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to a system of empirical treatment that has been uncritically accepted by many. are better explained as secondary hyperalgesia of peripheral neural origin. [1, 35,37,41,[80][81][82][83]In addition, hyperalgesia and allodynia are For the focus of this study on adherence to pain treatment guidelines, Diagnostic and treatment algorithm for noncardiac chest pain (NCCP). … Figures - uploaded by Visceral hyperalgesia is thought to be the primary under-. Treat underlying causes can be amplified by central secondary hyperalgesia and Treatment of pain associated with equine laminitis.

2016-05-11 2000-06-01 Opioid-induced hyperalgesia (OIH) is defined as a state of nociceptive sensitization caused by exposure to opioids. The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain could actually become more sensitive to certain painful stimuli. The type of pain experienced might be the Neuropathic pain affects 7–10% of people, but responds poorly to pharmacotherapy, indicating a need for better treatments. Mechanistic research on neuropathic pain frequently uses human surrogate models of the secondary hyperalgesia that is a common feature of neuropathic pain. Experimentally induced secondary hyperalgesia has been manipulated with pharmacological and non-pharmacological After heat stimulation the area of secondary hyperalgesia was quantified with a foam brush (allodynia) and a 26 g von Frey hair (mechanical hyperalgesia) by stimulating the skin distant from the treated area and slowly moving inward until the subject indicated the stimulus had become noxious or until the subject reported a definite change in sensation (i.e., burning, tenderness, more intense pricking). 2016-04-07 Allodynia (pain due to a stimulus that does not usually provoke pain) and hyperalgesia (increased pain from a stimulus that usually provokes pain) are prominent symptoms in patients with neuropathic pain. Both are seen in various peripheral neuropathies and central pain disorders, and affect 15–50% of patients with neuropathic pain.

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Hyperalgesia is defined as "An increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves". It is divided into 2 types, primary and secondary.

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He now finds that after the first or second treatment with HBOT, 50 to 75 percent of chronic regional pain syndrome (RSD/CRPS) patients get their normal sleep Treating Opioid-induced Hyperalgesia.

For example, bad sunburn can cause temporary allodynia, and touching sunburned skin, or running cold or warm water over it, can be very painful. Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues. Various studies of humans and animals have demonstrated that primary or secondary hyperalgesia can develop in response to both chronic and acute exposure to opioids. This side effect can be severe enough to warrant discontinuation of opioid treatment.
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Hyperalgesia was produced 2 days later by an intradermal injection of capsaicin (50 μg, 10 μl) at a point midway between the two treatment areas. Secondary hyperalgesia to noxious mechanical stimuli was investigated by using a blade probe (32 and 64 g) attached to a computer-controlled mechanical stimulator. Hyperalgesia, '-algesia' from Greek algos, ἄλγος) is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves. Tem Spread of hyperalgesia is likely due to central sensitization of nociceptive neurons in the spinal cord by primary nociceptive afferent input (neurogenic hyperalgesia), which is the basis of secondary hyperalgesia in the vicinity of any site of injury.
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For example, through a process of central sensitization, the firing of dorsal horn nociceptors can change dramatically in the setting of injury (produced by either tissue or nerve damage). Following an injury or cell damage two main things can occur. Primary hyperalgesia and secondary hyperalgesia. Secondary hyperalgesia is indicative of central sensitization. [1] Because secondary hyperalgesia is short-lived, persistent pain after surgery in large part may be primary hyperalgesia, perhaps amplified by central sensitization. The authors thank David Kramer for technical assistance during these experiments and Drs. Corey L. Cleland and Gerald F. Gebhart for reviewing the manuscript.