Department of Clinical Neurophysiology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
J Physiol. 2019 Jul;597(13):3457-3471. doi: 10.1113/JP277639. Epub 2019 Jun 6.
Ischaemic nerve block (INB) of the forearm rapidly reduces somatosensory input to a part of the body, which leads to the functional reorganization of the temporarily deafferented primary motor cortex (M1). We applied a novel modified INB (mINB) to the forearm, maintaining mean blood pressure, to assess cortical plasticity in the primary somatosensory cortex (S1) and the M1 regions associated with small hand muscles. S1 excitability was measured by median nerve somatosensory-evoked potentials (SEPs), while M1 excitability was evaluated by motor-evoked potentials (MEPS), using transcranial magnetic stimulation. The finding that S1 excitability increased and M1 excitability decreased after the mINB was removed reflects the differential short-term cortical plasticity of the S1 and M1 regions. These opposite effects observed for the S1 and M1 regions following the mINB may indicate a possible intra-hemispheric interaction between the S1 and M1 regions.
Ischaemic nerve block (INB) causes short-term sensory deprivation, leading to functional reorganization in the deafferented motor cortex (M1). We used a modified INB (mINB) to evaluate cortical plasticity in the somatosensory cortex (S1) and M1 region associated with small hand muscles, because INB strongly inhibits muscles distal to the tourniquet. Thirty-three healthy adults participated in different combinations of four experiments. A pneumatic tourniquet was placed just below the right elbow and inflated to induce a mINB. We recorded the median nerve somatosensory- and motor-evoked potentials (SEPs and MEPs) before, during and after mINB placement and assessed spinal cord excitability using F-wave measurements. SEPs at Erb's point (N9) were abolished during the mINB; those at cortical N20 were suppressed. After removing the mINB, N20 amplitudes increased significantly, while those at N9 did not fully recover. P14 amplitudes after tourniquet deflation immediately recovered to baseline levels. M1-MEP amplitudes decreased during the mINB, and Erb-MEPs were suppressed. After the mINB was removed, M1-MEPs remained suppressed, while Erb-MEPs fully recovered. F-waves were not affected by the intervention. Therefore, sensory, but not motor, nerve function was affected by the mINB. S1 excitability was enhanced after the mINB was removed, indicating that S1 and M1 excitability were modulated in opposing directions after deflation. These after-effects may reflect isolated effects or interactions between the S1 and M1 regions. Our findings may facilitate improved understanding of the sensorimotor modulations that occur distal to the tourniquet due to temporal deafferentation and lead to development of novel neuromodulation protocols.
前臂缺血性神经阻滞（INB）可迅速减少身体某部分的体感传入，导致暂时去传入的初级运动皮层（M1）的功能重组。我们应用一种新的改良 INB（mINB）在前臂，维持平均血压，以评估与小手部肌肉相关的初级体感皮层（S1）和 M1 区域的皮质可塑性。通过正中神经体感诱发电位（SEP）测量 S1 兴奋性，通过经颅磁刺激评估 M1 兴奋性。mINB 去除后 S1 兴奋性增加而 M1 兴奋性降低的发现反映了 S1 和 M1 区域的短期皮质可塑性的差异。mINB 后 S1 和 M1 区域观察到的相反影响可能表明 S1 和 M1 区域之间存在可能的半球内相互作用。
缺血性神经阻滞（INB）导致短期感觉剥夺，导致去传入运动皮层（M1）的功能重组。我们使用改良 INB（mINB）来评估与小手部肌肉相关的体感皮层（S1）和 M1 区域的皮质可塑性，因为 INB 强烈抑制止血带远端的肌肉。33 名健康成年人参与了四项实验的不同组合。在右肘下方放置一个气动止血带，并充气以诱导 mINB。我们在 mINB 放置前后和期间记录正中神经体感和运动诱发电位（SEP 和 MEP），并使用 F 波测量评估脊髓兴奋性。在 mINB 期间，Erb 点（N9）的 SEP 消失；皮质 N20 被抑制。去除 mINB 后，N20 振幅显著增加，而 N9 振幅未完全恢复。止血带放气后 P14 振幅立即恢复到基线水平。mINB 期间 M1-MEP 振幅降低，Erb-MEP 被抑制。去除 mINB 后，M1-MEP 仍然受到抑制，而 Erb-MEP 完全恢复。F 波不受干预影响。因此，感觉神经而不是运动神经功能受 mINB 影响。mINB 去除后 S1 兴奋性增强，表明 S1 和 M1 兴奋性在放气后以相反的方向调节。这些后效可能反映了 S1 和 M1 区域的孤立效应或相互作用。我们的发现可能有助于更好地理解由于时间去传入而导致止血带远端发生的感觉运动调节，并导致新的神经调节方案的发展。
