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AUD spring 2020 Electrophys II > Week 11: Late Latency Potentials > Flashcards

Week 11: Late Latency Potentials Flashcards

1
Q

what are the signal-related late potentials? (2)

A

N1-P2 and N2

*also known as exogenous

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2
Q

what are the event-related late potentials?

A

MMN and P3

*also known as endogenous

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3
Q

other terms for exogenous late potentials

A
  • late-latency AEPs
  • Late potentials (LPs)
  • auditory late responses (ALR)
  • slow cortical potentials (SCP)
  • vertex potentials
  • scalp cortical potential?
  • –positive and negative peaks that occur between 50 and 500 ms after onset of the eliciting signals
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4
Q

slow cortical potential waveforms (N1-P2 complex)

A
  • 1962-1972 used clinically and experimentally
  • potentials falling at 100 ms and beyond
  • –p1 latency is 50 ms and was traditionally included, its presence is a matter of filtering
  • P1-N1-P2 sequence occurs within the window of 50-200ms post stimulus
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5
Q

N1 of the N1-P2 complex

A

large negative wave

  • occurs about 80-120 ms after the stimulus
  • the largest negative wave in all EPs
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6
Q

P2 of the N1-P2 complex

A

large positive peak

*occurs around 175-200 ms

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7
Q

N1-P2 or SCP generators

A
  • more difficult to define
  • –higher brain centers receiving input from the auditory system
  • –most contributions likely from
  • —–primary auditory cortex itself
  • —–beyond projections to primary auditory cortex
  • —–secondary areas
  • N1 and P2 generators are different
  • –N1 wave primarily in the auditory cortex bilaterally
  • –P2 has multiple generators within the polysensory frontal areas
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8
Q

when do you get a robust N1, P2 response

A
  • if the patient state is held constant this will give stable and reliable responses
  • a robust response can be recorded with
  • –moderate to high intensity which will give a large N1-P2 amplitude over 2 microvolts
  • –loong duration (50-200 ms) narrow spectrum stimuli will give frequency specific responses
  • these responses are traceable to the limit of perception
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9
Q

how does intensity affect N1-P2 latencies

A
  • for higher intensity stimuli N1-P2 latency is 100 and 200ms respectively
  • at lower intensity levels latencies increase slightly
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10
Q

electrode montage for N1-P2

A

Cz, M2/M1/, Fpz as the ground

*not the Fz amplitude is only 60% of the vertex amplitude

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11
Q

N1-P2 filter settings

A

1-15 Hz

*can do 30 Hz if 15 is unavailable

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12
Q

N1-P2 epoch

A

500-1000 ms (the N1-P2 should be within 400 ms)

*250 ms if you want the window to include pre-stimulus

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13
Q

stimulus type for N1-P2

A
  • toneburst
  • –can use clicks and pips as well
  • 10-20-10 ms (50ms)
  • –avoid 100 ms as it can cause onset and offset responses to destructively interfere
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14
Q

number of sweeps/trials for N1-P2

A

5-20 sweeps per sub-average

  • –this number avoids adaptation and is less time consuming
  • do 2-3 traces then sum to form grand average
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15
Q

repetition rates for adults and children for N1-P2

A
  • 0.5/1.0/second for adults
  • 0.25-0.5/second for children
  • –for both randomize if possible
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16
Q

ways to enhance SCP (n1-p2) response

A
  • randomizing other aspects of the stimulus
  • –ear being tested
  • –test freq or intensity
  • pts should be kept alert
  • –giving a brief break
  • –making them more alert in some other clever way can re-evoke better responses
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17
Q

clinical applications of SVP (n1-p2)

