A Neurological Model for Childhood Autism

TLDR

The mesolimbic cortex and striatum together form the target area of dopaminergic mesencephalic neurons, a region distinct in cytoarchitecture, vasculature, and neurochemistry. The study analyzes behavioral and motor disturbances in childhood autism and proposes that the syndrome stems from dysfunction in bilateral neural structures including the mesolimbic cortex, neostriatum, and thalamic nuclei. This dysfunction may arise from macroscopic or microscopic changes in these structures or their functional partners, caused by perinatal viral infection, periventricular watershed insults, or genetic neurochemical abnormalities. The findings suggest that autism may be linked to neuromediator imbalance within these neural structures.

Abstract

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.