Pain
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Randomized Controlled Trial
Activation of the prostaglandin system in response to sleep loss in healthy humans: potential mediator of increased spontaneous pain.
Insufficient duration of sleep is a highly prevalent behavioral pattern in society that has been shown to cause an increase in spontaneous pain and sensitivity to noxious stimuli. Prostaglandins (PGs), in particular PGE2, are key mediators of inflammation and pain, and we investigated whether PGE2 is a potential mediator in sleep-loss-induced changes in nociceptive processing. Twenty-four participants (7 females, age 35.1+/-7.1 years) stayed for 7 days in the Clinical Research Center. ⋯ Urinary PGE2 metabolite significantly increased by about 30% in TSD over sleep condition. TSD-induced increase in spontaneous pain, in particular headache and muscle pain, was significantly correlated with increase in PGE2 metabolite. Activation of the PGE2 system appears to be a potential mediator of increased spontaneous pain in response to insufficient sleep.
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Clinical Trial
Momentary pain and coping in temporomandibular disorder pain: exploring mechanisms of cognitive behavioral treatment for chronic pain.
The purpose of this study was to determine whether cognitive-behavioral treatment (CBT) operates by effecting changes in cognitions, affects, and coping behaviors in the context of painful episodes. Patients were 54 men and women with temporomandibular dysfunction-related orofacial pain (TMD) enrolled in a study of brief (6 weeks) standard conservative treatment (STD) or standard treatment plus CBT (STD+CBT). Momentary affects, pain, and coping processes were recorded on a cell phone keypad four times per day for 7 days prior to treatment, and for 14 days after treatment had finished, in an experience sampling paradigm. ⋯ Concurrent catastrophization was strongly predictive of pain. Active behavioral coping and self-efficacy reported at the prior time point (about 3h previously) were also protective, while prior catastrophization and negative-high arousal mood were predictive of momentary pain. The results suggest that CB treatment for TMD pain can help patients alter their coping behaviors, and that these changes translate into improved outcomes.
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Recent meta-analyses find various magnitudes of placebo analgesia effects in placebo mechanism trials versus placebo control trials, which have led to debate. To further investigate the magnitude of placebo analgesia in placebo mechanism trials the databases "PubMed", "PsycINFO" and "Web of Science" (2002-2007) were searched with the term "placebo analgesia". Twenty-one articles including 24 studies fulfilled the selection criteria (concerning: mechanisms, control, placebo treatment, randomization and pain measures). ⋯ The magnitude of placebo effects was larger in studies that used long-term pain stimuli >20s (d=0.96) as opposed to short-term stimuli (d=0.81) and the largest placebo effects were found in studies wherein hyperalgesia was present (d=1.88). These results replicate our previous finding that placebo analgesic effects are higher in mechanism studies than in placebo control studies. However, since magnitudes of placebo analgesic effects are highly variable it may be valuable to investigate the factors and mechanisms that contribute to this variability as well as differences in magnitudes across types of studies.
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Earlier, we showed that streptozocin (STZ)-induced type 1 diabetes in rats leads to the development of painful peripheral diabetic neuropathy (PDN) manifested as thermal hyperalgesia and mechanical allodynia accompanied by significant enhancement of T-type calcium currents (T-currents) and cellular excitability in medium-sized dorsal root ganglion (DRG) neurons. Here, we studied the in vivo and in vitro effects of gene-silencing therapy specific for the Ca(V)3.2 isoform of T-channels, on thermal and mechanical hypersensitivities, and T-current expression in small- and medium-sized DRG neurons of STZ-treated rats. ⋯ Furthermore, treatments of diabetic rats with daily insulin injections reversed T-current alterations in DRG neurons in parallel with reversal of thermal and mechanical hypersensitivities in vivo. This confirms that Ca(V)3.2 T-channels, important signal amplifiers in peripheral sensory neurons, may contribute to the cellular hyperexcitability that ultimately leads to the development of painful PDN.
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In healthy adults, expectations can modulate the activity of inhibitory bulbo-spinal projections, and can even block the analgesic properties of counter-irritation - a phenomenon that triggers descending inhibition. Since descending inhibition is known to be deficient in fibromyalgia (FM) patients, we tested the possibility that expectancy-mediated analgesia would improve, or even kick-start, the deficient inhibitory responses of FM patients. By measuring subjective pain ratings, spinal withdrawal reflexes, and somatosensory evoked potentials (SEP), it was possible to test whether or not expectancy-mediated analgesia involved descending inhibition in FM patients. ⋯ However, even when analgesia was experienced, the spinal activity of FM patients was abnormal, showing heightened reflex responses. This demonstrates that, unlike healthy subjects, the modulation of pain by expectations in FM fails to influence spinal activity. These results indicate that FMs are capable of expectancy-induced analgesia but that, for them, this form of analgesia does not depend on the recruitment of descending inhibitory projections.