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
2
Q
what are the event-related late potentials?
A
MMN and P3
*also known as endogenous
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
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
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
6
Q
P2 of the N1-P2 complex
A
large positive peak
*occurs around 175-200 ms
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
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
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
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
11
Q
N1-P2 filter settings
A
1-15 Hz
*can do 30 Hz if 15 is unavailable
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
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
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
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
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
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
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
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
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
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
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
23
Q
what happens with Na-P2 of ‘“poor listeners”?
A
absent N2
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
25
Q
what event related (Endogenous) potential is rarely used
A
N400
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”
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
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
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
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
