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Showing papers on "Rapid eye movement sleep published in 1998"


Journal ArticleDOI
02 Jan 1998-Science
TL;DR: A model for brain mechanisms subserving REM sleep where visual association cortices and their paralimbic projections may operate as a closed system dissociated from the regions at either end of the visual hierarchy that mediate interactions with the external world is suggested.
Abstract: Positron emission tomography was used to measure cerebral activity and to evaluate regional interrelationships within visual cortices and their projections during rapid eye movement (REM) sleep in human subjects. REM sleep was associated with selective activation of extrastriate visual cortices, particularly within the ventral processing stream, and an unexpected attenuation of activity in the primary visual cortex; increases in regional cerebral blood flow in extrastriate areas were significantly correlated with decreases in the striate cortex. Extrastriate activity was also associated with concomitant activation of limbic and paralimbic regions, but with a marked reduction of activity in frontal association areas including lateral orbital and dorsolateral prefrontal cortices. This pattern suggests a model for brain mechanisms subserving REM sleep where visual association cortices and their paralimbic projections may operate as a closed system dissociated from the regions at either end of the visual hierarchy that mediate interactions with the external world.

453 citations


Journal ArticleDOI
TL;DR: The results underscore the importance of IL-6 in the cascade of cytokines for the neuroendocrine response during the acute phase reaction and appear to be involved in changes of sleep and behavior accompanying infection and inflammatory disorders.
Abstract: Interleukin-6 (IL-6) is a proinflammatory cytokine that has been shown to mediate, in addition to immune reactions, various endocrine and central nervous components of the acute phase response. In this context, the present study aimed to specify the contributions of IL-6 to the regulation of pituitary-adrenal secretory activity and GH and TSH secretion, as well as to the regulation of central nervous sleep and mood in healthy men. Effects of a low dose of IL-6 (0.5 microgram/kg body weight) were assessed, inducing plasma IL-6 concentrations closely comparable with those typically observed after infectious challenge. Each of the 16 male subjects participated in two 14-h sessions (between 1800 and 0800 h), receiving either placebo or human recombinant IL-6 sc at 1900 h. Blood was collected repeatedly to determine plasma hormone levels, serum concentrations of cytokines, and C-reactive protein. Moreover, mood was assessed, and sleep recordings were obtained between 2300 and 0700 h. The cytokine induced a prolonged increased in plasma concentrations of ACTH and cortisol (P < 0.001), but led to a decrease in TSH concentrations (P < 0.01). In response to IL-6, subjects reported fatigue and felt more inactive and less capable of concentrating than after placebo. Sleep architecture was altered significantly by the cytokine. Slow-wave sleep was decreased during the first half and increased during the second half of sleep. Rapid eye movement sleep during the entire nocturnal sleep time was significantly decreased. After IL-6, body temperature rose slightly. C-reactive protein concentrations were dramatically increased 12.5 h after substance administration (P < 0.001). IL-6 did not affect serum concentrations of IL-2, IL-8, interferon-alpha, and interferon-gamma. The results underscore the importance of IL-6 in the cascade of cytokines for the neuroendocrine response during the acute phase reaction. In addition, IL-6 appears to be involved in changes of sleep and behavior accompanying infection and inflammatory disorders.

412 citations


Journal ArticleDOI
TL;DR: In this article, PET imaging and brain lesion studies in humans are integrated with new basic research findings at the cellular level in animals to explain how the formal cognitive features of dreaming may be the combined product of a shift in neuromodulatory balance of the brain and a related redistribution of regional blood flow.
Abstract: Recent PET imaging and brain lesion studies in humans are integrated with new basic research findings at the cellular level in animals to explain how the formal cognitive features of dreaming may be the combined product of a shift in neuromodulatory balance of the brain and a related redistribution of regional blood flow. The human PET data indicate a preferential activation in REM of the pontine brain stem and of limbic and paralimbic cortical structures involved in mediating emotion and a corresponding deactivation of dorsolateral prefrontal cortical structures involved in the executive and mnemonic aspects of cognition. The pontine brainstem mechanisms controlling the neuromodulatory balance of the brain in rats and cats include noradrenergic and serotonergic influences which enhance waking and impede REM via anticholinergic mechanisms and cholinergic mechanisms which are essential to REM sleep and only come into full play when the serotonergic and noradrenergic systems are inhibited. In REM, the brain thus becomes activated but processes its internally generated data in a manner quite different from that of waking.

