Pathological changes such as cortical gliosis, infarction and calcification, subcortical vacuolization, and abnormal enlargement of large cerebral veins and connection with many fine arteries. Brain injury occurs mainly by mechanisms such as arterial blood theft, cerebral ischemia secondary to heart failure, hemorrhagic infarction, lesion compression and surgical trauma. The large cerebral vein originates from the venous return system that drains the intermediate structures of the choroid plexus. Initially, the vein does not communicate with the deep internal cerebral vein, and at about 11 weeks of embryonic development, the posterior part of the vein communicates with the internal cerebral vein to form the large cerebral vein, and the anterior part of the vein degenerates and eventually disappears. During the 6th to 11th week of embryonic development, if for some reason the embryo develops abnormally, the anterior part of the cerebral vein does not degenerate and occlude normally, an arteriovenous fistula can be formed. This embryological alteration may explain the arteriovenous traffic of the primary cerebral major vein that opens directly into the wall of the venous sac and is mostly located anteriorly and inferiorly to the sac wall. The arteries supplying the venous aneurysms may be derived from the paramedian choroid plexus vessels, posterior choroid plexus arteries, branches of the middle cerebral artery, superior cerebellar artery, and meningeal vessels; thalamic penetrating branches may also be involved in the blood supply due to siphoning action. The main pathological changes of cortical gliosis are short-circuiting between cerebral arteries and large cerebral veins, and a large amount of arterial blood enters directly into large cerebral veins, making them extremely dilated, round or ovoid, with grayish, thickened and tough walls; sometimes some thrombosis occurs, and the diameter is often more than 3 cm. The brain tissue within the lesion is degenerated, atrophied or softened. The artery supplying directly to the large cerebral vein involves 87% of the posterior cerebral artery, and 50% of the blood is supplied by the posterior cerebral artery alone, mostly unilaterally, and more often on the right side, but also bilaterally by the posterior cerebral artery. Other arteries may also be supplied by the anterior cerebral artery, middle cerebral artery, and superior cerebellar artery. Most of the patients belong to the above-mentioned cases, but there are some cases in which the draining veins of the cerebral arteriovenous malformation are introduced into the large cerebral vein, resulting in significant dilatation of the large cerebral vein, and in such cases, the arteriovenous malformation is usually larger and the arteriovenous fistula within the lesion is also larger. In conclusion, large cerebral venous aneurysms are the result of arterialization of the vein wall due to a series of hemodynamic changes induced by long-term high pressure arterial blood flow.