Vascular cognitive impairment and dementia Overview
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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]
Overview
- Vascular cognitive impairment and dementia (VCID) is cognitive impairment attributable predominantly to cerebrovascular disease, spanning a spectrum from mild vascular cognitive impairment (VCI) to vascular dementia (VaD), its most severe form.[1]
- VaD is the second most common dementia after Alzheimer disease (AD), accounting for 15–20% of cases when defined as a "pure" pathology.[1]
- The proportion attributed to vascular disease rises to up to ~75% when any vascular contribution (including mixed pathology) is counted, and a companion estimate places vascular co-pathology at 50–70% of dementia.[1][2]
- This wide range reflects definitional heterogeneity (pure VaD vs. any vascular contribution) rather than true disagreement between sources, and the two figures should not be read as contradictory.[1][2]
- VCID results from large- and small-vessel disease producing ischemic or hemorrhagic injury or hypoperfusion, with resultant network disruption manifesting as a predominantly "subcortical" syndrome of slowed processing, impaired attention/executive function, and emotional lability.[1]
- Diagnosis is a two-step process — establishing a cognitive syndrome, then a predominantly vascular etiology substantiated by neuroimaging, preferably MRI.[1]
- No cure exists; management centers on modest symptomatic pharmacotherapy and, most importantly, control of shared cardiovascular risk factors for prevention.[3]
Historical Perspective
- The concept of vascular dementia evolved from the 19th–20th century notion of "arteriosclerotic dementia," reframed by Hachinski and colleagues in the 1970s as "multi-infarct dementia" with the introduction of the Hachinski Ischemic Score.[4]
- Successive operational criteria (ADDTC, NINDS-AIREN) formalized diagnosis before the field shifted toward the broader vascular cognitive impairment/VCID construct, recognizing that vascular contributions extend well beyond discrete infarcts and frequently coexist with Alzheimer pathology.[1]
Classification
- VCID is classified along a severity spectrum — from mild VCI (vascular mild neurocognitive disorder in DSM-5-TR) to vascular dementia (vascular major neurocognitive disorder).[5][6]
- ICD-9/10 code only vascular dementia, whereas ICD-11 (not yet implemented in the United States) adds a code for vascular mild neurocognitive disorder.[5]
- By the 2017 VICCCS clinical-anatomic scheme, major VCI is divided into:[4]
- Post-stroke dementia (conventionally within 6 months of stroke)
- Multi-infarct (cortical) dementia
- Subcortical ischemic (small-vessel) vascular dementia
- Mixed dementia (coexisting VaD and AD), the most common neuropathologic substrate
Pathophysiology
- VCID arises from abnormalities of large and small cerebral vessels producing acute or chronic ischemic injury, hemorrhage, or hypoperfusion (including cardiac causes), leading to cumulative tissue damage and disruption of neural networks.[1]
- Key mechanisms include:[1][7]
- Endothelial dysfunction
- Neurovascular-unit breakdown with blood–brain barrier disruption
- Neuroinflammation
- White matter injury
- Preferential involvement of frontostriatal circuits explains the characteristic executive/processing-speed deficits.[1][7]
Causes
- VCID is caused by cerebrovascular diseases including:[1]
- Large-vessel atherosclerosis
- Small-vessel arteriolosclerosis (lacunes, white matter disease, microbleeds)
- Cerebral amyloid angiopathy
- Cardioembolic sources such as atrial fibrillation, heart failure, acute coronary syndrome, and valvular disease
- Hereditary small-vessel disease (e.g., CADASIL/NOTCH3) and vasculitides are less common causes.
