Phasic Rapid Eye Movement Research Articles

High frequency activities in the human orbitofrontal cortex in sleep–wake cycle

We recorded human orbitofrontal electrocorticogram during wakefulness and sleep in epileptic patients using subdural electrodes. During wakefulness and rapid eye movement (REM) sleep, we observed beta activity in the raw orbitofrontal signals. Power spectral analysis demonstrated beta enhancement during wakefulness and REM sleep when compared to slow wave sleep (SWS). During the phasic REM periods, the beta power was significantly lower than during the tonic REM periods. Gamma enhancement manifested itself in four out of six subjects during the phasic periods. This study is the first that has focused on electrical activity in the human orbitofrontal cortex. Although the role of the orbitofrontal cortex during sleep still remains unclear, high frequency activities give us important suggestions in elucidating the human sleep mechanism.

Different brain reactivity during phasic and tonic REM sleep: A simultaneous FMRI and EEG study

Different brain reactivity during phasic and tonic REM sleep: A simultaneous FMRI and EEG study

Rapid eye movement activity before spontaneous awakening in elderly subjects.

Previous research in young subjects found that rapid eye movement (REM) density is higher in those REM phases which are followed by an awakening (REM-W) than in those preceding NREM (REM-N), suggesting a 'gating role' of REM sleep toward the awakening. It is not yet known whether this evidence is maintained in elderly subjects, who display, relative to young subjects, more awakenings, different sleep states from which the awakenings come (NREM in a high proportion of cases) and a general impairment of rapid eye movement activity (REMA). To investigate this issue, we have compared in three different age groups (young, old and 'old old' subjects) the features of REMA, including REM density and the amount and duration of REM bursts, between REM-W and REM-N. Whereas in the young REM density is higher in REM-W than in REM-N, this difference is already reduced in the old group and fully cancelled in the old old subjects. The evidence that old individuals spontaneously wake up despite the absence of an increase of REMA could imply that in the aged awakening is not preceded by an increase of the arousal level (expressed in REM sleep by the REMA). The similar duration of REM bursts for REM-W and REM-N in both groups of old subjects suggests that with age a marked impairment occurs in the organizational aspects of REMs, independently from the following state.

Purpose of REM sleep: endogenous anti-epileptogenesis in man – a hypothesis

Neuro-scientists, worldwide, are endeavoring to elucidate the purpose of sleep which still remains largely elusive. There is, however, consensus on many aspects of sleep functions; one such aspect is its relationship with seizures/epilepsy. There is unequivocal agreement on increased susceptibility to epilepsy during nonrapid eye movement (NREM, slow-wave) sleep. Large number of studies have shown increased frequency of seizures and interictal epileptiform discharges in epileptic patients during NREM sleep (esp., stages I and II) which is associated with EEG synchronization. Similarly, there is widespread acceptance of de-synchronized brain-activity states being associated with rarity/total absence of epileptic potentials, one such state being rapid eye movement (REM) sleep. Certain drugs and substances which inhibit NREM sleep have been found to possess anti-convulsant properties. Not surprisingly, drugs/chemicals which enhance/promote NREM sleep or suppress/inhibit REM sleep are associated with increased susceptibility to seizures and are contraindicated in epilepsy. The manner and pattern in which REM phase occurs in sleep are also naturally programmed to exert anti-epileptogenic influence. This hypothesis-article highlights and conceptualizes the primary function of REM-sleep as endogenous anti-epileptogenic system in the body akin to the endogenous analgesia and immune systems man is born with.

Respiratory muscle activity during REM sleep in patients with diaphragm paralysis.

The diaphragm is the main inspiratory muscle during REM sleep. It was hypothesized that patients with isolated bilateral diaphragm paralysis (BDP) might not be able to sustain REM sleep. Polysomnography with EMG recordings was undertaken from accessory respiratory muscles in patients with BDP and normal subjects. Patients with BDP had a normal quantity of REM sleep (mean +/- SD, 18.6 +/- 7.5% of total sleep time) achieved by inspiratory recruitment of extradiaphragmatic muscles in both tonic and phasic REM, suggesting brainstem reorganization.

Antidepressant-induced insomnia: treatment options.

