1. VESTIBULAR DISORDERS 1

2. ANATOMY OF VESTIBULAR SYSTEM 2

3. Peripheral Vestibular System Functions: – To stabilize visual images on the fovea of the retina during head movement to allow clear vision – To maintain postural stability (esp. during the movement of the head) – Provide information used for spatial orientation 3

4. Labyrinth: (found within the temporal bone) has 2 types of movement sensors: – Semicircular canals (SCC): signals from these 3 SCCs are primarily used for gaze stability Anterior/superior Posterior/inferior Horizontal/lateral – Otolith organs: signals are primarily for postural stability Utricle saccule 4

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7. SCC: endolymph – fluid that moves freely within each canal in response to the direction of angular head movement – It bends the sensory receptor cells (hair cells) in the cupula as it moves Each SCC responds best to movement in its own plane (either superior, inferior, horizontal) 7

8. Otolith organs: Comprised of saccule and the utricle, respond to linear acceleration and to the pull of gravity Calcium carbonate crystals (otoconia) are embedded in a gelatinous matrix within them The sensory receptors/hair cells, project into this gelatinous matrix sign 8

9. angular (SCC) and linear velocity(otolith) input/informationVestibular nuclie in the brainstem (primarily medial & superior)Information is sent to ocular motor nuclei (VI, IV, III) Thalamus & cortex – for arousal & concious awareness of the head & body in space Medial & lateral vestibulo spinal tracts (MVST, LVST), PIVC, parieto insular vestibular cortex – for maintenance of postural control 9

10. Central Vestibular System Vestibular nuclei & its connections: – Reticular formation, thalamus, & vestibular cortex – contribute to the integration of arousal & concious awareness of the body; discerning between movement of self & the environment – Cerebellar connections – help to modulate the vestibulo ocular reflex (VOR); maintain posture during active & static activities, & coordinate lim movements 10

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13. Lesions in the central lower brainstem structures can mimic peripheral vestibular pathology Central lesions in the cortex & upper brainstem result in perceptual disorders such the abnormal perception of visual vertical 13

14. PHYSIOLOGY & MOTOR CONTROL 14

15. Important principles Tonic Firing Rate 80 pulses per second: normal tonic firing rate even when the head is stationary (e.g. sleep), the vestibular system is still active Angular or linear movement of the head can increase or decrease the firing rate of the vestibular system 15

16. Vestibulo-Ocular Reflex (VOR): Gaze stability during rapid head movement is maintained by VOR SCC afferent synapses with oculomotor nuclei producing a slow-phase eye movement (VOR) in the opposite direction of the head movement As the head moves in one direction, the eyes will move in the opposite direction with equal velocity -- vestibular gain (eye/head velocity = 1) 16

17. When the head is moving at velocities less than 60 degrees per second, gaze stability can be maintained using smooth pursuit When the head moves greater than 60 degrees per second, the vestibular system generates eye movement in the direction opposite the head movement to maintain gaze on the target VOR operate at head velocities of 350 – 400 deg per second > 400 degrees per second – VOR decreases and gaze stability degrades 17

18. Push – Pull Mechanism: UVL on the UVR SCCs - all work in pairs: (R) ant SCC paired with (L) post SCC & vice versa, then two horizontal canals Head turned to ® --» increased firing rate (depolarized) of ® horizontal SCC --» decreased firing rate (hyperpolarized) (L) horizontal SCC A faulty interpretation (from CNS) will lead to difficulties with gaze stabilization, motion perception, & postural stability 18

19. Inhibitory Cut Off Rotation of the head to the side depolarizes the hair cells of that labyrinth resulting in: – Increase in the firing rate of the vestibular neurons for head velocities of up to 350 to 400 deg per second – Concomittant hyperpolarization of the opposite labyrinth also occurs 19

20. Hyperpolarization of the hair cells in the opposite labyrinth can only decrease the firing rate to zero, point the inhibition is cut off (inhibitory cut off) The response to the head movements that hyperpolarize the hair cells is limited to a velocity range up to 80 deg per sec – E.g. rotation to ® of 120 per second, the ® ear increases its firng rate from 80 (tonic) to 200 deg per sec. – left ear decrease from 80 to zero not negative 40 20

