Category Archives: Autism

Time we identified cognitive phenotypes for the social deficits in autism

Social deficits? Their not the same as everyday difficulties in social situations. We all have experienced such difficulties, because the social world has as much potential for suffering as for happiness. But when we talk of social deficits in autism it’s about not being quite part of the social world. Yet, it’s not about deliberately withdrawing from this world and not about being antisocial.

I am not starting at the behavioural level to define the social deficits in autism. I would get lost in a maze where cause and effect can hardly be distinguished. For instance, there are people who often feel rejected, while others find them unbearably aggressive. Which comes first, the rejection or the aggression?


Continue reading Time we identified cognitive phenotypes for the social deficits in autism

Behaviour is determined by so many factors that a glitch in just one of these factors is incredibly hard to discover. It’s like being in the midst of climate change and generally rising temperatures, while being confounded by a cool summer. Like the observed cool temperatures, observed behaviour is potentially misleading if we want to learn something about what causes the behaviour.

Therefore I am starting at the cognitive level. I will only later go to the behavioural level when I know what signs to look out for. At the cognitive level I can let my thoughts range freely around the imagined mental machinery. I would like to poke into different bits and take them apart. I would like to see what would happen if a particular piece were missing or not working properly. Would the projected outcome resemble the real social problems that are experienced by autistic people?

What parts? What mental machinery? Well, its just a metaphor, and it may be better to talk of apps, perhaps. But here are some ideas. I believe evolution has endowed us from birth with a number of gadgets and these enable us to become the social creatures that we are. When any of them goes wrong, social deficits should result, – not to be confused with everyday social difficulties.

If we can find clues to the gadgets and what can go wrong, we are on the way to discover their neural basis and eventually their genetic origin. Progress! But how many are there? Can they each go wrong, separately or together? Here I am speculating and limit myself to 7 hypothetical mechanisms. Lets call them start-up kits, since they are subject to learning and development.


Start-up kits for a thoroughly social human being

  • Agency recognition (prey, predator, mate, friend, enemy
  • Affiliation (recognising kin, bonding, attachment)
  • Alignment (mimicry, resonance, contagion)
  • Belonging (identity, trust, loyalty, ingroup/outgroup distinction)
  • Hierarchy (knowing one’s place, dominance/submission, alliances)
  • Mentalising (mental state tracking, persuasion, deception, reputation)
  • Morality (fairness, equity, altruism, punishment)

I imagine these start-up kits run on the fuel of social emotions to regulate social behaviour (think guilt, shame, jealousy, pride, contempt). They depend on other social signals too, as displayed in eye gaze, voice and body language. For my money, its the last two, mentalising and morality, that have some claim for being uniquely human and being shaped by cultural learning. They also have some claim  for being broken in autism.

Perhaps any of the 7 mechanisms can be broken in autism. Perhaps this leads to different forms of social deficits and hence different cognitive phenotypes. This would go some way to explain the heterogeneity of the autism spectrum. It might also explain different degrees of severity – the more the worse, obviously. Perhaps testing different mechanisms separately would lead us to form subgroups in the autism spectrum. As far as I know this has not been done in any systematic way.

If they’re not broken, these hypothetical mechanisms work spontaneously and effortlessly, and are active throughout an individual’s life. This is reminiscent of instincts. They respond to a certain set of stimuli with a certain set of flexible responses. However, the responses can be suppressed or modified via conscious control.

To what extent these mechanisms are independent , or interacting with each other, is a matter for debate. If they were separate then, when one of them wasn’t working, a ‘hole’ in the mental architecture would appear, but the rest might function well. Do holes matter? It depends. Compensatory learning is a wonderful thing. If it works then the hole can be covered up to make it almost invisible in behaviour.

How then do you identify cognitive phenotypes?  You need to devise behavioural tests to capture the hypothesised cognitive deficit. Sadly, we don’t have the tests. This is not because they are impossible to design, but because nobody has made the necessary major effort to devise a systematic battery of tests that are reliable and sensitive.

Most of the tests we have so far give you a score that estimates a level of performance, but they don’t tell how that score was achieved. We need tests that can do precisely that. Moreover, we need to be able to detect how a score was achieved. It could be low, because of fatigue. It could be high, because of compensatory training. So, constructing valid and reliable tests is not a trivial task, they need a lot of man power and, of course, funding.  I expect this is why we haven’t got them yet..

