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APPENDIX 6–A. continued
ELECTROPHYSIOLOGIC
MEASURE DIAGNOSTIC OUTCOME AUDITORY STATUS
LLR Abnormal P1/N1/P2 amplitudes Abnormal maturation or function of
the auditory cortex
Absent P300 response Abnormality in top-down (decision
making) or bottom-up (difference
detection) processing; often seen
with cortical lesions or delayed
auditory development

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Vestibular Assessment and
Differential Diagnosis
Introduction
Chapter 7
Jamie M. Bogle
The vestibular system is a set of sensory end organs that detect angular and linear acceleration. This information is transmitted through various reflex pathways to maintain appropriate balance and visual stability.
Vestibular assessments use these pathways to identify weaknesses and to suggest possible diagnoses.
Vestibular System Anatomy and Physiology
Vestibular system end organs are housed within the inner ear. The membranous labyrinth is located
within the otic capsule and is filled with endolymph, a fluid with high potassium concentration (Smith
et al., 1965). There are five vestibular end organs: three semicircular canals (SCCs) and two otolith
organs (Figure 7–1). Each end organ contains its own sensory epithelium, the crista ampullaris for the
semicircular canals and the maculae for the otolith organs. The hair cells within the sensory epithelium
transmit mechanical energy into neural impulses encoding acceleration information. The superior vestibular nerve branch of cranial nerve VIII (CN VIII) innervates the horizontal and superior semicircular
canals and utricle, while the inferior vestibular nerve branch innervates the posterior canal and saccule.
Semicircular Canals (SCCs)
SCCs detect angular acceleration, meaning that they encode rotational movements. They are labeled
based on their orientation as the horizontal (or lateral), anterior (or superior), and posterior (or inferior)
SCC. Each SCC detects angular acceleration in a specific plane to create a three-dimensional model
of head movement.
n
Each SCC has a sensory epithelium at one end with the other open to the common vestibule.
The ampulla houses the sensory epithelium, called the crista ampullaris, and the cupula.
The cupula is a gelatinous structure that extends across the SCC to create a fluid-tight seal
(Lysakowski et al., 1998). Think of the cupula as a sail, deflecting when the head turns to
trigger the underlying sensory epithelium. The cupula only responds to angular acceleration
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FIGURE 7–1. Anatomy of the peripheral vestibular labyrinth. Source: From Lane JI, Witte RJ, Bolster B,
Bernstein MA, Johnson K & Morris J. AJNR Am J Neuroradiol. 2008 Sep;29(8):1436–1440; used with
permission of Mayo Foundation for Medical Education and Research, all rights reserved.
AUDIOLOGY NUGGET
The SCCs work together between ears as a pair — described as a co-planar or
push-pull mechanism. The horizontal SCCs form a pair. For example, as you
turn your head to the right, the right horizontal SCC experiences ampullopetal
flow (excitatory), while the left experiences ampullofugal flow (inhibitory). Each
anterior SCC is paired with the contralateral posterior SCC to describe the RALP
(right anterior/left posterior) and LARP (left anterior/right posterior) planes.
This co-planar relationship is vital to vestibular system performance because
each head movement transmits both excitatory and inhibitory information to
encode a range of accelerations.

