What the study also found was high level of autistic relatives and high scores on Autism spectrum for the prodigies. The relation between autism and prodigiousness was mediated by the endo-phenotype ‘paying attention to detail’ and none of the other symptoms of ASD seemed to play a role.
Many savants also are high on ASD and have exception working as well as long term memory. There too they pay excessive attention to details and are fascinated by speical interests.
Also, if one thinks about that for a minute, autism and ADHD seem to be opposed on a number of dimensions. The three basic features of ADHD are 1) inattentiveness and distractibility vs too much focus and fascination for an object shown by Autistic kid 2) impulsiveness vs restricted and repetitive motions and interests of the autistic kid and finally 3) hyperactivity vs restrained interactions and communications of the autistic kid.
I may even go ahead and stick my neck and say that while autism is primarily characterized by emotion of Interest/ fascination/ attention ; ADHD is characterized by emotion of Wonder/Awe/surprise.
One theory of autism suggests that the social and communicative difficulties arise as the child hides in a cocoon to prevent over-stimulation and sensory overload; a theory of ADHS says that the child is under-stimulated and needs stimulants like Ritalin to achieve baseline of activation and sensory stimulus.
Another popular theory of autism posits that it arises primarily due to ‘weak central coherence’, or inability to see the context/ gestalt/ ‘the big picture’. The ADHD kid on the other hand is hypothesized to use a lot of peripheral attention and daydreams missing what is being centrally taught in the classroom.
And that brings me to the root of the differences in my opinion; while the Autism spectrum is characterized by a local processing style, the ADHD-psychotic spectrum is characterized by a global processing style.
Some clarifications are due here. I believe ADHD to fall on the psychotic spectrum and have been proposing the autism and psychosis as opposites on a continuum model for close to eternity.
Also, when I say global/local processing styles I dont restrict the application to perception alone, but extend it to include cognitive style too.
There is a lot of work that has been done on global/ local processing styles with respect to perception, using Navon letter tasks and it is fairly established that normally people lean towards the global processing style.
Forrester et al extend this to cover there GLOMOSYS system that posits two basic types of perceptual/cognitive style- global and local.
It is also instructive to pause and note that similar to autism-psychosis continuum , it seems Intelligence and creativity are also in a sense opposed to each other. Also while creativity is associated with broad cognitive style that is divergent; intelligence is conceived of as narrow and focused application of abilities.
That brings me to my final analogy: while autistic kids may have pockets of intelligence and savantism and may be driving the evolution of intelligence; it is the ADHD kids who are more likely to be creative and are driving the evolution of creativity.
Joanne Ruthsatz, & Jourdan B. Urbach (2012). Child prodigy: A novel cognitive profile places elevated general intelligence,
exceptional working memory and attention to detail at the root
of prodigiousness Intelligence DOI: 10.1016/j.intell.2012.06.002 Jens F¨orster, & Laura Dannenberg (2010). GLOMOsys: A Systems Account of Global Versus Local Processing Psychological Inquiry, DOI: 10.1080/1047840X.2010.487849
It has been this blog’s thesis that autism and its milder form autism spectrum disorders (ASD) are diametrically opposed to psychosis and its milder form schizotypy. In no area is this more apparent than in the perception or attribution of minds to others. It thus gave me immense pleasure to read this new article by Wegner et al that looks at how the perception of others’ mind is affected in different sub-clinical conditions like ASD, Schizotypy and Psychopathy.
Wegner et al review a great deal of literature to come to the conclusion that others’ mind perception is a two dimensional construct and that we typically attribute mind to an entity depending on whether the entity can experience like us and whether they have goals and agency like us. Thus people can differ in the perception of either Agency or Experience when they attribute mind to an entity. Also b reviewing the available literature they came to the hypothesis that ASD folks should attribute less of agency , but perhaps equal experience to other humans and other entities as compared to controls; Schizotypals on the other hand have been shown to attribute more of mind and in particular agency to other entities than human. They also hypothesized that owing to lack of empathy the psychoptahs might perceive all animals/humans as lacking experience and thus mind-deficient to an extent and subject to manipulation.
They used online surveys to ascertain scores on ASD, schizotypy and psychopathy and correlated that with mind perception and attribution inclinations. How they assessed mind perception was by letting the subjects ascribe perceived experience and perceived agency to nine entities viz. baby, dead woman, dog, God, man , robot, Superman, tree and woman. They performed a confirmatory factor analysis that confirmed that indeed mind perception has two components- Experience and agency.
They got results in line with their hypothesis. ASD folks did not differ in ascribing Experience to fellow humans but did differ in ascribing agency. Schizotypals on the other hand ascribed too much agency to Robots/animals etc; and in general attributing min dto even things like tress , god and dead woman. Psychopaths on the other hand showed reduced ascription of Experience to other humans as well as animals. As an interesting aside, psychopaths attributed more mind to superman perhaps self-identifying with the fictional character
Thus, though mind perception in both ASD and Schizotypy is distorted it is tilted one way in autism and the other way in psychosis. With clinical populations the authors hope to get even stronger results. I am pleased because finally people have started taking the autism is opposed to psychosis paradigm seriously and have started doing research around it that is leading to fruitful results and confirmations.
