Mirror Neurons theory of autism refuted by fMRI study

14 May

Mirror neurons come up a lot in autism research. Perhaps the mirror neuron theory is, as one researcher put it, exaggerated with little evidence to support it.

This is discussed in the Simons Foundation sfari blog. Also, the authors have made a video to discuss the mirror neuron theory and their recent experiment (again, I found this on the sfari blog). I apologize that it is not closed captioned.

http://vimeo.com/moogaloop.swf?clip_id=11711513&server=vimeo.com&show_title=0&show_byline=0&show_portrait=0&color=6854a1&fullscreen=1

Normal Movement Selectivity in Autism from Simons Foundation on Vimeo.

I don’t want to just rephrase what has been said in these two presentations, so I will refer you to the sfari blog and the video from the researchers.

4 Responses to “Mirror Neurons theory of autism refuted by fMRI study”

  1. daedalus2u May 15, 2010 at 19:22 #

    Saying this “refutes” the mirror neuron hypothesis is (I think) an exaggeration. All of the subjects were pretty old, the youngest was 19. This is long after when development of a first language and most socialization occurs. The gestures used were not gestures used for communication. The groups were not matched either for IQ or gender.

    Mirror neurons are likely to be most important during language acquisition, where the brain “boot-straps” from primitive and generic neural structures present at birth to the developed and specialized neural structures that instantiate language including verbal, sign and body language(s). Small differences in mirror neurons could be important in the “boot-strapping” of language and then be lost later in life (after language acquisition) when they are no longer needed (and no longer available for acquisition of a first language).

    This is a “null” result, they didn’t observe significant differences in the mirror neuron things they looked at at a 0.05 significance level with 13 male subjects (3 data sets were rejected because of movement) and 10 controls (5 male + 5 female). What they were looking for and didn’t find was amplitude differences. They did find volume differences between the subjects and controls in each of the regions of interest that they looked at (figure 2 supplement). Where every single one of the ROIs was smaller in the autistic group, only one reached “statistical significance”. It sure seems to me that their lack of significance was due to small sample size, not that there was no difference. Using controls unmatched for gender and IQ may have increased the variability in the control group and lessened the apparent statistical significance of any differences.

    I think that amplitude is the wrong parameter to look at, and that volume is a better measure. It is volume that determines how much neural “hardware” is activated, not amplitude. In any case, the “amplitude” that is measured in BOLD fMRI is the difference in magnetic susceptibility caused by changes in perfusion changing the oxyHb and deoxyHb levels. It is increases in oxyHb that cause a decrease in magnetic susceptibility (oxyHb is diamagnetic). The amplitude is calculated by looking at some average magnetic susceptibility and then looking at deviations from that average. This has to be done individually. To a large extent, the selection of thresholds is arbitrary. There were some regions with increases in amplitude in the control brains, there were none in the autistic brains. They mention this in supplementary figure 1, where they also say “Reducing the threshold of the analysis yielded noisy meaningless differences throughout the whole brain as well as in voxels outside the brain.” I really don’t like it when people tell me that data is meaningless and then don’t tell me what the data is.

    I think this means that the dynamic range of the control brains was larger. Whether that is an actual result or a consequence of the weighting thresholds they used isn’t easy to figure out.

    In any case, this is not a compelling case to me that mirror neurons are not involved or are not important in autism.

  2. KWombles May 16, 2010 at 18:31 #

    It should be noted that in the end not all thirteen subjects’ fMRI datasets were used: “The presented analyses are, therefore, based on data collected from ten autistic and ten control subjects who completed the experiments successfully.”

    In addition, the authors argued the fact that their controls weren’t matched added to the weight of their claim, an assertion that makes no sense. I concur with Daedalus2u that this one study is “not a compelling case.” It’s certainly interesting, but that’s about all one can realistically say about it.

  3. daedalus2u May 16, 2010 at 22:33 #

    I have been thinking more about it, and amplitude of the BOLD fMRI signal is really not the way to compare different subjects. The BOLD fMRI signal is in blood flow, not neuronal activity. The degree of neuronal activity is (to some extent) independent of the degree of BOLD fMRI hemodynamic activation. In some cases they are close enough to be useful, but they are not identical.

    They say they do observe greater variability in the autistic subjects, even in the same subject. This suggests that there actually is a difference.

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