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Primary hyperalgesia

Increased responsiveness to noxious stimuli is termed hyperalgesia. It occurs following injury or disease and encompasses enhanced responses as well as reduced thresholds to a given noxious stimulus. Primary hyperalgesia occurs in the damaged area whereas secondary hyperalgesia occurs in the area surrounding it. [Pg.606]

Clinical manifestation Primary hyperalgesia, allodynia, spontaneous pain Secondary hyperalgesia, allodynia, spontaneous pain, aberrantly referred pain ... [Pg.929]

Distinguish between primary hyperalgesia and centrally mediated hyperalgesia... [Pg.77]

An injured area is typically more sensitive to subsequent stimuli. As a result, painful stimuli, or even normally nonpainful stimuli, may cause an excessive pain response. An increase in the sensitivity of nociceptors is referred to as primary hyperalgesia. A classic example of hyperalgesia is a bum. Even light touch of a burned area may be painful. [Pg.80]

Primary hyperalgesia occurs within the zone of injury and is caused by changes at the injury site itself. Secondary hyperalgesia occurs around the zone of injury and results from neuroplasticity and remodelling. [Pg.198]

Hyperalgesia describes a state of increased pain sensitivity and enhanced perception following acute injury which is related to peripheral release of intracellular or humoral noxious mediators [7,9-11]. Primary hyperalgesia (peripheral sensitization) describes an altered state of sensibility in which the intensity of painful sensation induced by noxious and non-noxious... [Pg.4]

Cytokines and interleukins released as part of the peripheral inflammatory response can circulate to and increase production of PCs in the brain. The accumulation of noxious mediators at the site of injury results in ongoing nociceptor stimulation, nociceptor recruitment and development of primary hyperalgesia. [Pg.8]

Hyperalgesia is defined by the International Association for the Study of Pain (lASP) as an increased response to a stimulus which is normally painful . Primary hyperalgesia or peripheral sensitization reflects the activation and sensitization of nociceptive A delta and polymodal C-fiber terminal endings within the injured area. Secondary hyperalgesia, or central sensitization, involves spinal neuroplasticity and facilitation... [Pg.17]

Primary hyperalgesia follows primary nociceptor activation (or transduction) in response to mechanical. [Pg.17]

Hyperalgesia may be observed following incision, crush, amputation, and blunt trauma Primary hyperalgesia... [Pg.20]

The recognition and control of nociceptor transduction and development of primary hyperalgesia are key to reducing the intensity and duration of acute pain. Nociceptor sensitization leads to reductions in noxious thresholds, increased pain disability, and delayed rehabilitation. The physiological response to transduction and the initiation of nociception can be limited or eliminated by peri operative administration of non-opioid analgesics and anti-inflammatory agents (e.g. NS AIDS, steroids). Although opioids can inhibit... [Pg.21]


See other pages where Primary hyperalgesia is mentioned: [Pg.929]    [Pg.456]    [Pg.933]    [Pg.6]    [Pg.929]    [Pg.521]    [Pg.17]    [Pg.17]    [Pg.18]    [Pg.21]    [Pg.23]    [Pg.44]   
See also in sourсe #XX -- [ Pg.18 , Pg.23 ]




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Hyperalgesia

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