Published online: 28.01.

2020

Acute Vestibular Syndrome

Kevin A. Kerber, MD, MS1

1 Department of Neurology, Health Services Research Program, Address for correspondence Kevin A. Kerber, MD, MS, Department of
University of Michigan, Ann Arbor, Michigan Neurology, Health Services Research Program, University of Michigan,
1500 E. Medical Center Dr, Ann Arbor, MI 48109
Semin Neurol (e-mail: kakerber@med.umich.edu).

Abstract The acute vestibular syndrome (AVS) is a label for presentations of new-onset severe
Keywords dizziness, vertigo, or imbalance, with examination findings of nystagmus or gait
► vertigo unsteadiness. The prototypical AVS presentation is the acute unilateral vestibulopathy
► acute vestibular due to vestibular neuritis. Stroke is also a serious concern in patients with AVS. Most
syndrome other peripheral vestibular disorders present as episodic or chronic syndromes. In this

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► vestibulopathy article, the diagnostic considerations, exam findings, and management of AVS are
► stroke reviewed.

Vestibular disorders are a common reason patients present for
medical care.1,2 There are three broad categories of vestibular
disorder presentations: the acute vestibular syndrome (AVS),
the episodic vestibular syndrome, and the chronic vestibular
syndrome. AVS is characterized by new-onset persistent dizzi-
ness which distinguishes it from the episodic and chronic
syndromes. At the time of an AVS presentation, patients
typically have severe and often disabling dizziness, nausea,
vomiting, and head motion intolerance. Other criteria for AVS
are examination findings of gait unsteadiness and/or nystag-
mus. Nearly all AVS patients report unsteadiness and most also
report vertigo.3 Other types of dizziness are also common
including lightheadedness, floating, and spacy or tilting sensa-
tions.3 It is important to keep in mind that patients with
dizziness usually report more than one type of dizziness,
reliability is low when patients select the primary type of
dizziness, and types of dizziness are not strong discriminators
of underlying disorders.4,5 The prototypical example of AVS is
the acute unilateral vestibulopathy (AUV) which is typically
attributed to vestibular neuritis. Stroke is also a serious concern.
Other vestibular disorders can initially present as AVS but
become more clearly episodic or chronic vestibular syndromes
over time. In this article, we review the epidemiology pertinent
to AVS, common causes of AVS including distinguishing fea-
tures, and AVS management.
Epidemiology
In the United States, there are more than 3 million visits to the
emergency department (ED) for dizziness every year and this
has been gradually increasing over time.1 There are numerous
potential causes of dizziness with approximately 3 to 4% of
visits receiving a diagnosis of ischemic stroke.1 Testing for
central causes with neuroimaging has substantially increased
over time, but the proportion of ED visits diagnosed with stroke
has not increased.1 At the population level, we do not know
what proportion of dizziness visits meets AVS criteria. However,
a single-center study found that approximately 10%
(373/3,296) of screened dizziness visits had AVS character-
istics.3 In AVS presentations, providers are concerned about
dangerous central causes such as stroke, and have uncertainty
regarding when to order neuroimaging.6 Most strokes that
present with dizziness symptoms have other neurologic fea-
tures such as face/arm weakness or numbness or speech/
language abnormalities to indicate a central lesion.2,7 However,
stroke can present with isolated dizziness and therefore should
still be considered when no other cause is obvious.2,3 Among all
patients presenting with isolated dizziness (not restricted to
AVS patients), a population-based study found that only 0.7%
(9/1297) had stroke identified as the diagnosis at the time of the
visit.2 Because it is possible that stroke might be missed at
the initial visit, several studies have also examined the cumu-
lative incidence of stroke following an ED dizziness visit that did
not receive a stroke diagnosis. Subsequent stroke in these
studies was approximately 0.3% (1 in 333) at 90 days.8–11 The
relatedness of the subsequent stroke events to the initial
dizziness visit is not certain. It is possible that the initial
dizziness visit was a missed stroke, transient ischemic attack,
some other warning precursor, or unrelated. A closer inspection
of the timing of the events suggests that approximately 60% or

