GC087 Sudden Hemiplegia Dysphagia
Sudden hemiplegia with dysphagia is an acute neurological presentation, typically due to a stroke affecting the middle cerebral artery or brainstem, resulting in unilateral motor weakness and impaired swallowing.
Sudden Hemiplegia & Dysphagia — Stroke and Cerebrovascular Disease
This lecture (GC 087) is one of the highest-yield neurology topics for HKUMed summative exams. It covers stroke — the most common adult neurological disease, the 2nd leading cause of death in China and 4th in HK, and a major cause of disability [1]. The lecture systematically walks through:
- Definitions — Stroke vs TIA (and why you must never say "CVA")
- Classification — Ischaemic vs haemorrhagic (ICH vs SAH), with subtypes
- Aetiology — Why strokes happen (atherosclerosis, cardioembolism, small vessel disease, uncommon causes)
- Risk factors — Modifiable vs unmodifiable
- Clinical presentation — Carotid vs vertebrobasilar territory symptoms
- Complications — Cerebral and systemic
- Investigations — Imaging, blood work, cardiac workup, vascular studies
- Management — General supportive care, acute therapies (tPA, thrombectomy), secondary prevention, surgical options
- Neuroradiology — CT and MRI temporal evolution of stroke, interventional neuroradiology
How this fits into exams: Past papers repeatedly test GCS calculation in stroke patients, localisation of lesions, CT findings, management principles (tPA window, antiplatelet choice), complications, and stroke syndromes. The 2025 SAQ Q1 directly tests hemiplegia localisation with cranial nerve deficits. The 2021 and 2022 MCQs test dense MCA sign, aphasia localisation, and seizure as a stroke complication.
Stroke = rapid onset clinical symptoms and signs of focal or global disturbances of cerebral functions due to non-traumatic vascular causes, symptoms lasting > 24 hrs or leading to death. [1]
Transient ischaemic attack (TIA) = ischaemic stroke but symptoms < 24 hrs [1]. The updated definition on the next slide refines this: TIA = focal neurologic symptoms < 1 hr without evidence of acute infarction [1].
DO NOT use "cerebrovascular accident" or "CVA." [1] This is explicitly stated on the lecture slide. Examiners may penalise you for using this term — it implies the event was accidental/random when it is actually a predictable vascular disease.
Exam Trap: Stroke vs TIA Definition
The lecture gives two slightly different definitions. The key exam-safe distinction: Ischaemic stroke = continuing symptoms > 24h OR fatal OR imaging evidence of acute infarction. Haemorrhagic stroke = fatal or imaging evidence. TIA = focal symptoms < 1h without acute infarction on imaging. Note the shift from "< 24h" to "< 1h" — the modern tissue-based definition means if DWI shows an infarct, it's a stroke even if symptoms resolved in 30 minutes.
Why "< 1 hour" matters: Most true TIAs resolve within minutes to an hour. If symptoms last hours, there is almost certainly tissue infarction even if CT is normal. MRI DWI can detect ischaemia within 30 minutes of onset [3].
| Type | Proportion | Subtypes |
|---|---|---|
| Ischaemic stroke (ISS) | 75-80% | Cortical, subcortical, posterior circulation, lacunar |
| Intracerebral haemorrhage (ICH) | 20% | Supratentorial, infratentorial |
| Subarachnoid haemorrhage (SAH) | < 5% | Aneurysmal (85%), other |
Mortality & Disability Hierarchy (High Yield)
Mortality: SAH (50% at 1 mo) > ICH (40% at 1 mo, 50% at 1 yr) > cortical infarct (20% at 1 mo, 35% at 1 yr) > lacunar infarct [1]
Disability: SAH (50% survivors with severe deficits) > cortical infarct > ICH > lacunar infarct [1]
Why SAH is the deadliest: SAH causes sudden catastrophic ICP rise, global cerebral hypoperfusion, and secondary vasospasm. ICH compresses brain tissue directly. Cortical infarcts affect large territories but don't always cause mass effect. Lacunar infarcts are small (< 1.5 cm) and typically don't cause death.
