Narcolepsy term papers

It usually occurs after eating, but may occur at any time, each sleep episode lasts for about fifteen minutes. The person then awakens refreshed, only to become tired within the next hour or so. I can somewhat relate to how narcoleptics feel because I have a somewhat similar, only not as severe sleeping disorder, sleep paralysis.

Narcolepsy represents a neurological problem of sleep wake mechanisms in the brain. As a result of the muscle paralysis, various muscles in the body are affected. Also, because of the dream-like hallucinations the brain and mental status of the person is also affected.

Though not all of these symptoms occur in all cases, in fact all of them occur in only ten percent of overall narcolepsy cases. Cataplexy is the most common symptom associated with narcolepsy, afflicting over seventy percent of patients. Sleep paralysis comes next, occurring in 30 percent of cases, and hallucination comes last, which is present in only 25 percent of cases. Narcolepsy is usually diagnosed between the ages of fifteen and twenty-five.

Unlike most diseases, narcolepsy affects men and women in equal numbers. Not only that, but the dream-like hallucinations that comes along with narcolepsy have caused some people to be driven mad, for they cannot discern what is reality and what is not. There are many ways of treating narcolepsy, both medical and non-medical. Some non-medical ways for narcoleptics to prevent sudden sleep attacks are; planning naps so that their body will feel rested when they need to stay awake.

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They can also take forced naps when they are drowsy to help them function normally. Consuming caffeine in moderation can also help a narcoleptic stay awake. Some medical treatments used for narcolepsy are stimulant pills such as dextroamphetamine, and methylphenidate. Recent research has revealed that narcolepsy with cataplexy is caused by a lack of hypocretins , key brain chemicals that help sustain alertness and prevent REM sleep from occurring at the wrong times.

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Hypocretins are neurotransmitters , chemicals that transmit signals from a neuron to a target neuron. Hypocretins are only produced by a small cluster of neurons in the hypothalamus , a brain region located roughly behind the eyes and between the ears. Of the billions of neurons in the brain, only about ,—, produce hypocretins.

Hypocretins are released from these neurons during wakefulness and bind to specific hypocretin receptors on target neurons, which increases the activity of these neurons. Hypocretins were first discovered in when two research groups independently identified them in the brain. Hypocretins and brain function In individuals without narcolepsy and whose sleep is well regulated, hypocretins are released during wakefulness and increase activity in target neurons that promote wakefulness and suppress rapid-eye-movement REM sleep.

In people who have narcolepsy with cataplexy, most of the hypocretin-producing neurons die off. The consequent lack of hypocretins results in lasting sleepiness and poor control of REM sleep.

What is narcolepsy?

In fact, REM sleep can become so poorly regulated that the paralysis or dreaming that normally occurs only in REM sleep can mix into wakefulness, causing cataplexy and dreamlike hallucinations. Though much has been learned about narcolepsy with cataplexy, considerably less is known about the cause of narcolepsy without cataplexy. Most likely, it is caused by less severe injury to the hypocretin neurons, resulting in fewer and less severe symptoms. See Key discoveries below for more on some of the studies that have shed light on the role of hypocretins in narcolepsy.

How hypocretin loss affects the brain In addition to revealing the normal role of hypocretin neurons in the brain, research has provided many insights into how a loss of hypocretin signaling causes sleepiness and cataplexy. During normal wakefulness, hypocretin neurons send signals that produce long-lasting increases in the activity of many other neurons essential for sustaining alertness and wakefulness. These neurons include those that produce key neurotransmitters such as norepinephrine, serotonin, and dopamine.

In narcolepsy, the loss of hypocretins may result in reduced or inconsistent activity in these target neurons. As a consequence, people with narcolepsy can be fully alert at times, but have great difficulty sustaining this alertness for long periods of time. Cataplexy and sleep paralysis are unusual states in which the brain circuits that produce paralysis during REM sleep become active during wakefulness.


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During REM sleep, most muscles are paralyzed by circuits in the lower brainstem and spinal cord. These paralysis circuits are normally blocked by norepinephrine and serotonin during wakefulness.

Narcolepsy - Brain Foundation

With loss of hypocretins, levels of these two neurotransmitters may be lower, permitting paralysis to occur even during wakefulness. This observation provides the main rationale for treating cataplexy with antidepressants that increase brain levels of norepinephrine and serotonin. Ongoing research is also beginning to reveal how cataplexy may be triggered by positive emotions. The amygdala and prefrontal cortex are brain regions that regulate emotional responses and connect with the paralysis pathways in the brainstem.

Neurons in the amygdala and prefrontal cortex are active during cataplexy, and inactivating either of these regions markedly reduces cataplexy in mice with narcolepsy. As these triggering pathways become better understood, it may be possible to target them with new medications. Understanding how narcolepsy develops Over the past several years, researchers have made good progress in understanding the process that kills the hypocretin neurons.

Genetic factors clearly play a role. Normally, the immune system kills off bacteria and viruses. These discoveries suggest that narcolepsy is an autoimmune disease in which the immune system accidentally kills off the hypocretin-producing neurons. Genetics Dr. Scammell discusses a gene that appears to play a role in narcolepsy with cataplexy.

The Science of Narcolepsy

Researchers are now beginning to identify some of the triggers for this autoimmune attack on the hypocretin neurons. Just after the onset of narcolepsy, people tend to have increased levels of antibodies against streptococcus, the bacteria that causes strep throat and other infections. The most compelling evidence that an immune process can kill the hypocretin neurons comes from a recent increase in narcolepsy in Finland and other northern European countries.