Head Trauma And Seizures

Head trauma can result in seizures of three types: immediate seizures, early posttraumatic seizures, and late posttraumatic seizures. Immediate seizures result from impact and presumably are due to traumatic depolarization of neurons. The risk of recurring seizures in these patients is minimal unless there are more serious prognostic factors such as prolonged coma and penetrating head injury.5 Anticonvulsants are sometimes used because of the unknown potential for immediate recurring seizures. In a patient who recovers rapidly, chronic anticonvulsant use is usually not indicated. An exception would be a patient with a prior seizure history or a family history of epilepsy.

Early posttraumatic seizures occur within the first week after trauma, and epilepsy results in 20 to 25 percent of these patients. These early seizures are presumed to result from the focal effects of contusions or lacerations and the associated hypoperfusion, which causes ischemia and related metabolic changes.

Treatment of immediate and early posttraumatic seizures requires the correction of neurologic problems, e.g., depressed fracture or hematoma, the reduction of cerebral edema, proper oxygenation (airway maintenance and correction of shock), and the careful administration of anticonvulsants. With immediate and early posttraumatic seizures when impaired consciousness already prevails, it is helpful to avoid the use of significantly sedative medication (barbiturates or diazepam), if possible. Phenytoin may be used successfully with relative safety (Table 121-4). The dosage is determined by the clinical presentation. Rapid loading is warranted to obtain immediate therapeutic levels in patients in whom repeated seizures are occurring or likely to recur, especially when a seizure may further aggravate associated medical or surgical conditions.

Immediate posttraumatic seizures warrant anticonvulsant therapy for initial control, whereas long-term management of immediate seizures remains controversial.

Late posttraumatic seizures occur after 1 week and may be seen as late as 10 years after the trauma. Structural changes such as atrophy with gliosis and permanent local vascular changes, altered dendrite branching, and presumably modified neurotransmitter function account for the development and permanence of these seizures. Of these seizures, 40 percent are focal or partial seizures and 50 percent are temporal lobe seizures, indicating the predilection for traumatic injury and known epileptogenic properties of this structure. The risk of recurring seizures in this group is reported to be as high as 70 percent.

Early and late posttraumatic seizures warrant long-term anticonvulsant therapy in view of the risk of immediate and later recurrence. Late-onset posttraumatic seizures are most likely to recur, and long-term anticonvulsant therapy is necessary. Patients at greater risk for chronic posttraumatic seizures include those with depressed skull fractures, posttraumatic amnesia more than 24 h after the trauma, dural penetration, acute intracranial hemorrhage, early posttraumatic epilepsy, and a foreign body in a cerebral wound. The more severe the seizure and the later the onset, the less likely remission will occur.

Emergency management of seizures related to trauma should emphasize neurosurgical assessment; the rapid, careful administration of nonsedative anticonvulsants; the interruption of the seizures; and the stabilization of the general medical condition.

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