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I Feinberg

Publications and source records attributed to I Feinberg.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1986

Sleep spindles in normal elderly: comparison with young adult patterns and relation to nocturnal awakening, cognitive function and brain atrophy.

Visual measurements of sleep spindles were carried out in 48 elderly and 20 young normal adults. Computed tomography brain scans and psychometric testing were also performed. Earlier findings of reduced spindle abundance, amplitude and duration in the elderly were confirmed. In addition, we demonstrated a linear increase in spindle density and duration across NREMPs in young adults that was absent in the elderly, indicating that age affects the temporal pattern as well as the quantity of spindles. Contrary to what seemed a highly plausible hypothesis, the amount of waking in the elderly was not inversely correlated with spindle abundance, confirming earlier observations (Feinberg et al. 1967) but in a much larger group. This finding suggests that spindle abundance does not reflect the integrity of the systems that maintain the brain in NREM sleep. We also were unable to show any clear evidence that relative preservation of spindles in the elderly is associated with relative preservation of cognitive skills: psychometric performance and spindle measures were, in most instances, not significantly correlated. However, the test of this hypothesis was limited by the high level of function and the narrow range of impairment of these Ss. One intriguing positive finding was the significant inverse relation between ratings of sulcal atrophy and spindle amplitude. This observation suggests an etiology for the reduced amplitude of the sleep EEG in old age. This change is one of the most striking effects of age on brain electrophysiology.

Adult↗
PubMed1985

Further evidence of abnormal non-rapid-eye-movement sleep in schizophrenia.

Very low levels of visually scored stage 4 sleep are found in 40% to 50% of acute and chronic schizophrenics. Stage 4 is a visual estimate of high-amplitude delta (0.5 to 3 Hz) electroencephalographic waves; these waves can now be measured directly and reliably by computer. In this pilot study, we carried out such measurement in the successive non-rapid-eye-movement periods (NREMPs). We also sampled and measured visually sleep spindles by NREMP; spindles constitute a second distinctive feature of the NREM electroencephalogram. In five unmedicated, recently rehospitalized schizophrenic patients we found reduced delta amplitude and abundance (and increased spindle density) in NREMP1 (also called "REM latency") as compared with ambulatory normal controls. NREMP1 was also abnormally short with an average length similar to that reported for major depression. These striking abnormalities of NREM sleep may underlie the abnormal rapid eye movement distributions sometimes found in schizophrenic and depressed patients. Further studies are required to evaluate the relation of these NREM abnormalities to psychopathology (and hence their utility as biological "markers") and to rule out confounding effects of hospitalization or undetected napping.

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↗