Localized cerebral hypoglycemia simulating stroke

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Abstract
Clinical and experimental evidence is presented to show that in the presence of a relative area of ischemia of the brain, hypoglycemia produces a localized reversible paralysis of neuronal function, with resultant motor and sensory deficit. During this stage of paralysis, metabolic utilization of O2 is impaired. Administration of glucose restores normal functional activity and O2 consumption to the area of hypoglycemic brain. It is presumed that the localized neuronal paralysis is the result of a reduced availability of glucose in the ischemic area, and that administration of glucose rapidly restores the deficient substrate. If sufficiently prolonged, localized hypoglycemia becomes irreversible and necrosis of nerve cells occurs.