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Neuro Rehab 2 > vestib - hypofunction & treatment > Flashcards

vestib - hypofunction & treatment Flashcards

1
Q

what does evidence say ab vestibular PT and vestib hypofunction

A

dec sx
improves gaze and postural stability
improve function

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2
Q

what are 6 possible etiologies for UVH

A

vestibular neuritis
labyrinthitis
acoustic neuroma
lesions of CN 8
temporal bone fx / head trauma
aging process

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3
Q

what is a consideration for neuritis and labyrinthitis as etiologies

A

often secondary to bacterial or viral infection -> leading to infections of nerve and of labyrinth

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4
Q

how can the aging process lead to UVH

A

weakens structures of inner ear
- possible degen changes can occur in only one labyrinth

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5
Q

clinical presentation of UVH

A

vertiginous crisis (AVS)
acute sx lasting 24-72

gradual return of mobility w lingering degree of vertigo, imbalance

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6
Q

what are characteristics of a vertiginous crisis

A

sudden onset of vertigo, n/v, and imbalance that warrants an ER visit

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7
Q

why do we initially label vertiginous crises as acute vestib syndrome (AVS) and not UVH

A

wait to determine if central or peripheral cause

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8
Q

why do acute sx last 24-72hrs in UVH

A

takes time for CNS to compensate for peripheral dysfunction
- compensation can lead to no sx present anymore at all

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9
Q

what are the 3 most common culprits of UVH

A

neuritis
labyrinthitis
neuronitis

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10
Q

what is neuritis and what are sx

A

inflammation of vestib nerve

affects vestibular branch of CN 8 associated w balance -> vertigo
- no change in hearing*

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11
Q

what is labyrinthitis and what are sx

A

inflammation of labyrinth

infection of both branches of CN 8 -> imbalance/vertigo and *hearing loss

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12
Q

what is neuronitis and what are sx

A

infection/damage to sensory neurons of vestibular ganglion

similar sx as neuritis/labyrinthitis
- vertigo

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13
Q

what is an acoustic neuroma (vestibular schwannoma)

A

noncancerous and usually slow-growing tumor that develops on main (vestib) nerve leading from inner ear to your brain

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14
Q

what are sx of acoustic neuromas

A

issues w balance / unsteadiness mostly

can cause hearing loss / tinnitus

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15
Q

what is the usual rate of growth for an acoustic neuroma and why is this problematic

A

slow growing -> might not realize until tumor is really large

dangerous if tumor is really large bc can cause CSF fluid to build up leading to hydrocephalus

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16
Q

what can happen if an acoustic neuroma gets really large and they remove it

A

when really large, CNS has learned to compensate for deficits in peripheral vestib system

resect tumor -> pts have less sx post op than those w smaller tumors
- surgery causes inflammation
- if larger tumor, CNS used to compensating as inflammation post op will now require
—> smaller tumors CNS might not be used to compensating and have to adjust to compensate for inflammation

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17
Q

what are the 7 key dx findings in UVH

A
  1. impaired VOR
  2. GEN
  3. (+) head thrust
  4. head shaking nystagmus
  5. dynamic visual acuity
  6. postural instability
  7. dec caloric response unilaterally per ENG
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18
Q

how does GEN present in UVH

A

beating toward intact side
horizontal non-direction changing

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19
Q

how does the (+) head thrust present in UVH

A

(+) to side of lesion w corrective saccade to unaffected side

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20
Q

how does head shaking nystagmus present in UVH

A

> /= 3 beats
horizontal nystagmus
fast beating to intact side

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21
Q

how does dynamic visual acuity present in UVH

A

> 3 line loss

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22
Q

how does postural instability present in UVH

A

> in acute phase

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23
Q

what is an important consideration w the use of vestibular suppressants

A

if you want to do a diff dx, don’t want them to be on vestib suppressants bc will interfere w our assesssment

if on the meds, want to see after half life

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24
Q

what are the 5 main UVH treatments

A

vestib suppressants (ie Meclizine)
adaptation exercises
balance training
test/ed pts on triggers
treat underlying cause
- ie steroids, antivirals, surgical resection

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25
Q

sx of BVH

A

oscillopsia
dizziness (not vertigo)
imbalance

particularly in dark/uneven surfaces

26
Q

what are the exam findings of BVH

A

significantly impaired VOR
(+) head thrust (B)**
free fall* w Romberger on foam
LOB amb w head turns
ataxia

27
Q

what are causes of BVH

A

ototoxicity
meneires dz
autoimmune ear dz
idiopathic/degen

28
Q

main interventions for BVH

A

adaptation if residual vestib function
substitution strategies if no vestib functions remain

29
Q

per strong research, what should clinicians NOT do in their intervention for vestib hypofunction and why

A

voluntary saccadic or smooth-pursuit eye mvmts in isolation (ie w/o head mvmt) to promote gaze stability

if have hypofunction, will have problems w VOR and gaze stability w head mvmts
- if going to do anything w head mvmts also include eye mvmts

30
Q

per strong research, what SHOULD clinicians include in interventions for vestib hypofunction

A

supervised vestib rehab

31
Q

what interventions is there only mod to strong evidence on in CPGs for vestib hypofunction

