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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum creatine phosphokinase (CPK) levels were studied in individuals: 40 psychotic children suffering from childhood autism, atypical personality development, and childhood schizophrenia; five children with childhood aphasia; 22 children with severe personality disorders; 29 normal children and normal siblings of psychotic children; and 14 normal parents of psychotic children. Creatine phosphokinase levels from the entire population of adults and children were normally disturbed, and the mean CPK levels for the eight diagnostic groups were within normal limits. Those 22 children with personality disorders had significantly higher CPK levels than the other diagnostic groups. This relatively higher level of CPK may be related to vulnerability to later development of schizophrenic spectrum disorders. There was no apparent relationship between CPK levels and motor activity, nor was there any change in the level of CPK during a trial of psychoactive medication. Creatine phosphokinase levels remained relatively stable on test-retest determination.
Arch Gen Psychiatry 1976 Jun
PMID:Creatine phosphokinase levels in children with severe developmental disturbances. 5 82

Comparison of the properties of blood platelets and serotonergic synaptosomes suggests that the human platelet can serve as an appropriate model for the transport, metabolism, and release of serotonin (5-HT) by CNS serotonergic neurons. The study of blood 5-HT levels and platelet 5-HT pharmacodynamics in patients with a variety of psychiatric and neurologic disorders has generated interesting leads into possible abnormalities of CNS 5-HT neurons in these patients. This article reviews the experimental evidence, which uses the human platelet model to investigate neurotransmitter-related abnormalities in Down syndrome, mental retardation, infantile autism, hyperactivity syndromes (minimal brain dysfunction), schizophrenia, affective disorders, Duchenne muscular dystrophy, Parkinson disease, Huntington chorea, and migraine headaches.
Arch Gen Psychiatry 1977 May
PMID:The human platelet. A diagnostic and research tool for the study of biogenic amines in psychiatric and neurologic disorders. 14 Jun 32

Patterns of parent-child interaction and family functioning were systematically examined in well-matched groups of 15 autistic and 14 dysphasic children. The measures used included the Douglas 24-hour standard day analysis, the Brown and Rutter interview measure of positive interaction, the Ittleson scales (based on a four- to six-hour period of home observation, specially developed time-sampled measures of observed mother-child interaction at home), and the Eysenck Personality Inventory. The findings from all measures agreed in showing that family life and interaction patterns were closely similar in the two groups. The results were compared with those of previous investigations; we concluded that autism is most unlikely to be due to abnormal psychogenic influences in the family.
Arch Gen Psychiatry 1979 Jun
PMID:Families of autistic and dysphasic children. I. Family life and interaction patterns. 44 21

Platelet monoamine oxidase (MAO) activity was studied in 31 individuals suffering from early childhood autism and was not significantly different from that found in normal children or adults. In the autistic children, MAO activity decreased with age, and there was a trend toward greater platelet MAO activity in prepubertal and pubertal male autistic children relative to normal male children. Total platelet counts were not elevated in autistic children.
Arch Gen Psychiatry 1977 May
PMID:Platelet monoamine oxidase in early childhood autism. 87 Dec 32

Blood pressure, peripheral blood flow, and peripheral vascular resistance were measured in normal adults and children and in children with autism and severe disturbances in personality development while the individuals were engaged in a variety of attentional tasks. The tasks were designed to elicit outward direction of attention (and intake of sensory input) or inward direction of attention (and relative rejection of external sensory input). During tasks involving sensory rejection, normal adults and normal children showed increased blood flow and decreased peripheral vascular resistance; with sensory intake, blood flow was decreased and resistance was increased. The most severely impaired children showed little alteration in their physiological response to task requirements. Autistic children had higher mean blood flow and lower peripheral vascular resistance than normal children and adults. Some autistic children characteristically may be in a state of sensory rejection associated with generally higher levels of arousal or defense against environmental bombardment.
Arch Gen Psychiatry 1977 May
PMID:Cardiovascular correlates of attention in normal and psychiatrically disturbed children. Blood pressure, peripheral blood flow, and peripheral vascular resistance. 87 Dec 33

