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GERICLINICS

GeriQBank · Paper III · Q4

Lacunar Infarcts

Moderate YieldAsked ×16-mark note
Chapter
Neurology, Neuro-ophthalmology & Environmental Emergencies
Years asked
Not recorded in the source
Frequency
Set 1× in Paper III (2009–2025)

As set in the university paper

  • Lacunar infarcts.

    Paper III · Neurology — Stroke, Coma, Seizures & Neuromuscular · asked ×1 · 6-mark note · see in paper list

Answer framework

  1. Definition and pathology — size and site; microatheroma and lipohyalinosis; share of strokes; related imaging findings; cognition; risk factors
  2. Classical lacunar syndromes — the four syndromes; the defining negative features; rarer syndromes
  3. Diagnosis — imaging; excluding haemorrhage; the stroke work-up
  4. Prognosis and management — prognosis; état lacunaire; acute treatment; BP control; statin; antiplatelets
  5. Recent updates — LACI-2; STRIVE-2; ESO guidelines; DAPT and genotype; BP targets; India

An exam answer plan drawn from the detailed answer below. Use it to attempt the question first.

Detailed answer

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Attempt it firstOutline your answer as a 6-mark note before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer

Short revision answer

  • A lacune is a deep subcortical infarct <15 mm from occlusion of a small perforating arteriole (basal ganglia, capsule, thalamus, pons), caused by microatheroma at the perforator origin or lipohyalinosis — together "small-vessel disease". Lacunes are about a quarter of ischaemic strokes.
  • The same process causes leukoaraiosis (white matter hyperintensity) and microbleeds (deep = hypertensive; lobar = amyloid angiopathy), each linked to cognitive impairment. Hypertension is the major risk factor, with age, diabetes, smoking and dyslipidaemia; still exclude cardioembolism and large-artery disease.
  • Syndromes: pure motor (commonest; face, arm and leg, at least two contiguous; posterior limb of the internal capsule or pons), pure sensory (thalamus, VPL nucleus), sensorimotor, and ataxic hemiparesis (including dysarthria–clumsy hand); rarely hemichorea or hemiballismus. The key negative: no cortical signs (aphasia, neglect, agnosia, apraxia) and no visual field defect.
  • Imaging separates capsular from pontine lesions (DWI most sensitive; CT often normal early) and excludes a small haemorrhage before antithrombotics. Complete the stroke work-up (ECG and rhythm monitoring, echo, carotid imaging, lipids, HbA1c, renal function, ESR).
  • Prognosis: one-year mortality about 10%, but 50% of survivors remain dependent; recurrent lacunes and white matter disease lead to vascular cognitive impairment, vascular parkinsonism, pseudobulbar palsy, gait apraxia and emotional lability (état lacunaire).
  • Treatment: thrombolysis within the window (benefit is preserved), antiplatelets and stroke-unit care. Secondary prevention: BP control matters most (PROGRESS; ≤130/80 in diabetes); atorvastatin 80 mg (SPARCL, about 20% fewer recurrent strokes); aspirin, clopidogrel or aspirin plus dipyridamole; glucose control and smoking cessation; no anticoagulation unless there is AF or a prosthetic valve.
  • Updates: LACI-2 (JAMA Neurology 2023; 363 patients) — isosorbide mononitrate reduced recurrent stroke (aOR 0.23) and cognitive impairment, cilostazol reduced dependence, both cheap (LACI-3 awaited); STRIVE-2 standardises terms ("white matter hyperintensity of presumed vascular origin" replaces leukoaraiosis); ESO small-vessel guidelines; short DAPT (INSPIRES 2024, started within 72 hours) and genotype-guided ticagrelor in CYP2C19 loss-of-function carriers (CHANCE-2; common in Indians); systolic <130 (SPS3). India: small-vessel and intracranial disease dominate; IHCI and NP-NCD frame prevention.

Condensed by GeriClinics from the detailed answer below, with no new facts added.

4.

Lacunar Infarcts Definition and pathology

1.

Lacunes are small infarcts resulting from occlusion of the small perforating arterioles supplying the basal ganglia, external and internal capsule, thalamus and pons. On brain imaging they are defined as deep subcortical infarcts less than 15 mm in maximum diameter.

