No abstract available.
Cerebral Amyloid Angiopathy ; Inflammation

No abstract available.
Alzheimer Disease* ; Animals ; Cerebral Amyloid Angiopathy* ; Mice*

No abstract available.
Cerebral Amyloid Angiopathy* ; Cerebral Hemorrhage* ; Humans ; Ischemic Attack, Transient*

Cerebral amyloid angiopathy(CAA) is a nonspecific disease entity that has been associated with a number of neuropathologic conditions, the most prominent being dementia and cerebral hemorrhage. It occurs more commonly than is generally appreciated, with implications that may be overlooked. As amyloid deposits are found in the vessels of the leptomeninges and cerebral cortex, the location and size of the hematoma, with cortical and subarachnoid extension, help to differentiate amyloid angiopathy from other causes of intracerebral hemorrhage in the elderly. It has, in addition, characteristic pathological features, and the existence of these, together with the occurance of nontraumatic normotensive spontaneous primary cerebral hemorrhage in the elderly, should indicate the existence of CAA. The authors report a case of cerebral amyloid angiopathy-related intracerebral hemorrhage.
Aged ; Amyloid* ; Cerebral Amyloid Angiopathy ; Cerebral Cortex ; Cerebral Hemorrhage* ; Dementia ; Hematoma ; Humans ; Plaque, Amyloid

Cerebral microbleeds (CMBs) are tiny, round dark-signal lesions that are most often detected on gradient-echo MR images. CMBs consist of extravasations of blood components through fragile microvascular walls characterized by lipohyalinosis and surrounding macrophages. The prevalence of CMBs in elderly subjects with no history of cerebrovascular disease is around 5%, but is much higher in patients with ischemic or hemorrhagic stroke. Development of CMBs is closely related to various vascular risk factors; in particular, lobar CMBs are thought to be associated with cerebral amyloid angiopathy. The presence of CMBs has been hypothesized to reflect cerebral-hemorrhage-prone status in patients with hypertension or amyloid microangiopathy. Stroke survivors with CMBs have been consistently found to have an elevated risk of subsequent hemorrhagic stroke or an antithrombotic-related hemorrhagic complication, although studies have failed to establish a link between CMBs and hemorrhagic transformation after thrombolytic treatment. A large prospective study is required to clarify the clinical significance of CMBs and their utility in a decision-making index.
Aged ; Aluminum Hydroxide ; Amyloid ; Carbonates ; Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage ; Humans ; Hypertension ; Macrophages ; Prevalence ; Stroke ; Survivors

Cerebral amyloid angiopathy-related inflammation (CAA-RI) is a rare but increasingly recognized subtype of CAA. CAA-RI consists of two subtypes: inflammatory cerebral amyloid angiopathy and amyloid β (Aβ)-related angiitis. Acute or subacute onset of cognitive decline or behavioral changes is the most common symptom of CAA-RI. Rapid progressive dementia, headache, seizures, or focal neurological deficits, with patchy or confluent hyperintensity on T2 or fluid-attenuated inversion recovery sequences and evidence of strictly lobar microbleeds or cortical superficial siderosis on susceptibility-weighted imaging imply CAA-RI. The gold standard for diagnosis is autopsy or brain biopsy. However, biopsy is invasive; consequently, most clinically diagnosed cases have been based on clinical and radiological data. Other diagnostic indexes include the apolipoprotein E ε4 allele, Aβ and anti-Aβ antibodies in cerebral spinal fluid and amyloid positron emission tomography. Many diseases with similar clinical manifestations should be carefully ruled out. Immunosuppressive therapy is effective both during initial presentation and in relapses. The use of glucocorticoids and immunosuppressants improves prognosis. This article reviews the pathology and pathogenesis, clinical and imaging manifestations, diagnostic criteria, treatment, and prognosis of CAA-RI, and highlights unsolved problems in the existing research.
Amyloid beta-Peptides ; Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage ; Humans ; Inflammation ; Magnetic Resonance Imaging ; Vasculitis

