دورية أكاديمية
Sensitivity and Specificity of the Boston Criteria Version 2.0 for the Diagnosis of Cerebral Amyloid Angiopathy in a Community-Based Sample.
العنوان: | Sensitivity and Specificity of the Boston Criteria Version 2.0 for the Diagnosis of Cerebral Amyloid Angiopathy in a Community-Based Sample. |
---|---|
المؤلفون: | Zanon Zotin MC; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago., Makkinejad N; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago., Schneider JA; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago., Arfanakis K; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago., Charidimou A; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago., Greenberg SM; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago., van Veluw SJ; From the J. Philip Kistler Stroke Research Center (M.C.Z.Z., N.M., A.C., S.M.G., S.J.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston; Center for Imaging Sciences and Medical Physics (M.C.Z.Z.), Department of Medical Imaging, Hematology and Clinical Oncology, Ribeirão Preto Medical School, University of São Paulo, Brazil; Rush Alzheimer's Disease Center (J.A.S., K.A.), Rush University Medical Center; and Department of Biomedical Engineering (K.A.), Illinois Institute of Technology, Chicago. |
المصدر: | Neurology [Neurology] 2024 Jan 09; Vol. 102 (1), pp. e207940. Date of Electronic Publication: 2023 Dec 13. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0401060 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1526-632X (Electronic) Linking ISSN: 00283878 NLM ISO Abbreviation: Neurology Subsets: MEDLINE |
أسماء مطبوعة: | Publication: Hagerstown, MD : Lippincott Williams & Wilkins Original Publication: Minneapolis. |
مواضيع طبية MeSH: | Cerebral Amyloid Angiopathy*/diagnostic imaging , Alzheimer Disease*, Humans ; Aged ; Aged, 80 and over ; Sensitivity and Specificity ; Aging ; Cerebral Hemorrhage |
مستخلص: | Background and Objectives: The Boston criteria are a set of clinical and neuroimaging features that enable accurate diagnosis of cerebral amyloid angiopathy (CAA) without invasive methods such as brain biopsies or autopsy. The last updates to the Boston criteria, named version 2.0, were recently released and incorporated new nonhemorrhagic MRI features. These criteria have been validated in symptomatic samples, with improved diagnostic yield. We set out to investigate the accuracy of the Boston criteria v2.0 for the diagnosis of CAA in a community-based sample. Methods: Participants were recruited from longitudinal clinical-pathologic studies of aging conducted at the Rush Alzheimer's Disease Center in Chicago: the Religious Orders Study and the Rush Memory and Aging Project. Deceased participants with in vivo 3T MRI and detailed pathologic data available were included in the analysis. We compared the diagnostic yield of the current and earlier versions of the Boston criteria in our sample. Among those classified as probable CAA according to the Boston criteria v2.0, we investigated the ability of each neuroimaging marker to distinguish between false-positive and true-positive cases. Results: In total, 134 individuals were included in the study (mean age = 82.4 ± 6.0 years; 69.4% F), and 49 of them were considered pathology-proven definite cases with CAA (mean age = 82.9 ± 6.0 years; 63.3% F). The Boston criteria versions 1.0 and 1.5 yielded similar sensitivity (26.5%, both), specificity (90.6% and 89.4%, respectively), and predictive values (negative: 68.1% and 67.9%; positive: 61.9% and 59.1%, respectively). The recently