In a 55‑year‑old right‑handed male smoker with hypertension and stable angina who now has persistent right‑sided facial weakness, right‑hand weakness, and aphasia (with prior transient ischemic attacks), what is the most likely anatomic pathophysiologic cause of his stroke?

Most Likely Pathophysiologic Mechanism

The most likely anatomic pathophysiologic explanation for this stroke is atherosclerotic disease of the left internal carotid artery (option 4).

Clinical Reasoning

This patient's presentation strongly points to large-artery atherosclerosis with artery-to-artery thromboembolism from the left internal carotid artery:

Key Clinical Features Supporting Left ICA Disease

• Right-sided symptoms with aphasia indicate left hemisphere involvement (language-dominant hemisphere in right-handed individuals) 1
• Progressive pattern: Two prior TIAs followed by completed stroke represents the classic "crescendo TIA" pattern characteristic of unstable carotid plaque with recurrent embolization 1
• Multiple vascular risk factors: Current smoking, hypertension (BP 170/95), and stable angina create the perfect milieu for accelerated carotid atherosclerosis 1
• Fourth heart sound (S4) indicates left ventricular hypertrophy from chronic hypertension, confirming long-standing vascular disease 1

Why This is Artery-to-Artery Embolism from Carotid Disease

Stroke and transient cerebrovascular ischemia arise from atherosclerotic extracranial cerebral arteries through several mechanisms, with embolism of thrombus formed on an atherosclerotic plaque being the most common 1. The stepwise progression over two months—brief hand weakness, then facial droop with partial aphasia, then persistent hemiparesis—reflects recurrent embolic showers from an unstable carotid plaque rather than a single catastrophic event 2, 3.

Excluding the Other Options

Option 1 (Cardiac embolism): While this patient has cardiovascular risk factors, several features argue against cardioembolism 4, 5:

• Regular pulse at 90 bpm makes atrial fibrillation unlikely 4
• No cardiac murmurs beyond the S4 (which reflects hypertensive heart disease, not valvular pathology) 4
• Progressive, stuttering course with multiple TIAs is atypical for cardioembolic stroke, which typically presents with maximal deficit at onset 4, 5
• The pattern of premonitory TIAs makes cardioembolic stroke less likely 4

Option 2 (Cerebral bleeding): Hemorrhagic stroke is excluded by 1:

• Progressive onset over days to weeks (hemorrhage is typically sudden)
• Prior transient episodes that resolved (hemorrhage doesn't spontaneously resolve)
• Clinical context requires imaging confirmation, but the question asks for pathophysiologic mechanism

Option 3 (Right MCA disease): This is anatomically incorrect 1:

• Right-sided weakness and aphasia localize to the left hemisphere, not right
• The right MCA supplies the left hemisphere's motor and language areas
• However, the pathology is upstream in the left internal carotid artery, which gives rise to the left MCA

Diagnostic Approach Required

Duplex ultrasonography is recommended to detect carotid stenosis in patients who develop focal neurological symptoms corresponding to the territory supplied by the left or right internal carotid artery 1. If ultrasound is equivocal, MRA or CTA should be obtained 1.

Critical Timing Consideration

In patients with ischemia in the territory of a stenotic carotid artery, carotid endarterectomy within the first 2 weeks reduces the risk of stroke, but the benefit of surgery diminishes with time after the initial event 1. This patient is already one week out from symptom onset, making urgent vascular imaging imperative 1.

Common Pitfall to Avoid

Do not assume this is small vessel (lacunar) disease despite the presence of hypertension and diabetes risk factors 6, 7. The presence of aphasia excludes lacunar stroke—lacunar syndromes by definition lack cortical signs such as language dysfunction 6. This patient requires evaluation for large-artery stenosis and potential cardiac sources 1, 8.

Additional Workup Still Needed

Even with presumed carotid disease, when extracranial or intracranial cerebrovascular disease is not severe enough to account for neurological symptoms of suspected ischemic origin, echocardiography should be performed to search for a source of cardiogenic embolism 1. Extended cardiac monitoring should also be considered to exclude paroxysmal atrial fibrillation 7, 8.