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VESTIBULAR SYSTEM

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					Vestibular Examination
     ANATOMY & FUNCTION



 Carmen Casanova Abbott PT, PhD
            Lecture Objectives

► Discuss  vestibular structure as it relates to
  vestibular function when examining a dizzy
  patient.
► Discuss signs and symptoms associated with
  vestibular disorders
► Differentiate between peripheral and central
  vestibular pathology
► Discuss components of a physical therapy
  vestibular examination.
   Vestibular System Function
► Provides  information concerning gravity,
  rotation and acceleration
► Serves as a reference for the somatosensory &
  visual systems
► Contributes to integration of arousal, conscious
  awareness of the body via connections with
  vestibular cortex, thalamus and reticular
  formation
► Allows for:
    gaze & postural stability
    sense of orientation
    detection of linear & angular acceleration
          Vestibular Anatomy
► Peripheral   sensory apparatus
   detects & relays information about head angular &
    linear velocity to central processing system
   orients the head with respect to gravity
► Central   processing system
   processes information in conjunction with other
    sensory inputs for position and movement of head in
    space
► Motor   output system
   generates compensatory eye movements and
    compensatory body movements during head &
    postural adjustments
         Peripheral Apparatus
► Membranous    Labyrinth
   Semicircular canals (SSC)
   Otolith organs
Netter ‘97
            Semicircular Canals
► Angular acceleration
► Ampulla contains sensory epithelium
        SSC Coplanar Pairing
► Spatial arrangement of the 6 SSC cause 3
  coplanar pairings
    R & L lateral, L anterior and R posterior; l
     posterior & R anterior; R & L horizontal
► Allows for a Push-Pull arrangement of the two
  sides (e.g., as head turns right, right SSC will
  increase firing rate & the left SSC will decrease
  firing rate)
► Advantages
    sensory redundancy
    common mode rejection/noise
           Inhibitory Cutoff
► Depolarization  of the ipsilateral hair cells
  occurs during angular head movements
► Hyperpolarization of contralateral hair cells
  occurs at the same time
► Hair cells are only able to hyperpolarize to
  what they were at rest = cut off of inhibitory
  influences from the movement going in the
  opposite direction even if the ipsilateral hair
  cells continue to spike higher firing rates
Purves 2001
                Otoliths
► Utricle and saccule
► Otolith sensory structures
   Maculae
   Otolithic membrane
   Otoconia
► Movement    of gel membrane & otoconia
  cause a shearing action to occur over
  the hair cells → sensitivity of otoliths
               Otolith Function
► Respond   to:
   Linear head motion on acceleration
   Static tilt
   Two organs respond to respective accelerations
    or tilts in their respective planes
    ►Saccule  has vertical orientation of maculae
    ►Utricle has horizontal orientation of maculae
Bear 1996
Purves 2001.
              Hair Cells
►2  types: kinocilium & stereocilia
► Sensory structures for the peripheral
  end organs (maculae and ampula)
► Hyperpolarized or depolarized
  depending upon the direction of
  deflection of the stereocilia (movement
 of stereocilia towards the kinocilium
 causes depolarization of the hair cell)
► Affectthe firing rate of the primary
 vestibular afferents to the brainstem
Bear 1996
       Striola of the Macula
► Striola serves as a structural landmark
► Contains otoconia arranged in narrow
  trenches, dividing each otolith
► Orientation of the hair cells change over
  the course of the macula
► Allows otoliths to have multidirectional
  sensitivity
Purves 2001.
Principles of the Vestibular System

