Hypertensive intracerebral hematomas were investigated using chromium Cr 51labeled erythrocytes. Patients underwent erythrocyte labeling shortly after admission following standard techniques for erythrocyte survival time. At postmortem examination the radioisotopic activity of the primary and secondary (Duret) hemorrhages were determined. In 11 patients with hypertensive hematomas no significant activity was found in the primary hematomas, suggesting that bleeding occurred over a short period of time and there was no rebleeding. Duret hemorrhages present in patients comatose on admission contained no significant actovity. The findings in the Duret hemorrhages suggest that patients comatose on arrival sustained these lesions as an almost immediate consequence of the initial primary hemorrhage. In two nonhypertensive patients, intracerebral hematomas secondary to a ruptured berry aneurysm and an arteriovenous malformation contained high levels of radioisotopic activity, suggesting a different pathophysiology of bleeding.