Cardiogenic cerebral infarction in the parietal lobe predicts the development of post-stroke epilepsy

Abstract

PurposePost-stroke epilepsy (PSE) is a major late complication of cardioembolic cerebral infarction. However, few studies have examined the epileptogenicity and characteristics of first-occurrence cardioembolic cerebral infarctions. MethodsThis retrospective study included 93 consecutive patients with old cardioembolic cerebral infarctions who were classified into two groups based on their epileptic history: patients presenting with PSE or stroke without seizure (SWS). Each patient was diagnosed with an epileptic seizure subtype and treated with appropriate anti-epileptic therapy after admission. We evaluated clinical characteristics, laboratory results, and intracranial infarct areas. The sizes of these areas were measured using MRI diffusion-weighted image (DWI) of each patient after their first stroke. The volume was calculated by multiplying the total slice area with the slice thickness. ResultsPSE was diagnosed in 43 (46.2 %) of 93 patients. The mean (± SD) time from infarction onset to the first seizure in the PSE group was 22.5 ± 31.6 months. The PSE group exhibited significantly more atrial fibrillation (p = 0.022) and higher glucose levels (p < 0.001) compared with the SWS group. The most common PSE seizure type was focal to bilateral tonic-clonic seizure (61.0 %). Although DWI did not reveal any significant differences in the volume of infarctions between the two groups, the involvement of the parietal lobe in infarction of the PSE group (69.8 %) upon first admission was significantly higher (p = 0.006) than that of the SWS group (40.0 %). Multiple logistic regression analysis revealed that parietal lobe involvement in infarction (OR 4.95; 95 % CI 1.25–19.60; p = 0.023) was a significant independent predictor of PSE. ConclusionThe involvement of the parietal lobe in infarction was a significant independent predictor of PSE. Dysfunction of the parietal lobe might play a critical role in the epileptogenesis of PSE.