A 58-year-old man with a 15-year history of poorly controlled hypertension (BP 160/95 mmHg) presents to the emergency department with acute onset of right-sided weakness affecting his face, arm, and leg equally. MRI brain with diffusion-weighted imaging shows a small acute infarct in the region marked **C** on the axial section through the internal capsule. Neurological examination reveals no aphasia, no visual field defects, and no sensory loss. Which of the following best describes the clinical syndrome and the mechanism of this stroke?

Explanation

## Why option 1 is correct The posterior limb of the internal capsule (marked **C**) contains corticospinal fibers arranged somatotopically (face → arm → trunk → leg from anterior to posterior). A lacunar infarct in this region, caused by lipohyalinosis of the lenticulostriate branches of the middle cerebral artery (MCA) secondary to chronic hypertension, produces **pure motor hemiparesis** — one of the five classic lacunar syndromes. The hallmark is equal motor weakness of the face, arm, and leg (unlike cortical strokes, which often spare the leg or disproportionately affect face/arm). Critically, there are NO cortical features: no aphasia, no neglect, no visual field defects, and no sensory loss. This patient's clinical presentation and imaging findings are pathognomonic for this syndrome. (Harrison 21e, Ch 426; Lacunar stroke classification.) ## Why each distractor is wrong - **Option 2 (Sensorimotor stroke from cardiac embolism)**: Sensorimotor stroke is a different lacunar syndrome (affecting both motor and sensory modalities) and is not caused by cardioembolic disease; it results from small vessel disease in the thalamus or internal capsule region. The absence of sensory loss in this patient rules out sensorimotor stroke. - **Option 3 (Cortical motor stroke with proximal MCA occlusion)**: Cortical strokes typically present with disproportionate weakness (face and arm more than leg), often accompanied by aphasia, neglect, or visual field defects. The equal distribution of weakness and absence of cortical signs exclude this diagnosis. Additionally, proximal MCA occlusion causes large vessel disease, not lacunar infarction. - **Option 4 (Ataxic hemiparesis from pontine infarct)**: Ataxic hemiparesis is a lacunar syndrome, but it originates from pontine infarcts (not internal capsule) and is characterized by cerebellar signs (ataxia) combined with motor weakness. The clinical presentation here lacks ataxia and dysarthria, and the imaging shows internal capsule involvement, not pontine pathology. **High-Yield:** Pure motor hemiparesis = posterior limb internal capsule lacunar infarct from lipohyalinosis (chronic HTN) → equal face + arm + leg weakness, NO cortical signs, NO sensory loss. [cite: Harrison 21e, Ch 426; Lacunar stroke syndromes and small vessel disease pathophysiology]