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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4612_Библиотеки_им_академика_М_И_Перельмана
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Audiology Review: Preparing for the Praxis and Comprehensive Examinations
https://t.me/medicina_free
342
TAB LE 7–11. Sensory Analysis Interpretation
SIGNIFICANCE OF ABNORMAL
RATIO NAME CALCULATION
Somatosensory Condition 2/Condition 1 Poor use of somatosensory cues
Visual Condition 4/Condition 1 Poor use of visual cues
Vestibular Condition 5/Condition 1 Poor use of vestibular cues
PERFORMANCE
Visual Preference Conditions 3 + 6/
Conditions 2 + 5
Overreliance on visual cues, even
when inaccurate
The composite score provides an overview of balance performance. This is a weighted
average considering Conditions 3 to 6 more heavily than Conditions 1 and 2.
Sensory analysis provides an understanding of which sensory system(s) may be contributing
to abnormal balance performance (Table 7–11).
n
Motor control test (MCT) evaluates the automatic postural reflexes elicited by abrupt
horizontal translations of the support surface. Patients are slid backward and forward in three
translational sizes (small, medium, large). The outcome measures are the active force latency
(ms), active force strength, and weight asymmetry.
n
Adaptation test (ADT) evaluates the adaptation of the automatic postural control system
by tilting the support surface toes up or toes down. Five identical trials of 8° rotations are
completed to evaluate the patient’s ability to adapt to this rotation. The outcome measure is
a sway energy score, defined as the magnitude of center of gravity sway immediately after a
forceplate rotation.
Functional VOR/Dynamic Visual Acuity Test (DVAT)
The VOR is key to maintaining clear vision with head movement. In patients with VOR pathway
abnormalities, turning the head in the plane of the deficient VOR will trigger dizziness and oscillopsia.
Functional VOR (DVAT) can be measured using bedside methodology or computerized systems that
document head acceleration. Both methods require establishing a visual acuity baseline measured when
the head is still and a subsequent visual acuity level obtained when the head is oscillating ±20° at a
frequency of 2 Hz. Visual acuity is measured in logMAR (log of minimal angle of resolution), with
logMAR of 0.00 equal to 20/20 visual acuity. There should not be a change of greater than 0.2 logMAR
between the conditions. Visual acuity changes greater than this suggest impaired VOR performance.
Additionally, the patient may report dizziness and nausea with this task.
Vestibular System Pathologies
There are innumerable underlying causes for dizziness and patient self-reported symptom characteristics are not always reliable for identifying the problem. Consider the case history and temporal (timing)
features of the patient’s symptoms to better identify possible etiologies (Table 7–12).
CHAPTER 7 Vestibular Assessment and Differential Diagnosis
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TABLE 7–12. Approach for Identifying Vestibular System Pathology Using Temporal Features
CATEGORY PERIPHERAL ETIOLOGY CENTRAL ETIOLOGY
Acute vestibular syndrome Vestibular neuritis Brainstem, cerebellar infarct
343
Recurrent vertigo Ménière disease
Superior semicircular canal
dehiscence (SSCD)
Positional vertigo Benign paroxysmal positional
vertigo (BPPV)
Chronic dizziness,
unsteadiness
Bilateral vestibulopathy
Vestibular schwannoma
Vestibular migraine
Transient ischemic attack (TIA)
Cerebellar disorder
Vestibular migraine
Persistent postural-perceptual
dizziness (PPPD)
Vestibular Neuritis
Vestibular neuritis occurs with an infection/inflammation of the vestibular nerve, most often involving
the superior branch. It is suspected in cases presenting with acute onset of vertigo, nausea/vomiting,
and generalized imbalance. The acute phase can last for hours to days, but imbalance may linger for
weeks after. There is no hearing loss or tinnitus associated with vestibular neuritis.
Consider this case example of suspected vestibular neuritis.
Patient was a 61-year-old male who reported waking up to rotational vertigo 2 months
before testing. He described rotational vertigo lasting for hours, with continued imbalance,
lightheadedness, and nausea with quick head movements. He denied other otologic symptoms.
VNG testing was abnormal. Gaze testing in neutral gaze without fixation demonstrated
right-beating nystagmus averaging 2°/second (Figure 7–14). This was not significant but likely
consistent with the remaining VNG battery and suggested a recent VOR insult. The remaining
oculomotor battery was within normal limits.
Caloric testing demonstrated significantly reduced responses in the left ear, with CP of
63%. TES for the left ear was 5°/second, suggesting minimal VOR performance in this ear.
There was no significant directional preponderance (Figure 7–15).
SHA testing demonstrated significantly reduced gain from 0.02 to 0.16 Hz, with significant phase lead from 0.02 to 0.04 Hz. Asymmetry was abnormal across all frequencies
(0.02–0.64 Hz), consistent with the underlying spontaneous nystagmus (Figure 7–16).
CVEMP responses were within expected limits for the right ear, with questionable left ear
response presence (Figure 7–17). These results are consistent with left peripheral loss.
Functional measures suggested that the patient had not yet compensated for his recent
vestibular loss. DVAT demonstrated a significant loss of visual acuity (logMAR loss = 0.6)
with leftward head movement. Rightward head movement was unimpaired. SOT results were
consistent with poor use of vestibular system information, with reduced performance noted on
Conditions 2, 5, and 6 (Figure7–18).
Overall findings suggested that the patient was experiencing uncompensated vestibular
symptoms associated with his vertigo episode 2 months prior. Medical consultation suggested
vestibular neuritis was the likely cause of his symptoms. He was referred to vestibular rehabilitation to facilitate compensation.
Audiology Review: Preparing for the Praxis and Comprehensive Examinations
https://t.me/medicina_free
344
FIGURE 7–14. Case example: vestibular neuritis; spontaneous nystagmus noted in neutral gaze without
fixation demonstrated right-beating nystagmus averaging 2°/second.
FIGURE 7–15. Case example: vestibular neuritis; caloric responses.
CHAPTER 7 Vestibular Assessment and Differential Diagnosis
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345
FIGURE 7–16. Case example: vestibular neuritis; SHA responses demonstrated low gain from 0.02 to 0.64 Hz, significant low-frequency
phase lead from 0.02 to 0.04 Hz, and significant asymmetry from
0.02 to 0.64 Hz.
Audiology Review: Preparing for the Praxis and Comprehensive Examinations
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FIGURE 7–17. Case example: vestibular neuritis; cVEMPs. Note that
waveforms are inverted (p1 is negatively deflected). The left cVEMP
response is significantly reduced (16.85 µV), with poor repeatability.
There is a significant amplitude asymmetry when compared to the
right cVEMP response (81.45 µV; 66% asymmetry to the left).
CHAPTER 7 Vestibular Assessment and Differential Diagnosis
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FIGURE 7–18. Case example: vestibular neuritis; SOT results.
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Labyrinthitis
The clinical presentation of labyrinthitis is similar to vestibular neuritis, except that the patient will also
report concurrent sudden hearing loss and tinnitus. The hearing loss and vertigo may occur simultaneously or within a few days of each other. Labyrinthitis occurs due to inflammation of the inner ear
and/or CN VIII.
Vestibulotoxicity
Various medications and chemicals cause vestibular hair cell death, leading to imbalance and oscillopsia. Common pharmaceutical agents include aminoglycosides (e.g., streptomycin, gentamicin)
and chemotherapeutics (e.g., cisplatin). Industrial or occupational exposure to chemical agents (e.g.,
xylene, toluene) can also occur. Because both ears are typically impacted, patients rarely report vertigo.
Not all individuals exposed to these agents will experience vestibular dysfunction, and modern dosing
methods for pharmaceuticals have aimed to reduce overall toxicity.
n
Clinical presentation of vestibulotoxicity
Bilaterally reduced VOR performance ranging from mild to areflexia
Reduced otolith reflex pathway responses
Reported oscillopsia, imbalance
May or may not present with bilateral hearing loss/tinnitus
Benign Paroxysmal Positional Vertigo (BPPV)
BPPV is the most common peripheral vestibular disorder. It occurs more often in women and has been
associated with advancing age, hormone changes, and head injury, and it may occur with other inner
ear disorders (e.g., labyrinthitis, vestibular neuritis) (Chen et al., 2021).
Audiology Review: Preparing for the Praxis and Comprehensive Examinations
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348
n
BPPV occurs when otoconia from the utricle is dislodged and migrates to a SCC (Figure7–19).
The otoconia change the function of the SCC, causing it to become sensitive to gravity. When
the patient makes an offending head movement, such as rolling over in bed or tipping the
head back, the gravity-sensitive SCC is triggered and the patient experiences vertigo.
n
The vast majority of BPPV involves the posterior SCC (90%), with horizontal SCC BPPV
diagnosed in approximately 10%. Rarely, BPPV has been reported in the anterior SCC. BPPV
can be easily identified using the Dix-Hallpike test for otoconia in the vertical canals and the
lateral head roll test for the horizontal canal.
