Meniere's disease. Causes, symptoms, diagnosis and treatment of pathology

List of diseases - M

Disease- a process resulting from the impact on the body of a harmful (emergency) stimulus of external or internal environment, characterized by a decrease in the adaptability of a living organism to the external environment while simultaneously mobilizing its defenses. The disease is manifested by an imbalance of the body with environment, expressed in the occurrence of adverse (inadequate) reactions, and in humans - a decrease in his ability to work for the duration of the illness.

Each disease is described in detail by our specialists in this section. medical portal EUROLAB - here you can find general information about each disease, learn it causes and characteristic external signs, you will learn how to recognize a dangerous disease and what types of diagnostics and analyzes should go through, you can see disease stages, her consequences and complications on the body, methods treatment and prevention this disease in general, you will find out when and which doctors you should contact, you can read doctor's consultations self-care, as well as themselves ask a doctor a question.

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Meniere's disease is a rare inner ear disease, manifested by a triad of symptoms - dizziness, hearing loss and noise in the ear / ears. The disease has a paroxysmal character, but the general dynamics of the disease is different. In most patients, the severity of all three of the above symptoms increases over time. In some patients, the disease does not progress even in the absence of treatment. There are also rare cases of a single attack of the disease without its subsequent repetitions and progression of hearing and balance disorders.

Due to the fact that exact reason disease is still unknown, the methods of its treatment are not targeted, and therefore are characterized by varying success. Although Meniere's disease does not lead to lethal outcome, hard-tolerated attacks rank it among the serious diseases that lead to the patient's disability and limit his occupation.

Anatomy of the inner ear and vestibular apparatus

Knowledge of the anatomy of the inner ear is extremely important for understanding the essence of Meniere's disease, since it is there that the peripheral sections of the auditory and balance analyzers are located.

The inner ear or labyrinth is a complex bony structure with an even more complex internal organization, located in the pyramid of the temporal bone between the internal auditory meatus and the cavity of the middle ear ( tympanic cavity). The labyrinth, in turn, is divided into two types - bone and membranous. The bony labyrinth determines the shape of the inner ear. The membranous labyrinth is located inside the bone labyrinth, repeats its shape and is the basis on which specific receptors are located. Lymph circulates in the cavity of the membranous labyrinth.

The inner ear is divided into three main parts - the vestibule, the cochlea and the semicircular canals. The vestibule is an intermediate section in direct contact with the tympanic cavity, cochlea and semicircular canals. The cochlea contains a peripheral section auditory analyzer– spiral ( Corti) an organ, and the semicircular canals are the peripheral part of the vestibular analyzer.

Anatomy of the bony labyrinth

The bony labyrinth of the inner ear is a system of interconnected cavities located in the pyramid of the temporal bone. Three parts of the bony labyrinth are divided - the vestibule, the cochlea and the semicircular canals. The cochlea is located in front, somewhat medially and downwards from the vestibule, and the semicircular arcs, respectively, posteriorly, outwards and upwards from the vestibule.

The vestibule is an elliptical cavity located between the cochlea and the semicircular arches. Communication with the cochlea occurs through the wide opening of the cochlear canal. Communication with the semicircular canals is carried out through 5 small holes. On the surface of the vestibule facing the tympanic cavity there are two openings - an oval and a round window. oval window ( vestibule window) has a central location and somewhat exceeds the diameter of a round window. The oval window contains the stirrup plate ( one of the three ossicles of the middle ear), the movements of which cause fluctuations in the lymph of the inner ear. round window ( snail window) is located closer to the entrance to the cochlea. It is tightened with a thin, elastic plate, the purpose of which is to dampen the fluctuations of the lymph after it passes through the cochlea, as well as to protect the spiral organ ( system of mechanoreceptors in the cavity of the cochlear canal, transforming mechanical vibrations lymph into electrical impulses) from mechanical damage. Also, this membrane prevents the reverse passage of the lymph wave through the cochlea, eliminating the "echo" effect.

The cochlea is represented by a spiral bone canal that performs 2.5 turns. Approximately in the middle of the bony canal of the cochlea, a spiral bone plate passes, dividing it into two sections. The first section is called the staircase of the vestibule. It communicates with the vestibule cavity through one wide opening. The second section is called the scala tympani because it communicates with the tympanic cavity through a round window. The inner terminal part of the cochlea is called its dome. In the area of ​​this dome, the spiral bone plate forms a hole called the helicotrema, which connects the scala vestibuli with the scala tympani.

