Molar quantitation of in vivo proton metabolites in human brain with 3D magnetic resonance spectroscopic imaging.

A method for molar quantitation of in vivo proton metabolites in human brain with three-dimensional (3D) proton magnetic resonance spectroscopic imaging (MRSI) is described. The method relies on comparison of brain and calibration phantom measurements, with corrections for coil loading, and spin-lattice and spin-spin relaxation times. A 3D proton MRSI pulse sequence was developed which acquires two echoes and enables acquisition of both the TMS coil loading reference phantom and proton metabolite signals from a single experiment. With the aqueous fraction (tissue water) taken into account, the calculated molar concentrations from 24 centrum semiovale white matter voxels from 4 control subjects were (mmol/l +/- SD): N-acetyl aspartate = 14.6 +/- 2.8, total creatine+phosphocreatine = 6.0 +/- 1.2, total choline = 1.9 +/- 0.4. These values are equivalent to previously reported results obtained from single volume localized proton magnetic resonance spectroscopy.

Elevated lactate and alkalosis in chronic human brain infarction observed by 1H and 31P MR spectroscopic imaging.

The goal of this study was to investigate lactate and pH distributions in subacutely and chronically infarcted human brains. Magnetic resonance spectroscopic imaging (MRSI) was used to map spatial distributions of 1H and 31P metabolites in 11 nonhemorrhagic subacute to chronic cerebral infarction patients and 11 controls. All six infarcts containing lactate were alkalotic (pHi = 7.20 +/- 0.04 vs. 7.05 +/- 0.01 contralateral, p less than 0.01). This finding of elevated lactate and alkalosis in chronic infarctions does not support the presence of chronic ischemia; however, it is consistent with the presence of phagocytic cells, gliosis, altered buffering mechanisms, and/or luxury perfusion. Total 1H and 31P metabolites were markedly reduced (about 50% on average) in subacute and chronic brain infarctions (p less than 0.01), and N-acetyl aspartate (NAA) was reduced more (approximately 75%) than other metabolites (p less than 0.01). Because NAA is localized in neurons, selective NAA reduction is consistent with pathological findings of a greater loss of neurons than glial cells in chronic infarctions.

Human brain infarction: proton MR spectroscopy.

Two-dimensional proton magnetic resonance (MR) spectroscopic imaging studies were performed of the distributions of the major hydrogen-1 metabolites of choline, creatine, N-acetyl aspartate (NAA) and lactate in normal (n = 6) and subacutely to chronically infarcted (n = 10) human brain. The two dimensions of phase encoding were applied over a 20-mm-thick section of brain tissue that had been selected with a double spin-echo localization method. Normal brain showed bilaterally symmetric metabolite distributions and no detectable lactate. Nine of 10 studies of brain infarction showed substantial decreases in NAA, creatine, and choline in the infarcted area compared with control areas; averaged for all studies, the decreases were 77% +/- 8, 63% +/- 11, and 54% +/- 12, respectively (mean +/- standard error). The decreased metabolite concentrations are probably due primarily to diminished cell density in the infarct. The decrease in NAA was larger than the decreases in choline and creatine. Findings in all of the studies showed lactate in the infarcted tissue and/or ventricles. The continued presence of lactate in the infarct indicates increased anaerobic glycolysis due to ischemia or other factors.

3D phase encoding 1H spectroscopic imaging of human brain.

A three-dimensional (3D) phase-encoding proton spectroscopic imaging method is presented for a whole body MRI/MRS system. Metabolite images at 2 T of choline, creatine, and N-acetyl aspartate (NAA) of normal brain were obtained with a spatial resolution of 1.5 cc. With PRESS volume preselection and outer volume suppression pulses, brain regions close to the skull could be studied without significant contamination by lipid and water signals.