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_4433_Библиотеки_им_академика_М_И_Перельмана
.pdf
174 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
center for 25 cycles at a frequency of 2 Hz. If a passive procedure is being employed, the same procedures
described for the active test should be undertaken;
however, in this case the examiner rotates the subject’s
head at the same frequency. The test is best performed
as a passive procedure (VEDGE, 2014). The passive
procedure allows the examiner to control the head
position, excursion, and frequency during shaking, as
well as the stillness of the head post-shaking.
A positive head-shake test can produce HSN with
three different qualitative characteristics (Hain & Spindler, 1993). First, the HSN can be monophasic or biphasic (i.e., it changes direction as it decays). Second, the
HSN can beat toward or away from the impaired side.
Finally, there can be a vertical component to the HSN,
which is referred to as cross-coupled nystagmus.
Results
Normal Result
Following head shaking, there are less than three beats
of post HSN.
Abnormal Result
The presence of post HSN is considered a pathologic
sign of imbalance in the vestibular inputs in the plane
of rotation. In most instances, a peripheral cause is
identified with the fast phase of the nystagmus directed
toward the side with increased neural firing. A small
reversal phase is sometimes observed. Signs of central
etiology include prolonged, vertical, and disconjugate
nystagmus.
Mechanism
in a single direction, there is an initial increase in neural
activity from vestibular afferents corresponding to the
initial deflection of the horizontal SCC cupula due to
angular acceleration. As the rotation is maintained but
acceleration drops to zero, the cupula slowly returns
to its neutral position due to the elasticity of the organ.
At this point, afferent activity in the nerve decreases
(Goldberg & Fernandez, 1971). These neural responses
are often described in terms of their time constant.
Time constant is defined as the interval after the onset
of a stimulus for the response to decline to 37% of the
initial value (Leigh & Zee, 1999). The time constant of
vestibular nerve fibers innervating the horizontal SCC
is approximately 6 s. However, the time constant of the
VOR (i.e., the compensatory eye movement generated
in response to stimulation of the horizontal SCCs) is
approximately 16 s. VS causes the VOR to persist two
to three times longer than the neural “drive” from the
periphery. Several groups have attributed a central
vestibular system construct called the “neural integrator” to account for this difference in the response
times between the VOR and peripheral neural activity
(Cohen, Henn, Raphan, & Dennett, 1981; Cohen, Matsuo, & Raphan, 1977; Raphan et al., 1979).
In patients with a unilateral peripheral vestibular
weakness, Hain et al. (1987) suggest that as the head
is oscillated side to side, there is an asymmetry in the
magnitude of peripheral neural input that results in an
asymmetric “charging” up of the neural integrator system. During each half-cycle of head movement toward
the impaired side, there is a lower level of neural activity transmitted to the central vestibular system than
when the head is rotated toward the intact side. Once
the head is stopped, the stored activity in the VS system
will discharge slowly through the VOR pathway and
produce HSN.
A popular and accepted theory regarding the mechanism for the peripheral pattern of HSN has been set forth
by Hain, Fetter, and Zee (1987). This theory combines
Ewald’s second law of canal function and the concept
of an asymmetrically charged velocity storage system.
Ewald’s second law states that ampulopetal endolymph
flow in the horizontal canal results in a greater electrical
output than ampullofugal endolymph flow.
HSN cannot be explained by Ewald’s law alone
because the law does not account for any nystagmus
that may persist after completion of the head shake.
The nystagmus that occurs when the head is abruptly
stopped after oscillating is thought to be due to a
central phenomenon known as velocity storage (VS)
(Raphan, Matsuo, & Cohen, 1979). When the head is
rotated at a constant velocity during earth-axis rotation
Test Performance
It is well known that HSN can occur in patients with
both peripheral and central vestibular system disorders. What is disputed is the sensitivity of the headshaking test to UVH, and how large of an asymmetry
must there be to observe HSN.
In this regard, Hain et al. (1987) examined patients
with complete unilateral loss of peripheral vestibular
function. This group of patients exhibited HSN with a
velocity of approximately 20 deg/s and a time course
lasting approximately 20 s with a small reversal lasting
an additional 100 s. The addition of a vertical component or “cross-coupling” was occasionally observed,
but was usually small if seen at all. Vertical head shaking has also been reported to elicit horizontal nystag-
9. BEDSIDE ASSESSMENT OF THE VESTIBULAR SYSTEM 175
https://t.me/medicina_free
mus that beats toward the impaired side (Hain et al.,
1987; Moritz, 1951). In peripheral disorders, it has
been shown that the amplitude of the nystagmus will
increase with an increased number of oscillations of the
head up to 30 cycles.
