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失神经、再神经支配和肌肉失衡对新生儿臂丛神经损伤后功能肌长度和肘屈曲挛缩的影响。

The effects of denervation, reinnervation, and muscle imbalance on functional muscle length and elbow flexion contracture following neonatal brachial plexus injury.

机构信息

Division of Orthopaedic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

出版信息

J Orthop Res. 2012 Aug;30(8):1335-42. doi: 10.1002/jor.22061. Epub 2012 Jan 6.

DOI:10.1002/jor.22061
PMID:22227960
Abstract

The pathophysiology of paradoxical elbow flexion contractures following neonatal brachial plexus injury (NBPI) is incompletely understood. The current study tests the hypothesis that this contracture occurs by denervation-induced impairment of elbow flexor muscle growth. Unilateral forelimb paralysis was created in mice in four neonatal (5-day-old) BPI groups (C5-6 excision, C5-6 neurotomy, C5-6 neurotomy/repair, and C5-T1 global excision), one non-neonatal BPI group (28-day-old C5-6 excision), and two neonatal muscle imbalance groups (triceps tenotomy ± C5-6 excision). Four weeks post-operatively, motor function, elbow range of motion, and biceps/brachialis functional lengths were assessed. Musculocutaneous nerve (MCN) denervation and reinnervation were assessed immunohistochemically. Elbow flexion motor recovery and elbow flexion contractures varied inversely among the neonatal BPI groups. Contracture severity correlated with biceps/brachialis shortening and MCN denervation (relative axon loss), with no contractures occurring in mice with MCN reinnervation (presence of growth cones). No contractures or biceps/brachialis shortening occurred following non-neonatal BPI, regardless of denervation or reinnervation. Neonatal triceps tenotomy did not cause contractures or biceps/brachialis shortening, nor did it worsen those following neonatal C5-6 excision. Denervation-induced functional shortening of elbow flexor muscles leads to variable elbow flexion contractures depending on the degree, permanence, and timing of denervation, independent of muscle imbalance.

摘要

新生儿臂丛神经损伤(NBPI)后出现的反常性肘屈挛缩的病理生理学机制尚不完全清楚。本研究通过检测下述假说来验证该挛缩的发生机制,即该挛缩是由失神经支配导致的肘屈肌生长受损引起的。在四个新生儿(5 天大)NBPI 组(C5-6 切除、C5-6 神经切断、C5-6 神经切断/修复和 C5-T1 全切除)、一个非新生儿 NBPI 组(28 天大的 C5-6 切除)和两个新生儿肌肉失衡组(三头肌肌腱切断术+ C5-6 切除)中,建立了单侧前肢瘫痪模型。术后 4 周,评估运动功能、肘活动范围和肱二头肌/肱肌功能长度。采用免疫组织化学法评估肌皮神经(MCN)失神经支配和再支配情况。肘屈肌运动恢复和肘屈挛缩在新生儿 NBPI 各组之间呈反向变化。挛缩的严重程度与肱二头肌/肱肌缩短和 MCN 失神经支配(相对轴突丢失)相关,MCN 有再支配(生长锥存在)的小鼠则不会出现挛缩。非新生儿 NBPI 无论是否失神经支配或再支配,均不会发生挛缩或肱二头肌/肱肌缩短。新生儿三头肌肌腱切断术不会引起挛缩或肱二头肌/肱肌缩短,也不会加重新生儿 C5-6 切除术后的挛缩。失神经支配导致肘屈肌的功能性缩短,导致可变的肘屈挛缩,这取决于失神经支配的程度、永久性和时间,而与肌肉失衡无关。

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