Western and Contemplative Sciences: a meeting with young neuroscientists

Earlier this week I was delighted, and honored, to sit in on a discussion with a small group of young neuroscientists. The topic was, “is the brain the mind; is the mind the brain?” They had gathered at the request of Dr. Dennis Phillips, a remarkably able and thoughtful professor at Dalhousie University. The conversation was held in a wonderful atmosphere of mutual respect in which all ideas expressed were considered and weighed in the light of existing evidence, theory and experience. There was an open minded, passionate interest in the topic, and all of its ramifications. The discussion roared on for nearly two hours, ending with an agreement to meet again soon, to continue on.

During the conversation I was struck with the parallels, often pointed out by the Dalai Lama, between western science and Buddhist psychology (what I would call contemplative science). Both ‘sciences’ involve gathering information and organizing it into a system of concepts that help us to better understand the nature of the world and of human experience. The goal is to get closer to ‘the truth’, to the way things actually are.

It’s interesting to consider that from this point of view there is no fundamental difference between spiritual (contemplative) and secular (scientific) intent.

Of course there are significant differences in methods. Contemplative science uses introspection (meditation) as the basic tool; individuals sit down and observe their own mind. From those experiences they develop concepts, and further refinements of the meditative techniques. These, in turn, are debated in a scholarly fashion, much like the ‘peer-review’ process in western science. Different ‘schools’ of thought arise and the entire enterprise moves forward, going through sequential ‘paradigm shifts’. (A concise description of this evolution in Buddhist thinking is available in the highly readable book, ‘Contemplating Reality’, by Andy Karr).

The young neuroscientists I met with were skeptical of introspection as a method, noting that it was inherently subjective and not amenable to the kind of ‘double-blind’ design that western science holds as an ideal. They also questioned whether the mind could actually observe itself; an interesting and useful point.

I suggested to them that contemplative science might, nonetheless, have something to offer to the current interest in correlating brain activity with mental experience (mind). It might be helpful, for example, to consider the various aspects or components of ‘mind’ that have been identified in the contemplative tradition as well as the concepts describing the overall structure and operation of mind.

In this regard, one view from contemplative science is that there is an ongoing, open ‘awareness’ that is continuous and that operates without conceptual or ‘dualistic’ thought. From this background of open awareness, suddenly arise the complex of thoughts and emotions with which we are so familiar, all based on a fundamental creation of the sense of self and other. Of particular interest is the view that the arising of thoughts and emotions occurs on a very short time scale, developing and elaborating over the course of perhaps 100 milliseconds and then dissolving back into the underlying open awareness. This arising occurs again and again, and yet again, so that it seems as if the thoughts and emotions are continuous. Yet, from the view of contemplative science, they are short duration, transitory phenomena; waves on the ocean of open awareness.

Is it this non-conceptual, open awareness that very experienced practitioners of meditation are able to access more consistently? Is this way of talking about the organization and function of ‘mind’ helpful in interpreting the current MRI and EEG studies of such practitioners?

It is no surprise that this two hour discussion did not lead to a definitive answer to the original question posed about the relationship of mind and brain. It was evident that there is no easy answer. Buddhist thought includes the concept of reincarnation, of some kind of continuation of mental experience after physical death. Most of the young neuroscientists preferred the idea that “mind is what the brain does”; that the brain produces mental experience. The end of brain function, in that view, is the end of mental experience. Importantly, this is the basis for determining the end of life in medical setting. If a person is ‘brain dead’, there is no further mental experience and the individual is ‘gone’.

Of course it is difficult to scientifically test this fundamental hypothesis; to do a double blind study. For the time being it seems each of us as western scientists or contemplative scientists (or both) will need to hold our own ‘working hypothesis’. Like a good Koan, the question of the relationship of brain and mind remains as a catalyst for sorting through our concepts and experiences and perhaps going beyond them to a more integrated understanding of our own mental experiences, so close at hand and yet so hard to fathom.

Summer time and the living is...hectic

Summer is supposed to be a time to relax. But it seems almost the opposite these days, atleast for me. My attention has been drawn away from this blog by other projects. But psychosis came back into focus yesterday when a friend called to talk about a long time mutual 'sister' who appears to have slipped, over the past year, into a serious psychosis with paranoid delusions and auditory hallucinations (hearing people talking about her).

Our 'sister' has a long history of psychological struggles along with difficulties in relationships. But her current mental state has clearly gone far beyond anything we've seen before.

Helping her has become problematic because she has incorporated her closest support people into her delusional system and now believes they are part of a massive conspiracy against her.

