Do you believe that an autistic person would make for a good standup comedian? The question was answered a few years ago at an AutismOne conference. A personal apearance along with a short video served to narrate the trials and tribulations of an adolescent autistic man trying to make his way through the standup comedy circuit. The young man wrote all of his material and was quite good at his delivery. From the presentation it became quite clear to me that some autistic individuals have no problems with imitation.
Probably at about the same time that the young standup comedian engaged my attention a small polemic erupted behind close doors within the autism community. A renowned psychologist used a passage in Temple Grandin’s book (i.e., Temple playing hide and seek as a child) to call into question her diagnosis. For a good player hide and seek requires some rudimentary knowledge of what others may think in order to find a good hiding spot. Instead of questioning the universality of Theory of Mind deficits among autistic individuals the psychologist called to question Temple’s diagnosis.
Theory of Mind is the ability to understand the mental state of others. It is now clear that not all autistic individuals have deficits of Theory of Mind. Still, the small polemic served to illustrate the psychologist’s biased way of thinking. It appears that some scientists have a tendency to dig themselves in ideological trenches from where they never surface again.
Imitation is clearly important in learning and developing social skills. It is therefore unsurprising that imitation has been discussed within a vast body of literature in autism. However, the evidence is in and the results are quite clear. An abnormality of imitation has long been discredited by clinicians as an overarching explanation for autism. Like in the examples above, some autistic individuals may do quite well at imitating and at intuitively gaging the state of mind of others. Furthermore, those individuals exhibiting such a deficit usually improve with aging. A book that I would highly recommend dealing with this and other similar issues is Laura Schreibman’s, “The Science and Fiction of Autism”.
The importance of imitation:
Probably the most popular theory trying to explain imitation deficits in autism postulates abnormalities in the workings of mirror neurons. The so-called “Broken Mirror Hypothesis” has attracted the attention of the public. It is an attractive idea that has been packaged and released to the layman press primarily by researchers initially coming from outside the field of autism.
In non-human primates electrophysiological studies have shown that mirror neurons have the ability to become activated when an animal acts or observes the same behavior in other animals. Although it is reasonable to speculate how imitation, acting through many downstream pathways, could provide for a core deficit of autism, the literature does not support this possibility. First, imitation as a defect in autism would have to spare imitation of speech despite some impairment of gestures. Think of ecolalia (the automatic repetition of vocalizations) that is frequently seen in autistic individuals. Isn’t this a type of imitation? Any theory trying to uphold imitation as a core deficit of autism would therefore have to postulate different brain mechanisms for different types of imitation, not simply mirror neurons. Second, children who exhibit imitation defects can have a reversal of the same if tested in an engaging/structured environment. The evidence attests to the fact that imitation deficits in autism are a functional deficit at the mercy of environmental exigencies rather than a stationary symptom due to an underlying pathology. Third, for many reported studies, it is not clear as to whether autistic patients have a deficit of imitation or an inability to express emotions (e.g., when imitating facial expressions). Lastly, the fact that imitation deficits are not universal nor persistent (they tend to diminish with aging) argues against their being considered a core deficit of the condition.
The mirror neuron system:
There is a large body of well publicized literature that has dismantled the theory of imitation in autism (e.g., Dinstein, I. et al. Neuron 13, 461-469 , Théoret H. et al. Curr. Biol. 15, R84-5 ). As reported in the literature, the broken mirror hypothesis relies on several unsupported assumptions: that the mirror system is responsible for understanding goals and imitation, that goal understanding and imitation are abnormal in autism, and that these deficits cause the social difficulties seen in autism (Hamilton A. F. et al. Neuropsychologia 45, 1859-1868 (2007). So the real question we should be asking ourselves is why are we still pursuing imitation theories of autism under various guises? Imitation may play an important role in social learning but it is certainly not a core deficit of autism. In this regard, therapeutic attempts at improving imitation in autistic individuals may provide for symptomatic treatment, never a cure.
[Addendum 4/17/13 Indeed the shallow view of popular scientists are still making rounds in the media. Ramachandran, whose practical experience with autistic individuals appears to be nill, tries to explain autism from the perspective of the broken mirror neuron hypothesis. Not only does he abstains from mentioning all of the negative evidence, he also stereotypes autistic individuals based on his imagination rather than clinical experience. See Ramachandran’s post: http://bigthink.com/in-their-own-words/pretend-youre-superman-the-magic-of-mirror-neurons See responses against the post: http://www.mfw.us/blog/2013/04/17/okay-im-superman/ ]
[Addendum 4/19/13 Just 1 day after Ramachandran’s speculative arguments were posted, they were taken down. Not surprising.]
[Addendum 4/24/13 An interview with the multifaceted and very talented Noah Britton is now available online: http://thautcast.com/drupal5/content/autistically-incorrect-conversation-noah-britton-part-one Noah Britton is most famous for co-founding the first comedy troupe composed entirely of people with Asperger’s: “Asperger’s Are Us”. He also performs music by himself and with the band “The Best Thing Ever”. In 2012 he was named as a public member of the federal government’s Interagency Autism Coordination Committee. In his spare time, he is a psychology professor in Boston, MA.]
Otro tema que sale una y otra vez relacionado con la teoría de la mente es el de la empatía. Esta es producto en mi opinión de la identificación que a su vez tiene que ver con la imitación. Pero la empatía es una función de alto nivel cuyo fallo no puede explicar fallos de nivel inferior. Simplemente se trataría de un síntoma frecuente en el autismo, -y en otros problemas como el tratorno bipolar o algunos trastornos de personalidad- y no siquiera está claro que ocurra siempre; yo he visto algún afectado con un exceso de empatía en ese sentido de imitación e identificación, si bien era una empatía más bien inapropiada.
