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VNNeurophysiologyDuringHeadTurn

(VelocityStorage)

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HeadTurntotheRight

H.

contraversiveneurons inhibits/decreasesthe acCvaConofthe ipsiversivetypeII inhibitoryneurons throughthe commissuralﬁber network

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VNNeurophysiologyDuringHeadTurn

(VelocityStorage)

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HeadTurntotheRight

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theipsiversivetypeII neuronsreleasesthe inhibitorycontrolofthe typeIIinhibitory neuronsonthe ipsiversivetypeI neurons

IncreasedAﬀerent

NeuralAcCvity

DecreasedAﬀerent

NeuralAcCvity

FIGURE 3–4. continues

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IncreasedAﬀerent

NeuralAcCvity

VNNeurophysiologyDuringHeadTurn

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

(VelocityStorage)

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controlonthe ipsiversivetypeI excitatoryneurons furtheraugmentsthe excitatoryenvironment

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NeuralAcCvity

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VNNeurophysiologyDuringHeadTurn

(VelocityStorage)

ThisincreasedexcitaConof

K.

I

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TypeIIinhibiCon

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HeadTurntotheRight

theipsiversiveexcitatory typeIneuronscreatesan augmented“neuraldrive” wheretheprocessrepeats itselfbyfurthersuppressing theinhibitorycontrolon thecontraversivetypeII neurons

IncreasedAﬀerent

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DecreasedAﬀerent

NeuralAcCvity

I

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FIGURE 3–4. continues

IncreasedAﬀerent

NeuralAcCvity

VNNeurophysiologyDuringHeadTurn

(VelocityStorage)

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drive”cycleisrepeated –thisprocessisknown asvelocitystorage mostacCveduringlow frequencyacceleraCons

Muchofthiscommissuralprocessis

governedthroughthecerebellum(nodulus/

ventraluvula)

VNNeurophysiologyDuringHeadTurn

I

TypeIexcitaCon

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M.

asis

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RepeaCngcycleof commissuralinhibiCon createsaugmented inhibitory(leB)and excitatory(right) environments

FIGURE 3–4. continued

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3. Anatomy and Physiology of the Central Vestibular System, Velocity Storage, and Central Compensation 71

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illustrates the various stages that occur during velocity storage.

Positive Feedback Loop. This process of afferent

augmentation (and preservation of the neural response), however, is not limitless or self-sustaining. Rather, the positive feedback loop is heavily mediated by the nodulus of the vermis and the vestibulocerebellum (Barin & Durrant, 2000; Curthoys & Halmagyi, 1996). Of course, we now know that the net effect of this positive feedback loop effectively augments a weak afferent signal beyond the primary peripheral input and is termed velocity storage (Baloh & Honrubia, 2001; Curthoys & Halmagyi, 2007; Markham, 1996). Augmentation of weak peripheral afferent signals is vital to the accurate perception and integration of low-frequency head movement, or more speciﬁcally, low frequency accelerations that are below

0.05 to 0.1

Hz (Highstein, 1996). Fundamentally, the process of velocity storage primarily exists to extend (or increase) the sensitivity (gain) of low frequency stimuli where the effectiveness of the VOR is less efﬁcient in transducing slow acceleration stimuli (Highstein, 1996). This loss of efﬁciency is primarily due to a decrease in the tuning of vestibular afferents below 0.1 Hz (as eluded to earlier in Highstein, 1996). Although there is some debate as to the degree of functional consequence that exists when the efﬁciency of the velocity storage no longer exists due to vestibular pathology, this concept is further discussed in Chapter 6.

The dependency on velocity storage mecha-

nisms for stimulus frequencies greater than 0.1

Hz is essentially zero. That is because the cupulae are accelerometers and respond (deﬂect) well to higher frequency stimuli. As the pendular model of semicircular canal function would dictate, deﬂection of the cupulae and underlying hair cells for more robust stimuli (>0.1 Hz) produces an afferent neural ﬁring rate (drive) that is sufﬁcient, by itself, to drive the VOR. Therefore, central augmentation is not needed for such mid-to-high frequency stimuli. It is only during low frequency accelerations that velocity storage mechanisms are required to augment an impuissant neural afferent drive that is, otherwise, not an issue with higher (more robust) frequency stimuli. This concept of

the vestibular afferent drive being a frequency dependent system is discussed and detailed again when reviewing VOR outcome measures (speciﬁcally VOR phase) during sinusoidal acceleration testing in Chapter 6.

