[Pain mechanisms in Complex Regional Pain Syndrome Type 1--a review]

The phenomenon of pain in the course of Complex Regional Pain Syndrome Type 1 is interesting, because its mechanism of its development and maintaining has not been definitively explain. The objective of this article was to review of contemporary knowledge in this issue. The following hypotheses were mentioned: 1) sensitization of dorsal root neurons on afferent barrage form site of injury, of which each, also non-nociceptive, can induce an activation of the nociceptive pathway; 2) interactions between the nervous and immune systems, when pain stimulation as a result of injury or inflammation activate microglia cells in central nerve system, what probably is responsible for development of spontaneous pain; 3) the role of of glutamatergic N-metyl-D-asparagin receptor (NMDA), which increased activity reduces pain experience due to changes of conductance and number of AMPA receptors, that mediate fast pain transmission; 4) the phenomenon of allodynia, when a touch stimuli, temperature or limb position change is experienced as a pain. This is probably caused by false interpretation of the stimuli due to its disturbed processing in the dorsal root ganglia; 5) a contribution of the cerebral cortex in the perception and processing of the pain, as a part of complex, homeostatic matrix; 6) a role of sympathetic pain component in Complex Regional Pain Syndrome. Afore-mentioned hypotheses do not allow to definitive identification of the major patophysiological mechanism which contribute in the development and maintaining of pain in CRPS, but they show a complexity of these processes.