Nighttime plasma cortisol secretion and EEG sleep—Are they associated?

Since the initial rise in plasma cortisol during sleep usually occurs near the second period of rapid eye movement (REM) sleep, a more precise association between the initial cortisol rise and electroencephalographic (EEG) sleep was examined in 22 normal control subjects. Our results indicate that the length of the total non-REM sleep period between the first and second REM period including awake time was significantly correlated to the cortisol rise time. However, the timing of the initial cortisol rise was not significantly related to the overall plasma cortisol levels during the night. But the second non-REM sleep period (minus awake time) is inversely related to overall cortisol levels during the night.     

Sleep in children with episodic sleep phenomena: a comparison with the normal child]

(1) The sleep pattern of 23 children, aged 5-12 years, with episodic nocturnal phenomena (night-terrors, somnambulism, rhythmic movements) was recorded during two successive nights. It was compared with that of a group of 21 normal children of the same age. (2) In the pathological group, slow wave sleep (SLP, stages 3 and 4) was significantly shortened during the 2 nights. This deficit mainly involved the first 3h of sleep. (3) As for the slow wave sleep, REM sleep (SP) modifications prevailed during the first hours of sleep. The first REM period was delayed and preceded by more numerous and atypical partial REM periods. The duration of the first REM period increased faster as a function of its latency than in the normal child. (4) In contrast with this difficulty for REM sleep to occur during the first part of the night, the subsequent REM sleep pattern was similar in the 2 groups (total REM sleep duration, mean REM period duration, mean REM cycle duration). For equal latencies, REM periods had similar duration. Finally, the total REM sleep amount was a linear function of the total sleep time, with more or less identical coefficients for the two groups. (5) The part played by these modifications during the first hours of sleep in the occurrence of night terrors and somnambulism is discussed.     

Nocturnal sleep in separated monkey infants.

Nocturnal sleep was recorded from ten unrestrained, group-living Macaca nemestrina (pigtail) monkey infants, using implantable multichannel biotelemetry systems, during the agitation-depression behavioral reaction that follows maternal separation. Sleep disturbances during the four nights of separation were characterized by decreases in rapid eye movement (REM) time and in the number of REM periods, and increases in REM latency. Time awake and number of arousals were increased. Slow-wave sleep was not significantly affected. Sleep pattern changes were most pronounced the first separation night, and tended to decrease as separation continued, whereas behavioral measures of depression tended to increase as separation continued (up to four days). Sleep patterns returned to normal following reunion with the mother. Those infants who had the most severe sleep disturbances the first separation night (more time awake, less total sleep, less REM) also tended to become most depressed behaviorally later in the separation period.     

Wakefulness-sleep transition: emerging electroencephalographic similarities with the rapid eye movement phase

The covert-rapid eye movement (REM) sleep hypothesis of dreaming suggests that elements of REM sleep emerge during sleep onset, leading to vivid hypnagogic imagery. We tested the physiological part of this hypothesis by analysing scalp-recorded electroencephalograms of 15 human subjects during wake–sleep transition and subsequent night time sleep. Wake–sleep transition was categorised semi-automatically as alpha activity, alpha dropout and as early Stage 2 sleep. The slow oscillation, the slow and the fast subdivisions of the delta and the theta frequencies respectively, as well as alpha and sigma bands were analysed. The similarity of individual-specific wake–sleep transition periods and the whole night Stage 2 or REM sleep periods was expressed in a composite similarity measure covering the spectral power of all analysed frequency bands and in frequency-specific similarities related to power values in single bands. A significant increase in composite similarity with the whole night REM sleep emerged in the period of alpha dropout and diminished in early Stage 2 sleep. The alpha dropout period was more similar to whole night REM sleep than to whole night Stage 2 sleep. These region-independent effects were mirrored in region-specific manner by frequency bands of the delta-slow theta range. Findings are in accordance with the covert REM sleep hypothesis, with previous electrocorticographic results and with the frequency range of the sawtooth waves in humans.     

REM architecture changes in bipolar and unipolar depression.

The authors compared total night sleep measures and REM sleep architecture values for normal control subjects (N = 36), unipolar depressed patients (N = 36), and bipolar depressed patients (N = 22). The unipolar and bipolar patients had significantly greater fragmentation of REM periods than control subjects, and bipolar patients showed greater fragmentation of REM periods than unipolar patients. In both the unipolar and bipolar samples, the duration of successive REM periods was related to the total number of REM periods during sleep.     

