Subacute electrical stimulation of the hippocampus blocks intractable XXXX and paroxysmal EEG activities.

@entity1 @entity410 @entity302
PURPOSE: To investigate the clinical, electroencephalographic (EEG), and histopathologic effects of subacute electrical stimulation of the hippocampal formation or gyrus (SAHCS) on 10 @entity1 with intractable @entity410 . METHODS: Bilateral, depth, hippocampal or unilateral, subdural, basotemporal electrodes were implanted in all 10 @entity1 for a topographic diagnosis of the site and extent of the @entity302 focus before a temporal lobectomy. In all patients, antiepileptic drugs (AEDs) were discontinued from 48 to 72 h before a program of continuous SAHCS, which was performed for 2-3 weeks. Stimulation parameters were biphasic Lilly wave pulses, 130/s in frequency, 450 micros in duration, and 200-400 microA in amplitude. The stimuli were delivered 23 of every 24 h for the 2-3-week SAHCS period. The effects of SAHCS on the number of clinical @entity410 per day and the percentage of interictal EEG spikes per 10-second samples of maximal paroxysmal activity at the @entity302 focus were determined daily during the 16 days of SAHCS. At the completion of this program, @entity1 underwent an en bloc temporal lobectomy, and the histopathologic effects of SAHCS on the stimulated tissue were analyzed by means of light-microscopy studies. RESULTS: In seven @entity1 whose stimulation electrode contacts were placed within the hippocampal formation or gyrus and who experienced no interruption in the stimulation program, SAHCS abolished clinical @entity410 and significantly decreased the number of interictal EEG spikes at the focus after 5-6 days. The most evident and fast responses were found by stimulating either the anterior pes hippocampus close to the amygdala or the anterior parahippocampal gyrus close to the entorhinal cortex. Other surface, hippocampal, and basotemporal EEG signs predicted and accompanied this antiepileptic response. These included an electropositive DC shift and monomorphic delta activity at the medial hippocampal and parahippocampal regions, and a normalization of the background EEG activity and signs of slow-wave sleep in surface. depth, and subdural regions. In contrast, no evident antiepileptic responses or no responses at all were found in three @entity1 when stimulation was either interrupted or when it was administered outside the hippocampus. Light microscopy analysis of the stimulated hippocampal tissue showed histopathological abnormalities attributable to the depth-electrode penetration damage or to the pial surface reaction to the subdural, Silastic electrode plate. However, no evident histopathological differences were found between the stimulated and nonstimulated hippocampal tissue. CONCLUSIONS: SAHCS appears to be a safe procedure that can suppress temporal lobe epileptogenesis with no additional damage to the stimulated tissue.
