Re: round shoulder 주인공(소흉근 신경포착 증후군) 생체역학 2022!!

[문형철]

JSES Rev Rep Tech

. 2022 Jun 30;2(4):469–488. doi: 10.1016/j.xrrt.2022.05.008

Pectoralis minor syndrome – review of pathoanatomy, diagnosis, and management of the primary cause of neurogenic thoracic outlet syndrome

Adil S Ahmed a, Alexander R Graf a, Anthony L Karzon a, Bethany L Graulich b, Anthony C Egger a, Sarah M Taub a, Michael B Gottschalk a, Robert L Bowers c, Eric R Wagner a,∗

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PMCID: PMC10426640  PMID: 37588453

Abstract

Thoracic outlet syndrome is an umbrella term for compressive pathologies in the supraclavicular and infraclavicular fossae, with the vast majority being neurogenic in nature. These compressive neuropathies, such as pectoralis minor syndrome, can be challenging problems for both patients and physicians. Robust understanding of thoracic outlet anatomy and scapulothoracic biomechanics are necessary to distinguish neurogenic vs. vascular disorders and properly diagnose affected patients. Repetitive overhead activity, particularly when combined with scapular dyskinesia, leads to pectoralis minor shortening, decreased volume of the retropectoralis minor space, and subsequent brachial plexus compression causing neurogenic thoracic outlet syndrome. Combining a thorough history, physical examination, and diagnostic modalities including ultrasound-guided injections are necessary to arrive at the correct diagnosis. Rigorous attention must be paid to rule out alternate etiologies such as peripheral neuropathies, vascular disorders, cervical radiculopathy, and space-occupying lesions. Initial nonoperative treatment with pectoralis minor stretching, as well as periscapular and postural retraining, is successful in the majority of patients. For patients that fail nonoperative management, surgical release of the pectoralis minor may be performed through a variety of approaches. Both open and arthroscopic pectoralis minor release may be performed safely with effective resolution of neurogenic symptoms. When further indicated by the preoperative workup, this can be combined with suprascapular nerve release and brachial plexus neurolysis for complete infraclavicular thoracic outlet decompression.

초록

흉곽출구증후군은

쇄골상 및 쇄골하 함요부에서 발생하는 압박성 병변을 포괄하는 용어로,

대부분 신경성 기원을 가집니다.

소흉근 증후군과 같은 이러한 압박성 신경병증은

환자와 의사 모두에게 어려운 문제가 될 수 있습니다.

신경성 장애와 혈관성 장애를 구분하고

영향을 받은 환자를 정확히 진단하기 위해서는

흉곽출구 해부학과 견갑흉부 생체역학에 대한 확고한 이해가 필요합니다.

반복적인 머리 위 동작, 특히 견갑골 운동 장애와 동반될 경우

소흉근 단축, 소흉근 후 공간의 용적 감소,

그리고 이에 따른 상완 신경총 압박을 유발하여 신경성 흉곽출구 증후군을 초래한다.

정확한 진단을 위해서는

철저한 병력 청취, 신체 검사, 초음파 유도 주사 등 진단적 검사를 종합적으로 수행해야 한다.

말초 신경병증, 혈관 질환, 경추 신경근병증, 공간 점유성 병변 등

다른 원인을 배제하기 위해 엄격한 주의가 필요합니다.

소흉근 스트레칭과 견갑골 주변 및 자세 재훈련을 포함한 초기 비수술적 치료는

대부분의 환자에서 성공적입니다.

비수술적 치료에 실패한 환자의 경우 다양한 접근법을 통해 소흉근의 외과적 이완술을 시행할 수 있습니다. 개방적 및 관절경적 소흉근 이완술 모두 신경성 증상을 효과적으로 해소하며 안전하게 시행될 수 있다. 수술 전 검사에 의해 추가적으로 필요한 경우, 견갑상신경 이완술 및 상완신경총 신경이완술과 병행하여 완전한 쇄골하 흉곽출구 감압술을 시행할 수 있다.

