Prevalence of Epilepsy and the Demographics, Clinical and Paraclinical Features in Patients with Multiple Sclerosis (P3.360)

2017 
Objective: To study prevalence of epilepsy and to examine the demographics, clinical and paraclinical characteristics of MS patients with diagnosis of epilepsy in a well defined cohort of MS patients. Background: Prevalence of epilepsy is 0.5–1% in general population. Emerging studies suggest prevalence and incidence of epilepsy is higher in patients with multiple sclerosis (MS), however the exact mechanism and underlying pathophysiology are still unknown. Design/Methods: Patients were identified in Comprehensive Longitudinal Investigation of Multiple Sclerosis at Brigham and Women’s Hospital database (CLIMB) by applying Research Patient Data Registry (RPDR) query, using key words; multiple sclerosis and Levetiracetam. We collected information on MS disease at seizure onset (age, MS type, duration, MS treatment and EDSS), seizure type and MRI and electroencephalography (EEG) features. Results: 47 MS patients with diagnosis of epilepsy were identified in our database (47/2288, 2%). 37/47 had epileptic seizure secondary to MS, 5/47 with primary brain tumor and 5/47 due to brain contusion/bleed. With regard to patients demographics; mean age and disease duration at seizure onset were 44.4y (range: 22–73) and 12y (range: 0–42) respectively. 64% (24/37) of patients had relapsing remitting MS at seizure onset and mean Expanded Disability Status Scale (EDSS) was 3.2 (range: 0–7.5). New MS lesions serving as possible seizure focus was identified in less than half of the patients (18/37, 48.6%). Majority of cases had either generalized seizure (19/37) or partial seizure with secondary generalization (7/37). Sharp waves/PLEDs (12/25) and focal slowing (10/25) were the most common EEG findings at seizure onset. Conclusions: Prevalence of epileptic seizure is increased in our MS database similar to other reports. About half of our patients had first onset seizure when in progressive disease stage and without an identifiable new MS plaques which suggest possible network failure or subclinical grey matter lesions as mechanisms of epileptic activity. Disclosure: Dr. Baharnoori has nothing to disclose. Dr. Stankiewicz has received personal compensation for activities with Teva Neuroscience, Novartis, Sanofi Genzyme, Biogen Idec, Genentech, and Bayer as a consultant. Dr. Chitnis received personal compensation for activities with Roche-Genentech and Sanofi-Genzyme. Dr. Chitnis received research support from EMD Serono, Biogen, Novartis and Verily.
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