The following review summarizes and examines Mark Solms's article Dreaming and REM Sleep are controlled by different brain mechanisms, which argues why the understanding of REM sleep as the physiological equivalent of dreaming needs to be re-analyzed. An analysis of Solms's article demonstrates that he makes a convincing argument against the paradigmatic activation-synthesis model proposed by Hobson and McCarley and provides provocative evidence to support his claim that REM and dreaming are dissociable states. In addition, to situate Solms's findings in concurrent research, other studies are mentioned that are further elucidated by his argument.

[Solms]

Sleep researchers in different disciplines disagree about how fully dreaming can be explained in terms of brain physiology. Debate has focused on whether REM sleep dreaming is qualitatively different from nonREM (NREM) sleep and waking. A review of psychophysiological studies shows clear quantitative differences between REM and NREM mentation and between REM and waking mentation. Recent neuroimaging and neurophysiological studies also differentiate REM, NREM, and waking in features with phenomenological implications. Both evidence and theory suggest that there are isomorphisms between the phenomenology and the physiology of dreams. We present a three-dimensional model with specific examples from normally and abnormally changing conscious states.

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.

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.

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.

Several theories claim that dreaming is a random by-product of REM sleep physiology and that it does not serve any natural function. Phenomenal dream content, however, is not as disorganized as such views imply. The form and content of dreams is not random but organized and selective: during dreaming, the brain constructs a complex model of the world in which certain types of elements, when compared to waking life, are underrepresented whereas others are over represented. Furthermore, dream content is consistently and powerfully modulated by certain types of waking experiences. On the basis of this evidence, I put forward the hypothesis that the biological function of dreaming is to simulate threatening events, and to rehearse threat perception and threat avoidance. To evaluate this hypothesis, we need to consider the original evolutionary context of dreaming and the possible traces it has left in the dream content of the present human population. In the ancestral environment human life was short and full of threats. Any behavioral advantage in dealing with highly dangerous events would have increased the probability of reproductive success. A dream-production mechanism that tends to select threatening waking events and simulate them over and over again in various combinations would have been valuable for the development and maintenance of threat-avoidance skills. Empirical evidence from normative dream content, children's dreams, recurrent dreams, nightmares, post traumatic dreams, and the dreams of hunter-gatherers indicates that our dream-production mechanisms are in fact specialized in the simulation of threatening events, and thus provides support to the threat simulation hypothesis of the function of dreaming.

Recent work on functional brain architecture during dreaming provides invaluable clues for an understanding of dreaming, but identifying active brain regions during dreaming, together with their waking cognitive and cognitive functions, informs a model that accounts for only the grossest characteristics of dreaming. Improved dreaming models require cross discipline apprehension of what it is we want dreaming models to “explain.”

[Hobson et al.; Neilsen; Revonsuo; Solms]

Although the work of Revonsuo is commendable for its attempt to use an evolutionary approach to formulate a hypothesis about the adaptive function of dreaming, the conclusions arrived at by this author cannot be fully shared. Particularly questionable is the idea that the specific function of dreaming is to simulate threatening events. I propose here a hypothesis in which the dream can have a different function.

[Revonsuo]

(1) Substituting (as Solms does) forebrain for brainstem in the search for a dream “controller” is counterproductive, since a distributed system need have no single controller. (2) Evidence against episodic memory consolidation does not show that REM sleep has no role in other types of memory, contra Vertes & Eastman. (3) A generalization of Revonsuo's “threat simulation” model in reverse is more plausible and is empirically testable.

[Hobson et al.; Solms; Revonsuo; Vertes & Eastman]

Solms shows the cortical basis for why dreams reflect waking concerns and goals, but with deficient volition. I argue the latter relates to Hobson et al.'s process I as well as M. A memory function for REM sleep is possible, but may be irrelevant to dream characteristics, which, contrary to Revonsuo, mirror the range of waking emotions, positive and negative.

[Hobson et al.; Nielsen; Solms; Revonsuo; Vertes & Eastman]

The advent of functional imaging has reinforced the attempts to define dreaming as a sleep state-dependent phenomenon. PET scans revealed major differences between nonREM sleep and REM sleep. However, because dreaming occurs throughout sleep, the common features of the two sleep states, rather than the differences, could help define the prerequisite for the occurrence of dreams.

