ICD-116D81

DEMENTIA DUE TO CEREBROVASCULAR DISEASE

Dementia due to cerebrovascular disease
ICD-10F01Vascular dementia
DSM-5-TRF01.5xMajor 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

  • 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 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

  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

ConditionDistinguishing feature
Alzheimer (6D80)Gradual, memory dominant.
Mixed Dementia (Alzheimer's + VaD)In many cases; clinically co-occurrent.
Lewy bodies (6D82)Visual hallucinations, parkinsonism.
Frontotemporal (6D83)Personality/behavior dominant.
Normal pressure hydrocephalusTriad (gait, urinary incontinence, cognitive impairment).
Depressive pseudodementiaAffective, improvement with antidepressants.

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.

8.1 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.

8.2 Differences between sources

  • NICE NG97 — vascular risk management.
  • 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 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.

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