Nervous System & Special Senses

Vascular dementia: workup and management

Clinical Overview and When to Suspect Vascular Dementia

— 2nd most common dementia after Alzheimer disease (AD); accounts for ~15–20% of dementias in North America, higher in Asia.

— Frequently coexists with AD pathology ("mixed dementia") in >40% of autopsy-confirmed cases over age 80.

— Cognitive decline in a patient with vascular risk burden: HTN, DM, AF, prior stroke/TIA, hyperlipidemia, smoking, CKD, OSA, PAD.

— Stepwise deterioration rather than insidious decline, or abrupt cognitive change temporally linked to a stroke.

— Early executive dysfunction and psychomotor slowing with relatively preserved episodic memory (contrast with AD).

— Gait disturbance (small-stepped, magnetic, or apraxic), urinary urgency, pseudobulbar affect, or focal neurologic signs.

— Multi-infarct dementia — cortical strokes, stepwise course.

— Subcortical ischemic VaD (Binswanger) — small vessel disease, executive/gait predominant.

— Strategic infarct dementia — thalamus, caudate, angular gyrus, hippocampus.

— Post-stroke dementia — within 3–6 months of an index stroke.

— CADASIL — autosomal dominant, NOTCH3, migraine with aura, early strokes, mood symptoms.

Board pearl: A patient with poorly controlled HTN, gait apraxia, urinary urgency, and executive dysfunction with subcortical white matter changes on MRI represents Binswanger-type subcortical VaD — anchor the differential here rather than AD or NPH. Step 3 favors recognizing the vascular risk profile + executive-predominant cognitive pattern as the trigger to pursue MRI brain and aggressive vascular risk factor optimization rather than starting a cholinesterase inhibitor as first move.

Definition: Vascular cognitive impairment (VCI) spans mild cognitive impairment to vascular dementia (VaD), caused by cerebrovascular disease producing ischemic, hemorrhagic, or hypoperfusive brain injury sufficient to impair ≥1 cognitive domain with functional decline.

Epidemiology:

When to suspect (Step 3 outpatient clues):

Subtypes to recognize:

Presentation Patterns and Key History

— Executive dysfunction (planning, set-shifting, multitasking) and slowed processing speed dominate early.

— Memory deficits are typically retrieval-based (improve with cueing), unlike AD storage failure.

— Language: reduced verbal fluency more than naming deficits.

— Apathy, depression, and emotional lability common; psychosis less common than in DLB.

— Stepwise decline with plateaus, or acute drop post-stroke that partially recovers then plateaus.

— Gradual subcortical decline can mimic AD; do not exclude VaD based on smooth trajectory alone.

— Prior TIA/stroke, AF, MI, CABG/PCI, carotid disease, PAD, CKD.

— Vascular risk factors: BP control history, A1c trends, LDL, tobacco pack-years, alcohol, sleep apnea symptoms (STOP-BANG).

— Medication review: anticholinergics, benzodiazepines, opioids, sedating antihistamines, antipsychotics — all can worsen cognition and falls.

— Functional status: IADLs (finances, medications, driving) before ADLs decline.

— Mood screen (PHQ-9) — depression is both a mimic and a comorbidity.

— Sleep: OSA worsens both vascular risk and cognition.

— Family history: early stroke, migraine with aura, dementia <60 → consider CADASIL.

— Rapid decline over weeks (consider CJD, autoimmune encephalitis, NPH, paraneoplastic).

— New focal deficits, seizures, headache → image urgently.

Step 3 management: At the initial visit, order MoCA (more sensitive than MMSE for executive/vascular dysfunction), PHQ-9, B12, TSH, CMP, CBC, and MRI brain. Schedule a dedicated caregiver-inclusive follow-up within 4 weeks to review results, discuss diagnosis, address driving safety, and initiate advance care planning before capacity declines further.

Cognitive phenotype:

Temporal course clues:

Targeted history to elicit:

Caregiver collateral: Essential — patients underreport. Ask about getting lost driving, missed bills, near-miss MVCs, leaving stove on, wandering.

Red flags requiring urgent workup:

Physical Exam Findings (and Hemodynamic Assessment)

— Office BP with proper technique, plus home BP monitoring — overtreatment causing orthostasis worsens hypoperfusion and cognition in elderly VaD.

— Orthostatic vitals (supine, 1 and 3 min standing) — falls risk; consider deprescribing antihypertensives if symptomatic.

— Irregularly irregular pulse → screen for AF with ECG (and consider extended monitoring).

— Carotid auscultation for bruits (low sensitivity but free).

— ABI if PAD suspected — strong marker of systemic atherosclerosis.

— Focal signs (hemiparesis, hyperreflexia, Babinski, hemianopia) support prior strokes.

— Pseudobulbar palsy: brisk jaw jerk, dysarthria, emotional incontinence — bilateral corticobulbar tract disease.

— Gait: small-stepped "marche à petits pas," magnetic gait (overlap with NPH), or apraxic gait; assess Timed Up and Go (>12 sec = fall risk).

— Frontal release signs (grasp, palmomental, snout) — nonspecific but support subcortical/frontal pathology.

— Cranial nerves: pseudobulbar features, conjugate gaze abnormalities from prior strokes.

— MoCA preferred — captures executive (trails B, clock draw, verbal fluency).