This column offers a question-and-answer forum to help nurses maintain their knowledge of advances in prescribing and psychopharmacology, and implications for safe psychiatric care. If you have a question related to prescribing psychotropic medications, please send it to the Editor, Mary Paquette at: mary@artwindows.com. ********** Question: I have been working with Margaret, a 39-year-old homemaker, for 1 month in individual psychotherapy. Because of persistent symptoms of major depressive illness, she was initially prescribed escitalopram 10 mg every morning. Over the past 1 to 2 weeks since initiation of this antidepressant, she has complained of worsening sleeping difficulties. What is the best approach to treating Margaret's persistent sleep disturbances? Deborah Antai-Otong answers: Sleep disturbances are common among people with major depression and are believed to occur in 90% of depressed clients (Thase, 2000). Sleep disorders associated with major depression are heterogeneous and range from hypersomnia to extreme difficulties maintaining sleep. The significance of resolving sleep problems in depressed clients is their potential to produce negative consequences on the quality of life, functional status, and psychiatric and medical co-morbidity and treatment outcomes. Most researchers submit that depression is a compelling predictor of disability, and insomnia is a principal contributor (Simon & VonKorff, 1997). Polysomnographic (PSG) analysis of people with depression reveals a pattern of sleep disturbance symptoms: disturbed sleep continuity, altered rapid eye movement (REM) sleep timing, and decreased slow-wave sleep (SWS) quantity. An early onset of the first episode of REM sleep and increased phasic REM sleep has been demonstrated on PSG recordings. Longitudinal data of electroencephalographic (EEG) sleep profiles of depressed clients indicate specific sleep disturbances (Buysse, Frank, Lowe, Cherry, & Kupfer, 1997; Thase & Howland 1995; Thase, Simons, & Reynolds, 1996): * Reduced SWS associated with reversible or state-dependent aberrations * Increased REM sleep and poor-quality sleep * Disinhibited REM sleep * Shortened REM latency * Prolonged first REM period * Increased REM density (Riemann, Berger, & Voderholzer, 2001) Additional sleep patterns include: * Frequent awakenings * Increased light sleep (stage 1) * Decreased deep sleep (stage 4) * Early morning wakening Although the precise pathogenesis of sleep disturbances in major depression is unknown, researchers submit that the same neurotransmitter systems that regulate mood, motivation, energy, and other functions may also be abnormal in depression and contribute to sleep disturbance. Serotonergic neurons play a vital part in the modulation of the onset and maintenance of sleep, and sleep disturbances in depression are linked to aberrations of serotonergic pathways. Depressed individuals successfully treated with various antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), often complain of persistent sleep disturbances. The effects of antidepressants on depression are significant because prolonged sleep problems increase the risk of relapse, recurrence, and suicide, with a need to add on new medications (Armitage, 1996; Buysse et al., 1997). Stimulation of serotonin type 2 (5-H[T.sub.2]) receptors appears to underlie insomnia and sleep disturbances in sleep architecture found in SSRIs or serotonin-norepinephrine reuptake inhibitors (SNRIs). In contrast, antidepressants that block 5-H[T.sub.2] receptor sites (e.g., nefazodone, mirtazapine) alleviate insomnia and improve sleep architecture (Thase, 2000). Based on this assumption, it is preferential to prescribe antidepressants with 5-H[T.sub.2]blocking properties as part of a treatment plan for depressed clients with significant insomnia. …

Spectral analysis of all-night human sleep EEG in narcoleptic patients and normal subjects.

