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AUDE 5410 Aud-Vestib Disorders > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

what are electrophysiologic audiometry

A

measures that record & analyze the as physiologic responses

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2
Q

another term for physiological responses

A

objective responses

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3
Q

what are types of electrophysiologic tests

A

immitance tests (tymps, reflexes & decay)
OAEs
auditory evoked responses (AERs)

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4
Q

what does in mean when we say the electrophysiologic tests are objective

A

they do not require the subject’s active participation, and are complementary to audiometry, which is subjective

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5
Q

is audiometry objective

A

no subjective

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6
Q

how do neurons in the brain communicate

A

rapid electrical impulses

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7
Q

what do the electral impulses allow the brain to do

A

coordinate behavior, sensation, thoughts, and emotion

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8
Q

what does the CNS do even in the absence of sensory stimulation

A

generates spontaneous and random neuroelectric activity

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9
Q

how can we record spontaneous and random neuroelectric activity

A

scalp electrodes

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10
Q

what happens to the brain once the sound goes in there?

A

auditory evoked responses

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11
Q

do neurons fire without stimulus

A

yes

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12
Q

what happens when there is a stimulus

A

neurons fire at a higher rate and amplitude

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13
Q

what forms the basis of electroencephalogram (EEG)

A

neuron firing spontaneously and random

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14
Q

are eeg good for us?

A

no
we have to look at tiny responses in the sea of large responses
we cannot remove eeg because that would mean the pt would be dead

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15
Q

what is a AEP

A

activity or response within the auditory system that is produced or stimulated (evoked) by sounds

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16
Q

where can the activity be

A

Cochlea
Auditory nerve
Central auditory nervous system (CANS)

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17
Q

AERs are an example of

A

neural activity in response to specific types of sensory stimulation, which are extracted from the EEG

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18
Q

The EEG response are huge while any other evoked response are relatively small. What does this mean

A

requires significant signal amplification and other mechanisms to read those responses

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19
Q

term physicians prefer for ABR

A

brainstem evoked auditory response
bear

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20
Q

What does the ABR consist of

A

sequential series of 5-7 peaks (responses)

The response occurs for ~ 5 to 10 ms following stimulus onset

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21
Q

clinically, focus is on what peaks

A

I-V in general
I, III, & V particular

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22
Q

what is latency

A

time frame signal is turned on and you see the response
time frame of the response of when you see the response occur

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23
Q

what is stimulus onset

A

signal turning on

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24
Q

what are the clinical applications of the ABR

A

can provide a close estimate of hearing threshold for specific frequencies

can predict a conductive, sensory, or neural site-of-lesion

screening tool for retrocochlear pathologies

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25
Q

The ABR is not a ________ but rather a measure of ________

A

test of hearing sensitivity but rather a measure of neural synchrony

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26
Q

why do we not focus on all peaks of I-V

A

if you see 1 and 3, 2 is assumed ot be there
if you see a 3 and 5, it is assumed 4 is there
4 can be right with 5 and that is not abnormal

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27
Q

why is ABR not a test of hearing sensitivity

A

because you are measuring nerve response, not sensory hair cell response
used as a test of hearing sensitivity in an indirect way because it tells how the system is hearing and a test of neural synchrony

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28
Q

what is neural synchrony

A

firing of all of the nerves
CN’s when they receive signal they fire, they do not fire randomly, they fire synchrony based on the signal they receive
low vs high frequency causes different neurons firing

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29
Q

synchronous firing and disruption causes clinically

A

speech understanding in general and more in speech in noise

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30
Q

why do they have difficulty hearing in noise?

A

they hear the noise with their ears but it doesn’t get to the brain so the brain cannot understand the information because the firing is

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31
Q

is the audio independent of neural dysynchrony

A

YES
audio can show anything, it is not a reflection of neural dysynchrony

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32
Q

audiogram tests

A

the integrity of the OHC & IHC

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33
Q

function of the ABR

A

neural synchrony

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34
Q

can you see hearing level on an ABR?

