Inflammation and endothelial dysfunction in Complex Regional Pain Syndrome

摘要

In literature dispute remains about the pathophysiology of Complex Regional Pain Syndrome (CRPS). A differentiation is made between afferent (e.g. inflammation), efferent (e.g. autonomic disturbance) and central mechanisms (e.g. cortical reorganisation) (Huygen et al. 2001). Although all these mechanisms play a role in CRPS, the relationship between them is not completely understood.Temperature asymmetry is one of the key signs and symptoms in CRPS. For years it was generally assumed that temperature asymmetry was a result of disturbances in the autonomic nervous system. Evidence for this mechanism is established in several experiences. The disturbance of the phasic sympathetic vasoconstrictor activity is shown by loss of the normal vasoconstrictive respons in the CRPS involved extremity on deep inhalation (5 breaths/minute). There is also a loss of the tonic sympathetic vasoconstrictive respons in the CRPS involved extremity on whole body cooling. It is shown that the disturbance in the phasic vasoconstrictive respons can restore (Wasner et al. 1999). Adrenergic supersensitivity is thought to play a role in the development of cold CRPS (Baron and Maier 1996)