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98 Rotational Vestibular Assessment
kinocilium is also located on the canalicular side of
the cupula. This orientation is significant because it
continues to allow the leading ear to displace the stereocilia toward the kinocilium, and depolarization
of the underlying hair cell ensues (Ewald’s third
law). With respect to the posterior canals, the lead-
ing ear would apply to the right ear during a backward pitching of the head over the right shoulder
(i.e., the LARP plane as described in Chapter 2),
and a backward pitching of the head over the left
shoulder for the left ear (RALP plane).
OTOLITH (MACULAR)
VESTIBULAR OCULAR REFLEX
Otolith Maculae VOR
Because the maculae of the otolith receptors sense
linear accelerations in the horizontal and vertical plane, it can be expected that the otolith VOR
would displace the eyes in the equal and opposite translational vector to that of head movement. This is, in fact, the case and is referred to
as the translational-VOR (t-VOR) (Leigh & Zee,
2006). The measurement of the t-VOR, however, is
fraught with complexities, because each macula’s
stereocilia organization produces both an excitatory and inhibitory response (Chapter 2). In light
of this multi-vector epithelial organization, compensation for unilateral peripheral macula damage is often extremely quick and void of persistent
or even short-term clinical effects (Gresty, Bronstein, Brandt, & Dieterich, 1992). Furthermore, the
precise neural pathways from the otolithic maculae to the ocular motor system are much more
difficult than they are for the semicircular canals.
This is primarily due to the kinocilium arrangement of the maculae epithelium and the subsequent fact that the macular nerves communicate
information about all conceivable directions of
linear movements (Schwarz & Tomlinson, 2005).
Because of this, clinical investigation of otolith
receptor function has proven to be difficult, and
remains a challenge to this day.
Effective and efficient clinical investigations into
otolith receptor function remain elusive. A simple
lateral head tilt should excite the macula and, in fact,
does generate an opposite torsional / rotational com-
pensatory eye movement within each orbit, known
as ocular counter-rolling (Baloh & Honrubia, 1998;
Gresty & Bronstein, 1992; Ödkvist, 2001; Tran Ba
Huy & Toupet, 2001). These compensation eye
movements, however, are highly inefficient in
counteracting the effect of head tilts. This is primarily because the amplitude (gain) of induced
eye torsion, even for large head tilts, is only around
10% of the amplitude of the actual head tilt (Barin
& Durrant, 2001). A centripetal force applied to a
single, off-centered macula of the utricle also produces a counter-rolling of the eyes equal to the
gravitational inertial forces with respect to the
velocity of the stimulus (Baloh & Honrubia, 1998).
This induced ocular counter-rolling produces an
increased subjective perceptual tilt with respect
to true vertical (normal perception within 2° to
4° of true gravitational vertical) (Baloh & Honrubia, 1998). Evidence for this is secondary to lateral forces applied to the maculae (utricle) during
off-center axis (centrifugation) rotational testing
(Böhmer & Mast, 1999). The degree of counterroll measured can be applied clinically; however,
the cost of equipment needed to investigate the
t-VOR counter-roll during centrifugation testing is expensive and, often prohibitive, beyond a
research setting. Off-axis centrifugation testing is
discussed in great detail later in Chapter 8.
Types of Compensatory
Maculo-Ocular Reflexes
Stimulation of the maculae causes two primary
reflexes that assist in the stabilization of the
head and eyes during linear acceleration and
static head tilt. First are maculo-spinal reflexes
that assist in the stabilization of the head during
postural changes. Second, are the maculo-ocular
reflexes. Similar to the vestibuloocular reflexes
generated by the SCCs, these otolith-generated
ocular reflexes assist in the stabilization of gaze
during movement (Tran Ba Huy & Toupet, 2001).
Both reflexes are fundamental in the stabilization
of gaze and posture during rapid translational
accelerations and/or static head tilts. First to be
discussed are the maculo-ocular reflexes.
