Accentuated cortico-cortical evoked potentials in neocortical epilepsy in areas of ictal onset

Epileptic Disorders - Tập 12 - Trang 292-302 - 2011
Masaki Iwasaki1,2, Rei Enatsu1, Riki Matsumoto1,3, Eric Novak4, Baburaj Thankappen1, Zhe Piao1, Tim O’Connor R1, Karl Horning1, William Bingaman1, Dileep Nair1,4
1Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, USA
2Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan
3Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
4Biostatistics, Department of Qualitative Health Sciences, Cleveland Clinic, Cleveland, USA

Tóm tắt

To determine whether patients with neocortical epilepsy show evidence for increased excitability measured by cortico-cortical evoked potentials (CCEPs) in ictal-onset regions. 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. 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. 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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