For the HSN test to be useful it must have a high
specificity and sensitivity. The number of patients
reporting to a dizziness clinic who will have complete
unilateral loss of vestibular system function will be rare
table 9–3. Comparison of Studies Evaluating the Head-Shake Test
Study n Controls Disorder Condition Sensitivity Specificity
Hain, Fetter, &
(1987)
Wei, Hain, & Proctor
(1989)
Vicini, Casani, &
Ghilardi (1989)
Takahashi,
Fetter, Koenig, &
Dichgans (1990)
Zee
6 7 Complete UVH Peripheral
108
277 73 Patients referred for
16 UVH 90% 64%
Dizziness No bilateral
ENG
in comparison to those presenting with varying degrees
of loss. Research pertinent to the sensitivity and specificity of the head-shake test in groups of patients who
have different degrees of peripheral dysfunction is presented in Table 9–3.
The studies in Table 9–3 demonstrate the variability and sensitivity of the head-shake test in groups of
patients with different degrees of vestibular weakness.
Although the research supports the notion that with
100% 43%
vestibular lesion
40% 60%
weaknesses
29% 90%
Hall & Laird (1992) 340 20 Dizziness 50%
Jacobson,
Newman, & Safadi
(1990)
Burgio, Blakley &
Myers (1991)
Goebel & Garcia
(1992)
Fujimoto, Rutka, &
Mai (1993)
Harvey, Wood, &
Feroah (1997)
Tseng & Chao
(1997)
Guidetti, Monzani,
& Civiero (2002)
Iwasaki, Ito, Abbey,
& Murofushi (2004)
116
115 17
214 Dizziness UVH
259
105 Dizziness 35% 92%
258 Canal paresis 90% 53%
273 Confirmed peripheral
132 Dizziness Six months of
Dizziness 27% 85%
Dizziness 44% 65%
B
VH
Vestibular weakness >20% UVH
UVH
>40%
>60% UVH
>80% UVH
Overall
Initial visit 74% Could not
weakness
recovery
42%
18%
50%
64%
68%
77%
49%
66 Could not
85%
85%
73%
72%
71%
70%
calculate
calculate
Totals 2219 117 UVH >20% 56% 71%
176 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
increasing peripheral vestibular system loss the sensitivity of the HSN test increases, there is no agreed on
criterion of how much loss is needed to observe a positive head-shake test. When utilizing the head-shake as
a screening tool for unilateral vestibular dysfunction,
the presence of HSN is a good indicator that the patient
should be referred for quantitative testing. The absence
of HSN but a case history positive for dizziness would
also warrant a referral for a complete balance function
assessment. However, the head-shake test in isolation
appears to be a poor predictor of low and moderate
levels of vestibular hypofunction. The body of research
(see Table 9–3) suggests that the head-shake test, therefore, should be used in conjunction with other bedside
tests or formal balance function testing.
A modification of the head-shake test (head-shaking tilt suppression) has been proposed by Zuma e
Maia et al. to assist with differentiating UVH from central pathology (Zuma e Maia, Cal, D’Albora, Carmona,
& Schubert, 2017). Tilting the head down after the
head-shake test suppressed the induced angular slow
phase velocity by more than 50% in individuals with
peripheral vestibular lesions. Individuals with central
vestibular lesions, however, had very little ability to
suppress the HSN. In patients with UVH, tilting the
head down suppresses the HSN via influence of the otolith organs. In patients with central pathology, there is
impairment of the otolith mediation on the VS system.
The VEDGE task force determined that the HSN
test was Reasonable to Recommend at this time for
patients with acute (zero to six weeks) and chronic
(greater than six weeks) vestibular disorders (Scherer
et al., 2014). The head-shake test was Reasonable to
Recommend at this time for patients with peripheral
or central dysfunction. The low sensitivity (22.5%
reported by Vicini, Casani, and Ghilardi [1989]) precluded a higher recommendation for use in diagnosing central vestibular dysfunction. Considering the
findings of the head-shake test in conjunction with
those of the HIT might be helpful during the bedside
assessment. The task force gave an Unable to Recommend at this time rating for use of the head-shake test
in individuals with BPPV.