Another new study that I came across recently and would like to link to found that VPA (valproic acid) treated mice were indeed an apt model of autism in mice and had the same brain correlates and signatures as in Autistic people. It is worth noting that VPA/sodium valproate is used to treat psychosis and I have pointed earlier too how this indicates that autism and psychosis are di\ametrically opposed. It is good that we are getting multiple confirmations of the important autism-psychosis opposition theory.
Autism is a spectrum disorder , better referred to as ASD, It has been known for some time that differences like autism are, multi-dimensional and not readily reducible to a single set of mechanisms or genetic causes. In the past we have discussed how the disorder may be related to structural differences in the brain like those due to minicolumnar differences.
A new study looked at structural differences in brains of people (adults) with ASD and instead of focusing piece-meal on one feature (like minicolumns) combined a multitude of structural features and used a multi-dimensional classification system to determine the accuracy and specificity of the structural differences to predict/aid in diagnoses.
They came uyp with five dimensions- two based on volumetric measurements (surface area and cortical thickness) and the other three on geometric features (average convexity/concavity, mean radial curvature and metric distortion. (the article is open access, so go read it to find what these mean:-) )
What they found was that cortical thickness was the strongest predictor and that predictive power was greater for Left hemisphere measures than for right hemisphere measures.
They also talk about what these measures may mean in terms of underlying neurons and substructures and I reproduce that here:
There is already evidence to suggest that several aspects of cerebral morphology are different in people with ASD—including both volumetric (i.e., cortical thickness, regional area) and geometric (i.e., cortical shape) features (Levitt et al., 2003; Nordahl et al., 2007); and that different morphological features may have different neuropathological and genetic underpinnings (Panizzon et al., 2009). For instance, cortical thickness is likely to reflect dendritic arborization (Huttenlocher, 1990), while cortical surface area has been linked to the number of minicolumns in the cortical layer (Rakic, 1988). Geometric features such as cortical folding pattern, on the other hand, may reflect an abnormal pattern of intrinsic as well as extrinsic connectivity (Van Essen, 1997). Thus, examining the relationship between such multiple cortical features could provide invaluable insights into the multifactorial etiology of ASD.
We know form previous work that all of the above (arborization, minicolumns, local and global connectivity) have been implicated in Autism. The important take-home for me from thi sstudy is the fact that all these are governed by possibly separate underlying genetic mechanisms and may thus be independent of each other. On its own variations in one dimension may not lead to full blown autism, but when variations in all five or more dimensions combine they may make one more susceptible to ASD diagnosis.
Remember we are only talking about structural change sin brains here; we haven’t even touched upon functional differences (default mode network?) and there is plethora of evidence that functional changes are also very important. Overall I believe the multi-dimensional nature of underlying structural and functional differences lend autism the spectrum property and also a continuum with normality. As always I would be eager to know how the SVM they used to classify Autistics fared when asked to classify Psychotics …did the pattern they see was reverse of Autism and inline with the Schizophrenia/psychosis as opposed to Autism theory?
Ecker, C., Marquand, A., Mourao-Miranda, J., Johnston, P., Daly, E., Brammer, M., Maltezos, S., Murphy, C., Robertson, D., Williams, S., & Murphy, D. (2010). Describing the Brain in Autism in Five Dimensions–Magnetic Resonance Imaging-Assisted Diagnosis of Autism Spectrum Disorder Using a Multiparameter Classification Approach Journal of Neuroscience, 30 (32), 10612-10623 DOI: 10.1523/JNEUROSCI.5413-09.2010
Dr Armstrong, was kind enough to answer a few questions for the benefit of our readers and these are reproduced below:
[SG] You have written a wonderful book on neurodiversity. Could you explain in brief, for the benefit of our readers, why neurodiversity has become so important in today’s context and why the focus on neurodiversity now when the differences that underlie the neurodiverse spectrum themselves are age-old?
[TA] I think neurodiversity is, as I’ve suggested in my book, “a concept whose time has come” because of the disability culture we live in. Almost half of us will have mental disorders sometime during our lifetime according to the National Institute of Mental Health, and even more will have “shadow syndromes” or minor versions of those disorders. When we get to the point where virtually everyone is seen as having a mental disorder to one degree or another, I think it’s time that we shift paradigms and use a diversity model instead of a disability model to account for those differences.
[SG] How much does neurodiversity owe to the Autistic advocacy movement and whether those beginnings are productive or counterproductive when one wants to bring other differences like mood or anxiety differences in the fold and talk about them as well?
[TA] I believe that the autistic advocacy movement deserves a great deal of credit for coining and developing the idea of neurodiversity. It’s rather amazing that a group of people who are known for their non-social attributes have made this contribution to our social understanding of brain differences. My hope is that my book Neurodiversity will help to broaden the concept of neurodiversity to include a wider range of abilities/disabilities. As far as I can see from looking at many sites online, there is an openness in the autism community to expanding the definition of neurodiversity beyond simply autism and Asperger’s syndrome.
