Direct tramadol application on sciatic nerve inhibits spinal somatosensoryevoked potentials in rats

We sought to determine the possible neural conduction blockade of tramadol and whether there is evidence of localized neural toxicity with spinal soma tosensory evoked potential (SSEP) measurements. Male Wistar rats were used. SSEP, elicited by supramaximally stimulating the hind paw and recorded fro m the thoracolumbar and the first and second lumbar interspinous ligaments, was monitored. SSEPs were obtained before drug application as the pretreat ment baseline and measured every 15 min after treatment for 2 h and at 60-m in intervals thereafter until SSEP returned to baseline or for another 4 h. Two small strips of Gelfoam (0.6 x 1.0 cm(2)) soaked with the drug were pl aced under and over the left sciatic nerve for a 30-min period. Gelfoam was prepared with tramadol hydrochloride (Tramal; the US trade name is Ultram) 5, 2.5, and 1.25 mg, diluted if needed with saline to a total volume of 10 0 muL (5%, 2.5%, and 1.25%, respectively). The control data were obtained f rom the right side limb with normal saline by following the same method. Sp inal SSEPs were measured after 48 h to detect the late neural damage. The r esults showed that direct tramadol application on sciatic nerves dose-depen dently reduced both the amplitude and conduction velocity of SSEPs when com pared with the pretreatment baseline. All SSEPs returned to pretreatment ba seline, and no significant changes of SSEP between bilateral limbs were not ed at the 48-h measurements. No evidence of irreversible conduction blockad e indicative of local neural toxicity was seen. Pretreatment with naloxone 1 mg/kg failed to block the changes of SSEP produced by 2.5% tramadol 100 m uL. We conclude that tramadol exerts a local anesthetic-type effect on peri pheral nerves.