Adrenal glucocorticoids, referred to as hormones, are the main hormones normally secreted by the adrenal cortical fasciculus, which can regulate the metabolism of sugar, protein and fat, especially playing an important role in the process of glucose metabolism, so they are called adrenal glucocorticoids. Glucocorticoids commonly used in clinical practice include: dexamethasone, prednisolone, methylprednisolone, hydrocortisone, betamethasone, etc. They have powerful anti-inflammatory, immunosuppressive and anti-allergic pharmacological effects and are widely used in the treatment of many clinical diseases. Glucocorticoids in neurosurgical emergencies are mainly used in the treatment of cerebral trauma, subretinal hemorrhage (SAH), hypertensive cerebral hemorrhage, cerebral fat embolism, hypopituitarism crisis, and severe intracranial infection. 1.Application of glucocorticoids after traumatic brain injury The main purpose of glucocorticoid use after traumatic brain injury is to reduce nerve injury, reduce cerebral edema and promote neurological function recovery. However, the effect of glucocorticoids in the treatment of traumatic brain injury has been controversial. Scholars who support the use of glucocorticoids believe that the application of glucocorticoids after traumatic brain injury, especially the early high-dose application, has significant cerebral protective effects, based on 1), high-dose glucocorticoids, especially methylprednisolone and dexamethasone, can effectively reduce the destruction of blood-brain barrier and endothelial cell damage after traumatic brain injury, and nearly reduce the degree of cerebral edema. 2), it can inhibit the lipid peroxidation of cell membrane after neurotrauma. 3) Stabilize brain cell membrane ion channels, maintain active membrane transport of Na+ and Ca2+, and rebuild the normal distribution of Na+ and Ca2+ inside and outside the cell. 4) Scavenge free radicals, a large number of experiments have confirmed that glucocorticoids can scavenge oxygen free radicals, inhibit neural cell membrane lipid peroxidation, and reduce brain edema. 5) Inhibit IL-1β, TNF-α and other pro-inflammatory expression of cytokines, reduce the inflammatory response after brain trauma, thus exerting cerebral protection. 6), reduce the production of endothelin, monoamines and prostaglandins, increase blood flow in the brain injury area and improve local microcirculation. 7), inhibit cerebrospinal fluid secretion. 8), diuretic effect, increase the elimination of Na+, K+ and Cl- in urine. 9), glucocorticoids have a short half-life in the blood (180 minutes for methylprednisolone, 200 minutes for dexamethasone, 100 minutes for hydrocortisone), if the therapeutic dose is applied for 3-5 days, decreasing to discontinuation for another 3-5 days, high-dose glucocorticoids are as safe as small doses, and the side effects of hormones are related to the duration of medication but not to the size of the daily dose. Scholars who oppose the use of glucocorticosteroids ask the following questions: 1. Can glucocorticosteroids reduce brain edema caused by trauma? (1), cerebral edema is divided into vasogenic, cytotoxic and interstitial cerebral edema, and experimental data show that the effect of glucocorticoids in reducing vasogenic cerebral edema is not satisfactory; (2), clinical studies show that high-dose glucocorticoids have no effect on reducing intracranial pressure (ICP). The effect of high-dose methylprednisolone and dexamethasone was studied in a double-blind way in several hundred patients with traumatic brain injury, and the changes in ICP were observed from 24 to 48 hours of drug administration. Experimental studies have found that the pathophysiological changes after central nerve injury progress rapidly, with rupture of neurons and axons occurring 6 hours after injury, accompanied by edema, ischemia and progressive degeneration of extensive neural structures. Most clinical studies have failed to confirm the ability of glucocorticoids to treat cerebral edema after neurological trauma, and it has been suggested that this is due to the low dose or late application of glucocorticoids, thus advocating high doses (i.e., methylprednisolone 15-30 mg kg-1 and dexamethasone 3-6 mg kg-1) and early (within 6 hours after injury) administration. However, Liangfu Zhou [1] summarized the literature from 1965 to 1988 and concluded that the literature after 1979 had a more elaborate design with a double-blind method, GCS as a measure of injury (GCS <7-8 points in the enrolled medical records), administration at the scene of injury or early post-injury (mostly 3-6 hours post-injury), and observation in