文献翻译：睡眠失调可能是帕金森氏症的前兆

[第1楼 PID5868] 2010-08-05 11:09 GoldenPig 写道:

文献翻译：睡眠失调可能是帕金森氏症的前兆

一项新的研究表明，睡眠失调可能是老年痴呆/帕金森氏症的前兆，而这类疾病最久会在睡眠失常的50年后被诊断出来。

这项研究结果发布在2010年7月28日Neurology杂志的在线版本上。

这项研究包括27位参与者，他们在发展形成帕金森氏疾病，痴呆或多系统萎缩之前，都经历了至少15年的快速动眼睡眠行为失常。其中多系统萎缩是一种症状与帕金森氏症类似的疾病。快速动眼睡眠行为失常的人经常会做伴有暴力行为的梦，比如打击行为，这通常会伤害他们自己或身边的人。

研究人员发现，睡眠失常开始到神经紊乱症状出现的时长能达50年，而平均时间跨度是25年。在这些患者中，有13人被诊断出患有痴呆，13人被诊断出患有帕金森氏症，还有1人被诊断出患有多系统萎缩。

"我们的发现表明，在一些患有帕金森氏症或痴呆的人中，其大脑活性有一个非常长的时间跨度，而这段时间并不会表现出其他的症状。"这项研究的作者Bradley F. Boeve表示，"接下来，我们还需要进行更多的研究，关注这个可能的关联，未来科学家或能用其开发出有效的疗法，以缓解或抑制帕金森氏症或痴呆这类疾病的发生。

文章来源： http://www.bioon.com/biology/neuroscience/449473.shtml

[第2楼 PID5868] 2012-08-20 19:27 Robot :

文献翻译：睡眠失调可能是帕金森氏症的前兆 相关

[第3楼 PID5869] 2010-08-05 11:10 GoldenPig 写道:

回复: 文献翻译：睡眠失调可能是帕金森氏症的前兆

英文原文：

REM sleep behavior disorder preceding other aspects of synucleinopathies by up to half a century

D. O. Claassen MD, K. A. Josephs MD, MST, J. E. Ahlskog MD, PhD, M. H. Silber MB, ChB, M. Tippmann-Peikert MD, and B. F. Boeve MD*

From the Department of Neurology (D.O.C., K.A.J., J.E.A., M.H.S., M.T.-P., B.F.B.) and Center for Sleep Medicine (M.H.S., M.T.-P., B.F.B.), Mayo Clinic College of Medicine, Rochester, MN.

Background: Idiopathic REM sleep behavior disorder (RBD) may be the initial manifestation of synucleinopathies (Parkinson disease [PD], multiple system atrophy [MSA], or dementia with Lewy bodies [DLB]).

Methods: We used the Mayo medical records linkage system to identify cases presenting from 2002 to 2006 meeting the criteria of idiopathic RBD at onset, plus at least 15 years between RBD and development of other neurodegenerative symptoms. All patients underwent evaluations by specialists in sleep medicine to confirm RBD, and behavioral neurology or movement disorders to confirm the subsequent neurodegenerative syndrome.

Results: Clinical criteria were met by 27 patients who experienced isolated RBD for at least 15 years before evolving into PD, PD dementia (PDD), DLB, or MSA. The interval between RBD and subsequent neurologic syndrome ranged up to 50 years, with the median interval 25 years. At initial presentation, primary motor symptoms occurred in 13 patients: 9 with PD, 3 with PD and mild cognitive impairment (MCI), and 1 with PDD. Primary cognitive symptoms occurred in 13 patients: 10 with probable DLB and 3 with MCI. One patient presented with primary autonomic symptoms, diagnosed as MSA. At most recent follow-up, 63% of patients progressed to develop dementia (PDD or DLB). Concomitant autonomic dysfunction was confirmed in 74% of all patients.

Conclusions: These cases illustrate that the -synuclein pathogenic process may start decades before the first symptoms of PD, DLB, or MSA. A long-duration preclinical phase has important implications for epidemiologic studies and future interventions designed to slow or halt the neurodegenerative process.