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week 1 Flashcards

1
Q

IHC innervation

A

radial afferents and lateral olivocochlear efferents

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2
Q

OHC innervation

A

spiral afferents and olivocochlear efferents

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3
Q

active OHC

A

increased selectivity- Area of BM responds
increased sensitivity- lower amplitudes can elicit response

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4
Q

somatic electromotility

A

this is the idea that the movement of the OHC and the depolarization/opening of tip link process to change the shaper of prestin at acoustic frequencies is what is measured when using OAEs

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5
Q

human auditory bandwidth

A
  • is steeper with the loss of OHC
  • steeper bandwidth cant ever achieve narrow bandwidth
  • to determine bandwidth frequency/8
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6
Q

how does bandwidth change with an increase in frequency

A

it gets bigger
- at higher frequencies wider bandwidth than at low

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7
Q

how is the CF spaced along the BM

A

logrithmically, so at the base (high freq) there are bigger changes in CF and at apex there is a smaller change

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8
Q

what are otoacoustic emissions

A

they are sounds that cross the middle ear and come back out (vibrations of OHC travelling outward) eardrum acting as speaker
- effects of outward transmission of OAEs differ by frequency

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9
Q

What sound elicits DPOAES

A

tones

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10
Q

the probe tip has what components

A
  1. a microphone to help with averaging and reducing noise
  2. two transducers (speakers)
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11
Q

T/F the probe tip has 1 channel

A

False there are 2 separate channels keeping the speaker to probe in one channel and the probe to mic in another
- we want to generate 1 tone on each transducer

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12
Q

what is forward pressure level

A

this would minimize standing waves, making probe insertion depth less important

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13
Q

TYPES of OAE

A

Spontaneous (SOAE)
stimulus frequency (SFOAE)
Distortion product (DPOAE)
Transient evoked (TEOAE)

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14
Q

spontaneous OAE

A

no stimulus no clinical use

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15
Q

stimulus frequency

A

tone, not clinically used because hard to separate tone from response since they are at the same frequency

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16
Q

transient evoked oae

A

click and tone
- good because gives info about whole length of cochlea but lots of info that needs to be separated
- response after stimulus bc travelling wave delays so we can separate

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17
Q

distortion product OAE

A

tone pair stimuli
- response and stimulus at different frequencies but occur at same time

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18
Q

what changes in a linear system

A

frequency

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19
Q

combination tone/distortion product

A

generates a new set of frequencies (distortion product)
- produced in cochlea and ANS
2f2-f1

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20
Q

Distortion generator

A

initiated where 2 frequencies travelling waves overlap
- motion of f1&f2 at f2 place

