عرض مصدر نوم قهري

{{معلومات مرض| الاسم=نوم قهري| صورة=1R02 crystallography.png
| تعليق=The neuropeptide [[orexin-A]] delivered to be reduced in the neurons of people with narcolepsy
| اختصاص=[[طب النوم]]| النطق=/ˈnɑːrkəˌlɛpsi/
        }}

'''السَّبَخ<ref name="المورد الحديث">{{استشهاد بويكي بيانات|Q112315598|صفحة=758}}</ref>''' أو '''التغفيق''' {{إنج|narcolepsy أو hypnolepsy}}، هو مرض عصبي مزمن يتمحور حول فقدان قدرة الدماغ على تنظيم دورات النوم والاستيقاظ بشكل طبيعي.<ref>{{استشهاد ويب|مسار=http://www.ninds.nih.gov/disorders/narcolepsy/narcolepsy.htm |عنوان=Narcolepsy Information Page: National Institute of Neurological Disorders and Stroke (NINDS) |ناشر=Ninds.nih.gov |تاريخ=18 July 2013 |تاريخ الوصول=3 March 2014| مسار أرشيف = https://web.archive.org/web/20161218135941/http://www.ninds.nih.gov/disorders/narcolepsy/narcolepsy.htm | تاريخ أرشيف = 18 ديسمبر 2016 |حالة المسار=dead}}</ref> يعاني المصابون بالتغفيق غالبا من نعاس شديد في النهار يشابه النعاس الذي يحدث بعد الحرمان من النوم لمدة 24-48 ساعة عند الأشخاص الطبيعيين،<ref name="wun">{{استشهاد ويب|مسار =//www.wakeupnarcolepsy.org/about-narcolepsy/what-is-narcolepsy/ |عنوان =What is Narcolepsy? |تاريخ الوصول= 23 June 2014| مسار أرشيف = https://web.archive.org/web/20180811165112/http://www.wakeupnarcolepsy.org:80/about-narcolepsy/what-is-narcolepsy/ | تاريخ أرشيف = 11 أغسطس 2018 }}</ref> ويعانون أيضا من اضطراب النوم ليلا، وغالبا ما يتم بشكل خاطئ تشخيص المريض بالإصابة بالأرق. يدخل مرضى التغفيق في مرحلة حركة العين السريعة خلال خمس دقائق من النوم، بينما يدخل الأشخاص الذين لا يعانون من التغفيق (إلا اذا كان لديهم حرمان شديد من النوم)<ref name="ninds1">{{استشهاد بدورية محكمة|مسار=//www.ncbi.nlm.nih.gov/pubmed/1697239 |عنوان=REM sleep deprivation during 5 hours leads to an immediate REM sleep rebound and to suppression of non-REM sleep intensity |عمل=Electroencephalogr Clin Neurophysiol. 1990 Aug;76(2):114-22. |ناشر=National Institutes of Health |تاريخ= Aug 1990|تاريخ الوصول=6 June 2014|pmid=1697239 |المجلد=76 |صفحات=114–22|مسار أرشيف= https://web.archive.org/web/20151116122757/http://www.ncbi.nlm.nih.gov/pubmed/1697239|تاريخ أرشيف=2015-11-16}}</ref> في مرحلة حركة العين السريعة بعد المرور بمرحلة النوم بطيء-الموجة، التي تدوم لمدة ساعة من بدء النوم.<ref name="ninds">{{استشهاد ويب|مسار=http://www.ninds.nih.gov/disorders/narcolepsy/detail_narcolepsy.htm |عنوان=Narcolepsy Fact Sheet - NIH Publication No. 03-1637 |عمل=National Institute of Neurological Disorders and Stroke |ناشر=National Institutes of Health |تاريخ الوصول=5 August 2010| مسار أرشيف = https://web.archive.org/web/20161119110559/http://www.ninds.nih.gov:80/disorders/narcolepsy/detail_narcolepsy.htm | تاريخ أرشيف = 19 نوفمبر 2016 }}</ref> من الأعراض الأخرى الشائعة لمرض التغفيق: الجمدة، وهي حدوث ضعف مفاجئ ومؤقت في العضلات مصحوبا بالوعي الكامل، وتحدث غالبا (وليس دائما) نتيجة لانفعالات مثل الضحك، البكاء، الخوف، إلخ.<ref>{{استشهاد بدورية محكمة|الأخير=Seigal|الأول=Jerome|عنوان=Narcolepsy|صحيفة=Scientific American|تاريخ=January 2001|صفحة=77}}</ref> ويحدث هذا العرض لـ70% من المصابين بمرض التغفيق.<ref>{{استشهاد ويب|مسار=http://www.ninds.nih.gov/disorders/narcolepsy/detail_narcolepsy.htm |عنوان=Narcolepsy Fact Sheet |تاريخ الوصول=2011-06-23| مسار أرشيف = https://web.archive.org/web/20161119110559/http://www.ninds.nih.gov:80/disorders/narcolepsy/detail_narcolepsy.htm | تاريخ أرشيف = 19 نوفمبر 2016 }}</ref>

