Related Experiment Video
Updated: May 31, 2026

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
Published on: March 14, 2017
Cerebral Blood Transit in Sickle Cell Anemia
Wesley T Richerson1, Megan A Aumann1, Alexander K Song1
1Department of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Sickle cell anemia patients exhibit increased venous blood volume and faster venous arrival time (VAT). These blood transit differences suggest complex vascular kinetics not solely tied to anemia severity.
Area of Science:
- Neuroimaging
- Vascular Biology
- Hematology
Background:
- Sickle cell anemia (SCA) involves increased cerebral blood flow due to reduced arterial oxygen content.
- This can lead to venous hyperintensities on ASL MRI, potentially indicating faster capillary transit, altered OEF, and stroke risk.
Purpose of the Study:
- Implement multi-delay ASL to quantify AAT, ATT, and VAT in SCA patients.
- Investigate if these parameters are reduced in SCA and correlate with disease severity.
Main Methods:
- Prospective, cross-sectional study of 40 SCA patients and 24 controls.
- Utilized multi-delay PASL MRI to measure AAT, gray matter ATT, VAT, and venous blood volume.
- Assessed OEF, infarcts, and vasculopathy via imaging and radiological review.
Main Results:
- SCA patients showed significantly increased venous labeled blood volume and reduced VAT compared to controls.
- AAT and gray matter ATT, but not VAT, correlated with hemoglobin levels.
- No significant relationships were found between AAT, ATT, VAT, and OEF or prior infarcts.
Conclusions:
- SCA patients demonstrate elevated venous blood volume and shorter VAT.
- Differential relationships between blood transit and hemoglobin across vascular compartments suggest complex venous blood kinetics in SCA.
Related Concept Videos
Hemorrhagic Stroke ll: Pathophysiology
Cerebral Edema ll: Pathophysiology
Transcellular Transport of Solutes
The Blood-brain Barrier
Hemorrhagic Stroke l: Introduction
Ischemic Stroke ll: Pathophysiology
