Kim H Mike, Galatz Leesa M, Patel Nikunj, Das Rosalina, Thomopoulos Stavros
Department of Orthopaedic Surgery, Washington University, One Barnes-Jewish Hospital Plaza, 11300 West Pavilion, Campus Box 8233, St. Louis, MO 63110, USA.
J Bone Joint Surg Am. 2009 Apr;91(4):879-91. doi: 10.2106/JBJS.H.00088.
Injury to the brachial plexus during birth results in paralysis of the upper extremity in as many as one in 250 births and can lead to substantial functional deficits in the shoulder. The goal of this study was to characterize the development of bone and joint deformities in paralyzed neonatal shoulders and to assess the improvement of these deformities after muscle function recovery with use of an animal model.
Intramuscular injections of botulinum toxin were used to paralyze the supraspinatus, infraspinatus, and posterior deltoid of the left shoulders of mice at birth. Seventy mice were divided into three groups: Botox, recovery, and normal. The twenty-five mice in the Botox group received botulinum toxin injections until they were killed. The twenty mice in the recovery group received botulinum toxin injections for different durations and then were allowed injection-free recovery periods until they were killed. The twenty-five mice in the normal group received saline solution injections until they were killed. Radiographs were used to measure shoulder and elbow contractures. Microcomputed tomography was used to examine anatomical parameters of the supraspinatus muscle, humerus, and scapula.
The Botox group showed bone and joint deformities including delayed mineralization and flattening of the humeral head, hypoplasia, and introversion (i.e., anteversion) of the humerus, contractures of the shoulder and elbow, hypoplasia of shoulder muscles, hypoplasia of the scapula, and hypoplasia and retroversion of the glenoid. In the recovery group, a significant trend toward normal properties was observed with longer recovery periods (p<0.05). However, only soft-tissue contractures of the shoulder and elbow were resolved completely with the longest recovery period.
This mouse model successfully simulates human neonatal brachial plexus palsy, reproducing most of the bone and joint deformities found in the human condition. The deformities started to develop early in the postnatal period in the paralyzed shoulders and progressed with longer durations of paralysis. Early restoration of muscle function completely resolved the soft-tissue contractures of the shoulder and elbow. However, osseous deformities of the humerus and scapula were never resolved completely. These findings demonstrate the time-dependence of reversibility of musculoskeletal deformities in developing shoulders with neurological deficits.
分娩时臂丛神经损伤导致高达每250例出生中就有1例上肢麻痹,并可能导致肩部严重功能缺陷。本研究的目的是描述麻痹新生儿肩部骨与关节畸形的发展情况,并评估使用动物模型在肌肉功能恢复后这些畸形的改善情况。
出生时对小鼠左肩部的冈上肌、冈下肌和三角肌后束进行肌肉注射肉毒杆菌毒素使其麻痹。70只小鼠分为三组:肉毒杆菌毒素组、恢复组和正常组。肉毒杆菌毒素组的25只小鼠接受肉毒杆菌毒素注射直至处死。恢复组的20只小鼠接受不同时长的肉毒杆菌毒素注射,然后有不注射的恢复期直至处死。正常组的25只小鼠接受生理盐水注射直至处死。使用X线片测量肩部和肘部挛缩。使用微型计算机断层扫描检查冈上肌、肱骨和肩胛骨的解剖参数。
肉毒杆菌毒素组出现骨与关节畸形,包括矿化延迟和肱骨头扁平、肱骨发育不全和内倾(即前倾)、肩部和肘部挛缩、肩部肌肉发育不全、肩胛骨发育不全以及关节盂发育不全和后倾。在恢复组中,随着恢复期延长,观察到向正常特性发展的显著趋势(p<0.05)。然而,只有在最长恢复期时肩部和肘部的软组织挛缩才完全得到解决。
该小鼠模型成功模拟了人类新生儿臂丛神经麻痹,重现了人类疾病中发现的大部分骨与关节畸形。这些畸形在麻痹肩部出生后早期开始发展,并随着麻痹时间延长而进展。肌肉功能的早期恢复完全解决了肩部和肘部的软组织挛缩。然而,肱骨和肩胛骨的骨性畸形从未完全解决。这些发现证明了发育中的肩部伴有神经功能缺损时肌肉骨骼畸形可逆性的时间依赖性。