1. VESTIBULAR DISORDERS AND VESTIBULAR REHABILITATION MCWAHAB, MD, MMHA, FPARM

2. ANATOMY OF THE PERIPHERAL AND CENTRAL VESTIBULAR SYSTEM MCWAHAB, MD, MMHA, FPARM

3. VESTIBULAR ANATOMY 1.Peripheral sensory apparatus – detects & relays information about head angular & linear velocity to central processing system – orients the head with respect to gravity 2.Central processing system – processes information in conjunction with other sensory inputs for position and movement of head in space 3.Motor output system – generates compensatory eye movements and compensatory body movements during head & postural adjustments MCWAHAB, MD, MMHA, FPARM

4. FUNCTION OF THE VESTIBULAR SYSTEM 1.Provides information concerning gravity, rotation and acceleration 2.Serves as a reference for the somatosensory & visual systems 3.Helps integrate arousal, conscious awareness of the body via connections with vestibular cortex, thalamus and reticular formation 4.Allows for: – gaze & postural stability – sense of orientation – detection of linear & angular acceleration MCWAHAB, MD, MMHA, FPARM

5. THE EAR MCWAHAB, MD, MMHA, FPARM

6. THE INNER EAR MCWAHAB, MD, MMHA, FPARM

7. PERIPHERAL APPARATUS Membranous Labyrinth – Semicircular canals (SSC) – Otolith organs MCWAHAB, MD, MMHA, FPARM

8. Netter ‘97 MCWAHAB, MD, MMHA, FPARM

9. SEMICIRCULAR CANALS Angular acceleration Ampulla contains sensory epithelium 1. Anterior semicircular canal 2. Ampulla (superior canal) 3. Ampulla (lateral canal) 4. Sacculus 5. Cochlear duct 6. Helicotrema 7. Lateral (horizontal) canal 8. Posterior canal 9. Ampulla (posterior canal) 10. Oval window 11. Round window 12. Vestibular duct (scala vestibuli) 13. Tympanic duct (scala tympani) 14. Utricule MCWAHAB, MD, MMHA, FPARM

10. ASCENDING PATHWAYS Vestibular nerve Vestibular nuclei Medulla Thalamus Vestibular Cortex Oculomotor complex Cerebellum MCWAHAB, MD, MMHA, FPARM

11. 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) MCWAHAB, MD, MMHA, FPARM

12. Netter 1997 MCWAHAB, MD, MMHA, FPARM

13. VESTIBULOSPINAL REFLEX Generates compensatory body movement to maintain head and postural stability, thereby preventing falls. MCWAHAB, MD, MMHA, FPARM

14. CEREBELLUM Monitors vestibular performance Readjusts central vestibular processing of static & dynamic postural activity Modulates VOR Provides inhibitory drive of VOR MCWAHAB, MD, MMHA, FPARM

15. Netter 1997 MCWAHAB, MD, MMHA, FPARM

16. SYMPTOMS OF VESTIBULAR DISEASE MCWAHAB, MD, MMHA, FPARM

17. SYMPTOMS OF VESTIBULAR DYSFUNCTION 1.Vertigo 2.Dizziness 3.Lightheadedness 4.Dysequilibrium 5.Oscillopia 6.Nystagmus MCWAHAB, MD, MMHA, FPARM

18. VERTIGO Feeling of being off balance/spinning sensation No. 1 reason for consult among patients >75 years old Significant risk factor for falls in the elderly In children, it may affect normal childhood activities MCWAHAB, MD, MMHA, FPARM

19. DIZZINESS Sensation of whirling or feeling a tendency to fall Vague sensation of light-headedness MCWAHAB, MD, MMHA, FPARM

20. LIGHTHEADEDNESS Feeling that fainting is about to occur It is vague It is less localizing than vertigo May be due to non-vestibular problem – Hypotension – Hypoglycemia – anxiety MCWAHAB, MD, MMHA, FPARM

21. DYSEQUILIBRIUM Sensation of being off balance Acute and chronic vestibular lesions will produce dysequilibrium Dysequilibrium is associated with decreased somatosensation or weakness in the lower extremities MCWAHAB, MD, MMHA, FPARM

22. OSCILLOPSIA Visual illusion of oscillating movement of stationary objects Subjective experience of motion of objects in the visual environment that are known to be stationary. Can arise with lesions of peripheral or central vestibular systems, vestibular hypofunction Indicative of diminished VOR gain – motion of images on fovea – diminished visual acuity MCWAHAB, MD, MMHA, FPARM

23. NYSTAGMUS Rapid alternating movement of eyes in response to continued rotation of the body Primary diagnostic indicator in identifying vestibular lesions Peripheral Vestibular Lesion – Composed of both slow and fast component eye movements. MCWAHAB, MD, MMHA, FPARM

