European Journal of Molecular & Clinical Medicine

Abstract

Amputation is often causing chronic postoperative pain with an incidence of 85%. Phantom limb pain or PLP is one of the post-amputation phenomena characterized by pain in the limb that has been removed, including the amputation. Neuropathic pain occurs due to hyperexcitability of damaged nerves and other functional nerves around them, causing changes in neuroma sensitivity, decreased potassium channel expression, and increased voltage-gate of sodium channel (VGSC) activity. VGSC buildup triggers cell membrane hyperexcitability, becomes an ectopic initiator of pain, and causes central and peripheral sensitization. Neuromas in the stump respond more to stimuli because they are sensitive to cytokines and amines, causes the massive process of nociceptive impulses and resulting in pain. Neural plasticity allows the nervous system to compensate for the damage after amputation, the brain undergoes a somatotopic map adjustment due to missing limbs. Plasticity is the brain's response to pain that causes the increase of pain signal transmission in the spinal cord. This is known as central sensitization and causes hyperalgesia and allodynia. The plasticity of nerve damage leads to ectopic discharge, it leads to spontaneous pain in the area innervated by the damaged nerve or the nerves surrounding the damaged nerve. Plasticity is the brain's response to pain that causes the transmission of pain signals in the spinal cord to increase. This mechanism is known as central sensitization, which causes hyperalgesia and allodynia. The plasticity of nerve damage leads to ectopic discharge, which can lead to spontaneous pain in the area innervated by the damaged nerve or the nerves surrounding the damaged nerve.