All the experimental tests we have at present are precarious. This is why I am not impressed when somebody tells me that, on tests in the lab, their autistic child is no different from any typically developing child, and hence there is no difference in underlying mental architecture. I think it would be beautiful to discover autism specific architecture, a whole city of familiar, yet different, structures.Urville18


Image credits:

Tup Wanders Flickr creative commons                                                          Chris Frith                                                                                                                                                            Gilles Trehin, Urville



This cognitive thing

Five years ago I wrote an opinion piece for the SPECTRUM (then SFARI) Autism website. I doubt that the message I wanted to get across  – did.

So I am trying again.Framework5With this simple framework I think we can declutter our thoughts about autism.

Continue reading This cognitive thing

What’s the problem with our current thinking about autism? If you have a Post-it note handy, we can start by drawing some lines to create spaces for what we already know and what we don’t. Framework1

We’ll reserve the top space for facts about the remote biological causes of autism. You could list an impressive number of risk factors here, such as susceptibility genes, and differences at the cellular level and differences in the size, activation and connectivity of brain structures, for example.Framework2

The space at the bottom is for all the behavioural observations,and performance on neuropsychological or psychometric tests. Behaviours reported by parents, behaviour assessed by questionnaires or interviews would be listed here as well. There is a huge amount of data: for recognition of faces alone, there are hundreds of papers.Framework3

The middle space between the two lines is the interesting one. It’s the ‘cognitive thing’.  This is for ideas about what is different about the mind of someone with autism — and the core of my obsession. Framework4

Here’s a hard question: How does an individual find meaning in the world and act on the world? Answer: Through cognitive mechanisms that allow the individual to learn and to adapt in its environment. These mechanisms have a basis in the brain and have been honed by evolution over millions of years. For the individual they come for free as  as start-up kits and they are active right from birth.

By the way, in this framework the term ‘cognitive’ describes everything that the mind does, consciously and unconsciously. It does not just refer to perception, attention, memory, reasoning. It refers to all aspects of mental life.  And this certainly includes emotion, motivation, reward learning.

The cognitive level is also the space for imagination and controversy. Here we can’t observe and measure facts; we can only propose hypotheses. Of course they have to be amenable to being tested both on the biological and the behavioural level. It seems to me that in our state of ignorance, we might as well be bold. I have already inserted two of my favourite hypotheses to explain what is different about the autistic mind, mentalising and detail focus.  I hope you will put forward your own hypotheses.

The  mentalising hypothesis is very bold. It proposes that  we are all born with a social GPS. The GPS tracks what others think and feel from moment to moment. This allows us to orient ourselves in social space without having to consciously think about it. Autism means not having this GPS, but instead having to rely on a map. This works, but is slower and more effortful. There are many tell-tale signs in behaviour and in the brain that seem to support this hypothesis.

Autism isn’t just about social communication. It is also about having a way of thinking, which can be described as ‘detail focussed’. The idea is that autism involves sticky attention to small parts at the expense of attention to the bigger picture. Thus local sensations can become overwhelming. This can be rephrased as giving less weight to prior expectations that prepare you to perceive a particular thing, and instead giving more weight to incoming information, both signal and noise. 

We need such bold hypotheses. Here’s why: Behavioural and biological data only become meaningful if they can be explained in terms of what the mind does. Understanding that a child lacks a social GPS is far more helpful to a teacher than knowing that he or she has a particular genetic abnormality (biological); or tends not to look at eyes (behavioural). Likewise a teacher can understand that a child who is overwhelmed by bitty information may be terrified by the smallest changes in his or her environment. 

We now have a structure that we can use to lay out what we have already learned about autism. I have drawn lines on Post-it notes, but if you want to insert all the facts that are already known, you will need a very large sheet of paper!

We can also use this simple layout to imagine how our knowledge might expand in the future. I have written about this with John Morton in 1995, and most recently in 2012.

The holy grail of autism research is to identify the commonalities of the autism spectrum. These commonalities should lead to defining cognitive phenotypes. Then it will be possible to trace causes of autism from genes to behaviour.

