Vestibular Examination
ANATOMY & FUNCTION
Carmen Casanova Abbott PT, PhD
Lecture Objectives
► Discuss
vestibular structure as it relates to
vestibular function when examining a dizzy
patient.
► Discuss signs and symptoms associated with
vestibular disorders
► Differentiate between peripheral and central
vestibular pathology
► Discuss components of a physical therapy
vestibular examination.
Vestibular System Function
► Provides
information concerning gravity,
rotation and acceleration
► Serves as a reference for the somatosensory &
visual systems
► Contributes to integration of arousal, conscious
awareness of the body via connections with
vestibular cortex, thalamus and reticular
formation
► Allows for:
 gaze & postural stability
 sense of orientation
 detection of linear & angular acceleration
Vestibular Anatomy
► Peripheral
sensory apparatus
 detects & relays information about head angular &
linear velocity to central processing system
 orients the head with respect to gravity
► Central
processing system
 processes information in conjunction with other
sensory inputs for position and movement of head in
space
► Motor
output system
 generates compensatory eye movements and
compensatory body movements during head &
postural adjustments
Peripheral Apparatus
► Membranous
Labyrinth
 Semicircular canals (SSC)
 Otolith organs
Netter ‘97
Semicircular Canals
► Angular
acceleration
► Ampulla contains sensory epithelium
SSC Coplanar Pairing
► Spatial
arrangement of the 6 SSC cause 3
coplanar pairings
 R & L lateral, L anterior and R posterior; l
posterior & R anterior; R & L horizontal
► Allows for a Push-Pull arrangement of the two
sides (e.g., as head turns right, right SSC will
increase firing rate & the left SSC will decrease
firing rate)
► Advantages
 sensory redundancy
 common mode rejection/noise
Inhibitory Cutoff
► Depolarization
of the ipsilateral hair cells
occurs during angular head movements
► Hyperpolarization of contralateral hair cells
occurs at the same time
► Hair cells are only able to hyperpolarize to
what they were at rest = cut off of inhibitory
influences from the movement going in the
opposite direction even if the ipsilateral hair
cells continue to spike higher firing rates
Purves 2001
Otoliths
► Utricle
and saccule
► Otolith sensory structures
 Maculae
 Otolithic membrane
 Otoconia
► Movement
of gel membrane & otoconia
cause a shearing action to occur over
the hair cells → sensitivity of otoliths
Otolith Function
► Respond
to:
 Linear head motion on acceleration
 Static tilt
 Two organs respond to respective accelerations
or tilts in their respective planes
►Saccule
has vertical orientation of maculae
►Utricle has horizontal orientation of maculae
Bear 1996
Purves 2001.
Hair Cells
►2
types: kinocilium & stereocilia
► Sensory structures for the peripheral
end organs (maculae and ampula)
► Hyperpolarized or depolarized
depending upon the direction of
deflection of the stereocilia (movement
of stereocilia towards the kinocilium
causes depolarization of the hair cell)
► Affect
the firing rate of the primary
vestibular afferents to the brainstem
Bear 1996
Striola of the Macula
► Striola
serves as a structural landmark
► Contains otoconia arranged in narrow
trenches, dividing each otolith
► Orientation of the hair cells change over
the course of the macula
► Allows otoliths to have multidirectional
sensitivity
Purves 2001.
Principles of the Vestibular System
► Tonic
firing rate
► Vestibular Ocular Reflex
► Push-pull mechanism
► Inhibitory cutoff
► Velocity storage system
Ascending Pathways
► Vestibular
nerve
► Vestibular nuclei
► Cerebellum
► Oculomotor complex
 CN 3, 4, and 6
 Along with vestibulospinal reflexes coordinate
head and eye movements
Relay Centers
► Thalamus
 Connection with vestibular cortex and reticular
formation → arousal and conscious awareness
of body; discrimination between self movement
vs. that of the environment
► Vestibular
Cortex
 Junction of parietal and insular lobe
 Target for afferents along with the cerebellum
►Both
process vestibular information with
somatosensory and visual input
Netter 1997
Tonic Firing Rate
► Vestibular
nerve and vestibular nuclei have a
normal resting firing rate (70-100 cycles/sec)
► Baseline firing rate present without head
movement
► Tonic firing is equal in both sides; if not, a
sense of motion is felt e.g., vertigo, tilt,
impulsion, spinning
► Excitation and inhibition of the vestibular
system can then occur from stimulation of the
hair cells
► Spontaneous recovery with light
Vestibular-Ocular Reflex
(VOR)
► Causes
eyes to move in the opposite
direction to head movement
► Speed of the eye movement equals that of
the head movement
► Allows objects to remain in focus during
head movements
Compensatory Eye Movements
► VOR
► Optokinetic
reflex
► Smooth pursuit reflex, saccades, vergence
► Neck reflexes
 combine to stabilize object on the same area of
the retina=visual stability
Purves 2001.
