From the Department of Neurology, The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, Guangdong Province, China (Qu, Liu, Wang, Chen); the Faculty of Neurology, Graduate School of Guangdong Medical University, Zhanjiang, Guangdong Province, China (Qu, Liu); the Faculty of Neurology, Graduate School of Southern Medical University, Guangzhou, Guangdong Province, China (Wang); the BrainNow Research Institute, Shenzhen, Guangdong Province, China (Luo, Shi); the School of Mathematics and Statistics, Huazhong University of Science and Technology, China (Gao); the Center for Mathematical Science, Huazhong University of Science and Technology, China (Gao); the Intelligent Brain Imaging and Brain Function Laboratory (Dongguan Key Laboratory), Dongguan People's Hospital, Dongguan, Guangdong, China (Qu, Chen); the Guangdong Provincial Key Laboratory of Mathematical and Neural Dynamical Systems, Great Bay University, Dongguan, Guangdong, China (Qu, Gao, Chen).
From the Department of Neurology, The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, Guangdong Province, China (Qu, Liu, Wang, Chen); the Faculty of Neurology, Graduate School of Guangdong Medical University, Zhanjiang, Guangdong Province, China (Qu, Liu); the Faculty of Neurology, Graduate School of Southern Medical University, Guangzhou, Guangdong Province, China (Wang); the BrainNow Research Institute, Shenzhen, Guangdong Province, China (Luo, Shi); the School of Mathematics and Statistics, Huazhong University of Science and Technology, China (Gao); the Center for Mathematical Science, Huazhong University of Science and Technology, China (Gao); the Intelligent Brain Imaging and Brain Function Laboratory (Dongguan Key Laboratory), Dongguan People's Hospital, Dongguan, Guangdong, China (Qu, Chen); the Guangdong Provincial Key Laboratory of Mathematical and Neural Dynamical Systems, Great Bay University, Dongguan, Guangdong, China (Qu, Gao, Chen)
J Psychiatry Neurosci. 2024 Oct 25;49(5):E345-E356. doi: 10.1503/jpn.240084. Print 2024 Sep-Oct.
The underlying functional alterations of brain structural changes among patients with empathy impairment following stroke remain unclear. We sought to investigate functional connectivity changes informed by brain structural abnormalities in multimodal magnetic resonance imaging (MRI) among patients with empathy impairment following stroke.
We enrolled people who had experienced their first ischemic stroke, along with healthy controls. We assessed empathy 3 months after stroke using the Chinese version of the Empathy Quotient (EQ). During the acute phase, all patients underwent basic magnetic resonance imaging (MRI), followed by multimodal MRI during follow-up. Our MRI analyses encompassed acute infarction segmentation, volumetric brain measurements, regional quantification of diffusion parameters, and both region-of-interest-based and seed-based functional connectivity assessments. We grouped patients based on the severity of their empathy impairment for comparative analysis.
We included 84 patients who had stroke and 22 healthy controls. Patients had lower EQ scores than controls. Patients with low empathy had larger left cortical infarcts (odds ratio [OR] 4.082, 95% confidence interval [CI] 1.183-14.088), more pronounced atrophy in the right cingulate cortex (OR 1.248, 95% CI 1.038-1.502), and lower scores on the Montreal Cognitive Assessment (OR 0.873, 95% CI 0.74-0.947). In addition, the cingulate cortex served as the seed in the seed-based analysis, which showed heightened functional connectivity between the anterior cingulate gyrus and the right superior parietal lobule, specifically in the low-empathy group.
We did not evaluate the relationship between specific network involvement and empathy impairment among patients following stroke.
Among patients with subacute ischemic stroke, reduced empathy was strongly associated with a more severe cognitive profile and atrophy of the right cingulate cortex. Our subsequent structural-informed functional MRI analysis suggests that the enhanced connectivity between the anterior cingulate gyrus and the superior parietal lobule may function as a compensatory mechanism for this atrophy.
中风后同理心受损患者的大脑结构变化的潜在功能改变尚不清楚。我们试图通过中风后同理心受损患者的多模态磁共振成像(MRI)中的脑结构异常来研究功能连接变化。
我们招募了经历首次缺血性中风的人和健康对照者。我们在中风后 3 个月使用中文同理心问卷(EQ)评估同理心。在急性期,所有患者都接受了基本的 MRI,然后在随访期间进行了多模态 MRI。我们的 MRI 分析包括急性梗塞分割、脑容积测量、弥散参数的区域量化以及基于感兴趣区和种子的功能连接评估。我们根据同理心受损的严重程度对患者进行分组,进行比较分析。
我们纳入了 84 名中风患者和 22 名健康对照者。患者的 EQ 评分低于对照组。同理心低的患者左皮质梗塞更大(比值比 [OR] 4.082,95%置信区间 [CI] 1.183-14.088),右侧扣带回皮质萎缩更明显(OR 1.248,95% CI 1.038-1.502),蒙特利尔认知评估(OR 0.873,95% CI 0.74-0.947)得分较低。此外,扣带作为种子在种子基础分析中,在前扣带回和右侧顶叶上回之间显示出更高的功能连接,特别是在低同理心组中。
我们没有评估特定网络参与与中风后患者同理心受损之间的关系。
在亚急性缺血性中风患者中,同理心的降低与更严重的认知特征和右侧扣带皮质萎缩密切相关。我们随后的结构信息功能 MRI 分析表明,前扣带回和顶叶上回之间增强的连接可能是这种萎缩的代偿机制。