Bedside Assessment of

Acute Dizziness and

Ver ti g o
Miriam S. Welgampola, MB BS, PhD, FRACP*, Andrew Phillip Bradshaw, BE, BSc,
Corinna Lechner, MPhil, Gabor Michael Halmagyi, MB BS, MD, FRACP

KEYWORDS
 Nystagmus  Vestibular neuritis  BPV  Meniere disease  Vestibular migraine

KEY POINTS
 Acute vertigo is accompanied by nystagmus that points to its underlying cause. A focused
history and careful bedside examination (with emphasis on spontaneous and positional
nystagmus characteristics and head impulse testing) yield the underlying diagnosis.
 An acute vestibular syndrome is a sudden severe and prolonged episode of vertigo that
could be caused by vestibular neuritis or a stroke. Typical vestibular neuritis is character-
ized by peripheral nystagmus, a positive bedside head impulse test, absence of skew de-
viation, and normal hearing. If all 4 conditions are not met, a stroke should be considered.
 Recurrent positional dizziness is most often due to benign positional vertigo (BPV), which
is characterized by exclusively positional, paroxysmal vertigo and nystagmus in the plane
of the affected semicircular canal.
 Recurrent spontaneous vertigo lasting hours could be due to vestibular migraine, often
accompanied by spontaneous horizontal, vertical, or torsional nystagmus, or by Meniere
disease, which typically begins with ipsiversive horizontal nystagmus and later progresses
to contraversive paretic nystagmus.
 Assessment of an acutely dizzy patient without a means of removing visual fixation is un-
rewarding, because spontaneous nystagmus is often missed.

Videos of a left peripheral vestibulopathy; cerebellar nystagmus; the effect of

visual fixation on central and peripheral nystagmus; left posterior canal BPV;
right horizontal canal BPV; nystagmus simulation created from 2-D video data;
paroxysmal torsional downbeat nystagmus; and nystagmus simulation created
from 2-D video data accompany this article at http://www.neurologic.
theclinics.com/

M.S. Welgampola’s and G.M. Halmagyi’s research is funded by the National Health and Medical
Research Council, Australia. A.P. Bradshaw and C. Lechner have nothing to declare.
Institute of Clinical Neurosciences, Royal Prince Alfred Hospital, Central Clinical School, Univer-
sity of Sydney, Sydney, New South Wales, Australia
* Corresponding author.
E-mail address: miriam@icn.usyd.edu.au

Neurol Clin 33 (2015) 551–564

http://dx.doi.org/10.1016/j.ncl.2015.04.001 neurologic.theclinics.com
0733-8619/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
552 Welgampola et al

INTRODUCTION

Acute vertigo is equally unpleasant and anxiety provoking for frontline physicians and
patients. Many physicians assessing a dizzy patient fear they might miss a life-
threatening brainstem stroke, perform a brain CT that almost never yields useful infor-
mation to exclude a central cause, administer antiemetics or vestibular suppressants,
and discharge a patient from care without a clear diagnosis or treatment. During the
past 150 years, the common causes of acute vertigo have been well characterized.
With a focused history and careful physical examination, it is now possible correctly
diagnose a majority of these disorders and offer useful treatment to patients present-
ing with acute vertigo. What questions must a clinician ask to determine the cause of
vertigo? What might the physical examination reveal? What additional resources could
help confirm the diagnosis? This review presents the essential history and bedside ex-
amination that can and should be performed in emergency departments, general
practice, and outpatient clinics.

