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Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration

Open access
Wardlaw, Joanna M, Smith, Eric E, Biessels, Geert J, Cordonnier, Charlotte, Fazekas, Franz, Frayne, Richard, Lindley, Richard I, O'Brien, John T +28 more·2013·The Lancet Neurology
DOI 10.1016/s1474-4422(13)70124-8PMC PMC3714437
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Abstract

Cerebral small vessel disease (SVD) is a common accompaniment of ageing. Features seen on neuroimaging include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. SVD can present as a stroke or cognitive decline, or can have few or no symptoms. SVD frequently coexists with neurodegenerative disease, and can exacerbate cognitive deficits, physical disabilities, and other symptoms of neurodegeneration. Terminology and definitions for imaging the features of SVD vary widely, which is also true for protocols for image acquisition and image analysis. This lack of consistency hampers progress in identifying the contribution of SVD to the pathophysiology and clinical features of common neurodegenerative diseases. We are an international working group from the Centres of Excellence in Neurodegeneration. We completed a structured process to develop definitions and imaging standards for markers and consequences of SVD. We aimed to achieve the following: first, to provide a common advisory about terms and definitions for features visible on MRI; second, to suggest minimum standards for image acquisition and analysis; third, to agree on standards for scientific reporting of changes related to SVD on neuroimaging; and fourth, to review emerging imaging methods for detection and quantification of preclinical manifestations of SVD. Our findings and recommendations apply to research studies, and can be used in the clinical setting to standardise image interpretation, acquisition, and reporting. This Position Paper summarises the main outcomes of this international effort to provide the STandards for ReportIng Vascular changes on nEuroimaging (STRIVE).

Integrity signals

Registry

Crossref · 10.1016/s1474-4422(13)70124-8

Cites

118 of 119 references verified0 citation errors · 1 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

19 of 116 cited sources checked · 11 supported · 1 flagged · accuracy not yet measured

  • Premisereasoning

    Neither of the previous guidelines includes advances in understanding the pathophysiology and measurement of cerebral small vessel disease.

    “neither include advances in understanding the pathophysiology and measurement of SVD”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [11] Hachinski, 2006, National Institute of Neurological Disorders and Stroke–Canadian Stroke Network vascular cognitive impairment harmonization standards, Stroke source
    • cites [12] Gorelick, 2011, Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association, Stroke source

      The cited statement discusses small-vessel disease pathophysiology in §6.3, including vascular risk factors and proposed mechanisms. It also describes methods for measuring small-artery remodeling there and the capabilities and limits of neuroimaging in §3.6. That is contrary to the claim that it does not include these topics. (LLM, conf=0.86)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
  • Premisereasoning

    Neither of the previous guidelines provides comprehensive recommendations for the many forms of cerebral small vessel disease seen on neuroimaging.

    “neither of these guidelines provide comprehensive recommendations for the many forms of SVD seen on neuroimaging”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [11] Hachinski, 2006, National Institute of Neurological Disorders and Stroke–Canadian Stroke Network vascular cognitive impairment harmonization standards, Stroke source
    • cites [12] Gorelick, 2011, Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association, Stroke source
  • Premisecitation

    White matter hyperintensities are strongly associated with cerebrovascular disease and vascular risk factors.

    “Although strongly associated with cerebrovascular disease and vascular risk factors,29”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [29] Debette, 2010, The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis, BMJ source
  • Premisecitation

    White matter hyperintensities are associated with covert neurological and cognitive symptoms and physical difficulties such as gait disturbance.

    “White matter hyperintensities are associated with covert neurological and cognitive symptoms and physical difficulties such as gait disturbance.31–35”
    Quote in the paperNot a substantial claim2 of 5 sources checked
    • cites [31] de Laat, 2011, Loss of white matter integrity is associated with gait disorders in cerebral small vessel disease, Brain source

      The paper reports that white matter lesions were associated with poorer gait measures in people with cerebral small vessel disease (p. 2). The Study population section (pp. 3–4) describes cognitive and motor disturbances as symptoms of small vessel disease, but does not establish an association between white matter hyperintensities specifically and covert neurological or cognitive symptoms. (LLM, conf=0.82)

      Experimental — accuracy not yet measured
    • cites [32] Windham, 2012, Covert neurological symptoms associated with silent infarcts from midlife to older age: the Atherosclerosis Risk in Communities study, Stroke source
    • cites [33] Saini, 2012, Silent stroke: not listened to rather than silent, Stroke source
    • cites [34] Haley, 2009, Subjective cognitive complaints relate to white matter hyperintensities and future cognitive decline in patients with cardiovascular disease, Am J Geriatr Psychiatry source
    • cites [35] Inzitari, 2009, Changes in white matter as determinant of global functional decline in older independent outpatients: three year follow-up of LADIS (leukoaraiosis and disability) study cohort, BMJ source
  • Premisecitation

    A consensus group from the US Alzheimer's Association has published standards for assessing microbleeds in the context of Alzheimer's disease or β-amyloid immunotherapies.

