vestib - hypofunction & treatment Flashcards by Jenn Cantilli

what does evidence say ab vestibular PT and vestib hypofunction

dec sx
improves gaze and postural stability
improve function

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what are 6 possible etiologies for UVH

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

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what is a consideration for neuritis and labyrinthitis as etiologies

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

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how can the aging process lead to UVH

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

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clinical presentation of UVH

vertiginous crisis (AVS)
acute sx lasting 24-72

gradual return of mobility w lingering degree of vertigo, imbalance

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what are characteristics of a vertiginous crisis

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

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

wait to determine if central or peripheral cause

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why do acute sx last 24-72hrs in UVH

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

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what are the 3 most common culprits of UVH

neuritis
labyrinthitis
neuronitis

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what is neuritis and what are sx

inflammation of vestib nerve

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

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what is labyrinthitis and what are sx

inflammation of labyrinth

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

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what is neuronitis and what are sx

infection/damage to sensory neurons of vestibular ganglion

similar sx as neuritis/labyrinthitis
- vertigo

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what is an acoustic neuroma (vestibular schwannoma)

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

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what are sx of acoustic neuromas

issues w balance / unsteadiness mostly

can cause hearing loss / tinnitus

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

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

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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what are the 7 key dx findings in UVH

impaired VOR
GEN
(+) head thrust
head shaking nystagmus
dynamic visual acuity
postural instability
dec caloric response unilaterally per ENG

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how does GEN present in UVH

beating toward intact side
horizontal non-direction changing

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how does the (+) head thrust present in UVH

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

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how does head shaking nystagmus present in UVH

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

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how does dynamic visual acuity present in UVH

> 3 line loss

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how does postural instability present in UVH

> in acute phase

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what is an important consideration w the use of vestibular suppressants

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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what are the 5 main UVH treatments

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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sx of BVH

oscillopsia dizziness (not vertigo) imbalance *particularly in dark/uneven surfaces*

what are the exam findings of BVH

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

what are causes of BVH

ototoxicity meneires dz autoimmune ear dz idiopathic/degen

main interventions for BVH

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

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

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

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

supervised vestib rehab

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

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

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

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

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

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)*

CPG for balance exercises in chronic UVH vs BVH

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

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

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

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

onset of sx comorbidities cog function use of meds

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

adaptation *** substitution habituation

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

hypofunction / peripheral dysfunction -> VOR impacted -> impacts gaze stabilization likely have gaze instability and adaptation exercise should always be included when treating that pop

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

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

what is an important target of adaptation interventions

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

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

need some residual vestibular function

VOR 1 vs VOR 2

VOR1 - target remaining stable and you turn head VOR2 - target and head are moving at same time

how do you progress from VOR1 exercises

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

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

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

what is habituation

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

what pts are habituation exercises apropriate for

UVH (if adaptation not succesful) CNS dysfunction

what is an outcome measure for habituation exercises

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

what is an important part of patient ed w habituation exercises

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

what are parameters for habituation exercises

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

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

eliminate exercise when pt reports 1-2days of sx free performance more tolerable 7-10days

what pt pop are adaptation exercises most appropriate for

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

what are substitution interventions and what do they improve

implements visual and somatosensory input to compensate for vestibular loss improves gaze and postural stability outcome is to improve vision stability w head mvmts

what is the main contributing factor targeted in substitution interventions

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

what pt pop is appropriate for substitution interventions

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

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

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*

what should postural stabilization/balance exercise do

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

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

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

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

w vision removed works to foster use of vestib cues

what is are important considerations ab vestib compensation

in some cases pts remain poorly compensated prolonged recovery w central vestib dysfunction may experience decompensation, or relapse

what are the main pieces of pt ed in UVH

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