Neuroanatomical correlates of cognitive impairment following basal ganglia-thalamic post-hemorrhagic stroke: Uncovering network-wide alterations in hemispheric gray matter asymmetry

Huan Wang; Minhua Yu; Jinxia Ren; Xiaoli Zhong; Dan Xu; Lei Gao; Haibo Xu

doi:10.1016/j.brainres.2023.148559

Neuroanatomical correlates of cognitive impairment following basal ganglia-thalamic post-hemorrhagic stroke: Uncovering network-wide alterations in hemispheric gray matter asymmetry

Brain Res. 2023 Dec 1:1820:148559. doi: 10.1016/j.brainres.2023.148559. Epub 2023 Aug 29.

Authors

Huan Wang¹, Minhua Yu¹, Jinxia Ren¹, Xiaoli Zhong¹, Dan Xu², Lei Gao³, Haibo Xu⁴

Affiliations

¹ Department of Radiology, Zhongnan Hospital of Wuhan University, Wuchang District, Wuhan City 430071, Hubei Province, China.
² Department of Nuclear Medicine, Zhongnan Hospital of Wuhan University, Wuchang District, Wuhan City 430071, Hubei Province, China.
³ Department of Radiology, Zhongnan Hospital of Wuhan University, Wuchang District, Wuhan City 430071, Hubei Province, China. Electronic address: ncu6096@126.com.
⁴ Department of Radiology, Zhongnan Hospital of Wuhan University, Wuchang District, Wuhan City 430071, Hubei Province, China. Electronic address: xuhaibo1120@hotmail.com.

PMID: 37652090
DOI: 10.1016/j.brainres.2023.148559

Abstract

Cognitive impairment and recovery are central issues in hemorrhagic stroke. This study aimed to investigate whether post-hemorrhagic stroke cognitive impairment (PhSCI) is associated with cortical gray matter (GM) loss and hemispheric asymmetry changes and whether these changes could predict improvements in cognitive function during the recovery. Nineteen patients with PhSCI, comprising 10 with basal ganglia hemorrhage and 9 with thalamic hemorrhage, were recruited. Among them, 9 completed a course of repetitive transcranial magnetic stimulation (rTMS). Additionally, 19 demographically and comorbidity-matched healthy controls were also included. Structural brain MRI and cognitive assessments were performed. Voxel-wise GM volume and hemispheric asymmetry were analyzed. The PhSCI patients exhibited bilateral, yet asymmetric, GM losses in the hippocampus, fusiform, lateral temporal, prefrontal, somatomotor, and inferior parietal regions. The analysis of GM asymmetry revealed that patients showed rightward GM in the lateral temporal, somatomotor, and inferior parietal regions. Among the 9 PhSCI patients who completed rTMS, there was a marginal trend of regional GM increase and leftward GM, and these changes were in parallel with the improvements in cognitive tests. Further lesion connectivity and metanalytic mapping identified two interconnected systems linked to the lesions, which were anchored in the default mode, somatomotor, and salience/cognitive control networks and in the cognitive domains of memory, language, decision-making, and executive function. In conclusion, PhSCI patients exhibited network-wide cortical GM losses, distal to subcortical hemorrhagic lesions, and hemisphere asymmetry changes. These changes appear to predict rTMS-related cognitive improvements, suggesting that even subcortical focal lesions can lead to alterations in distal cortical neuroanatomical architecture. Our preliminary findings provide new insights into the neuroanatomical basis of PhSCI.

Keywords: Cortical atrophy; Lesion network mapping; VBM; Vascular dementia; rTMS.