Among the multiple physical and psychological disabilities and sequels derived from landmines [6-8], one of the most important consequences is the chronic neuropathic pain secondary to amputation. Ketz conducted a retrospective study among 30 soldiers wounded in combat, finding a prevalence of 77% of Phantom Limb Pain (PLP) after traumatic amputation [9]. The factors associated with development of neuropathic pain in these patients include central and peripheral phenomena [10-12]. The direct damage to the involved tissue produces inflammation, and in some cases infection which induces the release of several molecules, such as hydrogen, potassium and arachidonic acid, which in turn, activate and sensitize pain receptors, leading to exaggerated responses to any minimal painful stimuli [11]. Another proposed mechanism for the development of PLP is the fact that damaged peripheral nerve tissues grows into so-called "neuromas" [13, 14]. These have shown to express a greater density of sodium channels in their cell membranes, increasing the activity of peripheral nociceptors [15]. This increased activity leads to changes in the synaptic structure of neurons located in the dorsal horn of the spinal cord, increasing their excitability as well as reducing the frequency and intensity of their inhibitory processes [11, 16]. Besides spinal and peripheral changes, encephalic alterations have also been found [17-24]. Melzack introduced the neuromatrix theory, which suggested that pain is a multidimensional experience, which involves a large neural network that enables the integration and simultaneous processing of information from multiple peripheral receptors with the processed information permanently in these neural circuits, emphasizing the importance of central structures in all aspects of pain [25]. In addition, Merzenich et al [26] conducted a study in adult monkeys, finding that after amputation of a limb, the primary somatosensory cortex seems to rearrange itself in the cortical areas representing the amputated limb.