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I./4.4.: Differentials by etiology
I./4.4.1.: Hypertensive hemorrhage
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Hypertensive hemorrhages origin from ruptured perforating arterioles. This fact corresponds with the typical localisation of the bleedings: basal ganglia, thalamus and pons supplied only by perforating arterioles, but rupture of arterioles could take place in the cortico-subcortical junction of the hemispheres and in the cerebellar nuclei as well. Distribution of the typical locations by frequency: putaminal– 30-40%, caudate– 10%, thalamic – 20-30%, pontine – 5-10%, cerebellar – 10%, subcortical – 20%.
I./4.4.2.: Hemorrhagic diathesis
This form result of oral anticoagulant therapy most often, occurs in 1-2% of anticoagulated patients. INR value above 4.5 brings higher frequency of bleedings, but cerebral hemorrhage could develop with the optimal treatment of INR 2-3. Hypertension is a risk factor for that. Most often, the hematoma enlarges for 6-12 hours, but hematoma progression over days was also observed. Hemorrhages as a result of coagulopathy have poor prognosis, two-third of the patients die. Cerebellar localization tends to be frequent. Treatment options are surgical if accessible (cerebellar, lobar hematomas) and causal, like factor substitution. Anticoagulant treatment could start with heparin (LMWH- low molecular weight heparin) after two weeks of the bleeding diathesis.
I./4.4.3.: Drug abuse
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Lobar hemorrhages in young patients (younger then 35 years) should raise the suspicion of drug abuse if there is no radiological sign of malformation. Drug use cause immidiate clinical symptoms because of the bleeding, so the ictus usually happens in places of amusement. Most bleedings caused by amphetamine and derivates followed by cocaine abuse. Sympathomymetic action manifest in hemorrhages.
I./4.4.4.: Amyloid angiopathy
Posterior, frequently parieto-occipital arterial watershed zone lobar bleedings are results of amyloid angiopathy after the sixth decade of life. Amyloid deposited in the walls of the arterioles and small arteries make the tissue broken, result in rupture even in normotensive patients. It is characteristic by multifocal bleeding and large size. Apart from the actual hemorrhage, residual multiple microbleeds as hemosiderine deposits are visible on highly sensitive gradient echo MRI scans.
I./4.4.5.: Other etiology
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More causes of intracerebral hemorrhages
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1) Tumor apoplexy, bleeding to the primary cerebral malignomas (e.g. gliobastoma multiforme),
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2) Cerebral metastases (bronchial carcinoma, melanoma malignum, renal carcinoma, thyroid- and colon-carcinomas),
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3) vasculitis,
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4) thrombosis of the sinuses and intracranial veins.
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