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... laboratory at the University of Chicago [1]; (2) he published the first case of polysomnography (PSG) documented acute REM sleep behavior disorder (RBD) that was triggered by sudden withdrawal from a monoamine oxidase inhibitor (MAOI) in 1978 [2], 8 years before the formal identification of RBD [3]; (3) he worked with Roffwarg and Dement on the early delineation of the ontogeny of the human sleep cycle [4]; (4) he first demonstrated that benzodiazepine (diazepam) therapy was effective in controlling night terrors together with suppression of stage 4 non-rapid eye movement (NREM) sleep [5], and he was also an early investigator of night terrors as phenomena emerging from stage 4 NREM sleep, without dreaming, as had been traditionally assumed [6,7]; (5) he collaborated with another pioneering sleep medicine physician, William C. Dement, MD, PhD, on studies focused on REM sleep deprivation and dreaming at Fisher's Mt. Sinai Hospital sleep laboratory [8,9], (6) he published the first PSG-documented case of sleep-related (psychogenic) dissociative disorder (SRDD) in 1976 [10]; (7) he first documented that typical nightmares ("anxiety dreams") occurred during REM sleep [11]; (8) he conducted some of the earliest research, beginning in 1965, that documented cycles of nocturnal penile tumescence emerging in conjunction with REM sleep cycles [12]; and (9) he conducted similar early studies of female sexual arousal during sleep that occurred predominantly in REM sleep [13]. ...
... In 1957, Fisher invited Dement to Mt. Sinai Hospital to do an internship, and following that they obtained grant funding and set up a sleep laboratory [15]. They began by doing the REM deprivation experiments, at that time thought of as "dream deprivation" [8,9]. ...
... Dement subsequently went to Stanford University where he established the renowned narcolepsy research program and clinical sleep medicine program. Although Dement and Fisher's original hypothesis that people deprived of "dreaming" would develop psychosis was not confirmed, they discovered that the longer subjects were deprived of REM sleep, the more frequent attempts they would make to enter REM sleep, and on recovery nights they demonstrated the important phenomenon of "REM rebound," including significant increases in REM sleep time and percentage [8,9]. The Fisher-Dement collaboration on this topic from Fisher's book chapter (pages 76-77) [2] is contained in Supplementary Material B. 6) First PSG-Documented Case of SRDD. ...
Charles Fisher is a pioneering historical figure in sleep laboratory research and sleep medicine who distinguished himself in nine areas: (1) he first documented nocturnal sleep-onset rapid eye movement (REM) sleep periods in narcoleptic patients; (2) he published the first case of polysomnography (PSG) documented acute REM sleep behavior disorder (RBD) that was triggered by sudden withdrawal from a monoamine oxidase inhibitor in 1978, 8 years before the formal identification of RBD; (3) he worked with Roffwarg and Dement on the early delineation of the ontogeny of the human sleep cycle; (4) he first demonstrated that benzodiazepine (diazepam) therapy was effective in controlling night terrors together with suppression of stage 4 non-rapid eye movement (NREM) sleep, and he was also an early investigator of night terrors as phenomena emerging from stage 4 NREM sleep, without dreaming, as had been traditionally assumed; (5) he collaborated with another pioneering sleep medicine physician, William C. Dement on studies focused on REM sleep deprivation and dreaming at Fisher’s Mt. Sinai Hospital sleep laboratory in New York City; (6) he published the first PSG-documented case of sleep-related (psychogenic) dissociative disorder in 1976; (7) he first documented that typical nightmares (“anxiety dreams”) occurred during REM sleep; (8) he conducted some of the earliest research, beginning in 1965, that documented cycles of nocturnal penile tumescence emerging in conjunction with REM sleep cycles; and (9) he conducted similar early studies of female sexual arousal during sleep that occurred predominantly in REM sleep.
... The quantity of REMS has been found to be affected in most of the diseases from simple fever to complex psycho-somatic disorders [21][22][23][24]. Experimental REMS loss has been reported to affect psycho-somatic behaviour including memory consolidation [25][26][27][28][29], irritability, concentration, mood and behaviour [8,30]. Based on these observations, as a unified hypothesis, we had proposed that REMS maintains brain excitability [31,32]. ...
