Tuesday, 8 November 2011

So many of these posts in a Roe.

Here's my Roehampton update: I got invited for an interview! Through some wonderful fortune an informal meeting and a decent proposal have opened up my first PhD interview opportunity. I've had job interviews before, but they were for lowest-rung manual labour positions usually, and all they were really looking for was some indication of me not being totally useless. This time, I fear my intellect will be under scrutiny from some pretty impressive researchers. My task for the next 6 days is to perfect my academic interview technique whilst learning the research around my proposed idea in sufficient detail. To this end, I have scheduled meetings with Fhionna and Vera, and I am looking into speaking to Abertay's career service.

As for the study portion, that's what this blog is for! Over the rest of this week I will take the basic proposal and elaborate upon its theoretical (and to some extent, methodological) basis. I have very little idea what questions I should expect, but the interview lasts for half an hour preceeded by a wee formal meeting with a current PhD student at Roehampton. Guess I should just cover every reasonable area.

Whilst we're talking interviews, what do you think of this for a smart but not too smart outfit?

Alright, let's start with a basic overview of my proposal: The thing that fascinated me most about mirror neuron research thus far, was Ramachandran's discussion of how only skin nerve signals prevented MN signals from being interpreted by the brain as actual sensation. I looked into this a little further and discovered that there was, in fact, a proposed mechanism through which this inhibition might actually occur. Baldissera et al. (2001) performed a wonderful study in which they found evidence that the spinal cord modulated brain signals according to whether the neurons activated were mirror or not. If the signals were sent by MNs, then the spine would send an opposite command to, in this case, the hand. For example, imagine you are observing an actor lift his hand. Mirror neurons would fire, but the spine would prevent the action being copied by coding for the individual to actually drop his hand. The equal signal for 'lift' and 'drop' cancel each other out, and no action is taken. This inhibition is not a perfect system, but it does seem to be a function of a healthy developed brain. Infants (developing brains) show a tendency to copy movements they observe a lot more readily, as do individuals with lesions in relevent brain regions . Even healthy folks sometimes copy without thinking. I can say with some level of certainty that anyone reading this will have accidentally made a facial expression in response to an imagined or observed expression at some point. The evidence for this is something I want to look into a lot more before my interview.

MN activity occurs with both motor actions, and observing 'touch'. Other studied human abilities show evidence of mirroring proporties, but as they are not motor areas, they are not called mirror neurons I don't believe. This is also something I need to examine more. When one performs a physical action (specifically touch or mouth actions) their motor neurons activate to code for that appropriate physical steps to perform that action. When that same person observes someone else making those movements, roughly 20% of their motor neurons activate in response. These are MNs, and one of the main theories for their purpose is the direct-matching theory . The theory suggests that mirror neurons allow individuals to compare an observed behaviour with an internal representation of how and perhaps why that individual would perform that action. The comparison allows the person to understand both the goal of the action, and the physical steps necessary to reproduce it. This theory has seen support in studies showing MN activity depends on life experience . Ferrari et al. (2003) found that humans who had never played the piano did not exhibit MN activity when watching a pianist. Those who were trained pianists did, as a fine example.

Tim Minchin's Mirror Neurons would be firing harder than dogs pulling a drive-by on a cattery.

Problem with the direct-matching theory is that it should find clear cut support in autism research, but it just doesn't. The Extreme Male Brain theory of autism follows the belief that autism is largely dependent on levels of "empathy" and "systemising". Empathy being the ability to share and understand the emotions and behaviours of others, systemising being one's desire to focus on systems with set rules and logic. Laughing and feeling a single (extremely manly) tear run down one's rugged gristly cheek whilst listening to a Tim Minchin love song, is an example of empathy. Completely overlooking the music to feel entranced at the complex system of black and white keys corresponding to different sounds etc, would be systemising. Males, through a fair amount of research using specially designed self-report questionnaires, have been shown to have more S than E. Females, the opposite. EMB theory follows on from findings that autistic individuals have much higher S and much lower S. They are like males, but...more so.

The reason I explained that, was because the Broken Mirror theory of autism is an overlapping theory that draws much of its theoretical basis from it. BM suggests that autistic folks have malfunctioning mirror neurons, preventing them from being able to 'direct-match' and thus understand the behaviours of other individuals. They would be crap at empathy, in other words. EMB finds this to be true, but very little research has discovered a clear cut link between measures of S / E and mirror neuron activity. It does appear that autistic individuals probably have abnormal MN activity though, so it could just be that measures of E and S are simply in need of a lot of alteration.

