Week 2 Highlights Flashcards
what is the pathophys of meniere’s dz
inc hydraulic pressure w/i inner ear endolymphatic system
what are 7 sx experienced during a Meniere’s attack
fullness of ear
reduction in hearing
tinnitus
vertigo
postural imbalance
nystagmus
followed by n/v
what is the duration of meniere’s attack
> 20min to <24hrs
what is the symptomology s/p a meniere’s attack
gradual abatement of sx
s/p severe attack - exhaustion, sleep for hours
generally ambulatory w/i 72hrs
may have some postural unsteadiness for days-weeks then will return to normal
how can hearing be impacted after a meniere’s attack and long term
hearing can return to baseline or may have residual permanent sensorineural hearing loss (SNHL) w/ lower frequencies
long term decline inhearing is expected
what is our main focus when treating someone w meniere’s
education
what role does vestibular play in treating meniere’s dz
not the primary treatment
when could vestib rehab be useful in treating meniere’s (3)
s/p vestib ablation procedure
hypofunction present
impaired postural control
what is vestibular “prehab”, when is it implemented in meniere’s and why
vestibular rehab 2wks prior to planned vestibular ablation (ITG)
induce compensation pre-op
enhance post op recovery
what are 3 other disorders associated w vestib migraines
motion sensitivity
meniere’s
idiopathic BPPV
per IHS criteria, what is a migraine w/o aura
lasts 4-72hrs if not treated
must have 2:
* U/L location
* pulsatile quality
* * mod to severe intensity*
* * aggravated by exertion/stair negotiation*
must have 1:
* n/v
* photophobia
* phonophobia
what is the HINTS exam
stroke suspected if any of the following exist:
* normal head thrust
* direction changing nystagmus in eccentric gaze
* skew deviation (vertical ocular misalignment)
what are the vestibular connections to oculomotor nuclei
3 neuron arc from SCC:
* vestibular nuclei
* ascending tracts (b/l via MLF)
* oculomotor nuclei in brainstem (CN III, IV, IV)
what function do several vestibular connections have and where are the majority located
autonomic functions
in midbrain, pons, and medulla
what oculomotor deficit is commonly seen in advanced PD
slow hypometric saccades
what are some examples of vestibular interventions appropriate for a pt w advanced PD
work on saccades
occular function
incorporate visual exercises into training (ie during balance training)
what is the relationship b/w slow saccades and fall risk in PD
turning performance is impaired in PD and may be influenced by saccade dysfunction
* association b/w saccade function and turning performance may be indicative of the key role saccades plays in initiating proper turning kinematics
what is the pathophys of cerebellopontine angle lesions
compression of brainstem and CNVIII
what is are the 2 most prevalent etiologies of cerebellopontine angle lesions
acoustic neuroma
meningioma
how are cerebellopontine angle lesions dx (5)
hearing loss
ringing in ear
sometimes: dizziness, fullness, imbalance
what imaging would show cerebellopontine angle lesions
MRI w contrast
what is subjective visual vertical
ability to detect subjective tilt
subjective visual vertical
impairments can be secondary to:
injury to otoliths or nerve connections
what are 2 impairments that result from subjective visual vertical
causes sensory conflict
can’t be used to assess utricular function U/L
normal vs abnormal subjective visual vertical
normal: adjust illuminated rod to vertical w mean error of <2.5deg
abnormal: >2.5 deg error noted in pts w central and peripheral path
what are 5 disorders that present with pathological subjective visual vertical
- acute peripheral neuritis
- wallenberg syndrome
- internuclear opthalmoplegia
- midbrain lesion
- vestib neuronitis
how is abnormal subjective visual vertical defined in children
> 2.13deg of deviation is significant (compared to >2deg using conventional testing)
what is internuclear opthalmoplegia and what are the 2 sx it is characterized by
specific gaze abnormality
- impaired horizontal eye mvmts w weak ADD in affected eye
- ABD nystagmus of contra eye
what is the pathophys of internuclear opthalmoplegia