Rapid eye movement sleep (REMS) is naturally expressed at least in all the mammals, including humans, studied so far. It is regulated by interplay among complex neuronal circuitry in the brain involving various neurotransmitters. Although the precise function and role of REMS is yet to be deciphered, loss of REMS increases brain excitability; however, the mechanism of action was unknown. As Na-K ATPase is the key molecule that maintains ionic homeostasis across neuronal membrane and modulates the excitability status of neurons, we proposed that REMS deprivation (REMSD) could affect the neuronal Na-K ATPase activity. On the other hand, evidences suggest that REMSD would elevate noradrenaline (NA) level in the brain and it has been proposed that REMS maintains brain NA at an optimum level. Therefore, while attempting to understand and explain the mechanism of action we hypothesized that REMSD-induced elevated NA could modulate Na-K ATPase activity in the brain and thus modulates the neuronal and brain excitability. In this chapter first we discuss the mechanism of increase in NA level in the brain after REMSD. Then we discuss the effect of such elevated NA on neuronal and glial Na-K ATPase activity. We observed that REMSD-induced increase in NA affected neuronal and glial Na-K ATPase activities in opposite manner, while it increased neuronal Na-K ATPase, and it decreased the same in glia. An intricate regulation of Na-K ATPase activity in neurons and glia is likely to be responsible for maintenance of ionic homeostasis in the brain during normal situation, which when disturbed including upon REMS loss patho-physiological changes and symptoms are expressed.
... Disturbed or loss of REMS has been associated with several psycho-somatic disorders and pathological conditions including schizophrenia, epilepsy, mood disorder, memory loss, etc. [37][38][39][40]. Experimental REMS loss has been correlated with loss of concentration and memory consolidation, increased irritability, fighting behaviour and altered neuronal firing rate [15,[41][42][43]. These led us to propose a unified hypothesis that REMSD alters neuronal excitability and as a corollary the function of REMS is to maintain brain excitability [4,18]; however, the underlying cellular mechanism for executing such changes was unknown. ...
Rapid eye movement sleep (REMS) modulates Na-K ATPase activity and maintains brain excitability. REMS deprivation (REMSD)-associated increased Na-K ATPase activity is mediated by noradrenaline (NA) acting on α1-adrenoceptor (AR) in the brain. It was shown that NA-induced increased Na-K ATPase activity was due to allosteric modulation as well as increased turnover of the enzyme. Although the former has been studied in detail, our understanding on the latter was lacking, which we have studied. Male Wistar rats were REMS deprived for 4-days by classical flower-pot method; suitable control experiments were conducted. In another set, α1-AR antagonist prazosin (PRZ) was i.p. injected 48 h REMSD onward. At the end of experiments rats were sacrificed by cervical dislocation and brains were removed. Synaptosomes prepared from the brains were used to estimate Na-K ATPase activity as well as protein expressions of different isoforms of the enzyme subunits using western blot. REMSD significantly increased synaptosomal Na-K ATPase activity and that was due to differential increase in the expressions of α1-, α2- and α3-isoforms, but not that of β1- and β2-isoforms. PRZ reduced the REMSD-induced increased Na-K ATPase activity and protein expressions. We also observed that the increased Na-K ATPase subunit expression was not due to enhanced mRNA synthesis, which suggests the possibility of post-transcriptional regulation. Thus, the findings suggest that REMSD-associated increased Na-K ATPase activity is due to elevated level of α-subunit of the enzyme and that is induced by NA acting on α1-AR mediated mRNA-stabilization.
... Drawing on the same psychiatric sources that later provided inspiration to the theorizing by Hobson and Solms, several laboratory dream researchers of the late 1950s and early 1960s explored the idea that dreaming might throw light on psychosis. They focused especially on a preliminary finding that depriving participants of REM sleep (which was called dream deprivation at the time) seemed to increase their hallucinatory thinking during the day (Dement, 1960;Dement & Fisher, 1963). However, it was soon shown that REM deprivation did not increase the cognitive pathology of schizophrenic patients (Zarcone, Gulevich, & Pivik, 1968) or have any negative effects on the thought patterns of nonclinical participants. ...
This article examines the ongoing debate between activation-synthesis theorist J. Allan Hobson and psychoanalytic theorist Mark Solms about the nature of dreaming and dream content. After discussing their neurophysiological disagreements, it argues that they are more similar than different in some important ways, especially in talking about dreams in the same breath as psychosis and in drawing conclusions about dream content on the basis of their neurophysiological assumptions, without any reference to the systematic findings on the issue. Evidence from inside and outside the sleep laboratory on the coherent nature of most dreams is presented to demonstrate that neither theorist is on solid ground in his main assertions. Dreaming is usually a far more realistic and understandable enactment of interests and concerns than the 2 researchers assume. In addition, several of Hobson's and Solms's claims concerning the neural basis of dreaming are challenged on the basis of neurophysiological evidence. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
... Second, there was also the fact of "REM rebound" after participants experienced what was then called dream deprivation, which seemed to support the idea of a need to dream in just the way Freudian dream theory might expect (Dement, 1960;Dement & Fisher, 1963). Third, there was preliminary evidence that the rise and fall of penile erections during REM related to dream content. ...
