VESTIBULAR DISORDERS

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ANATOMY OF VESTIBULAR
SYSTEM

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 Peripheral Vestibular
System
Functions:
To stabilize visual images on the
fovea of the retina during head
movement to allow clear vision
To maintain postural stability (esp.
during the movement of the head)
Provide information used for spatial
orientation

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 Labyrinth: (found within the temporal
bone) has 2 types of movement sensors:
Semicircular canals (SCC): signals from these
3 SCCs are primarily used for gaze stability
Anterior/superior
Posterior/inferior
Horizontal/lateral
Otolith organs: signals are primarily for
postural stability
Utricle
saccule

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 SCC:
endolymph fluid that moves freely
within each canal in response to the
direction of angular head movement
It bends the sensory receptor cells (hair
cells) in the cupula as it moves
Each SCC responds best to movement
in its own plane (either superior,
inferior, horizontal)
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 Otolith organs:
Comprised of saccule and the utricle,
respond to linear acceleration and to
the pull of gravity
Calcium carbonate crystals
(otoconia) are embedded in a
gelatinous matrix within them
The sensory receptors/hair cells,
project into this gelatinous matrix
sign 8
angular (SCC) and linear velocity(otolith) input/information

Vestibular nuclie in the brainstem (primarily medial &

superior)

Information is sent to ocular motor nuclei (VI, IV, III)

Thalamus & cortex for arousal & concious awareness of

the head & body in space

Medial & lateral vestibulo spinal tracts (MVST, LVST), PIVC,

parieto insular vestibular cortex for maintenance of
postural control
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 Central Vestibular System
Vestibular nuclei & its connections:
Reticular formation, thalamus, &
vestibular cortex contribute to the
integration of arousal & concious
awareness of the body; discerning
between movement of self & the
environment
Cerebellar connections help to
modulate the vestibulo ocular reflex
(VOR); maintain posture during active &
static activities, & coordinate lim 10
11
12
 Lesions in the central lower
brainstem structures can mimic
peripheral vestibular pathology

Central lesions in the cortex & upper

brainstem result in perceptual
disorders such the abnormal
perception of visual vertical

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PHYSIOLOGY & MOTOR
CONTROL

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 Important principles
Tonic Firing Rate
80 pulses per second: normal tonic
firing rate
even when the head is stationary
(e.g. sleep), the vestibular system is
still active
Angular or linear movement of the
head can increase or decrease the
firing rate of the vestibular system
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 Vestibulo-Ocular Reflex (VOR):
Gaze stability during rapid head movement is
maintained by VOR
SCC afferent synapses with oculomotor nuclei
producing a slow-phase eye movement (VOR)
in the opposite direction of the head movement
As the head moves in one direction, the eyes
will move in the opposite direction with equal
velocity -- vestibular gain (eye/head velocity
= 1)

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 When the head is moving at velocities less than
60 degrees per second, gaze stability can be
maintained using smooth pursuit
When the head moves greater than 60 degrees
per second, the vestibular system generates eye
movement in the direction opposite the head
movement to maintain gaze on the target
VOR operate at head velocities of 350 400 deg
per second
> 400 degrees per second VOR decreases and
gaze stability degrades

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 Push Pull Mechanism:
UVL on the UVR
SCCs - all work in pairs: (R) ant SCC paired with
(L) post SCC & vice versa, then two horizontal
canals
Head turned to -- increased firing rate
(depolarized) of horizontal SCC -- decreased
firing rate (hyperpolarized) (L) horizontal SCC
A faulty interpretation (from CNS) will lead to
difficulties with gaze stabilization, motion
perception, & postural stability

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 Inhibitory Cut Of
Rotation of the head to the side
depolarizes the hair cells of that
labyrinth resulting in:
Increase in the firing rate of the
vestibular neurons for head velocities of
up to 350 to 400 deg per second
Concomittant hyperpolarization of the
opposite labyrinth also occurs

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 Hyperpolarization of the hair cells in the
opposite labyrinth can only decrease the
firing rate to zero , point the inhibition is cut
off (inhibitory cut off)
The response to the head movements that
hyperpolarize the hair cells is limited to a
velocity range up to 80 deg per sec
E.g. rotation to of 120 per second, the ear
increases its firng rate from 80 (tonic) to 200 deg
per sec. left ear decrease from 80 to zero not
negative 40

