Vestibular Neuritis

Synonym: Vestibular neuronitis

Strictly speaking the term means inflammation of the vestibular nerve but the aetiology is often obscure and vestibular neuropathy may be a more accurate term. There is sudden disruption of afferent neural input so that acute vertigo results. Animal experiments and histology studies of temporal bone in individuals who have had vestibular neuritis suggest a viral cause. Reactivation of latent herpes virus is one possibility. However, local ischaemia may also be important at times.^1,2,3

There is no gender predominance and the mean age of onset is 41 years.³

History

• Onset is usually very abrupt.
• There is unsteadiness, nausea and vomiting.
• They feel as if the room is rotating.
• Moving the head aggravates symptoms.
• Distinguish between true rotational vertigo and giddiness, faintness or weakness. Patients are often very vague in the terms they use and may attempt medical terminology but get it wrong.

Examination

• Spontaneous, unidirectional, horizontal nystagmus is characteristic. The fast direction is towards the healthy ear. The fast direction may be the more obvious but it is really the correction of the pathological slow direction.
• Nystagmus may be apparent only on gazing away from the affected side or it may be suppressed by optic fixation.
• On walking or during the Rhomberg test, the patient tends to fall towards the affected side.

The following should be sought as their presence suggests that it is not vestibular neuritis:

• Nystagmus is multidirectional and does not fatigue on repetitive testing
• Hearing loss
• Abnormalities of cranial nerves other than VIII
• Red tympanic membrane
• Cerebellar ataxia
• Mastoid tenderness, nuchal rigidity or high fever

If it was not possible to demonstrate the vertigo the Hallpike manoeuvre may be employed:⁶

• Get the patient to sit on the couch with the head end flat.
• The patient should lie back from sitting to supine 3 times. The first time the head faces forward with the neck slightly extended. The second time the head is turned 45º to one side and the third time to the other side.
• The patient should keep both eyes open all the time. Each time check for signs of nystagmus and ask about feelings of vertigo.

There is usually a slight latent period of just seconds between the manoeuvre and the onset of symptoms and signs. There is also a tendency for them to fatigue with repeated testing. If these features are not present it suggests that the aetiology might be central, in the brain, rather than peripheral in the vestibular apparatus.

• The diagnosis can usually be made clinically and blood tests are usually unhelpful.
• Imaging studies (e.g. brain MRI or CT) may demonstrate tumours, haemorrhage or ischaemic stroke or demyelination. Imaging tends to be reserved for cases where more sinister pathology is suspected.

• Benign positional vertigo
• Labyrinthitis
• Ménière's disease
• Stroke, especially posterior inferior cerebellar artery syndrome (PICA)
• Multiple sclerosis
• Subarachnoid haemorrhage
• Tumours of the brain or acoustic neuroma
• Cervical spondylosis

• If the patient has marked vertigo with vomiting an antiemetic is useful and it may suppress the vertigo too. Nausea will retard gastric emptying and it may reverse and so an injection may be required.
• If the patient has recurrent attacks and needs self-administered medication, buccal prochlorperazine may be appropriate.
  Meclizine, promethazine, domperidone and other antihistamines may be useful.
• The speed of recovery can be improved by use of steroids, but a recent trial of prednisone failed to demonstrate any effect on long-term prognosis.^7,8
• Antiviral agents do not appear to help, either alone or with steroids.⁹

Most patients recover within a week but some suffer recurrent attacks.³ One study found a persistence of dizziness related to anxiety in one third of patients one year after the initial episode.¹⁰