Vestibular disorders

By: Dr. Aishwarya Mahajan

MPT in Neurophysiotherapy
 Anatomy
• The vestibular system is located within the
inner ear.

• The components of the system can be divided

into three parts:
1. Peripheral apparatus
2. Central processors
3. Motor output
 Parts of peripheral vestibular system

PVS

Membranous
Bony labyrinth
labyrinth

1. 3 semicircular canals 5 sensory organs:

2. Cochlea 1. 3 semicircular ducts
3. vestibule 2. 2 otolith organs (saccule and utricle).
 BONY LABYRINTH

Semicircular canals
• Help in controlling balance and stability by sensing rotation and orientation of head in 3D
space.
• The ducts are named in accordance with their location and the direction in which
they are optimized to register rotary movement:
1. Anterior (also: superior)
2. Posterior (also: inferior)
3.Lateral (also: horizontal)
• SCC are positioned right angles to one other.
• 6 individual SCC forms 3 coplanar pairs:
1. Right and left lateral
2. Left anterior and right posterior
3. Left posterior and right anterior
• Planes of the canals are close to the extraoccular muscles
• Coplaner positioning of canals is associated with the PUSH PULL
Mechanism
• E.g. when head rotates to right,
Hair cells on right horizontal canal are excited while left Haircells are
inhibited.
• SCC are filled with a fluid called ENDOLYMPH
• Endolymph moves freely within each canal in response to head
movement.
• Each SSC has an bulb like structure at the end known as AMPULLA.
• Within this ampulla there is a cone shaped structure known as
CUPULLA.
• Crista has haircells and supporting cells and CUPULLA.
• Each of the hair cells of the vestibular organs
is topped by a hair bundle.
• which consists of about fine nonmotile
stereocilia of graded lengths and a single
motile kinocilium.
• Longest stereocilia is called KINOCILIUM,
which extends upto to the cupulla.
 Otolith organs
• The two membranous sacs of the vestibule, the utricle
and the saccule, are known as the otolith organs.
• Because they respond to gravitational forces, they are
also called gravity receptors.

A. Saccule: Saggital plane, linear accelaration

B. Utricle: horizontal plane, lateral tilt of head
• Like SCC, PUSH PULL mechanism is also
incorporated into the geometry of each otolithic
membrane.
• Haircells of the Otolithic membrane known as MACULAE are
located on the medial wall of saccule and floor of utricle.
• The otolithic membrane are same as cupulla but are weighted.
• It contains Calcium carbonate crystals called OTOCONIA.
 Push pull mechanism:
• The crista is flexible.
• When the head moves, endolymph pushes the cupulla one way or the other, which
inturn displaces the hairs and alters the electrical potential of the hair cells.
• Change In potential is linked to the flow of potassium ions through mechanically gated
ion channels in steriocilia.
• when movement causes steriocilia to bend towards the kinocilium, ion channels open,
• Allowing the flow of potassium ions into the cell and resulting in DEPOLARISATION.
• When movement causes steriocilia to bend away from the kinocilium, ion channels
close-----resulting in HYPERPOLARISATION.
• The change in polarisation causes the corresponding neurons to send impulses to the

CNS.
 Vestibular ganglion
• The vestibular ganglion (ganglion of
Scarpa) lies within the fundus of the i
nternal auditory meatus.
• It is a cluster of bipolar sensory neurons,
that are the first-order neurons of the
vestibular pathway.
• The peripheral processes of vestibular
ganglion cells comprise the nerve fibers
that receive the stimuli from the hair
cells of the otolithic organs and
semicircular canals, respectively.
• The central processes of the vestibular
ganglion comprise the fibers of the
vestibular portion of
the vestibulocochlear nerve (CN VIII).
 Vestibular nerve
• The vestibular nerve transmits the equilibrium impulses from the vestibular
apparatus.

• It leaves the inner ear through the internal auditory meatus and enters the
posterior cranial fossa.

• Then, it synapses with the vestibular nuclei in the brainstem.

• Moreover, some of the fibers synapse directly with the cerebellum as well.

