Intracranial hypotension (IH) is a clinical syndrome of multiple neurological symptoms due to absolute or relative deficiency of cerebrospinal fluid; some patients with intracranial hypotension have normal intracranial pressure measurements and no characteristic changes in cranial magnetic resonance, but there is typical cerebrospinal fluid leakage, so this intracranial hypotension can also be called cerebrospinal fluid leakage disorder or cerebrospinal fluid volume reduction disorder. Etiologically, intracranial hypotension can be classified as (1) spontaneous or primary, and (2) secondary; the latter can be further classified as (2a) traumatic, mostly of medical origin, such as epidural puncture through the dura, arachnoid puncture, spinal surgery, nerve radiofrequency or destruction surgery, arachnoid implantation morphine pump removal, etc.; (2b) degenerative spinal changes; (2c) hypovolemia, mostly due to severe dehydration of the organism state; (2d) excessive drainage of cerebrospinal fluid, mostly from neurosurgical operations. Among the secondary intracranial hypotensions, the most common and clinically significant are medical intracranial hypotensions, such as epidural puncture through the dura, arachnoid puncture, spinal surgery tearing the dura, minimally invasive intervertebral disc surgery, nerve radiofrequency or destruction accidental damage to the dura, and non-healing of the dura after removal of the arachnoid-embedded morphine pump. Spontaneous Intracranial Hypotension (SIH) or also known as Primary Intracranial Hypotension (PIH) was first reported in Germany in 1938, but the pathogenesis was not clearly understood at that time. Since the early 1990s, spontaneous intracranial hypotension has been increasingly recognized based on the rapid development of imaging and some characteristic clinical manifestations of spontaneous intracranial hypotension, such as postural headache, decreased intracranial pressure and characteristic changes of cranial magnetic resonance (e.g., extensive dural enhancement, subdural fluid, hematoma and brain tissue subsidence); spontaneous intracranial hypotension has a wide range of clinical symptoms, in addition to the typical postural In addition to the typical postural headache, there are some other related clinical symptoms including dizziness, nausea and vomiting, diplopia, tinnitus, neck pain, altered consciousness, and even coma. The annual incidence of spontaneous intracranial hypotension is about 5/100,000 and is more common in women than men (about 2:1); current studies have confirmed that the pathogenesis of spontaneous intracranial hypotension is due to spontaneous rupture of abnormal structures in the spinal dura, such as diverticula, cysts and other weaknesses, resulting in cerebrospinal fluid leakage, and that such abnormal structures in the spinal dura are associated with underlying connective tissue diseases. Leakage is also spontaneous and usually occurs at the cervical or cervicothoracic junction, but can also occur in the mid and lower thoracic and lumbar segments, either singly or, more often, as a multisegmental cerebrospinal fluid leak. The treatment strategy for intracranial hypotension is currently a comprehensive phased treatment, starting with conservative treatment, such as bed rest, massive rehydration (oral plus intravenous fluids), caffeine intake and lap band abdominal compression, hormone and analgesic application, but bed rest and massive rehydration are the most basic and important conservative treatment measures. If conservative treatment is ineffective or recurrent, or if subdural fluid or hematoma progresses rapidly during conservative treatment, some invasive or minimally invasive treatments such as epidural autologous blood intervention, fibrin glue intervention, and open surgery to repair cerebrospinal fluid leaks are used; if spinal MRI shows multisegmental, massive cerebrospinal fluid leaks, conservative treatment can be shortened and epidural autologous blood intervention can be performed as early as possible Other controversial treatments include intermittent or continuous infusion of epidural saline, colloid, etc. There are no accurate data to confirm the effectiveness and safety of these measures. Intractable spontaneous intracranial hypotension: spontaneous intracranial hypotension without clinical effect or slow symptom relief after at least 2 weeks of strict conservative treatment (bed rest, heavy rehydration), or with altered consciousness, worsening headache, increased subdural hemorrhage, midline shift and evidence of cerebrospinal fluid leakage on cranial imaging during standard conservative treatment, or with no significant worsening of clinical symptoms during conservative treatment but with persistent multisegmental cerebral leakage on spinal imaging. There is persistent multisegmental cerebrospinal fluid leakage on spinal