Marsden C D, Obeso J A
University Department of Clinical Neurology, National Hospital for Neurology and Neurosurgery, London, UK.
Brain. 1994 Aug;117 ( Pt 4):877-97. doi: 10.1093/brain/117.4.877.
The basal ganglia play a role in controlling movement. The motor circuits within the striato-pallidal complex are thought to facilitate desired movement and inhibit unwanted movement through their influence via thalamus, mainly on precentral motor cortical regions. Lesions in the motor thalamus, or in the globus pallidus, therefore might be expected to impair voluntary movement. But stereotaxic lesions in patients with Parkinson's disease directed at the motor thalamus verified at autopsy, and lesions in the globus pallidus, which improve rigidity and tremor, apparently do not worsen parkinsonian hypokinesia and bradykinesia; nor do they regularly cause dyskinesias. Reasons for this discrepancy are reviewed. It is concluded that the motor circuits of the basal ganglia are part of a distributed motor system which can operate, albeit imperfectly, in the absence of striato-pallido-thalamo-cortical feedback. There may, however, be subtle defects in motor performance after thalamic and pallidal lesions which have escaped attention. Further consideration leads to two hypotheses concerning normal basal ganglia motor function. First, it seems most likely that it is a pause in firing of medial pallidal and substantia nigra reticulata neurons that, by disinhibition of thalamic targets, permits movements generated by cortical motor areas. An increase in firing of medial pallidal neurons, which so far has been the major focus of attention, may be more concerned with inhibition of unwanted movement. Secondly, we suggest that the basal ganglia play a particular role in motor control. A change in firing of medial pallidal neurons appears to occur too late to initiate a new movement. However, the motor circuit within the striato-pallidal system routinely receives a continuous delayed read-out of cortical motor activity and issues an output directed via thalamus mainly to premotor cortical regions. This may permit the routine automatic execution of sequences of movements generated in cortical motor areas. There is evidence that other regions of the striatum respond to significant external or internal cues as dictated by their cortical inputs, the significance being determined by memory, novelty, emotional and other contexts. We suggest that such events capture the attention of the non-motor striatum, which then interrupts the routine operation of the motor circuit, perhaps at the level of the medial pallidum and substantia nigra pars reticulata, to permit new cortical motor action.
基底神经节在控制运动中发挥作用。纹状体 - 苍白球复合体中的运动回路被认为通过其经丘脑主要对中央前运动皮层区域的影响来促进期望的运动并抑制不想要的运动。因此，运动丘脑或苍白球的损伤可能会损害自主运动。但是，对帕金森病患者进行的针对运动丘脑的立体定向损伤在尸检时得到证实，而苍白球的损伤虽能改善强直和震颤，但显然不会加重帕金森病的运动不能和运动迟缓；也不会经常引起运动障碍。本文对这种差异的原因进行了综述。得出的结论是，基底神经节的运动回路是分布式运动系统的一部分，该系统在没有纹状体 - 苍白球 - 丘脑 - 皮层反馈的情况下仍能运作，尽管并不完美。然而，丘脑和苍白球损伤后运动表现可能存在一些未被注意到的细微缺陷。进一步思考得出了关于基底神经节正常运动功能的两个假设。首先，似乎最有可能的是，内侧苍白球和黑质网状部神经元放电的暂停，通过解除对丘脑靶点的抑制，允许皮层运动区域产生运动。到目前为止一直是主要关注焦点的内侧苍白球神经元放电增加，可能更多地与抑制不想要的运动有关。其次，我们认为基底神经节在运动控制中起特殊作用。内侧苍白球神经元放电的变化似乎发生得太晚，无法启动新的运动。然而，纹状体 - 苍白球系统内的运动回路通常会持续接收皮层运动活动的延迟读出，并发出主要经丘脑指向运动前皮层区域的输出。这可能允许对皮层运动区域产生的运动序列进行常规自动执行。有证据表明，纹状体的其他区域会根据其皮层输入对重要的外部或内部线索做出反应，线索的重要性由记忆、新奇性、情绪和其他背景决定。我们认为，此类事件会引起非运动纹状体的注意，然后它可能在内侧苍白球和黑质网状部水平中断运动回路的常规运作，以允许新的皮层运动动作。