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because it has the same specific gravity as the surrounding endolymph. This also means that it
does not respond to linear acceleration.
n
For the horizontal SCC, as the head turns, endolymph lags and pushes on the cupula
to depolarize (i.e., excite) the sensory hair cells. This type of endolymph flow is called
ampullopetal. Conversely, a head turn in the opposite direction will hyperpolarize (i.e.,
inhibit) these same sensory hair cells. This type of endolymph flow is called ampullofugal.
The anterior and posterior SCCs are oriented differently — ampullopetal flow inhibits,
ampullofugal flow excites (Lysakowski et al., 1998).
Otolith Organs
The utricle and saccule are collectively known as the otolith organs. They are housed in the vestibular
labyrinth (see Figure 7–1). These end organs are responsible for detecting linear acceleration, including gravity. The utricle generally encodes horizontal acceleration while the saccule encodes vertical
acceleration.
n
Each otolith organ contains a sensory epithelium called the otolithic membrane. This
structure is embedded with calcium carbonate crystals called otoconia or otoliths (Lundberg
etal., 2006). The otoconia increase the specific weight of the otolithic membrane, causing
it to pull toward gravity or to lag during linear acceleration, thus triggering the underlying
sensory hair cells.
Vestibular Nerve
Cranial nerve VIII (CN VIII) innervates both the cochlea and vestibular system. The vestibular portion
further divides into two branches. The superior vestibular nerve branch innervates the horizontal SCC,
anterior SCC, and utricle. The inferior vestibular nerve innervates the posterior SCC and saccule
(Naito et al., 1995).
n
Both vestibular nerve branches travel from the peripheral vestibular system through the
internal auditory canal and cerebellar pontine angle to synapse at various vestibular nuclei in
the brainstem.
n
The vestibular nerve has a high spontaneous firing rate ranging from 70 to 100 spikes per
second (Goldberg & Férnandez, 1971; Lysakowski et al., 1995). When excited, the vestibular
nerve can fire up to 400 spikes per second (Uchino et al., 1982). Because of the high resting
neural firing rate, inhibition can be encoded, providing the mechanism for co-planar
stimulation.
Blood Supply
The labyrinthine artery supplies blood to the vestibular system. This artery typically arises from the
anterior inferior cerebellar artery (AICA) (Baloh & Honrubia, 2001). One branch (superior vestibular
artery) supplies the horizontal SCC, anterior SCC, and utricle, while the other (common cochlear
artery) supplies the posterior SCC, saccule, and cochlea. The blood supply to vestibular structures in
the brainstem and cerebellum is provided from various branches of the vertebrobasilar artery.

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Central Vestibular System
Once information from the vestibular end organs enters the brainstem, it synapses within the vestibular
nuclei (VN). The VN contains several substructures, including the superior VN, medial VN, lateral
VN, and inferior VN. Each of these substructures transmits specific end-organ information to the
appropriate reflex pathways.
n
Cerebellum: the superior VN and lateral VN are highly connected to the cerebellum, with
predominant information transmitted from the otolith organs (Carpenter & Sutin, 1983;
Pansky et al., 1988; Watson, 1991). The cerebellum transmits this information to the
reticulospinal tract, lateral vestibulospinal tract, and reticular formation (Pansky et al., 1988).
Information from the cerebellum is heavily used for motor control.
n
Reticular formation: the reticular formation uses information primarily from the otolith
organs and descends the length of the spinal cord (Fetter & Dichgans, 1996; Honrubia
& Hoffman, 1997). Vestibular system activation along this pathway may trigger sweating,
nausea, and vomiting (Pansky et al., 1988).
n
Thalamocortical projections: information from the VN ascends to the thalamus, further
projecting to the parietoinsular vestibular cortex (PIVC). The PIVC serves as a major
integration site for vestibular, visual, and motor system information. Thalamocortical
projections are also traced to the hippocampus, where they influence spatial perception and
cognition (Bigelow et al., 2016; Brandt et al., 2005; Semenov et al., 2016) and descend to the
VN/brainstem (Berthoz, 1996) to contribute to the efferent vestibular system.
n
Autonomic system: vestibular system information also influences autonomic system function.
The autonomic system controls various sympathetic and parasympathetic responses. The
otolith organs specifically contribute to blood pressure regulation during movement and
postural change (Goldberg et al., 2012; Yates et al., 2014).
Vestibular Reflexes
Reflex pathways are used to evaluate vestibular system performance. There are several basic vestibular
system reflexes.
n
Vestibulo-ocular reflex (VOR): enables visual stability during motion. The VOR is a reflex
pathway from the SCCs to specific extra ocular muscles to produce equal and opposite eye
movements in response to a head turn. If the VOR is not working properly, the patient
may experience oscillopsia — the perception of oscillating movement in the environment
during motion. Figure 7–2 provides the horizontal SCC VOR pathway. All SCCs provide
information to the VOR, but the horizontal SCC is the most evaluated pathway (e.g., caloric
testing, rotational chair testing, head impulse testing). The utricle also provides a translational
VOR (e.g., ocular vestibular evoked myogenic potentials).
n
Vestibulo-collic reflex (VCR): enables the head to remain still during movement (Hain &
Helminski, 2014). The proposed pathway for the VCR includes the saccule, inferior vestibular
nerve branch of CN VIII, medial VN, CN XI (spinal accessory), and ending in the trapezius
and sternocleidomastoid (SCM) muscles.

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FIGURE 7–2. The vestibulo-ocular reflex (VOR) pathway includes the vestibular nuclei (VN), cranial nerve
VI (CN VI), cranial nerve III (CN III), the medial longitudinal fasciculus (MLF), lateral rectus muscle (LR), and
medial rectus muscle (MR). Source: From Balance Function Assessment and Management, Third Edition
(pp. 1–717) by Jacobson, G. P., Shepard, N. T., Barin, K., Burkard, R. F., Janky, K., & McCaslin, D. L. Copyright
© 2021 Plural Publishing, Inc. All rights reserved.
n
Vestibulo-spinal reflex (VSR): triggers upper and lower limb responses to changes in balance
(Schubert & Shepard, 2016). Patients with damage to the vestibular system may demonstrate
imbalance acutely but should recover as vestibular compensation occurs. The VSR can
be evaluated using a range of bedside (e.g., Romberg test) and forceplate measures (e.g.,
computerized dynamic posturography).
Vestibular Nystagmus
Most vestibular diagnostic testing measures nystagmus — rapid, involuntary eye movements. Nystagmus allows the clinician to (1) evaluate a possible site of lesion in those with spontaneous nystagmus
and (2) define peripheral vestibular system performance as measured in induced nystagmus. Nystagmus represents the VOR (Figure 7–3). The slow phase component corresponds to vestibular system
information, while the fast phase is a reset saccade initiated to bring the eyes back to midline. Nystagmus is named by the fast phase for most analyses and is measured by the velocity (°/second) of the
slow phase.

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FIGURE 7–3. Vestibular nystagmus. In this example, the eyes drift slowly to the left
(slow phase; downward on the graph) and quickly reset to the right (fast phase;
upward on the graph). This tracing describes right-beating nystagmus.
KNOWLEDGE CHECKPOINT
Peripheral vestibular nystagmus follows Ewald’s laws (Ewald, 1882). These laws
describe how endolymph flow reliably influences the VOR to create predictable
nystagmus.
1. The axis of nystagmus parallels the axis of the SCC that generated it.
2. Ampullopetal endolymph flow produces a stronger response than
ampullofugal flow in the horizontal SCCs.
3. Ampullofugal endolymph flow produces a stronger response than
ampullopetal flow in the anterior and posterior SCCs.
Vestibular Case History and Questionnaires
The case history is one of the most important components of the vestibular assessment. A thorough
case history should include:
n
Temporal features of dizziness symptoms: timing, triggers
n
Dizziness characteristics: spinning, rocking, imbalance, lightheadedness, drunk feeling, spacey,
and so on
n
Additional symptoms: hearing loss, tinnitus, headache, nausea/vomiting, unsteadiness, other
neurological concerns

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n
Vascular risk factors: for example, cardiac syncope, atherosclerosis, heart disease,
319
vertebrobasilar artery insufficiency
n
Neurological risk factors: for example, migraine, stroke, transient ischemic attack (TIA),
concussion, multiple sclerosis
n
Medications (Table 7–1)
Some medications may cause vestibulotoxicity and many others cause dizziness/imbalance.
Many patients use multiple medications to manage various conditions. Polypharmacy — the
simultaneous use of >4 medications (Masnoon et al., 2017)
— is a common cause of
dizziness. Nearly 70% of patients presenting with dizziness and polypharmacy most often
have diagnoses including diabetes, hypertension, other cardiovascular abnormalities, and
depression (Jeong et al., 2022).
Questionnaires are useful tools to identify the patient’s self-perceived symptoms as well as how
symptoms impact quality of life. There are many questionnaires available, with commonly used options
provided in Table 7–2.
TABLE 7–1. Medications Associated With Vestibulotoxicity, Dizziness, and Imbalance
Classes of Vestibulotoxic
Medications
Classes of Medications
Associated With Dizziness/
Imbalance
Antibiotics (e.g., gentamicin)
Platinum-based chemotherapeutics
Loop diuretics
Antimalarial drugs
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Acetylsalicylic acid
Antispasmodics used for intestinal mobility disorders
Diuretics
Beta-blockers
Hypertension medications
Antihistamines
Hypnotic/anxiolytic medications
First-generation antipsychotics
Tricyclic antidepressants
Analgesics
Migraine medications
Antiepileptic medications
Parkinson medications
Antibiotics
HIV medications
Corticosteroids
Hormone therapies
Source: Altissimi et al. (2020).

