Abstract
Background. Because of disparate taxonomic arrays for classification, the American Academy of Pain Medicine has proposed categorizing pain on a neurobiologic basis as eudynia (nociceptive pain), Greek for “good pain,” or maldynia (maladaptive pain), Greek for “bad pain.” The latter has been viewed as maladaptive because it may occur in the absence of ongoing noxious stimuli and does not promote healing and repair.
Objective. To address recent findings on the pathogenesis of pain following neural injury and consider whether the development of maladaptive pain justifies its classification as a disease and to briefly discuss the scope of pharmacologic and non-pharmacologic approaches employed in patients with such pain.
Methods. English language reports on studies using human subjects were selected from a PubMed search of the literature from 1995 to August 2010 and from the Cochrane Library. Further information was obtained from Internet sites of medical specialty and other societies devoted to pain management.
Results. Neural damage to either the peripheral or central nervous system provokes multiple processes including peripheral and central sensitization, ectopic activity, neuronal cell death, disinhibition, altered gene expression, and abnormal sprouting and cellular connectivity. A series of neuro-immune interactions underlie many of these mechanisms. Imaging studies have shown that such damage is characterized by functional, structural, and chemical changes in the brain. Such pain is maladaptive in the sense that it occurs in the absence of ongoing noxious stimuli and does not promote healing and repair.
Conclusion. As defined, maldynia is a multidimensional process that may warrant consideration as a chronic disease not only affecting sensory and emotional processing but also producing an altered brain state based on both functional imaging and macroscopic measurements. However, the absolute clinical value of this definition is not established.
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