01Approach to the Critical Patient/attcp50

Immediate priorities

›Time-critical actions

›Activate stroke protocol immediately on arrival

›Door-to-CT target within 25 minutes

›Door-to-needle target within 60 minutes for eligible patients

›Last known well (LKW) time determination

›Precise time from witness or patient

›Wake-up strokes use time last seen normal

›Noncontrast CT head emergently

›Exclude hemorrhage before any thrombolytic

›CT often normal in acute lacunar stroke

›Point-of-care glucose immediately

›Hypoglycemia is the most common correctable stroke mimic

›Target glucose 7.8–10 mmol/l acutely

›Airway and oxygenation

›SpO2 target 94–99%

›Supplemental oxygen only if SpO2 <94%

›Routine supplemental oxygen not recommended in normoxic patients

›Airway compromise rare in pure lacunar stroke

›Dysphagia screen before oral intake

›NPO until swallow screen completed

›Hemodynamic management

›Permissive hypertension if NOT receiving thrombolysis

›Treat only if SBP >220 mmHg or DBP >120 mmHg

›Avoid aggressive BP lowering in first 24 hours

›Pre-thrombolysis BP target <185/110 mmHg

›Labetalol 10–20 mg IV over 1–2 minutes, may repeat once

›Nicardipine 5 mg/h IV, titrate by 2.5 mg/h every 5–15 minutes (max 15 mg/h)

02History/hx66

Presenting symptoms

›Classic lacunar syndromes

›Pure motor hemiparesis (55% of lacunar strokes)

›Unilateral face, arm, and leg weakness without sensory loss

›No aphasia, visual field cut, or cortical signs

›Localizes to posterior limb of internal capsule, corona radiata, or pons

›Pure sensory stroke (7%)

›Unilateral numbness or paresthesias without motor deficit

›Localizes to thalamus

›Sensorimotor stroke (20%)

›Combined hemiparesis and hemisensory loss

›Localizes to thalamocapsular junction

›Ataxic hemiparesis (10%)

›Ipsilateral weakness with cerebellar-type ataxia disproportionate to weakness

›Localizes to pons or internal capsule

›Dysarthria-clumsy hand syndrome (6%)

›Dysarthria with ipsilateral hand clumsiness

›Localizes to pons or internal capsule

Onset and timing

›Symptom onset characterization

›Abrupt focal neurological deficit typical

›Maximal at onset in most cases

›Stuttering or stepwise progression over hours in capsular warning syndrome

›LKW precision critical for thrombolytic eligibility

›Wake-up stroke defined as onset during sleep

›Prior TIA or stuttering symptoms suggest capsular warning syndrome

›Duration of symptoms

›TIA if resolution <24 hours (operationally <1 hour with no DWI lesion)

›Ongoing deficits beyond 24 hours confirm stroke

Risk factors and background

›Modifiable vascular risk factors

›Hypertension (OR 2.21 vs controls; strongest lacunar-specific risk)

›Long-standing poorly controlled hypertension most implicated

›Diabetes mellitus (OR 2.10)

›Microvascular disease promotes lipohyalinosis of penetrating arteries

›Hyperlipidemia (OR 1.74)

›Smoking (OR 1.65)

›Obstructive sleep apnea

›Non-modifiable risk factors

›Age >55 years

›Male sex

›Prior lacunes or white matter hyperintensities on imaging (OR 2.29 for recurrent lacunar infarct)

›Prior stroke and vascular history

›Prior lacunar stroke or TIA

›Coronary artery disease or peripheral vascular disease

›Atrial fibrillation or other arrhythmia

›Chronic kidney disease

Red flags and alarm features

›Features suggesting nonlacunar mechanism

›Aphasia, neglect, hemianopia, or gaze deviation

›Cortical signs absent in true lacunar stroke

›Presence mandates large vessel or cardioembolic workup

›NIHSS >7 or rapidly worsening deficit

›Consider large vessel occlusion requiring CTA and thrombectomy evaluation

›Decreased level of consciousness

›Atypical for lacunar stroke; consider hemorrhage or basilar occlusion

›Severe headache, vomiting, or seizure at onset

›Raises concern for hemorrhagic stroke or other etiology

›Rare genetic etiologies in younger patients

›CADASIL (cerebral autosomal dominant arteriopathy)

