Tomographic Mapping of CBF, CBV and Blood Brain Barrier Changes in Humans After Focal Head Injury Using SPECT-Mechanisms for Late Deterioration

Abstract

Ischemic brain damage due to reduced global cerebral perfusion pressure is a major determinant of outcome after head injury, and its recognition has led to major changes in management over the last few years (Graham et al. 1978). However, the effects of focal injury upon the local cerebral microcirculation has received little attention despite experimental evidence that progressive abnormalities can occur and may account for the delayed deterioration which often occurs in patients with cerebral contusions, intracerebral or subdural hematomas (Bullock et al. 1984). Serial CT scanning in patients with focal injury have shown hematoma enlargement in under 10% of patients while progression of surrounding brain edema occurs in one third of cases, and may cause raised intracranial pressure (Kobayashi et al. 1983). Hyperaemia has also been cited as a cause of raised ICP after diffuse injury and has been demonstrated after focal injury, but its role in causing later deterioration is not known (Kuhl et al. 1980).