We know a lot already, but how can we pull the existing findings together? We need to find a common pathway — the critical part in the system that is always affected, no matter which of the numerous genetic and environmental risk factors have placed an individual  on the autistic spectrum.


If we were to find a common pathway, this would define a distinctive property of the brain that is critically different in autism. The common pathway forms a node in a network of possible mappings: It pulls together all the strings from the data that are already available and from the data that are not yet available, but can be predicted.

If we can find a node at the cognitive level, animal models become more informative, for example. This is because one can look beyond behaviour, which is obviously very different in mouse and man.

To me there is something very appealing about pulling together the strings in a common pathway. No wonder I’m obsessed with this cognitive thing.

There is a thorny point here: The node would pinpoint both normal and abnormal function. But isn’t this too black and white? Isn’t everyone ‘a bit autistic?’

I happily agree with this at the behavioural level, where one thing always shades into another. A measure of amount of eye contact, for example, will vary continuously across different individuals — we can only make an artificial cut-off point to define what is ‘abnormal.’ The same goes for the biological level: If you assess neuro-chemical levels, you will get a continuous distribution, with clinical groups tending to lie at one extreme.

At the cognitive level, however, it is admissible to use categorical distinctions. We are free to theorise that there are functions that the typically developing mind automatically performs, which the mind of a person with autism performs in a qualitatively different way, or not at all — and vice versa.

So here’s my message: We shouldn’t despair of ever finding clarity in the ever more complex world of possible biological causes and dimensionally varying behaviours. If we focus on the mind, we can make sense of the enormous complexity by testing daring hypotheses that can pull the strings together.

Trust and regret – guardians of our decisions. What can go wrong?

Vaccination has been in the news again. Amongst others, science writer Virginia Hughes has given thoughtful comments on why ordinary people mistrust scientists on this issue.

I take this as a lesson in how science communication and public engagement can go wrong. As a scientist I feel hurt not to be trusted. As a mother I can imagine what it’s like when you are told you should vaccinate your child. I have been there and I have learned from the episode when the use of the triple MMR vaccine was blamed for the increase in autism, when Andrew Wakefield was celebrated as a hero speaking out for parents. The pharma industry, government and scientists were all accused of bias. What basic cognitive processes are involved in the way we make the decision to vaccinate or not to vaccinate? How can these processes undermine scientifically based advice?science-megaphone-300x226 Continue reading Trust and regret – guardians of our decisions. What can go wrong?

Why doesn’t rational explanation as provided by scientific evidence speak for itself? Here’s where our social minds play tricks with us. We basically prefer the inaccurate message given out by a trusted person over the accurate message given by a possibly untrustworthy person. But perhaps these are not tricks. Although it pains me to say this, trust can be more important than scientific truth. Here’s why. Evolution has endowed social creatures, including human beings, with the predisposition to cooperate. And for cooperation to work we need to trust each other. Many animals show reciprocal altruism: ‘I scratch your back and you scratch mine’, and human beings go one step further by showing indirect altruism: ‘I scratch your back, and one of your kin will scratch the back of one of mine. Thus, people help each other without the explicit idea to get something in return, but perhaps with the implicit belief that someone else will give help at another time. Because this belief is unspoken, and because helpers are often anonymous, free riding becomes very tempting. And as we know, if there are too many free riders, trust and cooperation will collapse.

Evolutionary theorists suggest that cycles of cooperation and trust alternate with lack of cooperation and distrust. To reinstate trust both forgiveness and punishment are needed. For instance, if people are prepared to punish free riders, then this eventually reinstates trust in the group. This is called altruistic punishment because it actually costs the person who does the punishment. At the very least, he attracts the dislike of the person he punishes.

Trust weighs heavily in the decision to vaccinate or not. We remember vividly the old family doctor who once mentioned that vaccination was not a good thing. But why is our memory so good for messages that tell us not to vaccinate?

When our social mind makes a choice then trust and the person making a recommendation, are not the only factors. The big players are our emotions. Our brain is particularly responsive to any kind of threat. But even more important may be an emotion known as anticipated regret.