Neuropsychologist and psychoanalyst Mark Solms (1997) made a major contribution to dream research through his clinico-anatomical studies, which reveal the outlines of the neural network that underlies dreaming. However, in more recent work (see record
2002-17656-000) he misunderstands the history of the rapid eye movement (REM)/non-REM (NREM) controversy in a Freudian-serving way and ignores the considerable systematic empirical evidence that contradicts the key claims of the Freudian dream theory he is trying to revive. After summarizing Solms's claims about the history of laboratory dream research, this article suggests a different version of that history and summarizes the empirical findings that explain why Freudian theory is not considered viable by most dream researchers. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
... Although several behavioral and neuroimaging studies have been carried out concerning the role of REM sleep in memory processes in humans (for review: Rauchs et al., 2005; Walker and Stickgold, 2006; Chuah and Chee, 2008), very few studies have directly investigated the role of selective REM-D on emotional regulation. Early studies found that, consistent with animal studies, subjects deprived of REM sleep showed irritability and anxiety (Dement and Fisher, 1963), deterioration in interpersonal relationships and increased signs of confusion and suspicion (Agnew et al., 1967), as well as poorer adaptation to stress-induced by viewing an emotionally arousing film (Greenberg et al., 1972). However, the consequences of REM-D on reactivity to threat-related stimuli and, in particular, its cerebral correlates have not yet been investigated in humans. ...
Converging evidence from animal and human studies suggest that rapid eye movement (REM) sleep modulates emotional processing. The aim of the present study was to explore the effects of selective REM sleep deprivation (REM-D) on emotional responses to threatening visual stimuli and their brain correlates using functional magnetic resonance imaging (fMRI). Twenty healthy subjects were randomly assigned to two groups: selective REM-D, by awakening them at each REM sleep onset, or non-rapid eye movement sleep interruptions (NREM-I) as control for potential non-specific effects of awakenings and lack of sleep. In a within-subject design, a visual emotional reactivity task was performed in the scanner before and 24 h after sleep manipulation. Behaviorally, emotional reactivity was enhanced relative to baseline (BL) in the REM deprived group only. In terms of fMRI signal, there was, as expected, an overall decrease in activity in the NREM-I group when subjects performed the task the second time, particularly in regions involved in emotional processing, such as occipital and temporal areas, as well as in the ventrolateral prefrontal cortex, involved in top-down emotion regulation. In contrast, activity in these areas remained the same level or even increased in the REM-D group, compared to their BL level. Taken together, these results suggest that lack of REM sleep in humans is associated with enhanced emotional reactivity, both at behavioral and neural levels, and thus highlight the specific role of REM sleep in regulating the neural substrates for emotional responsiveness.
... These data imply a homeostatic component in the regulation of REM sleep. Such homeostatic regulation is suggested by the occurrence of a "REM rebound" after nights of selective REM deprivation (18)(19)(20) and is recognized, although not specified, by Borbely (6). However, the loss of REM sleep at night is not completely compensated for during the morning (the sum of nocturnal and daytime REM sleep being 68.6, 78.8, and 94.8 min under Conditions A, B, and C, respectively). ...
Given the two-process model of sleep regulation, and the hypothesis that the sleep disorder in depressive illness is a consequence of a deficient Process S, it was predicted that relatively high levels of S would result in enhanced sleep continuity, increased slow-wave sleep (SWS), prolonged rapid-eye-movement (REM) latency, and less REM sleep. These predictions were tested in two studies. In Study 1, the level of Process S (at 0900 h prior to a 3-h sleep episode) was varied by altering the time and duration of prior nocturnal sleep (2400-0300 h, 0300-0600 h, 2400-0600 h). In Study 2, the leve of Process S (at 2400 h prior to an 8-h sleep episode) was varied by studying subjects when they had not napped or had taken 2-h naps beginning at either 1000 or 1900 h. As predicted by the model, SWS varied reliably depending on the level of S at bedrest, as did indices of sleep continuity at night. Contrary to prediction, however, REM sleep was either increased (Study 1) or did not change reliably (Study 2). It is suggested that, contrary to the other aspects of sleep, REM sleep is strongly influenced by circadian and homeostatic processes and that Process S plays a relatively minor role in its regulation.
... Based on anecdotal reports of mental disturbances produced in the earliest REM deprivation studies[73], it was suggested that REM sleep was important for discharging psychological tensions that would otherwise cause personality disturbances[74]. A comprehensive review by Vogel of subsequent controlled studies concluded that REM sleep deprivation did not produce psychological harm[34]. ...