Of course she does not recognize the delusional nature of her beliefs and see no need for professional help. So, how to help her? One possible avenue is that she is involved with some social service agencies. Perhaps by making the professionals in that agency aware of the depths of her mental issues will prompt them to get her to someone who can do a proper assessment and determine if she is psychotic (which appears to be the case) and begin the process of treatment.

This situation is certainly not unique; something like it is playing out in many, many families in the midst of this summer season.

May those who need help receive it.

Response to Dennis

Dennis,

Thanks so much for your interesting comments. I very much appreciate our shared interest and look forward to learning from, and with, you.

Your comment that ‘imposing our preconceptions’ on sensory data should not imply intentionality to do so certainly makes sense to me. Experientially, I seem to be totally unaware of this process. I wouldn’t have a clue as to how to ‘impose my preconceptions’ even if I wanted to. It just seems to happen naturally. I can talk about it intellectually, but experientially it just seems to roll along on its own; which means that I rarely question the validity of my sensory experiences. In the same way, I suppose, most people who have hallucinations, like hearing voices, assume that their experiences are ‘real’.

Your other comment, about Jill Taylor’s experience during a severe stroke, raises the question (among others) of the process by which a sense of separate ‘self’ is generated. Again, this seems to be something that happens without intention, and on a moment to moment basis I, for one, take the result to be ‘real’ without even thinking about it.

Recently there have been a couple of papers from Dr. Patrick McGorry and his Early Psychosis group in Melbourne, suggesting that a disturbance in this sense of self is an early and core aspect of the development of psychosis. Here is their latest abstract:

A disturbed sense of self in the psychosis prodrome: linking phenomenology and neurobiology. Neurosci Biobehav Rev. 2009 Jun;33(6):807-17. Epub 2009 Jan 20.
Nelson B, Fornito A, Harrison BJ, Yücel M, Sass LA, Yung AR, Thompson A, Wood SJ, Pantelis C, McGorry PD .ORYGEN Youth Health Research Centre, Department of Psychiatry, The University of Melbourne, Victoria, Australia. nelsonb@unimelb.edu.au

Interest in the early phase of psychotic disorders has risen dramatically in recent years. Neurobiological investigations have focused specifically on identifying brain changes associated with the onset of psychosis. The link between these neurobiological findings and the complex phenomenology of the early psychosis period is not well understood. In this article, we re-cast some of these observations, primarily from neuroimaging studies, in the context of phenomenological models of "the self" and disturbance thereof in psychotic illness. Specifically, we argue that disturbance of the basic or minimal self ("ipseity"), as articulated in phenomenological literature, may be associated with abnormalities in midline cortical structures as observed in neuroimaging studies of pre-onset and early psychotic patients. These findings are discussed with regards to current ideas on the neural basis of self-referential mental activity, including the notion of a putative "default-mode" of brain function, and its relation to distinguishing between self- and other-generated stimuli. Further empirical work examining the relationship between neurobiological and phenomenological variables may be of value in identifying risk markers for psychosis onset.

On posting comments

It seems that some people are unable to post comments on this blog. If you are in that situation, please feel free to email your comments to me (davidwhitehorn@eastlink.ca) and I will post them for you.

Below are two interesting comments sent to me from Dennis P. I will respond to them in a day or so. Thanks Dennis.

Re: An Optical Illusion and Psychosis (April 21, 2009)
Hello David:

This is a fascinating observation, but I think that we have to be a bit careful in how we interpret it. Saying that we "impose our preconceptions" on the sensory data is cognitively loaded and carries a connotation of intentionality, while the processes at work may not be particularly cognitive at all. Our brains have encountered thousands (millions?) of examples of faces in our experience, including under conditions of degraded sensory input, prior to exposure to the stimulus evoking the illusion. The hollow mask stimulus confronts us with sensory data that are somewhat ambiguous, and most intelligent perceivers (man or machine) would probably default to the interpretation that has been helpful so many times before. I'm reminded of the case of relative motion. When a small object and a large object move relative to each other in the absence of other disambiguating information, the default interpretation is that it is the smaller object which is moving because the perceptual system has encountered that scenario far more often than the alternative. In both the "hollow mask" illusion and relative motion cases, we don't need to postulate that the perceptual system is attempting to "match our past experiences"; rather, the perceptual system uses past experience to provide the most likely interpretation of incoming, impoverished sensory data.

