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Collateral circulation in symptomatic intracranial atherosclerosis

David S Liebeskind1, George A Cotsonis, Jeffrey L Saver

  • 1Department of Neurology, UCLA Stroke Center, University of California-Los Angeles, 710 Westwood Plaza, Los Angeles, CA 90095, USA. davidliebeskind@yahoo.com

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|December 16, 2010
PubMed

Insights

Collateral circulation in intracranial atherosclerosis is often absent or minimal, especially in less severe stenoses. More severe arterial narrowing drives greater collateral compensation, highlighting its role in disease pathophysiology.

Area of Science:

  • Neurology
  • Vascular Medicine
  • Radiology

Background:

  • Intracranial atherosclerosis (ICAS) pathophysiology is not fully understood.
  • Collateral circulation's role in ICAS has not been systematically characterized.

Purpose of the Study:

  • To systematically investigate and characterize collateral circulation in patients with symptomatic intracranial atherosclerosis.

Main Methods:

  • Multicenter trial analyzing baseline angiography in 569 patients.
  • Utilized angiographic scales to assess lesion characteristics, flow, perfusion, and collateral status.
  • Blinded review of collateral circulation in internal carotid, middle cerebral, vertebral, and basilar arteries.

Main Results:

  • Collateral data was available for 287 patients (50%) with stenoses from 50% to 99%.
  • 69% had absent/none collaterals; 4% had rapid, complete perfusion.
  • Collateral extent correlated significantly with stenosis severity (P<0.0001) and diminished antegrade flow (P<0.001).

Conclusions:

  • Collateral perfusion is a pivotal component in ICAS pathophysiology.
  • Findings suggest a need for further evaluation of collaterals in ongoing ICAS studies.
  • Detailed description of collaterals across various stenoses provides new insights.

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