• This makes the vestibular nerve unique, as it is the only cranial nerve whose
first-order neurons synapse with the cerebellum directly.

• The horizontal and superior semicircular canals, as well as the utricle, are all
innervated by the superior vestibular nerve, while the posterior semicircular
canal and the saccule are innervated by the inferior vestibular nerve.
 Central processes
• There are two main targets for vestibular input
from primary afferents:
1. the vestibular nuclear complex
2. the cerebellum
 Vestibular Nuclei

• The vestibular nuclei are the four nuclei that lie within the rhomboid

fossa of the brainstem.

• They contain the second-order neurons of the vestibular pathway that

synapse with the vestibular portion of the vestibulocochlear nerve.

Namely, the vestibular nuclei are:

• The superior vestibular nucleus (of Bechterew)

• The lateral vestibular nucleus (of Deiters)

• The inferior vestibular nucleus (of Roller)

• The medial vestibular nucleus (of Schwalbe)

• The superior and medial vestibular nuclei receive most
of the inputs from the cristae ampullares of the
semicircular canals.
• The inferior and lateral nuclei receive the remaining
fibers from posterior semicircular canals, as well as from
the utricle and saccule.
• The vestibular nuclei integrate inputs from the peripheral
vestibular structures, contralateral vestibular nuclei,
cerebellum and the other sensory systems (the visual and
somatosensory systems).
 Connections with the nuclei of the cranial nerves

• The superior and medial vestibular nuclei send fibers that join

the medial longitudinal fasciculus (MLF).

• Via this pathway, they synapse with the motor nuclei of the occulomotor

(CN III), trochlear (CN IV) and abducens (CN VI) nerves.

• This way, the vestibular system mediates the reflexive activity of the

extraocular muscles.

• More precisely, the vestibular system mediates the vestibulo-ocular

reflex, in which the movements of the eyes are adjusted to the

movements of the head.

Note the flow of information,
which starts with
depolarization of hair cells in
the inner ear sends
movement and positional
information to the vestibular
ganglia,
which transmits this
information to the vestibular
nuclei (also receives input
from the cerebellum).

From here, the vestibular

nuclei send information to
CN III, IV, & VI to dictate eye
movement.

The vestibular nuclei also

sends information to the
thalamus, cerebellum, and
medial and lateral
vestibulospinal tracts,
allowing for perception,
integration, and adjustments
of body position within
 Connections with the spinal cord
• The lateral vestibular nucleus sends axons via the lateral

vestibulospinal tract.

• This tract synapses with interneurons along the entire length of the

spinal cord, adjusting the posture of the body and tone of extensors
according to the vestibular stimuli (vestibulo-spinal reflex).

• The medial and inferior vestibular nuclei project their fibers via

the medial vestibulospinal tract.

• This tract terminates within the cervical spinal cord, adjusting the

posture of the head and neck (vestibulo-cervical reflex).

 Medial vestibulospinal tract
• The MVST neurons receive input from vestibular receptors and the cerebellum,
and somatosensory information from the spinal cord.
• MVST neurons carry both excitatory and inhibitory signals to innervate neck
flexor and extensor motor neurons in the spinal cord.
For example,
• if one trips over a crack in the pavement while walking, MVST neurons will
receive downward and forward linear acceleration signals from the otolith
receptors and forward rotation acceleration signals from the vertical semicircular
canals
• The VCR will compensate by providing excitatory signals to the dorsal neck flexor
muscles and inhibitory signals to the ventral neck extensor muscles, which moves
the head upward and opposite to the falling motion to protect it from impact.
Vestibulospinal reflex
 Connections with the cerebellum
1st mechanism
• The second-order neurons from the vestibular nuclei project to the inferior
olivary nucleus via the vestibulo-olivary tract.
• From here, the vestibular inputs are relayed via the lateral part of the
inferior cerebellar peduncle (restiform body) into the ipsilateral cerebellar
vermis, flocculonodular lobe.
• This connection enables the joint modulation of balance by the cerebellum
and vestibular system.
 2nd mechanism

