The mechanism of action of spinal mobilizations: a systematic review

Objective. To review the evidence regarding the mechanism of action of mobilizations.Summary of background data. Spinal mobilizations—low velocity passive oscillatory movements—reduce spinal pain in some patient subgroups. Identifying patients likely to respond remains a challenge since mobilizations’ mechanism(s) of action are unclear.Methods. Medline, Web of Science, Cinahl, Embase, and Scopus databases were searched for relevant studies. Reference lists of included studies were hand searched. Studies were included if the intervention was passive spinal mobilizations, participants were symptomatic, and outcomes evaluated possible mechanisms of action. Methodological quality was independently assessed by two assessors using a modified Cochrane Back Review Group tool.Results. Twenty-four studies were included in the review. Four were classified high risk, 14 moderate risk, and four low risk of bias. Commonest methodological limitations were lack of participant blinding, adequate randomization and allocation concealment, and sample size calculation. Evidence suggests that spinal mobilizations cause neurophysiological effects resulting in hypoalgesia (local and/or distal to mobilization site), sympathoexcitation, and improved muscle function. Mobilizations have no effect on temperature pain threshold. Three of four studies reported reduction in spinal stiffness, heterogeneous in location and timing. There is limited evidence (one study in each case) to suggest that mobilizations produce increased nociceptive flexion reflex threshold, improved posture, decreased concentration of substance P in saliva, and improved sway index measured in cervical extension. Evidence does not support an effect on segmental vertebral movement. Two studies investigated correlations between hypoalgesia and mechanism: one found a correlation with sympathoexcitatory changes, whereas the other found no correlation with change in stiffness.Conclusion. These findings suggest involvement of an endogenous pain inhibition system mediated by the central nervous system, although this is yet to be investigated directly. There is limited evidence regarding other possible mechanisms