Dreams and Dreamless Sleep

Dreamless sleep, as subjective experience, is mentioned primarily within Hindu and Buddhist contexts. In the Upanishads, dreamless sleep is presented for the most part as objectless consciousness. Tibetan Buddhists speak of dreamless sleep in terms of a progression of visual experiences consisting of darkness and light. Contemporary discussions of dreaming, unless concerned with Eastern religion or philosophy, do not tend to mention dreamless sleep. For some writers today, dreaming includes all subjective experience during sleep, leaving no room for an experience of dreamless sleep. Some writers describe dreaming as a simulation of waking life. Since not all experience during sleep is simulation, this concept allows for experiences during sleep that may be understood to be other than dreaming. The writer finds it useful to consider simulation as the determining characteristic of dreaming and finds certain other sleep experiences then that are best considered to be dreamless.     

A New Neurocognitive Theory of Dreams

Discoveries in three distinct areas of dream research make it possible to suggest the outlines of a new neurocognitive theory of dreaming. The first relevant findings come from assessments of patients with brain injuries, which show that lesions in different areas have differential effects on dreaming and thereby imply the contours of the neural network necessary for dreaming. The second set of results comes from work with children ages 3–15 in the sleep laboratory, which reveals that only 20–30% of REM period awakenings lead to dream reports up to age 9 and that the dreams of children under age 5 are bland and static in content. The third set of findings comes from a rigorous system of content analysis, which demonstrates the repetitive nature of much dream content and that dream content in general is continuous with waking conceptions and emotional preoccupations. Based on these findings, dreaming is best understood as a developmental cognitive achievement that depends upon the maturation and maintenance of a specific network of forebrain structures. The output of this neural network for dreaming is guided by a continuity principle linked to current personal concerns on the one hand and a repetition principle rooted in past emotional preoccupations on the other.     

Dreamed movement elicits activation in the sensorimotor cortex

Since the discovery of the close association between rapid eye movement (REM) sleep and dreaming, much effort has been devoted to link physiological signatures of REM sleep to the contents of associated dreams [1-4]. Due to the impossibility of experimentally controlling spontaneous dream activity, however, a direct demonstration of dream contents by neuroimaging methods is lacking. By combining brain imaging with polysomnography and exploiting the state of "lucid dreaming," we show here that a predefined motor task performed during dreaming elicits neuronal activation in the sensorimotor cortex. In lucid dreams, the subject is aware of the dreaming state and capable of performing predefined actions while all standard polysomnographic criteria of REM sleep are fulfilled [5, 6]. Using eye signals as temporal markers, neural activity measured by functional magnetic resonance imaging (fMRI) and near-infrared spectroscopy (NIRS) was related to dreamed hand movements during lucid REM sleep. Though preliminary, we provide first evidence that specific contents of REM-associated dreaming can be visualized by neuroimaging.     

Dream recall after night awakenings from tonic/phasic REM sleep

Eleven healthy subjects, 9 females and 2 males aged 21-23, were submitted to all night polygraphic recording and awaken in REM (Rapid Eye Movements) sleep, randomly upon tonic or phasic REM. Immediately upon awakening subjects were asked about possible dreaming according to the standardized questionnaire. Seventy-seven dreams, i.e. 79% of all 97 REM awakenings, were reported and analyzed. There were no significant differences in reported frequency of dreamings after awakening, mood and dream content due to phasic/tonic REM sleep. Dreams from phasic REM were a bit more colorful. Predictor of morning remembering of dreams was meaninglessness, not meaningfulness of dreams, and, in lesser extent, good mood, colorfulness, dreams with words and phasic REM sleep.     

Review of The Mind at Night: The New Science of How and Why We Dream.

