Articles: hyperalgesia.
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Central sensitization (CS) contributes to patient variability when treating pain in endometriosis. Targeting this process may alleviate hyperalgesia and allodynia in women refractory to current treatments. Currently, there has been no review of targeted treatments for central sensitization in women with endometriosis. Therefore, this review aims to identify and summarize the findings of studies regarding the availability and efficacy of targeted treatments for CS in women with endometriosis. ⋯ Given the lack of evidence for any treatment, all require further research to determine treatment efficacy before options will be available clinically. There is a clear need for consistency in defining and identifying CS in study populations. This review identifies areas of interest, particularly surgery and nerve stimulation, from which future research must stem.
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Resistance training-based exercise is commonly prescribed in the clinic for the treatment of chronic pain. Mechanisms of aerobic exercise for analgesia are frequently studied, while little is known regarding resistance training mechanisms. We developed a resistance training model in mice and hypothesized resistance training would protect against development of muscle pain, mediated through the activation of androgen receptors. ⋯ However, single administration of flutamide (1, 3, 10 mg/kg) in resistance-trained animals had no effect on existing exercise-induced protection against muscle pain. Therefore, resistance training acutely increases lactate and testosterone and strength overtime. Eight weeks of resistance training prevents the development of hyperalgesia through the activation of androgen receptors in an animal model of muscle pain.
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Randomized Controlled Trial
Predicting treatment response with sensory phenotyping in post-traumatic neuropathic pain.
Currently available treatments for neuropathic pain are only modestly efficacious when assessed in randomized clinical trials and work for only some patients in the clinic. Induced-pain or gain-of-function phenotypes have been shown to predict response to analgesics (vs placebos) in patients with neuropathic pain. However, the predictive value of these phenotypes has never been studied in post-traumatic neuropathic pain. ⋯ These data suggest that hyperalgesia, but not allodynia, predicts response to pregabalin in patients with chronic post-traumatic neuropathic pain. This study extends the growing data supporting the utility of induced-pain phenotypes to predict response to analgesics in post-traumatic neuropathic pain. Sensory phenotyping in large, multisite trials through the use of a structured clinical exam has the potential to accelerate the development of new analgesics and improve the generalizability of clinical trial results.
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Obese individuals report a higher susceptibility to chronic pain. Females are more likely to have chronic pain and excess adipose tissue. Chronic pain is associated with dysfunctional pain-modulatory mechanisms. Body composition differences may be associated with pain modulation differences in males and females. The purpose of this study was to investigate body composition (lean vs fat mass) differences and pain-modulatory functioning in healthy males and females. ⋯ Men and women exhibited similar CPM and EIH despite marked differences in body composition. Our findings suggest whole-body and limb-specific lean tissue mass and fat mass do not influence CPM and EIH in adults without chronic pain.
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We previously established a macaque model of central post-stroke pain (CPSP) and confirmed the involvement of increased activity of the posterior insular cortex (PIC) and secondary somatosensory cortex (SII) to somatosensory stimuli in mechanical allodynia by a combination of imaging techniques with local pharmacological inactivation. However, it is unclear whether the same intervention would be effective for thermal hyperalgesia. Therefore, using the macaque model, we examined behavioural responses to thermal stimuli following pharmacological inactivation of the PIC/SII. ⋯ CPSP is caused by stroke lesions in the sensory system and characterized by mechanical allodynia or thermal hyperalgesia. Inactivation of the PIC/SII has an analgesic effect on mechanical allodynia; however, it is not clear whether the same intervention could reduce thermal hyperalgesia. Here, using the macaque model, we demonstrated that inactivation of these cortices reduces hypersensitivity to thermal stimuli. This result emphasizes that increased PIC/SII activity can contribute to abnormal pain of multiple modalities.