21. Velocity Storage System: Signal generated by movement of the cupula is brief, lasting only as long as the cupula is deflected The response is sustained, by a circuit of neurons in the medial vestibular nucleus and lasts longer than 10 seconds. The purpose of sustaining the vestibular input may be to signal the brain that movement is still occurring even though the cupula is no longer reporting it 21

22. ASSESSMENT 22

23. History 3 key items in taking the history: Symptoms – Tempo – if the pt has had an acute attach of vertigo (within 3 days), chronic disequilibrium, or if the pt is having episodes of dizziness – episodic vertigo --- average duration of episodes in seconds, minutes or hours Circumstances – if with particular movements, positions or at rest 23

24. Symptoms Dizziness: sensation of whirling or feeling a tendency to fall – Vertigo: illusion of movement, most commonly a sense of spinning – Lightheadedness: vague and less localizing than vertigo. Defined as a sense of feeling as if about to fain – Disequilibrium: subjective sensation that the person is off balance Oscillopsia: visual instability with head movement in which images appear to move or bounce; due to decrease VOR gain 24

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26. SYMPTOMPOSSIBLE CAUSE VertigoBPPV (Benign paroxysmal positional vertigo), unilateral peripheral hypofunction, unilateral central lesion affecting the vestibular nuclei LightheadednessOrthostatic hypotension, hypoglycemia, anxiety, panic disorder DysequilibriumBilateral vestibular lesion, chronic unilateral vestibular lesion, lower extremity somatosensation loss, upper brainstem/vestibular cortex lesion, motor pathway lesions 26

27. Physical Examination Oculomotor tests: most localizing & diagnostic means to examine vestibular system. They include: – observation of nystagmus, – examination of the VOR at high acceleration (head thrust test), – head shaking induced nystagmus (HSN), – positional testing, – clinical dynamic visual acuity (DVA) test 27

28. Nystagmus – primary diagnostic indicator used in identifying most peripheral and central vestibular lesions An involuntary eye movement, nystagmus due to a peripheral vestibular lesion is composed of both slow and fast phase eye movements 28

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30. Its direction is named by the direction of fast phase of the eye movement In a vestibular lesion, the slow phase eye movement is due to a relative excitation of one side of the vestibular system The fast phase is simply a resetting eye movement 30

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32. Nystagmus due to a vestibular lesion is most commonly seen after an acute unilateral insult: – Spontaneous (at rest) nystagmus – occurs in the absence of motion because of the asymmetry between the functioning and non functioning sides of the vestibular systems – If its due to peripheral lesions, typically resolves after 7 days due to visual suppression as well as the adaptive capabilities of CNS 32

33. OBSERVATION OF NYSTAGMUS: Can be suppressed in light and when a person fixates on a target Should be performed under the conditions in which the person cannot visualize the surrounding environment: – Frenzel lenses – Infrared camera 33

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36. Infrared camera system 36

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38. HEAD TRUST TEST: VOR is examined using both slow (<60 deg/sec) & rapid head rotations Pt is asked to fixate on a near target  head moved in slow amplitude & attempts to fixate on the target  pt will be advised that head will be moved quickly  repeat with the pt fixating on target approximately 6 ft away Normal : will be able to maintain gaze on the target during head movement 38

39. Vestibular loss: will cause the eyes to move off the target (no VOR) & will to refixate on the target causing a saccade – fast eye movement – If unilateral peripheral or central vestibular lesion – pt will not be able to maintain gaze when head is rotated quickly toward the side of lesion – If bilateral peripheral vestibular lesion – results in refixation saccades when the head is thrust to either side 39

40. HEAD-SHAKING-INDUCED-NYSTAGMUS Useful in the dx of the unilateral vestibular defect Pt must wear frenzel lenses or use video infrared camera  instruct pt to close eyes  clinician flexes the head 30 deg (to place the horizontal SCC parallel with the ground)  oscillates the head horizontally 20 times at a frequency of 2 hertz  open eyes 40

41. Unilateral peripheral vestibular lesion: horizontal nystagmus with the quick phase toward the normal side and the slow phase toward the lesioned side Not all UVL will result in HSN Pt wil bilateral vestibular hypofunction will not have HSN bec of (-) asymmetry (+) vertical nystagmus after horizontal or vertical head shaking suggests a central lesion 41

42. POSITIONAL TESTING Used to identify vertigo and nystagmus Benign paroxysmal position vertigo (BPPV): – Most common cause of positional vertigo – Otoconia are dislodge and float into the SCC, causing an abnormal signal results in brief vertigo and nystagmus – The direction of the nystagmus is specific for which canal is involved 42

