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      Analysis of Fluctuation in Cerebral Venous Oxygenation Using MR Imaging: Quantitative Evaluation of Vasomotor Function of Arterioles

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          Abstract

          Purpose:

          Cerebral arteriolar vasomotor function plays an important role in brain health. Since respiratory changes in the partial arterial pressure of CO 2 (PaCO 2) cause arterioles to vasodilate or vasoconstrict, resting-state arteriolar vasomotion results in the fluctuation of venous blood oxygenation, which can be monitored by observing magnetic resonance (MR) signals. Focusing on the superior sagittal sinus as the largest cerebral vein, we developed a method to elucidate the respiratory fluctuation of cerebral venous oxygenation that may reflect the vasomotor function.

          Methods:

          Single slices of varying thickness (7–15 mm) taken perpendicular to the superior sagittal sinus of five volunteers were imaged by spin-echo echo-planar imaging using a 1.5-T MR system. The time series of the signal intensity at the superior sagittal sinus was Fourier-transformed, and the spectral fluctuation intensity (SFI) at respiratory frequency was obtained. The amplitude of the respiratory fluctuation in the cerebral venous oxygenation was calculated from the gradient of the relation between the SFI and the average signal intensity, which increased proportionally with an increase in slice thickness. The amplitude of the fluctuation in cerebral venous oxygenation at low (<0.1 Hz) and cardiac pulsation frequencies was also calculated for comparison with the respiratory fluctuation.

          Results:

          The amplitude of respiratory fluctuation in the cerebral venous oxygenation was quantified as 1.2%, demonstrating the validity of our method via the highest significant correlation ( r = 0.82) in the plot of SFI and average signal intensities; the correlations at low and cardiac pulsation frequencies were 0.60 and 0.63, respectively.

          Conclusion:

          We have successfully demonstrated cerebral venous oxygenation fluctuation at respiratory frequencies in the resting state. This fluctuation was non-invasively evaluated as 1.2%, representing the control value for the arteriolar vasomotor function of a healthy human.

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          Most cited references25

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          Separating respiratory-variation-related fluctuations from neuronal-activity-related fluctuations in fMRI.

          Subtle changes in a subject's breathing rate or depth, which occur naturally during rest at low frequencies (<0.1 Hz), have been shown to be significantly correlated with fMRI signal changes throughout gray matter and near large vessels. The goal of this study was to investigate the impact of these low-frequency respiration variations on both task activation fMRI studies and resting-state functional connectivity analysis. Unlike MR signal changes correlated with the breathing motion ( approximately 0.3 Hz), BOLD signal changes correlated with across-breath variations in respiratory volume ( approximately 0.03 Hz) appear localized to blood vessels and regions with high blood volume, such as gray matter, similar to changes seen in response to a breath-hold challenge. In addition, the respiration-variation-induced signal changes were found to coincide with many of the areas identified as part of the 'default mode' network, a set of brain regions hypothesized to be more active at rest. Regions could therefore be classified as being part of a resting network based on their similar respiration-induced changes rather than their synchronized neuronal activity. Monitoring and removing these respiration variations led to a significant improvement in the identification of task-related activation and deactivation and only slight differences in regions correlated with the posterior cingulate at rest. Regressing out global signal changes or cueing the subject to breathe at a constant rate and depth resulted in an improved spatial overlap between deactivations and resting-state correlations among areas that showed deactivation.
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            Measuring cerebrovascular reactivity: what stimulus to use?

            Cerebrovascular reactivity is the change in cerebral blood flow in response to a vasodilatory or vasoconstrictive stimulus. Measuring variations of cerebrovascular reactivity between different regions of the brain has the potential to not only advance understanding of how the cerebral vasculature controls the distribution of blood flow but also to detect cerebrovascular pathophysiology. While there are standardized and repeatable methods for estimating the changes in cerebral blood flow in response to a vasoactive stimulus, the same cannot be said for the stimulus itself. Indeed, the wide variety of vasoactive challenges currently employed in these studies impedes comparisons between them. This review therefore critically examines the vasoactive stimuli in current use for their ability to provide a standard repeatable challenge and for the practicality of their implementation. Such challenges include induced reductions in systemic blood pressure, and the administration of vasoactive substances such as acetazolamide and carbon dioxide. We conclude that many of the stimuli in current use do not provide a standard stimulus comparable between individuals and in the same individual over time. We suggest that carbon dioxide is the most suitable vasoactive stimulus. We describe recently developed computer-controlled MRI compatible gas delivery systems which are capable of administering reliable and repeatable vasoactive CO2 stimuli.
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              Microvasculature changes and cerebral amyloid angiopathy in Alzheimer's disease and their potential impact on therapy.

              The introduction of immunotherapy and its ultimate success will require re-evaluation of the pathogenesis of Alzheimer's disease particularly with regard to the role of the ageing microvasculature and the effects of APOE genotype. Arteries in the brain have two major functions (a) delivery of blood and (b) elimination of interstitial fluid and solutes, including amyloid-beta (Abeta), along perivascular pathways (lymphatic drainage). Both these functions fail with age and particularly severely in Alzheimer's disease and vascular dementia. Accumulation of Abeta as plaques in brain parenchyma and artery walls as cerebral amyloid angiopathy (CAA) is associated with failure of perivascular elimination of Abeta from the brain in the elderly and in Alzheimer's disease. High levels of soluble Abeta in the brain correlate with cognitive decline in Alzheimer's disease and reflect the failure of perivascular drainage of solutes from the brain and loss of homeostasis of the neuronal environment. Clinically and pathologically, there is a spectrum of disease related to functional failure of the ageing microvasculature with "pure" Alzheimer's disease at one end of the spectrum and vascular dementia at the other end. Changes in the cerebral microvasculature with age have a potential impact on therapy with cholinesterase inhibitors and especially on immunotherapy that removes Abeta from plaques in the brain, but results in an increase in severity of CAA and no clear improvement in cognition. Drainage of Abeta along perivascular pathways in ageing artery walls may need to be improved to maximise the potential for improvement of cognitive function with immunotherapy.
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                Author and article information

                Journal
                Magn Reson Med Sci
                Magn Reson Med Sci
                mrms
                Magnetic Resonance in Medical Sciences
                Japanese Society for Magnetic Resonance in Medicine
                1347-3182
                1880-2206
                2017
                28 April 2016
                : 16
                : 1
                : 45-53
                Affiliations
                [1 ]Graduate School of Health Sciences, Hokkaido University
                [2 ]Division of Biomedical Engineering and Science, Faculty of Health Sciences, Hokkaido University, Kita 12 Nishi 5, Kita-ku, Sapporo, Hokkaido 060-0812, Japan
                Author notes
                [* ]Corresponding author, Phone: +81-11-706-3412, Fax: +81-11-706-4916, E-mail: yamamoto@ 123456hs.hokudai.ac.jp
                Article
                mrms-16-045
                10.2463/mrms.mp.2015-0156
                5600043
                27151746
                629ec68d-d68d-492f-950c-a880d2752f41
                © 2016 Japanese Society for Magnetic Resonance in Medicine

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives International License.

                History
                : 06 July 2015
                : 30 March 2016
                Categories
                Major Paper

                blood oxygenation,carbon dioxide,arteriole,vasomotor
                blood oxygenation, carbon dioxide, arteriole, vasomotor

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