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PubMed2001

Oxytocin and autistic disorder: alterations in peptide forms.

BACKGROUND: Oxytocin (OT) is synthesized as a prohormone that is sequentially processed to peptides. These peptides are the bioactive amidated form (OT) and the C-terminal extended peptides, OT-Gly, OT-Gly-Lys and OT-Gly-Lys-Arg, which are designated together as OT-X. As an extension of our previous study finding decreased plasma OT in autism, studies were conducted to determine whether there were changes in OT peptide forms in autistic children. METHODS: Twenty eight male subjects (97 +/- 20 months; range, 70-139 months), diagnosed with DSM-IV autistic disorder through observation and semi-structured interview, were compared with 31 age-matched nonpsychiatric control subjects (106 +/- 22 months; range, 74-140 months). Using OT antisera with different specificity for the peptide forms, we measured plasma OT and OT-X in each group. RESULTS: T tests showed that there was a decrease in plasma OT (t = 4.4, p <.0001), an increase in OT-X (t = 2.3, p <.03) and an increase in the ratio of OT-X/OT (t = 4.5, p <.0001) in the autistic sample, compared with control subjects. CONCLUSIONS: The results suggest that children with autistic disorder show alterations in the endocrine OT system. Deficits in OT peptide processing in children with autism may be important in the development of this syndrome.

Adolescent↗
PubMed2001

No association between the 4g/5G polymorphism of the plasminogen activator inhibitor-1 gene promoter and autistic disorder.

Plasmin, a serine protease, is involved in many physiologically relevant processes, including haemostasis, cellular recruitment during immune response, tumour growth, and also neuronal migration and synaptic remodelling. Both tissue-type and urokinase-type plasminogen activators can be efficiently inhibited by plasminogen activator inhibitor-1 (PAI-1), a protease inhibitor of the serpin family. The human PAI-1 gene is located on chromosome 7q, within or close to a region that has been linked to autism in several linkage studies. Autism seems to be characterized by altered neuronal cytoarchitecture, synaptogenesis and possibly also cellular immune responses. We began addressing the potential involvement of the PAI-1 gene in autistic disorder with this linkage/association study, assessing transmission patterns of the 4G/5G polymorphism in the PAI-1 gene promoter that was previously shown to significantly affect PAI-1 plasma levels. No linkage/association was found in 167 trios with autistic probands, recruited in Italy and in the USA. We thus found no evidence that this polymorphism, or putative functionally relevant gene variants in linkage disequilibrium with it, confer vulnerability to autistic disorder.

Adolescent↗
PubMed1990

Fluvoxamine treatment of coincident autistic disorder and obsessive-compulsive disorder: a case report.

This is a single-case report of fluvoxamine treatment of comorbid autistic disorder (AD) and obsessive-compulsive disorder (OCD). Psychological, neuroanatomical, and neurochemical parallels are drawn between AD and OCD. The implications of this case of coincident AD and OCD, as well as the response to fluvoxamine, are discussed with respect to nosology, pathophysiology, and treatment of these disorders.

Adult↗
PubMed2004

Brief report: autistic disorder in three children with cytomegalovirus infection.

Previous research has identified a relationship between autistic disorder (autism) and specific congenital infections. Three cases of congenital or perinatal cytomegalovirus (CMV) infection occurring in association with autism are described. Hypothetical mechanisms relating congenital infection, such as CMV, to the development of autism are discussed. A better understanding of the immunologic response to certain congenital infections may provide important information pertaining to the pathophysiology and etiology of autism in vulnerable individuals.

Autistic Disorder↗
PubMed2003

Mutation screening of FOXP2 in individuals diagnosed with autistic disorder.

Although it is well established that genetic factors play an important role in the etiology of autistic disorder (AD), no specific genes have as yet been implicated. Genetic epidemiological data, particularly the sharp fall in concordance rates from monozygotic to dizygotic twins, indicate that the mode of transmission of this disorder is complex and may involve several genes. The 7q31 locus has been repeatedly linked to AD, suggesting that this chromosomal region is likely to harbor a susceptibility gene for AD. Recently, variations in the FOXP2 gene were reported to be responsible for a severe speech and language disorder. Because of the chromosomal location of FOXP2 (7q31) and the putative implication of the 7q31 region both in autistic and in language disorders (a feature of AD), it has been hypothesized that FOXP2 may be implicated in the pathophysiology of AD. To test this hypothesis, we screened the FOXP2 gene coding sequence for mutations in subjects diagnosed with AD and in normal controls. We identified four silent polymorphisms that were equally distributed between patients and controls. Using an intra-family association design, we identified no transmission disequilibrium in any of the four identified alleles, suggesting that the FOXP2 gene does not play a significant role in AD.

