Acute Subcortical Infarcts Cause Secondary Degeneration in the Remote Non-involved Cortex and Connecting Fiber Tracts

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.

Pattern of white matter degeneration in remote brain areas from the basal ganglion lesion of ischemic stroke patients with motor impairment

“…Similar to the previous study, infarcts cause motor area focal thinning in remote cortex via degeneration of inter-hemispheric connection ber of the corpus callosum [36,37], we found a change in the connection between the frontal hemispheres, and a small area in contralesional frontal cortex decreased in FA value. It has been reported that secondary degeneration occurred in the ipsilesional precentral gyrus after subcortical stroke involving the CST at the 6-month follow-up in stroke patients by calculating the mean kurtosis (MK) value of manually drawing ROI from Diffusion kurtosis imaging (DKI) imaging study [38]. Now we speculate the degeneration in remote parts of CST occurred in acute and subacute phases of stroke.…”

“…The connections between the cerebrum and the cerebellum pass through the cerebral peduncle in brainstem, so we assume that the weakening of connections to the cerebellum is partially consistent with the decrease in FA in brainstem. Previous DTI studies also found a decrease in FA in midbrain after stroke by manually plotting ROI [38]. A recent study found the role of the cerebellum for residual motor output by facilitating cortical excitability in chronic stroke [45].…”

Patterns of white matter degeneration in remote brain areas from the basal ganglion lesion of ischemic stroke patients with motor impairment

“…So we assume that the weakening of those connections is partially consistent with the decrease in FA in the brainstem. Previous DTI studies also found decreased FA in midbrain of the stroke patients by manually plotting ROI [38]. A recent study indicated that the cerebellum plays a role on residual motor output by facilitating cortical excitability in chronic stroke [45].…”

“…Similar to previous studies results showing infarct-related focal thinning of the motor area in remote cortex via degeneration of inter-hemispheric connection ber of the corpus callosum [36,37], we found changes in the connection between the frontal hemispheres, as well as reduced FA values in a small area located in the contralesional frontal cortex. It has been reported that secondary degeneration occurred in the ipsilesional precentral gyrus after subcortical stroke involving the CST at the 6-month follow-up in stroke patients by calculating the mean kurtosis (MK) value of manually drawing ROI from diffusion kurtosis imaging (DKI) imaging study [38]. We speculated that the degeneration in remote parts of the CST occurred in subacute phases of stroke.…”

Secondary Degeneration of White Matter After Focal Sensorimotor Cortical Ischemic Stroke in Rats

“…Indeed, both clinical studies on stroke patients and animal studies with stroke models reveal the critical role of infarct volume on functional outcome ( Peeling et al, 2001 ; Roof et al, 2001 ; Zaidi et al, 2012 ; Vagal et al, 2015 ; Turner et al, 2016 ). In addition, accumulating clinical evidence has shown that delayed secondary degeneration also occurs in remote non-ischemic cortical regions ( Duering et al, 2015 ; Wei et al, 2019 ). Axonal connectedness is believed to be the key linking remote neuronal damage to the primary lesion site ( Dikranian et al, 2008 ), suggesting that potential white matter (WM) degeneration also occurs after stroke.…”