43. – Hallpike-Dix test: this maneuver places the posterior SCC in a plane parallel with pull of gravity – This test can also be performed by moving into sidelying position – The ear toward the ground is the labyrinth being tested – Clinician should observe the eyes for nystagmus 43

44. SCC INVOLVEMENTNYSTAGMUS Posterior canalUp-beating and torsional Anterior canalDown- beating and torsional Horizontal canalHorizontal Vertical canalTorsional only * The torsional component occur because of the oblique muscle attachements the vertical SCCs synapse with 44

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47. CLINICAL DYNAMIC VISUAL ACUITY TEST Vestibular deficits: the eyes will not be stable in space during head movements Static acuity is determined first – the patient is asked to “Read the lowest line you can see” Pt then attempts to read the chart while the clinician horizontally oscillates the pt’s head at a frequency of 2 hertz. 47

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49. A metronome is useful to ensure correct frequency of oscillation A 3 or more line decrement in visual acuity during head movement  possible vestibular hypofunction 49

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51. BALANCE TEST BPPVUVLBVLCENTRAL LESION Romberg(-)Acute: (+) Chronic: (-) Acute: (+) Chronic: (-) Often (-) Tandem Romberg (-)Positive, eyes closed (+) Single legged stance (-)Maybe (+)Acute: (+) Chronic: (-) May be unable to perform GaitNormalAcute: wide-based, slow, decreased arm swing & trunk rotation Compensated: Normal Acute: wide-based, slow, decreased arm swing & trunk rotation Compensated; mild gait deviation May have pronounced ataxia Turn head while walking May produce ligh unsteadines s Acute: may not keep balance Compensated: Normal May not keep balance or slows cadence to perform May not keep balance, increased ataxia 51

52. VESTIBULAR FUNCTION TESTS: 2 most commonly used are: Caloric testing – involves infusing the external auditory canal with air or water – This stimulus introduces a temperature gradient causing movement of the endolymph within the horizontal SCC – The stimulated canal generates a horizontal nystagmus response 52

53. – Useful for determining the side of the side, bec each labyrinth is stimulated separately – Only the horizontal SCC is stimulated Rotary chair test – stimulates the vestibular system by rotating subjects in the dark – The VOR is measured is measured during rotation & compared during normal responses – Can actively stimulate both vestibular systems – Only assess vestibular function at frequencies up to 1 hertz 53

54. VESTIBULAR SYSTEM DYSFUNCTION 54

55. Mechanical BPPV: Biomechanical d/o is its most common cause s/sx: – vertigo with change in head position – Nausea with or without vomiting – Disequilibrium Latency of onset: 15 sec with duration of <60 sec The vertigo & nystagmus are direct impairments caused by misplaced otoconia 55

56. Indirect impairements: symptoms of nausea, vomiting, & imbalance Mechanisms: otoliths become dislodged from the utricle & fall into the SCCs – Cupulolithiasis – Canalithiasis 56

57. – Cupulolithiasis – fragments of otoconia breakaway and adhere to the cupula of one of the SCCs – head is moved into certain/provoking positions  weighted cupula is deflected by the pull of gravity  abnormal signal results in vertigo & nystagmus  these persist as long as in the provoking position – Does not explain the brief of vertigo in BPPV 57

58. – Canalithiasis – Otoconia are floating freely in one of the SCCs – Change in head positions  otoconia moves inside the SCC (because of pull of gravity)  endolymph movement & deflection of the cupula 58

59. Interventions of BPPV: Goals: – Replace the otoconia into the vestibule – Reduce the vertigo associated with head motion – Improve balance – Educate the pt about self treatment strategies in the advent of reoccurence – Return to daily activity involving head motion 59

60. Canalith repositioning treatment (CRT): – Based on the canalithiasis theory of free floating debris in the SCC – The pt’s head is moved is moved into different positions in a sequence that will move the debris out of the involved SCC and into the vestibule (location of saccule & utricle) -- Debris is in position, symptoms resolved – After the tx, px wear soft collar to avoid vertical head movt’s – Remain upright for 1 to 2 nights, avoid sleeping on the involved side for 5 additional nights – Horizontal movt of head to prevent stiffed neck 60

