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6
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Clinical Neurophysiology of
Vestibular Compensation
Kamran Barin
oVerVieW
Peripheral vestibular abnormalities affect the function
of both sensory and motor mechanisms and result in
different symptoms. These symptoms can be divided
into two distinct types (Halmagyi, Weber, & Curthoys,
2010). First, static symptoms are those that are present
in the absence of head movements. These symptoms
are commonly associated with a sudden unilateral loss
of vestibular function and include vertigo, imbalance,
nausea, and vomiting. Second, dynamic symptoms are
those that are present only during head movements.
These symptoms include blurry vision, loss of visual
acuity, and disorientation in complex sensory environments when the head is moving.
Vestibular symptoms become less intense over
several days and eventually disappear in many
patients even when the vestibular loss is persistent.
This process of functional recovery is called vestibu-
lar compensation and is related to the high degree of
plasticity within the central vestibular pathways
(Curthoys & Halmagyi, 1995). Vestibular compensation follows multiple and sometimes concurrent processes: adaptation of sensory and neural responses,
substitution of sensory mechanisms, and habituation to aberrant stimuli (Lacour, Helmchen, & Vidal,
2016). Vestibular compensation should not be mistaken
for recovery that sometimes occurs due to the resolution of the lesion and restoration of normal vestibular
function (Manzari, Burgess, MacDougall, & Curthoys,
2013).
Cellular, neural, and behavioral aspects of ves-
tibular compensation have been studied extensively in
recent years in both humans and animals (Curthoys,
2000; Darlington, Flohr, & Smith, 1991; Dutia, 2010).
These studies have provided a better understanding of
the time course of vestibular disorders and a basis for
devising effective rehabilitation protocols to expedite
recovery after a vestibular lesion. However, significant
gaps remain in our understanding of the vestibular
compensation process. For example, most of the studies on vestibular compensation so far have focused on
the functional recovery of the vestibulo-ocular reflex
(VOR) and primarily on the recovery of the horizontal VOR. There are very few studies that address vestibular compensation following isolated lesions in the
vertical canal or the otolith pathways (Aw et al., 1995).
Similarly, the compensation process for the human postural control deficits has been studied mainly from the
behavioral point of view with few considerations for
the neural or cellular aspects of recovery.
This chapter is a selective review of the neuro-
physiology of vestibular compensation following a
vestibular lesion. The focus of this review is on the
clinical findings during various stages after the onset
of the lesion. Disorders that cause transient effects
such as benign paroxysmal positional vertigo (BPPV)
are discussed elsewhere in this book and will not be
considered here.
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EFFECTS OF VESTIBULAR LESIONS
A general description of peripheral vestibular lesions
is provided in this section. There are several disorders that can cause vestibular abnormalities (Strupp
& Brandt, 2013). However, they all produce peripheral
vestibular lesions by one of two ways: either by affecting the function of hair cells within the labyrinth or
by affecting the function of nerve fibers that originate
from those hair cells.
Some of the more obvious causes of hair cell dysfunction include infections such as in labyrinthitis,
trauma such as in labyrinthine concussion, and exposure to toxic agents such as in gentamicin vestibulotoxicity (Magnusson & Karlberg, 2002; Strupp & Brandt,
2013). The mechanism of hair cell dysfunction is less
obvious in conditions such as Meniere’s disease (Carey,
2010). In a normal inner ear, there is no contact between
the endolymph, the fluid that fills the labyrinth, and
the perilymph, the fluid that surrounds the labyrinth.
It is believed that in patients with Meniere’s disease, for
reasons that are still unknown, the endolymph absorption becomes impaired and leads to increased pressure
in the inner ear. This condition, known as endolymphatic
hydrops, leads to the rupture of the labyrinthine membrane and exposure of the hair cells to perilymph. Mixing of the inner ear fluids apparently has a toxic effect
on the hair cells and causes them to briefly become
hyperactive, followed by a much longer period of deactivation. Once the rupture closes and the perilymph is
flushed out of the labyrinthine space, most but not all
of the hair cells regain function. As the cycle of increase
in the inner ear pressure followed by the rupture of the
membrane continues during Meniere’s attacks, more
and more hair cells may fail to regain normal function.
This explains both the fluctuating and progressive
nature of Meniere’s disease (Li & Lorenzo, 2013).
Another mechanism of hair cell dysfunction is
the disruption of the blood supply to the labyrinth
(Lee et al., 2014). The arteries that serve the inner ear
have no collateral connections and, therefore, the inner
ear hair cells are highly sensitive to ischemic events
that interrupt the blood flow to the labyrinth. Brief
interruptions can cause reversible deactivation of the
hair cells, but if the ischemia persists for more than
a few minutes, the damage will become permanent.
Depending on which branch of the labyrinthine artery
is involved, the hair cell damage may be confined to
specific structures within the labyrinth or may include
the entire labyrinth as well as the cochlea. Examples
of diseases that can affect the labyrinthine blood supply are infarcts and transient ischemic attacks (Cloutier
& Saliba, 2008). Brief changes in the blood flow, such
as the type commonly associated with migraine associated vertigo, can modulate the activity of the hair
cells and result in fluctuating auditory and vestibular symptoms (Karatas, 2011). It should be noted that
the vascular origin of migraines has been disputed
(Goadsby, 2009), but recent evidence confirms association between migraines and blood flow issues to the
central nervous system (Mason & Russo, 2018).
The most common cause of vestibular nerve
dysfunction is infection such as in vestibular neuritis
(Halmagyi et al., 2010). It is now clear that there are
different types of vestibular neuritis (Manzari et al.,
2013). For example, infection can cause inflammation
of the vestibular nerve, which results in a temporary
loss of vestibular function. The function is restored
once the inflammation goes away. However, the infection can also cause degeneration of the nerve fibers,
which results in a permanent and irreversible damage
to the vestibular nerve. In addition, vestibular neuritis can affect the superior branch, the inferior branch,
or both branches of the vestibular nerve (Kim & Kim,
2012; Manzari, Burgess, & Curthoys, 2012). The symptoms and the clinical presentation of the disease will
depend on which branch or branches of the vestibular
nerve are affected.
Another cause of vestibular nerve dysfunction is
compression of the nerve fibers by tumors such as vestibular schwannoma (Kutz, Roland, & Isaacson, 2012).
If the tumor becomes large, it can also compress the
brainstem or the cerebellum and generate both peripheral and central vestibular findings.
Finally, neurotoxic agents can also damage the
vestibular nerve fibers (Nevin, 2012). However, the
incidence of such damage is thought to be far less than
that of the toxic agents that damage the hair cells.
Regardless of the underlying cause of damage to
the peripheral vestibular system, the compensation
process appears to be the same. In the remainder of
this section, first a brief review of the normal vestibular
function in humans is presented. Then, the effects of
different types of lesion immediately after the onset of
the lesion will be discussed. The process of compensation for each type will be discussed in the next section.
As noted earlier, the focus of this chapter is on the compensation of the VOR pathways because of the limited
knowledge about the other aspects of compensation.
Vestibular Responses to Different
Types of Head Movements
The role of the VOR is to provide clear vision by stabilizing images on the retina during head movements.
This task requires moving the eyes such that the eye
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velocity matches the head velocity but in the opposite
direction. Figure 6–1 shows the neural activities of one
hair cell from the right lateral semicircular canal and
one hair cell from the left lateral semicircular canal in
response to different types of head movements. When
the head is at rest, each hair cell generates tonic neural
activity of approximately 80 to 100 spikes per second.
In the absence of head movements, the neural activities
received from the right and left labyrinths are approximately equal (Figure 6–1A).
When the head moves to one side in a manner
that resembles natural head movement, neural activities from both labyrinths are modulated from their
baseline level (Barin, 2009). The leading ear generates
figure 6–1. Responses of a normal individual to different types of head movements. Right and left vestibular nerve
(VN) activities, VOR neural command, and the final eye position are shown. The VOR neural command is the difference between the right and left VN activities that is further processed within the vestibular nuclei. Ideally, the VOR
command should be proportional to the head velocity. A. Head at rest. B. Rightward natural head movement.
