Vestibular neuronitis / neuritis Vestibular neuritis is The secondmost common cause of vertigo arising from a disorder of thelabyrinth is caused by inflammation of the vestibular nerve, thenerve that connects the balance portion of the inner ear to the brain.It is manifested by a sudden attack of rotatory vertigo often associated with nausea, vomiting, and sweating.
What are the causes? (Aetiology and pathology)
Vestibular Neuritis is thought to be caused by a viral infection of the balance nerve that runs from the inner ear to the brain. Various theories have been proposed to account for the cause of vestibular neuritis including inflammation of the vestibular nerve and ischemia of the labyrinth. Many of the histological features of vestibular neuritis when evalu¬ated in postmortem studies are similar to those observed in other sensory epithelia in known viral disorders. Herpes simplex virus type 1 (HSV -1) DNA has been detected on autopsy with the use of polymerase chain reaction in 66% of human vestibular ganglia. Reactivation of a latent infection with HSV -1 is presumed to account for the occurrence of vestibular neuritis.
The condition chiefly affects adults between the ages of 30 and 50 years without preference for sex.
Vestibular neuritis affects the superior division of the vestibular nerve more commonly than the inferior division. The superior division has a longer course through bone than does the inferior division and is therefore more liable to affection from ischemia, injury and entrapment.
Because of the association of the disorder with reactivation of HSV-l, the condition is also referred to as vestibular neuronitis.
Some patients will report having an upper respiratory infection (common cold) or a flu prior to the onset of the symptoms of vestibular neuritis, others will have no viral symptoms prior to the vertigo attack.
What are the symptoms?
The main symptom of vestibular neuronitis is vertigo, which appears suddenly, often with nausea and vomiting. Vertigo usually lasts for several days or weeks. It can come as a single attack or as a series of attacks of vertigo or a constant sense of balance carrying on for two to four weeks before diminishing. It may follow an upper respiratory tract infection. The cochlea (hearing portion) of the inner ear is unaffected and therefore the patient’s hearing function is normal.
Onset:- (The Acute phase) Vertigo is the leading symptom. The onset is sudden with, in some cases, transient paroxysms of vertigo accompanied by black-outs or drop-attacks, in others a feeling of imbalance, especially when walking or standing, aggravated by movements of the head indicating a sudden and partial or complete loss of vestibular function on one side,. Vertigo may be accompanied by nausea or vomiting but never by tinnitus or deafness. The presence of hearing loss in the affected ear may indicate labyrinthitis, an acute Meniere disease attack or infarct of the brainstem or cerebellum (often in the territory of the ante¬rior inferior cerebellar artery).
The patient should be made to walk, however difficult it may be, as severe gait ataxia strongly points to a central cerebrovascular event such as cerebellar infarction – especialli in the territory of the poste¬rior inferior cerebellar artery (PICA). Magnetic resonance imaging (MRI) with diffusion weighted images should be performed when indicated based upon clinical suspicion of an infarct.
Later:- (The Subacute phase) The intense vertigo of acute vestibular neuri¬tis can last from hours to days and rarely weeks. This phase is characterized by imbalance and disequilibrium that noticeably improves over this time. Patients will have sensitivity to motion and may avoid head turns and rapid movements.
They may develop brief attacks of vertigo that are not as intense as the initial attack. Vestibu1ar rehabilitation during this phase may speed recovery.
At the end of the subacute phase the patient will be near their baseline balance function but may notice small disturbances of equilibrium with rapid motions or in challenging environ¬ments. If evaluated for dizziness at this late stage, a diagnosis of vestibular neuritis is based largely on a suspicious history of severe vertigo within the prior months to year. Additional test¬ing, as described below, may also demonstrate a unilateral weakness confirming an insult to the inner ear. Commonly in this stage anxiety plays a major role in the patients perception of their debility. A significant portion of patients with acute vertigo will develop anxiety regarding their balance and potential for having recurring ver¬tigo. They will often limit activities such as driving, withdraw socially and become intensely fixated on any abnormal sensation of equilibrium. A psychological consultation in any vestibular neuritis patient with a dependent or insecure personality type is advisable.
In rare cases it can take months to go away entirely. Vestibular neuronitis does not lead to loss of hearing. One may notice that vision is disturbed or jumpy on looking to a particular side.
How is the diagnosis confirmed?
Pure tone Audiometry, Impedance bridge studies and vestibular (balance) tests – Electronystagmography is the gold standard by which the function of the balance organ is measured. A C.T.Scan or M.R.I.Scan of the brain is not required immediately and usually turns out to be normal.
Evaluation and Diagnostic Testing
Physical Examination. Findings on physi¬cal examination will generally depend upon the stage of vestibular neuritis. In the acute phase, the examiner will note spontaneous nystagmus the eyes move in the plane of the affected semicircular canal(s).
