FOCAL ISCHEMIA DUE TO TRAUMATIC CONTUSIONS DOCUMENTED BY STABLE XENON-CT AND ULTRASTRUCTURAL STUDIES

A traumatic cerebral contusion causes a zone of perifocal neuronal nec rosis, the cause of which is not known; the surgical management of the se lesions remains controversial. To determine the pathophysiological mechanisms responsible for brain damage after contusions, the authors performed cerebral blood now (CBF) mapping studies and related these t o change in local cerebral blood volume (CBV) and ultrastructure. In 1 1 severely head injured patients with contusion, CBF and CBV were meas ured in pericontusional areas using stable xenon-computerized tomograp hy (CT). These studies demonstrated a profound reduction in perilesion al CBF (mean 17.5 +/- 4 ml/100 g/min), which was always accompanied by a zone of edema defined by CT density measurements. Mean CBV in these regions was 2.3 +/- 0.4 ml/100 g, a reduction to approximately one-ha lf the value of 4.8 ml/100 g found in the nonedematous regions, and to approximately 35% of the value of 6.0 ml/100 g found in normal volunt eers. Ultrastructural analysis of the pericontusional tissue, taken at surgery in four patients with high intracranial pressure showed glial swelling with narrowing of the microvascular lumina due to massive po docytic process swelling. Additionally, some suggestion of vascular oc clusion due to erythrocyte and leukocyte stasis was seen. These data s upport the conclusion that microvascular compromise by compression and /or occlusion is a major event associated with profound perilesional h ypoperfusion, which is a uniform finding within edematous pericontusio nal tissue.