Wednesday, February 25, 2009

Linguistic effects on unconscious color perception

The post headline may seem an oxymoron , but it is indeed possible to perceive colors unconsciously. How do we know that someone has perceived a color, when he doesn't report the qualia. We do so by measuring the effects on subsequent behavior. Consider subliminal priming. Consider a subliminal stroop test, in which color patches are presented subliminally and then color lexical terms are presented consciously in neutral (say black) ink. I'm sure with this subliminal modified stroop test one could still get a color and lexical term interaction effect; the point is that color , when not perceived, may still influence subsequent behavior.

The experimental paradigm in this PNAS article did not go so far, but restricted itself to color stimuli that was not attended to; that is, the color was indeed perceived, but it was not attended to (the task involved attention to form rather than color) and so as the color was not attended to, they presumed that the effects that the color information would have on behavior would be completely unconscious. I'm not convinced, but that doesn't invalidate their otherwise very beautiful study that once again provides strong evidence for the milder version of the Sapir-Whorf hypothesis, at least as it relates to categorical color perception. 

Now, I have written previously about Sapir- Whorf hypothesis in general,  and in particular about the ability of Russians( who have two separate terms for light and dark blue) to visually discriminate between light and dark blue significantly better than their English counterparts, thanks to their rich color lexicon; so this new study that found that Greek-natives (who also have different lexical terms for light and dark blue) were superior to English-natives in terms of discriminating categorical color perception for light and dark blue color, did not come as a surprise or seemed ground-breaking; but there are important differences both in terms of the procedures used and the processes involved.

This study, works at pre-attentive level, uses physiological measures like ERP (they studied the vMMN - visual Mismatch Negativity) to determine whether the color stimuli had differential effect even at pre-attentive perception and thus provides independent evidence for the effect of Language on color perception. I'll now quote from the abstract and discussion section:

It is now established that native language affects one’s perception of the world. However, it is unknown whether this effect is merely driven by conscious, language-based evaluation of the environment or whether it reflects fundamental differences in perceptual processing between individuals speaking different languages. Using brain potentials, we demonstrate that the existence in Greek of 2 color terms—ghalazio and ble—distinguishing light and dark blue leads to greater and faster perceptual discrimination of these colors in native speakers of Greek than in native speakers of English. The visual mismatch negativity, an index of automatic and preattentive change detection, was similar for blue and green deviant stimuli during a color oddball detection task in English participants, but it was significantly larger for blue than green deviant stimuli in native speakers of Greek. These findings establish an implicit effect of language-specific terminology on human color perception.

This study tested potential effects of color terminology in different languages on early stages of visual perception using the vMMN, an electrophysiological index of perceptual deviancy detection. The vMMN findings show a greater distinction between different shades of blue than different shades of green in Greek participants, whereas English speakers show no such distinction. To our knowledge, this is the first demonstration of a relationship between native language and unconscious, preattentive color discrimination rather than simply conscious, overt color categorization.

To conclude, our electrophysiological findings reveal not only an effect of the native language on implicit color discrimination as indexed by preattentive change detection but even electrophysiological differences occurring as early as 100 ms after stimulus presentation, a time range associated with activity in the primary and secondary visual cortices (22). We therefore demonstrate that language-specific distinctions between 2 colors affect early visual processing, even when color is task irrelevant. At debriefing, none of the participants highlighted the critical stimulus dimension tested (luminance) or reported verbalizing the colors presented to them. The findings of the present study establish that early stages of color perception are unconsciously affected by the terminology specific to the native language. They lend strong support to the Whorfian hypothesis by demonstrating, for the first time, differences between speakers of different languages in early stages of color perception beyond the observation of high-level categorization and discrimination effects strategically and overtly contingent on language specific
distinctions.

I think this fits in with predictive models of perception, wherein, earlier stages of visual processing, that are unrelated to color discrimination, may still be primed by color information that one has obtained earlier and has processed pre-attentively. I, as always , am excited by this proof of whorfian hypotheses.

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An online personality guessing experiment

I came to know of You Just Get Me experiment today, courtsey PsychCentrals post on the top 10 online psychology experiments .

In a nutshell, the site lets you guess the personality of a person based on clues he provides. In my case the public clues I have provided are my photograph and my facebook profile. Now, as a fun experiment, I'll request all my readers to go to that site and try to guess my personality from these , as well as additional clues you might have got following my blogging practices and habits. Its bound to be fun and I believe the questionnaire has correctly guessed my personality (OCEAN based) and I have a separate application on facebook that profiles my personality (please do not take a sneak peak at it to guess my personality) and I found that the two personality characterizations do corroborate each other.

