BOLD delay times using group delay in sickle cell disease
Author(s) -
Julie Coloigner,
Chau Vu,
Adam Bush,
Matt Borzage,
Vidya Rajagopalan,
Natasha Leporé,
John C. Wood
Publication year - 2016
Publication title -
proceedings of spie, the international society for optical engineering/proceedings of spie
Language(s) - English
Resource type - Conference proceedings
SCImago Journal Rank - 0.192
H-Index - 176
eISSN - 1996-756X
pISSN - 0277-786X
DOI - 10.1117/12.2217263
Subject(s) - medicine , cardiology , magnetic resonance imaging , blood flow , neurovascular bundle , cerebral blood flow , oxygenation , ischemia , functional magnetic resonance imaging , disease , stenosis , biomarker , blood oxygen level dependent , pathology , radiology , biology , biochemistry
Sickle cell disease (SCD) is an inherited blood disorder that effects red blood cells, which can lead to vasoocclusion, ischemia and infarct. This disease often results in neurological damage and strokes, leading to morbidity and mortality. Functional Magnetic Resonance Imaging (fMRI) is a non-invasive technique for measuring and mapping the brain activity. Blood Oxygenation Level-Dependent (BOLD) signals contain also information about the neurovascular coupling, vascular reactivity, oxygenation and blood propagation. Temporal relationship between BOLD fluctuations in different parts of the brain provides also a mean to investigate the blood delay information. We used the induced desaturation as a label to profile transit times through different brain areas, reflecting oxygen utilization of tissue. In this study, we aimed to compare blood flow propagation delay times between these patients and healthy subjects in areas vascularized by anterior, middle and posterior cerebral arteries. In a group comparison analysis with control subjects, BOLD changes in these areas were found to be almost simultaneous and shorter in the SCD patients, because of their increased brain blood flow. Secondly, the analysis of a patient with a stenosis on the anterior cerebral artery indicated that signal of the area vascularized by this artery lagged the MCA signal. These findings suggest that sickle cell disease causes blood propagation modifications, and that these changes could be used as a biomarker of vascular damage.
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