Cross-sectional and Longitudinal Associations of Low-back Pain
and Related Disability with Psychological Distress Among
Patients Enrolled in the UCLA Low-Back Pain Study

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:    Frankp@chiro.org

FROM:   J Clin Epidemiol. 2003 (May); 56 (5): 463–471

Eric L. Hurwitz, DC, PhD, Hal Morgenstern, PhD

School of Public Health,
Department of Epidemiology,
University of California-Los Angeles,
Box 951772,
Los Angeles, CA 90095-1772, USA.
ehurwitz@ucla.edu

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The objectives of the study are to test the hypotheses that psychological distress affects subsequent low-back pain, and pain affects subsequent distress. Six hundred eighty-one participants in a randomized clinical trial of low-back pain treatments were followed for 18 months with assessments for pain, disability, and psychological distress at 6 weeks and 6, 12, and 18 months. Multivariable logistic regression modeling with generalized estimating equations was used to estimate effects.

Current pain and disability increased the odds of subsequent psychological distress [pain: adjusted odds ratio (OR)=1.36, 95% confidence interval (CI)=1.07, 1.72; disability: adjusted OR=1.23, 95% CI=0.98, 1.55], and current distress increased the odds of subsequent pain and disability (pain: adjusted OR=1.51, 95% CI=1.24, 1.86; disability: adjusted OR=1.49; 95% CI=1.20, 1.85).

Cross-sectional associations were much stronger than the longitudinal associations, suggesting bias in the former due to selection factors and/or temporal ambiguity. The longitudinal findings suggest that pain/disability and psychological distress may be causes and consequences of each other, although the associations are small.

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From the FULL TEXT Article:

Introduction

Low-back pain and depression are two of the most frequent reasons for seeking medical attention [1, 2] and are common comorbidities [3, 4], yet the temporal and causal directions and specific mechanisms linking pain with psychological distress and well-being remain elusive. [5]

Three primary nonmutually exclusive hypotheses have been put forth recently to explain the relationship between chronic pain and depression or depressive symptoms [5-7]:

(1)   depression increases the risk of pain (antecedent hypothesis),

(2)   pain increases the risk of depression (consequence hypothesis), and

(3)   a common mechanism influences the development of both chronic pain and depression (common pathogenetic mechanism).

Additional hypotheses, which are essentially variants of the consequence hypothesis and of each other, have also been described [5-7]: prior depressive episodes predispose subsequent pain sufferers to develop depression (scar hypothesis), thoughts and behaviors influence pain sufferers to develop depression (cognitive-behavioral mediation model), and pre-existing characteristics of individuals are activated following the onset of pain and the stressors associated with it, which then lead to the development of depression (diathesis-stress model). [6, 7]

Although the consequence hypothesis appears to be supported by the bulk of the limited published literature, with less support for the antecedent hypothesis [5], few prospective studies have examined the validity of these and other hypotheses. Many of the relevant studies are cross-sectional in nature, and thus the inherent temporal ambiguity between pain and depression complicates the interpretation of the findings. Such studies also preclude the simultaneous testing of hypotheses addressing each condition as a predictor of the other. Furthermore, given recent findings regarding the neurophysiology of physical and emotional pain and the common immune and neuroendocrine factors involved in pain perception and depression [5, 8–10], pain and psychological distress may be linked both bidirectionally and via common environmental, clinical, psychosocial, or other factors that mediate the association.

The purpose of this study is to estimate cross-sectional and longitudinal associations of low-back pain and related disability with psychological distress among primary-care low-back pain patients. The hypotheses are that psychological distress affects subsequent level of low-back pain, and level of low-back pain affects subsequent psychological distress among primary-care low-back pain patients. Because of lack of data on mental health history, exposure to stressors, and thoughts, behaviors, and other factors that may be associated with pain and psychological distress, this article does not address the other alternative (or complementary) hypotheses described above.

