Category Archives: psychosis

Psychosis and the City

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

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

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


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

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

To quote:

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

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

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

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

What neural mechanism may be involved?

To quote from the Suzzana et al paper again:

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

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

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

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

 


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

 

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Schizophrenia: 4 a’s and ABCD

The term Schizophrenia , as many of the readers will recall, was coined by Eugen Bleuler, a Swiss psychiatrist , who  intended the ‘split personality’ to reflect the fact that there was an underlying dissociation between various functions like memory, cognition, emotion that are normally integrated in normal people.

He also gave the famous 4 a’s that he presumed lied at the core of the schizophrenia and were fundamental aspects of the disorder.

To recall:

‘affect’: Inappropriate or flattened affect-emotions in-congruent to circumstances/situation.

‘autism’: social withdrawal- preferring to live in a fantasy world rather than interact with social world appropriately.

‘ambivalence’ : holding of conflicting attitudes and emotions towards others and self; lack of motivation and depersonalization.

‘associations’ : loosening of thought associations leading to word salad/ flight of ideas/ thought disorder.

Bleuler maintained that these distinctive and fundamental  features identified and formed the core of Schizophrenia while the manifest symptoms like hallucinations and delusions (first rank symptoms as per Schneider) were peripheral and not that important).

The readers of this blog will also be familiar with the ABCD model of psychology where Affect, Behavior (social aspects), Cognition and Desire (motivation/ dynamics)  are the four fundamental domains; it is easy to see how the four a’s of Bleuler map to the 4 domains of psychology and it seems that schizophrenics have major troubles in each domain:

affect: this directly maps to Affect dimension and inappropriate affect is a major core part of the syndrome.

autism: though named somewhat incorrectly the intent of autism was to catch the behavioral and social impediments of the schizophrenics.

ambivalence: here there are conflicts and ambiguities regarding what one desires; for self and for others; lack of motivation/conflicted motivation  is significant at this dimension.

associations: here the cognitive underpinnings are all too evident- the thought disorganization and flight of ideas is all too cognitive in nature.

It is amazing how the insights of Bleuler from a century before lend themselves so easily to fit the ABCD framework. What do you think, a bit stretched? or have I started making loose associations myself 🙂 ?

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

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Superman
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It has been this blog’s thesis that autism and its milder form autism spectrum disorders (ASD) are diametrically opposed to psychosis and its milder form schizotypy.  In no area is this more apparent than in the perception or attribution of minds to others. It thus gave me immense pleasure to read this new article by Wegner et al that looks at how the perception of others’ mind is affected in different sub-clinical conditions like ASD, Schizotypy and Psychopathy.

Wegner et al review a great deal of literature to come to the conclusion that others’ mind perception is a two dimensional construct and that we typically attribute mind to an entity depending on whether the entity can experience like us and whether they have goals and agency like us. Thus people can differ in the perception of either Agency or Experience when they attribute mind to an entity. Also b reviewing the available literature they came to the hypothesis that ASD folks should attribute less of agency , but perhaps equal experience to other humans and other entities as compared to controls; Schizotypals on the other hand have been shown to attribute more of mind and in particular agency to other entities than human. They also hypothesized that owing to lack of empathy the psychoptahs might perceive all animals/humans as lacking experience and thus mind-deficient to an extent and subject to manipulation.

They used online surveys to ascertain scores on ASD, schizotypy and psychopathy and correlated that with mind perception and attribution inclinations.  How they assessed mind perception was by letting the subjects ascribe perceived experience and perceived agency to nine entities viz.  baby, dead woman, dog, God, man , robot, Superman, tree and woman. They performed a confirmatory factor analysis that confirmed that indeed mind perception has two components- Experience and agency.

