Purpose: To evaluate reproducibility of total cerebral blood flow (CBF) measurements with phase contrast magnetic resonance imaging (pcMRI). Materials and Methods:We repeated total CBF measurements in 15 healthy volunteers with and without cardiac triggering, and with and without repositioning. In eight volunteers measurements were performed at two different occasions. In addition, measurement of flow in a phantom was performed to validate MR measurements. Results:A difference of 40.4 ml/minute was found between CBF measurements performed with and without triggering (P Ͻ 0.05). For repeated triggered measurements, the coefficient of variation (CV) was 7.1%, and for nontriggered measurements 10.3%. For repeated measurements with repositioning, the CV was 7.1% with and 11.2% without triggering. Repeated measurements at different occasions showed a CV of 8.8%. Comparing measured with real flow in the phantom, the triggered differed 4.9% and the nontriggered 8.3%. Conclusion:The findings of this study demonstrate that pcMRI is a reliable method to measure total CBF in terms of both accuracy and reproducibility. METHODS THAT CURRENTLY ARE USED to assess total cerebral blood flow (CBF) can be divided into two groups based on the underlying concepts. On the one hand, total CBF can be estimated based on information generated by flow in the capillaries; on the other hand, total CBF can be assessed by measuring flow in the supplying vessels of the brain. Methods that are based on measurements of flow in the capillaries are single positron emission computed tomography (SPECT), xenon-computed tomography (Xe-CT), and perfusion magnetic resonance imaging (MRI). Blood flow in the supplying vessels of the brain can be measured using Doppler ultrasound and phase contrast MRI (pcMRI). Advantages of both Doppler ultrasound and pcMRI are no need for using ionizing irradiation or administration of intravenous agents, and the possibility of repeated measurements on a short-term basis. However, limitations of Doppler ultrasound are its operator dependency and overestimation of total blood flow in a given vessel due to the fact that only the highest flow in the center of the vessel is assessed (1). Using pcMRI, total CBF can be assessed by simultaneously measuring flow in the internal carotid arteries and the basilar artery. As compared to Doppler ultrasound, pcMRI has the advantage of being operator independent and involving straightforward flow quantification. In addition, pcMRI can be added to morphologic MRI sequences, offering the option to correlate flow to morphology based on data generated during one examination.In vitro and in vivo studies have demonstrated that pcMRI provides reliable flow data (2-4). However, data on short-term and long-term reproducibility are scarce. Furthermore, there is an ongoing discussion whether total CBF should be measured using a cardiac-triggered or a nontriggered pcMRI technique (4 -6). Finally, using pc-MRI, considerable differences in total CBF have been found between healthy volunteers (7,8). ...

Nitric oxide (NO) plays a pivotal role in the regulation of peripheral vascular tone. Its role in the regulation of cerebral vascular tone in humans remains to be elucidated. This study investigates the role of NO in hypoxia-induced cerebral vasodilatation in young healthy volunteers. The effect of the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) on the cerebral blood flow (CBF) was assessed during normoxia and during hypoxia (peripheral O(2) saturation 97 and 80%, respectively). Subjects were positioned in a magnetic resonance scanner, breathing normal air (normoxia) or a N(2)-O(2) mixture (hypoxia). The CBF was measured before and after administration of L-NMMA (3 mg/kg) by use of phase-contrast magnetic resonance imaging techniques. Administration of L-NMMA during normoxia did not affect CBF. Hypoxia increased CBF from 1,049 +/- 113 to 1,209 +/- 143 ml/min (P < 0.05). After L-NMMA administration, the augmented CBF returned to baseline (1,050 +/- 161 ml/min; P < 0.05). Similarly, cerebral vascular resistance declined during hypoxia and returned to baseline after administration of L-NMMA (P < 0.05 for both). Use of phase-contrast magnetic resonance imaging shows that hypoxia-induced cerebral vasodilatation in humans is mediated by NO.

The accuracy of conditional or immediate MR imaging was similar to that of conditional CT in patients suspected of having appendicitis, which implied that strategies with MR imaging may replace conditional CT for appendicitis detection.

The normal intracranial venous system is adequately visualized with 3D phase-contrast and coronal 2D TOF MR angiography.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary small-vessel disease caused by mutations in the NOTCH3 gene on chromosome 19. On magnetic resonance imaging (MRI), subcortical white matter hyperintensities and lacunar infarcts are visualized. It is unknown whether a decrease in cerebral blood flow or cerebrovascular reactivity is primarily responsible for the development of white matter hyperintensities and lacunar infarcts. The authors used phase-contrast MRI in 40 NOTCH3 mutation carriers (mean age 45 +/- 10 years) and 22 nonmutated family members (mean age 39 +/- 12 years), to assess baseline total cerebral blood flow (TCBF) and cerebrovascular reactivity after acetazolamide. Mean baseline TCBF was significantly decreased in NOTCH3 mutation carriers. In young subjects, baseline TCBF was significantly lower than in nonmutation carriers (mean difference 124 mL/min). Furthermore, baseline TCBF did not differ significantly between mutation carriers with minimal and mutation carriers with moderate or severe white matter hyperintensities. No significant difference in mean cerebrovascular reactivity was found between mutation carriers and nonmutation carriers. This study suggests that a decrease in baseline TCBF in NOTCH3 mutation carriers precedes the development of white matter hyperintensities.

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The authors investigated the interaction between medial temporal lobe (MTL) atrophy and white matter hyperintensities (WMH) in Alzheimer disease (AD). They measured the MTL and WMH on MRI in 58 AD patients and 28 controls. MTL atrophy was associated with an increased risk of AD (OR = 6.2), but there was no significant association between WMH and AD. Moreover, there was an interaction between MTL and WMH (p = 0.045). These results suggest that vascular and Alzheimer-type pathology act in synergy in the clinical syndrome of AD.

Using whole brain volumetric magnetization transfer imaging, the authors demonstrated that cognitive decline in patients with mild cognitive impairment and AD is associated with widespread structural brain damage. As there were no specific relationships between regional brain damage and impairment of specific cognitive functions, pathology in AD and mild cognitive impairment is much more generalized than was expected.