Evaluation of Acute

D i z z i n e s s a n d Ve r t i g o
Anand K. Bery, MDa,1, David E. Hale, MDb,1,*,
David E. Newman-Toker, MD, PhDb,c,2,
Ali S. Saber Tehrani, MD, PhDb,2

KEYWORDS
 Dizziness  Vertigo  Nystagmus  Ischemic stroke  Vestibular neuritis
 Benign paroxysmal positional vertigo  Vestibular migraine

KEY POINTS
 The qualitative description of vestibular symptom “type” is generally unreliable and usually
of limited value in guiding diagnosis of acute dizziness and vertigo.
 Instead, ask patients about the timing and triggers of their vestibular symptoms to cate-
gorize their symptoms as continuous or episodic and triggered or spontaneous.
 Use the correct examination based upon vestibular syndrome. The Head Impulse,
Nystagmus, Test of Skew examination is used for the (spontaneous) acute vestibular syn-
drome. Orthostatic vital signs and Dix-Hallpike maneuver are used for triggered (posi-
tional) episodic vestibular syndrome (EVS). Episode history and associated symptoms
guide diagnosis in spontaneous EVS.

INTRODUCTION

Dizziness and vertigo are challenging clinical presentations to diagnose, particularly in

front-line settings such as the emergency department (ED) and primary care. A wide
variety of general medical conditions, medications, and toxic exposures produce dizzi-
ness as a symptom.1 Among vestibular causes of dizziness and vertigo, benign inner
ear conditions are most common, but differentiating these conditions from dangerous
mimics, namely stroke of the posterior cerebral circulation, is an immense challenge,
often depending critically on interpretation of subtle eye movement findings.2

a
Department of Otolaryngology, Massachusetts Eye and Ear, Boston, MA, USA; b Department
of Neurology, Division of Neuro-Visual & Vestibular Disorders, Johns Hopkins Hospital, Johns
Hopkins School of Medicine, Baltimore, MD, USA; c Armstrong Institute Center for Diagnostic
Excellence, Johns Hopkins School of Medicine, Baltimore, MD, USA
1
Drs A.K. Bery and D.E. Hale served as co–first authors and contributed equally to the work.
2
Drs D.E. Newman-Toker and A.S. Saber Tehrani served as co-senior authors and contributed
equally to the work.
* Corresponding author. 600 Wolfe Street, Pathology 2-210, Baltimore, MD 21287.
E-mail address: dhale12@jh.edu

Med Clin N Am 109 (2025) 373–388

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 374 Bery et al

Population-level studies corroborate the need to improve diagnosis of dizziness and

vertigo across settings, including both the ED3 and ambulatory clinics.4 In 2023, the
Society for Academic Emergency Medicine published the first clinical practice guide-
line for diagnosis and initial management of acute dizziness and vertigo. The guideline,
known as GRACE-3,5 underscores the importance of disseminating new, evidence-
based diagnostic approaches to dizziness. Though developed for use in the ED, the
recommendations of GRACE-3 have broad applicability and relevance across general
care settings; accordingly, we will cite specific GRACE-3 recommendations at relevant
points throughout this article.

APPROACH TO THE DIZZY PATIENT IN THE ACUTE SETTING

While dizziness and vertigo do have specific definitions published by an international

consensus committee of vestibular medicine specialists (Box 1),6 these terms will be
used interchangeably in this article, as evidence has shown that symptom type in the
acute care setting does not reliably predict localization or etiology.7,8 For instance, a pa-
tient who describes a false sense of motion (“vertigo”6), even if it is clearly described as a
sense that “the room is spinning,” could have either a vestibular or cardiac cause for
their symptoms.9 Conversely, a patient who describes a sense of impending faint (“pre-
syncope”) may have a posterior circulation transient ischemic attack (TIA), rather than
vasovagal presyncope.10 The exception is isolated gait unsteadiness (without either
dizziness or vertigo), which implies a wider differential diagnosis that will not be
addressed directly in this article. A more evidence-based diagnostic approach is to
use the Triage-TiTrATE (timing, triggers, and targeted examination)1 method, described
as follows (Fig. 1).

Step 1: Triage
The first step in approaching a patient with dizziness is to take a diagnostic “pause” to
consider red flags that might suggest a life-threatening cause of dizziness. For
example, does the patient have signs of hemodynamic instability to suggest aortic
dissection? Is there fever and hypoxia suggesting pneumonia or pulmonary embolus?

