Currently, there are two main treatment modalities for ruptured aneurysms: endovascular detachable spring coil treatment or surgical clamping. Many scholars and research institutions have conducted multicenter randomized studies to further investigate the differences in safety and efficacy between the two methods of treatment for aneurysms for which both methods of treatment are appropriate. At this year’s Stroke Congress, Peter A provided his insights into the choice of aneurysm treatment. He argued that clinicians have reached a consensus on the management of certain aneurysms, for example, 98% of MCA bifurcation aneurysms are treated surgically and 100% of basilar bifurcation aneurysms are treated endovascularly. Although the International Study of Aneurysm Therapy (ISAT) has made a significant contribution to the management of intracranial aneurysms, the results of the study cannot be generalized to the treatment of all aneurysms. It is estimated that approximately 80% of patients were excluded from the ISAT study, and further research is still needed on what to do for the other patients (elderly patients, unruptured aneurysms, posterior circulation aneurysms, giant aneurysms, and poorer grading). Endovascular treatment is mainly indicated for: elderly patients, presence of high-risk factors for anesthesia and surgery, poor HH grading, inability to clamp surgically, absence of intracerebral parenchymal hematoma (controversial), and aneurysms at sites that are either difficult to reach surgically or at high surgical risk (controversial). Aneurysms unsuitable for embolization include: giant aneurysms with or without thrombosis, cystic aneurysms, and aneurysms with neck body proportions unsuitable for embolization. Recent advances in medical imaging techniques have greatly increased the detection of unruptured intracranial aneurysms (UIAs). The annual chance of rupture for all UIAs is in the range of 1-2%, with some specific aneurysms having an increased risk of rupture, including increased aneurysm size, and site-specific aneurysms (e.g., aneurysms of the apex of the basilar artery). Because of the relatively constant risk of rupture, clinicians must pay close attention to the management of UIAs.The treatment of UIAs has not yet reached international unity of opinion, and extensive research has focused on the choice of microsurgical and endovascular interventions for UIAs. Michael Marks on the endovascular treatment of small unruptured aneurysms suggests that before endovascular treatment of small unruptured aneurysms, physicians need to consider whether such treatment can reduce the risk of rupture of the aneurysm, and whether such treatment can achieve the best efficacy (occlusion of the aneurysm) in a lower risk range. Although there have been great advances in endovascular treatment technology, including ① spring coil design: soft, ultra-soft, 3D design, tensile strength, bioactivity; ② development of embolization technology: balloon-assisted contouring technology, intracranial stenting; ③ advances in imaging: intraprocedural 2-dimensional images, 3D angiography. However, clinicians cannot ignore a series of serious complications associated with endovascular treatment: thrombosis, embolization, spring coil untwisting, spring coil entanglement; stenosis or occlusion of the aneurysm-carrying arteries; arterial entrapment, rupture of the aneurysm; incomplete embolization of the aneurysm or aneurysms that are more difficult to manage after embolization.Arthur L summarized the surgical treatment of small unruptured aneurysms. He noted that the major risks of surgical treatment of aneurysms include brain tissue traction injury, occlusion of the penetrating vessel, and stenosis of the aneurysm-carrying artery. Therefore, the choice of treatment for small unruptured aneurysms needs to be tailored. Asymptomatic small unruptured aneurysms can be monitored for changes at first. If the lesion continues to grow, it may produce a range of associated symptoms, such as stroke, occupational effects, and rupture hemorrhage. Treatment of small unruptured aneurysms that continue to grow needs to be considered. However, some asymptomatic unruptured aneurysms can rupture and bleed during observation, and this continues to be a source of confusion for clinicians in the treatment of their patients.The selection of patients with small unruptured aneurysms that are suitable for surgery is summarized by Arthur L. These include: young patients, wide-necked aneurysms, aneurysms with occupying effects, patients with a history of stenting of intracranial arteries, and surgeons who must be very experienced. Microsurgery is the traditional approach to the treatment of intracranial aneurysms. The surgical treatment of wide-necked, calcified, thrombosed, or saccular aneurysms can be challenging for the clinician, and Joshua Bederson summarizes the current approaches to this type of aneurysm surgery as follows: (1) aneurysm resection and occlusion of the aneurysm-carrying artery; (2) aneurysm clipping and reconstruction of the aneurysm-carrying artery; (3) aneurysm endarterectomy or thrombectomy; (4) aneurysm remodeling; (5) high- and low-flow bypass grafting; and (6) high- and low-flow bypass grafting. (i) Aneurysm closure and carrier artery reconstruction; (ii) Aneurysm endarterectomy or thrombectomy; (iii) Aneurysm remodeling; (iv) High- and low-flow bypass grafting; (v) Aneurysm closure and carrier artery reconstruction; (vi) Other. Endovascular intervention has become one of the most important methods of intracranial aneurysm treatment. The shortcomings of this treatment are the possibility of aneurysm neck remnants, untreatable part of the aneurysm, and recurrence of the aneurysm after treatment. Despite the use of state-of-the-art techniques and selection of the most suitable patients, the recurrence rate of aneurysms