VESTIBULAR DISORDERS

1. ANAPHY
II. ETIOLOGY et EPIDEMIOLOGY

III. CONDITIONS
PERIPHERAL CENTRAL
1° due to CWA insults
① BPPV /Benign Paroxysmal Positional Vertigo)
distention of
Onegin: Biomechanical ① Menier's Disease :
↑ undo lymphatic fluid → membranous tissues
leakage of
↳ displaced otoconia :
① Perilymph Fistula ruptured oval windows
: →
perilymph
A) benign tumor on @ located at
a. Cupulothiasic -
> 60sec ③ Vestibular Schwannomg :
CN 8 Schwann cell IAC

b. Canalithiasis ! ≤ 60sec ④ Motion sickness

"
:
sensory conflict theory

⑤ Migraine -
Related Sickness
② UHH / Unilateral Vestibular Hypofunction) ⑥ Cewicogenic Dizziness pathology :
in cervical spine
↳ soft tissue injury affectation
0Ñ9l Viral insults ; trauma ;
-

→
a- Afferent
joint dysfunction input
↳ ↓ receptor input

③ BVH /Bilateral Vestibular Hypofunction)

origin ◦to toxicity :
use of antibiotics
gentomyoin streptomycin
,

↳ ↓ receptor input

↳
RED FLAGS : suspect of central lesson involvement
① Horizontal / Vertical DIPLOPIA > 2 weeks i
① Persistent Pure Vertical Nystagmus
③ Spontaneous UP -

beating Nystagmus
④ Skew deviation
V. PT EXAMINATION
① Hx taking
② HAS
③ Motion Sensitive Quotient
④ Examination of EYE MOVEMENTS
⑤ Positional Testing
⑥ Gait and Balance

VI. PT MANAGEMENT

BPPV UVA BVH

i. Ep1eys(canalith) stability stability
Repositioning i. Gare i. Gare
2.
Libertorylsemont) (✗ i. XD (✗ i. XD
3.
Appaini / Gufoni) e. Postural stab :
2. Postural stab :

4. BBQ / Lampert) a.
Romberg a.
Romberg
5. Forced Prolonged Position b. Tandem b.Tandem
a. Casani maneuver 3. Habituation / 3.
Compensatory strategies
Brandt Banff Cawthorne Habituation ex
Cooksey
-

7. - _ -

NOT DONE
(Habituation Ex)

central Union DIO

i. Habituation ex .

2. Gait and Balance ex .

 I

14 DIFFERENTIAL DIAGNOSIS
.

1-

+
C
-

- - O - -
0

*
Ncfe component
① Slow Head position ISOLATE

② UDN Posterior SCC

→
= = neck ( r ) ill rdahm

DBN =
Anterior fec = neck ( v ) 4L rotation
 VESTIBULAR DISORDERS
 NYSTAGMUS:
 primary diagnostic indicator used in identifying most peripheral and central vestibular lesions
 composed of both slow and fast components
 direction of the nystagmus is named by the direction of the fast component.
 Normally, the subject’s eyes stay fixed on the examiner’s nose throughout the test
 (+) test = the eyes fall off the target and move with the head

Benign Paroxysmal Positional Unilateral Vestibular Bilateral Vestibular

Vertigo (BPPV) Hypofunction (UVH) Hypofunction (BVH)
Two Mechanisms: * Symptoms
Cupulolithiasis: Canalithiasis: M/C cause: ototoxicity
→ fragments of → otoconia are  Direct impairments of  gentamicin, streptomycin
otoconia floating vertigo Less common causes:
break away freely in one  Spontaneous nystagmus meningitis, autoimmune
and adhere to of the SCCs  Oscillopsia with head disorders, head trauma, tumors
the cupula of → M/C movements on each 8th CN, bilateral
one of the → </= 60 s  Postural instability vestibular schwannoma,
SCCs  Visual blurring transient ischemic episodes of
→ >60 seconds  Dysequilibrium vestibular vessels, sequential
* Symptoms unilateral vestibular neuronitis.
 the weighted cupula is deflected * symptoms :