high-dose, placebo, and low-dose groups for ICP, disability In addition to a few scholars who reported that glucocorticoids might be effective, most reported that there was no significant difference between the treatment group and the control group in terms of mortality, disability rate and quality of survival after six months. Therefore, it is concluded that glucocorticosteroids have no therapeutic effect on severe traumatic brain injury regardless of small or large dose, early or late post-injury administration.3. Glucocorticosteroids have side effects, especially long-term application is more obvious, and the common side effects are as follows: (1), the incidence of gastrointestinal bleeding reaches 50% [1], and the incidence is higher in those with original gastrointestinal bleeding or ulcers. (2), impaired sugar and nitrogen metabolism. Hyperglycemia is seen in 20-85% of patients and occurs especially after high dose application. Since increased ICP after brain trauma can cause neuronal hypoxia, hyperglycemia causing hyperlactatemia can aggravate neuronal hypoxia. Abnormal nitrogen metabolism will also aggravate metabolic acidosis, which is not conducive to the functional recovery of the nervous system and systemic tissues. (3), Immune system suppression. (4), Delayed healing of skin wounds and increased incidence of systemic infections. (5) Inhibition of the expression of neurotrophic factors in the brain after brain trauma [2]. A large number of clinical and experimental studies have proved that glucocorticoids have no therapeutic effect on brain trauma and traumatic brain edema, coupled with the fact that glucocorticoids themselves have more side effects, which are more likely to occur especially with long-term and high-dose applications. Therefore, high-dose glucocorticoids should not be used for severe traumatic brain injury, especially for those with obvious high cranial pressure [3]. 2. Application of glucocorticoids after SAH The main complication of SAH is cerebral vasospasm (CVS), and cerebral ischemia can occur in severe cases, which directly affects the surgical effect and patient prognosis. Vasodilators are usually used to treat delayed CVS after SAH, but clinical practice shows that the therapeutic effect of vasodilators is not very satisfactory. Kawano combined application of hydrocortisone, dextran and thionazepam has achieved satisfactory efficacy in the treatment of subretinal hemorrhage [4]. In China, Liu Baiyun [5] treated 11 patients with SAH with high-dose methylprednisolone and also achieved satisfactory results, and the onset of action was rapid, with improvement of clinical symptoms and signs seen on average 4-5 days after administration, and no significant drug side effects were found during the treatment period. Cui Qifu [6] conducted a small sample (40 cases) of patients with SAH treated with high-dose glucocorticoids and found that the mental, speech, and motor disorders in the hormone-treated group were significantly improved compared with the control group, and the main side effect was hyperglycemia. However, due to the small number of relevant studies, the final conclusion remains to be statistically analyzed in a large number of cases. 3.Application of glucocorticoids after cerebral fat embolism Fat embolism syndrome is a syndrome caused by traumatic and non-traumatic factors, in which fat and lipid-like substances from bone marrow and other tissues collect in the blood with weakened emulsification and abnormal physicochemical properties to form emboli, causing respiratory, neurological, hematological and skin involvement as the main manifestations, among which neurological symptoms are the main manifestations. The main manifestation is called cerebral fat embolism. The research on its pathogenesis has made great progress, and the following theories exist: 1, after the injury of the tissue containing fat cells, the cells rupture and release fat droplets, which can enter the blood circulation from the ruptured blood vessels; 2, after the trauma, the body is under acute stress, and the hypercoagulable state appears in the blood vessels, and the fatty celiac particles in the blood coagulate into large fat globules and form emboli; 3, the formation of emboli is related to the above two theories. The clinical manifestations of embolus formation are related to the size and number of embolism sites. In addition, the direct toxic effect of free fatty acids on lung parenchymal cells, capillary endothelial cells and alveolar surface active substances is also a major causative factor. The role of glucocorticoids in the treatment of fat embolism is well established. The significance of using glucocorticoids after cerebral fat embolism is: 1. Early application of glucocorticoids can significantly reduce the number of lipid droplets in the blood, and can make the diameter of lipid droplets smaller, thus eliminating or reducing the conditions of mechanical embolism. 