AFTER-DISCHARGES PROVOKED BY ELECTRICAL STIMULATION OF HUMAN CORTEX: PROPERTIES AND SIGNIFICANCE
Abstract number :
1.309
Submission category :
Year :
2002
Submission ID :
2657
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Parbeen K. Pathak, Daniel C. Jones, Warren T. Blume. Clinical Neurological Sciences, LHSC - University Campus, London, Ontario, Canada
RATIONALE: Although localising significance of electrically evoked clinical and subclinical seizures for epileptogenesis remains undetermined, whether scrutiny of after-discharge morphologies and other properties would clarify this issue remains undetermined. This report describes after-discharge (AD) properties from electrical cortical stimulation via subdural electrodes in 29 patients.
METHODS: We used biphasic usually monopolar stimuli at 0.3 msec, 50 Hz and 1-18 mAMP strengths in patients undergoing strip or grid subdural EEG for surgical candidature.
RESULTS: AD thresholds varied moderately among patients and only slightly among regions with mesial occipital and mesial frontal areas lower than convexity non-temporal regions. 33,058 stimuli evoked 402 (12%) ADs whose morphologies were: 1-4 Hz spike or polyspike bursts (163), sequential spikes (146), spike-waves (55), rhythmic waves (32) and rhythmic waves plus spikes (6). ADs lasted 1-20 seconds, those of 20/29 patients from 6-15 seconds. Morphological evolution as subclinical seizures (Blume et al., EEG Morphology of Partial Epileptic Seizures; Electroenceph. Clin. Neurophys (1984) 57:295-302) occurred in 39 (10%). Fourteen (44%) of 32 rhythmic wave ADs so evolved, more than from other AD morphologies (25 of 370 (7%)) (P[lt]0.0001). However, origin of such evolving ADs correlated with spontaneous seizure onset in only 6 (40%) while origins of electrically evoked clinical seizures correlated with spontaneous seizure origin in only 6 (46%) of 13 instances.
CONCLUSIONS: Subclinical or clinical seizures evoked by electrical stimulation of human cortex do not reliably localise epileptogenesis.