Adolescent↗
PubMed2006

The genetics of autistic disorders and its clinical relevance: a review of the literature.

Twin and family studies in autistic disorders (AD) have elucidated a high heritability of the narrow and broad phenotype of AD. In this review on the genetics of AD, we will initially delineate the phenotype of AD and discuss aspects of differential diagnosis, which are particularly relevant with regard to the genetics of autism. Cytogenetic and molecular genetic studies will be presented in detail, and the possibly involved aetiopathological pathways will be described. Implications of the different genetic findings for genetic counselling will be mentioned.

Autistic Disorder↗
PubMed2006

Case report: homicide by a 10-year-old girl with autistic disorder.

This case study presents a 10-year-old girl with a diagnosis of Autistic Disorder, who killed her 6-month-old sister by throwing her out of a window. Her aggressive-impulsive behavior had a persistent pattern. She had a history of epilepsy, and was frequently exposed to physical abuse. She never attended a structured treatment program. Here, we discuss the possible risk factors including history of epilepsy, unsupervised-disorganized home environment, existence of physical abuse-neglect and lack of appropriate treatment program leading to violent behavior.

Aggression↗
PubMed1993

A double-blind comparison of clomipramine, desipramine, and placebo in the treatment of autistic disorder.

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. DESIGN: Following a 2-week, single-blind placebo washout phase, 12 autistic subjects completed a 10-week, double-blind, crossover comparison of clomipramine and placebo, and 12 different subjects completed a similar comparison of clomipramine and desipramine. SETTING: Outpatient clinic. PATIENTS: A referral sample of 30 male and female autistic patients were enrolled, and 24 completed the study. MEASURES: Key outcome measures were the Autism Relevant Subscale of the Children's Psychiatric Rating Scale, the Modified Comprehensive Psychopathological Rating Scale-Obsessive-Compulsive Disorder Subscale, and the Clinical Global Impressions Scale. RESULTS: Clomipramine was superior to both placebo and desipramine on ratings of autistic symptoms (including stereotypies), anger, and compulsive, ritualized behaviors (P < .05), with no differences between desipramine and placebo. Clomipramine was equal to desipramine and both tricyclic agents were superior to placebo for amelioration of hyperactivity. CONCLUSION: Biological links between compulsions and stereotyped, repetitive behaviors in autistic disorder should be explored.

Adolescent↗
PubMed2006

A comparison of behavioral and emotional functioning in children and adolescents with Autistic Disorder and PDD-NOS.

Behavioral symptomatology was compared in 26 children and adolescents with Autistic Disorder ("autism") and 25 children and adolescents with Pervasive Developmental Disorder, Not Otherwise Specified ("PDD-NOS"). Relative to individuals with PDD-NOS, those with autism had more symptoms of depression, social withdrawal, atypical behavior, and immature social skills--and fewer family problems. These differences remained even when group differences in intellectual ability were statistically controlled. No group differences emerged in somatization, anxiety, or hyperactivity. Findings suggest that although both groups demonstrate considerable evidence of behavioral and emotional problems, those with autism are at particularly high risk for comorbid behavioral and emotional disabilities.

Adaptation, Psychological↗
PubMed1992

Autistic disorder: a neuropsychological enigma.

Autism is increasingly viewed as an expression of an unidentified neurological disorder. Because understanding of neurological dysfunction is basic to evaluation and treatment in occupational therapy, this article provides a comprehensive and critical review of the literature since 1985 concerning the neuropsychology of autistic disorder. The research is categorized into four basic types: (a) neuropsychological testing of functional abilities, (b) treatment studies based on neuropsychological hypotheses, (c) autistic-related diseases and genetic disorders, and (d) neuroanatomical and neurophysiological studies. The research shows a spectrum of neurological impairments within the brain stem, cerebellum, midbrain, and frontal lobe. These impairments are associated with deficits in socioemotional skills, sensory processing, motor planning, and cognitive flexibility. This research suggests that persons with autistic disorder need evaluation and treatment of a wide spectrum of functional deficits.

Autistic Disorder↗
PubMed2000

Case report: autistic disorder and chromosomal abnormality 46, XX duplication (4) p12-p13.

We report an 18-year-old female with a diagnosis of DSM-IV Autistic Disorder and moderate to severe mental retardation who was discovered to have a previously undescribed chromosomal abnormality 46, XX, duplication (4) p12-p13. We discuss her history and diagnosis, noting that the co-occurrence of her diagnoses have not previously been documented. The report adds to the literature supporting the argument that individuals with autistic spectrum disorders should be re-examined for chromosomal abnormalities.