Aetiology
| Category | Mechanism | Details |
|---|---|---|
| Atherosclerosis | Plaque → stenosis/occlusion | Large vessel disease (ICA, MCA, vertebral, basilar) |
| Thromboembolism | Clot from proximal artery | Artery-to-artery embolism |
| Cardioembolism | Clot from heart chambers | AF (most common), valvular disease, mural thrombus, PFO |
| Small vessel disease | Lipohyalinosis | Lacunar infarcts in penetrating arteries |
| Uncommon | Various | Dissection, inflammation, infection, hypotension, vasospasm, hypercoagulability, Moyamoya disease [1] |
Why cardioembolism matters so much: AF causes stasis in the left atrial appendage → thrombus formation → embolus to brain. This is the most common cause of cardioembolic stroke and is directly actionable (anticoagulation prevents recurrence). The 2021 SAQ tested a patient with untreated AF presenting with hemiplegia — the expected answer was hyperdense MCA sign on CT [5].
| ICH Causes | SAH Causes |
|---|---|
| Hypertension (most common) | Aneurysm (85%) |
| Bleeding tendency (warfarin, DOACs, thrombocytopenia) | Vascular malformation |
| Cerebral amyloid angiopathy (elderly, lobar) | Trauma |
| Aneurysm, vascular malformation, Moyamoya | Moyamoya disease |
Why hypertensive ICH occurs at specific locations: Chronic hypertension causes lipohyalinosis of small perforating arteries (lenticulostriate arteries off MCA, thalamoperforating arteries, pontine perforators). These weakened vessels rupture under high pressure. Classic locations: basal ganglia (putamen most common), thalamus, pons, cerebellum [1][3].
Cerebral amyloid angiopathy (CAA): Amyloid-beta deposits in cortical/leptomeningeal vessels of elderly patients → lobar ICH. Recurrent. On MRI SWI, multiple cortical microbleeds are characteristic. Important because anticoagulation is relatively contraindicated [1].
Unmodifiable: old age; male sex; history of TIA or stroke; peripheral vascular disease [1]
Modifiable: hypertension; heart disease; atrial fibrillation; diabetes mellitus; hyperlipidaemia; cigarette smoking; alcohol abuse; carotid artery stenosis; use of oral contraceptives; high plasma fibrinogen; high blood viscosity; obesity; lack of exercise; homocysteinaemia [1]
Why hypertension is the single most important modifiable risk factor: It accelerates atherosclerosis in large vessels AND causes lipohyalinosis in small vessels AND is the number one cause of ICH. Treating hypertension reduces stroke risk by approximately 40%.
Exam Pearl
The lecture specifically lists oral contraceptive use as a modifiable risk factor — this is often tested. Combined OCP increases risk of ischaemic stroke especially in women with migraine with aura. Also note homocysteinaemia — a less obvious risk factor that can be tested in SAQs.
Clinical Presentation
Hemiparesis, hemifacial weakness; hemisensory loss; language disturbances (dominant hemisphere); visuospatial disorientation (non-dominant hemisphere); visual disturbances (retinal stroke or amaurosis fugax); deviation of head & eyes towards the lesion side; dysarthria; dysphagia [1]
Understanding "eyes deviate towards the lesion": The frontal eye field (FEF) drives conjugate gaze to the contralateral side. When a hemispheric stroke destroys the FEF, the eyes deviate towards the lesion (away from the hemiplegia). Exception: in seizure, eyes deviate away from the lesion (towards the seizing side) because the FEF is firing abnormally.
Why language disturbances are in the dominant hemisphere: In > 95% of right-handed and ~70% of left-handed people, the left hemisphere is language-dominant. A left MCA stroke therefore causes aphasia. The 2024 MCQ Q12 tested this: non-fluent speech with impaired naming/repetition but intact comprehension = Broca's aphasia → left frontal [7].
Cortical blindness; homonymous visual field defects; diplopia; nystagmus; vertigo; Horner's syndrome; dysarthria; dysphagia; crossed hemiparesis; tetraparesis; crossed unilateral sensory loss; bilateral sensory loss; ataxia [1]
"Crossed" signs are the hallmark of brainstem lesions: Ipsilateral cranial nerve palsy + contralateral hemiplegia = the lesion is in the brainstem at the level of that cranial nerve. This is because cranial nerve nuclei are in the brainstem (ipsilateral), while the corticospinal tract has not yet decussated at the medullary pyramids (or has already partially crossed depending on level).
