VESTIBULAR DISORDERSJoannalyn B. Juego

ANATOMY: Peripheral Vestibular System

• Stabilizing the visual images on the fovea of the retina during head movements to allow clear vision

• Maintaining postural stability• Providing information used for spatial

orientation

ANATOMY: Peripheral Vestibular System

• Semicircular canals• Otolith organs• Central vestibular system

Vestibular System Dysfunction

• Peripheral Pathology

• Central Nervous System Pathology

Peripheral Pathology: Mechanical

• BPPV– Most common cause of vertigo– A biomechanical disorder– Nystagmus & vertigo without change in head

position; nausea with or without vomiting; & dysequilibrium

– Latency to onset of the vertigo & nystagmus occurs within 15 seconds once the head is in the provoking position; the duration is less than 60 seconds

Cupulolithiasis

• Fragments of the otoconia break away & adhere to the cupula of one of the SCCs

• When the head is moved into certain positions, the weighted cupula is deflected by the pull of gravity

• The abnormal signal results in vertigo & nystagmus, which persists as long as the patient is in the provoking position

Canalithiasis

• Otoconia are freely floating in one of the SCCs• When a patient changes head position, the

pull of gravity causes the freely floating otoconia to move inside the SCC resulting in endolymph movement & deflection of the cupula

Peripheral Pathology: Decreased Receptor Input

• UVH– Viral insults, trauma, & vascular events– Vertigo, spontaneous nystagmus, oscillopsia

during head movements, postural instability, & dysequilibrium

– Resolves within 3-7 days assuming the patient is exposed to common daylight conditions

Peripheral Pathology: Decreased Receptor Input

• BVH– Ototoxicity– Meningitis, autoimmune DO, head trauma, tumors

on the 8th CN, transient ischemic episodes of vessels supplying the vestibular system, & sequential unilateral vestibular neuronitis

– Dysequilibrium, oscillopsia, & gait ataxia

Central Nervous System Pathology

• Cerebrovascular insults involving the AICA, PICA, & vertebral artery

• Vertebrobasilar insufficiency (VBI)• TBI due to labyrinthine or skull fractures• Demyelinating diseases such as MS affecting

CN VIII

CENTRAL VESTIBULAR PATHOLOGY

PERIPHERAL VESTIBULAR PATHOLOGY

Ataxia often severe Ataxia mild

Abnormal smooth pursuit & abnormal saccadic eye movement tests

Smooth pursuit & saccades usually normal; positional testing may reproduce nystagmus

Sx usually do not include hearing loss; if so, it is often sudden & permanent

Sx may include hearing loss (insidious – may recover), fullness in ears, tinnitus

Sx might include diplopia, altered conscious, lateropulsion

Sx of acute vertigo not usually suppressed by visual fixation

Sx of acute vertigo usually suppressed by visual fixationSx of acute vertigo usually intense (more than central vestibular pathology)

Pendular nystagmus (eyes oscillate at equal speeds)

Nystagmus will incorporate slow & fast phases (jerk nystagmus)

Pure persistent vertical nystagmus persists regardless of positional testing

Spontaneous horizontal nystagmus usually resolves within 7 days in a patient with UVH

PHYSICAL THERAPY EXAMINATION

• History & Systems Review– Identification of symptoms– Duration & circumstances of symptoms

Identification of Symptoms

• Dizziness– Vaguely defined as the sensation of whirling or

feeling a tendency to fall– Patients should be directed away from using the

word & to use more precise terms – Vertigo, lightheadedness, dysequilibrium,

oscillopsia

Vertigo

• Illusion of movement• Episodic• Indicates pathology at one or more locations

along the vestibular pathways– Acute stage of UVH– Displaced otoconia (BPPV)– Acute unilateral brainstem lesion

Lightheadedness

• Feeling that fainting is about to occur • Causes– Orthostatic hypotension– Hypoglycemia– Anxiety– Panic disorder

Dysequilibrium

• Sensation of being off balance• Causes– BVH– Chronic unilateral vestibular hypofunction– Lower extremity somatosensation loss– Upper brainstem/vestibular cortex lesion– Cerebellar & motor pathway lesions

Oscillopsia

• Subjective experience of motion of objects in the visual environment that are known to be stationary

• Occur with head movements in patients with vestibular hypofunction since the vestibular system is not generating an adequate compensatory eye velocity during the head motion

Duration & Circumstances of Symptoms

• How recent the attacks happened• Whether the symptom is constant or episodic– Episodic: average duration of the episodes– Seconds to minutes – BPPV– Minutes to hours – Meniere’s disease– Days – vestibular neuronitis or migraine-

associated dizziness

Duration & Circumstances of Symptoms

• Whether the patient experiences symptoms with particular movements, positions, or at rest– Is the patient sensitive to motion as the passenger

in a moving car?– Does the patient experience a vigorous vertigo

when the head is moved into certain positions?