To investigate the pathophysiology of narcoleptic patients' sleep in detail, we analysed and compared the whole-night polysomnograms of narcoleptic patients and normal human subjects. Eight drug-naive narcoleptic patients and eight age-matched normal volunteers underwent polysomnography (PSG) on two consecutive nights. In addition to conventional visual scoring of the polysomnograms, rapid eye movement (REM)-density and electroencephalograph (EEG) power spectra analyses were also performed. Sleep onset REM periods and fragmented nocturnal sleep were observed as expected in our narcoleptic patients. In the narcoleptic patients, REM period duration across the night did not show the significant increasing trend that is usually observed in normal subjects. In all narcoleptic patient REM periods, eye movement densities were significantly increased. The power spectra of narcoleptic REM sleep significantly increased between 0.3 and 0.9 Hz and decreased between 1.0 and 5.4 Hz. Further analysis revealed that non-rapid eye movement (NREM) period duration and the declining trend of delta power density in the narcoleptic patients were not significantly different from the normal subjects. Compared with normal subjects, the power spectra of narcoleptic NREM sleep increased in the 1.0-1.4 Hz and 11.0-11.9 Hz frequency bands, and decreased in a 24.0-26.9 Hz frequency band. Thus, increased EEG delta and decreased beta power densities were commonly observed in both the NREM and REM sleep of the narcoleptic patients, although the decrease in beta power during REM sleep was not statistically significant. Our visual analysis revealed fragmented nocturnal sleep and increased phasic REM components in the narcoleptic patients, which suggest the disturbance of sleep maintenance mechanism(s) and excessive effects of the mechanism(s) underlying eye movement activities during REM sleep in narcolepsy. Spectral analysis revealed significant increases in delta components and decreases in beta components, which suggest decreased activity in central arousal mechanisms. These characteristics lead us to hypothesize that two countervailing mechanisms underlie narcoleptic sleep pathology.

Interictal Epileptic Spiking during Sleep and Wakefulness in Mesial Temporal Lobe Epilepsy: A Comparative Study of Scalp and Foramen Ovale Electrodes

To assess distribution of temporal lobe spikes across different states of sleep and wakefulness in simultaneous scalp and foramen ovale (Fo) recordings. The study included 12 patients with mesial temporal lobe epilepsy (MTLE). As part of their presurgical evaluation, patients underwent long-term video-EEG monitoring with combined scalp and foramen ovale electrodes (FoEs). In addition to traditional sleep scoring, waking was subdivided into eyes-opened and eyes-closed states, and rapid-eye-movement (REM) sleep was divided into phasic and tonic states. Spike counts were carried out visually for scalp and FoEs, and spiking rates were determined for each state. A ratio between FoE and scalp spiking rates also was calculated for each state. Scalp spiking showed a significant increase during NREM3,4, whereas FoE spiking increased during NREM2. The scalp/FoE ratio significantly increased during NREM3,4. A significant difference in spiking rate also was found between phasic and tonic REM states as well as between waking with eyes opened and closed in FoE recordings. Our data provide evidence of a discrepancy in spike distribution across different states of sleep and waking monitored by scalp and FoE recordings. We suggest that these discrepancies may reflect differences in archicortical and neocortical spike synchronization.

Sleep-Dependent Hippocampal Slow Activity Correlates with Waking Memory Performance in Humans

The positive effect of postlearning sleep on memory consolidation as well as the relationship between sleep-related memory processes and the hippocampal formation are increasingly clarified topics in neurobiology. However, the possibility of a stable relationship between waking mnemonic performance and sleep-dependent hippocampal electric activity is unexplored. Here we report a correlative analysis between sleep-dependent parahippocampal-hippocampal (pHip-Hip) electric activity recorded by foramen ovale (FO) electrodes and different types of memory performances in epileptic patients. Psychological testing was performed days or weeks before electrophysiological recordings. The relative spectral power of the slow activity (below 1.25 Hz) during deep non-REM (NREM) sleep at the right pHip-Hip region correlated positively with the visual memory performance according to Rey-Osterrieth Complex Figure Test (ROCFT). Along the posterior-anterior direction of the hippocampal formation a linear increasing of correlations was observed. The relative power of the activity below 1.25 Hz at the left pHip-Hip during phasic REM sleep correlated positively with verbal learning performance and mnemonic retention values according to ROCFT. It is concluded that the pHip-Hip structures' capacity of producing high amplitude and synchronized slow (< 1 Hz) oscillation during deep NREM sleep is related to the functional power of these structures. We hypothesize that the asymmetric (side-specific) propagation of ponto-geniculo-occipital (PGO) activity to the pHip-Hip region is related to the memory correlates of phasic REM sleep.

