REM rebound

Like the barbiturates, the benzodiazepines make it easier to fall asleep and to stay asleep through the night. However, they also suppress REM sleep, which can lead to REM rebound when they are discontinued. Tolerance to their sleep-promoting effects often develops after chronic use. Some long-acting benzodiazepines, such as flurazepam (Dalmane), are associated with pronounced hangover effects in the morning and are therefore problematic as sedative-hypnotics. Others, with a short-to-intermediate dnration of action, are more desirable as hypnotics. 

Many psychotropic drugs from various classes other than antidepressants have been shown over the years also to suppress REM sleep, but they do not have any antidepressant efficacy (Kales 1995). A review, however, indicated that, compared with other REM suppressant drugs, antidepressants produce a suppression of REM sleep that is larger, more persistent, and followed more frequently by REM rebound on drug discontinuation (G. W. Vogel et al. 1990). Thus, differences across drug classes indeed make antidepressants unique, with their REM suppressant effect paralleling only that of the arousal-induced REM sleep deprivation. 

Tolerance, physical dependence and addiction are possible with the benzodiazepines but less likely to occur than with barbiturates. In general this class of compounds does not cause induction. The potential for suicide is also lessened with these compounds. It has been estimated that physical dependence occurs in one person out of five million. Withdrawal symptoms are real but usually not life-threatening (fatigue due to REM rebound, dizziness, CNS disturbances). In general, benzodiazepines do not cause induction. 

Delta-9-tetrahydrocannabinol (THC), the main active ingredient in marijuana, reduces the amount of time spent in REM sleep, although tolerance to this effect can develop over time and the overall amount of time spent in REM sleep returns to normal levels. However, like people who constantly drink alcohol or take narcotic pain relievers, people who smoke marijuana daily can experience REM rebound after stopping the drug. 

But I won t budge. At some level, even in my deep REM rebound dream sleep, I am aware that my dream is a double vindication because it shows clearly how physiology and psychology intersect to form the general setting of the dream and how they interact to determine its particular dramatic form. So, yes, the wound clips really hurt, but, no, I don t really think they are real. 

In any case, it is quite clear that REM suppression is a robust consequence of prolonged alcohol abuse. This effect becomes increasingly problematic as the addiction is prolonged and the inevitable crisis is made worse even as it is postponed. Barbiturates, another CNS depressant sedative class of drug, offer a similar picture. When barbiturates are used experimentally to suppress REM—and they are very effective REM suppressants—their dose frequency and amount must be increased more and more over time until, at 3-4 weeks, it is virtually impossible to quell the REM rebound. When it finally occurs, it is characterized by such intense phasic activation (PGO waves) that the animals literally fly off their sleeping surfaces in convulsive spasms. 

Tolerance to the effects of marijuana clearly exist even though chronic users have described a reversed tolerance and claim that smaller doses of the drug are necessary to produce the desired effects. This effect is probably related to the manner of use and the expectations of the user. Chronic, high-dose cannabis users may experience an abstinence or withdrawal syndrome on abrupt discontinuation of use. Signs and symptoms include irritability, restlessness, nervousness, weight loss, insomnia, and rapid eye movement (REM) rebound. Onset of this syndrome is several hours after the last dose, and it lasts 4 to 5 d. Because withdrawal is not life-threatening, treatment involves little more than supportive therapy with short-term, low doses of benzodiazepines. 

To lessen the REM rebound effect, it is recommended that a person reduce barbiturate consumption by one therapeutic dosage over a period of five or six days, according to Physicians Desk Reference. Another method is to take two doses instead of three for a week. 

Drug administration is a common method to study neonatal RSD. Both subcutaneous injection and oral administration are applicable. The consequence of neonatal RSD by drug depends on the dose and the way that the drug was administered, such as the treatment duration (38,49). In contrast to an adult response, RSD in the rat at age 2 weeks or younger does not produce a REM rebound to REM suppression (50). Therefore, a dose-response relationship between drug and REM suppression is not as easy to differentiate as in adult models. For uniformity, an injection of a full dose once a day may not produce the same result as an injection of this dose split into a twice-daily dose (51). One to two weeks of total treatment duration with appropriate doses has been proven to be effective in producing long-term developmental abnormalities (38). 

Jimenez-Anguiano A, Baez-Saldana A, Drucker-Colin R. Cerebrospinal fluid (CSF) extracted immediately after REM sleep deprivation prevents REM rebound and contains vasoactive intestinal peptide (VIP). Brain Res 1993 63 345-348. 

Clonidine is one of the most widely used sedating medications in pediatric and child psychiatry practice, particularly in children with sleep onset delay and ADHD. It is a central alpha2 agonist. Pharmacokinetics show rapid absorption, with an onset action within 1 h, peak effects at 2-4 h and a half-life 6-24 h. Effects on sleep architecture are fairly minimal but may include decreased REM, so that discontinuation can lead to REM rebound. Clonidine has a narrow therapeutic index, and there has been a recent dramatic increase in reports of overdose with this medication. Potentially significant side effects including hypotension, bradycardia, anticholinergic effects, irritability, and dysphoria rebound hypertension may occur on abrupt discontinuation. Tolerance often develops, necessitating increases in dose. 

Most antidepressants decrease the quantity of REM sleep in the depressed patient, although it is difficult to say whether this is a reflection of the action of the drugs or due to the underlying pathology. Abrupt withdrawal of antidepressants, particularly the monoamine oxidase inhibitors, is often associated with REM rebound. 

REM rebound An increase in the rapid eye movement or REM stage of sleep when withdrawing from drugs that suppress REM time (Chapter 13). 

Hangover, REM Rebound, dependence, tolerance, excessive depression, respiratory depression, hypersensitivity... 

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