{"title":"Intracerebral haemorrhage.","authors":"C S Kase","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Intracerebral haemorrhage accounts for 15% of strokes. Its mechanisms include hypertension, cerebral amyloid angiopathy, rupture of vascular malformations, bleeding into primary or metastatic brain tumours, coagulopathies (due to the use of anticoagulants and thrombolytic agents), sympathomimetic drug effect (amphetamines, phenylpropanolamine, and cocaine), and vasculitis. The clinical presentation reflects both the general effects of increased intracranial pressure, and the neurological deficits that result from the specific location of the haemorrhage. Its diagnosis is based on computerized tomography, which identifies haemorrhage as a high-attenuation mass within the brain substance, and magnetic resonance imaging, which in addition estimates the age of the haemorrhage by identifying sequential patterns of transformation of the haemoglobin molecule within the haematoma. The mortality in intracerebral haemorrhage is dependent on the size and location of the haematoma. A reliable clinical parameter for the prediction of outcome is the Glasgow Coma Scale score at presentation. The management of intracerebral haemorrhage involves: (a) the prevention and treatment of increased intracranial pressure; and (b) the choice between surgical and nonsurgical treatment, a clinical decision that is still controversial as a result of the paucity of controlled clinical data comparing both treatment modalities.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"247-78"},"PeriodicalIF":0.0000,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bailliere's clinical neurology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Intracerebral haemorrhage accounts for 15% of strokes. Its mechanisms include hypertension, cerebral amyloid angiopathy, rupture of vascular malformations, bleeding into primary or metastatic brain tumours, coagulopathies (due to the use of anticoagulants and thrombolytic agents), sympathomimetic drug effect (amphetamines, phenylpropanolamine, and cocaine), and vasculitis. The clinical presentation reflects both the general effects of increased intracranial pressure, and the neurological deficits that result from the specific location of the haemorrhage. Its diagnosis is based on computerized tomography, which identifies haemorrhage as a high-attenuation mass within the brain substance, and magnetic resonance imaging, which in addition estimates the age of the haemorrhage by identifying sequential patterns of transformation of the haemoglobin molecule within the haematoma. The mortality in intracerebral haemorrhage is dependent on the size and location of the haematoma. A reliable clinical parameter for the prediction of outcome is the Glasgow Coma Scale score at presentation. The management of intracerebral haemorrhage involves: (a) the prevention and treatment of increased intracranial pressure; and (b) the choice between surgical and nonsurgical treatment, a clinical decision that is still controversial as a result of the paucity of controlled clinical data comparing both treatment modalities.