Evidence for heightened Agency in Schizophrenia

I have been maintaining that Autism and Schizophrenia are opposites on a continuum and one dimension on which they differ is Agency , with autistics attributing too less agency to themselves (and others), while schizophrenics attributing too much agency to themselves (and others).

The case for people with ASD is fairly settled. They have deficits in theory Of Mind (ToM) and one mechanism by which this deficit seems to arise is via their attributing less agency to themselves as well as others.

For Schizophrenics too, it was speculated that they have problems with agency , but a clear illustration that they have an enhanced agency attribution device was not firmly established. This study, which dates back to 2003, in my opinion, establishes the fact that their is hyper-agency attribution (or hyper-self-menatlizing) in schizophrenics.

The study in question is one by Haggard et al , and it uses an experimental paradigm to illustrate that schizophrenics indeed have problems with self- agency attribution, and that too in the hypothesized direction.

Here is the abstract:

An abnormal sense of agency is among the most characteristic yet perplexing positive symptoms of schizophrenia. Schizophrenics may either attribute the consequences of their own actions to the intentions of others (delusions of influence), or may perceive themselves as causing events which they do not in fact control (megalomania).Previous reports have often described inaccurate agency judgments in schizophrenia, but have not identified the disordered neural mechanisms or psychological processes underlying these judgments.We report the perceived time of a voluntary action and its consequence in eight schizophrenic patients and matched controls.The patients showed an unusually strong binding effect between actions and consequences. Specifically, the temporal interval between action and consequence appeared shorter for patients than for controls. Patients may overassociate their actions with subsequent events, experiencing their actions as having unusual causal efficacy.Disorders of agency may reflect an underlying abnormality in the experience of voluntary action.

Now, let us pause and recollect that Chris Frith had postulated that the voluntary action mechanism in Scizophrenics is somewhat malformed and specifically there is a disconnect between intention attribution and voluntary action manifestation. He however had not clearly stated that there would be over-attribution of intention to voluntary actions. We all know that dopamine is associated with voluntary action (voluntary movements) and that baseline dopamine is in excess in schizophrenics. This paper ties things in together showing that excess dopamine secretion in basal ganglia and cortical areas may lead to greater biding between intentions and subsequent actions (consequences) and by this mechanism may lead to over-attribution of agency. Of course the paper doe snot establish this mechanism but just speculates on it as one of the possible mechanisms. It is also important to pause and note that schizophrenics have a jumping-to-conclusions bias and thus if an intention and action were more tightly bound (occurred in time in close proximity)_, then they are more likely to judge the two events to be related and the intention to cause the action.

Now let me get to the actual experiment. Haggard et al asked schizophrenics as well as matched controls to note subjective time (using Libets approach) when they decided to voluntarily press a computer key, and also subjective time when they first heard an auditory tone . The tone was presented 250 ms after their voluntary key press. As has been established earlier, and using controls in this experiment, people advance the key press in future (shift it towards future time from the exact time they actually pressed the key) so that subjectively the key press happens after some time form the objective key press and in the direction of the tone presentation. Thus, the effective subjective time between the key press and the tone is reduced. This binding between a voluntary action and its consequence , happens in normal individuals too, but in schizophrenics this happened significantly more in magnitude ans was dependent on two factors. first, like in normals , the voluntary key press was advanced in time towards the tone presentation, but this advance was significantly greater than in the case of controls. Secondly, the subjective auditory tone was sort of anticipated and shifted back in time towards the voluntary key press in schizophrenics. Thus, in schizophrenics, it seemed to them that the auditory tone had occurred prior to when it was actually presented. This lead to overall very significant reduction in subjective time experienced between the voluntary key press and the tone hearing, thus binding the two events strongly and leading to stronger agency inferred. to quantize the things a bit, in normal controls the voluntary key press was on the average occurring 26 ms from the actual key press, the auditory tone was heard 5 ms from the actual presentation and thus the subjective difference between the key press (intention) and tone (consequence) was 250-(26+5)= 239 ms. In schizophrenics, the key press was deemed to occur 60 ms after the actual key press, however most importantly the tone was not heard subjectively after its presentation, but was heard anticipatory 139 ms before its actual presentation, thus the actual perceived subjective time between the key press (intention) and the tone (consequence) was 250-60-139 = 51 ms only. Now , one can easily see, that if perceived subjective time between tow events is shortened in schizophrenia, then wont they end up falsely clubbing many coincidental things too together, because they seem to follow each other in close temporal proximity.

To appreciate the results, one needs to put these results in the broader context of what we know about agency in schizophrenics:

Previous laboratory studies have investigated agency using action attribution tasks. In these tasks, the patient is asked to perform an action, and is shown a visual image corresponding to that action, for example, a line drawn with a pen , a video of a hand making a manual posture , or a computerised image of a joystick moving. By introducing a mismatch between the performed action and the visual feedback, experimenters investigate the accuracy of attribution judgments. The subject has to attribute the viewed image either to an action he has just been instructed to make or to some other source. Interestingly, all these studies have found schizophrenics abnormally willing to attribute to themselves actions which in fact differ from the ones they performed. Thus, they are less sensitive than control subjects to spatial, temporal or kinematic mismatches between actions and visual feedback. The direction of these results points towards an excessive, rather than a reduced, sense of agency. Such results have been interpreted in the context of an internal forward model. Schizophrenic patients’ errors involve mostly over-attribution, implying a forward model with an unusually tolerant comparator.

