Category Archives: ADHD

The Four Sub-Types of ADHD

Recently, I wrote a post about the four neural sub-types of depression. That classification was based on resting stage fMRI comparing depressive patients with controls; I hope someone does similar studies for other psychiatric conditions.

English: Symptoms of ADHD described by the lit...

English: Symptoms of ADHD described by the literature (Photo credit: Wikipedia)

The current post is an attempt to delineate what may come out in such a study if done for ADHD. I will be focusing on ADHD as it manifests in children, adolescents as well as adults.

I will be mostly relying on factor analytical studies of ADHD that have typically revealed 3 to 4 underlying factors.

ADHD has typically been diagnosed by looking at symptoms from inattentive or hyperactive-impulsive domains. You can find the DSM-5 criteria here. And its sub-types are combined presentation, predominantly inattentive presentation and predominantly hyperactive-impulsive presentation.

As per some studies, a majority (as much as 90 %) of ADHD subjects have inattentive symptoms while a few have hyperactive-impulsive symptoms. This is analogous to the depression findings that predominately depressive patients have a core pathology marked by low mood ; and subtypes marked by say anergia, anhedonia and anxiety.

However, factor analytical studies have presented a more nuanced picture. As per this study [pdf] there are four underlying factors of ADHD.

  1. Inattentive/ cognitive problems
  2. Hyperactivity/restlessness
  3. Impulsivity/ emotional lability
  4. Problems with self-concept

The first there factors are well established and quite apparent. To impulsivity description I may just add sensation-seeking too. The problems with self concept is something like low self-confidence/ self esteem, possibly due to continued underachievement and problems at school/ work. I would like to add another dimension to this fourth problems with self concept factor – that of disruptive/ defiant behavior possibly due to self-concept issues.

And I am sure in future, in future, when brain basis and neutral subtypes are more easily available for ADHD, we will find these four subtypes.

Before we leave, its important to note that ADHD lies on a continuum and its a matter of degree than a matter of kind .

Also, ADHD confers benefits too like enhanced creativity and some work has shown that creativity can be mistaken for ADHD in kids.

The above four sub-types may then be classified by their positive poles too:

  1. Daydreaming/broadened attention
  2. High energy and enthusiasm
  3. risk-taking and emotional sensitivity
  4. independent and idiosyncratic

All the above are also traits associated with the creative person. ADHD & creativity are indeed very closely related and its time we stopped seeing differences like ADHD in purely pathological terms.

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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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

Cognitive control: when less is more!

ResearchBlogging.org

Yesterday I wrote a post about ADHD and creativity and how the frontal lobes hypo-function and dopamine may be the mediating factors involved.  Today I serendipitously came across this article by Thomson-Schill et al in which they posit that frontal cortex hypofunction during childhood is beneficial, on average, as it enables convention learning and thus linguistic acquisition.

What they basically mean is that frontal cortex has been found to be involved in cognitive control i.e. in higher cognitive functions like planning, flexible thinking etc ; and the frontal cortex does this by biasing the competitive responses elicited by a stimuli by goals /existing beliefs / other task related information that is maintained in the working memory. To take an example, cognitive control is often measured by tasks such as the stroop task. the strrop task measures how well you are able to suppress the prepotent response tendency of naming the color-term itself by the task-relevant constraint that you name the color of the term instead. when a color term like ‘green’ is presented in Red color, then the green as well as red linguistic response compete with each other. In the absence of frontal biasing in teh direction of color ie.e red, we are apt to name the color-term itself i.e green by default which is the habitual response. Children , who have less well-developed frontal cortices generally perform poorer at the stroop task than adults as their frontal cortex does not bias or tilt the scales in favor of the color used rather than the color-term presented.

