Journal of Pain Research (Apr 2023)
Role of Sensory Pathway Injury in Central Post-Stroke Pain: A Narrative Review of Its Pathogenetic Mechanism
Abstract
Hai-Li Li,1,2 Min Lin,1,2 Xing-Ping Tan,1,2 Jiang-Lin Wang1,2 1Department of Pain Management, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, 646000, People’s Republic of China; 2Anesthesiology and Critical Care Medicine Key Laboratory of Luzhou, Southwest Medical University, Luzhou, Sichuan Province, 646000, People’s Republic of ChinaCorrespondence: Jiang-Lin Wang, Pain Department, The Affiliated Hospital of Southwest Medical University, No. 25 Pacific Street, Luzhou, Sichuan Province, 646000, People’s Republic of China, Tel +8618090880626, Fax +86830-3165469, Email [email protected]: Central post-stroke pain (CPSP) is a severe chronic neuropathic pain syndrome that is a direct result of cerebrovascular lesions affecting the central somatosensory system. The pathogenesis of this condition remains unclear owing to its extensive clinical manifestations. Nevertheless, clinical and animal experiments have allowed a comprehensive understanding of the mechanisms underlying CPSP occurrence, based on which different theoretical hypotheses have been proposed. We reviewed and collected the literature and on the mechanisms of CPSP by searching the English literature in PubMed and EMBASE databases for the period 2002– 2022. Recent studies have reported that CPSP occurrence is mainly due to post-stroke nerve injury and microglial activation, with an inflammatory response leading to central sensitization and de-inhibition. In addition to the primary injury at the stroke site, peripheral nerves, spinal cord, and brain regions outside the stroke site are involved in the occurrence and development of CPSP. In the present study, we reviewed the mechanism of action of CPSP from both clinical studies and basic research based on its sensory pathway. Through this review, we hope to increase the understanding of the mechanism of CPSP.Keywords: central post-stroke pain, pathogenetic mechanism, spinothalamic tract, thalamus
