Abstract
Much research in the philosophy of psychiatry has been devoted to the characterization of the normal and the pathological. In this article, we identify and deconstruct two postulates that have held sway in the philosophy of psychiatry. The first postulate concerns the belief that clinicians would benefit from conceiving of psychiatric disorders as stable entities with clear boundaries. By relying on a symptom-based approach, we support a conception of psychiatric disorders whose symptoms are the products of many activated mechanisms in mutual interactions. The second postulate concerns the way in which the philosophy of psychiatry has approached the question of harm. We posit that clinicians perceive harms primarily through networks of clinical manifestations. The identification and deconstruction of these two postulates leads us to propose a practical definition of a psychiatric disorder that is useful for the clinician, while adopting a principle of prudential conservatism that does not exclude other theoretical definitions of psychiatric disorder that are useful as an epistemic hub. Thus, we propose the following definition of a psychiatric disorder that is relevant to clinical practice: “a set of clinical manifestations belonging to the prototypical central core of psychiatry, organized in a causal network, involving at least one harm, and whose set of harms exceeds the traditional threshold of significance for a given psychiatric disorder, directly related to an activated mechanism. Such a network composed of clinical manifestations is frozen in a state that is unable to allow the deactivation of these manifestations spontaneously without a therapeutic intervention”.
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Notes
This would not preclude the existence of an underlying physiological cause, but at least it supposes the possibility of a “spectrum of essentiality” (Hitchcock et al., 2021) in which a cause could be identified for some disorders such as schizophrenia, while in others such as depression, it is the interaction of symptoms that is more relevant in naming the disorder.
However, we do not retain the definition of dysfunctional mechanisms of (Moghaddam-Taaheri, 2011) or (Darden, 2008). Of course, any dysfunction can account for a clinical manifestation. In this case, the mechanism would be based on a concept of role-function according to the account of Cummins (Cummins, 1975), which conceptualizes “functions as causal contributions of a component part to a capacity of a larger system”, or according to a “contextual system” as posited by Craver (Craver, 2001). However, we criticize this ‘broken-normal’ view and do not retain the notion of “failing function” (Nervi, 2010) owing to the lack of necessary and sufficient criteria (Krueger, 2015). We prefer to consider the potential robustness of a mechanism (see fourth part).
This example reinforces the idea of using a symptom-based approach, while debate in the philosophy of psychiatry is complicated by the analysis of the category of autism (diagnostic kind) in its entirety.
The weighting depends on the importance within the network. It refers especially to centrality and can be statistically and computationally measurable—there are more than 70 methods for compute centrality in complex networks.
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Acknowledgements
I am grateful to the three anonymous referees for helpful comments and discussion. I also warmly thank Prof. Elodie Giroux and Prof. Denis Forest for their inspiration, Prof. Jean-Arthur Micoulaud-Franchi for his wise advice, and Dr. Anne-Marie Gagné-Julien for her trust and support.
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Gauld, C. From psychiatric kinds to harmful symptoms. Synthese 200, 440 (2022). https://doi.org/10.1007/s11229-022-03922-5
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DOI: https://doi.org/10.1007/s11229-022-03922-5