Articles: hyperalgesia.
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Trigeminal neuropathic pain is due to lesion or dysfunction of the nervous system. Dynamic mechanical allodynia is a widespread symptom of neuropathic pain for which mechanisms are still poorly understood. Recent studies demonstrate that forebrain neurons, including neurons in the medial prefrontal cortex (mPFC) are important for the perception of acute and chronic pain. ⋯ Stimulus-evoked pERK-1/2 immunopositive cell bodies displayed a rostrocaudal gradient and layer-selective distribution in the ventral mPFC, being predominant in the rostral ventral mPFC and in layers II-III and V-VI of the ventral mPFC. In layers II-III, intense pERK-1/2 also extended into distal dendrites, up to layer I. These results demonstrate that trigeminal nerve injury induces a significant alteration in the ventral mPFC processing of tactile stimuli and suggest that ERK phosphorylation contributes to the mechanisms underlying abnormal pain perception under this condition.
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Evidence suggests large diameter afferents, presumably in response to centrally mediated changes, augment the mechanical allodynia or hyperalgesia seen in delayed onset muscle soreness (DOMS) conditions. Healthy males aged 18 to 30 (n = 16) performed eccentric exercise eliciting DOMS in the tibialis anterior muscle of a randomly assigned exercised leg. The contralateral leg served as a control. Mechanosensitivity was assessed on the exercised and control legs prior to and 24 hours postexercise via pressure pain thresholds (PPTs). PPTs were assessed at the muscle site, and at a distant segmentally related site, either without vibration or with vibration concurrently applied to the distant muscle, segmentally related, or control extra-segmentally related site. Participants completed a 6-point Likert scale providing a subjective measure of DOMS 5 days postexercise. Baseline mechanosensitivity was not significantly different at any site between the exercised and control legs prior to the exercise. Soreness ratings were higher 24 to 48 hours postexercise (P < .05), and baseline PPTs at the exercised legs muscle site decreased postexercise (P < .001). On day 1 following exercise, segmentally related site PPTs reduced significantly when vibration was applied concurrently to the DOMS affected tibialis anterior muscle (P < .04) compared to baseline mechanosensitivity or extrasegmental control vibration. ⋯ Further evidence is presented by this article indicating that large diameter afferents, presumably via centrally mediated mechanisms, augment the mechanical hyperalgesia seen in DOMS conditions. Future research examining eccentric activity in individuals with likely centrally sensitized conditions may be warranted.
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Nitecapone reduces development and symptoms of neuropathic pain after spinal nerve ligation in rats.
Neuropathic pain is caused by damage or malfunctioning of the nervous system. It is fairly common and more resistant to treatment than other types of pain. Since nitecapone, an inhibitor of catechol-O-methyl-transferase (COMT), has decreased neuropathic symptoms in diabetic rats, we studied its effects in another model of neuropathic pain, the spinal nerve ligation (SNL) model. ⋯ In nitecapone-naïve animals a single dose of nitecapone also reduced mechanical allodynia on the 14th day after the surgery. Nitecapone reduced the symptoms of neuropathic pain after the SNL, which is in line with the earlier study. Our results suggest that nitecapone and other COMT inhibitors should be studied further in the treatment of neuropathic pain.
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Anesthesia and analgesia · Aug 2011
The macrophage-mediated effects of the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone attenuate tactile allodynia in the early phase of neuropathic pain development.
Neuroinflammation triggered by macrophage infiltration into sites of peripheral nerve injury may result in neuropathic pain. Peroxisome proliferator-activated receptor (PPAR)γ signaling regulates the properties of macrophages. However, the macrophage-mediated effects of PPARγ signaling on neuropathic pain triggered by peripheral inflammation have not been investigated. ⋯ Rosiglitazone treatment in the early phase of neuropathic pain significantly alleviated the development of tactile allodynia by regulating macrophage infiltration and production of proinflammatory molecules at the inflamed site. Our results indicate that the activation of PPARγ signaling in macrophages during the early phase may suppress neuropathic pain development.
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Peripheral nerve injury-evoked neuropathic pain still remains a therapeutic challenge. Recent studies support the notion that progesterone, a neuroactive steroid, may offer a promising perspective in pain modulation. ⋯ Our results show that progesterone prevents allodynia in a rat model of sciatic nerve constriction and reinforce its role as a potential treatment for neuropathic pain.