Tag Archives: autism

How Cotard’s and other phenomena throw light on the self

indexCan the Cotard’s syndrome tell us something about the self? A person suffering from Cotard’s syndrome is likely to claim that he/ she is dead- can such a delusional experience make us appreciate what self is what it isn’t – and more importantly how the sense of self can go awry in some phenomena?

Anil Ananthaswamy, in his exquisitely written book ‘ The Man Who Wasn’t There‘ beautifully illustrates how Cotard’s and other such weird and not so weird phenomena can shed light on the true nature of self (provided the self exists and there is something it is like to have a self- more about this later).

The book is beautifully written, weaving narratives of actual patients suffering from various disorders, with cutting edge research in the field and at all times tying it back to the nature of the self.

Although the eight chapters talk about eight different phenomena- ranging from Cotard’s to deperosnalisation to Autism to schizophrenia to out-of-body experiences and ecstatic epilepsy to BIID ( or having a desire to amputate ones limbs) and Alzheimer’s – there doesn’t seem any discontinuity- nor does it seem as if disparate phenomena are being talked about. With self being the focus, each of these is used to approach the self from a different angle.

I am reminded of the parable of  blind men and the elephant – whereby each blind men could only grasp one part of the elephant. Self is such an elephant in the room. The various chapters do advance our understanding of the self and fortunately, this time, the sum is greater than the sum of the parts, and we are indeed able to get a  sense of the elephant/self!

It would be naive to assume that Anil would have solved the problem of self where great philosophers or scientists of past and present have failed to do so- but he does gives tantalizing glimpses of what the answer might me and at least brings us up to speed with what is being thought of in the philosophical / scientific circles.

The power of the book comes from its very approachable and readable writings style and the humane treatment of its subjects.  Whether its the isolation felt by a BID sufferer who has no means of getting his limb amputated legally or the strangeness felt by those suffering from deperosnailsation, Anil makes the stories vivid- loud and clear in one’s mind;s eyes.

The book is also chock full of interesting facts- some of which I was already familiar with, but got an opportunity to brush up on the latest happenings in the filed, others were new to me – for example I hadn’t realized that people with Cotard’s are typically depressed or that people remember more about their life from between 10 and 30 years (the reminiscence bump) and many such nuggets.

The book is immensely readable and holds your attention from chapter to chapter.  I was almost felling bad about having finished it as I wanted more of the treats to continue.  In a week in which we lost Oliver Sacks, it takes some solace to discover that there are others who are keeping the tradition alive.

Both the erudition , humanity and narration of Anil is superb. While reading the book, I thought he was himself a prominent neuroscientist- its only post reading it I realized he is a science journalist and has also written  a best seller in physics. Surprising how brilliant people are able to make their mark in whatever field they chose to focus on. Quiet coincidentally I had also reviewed ‘Subliminal’ by Leonord Mlodinow- who is also a physicist but has written a good book rooted in psychology.

My advice to readers of this blog- if you loved Sacks, if you loved VS Ramachandran,  or even if you didn’t or haven’t heard about them, do give this book a read- you are going to love the easy style- yet a lot of substance. I, for one , am eagerly looking forward to Anil’s next read.

Autism and ADHD: the intelligent and the creative child!

ResearchBlogging.org
A new study by Ruthsatz and Urbach is doing the rounds nowadays. That study has nothing to do with Autism or ADHD per se. The study focuses on child prodigies and finds that they have high levels of intelligence, enhanced working memory and that they pay attention to details.

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.

 

On the other hand there is gathering literature that suggests that the ADHD kid is basically on the creative side of the spectrum – restless, trying multiple strategies,  having diffused and peripheral attention, and to an extent novelty and sensation seeking.

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.

There is also some data from fly models that suggest that autism and ADHD are opposites in a sense.

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 instructive to pause and note here that psychosis is associated with a global processing style while autism with attention to details.

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.

The romantic notion that psychosis is the price for creativity may not be untrue.

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

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Psychosis and the City

English: Himba village about 15 km north of Op...

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ResearchBlogging.org
This post originally appeared on my Psychology Today blog “The Fundamental Four” on 15th Dec. 2011.  This is cross-posted from there.

