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9516 > week 1 > Flashcards

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
Q

DPgram fine structure

A

graph that looks at the complex changes in DPOAE level that occur for very specific stimulus conditions

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22
Q

When does DPOAE crash into noise floor

A

the tones have opposite phase and similar amplitude they cancel out and fall into noise floor

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23
Q

is DPOAE larger for normal hearing or people with damaged OHC

A

larger for normal

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24
Q

what frequency do we use for screening DPOAE of newborns

A

2-5KHz because their noise is high at low frequencies

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25
Q

auditory evoked potentials

A

arise in the order in which information reaches different layers of the auditory pathways
- early components from cochlea
late from cortical sources

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26
Q

ABR

A

measures potentials evoked from structures up to and including auditory brainstems

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27
Q

which waves are most replicable

A

I III and V

28
Q

what are the channels of ABR

A

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
Q

what is the purpose of using a differential amplifier

A

minimize 60Hz electrical noise and make sure its not sitting on time waveform
- amplifies signal and minimizing artefact

30
Q

how many inputs does a differential amplifier have?

A

3 but we only care about 2 (inverting and non-inverting)

31
Q

formula for differential amplifier

A

gain x (non-inverting-inverting)

32
Q

what is stimulus for neural ABR

A

high level clicks at low level presentation
- gives us good waveforms

33
Q

what stimulus for threshold ABR

A

near threshold bursts at medium sensation rates

34
Q

stimulus artificat

A

short duration electrical impulse drives acoustic membrane to create clicks and casts electromagnetic field that shows up on waveform

35
Q

absolute latencies

A

WAve 1- 1.5ms
Wave 3- 3.5ms
wave 5- 5.8ms

36
Q

IWI latencies

A

Wave I-III= 2.0ms
Wave III-IV= 2.3ms
Wave I-IV= 4.3ms

37
Q

absolute amplitude

A

Wave 1 0.4
Wave 5 0.75

38
Q

what causes delays

A

-stimulus travel delay
-travelling wave/filter delay
-synaptic delays
-excitatory post-synaptic potential time
- conduction velocity in auditory nerve fiber and tract

39
Q

amplitude (height of wave) varies according to

A

of neurons
degree of synchronization of neurons
- distance between neural generators and electrodes
-orientation of dendrites in neucli
dipole orientation

40
Q

what is the rule of thumb for travelling wave delay

A

period of 2 stimulus cycles

41
Q

moment by moment noise has a mean of

A

0
- it varies but moment to moment the mean is 0

42
Q

how do we estimate the size of the noise

A
  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
Q

how do we estimate the size of response?

A

can’t know till we average away noise but we do have norms

44
Q

CMRR

A

common mode rejection rate
- quantifies the reduction of noise by the differential amplifier
- amplitude noise vs the impedance b/w electrodes

45
Q

2 rules of impedance

A
  1. low absolute impedance (less 5Kohms)
  2. small difference between electrodes (less 2 Kohms)
46
Q

action potentials sum constructively when:

A
  1. there is a change in impedance (entering/exiting canal)
  2. or a change in neuron geometry (bending or branching)
47
Q

action potentials sum destructively:

A

because short duration of AP leads to problems with synchrony
- depolarization and repolarization represent opposite dipoles that cancel out

48
Q

categories of auditory nerve disorder

A
  1. Vascular compression of 8th auditory nerve
  2. auditory neuropathy syndrome disorder
  3. Vestibular schwanoma
49
Q

ANSD

A

auditory neuropathy syndrome disorder
- issues with synchronicity
- usually bilateral and effects IHC

50
Q

vestibular schwanoma

A

benign tumor from schwann cells
- usually unilateral
- slow growing
- high frequency HL
subtle vestib. symptoms

51
Q

whats an ABR limitation

A

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
Q

small tumor vs large tumor in terms of pathology

A

small tumor- preserve hearing/vestibular
large tumor- brainstem involved

53
Q

why do we have more high frequency dominating response

A

because high frequencies tend to sum consecutively and low frequencies sum destructively

54
Q

what happens when dominating fibers move apically

A

more fibers move to lower frequencies and wave 5 latencies get longer

55
Q

BIFID waveform

A

2 small bumps instead of 1 peak
- change stimulus rate or polarity to reduce this

56
Q

PAMR

A

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
Q

when are IWI abnormal

A

Wave I-III I 2.4ms
Wave III-V 2.3ms
Wave I-V 4.5ms

58
Q
A
59
Q

absent waves but present normal hearing threshold

A

retrocochlear lesion

60
Q

absent waves and absent threshold

A

cochlear HL or Cochlear HL and retrocohlear lesion

61
Q

interaural wave 5 latency

A

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
Q

Wave I and III present no 5

A

brainstem lesion

63
Q

wave I present and no III or 5

A

auditory nerve lesion
- if wave 2 is present it argues against this

64
Q

what are the stimulus factors that affect ABR

A
  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
Q

low frequency cochelear hearing loss

A

little effect on ABR

66
Q

flat cochlear hearing loss

A

normal ABR if sensation levels are high enough

67
Q

flat conductive hearing loss

A

amplitude decreases
absolute latencies longer
IWI dont change

68
Q

severe high frequency cochlear loss

A

IWI I-V shortened
wave 1 closer to apex

69
Q

why is Severe HL diagnosis hard

A

wave 1 absent or delayed
wave 5 delayed
morphology change

70
Q

how do we do a neurological assessment with cochlear loss

A
  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
Q

Goal of ABR threshold

A

predict audiometry PT behavioural threshold using objective measure

72
Q

What is the IHP correction factor for

A

to convert ABR threshold to estimate of PT audiometric threshold that can’t be measured

73
Q
A

9516 (1 decks)

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