COGNITIVE NEUROSCIENCE OF LANGUAGE - Postdoc in San Antonio

COGNITIVE NEUROSCIENCE OF LANGUAGE - Postdoctoral Position
Brain Cognition and Language Lab, Department of Biology, University of Texas at San Antonio

The Brain Cognition and Language lab at the University of Texas at San Antonio is seeking a postdoctoral researcher in the area of cognitive neuroscience of language. The research emphasis will be in understanding adult real time language comprehension. The primary technique used is Event Related Potentials (ERP). The lab also recently acquired a state-of-the-art eye-tracking system. Dr. Nicole Wicha is head of the lab, as well as Chief of the ERP lab at the Research Imaging Center at UT Health Science Center - San Antonio, where a variety of imaging techniques are available, including PET, fMRI and TMS.

Dr. Wicha is an Assistant Professor in Cognitive Neuroscience, and received her PhD in Cognitive Science in 2002 from the University of California at San Diego, under the mentorship of Drs. Marta Kutas and Elizabeth Bates.

Dr. Wicha's lab has several active research lines, many with a bilingual focus, including comprehension of language switches, influences of L1 on L2 comprehension, and the basis of bilingual arithmetic, and more general questions, such as understanding the predictive nature of sentence comprehension, uncovering interactions between different levels of language processing and the intersection between language and other aspects of cognition.

Applicants must have a PhD and a strong background in the cognitive psychology or neuroscience of language, or related fields, as well as statistics and experimental design. Experience with eye tracking, ERP, EEG or other neuroimaging methodologies and analyses is preferable. Proficiency in Spanish, or another language, is beneficial.

This position is available immediately, and will be funded by NICHD SC1 HD060435. Salary is commensurate with NIH guidelines. UTSA is an equal opportunity employer committed to creating a diverse, cooperative work environment. Women, members of under-represented minority groups and individuals with physical disabilities are encouraged to apply.

To apply please send a CV, statement of research interests and 3 letters of references to:
Nicole Y. Y. Wicha, Ph.D.
Department of Biology
University of Texas at San Antonio
One UTSA Circle
San Antonio, Texas 78249-0662

Nicole.Wicha@UTSA.edu
(210) 458-7013
http://www.bio.utsa.edu/faculty/wicha.html

Dispatches from the front of irrational reviewing

Here is a comment taken from a review that a friend just received. Given the reviews I have gotten over the years -- some on papers that Greg and I have written jointly -- I must admit that it takes the edge off a bit to see my friends get hassled this way ... :-) Of course, we all experience this kind of irritation. And it goes without saying that the bad reviews one receives about one's own work are always the most dumbass and irrational.

This stuff, though, is good, a real gem I just saw in a grant review: "they set their goals too high attempting to reveal the "holy grail" of cognitive neuroscience, the brain mechanisms of a particular psychological function."

HUH?? All I can think of is John McEnroe's line, yelled at the tennis umpire: "You can't be serious!! You can't be serious!!!!" My friend, a productive and creative scientist who has done new and cool stuff in cognitive neuroscience, has plenty of street cred. So where a reviewer gets off with this kind of comment is hard to imagine. My mirror neurons and my empathic system are unable to recreate this level of bs.

What was the reviewer hoping for? What is the credible alternative?? Are we looking, instead, for, say, 'just some vague hints concerning some general function'??? What would that even mean? If cognitive neuroscience reviewers think that ambitious and theoretically well-motivated research violates their religious predilections because of the holy-grail-iness of the research aim, they should recuse themselves.

Aren't specific mechanistic hypotheses about specific psychological functions (and their parts) exactly what we should be looking for? I thought we were in the business of identifying the 'parts list' of the mind/brain and figuring out how the parts relate and underlie perception, action, memory etc etc etc ...

And just to round things out ... Here a comment from a referee on a manuscript submission (different genre, different friend) -- equally unusual commentary, though: "The authors' disdain for language as it is used also becomes apparent when they construct their stimuli." Hmmm, really? Wow. Disdain for language, eh? In the stimuli. Right. This reviewer clearly has to stick with decaf ...

