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_4606_Библиотеки_им_академика_М_И_Перельмана
.pdf
52
https://t.me/medicina_free
A. Chern and L. Lustig
Fig. 3.17 Abnormal rotary chair results. Patient with an acute unilateral vestibular lesion. Results
indicate an increased low frequency phase and a right asymmetry, suggesting an uncompensated
vestibular lesion. Phase (a), gain (b), asymmetry (c), rotation: averaged cycles (d–g)
Video HIT
The video HIT (vHIT) is a type of high-frequency rotational test that is now a standard part of routine vestibular assessment [29]. It reveals vestibular hypofunction
using measured gain reduction and the presence of covert or overt saccades as a
quick, objective, and more sensitive version of the clinical HIT.The major disadvantage of the bedside HIT is its inability to detect covert saccades that are invisible
3 Tests toEvaluate theVestibular System
https://t.me/medicina_free
to the naked eye. As a result, commercial vHIT devices have been developed to
detect covert saccades and provide quantitative measures of VOR function. The
vHIT examines VOR using active or passive rotationary head movements (i.e., like
those used in everyday life) in both vertical and horizontal planes, enabling effective
assessments of the six SCCs. The high-frequency and high-acceleration stimuli help
unmask any asymmetries in the vestibular system. Compared to rotary chair testing,
the vHIT and other high-frequency rotational tests are more cost-effective—cheaper,
shorter test time, and lack heavy machinery [30].
If VOR eye movements are not adequate to keep the eyes on the target, then the
oculomotor pathway is activated. If there is a difference between the gaze and target
position, a catch-up saccade is generated after the head comes to a stop. Since higher
brain-level movements are involved, these overt saccades have long latencies
(≥250 ms). Some patients can initiate saccades during head movements—these
covert saccades have short latencies (≤200ms) that are not visible to the naked eye
during the bedside HIT. Covert saccades are usually followed by a small, overt
saccade.
53
Equipment
Equipment comprising the vHIT includes skin electrodes or a video recording system for eye movement, a headband with a motion sensor (i.e., for head movements),
and software calculating data. Several commercial versions of the vHIT are available with varied protocols [31].
Eye movements are measured using high-speed, high-resolution cameras. Head
movements are measured using sensors embedded in cameras. The device also
monitors the clinician’s ability to deliver appropriate impulses and provides feedback to improve performance.
Test Administration andParameters
Patients are instructed to keep their eyes on a target at a xed distance in front of
them while sitting upright. Head impulses are tested along the horizontal and vertical (i.e., right-anterior left-posterior and left-anterior and right-posterior) planes.
The head is supposed to be tilted downward by 30° to create a horizontal plane;
however, an upright head position may minimize artifacts and be better for recording eye movement for horizontal impulses. The clinician performing the head
impulses should make sure they are small-amplitude (between 10° and 20°), highvelocity (peak 200°/s), high-acceleration (peak 2000–6000°/s2), and unexpected as
patients are xed on stationary targets. The video recording will be evaluated for
eye movements and catch-up saccades.
54
https://t.me/medicina_free
Parameters for vHIT include VOR gain (ratio of eye velocity to the head impulse
velocity) for each SCC (similar to the rotary chair test). For healthy subjects, the
gain is close to 1 at low frequencies and declines at higher frequencies; vHIT cutoffs
of 0.68 or 0.8 and below have been recommended for the diagnosis of vestibular
loss [29, 32]. Corrective (both covert and overt) saccades are also reported; their
presence usually suggests a peripheral vestibular disease. Corrective saccades can
be characterized by their amplitude (or velocity), latency, and frequency. The amplitude of corrective saccades generally decreases with increasing vHIT gain. Generally
speaking, higher amplitude and greater corrective saccade frequency are suggestive
of vestibular loss [33, 42]. However, greater corrective frequency has also been
shown to be associated with increasing age [39].
A. Chern and L. Lustig
Clinical Application
The vHIT provides complementary information to existing vestibular tests and may
be helpful in evaluating suspected peripheral vestibular lesions [37]. The ability to
detect covert saccades makes the vHIT better than the clinical HIT test. It provides
high-frequency information. It can be used to distinguish stroke from peripheral
vestibular disease, distinguish unilateral versus bilateral vestibular hypofunction,
and monitor vestibulotoxicity and recovery from a vestibular insult. There are limitations to vHIT.Normal vHIT does not mean normal vestibular function; other vestibular tests such as VNG/ENG and vestibular-evoked myogenic potentials (VEMPs)
may show patterns demonstrating peripheral vestibular abnormalities.
There are several valid response patterns in vHIT.A normal vHIT is represented
by the absence of signicant catch-up saccades and VOR gains near 1.0 (greater
than ~0.8 bilaterally); a few small catch-up saccades may present with high-velocity
head impulses. A vHIT for a patient with a unilateral vestibular lesion or its corresponding vestibular nerve branch will demonstrate the presence of signicant catch up saccades (overt or covert) on one side accompanied by the asymmetric gain (side
of the lesion usually <0.8). Catch-up saccades can be present for impulses away
from the side of the lesion, but these are not as large in amplitude and usually start
at higher head velocities. Initial catch-up saccades are overt, but over time, covert
saccades may develop. Covert saccades are thought to be due to central compensation [34, 35]. Spontaneous nystagmus may be confounding—these appear as spikes
in eye velocity tracings. However, these may occur before or after head impulses,
are typically smaller in velocity compared to catch-up saccades, and for nystagmus
beating away from the side of the lesion, spikes appear opposite of VOR eye movements following head impulses toward the non-affected side.
3 Tests toEvaluate theVestibular System
https://t.me/medicina_free
55
Computerized Dynamic Posturography
Computerized dynamic posturography aims to examine postural stability through
quantitative assessment of individual and integrative patterns of visual, proprioceptive, and vestibular processing. Dysfunction of any of these necessary components
of balance results in a stronger reliance on other peripheral processes to maintain
balance. The test assesses overall balance function in response to ecologically simulated tasks. Computerized dynamic posturography measures the force applied by
the body to a platform. This strain gauge force platform measures postural sway
under different test conditions with the manipulation of somatosensory and visual
feedback. Several requirements are necessary prior to testing. Patients should be
able to stand still, unassisted, with their eyes open for a minimum of 1min to complete the test. A safety harness should be fastened so that the patient can move freely
with no external support. The patient’s feet should be positioned at designated
points on the force platform.
There are three primary protocols, including the (1) sensory organization test, (2)
posture-evoked response, and (3) motor control tests. Of these, the sensory organization test is most useful in the evaluation of patients with vestibular disorders.
Sensory Organization Test
The sensory organization test evaluates if an individual can appropriately utilize
visual, vestibular, and somatosensory cues and select the appropriate cue under conicting conditions in order to maintain balance.
Test Administration andParameters
There are six sensory conditions of increasing difculty that disrupt somatosensory
cues, visual cues, or both. In condition 1, the patient is asked to stand still on a stable
platform with eyes open in a stable visual environment (the patient has full use of
all information: visual, vestibular, and somatosensory). Condition 2 is similar to
condition 1, except the patient’s eyes are closed (the patient must rely on vestibular
and somatosensory information). Condition 3 incorporates a stable platform with
moving visual surroundings (the patient must suppress a false sense of visually
induced movement and rely on vestibular and somatosensory inputs). In condition
4, the patient must stand still on an unstable platform with eyes open in a stable
visual environment (the patient must rely on vestibular and visual inputs). In condition 5, the patient stands on an unstable platform with eyes closed (the patient must
rely on vestibular input only because visual and somatosensory feedback have been
56
https://t.me/medicina_free
eliminated). Condition 6 employs an unstable platform and visual environment (the
patient must rely on vestibular input alone and suppress a false sense of visually
induced movement).
Each sensory condition is tested three times. During each condition, force plates
monitor the sway of the patient’s center of gravity for 20s at a time. Stability is
quantied by an equilibrium score—the percentage score expressing the ratio of
anteroposterior peak-to-peak sway amplitude to the theoretical anteroposterior limits of stability. Equilibrium scores closer to 100% indicate minimal sway, while
scores closer to zero indicate a sway near the limits of stability. Theoretical limits of
stability are calculated on the basis of the maximum backward and forward center
of gravity sway angles to which healthy subjects can move without losing balance.
Primary testing parameters include the composite equilibrium score and sensory
analysis. Composite equilibrium score is the weighted average of all trials, which
provides an overall sense of the patient’s balance performance. Abnormally low
scores may be associated with malingering or a true vestibular, somatosensory, or
visual dysfunction. Sensory analysis computes the difference in equilibrium scores
between two conditions. The equilibrium score for sensory analysis is the average
of each of the three trials of conditions 1–6. Differences are calculated for four
ratios. Somatosensory ratio is a comparison of equilibrium scores for conditions 1
and 2. Abnormally low ratios are associated with somatosensory system dysfunction. Visual ratio is the ratio of equilibrium scores for conditions 1 and 4. Low
ratios are associated with poor processing of visual cues. Vestibular ratio is the
ratio of equilibrium scores for conditions 1 and 5. Low scores are associated with
vestibular system dysfunction. Vision preference ratio compares the sum of equi-
librium scores from conditions 3 and 6 with the sum of equilibrium scores from
conditions 2 and 5. It assesses whether inappropriate or inaccurate visual cues are
used. Low ratios are indicative of an abnormal preference for visual inputs. Normal
participants suppress inaccurate visual inputs, while participants with a vision preference exhibit unsteadiness when many stimuli are moving simultaneously. A free
fall is usually enough to rule out exaggeration or malingering—it is difcult for
participants to fall freely without a causative disorder.
A. Chern and L. Lustig
Posture-Evoked Response andMotor Control Tests
Evaluation of the posture-evoked response testing is based on electromyography
(EMG) activities recorded from the tibialis anterior and gastrocnemius muscles in
response to separate sequences of multiple, brief, and sudden up and down rotations
of the support surface. The upper and lower limits of the latencies of EMG responses
are obtained from healthy subjects and are used for comparison. Abnormal latencies
of responses are indicative of many types of lesions, ranging from peripheral nerve
lesions to lesions of the spinal cord and cerebellum.
Motor control tests include an evaluation of automatic postural responses to the
forward and backward horizontal translations of the support surface at three
3 Tests toEvaluate theVestibular System
https://t.me/medicina_free
57
different magnitudes. The primary testing parameters are weight symmetry, active
force latency, and active force strength, each averaged over several trials. Prolonged
latency in both sides and directions suggests CNS lesions, whereas unilateral prolonged latency may imply either a peripheral or localized CNS lesion. Prolonged
latencies in only one direction can be observed in CNS lesions affecting efferent
branches of the long-loop system. To measure the automatic response adaptation, a
series of “toes up” and “toes down” rotations of the support surface is presented
following the backward and forward translations.
Clinical Application
Computerized dynamic posturography is useful in the following situations: (1)
chronic disequilibrium, (2) persistent dizziness or vertigo despite treatment, (3)
patients with normal results in other vestibular tests, (4) measuring the baseline
postural control prior to treatment, (5) monitoring the results of vestibular ablative
treatments, and (6) selecting the most useful rehabilitative strategy [36].
A vestibular function pattern in sensory analysis is seen in patients with bilateral
or decompensated unilateral vestibular loss. In these cases, equilibrium scores are
within the normal range for conditions 1 through 4, but below the lower limits of the
range for conditions 5 and/or 6. However, a vestibular function pattern is not enough
to distinguish between peripheral and central vestibular lesions. Abnormal vision
preferences typically occur in patients after head trauma. It can be associated with a
vestibular dysfunction pattern, depending on whether vestibular compensation
develops. Multisensory dysfunction patterns, including combinations of vestibular
and vision systems or vestibular and somatosensory systems, suggest CNS lesions.
Certain decits are associated with specic patterns of dysfunction. Poor performance in conditions 5 and 6 is seen in patients with vestibular dysfunction. A visual
preference is seen when patients positively test for conditions 3 and 6. Because
patients in this visual preference group are not unstable when vision is taken away
(condition 5), vestibular dysfunction is not present. These patients have visualvestibular integration problems and need a neurological referral. Patients with poor
balance in conditions 4–6 have somatosensory dependence. They should be referred
for physical therapy assessment of strength and neurologic assessment of sensation
in the lower extremities. When patients fall into conditions 2, 3, 5, and 6, a visual
dependence pattern suggests that patients are overly reliant on visual information.
Therapy for these patients incorporates a gradual reduction in visual feedback while
performing exercises. Malingering patients often show difculty with all conditions
equally. This is different from the expected poorer results in more difcult situations.
Posturography has some limitations. Testing alone cannot localize or lateralize
the site of the lesion. Sometimes, results may be contradictory to VNG/ENT and
rotary chair testing results because posturography assesses the vestibulospinal and
postural control systems while the other two evaluate the VOR.
See Figs. 3.18 and 3.19 for examples of normal and abnormal posturography
results.
58
https://t.me/medicina_free
Fig. 3.18 Normal posturography results. Somatosensory, visual, and vestibular functions
are normal
A. Chern and L. Lustig
Fig. 3.19 Abnormal posturography results. Normal somatosensory and visual function with signicant vestibular dysfunction
3 Tests toEvaluate theVestibular System
https://t.me/medicina_free
59
VEMP Testing
VEMPs are short-latency EMGs evoked by acoustic stimuli. There are two types of
VEMP tests: cervical VEMP (cVEMP), in which surface electrodes are placed on
the tonically contracted bilateral sternocleidomastoid (SCM) muscles, and ocular
VEMP (oVEMP), which is recorded with electrodes placed on the bilateral inferior
oblique muscles. In cVEMP, a loud 95dB auditory click stimulus is provided, and
the EMG response of the ipsilateral SCM is measured. This pathway (sacculocolic
reex) is as follows: acoustic signal→saccule→inferior vestibular nerve→vestibular nucleus→ vestibulospinal tract→ SCM action potential. In oVEMP, the
EMG response of the contralateral ocular muscles in response to either boneconducted or air-conducted sound is measured. Air conduction induces a contralateral response, while bone conduction elicits bilateral responses. This pathway
(vestibulo-ocular pathway) is as follows: acoustic signal→utricle→superior vestibular nerve→contralateral inferior oblique (air conduction), or bilateral response
(bone vibration). Although the end organ origins of oVEMP are still being debated,
the strongest evidence supports the utricle being responsible for the oVEMP
response [37].
Test Administration andParameters
For cVEMP recording, EMG electrodes are applied to the middle third of the anterior neck muscles (SCM) and the supine patient holds their head up unsupported,
using the anterior neck muscles, while a ground electrode is placed on the forehead.
For an air-conducted stimulus, loud clicks (95–100dB or louder) or tone bursts
(7ms long at 500 or 750Hz and up to 140dB peak SPL) are repetitively presented
to each ear at 200ms intervals. Bone-conducted stimuli can also be utilized. The
EMG activity of the muscle is amplied and bandpass ltered for measurement. For
oVEMP recording, electrodes are applied just inferior to each eye, while grounding
electrodes are placed 1cm lower. Of note, the upward gaze direction enhances the
amplitude of oVEMP.Air and bone conduction can also be used to evoke oVEMP.An
intact middle-ear conduction system is necessary for quality VEMP responses.
The cVEMP waveform consists of an initial positivity (called P1 or P13 or wave
I) at 13 (13–15) ms and a negativity (called N1 or N23 or wave II) at 23 (21–24) ms.
Peak-to-peak amplitude from P13 to P23 is measured. The oVEMP waveform consists of an initial negativity (n1) at 10ms followed by a positivity (p1) at 15ms. [38]
Note that the scaling of cVEMP is larger than that of oVEMP due to the fact that the
SCM is a much larger muscle than the inferior oblique. See Fig.3.20 for an example
of a normal cVEMP waveform.
60
https://t.me/medicina_free
Fig. 3.20 Normal cervical
vestibular-evoked
myogenic potential
waveform
A. Chern and L. Lustig
Clinical Application
The main advantage of VEMP tests is their ability to assess a different part of the
vestibular system (i.e., the otolith end organs) compared to ENG/VNG, rotary chair
testing, and posturography (which assess the lateral SCC). Moreover, VEMP tests
are localizing, as they evaluate the right and left labyrinths separately. The tasks are
also relatively fast and tolerable for patients. One major limitation is the fact that
VEMP response rates decrease in older patients; as individuals age, the rate of bilateral absent VEMP waveforms increases, even in patients with no vestibular pathology [39, 40].
VEMP tests have been particularly useful in aiding the diagnosis of superior
canal dehiscence (SCD). VEMP tests are useful in detecting whether SCD is causing pathological pressure transmission in the vestibular phenomenon—both oVEMP
and CVEMP have been depicted to show lower thresholds (i.e., the Tullio effect)
and increased amplitudes in patients with SCD. The theory is that a dehiscence
superior SCC (or other third window disorder such as stula) lowers the impedance
of the vestibular system, resulting in lower resistance for pressure and sound transmission. Recent studies have suggested oVEMP is superior to cVEMP in the diagnosis of SCD [41].
Low amplitude or absent VEMPs may be found in the affected ear [42] of patients
with Meniere’s disease [43]. VEMP amplitudes can be increased in early Meniere’s
disease, perhaps due to saccular dilatation. Absent VEMPs in advanced disease may
represent a collapse of the saccule. It has recently been proposed that VEMPs that
increase glycerol loading or furosemide injection are suggestive of Meniere’s disease [44].
Prolonged latency of VEMPs has recently been suggested to be a sign of a retrocochlear (vestibular nerve) lesion, such as that found in vestibular neuritis. Abnormal
VEMPs (asymmetrical or long latency) are reported in about 25% of people diagnosed with vestibular neuritis [45]. VEMPs are generally absent or reduced in
patients with vestibular schwannomas.
