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 describes stroke as the most common adult neurological disease and, using the lecture-era regional rankings, the 2nd leading cause of death in China and 4th in Hong Kong [1]. Exact rankings change over time, but stroke remains a major cause of death and disability. The lecture systematically walks through:
- Definitions — Stroke vs TIA, including the lecture's older terminology
- 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 reperfusion, secondary prevention, surgical options
- Neuroradiology — CT and MRI temporal evolution of stroke, interventional neuroradiology
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 next slide proposes focal neurologic symptoms < 1 hr without evidence of acute infarction [1]. Both time cut-offs are now superseded by a tissue-based definition.
Prefer “stroke” to “cerebrovascular accident” or “CVA.” [1] “Stroke” is the clearer contemporary clinical term.
Exam Trap: Stroke vs TIA Definition
The lecture gives two time-based definitions, but current AHA framing does not define TIA by either 1 or 24 hours. TIA is an acute focal neurological syndrome attributable to a vascular territory that resolves completely without acute infarction; resolved symptoms with an acute DWI lesion are classified as ischaemic stroke. Symptoms often last under 60 minutes, but that is a clinical pattern rather than a defining threshold [10].
Practical implication: Even brief resolved focal symptoms are an emergency because early recurrent-stroke risk is front-loaded. MRI DWI is preferred for detecting acute infarction, but a negative DWI does not make a vascular event impossible; urgent brain and vessel imaging, rhythm assessment and secondary prevention still depend on the whole presentation [10].
Classification of Stroke
| 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 |
| Territory in the colour map | Main cortical/deep distribution | Deficit suggested by the map |
|---|---|---|
| ACA | Medial frontal/parietal surface | Contralateral leg-predominant weakness/sensory loss, abulia |
| MCA | Most of lateral cerebral convexity; deep lenticulostriate supply | Face/arm-predominant deficit, aphasia or neglect, visual-field loss |
| PCA | Occipital and inferomedial temporal cortex; thalamic/midbrain branches | Homonymous visual-field loss, memory or thalamic sensory syndromes |
| Anterior choroidal | Deep internal-capsular/optic pathway territory | Dense motor deficit ± hemisensory/visual-field loss |
The Circle of Willis links the two carotid systems through the ACom and links anterior to posterior circulation through the PCom arteries. Collateral flow varies greatly; a complete-looking textbook circle does not guarantee adequate real-world collateral perfusion.
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]
These figures communicate the slide's broad severity hierarchy, not current patient-specific prognoses. Outcome varies greatly with haemorrhage volume/site, infarct core and collaterals, age, consciousness, reperfusion, complications and treatment. Avoid using the percentages alone for counselling or treatment limitation.
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] |
The mechanism panel on the stroke-types image also depicts systemic hypoperfusion producing border-zone (watershed) infarction between major arterial territories. This differs from a single embolus: look for a compatible hypotensive episode and bilateral or junctional infarct pattern.
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].
- The common-carotid bifurcation is the commonest extracranial atheromatous site shown; other sites include the carotid siphon and intracranial ICA bifurcation.
- Cervical ICA dissection below the skull base can produce a tapered “string sign.” In a younger patient, ask about neck pain/headache, trauma or manipulation and ipsilateral Horner syndrome.
- Cardiac emboli may arise from AF/heart failure, mitral stenosis with atrial thrombus, recent MI or ventricular aneurysm with mural thrombus, infective-endocarditis vegetation, and prosthetic-valve thrombus.
- The aneurysm map concentrates most lesions in the anterior circulation, especially the ACom, MCA bifurcation and ICA/PCom region; posterior-circulation sites include the basilar apex and vertebral–PICA junction.
| ICH Causes | SAH Causes |
|---|---|
| Hypertensive arteriolosclerosis; uncontrolled hypertension is the major modifiable risk | Ruptured aneurysm (about 85% of spontaneous SAH in the lecture) |
| Bleeding tendency (warfarin, DOACs, thrombocytopenia) | Vascular malformation |
| Cerebral amyloid angiopathy (elderly, lobar) | Trauma |
| Aneurysm, vascular malformation, Moyamoya | Moyamoya disease |
Traumatic SAH is categorized and managed separately from spontaneous aneurysmal SAH. For spontaneous ICH, small-vessel arteriolosclerosis and cerebral amyloid angiopathy are the main vascular pathologies; “hypertension” is best understood as the dominant modifiable risk driving deep perforator arteriopathy [11].
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 older patients → lobar ICH. It can recur; lobar microbleeds or cortical superficial siderosis on susceptibility-sensitive MRI support the diagnosis. Antithrombotic decisions require individualized comparison of ischaemic and recurrent-haemorrhage risks rather than treating CAA as an automatic blanket contraindication.
