also legally blind. In comparison these other syndromes, boys with HHS had behavior that resembled autistic spectrum disorder. They were socially withdrawn, lacked interest in social contact, and manifested reduced seeking of attention from others, with hyperactivity and a need to maintain order. Though the boys with HHS showed decreased social interaction, they were not as socially impaired as in classic autism. Their language was delayed due to dual sensory impairment, cranial nerve deficits, and chronic medical problems, but their language style was not abnormal (no echolalia or jargon, no scripted phrases, and no pronoun reversal). Boys with HSS appeared frustrated, but they were not aggressive, or at risk for delinquency, manifesting few stereotypic behaviors or unusual preoccupations. They did not have a restricted repertoire of activities and interests. Their behavioral features appeared to be due to dual sensory impairment affecting hearing and vision, rather than to primary autistic spectrum disorder, but successful remediation requires similar educational interventions, which are discussed herein. (C) 2005 Wiley-Liss, Inc. C1 Univ Calif Los Angeles, Dept Pediat,Med Genet Birth Defects Ctr, Steven Spielberg Pediat Res Ctr,Ahmanson Pediat Ct, SHAREs Child Disabil Ctr,Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. Univ Calif Los Angeles, David Geffen Sch Med, Inst Neuropsychiat, Dept Psychiat, Los Angeles, CA 90048 USA. Vanderbilt Univ, John F Kennedy Ctr Res Human Dev, Nashville, TN USA. Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA 30322 USA. RP Graham, JM (reprint author), Cedars Sinai Med Ctr, 444 S San Vicente Blvd,Suite 1001, Los Angeles, CA 90048 USA. EM john.graham@cshs.org CR Achenbach TM, 1991, MANUAL CHILD BEHAV C Aman M., 1986, ABERRANT BEHAV CHECK Amiel J, 2001, AM J MED GENET, V99, P124, DOI 10.1002/1096-8628(20010301)99:2<124::AID-AJMG1114>3.0.CO;2-9 BERNSTEIN V, IN PRESS AM J MED GE BEST C, 1983, BRIT J VISUAL IMPAIR, V1, P11, DOI 10.1177/026461968300100205 Blake KD, 1998, CLIN PEDIATR, V37, P159, DOI 10.1177/000992289803700302 BLAKE KD, 1993, CHILD CARE HLTH DEV, V19, P395, DOI 10.1111/j.1365-2214.1993.tb00744.x BLAKE KD, 1990, ARCH DIS CHILD, V65, P217 BOND D, 1986, SENSORY IMPAIRMENTS BROWN D, 2004, IN PRESS AM J MED GE DAVENPORT SLH, 1986, INT J PEDIATR OTORHI, V12, P137, DOI 10.1016/S0165-5876(86)80071-4 Dykens EM, 1997, AM J MENT RETARD, V102, P228, DOI 10.1352/0895-8017(1997)102<0228:MBICWP>2.0.CO;2 FOX AM, 1983, P 1 CAN C ED DEV DEA GOLDSON E, 1986, AM J DIS CHILD, V140, P918 Graham JM, 2001, AM J MED GENET, V99, P120, DOI 10.1002/1096-8628(2000)9999:999<00::AID-AJMG1132>3.0.CO;2-J GUYOT JP, 1987, ARCH OTOLARYNGOL, V113, P321 HALL BD, 1979, J PEDIATR-US, V95, P395, DOI 10.1016/S0022-3476(79)80513-2 HARTSHORNE TS, 2004, IN PRESS AM J MED GE HARVEY AS, 1991, AM J MED GENET, V39, P48, DOI 10.1002/ajmg.1320390112 HITTNER HM, 1979, J PEDIAT OPHTH STRAB, V16, P122 ISSEKUTZ KA, 2004, IN PRESS INCIDENCE P Lalani SR, 2003, AM J MED GENET A, V118A, P260, DOI 10.1002/ajmg.a.20002 McInnes JM, 1982, DEAF BLIND INFANTS C Mitchell J A, 1985, J Med Syst, V9, P425, DOI 10.1007/BF00992578 NICHOLAS J, 2004, IN PRESS AM J MED GE PAGON RA, 1981, J PEDIATR-US, V99, P223, DOI 10.1016/S0022-3476(81)80454-4 Reiss S, 1998, PSYCHOL ASSESSMENT, V10, P97, DOI 10.1037//1040-3590.10.2.97 SALEMHARTSCHORN.N, 2004, IN PRESS AM J MED GE Sanlaville D, 2002, CLIN GENET, V61, P135, DOI 10.1034/j.1399-0004.2002.610208.x SMITH IM, 2004, IN PRESS AM J MED GE SOURIAU J, 2004, IN PRESS AM J MED GE Stromland K., 2003, Birth Defects Research, V67, P316 Tellier AL, 1998, AM J MED GENET, V76, P402, DOI 10.1002/(SICI)1096-8628(19980413)76:5<402::AID-AJMG7>3.0.CO;2-O THELIN J, 2004, IN PRESS AM J MED GE VANDIJK J, 2004, IN PRESS AM J MED GE VISSERS LEL, 2004, MUTATIONS NEW MEMBER Wiener-Vacher SR, 1999, ARCH OTOLARYNGOL, V125, P342 WILLIAMS G, 2004, IN PRESS J AM MED GE NR 38 TC 24 Z9 24 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD MAR 15 PY 2005 VL 133A IS 3 BP 240 EP 247 DI 10.1002/ajmg.a.30543 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 901DT UT WOS:000227263900004 PM 15637708 ER PT J AU Smith, IM Nichols, SL Issekutz, K Blake, K AF Smith, IM Nichols, SL Issekutz, K Blake, K TI Behavioral profiles and symptoms of autism in CHARGE syndrome: Preliminary Canadian epidemiological data SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE CHARGE syndrome; Canadian Pediatric Surveillance Program (CPSP); coloboma; choanal atresia; deafness; visual impairment; autism; behavior; development ID PERVASIVE DEVELOPMENTAL DISORDERS; CONGENITALLY BLIND-CHILDREN; SPECTRUM DISORDERS; MULTIPLE ANOMALIES; CHOANAL ATRESIA; HEART-DISEASE; ASSOCIATION; QUESTIONNAIRE; MALFORMATIONS; INDIVIDUALS AB Individuals with CHARGE syndrome were identified through the Canadian Pediatric Surveillance Program (CPSP). From this population-based cohort (n = 78), we present data on developmental and behavioral characteristics for the first 13 individuals (eight males, five females) for whom assessments are complete. Standardized parent questionnaires on development and behavior were followed by a structured telephone interview, with a specific emphasis on symptoms of autistic spectrum disorder (ASD). Preliminary results confirm that individuals with CHARGE syndrome have relatively low adaptive behavior skills, motor impairments being particularly significant. Most individuals did not present with significant behavior problems; however, evidence of ASD symptoms was judged to be moderate to strong in six of the ten children who were above the age of 4-5 years. Results are discussed with reference to the challenges inherent in the diagnosis of autism in individuals with sensory impairments, and to the implications for understanding the etiology of CHARGE syndrome and of ASD. (C) 2005 Wiley-Liss, Inc. C1 Dalhousie Univ, Dept Pediat, Halifax, NS, Canada. Dalhousie Univ, Dept Psychol, Halifax, NS, Canada. Dalhousie Univ, Fac Med, Halifax, NS, Canada. RP Smith, IM (reprint author), IWK Hlth Ctr, POB 9700, Halifax, NS B3K 6R8, Canada. 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J. Med. Genet. A PD MAR 15 PY 2005 VL 133A IS 3 BP 248 EP 256 DI 10.1002/ajmg.a.30544 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 901DT UT WOS:000227263900005 PM 15688419 ER PT J AU Hartshorne, TS Grialou, TL Parker, KR AF Hartshorne, TS Grialou, TL Parker, KR TI Autistic-like behavior in CHARGE syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE CHARGE; autism; deafblind; rubella; behavior ID DISORDERS; CHECKLIST; VALIDITY; CHILDREN AB Children with CHARGE syndrome frequently exhibit moderate to severe behavior difficulties, and are often diagnosed with obsessive-compulsive disorder, attention deficit disorder, Tourette syndrome, and autism. Hartshorne and Cypher (2004) surveyed parents of 100 children with CHARGE worldwide and confirmed the prevalence of behaviors that are associated with these disorders. They also found behaviors that could be described as typical of persons who are deafblind. The present study examined whether the autistic-like behaviors of children with CHARGE are more similar to those of children who are deafblind, to those of children who are autistic or are unique to CHARGE. Surveys including the Autism Behavior Checklist (ABC) were mailed to families of 204 children with CHARGE, and 160 usable surveys were returned (78%). Total scores on the ABC for children with CHARGE were significantly different from the norms for those with autism, and those who were deafblind. However, the variance for CHARGE was larger than for the normative groups, and 27.5% of those with CHARGE could be classified as autistic. The pattern of subscale scores for those with CHARGE differed from the other normative groups. (C) 2005 Wiley-Liss, Inc. C1 Cent Michigan Univ, Dept Psychol, Mt Pleasant, MI 48859 USA. RP Hartshorne, TS (reprint author), Cent Michigan Univ, Dept Psychol, Mt Pleasant, MI 48859 USA. EM tim.hartshorne@cmich.edu CR BROWN D, 2005, IN PRESS AM J MED GE DENNO LS, 1997, 3 INT CHARGE SYNDROM Eaves RC, 2000, PSYCHOL SCHOOLS, V37, P311, DOI 10.1002/1520-6807(200007)37:4<323::AID-PITS2>3.0.CO;2-S Fernell E, 1999, DEV MED CHILD NEUROL, V41, P270, DOI 10.1017/S0012162299000572 Hartshorne TS, 2004, MENT HLTH ASPEC DEV, V7, P41 Kabot S, 2003, PROF PSYCHOL-RES PR, V34, P26, DOI 10.1037/0735-7028.34.1.26 KAHN N, 1990, THESIS OHIO STATE U KATES L, 1981, VIEWPOINTS TEACHING, V57, P54 Krug DA, 1993, AUTISM SCREENING INS LENSKE PJ, 1980, J SPEC EDUC, V17, P86 LEWIS C, 2001, ED PSYCHOL PRACT, V17, P71 SALEMHARTSHORNE N, 2005, IN PRESS AM J MED GE Salem-Hartshorne N, 2004, J EARLY INTERVENTION, V26, P292, DOI 10.1177/105381510402600405 SISSON LA, 1993, BEHAV THER, V24, P553, DOI 10.1016/S0005-7894(05)80318-1 STURMEY P, 1992, J AUTISM DEV DISORD, V22, P321, DOI 10.1007/BF01058159 THELIN JW, 2005, IN PRESS AM J MED GE VANDIJK J, 1991, PERSONS HANDICAPPED VANHASSELT VB, 1989, BEHAV MODIF, V13, P257, DOI 10.1177/01454455890132007 WADDEN NPK, 1991, J AUTISM DEV DISORD, V21, P529, DOI 10.1007/BF02206875 NR 19 TC 24 Z9 24 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD MAR 15 PY 2005 VL 133A IS 3 BP 257 EP 261 DI 10.1002/ajmg.a.30545 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 901DT UT WOS:000227263900006 PM 15637726 ER PT J AU Lauger, K Cornelius, N Keedy, W AF Lauger, K Cornelius, N Keedy, W TI Behavioral features of CHARGE syndrome: Parents' perspectives of three children with CHARGE syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE CHARGE syndrome; behavior; deafblindness; autism; cortical visual impairment; executive function; OCD; limb apraxia; immune system; language impairment; metallothionein AB As the population first diagnosed with CHARGE Syndrome has aged, information has emerged about specific behavioral features of this syndrome. Once the medical features are managed, it is the behavioral features that interfere with our children's ability to form reciprocal relationships, to gain formal communication skills, to make the educational gains they are cognitively capable of, and to ultimately care for themselves. In telling the informal case studies of our children, we hope their behavioral commonalities, in spite of their medical and educational differences, will be apparent as well as the complexity of the multiple types of behavior observed. We remain hopeful that answers can be found that will help our children and our families cope with this very debilitating feature of CHARGE. (C) 2005 Wiley-Liss, Inc. C1 Arizona Deafblind Project, Tucson, AZ 85754 USA. Except Family Resource Ctr, San Diego, CA USA. Parent Links Program, San Diego, CA USA. RP Lauger, K (reprint author), Arizona Deafblind Project, POB 87010, Tucson, AZ 85754 USA. EM klauger@earthlink.net CR ALSOP L, 2000, INTERVENER EARLY INT ARWOOD EL, 1983, PRAGMATICISM THEORY Frost L., 2002, PICTURE EXCHANGE COM, V2nd LOVAAS OI, 1989, J BEHAV THER EXP PSY, V20, P17 RATNER V, 1994, UNDERSTANDING LANGUA, P330 WALSH WJ, 1996, BIOCH INDIVIDUALITY WALSH WJ, 2001, METALLOTHIONEIN AUTI NR 7 TC 3 Z9 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD MAR 15 PY 2005 VL 133A IS 3 BP 291 EP 299 DI 10.1002/ajmg.a.30557 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 901DT UT WOS:000227263900012 PM 15651089 ER PT J AU Stromland, K Sjogreen, L Johansson, M Joelsson, BME Miller, M Danielsson, S Billstedt, E Gillberg, C Jacobsson, C Norinder, JA Granstrom, G AF Stromland, K Sjogreen, L Johansson, M Joelsson, BME Miller, M Danielsson, S Billstedt, E Gillberg, C Jacobsson, C Norinder, JA Granstrom, G TI CHARGE association in Sweden: Malformations and functional deficits SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE CHARGE association; CA; visual and hearing impairment; autism; assisted fertilization; etiology; timing ID CONGENITAL HEART-DISEASE; CHOANAL ATRESIA; THALIDOMIDE EMBRYOPATHY; MULTIPLE ANOMALIES; AUTISTIC BEHAVIOR; MOBIUS SEQUENCE; CHILDREN; INDIVIDUALS; DISORDERS; SPECTRUM AB CHARGE association (CA) consists of a non-random association of ocular coloboma (C), heart anomaly (H), atresia of choanae (A), retarded growth and/or development (R), genital hypoplasia (G), and ear anomalies and/or hearing impairment (E). A prospective multidisciplinary study of 31 Swedish patients with CA was undertaken in order to describe the associated malformations and functional deficits, find possible etiological factors and identify critical time periods for the maldevelopment. The clinical files were analyzed, the mothers answered a questionnaire on history of prenatal events, and a clinical evaluation of systemic findings, vision, hearing, balance, speech, oral and swallowing function, and neuropsychiatric function, especially autism, was performed. The most frequent physical abnormalities affected ears (90%), eyes (90%), brain (61%), heart (52%), retarded growth (48%), genitals (38%), choanae (35%), and facial nerve (32%). Sixty-one percent of the patients were visually impaired or blind, and 74% had hearing loss or deafness. Problems in balance, speech, and eating were common. Forty percent of the patients had autism/atypical autism, and 82% had developmental delay. Three children were born following assisted fertilization and two mothers had diabetes. The mothers reported infections, bleedings, and drug use during pregnancy. Analysis of possible critical time periods suggested that most malformations were produced early in pregnancy, mainly during post conceptual weeks 4, 5, and 6. A multidisciplinary approach is essential in the assessment and management of CA. (C) 2005 Wiley-Liss, Inc. C1 Sahlgrenska Univ Hosp, Dept Ophthalmol, Gothenburg, Sweden. Univ Gothenburg, Dept Odontol, Mun H Ctr, Gothenburg, Sweden. Sahlgrenska Univ Hosp, Gothenburg, Sweden. Skaraborg Hosp, Dept Pediat, Skovde, Sweden. Univ Illinois, Eye & Ear Infirm, Dept Ophthalmol & Visual Sci, Chicago, IL USA. Univ London, Dept Psychiat, St Georges Hosp Med Sch, London, England. Sahlgrenska Univ Hosp, Dept Otolaryngol, Gothenburg, Sweden. RP Stromland, K (reprint author), Sahlgrenska Univ Hosp, Dept Pediat Ophthalmol, Queen Silvia Childrens Hosp, SE-41685 Gothenburg, Sweden. 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Methods: The Social Responsiveness Scale (SRS), a quantitative measure of autistic traits, was completed on 285 pairs of twins (by maternal report) and on their parents (by spouse report). Results: Correlation for social impairment or competence between parents and their children and between spouses was on the order of 4. In families in which both parents scored in the upper quartile for social impairment on the SRS, mean SRS score of offspring was significantly elevated (effect size 1.5). Estimated assortative mating explained approximately 30% of the variation in parent SRS scores. Conclusions: Children from families in which both parents manifest subthreshold autistic traits exhibit a substantial shift in the distribution of their scores for impairment in reciprocal social behavior, toward the pathological end. 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Psychiatry PD MAR 15 PY 2005 VL 57 IS 6 BP 655 EP 660 DI 10.1016/j.biopsych.2004.12.014 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 906FO UT WOS:000227626200011 PM 15780853 ER PT J AU Thatcher, KN Peddada, S Yasui, DH LaSalle, JM AF Thatcher, KN Peddada, S Yasui, DH LaSalle, JM TI Homologous pairing of 15q11-13 imprinted domains in brain is developmentally regulated but deficient in Rett and autism samples SO HUMAN MOLECULAR GENETICS LA English DT Article DE CMV infection; CMV disease; CMV prophylaxis; CMV monitoring; kidney transplantation ID CPG-BINDING-PROTEIN; PRADER-WILLI SYNDROMES; DNA METHYLATION; GENE-EXPRESSION; INTERPHASE NUCLEI; MECP2 MUTATIONS; NEURODEVELOPMENTAL DISORDERS; INSITU HYBRIDIZATION; HUMAN NEUROBLASTOMA; CHROMOSOME DOMAINS AB Rett syndrome (RTT), caused by mutations in MECP2 (encoding methyl CpG binding protein 2), and Angelman syndrome (AS), caused by maternal deficiency of chromosome 15q11-13, are autism-spectrum neurodevelopmental disorders. MeCP2 is a transcriptional repressor of methylated genes, but MECP2 mutation does not directly affect the imprinted expression of genes within 15q11-13. We tested a potential role for MeCP2 in the homologous pairing of imprinted 15q11-13 alleles in human brain tissue and differentiated neurons by fluorescence in situ hybridization (FISH). FISH analysis of control cerebral samples demonstrated a significant increase in homologous pairing specific to chromosome 15 from infant to juvenile brain samples. Significant and specific deficiencies in the percentage of paired chromosome 15 alleles were observed in RTT, AS and autism brain samples when compared with normal controls. SH-SY5Y neuroblastoma cells also showed a significant and specific increase in the percentage of chromosome 15q11-13 paired alleles following induced differentiation in vitro. 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Single intracisternal administration of bisphenol A, p-octylphenol, nonylphenol, dibutylphthalate (DBP), dicyclohexylphthalate (DCHP). or diethythexylphthalate (DEHP) into 5-day-old male Wistar rats caused significant hyperactivity at 4-5 weeks of age. It was about 1.3- to 1.6-fold more active in the nocturnal phase than control rats. Based on DNA macroarray analyses of the midbrain at 8 weeks of age, the endocrine disruptors altered the levels of gene, expression of G protein-coupled receptors that were involved in not only dopaminergic neurotransduction but also many peptidergic neurotransduction. The gene expression of dopamine receptor DIA was decreased by nonylphenol, DBP. or DEHP by 0.23- to 0.4-fold, whereas that of dopamine D2 was increased by nonylphenol or DBP by 2- to 2.8-fold. It was notable that four of six endocrine disruptors tested, i.e. nonylphenol, DBP, DCHP. and DEHP largely downregulated the levels of gene expression of galanin receptor 2 by 0.11- to 0.28-fold. Bisphenol A, DBP or DCHP significantly decreased the levels of gene expression of dopamine transporter at 8 weeks more than 0.5-fold. Immunohistochemical analyses revealed that p-octylphenol impaired the immunoreactivity for tyrosine hydroxylase in substantia nigra pars compacta. Thus, endocrine disruptors caused hyperactivity in the rat, probably regulating the levels not only of gene expression but also of proteins of both G-protein-coupled receptors systems and dopaminergic neurotransduction system. (C) 2004 Elsevier B.V. All rights reserved. C1 Natl Inst Environm Studies, Endocrine Disruptors & Dioxin Res Projects, Tsukuba, Ibaraki 3058506, Japan. Natl Inst Adv Ind Sci & Technol, Tsukuba, Ibaraki 3058566, Japan. RP Ishido, M (reprint author), Natl Inst Environm Studies, Endocrine Disruptors & Dioxin Res Projects, Tsukuba, Ibaraki 3058506, Japan. 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Pept. PD MAR 15 PY 2005 VL 126 IS 1-2 BP 145 EP 153 DI 10.1016/j.regpep.2004.08.035 PG 9 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 889DO UT WOS:000226423900023 PM 15620428 ER PT J AU Coghlan, A AF Coghlan, A TI Ending MMR shots does not halt rise in autism SO NEW SCIENTIST LA English DT News Item NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD MAR 5 PY 2005 VL 185 IS 2489 BP 16 EP 16 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 903RY UT WOS:000227444500018 ER PT J AU James, SJ Melnyk, S Jernigan, S AF James, SJ Melnyk, S Jernigan, S TI Low plasma methionine, cysteine, and glutathione levels are associated with increased frequency of common polymorphisms affecting methylation and glutathione pathways in children with autism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Arkansas Med Sci, Little Rock, AR 72202 USA. NR 0 TC 1 Z9 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A51 EP A52 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700240 ER PT J AU Jyonouchi, H Zimmerman-Bier, B Ruby, A Geng, L AF Jyonouchi, H Zimmerman-Bier, B Ruby, A Geng, L TI Changes in cellular immune reactivity to cow rectangle fs milk protein (CMP) following dietary intervention in children with autism apectium disorders (ASD) and positive gastrointestinal (GI) symptoms SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunologists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Expt Therapeut, Int Union Physiol Sci C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07101 USA. NR 0 TC 0 Z9 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A501 EP A501 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703388 ER PT J AU Jyonouchi, H Geng, L Ruby, A Zimmerman-Bier, B AF Jyonouchi, H Geng, L Ruby, A Zimmerman-Bier, B TI Aberrant inflammatory responses by peripheral blood derived macrophages and dendritic cells in children with autism spectrum disorders (ASD) and apparent immune abnormalities SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunologists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Expt Therapeut, Int Union Physiol Sci C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07101 USA. NR 0 TC 0 Z9 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A501 EP A501 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703389 ER PT J AU Vojdani, A O'Bryan, T Green, JA McCandless, J Woeller, KN Cooper, EL AF Vojdani, A O'Bryan, T Green, JA McCandless, J Woeller, KN Cooper, EL TI Immune response to dietary proteins, gliadin and cerebellar peptides in children with autism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Immunosci Lab Inc, Beverly Hills, CA 90211 USA. Omnis Grp, Libertyville, IL 60048 USA. Evergreen Ctr, Oregon City, OR 97045 USA. BioHlth Diagnost, San Diego, CA 92106 USA. Univ Calif Los Angeles, Dept Neurobiol, Los Angeles, CA 90095 USA. NR 0 TC 0 Z9 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A83 EP A83 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700382 ER PT J AU Bonati, MT Finelli, P Giardino, D Gottardi, G Roberts, W Larizza, L AF Bonati, MT Finelli, P Giardino, D Gottardi, G Roberts, W Larizza, L TI Trisomy 15q25.2-qter in an autistic child: Genotype-phenotype correlations SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE autism; complex neurodevelopmental disorder; duplication; FISH mapping; non homologous end joining; pure trisomy 15q25.2-qter ID PERVASIVE DEVELOPMENTAL DISORDERS; CHROMOSOME; DUPLICATION; GENE; IDENTIFICATION; HYBRIDIZATION; OVERGROWTH; TETRASOMY; DUPLICONS; DNA AB We report on the case of a male child with autistic disorder, postnatal overgrowth, and a minor brain malformation. Karyotyping and fluorescent in situ hybridization (FISH) analysis showed the presence of an extra copy of the distal portion of chromosome 15q (15q25.2-qter) transposed to chromosome 15p leading to 15q25.2-qter pure trisomy. This karyotype-phenotype study further supports the evidence for a specific phenotype related to trisomy 15q25 or 26-qter and suggests that distal chromosome 15q may be implicated in specific behavioral phenotypes. (C) 2005 Wiley-Liss, Inc. C1 Ist Auxol Italiano, Clin Med Genet, Milan, Italy. Ist Auxol Italiano, Lab Med Cytogenet & Mol Genet, Milan, Italy. Univ Milan, Dept Genet & Biol Med Sci, Milan, Italy. Univ Toronto, Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. RP Larizza, L (reprint author), Dipartimento Biol & Genet Sci Med, Via Viotti 3-5, I-20133 Milan, Italy. 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J. Med. Genet. A PD MAR 1 PY 2005 VL 133A IS 2 BP 184 EP 188 DI 10.1002/ajmg.a.30503 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 900CX UT WOS:000227194100013 PM 15666303 ER PT J AU Bar-Shalita, T Goldstand, S Hahn-Markowitz, J Parush, S AF Bar-Shalita, T Goldstand, S Hahn-Markowitz, J Parush, S TI Typical children's responsivity patterns of the tactile and vestibular systems SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID SENSORY PROFILE; ELECTRODERMAL RESPONSES; YOUNG-CHILDREN; DISABILITIES; PERFORMANCE; DEFENSIVENESS; BEHAVIORS; STIMULI; AUTISM; SAMPLE AB OBJECTIVES. The purposes of this study were to investigate the responsivity patterns of typical 3- and 4-year-old Israeli children to tactile or vestibular stimulation, or both, and to examine whether differences in these patterns exist between them with respect to age and gender. METHOD. The study sample consisted of one hundred seventeen 3-year-old and one hundred forty-three 4-year-old healthy Israeli children (N = 260). Mothers of these children completed a comprehensive tactile and vestibular responsivity questionnaire. RESULTS. The subjects' tactile and vestibular responsivity scores were neither hyperresponsive nor hyporesponsive. In addition, neither age nor gender was found to significantly differentiate between respective participant groups for hypo- or hyperresponsive behaviors. CONCLUSION. Typical Israeli children can be characterized by moderate responsivities to tactile and vestibular stimulation. Responsivity to tactile and vestibular input was similar for 3- and 4-year-olds, across genders. C1 Hebrew Univ Jerusalem, Sch Occupat Therapy, Dept Occupat Therapy, IL-91905 Jerusalem, Israel. Univ Haifa, IL-31999 Haifa, Israel. Teachers Coll, Kefar Sava, Israel. 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J. Occup. Ther. PD MAR-APR PY 2005 VL 59 IS 2 BP 148 EP 156 PG 9 WC Rehabilitation SC Rehabilitation GA 906YA UT WOS:000227679700004 PM 15830614 ER PT J AU Wilkinson, KM AF Wilkinson, KM TI Disambiguation and mapping of new word meanings by individuals with intellectual/developmental disabilities SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID SEVERE MENTAL-RETARDATION; CATEGORY N3C PRINCIPLE; YOUNG-CHILDREN; LANGUAGE IMPAIRMENT; DOWN-SYNDROME; LEXICAL PRINCIPLES; BASIC LEVEL; ACQUISITION; COMMUNICATION; AUTISM AB Wilkinson and Green (1998) reported that differences in the procedure by which new words were introduced to learners with cognitive impairments significantly affected their accuracy in later tests of receptive understanding of word meanings. However, a limited sample and no control group rendered the data preliminary. Here, I replicated and extended the research. 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E., 1989, MONOGRAPHS SOC RES C, V54/3-4 MERRIMAN WE, 1991, CHILD DEV, V62, P1288, DOI 10.1111/j.1467-8624.1991.tb01606.x MERVIS CB, 1994, CHILD DEV, V65, P1646, DOI 10.2307/1131285 MERVIS CB, 1995, AM J MENT RETARD, V100, P231 RICE ML, 1989, AM PSYCHOL, V44, P149, DOI 10.1037/0003-066X.44.2.149 RICE ML, 1990, CHILD LANG, V7, P171 RICE ML, 1990, J SPEECH HEAR DISORD, V55, P33 RICE ML, 1994, J SPEECH HEAR RES, V37, P106 Romski MA, 1996, AM J MENT RETARD, V100, P391 TAGERFLUSBERG H, 1985, CHILD DEV, V56, P1167, DOI 10.1111/j.1467-8624.1985.tb00185.x TAGERFLUSBERG H, 1990, J AUTISM DEV DISORD, V20, P1, DOI 10.1007/BF02206853 TAGERFLUSBERG H, 1985, J EXP CHILD PSYCHOL, V40, P450, DOI 10.1016/0022-0965(85)90077-3 Tomasello M, 1996, J CHILD LANG, V23, P157 WEISMER SE, 1993, J SPEECH HEAR RES, V36, P1013 Weismer SE, 1996, J SPEECH HEAR RES, V39, P177 Wilkinson K. M., 2001, AUGMENTATIVE ALTERNA, V17, P120, DOI 10.1080/714043374 Wilkinson KM, 1997, J EXP CHILD PSYCHOL, V67, P115, DOI 10.1006/jecp.1997.2402 Wilkinson K.M., 1998, AUGMENTATIVE ALTERNA, V14, P162, DOI 10.1080/07434619812331278336 Wilkinson KM, 1998, MENT RETARD DEV D R, V4, P73, DOI 10.1002/(SICI)1098-2779(1998)4:2<73::AID-MRDD3>3.0.CO;2-Y Wilkinson KM, 2003, J APPL DEV PSYCHOL, V24, P739, DOI 10.1016/j.appdev.2003.09.006 WILKINSON KM, 2001, P ANN GATL C RES THE WILKINSON KM, 1998, PSYCHOL REC, V48, P406 NR 46 TC 3 Z9 3 PU AMER ASSOC MENTAL RETARDATION PI WASHINGTON PA 444 N CAPITOL ST, NW, STE 846, WASHINGTON, DC 20001-1512 USA SN 0895-8017 J9 AM J MENT RETARD JI Am. J. Ment. Retard. PD MAR PY 2005 VL 110 IS 2 BP 71 EP 86 DI 10.1352/0895-8017(2005)110<71:DAMONW>2.0.CO;2 PG 16 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 910HC UT WOS:000227920600001 PM 15762826 ER PT J AU Leask, J Leask, A Silove, N AF Leask, J Leask, A Silove, N TI Evidence for autism in folklore? SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article C1 Childrens Hosp, Natl Ctr Immunisat Res & Surveillance Vaccine Pre, Westmead, NSW, Australia. Univ Sydney, Sydney, NSW 2006, Australia. Wentworth Area Hlth Serv, Populat Hlth Unit, Penrith, NSW, Australia. Childrens Hosp, Child Dev Unit, Westmead, NSW, Australia. RP Leask, J (reprint author), Natl Ctr Immunisat Res & Surveillance Vaccine Pre, Locked Bag 4001, Westmead, NSW 2145, Australia. EM Juliel_3@chw.edu.au CR Ashliman D. L., 1997, CHANGELINGS Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Kanner L, 1943, NERV CHILD, V2, P217 Lingam R, 2003, ARCH DIS CHILD, V88, P666, DOI 10.1136/adc.88.8.666 WINDLING T, 2003, J MYTHIC ARTS SPR Wing L., 1997, AUTISM, V1, P13, DOI 10.1177/1362361397011004 YEATS WB, 1973, FAIRY FOLK TALES IRE NR 7 TC 4 Z9 4 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 MAR PY 2005 VL 90 IS 3 BP 271 EP 271 DI 10.1136/adc.2003.044958 PG 1 WC Pediatrics SC Pediatrics GA 903OQ UT WOS:000227435800017 PM 15723914 ER PT J AU Miller, E Andrews, N Grant, A Stowe, J Taylor, B AF Miller, E Andrews, N Grant, A Stowe, J Taylor, B TI No evidence of an association between MMR vaccine and gait disturbance SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID RUBELLA VACCINE; ADVERSE REACTIONS; MEASLES; MUMPS AB Background: MMR vaccine has been reported to cause gait disturbance, and this possible association has been claimed to support the MMR-causes-autism theory. Aims: To determine whether any association between gait disturbance and MMR vaccination exceeds the age related background rate of gait disturbance, using record linkage and self control case series analyses. Methods: MMR vaccination records were linked to hospital admission and general practitioner attendance data. An increased rate of gait problems with onset in various intervals in the 60 day period after MMR vaccination was looked for in children aged 12 to <24 months. Results: No evidence of an increased rate of hospital admission or general practice consultations for gait disturbance was found in the putative post-vaccination risk periods. Conclusions: This study provides no evidence for a causal association between MMR and gait disturbance. C1 Publ Hlth Lab Serv, Hlth Protect Agcy, Immunisat Div, London NW9 5EQ, England. Royal Free Hosp, London NW3 2QG, England. RP Miller, E (reprint author), Publ Hlth Lab Serv, Hlth Protect Agcy, Immunisat Div, 61 Colindale Ave, London NW9 5EQ, England. EM liz.miller@hpa.org.uk CR ANDREWS N, UNPUB THIOMERSAL EXP BENJAMIN CM, 1992, BRIT MED J, V304, P1075 *DEP HLTH, 1996, IMM INF DIS, P99 *DEP HLTH, 2002, NHS IMM STAT ENGL 20 Farrington CP, 1996, AM J EPIDEMIOL, V143, P1165 Miller E, 1998, Dev Biol Stand, V95, P235 NASH JQ, 1995, EPIDEMIOL INFECT, V114, P475 PELTOLA H, 1986, LANCET, V1, P939 PLESNER AM, 1995, LANCET, V345, P316, DOI 10.1016/S0140-6736(95)90302-X Plesner AM, 2000, ACTA PAEDIATR, V89, P58, DOI 10.1080/080352500750029077 Virtanen M, 2000, PEDIATRICS, V106, part. no., DOI 10.1542/peds.106.5.e62 Wakefield Andrew J, 2003, N Engl J Med, V348, P951 Wakefield Andrew J., 2000, Adverse Drug Reactions and Toxicological Reviews, V19, P265 NR 13 TC 11 Z9 12 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 MAR PY 2005 VL 90 IS 3 BP 292 EP 296 DI 10.1136/adc.2003.048165 PG 5 WC Pediatrics SC Pediatrics GA 903OQ UT WOS:000227435800024 PM 15723921 ER PT J AU Stein, MT AF Stein, MT TI Repetitive movements are not seen only in children with autism SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Editorial Material CR Mahone EM, 2004, J PEDIATR-US, V145, P391, DOI 10.1016/j.jpeds.2004.06.014 NR 1 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD MAR PY 2005 VL 90 IS 3 BP 326 EP 326 PG 1 WC Pediatrics SC Pediatrics GA 903OQ UT WOS:000227435800039 ER PT J AU Ozonoff, S Garcia, N Clark, E Lainhart, JE AF Ozonoff, S Garcia, N Clark, E Lainhart, JE TI MMPI-2 personality profiles of high-functioning adults with autism spectrum disorders SO ASSESSMENT LA English DT Article DE personality; MMPI-2; autism; Asperger syndrome; diagnosis ID ASPERGER-SYNDROME; CHILDREN; INDIVIDUALS; TEMPERAMENT; RELATIVES; PARENTS; TRAITS; NEUROPSYCHOLOGY; SYMPTOMS; ANXIETY AB The Minnesota Multiphasic Personality Inventoty-Second Edition was administered to 20 adults with autism spectrum disorders (ASD) who fell in the average to above average range of intelligence and 24 age-, intelligence-, and gender-matched college students. Large group differences, with the ASD group scoring higher were found on the L validity scale, Clinical Scales 2 (D) and 0 (Si), Content scale Social Discomfort (SOD), Supplementary scale Repression (R), and Personality Psychopathology Five (PSY-5) scale INTR (Introversion). The proportion of ASD adults scoring in the clinical range on these scales was between 25% and 35%. High scores on these scales are consistent with the clinical picture of Asperger syndrome and high-functioning autism in adulthood. Future directions and implications for identifying adults in need of a specialized autism assessment are discussed. C1 UC Davis Med Ctr, MIND Inst, Sacramento, CA 95817 USA. Univ Utah, Salt Lake City, UT 84112 USA. RP Ozonoff, S (reprint author), UC Davis Med Ctr, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. EM sally.ozonoff@ucdmc.ucdavis.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 Bejerot S, 2001, NORD J PSYCHIAT, V55, P169 Blackshaw AJ, 2001, AUTISM, V5, P147, DOI 10.1177/1362361301005002005 Bryson S. 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J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Wechsler D, 1999, WECHSLER ABBREVIATED Wolff S, 1998, ASPERGER SYNDROME HI, P123 NR 48 TC 16 Z9 16 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1073-1911 J9 ASSESSMENT JI Assessment PD MAR PY 2005 VL 12 IS 1 BP 86 EP 95 DI 10.1177/1073191104273132 PG 10 WC Psychology, Clinical SC Psychology GA 901MM UT WOS:000227286600008 PM 15695746 ER PT J AU Dosani, S AF Dosani, S TI Autism and creativity: Is there a link between autism in men and exceptional ability? SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Book Review C1 Maudsley Hosp & Inst Psychiat, London SE5 8AZ, England. RP Dosani, S (reprint author), Maudsley Hosp & Inst Psychiat, 103 Denmark Hill, London SE5 8AZ, England. CR FITZGERALD M, 2003, AUTISM CREATIVITY IS NR 1 TC 2 Z9 2 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON SW1X 8PG, ENGLAND SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD MAR PY 2005 VL 186 BP 267 EP 267 DI 10.1192/bjp.186.3.267 PG 1 WC Psychiatry SC Psychiatry GA 906FW UT WOS:000227627000027 ER PT J AU Peterson, CC Wellman, HM Liu, D AF Peterson, CC Wellman, HM Liu, D TI Steps in theory-of-mind development for children with deafness or autism SO CHILD DEVELOPMENT LA English DT Article ID NORMAL-HEARING; FALSE BELIEF; EMOTION; METAANALYSIS; PERFORMANCE; STATES; REAL AB Prior research demonstrates that understanding theory of mind (ToM) is seriously and similarly delayed in late-signing deaf children and children with autism. Are these children simply delayed in timing relative to typical children, or do they demonstrate different patterns of development? The current research addressed this question by testing 145 children (ranging from 3 to 13 years) with deafness, autism, or typical development using a ToM scale. Results indicate that all groups followed the same sequence of steps, up to a point, but that children with autism showed an importantly different sequence of understandings (in the later steps of the progression) relative to all other groups. C1 Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. Univ Michigan, Ann Arbor, MI 48109 USA. RP Peterson, CC (reprint author), Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. EM candi@psy.uq.edu.au CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Andrich D, 1985, SOCIOL METHODOL, V15, P33, DOI 10.2307/270846 Astington JW, 2001, CHILD DEV, V72, P685, DOI 10.1111/1467-8624.00305 Baron-Cohen S., 2000, UNDERSTANDING OTHER, P3 BARONCOHEN S, 1995, BRIT J DEV PSYCHOL, V13, P379 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen S, 1995, MINDBLINDNESS BARONCOHEN S, 1991, CHILD DEV, V62, P385, DOI 10.1111/j.1467-8624.1991.tb01539.x BETTGER JG, 1997, J DEAF STUDIES DEAF, V2, P224 BLOOM P, 2000, COGNITION, V77, P825 Bock R. Darrell, 1997, ED MEASUREMENT ISSUE, V16, P21, DOI DOI 10.1111/J.1745-3992.1997.TB00605.X Courtin C, 1998, PSYCHOLOGICAL PERSPECTIVES ON DEAFNESS, VOL 2, P79 de Villiers J. G., 2000, CHILDRENS REASONING, P189 de Villiers J. G., 2000, UNDERSTANDING OTHER, P83 Dissanayake C., 2003, INDIVIDUAL DIFFERENC, P213 DUNN J, 1994, ORIGINS UNDERSTANDIN, P297 Dunn L. M., 1981, PEABODY PICTURE VOCA Embretson S. E., 2000, ITEM RESPONSE THEORY EMMOREY K, 1998, PSYCHOL PERSPECTIVES, P79 Flavell JH, 1999, ANNU REV PSYCHOL, V50, P21, DOI 10.1146/annurev.psych.50.1.21 FLAVELL JH, 1998, HDB CHILD PSYCHOL, V2, P857 Frith U., 1989, AUTISM EXPLAINING EN GOPNIK A, 1991, CHILD DEV, V62, P98, DOI 10.1111/j.1467-8624.1991.tb01517.x GREEN BF, 1956, PSYCHOMETRIKA, V21, P79, DOI 10.1007/BF02289088 HAPPE F, 1994, SOCIAL DEV, V3, P109 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Harris P. L., 2000, UNDERSTANDING OTHER, P182 HARRIS PL, 1986, CHILD DEV, V57, P895, DOI 10.1111/j.1467-8624.1986.tb00253.x Hillier A, 2002, J AUTISM DEV DISORD, V32, P583, DOI 10.1023/A:1021259115185 JACKSON AL, 2001, J DEAF STUDIES DEAF, V6, P158 LESLIE AM, 1992, COGNITION, V43, P225, DOI 10.1016/0010-0277(92)90013-8 LESLIE AM, 1994, COGNITION, V50, P211, DOI 10.1016/0010-0277(94)90029-9 Linacre J. 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M., 2002, HDB CHILDHOOD COGNIT, P167 WELLMAN HM, 1990, COGNITION, V35, P245, DOI 10.1016/0010-0277(90)90024-E Wellman HM, 2004, CHILD DEV, V75, P523, DOI 10.1111/j.1467-8624.2004.00691.x Wellman HM, 2002, AUTISM, V6, P343, DOI 10.1177/1362361302006004003 Wellman HM, 2001, CHILD DEV, V72, P655, DOI 10.1111/1467-8624.00304 WELLMAN HM, 1993, CHILDS THEORY MIND WILSON M, 1989, AUST J EDUC, V33, P127 Woolfe T, 2002, CHILD DEV, V73, P768, DOI 10.1111/1467-8624.00437 Wright B. D., 1982, RATING SCALE ANAL RA Wright B. D., 1979, BEST TEST DESIGN RAS Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 66 TC 118 Z9 123 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 MAR-APR PY 2005 VL 76 IS 2 BP 502 EP 517 DI 10.1111/j.1467-8624.2005.00859.x PG 16 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 908FZ UT WOS:000227774200013 PM 15784096 ER PT J AU Shamay-Tsoory, SG Tomer, R Berger, BD Goldsher, D Aharon-Peretz, J AF Shamay-Tsoory, SG Tomer, R Berger, BD Goldsher, D Aharon-Peretz, J TI Impaired "affective theory of mind" is associated with right ventromedial prefrontal damage SO COGNITIVE AND BEHAVIORAL NEUROLOGY LA English DT Article DE theory of mind; ventromedial cortex; prefrontal cortex; empathy; right hemisphere ID FRONTAL-LOBE; ASPERGER-SYNDROME; ORBITOFRONTAL CORTEX; EMPATHY DEFICITS; RHESUS-MONKEY; CHILDREN; AUTISM; BRAIN; REPRESENTATION; COMPREHENSION AB Objective: To examine the hypothesis that patients with ventromedial (VM) frontal lesions are impaired in the affective rather than cognitive facets of theory of mind (ToM). Background: Prefrontal brain damage may result in impaired social behavior, especially when the damage involves the orbitofrontal/VM prefrontal cortex (PFC). It has been previously suggested that deficits in ToM may account for such aberrant behavior. However, inconsistent results have been reported, and different regions within the frontal cortex have been associated with ToM impairment. Method: The performance of 26 patients with localized lesions in the PFC was compared with responses of 13 patients with posterior lesions and 13 normal control subjects. Three ToM tasks differing in the level of emotional processing involved were used: second-order false belief task, understanding ironic utterances, and identifying social faux pas. Results and Conclusions: The results indicated that patients with VM (but not dorsolateral) prefrontal lesions were significantly impaired in irony and faux pas but not in second-order false belief as compared with patients with posterior lesions and normal control subjects. Lesions in the right VM area were associated with the most severe ToM deficit. These results are discussed in terms of the cognitive and affective facets of "mind-reading" processes mediated by the VM cortex. C1 Univ Haifa, Dept Psychol, IL-31999 Haifa, Israel. Univ Haifa, Brain & Behav Res Ctr, IL-31999 Haifa, Israel. Rambam Med Ctr, Cognit Neurol Unit, Haifa, Israel. RP Shamay-Tsoory, SG (reprint author), Univ Haifa Mt Carmel, Dept Psychol, IL-31905 Haifa, Israel. 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PD MAR-APR PY 2005 VL 46 IS 2 BP 111 EP 116 DI 10.1016/j.comppsych.2004.07.030 PG 6 WC Psychiatry SC Psychiatry GA 906SE UT WOS:000227662200005 PM 15723027 ER PT J AU Verte, S Geurts, HM Roeyers, H Oosterlaan, J Sergeant, JA AF Verte, S Geurts, HM Roeyers, H Oosterlaan, J Sergeant, JA TI Executive functioning in children with autism and Tourette syndrome SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Review ID DEFICIT-HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; CARD-SORTING-TEST; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DIAGNOSTIC INTERVIEW SCHEDULE; OBSESSIVE-COMPULSIVE DISORDER; LATENT-VARIABLE ANALYSIS; FRONTAL-LOBE; YOUNG-CHILDREN; COMMUNICATION CHECKLIST AB The main aims of this study were to investigate if children with high-functioning autism (HFA) and children with Tourette syndrome (TS) can be differentiated in their executive functioning (EF) profile compared to normal controls (NCs) and compared to each other and to investigate whether children with HFA or children with TS and a comorbid group of children with both disorders are distinct conditions in terms of EF. 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T., 1989, SNIJDERSOOMEN NONVER Spencer T, 1998, J CHILD PSYCHOL PSYC, V39, P1037, DOI 10.1017/S0021963098002984 Stern E, 2000, ARCH GEN PSYCHIAT, V57, P741, DOI 10.1001/archpsyc.57.8.741 SVERD J, 1993, J AUTISM DEV DISORD, V23, P407, DOI 10.1007/BF01046229 SVERD J, 1991, AM J MED GENET, V39, P173, DOI 10.1002/ajmg.1320390212 Tabachnick B.G., 1996, USING MULTIVARIATE S, V2nd Tellegen P, 1993, EUROPEAN J PSYCHOL A, V9, P147 TRANEL D, 1994, HANDB NEUR, V9, P125 Turner M, 1999, J CHILD PSYCHOL PSYC, V40, P839, DOI 10.1017/S0021963099004278 Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 van Haasen P, 1986, WISC R WECHSLER INTE Volkmar Fred, 1999, Journal of the American Academy of Child and Adolescent Psychiatry, V38, p32S WELSH MC, 1988, DEV NEUROPSYCHOL, V4, P199 WEYNANDT LL, 1994, DEV NEUROPSYCHOL, V10, P27 Zelazo P. D., 2002, BLACKWELL HDB CHILDH, P445, DOI DOI 10.1002/9780470996652.CH20 Zelazo P. D., 1997, REV GEN PSYCHOL, V1, P198, DOI DOI 10.1037/1089-2680.1.2.198 Zelazo PD, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P195 NR 165 TC 59 Z9 60 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0954-5794 J9 DEV PSYCHOPATHOL JI Dev. Psychopathol. PD SPR PY 2005 VL 17 IS 2 BP 415 EP 445 DI 10.1017/S0954579405050200 PG 31 WC Psychology, Developmental SC Psychology GA 928AY UT WOS:000229244700007 PM 16761552 ER PT J AU Bishop, M Hobson, RP Lee, A AF Bishop, M Hobson, RP Lee, A TI Symbolic play in congenitally blind children SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID VISUAL IMPAIRMENT; SIGHTED CHILDREN; NURSERY-SCHOOL; AUTISM; INFANTS; PRESCHOOLERS; PATTERNS; BEHAVIOR; PRETEND; MIND AB There is controversy over the existence and nature of blind children's limitations in symbolic play. In this study we tested 13 5- to 9-year-old congenitally blind children for the ability to symbolize when an adult provided scaffolding for their play. The blind children were selected on the basis that they did not have the syndrome of autism, and they comprised two groups matched for age (MA) and verbal ability on the Wechsler Intelligence Scale for Children who contrasted in their ability to engage in social relations. We also tested a group of sighted children who were MA matched with the more socially able blind children. On the basis of an hypothesis about the social-developmental sources of symbolic play deficits in congenitally blind children, we predicted differences between the socially able and socially impaired groups of blind children in the following respects: the attribution of symbolic meanings to play materials, the ascription of individual roles to play figures, and the anchorage of play in the scenario as presented by the adult. The results accorded with these predictions. Whereas the more socially able blind children showed symbolic play that was very similar to that of sighted children, the MA- and IQ-matched socially impaired blind children were limited in the three aspects of their play. On the other hand, even the socially impaired children showed instances of symbolizing. The findings suggest a way to reconcile conflicting reports of symbolic play deficits in young blind children, and may be relevant for explaining the association between autism and congenital blindness. C1 Tavistock Clin, Adult Dept, London NW3 5BA, England. UCL, London WC1E 6BT, England. RP Hobson, RP (reprint author), Tavistock Clin, Adult Dept, 120 Belsize Lane, London NW3 5BA, England. EM r.hobson@ucl.ac.uk CR ANDERSEN ES, 1984, J CHILD LANG, V11, P645 BRETHERTON I, 1984, SYMBOLIC PLAY REPRES Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x BURLINGHAM D, 1961, PSYCHOANAL STUD CHIL, V16, P121 CASS HD, 1994, ARCH DIS CHILD, V70, P192 FEIN GG, 1981, CHILD DEV, V52, P1095, DOI 10.1111/j.1467-8624.1981.tb03157.x Ferguson R., 1995, BRIT J VISUAL IMPAIR, V13, P100, DOI 10.1177/026461969501300303 Fraiberg S., 1977, INSIGHTS BLIND Hobson R. P., 2000, REASONING MIND, P11 Hobson R. P., 1997, BLINDNESS PSYCHOL DE, P99 Hobson R. P., 2002, CRADLE THOUGHT Hobson R. Peter, 1993, PERCEIVED SELF ECOLO, P254 Hobson R. 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S., 1976, PLAY ITS ROLE DEV EV, P537 Werner H., 1984, SYMBOL FORMATION WILLS DM, 1968, BRIT J MED PSYCHOL, V41, P213 Wills D M, 1979, Psychoanal Study Child, V34, P31 Wills D M, 1979, Psychoanal Study Child, V34, P85 WILLS DM, 1965, PSYCHOANAL STUD CHIL, V20, P344 Wills D M, 1981, Psychoanal Study Child, V36, P217 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Winnicott D. W., 1971, PLAYING REALITY Wolf D., 1981, EARLY LANGUAGE ACQUI, P287 Wolf D. P., 1984, SYMBOLIC PLAY DEV SO, P195 WULFF SB, 1985, J AUTISM DEV DISORD, V15, P139, DOI 10.1007/BF01531600 NR 50 TC 6 Z9 6 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0954-5794 J9 DEV PSYCHOPATHOL JI Dev. Psychopathol. PD SPR PY 2005 VL 17 IS 2 BP 447 EP 465 DI 10.1017/S095457905050212 PG 19 WC Psychology, Developmental SC Psychology GA 928AY UT WOS:000229244700008 PM 16761553 ER PT J AU Coleman, M AF Coleman, M TI Advances in autism research SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Editorial Material CR Ahsgren I, 2005, DEV MED CHILD NEUROL, V47, P193, DOI 10.1017/S0012162205000356 Filipek PA, 2003, ANN NEUROL, V53, P801, DOI 10.1002/ana.10596 Fillano James J, 2002, J Child Neurol, V17, P435 Graf WD, 2000, J CHILD NEUROL, V15, P357, DOI 10.1177/088307380001500601 Oliveira G, 2005, DEV MED CHILD NEUROL, V47, P185, DOI 10.1017/S0012162205000332 Pons R, 2004, J PEDIATR-US, V144, P81, DOI 10.1016/j.jpeds.2003.10.023 Wright B, 2005, DEV MED CHILD NEUROL, V47, P190, DOI 10.1017/S0012162205000344 NR 7 TC 2 Z9 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD MAR PY 2005 VL 47 IS 3 BP 148 EP 148 DI 10.1017/S0012162205000277 PG 1 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 900SN UT WOS:000227234700002 PM 15739717 ER PT J AU Oliveira, G Diogo, L Grazina, M Garcia, P Ataide, A Marques, C Miguel, T Borges, L Vicente, AM Oliveira, CR AF Oliveira, G Diogo, L Grazina, M Garcia, P Ataide, A Marques, C Miguel, T Borges, L Vicente, AM Oliveira, CR TI Mitochondrial dysfunction in autism spectrum disorders: a population-based study SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CHILDREN; SCHIZOPHRENIA; LINKAGE; LACTATE AB A minority of cases of autism has been associated with several different organic conditions, including bioenergetic metabolism deficiency. In a population-based study, we screened associated medical conditions in a group of 120 children with autism (current age range 11y 5mo to 14y 4mo, mean age 12y 11mo [SD 9.6mo], male:female ratio 2.9:1). Children were diagnosed using Diagnostic and Statistical Manual of Mental Disorders criteria, the Autism Diagnostic Interview-Revised, and the Childhood Autism Rating Scale; 76% were diagnosed with typical autism and 24% with atypical autism. Cognitive functional level was assessed with the Griffiths scale and the Wechsler Intelligence Scale for Children and was in the normal range in 17%. Epilepsy was present in 19 patients. Plasma lactate levels were measured in 69 patients, and in 14 we found hyperlactacidemia. Five of 11 patients studied were classified with definite mitochondrial respiratory chain disorder, suggesting that this might be one of the most common disorders associated with autism (5 of 69; 7.2%) and warranting further investigation. C1 Hosp Pediat Coimbra, Ctr Desenvolvimento Crianca, Outpatient Clin Autism, P-3000076 Coimbra, Portugal. Hosp Pediat Coimbra, Ctr Desenvolvimento Crianca, Metab Clin, P-3000076 Coimbra, Portugal. Fac Med, Inst Biochem, Coimbra, Portugal. Gulbenkian Inst Sci, Oeiras, Portugal. RP Oliveira, G (reprint author), Hosp Pediat Coimbra, Ctr Desenvolvimento Crianca, Outpatient Clin Autism, P-3000076 Coimbra, Portugal. EM guiomar@hpc.chc.min-saude.pt RI Oliveira, Catarina/F-3685-2010 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bendall KE, 1996, AM J HUM GENET, V59, P1276 Ben-Shachar D, 2002, J NEUROCHEM, V83, P1241, DOI 10.1046/j.1471-4159.2002.01263.x Bernier FP, 2002, NEUROLOGY, V59, P1406 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Chakravarti A, 2002, P NATL ACAD SCI USA, V99, P4755, DOI 10.1073/pnas.092158299 Chugani DC, 1999, PROG NEURO-PSYCHOPH, V23, P635, DOI 10.1016/S0278-5846(99)00022-6 COLEMAN M, 1985, J AUTISM DEV DISORD, V15, P1, DOI 10.1007/BF01837894 DIOGO L, 1999, ACTA PEDIAT PORTUGUE, V30, P129 Duke T, 1999, ARCH DIS CHILD, V81, P343 FILANO JJ, 2002, J CHILD NEUROL, V17, P435 Filipek PA, 2003, ANN NEUROL, V53, P801, DOI 10.1002/ana.10596 Gardner A, 2003, ACTA PSYCHIAT SCAND, V107, P233, DOI 10.1034/j.1600-0447.2003.02188.x Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 GRAF W, 2000, J CHILD NEUROL, V6, P357 Griffiths R., 1984, ABILITIES YOUNG CHIL LASZLO A, 1994, CLIN CHIM ACTA, V229, P205, DOI 10.1016/0009-8981(94)90243-7 Lombard J, 1998, MED HYPOTHESES, V50, P497, DOI 10.1016/S0306-9877(98)90270-5 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MARQUES JHF, 1970, MANUAL ESCALA INTELL Pons R, 2004, J PEDIATR-US, V144, P81, DOI 10.1016/j.jpeds.2003.10.023 Ramoz N, 2004, AM J PSYCHIAT, V161, P662, DOI 10.1176/appi.ajp.161.4.662 RUSTIN P, 1994, CLIN CHIM ACTA, V228, P35, DOI 10.1016/0009-8981(94)90055-8 SHOPLER E, 1988, CHILDHOOD AUSTISM RA Vassault A., 1991, TECHNIQUES DIAGNOSTI, P285 NR 25 TC 103 Z9 104 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD MAR PY 2005 VL 47 IS 3 BP 185 EP 189 DI 10.1017/S0012162205000332 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 900SN UT WOS:000227234700008 PM 15739723 ER PT J AU Wright, B Brzozowski, AM Calvert, E Farnworth, H Goodall, DM Holbrook, I Imrie, G Jordan, J Kelly, A Miles, J Smith, R Town, J AF Wright, B Brzozowski, AM Calvert, E Farnworth, H Goodall, DM Holbrook, I Imrie, G Jordan, J Kelly, A Miles, J Smith, R Town, J TI Is the presence of urinary indolyl-3-acryloylglycine associated with autism spectrum disorder? SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article AB To test whether the presence of indolyl-3-acryloylglycine JAG) is associated with autism, we analyzed urine from population-based, blinded cohorts. All children in York, UK with autism spectrum disorders (ASDs), diagnosed using ICD-10 research diagnostic criteria, were invited to participate. Fifty-six children on the autism spectrum (mean age 9y 8mo, SD 3y 8mo; 79% male) agreed to participate, as did 155 children without ASDs (mean age 10y, SD 3y 2mo; 54% male) in mainstream and special schools (56 of whom were age-, sex-, and school-matched to children with ASDs). IAG was found at similar levels in the urine of all children, whether IAG concentrations or IAG:creatinine ratios were compared. There was no significant difference between the ASD and the comparison group, and no difference between children at mainstream schools and those at special schools. There is no association between presence of IAG in urine and autism; therefore, it is unlikely to be of help either diagnostically or as a basis for recommending therapeutic intervention with dietary manipulation. The significance of the presence of IAG in urine has yet to be determined. C1 Univ York, Child & Adolescent Mental Hlth Unit, York YO30 5RF, N Yorkshire, England. Univ York, Dept Chem, York YO30 5RF, N Yorkshire, England. York Hosp, Dept Biochem, York, N Yorkshire, England. York Bioanalyt Solut, York, N Yorkshire, England. York Hosp, Dept Paediat, York, N Yorkshire, England. Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England. RP Wright, B (reprint author), Univ York, Child & Adolescent Mental Hlth Unit, Limetrees,Shipton Rd, York YO30 5RF, N Yorkshire, England. EM Barry.Wright@sypct.nhs.uk CR Anderson RJ, 2002, J PHARM PHARMACOL, V54, P295, DOI 10.1211/0022357021778349 Bull G, 2003, MED SCI MONITOR, V9, P422 COOK JGH, 1971, CLIN CHIM ACTA, V32, P485, DOI 10.1016/0009-8981(71)90452-9 FITZGERALD M, 1999, AUTISM, V3, P193, DOI 10.1177/1362361399003002008 GENET R, 1995, J BIOL CHEM, V270, P23540 Hunter LC, 2003, DEV MED CHILD NEUROL, V45, P121, DOI 10.1017/S0012162203000227 IMRIE GA, 2004, CHROMATOGRAPHIA S2, V59, P209 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 Marklova E, 1999, AMINO ACIDS, V17, P401, DOI 10.1007/BF01361665 MCCARTHY DM, 1979, LANCET, V2, P877 Mills MJ, 1998, J CHROMATOGR B, V712, P51, DOI 10.1016/S0378-4347(98)00153-4 PANKSEPP J, 1979, TRENDS NEUROSCI, V2, P174, DOI 10.1016/0166-2236(79)90071-7 Pavone L, 1997, BIOL PSYCHIAT, V42, P72, DOI 10.1016/S0006-3223(97)00267-9 Reichelt Karl L., 1991, Brain Dysfunction, V4, P308 REICHELT KL, 1994, DEV BRAIN DYSFUNCT, V7, P71 ROBERTS J, 1977, J BIOL CHEM, V252, P2640 SHATTOCK P, 1990, Brain Dysfunction, V3, P328 Shattock Paul, 1991, Brain Dysfunction, V4, P323 Sher L, 1997, MED HYPOTHESES, V48, P413, DOI 10.1016/S0306-9877(97)90039-6 TILLEY K, 1994, J CHEM SOC P1, V21, P3079 United Stated Food and Drug Administration, 2001, GUID IND BIOAN METH WHO, 1993, ICD 10 CLASS MENT BE ZAVALA F, 1983, J BIOL CHEM, V258, P344 NR 24 TC 14 Z9 14 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD MAR PY 2005 VL 47 IS 3 BP 190 EP 192 DI 10.1017/S0012162205000344 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 900SN UT WOS:000227234700009 PM 15739724 ER PT J AU Ahsgren, I Baldwin, I Goetzinger-Falk, C Erikson, A Flodmark, O Gillberg, C AF Ahsgren, I Baldwin, I Goetzinger-Falk, C Erikson, A Flodmark, O Gillberg, C TI Ataxia, autism, and the cerebellum: a clinical study of 32 individuals with congenital ataxia SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID COGNITIVE-AFFECTIVE SYNDROME; CEREBRAL-PALSY; INFANTILE-AUTISM; TUMOR RESECTION; CHILDREN; IMPAIRMENTS; ABNORMALITIES; POPULATION; HYPOPLASIA AB The suggested link between autism and cerebellar dysfunction formed the background for a Swedish clinical study in 2001. Thirty-two children (17 females, 15 males; mean age 12y, SD 3y 10mo; range 6 to 21y) with a clinical suspicion of non-progressive congenital ataxia were examined, and parents were interviewed about the presence of neuropsychiatric problems in the child. Twelve children had simple ataxia, eight had ataxic diplegia, and 12 had 'borderline' ataxia. All but one of the 32 children had a mild to moderate gross motor disability according to Gross Motor Function Classification System (15 were categorized as level 1, 16 as level II, and one child as level IV). Neuroimaging and neuropsychological testing were achieved in most cases. There was a strong association between learning disability* and autism spectrum disorder (often combined with hyperactivity disorder) on the one hand, and both simple and borderline 'ataxia' on the other, but a weaker link between ataxic diplegia and neuropsychiatric disorders. A correlation between cerebellar macropathology on neuroimaging and neuropsychiatric disorders was not supported. Congenital ataxia might not be a clear-cut syndrome of cerebellar disease, but one of many signs of prenatal events or syndromes, leading to a complex neurodevelopmental disorder including autism and learning disability. C1 Sundsvall Hosp, Dept Child & Adolescent Neurol & Habilitat, SE-85186 Sundsvall, Sweden. Univ Umea Hosp, Dept Paediat, S-90185 Umea, Sweden. Karolinska Hosp, Dept Neuroradiol, S-10401 Stockholm, Sweden. Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41124 Gothenburg, Sweden. RP Ahsgren, I (reprint author), Sundsvall Hosp, Dept Child & Adolescent Neurol & Habilitat, SE-85186 Sundsvall, Sweden. EM ingegerd.ahsgren@lvn.se CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Badawi N, 1998, DEV MED CHILD NEUROL, V40, P520 Bauman ML, 1997, INT REV NEUROBIOL, V41, P367 Cans C, 2000, DEV MED CHILD NEUROL, V42, P816 Esscher E, 1996, DEV MED CHILD NEUROL, V38, P285 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Haas RH, 1996, J CHILD NEUROL, V11, P84 HAGBERG B, 1972, ACTA PAEDIAT S, V226 HAGBERG B, 1993, RECENT ADV PAEDIATRI, V11, P67 HARDING AE, 1984, HEREDITARY ATAXIAS R, P12 INGRAM T, 1963, CLIN DEV MED, V8, P70 Levisohn L, 2000, BRAIN, V123, P1041, DOI 10.1093/brain/123.5.1041 NORDBERG L, 1980, 11 HOGSK LAR I PED Nordin V, 1996, DEV MED CHILD NEUROL, V38, P297 Palisano R, 1997, DEV MED CHILD NEUROL, V39, P214 Riva D, 2000, BRAIN, V123, P1051, DOI 10.1093/brain/123.5.1051 Saitoh O, 1998, PSYCHIAT CLIN NEUROS, V52, P219 SANNER G, 1973, DYSEQUILIBRIUM SYNDR Schmahmann JD, 1997, INT REV NEUROBIOL, V41, P433 Schopler E., 1988, CHILDHOOD AUTISM RAT SCHOPLER E, 1992, PSYCHOEDUCATIONAL PR SCHUTT W, 1963, LITTLE CLUB CLIN DEV, V8, P83 Steinlin M, 1998, DEV MED CHILD NEUROL, V40, P148 Steinlin M, 2003, BRAIN, V126, P1998, DOI 10.1093/brain/awg195 Steinlin M, 1999, NEUROLOGY, V53, P966 Stromme P, 2000, DEV MED CHILD NEUROL, V42, P266, DOI 10.1017/S0012162200000451 Volpe JJ, 1995, NEUROLOGY NEWBORN, V3rd Wassmer E, 2003, PEDIATR NEUROL, V28, P347, DOI 10.1016/S0887-8994(03)00016-X Wechsler D., 1989, MANUAL WECHSLER PRES Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 31 TC 12 Z9 13 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD MAR PY 2005 VL 47 IS 3 BP 193 EP 198 DI 10.1017/S0012162205000356 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 900SN UT WOS:000227234700010 PM 15739725 ER PT J AU Boutot, EA Bryant, DP AF Boutot, EA Bryant, DP TI Social integration of students with autism in inclusive settings SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID LEARNING-DISABILITIES; CHILDREN; SCHOOL; ADOLESCENTS; FRIENDSHIP; ACCEPTANCE; CLASSROOMS; GENDER; GIRLS; BOYS AB Students with autism are increasingly being placed in general education "inclusion" settings for the purpose of improved social integration. This article presents information on the social integration Of ten students with autism in elementary inclusive settings. The purposes were to describe three social integration constructs of students with autism in inclusive classrooms, including their acceptance (social preference), visibility (social impact), and membership in a peer group (social network affiliation) and to identify the extent to which severity of autism characteristics contributed to these social integration constructs. Results suggest students with autism in inclusive settings are as accepted, visible, and members of peer groups, as well as both their peers without disabilities and those with other disabilities. Post hoc observations revealed further factors that may impact these constructs as well. C1 Univ Nevada, Dept Special Educ, Las Vegas, NV 89154 USA. Univ Texas, Austin, TX 78712 USA. RP Boutot, EA (reprint author), Univ Nevada, Dept Special Educ, 4505 Maryland Pkwy,Box 453014, Las Vegas, NV 89154 USA. 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Train. Dev. Disabil. PD MAR PY 2005 VL 40 IS 1 BP 14 EP 23 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 905ZR UT WOS:000227610800002 ER PT J AU Ganz, JB Sigafoos, J AF Ganz, JB Sigafoos, J TI Self-monitoring: Are young adults with MR and autism able to utilize cognitive strategies independently? SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID MANAGEMENT; CHILDREN; PRESCHOOLERS; TEENAGERS; SETTINGS; STUDENTS; BEHAVIOR; SKILLS AB Effectiveness of a self-monitoring procedure was evaluated for increasing work task completion and verbal requesting in two young adult men with autism and severe mental retardation. The study was conducted in a vocational training program at times when the men were expected to complete vocational tasks independently. A changing criterion design was used to evaluate the procedure on number of required tasks completed and number of verbal requests. When the self-monitoring procedure was applied to task completion and verbal requests for help, performance increased systematically and in line with the changing criteria design for each participant. Results suggest that individuals with autism and severe mental retardation can be taught to use a self-monitoring procedure to increase independent task completion and verbal requesting in a vocational training program. C1 Univ Texas, DISCI, COEHD, San Antonio, TX 78249 USA. Univ Texas, Austin, TX 78712 USA. RP Ganz, JB (reprint author), Univ Texas, DISCI, COEHD, 6900 N Loop 1604 W, San Antonio, TX 78249 USA. CR Gilberts GH, 2001, J ASSOC PERS SEVERE, V26, P25, DOI 10.2511/rpsd.26.1.25 HARTMANN DP, 1976, J APPL BEHAV ANAL, V9, P527, DOI 10.1901/jaba.1976.9-527 HOLLOWAY JB, 1999, EUROPEAN J MENTAL DI, V5, P13 Hughes C, 2002, EDUC TRAIN MENT RET, V37, P262 Hughes C. A., 1991, ED TREATMENT CHILDRE, V14, P96 Jitendra A. 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PD MAR PY 2005 VL 40 IS 1 BP 24 EP 33 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 905ZR UT WOS:000227610800003 ER PT J AU Mechling, LC Pridgen, LS Cronin, BA AF Mechling, LC Pridgen, LS Cronin, BA TI Computer-based video instruction to teach students with intellectual disabilities to verbally respond to questions and make purchases in fast food restaurants SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID COMMUNITY-BASED INSTRUCTION; MODERATE MENTAL-RETARDATION; HANDICAPPED STUDENTS; TIME-DELAY; SKILLS; CHILDREN; AUTISM; ACQUISITION; SIMULATION; SELF AB Computer-based video instruction (CBVI) was used to teach verbal responses to questions presented by cashiers and purchasing skills in fast food restaurants. A multiple probe design across participants was used to evaluate the effectiveness of CBVI. Instruction occurred through simulations of three fast food restaurants on the computer using video captions, still photographs, and voice recordings. Generalization and maintenance Of skills were measured within the three community fast food restaurants. Results indicate that verbal responses to questions and fast food restaurant purchasing skills can be taught to students with moderate to severe intellectual disabilities through CBVI. C1 Univ N Carolina, Dept Curriculum Studies, Wilmington, NC 28403 USA. RP Mechling, LC (reprint author), Univ N Carolina, Dept Curriculum Studies, 601 S Coll Rd, Wilmington, NC 28403 USA. CR Ayres K. M., 2002, J SPECIAL ED TECHNOL, V17, P15 Bates PE, 2001, RES DEV DISABIL, V22, P95, DOI 10.1016/S0891-4222(01)00060-9 BERG WK, 1989, NATL FORUM SPECIAL E, V1, P26 BILLINGSLEY F, 1980, BEHAV ASSESS, V2, P229 Brady M. P., 1995, ED TREATMENT CHILDRE, V18, P389 Branham RS, 1999, EDUC TRAIN MENT RET, V34, P170 Breen C. 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C., 2003, EXCEPTIONALITY, V11, P239, DOI 10.1207/S15327035EX1104_4 Mechling L. C., 2004, Journal of Special Education Technology, V19 Mechling LC, 2002, J SPEC EDUC, V35, P224, DOI 10.1177/002246690203500404 MECHLING LC, IN PRESS J SPECIAL E Mechling LC, 2003, EDUC TRAIN MENT RET, V38, P62 MORGAN RL, 1992, J APPL BEHAV ANAL, V25, P365, DOI 10.1901/jaba.1992.25-365 NEEF NA, 1990, J APPL BEHAV ANAL, V23, P447, DOI 10.1901/jaba.1990.23-447 NIETUPSKI J, 1984, EDUC TRAIN MENT RET, V19, P91 Norman J. M., 2001, Journal of Special Education Technology, V16 ROTHOLZ DA, 1989, J ASSOC PERS SEVERE, V14, P227 SCHLEIEN SJ, 1984, EDUC TRAIN MENT RET, V19, P297 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Snell M., 2000, INSTRUCTION STUDENTS SOWERS JA, 1995, MENT RETARD, V33, P209 SPRAGUE JR, 1984, J APPL BEHAV ANAL, V17, P273, DOI 10.1901/jaba.1984.17-273 Storey K., 1984, J ASSOC PERS SEVERE, V9, P178 Tawney J. W., 1984, SINGLE SUBJECT RES S Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 TEST DW, 1993, EDUC TRAIN MENT RET, V28, P232 Thiemann KS, 2001, J APPL BEHAV ANAL, V34, P425, DOI 10.1901/jaba.2001.34-425 TIONG SJ, 1992, BEHAV CHANGE, V9, P65 VANDENPOL RA, 1981, J APPL BEHAV ANAL, V14, P61, DOI 10.1901/jaba.1981.14-61 Wert BY, 2003, J POSIT BEHAV INTERV, V5, P30, DOI 10.1177/10983007030050010501 Westling DL, 2000, TEACHING STUDENTS SE WISSICK CA, 1992, J SPECIAL ED TECHNOL, V11, P207 NR 49 TC 35 Z9 35 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 1547-0350 J9 EDUC TRAIN DEV DISAB JI Educ. Train. Dev. Disabil. PD MAR PY 2005 VL 40 IS 1 BP 47 EP 59 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 905ZR UT WOS:000227610800005 ER PT J AU Howlin, P Karpf, J Turk, J AF Howlin, P Karpf, J Turk, J TI Behavioural characteristics and autistic features in individuals with Cohen Syndrome SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Cohen Syndrome; autistic disorder; behavioural characteristics ID NATURAL-HISTORY AB Diagnostic criteria for Cohen Syndrome are based largely on physical characteristics, and systematic information about behaviour and social functioning is limited. Typically, individuals with this condition are described as being very sociable and as showing low rates of pathology. However, recent studies have indicated that behavioural difficulties may occur more frequently than previously suggested and that autistic features may be relatively common. The present investigation of 45 individuals with Cohen Syndrome (age 4-48 years) found that, although 57% of the sample were reported as showing some behavioural disturbance, problems related mainly to anxiety and social interactions; marked anti-social behaviours were rare. Twenty-two individuals met criteria for autism on standardised diagnostic assessments, although the "autistic profile" was somewhat atypical. The implications of these findings for our understanding of Cohen Syndrome are discussed. C1 St George Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. Inst Psychiat, London SE5 8AE, England. RP Howlin, P (reprint author), St George Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. EM phowlin@sghms.ac.uk RI Howlin, Patricia/A-7622-2011 CR Chandler KE, 2003, J MED GENET, V40, P233, DOI 10.1136/jmg.40.4.233 Chandler KE, 2003, NEUROPEDIATRICS, V34, P7, DOI 10.1055/s-2003-38617 COHEN MM, 1973, J PEDIATR-US, V83, P280 Dunn L. 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L., 2002, MANUAL DEV BEHAV CHE Fryns JP, 1996, CLIN GENET, V49, P237 FRYNS JP, 1981, J GENET HUM, V29, P449 GARDNER MF, 1990, EXPRESSIVE ONE WORD Howlin P, 2001, DEV MED CHILD NEUROL, V43, P692, DOI 10.1017/S0012162201001244 KARPF J, 2004, CLIN GENET, V65, P1 Kivitie-Kallio S, 1999, NEUROPEDIATRICS, V30, P181, DOI 10.1055/s-2007-973488 KIVITIEKALLIO S, 2000, THESIS U HELSINKI Kivitie-Kallio S, 2001, AM J MED GENET, V102, P125, DOI 10.1002/1096-8628(20010801)102:2<125::AID-AJMG1439>3.0.CO;2-0 Kolehmainen J, 2003, AM J HUM GENET, V72, P1359, DOI 10.1086/375454 Lord C., 1999, AUTISM DIAGNOSTIC OB 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 NORIO R, 1984, CLIN GENET, V25, P1 NORTH KN, 1995, AM J MED GENET, V58, P54, DOI 10.1002/ajmg.1320580112 Raven JC., 1956, COLOURED PROGR MATRI Sparrow S, 1984, VINELAND ADAPTIVE BE Wechsler D, 1999, WECHSLER ABBREVIATED YOUNG ID, 1987, J MED GENET, V24, P488, DOI 10.1136/jmg.24.8.488 NR 23 TC 10 Z9 10 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 MAR PY 2005 VL 14 IS 2 BP 57 EP 64 DI 10.1007/s00787-005-0416-4 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 910RI UT WOS:000227949500001 PM 15793684 ER PT J AU Trillingsgaard, A Sorensen, EU Nemec, G Jorgensen, M AF Trillingsgaard, A Sorensen, EU Nemec, G Jorgensen, M TI What distinguishes autism spectrum disorders from other developmental disorders before the age of four years? SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism spectrum disorder; other developmental disorders; early identification; distinguishing features ID FAMILY HOME MOVIES; SYMPTOMS; INFANCY; POPULATION; CHILDREN; 1ST AB The increasing recognition of the benefits of early intervention for children with autism spectrum disorder (ASD) stresses the importance of early identification of children who might benefit from those programs. However, in the early years of life it may be difficult to distinguish children with ASD from children with other developmental disorders. The aim of the present study was to identify behavioural patterns that could facilitate this differentiation. Prior to diagnostic assessment, 2- and 3-year-old children (n = 30), all referred to a clinic for "possible autism", were observed in a semi-structured play interaction, and their parents were interviewed about the children's early development from 0 to 24 months. Following diagnostic assessment, the 17 children fulfilling the ICD-10 criteria for ASD were compared to the 13 children diagnosed with other developmental disorders (outside the autism spectrum). On the basis of parent reports only a few distinguishing signs of ASD were found before 24 months of age. on the basis of professional observations in a semi-structured play interaction several distinguishing signs were found for the 2- and 3-year-olds; smiles in response, responds to name, follows pointing, looks to "read" faces, initiates requesting verbal and nonverbal behaviours, and functional play. C1 Aarhus Univ Hosp, Psychiat Hosp Children & Adolescents, DK-8240 Risskov, Denmark. RP Trillingsgaard, A (reprint author), Aarhus Univ Hosp, Psychiat Hosp Children & Adolescents, Harald Selmersvej 66, DK-8240 Risskov, Denmark. EM Atr@buh.aaa.dk CR Adrien J L, 1992, Acta Paedopsychiatr, V55, P71 ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 ADRIEN JL, 1991, J AUTISM DEV DISORD, V21, P43, DOI 10.1007/BF02206996 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 Bernabei P., 1998, AUTISM, V2, P243, DOI 10.1177/1362361398023003 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 Charvin G, 2002, SINGLE MOL, V3, P43, DOI 10.1002/1438-5171(200204)3:1<43::AID-SIMO43>3.3.CO;2-J COX A, 1999, EUR ARCH PSY NEUR SC, V238, P169 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 GILLBERG C, 1990, J CHILD PSYCHOL PSYC, V31, P921, DOI 10.1111/j.1469-7610.1990.tb00834.x HWANG B, 2002, J AUTISM DEV DISORD, V30, P331 Lord C., 2000, AUTISM SPECTRUM DISO, P11 Lord C., 1995, J CHILD PSYCHOL PSYC, V36, P1 Lord C., 2002, AUTISM DIAGNOSTIC OB Mullen E, 1995, MULLEN SCALES EARLY OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 ROGERS SJ, 2001, INT REV RES MENT RET, P1 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 Williams AM, 2000, J SPORT SCI, V18, P737, DOI 10.1080/02640410050120113 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 World Health Organization, 1993, MENT DIS GLOSS GUID NR 27 TC 24 Z9 27 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 MAR PY 2005 VL 14 IS 2 BP 65 EP 72 DI 10.1007/s00787-005-0433-3 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 910RI UT WOS:000227949500002 PM 15793685 ER PT J AU Kaland, N Moller-Nielsen, A Smith, L Mortensen, EL Callesen, K Gottlieb, D AF Kaland, N Moller-Nielsen, A Smith, L Mortensen, EL Callesen, K Gottlieb, D TI The Strange Stories test - A replication study of children and adolescents with Asperger syndrome SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Asperger syndrome; autism spectrum disorders; Strange Stories test; theory of mind; social understanding ID AUTISM; MIND; ADULTS; DISORDERS; BELIEF; INDIVIDUALS; EXPLORATION; SPECTRUM; AGE AB The aim of the present study was to assess the ability of 21 children and adolescents with Asperger syndrome (AS) of normal intelligence to infer mental states in a Story context using Happe's [15] Strange Stories test. The participants in the AS group were compared with an age-matched control group (N = 20) of normally developing children and adolescents on a test of social understanding. The test material comprised social communication such as Pretence, joke, Lie, White Lie, Figure of Speech, Misunderstanding, Persuasion, irony, Double Bluff and Contrary Emotions, Appearance/Reality and Forgetting. As compared to the controls, the participants in the AS group performed less well on these tasks, and answered fewer correct mental state inferences, but performed well on a physical state control task. This study supports the main finding of earlier studies, showing that even individuals with AS of normal intelligence have problems in using mental state terms context-appropriately when tested on the Strange Stories test. C1 Lillehammer Univ Coll, Fac Social Sci, N-2624 Lillehammer, Norway. Danish Univ Educ, Dept Psychol & Special Educ, DK-2400 Copenhagen, Denmark. Univ Oslo, Inst Psychol, N-0317 Oslo, Norway. Univ Copenhagen, Inst Publ Hlth, Dept Hlth Psychol, DK-2200 Copenhagen, Denmark. RP Kaland, N (reprint author), Lillehammer Univ Coll, Fac Social Sci, Gudbrandsdalsvegen 350, N-2624 Lillehammer, Norway. 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PD MAR PY 2005 VL 20 SU 1 BP S9 EP S9 PG 1 WC Psychiatry SC Psychiatry GA 922WE UT WOS:000228869800031 ER PT J AU Nylander, L AF Nylander, L TI Self-assessed personality traits in adults with ADHD or autism spectrum disorders (ASD) - relevance for diagnosis'? SO EUROPEAN PSYCHIATRY LA English DT Meeting Abstract C1 Dept Neurosci, Lund, Sweden. NR 0 TC 0 Z9 0 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 MAR PY 2005 VL 20 SU 1 BP S191 EP S191 PG 1 WC Psychiatry SC Psychiatry GA 922WE UT WOS:000228869801242 ER PT J AU Steyaert, J Fryns, JP Devriendt, K AF Steyaert, J Fryns, JP Devriendt, K TI Genetic research in autism: What do we learn from it? SO EUROPEAN PSYCHIATRY LA English DT Meeting Abstract C1 Dept Neurowetensch & Psychiat, Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 NR 0 TC 0 Z9 0 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 MAR PY 2005 VL 20 SU 1 BP S191 EP S192 PG 2 WC Psychiatry SC Psychiatry GA 922WE UT WOS:000228869801243 ER PT J AU Tuinier, S Hamel, B Verhoeven, W AF Tuinier, S Hamel, B Verhoeven, W TI Communication impairments in mental retardation: Autism? SO EUROPEAN PSYCHIATRY LA English DT Meeting Abstract C1 Vincent Van Gogh Inst, Dept Psychiat, Venray, Netherlands. NR 0 TC 0 Z9 0 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 MAR PY 2005 VL 20 SU 1 BP S9 EP S9 PG 1 WC Psychiatry SC Psychiatry GA 922WE UT WOS:000228869800030 ER PT J AU Mutter, J Naumann, J Walach, H Daschner, F AF Mutter, J Naumann, J Walach, H Daschner, F TI Amalgam risk assessment with coverage of references up to 2005 SO GESUNDHEITSWESEN LA German DT Review DE amalgam; mercury; toxicity; adverse health effects; autoimmunity; neurodegenerative diseases ID SILVER DENTAL FILLINGS; IDIOPATHIC DILATED CARDIOMYOPATHY; AMYOTROPHIC-LATERAL-SCLEROSIS; SHSY5Y NEUROBLASTOMA-CELLS; BETA-AMYLOID SECRETION; BLOOD MERCURY LEVELS; LOW-LEVEL EXPOSURE; LOW-DOSE EXPOSURE; 1998 GERES-III; ALZHEIMERS-DISEASE AB Amalgam, which has been in use in dentistry for 150 years, consists of 50% elemental mercury and a mixture of silver, tin, copper and zinc. Minute amounts of mercury vapour are released continuously from amalgam. Amalgam contributes substantially to human mercury load. Mercury accumulates in some organs, particulary in the brain, where it can bind to protein more tightly than other heavy metals (e.g. lead, cadmium). Therefore, the elimination half time is assumed to be up to 1 - 18 years in the brain and bones. Mercury is assumed to be one of the most toxic non-radioactive elements. There are pointers to show that mercury vapour is more neurotoxic than methyl-mercury in fish. Review of recent literature suggests that mercury from dental amalgam may lead to nephrotoxicity, neurobehavioural changes, autoimmunity, oxidative stress, autism, skin and mucosa alterations or non-specific symptoms and complaints. The development of Alzheimer's disease or multiple sclerosis has also been linked to low-dose mercury exposure. There may be individual genetical or acquired susceptilities for negative effects from dental amalgam. Mercury levels in the blood, urine or other biomarkers do not reflect the mercury load in critical organs. Some studies regarding dental amalgam reveal substantial methodical flaws. Removal of dental amalgam leads to permanent improvement of various chronic complaints in a relevant number of patients in various trials. Summing up, available data suggests that dental amalgam is an unsuitable material for medical, occupational and ecological reasons. C1 Univ Klin Freiburg, Inst Umweltmed, D-79106 Freiburg, Germany. Univ Klin Freiburg, Krankenhaushyg, D-79106 Freiburg, Germany. Samueli Inst, European Off, Freiburg, Germany. RP Mutter, J (reprint author), Univ Klin Freiburg, Inst Umweltmed, Hugstetter Str 55, D-79106 Freiburg, Germany. 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Risks of a non-obvious disability SO HEALTH RISK & SOCIETY LA English DT Article DE Asperger's syndrome; autism; mental health; disability; risk; qualitative research; labelling; marginality ID AUTISM; DISORDERS AB In this paper the risks of having a non-obvious disability, Asperger's syndrome [AS], are explored. The key focus is the riskiness associated with being on the margins of normality, where personal experience (and theoretical concepts) of being 'different' and 'normal' merge. When labelling people in any way other than normal is unpopular, those on such margins remain at risk of being misunderstood and neglected. With AS there continues to be controversy over the diagnostic label, as well as a theoretical tension between the negative versus positive effects of applying such a diagnosis. The basis for this discussion is the findings of a qualitative study exploring the experiences of young adults with AS and those of their parents. Methods used include purposive sampling, unstructured interviews and constant comparative analysis-whereby analysis became organised around the core emergent category of 'not quite fitting'-and the kinds of risk associated with the subjectively felt experience, the perception on the part of others that behaviour is somehow curious or unusual. These risks are categorised into everyday and longer term risks. This paper also discusses comparable risks for other people who are marginally different whether as a result of disability, mental health problems or simply personality. C1 Western Sussex NHS Primary Care Trust, Arundel Surg, Arundel BN18 9HG, England. City Univ London, St Bartholomew Sch Nursing & Midwifery, London, England. RP Portway, SM (reprint author), Western Sussex NHS Primary Care Trust, Arundel Surg, Green Lane Close, Arundel BN18 9HG, England. 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PD MAR PY 2005 VL 7 IS 1 BP 73 EP 83 DI 10.1080/09500830500042086 PG 11 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA 911FF UT WOS:000227987300006 ER PT J AU Pearson, R Lewis, MB AF Pearson, R Lewis, MB TI Fear recognition across the menstrual cycle SO HORMONES AND BEHAVIOR LA English DT Article DE fear; oestrogen; menstrual cycle; sexual dimorphism; autism; depression ID HUMAN AMYGDALA; HORMONAL INFLUENCES; FACIAL EXPRESSIONS; TURNER-SYNDROME; DEPRESSION; EMOTION; DIFFERENTIATION; PERCEPTION; BRAIN; FACES AB This study assesses the mediating role of stage of menstrual cycle in the recognition of emotional expressions. It was hypothesised that fear recognition ability would be stronger at high-oestrogen stages of the menstrual cycle. The accuracy of recognising emotional expressions was compared across 50 women who were at different stages of their menstrual cycle. It was found that accuracy to recognise emotions was significantly affected by the interaction between stages of the menstrual cycle and the emotion being displayed. Further analysis revealed that for the emotion expression of fear alone, participants were significantly more accurate at the preovulatory surge (highest oestrogen levels) than at menstruation (oestrogen levels at lowest point). The results have implications for the processes that underlie fear processing and a possible insight into the sexual dimorphism of this ability and conditions that show variations in fear recognition (e.g., autism, Turner syndrome). (C) 2005 Elsevier Inc. All rights reserved. C1 Univ Wales Coll Cardiff, Sch Psychol, Cardiff CF10 3AT, S Glam, Wales. RP Lewis, MB (reprint author), Univ Wales Coll Cardiff, Sch Psychol, Pk Pl, Cardiff CF10 3AT, S Glam, Wales. EM LewisMB@cfac.uk RI Lewis, Michael/D-1488-2009 CR ADOLPHS R, 1995, J NEUROSCI, V15, P5879 Alliende ME, 2002, FERTIL STERIL, V78, P90, DOI 10.1016/S0015-0282(02)03167-9 Angold A, 1999, PSYCHOL MED, V29, P1043, DOI 10.1017/S0033291799008946 Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Bhagwagar Z, 2004, AM J PSYCHIAT, V161, P166, DOI 10.1176/appi.ajp.161.1.166 Calder AJ, 2001, NAT REV NEUROSCI, V2, P352, DOI 10.1038/35072584 Campbell R, 2002, NEUROPSYCHOLOGIA, V40, P575, DOI 10.1016/S0028-3932(01)00164-6 Collaer ML, 2002, HORM BEHAV, V41, P139, DOI 10.1006/hbeh.2001.1751 Creswell C. 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Behav. PD MAR PY 2005 VL 47 IS 3 BP 267 EP 271 DI 10.1016/j.yhbeh.2004.11.003 PG 5 WC Behavioral Sciences; Endocrinology & Metabolism SC Behavioral Sciences; Endocrinology & Metabolism GA 902BL UT WOS:000227326100004 PM 15708754 ER PT J AU Sidener, TM Carr, JE Firth, AM AF Sidener, TM Carr, JE Firth, AM TI Superimposition and withholding of edible consequences as treatment for automatically reinforced stereotypy SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE stereotypy; reinforcer displacement; environmental enrichment; super-imposition procedure ID FUNCTIONAL-ANALYSIS; SELF-INJURY; BEHAVIOR AB The delivery and subsequent withholding of tangible consequences has been previously investigated as an intervention for stereotypic behavior. The current investigation sought to extend previous research by evaluating its effectiveness and durability as treatment for stereotypy of 2 children who had been diagnosed with autism. Nonsocial functions for stereotypic behavior were identified via functional analysis. Edible items were then delivered contingent on stereotypy and were withheld in a subsequent condition. When the superimposition procedure failed to reduce stereotypy, environmental enrichment was implemented and was found to reduce the stereotypy of both participants. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RP Carr, JE (reprint author), Western Michigan Univ, Dept Psychol, 1902 W Michigan Ave, Kalamazoo, MI 49008 USA. EM jim.carr@wmich.edu CR FOXX RM, 1986, ANAL INTERVEN DEVEL, V6, P239, DOI 10.1016/S0270-4684(86)80004-0 FOXX RM, 1983, BEHAV ANAL LETT, V3, P371 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 IWATA BA, 1982, ANAL INTERVEN DEVEL, V2, P3, DOI 10.1016/0270-4684(82)90003-9 NEISWORTH JT, 1985, BEHAV MODIF, V9, P103, DOI 10.1177/01454455850091007 SCHMID TL, 1986, AM J MENT RETARD, V91, P286 NR 6 TC 14 Z9 14 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SPR PY 2005 VL 38 IS 1 BP 121 EP 124 DI 10.1901/jaba.2005.58-04 PG 4 WC Psychology, Clinical SC Psychology GA 914SE UT WOS:000228247100013 PM 15898482 ER PT J AU Bennett, HE Wood, CL Hare, DJ AF Bennett, HE Wood, CL Hare, DJ TI Providing care for adults with autistic spectrum disorders in Learning Disability Services: Needs-based or diagnosis-driven? SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE autistic spectrum disorders; needs-based assessment; quality of life; service provision ID PEOPLE AB Background This study assessed whether a Learning Disability Service should develop a specific autism strategy or provide services on a needs-led basis. Materials and methods An autism screening questionnaire had been used to identify individuals scoring above a cut-off who had (n = 9) or had not (n = 15) received a formal diagnosis of autism. A sample of low scorers (n = 22) were matched to these groups. Questionnaires assessing service provision, needs (disabilities and challenging behaviour), quality of life and knowledge of autism were sent to relatives of individuals living at home or key-workers for those living in supported housing. Results The high scoring groups had similar levels of needs. Those diagnosed with autism received more services in total while the high scoring group without autism diagnoses scored significantly lower on quality of life. Although these differences were not maintained when level of disability was taken into account, it appeared that there was some level of unmet need in the high scorers without autism diagnoses group. Conclusions It appeared that resources should be targeted at identifying and addressing the specific needs of individuals presenting with autistic spectrum difficulties. C1 Birmingham Childrens Hosp NHS Trust, Dept Clin Psychol, Parkview Clin, Birmingham B13 8QE, W Midlands, England. Pennine Care NHS Trust, Learning Disabil Serv, Dept Clin Psychol, Ashton Under Lyne, England. Univ Manchester, Acad Div Clin Psychol, Manchester, Lancs, England. RP Bennett, HE (reprint author), Birmingham Childrens Hosp NHS Trust, Dept Clin Psychol, Parkview Clin, 60 Queensbridge Rd, Birmingham B13 8QE, W Midlands, England. 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PD MAR PY 2005 VL 18 IS 1 BP 57 EP 64 DI 10.1111/j.1468-3148.2004.00219.x PG 8 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 894LC UT WOS:000226792200006 ER PT J AU Kagan-Kushnir, T Roberts, SW Snead, OC AF Kagan-Kushnir, T Roberts, SW Snead, OC TI Screening electroencephalograms in autism spectrum disorders: Evidence-based guideline SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the Canadian-Pediatric-Society CY JUN 17, 2001 CL VANCOUVER, CANADA SP Canadian Pediat Soc ID LANDAU-KLEFFNER-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDER; RISK-BENEFIT ASSESSMENT; SICKLE-CELL-ANEMIA; TERM-FOLLOW-UP; INFANTILE-AUTISM; DISINTEGRATIVE PSYCHOSIS; ANTIEPILEPTIC DRUGS; CONVULSIVE DISORDER; SEIZURE DISORDERS AB The purpose of this study was to establish guidelines for the use of screening electroencephalograms (EEGs) in autism spectrum disorders to identify subclinical epileptiform activity. MEDLINE and EMBASE were searched for relevant articles. The evidence was reviewed using the methodology of the Canadian Task Force on Preventive Health Care. A priori criteria were established for article selection and for grading the quality and strength of the evidence. Seizures are corm-non, occurring in 20 to 30% of patients based on the majority of studies. Epileptiform EEG abnormalities are present in 10.3% to 72.4% of patients and subclinical abnormalities in 6.1% to 31%. Evidence for the effectiveness of anticonvulsants and corticosteroids in reducing seizures and/or autistic symptoms is based primarily on case series and case reports, with only one published randomized trial. There is currently insufficient evidence to recommend for or against the use of screening EEGs in autistic patients. Given the frequency of seizure disorders in this patient population, a high index of clinical suspicion should be maintained for subtle symptoms of seizures. C1 Bloorview MacMillan Childrens Ctr, Toronto, ON M2J 4S9, Canada. Univ Toronto, Hosp Sick Children, Dept Pediat, Div Neurol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Hosp Sick Children, Dept Pediat, Brain & Behav Res Program, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Hlth Policy Management & Evaluat, Clin Epidemiol & Hlth Care Res Program, Toronto, ON, Canada. RP Kagan-Kushnir, T (reprint author), Bloorview MacMillan Childrens Ctr, 25 Buchan Court, Toronto, ON M2J 4S9, Canada. 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Child Neurol. PD MAR PY 2005 VL 20 IS 3 BP 197 EP 206 PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 914QQ UT WOS:000228243000006 PM 15832609 ER PT J AU de Bildt, A Sytema, S Kraijer, D Minderaa, R AF de Bildt, A Sytema, S Kraijer, D Minderaa, R TI Prevalence of pervasive developmental disorders in children and adolescents with mental retardation SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE prevalence; PDD; MR ID AUTISM DIAGNOSTIC INTERVIEW; ADAPTIVE-BEHAVIOR SCALES; PSYCHIATRIC-DISORDERS; OBSERVATION SCHEDULE; ADI-R; EPIDEMIOLOGY; CLASSIFICATION; INDIVIDUALS; IMPAIRMENTS; RELIABILITY AB Background: Insight into the prevalence of pervasive developmental disorder (PDD) in children and adolescents with mental retardation (MR) is known to be of clinical importance. However, estimating this prevalence is complicated. The literature reports prevalence rates ranging from 3% through 50%. This variation seems to be related to the concepts of PDD under study, the instruments used, and the studied populations. The present study aimed to estimate a reliable prevalence rate of PDD. Methods: A total population-based screening with the PDD-MRS and the ABC (n = 825) was followed by further assessment of children and adolescents at high risk for PDD according to these instruments, and for controls, with the ADI-R, ADDS-G and a DSM-IV-TR classification (n = 188). Results: The instruments lead to different prevalence rates that range from 7.8% to 19.8%. The differences in the estimated prevalence rates are related to the concept of PDD and the instruments they represent. The DSM-IV-TR prevalence (16.7%) seems to be the most reliable and well-founded estimate, since this prevalence rate is based on information from multiple informants and multiple time periods. Conclusions: The reported prevalence rates provide policy makers with an up-to-date and more substantiated guideline for the allocation of resources for children and adolescents with MR and PDD. The height of the prevalence should alert professionals that PDD is widespread in the population with MR. Keywords: Prevalence, PDD, MR. C1 Univ Groningen, NL-9700 AR Groningen, Netherlands. RP de Bildt, A (reprint author), Univ Groningen, POB 660, NL-9700 AR Groningen, Netherlands. EM a.de.bildt@accare.nl RI Sytema, Sjoerd/B-2058-2010 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bryson S. 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Child Psychol. Psychiatry PD MAR PY 2005 VL 46 IS 3 BP 275 EP 286 DI 10.1111/j.1469-7610.2004.00346.x PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 910SR UT WOS:000227953000007 PM 15755304 ER PT J AU Botting, N AF Botting, N TI Non-verbal cognitive development and language impairment SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE cognition; development; language disorder; longitudinal studies; non-verbal IQ; specific language impairment ID FOLLOW-UP; WORKING-MEMORY; CHILDREN; DISORDERS; OUTCOMES; AUTISM; SUBGROUPS; STABILITY; DEFICITS; UNITS AB Background: Specific language impairment (SLI) is currently partly defined by the presence of nonverbal IQ scores in the normal range. However, not only is there a debate concerning where 'normal thresholds' should be, but increasing information about the presence of processing deficits in SLI have led some researchers to question the use of IQ criteria in clinical diagnosis. In particular, little is known about the longitudinal and developmental patterns of cognitive performance in this population. Method: Data from a long-term follow-up study of SLI was examined in 82 children defined at original participation as having SLI who had IQ measurements at 7, 8, 11 and 14 years. Results: Analyses revealed a significant fall between 7 and 14 years of over 20 IQ points. This fall took place mainly between 8 and 11 years but was still continuing between 11 and 14 years. Further investigation revealed different groups of children showing different developmental patterns in IQ, even after controlling for baseline measurement. These groups also showed significantly different language outcomes at 14 years. Analyses controlling for IQ at 7 were also performed that suggested a dynamic process between language and cognitive development. 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Psychiatry PD MAR PY 2005 VL 46 IS 3 BP 317 EP 326 DI 10.1111/j.1469-7610.2004.00355.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 910SR UT WOS:000227953000010 PM 15755307 ER PT J AU Noens, ILJ van Berckelaer-Onnes, IA AF Noens, ILJ van Berckelaer-Onnes, IA TI Captured by details: sense-making, language and communication in autism SO JOURNAL OF COMMUNICATION DISORDERS LA English DT Review DE autism; language; communication; central coherence ID HIGH-FUNCTIONING CHILDREN; CENTRAL COHERENCE THEORY; WEAK CENTRAL COHERENCE; EARLY ADULT LIFE; ASPERGER-SYNDROME; JOINT ATTENTION; MENTAL-RETARDATION; EXECUTIVE FUNCTION; VISUAL ILLUSIONS; WORKING-MEMORY AB The communication of people with autism spectrum disorder (ASD) is characterized by a qualitative impairment in verbal and non-verbal communication. In past decades a growing body of descriptive studies has appeared on language and communication problems in ASD. Reviews suggest that the development of formal and semantic aspects is relatively spared, whereas pragmatic skills are considered to be specifically impaired. This unique profile was interpreted mainly within the framework of the theory of mind hypothesis, which links the social-communicative problems of people with autism to an incapacity to attribute mental states to themselves and others. This approach has proven useful, but has also left many questions unanswered. In more recent publications, limited intentionality and symbol formation have been identified as core problems in ASD. Problems in symbol formation in particular might be better understood from the viewpoint of the central coherence hypothesis, which conceptualizes ASD as a weaker drive for the integration of information. Possible links between cognitive findings and communication evoke new perspectives with respect to the complex of communication problems in ASD. 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A guide to medical, nutritional and behavioral issues. SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Book Review C1 Univ Sydney, Ctr Dev Disabil Studies, Sydney, NSW 2006, Australia. RP Roberts, J (reprint author), Univ Sydney, Ctr Dev Disabil Studies, Sydney, NSW 2006, Australia. CR VOLKMAR FR, 2004, HLTHCARE CHILDREN AU NR 1 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD MAR PY 2005 VL 30 IS 1 BP 63 EP 64 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 924QD UT WOS:000228992700013 ER PT J AU Kaplan, RS Steele, AL AF Kaplan, RS Steele, AL TI An analysis of music therapy program goals and outcomes for clients with diagnoses on the autism spectrum SO JOURNAL OF MUSIC THERAPY LA English DT Article ID ALZHEIMERS-DISEASE; DISORDERS; CHILDREN AB The researchers analyzed data related to goals and outcomes over 2 program years for 40 music therapy clients, ranging in age from 2-49 years, with diagnoses on the autism spectrum. They investigated music therapy interventions, session types, and formats most frequently used; goals most frequently addressed, assessed level of difficulty of clients and their situations; and generalization of skills attained in music therapy to other settings. The most common session type was individual, followed by partner small or large groups, peer model, or a combination. Primary goal areas were ranked from language/communication (41 %), behavioral/psychosocial (39%), cognitive (8%), and musical (7%), to perceptual/motor (5%). One hundred percent of subjects reached their initial objectives in these goal areas within one year or less, regardless of session type, level of difficulty, or goal area. Seventy-seven percent of intermediate objectives were reached within that time. The most frequently utilized interventions were interactive instrument playing, musical instrument instruction, interactive singing, instrument choices, and song choices. Specific interventions chosen did not affect accomplishment of initial objectives. However there was more variation among interventions in terms of achievement of intermediate objectives. Session formats were ranked from activity-based as most frequent to lesson-based, client-led/"shadow, " and ensemble format. All formats were successful when addressing initial objectives, with lesson-based format being most effective in reaching intermediate objectives. Lastly, 100% of parents and caregivers surveyed indicated subjects generalized skills/responses acquired in music therapy to nonmusic therapy environments. C1 Cleveland Mus Sch Settlement, Cleveland, OH USA. Ohio Univ, Athens, OH 45701 USA. RP Kaplan, RS (reprint author), Cleveland Mus Sch Settlement, Cleveland, OH USA. CR Brodsky W, 1997, J MUSIC THER, V34, P2 Cevasco AM, 2003, J MUSIC THER, V40, P41 EDGERTON CL, 1994, J MUSIC THER, V31, P31 Hanson N, 1996, J MUSIC THER, V33, P93 Mahlberg M, 1973, J MUSIC THER, V10, P189, DOI [10.1093/jmt/10.4.189, DOI 10.1093/JMT/10.4.189] NELSON DL, 1984, J MUSIC THER, V21, P100 Saperston B., 1973, J MUSIC THER, V10, P184 SHAW J, 1997, MUSIC THERAPY PERSPE, V15, P98 SNELLL AM, 1996, MODELS MUSIC THERAPY STANLEY JM, 1986, J MUSIC THER, V21, P184 Staum MJ, 1984, MUSIC THERAPY PERSPE, V1, P14 Stevens E, 1969, J MUSIC THER, V6, P98, DOI [10.1093/jmt/6.4.98, DOI 10.1093/JMT/6.4.98] Thaut M., 1984, MUSIC THERAPY PERSPE, V4, P7 THAUT M, 1999, INTRO MUSIC THERAPY, P163 Thaut M. H., 2000, SCI MODEL MUSIC THER TOIGO DA, 1992, MUSIC THERAPY PERSPE, V10, P13 Watson D., 1979, MISSOURI J RES MUSIC, V4, P8 1996, FOCUSING PROGRAM OUT 1996, MEASURING PROGRAM OU NR 19 TC 22 Z9 23 PU NATL ASSOC MUSIC THERAPY INC PI SILVER SPRING PA 8455 COLESVILLE RD, STE 1000, SILVER SPRING, MD 20910 USA SN 0022-2917 J9 J MUSIC THER JI J. Music Ther. PD SPR PY 2005 VL 42 IS 1 BP 2 EP 19 PG 18 WC Music; Rehabilitation SC Music; Rehabilitation GA 919ZJ UT WOS:000228656200001 PM 15839730 ER PT J AU Howard-Barr, EM Rienzo, BA Pigg, RM James, D AF Howard-Barr, EM Rienzo, BA Pigg, RM James, D TI Teacher beliefs, professional preparation, and practices regarding exceptional students and sexuality education SO JOURNAL OF SCHOOL HEALTH LA English DT Article ID SEX-EDUCATION; INTELLECTUAL DISABILITIES; SIECUS GUIDELINES; KNOWLEDGE; ATTITUDES; PEOPLE; AUTISM; NEEDS AB Sexuality education, part of the comprehensive school health education component of a Coordinated School Health Program, interests many health educators as well as special education teachers. In this study, Florida special educators reported their beliefs about teaching sexuality education to educable mentally disabled students, the range of sexuality topics the), teach, and their professional preparation in sexuality education. Respondents (n = 494) completed a mailed instrument that included the 36 sexuality content areas identified by the Sexuality Information and Education Council of the United States. Respondents believed strongly that many of the sexuality topics and content areas should be taught to educable mentally disabled students. However, most reported delivering only a modest amount of sexuality education, and they rated their professional preparation as inadequate. Regression analyses documented that respondents' beliefs predicted the topics they actually taught within 5 of the 6 key concepts. This study supports collaboration between health educators and special education teachers to adapt existing sexuality, curricula for students with special needs, improve professional preparation of special education teachers to teach sexuality education, and to more effectively implement comprehensive school health education through the Coordinated School Health Program model to special education students. C1 Univ N Florida, Coll Hlth, Dept Publ Hlth, Jacksonville, FL 32224 USA. Univ Florida, Dept Hlth Educ & Behav, Gainesville, FL 32611 USA. RP Howard-Barr, EM (reprint author), Univ N Florida, Coll Hlth, Dept Publ Hlth, 4567 St Johns Rd S, Jacksonville, FL 32224 USA. 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Health PD MAR PY 2005 VL 75 IS 3 BP 99 EP 104 DI 10.1111/j.1746-1561.2005.00004.x PG 6 WC Education & Educational Research; Education, Scientific Disciplines; Health Care Sciences & Services; Public, Environmental & Occupational Health SC Education & Educational Research; Health Care Sciences & Services; Public, Environmental & Occupational Health GA 921DB UT WOS:000228743300004 PM 15966552 ER PT J AU Williams, SK Johnson, C Sukhodolsky, DG AF Williams, SK Johnson, C Sukhodolsky, DG TI The role of the school psychologist in the inclusive education of school-age children with autism spectrum disorders SO JOURNAL OF SCHOOL PSYCHOLOGY LA English DT Review DE autism; autism spectrum disorders; inclusion; education; school ID HIGH-FUNCTIONING CHILDREN; PERVASIVE DEVELOPMENTAL DISORDERS; EVIDENCE-BASED INTERVENTIONS; POSITIVE BEHAVIORAL SUPPORT; EMBEDDED INSTRUCTION; SOCIAL-INTERACTION; PEER INTERACTIONS; STIMULUS-CONTROL; YOUNG-CHILDREN; SELF-INJURY AB Two independent trends are impacting school psychologists with regard to their involvement in the education of students with autism spectrum disorders (ASDs): increasing prevalence estimates of ASDs and an emphasis on the inclusion of students with special needs in regular education classrooms. In light of these trends and growing awareness of the need for evidence-based practices in the field, school psychologists can expect to be involved in the educational programming of students with ASDs and should be knowledgeable about empirically supported strategies relevant to inclusive education of these children. The purpose of this review is to familiarize school psychologists with currently available intervention techniques by describing each strategy and outlining the degree of empirical support for each. Strategies for managing disruptive behaviors, promoting learning, and facilitating social integration are reviewed. (c) 2005 Society for the Study of School Psychology. Published by Elsevier Ltd. All rights reserved. C1 Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA. Univ Pittsburgh, Dept Pediat, Sch Med, Pittsburgh, PA 15260 USA. RP Williams, SK (reprint author), Yale Univ, Ctr Child Study, Sch Med, POB 207900, New Haven, CT 06520 USA. 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PD MAR-APR PY 2005 VL 43 IS 2 BP 117 EP 136 DI 10.1016/j.jsp.2005.01.002 PG 20 WC Psychology, Educational SC Psychology GA 931NJ UT WOS:000229491700003 ER PT J AU McGreevy, D AF McGreevy, D TI Risks and benefits of the single versus the triple MMR vaccine: how can health professionals reassure parents? SO JOURNAL OF THE ROYAL SOCIETY FOR THE PROMOTION OF HEALTH LA English DT Article DE health professionals; measles, mumps and rubella; risks; single vaccination; triple vaccination ID RUBELLA VACCINE; MEASLES; MUMPS; AUTISM; POPULATION; CONFIDENCE AB Measles, mumps and rubella (MMR) are all preventable but infectious diseases caused by viruses. A particular study by Wakefield et all suggests that there are potentially adverse effects of having the triple MMR vaccine. This has been reported widely by the media and has caused alarm to parents of young children, probably contributing to the decline in its uptake.(2-5) in order to provide the context for the debate regarding the single versus the triple vaccine, this paper briefly appraises firstly, the Wakefield et al research paper(1) that has led to public health concerns and secondly, a more rigorous research study (Madsen et al(6)) that contradicts the findings; the paper then explores the risks and benefits of the single and the triple MMR vaccine programmes, finally providing a short discussion on factors that might influence the decision-making process by parents when faced with the dilemma of not having their child vaccinated, or opting for either the single or triple vaccination programme. C1 Univ Brighton, Clin Res Ctr, Eastbourne BN20 7UR, England. RP McGreevy, D (reprint author), Univ Brighton, Clin Res Ctr, 49 Darley Rd, Eastbourne BN20 7UR, England. EM d.mcgreevy@bton.ac.uk CR Andrews DN, 2002, BRIT MED J, V325, P597 Clements CJ, 2003, J MED ETHICS, V29, P22, DOI 10.1136/jme.29.1.22 COLLIER J, 2003, DRUGS THERAPEUTICS B, V41, P25 *DEP HLTH, 2001, MEASL MUMPS RUB VACC Eaton L, 2002, BRIT MED J, V324, P315 Elliman DAC, 2001, ARCH DIS CHILD, V85, P271, DOI 10.1136/adc.85.4.271 Evans M, 2001, BRIT J GEN PRACT, V51, P904 GOODMAN NW, 2001, HOSP MED, V62, P2 Horton R, 2004, LANCET, V363, P747, DOI 10.1016/S0140-6736(04)15714-0 Jansen VAA, 2003, SCIENCE, V301, P804, DOI 10.1126/science.1086726 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Mason BW, 2000, J EPIDEMIOL COMMUN H, V54, P473, DOI 10.1136/jech.54.6.473 Miller E, 2002, J INFECTION, V44, P1, DOI 10.1053/jinf.2001.0930 Moreton Judith, 2002, J Fam Health Care, V12, P151 Offit PA, 2002, PEDIATRICS, V109, P124, DOI 10.1542/peds.109.1.124 Owens SR, 2002, EMBO REP, V3, P406, DOI 10.1093/embo-reports/kvf106 Ramsay ME, 2002, BRIT J GEN PRACT, V52, P912 Smeeth L, 2001, BMC PUBLIC HEALTH, V1, DOI 10.1186/1471-2458-1-2 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2000, ADVERSE DRUG REACT T, V19, P284 Wakefield Andrew J., 2000, Adverse Drug Reactions and Toxicological Reviews, V19, P265 NR 21 TC 5 Z9 5 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. Health PD MAR PY 2005 VL 125 IS 2 BP 84 EP 86 DI 10.1177/146642400512500212 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 919OE UT WOS:000228626600008 PM 15819183 ER PT J AU Kahler, SG AF Kahler, SG TI A biochemical geneticist looks at Autism. SO MOLECULAR GENETICS AND METABOLISM LA English DT Meeting Abstract CT Annual Meeting of the Society-for-Inherited-Metabolic-Disorders (SIMD 2005) CY MAR 06-09, 2005 CL Pacific Grove, CA SP Genzyme Corp, Mead Johnson Nutr, NIDDK, NIH, Off Rare Dis, Dept Hlth & Human Serv, Ucyclyd Pharma, Actelion Pharmaceut US Inc, Abbott Labs, Ross Prod Div, SHS N Amer, Appl Biosyst, Appl Nutr Corp, BioMarin Pharmaceut Inc, Milupa N Amer, Vitaflo, Biochrom Inc, Cambrooke Foods, Hitachi High Technologies Amer Inc, Natl Urea Cycle Defects Fdn, Pickering Labs Inc, Rare Dis Therapeut Inc, Sigma Tau Pharmaceut, Transkarot Therapies Inc C1 Johns Hopkins Sch Med, Dept Pediat, Baltimore, MD USA. NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1096-7192 J9 MOL GENET METAB JI Mol. Genet. Metab. PD MAR PY 2005 VL 84 IS 3 BP 200 EP 200 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Genetics & Heredity; Research & Experimental Medicine GA 906NH UT WOS:000227648400013 ER PT J AU Arnold, GL Bowman, R Mooney, R McCall, K DeLuca, J Hyman, S AF Arnold, GL Bowman, R Mooney, R McCall, K DeLuca, J Hyman, S TI Organic acids and fungal metabolites in children with autism. SO MOLECULAR GENETICS AND METABOLISM LA English DT Meeting Abstract CT Annual Meeting of the Society-for-Inherited-Metabolic-Disorders (SIMD 2005) CY MAR 06-09, 2005 CL Pacific Grove, CA SP Genzyme Corp, Mead Johnson Nutr, NIDDK, NIH, Off Rare Dis, Dept Hlth & Human Serv, Ucyclyd Pharma, Actelion Pharmaceut US Inc, Abbott Labs, Ross Prod Div, SHS N Amer, Appl Biosyst, Appl Nutr Corp, BioMarin Pharmaceut Inc, Milupa N Amer, Vitaflo, Biochrom Inc, Cambrooke Foods, Hitachi High Technologies Amer Inc, Natl Urea Cycle Defects Fdn, Pickering Labs Inc, Rare Dis Therapeut Inc, Sigma Tau Pharmaceut, Transkarot Therapies Inc C1 Univ Rochester, Sch Med & Dent, Rochester, NY USA. NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1096-7192 J9 MOL GENET METAB JI Mol. Genet. Metab. PD MAR PY 2005 VL 84 IS 3 BP 213 EP 213 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Genetics & Heredity; Research & Experimental Medicine GA 906NH UT WOS:000227648400030 ER PT J AU Fatemi, SH AF Fatemi, SH TI Reelin glycoprotein: structure, biology and roles in health and disease SO MOLECULAR PSYCHIATRY LA English DT Review DE reelin; schizophrenia; autism; reeler mouse ID APOE RECEPTOR 2; BRAIN-DEVELOPMENT; EXTRACELLULAR-MATRIX; SPINAL-CORD; LIPOPROTEIN RECEPTORS; CORTICAL DEVELOPMENT; VULNERABILITY FACTOR; CEREBROSPINAL-FLUID; NEURONAL MIGRATION; ALZHEIMERS-DISEASE AB Reelin glycoprotein is a secretory serine protease with dual roles in mammalian brain: embryologically, it guides neurons and radial glial cells to their corrected positions in the developing brain; in adult brain, Reelin is involved in a signaling pathway which underlies neurotransmission, memory formation and synaptic plasticity. Disruption of Reelin signaling pathway by mutations and selective hypermethylation of the Reln gene promoter or following various pre- or postnatal insults may lead to cognitive deficits present in neuropsychiatric disorders like autism or schizophrenia. 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,MMC 392, Minneapolis, MN 55455 USA. 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The substantia nigra (SN) is involved in circling. We used unilateral SN pars reticulata (SNR) infusions of the GABA agonist muscimol to induce circling and deoxyglucose autoradiography mapping in adult and postnatal day (PN) 15 male and female rats to determine its substrates. In adults, muscimol infusions in posterior SNR induced a higher circling rate than in anterior SNR, after which males displayed faster circling than females. In contrast, PN15 female rats circled faster than PN15 male rats. Autoradiograms demonstrated age- and sex-specific alterations of deoxyglucose uptake in the SN pars compacta (SNC) associated with highest circling rates. The data suggest that there is a close relationship of the GABAergic SNR and dopaminergic SNC in the induction of circling; there is a topographic organization of the SNR in terms of circling behavior and associated deoxyglucose uptake, which is dependent on age and sex. (C) 2004 Elsevier Inc. All rights reserved. C1 Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Neurociencias, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Einstein Montefiore Epilepsy Management Ctr, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA. RP Velisek, L (reprint author), Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, 1410 Pelham Pkwy S, Bronx, NY 10461 USA. 