In this article I review "The Mind at Night: The New Science of How and Why We Dream," written by Andrea Rock. To begin with this book is an exciting journey through modern dream research. Scientific facts, which are skillfully explained, are complemented by personal accounts of well-known researchers in the field obtained through interviews. The diversity of the themes addressed in the book (e.g., sleep and memory, animal research, imaging studies, dream content analysis, consciousness research, creativity, and lucid dreaming) clearly shows the extensive "detective work" the author has accomplished. The major problem I had--as a researcher in this field--was the structure, or the lack of structure, within the book. Because of the way the book is organized, I decided to structure this review along the following themes: REM sleep, REM sleep and dreaming, biology of dreaming, dream content findings, and the integration of dream research into cognitive neuroscience in general. Despite the lack of structure of the book, Andrea Rock has written a wonderful book about modern dream research that is stimulating for researchers as well as for interested lay persons. I recommend it to everyone who is interested in dream research, the old question of the mind-body relationship, or understanding consciousness in general. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Temporally structured replay of awake hippocampal ensemble activity during rapid eye movement sleep

Human dreaming occurs during rapid eye movement (REM) sleep. To investigate the structure of neural activity during REM sleep, we simultaneously recorded the activity of multiple neurons in the rat hippocampus during both sleep and awake behavior. We show that temporally sequenced ensemble firing rate patterns reflecting tens of seconds to minutes of behavioral experience are reproduced during REM episodes at an equivalent timescale. Furthermore, within such REM episodes behavior-dependent modulation of the subcortically driven theta rhythm is also reproduced. These results demonstrate that long temporal sequences of patterned multineuronal activity suggestive of episodic memory traces are reactivated during REM sleep. Such reactivation may be important for memory processing and provides a basis for the electrophysiological examination of the content of dream states.     

The dream between neuroscience and psychoanalysis

The dream is tackled sometimes from the neurobiological viewpoint, sometimes from the neuropsychological angle, or from the positions of experimental and psychoanalytical psychology. Interest in dreams started with psychoanalysis in 1900, and 53 years later the discovery of REM sleep by Aserinski and Kleitman, and subsequent psychophysiological findings took the dream into the realm of biology. The dichotomous model of REM and non-REM sleep is described, as a basis for thought-like activity (non-REM sleep) and dreaming (REM sleep). This led to Hobson and McCarley's theory of activation-synthesis, suggesting that the mind while dreaming is simply the brain self-activated in REM sleep. Psychophysiological research has shown that people dream in all phases of sleep, from falling asleep to waking, but that the characteristics of the dreams may differ in the different phases. Bio-imaging studies indicate that during REM sleep there is activation of the pons, the amygdala bilaterally, and the anterior cingulate cortex, and disactivation of the posterior cingulate cortex and the prefrontal cortex. The images suggest there is a neuroanatomical frame within which dreams can be generated and then forgotten. Psychoanalysis studies the dream from a completely different angle. Freud believed it was the expression of hallucinatory satisfaction of repressed desires. Today it is interpreted as the expression of a representation of the transference in the hic et nunc of the session. At the same time it also has symbol-generating functions which provide an outlet by which affective experiences and fantasies and defences stored as parts of an unrepressed unconscious in the implicit memory can be represented in pictorial terms, then thought and rendered verbally. From the psychoanalytical point of view, the dream transcends neurobiological knowledge, and looks like a process of internal activation that is only apparently chaotic, but is actually rich in meanings, arising from the person's affective and emotional history.     

Psychophysiological correlates of lucid dreaming.

The main goal of the present study was to explore electrophysiological differences between lucid and nonlucid dreams in REM sleep. Seven men and four women experienced in lucid dreaming underwent polysomnographic recordings in the sleep laboratory on two consecutive nights. EEG signals were subjected to spectral analysis to obtain five different frequency bands between 1 and 20 Hz. Lucidity was determined by both subjective dream reports and eye-movement signals made by the subjects in response to light stimuli indicating a REM period. The main discrimination factor between lucid and nonlucid dreaming was found in the beta-1 frequency band (13-19 Hz), which in lucid dreaming was increased in both parietal regions. The ratio of frontal to parietal beta-1 activity was 1 to 1.16 in nonlucid and 1 to 1.77 in lucid dreaming. A tendency towards the greatest increase was observed in the left parietal lobe (P3), an area of the brain considered to be related to semantic understanding and self-awareness. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of Somatosensory Stimulation on Dream Content in Gymnasts and Control Participants: Evidence of Vestibulomotor Adaptation in REM Sleep