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Acute Vestibular Syndrome Kerber et al.
more of the 90-day strokes are likely related to the initial
dizziness presentation as these occurred within 7 days and
the short-term frequency of events was much higher than that
of comparison groups.8,9,11 It was surprising, however, that
only 13% (2/15) of the subsequent strokes were found to be in
the cerebellum or brainstem on neuroimaging in one study.9
The majority of these strokes (87%, 13/15) were instead in
regions (e.g., frontal lobe, parietal lobe) not typically felt to
cause AVS presentations.
Acute Unilateral Vestibulopathy (Vestibular
Neuritis)
Acute unilateral vestibulopathy presents with a rapid onset
of severe vertigo, nausea, vomiting, and imbalance. At pre-
sentation, patients are typically disabled by the symptoms as
demonstrated by very high disability scores (e.g., Dizziness
Handicap Index [DHI] >90).12,13
AUV is due to a lesion of the vestibular nerve on one side.
The vestibular nerve has a superior division, inferior division,
and a central trunk. A study of 43 AUV patients found that the
lesion usually involves both divisions based on the results of
canal-plane video head impulse tests.14 Traditionally, the
vestibulopathy has been attributed to a viral or postviral
etiology, making it analogous to an idiopathic cranial nerve 7
lesion (e.g., Bell’s palsy). However, an association with a
recent viral illness has not been previously shown with
AUV, recent upper respiratory infections are common in
the general population, and a viral basis cannot confirmed
in individual patients other than presentations of the
Ramsay-Hunt syndrome (see later).15 It is important to
note that other pathologies can also cause AUV, including
ischemia or demyelination of the nerve. The eighth cranial
nerve is second only to the optic nerve in the amount of
central myelin. It is not known what proportion of AUV might
be due to ischemic events. However, in an analogous condi-
tion affecting the auditory component of cranial nerve 8,
Lin et al used Taiwan National Health Insurance claims and
found that patients with sudden sensorineural hearing loss
(SSNHL) had an increased risk of stroke in the subsequent
5 years compared with a control group of appendectomy
patients, even controlling for vascular risk factors (hazard
ratio: 1.64, 95% confidence interval [CI]: 1.31–2.07; absolute
frequencies, 12.7 vs. 7.8%, respectively).16 In another study
that used Taiwan National Health Insurance claim data,
patients with SSNHL and vertigo had a higher risk of stroke
at 1 year (1.5%, 10/678) than did patients with SSNHL with-
out vertigo (0.6%, 11/1,998; hazard ratio: 1.75, 95% CI:
1.15–2.66).17 These studies emphasize that vascular causes
should be a concern in acute presentations of unilateral
cranial nerve 8 lesions. A genome-wide association study
(GWAS) in 131 AUV patients and 2,609 controls was recently
performed.18 The authors noted that this was a very small
number of cases for GWAS analysis, but found associations in
regions that were considered to be involved in viral disorders
and insulin metabolism. The findings also support the
general notion of both viral and vascular contributions to
AUV presentations.
Seminars in Neurology
The exam in AUV presentations has characteristic findings.
Simply based on symptoms, AUV presentations overlap with a
