Neuropathic pain can be induced by nerve injury or inflammation. An N-methyl-D-Aspartate (NMDA) antagonist (MK-801), and a sodium channel blocker (lidocaine) have been found to reduce mechanical allodynia. This study was conducted to determine whether intrathecal lidocaine or MK-801 had an antiallodynic effect on established mechanical allodynia in two well-characterized neuropathic pain rat models.

Male Sprague Dawley rats (n = 107) were anesthetized, and the left L5 and L6 spinal nerves were ligated (SNL group) or Freund complete adjuvant (FCA) was administrated to the same spinal nerves (FCA group) in order to cause neuropathic pain. A catheter was then implanted into the lumbar intrathecal space. After obtaining the baseline scores, time-effect curves of each drug were established for the antiallodynic effects of lidocaine (30µg, 100µg and 300µg) and MK-801 (1µg, 3µg, 10µg and 30µg). The allodynic thresholds for the left hind paw withdrawal to von Frey hairs were assessed and converted to %MPE, and the ED₅₀ value was then calculated using the %MPE. The antiallodynic effects of the two groups were then compared by analyzing the dose-response curves and the ED₅₀ values.

Both intrathecal lidocaine and MK-801 resulted in a dose dependent antiallodynic effect. ED₅₀ values and the analysis of dose response curves showed that intrathecal lidocaine provided more effective antiallodynia in the SNL group, whereas intrathecal MK-801 resulted in a greater antiallodynic effect in the FCA group.

In the SNL group, lidocaine had a better effect in reducing allodynic pain, whereas in the FCA group, MK-801 showed a greater antiallodynic effect.