They got results in line with their hypothesis. ASD folks did  not differ in ascribing Experience to fellow humans but did differ in ascribing agency. Schizotypals on the other hand ascribed too much agency to Robots/animals etc; and in general attributing min dto even things like tress , god and dead woman. Psychopaths on the other hand showed reduced ascription of Experience to other humans as well as animals. As an interesting aside, psychopaths attributed more mind to superman perhaps self-identifying with the fictional character

Thus,  though mind perception in both ASD and Schizotypy is distorted it is tilted one way in autism and the other way in psychosis. With clinical populations the authors hope to get even stronger results. I am pleased because finally people have started taking the autism is opposed to psychosis paradigm seriously and have started doing research around it that is leading to fruitful results and confirmations.

Another new study that I came across recently and would like to link to found that VPA (valproic acid) treated mice were indeed an apt model of autism in mice and had the same brain correlates and signatures as in Autistic people. It is worth noting that VPA/sodium valproate is used to treat psychosis and I have pointed earlier too how this indicates that autism and psychosis are di\ametrically opposed. It is good that we are getting multiple confirmations of the important autism-psychosis opposition theory.

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

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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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Autism, Psychosis and circadian clock

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Diagram illustrating the influence of dark-lig...
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I recently came across this post by Michelle Dawson that states the thesis that one of the abnormalities in Autism spectrum disorders is due to abnormal circadian clock functioning. More specifically, the clock is internally driven and has a greeter ‘free running’ period and does not entrain readily to environmental and social clues.

Autistics whose sleep-wake cycles carry on independently from environmental and social cues are said to be “freerunning.”
The usual response to freerunning in autism is to see this as an autism-related sleep disorder. There is very preliminary evidence that freerunning autistics can be successfully treated with melatonin. Bourgeron (2007) refers to a short case study about an autistic whose free-running was remediated by melatonin treatment.

If you feel a bit overwhelmed by all the circadian clock related terminologies, I wholeheartedly recommend BoraZ’s clock tutorial series , especially this one.

Dawson further says:

Glickman (2010) speculates that some autistics’ failure to chain our sleep-wake cycles to environmental cues may arise from our atypical perception. My totally wild guess might be that an extreme freerunning phenotype in autism may be contributed to in part by cognitive versatility in autism, which would result in perceived environmental cues affecting sleep-wake cycles in an optional rather than mandatory way.

I wont speculate about the reasons behind why autistics have a greater free-running period and less entrainment to social and environmental clue, but I woudl say that instead of giving them flexibility, I would presume that this locks them into their internal rhythms, while others are more responsive to environment and better adapted. That brings me to the opposite phenotype of ASD…the psychotic phenotype shown by Schizophrenics, depressives and Bipolars.

As per this PLOS Genetics article:

The contribution of the circadian regulatory system, arising from conflicts between internal biological clocks and environmental (solar) and social clocks, is evident in affective disorders. All major affective disorders (such as unipolar depression, OMIM #608516; bipolar disorder, and schizophrenia, OMIM #181500) include circadian phase disturbances in sleep, activity, temperature, and hormone levels (for reviews see [84]–[86]). Moreover, there is evidence that if rhythms can be altered/stabilised using relevant therapies, improvements in the primary symptoms can occur. For example, in some instances sleep deprivation has an antidepressant effect in patients [87]. Conversely, many disorders with a primary anomaly in the circadian system are associated with depressed mood. Seasonal affective disorder (SAD; OMIM #608516) is a common condition where depressive symptoms occur during shorter winter days [88]–[90]. Two inherited sleep phase disorders, familial advanced sleep phase syndrome (FASPS; OMIM #604348) and delayed sleep phase syndrome (DSPS), are both associated with abnormal affective states [91],[92]. Furthermore, individuals with a behavioural preference for “eveningness” have a greater tendency to develop depression [93].

The above to me seems hypersensitivity to social and environmental cues in affective/psychotic disorders. contrast this with ASD description by the same authors:

Other behavioural disorders with circadian and sleep-related disturbances include autism spectrum disorders (ASD) (OMIM %209850) [81]). Behavioural disturbances in ASD may arise in part from an inability of an individual’s circadian oscillator to entrain to environmental and social cues. One specific correlate of ASD is a low level of melatonin, and one of the enzymes critical in the synthesis of melatonin, acetylserotonin-O-methyltransferase (ASMT, OMIM *300015), is implicated as a susceptibility gene for ASD [82].