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 Velocity Storage System:
Signal generated by movement of the cupula is
brief, lasting only as long as the cupula is
deflected
The response is sustained, by a circuit of
neurons in the medial vestibular nucleus and
lasts longer than 10 seconds.
The purpose of sustaining the vestibular input
may be to signal the brain that movement is
still occurring even though the cupula is no
longer reporting it
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ASSESSMENT

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 History
3 key items in taking the history:
Symptoms
Tempo if the pt has had an acute attach
of vertigo (within 3 days), chronic
disequilibrium, or if the pt is having
episodes of dizziness episodic vertigo ---
average duration of episodes in seconds,
minutes or hours
Circumstances if with particular
movements, positions or at rest
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 Symptoms
Dizziness: sensation of whirling or feeling a
tendency to fall
Vertigo: illusion of movement, most commonly a
sense of spinning
Lightheadedness: vague and less localizing than
vertigo. Defined as a sense of feeling as if about to
fain
Disequilibrium: subjective sensation that the
person is off balance
Oscillopsia: visual instability with head
movement in which images appear to move or
bounce; due to decrease VOR gain
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SYMPTOM POSSIBLE CAUSE

Vertigo BPPV (Benign paroxysmal

positional vertigo), unilateral
peripheral hypofunction,
unilateral central lesion
affecting the vestibular nuclei

Lightheadedness Orthostatic hypotension,

hypoglycemia, anxiety, panic
disorder
Dysequilibrium Bilateral vestibular lesion,
chronic unilateral vestibular
lesion, lower extremity
somatosensation loss, upper
brainstem/vestibular cortex
lesion, motor pathway lesions
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 Physical Examination
Oculomotor tests: most localizing
& diagnostic means to examine
vestibular system. They include:
observation of nystagmus,
examination of the VOR at high
acceleration (head thrust test),
head shaking induced nystagmus (HSN),
positional testing,
clinical dynamic visual acuity (DVA) test
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 Nystagmus
primary diagnostic indicator used in
identifying most peripheral and
central vestibular lesions
An involuntary eye movement,
nystagmus due to a peripheral
vestibular lesion is composed of
both slow and fast phase eye
movements
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 Its direction is named by the
direction of fast phase of the eye
movement
In a vestibular lesion, the slow
phase eye movement is due to a
relative excitation of one side of the
vestibular system
The fast phase is simply a resetting
eye movement
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 Nystagmus due to a vestibular lesion is
most commonly seen after an acute
unilateral insult:
Spontaneous (at rest) nystagmus occurs
in the absence of motion because of the
asymmetry between the functioning and non
functioning sides of the vestibular systems
If its due to peripheral lesions, typically resolves
after 7 days due to visual suppression as well as
the adaptive capabilities of CNS

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 OBSERVATION OF NYSTAGMUS:
Can be suppressed in light and when
a person fixates on a target
Should be performed under the
conditions in which the person
cannot visualize the surrounding
environment:
Frenzel lenses
Infrared camera
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Frenzel lenses

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Infrared camera system

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 HEAD TRUST TEST:
VOR is examined using both slow (<60
deg/sec) & rapid head rotations
Pt is asked to fixate on a near target head
moved in slow amplitude & attempts to fixate
on the target pt will be advised that head
will be moved quickly repeat with the pt
fixating on target approximately 6 ft away
Normal : will be able to maintain gaze on the
target during head movement

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 Vestibular loss: will cause the eyes to
move off the target (no VOR) & will to
refixate on the target causing a saccade
fast eye movement
If unilateral peripheral or central vestibular
lesion pt will not be able to maintain gaze
when head is rotated quickly toward the side
of lesion
If bilateral peripheral vestibular lesion results
in refixation saccades when the head is thrust
to either side
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 HEAD-SHAKING-INDUCED-NYSTAGMUS
Useful in the dx of the unilateral vestibular
defect
Pt must wear frenzel lenses or use video
infrared camera instruct pt to close eyes
clinician flexes the head 30 deg (to place
the horizontal SCC parallel with the ground)
oscillates the head horizontally 20 times
at a frequency of 2 hertz open eyes

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 Unilateral peripheral vestibular lesion:
horizontal nystagmus with the quick phase
toward the normal side and the slow phase
toward the lesioned side
Not all UVL will result in HSN
Pt wil bilateral vestibular hypofunction will
not have HSN bec of (-) asymmetry
(+) vertical nystagmus after horizontal or
vertical head shaking suggests a central
lesion
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 POSITIONAL TESTING
Used to identify vertigo and nystagmus
Benign paroxysmal position vertigo
(BPPV):
Most common cause of positional vertigo
Otoconia are dislodge and float into the SCC,
causing an abnormal signal results in brief
vertigo and nystagmus
The direction of the nystagmus is specific for
which canal is involved