• A portion of the first-order neurons from the vestibular

ganglion of Scarpa pass through the medial part of the inferior
cerebellar peduncle.
• They enter the cerebellum as the mossy fibers and synapse
directly with the ipsilateral vestibulocerebellum, vermis and
fastigial nucleus.
• These connections enable cerebellar awareness of the
vestibular sensations and promote necessary movement
modifications by the cerebellum.
 Connections with the cortex
• The superior and lateral vestibular
nuclei project to the ventral posterior
nuclei of the thalamus to synapse with the
third-order neurons of the vestibular
pathway.
• The thalamus then relays the signals to
the primary vestibular cortex (Brodmann
area 3a), located in the cortex of the
parietal lobe adjacent to the primary
motor cortex.
• This area integrates the information from
the vestibular system with other
proprioceptive systems and passes that
information directly to the primary motor
cortex (Brodmann area 4).
• From here, the motor response to the
proprioceptive stimuli is generated.
 Motor output
1. VOR
• The vestibulo-ocular reflex is an involuntary motor activity
mediated by the vestibular system which serves for adjusting
the eye movements while the head moves in the horizontal
plane.
• It serves for fixing the gaze during head repositioning.
• The reflex arc is mediated by the medial longitudinal
fasciculus (MLF).
• Vestibular dysfunction is a disturbance in the body's balance system

due to an insult to the vestibular system of the inner ear, the central

nervous system processing centers, or both.

• Symptoms typically consist of vertigo, nausea, vomiting,

intolerance to head motion, unsteady gait, and postural instability,

with nystagmus often clinically apparent as well.

• The most common form of acute peripheral vestibular dysfunction

is benign paroxysmal positional vertigo, whereas an ischemic stroke

of the posterior fossa is the most common cause of acute central

vestibular dysfunction.
The term "peripheral" refers to a pathology of the vestibular system itself:
the membranous labyrinth and the superior and inferior vestibular nerves.
The term "central" refers to a pathology of the central nervous system
(CNS).
Central nervous system Peripheral vestibular system
pathology pathology
• CVA (AICA, PICA, SCA or • Benign paroxysmal
vertibrobasillar artery) positional vertigo (BPPV)
• TBI • Meniere's Syndrome
• Brainstem Strokes • Vestibular hypofunction
• Cerebellar Degeneration • Vestibular neuronitis
• Multiple Sclerosis • Acoustic Neuroma
 Central vestibular pathology
• Cerebrovascular insult involving the anterior-inferior
cerebellar artery (AICA), posterior inferior cerebellar
artery (PICA), and vertebral artery may cause vertigo
though other Signs associated with these infarcts are
present and help clarify the site of pathology.
• Lesion of the vertebral artery may affect the cerebellum
only and can mimic a peripheral vestibular hypofunction
in its clinical presentation.
• Most patients with cerebellar lesions however, will have
associated signs such as dysdiadochokinesia or past
pointing.
• Individuals with transient ischemic attach may
present with sudden vertigo that lasts minutes
and also include hearing loss.
• Patients with TBI with labyrinthine or skull
fracture may complain of vertigo.
• In MS, Cranial nerve VIII can present same
signs and symptoms as of UVH.An MRI scan
can be done to confirm MS.
 Peripheral vestibular system pathology

1. BPPV
• Benign Paroxysmal Positional Vertigo (BPPV) is the most common cause of
vertigo, which is a symptom of the condition.
• Paroxysmal positional vertigo is a mechanical disorder of the inner ear
causing short intervals of transient vertigo, often accompanied by autonomic
symptoms.
• (BPPV) accounts for at least 20% of individuals with moderate to severe
dizziness/vertigo and is the most common cause of brief, episodic, peripheral
vestibular dysfunction.
• Vertigo is a distressing, illusionary sensation of turning linked to impaired
perception of a stationary environment.
• It is an illusion of movement of self or environment resulting from sudden
imbalance of tonic neural activity in the vestibular cortical pathway
(Labyrinth, VIII nerve thalamus and vestibular cortex).
• Women and patients over age fifty are among the most commonly affected
• The average duration of symptoms is 2 weeks,
although individual episodes typically last less
than one minute and may occur several times
daily.
• Symptoms are caused by the stimulation of a
semicircular canal, usually the posterior
semicircular canal, and typically only affect
one side.
 BPPV can be classified as :

