Autonomic failure after stroke - is it indicative for pathophysiology of complex regional pain syndrome?

In order to find pieces of evidence for a central origin of autonomic failu re in complex regional pain syndrome I (CRPS I), the pattern of autonomic s ymptoms in CRPS I patients was compared to patients a few days after stroke . Autonomic failure in the latter group is assumed to represent definite CN S origin. Seventeen stroke patients, 21 patients in the acute and late stag e of CRPS I and a control group of 23 healthy subjects were investigated. D etailed neurological examination was performed, sweating was induced centra lly (thermoregulatory sweating, TST) and peripherally by carbachol iontopho resis (QSART) and quantified by evaporation hygrometry. Skin temperature wa s assessed by infrared thermography. The incidence of motor-sensory dysfunc tion (without pain) and the incidence of edema was strikingly similar in st roke and CRPS patients. Furthermore, stroke patients had increased TST but not QSART responses on the contralesional limb (P<0.05) and skin temperatur e was decreased (P<0.001). The same pattern of autonomic failure was found in late CRPS (TST: P<0.02, skin temperature: P<0.01) whereas in acute CRPS additional, presumably peripheral mechanisms, contribute to sympathetic sym ptoms. In conclusion, our investigation suggests that many clinical symptom s and the main features of sympathetic dysfunction in CRPS could be explain ed by a CNS pathophysiology.