EEG Energy Research Articles

Major unipolar depression and mild Alzheimer's disease: differentiation by quantitative tonic REM EEG

In a previous report, tonic REM sleep epochs from the all-night sleep EEG were processed and analyzed to produce a diagnostic that discriminated mild Alzheimer's disease (AD) from cognitively unimpaired control subjects. Here, we examine the specificity of this diagnostic in distinguishing depression from AD. Twenty-four cognitively unimpaired seniors (aged 63±1.3) with major depressive disorder (unipolar) were monitored for all-night EEG in a manner identical to that used in our previous report. Tonic REM EEG epochs were preconditioned, spectrally analyzed and compated with known populations of control and AD EEG spectra. Instances when a given depressed subject's spectra fell within spectral zones unique to control or AD populations formed a diagnostic score (control, AD, neither of these). Diagnostic scores correctly identified 88% ( 21 24 ) of cognitively unimpaired seniors with major depressive disorder (unipolar). This can be compared with 89% ( 31 35 ) of mild AD subjects and 100% ( 43 43 ) of control subjects correctly identified in our previous report. This diagnostic also correctly classified as to eventual clinical AD/not AD outcome 8 subjects with both major depressive disorder and validated memory complaints. The diagnostic discrimination of AD is based on the fact that AD subjects have significantly less tonic REM eEG energy in the 13–30 Hz frequency range and more in the 1–10 Hz range than control or depressed subjects, as shown in conventional spectral analysis.

Intracerebroventricular application of competitive and non-competitive NMDA antagonists induce similar effects upon rat hippocampal electroencephalogram and local cerebral glucose utilization

In this study we have used electrophysiological and metabolic markers to investigate the effects of competitive and non-competitive NMDA antagonists in rats after central or peripheral administration. The non-competitive antagonist, MK-801, induced dose-dependent suppression of rat hippocampal EEG energy both after intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) application. Similar effects were observed after i.p. and i.c.v. application of the competitive antagonist, dl-CPP-ene. Whereas the MK-801 was more potent after i.p. application, dl-CPP-ene was more potent after i.c.v. administration. Intracerebroventricular administration of MK-801 and dl-CPP-ene resulted in similar changes in the pattern of local cerebral glucose utilization in the olfactory tubercle and regions of the limbic system such as the anteroventral thalamus, hippocampus and entorhinal cortex. Intravenous (i.v.) administration of MK-801 induced increases in glucose metabolism similar to those observed after i.c.v. application. In contrast, i.v. administration of dl-CPP-ene induced only small decreases of glucose utilization in several regions of the central sensory system. Thus the blockade of glutametergic (NMDA) transmission results in decreased hippocampal EEG activity which is paralleled by increased metabolic activity in this area. We conclude from EEG recordings and [ 14C]2-deoxyglucose uptake experiments that both non-competitive and competitive NMDA antagonists produce the same pattern of alterations after i.c.v. administration. Apparent differences in efficacy after peripheral administration may be largely due to differences in bioavaliability.

The no-reflow phenomenon is a post-mortem artifact.

Post-ischemic reperfusion impairment, ("no-reflow phenomenon"), was studied in rats subjected to 8-30 minutes of global brain ischemia. During ischemia, rapid and complete loss of cerebral blood flow, EEG and 31P-high energy phosphates (ATP/PCr) was observed. Brain intravascular perfusion defects were examined by injecting carbon black intravenously in a group of rats with stable cardiopulmonary function and in another group subjected to rapid thoracotomy and intraarterial infusion of the carbon marker. Results indicate that global brain ischemic or non-ischemic control rats given intraarterial carbon black after thoracotomy had varying degrees of vessel filling defects in brain resulting in "pale tissue areas" suggestive of impaired perfusion (no-reflow). All rats given carbon black intravenously whether global brain ischemic or not, showed normal cerebrovascular filling of the carbon black and absence of "pale tissue areas". In addition, post-ischemic cerebral reperfusion following 8-30 minutes global brain ischemia can reverse neuroelectric, energy metabolite and cerebral blood flow loss in rats whose cardiopulmonary function is not compromised. These findings indicate that the "no-reflow phenomenon" is an agonal or post-mortem artifact observed in the presence of cardiopulmonary failure.

Effects of repeated sleep deprivation in the dark- or light-period on sleep in rats

This study was designed to examine the differences between sleep duration and EEG when sleep was restricted to the rest- or activity-phase for 5 successive days, achieved by repeated sleep deprivation in the dark (DSD) or light-period (LSD). In the DSD-experiment the percentages of the vigilance states were comparable to the level of the baseline light period. In LSD, the amounts of all sleep states increased substantially relative to baseline dark. The sleep episodes were lengthened in DSD and LSD. The duration of NREM-sleep and the sleep episodes remained longer in the light than in the dark, indicating circadian influences. In the first hours after sleep deprivation the delta activity during NREM-sleep was enhanced in LSD and to a lesser extent in DSD. This effect diminished over the consecutive days in both experiments. The EEG energy gained during sleep and its accumulation pattern on each day in DSD and LSD were strikingly similar, thereby reflecting a homeostatic process. After the sleep deprivation days, small changes were observed in the distribution of the vigilance states, the delta activity and EEG energy over the light- and dark-period.

