Crouch Dustin L, Plate Johannes F, Li Zhongyu, Saul Katherine R
Virginia Tech-Wake Forest University School of Biomedical Engineering and Sciences, Winston-Salem, NC 27157, USA.
J Hand Surg Am. 2013 Feb;38(2):241-9. doi: 10.1016/j.jhsa.2012.11.007. Epub 2013 Jan 5.
To determine whether transfer to only the anterior branch of the axillary nerve will restore useful function after axillary nerve injury with persistent posterior deltoid and teres minor paralysis.
We used a computational musculoskeletal model of the upper limb to determine the relative contributions of posterior deltoid and teres minor to maximum joint moment generated during a simulated static strength assessment and to joint moments during 3 submaximal shoulder movements. Movement simulations were performed with and without simulated posterior deltoid and teres minor paralysis to identify muscles that may compensate for their paralysis.
In the unimpaired limb model, teres minor and posterior deltoid accounted for 16% and 14% of the total isometric shoulder extension and external rotation joint moments, respectively. During the 3 movement simulations, posterior deltoid produced as much as 20% of the mean shoulder extension moment, whereas teres minor accounted for less than 5% of the mean joint moment in all directions of movement. When we paralyzed posterior deltoid and teres minor, the mean extension moments generated by the supraspinatus, long head of triceps, latissimus dorsi, and middle deltoid increased to compensate. Compensatory muscles were not fully activated during movement simulations when posterior deltoid and teres minor were paralyzed.
Reconstruction of the anterior branch of the axillary nerve only is an appropriate technique for restoring shoulder abduction strength after isolated axillary nerve injury. When shoulder extension strength is compromised by extensive neuromuscular shoulder injury, reconstruction of both the anterior and posterior branches of the axillary nerve should be considered.
By quantifying the biomechanical role of muscles during submaximal movement, in addition to quantifying muscle contributions to maximal shoulder strength, we can inform preoperative planning and permit more accurate predictions of functional outcomes.
确定在腋神经损伤后三角肌后束和小圆肌持续麻痹的情况下，仅将腋神经前支进行移位是否能恢复有用的功能。
我们使用上肢的计算肌肉骨骼模型来确定三角肌后束和小圆肌在模拟静态力量评估过程中产生的最大关节力矩以及在3次次最大肩部运动过程中对关节力矩的相对贡献。在有和没有模拟三角肌后束和小圆肌麻痹的情况下进行运动模拟，以识别可能代偿其麻痹的肌肉。
在未受损肢体模型中，小圆肌和三角肌后束分别占等长肩部伸展和外旋关节总力矩的16%和14%。在3次运动模拟中，三角肌后束产生的平均肩部伸展力矩高达20%，而小圆肌在所有运动方向上占平均关节力矩的比例均小于5%。当我们使三角肌后束和小圆肌麻痹时，冈上肌、肱三头肌长头、背阔肌和三角肌中束产生的平均伸展力矩增加以进行代偿。在三角肌后束和小圆肌麻痹的运动模拟过程中，代偿性肌肉并未完全激活。
仅重建腋神经前支是孤立性腋神经损伤后恢复肩部外展力量的合适技术。当广泛的神经肌肉肩部损伤导致肩部伸展力量受损时，应考虑重建腋神经的前支和后支。
通过量化次最大运动过程中肌肉的生物力学作用，除了量化肌肉对最大肩部力量的贡献外，我们可以为术前规划提供信息，并更准确地预测功能结果。
