Epidural Epinephrine and Clonidine: Segmental Analgesia and Effects on Different Pain Modalities

Background: It is not known whether epidural epinephrine has an analgesic effect per se. The segmental distribution of clonidine epidural analgesia and its effects on temporal summation and different types of noxious stimuli are unknown. The aim of this study was to clarify these issues.

Methods: Fifteen healthy volunteers received epidurally (L2-L3 or L3-L4) 20 ml of either epinephrine, 100 micro gram, in saline; clonidine, 8 micro gram/kg, in saline; or saline, 0.9%, alone, on three different days in a randomized, double-blind, cross-over fashion. Pain rating after electrical stimulation, pinprick, and cold perception were recorded on the dermatomes S1, L4, L1, T9, T6, T1, and forehead. Pressure pain tolerance threshold was recorded at S1, T6, and ear. Pain thresholds to single and repeated (temporal summation) electrical stimulation of the sural nerve were determined.

Results: Epinephrine significantly reduced sensitivity to pinprick at L1-L4-S1. Clonidine significantly decreased pain rating after electrical stimulation at L1-L4 and sensitivity to pinprick and cold at L1-L4-S1, increased pressure pain tolerance threshold at S1, and increased thresholds after single and repeated stimulation of the sural nerve.     

Muscle spasm induced sympathetic reflex bursts on microneurography in a case with pontine demyelination

Microneurography was performed in a 39-year-old woman with demyelination of the pontine white matter associated with muscle spasms in the lower extremities. Single bursts on the microneurogram were observed immediately after cessation of the spasm with no systemic changes in the blood pressure or heart rate. Voluntary tonic flexion of the lower extremities induced similar bursts with small amplitudes. These reflex bursts possessed a characteristic of muscle sympathetic nerve activity, because the latency between the peak of each burst and the prior R-wave on the electrocardiograph was constant. The occurrence of these bursts suggests that a segmental compensatory mechanism in the spinal cord may stabilize the muscle blood flow influenced by muscle contraction.