Abundant evidence exists that psychosis is more prevalent in urban areas as compared to rural areas. The fact that living in the city makes one vulnerable to psychosis is not up for debate – but healthy debate ensues about the mediating mechanisms.
Last year, Zammit et al claimed that the high incidence of psychosis in urban settings is a result of greater social fragmentation in urban areas.
Today I came across a study [pdf] that had nothing to do with psychosis and came up with this novel hypothesis that the mediating mechanism may be global versus local focus or processing style. If that seems farfetched, bear with me for a while.
First a bit of background, the new study was referenced by Christian Jarrett in a BPS research digest blog post in which he lucidly shows that it has been found that living in urban areas has been found to be associated with a propensity for global processing style (seeing the forest); while living in rural areas has been found to be associated with a local processing style (focusing on the trees and missing the forest).

The study itself is pretty straight forward; in one of the local/global task it used the famous Ebbinghaus illusion (see image) to measure the amount of bias towards global vis-a-vis local processing.


In the second task it used large, composite (global) shapes/letters made of small, parts (local) which were also themselves shapes/letters and then measured whether one was more drawn in making inferences/similarity based on global percepts or the local figurine.

The study measured this global vs. local bias in Himba society (Namibia) members who had varying level of exposure to urban environments as well as Japanese and British urbanites. What they found was that living in urban areas/ exposure to urban areas was significantly predictive of whether you would lean more towards more global mode of processing. The authors link this with more ‘visual clutter’ in the cities necessitating a global style of processing.
Christian mentions in passing the fact that autistic people have a very local bias of processing and are marked by weak central coherence; what he perhaps doesn’t realize is that psychotics, which have been conceptualized to lie diametrically opposed on a continuum from autistic, have a global processing bias and a strong central coherence.
Badcock and Crespi, and I even before them, have been crying from the rooftops to conceptualize psychosis and autism as diametrical disorders – and some investigators have paid heed. Suzzana N et al [pdf] have recently shown that as conceptualized by Badcock and Crespi , Autistics and Psychotics are actually at opposed ends of local vs global processing.

To quote:

We refer particularly to Crespi and Badcock (2008), who make the novel claim that the autism and positive schizophrenia spectra are diametrically opposed. They argue that individuals with autistic traits and individuals with positive symptoms of schizophrenia (e.g., magical ideation, unusual perceptual experiences and paranoia) should exhibit opposite cognitive profiles. The current investigation focuses specifically on their claim that autistic and positive schizophrenia traits contrastingly affect preference for local (i.e., piecemeal) versus global (i.e., integrative) processing.

Crespi and Badcock (2008) argue that while autistic traits are associated with a preference for local over global processing, positive schizophrenia traits are associated with a preference for global over local processing. That is, these authors claim that while individuals with autism show a tendency to focus on detail or process features in their isolation, individuals with traits of positive schizophrenia show a tendency to look at the ‘bigger picture’ or process features as an integrated whole. Although a preference for local processing fits theoretically with the tendency of individuals with autism to notice minor features or changes to the environment that are often overlooked by others (Hayes 1987), the link between traits of positive schizophrenia and a preference for global processing is less obvious. It is hypothesized though, that a global processing style could contribute to the complex delusions and enhanced creativity for individuals with positive schizophrenia (Nettle 2006; Oberman and Pascual-Leone 2008), as well as the tendency of these individuals to make ‘‘loose” associations between words and between aspects of the environment (Maher 1983; Spitzer 1997; Spitzer et al. 1993). Importantly, the effect of such loose associations is that one thought does not logically relate to the next, and thus these associations may be strongly linked to the hallucinations and delusions experienced by individuals with positive schizophrenia. However, while there are potential links of local and global processing to features of autism and positive schizotypy, the preferred processing styles for individuals with autistic and schizophrenic traits are yet to be examined together in the one investigation. Therefore, the current study aims to provide the first complete empirical test of Crespi and Badcock’s claim regarding local-global processing.

And this is exactly what they found. They used an embedded figural task to assess the global vs. Local bias and their results showed that indeed psychosis prone individuals had a more global style of processing.

Now one thing I am good at is putting two and two together and the moment I saw the new study correlating global style with urban living, a lot of pieces fell into place. Form the above it is apparent that global processing style may be an intermediate mediating factor that leads to association between urban living and psychosis.

What neural mechanism may be involved?

To quote from the Suzzana et al paper again:

The contrasting preferences for local versus global processing are identified with differences in brain connectivity in particular (Crespi and Badcock 2008). Reference is made to both structural (intrahemispheric and interhemispheric) and functional connectivity. Specifically, Crespi and Badcock argue that the preference for local over global processing displayed by individuals with autistic traits, compared to controls or individuals low on autistic traits, is a result of increased connectivity within neural regions relative to decreased connectivity across regions (Courchesne and Pierce 2005a, b; Happe´ and Frith 2006). Crespi and Badcock then argue that schizophrenia is associated with decreased connectivity within neural regions relative to an increased connectivity across brain regions (Colger and Serafetinides 1990; Siekmeier and Hoffman 2002), leading individuals with traits of positive schizophrenia to favor a global (over local) processing style, compared to controls or people low on these traits. These differences in brain connectivity for autism and positive schizophrenia are said to be mediated, at least in part, by genomic imprinting.