by the pull of gravity  Primary complaint is

 Vertigo and nystagmus with
change in head position
 Nausea with or without
vomiting
 Disequilibrium
GOALS:
a. The otoconia will be returned into
the vestibule.
b. The patient will demonstrate
reduced vertigo associated with
head motion.
c. The patient will demonstrate
improved balance.
d. The patient will demonstrate
enhanced decision-making skills
regarding self-treatment
strategies as a form of
prophylaxis.
e. The patient will demonstrate
independence in daily activity
(BADL, IADL) involving head
motion
I. Canalith Repositioning
Maneuver (CRM)
 Canalithiasis theory of free-
floating debris in the SCC
 The patient’s head is moved
into different positions in a
sequence that will move the
debris out of the involved
SCC and into the vestibule
(general term for the location
of the utricle and saccule)
Interventions
GOALS:
a. Improved stability of gaze
during head movement
b. Diminished sensitivity to
motion
c. Improved static and
dynamic postural stability
d. Independence in proper
performance of a home
exercise program that
includes walking
I. Gaze Stability
 Improves VOR and
other systems that are
used to assist gaze
stability with head
motion.
 Designed to expose
patient to retinal slip
 The patient must learn
to low the head
movement If the target
becomes blurred
Note! Retinal slip occurs when
the image of an object moves off IV. Tai chi: to improve
the fovea of the retina, resulting
in visual blurring
dysequilibrium; oscillopsia,
gait ataxia
 NO nausea, vertigo
(asymmetrical BVH)
 Patients can return to high
levels of activity (despite
permanent impairments)
GOALS:
a. Improved stability of gaze
during head movement
b. Reduced subjective
complaints of gaze
instability
c. Improved static and
dynamic balance
d. Independent in proper
performance of a HEP that
includes walking
e. Enhanced decision making
skills regarding
performance of daily
activity made more
challenging owing to the
disorder.
I. Balance exercises
II. Begin with a walking
program progressed to
ambulating on different
surfaces/environments
III. Pool exercises: buoyancy
allows the patient to move
safely w/o fall risks
balance, flexibility,and
increase strength
II. Liberatory (Semont) Maneuver
 First offered as a treatment
for posterior SCC BPPV
based on the cupulolithiasis
theory
 Involved rapidly moving the
patient through positions
designed to “dislodge” the
debris from the cupula.
 More difficult to for the patient
to tolerate but effective
alternative to treat
canalithiasis
III. Brandt-Daroff Exercises
 Habituate the CNS to the
provoking position
 May also act to dislodge
debris from the cupula
 Movements must be
performed rapidly hence will
provoke the patient’s vertigo
II. Postural Stability V. Vestibular adaptation
 To improve balance by exercise: excellent starting
encouraging the point for UVH/BVH patients
development of balance due to beneficial effects on
strategies within the gait, posture, and DVA
limitations of the patient
 Must challenge the
patient and be safe
enough to perform
independently
III. Motion Sensitivity
 To determine the
prescription, PT must
first identify the
“provoking position”,
this is by eliciting a mild
to moderate dizziness,
the patient remains in
provoking position for
30 seconds or less
intense feeling.
 Then a HEP will be
given to the patient
based on the results of
the positional testing.
 This is done 3-5x each,
2-3x/day.
 Habituation training:
warranted when a patient
with UVH has continual
complaints of dizziness
 CENTRAL NERVOUS SYSTEM PATHOLOGY
→ CVA Insults (AICA, PICA, Vertebral Artery) – causes vertigo though other signs associated with these
infarcts are present and help clarify the site of pathology
 AICA infarcts - hearing loss is usually more common
 Vertebral Artery – may affect the cerebellum only and can mimic a peripheral vestibular
hypofunction (dysdiadochokinesia or past pointing)
 Transient Ichemic Attacks (TIA) – sudden vertigo that lasts minutes, also hearing loss
 TBI – d/t skulls fractures may complain of vertigo , abnormal central processing causes the
perseveration of vertigo
 Vertebrobasilar insufficiency (VBI) – M/C cause is MVA; M/C symptom is visual field cuts,
also by cervical spondylosis
– does not involve classic signs and symptoms of vestibular pathology but involves drop
attacks, transient blindness, dysarthria
 Multiple Sclerosis (MS) – can affect CN 8