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Dis. PD MAR PY 2005 VL 18 IS 2 BP 346 EP 355 DI 10.1016/j.nbd.2004.10.012 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 896RC UT WOS:000226950200011 PM 15686963 ER PT J AU Williams, JHG Waiter, GD Perra, O Perrett, DI Whiten, A AF Williams, JHG Waiter, GD Perra, O Perrett, DI Whiten, A TI An fMRI study of joint attention experience SO NEUROIMAGE LA English DT Article DE joint attention; joint attention mechanism; fMRI; social cognition; autistic spectrum disorder ID COMMUNICATION DEFICITS; NEURAL REPRESENTATION; VISUAL-ATTENTION; PET EXPLORATION; EYE GAZE; AUTISM; MIND; PERCEPTION; MECHANISMS; CHILDREN AB Although much is now known about eye movement detection, little is known about the higher cognitive processes involved in joint attention. We developed video stimuli which when watched, engender an experience of joint attention in the observer. This allowed us to compare an experience of joint attention to nonjoint attention within an fMRI scanning environment. Joint attention was associated with activity in the ventromedial frontal cortex, the left superior frontal gyrus (BA10), cingulate cortex, and caudate nuclei. The ventromedial frontal cortex has been consistently shown to be activated during mental state attribution tasks. BA10 may serve a cognitive integration function, which in this case seems to utilize a perception-action matching process. The activation we identified in BA10 overlaps with a location of increased grey matter density that we recently found to be associated with autistic spectrum disorder. This study therefore constitutes evidence that the neural substrate of joint attention also serves a mentalizing function. The developmental failure of this substrate in the left anterior frontal lobe may be important in the etiology of autistic spectrum disorder. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Aberdeen, Sch Med, Dept Child Hlth, Royal Aberdeen Childrens Hosp, Aberdeen AB25 2ZG, Scotland. 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While the selective serotonin-receptive inhibitor fluvoxamine has been shown to be effective in adults with autism, as yet no published placebo controlled trials with these agents document safety and efficacy in children with autism. This study examines the selective serotonin reuptake inhibitor liquid fluoxetine in the treatment of repetitive behaviors in childhood and adolescent autism spectrum disorders (ASDs). In total, 45 child or adolescent patients with ASD were randomized into two acute 8-week phases in a double-blind placebo-controlled crossover study of liquid fluoxetine. Study design included two randomized 8-week fluoxetine and placebo phases separated by a 4-week washout phase. Outcome measures included measures of repetitive behaviors and global improvement. Low-dose liquid fluoxetine ( mean final dose: 9.9 +/- 4.35 mg/day) was superior to placebo in the treatment of repetitive behaviors by CY-BOCS compulsion scale. The effect size was in the moderate to large range, and the doses used were low. Liquid fluoxetine was only slightly, and not significantly, superior to placebo on CGI autism score partially due to a phase order effect. However, fluoxetine was marginally superior to placebo on a composite measure of global effectiveness. Liquid fluoxetine did not significantly differ from placebo on treatment emergent side effects. Liquid fluoxetine in low doses is more effective than placebo in the treatment of repetitive behaviors in childhood autism. Limitations include small sample size and the crossover design of the study. Further replication and long-term maintenance trials are needed. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Seaver & New York Autism Ctr Excellence, New York, NY USA. RP Hollander, E (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. 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This article offers basic guidelines for distinguishing scientifically supported from unsupported treatments for 3 important childhood psychiatric disorders: autistic disorder, attention-deficit/hyperactivity disorder, and conduct disorder. A key challenge for the future will be to place the treatment of childhood psychiatric disorders on firmer scientific footing. C1 Emory Univ, Dept Psychol, Atlanta, GA 30322 USA. RP Lilienfeld, SO (reprint author), Emory Univ, Dept Psychol, Room 206,532 Kilgo Circle, Atlanta, GA 30322 USA. EM slilien@emory.edu CR ABIKOFF H, 1991, J LEARN DISABIL, V24, P205 Alexander J., 1982, FUNCTIONAL FAMILY TH Ayres AJ, 1979, SENSORY INTEGRATION Bassarath L, 2003, CAN J PSYCHIAT, V48, P367 BIKLEN D, 1990, HARVARD EDUC REV, V60, P291 Brestan EV, 1998, J CLIN CHILD PSYCHOL, V27, P180, DOI 10.1207/s15374424jccp2702_5 CAMPBELL M, 1984, ARCH GEN PSYCHIAT, V41, P650 Chambless DL, 2001, ANNU REV PSYCHOL, V52, P685, DOI 10.1146/annurev.psych.52.1.685 Cooper WO, 2004, ARCH PEDIAT ADOL MED, V158, P753, DOI 10.1001/archpedi.158.8.753 Dawson G, 2000, J AUTISM DEV DISORD, V30, P415, DOI 10.1023/A:1005547422749 DELMOLINO LM, 1995, BEHAV THERAPIST, V18, P27 Dishion TJ, 1999, AM PSYCHOL, V54, P755, DOI 10.1037//0003-066X.54.9.755 GUALTIERI T, 1987, NEUROBIOLOGICAL ISSU, P373 Henggeler S. W., 1998, MULTISYSTEMIC TREATM Herbert J. 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A., 2003, SCI PSEUDOSCIENCE CL, P333, DOI DOI 10.1023/B:JOYO.0000025323.94929.D9 Wegner DM, 2002, BRADFORD BOOKS, P1 WEISNER DA, 2000, DEATH PSYCHOTHERAPY Weisz JR, 2004, CLIN PSYCHOL-SCI PR, V11, P300, DOI 10.1093/clipsy/bph085 Westen D, 2004, PSYCHOL BULL, V130, P631, DOI 10.1037/0033-2909.130.4.631 ZHANG SC, 1999, 189787 NCJ CAL STAT NR 44 TC 19 Z9 19 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 EI 1098-4275 J9 PEDIATRICS JI Pediatrics PD MAR PY 2005 VL 115 IS 3 BP 761 EP 764 DI 10.1542/peds.2004-1713 PG 4 WC Pediatrics SC Pediatrics GA 905UV UT WOS:000227596900038 PM 15741383 ER PT J AU Newschaffer, CJ Falb, MD Gurney, JG AF Newschaffer, CJ Falb, MD Gurney, JG TI National autism prevalence trends from United States special education data SO PEDIATRICS LA English DT Article DE autism; prevalence; trends AB Objective. Reports of large increases in autism prevalence have been a matter of great concern to clinicians, educators, and parents. This analysis uses a national data source to compare the prevalence of autism with that of other disabilities among successive birth cohorts of US school-aged children. Design. Comparison of birth cohort curves constructed from administrative data. Setting and Population. US children 6 to 17 years of age between 1992 and 2001. Main Outcome Measures. A disability category classification of autism, mental retardation, speech and language impairment, traumatic brain injury, or other health impairment, as documented by state departments of education and reported to the Office of Special Education Programs, US Department of Education. Results. Prevalences of disability category classifications for annual birth cohorts from 1975 to 1995 were calculated by using denominators from US Census Bureau estimates. For the autism classification, there were birth cohort differences, with prevalences increasing among successive (younger) cohorts. The increases were greatest for annual cohorts born from 1987 to 1992. For cohorts born after 1992, the prevalence increased with each successive year but the increases did not appear to be as great, although there were fewer data points available within cohorts. No concomitant decreases in categories of mental retardation or speech/language impairment were seen. Curves for other health impairments, the category including children with attention-deficit/hyperactivity disorder, also showed strong cohort differences. Conclusions. Cohort curves suggest that autism prevalence has been increasing with time, as evidenced by higher prevalences among younger birth cohorts. The narrowing in vertical separation of the cohort curves in recent years may mark a slowing in the autism prevalence increase. C1 Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Autism & Dev Disabilities Epidemiol, Dept Epidemiol, Baltimore, MD 21205 USA. Univ Minnesota, Div Epidemiol, Minneapolis, MN 55455 USA. Univ Minnesota, Div Clin Res, Minneapolis, MN 55455 USA. RP Newschaffer, CJ (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Autism & Dev Disabilities Epidemiol, Dept Epidemiol, 615 N Wolfe St,Suite E6030, Baltimore, MD 21205 USA. 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As a result, there are few professionals who are trained to treat the disorder. Although efforts are currently under way to determine the prevalence of autism in China, to date there are no reliable data that indicate the magnitude of the problem. There are no formalized education programs for children with autism and only a handful of treatment programs in larger city hospitals and private schools. Treatments range from herbal medicines and acupuncture to sensory integration training and, in rare instances, applied behavior analysis (ABA). This article provides an update on what is taking place in China for autism treatment, and the challenges that lie ahead as the Chinese Ministry of Education struggles to address the needs of children identified with the disorder. (C) 2005 Wiley Periodicals, Inc. C1 Univ Utah, Dept Educ Psychol, Salt Lake City, UT 84112 USA. RP Clark, E (reprint author), Univ Utah, Dept Educ Psychol, 1705 Campus Ctr Dr,Room 327, Salt Lake City, UT 84112 USA. 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Schools PD MAR PY 2005 VL 42 IS 3 BP 285 EP 295 DI 10.1002/pits.20079 PG 11 WC Psychology, Educational SC Psychology GA 903XG UT WOS:000227458300007 ER PT J AU Carter, EW Cushing, LS Clark, NM Kennedy, CH AF Carter, EW Cushing, LS Clark, NM Kennedy, CH TI Effects of peer support interventions on students' access to the general curriculum and social interactions SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE inclusion; peer supports; peer-mediated instruction; general education curriculum; social interaction; students with severe disabilities ID COOPERATIVE LEARNING GROUPS; EDUCATION CLASSROOMS; SIGNIFICANT DISABILITIES; PARAPROFESSIONALS; PARTICIPATION; PERSPECTIVES; ACHIEVEMENT; INCLUSION; TEACHERS; AUTISM AB Peer support interventions are emerging as an effective alternative to traditional paraprofessional models for assisting students with moderate to severe disabilities to access the general curriculum. To contribute to the refinement of peer support interventions, we evaluated the impact of altering the number of participating peers on the social and academic outcomes of students with and without disabilities. Our findings indicated that changes in the configuration of peer support arrangements differentially affected student outcomes. Specifically, higher levels of social interaction and contact with the general curriculum were observed when students with disabilities worked with two peers relative to one peer. The additive benefits of a second peer provide guidance to educators concerning the implementation of peer support interventions in inclusive classrooms. C1 Vanderbilt Univ, Dept Special Educ, Nashville, TN 37203 USA. Univ Wisconsin, Madison, WI USA. RP Kennedy, CH (reprint author), Vanderbilt Univ, Dept Special Educ, Box 328 Peabody, Nashville, TN 37203 USA. CR Agran M, 2002, EDUC TRAIN MENT RET, V37, P123 American Association on Mental Retardation, 2002, MENT RET DEF CLASS S BROER SM, IN PRESS EXCEPTIONAL Brown L, 1999, J ASSOC PERS SEVERE, V24, P250, DOI 10.2511/rpsd.24.4.250 BUKOWSKI WM, 1996, COMPANY KEEP FRIENDS CARTER EW, IN PRESS AM J MENTAL CAUSTONTHEOHARI, IN PRESS EXCEPTIONAL Cushing LS, 1997, J APPL BEHAV ANAL, V30, P139, DOI 10.1901/jaba.1997.30-139 CUSHING LS, 2003, TASH CONNECTIONS, V29, P8 CUSHING LS, 2004, INCLUDING STUDENTS S, P206 CUSHING LS, IN PRESS TEACHING EX DUGAN E, 1995, J APPL BEHAV ANAL, V28, P175, DOI 10.1901/jaba.1995.28-175 Fox NE, 1997, EXCEPT CHILDREN, V64, P81 French NK, 1999, J ASSOC PERS SEVERE, V24, P259, DOI 10.2511/rpsd.24.4.259 Garrison-Harrell L., 1997, FOCUS AUTISM OTHER D, V12, P241, DOI DOI 10.1177/108835769701200406 Gerber SB, 2001, EDUC EVAL POLICY AN, V23, P123, DOI 10.3102/01623737023002123 Giangreco MF, 2002, FOCUS EXCEPT CHILD, V34, P1 Giangreco MF, 1997, EXCEPT CHILDREN, V64, P7 Giangreco MF, 2001, EXCEPT CHILDREN, V68, P45 Giangreco MF, 2001, J ASSOC PERS SEVERE, V26, P75, DOI 10.2511/rpsd.26.2.75 Giangreco M.F., 2004, J SPECIAL ED LEADERS, V17, P82 Gilberts GH, 2001, J ASSOC PERS SEVERE, V26, P25, DOI 10.2511/rpsd.26.1.25 Goldstein H., 2002, PROMOTING SOCIAL COM GRANSTROM K, 1996, EDUC PSYCHOL, V16, P349, DOI 10.1080/0144341960160401 Harrower JK, 2001, BEHAV MODIF, V25, P762, DOI 10.1177/0145445501255006 Hemmingsson H, 2003, OTJR-OCCUP PART HEAL, V23, P88 HUNT P, 1994, J ASSOC PERS SEVERE, V19, P290 Kennedy C., 2004, INCLUDING STUDENTS S Kennedy C, 2005, SINGLE CASE DESIGNS Kennedy C. 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L., 2001, FDN INCLUSIVE ED COM SASSO GM, 1998, FOCUS AUTISM OTHER D, V13, P2 SCHMITT DR, 1984, J EXP ANAL BEHAV, V42, P377, DOI 10.1901/jeab.1984.42-377 SCHWARTZ IS, 1991, J APPL BEHAV ANAL, V24, P189, DOI 10.1901/jaba.1991.24-189 Shukla S., 1998, J BEHAV ED, V8, P397, DOI DOI 10.1023/A:1022801215119 Shukla S, 1999, J POSIT BEHAV INTERV, V1, P130, DOI DOI 10.1177/109830079900100301 York J, 1995, J ASSOC PERS SEVERE, V20, P31 *US DEP ED, 2002, 24 ANN REP C IMPL IN Werts MG, 1996, J APPL BEHAV ANAL, V29, P53, DOI 10.1901/jaba.1996.29-53 2004, INDIVIDUALS DISABILI, V118 NR 47 TC 36 Z9 36 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SPR PY 2005 VL 30 IS 1 BP 15 EP 25 DI 10.2511/rpsd.30.1.15 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 942HF UT WOS:000230272800004 ER PT J AU Cohen, S Taranto, D AF Cohen, S Taranto, D TI Autism spectrum disorders: Interventions and treatments for children and youth. SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Book Review C1 CUNY Hunter Coll, New York, NY 10021 USA. RP Cohen, S (reprint author), CUNY Hunter Coll, New York, NY 10021 USA. CR Greenspan SI, 1999, J ASSOC PERS SEVERE, V24, P147, DOI 10.2511/rpsd.24.3.147 HEFFLIN LJ, 1998, FOCUM AUTISM OTHER D, V13, P194 KOEGEL LK, 2004, OVERCOMING MUTISM FI SIMPSON RL, AUTISM SPECTRUM DISO NR 4 TC 0 Z9 0 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SPR PY 2005 VL 30 IS 1 BP 42 EP 43 DI 10.2511/rpsd.30.1.42 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 942HF UT WOS:000230272800007 ER PT J AU Reid, DH Parsons, MB Lattimore, LP Towery, DL Reade, KK AF Reid, DH Parsons, MB Lattimore, LP Towery, DL Reade, KK TI Improving staff performance through clinician application of outcome management SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE performance; outcome management; clinician application ID ORGANIZATIONAL-BEHAVIOR MANAGEMENT; DEVELOPMENTAL-DISABILITIES; FEEDBACK; ACCEPTABILITY; SETTINGS; PEOPLE AB In two studies, three clinicians were assisted in using an outcome management approach to supervision for improving the work performance of their staff assistants. Using vocal and written instructions, feedback, and modeling, each clinician was assisted in specifying an area of staff performance (or consumer activity related to staff performance) to improve, developing and implementing a performance monitoring system, training staff in the targeted performances using performance- and competency-based training, and providing on-the-job supportive and corrective feedback. In Study 1, a senior job coach was assisted in using the outcome management steps to improve prompting procedures of three staff job coaches working with supported workers with autism in a community job. Correct prompting improved for all three job coaches following implementation of the outcome management process by the senior job coach. In Study 2, two teachers in two adult education classrooms were assisted in using the process to improve the degree to which their assistants involved students with severe disabilities in meal-preparation activities. Student participation in the activities increased in both classrooms when the teachers implemented the outcome management steps. In both studies, improved performances maintained for at least a 14-week period. Results are discussed in regard to working with supervisors as representing one step in promoting the adoption of research-based supervisory strategies within human service organizations. (c) 2004 Elsevier Ltd. All rights reserved. C1 Carolina Behav Anal & Support Ctr, Morganton, NC 28680 USA. W Carolina Ctr, Morganton, NC USA. RP Reid, DH (reprint author), Carolina Behav Anal & Support Ctr, POB 425, Morganton, NC 28680 USA. EM drhmc@vistatech.net CR ALAVOSIUS MP, 1990, J APPL BEHAV ANAL, V23, P151, DOI 10.1901/jaba.1990.23-151 Alvero AM, 2001, J ORGAN BEHAV MANAGE, V21, P3, DOI 10.1300/J075v21n01_02 Babcock RA, 1998, J ORGAN BEHAV MANAGE, V18, P33, DOI 10.1300/J075v18n02_03 BRADLEY VJ, 1997, QUALITY LIFE, V2, P149 Daniels A. C., 1994, BRINGING OUT BEST PE FLYNN T, 1991, VOCATIONAL REHABILIT, V1, P25 GREEN CW, 1994, J DEV PHYS DISABIL, V6, P219, DOI 10.1007/BF02578412 Harchik AE, 1998, J ORGAN BEHAV MANAGE, V18, P83, DOI 10.1300/J075v18n02_05 Jahr E, 1998, RES DEV DISABIL, V19, P73, DOI 10.1016/S0891-4222(97)00030-9 Jensen JM, 1998, RES DEV DISABIL, V19, P449, DOI 10.1016/S0891-4222(98)00017-1 PAGE TJ, 1982, J APPL BEHAV ANAL, V15, P335, DOI 10.1901/jaba.1982.15-335 Parsons MB, 1998, J ORGAN BEHAV MANAGE, V18, P173, DOI 10.1300/J075v18n02_09 PARSONS MB, 1995, J APPL BEHAV ANAL, V28, P317, DOI 10.1901/jaba.1995.28-317 PECK CA, 1989, J APPL BEHAV ANAL, V22, P197, DOI 10.1901/jaba.1989.22-197 Phillips JF, 1998, J ORGAN BEHAV MANAGE, V18, P103, DOI 10.1300/J075v18n02_06 Reid D. H., 2004, POSITIVE BEHAV SUPPO Reid D. H., 2002, WORKING STAFF OVERCO REID DH, 1995, J APPL BEHAV ANAL, V28, P95, DOI 10.1901/jaba.1995.28-95 REID H, 2004, J APPL BEHAV ANAL, V36, P575 Schell RM, 1998, J ORGAN BEHAV MANAGE, V18, P157, DOI 10.1300/J075v18n02_08 SHORE BA, 1995, J APPL BEHAV ANAL, V28, P323, DOI 10.1901/jaba.1995.28-323 Sturmey P, 1998, J ORGAN BEHAV MANAGE, V18, P7, DOI 10.1300/J075v18n02_02 NR 22 TC 16 Z9 16 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD MAR-APR PY 2005 VL 26 IS 2 BP 101 EP 116 DI 10.1016/j.ridd.2004.05.002 PG 16 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 905NB UT WOS:000227574300001 PM 15590242 ER PT J AU Fisher, WW Adelinis, JD Volkert, VM Keeney, KM Neidert, PL Hovanetz, A AF Fisher, WW Adelinis, JD Volkert, VM Keeney, KM Neidert, PL Hovanetz, A TI Assessing preferences for positive and negative reinforcement during treatment of destructive behavior with functional communication training SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE autism; choice; functional analysis; positive reinforcement; negative reinforcement ID SELF-INJURIOUS-BEHAVIOR; ESCAPE BEHAVIOR; NONCONTINGENT REINFORCEMENT; DIFFERENTIAL REINFORCEMENT; FOOD REFUSAL; EXTINCTION; REFINEMENTS; PUNISHMENT; OPERATIONS AB Results of prior studies (e.g. [J. Appl. Behav. Anal. 32 (1999) 285]) showing that participants chose alternative behavior (compliance) over escape-reinforced destructive behavior when this latter response produced escape and the former response produced positive reinforcement may have been due to (a) the value of the positive reinforcer overriding the value of the negative reinforcer or (b) the presence of the positive reinforcer altering the value of the negative reinforcer (i.e., lessening the aversiveness of the demands). In this investigation we evaluated the relative contributions of these alternative mechanisms with two girls with autism. We compared the relative effects of positive and negative reinforcement using equivalent communication responses under both a restricted-choice condition (in which participants could choose positive or negative reinforcement, but not both) and an unrestricted-choice condition (in which participants could choose one or both reinforcers). Both participants often chose positive over negative reinforcement in the restricted-choice condition. However, in the unrestricted-choice condition (in which participants could choose one or both reinforcers), one participant consistently chose both reinforcers by the end of the analysis whereas the other primarily chose only positive reinforcement. Results suggested that for one participant the value of the positive reinforcer overrode the value of the negative reinforcer, whereas for the other participant, the presence of the positive reinforcer in the demand context lessened the aversiveness of the demands. (c) 2004 Elsevier Ltd. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Marcus Inst, Marcus Behav Ctr, Atlanta, GA 30329 USA. Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Atlanta, GA 30329 USA. RP Fisher, WW (reprint author), Johns Hopkins Univ, Sch Med, Marcus Inst, Marcus Behav Ctr, 1920 Briarcliff Rd, Atlanta, GA 30329 USA. 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Dev. Disabil. PD MAR-APR PY 2005 VL 26 IS 2 BP 153 EP 168 DI 10.1016/j.ridd.2004.01.007 PG 16 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 905NB UT WOS:000227574300005 PM 15590246 ER PT J AU Gabriels, RL Cuccaro, ML Hill, DE Ivers, BJ Goldson, E AF Gabriels, RL Cuccaro, ML Hill, DE Ivers, BJ Goldson, E TI Repetitive behaviors in autism: relationships with associated clinical features SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE repetitive behaviors; autism; NVIQ ID YOUNG-CHILDREN; SLEEP PROBLEMS; DEVELOPMENTAL DISORDERS; PREDICTORS; SYMPTOMS; INDIVIDUALS; FAMILIES AB Relationships between repetitive behaviors (RBs) and associated clinical features (i.e., cognitive and adaptive functioning levels, sleep problems, medication use, and other behavioral problems) were examined in two groups (High nonverbal IQ > 97 versus Low nonverbal IQ < 56) of children with autism spectrum disorders (n = 14; mean age = 10 years, 7 months). For the group as a whole, nonverbal cognitive ability (NVIQ) (as measured by the Leiter-R), adaptive functioning level, the presence of sleep problems, and three scales of the Aberrant Behavior Checklist (ABC) (Irritability, Lethargy, and Hyperactivity) were highly correlated with total RB scores on the Repetitive Behavior Scale-Revised (RBS-R). After controlling for NVIQ, adaptive level, sleep problems, and two scales of the ABC (Irritability and Lethargy) were not significantly associated with RB scores. However, there remained a significant positive correlation between the presence of RBs and the Hyperactivity scale of the ABC. Parent ratings of their stress levels and the presence of RBs in their children were highly correlated. The relationship between RBs and associated clinical features in autism is complex and future studies should control for cognitive ability when examining the direct and indirect relationships of these variables with RBs. (c) 2004 Elsevier Ltd. All rights reserved. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Childrens Hosp, Dept Psychiat, Denver, CO 80218 USA. Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC USA. Duke Univ, Med Ctr, Dept Psychiat, Durham, NC 27710 USA. Univ New Mexico, Dept Psychiat, Albuquerque, NM 87131 USA. Univ Denver, Sch Profess Psychol, Denver, CO USA. Childrens Hosp, Dept Pediat, Denver, CO 80218 USA. RP Gabriels, RL (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. 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Dev. Disabil. PD MAR-APR PY 2005 VL 26 IS 2 BP 169 EP 181 DI 10.1016/j.ridd.2004.05.003 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 905NB UT WOS:000227574300006 PM 15590247 ER PT J AU Ayvazo, S Ward, P AF Ayvazo, S Ward, P TI Effects of classwide peer tutoring on the catching performance of children with and without autism in physical education SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Ohio State Univ, Columbus, OH 43210 USA. EM ayvazo.1@osu.edu NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2005 VL 76 IS 1 SU S BP A112 EP A112 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 906NK UT WOS:000227648700303 ER PT J AU Hagar, KA Yun, JK AF Hagar, KA Yun, JK TI The relationship of sleep pattern and physical activity in children with autism SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Oregon State Univ, Corvallis, OR 97331 USA. EM kristinehagar@hotmail.com NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2005 VL 76 IS 1 SU S BP A114 EP A114 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 906NK UT WOS:000227648700309 ER PT J AU Pan, CY Frey, GC AF Pan, CY Frey, GC TI Identifying physical activity determinants in youth with autism spectrum disorders SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Indiana Univ, Bloomington, IN 47405 USA. EM chienyup@yahoo.com NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2005 VL 76 IS 1 SU S BP A116 EP A117 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 906NK UT WOS:000227648700315 ER PT J AU Pan, CY Frey, GC AF Pan, CY Frey, GC TI Physical activity patterns in youth with autism spectrum disorders SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Indiana Univ, Bloomington, IN 47405 USA. EM chienyup@yahoo.com NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2005 VL 76 IS 1 SU S BP A117 EP A117 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 906NK UT WOS:000227648700316 ER PT J AU Yilmaz, Y Birkan, B Konukman, F Agbuga, B AF Yilmaz, Y Birkan, B Konukman, F Agbuga, B TI Effects of progressive time delay method on teaching basic progression swimming skills for children with autism SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract C1 Texas A&M Univ, College Stn, TX 77843 USA. EM ilkery@anadolu.edu.tr NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2005 VL 76 IS 1 SU S BP A119 EP A120 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 906NK UT WOS:000227648700323 ER PT J AU Yilmaz, Y Birkan, B Konukman, F AF Yilmaz, Y Birkan, B Konukman, F TI Effects of least-to-most prompting on teaching prerequisite skills of tennis to children with autism in small group instructional arrangements SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Meeting Abstract EM ilkery@anadolu.edu.tr NR 0 TC 0 Z9 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 2005 VL 76 IS 1 SU S BP A120 EP A120 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 906NK UT WOS:000227648700324 ER PT J AU Sanjuan, J Tolosa, A Gonzalez, JC Aguilar, EJ Molto, MD Najera, C de Frutos, R AF Sanjuan, J Tolosa, A Gonzalez, JC Aguilar, EJ Molto, MD Najera, C de Frutos, R TI FOXP2 polymorphisms in patients with schizophrenia SO SCHIZOPHRENIA RESEARCH LA English DT Article DE FOXP2; schizophrenia; polymorphisms; language; evolutionary ID SUSCEPTIBILITY GENE; LANGUAGE; SPEECH; AUTISM; EVOLUTION; DISORDER AB Background: FOXP2 was described as the first gene involved in our ability to acquire spoken language. The main objective of this study was to compare the distribution of FOXP2 gene polymorphisms between patients with schizophrenia and healthy controls. Methods: Two FOXP2 polymorphisms, Intron3a and SNP 923875, and the G-->A transition in exon 14 were analysed in 149 patients with schizophrenia and schizoaffective disorders according to DSM-IV, as well as in 137 controls. All the patients showed a history of auditory hallucinations. Results: The transition G-->A at exon 14, detected in all the affected members in KE family, was not found in any of the analyzed samples from patients or controls. No significant differences were found between individual controls and patients for the two analysed polymorphisms. Conclusions: This study would not support a possible role of the two FOXP2 analyzed polymorphisms in the vulnerability to schizophrenia. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Valencia, Hosp CLin, Fac Med, Unidad Psiquiatria, E-46010 Valencia, Spain. Univ Valencia, Fac Biol, Dept Genet, E-46100 Burjassot, Valencia, Spain. Hosp Sagunto, Valencia 46520, Spain. RP Sanjuan, J (reprint author), Univ Valencia, Hosp CLin, Fac Med, Unidad Psiquiatria, Blasco Ibaez 15, E-46010 Valencia, Spain. 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RP Hussain, NK (reprint author), MIT, Howard Hughes Med Inst, RIKEN MIT Neurosci Res Ctr, Picower Ctr Learning & Memory, Cambridge, MA 02139 USA. 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Synapse formation is thought to be regulated by bidirectional signaling between pre- and postsynaptic cells. We demonstrate that members of the Neuroligin family promote postsynaptic differentiation in cultured rat hippocampal neurons. Down-regulation of neuroligin isoform expression by RNA interference results in a loss of excitatory and inhibitory synapses. Etectrophysiological analysis revealed a predominant reduction of inhibitory synaptic function. Thus, neuroligins control the formation and functional balance of excitatory and inhibitory synapses in hippocampal neurons. C1 Columbia Univ, Ctr Neurobiol & Behav, Dept Physiol & Cellular Biophys, New York, NY 10032 USA. RP Scheiffele, P (reprint author), Columbia Univ, Ctr Neurobiol & Behav, Dept Physiol & Cellular Biophys, New York, NY 10032 USA. 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Up until now a specific cognitive deficit in autism has not been found, although the majority of people with autism show intellectual impairment, verbal scores lower than manipulative measures and executive dysfunctions. Aims. A neuropsychological evaluation of children with AD was planned. These children had intellectual abilities in the normal range. They were compared with two other groups, one with pervasive developmental disorder not otherwise specified (PDD-NS), and the other from the general population. Subjects and methods. A battery of neuropsychological tests was carried out on five boys AD, five boys PDD-NS, and five boys of the general population. All of them were between 9 and 15 years old and their intellectual abilities were within the normal range. Results. The children AD obtained verbal scores lower than their visual-perception scores. They also showed good dynamic coordination of movement. 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MECP2 encodes methyl-CpG-binding protein 2 that acts as a transcriptional repressor for methylated gene constructs but is surprisingly not required for maintaining imprinted gene expression. Here, we test the hypothesis that MECP2 deficiency may affect the level of expression of UBE3A and neighboring autism candidate gene GABRB3 without necessarily affecting imprinted expression. Multiple quantitative methods were used including automated quantitation of immunofluorescence and in situ hybridization by laser scanning cytometry on tissue microarrays, immunoblot and TaqMan PCR. The results demonstrated significant defects in UBE3A/ E6AP expression in two different Mecp2 deficient mouse strains and human Rett, Angelman and autism brains compared with controls. Although no difference was observed in the allelic expression of several imprinted transcripts in Mecp2-null brain, Ube3a sense expression was significantly reduced, consistent with the decrease in protein. A non-imprinted gene from 15q11-q13, GABRB3, encoding the 03 subunit of the GABAA receptor, also showed significantly reduced expression in multiple Rett, Angelman and autism brain samples, and Mecp2 deficient mice by quantitative immunoblot. These results suggest an overlapping pathway of gene dysregulation within 15q11-q13 in Rett, Angelman and autism and implicate MeCP2 in the regulation of UBE3A and GABRB3 expressions in the postnatal mammalian brain. C1 Univ Calif Davis, Rowe Program Human Genet, Sch Med, Davis, CA 95616 USA. RP LaSalle, JM (reprint author), Univ Calif Davis, Rowe Program Human Genet, Sch Med, Davis, CA 95616 USA. 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Biol. PD FEB 8 PY 2005 VL 15 IS 3 BP R84 EP R85 DI 10.1016/j.cub.2005.01.022 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 897TI UT WOS:000227027700008 PM 15694294 ER PT J AU Molholm, S Foxe, JJ AF Molholm, S Foxe, JJ TI Look 'hear', primary auditory cortex is active during lip-reading SO NEUROREPORT LA English DT Editorial Material DE audio-visual; crossmodal; Heschl's gyrus; multisensory; sensory integration theory ID SPEECH-PERCEPTION; INTEGRATION; BINDING; AUTISM; FMRI C1 Nathan S Kline Inst Psychiat Res, Program Cognit Neurosci & Schizophrenia, Cognit Neurophysiol Lab, Orangeburg, NY 10962 USA. CUNY City Coll, Dept Psychol, Program Cognit Neurosci, New York, NY 10031 USA. RP Foxe, JJ (reprint author), Nathan S Kline Inst Psychiat Res, Program Cognit Neurosci & Schizophrenia, Cognit Neurophysiol Lab, 140 Old Orangeburg Rd, Orangeburg, NY 10962 USA. 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Setting: New South Wales (NSW) and Western Australia (WA), July 1999 to December 2000. Design: Data were obtained for WA from a prospective register and for NSW by active surveillance. Main outcome measures: Newly recognised cases of autism spectrum disorders (defined as autistic disorder, Asperger disorder and pervasive developmental disorder not otherwise specified [PDD-NOS]) in children aged 0-14 years; incidence was estimated in 5-year age bands (0-4 years, 5-9 years, 10-14 years). Results: In WA, 252 children aged 0-14 years were identified with autism spectrum disorder (169 with autistic disorder and 83 with Asperger disorder or PDD-NOS). Comparable figures in NSW were 532, 400 and 132, respectively. Most children were recognised with autistic disorder before school age (median age, 4 years in WA and 3 years in NSW). Incidence of autistic disorder in the 0-4-years age group was 5.5 per 10 000 in WA (95% Cl, 4.5-6.7) and 4.3 per 10 000 in NSW (95% Cl, 3.8-4.8). 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J. Aust. PD FEB 7 PY 2005 VL 182 IS 3 BP 108 EP 111 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 902HS UT WOS:000227346100006 PM 15698353 ER PT J AU Feng, JN Chen, JS Yan, J Jones, IR Craddock, N Cook, EH Goldman, D Heston, LL Sommer, SS AF Feng, JN Chen, JS Yan, J Jones, IR Craddock, N Cook, EH Goldman, D Heston, LL Sommer, SS TI Structural variants in the retinoid receptor genes in patients with schizophrenia and other psychiatric diseases SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE schizophrenia; retinoic acid receptors (RARs); retinoid X receptors (RXRs); NURR1 gene; mutation detection ID ALPHA GENES; NGFI-B; NURR1; EXPRESSION; MUTATIONS; SYSTEM; ACID; BETA AB Retinoid receptors (RARs and RXRs) regulate brain morphogenesis and function. Defects in these receptors may contribute to schizophrenia or other psychiatric diseases. To test the hypothesis that genetic variants of the retinoid receptor genes may predispose to schizophrenia and other psychiatric diseases, the six RAR and RXR genes and a heterodimer partner, the NURR1 gene, were scanned in 100 schizophrenia patients, along with pilot studies in 20-24 patients with bipolar disorder (BPD), attention-deficit hyperactivity disorder (ADHD), autism, or alcoholism. A total of 5.4 megabases of genomic sequence was scanned. No variants affecting protein structure or expression (VAPSEs) were found in four of the genes. One uncommon missense variant was found in each of the RARbeta, RARgamma, and RXRgamma genes. We conclude that structural variants in the RAR/RXR and NURR1 genes do not play a major role in the etiology of schizophrenia. (C) 2005 Wiley-Liss, Inc. C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. City Hope Natl Med Ctr, Dept Mol Diag, Duarte, CA 91010 USA. Univ Wales Coll Med, Dept Psychol Med, Cardiff CF4 4XN, S Glam, Wales. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. NIAAA, Dept Psychiat, NIH, Bethesda, MD USA. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. RP Sommer, SS (reprint author), City Hope Natl Med Ctr, Dept Mol Genet, 1500 E Duarte Rd, Duarte, CA 91010 USA. EM sommerlab@coh.org RI Jones, Ian/B-4925-2009; Goldman, David/F-9772-2010; turton, miranda/F-4682-2011 CR Aranda A, 2001, PHYSIOL REV, V81, P1269 Buervenich S, 2000, AM J MED GENET, V96, P808, DOI 10.1002/1096-8628(20001204)96:6<808::AID-AJMG23>3.0.CO;2-E Carmine A, 2003, AM J MED GENET B, V120B, P51, DOI 10.1002/ajmg.b.20033 Chambon P, 1996, FASEB J, V10, P940 Chiang MY, 1998, NEURON, V21, P1353, DOI 10.1016/S0896-6273(00)80654-6 Feng JN, 2001, AM J MED GENET, V105, P369, DOI 10.1002/ajmg.1364 Feng JN, 1998, AM J MED GENET, V81, P172 Goodman AB, 1998, P NATL ACAD SCI USA, V95, P7240, DOI 10.1073/pnas.95.13.7240 Goodman AB, 1996, SCHIZOPHR RES, V19, P163, DOI 10.1016/0920-9964(96)88523-9 Ishiguro H, 2002, AM J MED GENET, V114, P15, DOI 10.1002/ajmg.1620 Iwayama-Shigeno Y, 2003, AM J MED GENET B, V118B, P20, DOI 10.1002/ajmg.b.10053 Kastner P, 1997, DEVELOPMENT, V124, P313 Krezel W, 1998, SCIENCE, V279, P863 Maden M, 2002, NAT REV NEUROSCI, V3, P843, DOI 10.1038/nrn963 PERLMANN T, 1995, GENE DEV, V9, P769, DOI 10.1101/gad.9.7.769 Zetterstrom RH, 1996, MOL BRAIN RES, V41, P111, DOI 10.1016/0169-328X(96)00074-5 NR 16 TC 6 Z9 6 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. 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B PD FEB 5 PY 2005 VL 133B IS 1 BP 50 EP 53 DI 10.1002/ajmg.b.30113 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 891ZN UT WOS:000226619600009 PM 15635645 ER PT J AU Mulder, EJ Anderson, GM Kema, IP Brugman, AM Ketelaars, CEJ de Bildt, A van Lang, NDJ den Boer, JA Minderaa, RB AF Mulder, EJ Anderson, GM Kema, IP Brugman, AM Ketelaars, CEJ de Bildt, A van Lang, NDJ den Boer, JA Minderaa, RB TI Serotonin transporter intron 2 polymorphism associated with rigid-compulsive behaviors in Dutch individuals with pervasive developmental disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autistic disorder; serotonin transporter gene; HTT(SLC6A4); 5-HTTLPR; intron 2 VNTR ID GENE PROMOTER VARIANTS; HUMAN BLOOD-PLATELETS; AUTISTIC DISORDER; TRANSMISSION DISEQUILIBRIUM; DIAGNOSTIC INTERVIEW; GENOMEWIDE SCREEN; GENOMIC SCREEN; REGION; LINKAGE; FAMILIES AB Two putatively functional polymorphisms of the serotonin transporter gene (HTT, SLC6A4) were examined for associations with risk for pervasive developmental disorders (PDDs) and specific autism phenotypes. Dutch patients diagnosed with PDD (N = 125, age range 5-20 years, DSM-IV-TR based criteria, ADI-R and ADOS behavioral assessments) and their parents (N = 230) were genotyped for promoter ins/del (5-HTTLPR) and intron 2 variable number of tandem repeats (VNTR) alleles. Using the transmission disequilibrium test (TDT), no disorder-specific preferential transmission of promoter (long and short) or intron 2 (10- and 12-repeat) alleles was observed. However, multivariate analysis of continuous autism-related behavioral measures revealed that subjects with intron 2 12/12 genotype were significantly more impaired in the rigid-compulsive domain (P = 0.008). Quantitative TDT (QTDT) analysis also showed significant association of the intron 2 VNTR 12-repeat allele with rigid-compulsive behavior (P = 0.015). These results suggest that intron 2 VNTR alleles or nearby polymorphisms in linkage disequilibrium. may play a role in specific aspects of the behavioral phenotype of autism. (C) 2005 Wiley-Liss, Inc. C1 Univ Groningen, Child & Adolescent Psychiat Ctr, NL-9700 RB Groningen, Netherlands. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT USA. Univ Groningen Hosp, Dept Pathol & Lab Med, Groningen, Netherlands. Univ Groningen, Dept Biol Psychiat, Groningen, Netherlands. RP Mulder, EJ (reprint author), Univ Groningen, Child & Adolescent Psychiat Ctr, POB 660, NL-9700 RB Groningen, Netherlands. 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J. Med. Genet. B PD FEB 5 PY 2005 VL 133B IS 1 BP 93 EP 96 DI 10.1002/ajmg.b.30122 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 891ZN UT WOS:000226619600018 PM 15635668 ER PT J AU McDermott, S Moran, R Platt, T Issac, T Wood, H Dasari, S AF McDermott, S Moran, R Platt, T Issac, T Wood, H Dasari, S TI Depression in adults with disabilities, in primary care SO DISABILITY AND REHABILITATION LA English DT Article ID NATIONAL-COMORBIDITY-SURVEY; INTELLECTUAL DISABILITY; SYMPTOMS; EPIDEMIOLOGY; LIFETIME; INJURY; PEOPLE; RISK AB Purpose: This research was designed to answer the question: Does the prevalence of depression differ between adults with and without disability, in the same family medicine practice? Method: A retrospective cohort design was used, to study depression among adults, with and without primary disabling conditions, receiving primary care in either a university based urban or rural family practice setting. Results: When we compared individuals with disability to those without disability, and controlled for individual characteristics, the relative risk for depression was significantly lower for individuals with autism (Relative Risk (RR) 0.20: 95% Confidence Interval (CI) 0.05-0.55), cerebral palsy with mental retardation (RR 0.40: 95% CI: 0.24-0.65), and MR (RR 0.56: 95% CI: 0.39-0.77). The risk for depression was significantly higher for those with cerebral vascular accidents/stroke (RR 2.18: 95% CI: 1.72-3.76) and traumatic brain injury (RR 2.55: 95% CI: 1.72-2.77). The earliest onset of depression was among individuals with traumatic disabilities and mild mental retardation. Our estimate of depression prevalence for the non-disabled and disabled primary care patients was 22.8% and 24.9% respectively, when patients with disabilities were grouped together (p=0.008). Conclusion: It is important for physicians to recognize the higher prevalence of depression among patients with adult onset disabilities ( e. g. stroke, traumatic brain injury). In addition, they should be aware of lower prevalence of depression among many individuals with lifelong disabilities, such as mental retardation, cerebral palsy, and autism. C1 Univ S Carolina, Sch Med, Dept Family & Prevent Med, Columbia, SC USA. RP McDermott, S (reprint author), Family Practice Ctr, 3209 Colonial Dr, Columbia, SC 29208 USA. EM Suzanne.mcdermott@palmettohealth.org CR CHARLOT LR, 1993, AM J MENT RETARD, V98, P408 Chen LS, 2000, AM J PSYCHIAT, V157, P573, DOI 10.1176/appi.ajp.157.4.573 Davis JP, 1997, AUST NZ J PSYCHIAT, V31, P232, DOI 10.3109/00048679709073826 Dickens C, 2003, PSYCHOSOMATICS, V44, P209, DOI 10.1176/appi.psy.44.3.209 Everson SA, 2002, J PSYCHOSOM RES, V53, P891, DOI 10.1016/S0022-3999(02)00303-3 Glenn MB, 2001, BRAIN INJURY, V15, P811, DOI 10.1080/02699050010025777 Holsinger T, 2002, ARCH GEN PSYCHIAT, V59, P17, DOI 10.1001/archpsyc.59.1.17 KESSLER RC, 1994, ARCH GEN PSYCHIAT, V51, P8 Kessler RC, 2003, JAMA-J AM MED ASSOC, V289, P3095, DOI 10.1001/jama.289.23.3095 Labbate L A, 2000, Curr Psychiatry Rep, V2, P268, DOI 10.1007/s11920-996-0021-3 Marston GM, 1997, J INTELL DISABIL RES, V41, P476, DOI 10.1111/j.1365-2788.1997.tb00739.x McBrien JA, 2003, J INTELL DISABIL RES, V47, P1, DOI 10.1046/j.1365-2788.2003.00455.x MEINS W, 1995, J INTELL DISABIL RES, V39, P41 SAS Institute, 1999, SAS STAT US GUID VER Seel RT, 2003, ARCH PHYS MED REHAB, V84, P177, DOI 10.1053/apmr.2003.50106 STURMEY P, 1993, J INTELL DISABIL RES, V37, P437 Horwath Ewald, 1995, P317 *WHO, 1980, INT STAT CLASS DIS Whyte EM, 2002, BIOL PSYCHIAT, V52, P253, DOI 10.1016/S0006-3223(02)01424-5 Wu Lawrence R, 2002, J Am Board Fam Pract, V15, P183 NR 20 TC 13 Z9 13 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1464-5165 J9 DISABIL REHABIL JI Disabil. Rehabil. PD FEB 4 PY 2005 VL 27 IS 3 BP 117 EP 123 DI 10.1080/09638280400007380 PG 7 WC Rehabilitation SC Rehabilitation GA 903WL UT WOS:000227456200006 PM 15823993 ER PT J AU Takahashi, TN Farmer, JE Deidrick, KK Hsu, BS Miles, JH Maria, BL AF Takahashi, TN Farmer, JE Deidrick, KK Hsu, BS Miles, JH Maria, BL TI Joubert syndrome is not a cause of classical autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE Joubert; autism; recurrence risks ID UTAH EPIDEMIOLOGIC SURVEY; FAMILY HISTORY METHOD; PSYCHIATRIC-DISORDERS; BEHAVIOR CHECKLIST; MEDICAL CONDITIONS; CEREBELLAR VERMIS; INFANTILE-AUTISM; POSTERIOR-FOSSA; DISABILITY; HYPOPLASIA AB A previous report noted a 27% prevalence of autism in Joubert syndrome (JS), raising the question of overlapping etiologies. Family studies have shown that autism is characterized by family loading for a number of specific behavioral and psychiatric disorders and that the sib recurrence risk is around 4%. The purpose of this study is to determine whether children with Joubert and their families show behavioral or genetic characteristics similar to autism. Thirty-one volunteer Joubert families were identified. Parents completed a semi-structured family history interview and the Autism Behavioral Checklist. Rates of family loading for neuropsychiatric disorders in the JS families were compared to autism family history data and Down syndrome (DS) controls. The JS families had significantly lower rates of autism, alcoholism, cognitive, and language disorders than the autism families. Their rate of depression was lower, but not significantly different from that found in autism families. None of the JS children met the clinical cut-off for autism based on parental symptom report and the sib recurrence risk was 32% for the JS families compared to 4% for the autism and 0% for DS families. These data indicate that JS is a genetically distinct disorder from autism. Different genes with different inheritance patterns that affect neurodevelopment of the cerebellum could explain the clinical similarities previously reported in JS and autism. (C) 2005 Wiley-Liss, Inc. C1 Univ Missouri, Childrens Hosp, Div Med Genet, Columbia, MO 65212 USA. Med Univ S Carolina, Childrens Canc Inst, Charleston, SC 29425 USA. RP Takahashi, TN (reprint author), Univ Missouri, Childrens Hosp, Div Med Genet, 1 Hosp Dr, Columbia, MO 65212 USA. EM takahashin@missouri.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT ANDREASEN NC, 1986, ARCH GEN PSYCHIAT, V43, P421 Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 CANTANI A, 1989, RIV ITAL PED, V15, P102 CHAPMAN C, 2000, CYRILLIC 2 1 3 COURCHESNE E, 1988, NEW ENGL J MED, V318, P1349, DOI 10.1056/NEJM198805263182102 COURCHESNE E, 1994, AM J ROENTGENOL, V162, P123 Davies NJ, 1997, AM J MED GENET, V74, P12, DOI 10.1002/(SICI)1096-8628(19970221)74:1<12::AID-AJMG3>3.0.CO;2-X DEB S, 1994, BRIT J PSYCHIAT, V165, P395, DOI 10.1192/bjp.165.3.395 DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 Eaves RC, 2000, PSYCHOL SCHOOLS, V37, P311, DOI 10.1002/1520-6807(200007)37:4<323::AID-PITS2>3.0.CO;2-S Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 HASHIMOTO T, 1995, J AUTISM DEV DISORD, V25, P1, DOI 10.1007/BF02178163 HOLROYD S, 1991, BIOL PSYCHIAT, V29, P287, DOI 10.1016/0006-3223(91)91291-X HOLTTUM JR, 1992, BIOL PSYCHIAT, V32, P1091, DOI 10.1016/0006-3223(92)90189-7 KLEIMAN MD, 1992, NEUROLOGY, V42, P753 Krug DA, 1993, AUTISM SCREENING INS Maria BL, 1999, J CHILD NEUROL, V14, P368, DOI 10.1177/088307389901400605 Maria BL, 1997, J CHILD NEUROL, V12, P423 Miles JH, 2003, J AUTISM DEV DISORD, V33, P403, DOI 10.1023/A:1025010828304 Miles JH, 2000, AM J MED GENET, V91, P245, DOI 10.1002/(SICI)1096-8628(20000410)91:4<245::AID-AJMG1>3.0.CO;2-2 Miranda-Linne FM, 2002, J AUTISM DEV DISORD, V32, P181, DOI 10.1023/A:1015519413133 Nordin V, 1996, DEV MED CHILD NEUROL, V38, P297 ORVASCHEL H, 1982, J AFFECT DISORDERS, V4, P49, DOI 10.1016/0165-0327(82)90019-2 Ozonoff S, 1999, J CHILD NEUROL, V14, P636, DOI 10.1177/088307389901401003 Piven J, 1999, AM J PSYCHIAT, V156, P557 PIVEN J, 1991, J AM ACAD CHILD PSY, V30, P471, DOI 10.1097/00004583-199105000-00019 Piven J, 1997, NEUROLOGY, V49, P546 RICE JP, 1995, ALCOHOL CLIN EXP RES, V19, P1018, DOI 10.1111/j.1530-0277.1995.tb00983.x RITVO ER, 1990, AM J PSYCHIAT, V147, P1614 RITVO ER, 1989, AM J PSYCHIAT, V146, P1032 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x SARAIVA JM, 1992, AM J MED GENET, V43, P726, DOI 10.1002/ajmg.1320430415 Schaefer GB, 1996, ANN NEUROL, V39, P382, DOI 10.1002/ana.410390316 Schopler E., 1986, CHILDHOOD AUTISM RAT SMALLEY SL, 1995, AM J MED GENET, V60, P19, DOI 10.1002/ajmg.1320600105 STURMEY P, 1992, J AUTISM DEV DISORD, V22, P321, DOI 10.1007/BF01058159 THOMPSON WD, 1982, ARCH GEN PSYCHIAT, V39, P53 NR 41 TC 10 Z9 10 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD FEB 1 PY 2005 VL 132A IS 4 BP 347 EP 351 DI 10.1002/ajmg.a.30500 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 893HO UT WOS:000226710100002 PM 15633174 ER PT J AU Vargas, DL Nascimbene, C Krishnan, C Zimmerman, AW Pardo, CA AF Vargas, DL Nascimbene, C Krishnan, C Zimmerman, AW Pardo, CA TI Neuroglial activation and neuroinflammation in the brain of patients with autism (vol 57, pg 67, 2005) SO ANNALS OF NEUROLOGY LA English DT Correction CR Vargas DL, 2005, ANN NEUROL, V57, P67, DOI 10.1002/ana.20315 NR 1 TC 2 Z9 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD FEB PY 2005 VL 57 IS 2 BP 304 EP 304 DI 10.1002/ana.20397 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 892EW UT WOS:000226633800023 ER PT J AU Croen, LA Grether, JK Yoshida, CK Odouli, R Van de Water, J AF Croen, LA Grether, JK Yoshida, CK Odouli, R Van de Water, J TI Maternal autoimmune diseases, asthma and allergies, and childhood autism spectrum disorders - A case-control study SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID MULTIPLE-SCLEROSIS; FAMILIAL AUTOIMMUNITY; RHEUMATOID-ARTHRITIS; RISK-FACTORS; PREVALENCE; CYTOKINES; CHILDREN; EPIDEMIOLOGY; ASSOCIATION; POPULATION AB objective: To investigate the association between physician-documented diagnoses of maternal autoimmune diseases, allergies, and asthma around the time of pregnancy and subsequent diagnoses of autism in children. Design: A case-control study nested within a cohort of infants born between January 1995 and June 1999. Setting: Northern California Kaiser Permanente Medical Care Program. Participants: Cases (n = 420) were children with at least I diagnosis of an autism spectrum disorder (ASD) recorded in Kaiser Permanente outpatient clinical databases. Controls (n = 2100) were children without an ASD diagnosis who were frequency matched to cases on sex, birth year, and hospital of birth. Main Outcome Measures: Frequencies of maternal immunologic disorders were compared between cases and controls with a chi(2) statistic, and relative risks were estimated by crude and adjusted odds ratios and 95% confidence intervals using logistic regression. Results: The final study population included 407 cases and 2095 controls. A similar proportion of case and control mothers had a diagnosis of any autoimmune disease in the 4-year period surrounding pregnancy (10.3% vs 8.2%, P =. 15). After adjustment for maternal factors, only 1 autoimmune condition, psoriasis, was significantly associated with ASDs (adjusted odds ratio, 2.7; 95% confidence interval, 1.3-5.8). A greater than 2-fold elevated risk of ASD was observed for maternal asthma and allergy diagnoses recorded during the second trimester of pregnancy. Conclusions: These findings suggest that maternal antoimmune disorders present in women around the time of pregnancy are unlikely to contribute significantly to autism risk. Further etiologic investigations are needed to confirm these results and should include objective documentation of diagnoses and consider a larger set of maternal immune-related conditions, including asthma and allergies. C1 Kaiser Permanente, Div Res, Kaiser Fdn, Res Inst, Oakland, CA 94612 USA. Dept Hlth Serv, Environm Hlth Invest Branch, Oakland, CA USA. Univ Calif Davis, Div Rheumatol Allergy, Davis, CA 95616 USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, Kaiser Fdn, Res Inst, 2000 Broadway, Oakland, CA 94612 USA. 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Pediatr. Adolesc. Med. PD FEB PY 2005 VL 159 IS 2 BP 151 EP 157 DI 10.1001/archpedi.159.2.151 PG 7 WC Pediatrics SC Pediatrics GA 893YA UT WOS:000226755800009 PM 15699309 ER PT J AU Bishop, DVM Norbury, CF AF Bishop, DVM Norbury, CF TI Executive functions in children with communication impairments, in relation to autistic symptomatology - I: Generativity SO AUTISM LA English DT Article DE autism; executive functions; generativity; language impairment; pragmatics ID CONVERSATIONAL CHARACTERISTICS; LANGUAGE IMPAIRMENT; PRAGMATIC DISORDER; INDIVIDUALS; CHECKLIST; DEFICITS AB Previous research has found that people with autism generate few novel responses in ideational fluency tasks, and it has been suggested this deficit is a specific correlate of stereotyped/repetitive behavior. We assessed generativity in children with pragmatic language impairment (PLI) who showed communicative abnormalities resembling those seen in autism. We compared four groups: high-functioning autism; PLI; specific language impairment; and control. Generativity was measured using two fluency tasks previously shown to be sensitive to autistic disorder. Correlational analysis revealed a significant relationship between the percentage of correct responses on the fluency tasks and measures of communicative abnormality. It is often assumed that pragmatic difficulties are caused by limitations of social cognition. This study suggests that difficulties in generating relevant ideas can be another cause of autistic-like communicative abnormalities. 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. 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D., 2002, BLACKWELL HDB CHILDH, P445, DOI DOI 10.1002/9780470996652.CH20 NR 29 TC 53 Z9 55 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 FEB PY 2005 VL 9 IS 1 BP 7 EP 27 DI 10.1177/1362361305049027 PG 21 WC Psychology, Developmental SC Psychology GA 890UB UT WOS:000226535300002 PM 15618260 ER PT J AU Bishop, DVM Norbury, CF AF Bishop, DVM Norbury, CF TI Executive functions in children with communication impairments, in relation to autistic symptomatology - 2: Response inhibition SO AUTISM LA English DT Article DE autism; executive functions; inhibition; language impairment; pragmatics ID DEFICIT-HYPERACTIVITY DISORDER; LANGUAGE IMPAIRMENT; ATTENTION; SYMPTOMS AB Although impairment in executive functions has been described in autism, there has been debate as to whether response inhibition is specifically affected. We compared four groups: high-functioning autism; pragmatic language impairment; specific language impairment; and control. Inhibition was assessed using two subtests from the Test of Everyday Attention for Children, one requiring a verbal response and the other a non-verbal response. Although we found evidence of inhibitory deficits, these were neither specific to autism, nor linked to particular aspects of autistic symptomatology. Rather, they appeared to be associated with poor verbal skills and inattention. It is suggested that future studies need to control for structural language skills and attention deficit when evaluating cognitive deficits in autism. Reliance on control groups matched solely on vocabulary level or nonverbal mental age may obscure the important role played by language skills in executive functions. 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. EM dorothy.bishop@psy.ox.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Bishop D., 2000, SPEECH LANGUAGE IMPA, P99 Bishop D. V. 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In autistic this validation study, the CAST was distributed to 1925 children aged disorders; 5-11 in mainstream Cambridgeshire schools. A sample of participants childhood received a full diagnostic assessment, conducted blind to screen status. e sensitivity of the CAST, at a designated cut-point of 15 was 100, percent, the specificity was 97 percent and the positive predictive value disorders; was 50 percent, using the group's consensus diagnosis as the gold pervasive standard. The accuracy indices varied with the case definition used. The disorders; sensitivity of the accuracy statistics to case definition and to missing screening data was explored. The CAST is useful as a screening test for autism spectrum conditions in epidemiological research. There is not currently enough evidence to recommend the use of the CAST as a screening test within a public health screening programme in the general population. C1 Univ Cambridge, Cambridge CB2 1TN, England. RP Williams, J (reprint author), Inst Publ Hlth, Dept Publ Hlth & Primary Care, Univ Forvie Site,Robinson Way, Cambridge CB2 2SR, England. 