Vestibular Neuronitis

Travis Smith; Justin Rider; Steven Cen; Judith Borger.

Author Information

Last Update: July 11, 2022.

Continuing Education Activity

Vestibular neuritis is thought to be the result of inflammation of the vestibular portion of the
eighth cranial nerve and classically presents with vertigo, nausea, and gait imbalance. It is
considered a benign, self-limited condition that typically lasts several days, but can take
weeks to months for all vestibular symptoms to completely resolve. Vestibular neuritis is a
clinical diagnosis, and it’s the clinician's task to differentiate this benign self-limiting disease
from other central causes such as cerebrovascular syndromes. This activity reviews the
evaluation and treatment of vestibular neuritis and examines the role of the healthcare team in
evaluating and treating patients with this condition. 
Objectives:
 Identify the etiology of vestibular neuritis.
 Review the evaluation of vestibular neuritis.
 Outline the treatment and management options available for vestibular neuritis.
 Outline interprofessional team strategies for improving care coordination and
communication to advance the diagnosis and treatment of vestibular neuritis and
improve outcomes.

Introduction
Vestibular neuritis, also known by the name vestibular neuronitis, is thought to be caused by
inflammation of the vestibular portion of the eighth cranial nerve and classically presents
with vertigo, nausea, and gait imbalance. It is believed to be associated with preceding or
accompanying viral infection. It is considered a benign, self-limited condition that typically
lasts several days, but can take weeks to months for all vestibular symptoms to completely
resolve. Vestibular neuritis is a clinical diagnosis, and it’s the clinician's task to differentiate
this benign self-limiting disease from other central causes such as cerebrovascular
syndromes, which may share a similar history and physical exam findings. The mainstay in
medical treatment for vestibular neuritis is generally supportive, often consisting of
antiemetics, antihistamines, and benzodiazepines.[1][2] Vestibular rehabilitation should start
once the initial bouts of nausea and vomiting are under control.[3]
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Etiology
Vestibular neuritis is believed to be an inflammatory disorder selectively affecting the
vestibular portion of the eighth cranial nerve. The cause is presumed to be of viral origin.[2]
Epidemiology
The data is lacking regarding the incidence of acute vestibular neuritis, but it is known to be
the third most common cause of peripheral vertigo following BPPV and Meniere disease.
Estimates are that acute vestibular neuritis or labyrinthitis gets diagnosed in 6% of patients
who present to emergency departments in the USA the complaint of dizziness. This stat is
likely an under-representation of its true incidence as another 22% of the patients
complaining of dizziness are discharged without anything more specific than “dizziness” or
“vertigo.” A portion of these non-specific diagnoses likely includes actual cases of acute
vestibular neuritis.[1] It has no gender preference and usually affects those in their middle
ages. 

Pathophysiology
Vestibular neuritis is believed to be an inflammatory disorder selectively affecting the
vestibular portion of the 8th cranial nerve. The cause is presumed to be of viral origin (e.g.,
the reactivation of latent HSV infection), but other causes of vascular etiology and
immunologic in origin are proposals. Vestibular damage appears to have a predilection for
the superior portion of the vestibular labyrinth (supplied by the superior division of the
vestibular nerve) over the inferior aspect of the vestibular labyrinth (supplied by the inferior
portion of the vestibular nerve). The underlying mechanism is unclear, but this phenomenon
may be explainable by anatomical differences between the two vestibular divisions.[3]

