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Vestibular neuritis and labyrinthitis - UpToDate

Vestibular neuritis and labyrinthitis - UpToDate
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Vestibular neuritis and labyrinthitis
Author: Joseph M Furman, MD, PhD
Section Editors: Michael J Aminoff, MD, DSc, Daniel G Deschler, MD, FACS
Deputy Editor: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2019. | This topic last updated: Jul 18, 2018.
Vestibular neuritis is also known as vestibular neuronitis, labyrinthitis, neurolabyrinthitis, and acute
peripheral vestibulopathy. It is a benign disorder, self-limited, and associated with a complete
recovery in most patients. Nonetheless, its symptoms of vertigo, nausea, vomiting, and gait
impairment can be disabling in the short term.
Vestibular neuritis also shares clinical features with less benign disorders, particularly acute
vascular lesions of the central nervous system, from which it must be accurately differentiated in
order to avoid morbidity and mortality.
This topic will review the pathophysiology, clinical manifestations, diagnosis, and treatment of
vestibular neuritis. The evaluation and differential diagnosis of vertigo are discussed separately.
(See "Evaluation of the patient with vertigo" and "Causes of vertigo".)
Vestibular neuritis is generally understood to be a viral or postviral inflammatory disorder affecting
the vestibular portion of the eighth cranial nerve. This pathophysiologic mechanism is not
necessarily accurate [1]. There are few pathologic data to support this mechanism in patients with
this disorder, and a history of a preceding viral illness is elicited in less than one-half of patients [24].
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Vestibular neuritis, also known as vestibular neuronitis and labyrinthitis, represents an acute,
spontaneous, peripheral vestibular ailment, characterized by the rapid onset of severe vertigo with
nausea, vomiting, and gait instability.
Physical examination findings are consistent with an acute vestibular imbalance:
Spontaneous vestibular nystagmus that is unilateral, horizontal, or horizontal-torsional; that is
suppressed with visual fixation; and that does not change direction with gaze. The fast phase
of nystagmus beats away from the affected side.
Positive head thrust test. With rapid turning of the head toward the side of the lesion by the
examiner, the patient is unable to maintain visual fixation (figure 1). In one series, this was
present in 82 percent of patients [5]. Patients in this series with a positive head thrust sign
were also more likely to have persistent symptoms. While a positive head thrust test supports
the diagnosis of vestibular neuritis, it does not definitively rule out a central nervous system
disorder [6]. (See "Evaluation of the patient with vertigo", section on 'Other vestibular signs'.)
Gait instability with preserved ability to ambulate. If the patient sways or falls, it is opposite to
the direction of the fast component of the nystagmus, ie, toward the affected side.
Other neurologic signs and symptoms (dysarthria, dysphagia, weakness, sensory loss, facial
droop, limb dysmetria) are absent. Vertical diplopia or skew eye deviation may be present due
to an imbalance in otolithic-ocular reflexes, although its presence suggests that the patient
has had a stroke. (See "Evaluation of the patient with vertigo", section on 'Other vestibular
In pure vestibular neuritis, auditory function is preserved; when this syndrome is combined
with unilateral hearing loss, it is called labyrinthitis.
In one study of 101 patients, three clinical signs, in particular, were useful in distinguishing
vestibular neuritis from a cerebrovascular event [7]. The presence of either a normal head thrust
test, direction changing nystagmus, or a skew deviation had a 100 percent sensitivity and a 96
percent specificity for stroke. These findings, codified as the HINTS examination (Head Impulse
test, direction changing Nystagmus, Test of Skew), have been found to have a similarly high
sensitivity and specificity for distinguishing peripheral from central vertigo in patients with an acute
vestibular syndrome [8-12]. However, in all studies, examiners were either specialists or
specifically trained in this examination.
Many conditions cause vertigo (table 1). The clinical features of common causes of vertigo are
summarized in the table (table 2). The differential diagnosis of vertigo is discussed separately.
(See "Causes of vertigo" and "Evaluation of the patient with vertigo".)
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The principal differential diagnostic concern in a patient presenting with acute sustained vertigo is
a vascular event in the central nervous system affecting the cerebellum and/or brainstem [13,14].
This possibility should be considered in all patients with vascular risk factors, because of the
relatively high risk of recurrent vascular events [15].
