β频段同步——帕金森病的“坏小子”还是无辜旁观者？
Synchronisation in the beta frequency-band--the bad boy of parkinsonism or an innocent bystander?
作者信息
Eusebio Alexandre, Brown Peter
机构信息
Department of Neurology and Movement Disorders, CHU Timone, Marseille, France.
出版信息
Exp Neurol. 2009 May;217(1):1-3. doi: 10.1016/j.expneurol.2009.02.003. Epub 2009 Feb 20.
Abstract
Excessive synchronisation of basal ganglia neuronal activity in the beta frequency band has been implicated in Parkinson's disease. In a recent issue of Experimental Neurology, Bronte-Stewart, H., Barberini, C., Koop, M.M., Hill, B.C., Henderson, J.M., Wingeier, B., 2009. The STN beta-band profile in Parkinson's disease is stationary and shows prolonged attenuation after deep brain stimulation. Exp. Neurol. 215, 20-28. demonstrate that such activity is consistent over time and provide further evidence that deep brain stimulation is associated with its suppression. However, the extent to which beta synchrony has a mechanistic (rather than epiphenomenal) role in parkinsonism remains unclear, and the suppression of this activity by deep brain stimulation is contentious. This commentary discusses the evidence for and against a role for excessive beta synchrony in mediating the parkinsonian phenotype and in providing a possible mechanism to explain the therapeutic effects of deep brain stimulation in Parkinson's disease.
摘要
基底神经节神经元活动在β频段的过度同步化已被认为与帕金森病有关。在最近一期的《实验神经病学》杂志上，Bronte-Stewart, H., Barberini, C., Koop, M.M., Hill, B.C., Henderson, J.M., Wingeier, B.（2009年）发表了“帕金森病中丘脑底核β频段特征是稳定的，且在深部脑刺激后显示出延长的衰减”一文（《实验神经病学》第215卷，第20 - 28页）。该研究表明这种活动随时间是一致的，并提供了进一步证据证明深部脑刺激与其抑制有关。然而，β同步化在帕金森症中具有机制性（而非附带现象）作用的程度仍不清楚，并且深部脑刺激对这种活动的抑制存在争议。本评论讨论了支持和反对过度β同步化在介导帕金森病表型以及提供一种可能机制来解释深部脑刺激对帕金森病治疗效果方面作用的证据。
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本文引用的文献
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