Antoniades Chrystalina A, Rebelo Pedro, Kennard Christopher, Aziz Tipu Z, Green Alexander L, FitzGerald James J
Nuffield Department of Clinical Neurosciences and
Nuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 9DU, United Kingdom.
J Neurosci. 2015 Sep 23;35(38):13043-52. doi: 10.1523/JNEUROSCI.2317-15.2015.
The frontal cortex and basal ganglia form a set of parallel but mostly segregated circuits called cortico-basal ganglia loops. The oculomotor loop controls eye movements and can direct relatively simple movements, such as reflexive prosaccades, without external help but needs input from "higher" loops for more complex behaviors. The antisaccade task requires the dorsolateral prefrontal cortex, which is part of the prefrontal loop. Information flows from prefrontal to oculomotor circuits in the striatum, and directional errors in this task can be considered a measure of failure of prefrontal control over the oculomotor loop. The antisaccadic error rate (AER) is increased in Parkinson's disease (PD). Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has no effect on the AER, but a previous case suggested that DBS of the globus pallidus interna (GPi) might. Our aim was to compare the effects of STN DBS and GPi DBS on the AER. We tested eye movements in 14 human DBS patients and 10 controls. GPi DBS substantially reduced the AER, restoring lost higher control over oculomotor function. Interloop information flow involves striatal neurons that receive cortical input and project to pallidum. They are normally silent when quiescent, but in PD they fire randomly, creating noise that may account for the degradation in interloop control. The reduced AER with GPi DBS could be explained by retrograde stimulation of striatopallidal axons with consequent activation of inhibitory collaterals and reduction in background striatal firing rates. This study may help explain aspects of PD pathophysiology and the mechanism of action of GPi DBS. Significance statement: Parkinson's disease causes symptoms including stiffness, slowness of movement, and tremor. Electrical stimulation of specific areas deep in the brain can effectively treat these symptoms, but exactly how is not fully understood. Part of the cause of such symptoms may be impairments in the way information flows from one circuit within the brain to another, as a result of overactivity of certain nerve cells. By demonstrating that stimulation of an area called the globus pallidus interna partially reverses deficits in voluntary control of eye movements, this study shows that stimulation can improve information flow between circuits, probably by calming down the overactive cells.
额叶皮质和基底神经节形成了一组平行但大多相互分离的回路,称为皮质 - 基底神经节环路。动眼神经环路控制眼球运动,能够在没有外部帮助的情况下引导相对简单的运动,比如反射性的前跳视,但对于更复杂的行为则需要来自“更高层次”环路的输入。反跳视任务需要背外侧前额叶皮质,它是前额叶环路的一部分。信息从前额叶流向纹状体中的动眼神经回路,该任务中的方向错误可被视为前额叶对动眼神经环路控制失败的一种度量。帕金森病(PD)患者的反跳视错误率(AER)会升高。丘脑底核(STN)的深部脑刺激(DBS)对AER没有影响,但之前有一个病例表明苍白球内侧部(GPi)的DBS可能有影响。我们的目的是比较STN DBS和GPi DBS对AER的影响。我们测试了14名接受DBS治疗的人类患者和10名对照者的眼球运动。GPi DBS显著降低了AER,恢复了对动眼神经功能丧失的高级控制。环路间的信息流涉及接收皮质输入并投射到苍白球的纹状体神经元。它们在静止时通常是沉默的,但在PD中会随机放电,产生的噪声可能是环路间控制退化的原因。GPi DBS导致AER降低可以通过逆行刺激纹状体 - 苍白球轴突,继而激活抑制性侧支并降低纹状体背景放电率来解释。这项研究可能有助于解释PD病理生理学的各个方面以及GPi DBS的作用机制。意义声明:帕金森病会导致包括僵硬、运动迟缓及震颤等症状。对脑深部特定区域进行电刺激可有效治疗这些症状,但具体方式尚不完全清楚。此类症状的部分原因可能是由于某些神经细胞过度活跃,导致大脑内一个回路向另一个回路传递信息的方式出现障碍。通过证明刺激苍白球内侧部区域可部分逆转眼球运动自主控制方面的缺陷,本研究表明刺激可能通过使过度活跃的细胞平静下来来改善回路间的信息流。