24. NYSTAGMUS Physiologic nystagmus – vestibular, visual, extreme lateral gaze Pathologic nystagmus – spontaneous, positional, gaze evoked Labeled by the direction of the fast component MCWAHAB, MD, MMHA, FPARM

25. SXS OF VESTIBULAR DYSFUNCTION FALL HOSPITALIZATION (10% OF CASES) HOSPITALIZATION (10% OF CASES) DEATH (50% OF CASES) DEATH (50% OF CASES) PERIPHERAL (Inner ear & Vestibular nerve) -Benign Paroxysmal Positional Vertigo -Meniere’s Disease -Vestibular Neuritis -Labyrinthitis -Perilymphatic Fistula -Acoutic Neuroma CENTRAL -CVD -Cerebellar D/O -Migraine -Multiple Sclerosis -Posterior Fossa Tumor -Neurodegenerative D/O -Medications -Psychiatric D/O MCWAHAB, MD, MMHA, FPARM

26. DIFFERENTIATION BETWEEN PERIHERAL AND CENTRAL VERTIGO Peripheral Central Nauseasevere moderate Imbalancemild severe Hearing Losscommon rare Oscillopsiamild severe Neurologic Symptomsrare common Compensationrapid slow ( Furman JM, Whitney SL. 2000) MCWAHAB, MD, MMHA, FPARM

27. DIFFERENTIATION BETWEEN PERIHERAL AND CENTRAL VERTIGO CENTRAL Ataxia often severe Abnormal smooth pursuit and abnormal saccadic eye movements tests PERIPHERAL Ataxia mild Smooth pursuit and saccades usually normal; positional testing may reproduce nystagmus. MCWAHAB, MD, MMHA, FPARM

28. DIFFERENTIATION BETWEEN PERIHERAL AND CENTRAL VERTIGO CENTRAL SX of acute vertigo not usually suppressed by visual fixation PERIPHERAL SX of acute vertigo usually suppressed by visual fixation. SX of acute vertigo usually intense (more than central vestibular pathology) MCWAHAB, MD, MMHA, FPARM

29. DIFFERENTIATION BETWEEN PERIHERAL AND CENTRAL VERTIGO CENTRAL Pendular Nystagmus (Eyes oscillate at equal speeds) PERIPHERAL Nystagmus will incorporate slow and fast phases (jerk nystagmus) MCWAHAB, MD, MMHA, FPARM

30. PERIPHERAL CAUSES MCWAHAB, MD, MMHA, FPARM

31. BENIGN PAROXYSMAL POSITIONAL VERTIGO Otoconia (Calcium Carbonate crystals) normally embedded in the utricle Crystals dislodged into the canals and may block normal fluid movement that the canals used to sense head motion Fluids not affected by gravity but crystals do & when they move, fluids move and stimulates cupula to send false signals to the brain causing vertigo MCWAHAB, MD, MMHA, FPARM

32. BENIGN PAROXYSMAL POSITIONAL VERTIGO Most common cause of peripheral vestibular disorder Sign: Nystagmus Diagnosis – Dix-Hallpike test – Roll Tests 50% recurrence rate after treatment Treatment protocol may differ each time MCWAHAB, MD, MMHA, FPARM

33. DIX-HALL PIKE TEST MCWAHAB, MD, MMHA, FPARM

34. ROLL TEST MCWAHAB, MD, MMHA, FPARM

35. BENIGN PAROXYSMAL POSITIONAL VERTIGO CANALITHIASIS Loose crystals move freely n the fluid of the canal Symptom almost immediately stop when movement of the head ceases Treatment: Canalith Respositioning Maneuvers CUPOLOTHIASIS Crystals hung up on the bundle of nerves that sense the fluid movement Vertigo persists even when the head is not in the offending position Treatment: Liberatory Maneuver followed by Canalith Repositioning Maneuvers MCWAHAB, MD, MMHA, FPARM

36. CANALITH REPOSITIONING MANEUVER MCWAHAB, MD, MMHA, FPARM

37. LIBERATORY MANEUVER MCWAHAB, MD, MMHA, FPARM

38. MENIERE’S DISEASE Aka Idiopathic Endolymphatic Hydrops Most cases are unilateral 20-50 years old; M=F May be due to excessive production of fluid in the inner ear or inadequate absorption Attacks may be induce by fatigue and stress MCWAHAB, MD, MMHA, FPARM

39. MENIERE’S DISEASE Set of episodic symptoms including – Vertigo – Hearing loss intermittent occurring mainly at the time of the attacks of vertigo Initially involves lower pitches but may involve all pitches in chronic cases May become permanent – Tinnitus – Sensation of fullness in the affected ear Episodes last from 20 minutes up to 4 hours MCWAHAB, MD, MMHA, FPARM