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TABLE 7–2. Commonly Used Questionnaires to Evaluate Patients With Dizziness/Imbalance
QUESTIONNAIRE PURPOSE
General Scales
Hospital Anxiety and Depression Scale
(HADS) (Zigmond & Snaith, 1983)
Generalized Anxiety Disorder–7 (GAD-7)
(Spitzer et al., 2006)
Patient Health Questionnaire–9 (PHQ-9)
(Kroenke et al., 2001)
Dizziness Scales
Dizziness Handicap Inventory (DHI)
(Jacobson & Newman, 1990)
Activities-Specific Balance Confidence Scale
(ABC) (Powell & Myers, 1994)
Visual Vertigo Analog Scale (VVAS)
(Dannenbaum et al., 2011)
Dizziness Symptom Profile (DSP)
(Jacobson et al., 2019)
Bedside Evaluation
Determine levels of anxiety and depression in
an outpatient setting
Screen for generalized anxiety disorder
Screen for depression
Evaluate self-perceived handicap due to
dizziness
Assess balance confidence and determine fall
risk
Quantify dizziness symptoms to visually
provoking situations
Assist in identifying common vestibular
disorders
Patients presenting for audiometric testing may also report dizziness/imbalance. Bedside testing
provides clues to identify patients who may be experiencing vestibular system dysfunction (Table 7–3).
Electronystagmography/Videonystagmography (ENG/VNG)
The most common vestibular diagnostic battery is the ENG/VNG. The name of the test describes the
recording method; however, the subtests are the same for both.
ENG
ENG recording takes advantage of the corneoretinal potential (CP). Electrodes are placed on the
inner canthi, outer canthi, and above and below the eyes to record electrical activity. Measuring the
changes in electrical activity identifies nystagmus and other oculomotor movements. Most clinicians
use bitemporal electrode placement, with the horizontal electrodes placed on the outer canthus of each
eye (Figure 7–4). With this montage, the electrical activity between the eyes is averaged and the tracing
cannot identify disconjugate eye movements. Monocular (i.e., recording each eye individually) can also
be completed. ENG is rarely completed today due to advances in video recording technology.

TABLE 7–3. Bedside Evaluation Options Summary
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TEST PURPOSE TECHNIQUE INTERPRETATION
Spontaneous
vestibular
nystagmus
Identify a static
imbalance between
right and left peripheral
vestibular systems
Head impulse test Identify VOR
dysfunction
Head shake
nystagmus
Identify asymmetrical
neural integration
of VOR; measure of
compensation
Dynamic visual
acuity test
Identify oscillopsia with
head movement
Observe the patient’s eyes
for nystagmus in vision and
vision-denied conditions.
Examiner moves
the patient’s head in
low-amplitude, highvelocity head turns; observe
the patient’s eyes for loss of
visual fixation.
Patient oscillates the head
for 25 cycles at 2 Hz; vision
denied.
Patient reads to the lowest
level on an eye chart with
the head stable and with the
head oscillating at 2 Hz.
Normal:
no nystagmus
Abnormal: nystagmus;
determine if it follows
Alexander’s law
Normal:
no loss of fixation
Abnormal: loss of fixation;
patient demonstrates a
“catch-up” saccade to regain
fixation
Normal: <3 beats of postheadshake nystagmus
Abnormal:
> 3 beats of
post-headshake nystagmus;
fast phase typically beats
toward the better ear
Normal:
≤2 lines of change
on the eye chart
Abnormal:
> 2 lines of
change on the eye chart
Valsalva-induced
nystagmus
Identify the effect of
intracranial pressure
change on nystagmus
Modified Clinical
Test of Sensory
Interaction
Measure postural
control under various
conditions
on Balance
(mCTSIB)
Romberg Test Measure postural
control under various
conditions
Patient increases intracranial
pressure by performing
Valsalva maneuver for
10–15 seconds.
Patient maintains balance
for 30 seconds in four
conditions: (1) eyes open,
firm surface; (2) eyes closed,
firm surface; (3) eyes open,
foam surface; (4) eyes
closed, foam surface.
Patient maintains balance
for 30 seconds in two
conditions: (1) eyes open,
firm surface and (2) eyes
closed, firm surface.
Normal:
no dizziness or
nystagmus
Abnormal:
conjugate
eye movement toward
the contralesional ear;
nystagmus, dizziness
Normal: ability to maintain
balance in all conditions for
30 seconds
Abnormal: inability to
maintain balance in all
conditions for 30 seconds
Results may also be
compared to age-specific
normative values using
forceplate analyses.
Normal: ability to maintain
balance in all conditions for
30 seconds
Abnormal: inability to
maintain balance in all
conditions for 30 seconds
continues
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