Approach to the evaluation of the dizzy patient

ROBERT W. BALOH, MD, Los Angeles, California

Dizziness is a nonspecific symptom caused by many different pathophysiologic mechanisms.

Vertigo, an illusion of movement, indicates a lesion within the vestibular system. The duration
of attacks and associated symptoms helps to determine the site of lesion and likely diagnosis.
Examination of the dizzy patient should include a careful assessment of gait and balance and
a search for spontaneous and positional nystagmus. The vestibulo-ocular reflex can be
evaluated qualitatively at the bedside with the doll's eye, dynamic visual acuity, and ice water
caloric tests. Each test provides different information about vestibular function. [OTOkAR¥NGOL
HEAD NECK SURG 1995; 112:3-7.]

HISTORY lesions often liken the sensation to that of being

Dizziness is a difficult symptom to assess because
it is a subjective sensation that cannot be measured.
It often represents several different overlapping
sensations, and it can be caused by many different
pathophysiologic mechanisms and a variety of diag-
noses. Because the evaluation and treatment differ
markedly depending on the category of dizziness, it
is critical that the examining physician take a careful
history to determine the type of dizziness before
proceeding with diagnostic studies (Table 1). l
Distinguishing Between Vertigo and Other Types
of Dizziness
Although the description alone does not distin-
guish between vertigo and nonvestibular causes of
dizziness, certain words are commonly used to
describe each type of dizziness. A sensation of
spinning nearly always indicates a vestibular dis-
order. Patients with nonvestibular dizziness occa-
sionally report a sensation of spinning inside the
head, but the environment remains still, and they
do not have nystagmus. Patients with vestibular
From the Department of Neurology,Universityof California,Los
Angeles School of Medicine.
Dr. Baloh is supported by grants from the National Institute on
Aging (AG09683) and the National Institute on Deafness and
Other CommunicationDisorders (DC01404).
Presented at Clinical Applications of Vestibular Science, Uni-
versity of California, Los Angeles School of Medicine, Los
Angeles, Calif., Feb. 12-13, 1994.
Received for publication July 14, 1994; accepted July 15, 1994.
Reprint requests: Robert W. Baloh, MD, UCLA Department of
Neurology, Reed Neurological Research Center, 710 West-
wood Plaza, Los Angeles, CA 90024-1769.
Copyright © 1995by the American Academyof Otolaryngology-
Head and Neck Surgery Foundation, Inc.
0194-5998/95/$3.00 + 0 23/1/59198
drunk or having motion sickness. They describe
feelings of imbalance as though they are falling or
tilting to one side. Patients with nonvestibular
dizziness use terms such as "light-headed," "float-
ing," "giddy," or "swimming." The sensation that
one has left one's body is characteristic of psy-
chophysiologic dizziness.
Vertigo is an episodic phenomenon, whereas non-
vestibular dizziness is often continuous. An excep-
tion would be presyncopal light-headedness caused
by postural hypotension or cardiac arrhythmia. Pa-
tients with psychophysiologic dizziness often report
being dizzy from morning to night without change
for months to years at a time. Vertigo is typically
aggravated by head movements, whereas nonvesti-
bular dizziness is often aggravated by movements of
visual targets. Episodes of dizziness induced by po-
sition change suggest a vestibular lesion if postural
hypotension has been ruled out. Although stress can
aggravate both vestibular and nonvestibular dizzi-
ness, dizziness that is reliably precipitated by stress
suggests a nonvestibular cause. Finally, episodes of
dizziness occurring in specific situations (e.g., driv-
ing on a freeway, entering a crowded room, or
shopping in a busy supermarket) suggest a nonves-
fibular cause.
The presence of associated symptoms can also
help distinguish between vestibular and nonvesti-
bular causes of dizziness. Nausea and vomiting are
usual with vertigo but uncommon with other types
of dizziness. Associated auditory or neurologic
symptoms suggest a vestibular disorder, and pre-
syncopal symptoms and syncope suggest a non-
vestibular disorder. Multiple symptoms of acute
and chronic anxiety typically accompany psycho-
physiologic dizziness.
 Otolaryngology -
Head and Neck Surgery
4 BALOH January 1995