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62. 1.Pt’s head rotated toward the involved side 2.Then to Hallpike-Dix position 3.Head rotated 180 degrees to the opposite direction (unaffected side) – maintain the 30 deg neck extension 4.Pt is rolled onto shoulder (side of #3) 5.Slowly bring to sitting position, head still rotated 6.Pt then fitted with soft collar 62

63. Liberatory (Semont) maneuver: – Based on cupulolithiasis theory – Involves rapidly moving the pt through positions designed to dislodge the debris from the cupula – Similar to CRT, pt must avoid the provoking position & keep the head in upright position for 1 to 2 nights after the treatment 63

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65. 1.Starts in sitting – turns the head 45 deg to one side then quickly lies down on opposite shoulder 2.Remain for 30 sec or til vertigo stops 3.Pt slowly return to starting position 4.Maintain head in rotation until sitting upright 5.Pt turns to opposite direction – repeat the process 6.Do 10 to 20 times ; 3 x day until pt is without vertigo for 2 consecutive days 65

66. Brandt-Daroff exercises: – Designed to habituate the CNS to the provoking position, but may act by dislodging the debris from the cupula or by causing debris to move out of the canal – Should be performed for 10 to 20 repetitions (may decrease to 5), 3/day until the pt has no vertigo for 2 consecutive days – Movements must be performed rapidly 66

67. 1.Head is rotated 45 deg to one side – e.g. (L) 2.Pt moves from sitting to ® sidelying & stays in the position for 1 minute 3.Pt is then rapidly moved 180 deg from ® sidelying to (L) – head should be in original position 4.Pt returns to sitting – may be fitted with soft collar 67

68. BPPV Treatment Procedure Diagnosis/ Symptoms CRT BPPV due to canalithiasis Posterior SCC canalithiasis is the most common Liberatory maneuver BPPV due to cupullithiasis Posterior SCC cupulolithiasis is the most common Brandt – Daroff exercsies Persistent/ residual or mild vertigo (even after CRT) For pt who may not tolerate CRT 68

69. Decreased Receptor Input The most common causes of unilateral vestibular pathology are: viral insults, trauma, & vascular events s/sx of UVL: vertigo, spontaneous nystagmus, oscillopsia with head movements, postural instability, & dysequilibrium Vertigo & nystagmus initially resolves within 3 to 7 days assuming exposure to daylight conditions 69

70. Spontaneous nystagmus beyond 7 days may suggest possible central lesion or unstable peripheral lesion Symptoms of vertigo beyond 2 weeks should be considered and indirect impairments 70

71. Interventions for UVL: Goals: recovery time upon initiating vestibular rehabilitation averages 8 weeks – Improve stability of gaze during head movement – Decrease sensitivity to motion – Improve static & dynamic postural stability – Establish a home exercise program (HEP) that includes walking 71

72. Gaze stability - To improve the VOR & other systems that are used to assist gaze stability with head motion – a. X1 (times 1) – move the head horizontally (& vertically if appropriate) as quickly as possible while maintaining focus on a stable target – Retinal slip – occurs when the immage of an object moves off the fovea of the retina, resulting in visual blurring – Must learn to slow head movement if the target becomes blurred 72

73. – b. X2 (times 2) – pt move the head and target in opposite directions – Both should be made increasingly difficult as the patient improves 73

74. Postural stability – improve balance by encouraging the development of balance strategies within the limitations of the patient ( either somatosensory, visual or vestibular) – Should challenge the pt safe if done independently – Incorporate head movement into the exercises – most of these pt tend decrease their head movt 74

75. Motion sensitivity : habituation training – When pt has continual complaints of dizziness – Habituation is reduction in response to a repeatedly performed movement – Provoking position  mild to moderate dizzness  holds for 30 seconds or until symptoms abate  perform 3 to 5 times each, 2 to 3 times per day – Designed to reproduce dizziness and symptoms normally decrease within 2 weeks  if didn’t change, habituation should be change  if still no improvement then refer 75

76. Ototoxicity – The most common cause of a bilateral vestibular lesion (BVL) – Certain aminoglycosides (gentamycin, streptomycin) are readily taken up by the hair cells of the vestibular apparatus & continue to build in the system even after the person has stopped using the antibiotic – Dysequilibrium – primary complaint 76

