The SYMBIOME Project: An Exploratory Investigation of the Biological, Psychological, and Social Mechanisms that Contribute to the Transition from Acute to Chronic Musculoskeletal Pain

Abstract

This dissertation presents the initial findings of the SYMBIOME project; which attempts to combine the objective and subjective aspects of musculoskeletal pain to develop a prognostic clinical phenotype. Chapter 2 presents a moderator analysis of functional outcomes (pain interference and pain severity). Psychosocial moderators can affect the relationship between biomarkers and pain. For pain severity, TNF-α, TGF-β1, and CRP were moderated by employment status, pre-existing psychopathology, and sex. For pain interference, IL-1β, cortisol, TGF-β1, CRP, and IL-6 were moderated by pre-existing pain, peri-traumatic fear, region of injury, and peri-traumatic stress. Chapter 3 presents a latent growth curve analysis in determining the recovery trajectories of acute non-catastrophic musculoskeletal pain in the context of pain interference and severity over the course of 12 months. For pain interference, 3 distinct trajectories emerged: rapid recovery, delayed recovery, or minimal/no recovery. Pain severity favored a 2-trajectory model with rapid recovery or minimal/no recovery. Classification of recovery group depended on both baseline symptoms and relative rate of symptom decline. Recovery outcomes appeared to stabilize after a period of 3 months. Chapter 4 presents latent class analysis and growth mixture modeling as applied to a panel of 8 biomarkers (TNF-α, IL-1β, IL-6, CRP, IL-10, cortisol, BDNF, and TGF-β1). These markers may have the potential to discriminate between functional recovery outcomes. Using these markers, 3 meaningful groups or classes were identified. These groups could be adequately defined by using only 3 of the 8 markers (IL-1β, BDNF, and TGF-β1) where classes were organized by low concentration of markers in serum, average concentration, or high concentration of BDNF and TGF-β1. Those with high concentration of BDNF/TGF-β1 were more likely to score higher on self-report measures of pain and disability in their 6-month outcomes. These results support the claim that physiological factors are tied to pain through more than simple bivariate relationships. The context of the musculoskeletal trauma, both personal and social, can affect the behavior of biological systems

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