A preliminary study of cortical morphology changes in acute brainstem ischemic stroke patients

Abstract

The study aimed to explore the cortical thickness and gyrification abnormalities in acute brainstem ischemic patients in both the ipsilateral and contralateral hemisphere compared with healthy controls. Structural magnetic resonance imaging data were prospectively acquired in 48 acute brainstem ischemic patients, 21 patients with left lesion and 27 with right lesion, respectively. Thirty healthy controls were recruited. Cortical morphometry based on surface-based data analysis driven by CAT12 toolbox implemented in SPM12 was used to compare changes in cortical thickness and gyrification. Significant decreases of cortical thickness loss were found in bilateral cerebral hemispheres of the brainstem ischemic patients compared to the healthy controls (P < .05, family-wise error (FWE)-corrected). We also found significant gyrification decreases in the insula, transverse temporal, supramarginal of the ipsilateral on hemisphere in the right brainstem ischemic patients compared to the healthy controls (P < .05, FWE-corrected). Brainstem ischemic patients have widely morphological changes in the early phase and may be helpful in designing individualized rehabilitative strategies for these patients.

Cortical thinning 3 years after ischaemic stroke is associated with cognitive impairment and APOE ε4

“…( Daria, 2019 ) In acute (≤3-days) brainstem ischaemic stroke, significant bilateral thickness decreases were found compared to healthy controls. ( Chen, 2021 ) Remote focal cortical thinning and microstructural damage in white matter tracts connecting affected distant cortices to acute infarcts have also been reported. ( Duering, 2015 ) In a study of patients imaged hyper-acutely (<3-hours) and again 3 months post-stroke, we demonstrated no change in global average thickness, but found increases in cortical thickness in contralesional paracentral, superior-frontal, and insular regions, ( Brodtmann, 2012 ) corroborating the consistent involvement of contralesional motor areas reflecting cortical remodelling.…”

Retracted and Replaced: Altered microstructure of the contralesional ventral premotor cortex and motor output after stroke

“… 51-53 Data for structural changes in contralesional brain areas underlying PMV is sparse. Some reports did not find any significant alterations, 4 , 8 , 11 others showed increases in CT. 10 Likewise, also the association between CT of ipsilesional and contralesional brain regions and motor functions is still under debate given positive 6 , 11 , 12 , 14 and negative 2 , 4 , 5 , 9 , 10 study results.…”

Relationship Between Cortical Excitability Changes and Cortical Thickness in Subcortical Chronic Stroke

“…Moreover, cortices of the cingulate motor areas also showed a significant loss in CT. As cingulate motor areas are structurally and functionally connected with motor, premotor and also somatosensory areas ( 37 , 38 , 42 ), we speculate that network disconnection effects by the stroke lesion are likely to drive these CT reductions as well. In the literature, one study in acute ischemic brainstem strokes also found thinning of the cingulate cortices ( 18 ). Previous functional imaging studies have already shown that cingulate motor areas exhibit recovery-dependent increases in brain activation ( 43 , 44 ), potentially reflecting enhanced processing of somatosensory feedback after stroke ( 45 ).…”

“…Apart from important motor pathways, such as the CST, stroke-related alterations of brain structure also affect local cortical anatomy: For instance, cortical thinning has been observed in primary and secondary motor and non-motor brain regions of the ipsi-and contralesional hemispheres (5,(12)(13)(14)(15)(16)(17)(18), predominantly in cortices directly connected to the stroke lesion (14,19) or in the deepest layers of the motor cortices (13). By showing gradual cortical thickening in frontal and temporal cortices (20) or increases of cortical gray matter volume (21,22), other studies have argued for the existence of neuroplastic brain alterations after stroke to promote recovery processes.…”