Pulverenti Timothy S, Islam Md Anamul, Alsalman Ola, Murray Lynda M, Harel Noam Y, Knikou Maria
Klab4Recovery Research Laboratory, Department of Physical Therapy, College of Staten Island, The City University of New York, Staten Island, New York.
Bronx Veterans Medical Research Foundation at the James J. Peters Department of Veterans Affairs Medical Center, Bronx, New York.
J Neurophysiol. 2019 Dec 1;122(6):2331-2343. doi: 10.1152/jn.00554.2019. Epub 2019 Oct 2.
Locomotion requires the continuous integration of descending motor commands and sensory inputs from the legs by spinal central pattern generator circuits. Modulation of spinal neural circuits by transspinal stimulation is well documented, but how transspinal stimulation affects corticospinal excitability during walking in humans remains elusive. We measured the motor evoked potentials (MEPs) at multiple phases of the step cycle conditioned with transspinal stimulation delivered at sub- and suprathreshold intensities of the spinally mediated transspinal evoked potential (TEP). Transspinal stimulation was delivered before or after transcranial magnetic stimulation during which summation between MEP and TEP responses in the surface EMG was absent or present. Relationships between MEP amplitude and background EMG activity, silent period duration, and phase-dependent EMG amplitude modulation during and after stimulation were also determined. Ankle flexor and extensor MEPs were depressed by suprathreshold transspinal stimulation when descending volleys were timed to interact with transspinal stimulation-induced motoneuron depolarization at the spinal cord. MEP depression coincided with decreased MEP gain, unaltered MEP threshold, and unaltered silent period duration. Locomotor EMG activity of bilateral knee and ankle muscles was significantly depressed during the step at which transspinal stimulation was delivered but fully recovered at the subsequent step. The results support a model in which MEP depression by transspinal stimulation occurs via subcortical or spinal mechanisms. Transspinal stimulation disrupts the locomotor output of flexor and extensor motoneurons initially, but the intact nervous system has the ability to rapidly overcome this pronounced locomotor adaptation. In conclusion, transspinal stimulation directly affects spinal locomotor centers in healthy humans. Lumbar transspinal stimulation decreases ankle flexor and extensor motor evoked potentials (MEPs) during walking. The MEP depression coincides with decreased MEP gain, unaltered MEP threshold changes, and unaltered silent period duration. These findings indicate that MEP depression is subcortical or spinal in origin. Healthy subjects could rapidly overcome the pronounced depression of muscle activity during the step at which transspinal stimulation was delivered. Thus, transspinal stimulation directly affects the function of spinal locomotor networks in healthy humans.
运动需要脊髓中枢模式发生器电路持续整合下行运动指令和来自腿部的感觉输入。经脊髓刺激对脊髓神经回路的调制已有充分记录，但经脊髓刺激在人类行走过程中如何影响皮质脊髓兴奋性仍不清楚。我们在步周期的多个阶段测量了运动诱发电位（MEP），这些阶段以低于和高于脊髓介导的经脊髓诱发电位（TEP）阈值强度的经脊髓刺激为条件。在经颅磁刺激之前或之后施加经脊髓刺激，在此期间，表面肌电图中MEP和TEP反应之间不存在或存在总和。还确定了MEP幅度与背景肌电图活动、静息期持续时间以及刺激期间和之后的相位依赖性肌电图幅度调制之间的关系。当下行冲动的时间与经脊髓刺激在脊髓诱导的运动神经元去极化相互作用时，阈上经脊髓刺激会抑制踝部屈肌和伸肌的MEP。MEP抑制与MEP增益降低、MEP阈值不变以及静息期持续时间不变同时出现。在施加经脊髓刺激的那一步中，双侧膝关节和踝关节肌肉的运动肌电图活动明显受到抑制，但在随后的一步中完全恢复。结果支持一种模型，即经脊髓刺激引起的MEP抑制是通过皮质下或脊髓机制发生的。经脊髓刺激最初会破坏屈肌和伸肌运动神经元的运动输出，但完整的神经系统有能力迅速克服这种明显的运动适应性。总之，经脊髓刺激直接影响健康人类的脊髓运动中枢。腰部经脊髓刺激会降低行走过程中踝部屈肌和伸肌的运动诱发电位（MEP）。MEP抑制与MEP增益降低、MEP阈值变化不变以及静息期持续时间不变同时出现。这些发现表明MEP抑制起源于皮质下或脊髓。健康受试者能够迅速克服在施加经脊髓刺激的那一步中肌肉活动的明显抑制。因此，经脊髓刺激直接影响健康人类脊髓运动网络的功能。
