Makindo Medical Notes

🧠 Stroke = sudden focal neurological deficit due to vascular cause. ⚡ Always “Time is Brain”: prompt recognition, CT brain, and reperfusion therapy save neurons.

📊 Epidemiology

• 2nd leading cause of death worldwide 🌍.
• Most common cause of adult disability in the UK.
• ~85% ischaemic, ~15% haemorrhagic (intracerebral ± subarachnoid).

🧾 Risk Factors

• Modifiable: HTN (biggest), AF, diabetes, smoking 🚬, hyperlipidaemia, obesity, alcohol.
• Non-modifiable: age, male sex, family history, ethnicity (South Asian, Afro-Caribbean ↑ risk).

🧠 Causes of Stroke

Stroke = sudden onset of focal neurological deficit of vascular origin. ~85% are ischaemic and ~15% are haemorrhagic. Understanding the causes helps guide secondary prevention (antiplatelets, anticoagulation, BP control).

🟦 Causes of Ischaemic Stroke (≈85%)

• 🩸 Atherothromboembolism – Large artery disease (carotid stenosis, MCA, vertebrobasilar). – Plaque rupture → thrombosis → distal embolisation.
• ❤️ Cardioembolic – Atrial fibrillation (commonest cardiac cause). – Recent MI with mural thrombus. – Prosthetic valves, endocarditis (septic emboli). – Dilated cardiomyopathy.
• 🧪 Small vessel (Lacunar) disease – Lipohyalinosis & microatheroma in penetrating arteries (HTN, diabetes, smoking). – Leads to lacunar infarcts.
• 🧬 Other/uncommon causes – Arterial dissection (carotid/vertebral, esp. young pts, trauma, chiropractic manipulation). – Vasculitis (SLE, PAN, giant cell arteritis). – Thrombophilia (factor V Leiden, protein C/S deficiency, antiphospholipid). – Sickle cell disease. – Drugs (cocaine, amphetamines, OCP with smoking).

🟥 Causes of Haemorrhagic Stroke (≈15%)

• 📈 Hypertensive intracerebral haemorrhage – Chronic hypertension → lipohyalinosis, microaneurysms (Charcot–Bouchard) → rupture. – Common sites: basal ganglia, thalamus, pons, cerebellum.
• 🧬 Cerebral amyloid angiopathy – Deposition of β-amyloid in vessel walls (elderly). – Lobar haemorrhages, often recurrent.
• 💥 Aneurysm rupture – Berry aneurysm (esp. anterior communicating artery). – Causes subarachnoid haemorrhage (SAH).
• 🩸 Vascular malformations – Arteriovenous malformations (AVMs). – Cavernous haemangiomas.
• 💊 Anticoagulation / bleeding disorders – Warfarin, DOACs, thrombocytopenia, haemophilia, liver disease.
• 🧠 Neoplastic / metastatic haemorrhage – Melanoma, renal cell carcinoma, choriocarcinoma (highly vascular tumours).
• 🚬 Illicit drugs – Cocaine, amphetamines → severe HTN & vasospasm → ICH/SAH.

📊 Exam Tip

• Ischaemic = “plumbing blocked” 🚫🩸 (atherosclerosis, emboli, small vessels, dissection, clotting).
• Haemorrhagic = “pipe bursts” 💥🩸 (HTN, amyloid, aneurysm, anticoagulants, AVM, tumour).
• Always mention AF, carotid stenosis, hypertension — top 3 culprits in OSCEs.

📌 Oxford (Bamford) Stroke Classification

Type	Criteria	Vascular territory	Prognosis
🧠 TACS (Total Anterior Circulation Stroke)	All 3 of: Unilateral weakness/sensory deficit (face/arm/leg) Homonymous hemianopia Higher cortical dysfunction (dysphasia, neglect)	ICA or proximal MCA/ACA	Worst prognosis ⚠️ – high mortality, major disability
🧠 PACS (Partial Anterior Circulation Stroke)	2 of the 3 TACS features OR isolated higher cortical dysfunction OR isolated hemianopia	Distal MCA or ACA	Moderate outcome, variable disability
🧠 LACS (Lacunar Stroke)	One of the following, with no cortical signs: Pure motor stroke Pure sensory stroke Sensorimotor stroke Ataxic hemiparesis	Small vessel disease → penetrating arteries	Best prognosis 🙂, but can recur; risk of vascular dementia
🧠 POCS (Posterior Circulation Stroke)	Brainstem/cerebellar features: Cranial nerve palsy + contralateral motor/sensory deficit Bilateral motor/sensory deficit Disorders of conjugate eye movement Cerebellar dysfunction Isolated homonymous hemianopia	Vertebrobasilar circulation	Variable – can be mild (isolated visual loss) or catastrophic (locked-in)

💡 Exam Tip: - TACS = “all 3 features”. - PACS = “2 of 3” or isolated cortical/visual. - LACS = pure motor/sensory without cortical signs. - POCS = posterior circulation signs (cranial nerves, ataxia, vertigo).