يتكون النظام الذي ينظم النوم والاستيقاظ، والانتقال بين هاتين المرحلتين عند البشر من ثلاثة أنظمة فرعية متصلة وهي: منبثقات الأوريكسين من الوطاء الوحشي، الجهاز التنشيطي الشبكي، والنوية البطينية الوحشية قبل البصرية.<ref name="NHM sleep-narcolepsy" /> تكون هذه الأنظمة عند المرضى المصابين بالتغفيق مرتبطة باضطرابات وظيفية وذلك بسبب وجود نقص في انبثاقات الأعصاب المفرزة للأوريكسين من الوطاء، وبسبب أعداد الأوريكسين القليلة في السائل العصبي الخيشومي وفي الأنسجة العصبية، مقارنة بالمرضى الأصحاء.<ref name="NHM sleep-narcolepsy">{{استشهاد بكتاب |مؤلف = Malenka RC, Nestler EJ, Hyman SE | محرر = Sydor A, Brown RY | عنوان = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | سنة = 2009 | ناشر = McGraw-Hill Medical | مكان = New York |ردمك= 9780071481274 | صفحات = 294–296, 303 | إصدار = 2nd | الفصل = Chapter 12: Sleep and Arousal | اقتباس = <br />NEURAL SUBSTRATES OF SLEEP<br />Several neural systems mediate the switching between wakefulness and sleep and between the different stages of sleep. These systems include the ascending reticular activating system (ARAS), the ventrolateral pre-optic (VLPO) area, and the orexin/hypocretin system&nbsp;... The VLPO area of the anterior hypothalamus consists mainly of inhibitory neurons that release γ-aminobutyric acid (GABA) and the neuropeptide galanin. The VLPO neurons are likely to have reciprocal interactions with the ARAS and orexin neurons. The VLPO neurons inhibit and are inhibited by the TMN histamine neurons and REM-off monoamine neurons. Orexin neurons are located in the lateral hypothalamus. They are organized in a widely projecting manner, much like the monoamines, and innervate all of the components of the ARAS. They excite the REM-off monoaminergic neurons during wakefulness and the PT cholinergic neurons during REM sleep. They are inhibited by the VLPO neurons during NREM sleep.&nbsp;... During NREM sleep, the VLPO area neurons start inhibiting the orexin neurons of the lateral hypothalamus. Consequently, the norepinephrine and serotonin REM-off cells, which are excited by orexin neurons during wakefulness, start to wane in activity, which gradually releases the cholinergic REM-on cells from their inhibitory effect. At the end of NREM sleep, the VLPO area neurons directly inhibit the REM-off cells, which completely disinhibits the REM-on cholinergic neurons and initiates REM sleep. Consistent with the inhibition of REM on cells by serotonergic and noradrenergic inputs, antidepressant drugs, which increase the availability of synaptic serotonin or norepinephrine, reduce REM sleep.&nbsp;... <!--Narcolepsy 
Narcolepsy was first described during the late 1800s. It is characterized by abnormal transitions between REM and NREM sleep during the night and across the sleep–wake cycle. Narcoleptic patients do not sleep more than normal individuals; however, they have intrusive episodes of REM sleep during the day and fragmented sleep at night. The characteristic symptoms of narcolepsy, which include pathologic sleepiness, sleep paralysis, hypnagogic hallucinations (hallucinations that occur with the onset or termination of sleep), and cataplexy, are caused by the sudden intrusion of REM sleep into wakefulness. Cataplexy is pathognomonic for narcolepsy and is characterized by the sudden loss of muscle tone during wakefulness. During a cataplectic attack, a narcoleptic may suddenly fall to the floor from a standing position and be unable to move even though fully conscious. Interestingly, cataplectic attacks often are elicited by positive emotional stimuli. The primary treatment for narcolepsy consists of psychostimulants or modafinil to counter the hypersomnolence, and REM suppressing drugs, such as tricyclic antidepressants, which reduce cataplexy. Nonpharmacologic treatment, such as scheduled naps, also is effective for treating daytime hypersomnolence.