C.Sinusoidal head movements in the rotation chair testing. D. Rightward velocity-step head movement in the rota-
tion chair testing. E. Rightward head movement in the head impulse test. All responses are obtained in the absence
of fixation except for E. Note that time and amplitude scales are different for different stimuli. Also note that the
responses are approximate and are not intended to exactly match actual responses.
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excitation, whereas the lagging ear generates inhibition of neural activity. The change of neural activity is
approximately proportional to the head velocity (Figure 6–1B). The secondary vestibular neurons within
the vestibular nuclei relay the difference between the
right and left neural activities to the oculomotor nuclei,
which generates eye movements that are also proportional to the head velocity but in the opposite direction. It is important to note that the entire process takes
place at the brainstem level without the need for higher
cortical level involvement. As a result, VOR-generated
eye movements have a very short latency and are much
faster than tracking or pursuit eye movements that are
mediated by the higher cortical levels.
If the head moves sinusoidally side to side similarly to the type of head movements that occur during low-frequency rotation chair testing, the change in
the neural firing is also sinusoidal but differs from the
head velocity in two characteristics (Figure 6–1C). First,
the amplitude of the change is much less than the head
velocity, which results in a gain of lower than 1.0. Second, there is a time difference between the change in
the neural firing and the head velocity, which results in
a phase shift. The reason for these differences is related
to two factors (Barin, 2009). The first factor is the physical characteristics of the cupula and the endolymph.
That is, the inertia of the cupula and the viscosity of
the endolymph cause the hair cell responses to differ
from the head movements in low frequencies. The second factor is related to a neural integrator within the
vestibular nuclei, called the velocity storage mechanism
(VSM). The purpose of the VSM is to improve the lowfrequency performance of the cupula. The best analogy
for its function is a storage tank that has a large inlet
but a small outlet. As a result, the neural firing builds
up within the VSM and continues to discharge slowly
even after the stimulus has stopped. The combination
of the cupular dynamics and the VSM allows the VOR
to work well for natural head movements that are in
the mid- to high-frequency range but not so well for
very low frequency head movements as in Figure 6–1C.
As the frequency increases, the gain increases and the
phase shift decreases until the change in neural firing
becomes proportional to the head velocity during natural head movements.
The behavior of the cupula and the VSM is also
apparent when the head is accelerated rapidly and then
rotated at a constant velocity for a long time (Barin,
2009). This type of stimulus is similar to the velocity
step test in rotation chair testing. During the acceleration phase, the change in neural firing is proportional
to the head velocity (Figure 6–1D). After reaching the
final velocity and during the constant velocity rotation
phase, the cupula begins to return to its resting position and the neural firing declines toward the baseline
accordingly. In humans, it takes approximately 20 seconds for the cupula to return to its resting position but
the change in the neural firing persists for up to 60 seconds because of the influence of the VSM.
If the head is moved very rapidly to one side similarly to the type of head movements that occur during the head impulse test, the excitatory change in the
neural firing from the leading ear resembles the head
velocity (Figure 6–1E). However, the inhibitory change
in the neural firing from the opposite ear saturates and
the response is clipped at 0 spikes per second. During
the saturation phase, the labyrinth no longer provides
an accurate measure of the head movement. As a result
of this nonlinearity, the input to the oculomotor system is not proportional to the head velocity. Nonetheless, central vestibular pathways seem to place more
emphasis on the responses from the excitatory side,
which allows the VOR to function fairly effectively
because the excitatory labyrinth provides a more accurate measure of the head velocity (Weber, MacDougall,
Halmagyi, & Curthoys, 2009).
The above examples demonstrate that head movements generate an asymmetry between the right and
left neural activities. Determining which side is generating excitation and which side is generating inhibition identifies the direction of head movements. The
degree and the type of neural asymmetry determine
the amplitude and the type of head movements. For
example, the neural asymmetry for natural head movements mimics the head velocity, which can be relayed
to the oculomotor nuclei to generate compensatory eye
movements.