variety of other disorders such as ischemic stroke, and even
with general medical disorders such as gastroenteritis. The
nystagmus of AUV is a unidirectional horizontal pattern with a
dominant horizontal vector and typically a torsional compo-
nent. For example, a left-beat nystagmus will not change to
right-beat nystagmus even after looking at the right side. If
there is a change in the direction of the nystagmus based on
gaze, then the pattern is labeled as a bidirectional gaze-evoked
nystagmus which is a hallmark central pattern of nystagmus.
The velocity of the nystagmus in AUV will typically increase
when looking at the direction of the fast phase and decrease or
stop when looking at the opposite direction. The head impulse
test also helps localize the lesion. This test is a bedside assess-
ment of the vestibular-ocular reflex (VOR; ►Fig. 1).19 When the
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VOR is intact, quick movements of the head to either side result
in a nearly equal movement of the eyes in the opposite direction
so that the eyes remain fixed on the target. With a lesion of the
vestibular nerve on one side, the eyes will instead move with
the head so that at the end of the head movement the patient
will need to make a voluntary saccade back to the target. This
saccade is called a “corrective saccade” or a “catch-up saccade”
and is used at the bedside to identify reduction of the VOR.
Patients with AUV also do not typically have a skew deviation.
Collectively these examination elements and findings have
been labeled as the HINTS (Head Impulse Nystagmus Test of
Skew) exam.20,21 The HINTS findings that localize the lesion to
the vestibular nerve are unidirectional horizontal nystagmus,
an abnormal head impulse test to the side opposite to the fast
phase of the nystagmus, and the absence of a skew deviation. It
is possible that some patients with AUV have a milder vesti-
bulopathy so that the corrective saccade is not seen at the
bedside or is under the quantitative thresholds of impairment.
Less common variants of AUVare inferior vestibular neuritis,
labyrinthitis, and the Ramsay-Hunt syndrome. Inferior vestib-
ular neuritis is an AUV that affects only the inferior division of
the vestibular nerve. An inferior division of AUV is rarely
encountered and would be expected to cause spontaneous
downbeat torsional nystagmus since the inferior division inner-
vates the posterior canal which is in the vertical plane.14
Although a lesion of inferior division can present with down-
beat nystagmus, central lesions are the primary concern in any
AVS presentation with spontaneous or gaze-evoked downbeat
nystagmus. Labyrinthitis is a variant of AUV that involves both
the auditory and vestibular components. The Ramsay-Hunt
syndrome is characterized by vesicles on the concha of the
external ear, hearing loss, and facial palsy. For Ramsay-Hunt
syndrome, the vesicles indicate a viral process. The vesicles can
be unroofed and tested for varicella zoster virus (VZV) antigen
with direct immunofluorescence or VZV DNA with polymer-
ase-chain reaction.22
Brainstem or Cerebellar Ischemia/Infarction
Ischemic stroke of the brainstem or cerebellum can also
present as the AVS closely mimicking an AUV. Intracranial
hemorrhage causing isolated dizziness is very uncommon.23
 Acute Vestibular Syndrome Kerber et al.

