Biophysical Origins of the fMRI Signal
Kamil Uludag1,2
1Krembil Brain Institute, UHN, Canada, 2Medical Biophysics, University of Toronto, Toronto, ON, Canada

Synopsis

Keywords: Neuro: Brain function, Neuro: Brain connectivity, Contrast mechanisms: fMRI

I will describe the physiological processes underlying BOLD signal and discuss the generative biophysical model and its time course properties: It primarily results from changes in oxygen metabolism, cerebral blood flow, and volume, which affect paramagnetic deoxygenated hemoglobin. The physiological origin of BOLD signal transients, such as the initial overshoot, steady-state activation, and post-stimulus undershoot, will be explored. Incorrect physiological assumptions in the generative model of the BOLD signal can lead to incorrect inferences about local neuronal activity and effective connectivity between brain regions. The author also introduces the recent laminar BOLD signal model.

Abstract

In this talk, I will provide an overview of the physiological processes that contribute to the observed BOLD signal (i.e., the generative biophysical model), including their time course properties. The BOLD signal is primarily determined by the change in paramagnetic deoxygenated hemoglobin, which results from combination of changes in oxygen metabolism, and cerebral blood flow and volume. Specifically, the physiological origin of the so-called BOLD signal “transients” will be discussed, including the initial overshoot, steady-state activation and the post-stimulus undershoot. I argue that incorrect physiological assumptions in the generative model of the BOLD signal can lead to incorrect inferences pertaining to both local neuronal activity and effective connectivity between brain regions. In addition, I introduce the recent laminar BOLD signal model, which extends the generative to cortical depths-resolved BOLD signals, allowing for laminar neuronal activity to be determined using high-resolution fMRI data.

Acknowledgements

No acknowledgement found.

References

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Figures

Average BOLD time courses from early visual cortex in humans acquired at 3T for flickering in static checkerboards. After an initial overshoot, a new steady-state level is achieved followed by a post-stimulus undershoot variable in its amplitude depending on the stimulation. Figure from (Sadaghiani et al., 2009) with permission.

Chain of physiological events leading to the BOLD signal: Increase in neuronal activity is associated with increase in cerebral metabolic rate of oxygen (CMRO2) and leads to increase in cerebral blood flow and volume (CBF and CBV, respectively). While the increase in CMRO2 and CBV leads to increase in paramagnetic deoxygenated hemoglobin (dOHb), the increase in CBF leads to a decrease in dOHb. The combined effect of CMRO2, CBF and CBV results in a decrease in dOHb, which in turn lead to an increase in the blood oxygenation level-dependent (BOLD) signal.

Set-up of the physiologically-informed dynamic causal model (P-DCM). See text for description and details in Figure taken from (Havlicek et al., 2017c) with permission.

Intra-cortical vasculature (left): Pial arteries transport oxygenated hemoglobin to the cortex. Diving intra-cortical arteries branch into the arterioles and then capillaries. Deoxygenated blood is transported via venules and intra-cortical ascending veins to the surface of the cortex from where it is drained outside of the brain via pial veins. Dynamical mass balance model (right) of deoxygenated hemoglobin and cerebral blood volume (Q and V, respectively) in the micro-vasculature, and ascending and pial veins. Figure taken from (Havlicek and Uludağ, 2020) with permission.

Proc. Intl. Soc. Mag. Reson. Med. 31 (2023)