1. Vestibular Examination
ANATOMY & FUNCTION
Carmen Casanova Abbott PT, PhD

2. 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.

3. 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

4. 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

5. Peripheral Apparatus Membranous Labyrinth Semicircular canals (SSC)
Otolith organs

6. Netter ‘97

7. Semicircular Canals Angular acceleration
Ampulla contains sensory epithelium

8. 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
assist in compensation for sensor overload

9. 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

10. Purves 2001

11. 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

12. 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

13. Bear 1996

14. Purves 2001.

15. 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)
Affect the firing rate of the primary vestibular afferents to the brainstem

16. Bear 1996

17. 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

18. Purves 2001.

19. Principles of the Vestibular System
Tonic firing rate
Vestibular Ocular Reflex
Push-pull mechanism
Inhibitory cutoff
Velocity storage system

20. Ascending Pathways Vestibular nerve Vestibular nuclei Cerebellum
Oculomotor complex
CN 3, 4, and 6
Along with vestibulospinal reflexes coordinate head and eye movements

21. Relay Centers Thalamus Vestibular Cortex
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
Both process vestibular information with somatosensory and visual input

22. Netter 1997

23. Tonic Firing Rate
Vestibular nerve and vestibular nuclei have a normal resting firing rate ( 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

24. 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

25. 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

26. Purves 2001.

27. Vestibular Processing Gain
Keeps eye still in space while head is moving
Ratio of eye movement to head movement (equals 1)

28. 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

29. VOR Dysfunction Direction of gaze will shift with the head movement
Cause degradation of the visual image
In severe cases, visual world will move with each head movement

30. 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

31. Cerebellum Monitors vestibular performance
Readjusts central vestibular processing of static & dynamic postural activity
Modulates VOR
Provides inhibitory drive of VOR (allows for VORc)

32. 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)

33. Vestibulospinal Reflex (VSR)
Generates compensatory body movement to maintain head and postural stability, thereby preventing falls

34. Netter 1997

35. Vestibular Dysfunction

36. 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

37. 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

38. Fall Risk Factors ≥ 4 risk factors, 78% chance of falling in an older adult
Sedatives
Cognitive impairment
Palmomental reflex
LE disability
Foot problems
Balance abnormalities
Dizziness
↑ dependence on visual cues
Fear of falling
Orthostatic hypotension
(Tideiksaar R 1998)

39. Other Fall Risk Factors?

40. 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

41. 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)

42. 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)

43. Vestibular Pathophysiology
Disorders of tone & or gain (vertigo / movement- induced vertigo)
Vestibular nerve / 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

44. 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

45. 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…)

46. Differentiation Between Peripheral & Central Causes of Vertigo
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)

47. Peripheral Vestibular Disorders
Vestibular Neuronitis
Labyrinthitis
Meniere’s
Acoustic Neuroma
Fistula
Benign Paroxysmal Positional Vertigo (BPPV)

48. Central Vestibular Disorders
Vascular
Wallenberg’s Syndrome
Head Injury
Cerebellar Infarct
Postconcussive Syndrome
Demyelinating Disease
Congenital

49. Degenerative Cerebellar Disease
Signs & symptoms
abnormal ocular pursuit
gradual decline
irregular saccades
gaze end point nystagmus
ataxia

50. 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)

51. 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

52. Vestibular Function Tests
Caloric test
Rotary Chair test
Posturography

53. Results of Vestibular Function Tests
Presence of complete vs. incomplete loss
Presence of peripheral vs. central dysfunction
Direct patient management
Help in outcome prediction

54. Dizziness Handicap Inventory
Three subscales
function
emotion
physical aspects
Scoring
Yes 4 pts.
Sometimes 2 pts.
No pts.
Excellent test-retest reliability

55. 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

56. 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)

57. 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)

58. BPPV Cupulolithiasis
Debris, probably fragments of otoconia from the utricle, adhere to the cupula
Treatment
Brandt-Daroff habituation exercises
Semont, liberatory maneuver

59. 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)

60. 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

61. 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

62. 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

63. Balance Components
Steadiness
Symmetry
Dynamic stability

64. Balance Training: Postural Biofeedback
Postural symmetry & dynamic stability have been consistently improved by training using force platform systems

65. Clinical Test of Sensory Interaction In Balance (CTSIB)
Assesses pattern of sensory dependence for balance from timed stance tests during distortion of sensory environment

66. 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

67. 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)

68. General Therapeutic Intervention Objectives
Changing impairments
Improving functional performance
Improving capacity to adapt performance to changing task & environmental demands

69. 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

70. Result of Early Intervention
Gain returns quicker
Increased function
Decreased gait ataxia
Decreased perception of disequilibrium
(Herdman 2000)

71. 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

72. 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

73. 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)

74. 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

75. 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