Abstract: The traditional stimulus-response model of physiologic pain is conceptually appealing and has laid the foundation for a more comprehensive understanding of nociceptive pathways. However, physiologic pain alone is a rare entity in the clinical setting. In most situations, the noxious stimulus is not transient and may be associated with significant tissue inflammation and nerve injury. Under such circumstances, the classic “hard-wired” system becomes less relevant and dynamic changes in the processing of noxious input are evident in both peripheral and central nervous systems. This type of pain is called pathologic pain (because it implies that the tissue damage has already occurred) or clinical pain, as ongoing discomfort and abnormal sensitivity are features of the patient’s clinical symptomatology. Pathologic pain may manifest itself in several ways: spontaneous pain which may be dull, burning or stabbing (causalgia), exaggerated pain in response to a noxious stimulus (hyperalgesia), and pain produced by a stimulus which is not normally noxious (allodynia) (1). Pathologic pain may arise from injury to a variety of tissue types invoking distinct neural mechanisms, and it is often further classified into inflammatory pain (involving somatic or visceral structures) or neuropathic pain (involving lesions of the nervous system). In addition, it is useful to characterize clinical pain from a temporal perspective and make the distinction between recently occurring (acute) and long lasting (chronic) pain(1,2).
Publication Year: 2014
Publication Date: 2014-01-01
Language: en
Type: article
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Cited By Count: 2
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