Cerebral aneurysms occur at the branches of the bifurcation and main trunk of the intracranial arteries. The formation of aneurysms is associated with a congenital developmental defect in the middle layer of the arterial wall, the muscular layer, at this location. As a result of the impact of the blood flow, the weak point of the arterial wall protrudes outward and gradually expands to form a round, oval or spindle-shaped sac-like enlargement, which becomes an aneurysm. The rupture of aneurysm is not only due to the anatomical defects mentioned above, but also closely related to some acquired factors, such as hypertension and cerebral artery atherosclerosis. Fisher reported that ruptured aneurysm bleeding occurred during exertion, such as defecation, heavy lifting, sexual intercourse, bathing, stairs, etc., accounting for 55% and 29% of the cases. suddenly appearing during normal life and the rest during sleep. Due to the sudden increase in peripheral arterial pressure, obstruction of venous return in the head, and relative movement of brain tissue and Willis arterial rings to fixed structures in the skull, the pressure in the aneurysm rises in an instant and continues to increase, exceeding the weakness limit of the weak point of the aneurysm wall for a short period of time, and rupture at the weak point due to the turbulent flow pressure in the aneurysm. Therefore, these triggers are some risk factors, and proper attention to avoid them can prevent rupture and bleeding in patients with cerebral aneurysms. Clinical manifestations of cerebral aneurysm rupture aura symptoms: About 48.2%-60% of cerebral aneurysm rupture is preceded by aura symptoms. They are divided into 3 types of acuity; (1) symptoms of aneurysm enlargement, such as local headache, eye pain, visual impairment, extraocular muscle paralysis, etc., which vary with the site of aneurysm; (2) symptoms of small leakage of blood from aneurysm (anterior bleeding), such as anterior headache, nausea, vomiting, collar and back pain, shyness, drowsiness, etc.; (3) symptoms of local ischemia, such as motor and sensory impairment, vertigo, hallucination, balance disorder, etc. If a patient has these aura symptoms, especially if there is already leakage, transmicro or atypical subarachnoid hemorrhage, a cerebral angiogram should be performed as soon as possible to confirm the diagnosis, and preventive treatment such as lowering blood pressure to normal levels, and direct surgery should be taken. Signs and symptoms of a ruptured aneurysm: When an aneurysm ruptures and bleeds, symptoms of subarachnoid hemorrhage immediately appear, and in severe cases, the patient calls for a severe headache, then falls into a coma or deep coma, respiratory disturbances, increased blood pressure turns down, and can die within minutes or hours. Typical clinical manifestations are the signs and symptoms of acute subarachnoid hemorrhage. With headache, nausea and vomiting, restlessness, neck stiffness, with or without signs of impaired consciousness and neurological damage. In cases of excessive bleeding, patients become comatose, have altered vital signs, and even show signs of brain herniation. (1) Headache: It is the most common first symptom, 70% of which are severe full headache and 30% are localized headache or migraine. The headache is sometimes associated with the site of the aneurysm. In the case of internal carotid artery and posterior communicating artery aneurysm, the headache is mostly located in the frontal orbital region; in the case of internal carotid artery aneurysm, the headache is on one side of the head and face; in the case of anterior communicating artery aneurysm, the headache is often in the forehead on both sides; in the case of subscriptive artery aneurysm, the headache is often in the occipital region. Severe headache with “explosive” is the characteristic of headache in this kind of patients. (2) Disorders of consciousness: the incidence is 41%-81%. Coma occurs after the onset of headache, and after a few minutes or tens of minutes, the patient gradually wakes up. In some patients, the coma deepens until death. (3) Signs and symptoms of neurological impairment: Simple subarachnoid hemorrhage generally produces less lasting neurological impairment. Aneurysm rupture and bleeding with spasm of the aneurysm-carrying artery or drop in blood pressure leads to transient cerebral ischemia, which can show some transient neurological deficits. For example, ruptured anterior communicating aneurysms cause transient mild paralysis of both lower extremities, ruptured internal carotid aneurysms cause arteriovenous palsy and hemiparesis, ruptured posterior cerebral aneurysms cause visual distortion, and ruptured basilar aneurysms cause vertigo and brainstem symptoms. Ruptured aneurysms of the anterior half of the ring of Willis may also cause limited and generalized convulsions. As the disease progresses, certain persistent neurological deficits develop, especially in the presence of certain secondary pathological changes (e.g., hematoma, cerebral ischemia, cerebral infarction, etc.). These specific focal neurological signs are often of localized significance. (i) Hemiplegic aphasia: Most often seen in middle cerebral aneurysms, but also after rupture of internal carotid aneurysms and anterior communicating aneurysms. (ii) Actinic nerve palsy: often suggests rupture of the ipsilateral internal carotid artery – posterior communicating artery aneurysm. It can also be seen in internal carotid artery – anterior choroidal aneurysm and posterior cerebral artery – posterior communicating artery aneurysm rupture. (iii) Cavernous sinus syndrome: can arise after rupture of internal carotid artery aneurysm in the cavernous sinus segment. (iv) Bilateral abducens nerve palsy: seen in ruptured basilar aneurysm. It may be caused by brainstem displacement and compression of the abducens nerve between the anterior inferior cerebellar artery and the pontine brain. ⑤ Psychiatric symptoms: such as Korsakaff syndrome, personality changes, and memory deficits are seen in ruptured anterior communicating artery aneurysms. It is mostly a consequence of hematoma pressure near or ischemic damage to the medial frontal lobe, corpus callosum and hypothalamus bilaterally. About 1/3 of patients may present with ocular symptoms. (i) Vision loss: can follow rupture of internal carotid artery-ocular aneurysm or internal carotid artery-posterior communicating artery aneurysm. (ii) Visual field defects: most often seen in aneurysms of the bifurcation of the internal carotid artery or ruptured anterior communicating artery aneurysms. It is caused by the involvement of the optic cross. In addition, rupture of middle cerebral aneurysm followed by temporal lobe hematoma damage radiation, rupture of posterior cerebral aneurysm and basilar artery bifurcation aneurysm with occipital lobe ischemia can also cause ipsilateral partially blindness on the opposite side. (③) Fundus changes: retinal hemorrhage is mostly seen in ruptured ipsilateral middle cerebral aneurysm hemorrhage. Ruptured aneurysm hemorrhage often leads to subvitreous hemorrhage, which can spread to the vitreous and cause blindness. This is a result of central retinal vein hemorrhage following increased intracranial pressure and pressure on the optic nerve sheath. About 15% of patients may develop optic nerve papillary edema. (4) Systemic symptoms: In the early stage of aneurysm rupture, there may be transient increase in blood pressure, temperature, leukocytosis, hyperglycemia, glycosuria, proteinuria, etc., which may be related to the stimulation of hypothalamus by bleeding. When hypothalamic damage is aggravated, central hyperthermia, deep coma, upper gastrointestinal bleeding, cardiac arrhythmia, convulsions, Syndrome of inappropriate secretion of ADH (SIADH), hypertension, electrolyte disturbance, etc. may occur.