The document provides information on vestibular disorders and the anatomy and physiology of the vestibular system. It discusses the peripheral and central components, conditions that can cause vertigo such as benign paroxysmal positional vertigo, and therapeutic interventions for vestibular dysfunction including exercises to improve gaze stability and balance. Clinical examination techniques are outlined to evaluate vestibular lesions and develop individualized treatment plans.

1. Vestibular Disorders And dizzy 'tis to cast one's eyes … William Shakespeare

2. Review Of Function Provides information concerning gravity, rotation, and acceleration. Serves as a reference for the somatosensory and visual systems Contributes to integration of arousal, conscious awareness of the body via connections with vestibular cortex, thalmus, and reticular formation Allows for: Gaze & postural stability Sense of orientation Direction of linear & angular acceleration 08/18/10 Robert Niemeier, DPT

3. Review Of Anatomy Peripheral Sensory Apparatus Detects and relays information about head angular and 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 and postural adjustments 08/18/10 Robert Niemeier, DPT

4. Membranous Labyrinth Normal Membranous Labyrinth Semicircular canals Otolith Organs Utricle – detects linear acceleration and head tilts in the horizontal plane Saccule - detects linear acceleration and head tilts in the vertical plane 08/18/10 Robert Niemeier, DPT

5. Semicicular Canals Spatial arrangement of the 6 semicircular canals cause 3 coplanar pairings R and L Lateral L anterior and R posterior, L posterior and R anterior R and L Horizontal Detects angular acceleration Advantages: Common mode rejection/noise Sensory redundancy Assist in compensation for sensor overload 08/18/10 Robert Niemeier, DPT

6. Otoliths Hair Cells Sensory structures for peripheral end organs Affect firing rate of primary vestibular afferent to brainstem Striola Otoconia arranged in narrow trenches Allows otoliths to have multidirectional sensitivity Utricle and Saccule Otolith sensory structures Maculae Otolithic membrane Otoconia Movement of gel membrane and otoconia cause a shearing action 08/18/10 Robert Niemeier, DPT

7. Principles of the Vestibular System Tonic Firing Rate Vestibular Ocular Reflex Push-Pull Mechanism Inhibitory Cutoff Velocity Storage System 08/18/10 Robert Niemeier, DPT

8. Tonic Firing Rate Vestibular nerve and vestibular nuclei have a normal resting firing rate Baseline firing rate present without head movement Tonic firing equal in both sides if not results in vertigo, tilt, impulsion, and spinning Excitation and inhibition occur from stimulation of hair cells 08/18/10 Robert Niemeier, DPT

9. Vestibular-Ocular Reflex (VOR) Eyes move in opposite direction to head movement Speed of eye movement equals that of head movement Allows objects to remain in focus during head movements 08/18/10 Robert Niemeier, DPT

10. Compensatory Eye Movements Vestibular-Ocular Reflex Optokinetic Reflex - allows the eye to follow objects in motion when the head remains stationary Smooth Pursuit Reflex - allows the eye to closely follow a moving object Neck reflexes - reflex movement of the limbs that bring the body into the normal position in relation to the head Combine to stabilize object on the same area of the retina = visual stability 08/18/10 Robert Niemeier, DPT

11. VOR Dysfunction Direction of gaze will shift with head movements Causes degradation of visual image Visual world will move with each head movement 08/18/10 Robert Niemeier, DPT

12. Oscillopsia Visual illusion of oscillating movement of stationary objects Can arise with lesions of peripheral or central vestibular systems Indicative of diminished VOR gain (maintained fixation, dynamic visual acuity) Motion of images on fovea (f ovea (or fovea centralis ) denotes the pit in the retina which allows for maximum acuity of vision.) Diminished visual acuity 08/18/10 Robert Niemeier, DPT

13. Cerebellum Monitors vestibular performance Readjusts central vestibular processing of static and dynamic postural activity Modulates VOR Provides inhibitory drive of VOR 08/18/10 Robert Niemeier, DPT

14. Vestibulospinal Reflex (VSR) Generates compensatory body movement to maintain head and postural stability Helps prevents falls! 08/18/10 Robert Niemeier, DPT

15. Demographics Vestibular disorders manifested by vertigo are secondary only to low back pain NIH study estimates that 40% of population over 40 experience a dizziness disorder during lifetime 08/18/10 Robert Niemeier, DPT

16. Fall Demographics Fall experienced in community dwelling individuals 28 to 35 % over age 65 42 – 49% over age 75 Greater than 60% will have bilateral vestibular lesion (BVL) in the 65 to 75 year age range 08/18/10 Robert Niemeier, DPT

17. Fall Risk Factors 4 or more risk factors? 78% risk of fall in older adult Sedatives Cognitive impairment Palmomental reflex - The thenar eminence is stroked briskly with a thin stick, from proximal (edge of wrist) to distal (base of thumb) using moderate pressure. A positive response is considered if there is a single visible twitch of the ipsilateral mentalis muscle (chin muscle on the same side as the hand tested) Lower extremity disability Dizziness Increased dependence on visual cues Fear of falling Orthostatic hypotension Balance abnormalities Foot problems 08/18/10 Robert Niemeier, DPT

