A neurological model for childhood autism.
We analyze the behavioral and motor disturbances in childhood autism. On the basis of analogy to signs and conditions seen in adult neurology, we propose that the syndrome results from dysfunction in a system of bilateral neural structures that includes the ring of mesolimbic cortex located in the mesial frontal and temporal lobes, the neostriatum, and the anterior and medial nuclear groups of the thalamus. The mesolimbic cortex is cytoarchitectonically, angioarchitectonically, and neurochemically distinct and, along with the striatum, forms the entire target area of dopaminergic mesencephalic neurons. This raises the possibility that autism is related to neuromediator imbalance in those structures. Such dysfunction might be the result of macroscopic or microscopic changes in the target area or in structures functionally influencing them, consequent to a variety of causes such as perinatal viral infection, insult to the periventricular watershed area, or genetically determined neurochemical abnormalities.
D001288:Attention; D001321:Autistic Disorder / Q000209:etiology / Q000503:physiopathology; D001479:Basal Ganglia / Q000503:physiopathology; D002648:Child; D003192:Compulsive Behavior / Q000503:physiopathology; D005625:Frontal Lobe / Q000503:physiopathology; D006801:Humans; D008032:Limbic System / Q000503:physiopathology; D008959:Models, Neurological; D009069:Movement Disorders / Q000503:physiopathology; D010468:Perceptual Disorders / Q000503:physiopathology; D012920:Social Behavior Disorders / Q000503:physiopathology; D013064:Speech Disorders / Q000503:physiopathology; D013702:Temporal Lobe / Q000503:physiopathology; D013788:Thalamus / Q000503:physiopathology