Clinical diagnosis of cerebral amyloid angiopathy: Validation of the Boston Criteria

Knudsen, Katherine; Rosand, Jonathan; Karluk, Diane; Greenberg, Steven M.

doi:10.1212/wnl.56.4.537

Cited by 951 publications

(798 citation statements)

References 41 publications

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“…31 Radiologic manifestation of cerebral amyloid angiopathy: hemorrhagic and ischemic brain injury A definite diagnosis of CAA can only be made through biopsy or autopsy, however, clinical diagnostic criteria called the Boston criteria, allow researchers to diagnose CAA during life with high specificity (88% to 92%). 32,33 According to these criteria probable CAA is defined by the presence of multiple strictly lobar hemorrhages on T2* gradient-recalled echo or susceptibility weighted MRI. These may involve both macrohemorrhages and micro-hemorrhages, 34 herein referred to as 'ICH' and 'microbleeds', respectively.…”

Section: Pathologic Manifestation Of Cerebral Amyloid Angiopathymentioning

confidence: 99%

Ischemic brain injury in cerebral amyloid angiopathy

Reijmer

Veluw

Greenberg

2015

J Cereb Blood Flow Metab

124

102

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Cerebral amyloid angiopathy (CAA) is a common form of cerebral small vessel disease and an important risk factor for intracerebral hemorrhage and cognitive impairment. While the majority of research has focused on the hemorrhagic manifestation of CAA, its ischemic manifestations appear to have substantial clinical relevance as well. Findings from imaging and pathologic studies indicate that ischemic lesions are common in CAA, including white-matter hyperintensities, microinfarcts, and microstructural tissue abnormalities as detected with diffusion tensor imaging. Furthermore, imaging markers of ischemic disease show a robust association with cognition, independent of age, hemorrhagic lesions, and traditional vascular risk factors. Widespread ischemic tissue injury may affect cognition by disrupting white-matter connectivity, thereby hampering communication between brain regions. Challenges are to identify imaging markers that are able to capture widespread microvascular lesion burden in vivo and to further unravel the etiology of ischemic tissue injury by linking structural magnetic resonance imaging (MRI) abnormalities to their underlying pathophysiology and histopathology. A better understanding of the underlying mechanisms of ischemic brain injury in CAA will be a key step toward new interventions to improve long-term cognitive outcomes for patients with CAA.

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Section: Pathologic Manifestation Of Cerebral Amyloid Angiopathymentioning

confidence: 99%

Ischemic brain injury in cerebral amyloid angiopathy

Reijmer

Veluw

Greenberg

2015

J Cereb Blood Flow Metab

124

102

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“…Our results support the notion that histopathological examination of both cerebral cortex and hematoma is necessary to make a reliable diagnosis of CAA, as shown in the Boston criteria. 8,9 However, CAA distribution is characteristically patchy and segmental; it may lead to the possibility of having false-negative cases. 1,3,29 On the other hand, several attempts using amyloid imaging, such as 11 C-Pittsburgh compound B positron emission tomography ( 11 C-PiB PET), have been made to detect CAA as an underlying disease in several pathological conditions such as dementia, cortical SAH, and cerebral angitis.…”

Section: Factors That Influence the Detection Of Caa Pathologymentioning

confidence: 99%

“…3,7 Boston criteria were established for CAA-ICH by the Boston Cerebral Amyloid Angiopathy Group, and a definite diagnosis of CAA-ICH can be formulated only by demonstrating lobar or cortico-subcortical hemorrhage and severe CAA with vasculopathy after whole histological investigation of affected brain tissue is obtained at autopsy. 8,9 Biopsy of the evacuated hematoma or cerebral cortex contributes to premortem diagnosis of probable CAA-ICH with supporting pathology; however, the positive ratio of amyloid deposition in the specimens obtained from brain biopsy or hematoma evacuation has not been investigated enough. [9][10][11][12] We retrospectively searched the patients with clinically diagnosed CAA-ICH who underwent biopsy of evacuated hematoma, cerebral parenchyma, or both, and classified them into CAA-pathology positive and negative groups, depending on the pathological results.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 Biopsy of the evacuated hematoma or cerebral cortex contributes to premortem diagnosis of probable CAA-ICH with supporting pathology; however, the positive ratio of amyloid deposition in the specimens obtained from brain biopsy or hematoma evacuation has not been investigated enough. [9][10][11][12] We retrospectively searched the patients with clinically diagnosed CAA-ICH who underwent biopsy of evacuated hematoma, cerebral parenchyma, or both, and classified them into CAA-pathology positive and negative groups, depending on the pathological results. As a prerequisite, the CAA-pathology positive group could be estimated to have a higher ratio of definite CAA-ICH and a lower ratio of hypertensive ICH than the CAApathology negative group.…”

