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58 Rotational Vestibular Assessment
FIGURE 3–3. Cerebellum. A. Individual labeling of
the cerebellar lobules (1 to 9) (sagittal plane). (1) Lingula Cerebelli, (2) Lobulus Centralis, (3) Culmen, (4)
Declive, (5) Folium Vermis, (6) Tuber Vermis, (7) Pyramis
Vermis, (8) Uvula Vermis, and (9) Nodulus Vermis. From
Abolished tilt suppression of the vestibulo-ocular reflex
caused by selective uvulo-nodular lesion by G. Wiest,
L. Deecke, S. Trattnig, and C. Mueller, 1999, Neurology
52(2), 417–419. Reprinted with permission. continues
A
tions from the cerebellar cortex are exclusively
handled by a layer of cells known as Purkinje
cells (Brodal, 2004). Functionally, the cerebellum
is classified into the vestibulocerebellum, the
spinocerebellum, and the pontocerebellum with
each serving a primary need and responsibility
(Arslan, 2001).
Vestibulocerebellum (Lobule X)
The vestibulocerebellum is comprised solely of
the flocculonodular lobe (lobule X). The vestibulocerebellum is the most primitive and smallest part
of the cerebellum (Brodal, 2004) and is located
anteroventrally within the cerebellum just dorsal
to the fourth ventricle. The flocculonodular lobe
primarily receives neural fibers from the vestibular nuclei as well as directly from the vestibular
periphery (Brodal, 2004). The flocculonodular
lobe is comprised of the nodulus in the midline
and the two flocculi that flank either side (Figure
3–3B). The nodulus, located directly in the midline and anteroventrally within the cerebellum,
is actually the inferior most portion of the vermis. Each flocculus is connected via a thin stalk
that projects laterally from the nodulus, which
is known as the paraflocculus (Brodal, 2004). As
previously stated, the Purkinje cells of the vestibulocerebellum do not have axonal projections to
deep cerebellar nuclei, but rather send their axon
projections directly to the vestibular nuclei (Brodal,
2004). The vestibulocerebellum is therefore critical
to the vital components of vestibular physiology
and function, including VOR regulation, equilibrium, as well as central compensation (Brodal,
2004). Functionally, the flocculus, the nodulus,
and the vermis each have distinct responsibilities.
Cerebellar Flocculus. The overall responsibil-
ity of the flocculus is to maintain the gain of the
vestibular ocular reflex (Hain & Helminski, 2007).
The axonal fibers from the flocculus predominantly terminate in the superior and medial
vestibular nuclei. From there, ascending tracts
through the longitudinal medial fasciculus project
to the ocular motor nuclei which eventually innervate various ocular motor muscles for coordination of eye movement (Arslan, 2001). Therefore,
coordination between the flocculus and the vestibular nuclei provide a significant contribution to
maintaining an effective and efficient vestibular
ocular reflex.
3. Anatomy and Physiology of the Central Vestibular System, Velocity Storage, and Central Compensation 59
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B
FIGURE 3–3. continued B. Division of lobes and fissures (flattened transverse plane). Floccu-
lonodular lobe is also known as the vestibulocerebellum, which contains the nodulus, as well as
the flocculi and paraflocculi. These structures, along with the ventral nodulus, are critical to central
vestibular compensation. From Neuroscience for the Study of Communication Disorders (4th ed.)
by S. C. Bhatnagar, 2013, Baltimore, MD: Lippincott, Williams & Wilkins. Reprinted with permission.
Cerebellar Nodulus. The overall responsibility of
the cerebellar nodulus is to adjust the duration/
timing of the VOR as well as to process otolith
input (Hain & Helminski, 2007). Axonal projec-
tions from the nodulus are similar to that of the
flocculus with the exception of a further projection to the lateral and inferior nuclei. From there,
descending tracts form the vestibulospinal tracts
60 Rotational Vestibular Assessment
for coordination of posture and equilibrium. In
addition, strong evidence supports nodular projections to be critical for restoring and recalibrating
central vestibular neural symmetry following insult
during central compensation (Leigh & Zee, 2006).
