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Vascular Dementia

High EvidenceUpdated: 2025-12-24

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Red Flags

  • Rapidly progressive dementia (Creutzfeldt-Jakob, Autoimmune)
  • Sudden focal deficit (Acute Stroke)
  • Fluctuating consciousness (Delirium - treat cause)
  • Head injury (Subdural Haematoma)
Overview

Vascular Dementia

1. Clinical Overview

Summary

Vascular Dementia (VaD) is the second most common form of dementia, caused by cerebrovascular disease reducing blood flow to the brain. It encompasses a spectrum from "Multi-infarct dementia" (post-stroke) to "Subcortical ischaemic vascular dementia" (small vessel disease). Unlike Alzheimer's, VaD classically presents with a stepwise deterioration and prominent executive dysfunction (slowing of thought, planning difficulties) often preceding memory loss. Management focuses strictly on secondary prevention of cerebrovascular events to halt progression, as standard dementia drugs (cholinesterase inhibitors) have limited benefit unless mixed pathology exists. [1,2]

Key Facts

  • Prevalence: Accounts for ~15-20% of all dementia cases.
  • Pathology: Ischaemic or haemorrhagic brain damage. "Mixed Dementia" (Alzheimer's + Vascular) is extremely common in the elderly (>30%).
  • Presentation: "Subcortical" pattern: Slow processing speed (Bradyphrenia), Gait disturbance ("Marche à petits pas"), Mood changes/Lability, Early urinary urgency.
  • Imaging: MRI shows White Matter Hyperintensities (Leukoaraiosis) and lacunar infarcts.
  • Treatment Limitations: Donepezil/Memantine are NOT first-line for pure vascular dementia (NICE), unlike Alzheimer's.

Clinical Pearls

The "Stepwise" Course: The classic textbook description is a patient who is stable, has a "mini-stroke" or event, drops a level in function, stabilises, then drops again. (Reality: Small vessel disease can present as a smoother, gradual decline mimicking Alzheimer's).

Emotional Incontinence: Also known as Pseudobulbar Affect. The patient laughs or cries disproportionately to the stimulus (e.g., crying when asking for tea). It is a sign of bilateral upper motor neurone damage.

Gait is the clue: Alzheimer's patients often walk normally until late stages. Vascular patients often have an early "magnetic" or "shuffling" gait and falls.

Executive vs Memory: If a patient can't draw a clock (Executive/Visuospatial) but remembers three words (Memory), think Vascular or Lewy Body rather than early Alzheimer's.


2. Epidemiology

Risk Factors (The "Vascular" Factors)

Identical to Stroke risk factors.

  • Hypertension (Single most important treatable factor).
  • Smoking.
  • Diabetes Mellitus.
  • Atrial Fibrillation.
  • Hyperlipidaemia.
  • History of Stroke/TIA.

Demographics

  • Age: Incidence rises primarily >65.
  • Gender: Men > Women (converse of Alzheimer's).

3. Pathophysiology

Mechanisms

  1. Macrovascular (Multi-Infarct): Multiple large cortical strokes. Volume of brain tissue lost correlates with cognitive decline.
  2. Microvascular (Small Vessel Disease): Arteriolosclerosis of penetrating arteries supplying white matter and basal ganglia. Causes ischemia of connections (Subcortical).
  3. Strategically Placed Infarcts: A single small stroke in the Thalamus or Angular Gyrus can cause dementia.

Subcortical Ischaemia (Binswanger's)

  • Chronic hypoperfusion of deep white matter.
  • Disruption of frontal-subcortical circuits.
  • Leads to the "Frontal" features (Apathy, Executive dysfunction) and "Subcortical" features (Gait, Bladder).

