What Is the Connection Between the Inner Ear and Dizziness?

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Inner ear vertigo

Inner ear vertigo, also known as Meniere's disease, is an inner ear disease mainly due to episodic vertigo, fluctuating deafness, and tinnitus caused by labyrinthine edema.

Inner ear vertigo

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Except for ear causes caused by dizziness, please refer to the dizziness page of this site.

It is usually monotonic and more common in young adults. The cause of Meniere's disease is unknown and may be related to congenital inner ear abnormalities, autonomic dysfunction, viral infections, allergies, endocrine disorders, salt and water metabolism disorders, and so on. At present, it is generally believed that obstruction of endolymphatic reflux or malabsorption is the main cause of disease, such as narrowing or blockage of endolymphatic vessels; autonomic dysfunction can cause small blood vessels spasm in the inner ear, leading to labyrinth microcirculation disorder, tissue hypoxia, and endolymph biochemical properties. Changes, osmotic pressure increases and cause membrane stagnant water.

The pathological change of this disease is hydroponic membrane labyrinth, mainly involving the volute and balloon. Compression stimulates the cochlea to produce cochlea symptoms such as tinnitus and deafness, and compression stimulates the vestibular terminal organs to produce dizziness such as dizziness. Some people think that due to the increase of tension after membrane labyrinth hydromembrane, the vestibular membrane of membrane labyrinth finally ruptures, causing the concentration of potassium and sodium ions in the components of endolymph fluid to change, causing auditory nerve and vestibular nerve conduction block and causing symptoms. When the ruptured membrane labyrinth heals, the sensory nerves are at normal potassium and sodium levels and the symptoms disappear. Volatile symptoms occur as a result of membrane rupture and repair.

In the early stages of the disease, the nerves of the inner ear have not been degenerated. Therefore, hypofunction is still reversible. However, those with a longer course of disease have degeneration of inner ear receptors and basement membranes, sensorineural hearing loss, and permanent loss of vestibular function. In severe cases, although one or two episodes of vertigo occur, severe sensorineural hearing loss can also occur.

Inner ear vertigo

1. To determine whether it is Meniere's disease, pay attention to sudden deafness, labyrinthitis, ear drug poisoning, vestibular neuronitis, auditory neuroma, positional vertigo, sudden deafness, insufficient vertebral-basal artery blood supply, Identification of cardiovascular disease and hunt syndrome.

2. Vestibular function tests, hearing tests, glycerol tests, and cochlear electrocardiograms can be performed.

3.Treatment

(1) You should stay in bed during a seizure, eat a low-salt diet, and drink less water.

(2) Sedatives: Use diazepam during seizures to suppress dizziness and vomiting.

(3) Vasodilator drugs.

(4) Vitamins: Vitamin B1, Vitamin B6, Vitamin E and so on.

(5) Diuretics.

(6) Meniette stress treatment.

(7) Chemical labyrinth resection: Gentamicin is perfused in the tympanic chamber.

(8) Surgical treatment: It is not effective for frequent attacks and conservative treatment, and dizziness affects work and life. Consider surgical treatment. Including: decompression or drainage of endolymphatic sac, labyrinthectomy, vestibular neurotomy of posterior sigmoid sinus.

What are the typical symptoms of inner ear vertigo ?

(1) Vertigo (vertigo): It is characterized by sudden onset, severe dizziness, and rotation, that is, when you feel yourself or the surrounding objects rotate, you feel that the dizziness is aggravated when you move your head slightly. At the same time with nausea, vomiting, pale complexion and other symptoms of autonomic dysfunction. Dizziness diminishes and disappears after hours or days. The intermittent period can be weeks, months, or years, and usually the symptoms completely disappear during the intermittent period.

(Two) tinnitus (tinnitus): Most cases have tinnitus before vertigo, but often not noticed. Tinnitus is mostly low-frequency, varying in severity. Tinnitus usually worsens during the onset of vertigo.