Impaired judgement of agency can also be linked to the brain abnormalities underlying the disease. Agency involves forming a conscious mental association between one’s own intentional actions, and their consequences in the outside world. Thus, agency may be a conscious aspect of a more general system for instrumental or operant learning about environmental contingencies and rewards. Animal learning studies show that dopaminergic circuits, including the basal ganglia and medial forebrain are essential for associating actions with their effects, and for motivating behaviours. Brain imaging studies in man show that these same areas are active when a voluntary action produces a reward or other salient consequence . Moreover, these dopaminergic circuits are overactive in schizophrenia . Excessive dopaminergic activity might therefore explain abnormalities of conscious agency in schizophrenia, such as over-association between intentions and external events.

This is how they interpret their results:

More importantly, our schizophrenic patients seem to show an exaggerated version of the normal binding effect, or hyperbinding. These results could account for the findings of some action attribution experiments. Franck et al. asked patients and controls to move a joystick and then to observe their movements on a computer screen after a delay. The experimenters systematically varied the delay to investigate at what point the two groups ceased to accept the observed action as their own. Control subjects detected the temporal discrepancy between their action and the image with delays of around 100–150 ms. Schizophrenic subjects were much more tolerant, and accepted the viewed action as their own even for delays of 300 ms. Overall, the detection threshold for the relevant action was increased by about 150–200 ms for the patients compared to the controls. This value can be compared to the 180 ms difference between our patients and controls in the implied perceptual duration of the interval between action and tone.

The direction of the attribution effect is important: schizophrenics over-attributed events to their own agency. Our data suggests that schizophrenic patients have unusually strong associations between conscious representations of action and consequence. Thus, they might bind action and viewed image across the substantial delay periods imposed in the Franck et al. experiment, and be unaware of the artificially-induced lag between these events. There may be a critical period in which to perceive the consequence of an action. Actions and events falling in this period may be perceptually bound. A deficit in setting the duration of this critical period in schizophrenics could contribute to the shifts we found in their subjective temporal experience. This view would interpret abnormal conscious experience in schizophrenia as a problem in predicting the consequences of one’s own actions. Further work could investigate whether temporal analysis in schizophrenic patients is defective only when concerning their own actions, or also when observing actions made by others.

I am thrilled as usual and predict that if the same experimental paradigm is used with Autistic, then they will show very little or no forward movement of subjective time between their actual voluntary key-press and the subjective feel of when they decided to press the key. Also, there would be no anticipatory backwards movement of subjective time for when the tone was heard. Thus, Autistic would perceive the time gap as 250 ms only, or may even perceive the time to be more than 250 ms depending ion whether they move the voluntary key press subjective time back in time. No matter what they should show lesser binding between the intention (if they can form one) and consequence.
Haggard P, Martin F, Taylor-Clarke M, Jeannerod M, Franck N. (2003). Awareness of action in schizophrenia Neuroreport, 14 (7), 1081-1085

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4 thoughts on “Evidence for heightened Agency in Schizophrenia

  1. Anonymous

    Very interesting blog discussing a very subject area. Intuitively, there seems to be some sort of link between ASD and schizophrenia; I think it is reasonably well known that Kanner took the word ‘autism’ straight from the descriptive qualities of a symptom of schizophrenia. Further Autism was, until DSM III (?) a sub-category of schizophrenia (‘childhood type’). It strikes me as ironic that the two disorders should start together, be forcefully separated and then, perhaps, be brought back together in a completely different relationship in DSM V! Obviously no part of what I have just said makes the hypothesis you are putting forward wrong, but both schizophrenia and autism have, in my own opinion had a tendency to be the ‘playthings’ of academic psychology and as such the definition of these diseases have closely mirrored the paradigms of the day. Given the dominance of TOM at the moment, I’m not surprised that it is being utilised to explain these two keynote disorders. As you might’ve guessed, I’m a tad sceptical (not least because I have yet to see any really good evidence of TOM based interventions, which would be fantastic regardless of whether they pinned down the aetiology, as is the case with ABA) but it certainly is interesting and I’ll be watching closely. Thanks for the heads up.


  2. Sandy G

    Hi G,

    Thanks for your honest opinion; I agree that schizophrenia especially has been the plaything of academic psychology; yet I believe, with sincerity, that the juxtaposition of autism and schizophrenia and there acceptance as an extreme on a normal continuum would have significant clinical and academic implications; that said I don’t think my blog would be influential enough to get these characterized as opposed dimensional disorders in DSM V 🙂

  3. Anonymous

    ha ha maybe not. I would be surprised if people didn't go with this however. Baron-Cohen seems to be in the papers about, oh, twice a day discussing TOM and autism so I wouldn't be surprised if he'd pick this up and run with it. Further, it does absolutely stand to reason that if TOM is on a continuum, and if there is a disorder caused by a lack of TOM, that there should be disorder caused by too much TOM. It is an interesting idea for sure and as I say I am interested in it.

    I wonder though, why do you think that autism should have an age of onset <3years maybe from birth, and schizophrenia have an a.o.o around 20? Would this demonstrate that TOM is largely learnt? It would also mean that autism/schizophrenia could never be co-morbid? Interesting, testable questions certainly.


  4. Sandy G

    Hi G,
    yes, part of the answer lies in developmental time frame. ToM and levels/orders of intentionality/ perspective-taking develop in stages as per my view 9stage theories are another passion of mine) and I believe that while ToM related deficits would start becoming visible by age 3; the over development (excessive higher state toM abilities / disruption) of ToM may be visible only by adolescence/ early adulthood. That seems to be the developmental trajectory of autism and schizophrenia ; so seems to support my model partially!!

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