Allodynia is the elicitation of pain by light mechanical stimuli (such as touch or light pressure) which do not normally provoke pain (cf. hyperalgesia); this is a positive sensory phenomenon. Examples of allodynia include the trigger points of trigeminal neuralgia, the affected skin in areas of causalgia, and some peripheral neuropathies; it may also be provoked, paradoxically, by prolonged morphine use.
Various pathogenetic mechanisms are considered possible, including sensitization (lower threshold, hyperexcitability) of peripheral cutaneous nociceptive fibers (in which neurotrophins may play a role); ephaptic transmission ("cross-talk") between large and small (nociceptive) afferent fibers; and abnormal central processing.
The treatment of neuropathic pain is typically with agents, such as carbamazepine, amitriptyline, gabapentin and pregabalin. Interruption of sympathetic outflow, for example with regional guanethidine blocks, may sometimes help, but relapse may occur.