Jugular venous oxygen saturation (SjvO2) measures the balance between cerebral oxygen delivery and cerebral oxygen consumption. Abnormalities that increase oxygen consumption (e.g., fever or seizures) or that decrease oxygen delivery (e.g., increased ICP, hypotension, hypoxia, hypocapnia, or anemia) can decrease SjvO2. Measuring SjvO2 continuously in the ICU in 177 patients with severe head injury, jugular venous desaturation (SjvO2 < 50%) was identified at least once in 39% of the patients. Approximately half of the episodes of desaturation were due to intracranial hypertension and half were due to systemic causes. The occurrence of one or more episodes of desaturation was strongly associated with a poor outcome, suggesting that the reduction in oxygen delivery identified with the SjvO2 monitoring contributed to the neurological injury. In the operating room, jugular venous desaturation was identified in 6 of 8 patients who were monitored during emergency evacuation of a traumatic intracranial hematoma. The lowest SjvO2 observed was 28%. In all 8 cases, the SjvO2 increased, from 47 +/- 10% to 63 +/- 5% after evacuation of the hematoma. Additional data supporting the hypothesis that these secondary insults identified with the SjvO2 monitoring contribute to the patient's neurological injury come from measurement of the extracellular concentrations of lactate and excitatory amino acids in the brain using microdialysis. Lactate concentration increased from 0.9 +/- 0.3 to 2.4 +/- 0.5 mumol/L and glutamate increased from 11.5 +/- 8.5 to 55.0 +/- 10.4 mumol/L during 8 episodes of jugular venous desaturation in 7 of 22 patients monitored with microdialysis. SjvO2 identifies global reductions in cerebral oxygenation due to a variety of causes, and is useful as a monitor for secondary insults in patients with severe head injury.