Related Experiment Video
Updated: Aug 8, 2026

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats
Published on: January 21, 2020
Pathophysiology of complex regional pain syndrome
Robert J Schwartzman1, Guillermo M Alexander, John Grothusen
1Drexel University College of Medicine, Department of Neurology, 245 N. 15 Street, MS 423 Philadelphia, PA 19102, USA. robert.schwartzman@drexel.edu
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.
Related Concept Videos
Nociception
Analgesia and Pain Management
Pain
Degenerative Disc Disease ll: Pathophysiology
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation
Acute Inflammation III: Local and Systemic Effects