A
  • objective test–passive cooperation (alert) from the patient
  • –they must remain quiet and awake, have them do something like read a book during testing and monitor them to ensure they are awake
  • useful when the accuracy of the PTA results are in doubt
  • –psychogenic cases
  • –patients with learning difficulties
  • –non-organic HL (military, industrial, occupational)
  • responses will be within 10 dB of PTA thresholds
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18
Q

using N1-P2 in medicolegal cases

A
  • the cortical ERA technique is accepted by the british legal system as the definitive test of hearing status
  • SCP validates PTA thresholds
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19
Q

how will auditory CNS dysfunction affect N1-P2 responses

A
  • frontal lesion will have no effect on N1 or P2
  • tempro-parietal lobe lesions will give poor morphology of wave N1
  • auditory plasticity–post implantations means P1 is a good indicator of the extent of neural dys-synchrony that disrupts the cortical development and a good indicator to predict behavioral outcomes in children with ANSD
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20
Q

how to run threshold estimation with N1-P2

A
  • gives frequency specific estimates thresholds
  • -supre-threshold responses start at 60 dB HL
  • –record at lower intensities until threshold
  • –use bracketing technique (20 down, 10 up)
  • —–only need to do like 5 sweeps per trace and 3 traces prt freq
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21
Q

how to determine the threshold with N1-P2

A
  • the lowest intensity with a response present
  • an interpolation to the nearest 5 dB
  • some researchers use a 5 microvolt amplitude criterion
  • –if the response is less than this, that is the threshold intensity
  • –if greater the threshold is 5 dB lower
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22
Q

masking considerations with N1-P2 threshold estimation

A
  • need to consider masking with the same basis of masking as that is used in conventional PTA
  • narrow band noise is preferable if available
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23
Q

what happens with Na-P2 of ‘“poor listeners”?

A

absent N2

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24
Q

limitations of N1-P2

A
  • maturity
  • –an adult threshold estimation test
  • –not fully mature until late teens
  • –viable for children as young as 8 but have immature response with different morphology
  • —–N2 and P3 are often more dominant
  • —–a linger ISI (slower) RR is needed
  • variability
  • –considerable intra and inter subject variability
  • susceptibility to subject’s state and drugs
  • neuroanatomy
  • –is not precisely defined
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25
Q

what event related (Endogenous) potential is rarely used

A

N400

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26
Q

what is the MMN

A
  • mismatch negativity
  • negative component of the auditory event related potential occurring from 100-250 ms after stimulus onset
  • occurs after peripheral encoding–a central presentation
  • “pre-conscious” response (doesn’t require attention)
  • thought to represent detection of stimulus change or “sound discrimination accuracy”
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27
Q

how is the MMN response elicited

A
  • typically by an oddball paradigm
  • –a series of identical repeating stimuli (standard or frequency stimuli) is presented with an occasional “target” interspersed amongst the frequency stimuli
  • –target is different from frequent stimuli along some dimension
  • note responses to frequent and target waveforms are averaged separately
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28
Q

what are the 3 techniques used to “extract” the MMN wave

A
  • target in oddball–frequent in oddball
  • target in oddball–target alone
  • target in oddball–same target presented as a frequent in another oddball
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29
Q

MMN generators

A
  • supratemporal auditory cortex–major generator
  • –primary and secondary auditory cortices
  • –adult response=larger over frontocentral electrodes
  • frontal and subcortical sources possible
  • parallel processor may occur in separate generators
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30
Q

theoretical explanations of MMN

A
  • frequent stimulus forms a memory trace in the brain
  • –memory template is an automatic sensory event
  • MMN originates from a physiological mismatch or “change detection” when the target occurs
  • MMN generator initiates an attention switch when the target occurs
31
Q

factors that influence the MMN

A
  • development: recorded in infants
  • subject effects: age, gender, pathology
  • stimulus: interstimulus interval (ISI), magnitude of deviance, etc
  • for an MM elicited by musical stimuli, experience and training impact the response
32
Q

development of MMN in infants (newborn)

A
  • can be elicited at a few days of age
  • tonography is different from adults
  • –infant MMN is larger laterally, absent at midline
  • –midline is larger in adults increasing as you move laterally
  • –larger MMN at left temporal electrode than right for adults, no hemispheric asymmetry for infants
  • —–perhaps speech bias for adults?
33
Q

development of MMN in infants that are 10 months old

A
  • can tell difference in native and nonnative consonant contrast change trials
  • in native condition, MMN is present suggesting discrimination of auditory change is occurring
  • the ERP or the nonnative condition only shows a stable continuation of the curve
34
Q

development of MMN in children

A

*study of ids ages 7-11 was not significantly different in latency or amplitude from adults at Fz suggesting complete maturation by 11 yrs