    “A consensus group from the US Alzheimer's Association has published standards for assessing microbleeds in this specific clinical context,61”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [61] Sperling, 2011, Amyloid-related imaging abnormalities in amyloid-modifying therapeutic trials: recommendations from the Alzheimer's Association Research Roundtable Workgroup, Alzheimers Dement source
  • Classified as probably not a substantial claim. 43
  • May combine two claims. 21

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The American Heart Association statement included a class 2 recommendation for neuroimaging as part of clinical investigation of vascular cognitive impairment.

    “included a class 2 recommendation for neuroimaging as part of the clinical investigation of vascular cognitive impairment.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [12] Gorelick, 2011, Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association, Stroke source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    A scientific statement from the American Heart Association incorporated neuroimaging evidence for cerebral small vessel disease or stroke into criteria for probable vascular mild cognitive impairment and dementia.

    “a scientific statement from the American Heart Association incorporated neuroimaging evidence for SVD or stroke as part of the criteria for probable vascular mild cognitive impairment and dementia”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [12] Gorelick, 2011, Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association, Stroke source

  • May combine two claims.

    Premisecitation

    Alzheimer's disease and cerebral small vessel disease both lead to cognitive decline and dementia.

    “both lead to cognitive decline and dementia”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [5] Brayne, 2009, Neuropathological correlates of dementia in over-80-year-old brain donors from the population-based Cambridge City over-75s cohort (CC75C) study, J Alzheimers Dis source
    • cites [6] Matthews, 2009, Epidemiological pathology of dementia: attributable-risks at death in the Medical Research Council Cognitive Function and Ageing Study, PLoS Med source

      The Discussion links Alzheimer pathology and small vessel disease to dementia and describes small vessel disease as a contributor to vascular cognitive impairment. But the study assesses pathology in relation to dementia at death, not cognitive decline over time; its Limitations section explicitly says the analysis cannot establish causal directions. Thus, “lead to” is stronger than this study supports. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [7] 2001, Cognitive function and ageing study (MRC CFAS), Lancet

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Terms used to describe visible perivascular spaces include large, dilated, large dilated, or enlarged Virchow-Robin spaces or perivascular spaces.

    “Terms used to describe visible perivascular spaces include large, dilated, large dilated, or enlarged Virchow–Robin spaces or perivascular spaces.38,41,42,44–48”
    Quote in the paperNot a substantial claim2 of 8 sources checked
    • cites [38] Groeschel, 2006, Virchow-Robin spaces on magnetic resonance images: normative data, their dilatation, and a review of the literature, Neuroradiology source
    • cites [41] Zhu, 2010, Severity of dilated Virchow-Robin spaces is associated with age, blood pressure, and MRI markers of small vessel disease: a population-based study, Stroke source
    • cites [42] MacLullich, 2004, Enlarged perivascular spaces are associated with cognitive function in healthy elderly men, J Neurol Neurosurg Psychiatry source
    • cites [44] Heier, 1989, Large Virchow-Robin spaces: MR-clinical correlation, AJNR Am J Neuroradiol

      Not checked in the free run.

    • cites [45] Patankar, 2005, Dilatation of the Virchow-Robin space is a sensitive indicator of cerebral microvascular disease: study in elderly patients with dementia, AJNR Am J Neuroradiol
    • cites [46] Rouhl, 2008, Virchow-Robin spaces relate to cerebral small vessel disease severity, J Neurol source
    • cites [47] Zhu, 2011, Frequency and location of dilated Virchow-Robin spaces in elderly people: a population-based 3D MR imaging study, AJNR Am J Neuroradiol source
    • cites [48] Chen, 2011, Assessment of the Virchow-Robin Spaces in Alzheimer disease, mild cognitive impairment, and normal aging, using high-field MR imaging, AJNR Am J Neuroradiol source

  • May combine two claims.

    Premisecitation

    Non-lobar intracerebral haemorrhages are not thought to be caused by cerebral amyloid angiopathy and are mostly due to perforating arteriolar vasculopathy.

    “non-lobar intracerebral haemorrhages, which are not thought to be caused by cerebral amyloid angiopathy, and are mostly due to perforating arteriolar vasculopathy.64,65”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [64] Qureshi, 2001, Spontaneous intracerebral hemorrhage, N Engl J Med source
    • cites [65] Jackson, 2006, Is hypertension a more frequent risk factor for deep than for lobar supratentorial intracerebral haemorrhage?, J Neurol Neurosurg Psychiatry source

      The paper says cerebral amyloid angiopathy causes mainly lobar haemorrhages and describes a proposed link between deep haemorrhage and disease of small perforating vessels. It does not rule out amyloid angiopathy as a cause of non-lobar haemorrhage or establish that most non-lobar haemorrhages result from perforating arteriolar vasculopathy; it notes uncertainty about that vascular pathology (introductory passage and Discussion; page numbers unavailable). (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Combining clinical syndrome with MRI but without diffusion-weighted imaging, or with CT, is suboptimal; clinical syndrome by itself is the least dependable assessment approach.