The question of how the central nervous system
can determine the properties of head movement from
different patterns of neural firing is an important one
and has a profound implication regarding vestibular compensation. One hypothesis is the existence of
a lookup table or a database that for every pattern of
head movement contains a corresponding neural firing pattern (Borel, Lopez, Péruch, & Lacour, 2008). It is
possible that this database is formed early in life and
may explain why children and young adults engage
in the type of movements that may not be easily tolerated in older ages. In fact, part of the play activities
in childhood may be related to the formation of this
database. The support for this hypothesis comes from
the fact that the morphological development of the
labyrinthine structures seems to be complete within a
few months after birth but the central vestibular pathways continue to mature for several years (Casselbrant
et al., 2010).
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It should be noted that other oculomotor systems
interact with the vestibular system and participate in
controlling eye movements. For instance, in some of
the above examples, if the VOR drives the eyes close
to the orbital limit, the saccadic system moves the eyes
quickly in the opposite direction (Abadi, 2002). This is
the mechanism of generating nystagmus with the slow
phase mediated by the vestibular system and the
fast phase mediated by the saccadic system.
Effects of Acute Unilateral
Vestibular
Unilateral lesions are by far the most common type of
peripheral vestibular abnormalities. This type of lesion
generates asymmetries in the vestibular pathways that
mimic head movements. Figure 6–2 shows what happens when the hair cells or their afferent nerve fibers
are damaged in one of the lateral semicircular canals.
Lesions
Figure 6–2. Responses of an individual with right peripheral vestibular lesion to different types of head movements.
See Figure 6–1 for other details. The negative values for the VOR neural command indicate that the activity from
the left side is greater than the activity from the right side. Also, note that the spontaneous nystagmus (SP) in A is
superimposed on all of the other eye movements but they are not shown in the figure.
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Of course, the loss of a small number of hair cells or
nerve fibers will not cause significant consequences,
but if the damage is substantial, the neural activity
present at the vestibular nuclei of the damaged side
will be reduced proportional to the number of lost hair
cells or nerve fibers (Figure 6–2A). The resulting neural asymmetry is perceived as the head moving away
from the damaged ear in the plane of the affected
semicircular canal (Barin, 2009). Accordingly, spontaneous nystagmus is generated because the VOR moves
the eyes slowly toward the damaged ear followed by
the saccadic system resetting the eyes in the opposite
direction. The slow-phase velocity (SPV) of spontaneous nystagmus is an important parameter because it
reflects the velocity of the perceived head movements
and directly correlates with the patient’s static symptoms. At the onset of the lesion, the intensity of spontaneous nystagmus reflects the number of hair cells or
nerve fibers that are damaged. However, as we will
see, the intensity of spontaneous nystagmus and the
severity of static symptoms change quickly due to the
vestibular compensation process.
Because the perception of motion after a unilateral vestibular lesion is contradicted by other sensory
mechanisms, namely vision and proprioception, the
patient experiences vertigo and the associated autonomic symptoms in the absence of head movements.
Other static symptoms following a unilateral vestibular
lesion often include imbalance and tilting of the head
and body to one side.
When the patient moves his or her head following a unilateral vestibular lesion, the asymmetry in the
neural firing is not as large as that before the onset of
the lesion (Figure 6–2B). Therefore, the resulting eye
movements are not completely compensatory, which
causes the images not to be stationary on the retina. The
lack of coordination between head and eye movements
leads to dynamic symptoms such as blurry vision and
the loss of visual acuity during head movements.
Figure 6–2 shows the neural firing for different
types of head movements following an acute unilateral
lesion. As noted for natural head movements, neural
firing does not match head velocity, and the resulting
eye movements are smaller than the head movements
(Figure 6–2B). For low-frequency sinusoidal head
movements, the gain of VOR (amplitude) decreases
and the phase shift (timing) increases (Figure 6–2C).
