Pain response to perineuromal injection of normal saline, epinephrine, and lidocaine in humans.
In animal neuroma models the application of alpha-adrenergic agonists causes a burst of spontaneous afferent activity. The increased activity has been hypothesized to generate nociceptive input. Corroborative work in humans, however, has not been done. Nine subjects with chronic nerve end neuromas received perineuromal injections of normal saline, epinephrine (5 micrograms), and lidocaine in a blinded manner. Qualitative and quantitative pain assessments were performed with each injection. Epinephrine, but not saline, caused an intense increase in reported pain with subjects often commenting that the appendage was "on fire". Lidocaine significantly reduced but did not completely abolish the reported pain. The chemosensitivity of the neuroma to epinephrine may explain some of the clinical responses noted after sympathetic system manipulation. It is likely that alpha-adrenergic sensitivity is only one of many components sustaining or exacerbating pain after nerve injury.
Chabal
Charles
C
Anesthesiology Department, University of Washington School of Medicine and the Veterans Affairs Medical Center, Seattle, WA 98108 USA Neurological Surgery Department, University of Washington and the Veterans Affairs Medical Center, Seattle, WA 98108 USA Division of Neurosurgery, Oregon Health Sciences University, Portland, OR 97201-3098 USA.
Jacobson
Louis
L
Russell
Lisa C
LC
Burchiel
Kim J
KJ
D004837:Epinephrine / Q000008:administration & dosage*; D006801:Humans; D007267:Injections; D008012:Lidocaine / Q000008:administration & dosage*; D009463:Neuroma / Q000503:physiopathology*; D010146:Pain / Q000139:chemically induced* / Q000503:physiopathology; D010147:Pain Measurement; D012965:Sodium Chloride / Q000008:administration & dosage*
D012965:Sodium Chloride; D008012:Lidocaine; D004837:Epinephrine