Maculo-Ocular Reflexes
Compensatory maculo-ocular reflexes are generated by the otoliths in association with the ocular
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motor system in order to maintain gaze stability
during abrupt intra-aural linear translations and/
or static head tilts. Similar reflexes have been discussed with respect to maintaining gaze during
angular accelerations by the SCCs. During bilateral vestibulopathies impacting the SCCs, ocular
stabilization is less efficient or non-existent during
angular accelerations, and oscillopsia ensues. One
would assume that similar processes contributing
to SCC-engendered oscillopsia would also occur
in response to rapid translational accelerations if
the otoliths were equally damaged. This is, in fact,
true. Experimental evidence shows that, in the
presence of complete bilateral vestibulopathies, a
loss of visual acuity occurs when trying to fixate
on targets during abrupt linear accelerations (Lempert, Gianna, & Gresty, 1997). This evidence sup-
ports the presence of a linear or translational VOR,
and its relative importance in maintaining VOR
gaze fixation. Two primary maculo-ocular reflexes
occur: the linear or translational VOR (t-VOR) and
the ocular counterrolling VOR (c-VOR).
Maculo-Ocular Reflex Pathways. The anatomical
bases for the two distinct maculo-ocular reflexes
(t-VOR and c-VOR) have been well studied. Each
utricular macula can be subdivided into two hemimaculae, separated by the striola: the medial and
lateral halves (Figure 4–5) (Leigh & Zee, 2006).
As noted earlier, the kinocilium and associated
stereocilia hair cell bundle orientation between
the two hemimaculae are arranged such that the
polarities are in opposition to one another. Moreover, there is evidence to suggest that this oppos-
FIGURE 4–5. Utricular Vestibular Ocular Reflex pathways for tilt and translation. The medial hemi-
maculae (MED) contributes to counterrolling of the eyes by innervating the vertical torsional muscles.
The lateral hemimaculae (LAT) contributes to a contraversive horizontal slow phase by innervating
the horizontal muscles. LR (Lateral Rectus Muscle); MR (Medial Rectus Muscle); IR (Inferior Rectus
Muscle); IO (Inferior Oblique Muscle); SO (Superior Oblique Muscle); SR (Superior Rectus Muscle);
III (Ocular Motor Nucleus); IV Trochlear Nucleus); VI (Abducens Nucleus). From The Neurology of Eye
Movements (5th ed., p. 75) by R. J. Leigh and D. S. Zee, 2015, New York, NY: Oxford University Press.
Reprinted with permission.
100 Rotational Vestibular Assessment
ing polar relationship between one hemimacula to
its contralateral complement shares a semi-coplanar relationship, similar to that of the SCCs (Tran
Ba Huy & Toupet, 2001). That is, the medial half
of one utricle is a complement of the lateral half of
the opposing utricle in the opposite ear. As it pertains to the utricle, each hemimacula is responsible
for either the translational (t-VOR), or the counterrolling (c-VOR) compensatory ocular reflex (see
Figure 4–5). The lateral half of the utricle is likely
responsible for generating the t-VOR, thus making
it sensitive to translational accelerations (Leigh &
Zee, 2006). The medial half is likely responsible
for the ocular counterrolling reflex (c-VOR), thus
making it sensitive to static head tilt (Leigh & Zee,
2006). This subdivision of responsibilities within a
single macula provides a redundancy in the perception of translation versus static head tilt, and
may account for varied symptoms of vestibular
dysfunction, depending upon the location of macular insult. This functional subdivision also adds
further evidence to highlight the complex differences in the regional morphology and physiology
of the maculae cited earlier (Leigh & Zee, 2006).
In addition, the semicoplanar relationship ensures
that both a translational VOR as well as a counterrolling VOR would occur in response to a single
vector linear acceleration. These subdivisions of
responsibilities can also provide diagnostic insight
into which macula(e), (or portion of a macula), is
pathologic depending on whether the t-VOR or
the c-VOR is deficient, given a known linear acceleration or static head tilt. This becomes clinically
relevant insomuch that simple tests of sustained
static head tilting or abrupt linear accelerations in
the intra-aural vector can provide insight into the
laterality of (unilateral) utricular damage.
Translational Maculo-Ocular Reflex (t-VOR).
The t-VOR is a complementary horizontal nystagmus to the c-VOR that occurs in response to rapid
translational accelerations of the head. The precise
compensatory t-VOR is inversely proportional
to the distance of the visual target (Bronstein,
Gresty, & Rudge, 2004; Gresty & Lempert, 2001).
