Note that these are talking about small-e empathy; they in no way address any big vs small E issues. Still relevant, though.
Also - I'll probably (if I get approval) be doing my term paper for my other cogsci class on the same topic, except organized so as to prove a point rather than critique the studies' research methods (which was ostensibly the goal of this paper); I'll post that when it's done, probably in a month or so.
If I end up doing an honors thesis next semseter, there's a very high likelihood that it will be about some aspect of empathy - if at all possible, about big-vs-small -E issues. Who knows, I might even manage to snag some fMRI time if I can get one of the key-holding profs interested enough. :-P
The two articles I chose relate to empathy, and how it is likely based on a simulation model “run by” the mirror neuron system.
My first exposure to this explanation was in Neural Theory of Language, with an article by Vittorio Gallese on (as far as I know) the first discovery of mirror neurons in monkeys. As a research finding, this is interesting but not particularly compelling until you combine it with a few other things to get at a much more relevant big-picture. By using the mirror neuron system, monkeys – and humans – can create a sort of “simulation” of the person they’re watching… a simulation that is just short of being actual muscle movement (and actually is that in certain disorders).
The first article (Shenk et al.) takes a look at autistics – people who, among other things, have major impairment in their empathy – to see whether they have correlated mirror neuron deficits with EEG analysis. This is a correlational study only. In previous studies, the group has established that mu frequency band (8-13 Hz) oscillation suppression in prefrontal cortex areas (C3, C4, & CZ) is correlated with mirror neuron activity. They then measured the activity in these areas with EEG while two groups (one autistic, one normal) were exposed to four stimuli.
The first was white noise, used as a baseline; the second was a video of two bouncing balls; the third was a video of someone else’s hand moving; and the fourth was the subject moving their own hand in the same pattern as they’d seen in #3. In normals, the balls produce very little effect, watching another’s hand produces significant mu-band suppression, and moving their own hand produces very strong suppression. In the autistics, these were all virtually the same, with the significant exception that there was almost no mu-band suppression when watching another’s hand – an indication that there may be deficits in the underlying mirror neuron system.
Of course, this is a correlational study; it is difficult to see how it could be designed otherwise, as we can neither cause people to be autistic, nor (to my knowledge) directly suppress mu-band oscillations. However, their (very brief) conclusion is still justified; there is significant difference between the two groups, and only for the typically “mirror” activity
is possible that the non-suppression seen was somehow caused by a masking of other abnormal activity in the same area (since EEG is relatively imprecise spatially); this would be easily checked on an fMRI study. It is also possible that the autistic subjects had problems “earlier in the line” than the mirror neuron activity that would cause their mirror neurons to show abnormal suppression – for example, they might have visual abnormalities, or difficulty perceiving the hand in the picture as a human hand, or other errors in the prerequisites to mirror neuron activity. Again, fMRI study should be able to pick this up, by checking if there is abnormal activity anywhere but in the mirror neuron pathways themselves.
Lastly, it is possible that the abnormalities are linked to some other trait of autism disorders than the lack of empathy; one would have to look at a group of patients who exclusively had empathy deficiencies (or several groups from whom you could obtain a cross-section) to be certain that this is not the case.
The second article (Avenanti et al.) is actually a series of experiments. They use transcranial magnetic stimulation (TMS) of the left motor cortex to examine subjects’ reactions to watching videos of needles being stuck in someone’s hand. Two muscles in the subjects’ right hands were recorded for motor-evoked potentials (MEPs) – “the first dorsal interosseus (FDI) and the abductor digiti minimi (ADM).” These varied consistently with the location of the needle-penetration in the video – i.e. watching a needle to the FDI caused FDI MEP changes, but not ADM, and vice versa; were not significantly affected by videos of needle penetration of a foot or of a tomato, nor of a Q-tip touching the FDI or ADM; and was correlated with subjects’ subjective ratings of pain intensity and simulation, but not of other qualities (e.g. emotional reactions, compassion, etc).
The researchers use these results to support their hypothesis of a “pain resonance system” – one that topographically mirrors in motor neurons the somatic experiential qualities of what is perceived – i.e. pain intensity – but not any emotional or social factors.
The methods used in the Avenanti studies are sound, but have a couple holes I will mention later. The dissociations they were after to prove topographic representation were effective, though not close together enough to tell how fine a mapping it is (e.g. would the FDI samples also trigger a neighboring muscle?). The correlations with subjective scores are described and interpreted as such, and the researchers do not appear to be making any causal conclusions from those parts of the experiments.
As for the two holes: First, they do not directly address the question – discussed by the authors outside of their direct findings – of how another system of empathy, one that is correlated to emotional / social perceptions, might work; they simply point out that what they were observing (the MEP responses) did not correlate. Presumably this is an area for more research, into whether these are truly two separate systems, or whether they are generated by some sort of single underlying process.
Second, they did not choose a control that was similar a human hand to but obviously not human. It might be that pain empathy is purely a visual mapping – i.e. if it looks like a hand, then you get the result – but it might be that it requires a top-down conception that the target is “like me”. An easy way to do this would be to contrast the effects of two needle-insertions – one of an actual human hand (zoomed out enough to show that it is connected to an actual human, but not enough to add confounding information), and the second exact anatomical duplicate that is effectively visually identical, except that (with the same zoom) it is obviously not attached to an actual human. If this causes a difference, then you would need to posit some involvement of higher-order processes – ones that perhaps could be seen on an fMRI; if not, then this effect is a lower-level one.
Both of these studies support the hypothesis that mirror neurons, and a motor simulation of some sort, is behind empathy. They look at it from fairly different perspectives; the EEG study does not get into theorizing about two separate systems of empathy, nor topographic mapping or any such detail, so there is no direct opportunity for them to contradict on details.
I raised several questions that these studies do not address – though from what I know of the research in this area (which is, at present, “not much”) they are addressed in other studies. It would be good to have more research on exactly what the mirror neuron dysfunction is in autistics, and into whether this might be correctable (and if so, how much it would affect what symptoms). Likewise, the larger question of what the entire experience of empathy is – rather than exclusively the response to visual indications of pain – is somewhat outside the scope of the TMS study; it would require several more studies in series and substantial meta-analysis to tie together, since empathy is a rather complex phenomenon with low-level, cognitive, social, and other aspects.
1. Shenk, Hubbard, McCleery, Ramachandran, & Pineda – EEG evidence for motor neuron dysfunction in autism - http://psy.ucsd.edu/~lshenk/cnsfinal.pdf (print publication unknown)
2. Avenanti, Bueti, Galati & Aglioti - Transcranial magnetic stimulation highlights the sensorimotor side of empathy for pain; Nature Neuroscience 8, 955 - 960 (2005) - http://www.nature.com/neuro/journal/v8/n