1. Flight tickets, bus tickets, walking directions to Uni.
2. Printed copies of CV
3. Printed copy of dissertation?
4. Vera's poster for her research.
5. Notepad + Pen.
6. Snazzy outfit (got to be very snazzy).
Snazzy enough, for ya?
Top shop pose.
Sexy socks, pose.
7. Printed copy of application form / proposal (for fact checking. Possibly print out some of these blog articles to read on the plane?)
8. Will to live / sense of dignity.
Things to know:
1. My proposal, as much as possible.
2. The big studies in mirror neuron research. The basics.
3. Mirror neuron research in relation to direct-matching + Neurological evidence.
4. Mirror neuron research in relation to autism; broken mirrors theory and Southgate and Hamilton's (2008) imitation-based arguments.
5. Emotional Contagion, specifically automatic mimicry and feedback research.
6. Emotional Contagion research in relation to autism, linking it the findings that autistic individuals can imitate, just not automatically.
7. Vera Kempe's research, of which I am taking an active part. Sex differences in temporal resolution power.
8. The names, and general backgrounds of my interviewers; Jon Silas (mirror neurons and social cognition), Diane Bray (Forensic psychology), Michael Eysenck (Cognitive psychology in general, but most recently anxiety based work) and John Rae (Language based research).
9. Some information about Roehampton's fMRI facilities?
10. The building blocks of my answers to: "Why would you want to study here? / What would you do with the training, skills and qualifications you would gain? / Why would you be a more suitable candidate than the next guy?" sort of questions.
With only 2 days left (almost to the hour) before I am sitting across a table from a panel of interviewers, I know I can only retain so much information in my head at such short notice. As such, this will be my last article in preparation for the interview. I have covered all of the most important bases, I think. Mirror neurons in normal / autistic individuals. Emotional contagion in normal individual and today I will write about the research into emotional contagion in autistic folks. In addition to this list, I have a good basic understanding of what Vera is working on, which may come in handy if I'm asked any questions about my current research. After I'm done with this, it will be a case of fierce revision and working out roughly what I would say to the important questions.
"What would you say is your biggest weakness, James?" - "Interview technique. Everything else is brilliant... Promise."
Readers of yesterday's article will know that there is a lot of research yet very few firm conclusions as to how mirror neuron systems contribute towards autism. Southgate and Hamilton (2008) made a series of convincing arguments to suggest that the "broken mirrors" theory of autism was as of yet poorly supported, despite the number of researchers which had taken it on board. The theory relied upon Lacoboni et al.'s (1999) concept of direct-matching, suggesting that autistic individuals had impaired mirror neurons and that explained their less-than-average imitation abilities (e.g. Williams et al. 2004). The problem that S & H found with this, was that there was plenty of research showing autistic children could imitate just fine if they were specifically instructed to do so (Bird et al. 2007). Pretty much all MN research of the direct-matching sort involves participants being instructed to imitate, or to actively observe a specific action, so obviously involuntary 'automatic' imitation isn't required to exhibit the direct-matching system. Indeed automatic imitation fits under the mimicry mechanism of emotional contagion, with which direct-matching has an association but perhaps not direct control (Myself, a couple of days ago). S & H concluded that it was more likely that other characteristic traits of autism (lack of eye contact, less interest in infant-directed speech etc.) make it harder for autistic people to understand when and what to imitate.
Emotional contagion, according to Hatfield et al. (1993), occurs via two overlapping main mechanisms: mimicry and feedback. Mimicry describes the tendency for humans, even from infancy, to automatically copy the facial expressions (Dimberg, 1982), vocal speed and styles (Webb, 1972), and posture (LeFrance, 1979) amongst other physical expressive movements. Before the term was even coined, Condon and Ogston (1966) performed an experiment using high speed cameras to show that his college students would begin to automatically imitate their companions within 21msecs. Muhammed Ali, who was famous for his reaction times, could only manage a conscious reaction within 190msecs of a light cue. Mimicry, then, is a well established automatic reaction to emotional information displayed by a partner in interaction, whether it be direct or via TV etc. Many researchers have supported the evolutionary view, that automatic mimicry is an adaptation to allow us to build up rapport and familiarity with greater ease. Lakin and Chartrand (2003) showed that participants desire to be friends with a person correlated with the instances of automatic mimicry during their interaction. Additionally, individuals who had tried, and failed, to build a rapport with one person show more mimicry than those who have previously succeeded.
Feedback, the second process, makes use of mimicry. The brain notices that the expression/ tone of voice / posture is one of X emotion, so it thinks "oh, well I must be feeling X emotion then". Feedback is a matter of external then internal, rather than the other way around. Evidence for it comes from Laird and Bresler (1992) who found that manipulating participants' expressions did infact influence their self-reports of emotional state. Physiological evidence came from Ekman et al. (1983) who found similar responses in participants' autonomous nervous system when either internally summoning up and emotion or making the corresponding facial expression.
"Make yourself look really angry, then tell me how you feel." Try it yourself and let me know if it works.
So how do automatic mimicry and feedback processes differ in autistic individuals? I.e. do they experience emotional contagion in the same way? McIntosh et al. (2006) believed that as mimicry was fundamental to communication and social factors, it was likely that there would be some level of impairment. They examined automatic mimicry of facial expressions in autistic and non-autistic adults (matched as much as possible in all other attirbutes). There was no automatic mimicry in the autistic group at all. It did not occur, whilst it did in the non-autistic group at expected levels. Supporting Southgate and Hamilton's (2008) criticisms of the broken mirrors theory, voluntary imitation was not inhibited in either group. Beall et al. (2008) used electromyography (EMG) to check skeletal movements in the face showing changes in expressions. Between the years of 7-12 typically developing children showed automatic mimicry of happy, angry and even fear in response to the angry faces. (within 1000msecs of stimuli presentation). Autistic children betwene 8 and 13 showed no mimicry to fear, and inconsistent-but-low responses to happy or angry. Though older children had significantly more responses than younger, suggesting some development even if it is delayed. Hajikhani et al. (2007) and Dapretto et al. (2006) are two examples out of many, that have shown physical abnormalities in face-perception areas of the brain for both neutral and expressive faces.
There are far more examples of facial imitation deficits than in body posture or vocal style for autistic individuals, oddly. In fact there seems to be a series of arguments being made as to why posture mimicry should be studied as with typically developing individuals, but no studies existed that I had access to today. Disappointing, but the evidence above stands to show there are real known problems in mimicry. Indeed, there is some research into developing teaching methods to enable autistic children to learn to automatically imitate better (e.g. Ingersoll and Schreibman (2006). Something that may be related, is the evidence showing autistic individuals do not seem to experience contagious yawning! Senju et al. (2007) showed autistic and non-autistic children videos of people yawning in their experiment, and reported significantly less yawns in the autistic group both during and after the videos. Curious!
As for emotional feedback, impairment of that stems from more than just automatic processing difficulties. In typically developing people, feedback can be induced automatically or voluntarily. In autistic folks, according to Stel, Heuvel and Smeets (2008), it cannot be induced via either method. Unlike McIntosh et al.'s (2006) study they used visible automatic mimicry to judge to first conditions. Participants were videotaped by a hidden camera whilst they watched a video of a man talking about his adventures in a theme park and displaying happy expressions. Participants were then asked to rate their emotions when watching on a simple series of Likert scales. As expected, autistic children failed to display automatic mimicry. This procedure was repeated for the next test, but participants were directly asked to imitate expressions they saw. The results? Autistic individuals showed no significant emotional feedback through either of the studies, whilst typically developing individuals did. The self report measures weren't perfect for tracking emotional change, which is where neurological studies come in. There are numerous studies explaining the complex nature of emotion and the brain, and many to do with autism. Problem is none of them specifically relate to facial feedback that I have found. I will leave this door closed for the time-being, as there is such a thing as learning too much for an examination.
I typed "emotional feedback" into google image search, and this was one of the first results. Brilliant.
So, a brief summary. Autistic individuals display next to no automatic mimicry at all. Their voluntary mimicry is perfectly fine, but they do not recieve emotional feedback from (at least) their own facial expressions during either type of mimicry. All in all, emotional contagion is a highly impaired system for autistic folks and must have a very serious impact on their social lives given that EC seems to be an evolutionary adaptation allowing us to familiarise and affiliate ourselves with each other.
This has been my last study based interview-preparation article. I hope you've enjoyed the series as much as I have! Tomorrow is my last day to ready myself, and I will be studying what I have written and getting it as clear in my head as possible. It is quite likely I will write a brief final post about my last minute choices!
Any study that seeks to look into how something works in your everyday normal adult, is well served by examining how that thing works in people who have some sort of 'abnormal' condition. Abnormal, I should point out, is one of these words that has pretty rough connotations outside of the academic world. When I use the term, I mean "having some condition that the majority of humans don't have". Not "Having a condition which makes them sub-human". The other way round works just as well. When studying panic disorder (there is a faint chance someone might recall) I learned a lot about the condition by comparing how afflicated and unafflicted individuals dealt with their anxiety. It works for almost anything, and is a very good starting point.
In the last few weeks I have been writing about how mirror neurons and emotional contagion work in normal adults, without delving into equivalent research for abnormal folks. One of the main points of contention for MN theories is that it may or may not act as a tool for aiding the process of empathy. Emotional contagion, on the other hard, is widely considered to be a sort of automatic precursor to the full experience of empathy. Dr Silas, my potential PhD supervisor at Roehampton, worked with his colleagues to examine whether adults exhibited any difference in MN activation depending on their self-reported empatyh and systemising levels. Their results, like those of many other studies, answered with "sort of yes, sort of no" (Silas, Levy and Holmes, 2010). They looked at two types of EEG measurement: Evoked Readiness Potentials (nerve activations responding to a presented stimulus) and Induced Mu Desynchronisation (brain signals within the frequency range of 8-13 Hz that are inhibited when individuals observe, imagine or execute certain movements).
I love the look of this equipment so much, here's another picture. Dunno about you, but I'd be sitting there thinking: "Maybe they can actually read my thoughts. Don't think of tits. OH GOD now I'm thinking of them! Chairs! Chairs!"
They had participants go through a number of trials in which they had to press one of two buttons when the corresponding sound was played (execution). The same participants later had to watch another person perform the trial (observation). These simple tasks would allow the researchers to examine ERPs and IMD during aciton and observation. They had participants rate their levels of empathy and systemising using some standard tests that have been shown to fairly accurately measure both traits in previous studies (I am a little confused about which tests were used exactly, as there seem to be a number of different ones used in vairous experiments and I am unfamiliar with the differences between them). As expected given the vast majority of research, males had higher systemising and females had higher empathy to a statistically significant level. The researchers would have been glad to find that females showed stronger IMD during observation (indicating higher MN activity) but then were probably stumped at discovering that there was no correlation between IMD and the empathy/systemising scores. This result has been pretty typical of other studies, such as Cheng et al. (2008)'s.
The experiment had non-autistic adult males and females observing either a moving dot (non MN inducing control) or hand gestures (known to activate MNs). They also asked them to fill in three questionnaires: The Empathizing Quotient (pretty self explanatory for what it does), the Systemizing Quotient (again, self explanatory), and the Emotional Contagion Scale (Hah, now there's an interesting thing). Results? Males and females had significantly different empathy and systemising scores in the expected direction, and for both sexes higher systemising meant less IMD (thus less MN activity). Sounds like a step in the right direction, but although the correlation was statistically significant it was also very small, and measures of empathy did not correlate with MN activation in the main. Silas et al. (2010) mention several other studies which demonstrate some correlations but with many conditions which emphasise the current uncertainty about the relation between MNs and empathy.
Southgate and Hamilton (2008) examined the evidence for this theory that autistic people have abnormally functioning MNs (the broken mirrors theory), and came to the conclusion that it was not sufficient for explaining the difference between the imitation behaviour of un-autistic folks and the abnormal imitation of autistic people. They did not discount MNs as a contributor but just wanted to make clear that they believed the current explanations forwarded by many, to be premature. As my two examples had pretty uncertain results, they may be right. Focussing specifically on imitation abilities as a link between MNs and autism, the writers reviewed relevent studies and then offered their criticism. Imitation problems has been well documented as an issue in autistic individuals, with 21 studies involving 281 children with autism reviewed by Williams et al. (2004). The reviewers noted that overall, children with autism performed worse on imitative tasks. The nature of many of the tasks suggested that the issue was more to do with neural complications between sensing and motor control than with motivation or any other executive function. This is strongly supported by MN research, including that by Lacoboni et al. (1999) which identified the 'direct-matching' function of MNs. All in all, a good amount of research existed for Southgate and Hamilton (2008) to look into.
D'aaaaw. Imitation is awesome.
Along with all of the direct "Hey, people seem to have a mechanism for understanding and learning other people's movements" MN research, there are brain damage studies showing that lesions to important areas of the brain (in most cases, Broca's area) can mess with imitation abilities. Buxbaum, Kyle and Menon (2005) asked 44 patients who had had a stoke in their left hemisphere (where Broca's area is located in most brains) to observe and perform various pantomime movements. 21 of the participants had a condition called ideomotor apraxia which s characterised by the inability to imitate hand gestures or perform voluntarily pantomime actions. They were graded on how accurately they imitated what they observed. In both groups, the ability to recognise the movement they are observing (i.e. having experienced that movement in some way previously, and recall having done so) correlated positively with the ability to 'pretend' doing the movement. What this possibly showed was that destroying internal representations of an observed action corrupted MN activity and so buggered up the usual imitation system.
Southgate and Hamilton's (2008) first of two big arguments against the direct-matching theory of MN supporters is that there is more to imitation than simple mirroring. Young infants (who tend to be as of yet unaware that they are a separate being) have been shown to imitate a model adult doing an action with her head less often when her hands were also occupied. When the model had her hands free but still used her head to switch on a light, the children also used their heads in imitation. When the model occupied her hands with the blanket, the 14 month old infants seemed to decide the only reason she wasn't using her hands was that they were limited, so they used their hands to hit the switch (Gergely et al. (2002). Infants who were not communicated with by the model, would use their heads irrespective of conditions. This showed more complexity than mirroring. The children were influenced by communication and some form of reasoning. Autistic children given the imitation task were nto influenced by communication, and imitated with their head most of the time in either condition. Southgate and Hamilton suggested that this demonstrated that it was the acceptance of communication at fault rather than an impaired internal representation a la broken mirrors theory. Additionally, if direct-matching existed as a way of gradually replacing less efficient actions for more efficient ones as one develops new skills, why did the children swap efficient means (using hands) for inefficient ones (using head)?
The second of their arguments rested on the admission by MN researchers than the MN system is not purely involved in imitation. Rizzolatti and Craighero (2004) were involved in much of the initial macaque MN studies, and noted that although they definitely have them, they rarely imitated each other in the way humans do. Wilson et al. (2005) argued that MNs play a big role in predicting the behaviours of conspecifics (members of the same species). Rizzolati et al. (2001 and many other big names in the area) suggested that their primary role is the understanding, not the imitation, of other people's actions. Impaired MNs should thus impair not only imitation, but these other functions as well if broken mirrors theory is to be credible. In Buxbaum et al.'s (2005) study, the participants with ideomotor apraxia (lesions in MN-areas) showed significantly poorer action recognition as well as imitation abilities, but there is no evidence of similar problems existing in autistic individuals. Carpenter et al. (2001) gave autistic and non-autistic children (2 - 5 years old) a test which asked them to view actions which ultimately failed in their intended purpose. There was no significant difference in ability to identify what the intended action was between groups. I.e. both groups seemed to be able to understand the action purpose fine.
