title: Pathophysiology of complex regional pain syndrome.
abstract: Complex regional pain syndrome (CRPS) most often follows injury to peripheral nerves or their endings in soft tissue. A combination of prostanoids, kinins and cytokines cause peripheral nociceptive sensitization. In time, the Mg(2+) block of the N-methyl-D-aspartate receptor is removed, pain transmission neurons (PTN) are altered by an influx of Ca(2+) that activates kinases for excitation and phosphatases for depression, activity-dependent plasticity that alters the firing of PTN. In time, these neurons undergo central sensitization that lead to a major physiological change of the autonomic, pain and motor systems. The role of the immune system and the sickness response is becoming clearer as microglia are activated following injury and can induce central sensitization while astrocytes may maintain the process.
authors.affiliation: Drexel University College of Medicine, Department of Neurology, 245 N. 15 Street, MS 423 Philadelphia, PA 19102, USA. robert.schwartzman@drexel.edu
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Schwartzman
authors.forename: Guillermo M
authors.initials: GM
authors.lastname: Alexander
authors.forename: John
authors.initials: J
authors.lastname: Grothusen
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D020918:Complex Regional Pain Syndromes / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D004487:Edema / Q000209:etiology; D006801:Humans; D009069:Movement Disorders / Q000209:etiology