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Evidence from subcortical small infarcts suggests that motor fibers are somatotopically arranged in the human corona radiata. Following subtotal brain damage, localization of the corticofugal projection in the corona radiata and internal capsule can assist in evaluating a patient's residual motor capacity and predicting their potential for functional restitution.
The brain pia mater is reflected from the surface of the brain onto the surface of blood vessels in the subarachnoid space. In the brain, perivascular cuffs are regions of leukocyte aggregation in the perivascular spaces, usually found in patients with viral encephalitis. Perivascular spaces vary in dimension according to the type of blood vessel.
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]
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.
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
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]
Around the foci is generally defined area of other lesions of the brain white matter - the death of prooligodendrocytes, proliferation mikrogliocytes and astrocytes, swelling, bleeding, loss of capillaries, and others (the so-called "diffuse component PVL"). However, diffuse lesions without necrosis are not PVL.
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.