Narcolepsy Episodes

Narcolepsy episodes

Introduction

The brain is the headquarters of the relevant oscillators. Although he pointed out that hypothalamic lesions seemed to infer in circadian rhythms, he did not continue anatomically with this work. NSQ, in the hypothalamus, where the circadian oscillator is located. Sleep stadiums: the dream of slow or non -remit. 4 different phases. The dream of rapid ocular movements, or REM DREAM. Paradoxical dream. Circuits. Physiological Mechanisms Dream-Vigilia. (Special emphasis on the flip-flop mechanism.)

Developing

It is a unusual sleep disorder, which is inside the ReM dream. Narcolepsy is characterized by being episodes where, the person sleeps suddenly entering a few minutes into the REM phase. A person without disorder takes an average of 80-100 minutes to enter this sleep phase, because he has to go through the four phases of Nrem sleep. The duration of these events is as long as the duration of REM sleep, approximately.

The cause or origin of narcolepsia is not known, it is not yet clear if it is an autoimmune matter or if it is due to any other type of failure in another different mechanism. It is known that there is a loss of neurons in a localized site of the hypothalamus, these neurons are called hypocretins (HCRT-1) or orexins (Orexin-A). It is very important to take into account the loss of the hypocretins involved in the disorder, however, it is also necessary to say that it is not clear to what extent its deficiency defines the disorder.

There was talk that it can be or be an input autoimmune, explaining the massive loss of orexins in the hypothalamus. Some theories propose that there is a notable increase in REM pressure, decrease in the threshold in the transition to the REM sleep, deregulation of the brain mechanisms that normally coordinate the REM Dream. The Onset of the disorder is established around 16 years, not being necessary to take this age. It is hypothesized that it can be something immune, however, there is no record of this.

Obesity and weight gain among people with disorder. Cardinal Symptomatology: Catoplejía. Not all narcoleptic cases present this symptom. In fact, between 20 and 50% of the total cases diagnosed do not present it. It is also true that, within the disorder, most cases that do not present this cataplejía are usually badly diagnosed or without diagnosing. Sleep paralysis. Excessive daytime sleepiness. Hypnagogical hallucinations. Over time, this symptomatology, eds and cataplejía, however, improves the dream more and more.

It differs between two types of narcolepsy: type I. Narcolepsy with cataplejía. The pathognomic symptom par excellence is cataplejía. Catopling is the loss of muscle tone, they trigger emotions such as laughter or surprise. Mostly positive emotions. Type II. Narcolepsy without cataplejía. Much more heterogeneous. Both types differ by the presence or absence of cataplejía, however, there are also biological differences at oxins, or also called hypocretins. 

While in type I they are below the lower limit, 110 pm/ml, in the CSF, in type II we find normal levels. There is still much to discover about type II narcolepsy, since its operation is really unknown. There are times when it develops until it becomes a hypersomnia, or that evolves in such a way that it ends up being classified as type I.

Sleep paralysis, which can be given both to awakening and as falling asleep, as well as hypnagogical and hypnopompic hallucinations occur as part of the symptomatology, but it is not something exclusive to narcolepsia, it can occur in the general population, but it istrue that it is much more severe when this disorder is suffered. It is more difficult to know how Tii will develop than you. In fact, Tii sometimes presents cataplejía, having to relocate diagnosis to you.

Weight gain is symptomatology that occurs at the beginning of the disease. Patient cut treatments are usually made, since not everyone has the same symptomatology, or at least not in the same degree of urgency. The pharmacological treatment that is being carried out must be taken into account, since it will not be the same if it is being stimulating or not. For taking into account activities with some risk such as driving. Talk about what happens when they laugh. How could you solve.

What is usually used are: sleep control strategies. To program short naps throughout the day, or a long after food. Avoid sedentary activities. So they don’t sleep while they do them. Drugs used in the treatment of disorder. The pharmacology of the treatment of narcolepsy, as a disorder, does not have a medication that is capable of acting, in its entirety, on the disorder as such. It is not very clear, as we saw, the origin of narcolepsia, there are hypotheses about the loss of hypocretins.

As well as about the gene that is believed to be involved, but it is not known with total security what its origin is. In these cases, what is done is to follow a pharmacological treatment that focuses on symptomatology. We can see a difference of two large groups of drugs: on the one hand, those who are going to treat excessive diurnal sleep (eds), and, on the other hand, those who are focused on treat. Amphetamines considered as third line treatment for NT1. What they do is activate the increase in the concentration of certain monoamines, da and ne.

conclusion

Methylphenidate is used for excess day sleep, (EDS). It is the second therapeutic line treatment, when neither fadofinil nor sodium oxibato works. Much side effect, Pitolisant, is used for excess day sleep, (EDS). Sodium oxibato, improvement of sleep quality, increases slow sleep waves, anti -attack effects, fashion, first -line treatment in reducing symptomatology related to excess day sleep. For cataplejía. Sodium oxybate, is the best treatment, can be used for EDS and cataplejía. N1 and N2.