Risk Factors for Post-Traumatic Epilepsy in Adults

Abstract

Craniocerebral trauma (CCT) is the cause of 20% ofsymptomatic and 5% of all cases of epilepsy [23]. In Russia,CCT is the main cause (27.7%) of location-dependentepilepsy in adults [1, 18].Post-traumatic epilepsy (PTE) is one of the late and mostserious complications of CCT. CCT and, hence, the possiblerisk of PTE, is most common in the age range 15–34 years,where the number of cases is about 30% [30]. The mostimportant cause of CCT consists of transport accidents (most-ly traffic accidents), as well as domestic, sporting, and indus-trial accidents, as well as military injuries.Assessment of the morbidity of PTE involves use of var-ious definitions of CCT itself and PTE [17], as well as dif-ferent durations of studies. This is because the developmentof PTE requires a stably developed focus of epileptic activityresulting from organic brain injury [1, 29]. The mechanismsof epileptogenesis are tightly linked with the course of recov-ery processes after CCT or the occurrence of aberrant plas-ticity. The most important are changes in neurotransmitterprocesses, sprouting, the various mechanisms of neurondeath, changes in membrane and receptor properties, and theformation of hyperexcitable neuronal systems [19]. Whileepileptic activity during the acute phase of traumatic braininjuries results from cortical injury and the nonspecificresponse to intense physical actions (the mechanisms of pri-mary brain damage), in the later period of trauma, the harm-ful actions of free radicals and excitotoxicity due to gluta-mate accumulation (the mechanism of delayed secondarybrain damage) are probably more important [30]. An impor-tant role here is played by impairments to cellular andhumoral immunity and disintegration of the functions ofautonomic and humoral-endocrine regulation [1]. In allcases, genetic predisposition factors are of undoubted impor-tance, though they are complex and heterogeneous [17, 21].PTE should also be discriminated from post-traumaticseizures. PTE includes repeated, late (i.e., onset more thanone week after CCT) post-traumatic seizures [15, 23, 51].Post-traumatic epileptic seizures include any epilepticseizure developing as a result of CCT [21, 34, 35]. Epilepticseizures can develop at different times after CCT. In assess-ing the periods of onset of epileptic seizures, most authorsuse the Barolin et al. classification [5], initially developedfor epileptic seizures in cerebrovascular diseases. This clas-sification identifies the following types of epileptic seizures:immediate, developing within the first 24 h; early, develop-ing at 1–7 days from onset of illness; and late, starting atseven or more days.The time of onset and the frequency of development ofepileptic seizures depend on the type, location, and volumeof the focus of brain damage and the state of the premorbidbackground of the patient (presence of cerebrovascular dis-ease, repeated CCT in the history, genetic predisposition,chronic alcoholism, etc.) [1]. The incidence of early post-traumatic seizures is 3–5%, compared with an incidence of