Tag Archives: Attention-deficit hyperactivity disorder

ADHD and CNVs

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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

Neurodiversity:an interview with Dr. Thomas Armstrong

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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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Cognitive control: when less is more!

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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

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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!

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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 and ADHD as opposites based on fly models?

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Regular readers of this blog will know my fascination with autism and psychosis as opponents on a continuum theory . I have already been privately speculating that ADHD in childhood may be a risk factor for Psychosis in later adolescence, especially as both are supposed to have underling dopamine abnormalities, so this new study by Brembs et al caught my attention.

Recently I came cross this paper by Bjorn Brembs et al that investigated attention-like processes in mutant fly models that showed memory deficits. They weer aqble to show that despite overt similar olfactory memory deficits, the attention-like processes worked in opposite ways in the two mutant models. In the rutabaga/dunce model, the atention ws hyperfocussed , resembling human autism; while in radish models , attention was flexible and distract-able resembling human ADHD.

It is increasingly apparent that many classical Drosophila learning and memory mutants are also defective in short-term processes relevant to selective attention. Previous studies have shown that short-term memory as well as long-term memory mutants display attention-like defects (van Swinderen, 2007; van Swinderen et al., 2009), and the current study reveals radish mutants to be defective as well, albeit with distinctly different symptoms. The Drosophila mutants dunce1, rutabaga2080, and radish1 share olfactory memory defects but differ conspicuously for short-term processes relevant to visual attention. Whereas the more persistent optomotor behavior of dunce1 and rutabaga2080, both affecting the cAMP-associated pathways (Davis et al., 1995), are reminiscent of the persistent preoccupation of some patients afflicted with autism, the phenotype of radish mutant flies described here is similar to some of the symptoms of patients with ADHD.

They further speculate as o why these two phenotypes may be present and relate it to exploit/explore conundrum.

Attaining the right balance between persistence and flexibility is a crucial feature of adaptive behavior, because it reflects the balance between exploration and exploitation of natural resources. It is tempting to speculate that radish and dunce/rutabaga may constitute the two respective extremes of this balance. Recent work investigating torque behavior of wild-type flies (similar to our shorter experiments here) has shown that, during extended flights, the occurrence of turning maneuvers can be described by a Le´vi distribution (Maye et al., 2007). Such distributions of behavioral output, seen in foraging behavior in many animals, are characteristically long-tailed. This means that animals may occasionally persist with one behavioral choice for unusually long, but most often choices alternate at a more regular, normally distributed rate. The advantage of allowing for occasional long forays into one direction is presumably to chance on a new resource away from the proximal search space. Such behavior has been found to be ecologically advantageous, but mechanisms driving such alternation tendencies have not been documented in the Drosophila brain. One interpretation of our results is that the mushroom body circuits defined by dunce/ rutabaga/radish expression are involved in establishing the balance between persistence and flexibility [i.e., the explore/exploit dilemma (Daw et al., 2006)]. A separate set of results has independently also arrived at a similar conclusion, suggesting that the mushroom bodies could be involved in maintaining a period of behavioral flexibility (i.e., attention-like processes) before a longer-term transition to habit formation or motor learning
(Brembs, 2009).

To me, this research adds another intriguing possibility to the autism-psychosis dimension, that of ADHD as a childhood phenotype/risk factor for later psychosis.

van Swinderen, B., & Brembs, B. (2010). Attention-Like Deficit and Hyperactivity in a Drosophila Memory Mutant Journal of Neuroscience, 30 (3), 1003-1014 DOI: 10.1523/JNEUROSCI.4516-09.2010

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