Stroke Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Thompson is a 76-year-old man who presents with sudden onset right-sided weakness and inability to speak, witnessed by his wife 90 minutes before arrival. He has a background of persistent atrial fibrillation on apixaban 5 mg twice daily, hypertension, type 2 diabetes, and dyslipidaemia. [1]

On examination his blood pressure is 168/94, heart rate is 82 and irregularly irregular. He has global aphasia, a right homonymous hemianopia, right facial droop, right arm power of 1 out of 5, and right leg power of 3 out of 5. His NIHSS is 18. Finger-prick glucose is 8.2. [1]

Non-contrast CT shows loss of grey-white differentiation in the left insular ribbon with an ASPECTS score of 9. CT angiogram confirms a left M1 middle cerebral artery occlusion. CT perfusion shows an ischaemic core of 15 mL with a penumbra of 85 mL, giving a mismatch ratio of 5.7. [1]

His main problems are:

1. Acute left MCA territory ischaemic stroke with large vessel occlusion, NIHSS 18, presenting within the reperfusion window
2. Persistent atrial fibrillation on apixaban — this is a contraindication to IV thrombolysis but he remains thrombectomy-eligible
3. Favourable imaging profile with small core and large penumbra — strong candidate for mechanical thrombectomy
4. Comorbidities requiring integrated secondary prevention: hypertension, diabetes, dyslipidaemia
5. Dysphagia risk requiring formal swallow assessment before any oral intake" [1]

Examiner probing questions and model answers

Q1: "He is on apixaban. Can you give him thrombolysis?" [1]

"No. A direct oral anticoagulant is an absolute contraindication to IV thrombolysis because the anticoagulant effect cannot be rapidly or reliably excluded by standard coagulation tests. Even if his INR is normal, apixaban inhibits factor Xa directly and the INR does not reflect its activity. Specific reversal with andexanet alfa takes too long to administer in the acute thrombolysis window and is not indicated for the purpose of enabling thrombolysis. However, he still has a large vessel occlusion and should proceed directly to mechanical thrombectomy — thrombectomy does not require the absence of anticoagulation. The thrombolysis contraindication does not preclude thrombectomy." [1]

Q2: "What is the evidence for thrombectomy in a patient presenting within 6 hours?" [1]

"The MR CLEAN trial in 2015 was the first positive randomised controlled trial of intra-arterial thrombectomy within 6 hours of anterior circulation large vessel occlusion. This was followed by four more positive trials — ESCAPE, EXTEND-IA, SWIFT-PRIME, and REVASCAT. The HERMES meta-analysis pooled individual patient data from all five trials and showed that thrombectomy doubled the rate of functional independence at 90 days, with a number needed to treat of approximately 2.6. The benefit is greatest with early reperfusion and in patients with a favourable imaging profile — small core, good collaterals. This patient's ASPECTS of 9 and core-to-penumbra ratio of 5.7 place him in the highest-benefit category." [1]

Q3: "What is the difference between the 0-6 hour and 6-24 hour thrombectomy windows?" [1]

"In the 0-6 hour window, thrombectomy is indicated for any large vessel occlusion in the anterior circulation with a reasonable ASPECTS score — imaging-guided perfusion selection is not required because the time window itself is the selection criterion. The trials (MR CLEAN, HERMES) enrolled based on CT angiogram occlusion and ASPECTS. [1]

In the 6-24 hour window, the DAWN and DEFUSE-3 trials required imaging selection to demonstrate that salvageable penumbra still exists. DAWN used a clinical-imaging mismatch (core volume small relative to NIHSS). DEFUSE-3 used perfusion imaging with specific criteria: core under 70 mL, mismatch ratio at least 1.8, and mismatch volume at least 15 mL. The rationale is that beyond 6 hours, some patients have no salvageable penumbra (the tissue has infarcted) and reperfusion provides no benefit while increasing haemorrhagic risk. Imaging-guided selection identifies those who still have tissue to save." [1]

Q4: "His 24-hour CT shows successful reperfusion. When will you restart apixaban?" [1]

"He was already on apixaban when his stroke occurred, which means this was a treatment failure. Before restarting, I would verify his adherence, confirm the dose is correct — he should be on 5 mg twice daily, and dose reduction to 2.5 mg twice daily applies only if he meets two of three criteria: age over 80, weight under 60 kg, or creatinine over 133 micromoles per litre. At 76, he likely remains on the full dose. [1]

