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Meniere's disease

Under Meniere’s disease is understood the peripheral labyrinth syndrome of non-inflammatory genesis that occurs as a result of disturbance of the circulation of the ear lymph. In 1861, the French physician-paratrocologist, P. Meniere aia? Aua, reported an ear disease he had discovered, characterized by bouts of tinnitus, hearing loss, dizziness, ataxia, and autonomic disorders (nausea, vomiting, pallor of the skin, cold sweat) ) In this condition, the patients did not have seizures, loss of consciousness, brain diseases, purulent process in the middle ear, which gave the author grounds to indicate the localization of the pathological process in the ear maze. Before him, such symptoms were most often considered a manifestation of a stroke. P. Menier is considered the founder of clinical vestibulology.

Etiology. After P. Menier discovered the peripheral labyrinth syndrome, for a long time it was not possible to obtain any information about the nature of the pathological process in the ear labyrinth. The etiology of Meniere's disease has not yet been studied. Many authors, on the basis of sectional data obtained already in the middle of the 20th century, came to the conclusion that with Meniere's disease, hydrops of the ear labyrinth occurs, most likely associated with a violation of its blood supply.

Pathogenesis. The pathogenesis of the disease is based on a violation of the pressure regulation mechanism in the lymph spaces of the labyrinth. Increased labyrinth pressure makes it difficult to conduct a sound wave in the labyrinth fluids, and also worsens the trophy of labyrinth receptors. A periodically occurring significant increase in pressure is accompanied by a labyrinth crisis, due to the sharp inhibition of all sensory cells of the labyrinth. In this situation, the peripheral labyrinthine syndrome of oppression, characterized by hearing impairment and noise in the ear, as well as pathological spontaneous sensory, somatic and autonomic vestibular reactions, naturally manifests itself. Crises in Meniere's disease are more pronounced when one or mainly one of the labyrinths is affected.

Intralabyrinth pressure may increase for a number of reasons. These include hyperproduction of endolymph by the vascular stripe, impaired circulation through the endolymphatic ducts, as well as insufficient resorption in the endolymphatic sac. In addition, the intralabyrinth pressure (including endolymphatic) can increase as a result of an increase in perilymphatic pressure. Given the connection between the endolymphatic space through the cochlea’s water supply and the cerebrospinal subarachnoid space, it is impossible to exclude the possibility of an increase in intralabyrinth pressure due to an increase in intracranial pressure.

In the pathogenesis of increasing both the labyrinth and intracranial pressure, the vascular factor plays the main role. Its common features are the complex mechanism of regulation of vascular tone by the autonomic nervous system, abnormalities and asymmetries in the structure of the cerebral arteries (including options for the labyrinth artery to discharge from the anterior lower cerebellar and main arteries). The asymmetry of blood supply to the right and left hemispheres of the brain and labyrinths, functionally compensated by the system of the Wilisian circle and collaterals, can manifest itself under various adverse effects: irritation of the sympathetic periarterial nerve plexuses, hypertensive crisis, aggravation of hypotension, psychoemotional stresses. Increased permeability of the vascular wall occurs with a violation of water-salt metabolism and various hormonal disorders.

The complex structure of the vascular strip, the nutritional characteristics of the receptor cells of the ear labyrinth washed by the endolymph, the specific electrolyte composition of various lymphatic media, the presence of hormone-producing cells (apudocytes) in the labyrinth increase its vulnerability to various disorders of the neuroendocrine, vascular regulation in the body. If these disorders are manifested only by the peripheral labyrinth syndrome without signs of central dissociation and disharmonization of pathological reactions, then in this case we can talk about Meniere's disease.

Any dizziness or ataxia is not immediately attributable to Meniere's disease. This diagnosis can be established only after a thorough examination of the patient by an otolaryngologist, neuropathologist and therapist to exclude brain neoplasm, multiple sclerosis, atherosclerosis, vegetovascular dystonia, hypertension, hypotension, osteochondrosis of the cervical spine and many other diseases. The main task of the otolaryngologist in diagnosing Meniere's disease is to identify the peripheral labyrinth syndrome and the presence of signs of hydrops of the ear labyrinth.

Clinic. Characteristic signs of Meniere's disease are:

1)? Aoeaeae? O? Uee oa? Aeoa? ei? enooiiia? aciinou oa? aiey;

2) short duration of attacks;

3) the presence of all signs of the peripheral labyrinth syndrome;

4) the presence of signs of hydrops of the labyrinth and fluctuations in hearing;

5) well-being in the interictal period (disappearance of vestibular symptoms) with progressive hearing loss;

6) damage to mainly one ear.

The disease begins with a gradual decrease in hearing in one ear, which is not noticed by the patient and is detected only at the time of the first vestibular crisis. Even if the patient turns to the otolaryngologist with complaints of hearing loss, then in the absence of vestibular symptoms, this is not associated with the debut of Meniere's disease. Nevertheless, even according to tonal audiometry, one can note the hydrodynamic nature of the disturbance in sound conduction (rocky type of hearing loss).