Box 1
International consensus definitions for major vestibular symptoms

Dizziness is the sensation of disturbed or impaired spatial orientation without a false or

distorted sense of motion. This includes sensations sometimes referred to as giddiness,
lightheadedness, or nonspecific dizziness but does not include vertigo.
Presyncope (also near-syncope or faintness) is the sensation of impending loss of consciousness.
This sensation may or may not be followed by syncope. When patients report
“lightheadedness” (which is a very nonspecific term), it should be classified as presyncope,
dizziness, or both.
Syncope (also faint) is transient loss of consciousness due to transient global cerebral
hypoperfusion characterized by rapid onset, short duration, and spontaneous complete
recovery. Syncope usually leads to loss of postural control and falling.
Vertigo is the sensation of self-motion (of head/body) when no self-motion is occurring or the
sensation of distorted self-motion during an otherwise normal head movement.
Unsteadiness is the feeling of being unstable while seated, standing, or walking without a
particular directional preference. This sensation has previously been called disequilibrium or
imbalance.

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 Evaluation of Acute Dizziness and Vertigo 375

Fig. 1. An evidence-based approach to diagnosis of acute dizziness or vertigo emphasizing

TiTrATE (timing, triggers, and targeted examination).1 The history (timing, triggers) crucially
informs the targeted examination that will provide the highest diagnostic yield. For
example, HINTS is used in acute, continuous vertigo. Similarly, positional maneuvers such
as the Dix-Hallpike test are used in triggered, positional, episodic vertigo. BPPV, benign
paroxysmal positional vertigo; CPPV, central paroxysmal positional vertigo; DDx, differential
diagnosis; OH, orthostatic hypotension; TIA, transient ischemic attack.

Is consciousness altered in a way that may suggest intoxication, alcohol withdrawal,

or Wernicke’s syndrome? Table 1 outlines general medical “red flags” in dizziness
presentations that necessitate immediate attention.
Similarly, are there features that immediately point to a dangerous neurologic cause
of dizziness or vertigo (eg, lateralizing weakness or one of the “deadly D” symptoms
[Box 2])? Severe truncal or gait ataxia (for example, inability to sit upright or stand
without support) should also be considered a red flag. Lastly, new acute hearing
loss, when it accompanies acute vertigo (and is unaccompanied by obvious middle
or external ear pathology), should be considered cerebrovascular in etiology until
proven otherwise (see “Acute Vestibular Syndrome [AVS]” section). These neurologic
“red flags” should prompt a careful neurologic examination and strong consideration
of neuroimaging.
Step 2: Timing
Having appropriately triaged patients with obvious red flag features, we are left with
patients with isolated dizziness/vertigo. The next step is to consider the time course
of symptoms to begin pattern matching to one of the vestibular syndromes (Box 3).
Are symptoms still present at the time of assessment, and have they been continuous
since onset? If so, this is most likely the AVS.

ACUTE VESTIBULAR SYNDROME

AVS is defined as “a clinical syndrome of acute-onset, continuous vertigo, dizziness,

or unsteadiness lasting days to weeks, and generally including features suggestive of
new, ongoing vestibular system dysfunction (eg, vomiting, nystagmus, and severe
postural instability).”11 In AVS, localization is a key: do the symptoms come from a

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 376 Bery et al

Table 1
Prominent associated symptoms, signs, laboratory results, or exposures that may be available
at the initial triage step to inform diagnosis in dizziness/vertigo

Symptom or Finding Diagnoses that Are Suggested by the Finding

Altered mental status Wernicke encephalopathy; stroke; encephalitis; seizure;
hypertensive encephalopathy; intoxication with alcohol, illicit
drugs, carbon monoxide; alcohol withdrawal syndrome
Transient loss of Cardiac arrhythmia; acute coronary syndrome; aortic dissection;
consciousness pulmonary embolism; vasovagal syncope; hypovolemia;
stroke; subarachnoid hemorrhage; seizure
Headache Stroke; craniocervical vascular dissection; meningitis; carbon
monoxide exposure; VM; high or low intracranial pressure;
subarachnoid hemorrhage
Neck pain Craniocervical vascular dissection (especially of the vertebral
artery)
Chest/upper back pain Acute coronary syndrome; aortic dissection; pulmonary
embolism
Abdominal/low back pain Ruptured ectopic pregnancy; aortic dissection
Dyspnea or hypoxia Pulmonary embolism; pneumonia; anemia
Palpitations Arrhythmia; vasovagal syncope; panic disorder
Bleeding or fluid losses Hypovolemia; anemia
Fever or chills Systemic infection; encephalitis; mastoiditis; meningitis
Tachycardia Cardiac arrhythmia; pulmonary embolism; hypovolemia;
systemic infection; alcohol withdrawal syndrome
Abnormal glucose Symptomatic hypoglycemia; diabetic ketoacidosis
New/recent medication Medication side effects (eg, beta blocker) or toxicity (eg,
use gentamicin)
Recent otologic surgery Bacterial labyrinthitis; mastoiditis; perilymphatic fistula

Adapted from Newman-Toker DE, Edlow JA. TiTrATE: A Novel, Evidence-Based Approach to Diag-
nosing Acute Dizziness and Vertigo. Neurol Clin 2015;33(3):577-99; with permission.

