Abstract Details

Title The Pathogenesis and A Novel Surgical Approach to Treating Drug-Resistant Status Epilepticus Associated with Neurocysticercosis

Topic Epilepsy/Clinical Neurophysiology (EEG)

Presentation(s) P5 - Poster Session 5 (5:30 PM-6:30 PM)

Poster/Presentation
Number 6-027

Objective We describe a case of status epilepticus in the setting of neurocysticercosis that illuminates its potential pathophysiology and treatment.

Background Although neurocysticercosis (NCC) is implicated as a major cause of epilepsy worldwide, it is unknown whether NCC directly causes seizures, occurs as an incidental finding, or exists as part of a dual pathology in which a concomitant, unrelated brain lesion and a NCC lesion jointly contribute to epileptogenesis. Additionally, there is no clear consensus on treatments for antiepileptic drug (AED)-resistant epilepsy associated with NCC lesions.

Design/Methods Case report and literature review.

Results A 52-year-old right-handed man presented with recurrent seizures characterized by visual symptoms. His continuous video EEG monitoring showed subclinical status epilepticus arising from the right occipital region. His intracranial imaging revealed numerous scattered bilateral supratentorial ring-enhancing lesions presumed to be due to cysticercosis and encephalomalacia with ex-vacuo enlargement of the trigone and occipital horn secondary to a subdural hygroma. He was subsequently diagnosed with neurocysticercosis. Despite treatment with an optimized regimen of AEDs and anti-helminthic agents, his seizures persisted. As the seizures were well localized and refractory to medical management, further workup with a right occipital craniotomy was done with intraoperative corticography, which demonstrated frequent spikes in the right superior occipital gyrus. Right occipital and intraventricular lesions were excised for pathological analysis, which confirmed the presence of degenerated cysticercal organisms from the intraventricular cyst and the right occipital lesion. After the occipital lesion craniotomy, the patient achieved complete seizure-free remission, suggesting that the NCC lesion with gliosis was directly involved in the pathogenesis of epileptic seizures.

Conclusions

Our report elucidates a possible pathogenic relationship between calcified NCC cysts with perilesional gliosis and pharmacologically resistant epilepsy, and encourages the potential utilization of surgical resection of calcified NCC lesions localized to epileptogenic epicenters of seizure activity to pathologically confirm diagnosis and treat recalcitrant epilepsy.

Authors/Disclosures
Christina Law, NP (Sutter Health) PRESENTER	No disclosure on file
Jayant N. Acharya, MD, DM, FAAN (Southern Illinois University School of Medicine)	Dr. Acharya has nothing to disclose.
	No disclosure on file
	No disclosure on file
Vinita J. Acharya, MD, FAAN	Dr. Acharya has nothing to disclose.

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