Narcolepsy can be a heritable disorder, but in humans most cases appear sporadic. In some families, narcolepsy has been linked to a gene that is near the human leukocyte antigen (HLA) alleles DQB1 and DQA1 on chromosome 6, suggesting an autoimmune basis. In a dog model of narcolepsy, transmission is autosomal recessive, which is clearly different from human transmission, and is due to loss-of-function mutations in the orexin OX2 receptor gene. Disruption of the gene encoding orexin peptides in mice also causes a narcolepsy-like disorder.--> Orexin neurons, located in the lateral and posterior hypothalamus and excite monoaminergic neurons during wakefulness and cholinergic neurons during REM sleep. They are inhibited by VLPO during NREM sleep.

Orexin neurons are significantly decreased in number in narcoleptic patients. Hence, one hypothesis is that because of the small number of these neurons in narcolepsy there is less excitation of the monoaminergic neurons during wakefulness and consequently a tendency for the cholinergic neurons to escape from the monoaminergic inhibition resulting in sudden attacks of atonia and REM periods.&nbsp;... <!--This hypothesis is supported by the observation that administration of cholinomimetic agents exacerbates cataplexy in narcoleptic dogs, while administration of anticholinergic agents decreases cataplexy; drugs that block the reuptake of norepinephrine (ie, certain antidepressants)—and therefore enhance noradrenergic transmission at REM-off terminals—are powerful anticataleptic agents.
-->
Most cases of narcolepsy in humans are not linked to mutations in the genes encoding orexin peptides or receptors, but are associated with significantly reduced, often undetectable, levels of orexin in cerebrospinal fluid and brain tissues. Together, the linkage of narcolepsy with HLA alleles, its peak and trough incidence among those born in March and September, respectively (suggesting an environmental influence during the fetal or perinatal period), and the loss of orexin neurons raise the interesting possibility that narcolepsy may be caused by an autoimmune mediated destruction of these neurons in analogy with the autoimmune destruction of insulin-secreting β-islet cells in type I diabetes. A search for small-molecule agonists at orexin receptors is underway and could lead to a treatment for narcolepsy.-->}}</ref>

اشتق مصطلح التغفيق narcolepsy من الكلمة الفرنسية narcolepsie التي أوجدها الطبيب الفرنسي Jean-Baptidte-ÉdouardGélineay وذلك بالجمع بين الكلمة اليونانيةνάρκη narkē ("خدر" أو ذهول")،<ref>Entry [http://dictionary.reference.com/browse/Narcolepsy '''Narcolepsy.'''] in the '''Online Etymology Dictionary.''' Douglas Harper, Historian. 18 September 2007. {{Webarchive|url=http://web.archive.org/web/20160308154627/http://dictionary.reference.com:80/browse/narcolepsy? |date=08 مارس 2016}}</ref> وكلمة λῆψις) lepsis)، "هجمة" أو "نوبة".
[[ملف:Narcolepsy.webm|تصغير|upright=1.3|فيديو توضيحي]]