›Migraine with aura, recurrent lacunar strokes, family history of early dementia

›NOTCH3 gene mutation; confirmed by skin biopsy or genetic testing

›Fabry disease in unexplained young-onset small vessel disease

›Alpha-galactosidase A deficiency; skin manifestations, neuropathic pain

Review of systems

›Systemic review

›Neurological: Headache, visual changes, dysarthria, dysphagia, gait instability

›Cardiovascular: Palpitations, chest pain, dyspnea, claudication

›Endocrine: Polyuria, polydipsia suggesting undiagnosed diabetes

›Psychiatric: Depression or apathy common in small vessel disease

›Genitourinary: Urinary incontinence suggesting bilateral lacunar disease

03Physical Exam/exam44

Neurological assessment

›NIHSS scoring

›Median NIHSS 4–5 in typical lacunar stroke

›Score each of 11 domains systematically

›Baseline NIHSS guides thrombolytic eligibility and outcome prediction

›Classic lacunar syndrome pattern

›Proportional face-arm-leg involvement in pure motor hemiparesis

›Absence of cortical signs mandatory for lacunar diagnosis

›Cortical signs absence confirmation

›No aphasia (naming, repetition, fluency intact)

›No neglect (extinction to double simultaneous stimulation)

›No hemianopia on confrontation visual fields

›No gaze deviation or gaze preference

Motor and sensory examination

›Motor findings

›Unilateral upper and lower extremity weakness

›Face-arm-leg proportional weakness in pure motor hemiparesis

›Hemiplegia or hemiparesis severity graded on MRC scale

›Ataxia out of proportion to weakness

›Finger-nose-finger and heel-shin testing

›Gait ataxia with ipsilateral limb weakness in ataxic hemiparesis

›Sensory findings

›Unilateral hemisensory loss to pinprick and light touch

›Pure sensory stroke involves face, arm, and leg unilaterally

›Sensorimotor variant has both motor and sensory deficits

›Proprioception and vibration testing

›Thalamic infarcts may produce marked proprioceptive loss

04Differential Diagnosis/ddx43

Must-not-miss diagnoses

›Intracerebral hemorrhage (ICD-10: I61.9)

›Cannot be excluded clinically; requires noncontrast CT head

›May present with focal motor or sensory deficit identical to lacunar stroke

›Severe headache, vomiting, and rapid progression favor hemorrhage

›Large vessel occlusion stroke (ICD-10: I63.3)

›Cortical signs present: aphasia, neglect, gaze deviation, hemianopia

›NIHSS typically >7

›CTA required to identify large vessel occlusion amenable to thrombectomy

›Basilar artery occlusion (ICD-10: I63.09)

›Bilateral motor signs, locked-in syndrome, decreased consciousness

›Requires emergent CTA or MRA of posterior circulation

›Cardioembolic stroke (ICD-10: I63.4)

›May mimic lacunar syndrome in 5–11% of cases

›Concurrent atrial fibrillation, valvular disease, or intracardiac thrombus

›Cardiac and vascular workup required to exclude

Stroke mimics

›Hypoglycemia (ICD-10: E16.0)

›Most common correctable stroke mimic

›Immediate point-of-care glucose mandatory in all presentations

›Focal deficits may resolve with glucose correction

›Todd's paralysis (ICD-10: G83.89)

›Postictal focal motor deficit following witnessed or unwitnessed seizure

›History of seizure disorder or witnessed convulsive activity

›Deficits typically resolve within 24 hours

›Hemiplegic migraine (ICD-10: G43.4)

›Younger patients, prior similar episodes, gradual march of positive symptoms

›Visual aura, sensory spread, family history of hemiplegic migraine

05Laboratory Tests/lt45

Acute emergency labs

›Stat glucose

›Point-of-care glucose immediately on arrival

›Hypoglycemia correction before further workup if glucose <3.5 mmol/l

›Hyperglycemia associated with worse outcomes in acute stroke

›Target acutely 7.8–10 mmol/l

›Complete blood count

›Thrombocytopenia as contraindication to thrombolysis (platelets <100 x10^9/l)

