Lacunar Infarct

Definition

• Localization in Clinical Neurology, 8e, p. 1380
• Symptom to Diagnosis: An Evidence Based Guide, 4th Ed.

Pathophysiology

• Plum and Posner's Diagnosis and Treatment of Stupor and Coma, p. 278
• Adams and Victor's Principles of Neurology, 12th Ed.
• Localization in Clinical Neurology, 8e, p. 1380

Risk Factors

• Arterial hypertension (primary risk factor - ~80-90% of patients with lacunar stroke have hypertension)
• Diabetes mellitus
• Smoking
• Dyslipidemia
• African-American race (incidence approximately twice that in white population)
• Rarely: CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) - the most common monogenic cause of small vessel disease

Sites of Predilection

1. Putamen (most common)
2. Basis pontis
3. Thalamus
4. Posterior limb of the internal capsule
5. Caudate nucleus

• Localization in Clinical Neurology, 8e, p. 1380
• Rosen's Emergency Medicine, 9th Ed.

Classic Lacunar Syndromes (Five Classical)

1. Pure Motor Hemiplegia (PMH) - Most Common

• Frequency: 50-67% of lacunar strokes
• Location: Posterior limb of internal capsule, corona radiata, or basis pontis
• Features: Hemiparesis/hemiplegia of face, arm, AND leg. Mild dysarthria may be present at onset
• Absent features: No aphasia, apraxia, agnosia, sensory loss, visual, or higher cortical disturbances
• Capsular warning syndrome (crescendo TIAs) may precede it

2. Pure Sensory Stroke (PSS)

• Location: Ventroposterolateral nucleus of the thalamus (most common); also internal capsule/corona radiata, subthalamus, midbrain, parietal cortex
• Features: Numbness, paresthesias, and hemisensory deficit involving face, arm, trunk, and leg. Often cheiro-oral, cheiro-pedal, or cheiro-oral-pedal pattern
• In thalamic PSS: both spinothalamic AND medial lemniscal modalities affected
• In pontine PSS: vibration/position sense impaired, but pinprick/temperature preserved (selective medial lemniscal involvement)

3. Ataxic Hemiparesis (AH) - Second Most Common

• Location: Posterior limb of internal capsule, basis pontis, corona radiata
• Features: Combination of ipsilateral cerebellar ataxia AND contralateral hemiparesis (leg > arm), often with dysarthria ("dysarthria-clumsy hand syndrome" is a variant)

4. Sensorimotor Stroke

• Location: Posterolateral thalamus and adjacent internal capsule
• Features: Both hemiparesis and hemisensory loss

5. Dysarthria-Clumsy Hand Syndrome

• Location: Basis pontis or genu of internal capsule
• Features: Dysarthria + ipsilateral hand clumsiness/weakness, facial weakness, dysphagia
• Localization in Clinical Neurology, 8e, pp. 1380-1382

Key Clinical Features

• Onset: Typically abrupt or stuttering (can evolve over hours)
• Cortical signs are ABSENT: No aphasia, agnosia, apraxia, hemianopsia, or neglect
• Consciousness preserved (unless bilateral or strategically located)
• Size: Infarcts range from a few millimeters to 2 cm
• Preceding TIAs are common, especially the capsular warning syndrome

Neuroimaging

• Acute: small hypodensity in deep brain structures
• Chronic: hypodense cystic lesion

• Acute: DWI (diffusion-weighted imaging) shows restricted diffusion (bright signal)
• Chronic (FLAIR): Hyperintense rim surrounding a hypointense cavitated core, typically 3-15 mm diameter (Fig. 444-1A from Harrison's)
• Associated findings: white matter hyperintensities (periventricular leukoaraiosis), cerebral microbleeds on T2*/SWI sequences

MRI markers: A = Lacunar infarct (FLAIR - hyperintense rim, hypointense core, left thalamus); B = Acute microinfarct (DWI); C,D = Cerebral microbleeds; E = White matter hyperintensities (Harrison's Principles, 22nd Ed., Fig. 444-1)

• Harrison's Principles of Internal Medicine, 22E, p. 3533
• Neuroanatomy through Clinical Cases, 3rd Ed.

Diagnosis

• Diagnosis requires correlation of clinical lacunar syndrome + imaging
• The mere association of a lacunar syndrome with hypertension and DM is insufficient - other stroke causes (especially cardioembolic) must be excluded
• Embolic workup (echocardiography, cardiac monitoring for AF) should be performed even when lacunar mechanism is suspected
• TOAST classification categorizes this as "small vessel occlusion"

Management

• IV tPA (alteplase) if within 4.5 hours of onset and eligible (same criteria as other ischemic strokes)
• Aspirin is favored over warfarin for secondary prevention in cryptogenic/lacunar stroke (clinical trial evidence supports no difference between aspirin and warfarin)

• Aggressive hypertension control (primary target - SPRINT-MIND trial supports SBP <120 mmHg)
• Antiplatelet therapy (aspirin, clopidogrel, or aspirin + dipyridamole)
• Statin therapy (for associated dyslipidemia/atherosclerosis)
• Diabetes control
• Smoking cessation
• Neuroanatomy through Clinical Cases, 3rd Ed., p. 302
• Harrison's Principles of Internal Medicine, 22E, p. 3533

Prognosis and Complications

• Good short-term prognosis for individual lacunar strokes - deficits often improve significantly (as in the case from Neuroanatomy through Clinical Cases: numbness completely resolved in 5 days)
• Risk of recurrence (stroke recurrence rate ~1% per year for pure lacunar disease)
• Multiple lacunar infarcts over time can lead to vascular dementia - a multi-infarct dementia syndrome with dementia, gait abnormalities, and pseudobulbar signs (Binswanger disease in severe white-matter predominant form)
• Associated microbleeds and white matter hyperintensities indicate ongoing small vessel disease

Summary Table