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Pathological Pain

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In order to fully answer this question, it is important to understand the definition of pain. The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” (Mersky and Bogduk ed 1994). The physiological function of the pain sensory system is protective in nature, to shield the body from actual or potential tissue damage. Pathological pain, on the other hand, is described as “spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred” (Coderre et al 1993).
Nociceptors are peripheral sensory neurons that detect the physical sensation of …show more content…

There are many mechanisms for the sensitisation of nociceptors. A common scenario for this occurrence is when peripheral tissue is subjected to exogenous injury, whether it be mechanical, chemical, or toxic. Injury results in localised increase in inflammatory mediators, leading to the sensitisation of nociceptors. Upregulation and increased expression of various membrane receptors is the most common mechanism. Ionotropic receptors, Gq protein-coupled metabotropic receptors, Gs protein-coupled metabotropic receptors, and mitogen-activated protein kinase have been shown to be upregulated in nociceptors in response to the presence of inflammatory mediators (Sessle ed 2008). The resultant effect is increased conductance, lowered threshold for the initiation of action potentials, spontaneous depolarisation, and increased after-discharges to supra-threshold stimuli (Sessle ed 2008). Sprouting, or the growth of neuronal axons into the damaged tissue, also contributes to pathological pain. Increased number of nociceptive axons increases the opportunity for spatial and temporal summation and activation of nociceptors, which under normal conditions would not be activated. Sufficient concentration of inflammatory mediators can also lead to the activation of nociceptors which do not participate in the detection of noxious stimulus (Sessle ed 2008). With an increased number of nociceptors feeding back to the CNS, the sensation of pain is

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