A conjectured neural integrative defect (schizotaxia), due to a dominant schizogene completely penetrant for a parametric aberration in synaptic signal selectivity (hypokrisia), gives rise under ordinary social learning regimens to schizotypy, a personality showing ambivalence, aversive drift, dereism, autism, and cognitive slippage. Given unfavorable polygenic potentiators (eg, introversion, hypohedonia, and anxiety) and adverse life experiences (eg, childhood trauma or adult misfortune), around 10% develop schizophrenia. That schizophrenia is basically a neurologic disorder does not contradict whatever is known about its psychodynamics, nor preclude efficacy for psychotherapy or other psychosocial interventions. Research should concentrate on soft neurology and psychophysiology as indicators, being closer in the causal chain to the schizogene than psychometric, social, or high-level cognitive processes. Taxometric statistics are appropriate to testing a major locus model not simplistically formulated.
Arch Gen Psychiatry 1989 Oct
PMID:Schizotaxia revisited. 255 52

Altered serotonergic function has been postulated to exist in autistic disorder. Central serotonergic responsivity was assessed with a neuroendocrine challenge test in seven male young adults with autistic disorder and in seven age- and gender-matched healthy controls. Binding indexes and physiologic responsivity of the platelet serotonin-2 (5-HT2) receptor complex were also measured, as was whole-blood serotonin content. Compared with controls, autistic subjects had substantially blunted prolactin release in response to a 60-mg oral dose of fenfluramine hydrochloride, an indirect serotonin agonist [corrected]. Furthermore, the magnitude of serotonin-amplified platelet aggregation, mediated by the platelet 5-HT2 receptor complex, was reduced in the autistic group, as was the mean number of platelet 5-HT2 receptor sites. Among autistic subjects, fenfluramine-induced prolactin release correlated positively with the serotonin-amplified platelet aggregation response and negatively with whole-blood serotonin content. The results of the present study are compatible with the hypothesis that central serotonergic responsivity is decreased in male autistic young adults. Correlations between central and peripheral serotonergic measures in autistic subjects suggest that systemic alterations in serotonergic function may occur in autism.
Arch Gen Psychiatry 1989 Mar
PMID:Serotonergic responsivity in male young adults with autistic disorder. Results of a pilot study. 291 50

The last ten years of research on the genetics of infantile autism were critically reviewed. Epidemiologic findings have shown that autism is a rare disorder with a prevalence of two to five per 10,000, a male-female ratio of 3:1, and an association with mental retardation (66% to 75% of autistic subjects have full-scale IQ scores [70]). Autism is familial, as reflected in an empiric sibling recurrence risk of 3% and pooled monozygotic and dizygotic concordance rates of 64% and 9%, respectively, which are much greater than the population prevalence of 0.02% to 0.05%. Genetic heterogeneity is pronounced with potential genetic subgroups, including autosomal recessive inheritance, X-linked inheritance, and sporadic chromosomal anomalies. Studies of subclinical markers in autism have elucidated potential markers at various levels of phenotypic expression from the DNA to the behavioral level. Linkage and cytogenetic studies point to two chromosome regions as putative markers, 9q34 and Xq27. Results of family studies support a putative biochemical marker, low levels of plasma dopamine-beta-hydroxylase, and a putative cognitive marker, ie, normal visuospatial but low verbal functioning, in autism. The frequency of minor physical anomalies and presence or absence of mental retardation are two dimensions of the physical and behavioral phenotype that may demark etiologically distinct subgroups. Genetic heterogeneity is offered as one explanation of the observed sex difference in the prevalence of autism. Directions for potentially fruitful research should be considered.
Arch Gen Psychiatry 1988 Oct
PMID:Autism and genetics. A decade of research. 304 27

Subtypes of thought disorder and affective flattening were examined in 14 adults with clear DSM-III diagnoses of infantile autism or autism, residual state, using videotaped psychiatric interviews and objective rating scales. Schizophrenic, manic, and normal subjects constituted contrast groups. Autistic adults, most of whom were high functioning, showed a high incidence and severity of poverty of speech, poverty of content of speech, perseveration, and affective flattening. They showed significantly less derailment, illogicality, and other features of "positive thought disorder" than either the schizophrenic or manic group, but they did not differ from schizophrenics on any affective flattening variable.
Arch Gen Psychiatry 1986 Aug
PMID:Thought, language, communication, and affective flattening in autistic adults. 372 72

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. Positron emission tomography was completed during rest, with reduced visual and auditory stimulation. While the autistic group as a whole showed significantly elevated glucose utilization in widespread regions of the brain, there was considerable overlap between the two groups. No brain region showed a reduced metabolic rate in the autistic group. Significantly more autistic, as compared with control, subjects showed extreme relative metabolic rates (ratios of regional metabolic rates to whole brain rates and asymmetries) in one or more brain regions.
Arch Gen Psychiatry 1985 May
PMID:Brain metabolism in autism. Resting cerebral glucose utilization rates as measured with positron emission tomography. 387 50


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