DYNAMIC VISUAL ACUITY
TEST–(NON-INSTRUMENTED)
Introduction
Head movements may evoke dizziness or visual
blurring in patients with either unilateral or bilateral
vestibular hypofunction. This perception of objects
“bouncing” or “blurring” when the head is moving has
been termed oscillopsia, meaning “oscillating vision”
(Brickner, 1936). It can often be attributed to a defect in
the VOR. One of the primary functions of the VOR is
to keep the retina (fovea) stable on an object of interest
when the head is moving. When the vestibular labyrinths sense head movement, they produce (by way of
the VOR) equal and opposite compensatory eye movements that keep the eyes steady. This vestibular-driven
reflexive process allows the observer to retain visual
acuity with head movement and is known as dynamic
visual acuity (DVA) (Miller & Ludvigh, 1962). The VOR
is extremely precise and requires only a few degrees
of error per second between the retina and the target
to significantly degrade visual acuity and result in
oscillopsia (Westheimer & McKee, 1975). Barber (1984)
suggested that an examiner may be able to identify
an underlying vestibular disorder if DVA was abnormal. The “oscillopsia test” was his initial description
of a method to quantify the performance of a patient’s
DVA. This very simple test permitted the quantification of a patient’s visual acuity with and without oscillation of the head. The premise was that if there was
damage to the VOR, then a patient’s visual acuity
would be poorer with head movement than without.
Throughout the years there have been many variations
on the original oscillopsia test, or as it is often termed,
DVA test. For the purposes of this chapter it is referred
to as DVA.
Technique
It is suggested that commercially available computerized DVA systems greatly increase the sensitivity
of the test to vestibular dysfunction (Herdman, Tusa,
Blatt, Suzuki, Venuto, & Roberts, 1998). However, as
these systems are not available in all settings, a standard protocol that can be performed in most clinics
is described. The patient should perform the following test with best corrected vision (i.e., while wearing
glasses or contacts). First, position an Early Treatment
Diabetic Retinopathy Study (ETDRS) eye chart at a prescribed distance (typically 2.44 to 4 m). The threshold
is defined as the lowest line read without error. Gently
grasp the patient below the malar eminences and over
the parietal region and oscillate the head at a frequency
of 2 Hz and less than 20 degrees of arc displacement in
the yaw plane (Figure 9–2). The direction of line reading should be alternated to control for memorization
and the examiner must be careful not to pause when
the direction of head rotation is changed.
9. BEDSIDE ASSESSMENT OF THE VESTIBULAR SYSTEM 177
https://t.me/medicina_free
A
B
figure 9–2. A. An image illustrating correct hand placement for a patient
being tested during the dynamic visual acuity test. B. View from the
patient’s perspective while dynamic visual acuity is being assessed.
178 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
Results
Normal Result
A drop in best-corrected vision of no more than two lines
from baseline acuity with head rotation is obtained.
Abnormal Result
A drop in best-corrected vision of three or more lines
from baseline acuity with head rotation is obtained.
Mechanism
When the head is moved, the orbit of the eye moves as
well. The VOR provides a precisely calculated neural
input to contract or relax the appropriate oculomotor
muscles to adjust the eye in the orbit to retain the visual
target of interest on the fovea so that clear vision can be
maintained. Oscillation of the head left and right during the DVA test stimulates the lateral SCCs. The hair
cells in the lateral SCCs provide information regarding
rotational acceleration of the head in the yaw plane.
When the head is turned toward the right in the yaw
plane, there is an increase in neural firing rate in the
vestibular nerves on the right side and a slow deviation of the eye in the opposite direction. Simultaneously, there is a corresponding decrease in firing rate
in the afferent nerves on the left side. This asymmetry
in firing rates between the corresponding lateral SCCs
is proportionate to the acceleration of the head. The
vestibular end organs transduce this acceleration into
a neural code that the central vestibular system uses to
adjust the oculomotor muscles and move the eye in the
opposite direction of the head movement to retain the
visual target on the fovea for clear vision.