Is the mirror completely intact, then? Or perhaps just chipped a little.
Williams et al. (2004) mentioned above, did a big review and found that autistic kids weren't ace at imitation, but this has more recently been criticised by Hamilton, Brindley and Frith (2007). They asked autistic and non-autistic children to take part in a series of tasks designed to test their ability to copy actions. Both groups performed equally well, and the autistic children even had superior performance in action recognition tasks (though not by much). The reasoning behind the contrasting results? In Hamilton et al's study the children were explicitly instructed to imitate, rather than just hinted at as in Gergely et al's (2002) research. Bird et al. (2007) had the clever idea to pre-specifc the imitation that the participants should perform in reaction to a human or robotic hand making an action. The robot/human would hold their hand with thumb and fingers parallel and facing the roof, they would then either open or close their fingers and the participants (non/autistic) would have to imitate the action. In a second condition the participants were asked to do the opposite action. For both autistic and control groups the compatable imitations occured faster, and the reactions were faster when watching a human hand (animacy bias). All in all, there was no significant difference between the groups. So autistic children can imitate so long as they are specifically instructed to do so. Southgate and Hamilton (2008) suggested that their problems with imitation thus stem from knowing when and what to imitate (social problems) rather than any problem with the actual imitation mechanism. We know that autistic children tend to dislike making eye contact or engaging with infant-directed speech, so having an impaired ability to judge when it would be right to imitate is perfectly plausible.
So I will conclude, that on the basis of the reviewed papers the role of the mirror neuron system in autism is far from certain. Neurological studies have found no clear or reliable link between traditional measurements of empathy and systemising, and direct research of MNs in autistic people have found little to no reliable results. Autistic childen have been shown to have poor imitation, but more recent studies showing that direct instructions result in nromal levels of imitation bring that largely into quesstion. Additionally, if MN impairment was a major contributor to autism then more than just imitation would be impaired, there is little evidence that this is the case. Due to all of this, it very much seems like broken mirrors theory is premature and we have a lot of work to do to narrow down what contribution MNs make to autism.
I'll be looking deeper into the origins and current research findings around the idea of emotional contagion, today. In previous articles I mentioned studies involving the neurological examination of the sharing of disgust and pain, but I haven't yet explained any real background to the larger area. I can't pretend that when studying like that I don't feel the slightest bit anxious that I am going over too wide a range of stuff. I have my proposal, but that was like a surgical strike into the middle of several overlapping subjects that have been heavily researcher. What I am trying to do now is take a step back and do a little recon on the landscape. My interviewers will ask me questions about why I believe my proposal would be of use to the world, and whether it would indeed bring up any useful findings. It's very hard to confidentally claim that it will be successful from this position of what feels like complete ignorance. How are people ever certain about anything? Eesh, it shakes me. So my response is to go broad and hope that my interviewers will realise I have the dedication to spend a lot of time researching and planning carefully, if only I was given the time and facilities to do so effectively. One conversation with a qualified neuropsychologist and I know I would be able to rub out my mistakes and redirect my studies effectively.
For now, I will study and hope. 4 days from now I will be heading back home after my interview with the looming prospect of a 'yes' or a 'no'. How utterly, utterly frightening.
Emotional contagion is quite a lovely term for describing the (often) unconscious transferring of one human's emotional state to other humans. It seems to be one part of the complex phenomenon of empathy. By matching an observed emotion with an internal representation of what that emotion feels like, people often come to experience a ghost replica of that emotion. Paying attention to the replica can bring up the emotion for real. In this way, state Hatfield, Cacioppo and Rapsin way back in 1993; "people can and do 'feel themselves into' the emotional landscapes inhabited by their partners". In their initial defining of the term, Hatfield et al. sought to provide evidence that people mimic facial and vocal expressions, postures and behaviours of other persons around them. As a follow on from this, they attempted to show that people "caught" the emotions of others as a consequence of the facial, vocal and postural feedback. They believed that a mechanism for emotional contagion was important in humans because it would certainly aid coordinating group behaviours and help people keep track of the moods of those around them without heavy individual interaction. There is a lot of research on emotional contagion in the context of mob behaviour, which might be pretty interesting to look at.
A prime example of an angry mob.
Hatfield et al. (1993) noted that emotional contagion is thought to be substantionally different from empathy and sympathy. Primitive automatic transferrance of emotional state via unconscious cues such as posture and facial expression is one thing. Actively understanding an experience someone is going through and combining it with memories of similar experience is another. The two processes probably overlap, but it is important to make this distinction at an early stage. For emotional contagion you don't necessarily need context. See a cute girl cry, you're going to feel down even with absolutely no context. See the character Annie, from Community. I'm quite interesting in this difference in definition as one of the potential benefits of my proposal is to gain further insight into autism by seeing how heavily autistic individuals display emotional contagion if at all.
The researchers identified a number of mechanisms by which it takes place, the first being simple mimicry. They believed that during interactions, people automatically copied movements / facial expressions and coordinated them with the person they are itneracting with. I.e. John smiles a lot and gestures with his hands whilst talking to Sam. Sam picks up the smiling and also begins to make exaggerated communicative gestures. Certainly we have seen unconscious copying of movement reported in infants (mainly lip and tongue gestures, e.g. Meltzoff and Moore, 1977), and in studies showing individuals with lesions in frontal brain areas (Lhermitte et al. 1986). Many studies have noted anecdotal evidence of completely healthy adult participants mimicing actions from time to time, such as mirror neuron experiments where special controls had to be in place to stop identificaiton of MN activity being contamination by the participant copying the aciton they were observing. A chap named Ulf Dimberg (1982) used electromyographic (EMG) data to examine what participants did in reaction to watching happy or angry facial expressions. EMG measures skeletal movements, as opposed to EEG which measures brain activity. When the participants observed the happy faces they displayed an increased amount of muscle activity around their cheeks. When observing angry faces their brows had increased muscle activity instead. The visual signs of these movements were absolutely tiny, but it had been revealled that mimicry was in face taking place.
Mimicry in communicative sounds occurs too, quite interestingly. When individuals speak on their own, into a microphone for instance, their speed and style of speech tends to be a heck of a lot more individual than when they are speaking in a conversation. Coulson, Oviatt and Darves (1996) showed that 7 to 10 year old children changed the sound level of their speech when chatting to a computer controlled voice on 77% of occasions. Adults and children have both been shown to change the speed of their speech (Webb, 1972), and even the type of words they will use when speaking to others (Brennan, 1996). On top of all this, people have also been shown to mimic and synchronize their postures and movements with those of others. Bernieri (1988) described the tendency of students to mimic the stance sof tteachers during interactions, and LeFrance (lol, 1979) found similar amongst students. Both of them mentioned that those who shared their movements more, during interaction, tended to have a better rapport. Guegen (2009) went on to summarize most such research showing that mimicry seemed to be so intuitive and beneficial to human interactions that it had probably been an evolutionary selection. Everything from expressions, to movement, to infectious laughter (Provine, 1992).
A great demonstration of infectious laughter. Here is a video in Dutch without any context. You probably cant udnerstand the language, but will that stop you having a chuckle?
Back to Hatfield et al. (1993). Having outlined the mechanism of mimicry, they felt it necessary to note that conscious mimicry just cannot compete with the lightning fast automatic system that seems in place. They mentioned a test given to Muhammed Ali in which he was asked to detect a light and throw a punch in response. The fastest he could manage was 190msecs to detect and 40msecs more to punch. Condon and Ogston, in 1966, discovered that college students could synchronise their movements within 21 milliseconds (I tried to find this article but it's an oldie and sauntering into the Abertay library aint as easy when you live 50 miles away. For now I'll take their word for it). What this finding means, is that the automatic mimicry is a whole different process from any conscious attempt, and one either has it, or one does not. Remind me to look into whether autistic children show similar levels of it as healthy adults.
Hatfield et al's next proposal for how emotional contagion occurs is that individuals take feedback from their bodies that is both conscious and unconscious, which leads them to determine their emotional states based on what their bodies are doing. This links it to mimicry. If Person A has copied the angry expression of Person B, then Hatfield and co. suggest that Person A would make an un/conscious inference that because his face is showing anger, that he must indeed be angry. If this seems like it would be quite a difficult thing to test, you're not the only one to think so. It isn't impossible, and is one of many psychological testing problems which can be solved by ruthless trickery. A wonderful, wonderful experiment by Laird and Bresler in 1992 involved the researchers telling their participants that the purpose of the experiment was to take complicated measurements of the physiology behind their facial movements. Electrodes were connected to their expressive facial areas and then the experimenter, quite freely, arranged participants' faces into emotional expressions; "Hold still whilst I move your mouth into a smile". Asked to self report their emotional state after the expression shift, participants in the different conditions reported emotional attributes much more akin to the expression they were making. Hatfield et al. (1993) provided a brilliant quote from the study:
"When my jaw was clenched and my brows down, I tried not to be angry but it just fit the position. I'm not in any angry mood but I found my thoughts wandering to things that made me angry, which is sort of silly I guess. I knew I was in an experiment and I had no reason to feel that way, but I just lost control."
When participants were asked by Ekman et al. (1983) to either recall an experience of 6 individual emotions OR produce a facial expression matching the emotions, he found that either action prompted similar responses in participants' autonomous nervous system. This is essentially the 'secondary' nervous system that includes most nerves that are not part of the brain or spinal cord. It controls digestion, heart rate, perspiration etc. So, physiological manifestations of emotion were able to be provoked by making facial expressions as well as remembering an experience... I keep making an angry face to see if I feel more angry. It actually sort of works. Odd. Although feedback from posture and vocals has also been found to provoke emotional change, for the sake of focussing on more relevent material I will exclude it for now.
Here is a generic but rather pleasant artist's representation of neurons to warn you that we'll be moving onto neurological stuff again!
