一項(xiàng)新的研究表明,，睡眠失調(diào)可能是老年癡呆/帕金森氏癥的前兆，而這類疾病最久會(huì)在睡眠失常的50年后被診斷出來,。
這項(xiàng)研究結(jié)果發(fā)布在2010年7月28日Neurology雜志的在線版本上,。
這項(xiàng)研究包括27位參與者，他們?cè)诎l(fā)展形成帕金森氏疾病,，癡呆或多系統(tǒng)萎縮之前,，都經(jīng)歷了至少15年的快速動(dòng)眼睡眠行為失常。其中多系統(tǒng)萎縮是一種癥狀與帕金森氏癥類似的疾病,?？焖賱?dòng)眼睡眠行為失常的人經(jīng)常會(huì)做伴有暴力行為的夢(mèng)，比如打擊行為,，這通常會(huì)傷害他們自己或身邊的人,。
研究人員發(fā)現(xiàn)，睡眠失常開始到神經(jīng)紊亂癥狀出現(xiàn)的時(shí)長(zhǎng)能達(dá)50年,，而平均時(shí)間跨度是25年,。在這些患者中,，有13人被診斷出患有癡呆，13人被診斷出患有帕金森氏癥,，還有1人被診斷出患有多系統(tǒng)萎縮,。
"我們的發(fā)現(xiàn)表明，在一些患有帕金森氏癥或癡呆的人中,，其大腦活性有一個(gè)非常長(zhǎng)的時(shí)間跨度,，而這段時(shí)間并不會(huì)表現(xiàn)出其他的癥狀。"這項(xiàng)研究的作者Bradley F. Boeve表示,，"接下來,，我們還需要進(jìn)行更多的研究，關(guān)注這個(gè)可能的關(guān)聯(lián),，未來科學(xué)家或能用其開發(fā)出有效的療法,，以緩解或抑制帕金森氏癥或癡呆這類疾病的發(fā)生。（生物谷Bioon.com）
生物谷推薦原文出處：
Neurology 2010, doi:10.1212/WNL.0b013e3181ec7fac
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.
