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Cited by 456Cerebrovascular and genetic disordersIntracerebral and Subarachnoid Hemorrhage ResearchNeurological Disease Mechanisms and Treatments

Cerebral microinfarcts: the invisible lesions

Open access
Smith, Eric E, Schneider, Julie A, Wardlaw, Joanna M, Greenberg, Steven M·2012·The Lancet Neurology
DOI 10.1016/s1474-4422(11)70307-6PMC PMC3359329
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Abstract

The association between small but still visible lacunar infarcts and cognitive decline has been established by population-based radiological and pathological studies. Microscopic examination of brain sections shows even smaller but substantially more numerous microinfarcts, the focus of this Review. These lesions often result from small vessel pathologies such as arteriolosclerosis or cerebral amyloid angiopathy. They typically go undetected in clinical-radiological correlation studies that rely on conventional structural MRI, although the largest acute microinfarcts can be detected by diffusion-weighted imaging. In view of their high numbers and widespread distribution, microinfarcts could directly disrupt important cognitive networks and thus account for some of the neurological dysfunction associated with lesions visible on conventional MRI such as lacunar infarcts and white matter hyperintensities. Standardised neuropathological assessment criteria and the development of non-invasive means of detection during life would be major steps towards understanding the causes and consequences of otherwise macroscopically invisible microinfarcts.

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  • Microinfarcts are very small ischaemic lesions found mostly in the cortex at autopsy in older people, but they are occasionally visible on high-field MRI.

    “Microinfarcts are very small ischaemic lesions recorded mostly in the cortex during autopsy in older people, but are occasionally seen on high-field MRI.109,110”

    From Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration (2013) · cites this paper as [109]

    The Neuropathology section describes very small microinfarcts found in autopsy studies of older people, and the Neuroimaging section reports sub-millimeter infarcts demonstrated with 7-Tesla post-mortem MRI (pages unavailable). But the paper says pathological studies predominantly sampled the cortex, not that microinfarcts themselves are found mostly there; it also does not establish occasional detection on high-field MRI during life. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The consequences of SVD may extend into the cortex, manifesting both as microscopic vascular lesions and cortical atrophy.

    “However, the consequences of SVD may extend into the cortex, manifesting both as microscopic vascular lesions and cortical atrophy. 77-79”

    From Vascular Cognitive Impairment (2017) · cites this paper as [79]

  • Microinfarcts are emerging SVD features detectable at higher field strengths.

    “Other emerging features detectable at higher field strengths include microinfarcts.36,37”

    From Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging (2013) · cites this paper as [36]

  • Microinfarcts and microbleeds independently predict cognitive dysfunction.

    “Microscopic infarcts (microinfarcts) and hemorrhages (microbleeds) (fig. 5) are independent predictors of cognitive dysfunction, but are commonly associated with other vascular pathologies, such as leukoaraiosis, lacunar infarcts, large infarcts, and hemorrhage (Smith et al., 2012; van Norden et al., 2013), as well as CADASIL and AD (table 1).”

    From The Pathobiology of Vascular Dementia (2013) · cites this paper as Smith et al., 2012

  • Local cues such as blood-brain barrier compromise or microinfarcts could drive microglial state changes instead of a brain-wide shift.

    “local cues like blood brain barrier compromise (Montagne et al., 2015) or microinfarcts (Smith et al., 2012) could drive state changes rather than a brain-wide shift.”

    From Complex cell-state changes revealed by single cell RNA sequencing of 76,149 microglia throughout the mouse lifespan and in the injured brain (2018) · cites this paper as Smith et al., 2012

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Authors
Smith, E. E., Schneider, J. A., Wardlaw, J. M., & Greenberg, S. M.
Affiliations
  • University of Calgary (CA)
  • Rush University Medical Center (US)
  • University of Edinburgh (GB)
  • Massachusetts General Hospital (US)
Corresponding author
Greenberg, Steven M
ORCID
Venue
The Lancet Neurology
Publisher
Elsevier BV
Published
2012-03
Volume
11
Issue
3
Pages
272-282
ISSN
1474-4422 (ISSN-L)
DOI
10.1016/s1474-4422(11)70307-6
PMC
PMC3359329
OpenAlex
W2018721445
Cited by
456
References
100
Citations by year
2026: 8 · 2025: 23 · 2024: 26 · 2023: 21 · 2022: 26 · 2021: 37 · 2020: 31 · 2019: 27 · 2018: 35 · 2017: 43 · 2016: 49 · 2015: 48 · 2014: 39 · 2013: 32 · 2012: 9
FWCI
5.75
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • The Lancet Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
Funders
  • Scottish Funding Council
  • Alberta Innovates
  • National Institutes of Health
  • Canadian Institutes of Health Research
  • National Institute on Aging (R01AG026484, 2R01 AG26484-01, R01AG015819)
Topics
  • Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
  • Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
cerebral microinfarcts, cerebral small vessel disease, arteriolosclerosis, cerebral amyloid angiopathy, cognitive decline, lacunar infarction, white matter hyperintensities, diffusion-weighted imaging
MeSH terms
Brain, Cognition Disorders, Humans, Nerve Fibers, Myelinated, Brain Infarction

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