Vascular Neurocognitive Disorder (vascular NCD), historically called vascular dementia, is the second most common cause of acquired cognitive impairment in older adults after Alzheimer disease, and the most common cause clinicians can directly modify by treating cerebrovascular risk. DSM-5-TR classifies it under major or mild neurocognitive disorders and requires both objective cognitive decline and evidence that cerebrovascular disease is the dominant contributor, supported by history, examination, or neuroimaging. The clinical phenotype is heterogeneous: a stepwise post-stroke course, a slowly progressive subcortical syndrome from small-vessel disease, or a strategic single-infarct presentation can all qualify. Management has two parallel tracks — aggressive secondary prevention of further vascular injury, and symptomatic care for cognition, mood, and function. The clinical bottom line is that every patient with suspected vascular NCD needs a vascular workup the same day as the cognitive workup, because the windows to prevent the next stroke and the next cognitive step-down are the same window.

Vascular NCD is the second most prevalent neurocognitive disorder after Alzheimer disease in most Western populations, and may equal or exceed it in regions with high stroke burden such as East Asia.^[1-2] Cerebrovascular disease coexists with Alzheimer pathology in a large fraction of cases, making pure vascular dementia less common than mixed disease in autopsy series.^[3]

Prevalence and incidence

• Vascular cognitive impairment of any severity is present in approximately 1-4% of adults over age 65 in pooled estimates, rising sharply with age.^[1]
• Vascular NCD accounts for roughly 15-20% of dementia cases in North America and Europe and up to 30% in East Asia.^[2]
• Incidence approximately doubles every 5.3 years after age 65, paralleling the age curve of stroke.^[1]
• Up to one-third of stroke survivors meet criteria for cognitive impairment within 6 months, and roughly 20% meet criteria for major NCD.^[4]

Demographics and risk factors

• Men have a modestly higher incidence in midlife driven by earlier vascular disease; rates equalize or reverse with age.^[1]
• Black, Hispanic, and South Asian populations carry higher stroke risk and higher vascular NCD risk than white populations in U.S. and U.K. cohorts.^[5]
• Established modifiable risk factors include hypertension, diabetes mellitus, atrial fibrillation, hyperlipidemia, smoking, obesity, physical inactivity, and obstructive sleep apnea.^[6]
• Midlife hypertension is the single strongest modifiable risk factor and predicts late-life cognitive decline independent of clinical stroke.^[6-7]
• Depression, low educational attainment, and social isolation contribute additively to risk across both vascular and Alzheimer pathways.^[7]

Comorbidity

• Post-stroke depression occurs in 30-35% of stroke survivors and worsens cognitive trajectory.^[4,8]
• Anxiety disorders and apathy syndromes are common, particularly with subcortical disease.^[8]
• Coexisting Alzheimer pathology is present in 40-60% of older patients meeting clinical criteria for vascular NCD.^[3]

Vascular NCD is a final common pathway for any cerebrovascular process that disrupts cognitive networks. The dominant mechanisms are large-artery infarction, small-vessel disease, hypoperfusion, and hemorrhage, frequently in combination.^[2,9]

Vascular substrates

• Large-artery atherothromboembolic infarction, often producing cortical syndromes with abrupt onset.^[2]
• Cardioembolic infarction, classically from atrial fibrillation, with a predilection for strategic territories such as the thalamus, angular gyrus, and hippocampus.^[9]
• Small-vessel (lacunar) disease causing subcortical infarcts in basal ganglia, thalamus, internal capsule, and pontine base.^[9-10]
• Diffuse white matter ischemic injury (leukoaraiosis) from chronic arteriolosclerosis, the substrate of Binswanger disease.^[10]
• Cerebral amyloid angiopathy producing lobar microbleeds, superficial siderosis, and cortical microinfarcts, with high overlap with Alzheimer disease.^[10]
• Global hypoperfusion from cardiac arrest or severe hypotension producing watershed injury.^[10]
• Intracerebral hemorrhage, both deep hypertensive and lobar amyloid-related.^[10]

Anatomy and circuits

• Subcortical small-vessel disease preferentially disrupts frontal-subcortical circuits (dorsolateral prefrontal, anterior cingulate, orbitofrontal), producing the classic dysexecutive and apathetic phenotype.^[10,12]
• Strategic single-infarct dementia can follow lesions of the thalamus (especially paramedian), caudate, genu of the internal capsule, angular gyrus, or basal forebrain.^[12]
• Bilateral medial temporal infarcts (posterior cerebral artery territory) produce amnestic syndromes that closely mimic Alzheimer disease.^[12]