18. 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 08/18/10 Robert Niemeier, DPT

19. Vestibular Pathophysiology Disorders of tone and or gain (vertigo / movement produced vertigo) Vestibular nerve / nuclei give abnormal sensory information Tone automatically recovers in a few days, doesn’t need visual input Compensation for reduced gain depends on visual images, takes months to years to complete Nystagmus transient sign of vestibular lesion Movement induced symptoms can be chronic 08/18/10 Robert Niemeier, DPT

20. Dizzy Patient Presentation Medical referral Constant vertigo Lateropulsion - An involuntary movement of the body or turning of the gait toward one side; seen principally with unilateral infarction of a cerebellar hemisphere or lateral medulla. Facial asymmetry Speech & /or swallowing difficulties Oculomotor dysfunction - when one or both eyes do not move smoothly, accurately, and quickly across a line or from one word to another Vertical Nystagmus Severe headaches Recurrent Falls Unilateral hearing loss, tinnitus, fullness or ear pain 08/18/10 Robert Niemeier, DPT

21. Vertigo Vertigo - Hitchcock’s Finest An asymmetrical firing of the two vestibular systems Gives an illusion of spinning, movement 08/18/10 Robert Niemeier, DPT

22. Peripheral or Central Vertigo? Peripheral Severe Nausea Mild Imbalance Common Hearing Loss Mild Oscillopsia Rare Neurologic Symptoms Rapid Compensation Central Moderate Nausea Severe Imbalance Rare Hearing Loss Severe Oscillopsia Common Neurologic Symptoms Slow Compensation 08/18/10 Robert Niemeier, DPT

23. Peripheral Vestibular Disorders Vestibular Neuronitis - a paroxysmal, single attack of vertigo, a series of attacks, or a persistent condition which diminishes over three to six weeks. Labyrinthitis - an ear disorder that involves irritation and swelling of the inner ear Meniere’s - episodes of vertigo and tinnitus and progressive hearing loss, usually in one ear Acoustic Neuroma Fistula - abnormal connection or passageway between two epithelium-lined organs Benign Paroxysmal Positional Vertigo (BPPV) 08/18/10 Robert Niemeier, DPT

24. Central Vestibular Disorders Vascular Wallenberg’s Syndrome – Results in nystagmus and vertigo, which may result in falling, caused from involvement of the region of Deiters’ nucleusand other vestibular nuclei. Onset is usually acute with severe vertigo Head Injury Cerebellar Infarct Postconcussive Syndrome Demyelinating Disease Congenital 08/18/10 Robert Niemeier, DPT

25. Degenerative Cerebellar Disease Abnormal Ocular Pursuit Gradual Decline Irregular Saccades Gaze end point nystagmus Ataxia 08/18/10 Robert Niemeier, DPT

26. Clinical Exam Objectives Establish location and severity of lesion (Central or Peripheral) Examination History (hearing status) Cranial Nerves Vestibular Spontaneous Nystagmus (Imbalance in Tone) Postural Instability (Abnormal tone and gain, proprioceptive loss) VOR gain (maintained fixation, dynamic visual acuity) Head shaking (Compensated UVL; not necessarily PVL) Pressure Sensitivity (Fistula) Position nystagmus (Halpike – Dix Maneuver) Hyperventilation (Anxiety, acoustic neuroma) 08/18/10 Robert Niemeier, DPT

27. 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 direction of fast component 08/18/10 Robert Niemeier, DPT

28. Hallpike-Dix Maneuver Gold standard used to check for benign paroxysmal positional vertigo (BPPV) Nystagmus induced by this test we can determine SSC Dysfunction and assess a response to treatment 08/18/10 Robert Niemeier, DPT

29. Benign Paroxysmal Positional Vertigo (BPPV) Signs & Symptoms Sudden, severe attacks of vertigo precipitated by certain head positions and movements Lightheadedness; nausea Anxiety Avoids Movement Direction and duration of nystagmus differentiates between BPPV and Central Vestibular Lesion (CVL) Five Criteria in Diagnosis Torsional/linear-rotary nystagmus; reproduced by provocative positioning with affected ear down Nystagmus of 1-5 sec latency Nystagmus of brief duration (r-30 sec) Reversal of nystagmus direction on returning to upright position Response diminishes with repetition of maneuver (Fatigability) i.e. Hallpike-Dix Maneuver 08/18/10 Robert Niemeier, DPT

30. BPPV Cupulolithiasis Debris, probably form fragments of otoconia from the utricle, adhere to the cupula Treatment Brandt-Daroff - Habituation Exercises Semont - Liberatory Maneuver 08/18/10 Robert Niemeier, DPT

31. BPPV Canalithiasis Debris floating freely in the endolymph in the long arm of posterior SSC Treatment Canalith Reposition Maneuver (Epley) 84 – 90% remission rate 08/18/10 Robert Niemeier, DPT