Characteristics of rapid eye movement production during REM sleep in man: organization and rhythmicity

The purpose of this study was to verify statistically the existence of certain characteristics of rapid eye movement (REM) production during REM sleep: organization and rhythmicity. REM data were collected intermittently, over a period of 20 consecutive nights, from 6 normal adult subjects of both sexes. Results concerning the organization of REM production revealed the presence of 3 evolving slow trends: quadratic, linear and quasi-sinusoidal. The occurrence of a given trend type was not related to subject, night, time of night or length of REM sleep phase being analysed. Results of the analysis showed that it is possible for a series of REMs to contain one, two or more statistically significant rhythmic periods, or no significant rhythmic period. The rhythmic periods that were detected ranged from 1 to 21 min, and no predominant periods were present. As in the case of the slow trends, the occurrence of a given rhythmic period was not dependent on subject, night, time of night or length of the REM sleep phase.     

Premorbid polysomnographic signs in depressed adolescents: a reanalysis of EEG sleep after longitudinal follow-up in adulthood.

BACKGROUND: This is a report of a clinical follow-up study (10-15 years later as young adults) of adolescent major depressives and normal control subjects. Polysomnographic data were obtained during the original study period when the subjects were adolescent (time 1). With clinical follow-up (time 2) assessments in hand, our objective was to ascertain whether there were any premorbid polysomnographic signs associated with depression during adolescence. METHODS: Based upon initial (during adolescence) and follow-up clinical assessments (as adults), new subject groupings were generated: depression-free normal subjects and original normal subjects who experienced a depressive episode during the follow-up period (latent depressives). Suicidality and recurrence of depression were also examined. Multivariate analysis of covariance was used to analyze group differences in sleep measures and logistic regression for predicting three outcomes: lifetime depression, lifetime suicidality, and recurrence. RESULTS: Comparison of the depression-free normal subjects, the latent depressives, and the original major depressives revealed significant differences for sleep latency and sleep period time. Comparing all lifetime depressives (original major depressives and the latent depressives) to depression-free normal subjects revealed significantly more stages 3 and 4 combined (ST34) sleep and greater sleep period times among the depressives. An analysis involving the presence or absence of suicidality revealed no overall significant differences between the groups. Comparison of the lifetime depressives grouped by nonrecurrent and recurrent depressive course to the depression-free normal subjects revealed significant difference for sleep period time. Using logistic regression, we found that a longer sleep latency and sleep period time significantly predicted lifetime depression. Gender, ST34 sleep, and an interaction term for ST34 sleep and REM latency significantly predicted lifetime suicidality. CONCLUSIONS: There was evidence of premorbid sleep abnormalities during adolescence. A general pattern of sleep disruption around sleep onset and during the first 100 min of the sleep period and overall sleep was evident among the major and lifetime depressives, involving sleep latency (initial insomnia), sleep period time (hypersomnia), REM latency, and slow-wave sleep. This adds to the body of literature that highlights the importance of the first 100 min of the sleep period in depression.     

Are polysomnographic measures of sleep correlated to alexithymia?: A study on laboratory-adapted sleepers

Objective: Since recent findings have pointed to a correlation between alexithymia and measures of poor sleep quality during the first night of adaptation to a sleep laboratory, the aim of the current study was to assess the same relation in healthy laboratory-adapted sleepers. As a further measure of rapid eye movement (REM) sleep characteristics, REM density was also measured. Methods: Twenty-seven male subjects, without sleep or psychiatric disorders, filled out the 20-item Toronto Alexithymia Scale (TAS-20) and slept for two consecutive undisturbed nights. Polysomnography and REM density were measured in the postadaptation night. Results: Alexithymia scores did not correlate significantly with any polysomnographic variable or with REM density. Only the Externally Oriented Thinking (EOT) subscale showed a negative association with REM latency. Multiple regression on selected sleep measures as predictors confirmed these results. Conclusion: Results do not extend to normal sleep the association previously found between alexithymia and a poor quality of sleep during the adaptation night in the sleep laboratory. The only polysomnographic measure showing an association, albeit little, with one facet of alexithymia was REM latency.     

