Tanya Z. Fischer & Stephen G. Waxman
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.
Author affiliations
T. Z. Fischer & S. G. Waxman
Yale University Center for Neuroscience and Regeneration Research, Veterans Affairs Connecticut Healthcare System, 950 Campbell Avenue, West Haven, CT 06516, USA (T. Z. Fischer, S. G. Waxman).
Correspondence to: S. G. Waxman stephen.waxman@yale.edu
Published online 13 July 2010
Nature Reviews Neurology 6, 462-466 (August 2010) | doi:10.1038/nrneurol.2010.90
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