    “The combination of clinical syndrome plus MRI results but without diffusion-weighted imaging, or clinical syndrome plus CT results, is not optimal; clinical syndrome alone is the least reliable method of assessment.81”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [81] Potter, 2010, Associations of clinical stroke misclassification (‘clinical–imaging dissociation’) in acute ischemic stroke, Cerebrovasc Dis source

      The Discussion (page not provided) says clinical classification alone can misclassify mild strokes and that adding CT remains less sensitive than DWI for small acute infarcts. The Methods (page not provided) say all patients received MRI including DWI, so the paper does not assess MRI without DWI or establish a reliability ranking in which clinical assessment alone is definitively last. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    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”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [109] Smith, 2012, Cerebral microinfarcts: the invisible lesions, Lancet Neurol source

      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
    • cites [110] Brundel, 2012, Cerebral microinfarcts: a systematic review of neuropathological studies, J Cereb Blood Flow Metab source

  • May combine two claims.

    Premisecitation

    In the context of vascular disease and dementia, neuropathological substrates of atrophy include neuronal loss, cortical thinning, subcortical vascular pathology with white matter rarefaction and shrinkage, arteriolosclerosis, venous collagenosis, and secondary neurodegenerative changes.

    “neuropathological substrates of atrophy include neuronal loss,72 cortical thinning, subcortical vascular pathology with white matter rarefaction and shrinkage, arteriolosclerosis, venous collagenosis, and secondary neurodegenerative changes.73,74”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [72] Bobinski, 2000, The histological validation of post mortem magnetic resonance imaging-determined hippocampal volume in Alzheimer's disease, Neuroscience source
    • cites [73] Jagust, 2008, Neuropathological basis of magnetic resonance images in aging and dementia, Ann Neurol source

      The Abstract Results and Discussion (page not provided) link cortical gray matter atrophy to subcortical vascular pathology and arteriosclerosis, and describe white matter pathology associated with vascular disease. They do not establish white matter shrinkage, venous collagenosis, or secondary neurodegenerative changes as substrates of atrophy. Neuronal loss is followed by a different citation in the citing sentence. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [74] Black, 2009, Understanding white matter disease. Imaging–pathological correlations in vascular cognitive impairment, Stroke source

  • May combine two claims.

    Premisecitation

    Documented misclassifications include white matter hyperintensities as normal grey matter, lacunes as ventricle or white matter hyperintensity, and small subcortical infarcts as white matter hyperintensities.

    “Known examples to avoid are the misclassification of white matter hyperintensities as normal grey matter, of lacunes as ventricle or white matter hyperintensity, or of small subcortical infarcts as white matter hyperintensities.84”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [84] Wang, 2012, How much do focal infarcts distort white matter lesions and global cerebral atrophy measures?, Cerebrovasc Dis source

      The Introduction and Results (page unavailable) support the risk that stroke lesions, including lacunes, can be counted as white matter lesions; the paper also discusses stroke lesions being classified as CSF. Our copy does not document white matter hyperintensities being classified as normal grey matter or lacunes being classified specifically as ventricles. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim.

    Premisecitation

    Recommendations for imaging and reporting of microbleeds have been published.

    “Recommendations for imaging and reporting of microbleeds have been published,60”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [60] Greenberg, 2009, Cerebral microbleeds: a guide to detection and interpretation, Lancet Neurol source

  • Classified as probably not a substantial claim.

    Findingnone given

    Protocols for image acquisition and image analysis in cerebral small vessel disease research also vary widely.

    “which is also true for protocols for image acquisition and image analysis”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    The most common terms for recent small subcortical infarcts were lacunar infarcts, lacunar infarctions, and lacunar strokes.

    “the most common terms were lacunar infarcts, lacunar infarctions, and lacunar strokes”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    The most common terms for white matter hyperintensity were leukoaraiosis, white matter lesions, white matter hyperintensities, leukoencephalopathy, and white matter disease.

    “The most common terms were leukoaraiosis, white matter lesions, white matter hyperintensities, leukoencephalopathy (usually in the context of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and white matter disease”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    Commonly used terms for lacunes were lacune, lacunar stroke, and silent brain infarct.

    “Commonly used terms were lacune, lacunar stroke, and silent brain infarct.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Findingown data

    Microbleed was by far the most common term, followed by cerebral microbleed, then brain microbleed.

    “Microbleed was by far the most common term, followed by cerebral microbleed, then brain microbleed.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Findingown data

    A systematic review of studies on cerebral small vessel disease and atrophy revealed the use of many synonymous terms, including atrophy, brain volume, volume loss, and others.

