Since the discovery that the characteristics of dreaming sleep are far stronger in Stage 1 rapid eye movement sleep than in any other biological state, investigators have attempted to determine the relative responsibility of the tonic versus the phasic properties of REM sleep for the different characteristics of dreaming–features such as the amount of information in the dream report, the brightness and clarity of the visual images, shifts in thematic continuity, and incongruities of image and meaning. The present experiment is (...) designed to identify dream characteristics that are specifically associated with tonic changes in level of cortical activation within sleep. It samples reports of imagery and thought during spontaneous variations within one phase of the 24-h diurnal rhythm and across the REM-NREM sleep cycle in order to identify the independent and joint contributions of the two cycles to imagery and thought. The rising phase of the diurnal cycle in the late night and morning was estimated from clock time during the late night and early morning and was varied by delaying the sleep onset and waking time of the subjects. Considered together with other studies, the results suggest that the major determinant of vivid visual imagery and enhanced cognitive activity during sleep is a pattern of subcortical and cortical activation that is common to both the REM phase of the REM-NREM cycle and the activated phase of the 24-h diurnal wake-sleep cycle. (shrink)

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. Key Words: acetylcholine; brainstem; dopamine; dreaming; forebrain; NREM; REM; sleep. (shrink)

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. Key Words: cognition in sleep; dreaming; NREM sleep; REM sleep; sleep mentation. (shrink)

Building on the content, developmental, and neurological evidence that there are numerous parallels between waking cognition and dreaming, this article argues that the likely neural substrate that supports dreaming, which was discovered through converging lesion and neuroimaging studies, may be a subsystem of the waking default network, which is active during mind wandering, daydreaming, and simulation. Support for this hypothesis would strengthen the case for a more general neurocognitive theory of dreaming that starts with established findings and concepts derived from (...) studies of waking cognition and neurocognition. If this theory is correct, then dreaming may be the quintessential cognitive simulation because it is often highly complex, often includes a vivid sensory environment, unfolds over a duration of a few minutes to a half hour, and is usually experienced as real while it is happening. (shrink)