For the VOR to generate an appropriate compensatory eye movement, gain (the ratio of slow phase eye
velocity to head velocity) and phase (the temporal differ-
ence of slow phase eye velocity to head velocity) must
be accurate. When a vestibular end organ loses sensory
cells, the frequency response of the peripheral system
is reduced.
Take, for example, the case where one vestibular
end organ has been severely impaired and a large number of sensory hair cells in the lateral SCCs are damaged. With a quick head movement in the yaw plane,
fewer sensory cells respond in the damaged ear than in
a healthy ear for the same frequency. The leading ear
will produce less neural activity, which is insufficient to
drive the compensatory slow-phase eye velocity. This
would result in a head:eye movement ratio less than 1:1
and the eye would drift off target. This would result in
the eye moving to some degree with the head instead
of the normal compensatory eye deviation (via the
VOR) away from the direction of rotation of the head.
The ultimate result would be a reduction in visual acuity due to the slippage of the target from the fovea.
This relationship between the VOR and DVA
enables the clinician to make inferences regarding the
status of the vestibular system. For head movements
at frequencies above 2 Hz, or those that are associated with normal everyday movements, even a small
amount of retinal slippage during head movement can
be an indication of vestibular dysfunction. The effect
of oscillopsia is most often encountered in patients
with bilateral vestibular system hypofunction due to
ototoxicity, bilateral end-organ disease (e.g., bilateral
Ménière’s disease), or aging (Longridge & Mallinson,
1984). Patients with poorly compensated or severe
UVH can also have impaired dynamic visual acuity.
Test Performance
Results of investigations describing the ability of the
DVA test to differentiate between normal individuals
and those with vestibular disorders are mixed. When
the complete body of literature describing the use of
the DVA test to identify and quantify vestibular deficits
is examined, it becomes apparent that there are many
factors that can explain the differences in specificity
and sensitivity found between studies.
Several groups have described a positive relationship between peripheral vestibular dysfunction and
DVA performance (Demer, Honrubia, & Baloh, 1994;
Herdman et al., 1998; Longridge & Mallinson, 1984,
1987a, 1987b). In one of the first series of studies, Longridge and Mallinson (1984, 1987a, 1987b) described
a customized eye chart called the dynamic illegible E
(DIE) to assist in the detection of vestibular hypofunction. The authors designed a chart using only the “E”
from the Snellen chart oriented in different directions.
This was to control for the fact that some of the letters
in the standard Snellen chart are more readily identifiable than others. Each orientation was referred to as
an optotype. Using the DIE test procedure, the patient
indicates the direction of the optotype in each column
with the head still. This procedure was then repeated
while the patient’s head was oscillated back and forth
at a frequency of 1 Hz. The examiner recorded any
change in visual acuity during the dynamic phase of
the test.
9. BEdsidE AssEssmEnt oF tHE vEstiBulAr systEm 179
https://t.me/medicina_free
Using the DIE test, Longridge and Mallinson (1984)
reported the ability of the DVA test to screen for aminoglycoside vestibulotoxicity. A group of 8 subjects with
documented aminoglycoside toxicity were selected to
perform the DIE test. Six of these subjects were unable to
identify any of the optotypes from the DIE test with head
movement. One patient had normal caloric responses
and was able to perform the DIE test with abnormal
results, and one patient was unable to be tested due
to osteomyelitis. Interestingly, when blood serum was
monitored during therapy, none of this group had toxic
levels. According to the authors, these results provided
evidence that the DIE test was an appropriate screening
tool for aminoglycoside vestibulotoxicity.
Longridge and Mallinson (1987a, 1987b) provided
further support for use of the clinical DVA test in the
prediction of vestibular dysfunction. This investigation evaluated the relationship between DIE test performance and the magnitude of caloric reduction. The
authors recruited 244 patients with abnormal caloric
tests to undergo DIE testing. Multiple regression testing revealed a significant correlation between visual
acuity during head movement and degree of caloric
reduction. Specifically, the greater the degree of caloric
reduction, the poorer the DIE test score.
Demer et al. (1994) used a computerized paradigm
to measure DVA performance. The authors compared a
group of 13 normal subjects with 2 patients presenting
with complete bilateral vestibular system weakness.