It remains fascinating that schizophrenics may not generally behave this way (at least with regard to the hollow mask illusion), and your point that our past experience influences our present perceptions is well taken. The point I'm trying to make here is that the mechanism through which experience expresses its effect may be much more low-level than the cognitive one that the expression "impose our preconceptions" implies. As I type this, it occurs to me that a low-level account of the hollow mask illusion might speak to the "salience" issue raised in your earlier posts: is the finding with the hollow mask illusion evidence that schizophrenics have an impaired ability to weight the data from the various sources of information (bottom-up, top-down) normally used in perceptual judgements? I hope that this helps. Kind wishes,

DPP


Re: Separating 'this' from 'that' (February 26, 2009)

Hello David:
I wonder how much of this "duality" is a natural consequence of the human gift of language? As soon as we apply the (linguistic) label "chair," everything else becomes "not chair." On the one hand, as you imply, this skill is what makes our interactions with others, and with the world, so workable. On the other hand, the labels create a duality that runs counter to the reality of the interdependence of all things, or "interbeing," to borrow the term from Thich Nhat Hanh. A quite striking case supporting this view is the work of Jill Bolte Taylor (see "My Stroke of Insight"; see also her talk at ted.com), the neuroscientist who suffered a left hemisphere stroke which, among other things, left her temporarily with a severe language impairment. In her book, Taylor describes her perceptions at the time of the accident, which I might in turn describe as "perception stripped of language." In this state, Taylor experienced a loss of boundary between self and other, and something of a dissolution of ego as hard, separate, and permanent; instead, everything, including perceptions, became fluid, with a distinct sense of "flow." This afforded Taylor a quite profound insight. It also rendered her interaction with her world almost unworkable.

Jill Bolte Taylor's retrospective descriptions of her stroke experience use a language (so to speak) that is a little different to that offered by meditation masters trying to teach us about absolute and relative truth. It seemed to me, however, that the descriptions have common themes, and this made me wonder if one of the insights provided by the disciplined meditative practice is to "see" past the language layer that we automatically impose on what would otherwise be more direct perceptions. Perhaps the real gift of being human is the ability to have a heartfelt appreciation of interdependence and impermanence, balanced with a language facility that enables us to communicate effectively with our world.
Thanks for your blog. Kind wishes,
Dennis PP

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.

Treatment (Part 1)

In the conventional medical model, psychotic symptoms lead to dysfunction and, therefore, deserve treatment; interventions intended to reduce the symptoms and their impact on social function.

The recognized standard for treatment of psychosis in most developed countries of the world consists of antipsychotic medications coupled with support from professionals, family and friends and, in some cases, psychotherapy.

Before delving into the details of treatment it is worth asking whether the recognized standard treatment is always necessary and appropriate. There are two lines of logic that support the idea that the current standard treatment is not always necessary and appropriate.

The first logic is that there are a significant number of people who are, by virtue of their ability to function in society, considered ‘healthy’ (in terms of psychiatric conditions) and yet experience psychosis. The most common situation is a person who has auditory hallucinations. A recent study suggests that 10-15% of the general population report having auditory hallucinations (usually hearing a voice), from time to time. There is even an organized group of such people in the Netherlands who strongly believe the voices they hear are of value to them, and an important part of their life and who they are. These people are not at all interested in ‘treatment’.

The second line of logic comes from clinicians who believe that psychosis, even when it is severe enough to cause considerable social dysfunction, will, for at least some people, resolve or improve without medication if the person is in a supportive therapeutic environment.

Published research in recognized scientific journals examining the therapeutic environment approach for first episode psychosis is rare. One model, called ‘Soteria’ was developed in California in the 1970’s. Outcomes after one year were reported to be the same as for a comparator sample of patients receiving the convention care of the time. Unfortunately both groups had relatively poor outcomes by today’s standards. More recently a group in Berne has used a modified Soteria model, allowing some use of medication. (Soteria references: Carlton et al; Schizophr Bull. 2008 Jan;34(1):181-92. and Ciompi and Hoffman, World Psychiatry. 2004 Oct;3(3):140-6).

More recently a group in Finland tried to minimize use of medication in working with first-episode psychosis patients. They provided an intensive, high quality psychosocial intervention to two groups of patients. One of the groups received antipsychotic medication as usual while the other received the minimum medication consistent with ethical clinical practice. They reported that 40% of the patients in the minimal medication group recovered from the episode without ever taking anti-psychotic medication. (Finland references: Lehtinen et al Eur Psychiatry. 2000 Aug;15(5):312-20 and Bola et al J Nerv Ment Dis. 2006 Oct;194(10):732-9)

The overall lack of research makes it difficult to interpret these isolated findings. It has long been appreciated that there is a very wide range in terms of the inherent severity of conditions involving psychosis. It is not unreasonable to think that some young people experiencing a first episode of psychosis might have a relatively mild condition that could resolve without antipsychotic medication. It is likely, as well, that many people have gone through a psychotic episode and returned to social functionality without ever coming to the attention of the health care system.