[SG] Positive Psychology shares some of the same concerns as that of the Neurodiverse movement- the focus on strengths and what works and skepticism about the disease and pathology model- yet why hasn’t, in your opinion neurodiversity become center stage like the positive psychology movement has? Is it because in neurodiversity we are swinging the pendulum too much to the other side and perhaps blinding ourselves to underlying pathologies by claiming everything as differences?
[TA] No, I think it has to do with the credibility of the leadership of the Positive Psychology movement – spearheaded by a former president of the American Psychological Association and other famous professors of psychology. It’s essentially a top-down movement, whereas neurodiversity seems to me to be a bottom-up or “grass roots” movement that is coming from the people who are actually themselves neurodiverse. I don’t think of the neurodiversity movement as saying “we’re all different so leave us alone” I believe that attention needs to be given to ameliorating the disability part of neurodiversity, even as we focus the spotlight on the abilities.
[SG] For the benefit of our readers, if you could highlight the differences between the dimensional and categorical model of pathologies/differences. I believe neurodviversity leans towards the dimensional (continuum ) model. What can DSM V learn form the findings you have discussed in the Neurodiversity book? is a dimensional model of pathology a better one as compared to the categorical one? a necessary evil? or can the DSM mentality be done away with altogether?
[TA] One of the eight principles that I discuss in my book Neurodiversity is that everyone exists along “continuums of competence” with respect to a range of human processes including sociability, literacy, intelligence(s), attention, mood, and so forth. This is very similar to the DSM-V’s embracing of a dimensional perspective, and to that extent, I think the DSM-V is moving in the right direction. The problem is that the DSM-V will be a high stakes publication, and if people are put on a continuum from normal to pathological, the fuzzy line where normal becomes pathological (and vice versa) becomes very important, and may determine whether a person will be labeled with a disorder, given a drug treatment, and perhaps even stigmatized as a result. There’s a danger that many so-called normal people will be added to the ranks of the mentally disordered. Also, what’s missing from the DSM (in all its versions) is any kind of discussion of the positive dimensions of each of the disability categories.
[SG] Just like DSM, positive psychologists have come up with a list of character strengths and virtues as for ex can be seen on VIA signature strength website. Do you think those lists are sufficiently inclusive and give equal weighting to the special abilities found in neurodiverse individuals?
[TA] I think the VIA-IS (or Values in Action Inventory of Strengths) is a positive contribution to our understanding of human personality. It would be good to see someone take this inventory and map it onto the various pathologies taken up in the DSM-V. Wedding the two manuals would be a definite step in the right direction.
[SG] How much yours and your fathers experience of depression has been a driving force in your passion for psychology and especially instrumental in your focusing energies on the neurodiverse people.
[TA] I think it’s been very much a contributory factor. Seeing how my father’s depression affected our family’s functioning while growing up, and how my own depression has shaped my adult life, has been extremely influential in leading me to the field of psychology, and in trying to find the silver lining beyond the dark cloud.
[SG] People who are on extremes of the neurodiverse spectrum face immense stigma in our society. Your chapter on neurodiverstity in classroom talks about inclusive classrooms as you believe special classrooms for special ed programs end up labeling children. How practical you think is the concept of a neurodiverse classroom, esp in developing countries like India. Is a special ed class, even if it ends up labeling a child, better than no intervention at all and traditional classroom education only?
[TA] In a system based on traditional classroom learning, I believe that special education programs outside of the traditional classroom have a place, especially if they are using cutting-edge techniques for helping kids with special needs. But as an educational reformer, I am always pressing educators to expand beyond traditional learning environments for all kids, and when we utilize teaching methods that are good for all kids, we end up helping kids with special needs in the process.
[SG] Niche construction appears to be one of the special focus of your book. would you support or recommended special reservations in jobs/academics for neurodiverse people who may do especially well in those particular niches? For ex. would you favor a legislation that mandated for reservation for autistic people in computer testing industry. I’m thinking of cultural diversity guidelines in colleges, should we have similar neurodiversity guidelines too?
[TA] Are you talking about affirmative action for neurodiverse people? If so, then I believe there might be some merit in exploring how this might work. ([SG] note: yes, I was indeed talking about affirmative action; in India we typically refer to the issue as that of reservations!)
[SG] How did the writing of Neurodiversity enrich you as an individual. wWat can readers hope to take away from the book?
[TA] I wrote Neurodiversity while in the midst of a major depressive episode. At times I could hear myself saying “why are you looking at the strengths of these disorders, for God’s sake, when you know that they’re hell to deal with?” But there was another part of me, an intuitive part I believe, that instinctively believed it was important for me to bring strengths into the discourse about mental disabilities. I hope that readers will see this book as a supplementary guide to all the other books on disabilities that focus on the negatives. It’s important that we see both sides of the issue. We are, after all, whole human beings, with a great deal of complexity and richness. I hope that readers will take away a sense of this richness in the diversity of minds that make up humanity.
I would like to thank Dr Armstrong for taking some time off for the interview and would recommended the readers to read up some of his books, many of which focus on the special abilities and aptitudes of the neurodiverse people.
Today is Autistic Pride day celebrating the neurodiversity found among people. Neurodiversity , as a movement , has been traditionally associated with the autism community, but it is important to realize that when one speaks of neurodiversity one is also referring to other ‘differences’ in brain structure and organization like that seen in ADHD, dyslexia etc.