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Fig. 1 The head impulse test (HIT). The HIT is a bedside test of vestibular function. The HIT evaluates the vestibulo–ocular reflex (VOR), and can
help localize a lesion to the peripheral vestibular system. To perform the test, the patient is asked to maintain gaze on the examiner’s nose. The
examiner holds the patient’s head steady in the midline axis and then rapidly turns the head to
10–20 degrees off the midline. (A) The normal
response (intact VOR) is for the eyes to stay locked on the examiner’s nose. (B) An abnormal response (impaired VOR) is for the eyes to move with
the head, followed by a voluntary eye movement back to the examiner’s nose (a corrective or catch-up saccade). A normal response indicates
that the VOR is intact, making a lesion of the vestibular nerve less likely. The abnormal response indicates a lesion of the peripheral vestibular
system. (From Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial management of cerebellar infarction. The Lancet Neurology 2008;7
(10):951–964).

In a study of 272 AVS patients, 3 patients had intracranial
hemorrhage,3 2 of which were due to melanoma metastases
and 1 from a cavernoma. Ischemic stroke was more than
eight times as common as ICH in AVS presentations. The
stroke location in AVS presentations is typically in the
cerebellum (posterior inferior cerebellar artery > anterior
inferior cerebellar artery [AICA] distribution), medulla, or
pons.3 Thalamic infarcts have also been identified in AVS
presentations.
The ocular motor examination is performed to assess for
central patterns of eye movement findings. It is often underu-
tilized by frontline providers who also harbor important mis-
conceptions.24–26 The HINTS exam findings that indicate a
central lesion are any of the following: central patterns of
nystagmus, a normal head impulse test, and/or the presence
of skew deviation (►Table 1). A central lesion should be the
primary concern when there is bidirectional gaze-evoked
nystagmus or spontaneous or gaze-evoked vertical or pure
torsional nystagmus. Central lesions, however, can also cause
unidirectional horizontal nystagmus. Because central lesions
can also cause unidirectional horizontal nystagmus, the head
impulse test can further localize the lesion to the vestibular
nerve. If the result of the head impulse test is normal (no
corrective saccade to the side opposite the horizontal nystag-
mus) when unidirectional horizontal nystagmus is present,
then either a peripheral lesion is under the threshold for
detecting the vestibular lesion or there is a central lesion.
Corrective saccades in AUV presentations can be “covert”

Seminars in Neurology
Acute Vestibular Syndrome Kerber et al.

Table 1 Characteristics of presentations of acute unilateral vestibulopathy, stroke in the PICA distribution, and stroke in the AICA
distribution

Acute unilateral Stroke (PICA) Stroke (AICA)

vestibulopathy
Nystagmus Spontaneous unidirectional Central patterns Central patterns more common than
horizontal more common peripheral patternsa
than peripheral patternsa
Head impulse test, Abnormal to the direction Normal bilaterally Abnormal to the affected side
qualitative opposite to the nystagmus
fast phase
Head impulse test, Ipsilesional: 0.2–0.4 Ipsilesional: 0.7–0.8 Ipsilesional: 0.3–0.4
quantitative (gain)b Contralesional: 0.6–1.0 Contralesional: 0.7–0.8 Contralesional: 0.5–0.6
Skew deviation Typically absent May be present May be present
Vascular risk Typically low Typically high Typically high
Hearing loss Typically absent Absent Frequently present

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Abbreviations: AICA, anterior inferior cerebellar artery; PICA, posterior inferior cerebellar artery.
a
Central patterns of nystagmus include bidirectional gaze-evoked nystagmus, spontaneous or gaze vertical nystagmus (typically downbeat), and
spontaneous pure torsional nystagmus.
b
Summarized in Choi JY, Kim HJ, Kim JS. Recent advances in head impulse test findings in central vestibular disorders. Neurology 2018;90
(13):602–612.

