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

Smith, Eric E.; Greenberg, Steven M.

doi:10.1007/s11883-003-0048-4

Cited by 77 publications

(56 citation statements)

References 44 publications

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“…[31][32][33] The diagnosis of probable CAA by the Boston criteria has high specificity, but currently available methods are insensitive to the presence of CAA in situations such as occurrence of an isolated lobar ICH without microbleeds, hemorrhagic lesions in both deep and lobar locations, or cerebellar hemorrhages. 19,20 In our largest analyzed series of consecutive primary ICH patients who had MRI (n 5 526), patients with uncertain diagnoses were common (isolated lobar ICH, n 5 122, 23.2%; mixed location or cerebellar ICH, n 5 76, 14.5%) relative to the more definite diagnostic categories (probable CAA, n 5 191, 36.3%; HTN-ICH, n 5 137, 26%). 6 Older patients with multiple lobar microbleeds without ICH (lobar microbleed-only patients) show clinical, radiologic, and risk factor profiles of CAA, 26 but low microbleed counts on MRI are associated with a decreased probability of confirming CAA on autopsy.…”

Section: Resultsmentioning

confidence: 95%

“…Our sample was also restricted to participants able to come to the hospital for research imaging .6 months after their ICH; such survival bias might favor the null hypothesis, as these patients could be more likely to have less severe CAA. Finally, although we used previously validated diagnostic criteria, 19,20 we did not have pathologic evidence of underlying small vessel disease type. Again, any misclassification would tend to bias towards the null hypothesis rather than towards intergroup differences.…”

Section: Resultsmentioning

confidence: 99%

“…All 10 patients with CAA were diagnosed with probable CAA according to Boston criteria after presenting with symptomatic ICH. 19,20 Radiologic analyses were performed by separate study personnel (J.A.B., P.F.) and the results were recorded without knowledge of participants' clinical information.…”

Section: Classification Of Evidencementioning

confidence: 99%

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Florbetapir-PET to diagnose cerebral amyloid angiopathy

et al. 2016

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Objective: We hypothesized that florbetapir, a Food and Drug Administration-approved PET tracer, could distinguish cerebral amyloid angiopathy (CAA)-related intracerebral hemorrhage (ICH) from hypertensive ICH (HTN-ICH). Methods:We prospectively enrolled survivors of primary ICH related to probable CAA (per Boston Criteria, n 5 10) and HTN-ICH (n 5 9) without dementia. All patients underwent florbetapir-PET and multimodal MRI, and patients with CAA had additional Pittsburgh compound B (PiB) PET. Amyloid burden was assessed quantitatively (standard uptake value ratio [SUVR]) and visually classified as positive or negative. Results:The CAA and HTN-ICH groups had similar age (66.9 vs 67.1), sex, and leukoaraiosis volumes (31 vs 30 mL, all p . 0.8). Florbetapir uptake and PiB retention strongly correlated in patients with CAA both globally within cerebral cortex (r 5 0.96, p , 0.001) and regionally in lobar cortices (all r . 0.8, all p # 0.01). Mean global cortical florbetapir uptake was substantially higher in CAA than HTN-ICH (SUVR: 1.41 6 0.17 vs 1.15 6 0.08, p 5 0.001), as was mean occipital SUVR (1.44 6 0.12 vs 1.17 6 0.08, p , 0.001), even after correcting for global SUVR (p 5 0.03). Visual rating for positive/negative florbetapir demonstrated perfect interrater agreement (k 5 1) and was positive for all 10 patients with CAA vs 1 of 9 HTN-ICH patients (sensitivity 100%, specificity 89%).Conclusions: Florbetapir appears to label vascular amyloid in patients with CAA-related ICH. The approved florbetapir binary visual reading method can have diagnostic value in appropriate clinical settings. Classification of evidence:This study provides Class II evidence that florbetapir-PET provides a sensitivity of 100% (95% confidence interval [CI] 66%-100%) and specificity of 89% (95% CI 51%-99%) for determination of probable CAA among cognitively normal patients. Cerebral amyloid angiopathy (CAA), characterized by accumulation of b-amyloid (Ab) proteins in the walls of cortical/leptomeningeal vessels, is a common cause of vessel wall breakdown and vascular dysfunction in older adults, making it a major contributor to fatal or disabling intracerebral hemorrhages (ICH) as well as ischemic injury and dementia. 1,2 There currently is no specific treatment for CAA, in part because of our inability to identify this condition at early phases prior to appearance of multiple hemorrhagic brain lesions. 3 Accurate early diagnosis of CAA also has direct implications for stroke prevention, as this pathology is an important cause of anticoagulant-associated ICH and might dictate use of alternative nonpharmaceutical approaches such as left atrial appendage closure for patients with nonvalvular atrial fibrillation. 4,5

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 99%

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Florbetapir-PET to diagnose cerebral amyloid angiopathy

et al. 2016

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“…17 Thus, structural degenerations of the cortical and/or leptomeningeal vessel walls such as fibrinoid necrosis or microaneurysm formation exist in patients with CAA, and high blood pressure may trigger a rupture of the vessel walls, which results in lobar hemorrhage. We cannot exclude the possibility of CAA-ICH in the diagnosis of patients with lobar hemorrhage and hypertension, 12 and it is difficult to strictly distinguish CAA-ICH from hypertensive ICH solely based on clinical and radiological findings. 26…”

Section: Relationship Between Caa-ich and Hypertensionmentioning

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%

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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Statin Use Following Intracerebral Hemorrhage

Westover¹,

Bianchi²,

Eckman³

et al. 2011

Arch Neurol

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Context: Statins are widely prescribed for primary and secondary prevention of ischemic cardiac and cerebrovascular disease. Although serious adverse effects are uncommon, results from a recent clinical trial suggested increased risk of intracerebral hemorrhage (ICH) associated with statin use. For patients with baseline elevated risk of ICH, it is not known whether this potential adverse effect offsets the cardiovascular and cerebrovascular benefits.Objective: To address the following clinical question: Given a history of prior ICH, should statin therapy be avoided?Design: A Markov decision model was used to evaluate the risks and benefits of statin therapy in patients with prior ICH.Main Outcome Measure: Life expectancy, measured as quality-adjusted life-years. We investigated how statin use affects this outcome measure while varying a range of clinical parameters, including hemorrhage location (deep vs lobar), ischemic cardiac and cerebrovascular risks, and magnitude of ICH risk associated with statins.Results: Avoiding statins was favored over a wide range of values for many clinical parameters, particularly in survivors of lobar ICH who are at highest risk of ICH recurrence. InsurvivorsoflobarICHwithoutpriorcardiovascularevents, avoiding statins yielded a life expectancy gain of 2.2 qualityadjusted life-years compared with statin use. This net benefit persisted even at the lower 95% confidence interval of the relative risk of statin-associated ICH. In patients with lobar ICH who had prior cardiovascular events, the annual recurrence risk of myocardial infarction would have to exceed 90% to favor statin therapy. Avoiding statin therapy was also favored, although by a smaller margin, in both primary and secondary prevention settings for survivors of deep ICH. Conclusions: Avoiding statins should be considered for patients with a history of ICH, particularly those cases with a lobar location.

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

Cited by 77 publications

References 44 publications

Florbetapir-PET to diagnose cerebral amyloid angiopathy

Florbetapir-PET to diagnose cerebral amyloid angiopathy

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

Statin Use Following Intracerebral Hemorrhage

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