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Year 2: Neuromuscular II > Test 2: Intro to Vestibular Rehab > Flashcards

Test 2: Intro to Vestibular Rehab Flashcards

1
Q

purpose of the vestibular system

A

estimate body position and motion

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2
Q

incidence of vestibular dysfunction

A

15 million people in US

increases with age

can happen in kids (5.3% population) - only 29% treated

can occur secondary to other conditions; those with DM are 70% more likely; HTN also positively correlated

can be a result of trauma; 40-60% of those with head trauma who were not hospitalized had vestibular dysfunction

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3
Q

describe the general anatomy of the vestibular system

A

intricate network of accelerometers

peripheral and central components

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4
Q

labyrinth sits inside what bone

A

temporal

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5
Q

what are the bony portions of the 3 semicircular canals

A

cochlea
vestibule

filled with perilymphatic fluid

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6
Q

what makes up the membranous portions of the 3 semicircular canals

A

utricle
saccule

filled with endolymphatic fluid

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7
Q

the utricle and saccule detect what type of motion

A

utricle = horizontal linear acceleration

saccule = vertical linear

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8
Q

3 types semicircualr canals

A

anterior
posterior
horizontal

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9
Q

otolithic organs

A

utricle
saccue

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10
Q

what is an ampula

A

enlarged end of the semicircular canals

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11
Q

anatomy of semicircular canal

A

attached to utricle

filled with endolymphatic fluid; moves opposite of head motion

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12
Q

ampula anatomy

A

on utricular end of SCC

contains cupula

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13
Q

describe the hair cells and how direction is related to excitation/inhibition

A

tall ones all on one side; move toward tall ones = excitation

move toward little/away from tall ones = inhibition

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14
Q

cupula anatomy

A

gelatinous barrier that contains sensory hair cells

hair cells sit in crista ampullaris

cupula will detect when endolymph moves

cupula moves opposite of ampula?

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15
Q

what are stereocillia

A

supporting hair cells

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16
Q

what are kinocilia

A

main hair cells

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17
Q

what is caused when the stereocilia move toward the kiinocilia

A

exictation

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18
Q

what is caused when the stereocilia move away from the kinocilia

A

inhibition

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19
Q

what are otoconia

A

“crystals”

provide inertial mass for hte gelatinous matrix

made of calcium carbonate

can be impacted by nutrition

can get more brittle with age

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20
Q

otolithic organs contain what

A

otoconia
gelatinous matrix
hair cells
macula

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21
Q

examples of when utricle and saccule may be indicated

A

utricle = active with walking

saccule = active when riding elevator

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22
Q

describe CN VIII

A

cochlear portion goes to cochlea

vestibular portion splits to superior and inferior
- superior goes to utricle, AC, HC
- inferior goes to saccule and PC

CN VIII goes from inner ear to vestibular nuclei in medulla and pons

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23
Q

describe VOR (vestibulo-ocular reflex)

A

gaze stabilization

eye movements equal and opposite to head

head moves > CN VIII to vestibular nuclei > oculomotor nuclei > ocular mm

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24
Q

describe VSR (vestibulo-spinal reflex)

