• lacunar stroke (lacunar cerebral infarct – LACI) is defined as a small subcortical lesion ≤ 1.5 cm in diameter that is caused by occlusion of small penetrating arteries
    • penetrating arteries arise at sharp angles from major vessels and are thus anatomically prone to constriction and occlusion
    • the term “lacune” was first described in the late 19th and early 20th century – it usually describes a small, chronic cavity that represents the healed phase of lacunar infarction
    • etiology of lacunar infraction is not automatically of arteriolopathic origin ⇒ occlusion can be caused by different mechanisms!
    • most commonly basal ganglia (globus pallidus, putamen, thalamus, and caudate), the pons, and the subcortical white matter structures (internal capsule and corona radiate) are affected
  • lacunar stroke syndrome (LACS) is a clinical manifestation of lacunar stroke; the most common are:
    • pure motor hemiparesis
    • pure sensory stroke
    • sensorimotor stroke
    • ataxic hemiparesis
    • dysarthria-clumsy hand syndrome

Etiopathology

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Penetrating artery disease with a parent artery atherosclerosis
Arteriolopathy - small vessel disease (TOAST 3)

Clinical presentation

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  • a silent lacunar infarction (SLI) is an accidental finding on imaging methods without a history of stroke symptoms
  • silent strokes are much more common than previously thought
  • SLI increases the risk of a future major stroke, and multiple lesions can become symptomatic (lacunar state)
  • multiple lesions can affect various aspects of a person’s mood, personality, and cognitive functioning (lacunar state / Binswanger´s disease)

Diagnostic evaluation

  • brain imaging (CT/MRI)
    • excludes hemorrhage
    • DWI has higher sensitivity for acute infarcts when compared with other sequences or CT
    • in the acute phase, CT or even MRI can be negative; later, a small noncortical infarct can be visualized
  • vessel imaging (CTA/MRA)
    • excludes large vessel occlusion/stenosis
    • small perforating arteries are hard to visualize with CTA and MRA
    • high-res MRI can detect the ostial micro-atheroma of the penetrating artery; larger lesions are seen in such cases (Sun, 2018)
  • the definitive diagnosis is made by a combination of a typical lacunar syndrome + negative CTA/MRA + small, noncortical infarct seen on CT/MRI
    • typical is a history of long-standing diabetes, hypertension, and hyperlipidemia
    • such stroke is denoted to TOAST 3
  • in young patients with no risk factors, further investigation may be required to exclude embolic source
Lacunar stroke in the left thalamus
Thalamic lacunar strokes

Differential diagnosis

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Management

Acute stroke therapy

  • IV thrombolysis if eligible
  • for those patients not eligible for thrombolytic therapy, aspirin or dual antiplatelet therapy is recommended
  • routine symptomatic treatment of the acute stroke + early rehabilitation with speech and physical therapy

Prevention of cerebrovascular disease

  • antiplatelet therapy – according to CHANCE and POINT trials, dual antiplatelet therapy (DAPT – ASA+CLP) for 3 weeks followed by single antiplatelet provides the best results
    • prolonged DAPT doesn´t further decrease the risk of recurrent stroke and significantly increases the risk of bleeding
  • aggressive treatment of other vascular risk factors (typically hypertension, diabetes, hyperlipidemia, etc.)
    • high dose statin
    • aggressive hypertension treatment (target BP of 120/85 mmHg in the absence of significant extra-or intracranial stenosis)
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Lacunar stroke
link: https://www.stroke-manual.com/lacunar-stroke/