32. Vestibular Loss Balance and Gait Deficits Head movement-induced dizziness Head movement-induced visual blurring (Oscillopsia) LE dressing difficulty Driving deficits Disability related to work, social and leisure activities 08/18/10 Robert Niemeier, DPT

33. Systems Approach to Exam Examination of balance and mobility using a variety of tests & measurements to document functional abilities, determine underlying sensory, motor, and cognitive impairments that contribute to functional disabilities 08/18/10 Robert Niemeier, DPT

34. Balance Viewed as a motor skill that emerges from interaction of multiple systems Systems are organized to meet functional task goals and are constrained by type of environment Balance – like any skill, can improve with practice 08/18/10 Robert Niemeier, DPT

35. Balance Components Steadiness Symmetry Dynamic stability 08/18/10 Robert Niemeier, DPT

36. Balance Training Postural symmetry and dynamic stability have been consistently improved by training using force platform systems. Can be as simple as Wii Balance Games 08/18/10 Robert Niemeier, DPT

37. Clinical Test of Sensory Interaction in Balance (CTSIB) Assesses pattern of sensory dependence for balance from timed stance tests during distortion of sensory environment 08/18/10 Robert Niemeier, DPT

38. Berg Balance Scale Performance oriented balance assessment Interpretation: Greater than 45/56 score high specific (96%) for nonfallers Subjects who fell most frequently were those closer to cut off Correlates with other balance tests. 08/18/10 Robert Niemeier, DPT

39. Therapeutic Intervention Objectives Changing impairments Improving functional performance Improving capacity to adapt performance to changing task and environmental demands 08/18/10 Robert Niemeier, DPT

40. 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 and processing of visual, vestibular, and somatosensory stimuli 08/18/10 Robert Niemeier, DPT

41. Result of Early Intervention Functions are quicker to return Increased Function Decreased Gait Ataxia Decreased perception of disequilibrium 08/18/10 Robert Niemeier, DPT

42. Vestibular Exercise Program: Objectives Complement CNS natural compensation Diminish Dizziness & Vertigo Enhance gaze stabilization Enhance postural stability in static and dynamic situations Increase overall functional activities Patient education Nature of pathology Episodic nature, prognosis Control of exacerbations 08/18/10 Robert Niemeier, DPT

43. Vestibular Program Components Gaze stabilization exercises to retrain VOR function Balance retraining to retrain VSR Function Conditioning exercises to increase fitness level Habituation of canal repositioning maneuvers as indicated, e.g. Epley, Semont, Brandt-Daroff, etc 08/18/10 Robert Niemeier, DPT

44. Unilateral Vestibular Lesion (UVL) Adaptation is stimulated by producing an error signal; work at limit of abilities Incorporation of head movements and visual input Provide context specific stimulation to promote adaptation Adaptation is positively affected by voluntary muscle control 08/18/10 Robert Niemeier, DPT

45. Benign Paroxysmal Positional Vertigo (BPPV) Benign Paroxysmal Positional Vertigo (BPPV) dizziness is thought to be due to debris which has collected within a part of the inner ear. This debris can be thought of as "ear rocks", although the formal name is "otoconia". Ear rocks are small crystals of calcium carbonate derived from a structure in the ear called the "utricle" (figure1 ). While the saccule also contains otoconia, they are not able to migrate into the canal system. The utricle may have been damaged by head injury, infection, or other disorder of the inner ear, or may have degenerated because of advanced age. 08/18/10 Robert Niemeier, DPT

46. Bilateral Vestibular Disease (BVL) Bilateral peripheral vestibular disease with complete loss of function is characterized by symmetrical ataxia and loss of balance of either side, with strength preserved. Postural asymmetry is not present. A characteristic "side-to-side" head movement often accompanies these signs. Abnormal nystagmus is not observed, and with bilateral destruction of the receptor organs, normal vestibular nystagmus cannot be elicited by head movement or caloric testing. 08/18/10 Robert Niemeier, DPT

47. Central Vestibular Disease Any signs of brain stem disease in association with vestibular signs indicate that central involvement is present. The most frequent differentiating feature is a deficit in postural reactions, as central vestibular lesions most often result in paresis or loss of conscious proprioception. Alterations in mental status, or deficits in Vth or VIIth cranial nerves, also may be indicative of central disease. Nystagmus may be a key to differentiating central from peripheral disease. Nystagmus occurs in most central vestibular syndromes, and appears to be a permanent deficit. It is a positional nystagmus; therefore it may be present in some head positions (with respect to gravity), but not in others. Also the nystagmus may vary in direction with change in head position. Vertical nystagmus in any head position is most consistent with central vestibular disease. 08/18/10 Robert Niemeier, DPT

48. Vestibular Function Recovery Rates UVL: 6-8 weeks BPPV: remission in one/few treatments BVL: 6 months – 2 years CNS Lesion: 6 months – 2 years 08/18/10 Robert Niemeier, DPT

49. Prescription Individualized vestibular rehabilitation program Outpatient, 1-2 times/week for 4-6 weeks HEP, 5 minutes, 3 x / day Walking program (Health & Fitness prescription) Exercise graduated for possible increase of symptoms during first week 08/18/10 Robert Niemeier, DPT