Neurogenic pain is defined as pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the peripheral or central nervous system. Pain initiated or caused by a primary lesion or dysfunction in the nervous system is also called neuropathic pain. Postischemic pain is an example of neurogenic pain due to a transitory perturbation in the peripheral nerve. This is associated with abnormal burst discharges in primary afferent fibers, which may be due to two-stable states of axon membrane in high K+ environment. Carpal tunnel syndrome is an entrapment neuropathy. In the advanced stage of this syndrome, neuropathological changes responsible for pain are demyelinization, degeneration and regeneration of nerve fibers in the median nerve. Both demyelinated axons and sprouts of regenerating axons show spontaneous discharges and mechanosensitivity. Spontaneous discharges are due to accumulation of Na+ channels, and can be suppressed by Na+ channel blockers. Phantom limb pain is referred to a surgically removed limb or portion thereof. After amputation nearly all patients describe a persistent sensation of the missing limb (phantom limb). It is almost always associated with distorted image of lost part. Some patients additionally suffer from phantom limb pain. The neural networks for perceiving the body and its parts are built into the brain. Epidural anesthesia has been used for identifying whether the trigger for painful phantom is peripheral or central. If epidural anesthesia does not relieve chronic phantom limb pain, tigger mechanism is central; deafferentation of central neurons and their spontaneous and evoked hyperexcitability. Denervation hypersensitivity, damage to inhibitory mechanisms (disinhibition), glial neuronal interactions, and synaptic reorganization following collateral sprouting have been considered as possible mechanisms underlying hyperexcitability. Lesions anywhere along the course of the lateral ascending pain pathway (the spinothalamocortical pathway) can cause deafferentation pain. Neurons upstream in the spinothalamocortical pathway develop a state of hyperexcitability, when their major afferent input has been interrupted by a lesion. Hyperexcitable neurons discharge spontaneously in burst. The thalamic relay of this system is nucleus ventralis posterolateralis, and the somatosensory cortex receives painful impulses relayed through this thalamic nucleus. Local anesthesia or surgical removal of the somatosensoy cortex can only temporarily relieve phantom limb and deafferentation pains.