Quantitative T*2-mapping based on multi-slice multiple gradient echo flash imaging: retrospective correction for subject motion effects.

Numerous clinical and research applications for quantitative mapping of the effective transverse relaxation time T*(2) have been described. Subject motion can severely deteriorate the quality and accuracy of results. A correction method for T*(2) maps acquired with multi-slice multiple gradient echo FLASH imaging is presented, based on acquisition repetition with reduced spatial resolution (and consequently reduced acquisition time) and weighted averaging of both data sets, choosing weighting factors individually for each k-space line to reduce the influence of motion. In detail, the procedure is based on the fact that motion artifacts reduce the correlation between acquired and exponentially fitted data. A target data set is constructed in image space, choosing the data yielding best correlation from the two acquired data sets. The k-space representation of the target is subsequently approximated as linear combination of original raw data, yielding the required weighting factors. As this method only requires a single acquisition repetition with reduced spatial resolution, it can be employed on any clinical system offering a suitable sequence with export of modulus and phase images. Experimental results show that the method works well for sparse motion, but fails for strong motion affecting the same k-space lines in both acquisitions.

Exponential excitation pulses for improved water content mapping in the presence of background gradients.

Several water content mapping techniques are based on the acquisition of multiple gradient echoes (GE) with different echo times (TE). However, in the presence of linear magnetic field gradients G(susc) the signal decay is no longer exponential but in the case of a rectangular slice profile weighted by a sinc function, giving rise to erroneous initial amplitudes S(0) in monoexponential fitting. Generally, it can be shown that the signal decay is weighted by the time profile of the excitation pulse. Thus, for an excitation pulse with an exponential time profile, i.e., a Lorentzian slice profile, the signal decay remains exponential and exponential fitting still yields the correct amplitude S(0). Multiecho GE images of a gel phantom and five human volunteers were acquired at 3 T using a sinc-shaped and an exponential excitation pulse. In addition, simulations were performed to investigate the influence of saturation effects due to distortion of the ideal Lorentzian slice profile. A considerable overestimation of S(0) when using a sinc-shaped excitation pulse was observed. Errors were greatly reduced with an exponential excitation pulse. We thus propose the use of excitation pulses with exponential time profile to obtain accurate estimates for S(0) from exponential fitting.

Extended cortical activations during evaluating successive pain stimuli.

Comparing pain is done in daily life and involves short-term memorizing and attention focusing. This event-related functional magnetic resonance imaging study investigated the short-term brain activations associated with the comparison of pain stimuli using a delayed discrimination paradigm. Fourteen healthy young volunteers compared two successive pain stimuli administered at a 10 s interval to the same location at the nasal mucosa. Fourteen age- and sex-matched subjects received similar pain stimuli without performing the comparison task. With the comparison task, the activations associated with the second pain stimulus were significantly greater than with the first stimulus in the anterior insular cortex and the primary somatosensory area. This was observed on the background of a generally increased stimulus-associated brain activation in the presence of the comparison task that included regions of the pain matrix (insular cortex, primary and secondary somatosensory area, midcingulate cortex, supplemental motor area) and regions associated with attention, decision making, working memory and body recognition (frontal and temporal gyri, inferior parietal lobule, precuneus, lingual cortices). This data provides a cerebral correlate for the role of pain as a biological alerting system that gains the subject's attention and then dominates most other perceptions and activities involving pain-specific and non-pain-specific brain regions.

Bevacizumab impairs oxidative energy metabolism and shows antitumoral effects in recurrent glioblastomas: a 31P/1H MRSI and quantitative magnetic resonance imaging study.

Bevacizumab shows unprecedented rates of response in recurrent glioblastomas (GBM), but the detailed mechanisms are still unclear. We employed in vivo magnetic resonance spectroscopic imaging (MRSI) and quantitative magnetic resonance imaging to investigate whether bevacizumab alters oxygen and energy metabolism and whether this effect has antitumoral activity in recurrent GBM. (31)P and (1)H MRSI, apparent diffusion coefficient (ADC), and high-resolution T2 and T2' mapping (indirect marker of oxygen extraction) were investigated in 16 patients with recurrent GBM at 3 Tesla before and 1.5-2 months after initiation of therapy with bevacizumab. Changes of metabolite concentrations and of the quantitative values in the tumor and normal appearing brain tissue were calculated. The Wilcoxon signed-ranks test was used to evaluate differences for tumor/edema versus control as well as changes before versus after commencement of therapy. Survival analyses were performed for significant parameters. Tumor T2', pH, ADC, and T2 decreased significantly in patients responding to bevacizumab therapy (n = 10). Patients with at least 25% T2' decrease during treatment showed longer progression-free and overall survival durations. Levels of high-energy metabolites were lower at baseline; these persisted under therapy. Glycerophosphoethanolamine as catabolic phospholipid metabolite increased in responders. The MRSI data support the hypothesis that bevacizumab induces relative tumor hypoxia (T2' decrease) and affects energy homeostasis in recurrent GBM, suggesting that bevacizumab impairs vascular function. The antiangiogenic effect of bevacizumab is predictive of better outcome and seems to induce antitumoral activity in the responding GBMs.