The Journal of Emergency Medicine, Vol. -, No. -, pp.

1–15, 2018
Ó 2017 Elsevier Inc. All rights reserved.
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https://doi.org/10.1016/j.jemermed.2017.12.024

Clinical
Review

A NEW DIAGNOSTIC APPROACH TO THE ADULT PATIENT WITH ACUTE DIZZINESS

Jonathan A. Edlow, MD,*† Kiersten L. Gurley, MD,*†‡ and David E. Newman-Toker, MD, PHD§
*Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, †Harvard Medical School, Boston,
Massachusetts, ‡Department of Emergency Medicine, Mount Auburn Hospital, Cambridge, Massachusetts, and §Division of Neuro-Visual
and Vestibular Disorders, Department of Neurology, Otolaryngology, and Emergency Medicine, The Johns Hopkins University School of
Medicine, Baltimore, Maryland
Corresponding Address: Jonathan A. Edlow, MD, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, 330 Brookline
Avenue, Boston, MA 02215

, Abstract—Background: Dizziness, a common chief from posterior fossa structural lesions. Conclusions: The
complaint, has an extensive differential diagnosis that timing and triggers diagnostic approach for the acutely
includes both benign and serious conditions. Emergency dizzy patient derives from current best evidence and offers
physicians must distinguish the majority of patients with the potential to reduce misdiagnosis while simultaneously
self-limiting conditions from those with serious illnesses decreases diagnostic test overuse, unnecessary hospitaliza-
that require acute treatment. Objective of the Review: tion, and incorrect treatments. Ó 2017 Elsevier Inc. All
This article presents a new approach to diagnosis of the rights reserved.
acutely dizzy patient that emphasizes different aspects of
the history to guide a focused physical examination with , Keywords—dizziness; vertigo; diagnosis; misdiagnosis;
the goal of differentiating benign peripheral vestibular con- BPPV; vestibular neuritis; nystagmus; posterior circulation
ditions from dangerous posterior circulation strokes in the stroke
emergency department. Discussion: Currently, misdiagno-
ses are frequent and diagnostic testing costs are high. This
relates in part to use of an outdated, prevalent, diagnostic INTRODUCTION
paradigm. The traditional approach, which relies on dizzi-
ness symptom quality or type (i.e., vertigo, presyncope, or Approximately 3.5% of emergency department (ED) visits
disequilibrium) to guide inquiry, does not distinguish benign are for dizziness (1,2). Using the fewest possible resources,
from dangerous causes, and is inconsistent with current best physicians must distinguish between the large majority of
evidence. A new approach divides patients into three key dizzy patients with self-limiting or easily treatable condi-
categories using timing and triggers, guiding a differential tions and the minority with life- or brain-threatening con-
diagnosis and targeted bedside examination protocol: 1) ditions. Compared to those without dizziness, dizzy
acute vestibular syndrome, where bedside physical exami- patients undergo more testing, more imaging, have longer
nation differentiates vestibular neuritis from stroke; 2)
ED lengths of stay, and are more likely to be admitted (1).
spontaneous episodic vestibular syndrome, where associated
symptoms help differentiate vestibular migraine from tran-
In 2013, total health care–related costs for patients with
sient ischemic attack; and 3) triggered episodic vestibular dizziness in the United States was estimated to exceed
syndrome, where the Dix-Hallpike and supine roll test $10 billion (3,4). Additional ‘‘costs’’ included adverse
help differentiate benign paroxysmal positional vertigo events, such as patient anxiety, injuries from falls, and
preventable major strokes following misdiagnosed minor
Reprints are not available from the authors. cerebrovascular events (5).

RECEIVED: 20 June 2017; FINAL SUBMISSION RECEIVED: 21 October 2017;

ACCEPTED: 1 December 2017

1
2 J. A. Edlow et al.

Figure 1. Diagnostic approach to the acutely dizzy patient. ATTEST = A, associated symptoms; TT, timing and triggers; ES, ex-
amination signs; and T, additional testing as needed. The first step is to take a history focused on associated symptoms, timing
and triggers of the dizziness, and the overall context. Many patients’ histories will suggest a general medical cause (various toxic,
metabolic, infectious, or cardiovascular causes). In this group of patients, we recommend a very brief diagnostic ‘‘stop’’ in order
to reduce misdiagnosis. As part of this stop, first make sure there are no suspicious neurovestibular signs (nystagmus, limb
ataxia, or gait/truncal ataxia). If a general medical cause still seems likely, evaluate and treat for the presumed diagnosis or di-
agnoses. For patients with a positive stop or whose history does not suggest a general medical cause, ask questions aimed at
timing and triggers to place the patient into one of three categories. For patients in the acute vestibular syndrome (AVS) and trig-
gered, episodic vestibular syndrome (t-EVS), physical examination (see text) will often allow a specific diagnosis to be made. For
patients with the spontaneous episodic vestibular syndrome (s-EVS), use history to try to distinguish vestibular migraine from
transient ischemic attack (TIA) or other causes (see text) since, by definition, these patients will no longer have symptoms and
their dizziness cannot be triggered at the bedside. BPPV = benign paroxysmal positional vertigo.

The existing diagnostic paradigm for dizziness, based pass various words patients use to describe disturbed
on symptom quality or type of dizziness (i.e., asking the balance or spatial orientation, such as lightheaded, spin-
question ‘‘what do you mean ‘dizzy’?’’), is taught across ning, rocking, vertigo, off balance, and others.
specialties; however, newer research has questioned its
scientific basis (6). Taking a history from a dizzy patient
DISCUSSION
should be no different than taking a history in other pa-
tients. The timing, triggers, and evolution over time; asso- Differential Diagnosis
ciated symptoms; and context (and not the descriptor
used) best inform the differential diagnosis (7). Bedside Numerous conditions cause acute dizziness. A study from
examination can frequently establish a specific diagnosis a national database (National Hospital Ambulatory Med-
(8). A confident diagnosis of a peripheral vestibular prob- ical Care Survey), over a 13-year period, of 9472 patients
lem obviates the need for specialty consultation, expen- with dizziness reported general medical (including non-
sive imaging, and hospitalization. When the evaluation stroke cardiovascular) diagnoses (50%), otovestibular
suggests a central problem, especially stroke, steps can diagnoses (33%), and neurologic (including stroke) di-
be taken to prevent harm by early initiation of secondary agnoses (11%) (1). In this study, 22% of patients
stroke prevention for milder presentations or thromboly- received a symptom-only dizziness (not otherwise speci-
sis or surgical interventions for more malignant presenta- fied) diagnosis. Although assigning a symptom-only
tions (9). We propose a new diagnostic algorithm to guide diagnosis is common in emergency medicine practice,
one’s approach to the acutely dizzy patient (see Figure 1). this was much more common in dizzy patients than in
In this article, we use the general term dizziness to encom- non-dizzy controls (22.1% vs. 8.4%; odds ratio 3.1) (1).
Diagnostic Approach to Acute Dizziness in Adults 3