 ► Tonic  firing rate
 ► Vestibular Ocular Reflex
 ► Push-pull mechanism
 ► Inhibitory cutoff
 ► Velocity storage system
       Ascending Pathways
► Vestibular nerve
► Vestibular nuclei
► Cerebellum
► Oculomotor complex
   CN 3, 4, and 6
   Along with vestibulospinal reflexes coordinate
    head and eye movements
                Relay Centers
► Thalamus
   Connection with vestibular cortex and reticular
    formation → arousal and conscious awareness
    of body; discrimination between self movement
    vs. that of the environment
► Vestibular   Cortex
   Junction of parietal and insular lobe
   Target for afferents along with the cerebellum
     ►Bothprocess vestibular information with
      somatosensory and visual input
Netter 1997
          Tonic Firing Rate
► Vestibular  nerve and vestibular nuclei have a
  normal resting firing rate (70-100 cycles/sec)
► Baseline firing rate present without head
  movement
► Tonic firing is equal in both sides; if not, a
  sense of motion is felt e.g., vertigo, tilt,
  impulsion, spinning
► Excitation and inhibition of the vestibular
  system can then occur from stimulation of the
  hair cells
► Spontaneous recovery with light
      Vestibular-Ocular Reflex
               (VOR)
► Causes  eyes to move in the opposite
  direction to head movement
► Speed of the eye movement equals that of
  the head movement
► Allows objects to remain in focus during
  head movements
Compensatory Eye Movements
► VOR
► Optokinetic reflex
► Smooth pursuit reflex, saccades, vergence
► Neck reflexes
   combine to stabilize object on the same area of
    the retina=visual stability
Purves 2001.
      Vestibular Processing
              Gain
► Keeps  eye still in space while head is
  moving
► Ratio of eye movement to head movement
 (equals 1)
      Vestibular Processing
   Velocity Storage Mechanism
► Perseveration  of neural firing in the vestibular
  nerve by the brainstem after stimulation of SSC
  to increase time constant (10sec.)
    SSC respond by producing an exponentially
     decaying change in neural firing to sustained
     head movement
► Otolith & somatosensory input also drive
  mechanism
              VOR Dysfunction
► Directionof gaze will shift with the head
  movement
► Cause degradation of the visual image
► In severe cases, visual world will move with
  each head movement
              Oscillopsia

► Visual illusion of oscillating movement
  of stationary objects
► Can arise with lesions of peripheral or
  central vestibular systems
► Indicative of diminished VOR gain
   motion of images on fovea
   diminished visual acuity
             Cerebellum

► Monitors  vestibular performance
► Readjusts central vestibular processing
  of static & dynamic postural activity
► Modulates VOR
► Provides inhibitory drive of VOR (allows
 for VORc)
      Descending Pathways
► Provide motor output from the vestibular
  system to:
    Extraocular muscles (part of VOR)
    Spinal cord & skeletal muscles (generate
    antigravity postural activity to cervical,
    trunk & lower extremity muscles)
► Response  to changing head position with
  respect to gravity (righting, equilibrium
  responses)
  Vestibulospinal Reflex (VSR)

► Generates compensatory body movement
 to maintain head and postural stability,
 thereby preventing falls
Netter 1997
Vestibular Dysfunction
               Demographics
► Vestibular disorders manifested by vertigo
  are a significant health problem, secondary
  only to low back pain
► NIH study estimates that 40% of the
  population over the age of 40 will
  experience a dizziness disorder during their
  lifetime
           Fall Demographics
► Falls  will be experienced in community
    dwelling individuals:
     28-35 % over age 65
     42-49% over age 75
►    Greater than 60% will have bilateral
    vestibular lesion (BVL) in the <65 or >75
    years of age
              Fall Risk Factors

≥ 4 risk factors, 78% chance of falling in an older adult
► Sedatives                    ► Dizziness
► Cognitive  impairment        ►↑  dependence on
► Palmomental reflex             visual cues
► LE disability                ► Fear of falling
► Foot problems                ► Orthostatic
► Balance abnormalities
                                 hypotension
                                      (Tideiksaar R 1998)
Other Fall Risk Factors?
             Aging Changes
► Progressive   changes begin at age 40
   Decreased number of hair cells
   Decreased vestibular nerve fibers
► Lead to dizziness and vertigo
► Harder to deal with competing visual and
  somatosensory input
         Fear of Falling (FOF)
►   FOF affects willingness to participate in physical activity
    & exercise
►   FOF occurs in an average of 30% of older adults who
    have not fallen
►   FOF increases to an average of 60% of older adults who
    have fallen
►   FOF is higher among women
►   Prevalence of FOF is underestimated
►   Greater FOF associated with lower quality of life in
    mental health, social & leisure pursuits

                                                   (Legters, 2002)
          Falls Related Self-efficacy
► Falls Efficacy Scales (FES)
    better for frail
    indoor activities
► Activities-Specific Balance Confidence Scale (ABC)
    higher functioning
    indoor & outdoor activities
    > discrimination between fearful & nonfearful
                                   (Legters, 2002)
      Vestibular Pathophysiology

