Yet another model of REM, based on experimental studies and not dependent on cholinergic mechanism, has been offered by Lu and colleagues, in which two small populations of GABA-ergic neurons in the pontine tegmentum have reciprocal innervation and act as a “flip-flop” mechanism similar to the one proposed for sleep initiation. This REM system runs in parallel to the sleep-wake system but is integrated into its functioning and may offer insights into some of the dysfunction syndromes of REM sleep.
Solms (1995, 1996) and others have questioned the traditional view that dreaming and REM sleep are obligately or even closely connected and has presented an alternative perspective. Among patients with cerebral lesions that eliminate or disrupt REM sleep, he cites several cases, in which dreaming was retained. Conversely, in his patients with basal forebrain (frontal) lesions, dreaming was lost, at least for a time, while REM periods remained undisturbed through the night. This same observation had been made in patients who had prefrontal leukotomies. Solms has proposed that the dopaminergic systems in the basal forebrain areas elicit or modulate dreaming. This view is supported by reports of diminished dreaming in patients being treated with dopaminergic blockers and the enhancement of dreaming reported by patients taking l-dopa or dopamine agonsits. Notable in this regard is the fact that major intracortical dopaminergic pathways originate in the frontal lobes.
In regard to the neurophysiology of the EEG and sleep rhythms, much has been gleaned from intracellular recordings in animals. As with the earlier-described anatomic and neurochemical data, the degree to which similar electrophysiologic changes are reflected in humans is not known. Most of the integrated rhythms of sleep that are recorded at the surface of the brain, including the background activity of slow-wave sleep and the faster and more synchronized sleep spindles and vertex waves, have their origins in the thalamus. Steriade and colleagues have performed a substantial amount of the modern work in this area and summarize it in their review. They make clear that these complex EEG rhythms, while apparent in nascent form in certain isolated neurons, are oscillations that arise from integrated ensembles of cells, with the thalamus as a nexus. It is evident that there is as yet no agreement concerning the integration of all these brainstem and thalamic–hypothalamic mechanisms in the production of sleep or of dreams.
The Function of Sleep and Dreams
These questions have been pondered endlessly by physiologists and psychiatrists (and philosophers). Parkes has reviewed the main theories—body restitution, facilitation of motor function, consolidation of learning and memory—and tends to agree with the ungrammatical but unambiguous conclusion of Popper and Eccles that “Sleep is a natural repeated unconsciousness that we do not even know the reason for.” One cannot logically entertain the notion that the function of sleep is to produce dreams, at least until the utility and meaning of dreams become known. There is, however, considerable support for the popular notion that we stabilize learned material while asleep.
Regarding neurophysiologic changes during dreaming, Braun and colleagues used positron emission tomography (PET) to study REM sleep; they observed selective activation of the extrastriate visual cortices and limbic–paralimbic regions, with attenuation of activity in the primary visual cortex and frontal association areas. Based on these and similar studies, several authors have speculated that the suppression of frontal lobe activity during dreaming, at a time when visual association areas and their paralimbic connections are activated, might explain the uncritical acceptance of the bizarre visual content, the disordered temporal relationships, and the heightened emotionality that characterize dreams. This would be in keeping with Hobson’s view of dreams as a form of delirium.