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Neuropathic pain in diabetes—evidence for a central mechanism

Nature Reviews Neurology volume 6, pages 462–466 (2010)Cite this article

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Abstract

Hyperexcitability of and aberrant spontaneous impulse generation by damaged first-order sensory neurons and their peripheral axons are well-established processes that strongly contribute to pain associated with diabetic neuropathy. Studies in the past 5 years, however, suggest that, as in many neuropathic pain disorders, central neuropathic mechanisms can also contribute to pain experienced with diabetes. These studies have demonstrated that thalamic dysfunction occurs in patients with diabetes mellitus, and that in experimental models of this disease neurons in the ventral posterolateral thalamus can become hyperexcitable, firing at abnormally high frequencies and generating aberrant spontaneous activity. In this article, we discuss these findings, which suggest that thalamic neurons can act as central generators or amplifiers of pain in diabetes.

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Figure 1: VPL thalamic neuron activity in a model of painful diabetic neuropathy.
Figure 2: Models of neuropathic pain.

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Acknowledgements

This work was supported in part by the Rehabilitation Research Service and the Medical Research Service, US Department of Veterans Affairs, and the Erythromelalgia Association. The Center for Neuroscience and Regeneration Research is a collaboration of the Paralyzed Veterans of America and the United Spinal Association with Yale University.

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  1. Yale University Center for Neuroscience and Regeneration Research, Veterans Affairs Connecticut Healthcare System, 950 Campbell Avenue, West Haven, 06516, CT, USA

    Tanya Z. Fischer & Stephen G. Waxman

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Correspondence to Stephen G. Waxman.

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Fischer, T., Waxman, S. Neuropathic pain in diabetes—evidence for a central mechanism. Nat Rev Neurol 6, 462–466 (2010). https://doi.org/10.1038/nrneurol.2010.90

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