The role of melatonin seems to provide a clue. In autism, there seems to be low levels of melatonin and perhaps hypo-sensitivity to melatonin changes. In contrast Bipolar is marked by hypersensitivity of Melatonin receptors:

It has been suggested that a hypersensitivity of the melatonin receptors in the eye could be a reliable indicator of bipolar disorder, in studies called a trait marker, as it is not dependent on state (mood, time, etc.). In small studies, patients diagnosed as bipolar reliably showed a melatonin-receptor hypersensitivity to light during sleep, causing a rapid drop in sleeptime melatonin levels compared to controls.[58] Another study showed that drug-free, recovered, bipolar patients exhibited no hypersensitivity to light.[59] It has also been shown in humans that valproic acid, a mood stabilizer, increases transcription of melatonin receptors[60] and decreases eye melatonin-receptor sensitivity in healthy volunteers[61] while low-dose lithium, another mood stabilizer, in healthy volunteers, decreases sensitivity to light when sleeping, but doesn’t alter melatonin synthesis.[62] The extent to which melatonin alterations may be a cause or effect of bipolar disorder are not fully known.

The above is not the only source implicating Bipolar disorder and circadian clock dysfunction., See more here and here. The big question is not whether ASD and Affective disorders are both circadian rhythm disorders, but the big question is whether they show opposite phenotypes with respect to circadian clocks- one showing too little entrainment while the other too much?
Barnard, A., & Nolan, P. (2008). When Clocks Go Bad: Neurobehavioural Consequences of Disrupted Circadian Timing PLoS Genetics, 4 (5) DOI: 10.1371/journal.pgen.1000040

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

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A new paper by Ben Bashat et al extends their earlier findings that had found that there was accelerated maturation of white matter in children with Autism. In this new paper they use Tract Based Spatial statistics (TBSS) to determine the white matter integrity of children (age around 3 years) with Autism as compared to normal controls. Of course they used Diffusion tensor Imaging to find out Fractional anisotropy and other measures of white matter integrity.

Essentially they found that in some regions/tracts there was greater Fractional Anisotropy (FA) as compared to controls. These regions/tracts were genu and body of the corpus callosum (CC), left superior longitudinal fasciculus (SLF) and right and left cingulum (Cg). They also found that in areas of high FA there was corresponding decrease in Radial diffusivity (Dr). What this essentially means, to my naive mind, is that greater conductance or speed of action potential in axons would primarily be due to enhanced myelination which reduces leakage or lateral flow of AP.

I’ll like to contrast the results with an earlier study I had blogged about regarding creativity, psychopathology and white matter mylienation connection. As per that study an inverse relation was found between people high on creativity (divergent type) and Fractional anisotropy in frontal regions, i’e there was low FA. Also importantly there was increased Dr (radial diffusivity) in the same regions and thus the conclusion was that there was reduced myelination in those areas which meant reduced signal transmission speed and more signal leak . It is notable that that study too used DTI and Tract based Spatial statistics (TBSS) analysis method to arrive at their conclusions.

Regular readers of this blog will know my fanaticism for Autism and Psychosis as opposites on a continuum theory. This new paper nicely fits in with my last post linking creativity/psychosis and white matter/myelination, I had as much surmised that Autism would show the opposite effect and have high FA and decreased Dr. It is heartening to note when such a relation is found and reported- goes to show the strength and ability to make predictions of the theory.

However, I would also like to point out and highlight that I believe Autistic spectrum is characterized by another type of ability – the savantic intelligence– that may be directly due to this white matter /excess myelination effect. Perhaps the signals travel so fast that decisions are made locally without the time available to get other far-0off regions involved- thus giving attention to details but inability to link disparate regions and ideas.