So, please go ahead and guess me; and of course if yopu like put some data on the site for your personality analysis too. Go to this link to guess my personality.

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Thursday, February 19, 2009

Encephalon #64 up at the Neurocritic

The 64th edition of Encephalon is up at the Neurocritic and has been exceptionally well presented. Neurocritic embeds all the articles in context, sometimes linking to other external sources, and also providing a seamless flow between the varied topics that are covered. The articles themselves are very good, and include submissions from some new blogs other than the usual suspects.A couple of my favorites include a construal level-procrastination linkage study and a DAT-KO mice couldn't get high on cocaine study. There is more at the source, so head over to there.

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Tuesday, February 17, 2009

Support for the Aberrant Salience hypothesis of Psychosis

Last week I wrote about the aberrant salience theory of psychosis, and luckily, this week itself a new study has surfaced that corroborates that theory with some preliminary evidence.


Thanks to BPS research digest, I have come across this open source research article in Psychological Medicine, that has found evidence for the aberrant salience hypothesis.

What Rosier et al did was to administer a Salience Attribution Test to both patients with Schizophrenia and normal controls, and to look for differences in the adaptive and aberrant salience. It is important to realize that most of the patients were medicated on anti-psychotics, and as per the theory advocated by Shitij Kapur, the anti-psychotics would dampen the normal adaptive salience too as psychosis is due to hyper reactivity of dopamine system and anti-psychotics are supposed to work by attenuating that behavior. More specifically, the predictions were:

It has been hypothesized that dopamine antagonists reduce both adaptive and aberrant salience, and that in the absence of effective treatment patients with schizophrenia exhibit aberrant salience (Kapur, 2003). Therefore, our first prediction was that that medicated patients with schizophrenia would exhibit reduced adaptive salience relative to controls, representing an undesirable side-effect of anti-psychotic medication. Our second prediction was that medicated patients with schizophrenia would exhibit equivalent aberrant salience to controls, representing the beneficial effect of anti-psychotic medication, which is hypothesized to normalize aberrant salience from a previously elevated level (Kapur, 2003). Our third prediction was that those patients with persistent positive symptoms, in whom medication is not entirely effective, would exhibit greater aberrant salience than patients without positive symptoms. Our fourth prediction was that in the controls, individual differences in aberrant salience would be related to the personality trait of schizotypy, considered to be an index of psychosis proneness (Chapman et al. 1994; Claridge, 1994; Stefanis et al. 2004).

All of their predictions were supported by the test results. The SAT paradigm is really simple and depends on reaction time measures following CS+ and CS-; with CS+ reaction times quantifying adaptive salience and CS- reaction times quantifying aberrant salience attribution. Read the methods section for more on the SAT.
Interestingly in patients, those with persisting delusions as well as those high on Negative symptoms exhibited higher aberrant salience as compared to patients/ controls without any delusional symptoms.Also, in controls the introverted anhedonia subscale of schizotypy correlated signficantly with the aberrant salience, thus indicating a role for negative symptom formation/ explanation too as apart of the aberrant salience. This is how the authors interpret their findings:
Aberrant salience and positive symptoms of schizophrenia

One explanation of increased aberrant salience in patients with positive symptoms concerns aberrant dopamine signalling. Contemporary accounts of reward learning suggest that phasic dopamine firing codes reward prediction errors (Schultz et al. 1997), for example, those arising from temporal difference models of reinforcement learning (Dayan & Balleine, 2002). Such models elegantly account for changes in both the firing patterns of ventral tegmental area dopamine neurons in monkeys (Schultz, 1997), and ventral striatal responses in humans (Pessiglione et al. 2006; Seymour et al. 2007), as reward-learning progresses. If phasic dopamine release signals reinforcement prediction errors, any large stochastic fluctuation in dopamine release may disrupt learning about stimulus–reinforcement associations, generating a state in which motivational salience could be misattributed to neutral stimuli, or what might be termed a ‘false-positive’ phasic dopamine signal; such events have been proposed to result in positive symptoms (Kapur, 2003).
In the present study, patients for whom medication had effectively eliminated positive symptoms actually exhibited significantly less aberrant salience than controls, supporting the hypothesis that the beneficial effects of antipsychotic medications on positive symptoms are related to their ability to dampen-down aberrant salience (Kapur, 2003). However, independent of symptoms at the time of testing, the patients with schizophrenia exhibited significantly less adaptive salience than controls. Antipsychotic medication has long been considered to exacerbate negative symptoms in schizophrenia, which may be related to reduced adaptive salience [see discussion below and Schooler (1994) ]. Our findings support the suggestion of Kapur (2003) that this may be a necessary corollary to the beneficial effect of antipsychotic medication on positive symptoms.