35
Q

summary of pediatric development of MMN

A
  • most child studies indicate MMN is stable in latency and amplitude as compared to other late components of ERPs
  • MMNs in children are large than in adults and the distribution is different
  • –adult: frontocentral
  • –child: broader distribution, including parietal areas
36
Q

subject effects on MMN

A
  • MMN generators change with age
  • –middle aged subjects–larger over right hemisphere
  • –elderly–larger over left hemisphere
  • with complex stimuli, MMN latency is longer in females than males
  • can be elicited during sleep, but is not consistent
  • –when drowsy, latency and amplitude are increased
  • –during initial sleep stages, latency is increased and amplitude decreased
37
Q

stimulus parameters for MMN

A
  • many different feature changes elicit MMNs
  • –frequency, temporal (duration, rise/fall, ISI, pattern), intensity, spectro-temporal changes in speech stimuli (syllables; word/pseudo word pairs), timbre
  • –generally with simple stimuli, amplitude increases when ISI is shortened
38
Q

interstimulus interval (ISI) effect on MMN

A
  • amplitude decreases with age, especially at long ISI

* when short ISI are used, age does not affect MMN

39
Q

probability effect on MMN

A
  • probability of a target affects amplitude: lower probability yields greater amplitude
  • –lower probability also means longer recording time
40
Q

how different does the target need to be for MMN

A
  • generally the greater the magnitude of the difference between the target and frequent stimuli, the larger the response
  • –for MMN a difference of about 10% is usually good
  • MMN has also been elicited by just perceptible and imperceptible stimuli
41
Q

MMN stimulation rate

A
  • is the number of stimuli delivered per unit of time
  • fast rate is desirable
  • –ISI of 300 ms works well for simple stimuli
  • if rate is too fast, response will diminish
42
Q

randomization with MMN

A
  • pseudo-random
  • –meaning stimulation is random, with certain constraints
  • —–for example maybe having 3 standards precede a target
43
Q

MMN electrode montage

A
  • minimally you need the midlines (FZ, Cz, and Pz), an inverting, and extraocular
  • its nice to add Fpz, F4, F3, C4, C3, P4, P3 to see hemispheric effects
  • inverting= noise, mastoids, or linked lobes
44
Q

MMN recording parameters of filter, time, averages, ISI, and probability

A
  • filter: 0.1- 30 or 100 Hz
  • time (ms): -50 to 500 (response around 200ms?)
  • probability of oddball: 5-20%
  • ISI: 50-4000 ms
  • number of averages: at least 1400
45
Q

MMN are variability and replicability

A
  • variability: the dispersion of the data
  • replicability: can you obtain the same result more than once
  • –generally, replicable at group level but not individual level
  • –frequent and target waveforms are replicable, but difference waves are not
46
Q

MMN clinical applications

A
  • cognitive brain research unit says yes: they have looked at or are looking at
  • –alzheimers
  • –parkinsons
  • –schizophrenia
  • –dyslexia
  • –alcoholism
  • eval speech perception
  • assess pre-language function
  • assess auditory processing skills in infants (APD)
  • document neural plasticity with auditory, phonologic, and language intervention
  • assess benefit from hearing aids and CIs in children
  • determine capacity or talent for music and learning foreign languages
  • prognosis of outcome in comatose pts
47
Q

MMN in dyslexia

A
  • dyslexia is the inability of the auditory cortex to encode complex sound patterns with fast temporal variation
  • –reduced amplitude speech elicited MMN but not for tonal elicited MMNs
48
Q

alcoholism and MMN

A
  • seems to enhance MMN

- –possibly CNS neurons are hyper-excited due to neuroadaptive changes taking place during a heavy drinking bout

49
Q

alzheimers and MMN

A
  • decreased amplitude of MMN, especially with long inter-stimulus intervals
  • –thought to reflect reduces span of auditory sensory memory-fast decay of memory trace
  • –results in parkinsons disease are similar
50
Q

schizophrenia and MMN

A
  • reduced MMN for both long and short ISIs
  • –suggests that the memory trace for the standard is not adequately formed
  • –perceptual abnormality
51
Q