77. – Direct impairments: oscillopsia & gait ataxia are common clinical signs – No nausea or vertigo (no asymmetry in the tonic firing rate) – Gentamycin ototoxicity- posture & gait abnormalities, decreased visual acuity with head movement, & reduced VOR gains resulting in a (+) head thrust test – Impairments are likely permanent though pts can still return to high levels of activity 77

78. Interventions for BVL: Goals: – Reduce subjective complaints of gaze instability – Improve static & dynamic balance – Instruct the patient in a HEP that includes walking – Educate pt in activities that may be more difficult owing to the disorder 78

79. Gaze stability exercises: – May be similar to X1 but X2 is not recommended (may produce excessive retinal slip) – Pts with BVL depend on somtosensation &/or vision to maintain postural stability – Balance excercises should enhance the use of these cues – Should be performed safely – Begin with walking program, daily if tolerated 79

80. BVL Exercises to improve central reprogramming of eye movements Begin with 1.Hold two targets at arm’s length from your head. Look with your eyes first, then turn your head toward the target. Attempt to do this for 60 sec 2.Perform exercise 1 in the vertical direction Progress to 1.Progress to increasing the distance used to see the target. Use a busy background (checkeredboard, venetian blinds) 2.Same as horizontal exercise 80

81. Begin with Hold one target at arm’s length from your head. Close your eyes and turn your head away from the target, attempting to keep your eyes focused on the target. Open your eyes only after having turned your head Progress to Progress to doing this standing Progress to decreasing base of support 81

82. Balance Exercises Begin WithProgress ToPurpose 1. Stand with feet shoulder width apart, arms across the chest Bring feet closer together. Close eyes. Stand on a sofa cushion/pillow Enhance the use of vestibular signal form balance by decreasing BOS Eyes closed increases reliance on vestibular signals for balance 2. Practive ankle sways: ant-post & med- lat Doing circle sways. Close eyes Teaches the pt to use a correct ankle strategy. 82

83. Begin WithProgress ToPurpose 3. Attempt to walk with heel touching toe on firm surface Do the same exercise on carpet Enhance the use of vestibular signal for balance by decreasing BOS Doing exercise on carpet decreases proprioception, increasing difficulty 4. Practice walking & turning around Making smaller turns. Close eyes The turning stimulates & challenges the vestibular system 5. Walk & move your head side to side Counting backwards from 100 by threes Challenge balance & stimulate both vestibular system 83

84. Central Nervous System Lesion 1.Cerebrovascular insult particularly of the anterior-inferior cerebellar artery (AICA), posterior-inferior cerebellar artery (PICA), & vertebral artery 2.Traumatic brain injury 3.Vertebrobasilar insufficiency 4.Demyelinating disease such as multiple sclerosis (MS) 84

85. Common symptoms Central Abnormal smooth pursuit & abnormal saccadic eye movement tests SX usually do not include hearing loss SX migh include diploplia, altered conscious, lateropulsion, SX of acute vertigo not usually suppressed by visual fixation peripheral Smooth pursuit & saccades usually normal; positional testing may reproduce nystagmus SX may include hearing loss fullness in ears, tinnitus SX of acutevertigo usually intense (more than central vestibular pathology) 85

86. CENTRAL Pendular nystagmus Pure pesistent vertical nystagmus persists regarless of positional testing (persistent downbeat nystagmus in Hallpike Dix may indicate anterior canal BPPV PERIPHERAL Nystagmus will incoporate slow & fast phases (jerk nystagmus) Spontaneous persistent horizontal nystagmus will resolve within 7 days in a patent with UVL 86

87. Head trauma: – Another method of sustaining a peripheral vestibular lesion – Damage to the vestibule within its protective encasement – bony labyrinth – TBI pts commonly suffer from vertigo --- central processing of the vestibular input may also be the cause of their vertigo 87

88. Pendular nystagmus – eyes oscillate at equal speeds; often indicative of congenital disorders (e.g. absence of central central vision) Lateropulsion – person’s tendency to fall to one side Red flags: horizontal or vertical diplopia lasting longer than 2 weeks after the onset of unilateral vestibular loss; persistent pure vertical positional nystagmus (anterior canal cupulolithiasis should be r/o); & spontaneous up beating nystagmus (rare) 88

89. Ocular tilt reaction (OTR): – Ocular torsion – both eyes rotating downward the direction of tilt – Head tilting – Skew deviation – eyes appears as one eye being superiorly displaced in comparizon with the other eye 89