This emphasis on other differences than autism and continuum from neurotypicals in a neurodiversity spectrum is aptly highlighted by a timely book: Neurodiversity by Thomas Armstrong. The subtitle of the book reads ‘discovering the extraordinary gifts of autism, ADHD, dyslexia and other brain differences’ and Dr. Armstrong extends the neurodiversirty argument from traditionally seen ‘differences/diseases’ like Autism or ADHD or intellectual disabilities to the not-so-traditionally differences/diseases like Mood disorders, anxiety disorders and Schizophrenia.
The argument is that all these ‘differences’ are not to be conceptualized in a disease model where there are differences of kind, but in a differences and diversity model where things are in a continuum from normality to deviation and differences are of a degree rather than a kind. Also the emphasis is on the strengths and unique abilities of the people having different brains and not juts being focused or defining these conditions by what doesn’t work or is broken. thus Autism is not juts lack of sociability but must be conceptualized as a strength enabling interest and focus on objects vis-a-vis people.
In a way Neurodiversity is positive psychology on steroids. While positive psychology normally focuses on strengths of healthy or high functioning people, neurodiversity takes this one step forward and focuses on strengths of people traditionally classified as diseased in the disease model. By reconceptualizing this neurodiversity in terms of differences and variations that have evolved to make us better respond to changing environmental conditions puts a new spin to the differences debate and makes us appreciate and see these neurodiverse people in a new, non-stigmatized light.
Key to appreciating the neurodivesrity arguments spread throughout the book in the form of separate chapters for each of the seven differences that Armstrong focuses on (autism, adhd, dyslexia, intellectual disabilities, mood disorders, anxiety disorders and schizophrenia) is the view of the brain and the view of how neurodiverse individuals should be conceptualized and fit in with the society- be it by adapting to the society or doing niche construction. These principles, (eight of them) are elaborated and introduced in the first chapter and are thankfully available online in an abridged format. I would heavily recommend that interested people go read it.
I have just read the first few chapters relating to autism, ADHD and dyslexia till now, and they are written beautifully and capture the latest research while focusing on the positives and on niche construction. I am still to read the chapters on mood disorders and schizophrenia for example, and believe taht is they are as persuasive we are on the verge of e anew paradigm shift in ‘abnormal’ psychology as when one takes anxiety, mood and thinking disorders in its ambit, not much is left of traditional disease-based abnormal psychology. Im looking forward to reading the rest of the chapters and will post a follow up blog soon.
Meanwhile I whole heartedly recommend this book to the people who themselves or their near and dear ones are placed on the neurodiversiry spectrum be it as part of autistic pride movement or some other community. Going by the total incidence and prevalence of mental ill health in general , that means , this book is heavily recommended for everyone:-)
Full disclosure: I received a free review copy of this book.
I recently came across this post by Michelle Dawson that states the thesis that one of the abnormalities in Autism spectrum disorders is due to abnormal circadian clock functioning. More specifically, the clock is internally driven and has a greeter ‘free running’ period and does not entrain readily to environmental and social clues.
Autistics whose sleep-wake cycles carry on independently from environmental and social cues are said to be “freerunning.”
The usual response to freerunning in autism is to see this as an autism-related sleep disorder. There is very preliminary evidence that freerunning autistics can be successfully treated with melatonin. Bourgeron (2007) refers to a short case study about an autistic whose free-running was remediated by melatonin treatment.
If you feel a bit overwhelmed by all the circadian clock related terminologies, I wholeheartedly recommend BoraZ’s clock tutorial series , especially this one.
Dawson further says:
Glickman (2010) speculates that some autistics’ failure to chain our sleep-wake cycles to environmental cues may arise from our atypical perception. My totally wild guess might be that an extreme freerunning phenotype in autism may be contributed to in part by cognitive versatility in autism, which would result in perceived environmental cues affecting sleep-wake cycles in an optional rather than mandatory way.
I wont speculate about the reasons behind why autistics have a greater free-running period and less entrainment to social and environmental clue, but I woudl say that instead of giving them flexibility, I would presume that this locks them into their internal rhythms, while others are more responsive to environment and better adapted. That brings me to the opposite phenotype of ASD…the psychotic phenotype shown by Schizophrenics, depressives and Bipolars.
The contribution of the circadian regulatory system, arising from conflicts between internal biological clocks and environmental (solar) and social clocks, is evident in affective disorders. All major affective disorders (such as unipolar depression, OMIM #608516; bipolar disorder, and schizophrenia, OMIM #181500) include circadian phase disturbances in sleep, activity, temperature, and hormone levels (for reviews see –). Moreover, there is evidence that if rhythms can be altered/stabilised using relevant therapies, improvements in the primary symptoms can occur. For example, in some instances sleep deprivation has an antidepressant effect in patients . Conversely, many disorders with a primary anomaly in the circadian system are associated with depressed mood. Seasonal affective disorder (SAD; OMIM #608516) is a common condition where depressive symptoms occur during shorter winter days –. Two inherited sleep phase disorders, familial advanced sleep phase syndrome (FASPS; OMIM #604348) and delayed sleep phase syndrome (DSPS), are both associated with abnormal affective states ,. Furthermore, individuals with a behavioural preference for “eveningness” have a greater tendency to develop depression .
