We should pay enough attention to excessive sleep, because excessive sleep for any reason can extremely affect our daytime concentration, such as napping in class, at work, or on the highway can have very serious consequences and cause great social and economic losses. In the United States, more than 100,000 motor vehicle accidents each year are caused by drowsy drivers. And like the Three Mile Island nuclear power plant leak in Pennsylvania, the Exxon Valdez tanker spill, the Bhopal methyl isocyanate gas leak in India and the Challenger space shuttle accident are due to staff napping, inattentiveness caused by. The most common cause of all “oversleeping” patients is actually due to insufficient sleep. In fact, on average, we sleep 20% less than previous generations, but there is no clear evidence that they (previous generations) need more sleep than we do, or that we need less sleep than they do. The non-sleep-deficit causes of excessive sleep symptoms are basically identified as sleep disorders, and most of these patients will also have obstructive sleep apnea (OSA) or episodic sleep (narcolepsy). Obstructive sleep apnea is the most common cause of excessive sleepiness, with more than 2% of adult women and 4% of adult men suffering from this disorder. It is most commonly seen in loud snorers and is characterized by collapse of the upper airway during sleep, which leads to a decrease in blood oxygen levels, and the patient is thus awakened to restore the upper airway. Patients are constantly awakened throughout their sleep (up to 100 times per hour), which greatly affects their sleep quality, but they are not actually aware of this brief awakening process. Our in-depth study of obstructive sleep apnea revealed that it does not affect only middle-aged overweight men, as we first thought, but also children and adolescents (about 3% of children and adolescents suffer from it), women and people who are not overweight. Obstructive sleep apnea is now known to be a risk factor for hypertension, and is also associated with heart disease and type II diabetes, among other diseases. It has also been found that obesity, which has ravaged many countries, is a risk factor for obstructive sleep apnea. 2, episodic sleep disorder episodic sleep disorder is a relatively rare neurological disorder, an average of 1 in 2,000 people will suffer from this disorder. The most important characteristic of people with episodic sleep disorder is that although they get enough sleep the night before, they tend to fall asleep during the day the next day, especially when they are sedentary or engaged in a dull job. Episodic sleep is the only disorder that we currently know of that represents a sleep-wake disorder. If these symptoms are ordered by frequency, the most frequent symptom is sudden collapse (cataplexy), a sudden, brief episode of loss of muscle tone; the next most frequent symptom is pre-sleep hallucination (hypnagogic hallucination), a hallucination that occurs just before falling asleep, and The second symptom is hypnagogic hallucination, which occurs just before falling asleep, and hypnopompic hallucination, which occurs near the end of sleep; the third symptom is sleep paralysis, which occurs when patients wake up and find that they are unable to move other parts of their body except for breathing and moving their eyes; the fourth symptom is spontaneous movement (automatic behaviour). The fourth most frequent symptom is automatic behaviour, and the fifth most frequent symptom is sleep disruption at night. We have learned something about the separation of sleep states through the study of episodic sleep disorders: the waking and sleeping states are not completely separated from each other, and sometimes one state may intermingle with the other at an inappropriate time, leading to very serious consequences. More importantly we also found that patients with episodic sleep disorder do not sleep more than the general healthy population, they just cannot have very clearly distinguishable waking states, REM sleep states and NREM sleep states as normal people do. Various spontaneous activities, such as driving past a certain exit on the highway that one is supposed to leave, or putting clothes in the refrigerator, etc., indicate that the patient is in a situation where the waking state is mixed with the NREM sleep state. Patients with episodic sleep disorder are able to perform very complex activities, but they do not have sufficient cognitive ability to recognize the activities they are performing. Both sleep paralysis and sudden collapse occur during REM sleep, and they are associated with loss of muscle tone and arousal at this time. Sudden collapse can occur if the dystonic state “intrudes” into the awake state. Sleep paralysis can occur if the loss of tone state persists in the awake state. Hallucinations in the waking state or daytime hallucinations are actually caused by the dream state associated with sleep entering the waking state. The nighttime sleep disruption is also a manifestation of the loss of control of sleep-wake state boundaries in patients with episodic somnolence. In addition to sudden collapse, sleep paralysis, pre-sleep hallucinations, and pre-wake hallucinations are common symptoms in other people who do not suffer from episodic sleep disorder, especially when they lack sleep. We used to think of episodic sleepiness as a psychiatric disorder and have developed a set of psychodynamic theories (the main one being avoidance behavior) to explain the symptoms of episodic sleepiness, such as sudden collapse, sleep paralysis, and so on. But now we know that episodic somnolence is actually a disease caused by a disorder of the central nervous system. Episodic sleeping sickness has a very clear genetic cause, with more than 90% of people with episodic sleeping sickness carrying the HLA-DR2/DQ1 gene (now called HLA-DR15 and HLA-DQ6), compared to less than 30% of the normal population. We now believe that the DQ6 protein encoded by the DQB1*0602 region and the DQA1*0102 region of chromosome 6 is a molecular marker for episodic sleeping sickness. However, this association between DQ6 proteins and episodic sleeping sickness is inconsistent across races and is the most medically known HLA-linked phenomenon associated with the disease. Episodic sleeping sickness has a genetic predisposition. Although the incidence of episodic sleeping sickness is only 1 to 2 percent, it is still 10 to 40 times higher than in the general population. It is clear that there are genetic factors involved in the development of episodic sleeping sickness, but these genetic factors are not sufficient to cause the development of episodic sleeping sickness, nor are they necessary for the development of episodic sleeping sickness. One of the most important and exciting discoveries in the field of sleep-related medical research has been made through animal experiments on episodic sleepiness. In these experiments, we found a relationship between hypocretin-1, an appetite protein, and episodic sleepiness. Hypocretin-1 is a neuropeptide protein that is only produced by certain cells in the hypothalamus. It has been found that these neuronal cells that secrete hypothalamic secretin 1 protein appear to be lacking in the brains of patients with episodic sleeping sickness, and that the loss of these cells may be due to immune factors. In the cerebrospinal fluid (CSF) of HLA DQB1*0602 positive patients with narcolepsy, the concentration of hypocretin 1 protein is so low that it cannot be detected at all. However, other clinical conditions that may require differentiation from episodic sleeping sickness do not exhibit a lack of hypocretin 1 protein in the cerebrospinal fluid. This suggests that measuring the concentration of hypocretin 1 protein in the cerebrospinal fluid of patients is a very effective method of confirming the diagnosis of episodic somnolence.