Vascular cognitive impairment and dementia historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hasnain Ali Moryani, MBBS[2]
Historical Perspective
Overview
The concept of vascular cognitive impairment and dementia (VCID) has evolved through three broad eras: 19th-century recognition of discrete vascular brain lesions (Marie's état lacunaire; Binswanger's subcortical white matter disease), a mid-20th-century "arteriosclerotic dementia" hypothesis attributing late-life dementia to chronic global hypoperfusion, and a modern reconceptualization beginning in the 1970s.[1][2]
Demonstration that cerebral blood flow could still increase in demented patients disproved the global-hypoperfusion model, and introduction of the term "multi-infarct dementia" reframed vascular dementia as the cumulative result of discrete, potentially preventable strokes. "Vascular dementia" was subsequently judged too narrow, and "vascular cognitive impairment" was introduced around 2000 to capture the full spectrum from mild impairment to dementia. The umbrella term "VCID" reflects the current understanding that vascular and neurodegenerative processes usually coexist rather than representing distinct entities.[3]
Early descriptions of vascular brain injury (19th–early 20th century)
Vascular dementia was first suggested by pathologists identifying specific vascular brain lesions. Pierre Marie described the état lacunaire (lacunar state), and Otto Binswanger identified subcortical white matter lesions, later termed Binswanger disease. When Alois Alzheimer characterized the presenile degenerative disease bearing his name, most dementia in elderly patients was still attributed to "cerebral arteriosclerosis."[1]
The "arteriosclerotic dementia" / global hypoperfusion era
Alzheimer himself endorsed the view that dementia of the elderly resulted from cerebrovascular insufficiency — arterial "hardening" impairing the ability of cerebral vessels to dilate and match blood delivery to metabolic demand, causing chronic hypoperfusion, neuronal death, and dementia. This global-vasoparalysis hypothesis dominated clinical thinking into the 1970s.[1]
The shift to multi-infarct dementia (1970s)
Two developments overturned the global-hypoperfusion model:
- Cerebral blood flow measurement showed that cerebral vessels could still increase flow in cognitively impaired individuals, arguing against fixed global vasoparalysis.
- Pathological studies (Tomlinson and colleagues) and the clinical work of Hachinski and colleagues established multi-infarct dementia, in which dementia results from cumulative burden of multiple discrete infarcts rather than diffuse ischemia.
This reframing carried a key therapeutic implication: if strokes are preventable, a substantial fraction of dementia should likewise be preventable. The Hachinski Ischemic Score emerged from this era as a bedside tool to distinguish multi-infarct from degenerative dementia; it is now regarded as historically important rather than a primary diagnostic instrument.[1]
From vascular dementia to vascular cognitive impairment (circa 2000)
"Vascular dementia" was ultimately judged too restrictive, capturing only the severe end of the spectrum while failing to describe milder, often earlier, vascular-related cognitive change. Vascular cognitive impairment (VCI) was introduced at the start of the 2000s and widely adopted; vascular dementia is now understood as the most severe form of VCI along a continuum rather than a categorically separate disease.[4] The first major American Heart Association/American Stroke Association statement to consolidate the VCI construct across the full spectrum of vascular brain injury was published in 2011.[5]
Formalization of modern diagnostic criteria
Successive operational criteria formalized diagnosis, including the ADDTC and NINDS-AIREN criteria, followed by DSM-5 (vascular mild and major neurocognitive disorder) and the 2014 VASCOG criteria. The 2017 Vascular Impairment of Cognition Classification Consensus Study (VICCCS) produced the framework in wide current use, dividing VCI into mild and major subtypes; major VCI (vascular dementia) is subdivided into post-stroke dementia (cognitive decline beginning within 6 months of stroke), subcortical ischemic (small-vessel) vascular dementia, multi-infarct (cortical) dementia, and mixed dementia.[1][6] VICCCS designated MRI as the gold-standard imaging requirement and retained the "probable/possible" qualifiers.[6]
The VCID / neurovascular-unit era (present)
The umbrella term vascular contributions to cognitive impairment and dementia (VCID) reflects the contemporary shift away from viewing Alzheimer disease and vascular dementia as separate entities, emphasizing that neurovascular-unit dysfunction contributes across a broad range of neurodegenerative processes and impairment severities.[7][8] Pathological and epidemiological studies established that mixed vascular–degenerative pathology is the most common substrate of late-life dementia, and that vascular risk factors — notably midlife hypertension and diabetes — also increase Alzheimer disease risk, reinforcing a shared-prevention approach.[7]
Most recently, neuroimaging biomarkers of early vascular change — infarcts, white matter hyperintensities, microbleeds, cortical superficial siderosis, enlarged perivascular spaces — have been validated as predictors of future dementia, and updated criteria (VasCog-2-WSO, 2025–2026) formalize preclinical and vascular MCI stages using a neuroimaging-first approach.[9]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Iadecola C, Duering M, Hachinski V; et al. (2019). "Vascular Cognitive Impairment And Dementia: JACC Scientific Expert Panel". Journal of the American College of Cardiology. 73 (25): 3326–3344. doi:10.1016/j.jacc.2019.04.034.
- ↑ Korczyn AD (2005). "The Underdiagnosis of the Vascular Contribution to Dementia". Journal of the Neurological Sciences. 229-230: 3–6. doi:10.1016/j.jns.2004.11.011. PMID 15760612.
- ↑ Smith EE, Aparicio HJ, Gottesman RF; et al. (2025). "Vascular Contributions to Cognitive Impairment and Dementia in the United States: Prevalence and Incidence: A Scientific Statement From the American Heart Association". Stroke. doi:10.1161/STR.0000000000000494.
- ↑ Han X, Zhang J, Chen S; et al. (2023). "Mapping the Current Trends and Hotspots of Vascular Cognitive Impairment From 2000-2021: A Bibliometric Analysis". CNS Neuroscience & Therapeutics. 29 (3): 771–782. doi:10.1111/cns.14026.
- ↑ Gorelick PB, Scuteri A, Black SE; et al. (2011). "Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 42 (9): 2672–2713. doi:10.1161/STR.0b013e3182299496. PMID 21778438.
- ↑ 6.0 6.1 Battle CE, Abdul-Rahim AH, Shenkin SD, Hewitt J, Quinn TJ (2021). "Cholinesterase Inhibitors for Vascular Dementia and Other Vascular Cognitive Impairments: A Network Meta-Analysis". The Cochrane Database of Systematic Reviews. 2: CD013306. doi:10.1002/14651858.CD013306.pub2.
- ↑ 7.0 7.1 Sachdev PS, Bentvelzen AC, Gustafson D; et al. (2026). "Vascular Cognitive Impairment and Dementia: Clinical Features, Neuropathology, and Biomarkers". Journal of the American College of Cardiology. 87 (1): 52–76. doi:10.1016/j.jacc.2025.11.008.
- ↑ Iadecola C, Smith EE, Anrather J; et al. (2023). "The Neurovasculome: Key Roles in Brain Health and Cognitive Impairment: A Scientific Statement From the American Heart Association/American Stroke Association". Stroke. 54 (6): e251–e271. doi:10.1161/STR.0000000000000431.
- ↑ VasCog-2-WSO Criteria Consortium, Sachdev PS, Bentvelzen AC; et al. (2025). "Revised Diagnostic Criteria for Vascular Cognitive Impairment and Dementia-the VasCog-2-WSO Criteria". JAMA Neurology. 82 (11): 1103–1112. doi:10.1001/jamaneurol.2025.3242.