Genetics

• Most vascular NCD reflects polygenic vascular risk rather than monogenic disease.^[6]
• CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is caused by NOTCH3 mutations and presents with migraine with aura, recurrent lacunar strokes, mood disturbance, and progressive subcortical dementia, typically in the 4th-6th decades.^[13]
• CARASIL, COL4A1/A2-related disease, and Fabry disease are rarer monogenic causes worth recognizing when family history or atypical age is present.^[13]
• APOE ε4 increases risk for both Alzheimer disease and cerebral amyloid angiopathy, contributing to mixed pathology.^[7]

Integrative model

• Cumulative cerebrovascular injury reduces network reserve.^[2]
• Clinical impairment emerges when injury exceeds the individual's cognitive reserve, which is shaped by education, premorbid IQ, and concurrent neurodegenerative pathology.^[7]
• The two-hit model — vascular plus Alzheimer pathology — explains why vascular risk reduction lowers dementia incidence even in patients whose dominant pathology turns out to be Alzheimer.^[3,7]

DSM-5-TR places vascular NCD on the same continuum as other neurocognitive disorders, with the central question being whether cerebrovascular disease is the dominant driver of impairment.^[1,14] Severity (major vs mild) follows the same threshold rules used for Alzheimer-type and other NCDs.

DSM-5-TR criteria

• Evidence of significant (major NCD) or modest (mild NCD) cognitive decline from a prior level in one or more cognitive domains, established by concern from the patient, an informant, or clinician, and confirmed by standardized testing or quantified clinical assessment.^[1]
• For major NCD, cognitive deficits interfere with independence in everyday activities; for mild NCD, deficits do not interfere with independence but greater effort or compensation is required.^[1]
• Clinical features are consistent with a vascular etiology, suggested by either (a) onset of cognitive deficits temporally related to one or more cerebrovascular events, or (b) evidence of decline prominent in complex attention (including processing speed) and frontal-executive function.^[1]
• Evidence of cerebrovascular disease from history, physical examination, or neuroimaging is judged sufficient to account for the neurocognitive deficits.^[1]
• Symptoms are not better explained by another brain disease or systemic disorder.^[1]

Probable vs possible

• Probable vascular NCD requires neuroimaging evidence of significant parenchymal injury attributed to cerebrovascular disease, a temporal relationship between a cerebrovascular event and the neurocognitive deficits, or both clinical and genetic evidence of cerebrovascular disease (e.g., CADASIL).^[1]
• Possible vascular NCD is diagnosed when clinical criteria are met but neuroimaging is not available, or the temporal relationship cannot be established.^[1]

Specifiers

• Severity for major NCD: mild (instrumental activities affected), moderate (basic activities affected), severe (fully dependent).^[1]
• With or without behavioral disturbance (e.g., psychotic symptoms, mood disturbance, agitation, apathy, other behavioral symptoms).^[1]

ICD-11 differences

• ICD-11 codes vascular dementia under chapter 06 (Mental, behavioural and neurodevelopmental disorders) with a parallel etiologic code from chapter 08 for the underlying cerebrovascular disease.^[16]
• ICD-11 retains broadly compatible diagnostic logic and does not separate major from mild at the coding level but allows specification of severity.^[16]

Vascular NCD does not have one clinical face. The presentation depends on which vessels failed, which territory was injured, and how injury accumulated over time.^[2,12]

Cognitive profile

• Processing speed and executive function are typically affected earliest and most prominently, particularly in subcortical small-vessel disease.^[12]
• Episodic memory may be relatively preserved early, in contrast to amnestic Alzheimer disease; retrieval (cued recall improves performance) is more affected than encoding.^[12]
• Attention, working memory, and set-shifting deficits dominate; Anhedonia, apathy, and psychomotor slowing often accompany cognitive findings.^[12]
• Strategic infarct dementias can present with isolated amnestic, aphasic, or behavioral syndromes that depart from the typical subcortical picture.^[10]

Course patterns

• Stepwise decline temporally linked to discrete strokes, the historical prototype.^[2]
• Slowly progressive subcortical decline from accumulating small-vessel disease, often clinically indistinguishable from neurodegenerative dementia without imaging.^[10]
• Acute-onset post-stroke cognitive impairment with partial recovery over weeks to months, sometimes followed by gradual decline.^[4]

Motor and neurologic signs

• Gait disturbance (frontal/apraxic or small-stepped magnetic gait), early urinary urgency or incontinence, and pseudobulbar affect support subcortical vascular involvement.^[10,12]
• Focal neurologic signs — hemiparesis, hemisensory loss, hemianopia, dysarthria, extensor plantar response — are common and help anchor the vascular diagnosis.^[2]
• Parkinsonism (lower-body predominant, levodopa-poorly-responsive) can emerge from basal ganglia infarcts.^[10]

Neuropsychiatric features

• Depression and apathy are highly prevalent and often persistent; distinguishing them clinically matters because apathy responds poorly to antidepressants.^[4,8]
• Emotional incontinence (pathologic crying or laughing) is more common in vascular than Alzheimer disease.^[8]
• Delusions and visual hallucinations occur but are less prominent than in Lewy body disease.^[8]

The differential pivots on temporal pattern, imaging burden, and the symptom signature. Vascular NCD does not exclude co-pathology; mixed dementia (vascular plus Alzheimer) is the rule rather than the exception in older patients.^[1,9]

Entity-by-entity

• Alzheimer disease: dominant episodic memory deficit, hippocampal atrophy, and amyloid and tau biomarker positivity distinguish it; co-existence with vascular pathology is common in patients over 75.^[7]
• Dementia with Lewy bodies (DLB): fluctuating cognition, recurrent well-formed visual hallucinations, REM sleep behavior disorder, and spontaneous parkinsonism appearing within a year of cognitive decline support DLB over vascular NCD.^[17]
• Behavioral-variant frontotemporal dementia: early personality change, disinhibition, and language deficits in a patient under 65 favor bvFTD; vascular lesions are usually absent or incidental.^[18]
• Normal pressure hydrocephalus: the triad of gait apraxia, urinary incontinence, and cognitive slowing overlaps with subcortical vascular NCD; ventriculomegaly out of proportion to sulcal atrophy and improvement after large-volume lumbar puncture point to NPH.^[1]
• Depression with cognitive impairment: prominent anhedonia, diurnal mood variation, and effort-dependent rather than capacity-limited cognitive testing favor depression; the two often coexist and depression should be treated empirically before declaring irreversible decline.^[1]
• Delirium: acute onset, fluctuating attention, and an identifiable medical precipitant define delirium; in a patient with vascular NCD, a superimposed delirium is common and must be excluded before any new cognitive baseline is accepted.^[1]
• Medical mimics: hypothyroidism, vitamin B12 deficiency, neurosyphilis, HIV-associated neurocognitive disorder, chronic subdural hematoma, and obstructive sleep apnea can all mimic or worsen the picture and are part of the standard workup.^[1,9]
• Substance-induced neurocognitive disorder: chronic heavy alcohol use produces a syndrome with executive and memory deficits, often with cerebellar and frontal atrophy; benzodiazepine, anticholinergic, and opioid burden cause reversible deficits that must be subtracted before diagnosing vascular NCD.^[1]

Assessment proceeds on three parallel tracks: cognition, the vascular substrate, and reversible contributors. The diagnosis is rarely made on a single visit; serial assessment over 3-6 months separates fixed deficits from delirium, depression, and medication effects.^[1,9]

Interview and history

• Obtain a collateral history from a reliable informant; patient self-report underestimates deficits, especially with anosognosia.^[1]
• Map the temporal course explicitly: sudden, stepwise, fluctuating, or insidious onset reframes the differential.^[3-4]
• Document vascular risk factors: hypertension, diabetes, dyslipidemia, atrial fibrillation, smoking, prior stroke or TIA, sleep apnea, and family history of premature stroke.^[10]
• Screen for depression, sleep disorders, falls, and functional decline using a structured ADL and IADL inventory.^[1]
• Review the full medication list, including anticholinergic burden (using a scale such as the Anticholinergic Cognitive Burden scale), benzodiazepines, opioids, and over-the-counter sleep aids.^[30]

Physical and neurologic examination

• Measure blood pressure seated and standing; orthostatic hypotension worsens cerebral hypoperfusion and must be addressed before escalating antihypertensives.^[10]
• Auscultate for carotid bruits and assess cardiac rhythm; a new irregularly irregular rhythm prompts evaluation for atrial fibrillation.^[10]
• Document focal neurologic signs: hemiparesis, visual field defect, dysarthria, pseudobulbar affect, hyperreflexia, and extensor plantar responses suggest cortical or subcortical infarction.^[4]
• Assess gait: a wide-based, short-stepped magnetic gait suggests frontal-subcortical disease and predicts falls.^[4]

Cognitive testing

• Use a validated bedside instrument; the Montreal Cognitive Assessment (MoCA) is more sensitive than the Mini-Mental State Examination (MMSE) for executive dysfunction typical of vascular NCD.^[19,23]
• The MoCA includes trail-making, clock drawing, and verbal fluency tasks that probe the executive-processing-speed signature of small-vessel disease.^[20]
• Refer for formal neuropsychological testing when the clinical picture is ambiguous, when the patient is highly educated and screens normally despite functional decline, or when medicolegal capacity is in question.^[1]
• Reassess at 6 and 12 months; a documented decline of 3 or more points on the MoCA, paired with imaging or functional change, supports progression.^[20]

Laboratory and imaging workup

• Obtain CBC, comprehensive metabolic panel, TSH, vitamin B12, and HbA1c; add HIV and syphilis serology when the history suggests risk.^[1,9]
• Fasting lipid panel and ECG are standard; echocardiogram and ambulatory rhythm monitoring are indicated when cardioembolic source is suspected.^[10]
• Carotid duplex ultrasound or CT/MR angiography evaluates large-vessel stenosis in patients with cortical infarcts or carotid bruits.^[10]
• Structural neuroimaging is required; Magnetic Resonance Imaging (MRI) with FLAIR, T2, T2-star (GRE/SWI), and diffusion sequences outperforms CT for white-matter hyperintensities, lacunes, and microbleeds.^[5,15]
• The Fazekas scale rates white-matter hyperintensity severity; confluent periventricular and deep WMH (Fazekas 2-3) supports a vascular contribution.^[5]
• Reserve amyloid PET, CSF biomarkers, and FDG-PET for cases where Alzheimer or FTD pathology is suspected and would change management.^[5]

Rating scales

• The Hachinski Ischemic Score screens for vascular contribution; a score of 7 or above suggests vascular NCD, 4 or below suggests Alzheimer disease, with the caveat that mixed dementia is common.^[21]
• The Clinical Dementia Rating (CDR) stages severity and is widely used in trials.^[1]
• The Neuropsychiatric Inventory (NPI) quantifies behavioral and psychological symptoms and tracks response to intervention.^[22]

Treatment of vascular NCD runs on two parallel tracks: aggressive secondary prevention of further cerebrovascular injury to slow or prevent the next cognitive step-down, and symptomatic management of cognition, mood, and behavior. No disease-modifying therapy is approved specifically for vascular NCD, and pharmacologic gains on cognition are modest at best.^[25]

Vascular risk reduction

• Antihypertensive therapy targeting systolic blood pressure approximately 130 mmHg or lower reduces incident dementia and slows white-matter hyperintensity progression in older adults at vascular risk.^[26]
• Antiplatelet therapy with aspirin 81 mg PO QD is indicated after non-cardioembolic ischemic stroke or TIA; clopidogrel is an alternative.^[27]
• Anticoagulation is indicated when atrial fibrillation or another cardioembolic source is present, with direct oral anticoagulants preferred over warfarin in most patients.^[27]
• Statin therapy reduces recurrent stroke risk in patients with atherosclerotic disease and is recommended after ischemic stroke regardless of baseline LDL in most guidelines.^[27]
• Glycemic control, smoking cessation, weight management, and treatment of obstructive sleep apnea each contribute to vascular risk reduction, though their isolated effect on cognitive trajectory is less well established.^[3]
• Physical activity (aerobic exercise approximately 150 minutes per week of moderate intensity) is associated with reduced incident cognitive impairment in cohort studies and is broadly recommended in guidelines.^[28]

Pharmacotherapy

• Cholinesterase inhibitors show small, statistically detectable cognitive benefits in vascular NCD trials, most consistently for donepezil 5-10 mg PO QD; effect sizes are smaller than in Alzheimer disease and clinical global benefit is inconsistent.^[25,29]
• galantamine 16-24 mg PO QD has trial-level evidence in mixed Alzheimer-vascular dementia and is a reasonable option when a mixed pathology is suspected.^[29]
• memantine 10 mg PO BID has limited evidence in pure vascular NCD; some guidelines suggest a trial in moderate-to-severe disease, particularly mixed presentations.^[25]
• No agent has been shown to halt or reverse the underlying vascular pathology; framing pharmacologic gains as modest and symptomatic avoids overclaim and helps families calibrate expectations.^[25]

Psychotherapy

• Cognitive rehabilitation and structured cognitive stimulation programs show low-to-moderate evidence for short-term cognitive and functional benefit in mild-to-moderate dementia of mixed etiology.^[30]
• Behavioral interventions for depression and apathy, including behavioral activation and problem-solving therapy, are evidence-supported in older adults with cognitive impairment and avoid the anticholinergic burden of pharmacotherapy.^[31]
• Caregiver psychoeducation and skills training reduce caregiver burden and delay nursing-home placement in dementia of various etiologies.^[30]

Neuromodulation

• Repetitive transcranial magnetic stimulation has emerging but low-certainty evidence for cognitive symptoms and post-stroke depression; it is not standard care.^[32]
• Electroconvulsive therapy remains an option for severe, treatment-resistant depression complicating vascular NCD, with appropriate monitoring for post-ictal confusion and cardiovascular tolerance.^[33]

Adjunctive

• Treat depression with SSRIs as first-line; sertraline 25-100 mg PO QD and citalopram 10-20 mg PO QD are commonly used, with attention to QT prolongation at higher citalopram doses in older adults.^[31]
• Treat clinically significant apathy with structured behavioral activation; pharmacologic options (methylphenidate, dopaminergic agents) have limited and inconsistent evidence and should be reserved for refractory cases.^[31]
• For agitation and psychosis, prioritize non-pharmacologic strategies first; reserve antipsychotics for severe symptoms with risk of harm, use the lowest effective dose, and document the increased mortality and stroke risk in dementia.^[34]
• Avoid benzodiazepines, anticholinergic agents, and zolpidem-class hypnotics where possible; they worsen cognition and increase fall risk.^[34]

The table summarizes the central interventions in vascular NCD, drawn from cardiovascular secondary-prevention trials, pragmatic trials of intensive blood-pressure control, and meta-analyses of cholinesterase inhibitors and memantine in vascular and mixed cohorts.

Harms in vascular NCD cluster in two places: the cardiovascular treatments used to slow decline, and the symptomatic agents used to manage cognition and behavior. The evidence base is also narrower than the Alzheimer literature, and most trials enrolled mixed populations rather than pure vascular NCD.

Pharmacologic harms

• Antihypertensive intensification in frail older adults increases falls, orthostatic hypotension, syncope, and acute kidney injury, particularly in patients above 75 years or with diabetes ^[26].
• Antiplatelet and anticoagulant therapy increases major bleeding, including intracerebral hemorrhage, with risk rising sharply when both are combined or when cerebral microbleeds are present on MRI ^[27].
• Cholinesterase inhibitors cause cholinergic adverse effects (nausea, diarrhea, anorexia, bradycardia, syncope) and have precipitated syncope-related falls and hip fractures in older cohorts ^[25].
• Citalopram at doses above 20 mg in patients over 60 prolongs the QTc and increases torsades risk; escitalopram has a similar but lower-magnitude signal ^[31].
• Antipsychotic use in older adults with dementia carries an FDA boxed warning for increased all-cause mortality and a roughly two- to three-fold increase in cerebrovascular events ^[34].
• Benzodiazepines and Z-drugs in vascular NCD worsen cognition, raise fall and fracture risk, and should not be standing medications for sleep or agitation ^[30].

Monitoring and discontinuation considerations

• Cognitive trajectory should be reassessed at six to twelve month intervals to support meaningful conversations about goals of care, driving, and capacity ^[30].
• Deprescribing high-risk agents (anticholinergics, benzodiazepines, sedating antihistamines, long-acting sulfonylureas) is itself a cognitive intervention and is often higher-yield than adding a new drug ^[30].
• Antipsychotics started for an acute behavioral crisis should have a defined stop or taper date; long-term continuation drifts into the boxed-warning risk window ^[34].

