Stroke — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Margaret O'Sullivan, 72 years old, retired schoolteacher. [1]

Presenting complaint (4 weeks ago): Sudden onset right-sided weakness, slurred speech, and confusion, witnessed by her daughter. She was taken to hospital within 2 hours of symptom onset. Diagnosed with acute left MCA territory ischaemic stroke. Received IV thrombolysis and underwent mechanical thrombectomy (TICI 3 reperfusion). Discharged to inpatient rehabilitation 10 days ago; now being reviewed in the physician clinic for post-rehabilitation follow-up. [1]

Past history:

• Persistent atrial fibrillation (diagnosed 3 years ago; on apixaban 5 mg BD — confirmed adherent)
• Hypertension (15 years; on perindopril 10 mg, amlodipine 10 mg)
• Type 2 diabetes (12 years; on metformin 1g BD, empagliflozin 10 mg; HbA1c 62 mmol/mol)
• Dyslipidaemia (on atorvastatin 80 mg)
• Former smoker (ceased 3 years ago, 40 pack-year history)
• Cholecystectomy 2015 [1]

Current medications:

• Apixaban 5 mg BD
• Perindopril 10 mg OD
• Amlodipine 10 mg OD
• Metformin 1g BD
• Empagliflozin 10 mg OD
• Atorvastatin 80 mg OD
• Sertraline 50 mg OD (started for post-stroke depression 2 weeks ago) [1]

Current functional status:

• Walks with a single-point stick, moderate hemiparetic gait (circumduction of right leg)
• Right arm: proximal power 3/5, hand 1/5 (minimal function)
• Moderate expressive aphasia — can produce short phrases, comprehend complex commands
• Independent for transfers, requires assistance for dressing and showering
• Modified diet (soft, thickened fluids) due to residual mild dysphagia
• Continent of urine and bowel [1]

Examination findings (trainee elicits):

• Alert, cooperative, oriented. Speech is non-fluent with preserved comprehension (Broca-type aphasia)
• Cardiovascular: AF (irregularly irregular, 76/min), BP 148/86, no murmurs, JVP not elevated
• Neurological: right upper motor neuron facial weakness (forehead spared). Right arm: increased tone, power 3/5 proximal, 1/5 distal, brisk reflexes, extensor plantar. Right leg: power 4/5, mild spasticity, brisk reflexes. Right hemisensory loss to pinprick. No visual field defect (previously present, resolved). No neglect.
• Swallow: coughs on thin fluids at bedside [1]

Investigations (current):

• ECG: atrial fibrillation, rate 76, no acute ischaemic changes
• Lipid panel: total cholesterol 3.2, LDL 1.6, HDL 1.1
• HbA1c 62 mmol/mol
• eGFR 55
• CT head (1 month): established infarct in the left MCA territory (superior division) with mild ex-vacuo dilatation of the left lateral ventricle
• Echocardiogram (during admission): left atrial enlargement, LVEF 58%, no thrombus, no valvular lesion
• Carotid Doppler (during admission): no significant carotid stenosis (right 20%, left 15%) [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mrs O'Sullivan is a 72-year-old retired schoolteacher who sustained an acute left middle cerebral artery territory ischaemic stroke 4 weeks ago, treated with IV thrombolysis and mechanical thrombectomy with complete reperfusion. She has a background of persistent atrial fibrillation on therapeutic apixaban, hypertension, type 2 diabetes, dyslipidaemia, and a 40 pack-year smoking history. [1]

She is now 10 days into inpatient rehabilitation, making gradual progress with her gait and transfers, though her right hand function remains very limited. [1]

Her main problems are:

1. Post-stroke neurological deficit — right hemiparesis (arm worse than hand, recovering), Broca-type aphasia, mild residual dysphagia. She is making functional gains in rehabilitation
2. Persistent atrial fibrillation — she was on therapeutic apixaban when her stroke occurred, representing a treatment failure that requires evaluation
3. Suboptimal vascular risk factor control — BP 148/86 (target under 130/80 post-stroke), HbA1c 62 (target under 53)
4. Post-stroke depression — appropriately started on sertraline; needs ongoing monitoring
5. Residual dysphagia requiring thickened fluids — aspiration risk; needs reassessment
6. Medication regimen — polypharmacy; needs review and reconciliation" [1]

Management plan: [1]