A

large role in postural stability

adjusting limb motion appropriately for the position of the head

output is to the skeletal mm

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25
describe VCR (vestibulo-colic reflex)
use of neck musculature to stabilize the head in space output is to the cervical mm chickens!
26
where does the central vestibular system start
when CN VIII communicates with the vestibular nuclei in brainstem
27
describe the 4 vestibular nuclei
superior = controls VOR descending = connects to cerebellum and other nuclei medial = controls VOR and VSR lateral = controls VSR located in pons and medulla messages go to cerebellum, other VNs, and oculomotor nuclei
28
portions of the cerebellum and their role in the vestibular system
flocculus = required to adapt VOR gain nodulus = required for VOR duration anterior = superior vermis affects VSR
29
PICA feeds what
medulla and cerebellum
30
AICA feeds what
cerebellum
31
damage to AICA and PICA can be concerning for vestibular why
vestibular system may be intact but if there is a problem in the medulla/cerebellum it can affect processing of vestibular info
32
ocular nuclei purpose
take inpits from vestibular nuclei send outputs to the ocular mm via cranial nn II, IV, and VI located in midbrain
33
ocular mm determine what
nystagmus direction and output
34
eye mm that are single plane movements (larger mm) and their corresponding nerves
medial rectus - CN III lateral rectus - CN VI superior rectus - CN III inferior rectus - CN III
35
eye mm that are multiplane movements (smaller mm) and their corresponding nn
superior oblique (CN IV) inferior oblique (CN III) obliques are why torsional nystagmus is possible (up and to the side beat = sup oblique)
36
treatment differs for vestibular dysfunction depending on what
electrical = nn dysfunction (blood supply, compression, damage, etc) mechanical = putting something back (i.e. crystals) central vs peripheral vs both
37
what diagnostic findings can help you understand the type of vestibular dysfunction involved
eye movements postural movements sensory organization
38
nystagmus that indicates CNS
pure vertical and directional changing persistent
39
BPPV nystagmus
up beating torsional slowly goes away; not persistent posterior canal of SCC
40
how is nystagmus named
by the fast phase which side it goes to quickly easier to see looking at white of eye not pupil
41
geotropic horizontal
down toward ground with horizontal nystagmus
42
ageotropic horizontal
away from ground horizontal
43
horizontal nystagmus is what part of nervous system indicated
CNS or PNS
44
subjective hx to take with vestibular
describe the dizziness - spinning = vertigo - dysequilibrium/"off"/floaty = more balance related/VSR; not pure BPPV usually - lightheaded = cardiac or upper cervical instability duration - intermittent (peripheral)or constant (central) - seconds = BPPV -days/hours/min/moth = something else other S&S - gait, balance, N&V, sensation of motion at rest, limb weakness, sensory changes traumatic/precipitating factors? episodic? recent viral infection? tinnitis? (roaring = menniers) HA? drop attack? (turn head and fall over fully conscious; occluding vertebral artery) change with head turn?
45
PMH to look at with vestibular pts
HTN DM HAs migraine hearing changes autoimmune disease recent viral infections underlying CNS disorders vascular pharmacological cervical injuries falls
46
exam/vestibular screen
clear verterbral artery - SAFETY - modified vertebral artery position 5Ds and 3Ns saccades- central (CN III, IV, VI output) smooth pursuit - central (CN III, IV, VI) convergence/divergence - central (CN III, IV, VI) VOR cancel (central) VOR (central or peripheral) Head impulse (peripheral) position testing - dizzy/nystagmus when you put in plane of SCC balance/gait HINTS (to rule out central)
47
5 Ds and 3 Ns
numbness-face nystagmus N&V dizziness dysphagia drop attacks dysarthria diploplia
48
red flags for vestibular pts
direction changing nystagmus (central) positive HINTS (acute CVA) sustained nystagmus (central) vertical nystagmus (central) positive vertebral artery screen acute intractable N&V (send to hospital; may need steroids) UMN signs unstable vitals not responding to positioning maneuvers other S&S of stroke (FAST)
49
vestibular outcome measures
dizziness handicap index (DHI) ABC DGI FGA CTSIB fujuda step test (close eyes, march 30s, see if they turn)
50
what is BPPV
when otoconia in utricle get dislodged into SCC mechanical problem
51
canalithiasis vs cupulolithiasis and theories involved
controversial topic canalithiasis - otoconia are free floating in canal cupulolithiasis - otoconia adhered to cupula - theory lacks evidence another theory = fluid displacement from movement of otoconia past cupula causes excitation theory 3 = otoconia jam where many otoconia move together and get stuck no consensus
52
canalithiasis general S&S
latent onset of nystagmus (1-40 sec) nystagmus goes away within 60 sec sensation of vertigo lasts length of nystagmus most common form of BPPV
53
cupulolithiasis general S&S
immediate onset of nystagmus nystagmus persistent and may last for entire time the head is in the affected position sensation of vertigo lasts the length of nystagmus
54
nystagmus for posterior canal
up beating and torsional torsional toward affected side
55
horizontal canal nystagmus
with or without torsion ageotropic (cupulo) or geotropic (canal)
56
anterior (superior) canal nystagmus
down beating and torsional torsion toward affected side
57
assessment for PC and AC
dix hallpike
58
assessment for HC
roll test
59
PC repositioning maneuvers
Epley (canalithiasis) semont liberatory (canalithiasis or cupulolithiasis)
60
AC repositioning maneuvers
semont liberatory
61
HC repositioning maneuver
270 roll (BBQ roll) canalithiasis
62
unilateral hypofunctions
injury in peripheral component of vestibular system that changes input to the CNS from one side i.e. vestibular neuritis and labrynthitis
63
bilateral hypofunctions
injury to the peripheral component fo the vestibular system that changes the inpit coming to the CNS from both sides i.e B ototoxicity in setting of chemo agents
64
adaptation
change in vestibular response to certain stimuli neuroplastic change where there is a physiological balance of signaling
65
habituation
decreased response to stimulus with increased exposure get pt used to it
66
POC for BPPV
single canal, posterior canal, canalithiasis = 1-2 visits multi canal and or horizontal canal and or cupulolithiasis - may require more visits
67
POC for unilateral hypofunction
2-3 weeks in acute/sub acute phase 4-6 weeks in chronic phase gaze stability exercises 3x/day for 12 min for acute/subacute gaze stability exercises 3-5x/day for 20 min in chronic
68
bilateral hypofunction POC
5-7 weeks gaze stability 3-5 days for 20-40 min
69
central problems POC
depends on what causes the central and if you are doing remediation, compensation, and/or prevention
70

Year 2: Neuromuscular II (18 decks)

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