Description Interventions
Meniere’s Disease → Diagnosed by a documented:  Reducing or preventing
 Low-frequency hearing loss fluid build-up
 Episodic vertigo  Can be managed well
 Sense of fullness in the ear with controlled diet (2g/d
 Tinnitus (constant ringing sound in the or less sodium diet) –
absence of an external source) most important dietary
→ Symptoms gradually increase in severity restriction to follow
and then last 1-2 hrs per episode  Avoid caffeine and
→ During an episode, vestibular exercises are alcohol
not recommended  Diuretics to control the
→ Chronic Meniere can result to UVH for amount of fluid in the
which rehab is appropriate. body
 Surgery to prevent the
 Cause: fluid build up in the inner
 Increase in the endolymphatic fluid ear (endolymphatic
causing distention of the membranous shunt placement)
tissues  Physical therapy in
treating the effects of
UVH
Perilymphatic Fistula → A leakage of the perilymph into the middle  Treatment is ambiguous
ear resulting to vertigo and hearing loss  Treated usually with
→ PLF can happen during traumatic events bedrest in hopes of
such as deep-water diving, blunt head allowing the membranes
trauma without skull fracture, extremely to heal
loud noise.  Surgical patches of fistula

Vestibular → A benign tumor located on CN 8 schwann  Treatments usually

Schwannoma cell often in internal auditory canal (IAC) involves surgical incision
- aka Acoustic Neuroma of the tumor
Note! The IAC also contains the facial nerve  PT in early postoperative
(CN 7) and internal auditory artery period to help resolve
symptoms of
→ Complaints include: dysequilibrium and
 Unilateral hearing loss: M/C initial sign oscillopsia
 Progressive hearing loss  Outpatient treatment is
 Tinnitus similar for a UVH
 Disequilibrium
Motion Sickness → Normal sensation but is debilitating in some  Physical therapy reduces
people motion sensitivity
→ Sensory conflict theory  Cognitive behavioral
 sensory inputs of proprioception, management
vestibular, and visual information do  Biofeedback
not match stored neural patterns the  Habituation training
brain expects to recognize
→ Patient experiences:  Medications
 Pallor
 Nausea
 Emesis (vomiting)
 Diaphoresis (cold sweats)
 Motion sensitivity

Migraine-related → Deceptively similar to peripheral vestibular  Clinical examination can

Dizziness lesions (BBPV/UVH) help differentiate
→ Vertigo, dizziness, imbalance, motion vestibular pathology and
sickness migraine
→ If not controlled, may become worse with  Often well controlled with
vestibular rehabilitation medication and diet

Cervicogenic  Mechanism:  Persons suspected of

Dizziness 1. Soft tissue injury and joint dysfunction having VBI should be
- aka Cervical Vertigo might alter the afferent input referred to a neurologist
(proprioceptive input from the upper immediately
cervical spine) contributing to spatial
orientation
2. Pt might have VBI
 VBI Test: The VBI test can be
performed while the subject is
seated. The patient leans forward
and extends the neck. The neck is
then rotated 45° to the suspicious
side.

Contraindications to Physical Therapy

 Unstable vestibular disorders such as Ménière’s disease

 Uncontrolled migraine
 Perilymphatic fistula (PLF)
 An unrepaired superior semicircular canal dehiscence (burst).
 Sudden loss of hearing
 Increased feeling of pressure or fullness to the point of discomfort in one or both ears, and
severe ringing in one or both ears (Tinnitus)
 Postoperative pts must be observed for fluid discharge from the ears or nose = CSF leak
 Patients with acute neck injuries may not be able to tolerate some components of the physical
examination (CRM, gaze stability exercises)
 PT MANAGEMENT: EXAMINATION

