Abstracts

Rationale: Epileptic conditions are characterized by an altered balance between excitatory and inhibitory influences at the cortical level. Interictal "homeostasis" is maintained in part by intracortical inhibitory mechanisms. Intracortical excitation and inhibition can be investigated in vivo with cortico-cortical evoked potentials (CCEP). We hypothesized that during the interictal state, CCEPs obtained from stimulation of the ictal onset zone will have a relatively restricted distribution as compared to stimulation of cortices remote from this region. This may be due to a region of enhanced intracortical inhibition surrounding the ictal onset zone. Methods: We retrospectively reviewed CCEPs obtained in patients who underwent intracranial EEG evaluation with subdural grid electrodes (with or without additional depth electrodes) between 2008 and 2010. We identified patients with CCEPs recorded with similar stimulation parameters from both the ictal onset zone in addition to a region remote from the ictal onset zone (preferably a separate lobe). We then compared the distribution of CCEPs obtained from the highest stimulus intensity. For CCEP acquisition, we used bipolar electrical stimulation of adjacent paired subdural electrodes with a constant-current square wave pulse of 0.3 ms duration at a fixed frequency of 1 Hz. The polarity of the stimulus current was alternated. The stimulus intensity ranged from 1-15 mA. The electrocorticogram was then averaged 60 times with a time window of 200 ms time-locked to the stimulus. Results: We identified five patients who met our inclusion criteria. We studied the distribution of CCEPs obtained from five ictal onset zones in comparison to six remote regions of cortex. In four out of five of our patients, the distribution of CCEPs obtained from stimulation of the ictal onset zone was relatively restricted in comparison to that obtained from stimulation of remote cortices. Conclusions: Cortico-cortical evoked potentials provide a method of studying intracortical inhibition and excitation in epileptic patients. There appears to be a significant difference in the distribution of CCEPs recorded from the ictal onset zone as compared to cortical areas remote from this region. The restricted distribution of CCEPS recorded from the ictal onset zone during the interictal state may in part be a result of enhanced intracortical inhibitory mechanisms. Recognition of these CCEP patterns may help in identifying epileptogenic cortical regions.