Prospectively defined ‘‘dangerous’’ diagnoses (a mix of type (19). More than 60% of the patients endorsed more
medical and neurologic conditions for which a poor than one dizziness type. This finding alone severely un-
outcome was likely without treatment) were found in dercuts the logic of a diagnostic process based on dizzi-
15% of patients and were more common in older patients ness type. Beyond imprecision and inconsistency, the
(21% dangerous diagnoses in patients $50 years vs. 9.35 differential diagnosis is not tightly linked with the use
in patients < 50). The most common serious diagnoses of a given word. Use of the term vertigo was not associ-
were fluid and electrolyte disturbances (5.6%), cerebro- ated with stroke in a large series of ED patients with
vascular diseases (4.0%), cardiac dysrhythmias (3.2%), dizziness (20). Patients with a cardiovascular cause of
acute coronary syndromes (1.7%), anemia (1.6%), and dizziness describe ‘‘vertigo’’ in almost 40% of cases,
hypoglycemia (1.4%) (1). more than the fraction that described presyncope (21). Pa-
In a prospective single-institution study, 23 of 413 tients with benign paroxysmal positional vertigo (BPPV)
(6%) adult ED patients with dizziness had a central ner- often describe non-vertiginous dizziness, especially in
vous system (CNS) diagnosis (2). Another 3-year study elderly patients (22). Despite these newer data, most phy-
of 907 ED patients with dizziness, vertigo, or imbalance sicians still use a symptom-quality approach with dizzy
as a primary symptom reported that 1 in 5 were admitted patients without considering the timing and triggers
(68% to an intensive care unit) (10). Most patients had (6,23).
benign conditions, such as peripheral vestibular problems By way of analogy to another common medical
(32%), orthostatic hypotension (13%), and migraine complaint, patients with ‘‘sharp’’ chest pain are more
(4%). No specific diagnosis was made in 22% of cases. likely to have pulmonary embolism and those with
Serious neurologic disease was found in 49 (5%) patients, ‘‘dull’’’ chest pain are more likely to have acute coronary
of which 37 were cerebrovascular. Only 2 patients with syndromes, but one does not use the quality of the pain in
serious neurologic disease presented with isolated dizzi- such a binary way (17). Timing and triggers are more
ness, although patients were not systematically imaged, important in creating and rank-ordering a differential diag-
so some may have been missed. nosis. Intermittent exertional chest pain that resolves with
Thus, the overall incidence of important CNS disease rest suggests angina, whereas constant chest pain lasting
in adult ED patients with acute dizziness is approximately hours is more likely to be myocardial infarction. Chest
5%, most of which is stroke. Risk factors for CNS causes pain regularly triggered by swallowing suggests an esoph-
of dizziness include increasing age, history of vascular ageal problem. The history for virtually all chief com-
disease or previous stroke, the complaint of ‘‘instability,’’ plaints exploits the concept of timing and triggers.
abnormal gait, and focal neurologic findings (1,10–14). Patients are far more consistent in their responses to timing
and triggers than they are for dizziness type (19). Context
Origin and Flaws of the Traditional Approach and associated symptoms are also important in diagnosis;
for example, a smoker with chest pain, fever, and purulent
The symptom-quality paradigm comes from a methodo- sputum is conceptually different from a cancer patient
logically flawed study published in 1972 (Appendix 1) with chest pain, leg swelling, and dyspnea.
that was embraced by the medical establishment
(15,16). This approach is based on first asking a dizzy DIAGNOSTIC PITFALLS
patient, ‘‘What do you mean by, ‘dizzy’?’’ and then
using the response to generate a differential diagnosis In a retrospective German study of 475 consecutive ED
(e.g., vestibular problems if ‘‘vertigo,’’ cardiovascular dizzy patients seen by neurologists (who routinely per-
disorders if ‘‘presyncope’’ or ‘‘near-syncope,’’ formed a detailed ocular motor examination using Fren-
neurologic issues for ‘‘disequilibrium’’ and psychiatric, zel lenses), the neurologists diagnosed benign
or metabolic causes if ‘‘other’’). For this approach to conditions in 73% of cases and serious conditions (mostly
work, two facts must be true. Patients should be able to cerebrovascular and inflammatory CNS disease) in 27%
consistently choose one (and only one) dizziness type of cases (24). A neurologist masked to the initial ED visit
and each symptom type should be tightly linked with a changed the diagnosis at follow-up in 44% of those revis-
given differential diagnosis. Both are demonstrably iting within 30 days. Benign vestibular diagnoses were
false (6,16,17). deemed wrong in 58% (n = 21 of 36), including 17%
In a 2007 study, ED patients with dizziness were asked (n = 6 of 36) with missed ischemic stroke or transient
a series of questions aimed at determining the reliability ischemic attack (TIA).
and consistency of eliciting ‘‘symptom quality’’ and The most common reason for misdiagnosis was
timing and triggers of their dizziness (18). When the an evolution of the clinical course over time, which
main question was re-asked an average of 6 min later, factored in 70% of misdiagnoses (24). This is part and
half of the patients changed their primary dizziness parcel of emergency medicine; initially ambiguous (or
4 J. A. Edlow et al.

nonexistent) symptoms or signs evolve over time. There Not considering stroke in young patients is a particularly
has never been (and likely never will be) a head-to-head important contributing factor (30,35).
comparison of emergency physicians vs. neurologists
diagnosing patients with dizziness at the same phase of GOALS OF CARE
care, but this German study shows that diagnosing dizzi-
ness is complicated, even for those with specialized Primary goals of care in ED patients with dizziness not
training and focus. due to medical causes are to differentiate benign periph-
Posterior circulation strokes mimic peripheral causes eral vestibular conditions from posterior circulation
of dizziness (25–27). In one study from an ear, nose, strokes or other dangerous causes (rather than to make
and throat clinic, almost 3% of patients referred for a definitive diagnosis) and to manage symptoms appro-
vertigo had a missed cerebellar stroke (26). A missed priately before discharge in those who do not have serious
stroke diagnosis is important because the underlying diseases. It is usually the case that a definitive, final diag-
vascular pathology goes untreated (leaving the patient nosis is not the goal of ED care. However, with dizziness,
vulnerable to another stroke that might be prevented the most certain way to ‘‘rule out’’ dangerous causes is to
with secondary prophylaxis) and because patients can ‘‘rule in’’ one of two common, benign inner ear condi-
develop posterior fossa edema, which can be fatal tions (BPPV or vestibular neuritis) by bedside examina-
(28–30). Lost opportunity for thrombolysis is another tion. Furthermore, doing so leads to the correct choice
negative consequence of missing a posterior circulation of symptomatic treatment (repositioning maneuvers for
stroke; however, many cerebrovascular dizzy patients BPPV or vestibular suppressant medications for vestib-
have minor deficits and present late, and may not be ular neuritis).
thrombolysis candidates (31–33).
Younger age and vertebral dissection as the cause for A NEW DIAGNOSTIC PARADIGM
acute dizziness were found to be risk factors for missed
cerebellar stroke (34,35). Posterior circulation location A new diagnostic paradigm is based on the timing, trig-
is a risk factor for stroke misdiagnosis in general gers, associated symptoms, and context of the dizzy
(31,36–38). To put these data into context, only a very symptoms. Although the use of this new paradigm has
small proportion (0.18–0.7%) of ED patients diagnosed not yet been proven to reduce misdiagnosis in prospective
with a benign or peripheral vestibular diagnosis return clinical trials, it is supported by a very strong evidence
to the ED within 30 days and are hospitalized with a base in the specialty literature; it is also noteworthy that
cerebrovascular diagnosis (38–41). However, because the traditional paradigm is not evidence-based and likely
dizziness is so common, this very small percentage predisposes to misdiagnosis (16,44). We believe that this
probably translates into tens of thousands of missed new method allows one to confidently make an accurate
strokes and likely thousands of patients harmed each diagnosis more frequently than the traditional
year (42). paradigm. Although other acronyms have been used,
Knowledge gaps regarding eye-movement findings here we use the mnemonic: ATTEST (associated
also contribute to misdiagnosis (6). In a study of 1091 symptoms, timing and triggers, bedside examination
dizzy patients in U.S. EDs, physicians used templates signs, and additional testing as needed) (7).
to document the presence or absence of nystagmus in In the traditional paradigm, a patient endorsing vertigo
887 (80%). Nystagmus was said to be present in 185 would undergo an evaluation for peripheral vestibular vs.
(21%) (43). Of these 185 patients, sufficient information central causes of dizziness. This has led to confusion,
regarding the nystagmus to be diagnostically useful was such as using CT imaging for diagnosis and meclizine
recorded in only 10 (5.4%). Of patients given a peripheral for treatment of vertigo, no matter what the cause (45).
vestibular diagnosis, the nystagmus description Physicians tend to generalize their management of pa-
conflicted with the final diagnosis in 81%. Misdiagnosis tients with peripheral vertigo, whereas the 2 most com-
of common peripheral vestibular problems, such as mon causes (BPPV and vestibular neuritis) should be
BPPV and vestibular neuritis, leads to ineffective treat- managed very differently (42). We present three distinct
ments and resource overutilization (42). timing and triggers categories that are important for
Misdiagnosis of patients with dizziness results from emergency physicians to recognize (Table 1 and
five common pitfalls: over-reliance on a symptom- Figure 1).
quality approach to diagnosis, underuse of a timing and
triggers approach, lack of familiarity with key physical Acute Vestibular Syndrome
examination findings, overweighting traditional factors
such as age and vascular risk factors to screen patients, Spontaneous acute vestibular syndrome (AVS) is defined
and over-reliance on computed tomography (CT) (6). as the acute onset of persistent dizziness associated with
Diagnostic Approach to Acute Dizziness in Adults 5

Table 1. Timing-and-Trigger–Based ‘‘Vestibular* Syndromes’’ in Acute Dizziness†

Syndrome Description Common Benign Causes Common Serious Causes

AVS Acute, continuous dizziness lasting days, Vestibular neuritis Posterior circulation ischemic stroke
accompanied by nausea, vomiting, Labyrinthitis
nystagmus, head motion intolerance, and
gait unsteadiness
s-EVS Episodic dizziness that occurs Vestibular migraine TIA
spontaneously, is not triggered,‡ and Menière’s disease
usually last minutes to hours
t-EVS Episodic dizziness brought on by a specific, BPPV CPPV
obligate trigger (typically a change in head Orthostatic hypotension due to serious
position or standing up), and usually medical illness
lasting <1 min

AVS = acute vestibular syndrome; BPPV = benign paroxysmal positional vertigo; CPPV = central paroxysmal positional vertigo;
s-EVS = spontaneous, episodic vestibular syndrome; TIA = transient ischemic attack; t-EVS = triggered, episodic vestibular syndrome.
* Note that the use of the word vestibular here connotes vestibular symptoms (e.g., dizziness or vertigo or imbalance or lightheadedness),
rather than underlying vestibular diseases (e.g., benign paroxysmal positional vertigo, vestibular neuritis).
† This table lists the more common diseases causing these presenting syndromes and is not intended to be exhaustive.
‡ Dizziness is ‘‘triggered’’ (not dizzy at baseline, dizziness develops with movement), as in positional vertigo due to BPPV. This must be
distinguished from dizziness that is ‘‘exacerbated’’ (dizzy at baseline, worse with movement); such exacerbations are common in AVS,
whether peripheral (neuritis) or central (stroke).

