Abstract
Although changes in brain gray matter after stroke have been identified in some neuroimaging studies, lesion heterogeneity and individual variability make the detection of potential neuronal reorganization difficult. This study attempted to investigate the potential structural cortical reorganization after sub-cortical stroke using a longitudinal voxel-based gray matter volume (GMV) analysis. Eleven right-handed patients with first-onset, subcortical, ischemic infarctions involving the basal ganglia regions underwent structural magnetic resonance imaging in addition to National Institutes of Health Stroke Scale (NIHSS) and Motricity Index (MI) assessments in the acute (<5 days) and chronic stages (1 year later). The GMVs were calculated and compared between the two stages using nonparametric permutation paired t-tests. Moreover, the Spearman correlations between the GMV changes and clinical recoveries were analyzed. Compared with the acute stage, significant decreases in GMV were observed in the ipsilesional (IL) precentral gyrus (PreCG), paracentral gyrus (ParaCG), and contralesional (CL) cerebellar lobule VII in the chronic stage. Additionally, significant increases in GMV were found in the CL orbitofrontal cortex (OFC) and middle (MFG) and inferior frontal gyri (IFG). Furthermore, severe GMV atrophy in the IL PreCG predicted poorer clinical recovery, and greater GMV increases in the CL OFG and MFG predicted better clinical recovery. Our findings suggest that structural reorganization of the CL “cognitive” cortices might contribute to motor recovery after sub-cortical stroke.
Highlights
Brain damage after ischemic stroke can cause a greater variety of functional deficits
Secondary neurodegeneration has been identified in earlier studies using diffusion tensor imaging (DTI) in sub-cortical stroke patients (Liang et al, 2008; Crofts et al, 2011)
Diaschisis and degeneration can induce secondary atrophy in remote cortices (Yabuta and Callaway, 1998; Cheng et al, 2015) as observed in present study. These findings indicate that neurodegenerative atrophy in these ‘‘healthy’’ areas might partially account for permanent motor deficits
Summary
Brain damage after ischemic stroke can cause a greater variety of functional deficits. In addition to the evidence of secondary cortical atrophy, many early studies reported secondary degeneration of remote white matter tracts after damage to the motor pathway due to sub-cortical stroke (Thomalla et al, 2004, 2005; Liang et al, 2008; Yu et al, 2009; Rüber et al, 2012), and the severity of the degeneration predicts poor motor recovery (Yu et al, 2009; Lindenberg et al, 2010). Because early studies demonstrated widespread of functional reorganization of multiple brain network (Wang et al, 2010, 2014; Rehme et al, 2012), we hoped to observed increases in the GMVs of the remaining cortices and significant association between GMV increases and clinical recovery
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