6, 7 Hcrt1, which contains 33 amino acids, and Hcrt2, which contains 28 amino acids, are both encoded by the preprohypocretin gene. The Hcrt peptides were discovered in 1998. Finally, we will discuss the implications of these findings for the treatment of narcolepsy. We will review recent discoveries linking loss of Hcrt neurons to the genesis of human narcolepsy. In this paper, we will describe the anatomy, physiology, neurochemistry and behavioral role of the Hcrt system. In 2000, however, two simultaneously published papers determined that most human narcolepsy was linked to a loss of hypothalamic cells containing hypocretin (Hcrt, also known as orexin). It remains to be determined whether most cases of excessive sleepiness without cataplexy that are not attributable to another cause result from the same underlying disease process as most cases of narcolepsy with cataplexy.įor the 120 years following the identification of narcolepsy by Westphal 2 and its naming by Gelineau, 3 the cause of narcolepsy was a mystery, and the disorder was often attributed to psychiatric causes. Some patients classified as narcoleptic according to current sleep nosology 1 do not show cataplexy, and many experience this symptom only rarely. In most patients, sleepiness and cataplexy are the main complaints. The onset of narcolepsy is typically in the second or third decade of life. Narcolepsy is characterized by excessive daytime sleepiness, disrupted night-time sleep, cataplexy, sleep paralysis, hypnagogic hallucinations, and short latency from waking to rapid eye movement (REM) sleep initiation. Future treatments are likely to include Hcrt or Hcrt agonists to reverse the underlying neurochemical deficit. Sodium oxybate produces both reductions in cataplexy and improved waking alertness. Current treatments for narcolepsy include stimulants to combat sleepiness and antidepressants to reduce cataplexy. Cataplexy is caused by an episodic loss of activity in noradrenergic cells that support muscle tone, and a linked activation of a medial medullary cell population that suppresses muscle tone. Sleepiness results from the reduced activity of monoaminergic, cholinergic and other cells that are normally activated by Hcrt neurons, as well as from the loss of Hcrt itself. These cells normally serve to drive and synchronize the activity of monoaminergic and cholinergic cells. The underlying cause of most cases of human narcolepsy is a loss of neurons that produce hypocretin (Hcrt, also known as orexin). Narcolepsy is a neurological disorder that is characterized by excessive daytime sleepiness and cataplexy-a loss of muscle tone generally triggered by certain strong emotions with sudden onset.
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