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In most articles related to ERPs, we discuss in detail about the "peaks and troughs". Many often consider them of very little use saying they only reflect a final outcome of constructive and/or destructive interferences from different sources/dipoles..
I was wondering what information the transition portion from peaks to trough and vice versa give .. Anyone has any idea about this??
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Ali makes many excellent points on this issue. It is worth noting that he is drawing on the proper definition of transition state in the EEG literature, namely actual critical transition states typically assessed via modeling nonlinear dynamics (e.g. via measures of chaos, e.g. lyapunov exponents) often in epilepsy, seizures and other shifts in conscious mode.
I believe Anoop is referring to the time-interval of an ERP waveform that lies in-between a successive maxima (peak) and minima (trough) as a transition period.
Alas, I am not intimately familiar with the nuances of the N2/P3 complex so I'll abstain from recommending readings in that area. I'm certain you'll be able to find what you need with a quick lit search tgh! Or asking an expert on that topic.
It's absolutely true that the same issues that influence transitions influence peaks and troughs directly too. The problem just gets even more complicated when trying to changes in the "zones" between them.
The observation of an auditory "transition zone" being more stable (on what metrics if you don't mind me asking?) is an interesting one though. Do let me know when you get a paper out on that. I'd love to check it out.
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Hi everyone.
Recently, our lab wants to try recording auditory event-related potentials (FFR, MMN, & P300) from CI users. But we are a little confused about the recording techniques. Since CI transfers the sound it "hears" into electrical impulses, EEG recording may be severely interfered by the artifacts.
Our questions are:
1. Is there any way that we can eliminate such electrical artifacts?
2. Is it possible for us to record steady-state potentials like FFR or ASSR from CI users? (Since the FFR or the ASSR dynamically follows the stimulus sound like a "sound recorder" in the brain, we are afraid that the electrical artifacts from CI may totally swamp the brain activities.)
3. If we want to record MMN from CI users using an oddball paradigm, and we use stimulus sounds with long duration (e.g. 150~200 ms), will the electrical artifacts swamp the MMN? 
Thank you!
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Thank you very much! @Thomas Hörberg @Petter Kallioinen
I have a further question about CI-artifacts. Are they similar in temporal waveform to the corresponding stimulus sounds? Because we intend to record a brainstem potential that basically resembles the stimulus sound in temporal waveform. We are afraid that ICA might remove this brainstem activity.
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CE chirps evoke larger auditory evoked responses than the other stimuli such as pure tones. Larger responses could lead to better ASSR detection. Are there any studies or personal experience anyone would like to share?
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The above-referenced Wilson et al.,  2015 IJA paper concerns the 40-Hz ASSR (vs tone ABR)  in awake adults with normal hearing.  Its results are likely less applicable to infants.
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I have measured on the same subject auditory evoked potentials using two different stimulating apparatus and want to know if they are comparable or one better than the other. I am looking for methods that tell me about the morphology of the two waves in an objective fashion. Subjectively the two waves look alike, but need to back that up with some stats.
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Hi Jacinthe, yes I understand that, however, it is not possible to do a keyword search of your publications, thus making it impossible for me to find the relevant article or articles. If you could be so kind as to provide a title or a link or a year of publication I would be very thankful.. Kind regards
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I have read many papers and consult several books but one piece of information cannot be found. Imagine normal human ear is exposed to 1 kHz sine sound that causes normal audible loudness of say 40 db. What kind of electrical signals does cochlear send to the brain? If these are electric pulses all of the same shape, height and width, does their shape, height or width relate to the intensity of sound waves and how? If not, what does?
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Mario,
In the firing for shorter time periods, the rate varies stochastically, even if an auditory fibre is phase locked to a high degree (perfect phase locking is not observed, but vector strengths can be very high, meaning that the vast majority of intervals are locked to the phase of the stimulus). So it really is a question of what you mean by constant. The most exact spacing in time is only achieved during phase locking to high-level sounds at low frequencies – that is frequencies below the maximum firing rate of the fibre. Above that frequency, some of the cycles of the stimulus will be “missed”, i.e. the fibre will not be able to fire again that quickly. However, the spacing of the next firing will still be closely related to the phase (one, two, three cycles, etc). There is no minimum firing rate of auditory neurons in the cochlea – all of them have spontaneous activity that can be from below 1 spike/s up to about 100/s. During phase locking, such spontaneous firings become “locked” to the sound stimulus. The maximum firing rate of primary auditory neurons is somewhat higher than 300/second, pretty much irrespective of the best-response sound frequency. This maximum rate is not restricted to the auditory system but is true for all neurons of endothermic vertebrates. The longer the sound pulse, the more the rate will fall over time, often reaching a lower plateau rate after about 50 -100 ms (this is called adaptation). As I wrote before, it is likely that at low frequencies, the brain uses the spacing of the firings to derive the frequency of the sound (originally called the “volley theory”). Above frequencies where the spacing between firings no longer contains this information, i.e., above perhaps 1-2 kHz in humans (this is a guess), the information concerning the frequency of the sound is only conveyed by the place of origin of the fibres in the cochlea (tonotopic organization). What a firing neuron sounds like (the one in this video has a very variable rate and is not, I think, an auditory neuron) can be heard at:
I am not aware of a web site that offers a real sound recording of cochlear neurons firing, but some firing patterns are shown, for example in:
Geoff Manley
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I know Purdy et al have published reg MLR and CAEP but is there any other clinical application of auditory mid latency responses?
