Vestib 1 Final Flashcards

1
Q

what is caloric testing?

A

the most informative subtest of the VNG by being able to excite only 1 vestibular organ while the other one stays at rest

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2
Q

what are the advantages of calorics?

A

ear specificity, separating out the two ears without head movements, impacts the movements of endolymph and can show mild peripheral disorders

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3
Q

what are the disadvantages of calorics?

A

not a pleasant test, not testing at real world movements, not telling us about the whole end organ, cannot be performed on some patients and can infer but not definitively test for bilateral vestibular loss

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4
Q

how do calorics give a reponse

A

there is a convection change within the endolymph, causing it to become more or less dense
-with the change in density, this causes it to move differently

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5
Q

why will patients ultimately feel dizzy during calorics

A

we are hyperactivating one side while the other side stays normal, causing an asymmetry

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6
Q

does air or water give a bigger response

A

water, that is why we record for less time

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7
Q

how do warm and cool temperatures impact the endolymph density?

A

-warm stimulation decreases the density, creating an excitatory response in the test ear
-cool stimulation increases the density, creating an inhibitory response in the test ear

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8
Q

when we irrigate with warm, we will get a nystagmus that beats ________ the stimulated ear

A

towards

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9
Q

when we irrigate with cool, we will get a nystagmus that beats _________ the stimulated ear

A

away from

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10
Q

what is unilateral weakness (caloric paresis)?

A

comparing slow phase velocity (SPV) of the left ear to the SPV of the right ear, looking at the strengths between ears
-the weaker side, is the impacted side
-typically an indication of the end organ

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10
Q

when discussing the direction of nystagmus in relation to the temperature of calorics, what is the acronym that we use?

A

COWS
-cool opposite, warm same

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11
Q

what are the 4 recording parameters for calorics?

A

unilateral weakness, directional preponderance, fixation suppression, hyperactive/hypoactive responses

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12
Q

what is the equation for directional preponderance?

A

(RW+LC) - (LW+RC) / (RW+RC+LW+LC) x 100

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12
Q

what is directional preponderance?

A

comparing the slow phase velocity (SPV) of eye movements in the same direction, so using RW and LC to compare to LW and RC
-typically seen with a preexisting spontaneous nystagmus

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13
Q

what is the equation for unilateral weakness?

A

(RW+RC) - (LW+LC) / (RW+RC+LW+LC) x 100

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14
Q

what is fixation suppression?

A

observing if the nystagmus goes away/slows with the addition of a fixation
-failure of suppression indicates central

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15
Q

interpretation of calorics with norms

A

we look at a butterfly plot, showing data points based on COWS
-UW is abnormal if greater than 25%
-DP is abnormal if greater than 35%
-suppression is considered abnormal if less than 50%

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16
Q

what is the typical variation of calorics that is used

A

bithermal test

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17
Q

what type of system is used for our normal calorics that we do? how does it vary based on the balloon test?

A

we use an open system, meaning we are putting something in and it can come back out
-however, a balloon test is a closed system meaning that we are putting something in and it stays in there, creating not as large as a response

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18
Q

why are ice water calorics completed

A

completed to confirm the degree of loss or degree of function before/after a surgery
-helps dictate the level of invasiveness for surgery
-can also be completed to monitor vestibulotoxic drugs/injections with use of gentamicin

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19
Q

why can’t we rely on calorics alone

A

we are only getting low frequency information whereas normal head motion is in the middle to high range
-not relating/not generalizable to everyday head motion

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20
Q

what is caloric inversion?

A

caloric that beats in the opposite direction than what is expected
-getting an inverted response
-typically due to artifact or ME pathology (rarely will be CNS)

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21
Q

with acute vestibular injury patients, they do not want to be moving their head because it worsens those symptoms. however, over time ….

A

the acute vertigo goes away and they begin to experience static symptoms

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21
Q

what is caloric perversion?

A

generation of a oblique/vertical nystagmus following stimulation of the horizontal SCC during testing
-can occur if goggles are not placed properly

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22
Q

following a unilateral injury, they go through …..