›Polycythemia as stroke risk factor

›Leukocytosis suggests infectious etiology

›Coagulation studies

›PT/INR: Anticoagulant use precludes thrombolysis if INR >1.7

›aPTT: Heparin use within 48 hours is a thrombolysis contraindication

›Thrombolytics contraindicated if on direct oral anticoagulants within 48 hours

›Basic metabolic panel

›Electrolytes and renal function

›Creatinine and eGFR for contrast CTA planning and medication dosing

›Sodium disturbances as stroke mimics

›Hyponatremia and hypocalcemia may cause focal neurological deficits

Cardiac and risk factor labs

›Troponin

›Elevated in up to 20% of acute ischemic stroke

›Neurogenic cardiac injury mechanism

›Concurrent ACS must be considered and managed accordingly

›HbA1c

›Screens for diabetes and insulin resistance in all stroke patients

›Guides long-term glycemic management for secondary prevention

›Fasting lipid panel

06Diagnostic Tests/dt91

Scoring Systems

›NIHSS (National Institutes of Health Stroke Scale)

›11-domain standardized neurological severity score (range 0–42)

›Lacunar stroke typically NIHSS <7 (median 4–5)

›NIHSS >7 increases likelihood of large vessel or nonlacunar mechanism

›Required for thrombolysis eligibility and outcome monitoring

›Minor stroke threshold: NIHSS 0–5

›Eligible for DAPT protocol (POINT/CHANCE trials)

›Thrombolysis benefit maintained even in minor-moderate stroke

›ABCD2 score for TIA risk stratification

›Components: Age, BP, Clinical features, Duration, Diabetes

›Score 0–3 low risk, 4–5 moderate risk, 6–7 high risk

›High score (>4) warrants urgent inpatient workup

›ABCD3-I adds imaging and dual TIA for improved accuracy

›Modified Rankin Scale (mRS)

›Functional outcome scale 0 (no symptoms) to 6 (death)

›Baseline pre-stroke mRS essential for outcome comparison

›mRS 0–2 at discharge in approximately 78% of lacunar stroke patients

›Fazekas Scale for white matter hyperintensities

›Grades periventricular and deep white matter changes 0–3

›Higher Fazekas grade correlates with recurrence risk and cognitive decline

›Guides intensity of vascular risk factor management

MRI

›MRI brain with DWI protocol

›Gold standard for acute lacunar infarct detection

›Sensitivity 70–88% for lacunar infarcts within 24 hours

›Superiority over CT especially in posterior fossa and small cortical lesions

›ADC restriction confirms acute ischemia (dark on ADC, bright on DWI)

›Lacunar infarct definition on MRI

›Subcortical lesion <1.5 cm in diameter

›Located in territory of penetrating artery (internal capsule, thalamus, pons, basal ganglia)

›High DWI signal with corresponding ADC restriction

›MRI sequences for small vessel disease characterization

›FLAIR sequence

›White matter hyperintensities indicating chronic small vessel disease

›Periventricular and deep white matter involvement

›Fazekas grading applied to quantify burden

›SWI or GRE sequence

›Cerebral microbleeds identified as hypointense foci

›Multiple microbleeds increase hemorrhagic risk with antithrombotics

›Guides shared decision-making for antiplatelet therapy

›T1-weighted sequence

›Old lacunes appear as small hypointense cavities (lacunar cysts)

›Enlarged perivascular spaces (Virchow-Robin spaces) indicate small vessel disease

›MRA head and neck

›Excludes large artery stenosis >50% in head and neck vessels

›Required to confirm isolated lacunar mechanism

›Intracranial stenosis (branch atheromatous disease) may be missed without high-resolution MRI

CT

›Noncontrast CT head

›First-line imaging; primary role is exclusion of hemorrhage

›Sensitivity for acute lacunar infarct only approximately 50%

›Normal CT does not exclude lacunar stroke

›Early ischemic changes (sulcal effacement, loss of gray-white differentiation) may be subtle or absent