THE HISTORY

A focused history is a valuable contributor to a correct diagnosis. Sometimes a pa-

tient’s opening sentence might provide the diagnosis. “I spin whenever I turn over
to one side in bed” is an unmistakable history of BPV. When the open-ended history
does not yield the diagnosis, the following key questions need to be addressed.
Is It Truly Vertigo?
Vestibular vertigo is an illusion of movement (spinning, rocking, or tilting) of oneself or
one’s surroundings and implies a left-right asymmetry in the neural activity of the
vestibular nuclei. Light-headedness, fuzzy head, and presyncopal sensations are
more commonly reported in nonvestibular dizziness. In an ideal world, the quality of
dizziness should help separate vestibular from nonvestibular dizziness (postural hypo-
tension, cardiac rhythm disturbances, syncope, anemia, hypoglycemia, hypercalce-
mia, vitamin B12 deficiency, medication effects, and anxiety). Yet, patients’
descriptions are notoriously unreliable; therefore, it is best not to rely entirely on the
reported quality of dizziness.1
Is It the First Ever Attack or Is It Long-standing Recurrent Vertigo?
The first ever attack of acute spontaneous vertigo lasting 24 hours or longer (also
called an acute vestibular syndrome) is most commonly due to vestibular neuritis,
which is a benign and self-limiting disorder; however, it could also be due to a cere-
bellar infarct, which is potentially life threatening. To separate these 2 different entities
with a near-identical history, it is essential to learn to elicit the clinical signs of vestib-
ular neuritis.2,3 Episodic vertigo occurring over many years is harmless in origin and
could represent BPV, vestibular migraine, Meniere disease, or vestibular paroxysmia.
A recent history of recurrent episodes of vertigo, especially crescendo vertigo (epi-
sodes occurring with an increasing severity and frequency) lasting minutes, should
ring alarm bells for posterior circulation transient ischemic attacks (TIAs).
Is It Spontaneous or Positional?
All types of vertigo worsen with head movement. Vertigo that is present at rest and
worse with any head movement does not constitute positional vertigo. Vertigo that
is absent at rest and is brought on only by lying down, turning over in bed, bending
down, or arching back is likely to represent BPV. Less commonly, vestibular migraine
and vestibular paroxysmia could also present with positional vertigo.4,5 Postural
 Bedside Assessment of Acute Dizziness and Vertigo 553

hypotension can be triggered by arising from the supine or sitting to the upright posi-
tion. Spontaneous vertigo could be due to vestibular migraine, Meniere disease,
vestibular neuritis, and posterior circulation ischemia.
What Is the Duration of Each Spell?
Vertigo lasting only seconds is most commonly due to BPV but also could be due to
vestibular migraine or vestibular paroxysmia. Episodes lasting minutes raise the pos-
sibility of posterior circulation TIAs or vestibular migraine. Symptoms lasting hours
could be due to Meniere disease or vestibular migraine whereas a duration of 24 hours
or longer (also called an acute vestibular syndrome) is encountered in vestibular
neuritis, stroke, or vestibular migraine.
What Are the Associated Symptoms?
Conventional teaching has been that associated aural symptoms automatically imply
peripheral vertigo. Nothing could be further from the truth. Acute unilateral tinnitus and
hearing loss in the context of an acute vestibular syndrome could mean an anterior
inferior cerebellar artery (AICA) infarction.6 Aural fullness, tinnitus, and fluctuating
hearing loss that herald or accompany vertigo lasting hours are indicative of Meniere
disease.7
Vertigo associated with migraine headaches, photophobia, phonophobia, or visual
aura and a history of profound motion sensitivity make vestibular migraine more
likely.4 Vertigo from brainstem infarction or demyelination can present with associated
neurologic symptoms of diplopia, facial paresthesia or weakness, dysarthria,
dysphonia or hiccups, limb weakness, clumsiness, or sensory loss. Dizziness associ-
ated with panic symptoms triggered by specific situations (supermarkets or crowded
public places) could point to anxiety as an underlying cause. Undiagnosed and un-
treated vestibular vertigo, however, could also lead to subsequent anxiety symptoms
that take the foreground.
Do Recent Events Provide a Clue?
If there has been a recent head trauma, consider BPV, skull base fracture with vestib-
ular loss, perilymph fistula, and migraine.8 A recent introduction of or change in blood
pressure–lowering medication might imply postural hypotension. A recent salt load
from festive dining might imply the first episode of Meniere disease.

