title: On the origin of respiratory artifacts in BOLD-EPI of the human brain.
abstract: BOLD-based functional MRI (fMRI) can be used to explicitly measure hemodynamic aspects and functions of human neuro-physiology. As fMRI measures changes in regional cerebral blood flow and volume as well as blood oxygenation, rather than neuronal brain activity directly, other processes that may change the above parameters have to be examined closely to assess sensitivity and specificity of fMRI results. Physiological processes that can cause artifacts include cardiac action, breathing and vasomotion. Although there has been substantial research on physiological artifacts and appropriate compensation methods, controversy still remains on the mechanisms that cause the fMRI signal fluctuations. Respiratory-correlated fluctuations may either be induced by changes of the magnetic field homogeneity due to moving organs, intra-thoracic pressure differences, respiration-dependent vasodilation or oxygenation differences. The aim of this study was to characterize the impact of different breathing patterns by varying respiration frequency and/or tidal volume on EPI time courses of the resting human brain. The amount of respiration-related oscillations during three respiration patterns was quantified, and statistically significant differences were obtained in white matter only: p < 0.03 between 6 vs. 12 ml/kg body weight end tidal volume at a respiration frequency of 15/min, p < 0.03 between 12 vs. 6 ml/kg body weight and 15 vs. 10 respiration cycles/min. There was no significant difference between 15 vs. 10 respiration cycles/min at an end tidal volume of 6 ml/kg body weight (p = 0.917). In addition, the respiration-affected brain regions were very similar with EPI readout in the a-p and l-r direction. Based on our results and published literature we hypothesize that venous oxygenation oscillations due to changing intra-thoracic pressure represent a major factor for respiration-related signal fluctuations and increase significantly with increasing end tidal volume in white matter only.
authors.affiliation: Institute for Medical Physics, University of Vienna, Austria.
authors.forename: Christian
authors.initials: C
authors.lastname: Windischberger
authors.forename: Herbert
authors.initials: H
authors.lastname: Langenberger
authors.forename: Thomas
authors.initials: T
authors.lastname: Sycha
authors.forename: Edda M
authors.initials: EM
authors.lastname: Tschernko
authors.forename: Gabriele
authors.initials: G
authors.lastname: Fuchsjäger-Mayerl
authors.forename: Leopold
authors.initials: L
authors.lastname: Schmetterer
authors.forename: Ewald
authors.initials: E
authors.lastname: Moser
mesh_terms: D000328:Adult; D016477:Artifacts; D001921:Brain / Q000098:blood supply* / Q000502:physiology*; D002536:Cerebral Arteries / Q000502:physiology; D002550:Cerebral Veins / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D010865:Pilot Projects; D012680:Sensitivity and Specificity; D013990:Tidal Volume / Q000502:physiology*