Previous studies suggest that antipsychotic medication does not necessarily normalize abnormal dopamine signalling in psychotic patients. For example, functional neuroimaging studies have shown dopamine dysregulation in both medicated and unmedicated patients (Hietala et al. 1995; Abi-Dargham, 2004; McGowan et al. 2004). Therefore persistent symptoms in medicated patients might still be related to aberrant salience. Furthermore, the only other study investigating stimulus–reinforcement learning for appetitive outcomes in psychosis found that both medicated and unmedicated patients responded more quickly to a CS− than controls, a finding interpreted as aberrant salience (Murray et al. 2008). This study also reported that patients exhibited reduced haemodynamic correlates of reward prediction errors in the ventral striatum relative to controls, consistent with other findings in medicated patients (Juckel et al. 2006; Jensen et al. 2008). Nevertheless it will be important to confirm our findings in unmedicated patients.

Aberrant salience and negative symptoms of schizophrenia


Although positive symptoms were associated with increased aberrant salience, our data also suggest a link between aberrant salience and negative symptoms. Aberrant salience correlated not only with negative symptoms in the patients, but also with O-LIFE introvertive anhedonia, which relates to reduced interest and social withdrawal, in the controls. If dopamine transmission is dysregulated in psychosis (Abi-Dargham, 2004), it is possible that ‘false negatives’ in the phasic dopamine signal might occur, i.e. a reinforcement-related stimulus fails to elicit a sufficiently large phasic dopamine response. False negatives would decrease the value of motivationally salient stimuli, possibly leading to symptoms such as avolition, apathy and social withdrawal. Consistent with this explanation, other studies that investigated responses to emotionally salient images in medicated patients with schizophrenia reported decreased responding for (Heerey & Gold, 2007) and ventral striatal responses to (Taylor et al. 2005) positive emotional stimuli relative to controls.

This explanation is also consistent with data from a functional magnetic resonance imaging study investigating the effects of d-amphetamine on reward processing in healthy volunteers. Knutson et al. (2004) found that amphetamine administration paradoxically decreased the magnitude of phasic ventral striatal haemodynamic responses in response to a CS+ that signalled reward (i.e. increasing the potential for a false negative). In the same study, amphetamine administration caused significant phasic haemodynamic responses in the ventral striatum following CS+ that signalled potential monetary loss, an effect that was absent under placebo, possibly reflecting a loss of specificity of dopamine signalling (i.e. increasing the potential for a false positive). The aberrant salience model might therefore explain both positive and negative symptoms by appealing to a common neurobiological mechanism, namely a loss of signal:noise ratio in the mesolimbic dopamine system, possibly as a result of increased tonic dopamine activity (Grace, 1991; Winterer & Weinberger, 2004).
I believe they are on to something, but the explanation for negative symptoms is still not fully fleshed out or convincing. and of course one has to remember that these results are juts with 20 patients so need to be replicated before being put to use/ accepted as orthodoxy.
ResearchBlogging.org
J. P. Roiser, K. E. Stephan, H. E. M. den Ouden, T. R. E. Barnes, K. J. Friston, E. M. Joyce (2008). Do patients with schizophrenia exhibit aberrant salience? Psychological Medicine, 39 (02) DOI: 10.1017/S0033291708003863

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Sunday, February 15, 2009

On Reading Darwin

12 th of February was Darwin day, and I decided to study an original text of Darwin to honor the occasion. I chose the 'Expression of emotions in Man and animals' as my first text as I am familiar with the work of Paul Ekman and have had a deep fascination with the subject and wanted to find out how much Darwin had anticipated and got right in his times.I have only read the introduction and the first chapter till now, but am surprised at the level of modernity visible in Darwin's analysis.

Of course Darwin takes an evolutionary view on the subject and is also cognizant of the subtleness of the entire field.

