Structural plasticity of remote cortical brain regions is determined by connectivity to the primary lesion in subcortical stroke.
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ABSTRACT:
SUBMITTER: Cheng B
PROVIDER: S-EPMC4640340 | biostudies-literature | 2015 Sep
REPOSITORIES: biostudies-literature
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Project description:ObjectiveSubcortical stroke can cause a variety of language deficits. However, the neural mechanisms underlying subcortical aphasia after stroke remain incompletely elucidated. We aimed to determine the effects of distant cortical structures on aphasia outcomes and examine the correlation of cortical thickness measures with connecting tracts integrity after chronic left subcortical stroke.MethodsThirty-two patients and 30 healthy control subjects underwent MRI scanning and language assessment with the Western Aphasia Battery-Revised (WAB-R) subtests. Among patients, the cortical thickness in brain regions that related to language performance were assessed by the FreeSurfer software. Fiber tracts connecting the identified cortical regions to stroke lesions were reconstructed to determine its correlations with the cortical thickness measures across individual patient.ResultsCortical thickness in different parts of the left fronto-temporo-parietal (FTP) regions were positively related to auditory-verbal comprehension, spontaneous speech and naming/word finding abilities when controlling for key demographic variables and lesion size. Cortical thickness decline in the identified cortical regions was positively correlated with integrity loss of fiber tracts connected to stroke lesions. Additionally, no significant difference in cortical thickness was found across the left hemisphere between the subgroup of patients with hypoperfusion (HP) and those without HP at stroke onset.ConclusionsThese findings suggest that remote cortical atrophy independently predicts language outcomes in patients with chronic left subcortical stroke and aphasia and that cortical thinning in these regions might relate to integrity loss of fiber tracts connected to stroke lesions.
| S-EPMC9381815 | biostudies-literature
Project description:Background and purposePrevious studies have noted changes in resting-state functional connectivity during motor recovery following stroke. However, these studies always uncover various patterns of motor recovery. Moreover, subgroups of stroke patients with different outcomes in hand function have rarely been studied.Materials and methodsWe selected 24 patients who had a subcortical stroke in the left motor pathway and displayed only motor deficits. The patients were divided into two subgroups: completely paralyzed hands (CPH) (12 patients) and partially paralyzed hands (PPH) (12 patients). Twenty-four healthy controls (HC) were also recruited. We performed functional connectivity analysis in both the ipsilesional and contralesional primary motor cortex (M1) to explore the differences in the patterns between each pair of the three diagnostic groups.ResultsCompared with the HC, the PPH group displays reduced connectivity of both the ipsilesional and contralesional M1 with bilateral prefrontal gyrus and contralesional cerebellum posterior lobe. The connectivity of both the ipsilesional and contralesional M1 with contralateral primary sensorimotor cortex was reduced in the CPH group. Additionally, the connectivity of the ipsilesional M1 with contralesional postcentral gyrus, superior parietal lobule and ipsilesional inferior parietal lobule was reduced in the CPH group compared with the PPH group. Moreover, the connectivity of these regions was positively correlated with the Fugl-Meyer Assessment scores (hand+wrist) across all stroke patients.ConclusionsPatterns in cortical connectivity may serve as a potential biomarker for the neural substratum associated with outcomes in hand function after subcortical stroke.
| S-EPMC3527607 | biostudies-literature
Project description:Morphologic evolution of recent small subcortical infarcts (RSSI) ranges from lesion disappearance to lacune formation and the reasons for this variability are still poorly understood. We hypothesized that diffusion tensor imaging (DTI) and blood-brain-barrier (BBB) abnormalities early on can predict tissue damage 1 year after an RSSI. We studied prospectively recruited patients with a symptomatic MRI-defined RSSI who underwent baseline and two pre-specified MRI examinations at 1-3-month and 1-year post-stroke. We defined the extent of long-term tissue destruction, termed cavitation index, as the ratio of the 1-year T1-weighted cavity volume to the baseline RSSI volume on FLAIR. We calculated fractional anisotropy and mean diffusivity (MD) of the RSSI and normal-appearing white matter, and BBB leakage in different tissues on dynamic contrast-enhanced MRI. Amongst 60 patients, at 1-year post-stroke, 44 patients showed some degree of RSSI cavitation on FLAIR, increasing to 50 on T2- and 56 on T1-weighted high-resolution scans, with a median cavitation index of 7% (range, 1-36%). Demographic, clinical, and cerebral small vessel disease features were not associated with the cavitation index. While lower baseline MD of the RSSI (rs?=?-?0.371; p?=?0.004) and more contrast leakage into CSF (rs?=?0.347; p?=?0.007) were associated with the cavitation index in univariable analysis, only BBB leakage in CSF remained independently associated with cavitation (beta?=?0.315, p?=?0.046). Increased BBB leakage into CSF may indicate worse endothelial dysfunction and increased risk of tissue destruction post RSSI. Although cavitation was common, it only affected a small proportion of the original RSSI.