So. We know that emotional contagion happens, and we suspect it happens through a combination of A: Mimicry (as a way of expressing the emotion); and B: Feedback (as a way of actually experiencing the emotion). Do we know what neurological mechanisms are in place to facilitate both of these fairly automatic systems? After all, a highly sprung "PING - mimicry with 21msecs" system seems like it might be a pretty specific mechanism, and having the nervous systems take a hint from body posture or facial expressions alone and start exhibiting the emotions is...well... fascinating. How do these things occur? The question of why, we'll leave to speculation for now.
Well, if you've been reading my blog over the more recently entries, you'll perhaps be able to see the link between mirror neurons and mimicry. Certainly, more modern research into emotional contagion has started by referencing the existence of a mirroring system in motor-related brain areas, and gone on to look at the potential for similar systems in emotional segments of the brain. I've explained mirror neurons enough throughout my recent articles, so I will avoid doing so here. Mirror neuron studies on humans have shown that, without any corresponding movement, observers will exhibit activation of approximately 20% of the same neurons that they would use in order to copy the action they were observing (Lacoboni et al. 1999). One of the theories I find most convincing is that this neurological system is in place to aid understanding of both the purpose of actions, and the physical requirements of those actions. It isn't so hard to imagine the benefits of having a "quick learning" machine that allows an individual to practise skills without actually having to perform them. It's like physical revision. Indeed it might be of interest to you that imagery is a prominent therapy or preparation technique for atheletes. Mirror neurons have been shown to fire when individuals simply imagine the movements, in some experiments. So...imagining competing... theraputic, helps in practise.... see where I'm going with this?
"Direct-matching", the name for that theory, has been supported by enough evidence to be going on with. Primarily this support was given through studies like Lacoboni et al. (1999) where they discovered that there was mirror activation in both the parietal lobe (when observing odd movements) and in the left inferior frontal lobe (when trying to puzzle out the purpose of the movements). The mirror neuron system is very fast, of course. Studies in which neurons are directly hooked up to electrodes (Mukamel et al. 2010, for instance) are capable of showing that the system activates swiftly upon presentation of an appropriate stimuli. Similar, you might think, to the speed in which automatic emotional mimicry occurs a la the Muhammed Ali inspired study by Condon and Ogston (1966). Whilst I do not suspect that the mirror neuron system and emotional contagion are the same thing, I do believe it is possible that having a motor 'direct-matched' representation of, for example, a facial expression could be a precursor to the swift mimicry of that expression. I.e. Person A observes person B smiling. Person A's relevent mirror neurons fire, giving him an implicit understanding of the physical necessities etc. Person A then begins to smile, all within a minimal amount of time. Of course this is not always the case, but that's the whole point of my proposal, isn't it. What mediates that sort of contagion? Of additional interest in the mixed evidence that autistic individuals have a faulty direct-matching system; "Broken mirrors theory". If they do have impaired mirroring, do they also have impaired mimicry?
Having had personal experience of a man with autism, I am conflicted about causes which speak about "curing" or "facilitating the lives of" autistic people. It being a disorder in which there are many points on the spectrum, treating the condition like it is necessarily riddled with depression is almost insulting. None the less I absolutely encourage research into it, and trying to inform people a little more about what is involved.
Mimicry is, on a basic and not yet perfectly understood level, entwined with mirror neuron activity. I believe that, anyway. The systems seem so similar as to make it unlikely that they aren't both involved. As for emotional feedback it is definitely worth examining whether there are any studies showing 'mirror-like' systems in brain areas associated with the experiencing and production of emotion. I'll get back to that, after I've congratulated my Mum on passing her interview and getting a new job!!! Wow! That's got to be a good omen for my Roehampton thing! Brb, celebration.
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Alright, couple of hoursh later and I am... well... Let'sh jusht shay I had to copy/pashte "inebriated" to shpell it correctly. Letsh get back to it....hic!
There is a veritable treasure room of studies showing some extent of 'mirroring' of emotion in reaction to observing physical signs associated with certain emotions. These studies have been limited by how easy it is to provoke participants into giving baseline neural activity for when they show an emotion. It is relatively easy to immediately incite a disgust response, or pain for example. Ethical issues come into play for panic, terror or anger, and it is difficult to accurately prime someone to be happy or sad. Ekman et al. (1983) asked participants to think of a fond memory, which certainly might work but isn't a particularly controllable variable. Despite these issues there have been successful studies. Wicker et al. (2003) used disgust in their fMRI study due to the relative ease of getting participants to feel disgusted and the strong reactions to seeing other people experience it.
Food poisoning has always been a threat to humans. Developing a disgust response based on other human's avoidance of certain food would be a survival advantage and so that response is very pervasive even to this day. Wicker et al. noted that in a range of previous research the insula and the amygdala had been activated during exposure to disgusting smells or tastes. These findings have been supported by fMRI imagining and EEG studies. The insula appears to be activated when observing disgusted facial expressions (Krolak-Salmon et al. 2003). To verify whether the same areas of the insula and amygdala were activated both during disgust and observations of disgust, Wicker et al. gave participants a simple series of tasks. They were asked to observe a video of a small number of individuals smelling into a glass filled with coloured liquid. They either displayed an expression of disgust, pleasure or neutrality. The same participants were later asked to smell a pleasureable or disgusting gas. All tasks took place under an fMRI (so the design was especially clever as it involved little to no movement). Unlike with the pleasant conditions, observing and experiencing disgust did indeed activate the same areas of the anterior insula. The participants were all right handed healthy adult males, so although that study alone doesn't provide concrete evidence, adding all of their cited research makes a much stronger case.