Patients go to the doctor at the time of the labyrinth attack, which is characterized by noise in the ear, hearing loss, dizziness of a systemic nature, spontaneous horizontal rotator nystagmus towards the better hearing ear, tonic deviation of the hands and overshot, as well as deviation of the body to the side opposite to nystagmus, nausea , vomiting, blanching of the skin and cold sweat. They occupy a horizontal position, close their eyes and try not to make movements that dramatically worsen the condition, ktny and give the impression of detachment from the environment. The attack lasts several minutes, hours, less often - days, it often stops on its own. After an attack within 5-48 hours, patients note weakness, heaviness in the head, decreased working capacity, then their condition is fully normalized. Repeated attacks may be less pronounced in the case of a favorable course of the disease or, conversely, become more frequent and intensified. There are times when after one or two attacks they disappear forever, but hearing loss continues to progress slowly.

The pathological asymmetry of the vestibular apparatus that occurred during the attack is completely compensated by the central nervous system. With a temporary decrease in the labyrinth pressure, hearing improves slightly and noise in the ear decreases. Persistent disturbance of endolymph circulation leads to progressive hearing loss. The tonal audiogram is characterized by an increase in the thresholds of air and bone conduction at all frequencies (the curves run horizontally with a small bone-air interval), which is typical for the hydrodynamic nature of the violation of sound conduction. The eardrum is not changed.

In the reversible phase of the disease, the fluctuating nature of hearing loss (a slight periodic deterioration or improvement in hearing) is noted, which patients rarely pay attention to. Such fluctuation of hearing occurs due to the instability of increased intralabyrinth pressure.

Hydrops of the labyrinth is confirmed by a positive glycerol test. The patient drinks an empty stomach a mixture of pure medical glycerin (1-1.5 g per 1 kg of body weight), diluted in half with water or fruit juice. Before and 2-3 hours after taking glycerin, tonal audiometry is performed. A decrease in hearing thresholds of 10 dB or more confirms the presence of the labyrinth hydrops. A similar dehydrating effect is obtained by intramuscular administration of 1-2 ml of a 1% solution of furasemide (lasix test).

Hearing in Meniere's disease is initially disturbed by the conductive type, and then by the mixed type. The experiments of Rinne and Federichi do not give a clearly negative result due to the deterioration of bone conduction against the background of increased intralabyrinth pressure and inhibition of receptor cells of the Corti organ.
The defeat of the organ of Corti confirms a positive FUNG, which at the beginning of the disease may be unstable due to the periodic increase in pressure of the ear lymph. The excitability thresholds of the vestibular apparatus are increased, and the intensity of experimental reactions to strong stimuli is extremely high, which is a manifestation of vestibular recruitment, confirming the defeat of the receptors of the vestibular apparatus. Patients do not tolerate experimental vestibular tests.

Gradually, the disease goes into an irreversible stage, when the intra-maze pressure is constantly increased to a large extent. Against this background, fluctuations in hearing are not observed, the bone-air gap in the tonal audiogram disappears and the curves take a downward form, as with sensorineural hearing loss. Thresholds of bone conduction can reach 40 dB and above, and air conduction - more than 70 dB. The lower limit of perceived frequencies is increased to 60-80 Hz. With speech audiometry, 100% speech intelligibility is achieved. SISI test is 70-100%. With asymmetric hearing, lateralization of sound is noted in Weber's experiment in the best-hearing ear, and ultrasound is lateralized in the worse-hearing ear. Disturbed spatial hearing in the vertical and horizontal planes.

Treatment. During an attack, patients need emergency care, sparing transportation in a prone position. Strict bed rest is observed. After an attack, the volume of active head movements expands gradually.

Conservative treatment of Meniere's disease is aimed at stopping the labyrinth crisis and restoring the hydrodynamics of the labyrinth in the immediate period after the crisis. With preventive measures it is almost impossible to prevent an attack of Meniere's disease.

Relief of the labyrinth crisis is achieved by intramuscular injection of 1 ml of a 2% solution of promedol or a 2.5% solution of chlorpromazine in combination with 0.5-1 ml of a 0.1% solution of atropine sulfate and 1-2 ml of a 1% solution of diphenhydramine.

Promedol is a narcotic analgesic that reduces the summation ability of the central nervous system and has an anti-shock effect. Neuroleptic chlorpromazine, having a strong sedative effect, reduces spontaneous motor activity, inhibits motor defensive reflexes and, with a conscious mind, lowers reactivity to endogenous and exogenous stimuli. Atropine is an m-anticholinergic that has effects opposite to the stimulation of parasympathetic nerves, that is, it is parasympathetic. Its central cholinomimetic effect is manifested in a decrease in muscle tension. The antihistamine Dimedrol relieves spasm of smooth muscles, reduces capillary permeability, prevents the development of tissue edema, and also has a sedative effect, inhibits nervous excitation in the autonomic ganglia, and has a central cholinolytic effect.

