Pain
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Randomized Controlled Trial
The hidden effects of blinded, placebo-controlled randomized trials: an experimental investigation.
The knowledge of having only a 50% chance of receiving an active drug can result in reduced efficacy in blinded randomized clinical trials (RCTs) compared to clinical practice (reduced external validity). Moreover, minor onset sensations associated with the drug (but not with an inert placebo) can further challenge the attribution of group differences to drug-specific efficacy (internal validity). We used a randomized experimental study with inert placebos (inert substance) vs active placebos (inducing minor sensations), and different instructions about group allocation (probability of receiving drug: 0%, 50%, 100%). ⋯ Moreover, minor drug onset sensations can challenge internal validity. Effect sizes for these mechanisms are medium, and can substantially compete with specific drug effects. For clinical trials, new study designs are needed that better control for these effects.
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Facial expressions during infancy are important to examine, as infants do not have the language skills to describe their experiences. This is particularly vital in the context of pain, where infants depend solely on their caregivers for relief. The objective of the current study was to investigate the development of negative infant facial expressions in response to immunization pain over the first year of life. ⋯ Instead, infants displayed a variety of generalized pain and distress faces aimed at gaining caregiver aid. The development of nonverbal communication in infants, particularly facial expressions, remains an important area of inquiry. Further study into accurately measuring infant negative emotions, pain, and distress is warranted.
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The objective of this study was to evaluate the time-series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (<15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (≥15 days/month). We reanalyzed data from a 28-day observational study of chronic migraine (n=33) and chronic tension-type headache (n=22) sufferers. ⋯ When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days, denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.
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The aim of this study was to establish the somatosensory profiles of patients with cervical radiculopathy and patients with nonspecific neck-arm pain associated with heightened nerve mechanosensitivity (NSNAP). Sensory profiles were compared to healthy control (HC) subjects and a positive control group comprising patients with fibromyalgia (FM). Quantitative sensory testing (QST) of thermal and mechanical detection and pain thresholds, pain sensitivity and responsiveness to repetitive noxious mechanical stimulation was performed in the maximal pain area, the corresponding dermatome and foot of 23 patients with painful C6 or C7 cervical radiculopathy, 8 patients with NSNAP in a C6/7 dermatomal pain distribution, 31 HC and 22 patients with FM. ⋯ Both neck-arm pain groups demonstrated increased cold sensitivity in their maximal pain area (P<.03) and the foot (P<.009), and this was also the dominant sensory characteristic in patients with NSNAP. Both neck-arm pain groups differed from patients with FM, the latter characterised by a widespread gain of function in most nociceptive parameters (thermal, pressure, mechanical pain sensitivity P<.027). Despite commonalities in pain characteristics between the 2 neck-arm pain groups, distinct sensory profiles were demonstrated for each group.
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Motor cortex stimulation is generally suggested as a therapy for patients with chronic and refractory neuropathic pain. However, the mechanisms underlying its analgesic effects are still unknown. In a previous study, we demonstrated that cortical stimulation increases the nociceptive threshold of naive conscious rats with opioid participation. ⋯ Furthermore, motor cortex stimulation enhanced neuronal firing rate and Fos immunoreactivity in the ipsilateral periaqueductal gray. We have also observed a decreased Zif268, δ-aminobutyric acid (GABA), and glutamic acid decarboxylase expression within the same region, suggesting an inhibition of GABAergic interneurons of the midbrain periaqueductal gray, consequently activating neurons responsible for the descending pain inhibitory control system. Taken together, the present findings suggest that inhibition of thalamic sensory neurons and disinhibition of the neurons in periaqueductal gray are at least in part responsible for the motor cortex stimulation-induced antinociception.