AUDIOLOGY NUGGET
Clinical Presentation of Posterior SCC BPPV
n
Symptom latency occurs 1 to 10 seconds after a provoking movement,
such as rolling over in bed.
n
Symptom duration <1 minute
n
Torsional up-beating nystagmus beats toward the underneath ear,
changes direction when the patient sits up
n
Nystagmus and symptoms fatigue with repeated evaluation or
repositioning
FIGURE 7–19. Benign paroxysmal positional vertigo (BPPV). BPPV occurs when
otoconia are displaced and migrate into a semicircular canal, triggering vertigo with
position changes. This condition can be resolved with canalith repositioning. Source:
Used with permission of Mayo Foundation for Medical Education and Research, all
rights reserved.
CHAPTER 7 Vestibular Assessment and Differential Diagnosis
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TABLE 7–13. Nystagmus Associated With BPPV by Involved SCC
INVOLVED SCC RIGHT EAR LEFT EAR
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Posterior SCC Up-beating
Right-torsion
Anterior SCC Down-beating
Right-torsion
a
Horizontal SCC
Note. aCanalithiasis will present with geotropic nystagmus; cupulothiasis will
present with ageotropic nystagmus; nystagmus will generally occur bilaterally, with
the side with the larger velocity likely the suspect ear.
Geotropic/ageotropic Geotropic/ageotropic
Up-beating
Left-torsion
Down-beating
Left-torsion
Dix-Hallpike testing is a positioning test that evaluates for vertical canal BPPV. To complete
the test, the patient turns the head 45° to the right or left depending on the ear in question.
The patient is then laid back onto the examination table with the head hanging 30° below
horizontal off the table. The examiner holds the patient’s head in the appropriate position
and observes for nystagmus. The Dix-Hallpike test should be held for 30 to 60 seconds.
n
Because otoconia can migrate to any SCC, knowing the presenting nystagmus pattern will
help to identify the appropriate canal for management (Table 7–13).
Endolymphatic Hydrops/Ménière Disease
Endolymphatic hydrops includes any disorder associated with abnormal fluctuations in endolymph.
The most commonly discussed is Ménière disease. Ménière disease is an idiopathic disorder of the inner
ear that occurs when endolymph production or reabsorption is altered. Recent hypotheses suggest
that vertigo attacks may occur when endolymph either drains too quickly or overfills the labyrinth
(Gibson, 2010).
Q & A
Question: What are the diagnostic criteria for Ménière disease?
Answer: Patients must meet the following criteria to be diagnosed with Ménière
disease (Basura et al., 2020).
n
Two or more spontaneous episodes of vertigo each lasting 20 minutes to
12 hours
n
Audiometrically documented low- to mid-frequency sensorineural
hearing loss in one ear, defining the affected ear, on at least one occasion
before, during, or after one of the episodes of vertigo
n
Fluctuating aural symptoms (hearing loss, tinnitus, fullness) in the
affected ear
n
Not better accounted for by another vestibular diagnosis
Audiology Review: Preparing for the Praxis and Comprehensive Examinations
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350
n
Over time, damage to the underlying hair cells and support structures is more apparent.
Eventually, the ear may “burn out,” meaning that little hearing and/or vestibular function
remains. In these later stages, the patient may experience Tumarkin otolithic crises or “drop
attacks.” These episodes are described as a sudden perception of being pushed or knocked to
the ground and can lead to serious injury.
Consider this case of suspected Ménière disease.
Patient was a 64-year-old female reporting onset of hearing loss, tinnitus, aural fullness,
rotational vertigo, nausea, and vomiting 3 years ago. Episodes lasted several hours. She reported
that hearing loss in the left ear gets worse before her vertigo episodes but has not recovered as
well as it has before. The patient reported that her last episode was 4 months before testing.
Audiometric findings demonstrated normal hearing sensitivity sloping to moderate sensorineural hearing loss in the right ear and mild sloping to moderate sensorineural hearing loss
in the left ear (Figure 7–20).
Vestibular testing demonstrated findings consistent with significant left peripheral vestibulopathy. Caloric testing demonstrated a 55% CP in the left ear, with left ear TES of 11°/
second (Figure 7–21).
SHA testing demonstrated appropriate gain for 0.02 to 0.64 Hz stimuli. A significant
phase lead was noted for 0.02 to 0.04 Hz, consistent with the documented left peripheral
vestibulopathy (Figure 7–22).
The remaining VNG was within normal limits, with no evidence of acute vestibulopathy.
The overall clinical presentation is consistent with left peripheral vestibulopathy. The lesion
has compensated over the 4-month interval between her last vertigo episode and presentation
for testing. She continued to establish a management strategy with her ENT provider. She was
counseled regarding reducing salt intake and the possible use of a diuretic.
FIGURE 7–20. Case example: Ménière disease; audiometric presentation. Note the significant low-frequency
sensorineural hearing loss in the left ear consistent with Ménière disease presentation.
CHAPTER 7 Vestibular Assessment and Differential Diagnosis
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FIGURE 7–21. Case example: Ménière disease; caloric responses.
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