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adv neuro: vestibular > BPPV > Flashcards

BPPV Flashcards

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Preparativo Vestibular e ENEM flashcards
1
Q

what is the normal function of the SCCs and ampulla

A

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)

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2
Q

what can happen to otoconia when they degenerate w age

A

get more brittle, have more fissures
* more likely to break off matrix

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3
Q

how do the hair cells in the SCC work with the CN VIII’s excitation/inhbition

A

deflection away from kinocilium = inhibits

towards kinocilium = excites

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4
Q

why is the situation of the SCC planes significant

A

key for positional testing

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5
Q

what is the pathophys behind BPPV

A

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

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6
Q

what is the most common etiology of BPPV

A

idiopathic (58%)

can have correlations to other disorders
18.2% post-traumatic
8.5% viral neurolabyrinthitis

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7
Q

what questionnaire do you use w someone you suspect of BPPB

A

Dizziness Handicap Inventory (DHI)

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8
Q

what is significant prior medical hx to screen for in BPPV

A

vestib co-morbidities
* migraines
* inner ear

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9
Q

what are 4 types of special dx tests

A

neurologic tests
general med tests
x-rays
otologic tests

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10
Q

what are 6 vestibular co-morbidities for BPPV

A
  • otological hx
  • diabetes
  • osteopenia/porosis, Vit D deficiency
  • concussion
  • migraine
  • thryoid
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11
Q

why we not utilize Brandt-Daroff or self-CRP exercises

A

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

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12
Q

what is the clinical implication for the growing support for a correlation b/w DM2 and BPPV

A

screen for BPPV in those w DM2 and dizziness

additional research is needed to determine if this data is clearly meaningful

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13
Q

what is the thought behind why someone w DM2 and BPPV might also have HTN

A

HTN –> dec blood flow to labyrinth –> otolith dislodgement

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14
Q

if a woman is having recurrent BPPV what might be a nutritional recommendation and why

A

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

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15
Q

why is there thought to be a seasonality to BPPV

A

BPPV cases highest in months when serum Vit D levels lowest
* incidence is higher in autumn and winter over spring and summer

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16
Q

a migraine comorbity is most common in what BPPV etiology

A

idiopathic BPPV

3-4x more common in idiopathic BPPV than post traumatic

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17
Q

what autoimmune condition is most commonly associated w BPPV

A

thyroid dysfunction / hashimoto’s thyroiditis

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18
Q

what is the hypothesis for why autoimmune conditions may be correlated w BPPV

A

diffusion of immune-complexes in inner ear could change composition of endolympathic fluid exerting a mechanical stim of receptors and provoking typical vertigo

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19
Q

what are functional mvmts that if triggering may indicate BPPV vertical canal involvement

A
  • looks up (PC)
  • gets out of bed
  • moves head quickly
  • rolls over in bed
  • bends over
  • bends forward to read (AC)
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20
Q

what are functional mvmts that if triggering may indicate BPPV horizontal canal involvement

A
  • turning head in horizontal plane
  • bending forward in pitch plane
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21
Q

what is key to accurately dx BPPV

A

targeted hx
thorough clinical exam

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22
Q

why would you test for BPPV in an elderly pt w poor balance w/o classic BPPV subjective reports

A

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

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23
Q

what is cupulolithiasis

A

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

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24
Q

what is canalithiasis

A

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

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25
Q

is it possible for someone to have canalithiasis and no nystagmus?

A

if otoconia in constant contact w wall while it sediments -> produces no nystagmus

26
Q

what is the main way to differentiate between canalithiasis and cupulolithiasis

A

duration

27
Q

why is there a latency w canalithiasis

A

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

28
Q

how can vertigo and nystagmus change in cupulolithiasis? why?

A

vertigo and nystagmus may attentuate slightly d/t adaptation by the hair cell afferent complexes

29
Q

what direction does nystagmus beat to in BPPV and why

A

nystagmus to involved side

going to side of activation bc crystals moving and then activating (in different way bc of path of displaced otoconia)

30
Q

what is responsible for dictating the direction of the nystagmus associated w SCC

A

nerve correlation to eye muscles is why you get a specific direction w AC vs LC vs PC nystagmus

31
Q

what direction does nystagmus beat to in hypofunction and why

A

to not involved side

beating to the side that is working and activating

32
Q

what is reversal of nystagmus? why does this happen?

A

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

33
Q

what is the gold standard test for the dx of PC-BPPV

A

dix hallpike

34
Q

why is it significant to perform BPPV tests w fixation removed

A

prevents visual suppression of nystagmus

35
Q

how does nystagmus for PC-BPPV present

A

extorsional (toward dependent ear) and upward directed

36
Q

what are the 3 dx criteria for PC-BPPV

A
  1. (+) dix
  2. fixation removed
  3. extorsional and upbeating nystagmus
37
Q

why is loaded dix thought to have higher efficacy than standard dix

A

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

38
Q

what are the 2 dx criteria for AC-BPPV

A
  1. vertigo associated w ocular nystagmus
  2. nystagmus beating downward & maybe torsional (toward ear involved)
39
Q

BPPV-AC and Dix Hallpike

A

can get false (+) in the DHT
- if negative, do head hanging (more specific to AC)

40
Q

how does nystagmus present in BPPV-AC

A

down beating and intorsional toward dependent ear

41
Q

what is the key component to provocational testing of AC

A

as much extension as possible

42
Q

what is Ewald’s second law

A

response to excitatory stim is more intense than to inhibitory stim

seen in LC

43
Q

what is the dx criteria for LC-BPPV

A
  1. ocular nystagmus
  2. nystagmus associated w vertigo
  3. direction of DCPN (direction changing positional nystagmus ?) dependent on location of debris w/i LC
44
Q

how does LC-BPPV nystagmus present

A
  • geotropic or apogeotropic
  • horizontal
  • bidirectional changing
  • positional
45
Q

geotropic vs apogeotropic DCPN

location of debris

A

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

46
Q

geotropic nystagmus in BPPV vs migraine equivalent

A

if nystagmus geotropic and prolonged = likely migraine equivalent event
- will not be prolonged in BPPV, should be <60sec

47
Q

what can be noted for in the neutral position of bow and lean test

A

pseudospontaneous nystagmus

48
Q

what is pseudo-spontaneous nystagmus (PSN)

A

in neutral, lat SCC at 30deg angle in relation to horizontal plane –> otoliths can slowly move

49
Q

how will PSN present

A

geotropic beats away from affected ear (cupula deflection is inhibitory)

apogeotropic beats toward involved ear

50
Q

what is the only time when you would use brandt-daroffs to treat vertigo

A

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

51
Q

what should you do for pts w c/o subjective BPPV but no nystagmus?

A

showed benefits/improvement w BPPV treatments (based on what they were symptomatic from)

52
Q

what is the first choice for HSCC canalithiasis treatment

A

Gufoni

53
Q

what are the 2 go to treatments for HSCC BPPV canalithiasis

A

gufoni (less position changes)
BBQ

54
Q

what does the CPG say ab post-procedural restrictions in PSCC BPPV

A

no precautions

55
Q

although the CPG has no post-procedural restrictions, what are things you might tell your patient and when is this appropriate

A

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

56
Q

what is the most common type of canal conversion to see

A

posterior to horizontal

the stat on her slide says most common for AC to PC

57
Q

what can cause a canal jam

A

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

58
Q

if you suspect there are multiple canals involved, how do you proceed w treatment?

A

treat canal associated w most predominant and exaggerated presentation of nystagmus

59
Q

how will a canal jam present

A

sx: extreme vertigo

persistent nystagmus irrespective of head position

60
Q

tho self CRP’s are rarely given to pts, when would you give it to a pt

A
  • 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

adv neuro: vestibular (6 decks)

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