Cerebellar Vermis. The overall responsibility of
the cerebellar vermis is to assist in the coordination of the vestibulospinal system for effective
and efficient posture and equilibrium (Hain &
Helminski, 2007). Purkinje cells of the vermis as
well as the anterior and posterior cerebellar lobes
have prolific projections to the deep cerebellar
fastigial nuclei. From there, main axonal projections bypass the vestibulocerebellum (flocculonodular lobe) and directly terminate in the lateral
vestibular nuclei. From there, efferent projections
descend through the lateral vestibulospinal tract
and innervate the spinal cord (Arslan, 2001; Brodal, 2004). The cerebellar vermis and its efferent
projections are subsequently vital for postural
control (Brodal, 2004).
Spinocerebellum and Pontocerebellum
Besides the functional capacities offered by the
vestibulocerebellum, the cerebellum is further
divided into the spinocerebellum and the pontocerebellum (Brodal, 2004). Whereas the vestibulocerebellum is composed of the flocculonodular
lobe and nodulus, the spinocerebellum is composed of the entire anterior lobe and the paravermal lobules (intermediate hemispheres) of the
cerebellum (Brodal, 2004). The pontocerebellum,
or cerebrocerebellum, is composed of all the lateral aspects of the cerebellar hemispheres (Timmann & Diener, 2007). Both the pontocerebellum
and the spinocerebellum are named accordingly
in light of the heavy axonal projections from the
pontine nuclei and the spinal cord, respectively.
Although neither contains heavy projections to
or from the vestibular nuclei, both are believed
to collectively coordinate incoming sensory data
with the flocculonodular lobe in order to make
continuous and fine adjustments to movement
(Timmann & Diener, 2007). The spinocerebellum
tracts provide essential data regarding propulsive movements (e.g., ambulation) (Arslan, 2001).
The pontocerebellum and its pontine tracts saltate
neural responses from the cerebral motor areas;
most notably the primary motor cortex, somatosensory cortex, supplementary motor and premotor areas, the posterior parietal lobes, as well as
prefrontal and limbic areas (Timmann & Diener,
2007). Therefore, neural information is inundating the cerebellum and all its functional divisions
with sensory data pertaining to the analysis, planning, integration, and initiation of gross and fine
motor movements to ensure such movements are
performed both smoothly and accurately.
COMMISSURAL
VESTIBULAR FIBERS
Vestibular commissural fibers are a critical component to the function and efficiency of the central
vestibular system (Barin & Durrant, 2000; Baloh
& Honrubia, 2001). The commissural fibers play
a significant role in the functioning of the velocity
storage mechanism and with central compensation. Most of the commissural fibers arise and terminate within all four vestibular nuclei; however,
the superior and medial nuclei receive and send
most of the commissural neural tracts, with the
superior nucleus comprising the majority (Gacek,
2005). Because the commissural pathways predominantly involve the superior, inferior, and
medial vestibular nuclei, by default, the commissural neural activity is primarily provoked from
semicircular canal neural input. As we learned in
Chapter 2, the primary mechanism for this activity
is afforded by the opposite polarity of peripheral
hair cells in the cristae. Because maculae have an
opposite polarization of the hair cells between the
two halves of each sense organ (separated by the
striola), commissural projections may not be necessary to produce a differential effect from activation of these sensory end organs (Gacek, 2005).
Although heavy homologous commissural
projections are noted between vestibular nuclei
counterparts, the existence of many more variable
projections between disparate nuclei supports a
more complex commissural pathway structure
(Lysakowski et al., 1998). Overall, the relative
importance and function of these commissural
3. Anatomy and Physiology of the Central Vestibular System, Velocity Storage, and Central Compensation 61
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pathways should not be overlooked. The primary
role of the commissural pathway is largely inhibitory and compensatory (Curthoys & Halmagyi,
1996; Raphan & Cohen, 1996). The mere existence
of a commissural network largely facilitates two
of the most significant physiologic attributes of
the vestibular system, namely, velocity storage
and central compensation (Leigh & Zee, 2006).
