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Narcolepsy and traumatic brain injury: cause or consequence?

机译:发作性睡病和颅脑外伤:原因还是后果?

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Dear Sir, Narcolepsy with cataplexy is caused by a loss of hypothalamic hypocretin (orexin) neurons, but the etiology of this loss is unclear [1]. After traumatic brain injury (TBI), hypocretin neurons are partially reduced [2], and excessive daytime sleepiness (EDS) belongs to the most common posttraurnatic sleep-wake disturbances [3], In contrast, there are few, mostly ambiguous, reports on posttrau-matic narcolepsy [4]. We retrospectively assessed the frequency of TBI in 37 consecutive patients with well-diagnosed narcolepsy with cataplexy and characterized the TBI subgroup. We only included patients with positive HLA DQBl*0602 and low or undetectable cerebrospinal fluid hypocretin levels. TBI prior to the occurrence of narcolepsy symptoms was present in 7 out of 37 patients (19%) (Table 1). This number is considerably higher than most of the reported prevalences of TBI in the general population, which are about 1% [5]. Three of these patients were diagnosed with severe TBI. The others had mild injuries. Four patients had multiple TBIs throughout their lives. The interval between the last TBI and narcolepsy was up to 2 years in six patients, and 10 years in one patient. Clinical symptoms and sleep laboratory tests did not differ between narcolepsy patients with preceding TBI and those without brain trauma.
机译:亲爱的先生,发作性发作性发作性睡病是由下丘脑降钙素(orexin)神经元的丧失引起的,但是这种丧失的病因尚不清楚[1]。创伤性脑损伤(TBI)后,降钙素神经元部分减少[2],而白天过度嗜睡(EDS)则是最常见的创伤后睡眠-觉醒障碍[3]。创伤后发作性睡病[4]。我们回顾性评估了37例连续发作的发作性睡病并伴有脑瘫的患者的TBI频率,并对TBI亚组进行了特征分析。我们仅纳入HLA DQB1 * 0602阳性且脑脊液降血钙素水平低或无法检测到的患者。 37例患者中有7例(19%)出现发作性睡病症状之前的TBI(表1)。这个数字大大高于一般人群中大多数已报告的TBI患病率,约为1%[5]。其中三名患者被诊断出患有严重的TBI。其他人轻伤。四名患者一生中有多个TBI。最后一次TBI和发作性睡病之间的间隔在6例患者中最长为2年,在1例患者中为10年。先前有TBI的发作性睡病患者和没有脑外伤的发作性睡病患者之间,临床症状和睡眠实验室检查无差异。

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