An Optical Illusion and Psychosis

In an earlier posting we talked about the conclusion that the brain/mind creates our perceptions; an important insight that is accepted in western neuroscience and in eastern contemplative traditions.

Here is the link to the previous posting on this blog:
http://comingbacktoreality.blogspot.com/2009/01/constructing-reality.html

Optical illusions are an entertaining way to literally ‘see’ that what we see is not what is actually there. Instead, we tend to impose our preconceptions on the ‘data’ that has been presented to the brain by the sensory neurons and create perceptions that match our past experiences.

A posting on the website “Wired Science” provides an interesting example of such an optical illusion. The context is that in a recent research study people who had a diagnosis of schizophrenia actually were not able to see a particular optical illusion. They saw the visual object as it actually was while the ‘healthy controls’ experienced an optical illusion that fundamentally misinterpreted the actual visual object.

So, this is an interesting twist; people with psychosis see a visual object as it actually is, while people without psychosis are fooled.

The link to the Wired Science blog is as follows:

http://blog.wired.com/wiredscience/2009/04/schizoillusion.html

The optical illusion is demonstrated with a video that is available within the Wired Science blog.

The Dopamine Hypothesis, Version 3

The idea that psychosis involves hyperactivity of dopamine neurons has been generally accepted in psychiatry for nearly fifty years. A new review brings this hypothesis up to date. The authors (Howes and Kapur) incorporate results from a number of new techniques in molecular biology, genetics and brain imaging to define four major points.

Each of the points has interesting implications, some of which have already been mentioned in previous posting on this blog. For example, the first point in the review is that multiple factors, both genetic and environmental, interact, resulting in dopamine dysregulation. This point supports the idea we discussed that each person with psychosis has a unique path of causation and a unique condition. (Click below for the relevant previous posting on this blog).

http://comingbacktoreality.blogspot.com/2009/02/how-does-psychosis-arise-part-2.html

The second point is that the locus of the dopamine dysregulation is presynaptic, involving increased synthesis and tendency to release transmitter. The implication of this point is that current antipsychotic medications (which act postsynaptically) are acting ‘down stream’ from the point of actual dysregulation. Medications that act directly at the site of dysregulation may be preferable.

The third point is that dopamine dysregulation is linked specifically to the dimension ofpositive psychotic symptoms and 'psychosis proneness', regardless ofdiagnosis. This point is consistent with the idea that the current diagnostic system for psychotic disorders should be revised to emphasize symptom dimensions that are viewed as independent, each having its own particular underlying mechanisms. (Click below for the relevant previous posting on this blog).

http://comingbacktoreality.blogspot.com/2009/02/jim-van-os-and-salience-dysregulation.html

The fourth point is that dopamine dysregulation alters the appraisal of stimuli through the process of aberrant salience (stimuli that are not relevance are taken as relevant). This in turn leads to psychosis. This idea is extensively discussed in a previous posting on this blog; click below for that posting.

http://comingbacktoreality.blogspot.com/2009/01/salience-and-psychosis.html

Finally, there is no doubt much more to psychosis than dopamine. Still, the four major points in the updated hypothesis provide a helpful way to clarify issues in understanding psychosis.

Reference: OD Howes and S Kapur; The Dopamine Hypothesis of Schizophrenia:Version III - The Final Common Pathway. Schizophrenia Bulletin, March 2009.