Velocity Storage
The following review regarding the anatomical and physiologic processes of velocity storage
and central compensation has been synthesized
from Curthoys and Halmagyi (1996), Barin and
Durrant (2000), Baloh and Honrubia (2001), and
Leigh and Zee (2006). Much of what is known
regarding normal functioning of the velocity storage mechanism comes from single unit neuron
recordings from animals (primarily monkeys, rats,
and guinea pigs). The reader is strongly encouraged to review these sources for a complementary
and complete physiological understanding of the
velocity storage mechanism and its associated
neural pathways.
Velocity storage is a process of integration
and subsequent preservation and augmentation
of afferent signals sent from the various peripheral vestibular sensory receptors. Velocity storage
is particularly critical in the central augmentation
of low frequency stimuli that would otherwise
be too weak to effectively drive the VOR. It is
mediated within the vestibular nuclei by the commissural pathways and the cerebellum (Barin &
Durrant, 2000; Baloh & Honrubia, 2001). The process of velocity storage is integrated and mediated
primarily by specific neuronal cells within the vestibular nuclei (Curthoys & Halmagyi, 2007). These
highly specialized neuronal cells are type I and
type II neurons. The activation of these central
neuronal cells, however, is also heavily dependent
upon the peripheral afferent signal from the SCCs
and, to a lesser degree, the otoliths (Curthoys &
Halmagyi, 2007). Therefore, the functional dependence of the velocity storage mechanism is reliant
on adequate peripheral input. When such input
is altered, such as from a peripheral vestibular
lesion, the velocity storage mechanism responsibility is also modified.
Type I and Type II Vestibular Neurons
There are two types of primary neuronal cells
located within the vestibular nuclei complex, type
I
and type II neurons, (not to be confused with type
I and type II peripheral hair cells). These cell types
integrate and process the peripheral vestibular
sensory input (along with the cerebellum, higher
brainstem, and cortical structures) prior to sending efferent responses to the appropriate ocular
motor, postural motor, and vestibulocollic motor
reflexes. In addition, type I and type
II neurons
are essential to the velocity storage mechanism
as well as ensuring effective compensation for
peripheral vestibular disease. Individually, each
type of neuron has its own specialized function.
Collectively, type I and type II neurons, in association with the commissural fibers, work together to
form a complementary neurophysiologic network
that is vital to the efficiency of the central vestibular system.
Type I Vestibular Neurons. Within each vestibu-
lar nuclei, there exist type I neurons that are specialized to be either excitatory or inhibitory. That
is, some type I central neurons are only activated
with excitation, whereas others are only activated
with inhibition. This is generally dependent on the
direction of head rotation, such that rotations in
the yaw plane toward the right will activate primary horizontal semicircular canal afferents that
project and synapse directly with the appropriate
type I excitatory neurons in the right vestibular
nuclei. Conversely, type I inhibitory neurons located in the left vestibular nuclei will be simultaneously activated by primary vestibular afferents driven
by hyperpolarized (inhibited) hair cells originating from the crista in the left horizontal semicircular canal. Finally, type I neurons also show an
indirect synaptic cleft (“connection”) with type I
neurons located in the contralateral vestibular nuclei
through commissural projections (via contralateral
type II neurons). As mentioned previously, this
commissural network of decussating fibers is extensive and variable, often projecting to or away
from their respective homologous contralateral
nuclei division. Evidence shows that such commissural projections are inhibitory in nature (Curthoys
& Halmagyi, 1996, 2007; Raphan & Cohen, 1996).
62 Rotational Vestibular Assessment
Type II Vestibular Neurons. Type II neurons
differ from type I neurons is two primary ways.
