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. Prevention of cortical gliosis is mainly to avoid its triggering factors, and the prognosis of untreated large cerebral venous tumors is poor. Of 92 untreated patients in the statistical literature, 77.2% died, 3.3% were disabled, 12% remained intact, and 7.5% were lost to follow-up. The main cause of death was cardiac and cerebral ischemic damage. Untreated neonates have a higher morbidity and mortality rate of 96%. The prognosis for newborns with high efflux heart failure and children and adolescents presenting with subarachnoid hemorrhage is poor, regardless of treatment. However, in infants seen for hydrocephalus with increased head circumference or in patients with intracranial murmurs and no other clinical symptoms, surgical treatment has a better prognosis than other treatments, although it is difficult and the mortality rate is still high.