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Advanced Diagnostic Audiology > W8: MLR & LLR > Flashcards

W8: MLR & LLR Flashcards

1
Q

What does an EEG measure?

A

the electrical fields produced by large groups of neurons

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2
Q

An EEG signal is a ____ recording

A

line

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3
Q

An ERP is a type of ____

A

AEP

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4
Q

Auditory event related potentials (ERPs)/AEPs are ____ signals

A

EEG

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5
Q

What are the two types of recordings for an EEG?

A

1) passive recording: MMN response
2) active recording: auditory P3

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6
Q

Do AERPs/AEPs have high temporal resolution?

A

yes, with millisecond precision

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7
Q

What can ERPs/AEPs provide additional information about?

A

auditory perceptual and cognitive operations

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8
Q

Explain an active recording?

A

Attentive responses: when we give them instructions and they are focused (focused on cognitive details)
- P3
- Exogenic responses

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9
Q

Explain a passive recording?

A

Non attentive response: focused on physical aspects of auditory stimuli
- MMN
- Endogenic/internal responses

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10
Q

What are the 6 layers of the cerebral cortex?

A

1) molecular (plexiform) layer/ superficial layer
2) external granular layer
3) external pyramidal layer
4) internal granular layer
5) internal pyramidal layer
6) multiform (fusiform) layer

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11
Q

in the cerebral cortex, layers ____ are input stations

A

1-4

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12
Q

in the cerebral cortex, layers ____ and ____ are output terminals

A

5 and 6

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13
Q

What are th4e input stations responsible for?

A

sensory information, including info from the auditory system

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14
Q

What 2 things does an EEG reveal?

A

rhythmic brain activity in different frequency bands, depending on:
1) task complexity
2) brain state (mood, time of day, etc)

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15
Q

What are ERPs?

A
  • they are EEG signal epochs time locked to sensory or cogntive events
  • the capability of the brain to get locked at certain stimulus presentations
  • the brain is getting locked on a certain event
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16
Q

Is an ABR an ERP? What is?

A

No, we can record it during sleep
P3 is an ERP

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17
Q

With easier tasks ____ consumption is lower

A

oxygen

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18
Q

Explain the differences between ERP and AEP?

A

Clear instruction and demand to focus on certain parts of the stimulus = ERP

Tests that we can record during inattentiveness and low brain activity (alpha and below) = AEP

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19
Q

What are the 8 different brain waves?

A
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20
Q

What is temporal resolution

A

ability to track the occurrence of brain activity (ex: tracking the timing of ABR waves)

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21
Q

What is spatial resolution?

A

tracking the origin of the response (identifying lesion site/place of dysfunction)

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22
Q

Explain the temporal resolution and spatial resolution for EEG

A
  • high TR (no lag; the response follows the brain activity)
  • low SR
  • non invasive
  • relatively non expensive
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23
Q

Explain the temporal resolution and spatial resolution for MEG?

A
  • high TR
  • high SR
  • non invasive
  • expensive
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24
Q

Explain the temporal resolution and spatial resolution for fMRI and PET?

A
  • high SR
  • low TR (PET ~ 10s) - there is a lag from what has happened in the brain and what you are able to record
    • fMRI ~ 2s
  • minimally invasive (PET)
  • expensive
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25
Q

What do we currently use a combination of in research?

A

Currently in research we use a combination of fMRI and EEG to overcome spatial resolution weakness in EEG and temporal resolution weakness in fMRI

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26
Q

Why should an ABR be recorded alongside cortical AEPs?

A

to differentiate between peripheral and central hearing disorders

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27
Q

What are 4 EEG/AERPs?

A

1) auditory middle latency responses (AMLR)
2) auditory long-latency responses (ALLRs)
3) mismatch negativity (MMN)
4) P300

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28
Q

What is the time window, epoch, or wave latency for AMLR?

A

between 10-50ms after stimulus onset

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29
Q

What are the MLR peaks/waves?