A

yes you can predict CHL, SNHL or neural site of lesio

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35
Q

why is ABR a screening tool & not a diagnostic tool

A

it tells you something is wrong but it doesn’t tell you where the issue is arising

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36
Q

would dr send baby for an abr with symtpoms of vestib schwanoma

A

no they will go to an mri because it is more definitive

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37
Q

what are the generation sites of the ABR for each wave

A

1: distal viii n in the cochlea
3: cochlear nucleus, trapezoid body, superior olivary complex
5: lateral leminiscus

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38
Q

what is the blood supply of the cochlea

A

labyrinthine artery

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39
Q

where does the labyrinthine artery branch from

A

generally AICA
anterior inferior cerebellar artery

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40
Q

what is the blood supply of the brainstem

A

vertebrobasilar artery

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41
Q

how does the brain work

A

in unison

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42
Q

why do we want to look at blood supply?

A

problem could be here instead of a vestib schwanoma when problems show up on an abr

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43
Q

how long does it take before the waveform appears

A

latency

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44
Q

Absolute peak values at _______ nHL presentation level

A

Absolute peak values at ~80 dB nHL presentation level

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45
Q

nHL vs HL

A

normalized hearing level -

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46
Q

what is nHL

A

taking group of normal hearing young adults and looking at where the thresholds come in

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47
Q

what is the latency value for wave I

A

1.5 ms (mean)
(SD = + 0.25 ms)
(sd = standard deviation)

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48
Q

wave II

A

2.6 ms (mean)
(SD = + 0.25 ms)
about _____ latency above wave I

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49
Q

wave III latency

A

3.7 ms (mean)
(SD = + 0.25 ms)
about 1 ms above wave II

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50
Q

wave IV latency

A

4.7 ms (mean)
(SD = + 0.5 ms)

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51
Q

above 6 ms latency

A

start to get suspicious

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52
Q

wave V latency

A

5.5 ms (mean)
(SD = + 0.5 ms

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53
Q

latency norms can also be referred to as

A

jewitt norms

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54
Q

Inter-peak values at _____nHL presentation level

A

~80 dB

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55
Q

interpeak I-III

A

I - III IPL: 2.25 ms
(SD = + 0.5 ms)

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56
Q

interpeak III-V

A

2.0 ms
(SD = + 0.5 ms)

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57
Q

IPL I-V

A

4.0 ms
(SD = + 0.5 ms)

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58
Q

what are the transducer for ABR stim

A

inserts

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59
Q

stim type for ABR stim parameters

A

Clicks, chirp, tone burst (short frequency specific signal), and speech stimuli (/ba/, /da/)

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60
Q

what are the polarity for ABR stim paramaters

A

Rarefaction (-ve signal polarity)
Condensation (+ve signal polarity)
Alternating (combined polarity)

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61
Q

rate parameters for abr stim

A

> 20/s, e.g., 21.1 or 27.3/s
90/s useful for neurodiagnosis

typically is 21.1 or 27.7

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62
Q

intensity abr stim parameters

A

Variable in dB nHL – 10 to 90 dB

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63
Q

what are clicks

A

broadband very short signals
2000-4000 Hz

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64
Q

what are tone bursts

A

longer in duration and similar to tones and are frequency specific

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65
Q

which stim type for abr is frequency specific

A

tone bursts

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66
Q

rarefaction polarity

A

negative ve signal

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67
Q

condensation

A

positive ve signal

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68
Q

rate that the click/tone burst is delivered

A

rate

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69
Q

alternating polarity

A

alt on the computer, computer will math add condensation and rarefaction and give a waveform, instead of doing each individually and adding them together
gives better morphology and clearer signal

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70
Q

what is polarity

A

how sound goes in and whether it is pos or neg that it touches the membrane of the headphone

