The journal of pain : official journal of the American Pain Society
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Clinical Trial
Transcranial Alternating Current Stimulation at Alpha Frequency Reduces Pain When the Intensity of Pain is Uncertain.
Alpha activity directly before pain onset has been implicated in pain experience with higher prestimulus alpha associated with lower reported pain. However, expectations about pain intensity also seem to affect prestimulus alpha activity. To date, evidence for a relationship between alpha activity and pain experience has been largely correlational. ⋯ Visual cues preceding the pain stimulus were used to manipulate uncertainty. A significant tACS × Uncertainty × Stimulus intensity interaction was found for reported pain intensity (F2,44 = 4.50, P = .017, partial η2 = .17) and unpleasantness (F1,22 = 4.78, P = .040, partial η2 = .18). Pain experience during the application of somatosensory alpha tACS was significantly lowered compared with sham stimulation, but only when the intensity of an upcoming stimulus was uncertain.
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Previous studies have shown increased pain sensitivity in fertile-aged women with endometriosis in response to mechanical stimuli. As yet, population-based studies on the association of endometriosis with pain sensation and pain symptoms in late fertile age are lacking. The main objective of this population-based cohort study was to investigate whether a history of endometriosis is associated with altered pain sensation and musculoskeletal pain symptoms at age 46 years. ⋯ The results were adjusted for body mass index, smoking, depressive/anxiety symptoms, education, and use of hormonal contraceptives. These unique data revealed an altered pain sensation and a greater likelihood of reporting musculoskeletal pain at age 46 years among women with a history of endometriosis. The results imply that endometriosis has a long-term footprint on affected women, thus underlying the need for psychological support and medical treatment beyond fertile age.
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Although the clinical application of opioids for pain management is often hindered by undesired behavioral impairment, preclinical assays of antinociception typically do not provide information regarding the behaviorally disruptive effects of opioids that may accompany their antinociceptive effects. To address this, we modified a warm water tail withdrawal procedure to determine concurrently the effects of opioids on tail withdrawal latency (antinociception) and indices of food-maintained operant behavior (rates of responding and reinforcement density) in squirrel monkeys. Six opioid agonists were tested, and all produced dose-dependent antinociception and impairment of operant behavior. ⋯ Oxycodone, heroin, buprenorphine, and methadone all produced similar ED50 ratios (.82-1.14), whereas butorphanol yielded a significantly lower ED50 ratio (.17) reflecting behavioral disruption at doses producing only minimal antinociception. The antinociceptive and behaviorally disruptive effects of oxycodone and buprenorphine were further characterized using Schild analysis to calculate apparent pA2 values for antagonism of the 2 drugs by naltrexone. These analyses suggest that µ-receptor mechanisms likely mediate the antinociceptive as well as behaviorally disruptive effects of oxycodone (pA2 values: 8.13 and 8.57) and buprenorphine (pA2 values: 8.6 and 7.9).
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Experimental pain research frequently relies on the recruitment of volunteers. However, because experimental pain research often involves unpleasant and painful sensations, it may be especially susceptible to sampling bias. That is, volunteers in experimental pain research might differ from nonvolunteers on several relevant variables that could affect the generalizability and external validity of the research. ⋯ Study 1 showed that lower levels of fear of pain, higher levels of sensation-seeking, and older age predicted the perceived likelihood of participating in pain research. Study 2 showed significantly higher levels of sensation-seeking in participants who signed up for the pain study compared with those who signed up for the no-pain study. The implications of these findings for future research, as well as the clinical conclusions on the basis of experimental pain research, are discussed.
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Pain after spinal cord injury (SCI-Pain) is one of the most debilitating sequelae of spinal cord injury, characterized as relentless, excruciating pain that is largely refractory to treatments. Although it is generally agreed that SCI-Pain results from maladaptive plasticity in the pain processing pathway that includes the spinothalamic tract and somatosensory thalamus, the specific mechanisms underlying the development and maintenance of such pain are yet unclear. However, accumulating evidence suggests that SCI-Pain may be causally related to abnormal thalamic disinhibition, leading to hyperactivity in the posterior thalamic nucleus (PO), a higher-order nucleus involved in somatosensory and pain processing. ⋯ The substantial tonic activation of presynaptic GABAB receptors on GABAergic projections to PO-characteristic of normal animals-was absent in mice with SCI-Pain. Also absent in mice with SCI-Pain was the normal presynaptic regulation of glutamatergic projections to the PO by GABAB receptors. The loss of these regulatory presynaptic mechanisms in SCI-Pain may be an element of maladaptive plasticity leading to PO hyperexcitability and behavioral pain, and may suggest targets for development of novel treatments.