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GERICLINICS

GeriQBank · Paper II · Q27

Vascular dementia

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BPSD, Caregiver Support, Reversible Dementias, MCI & Vascular Dementia
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Attempt it firstOutline your answer before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer

7-Mark Answer

Textbook Core — 6 Points

1.

Definition and concept. Vascular dementia (VaD) is dementia resulting from cerebrovascular disease, having evolved from the older concept of arteriosclerotic dementia. The current and preferred umbrella term is vascular cognitive impairment (VCI), which spans the full spectrum from vascular MCI (Va-MCI) to VaD, and includes mixed vascular and AD pathology. About 5% of people over 65 have VCI, and in patients under 74 VCI may be the single most common cause of cognitive impairment. The inclusion of VCI-no dementia emphasises the preventable nature of VCI and the importance of early diagnosis; the asymptomatic susceptible host with risk factors is termed the “brain at risk”.

2.

Classification — seven subtypes. Multi-infarct (cortical) dementia from large cortical infarcts; small-vessel (subcortical) dementia from lacunes and white or deep grey matter lesions; strategic infarct dementia from a unilateral or bilateral infarct in a strategic area; hypoperfusion dementia; haemorrhagic dementia; Alzheimer’s disease with cerebrovascular disease (mixed); and hereditary dementia such as CADASIL, due to NOTCH3 mutation on chromosome 19. Subcortical ischaemic vascular disease (SIVD) — the lacunar state and Binswanger’s disease — is the commonest subtype (82.2% small-vessel versus 25.9% large-vessel in one study).

3.

Clinical features by vessel size. Large-vessel disease produces cortical infarcts in strategic locations giving a cortical dementia — frontal lobe (aphasia, apraxia, disinhibition, apathy), hippocampus and basal forebrain (amnesia), gyrus angularis (construction problems), parietal lobe (alexia, agraphia). Small-vessel disease affects thalamus, caudate nucleus and internal capsule, disrupting frontal–subcortical or thalamocortical circuits to give a subcortical dementia — executive dysfunction, attention deficit, apathy and personality change with comparatively milder memory deficit and slowed processing speed. “Lower-half parkinsonism” produces hesitation, marche à petit pas and diminished step height, and the triad of dementia, urinary incontinence and gait disturbance is more often produced by small-vessel VaD than by normal-pressure hydrocephalus.

4.

Course. Classically abrupt onset with stepwise deterioration and a fluctuating course with plateaus, but in practice 60% have a slow, less abrupt onset and 80% show slow progression with or without stepwise decline — so a gradual course does not exclude VaD.

5.

Diagnosis. NINDS-AIREN criteria for probable VaD require (i) dementia; (ii) cerebrovascular disease — focal neurological signs consistent with stroke plus neuroimaging evidence of clinically relevant vascular lesions; and (iii) a temporal relationship — onset of dementia within three months of a recognised stroke, abrupt deterioration, or fluctuating/stepwise progression. Supportive clinical features are early gait disturbance, unsteadiness with frequent unprovoked falls, early urinary frequency and urgency unexplained by urological disease, pseudobulbar palsy, and personality and mood change with abulia, depression, emotional incontinence, psychomotor retardation and abnormal executive function. Imaging severity criteria include white matter lesions affecting more than 25% of white matter. These criteria exclude about 90% of AD but have only modest sensitivity (50–70%) and misclassify mixed dementia as VaD (54% for ADDTC, 29% for NINDS-AIREN). MRI shows basal ganglionic and thalamic hyperintense foci, thromboembolic infarcts, confluent white matter and irregular periventricular hyperintensities (leukoencephalopathy); SPECT shows multiple focal deficits; and cerebral microbleed number independently predicts cognitive impairment and dementia severity.

6.

Management — four-pronged. (i) Symptomatic treatment for cognition: three donepezil and two galantamine studies show modest improvement of about two points on the VADAS-Cog, with inconsistent effects on activities of daily living, behaviour and global function; two memantine studies show modest cognitive benefit but no global benefit. There is no recommendation to prescribe cholinesterase inhibitors for pure VaD, but they should be used in mixed dementia once both AD and vascular components are demonstrated. (ii) Management of neuropsychiatric disturbance — depression is common with stroke and SIVD and is eminently treatable, so an antidepressant course is justified where suspected. (iii) Stroke prevention — control of vascular risk factors, especially hypertension, remains the most effective strategy; aspirin’s effect on cognition and prognosis remains unclear, and antithrombotics should be used with caution when lobar microbleeds are seen on MRI because of amyloid angiopathy. Neither pravastatin (PROSPER) nor atorvastatin (LEADe) improved cognition. (iv) Management of stroke-related disability — spasticity, parkinsonism and incontinence; levodopa can help apraxic gait in SIVD when the vascular burden lies in the basal ganglia or substantia nigra. Physical activity and multicomponent exercise combining aerobic and strength training have the most promising preventive evidence.

Latest Update — 1 Point

7.

The field has moved from “vascular dementia” to biologically and clinically harmonised vascular cognitive impairment. The VASCOG statement and the harmonised VICCCS criteria have superseded NINDS-AIREN and ADDTC, aligning with DSM-5 major and mild vascular neurocognitive disorder, and STRIVE-2 (2023) standardised the neuroimaging reporting of small-vessel disease (lacunes, white matter hyperintensities, perivascular spaces, microbleeds, cortical superficial siderosis, incidental infarcts). Therapeutically, intensive blood pressure lowering remains the only intervention with randomised evidence for cognitive benefit — SPRINT MIND reduced incident MCI and the combined MCI-plus-dementia outcome, and its extended follow-up supports sustained benefit — reinforced by the Lancet Commission 2024, which added high midlife LDL cholesterol (population attributable fraction 7%) to hypertension, diabetes, smoking, obesity and physical inactivity among the modifiable determinants of vascular brain injury.

Current Practice Update

Area Textbook Current recommendation Exam approach Nomenclature Vascular dementia; NINDS- Vascular cognitive Use VCI as the umbrella term AIREN and ADDTC criteria impairment (VCI); and NINDS-AIREN for the VASCOG/VICCCS criteria operational criteria aligned to DSM-5 Imaging reporting Descriptive leukoencephalopathy STRIVE-2 (2023) standardised Name the six STRIVE features and infarcts small-vessel disease terminology Prevention Vascular risk factor control, no SPRINT MIND — intensive BP Best single trial to quote for VaD randomised cognitive endpoint lowering reduced incident MCI prevention quoted Symptomatic drugs ChEIs not recommended for pure Unchanged State plainly; it is a common VaD; use in mixed dementia marking point Exam One-Liners VCI is the preferred umbrella term; ~5% of those over 65 have VCI; under 74 it may be the commonest cause of cognitive impairment.

Seven subtypes; SIVD (lacunar state and Binswanger’s) is commonest.

CADASIL = NOTCH3 mutation, chromosome 19.

Large vessel → cortical dementia; small vessel → subcortical dementia.

NINDS-AIREN needs dementia + cerebrovascular disease + temporal relationship (within 3 months of stroke, abrupt deterioration, or stepwise course).

White matter lesions must affect >25% of white matter.

Criteria exclude 90% of AD but have only 50–70% sensitivity for VaD.

60% have slow onset, 80% slow progression — stepwise decline is not obligatory.

The gait–incontinence–dementia triad is commoner in small-vessel VaD than in NPH. ChEIs are not recommended in pure VaD; use in mixed dementia; benefit ≈ 2 points on VADAS-Cog. PROSPER and LEADe negative for statins and cognition; SPRINT MIND positive for intensive BP lowering. Levodopa may help apraxic gait in SIVD.

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