He who admits on general grounds that the structure and habits of all animals have been gradually evolved, will look at the whole subject of Expression in a new and interesting light.

The study of Expression is difficult, owing to the movements being often extremely slight, and of a fleeting nature. A difference may be clearly perceived, and yet it may be impossible, at least I have found it so, to state in what the difference consists. When we witness any deep emotion, our sympathy is so strongly excited, that close observation is forgotten or rendered almost impossible; of which fact I have had many curious proofs. Our imagination is another and still more serious source of error; for if from the nature of the circumstances we expect to see any expression, we readily imagine its presence. Notwithstanding Dr. Duchenne's great experience, he for a long time fancied, as he states, that several muscles contracted under certain emotions, whereas he ultimately convinced himself that the movement was confined to a single muscle.

He then lists the various ways he plans to get to universal features of emotional expressions. These involve using questionnaires given to various anthropologists to discover if the emotions are expressed in a similar fashion all over the world ;and the study of infants and insane as they may have unadulterated / extreme emotional expressions respectively. He also briefly touches upon the usefulness of studying emotional expressions as depicted by Masters in painting in sculpture but finds the method wanting. Lats , but not the least, he studied emotional expression in other animals and treated emotional expression as a continuum.
Sixthly, and lastly, I have attended. as closely as I could, to the expression of the several passions in some of the commoner animals; and this I believe to be of paramount importance, not of course for deciding how far in man certain expressions are characteristic of certain states of mind, but as affording the safest basis for generalisation on the causes, or origin, of the various movements of Expression. In observing animals, we are not so likely to be biassed by our imagination; and we may feel safe that their expressions are not conventional.

He then lists the three basic principles of emotional expressions. I list them verbatim.

I. _The principle of serviceable associated Habits_.--Certain complex actions are of direct or indirect service under certain states of the mind, in order to relieve or gratify certain sensations, desires, &c.; and whenever the same state of mind is induced, however feebly, there is a tendency through the force of habit and association for the same movements to be performed, though they may not then be of the least use. Some actions ordinarily associated through habit with certain states of the mind may be partially repressed through the will, and in such cases the muscles which are least under the separate control of the will are the most liable still to act, causing movements which we recognize as expressive. In certain other cases the checking of one habitual movement requires other slight movements; and these are likewise expressive.

II. _The principle of Antithesis_.--Certain states of the mind lead to certain habitual actions, which are of service, as under our first principle. Now when a directly opposite state of mind is induced, there is a strong and involuntary tendency to the performance of movements of a directly opposite nature, though these are of no use; and such movements are in some cases highly expressive.

III. _The principle of actions due to the constitution of the Nervous System, independently from the first of the Will, and independently to a certain extent of Habit_.--- When the sensorium is strongly excited, nerve-force is generated in excess, and is transmitted in certain definite directions, depending on the connection of the nerve-cells, and partly on habit: or the supply of nerve-force may, as it appears, be interrupted. Effects are thus produced which we recognize as expressive. This third principle may, for the sake of brevity, be called that of the direct action of the nervous system
.

The first principal is easy to understand. It basically states that facial expression etc are associated with mental emotional states and do so by way of habit formation or association. Now, this should not exclude instinctual emotional expressions like smiling as they become fixed by the action of evolution.

The second principle has had only some relatively moderate success. I remember a recent study claiming that Fear and Disgust had opposite effects on facial muscle movements such that Fear led to movements (like broadening of eyes/ dilation of pupils)that allowed more information/material to be ingested; while disgust led to constriction of nose, eye, mouth etc. although Fear and disgust are not antithetical, one may discern similar patterns in other movements.

The third again, I believe has mixed success. It can be ralete to Jams-lange theory of emtoions, where nervous arousal happens first, and emotional feeling or expressions accompanying them follow next.


I am only thus far in my reading of Darwin, but surely will keep doing follow up posts.

