The association between cerebral amyloid angiopathy and atherosclerosis in patients with intracerebral hemorrhages (original) (raw)
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Journal of Zhejiang University Science, 2004
Objective: The purpose of this study was to differentiate between cerebral amyloid angiopathy (CAA) and hypertension (HTN) based on hemorrhage pattern interpretation. Methods: From June 1994 to Oct., 2000, 83 patients admitted to our service with acute intracerebral hemorrhage (ICH) were investigated retrospectively; 41 patients with histologically proven diagnosis of cerebral amyloid angiography and 42 patients with clear history of hypertension were investigated. Results: Patients with a CAA-related ICH were significantly older than patients with a HTN-related ICH (74.0 years vs 66.5 years, P<0.05). There was a significantly higher number of hematomas≥30 ml in CAA (85.3%) when compared with HTN (59.5%). No basal ganglional hemorrhage was seen in CAA, but in 40.5% in HTN. In CAA-related ICH, subarachnoid hemorrhage (SAH) was seen in 26 patients (63.4%) compared to only 11 patients (26.2%) in HTN-related ICH. Intraventricular hemorrhage was seen in 24.4% in CAA, and in 26.2% in HTN. Typical features of CAA-related ICH included lobar distribution affecting mainly the lobar superficial areas, lobulated appearance, rupture into the subarachnoid space, and secondary IVH from the lobar hemorrhage. More specifically, multiplicity of hemorrhage, bilaterality, and repeated episodes also strongly suggest the diagnosis of CAA. Multiple hemorrhages, defined as 2 or more separate hematomas in multiple lobes, accounted for 17.1% in CAA-related ICH. Conclusion: There are certain features in CAA on CT and MRI and in clinical settings. To some extent, these features may contribute to distinguishing CAA from HTN related ICH.
Folia neuropathologica, 2017
In patients with cerebral venous thrombosis (CVT) the incidence of intracerebral hemorrhage (ICH) is estimated at about 37% and subarachnoid hemorrhage (SAH) at 1% of patients. A case with coincident occurrence of ICH, SAH and CVT in a patient with cerebral amyloid angiopathy (CAA) is reported. A 79-year-old woman was admitted to the Neurological Department after the occurrence of generalized seizures, the first in her life. On admission she was unconscious with right hemiparesis and deviation of eyes to the left. On computed tomography (CT) scan many hemorrhagic infarcts were present in the frontal, parietal, temporal and left occipital lobes. Angio-CT revealed thrombosis in the right transverse sinus, right internal carotid vein and superior sagittal sinus. Her state slowly deteriorated. She died after 6 days. Neuropathologically, many hemorrhagic infarcts were observed in cortical regions in the vicinity of veins with thrombosis and in the white matter. The varied time of onset o...
Pathologic processes leading to cerebral hemorrhage in amyloid angiopathy
…, 1996
This report concerns a study undertaken to elucidate the pathogenesis of arterial rupture related to amyloid deposition. For this purpose, histochemical and immunohistochemical analyses were carried out on brain tissue specimens of a case of cerebral amyloid angiopathy (CAA) with multiple cortical hemorrhages. A small amount of amyloid P-protein was found in the tunica media vasorum in which the smooth muscle cells were well preserved. With increases in amyloid deposition, the entire arteriolar wall became concentrically thick, with amyloid largely occupying the tunica media; the number of smooth muscle cells was decreased and these cells were located in the intimal side of the vessel wall. Under these conditions, the elastic fibers and endothelial cells were relatively well preserved. In the advanced stage of amyloid deposition, the arterioles became devoid of smooth muscle cells and underwent either fibrous luminal occlusion or aneurysmal dilatation with fibrinoid necrosis and loss of elastic fibers; the latter would eventually rupture causing the hemorrhage. These findings suggest that amyloid P-protein-related loss of arteriolar smooth muscle cells could be the initial event, with the subsequent damage of the vascular wall leading to cerebral hemorrhages in CAA patients.
Polish Journal of Pathology, 2013
The process of β-amyloid accumulation in cerebral vessels is presented. Cerebral amyloid angiopathy (CAA) was confirmed during an autopsy. It was diagnosed according to the Boston criteria. Cerebral amyloid angiopathy can involve all kinds of cerebral vessels (cortical and leptomeningeal arterioles, capillaries and veins). The development of CAA is a progressive process. β-amyloid appears first in the tunica media, surrounding smooth muscle cells, and in the adventitia. β-amyloid is progressively accumulated, causing a gradual loss of smooth muscle cells in the vessel wall and finally replacing them. Then, the detachment and delamination of the outer part of the tunica media results in the "double barrel" appearance, fibrinoid necrosis, and microaneurysm formation. Microbleeding with perivascular deposition of erythrocytes and blood breakdown products can also occur. β-amyloid can also be deposited in the surrounding of the affected vessels of the brain parenchyma, known as "dysphoric CAA". Ultrastructurally, when deposits of amyloid fibers were localized in or outside the arteriolar wall, the degenerating vascular smooth muscle cells were observed. In the Institute of Psychiatry and Neurology the study was carried out in a group of 48 patients who died due to intracerebral hemorrhage caused by sporadic CAA.