297 citations


Journal ArticleDOI
15 Sep 1998-Sleep
TL;DR: Extensive evidence indicates the existence of a consistent relationship between SW sleep and increased GH secretion and, conversely, between awakenings and decreased GH release, and the concept of a dual control of daytime and sleep-related GH secretion remains to be directly demonstrated.
Abstract: In the human as in other mammals, growth hormone (GH) is secreted as a series of pulses. In normal young adults, a major secretory episode occurs shortly after sleep onset, in temporal association with the first period of slow-wave (SW) sleep. In men, approximately 70% of the daily GH output occurs during early sleep throughout adulthood. In women, the contribution of sleep-dependent GH release to the daily output is lower and more variable. Studies involving shifts of the sleep-wake cycle have consistently shown that sleep-wake homeostasis is the primary determinant of the temporal organization of human GH release. Effects of circadian rhythmicity may occasionally be detected. During nocturnal sleep, the sleep-onset GH pulse is caused by a surge of hypothalamic GHRH release which coincides with a circadian-dependent period of relative somatostatin disinhibition. Extensive evidence indicates the existence of a consistent relationship between SW sleep and increased GH secretion and, conversely, between awakenings and decreased GH release. There is a linear relationship between amounts of SW sleep--whether measured by visual scoring or by delta activity--and amounts of concomitant GH secretion, although dissociations may occur, most likely because of variable levels of somatostatin inhibition. Pharmacological stimulation of SW sleep results in increased GH release, and compounds which increase SW sleep may therefore represent a novel class of GH secretagogues. During aging, SW sleep and GH secretion decrease with the same chronology, raising the possibility that the peripheral effects of the hyposomatotropism of the elderly may partially reflect age-related alterations in sleep-wake homeostasis. While the association between sleep and GH release has been well documented, there is also evidence indicating that components of the somatotropic axis are involved in regulating sleep. The studies are most consistent in indicating a role for GHRH in promoting NREM and/or SW sleep via central, rather than peripheral, mechanisms. A role for GH in sleep regulation is less well-documented but seems to involve REM, rather than NREM, sleep. It has been proposed that the stimulation of GH release and the promotion of NREM sleep by GHRH are two separate processes which involve GHRH neurons located in two distinct areas of the hypothalamus. Somatostatinergic control of GH release appears to be weaker during sleep than during wake, suggesting that somatostatinergic tone is lower in the hypothalamic area(s) involved in sleep regulation and sleep-related GH release than in the area controlling daytime GH secretion. While the concept of a dual control of daytime and sleep-related GH secretion remains to be directly demonstrated, it allows for the reconciliation of a number of experimental observations.

237 citations


Journal ArticleDOI
TL;DR: It is concluded that subjective and objective measures of baseline sleep are predictors of relapse in treated alcoholic patients and neurophysiological dysfunction contributes strongly to the etiology of relapse, and sleep disturbance warrants clinical attention as a target of alcoholism treatment.
Abstract: Previous studies indicate that subjectively reported and objectively measured sleep abnormalities at baseline can increase the risk of relapse in treated alcoholics. However, previous studies did not include both subjective and objective sleep measures in the same group of patients. We utilized polysomnography and the Sleep Disorders Questionnaire to determine if baseline polysomnography increased the ability to predict relapse beyond the prediction with subjective measures alone, after controlling for nonsleep variables that were associated with relapse. We followed 74 patients with a DSM-III-R diagnosis of alcohol dependence, of whom 36 relapsed to at least some drinking during an average follow-up interval of 5 months. Univariate analyses revealed that relapsed patients did not differ from abstinent patients at baseline in demographics or psychiatric co-morbidity, but they had more prior treatment episodes for alcoholism, more difficulty falling asleep, more complaints of abnormal sleep, and, on polysomnography, longer sleep latencies, shorter rapid eye movement sleep latencies, and less stage 4 sleep percentage than abstinent patients. With a series of logistic regression analyses, which controlled for age and gender, we demonstrated that sleep measures improved the prediction model compared with nonsleep variables alone, and that polysomnography-measured sleep latency was the most significant predictor variable. We conclude that subjective and objective measures of baseline sleep are predictors of relapse in treated alcoholic patients. These data also suggest that neurophysiological dysfunction contributes strongly to the etiology of relapse. Finally, sleep disturbance warrants clinical attention as a target of alcoholism treatment.

