scholarly journals Relationship between White Matter Hyperintensities and Hematoma Volume in Patients with Intracerebral Hematoma

2018 ◽  
Vol 9 (6) ◽  
pp. 999 ◽  
Author(s):  
Xuemei Chen ◽  
Yuexinzi Jin ◽  
Jian Chen ◽  
Xin Chen ◽  
Xiang Cao ◽  
...  
Keyword(s):  
White Matter ◽  
White Matter Hyperintensities ◽  
Intracerebral Hematoma ◽  
Hematoma Volume

scholarly journals Relationship Between White-Matter Hyperintensities and Hematoma Volume and Growth in Patients With Intracerebral Hemorrhage

Stroke ◽  
2010 ◽  
Vol 41 (1) ◽  
pp. 34-40 ◽  
Author(s):  
Min Lou ◽  
Adel Al-Hazzani ◽  
Richard P. Goddeau ◽  
Vera Novak ◽  
Magdy Selim
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
White Matter Hyperintensities ◽  
Hematoma Volume

Intracerebral Hematoma, Perihemorrhagic Edema and Urinary Excreted Cysteinyl Leukotrienes Correlation Study

2014 ◽  
Vol 68 (2) ◽  
pp. 85-88
Author(s):  
Natalija Dolnenec-Baneva ◽  
Dijana Nikodijevic ◽  
Gordana Kiteva-Trenchevska ◽  
Igor Petrov ◽  
Dragana Petrovska-Cvetkovska ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Correlation Study ◽  
Intracerebral Hematoma ◽  
Moderate Correlation ◽  
Hematoma Volume ◽  
Cysteinyl Leukotrienes ◽  
Edema Volume ◽  
Perihemorrhagic Edema

AbstractIntroduction.Several mechanisms in formation of perihemorrhagic edema are activated after contact of brain tissue-extravasated blood in intracerebral hemorrhage. Cysteinyl leukotrienes (cysLT) (C4, D4, E4) are included in this process as significant edema factors and they determine the neurological deficit and outcome. The study aim was a 5-day follow-up (admission/3 day/5 day) of urinary cysLT, hematoma volume, edema volume values and their correlation in patients after spontaneous, primary supratentorial intracerebral hemorrhage.Methods.An enzyme immunoassay was used for urinary cysLT measured in 62 patients and 80 healthy controls. Hematoma and edema volumes were visualized and measured by computed tomography and mathematically calculated with a special spheroid shape formula (V=AxBxC/2).Results.CysLT of hemorrhagic patients (1842.20±1413.2, 1181.54±906.2, 982.30±774.2pg/ml/mg creatinine) were significantly excreted (p<0.01). Brain edema (12.86±13.5, 22.38±21.1, 28.45±29.4cm3) was significantly increased (p<0.01). Hematoma volume values (13.05±14.5, 13.13±14.7, 12.99±14.7cm3) were not significant (p>0.05). A high correlation (multiple regression) between cysLT, hematoma and edema was found on the 3rdday (R=0.6) and a moderate correlation at admission (R=0.3) and on the 5thday (R=0.3).Conclusion.In our 5-day follow-up study a significant cysLT brain synthesis and significant brain edema progression versus constant hematoma volume values in hemorrhagic patients was found. A high correlation between cysLT, hematoma and edema volume was found on the 3rdday, a moderate correlation on admission and on the 5thday, which means that high cysLT and hematoma values were associated with high/moderate edema values.

scholarly journals Sustained Opening of the Blood-Brain Barrier with Progressive Accumulation of White Matter Hyperintensities Following Ischemic Stroke

2019 ◽  
Vol 9 (1) ◽  
pp. 16 ◽  
Author(s):  
Imama Naqvi ◽  
Emi Hitomi ◽  
Richard Leigh
Keyword(s):  
Ischemic Stroke ◽  
White Matter ◽  
Acute Stroke ◽  
Blood Brain Barrier ◽  
White Matter Hyperintensities ◽  
Brain Barrier ◽  
Common Finding ◽  
Blood Brain ◽  
History Of ◽  
Iv Tpa

