Schieber Marc H, Lang C E, Reilly K T, McNulty P, Sirigu A
Department of Neurology, University of Rochester, 601 Elmwood Ave, Box 673, Rochester, NY 14642, USA.
Adv Exp Med Biol. 2009;629:559-75. doi: 10.1007/978-0-387-77064-2_30.
Individuated finger movements of the human hand require selective activation of particular sets of muscles. Such selective activation is controlled primarily by the motor cortex via the corticospinal tract. Is this selectivity therefore lost when lesions damage the corticospinal tract? Or when the motor cortex reorganizes after amputation? We studied finger movements in normal human subjects and in patients who had recovered substantially from pure motor hemiparesis caused by lacunar strokes, which damage the corticospinal tract without affecting other pathways. Even after substantial recovery from these strokes, individuation of finger movements remained reduced-both for flexion/extension and for adduction/ abduction motion of the fingers. Stroke subjects regained the ability to move the instructed digit through a normal range, but unintentional motion of other digits was increased. This increase did not result from a change in the passive biomechanical coupling of the fingers. Rather, voluntary contractions of muscles that move the intended digit were accompanied by inappropriate contractions in muscles acting on additional digits. These observations suggest that the normal corticospinal system produces individuated finger movements not only by selectively activating certain muscles, but also by suppressing activation of other muscles during voluntary effort to move a given digit. In a separate experiment, reversible amputation of the hand was produced in normal subjects by ischemic nerve block at the wrist. Motor output to the intrinsic muscles and sensory input both become blocked under these conditions, effectively amputating the hand from the nervous system. But the long extrinsic muscles that flex and extend the digits remain normally innervated, and thus flexion forces still can be generated at the fingertips. During reversible amputation of the hand produced by ischemic nerve block, the ability of subjects to activate subdivisions of extrinsic muscles and to exert flexion force at individual fingertips continued to show essentially normal selectivity. Voluntary activation of the remaining muscles thus continues to be selective after amputation, in spite of both the loss of sensory input from the amputated hand, and reorganization within the primary motor cortex. During cortical reorganization after amputation, then, voluntary patterns of motor output intended for finger muscles may not be lost. We therefore examined activity in the stump muscles of above-elbow amputees, who have no remaining hand muscles. Different movements of the phantom hand were accompanied by different patterns of EMG in remaining proximal muscles, distinct from the EMG patterns associated with movement of the phantom elbow. We infer that voluntary motor output patterns that normally control finger movements after amputation may become diverted to remaining proximal muscles.
人类手部的个体化手指运动需要特定肌群的选择性激活。这种选择性激活主要由运动皮层通过皮质脊髓束来控制。那么,当病变损伤皮质脊髓束时,这种选择性是否会丧失呢?或者在截肢后运动皮层发生重组时又会怎样呢?我们研究了正常人类受试者以及因腔隙性中风导致纯运动性偏瘫且已基本康复的患者的手指运动,腔隙性中风会损伤皮质脊髓束而不影响其他通路。即使从这些中风中大幅恢复后,手指运动的个体化仍然降低——无论是手指的屈伸运动还是内收/外展运动。中风患者恢复了将指令手指移动到正常范围的能力,但其他手指的无意运动增加了。这种增加并非源于手指被动生物力学耦合的变化。相反,移动目标手指的肌肉的自主收缩伴随着作用于其他手指的肌肉的不适当收缩。这些观察结果表明,正常的皮质脊髓系统产生个体化手指运动不仅是通过选择性激活某些肌肉,还通过在自主努力移动给定手指时抑制其他肌肉的激活。在另一个实验中,通过手腕处的缺血性神经阻滞在正常受试者中造成手部的可逆性截肢。在这些条件下,手部固有肌的运动输出和感觉输入都被阻断,有效地将手部与神经系统切断联系。但是使手指屈伸的长的外在肌仍保持正常的神经支配,因此指尖仍能产生屈力。在缺血性神经阻滞造成手部可逆性截肢期间,受试者激活外在肌亚群并在各个指尖施加屈力的能力继续表现出基本正常的选择性。尽管截肢后失去了来自被截肢手部的感觉输入且初级运动皮层内发生了重组,但剩余肌肉的自主激活在截肢后仍然具有选择性。那么,在截肢后的皮层重组过程中,用于手指肌肉的自主运动输出模式可能不会丧失。因此,我们检查了肘部以上截肢者残端肌肉的活动,这些截肢者已没有剩余的手部肌肉。幻手的不同运动伴随着剩余近端肌肉中不同的肌电图模式,这与幻肘运动相关的肌电图模式不同。我们推断,截肢后通常控制手指运动 的自主运动输出模式可能会转向剩余的近端肌肉。