Amputation is the removal of a body extremity which is generally caused by severe trauma, circulatory disorders, neoplasm, deformities and infection of the limb. In case of gangrene, infection or neoplasm, amputation is carried out as a control strategy for pre-operative pain or a disease process in the affected limb; in some cases, however, amputation surgery is performed as a preventative procedure for the abovementioned complications [
31]. Despite this attempt to alleviate patients’ pain and disability, up to 80 % of amputees report phantom limb pain (PLP) post-amputation surgery [
8]. PLP is defined as persistent painful sensations perceived in the missing portion of the amputated limb [
7]. Previous research associates PLP with peripheral changes such as increased nociceptive input from the residual limb [
39] and reduced near-surface blood-flow [
34]. However, recent evidence suggests that PLP is a sensory output primarily driven by cortical changes in the brain [
10]. Neuroimaging studies of patients with PLP revealed neuroplastic alterations of the somatotopic organization of the cortical and sub-cortical areas of the brain [
9,
13]. These changes are characterized by the anatomical shifting of neighbouring somatosensory [
18] and motor [
4] areas into a deafferented cortical area of the brain contralateral to the amputated limb. Furthermore, these neuroplastic changes are positively correlated to the severity of PLP [
15,
17]. These neuroplastic alterations can be reverted, with a correlation between the reversal of neuroplastic changes and pain relief in amputees with PLP [
1,
11,
20].