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The opposite suggests more involvement of the auditory portion of the eighth nerve. This information can
help with evaluating the chance of hearing preservation and the prognosis for the severity of post-surgery
vertigo symptoms.
Other examples of otological diseases that cause
unilateral caloric weakness include labyrinthitis and
labyrinthine concussion.
Pathologies that affect blood supply to peripheral vestibular structures can also produce a unilateral
weakness in the caloric test. The labyrinth receives
blood supply through one vessel only and therefore
is susceptible to ischemic events. Brief interruptions
of the blood supply to the labyrinth can cause reversible damage to the hair cells and result in fluctuating
vestibular symptoms. These symptoms can be attributed to etiologies such as migraine, if one accepts the
vascular component of such diseases. If the ischemia
persists beyond a few minutes, damage to the hair
cells in the affected vestibular structures will become
permanent (Baloh & Honrubia, 2001). For example, an
infarct of the internal auditory artery will damage both
the cochlea and the hair cells in the entire labyrinth and
produces test findings that are similar to those of labyrinthitis. Likewise, anterior vestibular artery infarctions damage the hair cells in the lateral and anterior
canals and produce caloric test findings that are similar to those produced by the superior nerve vestibular
neuritis. When the blood supply disruptions are caused
by infarcts and strokes of different kinds, usually the
imaging studies can identify the underlying pathology. However, in case of transient ischemic attacks, the
imaging studies are often not helpful. In those cases,
the only distinguishing factors between vascular and
nonvascular origins of vertigo and unilateral caloric
weakness are the patient history and the presence or
absence of risk factors for cerebrovascular disease.
Occasionally, central nervous system (CNS)
lesions can cause unilateral weakness in the caloric test
if they involve the root entry zone of the eighth nerve.
For example, approximately 50% of patients with multiple sclerosis experience vestibular symptoms some
time during the course of the disease (Marrie, Cutter,
& Tyry, 2013). This is likely due to the demyelination
process, which may cause blockage of neural transmission from the vestibular nerve to the central vestibular
structures. When the blockage is unilateral, the caloric
test will reveal unilateral weakness. One may be able
to differentiate between peripheral vestibular and CNS
lesions that cause unilateral caloric weakness because
the latter usually produce other central findings in the
ENG/VNG test.
Theoretically, a unilateral caloric weakness can
occur as a result of hyperactive responses from the
contralateral ear. However, this is extremely rare and
virtually indistinguishable from unilateral lesions that
damage the ipsilateral ear on the basis of caloric test
results. Huygen et al. (1989) reported 10 such cases in a
group of 600 patients. In 9 of those patients, there was
a hearing loss on the side of weaker caloric responses.
They attributed this finding to the loss of commissural
inhibition following temporary vestibular decompensation. When observed, the examiner must rule out
technical issues such as undetected TM perforation,
faulty irrigations, or faulty calibrations.
In summary, unilateral caloric weakness is a
highly significant finding that can localize the lesion to
the labyrinth or the vestibular nerve and further lateralize it to one ear. In the acute stage of the lesion, this
finding is usually accompanied by spontaneous nystagmus that causes a baseline shift in the caloric test.
Interpretation and Clinical Significance
Directional Preponderance
of
An abnormal directional preponderance exists when
nystagmus responses in one direction are significantly
stronger than nystagmus responses in the opposite
direction. It indicates the presence of an asymmetry in
the horizontal VOR pathways but provides no localizing information. That is, abnormal directional preponderance can originate from the labyrinths, vestibular
nerves, vestibular nuclei, or the CNS.
Early studies attributed directional preponderance to CNS lesions (Fitzgerald & Hallpike, 1942).
However, in these studies, what was called directional
preponderance was in fact asymmetric fixation suppression because caloric responses were observed with
eyes open and in the presence of vision. In later studies, directional preponderance was found in patients
with labyrinthine or vestibular nerve lesions as well
as in patients with CNS lesions (Baloh, Sills, & Honrubia, 1977; Coats, 1966). Furthermore, directional preponderance has also been reported in normal subjects
(Coats, 1965).
As noted, directional preponderance consists
of two different components: baseline shift and gain
asymmetry. Historically, these two components have
been interpreted together but their clinical implications
are quite different. A baseline shift, which accounts for
99% of abnormal directional preponderance findings
in the caloric test (Halmagyi et al., 2000), indicates the
presence of spontaneous nystagmus. Spontaneous nystagmus can be interpreted as a non-localizing finding.