A

specific exercise techniques to target identified activity limitations and participation restrictions
- including VR, augmented sensory feedback

32
Q

what is the significance of including gaze stabilization interventions w a pt w a hypofunction

A

almost all pts w hypofunction have a VOR impairment and thus gaze instability

33
Q

what are CPGs’ minimum parameters for gaze stabilization interventions in: acute/subacute UVH, chronic UVH, and BVH

A

acute/subacute UVH
- 3x/day for total of 12min daily

chronic UVH
- 3-5x/day for total of 20min daily for 4-6wks

BVH
- 3-5x/day for total of 20-40min daily for 5-7wks

the more chronic the hypofunction, the inc the frequency needed to tap into neuroplasticity -> same applies for (B)

34
Q

CPG for balance exercises in chronic UVH vs BVH

A

static and dynamic balance for min of 20min daily
- 4-6wks for UVH
- 6-9wks for BVH

35
Q

what is the CPGs’ reasons for stopping therapy in vestib hypofunction

A

achieve primary goals
resolution of sx
normalized balance and vestib fxn
plateau in progress

36
Q

what factors do the CPGs identify that modify rehab outcomes in vestib hypofunction

A

onset of sx
comorbidities
cog function
use of meds

37
Q

what are the 3 key categories of interventions for vestib hypofunction and which is arguably the most important to include

A

adaptation ***
substitution
habituation

38
Q

why are adaptation exercises arguably the most important to include when treating vestib hypofunction

A

hypofunction / peripheral dysfunction -> VOR impacted -> impacts gaze stabilization

likely have gaze instability and adaptation exercise should always be included when treating that pop

39
Q

how could central path or vestib hypofunction both lead to gaze instability

A

VOR starts peripheral and travels to CNS and then talks to ms on how to move ms

40
Q

what is an important target of adaptation interventions

A

to improve VOR gain by inducing retinal slip
- aka need to get ratio back to 1:1

41
Q

what function is needed for adaptation exercises working on gaze stability to be effective

A

need some residual vestibular function

42
Q

VOR 1 vs VOR 2

A

VOR1
- target remaining stable and you turn head

VOR2
- target and head are moving at same time

43
Q

how do you progress from VOR1 exercises

A

progress to VOR2 when can tolerate VOR1 exercises for at least 2min

44
Q

how can you alter VOR1 and 2 exercises for progressions and regressions

A

background: static -> busy
time -> inc duration
speed -> slow to fast
position: sit to stand, stances, support surfaces

45
Q

what is habituation

A

repeated exposure to provocative stim to reduce pathological response to stim thru inc the threshold of someone having sx

46
Q

what pts are habituation exercises apropriate for

A

UVH (if adaptation not succesful)
CNS dysfunction

47
Q

what is an outcome measure for habituation exercises

A

MSQ test
- able to ask what position changes induce sx and which ones make sx more intense
- use this to induce provocative motions that pt use in everyday life in habituation interventions

48
Q

what is an important part of patient ed w habituation exercises

A

tell them this is going to suck!!
- but that over time will feel better and dec sx

49
Q

what are parameters for habituation exercises

A

up to 4 provocative mvmts
- 2-3 sets
- 2-4x/day

50
Q

when do you stop habituation exercises and when is the typical timeline for that

A

eliminate exercise when pt reports 1-2days of sx free performance

more tolerable 7-10days

51
Q

what pt pop are adaptation exercises most appropriate for

A

always UVH
always if have VOR impairment
sometimes CNS bc VOR travels thru brain

52
Q

what are substitution interventions and what do they improve

A

implements visual and somatosensory input to compensate for vestibular loss

improves gaze and postural stability
outcome is to improve vision stability w head mvmts

53
Q

what is the main contributing factor targeted in substitution interventions

A

CNS compensates via COR
- driven by neck proprioception thru neck mvmts can impact eye mvmts
—> gives more info on how fast and direction of eye mvmt
—> insurance policy for VOR

54
Q

what pt pop is appropriate for substitution interventions

A

complete or severe (B) loss of vestib function or possibly CNS path

55
Q

what are 3 main substitution treatment strategies and what are these targeting

A
  1. imaginary target
    - imagine target to focus on
  2. active eye-head mvmt
    - move target, then move eys
  3. use of non compliant surfaces and series of foot placements to strengthen somatosensory

targeting visual or somatosensory systems

56
Q

what should postural stabilization/balance exercise do

A

should synthesize use of visual and somatosensory cues w use of vestib cues to improve postural stability

57
Q

when should you use non-compliant surfaces in postural stabilization /balance interventions

A

w vision removed and series of foot placements to strengthen somatosensory and vestibular

58
Q

when should you use compliant surfaces in postural stabilization /balance interventions

A

w vision removed works to foster use of vestib cues

59
Q

what is are important considerations ab vestib compensation

A

in some cases pts remain poorly compensated

prolonged recovery w central vestib dysfunction

may experience decompensation, or relapse

60
Q

what are the main pieces of pt ed in UVH

A

want them to be safe and environmental safety
- how can they be safe in community outside of HEP
- tell them what will be challenging and take more time

additional strategies such as using visual fixation on target

Neuro Rehab 2 (48 decks)

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