OBJECTIVE: To determine whether patients with neocortical epilepsy show evidence for increased excitability measured by cortico-cortical evoked potentials (CCEPs) in ictal-onset regions. METHODS: In patients undergoing intracranial recordings with subdural electrodes for epilepsy surgery, we measured amplitudes, latencies, and stimulus thresholds of CCEPs near ictal onset zones (iCCEPs), and compared with adjacent neocortex not associated with ictal EEG (nCCEP). CCEP amplitude and latency measurements were made with each stimulation site, using graded stimulation intensities. RESULTS: Ten patients were included in this study. CCEPs were recorded in eight of 10 patients. The first negative (N1) iCCEP amplitude was higher than that of nCCEP in seven of the eight patients. In the group analysis, this difference was statistically significant. In three of these patients, the difference was individually significant. In one patient, the amplitude was higher in nCCEP than iCCEP and the area selected as nCCEP was within primary eloquent cortex. There was no significant difference seen in latency changes or stimulus threshold. CONCLUSIONS: Accentuated CCEP amplitudes near ictal onset zones could reflect an increased excitability of the cortex associated with the epileptogenic zone in some patients with neocortical epilepsy. The response of the neocortex to low-frequency stimulation may vary depending on the presence or absence of intrinsic epileptogenicity.
OBJECTIVE: To determine whether patients with neocortical epilepsy show evidence for increased excitability measured by cortico-cortical evoked potentials (CCEPs) in ictal-onset regions. METHODS: In patients undergoing intracranial recordings with subdural electrodes for epilepsy surgery, we measured amplitudes, latencies, and stimulus thresholds of CCEPs near ictal onset zones (iCCEPs), and compared with adjacent neocortex not associated with ictal EEG (nCCEP). CCEP amplitude and latency measurements were made with each stimulation site, using graded stimulation intensities. RESULTS: Ten patients were included in this study. CCEPs were recorded in eight of 10 patients. The first negative (N1) iCCEP amplitude was higher than that of nCCEP in seven of the eight patients. In the group analysis, this difference was statistically significant. In three of these patients, the difference was individually significant. In one patient, the amplitude was higher in nCCEP than iCCEP and the area selected as nCCEP was within primary eloquent cortex. There was no significant difference seen in latency changes or stimulus threshold. CONCLUSIONS: Accentuated CCEP amplitudes near ictal onset zones could reflect an increased excitability of the cortex associated with the epileptogenic zone in some patients with neocortical epilepsy. The response of the neocortex to low-frequency stimulation may vary depending on the presence or absence of intrinsic epileptogenicity.
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