Cerebral amyloid angiopathy–associated intracerebral hemorrhage: pathology and management
Neurosurgical Focus, 2012
Amyloid angiopathy–associated intracerebral hemorrhage (ICH) comprises 12%–15% of lobar ICH in the elderly. This growing population has an increasing incidence of thrombolysis-related hemorrhages, causing the management of hemorrhages associated with cerebral amyloid angiopathy (CAA) to take center stage. A concise reference assimilating the pathology and management of this clinical entity does not exist. Amyloid angiopathy–associated hemorrhages are most often solitary, but the natural history often progresses to include multifocal and recurrent hemorrhages. Compared with other causes of ICH, patients with CAA-associated hemorrhages have a lower mortality rate but an increased risk of recurrence. Unlike hypertensive arteriolar hemorrhages that occur in penetrating subcortical vessels, CAA-associated hemorrhages are superficial in location due to preferential involvement of vessels in the cerebral cortex and meninges. This feature makes CAA-associated hemorrhages easier to access su...
Cerebral Amyloid Angiopathy: A Common Cause of Cerebral Hemorrhage
Current Medicinal Chemistry, 2009
Amyloid is a term used to describe protein deposits with circumscript physical characteristics:-pleated sheet configuration, apple green birefringence under polarized light after Congo red staining, fibrillary structure and high insolubility. Cerebral amyloid angiopathy (CAA) defines a clinicopathological phenomenon characterized by amyloid deposition in the walls of leptomeningeal and cortical arteries, arterioles, and, less often capillaries and veins of the central nervous system. CAAs are currently classified according to the protein deposited including amyloid peptide (A), cystatin C (ACys C), prion protein (PrP Sc), ABri/ADan, transthyretin (ATTR), and gelsolin (AGel). Most often amyloid deposition occurs in sporadic forms. In less common hereditary forms, a mutated variant protein or precursor protein is abnormally metabolized by proteolytic pathways in consequence of specific gene mutations, and accumulates as amyloid. The spectrum of clinical phenotypes associated with CAA-related vasculopathic changes includes both ischemic and hemorrhagic presentations, primary intracerebral hemorrhage (PICH) being probably the most well-recognized. However, in spite of accumulating data and recent progress in understanding the pathogenesis of CAA-related hemorrhage, the exact mechanisms leading to vessel rupture in these cases are yet to be established. This represents, at present, a major limitation to the identification of reliable biomarkers and the development of disease-specific treatment options. The present paper summarizes epidemiologic and clinical aspects of CAA, and highlights the presumed pathomechanisms of amyloid deposition in both sporadic and hereditary forms.
The Internet Journal of Internal Medicine, 2009
Cerebral amyloid angiopathy (CAA) is one of the important causes of primary intracerebral haemorrhage (PICH) in older people. Lobar, recurrent or multiple simultaneous hemorrhages in older patients should raise suspicion of its diagnosis. A definitive diagnosis of CAA requires pathological examination of the affected tissue. However, with modern imaging techniques, it is possible to make a diagnosis of 'probable CAA' in patients presenting with PICH.
Diagnosis and Treatment of Cerebral Amyloid Angiopathy
Clinics in Geriatric Medicine, 1991
Amyloid deposits in the cerebral vasculature are associated with a spectrum of overlapping clinicopathologic conditions distinguished from each other by their clinical presentation and anatomical distribution of amyloid fibril^.^,^^ The systemic vasculature is spared. Cerebral amyloid angiopathy (CAA) is being increasingly diagnosed in the normotensive elderly with intracerebral hemorrhage5 and has also been found in normal aging, Alzheimer's disease, hereditary cerebral hemorrhage, cerebral infarction, arteriovenous malformations, radiation necrosis, progressive demyelination syndromes, chronic vasculitis, dementia pugilistica, hereditary ataxia, the Parkinson-dementia complex of Guam, and spongiform encephal~pathies.~,~ The epidemiologic study of CAA is limited because confirmation of the diagnosis requires the examination of brain tissue. Thus, data on the prevalence of CAA are biased towards hospital-and autopsy-based populations rather than community studies.28 The data are also affected by the age of the subjects, the severity of the disease present, the diligence with which amyloid is sought, the extent of sampling, and the staining methods used.g The prevalence of CAA in normal people increases with age.5,28,38,47,48 Some degree of CAA was found in 36% of 84 autopsied brains in people ranging from 60 to 97 years of age. An increased proportion of brains contained CAA in each successive decade: 5% in the seventh decade, 43% in the eighth, 46% in the ninth, and 57% in
Sporadic cerebral amyloid angiopathy: An important cause of cerebral hemorrhage in the elderly
Journal of Neurosciences in Rural Practice, 2011
ABSTRACTCerebral amyloid angiopathy (CAA) is an important cause of primary intracerebral hemorrhage (PICH) in the elderly. Although there are no pathognomic clinical features of CAA-related PICH, the association of white matter changes with lobar, recurrent, or multiple simultaneous hemorrhages in older patients should raise the suspicion of its diagnosis. A defi nitive diagnosis of CAA requires pathologic examination of the aff ected tissue. However, with modern imaging techniques, it is possible to diagnose the “probable CAA” in patients presenting with PICH. Gradient-echo magnetic resonance imaging is a very sensitive, noninvasive technique for identifying microhemorrhages in life. The diagnosis of CAA is important because of the likely implication it has on future management targeted to reduce risk of future bleeding.