Quantitative scalp EEG from 32 channels and the cerebral glucose metabolic rate from the 32 underlying cortical positions as assessed by positron emission tomography (PET) with 18F-2-deoxyglucose (FDG) were obtained on 36 patients with mild to moderate senile dementia of the Alzheimer type and 17 age- and sex-matched normal control subjects. Subjects performed a verbal memory task during uptake of FDG. There were significant correlations between both delta amplitude and metabolic rate and memory performance during FDG uptake. Patients with Alzheimer’s disease had significantly greater left temporal delta amplitude and lower glucose metabolic rates. Both EEG delta in microvolts and metabolic rate had similar diagnostic sensitivity, but PET had fewer false positives among normals. The left amygdala had the highest sensitivity and percent correct diagnosis of any brain area. Temporal lobe EEG delta activity showed higher correlations with hippocampal metabolic rate than metabolic rate directly under the electrode.
In order to test the hypothesis that serotonergic mechanisms inhibit REM sleep via a 5HT1A receptor, we administered placebo and ipsapirone (10 and 20 mg by mouth 15 min before bedtime) to ten normal volunteers in a double blind fashion. Ipsapirone is a relatively selective 5HT1A receptor agonist. As predicted, ipsapirone prolonged REM latency and Mean Latency to Eye Movements (M-LEM), a measure of time between onset of REM sleep and the first eye movement of the REM period, and REM% at both doses compared with placebo. It also reduced sleep efficiency and total REM sleep time at the highest dose. These results support the hypothesis that systemic stimulation of 5HT1A receptors prolong REM latency and inhibit REM sleep.
Using positron emission tomography with fluorodeoxyglucose (18FDG or FDG), we compared the effects of zolpidem (10 mg), an imidazopyridine hypnotic, which is relatively selective for the BZ1 or omega receptor and placebo on cerebral glucose metabolism during the first non-REM sleep period of 12 young normal volunteers. Plasma zolpidem pharmacokinetics varied considerably among subjects, and plasma concentrations were lower than usually reported. In general, the effects of zolpidem on local cerebral glucose metabolism varied directly with plasma concentrations of zolpidem. Zolpidem induced changes in local cerebral glucose metabolism were unevenly distributed throughout the brain and were greater in subcortical areas than lateral cortical areas. Significant negative correlations were found between change in local absolute glucose metabolic rate (calculated by subtracting individual data on placebo nights from that on zolpidem nights) and plasma concentration of zolpidem for the following areas: medial frontal cortex, cingulate gyrus, putamen, thalamus, and hippocampus. The effects of zolpidem on local cerebral glucose metabolism were partially but not closely related to the reported density of BZ1 receptors.
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