Pain
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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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This study aimed to identify distinctive trajectories for pain/disability and posttraumatic stress disorder (PTSD) symptoms following whiplash injury and to examine the effect of injury compensation claim lodgement on the trajectories. In a prospective study, 155 individuals with whiplash were assessed at <1month, 3, 6 and 12months post injury. Outcomes at each time point were Neck Disability Index (NDI) and the Posttraumatic Stress Diagnostic Scale (PDS). ⋯ Following whiplash injury, there are distinct pathways of recovery for pain/ disability and PTSD symptoms. Management of whiplash should consider the detrimental association of compensation claim with psychological recovery and recovery of those with mild to moderate pain/disability levels. However, claim lodgement has no significant association with a more severe pain and disability trajectory.
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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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Muscular tension is assigned an important role in the development and maintenance of chronic pain syndromes. It is seen as a psychophysiological correlate of learned fear and avoidance behavior. Basic theoretical models emphasize classical conditioning of muscular responses as a mechanism of pain chronification. ⋯ Furthermore a significant relation was found between muscular responses and the experience of pain 1day after the experiment. Muscular responses can be learned via classical conditioning. TTH and BP patients revealed a higher number of unconditioned and conditioned responses.
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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.