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Low back pain is the second most frequently diagnosed pain condition in the United States, and although a majority of individuals have resolution of pain during the acute period, an estimated 40% of individuals will experience persistent pain. Given the heterogenous nature of low back pain, this study sought to describe and compare somatosensory and molecular (gene expression and metabolomic) profiles between individuals with acute low back pain and healthy no-pain controls
Methods:
Using a previously established protocol, we comprehensively assessed somatosensory parameters among 31 no-pain control participants, 31 participants with acute low back pain whose pain resolved within 6 weeks and 31 participants who transitioned from acute to chronic low back pain. Samples of whole blood were drawn to examine mRNA expression of candidate genes and metabolomic profiles of molecules involved in the transduction, maintenance, and modulation of pain.
Results:
During the acute stage of low back pain participants exhibited increased pain sensitivity to cold stimuli, mechanical stimuli, including mechanical temporal summation at both the painful back area and remote location suggesting a mechanism of enhanced central nervous system excitability.Participants who transitioned to chronic low back pain exhibited increased thermal detection thresholds. In addition, deep tissue specific peripheral sensitization was suggested due to significant differences in pressure pain threshold of the painful back area, but not the remote body site. Several genes that were differentially expressed were significantly associated with somatosensory alterations identified during the stage of acute low back pain and the metabolomic profiles suggest increased inflammatory activation with numerous proteins involved in modulating pain outcomes.
Conclusion:
Acute low back pain participants showed selective pain sensitivity enhancement and differential gene expression profiles compared to pain-free controls. Discussion will focus on how characterizing pain-associated somatosensory changes in the context of altered mRNA expression levels may provide insight on the molecular underpinnings of maladaptive chronic pain.