What is the role of sensory and motor dysfunction in 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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Answer

In both types of CRPS, peripheral and central sensitization explain the pathophysiology of spontaneous pain and hyperalgesia. [39] Clinical findings in patients consistently show sensory impairments that spread beyond the injured territory, and spontaneous pain that often engulfs a quadrant or hemisensory region. These abnormal patterns are due to altered central afferent processing and have been delineated with functional imaging studies. [40, 41, 42]

Likewise, the evidence to date supports the presence of similar mechanisms involving abnormalities of CNS motor processing (rather than pain, edema, disuse, trophic changes, or nerve injury) that are responsible for causing impairments of muscle strength in the involved distal extremity. Kinematic analysis studies suggest that motor deficits are probably due to impaired integration of visual and sensory afferent input within the parietal cortex. [43] Also, an increased amplitude of physiological tremor due to CNS mechanisms is common, occurring in about 50% of patients under observation. [44]

CRPS can also be linked to structural and functional changes in the brain cortex related to sensory and motor function. Patients with early-onset CRPS demonstrate decreased cerebral perfusion and grey matter volume in the somatosensory cortex. Patients with late-onset disease demonstrate decreased cerebral perfusion in the motor cortex. [45] These findings indicate CRPS has effects on higher level motor and sensory processing in the CNS.


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