Archive for February, 2009
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
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.
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.
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.
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.
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.
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
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.