🩺 Clinical Features

• Sudden weakness/numbness (face, arm, leg).
• Speech disturbance (dysphasia, dysarthria).
• Visual loss (hemianopia, amaurosis fugax).
• Ataxia, vertigo, diplopia (posterior circulation).
• Red flag = ↓ consciousness → consider intracerebral haemorrhage or large stroke.

🚑 Acute Assessment

• 🔎 Use FAST (Face–Arm–Speech–Time) in community.
• 🩺 ABCDE, O₂ if sats <94%, IV access, BM, ECG, BP, bloods.
• 🖥️ Urgent non-contrast CT head (<1 h of arrival): exclude bleed, guide thrombolysis.

💊 Acute Management

• Ischaemic stroke:
  • IV alteplase (0.9 mg/kg, max 90 mg) if within 4.5 h, no contraindications.
  • Mechanical thrombectomy if large vessel occlusion ≤6 h (≤24 h in select cases).
  • Aspirin 300 mg PO/NG after CT excludes bleed; switch to long-term secondary prevention later.
• Haemorrhagic stroke:
  • Stop anticoagulants, correct coagulopathy (e.g. PCC for warfarin, DOAC reversal).
  • Strict BP control (aim <140 mmHg systolic).
  • Neurosurgical input: evacuation if large/superficial bleed, hydrocephalus, or mass effect.

💉 Benefits of Thrombolysis (IV Alteplase / Tenecteplase)

• 🚑 Widely available & rapid: Can be given in most hospitals with a CT scanner → "door-to-needle" goal ≤ 60 minutes.
• ⏱️ Time window: Effective if started within 4.5 h of symptom onset (NICE/ESO guidelines).
• 🧠 Improves functional outcomes: ~30% more patients achieve independence at 3 months compared with no thrombolysis (NINDS, ECASS trials).
• 💡 Non-invasive: IV therapy, no need for interventional facilities.
• 🔎 Bridges to thrombectomy: “Bridging therapy” — patients eligible for thrombectomy often receive IV tPA first if within the window.

🩻 Benefits of Mechanical Thrombectomy

• 🎯 Superior for large vessel occlusion (LVO): MCA (M1/M2), ICA, basilar artery → where IV thrombolysis often fails.
• ⏱️ Wider treatment window: Up to 6 h routinely, and up to 24 h in selected patients with favourable perfusion imaging (DAWN, DEFUSE-3 trials).
• 💪 Much higher recanalisation rates: >70–80% successful reperfusion vs. ~30% with IV tPA alone.
• 🧠 Improves outcomes in severe strokes: Reduces disability, increases chance of independence, lowers mortality (absolute benefit ≈ 20–30%).
• 🌍 Can be given when thrombolysis contraindicated: e.g. anticoagulation, recent surgery, high bleed risk.

📊 Key Comparison (Finals Friendly)

	💉 IV Thrombolysis	🩻 Mechanical Thrombectomy
Route	IV alteplase / tenecteplase	Endovascular catheter retrieval
Time window	0–4.5 h (selected up to 6 h)	0–6 h; up to 24 h if favourable imaging
Best for	Smaller artery occlusion; early presenters	Large vessel occlusion (ICA, MCA, basilar)
Limitations	Risk of intracranial haemorrhage; contraindications	Needs specialist centre, interventional radiology
Benefit	↑ chance of independence at 90 days (NNT ≈ 8–10)	Major reduction in disability for LVO; NNT ≈ 3–4

📝 Exam Tip

• Always say: Thrombolysis = first-line if within 4.5 h and no contraindications.
• Thrombectomy = for LVO up to 6 h (24 h in select cases), often after thrombolysis (“bridging”).
• Both dramatically improve functional outcome → aim is disability reduction, not just survival.

🧩 Secondary Prevention

• 🩸 Antiplatelet: clopidogrel 75 mg OD (lifelong) or aspirin + dipyridamole if not tolerated.
• 💊 Statin: atorvastatin 80 mg (if non-haemorrhagic).
• 💊 Anticoagulation: if AF confirmed, start DOAC after 3–14 days (depending on stroke size).
• ⚖️ BP target: <140/90 mmHg, ACEi/diuretic first-line.
• Lifestyle: smoking cessation 🚭, exercise, diet.

