Examination of the Patient

with Dizziness or Imbalance

Gregory T. Whitman, MD

KEYWORDS
 Examination  Dizziness  Vertigo  Balance  Vestibular  Nystagmus  Gait

KEY POINTS
 Because of the multisensory nature of balance and vestibular function, the clinician seeing
a dizzy patient, must perform a comprehensive neurological assessment.
 Altered mental status and abnormalities of vision may disturb balance and gait.
 The direction and duration of any nystagmus should be recorded, and one should note
whether nystagmus is spontaneous, gaze evoked, or positional.
 Past pointing tests, Romberg tests, and the Fukuda stepping test may disclose
imbalance.

INTRODUCTION

“Dizziness” may signify vertigo (an illusory sense of movement of the environment or
self), lightheadedness (eg, a floating sensation), or other sensations that defy
description. Many people with dizziness have an abnormality of gait or postural stabil-
ity, necessitating inclusion of gait and balance in the clinical approach to dizziness.
Assessment of dizziness in US emergency rooms reportedly costs $4 billion per
year.1 Annual medical expenses due to falls in the United States were reported to
be $50.0 billion.2 Despite these high costs, many patients with dizziness or imbalance
are discharged from the hospital without a clear diagnosis, suggesting the need for
improved physical examination approaches.
One might reasonably ask: What is the rationale for combining dizziness and
imbalance into one category? Some patients with dizziness report their symptoms
are localized within or around the head and that their gait is normal. For others,
the main problem is abnormality of gait, the head feels normal. In practice, though,

Disclosure Statement: Dr G.T. Whitman has nothing to disclose with respect to relationships
with any commercial company that has a direct financial interest in subject matter or materials
discussed in article or with a company making a competing product.
Department of Otolaryngology, Harvard Medical School, Massachusetts Eye and Ear Infirmary,
Massachusetts Eye and Ear Balance and Vestibular Center, 250 Pond Street, Braintree, MA
02184, USA
E-mail address: gtw3@cornell.edu

Med Clin N Am 103 (2019) 191–201

https://doi.org/10.1016/j.mcna.2018.10.008 medical.theclinics.com
0025-7125/19/ª 2018 The Author. Published by Elsevier Inc. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
192 Whitman

most patients with dizziness or imbalance fall on a spectrum between the patient
with head-related symptoms alone, and the patient with balance and gait symptoms
alone.
The reader is assumed to be familiar with the basic neurologic examination.
This topic will not be reviewed in detail. The routine neurologic examination,
though, is critical, because of the extensive differential diagnosis. The differential
diagnosis of dizziness is reviewed elsewhere.3 The primary goals of this review
are as follows:
1. To outline a systematic approach to physical examination of the patient with dizzi-
ness or imbalance,
2. To discuss useful and frequently overlooked neurologic signs that are useful in clin-
ical practice for making a diagnosis.
First and foremost, one has to acknowledge the multisensory nature of balance and
vestibular function. Balance function may remain surprisingly normal (compensated),
until a large number of neurons and systems have been lost. One is surprised to
encounter patients with substantially absent peripheral vestibular reflexes but near
normal gait. Although the latter situation may be surprising, it is also common in other-
wise young, healthy patients who have lost vestibular function.
At the same time, a diverse array of neurologic disturbances may contribute to
imbalance. That is, gait disorders are commonly “multifactorial.” Consider a set of 3
disorders, as follows:
1. Unilateral benign paroxysmal positional vertigo (BPPV),
2. Mild diabetic peripheral neuropathy,
3. Bilateral impairment of visual acuity, due to cataracts.
It is by no means clear that any of the formerly mentioned 3 problems in isolation
would greatly disturb balance. Combined, however, the set of all 3 diagnoses would
almost assuredly cause imbalance. A critical principle, then, is that one must maintain
a high index of suspicion that imbalance is multifactorial.
As elsewhere in Neurology, the assessment of multiple coincident lesions is chal-
lenging and benefits from the experience of the examiner. For the nonspecialist, the
best approach to the possibility of multiple lesions may be to carefully catalog as
many abnormal neurological findings as possible, in as much detail as possible,
acknowledging that in the end, the combination of objective abnormalities may add
up to an explanation.