peripheral (ie, inner ear) or central (ie, brain) structure? Usually, peripheral processes
are benign in etiology (the most common being vestibular neuritis, caused by transient
inflammation of the eighth cranial nerve). The most important central cause to rule out
is a posterior fossa stroke.
Localization in AVS depends critically on the Head Impulse, Nystagmus, Test of Skew
(HINTS) examination, a well-validated and evidence-based bedside battery2 with 3
components: head impulse, nystagmus, and test of skew. In large, high-quality clinical

Box 2
The “Deadly D’s” that can indicate a central-localizing cause of vestibular symptoms

1. Diplopia: the patient is experiencing double vision

2. Dysarthria: the patient has slurring of speech
3. Dysphonia: the patient has voice hoarseness or change in quality of voice
4. Dysphagia: the patient has difficulty swallowing
5. Dysmetria: the patient has a lack of coordination with finger to nose or heel to shin testing

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 Evaluation of Acute Dizziness and Vertigo 377

Box 3
International consensus definitions for major vestibular syndromes11,22,56

Acute vestibular syndrome

 AVS is a clinical syndrome of acute-onset, continuous vertigo, dizziness, or unsteadiness
lasting days to weeks, and generally including features suggestive of new, ongoing
vestibular system dysfunction (eg, vomiting, nystagmus, and severe postural instability).
 There may also be symptoms or signs suggesting cochlear or central nervous system
dysfunction.
 AVS usually connotes a single, monophasic event, often caused by a one-time disorder, but it
may instead punctuate a relapsing-and-remitting or stepwise, progressive illness course.
 Disorders typically presenting this syndrome include vestibular neuritis, acute labyrinthitis,
traumatic vestibulopathy, demyelinating disease with vestibular involvement, and strokes
affecting central or peripheral vestibular structures.
Episodic vestibular syndrome
 EVS is a clinical syndrome of transient vertigo, dizziness, or unsteadiness lasting seconds to
hours, occasionally days, and generally including features suggestive of temporary, short-
lived vestibular system dysfunction (eg, nausea, nystagmus, sudden falls).
 There may also be symptoms or signs suggesting cochlear or central nervous system
dysfunction.
 Episodic vestibular syndrome usually connotes multiple, recurrent events caused by an
episodic disorder with repeated spells (triggered or spontaneous), but may initially present
after the first event.
Chronic vestibular syndrome
 CVS is a clinical syndrome of chronic vertigo, dizziness, or unsteadiness lasting months to
years and generally including features suggestive of persistent vestibular system
dysfunction (eg, oscillopsia, nystagmus, gait unsteadiness).
 There may also be symptoms or signs suggesting cochlear or central nervous system
dysfunction.
 CVS often connotes a progressive, deteriorating course, but sometimes instead reflects a
stable, incomplete recovery after an acute vestibular event, or persistent, lingering
symptoms between episodic vestibular events.

studies, HINTS, in the hands of trained examiners, has been shown to be more sensitive
than early MRI for detecting posterior fossa stroke in AVS, while maintaining very high
specificity.12 Box 4 provides practical guidance on performing and interpreting the
HINTS examination, and Fig. 2 outlines HINTS components and their interpretation (pe-
ripheral vs central). Note that HINTS is optimized for sensitivity to pick up a central lesion,
and thus ALL components must point to a peripheral localization for the screening ex-
amination to confidently exclude a central process. In other words, if any item points
central, further workup to exclude a central process (typically posterior fossa MRI) is
indicated. A key GRACE-3 recommendation is to use MRI as a confirmatory test in pa-
tients with central or equivocal HINTS examinations.5 GRACE-3 recommends the use
of HINTS (for clinicians trained in its use) in AVS with nystagmus,5 as HINTS has been
most extensively validated among AVS patients who have nystagmus.12 AVS patients
without nystagmus are at very high risk of having stroke as a cause, so they should
generally be imaged regardless.13
We address common questions about approaching patients with acute, continuous
vertigo in Box 5.

A Note About Hearing Loss

The posterior cerebral circulation also supplies blood to the inner ear (both the cochlea
[hearing] and the vestibular apparatus [balance]). Though rare, a stroke of the vestibular

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 378 Bery et al

Box 4
Practical tips on how to perform and interpret each component of the HINTS examination

