At present, there are more and more patients with vertigo in clinical practice, and as the causes of vertigo are traced, the proportion of otogenic vertigo is increasing, in addition to the well-known hypertension, cervical spondylosis and cranial occupational lesions, with the advancement of clinical and basic research. The common causes of otogenic vertigo are Meniere’s syndrome, labyrinthitis, vestibular neuritis, otoliths, etc. Vestibular neuronitis is a type of peripheral neuritis. The lesion occurs in the vestibular ganglion or the centripetal part of the vestibular pathway. There is a history of upper respiratory tract 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 were no other symptoms of cranial nerve damage. Hu Zhiqiang, Department of Otolaryngology, 113th Hospital of the Chinese People’s Liberation Army Sudden deafness with vertigo is common in 30-50 years old and may be caused by viral infection of the inner ear or vascular lesions or window membrane rupture. Patients have sudden onset of tinnitus and deafness on one side, and some of these cases are accompanied by vertigo and vomiting. The condition resembles Meniere’s disease, but the vertigo lasts longer and there are no recurrent attacks later. In some cases, the vestibular function may be impaired. The treatment of these diseases must be timely. At present, hormone, nerve nutrition and blood activation are usually performed, and if possible, hyperbaric oxygen therapy should be performed as soon as possible. In acute or chronic purulent otitis media, the infection may spread to the inner ear vagus and lead to plasmacythematous or purulent vaginitis. In this case, in addition to ear leakage, patients may have tinnitus, vertigo, nausea, vomiting and hearing loss, and spontaneous nystagmus to the affected side. When the disease progresses to septic labyrinthitis, not only is the vertigo severe and persistent, but also the hearing may decrease to total deafness, the spontaneous nystagmus may shift to the healthy side, and the vestibular function test on the affected side may disappear. When the above occurs, an ear mastoid x-ray should be taken, and preferably a CT scan of the temporal bone should be done to clarify the presence of mastoiditis, cholesteatoma, and vagal fistula. Viral labyrinthitis is mostly caused by herpes virus, mumps virus, and measles virus infections. Secondary to viral infection, patients present with vertigo, gait instability, marked nausea and vomiting, and mostly with severe deafness. Vestibular function tests are hypofunctional or absent on the affected side. The vertigo symptoms can gradually disappear completely after about 1 to 3 months due to normal vestibular function on the patient’s healthy side. Labyrinthine concussion Mostly caused by head trauma, often coexisting with concussion, due to the strong air wave impact after explosion, which can also cause inner ear labyrinthine concussion. After trauma, patients experience vertigo, nausea, vomiting, and significant hearing loss in the injured ear. Some of these are seen on otologic examination along with tympanic membrane trauma, with rupture or bleeding of the tympanic membrane. Hearing threshold changes of varying degrees and nature, either unilateral or bilateral, may be seen on audiological examination, and in severe cases, total deafness may be seen, with some acoustic conductance audiometry suggesting damage to the auditory chain and low vestibular function on the affected side. When diagnosing patients with concussion, especially those with hearing impairment and vertigo complaints, it should be noted that vagal concussion may also be present. Vestibular tract drug toxicity Most often, inner ear toxicity can be caused after the use of aminoglycoside antibiotics such as streptomycin, gentamicin, and kanamycin, or after an overdose with quinine or salicylic acid, or with phenytoinamide. The symptoms of vestibular toxicity usually appear a few days or weeks after drug administration, manifesting as dizziness, staggering gait, unsteadiness and difficulty in walking in children who used to walk, and difficulty in walking in adults who feel no roots under their feet, especially at night, and vertigo is not obvious when sitting or lying in bed, but worsens when moving, and some people have tinnitus and deafness, and symptoms of cochlear toxicity may appear simultaneously with or later than vestibular toxicity. If vestibular tract drug intoxication occurs in children, the prognosis is generally good because children are still developing and have strong compensatory ability, and walking difficulties can be significantly improved and symptoms eliminated after a few weeks. The higher the age, the slower the recovery, relative to the elderly. Otolithic membrane is a gelatinous membrane containing calcium carbonate particles that covers the surface of the oval saccule and balloon saccule, in which the calcium carbonate particles are called otoliths. When the head is struck by an external force, the otolith can be dislodged from its original position and roll into the semicircular canal, called otolith dislocation.