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.     

Neuropsychological function and REM sleep in schizophrenic patients.

To test the hypothesis that rapid eye movement (REM) sleep in schizophrenic patients is associated with cognitive function, we studied 18 schizophrenic inpatients by means of electroencephalograms taken during sleep in their own hospital beds after a minimum 2-wk medication withdrawal period. Patients underwent neuropsychological tests to measure memory function and other aspects of cognitive performance. REM sleep measures demonstrated positive and negative correlations with cognition and memory measures, depending on when REM occurred after sleep onset. Minutes of REM sleep and REM density in the first period correlated negatively with performance, while REM minutes occurring after the first REM period correlated positively with neuropsychological performance. Further work should test whether phasic REM sleep regulation at the beginning of the night plays a compensatory role for neuropsychological dysfunction in schizophrenics.     

REM sleep in primary depression: a computerized analysis.

REM sleep in 35 inpatients with primary depression was automatically analyzed for 7 consecutive nights during placebo administration. For the total night of sleep, as well as each individual REM period, the number of REMs, their total voltage integral over time, the sum of their durations and the average REM size were automatically calculated. Validity of these automated REM measures was established by significant correlations with manually scored REM measures. Changes in REM sleep across the night were also investigated. Similar to findings in normal subjects, REM time did not change from REM period to REM period. Average REM size increased significantly from REM period 2-3 and 3-4. Contrary to what is seen in normal subjects, REM frequency was high during the first REM period, significantly decreased from the first to second REM period and then remained constant. Finally, a significant inverse correlation between REM frequency for the first REM period and REM latency was noted. This pattern of REM sleep is interpreted as indicating a high pressure for phasic REM at the beginning of the night which is dissipated by the first REM period.     

Platform sleep deprivation affects deep slow wave sleep in addition to REM sleep

Rats were sleep deprived by the platform method to look for differential effects on light and deep slow wave sleep depending on platform size. Diameters of large and small platforms were 15 cm and 5.1 cm respectively. Sleep was recorded during a baseline light period (09.00-19.00 h), continuously during 48 h of sleep deprivation and during the first lights on recovery period (09.00-19.00 h). In both platform conditions REM sleep was virtually abolished during the first light period (hours 0-10 of sleep deprivation), while NREM sleep was reduced to approximately half of control values. During the second light period (hours 22-34 of sleep deprivation) REM sleep recovered somewhat in the large platform group. Light slow wave sleep (SWS-1) was comparable to baseline while deep slow wave sleep (SWS-2) was still significantly reduced. In the small platform group both SWS-2 and REM sleep was considerably reduced on day 2. Over the whole deprivation period there was an effect of platform size on SWS-1 (higher in the small platform group), and on SWS-2 and REM sleep (lower in the small platform group). During the 9 h light-time recovery sleep there was an REM sleep rebound in both groups. SWS-1 was reduced in both groups while SWS-2 was not significantly increased. The ratio SWS-2/SWS-1 was, however, significantly increased only in the small platform group recovery sleep. The results suggest that platform sleep deprivation deprives the animals of deep slow wave sleep in addition to REM sleep. This has implications for conclusions on REM sleep function based upon REM sleep deprivation.     

Electroencephalographic sleep findings in depressed outpatients

We compared the electroencephalographic (EEG) sleep characteristics of 20 outpatients with those of 20 age-matched inpatients with major primary depressive disorders. Both groups showed similar patterns of sleep disturbance: reduced rapid eye movement (REM) sleep latencies, sleep efficiencies, and slow wave sleep. While the inpatients had greater REM activity in the first REM period than did the outpatients, both groups showed evidence of greater REM sleep time and REM activity during the first half of the night than do normals. The outpatients demonstrated a level of adaptation in that more REM sleep time and activity were present on night 2 than on night 1.     

Rem sleep in depressed patients: Different attempts to achieve adaptation

Twenty-seven depressed patients and 10 healthy subjects were investigated in the sleep laboratory during two to three consecutive nights. Eleven of the 27 patients demonstrated the “first night effect” (group I) and 11 other patients demonstrated a clear absence of the “first night effect” (group II). Five of the 27 depressed patients were omitted from the study because they did not fit criteria for first night effect. The 10 healthy controls demonstrated a first night effect. In group I, the duration of the first rapid eye movement (REM) sleep episode was increased on the first night and on the second night the REM sleep latency was decreased, whereas REM sleep duration and eye movement (EM) density was increased. The number of the short sleep cycles (less than 40 minutes) was greater in group I versus group II and the percentage of slow-wave sleep (SWS) was also higher in group I. In depressed patients with the “first night effect” the enhanced REM sleep requirement is satisfied not only by an increased REM sleep duration but also by the improved REM sleep quality that is crucial for adaptation. The adaptive role of the increased first REM period and the increased EM density in this period is very limited.     

