Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Hypertension |Small Vessel Disease |CADASIL |CARASIL

Lacunar strokes are likely part of the spectrum of small vessel disease (SVD), which affects small arteries, arterioles, venules, and capillaries in the brain. SVD has long been associated with cognitive impairment and dementia. Lacunes are predictors of cognitive decline in cerebral small-vessel disease.

Historical Aspects

• The concept of lacunar stroke was first described by Dechambre in the early 1800s.
• Lacunes were initially identified as small cavities found at post-mortem examinations.
• Charles Miller Fisher further refined the clinical correlation in the 1960s, identifying about 15 clinical types of lacunar strokes.

Introduction

• Lacunar strokes account for 20% to 30% of all ischemic strokes.
• Short-term prognosis is generally good, but they indicate an increased risk of long-term mortality and cognitive decline.
• Lacunes involve small branches of larger arteries (<0.4 mm in diameter) and are typically end arteries without collaterals.
• These small vessels branch off larger arteries (4-8 mm in diameter), creating a 10-fold drop in size, making them more vulnerable to elevated blood pressure.
• Lacunar strokes overlap significantly with small vessel disease (SVD), with SVD being the underlying pathology and lacunar strokes as the clinical manifestation.
• The ostia of the penetrating vessels may become occluded by a thrombus within the main vessel's lumen, resulting in strokes larger than a typical lacune, which do not represent true penetrating artery disease.

Vessels and Sites

• Lenticulostriate arteries (MCA)
• Anterior striate arteries
• Heubner arteries
• Thalamoperforators (PCA)
• Deep perforators of the basilar artery
• Deep cerebral white matter
• Basal ganglia
• Basis pontis due to occlusion of a single small perforating artery supplying subcortical areas.

Aetiology

• Hypertension is documented in 90% of those with lacunar strokes, though this has been questioned in some studies.
• More common in individuals of African Caribbean descent, and those with diabetes and hypertension.
• Acute lesions are well visualized on MRI and sometimes on CT.
• Lacunar infarcts are typically rounded cavities <1.5 cm in diameter.
• Occlusion is caused by lipohyalinosis, fibrinoid necrosis, or microemboli.
• Microatheroma and arteriolosclerosis are associated with common vascular risk factors.
• Areas affected by lacunar infarcts are also prone to hypertensive bleeds and microbleeds, which may leave behind small cavities.

Anatomy of Lesions

• Centrum semiovale, caudate nucleus, internal capsule
• Globus pallidus, putamen, and thalamus
• Brainstem and midline cerebellum
• Rounded infarcts <1.5 cm in diameter
• Small vessels exposed to elevated blood pressures

Risk Factors

• 90% have a history of hypertension.
• More common in individuals of African Caribbean descent.
• Diabetes and smoking are also significant risk factors.

Vessels Affected

• Medial and lateral lenticulostriate branches of ACA/MCA
• Thalamogeniculate and thalamoperforant branches of PCA
• Paramedian branches of the basilar artery

Clinical Lacunar Syndromes

Lacunar strokes are typically subcortical, affecting white matter tracts. As a result, they often do not present with cognitive impairment, aphasia, or other higher cortical functions. However, they may present in a staggered or slow manner.

Differential Diagnosis

• Striatocapsular infarcts: Embolic occlusion of the MCA can affect penetrating branches, resulting in subcortical infarctions that are larger and more crescentic in shape compared to lacunar strokes.
• Microbleeds: These can occur in similar areas as lacunes and may leave behind small cavities. Gradient echo MRI may be needed for better differentiation.
• Vascular spaces: Non-pathological spaces seen in subcortical areas, which may be mistaken for lacunes.

Investigations

• Blood Tests: FBC, U&E, LFTs, ESR
• ECG: Look for evidence of LVH changes.
• CT Scan: Can detect lesions >2 mm. Lacunar infarcts appear as rounded lesions <15 mm in penetrating artery distributions (e.g., brainstem, thalamus, internal capsule).
• MRI: More sensitive, especially for pons lesions. Acute lesions show restricted diffusion and reduced ADC. Gradient echo sequences can help distinguish old ischemic from hemorrhagic cavities.
• Angiography: May reveal small vessel occlusion due to large vessel disease or non-occlusive thrombus.
• Screening for CADASIL: If clinically indicated.

Management

• Aggressive lifelong management of hypertension to <140/90 mmHg is crucial.
• Address coexisting conditions like diabetes, elevated lipids, and encourage smoking cessation.
• Consider antiplatelets and statins, although the evidence is less robust than for other ischemic stroke causes.

References

• What causes lacunar stroke?