Pain
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'Diffuse noxious inhibitory controls' (DNIC), a form of supraspinal descending endogenous analgesia, requires a noxious conditioning stimulus for pain attenuation. This may be partly dependent on a distraction effect. The term "conditioned pain modulation" (CPM) has recently been introduced to describe the psychophysical paradigm to test DNIC. ⋯ Post-hoc tests revealed a significant reduction in pain intensity ratings under Combined (21.2+/-2.3; mean+/-SEM) compared to CPM alone (16.0+/-2.3) (P<0.05). Furthermore, at all levels of distraction there were always a few subjects who were not distracted despite expressing CPM. Based on the additive effect of CPM and distraction on pain inhibition, and the cases of no distraction despite CPM, we suggest that CPM acts independently from distraction.
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It has been proposed that painful and non-painful referred sensations (RSs) are associated with reorganization of sensory pathways in patients with complete spinal cord injury (SCI). In order to investigate the referred sensation (RS) phenomenon and its correlation with neuropathic pain (NP) 48 patients with complete SCI, 24 with chronic NP and 24 without pain or paraesthesias were studied using clinical examination and neurophysiological tests. Patients reporting RSs were re-examined at 2 and 10weeks after the first examination. ⋯ None of the patients in the SCI group without NP presented RS. In conclusion, our results indicate that RS is relatively frequent in patients with complete SCI and NP. The common occurrence of RS in patients with NP and the location of the sensations in the same area as NP suggest that pain and RS share common pathophysiological mechanisms.
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The natural history of sensory function in the first 6months after herpes zoster (HZ) was determined in a cohort of 94 subjects at elevated risk for developing post-herpetic neuralgia (PHN). All four visits included ratings of pain and sensory symptoms, mapping areas of altered sensation and allodynia, and quantitative thermal and mechanical sensory testing. The last three visits included the capsaicin response test. ⋯ The hypothesis that PHN develops because of a failure to recover normal neural function was not supported. Sensory recovery proceeded at the same rate in eventual pain-free and eventual PHN subjects and is not a requirement for pain resolution. Early interventions that reduce neural injury or enhance recovery should be of benefit.
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Patients with chronic pain may have difficulties estimating their own physical activity level in daily life. Pain-related factors such as depression and pain intensity may affect a patients' ability to estimate their own daily life activity level. This study evaluates whether patients with Chronic Low Back Pain (CLBP) who are more depressed and/or report more pain indeed have a lower objectively assessed daily life activity level or whether they only perceive their activity level as lower. ⋯ There was a moderate association between the self-reported and objectively assessed activity levels (beta=0.39, p<0.01). The discrepancy between the two was significantly and negatively related to depression (beta=-0.19, p=0.01), indicating that patients who had higher levels of depression judged their own activity level to be relatively low compared to their objectively assessed activity level. Pain intensity was not associated with the perception of a patient's activity level (beta=0.12, ns).
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Behavioral studies have suggested that placebo analgesia is partly mediated by the endogenous opioid system. Expanding on these results we have shown that the opioid-receptor-rich rostral anterior cingulate cortex (rACC) is activated in both placebo and opioid analgesia. However, there are also differences between the two treatments. ⋯ Furthermore, the rACC activity co-varied with the prefrontal regions in the placebo condition specifically. A similar correlation between rACC and vlPFC was reproduced in another dataset involving emotional placebo and correlated with the degree of the placebo effect. Our results thus support that placebo is different from specific treatment with a prefrontal top-down influence on rACC.