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 refer to the alternative vascular pathways that can supply blood flow to brain tissue when primary vessels are occluded or stenosed. The presence and effectiveness of collateral circulation play a critical role in determining the extent of ischemic injury and the clinical outcome in patients with acute ischemic stroke. Adequate collateral circulation can maintain perfusion, delay infarct progression, and improve the potential for successful reperfusion therapies.

Anatomy and Physiology of Cerebral Collaterals

The cerebral collateral circulation consists of interconnected vascular networks that can compensate for reduced or blocked arterial flow. The primary collateral pathways include:

• Circle of Willis:
  • The anterior communicating artery connects the left and right anterior cerebral arteries (ACAs), allowing cross-flow between hemispheres.
  • The posterior communicating arteries connect the posterior cerebral arteries (PCAs) to the internal carotid arteries (ICAs), linking anterior and posterior circulations.
• Leptomeningeal (Pial) Collaterals:
  • Small arterioles on the brain's surface connecting distal branches of major cerebral arteries (e.g., between MCA and ACA or PCA territories).
  • Provide anastomotic channels that can reroute blood flow during arterial occlusion.
• Extracranial-Intracranial Collaterals:
  • Connections between external carotid artery (ECA) branches and intracranial vessels, such as through the ophthalmic artery.
  • Anastomoses from the facial, maxillary, and middle meningeal arteries can contribute to cerebral perfusion when ICAs are compromised.

Physiological Flow Needs

Cerebral blood flow (CBF) thresholds are critical in determining tissue viability:

• Normal CBF: Approximately 50-60 mL/100 g of brain tissue per minute.
• Benign Oligemia: CBF >17 mL/100 g/min; reduced flow without immediate risk of infarction.
• Ischemic Penumbra: CBF between 10-17 mL/100 g/min; viable tissue at risk of infarction without reperfusion.
• Infarct Core: CBF <10 mL/100 g/min; irreversible tissue damage.

Effective collateral circulation can maintain CBF above critical thresholds, preserving the penumbra and extending the therapeutic window for interventions.

Role of Collaterals in Stroke Pathophysiology

The presence and quality of collateral vessels influence stroke severity and outcomes:

• Good Collateral Circulation:
  • Maintains perfusion to ischemic areas, reducing infarct size.
  • Delays the progression of tissue injury, allowing more time for reperfusion therapies.
  • Associated with better functional outcomes and reduced risk of hemorrhagic transformation.
• Poor Collateral Circulation:
  • Leads to rapid infarct growth and larger infarct cores.
  • Increased risk of reperfusion injury and hemorrhagic transformation upon revascularization.
  • Associated with worse clinical outcomes and higher mortality.

Factors Influencing Collateral Circulation

• Anatomical Variations: Individual differences in vascular anatomy, such as completeness of the Circle of Willis, affect collateral potential.
• Chronic Ischemia: Conditions like atherosclerosis can stimulate arteriogenesis, enhancing collateral networks over time.
• Age and Comorbidities: Older age and conditions like diabetes mellitus may impair collateral vessel development and function.
• Acute Occlusion Dynamics: Sudden occlusions (e.g., embolism) may not allow time for collateral recruitment compared to gradual vessel narrowing.

Clinical Implications

Understanding collateral status has important clinical implications in stroke management:

• Prognosis Prediction: Collateral assessment helps predict stroke severity and potential recovery.
• Treatment Decisions: Patients with good collaterals may benefit more from reperfusion therapies like thrombolysis and mechanical thrombectomy.
• Risk Stratification: Identifying patients at risk of hemorrhagic transformation or reperfusion injury based on poor collaterals.

Investigations

Evaluating collateral circulation involves various imaging modalities:

• Computed Tomography Angiography (CTA):
  • Provides rapid assessment of vascular anatomy and collateral vessels.
  • Collateral grading systems (e.g., ASITN/SIR grading) can quantify collateral flow.
• Magnetic Resonance Angiography (MRA):
  • Non-invasive visualization of intracranial and extracranial vessels.
  • Time-resolved MRA techniques can assess dynamic collateral flow.
• Digital Subtraction Angiography (DSA):
  • Gold standard for detailed vascular imaging and collateral assessment.
  • Invasive procedure, typically used during endovascular interventions.
• Perfusion Imaging:
  • CT or MR perfusion studies evaluate cerebral blood flow, volume, and transit times.
  • Identify penumbral tissue and guide treatment decisions.
• Transcranial Doppler Ultrasound (TCD):
  • Assesses blood flow velocities in major cerebral arteries.
  • Can detect collateral flow via anterior and posterior communicating arteries.

Management Considerations

Management strategies should consider collateral status:

• Reperfusion Therapies:
  • Intravenous Thrombolysis: Timely administration can restore flow, especially beneficial in patients with good collaterals.
  • Mechanical Thrombectomy: Effective for large vessel occlusions; collateral status aids in patient selection and predicting outcomes.
• Blood Pressure Management:
  • Careful regulation to optimize cerebral perfusion without exacerbating edema or causing hemorrhagic transformation.
• Long-Term Risk Reduction:
  • Management of atherosclerotic risk factors to prevent further vascular compromise.
  • Antiplatelet therapy, statins, and lifestyle modifications.
• Monitoring and Supportive Care:
  • Close monitoring for neurological deterioration in patients with poor collaterals.
  • Rehabilitation services to maximize functional recovery.

Collateral Development in Chronic Ischemia

Chronic arterial stenosis or occlusion can stimulate the development of collateral vessels through arteriogenesis:

• Adaptation Over Time: Gradual vessel narrowing allows for compensatory collateral growth.
• Moyamoya Disease: A chronic condition characterized by progressive stenosis of intracranial arteries and development of fragile collateral networks prone to hemorrhage.
• Asymptomatic Occlusions: Patients with progressive carotid stenosis may remain symptom-free due to effective collateralization.
• Sudden Occlusions: Acute events like arterial dissection may result in severe deficits due to insufficient time for collateral recruitment.

Conclusion

The collateral circulation is a crucial determinant of stroke outcomes. Assessing collateral status provides valuable prognostic information and can guide therapeutic interventions. Enhancing our understanding of collateral dynamics may lead to improved strategies for managing acute ischemic stroke and optimizing patient recovery.

References

• Liebeskind DS. Collateral circulation. Stroke. 2003;34(9):2279-2284.
• Bang OY, Saver JL, Buck BH, et al. Cerebral atherothrombosis and collaterals. Stroke. 2008;39(6):1899-1904.
• Menon BK, d’Esterre CD, Qazi EM, et al. Multiphase CT angiography: a new tool for the imaging triage of patients with acute ischemic stroke. Radiology. 2015;275(2):510-520.
• Campbell BCV, Christensen S, Tress BM, et al. Failure of collateral blood flow is associated with infarct growth in ischemic stroke. J Cereb Blood Flow Metab. 2013;33(8):1168-1172.
• Schirmer SH, van Nooijen FC, Piek JJ, van Royen N. Collateral artery growth and angiogenesis require purinergic receptor P2Y2. Cardiovasc Res. 2004;63(4):678-685.