What are the neurologic manifestations of lacunar infarcts in older adults with hypertension, diabetes, or small‑vessel disease?

Neurologic Manifestations of Lacunar Infarcts

Lacunar infarcts present with one of five classical lacunar syndromes that reflect their characteristic location in deep brain structures supplied by single penetrating arteries, without cortical signs such as aphasia, neglect, or visual field defects. 1, 2

Classical Lacunar Syndromes (in order of frequency)

1. Pure Motor Hemiparesis (Most Common)

• Weakness affecting face, arm, and leg on one side without sensory loss, visual deficits, or higher cortical dysfunction 2, 3
• Results from infarction in the internal capsule, corona radiata, or basis pontis 1

2. Pure Sensory Syndrome

• Isolated hemisensory loss affecting face, arm, and leg without motor weakness 2, 3
• Typically caused by thalamic lacunar infarcts 4

3. Sensorimotor Stroke

• Combined motor weakness and sensory loss on the same side 2, 3
• Occurs with lesions affecting both motor and sensory pathways in close proximity 1

4. Ataxic Hemiparesis

• Combination of weakness and cerebellar-type ataxia on the same side, disproportionate to the degree of weakness 2, 3
• Results from lesions in the basis pontis, internal capsule, or corona radiata 1

5. Dysarthria-Clumsy Hand Syndrome

• Facial weakness, dysarthria, and dysphagia combined with mild hand weakness and clumsiness 2, 3
• Caused by lacunes in the basis pontis or genu of internal capsule 1

Key Distinguishing Features

The hallmark of lacunar syndromes is the absence of cortical signs, which differentiates them from cortical or large vessel strokes 1, 5:

• No aphasia (language dysfunction) 5
• No neglect (spatial inattention) 5
• No visual field defects (hemianopia) 5
• No apraxia (inability to perform learned movements) 1
• No agnosia (inability to recognize objects) 1

Atypical Presentations

While less common, patients may present with atypical lacunar syndromes that don't fit the five classical patterns but still lack cortical signs 2. These require careful imaging confirmation to distinguish from cortical involvement 4.

Long-Term Cognitive Manifestations

Beyond acute stroke syndromes, lacunar infarcts contribute to progressive neurologic decline 6:

• Vascular cognitive impairment develops in approximately 20% after first stroke and over one-third with recurrent strokes 6
• White matter hyperintensities are present in almost all elderly individuals with hypertension and lacunar disease, with variable severity 6
• Silent lacunar infarcts occur in 10-30% of patients, contributing to cognitive decline without obvious acute symptoms 6
• Increased risk of dementia in the mid- to long-term, even when initial presentation appears benign 2, 7

Critical Diagnostic Caveat

Facial numbness combined with facial weakness suggests cortical involvement and excludes lacunar classification, requiring different diagnostic workup and treatment considerations 5. The clinical syndrome alone is insufficient—imaging confirmation showing a small (<1.5 cm) subcortical infarct in basal ganglia, brainstem, or deep white matter is mandatory, along with exclusion of cardioembolic sources and large-artery stenosis >50% 1, 4.

Anatomic Locations

Lacunar infarcts are restricted to specific deep brain territories 1, 3:

• Basal ganglia (lentiform nucleus, caudate) 1
• Internal capsule 3
• Thalamus 1, 3
• Corona radiata 1
• Brainstem (basis pontis) 3
• Deep white matter (excluding cortex) 1

These locations correspond to territories supplied by small penetrating arteries (100-400 micrometers diameter) that branch at right angles from major cerebral vessels, making them uniquely vulnerable to hypertensive small vessel disease 3, 8.