The journal of pain : official journal of the American Pain Society
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In this research, we examined effects of higher versus lower threat contexts on attention biases in more and less pain-fearful chronic pain subgroups via eye-tracking methodology. Within a mixed chronic pain sample (69 women, 29 men), biases in orienting and maintenance of visual attention were assessed during the standardized image pair presentation phase (2,000 ms) of a modified visual dot probe task featuring painful-neutral (P-N) image pairs (lower threat context) and a parallel task in which these P-N pairs cued potential pain (higher threat context). ⋯ Although trait-based fear of pain was not related to any gaze bias index in either task, between task analyses indicated the sample reported more state fear, directed their initial gaze less often, and displayed longer overall gaze durations toward pain images in the higher threat context in which P-N trials signaled potential pain. Results supported the threat interpretation model premise that persons with chronic pain have difficulty disengaging from moderately threatening visual painful cues.
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Increased HCN Channel Activity in the Gasserian Ganglion Contributes to Trigeminal Neuropathic Pain.
Orofacial neuropathic pain caused by trigeminal nerve injury is a debilitating condition with limited therapeutic options. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability and are involved in the development and maintenance of chronic pain. However, the effect of HCN channel activity in the Gasserian ganglion on trigeminal neuropathic pain has not been examined. We evaluated nociceptive behaviors after microinjection of the HCN channel blockers ZD7288 or ivabradine into the Gasserian ganglion in rats with trigeminal nerve injury. Both blockers dose-dependently ameliorated evoked and spontaneous nociceptive behavior in rats with trigeminal neuropathic pain. Moreover, the clinically available HCN channel blocker ivabradine showed a prolonged antinociceptive effect. In the Gasserian ganglion, HCN1 and HCN2 are major HCN isoforms. After trigeminal nerve injury, the counts of HCN1 as well as HCN2 immuno-positive punctae were increased in the ipsilateral Gasserian ganglions. These results indicate that the increased HCN channel activity in the Gasserian ganglion directly contributes to neuropathic pain resulting from trigeminal nerve injury. ⋯ Trigeminal nerve damage-induced orofacial pain is severe and more resistant to standard pharmacological treatment than other types of neuropathic pain. Our study suggests that targeting HCN channel activities in the Gasserian ganglion may provide an alternative treatment of trigeminal neuropathy including trigeminal neuralgia.
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In recent years, the disappointing history of translation in pain research has undergone significant scrutiny. The escalation of knowledge and understanding related to presumed pain in neuropathic and inflammatory animal models contrasted with the unsatisfactory record of "bench-to-bedside" translation has raised many questions about the validity and clinical relevance of preclinical models and methods of behavioral assessment. Although many opinions have been expressed one of the overriding concerns and greatest barriers to the widening gap between preclinical research and the development of new interventions has been the underappreciated distinction between pain and nociception. ⋯ Other issues important to the discussion include but are not limited to the predictive validity of preclinical models, and the neglect of gender, age, and comorbidities in the design of preclinical studies. On the clinical side, the lack of sanitization of phenotypes in clinical trials has also contributed to the insufficient success of efforts to translate basic research to the clinic. The current review will discuss these and other issues believed to have contributed to the existing obstacles and challenges facing pain research along with making recommendations for the future.
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Conditioned pain modulation (CPM), a psychophysical paradigm that is commonly used to infer the integrity of endogenous pain-altering systems by observation of the effect of one noxious stimulus on another, has previously identified deficient endogenous analgesia in fibromyalgia (FM) and other chronic pain conditions. The mechanisms underlying this deficiency, be they insufficient inhibition and/or active facilitation, are largely unknown. ⋯ Higher resting connectivity between this cluster and cortical pain processing regions was associated with more efficient inhibitory CPM in both groups, whereas PAG connectivity with the dorsal pons was associated with greater CPM inhibition only in HC. Greater PAG connectivity to the caudal pons/rostral medulla, which was pain-inhibitory in HC, was associated with pain facilitation in FM patients.
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Musculoskeletal pain changes how people move. Although experimental pain is associated with increases in the variability of motor output, it is not clear whether motor-evoked pain in clinical conditions is also associated with increases in variability. In the current study, we measured jaw force production during a visually guided force paradigm in which individuals with chronic jaw pain and control subjects produced force at 2% of their maximum voluntary contraction (low target force level) and at 15% of their maximum voluntary contraction (high target force level). ⋯ We showed that the chronic jaw pain group exhibited greater force variability compared with controls irrespective of the force level, whereas the accuracy of force production did not differ between groups. Furthermore, predictors of force variability shifted from trait measures of pain intensity and pain interference at the low force level to state measures of pain intensity at the high force level. Our observations show that motor-evoked jaw pain is associated with increases in force variability that are predicted by a combination of trait measures and state measures of pain intensity and pain interference.