Vestibular neuronitis
By Dr.Imran Qazi
ENT A Ward TMO
18/12/19
Introduction
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.
Although vestibular neuronitis and labyrinthitis may be
closely related in some cases, vestibular neuronitis is
generally distinguished from labyrinthitis by preserved
auditory function.
Pathophysiology
Its etiology remains largely unknown, yet vestibular
neuronitis 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
Epidemiology
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. [2]
Sex
Studies have shown no consistent male or female
predominance. [3]
Age
This syndrome occurs most commonly in middle-aged adults;
mean age of onset is 41 years.
Causes
Viral infection of the vestibular nerve and/or labyrinth is
believed to be the most common cause of vestibular
neuronitis.
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.
Differential diagnoses
Benign Positional Vertigo
Central Vertigo
Labyrinthitis
Migraine Headache
Stroke, Hemorrhagic
Stroke, Ischemic
Workup
Laboratory studies
Radiological Imaging
Procedures
Laboratory Studies
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:
Cerebellar bleeds
Infarcts and tumors
Lesions of the brain stem
Cerebellopontine angle tumors
Multiple sclerosis
Because significant bony artifacts degrade CT images of the
posterior fossa, MRI is the preferred imaging modality when
available.
Performthe Hallpike maneuver on all patients who complain of vertigo but
do not exhibit nystagmus on routine examination of the extraocular
muscles.
Hallpikemaneuver 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.
History
History
Patients usually complain of abrupt onset of
severe, debilitating vertigo with associated
unsteadiness, nausea, and vomiting. [4] They
often describe their vertigo as a sense that
either they or their surroundings are
spinning. Vertigo increases with head
movement.
Physical
Physical
Spontaneous, unidirectional, horizontal nystagmus is the
most important physical finding. [5, 6] 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:
Multidirectional, nonfatiguing nystagmus suggesting vertigo
of central origin
Hearing loss
Other cranial nerve deficits
Truncal ataxia (suggests cerebellar disease or another CNS
process)
Inflamed tympanic membrane
Mastoid tenderness
High fever
Nuchal rigidity
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. [7, 8]
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. [8, 9, 10] 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.
Treatment
