To clarify the neural correlates and brain activity during the progression of human non-rapid eye movement (NREM) sleep, we examined the absolute regional cerebral blood flow (rCBF) during light and deep NREM sleep and during wakefulness in normal humans using positron emission tomography with H(2)(15)O. Relative changes in rCBF during light and deep NREM sleep in comparison to the rCBF during wakefulness were also analyzed. During light NREM sleep, the rCBF in the midbrain, in contrast to that in the pons and thalamic nuclei, did not decrease when compared to that during wakefulness, whereas rCBF decreased in the left medial frontal gyrus, left inferior frontal gyrus, and left inferior parietal gyrus of the neocortex. During deep NREM sleep, the rCBF in the midbrain tegmentum decreased, and there was a marked and bilateral decrease in the rCBF in all neocortical regions except for the perirolandic areas and the occipital lobe. There have been three groups of brain structures, each representing one type of deactivation during the progression of NREM sleep. The activity of the midbrain reticular formation is maintained during light NREM sleep and therefore represents a key distinguishing characteristic between light and deep NREM sleep. Selective deactivation of heteromodal association cortices, including those related to language, occurs with increasingly deep NREM sleep, which supports the recent theory that sleep is not a global, but it is a local process of the brain.

In 13 patients with central (thalamic) pain after stroke, CT, MRI, PET scan and intraoperative thalamic microrecordings were performed. Electrophysiological studies showed that irregular burst discharges were often encountered in the posterolateral thalamus. The more often the irregular burst discharges were encountered, the greater the decrease of sensory response in the posterolateral thalamus. Metabolic studies showed that regional cerebral glucose metabolism decreased in both the posterolateral thalamus and in the cortical postcentral area on the lesioned side in all cases. In the thalamic lesion cases in which many irregular burst discharges were found in the posterolateral thalamus, regional cerebral glucose metabolism and the relative value of glucose to oxygen metabolism increased in the cortical precentral area on the lesioned side. It was suggested that decreased activity with abnormal burst discharge in the posterolateral (sensory) thalamus associated with changes in cortical activity adjacent to the central sulcus might be related to the genesis of central (thalamic) pain. It is emphasized that cortical activity decreased in the postcentral area, but often increased in the precentral area.

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Eight patients with small gliomas (6 low-grade and 2 high-grade) localized in a single gyrus or less than 2 cm diameter were investigated using positron emission tomography and single photon emission computed tomography. All three tumors examined demonstrated hypermetabolism of amino acids. High-grade gliomas demonstrated hypermetabolism of glucose and high blood flow, but normal or low oxygen metabolism. High-grade gliomas also showed accumulation of 201Tl chloride and high or low accumulation of 123I-isopropyl iodoamphetamine. These indications allow preoperative diagnosis of the malignancy of small gliomas, which is important because small gliomas with high-grade malignancy need more extensive removal and adjuvant therapy.