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R., 1997, HDB AUTISM PERVASIVE, P5 *WHO, 1993, ICD10 INT STAT CLASS NR 36 TC 76 Z9 76 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 FEB PY 2005 VL 9 IS 1 BP 45 EP 68 DI 10.1177/136261305049029 PG 24 WC Psychology, Developmental SC Psychology GA 890UB UT WOS:000226535300004 PM 15618262 ER PT J AU Receveur, C Lenoir, P DeSombre, H Roux, S Barthelemy, C Malvy, J AF Receveur, C Lenoir, P DeSombre, H Roux, S Barthelemy, C Malvy, J TI Interaction and imitation deficits from infancy to 4 years of age in children with autism - A pilot study based on videotapes SO AUTISM LA English DT Article DE autism developmental delay; home videotapes; imitation disorders; interaction disorders ID DEVELOPMENTAL DISORDERS; SPECTRUM DISORDER; EARLY RECOGNITION; HOME VIDEOTAPES; BEHAVIOR; SENSORIMOTOR; RELIABILITY; SYMPTOMS; MOVIES; SCALE AB The present study investigated the influence of developmental level on interaction and imitation in infants and young children with autism on the basis of family videos and filmed consultation. The sample comprised 18 children with autism divided into groups according to their developmental quotient (DQ > 50 and DQ < 50). A quantitative evaluation was performed on video observations at four periods (10-12 months, 16-18 months, 24-26 months, after 4 years) using scales appropriate for the evaluation of interaction and imitation impairments. The findings showed that, at a very early age, infants later diagnosed as having autistic disorder show different intensities of interaction and imitation deficits according to developmental level. C1 Univ Tours, Psychiat Clin, Tours, France. Univ Tours, Serv Pedopsychiat, Tours 9, France. Hop Neurol, Lyon, France. Univ Tours, Serv Explorat Fonctionnelles & Neurophysiol Pedop, F-37041 Tours, France. RP Malvy, J (reprint author), CHU Bretonneau, Serv Pedopsychiat, 2 Bd Tonnelle, F-37044 Tours, France. 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K., 1989, ANAL QUANTITATIVE BE Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 NR 36 TC 20 Z9 20 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 FEB PY 2005 VL 9 IS 1 BP 69 EP 82 DI 10.1177/1362361305049030 PG 14 WC Psychology, Developmental SC Psychology GA 890UB UT WOS:000226535300005 PM 15618263 ER PT J AU Oyane, NMF Bjorvatn, B AF Oyane, NMF Bjorvatn, B TI Sleep disturbances in adolescents and young adults with autism and Asperger syndrome SO AUTISM LA English DT Article DE actigraphy; Asperger syndrome; autism; sleep diary; sleep disturbance ID CIRCADIAN-RHYTHMS; CHILDREN; DISORDER; PATTERNS; ACTIGRAPHY AB Sleep problems are commonly reported in children with autistic disorders. Most studies are based on sleep questionnaires and sleep diaries, but polysomnographic and actigraphic data have also been used. In this study we investigated sleep in older individuals (aged 15-25 years) with autism and Asperger syndrome, using sleep questionnaires, sleep diaries and actigraphy. Although the sleep questionnaires completed by parents and caretakers revealed only a moderate degree of sleep problems; greater sleep disturbance was recorded with actigraphy Using the latter method, low sleep efficiency (below 85 percent) or long sleep latency (more than 30 minutes) were found in 80 percent of the individuals. There was no early morning awakening, contrary to some earlier reports. This study suggests that even though subjective complaints of sleep disturbances are less common in adolescents and young adults with autism, this may be due to an adaptation process rather than an actual reduction in sleep disturbances. C1 Univ Bergen, Dept Publ Hlth & Primary Hlth Care, N-5009 Bergen, Norway. RP Bjorvatn, B (reprint author), Univ Bergen, Dept Publ Hlth & Primary Hlth Care, Ulriksdal 8C, N-5009 Bergen, Norway. 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RP Matthews, B (reprint author), Flinders Univ S Australia, Adelaide, SA 5001, Australia. CR SHORE S, 2003, BEYOND WALL PERSONAL NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD FEB PY 2005 VL 9 IS 1 BP 119 EP 119 DI 10.1177/1362361305049034 PG 1 WC Psychology, Developmental SC Psychology GA 890UB UT WOS:000226535300008 ER PT J AU Gilchrist, A AF Gilchrist, A TI Autism: Explaining the enigma SO AUTISM LA English DT Book Review C1 Royal Cornhill Hosp, Aberdeen, Scotland. RP Gilchrist, A (reprint author), Royal Cornhill Hosp, Aberdeen, Scotland. CR Frith U., 2003, AUTISM EXPLAINING EN NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD FEB PY 2005 VL 9 IS 1 BP 120 EP 120 DI 10.1177/136236130500900109 PG 1 WC Psychology, Developmental SC Psychology GA 890UB UT WOS:000226535300009 ER PT J AU Torsdottir, G Hreidarsson, S Kristinsson, J Snaedal, J Johannesson, T AF Torsdottir, G Hreidarsson, S Kristinsson, J Snaedal, J Johannesson, T TI Ceruloplasmin, superoxide dismutase and copper in autistic patients SO BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY LA English DT Article ID INFANTILE-AUTISM; DISORDER; CHILDREN; ENZYMES; DISEASE; BLOOD C1 Univ Iceland, Dept Pharmacol & Toxicol, Inst Pharm Pharmacol & Toxicol, IS-107 Reykjavik, Iceland. Univ Hosp, Dept Geriatr, Landspitali, Reykjavik, Iceland. State Diagnost & Counseling Ctr Handicapped, Reykjavik, Iceland. RP Torsdottir, G (reprint author), Univ Iceland, Dept Pharmacol & Toxicol, Inst Pharm Pharmacol & Toxicol, Hofsvallagata 53, IS-107 Reykjavik, Iceland. 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Pharmacol. Toxicol. PD FEB PY 2005 VL 96 IS 2 BP 146 EP 148 DI 10.1111/j.1742-7843.2005.pto960210.x PG 3 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 891GO UT WOS:000226569500010 PM 15679479 ER PT J AU McAlonan, GM Cheung, V Cheung, C Suckling, J Lam, GY Tai, KS Yip, L Murphy, DGM Chua, SE AF McAlonan, GM Cheung, V Cheung, C Suckling, J Lam, GY Tai, KS Yip, L Murphy, DGM Chua, SE TI Mapping the brain in autism. A voxel-based MRI study of volumetric differences and intercorrelations in autism SO BRAIN LA English DT Article DE autism; MRI; brain mapping ID FUSIFORM FACE AREA; WHITE-MATTER; CHINESE CHARACTERS; ASPERGER-SYNDROME; CEREBRAL-CORTEX; FUNCTIONAL MRI; NEURAL SYSTEMS; STRUCTURAL MRI; ACTIVATION; SCHIZOPHRENIA AB Autism is a disorder of neurodevelopment resulting in pervasive abnormalities in social interaction and communication, repetitive behaviours and restricted interests. There is evidence for functional abnormalities and metabolic dysconnectivity in 'social brain' circuitry in this condition, but its structural basis has proved difficult to establish reliably. Explanations for this include replication difficulties inherent in 'region of interest' approaches usually adopted, and variable inclusion criteria for subjects across the autism spectrum. Moreover, despite a consensus that autism probably affects widely distributed brain regions, the issue of anatomical connectivity has received little attention. Therefore, we planned a fully automated voxel-based whole brain volumetric analysis in children with autism and normal IQ. We predicted that brain structural changes would be similar to those previously shown in adults with autism spectrum disorder and that a correlation analysis would suggest structural dysconnectivity. We included 17 stringently diagnosed children with autism and 17 age-matched controls. All children had IQ >80. Using Brain Activation and Morphological Mapping (BAMM) software, we measured global brain and tissue class volumes and mapped regional grey and white matter differences across the whole brain. With the expectation that volumes of interconnected regions correlate positively, we carried out a preliminary exploration of 'connectivity' in autism by comparing the nature of inter-regional grey matter volume correlations with control. Children with autism had a significant reduction in total grey matter volume and significant increase in CSF volume. They had significant localized grey matter reductions within fronto-striatal and parietal networks similar to findings in our previous study, and additional decreases in ventral and superior temporal grey matter. White matter was reduced in the cerebellum, left internal capsule and fornices. Correlation analysis revealed significantly more numerous and more positive grey matter volumetric correlations in controls compared with children with autism. Thus, using similar diagnostic criteria and image analysis methods in otherwise healthy populations with an autistic spectrum disorder from different countries, cultures and age groups, we report a number of consistent findings. Taken together, our data suggest abnormalities in the anatomy and connectivity of limbic-striatal 'social' brain systems which may contribute to the brain metabolic differences and behavioural phenotype in autism. C1 Univ Hong Kong, Dept Psychiat, Pokfulam, Hong Kong, Peoples R China. Univ Hong Kong, Dept Diagnost Radiol, Pokfulam, Hong Kong, Peoples R China. Univ Cambridge, Cambridge Brain Mapping Unit, Cambridge CB2 1TN, England. Hong Kong Inst Educ, Sch Early Childhood Educ, Hong Kong, Hong Kong, Peoples R China. Inst Psychiat, Dept Psychol Med, London SE5 8AF, England. RP McAlonan, GM (reprint author), Univ Hong Kong, Dept Psychiat, Pokfulam, Hong Kong, Peoples R China. 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Affected individuals display a neurobehavioral phenotype that includes a significant impairment in social cognition alongside deficits in attentional control, inhibition and working memory. In contrast, relatively little is known about the trajectory and specificity of any cognitive impairment associated with the fragile X premutation ("carrier-status") (approximately 55-200 repeats). Here, we focus on one aspect of cognition that has been well documented in the fragile X full mutation, namely social cognition. The results suggest that premutation males display a pattern of deficit similar in profile, albeit milder in presentation, to that of the full mutation. However, little evidence emerged for a correlation between CGG repeat length and severity of phenotypic outcomes. The findings are discussed in the context of functional neuroimaging and brain-behaviour-molecular correlates. 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PD FEB PY 2005 VL 57 IS 1 BP 53 EP 60 DI 10.1016/j.bandc.2004.08.020 PG 8 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 888AQ UT WOS:000226347000011 PM 15629215 ER PT J AU Bayliss, AP Tipper, SP AF Bayliss, AP Tipper, SP TI Gaze and arrow cueing of attention reveals individual differences along the autism spectrum as a function of target context SO BRITISH JOURNAL OF PSYCHOLOGY LA English DT Article ID VISUAL-ATTENTION; SPATIAL ATTENTION; JOINT ATTENTION; SEX-DIFFERENCES; SOCIAL-PERCEPTION; EYE-GAZE; INHIBITION; CUES; DIRECTION; INFANTS AB Observing averted gaze results in a reflexive shift of attention to the gazed-at location. In two experiments, participants scoring high and low on the Autism-Spectrum Quotient questionnaire (AQ; Baron-Cohen, Wheelwright, Skinner, Martin, & Clubley, 200 1) observed arrow and gaze cues to investigate cueing effect magnitude as a function of the context in which peripheral targets could appear. While identical cueing effects were found with gaze and arrow cues, the more striking results concerned target stimuli. In Experiment 1, targets could appear on a peripheral face, or on scrambled face parts. Overall, greater cueing effects were found when the target appeared on a face. However, this face bias was only observed in participants with low AQ scores, whereas high AQ scorers oriented more to scrambled features. Experiment 2 found equal cueing to targets appearing on tools, as compared with tool parts. However, individual differences were again observed, where low AQ scorers showed larger cueing towards tools, while high scorers oriented more to scrambled parts, as in Experiment 1. These results support the idea that low AQ individuals orient strongly to objects attended by others. However, since the same results were found for arrow cues, this effect may generalize to all central cues to attention. 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J. Psychol. PD FEB PY 2005 VL 96 BP 95 EP 114 DI 10.1348/000712604X15626 PN 1 PG 20 WC Psychology, Multidisciplinary SC Psychology GA 899JR UT WOS:000227141200006 PM 15826326 ER PT J AU Milne, E Swettenham, J Campbell, R AF Milne, E Swettenham, J Campbell, R TI Motion perception and autistic spectrum disorder: A review SO CAHIERS DE PSYCHOLOGIE COGNITIVE-CURRENT PSYCHOLOGY OF COGNITION LA English DT Review DE autistic spectrum disorder; motion perception; visual system; developmental disorders ID HUMAN VISUAL-CORTEX; HIGH-FUNCTIONING AUTISM; DORSAL STREAM FUNCTION; FORM-FROM-MOTION; BIOLOGICAL-MOTION; DEVELOPMENTAL DISORDERS; WILLIAMS-SYNDROME; BRAIN-DAMAGE; SELECTIVE IMPAIRMENT; MENTAL-RETARDATION AB Recent evidence has indicated that some children with autistic spectrum disorder (ASD) show reduced ability to detect visual motion. The data suggest that this impairment is present in children with a range of autistic spectrum diagnoses, but not present in all children diagnosed with ASD. The occurrence of abnormal motion perception in children with ASD has led to speculation regarding the root of this impairment. Hypotheses regarding reduced sensitivity of the visual magnocellular system/cortical dorsal stream (Milne et al., 2002; Spencer et al., 2000) and reduced neuronal integration (Bertone et al., 2003), will be discussed. in this review. Clinical implications of the impairment, such as the degree to which motion perception may be related to diagnostic criteria and/or symptom severity in ASD, and the relationship between abnormal motion perception in autistic spectrum, and other, non-autistic spectrum developmental disorders will also be discussed. The conclusion is drawn that more research should be carried out including larger samples of participants, and that in future studies researchers should provide details of the variability of performance in their data, and investigate relationships between motion perception, diagnostic criteria, symptom severity and other potential correlates which, it is hoped will lead to further understanding of the implications of abnormal motion perception in ASD. C1 Univ Sheffield, Dept Psychol, Sheffield S10 2TP, S Yorkshire, England. UCL, Dept Human Commun Sci, London WC1N 1PF, England. RP Milne, E (reprint author), Univ Sheffield, Dept Psychol, Western Bank, Sheffield S10 2TP, S Yorkshire, England. 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Psychol. Cogn.-Curr. Psychol. Cogn. PD FEB-APR PY 2005 VL 23 IS 1-2 BP 189 EP 197 PG 9 WC Psychology, Experimental SC Psychology GA 025JR UT WOS:000236262300019 ER PT J AU Takarae, Y Minshew, NJ Sweeney, JA AF Takarae, Y Minshew, NJ Sweeney, JA TI Visual motion processing in autism: What studies on visuomotor behaviors tell us SO CAHIERS DE PSYCHOLOGIE COGNITIVE-CURRENT PSYCHOLOGY OF COGNITION LA English DT Editorial Material ID PURSUIT EYE-MOVEMENTS; POSTURAL CONTROL; MACAQUE MONKEY; CHILDREN; DEFICITS; COHERENCE; LESIONS; PERCEPTION; SIGNALS; AREA C1 Univ Illinois, Dept Psychiat, Ctr Cognit Med, Chicago, IL 60612 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. RP Sweeney, JA (reprint author), Univ Illinois, Dept Psychiat, Ctr Cognit Med, 912 S Wood St,Suite 235,MC913, Chicago, IL 60612 USA. 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Psychol. Cogn.-Curr. Psychol. Cogn. PD FEB-APR PY 2005 VL 23 IS 1-2 BP 205 EP 212 PG 8 WC Psychology, Experimental SC Psychology GA 025JR UT WOS:000236262300021 ER PT J AU Lajiness-O'Neill, RR Beaulieu, I Titus, JB Asamoah, A Bigler, ED Bawle, EV Pollack, R AF Lajiness-O'Neill, RR Beaulieu, I Titus, JB Asamoah, A Bigler, ED Bawle, EV Pollack, R TI Memory and learning in children with 22q11.2 Deletion Syndrome: Evidence for ventral and dorsal stream disruption? SO CHILD NEUROPSYCHOLOGY LA English DT Article DE neuropsychology; memory; 22q11 Deletion Syndrome; velocardiofacial syndrome; autism; genetics ID VELOCARDIOFACIAL-SYNDROME; WORKING-MEMORY; PREFRONTAL CORTEX; WILLIAMS-SYNDROME; 22Q11.2 MICRODELETION; DELETION 22Q11.2; VOLUMETRIC MRI; AUTISM; SCHIZOPHRENIA; ADOLESCENTS AB This study examined memory functioning in children and adolescents with 22q11.2 Deletion Syndrome (DS; velocardiofacial syndrome). An overall verbal better than nonverbal memory pattern was evident on the Test of Memory and Learning (TOMAL), with children with 22q11.2 DS performing significantly below their siblings and children with low average IQ but similar to children with autism on facial memory. Children with 22q11 DS also performed significantly below their siblings on tests of verbal working memory. Children with autism performed significantly poorer than the siblings of children with 22q11.2 DS only on their recall of stories. Delayed recall was significantly poorer in children with 22q11.2 DS and children with autism, compared to sibling controls. Although there were no significant group differences on tests of multiple trial verbal or visual learning, a relative weakness was noted with multiple trial visual learning in children with 22q11.2 DS and their siblings, suggesting that an alternative or interactive factor other than the deletion may account for the relatively better verbal compared to nonverbal memory abilities. Deficits in facial memory in children with both 22q11.2 DS and autism suggest disruptions in ventral temporal pathways such as between fusiform gyrus and parahippocampal/ hippocampal regions whereas deficits in verbal working memory in children with 22q11.2 DS implicates dorsolateral prefrontal regions, both intimating aberrant white matter pathways. C1 Henry Ford Hlth Syst, Dept Behav Hlth, Div Neuropsychol, Detroit, MI 48202 USA. Henry Ford Hlth Syst, Dept Genet, Detroit, MI USA. Wayne State Univ, Sch Med, Dept Psychiat, Detroit, MI USA. Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA. Brigham Young Univ, Dept Neurosci, Provo, UT 84602 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT USA. Univ Utah, Dept Radiol, Salt Lake City, UT 84132 USA. Childrens Hosp Michigan, Dept Pediat, Div Genet, Detroit, MI 48201 USA. RP Lajiness-O'Neill, RR (reprint author), Henry Ford Hlth Syst, Dept Behav Hlth, Div Neuropsychol, Detroit, MI 48202 USA. 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PD FEB PY 2005 VL 11 IS 1 BP 55 EP 71 DI 10.1080/09297040590911202 PG 17 WC Clinical Neurology SC Neurosciences & Neurology GA 920IZ UT WOS:000228683900005 PM 15823983 ER PT J AU Leslie, AM German, TP Polizzi, P AF Leslie, AM German, TP Polizzi, P TI Belief-desire reasoning as a process of selection SO COGNITIVE PSYCHOLOGY LA English DT Article DE belief desire reasoning theory of mind development inhibition domain-specificity ID OF-MIND DEVELOPMENT; FALSE BELIEF; EXECUTIVE FUNCTIONS; INHIBITORY CONTROL; CHILDS THEORY; AUTISM; REPRESENTATION; METAANALYSIS; INFERENCES; DECEPTION AB Human learning may depend upon domain specialized mechanisms. A plausible example is rapid, early learning about the thoughts and feelings of other people. A major achievement in this domain, at about age four in the typically developing child, is the ability to solve problems in which the child attributes false beliefs to other people and predicts their actions. The main focus of theorizing has been why 3-year-olds fail, and only recently have there been any models of how success is achieved in false-belief tasks. Leslie and Polizzi (Inhibitory processing in the false-belief task: Two conjectures. Developmental Science, 1, 247-254, 1998) proposed two competing models of success, which are the focus of the current paper. The models assume that belief-desire reasoning is a process which selects a content for an agent's belief and an action for the agent's desire. In false belief tasks, the theory of mind mechanism (ToMM) provides plausible candidate belief contents, among which will be a 'true-belief.' A second process reviews these candidates and by default will select the true-belief content for attribution. To succeed in a false-belief task, the default content must be inhibited so that attention shifts to another candidate belief. In traditional false-belief tasks, the protagonist's desire is to approach an object. Here we make use of tasks in which the protagonist has a desire to avoid an object, about which she has a false-belief. Children find such tasks much more difficult than traditional tasks. Our models explain the additional difficulty by assuming that predicting action from an avoidance desire also requires an inhibition. The two processing models differ in the way that belief and desire inhibitory processes combine to achieve successful action prediction. In six experiments we obtain evidence favoring one model, in which parallel inhibitory processes cancel out, over the other model, in which serial inhibitions force attention to a previously inhibited location. These results are discussed in terms of a set of simple proposals for the modus operandi of a domain specific learning mechanism. The learning mechanism is in part modular-the ToMM-and in part penetrable-the Selection Processor (SP). 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Psychol. PD FEB PY 2005 VL 50 IS 1 BP 45 EP 85 DI 10.1016/j.cogpsych.2004.06.002 PG 41 WC Psychology; Psychology, Experimental SC Psychology GA 885YE UT WOS:000226192500002 PM 15556129 ER PT J AU Hong, EJ West, AE Greenberg, ME AF Hong, EJ West, AE Greenberg, ME TI Transcriptional control of cognitive development SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Review ID RUBINSTEIN-TAYBI-SYNDROME; CPG-BINDING PROTEIN-2; LONG-TERM-MEMORY; RETT-SYNDROME; LANGUAGE DISORDER; WILLIAMS-SYNDROME; MENTAL-RETARDATION; GENE-EXPRESSION; MOLECULAR-GENETICS; BDNF TRANSCRIPTION AB Cognitive development is determined by both genetics and environment. One point of convergence of these two influences is the neural activity-dependent regulation of programs of gene expression that specify neuronal fate and function. Human genetic studies have linked several transcriptional regulators to neurodevelopmental disorders including mental retardation and autism spectrum disorders. 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Opin. Neurobiol. PD FEB PY 2005 VL 15 IS 1 BP 21 EP 28 DI 10.1016/j.conb.2005.01.002 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 906KQ UT WOS:000227640000004 PM 15721740 ER PT J AU Weiskop, S Richdale, A Matthews, J AF Weiskop, S Richdale, A Matthews, J TI Behavioural treatment to reduce sleep problems in children with autism or fragile X syndrome SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID INTELLECTUAL DISABILITY; BOY AB There are few well-controlled, published evaluations of sleep interventions for children with developmental disabilities. This paper evaluates a parent training programme using behavioural principles to reduce sleep problems in children with autism or fragile X syndrome (FXS). Training included bedtime routines, reinforcement, effective instructions, partner support, and extinction (removing reinforcement to reduce a behaviour). Programme efficacy was demonstrated by using a multiple baseline across-participant design. Social validity was also assessed. Five children with autism and one with Asperger syndrome (four males, two females; mean age 5y 6mo; age range 3y 5mo to 7y 4mo) and their parents; and seven children with FXS (six males, one female; mean age 4y 9mo; age range 1y 11mo to 9y 1mo) and their parents participated. Ten families completed intervention within the multiple baseline design. Most parents' goals were achieved and visual analysis of the sleep data indicated improvement. Settling problems, night waking, and co-sleeping were effectively reduced. The programme had high social validity and outcomes were clinically significant and maintained at follow-up. C1 RMIT Univ, Sch Hlth Sci, Bundoora, Vic 3083, Australia. RP Richdale, A (reprint author), RMIT Univ, Sch Hlth Sci, POB 71, Bundoora, Vic 3083, Australia. 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Screening for mutations in six genes mapping to 7q, CUTL1, SRPK2, SYPL, LAMB1, NRCAM and PTPRZ1 in 48 unrelated individuals with autism led to the identification of several new coding variants in the genes CUTL1, LAMB1 and PTPRZ1. Analysis of genetic variants provided evidence for association with autism for one of the new missense changes identified in LAMB1; this effect was stronger in a subgroup of affected male sibling pair families, implying a possible specific sex-related effect for this variant. Association was also detected for several polymorphisms in the promoter and untranslated region of NRCAM, suggesting that alterations in expression of this gene may be linked to autism susceptibility. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, D-6900 Heidelberg, Germany. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. Univ Bologna, Diparitmento Biol Evoluz Sperimentale, Bologna, Italy. Univ Bologna, Policlin S Orsola Malpighi, Med Genet Lab, Bologna, Italy. Stella Maris Clin Res Inst Child & Adolescent Neu, Calambrone, Italy. Vidensctr Ctr Autisme, Virum, Denmark. Borne Ungdomspsykiatrisk Hosp, Risskov, Denmark. John F Kennedy Inst, DK-2600 Glostrup, Denmark. Danish Tech Univ, Biophys Grp, Lyngby, Denmark. Dept Child & Adolescent Psychiat, Utrecht, Netherlands. Inst Psychiat, Ctr Social Genet & Dev Psychiat, London, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London, England. Pk Hosp Children, Sect Child & Adolescent Psychiat, Oxford, England. RP Monaco, AP (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. 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J. Hum. Genet. PD FEB PY 2005 VL 13 IS 2 BP 198 EP 207 DI 10.1038/sj.ejhg.5201315 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 888ZR UT WOS:000226413600014 PM 15523497 ER PT J AU Odell, D Maciulis, A Cutler, A Warren, L McMahon, WM Coon, H Stubbs, G Henley, K Torres, A AF Odell, D Maciulis, A Cutler, A Warren, L McMahon, WM Coon, H Stubbs, G Henley, K Torres, A TI Confirmation of the association of the C4B null allelle in autism SO HUMAN IMMUNOLOGY LA English DT Article DE autism; complement C4; autoimmunity; MHC; HLA ID COMPLEMENT COMPONENTS; CANDIDATE GENES; IMMUNE-SYSTEM; GENETICS; MHC; DISORDERS; CHILDREN; ANTIBODIES; DISEASE; PROTEIN AB The objective of this Study was to examine and attempt to confirm our previous findings of an increased frequency of the C4B null allele (C4BQ0) in subjects with autism. Newly identified subjects from Utah and Oregon were Studied. Families evaluated included 85 who had a child with autism and 69 control families. Of the subjects with autism studied, 42.4% carried at least one C4BQ0, compared with 14.5%;P( of the control subjects (p = 0.00013), with a relative risk of 4.33. Over half of the C4B null alleles in the subjects with autism involved C4A duplications. A marked increase in the ancestral haplotype 44.1 that lacks a C4B gene and has 2 C4A genes was also observed. The results of this study suggest that the human leukocyte antigen class III C4BQ0 significantly increases the risk for autism. (C) American Society for Histocompatibility and Immunogenetics, 2005. Published by Elsevier Inc. C1 Utah State Univ, Ctr Persons Disabilities, Logan, UT 84322 USA. Univ Utah, Salt Lake City, UT USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. RP Odell, D (reprint author), Utah State Univ, Ctr Persons Disabilities, 6895 Old Main Hill, Logan, UT 84322 USA. 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Immunol. PD FEB PY 2005 VL 66 IS 2 BP 140 EP 145 DI 10.1016/j.humimm.2004.11.002 PG 6 WC Immunology SC Immunology GA 899TJ UT WOS:000227167700006 PM 15694999 ER PT J AU Whitaker-Azmitia, PM AF Whitaker-Azmitia, PM TI Behavioral and cellular consequences of increasing serotonergic activity during brain development: a role in autism? SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE hyperserotonemia; CGRP; amygdala; oxytocin; hypothalamus ID GENE-RELATED PEPTIDE; PRENATAL COCAINE EXPOSURE; WHOLE-BLOOD SEROTONIN; DENTATE GRANULE CELLS; SOCIAL RECOGNITION; CENTRAL NUCLEUS; MONOAMINERGIC NEURONS; SOMATOSENSORY CORTEX; REPETITIVE BEHAVIORS; CORTICAL DEVELOPMENT AB The hypothesis explored in this review is that the high levels of serotonin in the blood seen in some autistic children (the so-called hyperserotonemia of autism) may lead to some of the behavioral and cellular changes also observed in the disorder. At early stages of development, when the blood-brain Barrier is not yet fully formed, the high levels of serotonin in the blood can enter the brain of a developing fetus and cause loss of serotonin terminals through a known negative feedback function of serotonin during development. The loss of serotonin innervation persists throughout subsequent development and the symptoms of autism appear. A review of the basic scientific literature on prenatal treatments affecting serotonin is given, in support of this hypothesis, with an emphasis on studies using the serotonin agonist, 5-methoxytryptamine (5-MT). In work using 5-MT to mimic hyperserotonemia, Sprague-Dawley rats are treated from gestational day 12 until postnatal 20. In published reports, these animals have been found to have a significant loss of serotonin terminals, decreased metabolic activity in cortex, changes in columnar development in cortex, changes in serotonin receptors, and "autistic-like" behaviors. In preliminary cellular findings given in this review, the animals have also been found to have cellular changes in two relevant brain regions: 1. Central nucleus of the amygdala, a brain region involved in fear-responding, where an increase in calcitonin gene related peptide (CGRP) was found 2. Paraventricular nucleus of the hypothalamus, a brain region involved in social memory and bonding, where a decrease in oxytocin was found. Both of these cellular changes could result from loss of serotonin innervation, possibly due to loss of terminal outgrowth from the same cells of the raphe nuclei. Thus, increased serotonergic activity during development could damage neurocircuitry involved in emotional responding to social stressors and may have relevance to the symptoms of autism. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved. C1 SUNY Stony Brook, Dept Psychol, Program Biopsychol, Stony Brook, NY 11794 USA. RP Whitaker-Azmitia, PM (reprint author), SUNY Stony Brook, Dept Psychol, Program Biopsychol, Stony Brook, NY 11794 USA. 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J. Dev. Neurosci. PD FEB PY 2005 VL 23 IS 1 BP 75 EP 83 DI 10.1016/j.ijdevneu.2004.07.022 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 907XW UT WOS:000227752500009 PM 15730889 ER PT J AU Heerey, EA Capps, LM Keltner, D Kring, AM AF Heerey, EA Capps, LM Keltner, D Kring, AM TI Understanding teasing: Lessons from children with autism SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE autism; social interaction; theory of mind; teasing ID HIGH-FUNCTIONING AUTISM; IDIOMATIC COMMUNICATION; DIAGNOSTIC INTERVIEW; JOINT ATTENTION; PRETEND PLAY; MIND; IMPAIRMENTS; DISTINCTION; AGGRESSION; DISORDERS AB Teasing requires the ability to understand intention, nonliteral communication, pretense, and social context. Children with autism experience difficulty with such skills, and consequently, are expected to have difficulty with teasing. To better understand teasing concepts and behaviors, children with autism, their parents, and age and Verbal-IQ-matched comparison children and parents described concepts and experiences of teasing and engaged in a parent-child teasing interaction. The teasing of children with autism was less playful and provocative and focused less on social norms than that of comparison children. Similarly, parents of children with autism teased in less playful ways. Scores on a theory of mind task accounted for several of the observed differences. Discussion focused on the importance of understanding social context and playful behavior during teasing. C1 Univ Maryland, Maryland Psychiat Res Ctr, Sch Med, Baltimore, MD 21201 USA. Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. RP Heerey, EA (reprint author), MIRECC, VAMHCS, Suite 6A,10 N Greene St, Baltimore, MD 21201 USA. 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Abnorm. Child Psychol. PD FEB PY 2005 VL 33 IS 1 BP 55 EP 68 DI 10.1007/s10802-005-0934-z PG 14 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 897BF UT WOS:000226978300005 PM 15759591 ER PT J AU Astor, J AF Astor, J TI A conversation with Dr Michael Fordham SO JOURNAL OF ANALYTICAL PSYCHOLOGY LA English DT Editorial Material DE autism; child analysis; child psychiatry; Fordham; individuation; primary self; transference-based approach AB In this interview in Dr Fordham's 83(rd) year he describes how he started to work with children, and how Mrs Jung was supportive. He talks about the initial suspicion this interest generated in the wider Jungian community. He refers to his acceptance of and interest in the psychotic elements in child analysis and his transference-based approach to working with these elements. He reflects on his own birth, his work with evacuee children in hostels during the war years and the politics of supervision. He describes the core Jungian concepts which underpinned his work and the theoretical differences from the Kleinian and Anna Freudian positions. CR FORDHAM M, 1965, J ANAL PSYCHOL, V10, P1 FORDHAM M, 1986, J ANAL PSYCHOL, V31, P3 FORDHAM M, 1977, J ANAL PSYCHOL, V22, P2 FORDHAM M, 1957, NEW DEV ANAL PSYHCOL Fordham M., 1985, EXPLORATIONS SELF, V7 Jung C. G, 1947, CW Jung C. G., 1963, MEMORIES DREAMS REFL JUNG CG, 1910, CW, V17 Klein M., 1975, NARRATIVE CHILD ANAL MCDOUFALL J, 1969, DIALOGUE SAMMY NR 10 TC 1 Z9 1 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-8774 J9 J ANAL PSYCHOL JI J. Anal. Psychol. PD FEB PY 2005 VL 50 IS 1 BP 9 EP 18 DI 10.1111/j.0021-8774.2005.00505.x PG 10 WC Psychology, Multidisciplinary SC Psychology GA 897DE UT WOS:000226983400002 ER PT J AU Ruble, LA Heflinger, CA Renfrew, JW Saunders, RC AF Ruble, LA Heflinger, CA Renfrew, JW Saunders, RC TI Access and service use by children with autism spectrum disorders in Medicaid Managed Care SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE services; medicaid managed care; mental health; behavioral health ID BEHAVIORAL HEALTH-CARE; PREVALENCE; DIAGNOSIS AB Although Medicaid is the largest public payer of behavioral health services, information on access and utilization of services is lacking, and no data on the frequency of service use or types of services provided for children with autism spectrum disorders (ASDs) are available. As states move toward managed care approaches for their Medicaid program, services information is critical. Behavioral health service data for children with autism spectrum disorders were collected from a state Medicaid Managed Care (MMC) program and analyzed from fiscal years 1995 through 2000. Findings revealed that the number of children who received services over time increased significantly; however, the rate of service use was only one tenth of what should be expected based on prevalence rates. The mean number of service days provided per child decreased significantly, about 40%, and the most prevalent forms of treatment changed. Day treatment vanished and medication and case management increased disproportionately to the number of children served. Explanations and implications of the findings are presented as well as recommendations for future research. C1 Univ Louisville, Dept Pediat, WCEC, Louisville, KY 40202 USA. Vanderbilt Univ, Dept Human & Org Dev, Nashville, TN USA. RP Ruble, LA (reprint author), Univ Louisville, Dept Pediat, WCEC, 571 S Floyd St,Ste 100, Louisville, KY 40202 USA. 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PD FEB PY 2005 VL 35 IS 1 BP 3 EP 13 DI 10.1007/s10803-004-1026-6 PG 11 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500002 PM 15796117 ER PT J AU Sigman, M McGovern, CW AF Sigman, M McGovern, CW TI Improvement in cognitive and language skills from preschool to adolescence in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE developmental change; communication; pretend play; language ID FOLLOW-UP; JOINT ATTENTION; DEVELOPMENTAL LEVEL; INFANTILE-AUTISM; SYMBOLIC PLAY; CHILDREN; STABILITY; COMMUNICATION; AGE AB This paper reports on the developmental progression of a sample of 48 adolescents and young adults with autism who were previously assessed at preschool age and again in the mid-school period. In contrast to the earlier period when about one-third of the children made dramatic gains, cognitive and language skills tended to remain stable or decline over this time span. The gain in mental and language age of the non-retarded adolescents with autism was less than half the change in their chronological age. The mentally retarded adolescents with autism showed some gain in mental age over time but this was far less than their change in chronological age, and they showed almost no gain in language age. Early childhood predictors of language skills in adolescence were functional play skills, responsiveness to others' bids for joint attention, and the frequency of requesting behaviors. C1 Univ Calif Los Angeles, Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA. RP Sigman, M (reprint author), Univ Calif Los Angeles, Sch Med, Dept Psychiat, 760 Westwood Plaza,Room 68-237, Los Angeles, CA 90095 USA. 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PD FEB PY 2005 VL 35 IS 1 BP 15 EP 23 DI 10.1007/s10803-004-1027-5 PG 9 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500003 PM 15796118 ER PT J AU Campbell, JM AF Campbell, JM TI Diagnostic assessment of Asperger's Disorder: A review of five third-party rating scales SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE Asperger's Disorder; assessment; validity; rating scales ID SCHOOL-AGE-CHILDREN; SCREENING QUESTIONNAIRE; CHILDHOOD; VALIDITY AB Five rating scales for screening and detection of Asperger's Disorder, three commercially available and two research instruments, are evaluated with reference to psychometric criteria outlined by Bracken in 1987 (Journal of Psychoeducational Assessment, 4, 313). Reliability and validity data reported in examiner's manuals or published reports are reviewed. The scales included in the review are the Asperger Syndrome Diagnostic Scale (ASDS), Autism Spectrum Screening Questionnaire (ASSQ), Childhood Asperger Syndrome Test (CAST), Gilliam Asperger's Disorder Scale (GADS), and Krug Asperger's Disorder Index (KADI). All published rating scales demonstrated significant weaknesses, particularly in the use of questionable normative samples. Among the published instruments, the KADI appears to be the most sound in terms of reliability and validity. The research instruments present incomplete psychometric data to date, but hold promise as clinical instruments. C1 Univ Georgia, Dept Educ Psychol, Athens, GA 30602 USA. RP Campbell, JM (reprint author), Univ Georgia, Dept Educ Psychol, 329 Aderhold Hall, Athens, GA 30602 USA. EM jcampbel@coe.uga.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Arick J. 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PD FEB PY 2005 VL 35 IS 1 BP 25 EP 35 DI 10.1007/s10803-004-1028-4 PG 11 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500004 PM 15796119 ER PT J AU Shek, DTL Tsang, SKM Lam, LL Tang, FLY Cheung, PMP AF Shek, DTL Tsang, SKM Lam, LL Tang, FLY Cheung, PMP TI Psychometric properties of the Chinese version of the Psycho-educational Profile-Revised (CPEP-R) SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Psycho-educational Profile-Revised (PEP-R); autistic disorder; Chinese; assessment; psychometric properties ID REPORT FAMILY INVENTORY; AUTISTIC-CHILDREN; RELIABILITY; BEHAVIOR; VALIDITY AB The purpose of this study was to examine the reliability and validity of the Chinese version of the Psycho-educational Profile-Revised (PEP-R). The Chinese PEP-R (CPEP-R) was administered to 63 preschool children with symptoms of autistic disorder recruited from special child-care centers in Hong Kong. Results showed that the scales of the CPEP-R were internally consistent, reliable across raters and temporally stable. Regarding the concurrent validity of the CPEP-R, the developmental score and developmental age assessed by the CPEP-R were significantly correlated with the Merrill-Palmer Scale of Mental Tests and the Hong Kong Based Adaptive Behavior Scale. The Behavioral Scale of the CPEP-R was also significantly related to the Childhood Autism Rating Scale. Besides replicating the findings in the Western context, the present study suggests that the psychometric properties of the PEP-R are stable across cultures and the related findings support the cross-cultural reliability of the tool. C1 Chinese Univ Hong Kong, Social Welfare Practice & Res Ctr, Dept Social Work, Shatin, Peoples R China. Univ Hong Kong, Dept Social Work & Social Adm, Hong Kong, Peoples R China. Heep Hong Soc, Hong Kong, Peoples R China. RP Shek, DTL (reprint author), Chinese Univ Hong Kong, Social Welfare Practice & Res Ctr, Dept Social Work, Shatin, Peoples R China. EM danielshek@cuhk.edu.hk RI Shek, Daniel/N-9576-2014 OI Shek, Daniel/0000-0003-3359-6229 CR ALPERN GD, 1967, J ABNORM PSYCHOL, V72, P478, DOI 10.1037/h0025240 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CRONBACH LJ, 1951, PSYCHOMETRIKA, V16, P297 *DEP HLTH, 1995, REP FIND LOC STUD ME DeVellis R. F., 1991, SCALE DEV Gillham JE, 2000, J AUTISM DEV DISORD, V30, P269, DOI 10.1023/A:1005571115268 Guilford J. P., 1978, FUNDAMENTAL STAT PSY HARTMANN DP, 1977, J APPL BEHAV ANAL, V10, P103, DOI 10.1901/jaba.1977.10-103 *HLTH WELF BUR, 1995, REP OV STUD VIS AUT *HLTH WELF BUR, 1994, REP WORK GROUP SERV Kwok J., 1989, HONG KONG BASED ADAP LAM MKT, 1993, J AUTISM DEV DISORD, V23, P273, DOI 10.1007/BF01046220 Muris P, 1997, J AUTISM DEV DISORD, V27, P621, DOI 10.1023/A:1025838312457 Parks S. 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Autism Dev. Disord. PD FEB PY 2005 VL 35 IS 1 BP 37 EP 44 DI 10.1007/s10803-004-1029-3 PG 8 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500005 PM 15796120 ER PT J AU Minshew, NJ Turner, CA Goldstein, G AF Minshew, NJ Turner, CA Goldstein, G TI The application of short forms of the Wechsler intelligence scales in adults and children with high functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE intelligence; short forms; assessment ID PERVASIVE DEVELOPMENTAL DISORDERS; WAIS-R; DIAGNOSTIC INTERVIEW; DEPRESSED SAMPLE; INDIVIDUALS; POPULATION; VALIDATION; INSTRUMENT; PRESCHOOL AB We evaluated the predictive accuracy of short forms of the Wechsler intelligence scales for individuals with high functioning autism. Several short forms were derived from participants who had received the full procedure. Stepwise multiple regression analyses were performed to determine the strength of association between the subtests included in the short form and IQ scores based upon the full test. These analyses were performed for all participants, and also for autism participants with atypical subtest profiles. In all analyses the percentages of explained variance were typically in the .8-9 range. It was concluded that short forms may be used with good predictive accuracy in individuals with high functioning autism, even when the subtest profile is atypical. C1 Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. VA Pittsburgh Hlth Care Syst, Pittsburgh, PA 15206 USA. RP Goldstein, G (reprint author), VA Pittsburgh Hlth Care Syst, 151R,7180 Highland Dr, Pittsburgh, PA 15206 USA. 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PD FEB PY 2005 VL 35 IS 1 BP 45 EP 52 DI 10.1007/s10803-004-1030-x PG 8 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500006 PM 15796121 ER PT J AU de Bildt, A Kraijer, D Sytema, S Minderaa, R AF de Bildt, A Kraijer, D Sytema, S Minderaa, R TI The psychometric properties of the Vineland Adaptive Behavior Scales in children and adolescents with mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Vineland Adaptive Behavior Scales; adaptive functioning; MR ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; DOWN-SYNDROME; INTELLECTUAL DISABILITY; FRAGILE-X; AUTISM; CHECKLIST; INDIVIDUALS; DEFICITS; MALES AB The psychometric properties of the Vineland Adaptive Behavior Scales Survey Form were studied in a total population of children and adolescents with MR, and in the specific levels of functioning (n = 826, age 4-18 years). The original division into (sub)domains, as assigned by the authors, was replicated in the total population and in the mild and moderate levels of functioning. In the severe and profound levels of functioning the structure was less well recognized. The reliability of the instrument proved to be good in the total population and the subgroups. The construct validity was high in all groups. The implications of these findings are discussed with respect to the usefulness of the Vineland for the population with MR. C1 Univ Groningen, Groningen, Netherlands. St Hendrik van Boeijen, Assen, Netherlands. RP de Bildt, A (reprint author), Accare Child & Adolescent Psychiat, POB 660, NL-9700 AR Groningen, Netherlands. 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PD FEB PY 2005 VL 35 IS 1 BP 53 EP 62 DI 10.1007/s10803-004-1033-7 PG 10 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500007 PM 15796122 ER PT J AU Burnette, CP Mundy, PC Meyer, JA Sutton, SK Vaughan, AE Charak, D AF Burnette, CP Mundy, PC Meyer, JA Sutton, SK Vaughan, AE Charak, D TI Weak central coherence and its relations to theory of mind and anxiety in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE weak central coherence; anxiety; theory of mind; high functioning autism; comorbidity; social-emotional functioning ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; BIOLOGICAL BASIS; CHILDS THEORY; PERFORMANCE; COMPREHENSION; INDIVIDUALS; DIAGNOSIS AB Recent theory and research suggests that weak central coherence, a specific perceptual-cognitive style, underlies the central disturbance in autism. This study sought to provide a test of the weak central coherence hypothesis. 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PD FEB PY 2005 VL 35 IS 1 BP 63 EP 73 DI 10.1007/s10803-004-1035-5 PG 11 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500008 PM 15796123 ER PT J AU Hala, S Rasmussen, C Henderson, AME AF Hala, S Rasmussen, C Henderson, AME TI Three types of source monitoring by children with and without autism: The role of executive function SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE austism; source monitoring; memory; cognitive development; school aged children ID IMAGINED ACTIONS; WORKING-MEMORY; SOURCE AMNESIA; INHIBITORY CONTROL; MIND; DEFICITS; DISORDERS; FAILURE; INTACT; TASKS AB Earlier investigations have found mixed evidence of source monitoring impairment in autism. The present study examined three types of source monitoring ability in children with autism and typically developing children. 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Autism Dev. Disord. PD FEB PY 2005 VL 35 IS 1 BP 75 EP 89 DI 10.1007/s10803-004-1036-4 PG 15 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500009 PM 15796124 ER PT J AU Vernazza-Martin, S Martin, N Vernazza, A Lepellec-Muller, A Rufo, M Massion, J Assaiante, C AF Vernazza-Martin, S Martin, N Vernazza, A Lepellec-Muller, A Rufo, M Massion, J Assaiante, C TI Goal directed locomotion and balance control in autistic children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE human; development; goal-directed locomotion; motor control; anticipation; coordination; autism ID CHILDHOOD AUTISM; HEAD STABILIZATION; AUTONOMOUS WALKING; MOVEMENT ANALYSIS; BASAL GANGLIA; BRAIN-STEM; INVOLVEMENT; HUMANS; MODEL; DISTURBANCES AB This article focuses on postural anticipation and multi-joint coordination during locomotion in healthy and autistic children. Three questions were addressed: (1) Are gait parameters modified in autistic children? (2) Is equilibrium control affected in autistic children? (3) Is locomotion adjusted to the experimenter-imposed goal? Six healthy children and nine autistic children were instructed to walk to a location (a child-sized playhouse) inside the psychomotor room of the pedopsychiatric centre located approximately 5 in in front of them. A kinematic analysis of gait (ELITE system) indicates that, rather than gait parameters or balance control, the main components affected in autistic children during locomotion are the goal of the action, the orientation towards this goal and the definition of the trajectory due probably to an impairment of movement planning. C1 Univ Paris 10, Lab Sport & Culture EA2931, F-92001 Nanterre, France. Univ Paris 06, Lodyc UMR 7617, F-75252 Paris, France. Hop St Marguerite, Ctr Medicopsychol Enfant & Famille, F-13009 Marseille, France. Univ Aix Marseille 1, CNRS, Lab Parole & Langage, F-13621 Aix En Provence, France. CNRS, Lab Dev & Pathol Mouvement, F-13402 Marseille, France. RP Vernazza-Martin, S (reprint author), 7 Bis Ave Auber, F-78360 Montesson, France. 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PD FEB PY 2005 VL 35 IS 1 BP 91 EP 102 DI 10.1007/s10803-004-1037-3 PG 12 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500010 PM 15796125 ER PT J AU Cohen, D Pichard, N Tordjman, S Baumann, C Burglen, L Excoffier, E Lazar, G Mazet, P Pinquier, C Verloes, A Heron, D AF Cohen, D Pichard, N Tordjman, S Baumann, C Burglen, L Excoffier, E Lazar, G Mazet, P Pinquier, C Verloes, A Heron, D TI Specific genetic disorders and autism: Clinical contribution towards their identification SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism; specific genetic disease; multidisciplinary approach ID LEMLI-OPITZ-SYNDROME; FRAGILE-X-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; PRADER-WILLI-SYNDROME; LINKED MENTAL-RETARDATION; 22Q13 DELETION SYNDROME; RETT-SYNDROME GENE; TUBEROUS SCLEROSIS; ANGELMAN SYNDROME; INFANTILE-AUTISM AB Autism is a heterogeneous disorder that can reveal a specific genetic disease. This paper describes several genetic diseases consistently associated with autism (fragile X, tuberous sclerosis, Angelman syndrome, duplication of 15q11-q13, Down syndrome, San Filippo syndrome, MECP2 related disorders, phenylketonuria, Smith-Magenis syndrome, 22q13 deletion, adenylosuccinate lyase deficiency, Cohen syndrome, and Smith-Lemli-Opitz syndrome) and proposes a consensual and economic diagnostic strategy to help practitioners to identify them. A rigorous initial clinical screening is presented to avoid unnecessary laboratory and imaging studies. Regarding psychiatric nosography, the concept of "syndromal autism"-autism associated with other clinical signs-should be promoted because it may help to distinguish patients who warrant a multidisciplinary approach and further investigation. C1 Grp Hosp Pitie Salpetriere, Serv Psychiat Enfant & Adolescent, F-75634 Paris, France. Hop Robert Debre, Unite Genet Clin, F-75019 Paris, France. 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Autism Dev. Disord. PD FEB PY 2005 VL 35 IS 1 BP 103 EP 116 DI 10.1007/s10803-004-1038-2 PG 14 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500011 PM 15796126 ER PT J AU Veltman, MWM Thompson, RJ Craig, EE Dennis, NR Roberts, SE Moore, V Brown, JA Bolton, PF AF Veltman, MWM Thompson, RJ Craig, EE Dennis, NR Roberts, SE Moore, V Brown, JA Bolton, PF TI A paternally inherited duplication in the Prader-Willi/Angelman syndrome critical region: A case and family study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE chromosome 15; Prader-Willi/Angelman Syndrome Critical Region; paternally inherited duplication; Pervasive Developmental Disorder ID PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; AUTISM; CHROMOSOME-15; SPECTRUM; PATIENT AB The Prader-Willi/Angelman Critical Region (PWACR; Chromosome 15q11-13) is of interest as a potential locus for genes conferring susceptibility to autism spectrum disorders (ASD). This report describes a female proband referred for evaluation of a possible ASD. Genetic analyses indicated that the proband, her father and one of her sisters, carried a paternally derived interstitial duplication involving 15q11-13. The proband showed evidence of ASD (PDD-NOS), borderline mental retardation, mild hypotonia and joint laxity. Her father and her sister were of normal intelligence and neither was thought to have an ASD, although speech/language difficulties and some autistic type behaviours were reported to have been present early in the development of the sister. This is one of the first reports of a child with a paternal duplication and an autism spectrum disorder. More research is required to determine whether paternally derived duplications that involve 15q11-13 are associated with developmental impairments. C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. Univ London, Inst Psychiat, London, England. Univ London, MRC Social Genet & Dev Psychiat Res Ctr, Inst Psychiat, London, England. Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England. Univ Southampton, Dept Human Genet, Southampton, Hants, England. Salisbury Dist Hosp, Wessex Reg Genet Lab, Salisbury, Wilts, England. Southampton Gen Hosp, Paediat Med Unit, Southampton SO9 4XY, Hants, England. RP Veltman, MWM (reprint author), Univ Cambridge, Dev Psychiat Sect, 18B Douglas House,Trumpington Rd, Cambridge CB2 2AH, England. EM mwmv2@cam.ac.uk RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR Adams WSD, 1995, WIDE RANGE ASSESSMEN Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Bolton PF, 2001, AM J MED GENET, V105, P675, DOI 10.1002/ajmg.1551 BOLTON PF, IN PRESS PSYCHIAT GE Borgatti R, 2001, PEDIATR NEUROL, V24, P111, DOI 10.1016/S0887-8994(00)00244-7 Browne CE, 1997, AM J HUM GENET, V61, P1342, DOI 10.1086/301624 BUNDEY S, 1994, DEV MED CHILD NEUROL, V36, P736 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Cook EH, 1997, AM J HUM GENET, V60, P928 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 1997, J CHILD PSYCHOL PSYC, V38, P667, DOI 10.1111/j.1469-7610.1997.tb01694.x GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P489, DOI 10.1097/00004583-199105000-00022 Harrison JE, 1997, J CHILD PSYCHOL PSYC, V38, P603, DOI 10.1111/j.1469-7610.1997.tb01687.x HOTOPF M, 1995, J AUTISM DEV DISORD, V25, P41, DOI 10.1007/BF02178166 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 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 Mullen E, 1995, MULLEN SCALES EARLY PINKEL D, 1986, P NATL ACAD SCI USA, V83, P2934, DOI 10.1073/pnas.83.9.2934 REPETTO GM, 1998, AM J MED GENET, V78, P82 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 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x Schroer RJ, 1998, AM J MED GENET, V76, P327, DOI 10.1002/(SICI)1096-8628(19980401)76:4<327::AID-AJMG8>3.0.CO;2-M The Psychological Corporation, 1999, WECHSL ABBR SCAL INT The Psychological Corporation, 2001, WECHSL IND ACH TEST Wassink T H, 2000, Curr Psychiatry Rep, V2, P170, DOI 10.1007/s11920-000-0063-x WASSINK TH, 2001, PSYCHIAT GENET, V1, P57 Zeschnigk M, 1997, EUR J HUM GENET, V5, P94 NR 30 TC 29 Z9 31 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 FEB PY 2005 VL 35 IS 1 BP 117 EP 127 DI 10.1007/s10803-004-1039-1 PG 11 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500012 PM 15796127 ER PT J AU Ho, A Todd, RD Constantino, JN AF Ho, A Todd, RD Constantino, JN TI Brief report: Autistic traits in twins vs. non-twins - A preliminary study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; twins; SRS; population genetics; PDD-NOS ID PERVASIVE DEVELOPMENTAL DISORDERS; RECIPROCAL SOCIAL-BEHAVIOR; AFFECTED SIBLING PAIRS; BROADER PHENOTYPE; POPULATION; CHILDREN; RISK AB Previous studies have suggested that among affected sib pairs with autism there is an increase in the frequency of twins over what would be expected in comparison to the prevalence of twins in the general population. In this study we sought to determine whether sub-threshold autistic traits were more pronounced in twins than in non-twins. The Social Responsiveness Scale (SRS) was administered in an epidemiologic twin sample (n = 802) and in a separate population-based sample of non-twins ascertained from a local school district (n = 255). For males (but not females), the mean SRS score was significantly higher among twins than among non-twins. As has been suggested for autism, twin status may incur increased liability to subthreshold autistic symptomatology, particularly in males. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Washington Univ, Dept Psychiat, St Louis, MO USA. Washington Univ, Dept Pediat, St Louis, MO 63130 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, Campus Box 8134,660 S Euclid Ave St, St Louis, MO 63110 USA. EM constantino@wustl.edu CR Betancur C, 2002, AM J HUM GENET, V70, P1381, DOI 10.1086/340364 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Constantino JN, 2003, J AM ACAD CHILD PSY, V42, P458, DOI 10.1097/01.CHI.0000046811.95464.21 Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2000, J DEV BEHAV PEDIATR, V21, P2 CONSTANTINO JN, 2004, J CHILD PSYCHOL PSYC Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Constantino JN, 2005, SOCIAL RESPONSIVENES Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 Greenberg DA, 2001, AM J HUM GENET, V69, P1062, DOI 10.1086/324191 Hallmayer J, 2002, AM J HUM GENET, V71, P941, DOI 10.1086/342990 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 Piven J, 1997, AM J PSYCHIAT, V154, P185 NR 15 TC 17 Z9 18 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 FEB PY 2005 VL 35 IS 1 BP 129 EP 133 DI 10.1007/s10803-004-1040-8 PG 5 WC Psychology, Developmental SC Psychology GA 909RD UT WOS:000227877500013 PM 15796128 ER PT J AU Vasanta, D AF Vasanta, D TI Language cannot be reduced to biology: Perspectives from neuro-developmental disorders affecting language learning SO JOURNAL OF BIOSCIENCES LA English DT Article DE cognitive modularity; developmental dyslexia; orthography; specific language impairment; Williams syndrome ID COGNITIVE NEUROSCIENCE; GENETICS; BRAIN; NEUROPSYCHOLOGY; MODULARITY; DYSLEXIA; CHILDREN; GESTURE AB The study of language knowledge guided by a purely biological perspective prioritizes the study of syntax. The essential process of syntax is recursion - the ability to generate an infinite array of expressions from a limited set of elements. Researchers working within the biological perspective argue that this ability is possible only because of an innately specified genetic makeup that is specific to human beings. Such a view of language knowledge may be fully justified in discussions on biolinguistics, and in evolutionary biology. However, it is grossly inadequate in understanding language-learning problems, particularly those experienced by children with neurodevelopmental disorders such as developmental dyslexia, Williams syndrome, specific language impairment and autism spectrum disorders. Specifically, syntax-centered definitions of language knowledge completely ignore certain crucial aspects of language learning and use, namely, that language is embedded in a social context; that the role of environmental triggering as a learning mechanism is grossly underestimated; that a considerable extent of visuo-spatial information accompanies speech in day-to-day communication; that the developmental process itself lies at the heart of knowledge acquisition; and that there is a tremendous variation in the orthographic systems associated with different languages. All these (socio-cultural) factors can influence the rate and quality of spoken and written language acquisition resulting in much variation in phenotypes associated with disorders known to have a genetic component. Delineation of such phenotypic variability requires inputs from varied disciplines such as neurobiology, neuropsychology, linguistics and communication disorders. In this paper, I discuss published research that questions cognitive modularity and emphasises the role of the environment for understanding linguistic capabilities of children with neuro-developmental disorders. The discussion pertains to two specific disorders, developmental dyslexia and Williams syndrome. C1 Osmania Univ, Dept Linguist, Hyderabad 500007, Andhra Pradesh, India. RP Vasanta, D (reprint author), Osmania Univ, Dept Linguist, Hyderabad 500007, Andhra Pradesh, India. 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PD FEB PY 2005 VL 30 IS 1 BP 129 EP 137 DI 10.1007/BF02705157 PG 9 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 920ZG UT WOS:000228733400015 PM 15824448 ER PT J AU Aman, MG Lam, KSL Van Bourgondien, ME AF Aman, MG Lam, KSL Van Bourgondien, ME TI Medication patterns in patients with autism: Temporal, regional, and demographic influences SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHOACTIVE MEDICINES; BEHAVIORAL SYMPTOMS; CHILDREN; PREVALENCE; DISABILITIES; INDIVIDUALS; DRUGS; HYPERACTIVITY; HALOPERIDOL AB To date, there have been relatively few surveys of psychotropic medicine use in individuals with autism. Data were analyzed from three statewide surveys that employed the same questionnaire and survey methodology. The first was done in the Autism Society of North Carolina in 1992-1993 (NC-1, n = 838; Aman et al. 1995); the second was done in the Autism Society of Ohio in 1999 (Ohio, n = 417; Aman et al. 2003), and the third was done again in the Autism Society of North Carolina in 2001 (NC-2, n = 1538; Langworthy-Lam et al. 2002). Response rates ranged from 48%-56%. Longitudinal trends were examined by comparing the NC-1 and NC-2 data, and regional effects were assessed by comparing the NC-2 and Ohio data. There was a very large increase in antidepressant utilization from 1993 to 2001, with significant increases also occurring for antipsychotics, psychostimulants, and alpha-agonists and beta-blockers. Among youths with autism, the use of any psychotropic increased from 30.5% in NC-1 to 45.2% in NC-2. Psychotropic medication patterns were remarkably consistent across North Carolina and Ohio, except that significantly more autism supplements were used in Ohio. We also examined subject and demographic variables across studies and found several robust correlates of psychotropic medication use. Greater age and handicap, and more restrictive placements, were associated with the use of several drug classes. Knowledge of these patterns may help families and medical planners anticipate future needs. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Univ N Carolina, Div TEACCH, Chapel Hill, NC USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr, Room 175,McCampbell Hall,1581 Dodd Dr, Columbus, OH 43210 USA. 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Child Adolesc. Psychopharmacol. PD FEB PY 2005 VL 15 IS 1 BP 116 EP 126 DI 10.1089/cap.2005.15.116 PG 11 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 907RW UT WOS:000227736600015 PM 15741793 ER PT J AU Clegg, J Hollis, C Mawhood, L Rutter, M AF Clegg, J Hollis, C Mawhood, L Rutter, M TI Developmental language disorders a follow-up in later adult life. Cognitive, language and psychosocial outcomes SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE developmental language disorder; cognitive profile; longitudinal; adult outcome; trajectory; psychosocial outcome; psychiatric morbidity; schizophrenia ID ASPERGER-SYNDROME; INFANTILE-AUTISM; NORMAL-CHILDREN; IMPAIRMENT; MIND; SPEECH; PRESCHOOLERS; INDIVIDUALS; RETARDATION; RELIABILITY AB mental language disorders (DLD) and on the prognostic predictors. Method: Seventeen men with a severe receptive DLD in childhood, reassessed in middle childhood and early adult life, were studied again in their mid-thirties with tests of intelligence (IQ), language, literacy, theory of mind and memory together with assessments of psychosocial outcome. They were compared with the non language disordered siblings of the DLD cohort to control for shared family background, adults matched to the DLD cohort on age and performance IQ (IQM group) and a cohort from the National Child Development Study (NCDS) matched to the DLD cohort on childhood IQ and social class. Results: The DLD men had normal intelligence with higher performance IQ than verbal IQ, a severe and persisting language disorder, severe literacy impairments and significant deficits in theory of mind and phonological processing. Within the DLD cohort higher childhood intelligence and language were associated with superior cognitive and language ability at final adult outcome. In their mid-thirties, the DLD cohort had significantly worse social adaptation (with prolonged unemployment and a paucity of close friendships and love relationships) compared with both their siblings and NCDS controls. Self-reports showed a higher rate of schizotypal features but not affective disorder. Four DLD adults had serious mental health problems (two had developed schizophrenia). Conclusion: A receptive developmental language disorder involves significant deficits in theory of mind, verbal short-term memory and phonological processing, together with substantial social adaptation difficulties and increased risk of psychiatric disorder in adult life. The theoretical and clinical implications of the findings are discussed. C1 Univ Sheffield, Sheffield S10 2TA, S Yorkshire, England. Univ Nottingham, Nottingham NG7 2RD, England. Inst Psychiat, London, England. RP Clegg, J (reprint author), Univ Sheffield, 31 Claremont Crescent, Sheffield S10 2TA, S Yorkshire, England. 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Psychiatry PD FEB PY 2005 VL 46 IS 2 BP 128 EP 149 DI 10.1111/j.1469-7610.2004.00342.x PG 22 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 895TW UT WOS:000226887600003 PM 15679523 ER PT J AU Knickmeyer, R Baron-Cohen, S Raggatt, P Taylor, K AF Knickmeyer, R Baron-Cohen, S Raggatt, P Taylor, K TI Foetal testosterone, social relationships, and restricted interests in children SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE testosterone; social relationships; restricted interests; sex-differences; autism ID CONGENITAL ADRENAL-HYPERPLASIA; HIGH-FUNCTIONING AUTISM; OPPOSITE-SEX TWINS; CENTRAL NERVOUS-SYSTEM; ASPERGER-SYNDROME; DIETHYLSTILBESTROL DES; COGNITIVE-ABILITIES; CEREBRAL LATERALIZATION; PRENATAL TESTOSTERONE; SPATIAL ABILITY AB Background: Sex-differences exist in some areas of human social behaviour. In animals, foetal testosterone (fT) plays a central role in organising the brain and in later social behaviour. fT has also been implicated in language development, eye-contact, and spatial ability in humans. Methods: Fifty-eight children (35 male and 23 female), whose fT was analysed in amniotic fluid, were followed up at age 4. Their mothers completed the Children's Communication Checklist, a questionnaire assessing language, quality of social relationships and restricted interests. Results: fT was negatively correlated to quality of social relationships, taking sex-differences into account. fT was also positively correlated with restricted interests in boys. Conclusions: These findings implicate fT in both social development and attentional focus. They may also have implications for understanding the sex ratio in autism. C1 Addenbrookes Hosp, Dept Clin Biochem, Cambridge, England. Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. 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Psychiatry PD FEB PY 2005 VL 46 IS 2 BP 198 EP 210 DI 10.1111/j.1469-7610.2004.00349.x PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 895TW UT WOS:000226887600008 PM 15679528 ER PT J AU Sutton, SK Burnette, CP Mundy, PC Meyer, J Vaughan, A Sanders, C Yale, M AF Sutton, SK Burnette, CP Mundy, PC Meyer, J Vaughan, A Sanders, C Yale, M TI Resting cortical brain activity and social behavior in higher functioning children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Asperger's disorder; autistic disorder; EEG; individual differences; social behavior; symptomatology ID PERVASIVE DEVELOPMENTAL DISORDER; ASPERGER-SYNDROME; SPECTRUM DISORDERS; JOINT ATTENTION; ANXIETY; SUBGROUPS; QUESTIONNAIRE; ACTIVATION; VALIDITY; CLASSIFICATION AB Background: Psychophysiological measurement of processes related to social behavior may be valuable for research on individual differences and subgroups among children with autism spectrum disorders (Coleman, 1987; Dawson, Klinger, Panagiotides, Lewy, &, Castelloe, 1995; Modahl et al., 1998). In particular, recent research and theory suggests that measures of resting anterior EEG asymmetry reflect complex brain processes associated with individual differences in approach or avoidance motivation that may be associated with social and emotional interaction tendencies among children with autism. Method: This hypothesis was examined in a study of the relations among resting anterior asymmetry, social impairment, and social anxiety in 23 high functioning children with autism (HFA) and 20 controls (age range 9-14 years). Results: These groups were significantly different on the measures of anterior asymmetry, social symptoms and anxiety-related measures. Moreover, HFA children who displayed right frontal asymmetry (RFA group) displayed more symptoms of social impairments and better visual analytic skills than did children who displayed left frontal asymmetry (LFA group). Alternatively, while the LFA group displayed fewer symptoms of social impairment they also reported greater levels of social anxiety, social stress, and lower satisfaction with interpersonal relations than did the RFA group. Conclusions: These observations indicate that anterior EEG asymmetry may be a marker of motivation and emotion processes that refract the autism taxon into important individual differences in social presentation among higher functioning children. C1 Univ Miami, Dept Psychol, Coral Gables, FL 33124 USA. UCL, Tavistock Clin, London, England. RP Sutton, SK (reprint author), Univ Miami, Dept Psychol, POB 248185, Coral Gables, FL 33124 USA. 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CR Ozonoff S, 2003, AUTISM SPECTRUM DISO Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 2 TC 0 Z9 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD FEB PY 2005 VL 66 IS 2 BP 271 EP 272 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 898LC UT WOS:000227077300024 ER PT J AU Norbury, CF AF Norbury, CF TI Barking up the wrong tree? Lexical ambiguity resolution in children with language impairments and autistic spectrum disorders SO JOURNAL OF EXPERIMENTAL CHILD PSYCHOLOGY LA English DT Article DE autism; language impairment; context; ambiguity ID GENERAL COMPREHENSION SKILL; HIGH-FUNCTIONING ADULTS; SENTENCE COMPREHENSION; CENTRAL COHERENCE; WORKING-MEMORY; SUPPRESSION; CONTEXT; READERS; WORDS; MIND AB Lexical ambiguity resolution was investigated in 9- to 17-year-olds with language impairment (LI, n = 20), autistic spectrum disorder (ASD) phis language impairment (ALI, n = 28), ASD and verbal abilities within the normal range (ASO, n = 20), and typically developing children (TD, n = 28). Experiment I investigated knowledge of dominant and subordinate meanings of ambiguous words. The LI and ALI groups knew fewer subordinate meanings than did the ASO and TD groups. Experiment 2 used a modified version of the Gernsbacher, Varner, and Faust (1990) paradigm to investigate contextual facilitation and suppression of irrelevant meanings. All groups demonstrated contextual facilitation, responding quickly and more accurately to words following a biased context. However, children with ALI and LI did not use context as efficiently as did their peers without language deficit. Furthermore, for the LI and ALI groups, errors in the suppression condition reflected poor contextual processing. These findings challenge the assumptions of weak central coherence theory and demonstrate the need for stringent language controls in the study of autistic cognition. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Norbury, CF (reprint author), Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. 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PD FEB PY 2005 VL 90 IS 2 BP 142 EP 171 DI 10.1016/j.jecp.2004.11.003 PG 30 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 898AH UT WOS:000227047500003 PM 15683860 ER PT J AU Krauss, MW Seltzer, MM Jacobson, HT AF Krauss, MW Seltzer, MM Jacobson, HT TI Adults with autism living at home or in non-family settings: positive and negative aspects of residential status SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; caregiving; residential status ID MENTAL-RETARDATION; AGING PARENTS; YOUNG-ADULTS; CHILDREN; DISABILITIES; TRANSITIONS; INVOLVEMENT; DISORDERS; LIFE AB Background Very little is known about the context of caregiving by parents of adults with autism or about the perceived impacts of continued patterns of co-residence vs. out-of-family living. In the present study, maternal assessments of residential status, involvement with adult children living in a non-family setting, and the impacts on mothers of their residential arrangements were examined. Methods Mothers from 133 families of adults (aged 22 years and older) with autism spectrum disorder (ASD) completed questionnaires as part of a longitudinal study on family caregiving. Mothers completed open-ended questions regarding the positive and negative aspects of their child's residential arrangement. Mothers also completed scaled questions regarding their satisfaction with their child's residential arrangements, the different ways in which people's lives change after a relative moves from the home, and the frequency of contact with their son or daughter. Results Mothers found co-residing with their adult child to be of greatest positive benefit to the family while those living apart found this residential arrangement of greatest benefit to the son or daughter with ASD. The greatest negative consequences for co-residing mothers were understood to fall on families, while mothers felt the majority of negative consequences for those that lived apart. There was a high level of contact and maternal involvement between the mother and adult child with ASD even after out-of-home placement. Conclusions Residential status, as appraised by mothers, has varying impacts on the individual with ASD. on the family, and on mothers as individuals and caregivers. The present analysis suggests the multifaceted and highly contingent maternal experience associated with where her child with ASD lives. Among families whose children live elsewhere, there is an impressive amount of continued contact between these families and their sort daughter. C1 Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02254 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Dept Sociol, Waltham, MA 02254 USA. RP Krauss, MW (reprint author), Brandeis Univ, Heller Sch Social Policy & Management, MS 035,POB 549110, Waltham, MA 02254 USA. EM krauss@brandeis.edu CR Aldous J., 1996, FAMILY CAREERS RETHI BAINE D, 1993, AUSTR NZ J DEV DISAB, V18, P1 Baker BL, 2002, MENT RETARD, V40, P1, DOI 10.1352/0047-6765(2002)040<0001:FBOWIO>2.0.CO;2 BAKER BL, 1993, HOSP COMMUNITY PSYCH, V44, P561 Carter E. A., 1980, FAMILY LIFE CYCLE FR, P3 FEATHERSTONE H, 1980, DIFFERENCE FAMILY LI Field S, 1999, FOCUS AUTISM OTHER D, V14, P36, DOI DOI 10.1177/108835769901400105 Fong L., 1993, INT J DISABIL DEV ED, V40, P105, DOI [10.1080/0156655930400204, DOI 10.1080/0156655930400204] Fujiura G. 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Res. PD FEB PY 2005 VL 49 BP 111 EP 124 DI 10.1111/j.1365-2788.2004.00599.x PN 2 PG 14 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 896JZ UT WOS:000226931700001 PM 15634320 ER PT J AU Symons, FJ Sperry, LA Dropik, RL Bodfish, JW AF Symons, FJ Sperry, LA Dropik, RL Bodfish, JW TI The early development of stereotypy and self-injury: a review of research methods SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE developmental disability; early development; self-injurious behavior; stereotypy ID PRADER-WILLI-SYNDROME; SMITH-MAGENIS-SYNDROME; NORMAL HUMAN INFANTS; LESCH-NYHAN DISEASE; FRAGILE-X-SYNDROME; MENTAL-RETARDATION; YOUNG-CHILDREN; RETARDED-CHILDREN; MALADAPTIVE BEHAVIOR; REPETITIVE BEHAVIOR AB Background The origin and developmental course of stereotypic and self-injurious behaviour among individuals with developmental disabilities such as intellectual disability (ID) or pervasive development disorders such as autism is not well understood. Method Twelve studies designed to document the prevalence, nature, or development of stereotypic and/or self-injurious behaviour in children under 5 years of age and identified as at risk for developmental delay or disability were reviewed. Comparisons were made with similar studies with typically developing children. Results It appears that the onset of naturally occurring rhythmic motor stereotypies is delayed in young at-risk children, but that the sequencing may be similar. A very small database, differences in samples, measures, and designs limited the degree to which comparisons could be made across studies. Conclusion Future work is needed based on appropriately designed prospective comparison studies and uniform quantitative measures to provide an empirical basis for new knowledge about the early development of one of the most serious behaviour disorders afflicting children with ID and related problems of development. 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PD FEB PY 2005 VL 49 BP 144 EP 158 DI 10.1111/j.1365-2788.2004.00632.x PN 2 PG 15 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 896JZ UT WOS:000226931700004 PM 15634323 ER PT J AU Lamb, JA Barnby, G Bonora, E Sykes, N Bacchelli, E Blasi, F Maestrini, E Broxholme, J Tzenova, J Weeks, D Bailey, AJ Monaco, AP AF Lamb, JA Barnby, G Bonora, E Sykes, N Bacchelli, E Blasi, F Maestrini, E Broxholme, J Tzenova, J Weeks, D Bailey, AJ Monaco, AP CA IMGSAC TI Analysis of IMGSAC autism susceptibility loci: evidence for sex limited and parent of origin specific effects SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; LINKAGE ANALYSIS; GENOMEWIDE SCREEN; GENETIC-LINKAGE; COMPLEX TRAITS; GENOMIC SCREEN; CHROMOSOME; REGION; ASSOCIATION AB Background and methods: Autism is a severe neurodevelopmental disorder, which has a complex genetic predisposition. The ratio of males to females affected by autism is approximately 4: 1, suggesting that sex specific factors are involved in its development. We reported previously the results of a genomewide screen for autism susceptibility loci in 83 affected sibling pairs ( ASP), and follow up analysis in 152 ASP. Here, we report analysis of an expanded sample of 219 ASP, using sex and parent of origin linkage modelling at loci on chromosomes 2, 7, 9, 15, and 16. Results: The results suggest that linkage to chromosomes 7q and 16p is contributed largely by the male male ASP (MLS = 2.55 v 0.12, and MLS = 2.48 v 0.00, for the 145 male - male and 74 male - female/ female - female ASP on chromosomes 7 and 16 respectively). Conversely linkage to chromosome 15q appears to be attributable to the male - female/ female - female ASP ( MLS = 2.62 v 0.00, for non-male and male - male ASP respectively). On chromosomes 2 and 9, all ASP contribute to linkage. These data, supported by permutation, suggest a possible sex limited effect of susceptibility loci on chromosomes 7, 15, and 16. Parent of origin linkage modelling indicates two distinct regions of paternal and maternal identity by descent sharing on chromosome 7 ( paternal MLS = 1.46 at similar to112 cM, and maternal MLS = 1.83 at similar to135 cM; corresponding maternal and paternal MLS = 0.53 and 0.28 respectively), and maternal specific sharing on chromosome 9 ( maternal MLS = 1.99 at,30 cM; paternal MLS = 0.02). Conclusion: These data support the possibility of two discrete loci underlying linkage of autism to chromosome 7, and implicate possible parent of origin specific effects in the aetiology of autism. C1 Univ Oxford, Wellcome Trust Ctr, Oxford OX3 7BN, England. Univ Bologna, Dipartimento Biol Evoluz Sperimentale, Bologna, Italy. Univ Bologna, Policlin S Orsola, Med Genet Lab, Bologna, Italy. Univ Oxford, Dept Cardiovasc Med, Oxford OX3 7BN, England. Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA. Univ Dept Psychiat, Pk Hosp Children, Sect Child & Adolescent Psychiat, Oxford, England. RP Monaco, AP (reprint author), Univ Oxford, Wellcome Trust Ctr, Roosevelt Dr, Oxford OX3 7BN, England. EM anthony.bailey@psychiatry.ox.ac.uk; anthony.monaco@well.ox.ac.uk RI Monaco, Anthony/A-4495-2010; Weeks, Daniel/B-2995-2012; Maestrini, Elena/K-7508-2012; Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Monaco, Anthony/0000-0001-7480-3197; Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X CR Abecasis GR, 2002, NAT GENET, V30, P97, DOI 10.1038/ng786 Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 Bartlett CW, 2002, AM J HUM GENET, V71, P45, DOI 10.1086/341095 Bonora E, 2003, MOL PSYCHIATR, V8, P885, DOI 10.1038/sj.mp.4001310 Bradford Y, 2001, AM J MED GENET, V105, P539, DOI 10.1002/ajmg.1497 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Buxbaum JD, 2004, MOL PSYCHIATR, V9, P144, DOI 10.1038/sj.mp.4001465 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Clayton-Smith J, 2003, J MED GENET, V40, P87, DOI 10.1136/jmg.40.2.87 Dunn L M., 1982, BRIT PICTURE VOCABUL Dunn L. 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Psychiatry PD FEB PY 2005 VL 76 IS 2 BP 205 EP 205 DI 10.1136/jnnp.2004.042820 PG 1 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 890WJ UT WOS:000226541500012 PM 15654033 ER PT J AU Hellings, JA Nickel, EJ Weckbaugh, M McCarter, K Mosier, M Schroeder, SR AF Hellings, JA Nickel, EJ Weckbaugh, M McCarter, K Mosier, M Schroeder, SR TI The overt aggression scale for rating aggression in outpatient youth with autistic disorder: Preliminary findings SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID BEHAVIOR; CHILDREN AB Aggression is a common and costly problem in youth with developmental disabilities. Rating scales that accurately capture and measure subtypes of aggression phenomenology, frequency and severity are urgently needed, in both clinical practice and research. The authors studied the Overt Aggression Scale (OAS) in a preliminary sample of eight outpatients who participated in an ongoing placebo-controlled study of valproate for aggression in autism. Subjects' OAS aggression scores showed significant correlation with the already validated retrospectively rated Aberrant Behavior Checklist Community Scale irritability subscale. Further study of the OAS in outpatients with aggression and developmental disabilities is warranted. C1 Univ Kansas, Med Ctr, Dept Psychiat, Kansas City, KS 66160 USA. RP Hellings, JA (reprint author), Univ Kansas, Med Ctr, Dept Psychiat, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. 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PD FEB PY 2005 VL 17 IS 1 BP 29 EP 35 DI 10.1176/appi.neuropsych.17.1.29 PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 902RP UT WOS:000227374500004 PM 15746480 ER PT J AU Libbey, JE Sweeten, TL McMahon, WM Fujinami, RS AF Libbey, JE Sweeten, TL McMahon, WM Fujinami, RS TI Autistic disorder and viral infections SO JOURNAL OF NEUROVIROLOGY LA English DT Review DE autism; immune response; virus; virus infection ID CONGENITAL CYTOMEGALOVIRUS-INFECTION; PERVASIVE DEVELOPMENTAL DISORDERS; HERPES-SIMPLEX ENCEPHALITIS; INFLAMMATORY-BOWEL-DISEASE; MUMPS-RUBELLA VACCINATION; MEASLES-VIRUS INFECTION; INFANTILE-AUTISM; MULTIPLE-SCLEROSIS; INTERFERON-GAMMA; HUMAN HERPESVIRUS-6 AB Autistic disorder (autism) is a behaviorally defined developmental disorder with a wide range of behaviors. Although the etiology of autism is unknown, data suggest that autism results from multiple etiologies with both genetic and environmental contributions, which may explain the spectrum of behaviors seen in this disorder. One proposed etiology for autism is viral infection very early in development. The mechanism, by which viral infection may lead to autism, be it through direct infection of the central nervous system (CNS), through infection elsewhere in the body acting as a trigger for disease in the CNS, through alteration of the immune response of the mother or offspring, or through a combination of these, is not yet known. Animal models in which early viral infection results in behavioral changes later in life include the influenza virus model in pregnant mice and the Borna disease virus model in newborn Lewis rats. Many studies over the years have presented evidence both for and against the association of autism with various viral infections. The best association to date has been made between congenital rubella and autism; however, members of the herpes virus family may also have a role in autism. Recently, controversy has arisen as to the involvement of measles virus and/or the measles, mumps, rubella (MMR) vaccine in the development of autism. Biological assays lend support to the association between measles virus or MMR and autism whereas epidemiologic studies show no association between MMR and autism. Further research is needed to clarify both the mechanisms whereby viral infection early in development may lead to autism and the possible involvement of the MMR vaccine in the development of autism. C1 Univ Utah, Dept Neurol, Salt Lake City, UT 84132 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT USA. RP Fujinami, RS (reprint author), Univ Utah, Dept Neurol, 30 N 1900 E,3R330 SOM, Salt Lake City, UT 84132 USA. 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Neurovirol. PD FEB PY 2005 VL 11 IS 1 BP 1 EP 10 DI 10.1080/13550280590900553 PG 10 WC Neurosciences; Virology SC Neurosciences & Neurology; Virology GA 903PR UT WOS:000227438600001 PM 15804954 ER PT J AU Vitiello, B Aman, MG Scahill, L McCracken, JT McDougle, CJ Tierney, E Davies, M Arnold, LE AF Vitiello, B Aman, MG Scahill, L McCracken, JT McDougle, CJ Tierney, E Davies, M Arnold, LE TI Research knowledge among parents of children participating in a randomized clinical trial SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ethics; clinical trials ID INFORMED-CONSENT; UNDERSTAND AB Objective: Parental permission is required for child research, but parents' understanding of research aims and procedures has not been well documented. Parental research knowledge was assessed during a clinical trial in autism. Method: Parents of 101 children (age 5-17 years) with autism participating in a placebo-controlled trial of risperidone were given a questionnaire at the end of the study. Results: Of the 95 parents completing the questionnaire, 99% knew of possible placebo assignment and that testing the medication efficacy was the main purpose of the investigators; 96% to 98% knew that research involved both risks and potential benefits, identified the study medication, and knew of their right to withdraw at any time; 90% to 95% knew of the medication's main side effects; 87% reported having been informed of possible alternatives to research participation; and 72% were aware that treatment was randomly assigned (whereas 27% reported that treatment was chosen based on individual needs to ensure best care). Parents with a college degree were more likely to recognize the random nature of treatment assignment. Conclusions: Overall, parents were highly knowledgeable of the main research components. About one fourth, however, seemed unaware that treatment was randomly determined and not personalized, suggesting that therapeutic misconception may affect some otherwise well-informed parents. C1 NIMH, Child & Adolescent Treatment & Prevent Intervent, Bethesda, MD 20892 USA. Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA USA. Indiana Univ, Div Child & Adolescent Psychiat, Indianapolis, IN 46204 USA. Kennedy Krieger Inst, Baltimore, MD USA. Columbia Univ, New York State Psychiat Inst, New York, NY 10027 USA. RP Vitiello, B (reprint author), NIMH, Child & Adolescent Treatment & Prevent Intervent, Room 7147,6001 Execut Blvd,MSC 9633, Bethesda, MD 20892 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD FEB PY 2005 VL 44 IS 2 BP 145 EP 149 DI 10.1097/00004583-200502000-00006 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 893HP UT WOS:000226710200006 PM 15689727 ER PT J AU Bourre, JM AF Bourre, JM TI omega-3 Fatty acids in psychiatry SO M S-MEDECINE SCIENCES LA French DT Article ID POLYUNSATURATED FATTY-ACIDS; ERYTHROCYTE-MEMBRANES; DOUBLE-BLIND; SCHIZOPHRENIC-PATIENTS; EICOSAPENTAENOIC ACID; POSTPARTUM DEPRESSION; DOCOSAHEXAENOIC ACID; SEAFOOD CONSUMPTION; FISH CONSUMPTION; CONTROLLED-TRIAL AB are of the omego-3 family, and are thus of dietary origin. The omega-3 fatty acids (mainly alpha-linolenic acid, ALA) participated in one of the first experimental demonstration of the effect of dietary substances (nutrients) on the structure and function of the brain. Experiments were first of all carried out on ex vivo cultured brain cells, then on in vivo brain cells (neurons, astrocytes and oligodendrocytes) from animals fed ALA deficient diet, finally on physicochemical (membrane fluidity), biochemical, physiological, neurosensory (vision an auditory responses), and behavioural or learning parameters. These findings indicated that the nature of polyunsaturated fatty acids (in particular omega-3) present in formula milks for human infants determines to a certain extend the visual, neurological, and intellectual abilities. Thus, in view of these results and of the high polyunsaturated fatty acid content of the brain, it is normal to consider that they could be involved in psychiatric diseases and in the cognitive decline of ageing. Omega-3 fatty acids appear effective in the prevention of stress, however their role as regulator of mood is a matter for discussion. Indeed, they play a role in the prevention of some disorders including depression (especially postpartum), as well as in dementia, particularly Alzheimer's disease. Their role in major depression and bipolar disorder (manic-depressive disease), only poorly documented, is not clearly demonstrated. The intervention of omega-3 dyslexia, autism, and schizophrenia has been suggested, but it does not necessarily infer a nutritional problems, The respective importance of the vascular system (where the omega-3 are actually active) and the cerebral parenchyma itself, remain to be resolved. However, the insufficient supply of omega-3 fatty acids in today diet in occidental (less than 50% of the recommended dietary intakes values for ALA) raises the problem of how to correct inadequate dietary habits, by prescribing mainly rapeseed (canola) and walnut oils on the one hand, fatty fish (wild, or formed, but the nature of fatty acids present in fish flesh is the direct consequence of the nature of fats with which they have been fed), and eggs from laying hens fed omego-3 fatty acids.The brain is one of the organs with the highest level of lipids (fats). Brain lipids, formed of fatty acids, participate in the structure of membranes, for instance 50% fatty acids are polyunsaturated in the gray matter, 1/3 C1 Hop Fernand Widal, Lab Neuropharmacol Nutr, INSERM, F-75475 Paris 10, France. RP Bourre, JM (reprint author), Hop Fernand Widal, Lab Neuropharmacol Nutr, INSERM, 200 Rue Faubourg, F-75475 Paris 10, France. 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Findings in neuropsychiatric disorders SO MOLECULAR PSYCHIATRY LA English DT Review DE hippocampus; MRI; volume; neurology; psychiatry ID TEMPORAL-LOBE EPILEPSY; POSTTRAUMATIC-STRESS-DISORDER; MILD COGNITIVE IMPAIRMENT; VOXEL-BASED MORPHOMETRY; TRAUMATIC BRAIN INJURY; BORDERLINE PERSONALITY-DISORDER; OBSESSIVE-COMPULSIVE DISORDER; CHILDHOOD-ONSET SCHIZOPHRENIA; APOLIPOPROTEIN-E EPSILON-4; 1ST EPISODE SCHIZOPHRENIA AB Magnetic resonance imaging (MRI) has opened a new window to the brain. Measuring hippocampal volume with MRI has provided important information about several neuropsychiatric disorders. We reviewed the literature and selected all English-language, human subject, data-driven papers on hippocampal volumetry, yielding a database of 423 records. Smaller hippocampal volumes have been reported in epilepsy, Alzheimer's disease, dementia, mild cognitive impairment, the aged, traumatic brain injury, cardiac arrest, Parkinson's disease, Huntington's disease, Cushing's disease, herpes simplex encephalitis, Turner's syndrome, Down's syndrome, survivors of low birth weight, schizophrenia, major depression, posttraumatic stress disorder, chronic alcoholism, borderline personality disorder, obsessive - compulsive disorder, and antisocial personality disorder. Significantly larger hippocampal volumes have been correlated with autism and children with fragile X syndrome. Preservation of hippocampal volume has been reported in congenital hyperplasia, children with fetal alcohol syndrome, anorexia nervosa, attention-deficit and hyperactivity disorder, bipolar disorder, and panic disorder. Possible mechanisms of hippocampal volume loss in neuropsychiatric disorders are discussed. C1 Cent Mil Hosp, Dept Mil Psychiat, NL-3584 CX Utrecht, Netherlands. Rudolf Magnus Inst Neurosci, Dept Psychiat, NL-3508 TA Utrecht, Netherlands. Emory Univ, Sch Med, Dept Psychiat, Atlanta, GA 30322 USA. Emory Univ, Sch Med, Dept Behav Sci & Radiol, Atlanta, GA 30322 USA. Ctr Positron Emiss Tomog, Decatur, GA USA. Atlanta VAMC, Decatur, GA USA. RP Geuze, E (reprint author), Cent Mil Hosp, Dept Mil Psychiat, Mailbox B-01-2-06,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. 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Psychiatr. PD FEB PY 2005 VL 10 IS 2 BP 160 EP 184 DI 10.1038/sj.mp.4001579 PG 25 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 891GN UT WOS:000226569400004 PM 15356639 ER PT J AU Koshino, H Carpenter, PA Minshew, NJ Cherkassky, VL Keller, TA Just, MA AF Koshino, H Carpenter, PA Minshew, NJ Cherkassky, VL Keller, TA Just, MA TI Functional connectivity in an fMRI working memory task in high-functioning autism SO NEUROIMAGE LA English DT Article DE autism; fMRI; working memory ID FRONTAL LOBES; HUMAN BRAIN; DIAGNOSTIC INTERVIEW; PREFRONTAL CORTEX; SOCIAL-BEHAVIOR; VISUAL-SEARCH; INDIVIDUALS; LANGUAGE; CHILDREN; MRI AB An fMRI study was used to measure the brain activation of a group of adults with high-functioning autism compared to a Full Scale and Verbal IQ and age-matched control group during an n-back working memory task with letters. The behavioral results showed comparable performance, but the fMRI results suggested that the normal controls might use verbal codes to perform the task, while the adults with autism might use visual codes. The control group demonstrated more activation in the left than the right parietal regions, whereas the autism group showed more right lateralized activation in the prefrontal and parietal regions. The autism group also had more activation than the control group in the posterior regions including inferior temporal and occipital regions. The analysis of functional connectivity yielded similar patterns for the two groups with different hemispheric correlations. The temporal profile of the activity in the prefrontal regions was more correlated with the left parietal regions for the control group, whereas it was more correlated with the right parietal regions for the autism group. (C) 2004 Elsevier Inc. All rights reserved. C1 Calif State Univ San Bernardino, Dept Psychol, San Bernardino, CA 92407 USA. Carnegie Mellon Univ, Ctr Cognit Brain Imaging, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Psychiat & Neurol, Pittsburgh, PA 15213 USA. RP Koshino, H (reprint author), Calif State Univ San Bernardino, Dept Psychol, 5500 Univ Pkwy, San Bernardino, CA 92407 USA. 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Topics include the pathology of alzheimer's disease,autism,epilepsy and parkinson's disease. Also discussed were gene regulation,gene expression, drug therapy and neurological biochemistry. NR 0 TC 0 Z9 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0143-4179 EI 1532-2785 J9 NEUROPEPTIDES JI Neuropeptides PD FEB PY 2005 VL 39 IS 1 BP 35 EP 65 DI 10.1016/j.npep.2004.09.002 PG 31 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 889QK UT WOS:000226457300005 ER PT J AU Dementieva, YA Vance, DD Donnelly, SL Elston, LA Wolpert, CM Ravan, SA DeLong, GR Abramson, RK Wright, HH Cuccaro, ML AF Dementieva, YA Vance, DD Donnelly, SL Elston, LA Wolpert, CM Ravan, SA DeLong, GR Abramson, RK Wright, HH Cuccaro, ML TI Accelerated head growth in early development of individuals with autism SO PEDIATRIC NEUROLOGY LA English DT Article ID CIRCUMFERENCE; DISORDERS; CHILDREN AB Macrocephaly is one of the most consistent physical findings reported in autistic individuals. Previous studies attempted to determine if macrocephaly is associated with risk for autism. This study hypothesizes that an abnormal acceleration in head growth during early development, rather than macrocephaly, is associated with autism risk. To investigate this hypothesis, head circumference data were examined in 251 individuals from 82 multiplex (at least two individuals with autism) and 113 sporadic (no family history) families with autism. This examination included longitudinal measurements for 79 individuals. Nineteen percent of the original 251 individuals were found to have macrocephaly (head circumference >97%). Abnormal acceleration in head growth was defined as an increase of 25 or more percentile points in head circumference between two consecutive measurements. Thirty-five percent of individuals with multiple head circumference records had an abnormal increase in head circumference. Furthermore, autistic individuals with accelerated head growth in early childhood displayed higher levels of adaptive functioning and less social impairment. This study confirms the presence of abnormal acceleration in head growth during the first and second months of life in a subgroup of autistic individuals. (C) 2005 by Elsevier Inc. All rights reserved. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Div Pediat, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Div Psychiat, Durham, NC 27710 USA. Marshall Univ, Div Math & Appl Sci, Huntington, WV USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. RP Dementieva, YA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Box 3445, Durham, NC 27710 USA. 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Neurol. PD FEB PY 2005 VL 32 IS 2 BP 102 EP 108 DI 10.1016/j.pediatrneurol.2004.08.005 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 896QP UT WOS:000226948900006 PM 15664769 ER PT J AU Croen, LA Yoshida, CK Odouli, R Newman, TB AF Croen, LA Yoshida, CK Odouli, R Newman, TB TI Neonatal hyperbilirubinemia and risk of autism spectrum disorders SO PEDIATRICS LA English DT Article DE autism spectrum disorders; hyperbilirubinemia; jaundice; pervasive developmental disorder; neonatal risk ID COMPLICATIONS; CHILDREN AB Objective. To investigate the association between neonatal hyperbilirubinemia and autism spectrum disorders (ASD). Methods. We conducted a large case-control study nested within the cohort of singleton term infants born between 1995 and 1998 at a northern California Kaiser Permanente hospital. Case subjects ( n = 338) were children with an ASD diagnosis recorded in Kaiser Permanente outpatient databases; control subjects ( n = 1817) were children without an ASD diagnosis, who were randomly sampled and frequency-matched to case subjects according to gender, birth year, and birth hospital. Results. Approximately 28% of case and control subjects received greater than or equal to 1 bilirubin test in the first 30 days of life. No case-control differences were observed for maximal bilirubin levels of greater than or equal to 15 mg/dL (10.1% vs 12.1%), greater than or equal to 20 mg/dL (2.1% vs 2.5%), or greater than or equal to 25 mg/ dL (0.3% vs 0.2%). Compared with children whose maximal neonatal bilirubin levels were < 15 mg/ dL or not measured, children with any degree of bilirubin level elevation were not at increased risk of ASD, after adjustment for gender, birth facility, maternal age, maternal race/ethnicity, maternal education, and gestational age ( for bilirubin levels of 15-19.9 mg/ dL: odds ratio: 0.7; 95% confidence interval: 0.5-1.2; for bilirubin levels of 20-24.9 mg/ dL: odds ratio: 0.7; 95% confidence interval: 0.3-1.6; for bilirubin levels of &GE; 25 mg/ dL: odds ratio: 1.1; 95% confidence interval: 0.1-11.2). Conclusion. These data suggest that neonatal hyperbilirubinemia is not a risk factor for ASD. C1 Kaiser Permanente, Div Res, Oakland, CA 94612 USA. Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94612 USA. 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In the present study, an ABAB design was used to assess the influence of proximity as a social stimulus. Close and distant proximity of a familiar adult was systematically manipulated to evaluate the effect of proximity on the on-task behavior of a 15-year-old male with autism. Baseline, experimental analysis, and intervention phases were conducted within a self-contained classroom. Pronounced effects of distant educator proximity to the participant were evident during both the experimental analysis and intervention, with increased on-task behavior occurring in the distant condition. Future recommendations for the investigation of proximity as a relevant social stimulus are forwarded. (C) 2005 Wiley Periodicals, Inc. C1 Munroe Meyer Inst Genet & Rehabil, Nebraska Med Ctr 985459, Omaha, NE 68198 USA. Univ So Mississippi, Hattiesburg, MS 39406 USA. Univ S Dakota, Sch Med, Vermillion, SD 57069 USA. 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Schools PD FEB PY 2005 VL 42 IS 2 BP 189 EP 196 DI 10.1002/pits.20055 PG 8 WC Psychology, Educational SC Psychology GA 897HI UT WOS:000226994200006 ER PT J AU Hampton, T AF Hampton, T TI Autism and the alphabet SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT News Item NR 0 TC 0 Z9 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JAN 26 PY 2005 VL 293 IS 4 BP 415 EP 415 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 890DW UT WOS:000226492900003 ER PT J AU Reddy, KS AF Reddy, KS TI Cytogenetic abnormalities and fragile-X syndrome in autism spectrum disorder SO BMC MEDICAL GENETICS LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; GENOTYPE-PHENOTYPE CORRELATIONS; CHROMOSOME REGION 15Q11Q13; PRADER-WILLI SYNDROMES; LINKAGE-DISEQUILIBRIUM; FMR1 GENE; MENTAL-RETARDATION; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; SUSCEPTIBILITY GENE AB Background: Autism is a behavioral disorder with impaired social interaction, communication, and repetitive and stereotypic behaviors. About 5-10 % of individuals with autism have 'secondary' autism in which an environmental agent, chromosome abnormality, or single gene disorder can be identified. Ninety percent have idiopathic autism and a major gene has not yet been identified. We have assessed the incidence of chromosome abnormalities and Fragile X syndrome in a population of autistic patients referred to our laboratory. Methods: Data was analyzed from 433 patients with autistic traits tested using chromosome analysis and/or fluorescence in situ hybridization ( FISH) and/or molecular testing for fragile X syndrome by Southern and PCR methods. Results: The median age was 4 years. Sex ratio was 4.5 males to 1 female [ 354: 79]. A chromosome (cs) abnormality was found in 14/421 [3.33 %] cases. The aberrations were: 4/14 [28%] supernumerary markers; 4/14 [ 28%] deletions; 1/14 [7%] duplication; 3/14 [21%] inversions; 2/14 [14%] translocations. FISH was performed on 23 cases for reasons other than to characterize a previously identified cytogenetic abnormality. All 23 cases were negative. Fragile-X testing by Southern blots and PCR analysis found 7/316 [2.2 %] with an abnormal result. The mutations detected were: a full mutation (fM) and abnormal methylation in 3 [43 %], mosaic mutations with partial methylation of variable clinical significance in 3 [43%] and a permutation carrier [14%]. The frequency of chromosome and fragile-X abnormalities appears to be within the range in reported surveys ( cs 4.8-1.7%, FRAX 2-4%). Limitations of our retrospective study include paucity of behavioral diagnostic information, and a specific clinical criterion for testing. Conclusions: Twenty-eight percent of chromosome abnormalities detected in our study were subtle; therefore a high resolution cytogenetic study with a scrutiny of 15q11.2q13, 2q37 and Xp23.3 region should be standard practice when the indication is autism. The higher incidence of mosaic fragile-X mutations with partial methylation compared to FRAXA positive population [50% vs 15-40%] suggests that faint bands and variations in the Southern band pattern may occur in autistic patients. C1 Genzyme Genet, Orange, CA 92868 USA. RP Reddy, KS (reprint author), Genzyme Genet, Orange, CA 92868 USA. 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Genet. PD JAN 18 PY 2005 VL 6 DI 10.1186/1471-2350-6-3 PG 16 WC Genetics & Heredity SC Genetics & Heredity GA 944CF UT WOS:000230401900001 ER PT J AU Sibbald, B AF Sibbald, B TI No autism coverage SO CANADIAN MEDICAL ASSOCIATION JOURNAL LA English DT News Item CR Cassels A, 2002, CAN MED ASSOC J, V167, P1278 NR 1 TC 0 Z9 0 PU CANADIAN MEDICAL ASSOCIATION PI OTTAWA PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 3Y6, CANADA SN 0820-3946 J9 CAN MED ASSOC J JI Can. Med. Assoc. J. PD JAN 18 PY 2005 VL 172 IS 2 BP 168 EP 168 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 886EA UT WOS:000226208500021 ER PT J AU Alonso-Navarro, H Jimenez-Jimenez, FJ Puertas-Munoz, I Rabano, J de Yebenes, JG Sarasa-Corral, JL AF Alonso-Navarro, H Jimenez-Jimenez, FJ Puertas-Munoz, I Rabano, J de Yebenes, JG Sarasa-Corral, JL TI Kluver-Bucy syndrome as the initial symptom of adult-type ceroid lipofuscinosis (Kufs'disease) SO REVISTA DE NEUROLOGIA LA Spanish DT Review DE ceroid lipofuscinosis; etiology; Kluver-Bucy syndrome; Kufs'disease ID DELAYED POSTIRRADIATION ENCEPHALOPATHY; HERPES-SIMPLEX ENCEPHALITIS; KUFS-DISEASE; TEMPORAL-LOBE; ALZHEIMERS-DISEASE; FRONTOTEMPORAL DEMENTIA; INFANTILE-AUTISM; II ENCEPHALITIS; NATURAL-HISTORY; FLUENT APHASIA AB Aims. The purpose of this paper is to report the case of a patient with Kluver-Bucy syndrome caused by adult-type ceroid lipofuscinosis (Kufs' disease) and to review the literature dealing with the causes of this syndrome. Case report. A 38-year-old male examined because of behavioural changes and cognitive impairment. Brain biopsy findings were characteristic of adult-type ceroid lipofuscinosis. This patient fulfilled the criteria of Kufs' disease, since he had mixed clinical features belonging to both type A (neuropsychiatric disorders) and B (aphasia-apraxia-agnosia syndrome) of the disease. The initial symptoms included several clinical features of Kluver-Bucy syndrome (probable visual agnosia, apathy, increased sexual activity, lack of sexual inhibition, hypermetamorphopsia, increased oral behaviour and changes in dietary habits). Conclusions. Adult-type ceroid lipofuscinosis is an infrequent clinical entity that is difficult to diagnose owing to the absence of peripheral biological markers and the need to confirm such a diagnosis by means of a histopathological study. C1 Univ Alcala de Henares, Dept Med Neurol, Hosp Principe Asturias, Alcala De Henares, Spain. Fdn Jimenez Diaz, Dept Neurol, Madrid, Spain. Fdn Jimenez Diaz, Dept Anat Patol, Madrid, Spain. RP Jimenez-Jimenez, FJ (reprint author), Marroquina 14-3B, E-28030 Madrid, Spain. 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Neurologia PD JAN 16 PY 2005 VL 40 IS 2 BP 93 EP 98 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 900BA UT WOS:000227189200009 PM 15712163 ER PT J AU Ylisaukko-Oja, T Rehnstrom, K Vanhala, R Kempas, E von Koskull, H Tengstrom, C Mustonen, A Ounap, K Lahdetie, J Jarvela, I AF Ylisaukko-Oja, T Rehnstrom, K Vanhala, R Kempas, E von Koskull, H Tengstrom, C Mustonen, A Ounap, K Lahdetie, J Jarvela, I TI MECP2 mutation analysis in patients with mental retardation SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE mental retardation; XLMR; Rett's syndrome; Angelman syndrome; mutation screening; X-chromosome ID CPG-BINDING-PROTEIN; RETT-SYNDROME; HOT-SPOT; GENE; MALES; IDENTIFICATION; POLYMORPHISMS; SEQUENCE; DOMAIN; DHPLC AB Mutations in the methyl-CpG-binding protein 2 (MECP2) gene are known to underlie Rett' syndrome, the most common cause of mental retardation (MR) in girls. Since the original report, phenotypes resulting from MECP2 mutations have been shown to extend, for example, to several Rett variants, autism, atypical Angelman syndrome, and nonspecific MR. It was earlier proposed that MECP2 mutations might account for similar to2% of the male cases with nonspecific MR. Thereby, the frequency of MECP2 mutations in the mentally retarded population would be comparable to that of Fragile-X syndrome. The aim of this study was to analyze well-characterized cases with MR and to clarify the role of the MECP2 gene in the etiology of MR and atypical Angelman syndrome. The coding sequence of the MECP2 gene was analyzed in a sample of 118 patients (103 males, 15 females) by direct sequencing. Two coding sequence variants, 602C > T (A201V) and 1189G > A(E397K), were identified. In addition, we identified four variants in the intronic or 3'UTR regions. None of these variants is likely to be causal. We conclude that the evidence across all the mutation screening studies implies that MECP2 mutations do not represent a major cause of nonspecific MR. (C) 2004 Wiley-Liss, Inc. C1 Natl Publ Hlth Inst, Dept Mol Med, Helsinki 00251, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Hosp Children & Adolescent, Unit Child Neurol, Helsinki, Finland. Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, Genet Lab, FIN-00290 Helsinki, Finland. Rinnekoti Fdn, Espoo, Finland. Oulu Univ Hosp, Dept Clin Genet, Oulu, Finland. Tartu Univ Clin, Ctr Med Genet, United Labs, Tartu, Estonia. Univ Helsinki, Cent Hosp, Genet Mol Lab, Helsinki, Finland. RP Ylisaukko-Oja, T (reprint author), Natl Publ Hlth Inst, Dept Mol Med, POB 104, Helsinki 00251, Finland. 