Inflammatory Mediators are Altered in the Acute Phase of Posttraumatic Complex Regional Pain Syndrome

Schinkel, Christian; Gaertner, Andreas; Zaspel, Johannes; Zedler, Siegfried; Faist, Eugen; Schuermann, Matthias

doi:10.1097/01.ajp.0000169669.70523.f0

Cited by 176 publications

(142 citation statements)

References 42 publications

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“…23 Other work indicates that plasma bradykinin levels are significantly higher in CRPS patients than in healthy controls. 24 It has also been observed that corticosteroids significantly diminished the clinical features of CRPS, indicating that inflammatory mechanisms might evolve into CRPS. 25 Furthermore, several small clinical studies demonstrated that, compared with controls and non-CRPS pain patients, CRPS patients display significant increases in proinflammatory cytokines, including interleukin (IL)-1b, IL-6, and tumour necrosis factor a (TNFa), and a decrease in antiinflammatory factors, including IL-10 cytokines in local blister fluid, circulating plasma, and cerebrospinal fluid.…”

Section: Inflammation Contributes To Crps Pathogenesismentioning

confidence: 99%

“…22 There is evidence demonstrating that neurogenic inflammation and activation of the immune system contributes to CRPS mechanisms. 23,24 It has been observed that an increased systemic level of calcitonin gene-related peptide in patients with CRPS plays a significant role in its pathogenesis. 23 Other work indicates that plasma bradykinin levels are significantly higher in CRPS patients than in healthy controls.…”

Section: Inflammation Contributes To Crps Pathogenesismentioning

confidence: 99%

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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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Section: Inflammation Contributes To Crps Pathogenesismentioning

confidence: 99%

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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“…3 Alexander et al 4 have demonstrated a significant increase of IL-1α and IL-6 in the cerebrospinal fluid (CSF) of CRPS patients as compared to control subjects. In contrast, Schinkel et al 5 showed that IL-8 and soluble TNF receptor 1/II, but not IL-6, were significantly elevated in the venous blood of CRPS patients. Sample differences may explain the discrepancies in IL-6 level in these reports.…”

mentioning

confidence: 84%

“…En revanche, Schinkel et coll. 5 ont montré que le IL-8 ainsi que le récepteur TNF 1/II, mais non pas le IL-6, étaient significativement plus élevés dans le sang artériel de patients à SDRC. Des différences d'échantillons pourraient expliquer les écarts dans les taux de IL-6 de ces deux études.…”

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

Taha

Blaise

2007

Can J Anesth/J Can Anesth

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“…This is precipitated and maintained by a pro-inflammatory cytokine profile (IL-1, IL-6, TNF-α, IL-1β) and depressed anti-inflammatory cytokines (IL-4 and IL-10) derived from extravasated leukocytes and recruited immune cells. [21][22][23][24][25][26] In GDS as well as CRPS, lesions may appear at a distance from the site of injury. The only CRPS patients that have undergone autopsy reveal microglial activation throughout the spinal cord which maybe a mechanism of spread and its distant effects.…”

Section: Case Reportmentioning

confidence: 99%

Gardner-Diamond syndrome associated with complex regional pain syndrome

Edinger¹,

Schwartzman²

2013

J Dermatol Case Rep

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Background: Gardner-Diamond syndrome (GDS) is also known as psychogenic purpura, autoerythrocyte sensitization syndrome and painful bruising syndrome.Main observation: This is a case report of 27-year-old woman who presented with unexplained bruising and intramuscular hematomas after a seven year history of complex regional pain syndrome. Her evaluation consisted of hematological studies, skin and muscle biopsy; it failed to reveal an underlying coagulopathy, vasculitis or other demonstrable cause. In the absence of any other etiology, she was diagnosed as Gardner-Diamond syndrome. Conclusion:This patient is unique because of intramuscular hematomas and the association of Complex regional pain syndrome with Gardner-Diamond syndro-

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Inflammatory Mediators are Altered in the Acute Phase of Posttraumatic Complex Regional Pain Syndrome

Cited by 176 publications

References 42 publications

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

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

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

Gardner-Diamond syndrome associated with complex regional pain syndrome

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