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 large-vessel atherosclerosis, drives small-vessel arteriolosclerosis and is the major modifiable risk for spontaneous ICH. Treating hypertension substantially reduces first and recurrent stroke risk; avoid treating the slide's older percentage estimates as universal for every patient.
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: an ipsilateral cranial-nerve deficit with a contralateral long-tract motor or sensory deficit localises to the brainstem. Corticospinal fibres in the brainstem are still above the pyramidal decussation, so a unilateral lesion there produces contralateral limb weakness.
| 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.
Lecture list of stroke mimics: intracranial tumour; chronic subdural haematoma; encephalitis; multiple sclerosis; seizure; “hysteria” [1]. The contemporary term for the last category is functional neurological disorder.
| 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 mimic must be considered without delaying a stroke code. Check immediately reversible mimics such as hypoglycaemia, then obtain urgent brain imaging before reperfusion or antithrombotic decisions; a non-contrast CT excludes haemorrhage but may remain normal in early ischaemia.
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 and larger infarcts because damaged microvasculature can bleed when perfusion returns. This is one reason the timing of therapeutic anticoagulation after AF-related stroke is individualized rather than immediate.
- Post-stroke seizures complicate 11% of stroke patients without previous history of seizure in the slide [1]. Treat this as a lecture-era figure: risk varies by stroke type, cortical involvement and follow-up interval.
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 coordinated swallowing and aspiration may be silent. Pneumonia is a major preventable cause of post-stroke morbidity and mortality. This is why a validated dysphagia screen is required before food, drink or oral medication, followed by formal assessment when failed or uncertain [9].
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 |
|---|---|
| Non-contrast CT head | Rule out haemorrhage (hyperdense on CT), identify early large-territory change and major mimics. A normal CT does not exclude early ischaemic stroke |
| MRI head (DWI) | Highly sensitive for acute ischaemia and can become abnormal within minutes; restricted diffusion is DWI-bright with a matching ADC drop. A negative early scan, especially in posterior circulation, does not completely exclude stroke |
| Acute bloods | Bedside glucose urgently; FBC, electrolytes/renal function and coagulation as clinically indicated. HbA1c and lipids help later risk assessment; ESR/CRP is targeted rather than universal |
| 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 | Persistent suspicion of SAH after non-diagnostic initial imaging, according to timing/local protocol; suspected CNS infection |
Swallow Screen Before Oral Intake
Keep the patient nil by mouth until a validated local swallow screen has been completed by trained staff. Do not improvise a large-volume water test in a drowsy patient or someone with obvious bulbar dysfunction. Failure or uncertainty requires speech-language therapist assessment and an alternative medication/nutrition route while aspiration risk is managed.
This is the lecture's simplified temporal table [1]. Early CT may be normal, but “normal up to 12 hours” is not a guaranteed phase: subtle signs may be visible earlier, and modern treatment must not wait for established hypodensity.
| 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 pairing: Acute ischaemia is typically DWI bright with corresponding ADC low. ADC later pseudonormalises and then becomes high as tissue evolves; persistent DWI brightness without low ADC may represent T2 shine-through. Always interpret DWI with ADC and the other sequences rather than using DWI brightness alone to date an infarct.
Posterior-fossa infarcts can be small and initially DWI-negative. If a convincing vertebrobasilar syndrome persists, do not dismiss it solely because the first MRI is negative; reassess clinically and discuss repeat/alternative vascular imaging.