Weinstein, M., Ben-Sira, L., Levy, Y., Zachor, D., Itzhak, E., Artzi, M., Tarrasch, R., Eksteine, P., Hendler, T., & Bashat, D. (2010). Abnormal white matter integrity in young children with autism Human Brain Mapping DOI: 10.1002/hbm.21042
Ben Bashat, D., Kronfeld-Duenias, V., Zachor, D., Ekstein, P., Hendler, T., Tarrasch, R., Even, A., Levy, Y., & Ben Sira, L. (2007). Accelerated maturation of white matter in young children with autism: A high b value DWI study NeuroImage, 37 (1), 40-47 DOI: 10.1016/j.neuroimage.2007.04.060
Jung, R., Grazioplene, R., Caprihan, A., Chavez, R., & Haier, R. (2010). White Matter Integrity, Creativity, and Psychopathology: Disentangling Constructs with Diffusion Tensor Imaging PLoS ONE, 5 (3) DOI: 10.1371/journal.pone.0009818

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More brains and bonkers connection: thinking out of a broken box

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We have covered many studies linking creativity with Psychosis and this new study by Manzano et al provides further corroborating evidence.

Dopamine has been linked with psychosis and is now also being increasingly being linked with creativity, especially divergent creativity and thinking style.

Divergent thinking is influenced by dopaminergic function. Reuter [6] found a correlation between divergent thinking (the Inventiveness battery of the Berliner Intelligenz Struktur Test) and polymorphisms of the dopamine D2 receptor gene–DRD2 TAQ IA. Higher creativity scores were observed in carriers of the A1 allele. This polymorphism is unrelated to general intelligence [7], [8], which suggests that it is more specifically related to Glr (“long-term storage and retrieval”). This finding is in line with functional imaging research showing the D2 system to be involved in attentional set shifting and response flexibility, which are important components of divergent thinking [9]. Furthermore, the finding indicates that divergent thinking is related to regional differences in D2 densities, since the DRD2 TAQ IA polymorphism has been shown to modulate D2 binding potential (D2BP) in both striatal [10] and extrastriatal regions [11].

Divergent thinking is traditionally measured using alternate uses test, for eg., in which a familiar object like brick is provided and subjects asked to name novel use for that object. The responses are marked for creativity as per the follwoing criterion:

  • Fluency–the number of valid responses;
  • Originality–how frequent the participant’s responses were among the responses of the rest of the sample;
  • Flexibility–the number of semantic categories produced;
  • Switching–the number of shifts between semantic categories;
  • and Elaboration–how extensive each response is (if the task involves producing more than single words)

The main findings of the study was that dopamine D2 binding potential (D2BP) receptor density in thalamus correlated negatively with divergent thinking and creativity scores. Here is how the authors interpret the results:

Based on the current findings, we suggest that a lower D2BP in the thalamus may be one factor that facilitates performance on divergent thinking tasks. The thalamus contains the highest levels of dopamine D2 receptors out of all extrastriatal brain regions [33], [45]. Decreased D2BP in the thalamus has been suggested, firstly, to lower thalamic gating thresholds, resulting in decreased filtering and autoregulation of information flow [31] and, secondly, to increase excitation of cortical regions through decreased inhibition of prefrontal pyramidal neurons [46], [47], [48]. The decreased prefrontal signal-to-noise ratio may place networks of cortical neurons in a more labile state, allowing them to more easily switch between representations and process multiple stimuli across a wider association range [49]. This state, which we hereforth will refer to as the “creative bias”, could benefit performance on tasks that involve continuous generation and (re-)combination of mental representations and switching between mind-sets. The creative bias could also explain why the different measures of divergent task performance correlate: A decreased signal-to-noise ratio in thalamus would decrease information gating and possibly increase fluency; decreased signal-to-noise ratio in cortical regions should better enable flexibility and switching between representations; similarly, the associative range should be widened and selectivity should be decreased which might spur originality and elaboration.