It can be caused by an asymmetry in the peripheral or
central vestibular pathways but is often seen in patients
with an acute vestibular lesion. Therefore, a finding of
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abnormal unilateral caloric weakness and baseline shift
in the direction of the weaker ear is consistent with an
uncompensated peripheral vestibular lesion on the
side of the weaker ear (see Figure 12–5A).
A gain asymmetry exists when caloric responses
are truly stronger in one direction without any preexisting nystagmus (see Figure 12–5B). Baloh and Honrubia (2001) have suggested that such an abnormality
is likely to be caused by a central lesion. However,
Halmagyi et al. (2000) found evidence of CNS lesions
in only 5% of patients with abnormal gain asymmetry.
Instead, about half of the patients had either benign
paroxysmal positioning vertigo or Meniere’s disease.
For the rest of these patients, no definitive diagnosis
could be established. Halmagyi and his associates
stated that gain asymmetry is a benign and transient
abnormality.
Gain asymmetry is an extremely rare finding.
Therefore, one must be cautious to rule out technical
errors. When confirmed, gain asymmetry still does not
provide definitive localizing information (Halmagyi
et al., 2000).
Overall, the clinical value of directional preponderance is marginal. It can originate from the labyrinths, vestibular nerves, central vestibular structures,
or the CNS. Because of its limited usefulness, the examiner is free not to include directional preponderance in
the interpretation of the caloric test.
Interpretation and Clinical
Significance of Bilateral Weakness
An abnormal bilateral weakness exists when total
caloric responses from both ears are absent or markedly
weak. This finding is far less common than an abnormal
unilateral caloric weakness and does not always indicate bilateral loss of vestibular function. Because of the
possibility of inadequate heat transfer to the labyrinth,
inadequate patient alertness, or suppression of caloric
responses by medications, an additional test is needed
to confirm the presence of bilateral vestibular hypoactivity (Furman & Kamerer, 1989; Stockwell, 1993).
The most effective procedure for confirming
bilateral vestibular hypoactivity is by using the rotation chair test (Jacobson & Newman, 1991). There are
three possible outcomes in rotation testing for patients
who have bilateral weakness in caloric testing (Baloh,
Sills, & Honrubia, 1979). The finding of below-normal
gains for all rotation frequencies confirms total bilateral
loss of horizontal vestibular function. The finding of
abnormal gains in low frequencies only (0.01–0.05 Hz)
suggests a partial loss of horizontal VOR. The gain in
very low frequencies (0.01 and 0.02 Hz) is better cor-
related with the presence of bilateral caloric weakness
compared with the gain at higher frequencies (Myers,
1992). Finally, the finding of normal gain in all frequencies indicates normal horizontal VOR and, most likely,
faulty caloric irrigations or lack of patient alertness.
Another alternative to rotation testing for confirming bilateral vestibular hypoactivity is the head impulse
test (Albernaz & Cusin, 2016; Levo, Aalto, & Hirvonen,
2017). Patients with bilateral vestibular hypoactivity
are expected to have corrective refixation saccades to
both right and left head impulses and lower overall
VOR gain (Judge, Janky, & Barin, 2017).
The most common symptom in patients with bilateral vestibular hypoactivity, also called Dandy’s syndrome, is unsteadiness. Some patients also complain
of oscillopsia and even episodic vertigo. Hearing loss
is present in some but not all patients (Vibert, Liard, &
Hausler, 1995). Compensation after a bilateral vestibular lesion is limited and the patients are more likely to
have impaired balance indefinitely (Telian, Shepard,
Smith-Wheelock, & Hoberg, 1991; Vibert et al., 1995).
Bilateral loss of vestibular function has been associated with several etiologies originating from both
peripheral and central vestibular pathways (Simmons,
1973). However, in many cases the cause is unknown
(Baloh, Jacobson, & Honrubia, 1989; Sargent, Goebel,
Hanson, & Beck, 1997). The most common pathology of
a peripheral origin is vestibulotoxicity (Brandt, 1996).
Infections that affect the labyrinths or vestibular nerves,
such as bilateral vestibular neuritis, meningitis, and
chronic otitis media, can also cause bilateral vestibular
hypoactivity (Telian et al., 1991). Other causes include
bilateral Meniere’s disease and congenital malformations (Honrubia et al., 1985). Bilateral loss of vestibular
responses can also be due to central pathologies such as
cerebellar degeneration and tumors (Rinne, Bronstein,
Rudge, Gresty, & Luxon, 1995). Head trauma, vascular diseases, and autoimmune diseases have also been
reported as possible causes for bilateral loss of vestibular function (Syms & House, 1997).
