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Autoradiographic Measurements of [14C]-Iodoantipyrine in Rat Brain Following Central Post-Stroke Pain
Published on: July 18, 2016
[Clinical manifestations and pathological mechanisms of central post-stroke pain at different lesion sites]
Xiao-Li Chen1, Jing Lei1,2, Hao-Jun You1,2
1Center for Translational Medicine Research on Sensory-Motor Diseases, Yan'an University, Yan'an 716000, China.
Abstract:
Central post-stroke pain (CPSP), a common sequela of stroke, is a type of central neuropathic pain characterized by spontaneous pain, hyperalgesia, and allodynia, which significantly hinders post-stroke rehabilitation. The pathophysiology of CPSP is complex, involving functional abnormalities in multiple neural pathways. Core mechanisms include central sensitization, central disinhibition, neuroglial overactivation, and neurotransmitter imbalances, all of which are associated with neuroinflammation and ion channel dysregulation. This review systematically summarizes the clinical manifestations and molecular mechanisms of CPSP induced by stroke lesions in different brain regions (brainstem, thalamus, and cortex), with a focus on maladaptive reorganization of pain pathways, neuroglia-mediated neuroinflammation, and ion channel modulation. The aim is to provide a theoretical foundation for targeted interventions in CPSP and explore potential therapeutic strategies.
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