| Syndrome | Location | Key Features |
|---|---|---|
| ACA stroke | Medial frontoparietal | Leg > arm weakness, personality change |
| MCA stroke | Lateral frontoparietal, temporal | Face/arm > leg weakness, homonymous hemianopia, aphasia (dominant) or neglect (non-dominant) |
| PCA stroke | Occipital, thalamus | Homonymous hemianopia with macular sparing, hemisensory loss without hemiplegia |
| Wallenberg (lateral medullary) | PICA/vertebral artery | Ipsilateral: Horner's, facial pain/temp loss, cerebellar ataxia, bulbar palsy; Contralateral: body pain/temp loss. NO hemiplegia [3][4] |
| Lacunar | Internal capsule, pons, thalamus | Pure motor, pure sensory, mixed sensorimotor, ataxic hemiparesis, dysarthria-clumsy hand. NO cortical signs [3] |
High Yield: Lacunar Syndromes Have NO Cortical Signs
If a question describes hemiparesis WITHOUT aphasia, neglect, hemianopia, or seizures — think lacunar infarct (small vessel disease). The absence of cortical signs is the discriminator. Lacunar infarcts are < 1.5 cm and occur in penetrating arteries.
DDx of stroke: intracranial tumour; chronic subdural haematoma; encephalitis; multiple sclerosis; seizure; hysteria [1]
| DDx | Key Distinguishing Feature |
|---|---|
| Intracranial tumour | Gradual onset, headache, papilloedema, progressive focal deficits |
| Chronic subdural haematoma | History of fall/trauma (may be trivial), fluctuating consciousness, elderly on anticoagulants |
| Encephalitis | Fever, seizures, altered consciousness, CSF pleocytosis |
| Multiple sclerosis | Young woman, relapsing-remitting, optic neuritis, periventricular white matter lesions |
| Seizure (Todd's paralysis) | Post-ictal weakness resolves in hours, witnessed seizure |
| Hysteria/functional | Non-anatomical distribution, Hoover's sign, inconsistency |
Why this matters: A "stroke mimic" can waste the tPA time window or, worse, lead to inappropriate thrombolysis. Always get a CT brain before treatment.
Complications of Stroke
Cerebral oedema; increased intracranial pressure; herniation; haemorrhagic transformation of cerebral infarction; seizures [1]
- Cerebral oedema peaks at days 3-5 (cytotoxic oedema). Large MCA territory infarcts in young patients can cause "malignant MCA syndrome" with uncal herniation → decompressive hemicraniectomy may be needed.
- Haemorrhagic transformation is more common with cardioembolic strokes (because when the embolus lyses and blood flow is restored, the infarcted vessels are leaky). This is why you avoid anticoagulation in large infarcts.
- Post-stroke seizures complicate 11% of stroke patients without previous history of seizure [1] — a specific number worth memorising.
Bronchopneumonia; aspiration pneumonia; deep vein thrombosis; pulmonary embolism; pressure sores; urinary tract infection; contractures; frozen shoulder; cardiovascular disturbances; fluid & electrolyte disturbances; anxiety & depression [1]
Why aspiration pneumonia is so important in stroke: Stroke frequently impairs the swallowing reflex (bulbar dysfunction). Dysphagia → silent aspiration → pneumonia is the leading cause of early death in stroke patients. This is why the swallowing test is mandatory before any oral feeding [3].
Investigations
The purpose of investigations is to confirm the clinical diagnosis, classify the types of stroke, define the underlying causes and risk factors, reveal any complications [1].
| Investigation | Purpose |
|---|---|
| CT head | Rule out haemorrhage (hyperintense on CT), identify large infarcts. Normal CT does NOT exclude ischaemic stroke in first 12 hours |
| MRI head (DWI) | Most sensitive for acute ischaemia — abnormal within 1 hour [1]. DWI shows restricted diffusion (bright) with corresponding ADC drop (dark) |
| Routine bloods | FBC, U&E, glucose, coagulation, ESR, fasting lipids, fasting glucose |
| ECG | AF, acute MI, LVH |
| CXR | Cardiomegaly, aspiration pneumonia |
| Investigation | When to Order |
|---|---|
| Tests for prothrombotic states | Young stroke, no obvious cause, recurrent stroke |
| Echocardiography (TTE or TOE) | Suspected cardioembolic source (AF, valvular disease, PFO) |
| Holter monitoring | Paroxysmal AF not captured on ECG |
| Ultrasound Doppler (extracranial, transcranial) | Carotid stenosis assessment |
| Cerebral angiography | Selected cases, endovascular intervention |
| Lumbar puncture | Suspected SAH with negative CT, suspected CNS infection |
Swallowing Test — Bedside Assessment
50 ml of water given in 5 ml portions. Observe for swallowing effort and choking. Fail if cannot complete in 1 minute or choking occurs. If fail → NG tube feeding [3]. This is done by a speech therapist or trained nurse before ANY oral intake is allowed. Dysphagia is in the lecture title for a reason — it is a critical early management step.