(3) Deafness: It is often unconscious in the early stage. Generally, hearing loss can be felt during the onset, and it is mostly unilateral. Although the patient is deaf, he feels harsh on high-frequency sounds, and even feels very harsh when he hears a loud sound. This phenomenon is called revitalization. Hearing often recovers during the intermittent period, but when the onset of hearing drops again, a unique hearing fluctuation phenomenon occurs. In the later stages, hearing can be sensorineural hearing loss.

(4) Others: At the onset of dizziness, there may be a feeling of ear fullness on the affected side, or a heavy, pressured head.

Diagnosis of inner ear vertigo

(1) Vestibular function test: It is not easy to see the climax of the vertigo attack clinically. When the patient came to the clinic, the symptoms and signs have mostly been reduced or disappeared. In the attack period, the horizontal type or horizontal rotation type can be found. Spontaneous nystagmus, the fast phase is multi-directional to the healthy side, but the direction of the nystagmus may change depending on the strength of the lesion, and sometimes worsened in some head positions. The Romberg test showed that the dumping was in the opposite direction to the nystagmus. Vestibular function tests may be performed on the affected side after repeated attacks, and may also appear normal or allergic.

(2) Hearing test: The affected side is often sensorineural hearing loss. Early hearing is dominated by low-frequency hearing loss. High-frequency hearing also decreases after repeated episodes, and high-frequency hearing decreases significantly in the later stages. Recruitment phenomenon It is often one of the characteristics of the disease, that is, the increase in ear loudness is faster than the increase in sound level.

(3) Glycerin test: After fasting for 2 hours, give 50% glycerol 3ml per kilogram of body weight, take once, take pure tone audiometry once an hour before and after taking the medicine. After 3 hours, a hearing increase of more than 15 dB is often positive, and other symptoms also temporarily improve. Positive is diagnostic, but negative does not rule out the disease.

(D) Cochlear electrogram examination: -SP / AP ratio> 40% is clinically significant.

Based on the above typical triad symptoms and signs, a diagnosis can be made clinically. However, because there are many diseases that cause dizziness, the reasons are complex, and they must be distinguished from the following diseases:

(A) labyrinthitis: purulent otitis media exists.

(2) Ototoxicity: There is a history of using ototoxic drugs such as streptomycin or gentamicin. Ototoxicity often affects both ears, and vertigo is mostly not hidden, less rotational, and has no recurrent features. Vestibular function was significantly diminished or disappeared on both sides. He was accompanied by hearing loss and tinnitus.

(3) Vestibular neuronitis: more than upper respiratory tract virus infection, which may be caused by the infection of the vestibular neurons. Clinically, it is characterized by sudden vertigo and spontaneous nystagmus with nausea and vomiting, without tinnitus and deafness. Dizziness lasts longer. Dizziness is mostly a sense of rocking instability, which can also be rotational, with a natural tendency to ease. Vestibular function tests significantly diminished and rarely recurred after healing.

(4) Auditory neuroma: dizziness is mild, it gradually occurs, and there is little rotation. Hearing loss and tinnitus often occur on the affected side at the time of onset, and gradually develop into severe sensorineural hearing loss, but there are also sudden deafness. . Ipsilateral vestibular dysfunction or disappearance. Trigeminal or facial nerve dysfunction may occur during the course of the disease. X-ray radiography and CT scan of the rock section showed enlarged inner auditory canal and mass. Cerebrospinal fluid protein content increased.

(5) Positional vertigo: The onset of vertigo is related to a specific head position, without tinnitus and deafness, and positional nystagmus can occur at the same time. Positional nystagmus can be divided into two types: central and peripheral. During the examination, the peripheral positional nystagmus manifestation has a latent period, mostly horizontal rotation. After several positional inspections in a short period of time, the direction of the nystagmus does not change, but it disappears or decreases quickly, which is fatigue. There is a type of peripheral prognosis with good prognosis and self-healing. It is called benign paroxysmal positional vertigo. The etiology is unknown. It is thought that it may be a terminal vestibular disease. Traction can induce dizziness and nystagmus on specific head positions. Centrality is characterized by nystagmus appearing immediately at a specific head position, no nystagmus latency, repeated trials with nystagmus without fatigue, nystagmus can be vertical, and direction can be changed.