The emergence of sleep precedes humanity and has always influenced human culture. The modern science of sleep and circadian rhythm medicine is foundationally based to address age old problems such as insomnia and nightmares. The pace of sleep scientific knowledge greatly accelerated with development of all-night sleep recordings and the subsequent illumination of the spectrum of clinical sleep disorders. Much of this fundamental work was influenced by Dr. William C. Dement and several other pioneers described in this article. The history of sleep and circadian science shows us the inexorable, and perhaps destined, path to know the functions of sleep and promote greater sleep health for society.
Resumen La privación de sueño se ha convertido en pandemia, debido a muchos factores, entre ellos, el ambiente industrializado. Las consecuencias de estos cambios son cada vez más evidentes en nuestra sociedad. Aunque todavía no se tiene un consenso acerca de la función del sueño, no es posible dudar de su esencial importancia para las funciones vitales, procesos cognitivos-emocionales y consolidación de la memoria, entre otras muchas. La privación de sueño interfiere con estas funciones, de manera temporal y permanente, por lo que es esencial darle el valor que tiene en la salud general de la población. Las áreas neuro-cognitivas particularmente afectadas son la velocidad psicomotora y cognitiva, la vigilia, la atención y la memoria de trabajo. Los experimentos de restricción crónica de sueño demuestran que el déficit cognitivo se acumula a varios niveles a través del tiempo. Muchas de las alteraciones del desempeño cognitivo se atribuyen a la somnolencia excesiva diurna provocada por la privación o disrupción del sueño, aunque esto es cierto, también hay alteraciones en el procesamiento de las tareas a nivel hipocampal que se afectan tanto con la restricción aguda como crónica de sueño. Palabras clave: privación de sueño, trastornos cognitivos, atención y memoria de trabajo.
Articles on sleep have only recently been incuded in compendia concerned primarily with experimental and physiological psychology. This change probably reflects the growing realization that processes regulating various waking behaviors and sleep are linked by common underlying physiological mechanisms. Waking behaviors are modulated by circadian and ultradian rhythms that are tied to sleep, and brain mechanisms concerned with the facilitation and suppression of sleep also control waking behaviors. Neural elements of the brainstem reticular formation and hypothalamus, including biogenic amine systems, appear to have multiple roles in both sleep and waking behavioral functions. Experimental manipulations such as brain lesions or drug treatments that modify sleep, also alter waking behaviors, and vice versa. Interactions between sleep, and feeding, temperature regulation, motor activity, and sensory function are noted throughout our review.
Sleep has been generally divided into rapid eye movement (REM) sleep and non-REM (NREM) sleep in higher order mammals, including humans. Several theories have proposed various functions of different stages of sleep. We hypothesized that REM sleep maintains brain excitability. In this chapter, we discuss the significance of REM sleep in the maintenance of neuronal electrochemical homeostasis, which governs brain excitability. Selective REM-sleep loss increases the activity of Na-K ATPase, a membrane-bound enzyme that maintains neuronal Na+ and K+ homeostasis and, thus, the neuronal resting membrane potential. Further, the REM sleep deprivation-induced increase in Na-K ATPase activity has been attributed to an increased level of norepinephrine in the brain.
Rapid eye movement (REM) sleep is a unique phenomenon within sleep-wakefulness cycle. It is associated with increased activity in certain group of neurons and decreased activity in certain other group of neurons and dreaming. It is likely to have evolved about 140 million years ago. Although mention of this stage can be traced back to as early as 11 century BC in the Hindu Vedic literature, the Upanishads, it has been defined in its present form in the mid-twentieth century. So far, neurobiology of its genesis, physiology and functional significance are not known satisfactorily and mostly remains hypothetical. Nevertheless, more and more studies have increasingly convinced us to accept that it is an important physiological phenomenon which cannot be ignored as a vestigial phenomenon. Although there are articles where different aspects of REM sleep have been dealt with, a review where the knowledge gathered by REM sleep deprivation studies to understand its significance is lacking. There is a need for such a review because a major portion of the knowledge about various aspects of REM sleep, specially its functional significance, has been acquired mostly from the REM sleep deprivation studies. Hence, in this review the knowledge gathered by REM sleep deprivation studies have been colated along with their importance so that it may be useful and referred to for information as well as while designing future studies.
