Is complex regional pain syndrome an inflammatory process? Theories and therapeutic implications

Taha, Rame; Blaise, Gilbert

doi:10.1007/bf03022768

Cited by 9 publications

(4 citation statements)

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“…Moreover, the sympathetic‐afferent coupling may sensitize the nociceptive primary afferents and lead to the release of neuropeptides (Substance P and CGRP) from peptidergic unmyelinated fibers . Neuropeptides (SP and CGRP), antidromically released from sensory terminals in the skin, evoke vasodilation and protein extravasation in the tissue, and the resulting signs (reddening, warming, and edema) are called neurogenic inflammation . The important contribution of inflammation to CRPS I is underlined by open‐label studies on treatments with infliximab (anti‐TNF), thalidomide, prednisone, and prednisolone …”

Section: Methodsmentioning

confidence: 99%

Complex regional pain syndrome type I: a comprehensive review

Bussa

Guttilla

Lucia

et al. 2015

Acta Anaesthesiol Scand

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Section: Methodsmentioning

confidence: 99%

Complex regional pain syndrome type I: a comprehensive review

Bussa

Guttilla

Lucia

et al. 2015

Acta Anaesthesiol Scand

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“…It has been suggested that enhanced peripheral neuronal inflammation, local and classic systemic inflammation, sympathetic nervous system dysfunction, and central nervous system abnormality are major mechanisms that contribute to the pathogenesis of CRPS in a genetically susceptible individual. [19][20][21] In fact, genetic predisposition and environmental stress are key factors in CRPS development and may explain the increased vulnerability of some individuals (Fig. 2).…”

Section: Inflammation Contributes To Crps Pathogenesismentioning

confidence: 99%

Update on the pathogenesis of complex regional pain syndrome: Role of oxidative stress

Taha

Blaise

2012

Can J Anesth/J Can Anesth

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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.

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“…Neuroplasticity, autonomic dysfunction, autoimmunity, oxidative stress, and other neuronal mechanisms have been postulated as pivotal factors in the pathogenesis of CRPS (54). Both genetic predisposition and environmental stress contribute to the development of CRPS and alterations in the PNS and the CNS are identified in patients (34,148). Inflammation and neuroimmune interactions play a critical role in the development of CRPS.…”

Section: Genetic Pathophysiologymentioning

confidence: 99%

Mechanisms of complex regional pain syndrome

Devarajan,

Mena,

Cheng

2024

Front. Pain Res.

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Complex Regional Pain Syndrome (CRPS) is a chronic pain disorder characterized by a diverse array of symptoms, including pain that is disproportionate to the initial triggering event, accompanied by autonomic, sensory, motor, and sudomotor disturbances. The primary pathology of both types of CRPS (Type I, also known as reflex sympathetic dystrophy, RSD; Type II, also known as causalgia) is featured by allodynia, edema, changes in skin color and temperature, and dystrophy, predominantly affecting extremities. Recent studies started to unravel the complex pathogenic mechanisms of CRPS, particularly from an autoimmune and neuroimmune interaction perspective. CRPS is now recognized as a systemic disease that stems from a complex interplay of inflammatory, immunologic, neurogenic, genetic, and psychologic factors. The relative contributions of these factors may vary among patients and even within a single patient over time. Key mechanisms underlying clinical manifestations include peripheral and central sensitization, sympathetic dysregulation, and alterations in somatosensory processing. Enhanced understanding of the mechanisms of CRPS is crucial for the development of effective therapeutic interventions. While our mechanistic understanding of CRPS remains incomplete, this article updates recent research advancements and sheds light on the etiology, pathogenesis, and molecular underpinnings of CRPS.

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Is complex regional pain syndrome an inflammatory process? Theories and therapeutic implications

Cited by 9 publications

References 15 publications

Complex regional pain syndrome type I: a comprehensive review

Complex regional pain syndrome type I: a comprehensive review

Update on the pathogenesis of complex regional pain syndrome: Role of oxidative stress

Mechanisms of complex regional pain syndrome

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