ABSTRACT
The growing understanding of the relationship between local brain edema as a dynamic response to the reduction of cerebral blood flow and early parenchymal hypodensities on plain CT has stimulated CT as a measure of choice for early stroke diagnosis.1-3 It is agreed that changes such as local brain swelling and gray matter hypodensity can become visible within the first few hours of stroke, depending on the severity of ischemia and the site and extent of perfusion impairment. Moreover, in acute stroke parenchymal hypodensity is considered a reliable indicator of tissue infarction even if demonstrated very early after symptom onset.4,5
This can be frequently seen in the case of middle cerebral artery stem occlusion with concomitant perfusion impairment of the basal ganglia, which inevitably leads to tissue necrosis due to the lack of collaterals. However, although the usefulness and prognostic value of early CT
Matthias König
changes for the detection of hemispheric infarcts has been confirmed in both clinical studies and daily routine, its overall sensitivity to ischemia is low during the first few hours of stroke.6-8 This might be in part the result of an insufficient skill of clinical physicians in interpreting very subtle signs on early CT scans.9 By far the most conclusive explanation, however, is that the development of brain swelling and tissue hypoattenuation is a time-dependent process, which means that these CT signs may require hours to develop fully. Taking into account that frequently morphological changes as shown on plain CT are the result of a preceding functional disturbance, in acute stroke the development of tissue hypodensity can be seen as the last step in a sequence of events primarily induced by the reduction of cerebral blood flow (CBF).