40. MENIERE’S DISEASE Diagnostics: Audiometric exam, Electronystagmogram, Rotational or balance platform testing, Electrocochleography Treatment – Low salt diet & diuretics – Anti-vertigo medications – Intratympanic injection with gentamicin or dexamethasone – Air pressure pulse generator – Surgery MCWAHAB, MD, MMHA, FPARM

41. INFECTION OF THE INNER EAR VESTIBULAR NEURITIS – Viral (Herpesviridae) infection of the vestibular nerve that causes vertigo LABYRINTHITIS – Infection, most commonly viral, of the labyrinth – Causes vertigo and sensory type hearing loss or tinnitus In both cases, sudden movement of the head causes the vertigo However, it is not generally related to the side of the head which is down (as in BPPV) but whether the patient is lying down or sitting up MCWAHAB, MD, MMHA, FPARM

42. INFECTION OF THE INNER EAR 95% of vestibular neuritis is one-time experience Treatment is symptomatic although if herpes infection is suspected, an anti-viral drug may be given Usually takes three weeks to recover from both Vestibular Neuritis and Labyrinthitis Recovery may be due to a successful immune system or brain getting used to the imbalance (Compensation) MCWAHAB, MD, MMHA, FPARM

43. PERILYMPHATIC FISTULA Abnormal connection (tear) in one or both of the small, thin membranes (the oval window and the round window) that separate the air filled middle ear and the fluid filled perilymphatic space of the inner ear Fluid leaks into the middle ear Due to the defect, changes in the pressure of the middle ear affects the inner ear stimulating the balance or hearing structures within Symptoms: ear fullness, fluctuating or sensitive hearing, dizziness, and motion intolerance Symptoms worse with changes in altitude (fast elevators, airplanes and high places) or increase in CSF pressure such as heavy lifting, bending over and coughing or sneezing MCWAHAB, MD, MMHA, FPARM

44. PERILYMPHATIC FISTULA Most common cause is head trauma usually a direct blow to the head or whiplash injury Other causes: Perforation of eardrum due to a strong nose blowing or sneezing, or anything that may increase the ICP, SCUBA diving Rarely congenital and usually unilateral If traumatic in cause, restrict physical activity for 7-14 days, further tests done if symptoms do not improve MCWAHAB, MD, MMHA, FPARM

45. PERILYMPHATIC FISTULA Perilymphatic space is connected to the CSF Perilymph fluid, which is high in Sodium, is similar with CSF Fistula causes perilymph in the inner ear escapes, due to the hydrostatic pressure of the CSF, and is replaced by CSF  lower levels of CSF in the brain and spinal cord  headache MCWAHAB, MD, MMHA, FPARM

46. PERILYMPHATIC FISTULA Treatment: Surgery – Surgery usually takes about an hour with minimal pain – After discharged, patients advised to stay at home for 3 days with limited activity – Sedentary work may be done after three days and to avoid lifting of more than 10 lbs as well as sporting activities for 1 month – Avoid contact sports, diving, weight lifting and roller coasters until cleared by physician MCWAHAB, MD, MMHA, FPARM

47. ACOUSTIC NEUROMA Intracranial, extra-axial tumors that arise from Schwann cell sheath investing either the vestibular or cochlear nerve Most common symptom is unilateral hearing loss In smaller lesion, there could be vertigo or balance problem MCWAHAB, MD, MMHA, FPARM

48. ACOUSTIC NEUROMA In patients presenting with unilateral hearing loss, consider acoustic neuroma until proven otherwise Definitive diagnosis is through a Gadolinium – enhanced MRI Treatment: – Surgical excision – Arrest tumor growth through radiation therapy – Careful serial observation MCWAHAB, MD, MMHA, FPARM

49. ACOUSTIC NEUROMA Observation is recommended for the following – Elderly patients – Patients with small tumors, especially if hearing is good – Patients with medical conditions that significantly increases the risk for operation – Patients who refuse treatment – Patients with a tumor on the side of an only hearing ear or only seeing eye MCWAHAB, MD, MMHA, FPARM

50. QUANTITATIVE VESTIBULAR TESTING MCWAHAB, MD, MMHA, FPARM

51. ELECTRONYSTAMOGRAPHY Diagnostic test to record involuntary movements of the eye caused by nystagmus Can also diagnose cause of tinnitus, vertigo, dizziness or balance dysfunction ENG measurements are based on the presence of corneoretinal potentials MCWAHAB, MD, MMHA, FPARM

53. QUANTIFIED DYNAMIC VISUAL ACUITY Behavioral measure of vestibular function that quantifies one’s ability to see clearly during predictable or unpredictable head movements Measuring visual acuity during head movements is one of the best functional tests in patients with unilateral and bilateral vestibular hypofunction It can identify the side of vestibular dysfunction and measure individual semicircular function MCWAHAB, MD, MMHA, FPARM