That is, as the target distance decreases, the size
of the t-VOR increases. In fact, linear compensation is only needed when the visual target is fairly
close since targets viewed from a distance require
negligible shifts of gaze to maintain visual acuity (Gresty & Lempert, 2001). Although these data
would suggest that the t-VOR is seldom requisite,
in instances where such a compensatory reflex
is essential, the latency of the t-VOR has been
recorded to be as fast as 20 ms in humans (Gresty
& Lempert, 2001).
The anatomical connections for the maculoocular reflexes are less well known than those of
the angular-VOR generated by the SCCs (Leigh
& Zee, 2006), largely due to the complexities of
developing lateral acceleration sleds that could
easily be used during clinical testing. As the maculo-ocular reflex pathways pertain to the utricle,
the t-VOR involves polysynaptic connections that
arise from the lateral portion of the macula, with
central connections that traverse to the contralateral vestibular nuclei possibly via the cerebellum
(Leigh & Zee, 2006). Together with other synaptic connections via the cerebral hemispheres, the
cerebellum, and the visual and somatosensory
systems, the vestibular nuclei coordinate compensatory ocular and motor responses during passive perturbations and self-generated movements
(Gresty & Lempert, 2001; Leigh & Zee, 2006).
Therefore, in response to an abrupt translational
acceleration to the left, the lateral hemimacula of
the left utricle is excited, which provides a lowgain compensatory horizontal eye movement to
the right via the right lateral rectus muscle and the
left medial rectus muscle (see Figure 4–5) (Leigh
& Zee, 2006). In addition, the medial hemimacula
of the right utricle is excited, causing a diminutive ocular rolling in the direction ipsiversive to
the linear acceleration. This ocular ipsi-roll reflex
is less robust (or non-existent) in response to
brief linear accelerations secondary to the longer
latency required to initiate the ocular-roll reflex
(Gresty & Lempert, 2001). However, in response
to a sustained linear acceleration, such as during
eccentric rotational testing, both the t-VOR and
the c-VOR are evident secondary to the sustained
applied force on the weighted otoconia (Gresty &
Lempert, 2001).
Counterrolling Macula-Ocular Reflex (c-VOR).
The c-VOR occurs in response to sustained tilting
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of the head in the lateral direction (roll axis) as
well as the sagittal plane (pitch axis). As the head
tilts laterally, the eyes counterroll in order to maintain the horizontal meridians of the retina toward
the earth horizontal plane (Tran Ba Huy & Toupet,
2001). One primary limitation to this reflex, however, is its fundamental low sensitivity or gain. As
Tran Ba Huy and Toupet (2001) explain, a lateral
tilting of the head by 90° yields an eye rotation of
only 6°. Such a physiologic response is the equivalent to the movement of the minute hand on a clock
by only 1 minute. This low-gain reflex is approximately 10% of actual head tilt (Ödkvist, 2001),
and occurs with a much longer latency than the
t-VOR, typically up to 300 ms (Gresty & Lempert,
2001). Provided the head tilt is static, the c-VOR
is largely dependent upon the otolith maculae,
specifically the utricle (Ödkvist, 2001). However,
under dynamic head bobbing or sustained lateral roll conditions, such as that of a sustained jet
fighter roll, the cyclotorsion of the c-VOR is under
the control of the vertical SCC (Ödkvist, 2001). Thus,
it is possible for the perception of tilt to be imparted from acceleration-induced canalicular activity
with virtually no otolith component (Gresty &
Lempert, 2001). Therefore, it is vital to understand
the various stimulus conditions that contribute
to a macular response in order to differentiate it
from a canalicular response. It is, however, possible to provoke a c-VOR of otolithic origin from
sustained eccentric linear acceleration, (to be discussed later under dynamic unilateral centrifugation testing in Chapter 8). In fact, this form of
eccentric linear acceleration causes a c-VOR that is
almost entirely “pure-otolithic.” This is largely due
to the fact that the eccentric counterroll VOR response is largely driven by the lateral centripetal
linear force directed across the outwardly displaced utricular macula, rather than the more robust
[dynamic] counterrolling VOR that can be produced by the vertical SCCs during dynamic head tilting
or dynamic lateral rolling (Gresty & Lempert, 2001).
