A number of risk factors for subarachnoid hemorrhage (SAH), country-specific, hypertension, smoking, and alcohol abuse, are considered independent risk factors, and winter and spring, being female, having a family history of cerebrovascular disease, and being postmenopausal are also associated with SAH. Aneurysmal subarachnoid hemorrhage is, in most cases, about 1.6 times more common in women than in men, and this difference is more pronounced in premenopausal women. Women’s hormone levels are also associated with the development of SAH, and the risk of SAH decreases with age at menarche and age at first childbearing. Diagnosis: Currently, the value of screening for aneurysms in high-risk individuals is uncertain. Noninvasive imaging tools are available to screen for aneurysms, as magnetic resonance angiography (MRA) and computed tomography angiography (CTA) examinations have limited accuracy and patient testing methods are not as accurate as they could be. Because magnetic resonance angiography (MRA) and computed tomography angiography (CTA) have limited accuracy, patients should follow individualized protocols. Digital subtraction angiography (DSA) remains the current gold standard. The main factors affecting the prognosis of SAH can be divided into 3 categories: patient, aneurysm, and hospital. Patient factors include severity of the first bleed, age, gender, duration of treatment, and comorbidities (e.g., hypertension, atrial fibrillation, bloody heart failure, coronary artery disease, and renal disease); aneurysm factors include size, location, and morphology of the aneurysm, among others; and hospital factors include the availability of endovascular, and therapeutic experience versus the equipment with which the patient was first evaluated). SAH causes a dramatic decrease in cerebral blood flow, decreased cerebral autoregulation, and acute cerebral ischemia. These pathophysiologic processes are also accompanied by increased intracranial pressure, decreased cerebral perfusion, decreased NO levels, acute vasoconstriction, microvascular platelet aggregation, collagenase activation, collagen loss, and decreased microvascular perfusion and increased permeability due to endothelial barrier antigens. Today, despite a better understanding of the mechanisms of brain damage in SAH, successful treatments are still lacking and more research is yet to be conducted. Rebleeding is also A serious problem with rebleeding from ruptured aneurysms, it is by far the leading cause of poor patient prognosis, with a mortality rate of up to 70%. Previous studies have described rebleeding. Studies have shown that rebleeding rates are highest at 4% on day 1 after hemorrhage, followed by daily rebleeding rates of 1% to 2% over the next 4 weeks. Several prospective follow-up cohort studies have shown rebleeding rates of 20% to 30% in the 1st month after conservative treatment, which then stabilizes at approximately 3% per year. Several prospective and retrospective studies have identified potential risk factors for rebleeding, including untimely treatment, high baseline blood pressure, and poor neurologic function at the time of hospitalization, all of which are associated with rebleeding within 2 weeks of SAH. The clinical presentation of subarachnoid hemorrhage is typical, with approximately 80% of patients who provide a history describing the symptom as “the most severe headache of their lives,” and another 20% experiencing headache episodes with aura. The majority of patients with intracranial aneurysms are asymptomatic until the aneurysm ruptures.SAH can occur at any time and can be triggered by factors such as heavy labor or exercise.In addition to headache, it may be accompanied by nausea, vomiting, nuchal rigidity, transient loss of consciousness, or focal neurologic deficits (including cerebral palsy).The symptoms of SAH can be described as “severe headache,” and the symptoms may include nausea, vomiting, neck stiffness, transient loss of consciousness, and neurologic deficits. In addition to the typical clinical manifestations, SAH has some other symptoms. Moreover, since the presentation of headache varies from patient to patient, misdiagnosis or delayed diagnosis often occurs. the misdiagnosis rate of DSA used to be 64% before 1985, and has recently decreased to about 12%. In patients with little or no neurologic symptoms, the 1-year mortality and disability rates are four times higher in misdiagnosed patients than in other patients. The most common reason for misdiagnosis is that patients do not receive a CT scan of the head. The basic diagnostic method for SAH is a CT scan of the head, the detection rate of which correlates with the patient’s clinical classification in relation to the time from the hemorrhage. The detection rate of CT is as high as 98%-100% within 12 days after SAH; it decreases to 93% after 24 h; and only 57%-85% at 6 d after bleeding. In the case of negative CT results, patients need to perform diagnostic lumbar puncture, the key points of the examination are: the ratio of red and white blood cells in the cerebrospinal fluid, whether the yellow staining, whether there is bilirubin and the time of lumbar puncture.