This is a classic exam table [1]:
| Time | CT Findings |
|---|---|
| Normal up to 12 hours | Hyperdense artery (dense MCA sign) or decreased density of lentiform nucleus |
| 12-24 hours | Loss of grey-white differentiation, insular ribbon sign, sulcal effacement |
| 1-3 days | Wedge-shaped hypodensity, cytotoxic oedema, haemorrhagic transformation |
| 4-7 days | Maximal cytotoxic oedema, gyral enhancement |
| 1-8 weeks | Subsiding oedema |
| > 8 weeks | Encephalomalacia |
Dense MCA Sign
The hyperdense MCA sign represents a thrombus/embolus within the MCA — it appears as a bright white vessel on non-contrast CT. The absence of 'dense MCA sign' does NOT exclude cerebral ischaemia [6] — this was directly tested in the 2022 MCQ Q68. The sign has moderate sensitivity but high specificity.
MRI Temporal Evolution
| Time | MRI Findings |
|---|---|
| Within 1 hour | Abnormal DWI and/or perfusion |
| 12-24 hours | T2W hyperintensity, loss of grey-white differentiation, meningeal enhancement |
| 1-3 days | Wedge-shaped T2W hyperintensity, haemorrhagic transformation |
| 4-7 days | Maximal cytotoxic oedema, gyral enhancement |
| 1-8 weeks → > 8 weeks | Subsiding oedema → encephalomalacia |
DWI-ADC mismatch: Acute ischaemia shows DWI bright (restricted diffusion because cytotoxic oedema traps water in cells) + ADC dark. Subacute/chronic infarcts show DWI bright with ADC bright ("T2 shine-through") — this is how you distinguish acute from old infarcts.
Management
This is extensively covered in the lecture and is a favourite SAQ topic [1]:
Keep the patient comfortable & avoid complications. Regular neuro-observation. [1]
| Aspect | Action | Why |
|---|---|---|
| Blood pressure | Avoid rapid lowering; induced hypertension? | Acute BP drop reduces cerebral perfusion to penumbra. Permissive hypertension maintains collateral flow. Only lower if > 220/120 (ischaemic) or > 180/110 (haemorrhagic, or if tPA given) |
| Electrolytes/fluids | Avoid imbalance, hypovolaemia, fluid overload | Hyponatraemia → cerebral oedema; dehydration → hypoperfusion |
| Dysphagia | Speech therapist assessment; Ryle's tube (NG) feeding if depressed consciousness or dysphagia | Prevents aspiration pneumonia — the #1 killer |
| Blood glucose | Monitor and maintain euglycaemia | Hyperglycaemia worsens ischaemic injury (lactic acidosis in penumbra); hypoglycaemia mimics stroke |
| Pulmonary | Careful feeding, early mobilisation, chest physiotherapy | Prevents pneumonia, atelectasis |
| DVT prophylaxis | Low dose SC heparin or sequential compression device | Immobilised hemiplegic patients are at high DVT/PE risk |
| Infection | Treat vigorously; reduce core temperature if fever | Fever increases metabolic demand and worsens infarct size |
| Bladder | Condom catheter (incontinent males) or IDC; intermittent catheterisation for PVR | Prevents overdistension, UTI |
| Bowels | High fibre diet, stool softeners, laxatives | Prevents constipation, faecal impaction |
| Pressure sores | Reposition, frequent turning, cushions, egg-crate/air mattress | Immobility + sensory loss → pressure ulcers |
| Physiotherapy/OT | Early PT, OT devices | Prevents contractures, frozen shoulder; aids recovery |
| Seizures | Anticonvulsants if seizures occur | Post-stroke seizures in 11% |
| Depression | Watch out for depression | Very common post-stroke; impairs rehabilitation |
| Iatrogenic | Avoid iatrogenic complications | Drug interactions, fluid errors, positioning injuries |
Acute Therapies for Ischaemic Stroke
Recombinant Tissue Plasminogen Activator within 3 (4.5) hours of the onset of stroke being effective; more haemorrhagic complications. Numerous contraindications. [1]
Intravenous streptokinase with unacceptable risk of haemorrhagic complications [1] — i.e., do NOT use IV streptokinase for stroke.
