Updated Diagnostic Criteria for Vascular Cognitive Impairment and Dementia

The International Society for Vascular Behavioural and Cognitive Disorders (VasCog) working group updated the diagnostic criteria for vascular cognitive impairment and dementia (VCID). This update was published in JAMA Neurology.

Since the VasCog criteria were published in 2014, advances in VCID research and biomarker development have driven the need for an update. The VasCog-2-World Stroke Organization (WSO) Criteria Consortium conducted a literature review for recent advancements in VCID and revisited published diagnostic guidelines. The 70 experts participating in the Consortium used a Delphi process comprising 3 rounds to determine the items that should be included in the VasCog-2-WSO criteria.

The VasCog-2-WSO criteria defines mild cognitive impairment (MCI) as an acquired cognitive decline in at least 1 cognitive domain that does not affect independence. Dementia is defined as substantial cognitive decline in at least 1 cognitive domain that affects independence.

The 6 consensus cognitive domains were defined as attention and processing speed, executive function, learning and memory, language, perceptual-motor function, and social cognition.

In order to be categorized as a vascular etiology of MCI or dementia, the cognitive deficits should be related with 1 or more clinical strokes, in which the onset of cognitive decline is sudden and continues to be observed more than 3 months after stroke. For patients without a stroke history, deficits should be related with subcortical ischemic pathology, which typically affects attention and processing speed or executive functioning.

To identify evidence of VCID, the Consortium recommends magnetic resonance imaging, which can reveal key qualifying features, such as strategically placed or numerous infarcts, at least 2 lacunes outside the brainstem or 1 lacune coupled with white matter hyperintensities, extensive white matter hyperintensities, or an intracerebral hemorrhage.

Alternative etiologies may better explain a patient’s symptoms than VCID, particularly when focal vascular lesions are absent or there is no history of vascular events. In addition, biomarkers such as amyloid β and phosphorylated tau-derived species, brain amyloid on positron emission tomography, or apolipoprotein E ε4 homozygosity, may indicate that Alzheimer Disease is the cause of cognitive symptoms. Similarly, biomarkers for Lewy body dementia, frontotemporal dementia, brain tumor, or traumatic brain injury should prompt evaluations for alternative diagnoses.

Further, the VasCog-2-WSO defines 3 subtypes of VCID: hemorrhagic, ischemic, and mixed. Patients with preclinical VCID or at risk for VCID are defined as having significant neuroimaging evidence of cerebrovascular disease but without MCI or dementia criteria met.

Future studies are needed to validate these updated criteria.

The Consortium authors concluded, “The VasCog-2-WSO criteria update the VasCog criteria for the diagnosis of VCID, providing operationalization and additional guidance on potential neuroimaging and fluid biomarkers. VasCog-2-WSO should provide an international standard for VCID diagnosis, facilitating diagnostic consistency among clinicians and researchers.”

Disclosures: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.