1. History-taking
a. Duration of vertigo?
 Seconds to minutes for BPPV
 Minutes to hours for Meniere’s Disease
 Several days for vestibular neuronitis/unilateral vestibular hypofunction
b. Medications? = antibiotics-aminoglycosides
c. Cause?
2. Visual Analogue Scale
 To check level of intensity of vertigo (environment), oscillopsia (objects), light-headedness (-) vestibular (could be OH), disequilibrium
 *if complain is “dizziness”, find what they specifically mean (describe): environment/objects moving? Light-headedness? Feeling of falling?
 Also used for subjective complaints (measure from 0-10)
 Effective in knowing: severity of complaint and in monitoring patient’s improvement
3. Motion Sensitivity Quotient
 Position patient in a provoking position where VOR/vertigo is activated (commonly used in BPPV)

Examination of Eye Movements Positional Testing Gait And Balance (Activity)

1. Smooth pursuit
 Ability to follow moving object
while head is stationary position
 Movement is not a vestibular
function but is used to rule out
central lesion (CVA?)
 If patient (+) vestibular disorder,
their smooth pursuit is normal
 Specifically, problem with
extraocular muscles
2. Saccadic movements
 Ability to jump vision from one
position to another
 (-) vestibular function
 Problem with saccadic
movements = problem with
extraocular muscles
1. Modified CTSIB
During Testing: 2. Dynamic Gait Index
 Keep eyes open and remain in provoking position 3. Gait speed
 Explain that the vertigo will stop or decrease if the 4. Physical Activities Scale for the Elderly
patient remains in the position
 If the patient's history suggests which side is
affected, start in unaffected side
 If the patient has severe nausea/emesis (vomiting),
the testing manuevers should be performed slowly.
 Perform in room light and use Frenzel lenses or
infrared camera system
Vertical canals
1. Dix-Hallpike maneuver/Barany maneuver/Nylen-
Barany maneuver
→ Gold standard test for BPPV
→ Also used to test Cranial Nerve 8
→ Check for UBN/DBN = assesses vertical canals
2. Sidelying test
→ Modification if patient cannot do Dix-Hallpike
→ Check for UBN/DBN
3. Skew deviation
 (+) central lesion vestibular
problems; (-) UVH/BVH
 Cover one eye and check, then
cover the other eye and check if
the eye has moved (up and
down) = skew deviation or eye
is not level
4. Nystagmus
a) Peripheral (jerky: slow /fast
phase)
b) Central origin (pendular -
equal velocity of nystagmus)
5. VOR:
 Head Impulse Test
a. UVH/central (corrective saccade
on side of the lesion)
b. BVH (corrective saccade on both
sides)
 Head-Shaking Induced Nystagmus
Test
a. Central lesion (vertical
nystagmus)
b. Peripheral (horizontal
nystagmus: direction towards
the affected side)
6. Dynamic Visual Acuity
 In static position, let patient
read the Snellen Chart (give
score – lines or letters patient
was able to read)
 Next, shake their head 20 times
quickly while they are ready
 Compare the difference with
lines they were not able to read
