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Neurology

Diagnosis, Imaging, and Tests

At a Glance

Vascular dementia is diagnosed by combining evidence of thinking and daily-function changes with brain imaging that shows blood-vessel damage and a clear connection between them. MRI is usually preferred, while cognitive and specialized tests help identify mixed dementia.

Diagnosing vascular dementia is like solving a three-part puzzle. It is not enough for a doctor to simply see a “bad scan” or note that you have high blood pressure. To confirm a diagnosis, your medical team looks for a cognitive syndrome (evidence of thinking changes), cerebrovascular disease (visible damage on a brain scan), and a clear, logical link between the two [1][2]. A proper assessment also includes a detailed functional history, a neurological examination, a medication review, and tests for potentially reversible contributors such as delirium, thyroid abnormalities, vitamin B12 deficiency, sleep apnea, or depression.

This process helps your doctor determine whether your symptoms are caused purely by blood vessel issues or if they are part of a mixed dementia involving other conditions like Alzheimer’s [1][3].

The Imaging “Map”: MRI vs. CT

Imaging is the most powerful tool for seeing how vascular disease has affected your brain. While a CT scan can be a helpful backup, the Magnetic Resonance Imaging (MRI) is considered the preferred imaging test because it can see much smaller and more subtle changes [4][5].

Doctors look for several specific markers on your MRI:

  • White-Matter Hyperintensities (WMH): These appear as bright white “clouds” or spots on certain MRI sequences (specifically the FLAIR sequence) [4]. They represent damage to the brain’s “wiring” caused by a chronic lack of blood flow [6]. They can indicate damage from vascular disease, but they are also common with typical aging, migraines, or inflammation, so their presence alone does not prove dementia.
  • Lacunar Infarcts: These are very small, deep strokes that leave behind tiny, fluid-filled cavities (lacunes) [4]. They are often “silent,” meaning you may not have realized they happened at the time [7].
  • Microbleeds: These are tiny, old leaks from fragile blood vessels deep in the brain. They can have different patterns and causes, including deep hypertensive arteriopathy or lobar cerebral amyloid angiopathy. Specialists use a specific sequence called susceptibility-weighted imaging to find these “ink spots” [4].
  • Strategic Infarcts: Sometimes, a single stroke in a “strategic” location—like the thalamus or caudate nucleus—can cause significant cognitive changes even if the stroke itself was small [8][9].

Importantly, there is no universal “threshold” or specific number of spots required for a diagnosis [10]. One person might have many spots and few symptoms, while another might have only a few spots in critical areas that cause significant trouble [11][8].

Measuring Thinking: MoCA vs. MMSE

To measure the “cognitive syndrome” part of the puzzle, doctors use screening tests. Two of the most common are the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA).

For vascular dementia, the MoCA is often preferred [12]. This is because vascular disease typically hits executive function—your ability to plan, organize, and focus—earlier than it hits short-term memory [6]. The MoCA includes tasks like “trail-making” (connecting dots) and clock-drawing that are much more sensitive to these specific vascular deficits [12][13]. The MMSE is still widely used and can be helpful in post-stroke settings, but it can sometimes miss the milder planning and attention issues common in vascular cognitive impairment [14][13]. Both are screening tools affected by factors like education, fatigue, hearing, and vision; they are not definitive diagnostic tests, and a functional history or formal neuropsychological testing is often needed to understand your true cognitive profile.

Distinguishing Pure vs. Mixed Dementia

Since mixed pathology is common [15], doctors may use biomarkers to see what else is happening in the brain [3].

  • Cerebrospinal Fluid (CSF) Testing: A lumbar puncture (spinal tap) allows doctors to collect cerebrospinal fluid, the liquid that bathes the brain. By measuring the ratios of specific proteins like amyloid and tau, they can determine if Alzheimer’s disease is co-existing with the vascular damage [16][17].
  • Amyloid PET Scans: This is a specialized brain scan where a tracer is injected into your vein to “light up” amyloid plaques, the hallmark of Alzheimer’s [18]. A positive scan doesn’t mean the vascular damage isn’t important; it shows amyloid pathology is present, but it does not by itself prove that Alzheimer’s disease is the primary cause of your symptoms, as amyloid becomes more common with age. These tests have costs and procedural considerations, and they are usually reserved for diagnostically uncertain cases where confirming Alzheimer’s pathology would alter your treatment plan [3].