Imagine you are bidding in an auction, and you do not get the item you bid for. You will show disappointment. Now imagine you are told that your bid was only very slightly less than that of the successful buyer. You will show regret. You regret that you did not offer a slightly higher bid. It has been shown that in auctions where the final price is revealed, buyers offer higher bids, than when it is not. This is a sign of anticipated regret. We feel this emotion automatically as a result of internal computations, of which we are not aware. Now it has also been shown that you are more likely to feel regret when you commit an act and something bad happens. You won’t feel so regretful when you omitted to do something. This is the case when you decide not to vaccinate. You didn’t commit something that might turn out to be wrong. You just omitted something.

The MMR story is a story of lack of trust, and a story of the wrong kind of anticipated regret. It is wrong because it disregards the consequences of not vaccinating. Several factors contributed to the lack of trust. To begin with, there may be a predisposition to distrust scientists who are often portrayed as callous and more interested in abstract generalisations rather than the fate of individual people. The decision to vaccinate means you are allowing a temporary hurt to your child, while your overarching inclination is to protect your child from hurt. Why should you allow this hurt, when you have no personal memory of the severity of illnesses such as mumps, measles and rubella. Protecting your child from these almost mythical illnesses seems somehow less pressing than protecting your child from an immediate danger. So, when Dr. Andrew Wakefield, came forward as taking a stand against vaccination, his opinion fell on fertile ground. Further, the possibility that the package of a triple vaccination – a triple injury – might cause a brain disorder, such as autism, seemed plausible.

As so often correlation turned into causation: autism had increased recently; the triple vaccination was introduced recently; ergo, the triple vaccination caused the increase. In the UK the Medical Research Council immediately set up projects designed to answer the question whether indeed there was a causal connection. The answer was no, and the scientific advice was that the triple vaccination is safe.

In spite of this advice, nobody believed it. This was strange and needs further explanation. Why was the trust in Wakefield continuing, when there was at the same time a lack of trust in scientific advice? Here is where the concept of anticipated regret comes in. Parents were ‘playing safe’, or so they thought, by not giving their children a single triple short vaccine. In fact, playing safe was an act of omission, and this is less linked to regret than commission. However, if you choose not to vaccinate your child, then you are a free rider, because the protection remains as long as everyone else (or the vast majority) does vaccinate their child. In order to be effective 90% of the population has to be vaccinated. Many middle class people thought they were justified in becoming free riders for the sake of their child. In consequence there have been outbreaks of measles.

Here is the gist of an interview that illustrates the role of anticipated regret in the MMR story. Interviewer: “Would you let your child get the controversial MMR vaccine?” Father: “Certainly not. If I let my child get the MMR vaccine and he later becomes autistic, I will never forgive myself.” Interviewer: “What, if your child then contracted the measles and died?” Father: “This would be an act of God. I would be very sad, but not feel guilty.”

We all know the end of the story. Remarkably, the reason that MMR vaccination became acceptable again for parents had nothing to do with the restoration of trust in scientists. Quite the opposite. It became known that Andrew Wakefield had a commercial stake in the development of single vaccines. Now, people who previously believed him to be a brave hero who spoke against powerful lobbies, such as big pharma, lost their trust in him. Another reason in favour of vaccination is the increase in measles, mumps and rubella outbreaks. This reminded people that these diseases are very dangerous. There are still people who firmly believe that their child’s autism was caused by vaccination and nothing will weaken them in this belief. However, our social nature strongly inclines us to do what others do, and to value what others value.

Image credit New Media Science Communication

Where is the crack in the mind machine: some insights from Bayesian theory into mental disorders by Pavel Voinov & József Arató

Where is the crack in the mind machine? Some insights from Bayesian theory into mental disorders.

Pavel Voinov and József Arató are PhD students in the Cognitive Sciences Programme at the Central European University, Budapest.

As cognitive scientists we keep asking ourselves what knowledge society expects from us and what the implications of this knowledge are. “Mind as a machine” is a good metaphor, as we feel it captures those expectations: to describe the principles of how the mind works, and, furthermore, to explain its failures and suggest ways to fix it.