A

central compensation
-resting neural activity on the damage side decreases explaining why we cannot measure a caloric
-producing a tonal imbalance, resulting in spontaneous nystagmus

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23
Q

how does the tonal imbalance following a unilateral deficit impact the nystagmus

A

drives the eyes slowly towards the weaker side leading to the fast phase beating in the opposite direction of the injury
-the compensatory mechanism is a rapid jerk back to the other direction

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24
Q

what is the process of central compensation

A

-resting neural activity of uninjured side is clamped down at the vestibular nuceli
-this reduces the asymmetry of VOR pathway and helps improve patients symptoms
-over time, clamping lets up as the resting activity is restored on the damaged side
-dynamic compensation is involved with reprogramming the VOR pathways to deal with long term effects

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25
Q

billing for VNG

A

-92540 basic vestibular bundle
-92537 caloric for two temps in both ears
-92538 caloric for one temp in both ears

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25
Q

best practices for VNG

A

-good oculography and calibration is key
-use threshold adjustment
-if you have abnormal results, reinstruct then repeat (a true abnormal result will remain abnormal)
-use a conservative criteria (the amount of abnormla data points should be more representative)
-be aware of potential patient confounding factors such as poor vision, medications or fatigue
-remove artifact from caloric data

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26
Q

when suddenly moving your head to the right, what happens in relation to the endolymph and your eyes

A

they move the opposite way
-the VOR serves to maintain a steady field so the eyes will travel opposite of the head motion

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27
Q

symptoms of an impacted VOR

A

head/eye coordination is out of sync, visual blurring, trouble reading signs when walking

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28
Q

when talking about an impulse, what are the three instances that occur

A

-head impulse starts (velocity exceeds 20%)
-head peak velocity or peak acceleration (reaches their peak)
-head impulse ends (velocity crosses 0%)

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29
Q

video head impulse (vHIT)

A

instrumented version of the bedside technique used to diagnose reduction in vestibular function
-can detect SCC dysfunction in all canals and is useful for the detection of peripheral vestibulopathy

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30
Q

background of the vHIT

A

originally described by halmagyi and curthoys within a study for 12 patients with unilateral vestibular neurectomy
-found altered VOR gain and presence of refixation saccades in abnormal individuals during head thrust

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31
Q

advantages of vHIT

A

can be performed from 10 months to elderly, gives a real world measure, evaluates HF reactivity, gives canal specific information, high sensitivity to vestibulopathy, can help track VRT progress and is site specific

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32
Q

limitations of vHIT

A

only analyses HF deficits, some studies suggest insensitvity to dysfunction secondary to menieres disease, techniques can be challenging, will miss mild unilateral vestibular origins

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33
Q

how to perform vHIT

A

patient is seated and the goggles are placed on, have patient focus on a fixed point, head then is moved rapidly in a 10-20 degree range
-conducting at least within the lateral plane, but can also do so in the LARP/RALP plane

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34
Q

two key aspects to remember when conducting vHIT

A

use quick acceleration and keep it unpredictable

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35
Q

gain of vHIT

A

eye movement relative to the target
-normative of 0.8 or greater (lateral) and 0.7 or greater (RALP or LARP)

36
Q

presence of refixation saccades

A

this occurs in people with abnormal VORs, either covert or overt

36
Q

2 parameters for vHIT

A

gain and presence of refixation saccades

37
Q

covert saccades

A

occurring during the head movement
-indicates compensated lesion
-too small to detect without recording them

38
Q

overt saccades

A

occurring after the head movement
-indicated uncompensated lesion

39
Q

SHIMP variant of vHIT

A

the head is the fixed target during this and patients are asked not to use their VOR

40
Q

vestibular nerve and canal connections

A

SVN: lateral and anterior canals
IVN: posterior canals

41
Q

vHIT vs. calorics

A

-calorics are highly variable, impacted by alertness/medications, unpleasant, telling us about the HSCC function and is reimbursed by insurance
-vHIT evaluates high frequency range, has greater specificity, fast/well tolerated, provides insight into compensation process

