Dexamethasone decreases blood flow in normal nerves and dorsal root ganglia.

Study Design: An experimental physiologic and histologic study of dexamethasone effects on peripheral nerves.

Objective: To characterize the effect of topically applied 0.4% dexamethasone on acute changes in nerve blood flow and subsequent histologic changes in rat sciatic nerve fibers.

Wallerian degeneration and hyperalgesia after peripheral nerve injury are glutathione-dependent.

Experimental inflammatory compression injury to the sciatic nerve (chronic constriction injury, CCI) induces Wallerian degeneration of axons and damages non-neuronal cells at the injury site in association with the development of exaggerated pain-like behavior, or hyperalgesia, to noxious thermal stimuli in the affected anatomical area. We examined whether glutathione, one of whose many functions is an important endogenous antioxidant, influenced resulting neuropathology and hyperalgesia following CCI. Dietary supplementation of the amino acid N-acetyl-cysteine (NAC), a rate-limiting component of glutathione production, beginning 1 day prior to CCI significantly diminished both Wallerian degeneration, measured by quantitative morphometry of myelinated fibers, and thermal hyperalgesia.