While genomic imprinting may be one mechanism, maybe there is something about exposure to urban environments (maybe it’s ‘visual clutter’) that also has a similar effect on pruning of synapses and unduly affect local pruning at the cost of pruning between widely separated regions thus leading to global processing bias.

Instructive to pause here and note that in children they start with local bias and around 6 year of age revert to global bias that adults typically have and this is mediated by synaptic pruning. See this open access PLOS one article.

Thus, it seems Psychosis and the City are intimately connected; and that, this is because, to live in a city, you need to (de)focus on ‘the big picture’.

 


Caparos, S., Ahmed, L., Bremner, A., de Fockert, J., Linnell, K., & Davidoff, J. (2012). Exposure to an urban environment alters the local bias of a remote culture Cognition, 122 (1), 80-85 DOI: 10.1016/j.cognition.2011.08.013
Crespi, B., & Badcock, C. (2008). Psychosis and autism as diametrical disorders of the social brain Behavioral and Brain Sciences, 31 (03) DOI: 10.1017/S0140525X08004214
Zammit, S., Lewis, G., Rasbash, J., Dalman, C., Gustafsson, J., & Allebeck, P. (2010). INDIVIDUALS, SCHOOLS AND NEIGHBOURHOODS; A MULTILEVEL LONGITUDINAL STUDY OF VARIATION IN INCIDENCE OF PSYCHOTIC DISORDERS Schizophrenia Research, 117 (2-3), 181-182 DOI: 10.1016/j.schres.2010.02.223
Russell-Smith, S., Maybery, M., & Bayliss, D. (2010). Are the Autism and Positive Schizotypy Spectra Diametrically Opposed in Local Versus Global Processing? Journal of Autism and Developmental Disorders, 40 (8), 968-977 DOI: 10.1007/s10803-010-0945-7

 

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Mind perception of others: opposing effects of having Autism/Psychosis

ResearchBlogging.org

Superman
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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.

Gray, K., Jenkins, A., Heberlein, A., & Wegner, D. (2010). Distortions of mind perception in psychopathology Proceedings of the National Academy of Sciences, 108 (2), 477-479 DOI: 10.1073/pnas.1015493108

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ADHD and CNVs

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By Richard Wheeler (Zephyris) 2007. The three ...
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I have written previously about CNV’s and how de novo CNV’s have been recently shown to correlate with disorders like autism and schizophrenia. I have also been militantly proposing that autism and psychosis are diametrically opposed disorders and have been gladdened to find that recent CNV data support that hypothesis.  I reported how 16p11.2 duplications were associated with schizophrenia while micro-deletions at same site associated with autism.  I also reported how a larger study which looked at multiple CNVs found the same reciprocal effects on CNV sites for autism and schizophrenia, thus bolstering the hypothesis that these are diametrically opposed.

By now you might be wondering what all this has to do with ADHD? Well, for one, early this year I started expanding my model and started conceptualizing ADHD as opposed to Autism in childhood and ADHD thus as belonging to psychotic spectrum; I mused that perhaps the same genetic vulnerability that leads to ADHD in childhood could lead to the manifestation of psychosis in teenage/adulthood. Its worthwhile noting that both ADHD and Psychosis are highly correlated with creativity.

So I could not stop my exuberance at finding that CNVs at another site 16p13.11 has been implicated in ADHD and the duplications are present in both ADHD and Schizophrenia. Also, as per the same study , ADHD children carry a large number of de novo CNV’s – a pattern similar ro Autism/schizophrenia. Some, for example the Neuroskeptic, have taken the same loci of CNVs to mean that these CNVs just confer a general risk of maladaptation, but I think they are missing the forest for the trees.  The pattern points to the diametrical model and how CNvs are one mechanism in which tug-of-wars are played (whether evolutionary variation or parent-offspring or between paternal and maternal genomes).

