Our results support the hypothesis that patients with epilepsy who die suddenly and unexpectedly have cardiac pathologic conditions that may be responsible for their deaths.

A double-blind crossover study of the effects of baclofen was conducted on 10 patients with typical trigeminal neuralgia. Baclofen significantly decreased the number of painful paroxysms in 7 of the 10 patients. An open trial in another 50 patients with trigeminal neuralgia refractory to or unable to tolerate carbamazepine showed that 37 (74%) were relieved of their attacks by baclofen, either alone (12 patients) or in combination with previously ineffective doses of carbamazepine or phenytoin (25). On long-term follow-up of one to five years (mean, 3.0 years), 18 of the 60 patients (30%) continued pain free while receiving baclofen; 10 (17%) went into remission after 3 to 6 months; 13 (22%) became refractory to baclofen after 1 to 18 months; and 2 (3%) elected operation despite a good response to baclofen. The results indicate that baclofen is a useful drug in the treatment of trigeminal neuralgia.

Eight cases of unexpected, unexplained death in young ambulatory epileptics were examined postmortem with special attention to the heart and lungs. Lung weights uniformly exceeded the expected value, with gross evidence of hemorrhagic pulmonary edema. Microscopic examination revealed moderate to severe pulmonary edema with protein-rich fluid as well as alveolar hemorrhage. There was no evidence of recent or old myocardial disease. Although death due to a seizure is usually thought to be almost instantaneous, the neurogenic pulmonary edema exemplified by these cases takes time to develop and may be remediable. The high frequency of absent or non-therapeutic anticonvulsant levels at the time of death in these patients may play a role in a possible centrally mediated adrenergic cause of neurogenic pulmonary edema and ventricular arrhythmia.

Thirty-seven cases of unexpected, unexplained death in epileptic patients were recorded by the Allegheny County Coroner's Office during the years 1969 through 1973. In no case was there anatomic or chemical evidence at autopsy sufficient to explain death. All patients had a duration of epilepsy greater than a year. All but two had less than one seizure per month. Blood levels of anticonvulsants at autopsy revealed only three patients with therapeutic levels of the drugs. Almost 50 percent of the cases studied had no demonstrable anticonvulsant. It is suggested that inadequate levels of anticonvulsant drugs are a significant factor associated with unexpected, unexplained death in epileptic patients.

We reviewed the clinical features of 12 patients with fat embolism seen in 10 years. Based on neurologic manifestations, patients were grouped into those with focal cerebral syndromes and those with diffuse encephalopathy. Patients with focal signs tended to present earlier with neurologic findings alone, did not have fever, and had less risk of pulmonary disorder than patients with encephalopathy.