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The exact pathophysiology of Monckeberg's arteriosclerosis remains uncertain. However, it is thought that the condition arises from the fatty degeneration of smooth muscle cells within the arterial media, leading to the formation of a mass that undergoes hyaline degeneration and eventually calcification.
Sclerosis (from Ancient Greek σκληρός (sklērós) 'hard') is the stiffening of a tissue or anatomical feature, usually caused by a replacement of the normal organ-specific tissue with connective tissue.
Drawing of sclerotic lesions from Babinski's thesis "Etude anatomique et clinique de la sclérose en plaques", 1885. Multiple sclerosis (MS) can be pathologically defined as the presence of distributed glial scars in the central nervous system that must show dissemination in time (DIT) and in space (DIS) to be considered MS lesions.
Atherosclerosis [a] is a pattern of the disease arteriosclerosis, [8] characterized by development of abnormalities called lesions in walls of arteries.This is a chronic inflammatory disease involving many different cell types and driven by elevated levels of cholesterol in the blood. [9]
This could indicate that some number of lesions exist, below which the brain is capable of repairing itself without producing noticeable consequences. [1] Another process involved in the creation of lesions is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons. [1] A number of lesion patterns have been ...
It is called tumefactive as the lesions are "tumor-like" and they mimic tumors clinically, radiologically and sometimes pathologically. [1] These atypical lesion characteristics include a large intracranial lesion of size greater than 2.0 cm with a mass effect, edema and an open ring enhancement. A mass effect is the effect of a mass on its ...
Focal segmental glomerulosclerosis (FSGS) is a histopathologic finding of scarring of glomeruli and damage to renal podocytes. [2] [3] This process damages the filtration function of the kidney, resulting in protein presence in the urine due to protein loss. [3]
In 1825, Bouchet and Cazauvieilh described palpable firmness and atrophy of the uncus and medial temporal lobe of brains from epileptic and non-epileptic individuals. [4]: 565 In 1880, Wilhelm Sommer investigated 90 brains and described the classical Ammon's horn sclerosis pattern, severe neuronal cell loss in hippocampal subfield cornum Ammonis 1 (CA1) and some neuronal cell loss in ...