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Wednesday, February 11, 2009

Psychosis and Salience dysregulation

Regular readers of this blog will know that I subscribe to the incentive salience theory of doapmaine propounded by Berridge et al. As per this theory dopamine mediates the salience of an internal/ external stimulus and endows and activates the motivational salience related to that stimulus. In simple words the mesolimbic dopamine systems serves to identify the importance of a stimulus to us- be it aversive or pleasurable. This conceptualization is different from the hedonic pleasure theory of dopamine and distinguishes between 'wanting/ dreading' and 'liking/ disliking'. Thus, the amount of doapminergic activity will affect the degree of dread or want associated with a stimulus, but not the actual liking/ disliking of the reward/punishment administered following the stimulus. Till now we have been talking mostly in terms of classical Pavlovian conditioning, but the same incentive salience can be extended to operant conditioning paradigm, with the external stimulus being replaced by an internal intention and the mesolimbic dopamine system activity determining whether, and to what degree,  one is motivated to perform the intended action. Again the motivational component should be separated from our actual liking/disliking of the expected outcomes of the behavioral measures.  Thus, we may actually like the reward at the end of operant behavior less , but still be highly motivated to perform the action depending on high dopaminergic activity that confers a very positive incentive salience to that operant behavior. Consider the gambler for whom winning the jackpot is motivationally very salient , but the actual pleasure he may derive or hedonistic value he may get from spending the lottery amount may not be that much. Or consider the carving of a drug addict for the dope- the drug administered may not feel that pleasurable ,  but the wanting is strong.

We also know about the reward error-prediction theory of dopamine, and that in my opinion is not incompatible with the incentive salience theory. The error coding signal of dopamine surge or ebb signals that the stimulus has become meaningful and salient and needs to be (re)coded. Thus, in most basic terms dopamine will signal whether the stimulus is meaningful for the organism and as it could be meaningful in both positive and negative sense , the dopamine activity will lead to subjective feelings of either alarm or significance associated with that stimulus. In either case, the stimulus would 'grab our attention' and become salient (this may happen unconsciously) and perhaps if the activity is sustained also become consciously significant and enter consciousness.

Now, consider a dysregulated mesolimbic dopamine system that is hyperactive and is characterized by excessive dopamine synthesis, release and synaptic presence. Here , for a given stimulus, that usually, and in normal individuals,  grabs the unconscious attention and is unconsciously and automatically evaluated , the dopamenirgic activity may be sustained and lead to conscious perception of/ attention to the stimulus and a conscious evaluation or appraisal of the stimulus. The individual with such a hyperactive dopaminergic system would start paying conscious attention to many stimulus that were earlier processed subliminally and start noticing a much deeper sensory (external) and cognitive( internal) world. But the effect would not just be a richness of sensation and distractibility, the dopamine surge will also label the stimulus to which the attention has thus been directed salient and the individual will try to reason why that stimulus is significant.So first sensory (vividness)  and cognitive (racing thoughts) richness arrives, along with an overwhelming subjective feeling that they are important and later with a need to create a story as to why the stimulus (internal/ external)  is important comes rationalizing and delusions that serve to jutify the significance of things that were earlier not consciously significant/threatening. Thus, the delusions of grandeur and persecution.  Also, sometimes the dopamine surges may happen without any associated external and internal stimulus. We know that when one is not task-oriented (either task involving external stimulus or internal goal-directed activity), then the default network that is usually associated with self-system and imagination takes over. In such conditions when the default network is active and one is just focused on self and internal imaginary world, a dopamine surge may signal that the self and imagination is very salient or important. The self thus becoming salient may get associated with other arbitrary external stimulus happening at that time and one may get delusions of reference whereby seemingly innocuous and impersonal external communications/ references are deemed to refer to the self.  thus, delusions may be partly explained by stimuli becoming consciously significant and also stimuli/ self becoming salient out of context.  Hallucinations might also be explained partly by the imaginative activity of the default newtrok becoming salient , meaningful, conscious and life-like and thus sort of 'real'. Thus, while many have outgrown the unconscious-becoming-conscious theories of psychosis, I see some scope for more work here and a possible mechanism too.

Of course the above incentive salience hyper activation can work in conjunction with other deficits/abnormalities like self-monitoring deficit, theory-of-mined hyperactivity, intentional attribution hyperactivity, need for more control in lieu of facing an unpredictable environment, jumping-to-conclusion bias etc to foster full fledged symptoms of psychosis in some individuals.

I am grateful to Mind Hacks for discovering the Shitij Kapur paper on the incentive dysregulation theory of psychosis and I now quote extensively form the paper.

First the paper establishes the dopamine theory of psychosis by looking at anti-psychotic drug action and also the effect of dopamine administration.