Somatosensory stimulation of the leg muscles in REM sleep appears to perturb virtual orientation in dream experiences. According to our model of vestibulomotor adaptation (Sauvageau, Nielsen, & Montplaisir, 1996), the dreaming mind attempts to compensate for such destabilizing stimulation by increasing eye movement activity or by modifying dream content, among other possible reactions. Effective compensation may be more easily achieved by participants who are adapted to the disruptive stimulation or who possess highly developed vestibulomotor skills. To examine this possibility, we studied the effects of Somatosensory stimulation on the dreams of 6 gymnasts and 6 control participants aged 9 to 16 years. Results provide some support for the expectations that 1) imposed Somatosensory information is processed by the central nervous system in REM sleep, 2) unilateral stimulation induces an upset in virtual orientation, 3) gymnasts are more resistant to these disruptive effects of stimulation than are control participants, and 4) because of long-term adaptation, the dream content of gymnasts does not differ markedly from that of controls. Though preliminary and in need of replication, the findings are compatible with the notion that the developed vestibular skills of gymnasts protects them to some extent from the effects of a disruptive Somatosensory stimulus during sleep.     

Dreaming and schizophrenia: a common neurobiological background?

Normal waking mentation is the outcome of the combined action of both electrophysiological and neurochemical antagonistic and complementary activating and inhibitory influences occurring mainly in the cerebral cortex. The chemical ones are supported principally by acetylcholine, and noradrenaline and serotonin, respectively. During rapid eye movement (REM) sleep, the monoaminergic silence - except dopaminergic ongoing activity - disrupts this equilibrium and seems to be responsible for disturbances of mental activity characteristic of dreaming. This imbalance could cause disconnectivity of cortical areas, failure of latent inhibition and possibly the concomitant prefrontal dorsolateral deactivation. Moreover, the decrease of prefrontal dopaminergic functioning could explain the loss of reflectiveness in this sleep stage. All these phenomena are also encountered in schizophrenia. The psychotic-like mentation of dreaming (hallucinations, delusions, bizarre thought processes) could result from the disinhibition of dopamine influence in the nucleus accumbens by the noradrenergic and serotonergic local silence and/or the lifting of glutamate influence from the prefrontal cortex and hippocampus. We hypothesize that, during REM sleep, the increase of dopamine and the decrease of glutamate release observed in nucleus accumbens reach the threshold values at which psychotic disturbances arise during wakefulness. Whatever the precise mechanism, it seems that the functional state of the prefrontal cortex and nucleus accumbens is the same during dreaming sleep stage and in schizophrenia. The convergent psychological, electrophysiological, tomographic, pharmacological and neurochemical criteria of REM sleep and schizophrenia suggest that this sleep stage could become a good neurobiological model of this psychiatric disease.     

Sleeping Dreams, Waking Hallucinations, and the Central Nervous System

Consciousness is now considered a primary function and activity of the brain itself. If so, consciousness is simply the brain's interpretation and integration of all the information made available to it at any given time. On the assumption that the brain is active across all states of being (wakefulness, REM sleep, and NREM sleep), this article proposes that dreaming and hallucinations represent variations on the same theme. Under usual circumstances during wakefulness, the brain ignores internally generated activity and attends to environmental sensory stimulation. During sleep, dreaming occurs because the brain attends to endogenously generated activity. In unusual settings, such as sleep-deprivation, sensory deprivation, or medication or drug ingestion, the brain attends to exogenous and endogenous activities simultaneously, resulting in hallucinations, or wakeful dreaming. This concept is supported by numerous neurologic conditions and syndromes that are associated with hallucinations.     

