Table of contentsVascular malformationPathophysiology of ICHHypertensive vascular changeAmyloid angiopathy (CAA)Molecular physiology of ICHDiagnosis of ICHClinical manifestationNeuroimagingTreatment of ICHSurgicalMedicalVascular malformationThe presence of vessel abnormalities bl in pain leads to an increased risk of intracranial hemorrhage. These anomalies include ruptured aneurysms, arteriovenous malformations, dural arteriovenous fistulas or cavernous angiomas (Di Tullio, Homma, 2002). Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay. Bleedings in this category eight occur after administration of thrombolytic drugs for treatment. Additionally, when a thrombus embolizes due to pain, it will usually be broken up after some time by the case's intrinsic process of thrombolysis. This often occurred after the point where the bl vessels themselves had become friable, leading to rupture of the vessel wall, extravasation of bl as hydrostatic pressure was restored (Nguyen et al., 2011). If a case develops a blood clot in a superficial or deep vein or venous sinus, hydrostatic pressure will increase upstream on the venous side of the capillary bed until water eventually penetrates through the capillary walls, into the interstitium of adjacent painful tissue. This process can cause edema, tissue dysaction leading to variable neurological deficits. If this continues hemorrhagic necrosis, vasogenic edema may develop in the affected area (Sagduyu et al., 2006). Intraparenchymal hemorrhages also occur in the setting of neoplastic disease, both in primary painful tumors, metA. S.Tatic disease. Additional causes in this category include hemorrhages due to sympathomimetic drugs such as cocaine, those due to systemic or primary arteriopathy (i.e., moyamoya), primary CNS, or systemic vasculitis (Burke et al., 2009). Pathophysiology of ICH Hypertensive vascular change ICH was generally caused by rupture of vessels that degenerated due to long-standing hypertension. The responsible arteries show significant media and smooth muscle degeneration. Fibrinoid necrosis of the subendothelium with microaneurysms, focal dilatations eight can be seen in some cases. Lipo-hyalinoses mainly linked to long-standing hypertension were most often round in non-lobar ICH (Charidimou et al., 2012). Amyloid angiopathy (CAA) CAA was characterized by the deposition of amyloid-β peptide in capillaries, arterioles, small, medium-sized arteries in the cortex, leptomeninges, cerebellum, making them stiff, brittle, predisposing them to to rupture (Rost et al., 2008). Molecular pathophysiology of ICHThe initial mechanism of ICH was compression of the painful parenchyma by the critical mass of the hematoma, which resulted in physical disruption of the parenchymal architecture. Increased intracranial pressure due to hematoma expansion can affect blood flow, mechanical deformation, neurotransmitter release, mitochondrial dysaction, and membrane depolarization. As a result, the neuron in the perihematomal area contains edema, environment by facts derived from the bl. Edema usually develops over the first 24 to 96 hours, slowly resolving over several weeks. Early edema was usually secondary to more present cases in the hematoma (Qureshi et al., 2003)..,