By combining these tests, your care team can move beyond a simple “vascular” or “Alzheimer’s” label and create a personalized plan that addresses every factor contributing to your cognitive health [1][19].

Common questions in this guide

How do doctors diagnose vascular dementia?
Doctors look for three things: changes in thinking and daily functioning, blood-vessel damage visible on brain imaging, and a clear connection between the damage and the symptoms. They may also review medications, perform a neurological examination, and test for reversible problems such as delirium, thyroid disease, vitamin B12 deficiency, sleep apnea, or depression.
Is an MRI better than a CT scan for finding vascular dementia?
MRI is usually preferred because it can detect smaller and subtler areas of brain damage than CT. CT can still be useful when MRI is not available or cannot be performed. Neither scan alone proves dementia, and there is no single number of spots that confirms the diagnosis.
What do white matter changes, lacunes, and microbleeds mean on an MRI?
White matter changes can reflect long-term reduced blood flow, lacunes are small cavities left by tiny strokes, and microbleeds are traces of old bleeding from fragile vessels. These findings can support vascular disease, but they may also occur with aging or other conditions. Doctors interpret them alongside cognitive changes and daily functioning.
Which cognitive test is better for vascular dementia, the MoCA or MMSE?
The MoCA is often more sensitive to problems with planning, organization, attention, and focus, which can occur early in vascular cognitive impairment. The MMSE is still useful in many settings, including after a stroke. Both are screening tools, so scores must be interpreted in light of education, fatigue, hearing, vision, and functional history.
Can testing show whether Alzheimer's disease is also contributing?
A spinal tap can measure amyloid and tau proteins in cerebrospinal fluid, and an amyloid PET scan can show amyloid plaques in the brain. A positive amyloid result indicates that Alzheimer’s-type changes are present, but it does not by itself prove they are the main cause of the symptoms. These tests are generally considered when the diagnosis is uncertain and the result could change care.

Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.Which specific MRI findings—like white matter changes, lacunes, or microbleeds—were most important for my diagnosis?
  2. 2.Given my education and background, how do you interpret my scores on the MoCA or MMSE?
  3. 3.Does my imaging show enough vascular damage to explain my current level of cognitive change, or is there a 'mismatch'?
  4. 4.Would a lumbar puncture or a PET scan be helpful to see if Alzheimer's is also contributing to my symptoms?
  5. 5.Are the vascular changes in a 'strategic' area of my brain, and how does that affect my specific symptoms like walking or planning?

Questions For You

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References

References (19)
  1. 1

    Vascular Cognitive Impairment.

    Smith E

    Continuum (Minneapolis, Minn.) 2016; (22(2 Dementia)):490-509 doi:10.1212/CON.0000000000000304.

    PMID: 27042905
  2. 2

    Vascular Cognitive Impairment.

    Dichgans M, Leys D

    Circulation research 2017; (120(3)):573-591 doi:10.1161/CIRCRESAHA.116.308426.

    PMID: 28154105
  3. 3

    Revised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup.

    Jack CR, Andrews JS, Beach TG, et al.

    Alzheimer's & dementia : the journal of the Alzheimer's Association 2024; (20(8)):5143-5169 doi:10.1002/alz.13859.

    PMID: 38934362
  4. 4

    Neuroimaging in vascular cognitive impairment: a state-of-the-art review.

    Heiss WD, Rosenberg GA, Thiel A, et al.

    BMC medicine 2016; (14(1)):174 doi:10.1186/s12916-016-0725-0.

    PMID: 27806705
  5. 5

    White matter degeneration in vascular and other ageing-related dementias.

    Hase Y, Horsburgh K, Ihara M, Kalaria RN

    Journal of neurochemistry 2018; (144(5)):617-633 doi:10.1111/jnc.14271.

    PMID: 29210074
  6. 6

    Vascular Cognitive Impairment and Dementia: Clinical Features, Neuropathology, and Biomarkers.

    Sachdev PS, Bentvelzen AC, Gustafson D, et al.

    Journal of the American College of Cardiology 2026; (87(1)):52-76 doi:10.1016/j.jacc.2025.11.008.

    PMID: 41498479
  7. 7

    Clinical presentations and epidemiology of vascular dementia.

