Water-suppressed localized proton NMR spectroscopy using stimulated echoes has been successfully applied to detect metabolites in the human brain in vivo. The STEAM spectroscopy sequence allows single-step localization by exciting three intersecting slices. Water suppression is achieved by preceding chemical-shift-selective (CHESS) rf pulses. High-resolution (0.05 ppm) proton NMR spectra of healthy volunteers have been High-resolution (0.05 ppm) proton NMR spectra of healthy volunteers have been obtained on a conventional 1.5-T whole-body MRI system (Siemens Magnetom). Volumes-of-interest (VOI) of 64 ml (4 x 4 x 4 cm3) were localized in the occipital area of the brain and spectra were recorded within measuring times ranging from 1 s (single scan) to about 10 min. The experimental procedure is described in detail. Resonance assignments include acetate, N-acetyl aspartate, gamma-amino butyrate, glutamine, glutamate, aspartate, creatine and phosphocreatine, choline-containing compounds, taurine, and inositols. Cerebral lactate was found to be at a maximum concentration of 0.5 mM when assuming N-acetyl aspartate in white matter to be 6 mM.

High-resolution proton NMR spectra of normal human brain in vivo have been obtained from selected 27- and 64-ml volumes-of-interest (VOI) localized in the insular area, the occipital area, the thalamus, and the cerebellum of normal volunteers. Localization was achieved by stimulated echo (STEAM) sequences using a conventional 1.5-T whole-body MRI system (Siemens Magnetom). The proton NMR spectra show resonances from lipids, lactate, acetate, N-acetylaspartate (NAA), gamma-aminobutyrate, glutamine, glutamate, aspartate, creatine and phosphocreatine, choline-containing compounds, taurine, and inositols. While T1 relaxation times of most of these metabolites were about 1100-1700 ms without significant regional differences, their T2 relaxation times varied between 100 and 500 ms. The longest T2 values of about (500 +/- 50) ms were observed for the methyl protons of NAA in the white matter of the occipital lobe compared to (320 +/- 30) ms in the other parts of the brain. No significant regional T2 differences were found for choline and creatine methyl resonances. The relative concentrations of NAA in gray and white matter were found to be 35% higher than those in the thalamus and cerebellum. Assuming a concentration of 10 mM for total creatine the resulting NAA concentrations of 13-18 mM are by a factor of 2-3 higher than previously reported using analytical techniques. Cerebral lactate reached a maximum concentration of about 1.0 mM.

Summary: In focal ischemia of rats, the volume of ischemic lesion correlates with the number of peri-infarct depolariza tions, To test the hypothesis that depolarizations accelerate in farct growth, we combined focal ischemia with externally evoked spreading depression (SD) waves, Ischemic brain in farcts were produced in halothane-anaesthetized rats by intra luminal thread occlusion of the middle cerebral artery (MCA), In one group of animals, repeated SDs were evoked at IS-min intervals by microinjections of potassium acetate into the fron tal cortex, In another group, the spread of the potassium-evoked depolarizations was prevented by application of the N-methyl D-aspartate (NMDA) receptor antagonist dizocilpine (MK-80 I), The volume of ischemic lesion was monitored for 2 h by diffusion-weighted imaging (DWI) and correlated with electro physiological recordings and biochemical imaging techniques, In untreated rats, each microinjection produced an SD wave and a stepwise rise of the volume and signal intensity of the In focal cerebral ischemia of rat infarct size correlates with the number of peri-infarct spreading depression (SD)-like depolarizations (Mies et aI., 1993; Chen et aI., 1993). These depolarizations are generated in the border zone of the ischemic lesion and spread into the peri infarct surrounding (Nedergaard and Hansen, 1993; Ne dergaard and Astrup, 1986). Glutamate antagonists such as dizocilpine (MK-801) or 2,3-dihydroxy-6-nitro-7-Received January I L 1996; final received May 3. 1996; accepted May 29, 1996.Address correspondence. and reprint requests to Prof. Dr. K.-A. Hossmann, Max-Planck-Institut fUr neurologische Forschung. Gleuelerstrasse 50, D-50931 Kiiln, FR Germany.Abbreviations used: ADC, apparent diffusion coefficient; ANOY A. analysis of variance; DC, direct current; DWl, diffusion-weighted im aging; MCA, middle carotid artery; MR, magnetic resonance; NBQX, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F)-quinoxaline; NMDA, N methyl-D-aspartate; RF, radiofrequency; ROI, region of interest; SD, spreading depression; TE. spin echo. 1090DWI-visible cortical lesion, The volume of this lesion in creased between IS min and 2 h of MCA occlusion from 19 ± 15% to 66 ± 16% of ipsilateral cortex, In dizocilpine-treated animals, microinjections of potassium did not evoke SDs, nor did the volume and signal intensity of the DWI-visible cortical lesion change, At 15 min after MCA occlusion, the DWI visible lesion was larger than in untreated animals-43 ± 16% of the ipsilateral cortex; however, after 2 h, it increased only slightly further to 49 ± 21 %. Slower lesion growth in the ab sence of SDs was also reflected by the volume of ATP-depleted tissue, which, after 2 h of MCA occlusion, involved 26 ± 12% of the ipsilateral cortex in treated and 49 ± 9% in untreated animals (p < 0.(1). These observations support the hypothesis that peri-infarct depolarizations accelerate cerebral infarct growth.

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A recently developed method for image-selected localized hydrogen-1 magnetic resonance (MR) spectroscopy was assessed in the differential diagnosis of nine primary and secondary cerebral tumors, including four gliomas, two meningiomas, one neurilemoma, one arachnoid cyst, and one metastasis of breast cancer. Well-resolved H-1 MR spectra of these tumors were obtained in vivo with a conventional 1.5-T whole-body MR imaging system. All tumor spectra were remarkably different from spectra from normal brain tissue. Spectra obtained from different tumors exhibited reproducible differences, while histologically similar tumors yielded characteristic spectra with only minor differences. The observed spectral alterations reflect variations in concentrations and relaxation times of the H-1 MR sensitive pool of free (mobile) metabolites within the tissues. In most cases, the concentrations of N-acetyl-aspartate and creatine/phosphocreatine are reduced below detectability, whereas choline-containing compounds are generally enhanced. The spectral differences between the tumors are mainly due to the differing concentrations of lipids, lactic acid, and carbohydrates. Localized H-1 MR spectroscopy may become an important clinical tool for the differentiation of tumors as well as for therapeutic control.