THE PHYSICAL EXAMINATION

The General Inspection
Look for a head tilt, which can be observed in superior oblique palsy (where the patient
tilts the head to the unaffected side to minimize diplopia) or in central and peripheral
vestibular disorders.9 Vertical misalignment of the eyes in the absence of an extraoc-
ular muscle palsy (skew deviation) can occur in peripheral and central vestibular loss
but is thought more common in the latter and has been identified as a useful discrim-
inator in the separation of central and peripheral causes of acute vestibular syn-
drome.10 Ocular tilt reaction (OTR) refers to the triad of skew deviation, head tilt
(toward the hypotropic eye), and ocular counter-roll (Fig. 1). These 3 findings are
attributed to a unilateral lesion of the so-called graviceptive pathways arising from
the utricle. A vestibular or lower brainstem lesion causes an ipsiversive OTR. To check
for skew deviation, a cover test should be performed. When each eye is covered in
turn (alternate cover test), a corrective vertical saccade occurs in the uncovered
eye, bringing the hypotropic (down) eye upwards or the hypertropic (up) eye down-
wards. The head tilt in OTR is toward the lower eye (see Fig. 1)
554 Welgampola et al

Fig. 1. Right ocular tilt response. A right-sided ocular tilt response characterized by a right
head tilt, skew deviation with right hypotropia, and left hypertropia, rightward ocular tilt
response.

Horner syndrome (unilateral ptosis, miosis, anhydrosis, and enophthalmos) is

caused by lesions affecting sympathetic pathways and must be sought especially in
patients with acute vestibular syndrome, because it can accompany brainstem
strokes (for example, lateral medullary infarction). The pupillary asymmetry enhances
in dim light; therefore, comparison of pupil size in the light and darkness is helpful.

Inspection for Spontaneous and Gaze-evoked Nystagmus

Vestibular vertigo is often associated with spontaneous nystagmus that could point to
its origin. First, observe the eyes as the subject fixes on a target and look for primary
position spontaneous nystagmus and saccadic intrusions. Next, observe the effect of
leftward and rightward gaze (15 from the primary position). Saccadic intrusions are
fast eye movements that take the eye away from the primary position. They include
square wave jerks, which are minute saccades (0.5 –3 , separated by an approxi-
mately 2000-ms interval) that make the eye oscillate to and from the primary position
(common in cerebellar disease and extrapyramidal disorders); ocular flutters, which
are high-frequency (10–15 Hz) showers of horizontal saccades without an interval;
and opsoclonus, which are flurries of vertical, horizontal, and torsional oscillations
 Bedside Assessment of Acute Dizziness and Vertigo 555

typically seen in infectious, paraneoplastic, and toxic pathologies affecting the brain-
stem and cerebellum.
Spontaneous nystagmus arising from an acute peripheral vestibular loss (eg, from
vestibular neuritis) gives rise to horizontal torsional nystagmus that beats away from
the lesioned ear (Fig. 2, Video 1). The nystagmus is unidirectional and maximal
when gazing in the direction of the fast phase (Alexander’s law) and suppresses
with visual fixation (see Figs. 2 and 3, Videos 1–3). To ensure spontaneous nystagmus
is not missed, visual fixation must be removed. This can be done using a pair of optical
or video Frenzel glasses (takeaway Frenzels)11 or using a penlight test. To do this, the
examiner could cover 1 eye and shine a penlight torch directly on the uncovered eye,
thus removing visual fixation. Nystagmus intensity is then compared for the illuminated
eye with the cover on and off.12 Failure to remove visual fixation might cause sponta-
neous nystagmus to be missed. Examining a dizzy patient without some means of
removing visual fixation is like trying to auscultate the heart without a stethoscope.
Typical central nystagmus could be bidirectional (left beating on left gaze, rights
beating on rightward gaze), vertical (primary position upbeat or downbeat), or purely
torsional. Although all these features immediately imply a central cause for acute
vertigo, the converse is not true (ie, typical peripheral nystagmus that is horizontal-
torsional, is unidirectional, and that suppresses with fixation does not assure the clini-
cian of an underlying peripheral cause because it can often be seen in central vertigo,
including cerebellar infarction and vestibular migraine).
Horizontal gaze-evoked nystagmus (see Video 3) is commonly encountered as a by-
product of anticonvulsant, lithium, or alcohol intoxication or brainstem (vestibular
nucleus or nucleus prepositus hypoglossi) or cerebellar disorders.