Gracias por el comentario. Creo que tanto la teoria de la mente como la de las neuronas de espejos para explicar el autismo han recibido mucha critica. Las mismas no cumplen con los dictados de generalizacion o universilidad dentro de la condicion. En el caso de la imitacion la persona afectada tiende a mejorar a travez de los anos. Tambien yo puedo hacer que un paciente con deficit de imitacion mejore al darle una recompensa a mismo. No creo que muchas de las teorias de base psicologicas hayan aportado nada al conocomiento del autismo
In the case of echolalia or echopraxia, isn’t the problem with mirror Neurons explanation of autism coming more from the inhibitory gaba system which refrains immediate imitation? Inhibitionprocess allows the interiorisation of the observed gesture or the words being heard. delayed echolalia or echopraxia can on the contrary be useful steps in the development of a pragmatic imitation, which immediate echolalia or echopraxia aren’t. Barry Prizant and Adriana Shuler published some years ago a paper on the positive use of echolalia to help language development in children with autism..
Thanks for the comment. I agree that imitation is of importance in learning and stated it so in the blog. As to the basis of echolalia/echopraxia and any relationship to the GABAergic system, I have not found much in the literature except for speculations. The relationship to mirror neurons, especially in humans, is even more of a stretch of the imagination.Some of the pieces that may need to be taken into account when trying to make sense of a pathophysiological mechanism are the facts that individuals on Depakote and those suffering from extensive damage to the frontal cortex may exhibit these symptoms. The widespread damage in the latter cases escapes the domain of the mirror neurons.
I know I am going on a tangent, but it is difficult to make sense out of the whole field of mirror neurons in humans and especially in autism. Evidence for their existence in humans is indirect. Even when a researcher proposed mu suppression as a way of testing this network, it was based on a supposition without concrete proof.
Thank you for the comment. Sorry if I rambled…one of those days.
Thanks for the article.
This is the problem, isn’t it? That some theories and hypotheses are attractive and catchy (‘mirror neurons deficit in autism’ – sounds fascinating, right?) but do not explain the phenomenon but rather mislead and create more misconceptions about it. I don’t think that those who live or work with individuals with autism would take the ‘broken mirror hypothesis’ seriously.
By the way, some other theories, though accepted, can lead to misconceptions as well. For example, Theory of Mind (and lack of it in autism). On the one hand, this theory is good – because it applies that we have to be explicit when interacting with autistic individuals (explaining what we mean when… etc.). On the other, however, it is one-sided, because it’s based on the assumption that there is only one possible ToM. But if their perception is so different from the ‘normal’ one, they develop their own ToM (Theory of Autistic Mind) and their reactions and interactions are normal for them. If we remove one-sidedness from this theory and re-examine our assumptions, we’ll see the misconceptions created by the theory – like, e.g. ‘lack of empathy in autism’ (if anything, some are more empathic than ‘normal’ population) or even a funnier one – ‘autistic people lack sense of humour’ (this one always makes me laugh).
It is a problem that permeates psychiatry. At a minimum, psychiatry has not been able to come up with a definition of what constitutes a mental illness. Attempts at providing boundaries by applying operational criteria fail as we do not have construct validity for the same. Furthermore conditions seem to be considered as mental illnesses depending on the biased thinking of some committees. One has only to remember the history of homosexuality or psychoanalysis in psychiatry to see how flimsy our criteria can be. Unfortunately in science nowadays the theory (and for that matter the research) that seems to matter the most is the one labeled with a catchy name or coming from a big academic institution. Then we will invest a lot of money on it doing genetics and neuroimaging work with little to show for the investment. The theories will then endure because there is no way of falsifying them. Their authors can answer criticisms by hiding behind wordy arguments rather than facts.
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Hello Manuel, Have you looked into VS Ramachandran further/familiar with his work? He offers compelling evidence, but so do people who disagree with him. It’s hard to know what is the answer. I believe people have also challenged your views of minicolumns.
A difference is you may have experience and know people on the spectrum with more insight into them than Ramachandran, but I don’t know. He may be wrong in the sense of saying everything in absolutes, but his motto is to go with an objective mind:
Are you familiar/read the entire hypothesis and/or looked at his book “The tell tale brain” .
Click to access 10.%20The%20Tell-Tale%20Brain%20-%20V%20S%20Ramachandran.pdf
His opinions may be wrong or too absolute, but his findings…I don’t know. I don’t believe or disbelieve. It may not be your area of research, If you have a speculation to why the MU tests came out the way they did I am curious, not what it is, but whether you do.
I believe that it’s important to fully understand what the other person is saying and disagree from your own scientific explanation rather than write it off (unless it’s a weird psychological theory like Baron Cohen’s systemizing one, that is not even incorrect). It’s better to argue against mirror neurons if that is what you believe or lack of theory of mind with some measurable evidence. Absence of proof is not proof of absence, nor is existence of evidence proof of existence.
It may not be your concern though to dedicate time and research just to disprove someone else or worthwhile to figure out more about Ramachandran’s entire set up viewpoint. I notice the above post is written as your own feelings and hunch and you may be right or wrong. This blog is not just for ncbi style studies, there is individually written opinion pieces.
I am not forcing you to reply or read anything. If you have anything to say and want to towards my stream of words, I would read it and maybe feel less confused. If not, no worries.
I have read his work and opinions in regards to autism. Always thought that it was extremely weak and based on his biased thinking as to what autism should be. The anatomical studies have already been done showing no mirror neuron deficit in the condition.
Just one (out of quite a few papers) that provides clear evidence against a simple mirror neuron hypothesis of autism – http://www.antoniahamilton.com/HamiltonBrindleyFrith_NPsy_2007.pdf
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