Pathophysiology of acute brain damage following epilepsy.
The possible pathophysiological mechanisms, both intrinsic and systemic, leading to acute brain damage following epilepsy are reviewed. In particular involvement of changes in blood brain barrier, alterations of acid base regulation in the brain, release of a variety of mediator compounds, such as arachidonic acid and glutamate, intracellular influx of calcium ions, and the inhibition of protein synthesis are discussed. Finally, pathophysiology of brain damage following epilepsy is compared with that following ischaemia and hypoglycaemia.
Baethmann
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Institute for Surgical Research, Ludwig-Maximilians-University of Munich, Federal Republic of Germany.
D000136:Acid-Base Equilibrium / Q000502:physiology; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000502:physiology; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D004828:Epilepsies, Partial / Q000503:physiopathology*; D006801:Humans; D009474:Neurons / Q000502:physiology
D001095:Arachidonic Acids; D016718:Arachidonic Acid