2.

Two underlying pathologies: microatheroma at the origin of the perforating artery, and more distal lipohyalinosis — degenerative change in the tunica media and adventitia of the arterioles. These cannot be distinguished clinically or radiologically and are together known as small-vessel disease (SVD).

3.

Lacunar strokes account for roughly a quarter of all ischaemic strokes.

4.

Other imaging manifestations of the same process: leukoaraiosis (patchy or confluent low attenuation on CT, high signal on T2 and FLAIR MRI in the white matter, also attributed to lipohyalinosis) and cerebral microhaemorrhages on gradient-echo (T2*) or susceptibility-weighted MRI.

5.

Leukoaraiosis, lacunes and microhaemorrhages are each independently associated with cognitive impairment.

6.

Hypertension is the major risk factor for lacunar infarction, leukoaraiosis and microhaemorrhage. Microhaemorrhages are also associated with cerebral amyloid angiopathy — deep/basal ganglia microbleeds suggest hypertensive arteriopathy, lobar microbleeds suggest amyloid angiopathy.

7.

Other risk factors: increasing age, diabetes mellitus, smoking and dyslipidaemia. Cardioembolism and large-artery atherosclerosis are usually not the mechanism, but must still be excluded.

Classical lacunar syndromes

8.

Pure motor stroke (commonest): unilateral face, arm and leg weakness. The weakness need not involve all three but should involve at least two contiguous sites — face and arm, or arm and leg. Lesion in the posterior limb of the internal capsule or the pons.

9.

Pure sensory stroke: contralateral hemisensory loss; lesion in the thalamus (ventral posterolateral nucleus).

10.

Sensorimotor stroke: a larger lacune producing mixed motor and sensory loss.

11.

Ataxic hemiparesis: limb ataxia combined with hemiparesis and/or dysarthria (including the dysarthria–clumsy hand variant); internal capsule or pons.

12.

The defining negative features (the marks-earning point): there is NO disturbance of higher cortical function and NO visual field deficit — no aphasia, neglect, agnosia or apraxia, and no hemianopia.

13.

Rarer lacunar syndromes include unilateral chorea and hemiballismus from lacunes in the basal ganglia.

Diagnosis

14.

Imaging is required to distinguish a capsular from a pontine site, as the syndromes are identical clinically. Diffusion-weighted MRI is most sensitive acutely; CT is frequently normal in the first hours.

15.

Occasionally a small haemorrhage produces an identical syndrome — imaging is essential before antithrombotic therapy.

16.

Complete the standard stroke workup: ECG and prolonged rhythm monitoring, echocardiography, carotid imaging, lipids, HbA1c, renal function, ESR — principally to exclude an alternative mechanism.

Prognosis and management

17.

Lacunar stroke carries a good prognosis for survival, with a one-year mortality of about 10%, but 50% of survivors remain dependent.

18.

Recurrent lacunes and progressive white matter change lead to vascular cognitive impairment, vascular parkinsonism, pseudobulbar palsy, gait apraxia and emotional lability ("état lacunaire").

19.

Acute treatment: intravenous thrombolysis if within the licensed window (benefit is preserved in lacunar stroke), antiplatelet therapy, and admission to a stroke unit for multidisciplinary care.

20.

Secondary prevention — blood pressure control is the single most important intervention (PROGRESS: perindopril-based regimen reduced recurrent stroke); target ≤130/80 mmHg in diabetic patients.

21.

Statin: high-dose atorvastatin 80 mg reduced recurrent ischaemic stroke by around 20% (SPARCL); treat cholesterol >3.5 mmol/L with dietetic input.

22.

Antiplatelet therapy (aspirin, clopidogrel, or aspirin with extended-release dipyridamole) plus glycaemic control, smoking cessation and lifestyle change. Anticoagulation is not indicated unless there is a separate indication such as atrial fibrillation or a prosthetic valve.

