Dreaming and REM sleep are controlled by different brain mechanisms

The paradigmatic assumption that REM sleep is the physiological equivalent of dreaming is in need of fundamental revision. A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms. Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism. The latter mechanism (and thus dreaming itself) can also be activated by a variety of nonREM triggers. Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density. Dreaming can also be induced by focal forebrain stimulation and by complex partial (forebrain) seizures during nonREM sleep, when the involvement of brainstem REM mechanisms is precluded. Likewise, dreaming is obliterated by focal lesions along a specific (probably dopaminergic) forebrain pathway, and these lesions do not have any appreciable effects on REM frequency, duration, and density. These findings suggest that the forebrain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism. The "REM-on" mechanism (like its various NREM equivalents) therefore stands outside the dream process itself, which is mediated by an independent, forebrain "dream-on" mechanism.     

Configuration of the dream in REM sleep

Dreams during REM sleep have a characteristic form. They are, so to speak, "chain dreams, in which the scenes follow consecutively and, although distinctly separate from each other, are welded into a coherent dream by the primary integrating thoughts underlying the dream. The contents of the different scenes are difficult to reconcile with the integrating thought behind the dream because they are not stimulated by the thought alone but, in a certain way, also by past experiences. The author describes a dream which apparently filled the REM phase from beginning to end. It has been possible to explain the background of the integrating thought and the origins of the different scenes. The peculiar character of such dreams should find more attention in scientific research.     

REM sleep: A social bonding mechanism

It is proposed that REm sleep evolved, in part, to promote social bonding between (1) a mammalian infant and the mother and (2) sexual partners. The bonding hypothesis is consistent with the available evidence from psychobiologic studies of the attachment process in infants, with the known physiologic correlates of REM sleep, with the facts concerning the ontogeny and the phylogeny of REM sleep, and with phenomenological properties of dreams.     

Spiral aftereffect durations following awakening from REM sleep and non-REM sleep

Nine Ss were awakened 2 min after the beginning of a REM period and 2 min after the beginning of a non-REM period (Stage 4), and were tested on a spiral aftereffect. The duration of the spiral aftereffect was found to be longer for the tests made following REM periods than for the tests made following non-REM periods. The results were interpreted to suggest a possible “carry over” effect from the particular sleep, stage into the waking state.     

Posttraining increases in REM sleep intensity implicate REM sleep in memory processing and provide a biological marker of learning potential

Posttraining rapid eye movement (REM) sleep has been reported to be important for efficient memory consolidation. The present results demonstrate increases in the intensity of REM sleep during the night of sleep following cognitive procedural/implicit task acquisition. These REM increases manifest as increases in total number of rapid eye movements (REMs) and REM densities, whereas the actual time spent in REM sleep did not change. Further, the participants with the higher intelligence (IQ) scores showed superior task acquisition scores as well as larger posttraining increases in number of REMs and REM density. No other sleep state changes were observed. None of the pretraining baseline measures of REM sleep were correlated with either measured IQ or task performance. Posttraining increases in REM sleep intensity implicate REM sleep mechanisms in further off-line memory processing, and provide a biological marker of learning potential.     

The case against memory consolidation in REM sleep

We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40-85%) and sustained (30-50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory.     

EEG asymmetry and sleep mentation during REM and NREM

The hypothesis that dreaming is mediated by the right hemisphere was evaluated by monitoring EEG power asymmetry during REM and NREM sleep, and obtaining mentation reports when short-term temporal shifts in the EEG indicated relative left- or right-hemispheric dominance. Content analyses provided no support for the right-hemisphere hypothesis; indeed, some scales showed higher content during relative left-hemispheric dominance. In contrast to earlier reports, no difference between REM and NREM in EEG asymmetry was observed.     

