ISCHEMIC STROKE / ETIOLOGY
Lacunar stroke
Created 02/12/2022, last revision 18/12/2022
- 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
Etiopathology| Content available only for logged-in subscribers (registration will be available soon) |
Clinical presentation
| Content available only for logged-in subscribers (registration will be available soon) |
| Content available only for logged-in subscribers (registration will be available soon) |
- 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
Differential diagnosis
| Content available only for logged-in subscribers (registration will be available soon) |
Management
Acute stroke therapy
- IV thrombolysis if eligible
- the contraindications to IV thrombolysis are the same as those for other types of acute strokes
- 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)