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 reflex rapid lowering; use the stroke-type/reperfusion-specific protocol | In ischaemic stroke, an abrupt fall may reduce penumbral perfusion. Reperfusion candidates require BP below the protocol threshold before treatment and close control afterwards; ICH has a different early-lowering strategy. Do not apply one number to every stroke. |
| Electrolytes/fluids | Avoid imbalance, hypovolaemia, fluid overload | Hyponatraemia → cerebral oedema; dehydration → hypoperfusion |
| Dysphagia | Validated screen before oral intake; speech-language assessment after a failed/uncertain screen; NG feeding/alternative medication route when unsafe | Reduces aspiration risk while maintaining nutrition and medication delivery |
| Blood glucose | Check immediately for hypoglycaemia and avoid marked hypo-/hyperglycaemia; do not target intensive 80–130 mg/dL control | Hypoglycaemia mimics stroke; intensive control increases severe hypoglycaemia without improving outcome [9] |
| Pulmonary/mobility | Aspiration precautions, oral care and mobilization/rehabilitation when medically stable | Prevents pneumonia, atelectasis and immobility complications; avoid aggressive mobilization in the first 24 hours after moderate ICH [11] |
| DVT prophylaxis | Intermittent pneumatic compression for immobile patients; pharmacological prophylaxis only after haemorrhage, infarct size and timing are reviewed | Immobilised hemiplegic patients are at high DVT/PE risk, but anticoagulant prophylaxis also carries intracranial bleeding risk |
| Infection/temperature | Search for and treat infection; treat fever according to protocol | Fever is associated with worse neurological injury; prophylactic antibiotics are not routine |
| Bladder | Bladder scan/timed toileting; intermittent catheterisation for retention when needed; avoid unnecessary indwelling catheters | Prevents overdistension while limiting catheter-associated UTI |
| Bowels | Individualized hydration/nutrition plus stool softener or laxative when needed | Prevents constipation and faecal impaction; “high fibre” is inappropriate until swallowing and hydration are safe |
| 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 | Treat clinical/electrographic seizures; do not give routine prophylaxis in the absence of seizures | The slide reports an 11% historical incidence; risk varies by stroke type, site and timing |
| 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.
Current update: The 2026 AHA/ASA guideline endorses either alteplase or tenecteplase within 4.5 hours for eligible patients with a disabling deficit, regardless of a low NIHSS score, and emphasizes treatment as fast as possible. Selected patients with unknown onset or presentation 4.5–9 hours from onset can receive imaging-selected thrombolysis using DWI–FLAIR or perfusion mismatch. For a non-disabling deficit in the 4.5-hour window, evidence does not support routine thrombolysis and dual antiplatelet therapy is preferred when otherwise eligible [9]. “Last known well,” deficit disability, imaging and the current local checklist all matter.
Key exclusions/checks in the lecture-era alteplase framework (not a substitute for the current local checklist):
- Active internal bleeding
- Recent (within 3 months) intracranial/spinal surgery or head trauma
- Blood pressure above the treatment protocol threshold (classically > 185/110 mmHg before alteplase)
- Known bleeding diathesis
- Platelet count < 100,000
- INR > 1.7 or PT > 15 seconds
- Blood glucose < 2.7 mmol/L
- Extensive established infarction/early ischaemic change on imaging
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): IV thrombolysis is less effective for a large ICA/MCA or basilar clot. A stent retriever expands through the thrombus and withdraws it into an aspiration catheter; direct aspiration is another modern approach. The historical visual progresses from intra-arterial fibrinolysis → ultrasound/coil retrievers → aspiration → stent retrievers. Selected patients can benefit beyond 6 hours, including up to 24 hours in imaging-selected pathways; activate the stroke/endovascular team rather than excluding from the slide's old 6-hour rule.
The slide's Merci retriever is an early corkscrew/coil-retriever design and is useful historically, but modern thrombectomy predominantly uses stent retrievers and/or aspiration. Current eligibility is broader than the slide: selected anterior-circulation patients with a large infarct core may still benefit, and the 2026 guideline strongly recommends EVT for basilar-artery occlusion presenting within 24 hours when NIHSS is ≥10 [9]. Do not delay indicated IV thrombolysis while arranging EVT.
Exam Answer: Acute Ischaemic Stroke Management
- CT brain to exclude haemorrhage
- Immediate vascular imaging/eligibility assessment; alteplase or tenecteplase as early as possible for an eligible disabling deficit
- Mechanical thrombectomy for eligible LVO, including selected late-window, large-core and basilar-occlusion patients
- Antiplatelet therapy after haemorrhage is excluded; if thrombolysis was given, wait for the protocol's post-treatment imaging/time point before antithrombotics
- 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: Do not use routine urgent therapeutic anticoagulation to prevent early recurrence or neurological worsening after arterial ischaemic stroke. When AF is the presumed cause, start long-term anticoagulation at a protocol-selected time after considering infarct size, haemorrhagic transformation and repeat imaging. Cerebral venous sinus thrombosis is a different disease in which anticoagulation is usually indicated even when venous infarction contains haemorrhage.
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/non-disabling stroke or high-risk TIA: Short-course aspirin plus clopidogrel can reduce early recurrence when started promptly in eligible non-cardioembolic patients. It is not long-term default therapy; a common guideline range is 21–90 days, followed by single antiplatelet therapy, with the exact regimen determined by the syndrome, vascular lesion and bleeding risk [9][13]. Do not start it at the bedside before excluding haemorrhage or at a time that conflicts with post-thrombolysis antithrombotic precautions.