The authors claim that this inability to bias results on the basis of pre-existing knowledge/beliefs leads to a greater ability to learn. They posit that learning conditions (that maximize competition )  are different from performance conditions (where one response needs to be selected or competition minimized) and the child’s brain is optimized for learning by not having frontal inhibition and control. An example they give is filtering noise form signal which the child are able to do, but adults can’t. for eg. if a new language has a phrase ‘et tu brute’ and 75 % of times it is in this form and 25% of times it is of the form ‘et tu vous Brute’, then adults will tend to probability match and select the utterance/ utter themselves phrase ‘et tu brute’ 75% of times and ‘et tu vous Brute’ 25 % of times. This is because when they want to utter the phrase their existing knowledge that sometimes the other phrase is also used, makes them sensitive to variations. In child’s brain on the other hand a competition between the two phrases takes place and as there is no moderating influence involved, the outcome hundred percent of the time is ‘et tu brute’. Thus, they are able to learn conventional meaning of a phrase/word etc more easily than an adult who gets bogged down by variations. Thus sometimes, less is more!

However the reason I got hooked to this study is the implications they draw for ADHD/Autism and creativity. I’ll quote them verbatim on the issue:

Central to our proposal is the claim that the timing of PFC development has been the target of selection and, therefore, that variations in timing are functionally meaningful. Recent neuroimaging studies have revealed potentially important differences in the timing of PFC development across typical and atypical individuals. Variations in the trajectory of PFC maturation (based on repeated measures of cortical thickness) have been associated with cognitive measures in typically developing children (Shaw et al., 2006). Children with attention-deficit hyperactivity disorder (ADHD) exhibit a delay in cortical maturation that is most prominent in the PFC (Shaw et al., 2007). In contrast, children with autism spectrum disorders (ASD) undergo early maturation of the PFC (Carper, Moses, Tigue, & Courchesne, 2002). A better understanding of the implications of these timing changes for both learning and performance may illuminate some of the behavioral and cognitive patterns associated with these diagnoses (e.g., impaired acquisition of social conventions in ASD), as well as offer a fertile ground for testing the validity of our hypothesis that typical PFC development involves a trade-off in favor of learning to the detriment of performance in infancy and early childhood.

This gels quite nicely with what I have been speculating for some time, that ADHD and Autism are opposed and that ADHD is childhood equivalent of psychosis. ADHD kids are bound to be good learners, more divergent creative and have better social and linguistic skills. Autistic kids on the other hand would be better performers (say child prodigies in memory etc) , more convergent thinkers, and have less social and linguistic skills- one mechanism of which may be lesser ability to learn social and linguistic conventions- like the usage of metaphorical terms.

On creativity this is what the authors say:

Creativity—the ability to approach an object or a situation from an alternative perspective—may benefit from the unsupervised competition that occurs in the absence of prefrontal control. Consider one common assessment of creative thinking, the Alternative Uses Task: When attempting to think of ways to use an object in some atypical way, adults struggle. In this case, an active PFC might, paradoxically, hinder flexible thinking, because the representation of the object is sculpted by prior experience and expectations. Interestingly, young children are immune to this kind of functional fixedness (German&Defeyter, 2000). Successful performance in similar tasks of ideational fluency has been associated with EEG changes in prefrontal regions (e.g., Mo¨lle, Marshall, Wolf, Fehm, & Born, 1999). Furthermore, patients with PFC damage solve insight-problemsolving tasks better than do their healthy counterparts (Reverberi, Toraldo, D’Agostini, & Skrap, 2005). This apparent flexibility of behavior can be interpreted as a stimulus-driven response: A mind that is at the mercy of its environment is not shaped by expectations or beliefs. This interpretation highlights a parallel between functional fixedness and probability matching, in that both of these ‘‘adult’’ phenomena involve biasing stimulus–response associations based on expectations. This proposal suggests new avenues of investigation into the processes that support creative thought and into putative relations between creativity and psychological disorders associated with hypometabolic prefrontal function (i.e., a state of lower energy consumption in the PFC, as in bipolar disorder, for example).

The above analysis of creativity in terms of hypofunction of frontal cortex bodes well for my theories of creativity-ADHD relationships as well as creativity-psychosis (bipolar etc) relationship, both of which involve developmental or functional hypofucnction of frontal cortex.

