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Brain, Vol. 125, No. 5, 1105-1115, May 2002
© 2002 Guarantors of Brain

Human regional cerebral glucose metabolism during non-rapid eye movement sleep in relation to waking

Eric A. Nofzinger1, Daniel J. Buysse1, Jean M. Miewald1, Carolyn C. Meltzer1,2, Julie C. Price2, Robert C. Sembrat2, Hernando Ombao4, Charles F. Reynolds1, Timothy H. Monk1, Martica Hall1, David J. Kupfer1 and Robert Y. Moore1,3

1 Department of Psychiatry, 2 Department of Radiology and 3 Department of Neurology, University of Pittsburgh School of Medicine and 4 Department of Statistics, University of Pittsburgh, PA, USA

Correspondence to: Eric A. Nofzinger, Department of Psychiatry, University of Pittsburgh School of Medicine, 3811 O’Hara Street, Pittsburgh, PA 15213-2593 USA E-mail: nofzingerea{at}msx.upmc.edu

Sleep is an essential human function. Although the function of sleep has generally been regarded to be restorative, recent data indicate that it also plays an important role in cognition. The neurobiology of human sleep is most effectively analysed with functional imaging, and PET studies have contributed substantially to our understanding of both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. In this study, PET was used to determine patterns of regional glucose metabolism in NREM sleep compared with waking. We hypothesized that brain structures related to waking cognitive function would show a persistence of function into the NREM sleep state. Fourteen healthy subjects (age range 21–49 years; 10 women, 4 men) underwent concurrent EEG sleep studies and [18F]fluoro-2-deoxy-D-glucose PET scans during waking and NREM sleep. Whole-brain glucose metabolism declined significantly from waking to NREM sleep. Relative decreases in regional metabolism from waking to NREM sleep occurred in wide areas of frontal, parietal, temporal and occipital association cortex, primary visual cortex, and in anterior/dorsomedial thalamus. After controlling for the whole-brain declines in absolute metabolism, relative increases in regional metabolism from waking to NREM were found bilaterally in the dorsal pontine tegmentum, hypothalamus, basal forebrain, ventral striatum, anterior cingulate cortex and extensive regions of the mesial temporal lobe, including the amygdala and hippocampus, and in the right dorsal parietal association cortex and primary somatosensory and motor cortices. The reductions in relative metabolism in NREM sleep compared with waking are consistent with prior findings from blood flow studies. The relative increases in glucose utilization in the basal forebrain, hypothalamus, ventral striatum, amygdala, hippocampus and pontine reticular formation are new observations that are in accordance with the view that NREM sleep is important to brain plasticity in homeostatic regulation and mnemonic processing.


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