Allostatic Self-Efficacy: A Metacognitive Theory of Dyshomeostasis-Induced Fatigue and Depression

Frontiers in Human Neuroscience

Klaas Enno Stephan¹  Marc Tittgemeyer¹  Zina Mary Manjaly²  Stephen M Fleming³  Christoph Daniel Mathys³  TIm Gard⁴  Anil K Seth⁵  Helene Haker⁶  Saee Paliwal⁶  Frederike Hermi Petzschner⁶  Lilian A.E. Weber⁶ 

[1] Max Planck Institute for Metabolism Research;Schulthess Clinic;University College London;University Hospital Zurich;University of Sussex;Unviersity of Zurich and ETH Zurich;

关键词: Allostasis;    Homeostasis;    Inflammation;    Multiple Sclerosis;    predictive coding;    effective connectivity;   

DOI  :  10.3389/fnhum.2016.00550

来源: DOAJ

【 摘 要 】

This paper outlines a hierarchical Bayesian framework for interoception, homeostatic/allostatic control, and meta-cognition that connects fatigue and depression to the experience of chronic dyshomeostasis. Specifically, viewing interoception as the inversion of a generative model of viscerosensory inputs allows for a formal definition of dyshomeostasis (as chronically enhanced surprise about bodily signals, or, equivalently, low evidence for the brain’s model of bodily states) and allostasis (as a change in prior beliefs or predictions which define setpoints for homeostatic reflex arcs). Critically, we propose that the performance of interoceptive-allostatic circuitry is monitored by a metacognitive layer that updates beliefs about the brain’s capacity to successfully regulate bodily states (allostatic self-efficacy). In this framework, fatigue and depression can be understood as sequential responses to the interoceptive experience of dyshomeostasis and the ensuing metacognitive diagnosis of low allostatic self-efficacy. While fatigue might represent an early response with adaptive value (cf. sickness behaviour), the experience of chronic dyshomeostasis may trigger a generalised belief of low self-efficacy and lack of control (cf. learned helplessness), resulting in depression.This perspective implies alternative pathophysiological mechanisms that are reflected by differential abnormalities in the effective connectivity of circuits for interoception and allostasis. We discuss suitably extended models of effective connectivity that could distinguish these connectivity patterns in individual patients and may help inform differential diagnosis of fatigue in the future.

【 授权许可】

Unknown