in some large-scale clinical studies still exceeds 20% (Raymond, Murayama). To reduce recurrence in the early postoperative period after aneurysm surgery, complete intraoperative occlusion of the aneurysm is important. This can be achieved with some advanced techniques, but some aneurysms still recur during long-term follow-up, suggesting that the mechanization of the thrombus in the lumen of the aneurysm may take a long time and that the mechanization may be partial. In experimental studies, incomplete endothelial coverage of the aneurysm neck and the presence of many open fissures are frequently seen. These endothelialized fissures are theorized to be an early sign of aneurysm recanalization and may be the histological etiology of aneurysm recurrence. Achieving closure of these endothelialized fissures through spring coil modifications can help improve the long-term outcome of endovascular treatment of aneurysms.Aquilla summarized the advances in bioactive spring coils. He categorized the new and improved spring coils currently in clinical use into the following three main types: (i) promoting thrombus mechanization: Matrix Boston, Cerecyte CMicrus Corp, Nexus CMTI/EV3, 32PIon Implanted Coils; (ii) increasing the degree of filling, reducing thrombus formation in the lumen and providing a point of attachment for intra-aneurysmal cell proliferation; and (iii) providing an attachment point for the endothelialized fissure to be closed by a new spring coil. (iii) Coexistence of two mechanisms of action: Biomerix Neurostring, NeuroVasx cPax. Vasospasm on angiography and symptomatic vasospasm are seen in about 50-70% and 20-40% of cases of SAH. Delayed cerebral ischemia affects the neurological function and prognosis of patients after SAH. Previous literature has shown that risk factors for developing vasospasm after aneurysmal SAH are: mean arterial pressure >112 mm Hg; bilateral lateral ventricular hemorrhage; mean flow velocity of the MCA on the TCD >140 cm/s within 5 days of the onset of SAH; hemorrhage with a thick layer in any of the cerebral pools; a decrease in the platelet count by >30%; a leukocyte count of >15,000/μl; hyperglycemia; and an age of <50 years. Good neurologic function score on admission; smoking. In a study of multisite symptomatic vasospasm after SAH, Katja noted that: 56% of patients with SAH presented with multisite symptomatic vasospasm; the vast majority of patients had a poor Hunt and Hess classification on admission; and early detection and early treatment of multisite vasospasm reduces the mortality rate of patients in the early stages of SAH and improves the prognosis of patients. In addition to the traditional "3-H" and nimodipine treatment for vasospasm after SAH, in recent years, many researchers and scholars have made in-depth studies on the anti-vasospasm treatment of other drugs.Ryszard reported the therapeutic effect of nitrite on cerebral vasospasm. He pointed out that the method of intraventricular injection of nitrite can provide a local source of NO release, and the method of preventing delayed cerebral vasospasm and preventing systemic hypotension by intraventricular injection of nitrite can be used as a new safe, inexpensive and desirable treatment. The neuroprotective effects of magnesium and other drugs (e.g., statins) have also been the focus of research in recent years in the pharmacologic treatment of SAH.Garcia reported on the neuroprotective effects of aminophen sulfone in patients with SAH. He concluded that aminophen sulfone has a clear neuroprotective effect in patients with Fisher grade 3-4, can effectively inhibit the emergence of DIND, and the current study did not find any serious side effects. He recommends 100 mg orally daily on days 5-15 post-SAH at a cost of less than$10 for the entire regimen. However, multicenter clinical studies are still needed to confirm this finding. From the results of previous experimental studies, he summarized the possible neuroprotective mechanisms of aminophen sulfone as: (i) inhibition of excitotoxic neuronal responses by antagonizing glutamate activity in the CNS; (ii) inhibition of inflammatory responses by acting as an irreversible inhibitor of myeloperoxidase, affecting neutrophil travel and migration, inhibiting peroxidase activity in eosinophils, and limiting neurotoxic oxygen free radicals by inhibiting the production of 5l-lipoxygenase products; and (iii) inhibition of the production of 5l-lipoxygenase products. generation limiting the generation of neurotoxic oxygen radicals. Intraluminal balloon angioplasty is currently one of the only surgical treatments for vasospasm after SAH.Marike summarized the efficacy and prognosis of prophylactic intraluminal balloon angioplasty for the treatment of cerebral vasospasm in patients with SAH of Fisher classification III. In a phase II, multicenter, randomized clinical study, Marike noted that: the prognosis of Fisher III patients treated with PTBA did not improve significantly; some patients developed vasospasm after PTBA, but the clinical course was not severe; the incidence of PTBA complications was similar to that of standard endovascular treatment; and experienced neurointerventionalists were able to improve the prognosis of their patients. He believes that the reasons for the poor outcome of the treatment are He suggested that the reasons for the poor outcome may be related to the fact that factors other than vasospasm may be contributing to the poor prognosis of these patients as well as insufficient numbers of patients. At the congress he gave directions for more in-depth research in the future: exploring other factors that can contribute to the poor prognosis of these patients; the number of vessels that need to be treated; the outcome of treatment in well-graded patients; and the need to carefully analyze the risks and trade-offs of treatment.