Purpose Complex regional pain syndrome (CRPS) is a chronic inflammatory pain syndrome that affects one or more extremities of the body. It is characterized by burning pain and abnormalities in the sensory, motor, and autonomic nervous systems. This review illustrates how oxidative stress and nuclear factor erythroid 2-related factor (Nrf2) activation might contribute to understanding the etiopathogenesis of CRPS.Principal findings The precise cause of CRPS remains unclear, and current treatments are not effective in many patients. The mechanism underlying CRPS may differ across patients and even within a single patient over time. Inflammatory and neuronal mechanisms have been suggested as key contributors to CRPS. Recent evidence demonstrates that oxidative stress is associated with clinical symptoms in patients with CRPS-I. Oxidative stress plays a key role in CRPS pathogenesis. The Nrf2 factor is a master regulator of the transcription of multiple antioxidants, which protects against oxidative stress and inflammation by inducing antioxidant and detoxifying genes through binding with an antioxidant response element. It has antinociceptive effects against inflammatory pain in an animal model. Conclusion This review summarises the effect of oxidative stress and mitochondrial dysfunction in the pathogenesis of CRPS. It also addresses the question of whether there is a potential role for Nrf2 (activated by pharmacological or nutritional activators) in alleviating the clinical features of CRPS or preventing its progression.
RésuméObjectif Le syndrome douloureux re´gional complexe (SDRC) est un syndrome de douleur inflammatoire chronique affectant un ou plusieurs membres; il est caracte´rise´par des douleurs de type bruˆlures et par des anomalies des syste`mes nerveux sensitif, moteur et autonome. La cause pre´cise du SDRC est encore inconnue et les traitements actuels sont inefficaces chez de nombreux patients. Le me´canisme sous-jacent du SDRC peut varier selon les patients et meˆme chez un meˆme patient au fil du temps. Des me´canismes inflammatoires et neuronaux ont e´te´propose´s comme jouant un rôle cle´dans la gene`se du SDRC. Les constatations tire´es des e´tudes re´centes montrent que le stress oxydatif est associe´aux symptômes cliniques du SDRC-1. L'objectif de cet article de synthe`se est d'illustrer comment le stress oxydatif et l'activation d'un facteur apparente´au facteur nucle´aire e´rythroı¨de-2 (Nrf2) pourraient contribuer a`la compre´hension de l'e´tiopathogene`se du SDRC. Constatations principales Le stress oxydatif joue un rôle essentiel dans la pathogene`se du SDRC. Le facteur apparente´au facteur nucle´aire e´rythroı¨de-2 est le maıˆtre re´gulateur de la transcription de multiples antioxydants prote´geant contre le stress oxydatif et l'inflammation par Author contributions Rame Taha and Gilbert Blaise have made substantial contributions to design and drafting the reviewand both of them have approved the final version to be published.