Effects of drugs on secondary epileptogenic lesions

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Abstract
Secondary epileptogenic lesions are electrically defined areas of paroxysmal discharge at least one synapse removed from a primary epileptogenic zone. The secondary region (mirror focus) arises as a result of continuous epilep-tiform bombardment from the primary lesion. It represents a true spread of epileptogenicity to an area untouched by the original experimental procedure. Previous work had shown that early surgical excision of the primary focus could prevent development of secondary lesions. However, since most patients are treated medically rather than surgically, it was of interest to determine whether chronic drug therapy in experimental animals, where the time course of secondary lesion development was known, would correspondingly, influence this process. Phenobarbital, Dilantin, and Thorazine were studied. Only phenobarbital was found to retard establishment of secondary lesions. The clinical implications of this observation were reviewed. The data suggest that secondary epileptogenesis is a specific result of synaptic bombardment and not of ephaptic recruitment of surrounding cells into epileptiform discharge. The differences in drug effect support the notion that separate physiologic mechanism subserve local as opposed to distant propagation of epileptic activity.

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