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71
Q

what is neurodiagnosis

A

not looking for hearing estimation sensitivity looking for problems at retro level
usually vestib schwanoma

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72
Q

why are higher rates useful for neurodiagnosis

A

at this higher rate you are stressing the system and causes the abr to fall apart because the system is already stressed with the tumor
stay at 75-80 dB

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73
Q

An ABR response showing all waves in a normal listener is best elicited with a

A

click stimulus at a high intensity (~ 75 to 90 dB nHL

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74
Q

Level in decibels relative to the subjective click threshold level for subjects with normal hearing

A

nHL

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75
Q
A
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76
Q

what happens as the intensity decreases

A

Wave 1 disappears first and with further intensity decrease (at ~ 55 to 65 dB nHL), all waves, except wave V, will disappear

latency of the waves (wave V) increases

morphology of the ABR response deteriorates

77
Q

is wave I disappearing with decrease in intensity normal

A

YES

78
Q

with further decrease in intensity waves disappear but V is this normal

A

yes

79
Q

why do the waves disappear?

A

I-III are tiny waves compared to wave V because the tech isnt available at the moment to keep amplifying without losing them

80
Q

what is the relationship bw latency and intensity

A

intensity and latency relationship - waveforms disappear and latency will increase

81
Q

a ____ in intensity causes a _____ in latency

A

decrease, increase

82
Q

what are the 3 important relationships to understand with decrease in intensity

A

as intensity goes down, earlier waveforms disappear and v stays
as intensity goes down, latency goes up (only wave v)
as intensity goes down, morphonly starts to deteriorate

83
Q

Actual hearing threshold is typically _____ dB HL better than the ABR threshold

A

~10 to 15

84
Q

if wave V threshold is 20 what is the actual threshold?

A

5-10 dB

85
Q

abr ____ threshold

A

overestimates

86
Q

how do you determine wave V and not the other wave shows in 40

A

because as you decrease intensity the latency should increase and on 40 the other wave did not shift to the right

87
Q

ABR threshold is determined at

A

lowest intensity that wave V can be recognized

88
Q

BC ABR resembles AC responses seen with lower intensity air-conducted clicks because

A

poor mechanical characteristics of bone-conduction transducers

89
Q

what can you note about bc abr

A

Morphology is poorer and rarely are five wave responses observed because bone-conducted output is limited
Wave V, however, is clearly visible, which is the one we need to assess

90
Q

limitation of the bone oscillator

A

you cannot go above a certain dB level

91
Q

Latency of wave V is slightly ___ for BC clicks

A

longer

92
Q

what are the increase latency of wave v in BC clicks

A

Adults = increase in wave V latency ~ 0.6 ms
Children = increase in wave V latency ~ 0.7 ms

93
Q

why is the dynamic range different in bc abr

A

With bone-conducted ABR, stimuli rarely exceed 55 dB nHL because you can’t deliver intensity greater than 55 to 60 dB HL via the bone oscillator

94
Q

are limitations of bc in audio also seen in abr

A

yes but worse with abr
cna only go up to 55-60

95
Q

why do we lose earlier waveforms in bc abr?

A

because we can only do low intensities and these low intensities causes those waves to disappear

96
Q

would almost 7 ms be normal in bc abr

A

yes but in ac abr would be abnormal

97
Q

what will you see in bc abr

A

poor morphology
loss of other waves regardless of normal/abnormal results
only see wave 5

98
Q

what is neuromaturation

A

nervous system is not fully mature when the baby is born
if it was, they would start walking and hold their head and sit up, etc.
because it is looking at the neurons and pathways it will affect the testing

99
Q

what does that mean for us testing children abr?

A

the norms we have are for adults so we hae to have baby norms
babies change week/week month/month, there is a chart of norms to reference

100
Q

why are abr affected by neuromaturation

A

because we are testing abr for children primarily so because of this we have to understand how their system works
different than adults due to neuromaturation

101
Q

how long until abr looks adult like?

