Chapter 35 – Posttraumatic epilepsy

Traumatic brain injury has been identified since antiquity as being associated with chronic seizures. Mechanisms of injury include blunt head trauma, high-velocity penetration of the brain during military conflict, and motor vehicle accidents, all causing cavitation and rotational forces with cortical laceration and contusion. Risks of an injured military veteran developing posttraumatic epilepsy are 40–50%. Among civilians, the incidence ranges from 7% to 25%. Risk factors for the development of epilepsy are important in clinical trials to interrupt epileptogenesis. Drug trials using valproic acid or phenytoin failed to interrupt epileptogenesis, although the latter drug did prevent seizures during the first weeks after injury. Methods of study in animals include focal injection of blood components into the neuropil, fluid percussion through a craniectomy, undercutting the cortex, and amygdalar kindling. Contusion and intracerebral hemorrhage cause focal encephalomalacia and hemosiderin deposition. Fluid percussion causes mechanical injury with isocortical encephalomalacia and ipsilateral hippocampal atrophy. Mossy fiber sprouting is observed in the hippocampus. Partial isolation of a neocortical island with intact circulation allows development of hyperexcitability and mimics epileptogenesis. Cortical regions are reorganized and this model allows longitudinal assessment as well as serving as a platform for evaluation of methods for interruption of epileptogenesis.