Vestibular neuritis is a selective lesion of the vestibular nerve, presumably having an inflammatory genesis and manifested by a single acute paroxysm of intense dizziness with balance disorder and complete hearing loss. Compensation of vestibular function after an episode of vertigo may take several weeks. Diagnosis is carried out by methods of examination of the vestibular analyzer, according to the indications, an MRI is performed. The basis of treatment is the appointment of vestibular suppressors in the first days and the subsequent use of vestibular gymnastics. The prognosis is favorable.
H81.2 Vestibular neuritis
Vestibular neuritis is a syndrome of acute vestibular dysfunction, not accompanied by a hearing disorder and occurring as a single episode of dizziness, lasting from 2-3 hours to several days. It was first described in 1909, then in more detail in 1924. The name “vestibular neuritis” was introduced into practical neurology in 1949. Vestibular neuritis is the 3rd most common acute vestibular vertigo syndrome. Mostly people in the age category from 30 to 60 years get sick. An increase in the incidence is observed in late spring. Recently, there has been a trend towards an increase in the number of patients turning to doctors for dizziness and balance disorders. In each case, it is important to correctly determine the cause of these symptoms and determine the form of the disease for the appointment of adequate treatment in the future.
The etiofactors of vestibular neuritis are not entirely clear. The substrate of the disease is considered to be an inflammatory process that selectively affects the vestibular nerve. Most likely, the inflammation has a viral etiology. This is confirmed by the manifestation of neuritis after undergoing acute respiratory infections. There are cases when herpetic encephalitis developed against the background of vestibular neuritis, and therefore it is assumed that one of the etiofactors is the herpes simplex virus. The described cases of the disease of several family members at once testify in favor of the infectious etiology.
A number of authors speak in favor of the infectious-allergic mechanism of development of vestibular neuritis, in which viruses are sensitizers and provoke a local autoimmune inflammatory process. Inflammation usually affects the upper branch of the vestibular nerve. Pathology of the lower branch is noted much less often. The auditory nerve remains completely intact. In addition, cases of vestibular neuritis of toxic genesis caused by the use of aminoglycoside antibiotics, in particular gentamicin, have been described.
Vestibular neuritis symptoms
The basis of the clinical picture is a paroxysm of transient systemic dizziness. The patient may feel the illusion of passive movement of his own body in space (circling, swaying on the waves, sinking) or imaginary movement of objects surrounding him. The latter is called “oscillopsia”. As a rule, the subjectively felt movement of objects around the patient occurs in the direction of the affected side. The intensity of dizziness increases with changes in posture and head movements; it may fall when the patient tries to fix his gaze at one point. Paroxysm is accompanied by nausea and vomiting, shakiness and instability due to an imbalance.
In some cases, patients indicate short-term episodes of instability or dizziness that preceded the attack. Such “harbingers” can be observed both a few days before the development of the main paroxysm of vestibular neuritis, and a couple of hours before it. The duration of acute vestibular paroxysm varies from several hours to 2-3 days. After it, some instability usually persists, lasting up to several weeks. In some patients, there is a persistent persistence of unilateral vestibular dysfunction, but over time it is compensated and does not lead to a clinically noticeable functional change.
Vestibular neuritis is not accompanied by a recurrence of vertigo paroxysms. Relapse is observed only in 2% of cases and affects only the previously healthy side. If a patient with a diagnosis of vestibular neuritis has new episodes of acute intense dizziness, then doctors should reconsider the diagnosis.
The systemic nature of dizziness indicates a lesion of the vestibular apparatus. In the neurological status, spontaneous nystagmus with a rapid phase in the direction from the affected ear is noted. It persists for 3-5 days after the end of the paroxysm. For another 2 weeks, nystagmus is detected, which occurs when the gaze is diverted towards the healthy side. In the Romberg pose, the patient is deflected to the affected side. The absence of general cerebral symptoms, signs of trunk damage and other focal manifestations excludes the central nature of the pathology (intracerebral tumor, stroke, encephalitis, meningitis, etc.). The study of the auditory analyzer using audiometry determines the complete preservation of hearing. The absence of hearing loss indicates a selective lesion of the vestibular analyzer.