›ASPECTS scoring

›Alberta Stroke Program Early CT Score for MCA territory changes

›Score 0–10; >6 favors thrombolytic eligibility

›Less applicable to isolated lacunar infarcts

›CT angiography (CTA) head and neck

›Required to exclude large vessel occlusion and identify lacunar mechanism

›CTA with contrast; assess intracranial and extracranial vessels

›Excludes proximal carotid stenosis >50% or intracranial occlusion

›Branch atheromatous disease identified as parent artery plaque at perforator origin

›CT perfusion (CTP)

›Not routinely indicated for small subcortical lacunar infarcts

›May identify mismatch in large vessel occlusion being differentiated from lacunar

›Follow-up CT

›Repeat NCCT at 24 hours post-thrombolysis

›Exclude hemorrhagic transformation

›Routine imaging after thrombolysis per AHA/ASA guidelines

Ultrasound

›Transthoracic echocardiography (TTE)

›Yield low in isolated confirmed lacunar stroke with clear small vessel disease mechanism

›Sensitivity for cardioembolic sources approximately 6% in isolated lacunar infarcts

›Guidelines recommend only if cardioembolic source suspected or mechanism uncertain

›Indications in lacunar stroke context

›Newly detected atrial fibrillation

›Young patient (<50) without traditional risk factors

›Clinical suspicion for endocarditis, PFO, intracardiac thrombus

›Transesophageal echocardiography (TEE)

›Higher sensitivity for PFO, LAA thrombus, and aortic arch atheroma

›Reserved for young patients with cryptogenic presentation and negative TTE

›PFO prevalence higher in younger lacunar stroke patients

›Carotid duplex ultrasound

›Screens for ipsilateral carotid stenosis >50%

›Large artery disease at carotid bifurcation may produce perforator ischemia

›Complementary to CTA or MRA for vascular imaging

›Cardiac monitoring

›12-lead ECG on all acute stroke patients

›Paroxysmal atrial fibrillation detection

›ST changes and T-wave inversions may represent neurogenic cardiac injury

›Continuous cardiac telemetry 24–48 hours minimum

›Paroxysmal AF detected in additional 5–10% with extended monitoring

›Implantable loop recorder if mechanism remains uncertain after standard workup

›30-day event monitor for outpatient cryptogenic workup

07Disposition/dispo28

Inpatient admission

›Admission criteria

›All acute lacunar strokes require hospital admission

›Stroke unit or monitored bed preferred (Class I recommendation)

›Stroke unit care reduces mortality and disability vs. general ward

›Monitored bed for telemetry

›Continuous cardiac monitoring minimum 24–48 hours

›Neurological monitoring and reassessment cadence

›Neurology consultation (vascular neurology preferred)

›All acute strokes require neurology involvement

›Facilitates thrombolysis decisions and secondary prevention planning

Transfer criteria

›Transfer to comprehensive stroke center

›Facilities without neurology or MRI capability

›If thrombolysis window open, do not delay transfer for thrombolysis

›Consider telestroke consultation to facilitate acute treatment

›Transfer timing

›Emergent transfer if thrombectomy consideration (though rare in lacunar)

›Urgent transfer within hours for ongoing workup and risk stratification

Discharge criteria

›Safe discharge requirements

›Neurologically stable or improving

›No evidence of capsular warning syndrome or progressive deficit

›Swallowing safe for oral intake

›Formal swallow assessment completed if any dysphagia concern

›Blood pressure controlled on oral regimen

›Secondary prevention medications initiated and tolerated

›Cardiac rhythm monitoring completed (minimum 24 hours)

08Treatment/t81

Acute reperfusion therapy

›IV thrombolysis eligibility

›Alteplase 0.9 mg/kg IV (maximum 90 mg)

›10% of total dose as bolus over 1 minute

›Remaining 90% as continuous infusion over 60 minutes

›Within 4.5 hours of LKW; lacunar stroke is eligible (not a contraindication)