Les patients souffrant de troubles bipolaires (TB) présentent cinq fois plus de risque de maladies cardiovasculaires que des sujets sans TB. Le syndrome métabolique est un facteur qui augmente significativement le risque de développer une maladie cardiovasculaire chez ces patients. Deux autres facteurs importants, mais néanmoins moins reconnus en pratique clinique, augmentent également le risque de maladie cardiovasculaire. Il s’agit des troubles de la réactivité émotionnelle et des pathologies du sommeil, avec en particulier le syndrome d’apnée obstructive du sommeil (SAOS). En effet, l’hyperréactivité émotionnelle semble favorisée par certains tempéraments dits « colériques », le TB et la privation de sommeil. Il est démontré que l’ensemble de ces variables interagissent et conduisent à une augmentation du risque cardiovasculaire. Par ailleurs, le SAOS est une pathologie du sommeil très fortement associée au TB, qui tend à fragmenter le sommeil et qui est également associée à un risque cardiovasculaire plus élevé. La synthèse de ces données souligne ainsi la place centrale des anomalies du sommeil et de la réactivité émotionnelle dans la vulnérabilité du TB aux maladies cardio-vasculaires. Ces données permettent également de rappeler l’importance d’identifier et de prendre en charge les anomalies du sommeil dans le TB, afin d’améliorer la morbidité et la mortalité de ce trouble.
This article (a) exposes some unnoticed implications of Jung's compensation theory of dreams, (b) integrates it with some facts discov- ered after Jung's time, (c) thereby makes that theory more useful in understanding the meaning and function of dreams, and also (d) points to the applicability of the same theory to Jungian psychotherapy in more ways than dream interpretation.
Four young adult subjects each slept ten consecutive nights in the laboratory without awakenings. The mean nightly REM sleep time was calculated for each subject and used as the baseline value for further procedures. Two subjects were allowed 75 per cent of their baseline REM sleep time for nineteen consecutive nights and slept without disturbance for the next five (recovery) nights. The first recovery nights were 54 per cent and 13 per cent respectively above the baseline with a more or less exponential decline to the basal level on subsequent nights. The compensatory rises in REM time were compatible with what might have been expected following five nights of complete deprivation and suggest that partial REM deprivation has a cumulative effect roughly proportional to the degree of partial deprivation. The other two subjects underwent complete REM sleep deprivation for five consecutive nights followed by five nights upon which REM sleep time was held to the baseline level. The next five nights were undisturbed and the REM sleep fraction was elevated 100 per cent and 66 per cent respectively above the baseline. These results suggest that the REM sleep deprivation effect can be reversed only by extra amounts of REM sleep and will persist if such compensation does not take place.
Dreaming has fascinated and mystified humankind for ages: the bizarre and evanescent qualities of dreams have invited boundless speculation about their origin, meaning and purpose. For most of the twentieth century, scientific dream theories were mainly psychological. Since the discovery of rapid eye movement (REM) sleep, the neural underpinnings of dreaming have become increasingly well understood, and it is now possible to complement the details of these brain mechanisms with a theory of consciousness that is derived from the study of dreaming. The theory advanced here emphasizes data that suggest that REM sleep may constitute a protoconscious state, providing a virtual reality model of the world that is of functional use to the development and maintenance of waking consciousness.
Studies on the behavioral consequences of rapid eye movement (REM) sleep deprivation in animals and humans are critically reviewed. In animals, converging evidence--some reasonably well controlled--indicates that REM sleep deprivation probably heightens central neural excitability and increased motivational behavior, but has nuclear or inconclusive effects on learning. In humans, evidence indicates that REM sleep deprivation is not dream deprivation and is not harmful to schizophrenic, depressed, or healthy subjects. Controversy continues about whether or not (some) schizophrenic patients respond abnormally to REM sleep deprivation by having no REM rebound. Controlled but unconfirmed work indicates that that endogenous, but not reactive, depressive patients are improved by REM sleep deprivation, a finding consistent with the animal behavioral consequences of the procedure and with the unique REM-depriving properties of efficacious antidepressant drugs.
To test the hypothesis that some schizophrenic patients fail to have a normal rapid eye movement (REM) sleep rebound following deprivation of REM sleep, 905 all night sleep recordings of the electroencephalogram, electrooculogram, and electromyogram were made on 26 psychiatric patients. The principal experiment studied the effects of 2 nights of partial deprivation of REM sleep on 8 actively ill schizophrenic patients and in 8 nonpsychotic, hospitalized psychiatric patients. REM sleep was also studied in 7 anxious depressed patients before, during, and after treatment with phenelzine, a monoamine oxidase inhibitor that suppresses REM sleep. In addition, 2 acute schizophrenics and 1 manic depressive patient were studied with nightly, longitudinal sleep recordings before, during, and after 6 psychotic episodes. The results support the hypothesis that most actively ill schizophrenic patients fail to have a normal REM rebound following deprivation of REM sleep. The evidence is most clear in the study of experimental deprivation of REM sleep, but it is also suggested by the longitudinal study of the 2 acute schizophrenic patients. Some overlap exists, however, between the actively ill schizophrenics and other psychiatric patients. The relationship between the abnormality of REM compensation of hypothesized biochemical abnormalities in schizophrenia is discussed.
In subjecting 14 healthy university students to partial differential rapid eye movement (REM) sleep deprivation (PDRD), the compensatory rebound of REM sleep during the next night was determined, and showed fairly substantial individual differences in the increased percentage of REM sleep time. This rate was approximately the same for the same individual for two sleep recordings. These individual differences had no positive correlation with the decreased rate of REM time in the PDRD nights or with the percentage of REM time in the baseline night. Therefore, the individual differences in the increased percentage of REM time can be presumed to reflect individual differences in need for deprived REM sleep. Next, we looked into the relationship between the individual subject's personality and behavior characteristics, and his increased percentage of REM time. This revealed that the individuals who were extrovertive, active, optimistic, showy, and who had many friends had significantly higher increases in the percentage of REM time than the individuals who were introvertive, neurotic, inactive, nervous, modest, and who had few friends. Also discussed was the neurophysiological and biochemical basis of the central nervous system as the background for the relationship between the personality and behavioral characteristics and the increased percentage of REM sleep time.
Based on the assumption that the mental aspect of REM sleep is an extreme state of divergent thinking, it was hypothesized that the psychological effect of REM deprivation varies on a dimension of creativity versus rote learning. On the creativity pole, REM deprivation has a damaging effect, while on the rote learning pole, it has a beneficial effect.
The subjects (.Ss) were 12 male undergraduate students. Each spent 3 nights in the laboratory. Ss served us their own controls, with 5 days separating the REM deprivation and the non‐REM deprivation nights.
Before going to bed, each of the Ss was given 4 tasks, on which testing took place the fallowing morning. Comparable tasks, in a balanced design, were used on the REM deprivation and on the non‐REM deprivation nights, The tasks given were: (a) serial memory, (b) “clustering” memory, (c) word fluency, and (d) Guilford's Utility Test.
Results showed a significant decrement in creativity (the Guilford's Utility Test), and a significant increment in role memory (the serial memory task), due to REM deprivation. No significant differences were found for the other 2 tasks used, which were somewhere in‐between the two extreme poles of creativity and role learning. These results might explain earlier, contradictory findings in this area.
These results lend further support to the general assumption that REM sleep is used by the organism for internal information processing. However, an additional assumption has to be. made, that this processing is divergent and not convergent.
Sleep physiological patterns were examined following a single oral dose (500 mg) of the hypnotic drug alpha chloralose. The drug increased SW sleep and decreased REM sleep without affecting total sleep time or the amount of stage 2. These changes were accompanied by a shift to slower frequencies and greater EEG synchrony, as well as a decrease in the number of spontaneous arousals in all stages of sleep, and throughout the night of medication. Except for a slight decrease in eye movement density, the drug had no systematic effects on phasic phenomena such as electrodermal or cardio-respiratory fluctuations, nor was there a systematic change in basal heart and breathing rates.
On the night following medication a “rebound” increase in percent stage REM was associated with a sharp decrease in SW sleep, and increases in spontaneous arousals and waking time. Such findings suggest that sleep stages are controlled by homeostatic mechanisms whose function is to maintain equilibrium.
A comparison of the effects of alpha chloralose with those of the barbiturate secobarbital revealed some striking differences. Although both alpha chloralose and the barbiturate reduced the amount of stage REM and the frequency of brief arousals, the latter compound enhanced EEG fast activity and desynchrony, and suppressed such phasic phenomena as rapid eye movements during stage REM, sigma spindles in stage 2, nonspecific electrodermal responses during SW sleep and cardio-respiratory variability in all sleep stages. For secobarbital, the decrease in percent stage REM was compensated by an increase in stage 2 rather than SW sleep.
Several studies in the cat suggest that in subanesthetic doses, alpha chloralose acts primarily on cortical inhibitory processes, causing release of the reticular activating system from inhibitory influences. The results of this study show that moderate doses in man probably act on both cortical and subcortical systems involved in the mediation of SW sleep, REM sleep and arousal.