In addition to an examination by a neurologist or an otoneurologist, a consultation with a vestibulologist with vestibulometry, electronystagmography and other studies of the vestibular analyzer is recommended to clarify the diagnosis. The diagnosis can be confirmed by the detection of unilateral vestibular areflexia or hyporeflexia when performing indirect otolithometry (caloric test). With negative results of the latter, a study of vestibular VP (evoked potentials) is carried out, since the pathology of the lower branch of the nerve does not lead to changes in the results of indirect otolithometry. In complex cases, MRI of the brain makes it possible to exclude intracranial pathology and identify indirect signs of neuritis.
In the course of the diagnostic search, it is necessary to differentiate the symptoms of neuritis from the manifestations of acute labyrinthitis, perilymphatic fistula, Meniere’s disease, transient ischemic attack, vertebral artery syndrome, first-time vestibular migraine paroxysm. The difference between acute labyrinthitis is its appearance against the background of acute otitis media or systemic infectious disease, the presence of hearing disorders in the clinical picture. In the anamnesis of patients with perilymphatic fistula, as a rule, there is a connection with barotrauma, traumatic brain injury, straining or severe cough; the diagnosis is clarified with the help of a fistula test.
It is most difficult to differentiate vestibular neuritis from the first episode of Meniere’s disease. In favor of the latter is a combination of dizziness with ear noise, hearing loss and a feeling of bursting inside the ear. A feature of migraine is the presence of a headache uncharacteristic for neuritis. Transient ischemic attack has a duration of up to 24 hours with the complete disappearance of neurological, including vestibular, symptoms after this period. Vertebral artery syndrome occurs with repeated episodes of dizziness of shorter duration, usually occurs against the background of pathology of the cervical spine (osteochondrosis, cervical spondylosis, Kimberly anomalies).
Treatment and prognosis
Drug therapy is symptomatic and is aimed at relieving dizziness and vestibular dysfunction. The main drugs are vestibulosuppressors: dimenhydrinate, metoclopramide, phenothiazines (fluorophenazine, thiethylperazine, thioridazine, promazine), benzodiazepine tranquilizers (nosepam, diazepam, gidazepam). Due to vomiting, these pharmaceuticals are administered intramuscularly or in the form of candles. The duration of their use is dictated by the severity of dizziness. It is usually limited to 3 days, since these drugs inhibit vestibular compensation.
Clinical studies have shown a greater percentage of complete vestibular recovery in patients who took methylprednisolone at a dose of 100 mg in parallel with the main treatment for the first 3 days, followed by a decrease in dosage by 20 mg every 3 days. The use of antiviral drugs, in particular antiherpetic agents) did not show a significant increase in the effectiveness of therapy. A number of clinicians suggest the use of betahistine as a drug that accelerates vestibular compensation. However, its reception does not replace the mandatory performance of vestibular gymnastics.
Vestibular gymnastics aims to achieve vestibular compensation as soon as possible. It is recommended from 3-5 days of illness, when the patient completely passes vomiting. Before this period, the patient should observe bed rest with immobilization of the head. The first exercises of vestibular gymnastics are turns in bed and sitting down. When the patient manages to suppress nystagmus by fixing the gaze, exercises with fixing the gaze from different angles of vision, smooth eye movements, horizontal and vertical movements of the head with fixed gaze are introduced. During this period, the patient is gradually allowed to stand and walk. As a training exercise, walking with closed eyes with support from the outside is used. On the 5th-7th day, provided there is no nystagmus with a direct view, exercises are introduced to train static and dynamic balance. On the 2nd and 3rd weeks, complex exercises exceeding the usual vestibular loads are recommended.
After suffering from neuritis, complete restoration of vestibular function is noted in about 40% of those who have been ill, incomplete — in 30%. The remaining patients have persistent vestibular areflexia. However, due to its unilateral nature and the development of vestibular compensation, it does not cause any discomfort in the daily life of patients.