Tests & Measures

• Visual Analogue Scale• Dizziness Handicap Inventory• Functional Disability Scale– Vestibular Rehabilitation Benefit Questionnaire

• Motion Sensitivity Quotient• Examination of Eye Movements

Observation for Nystagmus

• Nystagmus is the primary indicator used in identifying most peripheral & central vestibular lesions

• The direction of the nystagmus is named by the direction of the fast component– Left beating nsytagmus: eyes move slowly to the

right & the resetting eye movement is to the left

Head Impulse Test (Examination of the VOR at High Acceleration)

• Widely accepted clinical tool used to examine semicircular canal function

• Patient first fixates on a near target• When testing the horizontal SCC, the head is

flexed to 30 deg

Head Impulse Test (Examination of the VOR at High Acceleration)

• Patient is asked to keep their eyes focused on a target while his head is manually rotated in an unpredictable direction using a– Small amplitude (5 – 15 deg),– Moderate velocity (~200 deg/sec), and– High-acceleration (3,000 – 4,000/sec) angular

impulse

Head Impulse Test (Examination of the VOR at High Acceleration)

• Normal– Eyes will move in the direction opposite to the head

movement & gaze will remain on the target• With a loss of vestibular function– The VOR will not move the eyes as quickly as the head

rotation & the eyes will move off the target– The patient will then make a corrective saccade to

reposition the eyes on the target– Corrective saccade: rapid eye movement used to

reposition the eyes to the target of interest

Head Impulse Test (Examination of the VOR at High Acceleration)

• Unilateral peripheral lesion or pathology of the central vestibular neurons– Patient will not be able to maintain gaze when the

head is rotated quickly toward the side of the lesion

• Bilateral loss of vestibular function– Patient will make corrective saccades after a head

impulse to either side

Head-Shaking Induced Nystagmus Test (HSN)

• Useful aid in the diagnosis of a unilateral peripheral vestibular defect

• Patient is instructed to close his eyes• Clinician flexes the head 30 deg before

oscillating horizontally for 20 cycles at a frequency of 2 repetitions per second

• On stopping the oscillation, the patient opens the eyes & the clinician checks for nystagmus

Head-Shaking Induced Nystagmus Test (HSN)

• Normal– Nystagmus will not be present

• Presence of asymmetry between the peripheral vestibular inputs to central vestibular nuclei– May result in HSN

• UVH– Horizontal HSN– Quick phases of the nystagmus directed toward the

healthy ear & the slow phases directed toward the lesioned ear

Positional Testing• Commonly used to identify whether otoconia

have been displaced into the SCC, causing a condition referred to as Benign Paroxysmal Positional Vertigo (BPPV)

• Dix-Hallpike Test– Patient is moved from a long-sitting position with

the head rotated 45 deg to one side, to a supine position with the head extended to 30 deg beyond horizontal, head still rotated to 45 deg

– Observe the eyes for nystagmus

Positional Testing

• Dix-Hallpike Test Side-lying– Patient sits on the edge of the examination table– Clinician turns the head horizontally 45 deg– Patient is quickly brought down to the side

opposite the head rotation– Examiner checks for nystagmus & vertigo, & then

slowly brings the patient to the starting position– The other side is then tested

Positional Testing

• Roll test– If horizontal SCC BPPV is suspected– Patient is positioned supine with the head flexed

20 deg– Rapid rotations to the sides are done separately &

the clinician observes for nystagmus & vertigo

Dynamic Visual Acuity (DVA) Test• Measurement of visual acuity during horizontal

motion of the head• Static visual acuity is first determined– Patient is asked to “Read the lowest line you can see”

on a wall-mounted acuity chart– Lighthouse ETDRS (Early Treatment Diabetic

Retinopathy Study) wall charts are recommended• Patient then attempts to read the chart while the

clinician horizontally oscillates the patient’s head at a frequency of 2Hz

Dynamic Visual Acuity (DVA) Test• Normal– Head movement results in little or no change of visual

acuity compared with the head still (less than 1 line difference)

• Loss of vestibular function– Eyes will not be stable in space during head movements – Decrement in DVA compared with visual acuity when

the head is still– A 3-line or more decrement in visual acuity during head

movement is suggestive of vestibular hypofunction

Examination of Gait & BalanceTEST BPPV UVH BVH CENTRAL

LESION

Romberg (-) Acute: (+)Chronic: (-)

Acute: (+)Chronic: (-)

Often (-)

Tandem Romberg

(-) (+), eyes closed

(+) (+)

Single-legged stance

(-) May be (+) Acute: (+)Chronic: (-)

May be unable to perform

TEST BPPV UVH BVH CENTRAL LESION

Gait Normal Acute: wide-based, decreased arm swing, & rotationCompensated: (N)

Acute: wide-based, decreased arm swing, & rotationCompensated: mild gait deviation

May have pronounced ataxia

Turn head while walking

May produce slight unsteadiness

Acute: may not keep balanceCompensated: (N)

May not keep balance or slows cadence

May not keep balance, increased ataxia

Vestibular Function Tests: Semicircular Canal Tests

• Electronystamography (ENG) & Videonystamography (VNG)– Oculomotor & inner ear function