nausea or vomiting, gait instability, nystagmus, and head- Vestibular neuritis (the most common cause of an
motion intolerance lasting days to weeks (7,17,46). AVS) is a benign, self-limited, presumed viral or post-
Patients are usually symptomatic at presentation and viral inflammatory condition affecting the vestibular
focused physical examination is often diagnostic. The nerve (similar to Bell’s palsy affecting the facial nerve).
most common cause is vestibular neuritis (dizziness The diagnosis is therefore clinical and requires excluding
only) or labyrinthitis (dizziness plus hearing loss or other causes. Most cases are idiopathic, possibly linked to
tinnitus) (46). The most frequent dangerous cause is pos- herpes simplex infections (52). Ramsay Hunt Syndrome
terior circulation ischemic stroke, generally in the cere- due to herpes zoster presents with AVS, usually in
bellum or brainstem (46). A small minority are due to conjunction with hearing loss, facial palsy, and a vesicu-
multiple sclerosis (47,48). Rare causes of an isolated lar eruption in the ear or palate (53). While not recom-
AVS include cerebellar hemorrhage; thiamine mended in the diagnoses of vestibular neuritis, routine
deficiency; and various autoimmune, infectious, or magnetic resonance imaging (MRI) is usually normal in
other metabolic conditions (47,49,50). both cases (54).
A key concept is understanding the distinction be- Posterior fossa strokes can mimic vestibular neuritis or
tween symptoms that are exacerbated (dizzy at base- labyrinthitis (55). The prevalence of cerebrovascular
line, worse with movement) vs. triggered (not dizzy disease in patients presenting to the ED with dizziness
at baseline, dizziness develops with movement). Pa- is 3–5%, but among those with the AVS, it is estimated
tients with an AVS typically experience worse dizzi- at 25% (7,46). Almost all (96%) of these strokes are
ness with head movement (exacerbation), such as ischemic (46,49). Sensitivity of CT for acute posterior
when performing the Dix-Hallpike maneuver, but this fossa ischemic stroke may be as low as 7–16% in the
is not a sign of BPPV. Confusion on this point contrib- first 24 h (56,57). Therefore, CT cannot rule out
utes to difficulty differentiating BPPV from vestibular ischemic stroke in AVS, a factor contributing to
neuritis or stroke (6,7,23). Occasionally, BPPV misdiagnosis (6,23,30). Importantly, even MRI with
patients may endorse mild, persistent symptoms of diffusion-weighted imaging (DWI) misses 10–20% of
malaise or unsteadiness between triggered, brief strokes presenting with an AVS during the first 24–48 h
bouts of vertigo; this may be due to repeated after onset, more for small strokes (57–59). Delayed
symptoms triggered by small, inadvertent head MRI (3–7 days post symptom onset) may be required to
movements or anticipatory anxiety about moving, and confirm the presence of a new infarct (46,58,59).
is more common among older patients. This can Fortunately, the physical examination can make the
usually be teased out by careful history-taking. When distinction between vestibular neuritis and posterior cir-
such patients lack obvious features of vestibular culation stroke with greater sensitivity than early MRI
neuritis or stroke, the Dix-Hallpike and supine roll (58–60). These studies were conducted by neuro-
tests can be performed to assess for an atypical, otologists performing a targeted three-component ocular
AVS-like presentation of BPPV (51). motor examination—the head impulse test (HIT), gaze
6 J. A. Edlow et al.

testing for nystagmus, and alternate cover test for skew- cess. All or nearly all patients with an AVS due to a pe-
deviation (HINTS [head impulse, nystagmus, test of ripheral vestibular cause will have nystagmus if
skew]). Trained general neurologists may achieve similar carefully examined within the first days, so its absence
accuracy (61). Preliminary evidence suggests that makes the diagnosis of vestibular neuritis unlikely (65).
‘‘specially trained’’ emergency physicians using Frenzel Nystagmus may, however, be absent if vestibular suppres-
lenses can also successfully use components of this sant medications (e.g., benzodiazepines) are applied
approach (nystagmus testing and HIT) (62,63). Our before examination, so it is preferable to search for
own anecdotal experience also suggests that emergency nystagmus before appropriate medications to manage
physicians can learn to perform and interpret this symptoms are administered (45).
examination without any special lenses or equipment. Nystagmus is usually visible with the naked eye, but
However, because emergency physicians use of this normal visual fixation can completely suppress mild
approach has not been fully validated, we suggest nystagmus in patients with vestibular neuritis (66). Sub-
performing two additional components for the basic specialists often use Frenzel lenses to block visual fixa-
evaluation of the AVS patient—a targeted neurologic tion and magnify the view, making detection easier.
examination and gait testing. One simple technique that emergency physicians can
For several reasons, we perform these tests in the use to block visual fixation without the need for any spe-
following sequence (Table 2): 1) gaze testing; 2) alternate cial equipment is to simply place a piece of white paper
cover test; 3) HIT; 4) targeted neurologic examination, close to the patient’s eyes, and then instruct them to
focusing on cranial nerves (including hearing), cerebellar ‘‘look through the paper’’ and examine for nystagmus
testing, and long-tract signs; and 5) gait testing. from the side. This is only required if there is no
The major reason for gaze testing first is that nystagmus during the basic examination. If nystagmus
nystagmus is part of the definition of AVS, and the diag- is truly absent, an acute vestibular neuritis is very unlikely
nostic meaning of HIT differs dramatically in dizzy pa- and the HIT can yield false information (64).
tients without nystagmus (64). Gaze testing is also the Despite known pitfalls, bedside examination for
least intrusive part of the examination and represents an nystagmus is quite simple and, with practice, becomes
important branch point in decision-making based on the easy to interpret. The details of the nystagmus are diag-
presence or absence of nystagmus and its details. Thus, nostically important (45). Have the patient look straight
nystagmus helps to anchor and inform the rest of the pro- ahead (‘‘neutral’’ or ‘‘primary’’ gaze) and observe for

Table 2. Use of the Physical Examination to Diagnose Patients With Acute Vestibular Syndrome

Peripheral (All Must Be Present to Central (Any One of These Findings

Exam Component Diagnose Vestibular Neuritis) Suggests Posterior Fossa Stroke)

Nystagmus (straight-ahead gaze and Dominantly horizontal, direction-fixed, Dominantly vertical or torsional or
rightward and leftward gaze) beating away from the affected side* dominantly horizontal, direction-
changing on left/right gaze†
Test of Skew (alternate cover test) Normal vertical eye alignment and no Skew deviation (small vertical correction
corrective vertical movement (i.e., no on uncovering the eye)‡
skew deviation)
Head Impulse Test Unilaterally abnormal with head moving Usually bilaterally normal (no corrective
towards the affected side (presence of saccade)
a corrective re-fixation saccade
towards the normal side)§
Targeted neurologic examination (see No cranial nerve, brainstem, or cerebellar Presence of limb ataxia, dysarthria,
text) signs diplopia, ptosis, anisocoria, facial
sensory loss (pain/temperature),
unilateral decreased hearing
Gait and truncal ataxia Able to walk unassisted and to sit up in Unable to walk unassisted or sit up in
stretcher without holding on or leaning stretcher without holding on or leaning
against bed or rails against bed or rails

* Inferior branch vestibular neuritis will present with downbeat-torsional nystagmus, but this is a rare disorder. From the emergency med-
icine perspective, vertical nystagmus in a patient with an acute vestibular syndrome patient should be considered to be central (a stroke).
† More than half of posterior fossa strokes will have direction-fixed horizontal nystagmus that, alone, cannot be distinguished from that
typically seen with vestibular neuritis.
‡ More than half of posterior fossa strokes will have no skew deviation, so, on this criterion alone, cannot be distinguished from vestibular
neuritis.
§ Strokes in the anterior inferior cerebellar artery territory may produce a unilaterally abnormal head impulse test that mimics vestibular
neuritis, but hearing loss is usually present as a clue. If a patient has bilaterally abnormal Head Impulse Test, this is also suspicious for
a central lesion if nystagmus is present (as may be seen in Wernicke’s syndrome).
Diagnostic Approach to Acute Dizziness in Adults 7