Bone semicircular sea otters are three arcuate cavities located strictly perpendicular ( at a right angle) in relation to each other. The anterior semicircular canal is located vertically and perpendicular to the axis of the pyramid of the temporal bone. The posterior semicircular canal is also located vertically, but already almost parallel to the posterior surface of the temporal bone pyramid. The third - the lateral semicircular canal is located horizontally. Each channel has two legs. The legs of the anterior and posterior semicircular canals are connected on one side, forming a wider common pedicle. Thus, the communication of the semicircular canals with the vestibule occurs through only 5 small openings. Each leg has its own hole. At one end of each semicircular canal is an extension called the ampulla.

Anatomy of the membranous labyrinth

The membranous labyrinth is a thin translucent connective tissue membrane lining the inner surface of the bony labyrinth. It is tightly attached to the bone labyrinth by means of a large number of the finest threads. The cavity of the membranous labyrinth is filled with endolymph. The space between the bony and membranous labyrinths is filled with perilymph.

The electrolyte composition of endolymph and perilymph is different, which plays important role in providing a mechanism for perceiving sounds and maintaining balance. The formation of the perilymph is carried out by the wall of the membranous labyrinth. Endolymph is formed in the endolymphatic sac located in the solid meninges. Through the endolymphatic duct, which lies in the water supply of the vestibule, this fluid enters the spherical ( sacculus) and elliptical ( utriculus) sac, interconnected by a small duct. These sacs, in turn, communicate with the cochlear duct and the semicircular ducts located in the semicircular canals. Each semicircular duct forms its own ampulla ( extension before joining with vestibule), which contains the rectilinear and angular acceleration receptors. Auditory receptors are located in the cavity of the cochlear duct.

The volume of endolymph and perilymph is not constant, but tends to a certain reference value. Excess perilymph enters the middle ear through the round and oval fenestra. Excess endolymph enters the easily extensible endolymphatic sac located in the cranial cavity.

The mechanism of transmission and perception of sound

The internal structure of the cochlea and the principle of operation of the sound-receiving apparatus of the ear should be considered in more detail. Almost the entire length of the cochlear cavity is divided by two membranes - a thin vestibular membrane and a denser main membrane. These membranes divide the cochlear cavity into three passages - upper, middle and lower. Top and bottom moves ( scala vestibuli and scala tympani, respectively) communicate with each other through the opening of the dome of the cochlea - the helicotrema, while average stroke (membranous canal) is isolated from them. The perilymph circulates in the upper and lower canals, and the endolymph rich in potassium ions circulates in the middle canal, which is why it is positively charged with respect to the perilymph. On the main membrane in the cavity of the membranous canal is a spiral ( Corti) an organ that transforms the mechanical vibrations of the lymph into electrical impulses.

When a sound wave enters the external auditory canal, it causes the eardrum to vibrate. Through the system of sound ossicles in the middle ear, these mechanical vibrations are amplified approximately 20 times and transmitted to the stirrup, which tightly covers the oval window of the vestibule. Vibrations of the stirrup cause vibrations of the perilymph, which propagate to the scala vestibuli. Since the vestibule membrane separating the vestibule and the membranous canal is thin, the vibrations of the perilymph are transmitted unchanged to the endolymph of the membranous canal, which, in turn, causes vibrations of the main membrane on which the spiral organ is located.

The spiral organ consists of approximately 3,500 inner receptor hair cells and 12,000 to 20,000 outer hair cells. When the main membrane vibrates, the hairs of these receptors associated with the integumentary membrane ( component of the spiral organ - a thin plate hanging over the receptors) are deflected by less than half the diameter of a hydrogen atom. The deviation of these hairs causes the opening of ion channels, potassium ions penetrate into the receptor cell, causing its excitation and generation of a nerve impulse. Subsequently, impulses from internal and external receptors along the fibers of the VIII pair of cranial nerves enter the brain, where they are processed in the nuclei of the auditory analyzer and cause the corresponding sensations.

The mechanism of functioning of the vestibular apparatus

The structures of the vestibular apparatus are located in the semicircular canals and the vestibule of the labyrinth.

