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The World Health Organisation has defined stroke as: “A neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours.”
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· Thrombosis - thrombus forms locally, obstructing blood vessels within the brain, either veins or arteries. · Systemic hypoperfusion – such as in shock, for example hypovolemic, which results from inadequate blood volume for the continuation of satisfactory cardiac output, blood pressure, and tissue perfusion. | · Cerebral embolism - embolus forms in any blood vessel within the body and travels to the brain.
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· Penetrating head trauma
· Depressed skull fractures
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· Rupture of an aneurysm
| · Arteriovenous malformation · Bleeding within a tumour · Amyloid angiopathy · Cerebral venous sinus thrombosis |
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· Age · Gender (male > female, except in the very young and very old) · Race (Afro-Carribean > Asian > European) · Heredity · High fibrinogen · Previous vascular event, e.g. MI, stroke or peripheral embolism · Menopause | · High blood pressure · Heart disease (atrial fibrillation, heart failure) · Diabetes mellitus · Hyperlipidaemia · Smoking · Excess alcohol consumption (≥2/day) · Polycythaemia · Oral contraceptives · Social deprivation |
Kazuhiko et al., (2011) also suggest that infection with serotype k Streptococcus mutants expressing collagen-binding protein is a potential risk factor for haemorrhagic stroke.
Molecular mechanisms of neuronal ischaemia and infarction are depicted in Figure 4 and occur in the following order. Reduction of blood flow reduces supply of oxygen and glucose, hence ATP and H+ions. Energy-dependent membrane ionic pumps fail, leading to cytotoxic oedema and membrane depolarisation, allowing calcium entry and release of glutamate. Calcium enters cells via glutamate-gated channels and activates destructive intracellular enzymes, destroying intracellular organelles and cell membrane with release of free radicals. Free fatty acid release activates pro-coagulant pathways, which exacerbate local ischaemia. Glial cells take up H+ions and thus cannot take up extracellular glutamate and suffer cell death. The release of inflammatory mediators by microglia and astrocytes lead to necrosis of all cell types in the whole arterial territory.
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Introduction | | | Available treatments for stroke |