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 Hallpike-Dix test: this maneuver places
the posterior SCC in a plane parallel with
pull of gravity
This test can also be performed by
moving into sidelying position
The ear toward the ground is the
labyrinth being tested
Clinician should observe the eyes for
nystagmus

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SCC INVOLVEMENT NYSTAGMUS
Posterior canal Up-beating and torsional
Anterior canal Down- beating and
torsional
Horizontal canal Horizontal
Vertical canal Torsional only
* The torsional
component occur
because of the oblique
muscle attachements the
vertical SCCs synapse
with
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 CLINICAL DYNAMIC VISUAL
ACUITY TEST
Vestibular deficits: the eyes will not
be stable in space during head
movements
Static acuity is determined first the
patient is asked to Read the lowest
line you can see
Pt then attempts to read the chart
while the clinician horizontally 47
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 A metronome is useful to ensure
correct frequency of oscillation
A 3 or more line decrement in visual
acuity during head movement
possible vestibular hypofunction

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BALANC BPPV UVL BVL CENTRAL
E TEST LESION
Romberg (-) Acute: (+) Acute: (+) Often (-)
Chronic: (-) Chronic: (-)
Tandem (-) Positive, eyes (+) (+)
Romberg closed
Single (-) Maybe (+) Acute: (+) May be
legged Chronic: (-) unable to
stance perform
Gait Normal Acute: wide- Acute: wide- May have
based, slow, based, slow, pronounced
decreased arm decreased arm ataxia
swing & trunk swing & trunk
rotation rotation
Compensated: Compensated;
Normal mild gait
deviation
Turn head May Acute: may not May not keep May not
while produce keep balance balance or slows keep
walking ligh Compensated: cadence to balance,
unsteadin Normal perform increased
ess ataxia 51
 VESTIBULAR FUNCTION TESTS:
2 most commonly used are:
Caloric testing involves infusing the
external auditory canal with air or water
This stimulus introduces a temperature
gradient causing movement of the
endolymph within the horizontal SCC
The stimulated canal generates a horizontal
nystagmus response

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 Useful for determining the side of the side, bec
each labyrinth is stimulated separately
Only the horizontal SCC is stimulated

Rotary chair test stimulates the vestibular

system by rotating subjects in the dark
The VOR is measured is measured during rotation
& compared during normal responses
Can actively stimulate both vestibular systems
Only assess vestibular function at frequencies up
to 1 hertz

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VESTIBULAR SYSTEM
DYSFUNCTION

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 Mechanical
BPPV:
Biomechanical d/o is its most common cause
s/sx:
vertigo with change in head position
Nausea with or without vomiting
Disequilibrium
Latency of onset: 15 sec with duration of
<60 sec
The vertigo & nystagmus are direct
impairments caused by misplaced otoconia
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 Indirect impairements: symptoms of
nausea, vomiting, & imbalance
Mechanisms: otoliths become
dislodged from the utricle & fall into
the SCCs
Cupulolithiasis
Canalithiasis

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 Cupulolithiasis
fragments of otoconia breakaway and
adhere to the cupula of one of the SCCs
head is moved into certain/provoking
positions weighted cupula is deflected
by the pull of gravity abnormal signal
results in vertigo & nystagmus these
persist as long as in the provoking
position
Does not explain the brief of vertigo in
BPPV 57
 Canalithiasis
Otoconia are floating freely in one of the
SCCs
Change in head positions otoconia
moves inside the SCC (because of pull of
gravity) endolymph movement &
deflection of the cupula

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 Interventions of BPPV:
Goals:
Replace the otoconia into the vestibule
Reduce the vertigo associated with head
motion
Improve balance
Educate the pt about self treatment
strategies in the advent of reoccurence
Return to daily activity involving head
motion
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 Canalith repositioning treatment (CRT):
Based on the canalithiasis theory of free floating debris
in the SCC
The pts head is moved is moved into different positions
in a sequence that will move the debris out of the
involved SCC and into the vestibule (location of saccule
& utricle) -- Debris is in position, symptoms resolved
After the tx, px wear soft collar to avoid vertical head
movts
Remain upright for 1 to 2 nights, avoid sleeping on the
involved side for 5 additional nights
Horizontal movt of head to prevent stiffed neck