There are two sacs in the vestibule - elliptical ( matochka) and spherical. On the inner surface of each of the sacs there is an elevation formed by an accumulation of mechanoreceptors. One pole of these receptors is attached to the wall of the sac, and the second is facing its cavity and is free. At the free end of the receptor there is one long mobile hair and about 60 - 80 short and immobile hairs. Short hairs are located in the thickness of a jelly-like membrane containing a large number of microscopic otolith crystals ( calcium carbonate).

At rest, these crystals do not come into contact with the hairs and their irritation does not occur. However, at the beginning of a rectilinear movement in any direction, the otolithic membrane, being jelly-like, somewhat lags behind the underlying receptor cell, due to which the otolith crystals come into contact with short hairs, causing their irritation. The irritation of short hairs is summed up, and the cell generates a nerve impulse. The stronger the acceleration, the more otolith crystals are in contact with short hairs. Stronger irritation of the hairs leads to more frequent impulses of this nerve receptor. The higher the frequency of the sac receptor impulses, the stronger the feeling of acceleration or movement in space is felt.

Thus, the receptors of the sacs of the vestibule determine the intensity rectilinear acceleration. The direction of acceleration is determined by analyzing data from the receptors of the semicircular canals, the visual analyzer, and skeletal muscle mechanoreceptors.

The receptors of the semicircular ducts are concentrated only in the region of the ampullae and are located in the form of cristae ( ridges). These receptors are attached to the wall of the ampulla with one pole, and are immersed in the endolymph with the other free pole. Motile hairs are also located on the free pole of the receptor, but differ from the short and immobile hairs of the sacs. During the rotation of the head around one of the axes, the endolymph moves along the semicircular canals. Since each channel has only two openings, the movements of the endolymph can only be in two directions. When the endolymph moves, for example, forward, the hairs of the receptors deviate forward, ion channels for potassium open, the membrane of this receptor depolarizes and a nerve impulse is formed. When the endolymph moves into reverse direction the hairs of the receptors deviate backward, closing the ion channels and stopping the impulses of this receptor.

The above mechanism is approximate. In fact, impulses from the neurons of the vestibular system occur constantly at a certain frequency, which the brain perceives as a state of rest and balance. The movement of the endolymph in the semicircular canals leads to an increase or decrease in the frequency of impulses, depending on the direction of its movement.

Thus, the ampullae receptors of all three semicircular canals constantly send information to the brain about the position of the head relative to three axes - the frontal ( left right), vertical ( top bottom) and sagittal ( back and forth). These impulses fall into the centers of equilibrium in medulla oblongata (Bekhterev, Deiters and Schwalbe kernels) along the fibers of the VIII pair of cranial nerves. In the future, these nuclei coordinate the activities spinal cord, cerebellum, autonomic nerve ganglia, oculomotor nuclei, cerebral cortex, etc.

Causes and pathogenesis of Meniere's disease

The immediate cause of the development of the symptom complex of Meniere's disease is an increase in endolymph pressure in the labyrinth. This state otherwise referred to as endolymphatic hydrops or dropsy of the labyrinth. A clear causal relationship between the development of this disease and certain etiological factors not found. However, according to most researchers, angioedema, vegetative-vascular dystonia, middle ear infections, allergic diseases, beriberi, etc. There have been cases of the development of this disease through various periods of time after traumatic brain injuries.

It is believed that the above factors in one way or another lead to an increase in the amount of endolymph circulating in the inner ear. As possible mechanisms, an increase in the rate of endolymph production, a decrease in the rate of its resorption, and a violation of membrane permeability are considered. One way or another, high lymph pressure leads to protrusion of the stapes from the oval window of the vestibule, which makes it difficult for the transmission of a mechanical impulse from the tympanic membrane to the endolymphatic fluid. Besides, high blood pressure endolymph disrupts the ion channels of receptor cells and impairs their nutrition. As a result of the processes described above, these receptors gradually accumulate a certain potential, the discharge of which occurs at the time of an exacerbation of the disease and is manifested by a vestibular crisis.

Symptoms ( signs) Meniere's disease

Meniere's disease is described by three complaints:
  • systemic dizziness;
  • hearing loss;
  • tinnitus.
In most cases, there is a paroxysmal course with progressive hearing loss. However, the severity of the disease is determined not by auditory impairment, but by the severity of dizziness and autonomic disorders caused by it.

