BPPV Flashcards
what is the normal function of the SCCs and ampulla
fluid filled canals detecting rotation of the head
* rotation causes deflection of sensory hairs in crista ampullaris
* hair cells embedded w/i gelatinous membrane (cupula)
what can happen to otoconia when they degenerate w age
get more brittle, have more fissures
* more likely to break off matrix
how do the hair cells in the SCC work with the CN VIII’s excitation/inhbition
deflection away from kinocilium = inhibits
towards kinocilium = excites
why is the situation of the SCC planes significant
key for positional testing
what is the pathophys behind BPPV
mechanical disorder of inner ear caused by abnormal stim of 1 or more of 3 SCC w/i the ear
* otoconia break free from macula of utricle
* misplaced otoconia fall into SCC, change canal response to gravity
what is the most common etiology of BPPV
idiopathic (58%)
can have correlations to other disorders
18.2% post-traumatic
8.5% viral neurolabyrinthitis
what questionnaire do you use w someone you suspect of BPPB
Dizziness Handicap Inventory (DHI)
what is significant prior medical hx to screen for in BPPV
vestib co-morbidities
* migraines
* inner ear
what are 4 types of special dx tests
neurologic tests
general med tests
x-rays
otologic tests
what are 6 vestibular co-morbidities for BPPV
- otological hx
- diabetes
- osteopenia/porosis, Vit D deficiency
- concussion
- migraine
- thryoid
why we not utilize Brandt-Daroff or self-CRP exercises
there aren’t any exercises we can do to prevent recurrence
Brandt-Daroff can also result in multi-canal involvement
may use brandt-daroff for habituation purposes
what is the clinical implication for the growing support for a correlation b/w DM2 and BPPV
screen for BPPV in those w DM2 and dizziness
additional research is needed to determine if this data is clearly meaningful
what is the thought behind why someone w DM2 and BPPV might also have HTN
HTN –> dec blood flow to labyrinth –> otolith dislodgement
if a woman is having recurrent BPPV what might be a nutritional recommendation and why
Vit D and calcium supplements
lower bone mineral density and low serum Vit D may be a risk factor for BPPV
most notable in post-menopausal women
why is there thought to be a seasonality to BPPV
BPPV cases highest in months when serum Vit D levels lowest
* incidence is higher in autumn and winter over spring and summer
a migraine comorbity is most common in what BPPV etiology
idiopathic BPPV
3-4x more common in idiopathic BPPV than post traumatic
what autoimmune condition is most commonly associated w BPPV
thyroid dysfunction / hashimoto’s thyroiditis
what is the hypothesis for why autoimmune conditions may be correlated w BPPV
diffusion of immune-complexes in inner ear could change composition of endolympathic fluid exerting a mechanical stim of receptors and provoking typical vertigo
what are functional mvmts that if triggering may indicate BPPV vertical canal involvement
- looks up (PC)
- gets out of bed
- moves head quickly
- rolls over in bed
- bends over
- bends forward to read (AC)
what are functional mvmts that if triggering may indicate BPPV horizontal canal involvement
- turning head in horizontal plane
- bending forward in pitch plane
what is key to accurately dx BPPV
targeted hx
thorough clinical exam
why would you test for BPPV in an elderly pt w poor balance w/o classic BPPV subjective reports
elderly often don’t complain of true vertigo - “feel off”
* they also might move slow, so when they roll, they aren’t generating a robust response w positional changes to have a classic BPPV subjective report
what is cupulolithiasis
otoconia adhere to cupula itself inc the density of the particle –> producing inappropriate deflection of cupula in head when in provoking position
long duration
* otoconia adhere or hang down
what is canalithiasis
otoconia from utricle float into long arm of SCC
* when in provoking position, otoconia pulled by gravity to most dependent part of canal –> mvmt of otoconia overcomes the inertia of endolymph –> causes deflection of cupula
short duration sx, little latency
* otoconia move and create ripples, then settles
is it possible for someone to have canalithiasis and no nystagmus?
if otoconia in constant contact w wall while it sediments -> produces no nystagmus
what is the main way to differentiate between canalithiasis and cupulolithiasis
duration
why is there a latency w canalithiasis
takes 25sec for otoconium to traverse 1/4 of canal
don’t focus on this characteristic to differentiate from cupulo, focus on the shorter duration
how can vertigo and nystagmus change in cupulolithiasis? why?
