Dementia due to cerebrovascular disease

ICD-10F01	Vascular dementia
DSM-5-TRF01.5x	Major Vascular Neurocognitive Disorder

1. Definition and nosology

Dementia due to cerebrovascular disease (Vascular Dementia; ICD-11: 6D81; DSM-5-TR: F01.5x and similar) — cognitive decline and impairment of daily functioning developing as a result of cerebrovascular disease (stroke, small vessel disease, hypoperfusion). Second most common cause of dementia (~15–20%).

2. History

1. Binswanger O. (1894) — classic description of subcortical vascular dementia.
2. NINDS-AIREN (1993) — international diagnostic criteria.
3. VASCOG (2014) — Updated consensus (Vascular Cognitive Disorders).

3. Epidemiology

• 15–20% of dementia cases; often mixed with Alzheimer’s.
• Prevalence increases with age.
• Risk factors: hypertension, diabetes, hyperlipidemia, atrial fibrillation, smoking, history of stroke.

4. Etiology and pathogenesis

• Multi-infarct dementia.
• Small vessel disease (subcortical leukoaraiosis, lacunar infarcts — Binswanger).
• Strategic infarct (thalamic, hippocampal).
• Hypoperfusion (systemic hypotension, cardiac arrest).
• CADASIL (autosomal dominant cerebral arteriopathy, NOTCH3).

5. Clinical features

• “Stepwise” decline (as opposed to the gradual decline of Alzheimer’s).
• Executive function, processing speed and attention are predominantly affected — memory is relatively less impaired (difference from Alzheimer).
• Focal neurological signs — hemiparesis, dysarthria, extrapyramidal, visual field defect.
• Mood disorders (vascular depression), apathy, abulia frequent.
• Postural disturbances (gait, balance).

6. Diagnosis

6.1 Unified diagnostic criteria (NINDS-AIREN, VASCOG)

A. Meeting major NCD criteria.

B. Clinical features consistent with vascular etiology: either (1) stepwise decline + history of stroke or (2) executive function and processing speed predominant.

C. Brain imaging evidence of vascular pathology — infarcts, leukoaraiosis, microhemorrhages.

D. Temporal relationship between cognitive decline and vascular event (Probable VaD).

6.2 Differences between sources

• VASCOG 2014 (Sachdev P. et al. Alzheimer Dis Assoc Disord) — introduced the Vascular Cognitive Impairment umbrella term.
• NICE NG97 — management of vascular risk factors.

6.3 Diagnostic algorithm

• Clinical interview + informant.
• MoCA (attention to executive function subscales).
• Neurological examination — focal signs.
• Brain MRI (FLAIR — leukoaraiosis, DWI — acute infarcts, T2/SWI — microhemorrhages).
• Cardiovascular evaluation — blood pressure, ECG (atrial fibrillation), Holter, carotid ultrasound, echo.
• Laboratory — HbA1c, lipid, coagulation, hyperhomocysteinemia.

6.4 Differential diagnosis

7. Examination and assessment

1. MoCA, neuropsychological testing.
2. MRI, cardiovascular.
3. Laboratory panel.

8. Treatment

• Vascular risk factor management — first-line
  1. Hypertension (target SBP <140, sometimes <130);
  2. Diabetes HbA1c management;
  3. Statin (lipid);
  4. Antiplatelet (aspirin) or anticoagulant (atrial fibrillation — DOAC);
  5. Smoking cessation;
  6. Physical activity, diet.
• AChEI and memantine — evidence base limited for VaD, but may be effective in mixed dementia; NICE NG97 — considered in mixed cases.
• BPSD management — non-pharmacological first; antipsychotics limited (same FDA black box for Alzheimer’s).
• Depression (vascular depression) — SSRIs.
• Rehabilitation after stroke — physical, occupational, speech therapy.

8.1 Treatment methods

• Vascular Risk Management — Hypertension, diabetes, lipids, atrial fibrillation, smoking.
• AChEI/Memantine in Mixed Dementia — Donepezil, rivastigmine off-label in pure VaD; may be considered in mixed cases.
• Stroke Rehabilitation — Multidisciplinary.

8.2 Differences between sources

1. NICE NG97 — vascular risk management.
2. AHA/ASA stroke prophylaxis.

9. Prognosis

• Risk factor management reduces the rate of decline.
• Stroke history and comorbidity determine the prognosis.

10. Myths and misconceptions

Myth 1: “VaD is completely different from Alzheimer’s”

Evidence: In most dementia cases mixed pathology (Alzheimer + VaD); clinical differentiation sometimes difficult.

Myth 2: “There is no specific treatment for VaD”

Evidence: vascular risk factor management — first-line and effective intervention; prevention particularly strong.

Myth 3: “Aspirin for dementia prophylaxis”

Evidence: ASPREE trial (McNeil J.J. NEJM 2018) — aspirin in primary prevention showed no evidence of preventing dementia; only in specific stroke prophylaxis indications.

Myth 4: “Homocysteine-lowering vitamins prevent vascular dementia”

Evidence: the evidence for homocysteine-lowering vitamins as cognitive prophylaxis is weak.

Myth 5: “Stepwise decline is mandatory for diagnosing VaD”

Evidence: stepwise decline is typical only in multi-infarct form; in small vessel form decline is gradual.

11. Sources

• WHO. ICD-11. 6D81 Dementia due to cerebrovascular disease. 2024.
• APA. DSM-5-TR. 2022.
• NICE NG97. 2018.
• Sachdev P. et al. Diagnostic criteria for vascular cognitive disorders: a VASCOG statement. Alzheimer Dis Assoc Disord 2014;28(3):206–218.
• McNeil J.J. et al. Effect of Aspirin on Disability-free Survival in the Healthy Elderly (ASPREE). NEJM 2018;379(16):1499–1508.
• Livingston G. et al. Lancet Commission 2024.