Large dynamic fluctuations of the static magnetic field (B 0 ) are observed in the human body during MR scanning, compromising image quality and detection sensitivity in several MR imaging and spectroscopy sequences. Partially, these dynamic B 0 fluctuations are due to physiological motion such as breathing, but other sources of temporal B 0 field fluctuations are also present in the MR system (e.g., eddy currents). Especially at ultrahigh field (!7 T), the increased susceptibility effects lead to large B 0 field variations over time. Direct measurement and correction of these temporal field variations of up to 70 Hz will lead to a significant reduction of artifacts and improved measurement stability/reproducibility. For direct measurement of the temporally changing B 0 field, a simple field probe was developed, that was placed in proximity to the tissue of interest. In this work, it is shown how such a field probe system can be used to monitor temporal B 0 field variations in the human body during MRI and magnetic resonance spectroscopy. Furthermore, it is shown how the acquired temporal B 0 field information can drive a dynamic shim module to directly correct the B 0 magnetic field in real time. Magn Reson Med 67:586-591, 2012. V C 2011 Wiley Periodicals, Inc.Key words: 7 T; field correction; frequency correction; realtime shimming; breast Variation of the static magnetic field (B 0 ), and the resulting phase and frequency variations during MRI and magnetic resonance spectroscopy (MRS) sequences, can lead to a range of artifacts including ghosting, signal loss, phase corruption, and line broadening. Several sources of dynamic field variations during routine MRI scanning can be identified and are either attributed to scanner instability (e.g., eddy currents and drift), motion of the body, and the consequently changing susceptibility distribution in the magnet. Expansion of the chest during breathing not only causes severe artifacts in tissue close to the chest, such as the breast (1), but also affects imaging in body parts at further distance. In fact, breathinginduced phase changes are currently a limiting factor in high-resolution imaging of the brain (2). However, breathing is not the only source of these spatio-temporal field variation. Also cardiac pulsation (3) and motion of the extremities (4) can be a limiting factor in accurate MR image acquisition. As susceptibility effects scale with field strength, extreme field variations are expected at ultrahigh field (!7 T) resulting in uncontrolled frequency alterations. B 0 field variations of several hertz in the brain (2,5,6) and up to 40 Hz in the breast have been reported (7,8) at ultrahigh field. If not corrected, these B 0 fluctuations can lead to problems with localization and non-Lorentzian line broadening in MRS (9) and can cause severe signal loss or ghosting artifacts, for example in susceptibility-weighted imaging (2,4), diffusion tensor imaging (10), temperature measurements (3), phase-based perfusion imaging (11), spectroscopic imaging or spectra...

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The present study was designed to examine the effects of inhibition of nitric oxide synthase on cerebral energy metabolism after hypoxia-ischemia in newborn piglets. Ten 1- to 3-d-old piglets received N(omega)-nitro-L-arginine (NNLA), an inhibitor of nitric oxide synthase (NNLA-hypoxia, n = 5), or normal saline (hypoxia, n = 5) 1 h before cerebral hypoxia-ischemia. After the infusion, hypoxia-ischemia was induced by bilateral occlusion of the carotid arteries and decreasing FiO2 to 0.07 and maintained for 60 min. Thereafter, animals were resuscitated and ventilated for another 3 h. Using 1H- and 31P-magnetic resonance spectroscopy, cerebral energy metabolism was measured in vivo at 15-min intervals throughout the experiment. Phosphocreatine to inorganic phosphate ratios decreased from 2.74 +/- 0.14 to 0.74 +/- 0.36 (hypoxia group) and 2.32 +/- 0.17 to 0.18 +/- 0.10 (NNLA-hypoxia group) during hypoxia-ischemia. Thereafter, phosphocreatine to inorganic phosphate ratios returned rapidly to baseline values in the hypoxia group, but remained below baseline values in the NNLA-hypoxia group. Intracellular pH decreased during hypoxia-ischemia and returned to baseline values on reperfusion in both groups. Intracellular pH values were lower in the NNLA-hypoxia group (p < 0.001, ANOVA). Lactate was not present during the baseline period. After hypoxia-ischemia, lactate to N-acetylaspartate ratios increased to 1.34 +/- 0.28 (hypoxia group) and 2.22 +/- 0.46 (NNLA-hypoxia group). Lactate had disappeared after 3 h of reperfusion in the hypoxia group, whereas lactate to N-acetylaspartate ratios were 1.37 +/- 1.37 in the NNLA-hypoxia group. ANOVA demonstrated a significant effect of NNLA on lactate to N-acetylaspartate ratios (p < 0.001). Inhibition of nitric oxide synthase by NNLA tended to compromise cerebral energy status during and after cerebral hypoxia-ischemia in newborn piglets.

Recanalization therapy after acute ischemic stroke enables restoration of cerebral perfusion. However, a significant subset of patients has poor outcome, which may be caused by disruption of cerebral energy metabolism. To assess changes in glucose metabolism subacutely and chronically after recanalization, we applied two complementary imaging techniques, fluorodeoxyglucose (FDG) positron emission tomography (PET) and deuterium (2H) metabolic imaging (DMI), after 60-minute transient middle cerebral artery occlusion (tMCAO) in C57BL/6 mice. Glucose uptake, measured with FDG PET, was reduced at 48 hours after tMCAO and returned to baseline value after 11 days. DMI revealed effective glucose supply as well as elevated lactate production and reduced glutamate/glutamine synthesis in the lesion area at 48 hours post-tMCAO, of which the extent was dependent on stroke severity. A further decrease in oxidative metabolism was evident after 11 days. Immunohistochemistry revealed significant glial activation in and around the lesion, which may play a role in the observed metabolic profiles. Our findings indicate that imaging (altered) active glucose metabolism in and around reperfused stroke lesions can provide substantial information on (secondary) pathophysiological changes in post-ischemic brain tissue.