Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia

Haglund, Mattias; Passant, Ulla; Sjöbeck, Martin; Ghebremedhin, Estifanos; Englund, Elisabet

doi:10.1002/gps.1550

Cited by 108 publications

(97 citation statements)

References 30 publications

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“…Cerebral amyloid angiopathy, a microvasculopathy commonly found in the brains of individuals with Alzheimer disease, is now increasingly recognized as a likely contributing cause to cerebral microinfarcts and microbleeds. 43,111,112 Although microbleeds can be detected by special MRI sequences, their size may be overestimated; however, there is no reliable way to identify microinfarcts on neuroimaging. Microinfarcts can be detected in autopsy brain specimens, especially with the use of special immunohistochemical methods to detect collections of microglia/macrophages or astrocytes, a fairly reliable "footprint" of microfoci of ischemic change.…”

Section: Prognosismentioning

confidence: 99%

An Updated Definition of Stroke for the 21st Century

Sacco¹,

Kasner²,

Broderick³

et al. 2013

Stroke

2,718

1,029

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Despite the global impact and advances in understanding the pathophysiology of cerebrovascular diseases, the term “stroke” is not consistently defined in clinical practice, in clinical research, or in assessments of the public health. The classic definition is mainly clinical and does not account for advances in science and technology. The Stroke Council of the American Heart Association/American Stroke Association convened a writing group to develop an expert consensus document for an updated definition of stroke for the 21st century. Central nervous system infarction is defined as brain, spinal cord, or retinal cell death attributable to ischemia, based on neuropathological, neuroimaging, and/or clinical evidence of permanent injury. Central nervous system infarction occurs over a clinical spectrum: Ischemic stroke specifically refers to central nervous system infarction accompanied by overt symptoms, while silent infarction by definition causes no known symptoms. Stroke also broadly includes intracerebral hemorrhage and subarachnoid hemorrhage. The updated definition of stroke incorporates clinical and tissue criteria and can be incorporated into practice, research, and assessments of the public health.

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Section: Prognosismentioning

confidence: 99%

An Updated Definition of Stroke for the 21st Century

Sacco¹,

Kasner²,

Broderick³

et al. 2013

Stroke

2,718

1,029

View full text Add to dashboard Cite

show abstract

“…One possibility is that these neuroimaging lesions represent a subset of acute, relatively large cerebral microinfarcts (CMI), a widespread form of ischemic brain injury associated with advanced small vessel disease (SVD). [7][8][9][10] Given the brief time window (7-14 days 11 ) during which small incident infarcts remain detectable by DWI, the high frequency of ICH-associated lesions suggests that small DWI lesions may occur frequently in patients with SVD. Most reports have focused on the early post-ICH period, however, raising the question of whether these DWI lesions represent an ongoing process occurring throughout the course of SVD rather than a byproduct of the acute ICH.…”

mentioning

confidence: 99%

Characteristic distributions of intracerebral hemorrhage–associated diffusion-weighted lesions

