Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care

🧠 Introduction

Stroke collaterals are alternative vascular pathways that maintain perfusion when a main artery is blocked. They determine whether tissue becomes infarct core or preserved penumbra. Good collaterals ⏳ slow infarct growth, extend the treatment window, and improve outcomes.

🔬 Anatomy & Physiology

• 🔄 Circle of Willis: Anterior communicating artery (ACA ↔ ACA) & posterior communicating arteries (ICA ↔ PCA) link anterior & posterior flow.
• 🌐 Leptomeningeal (Pial) Collaterals: Tiny cortical arterioles connecting MCA ↔ ACA ↔ PCA territories.
• 🌉 Extracranial–Intracranial Collaterals: Ophthalmic artery, facial, maxillary, and middle meningeal anastomoses support intracranial flow when carotids fail.

📊 Flow Thresholds

• 💧 Normal: 50–60 mL/100g/min.
• 🟡 Benign oligemia: >17 mL/100g/min (no immediate infarction).
• 🟠 Penumbra: 10–17 mL/100g/min (viable if rescued).
• 🔴 Core: <10 mL/100g/min (irreversible damage).

✨ Collaterals keep penumbral tissue alive until reperfusion is achieved.

⚙️ Pathophysiological Impact

• ✅ Good Collaterals: Smaller infarcts, more time for thrombectomy, lower haemorrhagic risk.
• ❌ Poor Collaterals: Rapid core growth, worse outcomes, higher reperfusion injury risk.

🧾 Factors Influencing Collaterals

• 🧬 Anatomical variants: Completeness of Circle of Willis.
• 📈 Chronic ischaemia: Atherosclerosis promotes arteriogenesis.
• 👵 Age & comorbidities: Diabetes, HTN reduce vessel adaptability.
• ⚡ Acute occlusion: Embolic events give no time for recruitment → worse outcome.

🏥 Clinical Relevance

• 📉 Prognosis: Collateral grade predicts infarct size & functional recovery.
• 💉 Treatment selection: Strong collaterals = better response to tPA & thrombectomy.
• 🩸 Risk: Poor collaterals → higher risk of reperfusion haemorrhage.

🖼 Imaging Collaterals

• 🩻 CTA: Rapid grading (e.g. ASITN/SIR score).
• 🧲 MRA: Non-invasive, can show dynamic flow.
• 📡 DSA: Gold standard (often during thrombectomy).
• 📊 Perfusion Imaging: Defines core vs penumbra.
• 🔍 TCD: Detects flow diversion across ACom/PCom arteries.

🛠️ Management Considerations

• 🚑 Reperfusion: IV tPA & thrombectomy – outcomes strongly collateral-dependent.
• 💉 BP targets: Avoid dropping perfusion pressure in patients reliant on collaterals.
• 🫀 Risk reduction: Antiplatelets, statins, lifestyle to protect fragile networks.
• ♿ Support & Rehab: Intensive monitoring if collaterals are poor.

⏳ Chronic Collateral Development

• 🧩 Arteriogenesis: Gradual stenosis allows adaptive vessel growth.
• 🩸 Moyamoya disease: Fragile "smoke-like" collaterals prone to rupture.
• 🟢 Asymptomatic carotid occlusion: Often possible thanks to robust collaterals.
• ⚠️ Sudden occlusions: No time for adaptation → catastrophic deficits.

✅ Conclusion

Cerebral collaterals are the brain’s natural bypass system. They explain why two patients with the same occlusion may have dramatically different outcomes. Assessing collateral flow is central to modern stroke imaging, treatment selection, and prognosis.

📚 References

• Liebeskind DS. Collateral circulation. Stroke. 2003.
• Menon BK, et al. Multiphase CTA for stroke triage. Radiology. 2015.
• Campbell BCV, et al. Failure of collaterals predicts infarct growth. JCBFM. 2013.
• Schirmer SH, et al. Collateral artery growth & P2Y2 receptor. Cardiovasc Res. 2004.