A case of epilepsia partialis continua was caused by a subdural hematoma. Muscular contractions occurred primarily in the abdominal region. In this instance, the etiology of the syndrome is unique, and the primary involvement of the abdominal musculature is remarkable. Recent neurophysiological studies have shown the abdominal muscles to be separately represented in the cerebral cortex and to have a specific descending pathway in the spinal cord. The case reported here may be the clinical expression of activity in such a neural pathway.

SUMMARY The pathophysiological mechanisms responsible for KojevnikofFs syndrome are still not fully understood. In a family without any history of epilepsy in parents, grandparents or other relatives, three brothers died from unexplained brain disease accompanied by focal epileptic seizures at ages 17 months, 5 years and 20 years respectively. The oldest son, born 1948, was admitted to hospital with status epilep‐ticus in April, 1968. Focal epileptic attacks continued after the patient had recovered from his status. Ventriculography showed stenosis of the aqueduct and a Torkildsen's shunt was established. After three months with epilepsia partialis continua, mainly localized to the left arm, face and neck, his general condition détériorated. A craniotomy was performed and a subdural haematoma of recent origin was removed. An attempt was made after this operation to treat the epilepsy with intracarotid infusion of diphenylhydantoin during local cooling of the brain to 15oC through an extracorporeal carotid shunt. Although electroencephalography showed a resultant diminution in the amplitude, duration and frequency of paroxysmal discharges, the focal jerks persisted, indicating that they originated from the brain stem. RESUME Les mécanismes physiopathologiques du syndrome de Kojevnikoff ne sont pas encore complètement connus. Dans une famille sans histoire d'épilepsie chez les parents, les grand‐parents ou d'autres membres de la famille, trois frères, respectivement à 17 mois, 5 ans ½ et 20 ans, sont morts d'une affection cérébrale inconnue s'accompagnant de crises épileptiques focales. Le plus âgé, né en 1948, a été admis à l'hôpital en état de mal épileptique en avril 1968. Les crises épileptiques focales ont persisté après la fin de cet état de mal. Une ventriculographie a mis en évidence une sténose de l'acqueduc et on a pratiqué un shunt de Torkildsen. Après trois mois d'épilepsie partielle continue, intéressant surtout le bras gauche, le visage et le cou, son état s'est détérioré. Après crâniotomie on a évacué un hématome sous‐dural d'origine récente. Après cette opération on a essayé de traiter l'épilepsie par injection intracarotidienne de diphénylhydantoïne sous refroidissement local du cerveau à 15oC, réaliséà travers un shunt carotidien extracorporel. Bien que Ton ait observé une diminution de l'amplitude, de la durée et de la fréquence des décharges paroxystiques sur l'EEG, les secousses musculaires focales ont persisté, suggérant ainsi que leur point de départ était situé dans le tronc cérébral.

Various inflammatory diseases of central nervous system, including subacute sclerosing panencephalitis, could cause epilepsia partialis continua. Two boys with epilepsia partialis continua with onset in terminal phase of atypical subacute sclerosing panencephalitis have been reported. Children were not vaccinated against measles, and the second case had history of measles at an early age. In both cases, the onset of subacute sclerosing panencephalitis was characterized by altered behavior and cognitive decline with very fast mental and neurological deterioration. One boy was suffering from complex partial seizures and myoclonic jerks synchronous with periodic electroencephalographic pattern. Diagnosis was proved by increased titers of antimeasles antibodies in both serum and cerebrospinal fluid. In terminal phase of the disease, epilepsia partialis continua of localized group of the muscles was diagnosed, with good response to intravenous infusion of midazolam. Surface electroencephalographic recordings during epilepsia partialis continua did not show the epileptic discharges. During the terminal phase of the disease, no other type of seizures and movement disorders were recognized, except epilepsia partialis continua. In spite of the treatment, period from the onset of disease to death lasted less than 3 months, suggesting very fulminant course of subacute sclerosing panencephalitis.