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.

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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.

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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.

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