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REM sleep pressure

The ideas behind this question are not new and the answers are not yet clear, probably because of the complexity of drug effects and the intensely interactive nature of the intrinsic neuromodulatory systems. We should remember that from the earliest days of modern sleep research in the 1960s, studies showed that REM sleep parameters were normal in schizophrenia. This argued against the idea that increased REM pressure underlay schizophrenic psychosis and condemned the hypothesis to an early and perhaps premature oblivion. [Pg.239]

The other changes suggest a similar shift toward sympathetic activation. In Aserinsky and Kleitman s first published description of REM sleep (Science, 1953), they reported that heart rate and respiratory rate both increased. Soon thereafter, Frederick Snyder showed that systolic blood pressure also increased, sometimes to alarming levels, in REM. Psychotogens raise heart rate and blood pressure, too. [Pg.264]

Third, in REM sleep, at least, it is a well-established fact that the tonic increases in heart rate and blood pressure are associated with brain stem mediated activation and that the dramatic phasic blood pressure and heart rate increases are correlated with the clusters of eye movement that periodically punctuate each REM period, whereas heart rate pauses occur in the inter-REM intervals. [Pg.265]

Recent studies of dream emotion prove Kliiver and Bucy s point. They support the idea that it is the brain itself—and more specifically the limbic brain—that may generate fear (the number one dream affect), cosmic elation (number two), and anger (number three). To round out the picture, there are reports that an intensification of these same emotions colors the dreams of patients with temporal lobe epilepsy. Subjects may indeed evince rapid heart action, increases in blood pressure, and rises and falls of breathing efforts in REM sleep, but these are not sensed as part of the subjective experience of dream emotion. [Pg.293]

Noradrenaline - the EEG is aroused by stimulants such as the amphetamines and methylphenidate whereas drugs such as reserpine which deplete brain noradrenaline have the opposite effect. Similar effects to the stimulants may be obtained by the electrical stimulation of the locus coeruleus which has been shown to decrease in activity during the REM sleep phase of the sleep cycle. The precise role that noradrenaline plays in sleep is uncertain. While it may be involved in sleep induction, noradrenaline also has many other physiological functions including control of the heart rate, blood pressure, autonomic activity, etc. which play a role in the entraining process. [Pg.244]

This is quite different from the more typical experience that most of us have had at one time or another - to awaken from a dream in which we were trying to escape from imaginary pursuers, absolutely terrified. In the second case, which is more likely to occur in REM sleep, we have formed the perceptual scenario of an attack situation from which we are attempting to flee, and our emotion is appropriate to the dreamed action. Figure 7 shows the activation that is not in our control (i.e. autonomic activation) which is normally associated with REM sleep. As can be seen, increases in heart rate, blood pressure, and respiratory rate can begin in NREM sleep. [Pg.81]

Sleep cycle with activation. (A, B) Ultradian sleep cycle of NREM and REM sleep shown in detailed sleep-stage graphs of 3 human subjects (A) and REM sleep periodiagrams of 15 human subjects (B). In (C) one such sleep cycle is shown to illustrate the changes in eye movements (EM), EEG, blood pressure (SBP), respiration (resp.), pulse, and body movements (BM) that are associated with REM. [Pg.82]

Tranylcypromine (Parnate) Blocks metabolisni of biogenic amines (norepinephrine, serotonin, dopamine) increasing the synaptic concentration of these transmiTters. Suppresses REM sleep. Used tu tiedt depression if tricyclic antidepressants fail and when electroconvulsive therapy fails or is refused. Also used to treat narcolepsy, phobic/anxiety states and Parkinson s disease. Hepatotoxicity, excessive CNS stimulation, orthostatic hypoten -sion. Overdose may cause agitation, hallucinations, hyperreflexia, hyperpyrexia, convulsions, altered blood pressure. ... [Pg.38]

REM sleep, together with modifications in the autonomic functions (heart rate, blood pressure, vasoconstriction, and respiratory rate) ... [Pg.198]


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See also in sourсe #XX -- [ Pg.111 ]




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