released Boston criteria v2.0 offered higher sensitivity (38.8%) and slightly lower specificity (83.5%). Among those classified as probable CAA (v2.0), pathology-proven true-positive cases had higher numbers of strictly cortical lobar microbleeds compared with false-positive cases ( p = 0.004). Discussion: Similar to findings from symptomatic samples, the inclusion of nonhemorrhagic neuroimaging markers in the updated Boston criteria offered a 12.3% gain in sensitivity among community-dwelling individuals, at the expense of a 5.9% drop in specificity. In cases with probable CAA, the cortical location of microbleeds may represent a promising distinguishing feature between true-positive and false-positive cases. Despite its improved performance, the diagnostic sensitivity of the updated criteria in a community-based sample remains limited. Classification of Evidence: This study provides Class II evidence that the Boston criteria v2.0 accurately distinguishes people with CAA from those without CAA. |
References: | Alzheimers Dement. 2015 Dec;11(12):1480-1488. (PMID: 26079413) Ann Neurol. 1991 Nov;30(5):637-49. (PMID: 1763890) Curr Alzheimer Res. 2012 Jul;9(6):628-45. (PMID: 22471860) Stroke. 2018 Feb;49(2):491-497. (PMID: 29335334) Lancet Neurol. 2018 Mar;17(3):232-240. (PMID: 29331631) J Stroke. 2019 May;21(2):121-138. (PMID: 30991799) Ann Neurol. 1995 Aug;38(2):254-9. (PMID: 7654074) Neurology. 2013 Apr 23;80(17):1551-6. (PMID: 23553482) Cerebrovasc Dis. 2015;39(3-4):224-31. (PMID: 25823458) J Alzheimers Dis. 2020;73(1):333-345. (PMID: 31771057) Curr Opin Neurol. 2018 Feb;31(1):28-35. (PMID: 29120920) Stroke. 2007 Jun;38(6):1949-51. (PMID: 17510457) Lancet Neurol. 2022 Aug;21(8):714-725. (PMID: 35841910) Acta Neuropathol. 2018 Dec;136(6):887-900. (PMID: 30334074) Neurology. 2014 Dec 2;83(23):2116-23. (PMID: 25361776) Lancet Neurol. 2013 Aug;12(8):822-38. (PMID: 23867200) J Neurol Neurosurg Psychiatry. 2013 Jun;84(6):624-9. (PMID: 23412074) Neurology. 2016 Feb 9;86(6):505-11. (PMID: 26747886) Int J Stroke. 2019 Dec;14(9):956-971. (PMID: 31514686) Curr Alzheimer Res. 2012 Jul;9(6):646-63. (PMID: 22471867) Neurology. 2015 Dec 1;85(22):1930-6. (PMID: 26537052) Brain. 2017 Jul 1;140(7):1829-1850. (PMID: 28334869) Lancet Neurol. 2009 Feb;8(2):165-74. (PMID: 19161908) Am J Neurodegener Dis. 2014 Mar 28;3(1):19-32. (PMID: 24754000) Acta Neuropathol. 2017 Mar;133(3):409-415. (PMID: 27771772) J Alzheimers Dis. 2015;43(4):1325-30. (PMID: 25171715) Brain. 2016 Dec;139(Pt 12):3151-3162. (PMID: 27645801) Neurology. 2017 Mar 21;88(12):1157-1164. (PMID: 28228568) Neurology. 2010 Apr 27;74(17):1346-50. (PMID: 20421578) J Alzheimers Dis. 2018;64(s1):S161-S189. (PMID: 29865057) Neurobiol Aging. 2021 Apr;100:32-38. (PMID: 33477009) Neurology. 2001 Feb 27;56(4):537-9. (PMID: 11222803) Neurology. 2009 Nov 24;73(21):1759-66. (PMID: 19933977) Nat Rev Neurol. 2020 Jan;16(1):30-42. (PMID: 31827267) Neurology. 1984 Jul;34(7):939-44. (PMID: 6610841) Neurology. 2014 Jan 7;82(1):57-62. (PMID: 24285616) Radiology. 2018 Apr;287(1):11-28. (PMID: 29558307) N Engl J Med. 1996 Jul 18;335(3):189-96. (PMID: 8657218) J Alzheimers Dis. 2019;72(1):247-256. (PMID: 31561362) |
معلومات مُعتمدة: | P30 AG072975 United States AG NIA NIH HHS |
تواريخ الأحداث: | Date Created: 20240102 Date Completed: 20240103 Latest Revision: 20240425 |
رمز التحديث: | 20240425 |
مُعرف محوري في PubMed: | PMC10834125 |
DOI: | 10.1212/WNL.0000000000207940 |
PMID: | 38165367 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1526-632X |
---|---|
DOI: | 10.1212/WNL.0000000000207940 |