Neural-mechanical coupling of breathing in REM sleep

Smith, C. A., K. S. Henderson, L. Xi, C.-M. Chow, P. R. Eastwood, and J. A. Dempsey. Neural-mechanical coupling of breathing in REM sleep. J. Appl.Physiol. 83(6): 1923-1932, 1997.During rapid-eye-movement (REM) sleep theventilatory response to airway occlusion is reduced. Possiblemechanisms are reduced chemosensitivity, mechanical impairment of thechest wall secondary to the atonia of REM sleep, or phasic REM eventsthat interrupt or fractionate ongoing diaphragm electromyogram (EMG)activity. To differentiate between these possibilities, we studiedthree chronically instrumented dogs before, during, and after15-20 s of airway occlusion during non-REM (NREM) and phasic REMsleep. We found that 1) for a given inspiratory time the integrated diaphragm EMG(Di) was similar or reduced in REM sleep relativeto NREM sleep; 2) for a givenDi in response to airway occlusion and thehyperpnea following occlusion, the mechanical output (flow or pressure)was similar or reduced during REM sleep relative to NREM sleep;3) for comparable durations ofairway occlusion the Di and integratedinspiratory tracheal pressure tended to be smaller and more variable inREM than in NREM sleep, and 4)significant fractionations (caused visible changes in trachealpressure) of the diaphragm EMG during airway occlusion inREM sleep occurred in ~40% of breathing efforts. Thus reducedand/or erratic mechanical output during and after airwayocclusion in REM sleep in terms of flow rate, tidal volume, and/or pressure generation is attributable largely to reduced neural activity of the diaphragm, which in turn is likely attributable to REM effects, causing reduced chemosensitivity at the level of theperipheral chemoreceptors or, more likely, at the central integrator.Chest wall distortion secondary to the atonia of REM sleep maycontribute to the reduced mechanical output following airway occlusionwhen ventilatory drive is highest.

     

Brainstem and spinal cord circuitry regulating REM sleep and muscle atonia

Background

Previous work has suggested, but not demonstrated directly, a critical role for both glutamatergic and GABAergic neurons of the pontine tegmentum in the regulation of rapid eye movement (REM) sleep.

Methodology/Principal Findings

To determine the in vivo roles of these fast-acting neurotransmitters in putative REM pontine circuits, we injected an adeno-associated viral vector expressing Cre recombinase (AAV-Cre) into mice harboring lox-P modified alleles of either the vesicular glutamate transporter 2 (VGLUT2) or vesicular GABA-glycine transporter (VGAT) genes. Our results show that glutamatergic neurons of the sublaterodorsal nucleus (SLD) and glycinergic/GABAergic interneurons of the spinal ventral horn contribute to REM atonia, whereas a separate population of glutamatergic neurons in the caudal laterodorsal tegmental nucleus (cLDT) and SLD are important for REM sleep generation. Our results further suggest that presynaptic GABA release in the cLDT-SLD, ventrolateral periaqueductal gray matter (vlPAG) and lateral pontine tegmentum (LPT) are not critically involved in REM sleep control.

Conclusions/Significance

These findings reveal the critical and divergent in vivo role of pontine glutamate and spinal cord GABA/glycine in the regulation of REM sleep and atonia and suggest a possible etiological basis for REM sleep behavior disorder (RBD).     

Rem sleep without atonia--from cats to humans

Basic science research observations often lead to unexpected surprises. It is likely that in 1965 when Dr. Michel Jouvet placed bilateral peri-locus coeruleus lesions in cats and observed REM sleep without atonia (RWA) and "oneiric" behavior that could only be explained by "acting out dreams" (or "dreaming out acts"), he recognized that it was an important observation, but had little inkling of its true significance. Nor could he even imagine that it would lead to such greater understanding of wake/sleep phenomena in humans. Likely also, the first observation of REM sleep behavior disorder (RBD) in humans was felt to be interesting and novel - again with no true appreciation of what this seemingly simple observation would lead to important clinical relationships with numerous neurodegenerative disorders. The identification of RBD in humans also buttressed the concept of state dissociation, which has served to explain many previously unexplainable human behavioral phenomena.     