The above to me seems hypersensitivity to social and environmental cues in affective/psychotic disorders. contrast this with ASD description by the same authors:
Other behavioural disorders with circadian and sleep-related disturbances include autism spectrum disorders (ASD) (OMIM %209850) ). Behavioural disturbances in ASD may arise in part from an inability of an individual’s circadian oscillator to entrain to environmental and social cues. One specific correlate of ASD is a low level of melatonin, and one of the enzymes critical in the synthesis of melatonin, acetylserotonin-O-methyltransferase (ASMT, OMIM *300015), is implicated as a susceptibility gene for ASD .
The role of melatonin seems to provide a clue. In autism, there seems to be low levels of melatonin and perhaps hypo-sensitivity to melatonin changes. In contrast Bipolar is marked by hypersensitivity of Melatonin receptors:
It has been suggested that a hypersensitivity of the melatonin receptors in the eye could be a reliable indicator of bipolar disorder, in studies called a trait marker, as it is not dependent on state (mood, time, etc.). In small studies, patients diagnosed as bipolar reliably showed a melatonin-receptor hypersensitivity to light during sleep, causing a rapid drop in sleeptime melatonin levels compared to controls. Another study showed that drug-free, recovered, bipolar patients exhibited no hypersensitivity to light. It has also been shown in humans that valproic acid, a mood stabilizer, increases transcription of melatonin receptors and decreases eye melatonin-receptor sensitivity in healthy volunteers while low-dose lithium, another mood stabilizer, in healthy volunteers, decreases sensitivity to light when sleeping, but doesn’t alter melatonin synthesis. The extent to which melatonin alterations may be a cause or effect of bipolar disorder are not fully known.
The above is not the only source implicating Bipolar disorder and circadian clock dysfunction., See more here and here. The big question is not whether ASD and Affective disorders are both circadian rhythm disorders, but the big question is whether they show opposite phenotypes with respect to circadian clocks- one showing too little entrainment while the other too much? Barnard, A., & Nolan, P. (2008). When Clocks Go Bad: Neurobehavioural Consequences of Disrupted Circadian Timing PLoS Genetics, 4 (5) DOI: 10.1371/journal.pgen.1000040
A new paper by Ben Bashat et al extends their earlier findings that had found that there was accelerated maturation of white matter in children with Autism. In this new paper they use Tract Based Spatial statistics (TBSS) to determine the white matter integrity of children (age around 3 years) with Autism as compared to normal controls. Of course they used Diffusion tensor Imaging to find out Fractional anisotropy and other measures of white matter integrity.
Essentially they found that in some regions/tracts there was greater Fractional Anisotropy (FA) as compared to controls. These regions/tracts were genu and body of the corpus callosum (CC), left superior longitudinal fasciculus (SLF) and right and left cingulum (Cg). They also found that in areas of high FA there was corresponding decrease in Radial diffusivity (Dr). What this essentially means, to my naive mind, is that greater conductance or speed of action potential in axons would primarily be due to enhanced myelination which reduces leakage or lateral flow of AP.
I’ll like to contrast the results with an earlier study I had blogged about regarding creativity, psychopathology and white matter mylienation connection. As per that study an inverse relation was found between people high on creativity (divergent type) and Fractional anisotropy in frontal regions, i’e there was low FA. Also importantly there was increased Dr (radial diffusivity) in the same regions and thus the conclusion was that there was reduced myelination in those areas which meant reduced signal transmission speed and more signal leak . It is notable that that study too used DTI and Tract based Spatial statistics (TBSS) analysis method to arrive at their conclusions.
Regular readers of this blog will know my fanaticism for Autism and Psychosis as opposites on a continuum theory. This new paper nicely fits in with my last post linking creativity/psychosis and white matter/myelination, I had as much surmised that Autism would show the opposite effect and have high FA and decreased Dr. It is heartening to note when such a relation is found and reported- goes to show the strength and ability to make predictions of the theory.
However, I would also like to point out and highlight that I believe Autistic spectrum is characterized by another type of ability – the savantic intelligence– that may be directly due to this white matter /excess myelination effect. Perhaps the signals travel so fast that decisions are made locally without the time available to get other far-0off regions involved- thus giving attention to details but inability to link disparate regions and ideas.
Weinstein, M., Ben-Sira, L., Levy, Y., Zachor, D., Itzhak, E., Artzi, M., Tarrasch, R., Eksteine, P., Hendler, T., & Bashat, D. (2010). Abnormal white matter integrity in young children with autismHuman Brain Mapping DOI: 10.1002/hbm.21042 Ben Bashat, D., Kronfeld-Duenias, V., Zachor, D., Ekstein, P., Hendler, T., Tarrasch, R., Even, A., Levy, Y., & Ben Sira, L. (2007). Accelerated maturation of white matter in young children with autism: A high b value DWI study NeuroImage, 37 (1), 40-47 DOI: 10.1016/j.neuroimage.2007.04.060 Jung, R., Grazioplene, R., Caprihan, A., Chavez, R., & Haier, R. (2010). White Matter Integrity, Creativity, and Psychopathology: Disentangling Constructs with Diffusion Tensor Imaging PLoS ONE, 5 (3) DOI: 10.1371/journal.pone.0009818
There is a recent article in New Scientist about consciousness and its neural correlates and the article focuses on work of Stanislas Deheane and his colleagues and how they are trying to get evidence and proof for the Global workspace theory of consciousness as proposed by Beranrd Baars.