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20
Q

Distortion product

A

-has lower frequency (closer to apex)
smaller
- crosses middle ear

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21
Q

DPgram

A

looks at frequency and DPOAE level compared to noise

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21
Q

sound level

A

at F1 = L1
at F2=L2

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21
Q

T/F noise levels increase at high frequency but hidden by time averaging

A

FALSE noise levels decrease at higher frequency but is hidden by averaging time

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21
DPgram fine structure
graph that looks at the complex changes in DPOAE level that occur for very specific stimulus conditions
22
When does DPOAE crash into noise floor
the tones have opposite phase and similar amplitude they cancel out and fall into noise floor
23
is DPOAE larger for normal hearing or people with damaged OHC
larger for normal
24
what frequency do we use for screening DPOAE of newborns
2-5KHz because their noise is high at low frequencies
25
auditory evoked potentials
arise in the order in which information reaches different layers of the auditory pathways - early components from cochlea late from cortical sources
26
ABR
measures potentials evoked from structures up to and including auditory brainstems
27
which waves are most replicable
I III and V
28
what are the channels of ABR
Channel 1 (left side) has input1- non-inverting and input 2 inverting (blue) Channel 2 (right side) has input 1 non- inverting and input 2 inverting (red)
29
what is the purpose of using a differential amplifier
minimize 60Hz electrical noise and make sure its not sitting on time waveform - amplifies signal and minimizing artefact
30
how many inputs does a differential amplifier have?
3 but we only care about 2 (inverting and non-inverting)
31
formula for differential amplifier
gain x (non-inverting-inverting)
32
what is stimulus for neural ABR
high level clicks at low level presentation - gives us good waveforms
33
what stimulus for threshold ABR
near threshold bursts at medium sensation rates
34
stimulus artificat
short duration electrical impulse drives acoustic membrane to create clicks and casts electromagnetic field that shows up on waveform
35
absolute latencies
WAve 1- 1.5ms Wave 3- 3.5ms wave 5- 5.8ms
36
IWI latencies
Wave I-III= 2.0ms Wave III-IV= 2.3ms Wave I-IV= 4.3ms
37
absolute amplitude
Wave 1 0.4 Wave 5 0.75
38
what causes delays
-stimulus travel delay -travelling wave/filter delay -synaptic delays -excitatory post-synaptic potential time - conduction velocity in auditory nerve fiber and tract
39
amplitude (height of wave) varies according to
of neurons degree of synchronization of neurons - distance between neural generators and electrodes -orientation of dendrites in neucli dipole orientation
40
what is the rule of thumb for travelling wave delay
period of 2 stimulus cycles
41
moment by moment noise has a mean of
0 - it varies but moment to moment the mean is 0
42
how do we estimate the size of the noise
1. look at pre-stimulus time period (since no waveform) 2. observe variability from sweep to sweep 3. subtract 1/2 sweeps from other half cancelling invariant response leaving only noise
43
how do we estimate the size of response?
can't know till we average away noise but we do have norms
44
CMRR
common mode rejection rate - quantifies the reduction of noise by the differential amplifier - amplitude noise vs the impedance b/w electrodes
45
2 rules of impedance
1. low absolute impedance (less 5Kohms) 2. small difference between electrodes (less 2 Kohms)
46
action potentials sum constructively when:
1. there is a change in impedance (entering/exiting canal) 2. or a change in neuron geometry (bending or branching)
47
action potentials sum destructively:
because short duration of AP leads to problems with synchrony - depolarization and repolarization represent opposite dipoles that cancel out
48
categories of auditory nerve disorder
1. Vascular compression of 8th auditory nerve 2. auditory neuropathy syndrome disorder 3. Vestibular schwanoma
49
ANSD
auditory neuropathy syndrome disorder - issues with synchronicity - usually bilateral and effects IHC
50
vestibular schwanoma
benign tumor from schwann cells - usually unilateral - slow growing - high frequency HL subtle vestib. symptoms
51
whats an ABR limitation
has challenging time detecting smaller tumors - if the tumor only affects low frequency it may be undiagnosed because wave 5 latency is dominated by high frequency fibers
52
small tumor vs large tumor in terms of pathology
small tumor- preserve hearing/vestibular large tumor- brainstem involved
53
why do we have more high frequency dominating response
because high frequencies tend to sum consecutively and low frequencies sum destructively
54
what happens when dominating fibers move apically
more fibers move to lower frequencies and wave 5 latencies get longer
55
BIFID waveform
2 small bumps instead of 1 peak - change stimulus rate or polarity to reduce this
56
PAMR
post auricular muscule response initiated at 8-9ms, peak for neg 11-12 and peak for pos 13-15ms - attenuated by sleeping - afects ABR beyond 50 toneburst/second - indicates cochlea has transmitted sound to brain
57
when are IWI abnormal
Wave I-III I 2.4ms Wave III-V 2.3ms Wave I-V 4.5ms
58
59
absent waves but present normal hearing threshold
retrocochlear lesion
60
absent waves and absent threshold
cochlear HL or Cochlear HL and retrocohlear lesion
61
interaural wave 5 latency
difference b/w right and left ear latencies cant be larger than 0.3 or 0.4 or its considered abnormal - however 20% false positives and this is related to the fact cochlear hearing can have asymmetries
62
Wave I and III present no 5
brainstem lesion
63
wave I present and no III or 5
auditory nerve lesion - if wave 2 is present it argues against this
64
what are the stimulus factors that affect ABR
1. Basic stimulus factor (polarity/phase and stimulus- click, toneburst chirp) 2. stimulus rate 3. effect of stimulus level (as level decreases latencies increase and amplitude decrease)
65
low frequency cochelear hearing loss
little effect on ABR
66
flat cochlear hearing loss
normal ABR if sensation levels are high enough
67
flat conductive hearing loss
amplitude decreases absolute latencies longer IWI dont change
68
severe high frequency cochlear loss
IWI I-V shortened wave 1 closer to apex
69
why is Severe HL diagnosis hard
wave 1 absent or delayed wave 5 delayed morphology change
70
how do we do a neurological assessment with cochlear loss
1. Find Wave I the I-V IWI most important metric - try slower rate and alternating polarity 2. Wave V latency 3. compare between ears
71
Goal of ABR threshold
predict audiometry PT behavioural threshold using objective measure
72
What is the IHP correction factor for
to convert ABR threshold to estimate of PT audiometric threshold that can't be measured
73

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