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 when safe after considering infarct size, haemorrhagic transformation and repeat imaging. A DOAC is generally preferred for AF, except that warfarin is used for a mechanical valve or moderate-to-severe mitral stenosis [13] |
| 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]
Lecture/trial framing: NASCET/ECST showed the largest benefit for symptomatic ipsilateral 70–99% stenosis, smaller selected benefit at 50–69%, and no benefit below 50%. Contemporary selection also considers disability, age/sex, anatomy, peri-operative risk, modern medical therapy and timing; eligible severe symptomatic stenosis should be assessed for relatively early intervention rather than applying the old NNT in isolation [13].
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 | Immediate surgical removal ± EVD is recommended to reduce mortality with neurological deterioration, brainstem compression, obstructive hydrocephalus or volume ≥15 mL. EVD alone may be insufficient when the posterior fossa is compressed [11] |
| Deep basal-ganglia or brainstem ICH | Often managed medically, but obtain urgent neurosurgical/stroke input when there is deterioration, hydrocephalus or another actionable feature; the slide's blanket outcome statements are historical |
| Selected lobar ICH | Evacuation may be considered according to location, size, neurological deterioration and underlying lesion; it is not automatically recommended for every lobar bleed |
| IVH with hydrocephalus | External ventricular drainage may be required. Intraventricular thrombolysis is a specialist protocol/research-informed decision, not routine bedside use of streptokinase/urokinase/tPA |
| Malignant supratentorial infarction | Early decompressive hemicraniectomy improves survival and can improve the chance of a non-devastating functional outcome in selected patients; age, infarct extent, timing, premorbid function and patient values all matter. The slide's blanket “quality of life not improved” statement is outdated |
| 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]
The slide states that poor-grade patients were treated conservatively. This is historical framing: poor clinical grade alone should not prevent urgent neurovascular assessment, resuscitation and consideration of aneurysm securing. Current guidance recommends identifying and treating the ruptured aneurysm, preferably within 24 hours, with clipping versus coiling selected by an experienced multidisciplinary team based on patient and aneurysm anatomy [12].
Lecture-era treatment: angioplasty and intra-arterial papaverine for vasospasm [1]
SAH complications triad: Rebleeding (reduce by early aneurysm securing), hydrocephalus (may require CSF diversion) and delayed cerebral ischaemia/vasospasm. Start enteral nimodipine early and maintain euvolaemia; routine prophylactic hypervolaemia or haemodynamic augmentation is obsolete. Symptomatic delayed ischaemia may be treated with blood-pressure elevation and selected endovascular therapy in a specialist unit. Papaverine is not a routine modern bedside recommendation [12].
Neuroradiology & Interventional Procedures
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]
| Image/sequence | Visual lesson |
|---|---|
| Large ICA/MCA infarct on CT | Territory hypodensity, sulcal/ventricular effacement and mass effect indicate oedema and malignant-infarction risk |
| DWI + ADC | Acute infarct is bright on DWI with matching low ADC; the paired sequences distinguish true restriction from T2 shine-through |
| Acute lacune versus chronic white-matter disease | The tiny acute lesion is focally DWI-bright and ADC-dark; the much broader periventricular/deep burden is T2/FLAIR-bright chronic small-vessel disease. Do not call every FLAIR-bright focus an acute infarct |
| T2/FLAIR white-matter disease | Periventricular/deep hyperintensity reflects chronic small-vessel burden but is not by itself an acute infarct |
| SWI | Punctate susceptibility foci represent old blood products/microbleeds and help assess haemorrhagic small-vessel disease |
| PCA infarct on CT | Subacute occipital hypodensity evolves to chronic volume loss/encephalomalacia |
| Brainstem/PICA infarction | Axial posterior-fossa MRI may show pontine or cerebellar signal abnormality even when supratentorial CT is unrevealing; correlate with crossed signs, dysphagia, ataxia and the basilar/vertebral arteries |
| Brainstem/cerebellar ICH on CT | Acute blood is hyperdense; posterior-fossa lesions can obstruct CSF or compress the brainstem despite modest volume |
| SAH on CT | Hyperdense blood fills basal cisterns and sylvian fissures |
| CTA/DSA aneurysm panel | The sequence moves from cisternal SAH on non-contrast CT → ACom aneurysm on CTA → coil mass/parent-vessel anatomy on DSA. Other DSA examples show PCom and basilar-apex aneurysms |
| TOF MRA | Non-contrast flow-related signal depicts head/neck vessels and the Circle of Willis. Signal loss can represent thrombosis, but slow/turbulent or in-plane flow can mimic stenosis/occlusion; inspect source images and confirm when necessary |
Lecture list: transarterial thrombolysis; embolotherapy for AVM and aneurysm; angioplasty ± stenting for arterial stenosis [1]
Read this as a historical catalogue, not three routine interchangeable treatments. Modern acute LVO care centres on mechanical thrombectomy; aneurysm coiling and AVM embolisation are lesion-specific neurovascular procedures; and intracranial angioplasty/stenting is not first-line secondary prevention for severe symptomatic intracranial stenosis, where aggressive medical therapy is preferred [9][13].
