1043-3155 Pediatr Neurol Briefs pedneurbriefs Pediatr Neurol Briefs Pediatric Neurology Briefs Pediatr Neurol Briefs 2166-6482 1043-3155 2166-3155 Pediatric Neurology Briefs Publishers Chicago, IL, USA PNB-2-83-a 10.15844/pedneurbriefs-2-11-3 Metabolic Disorders Neurology Pediatrics Nervous System Diseases Child Development Brain Diseases Neurosurgery Child Infant Hypoglycemia and Brain Damage http://orcid.org/0000-0002-0173-7931 Millichap J. Gordon MD 1 2 * Division of Neurology, Children's Memorial Hospital, Chicago, IL Departments of Pediatrics and Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL Correspondence: Dr. J. Gordon Millichap, E-mail: jgmillichap@northwestern.edu 11 1988 01 08 2016 2 11 83 83 Copyright: © 1988 The Author(s) 1988 This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Biological differences between ischemia, hypoglycemia, and epilepsy

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.

 Cerebral Blood Flow Neurological Progress Report Lactic Acidosis

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.

 Auer RN Siesjö BK Biological differences between ischemia, hypoglycemia, and epilepsy Ann Neurol 1988 Dec 24 6 699 707 10.1002/ana.410240602 3061362