Abstracts

Rationale: Cerebral hyper perfusion syndrome (CHS) can occur after carotid endarterectomy (CEA) or carotid stenting. The initial clinical features include traditional triad of ipsilateral headache, transient focal motor seizures and cerebrovascular events. Most seizures may present up to three weeks after CEA. The classic semiology of seizures is focal motor seizures; although secondary generalized seizures may manifest. Status epilepticus is very rare and nonconvulsive status epilepticus has not been reported in literature. We report a case of refractory nonconvulsive status epilepticus as an initial manifestation after CEA.Methods: Hospital patients database were reviewed from 1980 to 2006. Patient’s diagnosis, complications after CEA, EEG recordings, hospitalization course and imaging findings were reviewed. One patient was identified who presented with nonconvulsive status epilepticus as a presenting manifestation of CHS.Results: Seventy four year old man with medical history of HTN and CAD who had right CEA 9 days before presenting to the ER with unilateral headache, impairment of consciousness and a generalized seizure. He was found to have right hemiparesis and was intubated. Initial MRI showed asymmetric diffusion hyperintensity within the cortex with subcortical white matter of the right frontal, parietal and temporal lobes. These changes were marked without any effect on ADC maps. There was prominent vasogenic edema over corresponding areas, as well as a small subarachnoid hemorrhage near the vasogenic edema. Considering the recent CEA and comatose patient, continuous video EEG monitoring was performed for several days. EEG showed hemispheric asymmetry and right hemisphere pseudo periodic to periodic, rhythmic, evolving waxing and waning electrographic discharges, which are epileptogenic. No clinical activities were noted during electrographic discharges. His nonconvulsive status epilepticus was initially refractory to antiepileptic medications. He was treated with dilantin, depakote, keppra, topomax, and maximum doses of propofol. His electrographic discharges were controlled with an addition of midazolam drip. After seizure control, his neurodeficits were improved and eventually had a nonfocal examination. He was transferred to rehabilitation.Conclusions: Seizures are frequent complaints of CHS, however refractory nonconvulsive status epilepticus has not been reported in literature. Appropriate management remains a cornerstone in CHS. The etiologies for seizures after CHS remain speculative. Damage to cerebral endothelium may attenuate or abolish the myogenic autoregulation. Release of nitric oxide, oxygen derived free radicals may damage the endothelium. The relative infrequency of CHS appears to be the main reason why this entity is poorly understood.