Canalithiasis-free-floating otoconia (calcium carbonate-protein crystals that have

become detached from the utricle or saccule) that move to the most dependent
position within the canal when the head changes position, thereby shifting the
endolymph and causing displacement of the cupula with a subsequent spinning
sensation.

• Cupulolithiasis-Less commonly, the particles may adhere to the cupula in the

ampulla of the semicircular canal and cause similar but longer-lasting symptoms
with head movements - this is termed "cupulolithiasis."

Additionally, the type of nystagmus that a patient may display can be classified as
geotropic or apogeotropic.
1. Geotropic describes the nystagmus towards the ground.
2. Apogeotropic describes the nystagmus is towards the ceiling.

BPPV symptoms are most obvious with changes in position and are usually worse in
the morning
 Etiology/Causes

• The most common cause of BPPV is idiopathic.

• The vestibular system of the inner ear can also

undergo degenerative changes as one ages.
• Under age 50, head injury is a common cause.

• Vestibular viruses and Meniere’s disease

• BPPV can also be a result of surgery due to

prolonged supine positioning and possible trauma
to the inner ear
It can be triggered by any action which stimulates the
posterior semi-circular canal which may be:
• Tilting the head
• Rolling over in bed
• Looking up or under
• Sudden head motion
BPPV may be made worse by any number of modifiers
which may vary between individuals:
• Changes in barometric pressure - patients often feel
symptoms approximately two days before rain or snow
• Lack of sleep (required amount of sleep may vary widely)
• Stress
 Clinical presentation
• Symptoms of BPPV include nystagmus and
vertigo with change in head position, and
occasionally nausea with or without vomiting, and
dysequilibrium.
• In the most common form, latency to onset of the
vertigo and nystagmus occurs within 15 seconds
once the head is in the provoking position.
• The duration is usually less than 60 seconds.
• The vertigo and nystagmus are direct impairments
caused by the misplaced otoconia.
• Diagnosis: DIX HALLPIKE MANEUVER
 Positional testing

1. Dix Hallpike test

• Most common positional test to
diagnose posterior canal BPPV.
• Result:

https://
www.youtube.com/watch?v=wgWOmuB1VFY
2. Supine head roll test
• Done for horizontal canal
BPPV.
• Result:

https://www.youtube.com/watch?
v=ns8XZ4rKiJc
 Vestibular Hypofunction

• The most common causes of UVH leading to decreased or

eliminated receptor input are viral insults, trauma, and
vascular events, tumors.
• Patients who sustain UVH experiences direct impairments of
vertigo, nystagmus, oscilloscopia, loss of balance,dizziness,
lightheadedness,nausea and vomitting.
• Initially patient will experience vertigo and nystagmus due to
asymmetry created when one vestibular system is not
functioning.
• This resolves in 3-7 days.
• Spontaneous nystagmus beyond this can be a sign of central
lesion or an unstable peripheral vestibular pathology.
• Pt have difficulty to walk in dark areas.
• The most common cause of a bilateral
vestibular hypo function (BVH) is ototoxicity.
• Certain classes of antibiotic such
aminoglycoside (gentamicin, streptomycin) are
taken up by the haircells of vestibular
apparatus and continue to build up in the
system even after the medication is stopped.
• The primary complaint is disequilibrium
though oscilloscopia and gait ataxia are
common clinical signs with BVH.
 Miniere’s disease
• Another common peripheral vestibular
disorder is Ménière disease, characterized by
episodes of vertigo lasting minutes to
hours that are accompanied by hearing loss
and roaring tinnitus.
• This condition is thought to be due to
endolymphatic hydrops with distortion and
distention of the endolymph portions of the
labyrinthine system.
 Theories

