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The dorsal root ganglion in chronic pain and as a target for neuromodulation: a review

PainSci » bibliography » Krames 2015
Tags: neurology, etiology, pro

PainSci notes on Krames 2015:

Neuropathic pain is the pain of distressed or malfunctioning nerves. A dorsal root ganglion is a bulge of neuron cell bodies close to the spinal cord, and, until quite recently, no one suspected it had anything to do with chronic neuropathic pain. Turns out it does: there are several observable changes in the DRG linked to neuropathic pain, suggesting that it’s probably actively involved in neuropathic pain, and not just the “messenger.”

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.

BACKGROUND: In the not-too-distant past, the dorsal root ganglion (DRG) was portrayed as a passive neural structure without involvement in the development or maintenance of chronic neuropathic pain (NP). The DRG was thought of as a structure that merely "supported" physiologic communication between the peripheral nervous system (PNS) and the central nervous system (CNS). Newer scientific information regarding the anatomic and physiologic changes that occur within the DRG as a result of environmental pressures has dispelled this concept and suggests that the DRG is an active participant in the development of NP. This new information, along with new clinical data showing that stimulation of the DRG reduces intensity of pain, suggests that the DRG can be a robust target for neuromodulation therapies.

METHODS: A review of the anatomical and physiological literature regarding the role of the DRG in the development of NP was performed utilizing SciBase, PubMed, and Google Scholar. The information gathered was used to lay an anatomic and physiologic foundation for establishing the DRG as a relevant target for neuromodulation therapies and to formulate a hypothesis as to how electrical stimulation of the DRG might reverse the process and perception of NP.

CONCLUSIONS: The DRG is an active participant in the development of NP. DRG stimulation has multiple effects on the abnormal changes that occur within the DRG as a result of peripheral afferent fiber injury. The sum total of these stimulation effects is to stabilize and decrease hyperexcitability of DRG neurons and thereby decrease NP.

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