— Clock-drawing test alone is a fast bedside screen for executive dysfunction.

— MMSE under-detects subcortical VaD because it weights memory and orientation.

— Funduscopy: hypertensive/diabetic retinopathy correlates with cerebral small vessel disease.

— Cardiac: murmurs, S3, JVD (CHF worsens cerebral perfusion).

— Skin/peripheral pulses, signs of prior MI scars.

Key distinction: AD patients typically have a normal neurologic exam aside from cognition; the presence of focal deficits, pseudobulbar signs, gait abnormality, or frontal release signs should shift you toward VaD or mixed dementia. Documenting these objective findings also strengthens the diagnostic case when ordering MRI and justifies vascular-targeted secondary prevention rather than dementia-only management.

Vital signs and hemodynamics:

Neurologic exam:

Cognitive bedside testing:

General exam:

Diagnostic Workup — Initial Labs and Imaging

— TSH, vitamin B12 — required minimum workup.

— CBC, CMP (Na, Ca, glucose, BUN/Cr, LFTs).

— HbA1c, fasting lipid panel — both diagnostic and risk-stratification.

— Consider RPR/HIV if risk factors or atypical features.

— Folate, homocysteine — selective; homocysteine is a vascular risk marker.

— UA if delirium suspected; urine drug screen if indicated.

— Findings supporting VaD:

— Multiple cortical/subcortical infarcts.

— Confluent periventricular and deep white matter hyperintensities (Fazekas 2–3) on FLAIR.

— Lacunes in basal ganglia, thalamus, pons.

— Cerebral microbleeds on SWI/GRE — lobar suggests CAA, deep suggests hypertensive arteriopathy.

— Strategic infarcts (thalamus, caudate, angular gyrus, hippocampus).

— Cortical superficial siderosis → CAA.

— CT acceptable if MRI contraindicated (pacemaker, claustrophobia) but less sensitive for small vessel disease.

Board pearl: Lobar microbleeds + superficial siderosis in an elderly normotensive patient = cerebral amyloid angiopathy (CAA) — a vascular dementia mimic where anticoagulation and antiplatelet therapy raise hemorrhage risk substantially. Recognize this pattern before reflexively starting aspirin or apixaban for "stroke prevention" — Step 3 will test the risk–benefit reversal that CAA imposes on standard vascular secondary prevention.

Reversible-cause labs (per AAN guideline for all new dementia):

ECG: Screen for AF, prior MI, LVH (hypertensive end-organ damage). If sinus but AF suspected → ambulatory monitoring (Holter, 14–30 day patch, or implantable loop in cryptogenic stroke).

Neuroimaging — MRI brain without contrast is preferred:

Carotid imaging: Duplex ultrasound if anterior circulation symptoms or bruit; CTA/MRA for confirmation before intervention.

Echocardiogram: Indicated when cardioembolic source suspected (prior stroke, AF, suspicious murmur).

Diagnostic Workup — Advanced or Confirmatory Studies

— Cognitive decline in ≥1 domain with functional impairment.

— Clinical features consistent with vascular etiology: onset temporally related to cerebrovascular event, OR predominant decline in processing speed/executive function.

— Evidence of cerebrovascular disease on imaging sufficient to account for deficits.

— Deficits not better explained by another disease.

— Indicated when diagnosis unclear, for baseline before therapy, or for capacity/disability determinations.

— Pattern: dysexecutive, slowed processing, preserved recognition memory.

— FDG-PET: AD shows temporoparietal hypometabolism; VaD shows patchy multifocal defects matching infarcts.

— Amyloid PET / CSF Aβ42, p-tau, t-tau: Use when AD vs VaD vs mixed is therapeutically relevant (e.g., considering anti-amyloid therapy or cholinesterase inhibitor trial).

— MRA/CTA: Intracranial stenosis, vasculitis pattern.

— Vessel wall MRI: Suspected CNS vasculitis.

— NOTCH3 for CADASIL: <60 yo, migraine with aura, recurrent subcortical strokes, anterior temporal pole and external capsule white matter lesions, positive family history.

— HTRA1 (CARASIL), COL4A1/A2 if phenotype fits.

— ESR/CRP, ANA, ANCA, complement, lupus anticoagulant, antiphospholipid antibodies.

— Lipoprotein(a), homocysteine.

— TEE with bubble study (PFO, endocarditis, aortic atheroma).

— LP if vasculitis or autoimmune encephalitis suspected.

Step 3 management: Reserve CSF AD biomarkers or amyloid PET for cases where distinguishing pure VaD from mixed/AD changes management — for example, deciding whether to add donepezil or pursue anti-amyloid monoclonal eligibility. Routine VaD diagnosis does not require CSF or PET; MRI plus clinical criteria suffice.

Diagnostic criteria (VASCOG/DSM-5 vascular NCD):

Neuropsychological testing:

Advanced imaging when atypical:

When to consider genetic testing:

Workup for younger or atypical patients (<65, rapid course, vasculopathy):

Risk Stratification and First-Line Management Logic

— BP: <130/80 mmHg for most adults with cerebrovascular disease; individualize in frail elderly to avoid orthostasis (target SBP 130–140 if recurrent falls). SPRINT-MIND signal: intensive BP control reduced MCI incidence.

