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.

Patients with drug-refractory temporal lobe epilepsy can be treated successfully with surgical resection of one temporal lobe, especially when the resection includes the hippocampus. Although intrahippocampal recordings usually localize seizure onsets to one hippocampus, there are bilaterally-independent interictal spikes, occasional contralateral seizure onsets and post-resection seizures that implicate contralateral damage and epileptogenicity. Post-mortem onquantified studies of both hippocampi in epileptics have revealed incidences of bilateral hippocampal sclerosis, mostly being asymmetric. The present paper reports on two post-mortem cases of bilateral, asymmetric cell loss in patients with physiologically-verified hippocampal epilepsy. In one patient the damage was severe bilaterally, but only slightly greater damage in one hippocampus. In the second patient, damage in one hippocampus was as severe as in the first patient; however the contralateral hippocampus appeared undamaged. However, cell counts revealed losses of over 30% in three different hippocampal subregions, indicating a mild form of asymmetric bilateral damage in patient two.

The effectiveness of long term EEG monitoring in the localization of the epileptic focus was studied in 37 patients with temporal lobe epilepsy comprising 190 recorded seizures, in 19 frontal lobe epileptic patients with 172 recorded seizures and in 12 additional patients which were classified as fronto-temporal. In the temporal lobe group, 49/190 seizures began focally (26%) and 20/190 seizures exhibited a regional onset (10%). In the frontal lobe group, only 21 out of 172 seizures (12%) had a focal ictal onset. 41/172 seizures began regionally (24%). In the fronto-temporal group, 31/55 seizures disclosed a focal EEG onset (57%). This study demonstrates that there is a two-fold increase in seizures beginning focally in the temporal lobe epilepsy group versus the frontal lobe group.