A 60-year-old male is admitted to the ICU for severe hypertension complicated by a headache. The patient has a past medical history of insulin-controlled diabetes, hypertension, and hyperlipidemia. He smokes 2 packs of cigarettes per day. He states that he forgot to take his medications yesterday and started getting a headache about one hour ago. His vitals on admission are the following: blood pressure of 160/110 mmHg, pulse 95/min, temperature 98.6 deg F (37.2 deg C), and respirations 20/min. On exam, the patient has an audible abdominal bruit. After administration of antihypertensive medications, the patient has a blood pressure of 178/120 mmHg. The patient reports his headache has increased to a 10/10 pain level, that he has trouble seeing, and he can't move his extremities. After stabilizing the patient, what is the best next step to diagnose the patient's condition?

CT head without intravenous contrast

Doppler ultrasound of the carotids

CT head with intravenous contrast

MRI head without intravenous contrast

MRI head with intravenous contrast

A 73-year-old man is brought to the emergency department by ambulance after being found to be non-communicative by his family during dinner. On presentation he appears to be alert, though he is confused and cannot follow instructions. When he tries to speak, he vocalizes a string of fluent but unintelligible syllables. Given this presentation, his physician decides to administer tissue plasminogen activator to this patient. This intervention best represents which of the following principles?

This does not represent prevention

A 75-year-old woman presents with sudden loss of vision. She says that she was reading when suddenly she was not able to see the print on half of the page. Her symptoms started 4 hours ago and are accompanied by a severe posterior headache. Vital signs reveal the following: blood pressure 119/76 mm Hg, pulse 89/min, SpO2 98% on room air. The patient was unable to recognize her niece when she arrived to see her. A noncontrast CT of the head shows no evidence of hemorrhagic stroke. What is the most likely diagnosis in this patient?

Posterior cerebral artery stroke

A 48-year-old woman presents with acute stroke symptoms 18 hours ago. MRI shows a right MCA M1 occlusion with large penumbra on perfusion imaging (mismatch ratio >1.8) and small infarct core (25 mL). Her NIHSS is 16. She has no significant comorbidities. Her family is concerned about disability but wants to pursue treatment if reasonable chance of benefit exists. Synthesize the evidence and evaluate the treatment approach.

Mechanical thrombectomy based on perfusion imaging criteria

Intravenous alteplase as salvageable tissue is present

Intra-arterial thrombolysis combined with mechanical device

No intervention as she is outside the standard treatment window

Medical management with antiplatelet and early rehabilitation

A 55-year-old man undergoes successful thrombectomy for left MCA occlusion. Post-procedure, he develops progressive lethargy and his blood pressure increases to 180/100 mmHg. CT shows hyperdensity in the treated territory without hemorrhage, and his symptoms worsen over 4 hours despite blood pressure control. Evaluate the most likely diagnosis and management priority.

Contrast extravasation from blood-brain barrier disruption; supportive care and avoid aggressive BP lowering

Hemorrhagic transformation; reverse anticoagulation immediately

Cerebral edema from large infarction; emergent decompressive hemicraniectomy

Reperfusion injury; start high-dose corticosteroids and osmotic therapy

Recurrent arterial occlusion; emergent repeat angiography and thrombectomy

An 80-year-old woman with atrial fibrillation presents 2 hours after acute ischemic stroke. NIHSS is 22. Imaging shows large left MCA territory infarction involving >1/3 of MCA territory with basilar artery occlusion. She lives alone but was independent before this event. Her family requests all possible interventions. Evaluate the management approach considering benefits versus risks.

Thrombectomy only for basilar occlusion, avoid thrombolysis due to large infarction

Comfort measures only given poor prognosis and age

Thrombolysis alone as thrombectomy unlikely to benefit with established large infarction

Proceed with thrombolysis and thrombectomy given the therapeutic window

Delay intervention and repeat imaging in 6 hours to assess progression

Ischemic vs hemorrhagic stroke differentiation for USMLE Step 3: High-Yield Management Lessons

Initial Triage - Scan, Don't Speculate

Core presentation: Sudden onset of a focal neurological deficit. The immediate priority is to differentiate between ischemic and hemorrhagic types, as treatments are diametrically opposed.

Clinical Features (FAST mnemonic 📌):
- Face Drooping
- Arm Weakness
- Speech Difficulty
- Time to call 911

Feature	Ischemic Stroke	Hemorrhagic Stroke
Pathophysiology	Vascular occlusion (thrombus/embolus)	Vessel rupture & bleeding
Initial CT	Often normal initially (hypodensity later)	Hyperdense (bright) blood
Acute Goal	Restore blood flow (e.g., tPA, thrombectomy)	Control bleeding, ↓ICP

Ischemic Stroke - The Clot Thickens

Pathophysiology: Brain tissue death from ↓ blood flow, creating a pale infarct. Surrounding salvageable tissue is the ischemic penumbra.
Etiology:
- Thrombotic: Local clot on an atherosclerotic plaque (e.g., carotid bifurcation).
- Embolic: Clot from a distant source (e.g., atrial fibrillation).

Vessel	Area Supplied	Clinical Deficit
MCA	Lateral cortex	Contralateral face/arm weakness, aphasia (dominant), neglect (non-dominant)
ACA	Medial cortex	Contralateral leg weakness, personality changes
PCA	Occipital lobe	Contralateral homonymous hemianopia w/ macular sparing

Acute Management: Thrombolysis with tPA if within <4.5 hours; BP must be <185/110 mmHg.

⭐ Lacunar Strokes: Small vessel strokes in deep brain structures (basal ganglia, thalamus) from hyaline arteriosclerosis, often due to hypertension or diabetes. They cause pure motor or pure sensory deficits.

Hemorrhagic Stroke - A Bloody Mess

Results from vessel rupture and bleeding into brain parenchyma or the subarachnoid space, creating a "red infarct." Management focuses on controlling bleeding and intracranial pressure (ICP).

Primary Causes:
- Chronic hypertension (most common for ICH)
- Ruptured saccular (berry) aneurysm (most common for SAH)
- Arteriovenous malformation (AVM)

CT scans of various intracranial hemorrhages

Feature	Intracerebral (ICH)	Subarachnoid (SAH)
Location	Brain parenchyma	Subarachnoid space
Cause	Hypertension, AVM	Aneurysm rupture
Presentation	Focal deficits, headache	"Worst headache of my life"
LP	Contraindicated (risk of herniation)	Blood/xanthochromia

⭐ Xanthochromia (yellow CSF) on lumbar puncture is a classic sign of SAH, appearing 6-12 hours after the bleed due to bilirubin from RBC breakdown.

The first and most critical step for all suspected strokes is a non-contrast head CT.

Ischemic stroke: CT is often normal in the first 6-24 hours, later showing a hypodense (dark) lesion.

Hemorrhagic stroke: CT immediately reveals hyperdense (bright) blood.

Hemorrhage often presents with severe headache, vomiting, and altered mental status.

This distinction is vital: tPA is for ischemic strokes and is contraindicated in hemorrhagic strokes.

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