Limitations of the evidence base

• Most modern trials enrolled mixed Alzheimer-vascular populations because pure vascular NCD is hard to ascertain antemortem, which dilutes intervention effect estimates ^[25,29].
• Trials of vascular risk-factor modification typically use composite cardiovascular endpoints, with cognitive outcomes as secondary or post-hoc analyses ^[26-27].
• Follow-up is usually less than three years, which is short relative to the natural history of vascular cognitive impairment ^[25].
• Older trials predate modern MRI subtyping (e.g. small vessel disease vs large artery), so the effect of an intervention in a specific vascular subtype is often unknown ^[10].

Vascular NCD intersects with several populations whose vascular biology, comorbidity burden, or social context changes management priorities.^[1]

Geriatric patients

• Frailty modifies the risk-benefit of intensive blood pressure lowering; orthostatic hypotension and falls can offset cognitive gains.^[26]
• Polypharmacy is the rule, not the exception; deprescribe anticholinergics, sedatives, and chronic benzodiazepines.^[30]
• Sensory impairment (hearing, vision) inflates cognitive test impairment and should be corrected before assigning a diagnosis.^[30]

Patients with diabetes and metabolic syndrome

• Diabetes accelerates small-vessel disease and approximately doubles dementia risk; tight but not aggressive glycemic control is appropriate in older adults.^[8]
• Severe hypoglycemia is an independent risk factor for dementia and worsens cognition acutely.^[8]

Atrial fibrillation and embolic disease

• Anticoagulation reduces stroke and likely slows cognitive decline in atrial fibrillation; balance against fall risk and bleeding.^[27]
• Cerebral amyloid angiopathy increases intracerebral hemorrhage risk on anticoagulation and is more common in mixed pathology.^[6]

Post-stroke patients

• Cognitive screening at three months post-stroke captures patients who fail to recover and identifies new vascular NCD diagnoses.^[2]
• Post-stroke depression and apathy overlap with cognitive symptoms and respond to SSRI treatment plus stroke rehabilitation.^[31]

Cultural and educational considerations

• Low education and limited literacy reduce performance on most cognitive instruments; use locally validated, education-adjusted norms.^[20]
• Premorbid Arabic-language and other non-English MoCA versions exist and should be used when appropriate to avoid misdiagnosis.^[20]

Vascular NCD has a more variable course than Alzheimer disease, ranging from stable plateaus between strokes to rapid decline after a single strategic infarct.^[3]

Natural history

• Median survival from diagnosis of major vascular NCD is approximately 3-5 years, shorter than Alzheimer disease in most cohorts, driven by cardiovascular and cerebrovascular mortality.^[3]
• A stepwise course is classic but not universal; subcortical small-vessel disease often progresses gradually and is clinically indistinguishable in trajectory from neurodegenerative dementias.^[6]

Response to treatment

• Aggressive vascular risk factor control can stabilize cognition for months to years in selected patients, particularly when initiated at the mild NCD stage.^[26]
• Cholinesterase inhibitors produce small cognitive improvements that are statistically significant but of uncertain clinical relevance.^[25]

Prognostic markers

• Higher white matter hyperintensity burden (Fazekas 3), lacune count, and microbleed burden predict faster decline.^[15]
• Recurrent stroke, uncontrolled hypertension, and atrial fibrillation predict step-wise deterioration.^[10]
• Coexisting Alzheimer pathology (mixed dementia) predicts faster progression than pure vascular disease.^[7]

Mortality

• Cardiovascular events and recurrent stroke are the leading causes of death, not the dementia itself.^[3]
• Pneumonia and complications of immobility dominate late-stage mortality, mirroring other dementias.^[3]

Acute changes in a patient with known or suspected vascular NCD require a stroke workup, not a behavioral one, until proven otherwise.^[27]

Acute neurologic change

• Any abrupt cognitive worsening, new focal deficit, or sudden behavioral change warrants urgent imaging to evaluate for new stroke or hemorrhage.^[27]
• Delirium superimposed on dementia is common and requires evaluation for infection, metabolic derangement, medication effect, and acute stroke.^[1]

Suicide risk

• Suicide risk is elevated in the first year after stroke, particularly with post-stroke depression and significant functional loss.^[31]
• Assess access to means, prior attempts, and current depressive symptoms at every visit during the first post-stroke year.^[31]

Agitation and behavioral emergencies

• First-line management of acute agitation is environmental and behavioral; identify and treat triggers (pain, constipation, urinary retention, delirium).^[30]
• Reserve pharmacologic restraint for imminent harm; antipsychotics carry stroke and mortality risk in this population.^[34]
• Avoid benzodiazepines except for specific indications (alcohol or benzodiazepine withdrawal); they worsen confusion and falls.^[30]

Driving and capacity

• Driving safety should be formally assessed in any patient with major NCD, and many with mild NCD; on-road testing is the gold standard.^[1]
• Decision-making capacity is task-specific; a patient may retain capacity for some decisions and lack it for others.^[1]

Several questions in vascular NCD remain unsettled and shape day-to-day decisions.^[7]

Diagnostic boundaries

• Pure vascular dementia is uncommon at autopsy; most older patients show mixed Alzheimer and vascular pathology, blurring categorical diagnosis.^[7]
• Competing diagnostic criteria (DSM-5-TR, NINDS-AIREN, VASCOG, AHA/ASA) yield meaningfully different prevalence estimates in the same population.^[2,5]

Treatment of cognitive symptoms

• Cholinesterase inhibitors and memantine produce modest benefits in vascular NCD but are not approved by the FDA for this indication, and effect sizes are smaller than in Alzheimer disease.^[25,29]
• Whether to offer a trial reflects clinician judgment about likely mixed pathology and patient preference rather than a clear evidence-based mandate.^[29]

Blood pressure targets

• SPRINT-MIND showed reduced incidence of mild cognitive impairment with intensive systolic blood pressure control (<120 mmHg) in non-frail older adults, but trials in established dementia are lacking.^[26]
• Optimal targets in frail patients, those with orthostatic hypotension, and those over 80 are debated; most guidelines accept systolic 130-140 mmHg in this group.^[26-27]

Multidomain prevention

• The FINGER trial supported a multidomain lifestyle intervention for cognitive maintenance in at-risk older adults, but replication trials (MAPT, preDIVA) had mixed results.^[24]
• The size and durability of benefit, and which patients gain the most, remain active research questions.^[24]

Emerging therapies

• Trials of cerebrolysin, nimodipine, and citicoline have shown inconsistent signals; none has guideline-level recommendation in major Western guidelines.^[30]
• Anti-amyloid monoclonal antibodies are not indicated for vascular NCD and increase amyloid-related imaging abnormality risk in patients with significant vascular pathology.^[7]

• Vascular NCD is the second most common cause of dementia in older adults after Alzheimer disease, and mixed pathology is the rule rather than the exception at autopsy.^[7]
• DSM-5-TR requires both cognitive decline and clinical or imaging evidence that cerebrovascular disease is sufficient to account for the deficits.^[1]
• The classic course is stepwise, but subcortical small-vessel disease typically produces a gradual, slowly progressive picture clinically indistinguishable from neurodegenerative dementia.^[6]
• Executive dysfunction and processing-speed slowing typically dominate the cognitive profile, with relative early sparing of episodic memory compared to Alzheimer disease.^[11]
• Binswanger disease is a small-vessel subcortical vascular NCD with extensive periventricular white matter hyperintensities and prominent gait apraxia and urinary urgency.^[6]
• CADASIL is an autosomal-dominant NOTCH3 mutation causing migraine with aura, recurrent subcortical strokes, mood disturbance, and early subcortical dementia.^[9]
• The Hachinski Ischemic Score above 7 favors vascular over Alzheimer etiology; a score below 4 favors Alzheimer disease.^[21]
• MoCA outperforms MMSE for detecting the executive and attentional deficits typical of vascular cognitive impairment.^[19]
• A strategic infarct in the thalamus, caudate, or angular gyrus can cause acute major NCD from a single small lesion.^[12]
• The SPRINT-MIND trial showed that intensive systolic blood pressure control to under 120 mmHg reduced the incidence of mild cognitive impairment in non-frail older adults.^[26]
• Cholinesterase inhibitors and memantine are not FDA-approved for vascular NCD; modest cognitive benefits are offset by gastrointestinal and cardiac adverse effects.^[25]
• Antipsychotics carry a boxed warning for increased mortality and stroke in older patients with dementia and should be a last resort for agitation.^[34]
• Post-stroke depression is common and treatable; sertraline and citalopram are reasonable first-line agents.^[31]
• Any acute cognitive worsening in a patient with vascular NCD warrants urgent imaging to evaluate for new stroke or hemorrhage before attributing it to behavioral causes.^[27]
• The leading causes of death in vascular NCD are recurrent stroke and cardiovascular events, not the dementia itself.^[3]

No external funding. No conflicts of interest declared. Peer-review status: pending.