Let me explain what I mean by tug-of-wars. Say you have a evolutionary trade-off between exploration and exploitation, with one extreme being useful in some extreme environmental niche (say food is abundant)  and the other strategy useful in the opposed environmental niche  (say food is scare) . The trait that gets stabilized  should have a bell cure distribution so that the a species can survive even if environment leans toward one extreme.  The way to archive this could be by having distribution of frequency of different alleles; or it can be via CNV mechanism.  You may have some gentic loci for exploration and have a  single popular gene allele that codes for exploration at that loci and CNVs that cause deletions here will lead to more exploitation while CNVs that are duplications will lead to more exploration.  Thus, by CNV mechanism one can have more of good thing or less of a good thing, good depending on context (i.e context says what is ‘good’).

To take the example of  16p13.11 – it seems it is somehow related to mental retardation/ creativity/intelligence. A deletion at this site causes mental retardation/multiple congenital anomalies.=, while duplications have benign effects. I would conjecture that duplications (associated with ADHD and schizophrenia) may actually increase intelligence/ creativity.   That woudl fit with the diametrical model and the finding that ADHD  kids are more creative nd develop language more readily than autistic kids of same age.

I am pasting the background and findings from the abstract below:

Large, rare chromosomal deletions and duplications known as copy number variants (CNVs) have been implicated in neurodevelopmental disorders similar to attention-deficit hyperactivity disorder (ADHD). We aimed to establish whether burden of CNVs was increased in ADHD, and to investigate whether identified CNVs were enriched for loci previously identified in autism and schizophrenia.
Data for full analyses were available for 366 children with ADHD and 1047 controls. 57 large, rare CNVs were identified in children with ADHD and 78 in controls, showing a significantly increased rate of CNVs in ADHD (0·156 vs 0·075; p=8·9×10?5). This increased rate of CNVs was particularly high in those with intellectual disability (0·424; p=2·0×10?6), although there was also a significant excess in cases with no such disability (0·125, p=0·0077). An excess of chromosome 16p13.11 duplications was noted in the ADHD group (p=0·0008 after correction for multiple testing), a finding that was replicated in the Icelandic sample (p=0·031). CNVs identified in our ADHD cohort were significantly enriched for loci previously reported in both autism (p=0·0095) and schizophrenia (p=0·010).

To some the fact that ADHD had the same loci as both Autism and Schizophrenia may speak against there being a diametrical relation; however the same was claimed when initially it was found that autism and schizophrenia CNVs were at the same loci; only after looking at the nature of CNV’s (whether duplications or deletions) were the researchers able to identify the diametrical nature of the CNV’s

I haven’t read the full paper yet (waiting for someone to send me the paper) and as and when I get my hands on the full paper, I’ll update this blog post with more details.

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Williams, N., Zaharieva, I., Martin, A., Langley, K., Mantripragada, K., Fossdal, R., Stefansson, H., Stefansson, K., Magnusson, P., & Gudmundsson, O. (2010). Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysis The Lancet DOI: 10.1016/S0140-6736(10)61109-9

The five dimensions of an autistic brain

ResearchBlogging.org

Major brain structures implicated in autism.
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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?

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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

Neurodiversity:an interview with Dr. Thomas Armstrong

Eight women representing prominent mental diag...
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I recently read Neurodiversity: discovering the extraordinary gifts of Autism, ADHD, Dyslexia and other brain differences(you can read a mini review here) by Dr. Thomas Armstrong and came away impressed. In the book Dr Armstrong makes a  strong case for viewing the traditional disabilities from a differences perspective and to focus on the different strengths and abilities of the neurodiverse people. A recurring theme of this blog has been that autism and schizophrenia/psychosis are opposites on a continuum model as proposed amongst others by Christopher Badcock and Beranard Crespi. Dr Armstrong touches on this model in his chapter on autism, though that not central to his theis .

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.

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Neurodiversity: more than just autism!

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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.

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Autism, Psychosis and circadian clock

ResearchBlogging.org

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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.

As per this PLOS Genetics article:

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 [84]–[86]). 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 [87]. 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 [88]–[90]. 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 [91],[92]. Furthermore, individuals with a behavioural preference for “eveningness” have a greater tendency to develop depression [93].

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) [81]). 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 [82].

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.[58] Another study showed that drug-free, recovered, bipolar patients exhibited no hypersensitivity to light.[59] It has also been shown in humans that valproic acid, a mood stabilizer, increases transcription of melatonin receptors[60] and decreases eye melatonin-receptor sensitivity in healthy volunteers[61] while low-dose lithium, another mood stabilizer, in healthy volunteers, decreases sensitivity to light when sleeping, but doesn’t alter melatonin synthesis.[62] 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

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Autism and white Matter/Myelination: the opposite of creativty/psychosis phenotype?

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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 autism Human 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

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