Why 3 (4.5) hours? The NINDS trial showed benefit up to 3 hours; ECASS III extended this to 4.5 hours with slightly less benefit and more bleeding risk. Beyond this window, the risk of haemorrhagic transformation outweighs the benefit of reperfusion.
Key contraindications (from lecture + GC 109):
- Active internal bleeding
- Recent (within 3 months) intracranial/spinal surgery or head trauma
- Uncontrolled hypertension (> 185/110 mmHg)
- Known bleeding diathesis
- Platelet count < 100,000
- INR > 1.7 or PT > 15 seconds
- Blood glucose < 2.7 mmol/L
- Large stroke on CT (> 1/3 MCA territory)
Mechanical thrombectomy within 6 hours of onset of stroke due to large artery occlusion [1]
Penumbra-based reperfusion therapy [1]
Why thrombectomy works for large vessel occlusion (LVO): tPA is less effective for large clots (e.g., ICA terminus, M1 MCA occlusion). Endovascular retrieval physically removes the clot. Multiple RCTs (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT PRIME, REVASCAT) showed dramatic benefit. Extended windows (up to 24 hours) are possible if perfusion imaging shows salvageable penumbra (DAWN, DEFUSE 3 trials).
Exam Answer: Acute Ischaemic Stroke Management
- CT brain to exclude haemorrhage
- IV rtPA within 3-4.5 hours if no contraindications
- Endovascular mechanical thrombectomy within 6 hours (up to 24h with perfusion mismatch) for large artery occlusion
- Aspirin 160-300 mg within 48 hours (after haemorrhage excluded)
- Admit to stroke unit
Avoid if extensive or haemorrhagic infarct, active or unidentified bleeding source, lack of monitoring, uncontrolled hypertension, infective endocarditis [1]
Clinical trials failed to show any beneficial effects of anticoagulation in acute stage [1]
Logical but unproven: (i) definite or probable cardiac emboli, (ii) prophylaxis of thrombus formation/propagation or embolisation distal to an occluded or severely stenotic large cerebral artery [1]
Indicated in cerebral venous thrombosis [1]
Translation: Don't routinely anticoagulate in acute ischaemic stroke. The IST and CAST trials showed aspirin is sufficient acutely. However, anticoagulation IS indicated for cerebral venous sinus thrombosis (even if there is haemorrhagic infarction — because the pathophysiology is venous congestion, not arterial bleeding).
International Stroke Trial: aspirin 300 mg daily within 48 hours — non-significant trend of benefit [1]
Chinese Acute Stroke Trial (CAST): aspirin 160 mg daily within 48 hours — significant 14% proportional risk reduction in mortality at 4 weeks [1]
Short-term dual antiplatelet for high risk TIA & ischaemic stroke cases [1]
DAPT in minor stroke/TIA: CHANCE trial (clopidogrel + aspirin for 21 days in minor stroke/high-risk TIA) showed significant reduction in recurrent stroke. This is now standard practice for NIHSS ≤ 3 or high-risk TIA.
Antiplatelet agents for non-cardioembolic ischaemic stroke: aspirin, clopidogrel, slow-release dipyridamole [1]
Anticoagulation for cardioembolic ischaemic stroke [1]
Healthy lifestyles, regular exercise, risk factor identification & control [1]
| Stroke Type | Secondary Prevention |
|---|---|
| Non-cardioembolic | Antiplatelet (aspirin OR clopidogrel) + statin + BP control + lifestyle |
| Cardioembolic (AF) | Anticoagulation (warfarin or DOAC) + rate/rhythm control |
| Carotid stenosis | Carotid endarterectomy (if symptomatic severe stenosis) |
Surgical Management
Carotid endarterectomy beneficial in symptomatic severe stenosis, but small benefit in asymptomatic severe stenosis [1]
NASCET/ECST data: Symptomatic carotid stenosis ≥ 70% — NNT ~6 to prevent one stroke over 2 years. For 50-69%, moderate benefit. For < 50%, no benefit. Asymptomatic stenosis — benefit is marginal and controversial.
