cerebral amyloid angiopathy/asthenia

A 75-year-old man with a history of atrial fibrillation (AF) and anticoagulant therapy presented with a headache. Cerebral amyloid angiopathy (CAA) was diagnosed after MRI of the brain revealed cortical superficial siderosis, lobar intracerebral hemorrhage, and lobar microbleeds. Anticoagulant

BACKGROUND Cerebral amyloid angiopathy is a well-known disease that is predominantly recognized in elderly people and repeatedly causes large subcortical hemorrhages. These hemorrhages may be derived from vessel wall weakness because of Abeta depositions in the wall of the cortical and

We describe a 68-year-old woman who presented with falls, mild limb bradykinesia, axial rigidity, and a severe supranuclear gaze palsy, which failed to benefit from levodopa. She subsequently developed severe apraxia, progressive dysarthria, dysphagia, and a frontal cognitive impairment. Pyramidal

OBJECTIVE Transient focal neurological episodes (TFNE) are recognized in cerebral amyloid angiopathy (CAA) and may herald a high risk of intracerebral hemorrhage (ICH). We aimed to determine their prevalence, clinical neuroimaging spectrum, and future ICH risk. METHODS This was a multicenter

The risk of anticoagulant-associated intracranial hemorrhage(ICH)is relatively low in patients treated with non-vitamin K antagonist oral anticoagulants(NOAC). The anticoagulant-associated ICH comprises mainly intraparenchimal hemorrhage. Subdural hematoma and subarachnoid hemorrhage(SAH)are rare

Amyloid-beta related angiitis (ABRA) of the central nervous system (CNS) is a rare disorder with overlapping features of primary angiitis of the CNS and cerebral amyloid angiopathy. We evaluated a 74-year-old man with intermittent left sided weakness and MRI findings of leptomeningeal enhancement,

The deposition of amyloid Abeta peptide in the wall of cerebral vessels (cerebral amyloid angiopathy), can lead to weakness and rupture of the vessel wall, resulting in hemorrhagic stroke. The Tg2576 transgenic mouse line, overexpressing mutant amyloid precursor protein in an age-dependent manner,

Three patients (of two unrelated Polish families) with early-adult onset dementia were subjects of the study. Two cases, previously diagnosed as familial Alzheimer's disease (FAD) with cerebral amyloid angiopathy (CAA), were confirmed by genetic and neuropathological studies, and one case of CADASIL