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Transient: Transient Middle Latency responses are used in monitoring Anesthesia during surgery.
Steady Sate:
1. The ASSR for low modulation rate 40Hz-60Hz are good for threshold estimation.  
2. FFR is considered as a possible tool for assessing auditory processing. 
In my view all the above are middle latency responses elicited with different stimuli and in different paradigm. 
If you are looking only at Transient MLR, as of now it has very limited advantages compared to ABR and CAEPs. 
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I have cum across loads of published research on MMN evoked by multiple deviants... Its just intruding to know if the same is applicable for P300?
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P300 is seen for both frequent and infrequent stimuli. As a motor response is expected for infrequent stimulus, sometimes it is hard to distinguish P300 from the mu response. See for more information about P300 with target and non-target stimulus. Katayama, J. I., & Polich, J. (1998). Stimulus context determines P3a and P3b. Psychophysiology, 35(1), 23-33.
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My dataset is to small to continue my research on automatic ABR analysis.
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So sorry Iwona Kostorz, our program is quite young but may be og assistance in the near future. I am sure other older centres might be of assistance
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I'm trying to understand how they work generally, no need for details:
- rate code = position in cochlear / on basiliar membrane with highest sensitivity for frequency (correct me if I got it wrong)
- temporal code / volley theory = unknown (neuron fire rate)?
- ensemble code = no idea
PS: What does phase locking mean in this context?
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The only thing I found is the influence of radii ratio: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2299218/
It's really interesting, but as human's cochlear doesn't vary in radii ratio that much, this should be neglectable.
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I am interested in hearing screening protocols that are standard practice in developed countries. What are standard hearing screening practices in your country?
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Hi there
There have been a number of high profile debates in the literature, especially in the States about this. See the paper by Bess and Paradise (Universal Screenings for Hearing Impairment: Not so Simple, Not Risk Free, Not Necessarily Beneficial and Not Presently Justified. Pediatrics, 93 (2) 330-334.) and the ensuing debate that raged!
In my opinion, the evidence is strong that early intervention (eg hearing aids or a CI) PLUS a committed family suggests much better outcomes for children born with a sensorineural hearing loss. This is supported by good evidence, eg Early intervention after universal neonatal hearing screening: Impact on outcomes by Christine Yoshinaga-Itano et al: Early Intervention and Language Development in Children Who Are Deaf and Hard of Hearing by Mary Pat Moeller, This suggests newborn hearing screening is better than say a health visitor screen at age 8 months.
To my thinking, a screening program is only as good as what happens to the children after they have failed the screen. there is loads of information about the English universal newborn hearing screening on their website, including all the protocols, and the ongoing Quality Assurance programme. The URL is http://hearing.screening.nhs.uk/ Without good diagnostic testing and appropriate remediation, then the screening process will never achieve all that it promised.
Thanks
Penny
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I am studying a rat model for schizophrenia and I am looking at an auditory-oddball paradigm. I am using EEG and ERP under anaesthesia on rats, and I based the study in order to get MMN data, but have since realized that it may also be useful for P3a (but not P3b). Can anyone elucidate the differences between MMN and P3a besides the differences in latency and amplitude?
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The MMN reflects violation of temporal regularity and represent automatic sensory discrimination and is a difference between two reactions:
1- response to unexpected deviant (novelty)
2- response to expected standard, which reflect a perceptual learning (induced by standards presentation).
The P3a represents the response to unexpected deviant (novelty) associated with a shift/orientation of the attention.
From this one can deduce that:
a) the MMN reflects also the perceptual learning while P3a does not;
b) P3a reflects attention shift, while the MMN does not.
However, it is possible to have both components in one ERP as the mechanisms are usually cooperating in healthy organism. I agree with Nike, you can modulate the P3a by inter-stimulus interval and different stimulus saliency. You can also modulate MMN by frequency and other odd-ball parameters.
As the P3a is attention related, it is not clear if you will be able to record it under anaesthesia, although there is some evidence that it is possible http://www.ncbi.nlm.nih.gov/pubmed/8457051 in humans. So it would be worth of trying :)
General comment to statement that MMN is a mechanism independent from attention (or preattentional). The process of perceptual can be modulated by attention and therefore it influences also MMN. For nice review by Sussman see: http://www.psycontent.com/content/l5g4m8504r414560/
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Is there a simple way to describe these as strategies?
What happens (birds / mammals) when hearing? What does each graph on the right side say?
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Daniel,
The bird system is simply a delay line. As the conduction speed of signals in nerves is low, much lower than the speed of electric signals in cables, a series of coincidence detectors as illustrated in the figure can code for interaural delay. The neurons in the delay line will only fire if a signal arrives at the same time from both ears, an by making the nerve fibre from one ear longer than the finbre from the other ear, the cell will fire at a preferred delay. Each coincidence detecting neuron has its own tuning curve (sinusoidal curves in b) and so cover the entire range of interaural delays.
In mammals, all delay-sensitive neurons are tuned with maximum sensitivity to delays outside the maximal possible delay between the ears and the interaural delay is thus directly coded in the level of response (straight part of curve in the purple part of the figure in d).
Coincidentally, the leading expert on this (and author of the paper) Benedict Grothe, happens to sit right across town from you!
Best regards
Jakob