IndexIntroductionNarcolepsy BasicsNarcolepsy in AnimalsNarcolepsy and Circadian RhythmsNarcolepsy and Emotions (1)Conclusion“I've heard that sometimes one version of you has to die before another version more enlightened I could have been born. I think that's true after seeing my dead body walking around. “Say no to plagiarism. Get a tailor-made essay on “Why violent video games should not be banned”? Get an original essay Introduction With over seven billion humans in the world, it is clear that human experience is a relatively independent thing and unique. However, there are some aspects of being human – or even being alive – that bind people and animals alike. The need to breathe, sleep, eat and propagate the species transcends time, culture and even taxonomic diversity mind, some processes constitute an interesting study of the functioning of both animals and humans. Relatedly, the phenomenon of narcolepsy in living beings – both humans and animals – constitutes a unique study of biological and circadian processes. Narcolepsy is the phenomenon of daytime drowsiness, cataplexy, and other related symptoms such as fragmented sleep. Much research has been conducted on this topic, so knowledge about narcolepsy – its characterizations, symptoms, diagnosis and physiology – is well established. This discussion paper examines narcolepsy both generally and in terms of three specific patterns of narcolepsy and how it manifests. First, the article provides an overview of narcolepsy, including its symptoms, diagnosis, and physiology. Secondly, the article discusses narcolepsy in animals; this second section is mainly about rats and mice. Third, the study examines narcolepsy in relation to the circadian rhythm and asks whether narcolepsy manifests itself equally during the day and at night. Finally, the article discusses the role of emotions in narcolepsy and what types of emotional feelings can serve as trigger events for a narcoleptic attack. While this discussion is not exhaustive, examining these various aspects of scientific knowledge related to narcolepsy will go a long way in establishing an understanding of the phenomenon. Narcolepsy Basics First, the general discussion will benefit if we move on to an overview of what narcolepsy is in scientific terms. and how it works. As noted above, narcolepsy is characterized by various symptoms, such as “excessive daytime sleepiness, cataplexy, [and] fragmented sleep” (Baumann, Bassetti, & Scammell, 2011, 5). In simple terms, cataplexy is a medical condition that causes individuals to collapse (while remaining conscious) after the onset of a very strong emotion or physical response to this emotion, such as laughter (Baumann, Bassetti, & Scammell, 2011 , 5). . As will be discussed, due to the confluence of both cataplexy and fragmented sleep, these two symptoms are believed to be indicators (if not pre-existing conditions) of narcolepsy. However, the debate is still open on this front. As the authors cited above state, “The prevalence of narcolepsy without cataplexy is largely unknown, as an adequate population-based study would require an MSLT of all subjects”; however, in case studies, it is also noted that patients with narcolepsy without cataplexy account for anywhere from 20% to 50% of all narcolepsy cases. Clearly, although there is some connection between cataplexy and narcolepsy, scientific knowledge so far has not established a direct link between the two types of symptoms. That isdespite the fact that scientists have been studying narcolepsy for over a century. As Baumann, Bassetti, and Scammell (2011) note, “until recently, its cause remained a mystery” (5). The biggest breakthrough occurred in 2000, when two independent research groups discovered the physiological cause of narcolepsy: “a selective loss of neurons in the hypothalamus that produce hypocretineuropetides (also known as orexins)” (Baumann, Bassetti and Scammell, 2011, 5). In other words, narcolepsy is not caused by a chemical imbalance or chemical response, but by the pre-existing configuration of neurons in an individual's brain. It was with this “innovative perspective” that “narcolepsy research has advanced in leaps and bounds, with new discoveries every year that have improved our understanding of the disorder” (Baumann, Bassetti, & Scammell, 2011, 6). Despite these advances, the main research question that remains is what "kills" these neurons that cause narcolepsy in the first place. But what are the consequences of narcolepsy? One of the main symptoms of narcolepsy is that it has "its major onset in adolescence" and often worsens with "the onset of puberty", with the main experience for early-onset patients being non-restorative sleep (Wehrle & Bruck , 2011, 32). The consequence of this timeline is as much social as it is psychological: “The widespread and often severe psychosocial effects are due in part to a delay in diagnosis. A common consequence was severe academic failure. Symptoms affected work and life goals. Increased social withdrawal and lower self-esteem were often evidence. Drowsiness was a problem for both public transport and driving, substantially impacting independent mobility” (Wehrle & Bruck, 2011, 32). With this in mind, it is clear that scientific knowledge about narcolepsy should be increased to improve recognition of the condition. As the authors state, “increased awareness of the disease and the provision of psychoeducational support, together with early diagnosis and medical treatment, are strongly justified to prevent the most common educational and psychosocial problems, including the risk of depression” (Wehrle & Bruck , 2011, 32). This is confirmed by another academic article, which also notes the rate of onset of narcolepsy: “it occurs in approximately 1 in 2,000 individuals, and usually begins in adolescents and early twenties” with a lifetime prevalence of 1 to 18 for every 1,000 people ( Kishi et al., 2004, 117; Ohayon et al., 2002). These two academic sources make it clear that, although a great deal of knowledge exists about narcolepsy, scientists are constantly learning more. The three specific models of narcolepsy discussed below should show how this knowledge is growing and what it means for narcoleptic patients. Narcolepsy in Animals First of all, examining narcolepsy in animals is a good first step in building knowledge of the phenomenon. The prevalence and symptoms of narcolepsy in animals can contribute greatly to building scientific knowledge about narcolepsy in humans. As one source states, “To facilitate further research, it is imperative that researchers reach a consensus regarding the assessment of narcoleptic behavior and EEG phenomenology in these models” – including animal models (Chen, Brown, McKenna & McCarley, 2009, 296 ). To address this issue, the authors examine various models of narcolepsy. The first concerns domestic animals such as sheep, horses, dogs and even bulls (Chen, Brown, McKenna & McCarley, 2009). The authors focus on dogs as the primary source of information on narcolepsy, as dogs have the highest ratehigh level of narcolepsy, particularly with cataplexy (Chen, Brown, McKenna & McCarley, 2009). The authors have a specific view regarding the canine model of narcolepsy: "Pedigree analysis indicated an autosomal recessive mode of inheritance with complete penetrance... it became clear that both familial and sporadic forms of canine narcolepsy exist" (Chen, Brown , McKenna & McCarley, 2009, 297). This insight provides one of the first steps towards understanding not only why narcolepsy occurs, but why there is a deficiency of the necessary neurons in the hippocampus in the first place – i.e. the genetic mutation. However, the authors clarify that “it should be noted that genetic mutation alone may not be sufficient for the full symptomatic development of narcolepsy,” since dogs treated with anti-inflammatory agents at an early age have reduced both cataplexy and narcolepsy (Chen, Brown , McKenna & McCarley, 2009, 297).The authors also delve into specific environments and triggers that can lead to the onset of narcolepsy in animal models. For example, the authors found that there were three distinct stages of cataplexy in dogs: “The early stage involved muscle atonia, waking-like EEG, and visual tracking… The second stage resembled REM sleep with hippocampal theta activity… The late stage was characterized by EEG with mixed frequency and amplitude before the transition to awake or asleep” (Chen, Brown, McKenna & McCarley, 2009, 298). These canine models represent a good start for researchers. A good resource for narcolepsy research are rodent models of the phenomenon. According to one study, episodes of narcolepsy in mice were characterized by the following symptoms: “the abrupt cessation of intentional motor activity associated with a sudden and prolonged change in posture that was maintained throughout the episode, ending abruptly with complete recovery of intentional motor activity" (Chen, Brown, McKenna, & McCarley, 2009, 301). Accounting for these symptoms, combined with consideration of what activities and events preceded the attacks, helps form a scientific idea of ​​how manifests narcolepsy and what can precipitate narcoleptic attacks. It also helps to understand how and when narcoleptic patients return to a normal state of wakefulness or sleep after a narcoleptic attack and how long they may last More Specific to the Animal Model of