ORTHOSTATIC VITAL SIGNS

Orthostatic vital signs are most useful when viewed as a stress test. The basic
routine of checking vitals lying down and then sitting up is insufficient. Prolonged
action of gravity may be necessary to cause enough pooling of blood below the
heart to elicit orthostatic intolerance, except in cases where orthostatic vital sign
measurements are hardly necessary. The patient who says, “When I stand up, I
get lightheaded,” should be encouraged to stand, for a few minutes, for example,
while history taking is continued. The examiner should ask about symptoms
(including blurred vision and dizziness) while the patient stands. Note should be
made of any deterioration in cognitive function while upright, and serial sets of
standing vital signs may be informative. It is common knowledge that a sustained
fall in systolic blood pressure of at least 20 mm Hg, after moving from the sitting
(or lying down) position to the standing position, is evidence for orthostatic
 Examination of the Patient with Dizziness 193

hypotension; however, one must not overlook the patient with possible orthostatic
cerebral hypoperfusion, and marked clinical symptoms in the standing position, but
who may not manifest overt hypotension. Although many approaches to orthostatic
vital signs would be acceptable, it is wise to routinely observe dizzy patients, in the
standing position, for at least 3 minutes, while monitoring for symptoms and/or
changes of vital signs. If overwhelming dizziness develops during such a test, the
patient should, for safety, be placed back into a sitting or lying down position
and allowed to recover.

CERVICAL SPINE

The neck provides proprioceptive information to the brain and is thus a potential
substrate for dizziness. Pain specialists are familiar with the dizziness occasionally
elicited with performance of bilateral cervical spine injection procedures.4 It is likely
that application of a combination of tests involving error in position sense of the
neck and nystagmus upon turning of the neck would improve diagnosis of patients
with cervical spine disorders plus dizziness.5,6 The best approach to the use of
such methods, in practice, remains to be clarified. At present, the best the busy
clinician can hope for with respect to diagnosing cervicogenic dizziness may be
to perform range-of-motion testing in the yaw (horizontal), pitch (sagittal), and
roll tilt (coronal) planes and ask the patient whether any of the “dizziness” symp-
toms are reproduced with certain neck positions or motions. If so, the clinician
can then look for treatable cervical spine disorders. One should remember to
consider the differential diagnosis of cervical artery dissection, of which neck
pain is a common early feature. For that reason, along with the possibility of cer-
vical myelopathy, the clinician considering a diagnosis of cervicogenic dizziness
must be sure to look for abnormal findings on the basic neurologic examination
that might lead one in a different direction.

MENTAL STATUS

Although the central vestibular system is often conceptualized in terms of

posterior fossa structures, widespread brain areas are needed to integrate multi-
sensory information in such a way as to create cues and impressions pertaining
to space and motion. Such integrative function inevitably involves the cerebral
cortex.
One should at least consider in passing the possibility that a chief complaint of
“dizziness” may be localized to the cerebral cortex. Indeed, it is not unusual for a pa-
tient with Alzheimer disease to report “dizziness” that defies explication, even in the
best of hands. This being the case, one should identify and record abnormal cognitive
behaviors such as repetitive questioning. If present, these suggest short-term memory
impairment. Cognitive function can be screened for by asking the patient to spell the
word “world” backward. If there is any doubt about the patient’s cognition, the clini-
cian can assess further with a brief cognitive test battery such as the Montreal Cogni-
tive Assessment.7
As part of the mental status examination, one should assess for anxiety. A common
clinical conundrum is anxiety, or more properly an anxiety disorder, may be formulated
as a cause of dizziness, a consequence of an inner ear disorder that causes dizziness,
or a product of aggravation of an underlying anxiety disorder by an inner ear disorder.8
In some cases, the anxiety is an important therapeutic target. A qualitative notation on
the chart about the examiner’s impressions of the patient’s mood and affect contrib-
utes to tracking of this component.
194 Whitman

VISION

Isolated loss of vision seldom causes a marked disturbance of balance. Like other
sensory channels, however, vision does contribute to balance, and visual impairment
contributes to imbalance. In particular, visual field cuts may be unobvious to the pa-
tient and may aggravate imbalance and increase fall risk.9 The standard confrontation
tests of visual fields are familiar to most physicians. In addition, visual fields can be
assessed in detail at the bedside, using a laser pointer and a wall.10 For patients
who are users of bifocal, trifocal, or progressive lenses, walking should be assessed
with and without the use of glasses. Declines in performance with the use of certain
lenses should be noted.

FACIAL NERVE FUNCTION

The Ramsay Hunt syndrome consists of facial nerve palsy, combined with a painful
rash involving the pinna or external auditory canal, plus vestibular and hearing defi-
cits in varying proportions. This syndrome is presumed to often be due to latent virus
reactivation. Treatment, which is beyond the scope of this review, is modeled after
that used in the setting of Bell palsy. It is important to recognize the facial palsy,
which may be relatively subtle in the context of severe dizziness. On examination,
eye closure is less vigorous on the involved side, and the ipsilesional nasolabial
fold is relatively flat. After some recovery, synkinesis may be noted, such that closure
of the eye on the affected side is associated with aberrant twitching of facial
muscles.

OTOSCOPY AND HEARING

Although a detailed ear examination is beyond the scope of this review, a few points
warrant brief discussion. Applying positive and negative pneumatic pressure
during otoscopy may elicit dizziness in pressure-sensitive disorders. These pres-
sure-sensitive disorders, including the superior semicircular canal dehiscence
syndrome11 and occasionally Meniere syndrome.12 In the instance of Ramsay
Hunt syndrome (see earlier), otoscopy may disclose vesicles in the external auditory
canal.
Hearing loss is a key feature of some disorders that cause dizziness. One must not,
however, immediately assume that hearing loss is sensorineural. For example,
cerumen blocking the external auditory canal may cause hearing impairment. At the
same time, one should try to make a diagnosis of sensorineural hearing loss as early
as possible, because of the potential need to treat sudden sensorineural hearing loss
with corticosteroid medication. Sensorineural hearing loss that involves loss of acuity
for low-frequency sound is a component of the diagnostic criteria for Meniere
disease. Interestingly, there are also emerging data suggesting that hearing loss of
any form may contribute to imbalance due to loss of sound cues about the spatial
environment.13,14
The well-known Rinne test is typically performed with a 512-Hz tuning fork. If the pa-
tient reports that sound is heard louder through bone than air, the result suggests
either a component of conductive hearing loss or a pseudoconductive hearing loss,
due to a third mobile window, such as superior semicircular canal dehiscence.15 It
is helpful to have a low-frequency (128 or 64 Hz) tuning fork, because hearing asym-
metries tend to be marked for this frequency when testing patients with Meniere. If
whispered speech is poorly understood in either ear, a retrocochlear lesion, for
example, vestibular schwannoma, should be considered.
 Examination of the Patient with Dizziness 195