MMN limitations

A
  • clinical application is not recommended at that time because of several reasons
  • -individual responses (very small) vs group responses
  • –efforts to improve recording techniques
  • —–needs better ways to extract MMN from the noise
  • —–improve SNR
52
Q

what is the P300

A
  • an endogenous potential
  • positive-going evoked potential with a centro-parietal maximum amplitude, and a peak-amplitude latency of 300-350 ms in young adults. peak can be from 250-400 ms
  • believes to reflect cognitive processing and used as a marker of cognitive changes with various clinical groups and in studies of life-span development
53
Q

factors involved in the generation of the P300

A
  • involves many cognitive processes including
  • –discrimination of sound characteristics
  • –temporal auditory processing
  • –attention
  • –memory
  • presence depends on detection of difference between target and frequent sound
54
Q

P300 background

A
  • discovered in the 1960’s and has contributed significantly to understanding of the brain processes underlying normal cognition
  • in 1965 sutton and more said evoked potential correlates of stimulus uncertainty
55
Q

how are p300 elicited

A
  • commonly elicited using an oddball paradigm
  • subject discriminates a target from a frequent stimulus by responding covertly or overtly
  • the target (infrequent) stimulus elicits a p300 which is absent for the standard (frequent) stimulus
56
Q

p300a and p300b (p3a and p3b)

A
  • p3a has a shorter latency than p300 and doesn’t require attention to the target
  • –more robust when predictability of target is low
  • –has a more anterior scalp distribution than the parieto-central distribution of the traditions p300, has a comparatively short peak latency (220-20 ms) and rapidly habituated
  • –is believed to reflect frontal lobe functioning
  • p3b is what we traditionally think of as a p300; it occurs with attention to a target stimulus
57
Q

theory of p300 amplitude

A
  • depends on synchronized firing of large numbers of neurons
  • when the neural representation of the stimulus environment changes due to a new sensory input (target) working memory updated
  • amplitude indexes attention resource allocation and the amount of attention resources engaged during information processing
58
Q

theory of p300 latency

A
  • reflects stimulus classification speed
  • since p300 latency is an index of stimulus processing, it can be used as a motor-free measure of cognitive function
  • p300 peak latency has been found to be negatively correlated with mental function (as measured by neurohyschological tests of attention and immediate memory)
59
Q

generators of p3a response

A
  • frontal lobe and hippocampus
  • p3a is produced when a demanding stimulus commands the frontal lobe attention
  • frontal lobe lessions and hippocampus diminish the p3a
60
Q

generators of p300/p3b response

A
  • temporopatietal pathway
  • p3b is produced when attention resources are used for stimulus evaluation/memory updating
  • studies on temporal lobotomy pts suggest that p3b originates in the medial temporal lobe
  • the p300 might originate in the right hemisphere and propagate to the left hemisphere through the corpus callusum
  • –larger amplitudes are recorded from the right frontal and parietal areas than from the left
61
Q

three ways to measure and interpret p300 response

A
  • amplitude (microvolt): voltage difference between the prestimulus baseline and the largest positive-going peak of the ERP waveform with a given latency window (ex 250-600 ms)
  • latency (ms): time from the stimulus onset to the point of maximum positive amplitude within the latency window
  • p300 area
62
Q

p300 scalp topography

A

*maximum amplitude in centro-parietal electrodes

63
Q

p300 stimulus parameters of intensity

A
  • amplitude increases and peak latency decreases with higher stimulus intensities
  • when the intensity of the infrequent event is increased from 10 dB SPL to 50 sB SPL,the average reduction in p300 latency was 29.3 ms
64
Q

p300 stimulus parameters of intensity and frequency

A
  • the increase in amplitude and decrease in latency with higher stimulus intensity seems to be more prominent for higher frequency tones than lower frequency tones
  • increased target tone frequency yielded p300 latency
  • –use of masking resulted in an increase in p300 latency
65
Q

p300 stimulus parameter of stimulus probability

A
  • the more improbable the event, the larger the amplitude of the p300
  • p300 amplitude is affected by the number of standard stimuli that precede the target stimuli (more standards= larger amplitude)
66
Q