    “Our systematic review of studies on SVD and atrophy revealed the use of many synonymous terms, including atrophy, brain volume, volume loss, and others.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Working groups developed standards for each of six key lesion types using established guideline-development principles from the Equator Network.

    “Working groups developed standards for each of the six key lesion types, using established principles for guideline development published by the Enhancing the QUAlity and Transparency Of health Research (Equator) Network.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Systematic searches were performed to identify relevant published work.

    “We did systematic searches to identify relevant published work”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    Variation in terms and definitions inhibits cross-study comparisons and obstructs research on risk factors, pathophysiology, pathological correlations, and clinical consequences of cerebral small vessel disease lesions.

    “This amount of variation inhibits cross-study comparisons and is a barrier to research on risk factors, pathophysiology, pathological correlations, and clinical consequences of these lesions.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Occasionally, a recent asymptomatic small subcortical infarct is found by chance on imaging and is called a silent cerebral infarct.

    “Occasionally, a recent asymptomatic small subcortical infarct is identified by chance on imaging,14,15 and is referred to as a silent cerebral infarct.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [14] Kang, 2012, New ischemic lesions coexisting with acute intracerebral hemorrhage, Neurology source
    • cites [15] Chowdhury, 2004, Are multiple acute small subcortical infarctions caused by embolic mechanisms?, J Neurol Neurosurg Psychiatry source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The working method used the Delphi principle with workshops at the beginning and end of the project and interim work assignments.

    “The working method was based on the Delphi principle with workshops at the beginning and end of the project, and with interim work assignments”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.

    Interpretationreasoning

    Standardisation could be used in clinical practice to improve diagnosis and better understand the cause of cognitive impairment in elderly patients.

    “such standardisation could be used in clinical practice to improve diagnosis and better understand the cause of cognitive impairment in elderly patients.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Cerebral small vessel disease causes about one fifth of all strokes worldwide.

    “the cause of about a fifth of all strokes worldwide.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [1] Norrving, 2008, Lacunar infarcts: no black holes in the brain are benign, Pract Neurol source
    • cites [2] Pantoni, 2010, Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges, Lancet Neurol source

  • Classified as probably not a substantial claim.

    Study design and conductown data

    The working group used a structured process to develop definitions and imaging standards for markers and consequences of cerebral small vessel disease.

    “We completed a structured process to develop definitions and imaging standards for markers and consequences of SVD.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    All participants reviewed and endorsed the final document.

    “All participants reviewed and endorsed the final document.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Interpretation of many reports is hindered by variable consequences of acute cerebral small vessel disease and related lesions and by convergence of lesions with different causes but similar late MRI appearances.

    “Interpretation of data from many reports is hampered by the variable consequences of acute SVD and related lesions and the convergence of lesions with different causes but similar late appearances on MRI”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S2 (checkable).

    Interpretationreasoning

    Visibility alone cannot serve as a uniform criterion for pathologically enlarged perivascular spaces.

    “Visibility alone cannot be a uniform criterion for pathologically enlarged perivascular spaces.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    The 15 mm maximum size boundary for lacunes of presumed vascular origin is not supported by much objective evidence.

    “we recognise that this size boundary is not supported by much objective evidence, and research is needed.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Synonymous terms for perivascular spaces include Virchow-Robin spaces, type 3 lacune, or état crible when located predominantly in the basal ganglia.

    “Synonymous terms for perivascular spaces include Virchow–Robin spaces,40 type 3 lacune,43 or état crible when located predominantly in the basal ganglia.38”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [38] Groeschel, 2006, Virchow-Robin spaces on magnetic resonance images: normative data, their dilatation, and a review of the literature, Neuroradiology source
    • cites [40] Kwee, 2007, Virchow-Robin spaces at MR imaging, Radiographics source
    • cites [43] Poirier, 1984, Cerebral lacunae. A proposed new classification, Clin Neuropathol

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    Whether the presence of several visible perivascular spaces is clinically significant remains controversial.

    “Whether the presence of several visible perivascular spaces is clinically significant remains controversial”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Perivascular spaces are extensions of the extracerebral fluid space around arteries, arterioles, veins, and venules as they course from the brain surface into and through the brain parenchyma.

    “Perivascular spaces are extensions of the extracerebral fluid space around arteries, arterioles, veins, and venules as they course from the brain surface into and through the brain parenchyma”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [37] Pollock, 1997, Perivascular spaces in the basal gangli of the human brain: their relationship to lacunes, J Anat source

  • Probably not a substantial claim: may not pass S4 (based). May combine two claims.

    Premisenone given

    Old infarcts are generally smaller than recent infarcts because of tissue loss and an ex-vacuo effect in old lesions, and because of swelling in new lesions.

    “since old infarcts are generally smaller than recent infarcts because of tissue loss and an ex-vacuo effect in old lesions, and because of swelling in new lesions.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Premisenone given

    The association between the size of perivascular spaces and clinical consequences is not well understood.

