REM Sleep Deprivation
The most notable finding from REM deprivation studies in humans is that the number of attempts that a person makes to go into REM while asleep greatly increases. After the deprivation is complete, the deprived person will experience a REM rebound, which is a significant increase in the percentage of time spent in REM over normal levels. This REM rebound can last for several nights. REM deprivation in humans is associated with a significant increase in stage 1 NREM during the deprivation period. Levels of stage 2 and 4 sleep remain relatively normal.
The initial REM deprivation study done by William Dement was reported in an article entitled “The Effect of Dream Deprivation”. Dement choose this title because at that time the relationship between dreams and NREM sleep was not clear, while dreams and REM tended to strongly correlate together. We now know that REM deprivation and dream deprivation are not synonymous. All REM periods do not yield reports of dreams, while some NREM periods do. Thus, dreams do not occur exclusively in REM. Nonetheless, Dement’s paper included reports of observances that are controversial to this day. The findings were that mild psychological disturbances developed. These disturbances included anxiety, irritability, and difficulty concentrating. Also noted was an increase in appetite. All of these psychological nuances were not observed in control participants, and in the REM deprived participants disappeared after a recovery night (of REM rebound. Studies including REM deprivation since Dement’s have reported participants experiencing confusion, suspicion, withdrawal, and being “less well integrated and less interpersonally effective”. The overall impression of REM deprived person is of anxiety, insecurity, and being introspective.
A crucial methodological point is that over the course of 4 nights REM deprivation, the authors estimated that the deprivation eliminated 65-75% of REM. The reason that so much REM (up to 1/3 of the normal amount of REM) was still experienced by participants was because once a person enters REM, it may take some time to identify that stage of sleep as REM. As a result, by the time the experimenters positively identify a person as being in REM, up to a minute or more could have elapsed.
While several studies suggest that REM deprivation can have adverse consequences, there are a number of studies that fail to confirm these findings. The most accepted position currently is that REM deprivation is not deleterious, and can even be beneficial. After it was demonstrated that REM deprivation did not produce mental instability, a question was raised concerning any positive consequences of REM deprivation. The following pieces of evidence suggest a link between depression and REM: Some symptoms of depression (decreased interest in sex and general pleasure seeking activity, decrease in aggression, and possibly decrease in eating) are opposite those of REM deprivation, which tends to produce “an excitability in the brain substrate for drive-related behavior”. Drugs that increase REM can produce depression. Antidepressants that can improve endogenous depression suppress (but not eliminate) REM. Of 25 drugs that are currently used to treat depression, 22 suppress REM. The other three anti-depressants have no effect on REM, but can still be effective in alleviating depression.
Animal studies of REM deprivation are markedly different than human studies. One of the most common ways to REM deprive a rat is to put the animal in a position (e.g., on a small platform) where it is able to experience slow wave sleep, but not REM. This is because muscle tone is still present during NREM sleep, and allows the animal to sit on the platform. The rat will be awakened immediately upon entering REM because the muscular atonia that prevails during REM will cause the rat to fall into a tank of water, waking it. Less noxious methods of REM depriving rats have recently been developed. (LINK TO Research methods).
There is evidence that REM sleep deprivation in animals has more serious consequences than in humans. This may be because the length of time animals have been REM deprived for is much longer than humans. Evidence suggests REM deprivation in rats impairs learning of new material, but does not effect existing memory. In one study, rats did not learn to avoid a painful stimulus after REM deprivation as well as they could before the deprivation. No learning impairments have been found in humans undergoing one night of REM deprivation. REM deprivation in rats produces an increase in attempts to enter REM, and after deprivation, REM rebound. In rats, as well as cats, REM sleep deprivation increased brain excitability (e.g. electrical amplification of sensory signals), and which lowered the threshold for waking seizures threshold. This increase in brain excitability seems to be similar in humans. One study also found a decrease in hindbrain sensory excitability. The hindbrain was less receptive overall to information in the afferent pathway, because of the increase in the amplification of those pathways that it is receptive to.
Ultimately, REM deprivation in rats is fatal. One of the main symptoms during this time was hypothermia, despite observable effects to increase heat production (e.g., by eating). This has led to the hypothesis that the function of REM is to prevent heat loss. This is interesting because one of the state characteristics of REM is loss of thermoregulation.
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Overview: Intro | SWS | REM | SWS vs REM | Effects