At present, it is believed that the cause of surgery-related cerebral venous infarction is injury to the cortical vein and venous sinus or cortical pial venous system [7-10]. ① Meningiomas often occur near the venous sinus and cortical drainage vein where arachnoid granules gather. During the operation, the vein around the meningioma or the related venous system is damaged, and there are no anastomotic veins in the injured area, which may lead to secondary cerebral venous infarction. ②Meningiomas are usually associated with dural vessels and cortical drainage veins or with the pial arteriovenous system. During the operation, the interface between the tumor and the arachnoid is separated, and the arachnoid and pia mater are destroyed, which may damage the venous system of the pia mater cortex and eventually lead to cerebral venous infarction. These two kinds of injury mechanisms are mutual cause and effect and they aggravate the degree of venous infarction. Statistical analysis showed that tumor location (superficial), peritumoral edema (moderate to severe), peritumoral vein (key vein) and histological grade (WHO II-III) were risk factors for cerebral venous infarction, and the risk factors were closely related to the mechanism of the cerebral venous infarction.
Tumor localization and peritumoral vein
Superficial meningioma refers to the convexity, parasagittal and falx, often accompanied by peritumoral veins. The growth pattern spreads along the cistern and embeds into the brain parenchyma, indicating that superficial meningioma has a wider contact surface between the tumor and brain parenchyma than deep meningioma and it lacks a cerebrospinal fluid barrier . Therefore, the probability of injuring the peritumoral vein and cortical pial system during resection is higher than that for deep or other meningiomas.
The previous literature has reported that the bifrontal or near midline approach is a risk factor for cerebral venous infarction. The essence of the approach is to remove the tumor through the bridging vein and sinus, which hinders the exposure or manipulation of the tumor during the resection process so that the operator has to block or accidentally damage the vein around the tumor. At the same time, the previous view was that the frontal cortical vein and the anterior 1/3 superior sagittal sinus could be sacrificed, but clinical cases confirmed that this is definitely not desirable and the risk of infarction after injury will be significantly increased, which may have catastrophic consequences. Previous research has shown predictors of positive motor function in rolandic meningomas, including venous involvement. To prevent cerebral venous infarction, the peritumoral veins and collateral veins of convexity, parasagittal and falx meningiomas can be classified [14-16]. It was suggested that the key veins should be avoided as much as possible, and the collateral veins should be selectively severed according to the degree of compensation to avoid the occurrence of cerebral venous infarction to the greatest extent.
Peritumoral edema and histological grade
Peritumoral edema is a common imaging manifestation in patients with meningioma and is a compensatory reaction of damaged brain tissue. The pathogenesis of peritumoral edema includes brain parenchymal compression, secretion of fluids, venous compression and hydrodynamics theory. The presence of brain parenchyma tumor interface-associated edema indicates a poor prognosis of the nervous system . The destruction of the tumor brain arachnoid layer interface leads to the formation of peritumoral edema. Dysplasia of the peritumoral drainage veins can also cause peritumoral edema. Meningiomas with peritumoral edema have a higher probability of destroying the cortical pial venous system. WHO grade II – III (atypical, anaplastic) meningiomas invade the arachnoid, pia mater, brain tissue and adjacent dura mater , increase the permeability of the meninges and blood vessels, aggravate the edema, and more easily damage the cortical venous system during the operation, resulting in increased postoperative edema and possibly venous infarction. Therefore, high-grade meningioma and peritumoral edema are risk factors for cerebral venous infarction. During the operation, we should try to separate along the tumor arachnoid boundary and retain part of the cortical venous system in order to reduce the incidence and severity of venous infarction.
Tumor size and the extent of resection
Previously, it was reported that tumor growth could destroy the arachnoid interface between tumors and meninges, and tumors ≥ 4 cm are a risk factor for cerebral venous infarction , but our data showed that there was no significant difference. Considering that tumors increase in volume, the brain tissue is compressed, the blood-brain barrier is destroyed, and peritumoral edema is formed, but there are still some tumors without peritumoral edema. In addition, its formation may be related to the operation. Usually, for large tumors, we should reduce the tension of the tumor on the vein first, and the possibility of injury is small, which is not different from that of tumors < 4 cm. The data from this group confirmed that there was no difference in the degree of tumor resection. Usually, the residual tumor is closely related to the sinus. For sindou  Ⅰ - Ⅲ tumors, total resection can be achieved, while for sindou Ⅵ - Ⅴ tumors, surgical resection is limited to reduce the risk. At the same time, the stenosis or occlusion of the sinus will be compensated for by collateral anastomosis. Therefore, the degree of resection is not a risk factor for cerebral venous infarction.
Injury to a key vein or the cortical pial vein system can cause cerebral venous infarction, but the severity of cerebral venous infarction after injury differs, and the symptoms of patients are also different, from no obvious symptoms to serious neurological impairment and even disturbances of consciousness. Robertson  divided cerebral venous infarction into the acute phase and chronic phase. Severe complications occurred in a short time after the operation in the acute stage and were life-threatening, while the chronic stage lasted for several days to months with mild symptoms. Generally, injury to the critical vein can cause serious complications in the acute stage, including postinfarction hemorrhage, limb and speech dysfunction, epilepsy, coma, etc. Timely review of CT and surgical intervention are needed. After cortical pial venous system injury, the symptoms of the patients gradually worsened, but the symptoms could be relieved after conservative treatment. The prognosis of patients with venous infarction is better if they are treated in time, but damage to a key vein will cause irreversible neurological damage.
In conclusion, superficial meningioma, moderate to severe peritumoral edema, peritumoral critical vein and WHO grade II-III are independent risk factors for cerebral venous infarction. We should realize that postoperative cerebral venous infarction may cause serious complications. The key peritumoral veins and collateral veins should be protected as much as possible to avoid the occurrence of a postoperative cerebral venous infarction. Separation should be performed according to the tumor arachnoid interface to prevent injury to the cortical venous system. If an adhesion between the tumor and brain parenchyma is obvious, selective electrocoagulation can be used to reduce the probability of a cerebral venous infarction. In short, patients with high-risk factors need to be closely observed for any changes and receive timely intervention when necessary to ensure a good prognosis.