Narcolepsy: How Genes Affect the Prevalence and Symptoms of Narcolepsy This is actually one of the original studies that demonstrated the importance of neurons and genes in causing narcolepsy in both animals and humans. As these authors state, “We report that a null mutation induced by targeted disruption of the mouse orexin gene results in an autosomal recessive phenotype with features remarkably similar to narcolepsy” (Chemelli et al., 1999, 437). In other words, the authors found that the appearance of narcolepsy in mice was directly related to a specific type of gene – or neuron. As the authors conclude, “These observations firmly identify orexins as neuropeptides with an important function in sleep regulation” (Chemelli et al., 1999, 437). This study, therefore, establishes the specific type of neuron, orexin, as the main factor influencing narcolepsy. Narcolepsy and Circadian Rhythms The other topic that provides some insight into how narcolepsy works is in relation to circadian rhythms. The main question here is whether narcolepsy is related to circadian rhythms; in other words, does narcolepsy manifest itself more during the day, at night or equally at all hours of the day? Since this is moreeasily observable compared to other aspects of narcolepsy, there is a great deal of knowledge on the topic. Regarding sleep and circadian rhythms in general, there is one source worth quoting at length: “A series of discoveries over the past decade have begun to identify the brain circuits and neurotransmitters that regulate our daily sleep cycles and watch. The latter depends on a network of cell groups that activate the thalamus and the cerebral cortex. A key switch in the hypothalamus turns off this arousal system during sleep. Other hypothalamic neurons stabilize the switch and their absence results in an inappropriate change in behavioral states, as occurs in narcolepsy” (Saper, Scammell and Lu, 2005, 1257). In other words, narcolepsy is directly influenced not so much by a human internal circadian rhythm, but rather by the internal processes of the hypothalamus. This is confirmed by another source, who states that “Mechanisms that potentially disrupt the circadian rhythm of leptin levels in hypocretin-deficient narcoleptic humans include abnormalities of the sleep-wake cycle and/or disruption of the circadian distribution of autonomic activity ” (Kok et al., 2001, 8246). In other words, the neurological process that affects narcoleptic humans is completely independent of the circadian rhythm. This is confirmed once again by a third study, which found that “the homeostatic process of sleep regulation is intact in narcoleptics… the circadian clock itself appears to function normally in narcoleptics” (Dantz, Edgar, & Derment, 1994, 24 ). With this in mind, one can safely conclude that narcoleptic attacks are just as likely to occur during the day as at night, since narcolepsy is not directly affected by the circadian rhythm. Narcolepsy and Emotion (1) The final topic relevant to understanding narcolepsy in both human and animal models is how narcoleptic attacks relate to emotional feelings. First, it is clear that emotion has a role to play in narcoleptic attacks; for example, one study found that “emotions were experienced more often and were more intense in narcoleptic SOREM than in nocturnal REM of narcoleptic or normal subjects, with anxiety/fear showing the strongest increase, followed by joy/euphoria.” (Fosse, Stickgold & Hobson, 2002, 724). In this regard, SOREM refers to REM that occurs in the early stages of daytime naps and nighttime sleep (Fosse, Stickgold & Hobson, 2002, 724). This finding makes it clear that extreme emotions of both varieties – both positive and negative – can play a role in the onset and duration of narcoleptic attacks, at least once sleep is already underway. As these authors conclude, “REM sleep in narcolepsy patients offers a unique opportunity to study emotions and analyze their psychophysiology,” and their study found that “narcolepsy intensifies REM dream emotions, particularly anxiety/ fear and joy/euphoria, and this is most clearly visible during SOREM sleep” (Fosse, Stickgold & Hobson, 2002, 724). In other words, emotions can trigger narcoleptic attacks even during sleep. But what about emotional triggers that, while patients are awake, cause cataplexy, which in turn causes narcolepsy? One study provides insight into this question, stating that “cataplexy is one of the most intriguing examples of how thought content can alter neurological functioning,” since patients in a state of cataplexy who also experience “an intense emotional state trigger objective transient muscle weakness verified by areflexia” (Krahn et al., 2005, 45). More.