Cerebellar hemorrhage or infarction — An important consideration in the differential diagnosis
of a patient with acute sustained vertigo is a vascular event (infarction or hemorrhage) in the
cerebellum [16,17]. As many as 25 percent of patients older than 50 years presenting to the
emergency department with this clinical picture have a cerebellar infarction rather than vestibular
neuritis, although the percentage is usually reported as much lower [18-20]. As this alternative
diagnosis represents a potentially immediately life-threatening condition, it is important to consider
this possibility in every patient who presents with acute sustained vertigo. Patients with acute
cerebellar lesions may have distinctive clinical features from that of vestibular neuritis [16,17,21]:
The nystagmus is not suppressed with visual fixation. It may be other than horizontal or
horizontal-torsional, and may change direction with gaze.
Patients are usually unable to stand or walk unsupported. The direction of falling is not
necessarily opposite to the direction of the nystagmus.
There may also be limb dysmetria, dysarthria, or headache.
Head thrust test is usually normal [6].
Symptoms may be unremitting for 72 hours or more.
Patients with a vascular event are typically older and/or have atherosclerosis risk factors
(hypertension, diabetes, smoking).
Despite these caveats, the distinction between vestibular neuritis and acute cerebellar lesions is
not always apparent; patients with acute vertigo are often quite ill, and the examination may be
limited. When the diagnosis is unclear, a neuroimaging study, typically magnetic resonance
imaging (MRI), may be necessary [2,17,22,23].
Brainstem infarction — The most common stroke syndrome producing vertigo is a lateral
medullary infarction producing a constellation of symptoms and signs known as a Wallenberg
Ipsilateral Horner syndrome
Dissociated sensory loss (loss of pain and temperature sensation on the ipsilateral face and
contralateral limbs and trunk)
Abnormal eye movements
Ipsilateral loss of corneal reflex
Hoarseness and dysphagia
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Ipsilateral limb ataxia
While these signs are usually apparent after a careful neurologic examination, these signs may be
overlooked by patients and non-neurologists because the vertigo, nausea, and vomiting may
overwhelm the clinical pictures. In one study, more than half of patients with an acute vertebral
syndrome subsequently found to be due to lateral medullary infarction did not have any of the
above signs documented on clinical examination [24]. (See "Posterior circulation cerebrovascular
syndromes", section on 'Lateral medullary infarction'.)
More restrictive brainstem infarctions have been described that affect isolated vestibular structures
[25]. Thus, their clinical manifestations are very similar to vestibular neuritis. While many of these
infarcts are due to small arterial disease, and are managed by atherosclerosis risk factor
management and antiplatelet therapy alone, some proportion (up to 50 percent in one series) has
been found to be due to nonlacunar mechanisms (vertebral artery dissection or atrial fibrillation),
suggesting that a high index of suspicion and accurate diagnosis is important [24].
A diagnosis of vestibular neuritis is largely based on the clinical presentation of an acute sustained
vestibular syndrome with examination features consistent with a peripheral lesion as discussed
above. There are no specific diagnostic tests.
Neuroimaging is indicated to rule out alternative diagnoses if the examination is not entirely
consistent with a peripheral lesion, if there are prominent risk factors for stroke, if there are focal
neurologic signs or symptoms, or if there is a new headache accompanying the vertigo [2,26]. A
younger patient with acute sustained vertigo, with no other neurologic signs or symptoms, and
with nystagmus and an examination that is consistent with a peripheral origin (see 'Clinical
manifestations' above) does not need imaging if there is improvement within 48 hours [2].
The procedure of choice is magnetic resonance imaging (MRI) with diffusion-weighted imaging
(DWI) and angiography (MRA). MRI with DWI can detect infarction in the posterior fossa on the
first day. MRA has a specificity and sensitivity exceeding 95 percent in detecting stenosis or
occlusion of the posterior circulation [27]. Small strokes in the brainstem or cerebellum may be
missed on the initial MRI-DWI; thus, if the initial MRI is negative and the diagnosis of a central
lesion is suspected, a repeat study should be ordered >72 hours after the onset of symptoms with
perfusion weighted sequences if available [12,24].
Computed tomography (CT) scanning with thin cuts through the cerebellum is an alternative when
MRI scanning is not available or in patients with metallic implants. The scan is usually normal in
the first hours after an infarct; however, intraparenchymal hemorrhage or significant edema
compressing the fourth ventricle will usually be evident immediately. A brain CT scan should
therefore be performed if an MRI scan is not immediately available.
