The biological behavior of Brainstem Cavernous Malformation (BSCM), especially the incidence and the rate of overt hemorrhage of the lesion calculated considering the brainstem volume, is different from that of other sites of cavernous hemangioma. With the popularity of MRI, many primary brainstem hemorrhages are found to be caused by BSCM. Early hemorrhages show a homogeneous hematoma signal or interspersed with a little irregular low signal, and in the following 1-6 weeks, as the hematoma liquefies and resorbs, it shows more typical features of cavernous hemangioma in a high signal background, but a few micro BSCM still show only small nodular foci attached to the lateral wall of the hematoma. Most of the so-called overt hemorrhages manifest as dizziness, vomiting, limb numbness or impaired mobility, facial paralysis, swallowing or dysphonia, with a few cases of drowsiness and very few life-threatening cases [1]. Symptoms usually peak within a few days and continue to resolve for several weeks thereafter, and sequelae may be very mild, but there is a high risk of rebleeding, especially within two years of the previous bleeding. Some patients may have recurrent bleeding for a short period of time, resulting in persistent or wavelike exacerbation of neurological function. In the distant future some patients are able to heal spontaneously. These advances in understanding come primarily from physician experience and lack scientifically designed studies of the natural history of BSCM. It is now broadly accepted that BSCM accounts for 9%-35% of all intracranial cavernous hemangiomas, has an annual bleeding rate of 0.5%-6%, and that the annual rebleeding rate increases significantly [1]. Recent medical advances for BSCM are more mainly reflected in surgical outcomes. On the one hand, although there is still some controversy about the surgical indications, timing and access, there has been a gradual convergence towards a unified understanding, which is beneficial for improving the surgical outcome; on the other hand, it has benefited from advances in surgical techniques and tools. I. Surgical indications and timing of BSCM Whether to operate? When to operate? This is a question that requires highly individualized consideration. In fact, for this type of disease, experienced surgeons have a very accurate prognosis of the patient’s postoperative status. lawton developed a 7-point grading scale for assessing the prognosis of BSCM surgery based on the size of the BSCM, whether it crosses the central point of the brainstem axis, the presence of venous malformations, whether it is older than 40 years, and the length of time after bleeding, which correlates well with the patient’s true prognosis [2 ]. In contrast, little is known about the current grasp of natural history instead. In the author’s experience, it is crucial to look at the patient’s symptoms and MR performance, and it is useful to ask three questions: (1) Are the symptoms persistently worse or life-threatening? (2) Can the BSCM lesion be distinguished from the high-signal hematoma background on MR? (3) Is there an appropriate access to the lesion? Answers are classified as yes (Y) or no (N). Recommendation: 1Y – Emergency surgical decompression [3, 4]. As the brainstem edema and glial proliferation zone are not formed, BSCM resection is not forced to avoid aggravating the acute brainstem injury; 2Y3Y – surgical resection of the lesion and pursuit of total resection; 1N2N3Y, MR only hematoma no BSCM lesion is found, it is recommended to be conservative and repeatedly review MR, which can be done once a week, after looking at the BSCM early surgery after visualizing the BSCM. The advantages of this are that the purpose of exploration is clearer, avoiding missed lesions, while the hematoma is liquefied and mechanization has not yet formed, facilitating decompression and separation of the lesion, and avoiding the peak edema period after brainstem hemorrhage [1, 5]. There is also a question of the appropriate level of answer to question 3, which needs to be weighed and decided. Surgery is certainly preferred for those with recurrent hemorrhage and simple access, especially if the lesion is superficial and grows outward to reach or protrude from the soft meningeal surface of the brainstem [2, 5]. For smaller lesions that are buried deep within the brainstem and have greater access damage, they can be conservative and operated on after the patient has had another or recurrent bleeding [1, 5, 6]. There is still a lack of evidence-based recommended protocols for asymptomatic BSCM found incidentally. Since the benefit to the patient is implicit and the surgical injury and risk are explicit, it is important to achieve full informed consent from the patient and family even when the lesion is located in a more accessible location for surgery and the estimated surgical injury is mild, with special attention to truthfully informing the patient of the unpredictability of the future bleeding risk of the lesion. The surgical approach to BSCM is also a highly individualized issue. Classically, the Two-point Method is used to find the closest line to the lesion and the best angle to the center of the lesion, and this is used to determine the surgical approach [7]. The newer Safe entry zone approach sometimes sacrifices proximity for distance, but is more conducive to protecting functional brainstem areas. Anatomically, from the spinal cord to the brainstem, the central duct opens dorsally to form the base of the quadrigeminal ventricle, accompanied by the displacement of the conduction tract and the formation of a functional column of gray matter nuclei. The open base of the quadrigeminal ventricle is characterized by important gray matter nuclei. Since the lateral conduction bundles are relatively minor, they should be utilized whenever possible. A posterior sigmoid sinus approach via a safe zone around the trigeminal roots is particularly recommended and is more effective than a transventricular floor approach for lesions that project both to the base of the quadrigeminal ventricle and to the lateral aspect of the pontine brain. To further reduce the surgical entry injury, the author proposes the safe entry point approach. With the advancement of microscopic techniques, it is no longer necessary to direct the entry point toward