In this post we will take the perspective of reverse mind-engineers. We will use one of the most prominent computational theories in contemporary cognitive science –  Continue reading Where is the crack in the mind machine: some insights from Bayesian theory into mental disorders by Pavel Voinov & József Arató

the Bayesian perspective, and show how it contributed to our understanding of two prevalent mental disorders – schizophrenia and autism. A distinctive feature of Bayesian theories of cognition is that they provide a formal description of the mind: it can be grasped with mathematical expressions, and thus be computationally modelled.Fig 1

Bayesian models of cognition can explain how people handle the uncertainty that is constantly present in the world. As we can never be sure what the true state of the world actually is, perception works by hypothesis testing. We continuously guess what we might expect to happen in the world. For these guesses we can use the accumulated knowledge we have acquired through past experience.

In other words, we evaluate newly incoming sensory information in the light of prior experience, and this is how we constantly make fresh predictions of what it is that we are seeing, hearing and feeling. What we actually perceive is not what is out there. Instead we perceive the most likely event out there. The most likely event is what we hypothesise given the new sensory signal (evidence) evaluated on the basis of the probabilities of past events (priors). We continuously update our expectations based on the differences between the predicted and experienced sensory stimuli (prediction error). The same model applies to belief formation: we update our beliefs based on the differences between expected and experienced events (Figure based on Van Boxtel & Lu).

Here’s an example how this works. ImagiFig 2ne you need to read a signboard at a distance. Even if you can’t discriminate individual letters, the context will help you, and you are likely to identify common words like “caution”, “danger”, “exit” etc., just by matching approximate length of a word or its salient features. Even if you can’t see any details at all, you may make a guess: this will be a case of relying solely on your priors. But when the context is not informative, and there are many probable alternatives, you will have to rely more on what your eyes deliver to the brain. Now you can’t guess the word and you need to distinguish the individual letters.

The Bayesian approach has been impressively powerful in modelling various aspects of human cognition: let’s see whether it has been useful for explaining malfunctions of the mind.


The most distinctive features of the schizophrenic mind are the so-called positive symptoms: delusions (abnormal beliefs) and hallucinations (false perceptions). Hence, a Bayesian framework is a promising tool for exploring these features.  After all, it was developed to deal with belief formation and perception – and these are precisely the cognitive functions that are most affected in schizophrenia.

Various experiments have shown that something goes wrong in the combination of prior knowledge and iFig 4ncoming sensory evidence. For example a weaker reliance on prior expectations can explain why schizophrenics are less susceptible to some visual illusion. Not being tricked by an illusion means, that in some situations, they perceive the world more veridically. So why does this not happen in healthy people? Healthy perception is optimally adapted to the environment, with the brain inferring the most likely patterns from raw sensory inputs. In contrast, schizophrenic patients are more influenced by what their eyes see, and less by the higher-level expectations their brain has derived from past experience. Look at the picture with two masks (image from: Grosjean et al., 2012). Our strong perceptual bias (or ‘prior’) for natural convex faces overrides competing information (such as shadows) and makes a concave hollow mask (bottom) perceived as a convex face (top). Schizophrenic patients are generally less susceptible to this illusion.

A weaker influence from higher-level expectations is also shown in tasks which involve uncertainty – for example in playing stone-paper-scissors game. Here schizophrenic patients take less account of the past history of their contestant’s decisions and as a result follow strategies based on only the most recent evidence. Patients were also more confident about their decisions, and raised the stakes after smaller number of sequential winnings than healthy players (Joyce et al, 2013).

Another important feature of decision-making under uncertainty in schizophrenic patients is their reduced sensitivity to negative feedback once they have formed their belief. In Bayesian terms they do not use the prediction error correctly to update their models of the world.

These findings are especially intriguing when linked to our knowledge about the neurotransmitter dopamine. Dopamine plays the key role in learning based on the prediction error. Abnormally high levels of dopamine found in the brains of schizophrenic patients may underlie their failures to integrate sensory (and higher order) error signals appropriately.  We are not surprised by outcomes of our actions because our brain foresees them. But absence or distortion of this prediction in the brain of schizophrenic patients may create strange experience and give rise to delusional beliefs about it (Fletcher  & Frith, 2009).

The Bayesian approach is also promising in modelling how this lower-level prediction error could give rise to false beliefs at higher – ’more cognitive’ – levels. In this case corrupted output from lower levels would feed into higher cognitive functions leading to faulty beliefs of a higher order. Altogether, within a Bayesian picture of the mind one can build a coherent story, which would explain positive symptoms of schizophrenia with strong links between neural, cognitive, and behavioural levels.


