Noncontrast mapping of arterial delay and functional connectivity using resting‐state functional MRI: A study in Moyamoya patients

Abstract

Purpose To investigate if delays in resting-state spontaneous fluctuations of the BOLD (sfBOLD) signal can be used to create maps similar to time-to-maximum of the residue function (Tmax) in Moyamoya patients and to determine whether sfBOLD delays affect the results of brain connectivity mapping. Methods Ten patients were scanned at 3T using a gradient-echo EPI sequence for sfBOLD imaging. Cross correlation analysis was performed between each brain voxel signal and a reference signal comprised of either the superior sagittal sinus (SSS) or whole brain (WB) average time course. sfBOLD delay maps were created based on the time shift necessary to maximize the correlation coefficient, and compared to dynamic susceptibility contrast Tmax maps. Standard and time-shifted resting-state BOLD connectivity analyses of the default mode network were compared. Results Good linear correlations were found between sfBOLD delays and Tmax using the SSS as reference (r2=0.8, slope=1.4, intercept=-4.6) or WB (r2=0.7, slope=0.8, intercept=-3.2). New nodes of connectivity were found in delayed regions when accounting for delays in the analysis. Conclusions Resting-state sfBOLD imaging can create delay maps similar to Tmax maps without the use of contrast agents in Moyamoya patients. Accounting for these delays may affect the results of functional connectivity maps.

Relationship Between Changes in the Temporal Dynamics of the Blood-Oxygen-Level-Dependent Signal and Hypoperfusion in Acute Ischemic Stroke

“…In DSC-MRI, this is analogous to Tmax, which is the time taken for the contrast bolus to pass from the vessel from which the arterial input function is measured to the tissue. 18 Indeed, several studies 5,10 have shown a close relationship between Tmax and BOLD delay. MTT, however, predominantly reflects microvascular perfusion.…”

The effects of hemodynamic lag on functional connectivity and behavior after stroke

“…Prior studies of hemodynamic lag have used various reference signals including the whole brain signal, 9,10 homotopic regions, 26 and superior sagittal sinus. 27 We additionally measured lags between homotopic regions and found that lag laterality measured with a global gray matter references was correlated to lag laterality measured with homotopic reference (r ¼ 0.55, P < 10 À9 ). The gray matter tissue compartment defines a time series representing the hemodynamic response to neural activity averaged over the whole brain.…”

“…Mean arterial transit time can be thought of as the static component of cerebral perfusion while the HDR represents responses to neural activity. Therefore, a previously reported association between hemodynamic lag and mean arterial transit time 10,27 could suggest that lag is attributable to static blood flow changes. However, static changes alone do not account for hemodynamic lag of the presently observed large magnitudes (>2 s) because changes in transit time typically are on the order of less than 1 s. 36 Altered neural activity theoretically could contribute to observed hemodynamic lags.…”

“…Following stroke, lag occurs in the vascular distribution of the infarct, and correlates with measures of clinical deficits, mean transit time 9,10,27 and with hypoperfusion. Prior studies have linked hemodynamic failure to infarct extent 43,44 and to risk of future ischemic stroke.…”

Quantitative mapping of cerebrovascular reactivity using resting-state BOLD fMRI: Validation in healthy adults

“…This approach was chosen as an additional measure because the global rs-fMRI signal has been linked to respiratory and cardiovascular fluctuations (Christen et al, 2015). Moreover, Liu et al (Liu et al, 2015) recently demonstrated strong associations between the global-signal correlation and CVR.…”