Kühn Andrea A, Tsui Alexander, Aziz Tipu, Ray Nicola, Brücke Christof, Kupsch Andreas, Schneider Gerd-Helge, Brown Peter
Department of Neurology, Charité, University Medicine Berlin, Campus Virchow, Berlin, Germany.
Exp Neurol. 2009 Feb;215(2):380-7. doi: 10.1016/j.expneurol.2008.11.008. Epub 2008 Nov 25.
Parkinson's disease (PD) is associated with exaggerated oscillatory synchrony in the basal ganglia at frequencies over 8-35 Hz. Studies have demonstrated a suppression of local field potential (LFP) activity in the subthalamic nucleus (STN) upon treatment with the dopamine prodrug, levodopa, with the degree of suppression of power in the 8-35 Hz band correlating with the improvement in combined measures of bradykinesia and rigidity. However, these studies do not explicitly address the question of what is more important in predicting clinical change - synchronisation of neuronal activity or the specific frequency within the 8-35 Hz band over which the latter occurs. In addition, they have not demonstrated a relationship between treatment-induced changes in synchronisation and changes in bradykinesia or rigidity on their own. To this end, we collected and analysed LFP and clinical data in 30 patients with PD. We found significant correlations between levodopa-induced power suppression and rigidity and bradykinesia, when these clinical features were considered separately, but only when power suppression profiles were re-aligned to the frequency of peak synchronisation. Under these circumstances correlations with rigidity persisted despite partialising out the effect of bradykinesia and vice versa. These data suggest that levodopa-induced improvements in both rigidity and bradykinesia scale with the degree of suppression of oscillatory power in the STN LFP, and that this is true irrespective of the frequency at which synchronisation occurs across a broad band from 8-35 Hz.
帕金森病(PD)与基底神经节在8 - 35赫兹以上频率的过度振荡同步有关。研究表明,使用多巴胺前体药物左旋多巴治疗后,丘脑底核(STN)的局部场电位(LFP)活动受到抑制,8 - 35赫兹频段的功率抑制程度与运动迟缓及僵硬综合指标的改善相关。然而,这些研究并未明确解决在预测临床变化中更重要的问题——神经元活动的同步化还是后者发生的8 - 35赫兹频段内的特定频率。此外,它们尚未证明治疗引起的同步化变化与运动迟缓或僵硬自身变化之间的关系。为此,我们收集并分析了30例帕金森病患者的LFP和临床数据。当分别考虑这些临床特征时,我们发现左旋多巴引起的功率抑制与僵硬和运动迟缓之间存在显著相关性,但前提是功率抑制曲线要重新校准到峰值同步频率。在这种情况下,尽管排除了运动迟缓的影响,与僵硬的相关性仍然存在,反之亦然。这些数据表明,左旋多巴引起的僵硬和运动迟缓的改善与STN LFP振荡功率的抑制程度成比例,并且无论在8 - 35赫兹宽带内同步发生的频率如何,都是如此。