A review of mentation in REM and NREM sleep: "covert" REM sleep as a possible reconciliation of two opposing models

Numerous studies have replicated the finding of mentation in both rapid eye movement (REM) and nonrapid eye movement (NREM) sleep. However, two different theoretical models have been proposed to account for this finding: (1) a one-generator model, in which mentation is generated by a single set of processes regardless of physiological differences between REM and NREM sleep; and (2) a two-generator model, in which qualitatively different generators produce cognitive activity in the two states. First, research is reviewed demonstrating conclusively that mentation can occur in NREM sleep; global estimates show an average mentation recall rate of about 50% from NREM sleep--a value that has increased substantially over the years. Second, nine different types of research on REM and NREM cognitive activity are examined for evidence supporting or refuting the two models. The evidence largely, but not completely, favors the two-generator model. Finally, in a preliminary attempt to reconcile the two models, an alternative model is proposed that assumes the existence of covert REM sleep processes during NREM sleep. Such covert activity may be responsible for much of the dreamlike cognitive activity occurring in NREM sleep.     

Dreaming

The aim is to discover a principle governing the formation of the dream. Now dreaming has an analogy with consciousness in that it is a seeming-consciousness. Meanwhile consciousness exhibits a tripartite structure consisting of (A) understanding oneself to be situated in a world endowed with given properties, (B) the mental processes responsible for the state, and (C) the concrete perceptual encounter of awareness with the world. The dream analogues of these three elements are investigated in the hope of discovering the source of the kinship between dream and consciousness. The dream world (A) proves to be a logically impossible world, limited by nothing more than sheer narratability. The internal world (B) of the dreamer is notable for the limitlessness of the scope allotted to the imagination (exactly taking over the offices of rational function), together with the presence of two important phenomena encountered in waking consciousness: a measure of interiority, and the positing of a world. Finally (C), the dream further replicates consciousness in so far as we seem in dreaming concretely to experience our physical surrounds in the form of perceptual imagining. These properties play their part in enabling the dream to be a seeming-consciousness. At the same time they are such as to necessitate its not being consciousness. It is proposed that in the light of these properties, and those composing the state of consciousness, the dream simply is the imagining of consciousness.     

Psychoanalytic dream theory and recent neurobiological findings about REM sleep

I have reviewed Hobson and McCarley's activation-synthesis hypothesis of dreaming which attempts to show that the instigation and certain formal aspects of dreaming are physiologically determined by a brainstem neuronal mechanism, their reasons for suggesting major revisions in psychoanalytic dream theory, and neurophysiological data that are inconsistent with their hypothesis. I then discussed the concept of mind-body isomorphism pointing out that they use this concept inconsistently, that despite their denials they regularly view physiology as primary and psychological processes as secondary, and that they frequently make the error of mixing the languages of physiology and psychology in their explanatory statements. Finally, in order to evaluate Hobson and McCarley's claim that their findings require revision of psychoanalytic dream theory, I examined their discussions of chase dreams, flying dreams, sexual dreams, the formal characteristics of dreams, the forgetting of dreams, and the instigation of dreams. I concluded that although their fascinating physiological findings may be central to understanding the neurobiology of REM sleep, they do not alter the meaning and interpretation of dreams gleaned through psychoanalytic study.     

Variable-interval reinforcement schedule value influences responding following REM sleep deprivation

The effects of rapid-eye movement sleep deprivation (REMSD) in rats were studied in relation to variable-interval (VI) reinforcement schedule value. Initially, lever pressing was maintained on a VI 30-s schedule of food pellet delivery. After a baseline was established, rats were repeatedly exposed to 96 hr of REMSD and control conditions of an equivalent duration. Responding decreased following REMSD but not after exposure to control conditions. Lever pressing was then maintained on a VI 15-s schedule of food pellet delivery and exposure to the REMSD and control conditions was repeated. Under this condition following repeated REMSD exposures, rates of lever pressing became similar to baseline responding. A VI 30-s schedule of food pellet delivery was then reinstated and REMSD and control conditions were repeated. Lever pressing following exposure to the REMSD condition decreased for 3 of 4 rats. Results suggest that VI schedule value influences the effects of REMSD on responding.