Similarly, for step-velocity movements, the amplitude
of neural responses immediately after the acceleration
phase is smaller and the decline of the response toward
the baseline (time constant) is faster (Figure 6–2D). The
effect is more noticeable for head movements toward
the side of lesion. Finally, the nonlinearity in the VOR
pathways causes the neural firing from the intact side
to saturate during head impulses toward the damaged
ear, and the eyes fall well short of head movements
(Figure 6–2E). In this case, the patient usually uses saccadic eye movements to refixate on the target (catch-up
saccades). The effect is present for movements toward
and away from the side of lesion but is far more noticeable for the movements toward the side of lesion.
In addition to the lateral semicircular canals,
damage to the other structures within the peripheral
vestibular system also causes asymmetries in the neural firings that mimic head movements in different
planes. The eye movements following a focal lesion in
different vestibular structures are shown in Figure 6–3
(Barin, 2009).
As noted, damage to one of the lateral canals is
perceived as the head moving toward the intact ear
and results in horizontal spontaneous nystagmus with
the fast phases beating away from the side of lesion
(Figure 6–3A).
A focal lesion of the anterior canal is perceived as
the head moving backward in the plane of anteriorposterior canal pairs and results in vertical nystagmus
beating up and torsional nystagmus beating away from
the side of lesion (Figure 6–3B). The rationale for vertical nystagmus is the same as the horizontal nystagmus
in lateral canal lesions. Presence of torsional nystagmus can be explained by the fact that the vertical canal
pairs are not aligned with the pitch plane. Torsional eye
movements are intended to bring the eyes to the plane
of canal pairs.
Because of the synergistic pairing of the vertical
canals, the same type of vertical and torsional nystagmus can be seen for excitation of the opposite posterior
canal. Such an excitation can happen for posterior canal
BPPV, but unlike BPPV-type nystagmus, the nystagmus
following damage to the anterior canal is persistent.
A focal lesion of the posterior canal is perceived as
the head moving downward in the plane of anteriorposterior canal pairs and results in vertical nystagmus
beating down and torsional nystagmus again beating
away from the side of lesion (Figure 6–3C). The same
type of nystagmus can be seen for BPPV of the opposite anterior canal, but again the resulting nystagmus
is transient.
Focal lesions of the utricle or saccule are not as
well understood as those of the semicircular canals
(Manzari, MacDougall, Burgess, & Curthoys, 2014).
One can assume that damage to one of the otolith
organs will cause loss of orientation with respect to
gravity and will be perceived as the head tilting away
from the damaged side (Figure 6–3D). Consistent with
that hypothesis, such a lesion has been shown to result
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figure 6–3. Eye movements following a focal lesion in different peripheral vestibular structures. A. Lateral semi-
circular canal (
E.
Superior branch of the vestibular nerve (SVN ). F. Inferior branch of the vestibular nerve (IVN ). G . Total labyrinthine
or vestibular nerve.
in a tonic torsion of the eyes toward the side of lesion
(Curthoys, Dai, & Halmagyi, 1991). This type of torsion
can be tested with the subjective visual vertical test. It is
not clear how common it is to have a focal lesion of the
otoliths. However, mild residual symptoms after a successful repositioning maneuver in BPPV patients may
be related to otolith abnormalities. After all, a substantial loss of otoconia from the utricle in these patients
can disrupt normal otolith function. This could explain
high incidence of ocular vestibular-evoked myogenic
potential (VEMP) abnormalities in this population (Xu
et al., 2016).
The manifestation of a lesion in different branches
of the vestibular nerve can be determined by combining the effects of lesions in different semicircular canals
LSCC ). B. Anterior semicircular canal (ASCC ). C. Posterior semicircular canal (PSCC ). D. Otoliths.
