What are the differences between lacunar strokes, lenticulostriate lesions, and anterior choroidal lesions in terms of presentation and management?

Distinguishing Lacunar Stroke, Lenticulostriate Lesions, and Anterior Choroidal Lesions

These three entities represent overlapping but distinct subcortical stroke patterns that differ primarily in their vascular territory, underlying mechanisms, clinical presentations, and management implications—with lenticulostriate and anterior choroidal lesions representing specific anatomic subtypes that may or may not qualify as true lacunar strokes depending on size, location, and etiology.

Lacunar Stroke: The Broader Category

Lacunar strokes are small (<1.5 cm) subcortical infarcts caused primarily by small vessel disease (lipohyalinosis), located in the basal ganglia, brain stem, or deep white matter, presenting with classic lacunar syndromes like pure motor hemiparesis. 1, 2

Key Defining Features:

• Size criterion: Must be <1 cm (some sources use <1.5 cm) in maximal dimension 3, 1
• Location restriction: Basal ganglia, brain stem, or deep white matter—NOT cerebral cortex 3
• Primary mechanism: Small vessel disease (lipohyalinosis) in 78% of cases, NOT large artery atherosclerosis 4
• Prognosis: Best survival among stroke subtypes (85% at 2 years) with lower early mortality and recurrence rates 3, 1

Clinical Presentation:

• Pure motor hemiparesis (most common) 1
• Sensorimotor stroke (when thalamic involvement) 5
• Ataxic hemiparesis 6
• Pure sensory stroke 3

Critical Diagnostic Requirements:

You cannot diagnose lacunar stroke on clinical syndrome alone—you must exclude cardioembolic sources and ipsilateral large artery stenosis >50%. 2 This requires:

• Transthoracic echocardiography 2
• Extended cardiac monitoring for atrial fibrillation 2
• Carotid imaging within 48 hours 2

Lenticulostriate Lesions: The Embolic Variant

Lenticulostriate infarcts involve the deep perforating branches of the middle cerebral artery (MCA) and are predominantly caused by cardioembolism rather than small vessel disease, making them mechanistically distinct from typical lacunar strokes. 7

Distinguishing Characteristics:

• Vascular territory: Supplied by lenticulostriate arteries arising from the MCA main trunk or cortical branches 7
• Primary mechanism: Cardiac embolism is the principal cause, NOT lipohyalinosis 7
• Anatomic location: Primarily affects the upper posterior limb of the internal capsule 6, 7
• Hemorrhagic risk: Higher risk of hemorrhagic transformation due to terminal arteries without anastomoses 7

Clinical Features:

• Motor deficit (most prominent) 7
• Sensory deficit 7
• Cognitive dysfunction 7
• Sensorimotor stroke when mild-to-moderate: 80% have lacunes when hemiparesis is incomplete, versus only 33% with complete motor/sensory impairment 5

Management Implications:

Because lenticulostriate infarcts are predominantly embolic, these patients require aggressive cardiac workup and may need anticoagulation rather than antiplatelet therapy alone. 2, 7 The prognosis depends primarily on damage intensity to the upper posterior limb of the internal capsule 7.

Anterior Choroidal Artery (AchA) Lesions: The Heterogeneous Group

Anterior choroidal artery infarctions represent a heterogeneous group where lesions confined to the posterior limb of internal capsule (pAchA) behave like small vessel disease, while those extending beyond (dAchA) are more often embolic with worse outcomes. 4

Two Critical Subtypes:

Probable AchA (pAchA) Infarction:

• Location: Confined to lower part of posterior limb of internal capsule (PLIC) 4
• Mechanism: Small artery disease in 78% of cases 4
• Clinical severity: Less severe neurologic deficits 4
• Caveat: May actually be supplied by lenticulostriate arteries rather than true AchA territory 4

Definite AchA (dAchA) Infarction:

• Location: Involves lateral geniculate body, uncus, or cerebral peduncle in addition to PLIC 4
• Mechanism: Cardioembolism (12% vs 2%, p=0.03) and distal internal carotid artery disease (35% vs 2%, p=0.001) much more common 4
• Clinical severity: Higher NIHSS scores and more severe limb weakness 4
• Small vessel disease: Only 56% (vs 78% in pAchA, p=0.02) 4

Anatomic Considerations:

The posterior limb of internal capsule and adjacent paraventricular region (70% of lacunar lesions) is the most frequently involved area, supplied predominantly by the anterior choroidal artery. 6 This makes AchA the predominant deep penetrating artery involved in lacunar stroke syndromes 6.

Clinical Syndromes by Tract Involvement:

• Corticospinal tract alone: Pure motor stroke 6
• Corticospinal + thalamocortical tracts: Sensorimotor stroke 6, 5
• Cerebellar pathways (dentatorubrothalamocortical/corticopontocerebellar): Ataxic hemiparesis 6

Management Algorithm Based on Lesion Type

Step 1: Confirm Lesion Size and Location

• If <1 cm in basal ganglia/brainstem/deep white matter: Proceed as potential lacunar stroke 3, 1
• If involves lateral geniculate/uncus/cerebral peduncle: Definite AchA—higher suspicion for large vessel or cardioembolic source 4

Step 2: Exclude Alternative Mechanisms

This is mandatory even when imaging suggests lacunar pattern: 2

• Echocardiography (minimum transthoracic) 2
• Extended cardiac monitoring 2
• Carotid imaging for stenosis >50% 2
• Lipid profile and HbA1c 2

Step 3: Mechanism-Based Treatment

• Small vessel disease confirmed: Antiplatelet therapy + aggressive risk factor modification (BP target <130 mmHg systolic) 3, 1, 8
• Cardioembolism identified: Anticoagulation required regardless of small infarct size 2
• Distal ICA stenosis (especially with dAchA): Consider more aggressive antiplatelet therapy or intervention 4

Critical Pitfalls to Avoid

The most dangerous error is assuming all small subcortical infarcts are lacunar strokes due to small vessel disease. 2, 4 This leads to:

• Undertreatment of patients with atrial fibrillation who need anticoagulation 2
• Missing significant carotid or intracranial stenosis requiring specific management 4
• Failure to recognize embolic mechanisms in lenticulostriate and definite AchA infarctions 4, 7

The inconsistent results in AchA infarction literature stem from variable inclusion of isolated PLIC lesions, which may actually be lenticulostriate territory rather than true AchA. 4 This explains why some studies show predominantly small vessel disease while others emphasize embolic mechanisms.

Sensorimotor stroke should only be classified as lacunar syndrome when hemiparesis and sensory loss are mild-to-moderate and incomplete—complete deficits suggest larger vessel involvement. 5