REMized clinically by a history of changes in the nature of the patients’ dreams
(they are more action-packed) and motor behavior (its is more action packed) during REM sleep that correlate with the
simultaneously occurring dream-mentation. The polysomnographic (PSG) findings consist of the intermittent appearance of
markedly increased tonic and phasic EMG activity during REM sleep Clinically, RBD usually responds exquisitely and persistently
to the nightly administration of clonazepam. While taking clonazepam, patients report that their dreams have reverted to a less
action-packed variety, and that their dream-enacting motor and verbal behaviors have ceased or are much less bothersome.
However, aside from some relatively subtle phasic EMG reduction,2 the REM sleep-related EMG activity remains relatively
unchanged following clonazepam administration. It is often impossible, by PSG study before and after clonazepam, to identify
which PSG is baseline, and which was performed following the administration of clonazepam.
It is clear from both animal experiments3 and from human conditions (notably narcolepsy and multi-system degenerative
disorders)4 that REM sleep may be associated with a lack of tonic or phasic atonia (REM without atonia) without there being
clinical symptoms of dream-enacting behaviors. Therefore, REM without atonia appears to be necessary, but not sufficient, for the
appearance of the full-blown RBD syndrome.
This raises an interesting question: What and/or where is the mechanism of action of clonazepam in the reduction of the
dream-related motor behavior during REM sleep? Is at the locomotor center, or some more rostral center(s) involved in the nature
REM Sleep Behavior Disorder
A 67-year old man developed a progressive sleep disorder in conjunction with a dementing illness over a five-year period. Limb
jerking, moaning, and talking appeared every night, and episodes of punching, kicking, falling out of bed, and running into furniture
occurred as frequently as three times nightly on as many as three nights per week. On one occasion, his wife saw him throw
punches while he dreamed of fighting a squirrel in an attic. The patient and his wife had received numerous injuries during his sleep
episodes. The onset of dementia was accompanied by aggressive wakeful behaviors that were controlled with the drug haloperidol;
however, this medication had no effect on his nocturnal behaviors. A computed tomographic brain scan was normal, and results of
a brief neurologic exam were unremarkable (Schenck 1987).
The above case study is not an abnormal description of what a person suffering from REM Sleep Behavior Disorder (RBD) goes
through each night. Other behaviors such as wrapping up their spouses in the sheets rodeo style, body jerking, leg twitching or
kicking, punching their partner, picking up a bedside telephone, leaping out of bed, or even leaving the bedroom entirely have all
been observed in RBD patients. RBD and the nocturnal actions that it provokes, may be associated with other neurological
problems, in some cases heralding the onset of something more serious. In a couple of reported cases, RBD has preceded
development of both Alzheimer’s and Parkinson’s disease (Schenck 1996), but it has also shown up in otherwise healthy,
neurologically sound people who behave quite normally in the waking world (Bamford 1992). What, then, is going on with people
suffering from RBD? The technical guidelines used to clinically diagnose RBD include the following:
1.Polysomnograph abnormality during REM sleep: elevated submental muscle tone (chin area) and/or excessive submental
2.Documentation of abnormal REM sleep behaviors during polysomnograph studies (prominent limb or truncal jerking;
complex, vigorous, or violent behaviors), or a history of injurious or disruptive sleep behaviors.(Schenck 1992).
Now that we are able to diagnose a patient as suffering from RBD, the next step is to figure out which specific areas
are responsible for producing these abnormal sleep behaviors. As it turns out, no one has yet pinned down a specific
mechanism for the action of RBD. However, the general area of interest appears to fall in the ponticular region of
the brain stem. It has been found in cats, that neuronal centers in the pontine tegmentum stimulate an inhibitory
outflow to spinal motoneurons that ordinarily is powerful enough to overcome a competing excitatory messages
calling for muscle tone during REM sleep. Thus, if this inhibition was disrupted from inadequate neuronal mass,
interruption of outflow pathways, or functional dysregulation, this would result in an increased level of muscle tone
(Schenck 1987). Thus, RBD is likely the result of the inability of inhibitory messages from the pontine tegmental
region to block the motor messages being sent out from other parts of the brain during REM sleep.
Interestingly, and is often the case with neurological problems, relief from the disorder can be provided without
thoroughly understanding the exact mechanism by which the disorder manifests itself. The potent benzodiazepine,
Clonazepam, has been wonderful in bringing RBD under control for those who suffer from it. The serotonergic
properties of this drug are likely what helps bring RBD under control (Schenck 1987). For a brief look at the role of
serotonin in sleep. Recognition of REM Sleep Behavior Disorder came first in the mid 1980’s and thus, their are
many research opportunities for looking at where this disorder shows up and the nature of the disorder itself. Since I
am a modest caffeine addict myself, it was interesting to stumble across an article relating RBD to caffeine abuse
(Stoltz 1991). The gentleman in question was quite a hard core coffee drinker, having 20-30 cups a day. During
polysomnograph observation the patient was found to have the classical definition of RBD (limb jerking, etc). He was
placed on clonazepam and advised to discontinue his coffee habit. He reported his symptoms to be gone, and after
being removed from the drug remained symptom free. Upon drinking coffee again, this time only about 1.5 cups per
week, he noticed more restlessness at night but did not have the acting out of dreams that he used to. Stoltz and
Aldrich concluded that in this particular patient, caffeine was associated with the expression of a latent tendency for
RBD, or that the caffeine “produced the syndrome de novo” (Stoltz 1991), which I believe means that it was directly
responsible for RBD expression. They do, however, admit that their follow up period has been short and further
observation must take place for confirmation of their postulations. However, the evidence they have gathered
indicates that it is probably a good idea for sufferers of RBD to be questioned about their caffeine intake, and
perhaps limiting this intake will help ease the symptoms of their RBD.
