Electroencephalographic sleep studies in depressed outpatients treated with interpersonal psychotherapy: II. Longitudinal studies at baseline and recovery.

Electroencephalographic (EEG) sleep studies may help to identify persistent versus episodic biological characteristics of major depressive disorder. This report examines longitudinal EEG sleep studies in depressed patients treated with psychotherapy alone. Nineteen patients were studied during a symptomatic baseline period and again during early remission after treatment with interpersonal psychotherapy (IPT). EEG sleep findings at baseline were not markedly abnormal, but they were similar to those in other published studies of young adult outpatients. No changes were found in visually scored EEG sleep measures between depression and early remission. Automated measures of delta sleep and rapid eye movement (REM) activity showed small state-related changes, with delta activity increasing from baseline to remission, and automated REM measures decreasing. Strong baseline-remission correlations were noted for most sleep measures, including slow wave sleep, phasic REM activity, and automated delta EEG counts; measures of sleep continuity and tonic REM sleep were not strongly correlated. Consistent adaptation effects across nights were observed for sleep continuity and REM measures during each clinical phase. These findings support the hypothesis that most visually scored EEG sleep measures, as well as the sleep adaptation process, are stable through the acute episode of depression, at least into early symptomatic remission. They also suggest that finer-grained automated analyses of delta and REM activity may provide more sensitive tools for examining state-related changes.     

Rapid eye movements, muscle twitches and sawtooth waves in the sleep of narcoleptic patients and controls

Seventeen unmedicated patients with narcolepsy-cataplexy and 17 age- and sex-matched controls were recorded polygraphically for 3 consecutive nights. Rapid eye movements (REMs), m. mentalis twitches and sawtooth waves in the EEG were visually scored. REM and twitch densities during REM sleep were significantly higher in the patients than in the controls. The distribution pattern of REMs and twitches was altered in the patients: twitch density peaked in the first REM period and density of REMs showed an even distribution across all the REM periods of the night. In the controls both REM and twitch density increased from the first to the second REM period. We therefore assume that in the narcoleptics phasic activity of REM sleep is disinhibited. Densities of REMs, twitches and sawtooth waves did not correlate with one another in patients and controls. They appear to be independently regulated. The REM periods of the patients contained 3 times as many waking epochs as those of the controls. This suggests that in narcolepsy the transition REM/waking is selectively facilitated. The REM/NREM ratio of twitch and sawtooth wave densities was the same in patients and controls.     

Genetics of rapid eye movement sleep in humans

The trait-like nature of electroencephalogram (EEG) is well established. Furthermore, EEG of wake and non-rapid eye movement (non-REM) sleep has been shown to be highly heritable. However, the genetic effects on REM sleep EEG microstructure are as yet unknown. REM sleep is of special interest since animal and human data suggest a connection between REM sleep abnormalities and the pathophysiology of psychiatric and neurological diseases. Here we report the results of a study in monozygotic (MZ) and dizygotic (DZ) twins examining the heritability of REM sleep EEG. We studied the architecture, spectral composition and phasic parameters of REM sleep and identified genetic effects on whole investigated EEG frequency spectrum as well as phasic REM parameters (REM density, REM activity and organization of REMs in bursts). In addition, cluster analysis based on the morphology of the EEG frequency spectrum revealed that the similarity among MZ twins is close to intra-individual stability. The observed strong genetic effects on REM sleep characteristics establish REM sleep as an important source of endophenotypes for psychiatric and neurological diseases.     

Concurrent occurrence of rapid eye movement with spindle burst during nocturnal sleep in mentally retarded children

Concurrence of REM and sleep spindle in 45 mentally retarded children (from 4 months to 8 years of age) was studied throughout nocturnal sleep, and the following results were obtained. (1) Twenty-five cases showed a single or burst of REMs during stage NREM with sleep spindles. (2) Twenty-nine cases showed sleep spindles at the beginning or toward the end of stage REM sleep. (3) No significant difference in DQ was found between the subjects with and without REMs during stage NREM sleep. The former subjects, however, had more normal clinical EEGs than the latter. (4) No significant difference in DQ or clinical EEG classification was revealed between the subjects with REMs during stage NREM sleep and those with spindles during stage REM sleep. (5) It was concluded that the concurrence of REM and sleep spindle during stage NREM is a useful sign for early diagnosis of mental retardation.     

