Abstract
Central post-stroke pain (CPSP) was first described by Dejerine and Roussy as a consequence of stroke-related lesions in the thalamus [1]. CPSP can develops after both haemorrhagic and ischemic lesions occurring at any level of somato-sensory pathway of the brain, including medulla, thalamus, and cerebral cortex. CPSP is characterized by either spontaneous or evoked unpleasant sensory described as allodynia, hyperalgesia, and dysesthesia, which severely affect the quality of life. The prevalence of CPSP has been reported to be 8–55%, which is due to different locations of the lesion in the brain. Evidences suggest that the occurrence of CPSP is particularly high after lateral medullary infarction or lesions in the ventroposterior thalamus [2]. In addition, lesions in other brain areas in the somatosensory pathway also result in CPSP [3-5].
Highlights
Central post-stroke pain (CPSP) was first described by Dejerine and Roussy as a consequence of stroke-related lesions in the thalamus [1]
CPSP is characterized by either spontaneous or evoked unpleasant sensory described as allodynia, hyperalgesia, and dysesthesia, which severely affect the quality of life
Based on basic and clinical studies, the following various neural circuit models have been proposed to illustrate the abnormal network of CPSP in the brain [4, 6]
Summary
Central post-stroke pain (CPSP) was first described by Dejerine and Roussy as a consequence of stroke-related lesions in the thalamus [1]. 2 The Institute for Brain Research (IBR), Huazhong University of Science and Technology, Wuhan, 430030, China CPSP can develops after both haemorrhagic and ischemic lesions occurring at any level of somato-sensory pathway of the brain, including medulla, thalamus, and cerebral cortex.
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