The 2 subjects with vestibular dysfunction demonstrated reduced DVA performance compared with the
normal group. The authors suggested that DVA testing during imposed head motion is a quantitative and
clinically feasible measure of oscillopsia that reflects
functionally significant abnormalities in the VOR.
Herdman et al. (1998) presented data describing
DVA performance in patients with bilateral and unilateral vestibular deficits using a computerized system.
DVA test performance was found to be significantly
different when scores obtained from patients with
unilateral and bilateral vestibular loss were compared
with those of their normal counterparts. Furthermore,
in the UVH group, there was a significant difference
in DVA performance for head movements toward the
affected side, compared with the unaffected side. When
the authors examined the sensitivity and specificity of
the test for age-matched normal controls compared
with the patient groups, the computerized DVA test
was shown to have a sensitivity of 94.5% and specificity of 95.2%.
However, evidence from other studies fails to support the reported relationship between DVA test per-
formance and vestibular dysfunction. Burgio, Blakely,
and Myers (1992) found a poor relationship between
vestibular dysfunction and DVA performance. This
study evaluated 115 patients referred to a dizziness
clinic and compared them with 17 control subjects.
The experimental group consisted of 25 patients with
unilateral caloric weakness (25% to 100%), 10 with a
bilateral weakness (total slow phase velocity of 0 to 21
deg/s), and 80 with normal ENGs who had complaints
of dizziness. The investigators found that the DVA test
was highly specific (100%) but had poor sensitivity.
Their results suggested that the DVA test did not detect
vestibular loss or subjective dizziness in more than 50%
of the cases with significant unilateral impairment.
The inconsistency in findings among the various
studies above is due to several factors. First, differences in methodology when performing the DVA test
exist between the aforementioned studies. Computerized DVA testing systems require that the head move
at or above a critical acceleration of the head prior to
exposure to visual stimuli. This prevents the subject
from reading the optotypes when the head is slowed
to change direction. Herdman et al. (1998) employed
such a system and reported high sensitivity for DVA
testing.
A second source of variability is the frequency of
head movement during the test. The pursuit system
has been shown to contribute to gaze stabilization at
lower frequencies. Lee, Dumford, and Crowley (1997)
assessed DVA performance from 27 normal patients
using voluntary head rotation at frequencies ranging
from 0.7 to 4 Hz. The authors found that there was a
natural decrement in visual acuity with increasing
frequency of horizontal head movement. The authors
suggested that the ocular motor system becomes an
ineffective system for ocular stabilization at frequencies
above 2 Hz and that the VOR functions as the primary
control system for visual stabilization during lower
frequencies associated with ambulation. According
to their results, to obtain an accurate measure of how
well the VOR is compensating for head movement, the
head should be oscillated no slower than 2 Hz. Many of
the studies described previously were performed with
head oscillations at frequencies below 2 Hz (Barber,
1984; Longridge & Mallinson, 1984, 1987a, 1987b).
In patients with UVH, the ability to read the optotype is improved when oscillating the head toward the
intact or better end organ. In paradigms where performance is not measured for each half-cycle, this may
result in spuriously good DVA performance. This variable can be controlled by computerized DVA systems,
where left and right head movement performance can
180 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
be assessed separately, thereby increasing the sensitivity of the test to unilateral end organ dysfunction.
A fourth source of interstudy variability is the
method used to calculate the DVA score. The two common methods are the traditional Snellen distance 20/
XX system (i.e., 20/20, 20/100, etc.) and the LogMAR
scale. Computerized DVA systems typically use the
measurement parameter “logarithm of the minimum
angle of resolution” or LogMAR. The LogMAR scale
is a conversion method that transforms the geometric
sequence of a traditional Snellen chart to a linear scale.
The LogMar scale describes performance as visual
acuity loss. Specifically, vision loss is represented by
a positive score, whereas better visual acuity is represented by a negative score. Many of the earlier studies
discussed above have described DVA performance by
indicating how many lines of the Snellen chart visual
acuity dropped with head movement. This interpretation of lines lost is only accurate when all steps
between lines are equal, which is not the case in the
Snellen chart. For this reason, use of an ETDRS eye
chart is recommended.
A fifth variable to consider in assessing the sensitivity of DVA is the degree of vestibular system compensation patients with UVH have attained. Herdman,
Schubert, Das, and Tusa (2003) reported the effect of
vestibular exercises on the recovery of DVA in patients
with UVH. The sample consisted of 21 patients with
UVH who were culled from an ambulatory referral center. Of this total, 13 of the patients performed
vestibular exercises designed to increase VOR gain,
whereas 8 of the patients performed placebo exercises.
