vestib - hypofunction & treatment Flashcards
what does evidence say ab vestibular PT and vestib hypofunction
dec sx
improves gaze and postural stability
improve function
what are 6 possible etiologies for UVH
vestibular neuritis
labyrinthitis
acoustic neuroma
lesions of CN 8
temporal bone fx / head trauma
aging process
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
how can the aging process lead to UVH
weakens structures of inner ear
- possible degen changes can occur in only one labyrinth
clinical presentation of UVH
vertiginous crisis (AVS)
acute sx lasting 24-72
gradual return of mobility w lingering degree of vertigo, imbalance
what are characteristics of a vertiginous crisis
sudden onset of vertigo, n/v, and imbalance that warrants an ER visit
why do we initially label vertiginous crises as acute vestib syndrome (AVS) and not UVH
wait to determine if central or peripheral cause
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
what are the 3 most common culprits of UVH
neuritis
labyrinthitis
neuronitis
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*
what is labyrinthitis and what are sx
inflammation of labyrinth
infection of both branches of CN 8 -> imbalance/vertigo and *hearing loss
what is neuronitis and what are sx
infection/damage to sensory neurons of vestibular ganglion
similar sx as neuritis/labyrinthitis
- vertigo
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
what are sx of acoustic neuromas
issues w balance / unsteadiness mostly
can cause hearing loss / tinnitus
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
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
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
how does GEN present in UVH
beating toward intact side
horizontal non-direction changing
how does the (+) head thrust present in UVH
(+) to side of lesion w corrective saccade to unaffected side
how does head shaking nystagmus present in UVH
> /= 3 beats
horizontal nystagmus
fast beating to intact side
how does dynamic visual acuity present in UVH
> 3 line loss
how does postural instability present in UVH
> in acute phase
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
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
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
- imaginary target
- imagine target to focus on - active eye-head mvmt
- move target, then move eys - 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
