Grumbles Robert M, Thomas Christine K
1 The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine , Miami, Florida.
2 Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
J Neurotrauma. 2017 Feb;34(3):581-590. doi: 10.1089/neu.2015.4374. Epub 2016 Aug 25.
The severe muscle weakness and atrophy measured after human spinal cord injury (SCI) may relate to chronic muscle denervation due to motoneuron death and/or altered muscle use. The aim of this study was to estimate motoneuron death after traumatic human SCI. The diameter and number of myelinated axons were measured in ventral roots post-mortem because ventral roots contain large diameter (> 7 μm) myelinated axons that typically arise from motoneurons and innervate skeletal muscle. In four cases (SCI levels C7, C8, T4, and L1) involving contusion (n = 3) or laceration (n = 1), there was a significant reduction in the number of large diameter myelinated axons at the lesion epicenter (mean ± standard error [SE]: 45 ± 11% Uninjured), one level above (51 ± 14%), and one (27 ± 12%), two (45 ± 40%), and three (54 ± 23%) levels below the epicenter. Reductions in motoneuron numbers varied by side and case. These deficits result from motoneuron death because the gray matter was destroyed at and near the lesion epicenter. Muscle denervation must ensue. In seven cases, ventral roots at or below the epicenter had large diameter myelinated axons with unusually thin myelin, a sign of incomplete remyelination. The mean ± SE g ratio (axon diameter/fiber diameter) was 0.60 ± 0.01 for axons of all diameters in five above-lesion ventral roots, but increased significantly for large diameter fibers (≥ 12 μm) in three roots at the lesion epicenter. Motoneuron death after human SCI will coarsen muscle force gradation and control, while extensive muscle denervation will stifle activity-based treatments.
人类脊髓损伤（SCI）后所测量到的严重肌肉无力和萎缩，可能与运动神经元死亡导致的慢性肌肉失神经支配和/或肌肉使用改变有关。本研究的目的是评估外伤性人类SCI后的运动神经元死亡情况。死后测量腹侧神经根中有髓轴突的直径和数量，因为腹侧神经根包含通常源自运动神经元并支配骨骼肌的大直径（>7μm）有髓轴突。在4例涉及挫伤（n = 3）或撕裂伤（n = 1）的病例（SCI节段为C7、C8、T4和L1）中，损伤中心处大直径有髓轴突数量显著减少（平均值±标准误[SE]：45±11%，未受伤侧），损伤中心上方一个节段（51±14%），以及损伤中心下方一个（27±12%）、两个（45±40%）和三个（54±23%）节段处。运动神经元数量的减少因侧别和病例而异。这些缺陷是由运动神经元死亡导致的，因为损伤中心及其附近的灰质被破坏。肌肉失神经支配必然随之发生。在7例病例中，损伤中心或其下方的腹侧神经根中有大直径有髓轴突，其髓鞘异常薄，这是髓鞘再生不完全的迹象。损伤上方5个腹侧神经根中所有直径轴突的平均±SE g比值（轴突直径/纤维直径）为0.60±0.01，但损伤中心3个神经根中≥12μm的大直径纤维的g比值显著增加。人类SCI后的运动神经元死亡将使肌肉力量分级和控制变得粗糙，而广泛的肌肉失神经支配将阻碍基于活动的治疗。