212 citations


Journal ArticleDOI
TL;DR: 87.9% of apnoea-associated bradyarrhythmias occur during rapid eye movement sleep; the vast majority of heart block episodes occur during a desaturation of at least 4% without a previously described threshold value of 72; and nasal continuous positive airway pressure or nasal bi-level positiveAirway pressure is the therapy of choice in patients with apnOEa- associated bradyARRhythmia.
Abstract: Heart block during sleep has been described in up to 10% of patients with obstructive sleep apnoea. The aim of this study was to determine the relationship between sleep stage, oxygen desaturation and apnoea-associated bradyarrhythmias as well as the effect of nasal continuous positive airway pressure (nCPAP)/nasal bi-level positive airway pressure (nBiPAP) therapy on these arrhythmias in patients without electrophysiological abnormalities. Sixteen patients (14 males and two females, mean age 49.6+/-10.4 yrs) with sleep apnoea and nocturnal heart block underwent polysomnography after exclusion of electrophysiological abnormalities of the sinus node function and atrioventricular (AV) conduction system by invasive electrophysiological evaluation. During sleep, 651 episodes of heart block were recorded, 572 (87.9%) occurred during rapid eye movement (REM) sleep and 79 (12.1%) during nonrapid eye movement (NREM) sleep stages 1 and 2. During REM sleep, the frequency of heart block was significantly higher than during NREM sleep: 0.69+/-0.99 versus 0.02+/-0.04 episodes of heart block x min(-1) of the respective sleep stage (p<0.001). During apnoeas or hypopnoeas, 609 bradyarrhythmias (93.5%) occurred with a desaturation of at least 4%. With nCPAP/ nBiPAP therapy, apnoea/hypopnoea index (AHI) decreased from 75.5+/-39.6 x h(-1) to 3.0+/-6.6 x h(-1) (p<0.01) and the number of arrhythmias from 651 to 72 (p<0.01). We conclude that: 1) 87.9% of apnoea-associated bradyarrhythmias occur during rapid eye movement sleep; 2) the vast majority of heart block episodes occur during a desaturation of at least 4% without a previously described threshold value of 72%; and 3) nasal continuous positive airway pressure or nasal bi-level positive airway pressure is the therapy of choice in patients with apnoea-associated bradyarrhythmias.

193 citations


Journal ArticleDOI
TL;DR: The high coherence of sleep spindles is an indication for their widespread and quasi-synchronous occurrence throughout the cortex and may point to their specific role in the sleep process, which may provide insights into large-scale functional connectivities of brain regions during sleep.

168 citations


Journal ArticleDOI
01 Dec 1998-Synapse
TL;DR: In this paper, the ponto-geniculo-occipital (PGO) wave-generating cells were mapped by microinjecting carbachol in 74 sites of the rat brainstem.
Abstract: A number of experimental and theoretical reports have suggested that the ponto-geniculo-occipital (PGO) wave-generating cells are involved in the generation of rapid eye movement (REM) sleep and REM sleep dependent cognitive functions. No studies to date have examined anatomical projections from PGO-generating cells to those brain structures involved in REM sleep generation and cognitive functions. In the present study, pontine PGO wave-generating sites were mapped by microinjecting carbachol in 74 sites of the rat brainstem. Those microinjections elicited PGO waves only when made in the dorsal part of the nucleus subcoeruleus of the pons. In six rats, the anterograde tracer biotinylated dextran amine (BDA) was microinjected into the physiologically identified cholinoceptive pontine PGO-generating site to identify brain structures receiving efferent projections from those PGO-generating sites. In all cases, small volume injections of BDA in the cholinoceptive pontine PGO-generating sites resulted in anterograde labeling of fibers and terminals in many regions of the brain. The most important output structures of those PGO-generating cells were the occipital cortex, entorhinal cortex, piriform cortex, amygdala, hippocampus, and many other thalamic, hypothalamic, and brainstem nuclei that participate in the generation of REM sleep. These findings provide anatomical evidence for the hypothesis that the PGO-generating cells in the pons could be involved in the generation of REM sleep. Since PGO-generating cells project to the entorhinal cortex, piriform cortex, amygdala, and hippocampus, these PGO-generating cells could also be involved in the modulation of cognitive functions.

