Cerebral circulation after head injury. Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury?

Abstract

✓ A series of comatose young patients with head injuries is presented in whom early regional cerebral blood flow (rCBF) is correlated with neurological outcome, and the critical threshold of rCBF compatible with recovery of responsive communicative interaction with the environment is estimated. Within the 1st week following injury, 63 patients had rCBF studies performed with radioactive xenon by the intracarotid bolus-injection technique and 35-channel external counting. A comparison was made between 2724 rCBF values from this group of patients with 381 from nine controls. Surviving patients were followed for 2 years to determine their eventual neurological outcome. When histograms of the frequency distribution of rCBF values were examined, it was evident that there was both a wider spread of rCBF and a shift to the left in all outcome groups. In awake controls, no rCBF values were less than 40 ml/100 gm/min, whereas in comatose patients the threshold for recovery of communicative brain function (with or without neurological deficits) was between 17 and 20 ml/100 gm/min. There was a clear difference, however, between patients who recovered communicative brain function (with or without neurological deficit) and those who did not (dying or surviving in a persistent vegetative state). In the latter two outcome groups, 14.5% of rCBF values were less than 20 ml/100 gm/min, with the highest incidence in those examined within the first few hours of injury. The distribution of ischemic rCBF was mainly in the frontal and parietal lobes. These investigations confirm previous postmortem pathological studies in revealing that cerebral ischemia in the frontoparietal “watershed” areas antemortem is a major factor leading to telencephalic brain death in the early hours after head injury. The pathophysiological mechanisms of this localized ischemia in patients with head injury are not well understood, but probably hemodynamic alterations resulting from increased intracranial pressure are a major factor. The critical threshold for survival of cortical function seems to be similar to that of normal brain, about 17 to 20 ml/100 gm/min.