HighlightsRubral branches were differentially involved in chronic capsular and pontine stroke.The impairment severity of each rubral branch was dependent on lesion locations.The integrity of the rubral branches is related to the severity of motor impairment.

Subcortical ischemic stroke can lead to persistent structural changes in the cerebral cortex. The evolution of cortical structural changes after subcortical stroke is largely unknown, as are their relations with motor recovery, lesion location, and early impairment of specific subsets of fibers in the corticospinal tract (CST). In this observational study, cortical structural changes were compared between 181 chronic patients with subcortical stroke involving the motor pathway and 113 healthy controls. The impacts of acute lesion location and early impairments of specific CSTs on cortical structural changes were investigated in the patients by combining voxel‐based correlation analysis with an association study that compared CST damage and cortical structural changes. Longitudinal patterns of cortical structural change were explored in a group of 81 patients with subcortical stroke using a linear mixed‐effects model. In the cross‐sectional analyses, patients with partial recovery showed more significant reductions in cortical thickness, surface area, or gray matter volume in the sensorimotor cortex, cingulate gyrus, and gyrus rectus than did patients with complete recovery; however, patients with complete recovery demonstrated more significant increases in the cortical structural measures in frontal, temporal, and occipital regions than did patients with partial recovery. Voxel‐based correlation analysis in these patients showed that acute stroke lesions involving the CST fibers originating from the primary motor cortex were associated with cortical thickness reductions in the ipsilesional motor cortex in the chronic stage. Acute stroke lesions in the putamen were correlated with increased surface area in the temporal pole in the chronic stage. The early impairment of the CST fibers originating from the primary sensory area was associated with increased cortical thickness in the occipital cortex. In the longitudinal analyses, patients with partial recovery showed gradually reduced cortical thickness, surface area, and gray matter volume in brain regions with significant structural damage in the chronic stage. Patients with complete recovery demonstrated gradually increasing cortical thickness, surface area, and gray‐matter volume in the frontal, temporal, and occipital regions. The directions of slow structural changes in the frontal, occipital, and cingulate cortices were completely different between patients with partial and complete recovery. Complex cortical structural changes and their dynamic evolution patterns were different, even contrasting, in patients with partial and complete recovery, and were associated with lesion location and with impairment of specific CST fiber subsets.

Numerous studies indicate altered static local and long‐range functional connectivity of multiple brain regions in schizophrenia patients with auditory verbal hallucinations (AVHs). However, the temporal dynamics of interhemispheric and intrahemispheric functional connectivity patterns remain unknown in schizophrenia patients with AVHs. We analyzed resting‐state functional magnetic resonance imaging data for drug‐naïve first‐episode schizophrenia patients, 50 with AVHs and 50 without AVH (NAVH), and 50 age‐ and sex‐matched healthy controls. Whole‐brain functional connectivity was decomposed into ipsilateral and contralateral parts, and sliding‐window analysis was used to calculate voxel‐wise interhemispheric and intrahemispheric dynamic functional connectivity density (dFCD). Finally, the correlation analysis was performed between abnormal dFCD variance and clinical measures in the AVH and NAVH groups. Compared with the NAVH group and healthy controls, the AVH group showed weaker interhemispheric dFCD variability in the left middle temporal gyrus ( p < .01; p < .001), as well as stronger interhemispheric dFCD variability in the right thalamus ( p < .001; p < .001) and right inferior temporal gyrus ( p < .01; p < .001) and stronger intrahemispheric dFCD variability in the left inferior frontal gyrus ( p < .001; p < .01). Moreover, abnormal contralateral dFCD variability of the left middle temporal gyrus correlated with the severity of AVHs in the AVH group ( r = −.319, p = .024). The findings demonstrate that abnormal temporal variability of interhemispheric and intrahemispheric dFCD in schizophrenia patients with AVHs mainly focus on the temporal and frontal cortices and thalamus that are pivotal components of auditory and language pathways.

Subcortical stroke may cause widespread structural changes to the cerebral cortex in multiple domains; however, the details of this process remain unclear. In this prospective observational study, we acquired two datasets to investigate the effect of lesion location on cortical structure. One was cross-sectional, comprising 269 patients with chronic stroke, either capsular stroke (CS) or pontine stroke (PS), and the other was longitudinal, comprising 119 patients with CS or PS. In the chronic-stage data, both CS and PS exhibited reduced cortical thickness in the precentral gyrus and increased cortical thickness and area in the frontal, temporal, occipital and insular cortices. Cortical thicknesses were correlated with motor outcomes in the precentral and lingual gyri, and early impairment of the corticospinal tract was associated with cortical thickness in the middle frontal gyrus. In the longitudinal dataset, CS showed gradually decreasing cortical thickness in the precentral gyrus, and both CS and PS showed gradually increasing cortical thickness and area in regions with significant structural reorganization. Subcortical stroke can therefore cause complex cortical structural changes in multi-domain regions involved in motor, primary and higher cognitive areas and have different evolution patterns depending on the subcortical level of the lesion affecting the motor pathways.