Cerebral microbleeds: a guide to detection and interpretation

Greenberg, Steven M.; Vernooij, Meike W.; Cordonnier, Charlotte; Viswanathan, Anand; Salman, Rustam Al-Shahi; Warach, Steven; Launer, Lenore J.; Buchem, Mark A. van; Breteler, Monique M.B.

doi:10.1016/s1474-4422(09)70013-4

Cited by 1,492 publications

(1,415 citation statements)

References 62 publications

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“…It has been suggested that intracortical microbleeds on MRI are associated with CAA, 13,14 whereas MRI microbleeds in subcortical areas are related to hypertension. 15 In light of these observations, it remains currently not feasible to distinguish a chronic gliotic CMI with hemorrhagic components from a primary hemorrhage on MRI. More studies should look into the histopathologic correlates and underlying etiology of MRI identified 'microbleeds'.…”

Section: Discussionmentioning

confidence: 99%

The Spectrum of MR Detectable Cortical Microinfarcts: A Classification Study with 7-Tesla Postmortem MRI and Histopathology

Veluw

Zwanenburg

Rozemüller

et al. 2015

J Cereb Blood Flow Metab

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Cerebral microinfarcts (CMIs) are common neuropathologic findings in aging and dementia. We explored the spectrum of cortical CMIs that can be visualized with 7T magnetic resonance imaging (MRI). Thirty-three coronal brain slices of 11 individuals with neuropathologically confirmed dementia were subjected to a high-resolution postmortem 7T MRI protocol. First, we identified all visible small (⩽5 mm) intracortical and juxtacortical lesions on postmortem MRI. Lesions were classified as CMI or nonCMI based on histology, and their MR features were recorded. Thirty lesions were identified on the initial MRI evaluation, of which twenty-three could be matched with histology. Histopathology classified 12 lesions as CMIs, all of which were located intracortically. On the basis of their MR features, they could be classified as chronic gliotic CMIs-with or without cavitation or hemorrhagic components-and acute CMIs. Eleven MRI identified lesions were not of ischemic nature and most commonly enlarged or atypically shaped perivascular spaces. Their MRI features were similar to gliotic CMIs with or without cavitation, but these 'CMI mimics' were always located juxtacortically. 7T postmortem MRI distinguishes different histopathologic types of cortical CMIs, with distinctive MR characteristics. On the basis of our findings, we propose in vivo rating criteria for the detection of intracortical CMIs.

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Section: Discussionmentioning

confidence: 99%

The Spectrum of MR Detectable Cortical Microinfarcts: A Classification Study with 7-Tesla Postmortem MRI and Histopathology

Veluw

Zwanenburg

Rozemüller

et al. 2015

J Cereb Blood Flow Metab

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“…3 Histopathological analyses of the small cerebral vessels associated with CMBs have generally identified vascular pathological changes indicative of hypertensive arteriolosclerosis. 4,5 Atherosclerosis of the systemic medium or large arteries is caused mainly by aging 6 and hypertensive wall damage. 7 Pulse wave velocity (PWV) is typically determined in the clinical setting to assess the grade of systemic atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Stroke patients with cerebral microbleeds on MRI scans have arteriolosclerosis as well as systemic atherosclerosis

et al. 2012

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Cerebral microbleeds (CMBs) are recognized as a manifestation of arteriolosclerosis in cerebral small vessels. However, little is known regarding whether stroke patients with CMBs often have systemic atherosclerosis. The aim of the present study was to elucidate this issue using the cardio-ankle vascular index (CAVI), a new index of systemic atherosclerosis, in acute ischemic stroke patients. We prospectively studied 105 patients (71 males, median age ¼ 70.0 years) with acute ischemic stroke. All of the patients were examined using T2*-weighted gradient echo magnetic resonance imaging (MRI) to look for and assess the CMBs and using fluid-attenuated inversion recovery to evaluate white matter hyperintensity (WMH). We assigned the patients into CMB and non-CMB groups and compared the clinical characteristics of these groups. The factors associated with CMBs were investigated using multivariate logistic regression analysis. T2*-weighted gradient echo MRI revealed CMBs in 47 patients (44.8%) and no CMBs in 58 patients (55.2%). The CAVI was significantly higher in the CMBs group (10.5 vs. 8.6, Po0.001).In the multivariate logistic regression analysis, CAVI per one point increase (odds ratio (OR), 1.50; 95% confidence interval (CI), 1.12-2.00; P ¼ 0.006), advanced WMH (OR, 4.78; 95% CI, 1.55-14.74; P ¼ 0.006) and impaired kidney function (OR, 3.31; 95% CI, 1.16-9.81; P ¼ 0.031) were independent factors associated with the presence of CMBs. A high CAVI was independently associated with CMBs in patients with acute ischemic stroke. Our results indicated that ischemic stroke patients with CMBs may have cerebral arteriolosclerosis as well as systemic atherosclerosis.