    “the association between the size of the perivascular spaces and clinical consequences is not well understood”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    The pathogenesis of white matter hyperintensities is not well understood and could be multifactorial.

    “the pathogenesis of these white matter lesions is not well understood and could be multifactorial.30”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [30] Gouw, 2011, Heterogeneity of small vessel disease: a systematic review of MRI and histopathology correlations, J Neurol Neurosurg Psychiatry source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Some studies have shown that small subcortical infarcts may evolve into a lacunar cavity or a hyperintensity without apparent cavitation on T2-weighted sequences, or may disappear with little visible consequence on conventional MRI.

    “some studies have shown that the small subcortical infarcts might have differing fates, evolving into a lacunar cavity or hyperintensity without apparent cavitation on T2-weighted sequences, or might disappear leaving little visible consequence on conventional MRI”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The cause of most lacunes is presumed to be small subcortical infarcts, either symptomatic or silent.

    “The cause of most lacunes is presumed to be small subcortical infarcts, either symptomatic or silent”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [26] Franke, 1991, Residual lesions on computed tomography after intracerebral hemorrhage, Stroke source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Leukoaraiosis was later adopted to denote hyperintensity on T2-weighted and FLAIR MRI, and sometimes also hypointensity on T1-weighted MRI.

    “this term was later adopted to denote hyperintensity on T2-weighted and FLAIR MRI, and sometimes also hypointensity on T1-weighted MRI”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [36] Hachinski, 1987, Leukoaraiosis, Arch Neurol source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Some studies have associated more prominent perivascular spaces with worse cognitive function.

    “some studies have associated more prominent perivascular spaces with worse cognitive function.42”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [42] MacLullich, 2004, Enlarged perivascular spaces are associated with cognitive function in healthy elderly men, J Neurol Neurosurg Psychiatry source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Lacunes are associated with an increased risk of stroke, gait impairment, and dementia.

    “are associated with an increased risk of stroke, gait impairment, and dementia.”
    Quote in the paperNot a substantial claim0 of 4 sources checked
    • cites [22] Vermeer, 2007, Silent brain infarcts: a systematic review, Lancet Neurol source
    • cites [23] Santos, 2009, Differential impact of lacunes and microvascular lesions on poststroke depression, Stroke source
    • cites [24] Choi, 2012, Silent infarcts and cerebral microbleeds modify the associations of white matter lesions with gait and postural stability: population-based study, Stroke source
    • cites [25] Snowdon, 1997, Brain infarction and the clinical expression of Alzheimer disease. The Nun Study, JAMA source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Leukoaraiosis describes a reduced area of x-ray attenuation on CT.

    “Leukoaraiosis describes a reduced area of x-ray attenuation on CT,36”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [36] Hachinski, 1987, Leukoaraiosis, Arch Neurol source

  • May combine two claims.

    Premisecitation

    In some cases, the central cavity fluid of a lacune is not suppressed on FLAIR, and the lesion can appear entirely hyperintense despite having clear CSF-like intensity on T1-weighted and T2-weighted MRI.

    “In some cases, the central cavity fluid is not suppressed on FLAIR, and the lesion can appear entirely hyperintense, despite MRI having a clear CSF-like intensity on other sequences such as T1-weighted and T2-weighted MRI.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [18] Moreau, 2012, Cavitation after acute symptomatic lacunar stroke depends on time, location, and MRI sequence, Stroke source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Estimates of the proportion of recent small subcortical infarcts that cavitate range from 28% to 94%.

    “Estimates of the proportion of recent small subcortical infarcts that cavitate range from 28%17 to 94%.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [17] Potter, 2010, Counting cavitating lacunes underestimates the burden of lacunar infarction, Stroke source
    • cites [18] Moreau, 2012, Cavitation after acute symptomatic lacunar stroke depends on time, location, and MRI sequence, Stroke source

  • May combine two claims.

    Premisecitation

    Intracerebral haemorrhage could be a manifestation of cerebral small vessel disease or secondary to other causes such as vascular malformations.

    “Intracerebral haemorrhage could be a manifestation of SVD62 or secondary to other causes such as vascular malformations.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [62] Lammie, 2000, Stress-related primary intracerebral hemorrhage: autopsy clues to underlying mechanism, Stroke source

  • May combine two claims.

    Premisecitation

    Superficial cortical siderosis could be a chronic consequence of subarachnoid bleeding or might result from very superficial cortical bleeding caused by vascular malformations, cerebral amyloid angiopathy, spinal dural defects, or it might be idiopathic.

    “Superficial cortical siderosis could be a chronic consequence of subarachnoid bleeding or might be the result of very superficial cortical bleeding caused by vascular malformations, cerebral amyloid angiopathy,67 spinal dural defects, or it might also be idiopathic.67,68”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [67] Linn, 2010, Prevalence of superficial siderosis in patients with cerebral amyloid angiopathy, Neurology source
    • cites [68] Kumar, 2006, Superficial siderosis, Neurology source

  • May combine two claims.

