Pain
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Complex regional pain syndrome (CRPS) is a painful condition affecting one or more extremities of the body, marked by a wide variety of symptoms and signs that are often difficult to manage because the pathophysiology is incompletely understood. Thus, diverse treatments might be ineffective. A recent report revealed the presence of autoantibodies against differentiated autonomic neurons in CRPS patients. ⋯ We identified these autoantibodies as immunoglobulin G directed against peptide sequences from the second extracellular loop of these receptors. The identification of functionally active autoantibodies in serum samples from CRPS patients supports an autoimmune pathogenesis of CRPS. Thus, our findings contribute to the further understanding of this disease, could help in the diagnosis in future, and encourage new treatment strategies focusing on the immune system.
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The human 'pain network' includes cortical areas that are activated during the response to painful stimuli (termed category 1) or during psychological processes that modulate pain, for example, distraction (termed category 2). These categories include parts of the parasylvian (PS), medial frontal (MF), and paracentral cortex (S1&M1). Here we test the hypothesis that causal interactions both within and between category 1 and category 2 modules occur during attention to a painful stimulus. ⋯ The proportion of contacts involved in interactions with PS was greater during distraction vs attention while activation was less, which suggests that distraction involves an inhibitory process in PS. Functional interactions between categories were overwhelmingly in the direction from category 2>1, particularly for contacts in MF which often had a driver role. These results demonstrate that MF is densely interconnected throughout the 'pain network' so that stimulation of MF might be used to disrupt the 'pain network' as a therapy for pain.