The activity that takes place in memory systems during sleep is likely to be related to the role of sleep in memory consolidation and learning, as well as to the generation of dream hallucinations. This study addressed the often-stated hypothesis that replay of whole episodic memories contributes to the multimodal hallucinations of sleep. Over a period of 14 days, 29 subjects kept a log of daytime activities, events, and concerns, wrote down any recalled dreams, and scored the dreams for incorporation of any waking experiences. While 65% of a total of 299 sleep mentation reports were judged to reflect aspects of recent waking life experiences, the episodic replay of waking events was found in no more than 1–2% of the dream reports. This finding has implications for understanding the unique memory processing that takes place during the night and is consistent with evidence that sleep has no role in episodic memory consolidation.

Performance on a visual discrimination task shows longterm improvement after a single training session. When tested within 24 hr of training, improvement, was not observed unless subjects obtained at least 6 hr of postraining sleep prior to retesting, in which case improvement was proportional to the amount of sleep in excess of 6 hr. For subjects averaging 8 hr of sleep, overnight improvement was proportional to the amount of slow wave sleep (SWS) in the first quarter of the night, as well as the amount of rapid eye movement sleep (REM) in the last quarter. REM during the intervening 4 hr did not appear to contribute to improvement. A two-step process, modeling throughput as the product of the amount of early SWS and late REM, accounts for 80 percent of intersubject variance. These results suggest that, in the case of this visual discrimination task, both SWS and REM are required to consolidate experience-dependent neuronal changes into a form that supports improved task performance.

The notion that dreaming might alter the strength of associative links in memory was first proposed almost 200 years ago. But no strong evidence of such altered associative links has been obtained. Semantic priming can be used to quantify the strength of associative links between pairs of words; it is thought to measure the automatic spread of activation from a “node” representing one word to nodes representing semantically related words. Semantic priming could thus be used to test for global alterations in the strengths of associative links across the wake-sleep cycle. Awakenings from REM and nonREM (NREM) sleep produce a period of state carry-over during which performance is altered as a result of the brain's slow transition to full wakefulness, and cognitive testing in this period can provide information about the functioning of the brain during the prior sleep period. When subjects were tested across the night—before and after a night's sleep as well as immediately following forced awakenings from REM and NREM sleep—weak priming (e.g., thief-wrong) was found to be state dependent ( p = 0.016), whereas strong priming (e.g., hot-cold) was not ( p = 0.89). Weak primes were most effective in the presleep and REM sleep conditions and least effective in NREM and postsleep conditions. Most striking are analyses comparing weak and strong priming within each wake-sleep state. Contrary to the normal pattern of priming, subjects awakened from REM sleep showed greater priming by weak primes than by strong primes ( p = 0.01). This result was seen in each of three protocols. In contrast, strong priming exceeded weak priming in NREM sleep. The shift in weak priming seen after REM sleep awakenings suggests that cognition during REM sleep is qualitatively different from that of waking and NREM sleep and may reflect a shift in associative memory systems, a shift that we hypothesize underlies the bizarre and hyperassociative character of REM-sleep dreaming. Known changes in brainstem activity that control the transition into and maintenance of REM sleep provide a possible explanation of this shift.

Bizarreness is a cognitive feature common to REM sleep dreams, which can be easily measured. Because bizarreness is highly specific to dreaming, we propose that it is most likely brought about by changes in neuronal activity that are specific to REM sleep. At the level of the dream plot, bizarreness can be defined as either discontinuity or incongruity. In addition, the dreamer's thoughts about the plot may be logically deficient. We propose that dream bizarreness is the cognitive concomitant of two kinds of changes in neuronal dynamics during REM sleep. One is the disinhibition of forebrain networks caused by the withdrawal of the modulatory influences of norepinephrine (NE) and serotonin (5HT) in REM sleep, secondary to cessation of firing of locus coeruleus and dorsal raphe neurons. This aminergic demodulation can be mathematically modeled as a shift toward increased error at the outputs from neural networks, and these errors might be represented cognitively as incongruities and/or discontinuities. We also consider the possibility that discontinuities are the cognitive concomitant of sudden bifurcations or “jumps” in the responses of forebrain neuronal networks. These bifurcations are caused by phasic discharge of pontogeniculooccipital (PGO) neurons during REM sleep, providing a source of cholinergic modulation to the forebrain which could evoke unpredictable network responses. When phasic PGO activity stops, the resultant activity in the brain may be wholly unrelated to patterns of activity dominant before such phasic stimulation began. Mathematically such sudden shifts from one pattern of activity to a second, unrelated one is called a bifurcation. We propose that the neuronal bifurcations brought about by PGO activity might be represented cognitively as bizarre discontinuities of dream plot. We regard these proposals as preliminary attempts to model the relationship between dream cognition and REM sleep neurophysiology. This neurophysiological model of dream bizarreness may also prove useful in understanding the contributions of REM sleep to the developmental and experiential plasticity of the cerebral cortex.