In patients with cerebral hemorrhage, including spontaneous cerebral hemorrhage, the receiving physician uses hemostatic drugs as a matter of course. However, in the case of thrombus formation in the cerebral venous return system, including the dural venous sinuses and cerebral veins, the use of hemostatic drugs only causes accelerated formation and prolongation of the thrombus, which leads to a rapid deterioration of the condition. The patient in this report was aggravated by the use of hemostatic drugs at the local hospital, whereas our bold treatment with heparinization and improvement of microcirculation did not aggravate the patient’s cerebral hemorrhage and resulted in a good prognosis. This result again shows that hemostatic drugs should never be used for cerebral venous return system thrombosis, instead heparinization therapy is safe and effective, even if the patient has intracranial hemorrhage.DSA examination can show the hemodynamic characteristics of cerebral circulation and can clearly diagnose cerebral venous return system thrombosis, which is also the gold standard for diagnosing cerebral venous return system thrombosis. However, the key is to be able to think about the possibility of cerebral venous return system thrombosis based on the patient’s clinical presentation and to perform further DSA examinations. Although the incidence of cerebral venous system thrombosis is small and the clinical manifestations vary greatly, there are still certain characteristics, especially the following: 1, seizures or cranial hypertension manifestation onset; 2, CT shows multiple spontaneous intracerebral hematomas, and when leukemia and other hematologic diseases are excluded; 3, CT shows hematomas with mixed high and low density and cotton ball-like changes, cerebral venous return system thrombosis should be highly suspected. Once cerebral venous return system thrombosis is suspected, in addition to disabling hemostatic drugs, DSA examination should be performed promptly to clarify the diagnosis. There is a causal relationship between dural arteriovenous fistula and venous sinus thrombosis. In the reported cases, it was difficult to determine whether the dural arteriovenous fistula caused the venous sinus thrombosis or the venous sinus thrombosis caused the dural arteriovenous fistula in the first case. From the second presentation, it is more likely that the dural arteriovenous fistula was caused by venous sinus thrombosis, on the grounds that the left transverse sinus was mechanized and almost occluded, while multiple (two) new fistulae appeared at the ends of the occluded transverse sinus. If a venous sinus thrombosis caused the dural arteriovenous fistula, what caused the recurrent thrombosis of the patient’s cerebral veins and sinuses? This is also a question that deserves deeper investigation. Until the cause is identified, the anticoagulant should be repeated orally for a long time, and this is what we have learned during the treatment.