Overall, the finding of bilateral caloric weakness is
of moderate clinical value. It is important to first determine if the finding is in fact due to bilateral loss of vestibular function. If so, it indicates bilateral lesion of the
lateral semicircular canals, their afferent pathways, or
the CNS.
Interpretation and Clinical Significance
of Hyperactive Responses
Caloric hyperactivity exists when total responses from
one or both ears exceed the normal limit. It is a rare
finding and the examiner must make sure that it is
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not due to technical errors or artifacts. For example,
heat transfer from the external auditory canal to the
labyrinth can be enhanced in patients with a TM perforation or with an open or altered mastoid (Barber &
Stockwell, 1980).
Once technical errors are ruled out, hyperactive
caloric responses indicate a central lesion most likely
caused by the loss of VOR inhibitory function at the
vestibular nuclei. Baloh, Konrad, and Honrubia (1975)
have demonstrated high incidence of hyperresponsive
calorics in patients with cerebellar atrophy. Animal
studies are consistent with the notion that lesions of
the cerebellar nodulus produce hyperactive caloric
responses (Fredrickson & Fernandez, 1964). However,
the results should be interpreted cautiously because the
responses were recorded without eliminating vision.
Caloric hyperactivity is usually bilateral but there
are reports of patients with hyperactive responses from
one ear only (Ikeda & Watanabe, 1997). Such a finding could be due to technical errors noted above. It is
also possible that the patient may have two different
lesions: a central lesion involving the vestibular nuclei
that produces hyperactive responses and a peripheral
vestibular lesion involving the weaker ear. Finally, it is
possible, but unlikely, that unilateral caloric hyperactivity can be caused by a peripheral vestibular lesion
on the hyperactive side (Huygen et al., 1989; Kimm &
Donaldson, 1980).
Overall, clinical value of caloric hyperactivity is
moderate because the results can be contaminated by
technical errors. The finding indicates a central lesion
most likely involving the cerebellum.
Interpretation and Clinical Significance
of
Failure of Fixation Suppression
Failure of fixation suppression exists when the intensity of caloric nystagmus is not sufficiently reduced
by fixation (Figure 12–7). It indicates a central lesion
involving the parietal-occipital cortex, the pons, or the
cerebellum. However, failure of fixation suppression is
most common with lesions of the midline cerebellum
(Baloh & Honrubia, 2001).
The fixation suppression test examines the interaction of visual and vestibular pathways. There is strong
evidence that the smooth pursuit system is involved
in suppressing vestibular nystagmus (Chambers &
Gresty, 1982; Halmagyi & Gresty, 1979). The pursuit
system makes it possible to track a small moving target by keeping its image on the fovea (the most sensitive part of the retina). When a target moves across the
Figure 12–7. Caloric responses of a patient with a unilateral failure of fixation suppression
(for left beating nystagmus). This patient also has unilateral defective smooth pursuit for
rightward target movements.
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retina, it causes retinal slip, which triggers the pursuit
system to move the eyes in a way that minimizes the
retinal slip and keeps the target image on the fovea.
When a patient is asked to fixate on a stationary target
during the caloric test, the slow phase of nystagmus
causes the target image to move across the retina and
generate retinal slip. The pursuit system will move
the eyes in the opposite direction of nystagmus slow
phases and suppress the nystagmus.
If the role of the smooth pursuit system in suppressing caloric nystagmus is accepted, one would
expect the findings in the fixation suppression test to
mimic those of the tracking test, essentially making
the fixation test redundant (Barnes, Benson, & Prior,
1978). For example, the patient in Figure 12–7 has failure of fixation suppression for caloric irrigations that
generate left-beating nystagmus. The same patient also
has unilateral defective pursuits for rightward target
movements.
The pathways that mediate fixation suppression of
vestibular nystagmus reside in different sites within the
CNS. As a result, many different etiologies of central
origin can cause failure of fixation suppression. Bilateral
cases are usually associated with diffuse lesions such
as cerebellar degeneration, whereas unilateral cases are
usually associated with more focal lesions such as cerebellopontine angle tumors (Jacobson et al., 1993).
Overall, failure of fixation suppression is a moderately significant finding that indicates a central lesion,
often involving the cerebellar flocculus or the surrounding structures. The fixation test is a simple test
to administer and can sometimes detect oculomotor
abnormalities that are not identified in other parts of
ENG/VNG. There are some limitations associated with
the fixation test that affect its usefulness and require
more careful interpretation of the results.
Rare Abnormalities in Caloric Testing
A number of highly unusual and rare findings have
been reported in the caloric test. They include caloric
inversion (all four irrigations produce responses that
beat opposite of the expected direction), caloric perversion (irrigations produce purely vertical nystagmus),
and premature caloric reversal (caloric responses
reverse direction much earlier than anticipated). Most
of these reported cases date back to the time before
sophisticated test equipment became available and
before our understanding of the underlying physiology had evolved. There have been no convincing cases
of such abnormalities in recent years. This raises the
possibility of technical issues with at least some of
these findings. Because these findings are extremely
rare, the examiner must assume a technical error unless
proven otherwise.
SPECIALIZED CALORIC TESTS
Two types of specialized caloric tests are discussed in
this section. These tests are not part of the standard
ENG/VNG test battery. They are reserved for specific
patient populations.
Ice Water Caloric Test
The need for ice water caloric testing has diminished
greatly as labyrinthectomy and vestibular neurectomy
cases have declined. In rare cases, when the standard
caloric stimulus fails to provoke a response from an ear,
ice water caloric testing is still needed (Proctor, 1992).
The purpose of the ice water caloric test is to determine
if there is any residual function remaining in the test ear.
Determining the absence of a caloric response is
not always easy, especially in the presence of spontaneous or positional nystagmus. When the total response
from either ear is very small — for example, less than
6 deg/sec (TotRE or TotLE < 6 deg/sec) — one can con-
sider the ear to be a candidate for ice water testing.
This value is derived empirically based on the inherent variability in identifying peak caloric responses of
each irrigation.
Before irrigating an ear with ice water, the patient’s
ear should be examined to make sure there is no TM
perforation. Ice water testing must not be performed
in an ear with a perforated eardrum. Then the examiner should mix some water with ice cubes and let it
stand for a few minutes. The patient should be placed
in the standard caloric position and the eye movements
calibrated. Visual fixation should be eliminated and the
patient’s head should be turned so that the test ear is
uppermost. The examiner can place an otoscope tip in
the ear and use it as a funnel to inject the water into
the ear canal. A towel should be placed on the patient’s
shoulder to catch the water after the irrigation. The eye
movement recording system should be started and the
patient should be given alerting tasks. At this time,
the examiner should draw 2 cc of ice water into the
syringe and inject it into the ear canal. It is best not
to deliver more than 2 cc because that is the average
volume of the ear canal. Any additional ice water is
likely to run out of the ear. After 20 seconds, the ice
water should be emptied out into the towel and the
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head should be placed in the standard caloric test position. The eye movement recording should continue
for 30 to 60 seconds while alerting the patient. The eye
movement tracings should be examined for any evidence of caloric-induced nystagmus. Absence of such
nystagmus indicates total loss of function in the lateral
semicircular canal or its afferent pathways. Sometimes
a small response is present indicating a severe but not
a complete loss of function.
BSA (2010) has recommended a procedure for the
basic ice water caloric testing that for the most part
matches the procedure described above. However,
sometimes a more comprehensive type of ice water
testing is needed. For example, interpretation of the ice
water caloric test becomes complicated if there is any
spontaneous or positional nystagmus. The intensity of
this nystagmus can change depending on the level of
alertness. Ice water caloric testing in the prone position can distinguish between caloric-induced responses
and changes in the intensity of spontaneous/positional
nystagmus due to different levels of alertness (Proctor,
1987). After administering the ice water in the supine
position and recording the eye movements for 30 to 40
seconds, the examiner should ask the patient to turn
into the prone position with the head hanging downward by 30 degrees (see Figure 12–1B). Alternatively,
the patient can sit up and bend forward to place the
head at an angle of 30 degrees with respect to the horizontal plane. Caloric-induced nystagmus will either
disappear or reverse directions in the prone position.
That will indicate presence of residual vestibular function in the test ear. If nystagmus does not change direction, it indicates total loss of function in the lateral
semicircular canal and its afferent pathways.
Caloric Test in Perforated Ear
Caloric testing of a patient with a perforated ear is possible, but a number of issues must be considered. First,
the use of water irrigations is contraindicated. When
air is used, warm irrigations of a perforated ear often
produce nystagmus that initially beats in the opposite
of the expected direction (Barber, Harmand, & Money,
1978). This is most likely due to the cooling effect that
dry air has on the moist mucous membrane within the
middle ear cavity. Second, the heat transfer from the
external auditory canal to the labyrinth is faster and
more intense in a perforated ear because the TM no
longer acts as a barrier. As a result, the onset of caloric
responses is usually much earlier and the intensity
is much stronger in a perforated ear compared with
those in an intact ear. Finally, caloric responses from
two ears cannot be compared quantitatively because
the main assumption of the caloric test — that both ears
are receiving equal stimulation — is no longer valid in
the case of a perforated ear. Therefore, the purpose of
caloric testing in a patient with a perforated ear is to
simply determine whether or not there is any response
from that ear.
Based on the above discussion, full caloric testing
in a patient with a perforated ear is not recommended.
A modified procedure can provide the necessary information and minimize patient discomfort. The examiner
should first perform a standard cool irrigation in the
ear with the intact TM. Next, the perforated ear should
be irrigated with cool temperature. If caloric nystagmus
appears (usually within the first 10 to 15 seconds), the
examiner should immediately stop the irrigation and
report that caloric responses are present in perforated
ear. If no nystagmus appears, the examiner should
report that there is no response from the perforated ear
to the standard air irrigation.
SUMMARY
Table 12–3 provides a summary of common abnormalities in the caloric test. The caloric test has been used
routinely in patients with dizziness and other balance
disorders. Although it does not identify a specific etiology, so far it has proved to be one of the most useful tests for detecting unilateral peripheral vestibular
lesions. With the introduction of vHIT and VEMPs, the
need for completing a full bithermal caloric test has
somewhat diminished. However, in some cases, the
caloric test is the only test that can determine the side
of lesion with a high level of confidence. The information from the caloric test must be used along with history, physical examination, and other tests to make a
diagnosis and devise management plans.
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Table 12–3. Common Abnormalities in the Caloric Test and Their Localization and Clinical Value
Abnormality Clinical Value Localization
Unilateral caloric
weakness
Directional
preponderance
Baseline shift
Gain asymmetry Unknown None. Indicates a peripheral vestibular lesion in either ear
Bilateral weakness
Hyperactivity Moderate Indicates a central lesion most likely involving the cerebellum.
Failure of fixation
suppression
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13
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Rotational Vestibular Assessment
Christopher K. Zalewski
introduCtion
Rotary chair testing provides an unparalleled clinical
assessment of the vestibular system. Modern rotational
chairs are capable of providing a variety of exacting
rotational stimuli that can effectively identify disorders
impacting both peripheral and central vestibular function. Moreover, vestibular compensation mechanisms
can be effectively evaluated and disease progression or
therapeutic processes can be efficiently monitored with
rotational testing. Its ability to evaluate peripheral and
central vestibular response across a broad frequency
range is vital to providing a more comprehensive vestibular phenotype for patients with suspected bilateral
vestibular weakness or areflexia as well as patients
with non-specific dizziness.
Although modern-day rotational chairs offer
a wide range of testing protocols, the most common
rotational test, sinusoidal harmonic acceleration (SHA)
testing, will be discussed at length in this chapter. The
salient outcome measures and the interpretation of this
test will be presented. Non-specific dizziness and clinically evasive vestibular disorders represent a growing
population within most otolaryngology and audiology
clinics, particularly in light of the exponential growth
of the geriatric population. The addition of rotational
testing in comprehensive vestibular assessment is critical to increasing the diagnostic sensitivity and specificity for vestibular pathology.
rotational testing and
the Vestibular
Similar to the auditory system, the vestibular system’s
sensitivity range is significantly broader than what is
needed for daily life activities. Although the vestibular system is capable of responding between 0.001 and
well over 20 Hz, the vestibular system’s response characteristics are principally efficient and effective for a
narrow range between 0.05 and 6 Hz (Goldberg et al.,
2012; Wilson & Jones, 1979). Figure 13–1 highlights the
vestibular system’s effectiveness for the narrow frequency range where natural head movements occur.
Within the frequency range of natural head movements, the responsiveness of the vestibular system can
be characterized as linear, capable of operating with
nearly perfect vestibular ocular reflex (VOR) gain and
phase (Goldberg et al., 2012; Wilson & Jones, 1979).
This is ideal, insomuch that the operating range of the
VOR is functionally matched to those activities that
are most common during ambulation, and particularly
those active head movements that are associated with
daily life activities.
Figure 13–1 also depicts the nonlinearity and lack
of response unity (i.e., perfect gain) of the VOR for frequencies that occur above and below those associated
with natural head movements. As can be seen, the efficiency of VOR gain and phase are significantly poorer
for these frequencies. Unfortunately, the test stimulus
system
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