JOURNAL ARTICLE
RANDOMIZED CONTROLLED TRIAL
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Changes in Cytokines, Sensory Tests, and Self-reported Pain Levels After Manual Treatment of Low Back Pain.

STUDY DESIGN: Unbalanced 3-factor design with repeated measures on 1 factor.

OBJECTIVE: To determine the effect of manual treatment (MT) on cytokine and pain sensations in those with and without low back pain (LBP).

SUMMARY OF BACKGROUND DATA: Evidence suggests that MT reduces LBP but by unknown mechanisms. Certain cytokines have been elevated in patients with LBP and may be affected by MT.

METHODS: Participants aged 20-60 years with chronic LBP or without LBP were recruited and randomly assigned to MT, sham ultrasound treatment, or no treatment groups. Venous blood samples were collected and pain levels assessed at baseline, 1 hour later, and 24 hours later. Blood was analyzed for interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and C-reactive protein. Pain levels were measured by pressure pain threshold (PPT), mechanical detection threshold (MDT), dynamic mechanical allodynia, and self-report.

RESULTS: Forty (30 women, age 36±11 y) participants completed the study, 33 with LBP (13 MT, 13 sham ultrasound treatment, and 7 no treatment) and 7 without LBP. Participants with or without LBP could not be differentiated on the basis of serum cytokine levels, PPT, or MDT (P≥0.08). There were no significant differences between the groups at 1 hour or 24 hours on serum cytokines, PPT, or MDT (P≥0.07). There was a significant decrease from baseline in IL-6 for the no treatment (LBP) group (P=0.04), in C-reactive protein for the sham ultrasound treatment group (P=0.03), in MDT for all 3 LBP groups (P≤0.02), and in self-reported pain for the MT and sham ultrasound treatment groups (P=0.03 and 0.01).

CONCLUSIONS: Self-reported pain was reduced with MT and sham ultrasound treatment 24 hours after treatment, but inflammatory markers within venous circulation and quantitative sensory tests were unable to differentiate between study groups. Therefore, we were unable to characterize mechanisms underlying chronic LBP.

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