Head impulse test

How to perform?
The patient is first asked to keep fixation on a target, such as the examiner’s nose. The head
is grasped and rotated quickly. See second part of Linked Video 1 for a demonstration of
the head impulse test. We recommend head impulses be made from lateral toward the
midline (centripetal). The direction and timing of impulses should be unpredictable—for
example, instead of “left, right, left, right,” consider a pattern such as “left, left, right.”
to prevent the patient from predicting the next direction and compensating for a possible
vestibular deficiency.
How to interpret?
Watch the patient’s eyes carefully during and immediately after each impulse. If the eyes
slip off the target, a rapid movement of the eyes (a “saccade”) is often seen, particularly in
the acute period of a peripheral vestibular process. It is the presence of this refixation or
“catch-up” saccade that is a hallmark of a PERIPHERAL-localizing head impulse test. In the
case of a RIGHT-sided peripheral vestibular process, the catch-up saccade will be seen
immediately after head impulses toward the RIGHT (and vice-versa for a LEFT-sided
process). If no catch-up saccade is seen, this portion of the exam localizes CENTRAL until
proven otherwise. Note that the absence of a sign here points CENTRAL, which is
counterintuitive and a common source of confusion. For this same reason, we recommend
always describing HINTS findings as “central” or “peripheral” rather than “positive” or
“negative.”
Linked Video 2 demonstrates the findings in a PERIPHERAL head impulse test (where a
corrective saccade is seen) for a right-sided peripheral vestibular process. Note that a
peripheral-appearing head impulse test result can be seen in a small minority of strokes,
often because the inner ear has itself been affected (ie, internal auditory artery infarction);
for this reason, a peripheral-appearing head impulse result must be followed up with the
other two HINTS test elements, which can catch most such stroke head impulse test
“exceptions.”
Nystagmus
Nystagmus is defined as an involuntary, rapid, rhythmic, oscillatory eye movement with at
least one slow phase.57 When patients have dizziness/vertigo, by far the most common type
of nystagmus is jerk nystagmus, which has one slow phase and one fast phase (aka “quick
phase”). The slow phase is the pathologic phase; the eyes slowly drift off target, and the fast
phase (ie, a saccade) is required to bring them back.
For the purposes of the HINTS examination, assessing the direction of the fast phase is crucial.
In a peripheral process, the dominant nystagmus trajectory is horizontal and the fast phase is
unidirectional (ie, does not change from left-beating to right-beating), regardless of where
the patient is looking. For example, in the case of a destructive right-sided acute PERIPHERAL
process, the nystagmus always has its fast phase to the left (ie, it beats away from the
affected side with the abnormal head impulse test). Nystagmus in peripheral AVS will almost
always be most intense when looking in the direction of the fast phase (eg, left-beating
nystagmus most intense in leftward gaze). Although the nystagmus may vanish when the
patient looks opposite the fast phase (in this example, when looking to the right), it should
not change direction (ie, it should generally not beat right-ward in right gaze, which
typically only occurs with a CENTRAL process).
Linked Video 3 demonstrates the nystagmus seen in a right-sided PERIPHERAL process. Note
that the refixation saccade that occurs during the head impulse test with an acute destructive
peripheral lesion will almost always be in the same direction as the nystagmus fast phase,
making it harder to identify as a discrete finding; however, the nystagmus will pause briefly
during the head impulse itself, such that the refixation saccade will be out of rhythm with an
otherwise steady nystagmus. If the refixation saccade instead goes opposite the nystagmus
fast phase (ie, the abnormal head impulse test is on the “wrong” side [eg, in the example
aforementioned, if the head impulse toward the left ear is abnormal, causing a rightward
refixation saccade in the setting of a left-beating, spontaneous nystagmus]), the lesion may
instead be CENTRAL.

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 Evaluation of Acute Dizziness and Vertigo 379

Any other pattern of nystagmus direction should be considered CENTRAL for the purposes of
the HINTS examination. This includes nystagmus that changes direction with gaze (often
referred to as direction-changing, gaze-evoked nystagmus, with left-beating on leftward
gaze and right-beating on rightward gaze). This also includes nystagmus that has a pure
vertical or pure torsional vector.
Assessing for presence of Test of Skew (using the alternate cover test)
How to Perform?
The patient is asked to fixate on a target across the room. The eyes are alternately covered
(using the examiner’s palm [to avoid peeking between the examiner’s fingers], a folded
piece of paper, etc.). In the case of a misalignment of the eyes, movement of the eye will be
seen when the eye is uncovered. The principle is that the eye moves to its resting/preferred
position when it is under cover. When it is uncovered, it moves back to pick up fixation. The
second part of Linked Video 4 shows how to correctly perform the test of skew.
How to Interpret?
The presence of a vertical movement (refixation) on the alternate cover test more often
results from CENTRAL pathology. Note that many normal subjects have a small horizontal
misalignment, and horizontal misalignments (even when large) are not of diagnostic
significance in this clinical context. That said, the comorbid presence of a horizontal
misalignment may make a vertical refixation appear diagonal, rather than purely vertical.
We are specifically looking for a vertical (or diagonal) refixation movement when one eye
or the other is uncovered (generally one eye will move upward when uncovered, and the
opposite eye will move downward when uncovered). The first part of Linked Video 5
demonstrates the classic vertical refixation movement seen when the eyes are misaligned
vertically.

apparatus itself (not necessarily of the brain) can yield a peripheral HINTS localization,
despite being a dangerous vascular event. Because the cochlea is usually involved,
hearing loss will usually co-occur. For this reason, an assessment of auditory function
by finger rub at the bedside should be added to the 3-step HINTS battery (so-called
“HINTS Plus”14). Under this paradigm (directly supported by GRACE-3 recommenda-
tions5), the presence of significant new, unilateral hearing loss with AVS should be
treated as a vascular event until proven otherwise.