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Discussion

Although many investigators have found cross-sectional and longitudinal associations of low-back and other musculoskeletal pain with depression and other psychological states and conditions [3, 31–45], this is the first longitudinal study of primary care low-back pain patients, to our knowledge, that shows low-back pain and psychological distress to be associated both cross-sectionally and longitudinally, suggesting the likelihood of multiple mechanisms linking pain and psychological distress. The findings indicate that

(1)   low-back pain and disability influence subsequent psychological distress,

(2)   psychological distress influences subsequent low-back pain and disability, and

(3)   each pain/disability–psychological distress longitudinal associations similar in magnitude to its sister psychological distress–pain/disability association.

The adjusted associations in the longitudinal analyses are fairly modest in magnitude, however. The cross-sectional associations are much stronger, suggesting that these associations are positively biased due to selection factors and/or temporal ambiguity.

As documented by others [43, 44, 46–50], prior back pain and disability, given their chronic-recurrent nature, were found to be associated with subsequent pain and disability, and prior psychological distress was associated with subsequent distress. We also found some evidence that pain or disability and psychological distress modify the effects of each other on the odds scale, suggesting that the effects of frequent pain or low-back disability on subsequent psychological distress are greater among distressed than nondistressed persons. Findings from this study, assuming no residual confounding, support both the antecedent and consequence hypotheses, and are not inconsistent with the scar, cognitive-behavioral mediation, diathesis-stress, and common pathogenetic mechanism hypotheses linking pain with depression or depressive symptoms.

Our findings are consistent with studies that have shown low-back pain to increase the risk of depression or psychological distress. [35, 41, 43] Among nondepressed subjects of the National Health and Nutrition Examination Survey I (NHANES I) and the National Health and Nutrition Epidemiologic Follow-Up Survey (NHEFS), chronic neck and back pain predicted depression after 8 years of follow-up (adjusted OR = 2.85). [41] Other investigators have shown first-time low-back pain to precede psychological distress [43] and chronic back pain to precede depressive symptoms. [35] Fishbain et al. [5] performed a comprehensive review of chronic pain and depression studies, 15 of which addressed and supported the consequence hypothesis that chronic pain influences the onset of depression.

Conversely, our findings are also consistent with investigations that have shown psychological distress or depression to influence the course of low-back and other musculoskeletal pain. [37, 41, 43–45, 51] Measures of psychological distress predicted the onset of low-back pain episodes during a 1-year follow-up period in a prospective cohort study (adjusted OR = 1.8). [51] A recent analysis of a subset of the 1958 British birth cohort found that psychological distress at 23 years of age predicted incident low-back pain at 32– 33 years of age (adjusted OR = 2.52). [45] Psychological distress was also a predictor of first-time low-back pain among health care workers after 18 and 36 months of followup. [43, 44] Leino and Magni [37] found in their longitudinal study of metal industry workers that depression predicted the onset of musculoskeletal pain, as did Magni et al. [41] in their analysis of NHANES I and NHEFS, finding that depression increased the likelihood of chronic musculoskeletal pain after 8 years (adjusted OR = 2.14).

However, other investigators have failed to find associations between mental health and back pain. [46, 52] During a 3-year period among enrollees of a health maintenance organization, episodes of low-back pain were no more common in depressed than nondepressed subjects. [46] Because major depression and other psychopathology was not predictive of return to work after 1 year among acutepain (6 weeks) patients in a prospective cohort study, the authors concluded that major psychopathology does not precede the onset of chronic low-back disability. [52] Fishbain et al. [5] found in their aforementioned review that of 13 studies that addressed the antecedent hypothesis in which depression precedes the onset of chronic pain, only three studies supported it. Interstudy differences in populations, length of follow-up, and in the definitions, diagnostic criteria, and measurements of back pain and mental health, as suggested by Fishbain [5] and others [7, 53], and statistical methods, may be responsible for some of the variability across studies.

