Wessel K, Verleger R, Nazarenus D, Vieregge P, Kömpf D
Department of Neurology, Medical University of Lübeck, Germany.
Electroencephalogr Clin Neurophysiol. 1994 Jul;92(4):331-41. doi: 10.1016/0168-5597(94)90101-5.
To determine the influence of cerebellar involvement on the preparatory state of the cerebral cortex for voluntary movements, we studied the movement-related cortical potentials (Bereitschaftspotential, BP) preceding sequential and goal-directed finger and arm movements in patients with cerebellar atrophy (CA). The first task (paradigm 1) consisted of a sequential finger movement at a self-paced rate of every 3 sec or longer, in which patients and control subjects pushed rapidly 7 keys on a keyboard in a sequence visually predetermined on a screen. The second task (paradigm 2) consisted of a goal-directed self-paced movement with visual feedback on a screen. In both paradigms, control subjects and patients had distinct movement-related cortical potentials, but peak amplitudes (close to movement onset) were reduced in the patient group (paradigm 2), whereas in the overall analysis the mean amplitude 600-800 msec before movement onset (NS1) was larger in the patient group (paradigms 1 and 2). Accordingly, the difference (NS2) between peak amplitude and NS1 was smaller in the patient group (paradigms 1 and 2). Whereas control subjects' peak amplitude (paradigm 2) and NS2 (paradigm 1) were focused at Cz, this topographical differentiation was abolished in the patient group. The onset of the BP was earlier in the patients than in the control subjects (paradigms 1 and 2). Our results suggest that pathways from the cerebellum to the cortex do play a role in generating movement-related cortical potentials. A strong input from the cerebellum seems to be crucial for the generation of a normal motor potential close to the movement onset, reflecting a specific deficit in patients with CA. Patients with CA may try to compensate for their motor deficits by a longer cortical activation preceding voluntary movements (earlier onset of the BP). The increased NS1 could be the result of larger effort, by which patients try to compensate for their motor deficits as well.
为了确定小脑受累对大脑皮层为自主运动做准备状态的影响，我们研究了小脑萎缩（CA）患者在进行连续且目标导向的手指和手臂运动之前的运动相关皮层电位（运动准备电位，BP）。第一项任务（范式1）包括以自定节奏每隔3秒或更长时间进行一次连续的手指运动，患者和对照受试者按照屏幕上预先视觉设定的顺序快速按下键盘上的7个按键。第二项任务（范式2）包括在屏幕上有视觉反馈的目标导向自定节奏运动。在这两种范式中，对照受试者和患者都有明显的运动相关皮层电位，但在患者组中（范式2），峰值幅度（接近运动开始时）降低，而在总体分析中，运动开始前600 - 800毫秒的平均幅度（NS1）在患者组中（范式1和2）更大。因此，患者组中（范式1和2）峰值幅度与NS1之间的差异（NS2）更小。对照受试者的峰值幅度（范式2）和NS2（范式1）集中在Cz，而在患者组中这种地形学差异消失了。患者的BP起始时间比对照受试者更早（范式1和2）。我们的结果表明，从小脑到皮层 的通路在产生运动相关皮层电位中确实发挥作用。来自小脑的强烈输入似乎对于接近运动开始时产生正常运动电位至关重要，这反映了CA患者的特定缺陷。CA患者可能试图通过在自主运动之前进行更长时间的皮层激活（BP起始更早）来补偿其运动缺陷。NS1增加可能也是患者试图补偿其运动缺陷而付出更大努力的结果。