The timing of restarting anticoagulation after a moderate stroke follows the 1-3-6-12 rule. His NIHSS was 18 on admission but improved to 8 after reperfusion. Using the post-reperfusion NIHSS of 8, he falls in the moderate category — start anticoagulation at approximately day 6. The 24-hour CT shows no haemorrhagic transformation, which supports safe resumption. I would restart apixaban and address adherence and dose. If the stroke was truly despite therapeutic apixaban, I would consider whether the mechanism is non-cardioembolic — but with persistent AF, cardioembolic is most likely, and anticoagulation remains the correct strategy." [1]

Q5: "What is his prognosis?" [1]

"His presenting NIHSS of 18 indicated a moderate-to-severe stroke with a poor prognosis without treatment — approximately 20 to 30 per cent chance of functional independence. However, successful reperfusion within 90 minutes significantly improves this — the probability of functional independence (modified Rankin Scale 0 to 2) rises to approximately 50 to 60 per cent with early complete reperfusion. His improvement from NIHSS 18 to 8 at 24 hours is a favourable early sign. Residual aphasia and right upper limb weakness will be the primary rehabilitation targets. His comorbidities — age, diabetes, and AF — are adverse prognostic factors for full recovery and increase his risk of recurrence. I would give the family an honest but cautiously optimistic assessment: early reperfusion was achieved, he is showing signs of improvement, and intensive rehabilitation gives him a reasonable chance of functional independence." [1]

Short Case Discussion

Scenario: "Examine this patient's neurological system. They were admitted 5 days ago."

Candidate presentation (model): [1]

"I examined Mrs Patel's neurological system. She is alert and cooperative, seated in a chair at 45 degrees. [1]

On general inspection, she has a left hemiparetic posture with the left arm held flexed across her chest and the left leg extended. She is attentive to her right side but ignores stimuli on her left. [1]

Cranial nerve examination reveals a left homonymous hemianopia on confrontation testing. Pupils are equal and reactive. There is a left upper motor neuron facial weakness with forehead sparing. Eye movements are full with no nystagmus. Tongue and palate are symmetrical. [1]

Motor examination of the upper limbs: tone is increased on the left with a spastic catch. Power is 2 out of 5 in the left arm and hand, 5 out of 5 on the right. In the lower limbs, tone is increased on the left. Power is 3 out of 5 in the left leg, 5 out of 5 on the right. Reflexes are brisk on the left with a left extensor plantar response. [1]

Sensory examination shows reduced light touch and pinprick sensation on the left side of the body. Joint position sense is impaired in the left fingers. On testing for extinction with double simultaneous stimulation, she extinguishes on the left — consistent with left-sided neglect. [1]

Coordination on the right is intact; it cannot be assessed on the left due to weakness. Speech is fluent with occasional word-finding difficulty but comprehension and repetition are preserved — consistent with mild anomic aphasia. [1]

In summary, these findings localise to a right middle cerebral artery territory infarct, producing a dense left hemiparesis, left hemisensory loss, left homonymous hemianopia, and left-sided neglect. The presence of neglect indicates right (non-dominant) hemisphere involvement. The dense arm weakness relative to the leg is consistent with MCA rather than ACA territory." [1]

Examiner: "What is the significance of neglect?" [1]

"Neglect is a disorder of spatial attention most commonly seen in right (non-dominant) hemisphere strokes. The right hemisphere is dominant for spatial attention for both sides of space, while the left hemisphere only attends to the right side. A right MCA stroke therefore produces left-sided neglect, whereas a left MCA stroke produces right-sided deficits but the intact right hemisphere can still attend to both sides, so neglect is uncommon. [1]

Neglect is a significant negative prognostic marker — it impairs rehabilitation participation, increases fall risk, and is associated with poorer functional outcomes. It may coexist with anosognosia (lack of awareness of the deficit). Treatment is intensive compensatory strategies and environmental modification during rehabilitation." [1]

Examiner: "How would you manage her spasticity?" [1]

"Her spasticity is at a subacute stage — 5 days post-stroke. At this early stage, the priority is maintaining range of motion with passive stretching and positioning to prevent contractures. If spasticity becomes functionally limiting or painful, I would use focal botulinum toxin injection to the affected muscles — typically the biceps, flexor carpi radialis, and finger flexors for an upper limb flexor pattern. I would avoid systemic antispasticity agents like baclofen or tizanidine at this stage because they can cause sedation and weakness that interfere with motor recovery. The goal is to treat focal spasticity that limits function while preserving motor recovery potential." [1]