First, while type I neurons are either excitatory or
inhibitory, type II neurons are always inhibitory
and only receive synaptic projections via the commissural pathways from excitatory type I neurons located in the contralateral vestibular nuclei
(Curthoys & Halmagyi, 1996; Raphan & Cohen,
1996). That is, type II inhibitory neurons are solely
activated by contralateral excitatory type I neurons via the commissural pathways, (and just to
be clear, activation of a type II inhibitory neurons
refers to the neuron exerting an increase in inhibition). The second way type II neurons differ from
type I neurons is that type II neurons always form
synaptic clefts with neighboring type I excitatory
neurons in the same vestibular nuclei (Curthoys &
Halmagyi, 1996; Raphan & Cohen, 1996). Therefore, type II inhibitory neurons share a rather
intimate relationship with type I excitatory neurons, insomuch that they share a direct synaptic
cleft with neighboring ipsilateral excitatory type
I neurons and also receive direct projections from
contralateral excitatory neurons via the commissural pathways, thereby forming an indirect
inhibitory “link” between excitatory type I neurons from opposing vestibular nuclei. The normal role of the type II inhibitory neurons is, therefore, to act as a facilitator between type I excitatory
neurons from both vestibular nuclei in order to
allow indirect inhibition (or even “silencing”) of
type I excitatory neurons located in the contralater-
al vestibular nuclei (Curthoys & Halmagyi, 1996;
Raphan & Cohen, 1996). Of course, it goes without
saying that the commissural fiber network plays
an integral role in this process. This processes of
“commissural inhibition” and the role of the type
II inhibitory neurons holds true when referring
to the process of velocity storage. However, the
role of type II inhibitory neurons changes slightly
during the “neural clamping” process that occurs
during central compensation (discussed later).
Type I and Type II Vestibular Neurons Complementary Physiology.
As previously stated, type II
inhibitory neurons are activated solely via the
commissural pathways from the contraversive
excitatory type I neurons, which are driven by
the semicircular canal afferents, (specifically horizontal canal afferents during yaw rotations). In
a healthy vestibular system, contraversive type
inhibitory II neurons are always activated (exert
stronger inhibition) when ipsiversive type I excitatory neurons are activated (Curthoys & Halmagyi, 1996; Raphan & Cohen, 1996). This is critical
when considering the relationship of type II inhibitory neurons with neighboring type I excitatory
neurons in the same vestibular nuclei. At its most
fundamental level, one could argue that it is this relationship that forms the foundation for the mechanism underlying velocity storage: specifically, the
further inhibition of the contraversive excitatory
type I neurons that are undergoing a transient reduction in the tonic resting neural vestibular firing
rate from the periphery due to the activation of
contraversive type I inhibitory neurons. Essentially, this serves to further lower the tonic neural
rate within the contraversive vestibular nuclei in
relation to the increased neural rate of the ipsiversive vestibular nuclei. Put simply, type I and type
II neurons are complementary with respect to
their inhibition and excitation. Overall, this process creates a larger tonic neural disparity between
the two vestibular nuclei than would have otherwise existed if it were not for this type I–type II
commissural relationship. As previously stated,
this process is particularly important for low-frequency acceleration stimuli that would otherwise
be too weak to effectively drive a functional VOR.
To summarize the relationship between type I
and type II central neurons thus far, let us consider
an example. When turning toward the right, type I
excitatory neurons located in the right vestibular
nuclei are activated by right (ipsiversive) horizontal canal afferents, which, in turn, activate type II
inhibitory neurons in the contraversive left vestibular nuclei. During the same rotation, toward the
right, type I inhibitory neurons in the left vestibular nuclei are activated (Barin & Durrant, 2000;
Baloh & Honrubia, 2001; Curthoys & Halmagyi,
1996). Simultaneously, type I excitatory neurons in
the contraversive left vestibular nuclei are inhibited
by their neighboring type II neurons secondary
to activation signals sent via commissural projections from the ipsiversive type I excitatory neurons located in the right vestibular nuclei. This
“commissural inhibition” is critical to the process
of velocity storage and central compensation.
However, this part of the complementary process
is only one-half of the “story.” The commissural
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relationship between type I excitatory neurons
and type II inhibitory neurons does not end here,
and is even more dramatic and complex than presented thus far. Let us now continue to dissect
how this commissural relationship forms the basis
for the velocity storage mechanism in the process
of augmenting a weak neural response.
