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Central mechanisms of pathological pain

Nature Medicine volume 16, pages 1258–1266 (2010)Cite this article

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Abstract

Chronic pain is a major challenge to clinical practice and basic science. The peripheral and central neural networks that mediate nociception show extensive plasticity in pathological disease states. Disease-induced plasticity can occur at both structural and functional levels and is manifest as changes in individual molecules, synapses, cellular function and network activity. Recent work has yielded a better understanding of communication within the neural matrix of physiological pain and has also brought important advances in concepts of injury-induced hyperalgesia and tactile allodynia and how these might contribute to the complex, multidimensional state of chronic pain. This review focuses on the molecular determinants of network plasticity in the central nervous system (CNS) and discusses their relevance to the development of new therapeutic approaches.

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Figure 1: Pain circuits.
Figure 2: Disease-induced functional and structural plasticity in neural substrates of pain.
Figure 3: Spinal mechanisms of physiological pain and disease-induced pain hypersensitivity.
Figure 4: Overview of typical signaling pathways used by pronociceptive molecules that mediate disease-induced pain hypersensitivity.

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Acknowledgements

I thank R. Lefaucheur for secretarial assistance and members of the laboratory for discussions.

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    Rohini Kuner

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Kuner, R. Central mechanisms of pathological pain. Nat Med 16, 1258–1266 (2010). https://doi.org/10.1038/nm.2231

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