A 58-year-old man with a 20-year history of poorly controlled hypertension presents with acute onset of weakness affecting his right face, arm, and leg equally, with preserved sensation and no speech disturbance. Imaging reveals a small lacunar infarct in the distribution of the lenticulostriate branches of the middle cerebral artery. The structure marked **C** in the diagram is responsible for this clinical presentation. Which of the following best explains why motor deficits in this location characteristically spare sensory function and language?

Explanation

## Why option 1 is right The posterior limb of the internal capsule (**C**) contains exclusively corticospinal tract fibers arranged in precise somatotopic order (face → upper limb → trunk → lower limb anteroposteriorly). A lacunar infarct here produces "pure motor hemiparesis" — motor deficits affecting face, arm, and leg equally — because all motor fibers are disrupted proportionally. Sensory function is preserved because thalamocortical sensory fibers travel in the posterior thalamic radiations and anterior limb of the internal capsule, not in the posterior limb. Language is preserved because Broca's area and its efferent connections (corticobulbar fibers in the genu) remain intact. This anatomical segregation is the hallmark of lacunar syndromes and distinguishes them from cortical strokes, where adjacent cortical areas may be affected, causing disproportionate deficits or additional cognitive/sensory loss (Gray's Anatomy 42e Ch 23; Harrison 21e Ch 426). ## Why each distractor is wrong - **Option 2**: While the genu does contain corticobulbar fibers, lacunar infarcts in the posterior limb do NOT preferentially spare the genu. The question describes a pure motor hemiparesis affecting face + arm + leg equally, which indicates the infarct involves the entire posterior limb somatotopy, not just sparing the genu. The facial weakness is present, not spared. - **Option 3**: Although the lenticulostriate arteries do supply the posterior limb, they also supply portions of the thalamus and other deep structures. More critically, this option misses the key anatomical point: sensory pathways (thalamocortical radiations) do NOT travel through the posterior limb of the internal capsule; they travel in different fiber bundles. The sparing of sensation is due to anatomical segregation of fiber tracts, not arterial supply patterns. - **Option 4**: Lipohyalinosis affects the small penetrating arteries (lenticulostriate branches) supplying the internal capsule itself, not brainstem motor neurons. The infarct is in the internal capsule, not the brainstem. This option confuses the location of the lesion and is anatomically incorrect. **High-Yield:** Pure motor hemiparesis = posterior limb internal capsule lacunar infarct; preserved sensation + language = proof that sensory and language pathways are NOT in the posterior limb. [cite: Gray's Anatomy 42e Ch 23; Harrison 21e Ch 426]