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Venous cerebral blood volume mapping in the whole brain using venous‐spin‐labeled 3D turbo spin echo
Author(s) -
Lee Hyunyeol,
Wehrli Felix W.
Publication year - 2020
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.28262
Subject(s) - hyperoxia , blood volume , pulse (music) , cerebral blood flow , cerebral blood volume , venous blood , arterial spin labeling , anesthesia , nuclear magnetic resonance , medicine , chemistry , cardiology , physics , lung , detector , optics
Purpose Venous cerebral blood volume (CBV v ) is a major contributor to BOLD contrast, and therefore is an important parameter for understanding the underlying mechanism. Here, we propose a velocity‐selective venous spin labeling (VS‐VSL)‐prepared 3D turbo spin echo pulse sequence for whole‐brain baseline CBV v mapping. Methods Unlike previous CBV v measurement techniques that exploit the interrelationship between BOLD signals and CBV v , in the proposed VS‐VSL technique both arterial blood and cerebrospinal fluid (CSF) signals were suppressed before the VS pulse train for exclusive labeling of venous blood, while a single‐slab 3D turbo spin echo readout was used because of its relative immunity to magnetic field variations. Furthermore, two approximations were made to the VS‐VSL signal model for simplified derivation of CBV v . In vivo studies were performed at 3T field strength in 8 healthy subjects. The performance of the proposed VS‐VSL method in baseline CBV v estimation was first evaluated in comparison to the existing, hyperoxia‐based method. Then, data were also acquired using VS‐VSL under hypercapnic and hyperoxic gas breathing challenges for further validation of the technique. Results The proposed technique yielded physiologically plausible baseline CBV v values, and when compared with the hyperoxia‐based method, showed no statistical difference. Furthermore, data acquired using VS‐VSL yielded average CBV v of 2.89%/1.78%, 3.71%/2.29%, and 2.88%/1.76% for baseline, hypercapnia, and hyperoxia, respectively, in gray/white matter regions. As expected, hyperoxia had negligible effect ( P > .8), whereas hypercapnia demonstrated vasodilation ( P  << .01). Conclusion Upon further validation of the quantification model, the method is expected to have merit for 3D CBV v measurements across the entire brain.

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