Post-Traumatic Stress Disorder Symptoms Are Associated With Incident Chronic Back Pain

A Longitudinal Twin Study of Older Male Veterans

Pradeep Suri, MD, MS; Edward J. Boyko, MD, MPH; Nicholas L. Smith, PhD; Jeffrey G. Jarvik, MD, MPH; Gail P. Jarvik, MD, PhD; Frances M.K. Williams, PhD; Rhonda Williams, PhD; Jodie Haselkorn, MD, MPH; Jack Goldberg, PhD

Disclosures

Spine. 2019;44(17):1220-1227. 

In This Article

Discussion

In this longitudinal study, baseline symptoms of PTSD were strongly associated with incident CBP at 5-year follow-up. This relationship was seen in within-MZ-pair analyses that control for genetics and early family environment, as well as unmeasured confounding factors. These results suggest that PTSD symptoms are a possible etiologic factor for CBP and not due to confounding by other factors.

Two prior longitudinal studies in clinical samples of patients with back pain have shown links with PTSD. In patients with incident low back pain in a military medical center, PTSD conferred a three-fold greater odds of acute back pain developing into CBP at 6 months follow-up.[44] PTSD also predicted a four-fold greater odds of future surgery in patients with CBP.[45] Our findings build upon this earlier work in two important ways. First, our study followed a nonclinical sample of those without back pain at baseline, establishing a clear temporal sequence of PTSD symptoms preceding the onset of CBP. Although in the military context PTSD and back pain may coexist due to combat-related physical injuries acting as the traumatic event triggering PTSD, while also directly injuring the spinal structures, this would not be expected in our study of older male Veterans who had left military service decades ago. Second, our work used a genetically informative sample that allowed us to determine that the PTSD-incident CBP association was present even after controlling for genetics, early family environment, and unmeasured confounders shared by MZ twins. These results add to findings from an earlier cross-sectional twin study by our group demonstrating that the association of PTSD and CBP persists once familial factors are accounted for,[25] and are consistent with studies of pain perception that show greater sensitivity to painful stimuli in subjects with PTSD and traumatic events compared with controls.[46,47] Taken together with prior work, the current findings suggest the possibility that PTSD symptoms may have causal effects on CBP. As effective psychologic and pharmacologic treatments exist for improving PTSD symptoms,[48–50] PTSD symptoms may be a potentially modifiable target of interventions to reduce the downstream risk of CBP. However, as PTSD symptoms should be treated for their mental health implications anyways, a more relevant implication for clinical practice may be that PTSD symptoms can be used to identify a subgroup of patients likely to experience future CBP; these at-risk individuals can be prepared to anticipate, respond to, and manage future back pain episodes. Such screening would be quite feasible to implement in the VA health care system, where PTSD symptoms are routinely screened for.[51]

To our knowledge, this is the first longitudinal cotwin control study to show a significant association between a psychological risk factor and incident back pain in within-MZ-pair analyses. A recent study by Pinheiro et al[22] found no significant associations between symptoms of depression/anxiety and incident chronic low back pain in longitudinal within-twin pair analyses, calling into question a causal effect of depression on future back pain. The contrasting results between our work and that of Pinheiro et al[22] may be because elevated PTSD symptoms affect back pain differently than do depression/anxiety. Another explanation for the null findings of Pinheiro et al,[22] as noted by the authors, was limited statistical power due to a small number of twin pairs discordant for the outcome of back pain.[22] This limitation is very common in longitudinal cotwin control studies of binary outcomes, where statistical power is driven mainly by the number of outcome-discordant twin pairs with complete data for exposures, outcomes, and covariates. Our study design resulted in exposure and outcome frequencies close to 50% and adequate statistical power, despite modest within-MZ-pair sample sizes.[22,23] Another potential limitation of the longitudinal cotwin control design using binary outcomes is the typical practice of restricting the baseline sample to twin pairs where both cotwins do not have the outcome at baseline, as was done in our study. Restriction to twin pairs concordant for absence of disease may define a baseline study sample that is enriched for those genetically predisposed to nothaving a particular disease,[52] and bias toward a null association in studies of environmental risk factors for a condition. This makes our finding of a significant association between PTSD and incident CBP all the more noteworthy. Multiple specific biological mechanisms have been proposed for how PTSD-related pathophysiologic changes may maintain or amplify the experience of pain, involving neurohormones, neurotransmitters, and inflammatory mechanisms, all of which are active areas of current research.[53]

Strengths of the current study include the longitudinal design, the unique ability of the cotwin control design to adjust for genetics and early family environment, and the use of accepted and validated measures for PTSD symptoms[36] and back pain.[38] Potential limitations include the use of surveys to ascertain CBP status, rather than structured interviews, and the reliance on recalled pain, the accuracy of which decreases according to the length of the recall period.[54] In addition, the definition used to identify a cohort free of CBP at the study baseline did not specify a minimum duration of pain needed to count as "chronic," and was formulated differently than the NIH task force recommended questions used at 5-year follow-up.[38] We expect that any such potential misclassification resulting from this would not occur differentially by current PTSD status, and therefore would have had minimal effects on our overall results, if any. Another potential limitation of our study was a low response rate at follow-up (66%), which was likely due in part to the long (5-year) follow-up period involved. Loss to follow-up could possibly create selection bias if the PTSD-back pain association differed in those lost to follow-up compared with those who completed follow-up. As our study included US Veterans only, and the majority of participants were white, further studies will be needed to see whether our findings are generalizable to non-Veterans, non-whites, and populations outside the US.

In summary, this cotwin control analysis demonstrated strong associations (RRs 1.5–2.7) between PTSD symptoms and the development of incident CBP even after accounting for familial factors. These data suggest that PTSD symptom severity might be a potential modifiable risk factor for chronic thoracolumbar back pain.

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