Fig. 2. Peripheral versus central findings on the HINTS examination in the acute vestibular
syndrome. HINTS is optimized for sensitivity at detecting stroke; thus, if any item is not in
a peripheral pattern, stroke workup is indicated.

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 380 Bery et al

Box 5
Frequently encountered situations in acute, continuous vertigo (and our practical responses)

What if my patient is too symptomatic to permit a close examination? Patients with the AVS are
often very symptomatic, especially soon after onset. We find it helpful to explain that a few
short minutes of examination are vital to reach a diagnosis. If there are any historic red flags,
then proceed to further targeted workup. Obtain what you can opportunistically—eg,
presence of nystagmus by observation. Prioritize screening neurologic examination,
coordination, ability to sit upright, HINTS, and bedside hearing assessment.
Since the head impulse test involves a relatively small amplitude rotation of the head (20 or
so), in our experience most patients tolerate it well. Encouragement is helpful. If at any point,
any item does not point toward a peripheral localization, have a low threshold for neurologic
workup, typically MRI brain with DWI. When in doubt, opt to observe the patient, obtain
further workup, and examine carefully when less symptomatic.
What if I am not sure about the head impulse test? This is a difficult maneuver comprising
psychomotor (the impulse) and cognitive (the interpretation) skills. We recommend practicing
this skill on all dizzy patients, even those who do not necessarily fit the AVS, to build expertise
and familiarity with normal and abnormal results.
Having a colleague record the patient’s eyes (eg, with a smartphone) while an impulse is
performed and playing the video in slow motion can assist with detecting a catch-up saccade if
one is unsure. If you lack confidence, focus on assessing gait severity, which is a reasonable
predictor (though not as good as HINTS).12,58

Etiologies that Produce Acute Vestibular Syndrome

Vestibular neuritis is inflammation of the vestibular portion of the eighth cranial nerve
that is usually transient and self-limited.15 It presents as acute dizziness or vertigo and
produces indistinguishable symptoms from a posterior fossa stroke causing isolated
dizziness or vertigo. Vestibular neuritis can be thought of as the eighth cranial nerve
analogue of an idiopathic facial nerve (“Bell’s”) palsy (which involves the seventh cra-
nial nerve). Annual incidence estimates range from 3.5 to 15.5 per 100,000 pa-
tients.16–18 The presumptive etiology in most cases of “typical” (idiopathic)
vestibular neuritis is viral or post-viral. The natural history is acute onset of dizzi-
ness/vertigo over hours to days, and slow improvement over weeks to months. Vestib-
ular rehabilitation can help with recovery, and early referral for vestibular physical
therapy is supported by available evidence.19
Ischemic stroke (of the brainstem or cerebellum) often causes isolated symptoms of
dizziness or vertigo without more obvious neurologic symptoms.20 Distinguishing this
kind of stroke from vestibular neuritis based on symptoms alone can be difficult or
impossible. In fact, dizziness is the symptom most tied to missed stroke, with roughly
40% of “pure vestibular” strokes missed by providers.21

EPISODIC VESTIBULAR SYNDROME

Episodic vestibular syndrome (EVS) is a clinical syndrome of transient vertigo, dizzi-

ness, or unsteadiness lasting seconds to hours, occasionally days, and generally
including features suggestive of temporary, short-lived vestibular system dysfunction
(eg, nausea, nystagmus, and sudden falls).22 EVS can occur either pursuant to a
trigger (t-EVS) or spontaneously (s-EVS).1 These, respectively, make up 30% and
20% of dizziness presentations in the acute setting, with EVS, overall, being the
most common presentation of dizziness in the ED.23

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 Evaluation of Acute Dizziness and Vertigo 381

Triggered Episodic Vestibular Syndrome

A trigger is a reliable action, movement, or situation that provokes the onset of symp-
toms.6 Most commonly, this includes a change in head or body position (eg, rolling
over in bed or arising from sitting to standing). Importantly, when approaching a pa-
tient with suspected t-EVS, the examiner must differentiate between actions that
exacerbate (ie, worsen) spontaneous symptoms from those that trigger (ie, cause
de novo) the symptoms to occur.24 This distinction allows the provider to differentiate,
for example, between continuous symptoms that worsen with head movements
(typical of AVS) and discrete episodic symptoms that begin after a head movement.
Episodes of t-EVS typically last from seconds to a minute.24 Fortunately, the 2 most
common causes of t-EVS—benign paroxysmal positional vertigo (BPPV) and ortho-
static hypotension (OH)—are benign in nature.25 Central paroxysmal positional vertigo
(CPPV) and OH secondary to serious medical causes are less frequent, yet important,
causes of t-EVS.25 To evaluate and differentiate these etiologies, the clinician can uti-
lize targeted examination maneuvers, including positional tests for BPPV and ortho-
static vital signs for OH, to recreate the patient’s symptoms while assessing for
associated physical examination signs.

