Late Post-infarction Epilepsy.
- Author:
Jae Moon KIM
1
;
In Beom SONG
;
Hee Jung SONG
;
Ae Young LEE
;
Chin Sang CHUNG
Author Information
1. Department of Neurology, College of Medicine, Chungnam National University, Korea.
- Publication Type:Original Article
- MeSH:
Brain Diseases;
Cerebral Infarction;
Diabetes Mellitus;
Epilepsy*;
Heart;
Humans;
Hypertension;
Motor Cortex;
Paresis;
Pathology;
Seizures
- From:Journal of the Korean Neurological Association
1994;12(4):675-685
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The clinical features of cerebral infarction (CI) which cause late post-infarct epilepsy (PIE), are not well understood. We tried to identify the clinical signs which might be associated with late PIE development. We analyzed 60 consecutive patients (PIE group) who had recurrent seizures at least a week after the CI. Neuroradiological findings, clinical features during the acute phase of CI, types of seizures, and the interval between CI and first seizure were analyzed. These data were compared with those of randonly sampled nonepikptic patients with CI (60 patients with CI group). In the epikptic patients who had the history of previous CI (46 patients), hemiparesis was frequent symptom during the acute phase of CI (93.5%). Diabetes mellitus and hypertension were frequent underlying illnesses and were not different between the groups. Heart diseaseswere common in PIE group (40% vs. 13.3%) and correspondingly, the cortical CI involving the superior division of the MCA including motor area was frequent brain pathology (46.7%). Seizures usually began with focamotor activity (50%), but generalized seizure ws also common (35%). In 14 patients, silent CI was identified after the first seizure. Their usual site of CI was subcortical (42.9%), whereas the subcortical CI was infrequent in those with history of CI (13.0%). Acute PIE occurred in six patients and persisted thereafter. These findings suggest that the cortical infarct involving the motor cortex is frequent pathology in the late PIE, that acute PIE may remains as late PIE, and that silent infarct may be an important cause in adult-onset epilepsy.