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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.
"Leukoaraiosis, or periventricular white matter disease, is the result of multiple small-vessel infarcts within the subcortical white matter... The pathophysiologic basis of the disease is lipohyalinosis of small penetrating arteries within the white matter, likely produced by chronic hypertension." [12]
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]
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population.
Others classify them as hippocampal, cortical, and WM lesions, [23] and finally, others give seven areas: intracortical, mixed white matter-gray matter, juxtacortical, deep gray matter, periventricular white matter, deep white matter, and infratentorial lesions. [24] The distribution of the lesions could be linked to the clinical evolution [25]
Periventricular leukomalacia (PVL) is a form of white-matter brain injury, characterized by the necrosis (more often coagulation) of white matter near the lateral ventricles. [ 1 ] [ 2 ] It can affect newborns and (less commonly) fetuses; premature infants are at the greatest risk of neonatal encephalopathy which may lead to this condition.
The finding of bilateral periventricular relatively asymmetrical lesions allied with deep white matter involvement, that may also be present in cortical gray-white matter junction, thalami, basal ganglia, cerebellum, and brainstem suggests an acute demyelination process. [22]
Compression of the brainstem as well as poor perfusion of the periventricular white matter in the prefrontal cortex are also thought to contribute to gait deviations in NPH. [14] Dementia in NPH is most likely caused by ventricular enlargement compressing the calvarium, which further leads to tearing of currently unidentified nerve fibers. [14]
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