PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Autistic Disorder”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed2003

Face processing in adolescents with autistic disorder: the inversion and composite effects.

Two experiments with upright and inverted face and object images were carried out to investigate whether face processing in autism is more feature-based than in individuals with typical development. Participants were 17 high-ability adolescents with autistic disorder (16-24 years), 24 typically developing children (9-10 years) and 16 adults (18-33 years). In Experiment 1, a normal inversion effect was found for the adolescents with autism in a standard face recognition paradigm with reduced memory demands, except for a subgroup with low social intelligence who were not better in recognizing upright relative to inverted photographs of faces. In Experiment 2, the group with autism did not show the composite effect like the adult group did: they recognized face halves as well in aligned composite faces as in non-aligned composite faces. The results on the inversion task suggest that most adolescents with autism form a normal configuration-based face representation, but the absence of the composite effect indicates that they are less prone to use the contextual information of the face in a visual-search task.

Adolescent↗
PubMed1991

Autistic disorder associated with an iso-dicentric Y chromosome.

The relationship between a fragile site on the X chromosome and autism has been well documented. The authors report a three-year-old child with partial duplication of the short arm of chromosome Y, who had an autistic disorder. He was microcephalic, but otherwise had a normal phenotype. There was a history of preterm birth and maternal diabetes. This is the sixth case of sex chromosome Y aneuploidy associated with autism, but the first with an isodicentric Y. In well-substantiated cases of autism, clinicians should now consider abnormalities of the Y as well as the X chromosome.

Autistic Disorder↗
PubMedDate not supplied

[Review of psychopharmacological treatments in adolescents and adults with autistic disorders].

Autism is an early developmental disorder. It leads to severe and durable disturbances. Given this problem, no treatment can be excluded a priori. Thus, many approaches are used to deal with autistic disorders. In France, pharmacological treatments are, for instance, largely and mostly used in adults. In the USA, these treatments concern 50% of persons with autism of any age. Nevertheless, they are rarely based on controlled studies. At the present, however, prescriptions and expected effects appear to be hard to localize. Furthermore, only few controlled studies validate their use. Aim - We offer a review of studies about medical treatments used in adolescents and adults with autism. They are classified in 3 categories: the first (category I) includes drugs used for their neurochemical effects focusing on autistic signs. The second (category II) covers drugs used for treatment of behavioural disorders frequently associated with autism. The third (category III) corresponds to a wide range of drugs or vitamins for wich only few case studies exist reporting irregular positive effects. The main hypothesis of this review is that autism involves a dysfunction of the neuromediation systems. This hypothesis opens new perspectives in the research of medical treatments in autism by focusing on molecules, which are supposed to have an effect on neuromediation systems. Method - Our review is based on studies, which have been published during the past twenty years. For many studies, data are limited to adolescents and adults. So we expanded our review to data available in children. The data bases that we have used are medline and psyclit. Keywords have been chosen according to: pharmacological considerations (psychotropic, psychoactive drugs, psychopharmacology) and clinical symptoms (autism, automutilations, aggressive behavior, and hyperactivity). Hypothesis of a dysfunction in the neuromediation systems in autism - Many studies exist about biochemical abnormalities in autism. As in schizophrenia and mental retardation, dysfunctions of the neuromediation systems are considered to be etiological factors. In 30% of people with autism the most regular dysfunction is the increase of serotonine. This led to the serotoninergic hypothesis in autism and to the use of active drugs in the serotonine system. However, the presence of other neurometabolic abnormalities also motivates the use of drugs, supposed to be active in other neuromediation systems. Pharmacological treatments in autism - Category I section sign 1 Active drugs in the dopamine system. Haloperidol (Dopamine antagonist): The effects of this molecule have been broadly studied in autism. Results indicate high efficiency in some symptoms of autism (lack in social behaviour, stereotypical behaviour) and in behavioural impairments that may be associated with autism (aggressive behaviour, hyperactivity). Its side effects, particulary the risk of late dyskinesy, make atypical antipsychotics preferable because of their lower risks. Risperidone (Dopamine and serotonine antagonist): Among several studies only few have been controlled. They indicate that Risperidone has positive effects on the behaviour and is quite well tolerated. section sign 2 Active drugs in the serotonine system. Clomipramine: after promising results, the medium-term efficiency has decreased and severe side effects have limited its use. Fluvoxamine, Fluoxétine, Sertraline (Specific serotonine drugs): Their efficiency has been mainly tested through open studies and their results are contrasted. In some cases, social behaviours have improved and aggressiveness and stereotyped behaviours have decreased. Fenfluramine: At present, this drug is removed from the market. Yet, some studies have suggested that it improves behavioural disturbances as well as performances in autism. section sign 3 Active drugs in the opiate system. Naltrexone: Several controlled studies have indicated an improvement in social and aggressive behaviours. Nevertheless, these studies have used small size sample and have not been replicated. Category II. This category correspond to drugs supposed to be active on neurochemical disturbances found in autism but their target symptoms are not autism specific signs as defined by the ICD 10. Buspirone: This serotonine agonist may have a good impact on emotional disorders and sleeping confusions. Methylphenidate: Most of the current studies about this noradrenergic drug concern children. The results are variable. Paradoxical effects may exist in children with severe mental retardation. Propanolol: Some isolated studies habe reported its efficiency on behavioural disturbances. Clonidine: This adrenergic drug treats efficiently some cases of aggressive behaviour and hyperactivity. Category III. This category contains a wide range of drugs, vitamins or method used in autism after sporadic observations of their positive effects. Secretine: An important improvement has been reported in isolated cases. However, controlled studies in children do not confirm these results. Vitamines B6, B12 and Magnesium: An improvement in socialization and in behavioural disorders have been reported in some cases, but these results are not yet confirmed. Lithium, Carbamazépine, Valproate: Results of some case studies have found it to be efficient in cyclic disorders. Gluten and casein free diet: An improvement of social behaviour have been reported by some parents after these diets. No controlled study has validated this observation. Conclusion - There is no consensus on the use of psychopharmacological treatments in autism. Although there exist many clinical observations, only few controlled studies have validated the efficiency and safety of these treatments. At the present time and until having sufficient studies, drugs are generally limited to severe disorders, for which usual psycho-educational approaches are insufficient.