42
Q

H.I.N.T.S for vestibular neuritis and stroke differentiation

A

head impulse, nystagmus, test of skew
-performing on patients who are having or days of continuous, ongoing vertigo and spontaneous nystagmus
-more sensitive and less costly than MRIs however requires expertise that is not routinely available

43
Q

head impulse in HINTS

A

keeping eyes on your nose and conducting head impulse
-if negative (no refixations) than central (stroke)
-if positive (refixations) than peripheral (vestibular neuritis)

44
Q

nystagmus in HINTS

A

looking for any signs in the primary or lateral gaze

45
Q

test of skew in HINTS

A

covering one eye and when you pull it down, you observe the eye movement
-if negative (eyes not snapping back) then peripheral
-if positive (eyes snapping back) then central

46
Q

common peripheral signs

A

sudden onset, intense severity, paroxysmal and intermittent pattern, worse with movement, will often show nausea, horizontal nystagmus, fatigue of signs, HL/tinnitus may occur

46
Q

common central signs

A

sudden or gradual onset, less intense severity, constant pattern, variability nausea, multi directional or vertical nystagmus, no fatigue of signs, typically no HL/tinnitus, CNS signs are typically present (such as headaches, changes in speech)

47
Q

billing for vHIT

A

there is no current approved codes for vHIT testing
-most will use 92700 (unlisted otoneurologic items or services with documentation)

48
Q

as a result of a concussion ….

A

nerve signals in the brain can be disrupted for months after a single concussion and during this time, people are more likely to have a secondary injury

48
Q

concussion

A

traumatic brain injury caused by a bump, blow or jolt to the head or by a hit to the body that causes the head/brain to move rapidly back and forth
-causes the brain to bounce or twist within the skills, creating a chemical change in the brain

49
Q

common symptoms experienced with a concussion that is also associated with vestibular injuries

A

dizziness/vertigo, imbalance or unsteadiness, blurred or bouncing vision, problems with coordination, headache, sensitivity to noise and fatigue

50
Q

how to differentiate between a TBI and vestibular etiology

A

by looking at the symptoms that are more common in vestibular pathologies than compared to TBIs
-vertigo as opposed to dizziness
-positionally evoked dizziness
-changes in hearing
-onset of tinnitus
-presence of spontaneous nystagmus

51
Q

assessment of concussions

A

there is no standard diagnostic testing
-based on a group of symptoms

52
Q

slow phase of nystagmus is driven by the ________ whereas fast phase of nystagmus is driven by the ________

A

ears ; CNS

53
Q

with rotational testing, we are looking at ….

A

how the VOR functions in regard to movements of the individual
-observing the function through head and eye velocity movement

54
Q

the expected response we should get with rotation

A

due to VOR function, we would expect that the eyes will move in opposite direction from the head
-gain should be lower than the head speed
-symmetry should be seen

55
Q

passive rotation

A

patient is moved by the examiner directly
-easier to control but limited to how fast we can move

56
Q

active rotation

A

patient is directed to move their own head/body
-more realistic, taking into components of musculoskeletal aspects

57
Q

rotational chair

A

a means to expand the evaluation of the VOR to include more velocities and provides a more natural physiologic representation of head movement/VOR function while being more tolerable by patients
-the axis of rotation is centered between both labyrinths

58
Q

within rotational testing, what direction results in which beating pattern

A

-counter clockwise (CCW) rotations results in LB
-clockwise (CW) rotations results in RB

59
Q

the rotational chair evaluates …
(anatomically)

A

HSCC, central systems and vestibular nuclei

60
Q

the direction in which you rotate excites the __________ canal (on that side)

A

horizontal
-CCW excites left HSCC
-CW excites right HSCC

61
Q

benefits of rotary chair

A

evaluates for bilateral vestibule loss, monitors for ototoxicity, evaluates for CNS disorders, infers degree of central compensation to peripheral disorders, makes determinations about rehabilitative therapy, evaluates vestibular function on those who cannot undergo caloric testing and can use on kids

