De Reuck J, Van de Velde E, Van Maele G, Wissaert W
Department of Neurology, Ghent University Hospital, Ghent, Belgium.
Cerebrovasc Dis. 2003;16(2):114-21. doi: 10.1159/000070590.
X-ray hypoattenuation on computed tomography (CT) reflects the severity of ischaemic damage after stroke. However, the clinical syndrome and the effect of time influence the visibility of infarcts. This prospective study analyses whether the degree of hypoattenuation on CT at two time intervals after stroke has a predictive value for the clinical outcome.
220 consecutive stroke patients were admitted within 24 h after onset with symptoms lasting more than 24 h. The study was restricted to 150 patients displaying an anterior circulation infarct or syndrome. All patients had CT scans without contrast enhancement on day 3 (+/-8 h) and day 10 (+/-8 h) after stroke onset. The degree of X-ray attenuation expressed in Hounsfield units was determined in the centre of the infarct area and compared to that in the corresponding zone of the contralateral hemisphere. The patients were divided into four groups according to their degree of disability at 3 months on the modified Rankin scale as follows: R 0-1, R 2-3, R 4-5 and R 6.
Patients in groups R 4-5 and R 6 had the most severe impairment on admission. The average decrease of X-ray attenuation on CT on day 3 was less in patients in group R 0-1, but was not different between the three other groups, while it was significantly correlated with the severity of the disability on day 10. CT X-ray attenuation increased between days 3 and 10 in group R 0-1, was unchanged in group R 2-3 and further decreased in groups R 4-5 and R 6.
The degree of X-ray attenuation on CT on day 3 allows us to distinguish those patients who will recover more or less completely from those with definite disability, while the CT findings on day 10 allow a more precise prediction of outcome. Increase of X-ray attenuation on day 10 is known as the fogging effect and appears to be a favourable prognostic factor. Fogging is generally considered to be due to macrophage invasion and proliferation of capillaries within the infarct area, but probably also represents partial restoration of some viable tissue.