Negative results of the EC-IC Co-operative study for extracranial to intracranial bypass; in patients with cerebral hypoperfusion? [1]
Synangiosis in young patients with Moyamoya disease: myo-encephalosynangiosis, duro-arterio-encephalosynangiosis, formal STA-MCA bypass [1]
| Scenario | Management |
|---|---|
| Cerebellar haemorrhage | Neurosurgical emergency: CSF drainage, clot evacuation [1]. Posterior fossa is small → rapid brainstem compression |
| Basal ganglia (hypertensive) ICH | Mortality improved with vegetative survival — surgery saves life but poor functional outcome |
| Brainstem haemorrhage | Very high mortality → conservative treatment [1] |
| Lobar haemorrhage | Evacuation + hematoma cavity microscopy (to exclude underlying tumour/AVM) — except amyloid angiopathy [1] |
| IVH with hydrocephalus | Ventricular drainage, chemical clot lysis (streptokinase/urokinase/tPA) [1] |
| Supratentorial infarct with oedema | Decompressive hemicraniectomy — quality of life not improved; young patients with non-dominant infarct [1] |
| Cerebellar infarct compressing brainstem | Drainage of hydrocephalus, infarctectomy, posterior fossa decompression [1] |
Ruptured cerebral aneurysm in 85%. High index of suspicion required, prompt referral, early treatment. [1]
Early microsurgical clipping or endovascular coiling as standard treatment in good surgical candidate [1]
Conservative treatment adopted for poor grade patients [1]
Angioplasty & intra-arterial papaverine for treatment of vasospasm [1]
SAH complications triad: Rebleeding (peak day 0-1, prevented by early clipping/coiling), hydrocephalus (acute from blood blocking CSF flow), vasospasm (peaks days 4-14, treat with nimodipine, triple-H therapy, angioplasty) [2].
CT or MRI is mandatory. Able to delineate blood vessels & assess brain perfusion (CTA, CTP, MRA, DWI, PWI) [1]
Ultrasonography applicable for neonatal brain, intraoperative imaging, or extracranial vascular imaging [1]
Conventional angiography invasive; reserved for selected cases, or for endovascular interventional therapy [1]
Interventional Neuroradiology
Transarterial thrombolysis; embolotherapy for AVM & aneurysm; angioplasty (+/- stenting) for arterial stenosis [1]
The lecture title is "Sudden Hemiplegia Dysphagia" — dysphagia is both a presenting feature AND a major complication.
Why stroke causes dysphagia:
- Bilateral cortical input is needed for coordinated swallowing. Unilateral stroke can disrupt this.
- Brainstem strokes (especially Wallenberg/lateral medullary syndrome) directly damage the nucleus ambiguus (CN IX, X) → loss of gag reflex, vocal cord paralysis, dysphagia [4].
- Pseudobulbar palsy from bilateral hemispheric strokes also causes dysphagia.
Management of dysphagia in stroke:
- Speech therapist assessment [1]
- Bedside water swallowing test (50 ml in 5 ml aliquots) [3]
- Ryle's tube (NG tube) feeding if depressed consciousness or dysphagia [1]
- Modified diet textures (thickened fluids, soft diet) if mild dysphagia
- PEG tube for prolonged dysphagia (> 4-6 weeks)
- Prevent aspiration pneumonia
- GC 109 (Headache and LOC): Covers acute stroke from the neurosurgical perspective — reinforces tPA within 3-4.5h, thrombectomy within 6h, SAH clipping/coiling, cervical artery dissection [2].
- GC 081 (Seizure and LOC): Post-stroke seizure (11%), status epilepticus, delirium vs stroke.
- GC 037 (Common neurological problems in older people): Vascular dementia, multi-infarct state.
- GC 241 (Dementia): Vascular cognitive impairment — artery of Percheron infarction causing bilateral thalamic infarcts.
- Cerebrovascular Disease (Surgery deck): Case-based — F/27 with right hemiplegia and dysphasia = think of uncommon causes (dissection, PFO, hypercoagulable state, Moyamoya) [8].