(6) Sudden Deafness: It is a sensorineural deafness that occurs suddenly for unknown reasons and is characterized by sudden hearing loss or loss. Tinnitus, accompanied by dizziness, nausea, and vomiting, but not recurrent. Hearing of some patients can be recovered on their own or partially.

(7) Insufficient blood supply to the vertebral-basal artery: Mostly caused by compression of the vertebral artery, such as cervical hyperplasia, or stimulation of the sympathetic plexus that governs the vertebral artery, causing arterial spasm and ischemia. Clinical manifestations are when turning or raising head, lowering head or changing posture. Sudden short-term dizziness, mostly a sense of rotation or rocking instability, may be blurred, reappeared or darkened, sometimes spontaneous nystagmus, tinnitus, deafness, and positional nystagmus may occur, X-rays Cervical spine radiographs often have bone changes. Arterial magnetic resonance (MRA) can determine if there is insufficient blood supply.

(8) Heart and vascular diseases: Hypertension, hypotension, heart disease, arteriosclerosis, etc. can cause dizziness, but all are accompanied by clinical manifestations of the primary disease.

(9) Thrombosis of the posterior inferior cerebellum: also known as dorsal lateral medullary syndrome, with severe vertigo, ipsilateral soft palate, pharyngeal muscle, laryngeal muscle paralysis, dysphagia, and language difficulties.

(10) Hunt syndrome is often accompanied by mild dizziness, tinnitus and hearing impairment, and severe ear pain. Herpes zoster and facial paralysis can help distinguish them.

What are the treatments for inner ear vertigo?

(1) Conservative treatment is generally a comprehensive treatment with the main purpose of adjusting autonomic nerve function, improving inner ear microcirculation, and removing membrane labyrinth. Bed breaks, low-salt diets, and less water should be used during the attack.

1. Sedatives: 2.5 to 5 mg of diazepam or 25 mg of promethazine, 50 mg of halotonin, 10 mg of riminine, and 30 mg of lumina are given orally during the onset. Difenidol (Difenidol) 25mg orally can suppress dizziness and vomiting.

2. Vasodilators:

(1) Haloperazine hydrochloride (sibilin) 5mg, 2 times a day, orally, can improve inner ear circulation.

(2) 1 to 2 mg of histamine phosphate is added to 200 ml of glucose solution, and intravenous infusion can improve the inner circulation microcirculation to relieve hydronephrosis.

(3) 500ml of low molecular weight dextran, intravenous drip, can increase blood volume, reduce blood viscosity, and improve cochlear microcirculation.

(4) Intravenous injection of 50% glucose can increase blood flow and have dehydration effect, but the maintenance time is short.

(5) 5 7% sodium bicarbonate 50ml, slowly and intravenously, 1 / day, can relieve inner ear arteriolar spasm, improve microcirculation, and increase cochlear blood flow.

(6) 105.2 mg of hydrobromide injection 654-2, intramuscularly, once a day. It is an anticholinergic drug that dilates the surrounding blood vessels.

(7) 10 to 20 mg of desbazol 3 times a day, orally; 4 to 8 mg of anti-vertizidine (petatadine) 3 times a day, orally.

(8) Traditional Chinese medicine preparations such as Pueraria flavonoids and Pueraria tablets, Salvia miltiorrhiza, Ligustrazine injection, etc. also have vasodilator action, which can be selected as appropriate.

3 Vitamins: Vitamin B1, Vitamin B6, Vitamin E, etc. taken orally.

4 Diuretics: chlorthalidone is better, 100mg daily or every other day, due to ototoxicity, it should not be used for a long time. Diuretic acid and furosemide should not be used due to ototoxicity.

(II) Surgical treatment: It is not effective for frequent attacks and conservative treatment, and dizziness may affect work and life, and surgical treatment may be considered.

The surgical methods are roughly divided into two categories: conservative surgery such as endolymphatic cystectomy, balloon incision and so on. Endolymphatic sac surgery is a physiological operation with an effective rate of 60 to 80%. It is the first choice for surgical treatment. Destructive surgery: such as labyrinthectomy, transcranial fossa or labyrinthic vestibular neurectomy can be performed as appropriate after lymphatic sac surgery is ineffective.