Arteriosclerosis and vasculitis are associated with the occurrence and development of aneurysms. Cerebral aneurysms are mostly seen at the bifurcation of the arteries at the base of the brain. According to its location, 4/5 of them are located in the anterior half of the cerebral artery ring, with the internal carotid artery, posterior communicating artery and anterior communicating artery being the most common ones; the posterior half of the cerebral artery ring accounts for about 1/5 of them, occurring in the vertebral basilar artery, posterior cerebral artery and its branches. Symptoms: When an aneurysm ruptures, there are often prodromal symptoms such as headache, followed by hemorrhagic symptoms, including severe headache, irritability, nausea and vomiting and other signs of meningeal irritation, followed by an increase in intracranial pressure. This may be accompanied by impaired consciousness and neurological localization of the corresponding area. Aneurysm hemorrhage forms larger hematomas intracranial aneurysms are mostly caused by localized congenital defects in the walls of cerebral arteries and on the basis of increased intraluminal pressure. In those with hypertension and cerebral motility, the condition mostly deteriorates sharply and brain herniation crisis occurs. According to statistics, after the first rupture of aneurysm, the mortality rate is as high as 30-40%, half of them die within 48 hours after the onset of the disease, and in 1/3 of the surviving cases, rebleeding may occur. CT scan can sometimes show the aneurysm lesion, and MRI examination can not only show the aneurysm, but also sometimes see the attached thrombus. Once the diagnosis of cerebral aneurysm is made, surgical treatment should be performed in order to cure it and avoid the risk of hemorrhage. The surgical approach is to treat the aneurysm directly by craniotomy. Intra-arterial embolization may also be used. Clinical manifestations 1. Symptoms of ruptured aneurysm and bleeding Small and medium-sized aneurysms without rupture and bleeding can be clinically asymptomatic. Once the aneurysm ruptures and bleeds, the clinical manifestation is severe subarachnoid hemorrhage, with rapid onset and severe headache, which is described as “head exploding”. Frequent vomiting, profuse sweating, elevated body temperature, neck stiffness, and a positive Creutzfeldt-Jakob sign. There may also be impaired consciousness and even coma. Some patients have triggers such as exertion and emotional excitement before bleeding, while others have no obvious triggers or develop during sleep. In about 1/3 of patients, aneurysm rupture results in death due to untimely diagnosis and treatment. Most aneurysm ruptures are closed by clotting and the bleeding stops, and the condition gradually stabilizes. As the blood clot around the aneurysm rupture dissolves, the aneurysm may rupture and bleed again. Secondary bleeding occurs within 2 weeks of the first bleed. In some patients, the hemorrhage may invade the vitreous through the optic nerve sheath causing visual impairment. After subarachnoid hemorrhage, erythrocyte destruction produces 5-hydroxytryptamine, catecholamines and other vasoactive substances that act on cerebral blood vessels, resulting in vasospasm, with an incidence of 21% to 62%, mostly occurring 3-15 days after the hemorrhage. Local vasospasm occurs only in the vicinity of the aneurysm, and the patient’s symptoms are not obvious and only show up on cerebral angiography. Extensive cerebral vasospasm can lead to the occurrence of cerebral infarction, patient’s impaired consciousness, hemiparesis, and even death. 2. Focal symptoms depend on the location of the aneurysm, the adjacent anatomy and the size of the aneurysm. Arteriovenous nerve palsy is commonly seen in internal carotid artery-posterior communicating artery aneurysms and aneurysms of the posterior cerebral artery, manifesting as unilateral eyelid ptosis, pupil dilatation, inability to internalize, up and down vision, and loss of direct and indirect light responses. Sometimes focal symptoms appear before subarachnoid hemorrhage and are considered precursors to aneurysm hemorrhage, such as mild migraine and orbital pain followed by arteriovenous nerve palsy, at which time one should be alert to the ensuing subarachnoid hemorrhage. If an aneurysm hemorrhage in the middle cerebral artery forms a hematoma; or an aneurysm hemorrhage in other parts of the brain followed by cerebral vasospasm cerebral infarction, the patient may develop hemiparesis, motor or sensory aphasia. If a giant aneurysm affects the visual pathway, the patient may have visual field impairment. After aneurysm hemorrhage, the condition varies in severity. In order to judge the condition, choose the timing of imaging and surgery, and evaluate the efficacy of treatment. Treatment Intracranial aneurysms should be treated surgically. Approximately 70% of patients who are treated conservatively will die from aneurysm rebleeding. Microsurgery has reduced the surgical mortality rate of aneurysms to less than 2%. For patients with Grade 1 or 2 disease, the imaging should be done as early as possible and the surgery should be performed within one week. If the condition is Grade 3 or above, it indicates serious bleeding, possible cerebral vasospasm and hydrocephalus, which is more dangerous to operate at this time, wait for a few days for the condition to improve and then operate. 2.Surgical method: Craniotomy is the most ideal method and should be preferred. It does not block the aneurysm-carrying artery, but completely eliminates the aneurysm. The isolation procedure is to clamp the aneurysm-carrying artery at both ends of the aneurysm, which should be used with caution when the lateral branch supply of the brain is not proven to be good. Aneurysm wall reinforcement has uncertain efficacy and should be used sparingly. For aneurysms that are not clinically suitable for surgery and are accessible by catheterization techniques, interventional treatment with balloon and spring-ring embolization is an option. Postoperative cerebral angiography should be reviewed to confirm whether the aneurysm disappears. 3. After the aneurysm rupture is treated during the operation period, the patient should be placed in absolute bed rest to minimize adverse sound and light stimulation, and it is better to place the patient in ICU monitoring. Transcranial Doppler ultrasonography can monitor the changes of cerebral blood flow, which is helpful to observe the progress of the disease. Constipation should be treated with laxatives, maintenance of normal blood pressure, and appropriate sedation. In case of combined cerebral vasospasm, early vascular protection therapy such as calcium antagonists can be tried. To prevent rebleeding from clot dissolution at the aneurysm rupture, larger doses of antifibrinolytic agents, such as aminocaproic acid, are used to inhibit the formation of fibrinolytic zymogens, but they should be used with caution in patients with renal dysfunction, as side effects may include thrombosis.