Both metabolic rate and protein catabolism are known to increase following severe head trauma, but the etiology of this hypermetabolism is unknown. To further investigate the problem, we studied the metabolism of 17 patients with indirect calorimetry who had severe craniocerebral trauma only and who required ICP monitoring for management. Patients were studied daily and immediately after ICP spikes greater than 20 mm Hg, prior to treatment with hyperventilation, osmotic diuretics, or barbiturates. Oxygen consumption (VO2) was correlated with ICP. Two groups of patients were identified. Group I patients were treated with hyperventilation and osmotic diuretics while Group II patients additionally received cerebral metabolic depressants. Group I had a significant correlation coefficient between VO2 and ICP. Significant hypercatabolism early in the post trauma period was demonstrated by increased urine urea nitrogen. Our observations suggest that in patients with craniocerebral trauma, elevated ICP is associated with increased oxygen consumption, protein catabolism and systemic hypermetabolism. Cerebral metabolic depressants blunted increases in VO2 which were seen with elevated ICP.