Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4382_Библиотеки_им_академика_М_И_Перельмана
.pdf
Higher
Higher
FIGURE 3–5. continues
“”
“
”
78
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
“
”
velocitystorage,
Higher
Higher
$*((%..3-'7'%.-*&)
7+6%/0*)
7+%)$%%0*)
7+)$%%/*-7
<)'..:
*3-)?/0
$)3-'3#()/
;
-%4%.-+/A/$%.
+-*..9.%(%'-/*
+-+/3')/-'
.7((/-7
-/.
.7((/-%
-)/3-'04%/7
.7((/-%
-)/3-'04%/7
OG OGP
@
@
FIGURE 3–5. continues
79
@@@@@@PPPPP
-.?(#
-)/3-'04%/7
GG
Higher
Higher
FIGURE 3–5. continues
80
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Higher
FIGURE 3–5. continues
81
FIGURE 3–5. continues
82
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
FIGURE 3–5. continues
83
Equalcentralneural
tone
“
”
Equalcentralneural
tone
FIGURE 3–5. continues
84
3. Anatomy and Physiology of the Central Vestibular System, Velocity Storage, and Central Compensation 85
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Equalcentralneural
tone
FIGURE 3–5. continued
Dynamic Compensation
Static compensation occurs at a much more efficient
rate than dynamic compensation. Unfortunately, patients with unilateral labyrinthine damage
exhibit difficulty integrating an accurate representation of the acceleration and velocity of head
movement for some time, (even following static
compensation), due to significant end organ asymmetry. Recall that the central compensation is just
that, central. The tonic balance is within the vestibular nuclei. However, during head movement, the
statically compensated central vestibular nuclei
will continue to receive asymmetric peripheral
input. It is this end organ imbalance that, despite
effective static compensation, continues to cause
considerable problems under dynamic (head
movement) conditions (Barin & Durrant, 2000).
Rotation of the head away from the lesioned labyrinth will quickly saturate the neural response to
zero spikes per second (if the system is not already
in this state). Conversely, the excitatory afferent
response from the intact side is unaffected. Consequently, integration of the asymmetric afferent
neural signals from the unbalanced peripheral
system, even in the presence of statically compensated central vestibular nuclei, will be ineffective
in generating an appropriate central neural asymmetry necessary for detecting the precise velocity
and direction required for an effective VOR.
The solution for dynamic compensation
is much more complex. Consider that the absolute magnitude difference in vestibular input is
approximately one-half of what it used to be prior
to the peripheral insult; that is, if one peripheral
labyrinth was completely lesioned only 50%, or
1/2 of the physiology remains. During dynamic
compensation, the vestibular pathways need to be
“recalibrated” to accept and process the new “onehalf” pattern of neural firing rates. Moreover, this
86 Rotational Vestibular Assessment
must be accomplished in relation to the laterality of lesion versus the direction of head movement (either toward or away from the peripheral
lesion). This must then be appropriately integrated and transformed into appropriate compensatory eye movements, exhibiting a VOR gain
that is adequate enough so as not to produce any
perceived dizziness by the patient. Certain VOR
pathways must be “doubled” during certain head
movements to compensate for the one-half loss of
peripheral input, whereas other head movements
may not require such compensation (Barin & Durrant, 2000). Dynamic compensation often involves
additional neural adaptations that facilitate the
process such as vestibulocollic reflex pathways.
Collectively, these processes can take a considerable amount of time, which largely depends on
a variety of different factors, from the degree of
severity of the peripheral vestibular lesion, to the
age and overall health, as well as the activity level
of the patient.
The Effects of Dynamic Compensation Is Also
Frequency Dependent.
integration of neural signals during dynamic head
changes, even following static compensation, is
more pronounced for low-acceleration stimuli.
The most efficient method of increasing the overall gain or sensitivity of the vestibular system,
given that half of the system is now extinguished,
is to increase the output (lessen the restriction/
control) of the central system’s ability to integrate
and coordinate the VOR response (Barin & Durrant, 2000). This method, however, is not without
significant consequence. By increasing the overall
integration and output of the VOR pathways, less
afferent peripheral input is effectively “stored” in
the neural integrator. That is, the mechanism and
efficiency of velocity storage is significantly and
permanently reduced (if not completely modified by the cerebellum to “zero” storage) and the
ability of the central system to propagate, extend,
or augment the neural output for low-frequency
stimuli is essentially disrupted or completely lost.
Consequently, the processing and integration of
low-frequency head movements is significantly
degraded more than any other stimuli. This
helps to explain why, despite effective static and
dynamic compensation, patients with non-acute
Generally, the ineffective
unilateral vestibular lesions often perceive slight
swaying and rocking sensations while standing and sitting still (low frequency stimulation),
and feel much better upon movement (higher
frequency stimulation) (Curthoys & Halmagyi,
2007). In addition, it is not surprising to see longstanding abnormalities during vestibular testing that incorporates low-frequency stimuli (i.e.,
prolonged low frequency VOR phase leads), as
the vestibular system’s ability to integrate and
process such stimuli often remains significantly
and, quite often, permanently modified. This is
true even following effective static and dynamic
compensation, because once the mechanisms for
central velocity storage are damaged, such processes are seldom, if ever, restored (Barin & Durrant, 2000). Moreover, the repair of such processes
(velocity storage) may not even be desired, as the
consequence of returning velocity storage to its
prelesion status may have consequences in VOR
gain that are greater than the alternative. This idea
is again discussed at greater length in Chapter 6
when reviewing sinusoidal acceleration testing.