The nystagmus will increase in amplitude with gaze toward the horizontal fast phase component, which is usu¬ally toward the nonaffected ear. The nystagmus should suppress with visual fixation but may be of such intensity as to be reduced in amplitude but remain noticeable. Direction changing nys¬tagmus and lack of visual suppression should raise the suspicion of a central event and prompt imaging for stroke evaluation. The presence of ataxia is also suggestive of central vestibular dys¬function or, rarely, a drug reaction.
Hearing should be checked during the acute phase A hearing loss is inconsis¬tent with vestibular neuritis, and the practitioner should consider labyrinthitis, Meniere disease, perilymphatic fistula, or acute otitis media among otologic causes of acute cochleovestibular symptoms.
The spontaneous nystagmus has usually resolved in the subacute phase although nys¬tagmus may be observed with gaze toward the unaffected ear
Electronystagmography Objective testing can be used to identify the unilateral vestibular hypofunction characteristic of vestibular neuritis. Caloric test¬ing showing an asymmetry is consistent with a history of unilateral vestibular insult. This test is more sensitive than either head thrust or head shake for identifying such an asymmetry. The ENG battery of tests can also be used to assess for the presence of.BPPV which occurs often after vestibular neuritis. In the acute and subacute phases, ENG can identify and document spontaneous and gaze evoked nys¬tagmus as well as determine their direction thus helping to identify the affected side. The ENG is important to distinguish a PICA thrombosis (in which ENG is normal) from Vestibular neuronitis in which it is always abnormal.
Imaging. The acute phase of vestibular neu¬ritis is of such severity and duration that clini¬cal examination alone may not be sufficient to rule-out central vascular events. Thus, computed tomography (CT) scan is the initial imaging test of choice to look for an acute hemorrhage involving the brainstem or cerebellum. MRI of the internal auditory canals during an acute phase of vestibu¬lar neuritis may show subtle enhancement of the superior vestibular nerve at the region of Scarpa ganglion. Beyond the acute phase, MRI with gadolinium enhancement is most useful for eval¬uating for other intracranial lesions that could account for an attack of vertigo or prolonged vestibular dysfunction. Tl-weighted images with contrast can demonstrate the presence of vestib¬ular schwannoma. Sudden vertigo is the initial presenting sign for vestibular schwannoma in approximately 15% of cases. It is rare in isolation and usually accompanies hearing loss. The presence of Chiari I malfor¬mation, cerebellar tumor, cerebellopontine angle arachnoid cyst, old brainstem infarct, or vascular loop can also be identified with MRI.
Management. Supportive treatment should also be given during the acute phase of vestibular neuritis.
Acute phase – Combination treatment of Methylprednisolone in a dosage of 48 mg. daily for the first 3 days tapered by 16 mg every 3 days for a total treatment time of 20 days and
Va1cyclovir admiistered as 1,000 mg three times per day for 1 week.
Patients should be hydrated if they are having significant vomiting and provided antiemetics.
Vestibular suppressants can also be prescribed to attenuate the severity of the attack. The treatment of vestibular neuronitis is medical, and depends entirely upon the severity of symptoms. Some patients’ will be so disabled as to require a period of rest in bed, others will be able to continue to get about, but all will probably require labyrinthine sedation to tide over the period of activity of the disease. As in Meniere’s disease promethazine theoclate (Avomine) or dimenhydrinate (Dramamine) tablets are useful drugs for suppressing the symptoms of vertigo and nausea.
Low dose valium is an effective vestibular suppressant, and mini¬mally sedating dosages of 2 mg every 6 hours as needed can be provided. Attempts should be made to wean the patient off of vestibular suppressants as soon as possible to allow central compensation of the unilateral hypofunction.
Once the patient has entered the subacuate phase of their attack, vestibular rehabilitation exercises should be recommended VOR exercises can speed central compensation for the unilateral weakness Patients experiencing chronic daily disequililibrium should be evaluated for psychogenic dizziness trigered by the initial neurotologic disorder. Additionally, an attack of vestibular neuritis may exacerbate underlying psychiatric or anxiety disorders.
The condition pursues a benign although sometimes protracted course and symptomatic recovery is the rule. Reassurance that recovery is confidently to be anticipated. Even when vertigo has been initially severe and immobilizing the recovery period does not often exceed 3 weeks.
Caloric responses generally remain permanently abnormal.
D.D. In Meniere’s disease deafness is always present, a feature which should immediately eliminate a diagnosis of vestibular neuronitis
Other forms of labyrinthitis, toxic, vascular or infective, may at times be difficult to differentiate, but if it is remembered that the diagnosis of vestibular neuronitis requires the stringent double verification of abnormal caloric reactions and normal cochlear audiograms.
How is an acute attack managed?
During an acute attack, lie down on a firm surface. Stay as motionless as possible and keep your eyes open and fixed on a stationery object in front of you. Do not try to sip or drink water as this may cause vomiting. Stay like this till the severity of vertigo subsides. Avoid the position causing the vertigo.
How is it treated?
Medical treatment based on results of investigations by a vertigo specialist usually involves a combination of medication and vestibular rehabilation therapy and course of exercises is advised. Also special exercises help to come back to normal early.
Appropriate Vestibular Rehabilitation Excersies help to recover quickly.