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Ictal neocortical slowing in temporal lobe epilepsy

From the Departments of Neurology (Drs. Blumenfeld, Rivera, McNally, Davis, and S. Spencer), Neurobiology (Dr. Blumenfeld), and Neurosurgery (Dr. D. Spencer), Yale University School of Medicine, New Haven, CT.

Address correspondence and reprint requests to Dr. Hal Blumenfeld, Yale Departments of Neurology and Neurobiology, 333 Cedar Street, New Haven, CT 06520-8018; e-mail: hal.blumenfeld{at}yale.edu

Background: Temporal lobe epilepsy (TLE) may affect brain regions outside the temporal lobe, causing impaired neocortical function during seizures.

Methods: The authors selected 11 consecutive patients with mesial TLE and hippocampal sclerosis who underwent intracranial EEG monitoring and had no seizures during a follow-up period of at least 1 year after temporal lobe resection. Secondarily generalized seizures were excluded, and up to three 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 postictal suppression.

Results: Mesial and lateral temporal contacts on the side of seizure onset showed significant increases in ictal patterns such as LVF and polyspike activity, followed by postictal suppression. Bilateral frontal and ipsilateral parietal cortex exhibited large amplitude irregular slow waves during seizures. This frontoparietal slowing persisted into the postictal period. Perirolandic and occipital cortex were relatively spared. These EEG patterns were accompanied by bland staring, minor automatisms, and unresponsiveness or amnesia in the majority of patients studied.

Conclusions: Prominent irregular slowing occurs in bilateral frontal and ipsilateral parietal association cortex during and after temporal lobe seizures. EEG slowing in the frontoparietal association cortex may signify physiologic impairment that contributes to widespread altered cerebral function during partial seizures.

Received December 29, 2003. Accepted in final form May 14, 2004.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the September 28 issue to find the title link for this article.

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