Pain
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Pain disrupts attention, which may have negative consequences for daily life for people with acute or chronic pain. It has been suggested that switching between tasks may leave us particularly susceptible to pain-related attentional disruption, because we need to disengage our attention from one task before shifting it onto another. Switching tasks typically elicit lower accuracies and/or longer reaction times when participants switch to a new task compared with repeating the same task, and pain may exacerbate this effect. ⋯ In studies 2 and 3, we also investigated the effects of type of pain, duration of pain, and analgesics on task performance. We conclude that pain has a small dampening effect on performance overall on switching tasks. This suggests that pain interrupts attention even when participants are engaged in a trial, not only when attention has been disengaged for shifting to a new task set.
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There is significant interest in the potential of Internet-delivered pain management programs for adults with chronic pain. Understanding the characteristics of people who do and do not benefit from Internet-delivered programs will help to guide their safe and effective use. Using a large sample from a previous randomised controlled trial of an established Internet-delivered pain management program, the Pain Course, this study (n = 463) examined whether several demographic, clinical, psychological, and treatment-related variables could be used to predict clinical response in levels of disability, depression, anxiety, or average pain. ⋯ However, no particularly decisive or dominant predictors emerged that were common across time points or across the outcome domains. Reflecting this, the identified predictors explained only 18.1%, 13.7%, 7.6%, and 9.5% of the variance in the likelihood of making a clinical improvement in disability, depression, anxiety, and average pain levels, respectively. The current findings suggest that a broad range of patients may benefit from emerging Internet-delivered pain management programs and that it may not be possible to predict who will or will not benefit on the basis of patients' demographic, clinical, and psychological characteristics.
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Nociceptive long-term potentiation, a use dependent increase in synaptic efficacy in the dorsal horn of the spinal cord is thought to contribute to the development of persistent pain states. So far, no study has analyzed the effects of high-frequency stimulation (HFS) of afferents from deep tissues (muscle and fascia) on pain perception in the back in humans. In 16 healthy volunteers, the multifidus muscle and the overlying thoracolumbar fascia were stimulated with electrical high-frequency pulses (5 × 100 pulses at 100 Hz) through bipolar concentric needle electrodes placed at lumbar level (L3/L4). ⋯ The HFS in muscle had no significant effect on muscle pain, but decreased pain sensitivity of the overlying fascia by 20% (P < 0.05). In additional experiments using the same electrodes and followed over >60 minutes post-HFS, potentiation by fascia HFS was similar to that of skin HFS. These findings show that the spinal input from the fascia can induce long-term changes in pain sensitivity for at least 60 minutes making it a candidate potentially contributing to nonspecific low back pain.
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Endogenous opioid system dysfunction potentially contributes to chronic pain in fibromyalgia (FM), but it is unknown if this dysfunction is related to established neurobiological markers of hyperalgesia. We previously reported that µ-opioid receptor (MOR) availability was reduced in patients with FM as compared with healthy controls in several pain-processing brain regions. In the present study, we compared pain-evoked functional magnetic resonance imaging with endogenous MOR binding and clinical pain ratings in female opioid-naive patients with FM (n = 18) using whole-brain analyses and regions of interest from our previous research. ⋯ These findings are the first to link endogenous opioid system tone to regional pain-evoked brain activity in a clinical pain population. Our data suggest that dysregulation of the endogenous opioid system in FM could lead to less excitation in antinociceptive brain regions by incoming noxious stimulation, resulting in the hyperalgesia and allodynia commonly observed in this population. We propose a conceptual model of affective pain dysregulation in FM.
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Individuals with Alzheimer's disease (AD) are in susceptible patient groups in which pain is an important clinical issue that is often underdiagnosed. However, it is unclear whether decreased pain complaints in patients with AD result from elevated pain tolerance or an impaired ability to communicate sensations. Here, we explored if AD-related pathology is present in key regions of the pain pathway and assessed whether nociceptive thresholds to acute noxious stimulation are altered in the double-mutant APPswe × PS1. ⋯ In the spinal cord, β-amyloid (APP/Aβ) immunoreactivity was observed in dorsal and ventral horn neurons, and the expression of vesicular glutamate transporter 2 (VGLUT2) was significantly reduced, while the expression of the inhibitory peptides enkephalins was increased in TASTPM dorsal horn, consistent with an increased inhibitory tone. TASTPM mice displayed reduced sensitivity to acute noxious heat, which was reversed by naloxone, an opioid antagonist. This study suggests that increased inhibition and decreased excitation in the spinal cord may be responsible for the reduced thermal sensitivity associated with AD-related pathology.