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]
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.
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.
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]
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.
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]
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]
Most patients experience complete recovery within a few weeks. A minority have recurrent vertiginous episodes following rapid head movement for years after onset.[7]
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]
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]
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.
Patients with vestibular neuritis 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.
Spontaneous, unidirectional, horizontal nystagmus is the most important physical finding in vestibular neuritis.[10, 11] Fast phase oscillations beat toward the healthy ear. Nystagmus may be positional and apparent only when gazing toward the healthy ear, or during Hallpike maneuvers. Patients may suppress their nystagmus by visual fixation.
Patient tends to fall toward his or her affected side when attempting ambulation or during Romberg tests.
Affected side has either unilaterally impaired or no response to caloric stimulation.
Vestibular neuronitis is unlikely if any of the following findings are present. The following symptoms should be absent:
The head impulse test is a test for normal ocular fixation in association with rapid passive head rotation. An abnormal response is indicated by an inability to maintain fixation during head rotation with a corrective gaze shift after the head stops moving. An abnormal test seems to be sensitive, but not perfectly specific, for a peripheral vestibular disorder.[12, 13]
One group has combined the head impulse test with an assessment of nystagmus type and a test of skew to form the HINTS test, a three-component eye movement battery of tests.[13, 14, 15] This clinical battery of tests appears helpful in differentiating vestibular neuritis from a more dangerous central process such as cerebellar stroke, though it awaits further independent confirmation.[13, 14]
Viral infection of the vestibular nerve and/or labyrinth is believed to be the most common cause of vestibular neuritis.[2]
Acute localized ischemia of these structures also may be an important cause.
Especially in children, vestibular neuritis may be preceded by symptoms of a common cold. However, the causative mechanism remains uncertain.
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.
Consider abnormal serum glucose, anemia, or any ongoing cardiac dysrhythmia when patients report feeling light-headed.
Cerebral imaging may be necessary to assess causes of central vertigo.
Possible causes of central vertigo include the following:
Because significant bony artifacts degrade CT images of the posterior fossa, MRI is the preferred imaging modality when available.
Imaging generally is not indicated in patients with isolated vertigo, in those with no history or physical findings that suggest any diagnosis other than vestibular neuritis, and in those without cerebrovascular disease risk factors. A lower threshold for imaging should be maintained for elderly patients or those with risk factors for cerebrovascular disease. These patients have a higher risk for a central cause of vertigo, even when no other symptoms manifest. In one study, 10% of patients with cerebellar infarction presented with isolated prolonged vertigo suggestive of vestibular neuritis.[16]
Perform the Hallpike maneuver on all patients who complain of vertigo but do not exhibit nystagmus on routine examination of the extraocular muscles.
Hallpike maneuver requires patient to lie back from sitting to supine position 3 times. The first time, have the patient lie back with the head facing forward and the neck slightly extended; repeat this movement with the patient's head turned 45 degrees to the right and a third time with the head turned 45 degrees to the left.
Instruct patient to keep both eyes open each time he or she lies back.
Check for nystagmus and ask patient about any symptoms of vertigo.
Among the characteristics of an elicited nystagmus that would suggest disease of peripheral origin are a pause before nystagmus appears (latency), unidirectional nystagmus, and fatiguing of nystagmus after approximately 1 minute or repeated inductions.
Failure either to observe or to provoke unidirectional nystagmus casts doubt on whether the process is localized to the peripheral vestibular system. Either finding suggests a need to consider other diagnostic alternatives.
Bedside tests (head-impulse, head-heave, head-shake, and vibration tests) are effective in the diagnosis and prediction of the time to recovery from vestibular neuritis.[9]
There is no standard treatment for vestibular neuritis. In most cases, the brain rapidly compensates and adjusts to the new vestibular deficit, or the inflammatory process resolves.
Multiple oral medicines that can help with dizziness and nausea are available (see Medication).
Evidence indicates many sedating medicines commonly used for this condition may slow recovery. Thus, medical treatment may reduce symptoms but prolong recovery.
Vestibular rehabilitation therapy (VRT), which includes balance exercises, appears to be equally as effective as corticosteroids in patients with vestibular neuritis.[4, 5]
ED physicians must first distinguish true vertigo from other types of dizziness. Then, after determining that the patient truly has vertigo, central vertigo must be ruled out through a careful history, physical examination, and, if still uncertain, imaging studies.
Regardless of the vertigo's etiology, ED physicians should attempt to alleviate patient suffering. An intravenous (IV) line often is started to rehydrate the patient, who should be allowed to lie still in bed as desired. Parenteral medicines then are administered.
Consider admission for patients who have persistent vomiting despite treatment and for patients unable to walk satisfactorily.
In cases of vestibular neuritis refractory to acute medical treatment, ED physicians may wish to consult with a neurologist or otolaryngologist.
Several types of medications have been used to treat vestibular neuritis. Treatment generally has been based on responses of patients with motion sickness, a related condition. Few controlled studies exist; treatment is often empiric. The results from one trial suggest a 3-week course of methylprednisolone tapered from 100 mg down to 10 mg daily may reduce long-term loss of vestibular function. Despite the evidence of viral infection in at least some patients, valacyclovir was found not to be helpful alone or in combination with methylprednisolone in the same study.[17] Conversely, other small outpatient trials suggested possible enhancement of early recovery but no long-term benefit from a course of steroid therapy.[18, 19, 20, 21] A rigorous Cochrane review that included four trials found no significant difference in the symptomatic resolution of vertigo at 24 hours, and no clear benefit in long-term recovery, though the sparsity of high-quality data was noted.[22]
Clinical Context: A 1:1 salt of 8 chlorotheophylline and diphenhydramine thought to be useful in treatment of vertigo. Diminishes vestibular stimulation and depresses labyrinthine function through central anticholinergic effects. However, prolonged treatment may decrease rate of recovery of vestibular injuries.
Clinical Context: For treatment and prophylaxis of vestibular disorders that may cause nausea and vomiting.
Clinical Context: Decreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. These effects associated with relief of nausea and vomiting.
Clinical Context: For symptomatic treatment of nausea in vestibular dysfunction.
These agents may suppress vestibular responses through an effect on the CNS, although their mechanism remains unknown. Some investigators believe this action is mediated primarily by central anticholinergic activity. Dimenhydrinate appears to be more effective and less sedating than lorazepam at the doses tested for the relief of acute vertigo.[23]
Clinical Context: Probably most commonly used benzodiazepine to treat vertigo, its CNS duration is relatively short as it is highly lipophilic and undergoes rapid redistribution after administration.
Clinical Context: Sedative hypnotic with short onset of effects and relatively long half-life. By increasing action of GABA, which is major inhibitory neurotransmitter in brain, may depress all levels of CNS, including limbic and reticular formation.
These agents centrally inhibit vestibular responses, presumably by potentiating inhibitory GABA receptors.
Clinical Context: Blocks action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and CNS. Antagonizes histamine and serotonin action. Transdermal scopolamine may be most effective agent for motion sickness. Use in vestibular neuronitis limited by its slow onset of action.
These agents are thought to work centrally by suppressing conduction in vestibular cerebellar pathways.
Clinical Context: Anti-inflammatory properties may reduce inflammation and edema of the vestibular nerve and associated apparatus, leading to faster recovery and less permanent damage.
Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli.