GeriQBank · Paper II · Q6
Lacunar Stroke
- Topic
- Stroke & Neurology
- Chapter
- Cerebrovascular Disease
- Years asked
- Not recorded in the source
- Frequency
- No university frequency data for this paper yet
Detailed answer
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Answer
Textbook Core – 6 Points
Definition and pathology. A small subcortical infarct, less than 15–20 mm in diameter, resulting from occlusion of a single deep penetrating artery (lenticulostriate, thalamoperforating or pontine perforator). It accounts for about 25% of all ischaemic strokes. The underlying pathology is lipohyalinosis and microatheroma of the small vessel, driven above all by hypertension and diabetes — not by embolism.
The five classical lacunar syndromes. Pure motor hemiparesis (posterior limb of the internal capsule or pons — the commonest); pure sensory stroke (ventral posterolateral thalamus); sensorimotor stroke; ataxic hemiparesis (pons or internal capsule); and dysarthria–clumsy hand syndrome (pons or genu of the internal capsule).
The defining negatives. There are no cortical signs — no aphasia, no neglect, no visual field defect, no altered consciousness and no seizure. In pure motor hemiparesis, the face, arm and leg are affected equally. These negatives are what earn marks and what distinguish a lacune from a cortical infarct.
Investigations. MRI with DWI is far superior to CT for small deep infarcts, which are frequently invisible on CT. Look also for the accompanying markers of cerebral small-vessel disease: white matter hyperintensities (leukoaraiosis), microbleeds on SWI, enlarged perivascular spaces and old silent lacunes. Still perform ECG, carotid Doppler and echocardiography to exclude a cardioembolic or large-artery source, though the cause is usually intrinsic small-vessel disease.
Treatment. Thrombolysis remains indicated within the time window — lacunar strokes benefit. Single antiplatelet therapy is the mainstay, with a 21-day course of dual therapy only for high-risk minor stroke. Add a high-intensity statin, and above all aggressive blood pressure control — the SPS3 trial showed that a systolic target below 130 mmHg reduced intracerebral haemorrhage. Control diabetes and stop smoking.
Prognosis and complications. Early functional recovery is usually good, but there is a high long-term risk of recurrence, vascular cognitive impairment and vascular parkinsonism. The accumulated multilacunar state produces pseudobulbar palsy, emotional lability, marche à petits pas, gait apraxia and falls. Long-term dual antiplatelet therapy must be avoided — SPS3 showed no benefit but significantly more bleeding and higher mortality.
Latest Update – 1 Point
AHA/ASA 2026 Acute Ischaemic Stroke Guideline — low NIHSS is no longer a reason to withhold thrombolysis. The guideline emphasises rapid thrombolysis for any eligible patient with a disabling deficit within 4.5 hours, regardless of NIHSS score and without waiting for advanced imaging. This matters specifically for lacunar stroke, which characteristically scores low on the NIHSS yet may be severely disabling (isolated hand weakness, ataxic hemiparesis, dysarthria–clumsy hand). Tenecteplase 0.25 mg/kg as a single bolus is now a Class 1 alternative to alteplase. The INSPIRES trial additionally supports starting dual antiplatelet therapy up to 72 hours in minor strokes of atherosclerotic origin.
Examiner’s Tip — Verbatim Mark-Earning Lines
“A lacunar syndrome is defined as much by what is absent as by what is present — no aphasia, no neglect, no field defect, no altered consciousness.”
“Blood pressure control is the single most important intervention in small-vessel disease.” “Do not continue dual antiplatelet therapy long term after a lacunar stroke — SPS3 showed harm.” Skeleton: Definition/lipohyalinosis → Five syndromes → Cortical-sign negatives → MRI + small-vessel markers → BP, statin, antiplatelet → Recurrence/vascular cognitive impairment → AHA/ASA 2026.
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References
- PAPERS-2-3-4_COMBINED.pdf — page 273
- GeriQBank source PDF — p. 273
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