1. Neurological rehabilitation:

   • Continue inpatient or intensive outpatient rehabilitation. Focus areas: right upper limb motor recovery (constraint-induced movement therapy if eligible), speech pathology for aphasia and swallow, gait re-education
   • Right hand function (1/5 distal power at 4 weeks) has a guarded prognosis — early hand recovery is the strongest predictor of final hand function. At 4 weeks with minimal distal movement, the probability of useful hand function is low. Prepare the patient and family for this while continuing therapy
   • Spasticity management: stretching, positioning, consider botulinum toxin for right wrist and finger flexors if functionally limiting [1]

2. Atrial fibrillation and anticoagulation:

   • This stroke occurred despite therapeutic apixaban — a true treatment failure. Confirm apixaban dose is correct (5 mg BD; dose reduction criteria not met). Verify adherence with pharmacy records
   • Continue apixaban. If the stroke mechanism is definitively cardioembolic from AF, switching to warfarin is not evidence-based for apixaban failures. Consider prolonged cardiac monitoring to exclude paroxysmal AF with high burden, though her AF is already persistent
   • Antiplatelets are NOT indicated in addition to anticoagulation (increases bleeding; this is cardioembolic stroke) [1]

3. Vascular risk factor optimisation:

   • Blood pressure: current 148/86 is above target. Increase perindopril or add a thiazide. Target under 130/80 (PROGRESS trial evidence)
   • Diabetes: HbA1c 62 is above target. Continue metformin and empagliflozin; consider adding a GLP-1 receptor agonist (liraglutide, semaglutide) which has demonstrated cardiovascular and potential stroke benefit. Target HbA1c under 53
   • Lipids: LDL 1.6 is excellent on atorvastatin 80 mg. Continue. No need to add ezetimibe unless LDL above 1.8 [1]

4. Swallow assessment:

   • Formal speech pathology review to reassess swallow safety. She is coughing on thin fluids, indicating ongoing aspiration risk
   • Maintain thickened fluids and texture-modified diet until safe swallow confirmed
   • If persistent at 3 months post-stroke, consider videofluoroscopic swallow study and PEG assessment [1]

5. Post-stroke depression:

   • Sertraline 50 mg is appropriate. Reassess at 4-6 weeks; titrate to 100-200 mg if response is partial
   • Monitor for improvement in mood, participation in rehabilitation, sleep, and appetite [1]

Examiner discussion questions

Q: "Her stroke occurred despite being on apixaban. What do you do?" [1]

"This is a treatment failure on a DOAC for AF-related stroke. The approach is: first, confirm the dose is correct and the patient is adherent — apixaban 5 mg BD is the standard dose, and she does not meet dose-reduction criteria. Check pharmacy dispensing records for adherence. Second, consider whether the stroke mechanism is truly cardioembolic — although she has AF, the possibility of a concomitant mechanism (e.g. intracranial atherosclerosis, patent foramen ovale in a paroxysmal pattern) should be considered, though her carotid Doppler was unremarkable and her echo showed no PFO or thrombus. Third, regarding anticoagulation choice — there is no trial-level evidence that switching from a DOAC to warfarin improves outcomes after a DOAC failure. I would continue apixaban at the full dose and ensure rigorous adherence. The risk factor profile (BP and diabetes control) is likely contributing and must be aggressively addressed." [1]

Q: "How would you manage her right hand function?" [1]

"At 4 weeks post-stroke with distal power of 1 out of 5, the prognosis for useful hand function is guarded. The strongest predictor of final hand function is early motor recovery — patients who show some voluntary finger extension within 72 hours have a high probability of good recovery. She had a severe MCA stroke with global aphasia and dense hemiplegia initially, so the baseline was poor. My approach: continue intensive task-specific upper limb therapy, including constraint-induced movement therapy if she has at least 20 degrees of active wrist extension and 10 degrees of finger extension. If not eligible, focus on passive range of motion, splinting to prevent contractures, and functional compensation with the left hand. I would set realistic expectations with the patient and family — the goal shifts from full hand recovery to independence with adaptive techniques. Serial assessments over the first 3 months will define the trajectory." [1]

Q: "Would you add an antiplatelet to her apixaban?" [1]

"No. Adding aspirin or clopidogrel to a DOAC in a patient with atrial fibrillation increases bleeding risk (particularly major and intracranial bleeding) without reducing stroke recurrence. This is a cardioembolic stroke, for which anticoagulation is the evidence-based therapy. The only situation where combined anticoagulation and antiplatelet therapy is indicated after stroke is if there is a separate cardiac indication — for example, recent coronary stent placement or mechanical heart valve. She has neither. The correct strategy is to optimise her anticoagulation and address her modifiable risk factors." [1]

