Vascular cognitive impairment (VCI) is often underrecognized. This guide for primary care physicians covers modern VCI concepts, clinical red flags and the role of neuroimaging to help you identify and manage at-risk patients and improve outcomes.

Published: October 8, 2025

Primary care physicians are frequently the first health care providers to encounter patients with cognitive concerns. While Alzheimer’s disease typically dominates discussions regarding dementia, vascular contributions to cognitive impairment and dementia, collectively referred to as vascular cognitive impairment (VCI), represent a critical but underrecognized cause of cognitive decline. Modern neuroimaging techniques readily allow for early identification of cerebrovascular disease that may contribute to cognitive dysfunction.

Although large strokes traditionally have been recognized as a cause of vascular dementia, cerebrovascular small vessel disease is actually the most common cause of VCI. By recognizing the various manifestations of cerebrovascular small vessel disease and its frequent coexistence with neurodegenerative pathology, primary care physicians can identify at-risk patients earlier and implement interventions that may significantly impact outcomes.

The key is moving beyond the traditional belief of vascular dementia as a stepwise decline in cognition after large strokes to recognizing other more common presentations, such as the insidious, multisystem impact of cerebrovascular small vessel disease.

Understanding the modern landscape of vascular cognitive impairment

Rather than stepwise decline, “vascular cognitive impairment” is an umbrella term encompassing cognitive impairment secondary to vascular brain injury from potentially multiple mechanisms. This includes both mild cognitive impairment due to vascular causes and vascular dementia.

“Pure vascular dementia accounts for only about 10% of all dementia cases. The reality is that mixed pathologies — combining vascular and neurodegenerative components — represent the most common scenario, particularly in older adults,” Kenneth Gregory Pugh, M.D., a geriatrician and memory disorders specialist at Norton Neuroscience Institute, said in a recent continuing medical education seminar.

Dr. Pugh presented on “Vascular Contributions to Cognitive Impairment.”

Cerebrovascular small vessel disease is the most important form of vascular cognitive impairment, typically occurring without overt clinical strokes. Unlike the dramatic presentation of large vessel strokes, small vessel disease often develops insidiously and may affect cognition, behavior, mood, gait and balance.

Clinical red flags for small vessel disease

Dr. Pugh advises watching for this constellation of symptoms that extends beyond typical memory complaints:

Cognitive pattern:

• Executive dysfunction and cognitive slowing
• Attention and working memory deficits
• “Forgetful” rather than truly amnesic (Patients improve with multiple choice or recognition tasks.)

Noncognitive manifestations:

• Gait disorders and balance problems
• Apathy or depression
• Urinary urgency, frequency or urge incontinence
• Increased falls

This multisystem presentation should raise suspicion for vascular contributions to cognitive decline, even in the absence of stroke history.

Leveraging neuroimaging for early detection

When ordering brain MRI for cognitive concerns, understanding what different sequences reveal is critical:

• T1 images: Assess atrophy patterns and regional volume loss
• T2-weighted fluid-attenuated inversion recovery (FLAIR) sequences: Critical for identifying white matter changes
• T2-susceptibility weighted imaging (SWI) sequences: Essential for detecting blood products such as microbleeds or superficial siderosis

Small vessel disease may manifest as several findings on MRI:

• White matter hyperintensities: Nearly ubiquitous with aging, but Grade 2 to Grade 3 changes on the Fazekas scale carry significant implications for cognitive decline and poor outcomes.
• Lacunar infarcts: These are small subcortical infarcts that can have profound cognitive impact depending on location.
• Cerebral microbleeds: Common, particularly with cerebral amyloid angiopathy and hypertensive arteriopathy, cerebral microbleeds are associated with cognitive impairment when numerous.
• Dilated perivascular spaces: These are increasingly recognized as a manifestation of small vessel disease linked to cognitive decline.
• Cortical superficial siderosis: This is a strong indicator of cerebral amyloid angiopathy.

The power of strategic infarcts

Don’t underestimate tiny lesions, according to Dr. Pugh. Strategic infarct dementia demonstrates how very small strokes or infarcts in key areas can cause acute, permanent and profound cognitive dysfunction. Lacunar infarcts in the thalamus, corpus callosum, caudate or left angular gyrus can result in dramatic cognitive deficits that may leave patients with significant impairment despite good recovery from motor symptoms.

This emphasizes why post-stroke cognitive assessment is crucial — even when physical recovery appears complete.

Addressing cerebral hypoperfusion

Consider chronic hypoperfusion as a treatable contributor to cognitive decline. Conditions associated with cognitive impairment through hypoperfusion mechanisms include:

• Atrial fibrillation and other arrhythmias
• Ischemic heart disease
• Carotid stenosis
• Heart failure
• Chronic lung disease
• Sleep apnea

Addressing these conditions may result in cognitive improvement in some patients.

Treatment considerations

While we lack specific therapies for pure vascular cognitive impairment, several approaches show promise:

Pharmacological interventions

• Cholinesterase inhibitors and memantine show small but significant benefits for vascular dementia in meta-analyses.
• Memantine particularly may help with apathy in vascular dementia.
• Given the high prevalence of mixed dementia, trials of these medications are often warranted.

Vascular risk management

• Blood pressure control remains the most important modifiable factor.
• However, traditional cardiovascular risk factors explain only about 16% of the variance of white matter disease changes.
• Current evidence suggests against routine antiplatelet therapy for asymptomatic or “covert” small vessel disease in patients over 70 without other indications, such as history of heart attack, transient ischemic attack or symptomatic stroke.

The synergistic effect: Why early recognition matters

Vascular disease can “unmask” Alzheimer’s pathology. Small subcortical infarcts increase dementia odds nearly fourfold, and patients with lacunar infarcts in key areas have a 20-fold greater risk of expressing clinical dementia with the same concentration of Alzheimer’s pathology.

This synergism means that preventing or treating vascular contributions may significantly delay or prevent clinical expression of dementia, even when some neurodegenerative pathology is present.