Practice Essentials
Vestibular neuritis, also referred to as vestibular neuronitis, may be described as acute, sustained dysfunction of the peripheral vestibular system with secondary nausea, vomiting, and vertigo. As this condition is not clearly inflammatory in nature, neurologists often refer to it as vestibular neuropathy. It results from inflammation of the vestibular nerve in the ear. [1, 2]
Signs and symptoms
Patients usually complain of abrupt onset of severe, debilitating vertigo with associated unsteadiness, nausea, and vomiting. [3] They often describe their vertigo as a sense that either they or their surroundings are spinning. Vertigo increases with head movement.
Diagnosis
Laboratory studies generally do not help determine the etiology or type of vertigo. However, laboratory studies may be useful to help distinguish between vertigo and other types of dizziness such as light-headedness.
Perform the Hallpike maneuver on all patients who complain of vertigo but do not exhibit nystagmus on routine examination of the extraocular muscles. Failure either to observe or to provoke unidirectional nystagmus casts doubt on whether the process is localized to the peripheral vestibular system.
Management
In most cases of vestibular neuritis, the brain rapidly compensates and adjusts to the new vestibular deficit, or the inflammatory process resolves. Oral medications can help with dizziness and nausea. Vestibular rehabilitation therapy (VRT), which includes balance exercises, appears to be equally as effective as corticosteroids in patients with vestibular neuritis. [4, 5]
Background
Vestibular neuritis, also referred to as vestibular neuronitis, may be described as acute, sustained dysfunction of the peripheral vestibular system with secondary nausea, vomiting, and vertigo. As this condition is not clearly inflammatory in nature, neurologists often refer to it as vestibular neuropathy. [1, 2]
Although vestibular neuritis and labyrinthitis may be closely related in some cases, vestibular neuritis is generally distinguished from labyrinthitis by preserved auditory function.
Pathophysiology
The etiology of vestibular neuritis remains largely unknown, yet it appears to be a sudden disruption of afferent neuronal input from 1 of the 2 vestibular apparatuses. This imbalance in vestibular neurologic input to the central nervous system (CNS) causes symptoms of vertigo. At least some cases are thought to be due to reactivation of latent herpes simplex virus type 1 in the vestibular ganglia. [2]
Epidemiology
Frequency
Dizziness is the primary ED complaint in 3.3% of US ED visits, and approximately 5.6% of these patients are diagnosed with vestibular neuritis or labyrinthitis. Thus, the annual incidence of these two diagnoses in US EDs is approximately 150,000 patients. [6]
Mortality/Morbidity
Most patients experience complete recovery within a few weeks. A minority have recurrent vertiginous episodes following rapid head movement for years after onset. [7]
Demographics
Studies have shown no consistent male or female predominance. [8] Vestibular neuritis occurs most commonly in middle-aged adults; mean age of onset is 41 years. [8]
Prognosis
Most patients recover from severe vertigo and imbalance within 1 week.
A minority have recurrent, less severe attacks or persistent symptoms. The likelihood of incomplete long-term recovery can be predicted based on initial bedside testing. [9]
Patient Education
In general, movement and activity, to the extent they can be tolerated by the patient, may hasten cerebral compensation and recovery. Eventually, patients can be taught exercises of the eyes and neck to hasten cerebral compensation and recovery. Exercises are seldom practical during the acute episode because of patient discomfort.