Dizziness

Dizziness in Meniere's disease is the most unpleasant of all symptoms and is paroxysmal in nature. The frequency of seizures can be different in the same patient, and as the disease progresses, their frequency may increase, remain unchanged, or even decrease. One of the factors leading to an increase in seizures is physical and mental overwork.

The development of an attack can occur regardless of the time of day, however, it has been noted that attacks are somewhat more common at night and in the morning. The duration of an attack of dizziness varies from several minutes to several days ( on average 2 - 6 hours). Some patients may anticipate the approach of an attack some time before its onset, as during an aura in epilepsy. The intensity of dizziness can also vary from mild to extremely severe. Autonomic symptoms associated with dizziness include nausea, vomiting, changes in blood pressure, sweating, and horizontal nystagmus ( involuntary oscillatory eye movements). In some cases, patients are forced to take a horizontal position immediately after the onset of an attack, since any turn of the head causes an increase in autonomic symptoms.

Such a patient not only experiences a sensation of rotation of objects, but cannot stand on his feet due to sudden loss balance. If the onset of an attack is simultaneous, then its passage, as a rule, takes some time - from 6 to 48 hours, during which dizziness and the vestibular symptoms associated with it gradually decrease. Nystagmus disappears last and can be observed up to a week from the moment the attack has passed. Also, for some time after the attack, the patient may experience severe general weakness. Nevertheless, a few days after the attack, the working capacity is completely restored, and during the period of remission the patient leads a full life.

Hearing loss

Hearing loss in Meniere's disease is progressive and often bilateral, although hearing loss is usually somewhat more pronounced on one side. In the early stages of the disease, only sound-conducting system ear with an intact sound-receiving apparatus. This is confirmed by the data of the audiogram, which shows signs of conductive hearing loss. As the disease progresses, damage to the helical ( Corti's) of the organ, and hearing impairments occur in a mixed type.

Initially, the perception of low and speech frequencies deteriorates with practically unchanged hearing in relation to high frequencies. During an attack of illness, hearing loss sharply increases, and after an attack, hearing is somewhat restored, but does not reach the level that was before the attack. In other words, with each attack of Meniere's disease, the hearing loss worsens.

Noise in ears

In the initial stages of the disease, tinnitus is episodic, low-pitched, buzzing ( not whistling). As the disease progresses, the frequency range of the noise may change, and its intensity may increase. It is constantly present, and during attacks it intensifies on the side of more serious organic disorders. Distinctive feature noise in Meniere's disease is its preservation when the carotid artery is clamped from the corresponding side. This maneuver helps to differentiate this disease from murmurs of vascular origin.

Clinical forms and stages

There are typical and atypical course of Meniere's disease.

In a typical course, the disease debuts with the appearance of a slight noise in the ears or one ear, after which, after a while, hearing and balance disorders appear simultaneously. Hearing impairment in this case is bilateral.

A different course of the disease is considered atypical, such as the onset of auditory disorders, and then vestibular ones, and vice versa.

There are three stages in the evolution of Meniere's disease:

  • reversible;
  • stage of severe clinical manifestations;
  • final ( terminal) stage.
These stages are established by the results of the audiogram. In the reversible stage, signs of dropsy of the labyrinth are found only before the attack.

In the stage of pronounced clinical manifestations, the pressure of the endolymph in the inner ear is constantly increased. A positive dehydration test confirms the presence of this particular stage, when hearing impairment proceeds mainly by the conductive type and the spiral organ is slightly damaged. Clinically, this stage is manifested by fluctuating ( intermittent) hearing loss - hearing loss during an attack and its improvement during remission.

In the final stage of the disease, hearing loss becomes mixed - conductive and neurosensory, which indicates an organic lesion of the spiral ( Corti's) organ. Hearing is permanently impaired and does not change during attacks, unlike vestibular symptoms and tinnitus. The dehydration test at this stage will be negative.

Diagnosis of Meniere's disease

Diagnosis of Meniere's disease is based on the determination of the relevant clinical picture, as well as on such an instrumental study as audiometry. Other instrumental methods ( magnetic resonance imaging, evoked potential method) are much less informative.