Shortening of the photoperiod affects sleep distribution, EEG and cortical temperature in the Djungarian hamster

To asses the influence of photoperiod on sleep regulation EEG, EMG, and cortical temperature were continuously recorded for two baseline days and after 4 h sleep deprivation in Djungarian hamsters (Phodopus sungorus) adapted to a short photoperiod (light dark 816). Comparison to previous data collected in a long photoperiod (lightdark 168) showed several major effects of photoperiod: 1. A prominent change in the 24-h distribution, duration and number of vigilance state episodes, whereas the total amount of sleep and waking was unchanged; 2. Cortical temperature was 0.7°C lower in the short photoperiod; 3. There was a significant negative correlation between cortical temperature and the frequency of REM sleep episodes; and 4. Absolute EEG power density showed a marked reduction in the short photoperiod. After sleep deprivation EEG slow-wave activity (mean power density 0.75–4.0 Hz) in NREM sleep showed a remarkably similar increase in both photoperiods demonstrating the robustness of the homeostatic regulation of sleep. Cortical temperature remained above baseline values after sleep deprivation in the short photoperiod whereas a negative rebound was present in the long photoperiod. Our results support the hypothesis that cortical temperature has a strong influence on REM sleep propensity and indicate the possibility of an optimum cortical temperature for recovery sleep after sleep deprivation. The lower EEG power density in the short photoperiod may contribute to energy conservation.Abbreviations LP long photoperiod - NREM non-rapid-eye-movement - REM rapid-eye-movement - SCN suprachiasmatic nucleus - SD sleep deprivation - SP short photoperiod - SWA slow-wave activity - T _CRT cortical temperature     

Conditioned Salivation and Associated Dreams from REM Sleep

Although research has investigated the feasibility of establishing classically conditioned physiological responses during sleep, very few experimental studies have considered whether classically conditioned cognitive associations are possible. Since dreams have previously been described as a state of hyper-association, an experiment involving classical conditioning of the human salivary response and associated dream content was conducted. During wakefulness, repeated pairings of a conditioned stimulus (CS; a red light) with an unconditioned stimulus (UCS; citrus juice) yielded a conditioned autonomic response (CR; salivation) on presentation of the CS alone. After exposure to the CS during REM sleep, salivary excretion rates measured upon awakening were significantly higher than measures taken from baseline REM awakenings. However, no CR-related dreams were reported by the participants. This result could be interpreted as evidence that participants in this experiment did not experience higher-order memory associations to the external stimuli presented during REM. Alternatively, the lack of CR-related dreams could be explained by previous findings that the autonomic nervous system often works independently of higher-order cognitive activity. Therefore, if an autonomic association is formed, this does not necessarily imply a cognitive one.     

Coupled Flip-Flop Model for REM Sleep Regulation in the Rat

Recent experimental studies investigating the neuronal regulation of rapid eye movement (REM) sleep have identified mutually inhibitory synaptic projections among REM sleep-promoting (REM-on) and REM sleep-inhibiting (REM-off) neuronal populations that act to maintain the REM sleep state and control its onset and offset. The control mechanism of mutually inhibitory synaptic interactions mirrors the proposed flip-flop switch for sleep-wake regulation consisting of mutually inhibitory synaptic projections between wake- and sleep-promoting neuronal populations. While a number of synaptic projections have been identified between these REM-on/REM-off populations and wake/sleep-promoting populations, the specific interactions that govern behavioral state transitions have not been completely determined. Using a minimal mathematical model, we investigated behavioral state transition dynamics dictated by a system of coupled flip-flops, one to control transitions between wake and sleep states, and another to control transitions into and out of REM sleep. The model describes the neurotransmitter-mediated inhibitory interactions between a wake- and sleep-promoting population, and between a REM-on and REM-off population. We proposed interactions between the wake/sleep and REM-on/REM-off flip-flops to replicate the behavioral state statistics and probabilities of behavioral state transitions measured from experimental recordings of rat sleep under ad libitum conditions and after 24 h of REM sleep deprivation. Reliable transitions from REM sleep to wake, as dictated by the data, indicated the necessity of an excitatory projection from the REM-on population to the wake-promoting population. To replicate the increase in REM-wake-REM transitions observed after 24 h REM sleep deprivation required that this excitatory projection promote transient activation of the wake-promoting population. Obtaining the reliable wake-nonREM sleep transitions observed in the data required that activity of the wake-promoting population modulated the interaction between the REM-on and REM-off populations. This analysis suggests neuronal processes to be targeted in further experimental studies of the regulatory mechanisms of REM sleep.     