Adolescent↗
PubMed1998

A double-blind, placebo-controlled study of risperidone in adults with autistic disorder and other pervasive developmental disorders.

BACKGROUND: Neurobiological research has implicated the dopamine and serotonin systems in the pathogenesis of autism. Open-label reports suggest that the serotonin2A-dopamine D2 antagonist risperidone may be safe and effective in reducing the interfering symptoms of patients with autism. METHODS: Thirty-one adults (age [mean+/-SD], 28.1+/-7.3 years) with autistic disorder (n=17) or pervasive developmental disorder not otherwise specified (n=14) participated in a 12-week double-blind, placebo-controlled trial of risperidone. Patients treated with placebo subsequently received a 12-week open-label trial of risperidone. RESULTS: For persons completing the study, 8 (57%) of 14 patients treated with risperidone were categorized as responders (daily dose [mean+/-SD], 2.9+/-1.4 mg) compared with none of 16 in the placebo group (P<.002). Risperidone was superior to placebo in reducing repetitive behavior (P<.001), aggression (P<.001), anxiety or nervousness (P<.02), depression (P<.03), irritability (P<.01), and the overall behavioral symptoms of autism (P<.02). Objective, measurable change in social behavior and language did not occur. Nine (60%) of 15 patients who received treatment with open-label risperidone following the double-blind placebo phase responded. Other than mild, transient sedation, risperidone was well tolerated, with no evidence of extrapyramidal effects, cardiac events, or seizures. CONCLUSION: Risperidone is more effective than placebo in the short-term treatment of symptoms of autism in adults.

Adolescent↗
PubMed2001

Clomipramine versus haloperidol in the treatment of autistic disorder: a double-blind, placebo-controlled, crossover study.