153 citations


Journal ArticleDOI
TL;DR: Narcolepsy was diagnosed in 51 children (29 boys) and all children presented at least once with depressive symptoms in reaction to their syndrome.
Abstract: Narcolepsy was diagnosed in 51 children (29 boys). The age range was 2.1 to 11.8 years (mean, 7.9 +/- 3.1 years). A mean of three referrals was made before narcolepsy was considered. In 10 children, cataplexy was the presenting symptom. Thirty-eight children acknowledged sleep paralysis and 30 acknowledged hypnagogic hallucinations. All children had sleep studies; 31 exhibited rapid eye movement at sleep onset. The mean sleep latency was 1.5 minutes +/- 39 seconds on the Multiple Sleep Latency Test. All children had at least two sleep-onset rapid eye movement sleep episodes in this test. Forty-six children were HLA class II-positive for DQw6, and 45 were also positive for DRw15. Thirty (65%) families refused referrals to support and counseling groups. Teachers often refused to acknowledge a medical problem. During follow-up, all children presented at least once with depressive symptoms in reaction to their syndrome. Narcolepsy should be considered when evaluating children with behavioral and depressive symptoms.

139 citations


Journal ArticleDOI
TL;DR: The results suggest that the brain cannabinoid system participates in the modulation of the vigilance states and mnemonic processes and that the effect on pain perception may be a peripheral rather than a central effect.

130 citations


Journal ArticleDOI
TL;DR: It is suggested that dreaming may actively moderate mood overnight in normal subjects, while those with some pre-sleep depressed mood showed a pattern of decreasing negative and increasing positive affect in dreams reported from successive REM periods.
Abstract: To test that REM sleep and/or dreaming aid in the overnight regulation of negative mood, 60 student subjects, selected to have no current or past episodes of depression, were tested with the Profile of Mood States (POMS) before and after two nights of laboratory sleep. There was a significant overnight effect of sleep on the Depression scale (Dep) both on a sleep-through night and a night of REM awakenings for dream recall. Pre-sleep Dep was significantly correlated with the affect in the first REM report. Although Dep scores were truncated due to the screening criteria, a subgroup of the 10 highest scorers differed from the 50 low scorers in the distribution of dream affect categories across the night. Low scorers displayed a flat distribution of positive and negative affect in dreams, while those with some pre-sleep depressed mood showed a pattern of decreasing negative and increasing positive affect in dreams reported from successive REM periods. This suggests that dreaming may actively moderate mood overnight in normal subjects.

Journal ArticleDOI
TL;DR: In an animal model of rapid eye movement sleep atonia, decrements in the activity of upper airway motoneurons are caused by withdrawal of excitation mediated by serotonin and other transmitters, rather than by state-dependent inhibition.
Abstract: The loss of tone in upper airway muscles contributes to disorders of breathing during sleep. In an animal model of rapid eye movement sleep atonia, decrements in the activity of upper airway motoneurons are caused by withdrawal of excitation mediated by serotonin and other transmitters, rather than by state-dependent inhibition.

Journal ArticleDOI
TL;DR: The rising REM sleep propensity, as reflected by the increase of interventions within and across RD nights, and the moderate REM sleep rebound during recovery can be accounted for by a compensatory response that serves REM sleep homeostasis.
Abstract: To investigate rapid eye movement (REM) sleep regulation, eight healthy young men were deprived of REM sleep for three consecutive nights. In a three-night control sleep deprivation (CD) session 2 wk later, the subjects were repeatedly awakened from non-REM sleep in an attempt to match the awakenings during the REM sleep deprivation (RD) nights. During the RD nights the number of sleep interruptions required to prevent REM sleep increased within and across consecutive nights. REM sleep was reduced to 9.2% of baseline (CD nights: 80.7%) and rose to 140.1% in the first recovery night. RD gave rise to changes in the EEG power spectra of REM sleep. Power in the 8.25- to 11-Hz range was reduced in the first recovery night, an effect that gradually subsided but was still present in the third recovery night. The rising REM sleep propensity, as reflected by the increase of interventions within and across RD nights, and the moderate REM sleep rebound during recovery can be accounted for by a compensatory response that serves REM sleep homeostasis. The changes in the electroencephalogram power spectra, which were observed during enhanced REM sleep propensity, may be a sign of an altered quality of REM sleep.