Yours from the grail-trail,
David

UNLV Postdoctoral Position: Perception and Cognitive Neuroscience

Postdoctoral Research: Perception and Cognitive Neuroscience (Postdoctoral Position)
Auditory Cognitive Neuroscience Laboratory, Psychology, University of Nevada, Las Vegas

The Auditory Cognitive Neuroscience Laboratory at the University of Nevada, Las Vegas invites applications for a one-year (renewable up to several years) postdoctoral fellowship to conduct research on the neural basis of auditory and visual perception in healthy individuals and in individuals with schizophrenia. Applicants are expected to have completed a Ph.D. in Psychology, Cognitive Science, or Neuroscience, and have published (or had accepted) research in one or more of these areas, with particular expertise and continuing interest in using psychophysical and/or non-invasive brain measurement techniques to understand mechanisms of perception and cognition. The salary range begins at approximately $36,000 annually, depending on years since Ph.D. according to the NIH post-doctoral scale. The ideal candidate will have experience carrying out research using some combination of psychophysical, ERP, MEG, structural MRI, and functional MRI techniques, using software such as Matlab/EEGLAB, Presentation, and BESA. Interviews will be conducted until the position is filled, and the position may begin as early as the Fall of 2009. Apply online at https://hrsearch.unlv.edu by submitting a detailed letter of interest, a detailed curriculum vita including a list of references, and relevant scholarly publications. For specific questions regarding the position, contact Dr. Joel Snyder at Joel.Snyder@unlv.edu. Information about the laboratory is available at http://faculty.unlv.edu/jsnyder/home.html. EEO/AA Employer

Contact Information:
Joel Snyder
Department of Psychology
University of Nevada, Las Vegas
4505 Maryland Parkway- Mail Stop 5030
Las Vegas, NV 89154-5030
joel.snyder@unlv.edu
http://psychology.unlv.edu/html/snyder.html

Can fMRI adaptation demonstrate (or refute) the existence of mirror neurons?

A recent fMRI study published by Caramazza and colleagues in PNAS used an adaptation paradigm and found no evidence for the existence of mirror neurons in humans. Basically, in brain regions that are thought to house mirror neurons, executing the same action twice in a row resulted in an attenuation of the fMRI response (the so-called adaptation effect) whereas executing and then observing the same action did not result in adaptation. The latter finding was taken to indicate that cells in these regions are not coding for both action execution and action observation, as one should find if mirror neurons exist.

Marco Iacoboni questioned this logic by arguing with the source of the underlying signal in adaptation studies:

adaptation paradigms ... change synaptic efficacy, which is invariably associated with a decoupling between action potentials and local field potential. When action potentials and local field potential do not correlate, the fMRI signal correlates with the local field potential, not the action potential. This means that Caramazza is not imaging action potentials. And guess what? Mirror neurons are defined by patterns of action potential activity. (see the full commentary here)

Iacoboni cited a paper by Bartels, Logothetis, and Moutoussis (2008) to support his claim. I wouldn't argue with Iacoboni's general argument that because fMRI may not be measuring spiking activity we cannot conclude from the PNAS study that mirror neurons do not exist (way too many negatives in that sentence but you get the idea). I would argue however with his apparent confidence regarding what the source of the fMRI adaptation signal is.

What Bartels et al. argue (convincingly) is that the BOLD response is complex, being driven by some combination of spiking activity and dendro-somatic activity, the later thought to be reflected in local field potentials. These two types of activity can dissociate and it is possible (likely even) that much of the BOLD signal under some circumstances reflects primarily non-spiking activity. In a specific case where detailed single-cell neurophysiology is available, namely direction of motion specificity in area MT, Bartels et al. argue that adaptation effects found in MT for direction selectivity do not reflect adaptation in spiking activity in MT but rather are a downstream reflection of such adaptation which happens elsewhere. The more general point they make is this:

the presence or absence of adaptation in an area measured using fMRI therefore does not allow for the conclusive inference of either the presence or absence of the neural property in question

So from the Caramazza study we cannot conclude whether cells in their ROIs exhibited adaptation or not in their spiking patterns because the adaption that was observed (e.g., for executing an action twice, the E-E condition) might be nothing more than a downstream reflection (inputs from) the site of the actual adaptation.

Let's run with this possibility. Suppose some upstream area outside the presumed human "mirror system" is actually where the E-E adaptation effect is occurring (note that the human mirror system has been identified using fMRI with its uncertain signal source). In this unidentified area that is sensitive to action execution we might expect to find not only adaptation for E-E events but, if mirror neurons exist, also for E-O (execute-observe) events. Yet no such adaptation was found.

Put differently, Bartels et al. arguments apply to making inferences about the cell properties within the adapting region identified with fMRI, not about making inferences regarding the existence of a cell population somewhere that shows adaptation.