Provocative Testing for Positional Nystagmus

Positional testing holds the key to the diagnosis of BPV, which is the most common
and correctable cause of vertigo worldwide. For example, in a patient with left

Fig. 2. Schematic diagram of typical nystagmus patterns observed in a left peripheral vesti-
bulopathy and in cerebellar pathology. The top panel shows typical peripheral right-
beating nystagmus that is unidirectional and enhances on rightward gaze. The bottom
panel shows typical gaze-evoked nystagmus, which beats leftward on left gaze and right-
ward on right gaze.
556 Welgampola et al

Fig. 3. Visual suppression of nystagmus. Typical peripheral nystagmus amplifies when the
subject dons a pair of Frenzel goggles (top panel) and is suppressed in bright light. Central
nystagmus is unaffected by visual fixation.

posterior canal BPV, in the upright position, the duct of the posterior canal aligns with
earth vertical and the otoconia gravitate toward the lowermost part of the duct to lie
close to the ampulla (Fig. 4A). When the head is rotated 45 to the left and rapidly
pitched backwards, the otoconia move along the left posterior canal to lie midway
along the duct (see Fig. 4B). The resultant plunger effect or negative pressure causes
ampullofugal movement of the cupula and briefly excites the posterior canal afferents,
producing the characteristic paroxysm of upbeat torsional geotropic nystagmus
(where the upper pole of the eye torts toward the lowermost ear) that is the hallmark
of posterior canal BPV (Video 4).
Horizontal canal BPV is a far less common cause of positional vertigo and is best
evoked by the supine roll test. The subject begins by assuming the supine position,
lying on a single pillow, with the head elevated 30 from horizontal, to align the horizon-
tal canals with earth vertical. Consider right horizontal canalithiasis where rotating to
the affected right side provokes a paroxysm of horizontal geotropic nystagmus
beating toward the right side (Fig. 5B, Video 5). Rotation to the left provokes a similar
but less intense paroxysm to the left. Lying face down from an initial upright position or
pitching the head down provokes horizontal right-beating nystagmus and lying supine
provokes left-beating nystagmus. To correctly identify the affected ear, nystagmus in-
tensity with either ear down can be compared. If an examiner has access to video gog-
gles, supine (contraversive) and prone (ipsiversive) nystagmus also helps identify the
affected side.13
Persistent, direction-changing horizontal positional nystagmus is observed in hori-
zontal canal BPV secondary to cupulolithiasis, where otoconia are adherent to the hor-
izontal canal cupula. In contrast to horizontal canalithiasis, the positional nystagmus is
apogeotropic, meaning that the nystagmus beats away from the lowermost ear during
supine testing. The nystagmus is more pronounced with the unaffected ear down.13
Persistent geotropic and apogeotropic horizontal positional nystagmus can also be
seen in central vestibular disorders, inclusive of vestibular migraine (Video 6).13
 Bedside Assessment of Acute Dizziness and Vertigo 557

Fig. 4. Left posterior canal BPV. (A) In the upright subject, the otoconia lie in the lowermost
part of the left posterior canal. No spontaneous nystagmus is seen. (B) As the head is turned
45 to the left and lowered to the Hallpike position, otoconia drift downward (ampullofu-
gally). Ampullofugal movement of the cupula excites vertical canal afferents. Left posterior
canal afferents are activated, briefly resulting in a paroxysm of upbeat geotropic torsional
nystagmus consistent with left posterior canal BPV. The panels on the right side illustrate eye
position and nystagmus slow-phase velocity in the vertical plane, with a crescendo-
decrescendo profile. (From Lechner C. Open Your Eyes! Video-oculography findings in
benign positional vertigo masters of philosophy [thesis]. University of Sydney. 2015; with
permission.)

