Search results
Results From The WOW.Com Content Network
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]
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.
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.
Seizures and delays in motor development are also prevalent. Additionally, mild mental retardation can be observed. Patients often exhibit diffuse swelling of the cerebral white matter and large subcortical cysts in the frontal and temporal lobes, with cysts developing on the tips of the temporal and subcortical areas.
In subcortical dementia, there is targeted damage to regions lying under the cortex. The pathological process that result in subcortical dementia shows neuronal changes that involve primarily the thalamus , basal ganglia , and rostral brain-stem nuclei and mostly, some projections in the white matter from these regions to the cortex, with ...
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.
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.
These small regions of high intensity are observed on T2 weighted MRI images (typically created using 3D FLAIR) within cerebral white matter (white matter lesions, white matter hyperintensities or WMH) [1] [2] or subcortical gray matter (gray matter hyperintensities or GMH). The volume and frequency is strongly associated with increasing age. [2]