Irwin Feinberg

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.

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.

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.

Computer-Detected Patterns of Electroencephalographic Delta Activity During and After Extended Sleep

Delta (0.5 to 3 hertz) waves are the electroencephalographic hallmark of human sleep. We measured their rate of production during and following an extended night of sleep. On the extended night, we confirmed previous observations of a linear decline in delta wave production across the first four periods of non-rapid-eye-movement (non-REM) sleep. An asymptote was reached in the fifth non-REM period, perhaps signifying that sleep processes reached completion. On the day after the extended night, subjects were allowed to remain awake 3.6 hours less than normal. During the next sleep session, amplitude and number of delta waves in non-REM periods 1 and 3 were significantly reduced. These findings illustrate the value of computer analysis of electroencephalographic waveforms in sleep. Systematic measurement of the amount and distribution of these waveforms as a function of preceding waking duration should provide clues to the kinetics of the metabolic processes underlying sleep.

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.