Disease relevance of Autistic Disorder

• METHOD: We conducted a chart review of 10 adults (mean +/- SD age = 43.8 +/- 6.0 years) with DSM-IV autistic disorder who were switched from other atypical antipsychotics to ziprasidone, primarily due to weight gain, but other reasons included hypercholesterolemia, maladaptive behaviors, drowsiness, and depression [1].
• Oral dyskinesia induced by fluoxetine therapy for infantile autism [2].
• Four boys with the combination of infantile autism and the fragile-X syndrome were given oral folic acid and placebo, according to a double-blind crossover design [3].
• Parents with normal whole blood serotonin levels who had children with autistic disorder and parents of children with Down's syndrome had significantly lower CES-D depression scores than parents with elevated whole blood serotonin levels who had children with autistic disorder [4].
• Future studies on the clinical associations of seizure disorders, mood disorders, and catatonia in autistic people may provide the necessary data to formulate a coherent theory of GABA dysfunction in Autistic Disorder [5].

Psychiatry related information on Autistic Disorder

• OBJECTIVE: Risperidone has been found efficacious for decreasing severe tantrums, aggression, and self-injurious behavior in children and adolescents with autistic disorder (autism) [6].
• Haloperidol in the treatment of infantile autism: effects on learning and behavioral symptoms [7].
• Sertraline response in adults with mental retardation and autistic disorder [8].
• Based on global improvement item criteria from the Clinical Global Impression Scale, 15 of 22 (68%) patients with autistic disorder, none of six (0%) patients with Asperger's disorder, and 9 of 14 (64%) patients with PDD NOS were categorized as treatment responders [9].
• In addition, treatment with fluvoxamine < or = 300 mg/day for > or = 8 weeks improved symptoms of social phobia (social anxiety disorder), post-traumatic stress disorder (PTSD), pathological gambling, compulsive buying, trichotillomania, kleptomania, body dysmorphic disorder, eating disorders and autistic disorder [10].

High impact information on Autistic Disorder

• A double-blind, placebo-controlled study of risperidone in adults with autistic disorder and other pervasive developmental disorders [11].
• Continued investigation into the role of serotonin in the pathogenesis and treatment of autistic disorder is warranted [12].
• A double-blind, placebo-controlled study of fluvoxamine in adults with autistic disorder [13].
• Effects of tryptophan depletion in drug-free adults with autistic disorder [12].
• OBJECTIVE: To determine whether clomipramine hydrochloride, a serotonin reuptake blocker with unique anti-obsessional properties, is differentially effective for obsessive-compulsive and stereotyped motor behaviors in autistic disorder compared with placebo and with the noradrenergic tricyclic antidepressant agent, desipramine hydrochloride [14].

Chemical compound and disease context of Autistic Disorder

• The cerebral metabolic rate for glucose was studied in ten men (mean age = 26 years) with well-documented histories of infantile autism and in 15 age-matched normal male controls using positron emission tomography and (F-18) 2-fluoro-2-deoxy-D-glucose [15].
• These findings support a role for genetic variants within the GABA receptor gene complex in 15q11-13 in autistic disorder [16].
• METHOD: Twenty-one pediatric subjects with diagnoses of autistic disorder or other pervasive developmental disorders, 6-15 years old and stabilized with a consistent dose of fluvoxamine or fluoxetine, were recruited for the study; 16 successfully completed the imaging protocol [17].
• High blood monocyte counts and neopterin levels in children with autistic disorder [18].
• METHOD: Following a 2-week, single-blind placebo lead-in phase, drug-free subjects with autistic disorder were administered three different doses of D-cycloserine during each of three 2-week periods [19].

Biological context of Autistic Disorder

• Use of the multiallelic transmission-disequilibrium test (MTDT), for nine loci on 15q11-13, revealed linkage disequilibrium between autistic disorder and a marker in the gamma-aminobutyric acidA receptor subunit gene, GABRB3 155CA-2 (MTDT 28.63, 10 df, P=.0014) [20].
• RESULTS: Linkage and association were observed between autistic disorder and the two SNPs, rs2056202 and rs2292813, found in SLC25A12 [21].
• BACKGROUND: Many studies in autistic disorder report sleep problems and altered circadian rhythms, suggesting abnormalities in melatonin physiology [22].
• No significant association was found between autistic disorder and the WNT2 genotypes in either the overall data set or in the language-impaired subset of families [23].
• Linkage/association between 5-HTT gene promoter alleles and autistic disorder was assessed using the transmission/disequilibrium test (TDT) and the haplotype-based haplotype relative risk (HHRR) [24].

Anatomical context of Autistic Disorder

• Anterior cingulate gyrus volume and glucose metabolism in autistic disorder [25].
• Cerebrospinal fluid (CSF) concentrations of the serotonin and dopamine metabolites, 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid (HVA), respectively, were measured in a group of 17 children with Autistic Disorder (DSM-III-R) [26].
• Blood platelet serotonin content was measured in 30 children with early infantile autism, as defined by Kanner, 30 age-matched normal subjects, and 45 children with various neurological and psychiatric disorders [27].
• Performance on Cambridge Neuropsychological Test Automated Battery subtests sensitive to frontal lobe function in people with autistic disorder: evidence from the Collaborative Programs of Excellence in Autism network [28].

Gene context of Autistic Disorder

• GFAP levels in children with infantile autism were higher than those in normal children of the same age range [29].
• Six previous family-based association studies of SLC6A4 in autistic disorder have been conducted, with four studies showing nominally significant transmission disequilibrium and two studies with no evidence of nominally significant transmission disequilibrium [30].
• Children with large RELN alleles did not show any difference in scores for questions related to the core symptoms of autistic disorder, but there was a tendency for children with at least one large RELN allele to have an earlier age at first phrase (chi(2) = 3.538, P = 0.06) [31].
• Mutation analysis of the coding sequence of the MECP2 gene in infantile autism [32].
• No association between the WNT2 gene and autistic disorder [23].

Analytical, diagnostic and therapeutic context of Autistic Disorder

• METHODS: Twenty drug-free adults with autistic disorder (16 men and 4 women) (mean [+/- SD] age, 30.5 +/- 8.5 years) underwent short-term tryptophan depletion in a double-blind, placebo-controlled, randomized crossover design [12].
• Functional deficits in autistic disorder: characterization by technetium-99m-HMPAO and SPECT [33].
• Effects of fenfluramine on EEG and brainstem average evoked response in infantile autism. Preliminary investigation [34].
• Hypothesis: is infantile autism a hypoglutamatergic disorder? Relevance of glutamate - serotonin interactions for pharmacotherapy [35].
• A number of controlled clinical trials did not show improvement in autistic symptoms with secretin compared with placebo, possibly indicating no role for the drug in autistic disorder [36].

References