Context: There is a common symptom pattern with most chronic low back pain (CLBP), suggesting that there is a common underlying etiology, belying the term “nonspecific.” Many studies of CLBP and its treatment have been conducted with the assumption of nonspecificity, and as a result, treatment has not been focused, thus there has not been a significant change in CLBP prevalence over the past several decades. It is the thesis of this study to show that there is an underlying, specific cause of CLBP and that the presumption that CLBP is nonspecific is misdirected. The lumbosacropelvic (LSP) region, including the sacroiliac joint (SIJ), is part of a neuromusculoskeletal (NMSK) feedback system, and it is proposed here that CLBP is the result of a change in the feedback (afferent) aspect in that system.
Objectives: The objectives of this study are to show that CLBP presents as a pattern of symptoms that actually represents the final common pathway for a dysfunctional LSP joint system. Rather than being “nonspecific,” the majority of CLBP has an underlying cause that is quite specific and predictable.
Methods: A total of 252 patients were seen for CLBP, 67% of whom were diagnosed with an SIJ dysfunction. The presence of pain was recorded from seven structures most closely associated with CLBP. The conditional probabilities of having each pain generator given a SIJ dysfunction and an SIJ dysfunction given the presence of the pain generator were estimated, and associations were analyzed utilizing chi-square tests. Phi coefficients and odds ratios were utilized to quantify the strength of the association. The multivariable logistic regression model was fit to relate the presence or absence of the SIJ dysfunction to the seven pain generators.
Results: The associations between SIJ dysfunction and each pain generator were statistically significant. Phi coefficients indicated moderate strengths of these bivariate associations. Iliolumbar ligament (ILL) and psoas muscle (PSM) were significant predictors of SIJ dysfunction in the multivariable model.
Conclusions: Seven pain generators had a strong association with SIJ dysfunction. This empirical clinical evidence supports our hypothesis that LSP system dysfunction, as evidenced by SIJ dysfunction, is a common source of symptom patterning associated with CLBP and is most likely the causal element. This is evidence that most CLBP is not “nonspecific” but rather the result of changes made by the NMSK control system for the LSP region.