›WAKE-UP trial confirmed no heterogeneity of treatment effect between lacunar and nonlacunar subtypes

›Tenecteplase 0.25 mg/kg IV (maximum 25 mg) as single bolus

›Non-inferior to alteplase for non-large vessel occlusion strokes

›Simpler single-bolus administration favored in many centers

›OPTION trial (2026): Benefit extended to 4.5–24-hour window with salvageable tissue

›Contraindications to thrombolysis

›Active internal bleeding or recent major surgery <14 days

›Prior intracranial hemorrhage

›Platelets <100 x10^9/l or INR >1.7

›SBP >185 mmHg or DBP >110 mmHg unresponsive to treatment

›Direct oral anticoagulant within 48 hours

›Mechanical thrombectomy

›Generally not applicable to lacunar stroke

›No large vessel occlusion identified as target

›Perforating arteries too small for catheter access

Antiplatelet therapy

›Acute antiplatelet protocol

›Minor stroke (NIHSS 0–5) not receiving thrombolysis

›Dual antiplatelet therapy (DAPT) within 24 hours of onset

›Aspirin 325 mg loading dose then 81 mg daily

›Clopidogrel 300 mg loading dose then 75 mg daily

›Continue DAPT for 21 days then transition to single antiplatelet

›Based on POINT and CHANCE trials (HR 0.51 for lacunar subset, 95% CI 0.33–0.79)

›If thrombolysis administered

›Hold all antiplatelets for 24 hours post-thrombolysis

›Initiate aspirin 81 mg daily at 24 hours

›Long-term antiplatelet monotherapy

›Aspirin 81 mg daily or clopidogrel 75 mg daily as single agent

›No preference for one over the other per current evidence

›Long-term DAPT NOT recommended (SPS3 trial: no additional benefit, increased major bleeding)

›Ticagrelor not superior to aspirin for lacunar stroke prevention

Blood pressure management

›Acute BP management

›No thrombolysis: Permissive hypertension up to SBP 220 mmHg, DBP 120 mmHg

›Autoregulation impaired; excessive lowering extends infarct

›Treat hypertensive emergency if end-organ damage (ACS, heart failure, aortic dissection)

›Pre-thrombolysis: SBP <185 mmHg, DBP <110 mmHg

›Labetalol 10–20 mg IV over 1–2 minutes (may repeat x1)

›Nicardipine 5–15 mg/h IV infusion

›Post-thrombolysis: Maintain SBP <180 mmHg, DBP <105 mmHg for 24 hours

›Secondary prevention BP target

›Target <130/80 mmHg (AHA/ASA 2021 guideline)

›Thiazide diuretics, ACE inhibitors, or ARBs preferred agents

›Aggressive BP reduction to <130/80 mmHg associated with 22% RRR in stroke recurrence

›Class I recommendation (AHA/ASA Stroke Prevention Guideline 2021)

Lipid-lowering therapy

›High-intensity statin therapy

›Atorvastatin 40–80 mg daily initiated acutely

›LDL-C target <1.8 mmol/l for secondary stroke prevention

›High-intensity statin reduces relative risk of recurrent stroke by 16–22%

›Class I recommendation (AHA/ASA 2021)

