Nina S. de Boer

In this paper, we explore the conceptual problems arising when using network analysis in person- centered care (PCC) in psychiatry. Personalized network models are potentially helpful tools for PCC, but we argue that using them in psychiatric practice raises boundary problems, i.e., problems in demarcating what should and should not be included in the model, which may limit their ability to provide clinically-relevant knowledge. Models can have explanatory and representational boundaries, among others. We argue that we can make more explicit what kind of questions personalized network models can address in PCC, given their representational and explanatory boundaries, using perspectival reasoning.

Borsboom and colleagues have recently proposed a “network theory” of psychiatric disorders that conceptualizes psychiatric disorders as relatively stable networks of causally interacting symptoms. They have also claimed that the network theory should include non-symptom variables such as environmental factors. How are environmental factors incorporated in the network theory, and what kind of explanations of psychiatric disorders can such an “extended” network theory provide? The aim of this article is to critically examine what explanatory strategies the network theory that includes both symptoms and environmental factors can accommodate. We first analyze how proponents of the network theory conceptualize the relations between symptoms and between symptoms and environmental factors. Their claims suggest that the network theory could provide insight into the causal mechanisms underlying psychiatric disorders. We assess these claims in light of network analysis, Woodward’s interventionist theory, and mechanistic explanation, and show that they can only be satisfied with additional assumptions and requirements. Then, we examine their claim that network characteristics may explain the dynamics of psychiatric disorders by means of a topological explanatory strategy. We argue that the network theory could accommodate topological explanations of symptom networks, but we also point out that this poses some difficulties. Finally, we suggest that a multilayer network account of psychiatric disorders might allow for the integration of symptoms and non-symptom factors related to psychiatric disorders and could accommodate both causal/mechanistic and topological explanations.