Pain
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Controlled Clinical Trial
Placebo analgesia is accompanied by large reductions in pain-related brain activity in irritable bowel syndrome patients.
Previous experiments found that placebos produced small decreases in neural activity of pain-related areas of the brain, yet decreases were only statistically significant after termination of stimuli and in proximity to when subjects rated them. These changes could reflect report bias rather than analgesia. This functional magnetic resonance imaging (fMRI) study examined whether placebo analgesia is accompanied by reductions in neural activity in pain-related areas of the brain during the time of stimulation. ⋯ Large reductions in pain and in brain activation within pain-related regions (thalamus, somatosensory cortices, insula, and anterior cingulate cortex) occurred during the placebo condition. Results indicate that decreases in activity were related to placebo suggestion and a second factor (habituation/attention/conditioning). Although many factors influence placebo analgesia, it is accompanied by reduction in pain processing within the brain in clinically relevant conditions.
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This study used positron emission tomography (PET) and [11C]diprenorphine to compare the in vivo distribution abnormalities of brain opioid receptors (OR) in patients with peripheral (n=7) and central post-stroke pain (CPSP, n=8), matched for intensity and duration. Compared with age- and sex-matched controls, peripheral neuropathic pain (NP) patients showed bilateral and symmetrical OR binding decrease, while in CPSP binding decrease predominated in the hemisphere contralateral to pain. In CPSP patients, interhemispheric comparison demonstrated a significant decrease in opioid binding in posterior midbrain, medial thalamus and the insular, temporal and prefrontal cortices contralateral to the painful side. ⋯ While bilateral binding decrease in both NP groups may reflect endogenous opioid release secondary to chronic pain, the more important and lateralised decrease specific to CPSP suggests opioid receptor loss or inactivation in receptor-bearing neurons. Opioid binding decrease was much more extensive than brain anatomical lesions, and was not co-localised with them; metabolic depression (diaschisis) and/or degeneration of OR neurons-bearing secondary to central lesions appears therefore as a likely mechanism. Central and peripheral forms of NP may differ in distribution of brain opioid system changes and this in turn might underlie their different sensitivity to opiates.
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The theory of chemical radiculitis had been put forward about 30 years ago, but as yet it has not been proved by clinical studies. The aim of the current studies was to determine whether the annular tear of a painful disc proved by discography is the cause of radiating leg pain (radiculopathy) in patients with discogenic low back pain. Forty-two patients with discogenic low back pain at single disc level with concomitant radiating leg pain were studied in order to analyse the relationship between site of annular tear and side of radiating leg pain. ⋯ The current studies found that there was a significant positive correlation between the site of annular tear and the side of radiation pain. Abnormalities of electromyogram and reduction of motor nerve conduction velocity were found on the side of radiating leg pain. The studies indicated that leakage of chemical mediators or inflammatory cytokines, which are produced in the painful disc, into epidural space through annular tear could lead to injury to adjacent nerve roots, and it might constitute the primary pathophysiologic mechanism of radiating leg pain in patients with discogenic low back pain but with no disc herniation.
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Despite the prominence of fear-avoidance models of chronic pain, there is a paucity of research regarding the origins of pain-related fear. Based on the premise that insecure attachment could be a developmentally based origin of elevated fear of pain, associations between adult attachment dimensions and constructs included in fear-avoidance models of chronic pain were investigated. Consistent with Bartholomew and Horowitz's [Bartholomew K, Horowitz LM. ⋯ The model of self dimension had significant positive associations with each of the fear-avoidance constructs. The model of others dimension had a significant positive association with pain catastrophizing, but was not significantly associated with fear of pain and pain hypervigilance. Future research directions and potential clinical implications are discussed.
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Previous studies using a primary task procedure have demonstrated that an experimental pain stimulus interrupts ongoing task performance in healthy volunteers and patients, and that this interruption is intensified by catastrophic thinking about pain and the perceived threat value of the pain stimulus. However, no studies have investigated the interruption of attention by relevant threatening stimuli in specific patient samples. ⋯ The patients showed a more pronounced deterioration of performance compared to controls when the neck rotation and extension fixations were introduced. Within the groups, neither catastrophic thinking nor fear predicted the magnitude of the performance deterioration.