Final Exam Study Guide (New Content) Flashcards

1
Q

who first described caloric reflexes? what did he earn? who is he

A

First described by Robert Bárány in 1906; earned the Nobel Prize in 1914.
Father of neurotology → first described caloric testing after noticing nystagmus during earwax irrigation

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2
Q

Most informative VNG subtest, isolating one vestibular organ at a time

A

calorics

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3
Q

Uses warm or cool water/air to stimulate

A

horizontal semicircular canal (HSCC) and induce nystagmus

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4
Q

describe what calorics primarily assesses

A

Primarily assesses vestibular function and detects asymmetries between ears
Assesses asymmetric vestibular function and peripheral vestibular pathways (up to CN VIII)
Normally, both sides work together. Stimulating one while the other is at rest induces vertigo

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5
Q

what can calorics also assess

A

Can also help assess brainstem function (e.g., in cases of brainstem death)

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6
Q

what is the bs critical for

A

cardiac, respiratory, and CNS regulation
Involved in all life-sustaining measures → heart rate, body temperature, sleep cycle, etc. (automatic things)

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7
Q

what is the major function of the flocculus

A

inhibit vor

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8
Q

More severe damage affects ____ responses first before impacting ______.

A

LF
HF

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9
Q

LF Tests

A

Calorics, Slow Rotary Chair.

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10
Q

HF tests

A

Head Impulse Test

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11
Q

Normal body temp

A

37 deg C or 98.6 deg F

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12
Q

types of caloric testing

A

bi-thermal tests (standard method)
mono-thermal
bilateral irrigation
balloon test
ice water

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13
Q

what is monothermal test

A

ice water irrigation in one ear → larger response further away from body temp you are

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14
Q

bilateral irrigation

A

both ears stimulated simultaneously

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15
Q

balloon test

A

water-filled balloon instead of direct irrigation

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16
Q

confirms complete vestibular loss

A

Ice water caloric test

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17
Q

Open systems/stimulations

A

Direct air/water irrigation

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18
Q

Closed loop systems

A

Inflated water-filled balloon transfers temperature

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19
Q

caloric testing position

A

The patient lies supine with head elevated 30° to align HSCCs perpendicular to gravity

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20
Q

what is included in irrigations

A

Cold & Warm Water or Air

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21
Q

describe water procedures

A

44/30 for 30 sec

Warm → 44oC
Cool → 30oC

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22
Q

describe air procedures

A

50/24 for 1 min

Warm → 50oC
Cool → 24o

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23
Q

6 up and 6 down

A

air and water calorics

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24
Q

Nystagmus response recorded for

A

90s

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25
Q

reversal

A

perform RW, LW, LC, RC or RC, LC, LW, RW

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26
Q

Allow around ____ min between each irrigation to let vertigo subside

A

5

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27
Q

should you task during calorics

A

YES

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28
Q

transfer effects endolymph density/neural firing rate around 6-10s post onset & we are stimulating HSCC

A

t

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29
Q

Physiological Responses

A

COWS

cold opposite
warm same

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30
Q

describe how physiological responses occur

A

Temp transfer changes density of endolymph; density changes causes movement w/in HSCC through convection; convection current generates excite/inhibit response in HSCC of TE

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31
Q

describe cold physiological responses

A

opposite/contralateral → nystagmus beats to the opposite side
I
ncreased endolymph density → ampullofugal flow → inhibitory response in TE

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32
Q

describe warm physiological responses

A

same/ipsilateral → nystagmus beats to the same side

decreased endolymph density → ampullopetal flow → excitatory response in TE

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33
Q

Cold in RE

A

LB nystagmus

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34
Q

Cold in LE

A

RB nystagmus

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35
Q

Warm in RE

A

RB nystagmus

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36
Q

Warm in LE

A

LB nystagmus

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37
Q

what are the metrics to measure/interpretation criteria

A

unilateral weakenss (UW)
directional preponderance (DP)
fixation suppression/fixation index
caloric inversion
caloric perversion
hyperactive/hypoactive
bilateral caloric weakness
total response