eye movements. By convention, the direction of move with the head, then snap back in a fast corrective
nystagmus is named by the direction of the fast compo- movement to again look at the examiner’s nose, as in-
nent. Patients whose eyes drift leftward and snap back structed) is a ‘‘positive’’ test (abnormal VOR), which
horizontally to the right have right-beating horizontal generally indicates a peripheral process, usually vestib-
nystagmus. After observing for nystagmus in primary ular neuritis. The HIT is performed to one side then the
gaze, look for ‘‘gaze-evoked’’ nystagmus by having the other, and the absence of a corrective saccade on both
patient look to the right and then to the left, each for sides suggests a stroke in AVS. It may seem counterintu-
several seconds. Again, observe for the presence of itive that a normal finding predicts a dangerous disease.
nystagmus and the direction of its fast-beating compo- This is why the HIT is only useful in patients with AVS
nent. Many normal individuals have a few beats of phys- (with nystagmus). A HIT done in a patient without
iologic horizontal nystagmus on extreme lateral gaze that nystagmus (e.g., a dizzy patient with urosepsis or dehy-
is very low amplitude, extinguishes quickly, beats in the dration), will be normal (i.e., worrisome for stroke)
direction of gaze and is symmetric to the two sides. and, therefore, misleading.
This finding does not ‘‘count’’ as pathologic nystagmus. Because the circuit of the VOR does not loop through
Table 2 shows the nystagmus findings for patients with the cerebellum, cerebellar stroke patients typically have a
the AVS. Two patterns suggest stroke: 1) dominantly ver- negative (normal) HIT (27,69). Occasional patients with
tical or torsional nystagmus in any gaze position; 2) posterior circulation stroke will have a falsely
dominantly horizontal nystagmus that changes direction ‘‘positive’’ (abnormal) HIT, usually from an infarct
in different gaze positions (e.g., bilateral, gaze-evoked involving the region where the vestibular nerve enters
nystagmus). Note, however, that the most common the brainstem or a stroke of the inner ear itself
pattern seen in stroke patients presenting AVS is (labyrinthine stroke) (67). When abnormal HITs occur
direction-fixed horizontal nystagmus (i.e., the same as in stroke, hearing is often also affected because blood
that seen in acute vestibular neuritis), which is why supply to both structures is generally from the anterior
further testing is often needed (46). inferior cerebellar artery (AICA), which also supplies
Skew deviation is a vertical misalignment of the eyes the cochlea (70). Adding a bedside test of hearing
due to imbalance in gravity-sensing vestibular pathways (‘‘HINTS plus’’) helps to diagnose these patients (60).
(67). Skew deviation is elicited using the ‘‘alternate This last point is important because traditional teaching
cover’’ test. With the patient looking directly at the exam- is that coincident hearing loss and dizziness is always pe-
iner’s nose, the physician covers one eye, then the other, ripheral (in the labyrinth). However, combined audio-
and continues alternating back and forth, roughly every vestibular loss is often a sign of stroke (71–73). The
1–2 s. If skew deviation is present, each time the covered relative frequency of labyrinthitis vs. AICA stroke is
eye is uncovered, a slight vertical correction occurs (one unknown (74). Because so-called ‘‘viral labyrinthitis’’
side corrects upward and the other corrects downward); if (i.e., AVS with unilateral hearing loss) is uncommon,
no vertical movement occurs, there is no skew (horizontal combined audiovestibular loss should be treated with
movements do not count). The amplitude of correction is extreme caution in the ED (7,60,75).
small (1–2 mm) and appears at the moment the eye is un- Patients with the AVS who have worrisome
covered; therefore, it is key for the examiner to focus on nystagmus, skew deviation, or a bilaterally normal
one eye (either one) for several cycles, rather than HIT have a presumed stroke and should be admitted.
following the uncovered eye. A normal response is no If all three tests are reassuring (direction-fixed, predom-
vertical correction, and an abnormal response suggests inantly horizontal nystagmus beating opposite a unilat-
a stroke in an AVS presentation. erally abnormal HIT, and without skew deviation),
The next component is the HIT, a test of the vestibulo- perform a targeted neurologic examination to search
ocular reflex (VOR) described in 1988 (68). Standing in for anisocoria, facial weakness or sensory asymmetry,
front of the patient, the examiner holds the patient’s dysarthria/dysphonia, or limb ataxia (8). Lateral medul-
head by each side, instructs the patient to focus on the ex- lary stroke (Wallenberg’s syndrome) merits special
aminer’s nose and to keep their head and neck loose. The attention. In addition to acute dizziness, patients may
examiner gently displaces the patient’s head about 10–20 complain of dysarthria, dysphagia, or hoarseness due
degrees from the midline to one side; from there, a flick of to lower cranial neuropathy. They may have Horner’s
the wrists brings the head back toward the center position syndrome with subtle ptosis and anisocoria only evident
rapidly (>120 degrees/s) where it stops ‘‘dead’’ at the in dim light (the normal larger pupil fully dilates,
midline, while the examiner observes the eyes carefully. accentuating the difference in pupil size) (76). The
The normal response (normal vestibular function) is physical finding of hemi-facial decreased pain and tem-
that the patient’s gaze remains locked on the examiner’s perature sensation may be missed if one only tests light
nose. The presence of a corrective saccade (the eyes touch.
8 J. A. Edlow et al.

Finally, if these four examination components headaches (81,90). Nausea, vomiting, photophobia,
(nystagmus, skew deviation, HIT, and targeted neurologic phonophobia, and visual auras may accompany
examination) are benign, test the gait. Ideally, have the vestibular migraine, but these features are often absent.
patient walk unassisted, but for severely nauseated pa- Hearing loss or tinnitus sometimes occurs, mimicking
tients too symptomatic to walk, test for truncal ataxia Meniere’s disease (91,92). Given the variable
by asking the patient to sit upright in the stretcher with presentations, the diagnosis of vestibular migraine is
arms crossed. Patients who cannot walk or sit up unas- made based on a combination of clinical findings, with
sisted are unsafe for discharge and are more likely to the most important benign feature being a history of
have a stroke (or other CNS pathology) rather than vestib- repeated recurrences over years without permanent
ular neuritis (27,44,77). Although American emergency sequelae (8,81).
physicians are uncomfortable using HINTS testing and Menière’s disease is a relatively uncommon cause of
instead overuse CT, one study reported that specially dizziness in the ED. Patients classically present with
trained emergency physicians using these bedside episodic vertigo accompanied by unilateral tinnitus and
examination elements decreased both CT use and aural fullness, often with reversible sensorineural hearing
hospitalization (62,63,78). loss (92). Episodes typically last minutes to hours. Only 1
The key takeaway is that bedside examination trumps in 4 patients initially present with the complete symptom
brain imaging in the early diagnosis of patients with the triad, and non-vertiginous dizziness is common (93,94).
AVS. Instructional videos are available at http://novel. Reflex (or neurocardiogenic) syncope includes vaso-
utah.edu/Newman-Toker/collection.php. vagal syncope, carotid sinus hypersensitivity, and situa-
tional syncope (e.g., micturition, defecation, cough)
Spontaneous Episodic Vestibular Syndrome (95). Presyncope without loss of consciousness
outnumber spells with full syncope (85). Dizziness is
The spontaneous episodic vestibular syndrome (s-EVS) is the most common presyncopal symptom and it may be
marked by recurrent, spontaneous episodes of dizziness of any type, including vertigo (21). Diagnosis is based
that range in duration from seconds to days, the majority on clinical history, excluding dangerous mimics (espe-
lasting minutes to hours. If patients are still symptomatic cially dysrhythmia), and can be confirmed by formal
at presentation (e.g., 3 h in), use this approach to AVS head-up tilt table testing (96).
(79). However, most are asymptomatic at the time of clin- Episodic dizziness from panic attacks (with or without
ical assessment and, by definition, the dizziness cannot be hyperventilation) begins rapidly, peaks within 10 min
triggered at the bedside, so the evaluation usually relies and, by definition, is accompanied by at least three other
entirely on the history. Perfusion-based imaging may symptoms (97). Although a situational precipitant (e.g.,
help diagnose some cerebrovascular causes when exami- claustrophobia) may be present, spells often occur
nation and history are inconclusive (79). without obvious reasons and classical symptoms are ab-
Spells sometimes occur up to several times a day, but sent in 30% of cases (87). Ictal panic attacks from tempo-
are usually less frequent and can be separated by months ral lobe epilepsy generally last only seconds, and altered
or even years, depending on the cause. The most mental status is frequent (86). Hypoglycemia, cardiac
common benign cause is vestibular migraine (80–82). dysrhythmias, pheochromocytoma, and basilar TIA can
The most common dangerous cause is posterior also mimic panic attacks by producing a combination
circulation TIA (83,84). Menière’s disease also presents of neurologic and autonomic features.
with the s-EVS, but is less common (81). Other causes The principal dangerous diagnosis presenting as s-
include reflex (e.g., vasovagal) syncope, and panic at- EVS is TIA (83). Traditionally, isolated vertigo was not
tacks (85,86). Diagnosis may be obvious but classical considered a TIA symptom, but epidemiologic evidence
features may be absent (87–89). Uncommon dangerous now suggests that isolated attacks of spontaneous dizzi-
causes of s-EVS are cardiovascular (cardiac ness are the most common vertebrobasilar TIAs
dysrhythmia, unstable angina pectoris, pulmonary (84,98). In a study of 86 patients with ‘‘acute transient
embolus), endocrine (hypoglycemia, neuro-humoral neo- vestibular syndrome’’ 23 (27%) were diagnosed with
plasms), or toxic (intermittent carbon monoxide expo- stroke or TIA (79). The authors defined ‘‘transient’’ as
sure). duration < 24 h and excluded BPPV and orthostatic hypo-
Vestibular migraine presentations are quite variable. tension (which are triggered); therefore, most (if not all)
Attack duration ranges from seconds to days (81). of these patients had s-EVS. Among 23 patients exam-
Nystagmus, if present, can be peripheral, central, or ined while still symptomatic (15 vestibular neuritis, 3
mixed type (90). Headache, often absent during the stroke, 5 undetermined), the HINTS plus approach was
attack, may begin before, during, or after the dizziness 100% sensitive and 75% specific for stroke; it could not
and may differ from the patient’s ‘‘typical’’ migraine be applied in the remaining 63 patients examined after
Diagnostic Approach to Acute Dizziness in Adults 9