Velocity Storage Central Mechanism
The complete process of velocity storage involves
an intricate, complex, and cyclical interaction
between the type I and type II neurons within
and between the VN, via the commissural fiber
network. It is the cyclical component to the velocity storage process that we must now discuss. In
doing so, we must continue to consider the interaction between type I and type II neurons, and
how they form the foundation for the velocity
storage mechanism within each vestibular nuclei
and across the commissural fiber network.
We have previously discussed how the efficiency of the peripheral vestibular system is frequency dependent. That is, because the cupulae
respond to acceleration, low frequency acceleration stimuli are less apt to provoke a robust
response than mid-to-high frequency stimuli
(greater than 0.05 Hz). However, that is not to say
that the vestibular system fails to respond to low
frequency acceleration stimuli. In fact, it is able
to respond to extremely low frequency stimuli. It
just so happens that the central processing of this
poorly integrated weak peripheral response requires a mechanism by which the impuissant neural response can be “amplified,” (not a concept too
far different than that of the cochlear amplifier).
That mechanism is known as velocity storage.
Velocity storage is critical for the processing
and augmentation of the weak neural response
produced from low frequency stimuli (in addition
to its integral involvement with central compensation). This reliance on the velocity storage mechanism for the processing of low frequency stimuli
will repeatedly be highlight during our discussion
of sinusoidal acceleration testing as it pertains to
low-frequency stimuli in Chapter 6. Let us consider the neurophysiological response to a low frequency angular stimulus applied to the horizontal
cristae. A depolarization of the peripheral vestibular receptor causes an increase in the ipsiversive
afferent vestibular neural firing rate, which activates type I excitatory neurons within the ipsilateral VN. The ipsiversive type I excitatory neurons
synapse directly with the contraversive type II
excitatory neurons via the commissural fibers.
Meanwhile, a concomitant and opposite signaling,
that originates from the contraversive hyperpolarized horizontal canal afferents, activates type I
inhibitory neurons within the contraversive VN.
The activation of the type II inhibitory neurons in the contraversive VN, in combination with
the activation of the type I inhibitory neurons, is
critical to the augmentation of the weak peripheral input. The increased activation of contraversive type II neurons, via the commissural fibers,
provides an indirect decrease in the activation
of type I excitatory neurons on the hyperpolarization side — that is, type II inhibitory neurons
exert increased inhibition on the contraversive
type I excitatory neurons. This occurs because the
increase in contraversive type II neuron activation
(increased inhibition) serves to reduce the excitatory nature of the type I excitatory neurons on
the hyperpolarization (inhibition) side, thus creating an even more inhibitory environment. This is
particularly true because type I inhibitory neurons
are concomitantly creating an inhibitory environment due to the decrease in resting neural tonic
activity signaled by the hyperpolarized periphery.
We have now reached a critical point in the
neurophysiology of the velocity storage mechanism. The next step is critical, as it pertains to a
further reduction of the contraversive type I excitatory neurons with a concomitant “augemented”
increase in the ipsiversive type I excitatory neurons. This next step in the commissural process
causes the neurophysiology of the velocity storage mechanism to become highly efficient in
augmenting weak neural responses. Because the
contraversive type
II inhibitory neurons have
reduced the activity of the contraversive type I
excitatory neurons, and because these contraversive excitatory neurons have an analogous direct
synapse back to the type II inhibitory neurons of
the ipsiversive side, the decrease in the excitatory
activity of the contraversive type I excitatory
neurons causes a subsequent decrease in the activation of type II ipsiversive neurons via the commissural pathways. This decrease in the activation
of ipsiversive type II inhibitory neurons (i.e., the
64 Rotational Vestibular Assessment
neurons are made less inhibitory) serves to reduce
the inhibition of the ipsiversive type I excitatory
neurons, which, in turn, allows them to further
increase their excitatory nature beyond that which
was already produced by the increase in the resting firing rate due to the depolarization of the
horizontal canal crista.
