Articles: hyperalgesia.
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The Journal of physiology · Nov 2010
Endogenous descending modulation: spatiotemporal effect of dynamic imbalance between descending facilitation and inhibition of nociception.
In conscious rats, we investigated the change of nociceptive paw withdrawal reflexes elicited by mechanical and heat stimuli during intramuscular (i.m.) 5.8% hypertonic (HT) saline elicited muscle nociception. i.m. injection of HT saline caused rapid onset, long lasting (around 7 days), bilateral mechanical hyperalgesia, while it induced bilateral, slower onset (1 day after the HT saline injection), long-term (about 1-2 weeks) heat hypoalgesia. Ipsilateral topical pre-treatment of the sciatic nerve with 1% capsaicin significantly prevented the occurrence of both the bilateral mechanical hyperalgesia and the contralateral heat hypoalgesia. Intrathecal administration of either 6-hydroxydopamine hydrobromide (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT), and intraperitoneal injection of naloxone all markedly attenuated the HT saline induced bilateral heat hypoalgesia, but not the mechanical hyperalgesia. ⋯ However, this discriminative function is physiologically silent or inactive, and can be triggered by stimulation of peripheral C-fibre afferents. Importantly, in contrast to the rapid onset of descending facilitation, the late occurrence of descending inhibition suggests a requirement of continuous C-fibre input and temporal summation. Thus, a reduction of C-fibre input using exogenous analgesic agents, i.e. opioids, may counteract the endogenous descending inhibition.
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J Orthop Sports Phys Ther · Nov 2010
Specific mechanical pain hypersensitivity over peripheral nerve trunks in women with either unilateral epicondylalgia or carpal tunnel syndrome.
Case-control study with blinded examiner. ⋯ Bilateral mechanical nerve pain hypersensitivity is related to specific and particular nerve trunks in women with either unilateral LE or CTS. Our results suggest the presence of central and peripheral sensitization mechanisms in individuals with either LE or CTS.
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To describe the presence of widespread pressure pain hyperalgesia and myofascial trigger points (TrPs) in neck and shoulder muscles in patients with postmastectomy pain. ⋯ Our findings revealed bilateral widespread pressure pain hypersensitivity in patients with postmastectomy pain. In addition, the local and referred pain elicited by active TrPs reproduced neck and shoulder/axillary complaints in these patients. These results suggest peripheral and central sensitization in patients with postmastectomy pain.
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Opioids are the most potent drugs for treatment of acute and chronic pain. However, accumulating evidence suggests that opioids may paradoxically also enhance pain, often referred to as opioid-induced hyperalgesia. Opioid-induced hyperalgesia is defined as an increased sensitivity to pain or a decreased pain threshold in response to opioid therapy. ⋯ However, it remains unclear whether opioid-induced hyperalgesia develops during continuous chronic application of opioids or on their withdrawal. This review provides a comprehensive summary of clinical research concerning opioid-induced hyperalgesia and the molecular mechanisms of opioid withdrawal and opioid tolerance and other potential mechanisms which might induce hyperalgesia during opioid therapy will be discussed. The status quo of our knowledge will be summarized and the clinical relevance of opioid-induced hyperalgesia will be discussed.