That led me to this excellent article by Raphaël Gaillard that uses iEEG (intracranial EEG) using electrodes placed in brain, but not doing single-cell recording but still working on aggregates but at a much higher spatial and temporal resolution than normal extra-cranial EEG. They used electrodes placed in epileptic patients undergoing surgery and determined the difference in neural activity during conscious and unconscious access.
For differentiating between the unconscious and conscious access they used the popular visual masking paradigm, whereby a target word is presented and then immediately afterwords (after a few ms only) a mask is presented; if the duration of stimuli presentation is less and it is immediately followed by a mask, then though the stimulus is processed unconsciously, it is not available for verbal report and is not processed consciously. In contrast, in the unmasked condition, the target is not followed by a mask and hence is available for conscious access. In the present experiment, the authors used a forward as well as a backward mask and also had a condition whereby a blank screen was present instead of target ; so that effects of processing target alone could be determined after subtracting the effect of masks. the paper is one access and very lucidly written so go have a look!
A quick detour: Bernard Baars global workspace theory posits that consciousness arises when neural representations of external stimuli, are made available wide spread to global areas of the brain and not restricted to the originating local areas. This has also been characterized as an attentional spotlight and whatever comes under the spotlight in global workspace, is widely visible to the rest of the audience (the other parts of the brain) and also gives rise to consciousness. In the absence of coming to focal awareness(spotlight), the processing/representation happens unconsciously by the many different parallel brain modules. Thus, while unconscious representations may arise in brain locally, to become conscious they need to become widespread and available to the entire (or most of) the brain. To boot:
We adopted a theory-driven approach, trying to test experimentally a set of explicit predictions derived from the global workspace model of conscious access. This model, in part inspired from Bernard Baars’ theory , proposes that at any given time, many modular cerebral networks are active in parallel and process information in an unconscious manner [22,23,31,32]. Incoming visual information becomes conscious, however, if and only if the three following conditions are met : Condition 1: information must be explicitly represented by the neuronal firing of perceptual networks located in visual cortical areas coding for the specific features of the conscious percept. Condition 2: this neuronal representation must reach a minimal threshold of duration and intensity necessary for access to a second stage of processing, associated with a distributed cortical network involved in particular parietal and prefrontal cortices. Condition 3: through joint bottom-up propagation and top-down attentional amplification, the ensuing brain-scale neural assembly must “ignite” into a self-sustained reverberant state of coherent activity that involves many neurons distributed throughout the brain.
Based on this theoretical framework, the following hypothesis were developed:
Neurophysiological Predictions Derived from the Global Workspace Model
In the light of our model, the masked–unmasked contrast corresponds to a comparison between a visual representation satisfying only condition 1 and a representation satisfying all three conditions for conscious access listed above. The global workspace model therefore leads to the following four predictions.
Prediction 1: a common early stage of processing.
Both masked and unmasked words should evoke similar neural activity within an early time window, reflecting a fast feedforward sweep propagating from posterior to anterior cortices. In particular, invisible masked words should induce transient event-related responses along the ventral visual pathway, as assessed by iERPs and ERSP.
Prediction 2: a temporal divergence.
Following this initial common stage, only unmasked words should be associated with sustained effects. We thus predict a divergence in cortical activation for unmasked and masked words. Given that we contrasted heavily masked stimuli with unmasked stimuli, we expect a progressive buildup of the divergence between these two conditions. In the light of recent high-resolution scalp electroencephalogram (EEG) studies in visual masking and attentional blink paradigms, this temporal divergence is expected to occur within a 200–500-ms window [1,2].
Prediction 3: an anatomical divergence.
The activation of frontal and parietal areas, which are allegedly dense in global workspace neurons, should be particularly sensitive to consciously perceived words (see  and Figure 1 of  for explicit simulations of this property). Although masked words may cause a small, transient and local activation within these regions, we predict that unmasked words should elicit a global and long-lasting activation of these regions, corresponding to a broadcasting process.
Prediction 4: phase synchrony and causality.
During this late time window, the long-lasting and long-distance neuronal assembly specific to conscious processing should be associated with an intense increase in bidirectional interelectrode communication. Measures of phase synchrony and Granger causality should be particularly apt at capturing this phenomenon.
And this is exactly what they found. They found that upto 200 ms activity in the unmasked and masked condition did not differ significantly and represented an early stage of processing. In the 200-500 ms window (post stimulus onset), there was temporal divergence with there being long-distance beta synchrony, sustained amplitudes and power in gamma band and Granger causality in the unmasked case, but not in the masked case. Further, there was anatomical divergence, with the unmasked condition showing more occipitotemporal activation, while the unmasked condition showing global (and especially frontal) activation. Lastly while local beta synchrony and reverse feed back causality (accounted perhaps by top-down attentional factors that try to focus more given the masking) was associated with the masked condition, long distance beta synchrony and causal imbalance in the feed-forward direction was only found in the unmasked condition, thereby validating the claim that in the unmasked condition the posterior local representations weer made globally available to anterior regions as well (these are my very brief summaries, you should read the original freely available article for nuances and details).
