Pathological changes such as cortical gliosis, infarction and calcification, subcortical vacuolization, and abnormal enlargement of the large cerebral veins, which are connected to many tiny arteries. The mechanisms by which brain injury occurs are mainly arterial steal, cerebral ischemia secondary to heart failure, hemorrhagic infarction, lesion compression, and surgical trauma. The diagnosis of cortical gliosis relies mainly on age of onset and clinical manifestations, but radiologic examination is required to confirm the diagnosis. Neonates with intractable heart failure with intracranial vascular murmur; infants with hydrocephalus should be considered the possibility of this disease, for those who can hear intracranial vascular murmur or the presence of subarachnoid hemorrhage, the diagnosis can be basically determined. Further diagnosis can be confirmed by cerebral angiography, CT scanning, or MRI. Cerebral large venous tumor, according to the age of onset of the clinical manifestations of the lesion can be divided into four age groups: 1. Neonatal group Typical manifestations of the disease are high-output, preloaded heart failure shortly after birth, which is present in almost all the sick children. The degree of heart failure is dependent on the size of the fistula and the presence of venous embolism. A sustained intracranial murmur is audible on cranial auscultation. Jugular venous oxygen saturation is markedly elevated. Cranial CR and MRI reveal aneurysmal lesions, and numerous small supplying arteries can be seen at the anterior and inferior margins of the lesions on angiography, mostly belonging to Yasargil type I, II and III, with type III being the most common. Ultrasonography also reveals persistent blood flow in the internal jugular vein, which is different from the normal fluctuating blood flow. Anechoic shadows can be detected in the lesion, and the flow is also persistent. Surgical treatment of intracranial lesions does not improve refractory heart failure and may precipitate myocardial infarction due to intraoperative lowering of blood pressure. Most children die of heart failure. Autopsy reveals pathological changes in the brain such as paraventricular softening foci, deep hemorrhage in the brain parenchyma, cortical gliosis, infarction and calcification, and subcortical vacuolization, and abnormally enlarged large cerebral veins that are connected to many tiny arteries. Mechanisms of brain injury occurring are mainly arterial blood theft, cerebral ischemia secondary to heart failure, hemorrhagic infarction, lesion compression and surgical trauma. 2. The infant group is clinically divided into two groups (1) Cardiac decompensation had occurred in the neonatal period, but it was relieved by treatment or relieved on its own. Subsequently (1 to 12 months after birth), there was an increase in head circumference and intracranial murmur, which was obvious on auscultation at the posterior lateral side of the head. (2) There was no history of cardiac decompensation. The infant is seen for increased head circumference and hydrocephalus is found. Chest X-ray may reveal cardiac hypertrophy. The ventricles of the brain may be markedly enlarged, involving the lateral and third ventricles. Previously, it was thought that the cause of ventricular enlargement was the compression of the midbrain aqueduct by the enlarged cerebral large veins, causing obstructive hydrocephalus. However, recent pathophysiologic and imaging studies have shown that the aqueducts often remain patent, and there is no clinical evidence of hydrocephalus, and there is no paraventricular edema on CT or MRI. Increased pressure in the sagittal sinus and venous system, which affects cerebrospinal fluid absorption, is now considered the main cause of ventricular enlargement. Usually cerebral angiography reveals a filling cystic lesion, and turbulence can be observed dynamically as the contrast agent washes into the cyst. Occasionally, thrombus formation within the lesion completely occludes the cystic cavity and fails to visualize it. If a thrombus forms in the wall of the capsule and the capsule lumen is present, a “target sign” can be seen on CT. Usually the fistula is smaller than in the neonatal group, and most of them have only one fistula, which is equivalent to Yasargil type I. The fistula is usually smaller than in the neonatal group, and most of them have only one fistula. Epilepsy is also the main clinical manifestation in this group. Prolonged intracerebral blood theft can cause cerebral ischemia. Cerebral infarction as well as degenerative changes are the pathologic basis of epilepsy. Children over 2 years old mostly develop with increased head circumference. Some patients may have subarachnoid hemorrhage, and the heart may also be mildly enlarged. Intracranial murmurs can be heard on cranial auscultation. However, it needs to be differentiated from physiologic intracranial murmurs in children. Generally in normal infants or children, the murmur can also be heard in the skull or ophthalmoplegia, with the ophthalmoplegia or the temporal side obvious, the murmur increases in systole, and the murmur disappears when the carotid artery is compressed. However, the murmur of large cerebral venous tumor is obvious near the parietal nodes and the posterior part of the midline, and it is stronger in newborns and infants, and it can be heard in both systole and diastole, or it can be continuous. 4.Adult group includes older children, adolescents or young adults Clinical manifestations are various: subarachnoid hemorrhage, pineal region occupation, high intracranial pressure and hydrocephalus. Head CT or MRI can be used for differential diagnosis. Pathophysiologically, the patient has a small arteriovenous fistula with low flow rate or belongs to secondary large cerebral venous tumor.