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NEUROLOGY 1984;34:927
© 1984 American Academy of Neurology

Enzyme changes in actively spiking areas of human epileptic cerebral cortex

Allan Sherwin, Felipe Quesney, Serge Gauthier, André Olivier, Yvon Robitaille, Patricia McQuaid, Christine Harvey and Nico van Gelder

From the Montreal Neurological Institute, the Department of Neurology and Neurosurgery (Drs. Sherwin, Quesney, Gauthier, Olivier, and Rohitaille, and Ms. McQuaid and Harvey), McGill University, et le Centre de recherche en sciences neurologiques, Département de physiologie (Dr. van Gelder), Faculté de médecine, Université de Montréal, Montreal, Québec, Canada.

Five enzymes involved in glutamic acid, GABA, and catecholamine metabolism were measured in epileptic human brain. Electrocorticographically defined areas of focal spiking were compared with samples from surrounding nonspiking cortex. Comparative enzyme activities were as follows (µmol/h/g wet wt): glutamic acid dehydrogenase (GDH)-spiking 135.77 ± 10.22 (mean ± SEM), nonspikingll8.58 ± 9.42 (p < 0.001, N = 17); gluotamicacid decarboxylase—spiking 10.63 ± 0.95, nonspiking 9.96 ± 1.10 (NS, N = 13); GABA-aminotransferase—spiking 36.49 ± 1.05, nonspiking 36.46 ± 1.48 (NS, N = 12); glutamine synthetase-spiking 96.94 ± 3.81, nonspiking 96.52 ± 4.10 (NS, N = 20); and tyrosine hydroxylase (TH; nmol/h/g)-spiking 16.23 ± 2.39, nonspiking 10.67 ± 1.95 (p < 0.001, N = 14). Increased activity of GDH and TH may prove useful to characterize further areas of active spiking in human focal epilepsy.

Address correspondence and reprint requests to Dr. Sherwin, Montreal Neurological Institute. 3801 University Street, Montreal, Quebec, Canada H3A 284.

Supported by the Medical Research Council of Canada.

Presented in part at the thirty-fourth annual meeting of the American Academy of Neurology, Washington, DC, May 1982.

Accepted for publication December 1, 1983.






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