For this reason, I think it is a serious mistake to dub Caramazza and colleagues study as fatally flawed and disregard it completely. It failed to identify any evidence of neural adaptation between action perception and action execution within the human "mirror system". Assuming a "downstream" argument for adaptation effects, what this might mean is that the human "mirror system" is treating action observation and action execution as distinct types of events either because there are no cells in this system that respond to both or because inputs to these regions treated these events as distinct.

At the same time, I think it would be a serious mistake to take this study as conclusive evidence that mirror neurons do not exist in humans. In fact, given our limited understanding of the source of the fMRI signal, I have a hard time taking any single fMRI study as conclusive evidence for anything. One needs converging results from multiple methods to make any kind of strong conclusions.

References

BARTELS, A., LOGOTHETIS, N., & MOUTOUSSIS, K. (2008). fMRI and its interpretations: an illustration on directional selectivity in area V5/MT Trends in Neurosciences, 31 (9), 444-453 DOI: 10.1016/j.tins.2008.06.004

Do mirror neurons exist in humans? A new study says 'no'

Already a new paper to appear in PNAS is generating a buzz in the press.

http://www.newscientist.com/article/dn17192-role-of-mirror-neurons-may-need-a-rethink.html

The study is by Alfonso Caramazza and colleagues who used an fMRI adaptation paradigm. Adaptation was assessed both for observing (O) and then executing (E) actions and executing and then observing (as well as O-O and E-E conditions). Assessing adaption in both directions, E->O and O->E, is critical because (i) if mirror neurons exist, adaptation should occur in both situations, and (ii) adaptation in the case of observing and then executing could be interpreted as motor priming during the observation event. The critical result was that in the regions they examined, fMRI adaptation was found for E-E conditions, showing that there is coding of information relevant to action execution, and also in O-E conditions suggesting prima facie that action observation and action execution are activating the same set of neurons in the ROIs. However, E-O trials did not exhibit adaption, which they should have if in fact there is a shared substrate for observation and execution (it shouldn’t matter what the order of presentation), and neither did O-O trials indicating that the ROIs were not coding perceptually driven information. This pattern of results can be explained if the ROIs are coding action execution information (E-E adaptation) and if observing an action that one might have to execute can prime these action coding regions (O-E adaptation).

This is a significant advance over previous attempts to find adaptation effects in the human mirror system because clear evidence of adaptation was identified, ruling out a power issue, and because they assessed observation-execution adaptation in both directions. This allows the authors to conclude with some degree of confidence that the direct matching hypothesis is incorrect.

So could it be possible that mirror neurons don't exist in humans? I have said that such an outcome would be surprising. But this new result makes me wonder whether there might be something funky about the training situation of macaques in which mirror neurons have been found that lead to the development of neurons with mirror properties. In other words, do mirror neurons even exist naturally in monkeys? ...

Do Broca's aphasics have trouble comprehending degraded speech?

Patients with Broca's aphasia are able to comprehend spoken words quite well, in fact, this preserved comprehension in the face of non-fluent speech production is a diagnostic criterion for the syndrome. This fact -- the dissociation between expressive and receptive speech -- demonstrates that the motor speech system is not critical to speech perception. Or does it?

A study by Moineau, Dronkers, & Bates (2005) suggests that Broca's aphasics have trouble comprehending single words under degraded acoustic listening conditions. This finding has been referred to as evidence supporting an important role for the motor system in speech perception. E.g., see this comment. But how solid is the finding?

Moineau et al. tested three aphasic groups (Broca's, Wernicke's, & anomic), right hemisphere non-aphasics (RHD), and control subjects on a word comprehension test under two listening conditions, clear speech and degraded speech (low-pass filtered and temporally compressed). The comprehension test was a picture-word verification test: Subjects heard a word and saw a picture that either matched or mismatched. They indicated match or mismatch by button press. Non-matching pictures were semantically and phonologically unrelated to the target (to the best of my reading).

In the clear speech condition only the Wernicke's patients showed any deficits on the comprehension task. In the degraded speech condition all subjects performed more poorly -- no surprise -- but now the Broca's patients performed statistically as poorly as the Wernicke's patients and both Broca's and Wernicke's performed worse than controls and RHD patients (Broca's did not differ from anomic aphasics, but Wernicke's did).