Sleep characteristics of menopausal insomnia: a polysomnographic study

Although menopausal insomnia is of clinical significance, the essential features of this form of disrupted sleep are poorly understood. The aim of the present study was to identify the sleep characteristics of menopausal insomnia by using overnight polysomnography (PSG). Twenty-one subjects with menopausal insomnia (MI) and 13 sex- and age-matched normal control (NC) subjects without sleep complaints took part in the present study. All MI and NC subjects underwent PSG on two consecutive nights. In comparison with NC, MI subjects had non-specific findings such as significantly shorter total sleep time, longer sleep latency, higher wake time after sleep onset, and lower sleep efficiency. As for rapid eye movement (REM) sleep variables, MI subjects had significantly shorter total REM sleep time, fewer numbers of REM sleep periods, longer REM latency, and higher REM density than did the NC subjects. As for the time course of REM density, REM density during the first 3 h period of nocturnal sleep was significantly higher for MI than for NC subjects. Unlike NC subjects, REM density for MI subjects did not tend to rise progressively during nocturnal sleep. The MI subjects had objective evidence of disrupted sleep and the most striking characteristics of this dysfunction were observed in REM sleep variables. The sleep characteristics of MI subjects were found to differ in REM sleep variables from those of patients with major depression (except for REM density). Menopausal insomnia patients appear to be similar to patients with generalized anxiety disorder accompanied by severe sleep disruption. These data lend support to the clinical distinction between menopausal insomnia and insomnia associated with major psychiatric disorders.     

Sleep studies on a 90-minute day.

After 2 adaptation and 2 baseline all-night sleep recordings, 5 normal young adult subjects (3 males) were placed on a schedule alternating 60 min of wakefulness and 30 min of sleep for 5 1/3 24-h periods. A 2-day recovery period followed. One male subject (MA15) was later placed on the identical protocol with the exception that he was allotted periods of 75 min of wakefulness and 15 min of sleep during the experimental period. One male narcolepsy-cataplexy patient was placed on the 60-30 schedule for 48 h. All subjects showed REM sleep during the schedule manipulation. REMM sleep occurred within 10 min of sleep onset (SOREMP) on 79 of 110 REM sleep occasions in the normals, on all 29 REM episodes in MA15, and on 16 of 17 REM periods in the narcoleptic. In the normals, REM sleep showed a tendency to recur on alternate 90-min cycles, while in the narcoleptic REM recurred on consecutive periods. Compared to baseline, REM sleep 24 h was decreased in the normals and increased in the narcoleptic. Time spent in slow wave sleep and stage 2 was also reduced in the normal subjects on the 90-min schedule, and stage 1 sleep time was increased. Peak sleep times for the 5 normals occurred between 09.00 and 12.30 and lowest sleep times from 21.00 to 02.00. During the first recovery night, sleep times ranged from 11.5 to 18.5 h, including significant increases of slow wave sleep and REM sleep. Except for SOREMPs, no signs of the narcolepsy-cataplexy syndrome were seen in any of the normal subjects.     

An automated analysis of REM sleep in primary depression.

The REM sleep of 23 nonpsychotic patients with primary depression was studied by means of an automated REM analyzer during a drug-free period and again during amitriptyline administration. Initial drug administration (50 mg) was associated with an immediate reduction in the number, average frequency, and average size of the rapid eye movements. The average REM size remained suppressed with continued drug administration while the average REM frequency showed a rebound which was responsible for a partial recovery of the number of REMs and total REM intensity to predrug levels. With regard to individual REM periods, REM frequency and REM intensity were redistributed during tricyclic administration so that the second REM period became more "intense" than the first REM period. This automated REM analysis technique provides an objective set of measures for characterizing discrete aspects of REM sleep during a depressive episode and for evaluating the changes in REM sleep during psychotropic trials.     

Changes in forebrain function from waking to REM sleep in depression: preliminary analyses of [18F]FDG PET studies.

Based on recent functional brain imaging studies of healthy human REM sleep, we hypothesized that alterations in REM sleep in mood disorder patients reflect a functional dysregulation within limbic and paralimbic forebrain structures during that sleep state. Six unipolar depressed subjects and eight healthy subjects underwent separate [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) PET scans during waking and during their first REM period of sleep. Statistical parametric mapping contrasts were performed to detect changes in relative regional cerebral glucose metabolism (rCMRglu) from waking to REM sleep in each group as well as interactions in patterns of change between groups. Clinical and EEG sleep comparisons from an undisturbed night of sleep were also performed. In contrast to healthy control subjects, depressed patients did not show increases in rCMRglu in anterior paralimbic structures in REM sleep compared to waking. Depressed subjects showed greater increases from waking to REM sleep in rCMRglu in the tectal area and a series of left hemispheric areas including sensorimotor cortex, inferior temporal cortex, uncal gyrus-amygdala, and subicular complex than did the control subjects. These observations indicate that changes in limbic and paralimbic function from waking to REM sleep differ significantly from normal in depressed patients.     