Benign paroxysmal positional vertigo

BPPV is a common cause of dizziness with a lifetime prevalence of 2.4% in the overall
population.26 In the ED, it likely accounts for approximately 10% to 20% of presenta-
tions.23,27 This common disorder can be diagnosed without the use of costly tests and
treated at the bedside by a trained clinician. Patients present with a brief (generally
less than 1 min) sensation of dizziness or vertigo triggered by a head movement or po-
sition change.28 Most classically, this occurs when a patient rolls over in bed, gets out
of bed, or tips the head backward at an angle (eg, reaching for a top shelf). Patients
with BPPV often experience nausea and occasionally vomiting; some (especially the
elderly) may also feel unsteady on their feet. Because these symptoms may linger be-
tween episodes, the clinician taking the history must carefully differentiate the length
of the dizziness and its after-effects to correctly identify the patient’s symptoms as
episodic, rather than continuous. BPPV is caused by otoconia, calcium carbonate
crystals normally located in the inner ear organ, that become displaced into the semi-
circular canals, the areas of the inner ear that sense rotations of the head. When the
head moves relative to gravity, the otoconia move activates signals within the vestib-
ular system to cause the sensation of false motion that patients experience.28 The oto-
conia typically become displaced to the posterior semicircular canal (pc-BPPV) of the
inner ear or the horizontal semicircular canal (hc-BPPV), leading to the 2 most com-
mon sub-types of BPPV.29 BPPV is diagnosed by completing positional testing spe-
cific to each canal (ie, the posterior canal or horizontal canal) and observing a
characteristic nystagmus. Classically, the nystagmus has a latency (begins briefly af-
ter the head position change), a crescendo phase (builds as the crystals move), and a
decrescendo phase (lessens as the crystals settle again), all in a time frame of gener-
ally less than 1 min.30 pc-BPPV is diagnosed after observing classical upbeat-torsional
nystagmus during the Dix-Hallpike test on the side of the affected ear; treatment is
with either the modified Epley (Linked Video 6) or Semont maneuver. Hc-BPPV is diag-
nosed after observing classical horizontal nystagmus (beating toward the ear facing
the ground [“geotropic”]) during the supine roll test (to either side, with the nystagmus
more prominent when rolling toward the affected ear); treatment is with either the Lem-
pert roll or Gufoni maneuver31 (Linked Video 7).
If, during positional testing, an unexpected pattern of nystagmus is observed, such
as downbeat or apogeotropic (away from the ground) horizontal nystagmus, or if the

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 382 Bery et al

nystagmus is persistent, the patient may have CPPV.32,33 CPPV can be caused by le-
sions of the posterior fossa that disrupt the graviceptive pathways that travel from the
inner ear structures through the brainstem and cerebellum.32 Therefore, these patients
often have other central-localizing findings on their general neurologic examinations,
while a patient with BPPV should have an otherwise normal examination. GRACE-3
guidelines support that patients who have BPPV should not undergo neuroimaging
unless atypical features are present that suggest a BPPV mimic, in which case MRI
with contrast is the preferred modality.5

Orthostatic hypotension
OH often causes dizziness or vertigo on arising (from lying to sitting or sitting to stand-
ing). Classical teaching suggests OH presents with lightheadedness or symptoms of
feeling faint (presyncope), but more than one-third of OH patients experience a spin-
ning vertigo sensation.9,34 This further emphasizes that in patients with episodic symp-
toms, especially if triggered by postural change, orthostatic vital signs should be
measured rather than relying solely upon symptom type. Triggers are likely to be help-
ful in distinguishing BPPV from OH; both cause symptoms on arising, but only BPPV
should cause symptoms when rolling in bed. OH, by definition, occurs with drop in
systolic (>20 mm Hg) or diastolic (>10 mm Hg) blood pressure within 3 min after stand-
ing after either sitting or lying.35 Numerous potential causes range from medication ef-
fects to vertebrobasilar insufficiency; in the acute setting more serious causes,
including cardiac diseases and blood loss, should be considered.36,37 Because medi-
cation effects (eg, with antihypertensives) commonly produce an orthostatic drop in
blood pressure, positional testing for BPPV may be warranted even when OH is
identified.

