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Head CT showing periventricular white matter lesions. Leukoaraiosis is a particular abnormal change in appearance of white matter near the lateral ventricles. It is often seen in aged individuals, but sometimes in young adults. [1] [2] On MRI, leukoaraiosis changes appear as white matter hyperintensities (WMHs) in T2 FLAIR images.
Deep white matter hyperintensities occur deep within white matter, periventricular white matter hyperintensities occur adjacent to the lateral ventricles and subcortical hyperintensities occur in the basal ganglia. [citation needed] Hyperintensities are often seen in auto immune diseases that have effects on the brain. [6]
The gray matter remains normal in all characteristics while the white matter changes texture, becoming soft and gelatinous. Rarefaction of the white matter is seen through light microscopy and the small number of axons and U-fibers that were affected can also be seen. Numerous small cavities in the white matter are also apparent.
The idea of DAI first came about as a result of studies by Sabina Strich on lesions of the white matter of individuals who had sustained head trauma years before. [37] Strich first proposed the idea in 1956, calling it diffuse degeneration of white matter; however, the more concise term "diffuse axonal injury" came to be preferred. [38]
Mild Moderate Severe ARIA-E Edema: FLAIR hyperintensity confined to sulcus and/or cortex/subcortical white matter in one location < 5 cm FLAIR hyperintensity 5 to 10 cm, or more than 1 site of involvement, each measuring < 10 cm FLAIR hyperintensity measuring > 10 cm, often with significant subcortical white matter and/or sulcal involvement.
White matter is the tissue through which messages pass between different areas of grey matter within the central nervous system. The white matter is white because of the fatty substance (myelin) that surrounds the nerve fibers (axons). This myelin is found in almost all long nerve fibers, and acts as an electrical insulation.
Diabetic microangiopathy, which is the most common cause of microangiopathy, is more prevalent in the kidney, retina and vascular endothelium since glucose transport in these sites isn’t regulated by insulin and these tissues cannot stop glucose from entering cells when blood sugar levels are high. [16]
A deficiency in GALC thus causes a buildup of these fatty acids, leading to an incursion by cells called "globoid macrophages" that destroy oligodendrocytes, thereby inhibiting any further myelin formation. [20] Given the presence of globoid macrophages clustered near white matter, Krabbe disease often is called globoid cell leukodystrophy.
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