A

2-3 yrs

102
Q

when can you use adult abrs norms for children

A

around age 3

103
Q

Interpretation should include consideration of chronological and developmental age
what does this mean

A

a child can be 3 mos old but was 6 mos premature, so the child chronologically is 3 mos old but biologically they are 6 weeks less

104
Q

what are the abr cautions

A

abr is affected by neuromaturation
abr normal itself doesn’t rule out all auditory abnormalities (low & high freq HL)
sedatioin is usually required for children between 6 mos and 4 yrs old unless they can sleep

105
Q

what is a corner audio

A

everything is no response and then 80-75 dB around 250-500Hz

106
Q

where is a click abr the most sensitive

A

bw 2-4 kHz

107
Q

what are the ideal situation for children with ABR

A

Sedation is generally required for children between ~ 6 months and 4 years of age unless child in a natural sleep stage

108
Q

what do we see with CHL in an abr

A

if whole wave shifts, the time bw I-V is the normal latency just shifted ot the right so the entire waveform is pushed out
to confirm it is CHL, you would need BC to determine

109
Q

why do they not sedate newborns for ABR anymore

A

respiratory depressant for sedation and the young babies would cause them to stop breathing which is why they do not do this on them anymore

110
Q

Wave V was replicable at 70 dB nHL, but disappeared at 60 dB nHL
what is the level of the hl? threshold?

A

55-60 dB

111
Q

Characteristic of SNHL ABR

A

wave 1 prolonged latency (around 2 ms)
relatively normal wave V normal latency
BC abr is normal

112
Q

list what you would see in abr with CHL

A

absolute latency is increased
mechanical issue in the middle ear, need more intensity to get the same levels so things shift out

113
Q

list what you would see in abr with SNHL

A

Wave 1: distal part of the 8th nerve

wave 1 may be absent or increased latency

may see all the wave latencies being higher too

114
Q

BS dysfunction in abr

A

only wave 1 is in tact and is intact and as you increase intensity it is still present (normally should disappear)

115
Q

most common type of spina bifida

A

myelomeningocele

116
Q

chiari ii malformation

A

congenital malformation of brain

117
Q

significant manifestations of chiari ii

A

include structural changes to the pons and 4th ventricle, and downward displacement of the medulla, 4th ventricle and cerebellum into the cervical spinal canal

118
Q

as latency increases, intensity

A

decreases

119
Q

what is stilulus rate

A

how fast the signal stim is delivered

120
Q

stimulus rate has no effect on abr waveforms

A

up to 20/s

121
Q

higher stim rates can ____ latency of ABR waveforms and ____ amp

A

increase, decrease

122
Q

what can be useful in diagnosing neurpathology like vestib schwannoma

A

increasing stim rate especially >90/s

123
Q

why does increase stim rate be useful for diagnosing neuropathology

A

because the nervous system is stressed beyond its functional capacity
Increasing rate with pathology can result in abnormal latency shifts or disappearance of later waveforms

124
Q

Increasing stimulus rate up to 50-90/second typically will have

A

little if any effect on a normal system

125
Q

waht can you see with increasing rate with pathology

A

esult in abnormal latency shifts or disappearance of later waveforms

126
Q

what do latency/intensity studies do

A

determine sensitivity

127
Q

what do rate studies do

A

neuropathology

128
Q

what would a normal rate study look like

A

want to see wave v, everything repeatable and all waveforms are present because you are not increasing intensity so everything is in tact

129
Q

what is the difference between nf 1 & 2

A

nf 2 transmission - dominant
vestib schwanomas
CNS tumors

nf1
cafe au leat spots
subcutaneous & cutaneous tumors (not CNS tumors

130
Q

abr with a vestibular schwannoma

A

tumor side will show wave 1 but no other waves
terrible morphology

131
Q

why do they not do surgery right away to remove it?