Vestibular Processing
Gain
► Keeps
eye still in space while head is
moving
► Ratio of eye movement to head movement
(equals 1)
Vestibular Processing
Velocity Storage Mechanism
► Perseveration
of neural firing in the vestibular
nerve by the brainstem after stimulation of SSC
to increase time constant (10sec.)
 SSC respond by producing an exponentially
decaying change in neural firing to sustained
head movement
► Otolith & somatosensory input also drive
mechanism
VOR Dysfunction
► Direction
of gaze will shift with the head
movement
► Cause degradation of the visual image
► In severe cases, visual world will move with
each head movement
Oscillopsia
► Visual
illusion of oscillating movement
of stationary objects
► Can arise with lesions of peripheral or
central vestibular systems
► Indicative of diminished VOR gain
 motion of images on fovea
 diminished visual acuity
Cerebellum
► Monitors
vestibular performance
► Readjusts central vestibular processing
of static & dynamic postural activity
► Modulates VOR
► Provides inhibitory drive of VOR (allows
for VORc)
Descending Pathways
► Provide
motor output from the vestibular
system to:
 Extraocular muscles (part of VOR)
 Spinal cord & skeletal muscles (generate
antigravity postural activity to cervical,
trunk & lower extremity muscles)
► Response
to changing head position with
respect to gravity (righting, equilibrium
responses)
Vestibulospinal Reflex (VSR)
► Generates
compensatory body movement
to maintain head and postural stability,
thereby preventing falls
Netter 1997
Vestibular Dysfunction
Demographics
► Vestibular
disorders manifested by vertigo
are a significant health problem, secondary
only to low back pain
► NIH study estimates that 40% of the
population over the age of 40 will
experience a dizziness disorder during their
lifetime
Fall Demographics
► Falls
will be experienced in community
dwelling individuals:
 28-35 % over age 65
 42-49% over age 75
►
Greater than 60% will have bilateral
vestibular lesion (BVL) in the <65 or >75
years of age
Fall Risk Factors
≥ 4 risk factors, 78% chance of falling in an older adult
► Sedatives
► Dizziness
► Cognitive
►↑
impairment
► Palmomental reflex
► LE disability
► Foot problems
► Balance abnormalities
dependence on
visual cues
► Fear of falling
► Orthostatic
hypotension
(Tideiksaar R 1998)
Other Fall Risk Factors?