Sleep and treatment response in depression: new findings using power spectral analysis

This study examined quantitative measures of sleep electroencephalogram (EEG) and phasic rapid eye movements (REM) as correlates of remission and recovery in depressed patients. To address correlates of remission, pre-treatment EEG sleep studies were examined in 130 women outpatients with major depressive disorder treated with interpersonal psychotherapy (IPT). To address correlates of recovery, baseline and post-treatment EEG sleep studies were examined in 23 women who recovered with IPT alone and 23 women who recovered with IPT+fluoxetine. Outcomes included EEG power spectra during non-rapid eye movement (NREM) sleep and REM sleep and quantitative REMs. IPT non-remitters had increased phasic REM compared with remitters, but no significant differences in EEG power spectra. IPT+fluoxetine recoverers, but not IPT recoverers, showed increases in phasic REM and REM percentage from baseline to recovery. In NREM sleep, the IPT+fluoxetine group showed a decrease in alpha power from baseline to recovery, while the IPT group showed a slight increase. The number of REMs was a more robust correlate of remission and recovery than modeled quantitative EEG spectra during NREM or REM sleep. Quantitative REMs may provide a more direct measure of brainstem function and dysfunction during REM sleep than quantitative sleep EEG measures.

Rhythmic hippocampal slow oscillation characterizes REM sleep in humans

Hippocampal rhythmic slow activity (RSA) is a well-known electrophysiological feature of exploratory behavior, spatial cognition, and rapid eye movement (REM) sleep in several mammalian species. Recently, RSA in humans during spatial navigation was reported, but systematic data regarding human REM sleep are lacking. Using mesio-temporal corticography with foramen ovale electrodes in epileptic patients, we report the presence of a 1.5-3-Hz synchronous rhythmic hippocampal oscillation seemingly specific to REM sleep. This oscillation is continuous during whole REM periods, is clearly observable by visual inspection, and appears in tonic and phasic REM sleep episodes equally. Quantitative analysis proved that this 1.5-3-Hz frequency band significantly differentiates REM sleep from waking and slow-wake sleep (SWS). No other frequency band proved to be significant or showed this high rhythmicity. Even in temporo-lateral surface recordings, although visually much less striking, the relative power of the 1.5-3-Hz frequency band differentiates REM sleep from other states with statistical significance. This could mean that the 1.5-3-Hz hippocampal RSA spreads over other cortical areas in humans as in other mammals. We suggest that this oscillation is the counterpart of the hippocampal theta of mammalian REM sleep, and that the 1.5-3-Hz delta EEG activity is a basic neurophysiological feature of human REM sleep.

Spectral Features of EEG Alpha Activity in Human REM Sleep: Two Variants with Different Functional Roles?

Evidence suggests that an important contribution of spectral power in the alpha range is characteristic of human REM sleep. This contribution is, in part, due to the appearance of well-defined bursts of alpha activity not associated with arousals during both tonic and phasic REM fragments. The present study aims at determining if the REM-alpha bursts constitute a different alpha variant from the REM background alpha activity. Since previous findings showed a selective suppression of background alpha activity over occipital regions during phasic REM fragments and, on the other hand, the density of alpha bursts seem to be independent of the presence or absence of rapid eye movements, one expects to find the same spectral power contribution of alpha bursts in tonic and phasic REM fragments. The results indicated that REM-alpha bursts showed a similar power contribution and topographic distribution (maximum energy over occipital regions) both in tonic and phasic REM fragments. This suggests that two variants of alpha activity with different functional roles are present during the human REM sleep: i) background alpha activity, modulated over occipital regions by the presence of rapid eye movements, which may be an electrophysiological correlate of the visual dream contents; and ii) REM-alpha bursts, independent of the presence of rapid eye movements, which could be facilitating the connection between the dreaming brain and the external world, working as a micro-arousal in this brain state.

The relationship between subjective sleep estimation and objective sleep variables in depressed patients

Introduction: To our knowledge there is no evidence in the literature about the relationship between subjective sleep estimation and objective sleep variables in depression. It is not known whether the subjective estimation of sleep quality and sleep duration is directly related to any objective sleep variable in depressed patients. Methods: Thirty patients with major depression and 10 healthy subjects have been investigated in our sleep laboratory during 1 or 2 consecutive nights after 1 night for adaptation. Every subject, after final awakening in the laboratory, answered questions concerning the subjective feelings about sleep duration, number of awakenings and sleep depth. We compared the sleep estimation in both groups and calculated the correlation between objective and subjective sleep variables in depressed patients. Results: The degree of a wrong sleep estimation in depressed patients is larger than in healthy subjects. Slow wave sleep (SWS) in depressed patients correlates positively with the subjective estimation of sleep duration. Eye movement density in REM sleep correlates with the subjective estimation of the number of awakenings. Conclusion: SWS in depression has a positive influence on the subjective feeling of sleep duration while phasic REM sleep activity has a negative influence.

