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The main symptom of vestibular neuronitis is a pronounced, acutely developing, paroxysmal, but prolonged systemic dizziness, which is usually accompanied by vomiting, imbalance. Often the development of symptoms is preceded by SARS.

Sometimes, some time before the full clinical picture, patients experience brief bouts of imbalance or dizziness. Symptoms of vestibular neuronitis increase during head movements or a change in body position in space. Some decrease in the severity of dizziness occurs when fixing the gaze on one point while maintaining a stationary position of the body. On examination, patients have a rather rough spontaneous nystagmus, while its fast phase will be strictly directed towards the diseased ear.

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At the same time, the imaginary systemic rotation of diclofenac around the patient in the classical versions is directed towards the healthy ear.

When conducting a test (pose) of Romberg, the patient deviates towards the lesion. Hearing with neuronitis is not significantly reduced. At the same time, a neurological examination does not reveal focal symptoms of damage to the brain stem or other parts of the brain. The duration of diclofenac pills is noted from 2-3 hours to several days and, in rare cases, even up to a week. Spontaneous nystagmus can be observed for about 4 days, horizontal nystagmus when the eyes follow the object towards the healthy ear when wearing Frenzel glasses (fixation of the gaze is turned off) is observed up to 3 weeks. After the vertigo attack stops, the patient may experience balance and gait disturbance for some time.

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Video about vestibular neuronitis.

The criteria for diagnosing vestibular neuronitis are the presence of characteristic symptoms: acute, paroxysmal and prolonged (more than 3 hours) systemic dizziness, which is accompanied by nausea and / or vomiting, as well as instability;nystagmus in the direction of the lesion, a positive Halmagi test. According to a number of authors, it is she who, as well as a test for the presence of hidden vertical strabismus (with central causes of acute dizziness, it is often detected) and the characteristics of nystagmus typical of a peripheral lesion (does not change direction depending on the direction of gaze, etc.), allow verify the diagnosis.

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The diagnosis is confirmed using a caloric test, in which there is an areflexia of the vestibular system on the side of the lesion.

In a rare variant, accompanied by damage to the lower branch of the vestibular nerve, such a test will be negative, however, vestibular neuronitis can be diagnosed by conducting a study of vestibular evoked potentials. Also, signs of diclofenac online are observed during MRI with gadolinium, the study will also exclude the diagnosis of stroke and multiple sclerosis.

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Treatment of vestibular neuronitis should be aimed at reducing the degree of dizziness, stopping vomiting (symptomatic therapy), as well as accelerating vestibular compensation.

Symptomatic therapy is reduced to the appointment of the so-called vestibular suppressants. The drug of choice in this case is dimenhydrinate in dosages of 50-100 mg 4 times a day at regular intervals. Metoclopramide, benzodiazepines, and phenothiazines can also be used. When vomiting, injectable forms of drugs are used (cerucal, latran i / m). The duration of therapy with vestibular suppressants is determined by the severity and duration of the presence of dizziness, they are rarely used for more than 3 days, because symptomatic therapy with drugs of this series inhibits recovery, although it brings relief to the patient.

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To restore vestibular function, the best way is to use vestibular gymnastics, you can learn more about the exercises by clicking on the appropriate link.

The combined work of the vestibular, visual and proprioceptive analyzers makes it possible to stop sensory mismatch. It should be remembered that the first days of exercise may lead to some deterioration in well-being, but therapy should not be stopped. The tactics of vestibular rehabilitation and the nature of the exercises directly correlate with the stage of neuronitis, in more detail you can see this relationship in the table in the figure below.

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The positive use of methylprednisolne in stepwise therapy with the gradual withdrawal of the drug has also been shown. The use of antiviral antiherpetic drugs (valacyclovir, acyclovir, etc.) did not show an improvement in the recovery of vestibular function.

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Recovery of impaired functions depends on many factors.

