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[Cerebral lacunae: still under debate].

C Derouesné¹, J Poirier

¹Service d'Urgences cérébrovasculaires, Groupe Hospitalier Pitié-Salpêtrière, Paris.

Revue Neurologique

|November 5, 1999

Summary

Cerebral lacunes, once thought to be specific stroke syndromes, are now understood to have diverse causes and clinical presentations. New research re-evaluates lacunar infarction, linking silent lacunes and white matter changes to cognitive impairment risks.

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Area of Science:

Neurology
Neuroimaging
Pathology

Context:

Advancements in Magnetic Resonance Imaging (MRI) have renewed interest in cerebral lacunes.
The traditional Fisher lacunar hypothesis is challenged by new clinical and epidemiological data.

Purpose:

To re-evaluate the concept of lacunar infarction based on recent clinical, epidemiological, and pathological findings.
To differentiate between types of lacunar infarcts and their underlying pathologies.

Summary:

Lacunar infarcts (type 1a) result from large perforating artery atherosclerosis.
Silent lacunar infarcts (type 1b) stem from microangiopathy affecting small perforating artery branches.
Silent lacunes and dilated perivascular spaces (type 3) correlate with white matter hyperintensities in elderly individuals, linked to small vessel disease and blood pressure dysregulation.

Impact:

Lacunar infarcts and white matter hyperintensities are significant risk factors for Vascular Cognitive Impairment.
These lesions are frequently associated with Alzheimer's disease.
The pathophysiology of giant or expanding type 3 lacunes remains an area for further investigation.

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