Alpha burst activity during human REM sleep: descriptive study and functional hypotheses

Objectives: Spectral power contribution in the range of alpha activity is a well-known electrophysiological feature of human REM sleep, which could be caused by the spontaneous bursts of alpha activity not associated with arousals that usually appear during this brain state. The present study was undertaken to determine the density of alpha bursts during tonic and phasic (oculomotor) REM periods for each REM cycle. In addition, this phasic brain event was also described from a spectral and topographical point of view.Methods: Ten healthy right-handed subjects (5 females) aged 19–25 years (mean 22.9 years, SD 2.6) participated in the present study. Each selected subject filled in a daily sleep log for 2 weeks before the experimental night to provide information on all 3 salient aspects of sleep pattern, sleep experience and sleep effects.Results: The results revealed that transient REM-alpha bursts, which lasted about 3 s and were accompanied by no increase in the EMG amplitude, appeared in all subjects who participated in this study, showing a higher density in the third and fourth REM cycle during phasic in comparison with tonic periods. The bandpass filtered signals showed the highest spectral contribution for the slower alpha components (8–9 Hz), the occipital scalp regions being the main generator source of this brain activity.Conclusions: The authors hypothesize that REM-alpha bursts may work as micro-arousals (or incomplete arousals) facilitating the brain connection with the external world in this cerebral state, whereas REM-alpha arousals – usually longer and accompanied by changes in the EMG amplitude – generate a shift of brain state associated with sleep fragmentation (complete arousal).

Sleep states alter ventral medullary surface responses to blood pressure challenges.

Ventral medullary surface (VMS) activity declines during rapid eye movement (REM) sleep, suggesting a potential for reduced VMS responsiveness to blood pressure challenges during that state. We measured VMS neural activity, assessed as changes in reflected 660-nm wavelength light, during pressor and depressor challenges within sleep/waking states in five adult, unrestrained, unanesthetized cats and in two control cats. Phenylephrine elevated blood pressure and elicited an initial VMS activity decline and a subsequent rise in VMS activity in all states, although the initial decline during quiet sleep occurred only in rostral placements. Phasic REM periods elicited a momentary recovery from the evoked activity rise, and arousals diminished the overall elevation in activity. A sodium nitroprusside depressor challenge increased VMS activity more in REM sleep than in quiet sleep, with the increase being even less in waking. Enhanced responses to depressor challenges during REM sleep suggest a loss of dampening of evoked activity during that state; state-related differential baroreflex sensitivity may result from sleep-waking changes in VMS responses to blood pressure challenges.

Ontogeny of REM sleep in rats: possible implications for endogenous depression

Nine neonatal Long–Evans rats had continuous (24 h/day) polysomnography for 2 weeks, from age 14 days through age 27 days. A new finding was that six more or less independent measures of REM sleep occurrence decreased in parallel from age 14 days to age 27 days. The measures included parallel decreases of four measures of 24-h REM duration (tonic REM sleep, phasic REM sleep, mean REM period duration, and number of REM periods) along with parallel increases of two measures of REM delay (REM latency and percent of nonsleep onset REM periods). A parsimonious interpretation of the correlated changes is that a common developmental REM sleep inhibitory process accounts for the six parallel changes over time. This hypothesis can be tested empirically by studying inhibitory processes that operate on the pedunculopontine tegmental/latero-dorsal tegmental nuclei, the generators of REM sleep. The study also noted that compared with (same species) normal adults, endogenous depressives had the same distinctive REM sleep characteristics as neonatal rats. The similarity suggests that an underdeveloped, relatively weak REM sleep inhibitory process may account for the REM sleep peculiarities of endogenous depression. This hypothesis can be tested in adult rats made “depressed” by neonatal treatment with antidepressant drugs. Thus, the ontogeny of REM sleep suggests a developmental process that may be altered in humans predisposed to endogenous depression, and may account for the (life-long) REM sleep abnormalities of the disorder.

Psychoanalysis and the neurosciences: a topical debate on dreams.