Journal ArticleDOI
TL;DR: It is shown for the first time that nicotine patches may be useful in the treatment of depression and nicotine increased REM sleep time in both groups and also on the WN.
Abstract: The role of repeated nicotine administration on sleep and major depression was studied. Six non-smoking normal volunteers (NV) and six non-smoking major depressed patients (MD) with a Hamilton Rating Scale for Depression > 18 served as subjects. All subjects underwent the following sleep procedures: acclimatization, control night, four nicotine nights (17.5 mg, transdermal patches) and one withdrawal night (WN). Nicotine increased REM sleep time in both groups and also on the WN. Hamilton scores showed an average reduction of 43.9% in the depressed patients. These findings suggest that nicotine receptor activation may be important in major depression and shows for the first time that nicotine patches may be useful in the treatment of depression.

Journal ArticleDOI
TL;DR: It is suggested that transitory increases in the pons of either acetylcholine or adenosine may underlie long-lasting elevations in the amount of rapid eye movement sleep, as well as following conditions of stress and learning.

Journal ArticleDOI
TL;DR: Results suggest that increased REM density and decreased total sleep time at about 2-4 weeks of abstinence predict relapse by 3 months in depressed alcoholics.

Journal ArticleDOI
TL;DR: Elevated awaking thresholds from sleep are a characteristic finding in chronic war-related PTSD patients, which may help to explain the diverse sleep laboratory findings in this syndrome.

Journal ArticleDOI
TL;DR: A positive correlation was found between EEG slowing during wakefulness and oxygen desaturation during the night, and this result may explain the wide range of neuropsychological deficits noted in patients with obstructive sleep apnoea syndrome, in addition to their poor performance in tasks of executive functioning.
Abstract: Neuropsychological investigations of patients with obstructive sleep apnoea syndrome (OSAS) have shown impairments in such basic functions as memory, attention and executive control. Since executive functions are known to be dependent on the integrity of the frontal lobe, it was hypothesized that OSAS may be associated with hypoxaemic frontal lobe dysfunction. To test this hypothesis, 21 apnoeic patients and 10 normal controls were studied with quantitative electroencephalographic (EEG) methods during rapid eye movement (REM) sleep, when most apnoeic events occur and during wakefulness. In apnoeic patients, EEG slowing in REM sleep was observed over frontal, central and parietal regions, while EEG slowing during wakefulness was observed over all cortical regions examined. A positive correlation was found between EEG slowing during wakefulness and oxygen desaturation during the night. Contrary to the hypothesis, these electroencephalographic changes were not localized only to the frontal region. This result may explain the wide range of neuropsychological deficits noted in patients with obstructive sleep apnoea syndrome, in addition to their poor performance in tasks of executive functioning.

Journal ArticleDOI
TL;DR: Findings indicate that polysomnographic abnormalities may precede the clinical expression of depression and may be useful in identifying those at highest risk for the illness.
Abstract: OBJECTIVE: This study presents polysomnographic data and psychiatric history for parents and siblings of probands with unipolar depression and short REM latency, probands with unipolar depression and normal REM latency, and normal comparison probands. METHOD: Parents and adult siblings (N=252) of probands (N=64) were evaluated for lifetime history of psychiatric disorders and were studied in the sleep laboratory for 3 nights. RESULTS: REM latency predicted lifetime history of major depression. Short REM latency was also associated with slow wave sleep deficits. Rate of short REM latency in relatives of depressed probands with short REM latency quadrupled the rate in relatives of both depressed probands with normal REM latency and normal probands. Lifetime risk of depression was almost twice as high in relatives of depressed probands with short REM latency as in relatives of depressed probands with normal REM latency. CONCLUSIONS: Short REM latency and slow wave sleep deficits are familial. Short REM laten...

Journal ArticleDOI
TL;DR: Lesions of the visual cortex or the superior colliculus-pretectal area were performed in albino rats to determine retinorecipient areas that mediate the effects of light on behavior, including rapid eye movementSleep triggering by lights-off and redistribution of non-rapid eye movement sleep in short light-dark cycles.
Abstract: Light and dark have immediate effects on sleep and wakefulness in mammals, but the neural mechanisms underlying these effects are poorly understood. Lesions of the visual cortex or the superior colliculus–pretectal area were performed in albino rats to determine retinorecipient areas that mediate the effects of light on behavior, including rapid eye movement sleep triggering by lights-off and redistribution of non-rapid eye movement sleep in short light–dark cycles. Acute responses to changes in light conditions were virtually eliminated by superior colliculus-pretectal area lesions but not by visual cortex lesions. Circadian entrainment was evident in both groups with lesions and in normal controls. Thus, acute light-dark effects on sleep and wakefulness appear to be mediated independently from cortical vision or circadian rhythms.

Journal ArticleDOI
TL;DR: The study of sleep and dreams has enjoyed a major breakthrough with recent findings from brain imaging studies in humans, and new brain lesion and electrophysiological recording data are complemented to give a detailed picture of the brain dynamics of changes in conscious state.

Journal ArticleDOI
TL;DR: The data demonstrate a slight role of periodic breathing in altering sleep architecture at high altitude and also show that periodic breathing induces only a minor improvement in arterial oxygen saturation during nonrapid eye movement sleep.
Abstract: This study aimed to investigate the effect of periodic breathing (PB) at high altitude on sleep structure and arterial oxygen saturation (Sa,O2). Five healthy subjects underwent polysomnographic studies at sea level, and during the first and the fourth week of sojourn at 5,050 m. Their breathing pattern, sleep architecture and Sa,O2 were analysed. PB was detected in the high-altitude studies during nonrapid eye movement (NREM) sleep and tended to increase from the first to the fourth week. Stages 3-4 were absent in four subjects at the first week, but only in one at the fourth week, irrespective of the amount of PB. The arousal index was 11.6+/-3.8 at sea level, 30.1+/-15.5 at the first week at altitude and 33.0+/-18.2 at the fourth week. At altitude, arousal index in NREM sleep was higher during PB than during regular breathing. In NREM sleep, the mean highest Sa,O2 levels in NREM epochs with PB were higher than in those with regular breathing by 2.8+/-1.7% at the first week and 2.9+/-1.5% at the fourth week (p<0.025). From the first to the fourth week, mean Sa,O2 increased significantly during wakefulness (5.6%), NREM (5.2% with regular breathing and 5.3% with PB) and rapid eye movement sleep (7.6%). The data demonstrate a slight role of periodic breathing in altering sleep architecture at high altitude and also show that periodic breathing induces only a minor improvement in arterial oxygen saturation during nonrapid eye movement sleep.

Journal ArticleDOI
TL;DR: Subjects reporting more negative dreams at the beginning and fewer at the night's end were more likely to be in remission 1 year later than were those with fewer negative Dreams at the Beginning and more at the end of the night.
Abstract: To test the hypothesis that REM sleep and/or dreams contribute to overnight mood regulation, 61 subjects were tested on the Beck Depression Inventory (BDI), and for 3 nights of monitored sleep on two occasions, once close to, and 1 year after, a marital separation. Forty-nine percent of the variance in the follow-up BDI could be accounted for by the initial BDI score, and three sleep and dream variables associated with the mood regulatory hypothesis: eye movement density in the first REM, strength of the affect in the first dream and total number of negative dreams recalled from REM awakenings. Among the 39 who met BDI depression criteria initially, 71.8% could be classified correctly as remitted or not remitted at follow-up by discriminant function analysis based on the presence of negative dreams the first vs. second half of the night. Subjects reporting more negative dreams at the beginning and fewer at the night's end were more likely to be in remission 1 year later than were those with fewer negative dreams at the beginning and more at the end of the night. Early negative dreams may reflect a within-sleep mood regulation process taking place, while those that occur later may indicate a failure in the completion of this process.

