Decisions about how to manage head-injured patients with regard to the development of epilepsy are confounded by the lack of specific information on which to base recommendations. Because long-term prophylaxis with currently available antiepileptic drugs has not been shown to be effective in preventing post-traumatic epilepsy, the following discussion provides a rational guide for the management of these patients:
Those patients with head injury of such severity that risk of seizures is high, and in whom the physiologic consequences would complicate management, should receive preventive phenytoin treatment. A loading dose of phenytoin should be given in the form of 18 mg/kg of fosphenytoin by peripheral vein at a rate not to exceed 100 phenytoin mEq per minute. A maintenance dose of 5 mg/kg per day should be given intravenously until oral administration is possible. If nasogastric tube feeding is used, simultaneous feeding and phenytoin administration should be avoided. Blood levels should be maintained within the recognized therapeutic range of 10–20 mg/mL.
Up to 10% of patients treated in this fashion may develop an allergic rash, so regular skin inspection must be performed. If such an allergic reaction occurs, then another parenteral form of anticonvulsant drug, such as phenobarbital, should be used.
Available data suggest that treatment with phenytoin is effective in preventing seizures for at least 1 month after injury. One method would be to maintain therapeutic plasma levels of phenytoin for at least that period. Then the drug should be tapered over the following 4 weeks.
Obtain an electroencephalogram (EEG) before drug taper. Although the EEG does not predict the potential for development of epilepsy immediately after injury, the observation of epileptiform patterns on the EEG after injury may be valuable in making a decision about whether to continue administering an anticonvulsant drug.
Patients occasionally are maintained on antiepileptic drugs for 6 months or more after injury. Because long-term treatment is not effective as prophylaxis, early taper is preferred.
Informed consent of patients and the members of their families is necessary before using an antiepileptic drug as a prophylactic treatment. Misunderstanding about the intent of treatment with antiepileptic drugs may cause problems with compliance or leave the impression that discontinuation of the medication has caused the patient to be vulnerable to the development of epilepsy.
If a patient ends up having been maintained on long-term prophylaxis even without having a seizure, then the patient and the physician face a clinically challenging problem. A patient may be anxious about such long-term treatment and may not be willing to risk discontinuing the drug. If the patient agrees to discontinue antiepileptic drug treatment, then special cautions regarding the prohibition of driving during the time of tapering of the drug must be individualized. The best course may be EEG assessment and a realistic discussion of risk, followed by discontinuation over 6 weeks.
As with other forms of epilepsy, those patients with few seizures that are easily controlled tend to have the best prognosis. Walker and Erculei30 observed that 50% of patients identified as having post-traumatic epilepsy would be in complete remission by 15 years after injury.
Assessment and decisions about discontinuation of medication after a long seizure-free interval should be governed by guidelines that apply to any patient who is a candidate for a trial off of medication.111,112
Patients with post-traumatic epilepsy may develop intractable epilepsy. Because such patients are unresponsive to antiepileptic drug therapy, the usual strategy is to evaluate the patient for resective surgery. The patient must understand the success rate of resective surgery and the potential for the need to pursue further assessment should the initial surgical effort fail.
The challenge of the monitoring process and accompanying planning for potential resective surgery is the unpredictable nature of the process of lesion formation after head injury. Head trauma of sufficient intensity to result in the development of post-traumatic epilepsy causes spatial dispersion of injured cortex in temporal and extratemporal regions.38 Location of the clinically important regions of injury causing epilepsy requires careful planning of intracranial electrode arrays. Knowledgeable observers, such as family members, should review videotaped seizures captured during epilepsy monitoring to ensure that the clinical events reflect the patient’s typical seizures.
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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