Rapid eye movement density shows trends across REM periods but is uncorrelated with NREM delta in young and elderly human subjects

Saccade-like eye movements are the most prominent phasic component of rapid eye movement (REM) sleep. Eye movement density (EMD) appears to be negatively related to sleep depth. Thus, EMD is depressed by sleep deprivation. We sought to determine in 19 young normal (YN) and 19 elderly normal (EN) subjects: (a) whether EMD is correlated with delta EEG in baseline sleep; (b) whether EMD is increased by daytime naps; and (c) whether EMD patterns across sleep cycles differ in the two age groups. Subjects participated in four separate 2-day recording sessions, each consisting of a baseline night, a daytime nap, and post nap night. EMD was measured as 0.3-2 Hz integrated amplitude (IA)/20 s stage REM. EMD was not correlated with rate of non rapid eye movement (NREM) delta production (power/min) in the baseline sleep of either group. Changes in EMD and delta power/min on post nap nights also were uncorrelated. These data indicate that very strong changes in sleep depth (state) are required to overcome the individual stability (traits) of NREM delta and eye movement density. ANOVA for EMD across REM periods 1-4 showed a significant cycle effect and a significant age x cycle interaction. These effects were mainly due to YNs having depressed EMD in the first REM period, likely due to the low arousal level early in sleep in these subjects. Compared with waking saccades the saccade eye movements of REM sleep have received little investigation. Further study of these movements could shed new light on neurophysiology of REM sleep. Such studies might also be clinically useful because the density of these movements appears to be related to depression and (independently) to cognitive function in individuals with brain impairment.     

Baseline and post-deprivation recovery sleep in SCN-lesioned rats

In humans, advancing age alters sleep patterns, reducing high voltage NREM sleep, sleep bout length, and delta power during NREM sleep. Although the mechanism by which these alterations occur is unknown, age-related changes in normal circadian processes may play a role. Increased age produces histological and functional changes in the suprachiasmatic nucleus (SCN), and alters the amplitude and phase of circadian rhythms. To examine the relationship between SCN function and age-related changes in sleep, we produced radiofrequency (RF) lesions of the SCN in rats of different ages and examined sleep behavior before and after sleep deprivation. Three-, 12- and 18-month-old rats received RF or sham lesions of the SCN. After verifying loss of circadian rhythm, 24-h EEG/EMG/temperature recordings were made in dim light before and after 24 h of sleep deprivation using the disk-over-water method. Age-related changes in NREM sleep, sleep bout length, and delta EEG power persisted despite SCN lesions. SCN lesions in all age groups increased baseline NREM sleep by 4% and NREM delta power by 15%, and decreased REM sleep by 10%. Although SCN lesions initially produced more REM and NREM sleep during recovery, 24-h values did not differ. Deteriorating SCN function is unlikely to cause the characteristic changes in sleep that occur with age. Our data also imply that an intact SCN slightly inhibits NREM sleep in the rat. Changes in NREM sleep and delta EEG power during recovery in lesioned rats suggest that the SCN may influence homeostatic regulation.     

Phasic EEG activities associated with rapid eye movements during REM sleep in man

Human cortical potentials associated with rapid eye movements (REMs) during REM sleep were recorded in 6 normal young adults by using the averaging technique. The potentials were compared with those recorded during voluntary saccades in the waking state in a dark or an illuminated room. A positive potential of relatively long duration with peak latency of about 200 msec and a wide spread bilateral distribution and of highest amplitude in the mid-parietal area appeared only during REM sleep. It is suggested that this positive potential is phasic EEG activity appearing in association with REMs during REM sleep in man. Comparison of this positive potential with P300s induced by task-irrelevant visual stimuli disclosed that they resemble each other. The possibility was discussed that this positive potential occurring in association with REMs during REM sleep is indeed a P300 appearing in response to visual images in dream.     