Differentiating Vascular Cognitive Impairment and Dementia from other Diseases
- VCID must be differentiated primarily from:[7]
- Alzheimer disease
- Dementia with Lewy bodies
- Frontotemporal dementia
- Normal-pressure hydrocephalus
- Depression (pseudodementia)
- Delirium
- Features favoring VCID include stepwise or fluctuating decline, a temporal link to stroke, executive/processing-speed-predominant deficits rather than early amnesia, and focal neurologic signs.[7][1]
- Mixed VaD-AD pathology remains a major overlap challenge.[7][1]
Epidemiology and Demographics
- VCID is the second most common dementia, comprising 15–20% of cases, with cerebrovascular disease contributing to up to ~75% of all dementia when mixed pathology is counted.[1]
- In the United States, an estimated 5.8 million people were living with dementia in 2020, projected to reach ~13.9 million by 2060.[5]
- Incidence rises steeply with age and is higher in populations with greater cardiovascular risk burden; shared risk factors mean cardiovascular clinicians frequently encounter it.[1]
Risk Factors
- The strongest and most consistent risk factors for VCID are modifiable cardiovascular factors:[8]
- Hypertension (particularly midlife)
- Diabetes mellitus
- Smoking
- Atrial fibrillation
- Obesity
- Physical inactivity
- Dyslipidemia (high LDL)
- Non-modifiable factors include age and prior stroke.[8]
Natural History, Complications and Prognosis
- The natural history of VCID is heterogeneous, ranging from acute/stepwise decline after strokes to gradual progression with cerebral small-vessel disease.[1]
- Average rates of cognitive decline are similar to AD, but mortality is higher — largely from cardiovascular and cerebrovascular causes — with recurrent stroke accelerating decline.[7]
- Complications include:[7]
- Progressive functional dependence
- Depression
- Apathy
- Neuropsychiatric symptoms
Diagnosis
- Diagnosis of VCID is a two-step process:[1]
- First, establishing a cognitive syndrome
- Then, establishing a predominantly vascular etiology through clinical history, examination, and neuroimaging (preferably MRI)
- A vascular cause is inferred from a temporal relationship between stroke and cognitive decline, or from a significant burden of cerebrovascular lesions on imaging.[1]
- The VasCog-2-WSO criteria (2025–2026) updated the 2014 VasCog criteria using a neuroimaging-first approach, formalizing preclinical VCID and vascular MCI stages.[9]
- Community-cohort validation showed a graded association with cardiovascular risk and mortality, detectable even at a neuroimaging-defined preclinical stage.[9]
History and Symptoms
- The history in VCID typically reveals:[1][7]
- Stroke or transient ischemic attack
- A stepwise or fluctuating course
- Early symptoms of slowed processing speed, impaired attention and executive function, and emotional lability (the subcortical syndrome), rather than the prominent early amnesia of Alzheimer disease
- Depression and apathy are especially common.[7]
Physical Examination
- Physical examination in VCID may reveal:[7]
- Focal neurologic deficits (motor or sensory findings)
- Gait and balance disturbance
- Pseudobulbar affect
- Primitive reflexes
- These findings reflect the underlying cerebrovascular lesions.[7]
Laboratory Findings
- There are no diagnostic laboratory tests for VCID.[1]
- Laboratory evaluation focuses on:[1]
- Excluding reversible causes of cognitive impairment
- Characterizing vascular risk factors (glucose/HbA1c, lipids)
- Emerging fluid biomarkers (e.g., neurofilament light, plasma amyloid/tau) are being investigated to detect coexisting Alzheimer pathology.[1]
Electrocardiogram
- The electrocardiogram has no direct role in diagnosing VCID.[1]
- It is useful for detecting atrial fibrillation and other cardioembolic sources that contribute to cerebrovascular injury.[1]
Chest X Ray
- Chest x-ray has no specific role in the diagnosis of VCID.
CT Scan
- Non-contrast CT can support the diagnosis of VCID by demonstrating:[1]
- Established infarcts
- White matter hypodensity
- Hemorrhage
- CT is useful when MRI is contraindicated, though it is less sensitive than MRI for small-vessel disease markers.[1]
MRI
- MRI is the preferred imaging modality and substantiates the diagnosis of VCID by demonstrating:[1]
- Large and small infarcts
- Lacunes
- White matter hyperintensities
- Enlarged perivascular spaces
- Cerebral microbleeds
- Cortical superficial siderosis
Echocardiography or Ultrasound
- Carotid ultrasound and echocardiography serve as adjuncts in VCID to identify treatable etiologic sources such as:[1]
- Large-vessel atherosclerosis
- Cardioembolic sources (thrombus, valvular disease)
Other Imaging Findings
- Amyloid/tau PET and FDG-PET can help identify coexisting Alzheimer pathology in VCID, informing prognosis and treatment expectations, particularly in suspected mixed dementia.[3]
Treatment
- Treatment of VCID is limited and centers on:[3][7]
- Modest symptomatic therapy
- Management of neuropsychiatric symptoms
- Treatment of comorbidities
- Caregiver support
- Most importantly, aggressive control of vascular risk factors for prevention
Medical Therapy
- Medical therapy for VCID includes cholinesterase inhibitors (donepezil, galantamine, rivastigmine) and memantine.[4][7][3]
- These produce small cognitive benefits — greatest when Alzheimer co-pathology is present — but inconsistent effects on global function.
