162 Chapter 6 heavily dependent on changes in CBF. Additionally, longer hemodynamic lag times were seen within regions with lower CBF. This has also been observed in healthy subjects and patients with white-matter hyperintensities, where reduced CBF was found alongside lower CVR and longer CVR time to peak.42–45 In the current study, however, in regions exhibiting vascular steal the negative CVR decreased further with increasing CBF. Even though the effect size of this relationship is considered small,46 this result is still striking. Previous research has likewise postulated that the relationship between CBF and CVR may be dependent on the staging of vascular reserve.8 This could be explained by the following: within non-steal regions (i.e. adequately responsive regions), the process of cerebral autoregulation ensures CBF is maintained through varying the vasodilation of the vessels. However, in vascular steal regions, vessels are likely to be maximally dilated. When this maximum vascular reserve capacity is able to compensate, adequate CBF could be maintained while CVR is negative. In even more vascularly comprised regions, this maximum vasodilation fails to compensate, leading to both low CBF and CVR values. These different associations could be reflective of the underlying vascular reserve clasifications as proposed by both Derdeyn and colleagues47 or Kuroda and colleagues48. The timing of the response as measured with CVR was related to the temporal metrics of the baseline CBF (i.e. AAT). In other words, regions in which the arrival time of labeled blood was longer also showed a longer vascular response delay to a hypercapnic stimulus. Since the timing of the CVR is related to the traveling duration of the blood, this positive relationship was to be expected. However, both the correlation analyses as well as visual inspection of the data suggest these two temporal measures are not identical. Within the same region, the hemodynamic lag time is longer than the AAT. This probably reflects the difference in the two temporal metrics. AAT solely reflects the arrival time of labeled blood in a physiological steady state on the arterial side. Hemodynamic lag, on the other hand, is a time measure in reaction to a hypercapnic stimulus, measured at the venous side and influenced by multiple factors like blood redistribution and vascular response speed.29 While prolonged AAT might be able to indicate areas with possible increased vascular collateralization49 and thereby also longer hemodynamic lag values, AAT cannot be used to identify regions at risk for decreased vascular response speed. When comparing ASL with BOLD MRI data, some technical limitations of both techniques should be considered. The main limitation of ASL is the short half-life of the endogenous tracer (~1-2 seconds), leading to possible underestimation of perfusion in areas with long transit delays.50 Additionally, the specific ASL
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