Seven patients with intractable narcolepsy were treated with the monoamine oxidase inhibitor, phenelzine. Striking reductions in the amount of cataplectic attacks, sleep paralysis and hypnagogic hallucinations were noted. In addition, daytime sleeping and hypersomnia were diminished, but side effects (hypotension, edema, impaired sexual function) were bothersome. Phenelzine almost completely suppressed rapid-eye-movement sleep and remained effective for periods of more than a year. Although dreams were frequently reported before drug treatment no dreams were reported when rapid-eye-movement sleep was completely absent. No adverse psychologic effects were noted during the period of total rapid-eye-movement suppression.
There are contradictory opinions on the consequences of REM deprivation. It is suggested that these contradictions are related to personality differences in the reaction to deprivation in general; that is, the reactions are triggered by the deprivation but not channeled by it, so that the REM deprivation functions as an impetus or drive, but the final results will not be understandable without taking account of the shaping effect of personality structure.Taking individual differences into account will not, of itself, help in understanding the function of REM/dream, unless we exercise greater precision in defining the relevant phenomena. It is doubtful whether behavioral changes usually registered after REM deprivation reveal the special nature of REM function. For example, hallucinations can be seen in subjects of particular personality make-up; but those persons will hallucinate in situations of sensory deprivation or thirst as well as REM deprivation. Such a phenomenon is hardly apt to tell us anything of the special function of REM or of dreaming.The evidence on REM as a diurnal cycle raises the question whether the existence of dream deprivation is a proven fact. On the other hand, the physiological aspect of REM deprivation (piling up of monoamine) can indicate something of the physiological function of this state of consciousness. The method of deprivation is therefore applicable here. But not as regards dreaming. Whether the dream serves drive discharge (Freud) or accumulation of kinesthetic experience (Lerner; a suggestion which gains some support from the above discussion), or whether it serves as a coding procedure by integrating recent input to existing structures (Breger2), the function of dreaming will have to be determined by methods other than deprivation.
This review conveys the extent of the sleep researcher's interest in, and potential contribution to, the resolution of some of the mysteries still surrounding many clinical disorders. In no area is there a complete understanding of the significance of the sleep disturbances to the overall clinical picture, and undoubtedly this must in part await a more complete understanding of the basic nature and function of sleep itself. The information obtained in the sleep laboratory has already added a new dimension to continuing exploration of many disease processes, and the authors are confident that future work will contribute to the elucidation both of the mechanisms of these disorders and of more rational treatments for them.
A review of some of the important recent findings on sleep and its disorders has been presented and they provide some insight into the mysterious process of sleep. Sleep is shown to be a very complex process which will require not only extension of the current researches but a revised approach into the areas covered by previous studies.
Sleep is a unique state quite different from other phenomena of loss or change of consciousness. It is distinguished from hypnosis which may involve more the specific arousal system of the thalamus. Hypnotic blindness for example does not involve sleep changes but rather a reversal of the electrical activity of the visual cortex (38).
Although there appears to be a system which alerts the sleeping organism to meaningful stimuli it seems that there is little evidence of significant new learning during sleep (12, 120, 153). Rather sleep involves the focusing of the activity of the central nervous system on its internal processes. Sleep produces a state of relative bodily inactivity but the central nervous system remains actively engaged in a restorative process not yet understood.
The discovery of the REM state has shown the complexity of sleep. No study of the effect of physical or chemical stimuli on the nervous system during sleep will be adequate without the examination of effects and responses in the different phases of sleep. The lack of success of continuous sleep therapy may be in part due to suppression of REM sleep by the sedatives used (23). It should be stated, however, that clinical studies are also needed to supplement the more sophisticated and expensive scientific procedures. There are still many areas of controversy on the phenomenology of sleep disorder which need investigation.
Reports that in hypophysectomized rats paradoxical sleep deprivation increases cerebral serotonin, tryptophan, and 5-hydroxyindoleacetic acid levels. (21 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Twenty Ss received, double blind, either a 15-mg dextroamphetamine sulfate (DA) spansule and pentobarbital (PB) 100 mg p.o. before bed on two nights or PB and a placebo (PL) on two other nights, all a week apart, in a balanced design. Fifteen of the Ss received DA and PB placebos on two additional nights. EEG and EOG recordings were obtained over a six-hour observation period on all nights.
DA + PB produced more body movements, spontaneous awakenings and stage-2 sleep and less delta sleep (stages 3 + 4) than did PB, while PB reduced time to sleep onset and produced less body movements and spontaneous awakenings than did PL. These findings were thought to indicate that DA decreases “soundness” and “depth” of sleep while PB increases them.
A decrease in emergent stage-1 sleep (activated sleep, AS) over the six-hour observation period with DA + PB was made up for by a corresponding increase in wakefulness (stage 0), while a decrease both in AS and stage 0 with PB was compensated for by a corresponding increase in nonactivated sleep (NAS).