Electroencephalographic correlates of cataplectic attacks in narcoleptic canines

Cataplectic attacks were monitored behaviorally and polygraphically in 4 narcoleptic dogs, of which three inherited the disorder. The recorded EEG signals were evaluated by power spectral analysis. We found 3 distinct stages of cataplexy: an initial stage which resembled wakefulness with tonic suppression of EMG activity, a later stage which was highly similar to REM sleep, and a final transitional stage to wakefulness or NREM sleep. The first stage of cataplexy was characterized by full postural collapse, a waking-like EEG spectrum, visual tracking, and a hypotonic EMG. The second stage of cataplexy differed electrographically from the previous stage by the onset of hypersynchronous hippocampal theta activity, a REM-like EEG spectrum, larger amplitude EEG signals, and a higher peak theta frequency. Glazed eyes, sporadic rapid eye movements and muscle twitches were also present. The final stage of cataplexy was characterized by mixed amplitude, mixed frequency EEG activity, and by the absence of rapid eye movements, visual tracking, directed movements, and muscle twitches. The EEG spectra of two other narcoleptic phenomena, sleep-onset REM periods and NREM sleep onsets from cataplexy, were nearly identical to the spectra of the normally occurring REM and NREM sleep periods.     

Loss of REM sleep features across nighttime in REM sleep behavior disorder

ObjectivesMelatonin is a chronobiotic treatment which also alleviates rapid eye movement (REM) sleep behavior disorder (RBD). Because the mechanisms of this benefit are unclear, we evaluated the clock-dependent REM sleep characteristics in patients with RBD, whether idiopathic (iRBD) or associated with Parkinson's Disease (PD), and we compared findings with PD patients without RBD and with healthy subjects.MethodsAn overnight videopolysomnography was performed in ten iRBD patients, ten PD patients with RBD (PD + RBD+), ten PD patients without RBD (PD + RBD−), and ten controls. The rapid eye movement frequency per minute (REMs index), the tonic and phasic electromyographic (EMG) activity of the levator menti muscle, and the duration of each REM sleep episode were evaluated. A generalized linear model was applied in each group, with the REM sleep cycle (four ordinal levels) as the dependent variable, as a function of REMs index, REM sleep duration, and tonic and phasic EMG activity.ResultsFrom the first to the fourth sleep cycle, REM sleep duration progressively increased in controls only, REMs index increased in subjects without RBD but not in patients with RBD, whether idiopathic or associated with PD, whereas tonic and phasic EMG activity did not change.ConclusionsPatients with PD or iRBD lost the physiologic nocturnal increase in REM sleep duration, and patients with RBD (either with or without PD) lost the increase of REMs frequency across the night, suggesting an alteration in the circadian system in RBD. This supports the hypothesis of a direct effect of melatonin on RBD symptoms by its chronobiotic activity.     

Internight reliability and benchmark values for computer analyses of non-rapid eye movement (NREM) and REM EEG in normal young adult and elderly subjects.

OBJECTIVE: To determine the reliability of computer measured non-rapid eye movement (NREM) and REM frequency bands in the 0.3-45 Hz range and to provide benchmark data for these measures in young normal (YN) and elderly normal (EN) subjects (Ss). METHODS: Sleep EEG was recorded in 19 YN and 19 EN Ss on 4 non-consecutive baseline nights and simultaneously quantified as fast Fourier transform (FFT) power and 3 zero-cross period-amplitude (PA) measures: integrated amplitude, time in band and average wave amplitude. RESULTS: The shapes of both the FFT and PA spectra differed among Ss but were highly consistent within individuals. Inter-night reliability of the separate frequency bands was correspondingly high. Despite substantial age effects, the reliability of computer-measured sleep EEG in the elderly equaled that of the YN Ss. Within both the YN and EN groups, the shapes of the NREM and REM spectral curves differed significantly. The NREM and REM also differed significantly in the two age groups. CONCLUSIONS: Computer-measured sleep EEG is highly reliable across non-consecutive nights in both young and elderly normal Ss. The trait-like stability of these measures suggests they are genetically determined. This possibility is supported by twin study data that show strong heritability for FFT-measured waking EEG. The different shapes of NREM and REM spectra add further evidence that these are fundamentally different states of brain organization. The age differences in spectral shape, along with PA data for wave incidence, demonstrate that age effects on sleep EEG are not caused by changes in skull impedance or other non-cerebral factors.     

Electroencephalographic sleep studies in depressed outpatients treated with interpersonal psychotherapy: I. Baseline studies in responders and nonresponders.

