9 Targeting GABA receptors may therefore enable regulation of sleep duration, 9 mediate muscle tone, 17 and prevent overstimulation.1 4 9 GABAergic neurons in the ventral medulla mediate the inhibition of motor neurons, 16 whereas those in the amygdala can trigger cataplexy upon evoking positive emotions. 9,15 GABA-containing neurons that originate in the ventrolateral and median preoptic areas of the hypothalamus inhibit wake-promoting neurons, which promotes non–rapid eye movement (REM) sleep. 1,13 The most important inhibitory neurotransmitter of the mammalian central nervous system (CNS) is γ-aminobutyric acid (GABA), 14 which can promote feelings of happiness and sedation. Sleep and wakefulness are regulated by interconnected brain circuits that modulate systems of neurotransmitters such as norepinephrine, serotonin, dopamine, histamine, and hypocretin ( FIGURE). 1,3,11,12 Consequently, those with type 1 narcolepsy can experience more severe symptoms. 1,2,9,10 Cataplexy is a particularly disruptive symptom that is unique to narcolepsy that can leave patients fully immobile while they maintain conscious awareness. 3,12 Narcolepsy is categorized into 2 major types based on the presence/absence of cataplexy and the level of hypocretin: type 1, cataplexy present and hypocretin low and type 2, cataplexy absent and hypocretin normal. 1-3,9-11 EDS affects all patients with narcolepsy and is often a primary symptom, 1-3,11 accompanied by bouts of irresistible “sleep attacks” that occur without warning and can last up to several minutes. Narcolepsy features excessive daytime sleepiness (EDS), sudden loss of muscle tone (cataplexy), disturbed nocturnal sleep, and hypnagogic and/or hypnopompic hallucinations. 5,6 Because of heterogeneity in the development and severity of symptoms, 6,7 many individuals do not receive narcolepsy diagnosis until years after onset. 4 However, the exact cause remains unknown genetic risk factors or environmental triggers may precede the loss of hypocretin neurons and subsequent hormone imbalances characteristic of the disorder. 4,5 Narcolepsy is increasingly recognized as an autoimmune disorder, 1 whereby the immune system reacts to an external trigger (eg, viral) in such a way that it attacks the brain cells (ie, hypocretin neurons) that synthesize a neuropeptide (ie, hypocretin) that regulates wakefulness and sleep. The disorder typically begins in childhood or adolescence, 1-3 with mild initial symptoms that can worsen with time. Early awakenings and dry mouth were the most common adverse effects.NARCOLEPSY IS A CHRONIC SLEEP DISORDER that can have debilitating consequences. Venlafaxine demonstrated significantly greater improvements in MSL in the MWT (p < 0.01). There were significant differences in the mean sleep latency (MSL) and sleep onset rapid eye movement periods (SOREMPs) in MWT and ESS scores, cataplexy and cataplexy-like episodes before and after treatment (p < 0.01). Improvement in sleepiness, cataplexy, cataplexy-like episodes, and antidepressant side effects were assessed. The subjects were followed for 1–6 years after treatment. One hundred forty-eight patients with narcolepsy were treated with antidepressants and administered the Epworth Sleepiness Scale (ESS) and the Maintenance of Wakefulness Test (MWT) before and after treatment from August 2012 to August 2017. At present, Sodium oxybate, modafinil, methylphenidate and other stimulants are recommended first-line therapies for narcolepsy but are difficult to obtain in China. Narcolepsy is a life-long neurological disorder characterized by excessive daytime sleepiness (EDS) and cataplexy.
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