Narcolepsy is a disease that affects the Central Nervous System with many symptoms that differ between each person with no cure that has been found. Narcolepsy has become known as a sleep disorder although it affects each person through the wakeful hours of the day. Symptoms that affect people with narcolepsy are excessive daytime sleepiness, disrupted night time sleep and when those affected fall asleep during the day, they experience sleep paralysis and hypnagogic hallucinations. Not every person who is diagnosed with narcolepsy experiences it with cataplexy. Cataplexy is a loss of skeletal muscle tone that causes people to lose function and can cause dangerous situations. Most of the time when this occurs it is partial and causes the head
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Regardless of the severity of the attack, the person stays awake and aware of their surroundings unless it lasts so long that they fall asleep. Some of the cataplexy attacks can be caused by a severe emotions such as fits of laughter, anger, and even sexual arousal. With the effect of the emotions, it causes some daily activities to be off limits for the person affected due to the attacks that can be caused. It is estimated that between 60-80% of patients with narcolepsy also experience cataplexy (3). Narcolepsy can also be described as an individual entering REM sleep after only ten minute form falling asleep whereas normal individuals do not enter REM sleep until about 100 minutes of NREM and a full sleep cycle (NREM and REM together) is about 110-120 …show more content…
About 15-30% of these patients suffer from sleep disorders. Narcolepsy-cataplexy is the main non-respiratory sleep disorder that causes EDS behind only sleep apnoea. The most understood hypersomnia is narcolepsy-cataplexy syndrome. The reason this syndrome is the most understood is due to the explanation of hypocretin (orexins) in the pathophysiology of human narcolepsy-cataplexy. The diagnosis of narcolepsy-cataplexy now includes the criteria of low CSF levels of hypocretin due to findings in recent studies. These findings included the discovery of hypocretin genes associated with animals with narcolepsy and post-mortem examinations of human subjects that suffered from narcolepsy during their lifetime showed them having loss of hypocretin-producing neurons in the hypothalamus and low levels of hypocretin-1 in the cerebrospinal fluid (CSF). More than 95% of patients that have definite cataplexy and carry the human leucocyte antigen (HLA) DQBI*06:02 can be predicted to show a deficiency of cerebrospinal fluid hypocretin. Due to the tight association, it implies that the destruction of hypocretin-secreting cells may be destroyed by the autoimmune process with the involvement of infections agents. Various hypothalamic functions involve hypocretins and therefore narcolepsy-cataplexy could be used a model disorder to understand rapid eye movement (REM) and the
Regardless of the severity of the attack, the person stays awake and aware of their surroundings unless it lasts so long that they fall asleep. Some of the cataplexy attacks can be caused by a severe emotions such as fits of laughter, anger, and even sexual arousal. With the effect of the emotions, it causes some daily activities to be off limits for the person affected due to the attacks that can be caused. It is estimated that between 60-80% of patients with narcolepsy also experience cataplexy (3). Narcolepsy can also be described as an individual entering REM sleep after only ten minute form falling asleep whereas normal individuals do not enter REM sleep until about 100 minutes of NREM and a full sleep cycle (NREM and REM together) is about 110-120 …show more content…
About 15-30% of these patients suffer from sleep disorders. Narcolepsy-cataplexy is the main non-respiratory sleep disorder that causes EDS behind only sleep apnoea. The most understood hypersomnia is narcolepsy-cataplexy syndrome. The reason this syndrome is the most understood is due to the explanation of hypocretin (orexins) in the pathophysiology of human narcolepsy-cataplexy. The diagnosis of narcolepsy-cataplexy now includes the criteria of low CSF levels of hypocretin due to findings in recent studies. These findings included the discovery of hypocretin genes associated with animals with narcolepsy and post-mortem examinations of human subjects that suffered from narcolepsy during their lifetime showed them having loss of hypocretin-producing neurons in the hypothalamus and low levels of hypocretin-1 in the cerebrospinal fluid (CSF). More than 95% of patients that have definite cataplexy and carry the human leucocyte antigen (HLA) DQBI*06:02 can be predicted to show a deficiency of cerebrospinal fluid hypocretin. Due to the tight association, it implies that the destruction of hypocretin-secreting cells may be destroyed by the autoimmune process with the involvement of infections agents. Various hypothalamic functions involve hypocretins and therefore narcolepsy-cataplexy could be used a model disorder to understand rapid eye movement (REM) and the