Adolescent↗
PubMed2001

Autistic disorder versus other pervasive developmental disorders in young children: same or different?

Eighteen preschool children diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders Third Edition Revised (DSM III-R) as having Pervasive Developmental Disorder-Not Otherwise Specified (PDD-NOS) were compared to 176 children with DSM III-R Autistic Disorder (AD), and to 311 non-autistic children with developmental language disorders (DLD) (N = 201) or low IQ (N = 110). All children were partitioned into "high" and "low" cognitive subgroups at a nonverbal IQ of 80. Within cognitive subgroups, the 18 PDD-NOS children did not differ significantly from either the DLD or the AD children in verbal and adaptive skills and obtained scores intermediate between those of these groups. The PDD-NOS did not differ from the AD children in maladaptive behaviors. Both the PDD-NOS and AD children had many more of these behaviors than the non-autistic comparison groups. Children in the "high" and "low" cognitive subgroups of AD, but not of PDD-NOS, differed substantially on most measures, with the children with lower cognitive scores significantly more impaired on all measures. Similarity of PDD-NOS children to AD children in maladaptive behaviors and an intermediate position between autistic and non-autistic groups on virtually all measures explains the difficulty clinicians encounter in classifying children with PDD and raises questions about the specificity of these diagnostic subtypes of the autistic spectrum.

Autistic Disorder↗
PubMed2002

Tetrasomy 15q11-q13 identified by fluorescence in situ hybridization in a patient with autistic disorder.

We report a female child with tetrasomy of the 15q11-q13 chromosomal region, and autistic disorder associated with mental retardation, developmental problems and behavioral disorders. Combining classical and molecular cytogenetic approaches by fluorescence in situ hybridization technique, the karyotype was demonstrated as 47,XX,+mar.ish der(15)(D15Z1++,D15S11++,GABRB3++,PML-). Duplication of the 15q proximal segment represents the most consistent chromosomal abnormality reported in association with autism. The contribution of the GABA receptor subunit genes, and other genes mapped to this region, to the clinical symptoms of the disease is discussed.

Adolescent↗
PubMed1996

Sertraline response in adults with mental retardation and autistic disorder.

BACKGROUND: Self-injury and aggression are common reasons for urgent psychiatric referral of persons with mental retardation and autistic spectrum disorders. Although the treatment prescribed for these problems has traditionally been neuroleptic medication, serotonin reuptake inhibitors such as sertraline may result in significant clinical improvement as well as fewer side effects. METHOD: The authors administered sertraline in an open trial to nine consecutively admitted adult mentally retarded outpatients presenting with target behaviors of self-injury and/or aggression. Most patients (N = 6) were mildly or moderately mentally retarded by DSM-III-R criteria; five had comorbid autistic disorder. Prescribed dosages ranged from 25 mg to 150 mg daily, based on observed clinical responses. Clinical Global Impressions (CGI) ratings were made at baseline and again after sertraline treatment for at least 28 days. RESULTS: Sertraline led to improvement in CGI ratings of overall clinical severity in eight of nine subjects; mean +/- SD improvement in CGI ratings was 2.44 points +/- 1.67. Discontinuation of the treatment was necessary in only one patient, after 18 weeks of sertraline treatment, because of agitation and worsening of self-picking. Side effects were otherwise minimal. CONCLUSION: These findings from a clinical sample suggest that sertraline is promising in the treatment of self-injury and aggression. Double-blind controlled studies of sertraline and other serotonin reuptake inhibitors in the treatment of self-injury and aggression in patients with mental retardation and with autistic disorder are warranted.

1-Naphthylamine↗
PubMed1996

Case study: comorbidity among Tourette's syndrome, autistic disorder, and bipolar disorder.

OBJECTIVE: Several studies report a greater than expected concurrence for Tourette's syndrome (TS) with autistic disorder (AD). TS and bipolar disorder (BD) also may co-occur at a greater than expected rate. The authors assess whether there is a greater than expected concurrence for TS+AD+BD. METHOD: Four patients who had at some time in their lives diagnoses of TS, AD, and BD were identified. Three of these had concurrent TS+AD+BD. Diagnoses were made according to DSM-III-R criteria. Each of these patients was living in North Dakota and was in the authors' care at the time of this study. RESULTS: The point prevalence (risk) for concurrent TS+AD+BD in North Dakota is not less than 4.6 x 10(-6). The developmental sequence of syndromes in these four patients was AD, then TS and then BD. Data from the authors' previously published, population-based prevalence studies indicate that TS+AD+BD co-occur at a greater than chance expectation. CONCLUSIONS: Common etiological factors may be involved in the greater than chance concurrence of TS+AD+BD.

Adolescent↗