Sleep and cortical temperature in the Djungarian hamster under baseline conditions and after sleep deprivation

The Djungarian hamster (Phodopus sungorus) is a markedly photoperiodic rodent which exhibits daily torpor under short photoperiod. Normative data were obtained on vigilance states, electroencephalogram (EEG) power spectra (0.25–25.0 Hz), and cortical temperature (T_CRT) under a 168 h light-dark schedule, in 7 Djungarian hamsters for 2 baseline days, 4 h sleep deprivation (SD) and 20 h recovery.During the baseline days total sleep time amounted to 59% of recording time, 67% in the light period and 43% in the dark period. The 4 h SD induced a small increase in the amount of non-rapid eye movement (NREM) sleep and a marked increase in EEG slow-wave activity (SWA; mean power density 0.75–4.0 Hz) within NREM sleep in the first hours of recovery. T_CRT was lower in the light period than in the dark period. It decreased at transitions from either waking or rapid eye movement (REM) sleep to NREM sleep, and increased at the transition from NREM sleep to waking or REM sleep. After SD, T_CRT was lower in all vigilance states.In conclusion, the sleep-wake pattern, EEG spectrum, and time course of T_CRT in the Djungarian hamster are similar to other nocturnal rodents. Also in the Djungarian hamster the time course of SWA seems to reflect a homeostatically regulated process as was formulated in the two-process model of sleep regulation.Abbreviations EEG electroencephalogram - EMG electromyogram - N NREM sleep - NREM non-rapid eye movement - R REM sleep - REM rapid eye movement - SD sleep deprivation - SWA slow-wave activity - T_CRT cortical temperature - TST total sleep time - VS vigilance state - W waking     

Association between Poor Glycemic Control,Impaired Sleep Quality,and Increased Arterial Thickening in Type 2 Diabetic Patients

Objective

Poor sleep quality is an independent predictor of cardiovascular events. However, little is known about the association between glycemic control and objective sleep architecture and its influence on arteriosclerosis in patients with type-2 diabetes mellitus (DM). The present study examined the association of objective sleep architecture with both glycemic control and arteriosclerosis in type-2 DM patients.

Design

Cross-sectional study in vascular laboratory.

Methods

The subjects were 63 type-2 DM inpatients (M/F, 32/31; age, 57.5±13.1) without taking any sleeping promoting drug and chronic kidney disease. We examined objective sleep architecture by single-channel electroencephalography and arteriosclerosis by carotid-artery intima-media thickness (CA-IMT).

Results

HbA1c was associated significantly in a negative manner with REM sleep latency (interval between sleep-onset and the first REM period) (β=-0.280, p=0.033), but not with other measurements of sleep quality. REM sleep latency associated significantly in a positive manner with log delta power (the marker of deep sleep) during that period (β=0.544, p=0.001). In the model including variables univariately correlated with CA-IMT (REM sleep latency, age, DM duration, systolic blood pressure, and HbA1c) as independent variables, REM sleep latency (β=-0.232, p=0.038), but not HbA1c were significantly associated with CA-IMT. When log delta power was included in place of REM sleep latency, log delta power (β=-0.257, p=0.023) emerged as a significant factor associated with CA-IMT.

Conclusions

In type-2 DM patients, poor glycemic control was independently associated with poor quality of sleep as represented by decrease of REM sleep latency which might be responsible for increased CA-IMT, a relevant marker for arterial wall thickening.     

A reply to Hobson (2005).

J. A. Hobson's (2005) commentary merely repeats his past theoretical assertions (see record 2005-02950-002). It asks questions that rest on the refuted hypothesis that real dreaming occurs only in REM sleep and that are already answered in the author's critique. Despite many studies, there is still no evidence that neurophysiological changes during REM are responsible for any unique formal features in dreams. As for the psychological consequences of the neuromodulatory environment during REM, there are no studies. Most important, Hobson overlooks a key point in regard to a new neurocognitive approach to dreams: The many parallels between dreaming and waking cognition raise the intriguing possibility that relatively small changes from waking to sleeping can account for the unique features of dreams, rendering his REM-based speculations irrelevant. (PsycINFO Database Record (c) 2010 APA, all rights reserved)