A

they sacrifice their hearing because they take away the 8th nerve
they usually leave them alone

132
Q

what are cochlear microphonics

A

characteristic: follows the stimulus exactly so when you change polarity the CM reverses, will see wave reversal
cochlear potential
from the OHCs
important for ANSD

133
Q

how to tell cm from a peak in abr

A

cm peaks will flip and abr always stays up

134
Q

A true ABR response will not reverse based on stimulus polarity

A

true

135
Q

A true ABR response in ANSD will reverse based on stimulus polarity

A

yes because it is not a true ABR

136
Q

what is abr a test of?

A

the nerve is generating the response, measuring neurosynchrony of the 8th nerve

137
Q

if there is dysynchrony, what is clinical manifestation of this

A

they have more difficulty hearing in noise but difficulty understanding in general

138
Q

why do PT with ansd have difficulties

A

because 8th nerve is not firing synchronously and we hear at the brain, 8th nerve is the first piece that goes from the cochlea and taking the information up and if it is effected everything following will get the same message and by brain, brain doesn’t understand the information

139
Q

rarefaction

A
  • polarity
    peak goes down
140
Q

condensation

A

+ polarity
upward peaks

141
Q

alternating polarity

A

sum of condensation & rarefaction

142
Q

how can cm mimic an abr and going all the way out?

A

we know it is a cm because when we reverse polarity can reverse so it is no longer an abr
because of the pathology - cm tends to ring longer

143
Q

how can you figure out if it is an cm or abr

A

waveform reversal

144
Q

what will cm look like in alternating polairty

A

flat line because they cancel each other out

145
Q

why do abr peaks stay up in rarefaction

A

because they are neural responses and that is what they do

146
Q

protocol for any child abr if they fail nbhs

A

start at higher intensity level (75-80)
start with two polarities and if waveform that doesn’t reverse, you are not looking at ansd
if they do reverse, = ansd
*do not start with alternating

146
Q

how do you look for ansd

A

you have to run both polarities first

147
Q

the CM mimics an ABR

A

true

148
Q

what are the guidelines for abr on infant who failed NBHS

A

Perform one run with either a rarefaction or condensation polarity followed by a second run of the other polarity at a 70 to 75 dB nHL intensity
If the waveforms reverse – STOP – ANSD diagnosed!
If waveforms do not reverse, proceed to a threshold search by decreasing intensity and using any polarity
Do NOT use an alternating polarity initially because the +ve and –ve responses will sum resulting in what appears as no response and an incorrect diagnosis of SNHL

149
Q

is management of snhl and ansd similar

A

NO they can be very different

150
Q

relationship between latency and intensity in abr

A

as intensity decreases, latency increases

151
Q

two ways you can diagnose ansd with ABR

A
  1. whole waveform reversal (two polarities)
  2. latency and intensity (latency will not shift to the right with an intensity decrease)
152
Q

Latency will not increase with decreasing intensity

A

ANSD

153
Q

what are clinical apps of abr

A

establish functional integrity of the auditory tract within the peripheral and central auditory nervous system (CANS)

Newborn infant hearing screening and threshold assessment

diagnose ANSD

confirm results of behavioral tests & establish site of lesion

Intra-operative monitoring of CN VIII

Assessment of difficult-to-test and non-cooperative patients such as sleeping/unresponsive patients & very young children

assess children & adults with intellectual disability and psychological disorders (mid and late AERs)

Detection of nonorganic hearing loss (NOHL)

Assessment of developmental disorders such as ADHD and (C)APD (mid and late AERs)

Assessment of dementias (mid and late AERs)

154
Q

te closer you are to the periphery, the____ the latency is

A

shorter

155
Q

AERs

A

auditory evoked responses

156
Q

OAEs are sounds generated within

A

normal cochlea

157
Q

OAEs are produced either n

A

spontaneously or in response to acoustic stimulation

158
Q

strongly implicated and widely accepted as generators of all types of OAEs

A

OHCs

159
Q

associated with absence of OAEs further supporting the hypothesis that OAEs are generated by these

