The neurochemical effects, patterns of cerebral blood flow derangement, time course and distribution of brain tissue damage, and selective neuronal necrosis resulting from hypoglycemia are compared to the biological effects of ischemia and epilepsy in a neurological progress report from the Departments of Pathology and Clinical Neurosciences, University of Calgary, Alberta, Canada, and the Laboratory for Experimental Brain Research, University Hospital, Lund, Sweden. Hypoglycemia interferes with cerebral energy production, causing membrane depolarization, loss of ion homeostasis, and lipolysis with accumulation of free fatty acids. Tissue aspartate and quinolinic acid levels rise and glutamate levels in CNS tissue fall during hypoglycemia. Cerebral blood flow is increased during the insult and decreased following the insult. Energy failure is moderate in degree with ATP levels dropping to 25 to 30% of control. Unlike ischemia and epilepsy, hypoglycemia is not accompanied by lactic acidosis. The duration of hypoglycemic insult required to produce selective neuronal necrosis is 10-20 min and neuronal death occurs within 1-8 hrs. [1]

COMMENT. Ischemia, hypoglycemia, and epilepsy, long thought to produce similar or identical brain damage, apparently have different mechanisms and effects on brain tissue. Insults of equal duration are not equipotent in causing brain damage. Ischemia is much more potent than hypoglycemia, and hypoglycemia is more potent than status epilepticus per minute of insult. The timing of neuronal necrosis evolves over hours to days in ischemia, minutes to hours in hypoglycemia, and during or very shortly after the insult of status epilepticus.