The use of antiepileptic drugs to prevent a posttraumatic seizure and subsequent epilepsy after closed or penetrating cranial injury has its proponents, and skeptics. In one study, patients receiving phenytoin developed fewer seizures at the end of the first year than a placebo group, but a year after medication was discontinued, the incidence was the same (and quite low) in the two groups. An extensive randomized study by Temkin and colleagues demonstrated that when administered within a day of injury and continuing for 2 years, phenytoin reduced the incidence of seizures in the first week, but not thereafter. Also, in a study of a large number of patients with penetrating head injuries, the prophylactic use of antiepileptic medications was ineffective in preventing early seizures (Rish and Caveness), and this is reflected in current guidelines (Chang and Lowenstein). Subsequent studies have come to much the same conclusion.
Usually, persistent seizures can be controlled by a single antiepileptic medication, and relatively few seizure disorders are recalcitrant to the point of requiring excision of the epileptic focus. In this small group, the surgical results vary according to the methods of patient selection and techniques of operation. Under the neurosurgical conditions of four decades ago, with careful selection of cases, Rasmussen (also Penfield and Jasper) was able to eradicate seizures in 50 to 75 percent of cases by excision of the focus; the results currently are somewhat better.
A worrisome consequence of severe head injury, which is observed in some comatose patients and particularly in the vegetative state, is a syndrome of episodic vigorous extensor posturing, profuse diaphoresis, hypertension, and tachycardia lasting minutes to an hour. A slight fever may accompany the spells. Families and staff are greatly disturbed by the display, particularly when the patient’s grimacing suggests suffering. These spells of excessive sympathetic activity and posturing may be precipitated by painful stimuli or by distention of a viscus, but often they arise spontaneously. The syndrome is often mistakenly identified as a seizure and in many texts is still referred to as “diencephalic epilepsy” but it is more likely the result of the removal of suppressive cortical influences on autonomic structures, allowing the hypothalamus to function independently of normal inhibitory mechanisms. A survey of 35 such patients by Baugley and colleagues identified diffuse axonal injury and a period of hypoxia as being the main associated injuries and this has been our experience as well.
Narcotics such as morphine and benzodiazepines have a slightly beneficial effect but bromocriptine, which may be used in combination with sedatives or with small doses of morphine, has been most effective according to Rossitch and Bullard.
The question of a causative relationship between cerebral trauma and the development of Parkinson disease has been a controversial issue for many years—usually with the conclusion that the condition does not exist and that any apparent relationship, particularly after a single brain injury, is coincidental. Some such patients probably had early symptoms of Parkinson disease brought to light by the head injury. There are, however, cases such as the one reported by Doder and colleagues, in which traumatic necrosis of the lenticular and caudate nuclei was followed after a period of 6 weeks by the onset of predominantly contralateral parkinsonian signs, including tremor, which progressed slowly and were unresponsive to l-dopa. There are also undoubted instances of parkinsonism following severe closed head injury and the vegetative state (Matsuda et al). An exception to these statements may be a parkinsonian syndrome in ex-boxers and in others who had frequent minor head injuries, as a manifestation of the “punch-drunk” syndrome, now subsumed under the term “chronic traumatic encephalopathy.” There remains the possibility that cranial trauma incites a series of cellular events that lead to the deposition of abnormal structural proteins such as synuclein (see below).