Alvarez-Argote Santiago, Gransee Heather M, Mora Juan C, Stowe Jessica M, Jorgenson Amy J, Sieck Gary C, Mantilla Carlos B
1 Department of Physiology and Biomedical Engineering, Mayo Clinic , Rochester, Minnesota.
2 Department of Anesthesiology, Mayo Clinic , Rochester, Minnesota.
J Neurotrauma. 2016 Mar 1;33(5):500-9. doi: 10.1089/neu.2015.4054. Epub 2015 Nov 19.
Midcervical contusion injuries disrupt descending ipsilateral excitatory bulbospinal projections to phrenic motoneurons, compromising ventilation. We hypothesized that a unilateral contusion injury at C3 versus C5 would differentially impact phrenic activity reflecting more prominent disruption of ipsilateral descending excitatory drive to more caudal segments of the phrenic motor pool with more cranial injuries. Phrenic motoneuron counts and evidence of diaphragm muscle denervation at individual neuromuscular junctions (NMJ) were evaluated at 14 days post-injury after unilateral contusion injury (100 kDynes). Whole body plethysmography and chronic diaphragm EMG were measured before the injury and at 3, 7, and 14 days post-injury. Contusion injuries at either level resulted in a similarly sized cavity. C3 contusion resulted in loss of 39 ± 13% of ipsilateral phrenic motoneurons compared with 13 ± 21% after C5 contusion (p = 0.003). Cervical contusion injuries resulted in diaphragm muscle denervation (C3 contusion: 17 ± 4%; C5 contusion: 7 ± 4%; p = 0.047). The pattern of denervation revealed segmental innervation of the diaphragm muscle, with greater denervation ventrally after C3 contusion and dorsally after C5 contusion. Overall, diaphragm root mean square electromyography activity did not change ipsilaterally after C3 or C5 contusion, but increased contralaterally (∼ 11%) after C3 contusion only on the first day post-injury (p = 0.026). Similarly, there were no significant changes in breathing parameters during eupnea or exposure to hypoxia (10% O2) - hypercapnia (5% CO2) at any time post-injury. Unilateral midcervical contusions minimally impair ventilatory behaviors despite phrenic motoneuron loss and diaphragm muscle denervation.
颈中部挫伤会破坏同侧下行至膈运动神经元的兴奋性延髓脊髓投射,从而损害通气功能。我们推测,与C5水平相比,C3水平的单侧挫伤对膈神经活动的影响会有所不同,这反映出随着损伤部位更靠近头端,同侧下行兴奋性驱动对膈运动神经元池更尾端节段的破坏更为显著。在单侧挫伤损伤(100达因)后14天,评估膈运动神经元数量以及单个神经肌肉接头处膈肌无力的证据。在损伤前以及损伤后3天、7天和14天测量全身体积描记法和慢性膈肌肌电图。两个水平的挫伤均导致大小相似的空洞。与C5挫伤后13±21%的同侧膈运动神经元损失相比,C3挫伤导致39±13%的同侧膈运动神经元损失(p = 0.003)。颈部挫伤导致膈肌无力(C3挫伤:17±4%;C5挫伤:7±4%;p = 0.047)。失神经模式显示了膈肌的节段性神经支配,C3挫伤后腹侧失神经更严重,C5挫伤后背侧失神经更严重。总体而言,C3或C5挫伤后同侧膈肌均方根肌电图活动没有变化,但仅在损伤后第一天,C3挫伤后对侧膈肌均方根肌电图活动增加(约11%)(p = 0.026)。同样,在损伤后的任何时间,在平静呼吸或暴露于低氧(10% O2)-高碳酸血症(5% CO2)期间,呼吸参数均无显著变化。尽管存在膈运动神经元损失和膈肌无力,单侧颈中部挫伤对通气行为的损害极小。