Finding
Paper
Abstract
Some, of the probable physiopathological mechanisms of post‐traumatic epilepsy have been reviewed and an hypothesis concerning an additional mechanism involving the decrease in inhibitory controls which might ensue with rupture of axon collaterals has been presented. Disruption of finely regulated vascular supply producing periodic or chronic functional ischaemia is considered of likely importance in chronic epileptogenic lesions which follow penetrating wounds of the brain. Mechanical distortion of dendrites caught in a glial cicatrix may also be of importance, as suggested by Ward, though it is not proven. Defects in the blood‐brain barrier and alterations in the buffering action of glial cells upon the maintenance of extracellular electrolyte balance may be also of importance. Finally it is proposed that the delicate collaterals which branch at right angles from axons of pyramidal cells may be particularly susceptible to the shearing forces of closed head injuries. Their rupture would result in a marked reduction in inhibitory controls permitting the recruitment of excessive synchronous discharge in large assemblies of neurones which is characteristic of the epileptic process.
Authors
H. Jasper
Journal
Epilepsia