Sleep and manipulations of the sleep-wake rhythm in depression

OBJECTIVE: Disturbed sleep is typical for most depressed patients and complaints about disordered sleep are the hallmarks of the disorder. Polysomnographic sleep research has demonstrated that besides impaired sleep continuity, sleep in depression is characterized by a reduction of slow wave sleep and a disinhibition of random eye movement (REM) sleep, with a shortening of REM latency, a prolongation of the first REM period and increased REM density. METHOD: Our own experimental work has focused on the reciprocal interaction hypothesis of non-REM and REM sleep regulation as a model to explain the characteristic features of depressed sleep. RESULTS: In agreement with the major tenet of this model, administration of cholinomimetics provoked shortened REM latency in healthy subjects and led to an even stronger REM sleep disinhibition in depressed patients. Manipulations of the sleep-wake cycle, such as sleep deprivation or a phase advance of the sleep period, alleviate depressive symptoms. CONCLUSION: These data indicate a strong bidirectional relationship between sleep, sleep alterations and depression.     

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.     

抑郁症患者可乐定快速眼运动睡眠抑制试验的对照研究

目的探讨重性抑郁症患者α2-肾上腺能受体功能状况。方法对15例重性抑郁症患者（抑郁症组）和15名正常人（正常对照组）分别进行多导睡眠脑电图检查。在第1个快速眼运动（REM）睡眠周期结束10min内,向所有被试者静脉注射可乐定（剂量按2mg/kg体重计算,并稀释于9ml生理盐水中）,比较两组的睡眠情况。结果可乐定注射前,抑郁症组的REM比例［（26.8±5.6）%］、REM次数［（6.8±1.2）次］及REM时间［（120.6±25.1）min］较正常对照组增加［分别为（19.2±3.3）%、（4.9±0.8）次、（78.8±14.4）min;P<0.05］,REM潜伏期缩短［（64.1±27.0）min,对照组为（96.1±27.0）min］;可乐定注射后,对两组非快速眼运动睡眠几乎无影响,而抑郁症组和对照组的REM比例［分别为（21.3±4.8）%和（13.6±2.7）%］、次数［分别为（5.3±1.2）次和（3.8±0.6）次］、时间［（101.0±24.0）min和（61.0±10.3）min］分别较注射前减少（P<0.05）,抑郁症组第1次和第2次REM间隔时间的差值小于正常对照组（P<0.01）;而两组REM潜伏期注射前后的差异均无显著性。提示抑郁症患者REM睡眠的可乐定反映较正常对照组迟钝。结论重性抑郁症患者可能存在α2-肾上腺能受体功能低下。     

Sleep and affective disorders. A minireview

The most predictable electroencephalographic sleep changes of major depression are a shortened first NREM sleep period, a prolonged first REM period (with increased density of rapid eye movements), sleep continuity disturbance, and diminished slow wave sleep (with shifting of delta activity from the first to the second NREM sleep period). The more rapid appearance of the first REM sleep period occurs in relation to sleep onset but not apparently in relation to clock time. The changes occurring in the first NREM-REM cycle of the night appear to be relatively specific to major (particularly endogenous) depression. Depressed men appear to have diminished nocturnal penile tumescence compared with healthy controls, but depressed patients generally do not have a higher incidence of sleep apnea or nocturnal myoclonus. The sleep physiologic changes of depression appear to persist into clinical remission, suggesting that they are trait-like. Published studies appear to support the conclusion that there is a close link between the regulation of sleep and the regulation of mood in affective illness.     