Table I. Mechanism and c o m m o n causes of different types of dizziness

Type Mechanism Common couses

Vertigo
Presyncopal light-headedness
Psychophysiologic dizziness
Disequilibrium
Ocular dizziness
Multisensory dizziness
Physiologic dizziness
Imbalance of tonic vestibular signals
Diffuse cerebral ischemia
Impaired central intergration of sensory
signals
Loss of vestibulospinal, proprioceptive, or
cerebellar function
Visual-vestibular mismatch due to impaired
vision
Partial loss of multiple sensory systems
Sensory conflict due to unusual combination
of sensory signals
Benign positional vertigo, Meniere's syn-
drome, neurolabyrinthitis, vertebrobasilar
insufficiency
Orthostatic hypotension, vasovagal episode,
cardiac arrhythmia, hyperventilation
Anxiety, panic attacks, phobias
Ototoxicity, peripheral neuropathy, stroke,
cerebellar atrophy
Correction of astigmatism, change in mag-
nification, oculomotor paresis
Diabetes mellitus, aging
Motion sickness, height vertigo, mal de
debarquement

Distinguishing Between Common Causes
of Vertigo
Vertigo can be caused by lesions of the peripheral
or central vestibular apparatus. In general, periph-
eral vertigo is more severe than central vertigo, is
more likely to be associated with hearing loss and
tinnitus, and often leads to nausea and vomiting.
Vertigo of central origin is typically associated with
neurologic symptoms such as diplopia, dysarthria,
incoordination, numbness, and weakness. Lesions
within the internal auditory canal produce a com-
bination of vertigo, hearing loss, and facial weakness
because of involvement of the seventh and eighth
nerves.
The duration of the episode of vertigo is one of the
most helpful differential features (Table 2). 2 Epi-
sodes of vertigo lasting seconds suggest the diagnosis
of benign positional vertigo. During the acute phase,
such patients may report a nonspecific feeling of
disorientation and imbalance along with nausea and
vomiting that last for hours to days, but with careful
questioning recurrent brief attacks of positional ver-
tigo interspersed with the more persistent nonspe-
cific dizziness can be identified. An episode of ver-
tigo coming on abruptly and lasting minutes is char-
acteristic of vertebrobasilar insufficiency and
migraine attacks (with or without headache). With
the typical bout of Meniere's syndrome, the vertigo
reaches a peak within minutes, remains severe for an
hour or two, and then gradually resolves during the
next few hours. Vertigo gradually developing over
several hours and then gradually resolving over sev-
eral days is characteristic of viral neurolabyrinthitis.
Vertigo caused by labyrinthine trauma and infarc-
tion of the labyrinth or lateral medulla comes on
suddenly but resolves very slowly over days to weeks.
Even with a complete unilateral loss of peripheral
vestibular function, vertigo will gradually resolve as
central compensation occurs. However, with some
central causes of vertigo, this compensation is slow
and incomplete when the pathways necessary for
compensation have been damaged.
EXAMINATION
Tests of Balance
Patients with damage to the vestibular system,
particularly when acute, have instability of the trunk
and lower limbs so that they sway back and forth or
even fall to the side. In 1846 Romberg noted that
patients with proprioceptive loss from tabes dorsalis
were unable to stand with their feet together and
eyes closed. In 1910, Bfir~iny emphasized the impor-
tance of vestibular influences on maintaining the
Romberg position. He noted that patients with acute
unilateral labyrinthine lesions swayed and fell to-
ward the diseased side, that is, in the direction of the
slow component of nystagmus. However, the Rom-
berg test is insensitive for chronic unilateral vestib-
ular lesions. 2 The sharpened Romberg test (the
patient stands with feet aligned in the tandem heel-
to-toe position) is a more sensitive indicator of
vestibular impairment, but many older normal sub-
jects cannot hold the position for more than 10
seconds.
Tandem gait tests are widely used as part of the
routine neurologic examination, and most clinicians
recognize normal and abnormal performances.
When performed with eyes open, tandem walking is
primarily a test of cerebellar function because vision
compensates for chronic vestibular and propriocep-
tive deficits. Acute vestibular lesions, however, may
impair tandem walking even with eyes open. Tan-
Otolaryngology -
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Volume 112 Number t
dem walking with eyes closed provides a better test
of vestibular function as long as cerebellar and
proprioceptive functions are intact. Patients with
acute or chronic vestibular disease often fail the test,