Both DA + PB reduced per cent AS sleep time and first AS period (ASP) latencies, DA + PB more markedly than PB. DA appeared to produce this effect primarily by increasing first ASP latencies, while PB did so as well by shortening the first two ASPs.
The tendency of PB to reduce rapid eye-movement (REM) density within ASPs (DA did not do so), to produce periods of emergent stage 1 without REMs, to shorten ASPs without changing the intervals between successive ASPs and to produce a maximum in the concentration of body movements in the 60–90 min interval after sleep onset suggested that it does not induce a basic alteration in the sleep cycle but rather suppresses certain manifestations of the first ASP (REMs and stage-1 sleep), while leaving others, such as body movements, unchanged to persist as a “REM-period residue.” Since DA was always administered with PB, it is not clear by what mechanisms the former delayed the appearance of first ASPs.
The acute effects of four drugs — pentobarbital, amitriptyline, chlordiazepoxide, and RO 5-6901 (a new benzodiazepine)—on sleep were investigated in 10 normal human subjects.
All the drugs produced a slight increase in total sleep time. D-time and D-time percent were moderately reduced by pentobarbital and greatly reduced by amitriptyline. The two benzodiazepines had no effect on these variables, i.e. they produced a night of normal or increased sleep without the reduced D-time found after most clinically used drugs.
The possibility is discussed that the effect of antidepressant agents on sleep patterns—specifically a reduction in the “need for D” —may be related to their clinical action.
From a brief review of studies of muscle tension during sleep it is concluded that the widely accepted positive correlation between cerebral and psychological activity and muscle tension does not hold during desynchronized sleep (DS). Some similarities between DS and extreme relaxation are postulated, and a check of this hypothesis is suggested. Possible peripheral mechanisms involved in changes in muscle tension are discussed, and a technique of investigation is suggested whereby further insight into these mechanisms may be gained.
The effect of reserpine on the sleep and dream patterns of six normal human subjects was investigated. All-night EEG and eye-movement recordings were obtained on about fifteen nights for each subject.
Results indicate that reserpine, in single doses of 1.0 to 2.0 mg increased the time spent in the D-state (“dreaming sleep”, “REM-sleep”) both in absolute terms and as a percentage of total time asleep. Reserpine also increased the number of awakenings but did not significantly affect the total amount of sleep.
It is suggested that the central effect of reserpine, its action in releasing serotonin and norephrine from storage in brain cells, is probably involved.
The EEGs and electrooculograms of 6 Ss were recorded for six hours on four nights in the laboratory. On two nights the Ss received methyl phenidate at a 5-mg dose level, and on two other nights they received a placebo. The drug significantly delayed the onset of the first REM period. It also significantly reduced the amount of REM sleep and increased the time spent in stage-2 sleep during the six-hour period of observation. It exerted these effects without significantly affecting any of the other parameters of the sleep cycle that were studied.
Although there were several premonitory signs of a sleep stage with dreaming, it was only in 1953 that such a stage was identified with certainty. This paper analyses the observations and research related to this dreaming stage (rapid eye movement sleep) until 1964. During these 11 years of research, the main psychological and physiological characteristics of this sleep stage were first described. Where the few results or discussions were later questioned, today's current state of knowledge is briefly outlined.
The discovery of the close association between rapid eye movement (REM) sleep and dreaming and development of sleep laboratory techniques ushered in a new era in the study of dreams. For the first time, direct and systematic investigation could be made of such topics as the occurrence, qualities, recollection, and childhood development of dreaming. Experimental methodologies permitted investigation of the responsiveness of dreams to external stimulation and the effects of deprivation of REM sleep. Much effort was devoted to searching for parallels between physiological aspects of REM sleep and characteristics of associated dreams, with modest results. The leading theory of dreaming in the early decades of this research was the psychoanalytic, which views dreams as highly meaningful reflections of unconscious mental functioning. With developments in understanding of the neurophysiology of REM sleep, new theories of dreaming were proposed. The most prominent, the activation-synthesis hypothesis, derived its view of dreaming directly from the neurophysiology of REM sleep, in particular the role of the brain stem, and in its original form regarded dreams as not essentially meaningful. Further developments in neurobiological research, including lesion and brain imaging studies, have established a clearer view of the functional neuroanatomy of REM sleep and dreaming. To what degree, and in what way, implications can be drawn from these findings for the psychology of dreaming is controversial. Some more recent theories of dreaming emphasize an adaptive function related to emotion and a role in learning and memory consolidation.