Subjects in the treatment group receiving vestibular
exercises showed a significant improvement in DVA
performance, whereas those performing the placebo
exercises did not. In contrast, Longridge and Mallinson (1987a, 1987b) used the conventional DVA test to
explore the relationship between DVA performance
and central nervous system compensation. The factors
of age, degree of caloric impairment, and time from
onset of disease process were compared with scores
from the DIE test. The investigators found no correlation between DIE test performance and central vestibular system compensation.
The clinical utility of the DVA test appears to be
influenced somewhat by technique and experience of
the examiner. The non-instrumented DVA test using an
ETDRS eye chart can be extremely useful in predicting
severe vestibular dysfunction. Specifically, the clinical
utility has been proven when the examiner suspects
bilateral vestibular dysfunction from aminoglycoside
vestibulotoxicity or a severe unilateral lesion (Burgio
et al., 1992; Demer et al., 1994; Longridge & Mallinson,
1984). However, computerized DVA systems, although
superior, are not always available in all balance clinics.
They allow the examiner to document central nervous
system compensation after rehabilitation, predict the
side of the lesion in unilateral involvement, and grossly
quantify the severity of bilateral vestibular hypofunction. As part of the National Institutes of Health Toolbox for the Assessment of Neurological and Behavioral
Function, a computerized DVA test was developed that
is valid, easy to administer, time- and cost-efficient
(Rine et al., 2012, 2013). Regardless of the system used,
it is important that whenever the results from the DVA
test are abnormal, a full balance function workup
should be recommended. When results are determined
to be normal, the referral should be made based on a
thorough case history.
The VEDGE task force determined that the noninstrumented DVA test was Reasonable to Recommend
at this time for patients with acute (zero to six weeks)
and chronic (greater than six weeks) vestibular disorders (Scherer et al., 2014). Serial testing may be useful to gauge the degree of rehabilitation effectiveness
(central compensation). The non-instrumented DVA
test was Reasonable to Recommend at this time for
patients with peripheral or central dysfunction, and
may be useful during the bedside assessment to corroborate HIT and HSN findings.
VALSALVA-INDUCED NYSTAGMUS
Introduction
The self-induced change of middle ear and intracranial
pressure commonly known as the Valsalva maneuver
(VM) is capable of inducing eye movements in patients
with craniocervical junction abnormalities and disorders affecting the inner ear. These anomalies may
include Arnold–Chiari malformation, perilymphatic
fistula, superior canal dehiscence, and other anomalies that involve the oval window, round window, saccule, or ossicles. The VM is named in honor of one of
its early proponents, Antonio Mario Valsalva (1666–
1723), although documentation of the technique exists
from the sixteenth century and earlier as a treatment
for deafness and method for removing foreign bodies
from the ear canal (Lustig & Jackler, 1999). Hennebert
first described eye movements induced by changes
in middle ear pressure in the early twentieth century.
This phenomenon is now known as Hennebert’s sign
and describes a conjugate eye movement away from
the affected ear with positive pressure applied to the
9. BEdsidE AssEssmEnt oF tHE vEstiBulAr systEm 181
https://t.me/medicina_free
external auditory meatus. A movement toward the
affected ear is expected with applied negative pressure.
The presence of such a movement allows the examiner
to deduce the presence of an anomalous connection
between the inner ear and the external environment
(Goebel, 2001).
Technique
Two variants of the VM should be performed by the
patient: one designed to increase air pressure in the
sinuses and middle ear, the other designed to increase
venous pressure in the cranium. In both cases, the subject should wear Frenzel or VNG goggles to prevent
VOR suppression and to permit the observation and
documentation of eye movements (Zee & Fletcher,
1996). The patient also should be instructed to report
any sensations of dizziness or vertigo induced by the
test procedure, including blurred vision, oscillopsia,
or diplopia (Brandt & Strupp, 2005). Eye movements
should be observed during and immediately following pressurization and relaxation for both tests. The
positive air pressure variant is performed by increasing barometric pressure in the sinuses, middle ear, and
pharynx. Patients should be instructed to take a deep
breath, pinch the nose, and close the mouth tightly,
then blow as if equalizing the pressure of the ears when
descending from altitude on an airplane. The patient
should maintain the pressure for 10 to 15 s. The result
is an increase in middle ear pressure (Walker & Zee,
2000). Following recovery from any elicited responses,
the patient should strain against a closed glottis and
lips for a similar duration, as if pressurizing the lungs
to help stabilize the trunk while lifting a heavy weight.