localizing brainstem syndrome resulting from lesion in the MLF in dorsomedial brainstem tegmentum of either pons or midbrain
what is the most common etiology for B/L internuclear opthalmoplegia in a young adult
MS
what is the most common etiology for U/L internuclear opthalmoplegia in middle aged and elderly adults
brainstem infarction
what is PPPD
persistent sensations of rocking/swayign and/or non-vertigo type dizziness on most days for >3 months
what 3 primary complaints in PPPD
hypersensitivity to visual flow (ie grocery stores, windshield wipers, busy flooring, computer images/scrolling)
head fullness
perception of veering
what is the frequency of sx in PPPD
min of 15days for every 30
majority daily sx
doesn’t need to be continuous
what are aggravating factors for PPPD (3)
- upright posture
- busy environments (complexity and/or motion)
- head or body mvmt (active or passive body motion w/o reguard to direction or position)
what are 2 nullifiers for PPPD
- avoidance of provoking environments/triggers
- lying down
how consistent is the severity of PPPD
fluctuates
what are 4 precipitating factors for PPPD
- medical, psychosocial, or environmental event causing acute vestib sx or imbalance
- coexisting vestib disorders
- h/o vertigo
- pre-existing anxiety disorder
what are psych or behavioral predisposing or coinciding factors for PPPD
- anxiety & depression
- other psychiatric disorders
- pre-existing anxiety
- heightened anxiety w vestib problem
- anxiety, cautiousness, neg expectation for recovery have greater chance of developing
how is PPPD dx
based on sx presentation:
* tempo
* aggravators
* triggering events
no specific test
tests tend to be normal, may be (+) for other conditions
no present neuro-otologic dysfunction
no ongoing med etiology
not a psychiatric condition
what improves the prognosis for PPPD
when migraine medically managed and psych care to address anxiety
psych probs and pt w dizziness
what is the challenge with getting a definitive dx
dizziness can lead to neg psych impact
psych disorders can result in profound dizziness
how does the incidence of psych disorders as primary cause of dizziness change
declines w inc age
what are general associations seen b/w psych problems and pt w dizziness
- psych probs often coexist w balance disorders
- common for anxiety to accompany vestib disorder
- depression more common in those w migraines/HAs than those w/o
- high prevalence of mood disorders and psych probs in pts w dizziness
what are general management strategies for psych problems and pts w dizziness
- recognize presence of disorder
- discuss w pt the disorder when appropriate and depending on dx
- provide reassurance
- relate emotions/stress can cause same sx as vestib disorder
- destigmatize by telling prevalence of disorder
- refer pt for med mgmt, CBT, etc.
- individualize HEP
- assure continued PT involvement
- wean inappropriate ADs
psych probs and pt w dizziness
at what point to you discuss the presence of one of the following disorders in the pt’s POC:
* anxiety
* depression
* CSD
* PPPD
* somatoform
* factitious
anxiet/depression/CSD/PPPD = early
somatoform - avoid in 1st visit
factitious - defer unless deemed clinically appropriate
* they don’t want to get better
what is MdDS
central vestib (neuro) disorder
*not a peripheral vestib (inner ear) disorder/dz
what are non-motion triggered MdDS (aka “rockers” or “spontaneous MdDS”)
individuals w similar sx w/o preceding motiono exposure
what is a challenge w treating non-motion triggered MdDS
possibly more difficult to treat w habituation but still able to cure >50%
what is the pathogenesis of MdDS
pathogenesis and lesion site unknown
no particular injury
most agree it is a variant of motion sickness
what are possible etiologies of MdDS
- otolith dysfunction
- d/t or exacerbated by anxiety/somatoform disorder
- variant of migraine
- processing error - inappropriate high weighting of somatosensory input for balance
what is a PT strategy for treating MdDS
work on pushing somatosensory reference back b/w vestib mechanism and somatosensory system
what is the Dai Protocol for in MdDS
established to address theory of Maladaption of VOR