Now we have come to a neurophysiologic
moment that creates a repeating cycle; a velocity storage cycle (if you will) that effectively can,
centrally, augment a weak peripheral afferent signal. As the ipsiversive type I excitatory neurons
are centrally driven to a higher tonic level, (due
to a decrease in their inhibition, complements of
the inhibited contraversive type I excitatory neurons and the commissural fibers), this in turn fur-
ther activates the contraversive type II neurons
inhibitory control over the contraversive type
I excitatory neurons. This process is similar to
that of the start of our discussion regarding the
initial commissural interaction between ipsiver-
sive excitatory type I neurons and contraversive
inhibitory type II neurons. This process, in turn,
creates a repeating effect of decreased activation
of ipsiversive type II neurons causing a further increase in ipsiversive type I excitatory neurons, all
while, concomitantly creating a centrally increased inhibitory neural-state in the contraversive
vestibular nuclei. And the cycle repeats itself.
And repeats itself. And repeats itself. And so on.
Thereby, creating a positive neural feedback loop.
In summary, ipsiversive type I excitatory neurons increase their tonic activity level by activation from the periphery, in addition to reduced
inhibitory control from neighboring ipsiversive
type II inhibitory neurons, (via the commissural
fibers from the inhibited contraversive type I
excitatory neurons). This creates an eloquent synergism between type I and type II central neurons,
and is the fundamental neurophysiological structure of the velocity storage mechanism. Figure 3–4
(A–M) complements the previous discussion and
NeuronalBuildingBlocksoftheVesCbularNuclei
I
TypeIexcitaCon
II
TypeIIinhibiCon
I
TypeIInhibitory
EqualTonicNeuralBalance
I
II
I
LVN
II
I
I
II
I
II
I
II
I
I
I
I
II
I
II
I
II
I
II
RVN
I
II
I
I
I
II
I
II
I
I
I
I
II
I
I
II
TypeIIinhibitory
A.
neuronsarealways
“paired”orassociated
withatypeIexcitatory
neuron(whichsharea
commissural“neural
link”withacontralateral
typeIexcitatoryneuron
FIGURE 3–4. A–M. Progressive stages associated with process of velocity storage. Large boxes
represent the right and left vestibular nuclei. continues
I
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TypeIexcitaCon
II
TypeIIinhibiCon
I
TypeIInhibitory
StaCcHeadPosiConing
EqualNeuralSymmetry
EqualTonicNeuralBalance
I
II
I
LVN
II
I
I
II
I
II
I
II
I
I
I
I
=
II
I
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I
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I
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RVN
I
II
I
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I
I
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I
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I
II
DuringstaCchead
B.
posiCons,thereexistsan
equalcentraltonic
neuralbalancethatis
governedbytheresCng
firingratefromthe
periphery,whichis
approximately90neural
spikes/second.
FIGURE 3–4. continues
65
VNNeurophysiologyDuringHeadTurn
(VelocityStorage)
I
TypeIexcitaCon
II
TypeIIinhibiCon
I
TypeIInhibitory
HeadTurntotheRight
AcCvaConofthe
D.
ipsiversivetypeI
excitatroyneurons
increasestheacCvaCon
ofthecontraversive
typeIIinhibitory
neuronsthroughthe
commissuralfiber
network
DecreasedAfferent
NeuralAcCvity
II
I
I
LVN
II
I
I
II
I
II
I
II
I
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RVN
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VNNeurophysiologyDuringHeadTurn
IncreasedAfferent
NeuralAcCvity
I
TypeIexcitaCon
II
TypeIIinhibiCon
I
TypeIInhibitory
DecreasedAfferent
NeuralAcCvity
FIGURE 3–4. continues
(VelocityStorage)
HeadTurntotheRight
II
I
I
LVN
II
I
I
II
I
II
I
II
I
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RVN
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AcCvaConofthe
E.
contraversivetypeII
inhibitoryneurons
increasestheirnatural
inhibitorycontrol
IncreasedAfferent
NeuralAcCvity
66
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FIGURE 3–4. continues
67
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