Targeting inflammation as a treatment modality for neuropathic pain in spinal cord injury: a randomized clinical trial. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Allison, David; Thomas, Aysha; Beaudry, Kayleigh; Ditor, David
• Is Part Of: Journal of neuroinflammation. Volume 13:Issue 1(2016)
• Page Start: 1
• Page End: 10
• Publication Date: 2016-12
• Subjects: Neuropathic pain -- Spinal cord injury -- Inflammation -- Anti-inflammatory diet; Central nervous system -- Diseases -- Periodicals; Inflammation -- Periodicals; 616.8
• DOI: 10.1186/s12974-016-0625-4
• Languages: English
• ISSNs: 1742-2094

Abstract

Abstract Background The purpose of the present study was to examine the effectiveness of an anti-inflammatory intervention as a treatment for neuropathic pain following spinal cord injury (SCI). Methods This randomized, parallel-group, controlled clinical trial (NCT02099890) examined 20 participants with varying levels and severities of SCI, randomized (3:2) to either a 12-week anti-inflammatory diet, or control group. Outcome measures consisted of self-determined indices of pain as assessed using the neuropathic pain questionnaire (NPQ) and markers of inflammation as assessed by various pro- and anti-inflammatory cytokines, as well as the eicosanoids PGE2 and LTB4. Results A significant group × time interaction was found for sensory pain scores (p < 0.01). A Mann-Whitney test revealed that the change scores (3-month baseline) were significantly different between groups for IFN-y (U = 13.0, p = 0.01), IL-1β (U = 14.0, p = 0.01), and IL-2 (U = 12.0, p = 0.01). A Friedman test revealed the treatment group had a significant reduction in IFN-y (x 2 = 8.67, p = 0.01), IL-1β (x 2 = 17.78, p < 0.01), IL-6 (x 2 = 6.17, p < 0.05), while the control group showed no significant change in any inflammatory mediator. A stepwise backward elimination multiple regression analysis showed that the change in sensory neuropathic pain was a function of the change in the proinflammatory cytokines IL-2 and IFN-y, as well as the eicosanoid PGE2 (R = 0.689, R 2 = 0.474). Conclusions Overall, the results of the study demonstrate the efficacy of targeting inflammation as a means of treating neuropathic pain in SCI, with a potential mechanism relating to the reduction in proinflammatory cytokines and PGE2. Trial registration ClinicalTrials.gov, NCT02099890