There are two practical problems to keep in mind. First, very few, if any clinical services have the resources and expertise to provide intensive, high quality therapeutic environment based support of the kind provided in the Finland study. The second is that, with current knowledge, we cannot determine with sufficient accuracy, at the time of the psychosis emerges, whether an individual has a relatively mild, or relatively severe condition. In a future blog I will talk about some of the research that might help sort that out.

In the meantime, the medical-legal environment in the developed nations (certainly in North America) is such that a psychiatrist who failed to recommend antipsychotic medication to a person with significant psychosis (impacting on their social function) would certainly face malpractice charges.

What this blog is about (revisited)

After a bit more than two months of creating this blog, it seemed useful to remind myself, and any readers who might wander by, about the purpose of the blog. Below is the very first posting, back in January.

"This blog is about psychosis and particularly psychosis as it is experienced by young people. From a psychiatric point of view the term psychosis refers to “a loss of contact with reality”. In psychiatric practice psychosis manifests in one, or all, of three ways; as hallucinations (‘false’ perceptions), as delusions (‘false’ beliefs) and as disorganization.

My interest in psychosis in young people stems most directly from the ten years (1996-2005) when I was Clinical Nurse Specialist and Coordinator of the Nova Scotia Early Psychosis Program. During that time I had the privilege of getting to know hundreds of young people who were experiencing psychosis, and their parents. As I tried to help these young people and their families understand what they were experiencing and how to deal with it, I found myself drawing upon two sources of information from my own background, the neurosciences and the study and practice of Buddhism.

In this blog I will try to bring together information from those two sources (and any others I can find) with the practicalities of clinical care and recovery to accomplish two objectives. The first is to open a door into the complex world of psychosis in young people. The second is to use the concept of psychosis as a focal point for exploring the nature of human mental experience".

I dont' know to what extent the objectives of the blog have been accomplished; it's certainly an ongoing challenge.

The web of delusion: a clinical vignette

Bill (not his real name) had been seeing a psychotherapist for several months. She told him he was delusional and needed to talk to someone (me) in the Early Psychosis Program. He didn’t like the idea, but eventually agreed. He and I met weekly for two months.

Bill told me that he was the focus of a global conspiracy; that his every move and every word were being monitored. When he left home (which he did rarely) he constantly saw doubles of his family and friends. These ‘people’ were clearly part of the conspiracy and had been placed along his route.

He was willing to talk about the idea that he might be delusional, and he said, when I asked, that he did not see me as part of the conspiracy. Nonetheless, on several occasions he noticed doubles in the hallway leading to my office.

I told him about the salience theory of psychosis. He was interested (he had taken a number of psychology courses). I suggested that he could conduct an experiment. Take a small amount of antipsychotic medication (to help improve his ability to discriminate relevant from irrelevant experiences) and see whether the doubles, and other signs of the conspiracy, were reduced. If so, he could conclude that they were not real.

He was not convinced. He felt the conspiracy was so pervasive and cleaver that they would know that he was taking medication and simply stay out of sight for a while, thus leading him to the false conclusion they weren’t real, and leaving him more open to attack. He also speculated that the conspiracy might be trying to get him to start on medication, which would, in some unknown way, play exactly into their plans for his destruction.

In the end he declined medication. We mutually agreed that our conversations, while quite interesting at times, were not leading to anything useful. We parted on good terms.

Separating 'this' from 'that'

My apologies for the length of the previous post (Jim van Os and the Salience Dysregulation Syndrome), I do think his ideas are important. He is talking about a major change in the way psychiatry thinks about diagnosis. What is diagnosis anyway but a process of putting a label on an individual condition?

From a Buddhist point of view, putting labels on phenomena is a very fundamental process that we all carry out, instant to instant, throughout our lives. The process of separating ‘this’ from ‘that’ is the root of dualistic thinking. This includes the basic split of ‘me’ and ‘other’ that creates the sense of separate self, the ego. In the Buddha’s first teachings after his own enlightenment, called the Four Noble Truths (suffering, the root of suffering, the cessation of suffering and the path), he identified the sense of separate self as the fundamental source of human suffering.

The idea that ‘I’ am separate from the rest of the phenomenal world is not accurate, from the view point of Buddhism or Western Science. Both systems of thought agree that all phenomena are interconnected and interdependent. There are no separate, independent entities. When we separate ‘this’ from ‘that’ (‘me’ from ‘other’) we are imposing an inaccurate way of thinking upon the actual nature of phenomena. It is not surprising that by starting with a fundamental flaw in our thinking, we end up in constant struggle with the world as it is. We see it as made up of separate independent entities when it actually isn’t that way

Although it is tempting to hope for our own enlightenment, when we could see beyond dualism, that is not our lot, nor our working ground. We are stuck with the way our mind works. We constantly fall into dualistic thinking. We walk around with a strong sense of ‘me’ being separate from everyone and everything else.

This dualistic way of understanding the world is called, by the Buddhist, ‘relative truth’, which sets it off from ‘absolute truth’, the way things actually are. (Of course ‘relative and absolute truth’ are dualistic constructs and so have no inherent existence in reality). In the cognitive world of relative truth it is possible to establish reference points from which judgments can be made, for example, as to how useful or helpful one or another concept (dualistic construct) may be for accomplishing a particular purpose.

In relative truth the idea of diagnosis makes sense. At its best, a diagnostic label can provide useful information to accomplish the goal of reducing suffering. It will still be relative truth (and therefore fundamentally inaccurate), but it can be helpful. (In physics it is agreed that Newtonian physics is highly simplified and inaccurate, but it is very useful in calculating the motion of planets and spaceships).

So a good diagnostic system (set of dualistic constructs) needs to be useful. It should help the person who is being diagnosed to understand what is happening to them and a diagnosis should guide the person and the health care professionals in determining how best to work with the situation.

What I like about the diagnostic system that van Os proposes is that it stays close to simply describing the phenomena (by rating each dimension). As well, by using the construct of a ‘syndrome’, it emphasizes that we are not talking about ‘diseases’ that have some self-existing reality, but we are simply talking about the clustering of phenomena.

Jim van Os and the ‘salience dysregulation syndrome’.

Jim van Os has long been one of my very favorite people in the world of psychosis. He is a professor of psychiatry at Maastricht, Netherlands and one of the truly innovative thinkers in the field.

Yesterday I came upon an editorial that he published this month (February 2009) in the British Journal of Psychiatry. In this concisely organized three-page article, van Os proposes a new diagnostic system for psychosis.

First he reminds the reader about the lack of validity of the current system, which is based on the construct of a disorder called ‘schizophrenia’. He reviews the evidence that this construct, on the one hand, lumps together people with widely different conditions and, on the other, separates people who have commonalities in terms of genetic and brain characteristics.

To replace the current diagnoses that are applied to people with psychosis, van Os proposed that everyone with psychosis (or sufficient severity to require psychiatric attention) be described as having a ‘salience dysregulation syndrome’. We have talked about salience in a previous posting of this blog. By adopting salience as a central construct van Os is using Kapur’s model in which psychosis (hallucinations and delusions) arise because the person has difficulty determining which of their mental experiences are relevant (and therefore need to be attended to and incorporated) and which are not. In Kapur’s model psychosis arises from an over inclusion of perceptions and experiences.

It is significant that van Os calls his construct a ‘syndrome’, rather than a ‘disorder’. He explains that a syndrome describes a set of signs and symptoms that tend to occur together but do not have a common cause (which would be the case for a true disorder).

A key point, as well, is that people with psychosis tend to experience other symptoms or have other characteristics. The hallucinations and delusions are, in fact, technically termed as ‘positive psychotic symptoms’ (positive meaning a symptom that is added to the usual human experience) to distinguish them from ‘negative symptoms’ (for example, an inability to experience pleasure or a lack of motivation). Disorganization tends to be present with psychosis and is included by some as a positive symptom, or seen as a separate dimension by others. As well, people with psychosis tend to have cognitive deficits in certain aspects of attention, memory and problem solving that appear to be present as part of development prior to the onset of psychosis. Depressive symptoms and manic symptoms also tend to co-occur with psychosis.

Using these six dimensions (positive symptoms, negative symptoms, disorganization, developmental cognitive deficits, depressive symptoms and manic symptoms), van Os constructs a diagram in which the severity of each symptom or deficit is rated for each individual person with psychosis. The ratings in all six dimensions provide a unique representation of the individual condition of each person.
The individual six dimension ratings provide, in the diagnostic system proposed by van Os, a way to divide the syndrome into three sub-categories.

The first category (salience dysregulation syndrome with developmental cognitive deficits) is used for people who have relative severe development cognitive deficits along with more severe negative symptoms and disorganization.

The second category (salience dysregulation syndrome with affective expression) is used for people who have relatively severe depressive and/or manic symptoms.

The third category (salience dysregulation syndrome ‘not otherwise specified’) is used for people who have relative severe positive psychotic symptoms and/or disorganization and relatively little in the way of cognitive deficits, negative symptoms or mood symptoms.

This new diagnostic system, that van Os is proposing, would encompass people who currently receive a diagnosis of schizophrenia or other ‘schizophrenia spectrum disorders’ and, as well, many who receive a diagnosis of bipolar disorder.

Whether this diagnostic proposal will ever be accepted and put into use in psychiatry certainly is not clear. It is timely in that both of the major diagnostic systems currently in use (DSM and ICD) are in the process of being revised. Dr. Van Os is, in fact, a member of the task force examining possible revisions to the DSM system in regard to psychosis.