The dopamine hypothesis of schizophrenia has comprised two distinct ideas: a dopamine hypothesis of antipsychotic action and a dopamine hypothesis of psychosis. The two are related but different. The dopamine hypothesis of antipsychotic medications can be traced to the early observation that antipsychotics increase the turnover of monoamines , more specifically, dopamine , and this observation anticipated the discovery of the "neuroleptic receptor" , now called the dopamine D2 receptor, providing a mechanistic basis for the dopamine hypothesis of antipsychotic action. A central role for D2 receptor occupancy in antipsychotic action is now well established, buttressed by neuroimaging studies using positron emission tomography and single photon emission computed tomography. However, the importance of dopamine receptors in the treatment of psychosis does not by itself constitute proof of the involvement of dopamine in psychosis .

Early evidence for a role of dopamine in psychosis was the observation that psychostimulant agents that trigger release of dopamine are associated with de novo psychosis and cause the worsening of psychotic symptoms in patients with partial remissions. Further evidence came from postmortem studies that showed abnormalities in dopaminergic indexes in schizophrenia, although the interpretation of these data was always confounded by drug effects . The most compelling evidence in favor of the dopamine hypothesis emerges from neuroimaging studies . Several studies have shown that patients with schizophrenia, when psychotic, show a heightened synthesis of dopamine , a heightened dopamine release in response to an impulse , and a heightened level of synaptic dopamine . While there are some indications of a change in the number of receptors , the claim remains controversial . Thus, on balance there is reasonable evidence of heightened dopaminergic transmission, more likely a presynaptic dysregulation than a change in receptor number, in patients with schizophrenia. This role of dopamine in psychosis and schizophrenia needs to be put in perspective. First, it is quite likely that the dopaminergic abnormality in schizophrenia is not exclusive (as other systems are involved), and it may not even be primary . Second, the dopaminergic disturbance is likely a "state" abnormality associated with the dimension of psychosis-in-schizophrenia, as opposed to being the fundamental abnormality in schizophrenia . As suggested by Laruelle and Abi-Dargham , "Dopamine [is] the wind of the psychotic fire." If so, how does dopamine, a neurochemical, stoke the experience of psychosis?

After this he looks at the incentive salience theory of dopamine.

Another account of the roles of dopamine is the incentive/motivational salience hypothesis of Berridge and Robinson and similar proposals by others . This latter conceptualization provides the most plausible framework for the current discussion and will be detailed further in this article.

The motivational salience hypothesis in its current form builds on the previous ideas of Bindra and Toates , who have written about incentive motivation, and of neurobiologists such as Fibiger and Phillips , Robbins and Everitt , Di Chiara , Panksepp , and others who have speculated on the role of dopamine in these motivated behaviors. According to this hypothesis, dopamine mediates the conversion of the neural representation of an external stimulus from a neutral and cold bit of information into an attractive or aversive entity . In particular, the mesolimbic dopamine system is seen as a critical component in the "attribution of salience," a process whereby events and thoughts come to grab attention, drive action, and influence goal-directed behavior because of their association with reward or punishment . This role of dopamine in the attribution of motivational salience does not exclude the roles suggested by previous theorists; instead it provides an interface whereby the hedonic subjective pleasure, the ability to predict reward, and the learning mechanisms allow the organism to focus its efforts on what it deems valuable and allows for the seamless conversion of motivation into action . When used in this sense, the concept of motivational salience brings us a step closer to concepts such as "decision utility" that are used to explain and understand the evaluations and choices that humans make . Conceived in this way, the role of dopamine as a mediator of motivational salience provides a valuable heuristic bridge to address the brain-mind question of psychosis-in-schizophrenia.

Then he goes to his main thesis that psychosis can be considered as a disorder of salience. Note the similarities as well as differences from my conceptualization as above.

It is postulated that before experiencing psychosis, patients develop an exaggerated release of dopamine, independent of and out of synchrony with the context. This leads to the assignment of inappropriate salience and motivational significance to external and internal stimuli. At its earliest stage this induces a somewhat novel and perplexing state marked by exaggerated importance of certain percepts and ideas. Given that most patients come to the attention of clinicians after the onset of psychosis, phenomenological accounts of the onset of psychosis are largely anecdotal or post hoc. However, patients report experiences such as, "‘I developed a greater awareness of.... My senses were sharpened. I became fascinated by the little insignificant things around me’" ; "Sights and sounds possessed a keenness that he had never experienced before" ; "‘It was as if parts of my brain awoke, which had been dormant’" ; or "‘My senses seemed alive.... Things seemed clearcut, I noticed things I had never noticed before’" . Most patients report that something in the world around them is changing, leaving them somewhat confused and looking for an explanation. This stage of perplexity and anxiety has been recognized by several authors and is best captured in the accounts of patients: "‘I felt that there was some overwhelming significance in this’" ; "‘I felt like I was putting a piece of the puzzle together’" .

