DIFFERENTIAL DIAGNOSIS OF PERIPHERAL VESTIBULAR DISORDERS

Differential Diagnosis of Peripheral Vestibular Disorders

PART 8: Vestibular Neuritis

Acute vestibular neuritis has also been known by many other names – vestibular neuronitis, neurolabyrinthitis, viral labyrinthitis, epidemic vertigo and acute vestibulopathy of unknown etiology. The clinical effects of this disorder are very dramatic and usually precipitate a visit to the emergency room. The patient experiences a sudden onset of severe whirling vertigo without a change in hearing. The vertigo is incapacitating and associated with nausea, vomiting and diaphoresis. Physical exam will show a distressed patient with spontaneous nystagmus with the fast phase beating away from the affected ear. The vertigo is persistent and the most severe symptoms will slowly resolve over several days to weeks after onset. The disease is mostly self-limited with most patients have complete resolution of their symptoms. Treatment is supportive with use of vestibular suppressant and anti-nausea medications at the onset of the disorder and vestibular rehabilitation exercises to hasten central vestibular compensation.

Clinical Presentation

Vestibular neuritis has such a dramatic presentation that when you have seen it once, you will never forget it. This patient is severely ill. There may be a history of a prior cold or upper respiratory infection in the days or weeks prior to the onset of the acute vertigo. It has been noted by many to have a seasonal occurrence and occur in epidemic fashion. The characteristic symptom is a single, acute, severe episode of vertigo without any associated auditory or neurologic symptoms. The vertigo will generally progress to a severe spinning sensation associated with nausea, vomiting and diaphoresis over the course of just a few minutes. Very often the patient (and often the physician) will be convinced that he is having a stroke or a heart attack, precipitating a visit to the emergency room.

There are almost never any auditory symptoms to suggest that the process is related to the ear and there are no other neurologic symptoms. The vertigo will be persistent and gradually improve over the course of several days to weeks. After this, the patient usually notes symptoms brought on only by quick head movements, particularly to the affected side. The patient may feel off balance for several months after the incident and in some cases may have symptoms persist for years. Additionally, it is not uncommon for patients to develop BPPV after a bout of vestibular neuritis.

Symptoms:

One severe, prolonged episode of vertigo, nausea, vomiting, and diaphoresis
No auditory symptoms, no other neurologic symptoms
May develop BPPV
No recurrence of vertigo

Pathophysiology

The pathophysiology is felt to be a viral inflammatory process of the superior division of the vestibular nerve or a vascular occlusive process resulting in sudden loss of superior division of the vestibular nerve function on the involved side. There is inflammatory cell infiltrate and edema. Eventually there is neural degeneration and replacement of neural elements with fibrous tissue. The end result is a significant loss of neural innervation of the vestibular end organ.

This denervation may be partial or complete. Because the superior division of the vestibular nerve is selectively affected, function of the endorgans innervated by the inferior vestibular nerve are preserved - namely the saccule and the posterior semicircular canal. Additionally, there may be degeneration of the vestibular end organ – the utricle, the horizontal and the superior semicircular canal ampullae. Degeneration of the otolithic organ (utricle) can result in the dispersement of otoconia, which can result in secondary BPPV.

Diagnosis

The diagnosis is made by a typical history and exclusion of other causes of sudden loss of unilateral vestibular input. This can be accomplished by history. Physical examination during the acute phase of vestibular neuritis will demonstrate horizontorotary nystagmus with the fast phase beating to the uninvolved side. An otherwise normal neurologic exam is important to distinguish this from an acute cerebellar hemorrhage or infarct. Imaging studies are usually normal, but high resolution MRI with Gd may show enhancement of the VIII^th nerve. ENG will demonstrate absent or significantly reduced caloric response on the involved side. Spontaneous nystagmus may or may not be seen on the ENG depending on how soon after the insult the ENG was performed.

Diagnosis:

Appropriate history and physical exam
Absent or significantly reduced caloric response on ENG
Normal imaging studies

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