Cerebral ischaemia is considered to be the central mechanism leading to secondary brain damage in patients with severe head injury. It would therefore seem appropriate to monitor cerebral oxygenation in these patients. The possibilities of continuous monitoring of brain tissue and CSF oxygen tension as parameters for cerebral oxygenation were evaluated. In experimental studies the influence of changed oxygen offer and decreased cerebral perfusion pressure on CSF and brain tissue pO2 were investigated. Fast changes in CSF pO2 were observed in response to decreasing oxygen offer. Slower changes were noted in response to hypo- and hyperventilation. An autoregulatory mechanism regulating CSF pO2 is postulated. Reducing cerebral perfusion pressure decreased both brain tissue and CSF pO2, but in the reperfusion phase after complete ischaemia a dissociation occurred between brain tissue and CSF pO2, CSF pO2 being restored, but brain tissue pO2 remaining low or even decreasing further. From these studies it is concluded that both CSF pO2 and brain tissue pO2 reflect changes in cerebral oxygenation caused by changes in oxygen offer as well as by changes in cerebral blood flow. Brain tissue pO2 is also sensitive to oxygen demand from the tissue. Preliminary studies of continuous monitoring of brain tissue pO2 in patients with severe head injury are reported.