Cerebral amyloid angiopathy(CAA) is characterized by the deposition of amyloid beta-protein in the walls of small to medium-sized arteries of the leptomeninges and cerebral cortex. While often asymptomatic, CAA can develop into intracerebral hemorrhage facilitated by arterial hypertension. We report the case of a 52-year-old man with CAA and arterial hypertension who developed recurrent cerebral hemorrhages on three different occasions and in multiple non-overlapping loci over a period of nine years. Based on our findings, we recommend brain biopsies for all patients undergoing evacuation of multiple recurrence or atypical pattern intracerebral hemorrhages.
Amyloid ; Amyloid beta-Peptides ; Arteries ; Biopsy ; Brain ; Cerebral Amyloid Angiopathy* ; Cerebral Cortex ; Cerebral Hemorrhage* ; Humans ; Hypertension* ; Middle Aged ; Recurrence

Superficial siderosis (SS) is a rare disorder characterized by deposition of hemosiderin in the leptomeninges and subpial layer of the central nervous system. Recently SS suggested a subtype of cerebral amyloid angiopathy which is an important cause of lobar intracerebral hemorrhage (ICH). We present a patient with cortical SS had seizure and cognitive dysfunction as symptom and lobar ICH in the existed area of cortical SS 4 years later. This case suggested cortical SS could be a warning sign of lobar ICH.
Central Nervous System ; Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage ; Hemosiderin ; Humans ; Seizures ; Siderosis

OBJECTIVE: In the so-called primary intracerebral hemorrhage (ICH), lobar and deep ICH were mainly due to cerebral amyloid angiopathy and deep perforating arterial disease. Our aim was to identify specifics of warfarin associated ICH (WAICH) and to focus on differences in susceptibility to warfarin according to the underlying vasculopathies, expressed by ICH location. MATERIALS AND METHODS: We identified all subjects aged > or = 18 years who were admitted with primary ICH between January 1, 2007 and September 30, 2012. We retrospectively collected demographic characteristics, the presence of vascular risk factors and pre-ICH medication by chart reviews. We categorized ICH into four types according to location: lobar, deep, posterior fossa, and undetermined. We investigated characteristics (including hematoma volume and expansion) of ICH according to the location of ICH. RESULTS: WAICH accounted for 35 patients (5.6%) of 622 ICH cases. In WAICH, 13 patients (37.1%) had lobar ICH and 22 patients (60.0%) had non-lobar ICH. Compared to other locations of ICH, lobar ICH showed an excess risk of WAICH (OR 2.53, 95% CI 1.03-6.21, p = 0.042). The predictors of lobar location of ICH were warfarin (OR 2.29, 95% CI 1.05-5.04, p = 0.038) and diabetes mellitus (DM) (OR 0.54, 95% CI 0.29-0.98, p = 0.044). The lobar location of ICH showed significant association with larger hematoma volume (p = 0.001) and high ratio of hematoma expansion (p = 0.037) compared with other locations of ICH. CONCLUSION: In our study, warfarin showed significant association with lobar ICH and it caused larger hematoma volume and more expansion of hematoma in lobar ICH.
Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage ; Diabetes Mellitus ; Hematoma ; Humans ; Intracranial Hemorrhages* ; Retrospective Studies ; Risk Factors ; Warfarin*

OBJECTIVE: The clinical and pathological characteristics of 10 cases of cerebral amyloid angiopathy (CAA)-related cerebral lobar hemorrhage (CLH) that was diagnosed at autopsy were investigated to facilitate the diagnosis of this condition. METHODS: The clinical characteristics of 10 cases of CAA-related CLH were retrospectively reviewed, and a neuropathological examination was performed on autopsy samples. RESULTS: The 10 cases included two with a single lobar hemorrhage and eight with multifocal lobar hemorrhages. In all of the cases, the hemorrhage bled into the subarachnoid space. Pathological examinations of the 10 cases revealed microaneurysms in two, double barrel-like changes in four, multifocal arteriolar clusters in five, obliterative onion skin-like intimal changes in four, fibrinoid necrosis of the vessels in seven, neurofibrillary tangles in eight, and senile plaques in five cases. CONCLUSION: CAA-related CLHs were located primarily in the parietal, temporal, and occipital lobes. These hemorrhages normally consisted of multiple repeated CLHs that frequently bled into the subarachnoid space. CAA-associated microvascular lesions may be the pathological factor underlying CLH.
Amyloid* ; Autopsy ; Cerebral Amyloid Angiopathy ; Diagnosis ; Hemorrhage* ; Necrosis ; Neurofibrillary Tangles ; Occipital Lobe ; Onions ; Plaque, Amyloid ; Rabeprazole ; Retrospective Studies ; Subarachnoid Space