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Patients with vestibular neuritis generally suffer from severe vestibular symptoms for one to two
days, followed by a gradual diminution of symptoms and a return of equilibrium. While the acute
illness rarely lasts more than several days to a few weeks, residual imbalance and nonspecific
dizziness may persist for months [1]. Early improvement in symptoms is believed to be largely due
to central compensation. Tests of vestibular function, such as caloric testing, show improvement
and ultimately recovery as well, but with a significant lag time compared with clinical symptoms [1].
A positive head thrust sign is of uncertain significance. Two studies have found that abnormal
head thrust testing correlates with ongoing symptoms and predicts a more protracted course,
especially if it remains positive in follow-up examinations [28,29], whereas another study found no
correlation between abnormal head thrust testing and persistent dizziness [30].
Usually patients suffer from vestibular neuritis only once. In one case series of 103 patients
followed for almost 10 years, just two patients had a recurrence, both in the contralateral ear [31].
However, in one series, 15 percent later developed benign paroxysmal positional vertigo (BPPV)
[32]. Panic disorder has been found to develop in 10 percent of patients with vestibular neuritis
over two years [33].
Potential treatments for vestibular neuritis include acute disease-specific treatment with
corticosteroids and antiviral agents, symptomatic treatments, and vestibular rehabilitation. There
are few formal studies of these therapies in patients with vestibular neuritis.
Acute disease-specific treatment — Treatment with corticosteroids during the acute period of
vertigo was shown in at least one clinical trial to improve the recovery of peripheral vestibular
function in patients with acute labyrinthitis. However, subsequent studies, albeit with many
limitations, have not found a clear benefit of corticosteroid therapy.
Despite these somewhat conflicting results and remaining questions, it seems reasonable to treat
presumed viral acute labyrinthitis with corticosteroid therapy. We typically prescribe a 10-day
course of prednisone; 60 mg daily on days 1 through 5, 40 mg on day 6, 30 mg on day 7, 20 mg
on day 8, 10 mg on day 9, and 5 mg on day 10. It is also reasonable not to treat with
corticosteroids in patients at risk for adverse effects.
A controlled trial randomly assigned 141 patients with vestibular neuritis to one of four treatment
groups: methylprednisolone, valacyclovir, methylprednisolone plus valacyclovir, or placebo [34].
The main outcome measure of vestibular function was the extent of unilateral caloric paresis; this
was determined by measuring the mean peak slow-phase nystagmus velocity after caloric
irrigation. The following observations were noted:
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Treatment with methylprednisolone (22-day tapering dose schedule) significantly improved
vestibular function at 12-month follow-up compared with placebo.
Treatment with valacyclovir 1000 mg three times daily for seven days did not improve
Treatment with the combination of methylprednisolone plus valacyclovir was no more effective
than methylprednisolone alone.
Although outcome as measured by caloric response was improved in the methylprednisolone
treatment groups, the study did not assess outcome by the duration and severity of symptoms
such as imbalance and chronic spatial disorientation. Therefore, it is not clear that corticosteroid
treatment provides long-term symptomatic relief, and further controlled trials are needed to
address this issue.
Another smaller, randomized, controlled study of 30 patients with vestibular neuritis found
somewhat different results [35]. Treatment with prednisone (1 mg/kg per day for 5 days, then a 15day taper) was associated with improved outcomes on some measures at three and six months,
but all objective and subjective outcomes were similar at 12 months. This suggests that
corticosteroid therapy may hasten recovery, but does not change the long-term prognosis.
A meta-analysis examined the efficacy of corticosteroids in four randomized controlled studies
(149 patients), including the two previously discussed [36]. There was an overall significant effect
of corticosteroid therapy on complete caloric recovery at 1 month but not at 12 months. They
found that the small sample size and methodologic issues with the included studies precluded firm
conclusions regarding the benefit of corticosteroids, particularly on long-term outcomes.
Subsequent small trials with similar methodologic problems have also not shown a clear benefit of
corticosteroid therapy [37-40].
Symptomatic treatment — Symptomatic treatments to reduce vertigo, nausea, and vomiting are
often employed in the first few days of vestibular neuritis. These include antiemetics,
antihistamines, anticholinergics, and benzodiazepines (table 3). A nonoral route is generally
preferred. Lower doses should be attempted, with upward titration as needed. (See "Treatment of
vertigo", section on 'Symptomatic treatment'.)