›Rosuvastatin 20–40 mg daily as alternative

›Lower myopathy risk compared to atorvastatin at high doses

Glycemic management

›Acute glucose control

›Target glucose 7.8–10 mmol/l in acute stroke

›Hyperglycemia (>10 mmol/l) worsens ischemic injury and outcomes

›Hypoglycemia (<3.5 mmol/l) must be corrected immediately

›Insulin infusion protocol if persistent hyperglycemia

›Avoid rapid glucose correction of hyperosmolar hyperglycemia

›Long-term diabetes management

›HbA1c target <53 mmol/mol (7%) for most patients with diabetes

›Tight glycemic control reduces microvascular complications

›Individualize targets in elderly or frail patients

Secondary prevention lifestyle modifications

›Lifestyle interventions

›Smoking cessation

›Pharmacotherapy with varenicline or nicotine replacement

›Cessation reduces recurrent stroke risk by 30–40%

›Physical activity

›At least 10 minutes of moderate-intensity aerobic activity 4 days per week

›Structured cardiac rehabilitation if concurrent cardiac disease

›Diet

›Mediterranean or DASH diet recommended

›Low-sodium diet (<2 g/day) for blood pressure control

›Weight management

›BMI target 18.5–24.9 kg/m2

›Structured weight-loss program if BMI >30 kg/m2

›OSA treatment

›CPAP therapy if OSA confirmed by sleep study

›OSA worsens BP control and vascular risk

09Special Populations/sp71

Pregnancy

›Lacunar stroke in pregnancy

›Rare but recognized; pregnancy is prothrombotic state

›Increased risk in third trimester and postpartum period

›Preeclampsia and eclampsia can mimic or cause lacunar syndrome

›Diagnostic approach modifications

›MRI preferred over CT to avoid fetal radiation

›DWI MRI safe in pregnancy; gadolinium avoided in first trimester

›CTA or MRA required if large vessel disease suspected

›Treatment in pregnancy

›Thrombolysis (alteplase) considered relative contraindication in pregnancy

›May be used if benefits clearly outweigh risks in life-threatening presentation

›Multidisciplinary team (neurology, MFM, hematology) required

›Antiplatelet therapy

›Low-dose aspirin 75–100 mg daily considered safer than standard doses

›Clopidogrel category B; limited safety data in pregnancy

›Antihypertensive management

›Labetalol and nifedipine preferred agents in pregnancy

›ACE inhibitors and ARBs contraindicated (teratogenic)

›Anticoagulation if concurrent AF

›Low molecular weight heparin preferred over warfarin in first trimester

›DOACs contraindicated in pregnancy

Geriatric

›Age-related considerations

›Lacunar stroke most common in patients >65 years

›Higher baseline comorbidity burden and polypharmacy

›Greater cognitive impairment at baseline complicates NIHSS assessment

›Frailty assessment

›Clinical frailty scale or equivalent

›Frailty modifies thrombolysis risk-benefit ratio

›Thrombolysis considerations in elderly

›No upper age limit for thrombolysis (Class I, AHA/ASA)

›IST-3 trial confirmed benefit in patients >80 years

›Higher hemorrhagic transformation risk in elderly; individualize decision

›Falls risk and microbleed burden

›Cerebral microbleeds on SWI increase hemorrhagic risk

›Falls risk informs antiplatelet choice and lifestyle counseling

›Secondary prevention modifications in elderly

›Aggressive BP lowering may increase fall and syncope risk

›Orthostatic hypotension assessment before and during treatment

›Gradual BP titration preferred

›Statin therapy tolerated in most elderly patients

›Myopathy risk increases with age; monitor CK and symptoms

›Cognitive assessment

›Vascular cognitive impairment common with lacunar disease

›Montreal Cognitive Assessment (MoCA) at follow-up visits

›Advance directive discussion if significant cognitive burden

Pediatrics

›Lacunar stroke in children

›Rare; accounts for approximately 10% of childhood arterial ischemic stroke

›Different risk factor profile from adults

›Genetic and hematologic etiologies predominate

›Pediatric-specific etiologies

›Sickle cell disease (most common identifiable cause of childhood stroke)

›CADASIL in familial cases with migraine and white matter disease

›Fabry disease in unexplained small vessel disease

›Vasculopathies (focal cerebral arteriopathy, moyamoya disease)

›Diagnostic approach in children

›MRI with DWI preferred (no radiation)

›Vascular imaging with MRA mandatory

›Echocardiography and cardiac workup in all children

›Hematologic workup

›Hemoglobin electrophoresis for sickle cell disease

›Hypercoagulability panel in all children (more likely than adults)