► Disorders    of tone & or gain (vertigo / movement-
  induced vertigo)
► Vestibularnerve / nuclei give abnormal sensory
  information
► Tone automatically recovers in a few days; does
  not need visual input
► Compensation for reduced gain depends on visual
  images; takes month to years to complete; high
  speeds & accelerations may never be complete
► Nystagmus usually transient sign of vestibular
  lesion; movement-induced symptoms can be
  chronic
Dizzy Patient Presentation: unexplained or
         new onset of symptoms

► Medical    referral is indicated
     constant vertigo
     lateralpulsion
     facial asymmetry
     speech & or swallowing difficulties
     oculomotor dysfunction
     vertical nystagmus
     severe headaches
     recurrent falls
     unilateral hearing loss, tinnitus, fullness, ear pain
                Vertigo
► An asymmetrical firing of the two
  vestibular systems
► Gives an illusion of spinning, movement
► Indicative of any one or combination of
  causes (acute UVH, BPPV, brainstem
 lesion, vascular hypotension…)
   Differentiation Between Peripheral &
         Central Causes of Vertigo
                      Peripheral               Central

Nausea                  severe                moderate
Imbalance               mild                  severe
Hearing Loss            common                rare
Oscillopsia             mild                  severe
Neurologic Symptoms     rare                  common
Compensation            rapid                 slow

                        (Furman JM, Whitney SL. 2000)
  Peripheral Vestibular Disorders
► Vestibular Neuronitis
► Labyrinthitis
► Meniere’s
► Acoustic Neuroma
► Fistula
► Benign Paroxysmal Positional Vertigo (BPPV)
  Central Vestibular Disorders
► Vascular
   Wallenberg’s Syndrome
   Head Injury
   Cerebellar Infarct
► PostconcussiveSyndrome
► Demyelinating Disease
► Congenital
Degenerative Cerebellar Disease
► Signs   & symptoms
     abnormal ocular pursuit
     gradual decline
     irregular saccades
     gaze end point nystagmus
     ataxia
       Objective of Clinical Exam
►   Establish location & severity of lesion (central or
    peripheral)
►   Typical examination
    - history (hearing status)
    - cranial nerves
    - vestibular
        spontaneous nystagmus (imbalance in tone)
        postural instability (abnormal tone & gain; proprioceptive loss)
        VOR gain (maintained fixation, dynamic visual acuity)
        head shaking (compensated UVL; not necessarily PVL)
        calorics
        pressure sensitivity (fistula)
        positional nystagmus (Hallpike-Dix test)
        hyperventilation (anxiety; acoustic neuroma)
                 Nystagmus
► Rapid alternating movement of eyes in
  response to continued rotation of the body
► Primary diagnostic indicator in identifying
  vestibular lesions
► Physiologic nystagmus
   vestibular, visual, extreme lateral gaze
► Pathologic   nystagmus
   spontaneous, positional, gaze evoked
► Labeled  by the direction of the fast
  component
► Central vs. peripheral cause differentiated by
  duration
Vestibular Function Tests

► Calorictest
► Rotary Chair test
► Posturography
  Results of Vestibular Function
              Tests
► Presence  of complete vs. incomplete loss
► Presence of peripheral vs. central
  dysfunction
► Direct patient management
► Help in outcome prediction
Dizziness Handicap Inventory
 ► Three   subscales
    function
    emotion
    physical aspects
 ► Scoring
    Yes       4 pts.
    Sometimes 2 pts.
    No        0 pts.
 ► Excellent   test-retest reliability
         Hallpike-Dix Maneuver
► Gold  standard used to check for the
  presence of benign paroxysmal positional
  vertigo (BPPV)
► Nystagmus induced by this test is an
  objective measurement from which we can
  determine SSC dysfunction and assess a
  response to treatment
Benign Paroxysmal Positional Vertigo
              (BPPV)
► Signs   & symptoms
   sudden, severe attacks of vertigo precipitated
    by certain head positions & movements
       ►e.g.,   rolling over, neck extension, bending forward
     lightheadedness; nausea
     anxiety
     avoids movement
     direction & duration of nystagmus
      differentiates between BPPV & a central
      vestibular lesion (CVL)
Benign Paroxysmal Positional Vertigo
              (BPPV)
►5  criteria crucial in diagnosis (Hallpike-Dix
  Test):
   torsional/linear-rotary nystagmus; reproduced by
    provocative positioning with affected ear down
   nystagmus of 1-5 sec. latency
   nystagmus of brief duration (5-30 sec.)
   reversal of nystagmus direction on returning to
    upright position
   response diminishes with repetition of maneuver
     (fatigability)
                               (Massoud ’96)
                 BPPV
              Cupulolithiasis
► Debris, probably fragments of otoconia from
  the utricle, adhere to the cupula
► Treatment
   Brandt-Daroff habituation exercises
   Semont, liberatory maneuver
                BPPV
             Canalithiasis
► Debris floating freely in the endolymph in
  the long arm of the posterior SSC
► Treatment
   Canalith repositioning maneuver (Epley)
   84-90% remission rate
   Sleep upright one night only (more severe
    cases)
       Problems Experienced with
             Vestibular Loss
► Balance& gait deficits
► Head movement-induced dizziness
► Head movement-induced visual blurring
  (oscillopsia)
► LE dressing difficulty
► Driving deficits
► Disability related to work, social & leisure
  activities
 Systems Approach to Examination

