Cerebral arteriovenous malformation is a congenital intracranial vascular malformation, which is an abnormal development of the structure between the arteries and veins in the brain, resulting in the replacement of the normal capillary network between them by “thread-like” vascular nests. As the walls of the vessels in these “thread-like” nests are thin, they communicate with each other a lot, leading to cerebral hemorrhage due to rupture of the vessel walls when a large amount of blood flow passes through the nests and impacts the vessel walls. However, the pathogenesis is still unclear, and some patients have a family history of genetic mutations that may affect the occurrence, development, and clinical course of arteriovenous malformations. It is possible that the arteriovenous malformation may grow and enlarge, remodeling or regressing the structure. Clinical manifestations Cerebral arteriovenous malformations (AVMs) account for 0.001%-0.01% of the population and 56.3%-80% of cerebrovascular malformations, and are the most common cerebrovascular malformation, with more males than females, approximately 2:1, and a peak age of onset of 20-39 years.41 Intracranial hemorrhage is manifested in ~79% of patients, and is more common in children. Cerebral hemorrhage The natural history of cerebral arteriovenous malformations has found an annual hemorrhage rate of 3% for unruptured hemorrhage, 4.5% for ruptured hemorrhage, and 0.7%-1% for untreated cerebral arteriovenous malformations. Concomitant aneurysms, deep venous drainage, and deep location are all high risk factors for their hemorrhage, and the relationship between the size of the arteriovenous malformation and hemorrhage is controversial. Sustained shock can cause localized sac-like bulging of the vessel wall at its weakest point, creating a flow-associated aneurysm, which is usually a high risk factor for arteriovenous malformation rupture, as well as a high-flow arteriovenous fistula within the malformed mass is also a high risk factor for hemorrhage. Epilepsy is the second most common symptom (11% to 33%), with cortical, large, superficial or multiple venous drains being a good cause of epilepsy. The type of epilepsy can be partial seizures or generalized tonic spastic seizures with loss of consciousness. An 8% 5-year incidence of epilepsy has been reported for incidentally detected intracranial arteriovenous malformations. Headache is not a specific manifestation of cerebral arteriovenous malformations, and one study reported that 0.2% of people with headache and no neurological abnormalities had intracranial arteriovenous malformations. It is not known whether pregnancy causes an increased risk of intracranial hemorrhage in cerebral arteriovenous malformations. Diagnosis CT or MRI of the brain can usually diagnose cerebral arteriovenous malformations, but only DSA is the gold standard for the diagnosis of cerebral arteriovenous malformations and is mandatory before treatment of cerebral arteriovenous malformations. DSA can clarify the configuration of the nest of malformed vessels, the relationship between the malformed mass and the surrounding vessels, the supplying arteries and the draining veins, the presence of associated aneurysms, arteriovenous fistulas, and the flow of the malformed mass, all of which are necessary for the treatment of arteriovenous malformations. The annualized hemorrhage rate for cerebral arteriovenous malformations is 4-18%, and the annualized mortality rate is 1%, with a rebleeding rate of over 30% in the first year in patients with hemorrhage as the first symptom. The mortality rate of patients with intracranial hemorrhage is 29% and the disability rate is 23%. Therefore, timely and effective treatment is the key to save patients’ lives and reduce the disability rate. The aim of treatment for cerebral AVM is to prevent and eliminate rupture and bleeding of the lesion, relieve neurological dysfunction, and improve the quality of life of patients. There is no controversy in the treatment of hemorrhagic cerebral AVM or symptomatic cerebral AVM, and active surgical management is advocated. In contrast, the treatment of unruptured cerebral AVM is controversial, but because of its risk of rupture, our opinion is to aggressively surgically manage it for cure with a low complication rate. The treatment of arteriovenous malformations is a comprehensive process, and endovascular treatment, gamma knife treatment, and craniotomy in conjunction with each other are the mainstream methods of treatment for intracranial arteriovenous malformations. Craniotomy: Surgery can cure the arteriovenous malformation if the malformed mass can be completely removed, but it is risky, especially if the arteriovenous malformation is located in the functional area, large, deep, or with deep drainage. (The left picture shows the malformed mass on preoperative angiography, the middle picture shows the excised malformed vessels, and the right picture shows the postoperative angiography indicating the disappearance of the malformed mass). This method has a high cure rate and can achieve a curative effect after total resection, but the surgical risk is high and intraoperative hemorrhage is life-threatening. Radiosurgery treatment: This method is used to irradiate the deformed vascular mass with high-energy radiation to induce spontaneous thrombus formation in the deformed mass and occlude the deformed vascular mass, the principle is that after irradiation, the fibrous endothelium of the vascular mass gradually forms thrombus to occlude the vascular mass. This includes gamma knife treatment and radiofrequency knife treatment. The process of occlusion of the vascular malformation mass after radiosurgery is long, often taking 2-3 years, and the risk of bleeding is generally said to decrease gradually, but remains controversial. Some studies also suggest that radiosurgical treatment of arteriovenous malformations after bleeding is superior to that of arteriovenous malformations without ruptured bleeding. Endovascular treatment: Endovascular embolization is an effective adjunctive treatment prior to surgical resection or radiosurgery, creating the conditions for surgery or radiosurgery by making the malformed mass smaller and embolizing the associated aneurysms and high-flow arteriovenous fistulas in one or several embolization sessions. This method is a minimally invasive interventional approach with fewer relative risks and complications than open surgery, but the cure rate is low with intervention alone. Only about 5% of patients can be completely cured of cerebral arteriovenous malformations by single-survival endovascular treatment. The PRESSURE COOKER technique may be a breakthrough in the development of curative embolization of intracranial arteriovenous malformations with the development of interventional embolization materials and techniques. The results of our study were published in the Chinese Journal of Cerebrovascular Diseases, “Proximal flow blocking and pressurization technique for the cure of cerebral arteriovenous malformations with embolization (Author: Donglei Brain Physicians Group, Yanting Gai, Donglei Song)”. The treatment plan for cerebral arteriovenous malformation requires a joint study and discussion between experienced neurosurgeons and neurointerventionists, and a decision based on the wishes of the family and the patient. In general, for large, deep-draining, high-grade, functional-area arteriovenous malformations, interventional combined with gamma knife or radio wave knife is recommended, while for small, non-functional, low-grade arteriovenous malformations, interventional embolization combined with surgical resection is recommended. Gamma knife or radiofrequency knife treatment alone is generally indicated for sites that cannot be embolized or surgically resected, such as the brainstem region.