| S-EPMC7235062 | biostudies-literature
Project description:The fate of subcortical diffusion-weighted imaging (DWI) lesions in stroke patients is highly variable, ranging from complete tissue loss to no visible lesion on follow-up. Little is known about within-lesion heterogeneity and its relevance for stroke outcome. Patients with subcortical stroke and recruited through the prospective DEDEMAS study (NCT01334749) were examined at baseline (n = 45), six months (n = 45), and three years (n = 28) post-stroke. We performed high-resolution structural MRI including DWI. Tissue fate was determined voxel-wise using fully automated tissue segmentation. Within-lesion heterogeneity at baseline was assessed by free water diffusion imaging measures. The majority of DWI lesions (66%) showed cavitation on six months follow-up but the proportion of tissue turning into a cavity was small (9 ± 13.5% of the DWI lesion). On average, 69 ± 25% of the initial lesion resolved without any visually apparent signal abnormality. The extent of cavitation at six months post-stroke was independently associated with clinical outcome, i.e. modified Rankin scale score at six months (OR = 4.71, p = 0.005). DWI lesion size and the free water-corrected tissue mean diffusivity at baseline independently predicted cavitation. In conclusion, the proportion of cavitating tissue is typically small, but relevant for clinical outcome. Within-lesion heterogeneity at baseline on advanced diffusion imaging is predictive of tissue fate.
| S-EPMC7308518 | biostudies-literature
Project description:BackgroundPrevious studies demonstrated that cerebellar subregions are involved in different functions. Especially the cerebellar anterior lobe (CAL) and cerebellar posterior lobe (CPL) have been postulated to primarily account for sensorimotor and cognitive function, respectively. However, the functional connectivity (FC) alterations of CAL and CPL, and their relationships with behavior performance in chronic stroke participants are unclear so far.Materials and methodsThe present study collected resting-state fMRI data from thirty-six subcortical chronic stroke participants and thirty-eight well-matched healthy controls (HCs). We performed the FC analysis with bilateral CAL and CPL as seeds for each participant. Then, we detected the FC difference between the two groups by using a two-sample t-test and evaluated the relationship between the FC and scores of motor and cognitive assessments across all post-stroke participants by using partial correlation analysis.ResultsThe CAL showed increased FCs in the prefrontal cortex, superior/inferior temporal gyrus, and lingual gyrus, while the CPL showed increased FCs in the inferior parietal lobule, precuneus, and cingulum gyrus in the stroke participants compared with HCs. Moreover, the FC alteration in the right CAL and the right CPL were negatively correlated with executive and memory functions across stroke participants, respectively.ConclusionThese findings shed light on the different increased FC alteration patterns of CAL and CPL that help understand the neuro-mechanisms underlying behavior performance in chronic stroke survivors.
| S-EPMC9691772 | biostudies-literature
Project description:Following acute ischemic stroke, isolated subcortical lesions induce gray matter atrophy in anatomically connected, yet distant cortical brain regions. We expand on previous studies by analyzing cortical thinning in contralesional, homologous regions indirectly linked to primary stroke lesions via ipsilesional cortical areas. For this purpose, stroke patients were serially studied by magnetic resonance imaging (diffusion tensor imaging and high-resolution anatomical imaging) in the acute (days 3-5) and late chronic stage one year after stroke. We analyzed changes of gray and white matter integrity in 18 stroke patients (median age 68 years) with subcortical stroke. We applied probabilistic fiber tractography to identify brain regions connected to stroke lesions and contralesional homologous areas. Cortical thickness was quantified by semi-automatic measurements, and fractional anisotropy was analyzed. One year after stroke, significant decrease of cortical thickness was detected in areas connected to ischemic lesions (mean -0.15 mm; 95% CI -0.23 to -0.07 mm) as well as homologous contralateral brain regions (mean -0.13 mm; 95% CI -0.07 to -0.19 mm). We detected reduced white matter integrity of inter- and intrahemispheric fiber tracts. There were no significant associations with clinical recovery. Our results indicate that impact of subcortical lesions extends to homologous brain areas via transcallosal diaschisis.
