The nature of discontent with the way we classify mental illness.
The following are remarks I made on a friend's post that concerned the recent announcement by the NIMH that it was going to encourage moving away from use of DSM criteria in research. I had posted on my Facebook page a news item about that decision.

The discussion, while it was philosophical and perhaps too scientifically oriented, it was interesting and I thought might be of interest to some of the fans of this page

I have long been a very harsh critic of the DSM approach to nosology. I am actually quite pleased that NIMH is promoting a move away from it. There are numerous problems with the current system, and the syndromal approach that is in current use lacks the necessary neurobiological markers to support it. I whole-heartedly believe that the mind is a product of brain activity, and as a neuroscientist I find it incomprehensible how we tend to parsimoniously categorize into disorders phenomena that are in most cases (and in all likelihood all cases) manifestations of variation in activity and functioning that fall on continua between extremes. It defies logic in my view to assume that the most complex structure known to us (the human brain) will decide to have its dysfunction fall into neat categories that simplicity-hungry classifiers seek. This is, by now, not at all a controversial position, and many highly respected "brains" in the field have concluded this.

However, it is an equally grave mistake to replace one form of artificial simplification of complexity with another. And that is what we often do when we, in the process of trying to deal with ambiguous and complex subjective experiences, reduce observations to physiological paradigms. While every subjective experience should potentially be traceable to biological activity, we are completely incapable, at present, to reduce subjective experiences to a discrete number of component biological activities. Even if we were able to do so at a cross-section in time, the almost infinite ways in which one "combined" subjective outcome could be generated, determined by genetic endowment, epigenetic modifications, the unique narrative history of environmental (both behavioural and biochemical) interactions with that molecular biology over the developmental trajectories of the individual in question, and the uniquely individualized and highly interactive "meanings" of all such subjective experiences (both expressed in, and secondarily interacting with the underlying molecular biology), essentially makes every clinical case (and every non-clinical one too) a completely unique example of how the brain could work. This is entirely consistent with the fact that we are dealing with the most complex structure we know. It is, in other words, much more complex than our capacity to study it. This is also why the psychoanalytic approach to psychopathology, while it often pays little attention to underlying biology, is quite possibly the most logical approach to mental dysfunction when biological/somatic treatment is not necessary or inadequate on its own. A uniquely individualized and custom-tailored approach is the way to go.

This would seam to lend credence to the symptom-based approach in which pharmocological/somatic treatments are custom-designed based on the constellation of symptoms and signs presented. As someone who does precisely that kind of work everyday, and have been for many years, I can tell you right away that it is the better approach, but that it is also inadequate.

What we can easily miss when we use that approach is the "Gestalt" of the subjective experience of the individual. This is a case of the whole being greater than the sum of its parts. The overall meaning of the subjective experience is indisputably important and, just as in all subjective experiences, result from and interact with underlying biology. Capturing it requires more than simply individualizing the approach to clinical symptoms. It requires more than the in-depth perspective a psychodynamic clinician would take and more than the symptom-focussed approach of a neuropsychiatrist. It requires a readiness and ability to utilize a"birds-eye-view" of the whole situation presenting itself to the clinician. And that is exceedingly difficult to do! To use this "whole-picture" approach, one must make use of the observed similarities between experiences of people, because without that mental tool, one would easily be overwhelmed with all the sources of individuality in the patient's experience. Such a "whole-picture" approach, along with the false medical notions of how Ockham's razor applies to human experience, is what has always driven the hunger to identify syndromes, then generalize them to populations and develop a set of epidemiological figures that, in turn, determine the nature and process of delivery of care. 

There is no doubt, for example, that there is no such thing as "autism" at a molecular biological level. Every child with "autism" is uniquely different from the other. We know of more than 250 genetic pathways that could lead to the manifestations of autism, and those explain less than 25% of cases identified with the syndrome. There are numerous ways in which the clever neuropsychiatrist can tailor-make a set of interventions to meet the specific needs of a specific patient that meets criteria for autism. The problem is that there are very real shared elements of the pathology, its impact on others and on the community and its relevance to educational and social services that necessitate the existence of an identifiable syndrome in order to be able to deliver services in an efficient manner that meets the needs of most individuals meeting the criteria of the syndrome. There is a need that results from that process in devising interventions that can be empirically demonstrated to be effective. However, just as the practical and pragmatic needs for syndromal classification can lead to determination of how care is provided, it interacts with human subjectivity: We progressively start to believe that the syndrome is real. This reification of phenomenological syndromes is another chapter in the narrative history of each individual with the syndrome with enormous practical as well as subjective (meaning) implications and consequences. Is that what we want? I don't know, but it is very difficult to see how efficient care could be delivered without "creating" these syndromes.

We create them and we think at the time that we are simply being empirical scientists that observe and report observations. Well, these reported observations present a reification of syndromes that do not necessarily represent really discrete pathologies, but then result in changing what we are observing, and modifying how we research what we observe and how we treat it and what we say to sufferers and what sufferers make of it and the meanings and implications of it all on the life of each one of them. It is impossible to extricate oneself from this complex interactive process. We are changing everything we study, observe or classify simply by studying, observing and classifying them.

It would seem on the surface that it would be better if we didn't engage in syndromal classification at all. It would seem that we could ultimately diagnose based on a biological marker or a set of markers. That is too simplistic and a delusionally optimistic perspective. It would seem to others that a syndromal classification is all we can do and all we need to do. That would be an incredibly foolish decision to go down a path of regularly exercising our observational skills to reclassify what we have already classified and thought of in scientific terms, which is a way of saying "we used to think we were scientifically accurate, but we definitely think that we are now... trust us!". 

The vast majority of so-called science we produce based on the syndromal approach is so highly suspect and of such poor quality and genralizabilty that it is either rendered largely useless or results in circular arguments that restrict the expansion of knowledge. For example, we coincidentally find that a dopamine blocker reduces some symptoms of psychosis, we conclude that psychosis is caused by dopaminergic dysfunction, we create a dopamine theory of schizophrenia and generate a series of medications based on that theory, we design trials that will prove the original observation of a dopamine-blocker resulting in improvement, then that reifies the dopamine theory in the minds of scientists who then go on to spend decades doing nothing significant to expand our understanding of psychosis. It is sad how we delude ourselves.

The alternative, a purely molecular approach that tries to start from the bottom up, runs into the devastating problem that a final subjective outcome can have, in many cases, infinite pathways and are influenced by infinite factors playing roles at different time-points during brain development. Those scientists are often all too eager to adopt a reductionistic approach that simplifies the problem in a rather sensational manner. All of a sudden, figuring out the details of one of the hundreds of molecular consequences of having the genetics of Fragile-X syndrome "has the potential to cure autism". We do end up producing much more reliable science, but we are still unable to put the different pieces together to solve an impossibly complex puzzle.

In other words, I believe that there are both merits and major deficiencies in both positions. Given that the "syndrome camp" is somewhat dominant, I find myself leaning toward and advocating for the alternative approach. But we have to realize that we are in no way truly addressing the complicated problems we are facing. We are simply trying to find useful ways that make us believe we are helpful clinicians, and make patients feel that their lives have better quality as a result of our work. Ultimately, it is the fact that we have those "subjective" motives that matters. 
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