    Smith EE

    Clinical science (London, England : 1979) 2017; (131(11)):1059-1068 doi:10.1042/CS20160607.

    PMID: 28515342
  8. 8

    Strategic white matter hyperintensity locations for cognitive impairment: A multicenter lesion-symptom mapping study in 3525 memory clinic patients.

    Coenen M, Kuijf HJ, Huenges Wajer IMC, et al.

    Alzheimer's & dementia : the journal of the Alzheimer's Association 2023; (19(6)):2420-2432 doi:10.1002/alz.12827.

    PMID: 36504357
  9. 9

    Strategic white matter hyperintensity locations associated with post-stroke cognitive impairment: A multicenter study in 1568 stroke patients.

    Coenen M, de Kort FA, Weaver NA, et al.

    International journal of stroke : official journal of the International Stroke Society 2024; (19(8)):916-924 doi:10.1177/17474930241252530.

    PMID: 38651756
  10. 10

    Reliability and validity of the total cerebral small vessel disease score: a systematic review and meta-analysis.

    Silva GD, Telles JPM, Rimkus CM, et al.

    Frontiers in neurology 2025; (16()):1593402 doi:10.3389/fneur.2025.1593402.

    PMID: 40656982
  11. 11

    Cerebral small vessel disease and vascular cognitive impairment: from diagnosis to management.

    Zanon Zotin MC, Sveikata L, Viswanathan A, Yilmaz P

    Current opinion in neurology 2021; (34(2)):246-257 doi:10.1097/WCO.0000000000000913.

    PMID: 33630769
  12. 12

    A comparison between the MoCA and the MMSE visuoexecutive sub-tests in detecting abnormalities in TIA/stroke patients.

    Mai LM, Sposato LA, Rothwell PM, et al.

    International journal of stroke : official journal of the International Stroke Society 2016; (11(4)):420-4 doi:10.1177/1747493016632238.

    PMID: 26865154
  13. 13

    Montreal Cognitive Assessment (MoCA) Scale: Strengths, Limitations, and Implication for Clinical Practice.

    Hadinezhad P, Noroozian M

    Iranian journal of psychiatry 2026; (21(1)):140-150 doi:10.18502/ijps.v21i1.20571.

    PMID: 42051279
  14. 14

    Brief Screening of Vascular Cognitive Impairment in Patients With Cerebral Autosomal-Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy Without Dementia.

    Brookes RL, Hollocks MJ, Tan RY, et al.

    Stroke 2016; (47(10)):2482-7 doi:10.1161/STROKEAHA.116.013761.

    PMID: 27625375
  15. 15

    Vascular cognitive impairment.

    van der Flier WM, Skoog I, Schneider JA, et al.

    Nature reviews. Disease primers 2018; (4()):18003 doi:10.1038/nrdp.2018.3.

    PMID: 29446769
  16. 16

    CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios: better diagnostic markers of Alzheimer disease.

    Janelidze S, Zetterberg H, Mattsson N, et al.

    Annals of clinical and translational neurology 2016; (3(3)):154-65 doi:10.1002/acn3.274.

    PMID: 27042676
  17. 17

    Diagnostic Biomarkers of Amyloid and Tau Pathology in Alzheimer's Disease: An Overview of Tests for Clinical Practice in the United States and Europe.

    Iaccarino L, Burnham SC, Dell'Agnello G, et al.

    The journal of prevention of Alzheimer's disease 2023; (10(3)):426-442 doi:10.14283/jpad.2023.43.

    PMID: 37357283
  18. 18

    Accuracy of Biomarker Testing for Neuropathologically Defined Alzheimer Disease in Older Adults With Dementia.

    Fink HA, Linskens EJ, Silverman PC, et al.

    Annals of internal medicine 2020; (172(10)):669-677 doi:10.7326/M19-3888.

    PMID: 32340038
  19. 19

    Considerations in the clinical use of amyloid PET and CSF biomarkers for Alzheimer's disease.

    Leuzy A, Bollack A, Pellegrino D, et al.

    Alzheimer's & dementia : the journal of the Alzheimer's Association 2025; (21(3)):e14528 doi:10.1002/alz.14528.

    PMID: 40042435

This page explains how vascular dementia is evaluated for educational purposes only and does not replace medical advice. Your clinician should interpret your MRI, cognitive scores, and biomarker results in the context of your symptoms and daily function.

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