4. Clinical Presentation

Cognitive Domain Profile

Neurological Signs

Psychiatric


Processing Speed
Slowed (Bradyphrenia).
Executive Function
Difficulty Planning, Organising, Sequencing.
Attention
Impaired.
Memory
Less affected initially than in Alzheimer's (Retreival deficit rather than Encoding deficit - cues help).
5. Clinical Examination

Cognitive Testing

  • MoCA / ACE-III: Preferred over MMSE. MMSE focuses on memory/language (Alzheimer's) and misses executive dysfunction. MoCA includes trails, abstraction, clock draw.

Cardiovascular

  • BP: Check for hypertension.
  • Pulse: Irregular (AF).
  • Carotid: Bruits.

Neurological

  • Focal weakness (previous stroke).
  • Parkinsonism (Lower body parkinsonism common in vascular).

6. Investigations

The "Dementia Screen" (Rule out reversible)

  • FBC, U&E, LFT, Calcium, Glucose/HbA1c.
  • Thyroid (TSH).
  • B12/Folate.
  • Syphilis/VIH (if indicated).

Neuroimaging (Essential)

  • CT Brain: Sufficient to show infarcts and significant atrophy.
  • MRI Brain (Gold Standard):
    • T2/FLAIR seq: Shows White Matter Hyperintensities (Leukoaraiosis).
    • DWI: Recent ischaemia.
    • Lacunes: Small dark holes in basal ganglia.

Vascular Work-up

  • ECG (AF).
  • Carotid Doppler (if previous TIA symptoms).

7. Management

Management Algorithm

        VASCULAR DEMENTIA DIAGNOSED
                  ↓
┌─────────────────────────────────────────────┐
│    SECONDARY PREVENTION (Crucial)           │
│  - Anti-hypertensives (Target less than 140/90)      │
│  - Statin (Atorvastatin)                    │
│  - Antiplatelet (Clopidogrel) or DOAC       │
│  - Smoking cessation                        │
└─────────────────────────────────────────────┘
                  ↓
┌─────────────────────────────────────────────┐
│    SYMPTOM MANAGEMENT                       │
│  - Depression: SSRI (Sertraline)            │
│  - Agitation: Non-drug first.               │
│  - Cognition: AChE Inhibitors??             │
└─────────────────────────────────────────────┘
                  ↓
       IS IT MIXED DEMENTIA?
       (Evidence of Alzheimer's too?)
       NO                 YES
       ↓                   ↓
  Prevention only     Consider Donepezil

1. Vascular Risk Reduction (The mainstay)

  • Blood Pressure: Tight control reduces progression.
  • Antithrombotics: Clopidogrel (75mg) or Anticoagulation (DOAC/Warfarin) if AF.
  • Statins: Atorvastatin 80mg usually indicated (Secondary prevention of stroke).
  • Lifestyle: Diet, Exercise, Smoking cessation.

2. Cognitive Enhancers (AChE Inhibitors)

  • Guidelines (NICE): Do NOT offer AChE inhibitors (Donepezil, Rivastigmine, Galantamine) or Memantine for pure vascular dementia. (Trials show minimal benefit and risk of side effects).
  • Exception: "Mixed Dementia" (Alzheimer's + Vascular). If Alzheimer's contributes to the picture, these drugs can be used.

3. Supportive Care

  • Occupational Therapy: Home modifications.
  • Physiotherapy: Gait safety, falls prevention.
  • Mental Capacity Act: Establish Power of Attorney early (while capacity remains).

8. Complications
  • Stroke: Recurrent large strokes.
  • Falls: High risk due to gait/executive issues. fractures.
  • Aspiration Pneumonia: Due to dysphagia (pseudobulbar). Major cause of death.
  • Sepsis: Urinary tract infections.

9. Prognosis and Outcomes

Survival

  • Median survival: 3-5 years from diagnosis.
  • Prognosis is generally worse than Alzheimer's Disease (due to high cardiovascular mortality burden).

Progression

  • Variable. Can be stable for years if no further strokes occur.
  • Acute deteriorations usually signal new vascular events or infection (delirium).