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1. Pts head rotated toward the involved
side
2. Then to Hallpike-Dix position
3. Head rotated 180 degrees to the
opposite direction (unaffected side)
maintain the 30 deg neck extension
4. Pt is rolled onto shoulder (side of #3)
5. Slowly bring to sitting position, head
still rotated
6. Pt then fitted with soft collar
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 Liberatory (Semont) maneuver:
Based on cupulolithiasis theory
Involves rapidly moving the pt through
positions designed to dislodge the
debris from the cupula
Similar to CRT, pt must avoid the
provoking position & keep the head in
upright position for 1 to 2 nights after
the treatment

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1. Starts in sitting turns the head 45 deg to
one side then quickly lies down on opposite
shoulder
2. Remain for 30 sec or til vertigo stops
3. Pt slowly return to starting position
4. Maintain head in rotation until sitting upright
5. Pt turns to opposite direction repeat the
process
6. Do 10 to 20 times ; 3 x day until pt is without
vertigo for 2 consecutive days

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 Brandt-Daroff exercises:
Designed to habituate the CNS to the
provoking position, but may act by
dislodging the debris from the cupula or
by causing debris to move out of the
canal
Should be performed for 10 to 20
repetitions (may decrease to 5), 3/day
until the pt has no vertigo for 2
consecutive days
Movements must be performed rapidly 66
1. Head is rotated 45 deg
to one side e.g. (L)
2. Pt moves from sitting to
sidelying & stays in
the position for 1 minute
3. Pt is then rapidly moved
180 deg from
sidelying to (L) head
should be in original
position
4. Pt returns to sitting
may be fitted with soft
collar

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BPPV Treatment Diagnosis/ Symptoms
Procedure

CRT BPPV due to canalithiasis

Posterior SCC canalithiasis is the
most common

Liberatory BPPV due to cupullithiasis

maneuver Posterior SCC cupulolithiasis is the
most common

Brandt Daroff Persistent/ residual or mild vertigo

exercsies (even after CRT)
For pt who may not tolerate CRT
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 Decreased Receptor Input
The most common causes of unilateral
vestibular pathology are: viral insults,
trauma, & vascular events
s/sx of UVL: vertigo, spontaneous
nystagmus, oscillopsia with head
movements, postural instability, &
dysequilibrium
Vertigo & nystagmus initially resolves
within 3 to 7 days assuming exposure to
daylight conditions
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 Spontaneous nystagmus beyond 7
days may suggest possible central
lesion or unstable peripheral lesion
Symptoms of vertigo beyond 2 weeks
should be considered and indirect
impairments

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 Interventions for UVL:
Goals: recovery time upon initiating
vestibular rehabilitation averages 8
weeks
Improve stability of gaze during head
movement
Decrease sensitivity to motion
Improve static & dynamic postural
stability
Establish a home exercise program 71
 Gaze stability - To improve the VOR &
other systems that are used to assist gaze
stability with head motion
a. X1 (times 1) move the head horizontally (&
vertically if appropriate) as quickly as possible
while maintaining focus on a stable target
Retinal slip occurs when the immage of an
object moves off the fovea of the retina,
resulting in visual blurring
Must learn to slow head movement if the target
becomes blurred

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 b. X2 (times 2) pt move the head and
target in opposite directions

Both should be made increasingly

difficult as the patient improves

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 Postural stability improve
balance by encouraging the
development of balance strategies
within the limitations of the patient
( either somatosensory, visual or
vestibular)
Should challenge the pt safe if done
independently
Incorporate head movement into the
exercises most of these pt tend
decrease their head movt 74
 Motion sensitivity : habituation training
When pt has continual complaints of dizziness
Habituation is reduction in response to a
repeatedly performed movement
Provoking position mild to moderate dizzness
holds for 30 seconds or until symptoms abate
perform 3 to 5 times each, 2 to 3 times per day
Designed to reproduce dizziness and symptoms
normally decrease within 2 weeks if didnt
change, habituation should be change if still no
improvement then refer

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 Ototoxicity
The most common cause of a bilateral
vestibular lesion (BVL)
Certain aminoglycosides (gentamycin,
streptomycin) are readily taken up by
the hair cells of the vestibular apparatus
& continue to build in the system even
after the person has stopped using the
antibiotic
Dysequilibrium primary complaint
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 Direct impairments: oscillopsia & gait
ataxia are common clinical signs
No nausea or vertigo (no asymmetry in the
tonic firing rate)
Gentamycin ototoxicity- posture & gait
abnormalities, decreased visual acuity
with head movement, & reduced VOR
gains resulting in a (+) head thrust test
Impairments are likely permanent though
pts can still return to high levels of activity

