Testing vascular contributions to BOLD spin-echo EPI signals with cortical B0 orientation effects

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Abstract Submission 


Olivia Viessmann1, Avery Berman1, W Scott Hoge2, Kawin Setsompop1,3, Lawrence Wald1,3, Jonathan Polimeni1,3


1A. A. Martinos Center for Biomedical Imaging, Harvard Medical School, Massachusetts General Hospital, Charlestown, Boston, MA, 2Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 3Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Cambridge, MA



Spin-echo (SE) BOLD is ideally sensitive to signal changes from the microvasculature and therfore provide enhanced spatial localisation of activation. However, SE EPI can be contaminated by T2* and therefore contributions from unspecific pial vessels on the cortical surface. The dependence of BOLD signal fluctuations on the orientation of the cortex relative to B0 has been proposed to disentangle micro- and macrovascular (i.e. capillary and pial) BOLD signal contributions[1,2].Pials generate extra- and intravascular field offsets of which the former are expected to introduce a sine-square and the latter a cosine-square signal dependence on cortical orientation. Two imaging parameters are thought to influence their relative contributions in SE-EPI:
1. Echo time (TE) dictates the time available for spins to diffuse in the extravascular field. Shorter TEs shift sensitivity to smaller vessel radii as spins in their vicinity experience broader ranges of field offsets compared to spins closer to large vessels[3]. Decreasing TE also increases the ratio of intra-to-extravascular signal contributions to the signal[4], but further reduces contrast-to-noise levels.
2. Echo train length (ETL) of the EPI readout: Ideally SE signals are governed by T2 relaxation, but pure T2 weighting is only achieved for kspace lines acquired at TE, the time of SE refocusing, and a T2' component from extravascular pial contributions is introduced during the EPI readout[5].
Here, we use cortical B0 orientation(Fig.1) to test if different TEs and ETLs produce distinguishable orientation profiles to disentangle vascular contributions in resting-state(rs) BOLD SE-EPI.


8 volunteers were scanned on a 7T scanner(Magnetom, Siemens, Germany). Each subject underwent 3×2 runs of BOLD SE-EPI with 2mm isotropic resolution,TR=3510ms,matrix=96×96×40,GRAPPA=4,105 volumes. Of these, 2 runs had a TE=25ms and ETL=13ms; 2 runs had a TE=55ms and ETL=13ms (only 3 out of the 8 subjects) and 2 runs had a TE=55ms and ETL=34ms. A T1-w MEMPRAGE (0.75mm isotropic resolution) was also acquired.
The T1-w image was processed with FreeSurfer to reconstruct the pial and white surfaces and an additional set of intracortical surfaces at 0.1 depth increments for cortical depth analysis. Surfaces were transformed into the subject's head position during the rs-fMRI runs and the orientation angle θB0 at each mesh vertex (Fig.1) was calculated and assigned to the EPI voxels[2]. tSNR, as a proxy for the BOLD signal amplitude, was calculated from the time series. EPI voxels were then sorted by orientation angle and relative cortical depth to plot tSNR vs. orientation for all depths.
Supporting Image: Fig1.png
   ·Figure 1: Cortical orientation to the main magnetic field B0 axis. Cortical orientation (and as such vascular orientation) varies between parallel and perpendicular alignment.


Fig.2 a-d show the tSNR orientation profiles for decreasing cortical depth for the three SE-EPI settings. Orientation profiles for the different TEs are clearly distinguishable. The longer TE shows larger orientation bias associated with pial vessels (sine-square dependence). The long TE data shows no intravascular (cosine-square dependence) component, but the short TE data has a maximum bias shifted away from 90º, in particular at the pial surface (Fig. 2 a/b). This suggests that an intravascular pial contribution may be added to the short TE SE-EPI signal. Longer ETL tends to enhance the sine-square dependence suggesting an overall increase in pial contribution.
Supporting Image: Figure2.png
   ·Figure 2: Orientation profiles for different TE and ETL (yellow shade is the std. dev. over all subjects). a) depth=0.9→ 1.2; b) depth=0.6 → 0.9; c) depth=0.3 → 0.6; d) depth=0.0 → 0.3.


This study reproduces the cortical B0 orientation dependence in SE-EPI that was recently demonstrated in BOLD gradient-echo EPI. We observe diverging orientation profiles for BOLD SE-EPI with different TE and ETL. Both shorter TE and ETL appear to decrease extravascular contributions from the pial vessels, but decreasing TE might introduce an additional intravascular component. Further simulation work is needed to understand the orientation signature of the capillary bed, presumed to have a static random orientation, although some orientation bias might even be present within the capillary network given its overall bulk flow parallel to the cortex.

Imaging Methods:


Modeling and Analysis Methods:

Task-Independent and Resting-State Analysis 2


Cortical Layers

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Was any human subjects research approved by the relevant Institutional Review Board or ethics panel? NOTE: Any human subjects studies without IRB approval will be automatically rejected.


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Functional MRI
Structural MRI

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Free Surfer

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[1] Gagnon et al., (2015) ‘Quantifying the Microvascular Origin of BOLD-fMRI from First Principles with Two-Photon Microscopy and an Oxygen-Sensitive Nanoprobe’, Journal of Neuroscience, 35(8):3663-3675
[2] Viessmann et al., (2018) ‘The EPI rs-fMRI signal shows an orientation effect with respect to B0 and phase-encode axis across cortical depth’, Proceedings of the ISMRM
[3] Boxerman et al., (1995) ‘MR Contrast Due to Intravascular Magnetic-Susceptibility Perturbations’, Magnetic Resonance in Medicine, 34(4);555-566
[4] Duong et al.,(2003) ‘Microvascular BOLD contribution at 4 and 7 T in the human brain: Gradient‐echo and spin‐echo fMRI with suppression of blood effects’, NeuroImage, 49(6): 1019-1026
[5] Goense and Logothetis, (2006) ‘Laminar specificity in monkey V1 using high-resolution SE-fMRI’, Magnetic Resonance in Medicine, 24(4):381-392.