Electroencephalographic (EEG) sleep measures have been examined as predictors of therapeutic response in patients with major depression. Although some studies have reported that EEG sleep measures are predictive of a favorable outcome with medications, two recent studies found no differences in the baseline sleep characteristics of responders and nonresponders to psychotherapy. To clarify this issue, we compared baseline EEG sleep in a group of patients with recurrent depression who responded to interpersonal psychotherapy (n = 19) and a comparable group who did not respond (n = 18). Baseline ratings of depression severity did not differ in the groups, but some differences in baseline sleep were noted. Psychotherapy nonresponders had longer sleep latencies, lower sleep efficiency, and increased automated measures of phasic rapid eye movement (REM) activity. In addition, the two groups had different EEG sleep adaptation patterns for REM latency and phasic REM density measures across the two study nights. These preliminary results suggest that baseline EEG sleep patterns, as well as the pattern of laboratory adaptation, may differ for depressed patients who respond to psychotherapy and those who do not.     

Sleep states and sleep electroencephalographic spectral power in mice lacking the beta 3 subunit of the GABA(A) receptor

Mice lacking the GABA(A) receptor beta(3) subunit exhibit a profound disruption in thalamic circuitry. We have studied sleep in these mice under baseline conditions and following treatment with the benzodiazepine midazolam. Under baseline conditions, NREM sleep time did not differ between beta(3) subunit knockout mice and wild type mice, while REM sleep time was significantly lower in knockout mice than in wild type mice during the light portion of a 24-h light-dark cycle. In constant dark conditions, circadian rhythmicity remained intact in mutant mice for a period of at least 9 days. EEG delta power (1-4 Hz) was significantly greater in the knockout than in wild type mice during NREM sleep but not during other states. A transient increase in EEG power in the 12-16 Hz range that occurred in wild type mice just prior to the transition from NREM to REM sleep was present but significantly blunted in the knockout. Midazolam decreased NREM delta power and REM time in wild type mice. The former but not the latter response to midazolam was intact in the knockout. These results further support a role for GABAergic transmission in regulating REM sleep and EEG spectral phenomena associated with NREM sleep.     

Eye Closure Sensitivity Without Photosensitivity in Juvenile Myoclonic Epilepsy: Polysomnographic Study of Electroencephalographic Epileptiform Discharge Rates

Two cases of juvenile myoclonic epilepsy (JME) presented with myoclonic jerks and EEG activation after eye closure, without sensitivity to intermittent photic stimulation. The effect of eye closure was computed by comparing discharge rates of polyspike-and-wave (PSW) complexes after eye closure and after eye opening. For one patient, never treated pharmacologically, a nocturnal polysomnograph was performed to study the variation of discharge rates of PSW complexes during wakefulness and sleep. The rate of PSW complexes was high during wakefulness before sleep onset, increased during spontaneous nocturnal awakenings, and became maximal during final morning awakening. Among nonrapid eye movement (NREM) sleep stages, EEG epileptiform activity was maximal during stages III and IV. Discharges were completely suppressed by rapid eye movement (REM) sleep. Awakenings following deep NREM sleep were very activating if no REM sleep was interposed. Awakenings from light NREM sleep were much less activating. There were no EEG abnormalities in awakenings immediately following REM sleep. Results suggest that REM sleep, similarly to eye opening, plays a role in inhibiting EEG manifestations of JME with eye closure sensitivity.     

Ischemic stroke selectively inhibits REM sleep of rats

Sleep disorders are important risk factors for stroke; conversely, stroke patients suffer from sleep disturbances including disruptions of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep and a decrease in total sleep. This study was performed to characterize the effect of stroke on sleep architecture of rats using continuous electroencephalography (EEG) and activity monitoring. Rats were implanted with transmitters which enabled continuous real time recording of EEG, electromyography (EMG), and locomotor activity. Baseline recordings were performed prior to induction of either transient middle cerebral artery (MCA) occlusion or sham surgery. Sleep recordings were obtained for 60 h after surgery to identify periods of wakefulness, NREM, and REM sleep before and after stroke. Spectral analysis was performed to assess the effects of stroke on state-dependent EEG. Finally, we quantified the time in wake, NREM, and REM sleep before and after stroke. Delta power, a measure of NREM sleep depth, was increased the day following stroke. At the same time, there was a significant shift in theta rhythms to a lower frequency during REM and wake periods. The awake EEG slowed after stroke over both hemispheres. The EEG of the ischemic hemisphere demonstrated diminished theta power specific to REM in excess of the slowing seen over the contralateral hemisphere. In contrast to rats exposed to sham surgery which had slightly increased total sleep, rats undergoing stroke experienced decreased total sleep. The decrease in total sleep after stroke was the result of dramatic reduction in the amount of REM sleep after ischemia. The suppression of REM after stroke was due to a decrease in the number of REM bouts; the length of the average REM bout did not change. We conclude that after stroke in this experimental model, REM sleep of rats is specifically and profoundly suppressed. Further experiments using this experimental model should be performed to investigate the mechanisms and consequences of REM suppression after stroke.     

