Pain
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Individual differences in interoceptive sensitivity are associated with differences in reported intensity of emotional experience, vulnerability to anxiety and mood disorder and capacity for emotional self-regulation. Enhanced sensitivity to autonomic state is often accompanied by increased autonomic reactivity. Here we tested the hypothesis that healthy people classified as more interoceptively sensitive, by their performance of a heartbeat monitoring task, will demonstrate enhanced perception of pain. ⋯ We observed significant relationships between heightened interoceptive sensitivity and both enhanced sensitivity and decreased tolerance to pain. These effects were accompanied by a more pronounced parasympathetic decrease and a change in sympathovagal balance during pain assessment in the high, compared to the low, interoceptively sensitive group. Our study provides novel evidence that interoceptive sensitivity is associated with the experience and tolerability of pain in conjunction with reactive changes in autonomic balance.
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This research examined selective biases in visual attention related to fear of pain by tracking eye movements (EM) toward pain-related stimuli among the pain-fearful. EM of 21 young adults scoring high on a fear of pain measure (H-FOP) and 20 lower-scoring (L-FOP) control participants were measured during a dot-probe task that featured sensory pain-neutral, health catastrophe-neutral and neutral-neutral word pairs. Analyses indicated that the H-FOP group was more likely to direct immediate visual attention toward sensory pain and health catastrophe words than was the L-FOP group. ⋯ Conversely, groups did not differ on EM indices of attentional maintenance (i.e., first fixation duration, gaze duration, and average fixation duration) or reaction times to dot probes. Finally, both groups showed a cycle of disengagement followed by re-engagement toward sensory pain words relative to other word types. In sum, this research is the first to reveal biases toward pain stimuli during very early stages of visual information processing among the highly pain-fearful and highlights the utility of EM tracking as a means to evaluate visual attention as a dynamic process in the context of FOP.
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Endurance exercise is known to promote sustained antinociceptive effects, and there is evidence that the reduction of pain perception mediated by exercise is driven by central opioidergic neurotransmission. To directly investigate the involved brain areas and the underlying neural mechanisms in humans, thermal heat-pain challenges were applied to 20 athletes during 4 separate functional magnetic resonance imaging (fMRI) scans, i.e., before and after 2 hours of running (exercise condition) and walking (control condition), respectively. Imaging revealed a reproducible pattern of distributed pain-related activation in all 4 conditions, including the mesial and lateral pain systems, and the periaqueductal gray (PAG) as a key region of the descending antinociceptive pathway. ⋯ The fact that running, but not walking, reproducibly elevated β-endorphin levels in plasma indicates involvement of the opioidergic system in exercise. This may argue for an elevated opioidergic tone in the brain of athletes, mediating antinociceptive mechanisms. Our findings provide the first evidence using functional imaging to support the role of endurance exercise in pain modulation.
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It has been recently described that disruption of the neural mechanisms of emotion-based decision making occurs in both chronic pain patients and in animal models of pain; moreover, it also has been shown that chronic pain causes morphological and functional changes in the prefrontal cortex that may be crucial for this decision-making dysfunction. However, it is not known whether pain alone is capable of altering the neuronal encoding of decision exhibited by prefrontal neurons. We have previously shown that naïve animals have risk-averse performance in the rodent gambling task, whereas chronic pain animals reverse their choice preference and become risk prone. ⋯ Our results show that the instantaneous neuronal firing rate was correlated with the probability of choosing a specific lever in 62.5% of the neurons; however, although in the control sessions 61% of the neurons encoded the reward magnitude, after the pain onset only 16% of the neurons differentiated small from large rewards. Moreover, we found that the fraction of risk-sensitive neurons recorded in each session predicted the overall risk bias of the animal. Our data suggest that orbitofrontal cortex encoding of risk preference is compromised in chronic pain animals.
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Oxaliplatin is a third-generation platinum-based chemotherapy drug that has gained importance in the treatment of advanced metastatic colorectal cancer. Its dose-limiting side effect is the production of chronic peripheral neuropathy. Using a modified model of oxaliplatin-induced sensory neuropathy, we investigated plastic changes at the cortical level as possible mechanisms underlying the chronicity of pain sensation in this model. ⋯ Quantification of the magnitude of neuronal extracellular signal-regulated kinase (ERK) phosphorylation in cortical neurons as a marker of neuronal activity revealed a 10-fold increase induced by oxaliplatin treatment, suggesting that neurons of cortical areas involved in transmission of painful stimuli undergo a chronic cortical excitability. We further demonstrated, using cortical injection of lentiviral vector shRNA against Kv2.2, that down-regulation of this potassium channel in naive animals induced a sustained thermal and mechanical hypersensitivity. In conclusion, although the detailed mechanisms leading to this cortical excitability are still unknown, our study demonstrated that a cortical down regulation of potassium channels could underlie pain chronicity in this model of chemotherapy-induced neuropathic pain.