A

two negative and two deflections labeled as:
- NA (~20ms), Pa (~30ms), Nb (~40ms), and Pb (~50ms)
- in some cases, Nb is followed by a positive wave called Pb, which is referred to as P1 in long latency evoked responses

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30
Q

What is the stimuli for AMLR?

A

clicks or tone pips (with clicks producing larger responses and shorter latencies)

31
Q

An AMLR is an ____ response

A

exogenous

32
Q

What is the AMLR sensitive to? (3)

A

Stimulus features:
1) increased amplitudes with increased stimulus intensity to a certain extent
2) shorter latency with increased stimulus frequency
3) change in amplitude and/or latency by sound source location

33
Q

To compare patients using AMLR, what do you need to use?

A

the same stimuli since AMLR is sensitive to stimulus features

34
Q

What is the origin of the AMLR?

A
  • generated in or near the PAC
  • modulated by prefrontal cortex
35
Q

Lesion based studies of the AMLR have shown what?

A
  • temporal lobe lesions can reduce Pa amplitude
  • unilateral prefrontal lesions can enhance Pa amplitude
36
Q

Why do prefrontal cortex lesions enhance Pa amplitude?

A

The prefrontal cortex modulates cortical activity in the auditory cortex (inhibitory impact)

AEPs are under control/modulation by higher cortical areas (when there is a lesion here, there is a loss of inhibitory activity, which causes a greater response/amplitude as there is nothing to inhibit auditory responses)

37
Q

What is the impact of aging on AMLR?

A
  • increased Pa amplitude and latency
  • it may reflect damage or involvement of:
    • 1) the auditory efferent system (top down pathways)
    • 2) prefrontal cortex and reduced inhibitory control
38
Q

AMLR: what is the cause of damage or involvement of the auditory efferent system?

A

APD due to the auditory system involvement (auditory driven)

39
Q

AMLR: what is the cause of damage or involvement of the prefrontal cortex?

A

APD due to the cognitive brain involvement (cognitive driven)

40
Q

Is it possible to differentiate damage in the auditory efferent system from damage in the prefrontal cortex for AMLR?

A

Yes, but very difficult

41
Q

AMLR clinical relevance (2)

A

MLR can be used to:
1) estimate hearing thresholds (showing good concordance with PTA)
2) to assess/differentiate central auditory disorders

42
Q

How can the AMLR be used to assess/differentiate central auditory disorders? (3)

A

1) reduced MLR amplitudes in PAC in auditory radiation lesions
2) reduced or absent Pa in tone deafness (non verbal auditory agnosia) despite normal ABR
3) no MLR change in pure word deafness (verbal auditory agnosis)

43
Q

What is auditory agnosia?

A
  • inability to recognize sounds despite intact hearing
44
Q

What is the place of involvement for auditory agnosis?

A

typically right temporal lesions

45
Q

What are the 4 subtypes of auditory agnosia?

A
46
Q

What is the time window for late auditory evoked potentials (LAEPs)

A

occur 50 to 600 ms after sound onset

47
Q

What is the stimulus for late auditory evoked potentials (LAEPs)

A

elicited using various auditory stimuli: clicks, pure tones, noise bursts, music, environmental sounds, and speech sounds

48
Q

What are the ALLR waves (as one of the LAEPs)?

A
  • P1, N1, P2, and N2, peak at approx 50, 100, 180, and 250 ms post stimulus
  • their recovery cycle is longer than MLRs, requiring a lower stimulus repetition rate (1-3 per sec)
49
Q

Among the ALR waves, the N1 is:

A
  • the most studied and reliable
  • often the largest response
  • easily observable
50
Q

ALLR: What are the brain generators of P1, N1, P2

A

1) thalamocortical projections
2) PAC and SAC

51
Q

ALLR: N1 potential generators based on lesion studies (6)

A

1) STG
2) anterior medial temporal bone
3) temporal parietal junction
4) temporal poles
5) orbital frontal cortex
6) posterior-superior temporal plane

52
Q

Reports of enhances P1 and N1 amplitude in patients with ____, suggesting what?

