Phantom limb pain (PLP) is a phenomenon in which the subjective sensation of an amputated limb still exists and has different degrees and nature of pain. There is no exact mechanism that can completely explain phantom limb pain. Various aspects of sensory afferents such as peripheral receptors, sensory afferent fibers, spinal conduction pathways, thalamus and even cortical changes are related to the occurrence of phantom limb pain, and the interaction between the nerve center and peripheral nerves plays an important role in the generation and maintenance of phantom limb pain. The possible pathogenesis includes: 1. damage to nociceptive receptors, sensory afferent nerve fibers, and dorsal root ganglion cells, resulting in abnormal sensitivity to mechanical, thermal, and chemical stimuli; 2. delayed sensitization and increased excitability of neurons in the posterior horn of the spinal cord that feel injurious impulses. Responses to non-injury stimuli also appear. 3, degeneration of neurons that feel injury, causing anatomical outgrowth of low-threshold mechanosensitive endings, thus forming a link with central sensory injury neurons, leading to functional synaptic remodeling in the posterior horn. 4, after amputation, due to the shortening of the length of peripheral nerves, the relationship between various thick and thin sensory fibers in terms of conduction time of impulses is dysregulated, forming in the paravertebral sympathetic ganglion or spinal cord The fixed excitation foci are formed in the paravertebral sympathetic ganglion or spinal cord, producing a pathological cortical-thalamic connection; 5. Phantom limb pain is also related to the patient’s psychological state. Phantom limb pain is related to the patient’s long-term memory of the painful experience of the amputation event. Psychological factors such as distraction, relaxation, fear, repression, previous pain experience, and family and cultural background influence the way pain is felt as well.