John B. Knowles

Psychometric evaluation of the Stanford Sleepiness Scale

SUMMARY  Two assumptions underlying the Stanford Sleepiness Scale (SSS) were evaluated: that the descriptors defining each level of the scale are equivalent ways of characterizing a particular level of sleepiness; and that sleepiness, thus measured, is an unidimensional construct. Twenty‐four True/False items were derived from the descriptors at each level of the SSS. This revised scale was administered to 340 undergraduates in a questionnaire which also included: the SSS; four visual analogue scales; items identifying the subjects age, sex, and circadian type; and the time of administration. Analyses of the responses indicated that endorsement of items on the revised scale was not consistent with the SSS level endorsed, indicating that the descriptors at each scale level are not equivalent. A principal components analysis revealed two components, tentatively identified as activation and sleepiness, accounting, respectively, for 24.2 and 20.6% of the variance. It was concluded that sleepiness is not an unidimensional construct. Further studies are necessary to elucidate the nature of its components.

The sleep of remitted bipolar depressives: comparison with sex and age-matched controls.

The sleep of 10 bipolar patients was recorded for five consecutive nights following their recovery from a depressive episode. In all respects except the number of arousals, their sleep did not differ reliably from that of 10 sex and age-matched control subjects. We conclude that sleep measures are unlikely to be useful as trait markers of a depressive diathesis in bipolar disorder.

Rapid eye movement latency and mood following a delay of bedtime in healthy subjects: do the effects mimic changes in depressive illness?

The phase advance hypothesis proposes that a phase advance of certain circadian rhythms (such as rapid eye movement (REM) sleep propensity) relative to the sleep‐wake cycle is implicated in the pathophysiology and pathogenesis of depression. In an earlier study, we reported that a 6‐h delay of sleep in normals produced REM changes that resembled the depressive pattern. Mood change was generally modest, although 2 of the 10 subjects became noticeably depressed. This study assessed the replicability of these results, and introduced a phase advance control condition. Predicted changes were observed in REM parameters. Modest but reliable mood change was confined to the first night of the phase delay, and was attributed to sleep loss. These results suggest that the effects of the phase shift were relatively benign, except in a minority of cases. Such individuals may have a susceptibility to depression that manifests itself under certain conducive physiological conditions.

Sleep deprivation: outcome of controlled single case studies of depressed patients.

Six drug-free depressed patients, each of whom acted as their own control, were studied for eleven consecutive days during which they were twice deprived of sleep for either 36 or 40 hours. The sequence of events was baseline (3 days), SD, recovery (3 days), SD, recovery (3 days). Blind ratings of clinical state were made on the basis of four-hourly interviews (standardized for each case), which were videotaped; sleep was monitored by conventional electrophysiological methods. Sleep deprivation had a beneficial, but transient, effect on four of the six patients studied. Changes in sleep were unrelated to changes in clinical state.

REM latency and depression: computer simulations based on the results of phase delay of sleep in normal subjects.

A phase advance of the circadian rhythm of rapid eye movement (REM) sleep propensity relative to the sleep-wake cycle has been hypothesized to account for the abnormalities of REM sleep in depression. One implication of this hypothesis is that an acute phase delay of sleep in normal subjects should produce the same abnormalities of REM sleep. A further implication is that changes in REM sleep that occur in normal subjects with delay shifts of sleep of progressively greater magnitude describe those that occur during the course of a depressive episode. This hypothesis was tested by computer simulation using two equations which, given the data derived from normal subjects experiencing phase delays of sleep, generated the REM latencies expected during successive stages of a depressive episode. For severely depressed patients, the computer-generated data matched those found empirically. The known correlation between severity of depression and REM latency, and the REM latencies of recovered patients, are consistent with the hypothesis.

Sleep and depression: a case study of EEG sleep prior to relapse.

By chance, we were able to record for five consecutive nights the sleep of a 61-year-old woman before each of two successive depressive episodes. In this patient, marked changes in EEG sleep (notably a decline in “sleep efficiency”) preceded both episodes. These changes are considered to be of predictive, but not of etiological, significance.

The influence of prior wakefulness on REM sleep.

Data from studies of naps and of shifted sleep were used to determine the relationship between two measures of rapid eye movement (REM) sleep (percentage of REM in the first 2 hr of sleep and REM latency) and prior wakefulness. For each sample, we calculated the difference between the observed value and that predicted by a cosine function that estimated the circadian rhythm of REM sleep propensity. The difference values were found to correlate reliably with hours and log hours of prior wakefulness. We conclude that while REM sleep is regulated in part by an endogenous circadian oscillator, it is also influenced by the duration of prior wakefulness.

REM sleep and depression: Further use of computer simulation to test the phase-advance hypothesis

A phase advance of the circadian rhythm of rapid eye movement (REM) sleep propensity relative to the sleep-wake cycle has been proposed to account for the abnormalities of REM sleep commonly found in depressed patients. One implication of this hypothesis is that a phase delay of sleep in normal subjects should produce the same abnormalities of REM sleep. The hypothesis was tested by computer simulation using equations based on data derived from normal subjects who had experienced phase shifts of their bedtime. At phase delays of between 4 and 6 hours (an estimate of the putative phase advance in depressed patients), the mean REM latency and the mean duration of the first REM period predicted by the equations did not differ significantly from those observed in depressed patients. The findings with respect to the distribution of REM latency were more equivocal.