Anterior canal BPV is rare and is also elicited with a Hallpike test. Left anterior canal
BPV could result in a positive right or left Hallpike test. The nystagmus, regardless of
which ear is down, is downbeat, with a torsional component that beats to the affected
left side (Video 7). Anterior canal BPV is so rare that torsional downbeat nystagmus on
positional testing should raise the possibility of an underlying central cause, unless the
nystagmus abolishes after a successful liberatory maneuver.
Spontaneous nystagmus can enhance in the supine position, leading to an incorrect
diagnosis of positional vertigo. For example, a subject with left vestibular neuritis could
demonstrate dramatic enhancement of subtle right-beating nystagmus in either Hall-
pike position. If the primary position spontaneous nystagmus is missed (during exam-
ination in a brightly lit emergency department), then enhanced spontaneous
nystagmus could be mistaken for BPV and inappropriately treated with repositioning
maneuvers, which would only lead to increasing nausea and motion sensitivity.
Enhanced spontaneous nystagmus distinctly differs from BPV in that it is persistent
rather than paroxysmal and is unidirectional (for example, right-beating nystagmus
is observed with the right ear down and the left ear down).
558 Welgampola et al

Fig. 5. Right horizontal canal BPV. (A) In the upright subject, otoconia lie along the lowest
part of the duct of the horizontal canal. No spontaneous nystagmus is seen. When lying on
the affected right side, the otoconia drift ampullopetally. For the horizontal canals, ampul-
lopetal movement of the cupula constitutes excitation and excitatory right-beating
nystagmus follows. The panel on the right side illustrates eye position and slow-phase veloc-
ity as a function of time. The nystagmus slow-phase velocity shows the typical rise and fall.
When lying on the unaffected left side, the otoconia drift ampullofugally and inhibit the
right horizontal anal afferents, and inhibitory (left-beating) nystagmus follows. The
nystagmus profiles with the affected and unaffected ears down are similar but the peak ve-
locity is higher with the affected ear down. The side with the more pronounced nystagmus
is considered the affected side. (From Lechner C. Open Your Eyes! Video-oculography find-
ings in benign positional vertigo masters of philosophy [thesis]. University of Sydney. 2015;
with permission.)

Head-shaking nystagmus
Head-shaking nystagmus is an additional method of demonstrating a left-right asym-
metry in dynamic vestibular function. While wearing Frenzel glasses, the patient’s
head is bent slightly forwards (30 ) to align the horizontal canals with earth horizontal.
The head is shaken in the yaw plane at 2 per second approximately 10 to 20 times. If
 Bedside Assessment of Acute Dizziness and Vertigo 559

there is a unilateral vestibular lesion, horizontal nystagmus with the quick phases
beating to the intact ear (contraversive head-shaking nystagmus) is seen at the end
of head shaking. Nystagmus may reverse thereafter. Normal subjects have no
head-shaking nystagmus or only 1 to 2 beats. Vertical nystagmus observed after hor-
izontal head shaking is a nonspecific sign, thought to imply central vestibulopathy.
Ipsiversive head-shaking nystagmus (with the fast phase beating toward the lesioned
ear) has been described in lateral medullary infarction.14

The Head Impulse

The head impulse test is a simple and effective method of assessing the integrity of the
horizontal vestibulo-ocular reflex (VOR) and is indispensable in the assessment of the
acute vestibular syndrome.15 It is within the capability of any clinician, but like any part
of the neurologic examination it is a skill acquired after much practice. To perform the
head impulse test, the patient fixates on a target approximately 1 m away. The exam-
iner firmly grasps the patient’s head with both hands and turns it briskly to the left or
the right (Fig. 6). The impulses should be unpredictable, low-amplitude (10 –20 ),
high-acceleration (2000 –4000 /s2) movements. When the VOR is intact, each head
movement is associated with an equal and opposite eye movement, thus maintaining
visual fixation on the target (see Figs. 6B, C). When the VOR is impaired unilaterally, a
head impulse to the affected side causes the head and eyes to initially move together,

