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Method to Correlate 1 H MRSI and 18 FDG-PET

The in vivo neuronal contribution to human cerebral metabolic rate of glucose (CMRglc), measured by 18 FDG-PET, is unknown. Examining the effect of 1 H MRSI-derived N-acetyl aspartate (NAA) concentration on positron emission tomography (PET) measures of metabolic activity might indicate the relationship of CMRglc to neuron density. In a population of 19 demented, cognitively impaired, and control subjects, the Muller-Gartner algorithm was applied to whole-brain PET data to isolate the PET signal originating in cortical gray matter alone (GMPET). An analogous procedure applied to multislice proton MRSI data yielded the N-acetyl aspartate concentration in cortical gray matter (GMNAA). In 18 of 19 subjects, a significant linear re- gression (P < 0.05) resulted when GMPET was plotted against GMNAA, whereby GMPET was higher for higher GMNAA. This suggests that CMRglc rises linearly with increasing neuron den- sity in gray matter. This method may be used to investigate the relationship of CMRglc to neurons in various conditions. Magn Reson Med 43:244-250, 2000. © 2000 Wiley-Liss, Inc. ( 18 F)Fluorodeoxyglucose positron emission tomography (PET) is widely used to measure the cerebral metabolic rate of glucose consumption (CMRglc) in the study of normal and diseased brain (1-3). Because glucose is the sole substrate for normal brain metabolism, values of CM- Rglc likely reflect overall levels of brain metabolic activity. But whether CMRglc directly represents the metabolic ac- tivity of neurons, and not of other cells, has yet to be established. It is difficult to address this question, partic- ularly in vivo in humans, with PET alone. PET data are acquired as averages over macroscopic volumes of tissue. Thus, the CMRglc values acquired by PET would be influ- enced by both neuronal metabolic rate and neuronal den- sity in the tissue volume. Further, realistic tissue volumes contain not only neurons, but also other cells, in particular neuroglia, that consume glucose. There is growing evi- dence that glia actually consume glucose at a higher rate than neurons do (4). The issue is important because both aging and disease may reduce neuron populations and so affect the measurement of metabolic rates. Atrophy correc- tion is only a partial solution because atrophy correction expresses cellular depletion in terms of gross tissue loss without regard to the type or density of cells present in the lost or in the remaining tissue. A method of indexing neuron density in vivo might permit more accurate assess- ment of these structural contributions to metabolic mea- surements, and therefore would improve the calculation of functional effects. The extent to which disease affects true metabolism could then be better understood. Proton magnetic resonance spectroscopic imaging of the brain ( 1 H MRSI) detects the amino acid N-acetyl aspartate (NAA), which is found in high concentrations only in neurons and is virtually undetectable in other cells, in- cluding glia (5,6). NAA resonance intensity in the 1 H MRSI spectrum is therefore related to neuron density and/or to NAA content per neuron. Thus, how CMRglc varies as a function of NAA concentration ((NAA)) should reflect the way in which brain glucose metabolism is affected by neuron density and/or by NAA content per neuron. The CMRglc-to-(NAA) relationship could be derived for an in- dividual subject by plotting local CMRglc against local (NAA) across that subject's brain. The CMGglc-to-(NAA) relationship might be expected to vary from subject to subject depending on factors such as subject cognitive status. However, there are limitations to this approach. First, although cortical gray matter is the tissue of primary interest in evaluating brain metabolic activity, PET and 1 H MRSI data are often expressed in terms of whole, unseg- mented brain tissue, rather than as values for cortical gray matter alone. Second, even if regional data are compared, the spatial resolution of MRSI is lower than that of PET, a source of possible signal infidelity. Therefore, the aims in this study were 1) to establish a method for the assessment of CMRglc and (NAA) in cortical gray matter, accounting for differences between PET and 1 H MRSI image resolu- tion; 2) to look for the quantitative relationship between gray matter CMRglc and (NAA) in individual cognitively normal, cognitively impaired, and demented subjects; and 3) to explore whether this CMRglc-to-(NAA) relation var- ies with cognitive status across subjects.