Alpha activity and cardiac correlates: three types of relationships during nocturnal sleep.

OBJECTIVE: We examined simultaneously alpha activity and cardiac changes during nocturnal sleep, in order to differentiate non-rapid eye movement (NREM) sleep, REM sleep, and intra-sleep awakening. METHODS: Ten male subjects displaying occasionally spontaneous intra-sleep awakenings underwent EEG and cardiac recordings during one experimental night. The heart rate and heart rate variability were calculated over 5 min periods. Heart rate variability was estimated: (1) by the ratio of low frequency (LF) to high frequency (HF) power calculated from spectral analysis of R-R intervals; and (2) by the interbeat autocorrelation coefficient of R-R intervals (rRR). EEG spectral analysis was performed using a fast Fourier transform algorithm. RESULTS: Three types of relationships between alpha waves (8-13 Hz) and cardiac correlates could be distinguished. During NREM sleep, alpha activity and cardiac correlates showed opposite variations, with high levels of alpha power associated with decreased heart rate, rRR and LF/HF ratio, indicating low sympathetic activity. Conversely, during REM sleep, alpha activity was low whereas heart rate, rRR, and the LF/HF ratio peaked, indicating high sympathetic activity. During intra-sleep awakenings, alpha activity and cardiac correlates both increased. No difference in time-course between alpha 1 (8-10 Hz) and alpha 2 (10-13 Hz) activity could be shown. Alpha waves occurred in fronto-central areas during slow wave sleep (SWS), migrated to posterior areas during REM sleep, and were localized in occipital areas during intra-sleep awakenings. CONCLUSIONS: These results suggest that alpha waves are not simply a sign of arousal, as is commonly thought. Fronto-central alpha waves, associated with decreased heart rate, possibly reflect sleep-maintaining processes.     

Diurnal variations in REM and NREM sleep EEG power spectra in the rat

Diurnal variations were observed in the EEG power spectra of REM sleep and non-REM (NREM) sleep in the rat. Diurnal variations occured in peak EEG frequency and spectral power (0–27 Hz and 5–9 Hz bands) during REM sleep. During NREM sleep diurnal variations were observed in spectral power in the 0–27 Hz and 0–4 Hz bands. The significance of these findings is discussed in terms of correlative data involving diurnal variations in neurotransmitters and hormones, all of which have been implicated in the induction or maintenance of sleep states.     

EEG activities during elicited sleep onset REM and NREM periods reflect different mechanisms of dream generation. Electroencephalograms. Rapid eye movement.

OBJECTIVE: To be the first to compare EEG power spectra during sleep onset REM periods (SOREMP) and sleep onset NREM periods (NREMP) in normal individuals and relate this to dream appearance processes underlying these different types of sleep periods. METHODS: Eight healthy undergraduates spent 7 consecutive nights in the sleep lab including 4 nights for SOREMP elicitation using the Sleep Interruption Technique. This enabled us to control preceding sleep processes between SOREMP and NREMP. EEG power spectra when participants did and did not report 'dreams' were compared between both types of sleep. Sleep stages, subjective measurements including dream property scores, sleepiness, mood, and tiredness after awakenings were also examined to determine their consistency with EEG findings. RESULTS: Increased alpha EEG activities (11.72-13.67 Hz) observed mainly in the central area were related to the absence of SOREMP dreams and appearance of NREMP dreams. Analyses of sleep stages combining two studies (16 participants) also supported the Fast Fourier Transform findings, showing that when dreams were reported there were decreased amounts of stage 2 and increased stage REM in SOREMP and increased stage W in NREMP. SOREMP dreams were more bizarre than NREMP dreams. Participants felt more tired after SOREMP with dreams than without dreams, while the opposite was observed after NREMP episodes. CONCLUSIONS: EEG power spectra patterns reflected different physiological mechanisms underlying generation of SOREMP and NREMP dreams. The same relationships were also reflected by sleep stage analyses as well as subjective measurements including dream properties and tiredness obtained after awakenings. This study not only supports the hypothesized relationships between REM mechanisms and REM dreams as well as arousal processes and NREM dreams, it also provides a new perspective to dream research due to its unique techniques to awaken participants and collect REM dreams during experimentally induced SOREMP.     