Besides carrying benefits related to fluency and switching, the decreased signal-to-noise ratio associated with the creative bias should be disadvantageous in relation to tasks that require high levels of selective attention. Some support for this prediction can be taken from Dorfman [50] who showed that the greater a person’s divergent thinking scores, the slower his or her reaction times were on a negative priming task requiring the inhibition of interfering information. Furthermore, the creative bias may also bring a risk of excessive excitatory signals from the thalamus overwhelming cortical neurotransmission, with ensuing cognitive disorganization and positive symptoms [30]. It is thus tempting to suggest that dopaminergic modulation of neurotransmission mediated through dopamine D2-receptors could be one of the mechanisms which associate creativity with positive psychotic symptoms. Interestingly, positive symptoms are not necessarily related to problems in executive function, at least not to the same extent as negative symptoms [51], which indicates that in the creative individual “blind variation” might be affected without a concomitant decline in “selective retention”. It can be speculated that aberrant thalamic function may promote unusual associations, as well as improved performance on divergent thinking tests in healthy individuals, in the absence of the detrimental effects typically associated with psychiatric disorders. In other words, thinking outside the box might be facilitated by having a somewhat less intact box.

In plain English speak, the same decreased signal-to-noise ratio in perfrontal regions that gives rise to creativity also gives rise to proneness to psychosis. The more the noise that is introduced the greater the chances that the ideas generated by ‘blind variation’ are more creative; if the ‘selective retention’ procedure is also defective or loosened to an extent, it may result in psychopathology and psychosis, while if intact it leads to creativity. Thus while one factor , that of loosening of associations, flexibility and set switching is common to both psychosis and creativity, the defects in selective retention may be the crucial factor that distinguishes brains from bonkers.

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de Manzano, ?., Cervenka, S., Karabanov, A., Farde, L., & Ullén, F. (2010). Thinking Outside a Less Intact Box: Thalamic Dopamine D2 Receptor Densities Are Negatively Related to Psychometric Creativity in Healthy Individuals PLoS ONE, 5 (5) DOI: 10.1371/journal.pone.0010670

The Creativity-dopamine (b)linkage: more brains and bonkers connections

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rh?zom?ng Cam?ra?Obscura pl?ats . .
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Creativity is certainly different from intelligence; it is usually gauged as the ability to make novel and useful unique contributions to a field. Creativity itself is not a unified construct but can be broken into convergent creativity (involving more focused approach) and divergent creativity (involving more widening and loosening of associations).

It has been evident for quite some time that there is a connection between insanity (especially bipolar/schizophrenia spectrum) and creativity , especially as evidenced by the creative bent of schizotypal people. See for example this article covering a recent study that looks at exactly the same issue. However, most of these studies rely on a unitary construct of creativity that does not do full justice to the correlations that could be found if convergent and divergent creativity was distinguished and effect of intelligence was factored out. The new study by Hommel, B. does just that.

Schizophrenia/psychosis as many will know from their elementary neuroscience knowledge is associated with dopamine dysfunction; specifically it is believed that high baseline dopamine levels are there in schizophrenics/psychotics. So it was not unreasonable for Hommel et al to hypothesize that dopamine should have some relation with creativity possible higher dopamine associated with high creativity. However, dopamine has shown an inverse U relation for many other factors and thus they were cautious and tried to fit both linear and quadratic graphs to their data. But we are moving ahead of ourselves. Before they could find the underlying relation between dopamine and creativity, they had to measure these things accurately.

They measured dopamine using Eye Blink Rate (EBR): that is how many time you blink in a minute. For creativity , they measured Convergent Creativity using a remote association task (don’t go by the name …the task has only one answer and measures convergent thinking) . for eg. a subject is given three words (say time, hair, stretch) and have to come up with a word that is commonly related to all three (answer: long) . this reliably measures creativity but of he convergent type. For Divergent thinking , they administered the Alternate Uses task (AUT),a task that requires one tocome up with novel uses of everyday objects like brick, toothpaste etc. The responses to AUT were further coded for fluency (how easily one could come up with alternatives measured by total no. of responses) , flexibility(the number of different categories used or how remote the mind wandered) and elaboration (the level of detail surrounding the use). They also measured fluid intelligence using Raven’s progressive matrices.

