Stress and Alterations in the Pain Matrix: A Biopsychosocial Perspective on Back Pain and Its Prevention and Treatment

Abstract

The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts.

Keywords: allostatic load; back pain; chronic pain; exercise; neuroplasticity; pain matrix; physical activity; relaxation; stress.

Figure 1

Overview of the complex and multidimensional changes in the central (red area) and peripheral nervous system (PNS, blue area) in patients with chronic pain. ↑ increased, ↓ decreased, ∆ change, + positive relation. Abbreviations: ACTH = adrenocorticotropic hormone, DHEA = dehydroepiandrosterone, GABA = γ-aminobutyric acid, MBSR = mindfulness-based stress reduction, PAG = periaqueductal grey, PFC = prefrontal cortex, TNF = tumor necrosis factor. The content of the picture is not exhaustive, but serves to demonstrate the complexity of chronic pain by listing relevant consequences, cofactors, and epiphenomena. Brain regions displayed on MNI template.