Insufficient Evidence for Load as the Primary Cause of Nonspecific (Chronic) Low Back Pain. A Scoping Review.

OBJECTIVE: To assess the causal role of the relationship between loading and the onset of nonspecific low back pain (NSLBP) and persistence of NSLBP (chronic low back pain [CLBP]). DESIGN: Scoping review. LITERATURE SEARCH: We searched the literature from 2010 until May 2021 using a combination of terms related to (spinal) load and the Bradford-Hill (BH) criteria. STUDY SELECTION CRITERIA: Operational definitions were developed for every criterion of the BH framework for causality. Study selection was based on the causal role of load in the onset of NSLBP and persistence of chronic low back pain. DATA SYNTHESIS: The BH criteria were operationalized, and causation was considered established when evidence supported the BH criteria strength, temporality, biological gradient, experiment, and biological plausibility. RESULTS: Twenty-two studies were included. There was no consistent support for an association between load and the incidence of NSLBP, or that more load increased the risk of NSLBP/CLBP. Half of the studies did not support specific load exposures to increase incidence of or increase pain in NSLBP/CLBP. Half of studies did not support load preceding NSLBP. No study supported plausible biological explanations to influence the relationship between load and NSLBP/CLBP, or that similar causes have similar effects on NSLBP. Nine of 10 experimental studies did not support that load results in NSLBP or that relieving load reduces NSLBP/CLBP. CONCLUSION: There was insufficient evidence to support a causal relationship between loading and the onset and persistence of NSLBP/CLBP based on the BH criteria. These results question the role of load management as the only/primary strategy to prevent onset and persistence of NSLBP/CLBP. J Orthop Sports Phys Ther 2024;54(3):1-15. Epub 25 January 2024. doi:10.2519/jospt.2024.11314.

How do we explain painful non-traumatic knee conditions to adolescents? A multiple-method study to develop credible explanations.

BACKGROUND: Perceived diagnostic uncertainty can leave adolescents confused about their condition and impede their ability to understand "what's wrong with me". Our aim is to develop credible explanations about the condition for adolescents suffering from non-traumatic knee pain. METHODS: This multiple-method study integrated findings from two systematic literature searches of qualitative and quantitative studies, an Argumentative Delphi with international experts (n = 16) and think-aloud interviews with adolescents (n = 16). Experts provided feedback with arguments on how to communicate credible explanations to meet adolescents' needs; we analysed feedback using thematic analysis. The explanations were tailored based on the adolescent end-users' input. RESULTS: We screened 3239 titles/abstracts and included 16 papers exploring diagnostic uncertainty from adolescents' and parents' perspectives. Five themes were generated: (1) understanding causes and contributors to the pain experience, (2) feeling stigmatized for having an invisible condition, (3) having a name for pain, (4) controllability of pain, and (5) worried about something being missed. The Argumentative Delphi identified the following themes: (1) multidimensional perspective, (2) tailored to adolescents, (3) validation and reassurance, and (4) careful wording. Merging findings from the systematic search and the Delphi developed three essential domains to address in credible explanations: "What is non-traumatic knee pain and what does it mean?", "What is causing my knee pain?" and "How do I manage my knee pain?" CONCLUSIONS: Six credible explanations for the six most common diagnoses of non-traumatic knee pain were developed. We identified three domains to consider when tailoring credible explanations to adolescents experiencing non-traumatic knee pain. SIGNIFICANCE: This study provides credible explanations for the six most common diagnoses of non-traumatic knee pain. Additionally, we identified three key domains that may need to be addressed to reduce diagnostic uncertainty in adolescents suffering from pain complaints. Based on our findings, we believe that clinicians will benefit from exploring adolescents' own perceptions of why they experience pain and perceived management strategies, as this information might capture important clinical information when managing these young individuals.

Effects of repeated conditioning pain modulation in healthy volunteers.

