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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 subcortical areas receiving projections are the amygdala, caudate nucleus and hippocampus. It is unknown if there are cortical regions that do not receive input from the claustrum. Additionally, large or small types of aspiny neurons are reported in the monkey brain, which are classified as “local circuit neurons".
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.
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.
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]
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
This formation is visible to the naked eye as a white strip running through the cortical grey matter, and is the reason the V1 in primates is also referred to as the "striate cortex." The line of Gennari is due to dense axonal input from the thalamus to layer IV of visual cortex.
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.