vertigo and nystagmus may attentuate slightly d/t adaptation by the hair cell afferent complexes
what direction does nystagmus beat to in BPPV and why
nystagmus to involved side
going to side of activation bc crystals moving and then activating (in different way bc of path of displaced otoconia)
what is responsible for dictating the direction of the nystagmus associated w SCC
nerve correlation to eye muscles is why you get a specific direction w AC vs LC vs PC nystagmus
what direction does nystagmus beat to in hypofunction and why
to not involved side
beating to the side that is working and activating
what is reversal of nystagmus? why does this happen?
if starts as up beat in provocative position, when you sit them back up the nystagmus reverses and down beats
think of ice moving as you pour water -> ice moves to displace water –> when you right it it and it reverses
don’t always see this, but nice to see it bc confirms dx so always watch them sit up
what is the gold standard test for the dx of PC-BPPV
dix hallpike
why is it significant to perform BPPV tests w fixation removed
prevents visual suppression of nystagmus
how does nystagmus for PC-BPPV present
extorsional (toward dependent ear) and upward directed
what are the 3 dx criteria for PC-BPPV
- (+) dix
- fixation removed
- extorsional and upbeating nystagmus
why is loaded dix thought to have higher efficacy than standard dix
starting in flexed position so you are providing a maximal range of motion for debris to go thru which results in:
* higher sx report
* longer nystagmus duration
* longer latency of nystagmus
what are the 2 dx criteria for AC-BPPV
- vertigo associated w ocular nystagmus
- nystagmus beating downward & maybe torsional (toward ear involved)
BPPV-AC and Dix Hallpike
can get false (+) in the DHT
- if negative, do head hanging (more specific to AC)
how does nystagmus present in BPPV-AC
down beating and intorsional toward dependent ear
what is the key component to provocational testing of AC
as much extension as possible
what is Ewald’s second law
response to excitatory stim is more intense than to inhibitory stim
seen in LC
what is the dx criteria for LC-BPPV
- ocular nystagmus
- nystagmus associated w vertigo
- direction of DCPN (direction changing positional nystagmus ?) dependent on location of debris w/i LC
how does LC-BPPV nystagmus present
- geotropic or apogeotropic
- horizontal
- bidirectional changing
- positional
geotropic vs apogeotropic DCPN
location of debris
geotropic:
* debris in long arm
apogeotropic: (possibilities)
* debris w/i ampullary segment or attached to cupula
* debris located on side of cupula adjacent to utricular vestibule or to long arm
* debris located w/i short arm
geotropic nystagmus in BPPV vs migraine equivalent
if nystagmus geotropic and prolonged = likely migraine equivalent event
- will not be prolonged in BPPV, should be <60sec
what can be noted for in the neutral position of bow and lean test
pseudospontaneous nystagmus
what is pseudo-spontaneous nystagmus (PSN)
in neutral, lat SCC at 30deg angle in relation to horizontal plane –> otoliths can slowly move
how will PSN present
geotropic beats away from affected ear (cupula deflection is inhibitory)
apogeotropic beats toward involved ear
what is the only time when you would use brandt-daroffs to treat vertigo
sitting up vertigo
* upbeating and ipsi torsion upon retrun to sit from dix
found that CRP wasn’t effective, but was resolved w Brandt Daroffs
what should you do for pts w c/o subjective BPPV but no nystagmus?
showed benefits/improvement w BPPV treatments (based on what they were symptomatic from)
what is the first choice for HSCC canalithiasis treatment
Gufoni
what are the 2 go to treatments for HSCC BPPV canalithiasis
gufoni (less position changes)
BBQ
what does the CPG say ab post-procedural restrictions in PSCC BPPV
no precautions
although the CPG has no post-procedural restrictions, what are things you might tell your patient and when is this appropriate
if they feel off - take it easy the rest of day, avoid excessive head motion FOR THAT DAY ONLY
if sx have been stubborn, maybe try to not sleep on that side ONLY FOR ONE NIGHT
* could sleep semi-recumbent on a few pillows for 1-2nights
she likes to have them rest after the maneuver to let things settle to make sure they are safe to walk out and drive
what is the most common type of canal conversion to see
posterior to horizontal
the stat on her slide says most common for AC to PC
what can cause a canal jam
if people trying all different maneuvers for wrong canal on wrong side, otoconia can get jammed up as they move from wider to more narrow segment
if you suspect there are multiple canals involved, how do you proceed w treatment?
treat canal associated w most predominant and exaggerated presentation of nystagmus
how will a canal jam present
sx: extreme vertigo
persistent nystagmus irrespective of head position
tho self CRP’s are rarely given to pts, when would you give it to a pt
- pt is competent in performing it
- cognitively intact
- recurrent BPPV in same canal
- going out of state
preference is for all maneuvers to be in clinic so can be reassessed