Thompson-Schill, S., Ramscar, M., & Chrysikou, E. (2009). Cognition Without Control: When a Little Frontal Lobe Goes a Long Way Current Directions in Psychological Science, 18 (5), 259-263 DOI: 10.1111/j.1467-8721.2009.01648.x

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ADHD and creativity

ResearchBlogging.org

Brainscan of brains with and without ADHD
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ADHD has traditionally been conceptualized in terms of deficits- that of attention , impulse control or motor restraint; but the new neurodiversity paradigm forces us to take a more balanced look and acknowledge the strengths that the ADHD kid may have- divergent thinking, spontaneity and high energy and vitality.

That brings me to research by Cramform that shows that the symptoms that define ADHD/ADD- hyperactivity, impulsivity and distractability are just the negative connotation and spin put on some of the traits that define highly creative and gifted child–  the traits of Vitality, spontaneity and daydreaming/wandering phenotype.

But first things first. ADHD , as many of the readers will know , is defined by three primary symptoms- hyperactivity or the restlessness and fidgety or squirming behavior of the kid; impulsiveness or the inability to control impulses manifest in overt behavior like getting up in class and interrupting;  and distractibility where the kid ends up paying too much attention, even to stimuli that are extraneous and should be ignored, thus leading to fleeting attention! ADHD is a traditional classroom misfit and thus a traditional teachers nightmare. However, one should note that a traditional teacher is not too much impressed by the highly creative kid too, who proves to be a bit too much to placate and who doesn’t conform too easily.

But what could be the mechanism why ADD/ADHD must be so closely related to and resembling creativity traits as to be indistinguishable from it by behavioral symptoms alone? I believe dopamine and frontal cortex are the culprit. We have seen in the past that dopamine is related to creativity and we have seen that frontal cortex is related to creativity; and we have also seen that dopamine is related to ADHD. As a  matter of fact ADHD on a neurotransmitter level is characterized by dopamine’s quirky behavior , while on the neuroanotomic level is known by the late development of frontal cortex that is an inhibitor to other areas like motor areas and impulsive areas (basal ganglia and sub-cortical regions)  thus leading to symptoms of  impulsivity and hyperactivity. In creative people too, especially in divergent form of creativity, we see that creativity manifest itself when dopamine comes into play and when frontal regions give up their control of other regions of the brain thus making remote associations more likely.

Of course dopamine is not just involved in ADHD, but also in Psychosis and thus my theory of Autism and Psychosis as opposites would claim that ADHD is childhood form of psychosis and is opposed to Autism. There is already some support for that idea with autism and ADHD being discovered as opposites and with ADHD more common in bipolar probands.

The dual symptoms of ADHD as inattention and as hyperactivity/ implusivity are easy to conceptualize when one sees that one is trying to maximize predictive ability / minimize surprise and also maximize rewards by being flexible in one;s behavior and taking risks rather that persevering on the well trodden path. Both attention-allocation and action-selection are sensitive to dopamine and in one particular phenotype result in more leaning towards flexibility, distracatibility, hyper energy and arousal and more novelty and thrill seeking. The desire is to explore and not to exploit. The hunter rather than the farmer as per Hartman’s model. These same are characteristics of the creative phenotype- those touched with fire- and thus on the move literally or figuratively- always seeking new combination and ideas and exploring uncharted territory.

Perhaps its time we stopped negatively labellings the gifted, creative ADDers as difficult kids, but rather design and structure classrooms around them that bring their potential to the fullest and make them bloom fully. Lets not stifle the creativity. Lets not devalue the immense energy and joy these child exhibit and the creative potential they embody.

Cramond, B. (1995). The Coincidence of Attention Deficit Hyperactivity Disorder and Creativity University of Connecticut, The National Research Center on the Gifted and Talented. Other: ED388016

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Neurodiversity: more than just autism!

Subject: Quinn, a boy with autism, and the lin...
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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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Attention allocation / Same as action selection/ New insight on ADHD #haiku #scaiku

The title of my above post is a scaiku (scientific haiku in 140 chars on twitter) that I posted last night on twitter.I am using this title as the inspiration for this post is twitter itself.