History and Physical

The typical presentation of vestibular neuritis is usually with the acute onset of the following:
 Vertigo
 Nausea
 Vomiting
 Balance problems
The symptoms in vestibular neuritis are typically constant, in contrast to the episodic
symptoms of other peripheral causes such as BPPV or Meniere's disease. Symptoms are
worsened with head movement but not triggered. Symptoms generally develop over several
hours, peak within the first 24 to 48 hours, and typically last several days before resolving
without intervention. Patients will likely note a preceding or concurrent viral illness, but it is
important to note that the lack of this history does not rule out the disease as it is reported to
be absent in up to 50% of patients [2].
Other symptoms, such as headaches, are usually absent. It is vital to ask the patient about
accompanying symptoms that may suggest central disorders of vertigo, such as visual
changes, somatosensory changes, weakness, dysarthria, incoordination, or an inability to
walk. If any of these are present, one must broaden the differential with to central causes of
vertigo. When the additional symptom of unilateral hearing loss is present, this shifts the
diagnosis towards labyrinthitis [2]. When attempting to differentiate this associated hearing
change from Meniere disease, it is important to know that Meniere disease also presents with
vestibular and auditory dysfunction. Still, patients with Meniere have more episodic and not
continuous symptoms lasting 20 minutes to usually no more than 12 hours.[3]
Physical Exam
Patients presenting with vestibular neuritis will have a normal physical exam and
neurological exam. The clinician needs to look for clues that might point to a central cause of
vertigo, warranting a more thorough evaluation. Central causes of vertigo are usually
continuous symptoms along with truncal instability, an unsteady gait, dysarthria, and other
focal neurological symptoms. Symptoms that are episodic in nature point to the more
common other peripheral causes like BPPV and Meniere’s disease. Other findings that are
consistent with peripheral causes of vertigo, like vestibular neuritis, include a negative HINTs
exam. The HINTS examination (see figure 1) consists of three components: Head Impulse,
Nystagmus, and Test of Skew. It has been found to have high sensitivity and specificity
(100% and 96%) for distinguishing peripheral from central vertigo in patients presenting with
acute vestibular syndrome when performed correctly by the experienced clinician.[1][2]
[4] Videos of this exam are available online. The following components make up this exam
are described as follows:
 The head impulse is performed with the patient sitting facing the examiner. Head
positioning is at about 20 degrees to the left and right from midline, and then the
examiner will briskly turn the head toward the midline. The examiner will then check
to see whether or not the patient can maintain visual fixation on the examiner. If the
patient’s eyes are not able to fixate on the examiner during the maneuver, their eyes
will be noted to saccade back toward the midline. When the saccade is present, the
test is considered a positive test and points towards a peripheral etiology such as
vestibular neuritis. If there is a corrective saccade in both directions, this is worrisome
for a central pathology. When the patient can fixate on the examiner’s nose during the
entire maneuver, the test is considered negative and points towards a central etiology.
 Nystagmus is another exam tool that is a part of the HINTS exam. It is important to
note that the naming of nystagmus is for the direction of the fast component.
Nystagmus follows a rule termed Alexander’s law, which states that the intensity of
nystagmus increases when the patient looks towards the direction of the fast phase.
The slow phase of the nystagmus beats towards the injured side. Spontaneous
nystagmus (when a patient is looking straight ahead without fixation) is determined to
be negative (peripheral) if it is described as horizontal beating or horizontal-torsional
and is unidirectional (fast phase beats towards one direction regardless of the
orientation of gaze, patient looking left or right). Vertigo that is observed to be
vertical and or bidirectional is considered a positive finding and points to a central
etiology.
 The test of skew is performed with the patient facing the examiner. The examiner then
covers and uncovers the patient's eye one at a time with his hand while the patient
attempts to fixate on the examiner.  Any deviation of one eye while it is covered,
followed by correction after uncovering the eye, is considered a positive or abnormal
test pointing to a central etiology. The patient with vestibular neuritis should be able
to maintain symmetrical eye alignment without deviation during the entire exam.
Other neurologic signs and symptoms: dysarthria, dysphagia, facial droop, dysmetria, motor
weakness, sensory loss, and abnormal reflexes are typically absent.[1][2] The auditory
function in patients with vestibular neuritis is usually preserved, but when there is combined
unilateral hearing loss, it is called labyrinthitis. It is crucial to assess the patient's gait and
posture as it can help localize the affected ear or be a signal of a more grave diagnosis. Their
seated posture should be normal, and while their gait is usually unaffected, they will tend to
veer or fall toward the affected side (opposite to nystagmus fast phase). 
Evaluation
The diagnostic basis is mostly on key signs and symptoms of acute vestibular dysfunction, as
mentioned above. However, because vestibular neuritis is a diagnosis of exclusion, the main
focus in patients presenting with acute spontaneous vertigo is to rule out a stroke or other
central causes. 
Neuroimaging of the brain with MRI or CT imaging is not indicated in most cases but can be
helpful when exam findings of a peripheral lesion are inconsistent if risk factors for stroke
exist and symptoms do not show improvement within 48 hours.[5] If a rule test is needed, an
MRI of the brain is more sensitive than a CT scan to rule out a CVA.
Other tests like cervical and ocular vestibular evoked myogenic potentials along with video
head impulse testing have made it possible to determine which vestibular division is involved
in vestibular neuritis.[6][7]

Treatment / Management
The treatment of vestibular neuritis usually consists of acute symptomatic treatment with
medications such as antiemetics (promethazine, metoclopramide), antihistamines
(diphenhydramine, meclizine), and benzodiazepines (diazepam, lorazepam). Following the
acute phase, other therapies, such as vestibular rehabilitation, are often recommendations.
[8] The utilization of the above antiemetics, antihistamines, and benzodiazepines should be
used for no more than three days or so as these medications can delay central compensation
and lead to chronic problems and recurrent vertigo.[3][8]   
In the past, the use of corticosteroids has been a therapeutic option, but their efficacy remains
controversial. This therapy was studied in a 2011 Cochrane review, which found insufficient
evidence to recommend their use in those with acute vestibular dysfunction.[9]
The viral etiology hypothesis has led to the theoretical benefit from antiviral medications;
however, the use of valacyclovir either alone or combined with a glucocorticoid has not
been shown to be effective.[10]