Likely Exam Questions
Q1: A 68-year-old woman with AF presents with sudden right-sided weakness. CT shows left basal ganglion haemorrhage. GCS: eyes open to pain (E2), inappropriate words (V3), flexion to pain (M4). (Past paper 2018/2019 Q8)
- (a) GCS = 2+3+4 = 9 [9][10]
- (b) Left dilated non-reactive pupil → uncal herniation compressing CN III (ipsilateral to lesion) [9]
- (c) Types of herniation: subfalcine, transtentorial (uncal), tonsillar [9]
- (d) Most common cause: hypertension [1]
- (e) Other causes: bleeding tendency/anticoagulation, cerebral amyloid angiopathy, vascular malformation, aneurysm [1]
Q2 (2025 SAQ Q1 style): A 42-year-old woman develops sudden right facial asymmetry, left arm/leg weakness, slurred speech, and choking on water.
- Neurological deficits: Right LMN facial palsy, left hemiplegia, dysarthria, dysphagia [11]
- Lesion: Right pons/brainstem (right facial nucleus affected = ipsilateral LMN VII; left corticospinal tract involved above decussation = contralateral hemiplegia) [11]
- Reflexes: Left-sided hyperreflexia, left upgoing plantar (Babinski), right normal [11]
Q3 (2022 MCQ Q68 style): "The absence of 'dense MCA sign' does not exclude cerebral ischaemia" → TRUE — this is the correct answer [6].
| Trap | Correct Answer |
|---|---|
| "CVA" used as a diagnosis | Never — use "stroke" or "ischaemic stroke" / "ICH" |
| tPA given after 6 hours | Wrong — window is 3 (max 4.5) hours |
| Streptokinase for stroke | Wrong — unacceptable haemorrhagic risk |
| Thrombectomy for small vessel disease | Wrong — only for large artery occlusion |
| Anticoagulation in acute stroke with large infarct | Wrong — avoid (risk of haemorrhagic transformation) |
| CT normal in first 6 hours = no stroke | Wrong — CT is often normal in early ischaemic stroke |
| Lacunar stroke with aphasia | Wrong — lacunar strokes have NO cortical signs |
| All stroke patients need carotid endarterectomy | Wrong — only symptomatic severe stenosis benefits significantly |
High Yield Summary
Stroke is the most common adult neurological disease. It is classified as ischaemic (75-80%), ICH (20%), or SAH (< 5%). Never say "CVA."
Ischaemic stroke is caused by atherosclerosis, cardioembolism (especially AF), small vessel disease, or uncommon causes (dissection, Moyamoya, hypercoagulability).
ICH is most commonly caused by hypertension. SAH by ruptured aneurysm (85%).
Mortality: SAH > ICH > cortical infarct > lacunar infarct.
Carotid territory = hemiparesis, hemisensory loss, aphasia/neglect, eyes deviate to lesion side. Vertebrobasilar = crossed signs, vertigo, diplopia, dysphagia, ataxia.
Investigations: CT brain first (rule out haemorrhage), MRI DWI most sensitive for acute ischaemia. ECG, bloods, echo, Doppler, Holter as needed.
Acute management: (1) IV rtPA within 3-4.5h, (2) thrombectomy within 6h for LVO, (3) aspirin within 48h, (4) swallowing assessment before feeding, (5) supportive care (BP, glucose, DVT prophylaxis, infection control). No routine anticoagulation acutely.
Secondary prevention: Antiplatelet for non-cardioembolic, anticoagulation for AF, risk factor control, CEA for symptomatic severe carotid stenosis.
CT evolution: Normal up to 12h → grey-white loss at 12-24h → wedge hypodensity at 1-3d → maximal oedema at 4-7d → encephalomalacia at > 8 weeks.
Post-stroke seizures occur in 11%. Watch for depression, aspiration pneumonia, DVT/PE, pressure sores.
Dysphagia management: Speech therapist, 50 ml water test, NG tube if fails, prevent aspiration.
Active Recall - Sudden Hemiplegia Dysphagia
[1] Lecture slides: GC 087. Sudden hemiplegia dysphagia.pdf (all pages) [2] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p25, p9) [3] Senior notes: Maksim Medicine Notes.pdf (p239-241) [4] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1110, p1239) [5] Past papers: 2021 Fourth Summative SAQ.pdf (Q8) [6] Past papers: 2022 Fourth Summative MCQ.pdf (Q68) [7] Past papers: 2024 Fourth Summative MCQ.pdf (Q12) [8] Lecture slides: Cererbrovascular disease.pdf (p51) [9] Past papers: 2018 Fourth Summative SAQ.pdf (Q8) [10] Past papers: 2019 Fourth Summative SAQ.pdf (Q8) [11] Past papers: 2025 Fourth Summative SAQ.pdf (Q1)
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