ICD-116D81	DEMENTIA DUE TO CEREBROVASCULAR DISEASE Dementia due to cerebrovascular disease
ICD-10F01	Vascular dementia
DSM-5-TRF01.5x	Major Vascular Neurocognitive Disorder

1. Definition and nosology

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

• Binswanger O. (1894) — classic description of subcortical vascular dementia.
• NINDS-AIREN (1993) — international diagnostic criteria.
• 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. Aetiology 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 subcortical dementia, 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 Source-specific clarifications

• 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

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

6.4 Differential diagnosis

7. Examination and assessment

• MoCA, neuropsychological testing.
• MRI, cardiovascular.
• Laboratory panel.

8. Treatment

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

Source-specific specifications

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

Treatment methods

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

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 potent 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: “Vitamins and homocysteine are prophylaxis for vascular dementia”

Evidence: cognitive prophylaxis with homocysteine-lowering vitamins evidence weak.

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

Evidence: Gradual decline typical in small vessel VaD; stepwise only in multi-infarct form.

11. Sources

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