Otogenic vertigo

Introduction Otogenic vertigo: refers to vertigo caused by abnormal vestibular vagus. When there is lost water (Ménière syndrome), motion sickness (sickness sickness), labyrinthitis, labyrinthine bleeding or poisoning, vestibular neuritis or damage, middle ear infections, etc. can cause postural balance disorders, vertigo. Because the vestibular nucleus is closely related to the nucleus of the oculomotor through the medial bundle, nystagmus often occurs when the current court is stimulated by pathology. When there is lost water (Ménière syndrome), motion sickness (sickness sickness), labyrinthitis, labyrinthine bleeding or poisoning, vestibular neuritis or damage, middle ear infections, etc. can cause postural balance disorders, vertigo.

Cause

When there is lost water (Ménière syndrome), motion sickness (sickness sickness), labyrinthitis, labyrinthine bleeding or poisoning, vestibular neuritis or damage, middle ear infections, etc. can cause postural balance disorders, vertigo.

The main manifestations of otogenic vertigo are paroxysmal vertigo, hearing loss and tinnitus. Severe cases are often accompanied by nausea, vomiting, pale, sweating and other vagus nerve stimulation. Horizontal or horizontal and rotational nystagmus can occur. The time of an episode is short, and the patient often feels that the object is rotating or rotating on its own. Walking may be skewed or dumped, and the episode is conscious.

an examination

Related inspection

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1. Audiological examination

(1) Pure tone audiometry: can understand whether hearing is declining, the degree and nature of hearing loss. In the early stage, most of the low-frequency sensorineural hearing loss, the hearing curve showed a slight rise. After multiple episodes, high-frequency hearing decreases, and the hearing curve can be flat or descending. Pure tone audiometry can also dynamically observe the continuous change of the patient's hearing.

(2) Cochlear electrogram: This examination can objectively understand whether there is water in the membrane labyrinth. The -SP/AP amplitude ratio >0.37 has diagnostic significance and can indirectly indicate the presence of membrane labyrinth.

(3) Otoacoustic emission (OAE): It can first reflect the cochlear function of patients with early Meniere's disease. When the early pure tone of the disease is not found abnormal, TEOAE (transient evoked otoacoustic emission) can be weakened or induced. Not out.

2. Ocular electrogram

During the high tide period, spontaneous nystagmus can be observed, and the horizontal sinusoidal and positional nystagmus can be observed or recorded by the nystagmus electrogram with neat rhythm, different intensity, first-term affected side and then turned to the healthy side. The nystagmus turns to the healthy side. Intermittent spontaneous nystagmus and various induced experimental results may be normal.

3. Glycerol test

It is mainly used to judge whether there is membrane lost water. Because the osmotic pressure of glycerol is high, and the molecular diameter is smaller than the diameter of the cytoplasmic serosal pores, it can diffuse to the cells of the inner ear margin, increasing the intracellular osmotic pressure, so that the water in the endolymph fluid enters the blood vessel of the vascular pattern through the cell pathway. Pressure effect.

4. Vestibular function experiment

(1) Cold and heat test: the early vestibular function of the affected side may be normal or mildly declining. After multiple episodes, the dominant side of the healthy side may appear, and the semicircular canal dislocation or loss of function may occur in the late stage.

(2) vestibular evoked myogenic potentials (VEMP): amplitude and threshold abnormalities may occur.

(3) Hennebert sign: When the tibial foot plate is adhered to the inflated balloon, vertigo and nystagmus can be induced when the external auditory canal pressure is increased or decreased. Menener's disease patients with Henenbert's sign can be positive.

5. Imaging examination

A CT scan of the tibia can show stenosis of the vestibular aqueduct. The inner eardrum labyrinth MRI under special contrast can show the lymphatic thinning in some patients.

6. Immunological examination

Raoch (1995) reported that 47% of patients with Meniere's disease had HSP70 antibody, which was 58.8% on both sides. Gottschlich (1995) used Western blotting to detect antibodies to bovine inner ear antigen in patients with Meniere's disease, showing that 30% of patients have 68 kD antigen antibodies.

Differential diagnosis

Commonly used in otogenic vertigo are Meniere's syndrome, labyrinthitis, vestibular neuronitis, otolithic disease, and the like.