Aside from the velocity storage mechanism extending the sensitivity of low frequency stimuli, this positive feedback loop can also manage tonic neural activity during conditions of sustained peripheral input. Most often, the vestibular system is subjected to brief head movements similar to those that occur during ambulation or conversations. However, the peripheral vestibular system can, at times, be subjected to sustained peripheral input such as that during sustained body rotation (ﬁgure skater or playing “dizzy bats”) or even during amusement park rides. This sustained peripheral afferent input must be appropriately managed by the central system, which also falls under the control of the velocity storage mechanism. As clinicians and researchers, we can also make use of this type of sustained stimulus and response scenario, which we will present in Chapter 7 when discussing velocity step testing.

Velocity Storage Dependency. The synergis-

tic process of velocity storage is complex and highly dependent on the integrity of certain neural processes and anatomical structures. As previously noted, commissural vestibular ﬁbers are undoubtedly essential for this process, because sectioning of commissural ﬁbers abolishes velocity storage (Leigh & Zee, 2006). Also paramount to this process is the effective down-regulation from the cerebellum, most notably from Purkinje cells within the cerebellar nodulus and uvula (Curthoys & Halmagyi, 1996; Highstein, 1996; Leigh & Zee, 2006). Finally, velocity storage is also dependent upon afferent signals from the vestibular periphery sensory end organs. Sectioning of the vestibular nerve or peripheral sensory end organ damage (either unilateral or bilateral) essentially abates velocity storage and signiﬁcantly shortens the neural output from the VN, similar to that of cupular mechanics or process alone (to be reviewed in Chapter 7 when discussing velocity step testing) (Leigh & Zee, 2006). Collectively, these mechanisms or processes are

72 Rotational Vestibular Assessment

not only responsible for producing velocity storage but are also essential for ensuring effective compensation of the vestibular neural balance following unilateral vestibular insult.

Vestibular Compensation

Vestibular compensation refers to the restoration of symmetry in the central neural tone between the vestibular nuclei following unilateral peripheral vestibular insult (Barin & Durrant, 2000). On a gross level, central compensation involves a series of steps, or processes, that occur at different rates, and at different degrees and stages. Speciﬁcally, static compensation will occur at a much faster rate than that of dynamic compensation, where motion-induced activity on asymmetric labyrinths exponentially complicates the central integration required to achieve and maintain neural rebalancing (Curthoys & Halmagyi, 2007). This is particularly true for low frequency information where velocity storage heavily contributes to the VOR response. Furthermore, the success of vestibular compensation is dependent on a number of physiologic factors. Such factors include commissural efﬁciency between the vestibular nuclei, effectiveness of cerebellar control (i.e., clamping) of the vestibular nuclei, adaptation of disinhibited contralesional excitatory activity, orbital position, changes in neural activity due to gaze changes, reweighting of spinal inputs, synaptogenesis (slow, long-term process), and denervation sensitivity (slow, long-term process) (Curthoys & Halmagyi, 1996; Zee, 2007). In short, because neurons located within the vestibular nuclei receive so many afferent ﬁbers other than the peripheral vestibular labyrinths (cerebellum, spinal, cortical, brainstem), the processes that modulate and regulate the recovery of neural symmetry are often complicated and sometimes slow to succeed.

Static Compensation

To understand the process of static central vestibular compensation, it is vital to understand the neurophysiologic basis of excitatory and inhibitory interactions of type I and type II neurons within

the vestibular nuclei (see discussion on velocity storage). Following acute vestibular insult, the average resting neural discharge rate of the VN on the intact side increases due to the lack of inhibition from the ipsilesional labyrinth (Barin & Durrant, 2000; Curthoys & Halmagyi, 2007). Concomitantly, the higher resting rate of intact VN only serves to further “silence” or inhibit the lesioned side. This, of course, is best illustrated by using the fundamental neurophysiological constructs that we just discussed for velocity storage and the inhibitory commissural network.

Following a unilateral peripheral vestibular lesion, the ipsilesional type I excitatory neurons are substantially reduced. Recalling the direct synaptic projections to the contralesional type II inhibitory neurons, the pathologic reduction of the ipsilesional type I excitatory neurons causes a decrease in the activation of the contralesional type II inhibitory neurons (i.e., less inhibitory control). Given the intimate neighboring relationship between the contralesional type II inhibitory neurons and the contralesional type I excitatory neurons, the reduction in activation of the contralesional type II inhibitory neurons (decrease of inhibitory control over the type I excitatory neurons) causes a subsequent increase in the tonic excitation level of the contralesional type I excitatory neurons, which occurs despite the lack of any head rotation or movement. This neurophysiologic process is what primarily drives the contralesional side to a higher tonic resting ﬁring rate, some level above the normal 90 neural spikes per second. However, the deleterious and insidious neurophysiologic process is not yet ﬁnished. Because the contralesional type I excitatory neurons have now assumed a higher level of tonic activation, they in turn project an increase in activation across the commissural network to the ipsilesional type II inhibitory neurons that are directly synapsed to their neighboring ipsilesional type I excitatory neurons, the very same type I excitatory neurons that have been negatively impacted due to the peripheral pathology. This signaling for an increase in activation of the ipsilesional type II inhibitory neurons only serves to increase their inhibitory control over the ipsilesional type I excitatory neurons, which in turn subsequently

3. Anatomy and Physiology of the Central Vestibular System, Velocity Storage, and Central Compensation 73

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drives their tonic neural activity even lower, if this is even possible (Curthoys & Halmagyi, 2007). Of course, this cycle of further-and-further inhibition of the ipsilesional type I excitatory neurons and increase in tonic excitation of the contralesional type I excitatory neurons will continue in a vicious cycle, similar to the process of velocity storage; thus continuously driving a higher level of tonic neural ﬁring rate in the contralesional VN concomitant to a decreasing level of tonic neural ﬁring rate in the ipsilesional VN.

Neural Clamping. As our discussion on velocity

storage would previously suggest, this cyclical commissural process, albeit pathological, would propagate and persist unless otherwise interrupted and regulated. Such regulation has been identiﬁed (at least in rats) within the cerebellum, speciﬁcally from the nodulus of the caudal vermis and the ﬂocculi during periods of early central vestibular asymmetry (Kitahara et al., 1998; Kitahara, Fukushima, Takeda, Saika, & Kubo,

2000). This intervention has been termed “neural clamping,” which involves the down regulation of neural activity within the intact VN (Barin & Durrant, 2000; Curthoys & Halmagyi, 2007). Evidence shows that a reduction in the efﬁciency of the neurotransmitter receptor for gamma-aminobutyric acid (GABA) on the type I excitatory neurons on the intact side would allow for greater (recovery) activity of ipsilesional type I neurons. This is because ipsilesional type I excitatory neurons would not be affected by as much inhibition from their synaptic neighboring type II inhibitory neurons due to a decrease (or elimination) of inhibition signaling from the now “stabilized” contralesional type I excitatory neurons (Curthoys & Halmagyi, 2007). In fact, this process of “neural clamping” can be clinically induced within hours of a non-pathologic vestibular asymmetry, such as that from sustained unilateral vestibular stimulation (Barin & Durrant, 2000). Within a week of a

unilateral vestibular lesion, neural activity from the type I excitatory neurons can be measured within the vestibular nuclei from the lesioned side. Supplemental evidence has also shown this “neural regeneration” to originate not from the afferent periphery, but rather from other sources within the CNS (Barin & Durrant, 2000).

During the later stages of asymmetric central repair, a progressive increase and rebalancing in neural activity is observed as the “neural clamping” from the cerebellum is adapted and modiﬁed. Kitahara and associates (1998; 2000) have proposed that neurons in the ﬂocculus may regulate the “hyperactive” type I excitatory neurons in the intact vestibular nucleus. In turn, and more importantly, this action would serve to regulate the inhibition of the type I excitatory neurons in the ipsilesional side, (via a reduction in the inhibition of the ipsilesional type II inhibitory neurons), thus allowing for a restoration of type I neural activity in the absence of any afferent peripheral input from the damaged labyrinth. This process likely continues and is continually modiﬁed by the cerebellum until the neural activity of the “clamped” contralesional side returns to prelesioned levels, and a symmetrical central neural tone is restored between the two vestibular nuclei. Figure 3–5 (A–V) complements the previous discussion on static compensation, and illustrates the various stages that occur during the compensation process.

This process of central compensation is most stable and effective when the lesion is stable and the environment (individual) is static. In fact, the process of static compensation is extremely robust, and very little appears to hasten or hinder it (Curthoys & Halmagyi, 2007). Conversely, the restoration of dynamic equilibrium, or the process of dynamic compensation, is much more complex and involves the integration of all systems involved with movement, such as the vestibulocollic reﬂex and the autonomic reﬂex system.

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FIGURE 3–5. A–V. Progressive stages associated with process of central vestibular compensa-

tion following a unilateral vestibular lesion. Large boxes represent the right and left vestibular nuclei. Smaller vertical rectangles (two ﬂanking each bottom side) represent the hypothetical level of neural tonic activity within the peripheral (P) and the central (C) vestibular systems. continues

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Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

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

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    





  

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

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

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   “”    

Higher



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

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FIGURE 3–5. continues





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



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

 

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“”     “ ”  





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

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

Higher



 

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  “ ”      





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FIGURE 3–5. continues

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

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/



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       

Higher

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

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         





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FIGURE 3–5. continues



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