Abstract
Background and Purpose: Remote white matter and cortex reorganization may contribute to functional reorganization and clinical outcome after acute infarcts. To determine the microstructural changes in the remote intact corticospinal tract (CST) and precentral gyrus cortex connected to the acute infarct after subcortical stroke involving the CST over 6 months.Methods: Twenty-two patients with subcortical stroke involving the CST underwent magnetic resonance imaging (MRI) and clinical assessment in the acute phase (baseline) and 6 months (follow–up) after the stroke. The MRI sequences included T1-weighted imaging, T2–weighted imaging, fluid-attenuated inversion recovery, diffusion tensor imaging (DTI), and diffusion kurtosis imaging. Fractional anisotropy (FA) and track–density imaging (TDI) values were generated using DTI data for the centrum semiovale, corona radiata, posterior limb of internal capsule, and cerebral peduncle. The mean kurtosis (MK) value of the precentral gyrus cortex was calculated. Changes in the FA, TDI, and MK values between the baseline and follow-up and the relationship between these changes were analyzed.Results: The TDI and FA values of all parts of the ipsilesional (IL) CST, including the noninvolved upper and lower parts, decreased at the 6-month follow-up (P < 0.001). The MK values of the stroke lesion (P < 0.001) and IL precentral gyrus cortex (P = 0.002) were lower at follow-up than at the baseline. The ΔTDI (r = 0.689, P < 0.001) and Δ FA values (r = 0.463, P = 0.03) of the noninvolved upper part of the IL CST were positively correlated with the ΔMK value of the IL precentral gyrus cortex.Conclusion: Secondary degeneration occurred in the remote part of the CST and the remote IL precentral gyrus cortex after subcortical stroke involving the CST. The secondary degeneration in the upper part of the CST was correlated with that in the IL precentral gyrus cortex.
Highlights
Ischemic stroke is a leading cause of death and long-term disability
A magnetic resonance spectroscopy (MRS) study showed that the N-acetylacetate (NAA) value of the intact primary motor cortex (M1) decreased after subcortical stroke, indicating neuronal depression, and dysfunction in the M1 area due to ischemia and/or diaschisis of the remote white-matter tracts connected to the acute ischemic infarcts [8]
The aim of this study was to use track-density imaging (TDI) and Diffusion tensor imaging (DTI) combined with diffusion kurtosis imaging (DKI) to explore the microstructural changes in the corticospinal tract (CST) involved by the stroke lesion as well as the remote intact CST and precentral gyrus cortex connected to the acute infarct during a 6-month follow-up period
Summary
Ischemic stroke is a leading cause of death and long-term disability. Motor disability is one of the most common sequelae of stroke. Secondary damage and degeneration of the remote white-matter tracts connected to the acute ischemic infarct as well as focal cortical thinning in remote cortical regions related to the infarct lesion have been reported after subcortical stroke [6, 7]. A magnetic resonance spectroscopy (MRS) study showed that the N-acetylacetate (NAA) value of the intact primary motor cortex (M1) decreased after subcortical stroke, indicating neuronal depression, and dysfunction in the M1 area due to ischemia and/or diaschisis of the remote white-matter tracts connected to the acute ischemic infarcts [8]. To determine the microstructural changes in the remote intact corticospinal tract (CST) and precentral gyrus cortex connected to the acute infarct after subcortical stroke involving the CST over 6 months
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