Department of Bioengineering, Imperial College London, London SW7 2AZ, United Kingdom
Department of Clinical and Movement Disorders, Institute of Neurology, University College London, London WC1N 3BG, United Kingdom.
J Neurosci. 2021 Jun 2;41(22):4867-4879. doi: 10.1523/JNEUROSCI.2908-20.2021. Epub 2021 Apr 23.
Human corticospinal transmission is commonly studied using brain stimulation. However, this approach is biased to activity in the fastest conducting axons. It is unclear whether conclusions obtained in this context are representative of volitional activity in mild-to-moderate contractions. An alternative to overcome this limitation may be to study the corticospinal transmission of endogenously generated brain activity. Here, we investigate in humans ( = 19; of either sex), the transmission speeds of cortical β rhythms (∼20 Hz) traveling to arm (first dorsal interosseous) and leg (tibialis anterior; TA) muscles during tonic mild contractions. For this purpose, we propose two improvements for the estimation of corticomuscular β transmission delays. First, we show that the cumulant density (cross-covariance) is more accurate than the commonly-used directed coherence to estimate transmission delays in bidirectional systems transmitting band-limited signals. Second, we show that when spiking motor unit activity is used instead of interference electromyography, corticomuscular transmission delay estimates are unaffected by the shapes of the motor unit action potentials (MUAPs). Applying these improvements, we show that descending corticomuscular β transmission is only 1-2 ms slower than expected from the fastest corticospinal pathways. In the last part of our work, we show results from simulations using estimated distributions of the conduction velocities for descending axons projecting to lower motoneurons (from macaque histologic measurements) to suggest two scenarios that can explain fast corticomuscular transmission: either only the fastest corticospinal axons selectively transmit β activity, or else the entire pool does. The implications of these two scenarios for our understanding of corticomuscular interactions are discussed. We present and validate an improved methodology to measure the delay in the transmission of cortical β activity to tonically-active muscles. The estimated corticomuscular β transmission delays obtained with this approach are remarkably similar to those expected from transmission in the fastest corticospinal axons. A simulation of β transmission along a pool of corticospinal axons using an estimated distribution of fiber diameters suggests two possible mechanisms by which fast corticomuscular transmission is achieved: either a very small fraction of the fastest descending axons transmits β activity to the muscles or, alternatively, the entire population does and natural cancellation of slow channels occurs because of the distribution of axon diameters in the corticospinal tract.
人类皮质脊髓传递通常使用脑刺激来研究。然而，这种方法偏向于最快传导轴突的活动。目前尚不清楚在这种情况下得出的结论是否代表轻度至中度收缩时的随意活动。克服这一限制的一种替代方法可能是研究内源性产生的脑活动的皮质脊髓传递。在这里，我们在人类（= 19；无论性别）中研究了皮质β节律（~20 Hz）在进行轻度紧张收缩时传向手臂（第一背间骨间肌）和腿部（胫骨前肌；TA）肌肉的传输速度。为此，我们提出了两种改进方法来估计皮质肌β传递延迟。首先，我们表明，累积密度（互协方差）比常用的有向相干性更准确，可用于估计双向系统中传输带限信号的传输延迟。其次，我们表明，当使用放电运动单位活动代替干扰肌电图时，皮质肌传递延迟估计不受运动单位动作电位（MUAP）形状的影响。应用这些改进方法，我们表明，下行皮质肌β传递仅比预期的最快皮质脊髓通路慢 1-2 ms。在我们工作的最后一部分，我们展示了使用来自灵长类动物组织学测量的较低运动神经元下行轴突的传导速度估计分布的模拟结果，以提出两种可以解释快速皮质肌传递的情景：要么只有最快的皮质脊髓轴突选择性地传递β活动，要么整个池都传递。讨论了这两种情景对我们理解皮质肌相互作用的影响。我们提出并验证了一种改进的方法来测量皮质β活动传至紧张活动肌肉的延迟。使用该方法获得的皮质肌β传递延迟与从最快皮质脊髓轴突传递中预期的延迟非常相似。使用估计的纤维直径分布对皮质脊髓轴突池的β传递进行模拟表明，实现快速皮质肌传递的两种可能机制：要么是一小部分最快的下行轴突将β活动传递到肌肉，要么是整个种群都传递，由于皮质脊髓束中轴突直径的分布，自然会消除慢通道。
