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Title:
Pain due to nerve damage: Are inflammatory mediators involved | Inflammation Research
Description:
Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones. A better understanding of the mechanisms involved should lead to improved therapies for neuropathic pain.
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Keywords {🔍}
google, scholar, pubmed, pain, peripheral, nerve, hyperalgesia, neurosci, rat, levine, sympathetic, article, injury, inflammation, inflammatory, cells, neuropathic, neuropathy, taiwo, lett, role, macrophages, experimental, model, privacy, cookies, content, research, mediators, tracey, neurophysiol, products, sci, publish, search, damage, postganglionic, mechanisms, access, res, rats, nature, neurons, goetzl, usa, glia, data, information, log, journal,
Topics {✒️}
month download article/chapter sympathetic neuron-derived prostaglandins post-injury pain hypersensitivity directly-acting hyperalgesic agent voltage-sensitive na+ channels mediated byα2-adrenergic receptors noradrenaline-induced prostalgandin production inflammatory mediators involved privacy choices/manage cookies sciatic nerve injury full article pdf denervation-induced inflammation peripheral nerve injury nerve injury depends peripheral neuropathy produced sympathetic postganglionic neurons postganglionic sympathic terminals causalgiform pain produced peri-axonal inflammation sectioned peripheral nerve mediation byα2 adrenoreceptors dorsal horn neurons painful constriction neuropathy nerve growth factor postganglionic sympathetic neurones sympathetically maintained pain sustained graded pain cutaneous nociceptive threshold nociceptive peripheral neurons formalin-induced nociception norepinephrine-induced increase paravertebral sympathetic ganglia reflex sympathetic dystrophy experimental peripheral neuropathy european economic area scope submit manuscript related subjects mediating mechanical allodynia tumour necrosis factorα amino-terminal octapeptide chemotactic proinflammatory cytokines intravenous regional block ngf-induced hyperalgesia pain due primary afferent nociceptors clonidine relieves hyperalgesia conditions privacy policy sympathetic nervous system enzyme histochemical study damaged peripheral nerves
Questions {❓}
- Epineurial peptides: a role in neuropathic pain?
- Human monocytes/macrophages: NO or no NO?
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headline:Pain due to nerve damage: Are inflammatory mediators involved
description:Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones. A better understanding of the mechanisms involved should lead to improved therapies for neuropathic pain.
datePublished:
dateModified:
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Pain
Hyperalgesia
Neuropathy
Nerve injury
Inflammatory mediators
Immunology
Pharmacology/Toxicology
Rheumatology
Allergology
Dermatology
Neurology
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headline:Pain due to nerve damage: Are inflammatory mediators involved
description:Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones. A better understanding of the mechanisms involved should lead to improved therapies for neuropathic pain.
datePublished:
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pageStart:407
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Pain
Hyperalgesia
Neuropathy
Nerve injury
Inflammatory mediators
Immunology
Pharmacology/Toxicology
Rheumatology
Allergology
Dermatology
Neurology
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