— LDL-C: High-intensity statin if prior ischemic stroke/TIA of atherosclerotic origin; goal LDL <70 mg/dL (SPARCL, recent guidelines).

— A1c: <7% generally; relax to <8% in advanced dementia/frail elderly to avoid hypoglycemia.

— Antiplatelet: Aspirin 81 mg or clopidogrel for non-cardioembolic ischemic stroke/TIA. DAPT only short-term (21–90 days) after minor stroke/high-risk TIA.

— Anticoagulation: DOAC preferred over warfarin for AF (CHA₂DS₂-VASc ≥2 in men, ≥3 in women) — weigh against fall risk and CAA microbleed burden.

— Smoking cessation, moderate alcohol, Mediterranean/DASH diet, ≥150 min/week aerobic activity.

— Structured aerobic exercise has the strongest evidence for cognitive benefit in VaD/MCI.

— Cognitive training, social engagement, hearing/vision correction.

— OSA treatment with CPAP.

— Depression treatment (SSRI preferred; avoid TCAs/paroxetine — anticholinergic).

CCS pearl: On a CCS-style case, after confirming VaD diagnosis, advance the clock to schedule: BP/lipid/A1c recheck at 4–6 weeks, MoCA at 6–12 months, medication reconciliation each visit, and caregiver support referral — these longitudinal orders score points.

Core management principle: There is no FDA-approved disease-modifying drug for VaD. The cornerstone is aggressive vascular risk factor control to slow progression and prevent further infarcts.

Targets (per AHA/ACC, ADA, ACC/AHA lipid, AAN secondary stroke prevention):

Non-pharmacologic cognitive/functional interventions:

Comprehensive geriatric assessment: Falls, polypharmacy (STOPP/START, Beers), nutrition, continence, caregiver burden.

Pharmacotherapy — First-Line Drug Regimen

— Antihypertensives: ACEi/ARB + thiazide or CCB preferred in stroke survivors (PROGRESS trial: perindopril/indapamide reduced recurrent stroke and dementia). Avoid centrally acting agents (clonidine, methyldopa) — sedation and cognitive worsening.

— Statin: Atorvastatin 40–80 mg or rosuvastatin 20–40 mg for atherosclerotic stroke/TIA. Add ezetimibe, then PCSK9 inhibitor if LDL not at goal.

— Antiplatelet: Aspirin 81 mg/day OR clopidogrel 75 mg/day. Do not combine chronically — increases bleeding without dementia benefit.

— DOACs for AF: Apixaban often preferred in elderly/CKD; dabigatran avoided in significant renal impairment and reduced in age >75.

— Diabetes: Metformin first-line; GLP-1 agonists and SGLT2 inhibitors add cardiovascular/stroke benefit (consider semaglutide, empagliflozin).

— Cholinesterase inhibitors (donepezil, galantamine, rivastigmine): Small cognitive benefits in VaD, particularly in mixed dementia. Reasonable trial when cholinergic deficit suspected or mixed AD/VaD likely. Monitor for bradycardia, syncope, GI upset, weight loss.

— Memantine: Modest benefit in moderate-severe disease; better tolerated.

— Discontinue if no functional benefit after 6–12 months or if adverse effects.

— Depression: SSRI (sertraline, escitalopram) first-line; avoid paroxetine (anticholinergic).

— Agitation: Non-pharm first. If needed, avoid antipsychotics when possible — black box warning: increased mortality and stroke in dementia. If unavoidable, lowest dose, shortest duration, document risk discussion.

— Avoid benzodiazepines, anticholinergics, Z-drugs.

Board pearl: Step 3 frequently tests deprescribing: an elderly VaD patient on diphenhydramine for sleep, oxybutynin for urge incontinence, and alprazolam for anxiety has an anticholinergic burden that worsens cognition and falls — switch oxybutynin to mirabegron, taper benzodiazepine, replace diphenhydramine with sleep hygiene/melatonin.

Vascular risk factor pharmacotherapy:

Cognitive symptom pharmacotherapy (off-label, modest benefit):

Neuropsychiatric symptoms:

Procedures and Advanced Interventions

— Symptomatic carotid stenosis 70–99% (ipsilateral TIA/stroke in last 6 months): CEA within 2 weeks of event reduces recurrent stroke (NASCET).

— Symptomatic 50–69%: CEA benefit modest; favor in men, older patients, hemispheric (not retinal) symptoms.

— Asymptomatic ≥70%: Carefully selected patients with life expectancy >5 years; benefit smaller in era of optimal medical therapy.

— Carotid artery stenting (CAS): Alternative if surgically high-risk anatomy or comorbidity; higher periprocedural stroke risk in elderly (>70).

— Consider in nonvalvular AF with absolute contraindication to long-term anticoagulation (e.g., recurrent GI bleed, severe CAA with prior ICH).

— In cryptogenic embolic stroke, age <60, with high-risk PFO features (large shunt, atrial septal aneurysm).

— IV thrombolysis (alteplase/tenecteplase) within 4.5 h; mechanical thrombectomy up to 24 h in select LVO with favorable imaging — preventing the next stroke prevents the next cognitive drop.

— Routine intracranial stenting for asymptomatic stenosis (SAMMPRIS — medical therapy superior).

— Anticoagulation for non-cardioembolic stroke (no benefit over antiplatelet, more bleeding).

— Vitamin E, ginkgo biloba, hormone replacement, NSAIDs — no cognitive benefit, potential harm.

Step 3 management: For a patient with symptomatic 80% left ICA stenosis presenting with TIA and new MoCA decline, arrange CEA within 14 days while simultaneously starting high-intensity statin, aspirin, and BP optimization. Delaying revascularization past 2 weeks substantially reduces the absolute risk reduction.

Carotid revascularization:

Atrial appendage occlusion (Watchman):

Patent foramen ovale (PFO) closure:

Acute stroke interventions (relevance to VaD progression):

Pacemaker/AF ablation: When AF burden contributes to recurrent embolism or hemodynamic compromise.

OSA — CPAP: Procedural-adjacent; titration study and adherence support.

Interventions NOT recommended:

Special Populations — Elderly and Renal/Hepatic Impairment

— Individualize BP targets: SBP 130–150 may be safer than <130 if orthostatic, falls, or syncope. STRICT BP control increases falls and AKI.

— Statin deprescribing: Reasonable in advanced dementia, limited life expectancy <1 year, or when goals shift to comfort.

— Anticoagulation in AF: Balance HAS-BLED vs CHA₂DS₂-VASc. Falls alone are NOT a contraindication — a patient must fall ~295 times/year for fall-related ICH risk to outweigh AF stroke prevention benefit. Consider apixaban 2.5 mg BID if ≥2 of: age ≥80, weight ≤60 kg, Cr ≥1.5.

— Avoid Beers list drugs: First-gen antihistamines, TCAs, benzodiazepines, long-acting sulfonylureas, muscle relaxants, antipsychotics for behavior.

— Metformin: Avoid if eGFR <30; reduce dose if 30–45.

— DOACs: Apixaban dose-adjust per criteria above; avoid dabigatran if CrCl <30; rivaroxaban 15 mg if CrCl 15–50.

— Statins: Atorvastatin and fluvastatin don't require renal adjustment; rosuvastatin reduce if eGFR <30.

— Contrast considerations: Weigh CTA contrast risk in CKD; MRA without gadolinium often suffices; gadolinium contraindicated if eGFR <30 (NSF).

— Cholinesterase inhibitors generally safe but rivastigmine is largely renally cleared metabolite — caution.

— Statins: avoid in active liver disease; mild elevations not contraindication.

— Apixaban contraindicated in Child-Pugh C; caution in B.

— Donepezil hepatically metabolized — caution.

Key distinction: A fall is not a reason to withhold anticoagulation; active major bleeding, severe thrombocytopenia, or extensive CAA microbleed burden is. Document the shared decision-making and reassess at each visit — this is a common Step 3 trap rewarding continuation of apixaban in an 85-year-old with AF and prior fall.

Frail elderly (>80, multiple comorbidities, limited life expectancy):

Renal impairment:

Hepatic impairment:

Special Populations — Younger Patients and Genetic Syndromes

— NOTCH3 mutation, chromosome 19.

— Presents 30s–50s with migraine with aura (often first symptom), recurrent subcortical strokes, mood disorders, progressive subcortical dementia.

— MRI: white matter hyperintensities in anterior temporal poles and external capsule are signature.

— Diagnosis: NOTCH3 gene testing; skin biopsy showing granular osmiophilic material (GOM) on EM if equivocal.

— Management: vascular risk factor control, avoid thrombolytics if possible (hemorrhage risk debated), antiplatelet for stroke prevention; anticoagulation generally avoided unless strong indication. Genetic counseling for first-degree relatives.

— Dutch-type (APP mutation): early-onset lobar ICH.

— Sporadic: elderly, lobar microbleeds, transient focal neurologic episodes ("amyloid spells") often mistaken for TIA — do not give antithrombotics empirically.

— Avoid statins, ACEi/ARBs, warfarin (1st trimester teratogen).

— Labetalol, nifedipine for BP; LMWH for anticoagulation; aspirin 81 mg generally safe.

Board pearl: A 40-year-old with migraine with aura, two lacunar strokes, family history of early stroke and dementia, and anterior temporal pole white matter lesions → order NOTCH3 genetic testing for CADASIL and refer for genetic counseling rather than working up traditional vascular risk factors alone.

CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy):

CARASIL: Autosomal recessive HTRA1 — alopecia, lumbago, early strokes/dementia.

CAA (sporadic and hereditary):

Sickle cell disease: Silent infarcts and overt strokes in children/young adults → transcranial Doppler screening, chronic transfusion or hydroxyurea.

Antiphospholipid syndrome: Recurrent strokes in young adults; long-term warfarin (INR 2–3) preferred over DOACs.

Pregnancy considerations (rare in VaD itself but relevant in young vasculopathies):

Pediatric vascular cognitive impairment: Post-stroke (often from moyamoya, sickle cell, cardiac disease) — neurorehab, schooling accommodations (IEP/504), neuropsychology.

Complications and Adverse Outcomes

— Each new infarct can drop cognition irreversibly. Aggressive secondary prevention is the highest-yield intervention.

— Gait disturbance, orthostasis from antihypertensives, polypharmacy, and impaired judgment combine.

— Hip fracture carries 20–30% 1-year mortality in elderly with dementia.

— Annual falls assessment, vitamin D supplementation, PT referral, home safety evaluation, removal of throw rugs, grab bars.

— Pseudobulbar dysfunction → silent aspiration. Speech-language pathology evaluation; bedside swallow exam.

— PEG tubes do NOT reduce aspiration risk or improve survival in advanced dementia — avoid; emphasize careful hand feeding and comfort.

— Depression (40%), apathy, anxiety, emotional incontinence (pseudobulbar affect — consider dextromethorphan-quinidine if disabling).

— Agitation, sundowning, psychosis — non-pharmacologic first.

— Urge incontinence common; avoid anticholinergics (worsen cognition). Use mirabegron, scheduled toileting, treat UTIs promptly.

— Depression, financial strain, social isolation. Screen with Zarit Burden Interview; refer to Alzheimer's Association (also serves VaD families), adult day programs, respite care.

— Bleeding on antithrombotics (especially with falls, CAA).

— Hypoglycemia from over-aggressive diabetes treatment.

— Orthostatic syncope from BP regimen.

— Cognitive impairment increases MVC risk. Refer for on-road driving evaluation when MoCA <22, getting lost, or family concern.

— Median survival 3–5 years from diagnosis; lower than AD due to vascular comorbidity.

Step 3 management: In an advanced VaD patient with recurrent aspiration pneumonia, do not order PEG placement — instead, initiate palliative care consultation, careful hand feeding, oral care, and family meeting to align goals; this is consistently the correct Step 3 answer.

Recurrent stroke and stepwise decline:

Falls and fractures:

Aspiration pneumonia and dysphagia:

Neuropsychiatric:

Incontinence:

Caregiver burden:

Medication-related:

Driving safety:

Mortality:

When to Escalate Care — Consults and Inpatient Triage

— Acute focal neurologic deficit → stroke alert, NIH stroke scale, CT/CTA, thrombolytic and thrombectomy candidacy. Time is brain.

— Sudden severe headache, vomiting → r/o ICH (especially CAA patients).

— New seizure → admit, EEG, MRI, address etiology.

— Rapid cognitive decline over days–weeks → admit for workup (autoimmune encephalitis, CJD, NPH, malignancy, metabolic, infection).

— Acute delirium superimposed on dementia → inpatient workup for UTI, pneumonia, electrolytes, medications, MI.

— Neurology: Diagnostic uncertainty, atypical features, age <65, recurrent strokes despite optimal medical therapy, suspected CADASIL or vasculitis, seizures.

— Vascular surgery: Symptomatic carotid stenosis ≥50% or asymptomatic ≥70% with reasonable life expectancy.

— Cardiology / electrophysiology: AF management, cryptogenic stroke (extended monitoring, possible PFO closure), Watchman candidacy.

— Geriatrics: Complex polypharmacy, falls, frailty, advance care planning.

— Psychiatry: Severe depression, refractory agitation, psychosis, safety concerns.

— Neuropsychology: Diagnostic clarification, capacity, baseline before treatment.

— Palliative care: Advanced disease, recurrent hospitalizations, caregiver distress, goals-of-care recalibration.

— PT/OT/SLP: Falls, ADL decline, dysphagia.

— Unable to ambulate, dress, bathe independently; incontinent; speech limited to ≤6 intelligible words; plus a qualifying comorbid event (aspiration pneumonia, pyelonephritis, sepsis, pressure ulcer stage 3–4, recurrent fever, weight loss >10% over 6 months).

CCS pearl: When the CCS clock shows acute focal weakness in a known VaD patient, immediately order: non-contrast head CT, CTA head/neck, glucose, CBC, BMP, coags, NIHSS, IV access, NPO, BP management per stroke protocol — then decide on alteplase/tenecteplase and thrombectomy. Don't anchor on "chronic dementia"; treat the acute stroke.

Emergency department / inpatient triage:

Specialty consultation triggers:

Hospice eligibility (FAST stage 7):

Key Differentials — Same-Category (Other Dementias)

— Insidious, gradual decline; early episodic memory loss with storage deficit (cued recall does not help).

— MRI: medial temporal lobe and hippocampal atrophy; minimal vascular changes.

— CSF: ↓Aβ42, ↑p-tau; amyloid PET positive.

— Treatment: cholinesterase inhibitors, memantine; lecanemab/donanemab in early AD (eligibility narrow, ApoE4 screening for ARIA risk).

— Most common in patients >80; treat both — vascular risk factors AND cholinesterase inhibitor trial.

— Core features: fluctuating cognition, visual hallucinations, REM sleep behavior disorder, parkinsonism.

— Severe neuroleptic sensitivity — antipsychotics can cause life-threatening rigidity.

— DaTscan helpful.

— Cholinesterase inhibitors (rivastigmine) often effective.

— Parkinsonism precedes dementia by >1 year (vs DLB <1 year).

— <65, behavioral disinhibition or progressive aphasia, frontal/temporal atrophy.

— Cholinesterase inhibitors can worsen behavior; SSRIs for behavior.

— Triad: gait apraxia (magnetic, "feet glued"), urinary incontinence, cognitive impairment (subcortical pattern).

— MRI: ventriculomegaly out of proportion to atrophy, DESH sign.

— Diagnosis: large-volume LP (tap test) — gait improvement supports VP shunt response.

— Major VaD mimic because both have gait + cognition + small vessel changes.

— Rapidly progressive (weeks–months), myoclonus, ataxia. MRI DWI cortical ribboning, basal ganglia hyperintensity; CSF RT-QuIC, 14-3-3.

Key distinction: VaD vs NPH — both have gait + cognition + incontinence, but NPH shows ventriculomegaly with tight high convexity sulci (DESH) and gait-predominant onset preceding cognitive change, whereas VaD shows extensive white matter disease, lacunes, and stepwise course. A high-volume LP confirms NPH.

Alzheimer disease (AD):

Mixed dementia (AD + VaD):

Dementia with Lewy bodies (DLB):

Parkinson disease dementia (PDD):

Frontotemporal dementia (FTD):

Normal pressure hydrocephalus (NPH):

Creutzfeldt-Jakob disease:

Key Differentials — Other-Category Causes

— Hypothyroidism — TSH.

— B12 deficiency — B12, methylmalonic acid; can also cause subacute combined degeneration.

— Neurosyphilis — RPR/FTA-ABS in risk groups; CSF VDRL.

— HIV-associated neurocognitive disorder — HIV testing.

— Chronic subdural hematoma — anticoagulant use, head trauma history, MRI/CT diagnosis; neurosurgical evacuation if symptomatic.

— Brain tumor — primary or metastatic; MRI with contrast.

— Hepatic or uremic encephalopathy — CMP, ammonia.

— Hyponatremia/hypercalcemia — BMP, calcium.

— Anticholinergics (diphenhydramine, oxybutynin, TCAs, paroxetine), benzodiazepines, opioids, sedating antiepileptics, antipsychotics, muscle relaxants, anti-emetics (promethazine). Compute anticholinergic burden score.

— Subacute, prominent complaints, poor effort on testing, "I don't know" answers; preserved orientation.

— Trial of SSRI; recheck cognition.

— Subacute (weeks), seizures, psychiatric features, autonomic instability.

— Anti-NMDAR, anti-LGI1, anti-CASPR2. CSF pleocytosis, MRI mesial temporal hyperintensity, EEG abnormal.

— Treat: steroids, IVIG, plasmapheresis, rituximab; screen for malignancy.

— Acute, fluctuating, inattention; identify trigger (infection, medication, metabolic, MI, stroke).

Board pearl: Always screen for and treat depression, OSA, and reversible deficiencies before finalizing a vascular dementia diagnosis. A patient who "improves dramatically on sertraline and CPAP" reveals the original diagnosis was depression + OSA, not VaD — Step 3 rewards this systematic reversibility check.

Reversible/secondary cognitive impairment to rule out (AAN minimum workup):

Medication-induced cognitive impairment:

Substance use: Alcohol use disorder (Wernicke-Korsakoff — thiamine), chronic cannabis, polysubstance.

Sleep disorders: OSA, chronic insomnia — treat first before labeling dementia.

Depression ("pseudodementia"):

Autoimmune/paraneoplastic encephalitis:

Delirium superimposed on dementia:

Secondary Prevention and Long-Term Plan

— BP <130/80 with ACEi/ARB ± thiazide or CCB (PROGRESS, SPRINT-MIND data).

— High-intensity statin for atherosclerotic stroke/TIA; add ezetimibe/PCSK9i if LDL not <70.

— Antiplatelet (aspirin or clopidogrel) for non-cardioembolic OR DOAC for AF.

— A1c <7% (relaxed in frailty); favor SGLT2i and GLP-1RA for cardiorenal/cerebrovascular benefit.

— Smoking cessation: varenicline, NRT, counseling.

— Moderate alcohol (≤1 drink/day women, ≤2 men; less in elderly).

— Mediterranean or DASH diet, ≥150 min/week moderate aerobic exercise, resistance training 2×/week.

— CPAP if OSA.

— Weight management: BMI 18.5–24.9 target.

— Annual influenza, pneumococcal (PCV20 or PCV15 + PPSV23), RSV (≥60), shingles (Shingrix ≥50), COVID-19 boosters, Tdap.

— Cognitive rehabilitation, structured routine, memory aids, calendars, pill organizers, automated medication dispensers.

— Hearing aids (treating hearing loss reduces dementia progression — ACHIEVE trial signal).

— Cataract surgery when indicated.

— Antiplatelet OR anticoagulant (not both unless specific indication), statin, BP regimen, glucose regimen.

— Deprescribe Beers-list drugs.

— Document indication and stop date for each med.

— POLST/MOLST, healthcare proxy, financial POA, code status — complete while capacity preserved.

Step 3 management: At every VaD follow-up, run the "ABCDE" checklist: Antiplatelet/anticoagulant, BP, Cholesterol (statin), Diabetes/diet/exercise, Education + advance directives. Missing any of these is the most common pimping point.

Vascular secondary prevention (the heart of VaD care):

Vaccinations (preventive medicine focus):

Cognitive and functional support:

Discharge medication reconciliation after stroke admission:

Advance care planning:

Follow-Up, Monitoring, and Rehab/Counseling

— Newly diagnosed: follow-up at 4–6 weeks to review labs, MRI, initiate/titrate therapy.

— Stable: every 3–6 months for vascular risk factor monitoring and functional reassessment.

— Post-stroke: at 1 week, 1 month, 3 months, then quarterly.

— BP: Home BP log; office check each visit; aim <130/80.

— Lipids: Lipid panel 4–12 weeks after statin start/change, then annually.

— A1c: Every 3 months until at goal, then every 6 months.

— Renal/liver: BMP and LFTs at baseline and periodically; check Cr before/after ACEi/ARB initiation and dose changes.

— CBC/INR: If on warfarin (INR every 2–4 weeks once stable); DOACs need annual Cr (more frequently if CKD or elderly).

— Cognition: MoCA every 6–12 months to track trajectory.

— Functional status: ADLs/IADLs, falls history each visit.

— Depression: PHQ-9 each visit.

— Driving: Annual assessment; refer for formal evaluation when concerns arise.

— Post-stroke: PT, OT, SLP — inpatient rehab vs SNF vs home health based on functional gain potential.

— Cardiac rehab if coexisting CAD.

— Pulmonary rehab if COPD overlap.

— Diagnosis disclosure with caregiver present.

— Discuss progression expectations, prognosis (median survival 3–5 years).

— Refer: Alzheimer's Association, Area Agency on Aging, adult day programs, respite care, support groups.

— Financial planning, long-term care insurance, Medicaid planning where appropriate.

— Safety: stove shut-offs, wandering (MedicAlert + Safe Return), firearm removal, medication lockboxes.

CCS pearl: Schedule the caregiver-inclusive visit explicitly on the CCS clock — disclosure of diagnosis, prognosis, and advance care planning is best done with the legally designated proxy present, and CCS rewards documentation of these conversations.

Visit cadence:

Monitoring parameters:

Rehabilitation:

Counseling and caregiver support:

Ethical, Legal, and Patient Safety Considerations

— Capacity is decision-specific, not global — a patient may consent to flu shot but lack capacity for complex surgery.

— Four components: understand, appreciate, reason, express choice.

— Document the assessment for major decisions (surgery, anticoagulation, code status, moving to facility).

— Capacity ≠ competency (legal determination).

— Use previously designated healthcare proxy / durable POA for healthcare.

— In absence, follow state hierarchy (typically spouse → adult children → parents → siblings).

— Apply substituted judgment (what would patient have wanted), then best interest if unknown.

— Initiate early — diagnosis is the trigger.

— POLST/MOLST for goals-of-care orders (CPR, intubation, artificial nutrition, hospitalization).

— State laws vary; some require physician reporting of dementia to DMV (e.g., California, Oregon, Pennsylvania).

— Know your state; document the discussion and any reporting.

— Physicians are mandated reporters in all states.

— Screen at each visit: unexplained bruises, weight loss, missed medications, financial exploitation, caregiver burnout signs.

— Report to Adult Protective Services even on suspicion.

— Inquire about home firearms; counsel on removal or secure storage when judgment is impaired. Document discussion.

— Hospital discharge in VaD patients carries high readmission risk.

— Medication reconciliation error rate is highest at transitions.

— Ensure: written discharge summary in plain language to caregiver, follow-up within 7 days, home health if needed, pill organizer, deprescribing of hospital-added sedatives.

— Informed consent for trials requires capacity; use legally authorized representative when impaired, with patient assent if possible.

Step 3 management: When a VaD patient with mild impairment refuses to stop driving and family is worried, assess capacity for the specific decision, perform office screen (clock-draw, Trails B, MoCA), refer for on-road driving evaluation, counsel patient and family, document and report per state law if mandated — never simply revoke the license unilaterally.

Decisional capacity assessment:

Surrogate decision-making:

Advance care planning:

Driving safety and mandatory reporting:

Mandatory reporting of elder abuse/neglect:

Firearm safety:

Transition-of-care risks (high Step 3 yield):

Research and experimental therapies:

High-Yield Associations and Rapid-Fire Clinical Facts

Board pearl: When you see gait disturbance + executive dysfunction + extensive white matter disease on MRI + vascular risk factors, the answer is almost always subcortical ischemic vascular dementia, and the next step is optimize BP, statin, antiplatelet, and treat OSA — not start donepezil first.

Stepwise decline + focal neuro findings + vascular risk factors = VaD until proven otherwise.

Executive dysfunction predominates in VaD; episodic memory loss in AD.

MoCA > MMSE for detecting vascular cognitive impairment (sensitive to executive dysfunction).

PROGRESS trial: perindopril/indapamide reduced recurrent stroke and dementia.

SPRINT-MIND: Intensive BP control (<120) reduced MCI; nonsignificant trend for probable dementia.

SPARCL trial: Atorvastatin 80 mg reduced recurrent stroke after non-cardioembolic stroke/TIA.

NASCET: CEA benefit for symptomatic 70–99% carotid stenosis; operate within 2 weeks of event.

Asymptomatic carotid stenosis ≥70%: CEA only if life expectancy >5 years; modern medical therapy narrows benefit.

AF + prior stroke = CHA₂DS₂-VASc ≥4 → anticoagulate; DOAC preferred over warfarin (except mechanical valves, severe mitral stenosis, antiphospholipid syndrome).