NYSTAGMUS

The most common type of nystagmus, called jerk nystagmus, is a rhythmic eye move-
ment having well-defined slow and fast phases. One should observe for the presence
of spontaneous nystagmus, while the patient is sitting, looking straight ahead. In the
case of acute unilateral peripheral vestibulopathy, and/or vestibular neuritis, and/or
labyrinthitis, spontaneous nystagmus is predominantly horizontal and unidirectional
with fast phases away from the lesion (a smaller torsional component may be evident).
The amplitude of spontaneous, unidirectional nystagmus typically increases with gaze
in the direction of fast phases.
The nystagmus of acute peripheral vestibulopathy becomes coarser when one elim-
inates fixation, using Frenzel video goggles. Alternatively, to eliminate fixation, one of
the patient’s eyes can be covered while the other eye is viewed with an ophthalmo-
scope and observed for nystagmus.
Smooth pursuit should be tested by asking the patient to slowly follow a finger to the
right and left, and up and down, noting smoothness of eye movements. Saccadic
smooth pursuit localizes to the brain. The specificity of the latter sign, however, is
greater in younger patients.16 Despite the high prevalence of saccadic smooth pursuit
with increasing age, excessive degeneration of smooth pursuit function is reported to
be associated with neurodegenerative brain diseases.17
Gaze-evoked and/or gaze-holding nystagmus may be defined as nystagmus that is
absent when looking straight but is present when looking (maintaining gaze) in some
directions. Gaze-evoked nystagmus may be seen in normal people with extreme eye
deviation, for example, all the way to the right, but there is no widely accepted
consensus on a definition of “extreme.” Suffice it to say that the specificity of gaze-
evoked nystagmus is highest when small deviations of eye position away from straight
ahead elicit nystagmus.
Direction switching nystagmus (eg, right beating with right gaze, and left beating
with left gaze) is a red flag for a possible brain lesion, as is pure vertical nystagmus,
or vertical nystagmus with only a subtle torsional component. If direction switching
nystagmus is asymmetric, that is, coarser with gaze in one particular direction, this
suggests a focal, structural brain lesion.
Persistent downbeat nystagmus may be spontaneous, but it tends to be coarser on
gaze to the right or left. It can be due to lesions of the cerebellum or at the craniocer-
vical junction, as in the case of Arnold Chiari malformations. Rebound nystagmus lo-
calizes to the cerebellum. It is recognized as follows: the patient first is asked to follow
a target such as the examiner’s finger to an eccentric position, for example, all the way
to the right, and then to make a saccade back to the midline, at which point a burst of
nystagmus is seen, in the direction of the saccade back toward the midline.
An important type of nystagmus is that observed in patients with BPPV. As implied
by the name of this condition, the nystagmus that is the hallmark of BPPV is parox-
ysmal and occurs in certain positions. The nystagmus occurs within seconds after
moving into a provocative position. The latency between adopting a provocative po-
sition and the onset of nystagmus is typically less than 15 seconds, but it can be
longer.
If all evidence points to BPPV, but nystagmus cannot be easily elicited, it may be
worth a try to maintain the patient in each provocative position for a longer period,
for example, 30 seconds, and observe for nystagmus. The latency between movement
of the head and onset of nystagmus is presumably due to a combination of the time
needed for freely floating particles to move around a semicircular canal and then sub-
sequently into and through the ampulla.
196 Whitman

The best single test for BPPV is the Dix-Hallpike test,18 which was originally
described by Dix and Hallpike.19 In brief, while the patient is seated, the head is turned
30 to 45 in the horizontal plane toward the ear to be tested. The patient next lies down
with the neck extended about 30 below the level of the examining surface. The exam-
iner observes for a paroxysmal burst of nystagmus. With the onset of nystagmus, most
patients feel anxious, some more than others. If the clinician anticipates such reactions,
anticipation of such reactions may facilitate counseling of the patient and talking the
patient through particle repositioning maneuvers, in a calm and reassuring manner.
In the most common form of BPPV, where debris is trapped in a posterior semicir-
cular canal, the nystagmus is a combination of upbeat and torsional with the upper
poles of the eyes beating toward the ground. The technical method of performance
of the Dix-Hallpike test has been described elsewhere in great detail.20,21
It is important to note that the Dix-Hallpike test will only be positive if there is debris
in one or more of the semicircular canals. If debris is instead primarily within the utricle,
the Dix-Hallpike test may be negative. The patient may, however, experience vertigo
again within a short timeframe, if the debris is transported from the utricle into a semi-
circular canal. The moral is that if BPPV is strongly suspected, but the Dix-Hallpike test
is negative, it may be advisable to repeat the test on a different day. Selected nystga-
mus types and associated abnormalities may be found in (Table 1).