EEG sleep in young depressives: first and second night effects

The sleep electroencephalogram (EEG) of young, drug-free, recurrently depressed outpatients was analyzed for 2 nights and was compared to age-matched controls using a variety of standard and computerized measures of sleep activity. On the first night, young depressives showed significantly greater difficulty in falling asleep and decreased sleep efficiency. Sleep architecture differences between the young depressives and controls were highlighted by increased percentages of Stage 2 sleep and major decreases in Stages 3 and 4 (delta wave) sleep among the depressives, as indicated by either period analyses or spectral analysis. The greatest differences in delta wave activity during night 1 were found in the first two (non-rapid eye movement (NREM) periods as measured by period analysis (NREM period 1, p less than 0.04; NREM period 2, p less than 0.001--average delta wave count) or by spectral analysis for the first 100 min of sleep (0.5-2.0 Hz). In contrast to the NREM sleep findings, various REM variables, including REM latency did not significantly distinguish the two subject groups for either night 1 or 2. Stepwise discriminant analysis demonstrated that night 1 sleep latency and delta wave counts during the second NREM period correctly classified 100% of all 16 individuals studied. The only differences between the young depressed patients and controls that remained on night 2 were significant reductions in slow-wave sleep as quantified by the computerized methods. Taken together, these findings suggest that the EEG response of young outpatients to the first night's stay in a sleep laboratory may be a useful tool for the diagnosis of depression in this age group. In addition, the use of computerized methods in this study point to an underlying deficit in delta sleep waveforms as being a prominent feature of the sleep of young depressed subjects.     

The first phase of nocturnal sleep in mentally retarded children

The first phase of sleep observed in 104 mentally retarded children (from 3 months to 8 years of age) was studied throughout nocturnal sleep, and the following results were obtained. In 4 out of 104 subjects, REM sleep onset was observed, and in the remaining 100 subjects NREM sleep onset was found at the first wakefulness-sleep transition of the night. Following awakenings (lasting 4 min or more) during the night, 170 (51.7%) out of a total of 329 samples were REM sleep onset, and 159 (48.3%) showed NREM sleep onset. The phases of sleep onset and those following awakenings evidenced no correlation between the frequency of NREM sleep onset and DQ or clinical EEG, whereas a positive correlation was found between the frequency of NREM sleep onset and age.     

Sleep in subjects with autistic disorder: a neurophysiological and psychological study

Polysomnography (EOG, EEG, EMG) was carried out in 17 male children and adolescents with autistic disorder, in seven patients with mental retardation and fragile X syndrome, and in five age- and sex-matched normal male subjects. Density of rapid eye movements was not significantly different in the three groups of subjects; however, some sleep parameters such as time in bed, sleep period time, and total sleep time were significantly lower in subjects with autistic disorder than in normal controls; moreover, patients with autistic disorder showed values of sleep period time, first REM latency and percent (%) sleep stage 1 lower than those of patients with fragile X syndrome with mental retardation. Density of muscle twitches was significantly higher in patients with autistic disorder than in normal controls. In contrast only minor differences were observed between patients with autistic disorder and those with fragile X syndrome with mental retardation. Furthermore, some psychoeducational profile-revised items such as perception and eye-hand coordination, showed significant correlation with some sleep parameters (time in bed, sleep latency, stage shifts, first REM latency and wakefulness after sleep onset). Childhood Autism Rating Scale (CARS) scores to visual response and non-verbal communication showed significant correlation with some tonic sleep parameters, such as sleep period time, wakefulness after sleep onset, and total sleep time. Relating to people and activity level items were found to be significantly correlated with rapid eye movement density. Our results suggest the existence of a sleep pattern in autistic patients different from that observed in subjects with mental retardation and from that of normal controls. In addition, these findings indicate that sleep parameters in these patients are correlated with some psychological indices generally used for the diagnosis of autistic disorder; for this reason, polysomnographies might be useful in the comprehension of the neurophysiological mechanisms underlying this condition.     

Dynamics of nap sleep during a 40 hour period.

Following 1 baseline night, the sleep of 8 adult males in equally space 1 h naps during a 40 h period was examined. Ten additional subjects were sleep-deprived for 40 h with 1 h periods of exercise given in place of naps. One recovery night followed the 40 h period for both groups. Total sleep time and the amount of stage REM during the naps were negatively related to the circadian-temperature cycle. Stage REM frequently appeared within 10 min of stage 1 onset and the normal sequence of stages REM and 4 were altered, demonstrating that the organization of sleep within a nap is quite different from that in monophasic nocturnal sleep. Auto-correlation and cross-correlation analyses showed that the relation of sleep stages from hour to hour in normal continuous baseline sleep was altered in nap-to-nap comparison. The timing of REM onset may be controlled by a sleep-dependent ultradian clock; the clock may stop upon awakening and resume at the next sleep onset. Naps had recuperative value in terms of maintaining the normal amounts of sleep stages on the recovery night; recovery sleep for the exercise group showed typical sleep-loss effects.     