The author begins by pointing out that, whereas Freud first turned his attention to dreams in 1895, they became an object of neuroscientific interest only in the 1950s, after the discovery of rapid-eye-movement (REM) sleep and the observation that a subject woken in an REM phase could remember and narrate them. He discusses the various brain structures found by the neuroscientists to be implicated in dreaming and the associated hypotheses about their involvement in the processes of remembering dreams, their spatial construction and semantic organisation, and the dreamer's emotional participation in and narration of dreams. Attention is drawn to recent psychophysiological research findings indicating that dreaming occurs in all sleep phases and not only in REM episodes. The cognitivist contribution is also discussed. The author goes on to demonstrate the difference between the neuroscientific and psychoanalytic approaches to dreams. Whereas the neuroscientists are interested in the structures involved in dream production and in dream organisation and narratability, psychoanalysis concentrates on the meaning of dreams and on placing them in the context of the analytic relationship in accordance with the affective history of the dreamer and the transference. The brain structures and functions of interest to the neurosciences, while constituting the physical and biological substrate of these aspects, are stated to be irrelevant to their psychoanalytic understanding.

Relationship between ethnicity and sleep patterns in normal controls: implications for psychopathology and treatment

The purpose of the study was to examine ethnic influences on sleep regulation. Seventy-three normal volunteers from four ethnic groups (17 African-Americans, 10 Asians, 30 Caucasians and 16 Hispanics) were studied for two consecutive nights with sleep polysomnography recordings in the laboratory. The subjects were in good physical and psychological health, and were asymptomatic with respect to sleep/wake complaints or sleep disorders. With the exception of minor differences, sleep continuity, sleep architecture and rapid eye movement (REM) sleep patterns were comparable among the four groups. African-Americans had evidence of more stages 1 and 2 and diminished stage 4 sleep, whereas the Hispanics had higher REM density. These preliminary findings suggest that sleep patterns are remarkably similar across cultures. There are, however, important cross-ethnic differences, specifically in the depth of sleep and in phasic REM measures. Because sleep disturbances are common symptoms of emotional disorders and since many psychoactive agents affect sleep, cross-ethnic differences in sleep patterns may have potential implications for the treatment and prevention of psychiatric disorders.

Effects of Prior Fluoxetine Treatment on EEG Sleep in Women with Recurrent Depression

We examined whether fluoxetine treatment has persistent effects on electroencephalographic sleep after drug discontinuation in patients with recurrent major depression. Age-matched groups of 23 women were treated with interpersonal psychotherapy alone (IPT) or fluoxetine plus interpersonal psychotherapy (IPT + FLU). Sleep studies were conducted when patients were depressed, and again at remission, at least four weeks after fluoxetine discontinuation. The groups did not differ in depression ratings pre- to post-treatment. Significant group*time interaction effects were noted for REM sleep (p = .04) and slow wave sleep (p = .02). REM percentage and phasic REM activity increased in the IPT + FLU group but decreased in the IPT group. The effects of fluoxetine treatment on electroencephalographic sleep can be observed for at least four weeks after drug discontinuation and appear to represent both drug discontinuation and neuroadaptation effects.

Manifestation of Pulmonary Hypertension During REM Sleep in Obstructive Sleep Apnea Syndrome

The effect of sleep stage change on pulmonary circulation has not been well documented in patients with obstructive sleep apnea syndrome (OSAS). We investigated whether or not stage-specific change can affect pulmonary artery pressure (Ppa) in patients with OSAS. Thirty-one patients with OSAS underwent right cardiac catheterization in the daytime and the following night, including 19 patients in whom Ppa could be measured throughout non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Ten of the 19 patients had daytime pulmonary hypertension (PH) defined by a mean Ppa (Ppa) >/= 20 mm Hg. Then we analyzed Ppa response to hypoxia spontaneously occurring during the period of sleep apnea. The slopes of the regression lines between arterial oxygen saturation measured by pulse oximeter (SpO2) and Ppa curves were almost the same in both NREM and REM patient groups with or without daytime PH, whereas the response curve was significantly shifted upward in REM compared with NREM patients with daytime PH. Furthermore, Ppa was elevated more markedly in association with REM burst, phasic REM, compared with tonic REM. We conclude that vascular tone of pulmonary artery could be elevated in association with REM sleep which is independent of the degree of hypoxia, and that this state-specific change is manifested in patients with daytime PH.