›Lipoprotein(a) as inherited risk factor

›Treatment in children

›Thrombolysis not routinely recommended in children <18 years

›Case series support use in selected severe presentations

›Pediatric stroke neurology consultation required

›Antiplatelet therapy

›Aspirin 3–5 mg/kg/day (maximum 100 mg) for secondary prevention

›Clopidogrel as alternative for aspirin-intolerant patients

›Anticoagulation for cardioembolic or hypercoagulable states

›Low molecular weight heparin or warfarin per hematology guidance

10Background/b75

Epidemiology

›Incidence and prevalence

›Lacunar stroke accounts for 20–25% of all ischemic strokes

›Approximately 1.5–2 per 1000 per year in adults >55 years

›Annual incidence increases with age and vascular risk factor burden

›Recurrence risk

›Annual recurrence rate 4–11%

›20% cumulative recurrence at 5 years

›Risk highest in first 90 days after index event

›Mortality and functional outcomes

›25% five-year mortality (higher than initially expected)

›Short-term prognosis relatively favorable

›78% achieve mild or no disability at discharge (mRS 0–2)

›Long-term morbidity

›Progressive vascular cognitive impairment and dementia

›Gait disorder and falls with accumulation of lesions

›Depression occurs in up to 30% post-lacunar stroke

›Demographics

›Mean age of onset approximately 65 years

›Higher prevalence in male sex

›Racial disparities: Higher rates in Black and Hispanic populations

›Associated with hypertension and diabetes more strongly than other stroke subtypes

Pathophysiology

›Mechanisms of lacunar infarction

›Lipohyalinosis (primary mechanism)

›Chronic hypertension causes segmental degeneration of small penetrating artery walls

›Hyaline material replaces smooth muscle in vessel wall

›Leads to stenosis and occlusion of penetrating arteries 100–400 microns in diameter

›Microatheroma (second major mechanism)

›Plaque formation at origin of penetrating artery from parent vessel

›Branch atheromatous disease: Plaque at parent artery occludes perforator ostium

›Embolism (contributing mechanism in subset)

›Cardioembolic or artery-to-artery emboli in 5–11% of cases

›Distinguishing lacunar from embolic mechanism requires full workup

›Vascular anatomy of penetrating arteries

›Lenticulostriate arteries from MCA

›Supply basal ganglia and internal capsule

›Infarction produces pure motor or sensorimotor syndromes

›Thalamogeniculate and thalamoperforating arteries from PCA and basilar tip

›Supply thalamus

›Infarction produces pure sensory or sensorimotor syndromes

›Paramedian basilar perforators

›Supply pons

›Infarction produces ataxic hemiparesis or dysarthria-clumsy hand syndrome

›Cerebral small vessel disease spectrum

›White matter hyperintensities (leukoaraiosis)

›Represent chronic ischemia and demyelination of periventricular white matter

›Correlate with recurrence risk, cognitive decline, and gait disorder

›Cerebral microbleeds

›Hemosiderin deposits from prior microhemorrhages

›Indicate blood-brain barrier disruption and vessel fragility

›Multiple microbleeds (>10) increase hemorrhagic stroke risk

›Enlarged perivascular spaces

›Marker of impaired glymphatic clearance

›Associated with brain atrophy and cognitive impairment

Therapeutic Considerations

›Evidence base for secondary prevention

›DAPT for minor stroke

›CHANCE trial (China): DAPT vs. aspirin alone in TIA/minor stroke; 32% relative risk reduction in stroke at 90 days

›POINT trial (USA/Canada): Confirmed CHANCE findings; NNT approximately 50 for 90-day stroke prevention

›THALES trial: Ticagrelor + aspirin vs. aspirin alone; modest benefit with increased bleeding

›Long-term antiplatelet evidence

›SPS3 trial: DAPT (aspirin + clopidogrel) vs. aspirin alone in lacunar stroke; no benefit of DAPT long-term, significantly increased major bleeding

›Supports 21-day DAPT followed by monotherapy

›Thrombolysis in lacunar stroke

›WAKE-UP trial (2019): IV alteplase in DWI-FLAIR mismatch; lacunar subgroup had equivalent benefit to nonlacunar

›OPTION trial (2026): Tenecteplase 0.25 mg/kg for non-LVO stroke 4.5–24 hours; extended treatment window

›Anticoagulation considerations

›Anticoagulation NOT indicated for lacunar mechanism without cardioembolic source