Aging Changes
► Progressive
changes begin at age 40
 Decreased number of hair cells
 Decreased vestibular nerve fibers
► Lead
to dizziness and vertigo
► Harder to deal with competing visual and
somatosensory input
Fear of Falling (FOF)
FOF affects willingness to participate in physical activity
& exercise
► FOF occurs in an average of 30% of older adults who
have not fallen
► FOF increases to an average of 60% of older adults who
have fallen
► FOF is higher among women
► Prevalence of FOF is underestimated
► Greater FOF associated with lower quality of life in
mental health, social & leisure pursuits
►
(Legters, 2002)
Falls Related Self-efficacy
► Falls
Efficacy Scales (FES)
 better for frail
 indoor activities
► Activities-Specific Balance Confidence Scale (ABC)
 higher functioning
 indoor & outdoor activities
 > discrimination between fearful & nonfearful
(Legters, 2002)
Vestibular Pathophysiology
► Disorders
of tone & or gain (vertigo / movement-
induced vertigo)
► Vestibular
nerve / nuclei give abnormal sensory
information
► Tone automatically recovers in a few days; does
not need visual input
► Compensation for reduced gain depends on visual
images; takes month to years to complete; high
speeds & accelerations may never be complete
► Nystagmus usually transient sign of vestibular
lesion; movement-induced symptoms can be
chronic
Dizzy Patient Presentation: unexplained or
new onset of symptoms
► Medical









referral is indicated
constant vertigo
lateralpulsion
facial asymmetry
speech & or swallowing difficulties
oculomotor dysfunction
vertical nystagmus
severe headaches
recurrent falls
unilateral hearing loss, tinnitus, fullness, ear pain
Vertigo
► An
asymmetrical firing of the two
vestibular systems
► Gives an illusion of spinning, movement
► Indicative of any one or combination of
causes (acute UVH, BPPV, brainstem
lesion, vascular hypotension…)
Differentiation Between Peripheral &
Central Causes of Vertigo
Peripheral
Nausea
Imbalance
Hearing Loss
Oscillopsia
Neurologic Symptoms
Compensation
severe
mild
common
mild
rare
rapid
Central
moderate
severe
rare
severe
common
slow
(Furman JM, Whitney SL. 2000)
Peripheral Vestibular Disorders
► Vestibular
Neuronitis
► Labyrinthitis
► Meniere’s
► Acoustic Neuroma
► Fistula
► Benign Paroxysmal Positional Vertigo (BPPV)
Central Vestibular Disorders
► Vascular
 Wallenberg’s Syndrome
 Head Injury
 Cerebellar Infarct
► Postconcussive
Syndrome
► Demyelinating Disease
► Congenital
Degenerative Cerebellar Disease
► Signs





& symptoms
abnormal ocular pursuit
gradual decline
irregular saccades
gaze end point nystagmus
ataxia
Objective of Clinical Exam
►
Establish location & severity of lesion (central or
►
Typical examination
- history (hearing status)
- cranial nerves
- vestibular
peripheral)
spontaneous nystagmus (imbalance in tone)
postural instability (abnormal tone & gain; proprioceptive loss)
VOR gain (maintained fixation, dynamic visual acuity)
head shaking (compensated UVL; not necessarily PVL)
calorics
pressure sensitivity (fistula)
positional nystagmus (Hallpike-Dix test)
hyperventilation (anxiety; acoustic neuroma)
Nystagmus
► Rapid
alternating movement of eyes in
response to continued rotation of the body
► Primary diagnostic indicator in identifying
vestibular lesions
► Physiologic nystagmus
 vestibular, visual, extreme lateral gaze
► Pathologic
nystagmus
 spontaneous, positional, gaze evoked
► Labeled
by the direction of the fast
component
► Central vs. peripheral cause differentiated by
duration
Vestibular Function Tests
► Caloric
test
► Rotary Chair test
► Posturography
Results of Vestibular Function
Tests
► Presence
of complete vs. incomplete loss
► Presence of peripheral vs. central
dysfunction
► Direct patient management
► Help in outcome prediction
Dizziness Handicap Inventory
► Three
subscales
 function
 emotion
 physical aspects
► Scoring
 Yes
4 pts.
 Sometimes 2 pts.
 No
0 pts.
► Excellent
test-retest reliability
Hallpike-Dix Maneuver
► Gold
standard used to check for the
presence of benign paroxysmal positional
vertigo (BPPV)
► Nystagmus induced by this test is an
objective measurement from which we can
determine SSC dysfunction and assess a
response to treatment
Benign Paroxysmal Positional Vertigo
(BPPV)
► Signs
& symptoms
 sudden, severe attacks of vertigo precipitated
by certain head positions & movements
►e.g.,




rolling over, neck extension, bending forward
lightheadedness; nausea
anxiety
avoids movement
direction & duration of nystagmus
differentiates between BPPV & a central
vestibular lesion (CVL)
Benign Paroxysmal Positional Vertigo
(BPPV)
►5
criteria crucial in diagnosis (Hallpike-Dix
Test):
 torsional/linear-rotary nystagmus; reproduced by
provocative positioning with affected ear down
 nystagmus of 1-5 sec. latency
 nystagmus of brief duration (5-30 sec.)