their symptoms had resolved. Although TIAs can last new dizziness not present at baseline). The most common
seconds to hours, the highest risk subgroup in this study etiologies of t-EVS are BPPV and orthostatic hypoten-
was those with symptoms lasting minutes (79,99). Focal sion. Dangerous causes include central (neurologic)
neurologic symptoms and head or neck pain were mimics of BPPV and serious causes of orthostatic hypo-
associated with stroke and TIA. Of the 27 patients tension. By definition, physicians should be able to repro-
diagnosed with a cerebrovascular cause, DWI imaging duce the dizziness at the bedside.
was only 58% sensitive, presumably because these BPPV, the most common vestibular cause of dizziness,
patients with transient symptoms had either smaller results from mobile crystalline debris in one or more
lesions or ischemia without infarction. The authors semicircular canals (‘‘canaliths’’) of the vestibular
found that perfusion-weighted MRI was able to nearly labyrinth. Classical symptoms are repetitive brief, trig-
double the proportion of patients in whom they could gered episodes of rotational vertigo lasting less than a
make a definite diagnosis. However, despite the intensive minute, though non-vertiginous dizziness is frequent
investigations these patients underwent, the authors could (22,107,108). The diagnosis is confirmed by
not determine a cause in 56% (79). reproducing symptoms using canal-specific positional
TIA causing dizziness or vertigo is easily missed; in a testing maneuvers and identifying a canal-specific
population-based study of transient symptoms preceding nystagmus (Table 3) (108–110). We recommend
vertebrobasilar stroke, 9 of 10 who sought medical atten- starting with the Dix-Hallpike maneuver, which tests
tion were initially missed (84). Dizziness is the most the posterior canal (most commonly involved) (111). A
common symptom in basilar artery occlusion occurring detailed recent review of these examination maneuvers
without other neurologic symptoms in 20% (100,101). includes instructive video clips (45). Should the Dix-
Dizziness is the most common presenting symptom of Hallpike maneuver not reproduce the symptoms, the
vertebral artery dissection, which affects younger supine head roll test (where one starts with the patient
patients, mimics migraine, and is easily misdiagnosed supine and turns, turning the head to 90 degrees right
(30,102). Because 5% of TIA patients suffer a stroke and left) can be attempted to diagnose horizontal canal
within 48 h, prompt diagnosis is critical (103). Patients BPPV. Once the correct canal is identified, bedside treat-
with posterior circulation TIA may have a higher stroke ment with canal repositioning maneuvers can follow
risk than those with anterior circulation TIA (104,105). (108). Although BPPV is common, emergency physicians
Prompt treatment lowers stroke risk after TIA by often do not use guideline-supported Dix-Hallpike (diag-
roughly 80% (28,29). Patients with new symptoms in nostic) or Epley (therapeutic) maneuvers (78,112,113).
the past 12 months, even if repetitive, should be Central mimics of BPPV (central paroxysmal posi-
considered ‘‘at risk’’ for cerebrovascular causes; extra tional vertigo [CPPV]) caused by posterior fossa
caution should be taken in those with ABCD2 risk neoplasm, infarction, hemorrhage, and demyelination
scores $ 3 or with sudden, severe, or sustained cranio- are rare. Distinguishing factors between BPPV from
cervical pain, as the latter may represent arterial dissec- CPPV are summarized in Table 4 (114).
tion (14,84,99,102). Orthostatic hypotension accounts for 24% of acute
Cardiac dysrhythmias should also be considered in pa- syncopal presentations (115). The classical symptom is
tients with s-EVS, particularly when true syncope occurs lightheadedness or presyncope on arising, but vertigo is
(106). Although some clinical features may increase or common and underappreciated (21,23). Orthostatic
decrease the odds of a cardiac cause, additional testing hypotension is a sustained decline in blood pressure of
(e.g., cardiac loop recording) is often required to confirm at least 20 mm Hg systolic or 10 mm Hg diastolic
the final diagnosis (95,96). within 3 min of standing (116). Optimal cutoffs may
need to be adjusted based on baseline blood pressure
Triggered Episodic Vestibular Syndrome (117). Emergency physicians are familiar with the com-
mon causes of orthostatic hypotension. Dangerous but
Patients with triggered episodic vestibular syndrome uncommon causes include myocardial infarction, occult
(t-EVS) have brief episodes of dizziness lasting seconds sepsis, adrenal insufficiency, and diabetic ketoacidosis
to minutes, depending on the underlying etiology. There (118).
is an ‘‘obligate’’ trigger; a specific trigger consistently Because BPPV produces dizziness on arising in 58%,
causes dizziness. Common triggers are changes in head it can mimic the postural lightheadedness of orthostatic
position or body posture. Patients with nausea and vom- hypotension, and often goes undiagnosed in the elderly
iting may overestimate episode duration. Again, clini- (22,119,120). Also, orthostatic hypotension may be
cians must distinguish exacerbating features (worsens incidental and misleading, especially in older patients
pre-existing baseline dizziness) from triggers (provokes taking antihypertensive medications (121). Positional
10 J. A. Edlow et al.

Table 3. Use of the Physical Examination to Diagnose Patients With Triggered Episodic Vestibular Syndrome

Positional Diagnostic Test in

t-EVS BPPV (Posterior Canal) BPPV (Horizontal Canal) Central

Dix-Hallpike test Upbeat-torsional* None† Variable direction (usually pure

5-30 s (crescendo- downbeat or horizontal;
decrescendo intensity pattern) almost never upbeat or
torsional)
Variable duration (often
persists >90 s if position is
held; rarely varies
significantly in intensity)
Supine roll test None† Pure horizontal‡ Variable direction (usually pure
30–90 s (crescendo- downbeat or horizontal;
decrescendo intensity pattern) rarely upbeat or torsional)
Variable duration (often
persists >90 s if position is
held; rarely varies
significantly in intensity)

BPPV = benign paroxysmal positional vertigo; t-EVS = triggered, episodic vestibular syndrome.
* The nystagmus of posterior canal BPPV will have a prominent torsional component, and the 12 o’clock pole of the eye will beat toward
the down-facing (tested) ear. Upon arising from the down (Dix-Hallpike) position, the nystagmus will reverse direction because the canal-
iths are now moving in the opposite direction. This reversal is not the same as gaze-evoked, direction-changing nystagmus seen in pa-
tients with acute vestibular syndrome, and does not imply central disease (see text describing HINTS).
† Although the Dix-Hallpike test is fairly specific to posterior canal BPPV and the supine roll test is fairly specific to horizontal canal BPPV,
the maneuvers may sometimes stimulate the other canal. If so, the nystagmus direction will depend on the affected canal, not on the type
of maneuver eliciting the nystagmus. The nystagmus may be considerably weaker and less obvious than if one were using the ‘‘correct’’
canal-specific maneuver.
‡ The nystagmus of horizontal canal BPPV may beat toward the down ear or away from it. It may spontaneously reverse after an initial
decay. When the other side is tested, the nystagmus will usually beat in the opposite direction (e.g., if right-beating initially with right
ear down, then it will usually be left-beating initially with left ear down). These reversals are not the same as gaze-evoked, direction-chang-
ing nystagmus seen in patients with acute vestibular syndrome, and does not imply central disease (see text describing HINTS).

triggers, such as rolling over in bed or reclining, are com- CONCLUSIONS

mon in BPPV, but should not occur with orthostatic hypo-
tension, helping to distinguish between these two entities. Dizziness, vertigo, and unsteadiness are common com-
Orthostatic dizziness and orthostatic hypotension are not plaints caused by numerous diseases that span organ sys-
always related (122,123). Orthostatic dizziness without tems. Diagnosis can be difficult. Misconceptions,
systemic orthostatic hypotension has been reported with resource overutilization, and misdiagnosis are common.
hemodynamic TIA (due low flow across a vascular The current ‘‘symptom quality’’ paradigm was created
stenosis) and in patients with intracranial hypotension 45 years ago and is not evidence-based; a newer para-
(124,125). digm, based on timing and triggers, is more consistent

Table 4. Characteristics of Patients With Triggered, Episodic Vestibular Syndrome that Suggest a Central Mimic (Central
Paroxysmal Positional Vertigo) rather than Typical Benign Paroxysmal Positional Vertigo

Presence of symptoms or signs that are not seen in BPPV

Headache
Diplopia
Abnormal cranial nerve or cerebellar function
Atypical nystagmus characteristics or symptoms during positional tests
Downbeating nystagmus*
Nystagmus that starts instantaneously, persists for >90 s, or lacks a crescendo-decrescendo pattern of intensity
Prominent nystagmus with mild or no associated dizziness or vertigo
Poor response to therapeutic maneuvers
Repetitive vomiting during positional maneuvers
Unable to cure patient with canal-specific canalith repositioning maneuver†
Frequent recurrent symptoms

BPPV = benign paroxysmal positional vertigo.

