IndexVascular malformationPathophysiology of ICHShypertensive vascular changesAmyloid angiopathy (CAA)Molecular pathophysiology of ICHCDiagnosis of ICHClinical manifestationNeuroimagingTreatment of ICHSurgicalMedicalVascular MalformationThe presence of blood vessel abnormalities 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 Shouldn't Be Banned"? Get Original Essay Hemorrhages in this category eight occur after administration of thrombolytic drugs for treatment. Furthermore, when a thrombus embolizes causing pain, it is usually destroyed after some time by the case's intrinsic thrombolysis process. This often occurred after the point at which the bl vessels themselves had become friable, leading to vessel wall rupture, extravasation of bl when hydrostatic pressure was restored (Nguyen et al., 2011). If a case develops a blood clot in a superficial or deep vein or venous sinus, the hydrostatic pressure will increase upstream on the venous side of the capillary bed until water has penetrated through the capillary walls, into the interstitium of the tissue painful adjacent. This process can cause edema, tissue dysfunction leading to variable neurological deficits. If hemorrhagic necrosis continues, vasogenic edema may develop in the affected area (Sagduyu et al., 2006). Eight intraparenchymal hemorrhages also occur in the context of neoplastic disease, both in tumors with primary pain, metA. St. Tatic's disease. Additional causes within this category include hemorrhage due to sympathomimetic drugs such as cocaine, those due to systemic or primary arterial disease (i.e., moyamoya), primary central nervous system, or systemic vasculitis (Burke et al., 2009). Pathophysiology of ICH Hypertensive vascular changes I.CH had usually caused by rupture of degenerated vessels due to long-standing hypertension. The responsible arteries show prominent degeneration of the middle and smooth muscles. In some cases, fibrinoid necrosis of the subendothelium with microaneurysms and focal dilations can be observed. Lipo-hyalinoses, predominantly related to long-standing hypertension, occurred more often in non-lobar IC (Charidimou et al., 2012). Amyloid angiopathy (CAA) CAA was characterized by the deposition of the amyloid-β peptide in the capillaries, arterioles, small, medium-sized arteries in the cortex, leptomeninges, cerebellum, making them rigid, fragile, predisposing them to rupture (Rost et al., 2008). Molecular pathophysiology of ICH The initial mechanism of ICH involved compression of the painful parenchyma by the critical mass of the hematoma, resulting in the physical destruction of the parenchymal architecture. Increased intracranial pressure due to hematoma expansion can affect bl flow, mechanical deformation, neurotransmitter release, mitochondrial desaction, membrane depolarization. As a result, the neuron in the peri-hematomal area contains edema, environment derived from bl facts. Edema typically develops in the first 24-96 hours, resolves slowly over several weeks, early edema was usually secondary to positive cases present in the hematoma (Qureshi et al., 2003). A secondary mechanism of pain was related to the coagulation cascade particularly thrombin. After endothelial damage, breakdown of hemoglobin, thrombin causes calls to infiltrate the pain. It binds to receptors activated by.,