(e.g., under the threshold of detection) in 30 to 70% of head
impulse trials,27 which is why a series of head impulses is
usually required. In patients with AUV, the frequency of correc-
tive saccades was also lower with low-velocity head impulse
tests (80 degree/s) compared with high-velocity head impulses
(240 degree/s).28 VOR deficits, both from bedside head impulse
tests and quantitative measures, have also been demonstrated
in central lesions, although these are typically mild unilateral
deficits or mild bilateral reductions.3,21,29 Stroke in the distri-
bution of the AICA is the closest mimicker of vestibular neuritis
as it is the vascular supply to the peripheral auditory and
vestibular structures.30 AICA strokes can therefore cause an
AUV. Considering that a case series of AICA infarct found that
68% (56/82) of infarcts had associated hearing loss,31 a revision
of the HINTS assessment added hearing loss as a central sign
and this HINTS-plus assessment correctly classified three of the
four stroke cases missed by HINTS alone.21
Vascular risk factors also contribute to the likelihood of
acute stroke. The ABCD2 score was developed to identify risk
of stroke after TIA presentations,32 but several studies indi-
cate that dizziness patients with increased vascular risk
measured using the ABCD2 score are more likely to have
stroke at the index dizziness visit even after adjusting for the
ocular motor examination.3,21,33 The ABCD2 score is com-
posed of age (>60 years ¼ 1 point), blood pressure (systolic
>140 or diastolic >90 ¼ 1 point), clinical features (unilateral
weakness ¼ 2 points; speech disturbance without weakness
¼ 1 point), diabetes (presence ¼ 1 point), and duration of
symptoms (60 minutes ¼ 2 points; 10–59 minutes ¼ 1
point).32 One study directly compared the ABCD2 score to
the HINTS ocular motor assessment and found that HINTS
outperformed the ABCD2 score when these were analyzed as
competing diagnostic tests.21 However, another study found
HINTS and ABCD2 score are both independent predictors of
stroke.3 Even if a provider has a preference for the HINTS
exam as the sole diagnostic test in AVS visits, vascular risk
factors should still inform the pretest probability of stroke
and thereby influence the posttest probability.
Other Potential Causes of Acute Vestibular
Syndrome
AVS presentations are less commonly caused by demyelinating
lesions, structural lesions, immune-mediated disorders such
as cerebellitis, or thiamine deficiency. Dizziness is very com-
mon with multiple sclerosis, and the eighth cranial nerve is
only second to the optic nerve in the amount of central myelin.
Structural lesions are typically gradual in onset, but could
result in sudden changes if, for example, there is hemorrhage
within a melanoma metastasis. Vestibular schwannoma is not
expected to cause AVS because these are slow-growing tumors
which usually present with gradual hearing loss. Cerebellitis,
either idiopathic or from an immune-mediated disorder,
is another potential cause of AVS. Patients with cerebellitis
present with more of a subacute onset of symptoms
over days to weeks, and have clear central oculomotor abnor-
malities, gait difficulties, and dysmetria on coordination test-
ing of the extremities. Thiamine deficiency can present with
gaze-evoked nystagmus and a bilateral vestibulopathy.34
Vestibular migraine, Meniere’s disease, and benign parox-
ysmal positional vertigo (BPPV) usually present as episodic
vestibular syndromes. However, these disorders should be
considered in AVS presentations when other causes are not
identified. Many patients with BPPV report constant symp-
toms and may not have experienced enough positional attacks
to make it a distinguishing feature at the time of an ED visit.35
For this reason, positional testing for BPPV is recommended
whenever there is no spontaneous or gaze nystagmus or
another clear cause. The positive finding for BPPV is the
hallmark nystagmus that is triggered and transient. Although

