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Exploring the post-stimulus undershoot with spin-echo fMRI: implications for models of neurovascular response
Benedikt A Poser1, Emily van Mierlo, David G Norris
1Erwin L. Hahn Institute for Magnetic Resonance Imaging, University Duisburg-Essen, Essen, Germany. benedikt.poser@donders.ru.nl
Human Brain Mapping
|July 13, 2010
Summary
The BOLD undershoot in fMRI is caused by elevated deoxyhemoglobin in small vessels post-stimulation. Delayed vascular compliance models do not fully explain this, suggesting a decoupling of oxygen metabolism and blood flow.
Area of Science:
- Neuroimaging
- Biophysics
- Physiology
Background:
- Functional MRI (fMRI) using gradient-echo echo-planar imaging (GE-EPI) detects neural activity via the Blood Oxygenation-Level Dependent (BOLD) contrast.
- A characteristic BOLD signal undershoot below baseline is commonly observed after stimulation with GE-EPI, but its origin remains debated.
- Existing hypotheses involve factors like delayed vascular compliance and blood volume changes, but lack definitive experimental support.
Purpose of the Study:
- To investigate the underlying mechanisms of the BOLD signal undershoot following visual stimulation.
- To differentiate between competing hypotheses for the BOLD undershoot using T₂-weighted fMRI at different field strengths (1.5 T and 3 T).
- To assess the validity of 'delayed vascular compliance' and blood volume changes in explaining the observed BOLD undershoot.
Main Methods:
- Utilized a purely T₂-weighted fMRI sequence to isolate BOLD signal changes.
- Conducted experiments at both 1.5 T and 3 T to leverage field strength-dependent T₂ contrast.
- Analyzed the undershoot-to-main response ratio across different field strengths and conditions.
Main Results:
- A significant BOLD undershoot was observed at both 1.5 T and 3 T, with a consistent undershoot-to-main response ratio.
- The findings strongly suggest the undershoot is driven by elevated post-stimulus deoxyhemoglobin concentration in small cerebral vessels.
- Neither 'delayed vascular compliance' (as per Balloon/Windkessel models) nor solely blood volume changes in arterioles/capillaries could fully account for the undershoot.
Conclusions:
- The BOLD undershoot is primarily attributed to increased deoxyhemoglobin in small vessels after neural stimulation.
- Current models of neurovascular response require refinement, particularly regarding the interplay between oxygen metabolism and blood flow.
- An 'arteriolar balloon' mechanism, representing delayed arterial compliance, may plausibly explain the temporal dynamics of the BOLD undershoot.