from static and with head
shaking
 (+) Vestibular/gaze stability
problems = >3 lines difference
Horizontal canals Participation (choose only one preferred scale but use
1. Roll test: commonly used test for horizontal canal ICF format)
→ Patient is in supine and head is rotated to one  Dizziness Handicap Inventory
side  Sickness Impact Profile
→ Wherever the head is rotated, that is the ear  Vestibular Disorders Activities of Daily Living Scale
you are testing.  Vestibular Activities and Participation Scale*
→ Determine if cupulolithiasis or canalithiasis
depends on the direction of the fast phase.
a) Geotropic – canalithiasis; fast
phase/fast beat is towards the ground
b) Ageotropic – cupulolithiasis; fast
phase/fast beat is away from the
ground (sends inhibitory signal)
→ Slow phase is still the VOR while fast phase is
the opposite or the repositioning
→ Ex: In checking left canal, the eye is positioned
to the right in slow-phase. Basically, the eye is
going away from the ground. Thus, it’s fast
phase will go towards the ground.
→ This means that the patient has (+) horizontal
canalithiasis
2. Bow and Lean test
 Diagnostic test for horizontal SCC
a) Bow: fast component beats toward affected
side (canalithiasis); away from affected side
(cupulolithiasis)
b) Lean: fast component beats away from
affected side (canalithiasis); towards
affected side (cupulolithiasis)
Testing sequence:
1. Dix-Hallpike Test (to check for vertical problem)
If first test is negative, proceed to:
2. Roll test (to check for horizontal problem; only the
duration is noted here)
3. Bow and Lean test (confirm if canalithiasis<60/
cupulolithiasis>60s) or Sidelying test (do this test if
previous test is negative because the condition
might actually be vertical)
4. Perform whatever movements that provoke sx
 PT MANAGEMENT
BPPV UVH BVH Central Lesion
1. Posterior: 1. Gaze stability exercise: 1. Gaze stability exercise 1. Habituation exercise
 Canalith Repositioning treatment / Epleys improve the VOR 2. Postural stability exercise 2. Gait and Balance
 Liberatory (Semont) maneuver  X1 3. Compensatory strategies: exercise
2. Anterior:  X2  learn to turn on lights at
 Canalith repositioning treatment / Epleys  use dynamic visual night if they have to get
3. Horizontal: acuity as outcome out of bed
a. Canalithiasis measure and to check  wait, sitting at the edge
 Appiani/Gufoni maneuver improvement of the bed, before
 Bar-B-Que Roll (Lempert) Maneuver getting up in the dark
 Forced Prolonged Position 2. Postural stability exercise  use lights that come on
b. Cupulolithiasis: Casani maneuver  Romberg positions automatically and to
4. Unknown problem (vertigo but no nystagmus):  Tandem walking or have emergency
 Brandt-Daroff maneuver (habituation Ex) standing lighting inside and
outside the house in
3. Habituation exercise (do case of a power failure
provoking position repeatedly
until they tolerate it because Note! No habituation exercise
patient is said to improve)
 Cawthorne-Cooksey
exercise