* Downbeating nystagmus can be seen with anterior canal BPPV. However, because BPPV of this canal is relatively rare and because
downbeating nystagmus is most often the result of central structural lesions, it is safer for emergency physicians to consider this finding
always worrisome prompting imaging or specialty consultation or referral.
† Modified Epley maneuver or equivalent for posterior canal BPPV. Supine roll test or equivalent for horizontal canal BPPV.
Diagnostic Approach to Acute Dizziness in Adults 11

with best evidence. History and physical examination are 15. Drachman DA, Hart CW. An approach to the dizzy patient.
Neurology 1972;22:323–34.
more accurate than imaging, and more likely to result in a 16. Newman-Toker D. Diagnosing Dizziness in the Emergency
specific diagnosis than the traditional paradigm. Department: Why ‘‘what do you mean by ’dizzy’?’’ Should Not
be the First Question You Ask [PhD]. Baltimore: Johns Hopkins
School of Medicine; 2007.
Acknowledgments—Dr. Newman-Toker’s effort was supported
17. Edlow J. Diagnosing dizziness: we are teaching the wrong para-
by a grant from the National Institutes of Health (NIDCD digm!. Acad Emerg Med 2013;20:1064–6.
U01 DC013778). The funding agency was not involved in 18. Newman-Toker DE. Charted records of dizzy patients suggest
design of the study, the collection, analysis, and interpretation emergency physicians emphasize symptom quality in diagnostic
of the data, or the decision to approve publication of the finished assessment. Ann Emerg Med 2007;50:204–5.
19. Newman-Toker DE, Cannon LM, Stofferahn ME, Rothman RE,
manuscript. Hsieh YH, Zee DS. Imprecision in patient reports of dizziness
Both Dr. Edlow and Dr. Newman-Toker review medical-legal symptom quality: a cross-sectional study conducted in an acute
cases for both plaintiff and defense firms in cases involving care setting. Mayo Clin Proc 2007;82:1329–40.
neurologic conditions, including dizziness and stroke. Dr. 20. Kerber KA, Brown DL, Lisabeth LD, Smith MA, Morgenstern LB.
Stroke among patients with dizziness, vertigo, and imbalance in
Newman-Toker has conducted funded research related to stroke
the emergency department: a population-based study. Stroke
misdiagnosis and has been loaned research equipment by two 2006;37:2484–7.
commercial companies (GN Otometrics and Interacoustics). 21. Newman-Toker DE, Dy FJ, Stanton VA, Zee DS, Calkins H,
Author contributions: JAE wrote the first draft and the diag- Robinson KA. How often is dizziness from primary cardiovascular
nostic algorithm. All authors reviewed and edited multiple revi- disease true vertigo? A systematic review. J Gen Intern Med 2008;
23:2087–94.
sions. JAE takes responsibility for the paper as a whole. 22. Lawson J, Johnson I, Bamiou DE, Newton JL. Benign paroxysmal
positional vertigo: clinical characteristics of dizzy patients
referred to a Falls and Syncope Unit. QJM 2005;98:357–64.
23. Stanton VA, Hsieh YH, Camargo CA Jr, et al. Overreliance on
symptom quality in diagnosing dizziness: results of a multicenter
REFERENCES survey of emergency physicians. Mayo Clin Proc 2007;82:1319–
28.
1. Newman-Toker DE, Hsieh YH, Camargo CA Jr, Pelletier AJ, 24. Royl G, Ploner CJ, Leithner C. Dizziness in the emergency room:
Butchy GT, Edlow JA. Spectrum of dizziness visits to US emer- diagnoses and misdiagnoses. Eur Neurol 2011;66:256–63.
gency departments: cross-sectional analysis from a nationally 25. Braun EM, Tomozik PV, Ropposch T, Nemetz U, Lackner A,
representative sample. Mayo Clin Proc 2008;83:765–775. Walch C. Misdiagnosis of acute peripheral vestibulopathy in cen-
2. Cheung CS, Mak PS, Manley KV, et al. Predictors of important tral nervous ischemic infarction. Otol Neurotol 2011;32:1518–21.
neurological causes of dizziness among patients presenting to 26. Casani AP, Dallan I, Cerchiai N, Lenzi R, Cosottini M, Sellari-
the emergency department. Emerg Med J 2010;27:517–521. Franceschini S. Cerebellar infarctions mimicking acute peripheral
3. Saber Tehrani AS, Coughlan D, Hsieh YH, et al. Rising annual vertigo: how to avoid misdiagnosis? Otolaryngol Head Neck Surg
costs of dizziness presentations to U.S. emergency departments. 2013;32:1518–21.
Acad Emerg Med 2013;20:689–696. 27. Lee H, Sohn SI, Cho WY, et al. Cerebellar infarction presenting
4. Newman-Toker DE. Missed stroke in acute vertigo a time for ac- with isolated vertigo: frequency and vascular topographical pat-
tion, not debate. Ann Neurol 2016;79:27–31. terns. Neurology 2006;67:1178–83.
5. Newman-Toker DE, McDonald KM, Meltzer DO. How much 28. Lavallée PC, Meseguer E, Abboud H, et al. A transient ischaemic
diagnostic safety can we afford, and how should we decide? A attack clinic with round-the-clock access (SOS-TIA): feasibility
health economics perspective. BMJ Qual Saf 2013;22(Suppl 2): and effects. Lancet Neurol 2007;6:953–60.
ii11–20. 29. Rothwell PM, Giles MF, Chandratheva A, et al. Effect of urgent
6. Kerber KA, Newman-Toker DE. Misdiagnosing dizzy patients: treatment of transient ischaemic attack and minor stroke on early
common pitfalls in clinical practice. Neurol Clin 2015;33:565–75. recurrent stroke (EXPRESS study): a prospective population-
7. Newman-Toker DE, Edlow JA. TiTrATE: a novel, evidence-based based sequential comparison. Lancet 2007;370:1432–42.
approach to diagnosing acute dizziness and vertigo. Neurol Clin 30. Savitz SI, Caplan LR, Edlow JA. Pitfalls in the diagnosis of cere-
2015;33:577–99. bellar infarction. Acad Emerg Med 2007;14:63–8.
8. Newman-Toker DE. Symptoms and signs of neuro-otologic disor- 31. Kuruvilla A, Bhattacharya P, Rajamani K, Chaturvedi S. Factors
ders. Continuum (Minneap Minn) 2012;18:1016–40. associated with misdiagnosis of acute stroke in young adults. J
9. Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial Stroke Cerebrovasc Dis 2011;20:523–7.
management of cerebellar infarction. Lancet Neurol 2008;7: 32. Martin-Schild S, Albright KC, Tanksley J, et al. Zero on the
951–64. NIHSS does not equal the absence of stroke. Ann Emerg Med
10. Navi BB, Kamel H, Shah MP, et al. Rate and predictors of serious 2011;57:42–5.
neurologic causes of dizziness in the emergency department. 33. Mandelzweig L, Goldbourt U, Boyko V, Tanne D. Perceptual, so-
Mayo Clin Proc 2012;87:1080–8. cial, and behavioral factors associated with delays in seeking med-
11. Chase M, Joyce NR, Carney E, et al. ED patients with vertigo: can ical care in patients with symptoms of acute stroke. Stroke 2006;
we identify clinical factors associated with acute stroke? Am J 37:1248–53.
Emerg Med 2012;30:587–91. 34. Masuda Y, Tei H, Shimizu S, Uchiyama S. Factors associated with
12. Moubayed SP, Saliba I. Vertebrobasilar insufficiency presenting as the misdiagnosis of cerebellar infarction. J Stroke Cerebrovasc Dis
isolated positional vertigo or dizziness: a double-blind retrospec- 2013;22:1125–30.
tive cohort study. Laryngoscope 2009;119:2071–6. 35. Newman-Toker DE, Moy E, Valente E, Coffey R, Hines AL.
13. Kerber KA, Meurer WJ, Brown DL, et al. Stroke risk stratification Misssed diagnosis of stroke in the ED: a cross-sectional analysis
in acute dizziness presentations: A prospective imaging-based of a large population based sample. Diagnosis (Berl) 2014;2:29–
study. Neurology 2015;85:1869–78. 40.
14. Navi BB, Kamel H, Shah MP, et al. Application of the ABCD2 36. Honda S, Inatomi Y, Yonehara T, et al. Discrimination of acute
score to identify cerebrovascular causes of dizziness in the emer- ischemic stroke from nonischemic vertigo in patients presenting
gency department. Stroke 2012;43:1484–9. with only imbalance. J Stroke Cerebrovasc Dis 2014;23:888–95.
12 J. A. Edlow et al.

