TY - JOUR
T1 - A mechanistic computational framework to investigate the hemodynamic fingerprint of the blood oxygenation level-dependent signal
AU - Báez-Yáñez, Mario Gilberto
AU - Siero, Jeroen C.W.
AU - Petridou, Natalia
N1 - Funding Information:
The authors would like to extend their thanks for the thoughtful commentary, suggestions, and revision help from Matthias van Osch (LUMC, The Netherlands). We would like to express our gratitude to the anonymous reviewers for their valuable comments and suggestions. This work was supported by the National Institute of Mental Health of the National Institutes of Health under the Award Number R01MH111417 and the Dutch Research Council under the Award Number 18969. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Publisher Copyright:
© 2023 The Authors. NMR in Biomedicine published by John Wiley & Sons Ltd.
PY - 2023/12
Y1 - 2023/12
N2 - Blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) is one of the most used imaging techniques to map brain activity or to obtain clinical information about human cortical vasculature, in both healthy and disease conditions. Nevertheless, BOLD fMRI is an indirect measurement of brain functioning triggered by neurovascular coupling. The origin of the BOLD signal is quite complex, and the signal formation thus depends, among other factors, on the topology of the cortical vasculature and the associated hemodynamic changes. To understand the hemodynamic evolution of the BOLD signal response in humans, it is beneficial to have a computational framework available that virtually resembles the human cortical vasculature, and simulates hemodynamic changes and corresponding MRI signal changes via interactions of intrinsic biophysical and magnetic properties of the tissues. To this end, we have developed a mechanistic computational framework that simulates the hemodynamic fingerprint of the BOLD signal based on a statistically defined, three-dimensional, vascular model that approaches the human cortical vascular architecture. The microvasculature is approximated through a Voronoi tessellation method and the macrovasculature is adapted from two-photon microscopy mice data. Using this computational framework, we simulated hemodynamic changes—cerebral blood flow, cerebral blood volume, and blood oxygen saturation—induced by virtual arterial dilation. Then we computed local magnetic field disturbances generated by the vascular topology and the corresponding blood oxygen saturation changes. This mechanistic computational framework also considers the intrinsic biophysical and magnetic properties of nearby tissue, such as water diffusion and relaxation properties, resulting in a dynamic BOLD signal response. The proposed mechanistic computational framework provides an integrated biophysical model that can offer better insights regarding the spatial and temporal properties of the BOLD signal changes.
AB - Blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) is one of the most used imaging techniques to map brain activity or to obtain clinical information about human cortical vasculature, in both healthy and disease conditions. Nevertheless, BOLD fMRI is an indirect measurement of brain functioning triggered by neurovascular coupling. The origin of the BOLD signal is quite complex, and the signal formation thus depends, among other factors, on the topology of the cortical vasculature and the associated hemodynamic changes. To understand the hemodynamic evolution of the BOLD signal response in humans, it is beneficial to have a computational framework available that virtually resembles the human cortical vasculature, and simulates hemodynamic changes and corresponding MRI signal changes via interactions of intrinsic biophysical and magnetic properties of the tissues. To this end, we have developed a mechanistic computational framework that simulates the hemodynamic fingerprint of the BOLD signal based on a statistically defined, three-dimensional, vascular model that approaches the human cortical vascular architecture. The microvasculature is approximated through a Voronoi tessellation method and the macrovasculature is adapted from two-photon microscopy mice data. Using this computational framework, we simulated hemodynamic changes—cerebral blood flow, cerebral blood volume, and blood oxygen saturation—induced by virtual arterial dilation. Then we computed local magnetic field disturbances generated by the vascular topology and the corresponding blood oxygen saturation changes. This mechanistic computational framework also considers the intrinsic biophysical and magnetic properties of nearby tissue, such as water diffusion and relaxation properties, resulting in a dynamic BOLD signal response. The proposed mechanistic computational framework provides an integrated biophysical model that can offer better insights regarding the spatial and temporal properties of the BOLD signal changes.
KW - biophysical modeling
KW - BOLD signal
KW - diffusion
KW - hemodynamic response
KW - microvasculature
KW - Monte Carlo simulation
KW - susceptibility
KW - Voronoi tessellation
UR - http://www.scopus.com/inward/record.url?scp=85168855662&partnerID=8YFLogxK
U2 - 10.1002/nbm.5026
DO - 10.1002/nbm.5026
M3 - Article
AN - SCOPUS:85168855662
SN - 0952-3480
VL - 36
JO - NMR in Biomedicine
JF - NMR in Biomedicine
IS - 12
M1 - e5026
ER -