Latest Updates (2023–Present)

LACI-2 trial (Wardlaw et al., JAMA Neurology 2023) — the single most examinable update. 363 patients with clinical lacunar ischaemic stroke, randomised 2×2 to isosorbide mononitrate (ISMN) 40–60 mg/day, cilostazol 200 mg/day, both, or neither, on top of guideline secondary prevention for one year. ISMN reduced recurrent stroke (adjusted OR 0.23, 95% CI 0.07–0.74) and cognitive impairment (aOR 0.55, 95% CI 0.36–0.86); cilostazol reduced dependence; the combination reduced the composite of vascular, dependence and cognitive outcomes. Retention was 99% with good adherence and no safety concerns. A prespecified 6-month analysis (2025) confirmed that benefit appears early. Both are inexpensive, licensed generic drugs; the definitive phase 3 trial (LACI-3) is awaited.

STRIVE-2 consensus (Lancet Neurology 2023) updated the neuroimaging standards for reporting cerebral small vessel disease — standardised terminology for recent small subcortical infarct, lacune of presumed vascular origin, white matter hyperintensity, perivascular space, microbleed, cortical superficial siderosis and brain atrophy. "Leukoaraiosis" is being retired in favour of "white matter hyperintensity of presumed vascular origin." European Stroke Organisation guidelines on cerebral small vessel disease — Part 1 (covert SVD, 2021) and Part 2 (lacunar ischaemic stroke) formalise management.

Antiplatelet intensification: INSPIRES (NEJM 2024) supports clopidogrel plus aspirin started within 72 hours for mild ischaemic stroke or high-risk TIA of atherosclerotic origin; CHANCE-2 showed genotype-guided ticagrelor is superior in CYP2C19 loss-of-function carriers — highly relevant, as this genotype is common in Indian and East Asian populations.

Blood pressure: SPS3 supported a systolic target <130 mmHg in lacunar stroke, particularly for reducing intracerebral haemorrhage; ESPRIT and 2024–2025 intensive-lowering trials reinforce this. Indian context: small-vessel disease and intracranial atherosclerosis account for a much larger share of Indian ischaemic stroke than extracranial carotid disease. ICMR-INDIAB and LASI data show very high prevalence and poor control of hypertension and diabetes in older Indians; the India Hypertension Control Initiative (IHCI) and the National Programme for Prevention and Control of Non-Communicable Diseases (NP-NCD) are the operative public-health frameworks for prevention.

Current Practice Update

Textbook Position (Pathy's 6th ed.) Current Evidence-Based Practice (2023–2026)

Secondary prevention is antiplatelet + statin + BP LACI-2 (2023) supports adding isosorbide mononitrate (reduces recurrent stroke control, identical to other ischaemic stroke and cognitive impairment) and cilostazol (reduces dependence) — endothelium-subtypes targeted therapy specific to small-vessel disease Terms "leukoaraiosis" and "lacune" used STRIVE-2 (2023) standardised terminology — "white matter hyperintensity of descriptively presumed vascular origin", "recent small subcortical infarct", "lacune of presumed vascular origin"

Aspirin or clopidogrel monotherapy after minor Short-course dual antiplatelet therapy (CHANCE, POINT, INSPIRES) for 21–30 stroke/TIA days; genotype-guided ticagrelor in CYP2C19 loss-of-function carriers (CHANCE-2) BP target ≤130/80 specified for diabetic patients Systolic <130 mmHg for all lacunar stroke (SPS3 and subsequent intensive-lowering trials), especially to reduce intracerebral haemorrhage Cognitive consequences noted as an association SVD is now recognised as the leading vascular contributor to dementia; cognitive outcome is a primary trial endpoint Examiner's Tip — say these lines verbatim:

"A lacune is a deep subcortical infarct less than 15 mm in maximum diameter from occlusion of a small perforating artery."

"The two pathologies are microatheroma at the perforator origin and lipohyalinosis of the tunica media and adventitia — indistinguishable clinically and radiologically, hence 'small-vessel disease'." "The four syndromes are pure motor, pure sensory, sensorimotor and ataxic hemiparesis." "The defining feature is absence of cortical signs and absence of a visual field defect." "Hypertension is the major risk factor for lacunes, leukoaraiosis and microhaemorrhages." "Prognosis: one-year mortality about 10%, but 50% of survivors remain dependent." "LACI-2 (2023) showed isosorbide mononitrate reduced recurrent stroke and cognitive impairment, and cilostazol reduced dependence — two cheap licensed drugs awaiting phase 3 confirmation."

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