Pain
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Patient characteristics associated with the course and severity of low back pain (LBP) and disability have been the focus of extensive research, however, known characteristics do not explain much of the variance in outcomes. The relationship between anterior trunk pain (ATP) and LBP has not been explored, though mechanisms for visceral referred pain have been described. Study objectives were: (1) determine prevalence of ATP in chronic LBP patients, (2) determine whether ATP is associated with increased pain and disability in these patients, and (3) evaluate whether ATP predicts the course of pain and disability in these patients. ⋯ The presence of ATP did not affect the clinical course of LBP outcomes. The results of this study suggest that patients who present with LBP and ATP have higher pain and disability levels than patients with localised LBP. Visceral referred pain mechanisms may help to explain some of this difference.
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Nocebo and placebo effects have been found to modulate several neurochemical systems, such as cholecystokinin, endogenous opioids, and endocannabinoids. Here we show that also the cyclooxygenase-prostaglandins pathway can be modulated by both nocebos and placebos. In fact, we found that negative expectation, the crucial element of the nocebo effect, about headache pain led to the enhancement of the cyclooxygenase-prostaglandins pathway, which, in turn, induced pain worsening. ⋯ We found a significant increase in headache and salivary prostaglandins and thromboxane in the nocebo group compared to the control group, suggesting that negative expectations enhance cyclooxygenase activity. In addition, placebo administration to headache sufferers at high altitude inhibited the nocebo-related component of pain and prostaglandins synthesis, which indicates that the cyclooxygenase pathway can be modulated by both nocebos and placebos. Our results show for the first time how nocebos and placebos affect the synthesis of prostaglandins, which represent an important target of analgesic drugs, thus emphasizing once again the notion that placebos and drugs may use common biochemical pathways.
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Therapeutic use of general sodium channel blockers, such as lidocaine, can substantially reduce the enhanced activity in sensory neurons that accompanies chronic pain after nerve or tissue injury. However, because these general blockers have significant side effects, there is great interest in developing inhibitors that specifically target subtypes of sodium channels. Moreover, some idiopathic small-fiber neuropathies are driven by gain-of-function mutations in specific sodium channel subtypes. ⋯ Moreover, mechanical stimuli initiated bursts of action potential firing in specific subpopulations that continued for minutes after removal of the force and were not susceptible to conduction failure. Surprisingly, despite the intense afferent firing, the behavioral effects of the Nav1.8 mutation were quite modest, as only frankly noxious stimuli elicited enhanced pain behavior. These data demonstrate that a Nav1.8 gain-of-function point mutation contributes to intense hyperexcitability along the afferent axon within distinct sensory neuron subtypes.
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Editorial Comment
To redistribute muscle activity in pain, or not: that is the question.