Mirror neurons refer only to action and touch at present, and my own perspective of autism (both from a non-informed perspective and from a research informed perspective) is that autism involves the incorrect (or indeed lack of) perception of emotions, more than the incorrect understanding of behaviour. I decided to look into a phenomenon called emotional contagion. This is the tendency for humans to experience the emotions of other humans around them to some extent. A good amount of research shows that this involves one part actual experience of the emotion, and one part copying of the facial features / gestures related to any given emotion. This latter part results in a sort of... "Why am I making this facial expression? Oh, I must be feeling X emotion" experience.

Don't believe me about emotional contagion? Watch the hell out of this, chum:



One of the most viewed videos on Youtube with almost 208 million views. You know emotional contagion exists, and so do 207,999,999 other people. If you aren't at least smiling, you've either watched this too much already or you've having a really bad day.

EC ties in very nicely with direct-matching theory in ways I will illustrate with a couple of great studies. Wicker et al. (2003) looked into the neural mechanisms underlying the experience of disgust and its seemingly contagious nature. Note the similarities between EC and mirror neurons. MN activation could easily be described as 'physical contagion' in another world. Participants were asked to lay in an fMRI machine and watch short clips of people looking into a glass filled with liquid and cringing in disgust after smelling it. The participants were then given a rank smelling fgas to inhale to envoke their own disgust reactions. They found the same area of participants' brains activated both during the experience and the observation (mainly the anterior insula) The researchers referred to MN research in their description of their findings:

"Thus, as observing hand actions activates the observer's motor representation of that action, observing an emotion [disgust] activates the neural representation of that emotion."

Using a different emotion, the experience of pain, Morrison et al. (2004) found very similar results in pain-related areas (right dorsal anterior cingulate cortext or ACC for short). Emotional contagion is not so clear cut as MN activity. The primary problem is that people can experience an emotion just because of an oberved stimuli, so the 'reflection' of an observed emotion might sometimes be a direct experience rather than just an empathetic understanding. With physical actions, when the brain activates in response to an observation, all a researcher has to do to identify whether it is just a 'reflection' is to watch if the participant is copying the movement instead of just observing it. Regardless, it is very clear that healthy adult humans are readily capable of sharing the emotions of others. Look at the laughing baby if you have forgotten, or explore the concept of anthropomorphic representations

Death, from Terry Pratchett's 'Discworld' series is as fine an example as one can get of the human tendency to apply human characteristics, primarily emotions, to non-human objects, beings or phenomenon. Oh bugger.

At this point, the purpose of my research proposal can be understood. Mirror neuron activity can be, and is, inhibited to prevent individuals flagrantly copying every action they observe which causes MN activity. Their activity is reliant upon experience; learning a new ability causes mirror neurons to fire when observing that ability where they did not previously / mirror neurons for one area can be trained to fire when an individual observes behaviour in a different area. Lesions to relevent brain areas can prevent mirror neuron inhibition, as can the loss of skin nerve signals through numbing or loss of skin. Autistic individuals, in many cases, display much less mirror neuron activation than unafflicted individuals.

Aaaaaaall of this research tells us that we have a mechanism for leanring and understanding behaviours than can be modulated by experience or various medical conditions. We are increasing our neurological understanding of how inhibition and modulation can occur and we are attempting to apply the findings to autistic individuals and other conditions in such a way where we can better understand and aid them. This research is wonderful, but neurological studies about how individuals 'mirror' emotions are lacking many important features. My proposed study is intended to examine possible neurological mechanisms for the inhibition of emotion contagion.

We are capable of ignoring emotional stimuli, or letting it affect us more than it should. We feel more emotional contagion for people we know well than people we do not, and some individuals are much more prone to it than others. If we feel one emotion very strongly when we are presented with emotional stimuli of an opposite kind, that may affect the way in which we are 'infected' with the opposite emotion. Learning how, when and where emotional contagion is inhibited may have valiable rammifications for the study of empathy and those who have an abnormally greater or lesser ability to experience it. If we can understand how / where emotional contagion is inhibited in different situations, that knowledge could be applied in treatment and care.

That is the basic overview of my proposal. My next article will be a deeper investigation into the current emotional contagion research and the backgorund of a bunch of mirror neuron stuff which informs some of the assumptions I have made. Until then!



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