Corticosteroids suppress ectopic neural discharge originating in experimental neuromas.
Some injured sensory fibers ending in an experimental neuroma in the rat sciatic nerve discharge spontaneously. Furthermore, many become sensitive to a range of physical and chemical stimuli. The resulting afferent barrage is thought to contribute to paresthesias and pain associated with peripheral nerve injury. We report that the development of such ectopic neuroma discharge is largely prevented when the freshly cut nerve end is treated with any of 3 commercially available corticosteroid preparations including two in depot form, triamcinolone hexacetonide (Lederspan) and triamcinolone diacetate (Ledercort), and one in soluble form, dexamethasone (Dexacort). These corticosteroids also produce a rapid and prolonged suppression of ongoing discharge in chronic neuromas that have already become active. The kinetics of corticosteroid suppression of neuroma discharge suggest a direct membrane action rather than an anti-inflammatory action.
D000200:Action Potentials; D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000672:Amputation Stumps; D000818:Animals; D003907:Dexamethasone / Q000627:therapeutic use; D008297:Male; D009463:Neuroma / Q000188:drug therapy* / Q000503:physiopathology; D010525:Peripheral Nerves / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D014221:Triamcinolone / Q000031:analogs & derivatives / Q000627:therapeutic use; D014222:Triamcinolone Acetonide / Q000031:analogs & derivatives / Q000627:therapeutic use
D000305:Adrenal Cortex Hormones; D014221:Triamcinolone; D003907:Dexamethasone; C030262:triamcinolone diacetate; D014222:Triamcinolone Acetonide; C005900:triamcinolone hexacetonide