62
Q

limitations of rotary chair

A

only testing the VOR at low/mid frequencies, only tells us about the function of HSCC and SVN, cannot be performed on some patients, poor ear specificity and takes up space within the clinic

63
Q

patient set up for rotary chair

A

seat subject in the chair and place the goggles on their head ensuring a snug fit, secure the patient with velcro straps to ensure no head movements (typically at a 30 degree angle downward)

64
Q

what two things need to occur prior to beginning rotational testing

A

calibration and spontaneous gaze

65
Q

4 subtests for rotational testing

A

SHA, step velocities, VFx and VVOR

66
Q

sinusoidal harmonic accelerations (SHA)

A

a test that brings the patient to a velocity of 60 degrees/second at various frequencies
-picks up where the calorics left off
-typically beginning with mid then highs then lows

67
Q

SHA testing protocol

A

-minimum of 2 to 3 cycles recorded for each frequencies
-performed in complete darkness
-must TASK the patient throughout

68
Q

why must you task the patient throughout the SHA test

A

they can try to correct the nystagmus during the test

69
Q

SHA phase

A

the timing component comparing timing of peak eye velocity to peak chair/head velocity
-how long it takes for VOR to become active

69
Q

recording parameters for SHA

A

gain, symmetry, phase and spectral purity

70
Q

SHA gain

A

ratio of SPV of the eyes to that of the head/chair
-if measure is less than .15 than no calculation of phase or symmetry will be made

70
Q

SHA symmetry

A

difference between peak RB and peak LB divided by the total sum of SPV
-most common with those that have pre existing spontaneous nystagmus or acute unilateral losses

71
Q

for slow rotations, the eyes will ______ the movement of the chair/head

72
Q

for fast rotations, the eyes will ______ the movement of the chair/head

A

lag behind

73
Q

SHA spectral purity

A

how clean the data is

74
Q

step velocities

A

taking the patient from rest to a very quick constant motion and examines the systems central velocity storage, then the patient is stopped abruptly and post rotary nystagmus is recorded

75
Q

step velocity test protocol

A

test is completed in darkness and without tasking, process is completed in one way then repeated in the other direction
-both initial nystagmus and post rotary nystagmus are measured and then compared

76
Q

expected nystagmus pattern within step velocities

A

-initial nystagmus should show a burst of nystagmus beating towards the direction of rotation
-this will dissipate over time as the subject maintains constant velocity
-the chair is then stopped and there will be a second burst of nystagmus but in the opposite direction

77
Q

recording parameters for step velocities

A

gain and time constant

78
Q

step velocity gain

A

initial peak gain SPV of nystagmus
-greater rotational velocities make gain measurements more ear specific

79
Q

step velocity time constant

A

time required for nystagmus to decay to 37% of the original peak gain SPV
-general rule is that 10 seconds or greater is normal

80
Q

visual suppression/fixation (VFx)

A

patient is asked to fixate on a point of light projected in front of them while being rotated, these visual targets will travel at the same speed as the chair
-subject should be able to maintain focus on the light, reducing vestibular induced nystagmus

81
Q

a failure to fixate is a _______ sign

81
Q

visual enhancement (VVOR)

A

patient is asked to look at the OPK stimulus while they rotate, the visual fixation will be stationary while the patient rotates
-usually completed if the patient has low gain for traditional SHA tests

82
Q

active head rotation (AHR)

A

created as a lower cost, easy to use, more space efficient tool to measure the VOR during rapid head movement where visual stability might be impaired in a patient with a vestibular deficit
-better assess moderate to high frequency head movement

83
Q

devices of AHR ….

A

-compare eye movements induced by active motion of the head rather than passive head/body movements induced by a chair
-assess mid to high frequency range whereas rotary chair assess low to mid frequency range

84
Q

typical frequency range for AHR

85
Q

problems with AHR

A

goggle slippage can cause HF phase to be incorrect, test retest reliability is insufficient and billing fraud since there is no code