Cortical EEG topography of REM onset: the posterior dominance of middle and high frequencies.

OBJECTIVES: To investigate the brain topography of human sleep electroencephalography (EEG) along the antero-posterior axis during rapid eye movement sleep (REM) onset and REM offset, by means of a quantitative analysis of EEG changes. METHODS: EEG power values were calculated across a 1.00-25.75 Hz frequency range during time intervals preceding and following REM onset of the first 4 sleep cycles of 10 normal subjects. Topographical changes were assessed through Fpz-A1, Fz-A1, Cz-A1, Pz-A1, Oz-A1 recordings during NREM-REM-NREM transitions. RESULTS: The temporal dynamics of REM onset is characterized by a specific topographical pattern of EEG changes with a relatively higher EEG activity at posterior sites: Oz does not show any clear change within the alpha and beta frequencies, at variance with the marked reductions of the other sites, while it shows reductions of power in the delta/theta and sigma frequency ranges of smaller size as compared to the other sites. REM offset does not appear as a mirror-image of REM onset, since the pattern of regional differences characterizing the NREM sleep preceding REM onset is not fully reached. CONCLUSIONS: REM onset is characterized by a general change of EEG activity toward a relative occipital diffusion of power, specifically distinguished by a posterior dominance of middle and high frequencies.     

Ultradian rhythms of alternating cerebral hemispheric EEG dominance are coupled to rapid eye movement and non-rapid eye movement stage 4 sleep in humans

Objective: To replicate the left minus right (L−R) hemisphere EEG power shifts coupled to rapid eye movement (REM) and non-rapid eye movement (NREM) sleep observed in 1972 by Goldstein (Physiol Behav (1972) 811), and to characterize the L−R EEG power spectra for total EEG, delta, theta, alpha and beta bands.Background: Ultradian alternating cerebral hemispheric dominance rhythms are observed using EEG during both waking and sleep, and with waking cognition. The question of whether this cerebral rhythm is coupled to the REM–NREM sleep cycle and the basic rest–activity cycle (BRAC) deserves attention.Methods: L−R EEG signals for ten young, normal adult males were converted to powers and the means were normalized, smoothed and subtracted. Sleep hypnograms were compared with L−R EEGs, and spectra were computed for C3, C4 and L−R EEG powers.Results: Significant peaks were found for all C3, C4 and L−R frequency bands at the 280–300, 75–125, 55–70 and 25–50 min bins, with power dominating in the 75–125 min bin. L−R EEG rhythms were observed for all bands. Greater right hemisphere EEG dominance was found during NREM stage 4 sleep, and greater left during REM for total EEG, delta and alpha bands (Chi-squares, P<0.001). Theta was similar, but not significant (P=0.163), and beta was equivocal.Conclusions: Earlier ultradian studies show that lateral EEG and L−R EEG power have a common pacemaker, or a mutually entrained pacemaker with the autonomic, cardiovascular, neuroendocrine and fuel-regulatory hormone systems. These results for L−R EEG coupling to sleep stages and multi-variate relations may present a new perspective for Kleitman's BRAC and for diagnosing variants of pathopsychophysiological states.     

Sleep and sleep regulation in the ferret (Mustela putorius furo)

We investigated sleep-wake (S-W) architecture and sleep regulation in the ferret: a phylogenetically primitive mammal increasingly used in neurobiological studies. Twenty-four hour S-W baseline data were collected in eight adult ferrets. Seven ferrets were then sleep deprived for 6h at the beginning of the light period. Like other placental mammals, ferrets exhibited the main vigilance states of wakefulness, rapid-eye-movement (REM) sleep and non-REM (NREM) sleep. Interestingly, the amount of REM sleep in the ferret was considerably higher (24.01+/-1.61% of total recording time) than typically reported in placental mammals. Ferret sleep was homeostatically regulated as sleep deprivation produced a significant increase in NREM EEG delta power during the recovery period. Therefore, ferret sleep in most respects is comparable to sleep in other placental mammals. However, the large amount of REM sleep in this phylogenetically more ancient species suggests that REM sleep may have been present in greater amounts in early stages of mammalian evolution.