but the direction of falling is not a reliable indicator
of the side of the lesion. The test's sensitivity can be
increased by having the patient walk on a rail a few
inches above the floor, but again the results are
nonspecific, and some normal subjects may not be
able to perform the test.
Spontaneous Nystagmus
An acute imbalance within the vestibular system
typically results in spontaneous nystagmus with a
slow phase toward the abnormal side and fast phase
toward the normal side. 2 Spontaneous nystagmus
may be present with fixation, or it may occur only
when fixation is inhibited. There are several simple
methods for inhibiting fixation at the bedside. Fren-
zel glasses consist of + 30 lenses mounted in a frame
that contains a light source on the inside so that the
patient's eyes are easily visualized and fixation is
blurred. An ophthalmoscope can also be used to
block fixation and bring out spontaneous nystagmus.
While the fundus of one eye is being visualized, the
patient is asked to lightly cover the other eye with
one hand. Occasionally nystagmus can be seen even
through closed lids. This can be misleading, how-
ever, because lid twitch movements often mimic
nystagmus.
Features that help distinguish between peripheral
and central causes of spontaneous nystagmus are
listed in Table 3. 2 Lesions of the peripheral vestib-
ular system (labyrinth or eighth nerve) typically
interrupt tonic afferent signals originating from all
the receptors of one labyrinth so that the resulting
nystagmus has combined torsional, horizontal, and
vertical components. The horizontal component
dominates because the tonic activity from the intact
vertical canals and otoliths partially cancels out.
Peripheral spontaneous nystagmus is strongly inhib-
ited by fixation. Unless the patient is seen within a
few days of the acute episode, spontaneous nystag-
mus will not be present unless fixation is inhibited by
one of the techniques described above. Gaze in the
direction of the fast component increases the fre-
quency and amplitude, whereas gaze in the opposite
direction has the reverse effect (Alexander's law).
By contrast, central spontaneous nystagmus is typi-
cally prominent with and without fixation. It may be
purely vertical, horizontal, or torsional or have some
combination of torsional and linear components. As
with peripheral spontaneous nystagmus, gaze in the
BALOH
Table 2. Duration of c o m m o n causes of vertigo
Duration Cause
Seconds Benign positional vertigo
Minutes Vertebrobasilar insufficiency, migraine
Hours Meniere's syndrome
Days Viral neurolabyrinthitis, infarction of labyrinth,
brain stem or cerebellum, labyrinthine trauma
Data from Baloh and Honrubia?
direction of the fast component usually increases
nystagmus frequency and amplitude, but unlike pe-
ripheral spontaneous nystagmus, gaze away from the
direction of the fast component will often change the
direction of the nystagmus. There is usually a null
region several degrees off center in the direction
opposite to that of the fast component where the
nystagmus is minimal or absent. Gaze beyond this
null region results in a reversal of nystagmus di-
rection.
Positional Testing
Two different types of positional testing are rou-
tinely used: a rapid change from the erect-sitting to
a supine head-hanging position (the so-called Dix-
Hallpike maneuver) and a quick turn of the head to
the side while the patient is supine (Fig. 1). Parox-
ysmal positional nystagmus occurs transiently after
the position is reached, whereas static positional
nystagmus persists as long as the position is held.
The most common type of paroxysmal positional
nystagmus (so-called benign positional nystagmus)
is induced by the Dix-Hallpike maneuver. It usually
has a 3- to 10-second latency before onset and rarely
lasts longer than 30 seconds. The nystagmus has
combined torsional and vertical components, con-
sistent with its originating from the posterior semi-
circular canal. 3 Although infrequent bilateral cases
have been reported, the nystagmus is usually promi-
nent only in one head-hanging position (the side of
the abnormal posterior canal), and a burst of nys-
tagmus occurs in the reverse direction when the
patient moves back to the sitting position. Another
key feature is that the patient has severe vertigo with
the initial positioning, but with repeated position-
ing vertigo and nystagmus rapidly disappear (fatig-
ability).
A less common peripheral variety of paroxysmal
positional nystagmus is induced by turning the head
to the side while the patient lies supine. 4 After a
brief latency, horizontal nystagmus beats toward the
ground on both sides, although it is always stronger
 Otolaryngology -
Head and Neck Surgery
BALOH January 1995