Theory 1:
 The blockage of the endolymphatic sac or duct.
 The entrance of the endolymphatic sac potentially becomes
blocked by saccular otoconia that detach from the membranes
and block the flow of endolymph.
Theory 2:
 A hypoplasia (under development) of the vestibular aqueduct,
leading to a reduction in the ability to regulate the volume of
fluid in the endolymphatic space.
Theory 3:
 The rupture of the dilated or distended endolymphatic sac
allows potassium-saturated endolymph into the perilymphatic
space. The result is that the biochemical gradient depolarizes the
cochlear and vestibular hair cells, leading to loss of function.
 Clinical presentation

1. Vertigo
• This feeling of dizziness can last anywhere from 20
minutes to a few days, with the average attack being two
to four hours.
• This sensation may produce nystagmus,nausea, vomiting
or sweating.
• An attack of vertigo can persist with a constant intensity
or may gradually increase in intensity.
• Recurrent vertigo often affects patients' daily activities
even during periods of remission.
• The episodes often force a person to lie down for several
hours and lose time from work or leisure activities.
• Vertigo can increase risk of falls, accidents while driving a
car or operating heavy machinery
 2. Hearing loss
• Usually affects one ear.
• The person will have a decline in ability to
hear during an attack but will regain hearing
when current episode has ended.
• When a person has had Ménière's for a
prolonged period, the hearing loss may
become permanent.
• Low frequency tones are most frequently lost,
but all tones may be affected as the disease
progresses.
 3.Tinnitus
• Sustained, loud ringing or buzzing in the ears.
The intensity of this may vary, but the symptom
is continual in people diagnosed with Ménière's.
4. Sensation of fullness in the ears.
• Typically the first symptom experienced
preceding an acute attack.
• This feeling is similar to what is felt when
changing altitudes (such as in an airplane) but
cannot be relieved by swallowing.
 Vestibular neuronitis
• Caused by an acute viral or post-viral inflammatory disorder.

• The inflammation affects the vestibular branch of the eighth

cranial nerve, resulting in hypofunctional vestibulopathy and
vertigo that can persist for days at a time.

