The dynamics of cerebrospinal fluid (CSF) circulation in 20 cases with hypertensive intracerebral hemorrhage was estimated with radioisotope cisternography (RIC) using In-111-DTPA. CT scan was performed simultaneously to observe the changes in the intracranial pathologies. The findings in RIC were classified into four types; normal circulation, ventricular reflux, ventricular stasis, and subarachnoid block over ipsilateral convexity. Among 20 cases examined with RIC in the acute stage, normal circulation was demonstrated in 11 cases (55.0%), ventricular reflux in 1 case (5.0%) and a subarachnoid block over ipsilateral convexity in 8 cases (40.0%). In the subacute stage, 11 out of 17 cases (64.6%) showed normal circulation, 3 (17.7%) ventricular reflux and 3 (17.7%) a subarachnoid block over ipsilateral convexity. Of 8 cases in the chronic stage, 5 cases (62.5%) showed normal circulation, 1 case ( 12.5%) ventricular reflux, 1 case (12.5%) ventricular stasis, and 1 case (12.5%) a subarachnoid block over ipsilateral convexity. Ventricular reflux and ventricular stasis which were demonstrated mainly in the later stage, seemed to be caused by blood in the CSF, because all cases with such abnormalities in RIC had a hematoma in the ventricle at the onset of hemorrhage, and none of the cases without rupture of the hematoma into the ventricle showed such abnormalities. A subarachnoid block over the ipsilateral convexity which was mainly observed in the acute stage and which frequently disappeared in the chronic stage was caused by the mass effect of the hematoma and the surrounding edema, because it was observed only in cases with larger hematomas. In 6 cases which developed ventricular dilatation in the chronic stage, 3 had a normal finding by RIC and the ventricular dilatation was probably caused by brain atrophy after absorption of a hematoma. The other 3 cases showed ventricular stasis by RIC and the disturbance in the CSF circulation may partly contribute to the ventricular dilatation. Thus, follow-up studies by RIC after a hypertensive intracerebral hemorrhage revealed consecutive pathophysiological changes in the CSF circulation in accordance with the intracranial pathological changes.