    Premisecitation

    The pathological changes of atrophy are heterogeneous and not necessarily indicative of neuronal loss.

    “The pathological changes of atrophy are heterogeneous and not necessarily indicative of neuronal loss.69–71”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [69] Jack, 2011, Alliance for aging research AD biomarkers work group: structural MRI, Neurobiol Aging source
    • cites [70] Walters, 2001, Haemodialysis and cerebral oedema, Nephron source
    • cites [71] Duning, 2005, Dehydration confounds the assessment of brain atrophy, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Results of a small study suggested good, but not perfect, inter-rater agreement on the site of origin of intracerebral haemorrhages.

    “Results of a small study66 suggested good, but not perfect, inter-rater agreement on the site of origin of intracerebral haemorrhages.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [66] Bhattathiri, 2003, Reliability assessment of computerized tomography scanning measurements in intracerebral hematoma, Neurosurg Focus source

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    A field strength of 3.0 T might be preferred, but images from modern 1.5 T MRI scanners are often of similarly high definition and are therefore acceptable.

    “A field strength of 3·0 T might be preferred, but images from modern 1·5 T MRI scanners are often of a similarly high definition,80 and are therefore acceptable”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [80] Wardlaw, 2012, A systematic review of the utility of 1·5 versus 3 Tesla magnetic resonance brain imaging in clinical practice and research, Eur Radiol source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Revised research criteria for cerebral amyloid angiopathy include superficial cortical siderosis as an additional haemorrhagic manifestation of cerebral amyloid angiopathy, equivalent to a lobar intracerebral haemorrhage.

    “Revised research criteria for cerebral amyloid angiopathy include superficial cortical siderosis as an additional haemorrhagic manifestation of cerebral amyloid angiopathy, equivalent to a lobar intracerebral haemorrhage.67”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [67] Linn, 2010, Prevalence of superficial siderosis in patients with cerebral amyloid angiopathy, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Comprehensive guidelines for the diagnosis and management of intracerebral haemorrhage have been published previously.

    “Comprehensive guidelines for the diagnosis and management of intracerebral haemorrhage have been published previously.63”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [63] Broderick, 2007, Stroke source

  • May combine two claims.

    Premisecitation

    Cerebral microbleeds are associated with cerebral small vessel disease and Alzheimer's disease.

    “Cerebral microbleeds are associated with SVD and Alzheimer's disease.57,58”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [57] Cordonnier, 2007, Spontaneous brain microbleeds: systematic review, subgroup analyses and standards for study design and reporting, Brain source
    • cites [58] Vernooij, 2008, Prevalence and risk factors of cerebral microbleeds: the Rotterdam Scan Study, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The presence or absence of strictly lobar microbleeds has been included in research criteria for cerebral amyloid angiopathy.

    “The presence or absence of strictly lobar microbleeds has been included in research criteria for cerebral amyloid angiopathy.59”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [59] Knudsen, 2001, Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Results of some studies suggest that MR-visible lesions correspond to haemosiderin-laden macrophages in perivascular tissue, consistent with vascular leakage of blood cells.

    “Results of some studies30,52,53 suggest that MR-visible lesions correspond to haemosiderin-laden macrophages in perivascular tissue, consistent with vascular leakage of blood cells.52,54–56”
    Quote in the paperNot a substantial claim0 of 6 sources checked
    • cites [30] Gouw, 2011, Heterogeneity of small vessel disease: a systematic review of MRI and histopathology correlations, J Neurol Neurosurg Psychiatry source
    • cites [52] Shoamanesh, 2011, Cerebral microbleeds: histopathological correlation of neuroimaging, Cerebrovasc Dis source
    • cites [53] De Reuck, 2011, Comparison of 7·0-T T*-magnetic resonance imaging of cerebral bleeds in post-mortem brain sections of Alzheimer patients with their neuropathological correlates, Cerebrovasc Dis source
    • cites [54] Fazekas, 1999, Histopathologic analysis of foci of signal loss on gradient-echo T2*-weighted MR images in patients with spontaneous intracerebral hemorrhage: evidence of microangiopathy-related microbleeds, AJNR Am J Neuroradiol

      Not checked in the free run.

    • cites [55] Dichgans, 2002, Cerebral microbleeds in CADASIL: a gradient-echo magnetic resonance imaging and autopsy study, Stroke source
    • cites [56] Tatsumi, 2008, Direct comparison of histology of microbleeds with postmortem MR images: a case report, Cerebrovasc Dis source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Combining diffusion tensor imaging with atrophy enables investigation of how vascular lesions affect distantly connected brain regions.