imaging, or conservative treatment is effective but prone to recurrence, or epidural intervention and surgical repair of cerebrospinal fluid leakage is effective but recurs after surgery. Epidural interventions were the first minimally invasive treatments used to repair cerebrospinal fluid leaks caused by epidural puncture through the dura, with epidural autologous blood interventions being the most commonly used. Definition of epidural intervention for intractable intracranial hypotension: The treatment of intracranial hypotension is achieved by injecting non-anticoagulated autologous venous whole blood, component blood (e.g. platelet-rich blood, fresh plasma, etc.), bioprotein glue, or a mixture of autologous blood and bioprotein glue from the epidural space under CT, X-ray or ultrasound guidance or non-direct vision. Bioprotein glue, autologous blood, or a mixture of autologous blood and bioprotein glue may be preferred for hypotension, and autologous blood is recommended for secondary intracranial hypotension, and bioprotein glue therapy or a mixture of autologous blood and bioprotein glue may be chosen after ineffectiveness. During epidural interventions, it is important to avoid penetrating the dura mater and aggravating the degree of cerebrospinal fluid leakage or brain herniation. When the patient experiences significant dizziness, headache, severe tinnitus, limb pain, numbness, respiratory depression, hemodynamic instability and any other discomfort affecting the cooperation with the treatment, then the injection should be stopped or slowed down immediately. When there is a rapid decrease in heart rate, the patient becomes indifferent, loses consciousness, or is agitated and unable to cooperate, the injection should be stopped immediately, the patient should be transferred to a supine position and given relevant supportive treatment, and a decision should be made whether to continue the treatment or to change the vertebral segment after the patient is in remission. The purpose of epidural intervention: to stop further leakage of cerebrospinal fluid, to restore cerebrospinal fluid pressure or volume, and to relieve the sinking of brain tissue and the dilated congested state of intracranial veins. Mechanism of Epidural Interventional Therapy: To seal the cerebrospinal fluid leak opening to the epidural cavity by using the coagulation of autologous blood after leaving the body and the adhesive property of bioprotein gel. Indications for epidural intervention: ineffective conservative treatment for more than two weeks, progressive subdural hematoma with massive subdural fluid accumulation, subdural herniation of the cerebellum (without impaired consciousness), multiple segments, large cerebrospinal fluid leaks, etc. Contraindications to epidural intervention: abnormal coagulation, bleeding tendency, or combined serious bleeding disorders puncture site infection, or systemic infection puncture site anatomical abnormalities massive subdural hemorrhage, impaired consciousness sacral cysts? Malignant tumors, including vertebral body tumors? Patients with leukemia. Complications of epidural intervention: transient spinal cord compression, respiratory, circulatory depression, spinal cord injury, dural puncture, aggravated cerebrospinal fluid leakage, cerebral hernia formation or aggravation, rebound increase in intracranial pressure (recumbent dizziness, headache), epidural hemorrhage, hematoma formation, compression of spinal nerve and spinal cord, paralysis epidural infection, abscess formation, systemic infection epidural cavity adhesions, spinal stenosis, chronic radicular neuralgia The above complications can be reduced and avoided as long as the indications for surgery are strictly controlled and the surgical operation is carefully regulated. At present, the interventional treatment of intracranial low pressure in China has achieved remarkable efficacy, and through strict compliance with the surgical operation specifications, serious neurological complications rarely occur and early recovery of patients with intracranial low pressure is facilitated; therefore, we also expect more research and clinical practice to confirm the safety and effectiveness of epidural interventional treatment of intracranial low pressure, especially spontaneous intracranial low pressure, and to develop relevant clinical Therefore, we also expect more research and clinical practice to confirm the safety and efficacy of intracranial low pressure, especially spontaneous intracranial low pressure epidural intervention, and to develop related clinical pathways, especially as well as epidural intervention strategies for large spontaneous cerebrospinal fluid leaks in multiple segments, in order to promote intracranial low pressure epidural intervention in a more standardized manner and reduce the occurrence of neurological related complications.