A triad of symptoms is clinically determined - vestibular disorders, hearing loss and tinnitus. Measurement of pulse and blood pressure during an attack can reveal associated vegetative-vascular disorders.

Audiometry

Audiometry is a key and almost the only method for diagnosing auditory disorders in Meniere's disease. This method is designed to study the thresholds of hearing during air and bone conduction of sound of various frequencies. The audiometric picture in Meniere's disease varies depending on the stage of the disease.

Audiometry in the initial stage of the disease
In the initial stage of the disease in the interictal period, there are no changes on the audiogram, that is, a normal audiogram is recorded. healthy person. Only some time before the attack and at the beginning of the attack, there is an increase in the sensitivity threshold of low sounds. At the same time, an air-bone interval is present, which indicates a conductive type of hearing loss. In other words, only air transmission of sound suffers, while bone conduction and auditory receptors are not affected.

Audiometry in the stage of advanced clinical manifestations
In the stage of advanced clinical manifestations in the interictal period, there is a constant decrease in hearing at low and speech frequencies with air conduction. Bone patency may be normal or slightly reduced. During an attack, hearing deteriorates significantly. The air-bone gap is still present. The condition of the sensory apparatus of the cochlea is normal or somewhat worsened.

It is at this stage of the disease that a dehydration test with furosemide is relevant ( diuretic). Its purpose is to temporarily reduce the pressure of the endolymphatic fluid and demonstrate an improvement in hearing on given background. For the test, the patient undergoes audiometry before intravenous administration of furosemide and after 2 to 3 hours, depending on the rate of development of the diuretic effect. If the speech frequency threshold decreases on the second audiogram ( hearing improves) by 10 dB ( decibel is a unit of sound intensity), the sample is considered positive.

A positive dehydration test is recorded only in the second stage of the disease, when air conduction is impaired due to an increase in endolymph pressure in the inner ear, and the spiral organ is not yet damaged. At the initial stage, such a test cannot be carried out, since in this case it will be positive only before the attack and in its initial period, and it is almost impossible to predict the time of the attack. In other words, in 99% of cases, this test will be negative, because most of the time, the pressure of the endolymph in the inner ear is not increased.

Audiometry in terminal stage diseases
In the terminal stage of the disease, there is a constant decrease in hearing in the interictal period and during an attack with both types of conduction. The air-bone interval disappears. The dehydration test is negative, because at this stage, a decrease in endolymph pressure in the inner ear does not improve the perception of sounds due to irreversible damage to the sensory apparatus of the cochlea.

In addition to the above changes in the audiogram according to the stages of the disease, there are also some of its changes that may be present at any of the stages. One of these changes is the phenomenon of sound bifurcation, that is, different frequency perception of sounds by the left and right ear. Also, in the initial stage of the disease, there may be a positive phenomenon of accelerating the increase in volume.

Treatment of Meniere's disease

Treatment of Meniere's disease is divided into treatment during an attack and treatment during remission ( interictal period). Due to the fact that the etiology of the disease remains unclear, mainly symptomatic and pathogenetic treatment is used, which can alleviate the patient's condition.

Treatment during an attack

The first aid during an attack of Meniere's disease is laying the patient in a comfortable position for him, in which dizziness and associated nausea would be minimal. The patient himself must choose this position. In addition, all possible stimuli should be eliminated, such as light, sounds, vibrations, etc. Applying a warm heating pad to the legs and mustard plasters to the cervical-occipital region leads to a rapid decrease in endolymph pressure in the inner ear by draining it into the endolymphatic sac.

From drug treatment apply:

  • atropine sulfate solution subcutaneously ( 1 ml - 0.1%);
  • intravenous glucose solution 20 ml - 40%);
  • novocaine solution intravenously ( 10 ml - 5%);
  • pipolfen solution ( 2 ml - 2.5%) or suprastin ( 20 mg/ml - 1 ml) intramuscularly;
  • promedol solution ( 1 ml - 2%) or chlorpromazine ( 1 ml - 2.5%) intramuscularly.
Intravenous administration of novocaine is allowed only if the patient has not previously been allergic to this drug. To eliminate this risk, a scarification allergy test. If no novocaine allergy is detected as a result of the test, then it intravenous administration should be carried out extremely slowly due to the arrhythmogenic effect ( ability to cause cardiac arrhythmias).