37. Nakajima MH, Hirano T, Uchino M. Patients with acute stroke 57. Choi JH, Kim HW, Choi KD, et al. Isolated vestibular syndrome in
admitted on the second visit. J Stroke Cerebrovasc Dis 2008;17: posterior circulation stroke: frequency and involved structures.
382–7. Neurol Clin Pract 2014;4:410–8.
38. Lee CC, Ho HC, Su YC, et al. Increased risk of vascular events in 58. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE.
emergency room patients discharged home with diagnosis of dizzi- HINTS to diagnose stroke in the acute vestibular syndrome: three-
ness or vertigo: a 3-year follow-up study. PLoS One 2012;7: step bedside oculomotor examination more sensitive than early
e35923. MRI diffusion-weighted imaging. Stroke 2009;40:3504–10.
39. Atzema CL, Grewal K, Lu H, Kapral MK, Kulkarni G, Austin PC. 59. Saber Tehrani AS, Kattah JC, Mantokoudis G, et al. Small strokes
Outcomes among patients discharged from the emergency depart- causing severe vertigo: frequency of false-negative MRIs and non-
ment with a diagnosis of peripheral vertigo. Ann Neurol 2016;79: lacunar mechanisms. Neurology 2014;83:169–73.
32–41. 60. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outper-
40. Kerber KA, Zahuranec DB, Brown DL, et al. Stroke risk af- forms ABCD2 to screen for stroke in acute continuous vertigo and
ter nonstroke emergency department dizziness presentations: a dizziness. Acad Emerg Med 2013;20:986–96.
population-based cohort study. Ann Neurol 2014;75:899–907. 61. Chen L, Lee W, Chambers BR, Dewey HM. Diagnostic accuracy
41. Kim AS, Fullerton HJ, Johnston SC. Risk of vascular events in of acute vestibular syndrome at the bedside in a stroke unit. J Neu-
emergency department patients discharged home with diagnosis rol 2011;258:855–61.
of dizziness or vertigo. Ann Emerg Med 2011;57:34–41. 62. Vanni S, Nazerian P, Casati C, et al. Can emergency physicians
42. Newman-Toker DE, Camargo CA Jr, Hsieh YH, Pelletier AJ, accurately and reliably assess acute vertigo in the emergency
Edlow JA. Disconnect between charted vestibular diagnoses and department? Emerg Med Australas 2015;27:126–31.
emergency department management decisions: a cross-sectional 63. Vanni SP, Pecci R, Casati C, et al. Standing, a four-step bedside al-
analysis from a nationally representative sample. Acad Emerg gorithm for differential diagnosis of acute vertigo in the emer-
Med 2009;16:970–7. gency department. ACTA Otorhinolaryngol Ital 2014;34:419–26.
43. Kerber KA, Morgenstern LB, Meurer WJ, et al. Nystagmus assess- 64. Newman-Toker DE, Kattah JC. In reply. Acad Emerg Med 2014;
ments documented by emergency physicians in acute dizziness 21:348–9.
presentations: a target for decision support? Acad Emerg Med 65. Taylor RL, McGarvie LA, Reid N, Young AS, Halmagyi GM,
2011;18:619–26. Welgampola MS. Vestibular neuritis affects both superior and infe-
44. Tarnutzer AA, Lee SH, Robinson KA, Wang Z, Edlow JA, New- rior vestibular nerves. Neurology 2016;87:1704–12.
man-Toker DE. ED misdiagnosis of cerebrovascular events in 66. Newman-Toker DE, Sharma P, Chowdhury M, Clemons TM,
the era of modern neuroimaging: a meta-analysis. Neurology Zee DS, Della Santina CC. Penlight-cover test: a new bedside
2017;88:1468–77. method to unmask nystagmus. J Neurol Neurosurg Psychiatry
45. Edlow JA, Newman-Toker D. Using the physical examination to 2009;80:900–3.
diagose patients with acute dizziness and vertigo. J Emerg Med 67. Newman-Toker DE, Curthoys IS, Halmagyi GM. Diagnosing
2016;50:617–8. stroke in acute vertigo: the HINTS family of eye movement tests
46. Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh YH, Newman- and the future of the ‘‘Eye ECG.’’ Semin Neurol 2015;35:506–21.
Toker DE. Does my dizzy patient have a stroke? A systematic re- 68. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch
view of bedside diagnosis in acute vestibular syndrome. CMAJ Neurol 1988;45:737–9.
2011;183:E571–92. 69. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal
47. Edlow JA, Newman-Toker DE. Medical and nonstroke neurologic head impulse test differentiates acute cerebellar strokes from
causes of acute, continuous vestibular symptoms. Neurol Clin vestibular neuritis. Neurology 2008;70:2378–85.
2015;33:699–716. 70. Hausler R, Levine RA. Auditory dysfunction in stroke. Acta Oto-
48. Pula JH, Newman-Toker DE, Kattah JC. Multiple sclerosis as a laryngol 2000;120:689–703.
cause of the acute vestibular syndrome. J Neurol 2013;260: 71. Lee H. Neuro-otological aspects of cerebellar stroke syndrome. J
1649–54. Clin Neurol 2009;5:65–73.
49. Kerber KA, Burke JF, Brown DL, et al. Does intracerebral haemor- 72. Lee H, Kim JS, Chung EJ, et al. Infarction in the territory of ante-
rhage mimic benign dizziness presentations? A population based rior inferior cerebellar artery: spectrum of audiovestibular loss.
study. Emerg Med J 2012;29:43–6. Stroke 2009;40:3745–51.
50. Kattah JC, Dhanani SS, Pula JH, Mantokoudis G, Saber 73. Lee SH, Kim JS. Acute diagnosis and management of stroke pre-
Tehrani AS, Newman-Toker D. Vestibular signs of thiamine defi- senting dizziness or vertigo. Neurol Clin 2015;33:687–98. xi.
ciency during the early phase of suspected Wernicke encephalop- 74. Newman-Toker DE, Reich SG. Wrong-way nystagmus in the
athy. Neurol Clin Pract 2013;3:260–468. AICA syndrome [letter to the editor]. Laryngoscope 2008;118:
51. Cutfield NJ, Seemungal BM, Millington H, Bronstein AM. Diag- 378–9.
nosis of acute vertigo in the emergency department. Emerg Med J 75. Pogson JM, Taylor RL, Young AS, et al. Vertigo with sudden hear-
2011;28:538–9. ing loss: audio-vestibular characteristics. J Neurol 2016;263:
52. Arbusow V, Theil D, Strupp M, Mascolo A, Brandt T. HSV-1 not 2086–96.
only in human vestibular ganglia but also in the vestibular laby- 76. Kim JS. Pure lateral medullary infarction: clinical-radiological
rinth. Audiol Neurootol 2001;6:259–62. correlation of 130 acute, consecutive patients. Brain 2003;126:
53. Lu YC, Young YH. Vertigo from herpes zoster oticus: superior 1864–72.
or inferior vestibular nerve origin? Laryngoscope 2003;113: 77. Carmona S, Martinez C, Zalazar G, et al. The diagnostic accuracy
307–11. of truncal ataxia and HINTS as cardinal signs for acute vestibular
54. Strupp M, Jager L, Muller-Lisse U, Arbusow V, Reiser M, syndrome. Front Neurol 2016;7:125.
Brandt T. High resolution Gd-DTPA MR imaging of the inner 78. Kene MV, Ballard DW, Vinson DR, Rauchwerger AS, Iskin HR,
ear in 60 patients with idiopathic vestibular neuritis: no evidence Kim AS. Emergency physician attitudes, preferences, and risk
for contrast enhancement of the labyrinth or vestibular nerve. J tolerance for stroke as a potential cause of dizziness symptoms.
Vestib Res 1998;8:427–33. West J Emerg Med 2015;16:768–76.
55. Baloh RW. Clinical practice. Vestibular neuritis. N Engl J Med 79. Choi JH, Park MG, Choi SY, et al. Acute transient vestibular syn-
2003;348:1027–32. drome: prevalence of stroke and efficacy of bedside evaluation.
56. Chalela JA, Kidwell CS, Nentwich LM, et al. Magnetic resonance Stroke 2017;48:556–62.
imaging and computed tomography in emergency assessment of 80. Neuhauser HK, Radtke A, von Brevern M, et al. Migrainous ver-
patients with suspected acute stroke: a prospective comparison. tigo: prevalence and impact on quality of life. Neurology 2006;
Lancet 2007;369:293–8. 67:1028–33.
Diagnostic Approach to Acute Dizziness in Adults 13

