Abstract

The “calibrated fMRI” technique requires a hypercapnia calibration experiment in order to estimate the factor “M”. It is desirable to be able to obtain the M value without the need of a gas challenge calibration. According to the analytical expression of M, it is a function of several baseline physiologic parameters, such as baseline venous oxygenation and CBF, both of which have recently been shown to be significant modulators of fMRI signal. Here we studied the relationship among hypercapnia-calibrated M, baseline venous oxygenation and CBF, and assessed the possibility of estimating M from the baseline physiologic parameters. It was found that baseline venous oxygenation and CBF are highly correlated (R2=0.77, P<0.0001) across subjects. However, the hypercapnia-calibrated M was not correlated with baseline venous oxygenation or CBF. The hypercapnia-calibrated M was not correlated with an estimation of M based on analytical expression either. The lack of correlation may be explained by the counteracting effect of venous oxygenation and CBF on the M factor, such that the actual M value of an individual may be mostly dependent on other parameters such as hematocrit. Potential biases in hypercapnia-based M estimation were also discussed in the context of possible reduction of CMRO2 during hypercapnia.

Highlights

  • Blood-Oxygenation-Level-Dependent (BOLD) fMRI is based on MRI signal changes associated with indirect effects of neural activation [1]

  • We found that the M factor is not correlated with either baseline venous oxygenation or baseline cerebral blood flow (CBF) (Fig. 5A and B)

  • Despite strong correlation among baseline venous oxygenation and CBF themselves, no apparent relationship was identified between them and the hypercapnia-calibrated M values. This was the case for the analysis of separate CBF or venous oxygenation or their combination according to the analytical expression

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Summary

Introduction

Blood-Oxygenation-Level-Dependent (BOLD) fMRI is based on MRI signal changes associated with indirect effects of neural activation [1]. The activated brain regions are “overperfused” and the blood oxygenation level is higher than that during baseline state This difference in blood oxygenation level can be related to MR signal intensity via the paramagnetic property of the deoxyhemoglobin molecules [5]. The relationship among MR signal, hemodynamic response, and metabolism has been studied with more success [5,8,9,10,11,12,13].

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