Last night, after a hard day full of tweeting (yes tweeting and keeping up with all the friends’ tweets is a lot of hard work- go check the 4-way conversation I had on cosnsciousness and free will), I was not able to relax myself, but found myself in a constant state of distraction and restlessness, and getting up in middle of night to update my status.  Of course I have heard of twitter addiction and would rubbish that off; but I could not rubbish off the unique demands on attention and juggling that twittering makes on you. First off, you need to read a lot of tweets and find the needle in the haystack- the tweets that need to be retweeted/replied to and ignore/forget the rest of them as soon as possible. Secondly, I at least, juggle constantly between windows and tabs of tweetdeck and other application trying to do optimal scavenging (feeding off good content tweeted by others) and foraging (finding a good tweetable link myself).

So to sum up, I found that twitter had taxed, at least yesterday, my attentional system- leading to a habitual distractibility and also my motor system hat had constantly flitted between open windows and tabs leading to a habitual distractibility. I am sure that was a very short term and temporary phenomenon, but that set me thinking  I have already devoted an entire post to how attention allocation and action selection may be similar and have drawn many parallels. The fundamental problem in  both the cases is to choose an action/ stimuli to attend to, that can maximize the rewards from the world/ predictability of the world.  At any given time, there are many more stimuli to attend to and acts to indulge in than are the attentional/intentional resources required for the same and thus one has to choose between alternatives. Mathematicaly, different acts have different probabilities associated with them that they would lead to a rewarding state- this wave function needs to be collapsed such that only one act is actually intended. One way to do is my maximizing Utility (ExV) associated with different acts and choosing the maximal one always; another solution is to randomly choose an act from the given set  in accordance with  the probability distribution  that is a function of their utilities.I believe that instead of maximizers most of us are staisficers and especially in time-sensitive decisions go for an undeliberate choice that does’nt actually maximize the utility over all possible behavioral acts, but choses one of them randomly/probabilistically as per their prior known probabilities of rewards. Thus, we can be both maximizers as well as satisficers and which system we engage depends both on situational factors as well as our personality tendencies/ habits.

Anyway that was a lot of digression from the main line of argument. To continue with the digression for some more time, if one extends the analogy to attending to stimuli, on can either attend to stimuli that leads to greatest predictability (P= ExR) ;  or one can attend to a stimuli from a given set in accordance with a probability distribution that is a function of their prior predictabilities. again I haven’t even got into Bayesian models where thing should get more complicated; suffice it to note for now that both attention-allocation and action-selection involve choosing an act / stimuli from a set.

A look at the Utility function of acts (U=ExV) and  Predictability function of stimuli (P = ExR) , immediately outlines the importance of dopamine in the above choosing mechanism as it encodes both (reward) expectancy as well as incentive salience/Value for acts;  on the attentional side of things, it should encode  both the strength of conditioned association (E) as well as (stimuli) Relevance for minimizing surprise. As such it should detect novelty in stimuli that can indicate that things have changed and the internal model needs updating. 

I also talked in my last post about a general energy level that leads to more propensity to indulge in operant acts and a general arousal level that leads to more propensity to attend to external stimuli. Today I want to elaborate on that concept using ADHD as a guide – ADHD has primarily two varieties (and in most general case both co-exist) – the inattentive type and the hyperactive-impulsive type. In the inattentive type, one is easily distracted or to put in my conceptualization – has a high baseline arousal leading to more frequent monitoring to the world/ external stimuli . The attention-reallocation happens faster than controls and may be triggered by irrelevant stimuli too. In the hyperactive-impulsive type,  one is overly active and impulsive or to put in mu conceptualization- has a high baseline energy level leading to more frequent shifts in activities and possibly triggering unvalued acts (impulses that are not really rewarding) .

It is important to note that dopamine and dopamine mediated regions like smaller PFC, cerebellum and basal ganglia, dopamine related genes like DAT1 and DRD4  and Ritalin that works primarily on dopamine have been implicated in ADHD.  All the above points to a dopamine signalling aberration in ADHD. Once one embraces the overarching framework of action-allocation and action-selection as similar in nature and possibly involving dopamine neurons, it is easy to see why ADHD children should have both hyperactive-impulsive and inattentive syndromes and subgroups.

cortex maturation: found the references

In my earlier post on cortex maturation, I was unable to find the references for the claims that in Autism cortex matures earlier during toddler phase and that even in adulthood, it may be thicker.