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38
Q

what is unilateral weakness

A

caloric paresis/relative vestibular reductin (RVR

comparison of bi-thermal RE responses to LE responses

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39
Q

significance of UW

A

abnormality is on the weaker side

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40
Q

abnormal UW & what does it suggest

A

≥ 25% interaural difference = clinically significant asymmetry (abn) → suggests pathology in the HSCC or superior vestibular nerve

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41
Q

what is the jongkees formula for UW

A

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

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42
Q

caution of UW

A

ensure good irrigations, no ‘stragglers’ (asymmetric)

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43
Q

causes of UW

A

Damage to the vestibular organ, vestibular nerve (VIII), or root entry zone of the VIII nerve

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44
Q

most common cause of UW

A

End organ disease

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45
Q

clinical significance of UW

A

Identifies the affected side but not the exact location of damage

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46
Q

what is directional preponderance

A

GA/BS
Comparison of right-beating to left-beating eye responses
exists when the nystagmus response is greater in one direction than the other

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47
Q

significance of DP

A

non-localizing finding, low diagnostic utility

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48
Q

produces right eye movement

A

RW & LC

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49
Q

produces left eye movement

A

LW & RC

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50
Q

clinically significant DP

A

> 30% difference in intensity of max SPV bw 2 RB responses and 2 LB responses
35% difference

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51
Q

DP references what side

A

Referencing the stronger side → eye has the desire to go in this direction

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52
Q

what is jongkee’s formula for DP

A

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

or right going +right going eyes - left going + left going eyes / total x100

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53
Q

caution with DP

A

most commonly seen with pre-existing spontaneous nystagmus or w/ asymmetric responses due to poor irrigation

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54
Q

what is fixation suppression

A

degree to which caloric nystagmus is attenuated by visual fixation → varies depending on lab data set used
After irrigation and eye movement is recorded, fixation light occurs and we are looking at what can the normal system do when a light is present (stops or goes low ) what was the max nystagmus we can induce

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55
Q

what is a normal fixation suppression/fixation index

A

> /=60% suppression of caloric-induced nystagmus w/ visual fixation

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56
Q

what does fixation suppressino check for

A

cerebellar fixation compression

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57
Q

what is a normal fixation

A

nystagmus lessens with fixation

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58
Q

assesses if connections bw vestibular nuclei and midline cerebellar structures are intact - cerebellar flocculus

A

functional index

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59
Q

what is caloric inversion

A

entire response is reversed
Entire caloric response that beats in the opposite direction to that expected
Rare & associated w/ BS disease
More commonly w/ technical error

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60
Q

example of caloric inversion

A

Irrgating R ear w/ warm should generate RB but here it will generate LB nystagmus

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61
Q

what is caloric perversion

A

generation of an oblique or vertical nystagmus
Linked to disease affecting BS structures @ 4th ventricle

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62
Q

Linked to disease affecting BS structures @ 4th ventricle

A

caloric perversion

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63
Q

Rare & associated w/ BS disease

A

caloric inversion

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64
Q

Measure that looks at the system as a whole
describes the general state of how sensitive or responsive the system is

A

Hyperactive/Hypoactive Responses

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65
Q

what is hyporesponsiveness

A

comparison of total responses from both ears (sum of all) → may indicate bilateral vestibular loss

non-localizing
Caution: alertness of PT (fatigue, meds), appropriate tasking

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66
Q

< 30 deg/s (Stockwell, 1980), < 26 deg/s (Jacobsen, 1993), < 20 deg/s Hain
< 12 deg/s per ear (Barin, 2008) accounts for UW bias

A

hyporesponsive

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67
Q

what is hyperresponsiveness

A

comparison of total response individually (sum of each ear) → may indicate central pathology (e.g., cerebellar dysfunction)
Rare finding
Caution: most common w/ bad calibration, abnormal ME (mastoid cavity, perf, PE tube) or bad irrigation temp

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68
Q

> 140 deg/s total RE responses, >140 deg/s total LE responses

A

hyperresponsiveness

69
Q

most common w/ bad calibration, abnormal ME (mastoid cavity, perf, PE tube) or bad irrigation temp

A

hyperresponsiveness

70
Q

alertness of PT (fatigue, meds), appropriate tasking

A

hyporesponsiveness

71
Q

what is total response

A

Useful to determine possible BVL (hypo) & hyper responsive even though used less clinically
Do not use calorics alone for bilateral diagnosis; rotary chair used to confirm
Total response / total eye speed
TR (RC + LC + RW + LW)