In other words, single word comprehension deficits in Broca's aphasia appear to be uncovered by presenting speech in an acoustically degraded form, and under these conditions they look as bad as Wernicke's aphasics. This is a pretty dramatic result! And it provides prima facie evidence in support of a role for the motor system in speech perception/comprehension.

But there's a problem. Two actually. The first is that the lesions in Broca's aphasia are not restricted to the motor system but also likely include many other frontal and parietal regions that may be important for attention, response selection, and other executive functions. Thus there is no direct evidence linking the motor speech system to the auditory comprehension deficit.

The other problem is the way Moineau et al. analyzed their data. Recall that the task is to detect matches and reject mismatches. This is a classic signal detection design. An important factor in signal detection experiments is response bias. Some subjects may have a bias toward responding "yes" and others may have a bias in the reverse direction. This affects the results. Luckily there are ways of correcting for response bias, for example the d-prime statistic which uses the proportion of hits (correct acceptances) versus the proportion of false alarms (incorrect acceptances) to correct for bias. Unfortunately Moineau et al. did not calculate d-primes in their analysis. Instead they simply took the proportion correct in the match and mismatch trials to calculate accuracy scores and this could lead to biased, possibly invalid results. In fact, when they looked at accuracy as a function of "congruence" (whether it was a match or mismatch condition) they reported that Broca's and Wernicke's patients have opposite biases! Wernicke's and control subjects performed better on the congruent trials (they tended toward "yes" responses) and Broca's and RHD subjects performed better on the incongruent trials (they tended toward "no" responses). Anomics showed no difference. These group differences in response bias suggest that the overall findings are indeed themselves biased.

To illustrate the problem consider the following graph. At each point along the x-axis is a different pair of hit and correct rejection scores (indicated on the y-axis) that average to equal the performance level (roughly 63%) for Broca's aphasics eyeballed from Moineau et al.'s graph. These are values that reflect the reported bias, incongruent>congruent. The x-axis labels are the A-prime scores for a given pair of hit/correct rejection scores. A-prime is a biased corrected estimate of proportion correct (it's more intuitive to think about than d-prime scores). Notice that for the same average accuracy, the corrected proportion correct scores (a-prime) vary from .7 to more than .8 and that all of the a-prime scores are greater than the reported accuracy of .63. Average uncorrected accuracy underestimates how well subjects are able to discriminate matches from mismatches in this range of values.



Here is the graph for the eyeballed Wernicke's score of ~53% average accuracy. These are the pairs of scores that reflect the reported bias, congruent > incongruent. Notice that most of the distribution of scores is in the 50-60% a-prime range (unlike Broca's which is higher) but also that there is an even wider spread of possible a-prime scores for the same average accuracy as reported by Moineau et al.



So it is really quite impossible to know how well these patients are performing on the comprehension test when response bias is not corrected. One might argue that even the most generous a-prime score for the Broca's patients is still in the low 80% range and that reflects comprehension deficits. True, but remember that this has to be compared against the a-primes for the control groups and since we can't know their bias corrected scores, we can't evaluate how poorly the Broca's patients are performing.

To be quite honest, this is a paper that never should have been published with this analysis. The concept behind the study is fantastic. It's a shame that we can't interpret the findings. So we still don't know whether Broca's aphasics have disproportionate difficulty comprehending acoustically degraded speech, and still no evidence that damage to the motor system produces significant deficits in single word comprehension.

Moineau, S., Dronkers, N.F., & Bates, E. (2005). Exploring the Processing Continuum of Single-Word Comprehension in Aphasia Journal of Speech, Language, and Hearing Research, 48 (4), 884-896 DOI: 10.1044/1092-4388(2005/061)

Another year of Talking Brains

May 16th marks the second anniversary of Talking Brains. We've gotten a decent amount of positive feedback which we very much appreciate, the online comments to some of our posts have been instructive, and our hit count continues to grow, doubling our monthly average in the last year.



So in general I'm pretty pleased with this little experiment. Again I would like to emphasize that we really want this blog to be a language science community forum and resource, and NOT just a place where David and I get speak our minds. This last year has seen a lot more interaction/commentary and that is a very positive development. Thank you very much to all the folks who have contributed! We hope in the next year to increase the contributions from the research community in a number of ways including more comments/discussion, sending us summaries of your recent pubs to post as guest entries (even an abstract and a figure would be great!), maybe more "interviews", and the less exciting but very useful job listings and conference announcements.

If anyone has any ideas on how to improve the blog please let us know!