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.