Keywords: Thoracic outlet syndrome, Neurogenic thoracic outlet syndrome, Pectoralis minor syndrome, Pectoralis minor release, Suprascapular neuropathy, Brachial plexus neurolysis

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Compressive neuropathies are among the most common conditions in the upper extremity.7,9,74 Compression proximal to the elbow, in the supraclavicular and infraclavicular fossae of the thoracic outlet, is less common. Neurovascular compression in the thoracic outlet is challenging to diagnose and treat.47 Thoracic outlet syndrome is categorized as neurogenic (NTOS) or vascular (VTOS), (Table I), with approximately 90%-95% of cases representing neurogenic etiology.52,91 As the brachial plexus and accompanying subclavian vessels traverse the transitioning anatomy of the neck, supraclavicular space, infraclavicular space, axilla, and finally the upper arm (Fig. 1), they are subject to multiple potential compressive sites.52 In the supraclavicular area, symptoms occur via narrowing of the scalene triangle and costoclavicular space as contraction of scalenes pulls the first rib superiorly toward the clavicle (Fig. 1, C and D). Inferior to the clavicle, compression is related to the pectoralis minor muscle (PM) (Fig. 1, A and B).91 Traditionally, brachial plexus symptoms were thought to stem from plexus compression between the anterior and middle scalenes or the clavicle and first rib, termed NTOS. However, recent understanding of the dynamic role of PM in scapular kinematics and nerve compression led to recognition of pectoralis minor syndrome (PMS) as the dominant etiology underlying NTOS.103 PMS presents diagnostic and treatment challenges for several reasons. The path of the brachial plexus through the supraclavicular and infraclavicular regions represents an anatomic watershed overlapping between treating sub-specialties. It has traditionally been a gray area between upper extremity, vascular, and neurosurgeons due to the anatomy and varying skill sets regarding nerve surgery, open exploration, and less-invasive arthroscopic approaches.24,35,54 Due to dearth of strong evidence or consistent diagnostic algorithms, patients with NTOS caused by PMS present with vague symptoms and are often shuffled between primary care, sports medicine, rheumatology, chiropractic, and pain clinics.102 This review provides a comprehensive overview of PMS, highlighting the anatomy, dynamic pathophysiology, reproducible diagnostic algorithm, and treatment of this underrecognized etiology of NTOS.

압박성 신경병증은

상지에서 가장 흔한 질환 중 하나이다.7,9,74

Compressive neuropathies

https://pubmed.ncbi.nlm.nih.gov/16679233/

팔꿈치 근위부,

즉 흉곽출구의 쇄골상 및 쇄골하 함요부에서의 압박은 상대적으로 드물다.

흉곽 출구에서의 신경혈관 압박은

진단과 치료가 까다롭다.47

흉곽 출구 증후군은 신경성(NTOS) 또는 혈관성(VTOS)으로 분류되며(표 I),

약 90~95%의 사례가 신경성 원인을 나타낸다.52,91

상완 신경총과 동반되는 쇄골하 혈관이 목, 쇄골상 공간, 쇄골하 공간, 겨드랑이,

그리고 최종적으로 상완부(그림 1)로 이동하는 과정에서

여러 잠재적 압박 부위에 노출됩니다.52

쇄골상부 영역에서는

사골근 삼각형과 늑골쇄골간 공간의 협착으로 증상이 발생하는데,

이는 사골근 수축이 제1늑골을 쇄골 쪽으로 상방으로 당기기 때문입니다(그림 1, C 및 D).

쇄골 아래에서는

압박이 소흉근(PM)과 관련이 있다(그림 1, A와 B).91

전통적으로 상완신경총 증상은

전경사근과 중경사근 사이 또는 쇄골과 제1늑골 사이에서 발생하는 신경총 압박(NTOS)에서 비롯된다고 여겨졌다.

그러나

최근 소흉근이 견갑골 운동학 및 신경 압박에서 수행하는 역동적 역할에 대한 이해가 깊어지면서,

소흉근 증후군(PMS)이 NTOS의 주요 원인이라는 점이 인정되었습니다.103

PMS는

여러 가지 이유로 진단 및 치료에 어려움을 줍니다.

견갑골 상부 및 하부를 통과하는 상완 신경총의 경로는

치료를 담당하는 세부 전문 분야 간에 중첩되는 해부학적 경계선을 나타낸다.

이는 신경 수술, 개방적 탐색술,

그리고 덜 침습적인 관절경적 접근법에 관한 해부학적 구조와 다양한 기술 세트 때문에

전통적으로 상지, 혈관, 신경외과 의사들 사이의 회색 지대였다.24,35, 54

강력한 증거나 일관된 진단 알고리즘이 부족하여 PMS로 인한 NTOS 환자들은

모호한 증상을 보이며,

종종 일반 진료, 스포츠 의학, 류마티스학, 카이로프랙틱, 통증 클리닉 사이를 전전하게 됩니다.102

본 리뷰는

PMS에 대한 포괄적인 개요를 제공하며,

NTOS의 이처럼 제대로 인식되지 않는 원인에 대한

해부학, 역동적 병리생리학, 재현 가능한 진단 알고리즘 및 치료법을 강조합니다.

Table I.

Overview of neurogenic versus vascular thoracic outlet syndrome.

                                   Neurogenic                                     Vascular

Distribution	90%-95%	5%-10% (venous >> arterial)
Demographics	Predominantly younger females	Predominantly younger, athletic males
Primary anatomic site	Retropectoralis minor space	Costoclavicular space, scalene triangle
Pathoanatomy	Pectoralis minor hyerpactivity results in shortening and fibrosis Scapula assumes chronically protracted posture, decreasing volume of retropectoralis minor space Compression during arm elevation on brachial plexus cords ± tethering of the suprascapular nerve at the suprascapular notch	Contraction of the anterior and middle scalene muscles superiorly elevates the first rib relative to the clavicle, decreasing costoclavicular space Primarily compresses the subclavian vein and to lesser extent, the subclavian artery Anatomic variations affecting costoclavicular space are common (ex: cervical rib, anomalous scalene, enlarged transverse process, etc.)
Primary Symptoms	Pain about the shoulder, neck, trapezius, and medial scapula, often accompanied by muscle spasms Subjective paresthesias in the arm or hand may be present, but are nonspecific	Hand and finger pain, cold intolerance, claudication, and episodic arm swelling Arm heaviness and easy fatiguability with use Subjective paresthesias in the arm or hand may be present, but are nonspecific
Examination Findings	Tenderness and + Tinel’s over pectoralis minor (and less commonly over scalenes) Scapular dyskinesia Hand atrophy – late presentation (Gilliatt-Sumner Hand)	Unilateral arm swelling and cyanosis Venous distention about the upper arm Raynaud’s-type appearance and skin changes in the fingers
Traditional Maneuvers	Multiple described provocative examinations (Adson, Wright, Roos, Cyriax, etc) are nonspecific, with high false-positive rates even in the normal population
Measurements (compared to contralateral side)	Pectoralis minor index Medial scapular distance Medial scapular angle Scapular protraction height
Diagnostic workup	Ultrasound-guided anesthetic injections – target pectoralis minor coracoid insertion ± suprascapular nerve at suprascapular notch ± scalene triangle MR angiogram of the chest – arms down/arms up protocol for dynamic vascular compression MRI of the brachial plexus EMG/NCS of bilateral upper extremities
Surgical Treatment	Pectoralis minor release (open or arthroscopic) ± Suprascapular nerve release ± Brachial plexus neurolysis	First rib resection (transaxillary or supraclavicular) ± Scalenectomy ± Resection of anomalous anatomy (if present)

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EMG, electromyography; MRI, magnetic resonance imaging; NCS, nerve conduction study.

Figure 1.

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Rendering of the brachial plexus and subclavian/axillary vessels passing through the thoracic outlet in a right shoulder. (A) Anterior view with subtraction of the deltoid, pectoralis major, trapezius, rotator cuff, and conjoint tendon. (B) Brachial plexus highlighted at the cord level deep to pectoralis minor, with subtraction of the vasculature. (C) Inlet view (looking from superior to inferior) of the thoracic outlet. The subclavian vein courses anterior to the anterior scalene in the costoclavicular space. The brachial plexus and subclavian artery pass between the anterior and middle scalenes. (D) Outlet view (looking from inferior to superior) of the thoracic outlet. 1, anterior scalene; 2, middle scalene; 3, first rib; 4, coracoid process; 5, pectoralis minor muscle; 6, brachial plexus; 7, subclavian artery; 8, subclavian vein.

우측 어깨에서 흉곽 출구를 통과하는 상완 신경총 및 쇄골하/액와 혈관의 렌더링.

(A) 삼각근, 대흉근, 승모근, 회전근개 및 공동건(conjoint tendon)을 제거한 정면 관점.

(B) 혈관 구조를 제거한 후 소흉근 깊은 부위의 신경다발 수준에서 강조 표시된 상완 신경총.

(C) 흉곽 출구 상부에서 하부로 바라본 유입부 관점. 쇄쇄골 공간에서 쇄쇄골 정맥은 전측 사골근 앞쪽을 지나간다. 상완 신경총과 쇄쇄골 동맥은 전측 사골근과 중측 사골근 사이를 통과한다.

(D) 흉곽출구 하부에서 상부로 바라본 출구면.

1, 전사골근; 2, 중사골근; 3, 제1늑골; 4, 쇄골상돌기; 5, 소흉근; 6, 상완신경총; 7, 쇄골하동맥; 8, 쇄골하정맥.

Thoracic outlet anatomy and biomechanics

Sound grasp of thoracic outlet anatomy is imperative to understand potential sites of compression and dynamic contribution of scapulothoracic kinematics that potentiate symptoms. Anatomic understanding further facilitates distinguishing NTOS vs. VTOS (Table I).

The thoracic outlet is broadly divided into supraclavicular and infraclavicular fossae (Fig. 1).

흉부 출구 해부학 및 생체역학

흉부 출구 해부학을 정확히 이해하는 것은

압박 발생 가능 부위와 증상을 악화시키는

견갑흉부 운동역학의 역학적 기여를 파악하는 데 필수적이다.

해부학적 이해는

NTOS와 VTOS를 구분하는 데 더욱 도움이 된다(표 I).

The supraclavicular fossa contains 2 anatomic spaces: the scalene triangle and costoclavicular space.26 The scalene triangle is the most proximal space, bound by the anterior and middle scalenes, and first rib, where the scalenes insert. Brachial plexus roots exit the vertebral foramina and traverse this space, uniting to become the upper (C5, C6), middle (C7), and lower (C8, T1) trunks.62 The subclavian artery courses inferiorly within the scalene triangle and anterior to the brachial plexus, in close proximity to the first rib.29,83 Of note, the subclavian vein does not pass through the scalene triangle, instead coursing anterior to the anterior scalene in close proximity to the first rib (Fig. 2).20,21 The scalenes elevate the first rib superiorly and tilt the neck to the ipsilateral side, as they originate from the transverse processes of the cervical vertebrae.78 As the first rib elevates, the volume of the scalene triangle shrinks.39 The subclavian artery is in the closest proximity to the first rib and is the first structure subject to compression during this dynamic process.26,68 The roots and trunks of the brachial plexus, particularly the upper and middle trunk, are further proximal and posterior, and less likely to be compromised (Fig. 2).46,79 Therefore, compression at the scalene triangle is more likely to create VTOS.

흉부 출구는 크게

쇄골상 및 쇄골하 함요부로 구분된다(그림 1).

쇄골상 함요부에는

사각근 삼각부와 쇄골늑간 공간이라는 두 해부학적 공간이 포함된다.26

사각근 삼각부는

가장 근위부에 위치한 공간으로, 전사각근과 중사각근,

그리고 이 근육들이 부착되는 제1늑골에 의해 경계된다.

https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-025-09048-2

상완 신경총 뿌리는

척추공을 빠져나와 이 공간을 가로지르며

상부(C5, C6), 중간(C7), 하부(C8, T1) 간지로 합쳐집니다.62

쇄골하동맥은 사골근 삼각부 내에서 하방으로,

상완 신경총의 전방으로, 제1늑골에 매우 근접하게 지나갑니다.29, 83

주목할 점은

쇄골하 정맥이 사골근 삼각형을 통과하지 않고,

대신 제1늑골에 근접하여 전사골근 앞쪽을 지나간다는 것이다(그림 2).20,21

사골근은 경추의 횡돌기에서 기시하므로

제1늑골을 상방으로 들어올리고

목을 동측으로 기울인다. 78

제1늑골이 상승함에 따라

사골근 삼각형의 공간은 축소됩니다.39

쇄골하동맥은

제1늑골에 가장 근접한 위치에 있어

이 역학적 과정에서 가장 먼저 압박을 받는 구조물입니다.26,68

상완신경총의 신경근과 간질,

특히 상간질과 중간간질은 더 근위부 및 후방에 위치하여 손상될 가능성이 낮습니다(그림 2). 46,79

따라서

사골근 삼각형에서의 압박이

VTOS를 유발할 가능성이 더 높다.

Figure 2.