- None is FDA-approved for VaD, and some guidelines and regulators advise against routine use.
- Antidepressants may help post-stroke depression but have poor efficacy in VaD-only depression.[3]
- Behavioral/environmental interventions are first-line for agitation and psychosis, with risperidone or quetiapine reserved as second-line.[3]
Surgery
- There is no surgical treatment specific to VCID.[3]
- Procedural interventions target underlying vascular sources (e.g., carotid revascularization, atrial fibrillation management), though direct evidence for cognitive endpoints is limited.[3]
Primary Prevention
- Primary prevention relies on managing cardiovascular risk factors — hypertension, diabetes, smoking, atrial fibrillation, obesity, and physical inactivity.[10]
- Intensive systolic blood-pressure lowering (SPRINT MIND):[11][12]
- Significantly reduced incident mild cognitive impairment and the composite outcome of mild cognitive impairment or probable dementia
- Did not significantly reduce probable dementia alone as a standalone endpoint — a nonsignificant trend that persisted through 7-year legacy follow-up and is reflected in the 2025 AHA/ACC hypertension guideline
- Multidomain lifestyle interventions (e.g., FINGER) have shown cognitive benefit in at-risk individuals.[3]
Secondary Prevention
- Secondary prevention in patients with established cerebrovascular disease or VaD centers on:[3]
- Antithrombotic therapy
- Aggressive post-stroke risk-factor optimization
- Continued lifestyle intervention to limit further vascular brain injury
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 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.
- ↑ 2.0 2.1 Biessels GJ, Debette S, Elahi FM; et al. (2026). "The Vascular Contribution to Dementia: World Stroke Organization Scientific Statement". International Journal of Stroke: 17474930261470506. doi:10.1177/17474930261470506.
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 Goodall LS, Lennon MJ, Sachdev PS; et al. (2026). "Current and Emerging Therapeutic Approaches for Vascular Cognitive Impairment and Dementia". Journal of the American College of Cardiology. 87 (1): 77–100. doi:10.1016/j.jacc.2025.09.1502.
- ↑ 4.0 4.1 4.2 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.
- ↑ 5.0 5.1 5.2 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.
- ↑ American Psychiatric Association (2022). Diagnostic and Statistical Manual of Mental Disorders (5th, text rev. ed.).
- ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 7.12 O'Brien JT, Thomas A (2015). "Vascular Dementia". Lancet (London, England). 386 (10004): 1698–706. doi:10.1016/S0140-6736(15)00463-8.
- ↑ 8.0 8.1 Sorond FA, Gorelick PB, Bae HJ; et al. (2026). "Vascular Contributions to Cognitive Impairment and Brain Health: Clinical Update and Mechanistic Considerations: A Scientific Statement From the American Heart Association". Stroke. 57 (7): e254–e270. doi:10.1161/STR.0000000000000524.
- ↑ 9.0 9.1 Lin YR, Lee WJ, Lee PL; et al. (2026). "Validation of the VasCog-2-WSO VCID Criteria in a Dementia-Free and Stroke-Free Community Cohort: Cardiovascular Risk and Mortality". Neurology. PMID 42531538 Check
|pmid=value (help). - ↑ Sabayan B, Boden-Albala B, Rost NS (2025). "An Ounce of Prevention: The Growing Need for Preventive Neurologists". Neurology. 105 (1): e213785. doi:10.1212/WNL.0000000000213785.
- ↑ Reboussin DM, Gaussoin SA, Pajewski NM; et al. (2025). "Long-Term Effect of Intensive vs Standard Blood Pressure Control on Mild Cognitive Impairment and Probable Dementia in SPRINT". Neurology. 104 (3): e213334. doi:10.1212/WNL.0000000000213334.
- ↑ Jones DW, Ferdinand KC, Taler SJ; et al. (2025). "2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults". Journal of the American College of Cardiology. 86 (18): 1567–1678. doi:10.1016/j.jacc.2025.05.007.