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Q1: TIA vs stroke (2 min)
"How do you define a TIA, and how is that definition different from how it used to be taught?"
- The old definition was purely time-based: a focal neurological deficit resolving within 24 hours.
- The modern, tissue-based definition instead relies on imaging — a TIA is a transient episode of neurological dysfunction without evidence of acute infarction on MRI, regardless of how quickly symptoms resolved.
- This matters because a substantial number of clinically "resolved" episodes under the old 24-hour rule actually show infarction on diffusion-weighted MRI — meaning they were small strokes, not TIAs, and carry different (higher) early recurrence risk.
- The ABCD2 score (Age, BP, Clinical features, Duration, Diabetes) still guides urgency of specialist assessment after a TIA regardless of which definition is used.
Q2: The CT-first principle (2 min)
"A patient presents with sudden hemiparesis. Why do you get a CT brain before an MRI, and what are you actually looking for?"
- CT is fast, universally available, and — critically — its main job in the acute setting is not to diagnose the ischaemic stroke (which can be entirely CT-silent in the first few hours) but to exclude haemorrhage.
- That single distinction — ischaemic versus haemorrhagic — determines the entire treatment pathway, and the two treatments are opposite: thrombolysis/antithrombotics for ischaemic stroke would be catastrophic if given for an undiagnosed bleed.
- Subtle early ischaemic signs on CT include a hyperdense MCA sign, loss of the insular ribbon, and sulcal effacement — but their absence does not exclude ischaemic stroke.
- CT angiography is added when a large-vessel occlusion is suspected, to select thrombectomy candidates.
Q3: The reperfusion algorithm (3 min)
"Walk me through the treatment of an ischaemic stroke presenting at 2 hours from onset with a dense hemiparesis and aphasia."
- Confirm the time window: within 4.5 hours for thrombolysis eligibility.
- Check BP is under 185/110 mmHg; treat with IV labetalol/nicardipine first if not.
- Give IV alteplase 0.9 mg/kg (max 90 mg) — 10% bolus over 1 minute, 90% infused over 1 hour — once haemorrhage and other contraindications are excluded.
- The clinical picture (dense hemiparesis + aphasia) raises suspicion of a large-vessel occlusion — obtain urgent CT angiography in parallel; if confirmed, proceed to mechanical thrombectomy, which can be offered from 0–6 hours without further selection, or up to 24 hours with a favourable imaging mismatch on CT perfusion or MRI.
- Thrombolysis and thrombectomy are not mutually exclusive — bridging therapy (thrombolysis followed by thrombectomy) is standard where both are available and the patient is eligible for each.
Q4: Blood pressure — the two opposite rules (2 min)
"Why do you treat blood pressure so differently in ischaemic stroke versus intracerebral haemorrhage?"
- In acute ischaemic stroke, blood pressure is generally managed permissively (the 185/110 threshold is only a ceiling required specifically to allow thrombolysis) — cerebral autoregulation is disrupted around the infarct, so aggressively lowering BP can drop perfusion to the vulnerable penumbra and worsen the infarct.
- In intracerebral haemorrhage, the opposite applies: blood pressure is actively lowered, with a systolic target under 140 mmHg, because higher pressure drives ongoing haematoma expansion, which is the dominant modifiable determinant of outcome in ICH.
- After successful thrombolysis, however, BP is actively kept under 180/105 mmHg for 24 hours — to limit the risk of haemorrhagic transformation of the newly reperfused, at-risk tissue.
Q5: Secondary prevention by mechanism (2 min)
"A patient has an ischaemic stroke. How does your secondary prevention differ if the cause is atrial fibrillation versus large-artery atherosclerosis?"
- Cardioembolic (AF): anticoagulation, typically started 2–14 days after the event (balancing haemorrhagic transformation risk against recurrence risk), with a DOAC generally preferred over warfarin.
- Non-cardioembolic (large-artery/lacunar): antiplatelet therapy — aspirin then long-term aspirin or clopidogrel monotherapy; for minor stroke or high-risk TIA, dual antiplatelet therapy for 21 days (aspirin + clopidogrel) then stepping down to monotherapy.
- Both groups also receive a high-intensity statin, blood-pressure control, glycaemic control, and smoking cessation — and symptomatic carotid stenosis over 70% is an indication for carotid endarterectomy regardless of antithrombotic choice.
Q6: The malignant MCA scenario (2 min)
"Day 2 after a large left MCA infarct, the patient's conscious level drops. What's happening, and what do you do?"
- This is the classic presentation of malignant MCA syndrome — massive cerebral oedema in a large territory infarct causing raised intracranial pressure and, if untreated, herniation.
- Urgent CT to confirm the extent of oedema/midline shift.
- Decompressive hemicraniectomy within 48 hours is the definitive treatment in appropriately selected (typically younger) patients — it substantially reduces mortality, though patients who survive may have significant residual disability, which is part of the shared decision-making conversation with family.