NOT where the disgusting gas was produced... as far as the participants knew.
In a fine example of international collaboration, Cheng, Yang, Lin, Lee and....Decety (2008) conducted an experiment following the same line of thought. Similar neural circuits had become associated with the observation and experience of pain and they wanted to look into it further. They mention in their introduction that the 'initial component' of human empathy is mimicry followed by feedback, the whole shebang that we've been discussing this whole time. Isn't it nice when you get a clue you are on the right path? Their experiment had participants observing static images of body parts in painful or non painful situations (one dreads to imagine). The results, like other studies of pain, showed similar 'mirrored' activity in a whoooole range of brain areas. This particular study focussed on the suppression of the somatosensory cortex but other pain research has spotted many others. The terminology is somewhat too complex for my purposes as of yet. Suffice to say, we have some real evidence of realistic experience of emotion in response to observation, not just physical mimicry.
In summary, emotiona contagion is the automatic transference of emotion between humans. Current research has established evidence for two mechanisms through which this occurs: mimicry and feedback. Humans incredibly swiftly adopt their posture, facial expressions, even vocal style to that of a person they are interacting with (unless consciously inhibited). The speed at which this happens is faster than any realistic conscious effort could manage. The whole phenomenon is heavily supported by mirror neuron research showing activation in motor-related brain areas occurs in response to the observation of certain behaviours (particularly mouth and hand movements...key expressive areas). Feedback draws, in part, from mimicry. It is the process through which the brain decides that because the individual has a certain facial expression / posture / tone then the individual must be experiencing that emotion. An actual experience of that emotion results. This phenomenon is supported by studies showing that simply forcing a certian facial expression can bias self-reports of emotional state towards the expressed emotion. Additionally, neurological studies showing that the same brain areas are activated during experience and observation of an emotion provide strong support. Also, my Mum is awesome!
Important questions: To what extent to autistic individuals experience emotional contagion? Are there any empirically examined differences? If so, what consequences might this have on empathy, given that mimicry and feedback are widely believed to be the precursors to full blown human empathy?
Thanks for reading. This has been a long but pretty fascinating one I hope.
Whilst all of this Roehampton stuff has been going on, I've also been in the initial stages of some voluntary and paid research up at Abertay. I had a meeting with my supervisor Vera today, and she suggested it might be a good idea to go over the subject area that we were delving into during the interview. As a sort of "I'm not a total lay-a-bout! Look what I'm involved with!" As a result, I'm going to write a brief overview of the subject and some of the projects that directly lead up to what I am currently helping Vera with. Bare in mind that as a recent graduate I am hardly fluent in all of this, in fact everything I have been going into in the past month or two has been pretty overwhelmingly 'fresh'. That said, I can feel my critical analytical training kicking in everytime I pick up a journal article, and there's no way to improve one's knowledge without pushing one's limits from time to time.
... or every day preceeding a terrifying important interview.
When individuals attempt to learn the sounds which underly speech, they are presented with the challenge of seperating quite similar sounding tones and understanding them as unique segments of that language's collection of speech sounds (phonemes / tonemes). Several research studies examining why some individuals are more adept at learning their native language then others have identified "temporal auditory sequence processing" as a heavily contributing factor to reading-impairing conditions such as dyslexia. This is a bit of a mouthful, but essentially refers to the ability of an individual to percieve sound information accurately. This is, when sounds begin / end and when very minute changes are made to them. Tallal (1980) performed a study in which she gave 'reading-impaired' and non-impaired children a series of tests which examined these abilities. Her test batteries involved the standard procedure of "are these sounds the same, or different?".
Now, imagine you hear two non-verbal tones one after the other in quick succession. Perhaps you have a "ding" and then a veeeeeery slightly different "deing". The difference in these sounds is so slight that it is far from obvious what the correct answer is. Not everyone would percieve that the "ding" sounds slightly more 'plucked' than the "deing", which is relatively more "bowed". Indeed, as we will come to find, there are large individual differences in participants' ability to differentiate. In Tallal's study, when the stimuli were presented as slow tones, there was no real difference in scores. When the experimenter upped the speed of the tones, suddenly the reading-impaired children started falling behind significantly. What this suggested was that the impaired children were less able to perceive what was essentially the speed at which a sound was faded in. Tricky to explain without a graph, I shall look for one, hang on.
...
Got one! This is the waveform of a 'plucked' violin string. Some tests of the ability of individuals to distinguish two very similar sounds involve the "amplitude envelope onset rise time". The envelop is the outline drawn around the waveform in red there, and the onset rise time is how quickly the amplitude increases at the start of the sound.
So, the boundary between a note sounding "plucked" and a note sounding "bowed" is an onset time of roughly 60msecs. This is a smaaaall time period. In Tallal's study, impaired children had a less accurate border between the two types of sounds, whilst unimpaired children could quite accurately seperate say.. an onset time of 40msec and one of 70msec. The relative abilities of individuals to distinguish these sounds is termed "Temporal resolution power". In Tallal's study there was a very distinct correlation between temporal resolution power and scores in a nonsense word reading task. In an EEG experiment examining brain areas relevent to processing auditory information like this, Stefanics et al. (2010) found a 'weaker than control' neural response during tests of onset time in dyslexic children between the ages of 8 to 10. The diminshed neural activity was consistently weaker across the years. My point is, temporal resolution power seems to be a predictor of the ability of children to learn to perceive word sounds correctly.