Objective: To report a patient in whom an acute ischemic stroke precipitated chronic blood-brain barrier (BBB) disruption and expansion of vascular white matter hyperintensities (WMH) into regions of normal appearing white matter (NAWM) during the following year. Background: WMH are a common finding in patients with vascular risk factors such as a history of stroke. The pathophysiology of WMH is not fully understood; however, there is growing evidence to suggest that the development of WMH may be preceded by the BBB disruption in the NAWM. Methods: We studied a patient enrolled in the National Institutes of Health Natural History of Stroke Study who was scanned with magnetic resonance imaging (MRI) after presenting to the emergency room with an acute stroke. After a treatment with IV tPA, she underwent further MRI scanning at 2 h, 24 h, 5 days, 30 days, 90 days, 6 months, and 1-year post stroke. BBB permeability images were generated from the perfusion weighted imaging (PWI) source images. MRIs from each time point were co-registered to track changes in BBB disruption and WMH over time. Results: An 84-year-old woman presented after acute onset right hemiparesis, right-sided numbness and aphasia with an initial NIHSS of 13. MRI showed diffusion restriction in the left frontal lobe and decreased blood flow on perfusion imaging. Fluid attenuated inversion recovery (FLAIR) imaging showed bilateral confluent WMH involving the deep white matter and periventricular regions. She was treated with IV tPA without complication and her NIHSS improved initially to 3 and ultimately to 0. Permeability maps identified multiple regions of chronic BBB disruption remote from the acute stroke, predominantly spanning the junction of WMH and NAWM. The severity of BBB disruption was greatest at 24 h after the stroke but persisted on subsequent MRI scans. Progression of WMH into NAWM over the year of observation was detected bilaterally but was most dramatic in the regions adjacent to the initial stroke. Conclusions: WMH-associated BBB disruption may be exacerbated by an acute stroke, even in the contralateral hemisphere, and can persist for months after the initial event. Transformation of NAWM to WMH may be evident in areas of BBB disruption within a year after the stroke. Further studies are needed to investigate the relationship between chronic BBB disruption and progressive WMH in patients with a history of cerebrovascular disease and the potential for acute stroke to trigger or exacerbate the process leading to the development of WMH.

scholarly journals Painting by lesions: White matter hyperintensities disrupt functional networks and global cognition

NeuroImage ◽  
2021 ◽  
Vol 236 ◽  
pp. 118089
Author(s):  
Rachel A. Crockett ◽  
Chun Liang Hsu ◽  
Elizabeth Dao ◽  
Roger Tam ◽  
Janice J. Eng ◽  
...  
Keyword(s):  
White Matter ◽  
White Matter Hyperintensities ◽  
Functional Networks ◽  
Global Cognition

scholarly journals Topographic patterns of white matter hyperintensities are associated with multimodal neuroimaging biomarkers of Alzheimer’s disease

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Malo Gaubert ◽  
Catharina Lange ◽  
Antoine Garnier-Crussard ◽  
Theresa Köbe ◽  
Salma Bougacha ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Glucose Metabolism ◽  
Corpus Callosum ◽  
Gray Matter ◽  
Fdg Pet ◽  
White Matter Hyperintensities ◽  
Gray Matter Volume ◽  
Matter Volume

Abstract Background White matter hyperintensities (WMH) are frequently found in Alzheimer’s disease (AD). Commonly considered as a marker of cerebrovascular disease, regional WMH may be related to pathological hallmarks of AD, including beta-amyloid (Aβ) plaques and neurodegeneration. The aim of this study was to examine the regional distribution of WMH associated with Aβ burden, glucose hypometabolism, and gray matter volume reduction. Methods In a total of 155 participants (IMAP+ cohort) across the cognitive continuum from normal cognition to AD dementia, FLAIR MRI, AV45-PET, FDG-PET, and T1 MRI were acquired. WMH were automatically segmented from FLAIR images. Mean levels of neocortical Aβ deposition (AV45-PET), temporo-parietal glucose metabolism (FDG-PET), and medial-temporal gray matter volume (GMV) were extracted from processed images using established AD meta-signature templates. Associations between AD brain biomarkers and WMH, as assessed in region-of-interest and voxel-wise, were examined, adjusting for age, sex, education, and systolic blood pressure. Results There were no significant associations between global Aβ burden and region-specific WMH. Voxel-wise WMH in the splenium of the corpus callosum correlated with greater Aβ deposition at a more liberal threshold. Region- and voxel-based WMH in the posterior corpus callosum, along with parietal, occipital, and frontal areas, were associated with lower temporo-parietal glucose metabolism. Similarly, lower medial-temporal GMV correlated with WMH in the posterior corpus callosum in addition to parietal, occipital, and fontal areas. Conclusions This study demonstrates that local white matter damage is correlated with multimodal brain biomarkers of AD. Our results highlight modality-specific topographic patterns of WMH, which converged in the posterior white matter. Overall, these cross-sectional findings corroborate associations of regional WMH with AD-typical Aß deposition and neurodegeneration.

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