Are polysomnographic measures of sleep correlated to alexithymia? A study on laboratory-adapted sleepers

Objective: Since recent findings have pointed to a correlation between alexithymia and measures of poor sleep quality during the first night of adaptation to a sleep laboratory, the aim of the current study was to assess the same relation in healthy laboratory-adapted sleepers. As a further measure of rapid eye movement (REM) sleep characteristics, REM density was also measured. Methods: Twenty-seven male subjects, without sleep or psychiatric disorders, filled out the 20-item Toronto Alexithymia Scale (TAS-20) and slept for two consecutive undisturbed nights. Polysomnography and REM density were measured in the postadaptation night. Results: Alexithymia scores did not correlate significantly with any polysomnographic variable or with REM density. Only the Externally Oriented Thinking (EOT) subscale showed a negative association with REM latency. Multiple regression on selected sleep measures as predictors confirmed these results. Conclusion: Results do not extend to normal sleep the association previously found between alexithymia and a poor quality of sleep during the adaptation night in the sleep laboratory. The only polysomnographic measure showing an association, albeit little, with one facet of alexithymia was REM latency.     

Rapid eye movement sleep cycle, clock time and sleep onset.

The phase of the REM sleep rhythm was studied in 10 normal subjects each of whom was sleep studied for 4 consecutive nights. For analysis, each night of sleep was aligned according to clock time and each minute was scored as REM or non-REM. With these data, REM probability was found as a function of clock time. Fractional harmonic analysis indicates a 90 min periodicity. The REM probability curve shows peaks occurring at 1:30 a.m., 3:15 a.m., 4:30 a.m., 5:45 a.m. and 7:00 a.m. Statistical measures comparing the time of REM sleep across subjects suggests that subjects tend to have REM sleep at the same time of the night as each other. The influence of elapsed time after sleep onset on REM sleep is also reestablished. Results indicate that the time of REM sleep is determined by both clock time and time of sleep onset, suggesting two clocks, one sleep dependent and the other related to the basic rest activity cycle (BRAC), which are responsible for driving REM sleep. Furthermore, the similarity of REM times across subjects indicates the possible existence of an extra-personae REM driving force linked to clock time and possibly the BRAC.     

Effects of auditory stimulation during rapid eye movement sleep in healthy volunteers and depressed patients.

Auditory and somesthesic forms of stimulation have substantially increased rapid eye movement (REM) sleep in cats. We investigated whether auditory stimulation, applied during REM sleep or outside REM sleep, would have similar effects in normal volunteers. We also administered auditory stimulation to depressed patients during REM sleep. Subjects were studied during 1 acclimatization night, 2 baseline nights, 4 consecutive nights with auditory stimulation, and 1 followup night without auditory stimulation. Normal volunteers were randomly divided into Group R, which received auditory stimulation during each REM sleep episode, and Group NR, which received auditory stimulation at the end of each REM sleep episode. Depressed patients (Group D) received auditory stimulation during each REM sleep period. Only Group R showed increased REM sleep time during the nights of auditory stimulation and throughout the followup night. This group also increased their sleep efficiency. Group NR showed reduced sleep efficiency due to an increase in both the duration and frequency of awakenings. Group D did not show increased REM sleep time, but did show shortened REM sleep episodes, increased REM sleep frequency, and increased duration of awakenings. Group D did not show clinical changes.     

EEG sleep studies in patients with generalized anxiety disorder

Sleep polygraphic recordings were performed during 3 consecutive nights in 12 inpatients with generalized anxiety disorder (GAD) in comparison with age- and sex-matched groups of patients with major depressive disorder (MDD) and normal subjects. GAD patients differed significantly from those with MDD. A lower number of awakenings and stage shifts in night 1 and the mean of the 3 nights and a shorter rapid eye movement (REM) duration in night 1 but longer REM latency in the mean of the 3 nights were observed in GAD in comparison to MDD. GAD patients also showed a significantly longer sleep onset latency and shorter duration of total sleep time and Stage 2 than control subjects. Electroencephalographic sleep recordings, as well as other laboratory tests, may help the clinician to differentiate anxiety from depressive disorders.