Sleep dreaming and

Solms (2000 see also Chapter 7) has observed that suppression of cortical dopaminergic afferents abolishes dreaming. Dopamine therefore appears to be a neurotransmitter keystone of the common features of REM sleep, dreaming and schizophrenia. 

Disturbance of arousal Disorders of sleep, dreaming and wakefulness... 

Needing emphasis is that voluntary movement is difficult or impossible in both REM sleep dreams and deep trance. It is this feature—the loss of volition—that may be a deeply unifying factor, even if it is caused by quite different mechanisms. In any case, the threshold to movement, like the threshold to external sensation, can be voluntarily or involuntarily raised so that immobility is guaranteed. But this does not mean that movement cannot be simulated, imagined, and perceived as real. It can. And it is perceived, with spectacular verisimilitude, in both states. 

At the same time that I was observing the effects of these drugs on people that I knew, I was investigating the neuropharmacological basis of sleep, especially REM sleep dreaming, and it occurred to me early on that there must be some common ground between these two areas of work. And that common ground is what this book is about. 

Better antihypertensive effect of P-adrenoceptor blockers is found in patients having high PRA and most are not efficacious in patients having low PRA or in elderly patients. P-Adrenoceptor blockers usually lower arterial blood pressure about 10 mm Hg (1.3 kPa). Side effects include lethargy, dyspnea, nausea, dizziness, headache, impotency, cold hands and feet, vivid dreams and nightmares, bronchospasm, bradycardia, and sleep disturbances. 

As we relax in preparation for and pass into sleep, the active desynchronised awake EEG characterised by the low-amplitude (5-10 pV) high-frequency (10-30 Hz) beta waves becomes progressively more synchronised giving larger (20-30 pV) and slower (8-12 Hz) alpha waves, and then even slower (1-4 Hz) and bigger (30-150 pV) delta waves. This so-called slow-wave sleep is interrupted at intervals of some 1-2h by the break-up and desynchronisation of the EEG into an awake-like pattern. Since this is accompanied by rapid eye movements, even though sleep persists and can be deeper, the phase is known as rapid eye movement, REM or paradoxical, sleep. It is a time when dreaming occurs and when memory may be secured. 

Wilkinson, R., Methods for research on sleep deprivation and sleep function. In, Sleep and Dreaming. (Hartmann,E., ed.). Boston Little and Brown, 1970. 

Solms, M. (2000). Dreaming and REM sleep are controlled by different brain mechanisms. Behav. Brain Sci. 23, 843-50 discussion 904-1121. 

Stickgold, R., Hobson, J. A., Fosse, R. Fosse, M. (2001). Sleep, learning, and dreams off-line memory reprocessing. Science 294, 1052-57. 

In REM sleep, there is a low-amplitude, mixed-frequency electroencephalogram, increased electric and metabolic activity, increased cerebral blood flow, muscle atonia, poikilothermia, vivid dreaming, and fluctuations in respiratory and cardiac rate. 

Those experiencing intoxication with Henbane feel a pressure in the head, a sensation as if someone were closing the eyelids by force sight becomes unclear, objects are distorted in shape, and the most unusual visual hallucinations are induced. Gustatory and olfactory hallucinations frequently accompany the intoxication. Eventually sleep, disturbed by dreams and hallucinations, ends the inebriation. 

Neuronal activity correlating with natural variations in conscious awareness from states of wakefulness, dreaming and non-dreaming sleep, and also with effects of drugs and diseases which affect consciousness. 

If dreaming is indeed stimulated by a mesocortical/mesolimbic DA mechanism, and not by the pontine cholinergic mechanism that triggers REM sleep, the question remains as to why dreaming and REM sleep should co-occur with such regularity ... 

All these drugs reduce sleep duration, decrease SWS and REM sleep, increase sleep latency and increase sleep fragmentation. They can cause a dose-related insomnia during use, and hypersomnia with increased dreaming and nightmares on withdrawal after chronic use. 

For some strictly occultist, fin de siecle discussions of dreams and the unconscious, see (among others) Blavatsky, Doctrine Secrete, vol. 1, 170 Bragdon, Four-Dimensional Vistas, chapter 6 ( Sleep and Dreams ) Carpenter, 72, 105 W. James, Varieties of Religious Experience, 405, 483-85 Ouspensky, Tertium Organum, 239. 

Another controversial but exciting area of research is the potential role of serotonin in sleep. 5-Hydroxytryptamine may trigger slow-wave sleep (non-REM sleep), whereas the muscarinic AChR and NE are involved in REM sleep (rapid-eye-movement sleep, paradoxical sleep, dream sleep). In addition to the aminergic regulation of sleep, recent research has identified several other presumed sleep factors delta-sleep-inducing peptide, sleep-promoting substance, interleukin-1, and muramyl peptides. 

Sleep disturbances and oppressive dreams become rarer. Daily mood swings with morning lows, lack of appetite and constipation cease. 

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