Although most interventional embolization treatments for cerebral arteriovenous malformations are less risky compared to surgical resection, there is still some risk of surgical accidents due to the complexity of the vascular malformation structure, the specific functionality of the cerebral vasculature, the unpredictability of cerebral blood flow alterations, and the uncontrollable nature of the embolization material. According to a group of cases analyzed by et al, the risk of death after cerebral arteriovenous malformation embolization was 1-2%, the risk of severe injury was 1.5%, the incidence of mild and transient injury was 9% and 11%, respectively, and the incidence of new onset epilepsy (i.e., no seizures before surgery and new seizure symptoms after surgery) was 3%. The causes of these outcomes may be cerebral hemorrhage, cerebral embolism, etc. Cerebral hemorrhage may occur during or after surgery. Intraoperative cerebral hemorrhage may be related to the operation or, more often, to the specific structure of the cerebral arteriovenous malformation; postoperative hemorrhage may be related to a “normal perfusion pressure breach” or to a residual malformed mass. The so-called “normal perfusion pressure breakthrough” refers to the inability of the small arteries and capillaries in the brain tissue surrounding the cerebral arteriovenous malformation to adapt to the sudden increase in blood flow and pressure after malformation embolization, resulting in bleeding. The severity of bleeding, whether intraoperative or postoperative, is related to the amount of bleeding, which may be life-threatening in severe cases and may require surgical removal of the hematoma if necessary, and depending on the situation, may require simultaneous resection of the malformation, which may leave some neurological dysfunction after surgery. If the hematoma is small, the doctor may also administer conservative medication under close observation depending on the situation. Cerebral infarction or cerebral embolism is more related to ectopic embolism of embolic material. Ectopic embolization is a complication of the embolization material causing embolization of the normal brain tissue or cranial nerve supply artery in the vicinity or distant part of the vascular malformation during the interventional embolization process, resulting in the corresponding neurological deficit. During insertion of the microcatheter into the malformed supply artery, it is expected to be as close to the malformed mass as possible. This is because the malformed supply artery may also have branches that supply blood to normal brain tissue proximal to the malformed mass, and the surgeon needs to avoid blockage of these normal supply arteries by the embolic material during embolization of the malformed mass, and therefore to be as close to the malformed mass as possible to reduce the risk of embolization of the normal cerebral supply artery. However, because of the high blood flow in arteriovenous malformations, some small normal supply arteries are poorly visualized or not visualized due to “blood theft”, and because malformed supply arteries are usually extremely tortuous, the deeper the insertion, the greater the risk of bleeding from these arteries. Therefore, in this case, earlier injection of embolic material may result in embolization of the normal supply arteries that were not originally visualized. In addition, because each blood supply artery has traffic through the aberrant mass, embolic material may diffuse to other blood supply arteries through one blood supply artery, which may cause embolization of the normal blood supply artery proximal to it if there is too much diffusion; in addition, liquid embolic material may diffuse forward along the blood flow, but may also return to the proximal end of the blood supply artery, which may cause embolization of the normal cerebral blood supply artery, and in the case of insufficient collateral In case of insufficient compensation, it may cause ischemic necrosis in the corresponding area of brain tissue and cause certain neurological deficits, and the severity of this complication is related to the site and area of malformation and ectopic embolization. In addition, when embolizing cerebral arteriovenous malformations with polymeric adhesive embolization material, the physician usually wishes to embolize as large an area of malformation as possible via one of the blood supplying arteries, which may require a longer duration of injection and may bring about reflux over a certain distance. In this case, the head end of the microcatheter may be stuck with polymeric adhesive. At this point, if the catheter is rashly removed, there is a high risk of excessive pulling of the glue within the malformed mass, which may lead to tearing of the small vessels around the malformed mass and bleeding. Therefore, after repeated attempts, the physician may choose to leave the microcatheter in place rather than remove it. But in any case, as mentioned earlier, the risk of such serious complications from interventional embolization is relatively small compared to the risks faced by the vascular malformation itself, and even if the above-mentioned accidents occur, most of them cause only minor or transient functional deficits; therefore, physicians will still recommend aggressive treatment for patients who are at greater risk in the natural course of their disease on the balance of pros and cons.