Fig. 6. The head impulse test. The top panel illustrates a normal (negative) head impulse
test. The subject fixes on a near target (the examiner’s nose). (A) When the head is turned
left, the intact left horizontal VOR produces an equal and opposite eye movement that re-
turns the eye to the target (B, C). The bottom panel shows a VOR deficit. (E) When the head
is turned leftward, the eyes initially move with the head. (F) A refixation saccade, or catch-
up saccade, returns the eye back to the target.
560 Welgampola et al

followed by a rapid corrective eye movement or catch-up saccade, which rapidly refix-
ates the eye (see Fig. 6F). A positive catch-up saccade in the horizontal canal plane is
usually evident in the subject presenting with an acute vestibular syndrome secondary
to superior vestibular neuritis.3,10,15
To confidently separate vestibular neuritis from an acute vestibular syndrome of
central origin, it is essential to demonstrate a positive HINTS plus battery test (horizon-
tal head, impulse test, typical peripheral nystagmus, absence of skew deviation, and
normal hearing), shown to separate central from peripheral causes of acute vestibular
syndrome.16 Sometimes, despite a significant horizontal canal deficit, the catch-up
saccade is not detectable at the bedside, because it actually occurs while the head
is still moving. These saccades, evident only on video head-impulse testing, are covert
saccades.17

Oculomotor Examination
Test horizontal and vertical saccades
Saccades are rapid eye movements that point the fovea at an object of interest. To
test saccades, ask the patient to rapidly fixate on 2 stationary objects (clinician’s
thumb and index finger) placed 50 cm apart and observe saccadic latency, velocity,
accuracy, and conjugacy. Saccadic abnormalities are not expected in peripheral
vestibular disorders. Slow saccades of restricted amplitude may reflect an ocular
muscle or ocular motor nerve paresis. Disconjugate slowing of horizontal saccades
is an abnormality observed in internuclear ophthalmoplegia, which is caused by le-
sions affecting the median longitudinal fasciculus (MLF). A unilateral MLF lesion re-
sults in selective slowing of adducting saccades on testing horizontal saccades to
the unaffected side. The abducting eye may sometimes demonstrate disconjugate
nystagmus (ie, the nystagmus is more marked in the abducting than the adducting
eye). In an acutely dizzy patient, an internuclear ophthalmoplegia might imply a brain-
stem stroke or demyelination. Saccadic dysmetria, in particular hypermetria, is seen
in cerebellar disease. The saccade overshoots and returns to the target. Ipsipulsion,
with hypermetria of ipsilateral saccades and hypometria of contralateral saccades,
occurs in a lateral medullary infarct and is due to interruption of olivocerebellar climb-
ing fibers in the inferior cerebellar peduncle and downstream inhibition of the ipsilat-
eral fastigial nucleus.

Test pursuit
To test smooth pursuit, ask the patient to follow an object (clinician’s finger) moving no
faster than 20 per second in both the horizontal and vertical directions. Look for
broken or saccadic pursuit. Because many parts of the neuraxis participate in smooth
pursuit, broken pursuit does not contribute greatly to identifying the site of a lesion.
Age, level of alertness, intoxication, and neurodegenerative disorders affecting the
cerebellum and basal ganglia can all impair smooth pursuit. Deficits in smooth pursuit
are usually accompanied by impaired visual cancellation of the VOR.

Visual cancellation of the vestibulo-ocular reflex

Ask the patient to sit on a swivel chair with arms extended, hands clasped and
thumbs pointing up. Rotate the patient en bloc in the yaw plane as the patient fixes
on his/her own thumbs. Inspect the eyes for quick phases. In a normal subject with
normal VOR cancellation, the eyes remain fixed on the target and no quick phases
are observed. In cerebellar disorders and in disorders of smooth pursuit, VOR
cancellation is impaired and quick phases toward the direction of rotation are
observed.
 Bedside Assessment of Acute Dizziness and Vertigo 561

