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Vestibular System (Ear) Lecture for students
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- 3. ANATOMY • Peripheral Vestibular System •Central Peripheral System
- 4. Peripheral Nervous System SemicircularCanals Otolithic Organs • Utricle & Saccule 3 SCC’s • Horizontal/Lateral • Posterior/Inferior • Anterior/Superior
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- 8. CENTRAL VESTIBULAR SYSTEM CORTEX -Parietal and insular lobes • Thalamus • Reticular System • Cerebellum
- 9. VESTIBULO-OCULAR REFLEX • Responsiblefor maintaining retinal stability • Rapid compensatory eye movement opposite direction of the head motion
- 10. PRIMARY AFFERENT SECONDARY NEURON MOTOR NEURON MUSCLE HORIZONTAL (L) Medial VN IpsiCNIII Contra CN VI Ipsi Medial Rectus Contra Lat Rectus POSTERIOR (L) Medial VN Ipsi CN IV Contra CN III Ipsi Superior Oblique Contra Inferior Rectus ANTERIOR (L) Lateral VN (B) CN III Ipsi Superior rectus Contra Inferior Oblique VESTIBULO-OCULAR REFLEX
- 11. EYE MOVEMENT; MUSCLE;CRANIAL NERVE RPSCC RHSCC LHSCC RASCC LASCC LPSCC
- 12. NYSTAGMUS • Involuntary eyemovement, with fast and slow component • Named by fast component • Spontaneous Nystagmus- acute unilateral vestibular lesion • Masked in light/visual fixation, elicited in dark
- 13. SYMPTOMS Vertigo • BPPV • UVH •Unilateral Central Lesion (Vestibular Nuclei) Lightheadedness • OH • Hypoglycemia • Anxiety • Panic Disorder Dysequilibrium • BVH • Chronic Unilateral Vestibular hypofuction • LE Somatosensation loss • Upper brainsterm/Vestibular Cortex lesion • cerebellar and motor pathway lesions Oscillopsia • VOR deficit
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- 15. PERIPHERAL PATHOLOGY BPPV • Mostcommon cause of vertigo • Onset: 15 sec • Duration: < 60 seconds CAUSE • Misplaced otoconia • Canalithiasis • Cupulolithiasis SYMPTOMS •Nystagmus •Vertigo •Nausea
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- 17. NYSTAGMUS PER SCCLOCATION AND MECHANISM OF BPPV SCC MECHANISM NYSTAGMUS Right posterior Cupulo Canal Persistent UBN c R torsion Transient UBN c R torsion Left Posterior Cupulo Canal Persistent UBN c L torsion Transient UBN c L torsion Horizontal Cupulo Canal Persistent ageotropic Transient geotropic Right Superior Cupulo Canal Persistent DBN c R torsion Persistent DBN c R torsion Left Superior Cupulo Canal Persistent DBN c L torsion Persistent DBN c L torsion
- 18. UNILATERAL VESTIBULAR HYPOFUNCTION • Decreasedor eliminated receptor input • Resolves within 3-7 days SYMPTOMS • Spontaneous nystagmus • Vertigo • Oscillopsia during head movement • Postural instability • Dysequilibrium* PERIPHERAL PATHOLOGY
- 19. BILATERAL VESTIBULAR HYPOFUNCTION • (B)affectation • Impairments are likely permanent • Can return to high levels of activity SYMPTOMS • Dysequilibrium* • Oscillopsia • Ataxia SYMMETRICAL • (-) nausea • (-) Vertigo • (-) nystagmus PERIPHERAL PATHOLOGY
- 20. • CVA ▪AICA ▪PICA ▪Vertebral artery •VBI • TBI • MS CENTRAL PATHOLOGY
- 21. CENTRAL VS PERIPHERALVESTIBULAR PATHOLOGY CENTRAL PERIPHERAL Ataxia Severe Mild Abn Eye Movement Smooth pursuit and Saccadic VOR Hearing Loss Rare but permanent More common but may recover (with tinnitus and fullness of ear) Vertigo - Not Suppressed by visual fixation - Can be suppressed by visual fixation - More intense Nystagmus - Pendular - Persistent - Pure vertical - Spontaneous - Horizontal - Transient Red flag - Diplopia, altered consciousness, lateropulsion
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- 25. HEAD IMPULSE TEST VerticalSemicircular Canal
- 26. HEAD SHAKING INDUCEDNYSTAGMUS • Tests unilateral peripheral vestibular defect INSTRUCTION: 1. Patient close eyes 2. Flex head 30 3. Oscillate horizontally 20 cycles (2 repetitions per second
- 27. DIX-HALLPIKE Test • Patientsits on the examination table • Manually rotate head 45 • Quickly brought to supine with neck 30 extended beyond neutral *ASCC & PSCC
- 28. • Patient sitson the examination table • Head rotated horizontally 45 degrees • Quickly bring patient down to side opposite to the side of head rotation DIX-HALLPIKE Test
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- 30. Caloric test • RESPONSE:COWS • Limitations • Only HSCC can be assessed • Stimulation corresponds to a frequency (0.025 Hz) that is much lower than the natural frequencies of head movement (1 to 20 Hz).
- 31. ROTATIONAL CHAIR TEST •Rotate subject in the dark/ Eyes closed using a chair. • Normal: Nystagmus should be generated • Compare VOR of each ear/direction • Considered the standard test for bilateral vestibular hypofunction • Limitation: -Only HSCC can be assessed
- 32. DYNAMIC VISUAL ACUITYTEST Measurement of visual acuity during horizontal movement of the head. Speed: >100deg/sec
- 33. CLINICAL TEST FORSENSORY INTERACTION OF BALANCE
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- 35. CANALITH REPOSITIONING MANEUVER •Anterior or posterior SCC
- 36. • For Rhorizontal SCC CANALITH REPOSITIONING MANEUVER
- 37. LIBERATORY (SEMONT) MANEUVER •R posterior SCC
- 38. BRANDT DAROFF • Rposterior SCC
- 39. BPPV TREATMENT TECHNIQUEINDICATIONS • CANALITHIASIS • Posterior SCC m/c CRM • CANALITH/CUPULOLITHIASIS • Posterior SCC m/c LIBERATORY (SEMONT) MANEUVER • Persistent/Residual mild vertigo • Cannot Tolerate CRM BRANDT-DAROFF
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- 41. GAZE STABILITY EXERCISE •ImproveVOR •Expose patient to “RETINAL SLIP”
- 42. HABITUATION EXERCISE •Find provokingposition and maintain for 30 seconds •Do 3-5 reps, 2-3x/day •Make activity diary •2 weeks
- 43. BALANCE EXERCISE •Develop balancestrategy •Challenging but safe enough to be done independently •INCORPORATE HEAD MOVEMENT
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- 45. •2x is notrecommended GAZE STABILITY TRAINING •Prone to fall BALANCE EXERCISE VESTIBULAR ADAPTATION
- 46. MENIERE’S DISEASE Tx: decreasingfluid build up or surgery Symptoms: Low frequency hearing loss + episodic vertigo Fullness of ear Tinnitus Due to increase in endolymphatic fluid
- 47. PERILYMPHATIC FISTULA • Cause:rupture of the oval or round windows. • MOI: trauma (loud noise, excessive pressure, head trauma) • Sx: Vertigo and Hearing Loss • Tx: • Bed rest • Surgical patches of fistula • PT: residual sx or hypofunction post-op