Abstract
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 prineuromal injections of normal saline, epinephrine (5 μg), 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.
Original language | English (US) |
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Pages (from-to) | 9-12 |
Number of pages | 4 |
Journal | Pain |
Volume | 49 |
Issue number | 1 |
DOIs | |
State | Published - Apr 1992 |
Keywords
- (Human)
- Chronic pain
- Epinephrine
- Neuroma pain
- Neuropathic pain
- Phantom limb pain
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Anesthesiology and Pain Medicine