or the otolith organs that are mediated through that
branch. For example, the superior portion of the vestibular nerve transmits information from the lateral and
anterior semicircular canals as well as the utricle. As a
result, damage to this branch of the vestibular nerve
results in horizontal nystagmus beating away from
the side of lesion, vertical nystagmus beating up, torsional nystagmus beating away from the side of lesion,
and tonic torsion of the eyes toward the side of lesion
(Figure 6–3E). Similarly, the inferior portion of the vestibular nerve is supplied by the posterior canal and
the saccule. Damage to this branch of the vestibular
nerve results in vertical nystagmus beating down, torsional nystagmus beating away from the side of lesion,
and tonic torsion of the eyes toward the side of lesion
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(Figure 6–3F). Finally, damage to both branches of the
vestibular nerve or a total labyrinthine lesion results
in combination of all lesions for individual structures
within the labyrinth. However, the vertical components
of the nystagmus are in opposite directions and cancel
out. As a result, total vestibular nerve or total labyrinthine lesions result in horizontal nystagmus beating
away from the side of lesion, torsional nystagmus beating away from the side of lesion, and tonic torsion of
the eyes toward the side of lesion (Figure 6–3G).
Effects of Acute Bilateral Vestibular Lesions
Bilateral vestibular lesions are rare compared with unilateral lesions. They can be present in one of two ways.
When the loss of function is approximately equal in
both peripheral vestibular systems, the patient exhibits very few of the static symptoms. That is, vertigo and
spontaneous nystagmus that are typical of unilateral
vestibular lesions are not present because of the absence
of neural asymmetries. Instead, these patients usually
experience dynamic symptoms such as unsteadiness,
oscillopsia (sensation of stationary objects moving during head movements), loss of visual acuity, and blurry
vision during head movements (Jen, 2009). Although
the acute symptoms may not appear to be as troublesome as those resulting from unilateral lesions, longterm functional consequences of bilateral lesions are far
more serious and more difficult to overcome (Kim, Oh,
Koo, & Kim, 2011).
When bilateral loss of function is present but is
more significant on one side, the patient exhibits both
symptoms associated with the unilateral vestibular
lesions as well as symptoms associated with the bilateral vestibular loss (Fujimoto et al., 2013). Again, the
consequences of this type of lesion both in the acute
and chronic phases of the lesion are very serious (Guinand, Boselie, Guyot, & Kingma, 2012).
Effects of Acute Central Vestibular Lesions
Very little is known about focal lesions affecting the
vestibular nuclei (Shepard, 2009). If damage to the
vestibular nuclei affects the tonic neural activity of the
secondary vestibular neurons on one side, then the
symptoms and presentation are expected to be similar to those for unilateral peripheral vestibular lesions.
However, the clinical picture is more complicated. In
humans, the majority of the conditions that damage the
vestibular nuclei are due to vascular diseases, tumors,
or trauma (Furman & Whitney, 2000). As a result, the
effects are not necessarily confined to the vestibular
nuclei and often involve other structures within the
brainstem, cerebellum, or cerebellar cortex. Animal
studies have demonstrated spontaneous nystagmus
following focal lesions within the vestibular nuclei
(Aldrich & Peusner, 2002). However, unlike peripheral
vestibular lesions, focal lesions of the vestibular nuclei
did not produce a caloric weakness. Instead, the caloric
findings included perverted nystagmus and other central findings.
It is clear that our understanding of central vestibular lesions is still emerging. Although compensation
following central vestibular lesions will be mentioned
briefly, a better understanding of the underlying pathophysiology of these disorders is needed before effective
rehabilitation methods can be devised.
VESTIBULAR COMPENSATION
Vestibular pathways possess a high degree of plasticity, which is essential to overcome the effects of environmental and developmental changes, such as aging
(Zee, 2000). The VOR adaptation after wearing special
prisms that reverse the visual field is a remarkable
demonstration of this plasticity (Melvill Jones, Guitton, & Berthoz, 1988). The same adaptive mechanisms
participate in the vestibular compensation process so
that the patients can recover functionally after a vestibular lesion. However, vestibular compensation is not
limited to the adaptation and may include substitution
by other oculomotor and postural control mechanisms
such as the saccadic system (Curthoys, 2000).
Figure 6–4 shows a highly simplified view of the
vestibular compensation mechanisms. The head movements are transduced into neural activity by the hair
cells within the labyrinth. The changes in neural activity are transmitted to the vestibular nuclei via the primary vestibular neurons within the vestibular nerve.
The secondary vestibular neurons usually relay the
neural activity to the motor centers such as the oculomotor nuclei and the spinal cord. The cerebellum
constantly monitors the changes in the neural activity
within the vestibular nuclei but does not intervene as
long as they are within the expected response of the
system. However, when changes in the neural activity do not match the expected responses, vestibular
compensation mechanisms alter the behavior of the
secondary vestibular neurons so that the motor centers receive a modified representation of the activity of
the primary vestibular neurons. The alteration at the
vestibular nuclei level may include reduction in gain,
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Figure 6–4. A simplified representation of the vestibular compensation process.
increase in gain, change in the timing, or other modification of neural activity. In this view of the vestibular compensation process, the cerebellum, namely the
cerebellar flocculus, plays an important role in initiating the compensation process (Courjon, Flandrin, Jeannerod, & Schmid, 1982; Johnston, Seckl, & Dutia, 2002).
It is now clear that vestibular compensation occurs
in different steps (Lacour, 2006). Static compensation
begins almost immediately after the onset of the lesion
in order to reduce the more distressing symptoms that
are present in the absence of head movements. Dynamic
compensation occurs later to reduce the longer-term negative effects of damage to the vestibular system. Dynamic
compensation appears to be a more complex process that
may never fully resolve the symptoms in some patients.
Compensation After Unilateral
Vestibular
It is well known that most patient complaints after a
sudden unilateral peripheral vestibular lesion follow
a typical pattern. The patients usually exhibit a few
days of severe and often disabling symptoms and a
few weeks of moderate and improving symptoms,
followed by a few months of mild and manageable
symptoms (Halmagyi et al., 2010). Of course, there are
individual differences depending on the age, activity
levels, and presence of other confounding conditions.
Nonetheless, this relatively universal pattern of recovery corresponds to the various stages of compensation
that are discussed in this section.
Figure 6–5 shows various steps of the static compensation process after the onset of a peripheral vestibular lesion. This is a highly simplified and somewhat
speculative presentation of the vestibular compensation process. Several assumptions are made for illustration purposes. First, only the recovery of horizontal
VOR is considered here, but the process is similar for
the VOR in other planes. Furthermore, it is assumed
that the damage to the peripheral vestibular system is
Lesion
complete. Finally, the neural activity of a single nerve
fiber is shown and it is assumed arbitrarily that its tonic
neural firing is 100 spikes/sec.
Prior to the Onset of Lesion
Figure 6–5A shows the neural activity at the vestibular
nuclei of a normal individual immediately following a
sudden horizontal head rotation toward the left ear. It
is assumed, again arbitrarily, that for the given change
in head velocity, the momentary change in neural firing
is 50 spikes/sec. The difference between the excitatory
response from the left side and the inhibitory response
from the right side immediately after the onset of rotation is 100 spikes/sec (2 × 50 spikes/sec). As the VOR
is functioning normally in this individual, head movements are extrapolated accurately from the pattern of
neural activities, and compensatory eye movements
are generated in the opposite direction of head movements, with the SPV matching the head velocity. As
the rotation continues, the saccadic system resets the
eyes when they approach the orbital limit and generates nystagmus with fast phases toward the direction
of head acceleration (left beating for this example).
Immediately After the Onset of Lesion
Figure 6–5B shows the neural activity at the vestibular
nuclei immediately following a lesion in the right lateral semicircular canal or its afferent neural pathway.
The neural asymmetry is perceived as the head rotation
to the left and spontaneous nystagmus is generated
with the fast phases directed toward the direction of
the perceived head motion and away from the side of
lesion (Fetter & Zee, 1988). Furthermore, the SPV of the
nystagmus is the same as that of Figure 6–5A because
the neural asymmetry of 100 spikes/sec is the same in
both conditions. It is important to note that the SPV of
spontaneous nystagmus reflects how fast the patient
perceives his or her head is rotating, and as a result it
relates directly to the severity of symptoms.
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