What is the pathophysiology of complex regional pain syndrome (CRPS)?

Updated: Jun 20, 2018
  • Author: Gaurav Gupta, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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In most cases, experts believe that CRPS develops when persistent noxious stimuli from an injured body region leads to peripheral and central sensitization, whereby primary afferent nociceptive mechanisms demonstrate abnormally heightened sensation, including spontaneous pain and hyperalgesia. Allodynia and hyperalgesia occur when central nervous system (CNS) somatosensory processing misinterprets normal nonpainful mechanical stimuli, such as light touching of the skin, as painful. Therefore, skin in the injured area becomes more sensitive to all stimuli, even nonpainful stimuli. In addition, the sensitization can extend beyond the originally injured area, thus enlarging the region of aberrant pain perception.

A similar impairment of CNS processing leads to motor aberrancies, such as weakness or tremor in the affected area. The peripheral and central sensitization associated with impaired CNS processing is linked to proposed disturbances within the sympathetic nervous system (SNS) that lead to sympathetic hyperactivity adversely affecting the injured area. Studies suggest that an augmented inflammatory response coupled with impaired healing further contribute to the refractory nature of malevolent CRPS. [9, 1, 10, 11, 12, 13]

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