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J D March

Publications and source records attributed to J D March.

15 recordsLinked to original sources
PubMed1999

A comparison of period amplitude analysis and FFT power spectral analysis of all-night human sleep EEG.

Zero-cross and zero-derivative period amplitude analysis (PAA) data were compared with power spectral analysis (PSA) data obtained with the fast Fourier transform in all-night sleep EEG from 10 subjects. Although PAA zero-cross-integrated amplitude showed good agreement with PSA power in 0.3-2 Hz, zero-cross analysis appears relatively ineffective in measuring 2-4 Hz and above waves. However, PAA zero-derivative measures of peak-trough amplitude correlated well with PSA power in 2-4 Hz. Thus, while PAA appears able to measure the entire EEG spectrum, the analytic technique should be changed from zero cross to zero derivative at about 2 Hz in human sleep EEG. PAA and PSA both demonstrate robust and interrelated across-night oscillations in three frequency bands: delta (0.3-4 Hz); sigma (12-16 Hz); and fast beta (20-10 Hz). The frequencies between delta and sigma, and between sigma and fast beta, did not show clear across-night oscillations using either method, and the two methods showed lower epoch-to-epoch agreement in these intermediate bands. The causes of this reduced agreement are not immediately clear, nor is it obvious which method gives more valid results. We believe that the three strongly oscillating frequency bands represent fundamental properties of the human sleep EEG that provide important clues to underlying physiological mechanisms. These mechanisms are more likely to be understood if their dynamic properties are preserved and measured naturalistically rather than being forced into arbitrary sleep stages or procrustean models. Both PAA and PSA can be employed for such naturalistic studies. PSA has the advantages of applying the same analytic method across the EEG spectrum and rests on more fully developed theory. Combined zero-cross and zero-derivative PAA demonstrates EEG oscillations that closely parallel those observed with spectral power, and the PAA measures do not rely on assumptions about the spectral composition of the signal. In addition, both PAA techniques can measure the relative contributions of wave amplitude and incidence to total power: These waveform characteristics represent different biological processes and respond differentially to a wide range of experimental conditions.

Adult↗
PubMed1992

Precise conservation of NREM period 1 (NREMP1) delta across naps and nocturnal sleep: implications for REM latency and NREM/REM alternation.

The delta integrated amplitude (DIA) in nonrapid eye movement period 1 (NREMP1) of daytime naps was precisely subtracted from the NREMP1s of ensuing nocturnal sleep, indicating that the brain can retain a record of DIA expressed in sleep episodes initiated 12.5 and 8.5 hours before nocturnal sleep onset. The DIA subtraction was primarily accomplished by reduced NREMP1 duration [earlier rapid eye movement (REM) onset], suggesting that the timing of REM period 1 (REMP1) onset is controlled by delta need. This result is consistent with the hypothesis that REM sleep occurs when a stimulus for NREM has been partially depleted.

Adult↗
PubMed1991

Sigma (12-15 Hz) and delta (0.3-3 Hz) EEG oscillate reciprocally within NREM sleep.

Sleep EEG in the sigma and delta frequency bands was subjected to spectral analysis in 8 normal young adults. In each subject, power density of sigma and delta oscillated reciprocally during NREM sleep, confirming an observation made initially with period/amplitude analysis. In REM sleep, power density for both frequency bands was at its lowest levels. Correlation coefficients between power density of delta vs. 1/sigma for all artifact-free 20-s epochs of NREM sleep/night were highly significant for each subject. These results show that cyclic oscillation of EEG within sleep is not limited to delta frequencies. The reciprocal relation of sigma to delta holds implications for the EEG mechanisms of NREM sleep. This dynamic pattern may also prove useful for sleep stage scoring and for a finer empirical analysis of sleep in psychiatric and neurological disorders.

Activity Cycles↗
PubMed1991

Acute deprivation of the terminal 3.5 hours of sleep does not increase delta (0-3-Hz) electroencephalograms in recovery sleep.

