Treatment of Post-Traumatic Epilepsy

Source: Pohlmann-Eden B, Bruchmeir J. Predictors and dynamics of posttraumatic epilepsy. Acta Neurol Scand 1997;95:257-262.

Post-traumatic epilepsy (pte), which occurs in up to 50% of cases of severe neurotrauma, represents a major residual complication. Pohlmann-Eden and Bruchmeir describe features of the acute injury which predict later PTE.

The authors located 57 patients with PTE in their seizure clinic over a 10-year period. They compared these with 50 sex- and age-matched controls who had "severe head trauma" (not defined) but no seizures. Recurrent "late" posttraumatic seizures (more than one week after the injury) were associated with the following head injury variables: posttraumatic amnesia lasting more than three days, loss of consciousness, focal signs on the first examination, missile injuries, frontal lesions, depressed skull fractures, intracerebral hemorrhages, diffuse cerebral contusions, and focal cerebral cortical lesions when they extended into subcortical areas (all P < 0.01).

Two-thirds of these patients developed PTE within two years of their injuries. PTE presented as status epilepticus in 11 of 57 (20%) of these cases. Of the 11, nine had CT-documented frontal lesions.


The Joint Section on Neurotrauma and Critical Care of the American Association of Neurological Surgeons has issued guidelines for the management of severe head injuries (reviewed in Neurol Alert 1997;15:68-69). They did not recommend universal posttraumatic use of prophylactic antiepileptic drugs (AEDs). In a widely cited, randomized, double-blind study of more than 400 patients, Temkin et al (N Engl J Med 1990;323:497-502) found phenytoin treatment effective in reducing the percent of patients who experienced one or more early posttraumatic seizures (less than one week after the injury), but ineffective in reducing the percent of patients who had at least one late posttraumatic seizure (in the following two years). After a late posttraumatic seizure, patients were removed from that study, and Temkin et al did not study the efficacy of AEDs in the treatment of recurrent posttraumatic seizures.

Pohlmann-Eden and Bruchmeir’s work points to a patient population at high risk for developing PTE and status epilepticus. Unfortunately, it appears that at least one carefully tested AED (phenytoin) cannot prevent the development of PTE, even if such a high-risk population were identified. This emphasizes the difference between "epileptogenesis" and "epilepsy." Epileptogenesis is the process by which abnormal neuronal functional reorganization occurs, ultimately leading to excess neuronal circuit excitability and clinical seizures. To date, no effective treatment strategies have been developed to impede epileptogenesis after severe head injuries. However, once epilepsy has started, AEDs reduce the probability of further recurrent seizures.

Regrettably, no specific data accompany these pronouncements, leaving their value, if any, up to the reader. —drl