the center of the lesion, but only to find a point where the lesion can be dragged out from the lateral side and completely resected by meticulous separation and traction, with the aid of neuroendoscopic exploration if necessary. In its specific application, the BSCM approach can be divided into two steps: (1) exposing the surface of the brainstem and (2) dissecting the surface of the brainstem to expose the lesion. The first step determines the body position and incision based on MR structural phases, including conduction bundle imaging, and image fusion with virtual reality can be used for inexperienced individuals [1, 8]. A transcallosal medullary approach can reduce cerebellar damage and reveal the base of the quadrigeminal ventricles and the dorsal aspect of the extended neck; an intercallosal approach can be used for the inferior medullary and extended neck junction; a subscallosal superior parietal median cerebellar approach in the prone position can reveal the dorsal and dorsolateral midbrain without traction, and the inferior border can reach the root of the talocrural nerve; an orbitozygomatic transcallosal approach is traditionally used for the ventral aspect of the brainstem, but an endoscopic transcallosal or transcallosal approach would be a better choice [9, 10]. For those located lateral to the brainstem, attention should be paid to its relationship to the nerve roots: for those located above the trigeminal nerve, a trans-lateral fissure or infratemporal approach can be used; for those located below the trigeminal, a posterior suboccipital ethmoid sinus approach is suitable; for those located near the posterior group of cranial nerves, especially ventral, a distal lateral approach is appropriate [1, 11]. In the second step, the location of the brainstem surface incision needs to be decided according to the local color, morphology, nucleus pulposus, or location of important conduction tracts. If the lesion is superficial and local yellow staining or elevation is visible under microscopy, localization is not difficult, while if the surface is normal the incision location needs to be decided based on anatomical markers or navigational positioning. It should be reminded that although the lesion will be more visible in the T2 phase, it will also be slightly larger in diameter than it actually is, appearing closer to or even protruding from the surface of the brainstem. To avoid misdirection, a combination of T1-enhanced navigation is advocated. The important motor structures such as the pyramidal fasciculus and facial nucleus near the incision should be precisely located and avoided by electrical stimulation. III. Technique of BSCM excision Meticulous and patient microscopic operation is required, and one should not be greedy for speed. The technical points are as follows: (1) Decompression first and then separation. By releasing the liquefied hematoma and gradually removing the sediment-like clot to reduce the tension and make room for retraction. (2) Separate along the light yellow soft glial proliferative zone, beyond which the brainstem can be damaged. However, care is also taken not to miss the lesion; certain follicles are concealed within the glial folds and should be peeled out. If left behind not only will not reduce the hemorrhage rate, but on the contrary the probability of recent hemorrhage will be high [1, 6, 12]. The point is to carefully maintain and separate the interface under direct vision, and the lesion can mostly be removed intact by blunt freeing. The brain cotton pulling method proposed by academician Liangfu Zhou is a very practical technique. (3) Avoid thermal injury. The heat generated during electrocoagulation for hemostasis can burn the brainstem tissue, so the power of electrocoagulation should be adjusted as low as possible and precisely electrocoagulated. bscm often has several tiny blood supply arteries and drainage veins, and the vessels themselves should be electrocoagulated instead of malformed masses or glia after clear differentiation. (4) Care should be taken to protect nearby relatively thick draining veins or venous malformations to avoid severe postoperative brainstem edema [5]. Reviewing the process of understanding BSCM, the brainstem was once considered a forbidden area for surgeons. Under the leadership of foreign masters such as Spetzler and Bertalanffy, and domestic masters such as Wang Loyal and Zhou Liangfu, breakthroughs in surgery have been achieved, and the development of neuronavigation, functional magnetic resonance, and neuroelectrophysiology have provided a strong guarantee for the safety of BSCM surgery [1,3, 6, 10, 11]. Currently, many units in China are able to perform such procedures, reflecting the improvement of the overall level of neurosurgery in China. Currently, the preferred treatment option for BSCM is still surgical resection [2-4], and we need to keep in mind that proper case selection, good access design, perfect intraoperative localization and monitoring are important prerequisites for successful BSCM surgery, and finally the surgical efficacy is ensured by fine microsurgical operations. It has been suggested that stereotactic radiotherapy (SRS, Stereotactic radiosurgery) can reduce the chance of bleeding in BSCM [13], but this meta-analysis calculates the annual bleeding rate before treatment by counting only the annualized bleeding rate during the time window from the appearance of symptoms or discovery of the lesion to the onset of SRS treatment, which can easily exaggerate the true risk, and it is easy to presume that the annual It is unscientific to assume that the annual bleeding rate decreases after treatment. When compared with the natural history of symptomatic BSCM, the annual rebleeding rate within 2 years after SRS treatment is 6.8%-12.5%, but the annual bleeding rate in symptomatic BSCM even without treatment is only 6.1%-16.3% within 2 years, which is not a significant difference [13, 14]. Therefore, there is insufficient evidence that SRS reduces the annual bleeding rate of BSCM. In addition, the evidence of side effects of SRS such as severe brainstem edema and the appearance of secondary angiomatous changes is more conclusive, with a rate of new neurological deficits of 11.8% [13]. Therefore, the use of radiation therapy is not recommended as a matter of urgency.