I was quite stunned to discover that is is also a predictor of working memory capacity (to the layman, short term memory capacity) and intelligence as can be judged by a whole variety of psychometric tests. I'm less than keen on the attempt to rate intelligence via tests that can't possibly include all of the things which really make up the unagreed upon definition of intelligence, but we'll ignore that misgiving for now. Rammsayer and Brandler (2007) examined the general intelligence (using a particular test that I wont go into, but think of it as an IQ test) of 100 participants. They then tested them on 8 temporal tasks similar in nature to the one I explained above. Participants scored roughly the same on all the tasks, strongly suggesting that it was indeed temporal resolution power being measured, rather than some other seperate task-specific skills. The findings showed TR to be a better predictor of intelligence scores than even physical reaction time, which is a strong predictor. Fascinating!
If you think the comment that reaction time correlated with general intelligence is strange, you're not alone. It is, however, surprisingly well documented. Deary, Der and Ford (2001) compared intelligence and reaction times using a 'Jensen's box' as shown above. 900 participants, and a strong as heck correlation. The reasoning behind this is that to react fast in a correct way, the brain must be adept at information processing.
Temporal resolution power shows prominent individual differences, as mentioned above. Men consistently show better TRP than women, so previous research has shown us. Rammsayer and Troche (2010) tested around 150 males and 150 females over a series of tasks examining their ability to identify the onset and offset of sounds. Males performed better to a degree only just falling short of statistical significance, which nonetheless indicated that they had slightly better TRP. McRoberts and Sanders (1992) showed that males had a slightly better ability (in some conditions) to identify increases or decreases in tones, and to differentiate between different 'contours' (changes in sound frequency). In many such studies males have been shown to have a slight, but never massive advantage and they rarely show that advantage consistently over all task types. Despite the nature of the advantage, it has been shown to exist in verbal tasks in which adults were asked to distinguish between non-native language sounds.
Kempe (My supervisor Vera) et al. have recently been working on a large study examining what cognitive abilities underly the ability of English speakers (in this particular study) to be able to distinguish between Norwegian "tonemes". Norwegian, being a tonal language, has certain words that are identical in every way apart from the tone which is used when pronouncing them. The tone can create an entirely new meaning, making it somewhat important to get things right lest you attempt to ask for someone to pass the salt and instead indicate your desire for someone to destroy it. Their experiment involved 6 different tasks which had particular contrasting themes between the sounds. Three of these were linguistic and Norwegian: 1. Changes in tone between two syllables of the same word. 2. Different pronounciations of Norsk vowels. 3. Different pronounciations of Norsk consonants. The other three were non-linguistic versions of the first three, essentially the same pitch changes, but without the presence of human speech.
This has been pretty tough going, even for one of my blog articles. For those of you who got this far, here's a lol.
As a way of checking how well Norwegians performed in the contrasts, 10 of them were examined. They performed better than the 90ish native English speakers who attempted the tasks. In terms of sex differences, males had a higher sensitivity to the contrasts in every condition, though as with previous research the advantage was miniscule. I'm talking a max of 5% more sensitive and most conditions closer to 1 or 2%. It was still statistically significant, so...hmmm. Clearly this sex difference needed addressing, what was causing it? As for the predictors of the ability to discern different Norwegian sounds, the best were the non-linguistic pitch contours extracted from the norwegian two-syllable words. The performance in THAT task was best predicted by: Gender, IQ (as determined by a 'culture fair' task) and musical ability self-rating. Folks who had already learned another language to a fair extent sometimes showed better scores in the Norwegian contrasts, suggesting they may have picked up Norwegian sounds that also exist in other non-English languages.
Right. so. The important findings are thus: There were sex differences in the sensitive to contrasts in Norwegian and non-lingual sounds, with males always having a slight advantage. This sensitivity, or temporal resolution power, had previously been strongly correlated with measures of intelligence and working memory capacity. Kempe et al. had shown that males and females had different temporal resolution abilities, but they did not find any difference in IQ between genders. If A predicts B, and males had slightly higher A, then shouldn't they also have slightly higher B? According to Vera's research there may be more than one temporal processing ability. She and her collaborators concluded that male advantages in temporal resolution power may be largely due to their slightly higher volume of white matter in their brains (Gur et al. 1999). Females have slightly smaller brains than males in general, and so must pack more grey matter (neurons) into the space whilst sacrificing white matter (conductive material that aids in the speedy transfer of electrical signals across neurons). It is possible, they figured, that the slight male advantage could correspond to this higher volume of conductive material. If this were true, it would be more likely that the male advantage was an evolutionary by-product of the pressures for different brain sizes than an actual selected-for adaptation.
And that's that! That was a summary of some of the work leading up to the project I am currently working on with Vera and her collaborators. Though for the interest of keeping research schtum until it has been published I want be going into more depth for now. Perhaps I'll be able to write it up in future!
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!