Section: Introductionmentioning

confidence: 99%

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Clinico-Radiological Characteristics and Pathological Diagnosis of Cerebral Amyloid Angiopathy-Related Intracerebral Hemorrhage

Doden

Sato

Sasahara

et al. 2016

Journal of Stroke and Cerebrovascular Diseases

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Objective: We aim to clarify the clinico-radiological characteristics of cerebral amyloid angiopathy-related intracerebral hemorrhage and to investigate the efficacy of pathological diagnosis using biopsy specimens. Method: We retrospectively reviewed 253 consecutive patients with cortico-subcortical hemorrhage who had been admitted to Aizawa Hospital between January 2006 and July 2013. We had performed craniotomy and hematoma evacuation in 48 patients, as well as biopsy of the evacuated hematoma, cerebral parenchyma adjacent to the hematoma, or both, and they were classified according to the histological results (positive or negative for vascular amyloid deposition) and to the Boston criteria. We compared the clinicoradiological characteristics of cerebral amyloid angiopathy-related intracerebral hemorrhage. We also investigated the detection rate of cerebral amyloid angiopathy with respect to the origins of the specimens. Results: Pathological examination revealed that 22 subjects were positive for vascular amyloid. The number of the cerebral microbleeds located in the deep or infratentorial region was significantly larger in the negative group than in the positive group (P < .05). There was no significant difference in the distribution of lobar cerebral microbleeds and in the prevalence of hypertension. In the probable cerebral amyloid angiopathyrelated intracerebral hemorrhage patients, the probability of having vascular amyloid detected by biopsy of both hematoma and parenchyma was 100%. Rebleeding in the postoperative periods was observed in 2 cases (9.1%) of the positive group.Conclusions: Our results demonstrate the importance and safety of biopsy simultaneously performed with hematoma evacuation. Deep or infratentorial microbleeds are less correlated with cerebral amyloid angiopathy-related intracerebral hemorrhage than with noncerebral amyloid angiopathy-related intracerebral hemorrhage.

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“…Brain microbleeds (BMB) are associated with ischemic and hemorrhagic stroke, cerebral amyloid angiopathy, neurotrauma, Alzheimer's disease, vascular dementia, cognitive decline, hypertension, and aging (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). The presence of BMB in ischemic stroke, intracerebral hemorrhage, and cerebral amyloid angiopathy is associated with future hemorrhage (2,(17)(18)(19).…”

mentioning

confidence: 99%

In vivo iron quantification in collagenase‐induced microbleeds in rat brain

McAuley

Schrag

Barnes

et al. 2011

Magnetic Resonance in Med

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Brain microbleeds (BMB) are associated with chronic and acute cerebrovascular disease. Because BMB present in the brain is a source of potentially cytotoxic iron proportional to the volume of extravasated blood, BMB iron content is a potentially valuable biomarker both to assess tissue risk and small cerebral vessel health. We recently reported methods to quantify focal iron sources using phase images that were tested in phantoms and BMB in postmortem tissue. In this study, we applied our methods to small hemorrhagic lesions induced in the in vivo rat brain using bacterial collagenase. As expected by theory, measurements of geometric features in phase images correlated with lesion iron content measured by graphite furnace atomic absorption spectrometry. Iron content estimation following BMB in an in vivo rodent model could shed light on the role and temporal evolution of ironmediated tissue damage and efficacy of potential treatments in cerebrovascular diseases associated with BMB. Magn Reson Med 67:711-717,

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Clinical diagnosis of cerebral amyloid angiopathy: Validation of the Boston Criteria

Cited by 951 publications

References 41 publications

Ischemic brain injury in cerebral amyloid angiopathy

Ischemic brain injury in cerebral amyloid angiopathy

Clinico-Radiological Characteristics and Pathological Diagnosis of Cerebral Amyloid Angiopathy-Related Intracerebral Hemorrhage

In vivo iron quantification in collagenase‐induced microbleeds in rat brain

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