Development of epilepsy after posterior reversible encephalopathy syndrome. (January 2016)

• Record Type: Journal Article
• Authors: Heo, Kyoung; Cho, Kyoo Ho; Lee, Moon Kyu; Chung, Su Jin; Cho, Yang-Je; Lee, Byung In
• Is Part Of: Seizure. Volume 34(2016)
• Page Start: 90
• Page End: 94
• Publication Date: 2016-01
• Subjects: PRES posterior reversible encephalopathy syndrome -- AED antiepileptic drug -- SE status epilepticus -- HS hippocampal sclerosis -- GTCS generalized tonic-clonic seizure -- PLED periodic lateralized epileptiform discharge -- FLAIR fluid-attenuated inversion recovery -- DW diffusion-weighted -- HE hypertensive encephalopathy -- TLE temporal lobe epilepsy; Epilepsy -- Seizure -- Posterior reversible encephalopathy syndrome -- Risk factors; Epilepsy -- Periodicals; Epilepsy -- Periodicals; Seizures -- Periodicals; Épilepsie -- Périodiques; Electronic journals; Electronic journals; 616.853
• DOI: 10.1016/j.seizure.2015.12.005
• Languages: English
• ISSNs: 1059-1311

Abstract

Highlights: Four out of 102 patients with PRES (3.9%) subsequently developed epilepsy. Cytotoxic edema and status epilepticus may predict the development of epilepsy. Epileptic foci corresponded to the regions with cytotoxic or severe vasogenic edema. Abstract: Purpose: This study was intended to describe the risk of epilepsy subsequent to posterior reversible encephalopathy syndrome (PRES) and the clinical features of post-PRES epilepsy. Method: We retrospectively identified all patients with PRES who were admitted to Severance Hospital and consulted with the Department of Neurology between 2001 and 2013 and the subgroup of these patients who subsequently developed epilepsy. We also describe clinical features of patients who were not treated with PRES as inpatients at our center but who presented later with post-PRES epilepsy during the study period. We studied clinical characteristics during the acute symptomatic phase of PRES and after the development of epilepsy. Results: During the study period 102 patients were treated at our center during the acute phase of PRES. Four of these patients (3.9%) subsequently developed epilepsy. Two additional patients with a history of PRES presented to our hospital after the acute phase of their illness with post-PRES epilepsy. During the acute phase, five of six patients had acute symptomatic seizures and four had convulsive or nonconvulsive status epilepticus (SE). Acute phase MRI showed cytotoxic edema in five patients, and follow-up MRI showed focal atrophic changes including hippocampal sclerosis in four. Presumptive epileptogenic foci were located in the left-side temporal, parietal and occipital lobes, corresponding to the regions that showed cytotoxic edema or severe vasogenic edema as well as with the location or lateralization of EEG abnormalities during the acute phase. Conclusion: Our findings indicate a small but not insignificant risk for the development of epilepsy after PRES. The presence of cytotoxic edema and severe, acute symptomatic seizures, such as SE suggests irreversible brain damage and may predict the development of epilepsy.