This is how the authors conclude:
The main motivation of our study was to probe the convergence of multiple neurophysiological measures of brain activity in order to define candidate neural signatures of conscious access. Conscious word processing was associated with the following four markers: (1) sustained iERPs within a late time window (>300 ms after stimulus presentation); (2) sustained and late spectral power changes, combining a high-gamma increase, beta suppression, and alpha blockage; (3) sustained and late increases in long-range phase coherence in the beta range; and (4) sustained and late increases in long-range causal relations.
Our results suggest that in the search for neural correlates of consciousness, time-domain, frequency-domain, and causality-based electrophysiological measures should not be seen as competing possibilities. Rather, all of these measures may provide distinct glimpses into the same distributed state of long-distance reverberation. Indeed, it seems to be the convergence of these measures in a late time window, rather than the mere presence of any single one of them, that best characterizes conscious trials.
That brings me back to the new scientist article:
Dehaene’s group had already shown that distant areas of the brain are connected to each other and, importantly, that these connections are especially dense in the prefrontal, cingulate and parietal regions of the cortex, which are involved in processes like planning and reasoning.
Considering Baars’s theory, the team suggested that these long-distance connections may be the architecture that links the many separate regions together during conscious experience. “So, you may have multiple local processes, but a single global conscious state,” says Dehaene. If so, the areas with especially dense connections would be prime candidates for key regions in the global workspace.
Now it is well known that in autism there are more local connections and more local processing; while psychosis/ schizophrenia spectrum is marked by more long-distance connections/ activity. If so , it is not unreasonable to conclude that psychotics may have higher p-conscious experiences while autistics may be stuck at more lower A-conscious experiences. I proposed something like that in my post titled ‘what it is like to be a zombie‘ and you are strongly encouraged to go read it now.
Certain regions of the brain’s global workspace, dubbed the default mode network (DMN), are active even when we are resting and not concentrating on any particular task. If the global workspace really is essential for conscious perception, Laureys’s team predicted that the activity of the DMN should be greatest in healthy volunteers and in people with locked-in-syndrome, who are conscious but can only move their eyes, and much less active in minimally conscious patients. Those in a vegetative state or in a coma should have even less activity in the DMN.
The researchers found just that when they scanned the brains of 14 people with brain damage and 14 healthy volunteers using fMRI. In a paper published in December 2009, they showed that the activity of the DMN dropped exponentially starting with healthy volunteers right down to those in a vegetative state (Brain, vol 133, p 161). “The difference between minimally conscious and vegetative state is not easy to make on the bedside and four times out of 10 we may get it wrong,” he says. “So this could be of diagnostic value.”
While the DMN may be important marker for brain damaged patients, it also has the potential to become a marker for different feels of consciousness sin brain intact but differently wired brains like those of autistics and psychotics.
I believe one way of conceptualizing autism is as a diminishing of consciousness/ subjective experience; while that of psychosis as overabundance of consciousness/ subjective feeling. Maybe that is why shamans of all ages have been closely identified with the psychotic spectrum.
If autistics have more local processing, then perhaps they should be better at tasks involving unconscious stimuli: perhaps that’s why despite their savantic abilities , much of what happens in the autistic mind is not only non-verbal , but also non-conscious and hence not juts not available for verbal report, but not accessible to consciousness.
I strongly feel that adding the consciousness dimension to autism/schizophrenia spectrum may be a good thing and lead to more clarity and new directions in research.
Gaillard, R., Dehaene, S., Adam, C., Clémenceau, S., Hasboun, D., Baulac, M., Cohen, L., & Naccache, L. (2009). Converging Intracranial Markers of Conscious Access PLoS Biology, 7 (3) DOI: 10.1371/journal.pbio.1000061
There is an article in press in Neuropsyhcologia by Lackner et al that related Dopamine (DA) levels as measured by Eye Blink Rate (EBR) to preschoolers (3-5 yrs old) Representational theory of Mind (RTM).
The authors hypothesized that as one of the neural correlates of RTM is dMPFC, and as dMPFC has dopamine receptors and is innervated by dopmainergic projections along the dopamine mesocortical pathways , hence perhaps it is the dopamine’s tonic and phasic levels that may be correlated with and have a causal role in the preschoolers’ developing RTM abilities.
3-5 years is a critical period in which the RTM abilities are developing in a normal kid and are first found to be deficient in autistic kids. another linkage the authors seem relevant, but which I don’t agree to much, is the error -prediction theory of dopamine. They believe that ToM/RTM abilities develop when one takes into account the behavior of others and finds discrepancies in ones own knowledge and why they act based on certain different assumptions and by realizing this error of prediction modifies ones understanding of others and starts attributing a mind to them. The authors believe that phasic dopamine which has error prediction functions may be affecting RTM via this pathway too; I find that not very convincing.