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 Interventions for BVL:
Goals:
Reduce subjective complaints of gaze
instability
Improve static & dynamic balance
Instruct the patient in a HEP that
includes walking
Educate pt in activities that may be
more difficult owing to the disorder
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 Gaze stability exercises:
May be similar to X1 but X2 is not
recommended (may produce excessive
retinal slip)
Pts with BVL depend on somtosensation
&/or vision to maintain postural stability
Balance excercises should enhance the
use of these cues

Should be performed safely

Begin with walking program, daily if 79
BVL Exercises to improve central
reprogramming of eye movements
Begin with Progress to
1. Hold two targets at
1. Progress to
arms length from
increasing the
your head. Look with
distance used to see
your eyes first, then
the target. Use a
turn your head
busy background
toward the target.
(checkeredboard,
Attempt to do this
venetian blinds)
for 60 sec
2. Perform exercise 1 in
the vertical direction 2. Same as horizontal
exercise

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Begin with Progress to
Hold one target at
arms length from
your head. Close your
eyes and turn your Progress to doing this
head away from the standing
target, attempting to
Progress to decreasing
keep your eyes
base of support
focused on the target.
Open your eyes only
after having turned
your head
81
 Balance Exercises
Begin With Progress To Purpose

1. Stand with feet Bring feet closer Enhance the use of

shoulder width together. vestibular signal
apart, arms across Close eyes. Stand form balance by
the chest on a sofa decreasing BOS
cushion/pillow Eyes closed
increases reliance
on vestibular
signals for balance

2. Practive ankle Doing circle sways. Teaches the pt to

sways: ant-post & Close eyes use a correct ankle
med- lat strategy.

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Begin With Progress To Purpose
3. Attempt to walk Do the same Enhance the use of
with heel touching exercise on carpet vestibular signal for
toe on firm surface balance by
decreasing BOS
Doing exercise on
carpet decreases
proprioception,
increasing difficulty

4. Practice walking Making smaller The turning

& turning around turns. Close eyes stimulates &
challenges the
vestibular system
5. Walk & move Counting Challenge balance
your head side to backwards from & stimulate both
side 100 by threes vestibular system
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 Central Nervous System
Lesion
1. Cerebrovascular insult particularly
of the anterior-inferior cerebellar
artery (AICA), posterior-inferior
cerebellar artery (PICA), & vertebral
artery
2. Traumatic brain injury
3. Vertebrobasilar insufficiency
4. Demyelinating disease such as
multiple sclerosis (MS)
84
Common symptoms
Central peripheral
Smooth pursuit &
Abnormal smooth pursuit saccades usually
& abnormal saccadic eye normal; positional
movement tests testing may reproduce
SX usually do not include nystagmus
hearing loss
SX may include
SX migh include diploplia
hearing loss fullness in
, altered conscious,
lateropulsion, ears, tinnitus
SX of acute vertigo not SX of acutevertigo
usually suppressed by usually intense (more
visual fixation than central vestibular
pathology)
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CENTRAL PERIPHERAL

Pendular nystagmus Nystagmus will

Pure pesistent vertical incoporate slow & fast
nystagmus persists phases (jerk
regarless of positional nystagmus)
testing (persistent Spontaneous
downbeat nystagmus persistent horizontal
in Hallpike Dix may nystagmus will resolve
indicate anterior canal within 7 days in a
BPPV patent with UVL

86
 Head trauma:
Another method of sustaining a
peripheral vestibular lesion
Damage to the vestibule within its
protective encasement bony labyrinth
TBI pts commonly suffer from vertigo ---
central processing of the vestibular
input may also be the cause of their
vertigo

87
 Pendular nystagmus eyes oscillate at equal
speeds; often indicative of congenital disorders
(e.g. absence of central central vision)
Lateropulsion persons tendency to fall to
one side
Red flags: horizontal or vertical diplopia lasting
longer than 2 weeks after the onset of unilateral
vestibular loss; persistent pure vertical
positional nystagmus (anterior canal
cupulolithiasis should be r/o); & spontaneous up
beating nystagmus (rare)