[Hobson et al.; Nielsen; Solms; Revonsuo; Vertes & Eastman]

There are obvious flaws in REM sleep suppression paradigms that do not allow any conclusion to be drawn either pro or contra the REM sleep-memory hypothesis. However, less intrusive investigations of REM sleep suggest that this sleep stage or its adjunct neuroendocrine characteristics exert a facilitating influence on certain aspects of ongoing memory formation during sleep.

[Nielsen; Vertes & Eastman]

Nielsen's model presents a new isomorphic brain-mind viewpoint, according to which the sole dream generator is found in a REM-on (explicit or covert REM) mechanism. Such a model cannot explain the dreamlike activity during SWS (slow wave sleep), SO (sleep onset) and in the last period of sleep. Moreover the hypothesis contrasts with Solms's data, which show that dreaming is present also in case of destruction of the REM generator.

[Nielsen; Solms]

The target articles in this volume address the three major questions about dreaming that have been most responsible for the delay in progress in this field over the past 25 years. These are: (1) Where in the brain is dreaming produced, given that dream reports can be elicited from sleep stages other than REM? (2) Do dream plots have any intrinsic meaning? (3) Does dreaming serve some specialized function? The answers offered here when added together support a new model of dreaming that is testable, and should revitalize this area of study.

[Hobson et al.; Nielsen; Revonsuo; Solms; Vertes & Eastman]

It has been widely demonstrated that dreaming occurs throughout human sleep. However, we once again are facing new variants of the equation “REM sleep = Dreaming.” Nielsen proposes a model that assumes covert REM processes in NREM sleep. I argue against this possibility, because dream research has shown that REM sleep is not a necessary condition for dreaming to occur.

[Nielson]

Relatively poor memory for dreams is important evidence for Hobson et al.'s model of conscious states. We describe the time-gap experience as evidence that everyday memory for waking states may not be as good as they assume. As well as being surprisingly sparse, everyday memories may themselves be systematically distorted in the same manner that Revonsuo attributes uniquely to dreams.

[Hobson et al.; Revonsuo]

The relationship between sleep and memory has been controversial since the 1950s. Studies on delayed dream recall and long-term retention of pre-sleep stimuli indicate that sleep may have a positive role in the consolidation of information. This positive indication counterbalances the negative one from the studies on the effects of REM deprivation.

[Vertes & Eastman]

Threat themes are clearly over-represented in dreams. Threat is, however, not the only theme with potential evolutionary significance. Even for hypnagogic and hypnopompic hallucinations during sleep paralysis, for which threat themes are far commoner than for ordinary dreaming, consistent non-threat themes have been reported. Revonsuo's simulation hypothesis represents an encouraging initiative to develop an evolutionary functional approach to dream-related experiences but it could be broadened to include evolutionarily relevant themes beyond threat. It is also suggested that Revonsuo's evolutionary re-interpretation of dreams might profitably be compared to arguments for, and models of, evolutionary functions of play.

[Revonsuo]

Information processing theories of memory and skills can be reformulated in terms of how categories are physically and temporally related, a process called conceptual coordination. Dreaming can then be understood as a story-understanding process in which two mechanisms found in everyday comprehension are missing: conceiving sequences (chunking categories in time as a higher-order categorization) and coordinating across modalities (e.g., relating the sound of a word and the image of its meaning). On this basis, we can readily identify isomorphisms between dream phenomenology and neurophysiology, and explain the function of dreaming as facilitating future coordination of sequential, cross-modal categorization (i.e., REM sleep lowers activation thresholds, “unlearning”).

[Hobson et al.; Nielsen; Solms; Revonsuo; Vertes & Eastman]

The validity of dream recall is discussed. What is the relation between the actual dream and its later reflection? Nielsen proposes differential sleep mentation, which is probably determined by dream accessibility. Solms argues that REM sleep and dreaming are double dissociable states. Dreaming occurs outside REM sleep when cerebral activation is high enough. That various active sleep states correlate with vivid dream reports implies that REM sleep and dreaming are single dissociable states. Vertes & Eastman reject that REM sleep is involved in memory consolidation. Considerable evidence for this was obtained by REM deprivation studies with the dubious water tank technique.

[Nielsen; Solms; Vertes & Eastman]