›No evidence of benefit for isolated small vessel disease

›Warfarin arm of SPS3 increased hemorrhagic risk without benefit

›Anticoagulation IS indicated if concurrent AF detected

›DOAC preferred over warfarin for AF-related stroke prevention

›Timing: Initiate 4–14 days post-stroke depending on infarct size

›Blood pressure reduction evidence

›SPS3 trial intensive arm: SBP target <130 mmHg associated with 19% reduction in recurrent stroke

›Significant reduction in intracerebral hemorrhage with intensive control

›Aggressive BP management central to lacunar stroke prevention

11Patient Discharge Instructions/pdi33

copy discharge instructions

›Discharge instructions for Ischemic Stroke (Lacunar)

›What happened to you

›You had a lacunar stroke, a type of stroke caused by blockage of a small blood vessel deep in the brain

›Your brain imaging showed the affected area and your doctors have begun treatment to prevent another stroke

›Your medications

›Take all prescribed medications exactly as directed

›Do not stop aspirin, clopidogrel, or blood thinners without calling your doctor

›Take your blood pressure medication every day even when you feel well

›Take your cholesterol medication (statin) as prescribed

›Blood pressure monitoring

›Check and record your blood pressure daily at home

›Target blood pressure is below 130/80 mmHg

›Contact your doctor if consistently above 150/90 mmHg

›Activity and driving

›Do not drive until cleared by your neurologist

›Light activity as tolerated; avoid strenuous activity until follow-up

›Resume exercise gradually after medical clearance

›Diet and lifestyle

›Follow a low-salt, heart-healthy diet (Mediterranean or DASH diet)

›Limit alcohol to no more than 1–2 drinks per day

›Stop smoking if you smoke; ask about cessation support

›Follow-up appointments

›Neurology follow-up within 1–2 weeks of discharge

›Primary care physician within 2–4 weeks

›Blood work for cholesterol and blood sugar at follow-up

›Return to the emergency department immediately for

›New or worsening weakness, numbness, or paralysis of face, arm, or leg

12References/r28

Guidelines and key sources

›AHA/ASA Guidelines

›Kleindorfer DO, et al. 2021 Guideline for the Prevention of Stroke in Patients with Stroke and TIA. Stroke. 2021

›Class I recommendation for dual antiplatelet therapy in minor stroke

›Blood pressure target <130/80 mmHg for secondary prevention

›Powers WJ. Acute Ischemic Stroke. NEJM. 2020

›Comprehensive review of acute stroke management

›Furie KL, Kelly PJ. Secondary Prevention after Ischemic Stroke. NEJM. 2026

›Updated evidence for secondary stroke prevention

Landmark trials

›Key clinical trials

›WAKE-UP Trial (Barow E, et al. JAMA Neurology. 2019)

›IV alteplase in DWI-FLAIR mismatch; equivalent benefit in lacunar subgroup

›SPS3 Trial (Del Brutto VJ, et al. JACC. 2019)

›DAPT no benefit over aspirin long-term in lacunar stroke; increased bleeding

›Intensive BP lowering to <130 mmHg reduced recurrent stroke by 19%

›POINT/CHANCE Trials

›Short-term DAPT significantly reduces 90-day stroke risk in minor stroke/TIA

›Lacunar subset: HR 0.51 (95% CI 0.33–0.79) for DAPT vs. aspirin

›OPTION Trial (Ma G, et al. JAMA. 2026)

›Tenecteplase benefit in non-LVO stroke in 4.5–24-hour window with imaging selection

Review articles and epidemiology

›Pathophysiology and mechanisms

›Yaghi S, et al. Lacunar Stroke: Mechanisms and Therapeutic Implications. J Neurol Neurosurg Psychiatry. 2021

›Comprehensive review of lacunar stroke mechanisms and management

›Regenhardt RW, et al. Advances in Understanding the Pathophysiology of Lacunar Stroke. JAMA Neurology. 2018

›Lipohyalinosis, microatheroma, and embolic mechanisms

›Wardlaw JM, et al. Small Vessel Disease: Mechanisms and Clinical Implications. Lancet Neurology. 2019

Evidence & Review

Evidence & Review