This variant serves to raise the intracranial pressure by
inducing increases in central venous pressure (Walker
& Zee, 2000). Either or both techniques may induce
nystagmus in patients with the anomalies described
above, and both should be included in the bedside
test battery.
Results
Normal Results
Although Hennebert’s sign has been reported in normal subjects, the VM should not elicit sensations of dizziness or vertigo in the great majority of patients. The
examiner, therefore, should be careful to distinguish
between a shift of the eyes (positive Hennebert’s sign)
and nystagmus. No elicited conjugate eye movements
should be observed under Frenzel or VNG goggles.
Abnormal Results
Increased middle ear or intracranial pressure as a
result of either variant of the VM will elicit a conjugate movement of the eyes toward the contralesional
ear in the cases of lateral and anterior canal involvement. If the patient maintains increased intracranial
pressure, a corrective saccade toward the ipsilateral ear
will be observed. Thus, nystagmus will “beat” toward
the affected ear. The direction of the fast phase of nystagmus may provide information regarding the site of
lesion. Horizontal nystagmus indicates involvement of
the lateral semicircular canal and will beat toward the
affected ear. Torsional and down-beating vertical nystagmus indicates a site of lesion in the anterior canal,
whereas torsional and up-beating vertical nystagmus
suggests involvement of the posterior canal (Davies,
2004). The direction of torsion provides information
regarding the laterality of the lesion; the fast phase of
the torsional nystagmus will beat in a clockwise direction for lesions of the left ear and a counterclockwise
direction for lesions of the right ear.
Mechanism
Increased pressure in the middle ear acts on abnormal
connections between the labyrinth and the external
environment to induce a pressure gradient within the
cochlea. These abnormalities may exist as a hypermobility of the oval and round window membranes,
defects of the bony structures surrounding the lateral
aspect of the membranous labyrinth such as erosion
due to cholesteatoma or chronic otitis media leading
to dehiscence or fistula of the posterior or lateral canal,
or defects of the floor of the middle cranial fossa leading to superior canal dehiscence (Brandt & Strupp,
2005; Goebel, 2001). The increased pressure within the
affected labyrinth simulates movement of the head as it
stimulates neural firing by displacing the cupula of the
semicircular canal. The increased neural discharge rate
drives the VOR such that a compensatory eye movement away from the affected ear is generated (Hennebert’s sign).
In the case of straining against a closed glottis,
increased pressure within the middle fossa is generated
through changes in central venous pressure. Increasing and maintaining pressure within the thoracic cavity decreases venous return through the jugular vein,
thereby raising intracranial pressure (Minor et al.,
2001). An abnormal connection between the middle
fossa and the vestibular labyrinth such as occurs in the
case of superior canal dehiscence will induce a pressure
182 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
change in the affected canal and elicit down-beating,
torsional nystagmus beating toward the affected ear.
Conversely, a dehiscence of the posterior canal will
elicit up-beating and torsional nystagmus with the
fast phase oriented toward the affected ear (Brantberg,
Bagger-Sjoback, Mathiesen, Witt, & Pansell, 2006).
Test Performance
A review of the literature suggests that the Valsalva
test is useful in screening for the presence of canal
dehiscence and perilymphatic fistula. The phenomenon, however, has also been reported in the presence
of several other disorders, including cholesteatoma.
Brantberg, Greitz, and Pansell (2004) reported a case
of superior canal dehiscence where abnormal bone
development in the middle cranial fossa was not the
cause of the dehiscence. The patient exhibited pressureinduced vertigo despite the location of the dehiscence
close to the common crus. Similarly, Tilikete, KrolakSalmon, Tuy, and Vighetto (2004) reported the case of
a subject with bilateral superior canal dehiscence. In
this case, both Valsalva-induced vertigo and Tullio’s
sign could be elicited, with upward and counterclockwise torsional beating nystagmus. Halmagyi et al.
