Focal Cooling Suppresses Continued Activity of Epileptic Focus in Patients with Partial Status Epilepticus

To the Editor: In a recent issue of Epilepsia, Kameel M. Karkar and colleagues (1) presented a patient with an oligoastrocytoma of the frontal lobe, partial motor and secondarily generalized seizures, and suppression of focal spike activity after local cortex cooling on an electrocorticogram. It is impossible to determinate the stability of this effect because the primary pathological formation was removed. Focal cerebral cortex cooling has been used in several cases of status epilepticus resistance. The first case was published by Y. Mazars et al., 1960 (2), and the second, by A.K. Ommaya and M. Baldwin, 1963 (3). My colleagues and I published the next two cases: symptomatic partial epilepsy with severe convulsive status epilepticus (4,5). The epileptogenic focus was localized in a functionally important part of the cortex, so attempts at its removal were not undertaken. Thus the opportunity appeared to ascertain the stability of the suppression of epileptic activity after local cooling of the epileptogenic focus. The facts of our first observations are as follows. A 14-year-old girl experienced right-side facial and brachial motor seizures for 7 years after a case of serous meningitis. She was admitted into the Emergency Institute unconscious with partial and secondarily generalized seizures that repeated every 3–4 min. Secondary respiratory disturbances of an occlusive type were observed. The anticonvulsive therapy undertaken included barbital anesthesia combined with syndromic interventions (removal respiration first). The procedure was ineffective, and her seizures were renewed. The next step was to administer muscle relaxants, artificial ventilation of lung, prolonged combined anesthesia by NO2/O2 inhalation, plus intravenous barbiturate. The attempt to stop this procedure was followed by the reappearance of her seizures. Because the aforementioned procedure brought only a temporary effect, a decision was made 44 h later to stop it and undertake a neurosurgical intervention instead. Massive cerebroarachnoidal adhesions were revealed at the left rolandic region, but the division of the adhesions was impossible because of intensive bleeding. (Only 10 years later, we revealed the disseminated intravascular syndrome as the obligatory disorder arising in status epilepticus). The epileptogenic zone was sprinkled with ethyl chloride. The temperature on the brain surface decreased from 38.8 to 30.2◦C. After the ethyl chloride application, the patient’s convulsions stopped and did not reappear. Antiepileptic drugs (hydantoin; phenytoin) were prescribed for the next 5 years. Gradually, the patient was taken off medication. We continued follow-up observations for 20 years. The patient graduated from college, was married, and had a child. In the second similar case, all manipulations were monitored by electrocorticography. After incomplete division of the cerebroarachnoidal adhesion (bleeding), epileptiform activity decreased insignificantly. After the next intervention, cortex cooling, epileptiform activity was stopped. The epileptic seizures did not reoccur. Thus the epileptiform activity and the epileptic seizures that accompanied it can be steadily suppressed by local cooling of the cortex epileptogenic focus. Recently it was shown that a connection exists between the cooling effect and the disruption of network synchrony necessary for epileptiform activity (6).