🛠️ Stroke Mimics

• Seizures (Todd’s paresis).
• Hypoglycaemia.
• Brain tumour.
• Functional neurological disorder.
• Complex migraine aura.

⚠️ Complications

• Aspiration pneumonia, dysphagia (do swallow screen in 4 h).
• Raised ICP → herniation.
• DVT/PE (immobility) → give prophylaxis (stockings + LMWH if safe).
• Depression, cognitive impairment.
• Epilepsy (post-stroke seizures).

📚 Key Exam Pearls

• “Time is Brain” ⏱️ – CT within 1 h, thrombolysis ≤4.5 h, thrombectomy ≤6 h.
• Lacunar stroke = no cortical signs.
• Thrombolysis contraindications: recent surgery, bleed, very high BP >185/110.
• Always screen swallow before giving oral meds/food 🍵.
• Secondary prevention = clopidogrel + statin + BP control.

🔗 References

• NICE NG128: Stroke & TIA (2019)
• Stroke Association UK
• RCP National Clinical Guideline for Stroke

🧠 Case 1 — Large-Artery Atherosclerosis

A 72-year-old man with hypertension, hyperlipidaemia, and smoking history presents with sudden left-sided weakness and dysarthria. CT head excludes haemorrhage, and carotid Doppler reveals >80% stenosis of the right internal carotid artery. 💡 Large-vessel atherosclerosis causes thrombotic occlusion or artery-to-artery embolism, most commonly at the carotid bifurcation. Management includes reperfusion (thrombolysis/thrombectomy if eligible), antiplatelets, statins, and carotid endarterectomy/stenting if severe symptomatic stenosis.

🧠 Case 2 — Cardioembolic Stroke

A 68-year-old woman with atrial fibrillation presents with sudden onset right hemiplegia and expressive aphasia. ECG shows irregularly irregular rhythm, and echocardiogram reveals left atrial enlargement. 💡 Atrial fibrillation predisposes to thrombus formation in the left atrial appendage, which can embolise to cerebral arteries, causing large territorial infarcts. Management focuses on reperfusion acutely and long-term anticoagulation to prevent recurrence.

🧠 Case 3 — Small Vessel (Lacunar) Stroke

A 60-year-old man with long-standing diabetes and hypertension develops sudden clumsy hand and dysarthria without cortical signs. MRI brain shows a small infarct in the internal capsule. 💡 Lacunar strokes result from lipohyalinosis and microatheroma affecting penetrating arteries, causing small deep infarcts. They typically present with pure motor or pure sensory syndromes. Secondary prevention involves tight blood pressure, diabetes, and lipid control alongside antiplatelet therapy.

🧠💥 Case 1 — Intracerebral Haemorrhage (Hypertensive)

A 66-year-old man with poorly controlled hypertension presents with sudden right-sided weakness, slurred speech, and reduced consciousness. CT brain shows a large basal ganglia haemorrhage. 💡 Chronic hypertension predisposes to rupture of deep perforating arteries, causing intraparenchymal bleeding, commonly in the basal ganglia, thalamus, or pons. Management is supportive with blood pressure control, neurosurgical review for large bleeds, and treatment of raised intracranial pressure, but prognosis is often poor.

🧠💥 Case 2 — Subarachnoid Haemorrhage (Aneurysmal)

A 54-year-old woman experiences a sudden “thunderclap” headache, vomiting, and photophobia while at work. Examination reveals neck stiffness but no focal deficits. CT brain confirms subarachnoid blood. 💡 Subarachnoid haemorrhage is most often due to rupture of a berry aneurysm at the circle of Willis. It presents dramatically with severe headache and meningism. Management includes urgent neurosurgical referral for aneurysm securing (clipping or coiling), nimodipine to prevent vasospasm, and supportive neurocritical care.

🧠💥 Case 3 — Lobar Haemorrhage (Cerebral Amyloid Angiopathy)

An 80-year-old woman with progressive memory decline develops sudden confusion, left-sided weakness, and seizure. CT head shows a lobar intracerebral haemorrhage in the parietal lobe. 💡 Cerebral amyloid angiopathy is a major cause of lobar haemorrhage in the elderly, due to amyloid deposition in cortical vessels, making them fragile. Unlike hypertensive bleeds, these are more superficial and recurrent. Management is supportive, with avoidance of anticoagulants/antiplatelets and consideration of neurosurgical evacuation in select cases.