    “For example, combining diffusion tensor imaging and atrophy allows the study of the effects of vascular lesions on distantly connected brain regions.108”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [108] Duering, 2012, Incident subcortical infarcts induce focal thinning in connected cortical regions, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    The mechanisms of the association between microbleeds and cognitive impairment, including whether microbleeds damage the brain and cause dysfunction, are not well understood.

    “although the mechanisms of this association, including whether microbleeds damage the brain and cause dysfunction, are not well understood.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    Emerging data show an association between microbleeds and cognitive impairment.

    “emerging data shows association between microbleeds and cognitive impairment”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Larger cortical microinfarcts have been visualised on 7.0 T MRI, and were sometimes visible on conventional 3.0 T MRI.

    “Larger cortical microinfarcts have been visualised on 7·0 T MRI, and these lesions were sometimes visible on conventional 3·0 T MRI.111”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [111] van Veluw, 2012, In vivo detection of cerebral cortical microinfarcts with high-resolution 7T MRI, J Cereb Blood Flow Metab source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The standards were developed through consensus among a large group of experts using rigorous methods.

    “These standards were developed on the basis of consensus in a large group of experts using rigorous methods.”
    Quote in the paperNot a substantial claim
57 of 57

  • The authors state this as an assumption.

    Tissue loss in brain atrophy is inferred from enlargement of peripheral and central CSF spaces relative to intracranial volume and other measures.

    “Tissue loss is assumed from the enlargement of peripheral (sulcal) and central (ventricular) CSF spaces in relation to intracranial volume and other measures”

  • The paper relies on this without support.

    The proposed standards reliably classify most manifestations of cerebral small vessel disease seen on neuroimaging.

    “These standards are expected to reliably classify most manifestations of SVD seen on neuroimaging”

  • The paper relies on this without support.

    Automated computational methods have not been developed for small vessel disease.

    “This validation step is crucial for studies of SVD because automated methods have not been developed for the disorder, and there is a high risk of misclassification of lesions, especially when unfamiliar pulse sequences are used or scanners are upgraded.”

  • The paper relies on this without support.

    Most scanners can now perform 3D acquisitions for T1, T2, GRE, and FLAIR.

    “These three-dimensional acquisitions are now possible on most scanners for T1-weighted, T2-weighted, GRE, and FLAIR techniques.”

  • The paper relies on this without support.

    Validation of 3D magnetisation-prepared T1-weighted protocols for major scanner types at 1.5 T and 3.0 T has been done by the Alzheimer's Disease Neuroimaging Initiative.

    “The Alzheimer's Disease Neuroimaging Initiative has validated three-dimensional magnetisation prepared T1-weighted sequence protocols for the major scanner types at 1·5 T and 3·0 T; sequence protocols are freely available.”

  • The paper relies on this without support.

    Sequences sensitive to paramagnetic content, like susceptibility-weighted imaging, produce more artifacts.

    “Other high-resolution sequences sensitive to paramagnetic content, such as susceptibility-weighted imaging and equivalents, should be considered for three-dimensional image acquisition, although these sequences increase the presence of artifacts.”

  • The paper relies on this without support.

    Regular recalibration against standard examples helps maintain consistency when rating many scans or scans from different sessions.

    “Regular recalibration against standard examples is useful to maintain consistency when rating large numbers of scans or when rating images from different sessions.”

  • The paper relies on this without support.

    A single sequence in the coronal or sagittal plane, rather than axial, aids visualisation of correct lesion dimensions.

    “The use of one sequence (usually T1-weighted MRI) in the coronal or sagittal plane instead of the axial plane helps to visualise the correct lesion dimensions (appendix).”
8 of 8

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In AD there is generalised atrophy with focal changes in the temporal lobe, especially the hippocampus.

    “For example, in AD there is generalised atrophy with focal changes in the temporal lobe, especially the hippocampus.”

    From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [12]

    The Brain atrophy section (page unavailable) says atrophy can be general or focal, including in the hippocampus. It does not identify generalised atrophy with focal temporal-lobe changes as a pattern in Alzheimer’s disease; its discussion of global and hippocampal atrophy concerns associations with small vessel disease. (LLM, conf=0.78)

    Experimental — accuracy not yet measured

  • Microbleeds develop in the absence of Aβ pathology and are associated with cognitive impairment and dementia, as shown in patients with small vessel disease of the brain that is estimated to contribute to 50% of all dementias worldwide including AD.

    “Importantly, microbleeds develop in the absence of A 𝛃 pathology and are associated with cognitive impairment and dementia, as shown in patients with small vessel disease of the brain that is estimated to contribute to 50% of all dementias wordwide including AD (224, 550, 637).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [637]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

  • Vascular cognitive impairment and VaD are associated with cortical and subcortical vascular changes including WMH, lacunes, enlarged perivascular spaces and microbleeds.

