Abstract
Chronic pain constitutes a challenge for the scientific community and a significant economic and social cost for modern societies. Given the failure of current drugs to effectively treat chronic pain, which are based on suppressing aberrant neuronal excitability, we propose in this review an integrated approach that views pain not solely originating from neuronal activation but also the result of a complex interaction between the nervous, immune, and endocrine systems. Pain assessment must also extend beyond measures of behavioural responses to noxious stimuli to a more developmentally informed assessment given the significant plasticity of the nociceptive system during the neonatal period. Finally integrating the concept of perinatal programming into the pain management field is a necessary step to develop and target interventions to reduce the suffering associated with chronic pain. We present clinical and animal findings from our laboratory (and others) demonstrating the importance of the microbial and relational environment in programming pain responsiveness later in life via action on hypothalamo-pituitary adrenal (HPA) axis activity, peripheral and central immune system, spinal and supraspinal mechanisms, and the autonomic nervous system.
Highlights
Physiological pain plays an essential and primordial function in our survival
While our understanding of the complex mechanisms involved in the development and maintenance of chronic pain has increased dramatically in recent decades, treatments in various modalities continue to be based on a reductionist approach that understanding the precise nociceptive mechanisms that cause pain, will result in more targeted and more effective treatments
We demonstrated that neonatal LPS exposure produced a developmentally regulated activation of hypothalamo-pituitary adrenal (HPA) axis activity following a noxious stimulus as indicated by increased plasma levels of corticosterone in PND 13 and 22 but not PND 7 rats [10]
Summary
Physiological pain plays an essential and primordial function in our survival. It signals potential damage to the body and produces a wide range of sophisticated actions to prevent this damage. While our understanding of the complex mechanisms involved in the development and maintenance of chronic pain has increased dramatically in recent decades, treatments in various modalities continue to be based on a reductionist approach that understanding the precise nociceptive mechanisms that cause pain, will result in more targeted and more effective treatments. From Galen to the gate-control theory developed by Melzack and Wall, pain has been viewed either as a separate, independent sensation, an emotion, or a result from activation of nociceptors, spinal and supraspinal pathways. This review proposes a shift in conceptualising the problem of chronic pain away from a dichotomous standpoint to an integrative view which captures both the sensory and the emotional-cognitive in a framework that emphasises the neuroendocrine to immune communication pathways and the relevance of early premorbid events as predictors. Chronic pain patients may be differentially predisposed to recovering (or not recovering) from a physical injury, infection or trauma because of their premorbid psychoneuroimmunological status
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