Clomipramine, haloperidol, and placebo were compared with baseline in the treatment of autism, and overall outcome, specific symptoms, and side effects were examined. It was hypothesized that clomipramine would be better tolerated than haloperidol and prove superior on a measure of stereotypy. Individuals with a DSM-IV diagnosis of autistic disorder (mean age, 16.3 years; range, 10-36 years) were randomly assigned, by using a Latin square design, to the following 7-week trials: placebo, clomipramine (mean daily dose, 128.4 mg; range, 100-150 mg), or haloperidol (mean daily dose, 1.3 mg; range, 1-1.5 mg). Data on 36 subjects were analyzed and taken together; the results favored haloperidol. In those patients who were able to complete a full therapeutic trial, clomipramine proved comparable to haloperidol in terms of improvement compared with baseline. However, significantly fewer individuals receiving clomipramine versus haloperidol were able to complete the trial (37.5% vs. 69.7%, respectively) for reasons related to both side effects and efficacy or behavior problems. In the intent-to-treat sample, which is perhaps more clinically relevant, only haloperidol proved superior to baseline on a global measure of autistic symptom severity, as well as specific measures for irritability and hyperactivity. Clomipramine did not seem more effective on a measure of stereotypy, nor was it better tolerated.

Adolescent↗
PubMed2005

Macrocephaly and the control of brain growth in autistic disorders.

Autism is a childhood-onset neuropsychiatric disorder characterized by marked impairments in social interactions and communication, with restricted stereotypic and repetitive patterns of behavior, interests, and activities. Genetic epidemiology studies indicate that a strong genetic component exists to this disease, but these same studies also implicate significant environmental influence. The disorder also displays symptomatologic heterogeneity, with broad individual differences and severity on a graded continuum. In the search for phenotypes to resolve heterogeneity and better grasp autism's underlying biology, investigators have noted a statistical overrepresentation of macrocephaly, an indicator of enlarged brain volume. This feature is one of the most widely replicated biological findings in autism. What then does brain enlargement signify? One hypothesis invoked for the origin of macrocephaly is a reduction in neuronal pruning and consolidation of synapses during development resulting in an overabundance of neurites. An increase in generation of cells is an additional mechanism for macrocephaly, though it is less frequently discussed in the literature. Here, we review neurodevelopmental mechanisms regulating brain growth and highlight one underconsidered potential causal mechanism for autism and macrocephaly--an increase in neurogenesis and/or gliogenesis. We review factors known to control these processes with an emphasis on nuclear receptor activation as one signaling control that may be abnormal and contribute to increased brain volume in autistic disorders.

Adaptation, Physiological↗
PubMed2002

Smaller left hemisphere planum temporale in adults with autistic disorder.

The structure of the planum temporale is often disturbed in disorders with associated communication problems, particularly in auditory and language processing areas in the brain. We hypothesized that people with autism would have reduced left hemisphere volumes in the planum temporale, a language related brain structure. We performed magnetic resonance imaging scans of 15 adults with autistic disorder and 15 comparison subjects, and measured the volume of gray matter in the planum temporale and Heschl's gyrus (HG) in both hemispheres. Planum temporale volume reduced in the left hemisphere of the autism group (P<0.003). No differences in HG volumes were observed between the two groups. The volume reduction seen in the left hemisphere of the autism group may suggest an early neurodevelopmental disturbance in autism that impacts language development.

Adolescent↗
PubMed2001

Association analysis of chromosome 15 gabaa receptor subunit genes in autistic disorder.

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain, acting via the GABAA receptors. The GABAA receptors are comprised of several different homologous subunits, forming a group of receptors that are both structurally and functionally diverse. Three of the GABAA receptor subunit genes (GABRB3, GABRA5 and GABRG3) form a cluster on chromosome 15q11-q13, in a region that has been genetically associated with autistic disorder (AutD). Based on these data, we examined 16 single nucleotide polymorphisms (SNPs) located within GABRB3, GABRA5 and GABRG3 for linkage disequilibrium (LD) in 226 AutD families (AutD patients and parents). Genotyping was performed using either OLA (oligonucleotide ligation assay), or SSCP (single strand conformation polymorphism) followed by DNA sequencing. We tested for LD using the Pedigree Disequilibrium Test (PDT). PDT results gave significant evidence that AutD is associated with two SNPs located within the GABRG3 gene (exon5_539T/C, p=0.02 and intron5_687T/C, p=0.03), suggesting that the GABRG3 gene or a gene nearby contributes to genetic risk in AutD.

