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MR spectroscopic imaging (MRSI) has become a valuable tool for quantifying metabolic abnormalities in human brain, prostate, breast and other organs. It is used in routine clinical imaging, particularly for cancer assessment, and in clinical research applications. This article describes basic principles of commonly used MRSI data acquisition and analysis methods and their impact on clinical applications. It also highlights technical advances, such as parallel imaging and newer high-speed MRSI approaches that are becoming viable alternatives to conventional MRSI methods. Although the main focus is on (1) H-MRSI, the principles described are applicable to other MR-compatible nuclei. This review of the state-of-the-art in MRSI methodology provides a framework for critically assessing the clinical utility of MRSI and for defining future technical development that is expected to lead to increased clinical use of MRSI. Future technical development will likely focus on ultra-high field MRI scanners, novel hyperpolarized contrast agents using metabolically active compounds, and ultra-fast MRSI techniques because these technologies offer unprecedented sensitivity and specificity for probing tissue metabolic status and dynamics., (Copyright © 2012 Wiley Periodicals, Inc.)

Purpose: To examine the relationships between the damaged macromolecular pool seen on magnetization transfer (MT) imaging and cerebral metabolic changes recorded by magnetic resonance spectroscopy (MRS), in frontal white and gray matter regions of late-life MDD patients., Materials and Methods: MT imaging and MRS were performed on eight patients with late-life MDD and eight age-matched healthy controls. MT ratios were calculated using the on-resonance and off-resonance images. Correlations were computed between MT ratios and the ratios of several metabolites, including choline (Cho), myo-inositol (mI), N-acetylaspartate (NAA), and N-acetylaspartylglutamate (NAAG), to creatine (Cr)., Results: Statistically significant correlations were found in white matter between the MT ratios and mI/Cr (r = -0.90, N = 7, P = 0.016), and between the MT ratios and (NAA + NAAG)/Cr (r = -0.89, N = 8, P = 0.007). No significant correlations were found in gray matter or between the MT ratios and NAA/Cr or Cho/Cr in white matter., Conclusion: Changes in the white matter macromolecular protein pool, observed as reduced MT ratios, may be related to changes in the mI and the total NAA pools. These findings may have implications for the pathophysiology of late-life major depression., (Copyright 2003 Wiley-Liss, Inc.)

Superparamagnetic iron oxide (SPIO) particles are used as a contrast agent in liver magnetic resonance imaging (MRI). SPIO particles exert their greatest influence on T2-weighted MR signal intensity. The time-to-echo (TE) value that provides optimal contrast has not been systematically studied over the range of clinically relevant field strengths. The purpose of this study was to quantitatively evaluate the TE dependence of the post-SPIO tumor to liver contrast-to-noise ratio (CNR). The hypothesis was that there is a TE that provides an optimal CNR. Subjects having probable metastatic hepatic lesions secondary to colorectal carcinoma were studied. Pre- and post-SPIO images were acquired at TE-effective (TE(eff)) equal to 46, 76, and 106 msec by using a turbo spin echo pulse sequence at 0.2 T and 1.5 T. The CNR for all lesions greater than 1 cm in diameter was determined in pre- and post-SPIO images. A paired statistical design was used to identify TE-related CNR dependencies. The primary findings were as follows. (1) CNR differences attributable to TE(eff) variation over the range of 46-106 msec were less than 34%. For 0.2 T, TE(eff) = 46 msec yielded a statistically significantly greater CNR than did TE(eff) = 76 or 106 msec. The same was true at the higher field strength, but differences were not significant. (2) Signal-to-noise measures suggested that SPIO reduced the lesion signal. (3) Post-SPIO CNR was significantly greater at 1.5 T than at 0.2 T. The observations indicate that over the field strength range of 0.2-1.5 T, CNR differences attributable to the TE(eff) variation, while being statistically significant in some cases, are small relative to those resulting from the SPIO administration., (Copyright 2001 Wiley-Liss, Inc.)

Diffusion magnetic resonance imaging provides an early marker of acute cerebral ischemic injury. Thrombolytic reversal of diffusion abnormalities has not previously been demonstrated in humans. Serial diffusion and perfusion imaging studies were acquired in patients experiencing acute hemispheric cerebral ischemia treated with intra-arterial thrombolytic therapy within 6 hours of symptom onset. Seven patients met inclusion criteria of prethrombolysis and postthrombolysis magnetic resonance studies, presence of large artery anterior circulation occlusion at angiography, and achievement of vessel recanalization. Mean diffusion-weighted imaging lesion volume at baseline was 23 cm3 (95% confidence interval [95% CI], 8-38 cm3) and decreased to 10 cm3 (95% CI, 3-17 cm3) 2.5 to 9.5 hours after thrombolysis. Mean apparent diffusion coefficient lesion volume decreased from 9 cm3 (95% CI, 2-16 cm3) at baseline to 1 cm3 (95% CI, 0.4-2 cm3) early after thrombolysis. A secondary increase in diffusion volumes was seen in 3 of 6 patients at day 7. In all 4 patients in whom perfusion imaging was obtained before and after treatment, complete resolution of the perfusion deficit was shown. Diffusion magnetic resonance signatures of early tissue ischemic injury can be reversed in humans by prompt thrombolytic vessel recanalization. The ischemic penumbra includes not only the region of diffusion/perfusion mismatch, but also portions of the region of initial diffusion abnormality.