2. Early application of glucocorticoids can reduce the concentration of free fatty acids in the plasma, thus reducing the damage of free fatty acids to parenchymal cells, capillary endothelial cells and alveolar surface active substances 3. Glucocorticoids can stabilize alveolar membrane type II cells and capillary endothelial cells, inhibit the production of inflammatory substances such as prostaglandins and leukotrienes, reduce exudative edema in lung tissue, improve respiratory function, increase arterial partial pressure of oxygen, relieve respiratory symptoms and reduce cerebral hypoxia. 4. Glucocorticoids can also stabilize the lysosomal membrane, inhibit the action of kinins, avoid pulmonary atelectasis, reduce cerebral edema, and promote patient wakefulness. 4.Application of glucocorticoids after hypertensive cerebral hemorrhage Some scholars believe that the combined application of mannitol, glucocorticoids and tachyphylaxis is more effective in treating acute cerebral edema, so hormones should be used as a routine measure for treating hypertensive cerebral hemorrhage. However, some scholars believe that the use of glucocorticoids is not conducive to the repair of local ruptured blood vessels, while patients with cerebral hemorrhage are often combined with infection, gastrointestinal bleeding and diabetes mellitus, all of which are unfavorable to the use of glucocorticoids. At present, there is no definite conclusion whether glucocorticoids should be applied routinely in hypertensive cerebral hemorrhage, but glucocorticoids can be considered in the following cases: 1. to inhibit various pathological abnormal reactions of brain tissue after cerebral hemorrhage; 2. to reduce intracranial pressure and rescue brain herniation with mannitol and tachyphylaxis, etc. 5, anterior pituitary hypopituitary crisis glucocorticoid application Patients with anterior pituitary lesions or postoperative pituitary tumor hypopituitary function, induced by various stresses such as infection, diarrhea, vomiting, dehydration, cold, surgery, trauma, anesthesia, sedatives, hypoglycemic drugs and other induced pituitary crisis, manifested by mental disorders, delirium, hyperthermia or hypothermia, nausea, vomiting, hypoglycemia, fainting, coma, convulsions or circulatory The symptoms include psychosis, delirium, hyperthermia or hypothermia, nausea, vomiting, hypoglycemia, syncope, coma, convulsion or circulatory failure. Glucocorticoid supplementation is the most important treatment measure. In severe intracranial infections such as postoperative infection and meningitis, glucocorticoids can be used in combination with antibiotics to reduce intracranial inflammation and systemic toxic reactions. The above briefly describes the use of glucocorticoids in neurosurgical emergencies, but they are best avoided in patients with systemic fungal infections, after live virus vaccination, active tuberculosis, hyperadrenocorticism (Cushing's syndrome), severe hypertension, stress ulcers, diabetes mellitus, and unexplained hyperthermia [11]. In conclusion, the use of glucocorticoids in the treatment of neurological disorders originated in the 1960s, but since the mid-1970s, the use of glucocorticoids in the field of neurosurgery has declined considerably. This is not simply due to poor efficacy, but also due to the side effects of hormones, which are more likely to occur especially with high doses of long-term application, and therefore the application of hormones should be strictly controlled for indications and should not be used routinely. However, glucocorticoids have many effects that cannot be replaced by other drugs, such as inhibiting lipid peroxidation in nerve cell membranes, stabilizing cell membrane permeability, inhibiting the production of vasoconstrictor substances, inhibiting the production of pro-inflammatory substances, and so on. Some synthetic glucocorticoids such as methylprednisolone have a strong anti-inflammatory effect, but the effect of sodium retention is smaller and the protective effect on brain cells is not mediated by glucocorticoid receptors, but by direct inhibition of lipid peroxidation. Therefore, in the absence of contraindications, glucocorticoids can still be applied in high doses, early and for short periods of time as drugs for the treatment of neurosurgical emergencies, with the aim of reducing the production of endogenous damage factors.