PubMed · 5104690
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
H Uwade. 1971-06-15. [Autism].. https://pubmed.ncbi.nlm.nih.gov/5104690/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Based upon the hypothesis that brain monoamine metabolism is disorganized in some children with an autistic disorder, we tried low dose levodopa therapy (0.5 mg/kg/day) proposed by Segawa, et al. We treated 20 patients with an autistic disorder diagnosed according to DSM-IV, and evaluated the effectiveness. A double blind cross over method was applied in this study because of the small number of patients. Drug effects were observed carefully by the psychologists and pediatric neurologists using an evaluation sheet consisting of twenty items. No significant effectiveness was observed in this study, although four cases (20%) showed some improvement. In conclusion, administration of low dose levodopa to autistic children resulted in no clear clinical improvements of autistic symptoms.
To study the relationships between clinical and biological data that are necessary for physiopathological analysis in the field of developmental disorders, we developed a quantified grouping system, based on four developmental assessment parameters. Parallel with this clinical research, we developed electrophysiological procedures adapted to the pathology of autism. In this paper, we report the utilization of an original multivariate descriptive statistical approach (correspondence analysis followed by cluster analysis) that allowed us to identify different bioclinical profiles using these clinical and electrophysiological data conjointly. These profiles are believed to be evidence for different underlying cerebral dysfunctions. This procedure proved effective in identifying two main bioclinical dimensions in a population of 145 developmentally disordered children. These dimensions reflect the association of intellectual impairment and centroparietal electrophysiological reactivity on the one hand, and autistic behavior and temporal electrophysiological reactivity on the other. This study, performed on a large population of children using objective methods of data analysis, provides validation of numerous multidisciplinary studies of autism and other developmental disorders carried out on small samples of children.
The autistic syndromes are caused by neurological dysfunctions. The capacity of autistic individuals to form representations of previous sensory impressions, useful for the processing of present information, is impaired. Self-organizing feature maps are mathematical models of cortical feature maps and may be used to simulate cortical processing. Dysfunctional self-organization, resulting in disability to extract features from stimuli, is proposed as a neural circuit theory of autism. The nature and a possible cause of dysfunction self-organization are examined. It is shown that impaired feature detection is valid for explaining the memory function in autism, the lack of drive for central coherence according to Frith's theory of autism, and a number of impairments from the diagnostic criteria. Unequal levels of impairment of different cortical feature maps can account for the typically uneven intelligence profile of autistic individuals. Excessive inhibitory lateral feedback synaptic connection strengths are presented as one factor impairing the development of feature maps. Strong or excessive inhibitory lateral feedback synaptic connection strengths also cause high sensory discrimination and abnormal sensory responses, both documented in autism. A neural circuit theory for autism has been presented. For a proof of this neural circuit theory neurological investigations are required.