In a recent PNAS commentary, reagarding the delay rather than deviance theory of ADHD, I came across the appropriate references to back the above observations, as well as the accelerated pruning in child-onset schizophrenia. Passing that along.

An important question is whether the delay of brain maturation is a specific characteristic of ADHD or is shared by other child psychiatric disorders. So far, none of the other major psychiatric disorders have been associated with a maturational delay of brain structure. However, to my knowledge, longitudinal structural studies have been conducted only in patients with ADHD, childhood-onset schizophrenia (COS), and autism, finding maturational deviance rather than delay. Adolescents with COS are characterized by a striking nonlinear, progressive acceleration of the normal gray matter and volume decrease in cortical regions that levels off in adulthood (22). In autism, there is an early left hemispheric overgrowth of gray and white matter at young toddler age with conflicting findings of either arrested growth or remaining brain enlargement in adolescence and adulthood (23). The findings of delayed structural brain maturation seem, thus far, to be specific to ADHD and may be an important neuroanatomic trait. However, further exploration of the developmental trajectories in other child psychiatric disorders is needed to establish the importance of a delay of brain maturation as a specific neuroanatomic marker for ADHD.
(emphasis mine, references below)
22. Greenstein D, Lerch J, Shaw P, Clasen L, Giedd J, Gochman P, Rapoport J, Gogtay N (2006) J Child Psychol Psychiatry 47:1003–1012.
23. Bashat DB, Kronfeld-Duenias V, Zachor DA, Ekstein PM, Hendler T, Tarrasch R, Even A, Levy Y, Sira LB (2007) NeuroImage 37:40–47.

cortex maturation: lag, span and thickness: ADHD, Schizophrenia, autism , IQ

There is an article making waves regarding the delayed maturation of the cortex of children with ADHD and so I thought I will throw in my two cents and try to simplify things.

First what is cortex maturation- the cortex of normal children first increases in size (as presumably new connections are made) , reaches a peak around 8 years of age and then the cortex thins (as spurious connections are pruned). We normally think of more connections being more beneficial, so it stands to reason why pruning should happen- but more connections do not translate into better connections- we only need to retain the right connections – the spurious connections need to be mercilessly pruned, if we are to function correctly. A theory based on this logic also asserts that we are born synaesthetes, but the spurious connections get pruned under normal development.

Now there are several things that can go wrong with this wiring and pruning process. Too much wiring can leave you with a thicker than normal cortex , too much pruning can leave you with lesser connections than required for normal functioning. Also the achievement of normal thickness, and subsequent thinnness can be developmentally shifted or lag from the normal developmental plan. Finally the thickening and thinnening may be squeezed in time and may happen at a faster rate for some individuals. Conversely, this may be spread over a broader time period and o9ccur at a relatively slower rate for other individuals. Considering the three factors of Size ( peak thichkness/ thinnness achieved), Lag (start and end of thickening and thinning process) and Rate (faster development over small time frame or longer span with slow rate of pruning/ initial connection formation) one gets 6 combinations (if we treat them as independent of each other) . Also considering that Thickening (initial connection formation) and Thinning (subsequent pruning) may also be independent one gets 12 combinations. these are sufficiently complex for me to abstain from making any sweeping generalizations. So I’ll go to data:
1. In ADHD, new research (as also highlighted above) reveals, that the development (thickening and thinning ) of cortex is similar to normal individuals- only it is slightly shifted and starts later. this explains why ADHD disappears after teenage and is a problem only in childhood.

2. Children with higher IQ have faster rate of thickening and thinning of cortex as seen from graphic below.

3. Research from Paul Thomsaon’s lab at UCLA has shown that in schizophrenia the normal pruning process does not stop in teenage as in normal adults, but continues beyond the early teenage resulting in more pruning than is normal.
4. I’ve read claims that in Autism the cortex is thicker and that it matures early. I’m tempted to posit Autism as a reverse trend of schizophrenic maturation, but need more accurate refernces and would be highly obliged if someone points me to appropriate resources.

All this seems very promising and I would be watching ne23s related to these developments more closely in future , considering that some of these are comorbid – like autism and IQ in high functioning ASDers and Creativity and Schizophrenia.