They then conducted experiments (administered the tests to subjects) , collected data and analyzed the results. The main findings of interest to us is that they found a inverse u shaped relation between dopamine (EBR) and flexibility dimension fo divergent thinking. This effect was present even when the effect of intelligence was factored out. thus both low dopamine, as well as too much dopamine is detrimental to flexible divergent thinking/creativity and schizotypals , placed precariously between normals and psychotics are best placed to be the most creative as they presumably have the optimum dopamine levels. the authors also argue that schizophrenics dopamine levels should not be brought down indiscreetly by using anti-psychotics (which reduce dopamine levels) but they should be brought in the optimum range of dopamine functioning. this obviously has immense importance and treatment implications. No wonder creative people feel stiffed when on anti-psychotics- their dopamine levels are being brought down way too much.

The other interesting finding was that dopamine (EBR) was negatively ad linearly related to convergent thinking. Thus, it is evident that convergent creativity and divergent creativity are different constructs and while dopamine has a complex quadratic relationship with divergent thinking, that with convergent thinking is linear though not very comforting. It seems that as dopamine levels increase the ability to narrow focus diminishes and this would be concordant with other studies linking dopamine to ADHD for example.

Overall, a view of how brains and bonkers are two sides of the same coin is emerging and it is exciting to note that many previous inconsistencies in literature around this issue may have to do with not differentiating and decomposing creativity into its many components and not looking for inverse u shaped effects.

Chermahini SA, & Hommel B (2010). The (b)link between creativity and dopamine: Spontaneous eye blink rates predict and dissociate divergent and convergent thinking. Cognition PMID: 20334856

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Creativity-psychosis linkage via reduced white matter /myelination

ResearchBlogging.org
I have been following, and am passionate about, the positive psychology movement for quite some time, but was surprised to discover that there was something called positive neuroscience also in place. I recently came across this new scientist article about the research paper of Rex Jung et al and was pleased to discover that Jung was working on the frontier of applying latest in neuroscience research to Positive brain states and substrates like that involved in creativity.

The article is in PLOSOne, an open access journal and is lucidly written , so you should go and read it now. I’ll anyway like to summarize their study results. First a bit of background about creativity psychopathology linkage.

Some research reports positive correlations between various definitions of creativity and a diagnosis of psychopathology [1], [2], [3], [4]. Other studies report that psychopathology is rarely, if ever, associated with creative insight, capacity, or productivity [5]. When artists are studied more carefully, certain personality characteristics appear to reside upon a continuum of both normal behavior and psychopathology. For example, creative expression in the visual arts and poetry has been linked with the overlapping personality traits of schizotypy and Openness to Experience (Openness), and particularly to self-reports of “unusual experiences” and “unconventional nonconformity”, but not the “introvertive anhedonia” characteristic of schizophrenia [6].

This is inline with what we have been covering at mouse trap regarding association of creativity with the psychotic spectrum especially the creativity that is artistic or revolutionary in nature rather than scientific and methodical in nature. This is how the authors distinguish between types of creativity inline with my views that one type of creativity is autistic (cognitive) in nature while the other is psychotic (emotional) and these are on a continuum.

First, there does not exist one “creativity”; rather, this construct is hypothesized to reside upon a continuum between cognitive (i.e., scientific) and emotional (i.e., artistic) behavioral domains [41], [42]. Thus, when comparing scientists and artists directly, researchers have found lower lifetime rates of psychopathology for: 1) scientists compared to artists, 2) natural scientists compared to social scientists, 3) nonfiction writers compared to fiction writers and poets, and 4) formal artists compared to “expressive” artists [3], [4], [43]. These findings have led researchers to hypothesize a hierarchical structure of creativity across disciplines [42], which echoes the notions of “paradigmatic” (i.e., a fundamental model of events) versus “revolutionary” (i.e., rejection of doctrines) approaches as applied to the sciences [44]. The benefits of working within the lines of a given field appear to be lower levels of psychopathology; alternately, individuals with lower levels of psychopathology may be attracted to such endeavors. Similarly, there is increasing evidence that the cost of “revolutionary” approaches to creative endeavors, whether it is in the arts or sciences, may be associated with increased levels of psychopathology although, again, causative links are weak at best.

