Background and Purpose-Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are relatively new MR techniques increasingly used in acute stroke. During the first hours of stroke evolution, the regions with abnormal perfusion are typically larger than the DWI lesions, and this mismatch region has been suggested to be "tissue at risk." The aim of this study was to evaluate the PWI/DWI mismatch region in acute stroke patients and find parameters indicative of both infarct progression and functional impairment. Methods-Twenty patients with nonlacunar ischemic stroke were imaged with DWI, PWI, and conventional MRI within 24 hours of symptom onset and after 1 week; in addition, the European Stroke Scale (ESS) score was recorded. With PWI, the volumes of regions with "time-to-peak" (TTP) delays of Ն2, 4, 6, 8, and 10 seconds were measured; these volumes were compared with the acute DWI lesion volumes, final infarct size, and ESS score. Results-In 80% of patients the acute DWI lesion was surrounded by regions with abnormal TTP delays (PWIϾDWI lesion). A TTP delay of Ն6 s in the mismatch region was found to be associated with lesion enlargement between the initial and follow-up MRI scans. Lesions increased in 9 of 12 patients (75%) in whom the area with TTP delay Ն6 s was larger than the DWI lesion, but they increased in only 1 of 8 (12.5%) of the remaining patients, in whom the area with a TTP delay Ն6 s was smaller than the DWI lesion.

Accurate and reliable quantification of brain metabolites measured in vivo using 1 H magnetic resonance spectroscopy (MRS) is a topic of continued interest in the field. Aside from differences in the basic approach to quantification, the quantification of metabolite data acquired at different sites and on different platforms poses an additional methodological challenge. In this study, we analyze spectrally edited -aminobutyric acid (GABA) MRS data and quantify GABA levels relative to an internal tissue water reference. Data from 284 volunteers scanned across 25 research sites were collected using standard GABA+ editing. Unsuppressed water acquisitions from the same volume of interest were acquired for signal referencing. Whole-brain T1-weighted structural images were acquired and tissue-segmented to determine gray matter, white matter and cerebrospinal fluid voxel tissue fractions. Water-referenced GABA+ measurements were fully corrected for tissue-dependent signal relaxation and water visibility effects. The cohort-wide coefficient of variation was 17%, which was largely driven by vendor-related differences according to a linear mixed-effects analysis. The mean within-site coefficient of variation was 9%. Vendor differences contributed 53% to the total variance in the data, while the remaining variance was attributed to site-(11%) and participant-level (36%) effects. Results from an exploratory analysis suggested that the vendor differences were related to the water signal acquisition. Discounting the observed vendor-specific effects, water-referenced GABA+ measurements exhibit levels of variance similar to creatine-referenced GABA+ measurements. It is concluded that quantification using internal tissue water referencing remains a viable and reliable method for the in vivo quantification of GABA+ levels.

Diffusion-weighted imaging helped to predict the size of the lesion on T2-weighted images obtained after about 8 days in patients with a symptom onset of more than 4 hours (r = 0.96), while in patients with a symptom onset of less than 4 hours, perfusion imaging provided important additional information about brain tissue with impaired perfusion.

In patients with intracerebral lesions supposed to be diffuse gliomas on MR imaging, FET-PET and MR spectroscopy analyses markedly improved the diagnostic efficacy of targeted biopsies.