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• W1543065462 abstract "To the Editor: Because of sudden onset of conscious disturbance and sphincter incontinence, a 74-year-old Chinese man without a past history of any systemic disease or dementia was sent to the emergency department (ED) of Far Eastern Memorial Hospital with suspected stroke. In the emergency department, he was found to have a Glasgow Coma Scale score of E4M6V1, global aphasia, and weakness of the right limbs; his blood pressure was 133/80 mmHg. Computed tomography (CT) of the brain showed a large lobar parenchymal hematoma (∼4.1 × 6.3 × 6.8 cm in size) in his left frontoparietal cortex and subcortical white matter with severe perifocal edema (Figure 1A). No brain atrophy was noted. Magnetic resonance imaging (MRI) of the brain showed a large left frontoparietal parenchymal hematoma with a fluid–fluid level including an upper bright layer and a dark sediment layer (presumably due to intracellular deoxyhemoglobin in red blood cells) and several small dark foci in the cortical layers in bilateral frontal lobes on three-dimensional T2*-weighted gradient-recalled echo images (T2*WGREI) (Figure 1B) and an enhanced rim on gadolinium-enhanced T1-weight images. What was the diagnosis? A case of cerebral amyloid angiopathy in a 74-year-old Chinese man. (A) Computed tomography (CT) of the brain shows a large lobar parenchymal hematoma (large arrows) in his left frontoparietal cortex and subcortical white matter with severe perifocal edema. (B) A three-dimensional T2*-weighted gradient-recalled echo axial image shows a large left frontoparietal parenchymal hematoma (arrowheads) with a fluid–fluid level including an upper bright layer and a dark sediment layer (presumably due to intracellular deoxyhemoglobin in red blood cells) and several small dark foci of microbleeds (small arrows) in the cortical layers in bilateral frontal lobes. Because of suspicion of brain tumor hemorrhage, a neurosurgeon performed a craniotomy and removal of the intracerebral hematoma but found no gross brain tumor. He took a biopsy of the parenchymal tissue around the hematoma. The pathological diagnosis was intracerebral hemorrhage (ICH) due to rupture of arterioles and amyloid (congophilic) angiopathy, which was proved using Congo red stain to highlight the involved vessel walls of arterioles and veins containing amyloid with yellow-green birefringence under polarized light (Figure 2). Histologic appearance of β-amyloid deposition in the media and adventitia of small and medium-sized cerebral cortical vessels (arterioles and veins) in a specimen in the case of cerebral amyloid angiopathy. (A) Photomicrograph (original magnification, × 100; hematoxylin and eosin stain) shows structural change (fibrinoid necrosis and fragmentation) of the vessel walls with the β-amyloid deposits (short arrows) and surrounding hematoma. (B) Photomicrograph (original magnification, × 100; Congo red stain) obtained with polarized light shows the classic yellow-green birefringence of β-amyloid deposits (long arrows). Cerebral amyloid angiopathy (CAA) is one cause of spontaneous ICH that occurs mainly in the cortical and subcortical areas of the cerebrum in elderly people, but hypertensive microangiopathy-related ICH can happen in the putamen, thalamus, midbrain, pons, and cerebellum.1-6 CAA, which is characterized by pathological deposition of β-amyloid protein in the media and adventitia of small and medium-sized vessels of the cerebral cortex, subcortex, and leptomeninges, is mostly sporadic and rarely hereditary.1, 4 The sporadic form usually happens in elderly people and has significantly greater prevalence and severity with increasing age, whereas the hereditary form occurs at younger ages, as early as the third decade.1, 4β-amyloid protein is congophilic, so pathologists require special Congo red stain to identify β-amyloid protein under polarized light.1, 4β-amyloid protein causes fibrinoid necrosis and fragmentation of vessel walls.1, 4 Most cases are asymptomatic. If symptomatic, patients with CAA may present with transient neurological events, progressive cognitive decline, or intracerebral macrohemorrhage (>5 mm in size).1 CAA is underrecognized in elderly Chinese patients with spontaneous cortical-subcortical and lobar ICH.7, 8 A neuropathology study showed the prevalence of CAA in the randomly selected autopsy brains in a Chinese population aged 40 and older was approximately 10%, but only 8.2% of the autopsy brains with spontaneous ICH had CAA.7 Another study showed that approximately 31.7% of the examined brains of elderly Chinese had CAA, with incidence increasing with age and no sex preponderance but a close relationship with Alzheimer's disease and multiple cerebrovascular lesions. The sites frequently involved are the frontal lobe, occipital lobe, parietal lobe, and cerebellar dentate nucleus, in descending order.9 CAA causes spontaneous ICH less frequently in elderly Chinese than Caucasians.3, 5, 7 Neuroimaging modalities play an important role in helping clinicians recognize CAA. The Boston Criteria for diagnosis of clinically suspected CAA includes possible CAA (only 1 cortical ICH), probable CAA (>1 cortical ICH), probable CAA with pathologic specimen proof, and definite CAA (with postmortem examination).1 If brain CT of a normotensive elderly patient reveals spontaneous cortical–subcortical ICH that may be associated with subarachnoid, subdural, or intraventricular hemorrhage, differential diagnoses should include trauma, neoplasm, CAA, coagulopathy, rupture of aneurysm, and vasculitis.1, 3, 4 CAA-related ICH occurs in an older age group than hypertension-related ICH and rarely in basal ganglia.6 MRI of the brain is helpful in detecting the presence of asymptomatic cerebral microbleeds (CMBs), focal deposits of hemosiderin (presenting as dark hypointense spots on T2*WGREI like that in Figure 1), which suggests past repeated episodes of spontaneous intracerebral microhemorrhage (≤5 mm).1, 10, 11 CMBs might indicate a higher risk of future intracerebral macrohemorrhage and may be a marker of cerebral hypertensive microangiopathy and CAA.12 According to the Rotterdam Scan Study, the overall prevalence of CMB is high, and supratentorial cortical–subcortical CMBs are related to CAA, whereas CMB, in the deep gray matter or an infratentorial location usually result from hypertensive or atherosclerotic microangiopathy.13 Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: Concept and design: Wing-Keung Cheung. Acquisition of subjects and data: Wing-Keung Cheung, Yao-Peng Shu, and Shei-Chain Tseng. Analysis and interpretation of data: Wing-Keung Cheung, Yao-Peng Shu, Shei-Chain Tseng, and Kao-Lun Wang. Preparation of manuscript: Wing-Keung Cheung. Critical review and approval: all authors. Sponsor's Role: None." @default.
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• W1543065462 date "2009-09-01" @default.
• W1543065462 modified "2023-09-25" @default.
• W1543065462 title "Spontaneous Intracerebral Hemorrhage Secondary to Cerebral Amyloid Angiopathy" @default.
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• W1543065462 doi "https://doi.org/10.1111/j.1532-5415.2009.02403.x" @default.
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