Precautions Contraindications
→ Modify position of patient/Do slow movements → Cannot prescribe vestibular rehabilitation
→ Can also allow patient to do it on their own for a controlled movement  Unstable vestibular disorders
 Cervical spine instability  Uncontrolled migraine
 Prolapsed intervertebral disk w/ radiculopathy  Unrepaired superior semicircular canal dehiscence
 Cervical myelopathy  Sudden loss of hearing
 Arnold Chiari malformation  Increased feeling of pressure/fullness to the point of discomfort
 Vascular dissection syndromes in one or both ears
 Previous cervical spine surgery  Severe ringing in one or both ears (Tinnitus)
 Acute trauma to neck (“whiplash”)
 Rheumatoid arthritis
 Carotid sinus syncope
 Aplasia of the odontoid process
992 SECTION II Intervention Strategies for Rehabilitation
■ DIAGNOSES INVOLVING
THE VESTIBULAR SYSTEM
Ménière’s Disease
Ménière’s disease is confirmed by a documented low-
frequency hearing loss and episodic vertigo. The
patient may also complain of a sense of fullness in the
ear and tinnitus. The symptoms gradually increase in
severity and can last several hours per episode. During
an episode, vestibular exercises are not recommended.
Chronic Ménière’s disease, however, can result in a
UVH, for which rehabilitation is appropriate. The
pathophysiology of Ménière’s disease, in part, probably
involves an increase in endolymphatic fluid causing
distention of the membranous tissues.130 Medical treat-
ment is therefore directed toward reducing or prevent-
ing fluid buildup. Many patients can manage the
symptoms well with a controlled diet. Patients with
Ménière’s disease are often placed on a 2 g/day or less
sodium diet. This is the most important dietary restric-
tion to follow. Other substances to be avoided are caf-
feine and alcohol. Sometimes medical management
includes use of a diuretic to control the amount of
water in the body. Surgery to either prevent the fluid
buildup in the inner ear (endolymphatic shunt place-
ment) or to stop the abnormal vestibular signal
r
(vestibular nerve section, or chemical ablation using cranial
transtympanic gentamicin injection) may be indicated NERVE
- the facial nerve (cranial nerve VII) and the internal
if the episodes are frequent enough to disturb daily
function. Physical therapy is beneficial in treating the
effects of a UVH owing to chronic Ménière’s disease,
although the therapy will not stop the episodes of ver-
tigo. Gaze and postural stability exercises may be ap-
propriate. Physical therapy is also useful in the
treatment of dysequilibrium occurring after a vestibular
neurectomy or chemical ablation.
Perilymphatic Fistula
Perilymphatic fistula (PLF) is most commonly caused
by a rupture of the oval or round windows, membranes
thatC separate the middle and inner ear. A A rupture of
these membranes results in leakage of the perilymph
into the middle ear. The result is vertigo and hearing
loss. Normally, perilymph bathes the SCCs and serves
as a protective barrier between the bony and membra-
nous labyrinth. PLF usually is caused from a traumatic
event, such as excessive pressure changes as in deep-
water diving, blunt head trauma without skull fracture,
or extremely loud noise.131 This diagnosis is much
debated and the treatment for PLF is similarly ambigu-
ous. Patients often are treated first with bedrest in
hopes of allowing the membrane to heal. Surgical
patches of the fistula are also performed. Physical ther-
apy is contraindicated for most patients with PLF;
however, it can be beneficial for those patients who
have continual dysequilibrium or develop a vestibular
hypofunction postoperatively. Medical management
will likely include strict limitations on activities, war-
ranting good communication between physical thera-
pist and physician.
A form of PLF not debated is superior semicircular
canal dehiscence. In this condition, the region of the
temporal bone normally covering the superior SCC is
thin or missing, rendering the membranous SCC sus-
ceptible to stimuli that it normally should not (e.g.,
sound, change of cranial pressure, vibrations).132 The
patient will notice a disturbing syndrome of vestibular
and auditory signs that may include eye movements
induced by loud noises or effort that increase intracranial
pressure (e.g., coughing), sudden or progressive hearing
loss, conductive hyperacusis, conductive hearing loss
that can mimic otosclerosis (abnormal bone growth near
middle ear), autophony (person’s own voice sounds
amplified), imbalance with noise, vertigo, or motion sen-
sitivity. Some patients even report hearing their eyeballs,
“as if scratching sandpaper!”
Vestibular Schwannoma
Vestibular schwannomas (VSs), historically known as
acoustic neuromas, are benign tumors arising from the
-0
Schwann cell of the eighth cranial nerve, often in the
internal auditory canal (IAC). The IAC also contains
auditory artery along with the vestibulocochlear nerve.
Symptom presentation is usually related to where the
tumor arises. If the tumor arises in the IAC, then tinnitus
and hearing loss are often the first symptoms. However,
if the growth occurs in the cerebellar-pontine angle, the
tumor may become quite large before symptoms of
hearing loss are revealed. Thus, although unilateral hear-
ing loss is often the initial sign of VS, the pathogenesis
of the associated structures within the space can some-
times result in vestibular (i.e., vertigo, imbalance), facial,
or even vascular symptoms. Generally, VS tumors grow
slowly. As a result, the extent of impaired vestibular or
facial nerve function is often not appreciated until the
tumor is removed. This is because the tumor gradually
compresses the cranial nerves, and in the case of vestibu-
lar function, allows the brain to compensate. However,
as the VS enlarges, symptoms of hearing loss, tinnitus,
and vestibular hypofunction worsen, resulting in the
primary deficits. Treatment usually involves surgical
excision of the tumor, though gamma knife radiation is
also an option. On tumor removal, most unilateral
vestibular afference is lost and the brain now perceives
asymmetrical vestibular input. Optimally, physical ther-
apy is initiated during the early postoperative period to
help the patient resolve symptoms of dysequilibrium and
oscillopsia.119 Outpatient treatment should be considered
similar to the treatment for a UVH.