Vestibulospinal Reflexes
Vision, proprioception, and vestibulospinal contributions enable upright stance; there-
fore, disturbances in any one of these contributors can affect gait and stance. Patients
with an acute unilateral vestibulopathy typically fall toward the side of the lesion. In the
acute vestibular syndrome, inability to maintain upright stance with the eyes open
should raise the possibility of a cerebellar infarct. Examine the patient’s normal gait,
then the tandem gait forward and backward. Look for a wide-based gait, which can
be observed in a cerebellar disorder but is not specific for it. Perform the standard
Romberg test, where the patient stands on flat ground with a normal stance width,
with the eyes shut; vestibular impairment does not cause a positive Romberg test
when proprioception is intact. Ask the patient to stand on a 20-cm thick foam cushion,
which interrupts proprioceptive information and causes inability to maintain upright
stance in subjects with bilateral vestibular loss. The Unterberger test is performed
by asking the patient to march in place with eyes closed for 30 seconds and noting
any excessive turning to the side of vestibular impairment.

General Neurologic Assessment

As with any other patient presenting with neurologic symptoms, a general neurologic
examination inclusive of a search for lateralizing cranial nerve signs, long tract signs,
cerebellar ataxia, and sensory loss should be undertaken.

Postural Blood Pressure, Pulse, and Auscultation

Lying and standing blood pressure and pulse measurement (20-mm systolic blood
pressure drop or 30 beats per minute heart rate rise) help identify orthostatic intoler-
ance as a cause of dizziness. Auscultation of the heart, neck, and supraclavicular
fossa is important to detect vascular bruits and cardiac murmurs that might be linked
with either lightheadedness (eg, aortic stenosis) or vertigo (eg, subclavian steal).

WHAT MIGHT BE SEEN IN A PATIENT PRESENTING WITH ACUTE VESTIBULAR

SYNDROME
Vestibular Neuritis
Vestibular neuritis is associated with horizontal torsional nystagmus that is unidirec-
tional, beats away from the affected ear, suppresses with visual fixation, and is
maximal on gazing in the direction of the quick phase. The nystagmus enhances
dramatically with either Hallpike test (if the patient allows the clinician to do this). A
positive horizontal head impulse test is seen on turning toward the lesioned side,
with a rapid corrective saccade or catch-up saccade. Hearing is uniformly normal in
vestibular neuritis. Abnormal hearing in the context of an acute vestibular syndrome
could imply an AICA infarction. An ipsilateral ocular tilt response rarely occurs in
vestibular neuritis, with head tilt toward the affected ear, skew deviation with hypotro-
pia on the side of the ear, and ocular torsion toward the side of the lesion. Because
skew deviation in the context of vertigo is seen more commonly with posterior circu-
lation strokes, it is considered a red flag for central vertigo.

Cerebellar Stroke
Although typical cerebellar nystagmus is bidirectional (left beating on left gaze and
right beating on right gaze), cerebellar strokes can present with second- or third-
degree spontaneous horizontal nystagmus (typical peripheral nystagmus).18 Typical
cerebellar nystagmus (see Video 2) is attributed to abnormalities in the cerebellar
flocculus (vestibulocerebellum) or the medial vestibular nucleus-nucleus prepositus
562 Welgampola et al

hypoglossus complex in the medulla. The head impulse test is negative except in
AICA infarcts and skew deviation may be evident. In recent studies by Chen and col-
leagues,19 62% of subjects with AICA infarcts had positive clinical head impulse
tests ipsilateral to the infarct. Even 20% of posterior inferior cerebellar artery/superior
cerebellar artery infarcts had a contralaterally positive clinical head impulses. On
quantitative testing, the amplitude of catch-up saccades observed in vestibular
neuritis were twice as large. In cases of an AICA infarct, hearing loss is evident on
the side with concurrent vestibular loss. Saccadic dysmetria, unilateral deficits in
VOR suppression, or appendicular cerebellar signs might help, but the key to iden-
tifying stroke is the failure to pass the HINTS battery. In patients with an acute vestib-
ular syndrome, any one of the following attributes should trigger a search for
cerebellar stroke: a normal head impulse, presence of skew, cerebellar nystagmus,
or a new hearing loss.

