What Do Our Brains Do When We're Dreaming?

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.

The Activation-Synthesis model of dream construction proposed that the phasic signals arising in the pontine brainstem during REM sleep and impinging upon the cortex and limbic forebrain led directly to the visual and motor hallucinations, emotion, and distinctively bizarre cognition that characterize dream mentation. In doing so, these chaotically generated signals arising from the brain stem acted as a physiological Rorschach test, initiating a process of image and narrative synthesis involving associative and language regions of the brain and resulting in the construction of the dream scenarios. In contrast, Mark Solms demonstrated that what is currently known about the dreaming brain is at least broadly consistent with Freud’s dream theory. He argued that it is generally accepted that brain stem activation is necessary, but not sufficient, to explain the particular characteristics of dream consciousness. What does explain the particular characteristics of dream consciousness, according to Solms, are the following features of brain activity during REM sleep the activation of core forebrain emotion and instinctual drive mechanisms, i.e., the limbic and paralimbic brain areas (the anterior cingulate, insula, hippocampus, parahippocampal gyrus, and temporal pole), and of the posterior perceptual system (the fusiform gyrus, superior, inferior and middle temporal gyrus, and angular gyrus) and the deactivation of executive dorsolateral frontal control mechanisms (the dorsolateral prefrontal cortex). He further argued that his lesion studies  are congruent with neuroimaging results because they showed that a total cessation of dreaming results from lesions in the medial part of the frontal lobe and in the temporoparietal junction (whereas no cessation of dreaming was observed for core brainstem lesions or for dorsolateral prefrontal lesions). Finally he emphasized that the activation of motivational mechanisms (such as drives and basic emotions) and of posterior perceptual system associated with deactivation of the executive control (i.e., reality oriented regulatory mechanism) during REM sleep, is broadly consistent with Freud’s dream theory which claims that our instinctual drive states (notably appetitive and libidinal drive system) are relatively disinhibited during sleep. Note that experimental results demonstrating the existence of unconscious representations that guide behavior could also have been cited in support of Freud’s dream theory.

Solms’ approach to dreaming and his experimental results fundamentally challenged our current understanding of dreaming. He proposes that dreaming and REM sleep are controlled by different brain mechanisms. According to Solms, REM sleep is controlled by cholinergic brain stem mechanisms, whereas dreaming is mediated by forebrain mechanisms that are probably dopaminergic. This implies that dreaming can be activated by a variety of NREM triggers. Several experimental results support this hypothesis.

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