Journal ArticleDOI
TL;DR: The present data suggest the involvement of the FR in the REM sleep processes by establishing prominent associations with the limbic and REM control mechanisms that involve the hippocampus and plausibly pontine ocular activity networks.

Journal ArticleDOI
TL;DR: The impact of the serotonergic system on sleep maintenance and on REM sleep is underlines, with significant effects on sleep EEG observed in terms of decreased non-rapid eye movement (non-REM) stage 2, increase of wake %, and of rapid eye movement density compared with baseline.

Journal ArticleDOI
TL;DR: The results suggest that the antidepressant effect of REM sleep deprivation and tricyclic antidepressants may share similar molecular changes in the norepinephrine system.

Journal ArticleDOI
01 Apr 1998-Chest
TL;DR: It is concluded that apneic events during REM and non-REM sleep probably contribute equally to sleepiness as measured by the Multiple Sleep Latency Test.

Journal ArticleDOI
TL;DR: The findings suggest not only that sleep is regulated in neonatal rats but that the accumulation and/or discharge of sleep need changes dramatically between the third and fourth postnatal weeks.
Abstract: This investigation represents the first systematic study of sleep homeostasis in developing mammals that spans the preweaning and postweaning periods. Neonatal rats from 12 to 24 days of postnatal ...

Journal ArticleDOI
TL;DR: It is suggested that uremia itself worsens the motor symptoms of RLS, probably as a result of increased excitability.
Abstract: In the present study, the nocturnal electroencephalographic sleep pattern, the number of periodic leg movements (PLM) during sleep and wakefulness, and the subjective sleep parameters of patients with uremic (n = 10) and idiopathic (n = 17) restless legs syndrome (RLS) were compared. The main finding was that the total number of PLM (p = 0.019), the PLM index (p = 0.018), and the PLM index while awake (p = 0.003) were significantly higher in patients with uremic RLS compared with patients who had idiopathic RLS. Additionally, both groups showed a distinct time-of-night pattern of PLM activity. Polysomnographic measures of sleep continuity (total sleep time, sleep efficiency, sleep onset latency, time awake) and sleep architecture (amount of nonrapid eye movement sleep stages 1, 2, 3, and 4 and the amount of rapid eye movement sleep) did not differ between uremic and idiopathic RLS patients. With regard to subjective parameters, sleep quality was estimated to be worse in uremic RLS (p = 0.033), whereas other parameters (for example, severity of RLS, quality of life) did not differ between the two groups. It is suggested that uremia itself worsens the motor symptoms of RLS, probably as a result of increased excitability.

Journal ArticleDOI
TL;DR: The results suggest that TFD-induced relapse in SSRI-treated patients in remission decreases as a function of treatment duration, degree of remission, or both.
Abstract: Background In previous studies, depletion of brain serotonin by administration of a tryptophan-free amino acid drink (TFD) (1) temporarily reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) in euthymic patients who had a history of major depression, and (2) enhanced rapid eye movement (REM) sleep in normal volunteers. In this study, we hypothesized that the TFD would not only increase depressive symptoms but also the propensity for REM sleep in euthymic patients treated with SSRIs. Methods Ten fully remitted, medicated male patients who had a history of major depressive episode ingested a 100-g TFD (the experimental dose) or a 25-g TFD (designed to be the control drink) in double-blind, random order on separate days. The effects were assessed with mood ratings, plasma tryptophan concentrations, and an all-night sleep electroencephalogram. Results The TFDs produced a dose-dependent reduction in plasma tryptophan concentrations, sleep latency, and REM latency, as well as increased REM percentage, REM minutes, REM density, and total sleep time. Neither strength of TFD altered mood to a clinically significant degree. Conclusions Although the TFD affected plasma tryptophan concentrations and various sleep measures, our study did not confirm previous reports that TFD temporarily reversed the antidepressant effects of SSRIs in euthymic patients. Our patients, however, had been treated for a longer period with SSRIs and were more fully remitted at the time of the study. Our results suggest that TFD-induced relapse in SSRI-treated patients in remission decreases as a function of treatment duration, degree of remission, or both.