10. Evidence and Guidelines

Key Guidelines

GuidelineOrganisationKey Recommendations
NG97NICE (2018)Diagnose using criteria. Do NOT use AChE inhibitors for pure VaD. Treat vascular risk.
Vascular Cognitive ImpairmentAHA / ASADefinition of VCI spectrum from mild impairment to dementia.
HypertensionNICETarget less than 140/90 (or less than 150/90 if >80y) to preserve cognition.

Landmark Studies

1. PROSPER Study (2002)

  • Result: Pravastatin reduced risk of TIA/Stroke in elderly.
  • Impact: Statins prevent the cause of VaD.

2. HYVET-COG (2008)

  • Question: Does treating HTN in over-80s reduce dementia?
  • Result: Trend towards reduction (reached significance when combined with other trials).
  • Impact: Treat BP even in the very elderly.

3. GAL-INT-6 (Galantamine in VaD)

  • Result: Small cognitive benefit but NO functional benefit.
  • Impact: Led to recommendation against routine use of AChE inhibitors.

11. Patient and Layperson Explanation

What is Vascular Dementia?

It is a decline in memory and thinking skills caused by reduced blood flow to the brain. This can be caused by a series of small strokes, one large stroke, or narrowing of the tiny blood vessels deep in the brain.

How is it different from Alzheimer's?

  • Alzheimer's: A build-up of proteins damages brain cells directly. Memory loss is usually the first sign.
  • Vascular: Lack of blood supply damages brain cells. Slow thinking/walking and mood changes often happen before memory loss. It can get worse in "steps" (sudden drops) rather than a smooth slide.

Can we treat it?

We cannot reverse the damage already done (dead brain cells won't grow back). However, we can stop it getting worse.

  • The Strategy: Protect the remaining brain tissue by stopping new strokes.
  • Medications: Blood Pressure tablets, Blood thinners, and Cholesterol tablets are the most important treatments.
  • Dementia pills: The pills used for Alzheimer's don't tend to work well for pure vascular dementia.

12. References

Primary Sources

  1. O'Brien JT, Thomas A. Vascular dementia. Lancet. 2015;386:1698-1706. PMID: 26590476.
  2. Iadecola C. The pathobiology of vascular dementia. Neuron. 2013;80:844-866. PMID: 24267647.
  3. NICE Guideline NG97. Dementia: assessment, management and support. 2018.
  4. Gorelick PB, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:2672-2713.

13. Examination Focus

Common Exam Questions

  1. Geriatrics: "Patient with step-wise decline, early incontinence, and broad-based gait. Diagnosis?"
    • Answer: Vascular Dementia (Subcortical type).
  2. Psychiatry: "Use of Donepezil in pure Vascular Dementia?"
    • Answer: Not recommended/Not effective. Only if mixed pathology.
  3. Neurology: "MRI shows extensive periventricular hyperintensities. Term for this?"
    • Answer: Leukoaraiosis (Small vessel disease).
  4. Pharmacology: "Best prevention for VaD?"
    • Answer: Antihypertensives.

Viva Points

  • Binswanger's Disease: Eponym for subcortical vascular dementia (white matter disease).
  • Hachinski Ischaemia Score: Old clinical tool to distinguish VaD from AD based on history (stepwise, somatic complaints, focal signs).
  • Pseudobulbar Affect: Mechanism? Disconnection of cortical inhibition of the brainstem emotional centres.

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • Rapidly progressive dementia (Creutzfeldt-Jakob, Autoimmune)
  • Sudden focal deficit (Acute Stroke)
  • Fluctuating consciousness (Delirium - treat cause)
  • Head injury (Subdural Haematoma)

Clinical Pearls

  • **Gait is the clue**: Alzheimer's patients often walk normally until late stages. Vascular patients often have an early "magnetic" or "shuffling" gait and falls.
  • **Executive vs Memory**: If a patient can't draw a clock (Executive/Visuospatial) but remembers three words (Memory), think Vascular or Lewy Body rather than early Alzheimer's.
  • Women (converse of Alzheimer's).

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines