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关键词：囊性黏连；麻醉；被动活动范围 摘要 研究设计：观察性：横断面研究。 背景：特发性冻结肩是造成严重和长期残疾的常见原因，其特点是自发性疼痛和进展性的肩关节运动受限。尽管特发性渐冻肩可以在预期中自然恢复，但其症状平均持续30个月。慢性炎症和盂肱关节周围囊状结构的各种纤维化和挛缩，被认为是冻结肩相关的体征和症状出现的原因，然而，这种衰弱状况的病理解剖学还没有被完全理解。 目的：探讨肌肉保护成分限制特发性冻结肩患者运动的可行性。 方法：计划手术患者在全身麻醉前、后分别测定被动肩外展活动度和外旋活动度（ROM） 结果：5例肩部疼痛和被动运动受限的患者自愿参加了这项研究。所有参与者在麻醉后被动外展活动度增加，从大约55°–110°的麻醉前活动度增加。其中3名参与者在麻醉后的被动外旋活动度显著增加，从大约15°- 40°的无感觉的ROM不等。 结论：本研究5例冻结肩的患者显示，主动肌保护，而不是囊膜挛缩，可能是导致某些特发性冻结肩的典型临床特征的患者运动受限的主要原因。这些发现强调了我们需要重新考虑对冻结肩病理解剖的理解。 证据级别：Level 4 ABSTRACT Study Design: Observational: cross-sectional study. Background: Idiopathic frozen shoulder is a common cause of severe and prolonged disability characterised by 1. 介绍 自19世纪晚期首次描述特发性冻结肩以来，它一直困扰着医学界。一般人群中约有8%–10%的人和29%的糖尿病人群中存在此现象（Walker-Bone et al., 2004; Balci et al., 1999）。其特征表现为自然发生间歇性疼痛，表现为明显的主动性和被动性关节僵硬stiffness（Lundberg, 1969; Nash and Hazelman, 1989），通常会导致功能的严重丧失（Jones et al., 2013）。大多数患者在1–3年后，肩关节疼痛功能逐渐恢复，这种情况被描述为自我限制（Hand et al., 2008）。 没有明确的肩部冻结的诊断试验，诊断依据是排除骨病、明显的肩袖损伤、锁定性脱位、骨折或以缺血性坏死为症状原因的体格检查（Lewis，2015）。如果患者在至少两个活动层面上有痛苦的主动和被动运动限制，其中一个是外部旋转，那么就可以对冻结的肩部进行临床诊断（Buchbinder et al，2004）。 冻结肩的病理解剖尚不完全清楚。冻结肩的组织学和关节镜研究表明，慢性炎症、纤维化和关节囊挛缩是造成疼痛和活动受限的原因（Ryan et al，2016）。因此，治疗通常是针对延长肩关节结构，以恢复肩关节活动度，同时管理疼痛。 冻结肩在最佳治疗方面没有共识（Lewis, 2015）。Evi-dence认为皮质类固醇注射可带来显著的短期效益（Buchbinder et al., 2003），但是，没有什么证据支持旨在延长盂肱关节囊的治疗措施。旨在增加ROM的理疗在短期内只比安慰剂注射略高一些（Carette et al., 2003）；关节镜下释放ROM没有随机对照试验的证据支持（Lewis，2015）；囊袋水化或膨胀仅与皮质类固醇注射（Tveita et al., 2008）。 也许目前的治疗方法是无效的，因为他们针对错误的结构？在其他疼痛的肌肉骨骼条件，如背部和颈部疼痛的关节活动往往是肌肉自我保护（痉挛）。这说明冻结肩患者肩关节活动度受限可能是由于肌肉收缩的反应，非皮肤的病理生理学或认知或情感因素，如害怕疼痛或焦虑。事实上，从解剖学的角度来看肩关节囊是强烈加强了旋转肌腱。肩关节内旋、前旋肌群（肩胛下肌）的收缩可以限制肩关节外旋的活动范围，这是诊断冻结肩的关键临床表现之一。考虑到在肩部提升时，为了防止这种运动，肱骨必须向外旋转，这也可能与肩外展和屈曲范围受限有关。这也可以解释为什么肩周炎患者的肩关节活动度会随着疼痛或焦虑的消退而自发改善。 本病例系列研究的目的是探讨肩关节冻结患者的肌肉保护成分对运动限制的作用。为此，我们比较了被动肩关节活动度在全身麻醉前后的使用情况。 Introduction Idiopathic frozen shoulder has puzzled the medical community since it was first described in the late 19th century. It occurs in ap-proximately 8%–10% of the general population and up to 29% of the diabetic population (Walker-Bone et al., 2004; Balci et al., 1999). It is characterised by spontaneous onset of pain with progressive, marked active and passive stiffness at the glenohumeral joint (Lundberg, 1969; Nash and Hazelman, 1989) usually resulting in gross loss of function(Jones et al., 2013). The condition is described as self-limiting with gradual return of painfree shoulder function after 1–3 years in most patients (Hand et al., 2008). There is no definitive diagnostic test for frozen shoulder and diag-nosis is based on physical examination following exclusion of osteoar-thritis, significant rotator cuff disease, locked dislocations, fractures or avascular necrosis as the cause of symptoms (Lewis, 2015). Clinical diagnosis of frozen shoulder is made if the patient has painful restric-tion of active and passive motion in at least two planes of movement, ofwhich one is external rotation (Buchbinder et al., 2004). The pathoanatomy of frozen shoulder is not fully understood. Histological and arthroscopic studies of frozen shoulder suggest chronic inflammation, fibrosis and glenohumeral joint capsule contracture is responsible for the pain and restricted range of movement (ROM) (Ryan et al., 2016). Consequently, treatment is most commonly aimed at lengthening glenohumeral joint structures to restore shoulder ROM while managing pain. Frozen shoulder is considered notoriously difficult to treat and there is no consensus regarding optimal management (Lewis, 2015). Evi-dence suggests that corticosteroid injection confers significant short term benefit (Buchbinder et al., 2003), however, there is little evidence to support the effectiveness of treatments aimed at lengthening the glenohumeral joint capsule. Physiotherapy aimed at increasing ROM is only slightly more effective than placebo injection in the short term (Carette et al., 2003); efficacy of arthroscopic capsular release is not supported by evidence from randomised control trials (Lewis, 2015); and capsular hydrodilation or distension is no more effective than corticosteroid injection alone (Tveita et al., 2008). Perhaps current treatment approaches are ineffective because they target the wrong structures? In other painful musculoskeletal condi-tions such as back and neck pain ROM is often restricted by muscle guarding (spasm). It may be that restricted shoulder ROM in people with frozen shoulder is due to muscle contraction in response to un-derlying pathophysiology or to cognitive or emotional factors such as fear of pain or anxiety. The fact that the glenohumeral joint capsule is strongly reinforced by the rotator cuff tendons makes this hypothesis plausible from an anatomical perspective. Contraction of the anterior rotator cuff (subscapularis), an internal rotator of the shoulder, could feasibly restrict shoulder external rotation range of motion, one of the crucial clinical findings required to make a diagnosis of frozen shoulder. Given that the humerus must externally rotate during shoulder eleva-tion muscle guarding to prevent this movement could also be associated with restricted shoulder abduction & flexion range. This could also explain why shoulder ROM improves spontaneously in patients suf-fering from frozen shoulder as pain and/or anxiety subsides. The aim of this case series, was to investigate a muscle guarding component to movement restriction in patients with frozen shoulder. To do so, we compared passive shoulder ROM before and after the administration of general anaesthesia.
2.方法 2.1.参与者 计划接受囊内释放手术治疗冻结肩的患者被告知这项研究。手术的适应症是参与的骨科外科医生对囊膜紧绷的临床印象。如果骨关节炎, 显著的肩袖损伤和肩部骨折或脱位被x线和MRI检查排除，同时站立位下所做的体格检查表明所有主动和被动肩关节活动完全性受限大于50% 正常的ROM，手术才予提供。如果患者在术前四星期内肩部有创伤史,受影响肩膀有过手术史, 肩部痛苦来自脊椎(定义为肩膀痛苦在颈椎活动和或触诊过程中加重) 或并发的炎症或神经系统疾病累及受影响的肩膀，则被排除。 2.2.结果测量 为了减少手术前在全身麻醉下参与者花费的时间，在全身麻醉前后只比较两个被动肩关节ROM 结果测量：外旋ROM，因为这个方向的被动限制是冻结肩的一个诊断标准(Bunker, 1997)；以及外展ROM，因为它可以很容易地在骨科医生要求的侧卧位下测量。便携式定制的臂架，内置电位器 (Vishay 型号 357, 德国) 和力传感器 (XTran, 型号 S1W 250N, 应用测量PTY，澳洲有限公司) 建立了记录扭矩应用到每个参与者的手臂实现最大的被动外旋ROM。参与者的手臂被捆绑到臂架上, 臂架主要保持肘部90度的屈曲，肩部45°外展。采用32位模拟器 (TX、美国) 和 LABVIEW 软件, 以100赫兹的采样率记录了肩外旋的角度和扭矩。通过被动地移动参与者的手臂来测量外展ROM。通过测量水平参考线与肩峰突起和外上髁之间的线的交叉处的角度，从数字照片测量实现的外展ROM。 2.3.步骤 在预定的手术当天, 研究人员会见了可能符合条件的病人, 并描述了研究的目的和设计。对于同意的患者, 主动和被动肩关节屈曲, 外展, 外旋与手臂侧向和手背向后在受损肩上进行，以确认资格。正如临床上常见的做法一样, 这些运动是在患者站立下进行，并用量角器 (内收, 屈曲, 外旋) 或卷尺 (手背后)来测量。在确认符合纳入和排除标准之后, 参与者签署了同意书, 同时收集人口统计数据, 包括年龄、惯用手和症状持续时间。为确定冷冻肩部对其生活质量的影响, 参与者完成了肩痛和伤残指数评定(SPADI)。 参与者侧卧,测量被动肩外展 ROM。其次是被动肩外旋测量;对三次重复的被动外旋ROM进行平均分析。要求每个参与者放松他们的受损肩膀, 同时测量人员慢慢地移动手臂通过有效范围。当感觉到运动阻力或剧烈的疼痛阻止进一步运动时，运动停止。 随后每位参赛者进入手术室并进行全身麻醉管理。研究人员随后进入手术室, 并重复被动肩关节ROM测量。对于不受麻醉前严重疼痛限制的外旋ROM 测量, 应用了类似于麻醉前情况下所达到的扭矩。对于那些在麻醉前经历限制外旋ROM严重疼痛的参与者, 逐渐增加扭矩直到感觉到运动阻力。在被动的外旋和外展 ROM 测量完成之后, 参与者被留在治疗肩部的外科医生的护理下。 3.结果 包括3名女性和2名男性。参与者的年龄从51岁到64岁，症状从6个月到30个月不等。没有一个参与者是糖尿病患者，3个参与者的非主导肩部受到影响。SPADI评分范围从67到87，显示中度至重度的疼痛和残疾。 所有受试者在麻醉后被动外展活动度增加，从53°到111°不等（表1，图1）。4名受试者在45°的侧卧位上测量时，表现出被动外旋ROM限制预麻醉。该ROM在3名参加者中增加了15°–41°（表1，图1a），一名参加者基本没有变化（图1，表1）。1c)麻醉后，在相同的力量水平。有一位参与者在站在一旁时符合严格限制的被动外部旋转ROM的包含标准，当在侧卧前麻醉下测量时，他在正常范围内（68°）显示了被动的外部旋转ROM。当施加同样的力时，经全身麻醉后，这个ROM非常相似（69°）（表1）。 4. 讨论 这是第一次关于肩周炎患者没有疼痛和肌肉收缩这些复杂变量参与的肩关节被动活动度的研究。5名参与者表示在麻醉后肩关节被动外展关节活动度增加53°-111°，增加60％-223％（表1；图1）。肩关节外展关节活动度的大幅增加表明肌肉防护可能是限制一些肩周炎患者外展关节活动度的重要原因。 本研究中被动肩关节外旋ROM的改善还指出了肌肉收缩在一些肩周炎患者运动受限中起的作用。5名患者中有3名表现出ROM的大幅度增加（表1，图1a）。对于参与者1和2，在麻醉前施加的外旋转扭矩大致相同的情况下，被动外旋ROM分别增加41°和20°。对于参与者3，其麻醉前被动外旋ROM受到剧烈疼痛的限制，当施加扭矩的速度与参与者1和2相似时，外旋ROM增加15°（表1，图1b）。 对于剩下的2名参与者，肩关节被动外旋关节活动度在麻醉下没有显著增加。参与者4也包括在内，因为他在侧面站立测量时满足了显着限制的被动外旋ROM的包含标准。然而，在麻醉之前使用臂架在侧卧位置测量时，被动外旋范围是68°，其在正常范围内。在全身麻醉下，该范围未改变（69°）（表1，图1b）。当参与者的手臂受到支撑并且在侧卧位置的手臂框架中放松时，减少肌肉防护可以解释这个结果。 参与者5具有有限的被动外肩旋转，其在麻醉下测量时几乎没有变化。该症状持续时间最长的受试者（30个月）记录了17°的被动外旋ROM预麻，受到剧烈疼痛的限制。在麻醉期间和施加的扭矩类似于应用于参与者1,2和3的外旋转ROM在20°时基本不变。这一发现表明缩短的结缔组织结构可能是该患者的运动受限的原因。虽然需要进一步的证据来证实这一假设，但该患者中的紧密结缔组织可能是长时间运动限制的功能。 虽然这项研究的目的不是回答为什么这组患者可能有肌肉防护导致严重的功能限制的问题，但可以推测。患有肩周炎的患者的肌肉保护可以是保护机制或响应潜在的病理生理学。在其他疼痛的肌肉骨骼疾病如背痛中观察到肌肉活动改变，尽管生理机制尚不清楚（vanDieën等，2003）。也可能存在导致运动受限的认知或情绪因素，例如恐惧（运动或疼痛），焦虑或对病症的灾难性评估。这些心理介导的因素被认为会影响其他痛苦条件下的行为。需要对更大的肩周炎患者进行研究，以确认这些发现的准确性。 准确评估被动肩部ROM对于确定致密结缔组织结构对肩部ROM缺陷的贡献至关重要，因为它是冷冻肩部诊断和指导治疗决策的关键标准。如果我们接受麻醉下的ROM测量反映了真正的被动ROM，那么这项研究表明，在存在疼痛的情况下被动肩部ROM的评估准确性很差。重要的是，这使人们质疑定义肩周炎诊断的物理评估程序的有效性。值得注意的是，这项研究并非旨在稳健地测试被动ROM评估的有效性，但研究结果表明，区分主动和被动ROM限制至关重要。 本研究的结论需要考虑到几个局限性。显然，五名接受手术治疗的患者的冻结肩的结果可能并不适用于一般的冻伤肩膀人群。此外，肩关节外展ROM测量没有稳定肩胛骨，因此不能准确反映肩关节的运动。在麻醉后外展ROM的增加可能是由于肩胛运动的增加，尽管这不可能解释一些参与者肩关节外展ROM几乎全面增加一倍的情况。 这项研究表明，肌肉保护可能是一些冻结肩患者肩运动缺陷的一个重要因素。鉴于许多当代的治疗方法都建立在肩关节活动限制是由于被动结构的收紧这样的假设上，所以这一发现值得进一步研究。 Discussion This is the first study to report passive shoulder ROM in patients diagnosed with frozen shoulder measured without the confounding variables of pain and muscle contraction. The five participants demonstrated increases of 53°–111° in passive shoulder abduction ROM following anaesthesia representing increases of between 60% and 223% (Table 1; Fig. 1). These large increases in abduction ROM suggest that muscle guarding is likely a significant contributor to abduction ROM restriction in some patients with frozen shoulder. Passive shoulder external rotation ROM improvement in this study also points to a role for muscle contraction in movement restriction in some patients diagnosed with frozen shoulder. Three of the five participants demonstrated large increases in ROM under anaesthesia (Table 1, Fig. 1a). For participants 1 and 2 passive external rotation ROM increased by 41° and 20° respectively at approximately the same external rotation torque applied pre-anaesthesia. For participant 3, whose pre-anaesthesia passive external rotation ROM was limited by severe pain, external rotation ROM increased by 15° when torque was applied at similar levels as for participants 1 and 2 (Table 1, Fig. 1b). For the remaining two participants, passive shoulder external ROM did not increase substantially under anaesthesia. Participant 4 was included in the study because he satisfied the inclusion criterion of significantly restricted passive external rotation ROM when measured in standing with the arm by the side. However, when measured in the side-lying position using the arm frame prior to anaesthesia, passive external rotation range was 68° which is within normal range. This range was unchanged (69°) under general anaesthesia (Table 1, Fig. 1b). Reduced muscle guarding when the participant's arm was supported and relaxed in the arm frame in the side-lying position could explain this result. Participant 5 had limited passive external shoulder rotation preanaesthesia which showed little change when measured under anaesthesia. This participant, who had the longest duration of symptoms (30 months), recorded a passive external rotation ROM pre-anaesthesia of 17° which was limited by severe pain. During anaesthesia and under applied torques similar to those applied to participants 1, 2 and 3 external rotation ROM was substantially unchanged at 20° This finding suggests that shortened connective tissue structures may be the cause of the movement restriction in this patient. It is possible that tight connective tissues in this patient are a function of prolonged restriction of movement, although further evidence is needed to confirm this hypothesis. While this study was not designed to answer the question of why this group of patients might have muscle guarding that results in such severe functional limitations, it is possible to speculate. Muscle guarding in patients suffering from frozen shoulder could be a protective mechanism or in response to underlying pathophysiology. Altered muscle activity has been observed in other painful musculoskeletal conditions, such as back pain, although physiological mechanisms are not clear (van Dieën et al., 2003). There may also be cognitive or emotional factors that result in limitations to movement such as fear (of movement or pain), anxiety or catastrophic appraisal of the condition. These psychologically-mediated factors are thought to influence behaviour in other painful conditions. Studies involving much larger groups of frozen shoulder patients are needed to confirm the veracity of these findings. Conclusions from this study need to be considered in light of several limitations. Most obviously, results from the five participants undergoing surgery for the treatment of their frozen shoulder may not generalise to the general frozen shoulder population. In addition, the shoulder abduction ROM measurements were performed without stabilising the scapula and so may not accurately reflect glenohumeral joint movement. It is possible that abduction ROM increases following anaesthesia could have been due to increased scapular movement, although this is unlikely to explain the one to twofold increases to virtually full range demonstrated by some participants. This study has demonstrated that muscle guarding may be a significant contributing factor to shoulder movement deficits in some patients suffering from frozen shoulder. Given that many contemporary treatment options rest on the assumption that restriction is due to tightening of passive structures, this finding is worthy of further investigation.
要点 结果:立即麻醉消除疼痛和肌肉收缩对肩关节功能有一定的影响，一些有特发性冻结肩关节典型临床特征的患者的被动肩外展和外旋ROM增加了约150% - 300%。 提示:在被诊断为冻结肩的病人中，麻醉后肩关节活动度增加的比例很大，这表明肌肉保护，可能是其中一些患者运动受限的主要原因，而不是囊膜挛缩。 注意:麻醉后被动肩关节ROM的增加仅在极少数冷冻肩患者中得到证实。为了证实这些发现的准确性，需要进一步研究更多的冷冻肩患者的肩关节ROM。 Key points Findings: Immediately following anaesthesia to eliminate the influence of pain and muscle contraction on shoulder function, passive shoulder abduction and external rotation ROM increased by approximately 150%–300% in some patients with the classical clinical features of idiopathic frozen shoulder. Implications: In patients diagnosed with frozen shoulder large percentage increases in shoulder ROM following anaesthesia indicate that muscle guarding, and not capsular contracture, may be the major contributing factor to movement restriction in some of these patients. Caution: Increases in passive shoulder ROM following anaesthesia have only been demonstrated in a very small number of frozen shoulder patients. Further studies concentrating on glenohumeral joint ROM in a larger group of frozen shoulder patients is required to confirm the veracity of these findings. 参考文献References
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