If this were an isolated incident, perhaps it would be no different from the everyday life experience of having one’s attention drawn to or distracted by something that is momentarily salient and then passes. What is unique about the aberrant saliences that lead to psychosis is their persistence in the absence of sustaining stimuli. This experience of aberrant salience is well captured by this patient’s account: "‘My capacities for aesthetic appreciation and heightened sensory receptiveness...were very keen at this time. I had had the same intensity of experience at other times when I was normal, but such periods were not sustained for long and had also been integrated with other feelings’" . From days to years (the prodrome) , patients continue in this state of subtly altered experience of the world, accumulating experiences of aberrant salience without a clear reason or explanation for the patient.

Delusions in this framework are a "top-down" cognitive explanation that the individual imposes on these experiences of aberrant salience in an effort to make sense of them. Since delusions are constructed by the individual, they are imbued with the psychodynamic themes relevant to the individual and are embedded in the cultural context of the individual. This explains how the same neurochemical dysregulation leads to variable phenomenological expression: a patient in Africa struggling to make sense of aberrant saliences is much more likely to accord them to the evil ministrations of a shaman, while the one living in Toronto is more likely to see them as the machinations of the Royal Canadian Mounted Police. Once the patient arrives at such an explanation, it provides an "insight relief" or a "psychotic insight" and serves as a guiding cognitive scheme for further thoughts and actions. It drives the patients to find further confirmatory evidence—in the glances of strangers, in the headlines of newspapers, and in the lapel pins of newscasters.

Hallucinations in this framework arise from a conceptually similar and more direct process: the abnormal salience of the internal representations of percepts and memories. This could account for the gradation in the severity of hallucinations, whereby to some people they seem like their own "internal thoughts," to others their own "voice," to others the voice of a third party, and to some others the voice of an alien coming from without . So long as these events (delusions and hallucinations) remain private affairs, they are not an illness by society’s standards . It is only when the patient chooses to share these mental experiences with others, or when these thoughts and percepts become so salient that they start affecting the behavior of the individual, that they cross over into the domain of clinical psychosis.

In the remaining part of the paper the author proposes how anti-psychotics work by dampening the salience of things and how they should be adjuncted with psychotherapy as the salience of delusional ideas/ hallucinations may be dampened immediately, but it takes traditional psychological work on the part of the patients to attenuate/overcome the already established beliefs/ perceptions that are no longer salient. I recommended reading the article in full as it has immense treatment implications.

Another implication of the paper is questioning the categorical diagnostic criteria of schizophrenia/ psychosis and making it more dimensional in nature by positing that the dysregulations of incentive salience happens in a continuum. this theme is more boldly covered in a recent BJP paper that argues that we rename schizophrenia to incentive dysregulation syndrome.

Analogous to the metabolic syndrome, although in need of improving on the weaknesses that since its introduction have become apparent, many people with positive psychotic experiences, that have been shown to constitute a fundamental alteration in salience attribution, also display evidence of alterations in other dimensions of psychopathology such as mania,disorganisation and developmental cognitive deficit. This may be referred to as the salience dysregulation syndrome. If the values of the dimensional components in this syndrome rise above a certain threshold, need for care (formal or informal) may arise. Depending on which combinations of dimensional psychopathology are most prominent in this salience dysregulation syndrome and taking into account which elements have been shown to possess the best diagnostic specificity, as discussed above, the categorical representation of this dimensional psychopathology may be expressed using three sub-categories: with affective expression (high in mania/depression dimension); with developmental expression (high in developmental cognitive deficit/negative symptoms); and not otherwise specified. The first two sub-categories are based on evidence of specificity and the more agnostic category of ‘not otherwise specified’ reflects the continuing gap in knowledge.

This I believe is welcome change and I have been arguing endlessly for psychosis to be seen as more of a dimensional syndrome (with autism at the other end) and in continuum with normality.
ResearchBlogging.org
Shitij Kapur (2003). Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. Am J Psychiatry. (160), 13-23
J. van Os (2009). A salience dysregulation syndrome The British Journal of Psychiatry, 194 (2), 101-103 DOI: 10.1192/bjp.bp.108.054254

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