Vestibular neuronitis is a type of peripheral neuritis. The lesion occurs in the vestibular ganglion or in the centripetal portion of the vestibular pathway. There is a history of upper respiratory viral infection about two weeks before the disease. Vertigo symptoms may occur suddenly, last for days or months, and worsen with activity. Symptoms of the vegetative nervous system are generally slightly less severe than in Meniere’s disease. There are no hearing changes, i.e., no complaints of tinnitus or deafness. Most patients have complete remission of symptoms after two or three months, and only a few cases have recurrent attacks. On examination, spontaneous nystagmus toward the healthy side, hypoacusis or hemianopsia on the affected side is seen. There are no other symptoms of cranial nerve damage. Etiology 1, viral infection: serum determination of herpes simplex zoster virus potency is significantly increased after the disease. 2, vestibular nerve stimulation: the vestibular nerve suffered vascular compression or arachnoid adhesions or even due to the narrowing of the internal auditory canal and caused nerve hypoxia degeneration due to the stimulation of nerve discharge and morbidity. 3, focal factors: there may be autoimmune reactions. 4.Diabetes mellitus: It is reported in the literature that diabetes mellitus can cause degeneration and atrophy of vestibular neurons leading to recurrent vertigo attacks. Some patients with vestibular nerve severed can be found to have arcuate or scattered degeneration and regeneration of vestibular nerve by pathological examination. Clinical manifestations 1. Single-episode type: sudden and intense rotational vertigo attacks and ataxia or imbalance, with obvious nausea and vomiting, horizontal rotational nystagmus, fast phase to the healthy side, without auditory and central nervous system lesion signs. The vertigo lasts for a few days or weeks (not more than 1-3 weeks), and usually decreases progressively after a few days, and the signs disappear completely after 6 months. 2. Multiple-onset type: The clinical manifestation is repeated episodes of rotational vertigo or balance disorder and unsteadiness without auditory or central nervous system lesions. The vertigo is not as intense as that of a single attack. The explanation for the appearance of this chronic form is that the vestibular nerve is only partially atrophied or that it is the result of a physiological disorder of nerve function. 3. The onset is often sudden, with vertigo and spontaneous nystagmus as its main clinical manifestations. 4.Severe cases may be accompanied by nausea and vomiting, but no tinnitus or deafness; the duration of vertigo is short. It is often gradually relieved within a few days, and usually can be completely recovered within 2 weeks; a few patients may have short-term residual dizziness, lightheadedness and unsteadiness of different degrees. 5.The vestibular function test (hot and cold water test, etc.) on the diseased side often shows hypofunction or disappearance, and sometimes it can spread to both sides. 6. Hearing tests are often unaffected. Diagnosis and differential diagnosis Diagnostic evaluation should include audiogram, nystagmography with hot and cold tests, gadolinium-enhanced cranial MRI, with special attention to the internal auditory tract to exclude other diagnostic possibilities, such as pontocerebellar horn tumor, brainstem hemorrhage or infarct formation. The diagnosis can be made based on the sudden onset of infection, severe vertigo, unsteadiness on standing, aggravated by head movement, without tinnitus or deafness, vestibular function tests showing unilateral or bilateral diminished response, and good prognosis. It can be differentiated from Meniere’s disease and Meniere’s syndrome based on a clear trigger of infection, without tinnitus and deafness, and with a good prognosis. Treatment For acute attacks of vertigo, symptom suppression can be performed according to the management of Ménière’s disease. For prolonged vomiting, intravenous rehydration and electrolytes are necessary for replenishment and supportive treatment. The best treatment is to target the cause, but since the pathophysiological mechanism of vertigo cannot be determined, symptomatic treatment is usually administered. Drugs can only reduce the symptoms of vertigo, but cannot completely eliminate it. Treatment is effective in most patients with vestibular neuritis, and Valium is commonly used. During acute attacks, intramuscular or intravenous administration is preferable due to nausea and decreased gastric motility. There is a clear dose-dependence of the patient’s response and the dose may be increased if the initial dose is ineffective. The exact mechanism of action of these drugs is unclear, but the site of action is clear, involving neurotransmitter and nerve impulse transmission from primary to secondary vestibular neurons, maintaining the level of tone in the vestibular nuclei. It also controls vomiting. All of these drugs have a sedative effect and should therefore be used with caution when patients are engaged in activities that require a high degree of alertness (driving, operating machinery, sports activities). Drugs with relatively weak sedative effects such as chlorpheniramine and scopolamine patches can be used as prophylaxis for mild vertigo control and motion sickness, but drug-drug interactions should be considered before application. Functional recovery of peripheral vestibular lesions is the result of both peripheral vestibular function and central vestibular compensation (recovery of vestibular tone imbalance). In other words, the patient’s function can be restored, but one side of the vestibular hypofunction still persists. Recovery from vestibular neuritis often takes several weeks, and longer recovery periods are common. The sooner a patient begins vestibular rehabilitation exercises, the faster and more complete the recovery of function. The goal of vestibular rehabilitation exercises is to accelerate the process of vestibular recovery and to improve the ultimate level of recovery. Vestibular rehabilitation programs generally include oculomotor training of the vestibulo-ocular reflex and balance training of the vestibulo-spinal reflex. Early on, nystagmus is present and the patient should attempt to suppress gaze nystagmus in all directions. After the nystagmus disappears, head-eye coordination exercises are started. Patients should try balance exercises and gait exercises. After symptoms improve head movement exercises in motion should be added, starting slowly and gradually speeding up. Tandem exercises are also gradually added. Since vestibular neuritis is currently considered to be a viral infection of the vestibular nerve, an antiviral combined with corticosteroids can be tried. Studies have shown that methylprednisolone significantly improves the symptoms of vestibular neuritis, that antiviral drugs are ineffective, and that the combination of the two does not help to improve the outcome. There are no accepted criteria for evaluating the efficacy of vestibular neuritis. Currently, the diagnosis of vestibular neuritis is still based on spontaneous and prolonged vertigo symptoms, with examination confirming one side of peripheral vestibular disease and no other neurological signs and symptoms. The first-line treatment is suppression of vertigo and vomiting. The effect of oral medication starts after 20-30 min, reaches its peak in 1-2 h and has a half-life of about 8 h. Vestibular rehabilitation should be started as soon as nausea and vomiting stop. Many exercises may cause an increase in vertigo, but vestibular compensation is necessary. Vestibular rehabilitation exercises should be performed at least twice a day for a few minutes each time, as often as the patient can tolerate, and with as little anti-dizziness medication as possible. The currently recommended treatment is symptomatic treatment in the acute phase, corticosteroid therapy and early vestibular rehabilitation. After diagnosis, intravenous aspergillus can be administered with significant effect.