Overall, the process of dynamic compensation is likely more complex than simply increasing
the overall gain of the VOR, or modifying velocity storage. The VCR and the VSR are intimately
involved in the process of signal integration, and
their involvement is undoubtedly vital to effective
dynamic compensation.
OTHER NON-VESTIBULAR
AFFERENT / EFFERENT
PROJECTIONS
The vestibular nerve and cerebellum are not the
only sources of afferent input to the vestibular
nuclei. Many nonvestibular afferent projections to
the vestibular nuclei are known to exist; however,
the function of each source of non-vestibular afferents is not always well understood. Such sources
include the visual system, cervical and spinal
cord neurons, as well as autonomic nervous system pathways. Many of the physiologic responses
from these neural centers have been clearly shown
to be affected by behaviors and stimuli not related
to vestibular nerve activity (Lysakowski et al.,
3. Anatomy and Physiology of the Central Vestibular System, Velocity Storage, and Central Compensation 87
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
1998). The more prevalent nonvestibular afferent
signals delivered to the vestibular nuclei are from
the visual system, as well as from cervicocollic
(neck) and cervicospinal pathways.
Visual Contributions
The visual system is fundamental to posture and
overall balance function (Nashner, 1997; Peterka,
2002). It is no surprise, therefore, that the visual
system has independent projections to the vestibular nuclei. As previously mentioned, there exists
a well-known and immensely critical efferent projection from the VN to the ocular motor system,
known as the VOR. However, it is also critical that
the visual system independently project afferent
fibers to the VN. These fibers provide a redundancy to the vestibular system but more importantly, supplement the perception of movement
for low frequencies, where the vestibular system
is less efficient (Lysakowski et al., 1998). Specifically, the efficiency of the cristae and the maculae to low-frequency movements (accelerations)
at or below 0.05 Hz is rather poor (Lysakowski
et al., 1998). In fact, the relative inefficiency of the
vestibular system to such low-frequency stimuli
often creates a significant physiological problem when attempting to produce an appropriate
ocular or postural reflex response, as the integration and processing of such impuissant stimuli
requires supplemental mechanisms that can augment the insufficient response (i.e., velocity storage). Although velocity storage is the primary
mechanism that addresses this deficiency, the
visual system is another key contributor, capable
of detecting extremely low-frequency movements
of the visual scene and incorporating that in the
VOR or postural reflex response. In doing so, the
brain uses low frequency visual information to
supplement the poorly integrated information
obtained from the labyrinth (Lysakowski et al.,
1998). In short, the inefficiencies of the vestibular
system to low (and very high) frequency stimuli
are compensated quite well by the visual system.
Specifically, this visual-vestibular enhancement is
largely mediated by the optokinetic system, and
effectively integrates “movement” information to
the vestibular nuclei when the peripheral vestibu-
lar system is unable to do so. Clinical assessment
of visual-vestibular enhancement during rotational testing is discussed in Chapter 8. (Leigh &
Zee, 2006). An “everday” example of such visualvestibular interaction is the physiological perception of movement in a stationary car when one
“perceives” the slow creeping advancement of a
neighboring car at a stoplight.
One final piece of evidence to support an integral connection between the visual system and the
vestibular system is motion sickness. Many people
experience motion sickness, which is essentially a
central conflict between the integration of visual
and vestibular signals. This association provides
further evidence for the existence of independent,
yet integrated, sensory pathways.
Cervical and Spinal Contributions
The spinal cord, particularly the cervical spinal
cord, provides another source of non-vestibular
afferent and efferent signals to and from the VN
(Lysakowski et al., 1998). As mentioned earlier,
projections from the cerebellar vermis help to
coordinate neck and postural movements within
the VN. Through this network, appropriate compensatory eye movements are also coordinated in
conjunction with head and neck movements via
the vestibulospinal and spinocerebellar neural
pathways. Without this network, effective maintenance of visual and head stabilization would
not be possible. The neural tracts within the cervicospinal region where the afferent and efferent
fibers travel are known as the medial and lateral
vestibular spinal tracts, or simply, the MVST and
LVST, respectively (Lysakowski et al., 1998). The
function of each tract, however, is unique. The
MVST is merely an extension of the medial longitudinal fasciculus. Its projections terminate in
the cervical regions of the spinal cord and serve
to stabilize and centrally position the head on the
shoulders by activating neck muscles that not only
resist passive movements of the head (e.g., during
ambulation), but also generate active head movements during intentional body movements. The
lateral vestibulospinal tract extends to the lower
lumbar regions of the spinal cord and provides
a persistent excitatory synaptic input to postural
Соседние файлы в папке Библиотека им академика М.И. Перельмана