There is little evidence supporting the use of one agent over another. In general, we prefer using
antihistamines and anticholinergics over the benzodiazepines, because they are somewhat less
sedating. One trial compared intravenous dimenhydrinate (50 mg) with lorazepam (2 mg) in 74
patients with acute peripheral vestibulopathy. After two hours, patients treated with dimenhydrinate
had better ability to ambulate and were more likely to feel ready to go home compared with
patients treated with lorazepam (86 versus 69 percent), who also felt drowsier after treatment [41].
Another study compared intramuscular dimenhydrinate (50 mg) with droperidol (2.5 mg) in 40
patients with acute peripheral vertigo and found similar efficacy of the two agents; after 30
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minutes, approximately 40 percent of patients felt sufficiently improved to go home without further
treatment [42].
While they provide necessary symptomatic relief in the first 24 to 48 hours, these medications are
believed to be somewhat contraindicated after that time. By suppressing vestibular activity, they
are believed to impair the central compensation response and delay long-term recovery.
Vestibular rehabilitation — Vestibular exercises have been shown to be efficacious in improving
symptoms and functioning as measured by a variety of symptom- and examination-based scores
in patients with unilateral peripheral vestibular injury [43]. In our clinical experience, these
measured improvements are clinically meaningful. (See "Treatment of vertigo", section on
'Vestibular rehabilitation'.)
Most studies of vestibular rehabilitation have not been specific to etiology. However, one study
randomly assigned 39 patients with vestibular neuritis to physical therapy versus standard care
[44]. Evaluation at 30 days revealed that balance function was substantially improved in treated
patients [44]. Other measures of central compensation appeared similar between the groups.
Vestibular rehabilitation is most likely to be efficacious when the patient is referred for a vestibular
physical therapy evaluation and completes an individually designed program.
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-toread materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
Basics topics (see "Patient education: Vertigo (a type of dizziness) (The Basics)" and "Patient
education: Labyrinthitis (The Basics)")
Beyond the Basics topics (see "Patient education: Dizziness and vertigo (Beyond the
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Vestibular neuritis is believed to be an acute viral or postviral inflammatory disorder of the
vestibular portion of the eighth cranial nerve. (See 'Pathophysiology' above.)
Vestibular neuritis presents with acute onset of vertigo with nausea, vomiting, and gait
impairment. In pure vestibular neuritis, auditory function is preserved; when this syndrome is
combined with unilateral hearing loss, it is called labyrinthitis. (See 'Clinical manifestations'
The clinical features of vestibular neuritis overlap with acute vascular events in the cerebellum
or brainstem. Clinical features may aid in the distinction of these entities (table 2). (See
'Clinical manifestations' above and 'Differential diagnosis' above.)
There is no confirmatory test for vestibular neuritis. However, an urgent neuroimaging study
(magnetic resonance imaging [MRI]) is required for patients with acute sustained vertigo
whose examination is not entirely consistent with vestibular neuritis, or in patients who are
older (>60 years), or have headache, any focal neurologic signs, or vascular risk factors. (See
'Diagnosis' above.)
In patients with clinical features entirely consistent with vestibular neuritis and no
contraindications to steroids, we suggest using a corticosteroid taper (Grade 2C). While
short-term recovery seems to be improved with this therapy, an effect on long-term outcomes
is more uncertain. It is reasonable to choose not to treat patients, particularly if there are risk
factors for adverse effects. (See 'Treatment' above.)
We suggest using vestibular suppressants and antiemetics to limit symptoms in the first 24 to
48 hours (Grade 2C). We stop acute symptomatic treatments within 48 hours if the patient's
symptoms allow, as some data suggest that these medications interfere with central
compensation and long-term recovery. (See 'Symptomatic treatment' above.)
We suggest early institution of a vestibular rehabilitation program after acute symptoms
subside, as this may hasten long-term recovery, particularly of balance (Grade 2B). (See
'Treatment' above and "Treatment of vertigo".)
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Topic 5102 Version 8.0
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Head thrust test
At rest, the patient is asked to fixate on a distant target. The patient's head is rotated
rapidly by the examiner, first to the left (A to B), then to the right (C to D). In a normal
response, the eyes remain on target (B). In an abnormal response, the eyes are dragged
off target (D), followed by a saccade back to the target (E). This response implies a
peripheral vestibular lesion on the right.
Graphic 52022 Version 4.0
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Causes of vertigo
Peripheral causes
Benign paroxysmal positional vertigo
Vestibular neuritis
Herpes zoster oticus (Ramsay Hunt syndrome)
Meniere disease
Labyrinthine concussion
Perilymphatic fistula
Semicircular canal dehiscence syndrome
Cogan's syndrome
Recurrent vestibulopathy
Acoustic neuroma
Aminoglycoside toxicity
Otitis media
Central causes
Vestibular migraine
Brainstem ischemia
Cerebellar infarction and hemorrhage
Chiari malformation
Multiple sclerosis
Episodic ataxia type 2
Graphic 66539 Version 8.0
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Clinical features of common causes of vertigo*
of nystagmus ¶
movements or
lasts days
Viral syndrome
accompany or
Falls toward
side of lesion,
no brainstem
Usually none
Head thrust
test usually
to several
Episodes may
be preceded
by ear
by vertigo,
hearing loss,
unilateral lowfrequency
hearing loss
to hours
History of
Central or
characteristics may
be present
and/or other
or following
Usually none
tests are
Single or
to hours
Older patient,
vascular risk
factors, and/or
Usually other
Usually none
MRI with DWI
over days
to weeks
As above
Usually other
Usually none;
an exception
is anterior
MRI will
infarction or
over days
to weeks
Older patient,
vascular risk
impairment is
may occur
Urgent MRI,
CT will
TIA: transient ischemic attack; MRI: magnetic resonance imaging; DWI: diffusion-weighted imaging; CT: computed
* For other diagnoses, refer to UpToDate topics on differential diagnosis of vertigo.
¶ Peripheral characteristics of nystagmus: horizontal or horizontal-torsional; suppresses with visual fixation; does not
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change direction with gaze. Central characteristics of nystagmus: may be horizontal, torsional, or vertical; does not
suppress with visual fixation; may change direction with gaze.
Graphic 81596 Version 11.0
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Medications for acute vertigo
Dose as-needed
Orally administered agents:
Antihistamines, first-generation
50 to 100 mg every 4 to 6 hours
25 to 50 mg every 4 to 6 hours
25 to 50 mg every 6 to 12 hours
0.5 mg immediate release every 8 hours
0.25 to 0.5 mg every 8 to 12 hours
1 mg every 12 hours
1 to 2 mg every 8 hours
Domperidone (not
available in United
10 mg every 8 hours
5 to 10 mg every 6 hours
Ondansetron ¶
4 mg every 8 to 12 hours
5 to 10 mg every 6 hours
12.5 to 25 mg every 8 hours
Parenterally administered agents for acute emergency ward use: Δ
Antihistamines, first-generation
10 to 50 mg IV
50 mg IV
10 mg IV
Ondansetron ¶
4 to 8 mg IV
2.5 to 10 mg IV
12.5 to 50 mg IM or IV (vesicant, use caution with IV administration; refer to
Lexicomp drug monograph included within UpToDate)
Medications for treatment of acute vertigo. Doses listed are for non-volume depleted adult or adolescent patients
with normal renal function. These agents may require dose adjustment in patients with reduced organ function
(eg, kidney or cardiac disease) and in older persons. For specific recommendations, refer to the Lexicomp drug
monographs included within UpToDate.
IV: intravenous; IM: intramuscular.
* Rare adverse cardiac reactions have been described with most antiemetics particularly following parenteral use. These
agents should be avoided in patients with known QT interval prolongation or other risk factors for torsades de pointes
(TdP) eg, hypomagnesemia, hypokalemia. Refer to topic review of acquired long QT syndrome, section on drug-induced
TdP within UpToDate. Phenothiazines and metoclopramide can cause extrapyramidal side effects (eg, akathisia, dystonia)
particularly with parenteral use. Refer to accompanying text.
¶ Other serotonin 5HT3 antagonist antiemetics (eg, dolasetron, granisetron) may be used if ondansetron is not available.
∆ If IV access is unavailable, these agents may be administered IM. However, with the exception of promethazine, IM use
is not preferred due to injection site pain.
Graphic 68052 Version 5.0
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Contributor Disclosures
Joseph M Furman, MD, PhD Nothing to disclose Michael J Aminoff, MD, DSc Equity Ownership/Stock
Options: Trust (The portfolio may include medical or drug companies). Equity Ownership/Stock Options
(Spouse): Trust (The portfolio may include medical or drug companies). Daniel G Deschler, MD,
FACS Nothing to disclose Janet L Wilterdink, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
Conflict of interest policy
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