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Establishing the “meaning” of microbleeds: Clinical context or lobar microbleed burden?
Author(s) -
Wilson Duncan,
Werring David J.
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.09.004
Subject(s) - meaning (existential) , context (archaeology) , medicine , psychology , history , psychotherapist , archaeology
We read with great interest the article by MartinezRamirez et al. [1] on the diagnostic value of cerebral microbleeds (MBs) in patients without intracerebral hemorrhage (ICH). The neuropathologic validation of the Boston criteria for cerebral amyloid angiopathy (CAA) to date has been mainly in cohorts of patients with symptomatic ICH [2,3]. This study makes a key contribution by expanding the application of these diagnostic criteria into a healthy older population, which could be important for testing potential new therapeutic approaches designed to slow CAA disease progression [4]. The authors correlated clinical and imaging features, based on the “classical” Boston criteria [2], with neuropathologic material to diagnose or exclude CAA pathology, in two distinct populations: a single-center specialist hospital cohort (n 5 55) and in a community sample from the Framingham Heart Study (n 5 47). The authors calculated the positive predictive values (PPV) of the presence of strictly lobar MBs in diagnosing pathologically proven CAA from each population: they found that lobar MBs had an 87.5% PPV for diagnosing CAA in hospital cohorts versus only 25% for the community cohort. Although the specificity of lobar MBs for CAAwas high in both cohorts, the sensitivity was much lower in the community sample. They conclude that “.strictly lobar microbleeds strongly predict cerebral amyloid angiopathy (CAA) in non-ICH individuals when found in hospital cohorts. However, their diagnostic accuracy in the general population appears limited.” This suggests lobar MBs are not a good diagnostic clue to detect CAA in patients without the clinical symptoms—e.g., cognitive decline, focal neurologic dysfunction—that might lead to a hospital referral. This finding is somewhat unexpected, given several indirect sources of evidence linking strictly lobar MBs to CAA. First, previous community-based studies show that strictly lobar MBs are associated with the apopli-