Clinical presentation and diagnosis of aSAH The clinical presentation of aSAH is very typical. About 80% of patients who provide a medical history describe the symptoms as “the most severe headache ever”, while another 20% have an aura of headache attack. SAH can occur at any time and can be triggered by factors such as heavy work or exercise. In addition to headache, symptoms may include nausea, vomiting, neck stiffness, transient loss of consciousness, or focal neurological deficits (including cerebral nerve palsy). In a retrospective study of 109 patients diagnosed with SAH, Fontanarosa found that 74% had headache, 77% had nausea or vomiting, 53% had loss of consciousness, and 35% had cervical akinesia. Twelve percent of these patients died before receiving treatment. In addition to the typical clinical manifestations, there are other symptoms of SAH. The rate of misdiagnosis of SAH, which used to be 64% before 1985, has recently decreased to about 12% [4, 21, 1922195 ]. Among patients with few or mild neurological symptoms, the 1-year mortality and disability rates of misdiagnosed patients are 4 times higher than those of other patients. The most common reason for misdiagnosis is that the patient did not receive a CT scan of the head. The patient’s history may show a small amount of bleeding before the hemorrhage occurred, called an “aura hemorrhage. Most aura hemorrhage headaches are not severe but last for several days, most occurring within 2 to 8 weeks before the hemorrhage [ 1982199 ]. Nausea and vomiting may also be present without signs of meningeal irritation. In three studies involving 1752 patients, 340 (15%-37%, mean 20%) had a history of sudden onset of headache before the onset of severe symptoms. Of course, we cannot overemphasize the importance of “aura hemorrhage”. SAH patients account for only 1% of all headache emergencies. More than 20% of patients with SAH have epilepsy, usually within 24 hours of bleeding, and most often in patients with combined cerebral hemorrhage, hypertension, and middle and anterior communicating cerebral aneurysms. The basic diagnostic method for SAH is CT scan of the head, and its detection rate is related to the clinical classification of the patient and the time to hemorrhage. The detection rate of CT is as high as 98%-100% within 12 h after SAH; it decreases to 93% after 24 h, while the detection rate is only 57%-85% at 6 d after bleeding. Since the detection rate of CT cannot be ensured to 100%, diagnostic lumbar puncture is required when the CT result is negative. Proper puncture technique, proper sample testing, and correct analysis of cerebrospinal fluid composition are essential to confirm the diagnosis. The key points of examination are: the ratio of red to white blood cells in the cerebrospinal fluid, the presence of yellow staining, the presence of bilirubin, and the timing of the lumbar puncture. The prognosis is generally good in patients who present with sudden severe headache and whose aura hemorrhage has been excluded by CT and cerebrospinal fluid examination. The use of techniques such as proton density-weighted imaging and fluid-attenuated inversion recovery sequences has significantly improved the detection of SAH in the acute phase, but there are still many limitations, such as the immediacy of MRI, sensitivity to motion artifacts, patient However, there are still many limitations, such as the immediacy of MRI, sensitivity to motion artifacts, patient compliance, and the long and costly time required for examination. In conclusion, these factors have limited the use of MRI as a routine test in the acute phase of SAH. MR I and MRA are more suitable for patients with negative head CT or angiogram and inconclusive lumbar puncture results.