Posts tagged autism
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
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.
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.
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 –). 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 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