81. Seemungal B, Kaski D, Lopez-Escamez JA. Early diagnosis and 106. Newman-Toker DE, Camargo CA Jr. ’Cardiogenic vertigo’—true
management of acute vertigo from vestibular migraine and me- vertigo as the presenting manifestation of primary cardiac disease.
niere’s disease. Neurol Clin 2015;33:619–628. ix. Nat Clin Pract Neurol 2006;2:167–172. quiz 73.
82. Strupp M, Versino M, Brandt T. Vestibular migraine. Handb Clin 107. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo:
Neurol 2010;97:755–771. clinical and oculographic features in 240 cases. Neurology 1987;
83. Blum CA, Kasner SE. Transient ischemic attacks presenting with 37:371–378.
dizziness or vertigo. Neurol Clin 2015;33:629–642. ix. 108. Fife TD, von Brevern M. Benign Paroxysmal positional vertigo in
84. Paul NL, Simoni M, Rothwell PM, Oxford Vascular S. Transient the acute care setting. Neurol Clin 2015;33:601–617. viii ix.
isolated brainstem symptoms preceding posterior circulation 109. Bhattacharyya N, Baugh RF, Orvidas L, et al. Clinical practice
stroke: a population-based study. Lancet Neurol 2013;12:65–71. guideline: benign paroxysmal positional vertigo. Otolaryngol
85. Romme JJ, van Dijk N, Boer KR, et al. Influence of age and gender Head Neck Surg 2008;139(Suppl):S47–81.
on the occurrence and presentation of reflex syncope. Clin Auton 110. Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: thera-
Res 2008;18:127–133. pies for benign paroxysmal positional vertigo (an evidence-
86. Kanner AM. Ictal panic and interictal panic attacks: diagnostic and based review): report of the Quality Standards Subcommittee of
therapeutic principles. Neurol Clin 2011;29:163–175. ix. the American Academy of Neurology. Neurology 2008;70:
87. Chen J, Tsuchiya M, Kawakami N, Furukawa TA. Non-fearful vs. 2067–2074.
fearful panic attacks: a general population study from the National 111. Welgampola MS, Bradshaw AP, Lechner C, Halmagyi GM.
Comorbidity Survey. J Affect Disord 2009;112:273–278. Bedside assessment of acute dizziness and vertigo. Neurol Clin
88. Dieterich M, Brandt T. Episodic vertigo related to migraine (90 2015;33:551–564. vii.
cases): vestibular migraine? J Neurol 1999;246:883–892. 112. Bashir K, Qotb MA, Alkahky S, Fathi AM, Mohamed MA,
89. Mathias CJ, Deguchi K, Schatz I. Observations on recurrent syn- Cameron PA. Are emergency physicians and paramedics
cope and presyncope in 641 patients. Lancet 2001;357:348–353. providing canalith repositioning manoeuvre for benign parox-
90. Lempert T, Neuhauser H, Daroff RB. Vertigo as a symptom of ysmal positional vertigo? Emerg Med Australasia 2015;27:179–
migraine. Ann N Y Acad Sci 2009;1164:242–251. 180.
91. Kayan A, Hood JD. Neuro-otological manifestations of migraine. 113. Kerber KA, Burke JF, Skolarus LE, et al. Use of BPPV processes in
Brain 1984;107(Pt 4):1123–1142. emergency department dizziness presentations: a population-
92. Sajjadi H, Paparella MM. Meniere’s disease. Lancet 2008;372: based study. Otolaryngol Head Neck Surg 2013;148:425–430.
406–414. 114. Soto-Varela A, Rossi-Izquierdo M, Sanchez-Sellero I, Santos-
93. Mancini F, Catalani M, Carru M, Monti B. History of Meniere’s Perez S. Revised criteria for suspicion of non-benign positional
disease and its clinical presentation. Otolaryngol Clin North Am vertigo. QJM 2013;106:317–321.
2002;35:565–580. 115. Sarasin FP, Louis-Simonet M, Carballo D, Slama S, Junod AF,
94. Faag C, Bergenius J, Forsberg C, Langius-Eklof A. Symptoms Unger PF. Prevalence of orthostatic hypotension among patients
experienced by patients with peripheral vestibular disorders: eval- presenting with syncope in the ED. Am J Emerg Med 2002;20:
uation of the Vertigo Symptom Scale for clinical application. Clin 497–501.
Otolaryngol 2007;32:440–446. 116. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on
95. van Dijk JG, Thijs RD, Benditt DG, Wieling W. A guide to disor- the definition of orthostatic hypotension, neurally mediated syn-
ders causing transient loss of consciousness: focus on syncope. Nat cope and the postural tachycardia syndrome. Clin Auton Res
Rev Neurol 2009;5:438–448. 2011;21:69–72.
96. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis 117. Fedorowski A, Burri P, Melander O. Orthostatic hypotension in
and management of syncope (version 2009). Eur Heart J 2009;30: genetically related hypertensive and normotensive individuals. J
2631–2671. Hypertens 2009;27:976–982.
97. Katon WJ. Clinical practice. Panic disorder. N Engl J Med 2006; 118. Gilbert VE. Immediate orthostatic hypotension: diagnostic value
354:2360–2367. in acutely ill patients. South Med J 1993;86:1028–1032.
98. Hoshino T, Nagao T, Mizuno S, Shimizu S, Uchiyama S. Transient 119. von Brevern M, Radtke A, Lezius F, et al. Epidemiology of benign
neurological attack before vertebrobasilar stroke. J Neurol Sci paroxysmal positional vertigo: a population based study. J Neurol
2013;325:39–42. Neurosurg Psychiatry 2007;78:710–715.
99. Grad A, Baloh RW. Vertigo of vascular origin. Clinical and elec- 120. Oghalai JS, Manolidis S, Barth JL, Stewart MG, Jenkins HA. Un-
tronystagmographic features in 84 cases. Arch Neurol 1989;46: recognized benign paroxysmal positional vertigo in elderly pa-
281–284. tients. Otolaryngol Head Neck Surg 2000;122:630–634.
100. von Campe G, Regli F, Bogousslavsky J. Heralding manifestations 121. Poon IO, Braun U. High prevalence of orthostatic hypotension and
of basilar artery occlusion with lethal or severe stroke. J Neurol its correlation with potentially causative medications among
Neurosurg Psychiatry 2003;74:1621–1626. elderly veterans. J Clin Pharm Ther 2005;30:173–178.
101. Fisher CM. Vertigo in cerebrovascular disease. Arch Otolaryngol 122. Radtke A, Lempert T, von Brevern M, Feldmann M, Lezius F,
1967;85:529–534. Neuhauser H. Prevalence and complications of orthostatic
102. Gottesman RF, Sharma P, Robinson KA, et al. Clinical character- dizziness in the general population. Clin Auton Res 2011;21:
istics of symptomatic vertebral artery dissection: a systematic re- 161–168.
view. Neurologist 2012;18:245–254. 123. Wu JS, Yang YC, Lu FH, Wu CH, Chang CJ. Population-based
103. Shah KH, Kleckner K, Edlow JA. Short-term prognosis of stroke study on the prevalence and correlates of orthostatic hypoten-
among patients diagnosed in the emergency department with a sion/hypertension and orthostatic dizziness. Hypertens Res 2008;
transient ischemic attack. Ann Emerg Med 2008;51:316–323. 31:897–904.
104. Flossmann E, Rothwell PM. Prognosis of vertebrobasilar transient 124. Stark RJ, Wodak J. Primary orthostatic cerebral ischaemia. J Neu-
ischaemic attack and minor stroke. Brain 2003;126:1940–1954. rol Neurosurg Psychiatry 1983;46:883–891.
105. Gulli G, Khan S, Markus HS. Vertebrobasilar stenosis predicts 125. Blank SC, Shakir RA, Bindoff LA, Bradey N. Spontaneous intra-
high early recurrent stroke risk in posterior circulation stroke cranial hypotension: clinical and magnetic resonance imaging
and TIA. Stroke 2009;40:2732–2737. characteristics. Clin Neurol Neurosurg 1997;99:199–204.
14 J. A. Edlow et al.

APPENDIX 1. SHORTCOMINGS OF THE 1972 Small, biased sample and lack of statistical rigor
SUBSPECIALTY REFERRAL CLINIC STUDY  Tertiary-care subspecialty referral clinic popula-
THAT LED TO ADOPTION AND PERSISTENCE tion limited to those fluent in English and avail-
OF THE ‘‘SYMPTOM QUALITY’’ able to return for four half days of laboratory
APPROACH (15,16). testing
 Small sample (n = 125 over 2 years) with large
Methodological weaknesses in study design fraction excluded in analysis or not diagnosed
and analysis (18%, n = 23 of 125; 12 inadequate data, 9 uncer-
Tautological hypothesis for primacy of symptom tain diagnoses, 2 inappropriate referrals)
quality  Very small subgroups for nonperipheral vestib-
 Methods placed patients into one of four cate- ular etiologies (e.g., psychiatric, n = 9; stroke,
gories of dizziness type by design n = 5; non-stroke neurologic, n = 4; cardiovascu-
 Related ‘‘appropriate’’ follow-up questions or lar, n = 4, other, n = 6).
special diagnostic tests applied selectively based  No quantitative analysis of type-etiology as-
on dizziness type assigned (work-up bias) sociation and exceptions ignored (e.g., ane-
 Dizziness type used to help determine final diag- mia classed as cardiovascular but symptoms
noses (e.g., ‘‘The diagnosis of a peripheral not ‘‘syncope-like’’; psychosis classed as psy-
vestibular disorder was, typically, applied to a chiatric but symptoms ‘‘variable and
patient who complained of unmistakable rota- numerous’’; 2 patients with hyperventilation
tional vertigo.’’) (incorporation bias) syndrome complained of ‘‘positional ver-
Weak standards for assignment of diagnoses tigo’’; multisensory dizziness [mostly periph-
 Diagnostic criteria not defined in detail (‘‘A dis- eral neuropathy combined with minor visual
cussion of the hierarchical ordering of criteria for or vestibular loss] complained of ‘‘light-head-
each diagnosis is beyond the scope of this pa- edness’’).
per.’’)
 Resident physicians (not senior consultants) per- Unavoidable issues related to era in which
formed most examinations study was performed
 Single individual assigned all final diagnoses; no Lack of modern imaging
independent verification  When the study was conducted, neither CT nor
 Individual assigning diagnoses not masked to MRI were available
dizziness type or other clinical features, nor to Era-specific lack of disease understanding
study hypothesis/objectives (risking diagnostic-  Vestibular migraine (a common cause of s-EVS)
review bias) had not yet been described
 No long-term follow-up of patients to verify ac-  Posterior circulation TIA/stroke presenting iso-
curacy of diagnoses lated dizziness not recognized
Diagnostic Approach to Acute Dizziness in Adults 15

ARTICLE SUMMARY
1. Why is this topic important?
Dizziness is an extremely common symptom that is
associated with numerous conditions. Distinguishing
serious from benign causes using the fewest possible re-
sources is key for emergency physicians. The ability to
make this distinction could reduce the current rate of
misdiagnosis for dangerous etiologies, including posterior
circulation stroke, while simultaneously improving the
care for patients with benign causes.
2. What does this review attempt to show?
This review shows that the traditional approach to diag-
nosing the dizzy patient based on the ‘‘type’’ of dizziness
is inconsistent with scientific evidence. By contrast, an
approach based on ‘‘timing and triggers’’ of the dizziness
coheres well with best evidence. Using this new approach,
physicians can more accurately identify patients with pos-
terior circulation stroke and more promptly diagnose and
treat the more common peripheral vestibular causes.
3. What are the key findings?
After first using history to place the patient into a
‘‘timing and triggers’’ category, physicians can apply a
diagnostic strategy that highly leverages the physical ex-
amination, utilizing specific bedside tests depending on
which category the patient fits within. This approach helps
to diagnose and treat common peripheral causes of dizzi-
ness and to confidently identify posterior circulation
stroke. Computed tomography is a poor test for ischemic
stroke, and even magnetic resonance imaging is not suffi-
ciently sensitive for detecting stroke in the first 48 h after
onset of dizziness symptoms.
4. How is patient care impacted?
Patients with peripheral vestibular causes of dizziness
can be managed according to best evidence and without
the need for specialty consultation or advanced imaging,
while those patients with posterior circulation stroke can
be correctly identified and treated appropriately.