Which pathophysiologic mechanism is characteristic of CRPS and helps maintain inflammation?

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CRPS maintains inflammation through a combined attack on pain processing: peripheral nociceptor sensitization together with central sensitization, driven by the release of inflammatory neuropeptides. When nociceptors become sensitized, they respond more readily to stimuli, lowering thresholds. This peripheral input then leads to central sensitization, where dorsal horn neurons become hyper-responsive, amplifying pain signals and spreading sensitivity. As these nerves fire, they release neuropeptides like substance P and CGRP, which promote neurogenic inflammation by causing vasodilation, plasma leakage, and recruitment of immune cells. This creates a self-perpetuating cycle of ongoing pain and inflammation in the affected region. So the best answer reflects both peripheral and central sensitization with neuropeptide-mediated inflammatory processes. The other options miss this dual sensitization and the role of neuropeptides, overstate the absence of sympathetic involvement, or focus on reduced blood flow rather than the inflammatory cycle driven by sensitization and neuropeptide release.