BACKGROUND: Conditioned pain modulation (CPM) may be impaired in chronic pain patients compared with healthy subjects. The CPM-effect is the difference between pain sensitivity assessments (test-stimuli) with and without a painful conditioning stimulus. CPM has been extensively explored but effects of repeated CPM-effects and differences between repeated CPM assessments and comparable control conditions are less studied. METHODS: In 20 healthy men, four 5-min bouts with a test-stimulus in the beginning and midway were applied by cuff-algometry to the dominant leg. The 2nd test-stimulus in each bout was conditioned in parallel by a painful cuff pressure on the contralateral leg. A control-session was performed without conditioning. The conditioning intensity was 70% of the pressure-pain tolerance threshold (PTT) assessed at baseline. Pain detection threshold (PDT) was extracted from test-stimuli. CPM/Control-effects were calculated as second minus first test-stimulus, and netCPM-effects were calculated as the difference between CPM-effects and Control-effects. RESULTS: Pain detection threshold increased in all four bouts (p < 0.02) compared to the unconditioned test-stimulus and compared to the 2nd test-stimulus in bout1, bout3 and bout4 of the control-session (p < 0.04). In the control-session, the 1st test-stimulus PDT increased from bout1 to bout2, bout3 and bout4 (p < 0.03). The netCPM-effect increased progressively over the four bouts (p = 0.03). CONCLUSION: Conditioned pain modulation-effects were maintained over four consecutive bouts and in the control-session repeated pain thresholds assessments habituated more than in the CPM-session leading to an increase in netCPM-effect over the four bouts. SIGNIFICANCE: Conditioning pain modulation can be assessed in 5-min intervals by cuff algometry with a fixed conditioning stimulus. Without applying conditioning stimuli the pain sensitivity of test-stimuli habituated. As a consequence, it can be speculated that the conditioning stimulus may negate the temporal habituation effects during repeated sessions, whereas this may not be the case for unconditioned stimuli. Applying both conditioned and unconditioned repeated test-stimuli may be a way to assess different parts of the pain modulatory system, and a model for measuring a netCPM-effect, which could indicate a balance between habituation and sensitization, is proposed.

Adiponectin in human pregnancy: implications for regulation of glucose and lipid metabolism.

AIMS/HYPOTHESIS: Adiponectin is upregulated during adipogenesis and downregulated in insulin-resistant states. The mechanism(s) governing the re-arrangements from adipogenesis to facilitated lipolysis during pregnancy are unknown. Our purpose was to analyse the role of adiponectin relative to the metabolic changes in human pregnancy. SUBJECTS, MATERIALS AND METHODS: Lean women (BMI <25 kg/m(2)) were evaluated longitudinally before conception, and in early (12-14 weeks) and late (34-36 weeks) pregnancy. Insulin sensitivity was measured using the glucose clamp technique. Venous blood and subcutaneous adipose tissue biopsies were obtained at each time point. RESULTS: Adiponectin concentrations were lower in the third trimester than in the pregravid condition (9.9+/-1.4 vs 13.5+/-1.8 microg/ml). The hypoadiponectinaemia was reflected by a 2.5-fold decrease in white adipose tissue adiponectin mRNA. These changes were associated with a 25% increase in fat mass (23.7+/-2.9 vs 18.9+/-2.9 kg). Insulin infusion decreased high molecular weight adiponectin complexes in pregravid women (9.9+/-0.6 vs 6.2+/-0.06) and the suppressive effect of insulin was lost during pregnancy. The pregnancy-mediated changes in adiponectin were strongly correlated with basal insulin levels and insulin sensitivity (p<0.0001). The relationship between adiponectin and insulin sensitivity was related to the decreased insulin regulation of glucose utilisation (r=0.55, p<0.001) but not of endogenous hepatic glucose production. CONCLUSIONS/INTERPRETATION: These data demonstrate that pregnancy is associated with adiponectin changes in lean women. Hypoadiponectinaemia is reflected by a lower amount of high molecular weight adiponectin and by the ratio of high to low molecular weight multimers. The adiponectin changes relate to decreased insulin sensitivity of glucose disposal rather than alterations of lipid metabolism.