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NCS Prep > 7 Vestibular Rehabilitation > Flashcards

7 Vestibular Rehabilitation Flashcards

1
Q

Sensory components of balance

A

Vision- to cortex, BG, ventrolateral thalamus, back to cortex
Vestibular- to brainstem/cerebellum, BG, ventrolateral thalamus, cortex
Somatosensory- to SC through DCML, to brainstem/cerebellum, etc.

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2
Q

Sensory processing occurs…

A

At vestibular nuclear complex and cerebellum

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3
Q

Two otolith organs

A

Respond to gravity and linear acceleration, send afferent information to vestibular ganglion
Utricle- horizontal
Saccule- vertical

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4
Q

Structure of semi-circular canals

A

Ampulla houses sensory hair cells, hair cells project into gelatinous mass (cupula), movement in plane of canal causes endolymph to push against cupula

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5
Q

Superior vestibular nerve innervates…

A

Anterior SCC, horizontal SCC, utricle

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6
Q

Inferior vestibular nerve innervates…

A

Posterior SCC, saccule

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7
Q

Vestibular nuclear complex projections

A

Spinal cord, cerebellum, nuclei of CN III, IV, VI for control of eye, head, and body movements

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8
Q

Vestibular nuclear complex components

A

Superior and medial nuclei- control gaze
Lateral (Deiter’s) nucleus- postural reflexed
Inferior nucleus- integration of vestibular and motor signals

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9
Q

Roles of vestibulocerebellum

A

Adaptation
Compensation for motor deficits
Motor learning
Regulation of balance and eye movements

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10
Q

Vestibular nuclear complex pathways

A

To thalamus and cortex- sensation and perception of head movement
Vestibulospinal pathways- motor commands to muscles of neck, upper torso, lower limbs to maintain balance and posture
Vestibulo-ocular pathways- to CN III, IV, VI for VOR

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11
Q

VOR

A

Maintains steady image on retina for high frequency head movements
VOR gain should be 1

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12
Q

Cervico-ocular reflex

A

Like VOR but slower speeds
Cervical proprioception drives eye movement
Used in presence of vestibular dysfunction

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13
Q

Other sources of dizziness (not central or peripheral vestibular)

A

Diabetes, hypoglycemia, infection, meds, emotional/psychological, hypotension, arrhythmias, multi-factorial fallers

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14
Q

Etiology and epidemiology of BPPV

A

Idiopathic in 50-70%, recurrence rate 27-41%, incidence increases with each decade of life

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15
Q

Clinical presentation of BPPV

A

Brief vertigo with position changes/head movements
<60 seconds for canalithiasis, >60 for cupulo
Latency of seconds
Nystagmus
Symptoms fatigue with repetition
Nystagmus quick beat towards involved side with Dix-Hallpike

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16
Q

Horizontal canal BPPV

A

Geotropic- canal affecting most symptomatic side
Ageotropic- if more than one minute, cupulo affecting least symptomatic; if less than one minute, canal affecting least symptomatic

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17
Q

Treating BPPV

A

Epley maneuver- posterior or anterior canalithiasis
Liberatory (Semont)- anterior or posterior cupulo
BBQ roll- horizontal canalithiasis
Modified Liberatory (Semont)- horizontal cupulo

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18
Q

Vestibular neuritis/labrynthitis presentation

A

Secondary to viral infection, neuritis = CN VIII, labrynth- endolymph fluids
Acute- severe vertigo and nausea lasting days, horizontal gaze-evoked nystagmus, abnormal VOR, impaired DVA
Sub-acute- prolonged disequilibrium without true vertigo, inadequate VOR, postural instability, gait, falls, deconditioning, CN VIII dysfunction

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19
Q

Vestibular neuritis/labyrnthitis treatment

A

Vesibular depressants in acute phase only

Vestibular rehab improves 80% of patients

20
Q

Meniere’s disease presntation

A

Over-accumulation of endolymph in inner ear causes abnormal firing of hair cells
Episodic exacerbations (vertigo) minutes to hours with full recovery, but over time get permanent damage and unilateral hypofunction
Rotary vertigo, low-tone sensorineuronal hearing loss, tinnitus, aural fullness, nausea and vomiting
Chronic- imbalance, dizziness with head turns

21
Q

Meniere’s disease treatment

A

Vestibular sedatives, anti-emetics (diazepam), intra-tympanic gentamycin
Endolymphatic sac surgery or ablative surgery for intractable symptoms
Low salt diet, avoidance of caffeine

22
Q

Vestibular schwannoma/ acoustic neuroma

A

Variable presentation

Dizziness, disequilibrium, unilateral hearing loss, tinnitus, +CN signs (V, VII, VIII)

23
Q

Trauma/skull fracture

A

Temporal bone fractures result in variable symptoms

24
Q

Perilymphatic fistula

A

Tear or deficit in small and/or round windows separating middle and inner ears allowing fluid to leak to air-filled middle ear
Changes in pressure (altitude, increased CSF pressure from lifting, bending, cough/sneeze) stimulate balance and/or hearing strucures
Aural fullness, fluctuating hearing, dizziness w/o true vertigo, motion sensitivity
Treatment- repair if symptoms don’t resolve

25
Q

Superior canal dehiscence

A

Opening in temporal bone overlying superior SCC from developmental abnormality (1-2%)
Vertigo and oscillopsia from loud noises and/or maneuvers that change middle ear of intracranial pressure (coughing/sneezing, straining)
Autophony, hypersensitivity to bone-conducted sounds, apparent conductive hearing loss
Avoid stimuli if possible, surgery for severe cases

26
Q

Bilateral hypofunction diagnoses

A 
Otoxic meds
Idiopathic vestibular loss
Bilateral Meniere's
Trauma
Autoimmune disease (RA, psoriasis)
Meningitis
Neurofibromatosis type 2
27
Q

Ototoxic meds

A

Gentamicin affects hair cells- irreversible damage

28
Q

Symptoms of bilateral hypofunction

A

Oscillopsia during head movement
Instability of gait
Disequilibrium
No vertigo!

