A 1H-decoupled 31P chemical shift imaging study of medicated schizophrenic patients and healthy controls.

BACKGROUND: Current 31P spectroscopy research in schizophrenia has examined phospholipid metabolism by measuring the sum of phosphomonoesters and the sum of phosphodiester-containing molecules. Proton decoupling was implemented to measure the individual phosphomonoester and phosphodiester components. This is the first study employing this technique to examine schizophrenic patients. METHODS: Multivoxel two-dimensional chemical shift in vivo phosphorous-31 magnetic resonance spectroscopy with proton decoupling was used to examine a 50-cm3 volume in prefrontal, motor, and parieto-occipital regions in the brain. Eleven chronic medicated schizophrenic patients were compared to 11 healthy controls of comparable gender, education, parental education, and handedness. RESULTS: A significant increase in the mobile phospholipid peak area and its full width at half maximum was observed in the medicated schizophrenic patients compared to the healthy controls in the prefrontal region. Inorganic orthophosphate and phosphocholine were lower in the schizophrenic group in the prefrontal region. CONCLUSIONS: The increased sum of phosphodiester [mobile phospholipid + glycerol-3-phosphoethanolamine (GPEth) + glycerol-3-phosphocholine (GPCh)] in schizophrenic patients, measured in earlier studies, arises from the phospholipid peak (MP) and not the more mobile phosphodiesters (GPEth, GPCh) as was originally suspected. A decrease in the phosphocholine component of the phosphomonoesters was also observed in the schizophrenic patients. These findings are consistent with an abnormality in membrane metabolism in the prefrontal region in schizophrenics.

Quantifying 1H decoupled in vivo 31P brain spectra.

Our objective was to develop a precise method for quantification of in vivo proton decoupled 31P spectra from the human brain. This objective required that an appropriate spectral model be created and that the quantification was performed using a non-subjective fitting technique. The precision of the quantification was assessed using Cramer-Rao standard deviations and compared using two different spectral models: one containing a pair of peaks representing 2,3-diphosphoglycerate, the other excluding this metabolite. The data was quantified using a Marquardt-Levenberg (ML) algorithm incorporating prior knowledge with a Hankel singular value decomposition (HSVD) performed initially to provide parameter estimates for the ML algorithm. Quantification was performed on two different in vivo 2-D CSI 31P data sets: the first examined 11 normal controls, the second examined a single individual six times. Spectra from a region in the parieto-occipital cortex were analyzed. The Cramer-Rao standard deviations were significantly lower for some metabolites with 2,3-diphosphoglycerate in the model: in the repeat study mobile phospholipids (p = 0.045) and phosphocholine (p = 0.034), and in the 11 controls mobile phospholipids (p = 0.003) and Pi (p = 0.002).

Effect of anaemia correction on skeletal muscle metabolism in patients with end-stage renal disease: 31P magnetic resonance spectroscopy assessment.

Skeletal muscle metabolism during exercise was compared in 5 patients with end-stage renal disease (ESRD) and 8 healthy controls, using a noninvasive technique, 31P magnetic resonance spectroscopy (MRS). After 3 months of anaemia correction with recombinant human erythropoietin (rHuEPO) these patients were re-evaluated. Maximal power achieved by the ESRD patients during a dynamic wrist flexion exercise test was 33% lower (p < 0.05) than the controls. Similarly in the ESRD group, the power at the onset of metabolic acidosis (the intracellular threshold) was 29% less than controls. The metabolic differences observed in the patients indicated a lower aerobic capacity. Three months of rHuEPO treatment resulted in a 55% increase in mean haematocrit but conferred no significant improvement in metabolic parameters at rest or during exercise. The lack of any significant changes in muscle metabolism following the correction of anaemia suggests that oxygen availability is not the exclusive limiting factor for aerobic metabolism in ESRD patients.

Transient changes in muscle high-energy phosphates during moderate exercise.

The purpose of this study was to use 31P-nuclear magnetic resonance spectroscopy to examine changes in wrist flexor muscle metabolism during the transitions from rest to steady-state exercise (on-transient) and back to rest (off-transient). Five healthy young males (mean age 25 +/- 2 yr) performed a series of square-wave exercise tests, each consisting of 5 min of moderate-intensity work followed by a 5-min recovery period. The subjects repeated this protocol six times, and each individual's results were pooled before analysis. ATP and intracellular pH did not change significantly during exercise or recovery. Phosphocreatine (PCr) declined progressively at the onset of exercise, reaching a plateau after approximately 2 min. A reciprocal increase in Pi occurred during the onset of exercise. During the recovery period PCr was resynthesized, whereas Pi returned to resting levels. The data were plotted as a function of time and fit with both first- and second-order exponential growth or decay models; however, the second-order model did not significantly improve the fit of the data. Time constants for the first-order model of the on- and off-transient responses for both PCr and Pi were approximately 30 s. These values are nearly identical to the time constants for oxygen consumption during submaximal exercise that have been reported previously by several authors. The results of this study show that the metabolism of muscle PCr during steady-state exercise and recovery can be accurately described by a monoexponential model and, further, suggest that a first-order proportionality exists between metabolic substrate utilization and oxygen consumption.