• Rotational chair test– Rotating subjects in the dark– Standard test for bilateral vestibular dysfunction

Vestibular Function Tests: Otolith Tests

• Vestibular-evoked myogenic potential (VEMP)– Cervical VEMP– Ocular VEMP

INTERVENTIONS

Benign Paroxysmal Positional Vertigo

• The otoconia will be returned into the vestibule

• The patient will demonstrate reduced vertigo associated with head motion

• The patient will demonstrate improved balance

• The patient will demonstrate independence in ADLs

Benign Paroxysmal Positional Vertigo

• Canalith repositioning maneuver (CRM)– BPPV due to canalithiasis, posterior SCC

canalithiasis is the most common• Liberatory (Semont) maneuver– BPPV due to cupulolithiasis, posterior SCC

cupulolithiasis is the most common• Brandt-Daroff exercises– Persistent/residual or mild vertigo (even after

CRM); for the patient who may not tolerate CRM

Unilateral Vestibular Hypofunction

• The patient will demonstrate improved stability of gaze during head movement

• The patient will demonstrate diminished sensitivity to motion

• The patient will demonstrate improved static & dynamic postural stability

• The patient will be independent in proper performance of a HEP that includes walking

Unilateral Vestibular Hypofunction

• Gaze Stability Exercises– Improve the VOR & other systems that are used to

assist gaze stability with head motion– Designed to expose patients to retinal slip

Retinal Slip

• Occurs when the image of an object moves off the fovea of the retina, resulting in visual blurring

• Necessary as this is the signal used to drive vestibular adaptation within the brain

• Because the brain can tolerate small amounts of retinal slip yet see a target clearly, the patient must try to keep the target in focus

• Otherwise, head motion that is too rapid will result in excessive retinal slip

Primary Paradigms of Vestibular Adaptation

• x1 exercises– Patient is asked to move the head horizontally as

quickly as possible while maintaining focus on a stable target

– Patient must learn how to slow the head movement if the target becomes blurred

– Starting target distance should be an arm’s length away

Primary Paradigms of Vestibular Adaptation

• x2 exercises– Requires the patient to move the head & the

target in opposite directions

Postural Stability Exercises

• Stand with feet shoulder-width apart, arms across the chest– Progress to: Bring feet closer together. Close eyes. Stand

on a sofa cushion or foam.• Practice ankle sways: medial-lateral & anterior-

posterior– Progress to: Doing circle sways. Close eyes.

• Attempt to walk with heel touching toe on firm surface– Progress to: Do the same exercise on carpet.

Postural Stability Exercises

• Practice walking 5 steps & turning 180 deg (left & right)– Progress to: Making smaller turns. Close eyes.

• Walk & move the head side to side, up & down– Progress to: Counting backward from 100 by

threes

Habituation Exercises

• Warranted when a patient with UVH has continual complaints of dizziness

• Habituation: reduction in response to a repeatedly performed movement

Habituation Exercises

• PT must determine the provoking positions first• When a position elicits a mild to moderate

dizziness, the patient remains in the provoking position for 30 seconds or until the symptoms abate, whichever comes first

• The patient is provided with a HEP based on the results of the positional test

• The provoking exercises are performed 3-5 times each, 2-3 times a day

Habituation Exercises

• Patient keeps an activity diary to monitor response to training

• The exercises are designed to reproduce the dizziness & the patient should be encouraged that the sxs normally decrease within 2 weeks

• If other 2 weeks the sxs are no better, the habituation exercises should be first changed

Bilateral Vestibular Hypofunction

• The patient will demonstrate improved stability of gaze during movement

• The patient will demonstrate reduced subjective complaints of gaze instability

• The patient will demonstrate improved static & dynamic balance

• The patient will be independent in proper performance of HEP that includes walking

• The patient will demonstrate enhanced decision-making skills regarding performance of ADLs

Bilateral Vestibular Hypofunction

• Gaze stability exercises similar to the x1 paradigm• Balance exercises• Walking program• Patient education is high priority– 2 years may be necessary to ensure as complete a

recovery as possible• Pool therapy• Tai Chi

Abnormal Central Vestibular Function

• The patient will demonstrate enhanced decision making skill regarding fall prevention strategies & necessary safety precautions to allow safe functioning within the home & the community

• The patient will demonstrate enhanced decision making skills regarding use of compensatory strategies to assist in gaze stability

• The patient will be independent in performance of an HEP that includes walking

Abnormal Central Vestibular Function

• Patient education– Time to recover will be 6 months or more, & may

be incomplete• Habituation exercises• Gait & balance exercises designed to

incorporate somatosensory, visual, & vestibular contributions

Diagnoses Involving the Vestibular System

• Meniere’s Disease• Perilymphatic Fistula• Vestibular Schwannoma• Motion Sickness• Migraine-Related Dizziness• Multiple Sclerosis• Multiple System Atrophy• Cervicogenic Dizziness