Motion Sickness
Motion sickness is a normal sensation that in some peo-
ple becomes debilitating. The predominant explanation
for motion sickness is the sensory conflict theory.133 The
three sensory inputs of proprioception, vestibular, and
visual information- do not match stored neural patterns
-
the brain expects to recognize. As a result, persons
experience pallor, nausea, emesis, diaphoresis, and
motion sensitivity. Physical therapy has been successfully
used to reduce motion sensitivity.134 Other methods
reported to combat motion sickness include the use of
cognitive-behavioral management, medications, biofeed-
back, and habituation training.135-138
Migraine-Related Dizziness
Migraine-related dizziness can be deceptively similar
to a peripheral vestibular lesion, be it BPPV or UVH.
Migraine-related symptoms include vertigo, dizziness,
imbalance, and motion sickness. A recent study reported
100% of migraineurs had abnormal nystagmus during a
migraine episode, if they were positionally tested as part
of an oculomotor examination.139 The prevalence of
migraine is significant, affecting 6% of men and 15% to
18% of women between the ages of 25 and 55.140 The
clinical examination will often provide the differential
diagnosis between vestibular pathology and migraine. The
history is crucial and important questions to patients in
whom migraine is suspected include asking if symptoms
worsen when barometric pressure changes, and whether
headache or eating certain foods are associated with any
of the symptoms. If the therapist suspects migraine the
patient should be referred to a neurologist, preferably one
with a special interest in headache. Migraine is often well
controlled with medication and diet. Migraine that is not
controlled may become worse with exercises such as
vestibular rehabilitation, which stimulate the peripheral
vestibular end organ and central VOR pathways.141
Vestibular rehabilitation in patients with migraine can be
very helpful, but patients with both vestibular hypofunc-
tion and migraine do not respond as well.142 Strupp et
al143 provide a thorough discussion of this topic.
Multiple Sclerosis
MS can affect cranial nerve VIII where it enters the
brainstem and causes identical symptoms to a unilateral
vestibular pathology. An MRI scan will ensure an accu-
rate diagnosis of MS.
Multiple System Atrophy
Multiple system atrophy (MSA) is a progressive
degenerative disease of the nervous system involving
CHAPTER 21 Vestibular Disorders 993
four clinical domains: cerebellar ataxia, autonomic
dysfunction, Parkinson’s disease–like symptoms, and
corticospinal dysfunction. MSA has been found to be
a cause of dizziness and imbalance.144 The effect of
physical therapy for persons with MSA has not been
thoroughly investigated, though a case study has been
reported.144
Cervicogenic Dizziness
Cervicogenic dizziness is a term meant to imply that the
cause of symptoms such as dizziness or imbalance arise
from pathology affecting the cervical spine or related soft
tissue. Unfortunately, cervical vertigo is a term still often
used, which implies true vertigo as a result of cervical
pathology, not documented in humans. The mecha-
nisms of involvement are believed to be from at least two
sources. First, the upper cervical spine sends propriocep-
tive input to the contralateral vestibular nucleus.145 Soft
tissue injury and joint dysfunction mighto alter the affer-
-
ent input contributing to spatial orientation. Vestibular
-
rehabilitation appears to be warranted for these individ-
uals.146 Second, a patient might have VBI (see above sec-
tion titled Central Nervous System Pathology). If VBI
is suspected, vascular compromise must first be ruled out
as a cause of the patient’s symptoms. The VBI test can
be performed while the subject is seated. The patient
leans forward and extends the neck. The neck is then ro-
tated 45° to the suspicious side. Persons suspected of
having VBI should be referred to a neurologist immedi-
ately. Repeated episodes of vertigo without the associ-
ated VBI symptoms usually suggest a peripheral
vestibular diagnosis.
■ CONTRAINDICATIONS TO
VESTIBULAR REHABILITATION
Physical therapy is not appropriate for unstable
vestibular disorders such as Ménière’s disease (with the
exception mentioned above), uncontrolled migraine,
PLF, or an unrepaired superior semicircular canal
dehiscence. Other contraindications the physical
therapist should be alert to include sudden loss of
hearing, increased feeling of pressure or fullness to
the point of discomfort in one or both ears, and
severe ringing in one or both ears. When treating
patients who have had a surgical procedure, the
clinician must be observant for discharge of fluid from
the ears or nose, which may indicate cerebrospinal
fluid leak. Patients with acute neck injuries may not
be able to tolerate some components of the physical
examination, the CRM, or some of the gaze stability
exercises.
 E.÷ *
:
.
:÷÷÷÷÷ ¥
.
¥
÷¥¥:11÷:÷
:
:÷÷;÷÷¥÷
$
at
}:
¥
÷ :÷÷
÷
Ei
÷÷÷÷ .
 BRIEF REVIEW OF VESTIBULAR SYSTEMS