The lecture title is "Sudden Hemiplegia Dysphagia" — dysphagia is both a presenting feature AND a major complication.
Why stroke causes dysphagia:
- Swallowing has bilateral cortical control, but a unilateral hemispheric lesion can still disrupt the distributed network.
- 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]
- Validated bedside swallow screen by trained staff before food, drink or oral medication
- Nasogastric feeding/alternative medication route when swallowing is unsafe, with aspiration precautions and reassessment [1]
- Modified diet textures (thickened fluids, soft diet) if mild dysphagia
- Consider gastrostomy for persistent dysphagia after multidisciplinary review; timing is individualised
- Prevent aspiration pneumonia
- GC 109 (Headache and LOC): Covers acute stroke from the neurosurgical perspective. Its alteplase and 6-hour thrombectomy windows are historical anchors; use the current time/imaging and vessel-specific pathways above [2][9].
- 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].
High Yield Summary
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Stroke
- is classified as ischaemic, ICH, or SAH. The slide's proportions and mortality figures are lecture-era estimates. Prefer “stroke” to “CVA.”
- TIA is tissue-based: resolved focal vascular symptoms without acute infarction, not “less than 1 hour” by definition.
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Ischaemic stroke
- is caused by atherosclerosis, cardioembolism (especially AF), small vessel disease, or uncommon causes (dissection, Moyamoya, hypercoagulability).
-
Haemorrhagic stroke
- Deep spontaneous ICH is strongly associated with hypertensive arteriolosclerosis; lobar ICH should also raise cerebral amyloid angiopathy and structural causes. The lecture attributes about 85% of spontaneous SAH to ruptured aneurysm.
-
Mortality
- SAH > ICH > cortical infarct > lacunar infarct.
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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
- Activate the stroke pathway immediately: non-contrast CT plus vascular/perfusion imaging as indicated. For an eligible disabling deficit, current guidance permits alteplase or tenecteplase within 4.5 hours and imaging-selected thrombolysis in some unknown/extended-window cases. Assess LVO thrombectomy eligibility, including selected large-core and basilar occlusions [9].
- For eligible non-disabling stroke, DAPT is preferred to thrombolysis; start any antithrombotic only at the protocol-safe time. Screen swallowing before oral intake and provide stroke-unit care.
- No routine anticoagulation acutely.
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Secondary prevention
- Antiplatelet for non-cardioembolic, anticoagulation for AF, risk factor control, CEA for symptomatic severe carotid stenosis.
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CT evolution
- The lecture's simplified sequence is early normal/subtle arterial or grey-white signs → territorial hypoattenuation and oedema → later encephalomalacia. Do not wait 12 hours for CT change before making reperfusion decisions.
-
Post-stroke seizures
- the slide reports 11%, but incidence varies. Treat seizures when they occur; do not use routine prophylactic antiseizure medication without an indication. Watch for depression, aspiration pneumonia, DVT/PE and pressure injury.
- Dysphagia management
- Nil by mouth until a validated screen; speech-language therapist review if failed/uncertain; use an alternative feeding and medication route when swallowing is unsafe.
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] American Heart Association/American Stroke Association: 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke [10] American Heart Association: 2023 Scientific Statement on Diagnosis, Workup and Risk Reduction of TIA in the Emergency Department [11] American Heart Association/American Stroke Association: 2022 Guideline for the Management of Spontaneous Intracerebral Hemorrhage [12] American Heart Association/American Stroke Association: 2023 Guideline for the Management of Aneurysmal Subarachnoid Hemorrhage [13] American Heart Association/American Stroke Association: 2021 Guideline for Prevention of Stroke in Patients With Stroke and TIA
GC086 Splenomegaly
Splenomegaly is the pathological enlargement of the spleen beyond its normal size, often resulting from infections, hematologic disorders, portal hypertension, or infiltrative diseases.
GC088 Sudden Severe Chest Pain
Sudden severe chest pain is an acute, intense thoracic pain of rapid onset that requires urgent evaluation to exclude life-threatening causes such as acute coronary syndrome, aortic dissection, pulmonary embolism, tension pneumothorax, or esophageal rupture.