et al. 2012

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Objectives: To determine whether small diffusion-weighted imaging (DWI) lesions occur beyond the acute posthemorrhage time window in patients with intracerebral hemorrhage (ICH) and to characterize their spatial distribution in patients with lobar and deep cerebral hemorrhages. Methods:In this cross-sectional study, we retrospectively analyzed 458 MRI scans obtained in the acute (#7 days after ICH) or nonacute (.14 days after ICH) phases from 392 subjects with strictly lobar (n 5 276) and deep (n 5 116) ICH (48.7% women; mean age 72.8 6 11.7 years). DWI, apparent diffusion coefficient maps, fluid-attenuated inversion recovery, and T2* MRIs were reviewed for the presence and location of DWI lesions. Results:We identified 103 DWI hyperintense lesions on scans from 62 subjects, located mostly in lobar brain regions (90 of 103, 87.4%). The lesions were not uniformly distributed throughout the brain lobes; patients with strictly lobar ICH had relative overrepresentation of lesions in frontal lobe, and patients with deep ICH in parietal lobe (p 5 0.002). Although the frequency of DWI lesions tended to be greater on scans performed within 7 days after ICH (39 of 214, 18.2%), they continued at high frequency in the nonacute period as well (23 of 178, 12.9%, odds ratio 1.5, 95% confidence interval 0.86-2.6 for acute vs nonacute). There was also no difference in frequency of lesions on acute and nonacute scans among 66 subjects with MRIs in both time periods (8 of 66 acute, 10 of 66 nonacute, odds ratio 0.77, 95% confidence interval 0.25-2.4). Conclusions:The high frequency of DWI lesions beyond the acute post-ICH period and their characteristic distributions suggest that they are products of the small vessel diseases that underlie ICH. Recent analyses of patients with primary intracerebral hemorrhage (ICH) have identified a surprisingly high incidence of small hyperintense lesions on diffusion-weighted imaging (DWI) sequences. 1-6Although the neuropathologic basis of these clinically asymptomatic DWI hyperintense lesions has not been determined, their imaging properties are suggestive of small cerebral infarcts. One possibility is that these neuroimaging lesions represent a subset of acute, relatively large cerebral microinfarcts (CMI), a widespread form of ischemic brain injury associated with advanced small vessel disease (SVD). 7-10Given the brief time window (7-14 days 11 ) during which small incident infarcts remain detectable by DWI, the high frequency of ICH-associated lesions suggests that small DWI lesions may occur frequently in patients with SVD. Most reports have focused on the early post-ICH period, however, raising the question of whether these DWI lesions represent an ongoing process occurring throughout the course of SVD rather than a byproduct of the acute ICH. Specific ties between the From the J. Philip

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“…In literature, a certain range of definitions of CMIs is used, deferring from invisible with the naked eye to o 5 mm. 8,17 Although, the feasibility of imaging CMIs at 3.0 T MRI would make it more applicable in clinical settings, the clinical value of these microscopic lesions must be clarified first, which also implies that it must be clarified which size is clinically relevant.…”

Section: Discussionmentioning

confidence: 99%

7.0 T MRI Detection of Cerebral Microinfarcts in Patients with a Symptomatic High-Grade Carotid artery Stenosis

Rotte

Köning

Hartog

et al. 2014

J Cereb Blood Flow Metab

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In the current study, the presence of cerebral cortical microinfarcts (CMIs) was evaluated in a series of 21 patients with a symptomatic high-grade 450% stenosis of the carotid artery. A T 2 -weighted fluid-attenuated inversion recovery sequence and a T 1 -weighted turbo field echo sequence of the brain were obtained at 7.0 Tesla magnetic resonance imaging. Primary study endpoint was the number of CMIs and macroinfarcts. In total, 53 cerebral infarcts (35 macroinfarcts; 18 CMIs) were found ipsilateral to the symptomatic carotid artery, in 14 patients (67%). In four of these patients, both CMIs and macroinfarcts were visible. In the contralateral hemisphere, seven infarcts (five macroinfarcts and two CMIs) were found in five patients (24%). In the ipsilateral hemispheres, the number of CMIs and macroinfarcts were significantly correlated (P = 0.02). Unpaired comparison of medians showed that the number of CMIs in the ipsilateral hemisphere was significantly higher than the number of CMIs in the contralateral hemisphere (P = 0.04). No significant correlation was found between stenosis grade and the number of any infarct. The current study shows that in symptomatic patients with significant extracranial carotid artery stenosis, CMIs are part of the total cerebrovascular burden and these CMIs prevail with a similar pattern as observed macroinfarcts.

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Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia

Cited by 108 publications

References 30 publications

An Updated Definition of Stroke for the 21st Century

An Updated Definition of Stroke for the 21st Century

Characteristic distributions of intracerebral hemorrhage–associated diffusion-weighted lesions

7.0 T MRI Detection of Cerebral Microinfarcts in Patients with a Symptomatic High-Grade Carotid artery Stenosis

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