An article in the Scientific American, by Jerome M. Siegel, focused on a
dangerous sleeping disorder called Narcolepsy. A Narcoleptic has Symptoms such
as cataplexy, which is the loss of skeletal muscle tone, and always feeling
sleepy during daytime hours. The people suffering from this disorder tend to
feel as if they hadn't gone to sleep for 48 hours. In addition, they sleep
poorly at night. Laughter, embarrassment, sudden anger, social interactions with
strangers, and sexual intercourse may trigger a cataplectic attack. A
Narcoleptic may even fall asleep at the most dangerous times. For example,
driving a car with this untreated disorder puts a person at high risk of an
automobile accident. The disorder makes it difficult for them to focus on
specific things, such as schoolwork or work in the workplace. Sleep paralysis
and hypnagognic hallucinations are among two other symptoms of narcolepsy. Sleep
paralysis is an ability to move when you fall asleep or awaken. This occurs
daily. On the other hand, hypnagogic hallucinations are dreamlike experiences
during waking that sometimes incorporate elements of the environment. These
symptoms occur when narcoleptics are most sleepy. In addition, not every person
suffers from the symptoms the same way. Also, this article pointed out that
Narcolepsy affects between one and one thousand and one and two thousand people
in the U.S. In contrast, one in 600 in Japan to one in 500,000 in Israel. It
also stated that the environment and ethnic backgrounds are the reason for the
number differences of these countries. The first signs of Narcolepsy appear in
the teens or 20's. The symptoms do get worse after a few years and then they
plateau. The causes or Narcolepsy is linked to a disruption of the sleep control
mechanism in our brain. Our sleep cycle normally has two stages, Rapid-Eye
movement Sleep (REM), and Non-Rapid Eye Movement Sleep (NREM). When we’re
experiencing NREM sleep, our muscles are relaxed, breathing is normal, the
cerebral cortex generates high-voltage waves and the energy consumed by the
brain is minimized. In contrast, in REM sleep, breathing and heart rate are
irregular, rapid eye movements occur; the cortex generates fast, irregular, low
voltage waves. Non-Narcoleptics tend to begin to sleep with NREM sleep. After 90
minutes or so, they're in REM sleep. When this happens, they experience loss of
muscle tone and dreamlike hallucinations that usually occur during REM sleep.
Researchers stated that being sleepy is normal, but it’s the large amount of
sleep in Narcoleptics that’s very abnormal. In the early 1970's, advanced
research in Narcolepsy began. Researchers discovered that some dogs showed that
they had very similar symptoms to human narcoleptics. William C. Demit of
Stanford University stated that the disease in the dogs was inherited by both
the mother and father to their offspring. In the 1940's, Horace W. Magnoun of
Northwestern University discovered when he electrically stimulated the medulla
(part of the brain stem) the muscle tone disappeared. He didn't connect his
studies to sleep. The studies in animals show us that the main function of the
muscle-tone control system in the medulla suppresses muscle activity in REM
sleep. In addition, it regulates the level of muscle tone in waking. This part
doesn’t work when the animals are moving. This explains the notion of when we
try to relax or “turn off” our muscles; we are actually trying to “turn
on” this specific section of the brain. REM sleep is the only time when normal
individuals lose all muscle tone. Another study by Frank Wu indicated that there
was another group of nerve cells in the brainstem called the Locus Coeruleus.
The locus coeruleus also plays a role in REM sleep and narcolepsy. It releases a
neurotransmitter called norepinephrine, which communicates with another neurons.
Both these nerve cells are active in animals in waking, but inactive when
they’re in REM sleep. In REM sleep the reduced amount of motor neurons
prevents them from moving or responding to their dreams. In cataplexy, the same
reduction prevents the motor neurons from responding to a narcoleptics attempt
to move. Researchers also concluded that unknown agents in the environment may
cause an autoimmune reaction that ends up damaging neurons in the brain that
control arousal and muscle tone. After narcoleptic symptoms occur, the patients
don’t get any worse or any better. This tells us that the damage might show up
for a short time; during the time the patients first develop the signs of this
sleep disorder. The brains supports cells later removed the damaged cells left
over from this sleeping disorder in the brain of the patient as they aged and
before most patients died. Siegel also supported his hypothesis by stating that
the degeneration in dogs was in the amygdala. The amygdala is a brain structure
involved in emotion and inducing sleep. The damage to the amygdala can cause the
symptoms of narcolepsy by inappropriately activating brain-stem circuits that
are undamaged. At this time, patients are given stimulants such as Ritalin and
Cylert or amphetamines. Their purpose is to reduce the sleepiness experienced by
the narcoleptics. These drugs only are affective for a short period of time and
cause side affects such as agitation, dry mouth, and anxiety. Doctors also
prescribe monoamine oxidase inhibitors. The purpose is to prevent cataplectic
attacks of narcolepsy. They’re still hoping for new treatments that will
improve the treatment of this disease. So far, the results of the research look
very promising.