► Examination  of balance & mobility using a
 variety of tests & measurements to
 document functional abilities, determine
 underlying sensory, motor, & cognitive
 impairments contributing to functional
 disabilities
                Balance
► Can  be viewed as a motor skill that
  emerges from the interaction of multiple
  systems
► These systems are organized to meet
  functional task goals & are constrained by
  the type of environment
► Balance, like any skill, can improve with
  practice
  Balance Components
► Steadiness
► Symmetry
► Dynamic   stability
    Balance Training: Postural
          Biofeedback
► Posturalsymmetry & dynamic stability
 have been consistently improved by
 training using force platform systems
    Clinical Test of Sensory
Interaction In Balance (CTSIB)

► Assesses pattern of sensory dependence
 for balance from timed stance tests
 during distortion of sensory environment
         Berg Balance Scale
► Performance    -orientated balance
  assessment
► Interpretation:
   > 45/56 score highly specific (96%) for
    nonfallers
   subjects who fell most frequently were those
    closer to cut off
► Correlates   with other balance tests
Functional Gait Assessment (FGA)
► Assesses postural stability during walking
► Modified version of the Dynamic Gait Index
► Added 3 new tasks to increase challenge
  and sensitivity of the test to minor changes
  in gait
► Stronger vestibular components (head
 turns, narrow BOS, ambulating backwards
 and with eyes closed)
General Therapeutic Intervention
          Objectives
► Changing  impairments
► Improving functional performance
► Improving capacity to adapt performance
  to changing task & environmental
  demands
       Mechanism of Recovery:
           Compensation
► Results   from changes in CNS
   rebalancing of tonic activity within vestibular nuclei
    (spontaneous recovery)
   recovery of VOR (vestibular adaptation)
   habituation (progressive decline in response to same
    stimulus)
   alternative strategies/substitution; in complete loss of
    vestibular function
► Enhanced   by active movements & processing of
  visual, vestibular, & somatosensory stimuli
    Result of Early Intervention
► Gain returns quicker
► Increased function
► Decreased gait ataxia
► Decreased perception of disequilibrium
                         (Herdman 2000)
  Vestibular Exercise Program
          Objectives
► Complement     CNS natural compensation
    diminish dizziness & vertigo
    enhance gaze stabilization
    enhance postural stability in static & dynamic
     situations
► Increase overall functional activities
► Patient education
    nature of pathology
    episodic nature, prognosis
    control of exacerbations
Vestibular Program Components
► Gaze  stabilization exercises to retrain VOR
  function
► Balance retraining to retrain VSR function
► Conditioning exercises to increase fitness
  level
► Habituation or canal repositioning
  maneuvers as indicated
e.g., Unilateral Vestibular Lesion:
       Exercise Guidelines

► Adaptation  is best stimulated by producing an
  error signal; work at limit of abilities
► Incorporation of head movements & visual
  input
► Provide context specific stimulation to
  promote adaptation
► Adaptation is positively affected by voluntary
  muscle control
           ►                     (Herdman 2000)
Vestibular Function Recovery Rates

► UVL: 6-8 weeks
► BPPV: remission in 1/few treatments
► BVL: 6 months - 2 years
► CNS Lesion: 6 months - 2 years
  Physical Therapy Intervention:
            Prescription
► Individualized    vestibular rehabilitation
 program:
   Outpatient, 1-2 times / week (4-6 weeks)
   HEP, 5 minutes, 3x / day
   Walking program (health & fitness prescription)
► Compliance     to daily program essential
  to success
► Exercise graduated for possible increase
  of symptoms during the first week

				
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posted:5/23/2011
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