S.Ya. Kosyakov, G.Z. Piskunov. This lecture examines current treatment methods for acute sensorineural hearing loss from the perspective of a possible etiologic agent and evidence-based medicine criteria. The term idiopathic acute sensorineural hearing loss (IASH) is used to define sensorineural hearing loss that develops suddenly and for an unknown reason. IASH is typically defined as a sensorineural hearing loss of 30 dB or more at three consecutive frequencies, occurring within three days. The incidence of IASH ranges from 5 to 20 cases per 100,000 population. The true incidence is likely higher, as many patients experience spontaneous recovery. IASH most often occurs between the ages of 50 and 60. The true cause of IASH is often unknown. There are three main causes of IOST: 1. Infectious etiology - IOST can be caused by cytomegalovirus, Herpes simplex types 1 and 2, Epstein-Barr virus, herpes virus type 6, varicella zoster, and many others. Viral etiology is confirmed by virus identification in the inner ear using indirect immunofluorescence. 2. Vascular etiology - IOST can be caused by vascular spasm or occlusion. The microcirculation of the inner ear is unique, especially in the intraosseous part and terminal sections, which leads to increased sensitivity of the cochlea to anoxia. 3. Ruptures of membranous structures - the cochlear membranes are very delicate, and a history of IOST association with increased physical activity or a sharp change in barometric pressure suggests the possibility of membrane ruptures. The development of IOST and treatment require urgent action in relation to this pathology. Diagnosis of IOST is based on a thorough medical history, a high index of suspicion, and an appropriate set of diagnostic tests. The earlier the diagnosis, the sooner appropriate therapy is administered, and the better the outcome. Unfortunately, the patient is often the limiting factor, as the time from the onset of the first symptoms to seeking specialist attention can vary. The medical history should include all possible associated events preceding the hearing loss (e.g., air travel, scuba diving, viral infections, medication use). It is important to determine the rate of development, the duration of hearing loss, and all associated symptoms: tinnitus, dizziness, headache, and visual impairment. A general neurological examination focusing on the cranial nerves and vestibular system is essential. The audiological examination should include pure-tone audiometry and speech intelligibility testing, acoustic reflex recording, and tympanometry. According to the literature, spontaneous recovery rates range from 50 to 70%. Most cases of spontaneous hearing recovery occur within the first 2 weeks. There are 5 main factors affecting the prognosis in patients with SSHL: 1. The degree of initial hearing loss - a profound degree of more than 80 dB has a poor prognosis. 2. The frequencies involved - low-frequency hearing loss recovers better than high-frequency hearing loss. 3. The presence of vestibular reactions worsens the prognosis. 4. The patient's age - children and elderly patients have a worse prognosis. 5. The time since the onset of the disease - a delay in treatment worsens the results. Many regimens have been proposed for the treatment of acute sensorineural hearing loss, but independent studies have not found an evidence base for any of them. As a rule, vasodilators, diuretics, anticoagulants, plasma substitutes, corticosteroids, carbon dioxide inhalation, vitamins, and combination therapy are used. The list of drugs used to treat SSHL contains more than 60 names! Treatment for HSCT is often carried out out of inertia, according to regimens adopted in various clinics for decades, although these regimens were developed at a time when the foundations of evidence-based medicine had not yet been established. Systematic reviews of the literature on therapeutic strategies for HSCT treatment revealed only two evidence-based studies (Wilson et al. 1980, Moskowitz et al. 1984), which addressed the limited beneficial effect of early steroid administration on the prognosis of hearing recovery in HSCT. Given the significance of the infectious theory of HSCT genesis, and particularly the influence of the viral agent, these studies are particularly significant. Herpes infection leads to a complex immune response. The body's defense mechanisms in response to the intracellular action of the herpes virus involve specific and non-specific immunity. Cells infected with the herpes virus are recognized by specialized T cells, which directly destroy the infected cells. Accordingly, the immune response activated by herpes ultimately leads to the destruction and loss of function of the infected sensory epithelium. Based on the above, the following treatments may be proposed: - antiviral treatment with acyclovir; - immunosuppression with glucocorticoids. Antiviral treatment with acyclovir. Acyclovir is an effective antiviral agent for the treatment of herpes virus infection, disrupting and preventing the replication of viral DNA. Acyclovir affects all cells but can only be activated through phosphorylation by a specific enzyme of the herpes virus, thymidine kinase. This means that acyclovir is specific only to cells infected with the herpes virus. Acyclovir forms an inert and irreversible complex between viral DNA and DNA polymerase, which leads to the direct destruction of replicant DNA. A prospective, double-blind, randomized clinical trial by Albers F. (2002) examined the treatment of HSV-1 with a combination of acyclovir and corticosteroids versus corticosteroids alone. It was found that antiviral treatment with acyclovir alone cannot prevent the destructive cytotoxic immune response due to herpes virus reactivation. Therefore, the use of immunosuppressants is also necessary. Glucocorticoid immunosuppression. Corticosteroids are pharmacological analogues of the glucocorticoid family of steroid hormones and have a strong anti-inflammatory and immunosuppressive effect. Corticosteroids act through intracellular receptors, which are present in almost all cells of the human body. After binding to these receptors, the transcription of specific genes is regulated. The