Autistic Disorder↗
PubMed1997

High-dose pyridoxine and magnesium administration in children with autistic disorder: an absence of salutary effects in a double-blind, placebo-controlled study.

Several reports have described salutary effects such as decreased physical aggression and improved social responsiveness being associated with the administration of high doses of pyridoxine and magnesium (HDPM) in open-labeled and controlled studies of patients with autism. Despite this fact, this intervention remains controversial. A 10-week double-blind, placebo-controlled trial was undertaken to examine both the efficacy and safety of HDPM in autism. Twelve patients were enrolled, and 10 patients (mean age 6 years 3 months) were able to complete the study. HDPM at an average dose of 638.9 mg of pyridoxine and 216.3 mg of magnesium oxide was ineffective in ameliorating autistic behaviors as assessed by the Children's Psychiatric Rating Scale (CPRS), the Clinical Global Impression Scale, and the NIMH Global Obsessive Compulsive Scale. Furthermore, no clinically significant side effects were noted during HDPM administration. A trend for a transient change on the CPRS was found that was possibly due to a placebo response. This study raises doubts about the clinical effectiveness of HDPM in autistic disorder.

Adolescent↗
PubMed1996

Cytogenetic and molecular analysis of inv dup(15) chromosomes observed in two patients with autistic disorder and mental retardation.

A variety of distinct phenotypes has been associated with supernumerary inv dup(15) chromosomes. Although different cytogenetic rearrangements have been associated with distinguishable clinical syndromes, precise genotype-phenotype correlations have not been determined. However, the availability of chromosome 15 DNA markers provides a means to characterize inv dup(15) chromosomes in detail to facilitate the determination of specific genotype-phenotype associations. We describe 2 patients with an autistic disorder, mental retardation, developmental delay, seizures, and supernumerary inv dup(15) chromosomes. Conventional and molecular cytogenetic studies confirmed the chromosomal origin of the supernumerary chromosomes and showed that the duplicated region extended to at least band 15q13. An analysis of chromosome 15 microsatellite CA polymorphisms suggested a maternal origin of the inv dup(15) chromosomes and biparental inheritance of the two intact chromosome 15 homologs. The results of this study add to the existing literature which suggests that the clinical phenotype of patients with a supernumerary inv dup(15) chromosome is determined not only by the extent of the duplicated region, but by the dosage of genes located within band 15q13 and the origin of the normal chromosomes 15.

Adolescent↗
PubMed1999

Physical mapping of the serotonin 5-HT(7) receptor gene (HTR7) to chromosome 10 and pseudogene (HTR7P) to chromosome 12, and testing of linkage disequilibrium between HTR7 and autistic disorder.

The gene encoding the serotonin 5-HT(7) receptor (HTR7) has been considered as a candidate locus in several neuropsychiatric disorders, based on pharmacological evidence and ligand-binding studies. After determining over 3 kb of previously unpublished sequence from introns 1 and 2 of HTR7, a single base (C/T) polymorphism in the second intron of HTR7 was found. Allele-specific PCR was used to genotype the HTR7 marker in 53 trios consisting of subjects with autistic disorder and both parents. Using the transmission disequilibrium test (TDT), no evidence of preferential transmission of either allele was found (TDT chi(2) = 0.252, p = 0.602). Sequence data obtained from both intron 1 and intron 2 of HTR7, and from the 5-HT(7) pseudogene (HTR7P), was used to confirm localization of HTR7 to 10q23 and HTR7P to 12p13 using radiation hybrid analyses.

Autistic Disorder↗
PubMed2002

Some aspects of treatment and habilitation of children and adolescents with autistic disorder in Northern-Finland.