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J. Med. Genet. A PD JAN 15 PY 2005 VL 132A IS 2 BP 121 EP 124 DI 10.1002/ajmg.a.30416 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 888NJ UT WOS:000226381200002 PM 15578581 ER PT J AU Carper, RA Courchesne, E AF Carper, RA Courchesne, E TI Localized enlargement of the frontal cortex in early autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE gray matter; white matter; MRI; orbital cortex; dorsolateral; motor ID CEREBRAL-BLOOD-FLOW; MAGNETIC-RESONANCE; MENTAL-RETARDATION; EXECUTIVE FUNCTION; CHILDHOOD AUTISM; INFANTILE-AUTISM; CELL COUNTS; BRAIN; CHILDREN; INDIVIDUALS AB Background. Evidence from behavioral, imaging, and postmortem studies indicates that the frontal lobe, as well as other brain regions such as the cerebellum and limbic system, develops abnormally in children with autism, It is not yet clear to what extent the frontal lobe is affected; that is, whether all regions of frontal cortex show the same signs of structural maldevelopment. Methods. In the present study, we measured cortical volume in four subregions of the frontal cortex in 2-year-old to 9-year-old boys with autism and normal control boys. Results: The dorsolateral region showed a reduced age effect inpatients when compared with control subjects, with a predicted 10016 increase in volume from 2 years of age to 9 years of age compared with a predicted 48016 increase for control subjects. In a separate analysis, dorsolateral and medial frontal regions were significantly enlarged in patients aged 2 to 5 years compared with control subjects of the same age, but the precentral gyrus and orbital cortex were not. Conclusions: These data indicate regional variation in the degree of frontocortical overgrowth with a possible bias toward later developing or association areas. Possible mechanisms for these regional differences are discussed. C1 Univ Calif San Diego, Ctr Autism Res, Childrens Hosp, Res Ctr, San Diego, CA 92103 USA. Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. RP Carper, RA (reprint author), 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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Psychiatry PD JAN 15 PY 2005 VL 57 IS 2 BP 126 EP 133 DI 10.1016/j.biopsych.2004.11.005 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 888BQ UT WOS:000226349600003 PM 15652870 ER PT J AU Tordjman, S Anderson, GM Pichard, N Charbuy, H Touitou, Y AF Tordjman, S Anderson, GM Pichard, N Charbuy, H Touitou, Y TI Nocturnal excretion of 6-sulphatoxymelatonin in children and adolescents with autistic disorder SO BIOLOGICAL PSYCHIATRY LA English DT Article DE 6-sulphatoxymelatonin; melatonin; autistic disorder; autism severity; pineal; circadian sleep-wake rhythm ID HUMAN-PLASMA MELATONIN; SLEEP-WAKE RHYTHM; 6-HYDROXYMELATONIN SULFATE; YOUNG-ADULTS; BLIND; HORMONE; METABOLITE; CHILDHOOD; SEROTONIN; CORTISOL AB Background: Many studies in autistic disorder report sleep problems and altered circadian rhythms, suggesting abnormalities in melatonin physiology. Additionally, melatonin, a pineal gland hormone produced from serotonin, is of special interest in autistic disorder given reported alterations in central and peripheral serotonin neurobiology. Methods: Nocturnal urinary excretion of 6-sulphatoxymelatonin was measured by radioimmunoassay in groups of children and adolescents with autistic disorder (n = 49) and normal control individuals (n = 88) matched on age, sex, and Tanner stage of puberty. Results: Nocturnal 6-sulphatoxymelatonin excretion rate was significantly and substantially lower in patients with autism than in normal controls (mean +/- SEM, .75 +/- .11 vs. 1.80 +/- .17 mug/hr, p = .0001), and was significantly negatively correlated with severity of autistic impairments in verbal communication and play (p < .05). Conclusions: These findings indicate clearly that nocturnal production of melatonin is reduced in autism. Further research is warranted in order to understand the mechanisms underlying the lower melatonin production, to assess the impact of altered melatonin on the pathophysiology and behavioral expression of autistic disorder, and to determine the utility of melatonin administration in individuals with autism. C1 Univ Rennes 1, Fac Med, Ctr Hosp Guillaume Regnier, Ctr Sci Res,URM 7593,Hop Pitie Salpetriere, F-35200 Rennes, France. Univ Paris 06, Dept Med Biochem & Mol Biol, Paris, France. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. RP Tordjman, S (reprint author), Univ Rennes 1, Fac Med, Ctr Hosp Guillaume Regnier, Ctr Sci Res,URM 7593,Hop Pitie Salpetriere, 154 Rue Chatillon, F-35200 Rennes, France. 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Psychiatry PD JAN 15 PY 2005 VL 57 IS 2 BP 134 EP 138 DI 10.1016/j.biopsych.2004.11.003 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 888BQ UT WOS:000226349600004 PM 15652871 ER PT J AU Waiter, GD Williams, JHG Murray, AD Gilchrist, A Perrett, DI Whiten, A AF Waiter, GD Williams, JHG Murray, AD Gilchrist, A Perrett, DI Whiten, A TI Structural white matter deficits in high-functioning individuals with autistic spectrum disorder: a voxel-based investigation SO NEUROIMAGE LA English DT Article DE autistic disorder; MRI; brain structure; cerebral white matter; morphometry ID FUSIFORM FACE AREA; RIGHT-HEMISPHERE; ASPERGER-SYNDROME; MAGNETIC-RESONANCE; FACIAL EXPRESSIONS; CORPUS-CALLOSUM; BRAIN; MIND; MRI; COMMUNICATION AB A number of imaging and neuropathological studies have reported structural abnormalities in white matter areas such as the corpus callosum in autism spectrum disorder (ASD). Differences in both global brain volume and the size of specific neural structures have been reported. In order to expand these previously reported findings and to describe more precisely the nature of such structural changes, we performed a voxel-based morphometric whole brain analysis, using a group-specific template, in male adolescents with ASD. Fifteen individuals with normal intelligence and ASD, and a group of 16 controls, matched for age, sex, and IQ, were investigated. High-resolution T1-weighted 3D data sets were acquired and analysed. Local white matter volume deficits were found in the corpus callosum, particularly in the anterior splenium and isthmus, and right hemisphere. White matter volume deficits were also found in the left middle temporal, right middle frontal, and left superior frontal gyri. No significant areas of increased white matter volume were found. Our findings support the hypothesis that reduced white matter volume in the corpus callosum and right hemisphere may play a role in the pathophysiology of ASD. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Aberdeen, Dept Radiol, Res MRI Ctr, Aberdeen AB25 2ZD, Scotland. Univ Aberdeen, Dept Child Hlth, Aberdeen AB25 2ZD, Scotland. Royal Cornhill Hosp, Young Peoples Dept, Aberdeen, Scotland. Univ St Andrews, Sch Psychol, St Andrews, Fife, Scotland. RP Waiter, GD (reprint author), Univ Aberdeen, Dept Radiol, Res MRI Ctr, Lilian Sutton Bldg,Foresterhill, Aberdeen AB25 2ZD, Scotland. 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Twin and family studies point to a significant genetic etiology, and several groups have performed genomic linkage screens to identify susceptibility loci. Methods: We performed a genome-wide linkage screen in 158 combined Tufts, Vanderbilt and AGRE (Autism Genetics Research Exchange) multiplex autism families using parametric and nonparametric methods with a categorical autism diagnosis to identify loci of main effect. Hypothesizing interdependence of genetic risk factors prompted us to perform exploratory studies applying the Ordered-Subset Analysis (OSA) approach using LOD scores as the trait covariate for ranking families. We employed OSA to test for interlocus correlations between loci with LOD scores >= 1.5, and empirically determined significance of linkage in optimal OSA subsets using permutation testing. Exploring phenotypic correlates as the basis for linkage increases involved comparison of mean scores for quantitative trait-based subsets of autism between optimal subsets and the remaining families. Results: A genome-wide screen for autism loci identified the best evidence for linkage to 17q11.2 and 19p13, with maximum multipoint heterogeneity LOD scores of 2.9 and 2.6, respectively. Suggestive linkage ( LOD scores >= 1.5) at other loci included 3p, 6q, 7q, 12p, and 16p. OSA revealed positive correlations of linkage between the 19p locus and 17q, between 19p and 6q, and between 7q and 5p. While potential phenotypic correlates for these findings were not identified for the chromosome 7/5 combination, differences indicating more rapid achievement of "developmental milestones" was apparent in the chromosome 19 OSA-defined subsets for 17q and 6q. OSA was used to test the hypothesis that 19p linkage involved more rapid achievement of these milestones and it revealed significantly increased LOD* scores at 19p13. Conclusions: Our results further support 19p13 as harboring an autism susceptibility locus, confirm other linkage findings at 17q11.2, and demonstrate the need to analyze more discreet trait-wbased subsets of complex phenotypes to improve ability to detect genetic effects. 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Genet. PD JAN 12 PY 2005 VL 6 AR 1 DI 10.1186/1471-2350-6-1 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 943XB UT WOS:000230387700001 PM 15647115 ER PT J AU Adolphs, R Gosselin, F Buchanan, TW Tranel, D Schyns, P Damasio, AR AF Adolphs, R Gosselin, F Buchanan, TW Tranel, D Schyns, P Damasio, AR TI A mechanism for impaired fear recognition after amygdala damage SO NATURE LA English DT Article ID FACIAL EMOTION; BILATERAL DAMAGE; AUTISM; FACES; GAZE; INDIVIDUALS; EXPRESSIONS; INFORMATION; PERCEPTION; PATTERNS AB Ten years ago, we reported that SM, a patient with rare bilateral amygdala damage, showed an intriguing impairment in her ability to recognize fear from facial expressions(1). Since then, the importance of the amygdala in processing information about facial emotions has been borne out by a number of lesion(2-4) and functional imaging studies(5,6). Yet the mechanism by which amygdala damage compromises fear recognition has not been identified. Returning to patient SM, we now show that her impairment stems from an inability to make normal use of information from the eye region of faces when judging emotions, a defect we trace to a lack of spontaneous fixations on the eyes during free viewing of faces. Although SM fails to look normally at the eye region in all facial expressions, her selective impairment in recognizing fear is explained by the fact that the eyes are the most important feature for identifying this emotion. Notably, SM's recognition of fearful faces became entirely normal when she was instructed explicitly to look at the eyes. This finding provides a mechanism to explain the amygdala's role in fear recognition, and points to new approaches for the possible rehabilitation of patients with defective emotion perception. C1 Univ Iowa, Dept Neurol, Iowa City, IA 52242 USA. CALTECH, Div Humanities & Social Sci, Pasadena, CA 91125 USA. Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. Univ Glasgow, Dept Psychol, Glasgow G12 8QB, Lanark, Scotland. RP Adolphs, R (reprint author), Univ Iowa, Dept Neurol, Iowa City, IA 52242 USA. 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In order to confirm these causative mutations in our autistic population and to determine their frequency we screened 96 individuals affected with autism. We found no mutations in these X-linked genes. These results indicate that mutations in NLGN3 and NLGN4 genes are responsible for at most a small fraction of autism cases and additional screenings in other autistic populations are needed to better determine the frequency with which mutations in NLGN3 and NLGN4 occur in autism. (C) 2004 Wiley-Liss, Inc. C1 McGill Univ, Inst Res, Hlth Ctr TI MUHC, Montreal, PQ H3G 1A4, Canada. McGill Univ, Douglas Hosp, Res Ctr, Verdun, PQ H4H 1R3, Canada. Hop Riviere Praires, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ, Canada. McGill Univ, Dept Psychiat, Montreal Childrens Hosp, Montreal, PQ, Canada. RP Rouleau, GA (reprint author), McGill Univ, Inst Res, Hlth Ctr TI MUHC, L7 224,1650 Cedar Ave, Montreal, PQ H3G 1A4, Canada. 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The main aims of this paper are: 1) to use published empirical findings to consider whether the rise reflects a true increase in incidence, as distinct from the consequences of better ascertainment and a broadening of the diagnostic concept; and 2) to consider how epidemiological data may be used to test hypotheses about possible causal influences, using MMR and thimerosal as examples. Methods: Search of the literature for studies with a large epidemiological base population, systematic standardized screening, a focus on an age group for which diagnostic assessments are reliable and valid, and diagnosis by trained professionals using high-quality research assessments. Also, search of a broader literature to consider the evidence from all epidemiological studies with respect to the hypothesized causal effect of MMR and thimerosal on autism spectrum disorders. Results: The true incidence of autism spectrum disorders is likely to be within the range of 30-60 cases per 10 000, a huge increase over the original estimate 40 years ago of 4 per 10 000. The increase is largely a consequence of improved ascertainment and a considerable broadening of the diagnostic concept. However, a true risk due to some, as yet to be identified, environmental risk factor cannot be ruled out. There is no support for the hypothesis for a role of either MMR or thimerosal in causation, but the evidence on the latter is more limited. Conclusion: Progress in testing environmental risk hypotheses will require the integration of epidemiological and biological studies. C1 Kings Coll London, SGDP Ctr, Inst Psychiat, London SE5 9AF, England. RP Rutter, M (reprint author), Kings Coll London, SGDP Ctr, Inst Psychiat, De Crespigny Pk,POB 80,Denmark Hill, London SE5 9AF, England. 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Here, we provide evidence for a genetic basis of several quantitative traits that are related to autism. These traits, from the Broader Phenotype Autism Symptom Scale (BPASS), were measured in nuclear families, each ascertained through two probands affected by autism spectrum disorder. The BPASS traits capture the continuum of severity of impairments and may be more informative for genetic studies than are the discrete diagnoses of autism that have been used by others. Using a sample of 201 nuclear families consisting of a total of 694 individuals, we implemented multivariate polygenic models with ascertainment adjustment to estimate heritabilities and genetic and environmental correlations between these traits. Our ascertainment adjustment uses conditioning on the phenotypes of probands, requires no modeling of the ascertainment process, and is applicable to multiplex ascertainment and multivariate traits. This appears to be the first such implementation for multivariate quantitative traits. The marked difference between heritability estimates of the trait for language onset with and without an ascertainment adjustment (0.08 and 0.22, respectively) shows that conclusions are sensitive to whether or not an ascertainment adjustment is used. Among the five BPASS traits that were analyzed, the traits for social motivation and range of interest/flexibility show the highest heritability (0.19 and 0.16, respectively) and also have the highest genetic correlation (0.92). This finding suggests a shared genetic basis of these two traits and that they may be most promising for future gene mapping and for extending pedigrees by phenotyping additional relatives. C1 Univ Washington, Div Med Genet, Autism Ctr, Seattle, WA 98195 USA. Univ Washington, Div Gerontol & Geriatr Med, Autism Ctr, Dept Med, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Autism Ctr, Seattle, WA 98195 USA. Univ Washington, Dept Pharmacol & Neurol, Seattle, WA 98195 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. Vet Affairs Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle, WA USA. RP Wijsman, EM (reprint author), Univ Washington, Div Med Genet, Autism Ctr, Box 357720, Seattle, WA 98195 USA. 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J. Hum. Genet. PD JAN PY 2005 VL 76 IS 1 BP 68 EP 81 DI 10.1086/426951 PG 14 WC Genetics & Heredity SC Genetics & Heredity GA 878JR UT WOS:000225643600006 PM 15547804 ER PT J AU Baranek, GT Barnett, CR Adams, EM Wolcott, NA Watson, LR Crais, ER AF Baranek, GT Barnett, CR Adams, EM Wolcott, NA Watson, LR Crais, ER TI Object play in infants with autism: Methodological issues in retrospective video analysis SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID YOUNG-CHILDREN; MIND; AGE; EXPLORATION; DIAGNOSIS AB OBJECTIVES. Using a taxonomy of object play, this study describes methodological issues in using retrospective video analysis and computer-based coding as a research tool for early identification of autism. METHOD. Home videos of 32 infants with autism (n= 11), developmental delay (n = 10), and typical development (n = 11) were edited and analyzed for duration and highest level of object play in four hierarchical categories (exploratory, relational, functional, symbolic) using The Observer 3.0. RESULTS. The three groups had similar levels of engagement with objects, and no statistically significant differences in duration of exploratory play. Higher levels of play were rarely evident at 9-12 months, however, the highest level achieved (functional play) was apparent only in the typical group. CONCLUSION. This study provides the first naturalistic investigation of object play skills in infants with autism ages 9-12 months. It also demonstrates feasibility for using computer-based coding technology within the context of retrospective video analysis methods. Duration of exploratory play was not a discriminating feature of autism at this early age. C1 UNC, Div Occupat Sci, Chapel Hill, NC 27599 USA. Durham Publ Sch, Durham, NC USA. Lynne Israel & Associates, Washington, DC USA. Univ N Carolina, Div Speech & Hearing Sci, Chapel Hill, NC USA. RP Baranek, GT (reprint author), UNC, Div Occupat Sci, CB 7120, Chapel Hill, NC 27599 USA. 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PD JAN-FEB PY 2005 VL 59 IS 1 BP 20 EP 30 PG 11 WC Rehabilitation SC Rehabilitation GA 888RV UT WOS:000226392800003 PM 15707120 ER PT J AU Santangelo, SL Tsatsanis, K AF Santangelo, SL Tsatsanis, K TI What is known about autism - Genes, brain, and behavior SO AMERICAN JOURNAL OF PHARMACOGENOMICS LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER GENE; OBSESSIVE-COMPULSIVE BEHAVIORS; PLACEBO-CONTROLLED TRIAL; HIGH-FUNCTIONING AUTISM; RETT-SYNDROME; LINKAGE-DISEQUILIBRIUM; SUSCEPTIBILITY GENE; SPECTRUM DISORDERS; TRANSMISSION DISEQUILIBRIUM AB Autism is a neurodevelopmental disorder of genetic origins, with a heritability of about 90%. Autistic disorder is classed within the broad domain of pervasive developmental disorders (PDD) that also includes Rett syndrome, childhood disintegrative disorder, Asperger syndrome, and PDD not otherwise specified (PDD-NOS). Prevalence estimates suggest a rate of 0.1-0.2% for autism and 0.6% for the range of PDD disorders. There is considerable phenotypic heterogeneity within this class of disorders as well as continued debate regarding their clinical boundaries. Autism is the prototypical PDD, and is characterized by impairments in three core domains: social interaction, language development, and patterns of behavior (restricted and stereotyped). Clinical pattern and severity of impairment vary along these dimensions, and the level of cognitive functioning of individuals with autism spans the entire range, from profound mental retardation to superior intellect. There is no single biological or clinical marker for autism, nor is it expected that a single gene is responsible for its expression; as many as 15+ genes may be involved. However, environmental influences are also important, as concordance in monozygotic twins is less than 100% and the phenotypic expression of the disorder varies widely, even within monozygotic twins. Multiple susceptibility factors are being explored using varied methodologies, including genome-wide linkage studies, and family- and case-control candidate gene association studies. This paper reviews what is currently known about the genetic and environmental risk factors, neuropathology, and psychopharmacology of autism. Discussion of genetic factors focuses on the findings from linkage and association studies, the results of which have implicated the involvement of nearly every chromosome in the human genome. However, the most consistently replicated linkage findings have been on chromosome 7q, 2q, and 15q. The positive associations from candidate gene studies are largely unreplicated, with the possible exceptions of the GABRB3 and serotonin transporter genes. No single region of the brain or pathophysiological mechanism has yet been identified as being associated with autism. Postmortem findings, animal models, and neuroimaging studies have focused on the cerebellum, frontal cortex, hippocampus, and especially the amygdala. The cerebello-thalamo-cortical circuit may also be influential in autism. There is evidence that overall brain size is increased in some individuals with autism. Presently there are no drugs that produce major improvements in the core social or pragmatic language deficits in autism, although several have limited effects on associated behavioral features. The application of new techniques in autism research is being proposed, including the investigation of abnormal regulation of gene expression, proteomics, and the use of MRI and Postmortem analysis of the brain. C1 Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT USA. Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, Boston, MA 02115 USA. RP Santangelo, SL (reprint author), Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, 149 13th St, Charlestown, MA 02129 USA. 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J. Pharmacogenomics PY 2005 VL 5 IS 2 BP 71 EP 92 DI 10.2165/00129785-200505020-00001 PG 22 WC Genetics & Heredity; Pharmacology & Pharmacy SC Genetics & Heredity; Pharmacology & Pharmacy GA 961XS UT WOS:000231695700001 PM 15813671 ER PT J AU Hu-Lince, D Craig, DW Huentelman, MJ Stephan, DA AF Hu-Lince, D Craig, DW Huentelman, MJ Stephan, DA TI The autism genome project - Goals and strategies SO AMERICAN JOURNAL OF PHARMACOGENOMICS LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; SINGLE-NUCLEOTIDE POLYMORPHISMS; SEROTONIN TRANSPORTER 5-HTT; RECEPTOR SUBUNIT GENES; LINKAGE-DISEQUILIBRIUM; SUSCEPTIBILITY GENE; SPECTRUM DISORDERS; INFANTILE-AUTISM; COMPLEX DISEASE; CHROMOSOME 7Q AB Autism is a complex neurodevelopmental disorder with a broad spectrum of symptoms and varying severity. Currently, no biological diagnosis exists. Although there has been a significant increase in autism genetics research recently, validated susceptibility genes for the most common, sporadic forms of autistic disorder, as well as familial autism, have yet to be identified. The identification of autism-susceptibility genes will not only assist in the identification and/or development of better medications that can help improve the health and neurodevelopment of children with autism, but will also allow for better perinatal diagnosis. The Autism Genome Project (AGP) is a large-scale, collaborative genetics research project initiated by the National Alliance for Autism Research and the National Institutes of Health, and is aimed at sifting through the human genome in search of autism-susceptibility genes. Phase I of the AGP will consist of genome-wide scans utilizing both SNP array and microsatellite technologies. Linkage analysis will subsequently be performed on approximately 1500 pedigrees as will downstream fine-mapping and sequencing of the critical linkage intervals. Ultimately, the vision will be to identify the exact nucleotide variants within genes which give rise to predisposition. The AGP intends to move the field of autism clinical management forward by answering questions about the causal mechanisms underlying the pathophysiology of autism. From this knowledge, therapeutic targets for drug treatments, and ultimately, a newborn screening diagnostic that would allow for early intervention, can begin to be developed. C1 Translat Genom Res Inst, Neurogenom Div, Phoenix, AZ 85004 USA. RP Stephan, DA (reprint author), Translat Genom Res Inst, Neurogenom Div, 445 N 5th St,5th Floor, Phoenix, AZ 85004 USA. 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J. Pharmacogenomics PY 2005 VL 5 IS 4 BP 233 EP 246 DI 10.2165/00129785-200505040-00004 PG 14 WC Genetics & Heredity; Pharmacology & Pharmacy SC Genetics & Heredity; Pharmacology & Pharmacy GA 963YH UT WOS:000231842000004 PM 16078860 ER PT J AU Schindler, HR Horner, RH AF Schindler, HR Horner, RH TI Generalized reduction of problem behavior of young children with autism: Building trans-situational interventions SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID NATURAL COMMUNITIES; REINFORCEMENT; MAINTENANCE; DISORDERS; SUPPORT AB The effects of functional communication training on the generalized reduction of problem behavior with three 4- to 5-year-old children with autism and problem behavior were evaluated. Participants were assessed in primary teaching settings and in three secondary, generalization settings. Through baseline analysis, lower effort interventions in the secondary settings were documented as ineffective when Implemented alone. 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PD JAN PY 2005 VL 110 IS 1 BP 36 EP 47 DI 10.1352/0895-8017(2005)110<36:GROPBO>2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 884KK UT WOS:000226083400005 PM 15568965 ER PT J AU McDermott, S Moran, R Platt, T Wood, H Isaac, T Dasari, S AF McDermott, S Moran, R Platt, T Wood, H Isaac, T Dasari, S TI Prevalence of epilepsy in adults with mental retardation and related disabilities in primary care SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID INTELLECTUAL DISABILITY; SEIZURE DISORDERS; DOWN-SYNDROME; AGE; CLASSIFICATION; POPULATION; CHILDREN; AUTISM; ONSET AB Two primary care practices were used to recruit adults with and without disability. Disability groups included autism, Down syndrome, cerebral palsy, and mental retardation. The patients without disability had an epilepsy prevalence rate of 1%. The prevalence of epilepsy within the disability groups was 13% for cerebral palsy, 13.6% for Down syndrome; 25.4% for autism, 25.5% for mental retardation, and 40% for adults with both cerebral palsy and mental retardation. During the decades of adulthood, the prevalence of epilepsy declined for those with cerebral palsy and mental retardation. The prevalence of epilepsy increased with advancing years for adults with Down syndrome, autism, and those without disability. Nonetheless, during each decade the prevalence of epilepsy was higher in all of the disability groups compared to those without disability. C1 Univ S Carolina, Sch Med, Columbia, SC 29208 USA. RP McDermott, S (reprint author), Family Practice Ctr, Dept Family & Prevent Med, 3209 Colonial Dr, Columbia, SC 29203 USA. 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J. Ment. Retard. PD JAN PY 2005 VL 110 IS 1 BP 48 EP 56 DI 10.1352/0895-8017(2005)110<48:POEIAW>2.0.CO;2 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 884KK UT WOS:000226083400006 PM 15568966 ER PT J AU Lee-Wong, M Resnick, D Chong, K AF Lee-Wong, M Resnick, D Chong, K TI A generalized reaction to thimerosal from an influenza vaccine SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY LA English DT Article ID CONTACT-DERMATITIS; AUTISM; HYPERSENSITIVITY; SENSITIVITY; ASSOCIATION; THIOMERSAL AB Background: Thimerosal is a preservative commonly used in ophthalmic solutions, otic drops, and vaccines because of its bactericidal property. Objective: To report a case of a generalized reaction to thimerosal in a patient who received an influenza vaccine. Methods: We describe a patient who developed a generalized maculopapular eruption after receiving a thimerosal-containing influenza vaccine. 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PY 2005 VL 58 SU 9 BP S88 EP S88 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 982YG UT WOS:000233197600311 ER PT J AU Serajee, FJ Nabi, R Zhong, H Huq, AHMM AF Serajee, FJ Nabi, R Zhong, H Huq, AHMM TI Association of mitochondrial aspartate/glutamate carrier SLC25A12 and SLC25A13 genes with autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 34th Annual Meeting of the Child-Neurology-Society CY SEP 28-OCT 01, 2005 CL Los Angeles, CA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2005 VL 58 SU 9 BP S105 EP S105 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 982YG UT WOS:000233197600371 ER PT J AU Serajee, FJ Nabi, R Zhong, H Huq, AHMM AF Serajee, FJ Nabi, R Zhong, H Huq, AHMM TI Association of Y-chromosome haplotypes with autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 34th Annual Meeting of the Child-Neurology-Society CY SEP 28-OCT 01, 2005 CL Los Angeles, CA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2005 VL 58 SU 9 BP S82 EP S82 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 982YG UT WOS:000233197600289 ER PT J AU Vargas, DL Nascimbene, C Krishnan, C Zimmerman, AW Pardo, CA AF Vargas, DL Nascimbene, C Krishnan, C Zimmerman, AW Pardo, CA TI Neuroglial activation and neuroinflammation in the brain of patients with autism SO ANNALS OF NEUROLOGY LA English DT Article ID MONOCYTE CHEMOATTRACTANT PROTEIN-1; ADAPTIVE IMMUNE-RESPONSES; SPECTRUM DISORDERS; MULTIPLE-SCLEROSIS; CEREBROSPINAL-FLUID; GLIAL-CELLS; SPINAL-CORD; MCP-1 CCL2; TGF-BETA; T-CELLS AB Autism is a neurodevelopmental disorder characterized by impaired communication and social interaction and may be accompanied by mental retardation and epilepsy. Its cause remains unknown, despite evidence that genetic, environmental, and immunological factors may play a role in its pathogenesis. To investigate whether immune-mediated mechanisms are involved in the pathogenesis of autism, we used immunocytochemistry, cytokine protein arrays, and enzyme-linked immunosorbent assays to study brain tissues and cerebrospinal fluid (CSF) from autistic patients and determined the magnitude of neuroglial and inflammatory reactions and their cytokine expression profiles. Brain tissues from cerebellum, midfrontal, and cingulate gyrus; obtained at autopsy from 11 patients with autism were used for morphological studies. Fresh-frozen tissues available from seven patients and CSF from six living autistic patients were used for cytokine protein profiling. We demonstrate an active neuroinflammatory process in the cerebral cortex, white matter, and notably in cerebellum of autistic patients. Immunocytochemical studies showed marked activation of microglia and astroglia, and cytokine profiling indicated that macrophage chemoattractant protein (MCP)-1 and tumor growth factor-beta1, derived from neuroglia, were the most prevalent cytokines in brain tissues. CSF showed a unique proinflammatory profile of cytokines, including a marked increase in MCP-1. Our findings indicate that innate neuroimmune reactions play, a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain. C1 Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Div Neuroimmunol & Infect Disorders, Baltimore, MD 21287 USA. Univ Milan, Dept Neurol, Milan, Italy. Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. RP Pardo, CA (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurol, 600 N Wolfe St, Baltimore, MD 21287 USA. 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Rev. Neurosci. PY 2005 VL 28 BP 109 EP 126 DI 10.1146/annurev.neuro.27.070203.144137 PG 18 WC Neurosciences SC Neurosciences & Neurology GA 955ON UT WOS:000231235700005 PM 16033325 ER PT S AU Gottesman, II Hanson, DR AF Gottesman, II Hanson, DR TI Human development: Biological and genetic processes SO ANNUAL REVIEW OF PSYCHOLOGY SE Annual Review of Psychology LA English DT Review; Book Chapter DE adaptive systems; endophenotypes; CNS plasticity; schizophrenia; autism ID CHILDHOOD-ONSET SCHIZOPHRENIA; AFFECTED SIBLING PAIRS; CEREBRAL-PALSY; HUMAN BRAIN; NEUROBIOLOGICAL DEVELOPMENT; RECEPTOR SUBTYPES; BIPOLAR DISORDER; TWINS DISCORDANT; CELL-BIOLOGY; AUTISM AB Adaptation is a central organizing principle throughout biology, whether we are studying species, populations, or individuals. Adaptation in biological systems occurs in response to molar and molecular environments. Thus, we would predict that genetic systems and nervous systems would be dynamic (cybernetic) in contrast to previous conceptualizations with genes and brains fixed in form and function. Questions of nature versus nurture are meaningless, and we must turn to epigenetics-the way in which biology and experience work together to enhance adaptation throughout thick and thin. Defining endophenotypes-road markers that bring us closer to the biological origins of the developmental joumey-facilitates our understanding of adaptive or maladaptive processes. For human behavioral disorders such as schizophrenia and autism, the inherent plasticity of the nervous system requires a systems approach to incorporate all of the myriad epigenetic factors that can influence such outcomes. C1 Univ Minnesota, Dept Psychiat, Minneapolis, MN 55454 USA. Univ Minnesota, Dept Psychol, Minneapolis, MN 55454 USA. Univ Minnesota, Dept Psychiat, Minneapolis, MN 55417 USA. Univ Minnesota, Dept Psychol, Minneapolis, MN 55417 USA. Vet Adm Hosp, Minneapolis, MN 55417 USA. RP Gottesman, II (reprint author), Univ Minnesota, Dept Psychiat, Minneapolis, MN 55454 USA. 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PY 2005 VL 56 BP 263 EP 286 DI 10.1146/annurev.psych.56.091103.070208 PG 26 WC Psychology; Psychology, Multidisciplinary SC Psychology GA 904NA UT WOS:000227503800011 PM 15709936 ER PT J AU Volkmar, F Chawarska, K Klin, A AF Volkmar, F Chawarska, K Klin, A TI Autism in infancy and early childhood SO ANNUAL REVIEW OF PSYCHOLOGY SE Annual Review of Psychology LA English DT Review; Book Chapter DE psychopathology; pervasive developmental disorders; joint attention ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; 6-YEAR FOLLOW-UP; YOUNG-CHILDREN; JOINT ATTENTION; SPECTRUM DISORDER; PRESCHOOL-CHILDREN; EARLY INTERVENTION; EARLY RECOGNITION; ASPERGER-SYNDROME AB Although initially described as an inborn disorder of affective contact, information on autism as it exists in infants has been limited. Delays in diagnosis, lack of information about the condition, and reliance on retrospective research strategies have been problematic. An awareness of the increased risk for siblings is now allowing the development of new, prospective approaches. Consistent with Kanner's original hypothesis, the available information strongly suggests a fundamental difficulty in the earliest social processes, which, in turn, impacts many other areas of development. New approaches to screening have lowered the age of initial diagnosis; this presents new challenges for early intervention. Directions for future research are highlighted. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. RP Volkmar, F (reprint author), Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. 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PY 2005 VL 56 BP 315 EP 336 DI 10.1146/annurev.psych.56.091103.070159 PG 24 WC Psychology; Psychology, Multidisciplinary SC Psychology GA 904NA UT WOS:000227503800013 PM 15709938 ER PT J AU Prothmann, A Albrecht, K Dietrich, S Hornfeck, U Stieber, S Ettrich, C AF Prothmann, A Albrecht, K Dietrich, S Hornfeck, U Stieber, S Ettrich, C TI Analysis of child-dog play behavior in child psychiatry SO ANTHROZOOS LA English DT Review DE animal-assisted therapy; child-dog interaction; interaction patterns; interspecific communication; mental disorders ID PET-FACILITATED THERAPY AB Children have a natural affinity for animals and most often communicate with them nonverbally; nonverbal communication is authentic and difficult to influence deliberately. This study examines whether characteristic interaction patterns exist during pet-facilitated therapy with dogs, and whether these call be used for diagnosing psychiatric disorders in children and adolescents. Forty children and adolescents with anorexia, bulimia, anxiety disorder or autism (classified according to the International Classification of Diseases - ICD 10) were monitored while in the same room as a therapy dog; their behavior during a 25-minute encounter was video-recorded and analyzed The patients demonstrated significant diagnosis-specific behavioral differences; the greatest differences were found when the autistic patients were compared with the anxiety and eating disorder patients. The autistic children's behavior was characterized by many brief interaction phases, whereas anxiety disorder patients interacted less often, with longer lasting episodes. While autistic children showed greater fear of the dog, anxiety disorder patients were more afraid of inter-human contact. A discriminant analysis assigned 77.5% of the patients to the correct diagnostic group. 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Down syndrome, fragile X syndrome, specific language impairment, and Williams syndrome. This paper describes the specific pattern of linguistic deficits in each of these disorders in terms of speech production, semantic, and syntactic abilities as well as the relationship between cognitive and linguistic skills and the presence of a deviant or delayed pattern of development. In the spirit of synthesis across diverse literatures, preliminary comparisons among the language profiles of these disorders are made. The full picture, however. is incomplete given the current state of the literature. which tends to focus on the analysis of a narrow range of linguistic phenomena within a single disorder. The field is in need of research that systematically compares these disorders and leads to detailed descriptions of linguistic phenotypes of each disorder. C1 Univ Kansas, Child Language Doctoral Program, Lawrence, KS 66045 USA. 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PD JAN PY 2005 VL 26 IS 1 BP 7 EP 27 DI 10.1017/S0142716405050034 PG 21 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 892ED UT WOS:000226631800003 ER PT J AU Tager-Flusberg, H AF Tager-Flusberg, H TI Designing studies to investigate the relationships between genes, environments, and developmental language disorders SO APPLIED PSYCHOLINGUISTICS LA English DT Article ID METHODOLOGICAL ISSUES; AUTISM; COMMUNICATION; IMPAIRMENT; DEFICITS AB This paper focuses on designing studies that will compare children with developmental language disorders (DLD) drawn from several syndromes in which there are primary impairments in the acquisition of language. This kind of research can be used to address four key questions: (a) What are the developing language phenotypes that characterize specific disorders? (b) What factors are key precursors and predictors of language acquisition in DLD? (c) What are the genes that contribute to DLD in different syndromes? (d) What environmental factors influence the trajectories of language development in DLD? Several design issues are discussed including an overall study design. subject selection and recruitment, matching and comparisons across groups, and methodologies. A number of important challenges to the design and implementation of these kinds of studies are presented in the final section of the paper. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Tager-Flusberg, H (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,L-814, Boston, MA 02118 USA. 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PD JAN PY 2005 VL 26 IS 1 BP 29 EP 39 DI 10.1017/S0142716405050046 PG 11 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 892ED UT WOS:000226631800004 ER PT J AU Muller, RA AF Muller, RA TI Neurocognitive studies of language impairments: The bottom-up approach SO APPLIED PSYCHOLINGUISTICS LA English DT Article ID WILLIAMS-SYNDROME; SEVERE SPEECH; HUMAN BRAIN; AUTISM; DISORDER; CHILDREN; MORPHOLOGY; CORTEX; FMRI; CONSEQUENCES AB Neurocognitive studies can approach gene-based developmental language impairments from two angles, which are complementary and ideally combined in a research program. One approach aims at an optimal phenotypic description of a disorder and from there proceeds to a biological and developmental understanding. Complementary to such a top-down approach, a bottom-up perspective will primarily focus on potential etiological pathways and attempt to explain complex outcome phenotypes m terms of elementary developmental disturbances. My paper is dedicated to this latter approach. I argue that in behaviorally defined disorders (such as specific language impairment or autism) shared genetic risk and common etiology can at best be expected for specific aspects of language deficit and that such shared etiology will only apply to subtypes of these disorders. One reason for this skepticism is that the emerging language system in children can he affected in many different ways via more elementary sensory, perceptual, cognitive, and motor impairments. Neurocognitive research on developmental language disorders relies on an understanding of such potential elementary disturbances before it can confidently proceed to the study of complex linguistic impairments. C1 San Diego State Univ, Dept Psychol, San Diego, CA 92120 USA. RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, 6363 Alvarado Ct,225 E, San Diego, CA 92120 USA. 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Psycholinguist. PD JAN PY 2005 VL 26 IS 1 BP 97 EP 110 DI 10.1017/S0142716405050083 PG 14 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 892ED UT WOS:000226631800008 ER PT J AU Williams, DL Goldstein, G Minshew, NJ AF Williams, DL Goldstein, G Minshew, NJ TI Impaired memory for faces and social scenes in autism: clinical implications of memory dysfunction SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Article DE autism; memory; information processing ID WORKING-MEMORY; DIAGNOSTIC INTERVIEW; RETRIEVAL SCHEMES; YOUNG-CHILDREN; VISUAL MEMORY; INDIVIDUALS; DISORDER; INTACT; RECALL; DISCRIMINATION AB A clinical memory test, the Wechsler Memory Scale-III (WMS-III), was used to study the auditory and visual memory of 29 high-functioning adults with autism and 34 group-matched normal controls. The individuals with autism performed as well as the controls on immediate and delayed memory for word pairs and stories and on a verbal working memory task. The autism group was impaired on immediate and delayed recall of faces and of family scenes and had impaired spatial working memory. The integrity of verbal working memory and impaired spatial working memory is consistent with the findings of other studies and may reflect the greater computational demands of the spatial task. Most importantly, the deficits in memory for faces and common social scenes, complex visual/spatial stimuli, demonstrate the contribution of memory dysfunction in autism to deficits in real life function. (C) 2004 National Academy of Neuropsychology. Published by Elsevier Ltd. All rights reserved. C1 Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA. RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, Webster Hall Suite 300,3811 O Hara St, Pittsburgh, PA 15213 USA. 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PD JAN PY 2005 VL 20 IS 1 BP 1 EP 15 DI 10.1016/j.acn.2002.08.001 PG 15 WC Psychology, Clinical; Psychology SC Psychology GA 886WI UT WOS:000226263200001 PM 15620811 ER PT J AU Barbaresi, WJ Katusic, SK Colligan, RC Weaver, AL Jacobsen, SJ AF Barbaresi, WJ Katusic, SK Colligan, RC Weaver, AL Jacobsen, SJ TI The incidence of autism in Olmsted County, Minnesota, 1976-1997 Results from a population-based study SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; SPECTRUM DISORDER; MENTAL-HEALTH; PREVALENCE; CHILDREN; EPIDEMIOLOGY; ASSOCIATION; THIMEROSAL; MEASLES AB Objective: To determine the incidence of autism among children in Olmsted County, Minnesota. Design: Through the Rochester Epidemiology Project, all inpatient and outpatient diagnoses are indexed for computerized retrieval. This computerized diagnostic index was used to identify children with any developmental disorder. A glossary of symptoms of autism was used to review medical and school records of these children for symptoms consistent with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for autistic disorder. Setting: Olmsted County, Minnesota. Subjects: All residents of Olmsted County 21. years or younger between 1976 and 1997. Main Outcome Measure: The incidence of research-identified autism based on DSM-IV criteria for autistic disorder. Results: The age-adjusted incidence of research-identified autism was 5.5 (95% confidence interval, 1.4-9.5) per 100 000 chidren from 1980 to 1983 and 44.9 (95% confidence interval, 32.9-56.9) from 1995 to 1997 (8.2-fold increase). This increase was confined to children younger than 10 years who were born after 1987. Conclusions: The incidence of research-identified autism increased in Olmsted County from 1976 to 1997, with the increase occurring among young children after the introduction of broader, more precise diagnostic criteria, increased availability of services, and increased awareness of autism. Although it is possible that unidentified environmental factors have contributed to an increase in autism, the timing of the increase suggests that it may be due to improved awareness, changes in diagnostic criteria, and availability of services, leading to identification of previously unrecognized young children with autism. C1 Mayo Clin, Coll Med, Dept Pediat & Adolescent Med, Div Dev & Behav Pediat, Rochester, MN 55905 USA. Mayo Clin, Coll Med, Dept Hlth Sci Res, Div Epidemiol, Rochester, MN 55905 USA. Mayo Clin, Coll Med, Div Biostat, Rochester, MN 55905 USA. Mayo Clin, Coll Med, Dept Psychiat & Psychol, Rochester, MN 55905 USA. 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PY 2005 VL 57 SU S BP 254 EP 254 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 001SD UT WOS:000234555702224 ER PT J AU Crifo, C Siems, W Soro, S Salerno, C AF Crifo, C Siems, W Soro, S Salerno, C TI Inhibition of defective adenylosuccinate lyase by HNE: A neurological disease that may be affected by oxidative stress SO BIOFACTORS LA English DT Article; Proceedings Paper CT Berlin Meeting on NNE and Further Lipid Peroxidation Products - From Basic Science to Medicine CY JUL 06-09, 2004 CL Berlin, GERMANY DE purine metabolism; inherited disease; lipid peroxidation; psychomotor retardation; autism ID DEFICIENCY; ENZYME; PATIENT; MUSCLE AB Adenylosuccinate lyase is an enzyme of fumarase superfamily that participates in the purine biosynthetic pathway, catalysing the nonhydrolytic cleavage of succinyl groups from SAICA ribotide and adenylosuccinate. Enzyme defects are associated with a human inherited disease, which arises from single point mutations to the gene and results in mild to severe psychomotor retardation, epilepsy, muscle wasting, and autistic features. Adenylosuccinate lyase activity is lost to a different extent in the patients. Diminished levels of enzyme have been attributed to loss of catalytic activity, protein instability, or environmental factors. P100A/D422Y mutation represents a feasible model for studying the effect of cell milieu on the activity of the impaired enzyme. The defective enzyme is inhibited by micromolar concentrations of trans-4-hydroxy-2- nonenal (HNE), a major product of membrane peroxidation that has been found to accumulate in brain tissues of patients with neurodegenerative disorders. It is suggested that inactivation of defective adenylosuccinate lyase by HNE and other membrane peroxidation products may account, at least in part, for the impairment of neurological functions and recurrent worsening of the symptoms. C1 Univ Roma La Sapienza, Lab Clin Biochem, I-00185 Rome, Italy. Univ Roma La Sapienza, Dept Biochem Sci, I-00185 Rome, Italy. Loges Sch Phys Med, Bad Harzburg, Germany. RP Salerno, C (reprint author), Univ Roma La Sapienza, Lab Clin Biochem, Via Sardi 58, I-00185 Rome, Italy. 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Alison Jimenez Gonzalez, Patricia Manghi, Elina R. Esquivel, Marcela Monge, Silvia Fallas Delgado, Marietha Fournier, Eduardo Bondy, Pamela Castelle, Kathryn TI A genetic study of autism in Costa Rica: multiple variables affecting IQ scores observed in a preliminary sample of autistic cases SO BMC PSYCHIATRY LA English DT Article AB Background: Autism is a heritable developmental disorder of communication and socialization that has not been well studied in Hispanic populations. Therefore, we are collecting and evaluating all possible cases of autism from a population isolate in the Central Valley of Costa Rica (CVCR) for a clinical and genetic study. Methods: We are assessing all subjects and parents, as appropriate, using the newly translated Spanish versions of the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) as well as tests of intelligence and adaptive behavior. Detailed obstetric and family medical/psychiatric histories are taken. All cases are tested for Fragile X and will be extensively evaluated for cytogenetic abnormalities. Results: To date we have obtained clinical evaluations on over 76 cases of possible autism referred to our study and report data for the initial 35 complete cases. The mean age of the probands is 6.7 years, and 31 of the 35 cases are male. Twenty-one of the cases have IQs <50 and only 6 cases have IQs >= 70. Over half of the mothers had complications during pregnancy and/or delivery. No cases have tested positively for Fragile X or PKU. Chromosomal G-banding is not yet complete for all cases. Conclusion: Diagnostic data gathered on cases of autism in the CVCR using Spanish versions of the ADI-R and ADOS look similar to that generated by studies of English-speaking cases. However, only 17% of our cases have IQs within the normal range, compared to the figure of 25% seen in most studies. This result reflects an ascertainment bias in that only severe cases of autism come to treatment in the CVCR because there are no government-sponsored support programs or early intervention programs providing an incentive to diagnose autism. The severity of mental retardation seen in most of our cases may also be exaggerated by the lack of early intervention programs and the use of IQ tests without Costa Rican norms. Still, we must formally train healthcare providers and teachers to recognize and refer autistic cases with normal or near normal IQs that are not seen in treatment. C1 [McInnes, L. Alison; Castelle, Kathryn] Mt Sinai Sch Med, New York, NY 10029 USA. [Jimenez Gonzalez, Patricia; Esquivel, Marcela; Monge, Silvia; Fallas Delgado, Marietha; Fournier, Eduardo] Hosp Nacl Ninos Dr Carlos Saenz Herrera, San Jose, Costa Rica. [Jimenez Gonzalez, Patricia; Esquivel, Marcela; Monge, Silvia; Fallas Delgado, Marietha; Fournier, Eduardo] CCSS, Child Dev & Behav Unit, San Jose, Costa Rica. [Manghi, Elina R.; Bondy, Pamela] Univ Illinois, Chicago, IL USA. RP McInnes, LA (reprint author), Mt Sinai Sch Med, New York, NY 10029 USA. EM alison.mcinnes@mssm.edu; pjimenezg@hnn.sa.cr; elina25@uic.edu; esquivel_marcela@yahoo.com; smongeq@racsa.co.cr; mariethafallas@yahoo.com; urefor@racsa.co.cr; pbondy@uic.edu; kathryn.castelle@mssm.edu FU NINDS [R01 043540] FX LAM is supported by NINDS grant number R01 043540. 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Horstmann, Vibeke Avarseji, Hassan Sivberg, Bengt V. TI Alterations of prolyl endopeptidase activity in the plasma of children with autistic spectrum disorders SO BMC PSYCHIATRY LA English DT Article AB Background: Prolyl Endopeptidase (PEP, EC 3.4.21.26), a cytosolic endopeptidase, hydrolyses peptide bonds on the carboxyl side of proline residue in proteins with a relatively small molecular weight. It has been shown that altered PEP activity is associated with various psychological diseases such as schizophrenia, mania and depression. Autistic Spectrum Disorders (ASD) are neuropsychiatric and behavioural syndromes affecting social behaviours and communication development. They are classified as developmental disorders. The aim of this study was to examine the hypothesis that PEP activity is also associated with ASDs. Methods: Fluorometric assay was used to measure PEP activity in EDTA plasma in children with ASD (n = 18) aged 4-12 years (mean +/- SD: 7.9 +/- 2.5). These results were then compared to PEP activity in a control group of non-ASD children (n = 15) aged 2-10 years (mean +/- SD: 6.4 +/- 2.2). Results: An alteration in PEP activity was found in the children with ASD compared to the control group. There was much greater variation of PEP activity in the group of ASD children when compared to the controls (SD= 39.9 and SD 9.6, respectively). This variation was significant (p < 0.0005), although the mean level of PEP activity in the group of ASD children was slightly higher than in the control group (124.4 and 134.1, respectively). Conclusion: Our preliminary finding suggests a role for PEP enzyme in the pathophysiology of autism but further research should be conducted to establish its role in the aetiology of psychiatric and neurological disorders, including autism and related spectrum disorders. C1 [Momeni, Naghi; Nordstroem, Berit M.; Horstmann, Vibeke; Sivberg, Bengt V.] Lund Univ, Dept Hlth Sci, Lund, Sweden. [Avarseji, Hassan] Golestan Univ Med Sci, Dept Neurol, Gorgan, Iran. RP Sivberg, BV (reprint author), Lund Univ, Dept Hlth Sci, Lund, Sweden. EM naghi.momeni@spray.se; Berit.Nordstrom@med.lu.se; vikeke.horstmann@med.lu.se; hassan_avarseji@yahoo.com; Bengt.Sivberg@med.lu.se CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BAUMAN ML, 1991, PEDIATRICS, V87, P791 Cook Edwin H. 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Subjects included 46 boys of normal intelligence aged 5.7-11.3 years (16 autistic, 15 DLD, 15 controls). Imaging analysis included grey-white segmentation and cortical parcellation. Asymmetry was assessed at a series of nested levels. We found that asymmetries were masked with larger units of analysis but progressively more apparent with smaller units, and that within the cerebral cortex the differences were greatest in higher-order association cortex. The larger units of analysis, including the cerebral hemispheres, the major grey and white matter structures and the cortical lobes, showed no asymmetries in autism or DLD and few asymmetries in controls. However, at the level of cortical parcellation units, autism and DLD showed more asymmetry than controls. They had a greater aggregate volume of significantly asymmetrical cortical parcellation units (leftward plus rightward), as well as a substantially larger aggregate volume of right-asymmetrical cortex in DLD and autism than in controls; this rightward bias was more pronounced in autism than in DLD. DLD, but not autism, showed a small but significant loss of leftward asymmetry compared with controls. Right : left ratios were reversed, autism and DLD having twice as much right- as left-asymmetrical cortex, while the reverse was found in the control sample. Asymmetry differences between groups were most significant in the higher-order association areas. Autism and DLD were much more similar to each other in patterns of asymmetry throughout the cerebral cortex than either was to controls; this similarity suggests systematic and related alterations rather than random neural systems alterations. We review these findings in relation to previously reported volumetric features in these two samples of brains, including increased total brain and white matter volumes and lack of increase in the size of the corpus callosum. Larger brain volume has previously been associated with increased lateralization. The sizeable right-asymmetry increase reported here may be a consequence of early abnormal brain growth trajectories in these disorders, while higher-order association areas may be most vulnerable to connectivity abnormalities associated with white matter increases. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Morphometr Anal, Boston, MA USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Boston, MA USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA. Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Psychobiol Program, Waltham, MA 02154 USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Med Genet Program, Waltham, MA 02154 USA. McLean Hosp, Dept Neurol, Belmont, MA 02178 USA. McLean Hosp, Mailman Res Ctr, Belmont, MA 02178 USA. MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. Colby Coll, Dept Math, Waterville, ME 04901 USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. Childrens Hosp Oakland, Dept Infect Dis, Oakland, CA USA. Middle Tennessee State Univ, Tennessee Ctr Study & Treatment Dyslexia, Murfreesboro, TN 37130 USA. RP Herbert, MR (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Morphometr Anal, 149 13th St,Room 6012, Charlestown, MA 02129 USA. 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As the cerebellum controls sensorimotor coordination and lesions here typically cause hypotonia, dysmetria and dyscoordination, we performed a series of quantitative tests aimed at investigating cerebellar function in Asperger individuals. Tests examining visually guided movement (rapid pointing), speeded complex movement (finger tapping, rapid hand turning), muscle tone (catching dropped weight), prediction, coordination and timing (balance, grip force and interval timing) were conducted on 12 Asperger subjects and 12 age and IQ matched controls. In comparison to control subjects, Asperger subject's demonstrated: (i) decreased pointing accuracy and rate, (ii) increased postural instability, and (iii) decreased timing accuracy. IQ was found to co-vary with some parameters of each of these tasks and no further impairments were found on the remaining tests. 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Parents of children with cancer and autism have been shown to find social support online, and many parents of healthy infants and children seek information about parenting online. However, access and use of the Internet is greater among socio-economically advantaged groups, a phenomenon known as the 'digital divide'. Our aim was to investigate whether users of a Swedish general parenting website perceived support in the parenting role and, if so, whether this support was socially biased because of the digital divide phenomenon. Methods Users of the largest Swedish parenting website were asked to participate in the study. A total of 2221 users completed the anonymous survey posted on the website during a one-week period. Results Most respondents (95%) were female (mean age 30.6 years). Respondents' educational level was slightly, but not significantly, higher than that in the general population, whereas 68% had income levels at or under the national average, contradicting the intuitive hypothesis that users would be socio-economically privileged. Perceived social support, measured by the Interpersonal Support Evaluation List (ISEL) appraisal subscale, indicated high perceived support. Living without a partner and having lower levels of income and education increased perceived support. The perception that other parents' opinions are more valuable than the advice of experts was influential in the regression equation for ISEL scores, indicating that peer help is important in online social support. Conclusions Internet use for general parenting issues in Sweden, mainly by women, does not seem to follow the digital divide phenomenon. Therefore, the internet provides an exciting opportunity for future infant and child public health work. 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PD JAN PY 2005 VL 31 IS 1 BP 43 EP 52 PG 10 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 889JK UT WOS:000226439100008 PM 15658965 ER PT J AU Parker, SW Nelson, CA AF Parker, SW Nelson, CA CA Bucharest Early Intervention Proje TI The impact of early institutional rearing on the ability to discriminate facial expressions of emotion: An event-related potential study SO CHILD DEVELOPMENT LA English DT Article ID EARLY SEVERE DEPRIVATION; RECOGNITION MEMORY; AMYGDALA RESPONSE; SOCIAL-BEHAVIOR; CHILDREN; BRAIN; INFANTS; AUTISM; FACES; CHILDHOOD AB Event-related potentials (ERPs), in response to 4 facial expressions of fear, angry, happy, and sad, were collected from 72 institutionalized children (IG), ages 7 to 32 months, in Bucharest, Romania, and compared with ERPs from 33 children, ages 8 to 32 months, who had never been institutionalized (NIG). The NIG and IG exhibited different patterns of responding in early latency components. Moreover, group differences in amplitude were evident across all components. Such differences may point to the role of early deprivation in disrupting the development of the neural circuitry involved in the recognition of facial expressions. C1 Univ Minnesota, Inst Child Dev, Minneapolis, MN 55455 USA. RP Nelson, CA (reprint author), Univ Minnesota, Inst Child Dev, 51 E River Rd, Minneapolis, MN 55455 USA. 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PD JAN-FEB PY 2005 VL 76 IS 1 BP 54 EP 72 DI 10.1111/j.1467-8624.2005.00829.x PG 19 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 894DU UT WOS:000226771500004 PM 15693757 ER PT J AU Luiselli, JK Cochran, ML Huber, SA AF Luiselli, JK Cochran, ML Huber, SA TI Effects of otitis media on a child with autism receiving behavioral intervention for self-injury SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE autism; self-injury; otitis media; behavioral intervention; child ID FUNCTIONAL-ANALYSIS; SLEEP-DEPRIVATION AB We report the case of a five-year old boy with autism who demonstrated unanticipated increases in self-injurious behavior that had decreased following intervention. On these occasions, elevated self-injury was linked to physician diagnosed otitis media. The findings support an emerging clinical literature documenting possible negative effects from medical influences on challenging behaviors. C1 May Inst, Clin Training & Peer Review, Norwood, MA 02062 USA. May Ctr Early Childhood Educ, Arlington, MA 02476 USA. RP Luiselli, JK (reprint author), May Inst, Clin Training & Peer Review, 1 Commerce Way, Norwood, MA 02062 USA. EM jluiselli@mayinstitute.org CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bondy A, 2001, BEHAV MODIF, V25, P725, DOI 10.1177/0145445501255004 Carr E., 1995, MENTAL RETARDATION D, V1, P94, DOI DOI 10.1002/MRDD.1410010204 CARR EG, 2003, AM J MENT RETARD, V2, P177 IWATA BA, 1982, ANAL INTERVEN DEVEL, V2, P3, DOI 10.1016/0270-4684(82)90003-9 Kennedy CH, 1996, J APPL BEHAV ANAL, V29, P133, DOI 10.1901/jaba.1996.29-133 Lerman DC, 2003, J APPL BEHAV ANAL, V36, P119, DOI 10.1901/jaba.2003.36-119 OREILLY MF, 1995, J APPL BEHAV ANAL, V28, P225, DOI 10.1901/jaba.1995.28-225 OReilly MF, 1997, J APPL BEHAV ANAL, V30, P165, DOI 10.1901/jaba.1997.30-165 NR 9 TC 5 Z9 5 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 0731-7107 J9 CHILD FAM BEHAV THER JI Child Fam. Behav. Ther. PY 2005 VL 27 IS 2 BP 51 EP 56 DI 10.1300/J019v27n02_05 PG 6 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 955TQ UT WOS:000231250900005 ER PT J AU Paul, HA AF Paul, HA TI Bipolar disorders in childhood and early adolescence SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Book Review ID AUTISM C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, N Brunswick, NJ 08902 USA. RP Paul, HA (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, 1 Wedgewood Dr, N Brunswick, NJ 08902 USA. EM happhd@optonline.net CR BACHEVALIER J, 1994, NEUROPSYCHOLOGIA, V32, P627, DOI 10.1016/0028-3932(94)90025-6 BELLER B, 2003, BIPOLAR DISORDERS CH DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 KAGEN J, 1988, SCIENCE, V240, P167 WOZNIAK J, 1995, J AM ACAD CHILD PSY, V34, P1577, DOI 10.1097/00004583-199512000-00007 NR 5 TC 0 Z9 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 0731-7107 J9 CHILD FAM BEHAV THER JI Child Fam. Behav. Ther. PY 2005 VL 27 IS 3 BP 79 EP 84 PG 6 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 984UA UT WOS:000233328600007 ER PT J AU Paul, HA AF Paul, HA TI Siblings of children with autism: A guide for families, 2nd edition. SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Book Review C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Newark, NJ 07103 USA. RP Paul, HA (reprint author), 1 Wedgewood Dr, N Brunswick, NJ 08902 USA. EM happhd@optonline.net CR Harris S. L., 2003, SIBLINGS CHILDREN AU NR 1 TC 0 Z9 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 0731-7107 J9 CHILD FAM BEHAV THER JI Child Fam. Behav. Ther. PY 2005 VL 27 IS 4 BP 85 EP 87 DI 10.1300/J019v27n04_05 PG 3 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 011RF UT WOS:000235285100005 ER PT J AU Hughes, JR Melyn, M AF Hughes, JR Melyn, M TI EEG and seizures in autistic children and adolescents: Further findings with therapeutic implications SO CLINICAL EEG AND NEUROSCIENCE LA English DT Article DE autism; electroencephalography; epilepsy; seizures; slow waves; spikes ID INFANTILE-AUTISM; SPECTRUM DISORDERS; EPILEPTIFORM EEG; EPILEPSY; BIRTH; SEASON AB The goal of this study was to investigate the incidence of epilepsy and also the EEG findings among children with autism (A), a devastating disorder, and to compare these data to an EEG control group. EEGs were quantified as to the degree of epileptiform activity and also slow wave abnormalities. Abnormal EEGs were found in 75% of the 59 A children and 82% of their 151 EEGs; 46% had clinical seizures. Nearly all children with seizures had epileptiform activity, but almost 20% of those with spike discharges did not have clinical attacks. Slow wave abnormalities were more frequent and of a greater degree of severity in the A group, compared to controls. One new finding was that a greater variability of EEG abnormalities was found in the A group. Therapeutic implications, based on these latter findings, are discussed. C1 Univ Illinois, Sch Med, Med Ctr MC 796, Dept Neurol,Div Clin Neurophysiol & Epilepsy, Chicago, IL 60612 USA. Univ Illinois, Sch Med, Dept Neurol, Div Pediat Neurol, Chicago, IL 60612 USA. RP Hughes, JR (reprint author), Univ Illinois, Sch Med, Med Ctr MC 796, Dept Neurol,Div Clin Neurophysiol & Epilepsy, 912 S Wood St,Rm 862N, Chicago, IL 60612 USA. 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EEG Neurosci. PD JAN PY 2005 VL 36 IS 1 BP 15 EP 20 PG 6 WC Clinical Neurology; Neurosciences; Neuroimaging SC Neurosciences & Neurology GA 892NV UT WOS:000226658200003 PM 15683193 ER PT J AU Malone, RP Gratz, SS Delaney, MA Hyman, SB AF Malone, RP Gratz, SS Delaney, MA Hyman, SB TI Advances in drug treatments for children and adolescents with autism and other pervasive developmental disorders SO CNS DRUGS LA English DT Review ID PLACEBO-CONTROLLED TRIAL; DEFICIT HYPERACTIVITY DISORDER; LONG-TERM TREATMENT; DOUBLE-BLIND; CONTROLLED CROSSOVER; RISPERIDONE TREATMENT; BEHAVIORAL SYMPTOMS; PORCINE SECRETIN; YOUNG-CHILDREN; SCHIZOPHRENIC CHILDREN AB Autism is a disorder characterised by abnormalities in language and social development, and repetitive behaviours. Antipsychotics, including haloperidol and risperidone, are the most widely studied drugs for reducing symptoms in children and adolescents with autism. When administered at relatively low dosages, antipsychotics have been shown to reduce repetitive behaviours (stereotypies) and social withdrawal, as well as a number of related symptoms, such as hyperactivity, aggression, self-abusive behaviour, temper tantrums, lability of mood and irritability. Adverse effects of antipsychotics include sedation, dizziness, increased appetite, weight gain, changes in the electrocardiogram parameters, drooling, hyperprolactinemia and a risk of drug-related dyskinesias. Other agents have been less well studied for the treatment of autism, but there are suggestive data regarding their safety and efficacy. Of these agents, a number have been investigated, based on theories about the aetiology of autism, including SSRIs and naltrexone, although the efficacy of these agents has been limited. Stimulant drugs have been shown to reduce hyperactivity and improve focus, but they may cause behavioural worsening, weight loss and stereotypies de novo. 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Rivetti, A. Price, D. TI Vaccines for measles, mumps and rubella in children SO COCHRANE DATABASE OF SYSTEMATIC REVIEWS LA English DT Review ID INFLAMMATORY-BOWEL-DISEASE; IDIOPATHIC THROMBOCYTOPENIC PURPURA; PERVASIVE DEVELOPMENTAL DISORDER; LYMPHOID-NODULAR HYPERPLASIA; DIPHTHERIA-TETANUS-PERTUSSIS; PLACEBO-CONTROLLED TRIAL; SAFETY DATALINK PROJECT; COMBINED LIVE MEASLES; MMR MASS VACCINATION; ASEPTIC-MENINGITIS AB Background Public debate over the safety of the trivalent measles, mumps and rubella (MMR) vaccine, and the resultant drop in vaccination rates in several countries, persists despite its almost universal use and accepted effectiveness. Objectives We carried out a systematic review to assess the evidence of effectiveness and unintended effects associated with MMR. Search strategy We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 4, 2004), MEDLINE (1966 to December 2004), EMBASE (1974 to December 2004), Biological Abstracts (from 1985 to December 2004), and Science Citation Index (from 1980 to December 2004). Results from reviews, handsearching and from the consultation of manufacturers and authors were also used. Selection criteria Eligible studies were comparative prospective or retrospective trials testing the effects of MMR compared to placebo, do-nothing or a combination of measles, mumps and rubella antigens on healthy individuals up to 15 years of age. These studies were carried out or published by 2004. Data collection and analysis We identified 139 articles possibly satisfying our inclusion criteria and included 31 in the review. Main results MMR was associated with a lower incidence of upper respiratory tract infections, a higher incidence of irritability, and similar incidence of other adverse effects compared to placebo. The vaccine was likely to be associated with benign thrombocytopenic purpura, parotitis, joint and limb complaints, febrile convulsions within two weeks of vaccination and aseptic meningitis (mumps) (Urabe strain-containing MMR). Exposure to MMR was unlikely to be associated with Crohn's disease, ulcerative colitis, autism or aseptic meningitis (mumps) (Jeryl-Lynn strain-containing MMR). We could not identify studies assessing the effectiveness of MMR that fulfilled our inclusion criteria even though the impact of mass immunisation on the elimination of the diseases has been largely demonstrated. Authors' conclusions The design and reporting of safety outcomes in MMR vaccine studies, both pre- and post-marketing, are largely inadequate. The evidence of adverse events following immunisation with MMR cannot be separated from its role in preventing the target diseases. C1 Serv Sovrazonale Epidemiol, I-15100 Alessandria, Italy. RP Demicheli, V (reprint author), Serv Sovrazonale Epidemiol, ASL 20,Via Venezia 6, I-15100 Alessandria, Italy. 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PY 2005 IS 4 AR CD004407 DI 10.1002/14651858.CD004407.pub2 PG 33 WC Medicine, General & Internal SC General & Internal Medicine GA 096UK UT WOS:000241402100044 ER PT J AU Nye, C Brice, A AF Nye, C. Brice, A. TI Combined vitamin B6-magnesium treatment in autism spectrum disorder SO COCHRANE DATABASE OF SYSTEMATIC REVIEWS LA English DT Review ID INFANTILE-AUTISM; CHILDHOOD AUTISM; DOUBLE-BLIND; RATING-SCALE; MAGNESIUM; CHILDREN; PYRIDOXINE; ACID; SCHIZOPHRENIA; SYMPTOMS AB Background The use of mega-vitamin intervention began in the 1950s with the treatment of schizophrenic patients. Pyroxidine (vitamin B6) was first used with children diagnosed with "autism syndrome" when speech and language improvement was observed in some children as a result of large doses of B6. A number of studies attempted to assess the effects of vitamin B6-Magnesium (Mg) was found to reduce undesirable side effects from B6) on characteristics such as verbal communication, non-verbal communication, interpersonal skills, and physiological function, in individuals with autism. Objectives To determine the efficacy of vitamin B6 and magnesium (B6-Mg) for treating social, communication, and behavioural responses of children and adults with autism. Search strategy We searched the Cochrane Controlled Trials Register (Cochrane Library, Issue 2, 2002), MEDLINE (1966 to January 2002), EMBASE (1980 to January 2002), PsycINFO (1887 to January 2002), Dissertation Abstracts International (1861 to January 2002). The search engine FirstSearch was also used (January 2002). All searches were updated in April 2005. Reference lists for all the obtained studies and other review articles were examined for additional studies. Selection criteria All studies in which the participants had been diagnosed with autistic spectrum disorder were randomly allocated prior to intervention and in which outcomes were compared to either a placebo or non-treated group were included. Data collection and analysis Two reviewers independently evaluated and extracted data from all potential studies identified for inclusion. Main results This update includes a new trial (Kuriyama 2002) to bring the total of included studies to three (total n = 33). One study, which used a cross-over design (Tolbert 1993) provided insufficient data to conduct an analysis. Another crossover study (Findling 1997) yielded no significant differences between treatment and placebo group performances following the B6 intervention on measures of social interaction, communication, compulsivity, impulsivity, or hyperactivity. The latest study (Kuriyama 2002) was motivated by evidence from epilepsy research and was focussed on a subgroup of children with pervasive developmental disorders (PDDs) who exhibited clinical features similar to those with pyroxidine-dependent epilepsy. This small study (n = 8) only measured IQ and 'Social Quotient' and found a statistically significant benefit for IQ (5.2, 95% CI = [0.2 to 10.3]) when in the treated group, by using change scores. Authors' conclusions Due to the small number of studies, the methodological quality of studies, and small sample sizes, no recommendation can be advanced regarding the use of B6-Mg as a treatment for autism. C1 Univ Cent Florida, Ctr Austism & Related Disabil, Orlando, FL 32826 USA. RP Nye, C (reprint author), Univ Cent Florida, Ctr Austism & Related Disabil, 12001 Sci Dr,Suite 145, Orlando, FL 32826 USA. 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PY 2005 IS 4 AR CD003497 DI 10.1002/14651858.CD003497 PG 16 WC Medicine, General & Internal SC General & Internal Medicine GA 096UK UT WOS:000241402100127 ER PT J AU Williams, KW Wray, JJ Wheeler, DM AF Williams, KW Wray, JJ Wheeler, DM TI Intravenous secretin for autism spectrum disorder SO COCHRANE DATABASE OF SYSTEMATIC REVIEWS LA English DT Review ID PLACEBO-CONTROLLED TRIAL; PERVASIVE DEVELOPMENTAL DISORDER; SYNTHETIC HUMAN SECRETIN; DOUBLE-BLIND; PORCINE SECRETIN; CHILDREN; SYMPTOMS; METAANALYSIS; PREVALENCE; BEHAVIOR AB Background Secretin is a gastro-intestinal hormone which has been presented as an effective treatment for autism based on anecdotal evidence. Objectives To determine if intravenous secretin: 1. improves the core features of autism (social interaction, communication and behaviour problems); 2. improves the non-core aspects of behaviour or function such as self injurious behaviour; 3. improves the quality of life of affected individuals and their carers; 4. has short term and long term effects on outcome; 5. causes harm. Search strategy Results of electronic searches of CENTRAL, MEDLINE, EMBASE, PsycINFO, CINAHL, ERIC, HealthStar and Sociofile (1998 March 2005) were independently examined by two authors. Reference lists of trials and reviews were searched; experts and trialists were contacted to find unpublished studies. Selection criteria Randomised controlled trials of intravenous secretin comparing secretin with a placebo treatment in children or adults diagnosed with autism spectrum disorders, where at least one standardised outcome measure was reported. Data collection and analysis Fourteen studies met inclusion criteria. All outcome data were continuous. Where trials used cross-over designs, analysis was conducted on results from first treatment phase, allowing combined analysis with parallel design trials. Where standardised assessment tools generated scores as outcome measures, comparisons were made between means of these scores. Where baseline means were reported, differences between treatment and control were determined to assess possible bias. Where mean change from baseline was reported, this was used in preference to post-treatment scores for meta-analyses or forest plots. As meta-analysis was possible for only one outcome (Childhood Autism Rating Scale), it was impossible to use sensitivity or subgroup analyses to assess impact of study quality, clinical differences in the intervention, or clinically relevant differences between groups, such as age or presence of gastrointestinal symptoms. Main results Twenty-five established standardised outcome measures were reported to assess core features of autism, communication, behaviour, visio-spatial skills, affect and adverse events within fourteen included studies. No more than four studies used any one outcome measure similarly. Outcomes were reported between three and six weeks. RCTs of efficacy of secretin in autism have not shown improvements for core features of autism. Authors' conclusions There is no evidence that single or multiple dose intravenous secretin is effective and as such it should not currently be recommended or administered as a treatment for autism. Further experimental assessment of secretin's effectiveness for autism can only be justified if methodological problems of existing research can be overcome. SYNOPSIS Secretin is a gastro-intestinal hormone which has been presented as an effective treatment for autism based on anecdotal evidence. This review of thirteen randomised studies found no evidence that single or multiple dose intravenous secretin is effective across a range of outcomes, and concludes that as such it should not currently be recommended or administered as a treatment for autism. Further experimental assessment of secretin's effectiveness for autism can only be justified if methodological problems of existing research can be overcome. C1 Childrens Hosp, Westmead, NSW 2145, Australia. RP Williams, KW (reprint author), Childrens Hosp, Locked Bag 4001, Westmead, NSW 2145, Australia. 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PY 2005 IS 3 AR CD003495.pub2 DI 10.1002/14651858.CD003495.pub2 PG 36 WC Medicine, General & Internal SC General & Internal Medicine GA 968ZI UT WOS:000232202500016 ER PT S AU Paplinski, AP Gustafsson, L AF Paplinski, AP Gustafsson, L TI Multimodal feedforward self-organizing maps SO COMPUTATIONAL INTELLIGENCE AND SECURITY, PT 1, PROCEEDINGS SE LECTURE NOTES IN ARTIFICIAL INTELLIGENCE LA English DT Article; Proceedings Paper CT International Conference on Computational Intelligence and Security CY DEC 15-19, 2005 CL Xi'an, PEOPLES R CHINA SP IEEE Computat Intelligence, Hong Kong Chapter, Xidian Univ, Hong Kong Baptist Univ, Natl Nat Sci Fdn China, Guangdong Univ Technol ID ORGANIZATION; AUTISM AB We introduce a novel system of interconnected Self-Organizing Maps that can be used to build feedforward and recurrent networks of maps. Prime application of interconnected maps is in modelling systems that operate with multimodal data as for example in visual and auditory cortices and multimodal association areas in cortex. A detailed example of animal categorization in which the feedworward network of self-organizing maps is employed is presented. In the example we operate with 18-dimensional data projected up on the 19-dimensional hyper-sphere so that the "dot-product" learning law can be used. One potential benefit of the multimodal map is that it allows a rich structure of parallel unimodal processing with many maps involved, followed by convergence into multimodal maps. More complex stimuli can therefore be processed without a growing map size. C1 Monash Univ, Clayton Sch Informat Technol, Clayton, Vic 3800, Australia. Lulea Univ Technol, S-97187 Lulea, Sweden. RP Paplinski, AP (reprint author), Monash Univ, Clayton Sch Informat Technol, Clayton, Vic 3800, Australia. 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ID DEFICIT HYPERACTIVITY DISORDER; POSITRON-EMISSION-TOMOGRAPHY; HEALTHY-HUMAN SUBJECTS; I-123 BETA-CIT; DOPAMINE TRANSPORTER; SEROTONIN TRANSPORTER; PARKINSONS-DISEASE; IN-VIVO; HIGH-AFFINITY; MICE LACKING AB Membrane and vesicular monoaminergic transporters, responsible for the homeostasis of neurotransmitter pools at nerve endings, are very involved in the physiology and diseases of central nervous system. Recent progresses of cerebral molecular imaging using SPECT and PET methods allow the extend of in vivo exploration of these transporters. For this aim, an increasing number of radiopharmaceuticals labelled with [(123)I], [(99)mTc], [(11)C] or [(18)F] have been developed such as cocaine derivatives for the DAT, compounds from the diphenyl sulfide family for the SERT, and dihydrotetrabenazine derivatives for the VMAT(2). These functional imaging methods can be very useful in several neurological and psychiatric disorders which involve the monoaminergic neurotransmission systems such as Parkinson's disease, ADHD, depression and autism. For example, the DAT is a specific index of the density of dopaminergic endings which progressively degenerate in Parkinson's disease. In vivo exploration of this transporter can therefore be a relevant way (i) to realize an early detection of the loss of dopaminergic neurons, (ii) to assess the progression of the disease, (iii) to validate and improve the efficacy of new therapeutic strategies such as neuroprotection and neuroreparation. 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Pharm. Design PY 2005 VL 11 IS 25 BP 3237 EP 3245 DI 10.2174/138161205774424744 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 960UC UT WOS:000231617700004 PM 16250852 ER PT J AU Honda, H Shimizu, Y Imai, M Nitto, Y AF Honda, H Shimizu, Y Imai, M Nitto, Y TI Cumulative incidence of childhood autism: a total population study of better accuracy and precision SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; PRESCHOOL-CHILDREN; CHANGING PREVALENCE; RUBELLA VACCINE; EPIDEMIOLOGY; CALIFORNIA; MEASLES; SYSTEM; JAPAN AB Most studies on the frequency of autism have had methodological problems. Most notable of these have been differences in diagnostic criteria between studies, degree of cases overlooked by the initial screening, and type of measurement. This study aimed to replicate the first report on childhood autism to address cumulative incidence as well as prevalence, as defined in the International Statistical Classification of Diseases and Related Health Problems, 10th revision (ICD-10) Diagnostic Criteria for Research. Here, the same methodological accuracy (exactness of a measurement to the true value) as the first study was used, but population size was four times larger to achieve greater precision (reduction of random error). A community-oriented system of early detection and early intervention for developmental disorders was established in the northern part of Yokohama, Japan. The city's routine health checkup for 18-month-old children served as the initial mass screening, and all facilities that provided child care services aimed to detect all cases of childhood autism and refer them to the Yokohama Rehabilitation Center. Cumulative incidence up to age 5 years was calculated for childhood autism among a birth cohort from four successive years (1988 to 1991). Cumulative incidence of childhood autism was 27.2 per 10 000. Cumulative incidences by sex were 38.4 per 10 000 in males, and 15.5 per 10 000 in females. The male:female ratio was 2.5:1. The proportions of children with high-functioning autism who had Binet IQs of 70 and over and those with Binet IQs of 85 and over were 25.3% and 13.7% respectively. Data on cumulative incidence of childhood autism derived from this study are the first to be drawn from an accurate, as well as precise, screening methodology. C1 Yokohama Rehabil Ctr, Dev Psychiat Unit, Kohoku Ku, Yokohama, Kanagawa 2220035, Japan. RP Honda, H (reprint author), Yokohama Rehabil Ctr, Dev Psychiat Unit, Kohoku Ku, 1770 Toriyama Cho, Yokohama, Kanagawa 2220035, Japan. 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PY 2005 VL 28 IS 3 BP 809 EP 827 DI 10.1207/s15326942dn2803_4 PG 19 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 987UC UT WOS:000233541800004 PM 16266250 ER PT J AU Luyster, R Richler, J Risi, S Hsu, WL Dawson, G Bernier, R Dunn, M Hepburn, S Hyman, SL McMahon, WM Goudie-Nice, J Minshew, N Rogers, S Sigman, M Spence, MA Goldberg, WA Volkmar, FR Lord, C AF Luyster, R Richler, J Risi, S Hsu, WL Dawson, G Bernier, R Dunn, M Hepburn, S Hyman, SL McMahon, WM Goudie-Nice, J Minshew, N Rogers, S Sigman, M Spence, MA Goldberg, WA Volkmar, FR Lord, C TI Early regression in social communication in autism spectrum disorders: A CPEA study SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; SPEECH LOSS; DISINTEGRATIVE PSYCHOSIS; RUBELLA VACCINATION; LANGUAGE REGRESSION; NO EVIDENCE; CHILDREN; MEASLES; POPULATION AB In a multisite study of 351 children with autism spectrum disorders, 21 children with developmental delays, and 31 children with typical development, this study used caregiver interviews (i.e., the Autism Diagnostic Interview Revised) at the time of entry into other research projects and follow-up telephone interviews designed for this project to describe the children's early acquisition and loss of social-communication milestones. Children who had used words spontaneously and meaningfully and then stopped talking were described by their caregivers as showing more gestures, greater participation in social games, and better receptive language before the loss and fewer of these skills after the loss than other children with autism spectrum disorders. A significant minority of children with autism without word loss showed a very similar pattern of loss of social-communication skills, a pattern not observed in the children with developmental delays or typical development. C1 Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10461 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Boulder, CO 80309 USA. Univ Rochester, Dept Pediat, Rochester, NY 14627 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. 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PY 2005 VL 27 IS 3 BP 311 EP 336 DI 10.1207/s15326942dn2703_2 PG 26 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 928AN UT WOS:000229243600002 PM 15843100 ER PT J AU O'Shea, AG Fein, DA Cillessen, AHN Klin, A Schultz, RT AF O'Shea, AG Fein, DA Cillessen, AHN Klin, A Schultz, RT TI Source memory in children with autism spectrum disorders SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article; Proceedings Paper CT 112th Annual Convention of the American-Psychological-Association CY JUL 28-AUG 01, 2004 CL Honolulu, HI SP Amer Psychol Assoc ID EXECUTIVE FUNCTION; INDIVIDUALS; MIND; DEFICITS; PERFORMANCE; SAMPLE AB The evidence to date regarding memory processes in children with autism spectrum disorders (ASD) remains equivocal. Although children with these neuro-developmental disorders have been shown to display exceptional memories for fact-based information, they seem to be less able to attach meaning or context to their memories. Thus, this study investigated the specific role of source memory in autism. Children with ASD were compared to a chronological and mental age-matched comparison group of typically developing children. Although children with autism performed similarly to controls on a fact recognition measure, their performance on a source memory task was significantly lower. The findings indicated, however, that the nature of source memory confusion in children with autism does not appear to reflect a generalized deficit in attaching context to memories but rather is dependent on the specific to-be-remembered information that, in this study, involves social aspects of context. C1 Yale Univ, Sch Med, Dept Neurosurg, Neuropsychol Serv, New Haven, CT 06510 USA. Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. RP O'Shea, AG (reprint author), Yale Univ, Sch Med, Dept Neurosurg, Neuropsychol Serv, 60 Temple St,Ground Floor, New Haven, CT 06510 USA. EM angela.oshea@yale.edu RI Cillessen, Antonius/A-5978-2010 CR AMELI R, 1988, J AUTISM DEV DISORD, V18, P601, DOI 10.1007/BF02211878 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Archibald SJ, 1999, CHILD NEUROPSYCHOL, V5, P115, DOI 10.1076/chin.5.2.115.3167 BARTH C, 1995, DEV NEUROPSYCHOL, V11, P53 Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x BOUCHER J, 1976, BRIT J PSYCHOL, V67, P73 BOUCHER J, 1981, J AUTISM DEV DISORD, V11, P293, DOI 10.1007/BF01531512 Butters M. 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PY 2005 VL 27 IS 3 BP 337 EP 360 DI 10.1207/s15326942dn2703_3 PG 24 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 928AN UT WOS:000229243600003 PM 15843101 ER PT J AU Joseph, RM McGrath, LM Tager-Flusberg, H AF Joseph, RM McGrath, LM Tager-Flusberg, H TI Executive dysfunction and its relation to language ability in verbal school-age children with autism SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID FRONTAL-LOBE FUNCTION; WORKING-MEMORY; NONRETARDED-CHILDREN; PERFORMANCE; IMPAIRMENT; DEFICITS; INTACT; TOWER; INDIVIDUALS; DISORDERS AB This study examined executive dysfunction and its relation to language ability in verbal school-age children with autism. Participants were 37 children with autism and 31 nonautistic comparison participants who were matched on age and on verbal and nonverbal IQ but not on language ability, which was lower in the autism group. Children with autism exhibited deficits compared to the comparison group across all 3 domains of executive function that were assessed including working memory (Block Span Backward; Isaacs & Vargha-Khadem, 1989), working memory and inhibitory control (NEPSY Knock-Tap; Korkman, Kirk, & Kemp, 1998), and planning (NEPSY Tower; Korkman et al., 1998). Children with autism were less developed than the comparison group in their language skills, but correlational analyses revealed no specific association between language ability and executive performance in the autism group. In contrast, executive performance was positively correlated with language ability in the comparison group. This pattern of findings suggest that executive dysfunction in autism is not directly related to language impairment per se but rather involves an executive failure to use of language for self-regulation. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Univ Denver, Dept Psychol, Denver, CO 80208 USA. RP Joseph, RM (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,L-814, Boston, MA 02118 USA. 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PY 2005 VL 27 IS 3 BP 361 EP 378 DI 10.1207/s15326942dn2703_4 PG 18 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 928AN UT WOS:000229243600004 PM 15843102 ER PT J AU Kleinhans, N Akshoomoff, N Delis, DC AF Kleinhans, N Akshoomoff, N Delis, DC TI Executive functions in autism and Asperger's disorder: Flexibility, fluency, and inhibition SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article; Proceedings Paper CT 31st Annual Meeting of the International-Neuropsychological-Society CY FEB 05-08, 2003 CL HONOLULU, HI SP Int Neuropsychol Soc ID DEVELOPMENTAL CEREBELLAR ABNORMALITY; COMMUNICATION DEFICITS; SHIFTING ATTENTION; VISUAL-SEARCH; WORD FLUENCY; CHILDREN; INDIVIDUALS; SPECTRUM; COMPREHENSION; INTERFERENCE AB The Color-Word Interference Test, Trail Making Test, Verbal Fluency Test, and Design Fluency Test from the Delis-Kaplan Executive Function System (Delis, Kaplan, & Kramer, 2001) were administered to 12 high-functioning adults and adolescents with autistic disorder or Asperger's disorder. Each test included a switching condition in addition to baseline and/or other executive-function conditions. Participants performed significantly below average on a composite measure of executive functioning adjusted for baseline cognitive ability. Complex verbal tasks that required cognitive switching and initiation of efficient lexical retrieval strategies produced the most consistent deficits, whereas cognitive inhibition was intact. We discuss implications of these findings for understanding the neurocognitive substrates of autistic spectrum disorders. C1 San Diego State Univ, Joint Doctoral Program Clin Psychol, La Jolla, CA 92037 USA. Univ Calif San Diego, Dept Psychiat, Sch Med, San Diego, CA 92103 USA. Childrens Hosp, Child & Adolescent Serv Res Ctr, San Diego, CA USA. RP Kleinhans, N (reprint author), San Diego State Univ, Joint Doctoral Program Clin Psychol, 8110 La Jolla Shores Dr,Suite 201, La Jolla, CA 92037 USA. 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PY 2005 VL 27 IS 3 BP 379 EP 401 DI 10.1207/s15326942dn2703_5 PG 23 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 928AN UT WOS:000229243600005 PM 15843103 ER PT J AU Dawson, G Webb, SJ McPartland, J AF Dawson, G Webb, SJ McPartland, J TI Understanding the nature of face processing impairment in autism: Insights from behavioral and electrophysiological studies SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDER; EVENT-RELATED POTENTIALS; GAMMA-BAND ACTIVITY; CAT VISUAL-CORTEX; SPECTRUM DISORDER; BRAIN ACTIVITY; JOINT ATTENTION; YOUNG-CHILDREN; COGNITIVE NEUROSCIENCE; SELECTIVE ATTENTION AB This article reviews behavioral and electrophysiological studies of face processing and discusses hypotheses for understanding the nature of face processing impairments in autism. Based on results of behavioral studies, this study demonstrates that individuals with autism have impaired face discrimination and recognition and use atypical strategies for processing faces characterized by reduced attention to the eyes and piecemeal rather than configural strategies. Based on results of electrophysiological studies, this article concludes that face processing impairments are present early in autism, by 3 years of age. Such studies have detected abnormalities in both early (N170 reflecting structural encoding) and late (NC reflecting recognition memory) stages of face processing. Event-related potential studies of young children and adults with autism have found slower speed of processing of faces, a failure to show the expected speed advantage of processing faces versus nonface stimuli, and atypical scalp topography suggesting abnormal cortical specialization for face processing. Other electrophysiological studies have suggested that autism is associated with early and late stage processing impairments of facial expressions of emotion (fear) and decreased perceptual binding as reflected in reduced gamma during face processing. This article describes two types of hypotheses-cognitive/perceptual and motivational/affective-that offer frameworks for understanding the nature of face processing impairments in autism. This article discusses implications for intervention. C1 Univ Washington, Autism Ctr, Seattle, WA 98195 USA. RP Dawson, G (reprint author), Univ Washington, Autism Ctr, Box 357920, Seattle, WA 98195 USA. 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Neuropsychol. PY 2005 VL 27 IS 3 BP 403 EP 424 DI 10.1207/s15326942dn2703_6 PG 22 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 928AN UT WOS:000229243600006 PM 15843104 ER PT J AU Haist, F Adamo, M Westerfield, M Courchesne, E Townsend, J AF Haist, F Adamo, M Westerfield, M Courchesne, E Townsend, J TI The functional neuroanatomy of spatial attention in autism spectrum disorder SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID ORIENTING GAZE SHIFTS; SELECTIVE ATTENTION; VISUAL-ATTENTION; EYE-MOVEMENTS; CORPUS-CALLOSUM; DIRECTING ATTENTION; INFANTILE-AUTISM; NEURAL SYSTEMS; CHILDREN; FMRI AB This study investigated the functional neuroanatomical correlates of spatial attention impairments in autism spectrum disorders (AS[)) using an event-related functional magnetic resonance imaging (FMRI) design. Eight ASD participants and 8 normai comparison (NC) participants were tested with a task that required stimulus discrimination following a spatial cue that preceded target presentation by 100 msec (short interstimulus interval [ISI]) or 800 msec (long ISI). The ASD group showed significant behavioral spatial attention impairment in the short ISI condition. The FMRI results showed a reduction in activity within frontal, parietal, and occipital regions in ASD relative to the NC group, most notably within the inferior parietal lobule. ASD behavioral performance improved in the long ISI condition but was still impaired relative to the NC group. ASD FMRI activity in the long ISI condition suggested that the rudimentary framework of normal attention networks were engaged in ASD including bilateral activation within the frontal, parietal, and occipital lobes. Notable activation increases were observed in the superior parietal lobule and extrastriate cortex. No reliable activation was observed in the posterior cerebellar vermis in ASD participants during either long or short ISI conditions. In addition, no frontal activation during short ISl and severely reduced frontal activation during long ISI was observed in the ASD group. Taken together, these findings suggest a dysfunctional cerebello-frontal spatial attention system in ASD. The pattern of findings suggests that ASD is associated with a profound deficit in automatic spatial attention abilities and abnormal voluntary spatial attention abilities. This article also describes a method for reducing the contribution of physical eye movements to the blood-oxygenation level dependent activity in studies of ASD. C1 Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Childrens Hosp Res Ctr, La Jolla, CA USA. RP Haist, F (reprint author), Univ Calif San Diego, Dept Psychiat, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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Neuropsychol. PY 2005 VL 27 IS 3 BP 425 EP 458 DI 10.1207/s15326942dn2703_7 PG 36 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 928AN UT WOS:000229243600007 PM 15843105 ER PT J AU Waage-Baudet, H Dunty, WC Dehart, DB Hiller, S Sulik, KK AF Waage-Baudet, H Dunty, WC Dehart, DB Hiller, S Sulik, KK TI Immunohistochemical and microarray analyses of a mouse model for the Smith-Lemli-Opitz syndrome SO DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE Smith-Lemli-Opitz syndrome; autism; sonic hedgehog; netrin; microarray; cholesterol biosynthesis ID CILIARY NEUROTROPHIC FACTOR; DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; MICROTUBULE-ASSOCIATED PROTEINS; MULTIPLE CONGENITAL-ANOMALIES; COLORECTAL-CANCER DCC; II-DEFICIENT MICE; ALZHEIMERS-DISEASE; AXON GUIDANCE; SONIC-HEDGEHOG; OLIGONUCLEOTIDE ARRAYS AB The Smith-Lemli-Opitz syndrome is a mental retardation/malformation syndrome with behavioral components of autism. It is caused by a deficiency in 3 beta-hydroxysteroid-Delta(7)-reductase (DHCR7), the enzyme required for the terminal enzymatic step of cholesterol biosynthesis. The availability of Smith-Lemli-Opitz syndrome mouse models has made it possible to investigate the genesis of the malformations associated with this syndrome. Dhcr7 gene modification (Dhcr7-/-) results in neonatal lethality and multiple organ system malformations. Pathology includes cleft palate, pulmonary hypoplasia, cyanosis, impaired cortical response to glutamate, and hypermorphic development of hindbrain serotonergic neurons. For the current study, hindbrain regions microdissected from gestational day 14 Dhcr7-/-, Dhcr7+/- and Dhcr7+/+ fetuses were processed for expression profiling analyses using Affymetrix oligonucleotide arrays and filtered using statistical significance (S-score) of change in gene expression. Of the 12,000 genes analyzed, 91 were upregulated and 98 were downregulated in the Dhcr7-/- hindbrains when compared to wild-type animals. Fewer affected genes, representing a reduced affect on these pathways, were identified in heterozygous animals. Hierarchical clustering identified altered expression of genes associated with cholesterol homeostasis, cell cycle control and apoptosis, neurodifferentiation and embryogenesis, transcription and translation, cellular transport, neurodegeneration, and neuronal cytoskeleton. Of particular interest, Dhcr7 gene modification elicited dynamic changes in genes involved in axonal guidance. In support of the microarray findings, immunohistochemical analyses of the netrin/deleted in colorectal cancer axon guidance pathway illustrated midline commissural deficiencies and hippocampal pathfinding errors in Dhcr7-/- mice. The results of these studies aid in providing insight into the genesis of human cholesterol-related birth defects and neurodevelopmental disorders and highlight specific areas for future investigation. Copyright (c) 2005 S. Karger AG, Basel. C1 Univ N Carolina, Dept Cell & Dev Biol, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Pathol, Chapel Hill, NC 27599 USA. Univ N Carolina, Bowles Ctr Alcohol Studies, Chapel Hill, NC 27599 USA. NCI, Canc & Dev Biol Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA. RP Sulik, KK (reprint author), Univ N Carolina, Sch Med, Ctr Alcohol Studies, 3019A Thurston Bowles Bldg,CB 7178, Chapel Hill, NC 27599 USA. 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Neurosci. PY 2005 VL 27 IS 6 BP 378 EP 396 DI 10.1159/000088453 PG 19 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 982ZT UT WOS:000233201600003 PM 16280635 ER PT J AU Kuhl, PK Coffey-Corina, S Padden, D Dawson, G AF Kuhl, PK Coffey-Corina, S Padden, D Dawson, G TI Links between social and linguistic processing of speech in preschool children with autism: behavioral and electrophysiological measures SO DEVELOPMENTAL SCIENCE LA English DT Article ID LISTENING PREFERENCES; LANGUAGE-ACQUISITION; AUDITORY INFORMATION; 4-MONTH-OLD INFANTS; DISABLED-CHILDREN; SPECTRUM DISORDER; EARLY RECOGNITION; BRAIN POTENTIALS; HOME VIDEOTAPES; DIRECTED SPEECH AB Data on typically developing children suggest a link between social interaction and language learning, a finding of interest both to theories of language and theories of autism. In this study, we examined social and linguistic processing of speech in preschool children with autism spectrum disorder (ASD) and typically developing chronologically matched (TDCA) and mental age matched (TDMA) children. The social measure was an auditory preference test that pitted 'motherese' speech samples against non-speech analogs of the same signals. The linguistic measure was phonetic discrimination assessed with mismatch negativity (MMN), an event-related potential (ERP). As a group, children with ASD differed from controls by: (a) demonstrating a preference for the non-speech analog signals, and (b) failing to show a significant MMN in response to a syllable change. When ASD children were divided into subgroups based on auditory preference, and the ERP data reanalyzed, ASD children who preferred non-speech still failed to show an MMN whereas ASD children who preferred motherese did not differ from the controls. The data support the hypothesis of an association between social and linguistic processing in children with ASD. C1 Univ Washington, Ctr Dev & Disabilities, Seattle, WA 98195 USA. Univ Washington, Dept Speech & Hearing Sci, Seattle, WA 98195 USA. Univ Washington, UW Autism Ctr, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. RP Kuhl, PK (reprint author), Univ Washington, Ctr Dev & Disabilities, Seattle, WA 98195 USA. 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PD JAN PY 2005 VL 8 IS 1 BP F1 EP F12 DI 10.1111/j.1467-7687.2004.00384.x PG 12 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 894HD UT WOS:000226780700001 PM 15647058 ER PT J AU Sperner-Unterweger, B AF Sperner-Unterweger, B TI Immunological aetiology of major psychiatric disorders - Evidence and therapeutic implications SO DRUGS LA English DT Review ID NECROSIS-FACTOR-ALPHA; INFLAMMATORY RESPONSE SYSTEM; HERPES-SIMPLEX-VIRUS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; SCHIZOPHRENIC-PATIENTS RESISTANT; NEUROTROPHIN-3 MESSENGER-RNA; AFRICAN-AMERICAN ETHNICITY; LYMPHOCYTE SUB-POPULATIONS; ALCOHOL-DEPENDENT PATIENTS; AMYLOID PRECURSOR PROTEIN AB Historically, immunological research in psychiatry was based on empirical findings and early epidemiological studies indicating a possible relationship between psychiatric symptoms and acute infectious diseases. However, aetiopathological explanations for psychiatric disorders are no longer closely related to acute infection. Nevertheless, immune hypotheses have been discussed in schizophrenia, affective disorders and infantile autism in the last decades. Although the variability between the results of the epidemiological studies conducted to date is strikingly high, there is still some evidence that the immune system might play a role in the aetiopathogenesis of these three psychiatric diseases, at least in subgroups of patients. In anxiety disorders immunological research is still very much in its infancy, and the few and inconsistent data of immune changes in these patients are believed to reflect the influence of short- or long-term stress exposure. Nevertheless, there are also some hints raising the possibility that autoimmune mechanisms could interrupt neurotransmission, which would be of significance in certain patients with anxiety and panic disorders. Drug and alcohol (ethanol) dependence are not believed to be primarily influenced by an immunological aetiology. On the other hand, immune reactions due to different drugs of abuse and alcohol may directly or indirectly influence the course of concomitant somatic diseases. In different organic brain disorders the underlying somatic disease is defined as a primary immune or autoimmune disorder, for instance HIV infection or systemic lupus erythematosus (SLE). For other neurodegenerative disorders, such as Alzheimer's disease, immunoaetiopathological mechanisms are supported by experimental and clinical studies. Treatment strategies based on immune mechanisms have been investigated in patients with schizophrenia and affective disorders. Furthermore, some antipsychotics and most antidepressants are known to have direct or indirect effects on the immune system. Different immunotherapies have been used in autism, including transfer factor, pentoxifylline, intravenous immunoglobulins and corticosteroids. Immunosuppressive and/or immunomodulating agents are well established methods for treating the neuropsychiatric sequelae of immune or autoimmune disorders, for example AIDS and SLE. Therapeutic approaches in Alzheimer's disease also apply immunological methods such as strategies of active/passive immunisation and NSAIDs. Considering the comprehensive interactive network between mind and body, future research should focus on approaches linking targets of the different involved systems. C1 Innsbruck Univ Clin, Dept Biol Psychiat, A-6020 Innsbruck, Austria. RP Sperner-Unterweger, B (reprint author), Innsbruck Univ Clin, Dept Biol Psychiat, Anichstr 35, A-6020 Innsbruck, Austria. 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We report the case of a 36 year old woman with bipolar disorder and alpha-thalassemia. The patient, native of Reunion Island, has a family history of bipolar disorder (both parents, one brother, and a paternal uncle). The severity of the bipolar disorder type I in her family, is illustrated by the suicides of both parents, one brother and the paternal uncle, in intervals of only a few years. After a Medline review (1980-2004) we found only two studies suggesting a possible relationship between bipolar disorders and alpha-thalassemias (3, 4), but without clinical case report information. Some genetic studies described the existence of possible genetic susceptibility for bipolar disorder (6, 7, 13) on the short arm of chromosome 16, close to the gene involved in certain alpha-thalassemias, on the region 16p13.3. An interesting finding is that the sequencing of 258 kb of the chromosome region 16p13.3 not only allowed the identification of genes involved in the alpha-thalassemia and in the vulnerability to bipolar disorders, but also the identification of genes implicated in tuberous sclerosis, in polycystic kidney disease, in cataract with microophtalmia, and in vulnerability genetic factors for ATR-16 syndrome, asthma, epilepsy, certain forms of autism and mental retardation (3, 23). Numerous clinical descriptions and some familial studies on linkage suggested a possible relationship between tuberous sclerosis, polycystic kidney disease, cataract with microophtalmia, ATR-16 syndrome, asthma, epilepsy, certain forms of autism, mental retardation and bipolar disorder, given the closeness of these vulnerability genes on the short arm of the chromosome 16 (8, 9, 11, 12, 24). A vulnerability gene of alcohol dependence was also identified on this same chromosome region (16p13.3), by a study concerning 105 families (17). Taking into account the methodological difficulties due to the clinical and genetic heterogeneity of bipolar disorder, we suggest that linkage techniques should be used to confirm the presence of susceptibility genetic factor for bipolar disorders on chromosome 16. Thus a known genetic disease (alpha-thalassemia) could contribute to confirming the presence on the short arm of chromosome 16 of a susceptibility genetic factor for bipolar disorders. Linkage studies should be performed in families with a strong association for both diseases. Thanks to linkage techniques, one could hope for an improvement in understanding the physiopathology of bipolar disorder, with possible implications at a therapeutic level. C1 Hop Cantonal Univ Geneva, CH-1211 Geneva, Switzerland. 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Hepatocyte growth factor/scatter factor (HGF/SF) has been identified as an important molecular cue that may guide the movement of interneurons from their birthplace in the ganglionic eminences (GE) to their final resting place in the neocortex. In vitro studies demonstrate that decreased HGF/SF bioactivity in pallial and subpallial tissues is associated with a reduction in the number of cells migrating out of GE explants. The uPAR knockout mouse provides a unique opportunity to study the effects of interneuron disruption in vivo. uPAR(-/-) mice have reduced HGF/SF bioactivity in the GE during the period of interneuron development and a concomitant 50% reduction in the number of GABAergic interneurons seeding frontal and parietal regions of the cerebral cortex. Behaviorally, these mice display an increased susceptibility to seizures, heightened anxiety, and diminished social interaction. This article discusses the commonalities between the functional defects seen in uPAR-/- mice and those of humans with developmental disorders, such as epilepsy, schizophrenia, and autism. It is suggested that disruption of GABAergic interneuron development may represent a common point of convergence underlying the etiologies of many of these developmental disorders. C1 Vanderbilt Univ, Vanderbilt Kennedy Ctr Res Human Dev, Nashville, TN 37203 USA. RP Levitt, P (reprint author), Vanderbilt Univ, Vanderbilt Kennedy Ctr Res Human Dev, POB 40,230 Appleton Pl, Nashville, TN 37203 USA. 