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Cerebral amyloid angiopathy may cause intraparenchymal hemorrhage even in patients without elevated blood pressure. Unlike hypertension, cerebral amyloid angiopathy does not typically affect blood vessels to deep brain structures. Instead, it is most commonly associated with hemorrhage of small vessels in the cerebral cortex. [2]
Hemorrhagic stroke may occur on the background of alterations to the blood vessels in the brain, such as cerebral arteriolosclerosis, cerebral amyloid angiopathy, cerebral arteriovenous malformation, brain trauma, brain tumors and an intracranial aneurysm, which can cause intraparenchymal or subarachnoid hemorrhage. [1]
Cerebral softening, also known as encephalomalacia, is a localized softening of the substance of the brain, due to bleeding or inflammation. Three varieties, distinguished by their color and representing different stages of the disease progress, are known respectively as red, yellow, and white softening.
Once ruptured, it results in intraparenchymal hemorrhage, intraventricular hemorrhage and SAH. Rupture of cerebral AVM often occurs in young people and children. Cerebral AVM can be diagnosed by computed tomography angiography (CTA) brain, magnetic resonance angiography (MRA) brain, or digital subtraction angiography (DSA). DSA is important to ...
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.
Other common locations for DAI include the white matter in the cerebral cortex, the superior cerebral peduncles, [16] basal ganglia, thalamus, and deep hemispheric nuclei. [clarification needed] [20] These areas may be more easily damaged because of the difference in density between them and the other regions of the brain. [20]
Microinfarcts are microscopic lesions, of cellular death or tissue necrosis, which are a result of pathologies involving small vessels. Such pathologies are arteriosclerosis or cerebral amyloid angiopathy. [5] Microinfarcts take longer to affect neuronal death progress, at up to 28 days, rather than hours. [6]
ARIA-E refers to cerebral edema, involving the breakdown of the tight endothelial junctions of the blood-brain barrier and subsequent accumulation of fluid. [3] In a double-blind trial of the humanised monoclonal antibody solanezumab (n = 2042), sixteen patients (11 taking the drug, 5 taking a placebo), or 0.78% developed ARIA-E.