Hospital records and data on the treatment/habilitation status of 187 children with autism aged 3-18 years were gathered from Northern Finland. The treatment programs and therapies varied, depending on the trained staff available. One-hundred and fifty-two (82.9%) children and adolescents with autism received more than one therapeutic intervention or specific training program. The most common therapies were physiotherapy as well as speech, occupational and music therapy. 43.9% of the children and adolescents with autism received specific training according to TEACCH (Treatment and Education of Autistic and related Communication-Handicapped Children), 10.2% according to Lovaas and 30.5% according to the Portage program. Antiepileptic medication had been prescribed to 23.9% and psychopharmacological interventions to 14.9% of the individuals with autistic disorder (AD). One hundred and seventy-eight subjects out of 187 showed some improvement on the Childhood Autism Rating Scale (CARS), even if no statistically significant difference was found between the outcome of the available habilitation methods.

Adolescent↗
PubMed2006

Development of multi-agency referral pathways for attention-deficit hyperactivity disorder, developmental coordination disorder and autistic spectrum disorders: reflections on the process and suggestions for new ways of working.

This article summarizes the rationale for multi-agency working when assessing children and young people with suspected neurodevelopmental disorders such as attention-deficit hyperactivity disorder, developmental coordination disorder and autistic spectrum disorders. Details of referral pathways that have been drawn up for each separate disorder are given and the process through which multi-agency agreement was reached is described. Key features thought to be common to all three pathways are discussed and factors thought to have contributed to successful multi-agency working highlighted. The work is described in the context of existing national policy documents in the UK.

Attention Deficit Disorder with Hyperactivity↗
PubMed2001

Double-blind, placebo-controlled study of amantadine hydrochloride in the treatment of children with autistic disorder.

OBJECTIVE: To test the hypothesis that amantadine hydrochloride is a safe and effective treatment for behavioral disturbances--for example, hyperactivity and irritability--in children with autism. METHOD: Thirty-nine subjects (intent to treat; 5-19 years old; IQ > 35) had autism diagnosed according to DSM-IV and ICD-10 criteria using the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule-Generic. The Aberrant Behavior Checklist-Community Version (ABC-CV) and Clinical Global Impressions (CGI) scale were used as outcome variables. After a 1-week, single-blind placebo run-in, patients received a single daily dose of amantadine (2.5 mg/kg per day) or placebo for the next week, and then bid dosing (5.0 mg/kg per day) for the subsequent 3 weeks. RESULTS: When assessed on the basis of parent-rated ABC-CV ratings of irritability and hyperactivity, the mean placebo response rate was 37% versus amantadine at 47% (not significant). However, in the amantadine-treated group there were statistically significant improvements in absolute changes in clinician-rated ABC-CVs for hyperactivity (amantadine -6.4 versus placebo -2.1; p = .046) and inappropriate speech (-1.9 versus 0.4; p = .008). CGI scale ratings were higher in the amantadine group: 53% improved versus 25% (p = .076). Amantadine was well tolerated. CONCLUSIONS: Parents did not report statistically significant behavioral change with amantadine. However, clinician-rated improvements in behavioral ratings following treatment with amantadine suggest that further studies with this or other drugs acting on the glutamatergic system are warranted. The design of these and similar drug trials in children with autistic disorder must take into account the possibility of a large placebo response.

Adolescent↗
PubMed1999

A Double-Blind, Placebo-Controlled Trial of Secretin for the Treatment of Autistic Disorder.

OBJECTIVE: This study examines the efficacy of intravenous porcine secretin for the treatment of autism. METHODS: Using a randomized, double-blind, placebo-controlled crossover design, 20 subjects with autistic disorder received either a secretin or placebo infusion at baseline and the other substance at week 4. Subjects were given the Autism Diagnostic Interview-Revised, the Autism Diagnostic Observation Schedule-Generic (ADOS-G), and other pertinent developmental measures at baseline and at weeks 4 and 8 to assess drug effects. RESULTS: For the primary efficacy analysis, change of ADOS-G social-communication total score from week 0 to week 4, no statistically significant difference was obtained between placebo (-1.0 +/- 2.4) and secretin groups (-0.7 +/- 1.4; t 0.34, df 18, P less than.74). No significant differences were obtained for the other measures, including when all 20 subjects were compared by paired t-test from baseline to 4 weeks after secretin infusion. CONCLUSION: There was no evidence for efficacy of secretin in this preliminary randomized controlled trial. These data were collected as part of a multicenter study with the University of California-Irvine and the University of Utah.

Journal Article↗