The underlying cause of neuropathic pain associated with other sensory disturbances such as hyperalgesia or allodynia frequently is peripheral nerve damage which can be documented. The study of its pathological mechanism is based on animal models of neuropathy in which changes are studied in the responses to sensory stimuli following severing, ligation or freezing of nerves. The changes of sensory reactivity can be due to a number of structural, physiological and neurochemical changes observed in these animal experiments. Acute changes (stimulation of neurons in sensory pathways, release of neuropeptides: substance P, CGRP and other neurotransmitters, neurogenic inflammation, vascular lesions) produce physiological processes of chronic character (inflammation of nerve and tissues, degeneration, regeneration) leading to functional, neurochemical (increase of receptor number, release of mediators of inflammatory process: bradykinin, histamine, serotonin, prostaglandins, cytokines, nerve growth factors), structural anatomic (loss of myelinated fibres, growth of axonal processes in sensory and sympathetic neurons). All these factors should be considered in the principles of neuropathic pain therapy.