WHAT MIGHT BE SEEN IN EPISODIC SPONTANEOUS VERTIGO

Meniere Disease
An episode of acute vertigo in Meniere disease is characterized by typical peripheral
nystagmus that is unidirectional, obeys Alexander’s law, and is enhanced in the dark.
In contrast to other peripheral vestibular disorders, the nystagmus could first beat to-
ward the affected ear (irritative nystagmus), within seconds to minutes change direc-
tion to beat toward the unaffected ear (paretic nystagmus) (Video 8),20,21 and finally
change direction once more (recovery nystagmus) to beat to the affected ear. This
sequence of direction change in primary position spontaneous nystagmus has only
been reported in endolymphatic hydrops.

Vestibular Migraine
An acutely dizzy patient with vestibular migraine could present with spontaneous hor-
izontal, vertical, or pure torsional nystagmus.22 Additionally both horizontal and verti-
cal positional nystagmus can be observed in vestibular migraine. In contrast to BPV,
the positional nystagmus of vestibular migraine is persistent and remains as long as
the head remains in the provocative position (see Video 6).23 When the nystagmus
is horizontal, both geotropic and apogeotropic positional nystagmus can be
observed.13,23

WHAT MIGHT BE SEEN IN THE PATIENT WITH RECURRENT POSITIONAL VERTIGO

Benign Positional Vertigo
Typical posterior canal BPV is not associated with primary position spontaneous
nystagmus; during Hallpike testing with the affected ear down, paroxysmal positional
nystagmus with a vertical upbeating torsional geotropic eye movement is observed
(see Fig. 4, Video 4). The nystagmus could begin after a 5- to 10-second latency
and rapidly rises to a crescendo, completely abating by 60 seconds. Hallpike testing
with the unaffected ear down generally yields no nystagmus but rarely could produce
low-amplitude nystagmus similar to that observed with the affected ear down.
Returning the patient from the Hallpike position to an upright position causes reverse
flow of otoconia (ampullopetally) and torsional downbeat nystagmus with torsion to-
ward the unaffected ear. Horizontal canal BPV, anterior canal BPV, and central
vestibular disorders can also present with recurrent positional vertigo. Annotated
videos of these less common presentations of positional vertigo are included (see
Videos 5–7).
 Bedside Assessment of Acute Dizziness and Vertigo 563

WHEN THE PATIENT IS ACUTELY DIZZY AND THERE ARE NO PHYSICAL SIGNS TO FIND

Failure to demonstrate nystagmus in a brightly lit room is of no diagnostic value. In an

acutely dizzy patient, however, the absence of nystagmus when examined without vi-
sual fixation implies a nonvestibular cause for vertigo. Consider hypotension, cardiac
rhythm disturbances, hypoglycemia, anemia, and anxiety, especially if associated with
other panic symptoms and reproducible with hyperventilation.

FUTURE DIRECTIONS IN ACUTE VERTIGO

A majority of acutely vertiginous patients present to an emergency department and

general practice rather than a specialty clinic. Frontline practitioners have the unique
opportunity of observing ictal nystagmus, which provides critical information that
could streamline the diagnostic process, but they lack the expertise and the equip-
ment to elicit, record, or interpret nystagmus. Conversely, expert clinicians who
have all of these seldom have the opportunity of assessing an acutely vertiginous pa-
tient. The use of inexpensive methods of removing visual fixation11 and portable video
recording devices in emergency departments and general practice settings could cor-
rect this discrepancy. In an era when many adults own a handheld device with a digital
camera, it is inconceivable that a general practitioner or emergency physician has no
access to a simple video Frenzel device or its equivalent. Easy access to the correct
tools and greater familiarity with cardinal eye signs of common vestibular disorders
promote early diagnosis and better management of acutely dizzy patients in the
frontline.

SUPPLEMENTARY DATA

Supplementary data related to this article can be found online at http://dx.doi.org/10.

1016/j.ncl.2015.04.001.

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