90. Interventions for CVL: Goals: – Ensure fall prevention strategies & necessary safety precautions are in place to allow safe functioning within the home & community – Educate pt in compensatory strategies to assist in gaze stability – Instruct the pt in a HEP that includes walking 90

91. TBI pts may not be ideal for vestibular rehabiliatation due to its irritating nature & further disorienting the pt At the level of the brainstem (vestibular nuclei) – similar expectations for recovery with UVL Vestibular cortical lesions may also recover similar to the process of CVA 91

92. Common Vestibular Diagnoses MENIERE’S DISEASE: – Low frequency hearing loss & episodic vertigo – May also complain of tinnitus – sense of fullness in the ear – SX gradually increase in severity & then last 1 to 2 hours per episode – Chronic type can result to UPV hypofunction (requires rehabilitation) 92

93. – Pathophysiology: probably involves an increase in endolymphatic fluid causing distension of the membranous tissues – Medical intervention to reduce fluid build up – Many pts can manage the SX well with controlled diet – 2 grams or less per day of sodium diet (most important dietary restriction to follow) – Avoid caffeine & alcohol – Sometimes managed with diuretic to control the amount of fluid in the body 93

94. – Surgery: endolymphatic shunt placement – prevent fluid buildup in the inner ear; vestibular nerve section – stop abnormal vestibular signal – PT: most beneficial for unilateral vestibular hypofunction – therapy will not stop vertigo; gaze & postural stability exercise; tx of disequilibrium occuring after neurectomy 94

95. PERILYMPHATIC FISTULA (PFL): – Most commonly caused by rupture of the oval or round windows, membranes that separate the middle & inner ear – Rupture  leakage of the perilymph into the middle ear  vertigo & hearing loss – Perilymph bathes the SCC, serving as a protective barrier between the bony & membranous labyrinth 95

96. – Usually caused by a traumatic event – e.g. excessive pressure changes as in deep water diving, blunt head trauma without skull fracture; or extremely loud noise – Tx: initially with bed rest – hopes of allowing the membrane to heal – PT: contrainicated in most cases with PLF – Medical mx: strict limitations on activities, warranting good communication between PT & MD 96

97. ACOUSTIC NEUROMA: – A.k.a Vestibular schwannoma – Benign tumor located on CN VIII – S/SX: progressive hearing loss; tinnitus; & disequilibrium – TX: usually surgical excision of the tumor – PT: early post-op to help the resolve SXs of disequilibrium & oscillopsia; OPD should be considered similar to tx of UVL 97

98. MOTION SICKNESS: – Normal sensation but in some people becomes debilitating – Sensory conflict theory – proprioception, vestibular, & visual information do not match stored neural patterns the brain expects to recognize  pallor, nausea, emesis, diaphoresis, & motion sensitivity – TX: cognitive behavioral management, medications, biofeedback, & habituation training using ground & flight situations 98

99. Common Nonvestibular Diagnoses MIGRAINE-RELATED DIZZINESS: – Can be deceptively similar to a peripheral vestibular lesion – vascular event occurs in a vestibular structure (vestibular nuclei) – SX: vertigo, dizzines, & motion sickness – Women between 35 & 45 are more prone – Often well controlled with medication & diet 99

100. MULTIPLE SCLEROSIS: – MS can affect CN VIII where it enters the brainstem & causes identical symptoms to a unilateral vestibular pathology. 100

101. CERVICAL VERTIGO: – Commonly used in Europe – Mechanisms; – 1. upper cervical spine sends proprioception input to the C/L vestibular nucleus  soft tissue injury & joint dysfunction might alter the afferent input contributing to spatial orientation – 2. (+) vertebrobasilar insufficiency – pt is seated then leands forward & extends the neck then rotate 45 deg to suspicious side  SX: diplopia, dysarthria, syncope, headache, visual field deficits, vertigo & nystagmus 101

102. C/I for Vestibular Rehabilitation Unstable vestibular d/o (Meniere’s dse, PLF) Sudden loss of hearing Increased feeling of pressure or fullness to the point of discomfort in one or both ears Severe ringing in one or both ears When treating for post op: observe for d/charge of fluid from ears or nose (CSF leak); Pt with acute neck injuries may not be able to tolerate either CRT or some of the gaze stability exercises 102