| S-EPMC7026841 | biostudies-literature
Project description:In order to investigate the role of circulating extracellular vesicles (EVs), proteins, and microRNAs as damage and repair markers in ischaemic stroke depending on its topography, subcortical (SC), and cortical-subcortical (CSC) involvement, we quantified the total amount of EVs using an enzyme-linked immunosorbent assay technique and analysed their global protein content using proteomics. We also employed a polymerase chain reaction to evaluate the circulating microRNA profile. The study included 81 patients with ischaemic stroke (26 SC and 55 CSC) and 22 healthy controls (HCs). No differences were found in circulating EV levels between the SC, CSC, and HC groups. We detected the specific expression of C1QA and Casp14 in the EVs of patients with CSC ischaemic stroke and the specific expression of ANXA2 in the EVs of patients with SC involvement. Patients with CSC ischaemic stroke showed a lower expression of miR-15a, miR-424, miR-100, and miR-339 compared with those with SC ischaemic stroke, and the levels of miR-339, miR-100, miR-199a, miR-369a, miR-424, and miR-15a were lower than those of the HCs. Circulating EV proteins and microRNAs from patients with CSC ischaemic stroke could be considered markers of neurite outgrowth, neurogenesis, inflammation process, and atherosclerosis. On the other hand, EV proteins and microRNAs from patients with SC ischaemic stroke might be markers of an anti-inflammatory process and blood-brain barrier disruption reduction.
| S-EPMC8301391 | biostudies-literature
Project description:The authors investigated the changes in connectivity networks of the bilateral primary motor cortex (M1) of subcortical stroke patients using a multimodal neuroimaging approach with antiplatelet therapy. Nineteen patients were scanned at 2 time points: before and 1 month after the treatment. The authors assessed the resting-state functional connectivity (FC) and probabilistic fiber tracking of left and right M1 of every patient, and then compared these results to the 15 healthy controls. The authors also evaluated the correlations between the neuroimaging results and clinical scores.Compared with the controls, the patients showed a significant decrease of FC in the contralateral motor cortex before treatment, and the disrupted FC was restored after treatment. The fiber tracking results in the controls indicated that the body of the corpus callosum should be the main pathway connecting the M1 and contralateral hemispheres. All patients exhibited reduced probability of structural connectivity within this pathway before treatment and which was restored after treatment. Significant correlations were also found in these patients between the connectivity results and clinical scores, which might imply that the connectivity of M1 can be used to evaluate the motor skills in stroke patients.These findings can help elucidate the neural mechanisms responsible for the brain connectivity recovery after stroke.
| S-EPMC4753872 | biostudies-other
Project description:Stimulus presentation is believed to quench neural response variability as measured by fano-factor (FF). However, the relative contributions of within-trial spike irregularity and trial-to-trial rate variability to FF fluctuations have remained elusive. Here, we introduce a principled approach for accurate estimation of spiking irregularity and rate variability in time for doubly stochastic point processes. Consistent with previous evidence, analysis showed stimulus-induced reduction in rate variability across multiple cortical and subcortical areas. However, unlike what was previously thought, spiking irregularity, was not constant in time but could be enhanced due to factors such as bursting abating the quench in the post-stimulus FF. Simulations confirmed plausibility of a time varying spiking irregularity arising from within and between pool correlations of excitatory and inhibitory neural inputs. By accurate parsing of neural variability, our approach reveals previously unnoticed changes in neural response variability and constrains candidate mechanisms that give rise to observed rate variability and spiking irregularity within brain regions.
| S-EPMC9286274 | biostudies-literature
Project description:Some efforts were done to investigate the disruption of brain causal connectivity networks involved in major depressive disorder (MDD) using Granger causality (GC) analysis. However, the homogenous hemodynamic response function (HRF) assumption over the brain may disturb the inference of temporal precedence. Here we applied a blind deconvolution approach to examine the altered HRF shape in first-episode, drug-naïve MDD patients. The regions with abnormal HRF shape in patients were chosen as seeds to detect the GC alterations in MDD. The results demonstrated significantly decreased magnitude of spontaneous hemodynamic response of the orbital frontal cortex (OFC) and the caudate nucleus (CAU) in MDD comparing to healthy controls, suggesting MDD patients likely had alterations in neurovascular coupling and cerebrovascular physiology in these two regions. GC mapping showed increased/decreased GC in OFC-/CAU centered networks in MDD. The outgoing GC values from OFC to anterior cingulate cortex and occipital regions were positively correlated with Hamilton Depression Scale (HAMD) scores, while the incoming GC from insula, middle and superior temporal gyrus to CAU were negatively correlated with HAMD scores of MDD. The abnormalities of directional connections in the cortico-subcortico-cerebellar network may lead to unbalanced integrating the emotional-related information for MDD, and further exacerbating depressive symptoms.
| S-EPMC4766513 | biostudies-other