The interval between the head injury and the first seizure varies greatly. A small number of patients have convulsive movements within moments of the injury (immediate epilepsy). Usually this amounts to a brief tonic extension of the limbs, with slight shaking movements immediately after concussion, followed by awakening in a mild confusional state. Whether this represents a true epileptic phenomenon or, as appears more likely, is the result of arrest of cerebral blood flow or a transient brainstem dysfunction is unclear. Some 4 to 5 percent of hospitalized head-injured individuals are said to have one or more seizures within the first week of their injury (early epilepsy). The immediate seizures have a good prognosis and we tend not to treat them as if they represented epilepsy; on the other hand, late seizures are significantly more frequent in patients who had experienced epilepsy in the first week after injury (not including the convulsions of the immediate injury; Jennett). Seizures occurring minutes or hours after the injury in an otherwise fully awake patient have sometimes turned out to be factitious in our experience.
The term “posttraumatic epilepsy” usually refers to late epilepsy, that is, to seizures that develop several weeks or months after closed head injury (1 to 3 months in most cases). Approximately 6 months after injury, half the patients who will develop epilepsy have had their first episode; by the end of 2 years, the figure rises to 80 percent (Walker). Data derived from a 15-year study of military personnel with severe (penetrating) brain wounds indicate that patients who escape seizures for 1 year after injury can be 75 percent certain of remaining seizure free; patients without seizures for 2 years can be 90 percent certain; and for 3 years, 95 percent certain. For the less-severely injured (mainly closed head injuries), the corresponding times are 2 to 6 months, 12 to 17 months, and 21 to 25 months (Weiss et al). Despite this, there is no doubt that seizures in adulthood occur for which there is no other explanation than a small scarred cortical contusion that had been acquired decades before. The interval between head injury and development of seizures is said to be longer in children.
Posttraumatic seizures (both focal and generalized) tend to decrease in frequency as the years pass, and a significant number of patients (10 to 30 percent, according to Caviness) eventually stop having them. Status epilepticus is uncommon. Individuals who have early attacks (within a week of injury) are more likely to have a complete remission of their seizures than those whose attacks begin a year or so after injury. A low frequency of attacks is another favorable prognostic sign. Alcoholism is considered to have an adverse effect on this seizure state, but there are no systematic studies of this subject. Our colleague, M. Victor, observed some 25 patients with posttraumatic epilepsy in whom seizures had ceased altogether for several years, only to recur in relation to drinking. In these patients the seizures were precipitated by a weekend or even one evening of heavy drinking and occurred, as a rule, not when the patient was intoxicated but in the withdrawal period.
The nature of the epileptogenic lesion has been a cortical scar in most instances, but in some cases, particularly in alcoholics, it has been elusive. From the examination of old cortical contusions (plaques jaunes), one cannot, on morphologic grounds, determine whether a lesion had or had not been epileptogenic. Electrocorticograms of the brain in regions adjacent to old traumatic foci reveal a number of spontaneously electrically active zones adjacent to the scars.