The anatomical connections for the c-VOR
have received a greater degree of investigation
than those of the t-VOR due to the advancements
of eye recording techniques and better rotational
testing (Leigh & Zee, 2006). As they pertain to the
utricle, the c-VOR involves synaptic connections
that arise from the medial portion of the utricle.
The medial hemimaculae has been shown to be
more important for signaling head tilt, which produces a compensatory counterrolling using vertical torsional ocular muscles (Leigh & Zee, 2006)
(see Figure 4–5). Therefore, in response to a static
head tilt or sustained eccentric rotation to the
left, the medial hemimacula of the left utricle is
excited which provides a low-gain compensatory
cyclotorsional eye movement to the right via the
right inferior rectus and inferior oblique muscles
and the left superior oblique and superior rectus
muscles (Leigh & Zee, 2006).
Maculo-Spinal Reflexes
Maculo-spinal reflexes are generated by the otoliths in association with spinal reflexes in order
to maintain postural stability during abrupt linear
translations. During unexpected perturbations,
these reflexes are generated in order to provide
rapid muscular responses that counteract opposing linear forces. This maculo-spinal reflex has been
described as a startle reflex. However, as Gresty
and Lempert (2001) explain, “the earliest part of
this startle response is purely vestibular in origin.
It is very likely that this response is triggered by
stimulation of the otolith apparatus, as one could
tentatively suggest by the irregular units” (p. 25).
Specifically, the type I striolar, non-coherent hair
cells would provide the required irregular afferent
response. In addition, Brandt (1999) demonstrated
that these otolith-generated reflexes are critical in
providing ongoing anti-gravity muscle activation.
Brandt (1999) hypothesized that it is a loss of this
tonic activation through the lateral vestibulospinal reflex during a crisis of Tumarkin. During such
crises, patients are noted to inexplicably fall to
the ground without a loss of consciousness, often
describing a complete loss of postural muscle
tone resulting in the inability to maintain upright
stance (Brandt, 1999). Such maculo-spinal reflexes
are also experienced on a daily basis by commuters who stand on a moving train. During abrupt
starts and stops, maculo-spinal reflexes provide
the necessary counterbalanced postural reflexes
required to avoid falling. Clinically, it is this reflex
that is evaluated during VEMP testing (Colebatch,
102 Rotational Vestibular Assessment
2001). Although both the saccule and the utricle
are capable of producing such a reflex, the utricle
is the more relevant anatomy for vestibulospinal
mechanisms because most perturbations experienced in the environment occur in the horizontal
rather than the vertical plane (Leigh & Zee, 2006).
Vestibulocollic Reflex (VCR)
Recently, investigation into a saccular reflex has
brought new light to the examination of saccular
physiology and function. Saccular function has
been shown to be responsible for providing a significant contribution to the vestibulocollic reflex
(VCR) (Colebatch & Halmagyi, 1992; Colebatch,
Halmagyi, & Skuse 1994). Inputs from the saccule,
cervical spinal cord, and cerebellum are important
for mediating the cervical ocular reflex (COR),
which coordinates head, neck, and eye reflexes
for image stabilization. Afferent projections from
the saccule course through the inferior branch of
the vestibular nerve in order to innervate interneurons within the MVN and LVN (Lysakowski et
al., 1998). From there, efferent fibers are sent down
the descending MLF to innervate interneurons
within the cervical and spinal cord via the MVST
and, to a much lesser extent, the LVST. From there,
synaptic connections extend to cervical anterior
horn cells and both flexor and extensor cervical
motor neurons within the neck (spinal accessory
nuclei of CN XI) (Figure 4–6). This vestibulocollic reflex arc helps to stabilize the head on the
shoulders by coordinating neck muscle contractions that resist passive movements of the head
(Lysakowski et al., 1998). Stimulation of the saccule can, therefore, produce measurable responses
from neck muscles known as vestibular evoked
myogenic muscle potentials (VEMP). Clinically,
this vestibulocollic reflex arc can provide valuable
information regarding the neural integrity of the
MVST, as well as saccular and inferior vestibular
nerve function.