Apixaban dose reduction (2.5 mg BID): ≥2 of: age ≥80, weight ≤60 kg, Cr ≥1.5.

Antipsychotics in dementia: Black box — increased mortality and stroke; non-pharm first.

CADASIL: NOTCH3, migraine with aura, anterior temporal pole white matter changes.

CAA: Lobar microbleeds, cortical superficial siderosis, "amyloid spells" — avoid antithrombotics if possible.

Binswanger disease: Subcortical ischemic VaD with confluent white matter lesions, HTN, gait/executive dysfunction.

PEG tube in advanced dementia: No survival or aspiration benefit — do not place.

Cholinesterase inhibitors in pure VaD: Modest benefit; better evidence in mixed dementia.

Falls alone do not contraindicate anticoagulation in AF — the math favors continuing.

Treat OSA, depression, hearing loss — modifiable contributors to cognitive decline.

Hospice eligibility: FAST 7c + qualifying comorbidity (aspiration pneumonia, stage 3–4 ulcer, recurrent UTI, weight loss).

Mixed dementia is the most common dementia in patients >80 — treat vascular risk AND cognitive symptoms.

Board Question Stem Patterns

— 78-year-old with HTN, DM, AF on warfarin had a left MCA stroke 2 years ago; cognition has worsened "in steps" with each subsequent TIA. MRI shows multiple cortical and lacunar infarcts. → Vascular dementia. Next step: optimize secondary prevention; switch warfarin to apixaban if non-valvular AF and reasonable kidney function.

— 72-year-old with chronic uncontrolled HTN, gait apraxia, urinary urgency, executive dysfunction; MRI shows confluent periventricular white matter hyperintensities and multiple lacunes. → Binswanger subcortical ischemic VaD. Best initial step: intensive BP control, not VP shunt.

— 42-year-old with migraine with aura, two lacunar strokes, mother with early dementia. MRI shows anterior temporal pole hyperintensities. → CADASIL; next test NOTCH3 genetic testing.

— 81-year-old normotensive with transient focal episodes and lobar microbleeds. → CAA; avoid anticoagulation/antiplatelet when possible; do not lyse if questionable.

— 84-year-old with AF (CHA₂DS₂-VASc 5) and 2 falls last year. → Continue apixaban; address fall risk separately.

— Family asks for haloperidol for sundowning. → Non-pharm first (environment, routine, treat pain/UTI); avoid antipsychotics due to black box mortality/stroke risk.

— → Do not place PEG; careful hand feeding, palliative care consultation.

— Mild VaD, family worried. → Formal on-road driving evaluation; report per state law.

— Insidious memory loss plus stepwise vascular insults, hippocampal atrophy plus white matter disease. → Treat both — vascular prevention plus cholinesterase inhibitor trial.

— 75% symptomatic ICA stenosis 1 week post-TIA. → CEA within 2 weeks, plus statin/antiplatelet/BP control.

Key distinction: Step 3 stems often pair a vascular risk profile with a specific cognitive/exam pattern; anchor on the executive-predominant phenotype + imaging pattern to choose VaD over AD, and then select the secondary prevention or deprescribing action as the next best step rather than a cognitive enhancer.

"Stepwise decline" stem:

"Subcortical pattern" stem:

"Young patient with migraines and strokes" stem:

"Lobar microbleeds" stem:

"Falls and anticoagulation" stem:

"Antipsychotic for agitation" stem:

"PEG for advanced dementia with aspiration" stem:

"Driving" stem:

"Mixed dementia" stem:

"Carotid stenosis after TIA" stem:

One-Line Recap

Vascular dementia is a clinical-radiographic diagnosis of cognitive decline driven by cerebrovascular disease whose management is fundamentally about aggressive vascular risk factor control, secondary stroke prevention, deprescribing of cognition-impairing drugs, and longitudinal caregiver-inclusive functional support — not a single pill.

Board pearl: The single most exam-rewarded action in vascular dementia is aggressive control of modifiable vascular risk factors — that one move prevents the next stroke that would have caused the next step down.

Diagnosis: Vascular risk factors + executive-predominant cognitive decline + MRI evidence of infarcts, lacunes, confluent white matter disease, or microbleeds; rule out reversible causes (TSH, B12, depression, OSA, meds, NPH, SDH) before finalizing.

Treatment pillars: BP <130/80 (ACEi/ARB-based), high-intensity statin (LDL <70), antiplatelet for non-cardioembolic stroke or DOAC for AF, A1c <7%, smoking cessation, Mediterranean/DASH diet, ≥150 min/week aerobic exercise, CPAP for OSA, treat depression and hearing loss; cholinesterase inhibitor trial reasonable in mixed dementia.

Avoid: Anticholinergics, benzodiazepines, antipsychotics for behavior (black box), PEG tubes in advanced disease, dual antiplatelet long-term, anticoagulation in CAA when avoidable; do not withhold anticoagulation in AF solely because of fall risk.

Longitudinal care: MoCA every 6–12 months, BP/lipid/A1c monitoring, annual driving and capacity reassessment, advance care planning early, caregiver support and hospice referral when FAST 7c with qualifying comorbidity emerges — and act fast on symptomatic carotid stenosis (CEA within 2 weeks) and acute stroke (alteplase/thrombectomy) because every recurrent infarct ratchets cognition downward irreversibly.