We conclude that PiB-positron emission tomography can detect cerebrovascular beta-amyloid and may serve as a method for identifying the extent of CAA in living subjects.

Cerebral amyloid angiopathy-related inflammation represents a clinically, pathologically, radiographically, and genetically distinct disease subtype with implications for clinical practice and ongoing immunotherapeutic approaches to Alzheimer disease.

Introduction Intracerebral hemorrhage (ICH) is the most feared complication of oral anticoagulant therapy (OAT). While anticoagulated patients have increased severity of bleeding following ICH, they may also be at increased risk for thromboembolic events (TEs) given that they had been prescribed OAT prior to their ICH. We hypothesized that TEs are relatively common following ICH, and that anticoagulated patients are at higher risk for these complications. Methods Consecutive patients with primary ICH presenting to a tertiary care hospital from 1994 to 2006 were prospectively characterized and followed. Hospital records were retrospectively reviewed for clinically relevant inhospital TEs and patients were prospectively followed for 90 day mortality. Results For 988 patients of whom 218 (22%) were on OAT at presentation, median hospital length of stay was 7 (IQR 4–13) days and 90-day mortality was 36%. TEs were diagnosed in 71 patients (7.2%) including pulmonary embolism (1.8%), deep venous thrombosis (1.1%), myocardial ischemia (1.6%), and cerebrovascular ischemia (3.0%). Mean time to event was 8.4 ± 7.0 days. Rates of TE were 5% among those with OAT-related ICH and 8% among those with non-OAT ICH (P = 0.2). After multivariable Cox regression, the only independent risk factor for developing a TE was external ventricular drain placement (HR 2.1, 95% CI 1.1–4.1, P = 0.03). TEs had no effect on 90-day mortality (HR 0.7, 95% CI 0.5–1.1, P = 0.1). Conclusions The incidence of TEs in an unselected ICH population was 7.2%. Patients with OAT-related ICH were not at increased risk of TEs.

Background and Purpose-Cerebral amyloid angiopathy (CAA) is a major cause of lobar intracerebral hemorrhage and cognitive impairment and is associated with white matter hyperintensities and cerebral microbleeds. MRI diffusion tensor imaging detects microstructural tissue damage in advanced CAA even in areas that appear normal on conventional MRI. We hypothesized that higher global mean apparent diffusion coefficient (mean ADC), reflecting a higher amount of chronic tissue disruption caused by CAA, would be independently associated with CAA-related cognitive impairment. Methods-Preintracerebral hemorrhage cognitive impairment was systematically assessed using a standardized questionnaire (IQCODE) in 49 patients. Volume of white matter hyperintensities, number of microbleeds, and mean ADC were determined from MRIs obtained within 14.0Ϯ22.5 days of intracerebral hemorrhage cognitive impairment. White matter hyperintensities and mean ADC were measured in the hemisphere uninvolved by intracerebral hemorrhage to avoid confounding. Results-Preintracerebral hemorrhage cognitive impairment was identified in 10 of 49 subjects. Mean ADC was the only variable associated with preintracerebral hemorrhage cognitive impairment and was elevated in those with preintracerebral hemorrhage cognitive impairment compared with those without (12.4ϫ10 Ϫ4 versus 11.7ϫ10 Ϫ4 mm 2 /s; Pϭ0.03). Mean ADC positively correlated with age but not white matter hyperintensities or number of microbleeds. In logistic regression controlling for age and visible cerebral atrophy, mean ADC was independently associated with preintracerebral hemorrhage cognitive impairment (OR per 1ϫ10 Ϫ4 mm 2 /s increaseϭ2.45, 95% CI 1.11 to 5.40, Pϭ0.04). Conclusions-Mean ADC is independently associated with preintracerebral hemorrhage cognitive impairment in CAA.The lack of correlation with other MRI markers of CAA suggests that mean ADC may be sensitive to distinct aspects of CAA pathology and its tissue consequences. These results suggest that global MRI diffusion changes are sensitive to clinically relevant microstructural alterations and may be useful markers of CAA-related tissue damage. Key Words: cerebral amyloid angiopathy Ⅲ cerebral microhemorrhage Ⅲ cognitive impairment Ⅲ dementia Ⅲ diffusion Ⅲ microbleeds Ⅲ white matter disease C erebral amyloid angiopathy (CAA) is a major cause of lobar intracerebral hemorrhage (ICH) and cognitive impairment in the elderly and is associated with a high prevalence of markers of small vessel disease, including white matter hyperintensities (WMH) and cerebral microbleeds (MB). [1][2][3][4] ICH in sporadic CAA is likely caused by vessel fragility and rupture due to the deposition of amyloid within the media and adventitia of small-to medium-sized cerebral arteries. 5 The presence of WMH visualized on conventional MRI sequences 4 suggests that vascular amyloid deposition may alter white matter perfusion by causing stenosis or vascular dysfunction. 6 This hypothesis is supported by the observations of extensive white matter damage ...