Phantom limb pain refers to the presence of painful sensations in an absent limb parts and it has been classified as neuropathic pain syndrome[1-3]. The first medical description of post amputation sensation was given in 1552 by Ambroise Pare, a French military surgeon, who noticed that patients complain of severe pain in the missing limb following amputation[4]. Phantom limb pain and sensations may have its onset immediately or years after the amputation. There are reports of two peak periods of onset, the first within a month and the second a year after amputation[5]. Generally, pain diminishes in both frequency and duration during the first 6 months after amputation[6].

          Although 80% of patients may experience phantom limb pain after lower limb amputation[4, 7], its reported incidence varies widely due to the absence of a unified definition of phantom limb pain or to the fact that many patients don’t report their pain for fear of being stigmatized as mentally ill.

        The underlying mechanisms of development of phantom limb pain are poorly understood, however major changes in both central and peripheral nervous system in response to peripheral nerve injury and subsequent alterations in the peripheral sensory input are postulated for the development of phantom sensations. Central sensitization, occurring at the level of spinal cord is likely to play a important role in ongoing pain[8-10]. Animal models of peripheral nerve injury have shown that activation of the N-methyl D-aspartate (NMDA) receptor is integral to the process of central sensitization, particularly in nerve injury models[11,12]. Laboratory studies implicate that sensory input from noxious stimuli at the time of nerve injury with acute central neural plasticity leads to persistent neuropathic pain. NMDA antagonists administered to animals prior to nerve injury significantly reduced behavioral signs of neuropathic pain and associated neurochemical changes[13,14]. The mechanism of action is thought to be prevention of spinal cord sensitization.

                In a randomized study assessing the effect of pre-emptively modulating sensory input with epidural ketamine on post-amputation pain and sensory processing, Wilson and others demonstrated that epidural ketamine didn’t affect significantly onset of phantom pain and stump pain after one year of observation. But postoperative analgesia was significantly better in ketamine group with reduced stump sensitivity[8]. This study defined role of NMDA receptors in the development of pain following amputation, but warrants further studies to confirm its role in persistent phantom limb pain.

       In this study, we assess the effect of pre-emptive treatment with intrathecally administered NMDA antagonist, Ketamine in combination with local anaesthetic on reducing spinal sensory transmission triggering hyperplastic changes, acute central sensitization and the development of persistent phantom limb pain.