Differential Diagnosis
The differential diagnosis in patients presenting with vertigo can be broken down to that of
peripheral or central etiologies as well as those with or without hearing loss:
Peripheral Causes:
 Benign paroxysmal positional vertigo (BPPV): Presents with episodic vertigo
following predictable head movements that trigger symptoms. It is usually an acute
onset with a duration of seconds to minutes. 
 Meniere disease: Presents acutely with recurrent episodes of vertigo along with
sensory symptoms (e.g., ear fullness, tinnitus, low-frequency hearing loss). Symptoms
last minutes to hours. 
 Labyrinthitis: Presents with similar symptoms to vestibular neuritis but will also
include auditory symptoms such as unilateral hearing loss. Symptom duration lasts
days to weeks.[2]
Central Causes:
  Vestibular migraine: Can present with central or peripheral signs/symptoms. Patients
will have a headache and will note recurrent episodes and must have a documented
diagnosis of migraine. Symptoms duration is minutes to hours. 
 Vertebrobasilar TIA: Patients will usually have vascular risk factors. Symptoms are
shorter and of acute onset. Symptoms duration is minutes to hours
 Brainstem ischemia/infarct: Patients will often have vascular risk factors or a history
of trauma. There is commonly noted to be a constellation of neurological symptoms
along with vertigo present, known as a Wallenberg syndrome, which is an infarct of
the lateral medulla. The onset is acute, and the duration of symptoms is days to weeks.
 Cerebellar infarct or hemorrhage - There are usually vascular risk factors or trauma
present. Symptom onset is acute, and the duration is days to weeks.[2] There are
typically associated neurological deficits present along with an abnormal HINTS
exam, truncal instability, headache, ipsilateral Horner syndrome, limb ataxia,
abnormal pupillary response, and other neurological abnormalities.
Hearing Loss Present: 
 Perilymphatic fistula
 Cholesteatoma
 Meniere disease
 Labyrinthitis
 Acoustic neuroma
 Autoimmune processes
 Psychogenic
Hearing Loss Absent:
 Benign positional paroxysmal vertigo
 Vertebral basilar insufficiency
 Migraines
 Vestibulopathy
 Vestibular neuronitis
 Central nervous system disorders
 Lyme disease
 Multiple sclerosis

Prognosis
The natural history of this disease is uncomplicated with complete resolution in most cases.
Some can have incomplete resolution and with a study showing 15% with persistent
symptoms at one year.[2] Recurrence of vestibular neuritis is infrequent, with studies that
have shown its recurrence in only 2 to 11% of patients.[11][12]

Complications
Two important complications associated with vestibular neuritis are benign paroxysmal
positional vertigo (BPPV) and persistent postural-perceptual dizziness (PPPD), a relatively
new term. Research has found that 10 to 15% of patients with vestibular neuritis will develop
BPPV in the affected ear within a few weeks.[11][12] PPPD is a new diagnostic syndrome of
non-spinning vertigo and unsteadiness, which combines significant features of chronic
subjective dizziness, phobic postural vertigo, and other related disorders.[13] One study
found PPPD in 25% of patients who were followed 3 to 12 months after acute or episodic
vestibular disorders.[14]

Deterrence and Patient Education

One should suspect vestibular neuritis if the patient experiences an acute onset of persistent
vertigo that lasts hours to several days.
Patients who experience the above seek consultation with their primary care, emergency, or
ENT physician.
Physicians will primarily exclude vertigo secondary to another more severe disease of the
brain or its blood vessels, and refer the patient to an ENT (otolaryngologist) for further
testing and treatment.

Enhancing Healthcare Team Outcomes 

The word “dizziness” is very vague and may be described differently among patients.
Patients may characterize it as light-headedness, faintness, nausea, or an unsteady feeling. On
the other hand, true vertigo is a spinning sensation of movement and more suggestive of
vestibular disease. Complicating the diagnosis of vertigo is the fact that the above sensations
often accompany vestibular disease. These demonstrate is why the management of vestibular
vertigo requires the effort of a collaborative interprofessional healthcare team.
The main concern in a patient presenting with acute vertigo is a vascular accident of the
cerebellum or brainstem. However, vestibular neuritis is distinguishable from a central cause
such as a cerebrovascular event with the use of the HINTS exam either by a specialist or
someone specifically trained in the examination. In these patients, a referral to an ENT
colleague is a strong recommendation.
A pharmacist can perform medication reconciliation to see if any drugs are known to cause
vertigo, and if the clinician initiates pharmaceutical therapy for the vertigo, the pharmacist
can verify dosing and counsel the patient on administration, adverse effects, etc. Nursing can
monitor treatment progress, answer patient questions, check and reinforce administration, and
report any concerns to the treating clinician.
Vestibular neuritis is a self-limiting disease with vestibular symptoms lasting for one to two
days, followed by a gradual reduction in symptoms. Rarely does the illness lasts more than
several days to a few weeks. Early improvement in symptoms is believed mainly due to
central compensation. For this reason, symptomatic treatment with medications is stopped
within the first 48 to  72 hours of the patient’s symptoms as it may interfere with central
compensation and long-term recovery.
Most patients will experience vestibular neuritis only once, with some experiencing a residual
imbalance and nonspecific dizziness persisting for months. If this occurs, the vestibular
function can substantially be improved if patients follow through an individually designed
vestibular rehabilitation program. The interprofessional team can guide these cases to their
optimal result through open communication and collaborative teamwork. [Level 5]

Review Questions
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References
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