{"title":"[A case of unilateral chorea associated with cortical infarction with transient cortical and striatal hyperperfusion].","authors":"Yuta Madokoro, Hiroyasu Inoue, Teppei Fujioka, Masayuki Mizuno, Masahiro Oomura, Noriyuki Matsukawa","doi":"10.5692/clinicalneurol.cn-002037","DOIUrl":null,"url":null,"abstract":"<p><p>Although disruption of basal ganglia loops due to reduced cortical blood flow has been postulated as a possible mechanism for chorea after cortical infarction, detailed studies have not been conducted. We report a case of cardiogenic cerebral embolism of the right frontal to insular cortex due to occlusion of the right M2 branch, followed by the appearance of chorea in the left upper limb on the next day, recanalization of the occluded vessel, and hyperperfusion detected in the same area of brain via single-photon emission computed tomography (SPECT). Interestingly, the blood flow to the right striatum, which was not infarcted, was increased; however, this was not observed after the disappearance of chorea. We speculated that hyperperfusion after cortical infarction affected the striatum, which resulted in the emergence of chorea. In addition to cortical infarction, increased cortical blood flow due to recanalization should be considered as a possible mechanism for chorea development due to cortical infarction.</p>","PeriodicalId":39292,"journal":{"name":"Clinical Neurology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Neurology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5692/clinicalneurol.cn-002037","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
[A case of unilateral chorea associated with cortical infarction with transient cortical and striatal hyperperfusion].
Although disruption of basal ganglia loops due to reduced cortical blood flow has been postulated as a possible mechanism for chorea after cortical infarction, detailed studies have not been conducted. We report a case of cardiogenic cerebral embolism of the right frontal to insular cortex due to occlusion of the right M2 branch, followed by the appearance of chorea in the left upper limb on the next day, recanalization of the occluded vessel, and hyperperfusion detected in the same area of brain via single-photon emission computed tomography (SPECT). Interestingly, the blood flow to the right striatum, which was not infarcted, was increased; however, this was not observed after the disappearance of chorea. We speculated that hyperperfusion after cortical infarction affected the striatum, which resulted in the emergence of chorea. In addition to cortical infarction, increased cortical blood flow due to recanalization should be considered as a possible mechanism for chorea development due to cortical infarction.