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CT image showing extensive low attenuation in the right hemispheric white matter due to dilated Type 2 perivascular spaces Axial fat-suppressed T2-weighted MRI image in the same patient as above demonstrating extensive dilated Type 2 perivascular spaces in the right hemisphere Perivascular space is depicted in the inset box.
Binswanger's disease, also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy, [1] is a form of small-vessel vascular dementia caused by damage to the white brain matter. [2] White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. [3]
The claustrum (Latin, meaning "to close" or "to shut") is a thin sheet of neurons and supporting glial cells in the brain, that connects to the cerebral cortex and subcortical regions including the amygdala, hippocampus and thalamus.
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.
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.
Subcortical areas: Septal nuclei; Amygdala; Nucleus accumbens; Diencephalic structures: Hypothalamus; Mammillary bodies; Anterior nuclei of thalamus; Other areas that have been included in the limbic system include the: Stria medullaris; Central gray and dorsal and ventral nuclei of Gudden
Leukoencephalopathy (leukodystrophy-like diseases) is a term that describes all of the brain white matter diseases, whether their molecular cause is known or unknown. [1] It can refer specifically to any of these diseases: Progressive multifocal leukoencephalopathy; Toxic leukoencephalopathy
They do not spread into the subcortical white matter and never show gadolinium enhancement. Over a one-year period, CLs can increase their number and size in a relevant proportion of MS patients, without spreading into the subcortical white matter or showing inflammatory features similar to those of white matter lesions.