Vestibular neuritis

Vestibular neuritis

Updated 2020

What is vestibular neuritis?

Vestibular neuritis is the sudden loss in function of the vestibular nerve. It is caused by a virus which attacks and damages one of two branches of the vestibular nerve. Due to the fact that the left and the right vestibular organs are in balance, the sudden loss of function in one causes the patient to experience vertigo, dizziness and loss of balance.

How common is vestibular neuritis and who is at risk?

It is estimated that 5% of all dizziness and 15% of all vertigo occur due to vestibular neuritis. It occurs equally in males and females but is rare in children.

Vestibular neuritis
Vestibular neuritis

What is the cause of vestibular neuritis?

It is most believed that the Herpes simplex type 1 (HSV-1) or cold sore virus attacks the vestibular nerve of the inner ear and causes the condition. In some cases, Varicella Zoster (the shingles virus) can cause vestibular neuritis. Vestibular neuritis often follows a viral upper respiratory tract infection. It usually occurs in spring and early summer and may affect more than one family member.

Another possible cause of vestibular neuritis may be the sudden loss of blood flow to the inner ear as seen with small clots or spasm.

What is the difference between vestibular neuritis, vestibular neuronitis and labyrinthitis?

Vestibular neuritis implies that there is inflammation (neuritis) of the vestibular nerve. It is more common to involve the superior vestibular nerve (85% of cases). In 15% of cases the inferior vestibular nerve is involved.

The term neuronitis is used if the site of involvement is the sensory nerves of the vestibular ganglion or in the brainstem vestibular nucleus.

If hearing loss is also present it is referred to as labyrinthitis. The inflammation affects the whole labyrinth is usually caused by an infection. It may also describe involvement of the whole 8th cranial nerve.

The different terms used above indicate that we are still not exactly sure which part(s) are involved in each case and that different sites may be involved, leading to the same clinical picture.

Acute vestibular syndrome.

Nowadays, some experts prefer to use the term acute vestibular syndrome (AVS) in all patients that present with acute (sudden onset) vertigo without hearing loss suggestive of vestibular neuritis. The reason for this is that 25% of brainstem and cerebellar strokes may mimic vestibular neuritis. It is estimated that 1 in 5 strokes causing AVS effects patients aged 50 years. Therefore, before calling it vestibular neuritis, stroke must be excluded!

How does a patient with vestibular neuritis present?

Symptoms include sudden onset of rotational vertigo, dizziness, disequilibrium and a tendency to fall to one side. Sweating, nausea, vomiting may be present, but pain is not typical and may indicate infection. Patients display nystagmus (repetitive involuntary jerking eye movements). Hearing loss is absent. The symptoms may be severe for a few days and it is common for patients to experience dizziness and motion sensitivity for a few weeks.

Which other conditions should be considered in a patient with vestibular neuritis?

The most important condition to rule out in AVS is stroke.
Other conditions include:

  • Transient ischaemic attacks (TIA)
  • Migraine associated vertigo (MAV)
  • Meniere’s disease (MD),
  • Vestibular schwannoma and other inner ear tumours
  • Multiple sclerosis (MS)
  • Labyrinthitis

Special investigation for vestibular neuritis.

Videonystagmography (VNG) can be used to record and analyse the nystagmus.

The video head impulse test (VHIT) has emerged as one of the most helpful tests in differentiating vestibular neuritis from other conditions. It may help to distinguish vestibular neuritis from stroke. The VHIT can help to localize the damage and can also be used in monitoring recovery and response to vestibular rehabilitation.

Vestibular evoked myogenic potential (VEMP) testing may help to confirm the specific branch of the vestibular nerve that is affected but is seldom used in the acute setting.

Magnetic resonance imaging (MRI) may be required to rule out other brain pathology. In vestibular neuritis it may show inflammation of the vestibular nerve.

Blood tests are rarely of value and indicated more often to exclude other conditions. If hearing loss is suspected an audiogram may be requested.

Management of vestibular neuritis.

Initial management with medication is mainly symptomatic and includes vestibular suppressants, anti-nausea medication, anti-viral, betahistine and steroids. If infection is suspected antibiotics will be added and if a stroke, an anti-clotting agent is an option. Patients usually must be admitted in order to treat dehydration with intravenous fluids.

After the acute stage of vertigo and nausea has settled vestibular rehabilitation exercises are indicated. Depending on the severity of the damage to the nerve, it can take weeks to recover.

Vestibular rehabilitation exercises aim to help the brain to compensate for the damaged nerve. The more meticulously it is performed, the better the outcome. The vestibular rehabilitation exercises may lead to dizziness and even nausea in the beginning but as time goes on and the brain compensates symptoms will improve. It may also be advisable to ‘push’ yourself in order to maximise the point of recovery.

Prognosis of vestibular neuritis.

The recovery is variable but overall, the prognosis is good. The level of recovery depends on 3 factors namely:

  • the severity of the damage
  • the level of recovery of the vestibular function
  • the level of central compensation that occurs

Recovery usually occurs within a few weeks but may take up to 1 year and be incomplete. It may impact more on patients in certain professions, such as pilots. Vestibular neuritis may recur in cases of incomplete damage, but luckily recurrent vestibular neuritis is quite rare.

It is more common, however, for patients who suffered from vestibular neuritis to develop benign paroxysmal positional vertigo (BPPV) at a later stage. If the cause was loss of blood flow to inner ear it is then referred to as the Lindsay-Hemenway syndrome.