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density.

The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Spectral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25-15.0 Hz) over successive nonrapid eye movement--rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.

Reduction of human sleep duration after bright light exposure in the morning

In 8 subjects the spontaneous termination of sleep was determined after repetitive exposure to either bright or dim light, between 6.00 and 9.00 h, on 3 days preceding sleep assessment. Sleep duration was significantly shorter following bright light than following dim light. During sleep the time course of EEG energy was not affected by the light treatment. Analysis of the time course of body temperature during sleep indicated an earlier rise of body temperature following the bright light treatment. In terms of the two-process model of sleep regulation this can be interpreted as a direct effect of light on the circadian phase of the wake up threshold.

Stages in human brain development

In a 1974 survey of data on human brain and head growth statistically significant peaks in growth rates of human brains were found around ages 11 years and 15 years. In addition, correlations were found in that almost all studies had non-significant peaks around ages 3, 7, 11–12 and 15 years; troughs were found at the intermediate ages (5, 9, and 13 years). More recent data include a very extensive collection of head circumference data from a dozen countries which showed statistically significant peaks around ages 7, 12, and 15 years. Confirmation of those results have been found in data on cortical thickness, photographs of neuronal arbors, and the percent of EEG energy found in the α-frequencies (8–13 cps). The proposed peak around age 3 years cannot be decided from existing brain weight and head circumference data bases, but the EEG data and the cortical thickness data supply significant support. Overall, there are statistically significant peaks in brain growth rates at age 7, 11–12, and 15 years, though the latter holds only for males at present. The significance of the stages for development of brain functions is being explored.

Stages in human brain development

In a 1974 survey of data on human brain and head growth statistically significant peaks in growth rates of human brains were found around ages 11 years and 15 years. In addition, correlations were found in that almost all studies had non-significant peaks around ages 3, 7, 11-12 and 15 years; troughs were found at the intermediate ages (5, 9, and 13 years). More recent data include a very extensive collection of head circumference data from a dozen countries which showed statistically significant peaks around ages 7, 12, and 15 years. Confirmation of those results have been found in data on cortical thickness, photographs of neuronal arbors, and the percent of EEG energy found in the alpha-frequencies (8-13 cps). The proposed peak around age 3 years cannot be decided from existing brain weight and head circumference data bases, but the EEG data and the cortical thickness data supply significant support. Overall, there are statistically significant peaks in brain growth rates at age 7, 11-12, and 15 years, though the latter holds only for males at present. The significance of the stages for development of brain functions is being explored.

The EEG's of chronic schizophrenic patients in hospital and in the community

EEG's were recorded from chronic schizophrenic impatients, remitted patients living in the community and normal controls, during resting and auditory stimulation conditions. Chronic inpatients had more energy in the slower and fastest wave bands than either remitted patients or normal controls. No differences were found in overall EEG energy and variability between groups of subjects or between sides of the head. It was concluded that any abnormalities were associated with behavioural differences and not with schizophrenic process changes.

Pharmacological Aspects of Dihydrogenated Ergot Alkaloids in Experimental Brain Research

In three different experimental series with 22 experimental and 21 control cats it is demonstrated that DH-ergotoxine mesylate (Hydergine®) improves EEG energy, disturbed by temporary ischemia, in the isolated perfused cat head. It could be shown that improvement of EEG energy and lowering of arteriovenous lactate difference can be directly correlated. DH-ergonine improves experimentally induced metabolic decline as does DH-ergotoxine, but at one tenth of the dosage.

Telemetry and continuous energy analysis of hypothalamic eeg changes in female cats during intromission by the male

(1) Hypothalamic and cortical macro-electrode (EEG) records were telemetered from freely-moving, ovariectomized cats treated with estrogen during mating tests with males, and records were analysed for EEG energy changes in 3 frequency bands (4–8, 8–16 and 16–32 Hz). The methods used for telemetry and EEG analysis are fully described. (2) Synchronous with the male's intromission, there was a flattening of the amplitude of the already activated EEG (Suppression response) in hypothalamic ventromedial nucleus (Hvm) which was not observed in other hypothalamic or cortical sites. (3) EEG energy analysis showed that the effect was most marked in the 16–32 Hz band, and confirmed that it was localized to Hvm. (4) Similar, but not identical, suppression responses were observed during vaginal probing both before and during estrogen treatment: the response was not, therefore, a hormone-dependent one. (5) The suppression response in Hvm was considered to be a neural correlate of intromission by the male and, together with changes in the background level of the EEG, may play a role in determining the affective responses of the female cat to the male's copulatory activity.