Articles: hyperalgesia.
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J. Peripher. Nerv. Syst. · Mar 2019
Anti-allodynic and anti-inflammatory effects of 17α-hydroxyprogesterone caproate in oxaliplatin-induced peripheral neuropathy.
Chemotherapy-induced peripheral neuropathy is a disabling condition induced by several frequently used chemotherapeutic drugs including the front-line agent oxaliplatin (OXA). Symptoms are predominantly sensory with the development of neuropathic pain. Alternative dosing protocols and treatment discontinuation are the only available therapeutic strategies. ⋯ Animals treated with HPGCp showed patterns of response similar to those detected in control animals, while those treated with HPGCt showed a suppression of both hypersensitivities after HPGC administration. We also observed a significant increase in the mRNA levels of activating transcription factor 3, the transcription factor (c-fos), glial fibrillary acidic protein, ionized calcium binding adaptor protein 1, interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNFα) in DRG and spinal cord of OXA-injected animals, and significantly lower levels in rats receiving OXA and HPGC. These results show that HPGC administration reduces neuronal and glial activation markers and is able to both prevent and suppress OXA-induced allodynia, suggesting a promising therapeutic strategy.
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Zhonghua Wei Zhong Bing Ji Jiu Yi Xue · Mar 2019
[Effect of autophagy on N-methy-D-aspartate receptor and hyperalgesia in a rat model of neuropathic pain].
To investigate the effects of autophagy on N-methy-D-aspartate (NMDA) receptor and its subunit NR2B and behavioral test in a rat model of neuropathic pain (NP). ⋯ NP could regulate the variety of NMDA/NR2B and hyperalgesia via increasing autophagy.
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Administration of endogenous mediators or exogenous chemicals in migraine patients provoke early headaches and delayed migraine-like attacks. Although migraine provoking substances are normally vasodilators, dilation of arterial vessels does not seem to be the sole contributing factor, and the underlying mechanisms of the delayed migraine pain are mostly unknown. Sustained mechanical allodynia is a common response associated with the local administration of various proalgesic substances in experimental animals and humans. Here, we investigated the ability of a series of endogenous mediators which provoke or do not provoke migraine in patients, to cause or not cause mechanical allodynia upon their injection in the mouse periorbital area. ⋯ The correspondence between substances that provoke (CGRP; PACAP, histamine, PGE2, PGI2), or do not provoke (VIP and PGF2α), migraine-like attacks in patients and periorbital allodynia in mice suggests that the study of allodynia in mice may provide information on the proalgesic mechanisms of migraine-provoking agents in humans. Results underline the ability of migraine-provoking substances to initiate mechanical allodynia by acting on peripheral terminals of trigeminal afferents.
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Previous reviews have reported that manifestations of pain sensitization may play an important role in the pain experienced by people with knee osteoarthritis. However, it is unknown if manifestations of pain sensitization are common features across other painful knee disorders or if sensitization requires targeted intervention. This review aims to synthesize the published research investigating manifestations of pain sensitization in painful knee disorders and to evaluate if the manifestations of pain sensitization change in response to treatment. ⋯ Our meta-analysis provides evidence of pain sensitization in people with knee osteoarthritis (strong evidence), people with patellofemoral pain (moderate evidence), and postmeniscectomy patients (very limited evidence). However, conflicting evidence exists in patellar tendinopathy. Metaregression indicates that pain is associated with pressure pain thresholds in knee osteoarthritis. In people with knee osteoarthritis and patellofemoral pain, several interventions were found to reduce manifestations of pain sensitization. This review highlights that pain sensitization may be amenable to treatment through exercise therapy, mobilization, and pharmacological and surgical intervention.
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Emerging evidence suggests that opioid use immediately after surgery and trauma may worsen outcomes. In these studies, the authors aimed to determine whether morphine administered for a clinically relevant time period (7 days) in a tibia fracture orthopedic surgery model had adverse effects on postoperative recovery. ⋯ Morphine treatment beginning at the time of injury impairs nociceptive recovery and other outcomes. Measures preventing glial activation through Toll-like receptor 4 signaling may reduce the adverse consequences of postoperative opioid administration.