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		题名	作者	年代	出处	被引量
	1	SLC20A2 and THAP1 deletion in familial basal ganglia calci- fication with dystonia显示文摘	Baker M Strongosky AJ Sanchez-Contreras MY	2014	Neurogenetics2014，15，1：	1
	2	Autosomal dominant dystonia-plus with cerebral calcifications显示文摘	Z K. Wszolek Y Baba I R. Mackenzie R J. Uitti A J. Strongosky D F. Broderick M C. Baker S Melquist M L. Hutton Y Tsuboi J E. Allanson J Carr A Kumar S M. Calne J Miklossy P L. McGeer D B. Calne A J. Stoessl	2006	Neurology2006，，4：	1
	3	苍白球脑桥黑质变性家族11例成员的快动眼睡眠行为障碍缺失显示文摘Background: Rapid eye movement sleep behavior disorder (RBD) is a parasomnia that is manifested by dream enactment behavior. The electrophysiologic substrate for RBD on polysomnography is rapid eye movement sleep without atonia. Rapid eye movement sleep behavior disorder likely stems from neuronal network dysfunction in the brainstem, although it is not yet clear which specific networks are involved. Rapid eye movement sleep behavior disorder is often associated with the sporadic synucleinopathies but rarely associated with the sporadic tauopathies. There are no reports on the possible association of rapid eye movement sleep without atonia and RBD with any familial tauopathy. Objective: To characterize the clinical sleep and polysomnography features in a kindred with a familial tauopathy. Methods: We performed standard polysomnography in 11 members of the pallidopontonigral degeneration kindred irrespective of any sleep-related complaints. Neuropathologic findings were analyzed in those who subsequently underwent autopsy. Results: Six affected and 5 genealogically at-risk family members were studied. None of the 11 had a history of dream enactment behavior. Nine of the 11 members attained sufficient rapid eye movement sleep on polysomnography, and the electrophysiologic features of rapid eye movement sleep without atonia and behavioral manifestations of RBD were absent in all subjects. Neuropathologic examination of 4 affected individuals revealed marked nigral degeneration in 3 along with mild degenerative changes in the locus coeruleus, pontine nuclei and tegmentum, and medullary tegmentum. Conclusions: These findings argue against nigral degeneration being the primary cause of RBD. The absence of the historical, electrophysiologic, and behavioral manifestations of RBD in this kindred provides further evidence that RBD is rare in the sporadic and familial tauopathies. The difference in frequencies of RBD associated with the synucleinopathies compared with the tauopathies suggests differences in the selective vulnerability of brainstem circuits between the synucle inopathies and tauopathies.	Boeve B.F. Strongosky A. 邱伟庆	2006	世界核心医学期刊文摘(神经病学分册)2006，2，6：	0

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