Seminars in Neurology

posterior canal BPPV is the dominant form of BPPV when this
has been described in the outpatient setting, it is possible that
the horizontal canal variant represents a larger proportion that
expected with acute presentations.
Imaging
Brain imaging is commonly ordered in AVS patients. Use of CT
in the ED for dizziness increased from 10% of patients in 1995 to
25% by 2004.1 CT is a highly accurate test for intracranial
hemorrhage; however, a meta-analysis of seven studies found
that the sensitivity of CT for ischemic stroke is only 39% when
performed within 12 hours of symptom onset.36 The sensitivity
did not increase in one study that analyzed CT sensitivity after
12 hours of onset.37 MRI with diffusion-weighted imaging
(DWI) is much more accurate, with a sensitivity of 99% from
a meta-analysis of seven studies.36 Other studies, however,
found that the sensitivity of MRI is lower with small strokes,
strokes in the posterior fossa, and when MRI is performed
<24 hours from symptom onset compared with MRI per-
formed >24 hours from onset.38–41 Part of the lower accuracy
could relate to MRI-DWI protocols that use a slice thickness of
4 mm or gaps 2 mm.37,39 The study with the lowest sensi-
tivity for infarct used a DWI slice thickness of 7 mm and did not
report gap thickness.37 In one AVS study that used MRI-DWI
protocol with gaps of 0 to 1 mm, incidental infarcts on MRI
were actually more frequent than false-negative early MRI
(3/29 strokes with incidental infarct on MRI; 1/29 with false-
negative infarct on early MRI).3
Approach to the Acute Vestibular Syndrome
Presentation
The frequency of acute stroke was 11% (95% CI: 7–15%;
29/272) in a prospective single-center study of AVS that
used active surveillance and research MRIs in patients who
did not receive them clinically or if a clinical MRI was
performed <24 hours from onset.3 In this study, patients
were excluded for posterior canal BPPV, obvious medical
causes, or a history of similar recurrent episodes. This
frequency of stroke in AVS was much higher than the 3 to
4% prevalence of stroke diagnosis in the broader population
of all patients with dizziness as a reason for visiting the ED.1,2
In the AVS population, the probability of having a stroke on
MRI increases in the presence of vascular risk factors, any
possible or other mild central features, and central ocular
motor findings.3 If a unidirectional horizontal pattern of
nystagmus is identified, then a lesion of the peripheral
vestibular nerve is the most likely cause, although an infarct
of the brainstem or cerebellum is still possible. In the absence
of a central pattern of nystagmus, a prospective study found
that only 1 of 109 (<1%) patients had a stroke on MRI when
the vascular risk assessed using the ABCD2 score was 4 and
there were no other obvious focal findings on the general
neurologic examination.3 This misclassified patient had an
ABCD2 score of 4 but had a history of prior stroke, atrial
fibrillation, and diabetes. In another study of AVS presenta-
tions, all of the stroke patients (42/42) had either central
Acute Vestibular Syndrome Kerber et al.
nystagmus or severe imbalance defined as inability to walk
without support.42 The head impulse test and test of skew
deviation can also inform the likelihood of stroke. In a single-
center study with two neuro-ophthalmologists performing
the bedside examination, the HINTS examination alone had a
sensitivity of 97% (109/113: 95% CI, 92–99%) and specificity
of 84% (65/77: 95% CI, 75–91%).21 Four of the 113 (4%) stroke
patients had a HINTS exam suggesting a peripheral vestibu-
lar lesion (i.e., false negative for stroke). It is not clear if the
very high HINTS accuracy rates are generalizable outside of
the study’s examiners. Reliability of HINTS in a separate
study was only fair.3 It is possible that spectrum bias also
influenced the very high accuracy rates, and since the
population was referral-based, nearly all patients underwent
clinical MRI, and the frequency of stroke in this study was
very high (60%).21 When hearing loss was added to the HINTS
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exam as a symptom suggesting stroke, three of the four
HINTS false-negative cases were correctly classified.3 A
separate study found no patients with stroke on MRI
(0/86) when the HINTS exam was noncentral, vascular risk
was low, and no other obvious central deficits were present.3
There is currently an ongoing multicenter randomized clini-
cal trial of a bedside assessment using video-oculography
(including the HINTS assessment) to guide care in patients
who present to the ED for dizziness and have nystagmus or
pathologic ataxia (gait, trunk, stance, limbs; ClinicalTrials.
gov Identifier: NCT02483429). Because AVS presentations
are high risk for ischemic origin of central or peripheral
vestibular structures and MRI can miss small strokes in the
posterior fossa, clinicians should address cardiovascular risk
factors regardless of whether an infarct is identified on
imaging or not. Some patients with AVS and a negative acute
stroke evaluation may still benefit from 6 to 12 weeks of
aspirin, as this time period is the highest risk for a subse-
quent stroke and is the time period that aspirin
reduces secondary stroke events.43
Treatment of the Acute Vestibular Syndrome
The course of symptoms for AUV is gradual improvement
over days to weeks. About 20% of patients report some dizziness
even 12 months later.44 The primary treatment for unilateral
vestibulopathy is vestibular physical therapy (principally gaze-
stabilization exercises) which is supported by a meta-analysis
of 39 trials and a clinical practice guideline.45,46 Although the
population was postsurgical vestibulopathy in most of the
studies, trials specifically in nonsurgical AUV (e.g., vestibular
neuritis) found that physical therapy reduced dizziness severity
by 64 to 81% at 1 week to 1 month, compared with 42 to 58% in
controls.47,48 A Cochrane Collaboration meta-analysis of a short
course of corticosteroids concluded that there is insufficient
evidence to support their use in AUV.49 Although some studies
found improved recovery of the vestibular system measured by
caloric testing in treated versus controls,13,50 other studies did
not.12,44 In three trials that measured dizziness disability with
the DHI as the outcome, there was no evidence of benefit to
corticosteroids compared with placebo, and the trends favored
placebo.12,13,44 Furthermore, the caloric asymmetry only
Seminars in Neurology
Acute Vestibular Syndrome Kerber et al.

