Articles: hyperalgesia.
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Neurogastroenterol. Motil. · Jul 2020
Peripheral mechanisms contribute to comorbid visceral hypersensitivity induced by preexisting orofacial pain and stress in female rats.
Stress exacerbates many chronic pain syndromes including irritable bowel syndrome (IBS). Among these patient populations, many suffer from comorbid or chronic overlapping pain conditions and are predominantly female. Nevertheless, basic studies investigating chronic psychological stress-induced changes in pain sensitivity have been mostly carried out in male rodents. Our laboratory developed a model of comorbid pain hypersensitivity (CPH) (stress in the presence of preexisting orofacial pain inducing chronic visceral pain hypersensitivity that significantly outlasts transient stress-induced pain hypersensitivity (SIH)) facilitating the study of pain associated with IBS. Since CPH and SIH are phenotypically similar until SIH resolves and CPH persists, it is unclear if underlying mechanisms are similar. ⋯ The data indicate many similarities but some differences in mechanisms contributing to comorbid pain conditions compared to transient stress-induced pain.
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Randomized Controlled Trial Comparative Study Observational Study
Pressure pain threshold and temporal summation in adults with episodic and persistent low back pain trajectories: a secondary analysis at baseline and after lumbar manipulation or sham.
People with chronic low back pain (LBP) typically have increased pain sensitivity compared to healthy controls, however its unknown if pain sensitivity differs based on LBP trajectory at baseline or after manual therapy interventions. We aimed to compare baseline pressure pain threshold (PPT) and temporal summation (TS) between people without LBP, with episodic LBP, and with persistent LBP, and to compare changes over time in PPT and TS after a lumbar spinal manipulation or sham manipulation in those with LBP. ⋯ We found no differences between people with no LBP, episodic LBP, or persistent LBP in baseline PPT or TS. Changes in PPT and TS following a lumbar manual therapy intervention do not appear to differ between LBP trajectories.
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Patients undergoing cancer treatment often experience chemotherapy-induced neuropathic pain at their extremities, for which there is no U.S. Food and Drug Administration-approved drug. The authors hypothesized that local sympathetic blockade, which is used in the clinic to treat various pain conditions, can also be effective to treat chemotherapy-induced neuropathic pain. ⋯ Local sympathetic nerves control the progression of immune responses in dorsal root ganglia and pain-like behaviors in mice after paclitaxel, raising the possibility that clinical strategies already in use for local sympathetic blockade may also offer an effective treatment for patients experiencing chemotherapy-induced neuropathic pain.
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Persistent post-traumatic headache remains a poorly understood clinical entity. Although there are currently no accepted therapies for persistent post-traumatic headache, its clinical symptoms, which primarily resemble those of migraine or tension-type headache, often serve to guide treatment. However, evidence-based justification for this treatment approach remains lacking given the paucity of knowledge regarding the characteristics of these two major persistent post-traumatic headache phenotypes and their etiology. ⋯ Distinct persistent post-traumatic headache symptoms and quantitative sensory testing profiles may be linked to different etiologies, potentially involving various levels of neuropathic and inflammatory pain, and if confirmed in a larger cohort, could be used to further characterize and differentiate between persistent post-traumatic headache subgroups in studies aimed to improve treatment.
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Myofascial pain syndrome (MPS) is a type of skeletal pain identified by myofascial trigger points (MTrPs). The formation of MTrPs is linked to muscle damage. The fibroblast growth factor receptor (FGFR1) has been found to cause pain sensitivity while repairing tissue damage. ⋯ PD173074 increased the mechanical pain threshold of the MTrPs group, and inhibited the expression of p-FGFR1, PI3K-p110γ, and p-AKT. Moreover, LY294002 increased the mechanical pain threshold of the MTrPs group. These findings suggest that FGFR1 may regulate myofascial pain in rats through the PI3K/AKT pathway.