Pain
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Fibromyalgia (FM) tends to coexist with gastroesophageal reflux disease (GERD). This retrospective cohort study was conducted to determine the bidirectional association between FM and GERD, using a nationwide database, the National Health Insurance of Taiwan. We established 2 study arms, including 35,117 patients with FM in arm 1 and 34,630 patients with GERD in arm 2, newly diagnosed between 2000 and 2010. ⋯ The GERD cohort ultimately had a 1.5-fold higher incidence of FM than the non-GERD cohort (5.76 vs 3.96 per 1000 person-years), with an aHR of 1.44 (95% CI = 1.29-1.60). The present study suggests a bidirectional relationship between FM and GERD. There is a greater risk of developing GERD for patients with FM than developing FM for patients with GERD.
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Contextual influences on pain communication in couples with and without a partner with chronic pain.
This is an experimental study of pain communication in couples. Despite evidence that chronic pain in one partner impacts both members of the dyad, dyadic influences on pain communication have not been sufficiently examined and are typically studied based on retrospective reports. Our goal was to directly study contextual influences (ie, presence of chronic pain, gender, relationship quality, and pain catastrophizing) on self-reported and nonverbal (ie, facial expressions) pain responses. ⋯ None of the examined variables predicted self-reported pain. Results suggest that contextual variables influence pain communication in couples, with distinct influences for PTs and POs. Moreover, self-report and nonverbal responses are not displayed in a parallel manner.
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Offset analgesia (OA) represents a disproportionately large decrease of pain perception after a brief, temporary increment of thermal pain stimulus and was reported attenuated in patients with neuropathic pain. We examined whether OA depends on the increment duration before offset, and whether individual features of OA distinguish patients with chronic pain and healthy controls. We used a Peltier-type thermal stimulator and OA paradigms including 5-, 10-, or 15-s duration of 1°C-increment (T2) over 45°C. ⋯ Maximum VAS latency was longer in patients than in controls and negatively correlated with [INCREMENT]OA in patients. An OA index ([INCREMENT]OA/[maximum VAS latency]) proved diagnostic of chronic pain with an area under the receiver operating characteristic curve at 0.897. Patients with chronic pain showed impairment of OA and reduced temporal sharpening of pain perception, which might imply possible disturbance of the endogenous pain modulatory system.
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The dynamics of noxious sensation shapes pain perception, yet the memory of the temporal dimension of pain remains almost completely unexplored. Here, brain activity during the memory of pain duration was contrasted with that associated with the memory of pain intensity using functional magnetic resonance imaging and a delayed reproduction task. Participants encoded, maintained during a short delay, and reproduced (1) the "duration" of pain (ie, onset-to-offset), (2) the "dynamics" of pain (ie, evolution of pain over time), or (3) the intensity of pain (ie, control with no explicit temporal processing required). ⋯ In contrast, the memory delay of the dynamic task involved the bilateral supplementary motor area and the frontoparietal attentional network. Although SI, SII, and insula may contribute to the memory trace of pain sensation, other areas less commonly reported in pain studies are associated with time processing and may therefore contribute to the processing of temporal aspects of pain. Results further suggest a differential role of core timing regions of the brain depending on specific task instructions and attentional allocations to the single dimension of time, as compared to the joint processing of both time and intensity.
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Along with the well-known rewarding effects, activation of nicotinic acetylcholine receptors (nAChRs) can also relieve pain, and some nicotinic agonists have analgesic efficacy similar to opioids. A major target of analgesic drugs is the descending pain modulatory pathway, including the ventrolateral periaqueductal gray (vlPAG) and the rostral ventromedial medulla (RVM). Although activating nAChRs within this circuitry can be analgesic, little is known about the subunit composition and cellular effects of these receptors, particularly within the vlPAG. ⋯ Furthermore, intra-vlPAG α7 antagonist pretreatment blocked PHA-543,613-induced antinociception via either administration method. Systemic administration of submaximal doses of the α7 agonist and morphine produced additive antinociceptive effects. Together, our findings indicate that the vlPAG is a key site of action for α7 nAChR-mediated antinociception.