1. Vestibular neuronitis

This disease is a type of peripheral neuritis. The lesion occurs in the centripetal portion of the vestibular ganglion or vestibular pathway. More than two weeks before the illness, there was a history of upper respiratory tract infection. Symptoms of vertigo can occur suddenly and last for days or months, with increased symptoms during activity. Symptoms of the autonomic nervous system are generally slightly milder than Meniere's disease. No hearing change, that is, the chief complaint without tinnitus and deafness. Most patients have complete remission after two or three months, and only a few cases have recurrent episodes. During the examination, there may be spontaneous nystagmus to the healthy side, low vestibular function or semicircular canal palsy on the affected side. No other symptoms of cranial nerve damage.

2, sudden deafness with vertigo

More common in 30-50 years old, may be caused by inner ear virus infection or vascular disease or rupture of the window membrane. The patient suddenly had tinnitus and deafness on one side. Some of the cases were accompanied by vertigo and vomiting. The condition was like Meniere's disease, but the vertigo lasted for a long time and there was no recurrent episode. Hearing tests showed severe sensorineural spasm (more than 60 dB), and vestibular function with vertigo may be impaired. The treatment of such diseases must be timely. At present, general treatments such as hormones, nutritional nerves and blood circulation are generally carried out, and hyperbaric oxygen therapy should be performed as soon as possible.

3, labyrinthitis

In patients with acute or chronic suppurative otitis media, the spread of infection may affect the inner ear and get lost, and serous or purulent labyrinthitis occurs. In addition to ear leaks, patients with tinnitus, dizziness, nausea, vomiting and hearing loss may appear to the patient. Spontaneous nystagmus on the side, when there is a pupil in the labyrinth, the external ear canal pressure can cause dizziness, and the nystagmus is more obvious, that is, the fistula test is positive. When the disease progresses to suppurative labyrinthitis, not only vertigo is serious, but persistence, hearing can be reduced to full sputum, spontaneous nystagmus is turned to the healthy side, and the vestibular function test disappears. When the above situation occurs, the ear mastoid X-ray film should be taken. It is best to do a CT scan of the humerus to determine whether there is mastoiditis, cholesteatoma, or labyrinth. Viral labyrinthitis is caused by herpes virus, mumps virus, and measles virus infection. After the virus infection, the patient developed dizziness, gait instability, obvious nausea and vomiting, and more often accompanied by severe deafness. The vestibular function checks for poor or absent function on the affected side. Symptoms of vertigo due to normal vestibular function in patients with vaginal symptoms can gradually disappear completely after 1 to 3 months.

4, lost in shock

Mostly due to head trauma, often with concussion at the same time, due to the impact of a strong air and gas waves after the explosion, can also cause the inner ear to get lost. After trauma, the patient developed dizziness, nausea, vomiting, and hearing ear hearing loss. Part of the otological examination may be accompanied by tympanic membrane trauma, rupture or bleeding of the tympanic membrane. Hearing examination can be seen in different degrees and different characteristics of unilateral or bilateral hearing threshold changes, severe cases can be full sputum, and some acoustic impedance test can indicate ossicular chain damage, the affected side vestibular function is low. In the diagnosis of concussed patients, especially those with hearing impairment and vertigo, it should be noted that there may be a labyrinth.

5, vestibular drug poisoning

Most use of streptomycin, gentamicin, kanamycin and other amino glycoside antibiotics, or use quinine, salicylic acid drugs, or phenytoin overdose, can cause inner ear poisoning. Generally, vestibular poisoning symptoms appear in the days or weeks after administration. The symptoms are dizziness and gait. Children who walk will have unstable standing and difficulty walking. Adults will feel no roots and difficulty walking, especially at night. Dizziness is not obvious when sitting or lying in bed, vertigo is aggravated during activities, some people are accompanied by tinnitus, deafness, and symptoms of cochlear poisoning may occur simultaneously or later in vestibular poisoning. For example, vestibular drug poisoning occurs in childhood. Because children are still in development, they have strong compensatory ability. After several weeks, walking difficulties can be significantly improved, symptoms are eliminated, and the general prognosis is good. Relative to the elderly, the higher the age, the slower the recovery.

6. The otolith film refers to a colloidal film containing calcium carbonate particles covering the surface of the elliptical sac and the sac plaque, wherein the calcium carbonate particles are called otolith. When the head is hit by an external force, the otolith will be out of position and rolled into the semicircular canal, called the otolith dislocation.

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