A

Absence or damage of OHCs

160
Q

OAEs are vulnerable to

A

noxious agents all of which can negatively affect the cochlea

161
Q

what could affect/damage the OHCs

A

ototoxic drugs
intense noise
hypoxia (usually babies)

162
Q

give a brief description of what OAEs are

A

pre neural
present when hearing sensitivity is normal
absent in frequency regions where cochlear hearing loss is >/= 30-40 dB HL

163
Q

reliable OAEs are abtained between

A

around 500-8000 Hz

164
Q

provides the mechanical source of OAE energy

A

motility of OHCs

165
Q

can OAEs be absent in normal ears

A

yes, but very rare

166
Q

why are they not affected by neuromaturation?

A

because they are developed by month 5, when you do oaes it doesn’t matter if they are a newborn or not you will still see them due to fully development of them

167
Q

when does abr start to look adult like and use their data

A

2-3 yrs old

168
Q

what is a limitation of OAEs

A

PT must sit/sleep quietly for a few min to complete the test
only allow for prediction of HL

169
Q

what could an absent oae predict

A

anything from mild to severe snhl or middle ear disorder

170
Q

present OAEs do not rule out

A

mild snhl, auditory processing disorders, or cn viii disorders

171
Q

why are OAEs great screening tools but not diagnostically

A

because they cannot determine the severity of HL

172
Q

what are soaes

A

spontaneous oaes
elicited without external stim

173
Q

how are soaes measured

A

place a sensitive miniature microphone in ear canal

174
Q

is there a correlation bw tinnitus and soaes

A

NO

175
Q

what are teoaes

A

transient evoked otoacoustic emissions
occurs in response to a brief acoust stim (click/tone burst)
age dependent

176
Q

how are teoaes age dependent

A

decreased amp as fxn of age with normal hearing

177
Q

waht are dpoaes

A

distortion product oaes
these are a result of the nonlinear behavior of a healthy cochlea fxning as a nonlinear system

178
Q

how are dpoaes administered

A

simultaneously presenting pure tones of two appropriate frequencies (f1 & f2) presented at two intensity levels (L1 & L2)

179
Q

what elicits the best DPOAEs response in humans

A

2*f1-f2

180
Q

why are oaes not measurable with ME pathology

A

responses are attenuated by ME pathology because it is not effectively transmitted through the ME system to be measured in the ear canal

181
Q

what would you expect to see in OAEs with PE tubes?

A

may see responses or may see nothing
cannot say they failed because you know they have a tube

182
Q

what are ME paths that could affect OAEs

A

pe tubes
negative me pressure (C)
collapsed ear canals

183
Q

should you repeat OAEs after ME is healhty again?

A

YES

184
Q

what would you get in OAE of negative type c tymp

A

variable responses

185
Q

can you meausre oae in type b

A

do not do oaes
due to fluid and will attenuate the stimulus so they cannot be measured

186
Q

what are collapsed ear canals? who gets them?

A

kids (up to 2 years of age)
cartilage isn’t fully formed so it is not hard and it causes a problem when headphones are used because it will close the canal with the tragus

old people
as we grow older skin loses elasticity and the cartilage isn’t as firm so when you put the headphone on you collapse the canal with the headphone or you push the enlarged tragus into their canal

187
Q

what should you do before performing oaes

A

otoscopy and tymps

188
Q

clinical uses of oaes

A

NBHS
hereditary HL
monitor cochlear status (noise exposure/ototoxicity)
difficult to test populations (young kids, NOHL, unresponsive PTs etc.)
site of lesion testing (cochlear vs retro)
diagnosis of ANSD)
confirmation of results of behavioral tests

AUDE 5410 Aud-Vestib Disorders (18 decks)

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