Table 2 Summary of clinical trials of pharmacologic symptomatic treatment in acute presentations of vertigo with outcomes
assessed at 30 min to 2 h from treatment

Author, year Population Intervention Outcome

Marill et al, 2000 Emergency department
vertigo patients
Irving et al, 2002 Vertigo, worsened
with movement,
and sudden in onset
Amini et al, 2014 Signs and symptoms
consistent
with peripheral vertigo
IV lorazepam 2 mg vs. 35% decrease in vertigo with ambulation
dimenhydrinate 50 mg (10-point scale) with lorazepam vs. 59%
decrease with dimenhydrinate (p ¼ 0.04)
56% increase in drowsiness (10-point scale)
with lorazepam vs. 0% increase with
dimenhydrinate
IM dimenhydrinate vs. 42% decrease in 10-point VAS for
IM droperidol dimenhydrinate vs. 46% decrease for
droperidol (p ¼ 0.9)
IV 25 mg promethazine vs. 66% decrease in severity on vertigo VAS for
IV 2 m lorazepam promethazine vs. 38% decrease for
lorazepam (p < 0.001). Adverse event of
lethargy in 4% of promethazine group vs.

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14% of lorazepam
Dogan, 201459 Acute vertigo IV dimenhydrinate 100 mg vs. 40% reduction in severity of vertigo on
IV piracetam 2,000 mg 10-point scale at 30 min in dimenhydrinate
vs. 45% reduction with piracetam (NS)
Shafipour et al, Acute peripheral vertigo IV 5 mg diazepam vs. 95% (71/75) with “excellent” improvement
2017 IV 25 mg promethazine with promethazine vs. 17% (13/75) with
“good” improvement with diazepam
Saberi et al, 2019 Acute peripheral vertigo IM promethazine 25 mg vs. 51% reduction with promethazine in
IV ondansetron 4 mg severity of vertigo on 10-point VAS at
2 h vs. 37% reduction with ondansetron

Abbreviations: IM, intramuscular; IV, intravenous; VAS, visual analog scale.

weakly correlates with the DHI,13,51 which is a validated
questionnaire of self-reported dizziness severity and associated
disability.52 If a short course of corticosteroids is discussed with
the patient, then the risks of possible adverse events should also
be considered including infections, blood clots, fractures, hy-
perglycemia, and hypertension.53
There are few high-grade clinical trials of pharmacologic
treatments of vertigo in acute presentations.54–58 Available
studies focus on heterogenous vertigo populations or acute
peripheral vertigo presentations without other criteria to
make it more specific to certain entitles. The studies are also
limited by their outcome measures, which were typically
10-point severity scales obtained 30 minutes to 2 hours after
treatment. Considering these limitations, the available studies
indicate that dimenhydrinate or promethazine is more effec-
tive in reducing vertigo severity compared with benzodiaze-
pines (►Table 2). Dimenhydrinate or promethazine also had
less sedation than benzodiazepines. For this reason, an initial
treatment with dimenhydrinate or promethazine is preferred.
The goal with all symptomatic medicines should be to reduce
their use after the first 1 to 2 days. Otherwise, the continued
use of the medicines can impair central compensation.
Conclusions
The AVS presentation is a unique type of dizziness presentation
with severe symptoms and nystagmus or imbalance. The most
likely causes are an AUV or stroke. Other causes such as
cerebellitis, peripheral vestibular disorders, or vestibular
migraine, are also possible. Stroke is very unlikely in the
absence of a central pattern of nystagmus, low vascular risk,
and no mild or possible other central findings on the general
neurologic examination. As a standalone diagnostic test, the
HINTS examination has been found to have high accuracy, but
the generalizability of the exam performance is not clear. The
natural history of AVS is gradual improvement with time and
vestibular physical therapy is an evidence-based treatment.
Conflict of Interest
None declared.
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