FIGURE 4–6. Vestibulospinal pathways from the
maculae. Utricular neural pathways innervate the ocular
motor system, whereas the saccular pathways project
down the ipsilateral medial vestibulospinal tract (MVST)
to innervate the anterior horn cells (AHC) of the spinal
cord and the ipsilateral sternocleidomastoid muscle
(SCM). Medial longitudinal fasciculus (MLF); IO (Inferior Oblique Muscle). From Vestibular-Evoked Myogenic
Potentials (VEMPs) by D. L. McCaslin and G. P. Jacobson, 2016. In G. P. Jacobson and N. T. Shepard (Eds.),
Balance Function Assessment and Management, (pp.
533–579). San Diego, CA: Plural Publishing. Reprinted
with permission.
Vestibulospinal Reflex (VSR)
Vestibulospinal function is predominantly governed through the lateral vestibulospinal tract
(LVST). Projections within the LVST predominantly originate from the utricle macula, as well
as the vermis and fastigial nuclei, via the interneurons of the lateral vestibular nuclei. The neural input delivered through the LVST is constantly
4. The Vestibular Ocular Reflex and Vestibular Nystagmus 103
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held active. This constant tonic contraction provides a dominant, and much needed, excitatory
synaptic input to lower postural extensor motor
neurons and muscles, which serves to hold upright
posture in the presence of a continuous gravitational vector (Lysakowski et al., 1998). This excitatory pathway is known as the vestibulospinal
reflex (VSR). Clinically speaking, loss of such input
from a unilateral vestibular lesion significantly
reduces extensor output. This creates a “weaker”
side ipsilateral to the lesioned side with a tendency
for patients to fall or veer to this weaker side such
as that observed during the Fakuda Stepping Test.
A
VESTIBULAR NYSTAGMUS
Nystagmus Defined
Baloh and Honubia (2001) define nystagmus as
a nonvoluntary rhythmic oscillation [jerking] of
the eyes. Nystagmus has an abnormal slow phase
deviation of the eyes in the orbit that often has
its origins from the vestibular system. The slow
phase is followed by a quick “resetting” phase,
which brings the eyes back to the primary position within the orbit. This fast (resetting) phase
is mediated by the paramedian pontine reticular
nuclei and MVN within the brainstem (Leigh &
Zee, 2006). Although the slow phase component
of the nystagmus is vestibular in origin, nystagmus is always named by the fast phase. That is,
a right-beating vestibular nystagmus has a leftward moving vestibular slow-phase followed by
a rightward fast-phase (Figure 4–7). During vestibular testing, VOR nystagmus is often induced;
however, the presence of nystagmus in the absence of any head movement or clinical induction is often pathologic. Vestibular nystagmus is
seldom purely unidirectional and often exhibits
elements in the horizontal, vertical, and even torsional plane (Leigh & Zee, 2006). Although nystagmus can occur in any plane within the orbit,
according to Ewald’s first law, resulting nystagmus will always occur in the same plane as the
affected canal. Horizontal nystagmus, however,
is generally the most common presentation. This
B
FIGURE 4–7. Right-Beating (A), and Left-Beating (B)
nystagmus. Nystagmus is quantified by determining
the slope of the slow-phase component, and qualified
(named) according to the fast phase component. The
slope of the nystagmus is determined by calculating
the degree of eye movement that usually occurs over
a 1-second interval. Upward on the graph is rightward
eye movement and downward on the graph is leftward
eye movement.
is because any neural imbalance produced by the
damaged vertical SCCs is usually cancelled out
by the coplanar intact SCCs, leaving a dominant
horizontal nystagmus (Leigh & Zee, 2006). Understanding the physiology of vestibular nystagmus
is best discussed in relation to h-SCC VOR physiology. Therefore, only horizontal vestibular nystagmus
will be discussed here, as it is most relevant during physiologic testing of the vestibular system.
Nystagmus from Unilateral
Vestibular Lesions
As stated earlier, vestibular nystagmus can be
clinically provoked, or it can occur in response to
104 Rotational Vestibular Assessment
a pathologic imbalance in the vestibular system.
The neurophysiology underlying pathologic nystagmus parallels that of the neural substrate of the
h-VOR discussed earlier.