72
Q

Rotary chair testing is the only true way to diagnose a bilateral vestibular loss - reduced calorics DOES NOT indicate BVL (hypo)

73
Q

causes of bilateral vestibular loss

A

Systemic infections
CNS disease (benign intracranial hypertension, inherited and acquired BS & cerebellar neurodegenerative diseases (Friedreich’s ataxia, Wernick-Korsakoff syndrome)

74
Q

bell’s phenomenon

A

(doll eyes)
Reflex averting (rolling up) and adducting (moving laterally toward one another) of the eyes that occur upon eye closure - ENG only w/ eyes closed

75
Q

common errors of calorics

A

Was the irrigation good? - operator error is the most common
Visualize the ™ to direct water/air to it to ensure adequate temperature

76
Q

What can affect the temp transfer

A

wax, hair like a jungle, ME effusion,

77
Q

If you have three responses that look good and one that doesn’t, the assumption must be made that the one irrigation was bad and you should re-do it. If you have 2 of 4 bad, on the same side, it is more likely a unilateral weakness

78
Q

advantages of calorics

A

Ear specificity/laterality of the test → physiologic integrity of L & R horizontal canal; periphery can be directly assessed
Caloric stimulus is nonphysiologic →The caloric test isn’t a natural way to stimulate the balance system because, in everyday life, both sides of the inner ear work together when we move our head and body. However, when we put warm or cool water in one ear, it changes the movement of fluid in the nearby balance canal on that side. This, in turn, affects the signals sent from that ear’s balance system to the brain

Can rule out mild deficits
Affects LF first

79
Q

limitations of calorics

A

Level of stimulation reaching the system varies
Only assesses LF VOR function (0.002–0.004 Hz)
Not suitable for some patients (e.g., young children, surgical ears, severe middle ear pathology, microtia/anotia, otorhhea, etc.)
Variable & slightly uncomfy
Can infer but not definitely diagnose for BVL - no statement about VOR & BVL should be based on calorics alone

80
Q

Central compensation can restore function over time, but caloric testing will always show past damage & cannot determine level of functional compensation (rotary chair can help)

81
Q

what is ice water calorics used for

A

Primarily used when bi-thermal irrigations are very low or to confirm diagnosis of BVL
Rotary chair is still gold standard

Useful in confirming ablative procedures - gentamicin injections & vestibular nerve section
Sees if there is any function of the vestibular system left

82
Q

gold standard for BVL

A

rotary chair

83
Q

No universally standardized procedure or temperature but typically a single bolus approximately 2cc of ice water (~18℃) is delivered to the ear

84
Q

why would you do ice water calorics

A

confirm BVL

PT undergoing ablative surgery for intractable vertigo - If PTis getting surgery to disable one side of their balance system because of severe vertigo, having some remaining function in that ear means they will likely feel very sick after the procedure. Knowing this ahead of time helps the doctor prepare for their recovery and manage their symptoms right after surgery

Good to know if there is any residual vestibular function when PTs are treated with vestibulotoxic medications to the peripheral vestibular system

85
Q

Vestibular pathways undergo ________ following a unilateral damage

A

compensatory changes

86
Q

Stages of Compensation:

A

Clamping Down - minimizes tonic imbalance & PT symptoms
Static compensation: Reduces spontaneous nystagmus at rest
Dynamic compensation: Reprograms the VOR to adjust for movement
Full compensation: Requires an intact cerebellum; vestibular rehabilitation can speed up adaptation

87
Q

describe the process initally after acute unilateral vestibular loss

A

After insult, resting neural activity on damaged side decreases & is why we can measure caloric weakness on that same side & why person perceives vertigo
Tonal imbalance produces spontaneous nystagmus accompanying weakness

uncompensated (partially-compnesated) peripheral loss

88
Q

how do we see nystagmus in acute vestib loss (uni)

A

Tonal imbalance of strong side drives the eyes slowly toward the weaker side & the brain’s compensatory mechanism rapidly jerks it back in the other direction
Causes a spontaneous nystagmus with fast-phase movement beating away from the damaged ear
Ex: L caloric weakness causes a RB spontaneous nystagmus

