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.
Thursday, February 26, 2009
Monday, February 23, 2009
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.
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.
Friday, February 20, 2009
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?
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?
Saturday, February 7, 2009
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).
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).
Monday, February 2, 2009
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”.
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”.
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