However, there is a great deal of resistance to any major change in the diagnostic system for psychosis and the idea of putting aside the construct of schizophrenia, that has been so important to psychiatry for 100 years, is probably much too radical to be accepted.

Most people in psychiatry cling to the view that schizophrenia is a real disorder and forget that it is simply a construct used to try and bring order to the great range of mental conditions that include, as one of their features, the experience of psychosis.

Reference: Jim van Os (2009). A salience dysregulation syndrome. British Journal of Psychiatry 194, 101-103.

How does psychosis arise (part 2)

In discussing explanatory models for how psychosis arises a key issue, in my view, is that psychosis is not one ‘thing’. Everyone who experiences psychosis does not have the same condition. I would suggest, to the contrary, that each person who experiences psychosis is different and unique. The experiences are different and the evolving causes and conditions are different. Therefore, the explanations will be different.

If you accept the view of individual uniqueness then the kind of explanatory model(s) we are looking for are going to be quite general in nature. They will identify the kinds of causes and conditions that could lead to psychosis. There will be multiple factors that could interact with one another in a variety of ways. Only rarely, if ever, will the models explain what happened to a particular individual.

Perhaps the closest to a simple explanation would be for psychosis that is associated with a particular genetic variant, the 22q11.2 deletion. People who have this relatively rare genetic condition (1 in 2000) have, to varying degrees, a number of abnormalities in development, including the heart, the structure of palate and general intelligence. They also have a high rate of psychosis (as high as 30% compared with 3% in the general population).

In 22q11.2 deletion, a small number of genes on chromosome 22 are missing. One is the COMT gene that guides production of the enzyme COMT, a key enzyme in regulating dopamine metabolism in the brain.

So if we find someone with this genetic condition, and they become psychotic, our explanation would certainly include the gene deletion. But why is it that only 30% of people with the deletion develop psychosis. Why not 100%?

Clearly, when we are talking about causes and conditions leading to psychosis, the story is complex. As well, the 22q11.2 deletion syndrome accounts for a minute percentage of all cases of psychosis. In the other cases the genetics appears to be even more complex.

Years of trying to find ‘the gene for schizophrenia (or psychosis)’ has resulted in identification of a large number of genes that seem to be very weakly associated with psychosis. Researchers have come to call them ‘susceptibility genes’ to emphasize that alterations in any one of these genes cannot, alone, explain psychosis. Instead, the idea is that each gene provides some increased susceptibility, and that a person with a combination of a number of these genes (under particular conditions) becomes highly likely to experience psychosis.

This supports the view of individual uniqueness; each person with psychosis will have a different set of susceptibility genes and encounter different conditions in which those genes are expressed.

Are we getting anywhere in terms of explanatory models? Is recognizing individuality and complexity useful?

How does psychosis arise (part 1)

I want to get back to Basia’s question: why do people become psychotic? The honest answer is, ‘no one knows’, or as my father (who was a physician-scientist) used to say, ‘if I knew the answer to that I would win the Nobel Prize’. But there are certainly a number of useful ways to think about how psychosis arises.

It’s interesting that western science (including neuroscience) and the contemplative sciences (like Buddhism) share the view that events and conditions arise as a result of previous events and conditions. It’s called cause and effect. So the answer to why or how something happened involves identifying a set of factors that interacted over time.

Western and Eastern thought also agree that cause and effect is very complex; a web of constantly changing, interacting phenomena. Multi-factorial interactions are the name of the game for any explanatory model.

A prime example is the ‘Stress-Vulnerability’ model that is commonly used in psychiatry and neuroscience (and in western medicine in general). The idea is that each person has some particular degree of vulnerability to develop (in this case) psychosis. Some people are very vulnerable. Others have a very low vulnerability. The key point is that there is an interaction between whatever vulnerability there is and the degree of stress that they have encountered over time (including the present). High vulnerability and high stress makes it very likely that psychosis will manifest, much more so than if there is, for example, high vulnerability and low stress.

In the Stress-Vulnerability model, stress refers to any environmental factor (psychosocial, physical or chemical). So this model is basically pointing out the interaction of ‘nature’ (biological vulnerability) and ‘nurture’ (environmental exposure),

I found the model is useful in clinical practice. We worked with a young man who smoked a lot of marijuana (for months) and became psychotic. We showed him research data indicating that using marijuana increases a person’s risk of psychosis. His questions was, “I have three friends who smoked even more than me, but they didn’t become psychotic; how come”? Our answer was, ‘because you are more vulnerable to the chemical stress that marijuana represents”.

