1987 Volume 9 Issue 4 Pages 334-339
Ring form contrast enhancement of CT scans are frequently observed in the cases of hypertensive cerebral hemorrhage in subacute stage.
A mechanism of the appearance of ring enhancement was investigated by multiparameter analysis of local cerebral circulation in ten patients, including one case with thalamic hemorrhage and nine with putaminal hemorrhage. Mean age of the cases was 57 years old. The size of hematoma observed in CT scans was moderate in all cases. hemodynamic indices were measured 2-96 days after the onset. The instrument used was GE CT/T 8800 scanner.
The local cerebral blood flow (L-CBF) was estimated by the inhalation of high concentration (65%) of nonradioactive Xenon. And local mean transit time was measured by dynamic CT scans after intravenous bolus injection of Iodine. The width value calculated from the time concentration curve was used as an index of mean transit time. The map of local cerebral blood volume (L-CBV) index was prepared by multiplying L-CBF map by width map in each pixels.
The degrees of brain edema, contrast effects, and local vascular bed volume in each maps were estimated as minor; 1, moderate; 2 and severe; 3 grades. The maps were evaluated by those multiple parameters, and following results were obtained. : 1) Brain edema tended to increased until around 20 days after the onset and gradually decreased thereafter. 2) Contrast ring enhancement showed two peaks around 20 and 40 days after the onset. 3) The local vascular bed volume of perihematoma was increased around 40 days after the onset.
1) Ring form contrast effect in subacute stage of hypertensive cerebral hemorrhage was biphasic, showing early and late enhancement. 2) The early contrast enhancement was related to extravasation of contrast medium, which coincided with deterioration of brain edema. And 3) the late contrast enhancement was closely related to an increase of local vascular bed volume.
Assessment by simultaneous use of CT, nonradioactive Xenon, and Iodine enables more detailed in vivo evaluation of the pathophysiology of hypertensive cerebral hemorrhage.
