This study systematically reviewed differences in pain perception between athletes and normally active controls. We screened MEDLINE, Sport-Discus, EMBASE, Web of Science, PsycINFO, PSYNDEX, and the citations of original studies and systematic reviews. All studies on experimentally induced pain that compared pain perception between athletes and normally active controls were eligible. The main outcome measures were pain tolerance and pain threshold. Effects are described as standardized mean differences and were pooled using random-effects models. Fifteen studies including 899 subjects met the inclusion criteria. Twelve of these studies assessed pain tolerance, and 9 studies examined pain threshold. A meta-analysis of these studies revealed that athletes possessed higher pain tolerance compared to normally active controls (effect size calculated as Hedges' g=0.87, 95% confidence interval [CI(95)] 0.53-1.21; P<0.00001), whereas available data on pain threshold were less uniform (Hedges' g=0.69, CI(95) 0.16-1.21; P=0.01). After exclusion of studies with high risk of bias, differences between groups in pain threshold were not significant any longer. Our data suggest that regular physical activity is associated with specific alterations in pain perception. Psychological and biological factors that may be responsible for these alterations are discussed.
Age- and gender-matched reference values are essential for the clinical use of quantitative sensory testing (QST). To extend the standard test sites for QST-according to the German Research Network on Neuropathic Pain-to the trunk, we collected QST profiles on the back in 162 healthy subjects. Sensory profiles for standard test sites were within normal interlaboratory differences. QST revealed lower sensitivity on the upper back than the hand, and higher sensitivity on the lower back than the foot, but no systematic differences between these trunk sites. Age effects were significant for most parameters. Females exhibited lower pressure pain thresholds (PPT) than males, which was the only significant gender difference. Values outside the 95% confidence interval of healthy subjects (considered abnormal) required temperature changes of >3.3-8.2 °C for thermal detection. For cold pain thresholds, confidence intervals extended mostly beyond safety cutoffs, hence only relative reference data (left-right differences, hand-trunk differences) were sufficiently sensitive. For mechanical detection and pain thresholds, left-right differences were 1.5-2.3 times more sensitive than absolute reference data. The most sensitive parameter was PPT, where already side-to-side differences >35% were abnormal. Compared to trunk reference data, patients with postherpetic neuralgia exhibited thermal and tactile deficits and dynamic mechanical allodynia, mostly without reduced mechanical pain thresholds. This pattern deviates from other types of neuropathic pain. QST reference data for the trunk will also be useful for patients with postthoracotomy pain or chronic back pain.
FMS patients showed increased sensitivity for different pain modalities at all measured body areas, suggesting central disinhibition as a potential mechanism. CBP participants in contrast, showed localized alterations within the affected segment possibly due to peripheral sensitization.
Findings considering conditioned pain modulation (CPM) in chronic back pain (CBP) are contradictory. This might be because many patients with CBP report pain in further areas of the body, and altered CPM might influence spatial extent of pain rather than CBP per se. Therefore, we compared CPM in patients with CBP with different pain extent. Patients with fibromyalgia syndrome (FMS), for whom CPM impairment is reported most consistently, were measured for comparison. Based on clinical evaluation and pain drawings, patients were categorized into chronic local back pain (CLP; n = 53), chronic widespread back pain (CWP; n = 32), and FMS (n = 92). Conditioned pain modulation was measured by the difference in pressure pain threshold (test stimuli) at the lower back before and after tonic heat pain (conditioning stimulus). We also measured psychosocial variables. Pressure pain threshold was significantly increased in CLP patients after tonic heat pain (P < 0.001) indicating induction of CPM. Conditioned pain modulation in CLP was significantly higher than that in CWP and FMS (P < 0.001), but CPM in CWP and FMS did not differ. Interestingly, a higher number of painful areas (0-10) were associated with lower CPM (r = 0.346, P = 0.001) in CBP but not in FMS (r = -0.013, P = 0.903). Anxiety and depression were more pronounced in FMS than in CLP or CWP (P values <0.01). Our findings suggest that CPM dysfunction is associated with CWP and not with FMS as suggested previously. FMS seems to differ from CWP without FMS by higher psychosocial burden. Moreover, patients with CBP should be stratified into CLP and CWP, and centrally acting treatments targeting endogenous pain inhibition seem to be more indicated the higher the pain extent.
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