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Neuropathic pain: a maladaptive response of the nervous system to damage

PainSci » bibliography » Costigan et al 2009
Tags: chronic pain, etiology, biology, mind, neurology, pain problems, pro

One article on PainSci cites Costigan 2009: Sensitization in Chronic Pain

PainSci notes on Costigan 2009:

Researchers are looking at where pain is located and how it is triggered. Most likely, pain “is an expression of maladaptive plasticity within the nociceptive system.” This, essentially, is a neural disease state.

Other things affect neuropathic pain, including genetics, gender, and age.

Treatment, then, needs to address these issues, not by just suppressing symptoms by preventing the “maladaptive plasticity” and reducing the other risks.

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Neuropathic pain is triggered by lesions to the somatosensory nervous system that alter its structure and function so that pain occurs spontaneously and responses to noxious and innocuous stimuli are pathologically amplified. The pain is an expression of maladaptive plasticity within the nociceptive system, a series of changes that constitute a neural disease state. Multiple alterations distributed widely across the nervous system contribute to complex pain phenotypes. These alterations include ectopic generation of action potentials, facilitation and disinhibition of synaptic transmission, loss of synaptic connectivity and formation of new synaptic circuits, and neuroimmune interactions. Although neural lesions are necessary, they are not sufficient to generate neuropathic pain; genetic polymorphisms, gender, and age all influence the risk of developing persistent pain. Treatment needs to move from merely suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk.

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