89
Q

describe central compensation & its stages

A

First step - clamping down on resting neural activity on the healthy side to minimize tonic imbalance
Reduces asymmetry of VOR pathway and decreases vertigo symptoms
Over time clamping of the good side lets up as resting activity on the damaged side is restored
Static compensation - spontaneous nystagmus disappears & PT symptoms improve as long as their head is still
Patients with acute VOR deficits typically complain of vertigo whereas those with chronic VOR deficits complain of motion-provoked disequilibrium or disorientation as head movement results in blurring of the visual environment.
Last stage - dynamic compensation - involves reprogramming of VOR pathways to deal with long-term effects of labyrinthine loss on damaged side
Individual returns functionally to normal
Can be sped up by VRT/VR exercises
Good compensation relies on intact cerebellum (flocculus & paraflocculus specifically)

90
Q

calorics will not always show weakness after compensation

A

F

Calorics will always still show weakness through the process and permanently after compensation

91
Q

Abnormal findings on oculomotor exams
what should you do

A

Re-instruct
Repeat the test
True abn is always abn

92
Q

Oculomotor data points

A

Use conservative criteria - 50% or more points for abn/normal criteria

93
Q

what are patient confounding factors

A

Poor vision, eye abnormalities, fatigue, medications, inability to perform tasks

94
Q

Textbook Feature - DOCUMENT

A

Use to take notes about subjective complaints or patient inability to perform tests or anatomical or other factors that might skew results

95
Q

positional testing best practices

A

Turn PT head BEFORE recording to avoid appearance of nystagmus tracings
Be quick
Instruct PT to keep eyes open during positional testing

96
Q

calorics best practices

A

Clean up & verify caloric data bw irrigations
Give PT 4-5 in between irrigations and work in reverse order
Avoids two irrigations in a row for same direction

97
Q

Basic vestibular evaluation
includes: spontaneous nystagmus test with eccentric gaze fixation test, with recording, positional nystagmus test (minimum of 4 positions) with recording, optokinetic nystagmus test, bidirectional foveal and peripheral stimulation, with recording and osciallting tracking test, with recording

98
Q

In order for 92540 to be billed correctly, each procedural component listed under that code must be completed in their entirety (for example; 4 positional tests = Dix Hallpike, positional each position)

what can you do if you do not perform them all under that code

A

Add -52 modifier if only perform part of a code (e.g. only 3 irrigations for 92537) and -22 modifier if perform more than four irrigations (for example ice water also

99
Q

Caloric vestibular test with recording, bilateral; bi-thermal

100
Q

Caloric vestibular test with recording, bilateral; monothermal (ie, one irrigation in each ear for a total of two irrigations)

A

CPT 92538:

101
Q

reimbursement for VNG

A

Reimbursement 2020: ~$150 for CMS

102
Q

If entire ENG/VNG is not performed, may be able to bill individual components rather than bundled (92540) code

103
Q

Spontaneous nystagmus test, including gaze and fixation nystagmus, with recording

104
Q

Positional nystagmus test, minimum of 4 positions, with recording

105
Q

Optokinetic nystagmus test, bidirectional, foveal or peripheral stimulation, with recording

106
Q

Oscillating tracking test, with recording

107
Q

Add the -59 modifier if bill two or three of 92541, 92542, 92543, or 92544 on the same patient on the same date of service
Billing multiple vestibular tests on the same day

108
Q

Canalith Repositioning Procedure(s) (e.g., Epley maneuver, Semont), per day

109
Q

reimbursement for canalith repositioning

A

Reimbursement 2020: ~$50 for CMS Not covered under Audiology benefit

110
Q

what is the code for saccades

A

there is no code

111
Q

how does VOR work if you turn head to R

A

Acceleration to the right, endolymph flow to the left, eyes stay to the left

SCC work in pairs
Senses strength & direction of acceleration and deceleration

112
Q

describe 3 instances during an impulse

vor slow phase (latency & gain)

A
  1. head impulse start - time when the head velcoty exceeds 20 deg/s
  2. peak acceleration/velocity - where velocity/acceleration reaches max values
  3. head impulse end - head velocity crosses 0 deg/s & usually repounds
113
Q

computerized way to look at how the eyes are moving relative to the head movement

114
Q

what is the head impulse test / head thrust test

A

Bedside screening to detect SCC dysfunction in ALL canals
Useful to detect peripheral vestibulopathy

115
Q

who discovered HIT? what did they do and find

A

Described by Halmagyi & Curthoys 1988 in study of 12 PTs w/ unilateral vestibular neurectomy
Found altered VOR gain and re-fixation (catch-up) saccades in abn individuals during head thrus

116
Q

how to perform vHIT

A

Patient keeps eyes focused on fixed point
Head moved rapidly (200+degrees/second), 10-20 deg range only
Keep unpredictable
Can be performed from 10 months old to elderly

117
Q

what are covert saccades

A

saccades happening DURING head movement; unable to see w/ naked eye
Hidden when head moves; cannot see
Compensated lesions

118
Q

what are overt saccades

A

saccades happening AFTER head movement; can see w/ naked eye
See after head stops; through instrumentation or bedside
Uncompensated lesion

119
Q

Instrumented version of the bedside technique (Halmagyi) used to diagnose reduction in vestibular function
Quantifies gain measures & detects both overt and covert

120
Q

best way to perform vHIT

A

Head rotations should be rapid & unpredictable in direction and time, small amplitude (10-15 deg), and peak head velocity (150+ deg/s

121
Q

lateral/horizontal vHIT

A

right and left (typical)

122
Q

RALP vHIT

A

right anterior and left posterior
head turned to the left

123
Q

LARP

A

left anterior and right posterior
head turned to the right

124
Q

how to analyze vHIT

A

Gain → eye movement relative to the head movement
Normative >0.7 some systems, >0.8 other systems
Presence of re-fixation saccades (covert & overt)

125
Q

vHIT gives site specificity about where the damage is located

126
Q

adv of vHIT

A

fast, easy to do, anyone can tolerate it, gives us more anatomical information (multiple canals & nerve branches), in line with how our system normally functions, ear pathology, compensation status, VRT, portable

127
Q

disadv of vHIT

A

HF information only (can have mild and miss it), no cpt codes so reimbursement is either free or OOP for the PT (advanced beneficiary notice - says ins might not cover something) technique is challenging, some research suggests dysfunction secondary to meniere’s disease

128
Q

dysfunction secondary to meniere’s disease

129
Q

how does calorics differ from vHIT

A

Highly variable, affected by alertness & meds, unpleasant, time consuming, only tells about HSCC fxn, not portable & need dark environment, & are reimbursable by insurance, and catches milder UW

130
Q

what are the disadv of calorics compared to vhit

A

Evaluates VOR in frequency below physiological range (.003 Hz)
Induces non-physiologic endolymphatic flow in HSCC & creates technique problems (failed irrigation, asymmetrical transmission of thermal energy or persistent stimulation bw irrigations & alertness)
Time consuming, discomfort to PTs
Results cannot determine compensation

131
Q

how does vHIT differ from calorics

A

Not reimbursable by insurance, misses milder UW (~<40%), insensitive & not performing as well as calorics, greater specificity than calorics
Evaluates physiological HF range of VOR in HSCC, ASCC, PSCC (up to 5 Hz)
Fast & well tolerated, allows for re-testing
Results can determine compensation process
Instantaneous gain analysis gives direct measure of how balance system controls eye movement because it isn’t affected by slower brain or eye movement adjustments but position gain analysis can be influenced by these factors and makes it less of a pure test of function

132
Q

what does HINTS stand for

A

Head Impulse, Nystagmus, Test of Skew

133
Q

what is hints

A

Strokes can be distinguished from benign acute vestibulopathies using bedside oculomotor tests
Pro → more sensitive (<24hrs) and less costly than early stage MRI for stroke
Con → requires expertise not routinely available in ER
Conceptually similar to ECG to diagnose acute cardiac ischemia

134
Q

interpretation of HINTS

A

Head impulse = - central
Head impulse = + peripheral
Test of skew = - peripheral
Test of skew = + central

