How Does Narcolepsy Affect The Nervous System – Responding to autism in low- and middle-income countries (Lmic): what to do and what not to do
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How Does Narcolepsy Affect The Nervous System
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Increased Very Low Frequency Pulsations And Decreased Cardiorespiratory Pulsations Suggest Altered Brain Clearance In Narcolepsy
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Department of Neurosurgery, American College of Surgeons, Trauma and Gamma Knife Center, Cannizzaro Hospital, Catania, 95100 Catania, Italy
Received: September 5, 2022 / Revised: October 22, 2022 / Accepted: October 28, 2022 / Published: October 30, 2022
Narcolepsy is a chronic, long-term neurological disorder characterized by a decreased ability to regulate sleep-wake cycles. Some clinical symptoms are included in the differential diagnosis with other neurological diseases. Excessive daytime sleepiness and brief episodes of involuntary sleep are the main clinical symptoms. Most people with narcolepsy experience cataplexy, which is a loss of muscle tone. Many people experience neurological problems, such as sleep cycle disorders, hallucinations, or sleep paralysis. Due to the neurological conditions involved, the exact pathophysiology of narcolepsy is unknown. Differential diagnosis is important because the relative clinical symptoms of narcolepsy are easily diagnosed when all symptoms are present, but it is more difficult when sleep attacks are isolated and cataplexy is episodic or absent. Treatment is adapted to the patient’s symptoms and clinical diagnosis. With the aim of facilitating the diagnosis and treatment of sleep disorders and better understanding the neuropathological mechanisms of these sleep disorders, this review summarizes current knowledge about narcolepsy, in particular the genetic and non-genetic associations of narcolepsy, the pathophysiology of pre – inflammatory response, the neuromorphological characteristics of narcolepsy and other conditions such as diabetes, ischemic stroke and Alzheimer’s disease. Possible links to disease. This review also reports on the most recent research and therapeutic advances in narcolepsy. Significant advances have been made in elucidating the pathogenesis of narcolepsy, with substantial evidence of an autoimmune response against hypocretin neurons; but there are some gaps that need to be filled. Further research should focus on identifying molecular targets and novel self-antigens for the treatment of narcolepsy. Despite therapeutic advances, standardized criteria for narcolepsy and diagnostic measures are widely accepted, but can be revised and updated in the future with understanding. Treatment should be tailored to the patient’s symptoms and clinical diagnosis, and future treatments with hypocretin agonists, GABA agonists, histamine receptor antagonists, and immunomodulatory medications should be directed to address the underlying cause of narcolepsy.
Narcolepsy is a chronic, lifelong neurological disorder that interferes with a person’s daily sleep and wake cycles. It mainly affects REM and NREM sleep cycles and is associated with several neurological disorders [1]. Episodic daytime sleepiness and nighttime awakenings are differentiated by difficulty sleeping. It is characterized by abnormal rapid eye movements, cataplexy, and mild muscle weakness, which lead to collapse or paralysis [2, 3, 4]. Narcolepsy affects people of all ages, including children, teenagers, adults and the elderly, and symptoms range from mild to severe. A person with narcolepsy may fall asleep at any time, such as while talking or driving. Narcolepsy, also known as hypersomnia, is a chronic REM sleep disorder characterized by excessive daytime sleepiness [3, 4, 5]. In the classic sleep cycle, the individual enters the early stages of sleep, followed by a 90-minute period of deep sleep, in which REM sleep ends. Patients with narcolepsy, on the other hand, can enter REM sleep 15 minutes after the start of the daytime sleep cycle [1]. Thus, REM sleep causes daydreaming and muscle paralysis. Narcolepsy and its associated pathology are caused by several factors [1]. Traumatic brain injuries such as stroke, hypothalamic injury and loss of hypocretin receptors, major neurological complications such as major depressive disorder and schizophrenia, metabolic disorders such as diabetes, and other factors contribute to the development of narcolepsy. The exact cause and pathophysiology of narcolepsy pathology are unknown, but based on research and clinical experience, it is divided into three main types: (1) narcolepsy with cataplexy; (2) narcolepsy without cataplexy, characterized by daytime drowsiness; and (3) secondary narcolepsy, resulting from hypothalamic injury and imbalance of neuronal distribution [6, 7]. The Board of Directors of the American Academy of Sleep Medicine published the International Classification of Sleep Disorders, 3rd Edition (ICSD-3) in 2014. In the third edition, the most dramatic change in content was the consolidation of the secondary categories of insomnia into one single category. chronic insomnia category”. The narcolepsy nomenclature in the central hypersomnolence disorder section was changed to narcolepsy type 1 and 2 [8]. The nosology of narcolepsy was also revised, dividing the disorder into type 1 and type 2, replacing narcolepsy with and no cataplexy. This reflects a shift in focus from symptom-based diagnosis to pathophysiology-based diagnosis, in this case the hypocretin (orexin) deficiency state. This shift is based on the notion that almost all patients with cataplexy present hypocretin deficiency. Additionally, “narcolepsy with cataplexy” is incorrect because some patients with hypocretin deficiency do not experience cataplexy or do not develop cataplexy [8]. To facilitate the diagnosis and treatment of sleep disorders and to better understand the neuropathological mechanisms of this sleep disorder Since the number of studies on treatment options for narcolepsy has increased in the last decade, we have summarized all current knowledge about narcolepsy in this review. in particular, the genetic and non-genetic associations of narcolepsy, the pathophysiology of the pre-inflammatory response, the neuromorphological features of narcolepsy and possible associations with other diseases such as diabetes, ischemic stroke and Alzheimer’s disease. This review also reports on the most recent research and therapeutic advances in narcolepsy.
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Several studies have been carried out to determine the exact prevalence of narcolepsy, which has been found to be between 25 and 50 per 100,000 people in Europe, Japan and the United States [9, 10, 11]. As a result, narcolepsy is a rare disease. Due to the lack of specific diagnosis and symptoms that mimic other diseases, the exact epidemiology is unknown. Narcolepsy affects between 50 and 67 per 100,000 people in North America, Western Europe, and Asia [12]. In India and other Asian countries, the prevalence of narcolepsy is very low and there are very few confirmed cases of narcolepsy with careful investigation. The prevalence in India is very low because cases are misdiagnosed, underdiagnosed, or only partially diagnosed to confirm narcolepsy [13]. Due to mixed symptoms and other neurological disorders, it is often misdiagnosed as seizures or obstructive sleep apnea, therefore, the exact prevalence of narcolepsy worldwide is believed to be low. However, if each patient is screened and differentially diagnosed, the true prevalence is higher than reported [14].
Although 2–3% of familial cases are reported, narcolepsy is mostly a sporadic disorder. In several families with familial narcolepsy, incomplete transmission with an autosomal dominant mode of inheritance and a heterogeneous single gene mutation has been observed [15]. The risk of developing narcolepsy in first-degree relatives of patients is 10 to 40 times higher than in the general population. And identification of the defective genes can provide important information about pathological mechanisms (e.g., the hypocretin receptor type 2 mutation reported in autosomal recessive narcolepsy in dogs).
Sporadic narcolepsy, like most complex disorders, is believed to be the result of a complex interaction of environmental factors and multiple genetic variants. There was an HLA association
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