So that fits in with broader creativity/ psychopathology linkage, but to get back to the current study the authors had already established earlier that performance on Divergent Thinking (DT) (a measure of creativity) “exhibited significant inverse relationships with both cortical thickness in frontal lobe regions and metabolite concentration of N-acetyl-aspartate (NAA) in the anterior cingulate cortex in normal young subjects “. Thus, some theoretical relationship between creativity and underlying brain circuitry in the frontal reagion was available a priori. Also, research by other researchers has already established that ” Both schizophrenic and bipolar patients have been shown to have reduced fractional anisotropy (FA) in the anterior thalamic radiation [12], [13] and uncinate fasciculus [14] within frontal brain regions. Similarly, reduced FA was observed within the uncinate fasciculus of a cohort with schizotypal personality disorder, providing strong support for the hypothesis that similar neural phenotypes may not result in full-blown clinical symptoms [15]. Finally, in normal subjects, the Neuroregulin-1 (NRG1) single nucleotide polymorphisms (SNP’s) SNP8NRG243177 and SNP8NRG221533 were found to predict lower FA in the left anterior thalamic radiation [16]. As NRG1 has been found to predict higher risk of schizophrenia [17], [18] and bipolar disorder [19], and is linked with axonal myelination and migration [20], these authors hypothesize a mechanistic link between NRG1 within the anterior thalamic radiation and risk for psychotic disorders [16].”

Thus, from the above it is easy to see that there should be a inverse relationship between Fractional Anisotropy (a construct related to myelination of axons) in the frontal regions and creativity if one assumes that creativity and psychopathology are related and are on one end of a continuum. And this inverse relationship between creativity and FA is exactly what they found:

Our results suggest a convergence between a cognitive measure of divergent thinking, a personality measure of Openness, and a white matter integrity measure within the inferior frontal lobes. We found that normal young subjects with lower levels of FA within predominantly left inferior frontal white matter (i.e., regions overlapping the uncinate fasciculus and anterior thalamic radiation) scored higher on the CCI; similarly subjects with lower levels of FA within the right frontal white matter (i.e., regions overlapping the uncinate fasciculus and anterior thalamic radiation) scored higher on self-reported measures of Openness. These two regions of white matter overlap with those reported by other researchers who found lower FA in both schizophrenia and bipolar disorder [13], [14], [30].

They could also nail the reduced FA to reduced myelination as radial diffusion was affected more than axial diffusion. As reduced myelination has been shown as a diatheisis for psychosis, this fits in with previous research linking risk factors common to psychosis and creativity.

Whereas more neural resources are often associated with higher intellectual capacity in a parieto-frontal network of brain regions [39], studies in DT appear to suggest that less is often better in a different network of brain regions, particularly fronto-cingulate-subcortical networks linked via white matter loops [40].

One can speculate that frontal region, more concerned with executive control , when with reduced activity or functional connectivity , may not inhibit the other brain regions that much, and may thus lead to flowering of inherent creativity and cross-talk amongst different brain regions. On the other hand too much white matter/ gray matter in this region may lead to too much control and leave little room for flexibility and creativity.

However, while lower FA is commonly seen in diseases where both cognition and white matter integrity are impaired (e.g., Traumatic Brain Injury, Schizophrenia, Alzheimer’s disease) [45], [46], [47], evidence is accumulating that higher FA in particular brain regions may also be associated with clinical disorders including post-traumatic stress disorder [48], obsessive-compulsive disorder [49], panic disorder [50], synaesthesia [51], and Williams syndrome [52].