DCE Short Case — Neurological Examination

Instruction

"Examine this patient's neurological system. They had a stroke 6 weeks ago. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Right hemiparetic posture — arm flexed, adducted, internally rotated; leg extended
• Right upper motor neuron facial weakness — lower face only, forehead spared
• Right arm: increased tone (spastic), power reduced proximally (3/5) and distally (1/5), brisk reflexes, extensor plantar
• Right leg: power 4/5, mild spasticity, brisk reflexes
• Right hemisensory loss to pinprick and light touch
• Broca-type aphasia — non-fluent speech, preserved comprehension
• Arm-worse-than-leg gradient — consistent with MCA (not ACA) territory
• No visual field defect, no neglect (previously present, resolved) [1]

Systematic examination routine

1. Observe from the end of the bed: hemiparetic posture, communication style (non-fluent speech), attention to environment
2. Cranial nerves: facial symmetry (UMN pattern), visual fields (confrontation), pupils, eye movements, tongue, palate
3. Motor system (compare side to side):
   • Tone: roll the limbs, test at elbow/wrist and knee/ankle; look for a spastic catch or clasp-knife phenomenon
   • Power: MRC scale, document the face/arm/leg gradient. Test key movements (shoulder abduction, elbow flexion/extension, wrist extension, finger flexion/extension, hip flexion, knee flexion/extension, ankle dorsiflexion/plantarflexion)
   • Reflexes: biceps, triceps, supinator, knee, ankle. Compare sides. Plantar response (Babinski)
4. Sensory: pinprick and light touch (compare sides and dermatomes), joint position sense (great toe), vibration sense (if posterior column lesion suspected)
5. Coordination: finger-nose, heel-shin — cerebellar signs suggest posterior circulation or cerebellar connections. May be limited by weakness on the affected side
6. Higher cortical function: language (fluency, comprehension, naming, repetition — distinguish Broca from Wernicke aphasia), neglect (double simultaneous stimulation), executive function
7. Gait: observe hemiparetic gait — circumduction of the affected leg, reduced arm swing [1]

Presentation template

"I examined Mrs O'Sullivan's neurological system. She is alert and cooperative but has non-fluent speech with frequent pauses and effortful word production, while comprehension appears preserved. [1]

On general inspection she has a right hemiparetic posture with the right arm flexed and adducted. [1]

Cranial nerve examination reveals a right upper motor neuron facial weakness with forehead sparing. Visual fields are full to confrontation. Pupils are equal and reactive. Eye movements, tongue, and palate are normal. [1]

In the upper limbs, tone is increased on the right with a spastic catch. Power on the right is 3 out of 5 proximally and 1 out of 5 distally. The left arm is normal at 5 out of 5. Reflexes are brisk on the right with a right extensor plantar response. [1]

In the lower limbs, tone is mildly increased on the right. Power is 4 out of 5 in the right leg and 5 out of 5 on the left. Reflexes are brisk on the right. [1]

Sensory examination reveals reduced pinprick and light touch sensation on the right side of the body. Coordination is intact on the left but limited on the right by weakness. [1]

Her speech pattern is consistent with Broca aphasia — non-fluent with preserved comprehension. [1]

In summary, these findings are consistent with a left middle cerebral artery territory infarct producing right hemiparesis with an arm-worse-than-leg gradient, right hemisensory loss, and Broca aphasia. The cortical sign of aphasia confirms this is a cortical, not lacunar, stroke." [1]

Discussion questions

Q: "Localise the lesion." [1]

"The combination of right hemiparesis with arm worse than leg, right hemisensory loss, and Broca aphasia localises to the left middle cerebral artery territory — specifically the superior division, which supplies the motor and sensory cortex for the face and arm, as well as Broca's area in the inferior frontal gyrus. The leg is relatively spared because the leg motor cortex (paracentral lobule) is supplied by the anterior cerebral artery. The absence of a visual field defect suggests the posterior division (occipital projections) was not significantly involved or has recovered." [1]

Q: "What would you do differently if she also had a right homonymous hemianopia?" [1]

"The addition of a right homonymous hemianopia would indicate either more extensive MCA involvement (with deep white matter optic radiations affected) or involvement of the posterior cerebral artery territory. If the infarct spanned both MCA and PCA territories, I would consider a proximal large vessel occlusion — such as an internal carotid artery terminus occlusion, which can affect both territories simultaneously. This would be important for the acute management decision because ICA terminus occlusions are thrombectomy-eligible. The presence of a complete MCA-plus-PCA syndrome at presentation indicates a larger infarct and potentially worse prognosis." [1]