VERTICAL OCULAR MISALIGNMENT

The search for skew deviation is becoming a routine part of the neurologic examina-
tion in some emergency departments.22 The key point for the nonspecialist is that any
new vertical misalignment of the eyes should be considered a potential central sign,
for example, due to involvement of the brainstem. To probe for ocular misalignment,
one can simply ask the patient whether there is a history of double vision. Ocular
misalignment can be revealed on examination through use of the alternate cover
test, in which a patient fixates on a target, such as the examiner’s nose, while each
of the patient’s eyes is alternately covered. This procedure is repeated several times,
alternating between the right and left eye. The examiner should observe for readjust-
ment of eye position when either eye is uncovered.

ABNORMAL SACCADIC EYE MOVEMENTS

Fixation may be derailed by inappropriate saccades referred to as saccadic intrusions.

One common saccadic intrusion is the square wave jerk. The square wave jerk is an

Table 1
Selected abnormal examination findings and the differential diagnosis

Examination Finding Differential Diagnosis

Dix-Hallpike test shows paroxysmal upbeat BPPV involving the posterior (or horizontal or
torsional (or horizontal or downbeat) anterior) semicircular canal, respectively
nystagmus
Spontaneous, unidirectional, predominantly Acute peripheral vestibulopathy and/or
horizontal nystagmus vestibular neuritis and/or labyrinthitis
Gaze evoked, direction switching nystagmus Posterior fossa lesion
Skew deviation Posterior fossa lesion
Facial palsy and vesicles in the external Ramsay Hunt syndrome
auditory canal
Asymmetric loss of hearing acuity Meniere syndrome, vestibular schwannoma
 Examination of the Patient with Dizziness 197

eye movement in which a small, single saccade, in random direction, is followed by a

saccade back to the direction of fixation. Square wave jerks are nonspecific. Their
presence may signify basal ganglia or cerebellar disease, but they are also seen in
older people without evident neurologic disease. Unlike jerk nystagmus, saccades
may be distinguished by the absence of well defined, rhythmic fast and slow phases.

VESTIBULO-OCULAR REFLEX TESTS

A focused assessment of the semicircular canal function, at least for the horizontal ca-
nal, can be performed at the bedside. The head impulse test was developed to assess
the horizontal angular vestibulo-ocular reflex. The technical method of the head im-
pulse test has been described in detail elsewhere.23 In brief, the patient fixates on
the examiner’s nose, typically starting with the patient’s head turned about 10 to
the right or left of midline. The head is then abruptly, passively, and unpredictably
turned by the examiner, toward one side or the other, through about 20 , using caution
to avoid injury. The examiner watches for catch up saccades back toward the midline.
In the case of peripheral vestibulopathy, the eyes move passively with the head during
head impulses, resulting in the need for a catch up saccade, away from the weak ear,
toward the examiner’s nose. An assumption of this test, and a fairly good one, is that in
some disorders, such as acute vestibular neuritis, peripheral vestibular involvement is
substantially diffuse and would thus be expected to involve the horizontal semicircular
canals.
Like the head impulse test, dynamic visual acuity tests assess the vestibulo-ocular
reflex. First, the patient’s best near vision is determined. Then, the examiner passively
oscillates the patient’s head to the right and left in the yaw (horizontal) plane at about
2 Hz. If the patient loses more than 2 lines of vision, vestibular weakness should be
suspected. It is best to use a near card, because the demands on the vestibulo-
ocular reflex are greater with near viewing.24

LIMB MOTOR TESTS

The title of this section is deliberately noncommittal and meant to encompass what
physicians typically call motor and cerebellar tests. Labeling tests as “motor” (by
which many neurologists would mean muscle bulk, tone, and strength) or “cerebellar,”
as is often done in practice, belies the inherent multisystem and poorly localized na-
ture of the functions being tested.
Moreover, many techniques involving limbs depend on substantial sensory inputs
for which any test interpretation must (but usually does not) account. Thus, it is wise
to choose tests that are as simple as possible, on both the afferent and efferent sides,
in order to limit the amount of information given to the patient and increase the sensi-
tivity of the test.
The finger-to-nose tests familiar to every medical student are flawed. They give the
patient abundant sensory information, potentially disguising deficits. More sensitive
for detection of peripheral vestibulopathy are past pointing tests. These past pointing
tests that require a patient (with eyes closed) to extend both arms and repeatedly
touch the examiner’s fingers approaching the examiner’s fingers either from above
or below. Past pointing tests were studied by Róbert Bárány,25 who described his
method as follows26:

The patient is asked to close his eyes and touch the doctor’s finger with.index
finger, then.keeping the arm outstretched.lower it to knee-level, then raise it
again and touch the doctor’s finger once more.The direction of.deviation will
198 Whitman

differ according to the direction of the nystagmus.always in an opposite direc-

tion to the nystagmus.

The muscle power examination has obvious relationships to balance and gait.
Particularly important is to test both foot dorsiflexor27 and plantarflexor28 power. Def-
icits of either may cause critical gait and balance impairment. Strength can be
assessed either with manual muscle power examination, or at times more revealingly,
by asking the patient to perform tasks using the patient’s own body weight, such as
standing on the toes, while the examiner observes the vigor with which this maneuver
is completed.

BALANCE AND GAIT TESTS

The Romberg sign is a well-known indicator of visual dependence that implies loss of
normal proprioception or loss of peripheral vestibular function.29 Originally developed
for diagnosis of myelopathy, namely tabes dorsalis, the Romberg sign is also encoun-
tered in clinical practice when testing patients with bilateral peripheral vestibular
hypofunction,30 and those with vitamin B12 deficiency, copper deficiency, or
hyperzincemia.31
The Romberg test can be made more difficult and thus more sensitive to balance-
related issues by asking the patient to stand in tandem with eyes closed. The examiner
should note whether the patient can confidently maintain this posture for several sec-
onds. There are many variations of the Romberg test. In general, these tests have been
somewhat unduly criticized, as a result of their less than excellent sensitivity (due in
part to vestibular compensation) and specificity (many different types of disorders
and aging affect balance).
As is the case with respect to other clinical neurologic tests, any one isolated abnor-
mality must be interpreted with caution. Combined with other tests, though, the Rom-
berg test contributes sensitivity to the neurologic examination. For example, a patient
who presents after an acute vertiginous illness, and who falls strongly to the left, has
mild left-sided hearing loss and has right beating nystagmus on extreme rightward
gaze, might be suspected to have had left-sided labyrinthitis. Any one of these findings
alone, in isolation, might be discounted, but together, they form an important pattern.
Similar comments might be made about the Fukuda stepping test. In this test, a pa-
tient is asked to march in place with arms outstretched and eyes closed for about
1 minute, and the examiner observes for abnormal turning toward the right or left
greater than 20 .32 If used as a stand-alone test, it is not likely to have high sensitivity
or specificity for any particular disorder. However, when combined with other tests
described in this review, the Fukuda test increases the likelihood of recognition of a
diagnostically useful pattern.
In the examination of gait, one should ask the patient to walk outside the examina-
tion room and look for potential signs of central nervous system dysfunction, for
example, small step length, irregular step length, and asymmetric arm swing. The
“walking Romberg” test gauges postural stability during a 5-m walk with the patient’s
eyes closed. Most patients with clinically significant cervical myelopathy were re-
ported to manifest either a Romberg sign or a walking Romberg sign.33
Recently, there has been increasing interest in dual-task paradigms that simulta-
neously assess cognition and gait.34 Balance places phenomenal demands on atten-
tion. If a patient has an underlying cognitive disorder, an abnormality of gait, or both,
the gait and balance dysfunction can in some cases be unmasked by placing cognitive
demands on the patient while simultaneously also asking the patient to perform a bal-
ance or gait task. The breakdown of gait function during a cognitively challenging task
 Examination of the Patient with Dizziness 199

may be expressed in terms of the dual task cost (DTC) of walking while performing a
cognitively demanding task, for example:

DTC 5 ([single-task gait velocity – dual-task gait velocity]/single-task gait

velocity)  100.35

One of the first reported clinical tests in this category was the “Stops walking when
talking” test that was reported to predict fall risk.36 The clinician can glean helpful in-
formation through careful observation of the patient’s gait in the hallway during con-
versation, in comparison to that when the patient is concentrating on walking. One
definition of high DTC that might reasonably be used in practice would be a decrease
in gait velocity of greater than 20% when performing a cognitive task, such as count-
ing backward from 100 while walking.37 If a patient’s performance declines markedly
during conversation or performance of a cognitive task such as counting backward
(reflecting a high DTC), then cognitive impairment and a risk for falls38 should both
be suspected.

SUMMARY

Through performance of a neurologic and ear examination, objective data can be

gleaned that narrow the differential diagnosis of “dizziness.” The multisensory and
integrative nature of balance places distinct demands on the diagnostic process.
Accordingly, the combination of multiple types of physical examination methods
may be expected to increase the sensitivity of one’s approach to detection of
disorders.

REFERENCES

1. Saber Tehrani AS, Coughlan D, Hsieh YH, et al. Rising annual costs of dizziness
presentations to U.S. emergency departments. Acad Emerg Med 2013;20:
689–96.
2. Florence CS, Bergen G, Atherly A, et al. Medical costs of fatal and nonfatal falls in
older adults. J Am Geriatr Soc 2018;66(4):693–8.
3. Whitman GT. Dizziness [review]. Am J Med 2018. https://doi.org/10.1016/j.
amjmed.2018.05.014.
4. Zhu X, Grover MJ. Cervicogenic dizziness successfully treated with upper cervi-
cal medial branch nerve radiofrequency ablation: a case report. A A Pract 2018;
10(6):150–3.
5. L’Heureux-Lebeau B, Godbout A, Berbiche D, et al. Evaluation of paraclinical
tests in the diagnosis of cervicogenic dizziness. Otol Neurotol 2014;35(10):
1858–65.
6. Reiley AS, Vickory FM, Funderburg SE, et al. How to diagnose cervicogenic dizzi-
ness. Arch Physiother 2017;7:12.
7. Hobson J. The montreal cognitive assessment (MoCA). Occup Med (Lond) 2015;
65(9):764–5.
8. Staab JP, Ruckenstein MJ. Which comes first? Psychogenic dizziness versus oto-
genic anxiety. Laryngoscope 2003;113(10):1714–8.
9. Mihailovic A, Swenor BK, Friedman DS, et al. Gait implications of visual field dam-
age from glaucoma. Transl Vis Sci Technol 2017;6(3):23.
10. Stark R. Clinical testing of visual fields using a laser pointer and a wall. Pract Neu-
rol 2013;13(4):258–9.
200 Whitman

