Knowledge of cerebral metabolic variables increases the information available for managing the head-injured patient. This article reviews normal cerebral metabolism and describes the derangement of metabolism observed in patients with head trauma. Cerebral metabolism is globally decreased by one third to one half in the severely head-injured patient, usually because of the lower metabolic expenditure associated with coma, but sometimes because of superimposed hypoxia/ischemia, primarily due to secondary insults. Measurement of jugular venous oxygen saturation has become the most useful method for monitoring cerebral metabolism in the ICU. Although jugular venous oxygen saturation does not provide quantitative information about either cerebral blood flow or cerebral metabolism, it reflects the ratio between these two variables. To maintain a sufficient level of available oxygen and energy production at the cellular level, there are two therapeutic strategies: a) hemodynamic and b) metabolic. Treatments can be directed at both increasing oxygen delivery and integrating hemodynamic handling, and at various pharmacologic or physical methods intended to reduce the cerebral metabolic demand. The latter strategy is designed to depress either the basal or activation components of cerebral metabolism. This strategy includes manipulations of brain temperature and the use of central nervous system-depressant, barbiturate, and similar drugs.