Pain
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Recent evidence points to a possible overlap in the neural systems underlying the distressing experience that accompanies physical pain and social rejection (Eisenberger et al., 2003). The present study tested two hypotheses that stem from this suggested overlap, namely: (1) that baseline sensitivity to physical pain will predict sensitivity to social rejection and (2) that experiences that heighten social distress will heighten sensitivity to physical pain as well. In the current study, participants' baseline cutaneous heat pain unpleasantness thresholds were assessed prior to the completion of a task that manipulated feelings of social distress. ⋯ Additionally, for those in the social rejection conditions, greater reports of social distress were associated with greater reports of pain unpleasantness to the thermal stimuli delivered at the end of the game. These results provide additional support for the hypothesis that pain distress and social distress share neurocognitive substrates. Implications for clinical populations are discussed.
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Low back pain is considered to fluctuate over time, and related prognostic factors may behave similarly, therefore classification of prognosis may be affected by timing of assessment. We aimed to investigate the implications of timing of assessment of prognosis in low back pain. In a prospective cohort of primary care low back pain consulters aged 30-59 years, 359 returned questionnaires at baseline, one-month and one-year. ⋯ Presence of the indicators at both time points was associated with even higher risk; people with persistent high pain intensity had 15 times the risk of a poor outcome (relative risk 15.1; 95% confidence interval 6.7-33.8) compared with people not reporting high pain at either point. Combining information on prognostic indicators from two time points provides better classification of low back pain patients' eventual outcome than a single measurement alone. This increased accuracy in predicting prognosis is relevant to both clinical and research practice.
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Recent evidence suggests that emotional picture-viewing is a reliable method of engaging descending modulation of spinal nociception. The present study attempted to replicate these findings and determine the effect of noxious stimulus predictability. Participants viewed pictures from the International Affective Picture System (IAPS), during which pain and nociceptive flexion reflexes (NFR) were elicited by electric shocks delivered to the sural nerve. ⋯ However, descending modulation could not be detected in NFRs resulting from predictable noxious stimuli. Although preliminary, this study implies that separate mechanisms are responsible for emotional modulation of nociception at spinal vs. supraspinal levels, and that predictable noxious events may disengage modulation at the spinal level. The current paradigm could serve as a useful tool for studying descending modulation.
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Functional magnetic resonance imaging (fMRI) of blood oxygen level dependent (BOLD) haemodynamic responses was used to study the effects of the noxious substance capsaicin on whole brain activation in isofluorane anaesthetised rats. Rats (n=8) received intradermal injection of capsaicin (30 microg/5 microl), or topical cream (0.1%) capsaicin and BOLD responses were acquired for up to 120 min. Effects of capsaicin versus placebo cream treatment on the BOLD response to a 15 g mechanical stimulus applied adjacent to the site of cream application were also studied. ⋯ Capsaicin also produced increases in BOLD signal intensity in other regions that contribute to pain processing, such as the parabrachial nucleus and superior colliculus. Mechanical stimulation in capsaicin-treated rats, but not placebo-treated rats, induced a significant decrease in BOLD signal intensity in the PAG (p<0.001). These data demonstrate that the noxious substance capsaicin produces brain activation in the midbrain regions and reveals the importance of the PAG in central sensitization.
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Studies implicate endocannabinoids in the acute and chronic actions of opioid drugs, including the genesis of physical dependence. Previous evidence suggests that spinal release of calcitonin gene-related peptide (CGRP) and activation of its receptors contribute to opioid physical dependence. The release of CGRP at the spinal level is modulated by cannabinoid (CB1)-receptors. ⋯ Intrathecal co-administration of CB1-receptor antagonists, AM-251 or SR141716A, with daily morphine attenuated the behavioral manifestations of withdrawal. Treatment with AM-251 also reduced the depletion of CGRP, suppressed Fos-induction, and prevented the increase in capsaicin-evoked spinal CGRP release. Altogether, this study suggests that endocannabinoid activity, expressed via CB1-receptors, contributes to the induction of opioid physical dependence through spinal modulation of CGRP.