Chapter

Dysfunction of the Hypothalamic–Pituitary–Adrenal Axis and Associated Stress Axes in the Development of Chronic Low Back Pain

John McBeth and Andrea Power

in From Acute to Chronic Back Pain

Published on behalf of Oxford University Press

Published in print January 2012 | ISBN: 9780199558902
Published online November 2012 | e-ISBN: 9780191753343 | DOI: http://dx.doi.org/10.1093/med/9780199558902.003.0026
Dysfunction of the Hypothalamic–Pituitary–Adrenal Axis and Associated Stress Axes in the Development of Chronic Low Back Pain

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As discussed in Parts 2 to 4 of this volume, low back pain (LBP) is a complex disorder whose aetiology is associated with a host of factors across multiple domains that include biological, psychological, and individual- and higher-order social factors. By definition chronic LBP is LBP that persists beyond the normal healing time required for any insult or injury that may have preceded the onset of symptoms (IASP 2002). That is, for most cases, LBP in the absence of obvious pathology. The challenge then is to identify the factors that are associated with symptom perpetuation, or chronification.

It is clear that to determine the factors that are associated with the transition from acute to chronic LBP, we cannot limit our perspective. Focusing on the role of the biological determinants of chronicity in isolation from psychological and social factors would be meaningless. The inter-relationships between risk factors for chronicity can be usefully conceptualized through a traditional biopsychosocial model. However in an excellent theoretical paper (Deary et al. 2007) the biopsychosocial model has been expanded to develop a model of symptom perpetuation that is autopoietic (a term borrowed from systems theory and cell biology that literally means ‘self-creating’) (see Figure 5.1). The core tenet of that model is a multifactorial autopoietic cycle that underlies the perpetuation of symptoms. The strength of this conceptualization is that while across groups of individuals there may be similarities in the factors associated with the chronification of LBP, the model allows for interactions between these factors that may be unique to subgroups or even the individual experience and addresses the important issue of phenotypic heterogeneity. Expanding beyond the original aim of the Deary et al. (2007) paper (to explore the onset and perpetuation of ‘medically unexplained’ symptoms such as chronic fatigue and irritable bowel syndrome) this model can usefully focus our thoughts on the role of multiple factors in the perpetuation of LBP. The reader is encouraged to place the findings reported below in the context of the model outlined in Figure 5.1.

Stress response systems are notoriously sensitive to multiple factors: prior experience and life stress (Faravelli et al. 2010), psychological distress, cognitive and behavioural factors (Geiss et al. 2005), and body composition (Vicennati et al. 2009) to name a few. In this chapter we will outline the putative role of innate stress response systems in the perpetuation of pain. The main focus will be the primary stress response system in humans the hypothalamic–pituitary–adrenal (HPA) axis. We will also briefly explore the relationship with other related systems; the hypothalamic–pituitary–gonadal (HPG) and hypothalamic–pituitary–growth hormone (HPGH) axes. We will argue that these stress response systems may bring about the transition from acute to chronic LBP.

However, while the available data is suggestive, these relationships have not been adequately tested in well-conducted longitudinal epidemiological studies. Data from other disorders that are strongly associated with stress and that have pain as the cardinal symptom will occasionally be included in the discussion where data is not directly available on LBP. We conclude with a research recommendation that outlines a testable hypothesis to establish the true relationship between functioning of stress response systems and the chronification of LBP.

Chapter.  10504 words.  Illustrated.

Subjects: Neuroscience ; Pain Medicine

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