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“…It has been increasingly acknowledged that the location of CMBs either in the lobar or nonlobar territories may reflect their underlying etiology. Strictly lobar CMBs (SL‐CMBs) are thought to be caused by cerebral amyloid angiopathy (CAA) frequently in patients with Alzheimer's disease (AD), whereas nonlobar CMBs (deep or infratentorial) are thought to be due to hypertensive vasculopathy (HV) (Greenberg et al., 2009; van Rooden et al., 2009). Mixed (deep/infratentorial with lobar) CMBs (M‐CMBs) are also thought to reflect HV (Greenberg et al., 2009; Vernooij et al., 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Strictly lobar CMBs (SL‐CMBs) are thought to be caused by cerebral amyloid angiopathy (CAA) frequently in patients with Alzheimer's disease (AD), whereas nonlobar CMBs (deep or infratentorial) are thought to be due to hypertensive vasculopathy (HV) (Greenberg et al., 2009; van Rooden et al., 2009). Mixed (deep/infratentorial with lobar) CMBs (M‐CMBs) are also thought to reflect HV (Greenberg et al., 2009; Vernooij et al., 2008). HV and CAA may synergistically contribute to the development of lobar CMBs (Cordonnier & van der Flier, 2011; Fazekas et al., 1999; Kim et al., 2016; Lee, Kim, Kim, Yoon, & Roh, 2007; Park et al., 2013; Smith et al., 2010).…”

Section: Introductionmentioning

confidence: 99%

Background and distribution of lobar microbleeds in cognitive dysfunction

et al. 2017

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ObjectivesCerebral microbleeds (CMBs) are often observed in memory clinic patients. It has been generally accepted that deep CMBs (D‐CMBs) result from hypertensive vasculopathy (HV), whereas strictly lobar CMBs (SL‐CMBs) result from cerebral amyloid angiopathy (CAA) which frequently coexists with Alzheimer's disease (AD). Mixed CMBs (M‐CMBs) have been partially attributed to HV and also partially attributed to CAA. The aim of this study was to elucidate the differences between SL‐CMBs and M‐CMBs in terms of clinical features and regional distribution.MaterialsWe examined 176 sequential patients in our memory clinic for clinical features and CMB location using susceptibility‐weighted images obtained on a 3T‐MRI. The number of lobar CMBs in SL‐CMBs and M‐CMBs was counted in each cerebral lobe and their regional density was adjusted according to the volume of each lobe.ResultsOf the total 176 patients, 111 patients (63.1%) had CMBs. Within the patients who had CMBs, M‐CMBs were found in 54 patients (48.6%), followed by SL‐CMBs in 35 (31.5%) and D‐CMBs in 19 (17.1%). The SL‐CMB group showed a significantly higher prevalence of family history of dementia, whereas the M‐CMB group showed an increasing trend toward hypertension and smoking. The prevalence of AD was significantly higher in the SL‐CMBs group, whereas the prevalence of AD with cerebrovascular disease was higher in the M‐CMBs group. The regional density of lobar CMBs was significantly higher in the occipital lobe in the M‐CMB group, whereas the SL‐CMB group showed higher regional density between regions an increasing tendency in the parietal and occipital lobe.ConclusionThe between‐group differences in clinical features and regional distribution indicate there to be an etiological relationship of SL‐CMBs to AD and CAA, and M‐CMBs to both HV and CAA.

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Cerebral microbleeds: a guide to detection and interpretation

Cited by 1,492 publications

References 62 publications

The Spectrum of MR Detectable Cortical Microinfarcts: A Classification Study with 7-Tesla Postmortem MRI and Histopathology

The Spectrum of MR Detectable Cortical Microinfarcts: A Classification Study with 7-Tesla Postmortem MRI and Histopathology

Stroke patients with cerebral microbleeds on MRI scans have arteriolosclerosis as well as systemic atherosclerosis

Background and distribution of lobar microbleeds in cognitive dysfunction

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