88
 Ocular tilt
reaction (OTR):
Ocular torsion
both eyes rotating
downward the
direction of tilt
Head tilting
Skew deviation
eyes appears as
one eye being
superiorly displaced
in comparizon with
the other eye 89
 Interventions for CVL:
Goals:
Ensure fall prevention strategies &
necessary safety precautions are in
place to allow safe functioning within
the home & community
Educate pt in compensatory strategies
to assist in gaze stability
Instruct the pt in a HEP that includes
walking
90
 TBI pts may not be ideal for
vestibular rehabiliatation due to its
irritating nature & further
disorienting the pt
At the level of the brainstem
(vestibular nuclei) similar
expectations for recovery with UVL
Vestibular cortical lesions may also
recover similar to the process of CVA
91
 Common Vestibular
Diagnoses
MENIERES DISEASE:
Low frequency hearing loss & episodic
vertigo
May also complain of tinnitus sense
of fullness in the ear
SX gradually increase in severity & then
last 1 to 2 hours per episode
Chronic type can result to UPV
hypofunction (requires rehabilitation)

92
 Pathophysiology: probably involves an
increase in endolymphatic fluid causing
distension of the membranous tissues
Medical intervention to reduce fluid build up
Many pts can manage the SX well with
controlled diet 2 grams or less per day of
sodium diet (most important dietary
restriction to follow)
Avoid caffeine & alcohol
Sometimes managed with diuretic to control
the amount of fluid in the body
93
 Surgery: endolymphatic shunt
placement prevent fluid buildup in
the inner ear; vestibular nerve
section stop abnormal vestibular
signal
PT: most beneficial for unilateral
vestibular hypofunction therapy will
not stop vertigo; gaze & postural
stability exercise; tx of disequilibrium
occuring after neurectomy
94
 PERILYMPHATIC FISTULA (PFL):
Most commonly caused by rupture of
the oval or round windows, membranes
that separate the middle & inner ear
Rupture leakage of the perilymph into
the middle ear vertigo & hearing loss
Perilymph bathes the SCC, serving as a
protective barrier between the bony &
membranous labyrinth

95
 Usually caused by a traumatic event e.g.
excessive pressure changes as in deep
water diving, blunt head trauma without
skull fracture; or extremely loud noise
Tx: initially with bed rest hopes of
allowing the membrane to heal
PT: contrainicated in most cases with PLF
Medical mx: strict limitations on activities,
warranting good communication between
PT & MD

96
 ACOUSTIC NEUROMA:
A.k.a Vestibular schwannoma
Benign tumor located on CN VIII
S/SX: progressive hearing loss; tinnitus;
& disequilibrium
TX: usually surgical excision of the
tumor
PT: early post-op to help the resolve SXs
of disequilibrium & oscillopsia; OPD
should be considered similar to tx of UVL
97
 MOTION SICKNESS:
Normal sensation but in some people
becomes debilitating
Sensory conflict theory proprioception,
vestibular, & visual information do not match
stored neural patterns the brain expects to
recognize pallor, nausea, emesis,
diaphoresis, & motion sensitivity
TX: cognitive behavioral management,
medications, biofeedback, & habituation
training using ground & flight situations
98
Common Nonvestibular Diagnoses

MIGRAINE-RELATED DIZZINESS:
Can be deceptively similar to a
peripheral vestibular lesion vascular
event occurs in a vestibular structure
(vestibular nuclei)
SX: vertigo, dizzines, & motion sickness
Women between 35 & 45 are more
prone
Often well controlled with medication &
diet
99
 MULTIPLE SCLEROSIS:
MS can affect CN VIII where it enters the
brainstem & causes identical symptoms
to a unilateral vestibular pathology.

100
 CERVICAL VERTIGO:
Commonly used in Europe
Mechanisms;
1. upper cervical spine sends proprioception input
to the C/L vestibular nucleus soft tissue injury &
joint dysfunction might alter the afferent input
contributing to spatial orientation
2. (+) vertebrobasilar insufficiency pt is seated
then leands forward & extends the neck then rotate
45 deg to suspicious side SX: diplopia,
dysarthria, syncope, headache, visual field deficits,
vertigo & nystagmus

101
 C/I for Vestibular
Rehabilitation
Unstable vestibular d/o (Menieres dse, PLF)
Sudden loss of hearing
Increased feeling of pressure or fullness to
the point of discomfort in one or both ears
Severe ringing in one or both ears
When treating for post op: observe for
d/charge of fluid from ears or nose (CSF leak);
Pt with acute neck injuries may not be able to
tolerate either CRT or some of the gaze
stability exercises

102