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Abstract Cerebrovascular reactivity (CVR) is an indicator of cerebrovascular reserve and provides important information about vascular health in a range of brain conditions and diseases. Unlike steady-state vascular parameters, such as cerebral blood flow (CBF) and cerebral blood volume (CBV), CVR measures the ability of cerebral vessels to dilate or constrict in response to challenges or maneuvers. Therefore, CVR mapping requires a physiological challenge while monitoring the corresponding hemodynamic changes in the brain. The present review primarily focuses on methods that use CO2 inhalation as a physiological challenge while monitoring changes in hemodynamic MRI signals. CO2 inhalation has been increasingly used in CVR mapping in recent literature due to its potency in causing vasodilation, rapid onset and cessation of the effect, as well as advances in MRI-compatible gas delivery apparatus. In this review, we first discuss the physiological basis of CVR mapping using CO2 inhalation. We then review the methodological aspects of CVR mapping, including gas delivery apparatus, the timing paradigm of the breathing challenge, the MRI imaging sequence, and data analysis. In addition, we review alternative approaches for CVR mapping that do not require CO2 inhalation. Highlights • Cerebrovascular reactivity (CVR) can be measured by MRI with CO2 challenge. • Physiological basis and methodological aspects of this method will be reviewed. • Alternative approaches for CVR mapping without CO2 inhalation will be reviewed. [ABSTRACT FROM AUTHOR]

Background and purpose The BOLD signal amplitude as a response to a hypercapnia stimulus is commonly used to assess cerebrovascular reserve. Despite recent advances, the implementation remains cumbersome and alternative ways to assess hemodynamic impairment are desirable. Resting-state BOLD signal fluctuations (rsBOLD) have been proposed however data on its sensitivity and dependence on baseline venous cerebral blood volume (vCBV) is limited. The primary aim of this study was to compare the effect sizes of resting-state and hypercapnia induced BOLD signal changes in the detection of hemodynamic impairment. The second aim of the study was to assess the dependence of BOLD signal variability on vCBV. Materials and methods Fifteen patients with internal carotid artery occlusive disease and 15 matched healthy controls were included in this study. The BOLD signal was derived from a dual-echo gradient-echo echo-planar sequence during hypercapnia (HC) and hyperoxia (HO) gas modulations. BOLD (fractional) amplitude of low frequency fluctuations ((f)ALFF) was compared to HC-BOLD, BOLD response delays derived from time delay analysis and ΔBOLD in response to progressively increasing HC. Effect sizes (i.e. the standard mean difference between patients and controls) were calculated. HO-BOLD was used to estimate vCBV, and its contribution to the variability in rsBOLD signal was evaluated. Results The effect sizes of ALFF and fALFF (0.61 and 0.72) were lower than the effect sizes related to hypercapnia-based hemodynamic assessment analysis; 1.62, 1.56 and 0.90 for HC-BOLD, BOLD response delays and ΔBOLD in response to progressively increasing HC. A moderate relation was found between (f)ALFF and HC-BOLD in controls (R 2 of 0.61 and 0.42), but this relation decreased in patients (R 2 of 0.33 and 0.15). (f)ALFF did not differ between patients and controls whereas HC-BOLD did (p < 0.005). The ΔBOLD response to progressively increasing HC was significantly different in between patients and controls for ΔEtCO 2 values ≥ 2 mmHg (at +2 mmHg F(1, 18) = 5.85, p = 0.026). Up to 31% and 53% of the variance in the ALFF and HC-BOLD spatial distribution could be explained by HO-BOLD. Conclusion ALFF and fALFF demonstrated a moderate effect size to detect hemodynamic impairment whereas the effect size was large for methods employing a hypercapnia-based vascular stress stimulus. Based on our analysis of BOLD signal change as a response to a progressively increasing hypercapnia stimulus we can argue that a hypercapnia stimulus of at least 2 mmHg above baseline EtCO 2 is necessary to evaluate hemodynamic impairment. We also demonstrated that a substantial amount of information imbedded in the rsBOLD and HC-BOLD was explained by HO-BOLD. HO-BOLD can serve as a proxy for vCBV and this thus indicates that one should be careful when adopting these techniques in disease cases with compromised CBV. [ABSTRACT FROM AUTHOR]