    “vascular cognitive impairment and VaD are associated with cortical and subcortical vascular changes (latter including white matter hyperintensities (WMH), lacunes, enlarged perivascular spaces and microbleeds) [11, 12].”

    From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [12]

  • FTD is associated with anterior temporal pole and frontal atrophy, with semantic dementia subtype associated with asymmetric temporal atrophy.

    “FTD is associated with anterior temporal pole and frontal atrophy, with semantic dementia subtype associated with asymmetric temporal atrophy.”

    From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [12]

    The Brain atrophy section (page not available in our copy) says atrophy can be focal or asymmetrical, but discusses it in the context of small-vessel disease rather than FTD. Searches for FTD, anterior temporal pole, and semantic dementia found no passage linking those diagnoses to the claimed atrophy patterns. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

  • DLB shows relative preservation of the hippocampus and occipital and subcortical atrophy.

    “DLB shows relative preservation of the hippocampus and occipital and subcortical atrophy”

    From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [12]

    The Brain atrophy section discusses hippocampal and subcortical atrophy in the context of small vessel disease, but does not describe an atrophy pattern in DLB. Searches for DLB, dementia with Lewy bodies, and occipital atrophy found no passage addressing the claim. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Two volumes are given for Stroke in 2009

    Minor

    Reference 100 lists Stroke as volume 49 in 2009, while reference 23 lists it as volume 40 in 2009.

  • Two volumes are given for Stroke in 2012

    Minor

    Reference 33 lists Stroke as volume 3 in 2012, whereas reference 18 lists it as volume 43 in the same year.

2 of 2

Cites

Flagged first, then by citations

6 of the 125 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. 2001, Cognitive function and ageing study (MRC CFAS), Lancet, 357, 169

Cited by

Sorted by citations

Related

Authors
Wardlaw, J. M., Smith, E. E., Biessels, G. J., Cordonnier, C., Fazekas, F., Frayne, R., Lindley, R. I., O'Brien, J. T., Barkhof, F., Benavente, O. R., Black, S. E., Brayne, C., Breteler, M., Chabriat, H., DeCarli, C., de Leeuw, F.-E., Doubal, F., Duering, M., Fox, N. C., Greenberg, S., Hachinski, V., Kilimann, I., Mok, V., Oostenbrugge, R. V., Pantoni, L., Speck, O., Stephan, B. C. M., Teipel, S., Viswanathan, A., Werring, D., Chen, C., Smith, C., van Buchem, M., Norrving, B., Gorelick, P. B., & Dichgans, M.
Affiliations
  • University of Edinburgh (GB)
  • University of Calgary (CA)
  • University Medical Center Utrecht (NL)
  • Centre Hospitalier Universitaire de Lille (FR)
  • Medical University of Graz (AT)
  • The University of Sydney (AU)
  • University of Cambridge (GB)
  • Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
  • University of British Columbia (CA)
  • Sunnybrook Health Science Centre (CA)
  • German Center for Neurodegenerative Diseases (DE)
  • Inserm (FR)
  • University of California, Davis (US)
  • Institut für Schlaganfall- und Demenzforschung (DE)
  • UCL Queen Square Institute of Neurology (GB)
  • Massachusetts General Hospital (US)
  • Western University (CA)
  • Chinese University of Hong Kong (HK)
  • Maastricht University Medical Centre (NL)
  • Azienda Ospedaliero-Universitaria Careggi (IT)
Corresponding author
Wardlaw, Joanna M
ORCID
Venue
The Lancet Neurology
Publisher
Elsevier BV
Published
2013-08
Volume
12
Issue
8
Pages
822-838
ISSN
1474-4422 (ISSN-L)
DOI
10.1016/s1474-4422(13)70124-8
PMC
PMC3714437
OpenAlex
W2158742097
Cited by
5,560
References
125
Citations by year
2026: 395 · 2025: 490 · 2024: 604 · 2023: 578 · 2022: 667 · 2021: 570 · 2020: 479 · 2019: 443 · 2018: 322 · 2017: 289 · 2016: 227 · 2015: 188 · 2014: 128 · 2013: 18
FWCI
108.93
Type
journal article
Language
en
Open access
Licence
Locations
  • The Lancet Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion, other-oa)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
  • Europe PMC (PubMed Central) (submittedVersion)
  • PubMed Central (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Florence Research (University of Florence) (submittedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
  • Leiden Repository (Leiden University) (submittedVersion)
  • DZNE Pub (submittedVersion)
  • Pure Amsterdam UMC (submittedVersion)
  • Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
  • Radboud Repository (Radboud University) (submittedVersion)
  • Research Publications (Maastricht University) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
  • Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
  • Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
Keywords
cerebral small vessel disease, neurodegeneration, aging, white matter hyperintensities, lacunes, microbleeds, perivascular spaces, brain atrophy
MeSH terms
Aging, Female, Humans, Image Processing, Computer-Assisted, International Cooperation, Male, Terminology as Topic

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-04.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-04.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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