Neuropathic pain arises from lesions or diseases affecting the somatosensory nervous system, producing pain through fundamentally different mechanisms than nociceptive pain. Understanding these mechanisms is essential for selecting appropriate pharmacotherapy. Peripheral sensitization occurs when nerve injury triggers ectopic firing in damaged primary afferent neurons. Injured axons develop abnormal accumulations of voltage-gated sodium channels (Nav1.7, Nav1.8, Nav1.9) at injury sites and along the axon, creating spontaneous depolarization and pain signaling without external stimuli. Wallerian degeneration releases inflammatory mediators (TNF-alpha, IL-1, IL-6, prostaglandins, nerve growth factor) that further sensitize nociceptors and recruit immune cells. Dorsal root ganglion (DRG) neurons undergo phenotypic switching: large-diameter A-beta fibers (normally carrying touch information) begin expressing substance P and CGRP, effectively becoming nociceptors -- this is the cellular basis of allodynia (pain from normally non-painful touch). Central sensitization develops as persistent nociceptive input from damaged peripheral nerves produces long-term potentiation (LTP) in dorsal horn neurons. Excessive glutamate release activates NMDA receptors, causing massive calcium influx that triggers intracellular kinase cascades (PKC, ERK, CREB), upregulating receptor expression and reducing inhibitory GABA-ergic interneuron activity. This wind-up phenomenon amplifies pain...