A 72-year-old woman with a history of atrial fibrillation (not on anticoagulation) presents with acute onset of right-sided weakness and speech difficulty. Non-contrast CT head shows a 3 cm hyperdense lesion in the left putamen with 5 mm midline shift and intraventricular extension into the left lateral ventricle. CT angiography of the head and neck is normal. Which of the following is the most likely source of this hemorrhage?

Explanation

## Hypertensive Intracerebral Hemorrhage — Putaminal Location **Key Point:** A hyperdense lesion in the **left putamen** with intraventricular extension and a normal CT angiography is the classic presentation of **hypertensive intracerebral hemorrhage (ICH)** due to rupture of **Charcot–Bouchard microaneurysms** — NOT hemorrhagic transformation of an ischemic stroke. ### Why Option B is Correct - **Putaminal location** is the single most common site (~35–50%) of hypertensive ICH. The lenticulostriate arteries supplying the putamen are end-arteries subjected to high pulsatile pressure, making them the prototypical site for Charcot–Bouchard aneurysm formation. - **Charcot–Bouchard aneurysms** (microaneurysms, 0.3–1 mm) form on small penetrating arteries (lenticulostriate, thalamoperforating) in the setting of chronic hypertension. Their rupture produces a well-defined hematoma in the basal ganglia/thalamus. - **Normal CT angiography** is expected — these are microaneurysms on small vessels below CTA resolution; CTA is performed to exclude macrovascular causes (AVM, saccular aneurysm). - **Intraventricular extension** is a common complication of putaminal ICH (blood tracks into the lateral ventricle via the caudate), consistent with hypertensive ICH. - The history of **atrial fibrillation** is a red herring; AF causes cardioembolic *ischemic* stroke, not primary ICH. The patient is NOT on anticoagulation, further reducing hemorrhagic risk from AF. ### Why the Other Options Are Incorrect | Option | Reason Incorrect | |--------|-----------------| | **A — Hemorrhagic transformation (HT)** | HT of an ischemic stroke produces petechial or confluent hemorrhage *within* an ischemic territory, typically with surrounding low-density edema. A 3 cm well-defined hyperdense putaminal hematoma with mass effect is primary ICH morphology, not HT. HT also requires a preceding ischemic event (no prior imaging evidence here). | | **C — AVM rupture** | AVM would show an abnormal vascular nidus, early draining vein, or feeding artery on CTA. CTA is normal here. | | **D — Amyloid angiopathy** | Cerebral amyloid angiopathy (CAA) causes **lobar** hemorrhages (cortical/subcortical) in elderly patients, NOT deep basal ganglia hemorrhages. Putaminal location strongly argues against CAA. | ### Classic Hypertensive ICH Locations (High-Yield) 1. **Putamen/external capsule** — 35–50% (lenticulostriate arteries) 2. **Thalamus** — 15–25% (thalamoperforating arteries) 3. **Cerebellum** — 10–15% 4. **Pons** — 5–10% 5. **Lobar** — 10–20% (often amyloid angiopathy in elderly) **Clinical Pearl:** The triad of **putaminal location + normal CTA + hypertensive history** = hypertensive ICH until proven otherwise. Atrial fibrillation causes ischemic stroke; it does not predispose to primary ICH in the absence of anticoagulation. [cite: Harrison's Principles of Internal Medicine, 21e, Ch. 430; Adams & Victor's Principles of Neurology, 11e; Robbins & Cotran Pathologic Basis of Disease, 10e, Ch. 28]