To accelerate the development of mechanisms of vestibular compensation of a central nature in combination with vestibular gymnastics, it is recommended to use betahistine hydrochloride preparations (original drug Betaserc) in a course with a daily dosage of 48 mg (24 mg 2 times a day or 16 mg 3 times a day). Due to the agonistic effect on H3 histamine receptors, an increase in the release of neurotransmitters occurs, exerting an inhibitory effect on the vestibular nuclei in the brainstem. Studies show that betahistine can accelerate vestibular compensation mechanisms.
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Among them are the degree of nerve damage, the rate of compensation of the mechanisms of the central nervous system, the adequacy and timeliness of the prescribed treatment, the usefulness of performing vestibular gymnastics.

It should also be noted that often sick people for a long time note bouts of mild dizziness when changing body position and sharp turns of the head after the illness. A more complete restoration of nerve functions, according to different authors, is observed in about half of the patients after 1 year, 30% have a partial restoration of functions, while the rest retain unilateral vestibular areflexia, which, however, does not cause significant discomfort, due to the mechanisms of vestibular compensation. At the same time, the presence of ongoing complaints can be a sign of a psychogenic state of a person.
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According to the latest data, relapses are not very common, about 5-15% according to different authors, while a healthy nerve can be affected, as well as an already affected nerve (in case of its complete recovery).

(According to early data, relapses are extremely rare (no more than 1-2%), while a healthy nerve is more often affected). It is more logical to look for other causes in case of repeated attacks of systemic dizziness (BPPV, vestibular migraine, Meniere's disease, etc.). Vestibular neuronitis (neuronitis vestibularis, neuropathia vestibularis, acute peripheral vestibulopathy, vestibular neuritis) is an inflammation of the vestibular ganglion, characterized by paroxysmal systemic dizziness *, autonomic disorders, a sharp imbalance, spontaneous nystagmus in the absence of hearing impairment.
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As an independent nosology, it is rarely diagnosed, since the pathology often manifests itself with neuroinfection - measles, influenza, rubella, etc.

The cause of vestibular neuronitis is not known. A viral or infectious-allergic etiology is suspected (as in Bell's palsy), but there is no conclusive evidence for this. In favor of the viral etiology (most often the herpes simplex virus of the first type) of vestibular neuronitis is evidenced by the frequent development of the disease after a respiratory viral infection, the epidemic nature of the disease with a peak incidence in late spring and early summer, as well as cases of simultaneous illness of several members described in the literature. families. The role of the herpes virus is confirmed by cases of the development of herpetic encephalitis with vestibular neuronitis. Vestibular neuronitis is more of a syndrome than a separate nosological form.
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Much less common is the defeat of the lower branch of the vestibular nerve.

With vestibular neuronitis, the upper branch of the vestibular nerve, which innervates the horizontal and anterior semicircular canals, as well as the elliptical sac of the vestibule of the labyrinth, is usually affected, as indicated by the frequent combination of vestibular neuronitis with benign paroxysmal positional vertigo, which is usually caused by otolithiasis of the posterior semicircular canal innervated by the inferior branch of the vestibular nerve.
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Men and women get sick equally often. The disease may be preceded by a respiratory viral infection.

The disease occurs in adults of any age. Sometimes a few hours or days before the onset of an acute vestibular attack, patients experience brief episodes of dizziness or unsteadiness. Vestibular neuronitis presents with a sudden, prolonged attack of dizziness that is often accompanied by nausea, vomiting, imbalance, and fear. Dizziness may decrease with fixation of the gaze. Symptoms are aggravated by head movements or changes in body position. Patients endure this condition extremely hard and often do not get out of bed. Spontaneous nystagmus is characteristic, the slow phase of which is directed towards the affected ear.
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The imaginary rotation of objects around the patient is also typically directed towards the healthy ear.

On the same side, the reaction to a cold test decreases. Positional nystagmus is often noted. In the Romberg test, the patient deviates towards the affected ear. Sometimes there is noise and congestion in the ear. Hearing is not reduced. The audiogram is normal. There are no focal symptoms indicating damage to the brain stem (paresis, diplopia, dysarthria, sensory disturbances).
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