In case of refractoriness ( decrease in efficiency) of the ongoing treatment, repeated administration of atropine, chlorpromazine and novocaine is carried out. If you have skills behind the ear drug administration, you can enter a mixture of novocaine, atropine and caffeine ( 1 ml - 10%). Thus, the effectiveness of drugs increases, and their systemic side effects decrease.

In the interval between the appointment of the above funds, not earlier than one hour after the administration of the last drug, a drip injection of a sodium bicarbonate solution is recommended ( 50 ml - 5%). Repeated injections of this drug are performed only under the control of the acid-base balance of the blood.

Treatment during remission

Treatment of Meniere's disease during remission consists in prescribing:
  • betahistine ( vertran, betaserc, tagista - 16 mg) by mouth daily for at least 3 to 4 months;
  • rheopolyglucin ( 100 mg/ml - 100 ml) intravenous drip 1-2 times a week for 3-4 months;
  • vinpocetine ( 5 mg a) by mouth daily for 2 to 3 months;
  • papaverine ( 40 mg) inside in short courses of 10-14 days with a break of 1-2 months;
  • piracetam ( 800 mg) courses of 10 - 14 days with breaks of several months, etc.

All of the above drugs are serious drugs. Due to high risks side effects be sure to consult with your doctor otorhinolaryngologist/ENT) on the need for their use, as well as on the individual dosage and combination regimen.

The practice of treating this pathology with alternative medicine methods, such as acupuncture, laser puncture, etc., is considered positive. A healthy and moderate lifestyle allows you to prolong the remission of the disease and make attacks less painful.

Surgical treatments

These methods of treatment are resorted to as the last stage, when other methods have not had the desired effect.

Surgical methods of treatment are developing in three directions:

  • dissection of the nerves responsible for the regulation of pressure in the labyrinth;
  • decompression operations;
  • destructive operations.
Dissection of the nerves responsible for the regulation of endolymph pressure in the labyrinth
This type surgical intervention is indicated at the initial stage of the disease, since it usually gives a temporary effect and somewhat delays the progression of the disease. In particular, the drum string is dissected and the nerve plexus of the promontorium is destroyed ( small middle ear structure).

Decompression operations
This type of surgical intervention is indicated in the second and third stages of the disease. Their effectiveness is high, and there are not many side effects compared to destructive operations. The essence of these operations is to form a hole or a small gap in one or more structures in which the endolymph circulates ( vestibular sacs, cochlear duct, endolymphatic sac). As a result, excess fluid will constantly bleed into the cavity of the skull or middle ear, from where naturally will dissolve.

Destructive operations
This type of surgical intervention is rarely used, only when other methods of medical and surgical intervention have not brought the desired result. Its essence lies in the unilateral or bilateral destruction of the labyrinth, after which the pathological impulses from it cease, and the attacks of dizziness disappear. Some time after the operation, the brain partially compensates for the vestibular function of the lost organ due to the joint work of the visual analyzer, the cerebellum and the cerebral cortex. Unfortunately, hearing during these operations is irretrievably lost, and therefore such operations are recommended only at the third stage of the disease, when hearing is already lost.

Prognosis for Meniere's disease

Despite the fact that Meniere's disease is not fatal, it brings considerable suffering to its owners, so it belongs to the category of severe, disabling diseases. Constant attacks of dizziness, nausea and vomiting, jumps in blood pressure and progressive hearing loss up to complete deafness lead to a serious deterioration in the quality of life.




Is Meniere's disease treated with folk remedies?

Meniere's disease is one of the diseases in which the treatment of folk remedies ( herbs, roots, bee products, etc.) has almost no effect.

The main purpose of traditional medicine is to relieve the inflammatory process and antispasmodic effect. Because Meniere's disease is not inflammatory diseases, then the means of traditional medicine in most cases are powerless. Moreover, their use increases the risk of excess fluid intake and impaired electrolyte balance, which can enhance hydrops ( dropsy) of the labyrinth and cause another attack of the disease.

