an autodidact meets a dilettante…

The term ‘autism’ was coined in the 1940s by two physicians working independently of each other, Hans Asperger in Austria and Leo Kanner in the USA, to describe a syndrome the key feature of which was a problem with interacting with others in ‘normal’ ways. Sounds vague, but the problem was anything but wishy-washy to these individuals’ parents and families, and over time a more detailed profile has built up.

The term itself is from the Greek autos, or ‘self’, because those with the syndrome had clear difficulties in interpreting others’ moods and responses, resulting in a withdrawn, often antisocial state. Autistic kids often avoid eye contact and are all at sea over the simplest communication.

Already though, I feel I’m saying too much. When describing autism, it’s common to use words like ‘often’ or ‘sometimes’ or ‘some’, because the symptoms are seemingly so disparate. Much of what follows relies on the neurologist V S Ramachandran’s book The tell-tale brain, especially chapter 5, ‘Where is Steven? The riddle of autism’.

Autistic symptoms can be categorised in two major groups, social-cognitive and sensorimotor. The social-cognitive symptoms include mental aloneness and a lack of contact with the world of other humans, an inability to engage in conversation and a lack of emotional empathy. Also a lack of any overt ‘playfulness’ or sense of make-believe in childhood. These symptoms can be ‘countered’ by heightened, sometimes obsessive interest in the inanimate world – e.g. the memorising of ostensibly useless data, such as lists of phone numbers.

On the sensorimotor side, symptoms include over-sensitivity and intolerance to noise, a fear of change or novelty, and an intense devotion to routine. There’s also a physical repetitiveness of actions and performances, and regular rocking motions.

These two types of symptoms raise an obvious question – how are the two types connected to each other? We’ll return to that.

Another motor symptom, which Ramachandran thinks is key, is a difficulty in physically imitating the actions of others. This has led him to pursue the hypothesis that autism is essentially the result of a deficiency in the mirror neuron system.

In recent years there’s been a lot of excitement about mirror neurons – possibly too much, according to some neurologists. A mirror neuron is one that fires not only when we perform an action but also when we observe it being performed by others. They’ve been found to act in mammals and also, it seems, in birds, and in humans they’ve been found in the premotor cortex, the supplementary motor area, the primary somatosensory cortex and the inferior parietal cortex. It’s easier, however, to locate them than it is to determine their function. Clearly, to describe them as ‘responsible’ for empathy, or intention, is to go too far. As Patricia Churchland points out, ‘a neuron is just a neuron’, and what we describe as empathy or intention will likely involve a plethora of high-order processes and connections, in which mirror neurons will play their part.

With that caveat in mind, let’s continue with Ramachandran’s speculations on autism and mirror neurons. First, we’ll need to be reminded of the term ‘theory of mind’, used regularly in psychology. It’s basically the idea that we attribute to others the same sorts of intentions and desires that we have because of the assumption that they, like us, have that internal feeling and processing and regulating system we call a ‘mind’. A sophisticated theory of mind is one of the most distinctive features of the human species, one which gives us a unique kind of social intelligence. That autism would be related to theory-of-mind deficiencies seems a reasonable assumption, so what is the brain circuitry behind theory of mind, and how do mirror neurons fit into this picture?

Although neuro-imaging has revealed that autistic children have larger brains with larger ventricles (brain cavities) and notably different activity within the cerebellum, this hasn’t helped researchers much, because autism sufferers don’t present any of the usual symptoms of cerebellum damage. It could be that these changes are simply the side effects of genes which produce autism. Some researchers felt it was better to focus on mirror neurons straight-off, as obvious suspects, and to see how they fired and where they connected in particular situations. They used EEG (electroencephalography) as a non-invasive way to observe mirror neuron activity. They focused on the suppression of mu waves, a type of brain wave. It has long been known that mu waves are suppressed when a person makes any volitional movement, and more recently it has been discovered that the same suppression occurs when we watch others performing such movements.

So researchers used EEG (involving electrodes placed on the scalp) to monitor neuronal activity in a medium-functioning autistic child, Justin. Justin exhibited a suppressed mu wave, as expected, when asked to make voluntary movements. However, he didn’t show the same suppression when watching others perform those movements, as ‘neurotypical’ children do. It seemed that his motor-command system was functioning more or less normally, but his mirror-neuron system was deficient. This finding has been replicated many times, using a variety of techniques, including MEG (magnetoencephalography). fMRI, and TMS (transcranial magnetic stimulation). Reading about all these techniques would be a mind-altering experience in itself.

According to Ramachandran, all these confirmations ‘provide conclusive evidence that the [mirror neuron] hypothesis is correct.’ It certainly helps to explain why a subset of autistic children have trouble with metaphors and literality. They have difficulty separating the physical and the referential, a separation that mirror neurons appear to mediate somehow.

A well-developed theory of mind which can anticipate the behaviour of others is clearly a feature of understanding our own minds better. In Ramachandran’s words:

If the mirror-neuron system underlies theory of mind and if theory of mind in normal humans is supercharged by being applied inward, towards the self, this would explain why autistic individuals find social interaction and strong self-identification so difficult, and why so many autistic children have a hard time correctly using the pronouns ‘I’ and ‘you’ in conversation. They may lack a mature-enough self-representation to understand the distinction.

Of course, tons more can be said about the ‘mirror network’ and tons more research remains to be done, but there are many promising signs. For example, the findings about lack of mu wave suppression could be used as a diagnostic tool for the early detection of autism, and some interesting work is being done on the use of biofeedback to treat the disorder. Biofeedback is a process whereby physiological signals picked up by a machine from the brain or body of a subject are represented to the subject in such a way that he or she might be able to affect or manipulate that signal by a conscious change of behaviour or thinking. Experiments have been done to show that subjects can alter their own brain waves through this process. Some experimental work is also being done with drugs such as MDMA (otherwise known as the party drug ‘ecstacy’) which appear to enhance empathy through their action on neurotransmitter release.

So that’s a very brief introduction to autism. Hopefully I’ll come back to it in the future to explore the progress being made in understanding and treating the syndrome.