 reversal of nystagmus direction on returning to
upright position
 response diminishes with repetition of maneuver
(fatigability)
(Massoud ’96)
BPPV
Cupulolithiasis
► Debris,
probably fragments of otoconia from
the utricle, adhere to the cupula
► Treatment
 Brandt-Daroff habituation exercises
 Semont, liberatory maneuver
BPPV
Canalithiasis
► Debris
floating freely in the endolymph in
the long arm of the posterior SSC
► Treatment
 Canalith repositioning maneuver (Epley)
 84-90% remission rate
 Sleep upright one night only (more severe
cases)
Problems Experienced with
Vestibular Loss
► Balance
& gait deficits
► Head movement-induced dizziness
► Head movement-induced visual blurring
(oscillopsia)
► LE
dressing difficulty
► Driving deficits
► Disability related to work, social & leisure
activities
Systems Approach to Examination
► Examination
of balance & mobility using a
variety of tests & measurements to
document functional abilities, determine
underlying sensory, motor, & cognitive
impairments contributing to functional
disabilities
Balance
► Can
be viewed as a motor skill that
emerges from the interaction of multiple
systems
► These systems are organized to meet
functional task goals & are constrained by
the type of environment
► Balance, like any skill, can improve with
practice
Balance Components
► Steadiness
► Symmetry
► Dynamic
stability
Balance Training: Postural
Biofeedback
► Postural
symmetry & dynamic stability
have been consistently improved by
training using force platform systems
Clinical Test of Sensory
Interaction In Balance (CTSIB)
► Assesses
pattern of sensory dependence
for balance from timed stance tests
during distortion of sensory environment
Berg Balance Scale
► Performance
-orientated balance
assessment
► Interpretation:
 > 45/56 score highly specific (96%) for
nonfallers
 subjects who fell most frequently were those
closer to cut off
► Correlates
with other balance tests
Functional Gait Assessment (FGA)
► Assesses
postural stability during walking
► Modified version of the Dynamic Gait Index
► Added 3 new tasks to increase challenge
and sensitivity of the test to minor changes
in gait
► Stronger vestibular components (head
turns, narrow BOS, ambulating backwards
and with eyes closed)
General Therapeutic Intervention
Objectives
► Changing
impairments
► Improving functional performance
► Improving capacity to adapt performance
to changing task & environmental
demands
Mechanism of Recovery:
Compensation
► Results
from changes in CNS
 rebalancing of tonic activity within vestibular nuclei
(spontaneous recovery)
 recovery of VOR (vestibular adaptation)
 habituation (progressive decline in response to same
stimulus)
 alternative strategies/substitution; in complete loss of
vestibular function
► Enhanced
by active movements & processing of
visual, vestibular, & somatosensory stimuli
Result of Early Intervention
► Gain
returns quicker
► Increased function
► Decreased gait ataxia
► Decreased perception of disequilibrium
(Herdman 2000)
Vestibular Exercise Program
Objectives
► Complement
CNS natural compensation
 diminish dizziness & vertigo
 enhance gaze stabilization
 enhance postural stability in static & dynamic
situations
► Increase
overall functional activities
► Patient education
 nature of pathology
 episodic nature, prognosis
 control of exacerbations
Vestibular Program Components
► Gaze
stabilization exercises to retrain VOR
function
► Balance retraining to retrain VSR function
► Conditioning exercises to increase fitness
level
► Habituation or canal repositioning
maneuvers as indicated
e.g., Unilateral Vestibular Lesion:
Exercise Guidelines
► Adaptation
is best stimulated by producing an
error signal; work at limit of abilities
► Incorporation of head movements & visual
input
► Provide context specific stimulation to
promote adaptation
► Adaptation is positively affected by voluntary
muscle control
►
(Herdman 2000)
Vestibular Function Recovery Rates
► UVL:
6-8 weeks
► BPPV: remission in 1/few treatments
► BVL: 6 months - 2 years
► CNS Lesion: 6 months - 2 years
Physical Therapy Intervention:
Prescription
► Individualized
program:
vestibular rehabilitation
 Outpatient, 1-2 times / week (4-6 weeks)
 HEP, 5 minutes, 3x / day
 Walking program (health & fitness prescription)
► Compliance
to daily program essential
to success
► Exercise graduated for possible increase
of symptoms during the first week