Progressive hemorrhagic injury (PHI) can be divided into coagulopathy-related PHI and normal coagu- lation PHI. Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy (TIC). Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality. In this review, we discussed some mechanisms in TIC, which is of great importance in the development of PHI, including tissue factor (TF) hypothesis, protein C pathway and thrombocytopenia. The main mechanism in the relation of TIC to PHI is hypocoagulability. We also reviewed some coagulopathy parameters and proposed some possible risk factors, predictors and therapies.
Blood Coagulation Disorders ; epidemiology ; etiology ; Brain Injuries, Traumatic ; complications ; Cerebral Hemorrhage ; epidemiology ; etiology ; therapy ; Fibrin Fibrinogen Degradation Products ; analysis ; Humans ; Incidence ; Protein C ; physiology ; Risk Factors ; Thromboplastin ; physiology

BACKGROUND/AIMS: The clinical implications of hypocholesterolemia have not been well studied, although some studies have revealed an association between hypocholesterolemia and intracerebral hemorrhage (ICH). We evaluated the clinical characteristics of subjects with very low-density lipoprotein cholesterol (LDL-C) and compared the risk for ICH using various clinical parameters. METHODS: Using hospital records, we evaluated the clinical characteristics of subjects with LDL-C levels < or = 40 mg/dL (very low LDL-C group). We also evaluated the risk for ICH in this very low LDL-C group and in subjects with low LDL-C < or = 70 mg/dL (low LDL-C group). RESULTS: Among 34,415 subjects who presented at the laboratory for serum LDL-C measurements, 250 subjects had a very low serum LDL-C level (< or = 40 mg/dL). About half of the subjects were statin users; the very low LDL levels in the other subjects were likely attributable to alcohol consumption or a various chronic illness such as liver disease or end-stage renal disease (ESRD). ICH occurred in three subjects with very low LDL-C, all of whom had no history of statin use. ESRD tended to be associated with ICH in subjects with serum LDL-C < or = 70 mg/dL. CONCLUSIONS: About 1% of the subjects whose LDL-C was measured in the hospital had a LDL-C level < or = 40 mg/dL, and about half of these subjects had no history of hypolipidemic therapy. ICH incidence was not related to LDL-C level or statin use.
Aged ; Alcohol Drinking/adverse effects/epidemiology ; Biological Markers/blood ; Cerebral Hemorrhage/blood/*epidemiology ; Cholesterol, LDL/*blood ; Down-Regulation ; Dyslipidemias/blood/*epidemiology ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects ; Incidence ; Kidney Failure, Chronic/epidemiology ; Liver Diseases/epidemiology ; Male ; Middle Aged ; Republic of Korea/epidemiology ; Retrospective Studies ; Risk Assessment ; Risk Factors ; Time Factors

Cerebral amyloid angiopathy (CAA) involves cerebrovascular amyloid deposition and is classified into several types according to the amyloid protein involved. Of these, sporadic amyloid beta-protein (Abeta)-type CAA is most commonly found in older individuals and in patients with Alzheimer's disease (AD). Cerebrovascular Abeta deposits accompany functional and pathological changes in cerebral blood vessels (CAA-associated vasculopathies). CAA-associated vasculopathies lead to development of hemorrhagic lesions [lobar intracerebral macrohemorrhage, cortical microhemorrhage, and cortical superficial siderosis (cSS)/focal convexity subarachnoid hemorrhage (SAH)], ischemic lesions (cortical infarction and ischemic changes of the white matter), and encephalopathies that include subacute leukoencephalopathy caused by CAA-associated inflammation/angiitis. Thus, CAA is related to dementia, stroke, and encephalopathies. Recent advances in diagnostic procedures, particularly neuroimaging, have enabled us to establish a clinical diagnosis of CAA without brain biopsies. Sensitive magnetic resonance imaging (MRI) methods, such as gradient-echo T2* imaging and susceptibility-weighted imaging, are useful for detecting cortical microhemorrhages and cSS. Amyloid imaging with amyloid-binding positron emission tomography (PET) ligands, such as Pittsburgh Compound B, can detect CAA, although they cannot discriminate vascular from parenchymal amyloid deposits. In addition, cerebrospinal fluid markers may be useful, including levels of Abeta40 for CAA and anti-Abeta antibody for CAA-related inflammation. Moreover, cSS is closely associated with transient focal neurological episodes (TFNE). CAA-related inflammation/angiitis shares pathophysiology with amyloid-related imaging abnormalities (ARIA) induced by Abeta immunotherapies in AD patients. This article reviews CAA and CAA-related disorders with respect to their epidemiology, pathology, pathophysiology, clinical features, biomarkers, diagnosis, treatment, risk factors, and future perspectives.
Alzheimer Disease ; Amyloid ; Amyloid beta-Peptides ; Biomarkers ; Biopsy ; Blood Vessels ; Brain ; Cerebral Amyloid Angiopathy* ; Cerebrospinal Fluid ; Cerebrovascular Disorders ; Dementia ; Diagnosis ; Epidemiology ; Humans ; Immunotherapy ; Infarction ; Inflammation ; Leukoencephalopathies ; Ligands ; Magnetic Resonance Imaging ; Neuroimaging ; Pathology ; Plaque, Amyloid ; Positron-Emission Tomography ; Risk Factors ; Siderosis ; Stroke ; Subarachnoid Hemorrhage