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We measured biochemical markers of excitability in brain excised for neurosurgical therapy of epilepsy. Intraoperative electrocorticography was used to identify and compare samples from regions of persistent interictal spike discharges and areas of the cerebral convexity which were free of interictal piking. We found that interictal spiking was associated with elevated tissue levels of the excitatory amino acids glutamic acid (26%, p < 0.001) and aspartic acid (25%, p < 0.05). There was also a significant increase in the activity of the enzymes glutamic acid dehydrogenase (20%, p < 0.01) and aspartate acid aminotransferase (18%, p < 0.01) which are involved in their formation. There was no change in the levels of the inhibitory neurotransmitters GABA or taurine. We also found a significant increase in the activity of tyrosine hydroxylase (52%, p < 0.001), the rate controlling enzyme in catecholamine biosynthesis. There was a reduction in the density (Bmax) of cortical alpha-1 adrenoceptors (26%, p < 0.01) and a concommitant diminution of receptor coupled phosphatidylinositide metabolism (21%, p < 0.01). This blunting of inhibitory noradrenergic transmembrane signaling may contribute to a relative imbalance between excitatory and inhibitory mechanisms in epileptogenic neocortex.
Consecutive craniotomies (118) drawn from major hospitals, and performed for disorders other than epilepsy or acute trauma were reviewed. The final diagnosis included tumor (70), subdural hematoma (13), aneurysm (10), arteriovenous malformation (7), and miscellaneous lesions (18). Eighty-seven (73.7%) patients had not experienced seizures prior to neurosurgery, II of these (12.6%) had a seizure within the first week, in six the attack occurred within 24 hours, and of these three had further attacks. In contrast, of the 31 patients (26.3%) that had one or more seizures prior to operation, II patients (35.5%) had seizures within the first week. In ten patients seizures occurred within the first 24 hours and of these seven had one or more recurrences later in the week. Anticonvulsant drugs were administered to 72 patients before operation, including all those with a history of seizures, hut loading doses were not utilized to ensure therapeutic levels. In patients with predisposing factors to postoperative seizures, anticonvulsant drugs should be administered before or immediately following craniotomy in adequate dosage to rapidly achieve and maintain effective plasma levels. Phenytoin, owing to its minimal sedative effects is the drug of choice. A loading dose of18 milligrams per kilogram can be safely administered as an admixture to an intravenous infusion of 0.9% saline with careful monitoring of cardiopulmonary function.
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