3 Tests toEvaluate theVestibular System
https://t.me/medicina_free
61
References
1. Hajioff D, Barr-Hamilton RM, Collegde NR, Lewis SJ, Wilson JA.Is electronystagmography
of diagnostic value in the elderly? Clin Otolarygol Allied Sci. 2002;27(1):27–31.
2. Baloh RW, Honrubia V.Clinical neurophysiology of the vestibular system. Philadelphia, PA:
FA Davis; 1989.
3. Fife TD, Tusa RJ, Furman JM, Zee DS, Frohman E, Baloh RW, Hain T, Goebel J, Demer J,
Eviatar L.Assessment: vestibular testing techniques in adults and children: report of the therapeutic and technology subcommittee of the American Academy of Neurology. Neurology.
2000;55(10):1431–41.
4. Halmagyi GM, Curthoys IS.A clinical sign of canal paresis. Arch Neurol. 1988;45:737–9.
5. Halmagyi GM, Yavor RA, Colebatch JG.Tapping the head activates the vestibular system: a
new use for the clinical reex hammer. Neurology. 1995;45:1927–9.
6. Hamman KF, Schuster EM.Vibration induced nystagmus: a sign of unilateral vestibular decit. J Otorhinolaryngol Relat Spec. 1999;61:74–9.
7. Burgio DL, Blakley BW, Myers SF. The high frequency oscillopsia test. J Vest Res.
1992;2:221–6.
8. Walker MF, Zee DS.The effect of hyperventilation of downbeat nystagmus in cerebellar disorders. Neurology. 1999;53:1576–9.
9. Minor LB, Haslwanter T, Strautmann D, Zee DS. Hyperventilation-induced nystagmus in
patients with vestibular schwannoma. Neurology. 1999;53:2158–68.
10. Vibert D, Hausler R, Safran AB.Subjective visual vertical in peripheral unilateral vestibular
diseases. J Vestib Res. 1999;9:144.
11. Tribukait A, Bergenius J, Brantberg K.Subjective visual horizontal during follow-up after
unilateral vestibular deafferentation with gentamicin. Acta Otolaryngol. 1998;118:479.
12. Vital D, Hegemann SC, Straumann D, Bergamin O, Bockisch CJ, Angehrn D, Schmitt KU,
Probst R. A new dynamic visual acuity test to assess peripheral vestibular function. Arch
Otolaryngol Head Neck Surg. 2010;136(7):686–91.
13. Gordon CR, Shupak A, Spitzer O, Melamed Y.Nonspecic vertigo with normal otoneurological examination. The role of vestibular laboratory tests. J Laryngol Otol. 1996;110(2):1133–7.
14. Stewart MG. Cost effectiveness of the diagnostic evaluation of vertigo. Laryngoscope.
1999;109:600–5.
15. Frohman TC, Em F, O’Suilleabhain P, Salter A, Dewey RB, Hogan N, Galetta S, Lee AG,
Straumann D, Noseworthy J, Zee D, Corbett J, Corboy J, Rivera VM, Kramer PD.Accuracy
of clinical detection of INO in MS: corroboration with quantitative infrared oculography.
Neurology. 2003;61(6):848–50.
16. Levy RA, Arts HA.Predicting neuroradiologic outcomes in patients referred for audiovestibular dysfunction. Am J Neuroradiol. 1996;17:1717–24.
17. Barber HO, Stockwell CW.Electronystagmography. St Louis, MO: CV Mosby; 1980.
18. Eckert AM, Gizza M. Video-oculography as part of the ENG test battery. Br J Audiol.
1998;32:411.
19. Vitte E, Semont A. Assessment of vestibular function by videonystagmoscopy. J Vest Res.
1995;5:377–83.
20. Kinney WC, Wallace RC, Ross JS, Hamid MA. Retrospective blinded review of magnetic
resonance imaging in patients with central electronystagmography ndings. Am J Otol.
1998;19:341.
21. Stoddard RL, Baguley DM, Beynon GJ, Chang P, Moffat DA.Magnetic resonance imaging
results in patients with central electronystagmography ndings. Clin Otolaryngol. 2000;25:293.
22. Bhansali SA, Honrubia V.Current status of electronystagmography testing. Otolaryngol Head
Neck Surg. 1999;120:419.
23. Assessment: electronystagmography report of the Therapeutics and Technology Assessment
Subcommittee. Neurology. 1996;46:1763–6.
24. Jongkees LBW, Philipszoon AJ.Electronystagmography. Acta Otolaryngol. 1964;189:1–111.
Соседние файлы в папке Библиотека им академика М.И. Перельмана