Autism spectrum disorder has a clinical picture distinctively different from schizophrenia. The characteristic symptoms of this condition are repetitive behaviours and problems in social interaction and communication. Furthermore, autism is usually accompanied by a range of sensory peculiarities. The origin of these differences and its relation to the core symptoms of autism is still a mystery for psychologists. Atypical features of autistic perception include hyper-sensitivity to ordinary incoming stimuli, enhanced focus on details, and more fragmented perception. On the picture with kiwi fruits people with autism would likely see three separate objects rather than a triangle.Fig 3

Recently, Pellicano and Burr (2012) have proposed a Bayesian account of abnormal perception in autism. According to this account, perception in autism is shaped by weak priors. As we remember, a prior basically means accumulated information about the environment, and a weak prior means that less account is taken of this accumulated information. Hence we can say that the brain is not tuned appropriately to the environment. As a consequence, the perceived reality would be dominated by new incoming stimuli, and would be less influenced by internal information (priors). This would explain why autistic children are less susceptible to visual illusions and are often better at accurate copying of unusual images.

On the other hand, weak priors would also explain the phenomenon of sensory overload, that is hyper-sensitivity to ordinary sensory stimuli, like human voices or lamplight. While our sensitivity is modulated by the context, – we would be surprised if we heard a human voice in the middle of a forest, but not in the street. This contextual information does not seem to work for people living with autism. For ordinary people the brain would filter out most of incoming information. For autistic people everything from the sensory stream would be preserved, and this might lead to blurring of the figure with the background in their perception.

However, a theory has low scientific value if it can only incorporate already known facts, but can’t make predictions for new findings. What empirical prediction can the Bayesian theory make? The weak priors hypothesis can be tested against the sensory enhancement hypothesis: while the former suggests reduced influence of contextual information on perception, the latter predicts less noise in the sensory input for autistics. Joshua Skewes and colleagues (2014) tested this prediction in an experiment probing acuity of visual perception in ordinary people. The experiment demonstrated that people with higher scores on a scale measuring autistic traits, the AQ,  were less sensitive to the context information, but were as sensitive to the noise in stimuli as the control group. This result favours the weak priors hypothesis. However, it has not yet been tested with autistic individuals.

Conclusion. If you read the two stories carefully you can see surprising similarities between them: faulty functioning of prior knowledge is suggested as an explanatory cause for both conditions, and this cause is described in almost identical words. This is the weak part of the story: the theory seems to be so unspecified at the moment that it apparently fails to account for qualitative differences between two conditions, which a clinician would never confuse. We seem to be at the stage of trying to embed things in vague and extensively general principles, but small pieces of the big puzzle are yet to be defined. Perhaps this would sound disappointing if you expected a story like “There is a function in the normal brain which checks whether or not our beliefs are realistic. The part of the brain responsible for this function is broken in schizophrenics and that’s why you believe I’m an alien”. Unfortunately, we are not even close to the mechanical description of the “Mind as a machine”. But our first steps indicate that we’re on the right path…






On Andrassy Ut

This is the Champs-Elysée of Budapest: a grand tree lined avenue, framed by glamorous buildings, and with some famous coffee houses. We are sitting outside the classic Café Müvesz, with a splendid view of the Opera: Ildiko Kiraly, Kata Egyed, Chris and me after a nice open air lunch at Liszt Ferenc Tér, not more than two hundred yards away.
-You used your famous “Head-touch” experiment with autistic children. You found in a new experiment that young autistic children, unlike carefully matched children with Down Syndrome, disregarded the experimenter’s intention as indicated by ostensive gestures. This is a strong indication that we cannot rely on what  Gergely and  Csibra called natural pedagogy when teaching autistic children.

Continue reading On Andrassy Ut

The waitress brought cups of coffee and glasses of water. I took up a previous threat of our conversation:

-Your colleagues made the stunning discovery that the A not B error in young  infants was much reduced if the experimenter did not use ostensive gestures. Let me see if I got this right: It is precisely the communicative setting that makes infants perseverate in their error. It is as if they assume the experimenter has taught them to go to a particular hiding place – and this is what they reach for. If the experimenter does not use ostensive gestures, they don’t learn this and consequently don’t make the error. Instead they go for the new hiding place where the object really is.

