scholarly journals Impact of White Matter Damage After Stroke

10.5772/23204 ◽  
2012 ◽  
Author(s):  
Robert Lindenberg ◽  
Rdiger J.
Keyword(s):  
White Matter ◽  
White Matter Damage

Accumulation of 4-hydroxy-2-nonenal-modified proteins in the white matter damage in chronic cerebral hypo-perfusion rat mode

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S262-S262
Author(s):  
Terubumi Watanabe ◽  
Yoshiko Yanagi ◽  
Takao Urabe ◽  
Yoshikuni Mizuno
Keyword(s):  
White Matter ◽  
White Matter Damage ◽  
Modified Proteins

Cognitive dysfunctions associated with white matter damage due to cardiovascular burden – determinants and interpretations

2014 ◽  
Vol 45 (3) ◽  
pp. 334-345 ◽  
Author(s):  
Paweł Krukow
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Cardiovascular Diseases ◽  
Cognitive Disorder ◽  
Theoretical Background ◽  
Dynamic Aspect ◽  
Pathological Changes ◽  
White Matter Damage ◽  
Neuropsychological Disorders ◽  
Considerable Research

AbstractAlthough considerable research has been devoted to cognitive functions deteriorating due to diseases of cardiovascular system, rather less attention has been paid to their theoretical background. Progressive vascular disorders as hypertension, atherosclerosis and carotid artery stenosis generate most of all pathological changes in the white matter, that cause specific cognitive disorder: disconnection syndromes, and disturbances in the dynamic aspect of information processing. These features made neuropsychological disorders secondary to cardiovascular diseases different than the effects of cerebral cortex damage, which may be interpreted modularly.

scholarly journals Diffuse White Matter Damage Is Absent in Neuromyelitis Optica

2009 ◽  
Vol 31 (1) ◽  
pp. 76-79 ◽  
Author(s):  
F. Aboul-Enein ◽  
M. Krššák ◽  
R. Höftberger ◽  
D. Prayer ◽  
W. Kristoferitsch
Keyword(s):  
White Matter ◽  
Neuromyelitis Optica ◽  
White Matter Damage ◽  
Diffuse White Matter

Abstract WP103: Endothelial Nitric Oxide Synthase Regulates White Matter Changes after Stroke

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Xu Cui ◽  
Michael Chopp ◽  
Tao Yan ◽  
Ruizhuo Ning ◽  
Cynthia Roberts ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
White Matter ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Wild Type ◽  
White Matter Damage ◽  
White Matter Changes ◽  
Significant Difference ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background: Stroke induced white matter damage is associated with neurological functional deficits, but the underlying mechanisms are not well understood. Endothelial nitric oxide synthase knockout (eNOS-/-) mice exhibited a higher mortality, more severe neurological functional deficit, and decreased neurogenesis, angiogenesis and arteriogenesis after stroke than wild type mice. There are no reports as to whether eNOS is related to the white matter change post-stroke. Methods: Adult male C57BL/6 WT and eNOS -/- mice were subjected to permanent middle cerebral artery occlusion (MCAo) by a filament and sacrificed 7 days after MCAo. Functional evaluation, infarct volume measurement, and immunostaining for analysis of white matter changes were performed. Results: There is no significant difference in the infarction volume between wild type and eNOS -/- (wild type : 23.09%±3.32%; eNOS-/-: 27.83%±4.92%, p=0.436, n=9/group). However, eNOS -/- mice showed significantly decreased functional outcome tested by the singal pellet reaching test (wild type: 38.46%%±1.43%, eNOS-/-: 27.45%±2.41%, p=0.0017). eNOS -/- mice also exhibited increased white matter damage compared to wild type mice, including decrease: 1. Axonal density stained by Bielshowsky Silver in the ipsilateral striatal bundles (wild type: 22.06%±3.0%, eNOS-/-: 13.32%±2.18%,, p=0.031), and in the contralateral striatal bundles (wild type: 65.35%±3.97%, eNOS-/-: 29.38%±5.84%, p=0.02); 2. Density of phasphorylated neurofilament by SMI31-immunoflureoscent staining (wild type: 24.11%±2.06%, eNOS-/-: 7.90%±1.70%, p=0.009); 3. The number of CNPase-positive oligodendrocytes in the ischemic border (wild type: 52.23±5.10, eNOS-/-: 35.59±5.33, p=0.041); 4. The number of NG2-positive oligodendrocyte progenitors in the ischemic border (wild type: 26.22±2.31, eNOS-/-: 18.38±1.95, p=0.0187). There is no significant difference in the density of Luxol fast blue stained myelin in the ipsilateral striatal bundles between wild type and eNOS -/- mice (wild type: 25.21%±3.64%; eNOS-/-: 21.39%±6.29%, p=0.260). Conclusions: We are the first to report that eNOS not only regulates vascular changes and neurogenesis, but also plays an important role in white matter changes after stroke.

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