The main directions of further conservative treatment are the elimination of metabolic acidosis, dehydrating therapy and the improvement of intracranial hemodynamics.

An increase in the alkaline reserve of blood is produced by intravenous infusion of a 5% solution of sodium bicarbonate. During the first infusion, 50 ml of the solution is administered, and with subsequent infusions, the dose is increased to 150 ml. The course consists of 7-10 infusions. Instead of sodium bicarbonate, trisamine buffer (THAM) can be used. Its maximum dose should not exceed 1.5 g / kg per day.

The dehydrating effect is obtained by intravenous administration of 10-20 ml of a 40% glucose solution or by intramuscular administration of 1 ml of a 1% solution of furasemide.

Glucocorticoids have a powerful decongestant, anti-shock and stimulating effect. Given that in Meniere's disease, the function of the adrenal cortex is slightly reduced, their use is justified. It is advisable to administer 60 mg of prednisolone intravenously, dissolving in 200 ml of an isotonic sodium chloride solution. 10 ml of panangin, 5 ml of 5% ascorbic acid solution and 3 ml of cocarboxylase can be added to the solution.

Microcirculation of cerebral vessels is improved by intravenous administration of various blood substitutes (reopoliglyukin, reogluman, mannitol, etc.) in an amount of 200-400 ml.

At the end of an intravenous infusion of a solution of prednisolone and blood substitutes, 1 ml of furasemide is administered to remove excess fluid from the body.

Intravenous administration of drugs of different mechanisms of action is performed with an interval of more than 12-24 hours.

Drugs that improve cerebral circulation are cinnarizine (stugeron), cavinton (vinpocetine), trental. They are administered intravenously, intramuscularly and orally. Nootropil and bemitil have a good adaptogenic effect on brain tissue that stimulates central compensation.

In the treatment of Meniere's disease, antispasmodics (dibazole, papaverine), nicotinic acid (Vit. B3), which have a vasodilating effect and other vitamins that affect tissue metabolism (A, E, B1, B2, B6, B12) are used.

It is advisable to use drugs of a different mechanism of action and combine various methods of their administration, but at the same time, the correspondence of the intensity of therapy to the clinical manifestations of the disease is taken into account, since excessively active therapy can have a destabilizing effect on the compensation processes. Polypharmacy should also not be allowed. The introduction of each drug is logically justified.

IB Soldatov (1961) proposed a method for creating a depot of pharmacological preparations in the immediate vicinity of the labyrinth. In case of metatympanal blockade, atropine and caffeine are introduced parameatally after novocaine.

V.E. Koryukin (1973) applies a blockade of the upper cervical sympathetic plexus, which has a pronounced vasodilating effect, increases intracranial blood supply and increases blood flow velocity, thereby intensifying metabolic processes. With the correct blockade technique, redness of the skin of the corresponding half of the face and Horner's syndrome occur.

In the surgical treatment of Meniere's disease, three groups of operations can be distinguished.

1. Surgery on the nerves of the tympanic cavity.

2. Decompression operations.

3. Destructive operations.

Surgery on the nerves of the tympanic cavity consists in interrupting the pathological impulse from the autonomic nervous system. These include resection of the drum string and drum plexus. These interventions are effective for ear noise in the initial stage of Meniere's disease.

Decompression operations include drainage and shunting of the endolymphatic sac, cochlear passage, and vestibule sacs. Drainage involves the imposition of a fistula, and bypass surgery involves the removal of endolymph through it with a plastic shunt. Currently, surgery on the endolymphatic sac with the creation of a stable drainage hole using a laser is most often used. It can be carried out at any stage of Meniere's disease. Drainage of the cochlear passage and vestibule sacs is more easily technically feasible, but more traumatic for the structures of the labyrinth, so they are performed in patients with severe hearing loss to prevent vestibular disorders.

Destructive operations on the labyrinth and vestibular portion of the vestibular cochlear nerve consist in the removal of vestibular sacs through the oval window and the destruction of the vestibular ganglion in the depths of the internal auditory canal. They are performed only in a hopeless situation when all other operations have been ineffective.

Meniere's disease does not lead to death, but labyrinth crises are painful for patients, impair their ability to work, and lead to severe hearing loss and even disability. Such patients have limitations of fitness for military service due to hearing and vestibular dysfunction. They cannot perform work in extreme conditions (sensory deprivation, hypoxia, severe physical and psycho-emotional stress, optokinetic stimulation). Due to inhibition and asymmetry of the function of the vestibular apparatus, these persons cannot work in the dark, at height and under water, and also be operators of moving devices. They cannot fulfill the duties of military service related to the impact on the human body of accelerations (flight personnel, crew, drivers of military vehicles, etc.)

Survey of military personnel is carried out according to Art. 39 orders of the Ministry of Defense of the Russian Federation N 315 1995
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Meniere's disease

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