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NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 6 BP 34 EP 34 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 964MN UT WOS:000231885300118 ER PT J AU Tuchman, R AF Tuchman, R TI Epilepsy in autism SO EPILEPSIA LA English DT Meeting Abstract CT 26th International Epilepsy Congress CY AUG 28-SEP 01, 2005 CL Paris, FRANCE SP Int League Against Epilepsy, Int Bureau Epilepsy C1 Miami Childrens Hosp, Dan Marino Ctr, Dept Neurol, Miami, FL USA. 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NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 8 BP 78 EP 78 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 973RK UT WOS:000232540100228 ER PT J AU Kim, HL Filipek, P Donnelly, JH Tournay, AE Book, TM AF Kim, HL Filipek, P Donnelly, JH Tournay, AE Book, TM TI Intrinsic features of epileptiform EEG abnormalities in children with autism SO EPILEPSIA LA English DT Meeting Abstract CT Joint Annual Meeting of the American-Epilepsy-Society/American-Clinical-Neurophsiology-Society CY DEC 02-06, 2005 CL Washington, DC SP Amer Epilepsy Soc, Amer Clin Neurophysiol Soc C1 Univ Calif Irvine, Coll Med, Irvine, CA 92717 USA. OC Kids, Orange, CA USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 8 BP 137 EP 137 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 973RK UT WOS:000232540100401 ER PT J AU Danielsson, S Gillberg, IC Billstedt, E Gillberg, C Olsson, I AF Danielsson, S Gillberg, IC Billstedt, E Gillberg, C Olsson, I TI Long-term outcome for individuals with autism and early onset epilepsy in a community-based cohort SO EPILEPSIA LA English DT Meeting Abstract CT 26th International Epilepsy Congress CY AUG 28-SEP 01, 2005 CL Paris, FRANCE SP Int League Against Epilepsy, Int Bureau Epilepsy C1 Univ Gothenburg, Inst Hlth Women & Children, Dept Paediat, Gothenburg, Sweden. Univ Gothenburg, Inst Hlth Women & Children, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 6 BP 178 EP 178 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 964MN UT WOS:000231885300650 ER PT J AU Wenzel, HJ Berman, RF Katleba, K Lo, Y Jaubert, P Wenzel, M Altangerel, A Schwartzkroin, PA AF Wenzel, HJ Berman, RF Katleba, K Lo, Y Jaubert, P Wenzel, M Altangerel, A Schwartzkroin, PA TI Characterization of an animal model of autism: Potential relevance to brain hyperexcitability and seizures SO EPILEPSIA LA English DT Meeting Abstract CT Joint Annual Meeting of the American-Epilepsy-Society/American-Clinical-Neurophsiology-Society CY DEC 02-06, 2005 CL Washington, DC SP Amer Epilepsy Soc, Amer Clin Neurophysiol Soc C1 Univ Calif Davis, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 8 BP 305 EP 305 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 973RK UT WOS:000232540101272 ER PT J AU Lewine, JD Nowack, WJ AF Lewine, JD Nowack, WJ TI Magnetoencephalography in adults with autism spectrum disorder SO EPILEPSIA LA English DT Meeting Abstract CT Joint Annual Meeting of the American-Epilepsy-Society/American-Clinical-Neurophsiology-Society CY DEC 02-06, 2005 CL Washington, DC SP Amer Epilepsy Soc, Amer Clin Neurophysiol Soc C1 Univ Kansas, Med Ctr, Hoglund Brain Imaging Ctr, Kansas City, KS 66103 USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 8 BP 326 EP 327 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 973RK UT WOS:000232540101334 ER PT J AU Padilla, LA Gutierrez, J AF Padilla, LA Gutierrez, J TI Comparison of epilepsy frequency, seizure type, and electroencephalographic abnormalities in patients with primary autism and patients with secondary autism SO EPILEPSIA LA English DT Meeting Abstract CT 26th International Epilepsy Congress CY AUG 28-SEP 01, 2005 CL Paris, FRANCE SP Int League Against Epilepsy, Int Bureau Epilepsy C1 Natl Med Ctr, Mexico City, DF, Mexico. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2005 VL 46 SU 6 BP 400 EP 401 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 964MN UT WOS:000231885302277 ER PT J AU Ylisaukko-oja, T Peyrard-Janvid, M Lindgren, CM Rehnstrom, K Vanhala, R Peltonen, L Jarvela, I Kere, J AF Ylisaukko-oja, T Peyrard-Janvid, M Lindgren, CM Rehnstrom, K Vanhala, R Peltonen, L Jarvela, I Kere, J TI Family-based association study of DYX1C1 variants in autism SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE dyslexia; hyperlexia; specific language impairment; DYX1; 15q; FBAT ID MAJOR SUSCEPTIBILITY LOCUS; LANGUAGE IMPAIRMENT; DEVELOPMENTAL DYSLEXIA; CHROMOSOME 7Q; CANDIDATE GENE; SEVERE SPEECH; DISORDER; LINKAGE; REGION; FOXP2 AB DYX1C1 was recently identified as a candidate gene for developmental dyslexia, which is characterized by an unexpected difficulty in learning to read and write despite adequate intelligence, motivation, and education. It will be important to clarify, whether the phenotype caused by DYX1C1 extends to other language-related or comorbid disorders. Impaired language development is one of the essential features in autism. Therefore, we analyzed the allelic distribution of the DYX1C1 gene by family-based association method in 100 Finnish autism families. No evidence for association was observed with any intragenic marker or with haplotypes constructed from alleles of several adjacent markers. No evidence for deviated allelic diversity was either observed: the frequency of expected dyslexia risk haplotype was comparable to its frequency in Finnish controls. Thus it seems unlikely that DYX1C1 gene would be involved in the genetic etiology of autism in Finnish patients. C1 Natl Publ Hlth Inst, Biomedicum Helsinki, Dept Mol Med, Helsinki 00290, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Karolinska Inst, Novum, Clin Res Ctr, Dept Biosci, Huddinge, Sweden. Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. HUSLAB, Mol Genet Lab, Helsinki, Finland. RP Ylisaukko-oja, T (reprint author), Natl Publ Hlth Inst, Biomedicum Helsinki, Dept Mol Med, Haartmaninkatu 8, Helsinki 00290, Finland. EM tero.ylisaukko-oja@ktl.fi RI Kere, Juha/A-9179-2008; Jarvela, Irma/L-5836-2013 OI Kere, Juha/0000-0003-1974-0271; CR Alarcon M, 2002, AM J HUM GENET, V70, P60, DOI 10.1086/338241 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 BAILEY A, 1995, PSYCHOL MED, V25, P63 Bartlett CW, 2002, AM J HUM GENET, V71, P45, DOI 10.1086/341095 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Bradford Y, 2001, AM J MED GENET, V105, P539, DOI 10.1002/ajmg.1497 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 Gauthier J, 2003, AM J MED GENET A, V118A, P172, DOI 10.1002/ajmg.a.10105 Grigorenko EL, 1997, AM J HUM GENET, V60, P27 Grigorenko EL, 2003, P NATL ACAD SCI USA, V100, P11190, DOI 10.1073/pnas.2134926100 Grigorenko EL, 2002, J AUTISM DEV DISORD, V32, P3, DOI 10.1023/A:1017995805511 Horvath S, 2001, EUR J HUM GENET, V9, P301, DOI 10.1038/sj.ejhg.5200625 Bailey A, 1998, HUM MOL GENET, V7, P571 Palferman S, 2001, HUM MOL GENET, V10, P973 Jurinke Christian, 2002, Methods Mol Biol, V187, P179 Kaminen N, 2003, J MED GENET, V40, P340, DOI 10.1136/jmg.40.5.340 Lai CSL, 2001, NATURE, V413, P519, DOI 10.1038/35097076 Lai CSL, 2000, AM J HUM GENET, V67, P357, DOI 10.1086/303011 Lake SL, 2000, AM J HUM GENET, V67, P1515, DOI 10.1086/316895 Morris DW, 2000, HUM MOL GENET, V9, P843, DOI 10.1093/hmg/9.5.843 Newbury DF, 2002, AM J HUM GENET, V70, P1318, DOI 10.1086/339931 Nopola-Hemmi J, 2000, J MED GENET, V37, P771, DOI 10.1136/jmg.37.10.771 O'Brien EK, 2003, AM J HUM GENET, V72, P1536, DOI 10.1086/375403 Peltonen L, 2000, NAT REV GENET, V1, P182, DOI 10.1038/35042049 Schulte-Korne G, 1998, AM J HUM GENET, V63, P279, DOI 10.1086/301919 Shao YJ, 2002, AM J HUM GENET, V70, P1058, DOI 10.1086/339765 SHAYWITZ SE, 1998, NEW ENGL J MED, V338, P30 Newbury DF, 2002, AM J HUM GENET, V70, P384 Taipale M, 2003, P NATL ACAD SCI USA, V100, P11553, DOI 10.1073/pnas.1833911100 Turkeltaub PE, 2004, NEURON, V41, P11, DOI 10.1016/S0896-6273(03)00803-1 VEENSTRAVANDERW.J, 2004, MOL PSYCHIAT 0616 Wassink TH, 2002, AM J MED GENET, V114, P566, DOI 10.1002/ajmg.10415 World Health Organisation (WHO), 1993, INT CLASS DIS NR 35 TC 7 Z9 7 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PD JAN PY 2005 VL 13 IS 1 BP 127 EP 130 DI 10.1038/sj.ejhg.5201272 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 880EV UT WOS:000225772700019 PM 15470369 ER PT J AU Broussolle, P AF Broussolle, P TI Clinical and practical aspects of the prevention of autism SO EVOLUTION PSYCHIATRIQUE LA French DT Book Review CR CRESPIN GC, 2004, ASPECTS CLIN PRATIQU NR 1 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JAN-MAR PY 2005 VL 70 IS 1 BP 196 EP 197 PG 2 WC Psychiatry SC Psychiatry GA 911RM UT WOS:000228022300021 ER PT J AU Schmitz, C van Kooten, LAJ Hof, PR van Engeland, H Patterson, PH Steinbusch, HWM AF Schmitz, C van Kooten, LAJ Hof, PR van Engeland, H Patterson, PH Steinbusch, HWM TI Autism: Neuropathology, alterations of the GABAergic system, and animal models SO GABA IN AUTISM AND RELATED DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID GAMMA-AMINOBUTYRIC-ACID; BORNA-DISEASE-VIRUS; RECEPTOR SUBUNIT GENES; GABA-A RECEPTORS; RAT SPINAL-CORD; MENTAL-RETARDATION; BRAIN-DEVELOPMENT; NERVOUS-SYSTEM; TANGENTIAL MIGRATION; CORTICAL DEVELOPMENT AB Autism is a neurodevelopmental disorder with a strong genetic component and several known environmental risk factors. Neuropathological studies have shown consistent abnormalities in the limbic system, cerebellum, and cerebral cortex. Several findings suggest a role for the GABAergic system in autism neuropathology. There are reports of elevated plasma GABA levels, reduction of the GABAergic system enzymes, and decreased availability of GABA in autistic patients. Autism has a reported heritability of 60-90%. Abnormalities in the 15q11-13 region have been found in autistic people, and the GABA(A) receptor genes are located in this region. In addition, GABA dysfunction may occur in coni unction with Reelin. Abnormalities in the gene encoding for Reelin have been implicated in autism, and Reelin and GABA play an important role in the development of minicolumns. Compared to controls, minicolumns are more numerous, smaller, and less compact in autistic patients. Several studies provided evidence for the role of GABA receptors in tangential migration of neurons. Furthermore, GABA regulates cell proliferation in some brain regions. Because the underlying causes of the reduced GABA system function in autism are not well understood, it is important to develop animal models of autism, which can give more insights into the neuropathology and behavioral aspects of the disease. Animal models of autism include misregulation of genes implicated in the disorder, as well as the use of known environmental risk factors. In the future, investigation of human autism tissues and animal models, in combination With implementation of new techniques such as design-based stereology and gene expression, may result in the elucidation of the etiology of autism. C1 Maastricht Univ, Div Cellular Neurosci, Dept Psychiat & Neuropsychol, NL-6100 MD Maastricht, Netherlands. Univ Utrecht, Ctr Med, Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, NL-3508 GA Utrecht, Netherlands. EURON, NL-6200 MD Limburg, Netherlands. Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA. CALTECH, Div Biol, Pasadena, CA 91125 USA. RP Schmitz, C (reprint author), Maastricht Univ, Div Cellular Neurosci, Dept Psychiat & Neuropsychol, NL-6100 MD Maastricht, Netherlands. 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signaling in the developing cerebellum SO GABA IN AUTISM AND RELATED DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID SUBUNIT MESSENGER-RNAS; RECEPTOR ALPHA-6 SUBUNIT; AFFINITY GABA-RECEPTORS; CULTURED HIPPOCAMPAL-NEURONS; GLUTAMIC-ACID DECARBOXYLASE; CENTRAL-NERVOUS-SYSTEM; REELER MUTANT MOUSE; K-CL COTRANSPORTER; GRANULE CELLS; RAT-BRAIN AB In the adult central nervous system (CNS), gamma-amino butyric acid (GABA) is the predominant inhibitory neurotransmitter, and it regulates glutamatergic activity. Recent studies have revealed that GABA serves as an excitatory transmitter in the immature CNS, and acts as a trophic factor For brain development. Furthermore, normal formation of GABAergic synapses is crucial for the expression of higher brain functions such as memory, learning, and motor coordination, and various psychiatric diseases such as anxiety disorders, epilepsy, schizophrenia, and autism are partly caused by the dysfunction of GABA in the developing and mature brain. These results indicate that the GABAergic roles change developmentally with special references to alterations in GABAergic transmission and signaling, and that GABA plays various roles in the expression of almost all brain functions. We morphologically investigated the developmental changes in the GABAergic transmission system and the key factors for the formation of GABAergic synapses and networks. Here, we focus on the cerebellar cortex, which provides an ideal system for the investigation of brain development, and review four points: (1) The GABAergic system in the adult cerebellum, (2) GABAergic signaling before synaptogenesis-the mechanisms by which GABA exerts its effect on developing neurons, (3) Formation of GABAergic synapses-mechanisms underlying formation of functional GABAergic synapses, and (4) Functions of GABAergic synapses. C1 Hokkaido Univ, Sch Med, Dept Mol Neuroanat, Sapporo, Hokkaido 0608638, Japan. RP Takayama, C (reprint author), Hokkaido Univ, Sch Med, Dept Mol Neuroanat, Sapporo, Hokkaido 0608638, Japan. 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LHRH neurons in the hypothalamus of female rhesus monkeys are already active during the neonatal period, but subsequently enter a dormant state in the juvenile/prepubertal period because of an elevated level of GABA in the stalk-median eminence (S-ME). The developmental reduction in tonic GABA inhibition results in an increase in LHRH release in the S-ME, triggering puberty. The reduction in GABA also appears to allow all increase in glutamate release in the S-ME and this glutamate seems to further contribute to the pubertal increase in LHRH release. These observations conducted in nonhuman primates, as a model for humans, provide sonic insights into future studies of the importance of GABAergic mechanisms in the relation between onset of puberty and neurodevelopmental disorders including autism. C1 Univ Wisconsin, Dept Pediat, Madison, WI 53715 USA. Univ Wisconsin, Wisconsin Natl Primate Res Ctr, Madison, WI 53715 USA. 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Rev. Neurobiol. PY 2005 VL 71 BP 113 EP 129 DI 10.1016/S0074-7742(05)71005-9 PG 17 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA BDS43 UT WOS:000235180000005 PM 16512348 ER PT J AU LaSalle, JM Hogart, A Thatcher, KN AF LaSalle, JM Hogart, A Thatcher, KN TI Rett syndrome: A Rosetta stone for understanding the molecular pathogenesis of autism SO GABA IN AUTISM AND RELATED DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID CPG-BINDING-PROTEIN; X-CHROMOSOME INACTIVATION; PRADER-WILLI-SYNDROME; AMINOBUTYRIC-ACID RECEPTOR; ANGELMAN-SYNDROME GENE; ACTIVE CHROMATIN HUB; LINKAGE-DISEQUILIBRIUM; DNA METHYLATION; GABA(A) RECEPTOR; IMPRINTING CENTER AB Autism is a common but complex disorder, showing high heritability but elusive genetic etiology. One approach to "deciphering" the etiology of autism is to investigate overlapping pathways with other autism spectrum-disorders with known genetic causes. Rett syndrome, an X-linked disorder caused by Mutations in MECP2, and Angelman syndrome, an imprinted disorder caused by maternal 15q11-13 deficiency, share many features with autism. Furthermore, maternal 15q11-13 duplications in autism and rare MECP2 mutations in autism and Angelman syndrome point to genetic overlap between these three disorders. Recent studies on human postmortem brain samples and Mecp2-deficient mouse models have demonstrated overlapping pathways in the molecular pathogenesis of these disorders. Although originally described as a transcriptional repressor of methylated genes, new roles for MeCP2 in chromatin organization have recently emerged. In addition, the recent demonstration of MeCP2 as a regulator of both UBE3A (the Angelman gene) and GABRB3 (encoding a GABA(A) receptor subunit) expression within 15q11-13 has revealed some interesting insights into the genetic and epigenetic pathways common to all three disorders. The discovery of mutations in MECP2, the gene encoding methyl-CpG binding protein 2, as the cause of Rett syndrome (RTT) in 1999 (Amir et al., 1999) has opened up an entirely new line Of investigations about the role of DNA methylation and chromatin in the development of the mammalian brain. Furthermore, of the five pervasive developmental disorders (PDD) subtypes, including autistic disorder, RTT, Asperger disorder, disintegrative disorder, and PDD Not Otherwise Specified (PDD-NOS), RTT is the only one with a known genetic cause (Zoghbi, 2003). Could the emerging information from the rapidly progressing field of MeCP2 research therefore be applied to autism in a "Rosetta Stone" approach to understanding the complex genetics of autism? The Rosetta stone was a small but significant stone tablet containing the same message written in Greek and two different Egyptian scripts that was essential to deciphering Egyptian hieroglyphics. 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ER PT J AU Blatt, GJ AF Blatt, GJ TI GABAergic cerebellar system in autism: A neuropathological and developmental perspective SO GABA IN AUTISM AND RELATED DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID INFERIOR OLIVARY COMPLEX; COGNITIVE-AFFECTIVE SYNDROME; OLIVOCEREBELLAR PROJECTION; CEREBROCEREBELLAR SYSTEM; INFANTILE-AUTISM; POPULATION; DISORDER; CHILDREN; THOUGHT; BRAIN AB Alterations in the GABAergic system in autism only recently became evident affecting specific receptors in die hippocampus, GAD protein levels in parietal cortex and cerebellum and a decreased number of GABAergic Purkinje cells evident in a subset of autistic cases. A candidate gene for the GABA-A beta 3 subunit has remained attractive on the chromosome 15q11-q13 region in a subset of individuals. Current Studies are revealing valuable data toward understanding how cerebellar circuitry may be altered in autism as better markers and techniques become available. In particular, immunostaining of Purkinje cells demonstrated that previous Nissl studies may have overlooked agonal effects on the efficacy of tissue sections bringing into question results of previous Studies, sonic of which also did not control for age. It appears that: the cerebellum in autism shows variability in neuropathology similar to that described for other affected brain areas in autism. Decreased Purkinje cells arc present in about half of cases in the posterior lateral cerebellar cortex yet normal cytoarchitecture persists throughout the cerebellum indicating completion of migration of both Purkinje cell and granule cell populations. 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Reelin mutations or deficiency of the protein product could cause abnormal cortical development and/or Reelin-induced signal transduction impairment in brain. Reelin abnormalities in several neuropsychiatric disorders, such as autism and schizophrenia, may provide mechanistic explanations for etiologies of these disorders. C1 Univ Minnesota, Sch Med, Dept Psychiat, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Minneapolis, MN 55455 USA. 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SO GABA IN AUTISM AND RELATED DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID GAMMA-AMINOBUTYRIC-ACID; INVERTED DUPLICATED CHROMOSOME-15; BENZODIAZEPINE-RECEPTOR-BINDING; MATERNAL UNIPARENTAL DISOMY; PLASMA GABA; CEREBROSPINAL-FLUID; DEPRESSED-PATIENTS; ANGELMAN-SYNDROME; SUBUNIT GENE; ELECTROCONVULSIVE-THERAPY AB Research advances in autism, Prader-Willi syndrome, and catatonia allow new inferences about their mutual relations. Catatonia has been described in both people with autism and Prader-Willi syndrome, but remains unaccounted. Although autism and Prader-Willi syndrome have been considered entities In their own right, clinlical observations suggest common ground and point to GABA dysfunction as a putative shared risk factor. The knowledge base on GABA abnormalities in autism, Prader-Willi syndrome, and catatonia is limited but expanding, and is summarized in this chapter. 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English DT Review ID ANGIOTENSIN-II AT(1); RECEPTOR SUBUNIT EXPRESSION; INFLAMMATORY BOWEL-DISEASE; PLACEBO-CONTROLLED TRIAL; NITRIC-OXIDE PRODUCTION; CEREBRAL-BLOOD-FLOW; MATERNAL-BEHAVIOR; PANCREATIC-SECRETION; DEPENDENT MECHANISM; CROHNS-DISEASE AB The long-term goal of our work is to create a novel treatment for autism and to explain its pathogenesis. Based on a theory that views emotions and emotional behavior as stemming from dysregulations of a unified brain/gut network, we propose a new paradigm for the treatment of mental illness. This chapter reviews evidence that two neuropeptides, secretin and oxytocin, are critical in the conditioning OF infant adaptive behavioral patterns and that peptidergic mechanisms are abnormal in developmental disorders such as autism. Our clinical observations in the treatment of autism justify our laboratory investigations into the role of peptides in the neurological manifestations of visceral diseases encompassing emotional/visceral brain regions abnormal in autism. Importantly, our studies have thus far demonstrated that (1) visceral inflammation activates visceral/emotional brain regions in areas known to be abnormal in autism; (2) secretin, like oxytocin, activates many of the same visceral/emotional brain regions that are dysregulated in chronic cerebral and visceral disorders such as autism; (3) a structural basis for the mechanisms of action of secretin and oxytocin was clarified; (4) secretin as well as oxytocin is synthesized in the hypothalamus and may act on structures involved in the pathophysiology of autism; (5) secretin and oxytocin localize to perivascular and subependymal regions of the paraventricular hypothalamus, suggesting a chemosensory and secretory function. We believe autism is the result of an adverse cascade of events that sterns From one or more genetic/environmental insults. Over time, if uncompensated, the cascade leads to adverse conditioning of stress adaptation networks and results ill various interrelated developmental psychological, neurological and immunological pathology, including autism. Our laboratory is engaged in efforts to translate clinical experience in the treatment of autistic patients into bench findings. We believe that it is possible, regardless of etiology, to treat autism and related developmental disorders by intervening in stress response mechanisms With exogenous administration of peptide combinations. C1 Columbia Univ, Coll Phys & Surg, Div Neurosci, Dept Psychiat, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Dept Anat & Cell Biol, New York, NY 10032 USA. RP Welch, MG (reprint author), Columbia Univ, Coll Phys & Surg, Div Neurosci, Dept Psychiat, New York, NY 10032 USA. 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The current diagnostic classification system, the DSM-IV-TR, includes the presence of stereotypical behaviors of interest in its criteria for autism. Rescarch suggests that as many as 85% of children with autism exhibit relative behaviors or mannerisms. However, stereotypical behaviors are not specific to autism and are associated with other disorders such as Tourette's syndrome, schlzophrenia, and mental retardation. Although the DSM-IV-TR criteria for stereotypical behaviors, as outlined in the diagnostic criteria for autistic disorder, focuses on motor symptoms that tend to occur in excess (e.g., twirling, spinning, head-banging), a broader conceptualization of the types of motor abnormalities observed in individuals with autism has been proposed more recently. Stereotyped patterns of behavior include not only excessive atypical movement but also the loss of typical movement (e.g., catatonia) in this broader definition. support for this definition is evidenced by both clinical observations and empirical research. Research examining the overlap between catatonia and other stereotypic behaviors among individuals with autism suggest that the greatest risk for catatonic behaviors occurs in adolescence and may be precipitated by stressful events. Assessment tools for autism often include some measure of stereotyped behaviors and interest, but the presence of stereotypy is not in and of itself a pathiognomonic sign of autism. Focusing primarily on the presence of classic stereotypical behaviors in diagnoses may subsequently lead to overidentifying autism in very young or mentally retarded individuals. A number of theories have been proposed over the years to explain the function and etiology of stereotypical behaviors. Lovaas and his colleagues, for example, proposed that the sensory and perceptual stimuli created through repetitive behaviors may be self stimulating. Others suggest that stereotypical behaviors are maintained by socially mediated positive and negative reinforcers; whereas biological theories focus on dysfunctions in the serotonin, opioid, and dopaminergic systems in the brain. C1 Univ Mississippi, Ctr Med, Dept Psychiat, Jackson, MS 39216 USA. Univ So Mississippi, Dept Psychol, Hattiesburg, MS 39406 USA. RP Stoppelbein, L (reprint author), Univ Mississippi, Ctr Med, Dept Psychiat, Jackson, MS 39216 USA. 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A number of genes have been identified within this region including a cluster of gamma-amino butyric acid type A receptor subunit genes, GABRB3, GABRA5, and GABRG3 (encoding the beta(3), alpha(5), and gamma(3) subunits, respectively). Numerous studies have demonstrated the importance of the GABAergic system in neurodevelopment; therefore the presence of a group of GABA(A) receptor genes within the locus is intriguing. The beta(3) subunit is widely expressed during the late embryonic to early postnatal period of brain development. A deficiently in the beta(3) subunit during this critical period would be expected to negatively impact the temporal ordering of neurogenesis and synaptogenesis. This would have subsequent ramifications in the maturation of circuts involved in supporting complex behaviours, motors skills, and cognition. As expected, mice deficient in the gabrb3 gene exhibit a wide assortment of neurochemical, electrophysiological, and behavioral abnormalities, many overlapping with traits typically observed in autism spectrum disorder and Angelman syndrome. These findings suggest a potential involvement of the GABRB3 gene in the etiology of these neurodevelopmental disorders. The gabrb3 gene deficient mouse has proved to be a valuable model in the critical examination of the interconnection between development, pathology, and behaviour as they relate to disorders of neurodevelopment. C1 Mol Res Inst, Mountain View, CA 94043 USA. RP Delorey, TM (reprint author), Mol Res Inst, Mountain View, CA 94043 USA. 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CORRELATIONS; SEROTONIN TRANSPORTER 5-HTT; GENETIC RISK-FACTORS; LINKAGE-DISEQUILIBRIUM; PERIODIC CATATONIA; SCHIZOPHRENIA SUSCEPTIBILITY; DYSBINDIN GENE AB We have compiled significant results from 53 genome scans for five different mental disorders Including autism syndrome disorder (ASD), schizophrenia (SZ) and catatonia, bipolar disorder (BP), attention-deficit/hyperactivity disorder (ADHD), and alcoholism. Eight autosomal chromosomes (1, 2, 3, 7, 9, 13, 15, and 17) showed significant linkages with ASD while five of these chromosomes (1, 7, 13, 15, and 17) shared common susceptibility loci with other mental disorders mostly SZ and BP. Chromosome 15 is particularly rich in shared regions, three to four being detected where all four other mental disorders are involved in one or the other of these regions. Chromosome 15 is a particularly unstable chromosome where numerous chromosomal rearrangement and abnormalities have been associated with ASD. Strong candidate genes such as gamma-amino-butyric acid (GABA) receptor B3, A5, and G3 have shown associations with ASD on this chromosome. Some susceptibility loci for different mental disorders have also been assigned to chromosome 15 such as schizophrenia 10, major depressive disorder 2, dyslexia 1, epilepsy.) juvenile myotonic 2, and spinocerebellar ataxia 11. 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V120B, P47, DOI 10.1002/ajmg.b.20037 Yirmiya N, 2001, AM J MED GENET, V105, P381, DOI 10.1002/ajmg.1365 Ylisaukko-oja T, 2004, MOL PSYCHIATR, V9, P161, DOI 10.1038/sj.mp.4001385 Zhong N, 1999, NEUROGENETICS, V2, P129, DOI 10.1007/s100480050064 Zinn-Justin A, 1999, GENET EPIDEMIOL, V17, pS421 NR 147 TC 8 Z9 8 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2005 VL 71 BP 419 EP 443 DI 10.1016/S0074-7742(05)71017-5 PG 25 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA BDS43 UT WOS:000235180000017 PM 16512360 ER PT S AU Francis, P Firth, L Mellor, D AF Francis, P Firth, L Mellor, D BE Costabile, MF Paterno, F TI Reducing the risk of abandonment of assistive technologies for people with autism SO HUMAN-COMPUTER INTERACTION - INTERACT 2005, PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT International Conference on Human-Computer Interaction CY SEP 12-16, 2005 CL Rome, ITALY SP Soc Gen Informat SPA, Microsoft Res, SAP, AICA, PHILIP, NOKIA, Sriabs, ERCIM, Inst Sci Technol Informat FAEDO, Univ Barensis Sigillum, La Sapienza AB This paper reports on an investigation that found that conventional techniques for including users in technology design are likely to fail if the user has autism. The heterogeneity of autistic symptomatology across cognitive, social, behavioural and communication domains suggests a 'single user' environment, while rendering typical design interaction techniques meaningless, making the need for assistive technologies great, and the risk of abandonment high. This complex problem of urgency and constraint was addressed through a Delphi study with a panel of psychologists critiquing design activities for people with autism. The major finding is that while each of the activities may work if modified, all require that the designer is well acquainted with autism in general and has a close working relationship based on trust with the individual user. If these requirements are met, there is no reason that the abandonment rate cannot be reduced. C1 Univ Melbourne, Dept Informat Syst, Parkville, Vic 3052, Australia. Deakin Univ, Dept Psychol, Geelong, Vic 3217, Australia. 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We tested for linkage in a candidate region on chromosome 3q25 27 first identified in Finnish autism families [ 1]. The peak in this previous study was at D3S3037 ( 183.9 cM). We tested this region in seven affected family members and 24 of their relatives from a single large extended Utah pedigree of Northern European ancestry. A total of 70 single nucleotide polymorphisms ( SNPs) were analyzed from 165 to 204 cM. The maximum NPL-all nonparametric score using SimWalk2snp was 3.53 ( empirical p value = 0.0003) at 185.2 cM ( SNP rs1402229), close to the Finnish peak. A secondary analysis using MCLINK supported this result, with a maximum of 3.92 at 184.6 cM ( SNP rs1362645). We tested for alterations in a candidate gene in this region, the fragile X autosomal homolog, FXR1. No variants likely to contribute to autism were found in the coding sequence, exon-intron boundaries, or the promoter region of this gene. 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Hered. PY 2005 VL 60 IS 4 BP 220 EP 226 DI 10.1159/000090546 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 010QC UT WOS:000235208200005 PM 16391490 ER PT J AU Andreae, MC Freed, GL Katz, SL AF Andreae, Margie C. Freed, Gary L. Katz, Samuel L. TI Safety Concerns Regarding Combination Vaccines Perspective of Select European Countries SO HUMAN VACCINES LA English DT Review DE autism; combination vaccines; immunization policy; MMR; safety AB This study explored health officials' perception of parental concern regarding the safety of combination vaccines and its impact on policy decisions in different European countries. Interviews were conducted with governmental and nongovernmental health officials in the United Kingdom, France, Ireland and Sweden over a four-month period. Parental concern regarding the safety of combination vaccines was perceived to be prevalent in the United Kingdom, Ireland and Sweden while no such concern was evident in France. 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Vaccines PD JAN PY 2005 VL 1 IS 1 BP 1 EP 5 DI 10.4161/hv.1.1.1422 PG 5 WC Biotechnology & Applied Microbiology; Immunology SC Biotechnology & Applied Microbiology; Immunology GA V19ZR UT WOS:000208110800001 PM 17038825 ER PT J AU Demir, SS AF Demir, SS TI Talking to the autism community SO IEEE ENGINEERING IN MEDICINE AND BIOLOGY MAGAZINE LA English DT Editorial Material NR 0 TC 0 Z9 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 0739-5175 J9 IEEE ENG MED BIOL JI IEEE Eng. Med. Biol. Mag. PD JAN-FEB PY 2005 VL 24 IS 1 BP 14 EP + DI 10.1109/MEMB.2005.1384093 PG 3 WC Engineering, Biomedical; Medical Informatics SC Engineering; Medical Informatics GA 888IC UT WOS:000226366400005 ER PT J AU Carpenter, M Tomasello, M Striano, T AF Carpenter, M Tomasello, M Striano, T TI Role reversal imitation and language in typically developing infants and children with autism SO INFANCY LA English DT Article ID INTENTIONS; GESTURES; GOALS; GAMES AB Three types of role reversal imitation were investigated in typically developing 12-and 18-month-old infants and in children with autism and other developmental delays. Many typically developing infants at both ages engaged in each of the 2 types of dyadic, body-oriented role reversal imitation: self-self reversals, in which the adult acted on herself and the child then acted on himself, and other-other reversals. in which the adult acted on the child and the child then acted back on the adult. However, 12-month-olds had more difficulty than 18-month-olds with triadic, object-mediated role reversals involving interactions around objects. There was little evidence of any type of role reversal imitation in children with autism. Positive relations were found between role reversal imitation and various measures of language development for 18-month-olds and children with autism. C1 Max Planck Inst Evolutionary Anthropol, D-04103 Leipzig, Germany. RP Carpenter, M (reprint author), Max Planck Inst Evolutionary Anthropol, Deutsch Pl 6, D-04103 Leipzig, Germany. EM carpenter@eva.mpg.de CR Behne T, 2005, DEV PSYCHOL, V41, P328, DOI 10.1037/0012-1649.41.2.328 Bekkering H, 2000, Q J EXP PSYCHOL-A, V53, P153, DOI 10.1080/027249800390718 Bellagamba F, 1999, INFANT BEHAV DEV, V22, P277, DOI 10.1016/S0163-6383(99)00002-8 Brown J. 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Data from a recent study of young children with autism suggests that performance on a delay nonmatch to sample (DNMS) task associated with ventromedial prefrontal functions, but not an A-not-B/delayed response task associated with dorsolateral prefrontal cortex, was related to joint attention skills (Dawson et al., 2002). Recent research also suggests that joint attention is associated with dorsalmedial brain systems linked to self-monitoring (Mundy, 2003). This study investigated the relations among joint attention, DNMS, and self-recognition performance in a longitudinal study of 39 normally developing toddlers from 14 to 18 months. The results indicated that development on the DNMS and self-recognition tasks, but not a means end task, predicted joint attention at 18 months. Further analysis showed that the model was only significant for initiating joint attention (IJA). The implications of these results for the neuro-development of IJA are discussed. C1 Univ Maryland, Dept Human Dev, College Pk, MD 20742 USA. Univ Miami, Dept Psychol, Miami, FL 33152 USA. RP Nichols, KE (reprint author), Univ Maryland, Dept Human Dev, College Pk, MD 20742 USA. 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The system, based on the Story-Table developed by IRST-itc, is aimed at supporting a group of children in the activity of storytelling. The system is based on a unique multi-user touchable device (the MERL Diamond Touch) designed with the purpose of enforcing collaboration between users. The instructions were simplified in order to allow children with communication disabilities to learn and operate the story table. First pilot results are very encouraging. The children were enthusiastic about communicating through the ST and appeared to be able to learn to operate it with little difficulty. C1 Univ Haifa, LIRT, Har Hakarmel, Israel. IRST, ITC, I-38050 Trento, Italy. Bar Ilan Univ, Sch Educ, Ramat Gan, Israel. RP Gal, E (reprint author), Univ Haifa, LIRT, Har Hakarmel, Israel. EM egal@univ.haifa.ac.il; gorenbar@itc.it; gazit@cri.haifa.ac.il; bauminn@biu.ac.il; cappelle@itc.it; pianesi@itc.it; stock@itc.it; zancana@itc.it; stock@itc.it CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT BARONCOHEN S, 1999, AUTISM FACTS CAPPELLETTI A., 2004, P INT C ADV LEARN TE DIETZ P. H., 2001, P ACM S US INT SOFTW ZANCANARO M., 2003, P INT C US INT SOFTW NR 5 TC 8 Z9 8 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-30509-2 J9 LECT NOTES COMPUT SC PY 2005 VL 3814 BP 320 EP 323 PG 4 WC Computer Science, Artificial Intelligence SC Computer Science GA BDU60 UT WOS:000235474700043 ER PT S AU Grynszpan, O Martin, JC Nadel, J AF Grynszpan, O Martin, JC Nadel, J BE Panayiotopoulos, T Gratch, J Aylett, R Ballin, D Olivier, P Rist, T TI Using facial expressions depicting emotions in a human-computer interface intended for people with autism SO INTELLIGENT VIRTUAL AGENTS, PROCEEDINGS SE LECTURE NOTES IN ARTIFICIAL INTELLIGENCE LA English DT Article; Proceedings Paper CT 5th International Working Confernece on Intelligent Virtural Agents CY SEP 12-14, 2005 CL Kos, GREECE SP Univ Piraeus Res Ctr, AgentLink, Hellen Artificial Intelligence Soc, Medicon SA, Focus Magazine C1 CNRS, LIMSI, F-91403 Orsay, France. Hop La Pitie Salpetriere, CNRS, UMR 7593, F-75013 Paris, France. RP Grynszpan, O (reprint author), CNRS, LIMSI, BP 133, F-91403 Orsay, France. EM ouriel@limsi.fr; martin@limsi.fr; jnadel@ext.jussieu.fr NR 0 TC 0 Z9 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-28738-8 J9 LECT NOTES ARTIF INT PY 2005 VL 3661 BP 489 EP 489 PG 1 WC Computer Science, Artificial Intelligence; Computer Science, Cybernetics SC Computer Science GA BDA48 UT WOS:000232267200041 ER PT J AU Mutter, J Naumann, J Sadaghiani, C Walach, H Drasch, G AF Mutter, J Naumann, J Sadaghiani, C Walach, H Drasch, G TI Mercury and autism: Response to the letter of K. E. V. Muhlendahl [Int. J. Hyg. Environ. Health 208 (2005) 435] SO INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH LA English DT Letter ID THIMEROSAL; AMALGAM C1 Univ Hosp, Inst Environm Med & Hosp Epidemiol, D-79106 Freiburg, Germany. European Off, Samueli Inst, Freiburg, Germany. Univ Munich, Inst Forens Med, Munich, Germany. RP Mutter, J (reprint author), Univ Hosp, Inst Environm Med & Hosp Epidemiol, Hugstetter Str 55, D-79106 Freiburg, Germany. EM joachim.mutter@uniklinik-freiburg.de CR ADAMS J, 2004, DEF AUT NOW C DAN 1 *BFARM, 2003, AM ZAHN THER GASSET AR, 1975, ARCH OPHTHALMOL-CHIC, V93, P52 GRANDJEAN P, 1995, NEUROTOXICOLOGY, V16, P27 Holmes AS, 2003, INT J TOXICOL, V22, P277, DOI 10.1080/10915810390220054 Hu LW, 2003, T AM NUCL SOC, V89, P681 *LIF SCI RES OFF, 2004, REV AN LIT HLTH EFF MEISTER A, 1995, METHOD ENZYMOL, V251, P3 Mutter J, 2005, GESUNDHEITSWESEN, V67, P204, DOI 10.1055/s-2005-857962 Mutter J, 2004, INT J HYG ENVIR HEAL, V207, P391, DOI 10.1078/1438-4639-00305 Nelson KB, 2003, PEDIATRICS, V111, P674, DOI 10.1542/peds.111.3.674 von Muhlendahl K. E., 2004, INT J HYG ENVIR HEAL, V207, P391 NR 12 TC 5 Z9 5 PU URBAN & FISCHER VERLAG PI JENA PA BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY SN 1438-4639 J9 INT J HYG ENVIR HEAL JI Int. J. Hyg. Environ. Health. PY 2005 VL 208 IS 5 BP 437 EP 438 DI 10.1016/j.ijheh.2005.06.001 PG 2 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA 970AC UT WOS:000232276600013 ER PT J AU Botting, N Adams, C AF Botting, N Adams, C TI Semantic and inferencing abilities in children with communication disorders SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE semantic; inference; assessment; language impairment; communication disorders ID LANGUAGE IMPAIRMENT; YOUNG-CHILDREN; CHECKLIST CCC; COMPREHENSION; AUTISM; REPRESENTATION; CLASSIFICATION; KNOWLEDGE; SCORES; SLI AB Background: Semantic and inferencing abilities have not been fully examined in children with communication difficulties. Aims: To investigate the inferential and semantic abilities of children with communication difficulties using newly designed tasks. Methods & Procedures: Children with different types of communication disorder were compared with each other and with three groups of typically developing children: those of the same chronological age and two groups of younger children. In total, 25 children aged 11 years with specific language impairment and 22 children, also 11 years of age, with primary pragmatic difficulties were recruited. Typically developing groups aged 11 (n = 35: age-match). and those aged 9 (n = 40) and 7 (n = 37; language similar) also participated as comparisons. Outcomes & Results: For Semantic Choices, children with specific language impairment performed significantly more poorly than 9- and 11 -year-olds, whilst the pragmatic difficulties group scored significantly lower than all the typically developing groups. Borderline differences between specific language impairment and pragmatic difficulties groups were found. For inferencing, children with communication impairments performed significantly below the 11-year-old peers, but not poorer than 9- and 7-year-olds, suggesting that this skill is in fine with language ability. Six children in the pragmatic difficulties. group who met diagnosis for autism performed more poorly than the other two clinical groups on both tasks, but not statistically significantly so. Conclusions: Both tasks were more difficult for those with communication impairments compared with peers. Semantic but not inferencing abilities showed a non-significant trend for differences between the two clinical groups and children with pragmatic difficulties performed more poorly than all typically developing groups. The tasks may relate to each other in varying ways according to type of communication difficulty. C1 Univ Manchester, Sch Educ, Manchester M13 9PL, Lancs, England. RP Botting, N (reprint author), Univ Manchester, Sch Educ, Oxford Rd, Manchester M13 9PL, Lancs, England. 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PD JAN-MAR PY 2005 VL 40 IS 1 BP 49 EP 66 DI 10.1080/13682820410001723390 PG 18 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 890OF UT WOS:000226520000003 PM 15832525 ER PT J AU Jayachandra, S AF Jayachandra, S TI Is secretin effective in treatment for autism spectrum disorders (ASD)? SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Letter ID PERVASIVE DEVELOPMENTAL DISORDER; CHILDREN C1 Monash Univ, Dept Med Biosci, Petaling Jaya 46150, Selangor, Malaysia. RP Jayachandra, S (reprint author), Monash Univ, Dept Med Biosci, 2 Jalan Kolej,Bandar Sunway, Petaling Jaya 46150, Selangor, Malaysia. EM sjayacha@monash.edu.my CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Kern JK, 2002, J AUTISM DEV DISORD, V32, P153, DOI 10.1023/A:1015441428154 McQueen JM, 2002, ANN PHARMACOTHER, V36, P305 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Sponheim E, 2002, ACTA PAEDIATR, V91, P540, DOI 10.1080/080352502753711669 NR 8 TC 1 Z9 1 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 USA SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 2005 VL 35 IS 1 BP 99 EP 101 DI 10.2190/Q1D2-5DNB-V4FJ-J9M5 PG 3 WC Psychiatry SC Psychiatry GA 936PL UT WOS:000229867800008 PM 15977948 ER PT J AU Canitano, R Luchetti, A Zappella, M AF Canitano, R Luchetti, A Zappella, M TI Epilepsy, electroencephalographic abnormalities, and regression in children with autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT Meeting of the Mariani-Foundation on Development Neurosciences and Cognitive Phenotypes CY NOV 22-24, 2002 CL Portofino, ITALY SP Mariani Fdn ID LANDAU-KLEFFNER-SYNDROME; SPECTRUM DISORDERS; MENTAL-RETARDATION; SEIZURE DISORDERS; ADOLESCENTS; CHILDHOOD AB The association of epilepsy and autism is recognized, and it has been reported at a percentage that varies between 8 and 42%, depending on age and diagnostic criteria. One third of autistic children undergo a regression of language and behavior between 2 and 3 years, and epileptiform abnormalities and epilepsy can be concomitant in an undetermined percentage of them. The aim of this study was to investigate the prevalence of epilepsy and paroxysmal abnormalities in a group of children with autism and to determine the percentage of regression course in this group. Forty-six patients with autism (mean age 7.8 +/- 2.7 years; 34 boys and 12 girls) were consecutively examined, and clinical evaluation, assessment, and electroencephalographic (EEG) recordings were performed in all of them. Thirty-five percent showed paroxysmal abnormalities and epilepsy, 22% had only paroxysmal abnormalities without seizures, and 13% of the children suffered from epilepsy. Sixty-five percent had a normal EEG. No difference in regression rate was observed between patients with paroxysmal abnormalities and epilepsy and those with a normal EEG and without seizures. In the study group, the prevalence of epilepsy was in the low range of individuals with autism, and different types of epilepsy were observed. Autism with regression was not influenced by paroxysmal abnormalities and epilepsy. C1 Gen Univ Hosp Siena, Div Child Neuropsychiat, Siena, Italy. RP Canitano, R (reprint author), Gen Univ Hosp Siena, Div Child Neuropsychiat, Viale Bracci 1, Siena, Italy. EM canitano@unisi.it CR AICARDI J, 1994, EPILEPSY CHILDREN, P176 *AM PSYCHOL ASS, 1994, DIAGN STAT MAN MENT BAILEY A, 1995, PSYCHOL MED, V25, P63 BEAUMANOIR A, 1995, MARIANI FDN PAED NEU, P260 Commission on Classification and Terminology of the International League Against Epilepsy, 1989, EPILEPSIA, V30, P389 DEONNA T, 1991, J CLIN NEUROPHYSIOL, V8, P263 DEYKIN EY, 1979, AM J PSYCHIAT, V136, P1310 ELIA M, 1995, AM J MENT RETARD, V100, P6 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 GILLBERG C, 1991, J AUTISM DEV DISORD, V21, P61, DOI 10.1007/BF02206998 Rossi PG, 2000, BRAIN DEV-JPN, V22, P102 Gordon N, 1997, BRAIN DEV-JPN, V19, P311, DOI 10.1016/S0387-7604(97)00031-4 KANNER A, 2000, J AUTISM DEV DISORD, V20, P491 Kawasaki Y, 1997, J AUTISM DEV DISORD, V27, P605, DOI 10.1023/A:1025886228387 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 Mantovani JF, 2000, DEV MED CHILD NEUROL, V42, P349, DOI 10.1017/S0012162200210621 Mouridsen SE, 1999, DEV MED CHILD NEUROL, V41, P110, DOI 10.1017/S0012162299000213 Nass R, 1998, DEV MED CHILD NEUROL, V40, P453 OLSSON I, 1988, ARCH NEUROL-CHICAGO, V45, P666 Rapin I, 1995, Semin Pediatr Neurol, V2, P278, DOI 10.1016/S1071-9091(95)80007-7 ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 ROSSI PG, 1995, BRAIN DEV-JPN, V17, P169, DOI 10.1016/0387-7604(95)00019-8 Shinnar S, 2001, PEDIATR NEUROL, V24, P183 Steffenburg S, 1996, ARCH NEUROL-CHICAGO, V53, P904 Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 Tuchman R, 1991, PEDIATRICS, V6, P1219 TUCHMAN R, 1997, PEDIATRICS, V4, P560 Tuchman R, 2000, J AUTISM DEV DISORD, V30, P485, DOI 10.1023/A:1005572128200 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 WONG V, 1993, J CHILD NEUROL, V8, P313 NR 30 TC 68 Z9 68 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0883-0738 EI 1708-8283 J9 J CHILD NEUROL JI J. Child Neurol. PD JAN PY 2005 VL 20 IS 1 BP 27 EP 31 DI 10.1177/08830738050200010401 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 903HA UT WOS:000227415300005 PM 15791919 ER PT J AU Rice, SA Bigler, ED Cleavinger, HB Tate, DF Sayer, J McMahon, W Ozonoff, S Lu, J Lainhart, JE AF Rice, SA Bigler, ED Cleavinger, HB Tate, DF Sayer, J McMahon, W Ozonoff, S Lu, J Lainhart, JE TI Macrocephaly, corpus callosum morphology, and autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID WHITE-MATTER; ASPERGER-SYNDROME; SEX-DIFFERENCES; BRAIN VOLUME; MRI; ABNORMALITIES; CHILDREN; SPECTRUM; GROWTH; SIZE AB Although the cause of autism is undetermined, a general consensus has been that some type of early aberrant neural development underlies the disorder. Given the increased prevalence of macrocephaly in autism, one theory of abnormal neural development implicates early brain growth resulting in larger brain and head size in autism. Surface area measurements of the midsagittal section of the corpus callosum can be used as an index of neural development and white-matter integrity because the corpus callosum is the major white-matter structure that interconnects the two cerebral hemispheres. The purpose of this study was to obtain corpus callosum surface area, shape, and contour in a sample of non-mentally retarded autistic subjects with macrocephaly (n = 12) and compare them with those of matched (n = 8), typically developing control subjects with benign macrocephaly. No significant differences were found in surface area, shape, or contour between groups, nor did corpus callosum surface area relate to measures of IQ or picture vocabulary. These findings suggest no unique difference in overall regional corpus callosum surface area in autism with macrocephaly. C1 Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA. Brigham Young Univ, Dept Neurosci, Provo, UT 84602 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT USA. Univ Utah, Dept Radiol, Salt Lake City, UT USA. Brown Univ Training Consortium, Providence, RI USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. RP Rice, SA (reprint author), Brigham Young Univ, Dept Psychol, 1001 SWKT, Provo, UT 84602 USA. RI Tate, David/G-5166-2011 OI Tate, David/0000-0003-0213-1920 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Aylward EH, 2002, NEUROLOGY, V59, P175 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 Bailey DB, 2000, J AUTISM DEV DISORD, V30, P49 BARKOVICH AJ, 1988, AM J NEURORADIOL, V9, P487 BARKOVICH J, 1996, AM J NEURORADIOL, V17, P1643 BELMONTE M, 1995, NEUROREPORT, V6, P1253 Bigler ED, 2003, AM J NEURORADIOL, V24, P2066 Carpenter MB, 1983, HUMAN NEUROANATOMY Courchesne E, 2001, NEUROLOGY, V57, P245 COURCHESNE E, 1993, AM J ROENTGENOL, V160, P387 Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Courchesne E, 1999, NEUROLOGY, V52, P1057 DeLong GR, 1999, NEUROLOGY, V52, P911 Dunn L. 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Child Neurol. PD JAN PY 2005 VL 20 IS 1 BP 34 EP 41 DI 10.1177/08830738050200010601 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 903HA UT WOS:000227415300007 PM 15791921 ER PT J AU Yirmiya, N Shaked, M AF Yirmiya, N Shaked, M TI Psychiatric disorders in parents of children with autism: a meta-analysis SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autistic disorder; broad phenotype; behavioral genetics; meta-analysis; parents; psychiatric disorders ID DIAGNOSTIC OBSERVATION SCHEDULE; FAMILY HISTORY; LANGUAGE DISORDER; CHILDHOOD PSYCHOSES; COGNITIVE PHENOTYPE; INFANTILE-AUTISM; GENETICS; PERSONALITY; RELATIVES; SIBLINGS AB Background: The genetic basis of autism has received great attention during the last few years. The psychiatric status of parents of persons with autism has been studied as part of the broad phenotype of autism. Methods: In the current study we examined all studies in which psychiatric difficulties of parents of children with autism were compared to those of parents of other children, as part off the broad phenotype of autism. Results: Overall, when parents of children with autism were compared to all other parents taken together, i.e., parents of typically developing children grouped together with parents of children with diagnoses other than autism, they were found to have more psychiatric difficulties. but this finding was inconsistent. Once type of comparison group (e.g... Down Syndrome: learning disabilities) and method of assessing psychiatric difficulties (e.g... self-report, clinical measures) were taken into account, different findings were yielded for the various comparison groups and methods of assessing psychiatric difficulties in parents, suggesting that parents of children with autism present more psychiatric difficulties, mostly in comparisons involving samples of parents of children with no known genetic risk (e.g., Down Syndrome). Conclusions: These findings suggest that in future studies. researchers should carefully consider the advantages and disadvantages of various comparison groups and other characteristics, such as method of assessment.. gender, and level of functioning, m attempting to delineate the specificity and universality of the broad phenotype of autism. C1 Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Sch Educ, IL-91905 Jerusalem, Israel. 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Child Psychol. Psychiatry PD JAN PY 2005 VL 46 IS 1 BP 69 EP 83 DI 10.1111/j.1469-7610.2004.00334.x PG 15 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 892GG UT WOS:000226637500007 PM 15660645 ER PT J AU Fombonne, E AF Fombonne, E TI Epidemiology of autistic disorder and other pervasive developmental disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID INFANTILE-AUTISM; CHILDHOOD AUTISM; PRESCHOOL-CHILDREN; TOTAL POPULATION; CHANGING PREVALENCE; ASPERGER-SYNDROME; SPECTRUM; JAPAN; FRENCH; INSTRUMENT AB Is the incidence of autistic disorder and other pervasive developmental disorders (PDDs) increasing? Recent epidemiological surveys of autistic disorder and other PDDs have heightened awareness of and concern about the prevalence of these disorders; however, differences in survey methodology, particularly changes in case definition and case identification over time, have made comparisons between surveys difficult to perform and interpret. Recent surveys suggest that the rate of all PDDs is about 60 per 10,000. The prevalence of autism today is estimated at 13 per 10,000, Asperger's disorder is approximately 3 per 10,000, and childhood disintegrative disorder is very rare at about 0.2 per 10,000. The assessment process, sample size, publication year, and geographic location of studies all have an effect on prevalence estimates. In addition, data from many of these surveys indicate correlates of autistic disorder and other PDDs with IQ, gender, and other medical disorders. C1 McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3Z 1P2, Canada. 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This article reviews neurochemical contributions to the pathophysiology of autism with a focus on monoamines, glutamate/gamma-aminobutyric acid systems, and neuropeptides. As these efforts move forward, it will be important to begin to integrate genetic studies with those involving neuroimaging and postmortem research in each of these 3 areas, as well as with pharmacologic treatment approaches. C1 Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, Indianapolis, IN 46202 USA. James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, 1111 W 10th St,PB 2nd Floor, Indianapolis, IN 46202 USA. 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