135
Q

onset from per and cen

A

sudden

sudden or gradual

136
Q

severity of peri and cent

A

intense

ill-defined, less intense

137
Q

pattern of peri and cent

A

paroxysmal, intermittent

constant

138
Q

worse w/ movement for per and cen

A

yes in peri

variable in cent

139
Q

nausea/diaphoresis peri and cent

A

frequenty in per

variable in cent

140
Q

nystagmus in peri and cent

A

horizontal

vertical or multi-directional

141
Q

fatigue signs in peri and cent

142
Q

HL or tinnitus in peri or cent

A

maybe in peri
no in cent

143
Q

CNS signs

A

peri no

central usualy present

144
Q

what is the variant to vhit and who reported it

A

SHIMP

macdougall 2016

145
Q

what is SHIMP variant to vHIT

A

PTs view a laser dot that moves with their head and PTs turn off their VOR than to use it
Anticompensatory saccades are elicited in normal controls but less commonly found in those who have less VOR to suppress

146
Q

If vHIT is normal

A

perform other vestibular function tests
vHIT alone doesn’t conclude normal vestibular function

147
Q

If vHIT is abnormal

A

use hx, symptoms, medical hsitory and other testing to triage PT

148
Q

vHIT is a great quick easy test to tell about function of the VOR for all 6 SCCs, state of superior & inferior VN, and can indicate if the issue may be central

149
Q

what is a concussion

A

type of traumatic brain injury (TBI) caused by bump, blow or jolt to the head or a hit to the body that causes the head and brain to move rapidly back and forth

doesn’t appear on mri or ct

no diagnostic test for it

150
Q

how does a concussion happen

A

Sudden movement causes the brain to bounce around and twist in the skull creating chemical changes in the brain and sometimes stretching and damaging brain cells

151
Q

how do you daignose concussion

A

based on groups of symptoms or signs that may be immediately present or arise over weeks after
Some develop no symptoms after a concussive event and some can takes weeks

152
Q

what symptoms of vestibular disorders aligns with concussion/TBI

A

Dizziness / Vertigo
#2 Imbalance or unsteadiness
Blurred or bouncing vision
Problems with coordination, thinking, memory
#8 Headache
#9 Sensitivity to noise / bright lights
#10 Fatigue

153
Q

only test we have to split the vestibular system and test each ear individually
ear specificity

154
Q

the only true way to diagnose a bilateral vestibular loss

A

rotary chair

155
Q

hypo responsiveness indicates a bilateral VL

A

FALSE
does not

156
Q

who had the earliest written acount of vertigo

A

Aristotle (384-322 BC)

157
Q

Normal daily activities - produce head velocities up to ______, accelerations up to _______and frequency from _____

A

550 deg/s
6000 deg/s
0-20Hz

158
Q

Best way to evaluate VOR

A

Very LFs - calorics
Low & mid frequencies - rotary chair
HFs - active head rotation
f

159
Q

what is the VOR

A

reflexive eye movement occurring in response to head movement
allows for stable gaze

160
Q

who is barany? what did he win? who was he? what did he create

A

Barany chair- 1876-1936; nobel prize in 1914
Hungarian physiologist
Device stimulating SCC through controlled rotation

161
Q

types of rotational tests

A

passive
active

162
Q

passive rotational tests

A

PT is moved by the examiner directly
Head or whole body
HIT/Head thrust, rotary chair tests, off-axis rotations (SVV & SVH)

163
Q

active rotational test

A

PT moves their own head
Can be active or passive headshake
Vestibulo-authorotation test (VAT/Vorteq)

164
Q

eval parameters of VOR

A

gain, symmetry & phase

165
Q

axis of rotation of rotational tests

A

centered bw both labyrinths (bilateral stimulation)

166
Q

CCW rotations

A

LB nystagmus - L HSCC excites & R HSCC inhibits

167
Q

CW rotations

A

RB nystagmus - R HSCC excites & L HSCC inhibits

168
Q

what does rotational chairs evaluate

A

Examines HSCC, central systems & vestibular nuclei
Only concerned w/ slow phases & all are combined in sinusoidal form for analysis

169
Q

what are the clinical applications of rotational testing

A

Evaluates for BVL or PT w/ low calorics
Monitors ototoxicity
Evaluates for CNS disorders
determine compensation status and rehab recommendations
Evaluates vestibular function on those who can’t undergo caloric testing (Surgical ears (mastoid cavity, PE tubes, perf, otorhea)
microtia/anotia
Young kids or handicapped)