p300 recording parameters

A
  • can be recorded with eyes open or closed
  • –eyes closed produces less artifact by may cause sleepiness
  • amplitude filter settings 0.1-30 Hz to remove the 50/60 Hz cycle activity
  • electrode montage: at least Fz, Cz, and Pz midline sites to facilitate correct identification of the peak
  • –especially important in the case of elderly or clinical populations where identifying the peak is hard
  • –large electrode arrays (32, 64, 128) can be used to construct 3D tonographic maps and modeling the underlying neural sources
  • inverting electrode site–typically a non-cephalic site such as linked earlobes or mastoids
  • ground electrode- forehead Fpz)
  • electro-ocular activity (EOG) is recorded with bipolar electrodes to monitor ocular artifacts
  • recording epochs range from 800-1200ms depending on test conditions
  • prestimulus interval of 50-100ms
  • minimum number of artifact-free single trials of target= 20
  • stimulus habitation or long testing periods appear to affect the p3a component while the p3b component is more stable
67
Q

response effect of p300

A
  • the mode of response influences the recorded p300

* have silently count or silently count and press a button will give better amplitude than just mentally acknowledge

68
Q

p300 subject parameters

A
  • a number of biological factors directly or indirectly influence the p300
  • in general factors that affect general alertness or arousal levels result in an increase in p300 amplitude and decrease in latency
  • –exercise, drugs lie caffeine and nicotine, food intake, etc
  • gender has small effects
  • –amplitude: females is larger than males
  • –latency for females is smaller than males
  • personality: introverts have smaller amplitude than extroverts
  • genetics: p300 amplitude and latency genetically determined
69
Q

effect of age on p300

A
  • significant negative correlation between age and p300 latency for 6-23 year olds
  • –concluded that latency decreases with increasing age during childhood until it reaches an asymptote during the second decade of life
  • increased myelinization and dendritic aborization
70
Q

effects of aging and auditory thresholds on p300

A
  • studies investigating cognitive function should ensure that all subjects can accurately discriminate the stimuli behaviorally
  • to compensate for the differences in hearing acuity, some investigators have used higher stimulus intensities
71
Q

p300 clinical applications

A
  • practical interpretation of the p300 is that it is an index of general cognitive efficiency
  • –how well an individual can process incoming information
  • p300 peak latencies are prolonged with dementing illness
  • p300 amplitude is reduces and latency increased with intellectual impairment
  • p300 latency may differentiate dementia from depression-associated pseudodementia
  • p300 may be effective for evaluating therapeutic strategies involving cognitive medications or interventions
  • but despite group differences between cognitively impaired populations and controls, p300 isnt sensitive enough to differentiate patients on an individual basis, especially during initial stages of the disorder
  • –similar findings reported for other cognitively impaired pops (autism, minor TBI, MS, epilepsy, aphasia)
72
Q

auditory perception and the p300

A
  • since the p300 is a response to a stimuli that is in some way relevant, it has been used to test some difficult pops for auditory processing problems
  • for these applications, one would be concerned more with the presence/absences of a response rather than the response characteristics
73
Q

clinical application of p300 for CI

A
  • recorded earlier ERPs and 300 for children with CI with both passive and active task paradigms
  • results showed that some children demonstrated they could discriminate the stimuli with the presence of distinct reproducible p300s
  • –for both active and passive conditions
  • for children what did not demonstrate a reliable p300 the presence of a robust n1-p2 complexes supported the audibility of the stimuli
  • suggested p300 may also be used with phonetic and phonemic stimuli and for monitoring the progress of young CI populations
  • ***also reported by another dude that you can use p300 to differentiate pts with functional cortical or auditory processing problems
74
Q

disadvantages of p300

A
  • high inter subject variability and poor spatial resolution
  • –allowing localization of an active site only to within several centimeters
  • although p300 is not sensitive enough to diagnose or deferentially diagnose cognitively impaired populations, it seems to ave potential for applications in the evaluation of specific auditory perceptual skills

AUD spring 2020 Electrophys II (13 decks)

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