Central Tonic Neural Asymmetry
The physiologic symmetry of the vestibular system is ultimately determined by the tonic neural
balance of the central vestibular nuclei (Baloh &
Honrubia, 1996; Barin & Durrant, 2000; Curthoys
& Halmagyi, 1996). Under normal physiology,
an equal afferent signal is delivered to each vestibular nuclei complex, thus creating a tonic neural
balance within the central vestibular system (see
Figure 3–5A). A change in normal physiologic balance of the central vestibular system at rest dictates
that an alteration, (increase or decrease), in the
symmetry of the vestibular periphery sensory end
organs exists. Therefore, in the state of a peripheral afferent asymmetry, a subsequent asymmetry
in interneuron activity is created between the VN
(Barin & Durrant, 2000) (see Figure 3–5C). Secondary to this central tonic asymmetry, an enduring spontaneous nystagmus is manifested, with
concomitant vegetative symptoms of nausea and
vomiting. In addition, associated or frank vertigo
is often present. The vertigo is often debilitating in
this stage with the patients reporting a perceptual
rotation toward the non-lesioned labyrinth (Barin
& Durrant, 2000). Within days or weeks, however,
tonic rebalancing of the VN is possible following
successful central compensation. Following complete central compensation, a tonic asymmetry no
longer exists within the central VN and the spontaneous nystagmus slowly abates.
Pathoneurophysiology of
Spontaneous Nystagmus
The pathophysiology of an acute spontaneous
nystagmus in response to an acute unilateral vestibular insult is secondary to an asymmetrical
neural tone within the central VN. In the absence
of an afferent peripheral input, type I neurons
within the ipsilesional VN quickly lose their
input and neuronal activity. Concomitantly in
the contralesional intact VN, there is a significant
increase in the average central resting rate (Cur-
thoys & Halmagyi, 1996). This dramatic increase
in resting neural activity in the contralesional VN
is due to the lack of ongoing commissural inhibition from the ipsilesional VN. Unfortunately, the
increase of resting activity in the contralesional
VN serves to further increase their neural inhibition on the lesion side via the commissural fibers,
thus silencing it even more, (if possible) (Curthoys
& Halmagyi, 1996). This augmented tonic neural
asymmetry within the VN is similar in physiology
to that of a high velocity head acceleration toward
the contralesional ear. Secondary to this asymmetry, neural stimuli are sent via the second and
third-order neurons to excite the motor neuron
units of the extraocular muscles causing a subsequent slow deviation of the eyes in the ipsilesional
direction, (slow phase vestibular component). The
slow phase deviation is followed by a quick resetting of the eyes in the contralesional direction back
to their primary ocular position (fast phase component). Until central compensation is complete,
a neural asymmetry will persist and an enduring spontaneous nystagmus continues. It is only
when central compensation of the central VN is
achieved, that tonic neural symmetry returns and
the spontaneous nystagmus abates.
Nystagmus from Bilateral
Peripheral Vestibular Lesions
An acute unilateral vestibular neural asymmetry
will always produce a spontaneous nystagmus
secondary to the tonic imbalance of the afferent
system (Baloh & Honrubia, 1996; Barin & Durrant, 2000; Curthoys & Halmagyi, 1996). However, if both vestibular peripheries were affected
equally and simultaneously, a neural asymmetry would fail to exist. In this case, spontaneous
nystagmus would not occur because the afferent
inputs between the vestibular nuclei remain balanced. In fact, in the most extreme case, where the
overall sensitivity (response or gain) of the system
becomes acutely absent in each ear, there is also a
lack of spontaneous nystagmus, as the tonic afferent peripheral drive continues to remain equal,
albeit at 0 spikes/second.
Despite the absence of any spontaneous nys-
tagmus in cases of acute bilateral labyrinthine are-
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flexia, the absence of a vestibular afferent neural
drive is not without complication and functional
impact. In the absence of any vestibular afferent
input, an effective VOR cannot exist. As a consequence, a compensatory eye movement in the
equal and opposite direction cannot be produced,
and a resulting blurring of the visual field occurs
with any head movement. In short, the VOR fails to
integrate any head movement in order to produce
an appropriate compensatory ocular response to
maintain visual stability. Even in response to the
smallest of head movements, fixation of a particular image momentarily slips off the retina. At this
point, fixation must be redirected back onto the
intended target, with a latency no shorter than 200
ms (Leigh & Zee, 2006). This is known as a corrective saccade, and can easily be identified during head impulse testing. The resulting dilemma
from such a loss of bilateral peripheral vestibular
input is an inability to maintain visual fixation of
an intended target on the retina whenever brief
head movements are introduced. The lack of
visual fixation during repeated head movements,
such as that during ambulation, often creates a
continuous inability to maintain visual fixation
of the environment. This creates a “shaking” or
“jumping” of the visual environment, which is
known as oscillopsia, and is a common indicator
of bilateral peripheral vestibular damage, such as
that encountered during vestibulotoxicity (Leigh
& Zee, 2006).
