Abstract
Context: Depression and somatization are often present in patients with chronic low back pain (LBP).
Objectives: To measure the presence of depression and somatization in patients with chronic LBP and to study the associations of depression and somatization with somatic dysfunction, LBP severity, back-specific functioning, and general health.
Design: Cross-sectional study using baseline measures collected within a randomized controlled trial.
Setting: University-based study in Dallas-Fort Worth, Texas.
Patients: A total of 202 adult research participants with nonspecific chronic LBP.
Main Study Measures: Depression was self-reported and also measured with the Modified Zung Depression Index (MZDI). Somatization was measured with the Modified Somatic Perception Questionnaire (MSPQ). The MZDI and MSPQ scores were used to classify patients as “normal,” “at risk,” or “distressed” using the Distress and Risk Assessment Method. Somatic dysfunction was assessed using the Outpatient Osteopathic SOAP Note Form. A 100-mm visual analog scale (VAS), the Roland-Morris Disability Questionnaire (RMDQ), and the Medical Outcomes Study Short Form-36 Health Survey (SF-36) were used to measure LBP severity, back-specific functioning, and general health, respectively.
Results: There were 53 patients (26%) and 44 patients (22%) who were classified as having depression on the basis of self-reports and the MZDI cut point, respectively. A total of 38 patients (19%) were classified as having somatization on the basis of the MSPQ cut point. There were significant correlations among self-reported depression and the MZDI and MSPQ scores (P<.001 for each pairwise correlation). Similarly, the MZDI and MSPQ scores were both correlated with LBP severity and back-specific disability, and they were inversely correlated with general health (P<.001 for each pairwise correlation). Depression and the number of key osteopathic lesions were also each correlated with back-specific disability and inversely correlated with general health (P<.001 for each pairwise correlation). The MZDI (P=.006) and MSPQ (P=.004) scores were also correlated with the number of key osteopathic lesions.
Conclusions: The associations among depression, somatization, and LBP in this study are consistent with the findings of previous studies. These associations, coupled with the findings that MZDI and MSPQ scores are correlated with somatic dysfunction, may have important implications for the use of osteopathic manual treatment in patients with chronic LBP.
Chronic low back pain (LBP) frequently involves a multifactorial etiology and requires ongoing medical management. As depicted in
Figure 1, the biopsychosocial model has been widely used to reflect the complexity of factors that may be associated with chronic medical conditions.
1 Therein, disease is defined as an objective biological event involving the disruption of specific body structures or organ systems by means of anatomical, pathological, or physiological changes. In contrast, illness generally refers to a subjective experience or self-attribution that a disease is present. Thus, with regard to chronic LBP, the biopsychosocial model views it as a complex interaction of biological, psychological, and social factors, with each individual having unique interactions that affect processing of nociceptive input to derive a global perception of pain.
Correspondingly, the osteopathic approach to the treatment of patients with chronic LBP includes consideration of body unity, homeostasis, and structure-function relationships.
2 Cardinal manifestations within each of these 3 domains include depression, dysregulation of the autonomic nervous system, and somatic dysfunction, respectively. A better understanding of the interrelationships among these factors is crucial in developing better treatment options for patients with chronic LBP, including osteopathic manual treatment (OMT). The purpose of the present study was to explore these interrelationships and their associations with LBP severity, back-specific functioning, and general health using baseline data from the OSTEOPAThic Health outcomes In Chronic low back pain (OSTEOPATHIC) Trial.
3
Association of MZDI Scores With Low Back Pain Severity, Back-Specific Functioning, and General Health
Association of MSPQ Scores With Low Back Pain Severity, Back-Specific Functioning, and General Health
Depression and somatization have been implicated in the transition from acute to chronic LBP,
12 and also appear to be influential in the development of disability in patients with LBP.
13 The occurrence of depression and somatization in our patients was similar to that previously observed in patients with chronic LBP,
14-16 and greater than that of general population controls.
14,15 The correlations among depression, somatization, and pain duration and ratings in our study were also similar to those previously reported in chronic LBP patients.
16
Patients with pain or depression frequently exhibit common clinical features, suggesting that they may share some aspects of pathophysiology represented by common pathways and neurotransmitters.