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Fig. 1. Technique for performing oositional testing. A, Patient is rapidly taken from sifting to
head-hanging position. B, Patient lies supine, and head is quickly turned to each side.

Table 3. Differentiation between spontaneous nystagmus of peripheral and central origin

Origin Appearance Fixation Gaze Mechanism Localization

Peripheral Combined torsional, Inhibited Unidirectional (Alexan- Asymmetric loss of periph- Labyrinthine or
horizontal der's law) eral vestibular tone vestibular nerve
Central Often pure vertical, Usually little May change direction imbalance in central oeulo- CNS, usually brain
horizontal, effect motor tone; usually cen- stem or cerebellum
or torsional tral vestibular, may be
pursuit or OKN

From Baloh RW, Honrubia V. Clinical neurophysiologyof the vestibular system. 2nd ed. Philadelphia: FA Davis, 1992;1990:1-301.
OKN,Optokinetic nystagmus; CNS,central nervous system.

on one side (the side with an abnormal horizontal
canal). It lasts about a minute and does not fatigue
with repeated positioning. Both peripheral varieties
of paroxysmal positional nystagmus are thought to
result from deposits of calcium carbonate crystals
that enter the semicircular canal?
Paroxysmal positional nystagmus can also result
from brain stem and cerebellar lesions. 2The central
type does not decrease in amplitude or duration with
repeated positioning, does not have a clear latency,
and usually lasts longer than a minute. The direction
is unpredictable and may be different in each posi-
tion. It is often purely vertical with fast phase di-
rected downward (i.e., toward the cheeks).
Static positional nystagmus remains as long as the
position is held, although it may fluctuate in fre-
quency and amplitude. It may be in the same direc-
tion in all positions or change directions in different
positions. Despite earlier reports to the contrary, it
is now generally accepted that direction-changing
Otolaryngology -
Head a n d N e c k Surgery
Volume 112 Number I
nystagmus and direction-fixed static positional nys-
tagmus are most commonly associated with periph-
eral vestibular disorders, although both also occur
with central lesions. 6 Their presence indicates a
dysfunction in the vestibular system without local-
izing value. As with spontaneous nystagmus, how-
ever, lack of suppression with fixation and signs of
associated brain stem dysfunction suggest a central
lesion.
Bedside Assessment of Vestibulo-ocular Reflex
The doll's eye test induces reflex eye movements
by moving the patient's head back and forth in the
horizontal or vertical plane. In an alert patient,
these eye movements result from combined visual
and vestibular stimulation. Therefore patients with
complete loss of vestibular function will have com-
pensatory eye movements on the test if their visuo-
motor systems are intact. However, if the head is
moved at high frequencies ( > 1 Hz) above the range
of the smooth pursuit system, a patient with bilateral
vestibular loss will make jerking corrective move-
ments with saccades rather than the smooth correc-
tive movements characteristic of the vestibulo-ocu-
lar reflex (VOR). Asymmetries in smooth compen-
satory movements can be seen in patients with
unilateral peripheral lesions. ~ The doll's eye test is a
good bedside test of the V O R in comatose patients
because their visuomotor systems are not function-
ing. Conjugate compensatory eye movements indi-
cate normal vestibulo-ocular pathways. Disconju-
gate eye movements may indicate a lesion of the
medial longitudinal fasciculus, the oculomotor neu-
rons, or the ocular muscles. Absence of reflex eye
movements in a comatose patient is usually an omi-
nous sign indicating massive brain stem damage if
acute drug intoxication or metabolic disorders can
be ruled out.
The dynamic visual acuity test is performed by
BALOH 7
having the patient shake the head rapidly back and
forth in the horizontal plane at approximately 2 Hz
while reading a Snellen visual acuity chart at the
standard distance. Because the smooth pursuit sys-
tem functions best below 1 Hz and almost not at all
at 2 Hz, this is primarily a test of the horizontal
VOR. A drop in acuity of more than one line on the
Snellen chart suggests an abnormal VOR, usually
because of bilateral symmetrical damage.
Bedside ice water caloric tests are not routinely
used because they are uncomfortable to the patient
and prone to artifacts. Because of its ready avail-
ability, ice water (approximately 0° C) is usually
used. In a comatose patient, only a slow tonic de-
viation toward the side of stimulation is observed. In
alert subjects, duration and speed of induced nys-
tagmus vary greatly, but greater than 20% asymme-
try in nystagmus duration suggests the possibility of
a lesion on the side of the decreased response. This
should always be confirmed with standard bithermat
caloric testing and electronystagmography.
REFERENCES
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1992:15-28.
2. Baloh RW, Honrubia V. Clinical neurophysiologyof the ves-
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3. Baloh RW, Honrubia V, JacobsonK. Benignpositionalvertigo:
clinical and oculographic features in 240 cases. Neurology
1987;37:371-8.
4. Baloh RW, Jacobson K, Honrubia V. Horizontal semicircular
canal variant of benign positionalvertigo.Neurology,1993;43:
2542-9.
5. Brandt T, Steddin S. Current viewof the mechanismof benign
paroxysmalpositioningvertigo:cupulolithiasisor canalithiasis.
J Vestib Res 1993;3:373-82.
6. Lin J, Elidan J, Baloh RW, Honrubia V. Direction-changing
positional nystagmus: incidenceand meaning. Am J Otolaryn-
gol 1986;7:306-10.
7. HalmagyiM, CurthoysIS. A clinicalsign of canal paresis. Arch
Neurol 1988;45:737-9.