29
Q

Central dysfunction signs

A 
Constant symptoms
Nystagmus not suppressed by visual fixation
Pure vertical nystagmus
Impairments in smooth pursuits/saccades
Impaired VOR cancellation
30
Q

Vertiginous migraine

A

Vascular origin, about 25% of those with migraine have vertigo
Can occur with or without headache
Symptoms seconds to days
Treatment- trigger avoidance, migraine preventative meds, vestibular rehab
PT- VOR exercises, COR reflex, depth perception, sensory integration for balance, gait, aerobic exercise

31
Q

Concussion

A

Anxiety, cognitive problems, depression, fatigue, HA, irritability, photo/phono-sensitive, sleep disturbances
Dizziness, imbalance, visual disturbances
23-81% of people have dizziness in first few days
PT- VOR exercises, static standing balance, gait exercises, cervical spine interventions

32
Q

Multiple sclerosis

A

Plaques in brainstem, visual pathways, cerebellum can cause vestibular symptoms
34.7-50.9% of those with MS have brainstem and cerebellum lesions
Peripheral vestibulopathy in up to 85% of those with MS
PT- can improve fatigue, balance, disability by DHI

33
Q

Cervicogenic dizziness

A

Non-specific sensation of altered orientation in space and disequilibrium from abnormal afferent activity from neck
Mis-match of proprioceptive and vestibular input
Symptoms- unsteadiness, imbalance, light-headed, disorientation minutes to hours; neck pain, HA, jaw pain, tinnitus

34
Q

Electronystagmography/ videonystagmography

A

Caloric test- gold standard
Irrigate external canal with cold or warm water/air and watch nystagmus
Cold = away from irrigated ear
Warm = toward irrigated ear

35
Q

Sinusoidal harmonic acceleration test

A

Rotary chair test
VOR measured during rotation of body in dark
Assesses horizontal canal and/or superior vestibular nerve
Identifies central impairment, bilateral vestibular dysfunction, and central compensation

36
Q

Vestibular evoked myogenic potential (VEMP)

A

Tones in ears while evoking responses from specific muscles
Cervical VEMP- saccule and inferior nerve
Ocular VEMP- utricle and superior nerve

37
Q

Oculomotor exam components

A 
Alignment- tropia, phoria, exo-, eso-
ROM
Convergence
Nystagmus (spontaneous, gaze-holding)- unable to suppress with visual fixation in central dysfunction
Smooth pursuit, saccadic movement
Head impulse test
VOR cancellation
DVA (>2 line drop can indicate deficit)
38
Q

Dizziness handicap inventory

A

0-100 (higher number is greater handicap)
0-30 mild
31-60 moderate
61-100 severe handicap

39
Q

Sensory organization test

A

1- fixed support and surround/ EO
2- fixed support and surround/ EC
3- fixed support, responsive surround/ EO
4- responsive support, fixed surround/ EO
5- responsive support, fixed surround/ EC
6- responsive support and surround/ EO

40
Q

Clinical test of sensory interaction and balance

A 
1- firm EO
2- firm EC
3- firm visual conflict
4- foam EO
5- foam EC
6- foam visual conflict
41
Q

Modified CTSIB

A

1- firm EO
2- firm EC
3- foam EO
4- foam EC

42
Q

Motion sensitivity quotient

A 
16 changes of head or body position
0 (no dizziness) to 5 (severe)
Duration- 1 (5-10 sec), 2 (11-30 sec), 3 (>30 sec)
0-10%- mild
11-30%- moderate
31-100%- severe motion sensitivity
43
Q

Adaptation

A

Induce CNS plasticity by creating error signal (retinal slip) to change VOR gain
VORx1, VORx2
For unilateral hypofunction, bilateral if residual function, central if appropriate
Can add visual stimulation, duration/rate up to 2 Hz for 2 minutes

44
Q

Substitution

A

Use alternative strategies- saccadic movements dissociated from head movement
Pts may need AD for somatosensory input
For bilateral hypofunction, central

45
Q

Habituation

A

Desensitization to provocative stimuli via repetitive exposure
Visual vertigo- exposure to optokinetic stimulation can help in cases where over-reliance on visual input creates symptoms in visual/vestibular conflict
For unilateral hypofunction and central vestibular dysfunction

46
Q

Rehab effects for bilateral hypofunction

A

Adaptation, gait, and balance activities
Significantly improves DVA similar to unilateral hypofunction
Age not a factor in recovery
Recovery in approximately 5 weeks of exercise

NCS Prep (19 decks)

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