A procedure is described for combining anatomical information from magnetic resonance imaging (MRI) or computerized tomography (CT) and functional information from positron emission tomography (PET) in a rapid fashion. MRI data are combined with a procedure for the definition, storage, and recall of anatomically based regions of interest. An atlas of standard regions of interest, defined for a set of 18 parallel planes spaced at 6-mm intervals, provides an initial region of interest template for each patient slice. Global adjustments to scale, orientation, and position are applied to obtain an initial match. Individual regions of interest may then be moved, deleted, or redrawn as needed. The ability to store region of interest templates ensures reproducibility of analysis over long periods and introduces a standardization of analysis technique. In 25 brain structures, the mean coefficient of variation in cerebral glucose utilization rate (CMRGlc) measurements among five neuroanatomically trained observers was reduced from 8.1% for manual region of interest definition to 4.0% using the template approach with MRI. Template analysis for space-occupying lesions such as tumors or infarcts is illustrated with PET data from a stroke study, emphasizing the facility for rapid, reproducible analysis of multifunctional studies. MRI-PET matching for a structurally intact caudate nucleus having reduced CMRGlc in Huntington's disease emphasizes the accuracy of anatomical localization required to quantify small structures.

In prolonged fasting, the brain derives a large portion of its oxidative energy from the ketone bodies, beta-hydroxybutyrate and acetoacetate, thereby reducing whole body glucose consumption. Energy substrate utilization differs regionally in the brain of fasting rat, but comparable information has hitherto been unavailable in humans. We used positron emission tomography (PET) to study regional brain glucose and oxygen metabolism, blood flow, and blood volume in four obese subjects before and after a 3-wk total fast. Whole brain glucose utilization fell to 54% of control (postabsorptive) values (P less than 0.002). The whole brain rate constant for glucose tracer phosphorylation fell to 51% of control values (P less than 0.002). Both parameters decreased uniformly throughout the brain. The 2-fluoro-2-deoxy-D-glucose lumped constant decreased from a control value of 0.57 to 0.43 (P less than 0.01). Regional blood-brain barrier transfer coefficients for glucose tracer, regional oxygen utilization, blood flow, and blood volume were unchanged.

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In 8 patients who had clinically diagnosed presenile dementia (Alzheimer's disease) the cerebral glucose metabolism was repeatedly determined via FDG-PET under therapy with a muscarinergic choline agonist. The pattern of glucose metabolism disturbance characteristic of Alzheimer's disease, which had been determined previously by examining the metabolism, was confirmed. Whereas the total cortical glucose metabolism was significantly reduced, the regions of the parietal and the adjacent regions of the temporal and occipital association cortex were preferably affected. The primary somatosensory and visual cortex were largely excepted from the reduction in metabolism or showed slightly enhanced metabolic rates, as for example the cerebellum. The disturbance was not equilaterally pronounced and correlated with the neuropsychological deficiency. Despite biochemically "on target" therapy the glucose metabolism decreased progressively (mean value with large interindividual and intraindividual variations. No relationship between the degree of reduced metabolism and the clinical pattern was seen. Rather, it appears that the clinical pattern is much more strongly influenced by mutual adjustment of metabolic differences in various areas of the brain. Results obtained by the authors are communicated besides a review of update knowledge and interpretation of pathophysiological and biochemical linkups in Alzheimer's disease, taking into consideration the glucose metabolism studies published in the literature.

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Regional cerebral blood flow (rCBF) and glucose metabolism (rCMRglc) were measured in 44 patients with various kinds of focal vascular brain lesions, using multislice positron emission tomography (PET). Haemodynamic data were obtained by a recently developed, non-invasive clearance method utilizing (18F)-methyl fluoride as a diffusible, gaseous indicator. Shortly after completion of each flow study, rCMRglc was dynamically determined by standard procedures using 2(18F)-fluorodeoxyglucose. While blood flow and glucose consumption in the structurally damaged area were often uncoupled during the acute phase, metabolism-to-flow ratios were markedly less scattered at later stages of cerebrovascular disease. Individual maximum-likelihood cluster analysis of brain regions revealed remarkable similarity between deactivation patterns of rCBF and rCMRglc, with Tanimoto coefficients averaging 0.56. This similarity was inversely related to the residual rCMRglc of the lesion. These findings are in line with results obtained by PET of other tracers, suggesting that the pair of methods provides valuable and somewhat complementary information on brain function and mechanisms of cerebral vascular disease.

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