immunosuppressive effect of corticosteroids is complex: they reduce the production of inflammatory mediators, inhibit the migration of inflammatory cells, and promote apoptotic death of leukocytes and lymphocytes. Typically, treatment is with prednisolone at a dose of 1 mg/kg of body weight for 7 days, gradually tapering the dose by the 7th day. However, a strong anti-inflammatory and immunosuppressive effect can be achieved with high-dose glucocorticoid pulse therapy: 10-20 mg/kg methylprednisolone or 2-5 mg/kg dexamethasone orally, daily or every other day, for a maximum of 5 doses. Controlled studies of this treatment for optic neuritis are encouraging. The following adverse effects are known to occur with glucocorticoid pulse therapy: sleep disturbances, mood changes, gastrointestinal disturbances, facial twitching, and transient weight gain. Serious adverse events (anaphylaxis, seizures, sepsis, aseptic osteonecrosis, arrhythmias, and sudden death) are extremely rare and typically occur in patients with significant risk factors. Continuing with the discussion of the use of corticosteroids in the treatment of IOTS, a method of intratympanic dexamethasone injection into the tympanic cavity, proposed in 2001, is noteworthy. The dose was 0.25 ml of dexamethasone injection solution. Under local anesthesia, a tympanic puncture was performed with a thin injection needle in the anterior-superior quadrant of the tympanic membrane. A second tympanic puncture was performed in the anterior-inferior quadrant, and 0.25 ml of dexamethasone solution was injected. The patient's head was oriented so that the solution covered the round window niche for 20 minutes; the patient was instructed not to swallow. This treatment method was based on animal experiments that demonstrated that dexamethasone concentrations in the perilymph are significantly higher with intratympanic administration than with systemic administration. We modified this method and, for viral-associated tympanic otitis media, place a shunt in the posteroinferior quadrant of the tympanic membrane and administer a dexamethasone solution. A more comprehensive evaluation of this treatment method is required than has been published and is currently available. Vascular therapy. As mentioned above, tympanic otitis media treatment is most often performed using combinations of various drugs, attributed to their vasodilatory, antiplatelet, and other effects, which generally improve cochlear blood flow. According to a meta-analysis of 5 retrospective studies (488 patients) (Stokroos R J, Albers F W I996), none of the following drugs had an effect on improving cochlear blood flow: procaine, dextran, bacstroban, betamethasone, pentoxifylline, novocaine, nicotinic acid, vitamin B, a mixture of carbon dioxide and oxygen inhalations, and papaverine. However, to date, only betahistine (a structural and pharmacological analogue of histamine) has a proven effect on cochlear blood flow. Histamine is both a local hormone and a neurotransmitter. Intravenous administration of histamine causes a vasodilatory effect on the microcirculation. However, histamine has very narrow therapeutic margins and, therefore, its use in the treatment of IOST has been abandoned. Betahistine has a structural and pharmacological similarity to histamine and is a potent H3 receptor antagonist. Experiments have shown that betahistine causes cerebral and peripheral vasodilation with a 54% increase in microcirculation in the inner ear, specifically in the stria vascularis and spiral ligament. Furthermore, betahistine displaces histamine from its binding to the H3 receptor and increases the release of neurotransmitters into the synapse, which normalizes the excitation of peripheral receptors. The advantage of betahistine over histamine in treatment is its simpler administration. Furthermore, betahistine is effective when taken orally, whereas histamine is degraded. The effect of betahistine on cochlear blood flow occurs at lower doses than the systemic effect, meaning there is no effect on systemic blood pressure, no extrapyramidal symptoms, no sedation, and no drowsiness. The cost-effectiveness of this treatment method is undeniable: the total cost of a standard intravenous drug regimen for 10 days, including the cost of a disposable system, is 826 rubles per course. To this must be added the cost of a hospital stay (an average of 600 rubles x 10 days = 6,000 rubles). The total cost of a course of traditional vascular treatment with IOST is 6,826 rubles, excluding the cost of a nurse. In comparison, a monthly course of Betaserc at a dose of 16 mg costs an average of 900 rubles. Magnesium treatment with IOST. The emergence of placebo-controlled studies on the use of magnesium in the treatment of IOST has revived the interest of this well-known and well-known drug. Mg2+ is involved in several vital processes in the human body. Mg2+ is the main factor regulating the permeability of cell membranes during energy delivery and consumption. Several studies in recent decades have revealed a link between Mg2+ and noise-induced hearing loss. Thus, Attias et al. (1994) determined in a placebo-controlled study that prophylactic administration of Mg2+ has a preventive effect on the shift in hearing thresholds caused by exposure to high-intensity noise. Scheibe F. et al. (2000) found that preventive administration of Mg2+ reduces the degree of sensorineural hearing loss of ischemic etiology. The treatment method is as follows: MgSC>4 solution is administered intravenously by drip (14 drops per minute) at a rate of 2 g per 500 ml of saline, which, converted to a 25% magnesium solution, is equal to 8 ml of a 25% solution per 500 ml of saline. The course consists of 10 infusions. This dose is a percentage of the dose administered, for example, for eclampsia and is considered safe, with no cardiovascular or nervous system side effects. The only potential adverse effect of this drug is transient hypotension. Therefore, for the treatment of SIOS, there is likely no need to use a combination of medications with questionable efficacy. Instead, it is necessary to consider the possible etiology of the process and medications whose effectiveness is based on evidence-based medicine.