We sought to determine the possible neural conduction blockade of tramadol and whether there is evidence of localized neural toxicity with spinal somatosensory evoked potential (SSEP) measurements. Male Wistar rats were used. SSEP, elicited by supramaximally stimulating the hind paw and recorded from the thoracolumbar and the first and second lumbar interspinous ligaments, was monitored. SSEPs were obtained before drug application as the pretreatment baseline and measured every 15 min after treatment for 2 h and at 60-min 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 placed 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 100 microL (5%, 2.5%, and 1.25%, respectively). The control data were obtained from the right side limb with normal saline by following the same method. Spinal SSEPs were measured after 48 h to detect the late neural damage. The results showed that direct tramadol application on sciatic nerves dose-dependently reduced both the amplitude and conduction velocity of SSEPs when compared with the pretreatment baseline. All SSEPs returned to pretreatment baseline, and no significant changes of SSEP between bilateral limbs were noted at the 48-h measurements. No evidence of irreversible conduction blockade 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 microL. We conclude that tramadol exerts a local anesthetic-type effect on peripheral nerves.

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.

The hydrophobic hydration of dimethylsulfoxide (DMSO)/D2O was explored using a combination of the high-pressure method and ab initio calculations. The frequencies of the C–H stretching vibration of DMSO increase as the mole fraction of D2O increases, while no appreciable changes in spectral shapes are observed upon dilution. Interestingly, the infrared spectra of DMSO/D2O observed under high-pressure exhibits dramatic changes, while the new spectral features locating at ∼2942 and ∼3033 cm−1 appear. The spectral changes were attributed to the combined effect of C–H–O hydrogen bonding between C–H in DMSO and oxygen atom in D2O, a phase change, pressure increase, etc. Ab initio calculation results, forecasting the frequency shift of the C–H stretching vibration as C–H–O is interacting via hydrogen bonding, are discussed. The reorganization of the hydrogen-bond network or geometry may be responsible for spectral changes as the pressure was elevated.

The present study was designed to test whether tramadol is effective in the control of neuropathic pain in rats. Chronic constriction injury (CCI) of the sciatic nerve was induced over the left hind limb in male Sprague-Dawley rats. Identical surgery was performed on the opposite side except that the sciatic nerve was not ligated (sham surgery). Paw withdrawal latency (PWL) to heat was tested for each hind paw 1 day before surgery and on the 4th day after surgery to ensure the development of thermal hyperalgesia. In the acute treatment groups, saline or tramadol was administered subcutaneously at doses of 10, 20 or 30 mg/kg, and PWLs were measured 30, 60, 90, 120, 150 and 180 min after treatment. In the semi-chronic treatment groups, continuous systemic administration of tramadol 40 mg/kg/day or saline for 7 days was provided at a uniform rate via osmotic mini pumps. Tramadol reversed PWL in a dose-dependent manner in the acute treatment groups. PWLs were significantly reversed at 2 days after tramadol infusion, and this effect was sustained throughout the remainder of the treatment period in comparison with the saline group. Tramadol also resulted in a decreased sensitivity to thermal stimulus on the sham limb both in acute and semi-chronic administration. We conclude that both acute and semi-chronic tramadol treatment relieves thermal hyperalgesia effectively in rats with CCI of the sciatic nerve. This indicates that tramadol shows promise as a potential treatment for relief of neuropathic pain in humans.

A 32‐year‐old man who suffered from complex regional pain syndrome type I (CRPS I) of the right upper limb after surgical release of carpal tunnel syndrome of the right hand is the subject of this case report. Symptoms and signs over the right hand were alleviated under rehabilitation and conventional pharmacological management, but severe painful swelling of the right wrist persisted. Axillary brachial plexus block (BPB) with patient controlled analgesia (PCA) was performed on the 32nd postoperative day, which soon resulted in significant reduction of pain with gradual improvement of function of the right wrist. Conclude that axillary BPB with PCA may provide patients with CRPS I of the upper limb a feasible and effective treatment.