We have discussed the consequences of symmetrical, bilateral vestibular lesions; however,
what are the consequences of asymmetrical, vestibular lesions? In theory, labyrinthine destruction
that occurs asymmetrically should produce a spontaneous nystagmus that beats toward the healthier
ear, or at least the higher tonic neural firing rate.
However, the temporal aspects of an asymmetrical,
bilateral vestibular insult are critically important
in determining the onset of any spontaneous nystagmus (and vertigo). Interestingly, there are conditions where asymmetric labyrinthine lesions
could fail to produce spontaneous nystagmus and
vertigo. One such clinical condition is an asymmetric decline of the peripheral afferent neural
drives that specifically occur at different rates, but
does so in a very chronic, and slow manner. The
lack of spontaneous nystagmus and vertigo during such slow progression of clinical disease is due
to the concomitant and ubiquitous central vestibular compensation process (Carin & Durrant, 2000;
Curthoys & Halmagyi, 1996). The efficient, physiologic compensation process allows for a continu-
ous rebalancing of the central neural activity that
is omnipresent during the slow, pathologic, asymmetric change in afferent peripheral neural drive.
In short, the rate of asymmetrical neural decline
is equaled by the rate of central compensation.
An example of such a pathologic process would
be that of neurofibromatosis type II, where slowgrowing bilateral vestibular schwannomas can
grow and impact vestibular afferent function at
significantly different rates. However, due to the
slow growth patterns of the vestibular schwannomas (albeit asymmetric), acute vestibular nystagmus and vertigo are often absent, secondary
to the effectiveness, and efficiency of the central
compensation process. If the schwannomas were
to alter their growth pattern in such a way that the
afferent neural drive became acutely asymmetric, it is likely that spontaneous nystagmus (and
vertigo) would ensue (depending on the residual
level of remaining afferent neural drive).
5
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The Clinical Utility of
Rotational Testing
INTRODUCTION TO
ROTATIONAL TESTING
Now that we have a thorough understanding and
foundation of the vestibular system’s anatomy
and physiology, we can begin to discuss the relevance and overall physiological responses generated by rotational testing. Just as the cochlea
responds to a broad range of acoustic frequencies,
the vestibular system equally responds to a broad
range of acceleration stimuli (frequencies). Similar to the auditory system, the vestibular system’s
sensitivity range is significantly broader than
what is needed for daily life activities. Specifically,
the vestibular system’s response characteristics
are principally efficient and effective for a narrow range between 0.05 and 6 Hz, even though its
detection sensitivity for acceleration stimuli can
extend well beyond this range. Figure 5–1 illustrates this point and highlights the system’s effectiveness for the narrow frequency range where
natural head movements occur. Within this frequency range, the responsiveness of the vestibular system can be characterized as a linear system
capable of operating with nearly perfect 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,
approximately 1 to 5 Hz.
Figure 5–1 also depicts the nonlinearity and
lack of response unity (perfect gain) for frequencies that occur above and below those associated
with natural head movements. For these frequencies, VOR gain and phase are significantly poorer.
Unfortunately, the test stimulus that is most commonly used to clinically evaluate the vestibular
system, the caloric stimulus, falls within this range
and is, therefore, neither truly ideal nor representative of daily life activities. This can be seen in
Figure 5–1 where the gain and phase of the vestibular system at the frequency of the caloric stimulus is quite poor. This is not to say that the caloric
response fails to deliver a useful clinical result. As
many clinicians who assess the vestibular system
know, the caloric test offers a distinct advantage
for determining laterality of vestibular pathology.
However, one of the primary disadvantages of the
impuissance of the caloric stimulus is that even
the slightest vestibular pathology is often sufficient to deleteriously impact its ability to provoke a vestibular response. This may seem like a
positive advantage of the caloric stimulus, as its
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