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The relationship between high sensitivity C-reactive protein and migraine is unclear. The aim of this cross-sectional population-based study was to investigate the association between high sensitivity C-reactive protein and types of headache, and to evaluate the impact of insomnia on this association.
Learn More >Therapeutic interventions for neuropathic pain (NP), such as the NMDA-antagonist ketamine, can vary widely in effectiveness; Here, we conducted a longitudinal functional MRI study to test the hypothesis that the pain relieving effect of ketamine is due to reversal of abnormalities in regional low frequency brain oscillations (LFOs) and abnormal cross-network functional connectivity (FC) of the dynamic pain connectome. We found that: 1) ketamine decreased regional LFOs in the posterior cingulate cortex (PCC) of the default mode network (DMN), 2) a machine learning algorithm demonstrated that treatment-induced brain changes could be used to make generalizable inferences about pain relief, 3) treatment responders exhibited a significant decrease in cross-network static FC between the PCC and regions of the sensorimotor (SM) and salience networks following treatment, 4) the degree of reduced cross-network FC was correlated with the amount of pain relief, and 5) ketamine treatment did not produce significant differences in static or dynamic FC within the ascending nociceptive- or descending antinociceptive pathway. These findings support the proposition that regional LFOs contribute to cross-network connectivity that underlie the effectiveness of ketamine to produce significant relief of neuropathic pain. Together with our recent findings that pre-treatment dynamic FC of the descending antinociceptive pathway can predict ketamine treatment outcomes, these new findings indicate that pain relief from ketamine arises from a combination of a strong and flexible pre-treatment FC of the descending antinocieptive pathway together with plasticity (reduction) of cross-network connectivity of the DMN with SM and salience networks.
Learn More >Pain affects over 70% of individuals with inflammatory bowel disease (IBD), with abdominal and musculoskeletal pain representing the most common complaints. Musculoskeletal pain in IBD is reported to be associated with multiple clinical features, however the scope and nature of pain is not well understood. Primary aims were to identify subgroups of musculoskeletal pain in individuals with IBD based on clinical features of pain, and assess how these subgroups differ in aspects of demographics, comorbidity, and IBD characteristics.
Learn More >Most studies fail to show an association between higher levels of pain-related fear and protective movement behavior in patients with chronic low back pain (CLBP). This may be explained by the fact that only general measures of pain-related fear have been used to examine the association with movement patterns. This study explored whether task-specific, instead of general measures of pain-related fear can predict movement behavior.
Learn More >Perception of sensory stimulation is influenced by numerous psychological variables. One example is placebo analgesia, where expecting low pain causes a painful stimulus to feel less painful. Yet, because pain evolved to signal threats to survival, it should be maladaptive for highly-erroneous expectations to yield unrealistic pain experiences. Therefore, we hypothesised that a cue followed by a highly discrepant stimulus intensity, which generates a large prediction error, will have a weaker influence on the perception of that stimulus. To test this hypothesis we collected two independent pain-cueing datasets. The second dataset and the analysis plan were preregistered ( https://osf.io/5r6z7/ ). Regression modelling revealed that reported pain intensities were best explained by a quartic polynomial model of the prediction error. The results indicated that the influence of cues on perceived pain decreased when stimulus intensity was very different from expectations, suggesting that prediction error size has an immediate functional role in pain perception.
Learn More >Efficacy of galcanezumab in chronic migraine has been demonstrated in a pivotal Phase 3 study. Here, we assess efficacy in patients who have failed ≥2 and ≥1 prior migraine preventives for efficacy and/or safety reasons, and in those who never failed.
Learn More >To investigate whether the two briefest validated ICF-based (International Classification of Functioning, Disability and Health) tools can detect differences between different spinal conditions.
Learn More >Chronic pain affects 1 in 5 people and has been shown to disrupt attention. Here, we investigated whether pain disrupts everyday decision making. In Study 1, 1322 participants completed two tasks online: a shopping decisions task and a measure of decision outcomes over the previous 10 years. Participants who were in pain during the study made more errors on the shopping task than those who were pain-free. Participants with a recurrent pain condition reported more negative outcomes from their past decisions than those without recurrent pain. In Study 2, 44 healthy participants completed the shopping decisions task with and without experimentally-induced pain. Participants made more errors while in pain than while pain-free. We suggest that the disruptive effect of pain on attending translates into poorer decisions in more complex and ecologically valid contexts, that the effect is causal, and that the consequences are not only attentional, but financial.
Learn More >Neuropathic mechanisms are involved in burning mouth syndrome (BMS), and variation of the dopamine D2 receptor (DRD2) gene contributes to experimental pain perception. We investigated whether neurophysiologic findings differ in BMS patients compared to healthy controls, and whether 957C>T polymorphism of the DRD2 gene influences thermal sensitivity or pain experience in BMS.
Learn More >Sensory neuron nicotinic acetylcholine receptors (nAChRs) contribute to pain associated with tissue injury. However, there are marked differences between rats and mice with respect to both the properties and distribution of nAChR currents in sensory neurons. Since both species are used to understand pain signaling in humans, we sought to determine whether the currents present in either species was reflective of those present in human sensory neurons. Neurons from lumbar 4/5 dorsal root ganglia were obtained from adult male and female organ donors. Nicotine-evoked currents were detected in 40 of 47 neurons (85%). In contrast to the naïve mouse, in which almost all nAChR currents are transient, or the rat, in which both mouse-like transient and more slowly activating and inactivating currents are detected, all the currents in human DRG neurons were slow, but slower than those in the rat. Currents were blocked by the nAChR antagonists mecamylamine (30 µM), but not by the TRPA1 selective antagonist HC-030031 (10µM). Single cell PCR analysis of nicotinic receptor subunit expression in human DRG neurons are consistent with functional data indicating that receptor expression is detected 85 ± 2.1% of neurons assessed (n = 48, from 4 donors). The most prevalent co-expression pattern was α3/β2 (95 ± 4% of neurons with subunits), but α7 subunits were detected in 70 ± 3.4% of neurons. These results suggest that there are not only species differences in the sensory neuron distribution of nAChR currents between rodent and human, but that the subunit composition of the channel underlying human nAChR currents may be different from those in the mouse or rat. PERSPECTIVE: The properties and distribution of nicotine-evoked currents in human sensory neurons were markedly different from those previously observed in mice and rats. These observations add additional support to the suggestion human sensory neurons maybe an essential screening tool for those considering moving novel therapeutics targeting primary afferents into clinical trials.
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