Multiple Sclerosis (MS) is an inflammatory disease of the central nervous system with pathological changes in grey, and particularly in white matter, where it causes demyelinization. Yet, the exact pathogenesis of the disease remains unknown. Conventional MRI provides high detection sensitivity for MS lesions, but its pathological specificity is limited. MR spectroscopic imaging, in particular at higher field strength, on the other hand can detect metabolites that were shown to play a role in the biochemistry of the disease, such as N-Acetyl-Aspartate (NAA), Choline (Cho), Creatine (Cr), myo-Inositol (Ins), Glutamate and Glutamine (Glx), Glutathione, Lactate and lipids.Fourteen MS patients were measured on a 7T Siemens Magnetom MR scanner with a 32-channel head coil (Nova Medical). The IRB approved this study, and written, informed consent was obtained from all patients. Three patient data sets had to be excluded due to strong motion artifacts. The sequence [1] directly acquired the free induction decay with an acquisition delay of 1.3 ms, 64x64 matrix size, 220x220x8mm³ FOV. In six patients, an MRSI data set of a 100x100 resolution was additionally measured. The TRs were 600 ms (64x64) and 200 ms (100x100). The measurement time was reduced to 6 minutes via 2D-CAIPIRINHA [2]. The data were Hamming filtered, lipid decontaminated using an L2-regularization [3], and fitted with LCModel. Metabolic maps of total NAA (tNAA), total Choline (tCho), total Creatine (tCr), and Ins were compared to FLAIR images. MS lesions as well as normal appearing white matter (NAWM) were marked as ROIs on FLAIR images using MINC tools. If possible, the NAWM ROIs were chosen on the contra-lateral side of the brain. The relative metabolic concentration differences between the lesion and the NAWM regions were calculated for all 11 patients, and the mean and the standard deviation over the patients was calculated.A qualitative assessment showed a decrease in tNAA in all patients in comparison to NAWM. However, not all MS plaques were visible on the tNAA maps. In two patients, decreases in tNAA were visible, but no corresponding lesion was seen on the FLAIR image. Ins was increased in 8 of all 11 patient data sets. Increased levels of tCho were measured in 3 of 11 patients, and increased in 3 other patients, while tCr was increased in 1, and decreased in another patient. Example metabolic maps and spectra are shown in figures 1-4. The qualitative assessment showed a decrease of (25.8±13.4)% of tNAA, and (2.3±15.7)% of tCr, while Ins increased by (41.8±34.2)% and tCho by (2.3±16.5)%. In three patients, metabolic changes were visually not or hardly seen on the 64x64 resolution data, but were clearly visible on the 100x100 data. Such an example is shown in figure 5.tNAA is a specific marker of neurons, axons, and dendrites. Reduced NAA was confirmed by MRS and histology studies on biopsied samples of MS patients [4]. However, tNAA can partially normalize after the lesion formation, explaining the observed tNAA drops only in some MS lesions. Ins is a precursor of phospholipid membrane constituents, and its concentration is affected by the formation and breakdown of myelin. Thus, changes in Ins are expected in MS lesions, as was shown in our study. tCho is a marker for heightened cell membrane turnover as seen in demyelination, remyelination, inflammation and gliosis [5]. With that, the diverse changes found in our study can be interpreted as different phases of de- and remyelination of the investigated MS lesions during the period of the MR examinations. Other metabolites, such as Glutathione, lactate, lipids and Glx were not reliably detected in the WM of all patients, and were thus not included in our study. When comparing the 64x64 with the 100x100 data sets, the necessity for even higher resolutions than 64x64 is apparent.