Cardiopulmonary Interactions Following REM Sleep Deprivation in Sprague–Dawley Rats

We characterized the effects of 48 h of rapid-eye-movement (REM) sleep deprivation on cardiovascular and respiratory variables and on sleep-related cardiopulmonary interactions in adult male Sprague–Dawley rats. Rats were instrumented for monitoring EEG, EMG, and aortic blood pressure. Respiratory rate and minute ventilation were measured by unrestrained single-chamber plethysmography. By using radiotelemetry to monitor blood pressure we clearly demonstrated progressive decreases in mean blood pressure with transitions from wakefulness to non-rapid-eye-movement and REM sleep which were unaffected by REM sleep deprivation. Mirror-image state-dependent increases in heart period suggest that baroreflexes were augmented during sleep with respect to wakefulness. REM sleep deprivation was also associated with lower blood pressure and longer heart period over all sleep/wake states, although this achieved statistical significance only during REM sleep and only during the first hour of recovery sleep. These cardiovascular changes coupled with the observed decreases in respiratory rate and minute ventilation suggest a further augmentation of baroreflexes following REM sleep deprivation.     

Electroencephalographic sleep of adolescents with major depression and normal controls

Forty-nine, mostly outpatient (86%), nonbipolar adolescents, aged Tanner stage III to 18 years, with a current diagnosis of major depressive disorder and 40 adolescents without current presence or history of psychiatric disorder were studied polysomnographically for three consecutive nights. Sleep latency was significantly longer in the depressive groups. The nonendogenous depressive patients exhibited significantly more awake time and lower sleep efficiency during the sleep period. No significant group differences were found for first rapid eye movement (REM) period latency, REM density, or any other REM sleep measures. Age correlated significantly with REM latency and delta sleep time, especially among depressive patients. No significant correlations between sleep measures and severity of illness were found. It appears that the classic REM sleep findings associated with the adult depressive syndrome are not present among depressive adolescents, indicating a later ontogeny for these abnormalities.     

Electroencephalographic sleep of younger depressives. Comparison with normals

The electroencephalographic sleep of younger depressives (aged 20 to 44 years) was compared with that of an age-matched group of normals. The patients demonstrated many of the typical sleep changes reported for older depressed populations: shortened rapid-eye-movement (REM) latency; REM sleep activity alterations, with a shift to the early portion of the night (first REM period); reduced delta sleep; and sleep efficiency reductions marked by sleep-onset difficulties. The traditional scoring procedures were supplemented by automated REM and delta-sleep analyses that provided more precise delineation of these differences between patients and normals, particularly the distributions of REM activity and delta-wave patterning.     

REM sleep deprivation during 5 hours leads to an immediate REM sleep rebound and to suppression of non-REM sleep intensity.

Nine healthy male subjects were deprived of REM sleep during the first 5 h after sleep onset. Afterwards recovery sleep was undisturbed. During the deprivation period the non-REM EEG power spectrum was reduced when compared to baseline for the frequencies up to 7 Hz, despite the fact that non-REM sleep was not experimentally disturbed. During the recovery interval a significant rebound of REM sleep was observed, which was only accompanied by a very slight increase of power in the lower non-REM EEG frequencies. In order to control for intermittent wakefulness, the same subjects were subjected to non-REM sleep interruption during the first 5 h after sleep onset 2 weeks later. Again subsequent recovery sleep was undisturbed. The interventions resulted in a similar amount of wakefulness in both conditions. During the intervention period, the non-REM EEG power spectrum was only marginally reduced in the delta frequency range. REM sleep duration was only slightly reduced. During the recovery interval, however, a substantial increase in EEG power in the delta frequency range was noted, without notable changes in REM time. It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.     

Pilocarpine, an orally active muscarinic cholinergic agonist, induces REM sleep and reduces delta sleep in normal volunteers

The effect of oral pilocarpine, a direct-acting muscarinic, cholinergic agonist, on polygraphic sleep parameters was studied in 13 healthy male volunteers. Subjects received placebo and oral pilocarpine (25 mg) in a double-blind, counterbalanced, crossover design. Pilocarpine shortened the latency of rapid eye movement (REM) sleep and increased total REM time, REM%, and the duration of the first REM period. In addition, it reduced Stage 4 sleep and Delta sleep. Pulse rate was not significantly changed during the first hour of darkness after administration of pilocarpine. Subjective sleep experience and the subjects' condition in the morning were not altered. These results suggest that pilocarpine has central effects (i.e., induction of REM sleep) that are similar to those of other centrally acting muscarinic cholinomimetic agents.     