However, their basic premise that tonic or baseline dopamine affects RTM abilite seems to be on firm ground and they found support for this hypothesis. They did not measure DA levels directly , but instead relied on Eye Bink Rate (EBR) which is a robuts predictor of overall dopamine in the mesolimbic pathways via the caudate nucleus dopamine levels. They also did not measure EBR directly but measured it using EEG waveforms of relevant brain regions above the eyes.
The RTM tasks they used and the Response -conflict executive function (RC-EF) tasks they used are very simple and intuitive and I refer the reader to methods section to pursue them in detail. For our purpose it is sufficient to mention that RTM did not include the famous anne-sally false belief task but had other variants like false belief location task etc.
Their findings were unequivocal. They found that DA levels as gauged from EBR were a significant predictors of RTM abilities and the effect was not mediated by a possible confound- that of RTM and RC-EF linkages and correlations.
For our purposes what is most important is the direction of the effect . More DA levels were associated with better RTM ; while lower DA was associated with lower RTM performance. This is consistent with the DA relation of Schizophrenia/Autism one of which has higher DA levels and better ToM; while the other both poorer ToM and lower baseline DA. To quote:
These findings dovetail with other research connecting dopamine and representational theory of mind in autistic and schizophrenic populations. Both autism and schizophrenia have been associated with RTM impairment (Pickup, 2008; Sabbagh,2004; Savina & Beninger, 2007) and dysregulation of DA (Braver, Barch, & Cohen, 1999; Lam, Aman, & Arnold, 2006). For instance, in the case of schizophrenia there is some evidence that increased levels of frontal dopamine, as a consequence of the pharmacological activity of some atypical antipsychotics, leads to increased performance on RTM tasks (Savina & Beninger, 2007). The present study added to this body of literature by demonstrating associations between RTM and DA in typically developing children. Considered together, this further supports the hypothesis that dopaminergic functioning plays a role in RTM development.
As always, I am excited by more support for Autism and Psychosis as opposites theory and belive this further cements the case and shows possible neurochemichal mechanisms underlying the difference.
Regular readers of this blog will know my fascination with autism and psychosis as opponents on a continuum theory . I have already been privately speculating that ADHD in childhood may be a risk factor for Psychosis in later adolescence, especially as both are supposed to have underling dopamine abnormalities, so this new study by Brembs et al caught my attention.
Recently I came cross this paper by Bjorn Brembs et al that investigated attention-like processes in mutant fly models that showed memory deficits. They weer aqble to show that despite overt similar olfactory memory deficits, the attention-like processes worked in opposite ways in the two mutant models. In the rutabaga/dunce model, the atention ws hyperfocussed , resembling human autism; while in radish models , attention was flexible and distract-able resembling human ADHD.
It is increasingly apparent that many classical Drosophila learning and memory mutants are also defective in short-term processes relevant to selective attention. Previous studies have shown that short-term memory as well as long-term memory mutants display attention-like defects (van Swinderen, 2007; van Swinderen et al., 2009), and the current study reveals radish mutants to be defective as well, albeit with distinctly different symptoms. The Drosophila mutants dunce1, rutabaga2080, and radish1 share olfactory memory defects but differ conspicuously for short-term processes relevant to visual attention. Whereas the more persistent optomotor behavior of dunce1 and rutabaga2080, both affecting the cAMP-associated pathways (Davis et al., 1995), are reminiscent of the persistent preoccupation of some patients afflicted with autism, the phenotype of radish mutant flies described here is similar to some of the symptoms of patients with ADHD.
They further speculate as o why these two phenotypes may be present and relate it to exploit/explore conundrum.
Attaining the right balance between persistence and flexibility is a crucial feature of adaptive behavior, because it reflects the balance between exploration and exploitation of natural resources. It is tempting to speculate that radish and dunce/rutabaga may constitute the two respective extremes of this balance. Recent work investigating torque behavior of wild-type flies (similar to our shorter experiments here) has shown that, during extended flights, the occurrence of turning maneuvers can be described by a Le´vi distribution (Maye et al., 2007). Such distributions of behavioral output, seen in foraging behavior in many animals, are characteristically long-tailed. This means that animals may occasionally persist with one behavioral choice for unusually long, but most often choices alternate at a more regular, normally distributed rate. The advantage of allowing for occasional long forays into one direction is presumably to chance on a new resource away from the proximal search space. Such behavior has been found to be ecologically advantageous, but mechanisms driving such alternation tendencies have not been documented in the Drosophila brain. One interpretation of our results is that the mushroom body circuits defined by dunce/ rutabaga/radish expression are involved in establishing the balance between persistence and flexibility [i.e., the explore/exploit dilemma (Daw et al., 2006)]. A separate set of results has independently also arrived at a similar conclusion, suggesting that the mushroom bodies could be involved in maintaining a period of behavioral flexibility (i.e., attention-like processes) before a longer-term transition to habit formation or motor learning
To me, this research adds another intriguing possibility to the autism-psychosis dimension, that of ADHD as a childhood phenotype/risk factor for later psychosis.
van Swinderen, B., & Brembs, B. (2010). Attention-Like Deficit and Hyperactivity in a Drosophila Memory Mutant Journal of Neuroscience, 30 (3), 1003-1014 DOI: 10.1523/JNEUROSCI.4516-09.2010
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