Spontaneous Episodic Vestibular Syndrome

Spontaneous EVS occurs unprovoked, without a clear or reliable trigger. Most s-EVS
episodes occur on a time frame of minutes to hours; thus, they typically resolve prior to
the patient’s evaluation and cannot be reproduced during examination (as with t-EVS).
Consequently, the goal of evaluating s-EVS is taking a detailed history to understand
the context surrounding the episode and any associated symptoms during the
episode. The most common, benign cause of s-EVS is vestibular migraine (VM); other
benign causes include vasovagal syncope and panic attack. Menière disease is a
classic cause of s-EVS, but it is nearly 5-fold less common than VM.23 The most com-
mon "cannot-miss" diagnosis is TIA with other serious causes including cardiac
arrhythmia and hypoglycemia. Again, as is the case for t-EVS, the symptom type is
generally uninformative. Cardiovascular etiologies, including cardiac arrhythmia, often
present with vertigo, as opposed to presyncope.9,38 Instead, the timing (onset, dura-
tion) of the episode and associated symptoms help identify the diagnosis. Lastly, if the
spontaneous episode is still present at the time of evaluation, the examination
described in the AVS section can differentiate central- and peripheral-localizing
etiologies.39

Vestibular migraine
Vestibular migraine (VM), a common cause of s-EVS, is estimated to affect 6.1 million
individuals, with a 1-y prevalence of approximately 2.7%.40 Diagnostic criteria arise
from consensus criteria from the International Headache Society and International
Classification of Vestibular Disorders of the Bárány Society.41,42 To be diagnosed
with VM, a patient must have at least 5 episodes of vestibular symptoms that can range
from 5 min to 72 h with at least 50% of episodes associated with a migraine-type

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 Evaluation of Acute Dizziness and Vertigo 383

headache, photophobia and phonophobia, or visual aura. Patients must also have a
current or prior diagnosis of migraine with or without aura according to the International
Classification of Headache Disorders’ definition of migraine. Clinically, patients often
also experience motion sensitivity and feelings of imbalance or tilt.43 It is important to
note patients with VM can experience any vestibular symptom, which again empha-
sizes the importance of understanding the episode timing and associated symptoms,
rather than making a diagnosis based upon symptom type alone. Many patients with
VM have predisposing factors for their symptoms (eg, lack of sleep)—this is not defined
as a direct trigger of their symptoms (as a position change would be in BPPV). Although
patients must have at least 5 episodes of vestibular symptoms to be diagnosed with
VM, all patients with VM will have a first episode of VM. These troubling first-time symp-
toms may result in a presentation to the ED, and, if evaluated acutely, patients can have
a range of ictal ocular motor findings, including nystagmus that may appear central-
localizing.44,45 When central findings are identified in a patient who has not previously
been imaged, MRI with diffusion-weighted images (DWI) is warranted to search for ev-
idence that might suggest a diagnosis of TIA instead of VM. Interictally, patients with VM
often have non-specific examination findings, and the diagnosis is made based upon
the patient’s history with a focus on timing, triggers, and associated symptoms.

Menière’s disease
Menière’s disease (MD) is a less common cause of s-EVS. Although commonly taught
as the prototypical cause of spontaneous vertigo, it is far less common than VM with
an estimated prevalence of 34 to 190 per 100,000.46 Similar to VM, diagnostic criteria
have been defined by consensus across multiple national and international neuro-
otology societies.47 The patient must have 2 or more spontaneous episodes of vertigo
of 20 min to 12 h duration, documented low-to medium-frequency sensorineural hear-
ing loss surrounding the episode of dizziness, and fluctuating aural symptoms (hearing
changes, tinnitus, and fullness) in the affected ear. During episodes, patients classi-
cally go through 2 nystagmus phases: an “irritative” phase in which horizontal
nystagmus beats toward the affected ear and a “recovery” phase in which it beats
away from the affected ear.46,48 Aside from the classic horizontal nystagmus, other
patterns of nystagmus, including ictal downbeat nystagmus, have been reported as
well.49 Importantly, patients who are evaluated for dizziness may have a longstanding
history of mild, subjective transient auditory symptoms, but this by itself does not point
to MD and, instead, may suggest migraine.42,43,50 There is thought to be an overlap
between MD and VM, with a higher prevalence of migraine in patients with MD
when compared with the prevalence of migraine in the general population, and vice
versa.51–53 Careful history taking and correct supportive evaluations, including audi-
ometry, can usually help differentiate these 2 related disorders.

Transient ischemic attack

Just as ischemic strokes can present with isolated vertigo, TIA can as well. Roughly
12% of patients with vertebrobasilar stroke report a preceding episode of isolated
vertigo or imbalance without focal neurologic findings,20,54 and up to 10% of patients
with s-EVS are diagnosed with TIA as a cause.23 History-taking should include an
assessment for comorbid neurologic symptoms during the episode (or as part of
other recent spells), including focal weakness or “deadly D’s” (see Box 2), and un-
derlying vascular risk factors. If present, these features substantially increase the
odds of TIA as the cause of dizziness or vertigo, but their absence does not rule
out TIA.12,20 Patients with a suspected TIA should be evaluated with appropriate
neuro-vascular imaging, including computed tomography (CT) angiography (CTA)

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 384 Bery et al

or magnetic resonance angiography (MRA). MRI with DWI may identify small
ischemic lesions.55 Non-contrast CT scans should be avoided due to their low diag-
nostic yield (a GRACE-3 recommendation5).