He wasn’t convinced, of course, but he did ask the obvious next question; ‘why am I more vulnerable’? Good question; perhaps we should rephrase Basia’s question to be: why do some people become psychotic and others don’t? I’ll take a shot at that in ‘part 2’ (stay tuned).

On the nature of explanations

My friend Basia stopped by this morning. She had read the posting on ‘salience’ on this blog and asked for an explanation as to why a person experiencing psychosis has difficulty determining salience. Thinking about her question led me into this digression about the process of developing explanations.

It’s interesting that we humans seem to have such a strong need to have explanations. After all, what is an explanation other than a set of concepts that appear to make sense out of some observations and experiences we have had, (the same process, by the way, that, according to salience model, leads to delusions).

If explanations are concepts, it’s worth thinking about concepts for a moment. The cognitive neurosciences view our mental world as being made up of a complex framework of interconnected concepts that are, of course, our own creation.

Contemplative science agrees but adds the insight that concepts are inherently dualistic. For example, ‘psychosis’ is a concept. By creating ‘psychosis’, we automatically create ‘non-psychosis’. Concepts separate off ‘entities’, defined sections of phenomena, from what is actually an interconnected web.

The contemplative sciences emphasize the difference between the kinds of ‘truth’ (explanation) we can discover with concepts (relative truth) and the actual ‘truth’ of how the world functions (absolute truth). The latter is beyond concept.

Relative truth, the use of concepts, is seen as useful, but it becomes problematic when we mistake relative truth for absolute, which we do all the time. We forget that we ‘made up’ the concepts and we believe that they are inherently ‘real’.

A final thought for this digression: perhaps we don’t always need a firm (and certainly not a fixed) explanation for everything. As the old saying goes “it’s not what you don’t know that hurts you, it’s what you think you know that ain’t so”.

Salience and psychosis

Dr. Shitij Kapur is a psychiatrist-neuroscientist at the University of Toronto. He is articulate and creative. Among a number of contributions to a better understanding of psychosis, he has recently proposed a model of psychosis that focuses on the concept of ‘salience’.

Salience, in this model, is defined as a determination, by the brain, as to the relevance, to the person (organism), of any mental experience. Some mental experiences are significant, others are not. The latter can be ignored.

Experiences that are salient, on the other hand, are added to our conceptual framework, our understanding of the world, our beliefs about what is happening.

The heart of Kapur’s model is the idea that psychosis arises from a relative inability of the brain to determine salience. The brain can’t tell the differences between relevant and irrelevant information. There are obvious implications of this inability on the resulting conceptual frameworks, our belief systems.

Let’s look at a simple example. Walking down the street I notice a man sitting in a car, smoking a cigarette. A moment later a woman walks past the car, stops and answers a call on her cell phone. I think nothing of it; no salience to me.

But suppose I couldn’t tell if those two events were salient or not and I assumed, therefore, that they might be. This could start me off a train of thought and speculation. To begin, if these experiences are salient, there must be some reason, related to me, that the man is in the car as I walk by. Was he there to watch me? Was it the man in the car who called the woman? If so, are they working together to spy on me? As you can see, I am well on my way to paranoid delusional system, a belief system that is based on fundamentally flawed ‘evidence’; evidence that is flawed because I am unable to determine salience.

It is interesting that Kapur’s model proposes that psychotic experiences, delusion beliefs in this case, are actually formed in exactly the same way as non-psychotic beliefs. The only difference is that delusions incorporate experiences (information) that are not actually relevant (salient).

One clinical implication is that the person who has formed the delusional belief is as sure that it is true as they are about any non-psychotic belief they hold. Why shouldn’t they be; the belief was formed through the same process.

Psychosis as an extreme state

‘The mind of a person who is psychotic works exactly the same way as the mind of anyone else. The difference is a matter of intensity and duration’.

This assertion, paraphrased from an unpublished presentation in 1985 by Dr. Antonio Wood, a psychiatrist and Buddhist practitioner, points to what I would suggests is a key concept: psychosis does not involve a fundamental change in the way mind operates. Instead, psychosis represents an intensification and extension of experiences that are common to all human beings.

Dr. Wood’s logic begins by pointing out the basic sanity of mind, a state of ‘basic healthiness’ that is, from a Buddhist point of view, the inherent state of mind. Insanity, then, is any departure from basic sanity.

On a moment-to-moment basis all of us (who take the time to notice) frequently and repeatedly lose track of basic sanity, of being present, and drift off into thoughts and emotions of the past or the future. Dr. Wood terms those moments in which we are not fully present as ‘temporary insanity’.

