Abstracts

Temporal lobe epilepsy (TLE) may cause impaired function of extratemporal association cortex during seizures. Prior neuroimaging using ictal SPECT has demonstrated decreased perfusion in frontoparietal association cortex during temporal lobe seizures, suggesting impaired function in these regions. Using intracranial EEG in patients with surgically confirmed mesial TLE, we sought to investigate remote electrographic effects of temporal lobe seizures on the association cortex. We selected 11 consecutive patients with mesial TLE and hippocampal sclerosis who had no seizures during a follow-up period of one year following surgery. Secondarily generalized seizures were excluded and up to 3 seizures were analyzed per patient (31 seizures total). Electrode contacts were assigned to one of nine cortical regions based on MRI surface reconstructions. EEG during seizures was analyzed for specific patterns including low voltage fast (LVF), rhythmic polyspike, spike-wave, irregular slowing, and post-ictal suppression. Behavioral analysis was also performed based on review of videotapes during seizures. Statistical analyses were performed by concordance of parametric (ANOVA followed by two-tailed t-tests) and nonparametric (Friedman followed by Wilcoxon) tests with a Bonferroni corrected significance threshold of 0.05. 31 seizures were analyzed in 11 patients (6 left temporal onset, 5 right). Significant increases in ictal EEG patterns (LVF and polyspike activity) were observed in mesial and lateral temporal contacts ipsilateral to seizure onset, followed by post-ictal suppression. Interestingly, bilateral frontal and ipsilateral parietal cortex exhibited large amplitude irregular slow waves during seizures which persisted into the post-ictal period. Peri-Rolandic and occipital cortex were relatively spared. These EEG patterns were accompanied by bland staring, minor automatisms, and unresponsiveness in the majority of patients. Prominent irregular intracranial EEG slowing was observed in bilateral frontal and ipsilateral parietal association cortex during and following temporal lobe seizures. We propose that this irregular slowing does not represent ictal activity, but rather, more closely resembles the EEG slowing seen in coma, sleep, or encephalopathy. EEG slowing in the frontoparietal association cortex may signify physiological impairment that contributes importantly to altered cerebral function during complex partial seizures. (Supported by Dana Foundation Clinical Hypotheses in Neuroscience award (HB).)