In another case of substance abuse relating to RBD expression, Schenck and Horwitz found that a patient had RBD
onset after stopping a long habit of alcohol and amphetamine abuse. Since both ethanol and amphetamines have been
shown to inhibit REM sleep, they hypothesized that this case could represent a pathological REM rebound effect
(Schenck 1988). The rebound effect is quite simple: if you do not get enough of something you need, REM sleep in
this case, when the chance arises, you will get more than you would normally get in a typical nights sleep so as to
‘replenish’ yourself with REM sleep. This whole rebound effect has been the cause of much speculation regarding
the purpose of REM sleep and whether or not it produces something our bodies need, or destroys something that, in
high levels, is bad for our health.
It is here that I will conclude this last of my essays devoted to sleep and sleep disorders. This independent study of
mine has been fabulous for looking into something that I had a lot of personal interest in and for learning a lot about
the mechanisms in our body that give us those beautiful hours of rest each night. This study also helped me
appreciate even more what a fine line it is that separates the healthy from the ill; how just a little malfunction can turn
an exciting dream enjoyed by one, to an act of violence which poses a threat not only to the dreamer, but those
around the dreamer as well. To think that, during sleep, we might be able to jump out of bed, hop in our car and drive
off into a tree or lake….it certainly poses questions in my mind about the way I perceive states of consciousness. I
hope to continue learning more about the functions of sleep and the purpose it serves in our survival. Good night and
The Stages of Sleep
Stage 1 of our sleep cycle is characterized by Theta Activity, pulses of 3.5 to 7.5 Hz. This is the transitional period between sleep
and wakefulness. After about 10 minutes, we move on to the next stage.
Stage 2 also shows the Theta Activity of stage 1, but also contains “sleep spindles”(small bursts of 12-14 Hz waves that occur
between 2 and 5 times a minute throughout stages 1-4 of the sleep cycle) and “K-Complexes”(sudden, sharp, high amplitude waves
which are unique to stage 2 sleep). If a person is forced awake at this stage, they will often deny that they’ve been sleeping. After
about 15 min. we move into the third stage of the sleep cycle.
Stage 3 is characterized by high amplitude Delta waves, which have a frequency below 3.5 Hz, mixed in with the Theta activity of
stages 1 and 2. There is a easy, ill-defined transition between stages 3 and 4.
Stage 4 is signaled by greater that 50% Delta Activity and typically lasts for about 45 minutes in a healthy individual. This is the
deepest part of our sleep cycle and is the stage in which nightmares typically come out of the closet to visit the hapless sleeper.
Stage 5 is better known as REM sleep and typically begins about 90 minutes after the onset of sleep. REM sleep is associated with
a desynchronicity in EEG readings reminiscent of the waking state, and has Theta waves as in stage 1 of the sleep cycle. A person
typically carries out storyline type dreaming in this stage of the sleep cycle(storyline dreams differ from nightmares in that
nightmares often are just a single, fixed and oppressive situation that the sleeper experiences whereas a dream often runs like a
movie) and is very easily waken up. Interestingly, except for the eyes and diaphragm, skeletal muscle tone is lost, essentially
paralyzing us while our eyes dart back and forth beneath our eye lids.
That, then, is a summary of the 5 stages of the sleep cycle. Stages 1-4 are commonly called the slow wave, or non-REM stages
and occur mostly in the first half of the night, which brings up another interesting little bit of information. As the night progresses,
we fail to sink as far down in sleep as we did in the previous sleep cycle such that the time we spend in stages 3 and 4 are reduced
while the time, or frequency in which we visit REM increases(Carlson).
In my very uneducated opinion, this is why we can get by with just a few hours of sleep. The majority of the really deep sleeping
comes in the first half of the night, so by getting 4 hours or so, we can still extract enough of the restorative benefits that deep
sleep gives us. There is a lot of literature available on how various conditions or chemicals effect the amount of time we spend in
either Slow-Wave or REM sleep, and I hope future essays will delve more fully into these subjects. Luckily for researchers
studying the subject, the origins in the brain responsible for sleep are still not fully understood and thus, facilitate continual probes
into how different parts of the brain are behaving during sleep and how to influence those parts to give us the best or worst
possible night of sleep. In the next section, I will look at a couple of hypotheses on:
There is nothing better for getting the day started off right than waking up in a good mood. This is especially true if we weren’t in
the best of moods when we went to sleep. To view the rest of this essay you must be a screwschool member click here to become