 |
|
Human Epileptic BrainNa, K ATPase Activity and Phenytoin Concentrations
Richard L. Rapport II, MD;
A. Basil Harris, MD;
Patrick N. Friel;
George A. Ojemann, MD
Arch Neurol. 1975;32(8):549-554.
Abstract
An abnormal flux of monovalent cations may be related to the epileptogenic process in man. One possible mechanism for deranged electrolyte metabolism in epileptic brain is an abnormality in sodium, potassium-dependent adenosine triphosphatase (Na, K ATPase). We found the activity of Na, K ATPase to be significantly less in epileptic human cortex than in nonepileptic cortex. Histological changes have been simultaneously evaluated in epileptic brain. A second membrane-bound enzyme, acetylcholinesterase (AChE), was also assayed as a marker for neuronal membranes and found not to correlate with the epileptogenicity of human brain. In addition, the concentrations of the anticonvulsant compound phenytoin have been determined in the serum and cerebral cortex of epileptic and nonepileptic patients. The ratio of phenytoin in cortex to serum concentration is significantly lower in epileptic patients than in nonepileptic controls.
Author Affiliations
From the Department of Neurological Surgery, University of Washington School of Medicine, Seattle.
Footnotes
Accepted for publication Oct 14, 1974.
Reprint requests to Department of Neurological Surgery, University of Washington School of Medicine, Seattle, WA 98195 (Dr. Rapport).
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Intravenous Lidocaine in the Treatment of Convulsions
Lemmen et al.
JAMA 1978;239:2025-2025.
ABSTRACT
Prophylactically Administered Phenytoin: Effects on the Development of Chronic Cobalt-Induced Epilepsy in the Cat
Rapport and Ojemann
Arch Neurol 1975;32:539-548.
ABSTRACT
|