SUMMARY

Dizziness and vertigo are challenging clinical presentations, given the multitude of
medical, neurologic, and otolaryngologic causes of such symptoms. This diagnostic
challenge is compounded by the fact that cannot-miss diseases can present with
the same symptoms as self-limited diseases. The framework we provide—supported
by practical guidelines, pearls, and tips—will guide clinicians toward the correct
diagnosis.

CLINICS CARE POINTS

Pearls
 Focus your history on the timing and triggers of the patient’s vestibular symptoms rather
than on symptom “type” (ie, qualitative description as dizziness, vertigo, unsteadiness,
etc.). Note that vestibular symptoms do not necessarily imply a primary vestibular etiology.
First, determine whether the symptoms are acute and continuous or episodic.
 If symptoms are new, continuous, and accompanied by other peri-vestibular symptoms (eg,
nausea/vomiting, gait unsteadiness), this is the AVS. Most AVS is “spontaneous” (ie, not post-
exposure). In isolated AVS with nystagmus, apply the HINTS examination to differentiate
between peripheral (eg, vestibular neuritis) and central (eg, stroke) localizations.
 If symptoms are brief, and especially if they are recurrent, this is the “EVS”. EVS is often
triggered, and the most common trigger is a change in head position or body posture.
The 2 most common causes of positional EVS are OH and BPPV. If triggered only on arising
without symptoms when rolling in bed, measure orthostatic vital signs. Regardless, complete
positional tests (Dix-Hallpike, supine roll) to evaluate for BPPV.
 If an EVS is spontaneous, the most common causes are vasovagal presyncope and VM, but the
“cannot miss” diagnosis is TIA. Focus your history taking on the pattern of prior dizziness
episodes, and leverage any associated symptoms (then or now) that are neurologic, auditory/
aural, or cardiovascular. Always ask about the “deadly D’s” (diplopia, dysarthria, dysphonia,
dysphagia, and dysmetria), which are red flags and frequent harbingers of brainstem or
cerebellar TIA.
Pitfalls
 Symptom quality (“type”) is unreliable as a diagnostic tool; for example, patients with BPPV
may describe postural lightheadedness while those with a cardiac cause for their dizziness
frequently describe room-spinning vertigo.
 Patients with BPPV may initially describe symptoms that seem to be continuous because
patients feel nauseated or slightly off balance between frequent, triggered episodes. Be
sure to differentiate truly continuous vestibular symptoms exacerbated by head movement
in AVS from episodic symptoms triggered by head movement in EVS.
 To conclude a HINTS examination supports a peripheral localization in AVS, all three
components must point to a peripheral lesion. In other words, if any 1 component
localizes centrally, assessment for stroke by MRI with DWI is warranted.
 Although auditory symptoms usually point to a peripheral localization, take care with new,
unilateral hearing loss in patients with AVS, who may have inner ear infarction. In these
patients, even MRI with DWI may not demonstrate the lesion.
 Many patients have OH from medications, but the presence of OH does not always indicate
orthostatic dizziness. Before diagnosing OH as the cause, be sure symptoms correspond to
the OH and do not occur when supine (eg, rolling in bed).
 Positional vertigo is usually due to BPPV. However, beware of cases demonstrating downbeat
or apogeotropic (away from the floor) horizontal nystagmus on positional testing. These
patients may harbor structural brain lesions in the posterior cranial fossa.

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 Evaluation of Acute Dizziness and Vertigo 385

 CT scans are commonly used to search for “central causes,” but often provide only false
reassurance when they show no ischemic stroke, since their sensitivity is very low.
Excluding small posterior fossa strokes requires MRI with DWI in an appropriate time
window (roughly 3–7 days post onset of persistent symptoms). Excluding TIA requires a full
stroke workup, including vascular imaging by CTA or contrast-enhanced MRA.

ACKNOWLEDGMENTS

The authors thank Megan Clark, MWC, for editing assistance funded by the Armstrong
Institute Center for Diagnostic Excellence.

DISCLOSURE

Dr D.E. Newman-Toker reports grants and contracts related to dizziness/stroke diag-

nosis and diagnostic error from the Agency for Healthcare Research and Quality,
United States, Gordon and Betty Moore Foundation, United States, Society to
Improve Diagnosis in Medicine, United States, and Natus Inc.; medicolegal consulting
for both plaintiff and defense firms related to misdiagnosis of neurologic conditions,
including dizziness and stroke; and honoraria for lectures on these topics; outside
the submitted work. He has a patent (US Appl. No. 17/597,213; filed Dec. 29, 2021)
pending for smartphone-based stroke diagnosis in patients with dizziness. All other
authors have nothing to disclose.

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