While ‘temporary insanity’ comes and goes, more intensive and long lasting loss of basic sanity occurs in relation to particular areas of our life. These are the life situations and issues that ‘push our buttons’. Our neuroses, the habitual patterns that we experience in these situations, involve a disconnection from what is actually happening around us. Dr. Wood calls this ‘permanent partial insanity’.

Finally, Dr. Wood describes clinical psychosis as ‘extreme neurosis’. In psychosis the loss of connection with basic sanity is more frequent and pervasive. How frequent and how pervasive will differ for each individual.

So, from this point of view, people who experience psychosis are not aliens from another mental planet. They are ordinary human beings who are experiencing an extreme version of what we all experience every moment of every day.

Note: My apologies to Dr. Wood. I have taken his unpublished ideas and presented them in a way that makes sense, and seems helpful, to me (without consulting him). He is certainly not responsible for my misunderstandings.

How is psychosis a problem?

Steve, a university student, begins smelling an intense obnoxious odor emanating from his own body. Despite frequent showers and application of deodorants, the smell persists. Embarrassed, he stops going to classes and is forced to drop out of school.

Marion works in a flower shop to support herself while taking art school classes. She has recently received a raise in pay but over hears, on repeated occasions, her supervisor telling other employees that she is going to be fired. Confused and upset, Marion has difficult sleeping and begins to call in sick to work.

Barry, a young businessman, hears God saying “you can not be harmed, I will protect you”. Not sure if he can believe what God has said, Barry drives his car off a highway at high speed. The car rolls over three times and sustains serious damage. Barry is not hurt.

James becomes convinced over a period of nearly a year that a terrorist organization is stalking him. One day on the street he hears a passerby say “it’s time to grab him”. Convinced that the terrorist are about to abduct and torture him he decides to take control of his fate. He goes to a nearby bridge and jumps. Landing on rocks below, James is paralyzed from the waist down.

Shelia believes that her thoughts cause major world events. On the morning of September 11, 2001 she turns on the TV. Seeing the collapse of the twin towers she is overwhelmed with guilt. Going to the garage, Shelia finds a rope and hangs herself from a rafter.

Note: These five vignettes are based on actual experiences but have been somewhat altered to protect confidentiality.

Constructing Reality

In psychiatry, psychosis is defined as a loss of contact with reality. Perhaps the most obvious interpretation of this definition would be that there is some kind of objective reality ‘out there’ that most of us (‘normal’ people) are in contact with. However, in this post-modern world it is probably no surprise if I suggest that, instead of there being an objective reality, each of us constructs our own experience of what is ‘real’.

The view that there is no objective reality is strongly supported by the neurosciences and what we could call the contemplative sciences, the latter representing the concepts and methods that have arisen during the 2500 year history of introspective observation and scholarly debates by practitioners of Buddhist (and related) meditation.

The neurosciences, using experimental and clinical observations, have demonstrated that perceptual experiences (seeing, hearing, etc) are constructed. Unlike a camera that reproduces a scene, the sensory systems of the brain sample information about the world around us, code it in neural activity, carry out analysis of key features and then construct (and project) a perceptual experience. What we hear, see and feel is a constructed simulation.

In regard to our belief systems, the cognitive neurosciences have explored how we put together concepts and information to create conceptual frameworks that we call our beliefs. From the point of view of contemplative sciences all concepts, indeed all experiences of the phenomenal world, are insubstantial and have no ‘reality’; no independent essence.

Going further, the contemplative sciences have concluded that all mental experiences are created by mind. Our moment-to-moment mental experiences are viewed as being dominated by “primitive beliefs about reality” and are described as being like a dream that we have while awake.

Given these conclusion from western and eastern traditions, perhaps it would be helpful to define psychosis not as a loss of contact with reality, but as an alteration in the way the experience of reality is constructed.

What this blog is about.

This blog is about psychosis and particularly psychosis as it is experienced by young people. From a psychiatric point of view the term psychosis refers to “a loss of contact with reality”. In psychiatric practice psychosis manifests in one, or all, of three ways; as hallucinations (‘false’ perceptions), as delusions (‘false’ beliefs) and as disorganization.

My interest in psychosis in young people stems most directly from the ten years (1996-2005) when I was Clinical Nurse Specialist and Coordinator of the Nova Scotia Early Psychosis Program. During that time I had the privilege of getting to know hundreds of young people who were experiencing psychosis, and their parents.

As I tried to help these young people and their families understand what they were experiencing and how to deal with it, I found myself drawing upon two sources of information from my own background, the neurosciences and the study and practice of Buddhism.

In this blog I will try to bring together information from those two sources (and any others I can find) with the practicalities of clinical care and recovery to accomplish two objectives. The first is to open a door into the complex world of psychosis in young people. The second is to use the concept of psychosis as a focal point for exploring the nature of human mental experience.