The risk of developing post-traumatic epilepsy (PTE) is related to the severity of injury.3–5 Within the first year after head trauma, the incidence of seizures is 12 times as great as for the population.3 Patients with severe head trauma and cortical injury with neurologic deficits on physical examination, but with the dura mater remaining intact, have an incidence of epilepsy from 7% to 39%. Increased severity of trauma, as indicated by dural penetration and neurologic abnormalities, yields a range of epilepsy incidence of 20–57%.3,6 Guidelines for identifying patients at risk for late epilepsy (see Table: Factors of Late Epilepsy) include those factors associated with the severity of neocortical contusion, including presence of an intracerebral hematoma and the need for surgical repair of a depressed skull fracture.1
An attempt was made to improve the prediction of who might be liable to develop PTE, applying a formula using weighted trauma categories.7 The formula included the brain location, the agent of injury, severity, complications, and the presence of focal neurologic deficits.7 The highest numeric values of risk were associated with:
Predictive factors associated with epilepsy risk in the Vietnam Head Injury Survey8 included:
Other studies of patients with PTE showed prolonged post-traumatic amnesia, the presence of a cortical laceration occurring with a depressed skull fracture with dural laceration, and intracerebral hematoma to be predictive.9,10 The risk of development of seizures is increased after hemorrhagic cerebral infarction11,12 and spontaneous intracerebral hematoma.13 These data resulted in the development of a hypothesis by Willmore and colleagues that suggested that trauma-induced hemorrhage with blood in contact with the neuropil is an important etiologic factor in the development of PTE.14–16
Latency from head injury to the development of epilepsy varies, although 57% of patients have onset of seizure within 1 year of injury.8 Whether a seizure occurs immediately after injury, within the first week, or beyond the first week may have prognostic significance for the development of epilepsy.1
Immediate seizures, occurring within hours after trauma, or a sequence of seizures with development of post-traumatic status epilepticus complicates management of an injured patient by causing hypoxia, hypertension, and metabolic changes. An immediate seizure may be a nonspecific reaction to head trauma, but an intracranial hematoma also may present this way and must be excluded. An early seizure, occurring during the first week after injury, increases the incidence of late epilepsy.1
Closed head injury of such severity to cause hospitalization results in an overincidence of PTE of 4–7%.1,17 The incidence of PTE is considerably higher among patients undergoing rehabilitation for head injury.18–20 Patients with penetrating head injury have an epilepsy incidence of 35–50%.3,8,21–23 Not all factors are understood, however, because trivial head injury also has been associated with development of PTE.24
Occurrence of a seizure after head injury is not always predictive for development of epilepsy, nor does such a complication predict an eventual enduring problem with chronic epilepsy. Between 50% and 65% of patients who have seizures do so within 12 months of injury.8,23,25 Approximately 80% have seizures by 2 years after injury.26,27
About half of all patients have single seizures, without recurrence, and another 25% have just two or even three seizures followed by abatement of that clinical problem. Timing of a seizure in relationship to head injury provides some predictive information. Of patients with a seizure within 1 week of injury, 20–30% have late seizures, beyond 1 week of injury.8,26,28,29 Such later seizure recurrence seems better correlated with seizure frequency during the first year. Although these observations suggest that the overall prognosis is good,30 intractability becomes a major clinical problem for some patients.
Nonepileptic seizures also have complicated head trauma, with up to 32% of one series of pseudoseizure patients having a history of head injury.31
History of febrile seizures is found as part of the pattern of risk for development of typical mesial temporal sclerosis and the clinical problem of complex partial seizures. However, head injury, particularly during childhood, is a factor in some cases.32 Indeed, the University of California at Los Angeles series33,34 found head trauma as an associate event in 16% of their cases with mesial temporal sclerosis. Such an occurrence is not typically dual in pathology35,36 but may represent the consequences of transmitted forces with selective vulnerability of the hippocampus, as has been observed in animals.37
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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