A

dorsolateral prefrontal cortex lesions, suggesting the inhibitory impact of this brain area on the auditory cortex

53
Q

What is the impact of aging on ALLR?

A

increased P1 and N1 wave amplitude and latency (older vs younger)

54
Q

What are the 2 potential mechanisms involved that affect the ALLR in aging?

A

1) impaired inhibitory functions
2) general slowing in perceptual and cognitive processing

55
Q

The oddball paradigm is an ____ response

A

endogenous

56
Q

How does the oddball paradigm work?

A

when target/deviant stimuli are presented infrequently and irregularly (10% ga) within a series of standard stimuli (90% da)

57
Q

What two populations report abnormal N1 and P2 with ALLR?

A
  • older adults with or without ARHL (age related hearing loss)
  • children with auditory based learning problems (dyslexia, SLI)
58
Q

What are the 5 clinical applications of ALLR?

A

1) monitoring auditory aging/ARHL
2) monitoring the aging impact
3) evaluating individuals with a loss of cooperation
4) monitoring ABLPs and treatment impact
5) monitoring intervention outcomes: in cochlear implant or hearing aid users

59
Q

What is the time window for MMN?

A

a negative LAEP, overlapping with N1 and P2 waves (100-300ms)

60
Q

What are the primary generators for MMN?

A

auditory cortices, specifically the supratemporal area

61
Q

How is the MMN recorded?

A
  • using oddball paradigms (endogenous response)
  • under a passive (inattentive) state, such as watching a movie or reading a book (reflects concurrent sound segregation independent of attention)
62
Q

MMN is a measure of (2)

A
  • discrimination ability in a passive state
  • immediate sensory memory
63
Q

What is the impact of aging in older vs younger adults for MMN?

A
  • reduced MMN amplitude
    • found this using different types of deviant stimuli: such as frequency, duration, and complex tone sequences
    • reflecting reduced discrimination ability in passive hearing
64
Q

Why is there inconsistent results for MMN latency?

A
  • the response is commonly wide, leading to challenges for accurately measuring latency
  • variability is greater
65
Q

MMN has been investigated in what 5 clinical populations?

A
  1. individuals with hearing loss
  2. CI recipients
  3. older adults with cognitive impairments
  4. patients with stroke
  5. children with attention, learning, and language impairments
66
Q

Like other AEPs, MMN is not often used in clinical practice due to what 5 things?

A

1) testing time
2) lack of studies on sensitivity and specificity for APD
3) LACK OF NORMATIVE DATA
4) lack of expertise
5) associated costs for clinics and patients

67
Q

Explain the p300 response (3)

A
  • a positive large response peaking around 300 ms
  • actively elicited using oddball paradigms (endogenous response)
  • recorded using 10-100 trials, depending on target discriminability and participant age
68
Q

What are the 3 neuronal resources for the p300?

A
  • the medial temporal lobe
  • parietal cortex
  • prefrontal cortex
69
Q

Aging impact of p300

A

reduced amplitude and increased latency (reflecting age related difficulty in actively discriminating target stimuli)

70
Q

What is the clinical relevance of p300 (3)?

A

Can be used to investigate auditory disorders involving higher order processes:
- verbal agnosia
- congenital amusia
- language impairment

71
Q

P3 is not affected by ____

A

mild to moderate HL (this is the only AEP that isn’t affected by HL).

72
Q

C: AMLR and N1 (2)

A
  • are mainly related to audibility
  • they are stimulus driven AEPs/exogenous AEPs
73
Q

C: P2, MMN, P3 (3)

A
  • are mainly related to discriminability (passive or active)
  • are cognitive driven AEPs/endogenous AEPs
  • could be used to assess the impact of auditory disorders on discriminating complex auditory stimuli (APD)
74
Q

What are the 5 challenges for clinical use (in general)?

A

1) lack of widely used valid and reliable simulus paradigms
2) lack of norms with sensitivity, specificity, validity, and reliability
3) time consuming
4) expensive/cost associated
5) require training and expertise

Advanced Diagnostic Audiology (10 decks)

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