The effects of intrathecal tramadol on spinal somatosensory-evoked potentials and motor-evoked responses in rats.

Abstract

Tramadol has been proven to exert a local anesthetic-type effect on peripheral nerves in both clinical and laboratory studies. In this study, we evaluated the effects of tramadol on sensory and motor neural conduction when administered intrathecally in the rat. Tramadol (0, 1, or 2 mg) was administered through an intrathecal catheter. Spinal somatosensory-evoked potentials (SSEPs) were recorded at the thoracolumbar junction after stimulation of the sciatic nerve. An evoked compound muscle action potential (CMAP) was recorded in the intrinsic muscles of the foot in response to electric stimulation of the lower thoracic (T1213) interspinous space. Both SSEP and CMAP were obtained before drug application as the pretreatment baseline and at 5, 15, and 30 min after treatment, and at 30- or 60-min intervals thereafter for another 4.5 h. SSEP was averaged from 20 responses, whereas CMAP was obtained from a single stimulation. Reproducible SSEPs and CMAP were consistently recorded in all rats. Intrathecal tramadol dose-dependently reduced the amplitude and delayed the latency in both SSEPs and CMAP. Generally, the suppressive effects occurred immediately after injection and recovered over 2 h. Combined administration with 20 micro g of intrathecal naloxone did not attenuate the inhibition of spinal SSEPs. We conclude that intrathecal tramadol causes a dose-related suppressive effect on both sensory and motor neural conduction in the spinal cord. Spinal somatosensory-evoked potentials and evoked compound muscle action potential were used to evaluate the effects of intrathecal tramadol on sensory and motor neural conduction. Intrathecal tramadol dose-dependently reduced the amplitude and delayed the latency of both spinal somatosensory-evoked potentials and compound muscle action potential. These results indicate that tramadol exerts a dose-related central neural blockade.