However, one of effective methods, used to urgently reduce pressure in the cavity of the labyrinth, is the application of mustard plasters to the cervical-occipital region and the application of a warm heating pad to the legs. These manipulations lead to the expansion of the vessels of the head, neck and lower extremities, as well as to the redistribution of fluid from the head to the body. This, in turn, leads to a decrease in the rate of endolymph formation and an acceleration in the rate of its evacuation. In addition, under the action of mustard plasters, a reflex expansion of the endolymphatic sac occurs, into which excess endolymph flows, reducing pressure in the cavity of the inner ear and stopping the attack of the disease.

It is difficult to say whether this method to traditional medicine. On the one hand, mustard plasters are less and less considered traditional medicine due to the controversial mechanism of action, unlike conventional medicines. On the other hand, the above method of stopping an attack of Meniere's disease is described in serious medical sources, which does not allow doubting its reliability.

What is the most effective medicine for Meniere's disease?

The most effective treatment for Meniere's disease is a drug called betahistine. It also exists on the market under the commercial name betaserk, tagista, vertran, etc.

Despite the fact that the etiology of Meniere's disease is unknown, and therefore the cause that needs to be eradicated for a complete cure is unknown, betahistine showed the best and most stable effect compared to other groups of drugs used for the complex treatment of this disease. To develop the effect, betahistine should be taken continuously throughout life, if it does not cause significant side effects. The result of the treatment does not appear immediately, but after 3-4 months of taking the drug, when its sufficient concentration is created in the structures of the inner ear.

As a result of clinical studies, patients with Meniere's disease who took this drug according to all recommendations for many years developed attacks of the disease several times less often. The duration of the attack and its severity also decreased, and the tinnitus became quieter and even completely disappeared. The progression of hearing loss slowed down, but did not stop completely. Thus, betahistine is not able to cure Meniere's disease, but greatly facilitates its course and delays the patient's disability due to hearing loss.

Despite the fact that this drug is recommended for use throughout life, it should be temporarily discontinued during an exacerbation of peptic ulcer of the stomach and duodenum. Treatment can be resumed only after endoscopic confirmation of ulcer healing. In addition, this drug is absolutely contraindicated in pheochromocytoma ( benign tumor of the adrenal gland that secretes epinephrine and its analogs) due to an increase in the rate of secretion of biologically active substances. Tumor releases large amounts of adrenaline into the bloodstream leading to life-threatening surges in blood pressure and heart rate. Thus, you can take betahistine only after surgical removal this tumor. With the development of an allergic reaction to the components of the drug, it should be immediately canceled.

Are Meniere's Disease Disabled?

In Meniere's disease, the first or second degree of disability is indicated, depending on the severity of clinical disorders.

When assessing the severity of this pathology, the patient's condition is examined during an attack and in the interictal period ( remission period). Audiometry is performed to determine the severity of hearing impairment. To assess vestibular disorders, an objective neurological examination is performed with mandatory positional tests ( finger-nose test, Romberg test, etc.). An objective assessment of tinnitus is not possible, therefore, they take into account subjective feelings the patient about the frequency and loudness of the noise. Patients in the terminal stage of the disease usually receive a second or even a first degree of disability.

Do I need a diet for Meniere's disease?

According to most researchers, the diet in Meniere's disease does not play a big role, but is welcomed as integrated approach to the treatment of this disease.

With Meniere's disease, constant abstinence from spicy and salty foods is recommended. For one week of each month, the diet should be tightened. Salt must be completely excluded, water consumption should be limited to half a liter per day and one liter on hot days. With active physical work fluid intake may increase, but the patient should be constantly slightly thirsty. It is recommended to increase the proportion of fruits and vegetables in the diet. Dairy products should be present in at least one meal a day. Meat and fish are allowed only boiled 2-3 times a week. Complying with the data simple recommendations on nutrition, in most cases it is possible to increase the remission period for Meniere's disease.

Are there exercises for Meniere's disease?

Exercises for Meniere's disease exist, and they are aimed mainly at restoring the vestibular apparatus after an attack. Exercises to restore hearing, if they exist, most likely do not have the desired effect due to the fact that organic damage to the spiral organ, which develops due to high pressure endolymphs in the labyrinth are irreversible.

Organic damage to the structures of the vestibular apparatus is also practically not restored, however, unlike the auditory analyzer vestibular analyzer can partially compensate for lost functions due to the joint work of the visual analyzer, proprioceptive receptors ( receptors that measure tension in muscles, tendons, and ligaments), cerebellum and reticular formation of the brain.

Exercises for Meniere's disease are aimed at accelerating the body's adaptation to the loss of vestibular apparatus receptors after another bout of dizziness. Such exercises include squatting with support, lifting the head and then the trunk from a supine position, rotation around the axis with support, gymnastics for the eyes, etc. Any exercise that causes the patient moderate dizziness, but not nausea, will do. and vomiting.

You need to start such exercises 2-3 days after the attack. It is advisable to give them a total of at least two hours a day. Of course, you need to do not two hours in a row, but approaches for 20-30 minutes. Daily exercises can reduce the time to restore the previous balance 2 - 3 times faster than it happens when the patient does not exercise.

Mild leukoplakia was first described by B.M. Pashkov and E.F. Belyaeva (1964), differs from regular forms leukoplakia - the presence of slightly elevated foci on the mucous membrane of the cheeks, lips and tongue white color covered with soft scales, easily removed with a spatula.

Acidum arsenicosum is used in dentistry to treat inflamed pulp. This is a sympathetic poison that acts on the smallest blood vessels, they burst, as a result, the nutrition of the pulp tissue is disturbed and it becomes necrotic. Arsenic periodontitis is a consequence of incorrect treatment of acute pulpitis.

Most of the diseases discussed here result in bilateral proximal weakness and atrophy of a symmetrical pattern (with the exception of proximal diabetic polyneuropathy, neuralgic amyotrophy, and, in part, amyotrophic lateral sclerosis) in the arms and legs.

Prothrombin, or factor II, under the influence of factors X and Xa, becomes active, which activates the formation of fibrin from fibrinogen. This mutation is thought to account for 10–15% of hereditary thrombophilias, but occurs in approximately 1–9% of mutations without thrombophilia.

The mucocele of the paranasal sinuses is a kind of retention saccular cyst of any one paranasal sinus, which is formed as a result of obliteration of the nasal excretory duct and the accumulation of mucous and hyaline secretion inside the sinus, as well as elements of desquamation of the epithelium

Mucopolysaccharidoses (MPS) are hereditary metabolic diseases from the group of lysosomal storage diseases. The development of hereditary mucopolysaccharidoses is due to a dysfunction of lysosomal enzymes involved in the degradation of glycosaminoglycans (GAGs) - important structural components of the intracellular matrix.

Mucopolysaccharidosis IV is an autosomal recessive progressive genetically heterogeneous disease resulting from mutations in the genes encoding galactose-6-sulfatase (N-acetylgalactosamine-6-sulfatase), which is involved in the metabolism of keratan sulfate and chondroitin sulfate or in the beta-galactosidase gene (this form is an allelic variant of Gml-gangliosidosis), leading to the manifestation of mucopolysaccharidosis IVA and mucopolysaccharidosis IVB, respectively.

Mucopolysaccharidosis type III is a genetically heterogeneous group of diseases inherited in an autosomal recessive manner. Four nosological forms are distinguished, differing in the severity of clinical manifestations and the primary biochemical defect.

Mucopolysaccharidosis type II is an X-linked recessive disease resulting from a decrease in the activity of lysosomal iduronate-2-sulfatase, which is involved in the metabolism of glycosaminoglycans. Mucopolysaccharidosis II is characterized by progressive neuropsychiatric disorders, hepatosplenomegaly, cardiopulmonary disorders, and bone deformities. To date, 2 cases have been described in girls associated with inactivation of the second, normal, X chromosome.

Mucopolysaccharidosis type I is an autosomal recessive disease resulting from a decrease in the activity of lysosomal a-L-iduronidase, which is involved in the metabolism of glycosaminoglycans. The disease is characterized by progressive disorders of the internal organs, skeletal system, neuropsychiatric and cardiopulmonary disorders.

Cystic fibrosis is hereditary disease that affects the exocrine glands, mainly the gastrointestinal tract and respiratory system. As a result, COPD, exocrine pancreatic insufficiency and abnormal high content electrolytes in sweat. Diagnosis is based on a sweat test or identification of 2 mutations that cause cystic fibrosis in patients with characteristic symptoms.

Cystic fibrosis is a genetic autosomal recessive monogenic disease characterized by a violation of the secretion of exocrine glands of vital important organs with damage primarily to the respiratory and digestive systems, severe course and poor prognosis.

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