-Yes, that’s correct, said Ildiko, -and this was the same in dogs, but not in wolves, as shown in the paper with Topal. So natural pedagogy is something that works for dogs too, probably because they have been social companions of humans for millenia.

Chris and I had been extremely interested in studies testing the theory of ‘Natural pedagogy’, introduced by Gergely and Csibra (aka the rockstar Hungarian developmental psychologists). It is a fascinating theory that suggests that humans have a means to acquire culturally relevant information from each other, that makes learning incredibly fast and powerful. The trick that evolution has provided is ‘ostensive communication’.

Chris: – There are two ways of learning from others.  They can address you ostensively, perhaps call you by your name, look at you directly, flash their eye brows at you. But you can also learn by just observing them.

When  our coffee was almost finished, the conversation strayed towards a Bayesian theme. Chris asked: -Why do we pay so much attention to the information that comes from our own senses? When does this start in development?

Ildiko and Katalin both considered this question. -It seems very possible that at first young infants do not pay so much attention to their own sensory information. Take the A not B error. They follow the object with their eyes, and they therefore know where it has been put. But this information counts for less than the information conveyed by the adult’s communication. So it is another person’s perception that seems to win over their own.

-Interesting! So it is not so obvious that we first and foremost regard our own sensory perceptions when making any inferences about the world. Perhaps we are taught that the evidence of our own eyes is the best.

Chris added: – I have just seen a paper by Jaswal who studied children’s trust in information provided by adults. Toddlers believe what an adult says even though they have just seen something different.

My thoughts strayed to “nullius in verba” -take nobody’s word for it- the motto of the Royal Society.

– So is it only since the enlightenment that we feel we must see for ourselves to believe? It was clearly a huge cultural change that brought about the attitude that we should not put our trust in the evidence transmitted to us by others.

-But then aren’t there lots of pitfalls when we put all our trust into our own senses? And by implication, our own experiments?

– Hmmm, we have a conundrum and this relates to our earlier and rather controversial post “Not to be found in any methods section.”



An autism walk in Budapest

On 5th April we all met up in front of the National Academy of Sciences, about 400 people, friends and parents and children, holding blue balloons. The light rain soon stopped as we walked along the river bank, the famous Duna Corso. It was a leisurely walk and I could talk to a number of parents involved in the Hungarian autism association. Like parents everywhere they talked about good times and bad, worries and expectations about their children, all mixed with funny anecdotes. Continue reading An autism walk in Budapest

Uta, Eustacia and Connie BudapestOne of the participants was Eustacia Cutler, mother of Temple Grandin, to the left of the photo, looking absolutely regal aged 89 years. She  had given an inspiring talk the day before. So had Connie Kasari from UCLA, who is in the middle of the photo.  I am on the right holding a biscuit made in the shape of a puzzle piece with blue icing made by a parent.

It was a delight to be in the company of these great women. Many people might be surprised to learn that Temple Grandin’s mother is a Grande Dame of the old school, a one-time actress and still a star performer, and above all a sparklingly intelligent advocate for autism. But it is not so surprising, if you consider that fiercely intelligent Temple too has the quality of a performer. However, it is only Eustacia  – [oh what an apt name] – who has the recognizable charm that radiates from great performers.

What is charm? An intangible quality, far beyond the reach of research in social cognition.

I found only one paper in a Social Psychology journal with reference to charm in the title: Feminine charm: An experimental analysis of its cost and benefits in negotiations. By Laura Kray, Connson C. Locke and Alex B. van Zant.  I was struck by something in the abstract:

…[The authors] expected that the degree to which females were perceived as flirtatious (signaling a concern for self), rather than merely friendly (signaling a concern for other), would predict better economic deals for females.

So it could be that charm is ‘signaling a concern for self’,  while friendliness is ‘signaling a concern for other. What an interesting idea! It seemed to speak to the difference between charming Eustacia on the one side, and friendly Connie and me on the other. It also seemed to hint at an explanation of why autistic children so often strike us as simply charming. But, of course you can be autistic without being charming, just as much as you can be charming without being autistic.