It is interesting to note that enhanced FA is associated with clinical disorder of Williams syndrome, which is associated with Autism; on the other end of continuum, reduced FA in particular brain region is associated with psychosis proneness, thus providing another convergent linkage of autism and psychosis as opposites.

Jung, R., Grazioplene, R., Caprihan, A., Chavez, R., & Haier, R. (2010). White Matter Integrity, Creativity, and Psychopathology: Disentangling Constructs with Diffusion Tensor Imaging PLoS ONE, 5 (3) DOI: 10.1371/journal.pone.0009818

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Dopamine and theory of mind: another autism/schizophrenia dichotomy

ResearchBlogging.org

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There is an article in press in Neuropsyhcologia by Lackner et al that related Dopamine (DA) levels as measured by Eye Blink Rate (EBR) to preschoolers (3-5 yrs old) Representational theory of Mind (RTM).

The authors hypothesized that as one of the neural correlates of RTM is dMPFC, and as dMPFC has dopamine receptors and is innervated by dopmainergic projections along the dopamine mesocortical pathways , hence perhaps it is the dopamine’s tonic and phasic levels that may be correlated with and have a causal role in the preschoolers’ developing RTM abilities.

3-5 years is a critical period in which the RTM abilities are developing in a normal kid and are first found to be deficient in autistic kids. another linkage the authors seem relevant, but which I don’t agree to much, is the error -prediction theory of dopamine. They believe that ToM/RTM abilities develop when one takes into account the behavior of others and finds discrepancies in ones own knowledge and why they act based on certain different assumptions and by realizing this error of prediction modifies ones understanding of others and starts attributing a mind to them. The authors believe that phasic dopamine which has error prediction functions may be affecting RTM via this pathway too; I find that not very convincing.

However, their basic premise that tonic or baseline dopamine affects RTM abilite seems to be on firm ground and they found support for this hypothesis. They did not measure DA levels directly , but instead relied on Eye Bink Rate (EBR) which is a robuts predictor of overall dopamine in the mesolimbic pathways via the caudate nucleus dopamine levels. They also did not measure EBR directly but measured it using EEG waveforms of relevant brain regions above the eyes.

The RTM tasks they used and the Response -conflict executive function (RC-EF) tasks they used are very simple and intuitive and I refer the reader to methods section to pursue them in detail. For our purpose it is sufficient to mention that RTM did not include the famous anne-sally false belief task but had other variants like false belief location task etc.

Their findings were unequivocal. They found that DA levels as gauged from EBR were a significant predictors of RTM abilities and the effect was not mediated by a possible confound- that of RTM and RC-EF linkages and correlations.

For our purposes what is most important is the direction of the effect . More DA levels were associated with better RTM ; while lower DA was associated with lower RTM performance. This is consistent with the DA relation of Schizophrenia/Autism one of which has higher DA levels and better ToM; while the other both poorer ToM and lower baseline DA. To quote:

These findings dovetail with other research connecting dopamine and representational theory of mind in autistic and schizophrenic populations. Both autism and schizophrenia have been associated with RTM impairment (Pickup, 2008; Sabbagh,2004; Savina & Beninger, 2007) and dysregulation of DA (Braver, Barch, & Cohen, 1999; Lam, Aman, & Arnold, 2006). For instance, in the case of schizophrenia there is some evidence that increased levels of frontal dopamine, as a consequence of the pharmacological activity of some atypical antipsychotics, leads to increased performance on RTM tasks (Savina & Beninger, 2007). The present study added to this body of literature by demonstrating associations between RTM and DA in typically developing children. Considered together, this further supports the hypothesis that dopaminergic functioning plays a role in RTM development.

As always, I am excited by more support for Autism and Psychosis as opposites theory and belive this further cements the case and shows possible neurochemichal mechanisms underlying the difference.

Lackner, C., Bowman, L., & Sabbagh, M. (2010). Dopaminergic functioning and preschoolers’ theory of mind Neuropsychologia DOI: 10.1016/j.neuropsychologia.2010.02.027

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