Sleep electroencephalograms (EEG) and electrooculograms were recorded in nine young adult males on a baseline night, a night in which they were deprived of an average of 3 hr 27 min of sleep by early awakening, and on a recovery night. Records were analyzed by visual sleep stage scoring and period-amplitude analysis; the results of both were tabulated by successive nonrapid eye movement periods (NREMPs) and rapid eye movement (REM) periods. Neither visually scored delta nor REM measures were affected by this substitution of waking for sleep. Although there was a significant increase in the 0-3-Hz time/epoch on the recovery night, this finding was not confirmed in the accompanying report. These results, taken in association with data from previous studies, are consistent with the hypothesis that, in an acute experiment, visually scored delta and computer-measured 0-3-Hz EEGs increase above the baseline levels only if there has been loss of stage 3/4 EEG (or of sleep) from the first two NREMPs. The findings here are inconsistent with older reports and indicate that further parametric data are required to construct a quantitative model of the relation of sleep EEG waveforms to the duration of prior waking.

Adult↗
PubMed1991

Acute deprivation of the terminal four hours of sleep does not increase delta (0-3-Hz) electroencephalograms: a replication.

This experiment evaluated further our previous finding that substitution of waking for the terminal 3-4 hr of sleep produces little or no increase in either visually scored or computer measures of delta sleep. Eleven young adults (mean age 24.5 yr) were studied on a baseline night, a night with sleep limited to an average of 188 min, and a recovery night. Visually scored sleep stages, eye movement activity and computer measures of 0-3 Hz were analyzed by nonrapid eye movement periods (NREMPs) and for all recorded sleep in each condition. In addition, we measured the heights, durations and areas under the curve manifested by the cyclic waxing and waning of 0-3-Hz integrated amplitude across sleep. Acute loss of 3.9 hr of sleep did not increase either visual or computer measures of delta electroencephalograms (EEG) on the recovery night, essentially confirming our previous findings. We hypothesize that augmentation of delta EEG above baseline levels after acute (one night's) sleep loss requires that disruption or loss of sleep from the first two NREMPs (or delta cycles). Rapid eye movement (REM) sleep durations on the recovery night were unaffected by the marked loss of REM sleep caused by partial deprivation. Although eye movements as well as stage REM were lost in the deprivation condition, eye movement density was significantly reduced rather than increased on the recovery night. This reduction is consistent with the hypothesis that REM activity varies inversely with sleep depth (or directly with central arousal level). The observations here, taken in association with previous results, suggest that a threshold for eye movement suppression by sleep deprivation in young adults lies in the range of 3-4 hr of prior sleep loss.

Adult↗
PubMed1990

Gamma distribution model describes maturational curves for delta wave amplitude, cortical metabolic rate and synaptic density.

We analyzed the available ontogenetic data (birth to 30 years of age) for: amplitude of delta EEG (DA) waves during sleep; cortical metabolic rate (CMR) measured with positron emission tomography; and synaptic density (SD) in frontal cortex. Each is at the adult level at birth, increases to about twice this level by 3 years of age, and then gradually falls back to the adult level over the next two decades. Statistical analyses revealed that individual gamma distribution models fit each data set as well as did the best ad hoc polynomial. A test of whether a single gamma distribution model could describe all three data sets gave good results for DA and CMR but the fit was unsatisfactory for SD. However, because so few data were available for SD, this test was not conclusive. We proposed the following model to account for these changes. First, cortical neurons are stimulated by birth to enter a proliferative state (PS) that creates many connections. Next, as a result of interactions in the PS, neurons are triggered into a transient organizational state (OS) in which they make enduring connections. The OS has a finite duration (minutes to years), and is characterized by high rates of information-processing and metabolism. Levels of CMR, SD and DA, therefore, are proportional to the number of neurons in the OS at any time. Thus, the cortex after birth duplicates, over a vastly greater time scale, the overproduction and regression of neural elements that occurs repeatedly in embryonic development. Finally, we discussed the implications of post-natal brain changes for normal and abnormal brain function. Mental disorders that have their onset after puberty (notably schizophrenia and manic-depressive psychoses) might be caused by errors in these late maturational processes. In addition to age of onset, this neurodevelopmental hypothesis might explain several other puzzling features of these subtle disorders.

Adolescent↗
PubMed1988

Response of delta (0-3 Hz) EEG and eye movement density to a night with 100 minutes of sleep.

In one of a series of experiments aimed at gathering the empirical data required to formulate mathematically our recovery model of sleep, we recently (1) measured the increase in delta electroencephalogram (EEG) following one night of total sleep deprivation (TSD). We found that the delta rebound was confined to the first non-rapid eye movement period (NREM-P1) of recovery sleep; this unexpected result was documented with direct computer measurement of 0-3 Hz EEG, as well as with visual scoring of stages 3 and 4. We also found a robust decrease in eye movement density during the second and third REM periods, which we hypothesized to be due to the increased depth of recovery sleep. In the present experiment, we awakened young adult subjects after 100 min of sleep, a duration that includes the first cycle for this age group, and analyzed visual and computer measures of delta and eye movement density during recovery sleep. We again found eye movement density to be significantly reduced in REM-P2 and P3, but to a lesser degree than after total sleep deprivation, a condition that may be presumed to produce a greater increase in sleep depth. Delta increases were again limited to the first cycle, although all subjects completed this cycle on the 100-min night. The major difference between recovery sleep patterns following the total deprivation and the 100-min sleep conditions was that 0-3-Hz wave amplitude increased significantly after the former, but not after the latter. In both studies, recovery sleep showed increased 0-3-Hz wave density. The neurophysiological implications of a response of EEG amplitude as opposed to wave density are briefly considered; separate measurement of these variables is more readily accomplished with period-amplitude than with spectral analysis. Our results further illustrate the importance of measuring sleep by physiological units, such as the successive NREMPs and REMPs. They also support other data that indicate that NREM-P1 plays a special role in human sleep: it responds selectively to sleep deprivation, shows the greatest ontogenetic variation across the human lifespan, and is the component of sleep that is most frequently abnormal in psychiatric patients. As we have long argued, it is inappropriate to conceptualize this high priority component of NREM sleep as "REM latency" and as a measure of REM "pressure" exclusively.

Adult↗
PubMed1987

Effects of sleep loss on delta (0.3-3 Hz) EEG and eye movement density: new observations and hypotheses.

One night's sleep loss in young adults increased delta (0.3-3 Hz) EEG only in the first non-REM period of recovery sleep. The delta increase was limited to frequencies 0.3-4 Hz; within this range, the effects on wave form periods and amplitudes differed by frequency band. These results illustrate the value of computer analysis applied to the physiological units of sleep (the successive non-REM and REM periods of each sleep cycle). The finding that all of the delta increase occurred in the first sleep cycle appears inconsistent with the exponential decline of delta across cycles predicted by 'recovery' models of sleep. The fact that wave periods and amplitudes are differentially affected by sleep loss indicates that it is premature to adopt any single wave form characteristic (e.g., power spectral density) to index delta sleep. Our data also confirm a recent report that eye movement density decreases after sleep loss; we hypothesize that this change results from greater depth of sleep; an inverse relation of depth of sleep to eye movement density provides a coherent explanation for a range of otherwise disparate observations. Lastly, we propose a new hypothesis to account for the presence of eye movement during REM sleep.

Adult↗
PubMed1985

Homeostatic changes during post-nap sleep maintain baseline levels of delta EEG.

It has been hypothesized that visually scored stage 4 EEG (dense, high amplitude 0.5-3 Hz (delta) waves) is a correlate of a metabolic process that reverses some of the effects of waking on the brain. The results of nap studies appear inconsistent with this hypothesis since late naps produce a disproportionate loss of stage 4 during subsequent sleep. We show here with direct computer measurement that the integrated amplitude (and other measures) of 0.5-3 Hz EEG waves are conserved across a nap and post-nap sleep. Thus, the metabolic model remains tenable. However, the homeostatic adjustments involve changes in the periods, durations and distributions of delta waves that are not predictable by any existing model. This study also demonstrates the limitations inherent in visual estimates (sleep stage scoring) of delta wave amplitude and abundance.

Adult↗
PubMed1984

Log amplitude is a linear function of log frequency in NREM sleep eeg of young and elderly normal subjects.

The log of the amplitude of EEG waves during NREM sleep is a linear function of the log of their frequency. The slope of this function is reliable within individuals, is significantly less steep in elderly than in young subjects and, in both groups, becomes flatter across successive NREM periods. We interpret these results as consistent with the hypothesis that the function of NREM sleep is to reverse the effects of waking on the brain. According to this model the decreased steepness of slope in the elderly and in later NREM periods reflects the diminishing intensity of these processes. Whatever the correct interpretation, the within-subject consistency of slope values permits their empirical study as a function of experimental manipulations. In addition, the quantitative F-A function established here (A = c/Fb) sets constraints that may prove useful for physiologic models of EEG waves during sleep.

Adult↗
PubMed1979

Flurazepam effects on sleep EEG. Visual, computer, and cycle analysis.

Analysis of sleep effects of flurazepam hydrochloride on four normal subjects confirmed that this drug substantially suppresses both REM and stage 4 sleep. Computer analysis disclosed that delta wave amplitude was greatly reduced by flurazepam. However, low density delta wave activity (ie, stage 2 sleep, which was increased in duration beyond the reduction in stage 4), permitted the number of delta waves and the time they occupied per night to remain at baseline levels. This finding suggests that sedative-hypnotics increase total sleep time by slowing the metabolic processes of sleep so that a longer sleep duration is required for the same biological effects. New observations on the induction times of REM and stage 4 effects are also presented. In general, the distortions in sleep EEG produced by flurazepam qualitatively resemble, but are quantitatively greater than, those produced by barbiturates in equivalent hypnotic doses.

Adult↗
PubMed1977

Flurazepam effects on slow-wave sleep: stage 4 suppressed but number of delta waves constant.

Repeated administration of flurazepam reduced stage 4 sleep (high delta-wave concentration) but produced a greater increase in stage 2 duration so that total sleep time was increased. Computer analysis revealed that the increased amount of stage 2 (low delta-wave concentration) sleep provided a number and duration of delta waves sufficient to offset the loss of delta activity in stage 4. However, the amplitude of the average delta wave was reduced. These results demonstrate the value of direct quantification of delta-wave activity, the variable that underlies visual classification of slow-wave sleep into stages 2 to 4. They also give rise to new hypotheses regarding the relative absence of side effects in spite of profound stage 4 suppression by flurazepam and the mechanisms by which total sleep time is increased by this drug.

Anti-Anxiety Agents↗
PubMedDate not supplied

Observations on delta homeostasis, the one-stimulus model of NREM-REM alternation and the neurobiologic implications of experimental dream studies.

We first review the concept of delta homeostasis as formulated in our 1974 model and as developed quantitatively by Borbely and colleagues in several versions of the two-process model. We illustrate difficulties in the application of this quantitative model to the negative delta rebound in the rat and we put forward additional evidence that the negative rebound is a pathological rather than a homeostatic response to sleep deprivation. We next review experiments on rats in which the waking metabolic rate of limbic structures was increased by blockade of the NMDA-gated cation channel with ketamine and MK-801. As predicted by the 1974 homeostatic model, NREM delta increased during subsequent sleep. However, it remains to be shown that this powerful effect is actually caused by the metabolic change and that it is an intensification of physiological sleep rather than a non-specific increase in EEG slow waves caused by neurotoxicity. We then outline our one-stimulus model of NREM/REM alternation. In this model NREM sleep is induced by periodic (neuroendocrine?) pulses. These pulses increase delta EEG amplitude and density, depress arousal level and inhibit neural activity. When the strength of the pulsatile stimulus falls below a critical level, REM emerges as neuronal escape. Last, we discuss the neurobiologic implications of two robust findings in experimental dream studies: the relation of dream reports to arousal and the consistent failure of controlled studies to demonstrate qualitative differences between NREM and REM mentation.

Animals↗