Mechanism for chronic pain generation

Neuropathic pain and the other abnormalities of sensation induced by axon injury or by peripheral nerve inflammation should result from functional compensations of the injured neurons during their regeneration. Ectopic distribution of proteins related to Na⁺, K⁺ and Ca²⁺ channels as well as of receptors on both membranes of injured axon and its cell body becomes a main pacemaker from which spontaneous ectopic afferent of primary sensatory neurons and crosstalk between neurons occur. Abnormal ectopic afferent activities lead to disorders of the sensation, such as hyperalgesia, allodynia, spontaneous pain and paraesthesia. Administration of some ion channel agents and/or α2-adrenergic blockers has shown efficiency in preventing neuropathic pain development and in relieving neuropathic pain.