Blood Oxygenation Level Dependent (BOLD) imaging in combination with vasoactive stimuli can be used to probe cerebrovascular reactivity (CVR). Characterizing the healthy, age-related changes in the BOLD-CVR response can provide a reference point from which to distinguish abnormal CVR from the otherwise normal effects of ageing. Using a computer controlled gas delivery system, we examine differences in BOLD-CVR response to progressive hypercapnia between 16 young (28 ± 3 years, 9 female) and 30 elderly subjects (66 ± 4 years, 13 female). Furthermore, we incorporate baseline T 2 * information to broaden our interpretation of the BOLD-CVR response. Significant age-related differences were observed. Grey matter CVR at 7 mm Hg above resting PetCO 2 was lower amongst elderly (0.19 ± 0.06%ΔBOLD/mm Hg) as compared to young subjects (0.26 ± 0.07%ΔBOLD/mm Hg). White matter CVR at 7 mm Hg above baseline PetCO 2 showed no significant difference between young (0.04 ± 0.02%ΔBOLD/mm Hg) and elderly subjects (0.05 ± 0.03%ΔBOLD/mm Hg). We saw no significant differences in the BOLD signal response to progressive hypercapnia between male and female subjects in either grey or white matter. The observed differences in the healthy BOLD-CVR response could be explained by age-related changes in vascular mechanical properties. [ABSTRACT FROM AUTHOR]

Background and aim Disturbances in cerebral oxygenation saturation (SO 2 ) have been linked to adverse outcome in adults, children, and neonates. In intensive care, the cerebral SO 2 is increasingly being monitored by Near-InfraRed Spectroscopy (NIRS). Unfortunately NIRS has a limited penetration depth. The “modified T 2 -prepared Blood Imaging of Oxygen Saturation” (T 2 -BIOS) MR sequence provides a step towards full brain SO 2 measurement. Materials and methods Tissue SO 2 , and venous SO 2 (S v O 2 ) were obtained simultaneously by T 2 -BIOS during a respiratory challenge in ten healthy volunteers. These two measures were compared to SO 2 that was obtained by a single probe MR-compatible NIRS setup, and to cerebral blood flow and venous SO 2 that were obtained by arterial spin labelling and T 2 -TRIR, respectively. Results SO 2-T2-BIOS and SO 2-NIRS had a mean bias of − 4.0% (95% CI − 21.3% to 13.3%). S v O 2-T2-BIOS correlated with SO 2-NIRS (R 2 = 0.41, p = 0.002) and S v O 2-T2-TRIR (R 2 = 0.87, p = 0.002). In addition, SO 2-NIRS correlated with S v O 2-T2-TRIR (R 2 = 0.85, p = 0.003) Frontal cerebral blood flow correlated with SO 2-T2-BIOS (R 2 = 0.21, p = 0.04), but was not significant in relation to SO 2-NIRS . Discussion/conclusion Full brain SO 2 assessment by any technique may help validating NIRS and may prove useful in guiding the clinical management of patient populations with cerebral injury following hypoxic-ischaemic events. The agreement between NIRS and T 2 -BIOS provides confidence in measuring cerebral SO 2 by either technique. As it stands now, the T 2 -BIOS represents a novel idea and future work will focus on improvements to make it a reliable tool for SO 2 assessment. [ABSTRACT FROM AUTHOR]

Cerebrovascular reactivity (CVR) mapping using CO 2 -inhalation can provide important insight into vascular health. At present, blood-oxygenation-level-dependent (BOLD) MRI acquisition is the most commonly used CVR method due to its high sensitivity, high spatial resolution, and relatively straightforward processing. However, large variations in CVR across subjects and across different sessions of the same subject are often observed, which can cloud the ability of this promising measure in detecting diseases or monitoring treatment responses. The present work aims to identify the physiological components underlying the observed variability in CVR data. When studying the association between CVR value and the subject's CO 2 levels in a total of N = 253 healthy participants, we found that CVR was lower in individuals with a higher basal end-tidal CO 2 , EtCO 2 (slope = −0.0036 ± 0.0008%/mmHg2, p < 0.001), or with a greater EtCO 2 change (ΔEtCO 2) with hypercapnic condition (slope = −0.0072 ± 0.0018%/mmHg2, p < 0.001). In a within-subject setting, when studying the CVR difference between two repeated scans (with repositioning) in relation to the corresponding differences in basal EtCO 2 and ΔEtCO 2 (n = 11), it was found that CVR values were lower if the basal EtCO 2 or ΔEtCO 2 during that particular scan session was greater. The present work suggests that basal physiological state and the level of hypercapnic stimulus intensity should be considered in application studies of CVR in order to reduce inter-subject and intra-subject variations in the data. Potential approaches to use these findings to reduce noise and augment sensitivity are proposed. • Individuals with higher baseline end-tidal (Et) CO 2 had lower CVR. • Individuals with greater Et-CO 2 change due to hypercapnia had lower CVR. • Similar relationship was present in an intra-subject setting. • These relationships were observed in multiple studies in different cohorts. [ABSTRACT FROM AUTHOR]