Causality in Psychiatry: A Hybrid Symptom Network Construct Model

Abstract

Causality or etiology in psychiatry is marked by standard biomedical, reductionistic models (symptoms reflect the construct involved) that inform approaches to nosology, or classification, such as in the DSM-5 [Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition; (1)]. However, network approaches to symptom interaction [i.e., symptoms are formative of the construct; e.g., (2), for posttraumatic stress disorder (PTSD)] are being developed that speak to bottom-up processes in mental disorder, in contrast to the typical top-down psychological construct approach. The present article presents a hybrid top-down, bottom-up model of the relationship between symptoms and mental disorder, viewing symptom expression and their causal complex as a reciprocally dynamic system with multiple levels, from lower-order symptoms in interaction to higher-order constructs affecting them. The hybrid model hinges on good understanding of systems theory in which it is embedded, so that the article reviews in depth non-linear dynamical systems theory (NLDST). The article applies the concept of emergent circular causality (3) to symptom development, as well. Conclusions consider that symptoms vary over several dimensions, including: subjectivity; objectivity; conscious motivation effort; and unconscious influences, and the degree to which individual (e.g., meaning) and universal (e.g., causal) processes are involved. The opposition between science and skepticism is a complex one that the article addresses in final comments.

A Complex Network Perspective on Clinical Science

“…In contrast, the complex network perspective acknowledges environmental (and genetic) causes, but as triggers activating individual features of a disorder, which, in turn, activate other elements of the network. Moreover, the arrow of causation may emerge as self-reinforcing, homeostatic loops, such as hypervigilance fostering exaggerated startle responses in trauma survivors which, in turn, maintain their hypervigilance (see McNally et al, 2015). Unlike theoretical diagrams common in 20 th century psychology (e.g., stimulus > organism > response models of neobehaviorism; causal flowcharts of cognitive psychology), the graphs produced by network analysis are empirically derived.…”

Evidence that psychopathology symptom networks have limited replicability.

“…Analyzing broader constructs—such a symptom clusters (e.g., Anker et al, 2017)—versus single symptoms would also be amenable to this approach. Specifically, we would suggest—as others have (Eaton, 2015; Epskamp et al, in press; Markus, 2010; Stapel, 2015; Young, 2015)—that integrating latent variables into network analysis is the best way forward. We echo the suggestions made by Epskamp et al (in press), who recently proposed latent network modeling , in which latent variables are used to extract the most reliable variance from multiple measures of a symptom, and these latent variables subsequently act as the nodes in a network analysis.…”

“…Most importantly, to avoid making misleading conclusions, there is a fundamental assumption that all nodes that may have a causal role are included in the network (i.e., every common cause that two or more variables share; Dawid, 2008; Glymour, 1997). In psychopathology research, it is unfortunately inevitable that there are external factors with direct and indirect effects on the nodes that have not been modelled (Borsboom, Epskamp, Kievit, Cramer & Schmittmann, 2011b; Young, 2015). Ultimately, psychopathology networks do not and cannot illuminate causal relationships among psychopathology symptoms in cross-sectional data.…”

Anxiety disorder symptoms at age 10 predict eating disorder symptoms and diagnoses in adolescence

“…While the majority of research has investigated anxiety and ED comorbidity at a diagnostic level, models of comorbidity in mental illness posit that latent liability may impact symptoms of multiple disorders (Krueger & Markon, ), and that symptoms of disorders themselves (e.g., affective experiences, behaviors) may influence disorder presentation and progression (e.g., the likelihood that a disorder will increase in severity over time or that symptoms of comorbid psychiatric disorders will arise; Young, ). As such, it is pertinent to investigate comorbidity of anxiety and EDs at the symptom level.…”