Although there is disagreement regarding the effect of mental health on the risk of low-back pain, a number of recent studies have consistently shown depression to be a prognostic factor in recovery from low-back pain. [31, 32, 46, 54] Dionne et al. [31] demonstrated that depression was one of the strongest predictors of low-back pain-related functional limitations at 2 years among primary care back-pain patients. Baseline depression was also a major predictor of patient’s self report of poor outcome at 7 weeks and 1 year (adjusted OR = 2.3) among primary care low-back pain patients of a health maintenance organization. [32] Among patients receiving care for lumbar disc prolapse or protrusion, depression was found to be one of the most important predictors of persistent pain 6 months after initial treatment. [87]

Our study has a few limitations. The relative generalizability of the findings, which are based on a clinical rather than a population-based sample, is the study’s major limitation. Our study population is similar to other outpatient lowback pain populations with respect to baseline level of back pain [55–57] and related disability [14, 56–60]; however, we did not follow a population that was free of low-back pain and psychological distress at baseline; thus, we cannot draw inferences regarding the relations between pain, related disability, and psychological distress among initially diseasefree persons. Furthermore, because of the relatively high nonparticipation rate, we did not necessarily obtain a representative sample of all eligible persons presenting with low-back pain at the health care facility, thus affecting the generalizability of our results from the longitudinal and cross-sectional analyses.

Selection bias might have been a threat to internal validity in the cross-sectional analyses if selection into the study was associated with both psychological distress and pain or disability level. In fact, selection bias in the cross-sectional analyses is one possible explanation for the difference in results between cross-sectional and longitudinal analyses. However, selection bias probably did not affect our estimates of effect from the longitudinal analyses because 90% of the 681 enrolled subjects were followed up through 18 months, and it is very unlikely that the outcomes (which were observed during the follow-up period) could have influenced the selection of subjects. [61] Although it is true that both baseline outcome measures and the main predictor might have affected the selection of subjects, we controlled for the baseline measure of each outcome variable in our analyses. Thus, our effect estimates would not be biased because of these selection patterns. There may be other risk factors that might have influenced subject selection, but we have attempted to measure and control for those potential confounders as well. Selection (or nonparticipation) of potentially eligible persons would not be expected to introduce bias in effect estimation because the outcome observed during follow-up is not likely to be associated with the probability of selection, conditional on those other factors that we controlled through statistical adjustment.

Other limitations include our use of short self-report instruments and our definitions of psychological distress, pain, and disability, and residual confounding. Although more comprehensive measures of psychological distress and depression would have been preferable, the MHI-5 correlates well with many other well-known mental health scales [21, 23, 24], and the pain and disability measures have been previously validated. [12–19] Furthermore, the estimates of association were not substantially different across each of the pain and disability measures, and defining pain, disability, and psychological distress more strictly by moving the cut points did not materially affect the results. Although we controlled for the effects of some potential confounders by multivariable modeling, confounding by known and unknown factors, given the complex, multifactorial nature of pain and psychological distress, remains a possibility.

Finally, we could not directly test the scar, cognitive-behavioral, and diathesis-stress hypotheses because of lack of data on prior history of psychological distress or depression, thoughts and behaviors, and stressors that may be associated with the onset and maintenance of pain. The results of this study coupled with recent evidence from human and animal research suggest the validity of these and other hypotheses may vary by subgroups defined according to genetic, environmental, clinical, behavioral, and other characteristics. [62, 63] Effect estimation of potential predictors of pain with and without comorbid depression (and depression with and without comorbid pain) may be helpful in addressing the common pathogenetic mechanism hypothesis. The design of multiple studies to directly test each hypothesis in a variety of populations should be the focus of future research.

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Conclusion

Among a population of primary care patients presenting with low-back pain and enrolled in a randomized clinical trial with 18 months of follow-up, level of low-back pain influences subsequent psychological distress, and psychological distress influences subsequent level of low-back pain and disability. These longitudinal associations are small in magnitude relative to the much larger cross-sectional associations, the latter estimates reflecting effects in both directions and possible bias due to selection factors. Large, long-term prospective, population-based studies should be conducted to identify factors that predict the onset, progression, and recurrence of pain, disability, and psychological distress, as well as cognitive, behavioral, and other modifiable factors that may influence the associations between pain, related disability, and psychological distress.

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