54. QUANTIFIED DYNAMIC VISUAL ACUITY MCWAHAB, MD, MMHA, FPARM

55. VESTIBULAR EVOKED MYOGENIC POTENTIAL TESTS Assess the saccule and its central projection (inferior vestibular nerve) to evaluating the CN XI circuit Series of tones are presented to each ear individually, and the corresponding evoked sternocleidomastoid responses are recorded during the patient’s neck flexion Absence of response reflects damage to that side CANNOT be used in patients with conducting hearing loss MCWAHAB, MD, MMHA, FPARM

57. COMPUTER DYNAMIC POSTUROGRAPHY Test the vestibulospinal reflexes and assess balance maintenance Assess the major senses involved in balance: vestibular, vision and proprioception Gives insight to patient’s functional status, compensation and fall risk A force plate measures body sway under different visual and postural conditions MCWAHAB, MD, MMHA, FPARM

59. VESTIBULAR REHABILITATION MCWAHAB, MD, MMHA, FPARM

60. VESTIBULAR REHABILITATION Is a specific form of physical therapy designed to habituate symptoms and promote adaptation to and substitution for various aspect of deficits related to a wide variety of balance disorder It is effective both in peripheral and central vestibular disorders Protocol should be individualized Basis for success is through the use of existing neural mechanism for adaptation, plasticity & compensation MCWAHAB, MD, MMHA, FPARM

61. STRATEGIES IN VRT Habituation for positional or motion-provoked symptoms Adapting to improve the gain of the vestibuloocular or the vestibulospinal reflexes Substituting alternative senses to replace lost vestibular function by biasing use away from the dysfunctional vestibular input MCWAHAB, MD, MMHA, FPARM

62. GOALS OF VRT Improve balance Minimize falls Decrease subjective sensations of dizziness Improve stability during locomotion Reduce over dependency on visual and somatosensory inputs Improve neuromuscular coordination Decrease anxiety and somatization due to vestibular disorientation MCWAHAB, MD, MMHA, FPARM

63. COMPONETS OF VRT 1.Coordinated team of clinicians 2.Accurate diagnosis & assessment  Quantifying the degree of damage to peripheral and central vestibular pathways  Evaluation of physiologic and neurologic compensation  Detailed medical history and balance symptoms  Evaluation of gait, ambulation, head movement, balance under altered sensory cues under static and dynamic conditions *Timed Up and Go Test is the most reliable test of balance *Unipedal Stance Test is the best predictor of falls MCWAHAB, MD, MMHA, FPARM

64. COMPONETS OF VRT 1.Coordinated team of clinicians 2.Accurate diagnosis & assessment  Sensory evaluation to include visual and proprioceptive abilities  Posturography to differentiate balance dysfunction due to vestibular from proprioceptive loss by measuring shoulder and pelvis sway  Evaluation of impact of symptoms to daily activities *Dizziness Handicap Inventory *Activities-Specific Balance Confidence Scale MCWAHAB, MD, MMHA, FPARM

65. COMPONETS OF VRT 1.Coordinated team of clinicians 2.Accurate diagnosis & assessment 3.Outcome measurement after VRT  Computerized Dynamic Posturography (Vestibulospinal Reflex)  Dynamic Visual Acuity Test & Gaze Stabilization Test (Vestibuloocular Reflex)  VRT Benefit Questionnaire  Dynamic Gait Index (Risk for Fall after VRT) MCWAHAB, MD, MMHA, FPARM

66. 2016 EVIDENCE-BASED CPG FROM APTA (Strong Evidence) VRT should be offered to patients with unilateral & bilateral vestibular hypofunction who have vestibular deficit-associated impairments and functional limitations Voluntary saccadic or smooth-pursuit eye movements should NOT be performed in isolation (without head movement) for gaze stability in rehab MCWAHAB, MD, MMHA, FPARM

67. 2016 EVIDENCE-BASED CPG FROM APTA (Moderate Evidence) Specific exercise techniques aimed at identified impairments or functional limitations may be offered Based on patients preference, supervised VRT may be provided MCWAHAB, MD, MMHA, FPARM

68. 2016 EVIDENCE-BASED CPG FROM APTA (Expert Opinion) Gaze stability exercise, as one part of home exercise program may be prescribed a minimum of 3x/day Adequate supervised VRT that allow patients to comprehend the programs’ goals and understand how to independently manage themselves and progress can be considered MCWAHAB, MD, MMHA, FPARM

69. FACTORS AFFECTING SUCCESS OF VRT Extent and location of damage to vestibular system Status of visual and proprioceptive system Physical strength Motor skills Integrity of Cerebellum General physical health Decision making and cognitive abilities Age Memory Presence of psychological and anxiety disorder MCWAHAB, MD, MMHA, FPARM