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bibliography * The PainScience Bibliography contains plain language summaries of thousands of scientific papers and others sources, like a specialized blog. This page is about a single scientific paper in the bibliography, Costigan 2009.

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

updated
Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci. 2009;32:1–32. PubMed #19400724.
Tags: chronic pain, etiology, biology, mind, neurology, pain problems, pro

PainSci summary of Costigan 2009?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focussed on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★★☆?4-star ratings are for bigger/better studies and reviews published in more prestigious journals, with only quibbles. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.

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 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

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.

related content

One article on PainScience.com cites Costigan 2009 as a source:


This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog.