A 58-year-old man with a 12-year history of poorly controlled hypertension and type 2 diabetes presents with acute onset weakness of the right face, arm, and leg occurring 2 hours ago. CT brain shows a small hypodense lesion in the region marked **C** on the axial basal ganglia level image. Neurological examination reveals equal weakness across face, arm, and leg with intact language, normal visual fields, and normal sensation. Which of the following best explains the clinical presentation and guides acute management?

Explanation

## Why option 1 is right The internal capsule (structure **C**) is the most common site of lacunar infarcts due to lipohyalinosis of small penetrating lenticulostriate branches of the MCA. This is strongly associated with chronic hypertension and diabetes, both present in this patient. The posterior limb of the internal capsule carries corticospinal tract fibers in somatotopic arrangement (face → arm → trunk → leg anteroposteriorly), explaining why this patient has equal weakness of face, arm, and leg—the hallmark of "pure motor hemiparesis," one of the five classic lacunar syndromes. Critically, there are NO cortical features (no aphasia, no visual field defect, no sensory loss), which distinguishes this from cortical MCA strokes. Modern evidence (post-2015) shows that lacunar infarcts are NO LONGER excluded from IV thrombolysis and can be treated within the 4.5-hour window like other acute ischemic strokes. [Gray's Anatomy 42e Ch 23; Harrison 21e Ch 426] ## Why each distractor is wrong - **Option 2**: While MCA occlusion can cause hemiparesis, cortical strokes typically present with disproportionate weakness (face/arm > leg) and cortical features such as aphasia, neglect, or visual field defects—none of which are present here. Mechanical thrombectomy is indicated for large vessel occlusion, not small vessel lacunar disease. - **Option 3**: Pure sensory stroke is a different lacunar syndrome caused by thalamic infarction (structure **D**), not internal capsule involvement. This patient has motor, not sensory, deficits. - **Option 4**: Pontine infarcts present with crossed syndromes (ipsilateral cranial nerve + contralateral limb signs) and are caused by basilar artery disease, not lenticulostriate branch disease. Anticoagulation is not standard for lacunar infarcts; antiplatelet therapy is preferred. **High-Yield:** Internal capsule lacunar infarcts → pure motor hemiparesis with equal face/arm/leg weakness, no cortical signs; eligible for IV thrombolysis within 4.5 hours; secondary prevention focuses on aggressive BP control, statin, and antiplatelet therapy. [Gray's Anatomy 42e Ch 23; Harrison 21e Ch 426]