• When the inflammation also affects the cochlea and causes

hearing loss, the syndrome is referred to as labyrinthitis.
 Vestibular schwannoma
• These are acoustic neuromas which are benign in nature
• They arise from the schwan cells of 8th CN often in the
IAC.
Symptoms:
• tumor in IAC: tinnitus and hearing loss
• Cerebro pontine angle: hearing loss, imbalance, facial
palsy, vertigo
Management:
Post sx PT- Facial muscle rehab
strengthening of cervical muscles
balance and postural stability exs
 Differentiating signs
• The most important part of the clinical history is the length of the symptomatic
episodes, determining which will differentiate peripheral from central causes and
potentially indicate the most likely peripheral cause.
• Recurrent episodes lasting under one minute are usually BPPV.
• A single episode of vertigo lasting several minutes to hours may be due to a
vestibular migraine or a TIA that is related to the vascular areas of the labyrinth or
brainstem.
• Recurrent episodes that last minutes to hours are associated with Ménière disease,
particularly when accompanied by roaring tinnitus and hearing loss.
• Vertiginous episodes that last for days can occur with vestibular neuronitis,
labyrinthitis, multiple sclerosis, and infection or infarction of the brainstem or
cerebellum.
• Patients presenting with vertigo, diplopia, dysarthria,
weakness, or numbness should be evaluated for CNS
etiologies like acute ischemic stroke and demyelinating
disorders like multiple sclerosis.
• These neurologic symptoms may precede, accompany, or
follow the onset of vertigo.
• Ménière disease is often accompanied by low-frequency
sensorineural hearing loss and a tinnitus which is described as
a "roaring" or "whooshing" sound in addition to a sensation of
pressure in the ear.
 Assessment
• Examination of CN function
• Examination of tone
• Examination of reflex
• Posture: observe for asymmetry, head tilt or
rotation
• Examination of balance and gait
• Examination of nystagmus
• Examination of saccades and smooth pursiuts
• Occular alignment
 Observation of nystagmus:
• It is a primary diagnostic indicator for identifying peripheral and central
vestibular lesions.
• Commonly, patients who present with vertigo will also demonstrate
nystagmus on physical examination.
• Peripheral vestibular nystagmus: both slow and fast components.
• The direction of nystagmus is named by the direction of fast component.
• Spontaneous nystagmus is a slow drift of the eyes away from the target in
one direction followed by a fast corrective movement in the reverse
direction.
• Eg: a "right beating" nystagmus drifts slowly to the left and then corrects
rapidly back to the right.
• Spontaneous nystagmus results from imbalance in the vestibular signals
through their transmission to the oculomotor neurons.
A. Spontaneous nystagmus:
• Horizontal nystagmus results from a horizontal semicircular
canal lesion, and torsional nystagmus results from superior
or posterior semicircular canal involvement.
• Mixed horizontal-torsional nystagmus results if a peripheral
lesion affects all three semicircular canals on one side.
• Visual fixation, however, should suppress nystagmus if it is
due to a peripheral lesion
B. Positional nystagmus:
Positional nystagmus is induced by a change in head position.
Nystagmus caused by stimulation of the peripheral semicircular
canals from movement of the otoconia or canaliths typically
lasts up to 30 seconds and then dissipates.
C. Static nystagmus: occurs with lesions to the peripheral otolith
system through connections in the vestibular nuclei and
cerebellum.
• It is provoked with change of head position in relation to
gravity and continues as long as the position is maintained.
• Nystagmus caused by central vestibular system damage lasts
minutes or longer before abating.
D. Gaze-evoked nystagmus: occurs when clients shift the eyes
from a primary central position to a second location.
• It is caused by the inability to maintain stable gaze position,
and the eye drifts back toward the center or primary position.
• Usually indicative of a CNS problem, it is common in MS,
brain injury, and congenital lesions.
E. Head shaking nystagmus: To test, head is placed in 30 degrees of flexion. Then
rotate to 45 degrees to both the sides while fixing on an object.(30 times each side)
Normally: no nystagmus
Vestibular involvement: nystagmus with or without latency which lasts for 5 to 20
secs.

F. Check for smooth pursuit and saccades:

Saccades are rapid eye movements that allow us to quickly scan a visual scene.
Contrary to the rapid, jerking movements of saccades, smooth pursuit visual
behavior involves the eyes tracking a stimulus in a linear fashion.

• Track a moving object with eyes with the head stationary.

• It tests the motor function of CN III,IV and VI.
• During this test, observe for gaze evoked nystagmus quality of eye movement.
G. Occular alignment:
• Skew deviations (loss of tonic otoliths input from one
side.
• Seen in acute UVL.
• Should resolve within 3 to 7 days after onset.
 Balance Assessment:

1.Test of quit standing:

• Rhomberg test
• Sharpened rhomberg test
• One legged stance test
• Response to perturbations:
 Unpredictable- Nudge test (observe Automatic
postural reactions)
 Predictable: ‘don’t let me push you’
• Postural sway on balance master (force plate)
2.Active standing:
• Functional reach test
• Multidirectional reach test
3.Sensory Manipulation
• Sensory organization test or Clinical test of sensory integration and balance
4. Functional balance scale
• Berg balance scale
• Dynamic gait index
• Fukuda stepping test
• Timed up and go test
• Tinnetti scale of balance and gait
• Dizziness handicap inventory
• Activities-specific Balance Confidence Scale
 Gait

• The gait pattern reflected by vestibular dysfunction, or lack of integration, involves

flat-foot gait with minimal heel strike, abnormal foot placement requiring larger-
than-normal trunk adjustment.
• In order to control the position of the trunk, the base of support is widened.
• Speed of gait is another indication of vestibular function from the perspective that
patients with bilateral vestibular loss demonstrate a slower self-selected speed.
• Typically, increased double-limb stance time and decreased stability at heel strike
are present.
• Walking with head turns becomes even more challenging as the vestibular system is
activated and the somatosensory and visual systems are disadvantaged.
• Vestibular contributions to stability during transitions from sitting to standing,
initiation of gait, and abnormal foot placement can be identified during standard
tests such as the TUG, Tinetti, DGI and FGA.
 Management
Goals
• Otoconia will be returned to the vestibule.
• Patient will demonstrated reduced vertigo
associated with head movements.
• Patient will demonstrate improved balance.
• Patient will demonstrate imrpoved
independence in ADLs and IADLs with head
motions
 Clinical decision making
1. Temporary: extent of potential improvement
and how soon?
So accordingly: Habituate, stimulate,facilitate
and force use
2. Permanent:
• internal substitution by remaining system.
• External substitution by a supporting device
So accordingly substitute, compensate,educate
Physiological basis for vestibular rehabilitation:
1. Adaptation
2. Habituation
3. Substitution
4. Compensation
 Physiotherapy Management

Canalith repositioning procedure

(Epley maneuver)
• Can be used for anterior and posterior SCC canalithiasis
• Can also be applied for horizontal SCC, but anterior
and horizontal canal BPPV is rare.
• Post to CRM, pt is asked to remain upright for 1 or 2
nights (sleep in recliner chair)
• And then avoid sleeping on the involved side for 5
additional nights.

https://www.youtube.com/watch?v=9SLm76jQg3g
Liberatory Semont maneuver
• Used for posterior canal BPPV Cupulolithiasis

https://www.youtube.com/watch?v=-
omE6Vs6ZuU
Brandt Daroff exercises:
• Used to habituate the patients with the provoking
positions.
• Exercise should be performed for 5 to 10 repetitions, 3
times in a day until the patient has no vertigo for 2
consecutive days.
• If pt has severe vertigo or complains of nausea
perform the exs for 3 reps*3 times in a day.

https://www.youtube.com/watch?v=JdCCEGtfYUo
Gaze stabilisation exercises
 Habituation exercises
Cawthorne Cooksey exercises
• The purpose of these exercises is to build up a tolerance mechanism and the
more diligently and regularly they are carried out, the sooner the symptoms
will disappear.
• The exercises should be performed three times each day.
• Begin with exercise 1A.
• This should be performed in three sets of five, three times a day.
• Grade the severity of your symptoms as you do this exercise, using the
following scale:
0 symptom free
1 mild discomfort
2 discomfort
3 severe

Only when the symptoms clear, or after two weeks, move on to the next exercise
1B.
 Substitution

• These exercises synthesize use of vision and

somatosensory cues with vestibular cues to enhance
central programming to improve gaze stability and
postural stability.
• Patients with B/L vestibular loss substitute vision and
proprioception for use of vestibular information.
• Such patients are increasingly incapacitated in the dark
(dazzling lights from vehicles while walking on a rough
terrain)
Mx:
• Perform exercises in environments with altered sensory
information.
• Sensory organization training VR.
Balance and gait training
2. Educate patients on how to avoid injury due to imbalance or vertigo, techniques
on how to fall to minimize injury
Home Modification
• Add grab bars to the shower or tub, both horizontal and vertical
• Add a shower or tub seat
• Add anti-slip strips in showers or tubs
• Consider an elevated toilet seat
• Add ramps and reduce threshold heights in doorways for anyone ambulating
with the assistance of a wheeled device (rolling walkers, wheelchairs, scooters,
etc)
• Add handrails or secure hand holds at steps or stairs
• Place risers or blocks under the legs of couches or chairs
• Remove throw rugs throughout the house
• Clear out clutter. Set a goal to clear a pathway 36 inches wide, which leaves
enough room to easily handle a walker or wheelchair
• Add light sensor night-lights in hallways and bathrooms
• Add motion-sensor alarms that alert care providers when loved ones start to get
out of bed
• Carry small loads, as heavy ones throw off your balance
• Keep items you use often in easy-to-reach places
• Task analysis
• Functional task training
• Feedback from the patient
• Interdiscipinary