17 Three cytokines—interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α—have been characterized as typical pro-inflammatory cytokines that are central to clinical manifestations of the “sickness response.”
18 The latter subsumes both pain and depression. It is hypothesized that the normal, adaptive mechanisms of the sickness response are altered over time in chronic conditions, such that signaling is no longer providing contextually appropriate information. Interventions that attenuate this cascade of cellular events initiated by pro-inflammatory cytokines may prove helpful in preventing or managing pathological depression and chronic pain.
18 A recent study found no differences in TNF-α serum concentrations between chronic LBP patients with and without depression, although both groups of patients had significantly higher TNF-α concentrations than healthy controls.
17 On the basis of these and previous results, the study authors concluded that TNF-α acts as a mediator, by similar mechanisms, in both chronic LBP and depression. These findings may have potentially important clinical implications, as TNF-α concentrations decreased significantly after 12 weeks in patients with chronic LBP in response to a 6-session regimen of OMT.
19
Recently, there has been a greater recognition of the role that “central sensitization” plays in patients with musculoskeletal pain.
20 As distinct from nociceptive or peripheral neuropathic pain, central sensitization refers specifically to neurophysiological processes occurring at a cellular level throughout a widely distributed central nervous system.
21 Aside from altered processing in the brain, there are also “bottom-up” mechanisms involved in the pathophysiology of central sensitization. For example, peripheral injury and other forms of stressors may trigger the release of pro-inflammatory cytokines, thereby activating spinal cord glia with cyclooxygenase-2 and prostaglandin E2 expression in the central nervous system.
20 Interestingly, we have also found statistical associations between IL-1β and IL-6 serum concentrations and the severity of somatic dysfunction, as manifested by the number of key osteopathic lesions, in patients with chronic LBP.
19 Nevertheless, on the basis of self-reported LBP severity, disability, health status, depression, and anxiety, central sensitization has been classified as the mechanism for LBP in less than one-fourth of patients, as compared with nociception in more than one-half of patients.
22 Similarly, using the same discriminant validity classification scheme,
22 the baseline scores for VAS pain, RMDQ, SF-36 general health, work status, and LBP chronicity of our patients were consistent with a predominant nociceptive mechanism of pain.
To our knowledge, the present study is the first to find empirical evidence suggesting a statistical correlation between depression and somatization, as measured by MZDI and MSPQ scores, and the severity of somatic dysfunction as determined by the number of key osteopathic lesions in the T10-12, ribs, lumbar, sacrum/pelvis, and pelvis/innominate anatomical regions. Further analyses of these results, using cut points based on the DRAM classification system, found the strongest association with number of key osteopathic lesions among patients having MZDI scores from 17 to 33 and among those classified by the DRAM as “at risk.” There was no significant association with the number of key osteopathic lesions in patients with self-reported depression, nor in the subgroups of patients with high MZDI scores (≥34), high MPSQ scores (≥12), or a classification of “distressed” on the DRAM. Future analyses of these baseline measures, coupled with longitudinal assessments of depression and somatization and the OSTEOPATHIC Trial outcomes, may provide more insight on the utility of OMT in the treatment of patients with chronic LBP.
There are potential limitations of our study. First, as indicated above, self-reported depression generally was not subjected to corroboration by medical records. Thus, there may have been some misclassification of depression on the basis of self-reports of patients. Nevertheless, the self-reporting of depression in our study was comparable to that reported in other studies of patients with chronic LBP, and we also observed a significant correlation between self-reported depression and MZDI scores in our study. Second, it is possible that some significant findings may represent type I errors because of multiple comparisons, particularly in our correlational analyses. However, because this was an exploratory study, we elected not to adjust for multiple comparisons. Third, there may have been interexaminer variability in diagnosing somatic dysfunction using the musculoskeletal table of the Outpatient Osteopathic SOAP Note Form,
7 particularly in distinguishing between “obvious” TART elements (severity defined as “moderate” and not considered key lesions) and key lesions that “stand out” (severity defined as “severe”). Although we provided fidelity training for OMT providers during the study,
23 we did not formally assess provider performance or interexaminer reliability.