Predicting mortality in mixed depression and dementia using EEG sleep variables

The authors report a study of electroencephalographic (EEG) sleep predictors of two-year mortality in 26 elderly patients with mixed symptoms of depression and cognitive impairment. Patients who had died by two-year follow-up were characterized by significantly longer rapid eye movement (REM) sleep latencies at baseline, less robust REM sleep rebound following all-night sleep deprivation, and baseline apnea-hypopnea indexes greater than 3. Logistic regression analysis using the apnea-hypopnea index value and REM latency correctly predicted 77% of survivors and non-survivors. Survival time following initial measurements was significantly correlated with REM sleep time (r = 0.78, p less than .02) and duration of first REM sleep period (r = 0.75, p less than .02). The authors speculate that changes in these predictor variables may indicate impairment in the cholinergic control of cognitive function, REM sleep, and respiratory function.     

Sleep and suicidality in psychotic patients

The purpose of the study was to determine whether polysomnographic rapid eye movement (REM) sleep parameters distinguish between psychotic patients with and without a history of suicidal behavior. We examined both hand-scored and automated measures of rapid eye movement (REM) sleep in psychotic patients with and without a history of suicidal ideation or attempts. Patients with suicidal behavior had significantly increased REM activity and time both in the whole night data and in the first REM period. These findings suggest an association between REM sleep abnormalities and suicidal behavior, perhaps related to alteration in serotonergic function.     

Relationship between Delta, Sigma, Beta, and Gamma EEG bands at REM sleep onset and REM sleep end.

OBJECTIVE: The aim of the present study was to analyze in detail the relationship of two newly introduced measures, related to the Beta and Gamma EEG bands during REM sleep, with Delta and Sigma activity at REM sleep onset and REM sleep end, in order to understand their eventual role in the sleep modulation mechanism. METHODS: For this purpose, power spectra of 1 EEG channel (C4, referred to A1) were obtained by means of the fast Fourier transform and the power of the bands ranging 0.75-4.50 Hz (Delta), 4.75-7.75 (Theta), 8.00-12.25 (Alpha), 12.50-15.00 (Sigma), 15.25-24.75 (Beta), 25.00-34.75 (Gamma 1), and 35.00-44.75 (Gamma 2) was calculated for the whole period of analysis (7 h), in 10 healthy subjects. Additionally, two other time series were calculated: the ratio between Beta and Gamma2, and between Gamma1 and Gamma2 (Beta and Gamma ratios). For each subject, we extracted 3 epochs of 30 min corresponding to the 15 min preceding and the 15 min following the onset of the first 3 REM episodes. Data were then averaged in order to obtain group mean values and standard deviation. The same process was applied to the 30-min epochs around REM sleep end. RESULTS: The course of the Delta band around REM sleep onset was found to be characterized by a first phase of slow decline lasting from the beginning of our window up to a few seconds before REM onset; this phase was followed by a sudden, short decrease centered around REM onset, lasting for approximately 1.5-2 min. At the end of this phase, the Delta band reached its lowest values and remained stable up to the end of the time window. The Sigma band showed a similar course with stable values before and after REM sleep onset. The Beta and Gamma ratios also showed a 3-phase course; the first phase, in this case, was characterized by stable low values, from the beginning of our window up to approximately 5 min before REM onset. The following second phase was characterized by an increase which reached its maximum shortly after REM sleep onset (approximately 1 min). In the last phase, both Beta and Gamma ratios showed stable high values, up to the end of our time window. At REM sleep end, the Delta band only showed a very small gradual increase, the Sigma band presented a more evident gradual increase; on the contrary, both Beta and Gamma ratios showed a small gradual decrease. CONCLUSIONS: The results of the present study show a different time synchronization of the changes in the Delta band and in Beta and Gamma ratios, at around REM sleep onset, and seem to suggest that the oscillations of these parameters might be modulated by mechanisms more complex than a simple reciprocity. All these considerations point to the fact that REM sleep can be considered as a complex phenomenon and the analysis of high-frequency EEG bands and of our Beta and Gamma ratios represent an additional important element to include in the study of this sleep stage.     

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.     

Multiple Sleep Latency Test findings in Kleine-Levin syndrome

Multiple Sleep Latency Test (MSLT) findings in a case of Kleine-Levin syndrome are reported for the first time. MSLT data indicate sleepiness as severe as in narcolepsy or obstructive sleep apnea and the occurrence of four sleep onset rapid eye movement (REM) periods, with a greater REM propensity at 2:00 p.m. and 4:00 p.m. than at 10:00 a.m. and 12:00 noon. The replication of such findings might suggest that Kleine-Levin syndrome could be considered a form of periodic REM sleep disinhibition. Therefore, the traditional hypothesis of diencephalic dysfunction may require modification to include the role of more caudal brain stem structures specifically activated during REM sleep.