3 primary functions: B. Otolith (vestibule) Organs

1. Stabilizing visual images on the fovea of the
retina during head movement to allow clear
vision  the VOR stabilizes an image seen
while the head is moving
2. Maintaining postural stability, especially during
movement of the head  VCR and VSR
3. Providing information used for spatial
orientation  SCCs and Otolith organs

VESTIBULAR APPARATUS

→ For balance, equilibrium, spatial orientation → Sensitive to LINEAR Acceleration/

→ Consists of 2 main structures:
 Semi-Circular Canals (SCCs)
 Otolith Organs (Utricle and Saccule)
A. Semi-Circular Canals (SCCs)
Deceleration movements and Gravitational Pull
→ Are like “sacs” made up of hair cells (similar
to SCCs) and have otoconia (calcium
carbonate crystals)
→ Linear acceleration/deceleration and
gravitational pull motions move the otoconia
inside the utricle and saccule

→ Sensitive to ROTATIONAL/ANGULAR
movements
→ 3 SCCs that are oriented in 3 planes:
1. Lateral (Horizontal) SCC
 Side-to-side movements; “No”
2. Anterior (Superior) SCC
 Up and down; “Yes”
3. Posterior SCC
 Movement like extending neck
→ All 3 SCCs are filled with endolymph fluid
→ Note! They are have different orientations
anatomically:
 Horizontal Canal: 30 degrees from
horizontal/transverse plane
 Anterior/Posterior Canal: 45 degrees away
from the pure sagittal plane
1. Utricle
 orientation and static balance particularly
in horizontal tilt
 Linear horizontal acceleration (Ex: riding a
car – there’s greater velocity)
 Ex: prolonged position of head to the side
is perceived by the utricle
2. Saccule
 orientation and static balance particularly
in vertical tilt
 Linear vertical acceleration (Ex: riding an
elevator, airplane accelerating)
 Motion sickness - brain is confused when the
vestibular system experiences something for
the first time; example: space is enclosed, our
eyes are not moving but the vestibular system
perceives something due to the acceleration

Clinical significance: To check for the specific

canals/to move the otoconia, position the canals on
the pure sagittal plane by rotating the head
 Anterior SCC: rotate head to C/L side @ 450
 Posterior SCC: rotate head to I/L side @ 450
 Horizontal SCC: Neck flexion @ 30 degrees
 CtN-
Pwc parieto -
insular →
vestibular cortex

plocculondular
a. the
lobe
cerebellum * AWARENESS ④
maintain
Fx
:

calibration of
eye movements
① Vestibule ocular reflex
-
③
( VOR)

② this INFO is
sent to
the OCULAR Motor
NUCLEI
{
↑ /

=
① iniqY%%F "
vestibular spinal
a-
ltpamti on
SPACE ↓N8
nuclei

- r

① Peripheral vestibular system sends INPUT

↓
② medial and lateral
vettibnto spinal TRACTS
-

}
↓
③ activation of
2 types of VCR } VSR
REFLEXES
↳ maintain BALANCE 9
EQUILIBRIUM through :

① mm .
contraction
① HIP & STEP STRATEGY