11. Shuman AG, Rizvi SS, Pirouet CW, et al. Hennebert’s sign in superior semicircular
canal dehiscence syndrome: a video case report. Laryngoscope 2012;122(2):
412–4.
12. Nadol JB Jr. Positive Hennebert’s sign in Meniere’s disease. Arch Otolaryngol
1977;103(9):524–30.
13. Zhong X, Yost WA. Relationship between postural stability and spatial hearing.
J Am Acad Audiol 2013;24(9):782–8.
14. Vitkovic J, Le C, Lee SL, et al. The contribution of hearing and hearing loss to bal-
ance control. Audiol Neurootol 2016;21(4):195–202.
15. Bance M. When is a conductive hearing loss not a conductive hearing loss?
Causes of a mismatch in air-bone threshold measurements or a "pseudoconduc-
tive" hearing loss. J Otolaryngol 2004;33(2):135–8.
16. Maruta J, Spielman LA, Rajashekar U, et al. Visual tracking in development and
aging. Front Neurol 2017;8:640.
17. Shakespeare TJ, Kaski D, Yong KXX, et al. Abnormalities of fixation, saccade and
pursuit in posterior cortical atrophy. Brain 2015;138(Pt 7):1976–91.
18. Bhattacharyya N, Gubbels SP, Schwartz SR, et al. Clinical practice guideline:
benign paroxysmal positional vertigo (update). Otolaryngol Head Neck Surg
2017;156(3_suppl):S1–47.
19. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis of certain
common disorders of the vestibular system. Proc R Soc Med 1952;45(6):341–54.
20. Muncie HL, Sirmans SM, James E. Dizziness: approach to evaluation and man-
agement. Am Fam Physician 2017;95(3):154–62.
21. Kim JS, Zee DS. Clinical practice. Benign paroxysmal positional vertigo. N Engl J
Med 2014;370(12):1138–47.
22. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to
screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med
2013;20(10):986–96.
23. Spiegel R, Kirsch M, Rosin C, et al. Dizziness in the emergency department: an
update on diagnosis. Swiss Med Wkly 2017;147:w14565.
24. Viirre E, Tweed D, Milner K, et al. A reexamination of the gain of the vestibulooc-
ular reflex. J Neurophysiol 1986;56(2):439–50.
25. Behrman W. The pointing test of barany. Br Med J 1938;1(4033):898.
26. Robert Bárány - Nobel Lecture. Available at: https://www.nobelprize.org/nobel_
prizes/medicine/laureates/1914/barany-lecture.html. Accessed June 6, 2018.
27. Poppler LH, Groves AP, Sacks G, et al. Subclinical peroneal neuropathy: a com-
mon, unrecognized, and preventable finding associated with a recent history of
falling in hospitalized patients. Ann Fam Med 2016;4(6):526–33.
28. Macgilchrist C, Paul L, Ellis BM, et al. Lower-limb risk factors for falls in people
with diabetes mellitus. Diabet Med 2010;27(2):162–8.
29. Cheng HM, Park JH, Hernstadt D. Subacute combined degeneration of the spinal
cord following recreational nitrous oxide use. BMJ Case Rep 2013. https://doi.
org/10.1136/bcr-2012-008509.
30. Strupp M, Kim JS, Murofushi T, et al. Bilateral vestibulopathy: diagnostic criteria
consensus document of the classification Committee of the Bárány Society.
J Vestib Res 2017;27(4):177–89.
31. Verma R, Praharaj HN, Khanna VK, et al. Study of micronutrients (copper, zinc
and vitamin B12) in posterolateral myelopathies. J Neurol Sci 2013;329(1–2):
11–6.
32. Dai M, Cohen B, Smouha E, et al. Readaptation of the vestibulo-ocular reflex re-
lieves the mal de debarquement syndrome. Front Neurol 2014;5:124.
 Examination of the Patient with Dizziness 201

33. Findlay GF, Balain B, Trivedi JM, et al. Does walking change the Romberg sign?
Eur Spine J 2009;18(10):1528–31.
34. Fritz NE, Cheek FM, Nichols-Larsen DS. Motor-cognitive dual-task training in per-
sons with neurologic disorders: a systematic review. J Neurol Phys Ther 2015;
39(3):142–53.
35. Montero-Odasso MM, Sarquis-Adamson Y, Speechley M, et al. Association of
dual-task gait with incident dementia in mild cognitive impairment: results from
the gait and brain study. JAMA Neurol 2017;74(7):857–65.
36. Hyndman D, Ashburn A. Stops walking when talking as a predictor of falls in peo-
ple with stroke living in the community. J Neurol Neurosurg Psychiatry 2004;75(7):
994–7.
37. Sakurai R, Bartha R, Montero-Odasso M. Entorhinal cortex volume is associated
with dual-task gait cost among older adults with MCI: results from the gait and
brain study. J Gerontol A Biol Sci Med Sci 2018. https://doi.org/10.1093/
gerona/gly084.
38. Yamada M, Aoyama T, Arai H, et al. Dual-task walk is a reliable predictor of falls in
robust elderly adults. J Am Geriatr Soc 2011;59(1):163–4.