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Metabolic Factors Interest has focused on the role of excitatory neurotransmitters, particularly glutamate and aspartate, which are formed from glycolytic intermediates of the Krebs cycle It has been found that these neurotransmitters, released by ischemic cells, excite neurons and produce an intracellular in ux of Na and Ca These changes are said to be responsible for irreversible cell injury This is presently a subject of active biochemical and clinical research Some current attempts at therapy, for example, are directed at limiting the extent of infarction by blocking the glutamate receptor, particularly the NMDA (N-methyl-D-aspartate) channel one of several calcium channels that open under conditions of ischemia and set in motion a cascade of cellular events, eventuating in neuronal death However, even complete blockade of the NMDA channels has so far not prevented cellular death, presumably because dysfunction of several other types of calcium channels continues Novel strategies have been suggested to prevent calcium in ux, but the drugs that block the various calcium channels seem to work only if given before the stroke, making this approach impractical in most situations Additional biochemical events must be induced by ischemia, including the production of free radicals, which leads to peroxidation and disruption of the outer cell membrane Clearly, the cascade of intracellular events that lead to neu-

that project to and from the basal ganglia and pass through it on their way to cortical and limbic areas certainly play a role in the creation of abnormal movements In other words, strict localization of basal ganglionic function is not likely to stand up to critical analysis Furthermore, a role for the basal ganglia in cognitive function and abnormal behavior is hinted at provocatively in Parkinson disease, progressive supranuclear palsy, Tourette syndrome, and other processes, as summarized by Ring and Serra-Mestres A certain slowness in thinking has been alluded to earlier, but it is quite

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inconsistent Again, it would be an oversimpli cation to assign primary importance to the presence of depression, dementia, psychosis, and other disturbances in disease of the basal ganglia or to view changes in these structures as proximate causes of obsessivecompulsive and other behavioral disorders, but some role as part of a larger circuitry is likely All that can be stated is that such a role is likely in complex behavior, but its precise nature is not known at this time

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