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#35904 Mitochondrial dysfunction as triggering in complex regional pain syndrome
  1. Paola María Robert Vélez1,
  2. Lucia Elizabeth Alvarez Palazuelos2,
  3. Andrea Virginia Ruiz-Ramírez2,
  4. Carlos Francisco Rivera Quiles3,
  5. Miguel Alejandro Dávalos Benítez1 and
  6. Moctezuma Ilhuicamina Cabrera Salaiza1
  1. 1Universidad Autónoma de Guadalajara, Guadalajara, Mexico
  2. 2Departamento de Neurología, Universidad Autónoma de Guadalajara, Guadalajara, Mexico
  3. 3Universidad Autónoma de Guadalajara, Guadajalara, Mexico


Please confirm that an ethics committee approval has been applied for or granted: Not relevant (see information at the bottom of this page)

Background and Aims Complex regional pain syndrome (CRPS) is characterized by being disproportionate to the triggering event; the associated characteristics are autonomic dysfunction, swelling of the zone of affection, and even changes in the skin, such as dystrophy and rigidity. The pathophysiology is still unknown; it has been mentioned as a multifactorial disorder, with an exaggerated immune response to the triggering event, abnormal vasomotor function, and even maladaptive neuroplasticity. This study aimed to evaluate the differently expressed genes (DEG) between 4 patients with complex regional pain syndrome vs. healthy controls and analyze the pathways intervening.

Methods Material/Methods: The gene expression dataset GSE47603 was downloaded from the GEO database, and DEG obtained. The highest up-regulated genes were examined in the String platform for the protein-protein interaction (PPI) network.

Results Results: 60 primary genes up-regulated were identified according to the Log2-fold change statistics. The network for the 60 genes was sub-selected in clusters in STRING, obtaining a network of 20 nodes, 24 edges, and a PPI enrichment p-value of 3.73e-11. The principal intervening pathways were mitochondrial ATP synthesis, the electron transport chain, and lysosome vesicle biogenesis.

Abstract #35904 Figure 1

Meandiff plot of genes expressed in CRPS Vs controls

Abstract #35904 Figure 2

CRPS cluster of 20 nodes, with the principal proteins involved in mitochondrial functions

Conclusions We found a relevant participation of mitochondrial metabolism in the PPI network that has not been mentioned before as a pain onset in CRPS, but at the same time presence of pain has been reported in patients with mitochondrial disease, the essential role that it could play in the sudden development of pain in CRPS needs to be further analyzed.

  • CRPS
  • Complex regional pain syndrome
  • pain
  • triggering of CRPS
  • Mitochondrial Dysfunction

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