Pain
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We hypothesised that the relative importance of physical and psychological risk factors for mechanical low back pain (LBP) might differ importantly according to whether there is underlying spinal pathology, psychological risk factors being more common in patients without demonstrable pathology. If so, epidemiological studies of LBP could benefit from tighter case definitions. To test the hypothesis, we used data from an earlier case-control study on patients with mechanical LBP who had undergone magnetic resonance imaging (MRI) of the lumbosacral spine. ⋯ Radiation of pain below the knee (280 patients) and weakness or numbness below the knee (257 patients) were both associated with nerve root deviation/compression (OR 2.5, 95% CI 1.4 to 4.5; and OR 1.8, 95% CI 1.1 to 3.1, respectively). However, we found no evidence for the hypothesised differences in risk factors between patients with and without demonstrable spinal pathology. This suggests that when researching the causes and primary prevention of mechanical LBP, there may be little value in distinguishing between cases according to the presence or absence of the more common forms of potentially underlying spinal pathology.
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Multicenter Study
Elevated levels of gonadotrophins but not sex steroids are associated with musculoskeletal pain in middle-aged and older European men.
The aim of this study was to determine the association of hormone levels with the occurrence of musculoskeletal pain. Men ages 40 to 79 years were recruited from population registers in 8 European centres. Subjects were asked to complete a postal questionnaire, which enquired about lifestyle and the occurrence of musculoskeletal pain over the past month. ⋯ Compared with those in the lowest tertile of LH, those in the highest tertile were more likely to report some pain (vs no pain, RRR=1.28; 95% CI 1.09 to 1.50) and also CWP (vs no pain, RRR=1.51; 95% CI 1.10 to 2.07). Similar results were found for FSH. Gonadotrophins, but not sex steroid hormone levels, are associated with musculoskeletal pain in men.
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For most healthy subjects, both subjective pain ratings and pain-evoked potentials are attenuated under conditioned pain modulation (CPM; formerly termed diffuse noxious inhibitory controls, or DNIC). Although essentially spinal-bulbar, this inhibition is under cortical control. This is the first study to observe temporal as well as spatial changes in cortical activations under CPM. ⋯ This was followed by reduced activations in the primary and secondary somatosensory cortices, supplementary motor area, posterior insula, and anterior cingulate cortex from 400 ms poststimulus. Our findings show that the prefrontal pain-controlling areas of OFC and amygdala increase their activity in parallel with subjective pain reduction under CPM, and that this increased activity occurs prior to reductions in activations of the pain sensory areas. In conclusion, achieving pain inhibition by the CPM process seems to be under control of the OFC and the amygdala.
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The current study examined the relationship between pain-related fear, physical performance, and pain-related interference in the context of experimentally induced pain to the lower back. Thirty healthy participants completed a test of maximal trunk strength before and after induction of delayed-onset muscle soreness (DOMS) to the trunk extensors. Pain-related fear (Tampa Scale of Kinesiophobia and Pain Anxiety Symptom Scale) was assessed prior to DOMS induction, and measures of current pain and pain-related interference with life activities were obtained 1 day after DOMS induction. ⋯ Current pain intensity and anthropometric factors did not contribute significantly to these outcome measures. To our knowledge, this is the first study to identify the impact of pain-related fear on physical performance among a healthy group of individuals following experimental acute low back injury. The findings extend previous research on psychological variables and simulated injury, and suggest that pain-related fear may be an important vulnerability factor in development of disability following acute pain experience.
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Transient receptor potential ion channel melastatin subtype 8 (TRPM8) is activated by cold temperatures and cooling agents, such as menthol and icilin. Compounds containing peppermint are reported to reduce symptoms of bowel hypersensitivity; however, the underlying mechanisms of action are unclear. Here we determined the role of TRPM8 in colonic sensory pathways. ⋯ Icilin also prevented mechanosensory desensitization and sensitization induced by capsaicin and the TRPA1 agonist AITC (40 μmol/L), respectively. TRPM8 is present on a select population of colonic high threshold sensory neurons, which may also co-express TRPV1. TRPM8 couples to TRPV1 and TRPA1 to inhibit their downstream chemosensory and mechanosensory actions.