Central post-stroke pain due to injury of the spinothalamic tract in patients with cerebral infarction： a diffusion tensor tractography imaging study

作     者：Sung Ho Jang Jun Lee Sang Seok Yeo 

作者机构：Department of Physical Medicine and Rehabilitation College of Medicine Yeungnam University Namku Daegu Republic of Korea Department of Neurology College of Medicine Yeungnam University Namku Daegu Republic of Korea Department of Physical Therapy College of Health Sciences Dankook University Chungnam Republic of Korea 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2017年第12卷第12期

页      面：2021-2024页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

基　　金：supported by the National Research Foundation(NRF)of Korea Grant funded by the Korean Government(MSIP) No.NRF-2015R1D1A1A01060314 

主　　题：nerve regeneration central post-stroke pain cerebral infarction spinothalamic tract diffusion tensorimaging neural regeneration 

摘      要：Many studies using diffusion tensor tractography（DTT） have demonstrated that injury of the spinothalamic tract（STT） is the pathogenetic mechanism of central post-stroke pain（CPSP） in intracerebral hemorrhage; however, there is no DTT study reporting the pathogenetic mechanism of CPSP in cerebral infarction. In this study, we investigated injury of the STT in patients with CPSP following cerebral infarction, using DTT. Five patients with CPSP following cerebral infarction and eight age-and sex-matched healthy control subjects were recruited for this study. STT was examined using DTT. Among DTT parameters of the affected STT, fractional anisotropy and tract volume were decreased by more than two standard deviations in two patients（patients 1 and 2） and three patients（patients 3, 4, and 5）, respectively, compared with those of the control subjects, while mean diffusivity value was increased by more than two standard deviations in one patient（patient 2）. Regarding DTT configuration, all affected STTs passed through adjacent part of the infarct and three STTs showed narrowing. These findings suggest that injury of the STT might be a pathogenetic etiology of CPSP in patients with cerebral infarction.