The location and possible lateralization of structures mediating autonomic processing are not well-described in the human. Functional magnetic resonance imaging procedures were used to demonstrate signal changes in multiple brain sites during blood pressure challenges. Magnetic resonance signals in brain tissue were visualized with a 1.5 Tesla scanner in 11 healthy volunteers (22-37 years), by using echo-planar procedures. Images were collected during baseline states and three pressor challenges: cold application to the hand or forehead, and a Valsalva maneuver. Image values from experimental conditions were compared with corresponding baseline values on a voxel-by-voxel basis to identify brain regions responsive to physiologic activation. Probability maps (P < 0.01) of voxel changes, with Bonferroni corrections for multiple comparisons, were determined, and amplitude of signal changes associated with significance maps were pseudocolored and overlaid on anatomic images. The time courses and extent of signal alterations in defined unilateral regions were followed and compared with changes in corresponding regions on the contralateral side. Pressor challenges elicited significant regional signal intensity changes within the orbitomedial prefrontal cortex, temporal cortex, amygdala, hippocampal formation, thalamus, and hypothalamus. Cerebellar, midbrain, and pontine areas were also recruited. Signal changes, especially at forebrain sites, were often highly lateralized. The findings indicate that (1) transient, behaviorally-coupled cardiovascular challenges elicit discrete activity changes over multiple brain sites, and (2) these activity changes, especially in specific prefrontal and temporal forebrain regions and cerebellum, are often expressed unilaterally, even to a bilateral challenge.

Using proton magnetic resonance spectroscopic imaging, we studied the cerebellum of 9 patients with cerebellar degeneration and of 9 age-matched normal control subjects. This technique permits the simultaneous measurement of N-acetylaspartate, choline-containing compounds, creatine/phosphocreatine, and lactate signal intensities from four 15-mm slices divided into 0.84-ml single-volume elements. Because patients with cerebellar degeneration often show substantial atrophy on magnetic resonance imaging (MRI), we specifically chose to analyze the spectroscopic signals only from tissue that did not have an atrophic appearance on the MRI. The spectroscopic findings showed a significant reduction of N-acetylaspartate in all parts of the cerebellum, a significant correlation with MRI scores of cerebellar atrophy, and a significant correlation with clinical rating scores of cerebellar disturbance. Our method of analysis suggests the presence of a neurodegenerative process in cerebellar areas that do not appear to be atrophic on the MRI. Some limitations of proton magnetic resonance spectroscopic imaging in the present study were related to the partial field inhomogeneity characteristics of the posterior fossa, the anatomical location of the cerebellum, and the particularly severe cerebellar atrophy in some of the patients.

A significant number of patients with progressive leukodystrophy do not have a definitive diagnosis. This report describes the clinical, morphological, and biochemical characteristics of 4 unrelated girls with progressive ataxic diplegia of unknown etiology. These patients had normal development until the ages of 1.5 to 5 years. A diffuse confluent abnormality of the white matter of the central nervous system was present on computed tomography and magnetic resonance scans obtained early in the course of the illness. Dementia was not present and peripheral nerves were normal. All patients were evaluated for known metabolic and degenerative diseases and no abnormalities were observed. Light and electron microscopy of open-brain biopsy specimens from 2 girls showed selective white matter abnormalities including hypomyelination, demyelination, and gliosis. Myelin-specific proteins in the subcortical white matter were examined immunocytochemically and by Western blot analysis. They were of normal molecular size but were markedly reduced in quantity in both patients compared to control subjects. Lipid analysis revealed decreased levels of characteristic myelin lipids. When examined by magnetic resonance spectroscopic imaging, all patients showed a marked decrease of N-acetylaspartic acid, choline, and creatine in white matter only. The magnetic resonance spectroscopic imaging profile is a unique diagnostic feature of this clinicopathological syndrome.

Bicuculline-induced status epilepticus was studied in paralyzed rabbits ventilated with an oxygen and nitrous oxide mixture. An Oxford Instruments TMR 32-200 spectrometer was used to record phosphorus 31 nuclear magnetic resonance spectra of the in vivo brain. An array of conventional physiological variables including the electroencephalogram was simultaneously recorded. Several features were consistently observed during status epilepticus: (1) Phosphocreatine levels fell to about two-thirds of their control values and remained at that level despite a gradual decline in seizure activity; (2) intracellular pH declined and then remained constant, whereas seizure discharges declined; (3) adenosine triphosphate levels remained constant at their control values. These new, lower levels of brain phosphocreatine and intracellular pH were largely unaffected by increases in seizure activity brought about by elevation of blood pressure from levels too low to support adequate cerebral perfusion, by waning of anticonvulsant drug effect, or by repeated doses of bicuculline.

Using a 1.89-Tesla spectrometer, 1H and 31P nuclear magnetic resonance spectra were acquired from the brains of paralyzed rabbits ventilated with 30% oxygen in nitrous oxide. Intracellular pH and changes in lactate concentration in the cerebrum were monitored by nuclear magnetic resonance methods during and after bicuculline-induced seizures, together with the electroencephalogram, heart rate, and arterial blood pressure. During seizures lasting more than an hour, cerebral intracellular pH became acidic, the cerebral lactate level rose rapidly, and both changes persisted as long as 2 hours without signs of recovery. After less prolonged seizures, lactate elevations were no less persistent, despite nearly complete recovery of intracellular pH and the electroencephalogram.