A 66 year old male with hypertension, diabetes, hypercholesterolemia, and TIA is admitted after an episode of acute confusion and left hemiparesis. He was found down at home by his wife stuporous without recall of the event with a deficit that resolved within 1 hour. Retrospectively the patient had brief monthly episodes of "confusion" for 4 years since his TIA that would make him sleepy though he did not recall them. MRI brain, laboratory, and cardiac evaluations were unrevealing. Carotid ultrasound showed left carotid stenosis < 50% and right carotid stenosis (50-69%). This was validated by CT angiography with a right carotid cross-sectional stenosis of 60-70%. He was diagnosed with crescendo TIAs and underwent right carotid surgery with intraoperative EEG.
Figure: Intraoperative EEG demonstrating diffuse suppression on initial carotid clamping.
Patients > 65 years of age with epilepsy represent the most rapidly growing segment of the population. The predominance of cerebrovascular disease and other co-morbidities imply risk for a structural etiology. Focal seizures may commonly be associated with amnesia and mimic other neurological conditions1. In our patient stroke was suspected due to risk factors coupled with a post-ictal focal neurological deficit (Todd’s phenomenon). Carotid endarterectomy was performed with the intraoperative EEG demonstrating a diffuse suppression during clamping created by focal ischemia. Shunting was performed, the EEG resolved, and the patient recovered. Leviteracetam was later begun and he has remained seizure free on a follow-up 24 hour ambulatory EEG. Seizures may be distinguished from TIAs by their paroxysmal brief duration, impaired consciousness, and post-ictal state despite the absence of awareness.
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