Abstracts

Rationale: Although a number of novel antiepileptic drugs have been introduced in recent years, they remain inadequate for the control of focal neocortical epilepsy in many patients. Even with advancements in surgical technique, many patients remain poor candidates for potentially curative surgical intervention. Recently, focal cortical cooling has been shown to stop seizures and inhibit epileptogenesis in rodents. To investigate the potential clinical utility of this approach, we examined the thermal characteristics of canine and human brain undergoing active and passive surface cooling. Methods: Four patients with intractable epilepsy were treated in standard fashion. Before the resection of a neocortical epileptogenic focus, multiple intraoperative studies of cooling using active (perfused grid) and passive (stainless steel probe) methods, as well as directly applied iced saline irrigation, were performed. Temperatures were 4°C for iced saline used in irrigation and the perfused grid, and 23°C for the passive cooling probe. Measurements were taken using four sterile clinical brain temperature probes at depths of 0, 5, 10 and 15 mm into the cortex. We also actively cooled the neocortices of two dogs with temporarily implanted perfused grids. In the dogs, temperatures were measured within the bladder and at the interface between the bladder and the neocortex. Results: Focal surface cooling of human brain causes predictable, depth dependent cooling of the underlying brain tissue. Cooling of 0.6 to 2°C was achieved both actively and passively to a depth of 10 to 15 mm from the cortical surface. The perfused grid produced comparable cooling of dog neocortex when the craniotomy was closed. Conclusions: The human cortex can easily be cooled during invasive monitoring with the use of simple devices such as a cooling grid or a small passive probe. These techniques provide pilot data for the design of a implantable device to control intractable epilepsy. The possible uses of such a device include the preoperative confirmation of the accurate localization of an epileptogenic focus, the identification of neurologic deficits that could result from the removal of epileptogenic cortex, and the possible treatment or prevention of epilepsy.