Loss of hypocretin (orexin) neurons with traumatic brain injury.
Loss of hypocretin (orexin) neurons with traumatic brain injury.
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DOI：
10.1002/ana.21836
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发表时间：
2009-10
影响因子：
11.2
通讯作者：
Scammell, Thomas E.
中科院分区：
文献类型：
--
作者：
Baumann, Christian R.;Bassetti, Claudio L.;Valko, Philipp O.;Haybaeck, Johannes;Keller, Morten;Clark, Erika;Stocker, Reto;Tolnay, Markus;Scammell, Thomas E.
慢性日间嗜睡是许多创伤性脑损伤（TBI）患者的主要致残症状，但到目前为止，其病因尚不清楚。产生促进觉醒的神经肽下丘脑视丘素（食欲素）的下丘脑神经元的大量损失导致发作性睡病的严重嗜睡，并且这些细胞的部分损失可能导致帕金森病和其他疾病的嗜睡。我们已经发现，下丘脑泌素神经元的数量在严重TBI患者中显著减少。这一观察结果突出了TBI中经常被忽视的下丘脑损伤，并为TBI患者慢性嗜睡的原因提供了新的见解。
Chronic, daytime sleepiness is a major, disabling symptom for many patients with traumatic brain injury (TBI), but thus far, its etiology is not well understood. Extensive loss of the hypothalamic neurons that produce the wake-promoting neuropeptide hypocretin (orexin) causes the severe sleepiness of narcolepsy, and partial loss of these cells may contribute to the sleepiness of Parkinson’s disease and other disorders. We have found that the number of hypocretin neurons is significantly reduced in patients with severe TBI. This observation highlights the often overlooked hypothalamic injury in TBI and provides new insights into the causes of chronic sleepiness in patients with TBI.
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