The Spine Journal
VOLUME 22, ISSUE 2, P214-225, FEBRUARY 01, 2022
Highlights
• Early transiently raised C-reactive protein associated with good long-term recovery after acute back pain.
• Persistent tumor necrosis factor overexpression associated with poor long-term recovery after acute back pain.
• Psychological and sleep status during acute back pain did not predict future inflammation.
• The acute phase inflammatory response appears a key determinant of back pain outcome.
Abstract
BACKGROUND CONTEXT
Individual characteristics can influence outcomes after injury. Our previous work in individuals with early-acute low back pain (LBP) identified subgroups (clusters) with specific biopsychosocial features that recovered poorly or well by 6 months.
PURPOSE
This study extends on that work by revealing the short- and long-term trajectories of recovery and systemic inflammation of these participant clusters: (1) “inflammatory & poor sleep” (Cluster 1), “high TNF & depression” (Cluster 2), “high pain & high pain-related fear” (Cluster 3), and “low pain & low pain-related fear” (Cluster 4).
STUDY DESIGN/SETTING
Longitudinal cohort study.
PATIENT SAMPLE
Eighty-three individuals within 2 weeks of an acute episode of LBP – grouped into their a priori-defined cluster.
OUTCOME MEASURES
General participant characteristics (sex, age, body mass index, smoking history, previous LBP history); self-reported LBP (0–10 numerical rating scale, LBP-related disability (Roland-Morris Disability Questionnaire), depression (Center for Epidemiological Studies Depression Scale, pain catastrophizing (Pain Catastrophizing Scale), fear avoidance (Fear Avoidance Beliefs Questionnaire), pain self-efficacy (Pain Self-Efficacy Questionnaire), and sleep (Pittsburgh Sleep Quality Index); systemic inflammatory biomarkers (C-reactive protein [CRP], interleukin-6 [IL-6], interleukin-1β, tumor necrosis factor [TNF]).
METHODS
Participants provided blood for the measurement of CRP/cytokines, and completed questionnaires related to their pain/disability, psychological and sleep status. Blood measures were repeated 3-monthly for 9 months, and pain/disability were self-reported fortnightly for 12 months. Recovery (change in pain) and CRP/cytokines were longitudinally compared between clusters using mixed-models. Associations between baseline factors and follow-up CRP/cytokines levels were assessed with multiple regression.
RESULTS
Clusters 1 and 2 were associated, but oppositely, with recovery over the 12-months. Cluster 1 reported most recovery at every 3-monthly interval, whereas Cluster 2 reported least recovery. Cluster 1 had elevated CRP (and IL-6) at baseline that continued to decrease from 3 to 9 months. TNF was elevated early and persistently in Cluster 2. Baseline factors other than inflammation generally failed to predict follow-up inflammation.
CONCLUSIONS
Findings support the early role of CRP (and perhaps IL-6) in control of inflammation and recovery, and a pathological role of persistent TNF overexpression, which may be perpetuated by depressive-like behaviors.