A new hypothesis for the pathophysiology of complex regional pain syndrome.
Complex Regional Pain Syndrome (CRPS) has defied a clear unified pathological explanation to date. Not surprisingly, treatments for the condition are limited in number, efficacy and their ability to enact a cure. Whilst many observations have been made of physiological abnormalities, how these explain the condition and who does and doesn't develop CRPS remains unclear. We propose a new overarching hypothesis to explain the condition that invokes four dynamically changing and interacting components of tissue trauma, pathological pain processing, autonomic dysfunction (both peripheral and central) and immune dysfunction, primarily involving excessive and pathological activation of dendritic cells following trauma or atrophy. We outline pathophysiological changes that may initiate a cascade of events involving dendritic cells and the cholinergic anti-inflammatory pathway resulting in the condition, and the changes that maintain the condition into its chronic phase. This hypothesis should provide fertile ground for further investigations and development of new treatments that holistically address the nature of the disorder along its developmental continuum.
['Russo|Marc|M|', 'Georgius|Peter|P|', 'Santarelli|Danielle M|DM|']
D000818:Animals D015551:Autoimmunity D001341:Autonomic Nervous System D001479:Basal Ganglia D020918:Complex Regional Pain Syndromes D003713:Dendritic Cells D006801:Humans D007107:Immune System D008198:Lymph Nodes D017628:Microglia D009437:Neuralgia D013116:Spinal Cord
Complex regional pain syndrome CRPS Dendritic cell Immune system Reflex sympathetic dystrophy