(2003) described a patient who underwent three stapedectomy surgeries despite the audiometric finding of
conductive hearing loss with preserved ipsilateral and
contralateral acoustic reflexes, symptoms of superior
canal dehiscence. The patient reported hypersensitivity to bone-conducted sounds (Tullio’s phenomenon)
and exhibited a vestibular evoked myogenic potential (VEMP) at abnormally soft sound intensities and
Valsalva-induced vertigo. Rambold, Heide, Sprenger,
Haendler, and Helmchen (2001) reported the case of a
patient who experienced VM-elicited contralateral horizontal nystagmus with the diagnosis of perilymphatic
fistula. The patient also exhibited pulse synchronous
oscillations of the eyes.
Several studies have been conducted investigating
the sensitivity of the Valsalva test. Reported sensitivity has varied. Hillman, Kertesz, Hadley, and Shelton
(2006) reported vertigo evoked by VM in only 12 of 27
(44%) subjects with superior canal dehiscence. Of the
12 subjects, 8 could elicit nystagmus during Valsalva
or simulated heavy lifting, corresponding to a sensitivity of 29%. Minor (2000) reported Valsalva-induced
nystagmus in 10 of 17 subjects (i.e., a sensitivity of 58%)
subsequently identified with superior canal dehiscence.
In a later study the VM showed 82% sensitivity in a
cohort of 28 patients previously diagnosed with supe-
rior canal dehiscence (Minor et al., 2001). Symptoms
could be evoked in some of these patients by pressing
on the tragus of the ear. The authors noted that nystagmus could continue for several beats after the release
of pressure. Cremer, Minor, Carey, and Della Santina
(2000) reported that 8 of 11 subjects with superior canal
dehiscence exhibited nystagmus following VM (i.e.,
73% sensitivity). Brantberg et al. (2001) reported that
8 of 8 (100%) subjects with superior canal dehiscence
experienced pressure-induced vertigo. The subjects
reported that the vertigo worsened during periods of
upper respiratory infection.
The presence of a positive Valsalva test, therefore,
should be considered evidence of an abnormal connection between the middle ear and the inner ear, or the
intracranial space and the middle ear.
MODIFIED CLINICAL TEST OF SENSORY
INTERACTION ON BALANCE
Introduction
There are three main systems that contribute to balance
and postural control. We use our visual system to orient
ourselves to things we know to be vertical in our world
such as door frames, windows, corners of rooms, etc.
We use input from the somatosensory system (information from joint receptions and Golgi tendon organs) to
give us information about the support surface. Lastly,
we use information from the vestibular system to gain
awareness of spatial orientation relative to gravity.
The Modified Clinical Test of Sensory Interaction
on Balance (mCTSIB) is a bedside test of postural control under various sensory conditions. The mCTSIB is a
modification of the Clinical Test of Sensory Interaction
on Balance (CTSIB) that originally used six sensory conditions, including a visual conflict dome to introduce
visual conflict (Cohen, Blatchly, & Gombash, 1993). The
mCTSIB retains conditions 1 (eyes open, firm surface),
2 (eyes closed, firm surface), 4 (eyes open, foam surface), and 5 (eyes closed, foam surface) from the original CTSIB (Figure 9–3). This test gives the examiner
insight into an individual’s ability to maintain postural
control during four different sensory conditions. It cannot be used to diagnose a vestibular disorder; however,
in the last condition with vision removed (eyes closed)
and inaccurate somatosensory input (foam surface), the
only system giving accurate sensory input is the vestibular system. Individuals with impairments in vestibular function tend to have difficulty with the eyes closed,
9. BEDSIDE ASSESSMENT OF THE VESTIBULAR SYSTEM 183
https://t.me/medicina_free
A B
C D
figure 9–3. A. Condition 1— Eyes open on a firm surface B. Condition 2 — Eyes closed
on a firm surface C. Condition 3 — Eye open on a foam surface D. Condition 4 — Eyes
closed on a foam surface.
foam surface condition. However, it must be noted that
there are many other reasons that an individual may
experience difficulty in that, or any of the other, condi-
tions. If an individual has deficits of postural control
during any of the mCTSIB conditions, a more in-depth
balance assessment is warranted.
Соседние файлы в папке Библиотека им академика М.И. Перельмана