Coma and Epilepsy

Coma, regardless of its etiology, is associated with reductions in brain metabolism. In the case of lesions occurring in the reticular activating system, the reduction in CMR probably represents a normal physiologic adjustment to reduced functional activity. During generalized seizure activity, CMR and CBF may increase dramatically.^[411] The intensive motor and brain activity associated with generalized seizures leads to the development of systemic and cerebral acidosis, often accompanied by a reduction in arterial oxygenation, an increase in PaCO₂ , and peripheral lactic acidosis. If generalized seizure activity continues unabated, arterial hypotension ensues. With muscular relaxation and measures ensuring adequate oxygenation and ventilation, the systemic acidosis and hypotension can be avoided and the severity of cerebral acidosis diminished. During relatively brief episodes of continuous seizures, the brain seems able to meet the high metabolic demands.^[411] However, even with effective ventilation and maintenance of perfusion pressure, when seizures continue for a prolonged period, they can lead to the development of irreversible neuronal damage.^[597] Therapy aimed at interrupting the seizure and restoring a normal balance between cerebral metabolic demand and blood flow is indicated. Barbiturates, benzodiazepines, or other potent anticonvulsants are appropriate. Adequate ventilation, oxygenation, and maintenance of blood pressure are important adjunctive measures. Muscle relaxants must be viewed as purely symptomatic therapy because they do not alter the abnormal cerebral electrical activity.

The potentially injurious nature of seizures justifies attention to prevention. Practices vary. However, patients who have sustained a severe head injury or subarachnoid hemorrhage and any patient in whom a substantial cortical incision is planned are at risk, and prophylactic anticonvulsants should be considered.