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Inlet and outlet renderings illustrating anatomic relationships of the neurovascular bundle and osseous structures. (A) Inlet view with subtraction of the brachial plexus, demonstrating proximity of the subclavian vessels between the clavicle and first rib. (B) Outlet view depicting similar relationship between the vessels and osseous anatomy. (C) Inlet view with the brachial plexus. Note the relatively posterior position of the plexus and increased distance between the clavicle and first rib at this location. (D) Outlet view the brachial plexus. Again, note the markedly increased distance between the clavicle and first rib at the posterior location of the plexus.

신경혈관 다발과 골격 구조의 해부학적 관계를 보여주는 유입부 및 유출부 렌더링.

(A) 상완 신경총을 제거한 유입부 뷰로, 쇄골과 제1늑골 사이의 쇄골하 혈관 근접성을 보여준다. (B) 혈관과 골격 해부학적 구조 간의 유사한 관계를 묘사한 출구 뷰. (C) 상완 신경총이 포함된 입구 뷰. 신경총의 상대적으로 후방 위치와 이 부위에서 쇄골과 제1늑골 사이의 증가된 거리를 주목하십시오. (D) 상완 신경총이 포함된 출구 뷰.

다시 한번, 신경총의 후방 위치에서 쇄골과 제1늑골 사이의 현저히 증가된 거리를 주목하십시오.

Beyond the scalene triangle, the neurovascular bundle enters the costoclavicular space. This is anterior and inferior relative to the scalene triangle, but due to the curved anatomy of the thoracic wall and clavicle, the long axis of this space is superior-anteromedial to inferior-posterolateral.32,48 The costoclavicular space is bound anteriorly and superiorly by the clavicle and subclavius muscle (originating at the first costal cartilage, inserting on the inferior clavicular surface), medially by the costoclavicular ligament, and posteriorly and inferiorly by the anterior and middle scalene insertions and first rib (Fig. 1).28 As the first rib elevates through scalene contraction, the subclavian vein (and lesser extent the subclavian artery) is compressed against the undersurface of the clavicle (Fig. 2).8,48 Simultaneous subclavius muscle contraction or hypertrophy exacerbates this phenomenon.2,66 Variant anatomy at this level, such as cervical ribs or enlarged vertebral transverse processes, preferentially decreases volume in the anterior aspect of the costoclavicular space,23,31 exerting compression on the subclavian vessels. Given the aforementioned orientation and dimensions of the costoclavicular space, the brachial plexus is relatively posterior and less likely to undergo dynamic compression (Fig. 2). Consequently, pathology affecting the costoclavicular space produces VTOS.

The neurovascular bundle continues inferolaterally from the supraclavicular to infraclavicular fossa. Brachial plexus trunks split into anterior and posterior divisions, and subclavian vessels become axillary vessels beyond the first rib lateral margin.58 The prime space in the infraclavicular thoracic outlet is the retropecotralis minor space (Fig. 1).42 This is bound by the coracoid process superiorly, second through fourth ribs posteriorly, and PM anteriorly (Fig. 3).89 Within this space, plexus divisions rejoin to form lateral, medial, and posterior cords, and the second stage of the axillary artery continues deep to PM.100 The PM is the principal dynamic driver controlling retropecotralis minor space.89,91,94

사각근 삼각형 너머로 신경혈관 다발은

늑골쇄골 공간으로 진입한다.

이 공간은

사각근 삼각형에 비해 전방 및 하방에 위치하지만,

흉벽과 쇄골의 곡선형 해부학적 구조로 인해

이 공간의 장축은 하방-후측외측보다 상방-전내측에 위치한다.32,48

쇄쇄골간 공간은

전방 및 상방으로는 쇄골과 쇄골하근(제1 늑연골에서 기시하여 쇄골 하면에 부착),

내측으로는 늑쇄골 인대에 의해,

후방 및 하방으로는 전경사근과 중경사근의 부착부와 제1늑골에 의해 경계된다(그림 1).28

제1늑골이 경사근 수축에 의해 상승함에 따라, 쇄골하 정맥(그리고 상대적으로 쇄골하 동맥)은 쇄골의 하부 표면에 압박된다(그림 2). 8,48 동시에 쇄골하근이 수축하거나 비대해지면 이 현상이 악화된다.2,66 이 부위의 변이 해부학적 구조(예: 경추 늑골 또는 비대해진 척추 횡돌기)는 늑쇄골 공간의 전방 부피를 우선적으로 감소시켜23,31 쇄골하 혈관에 압박을 가한다. 앞서 언급한 늑골쇄골 공간의 방향과 치수를 고려할 때, 상완 신경총은 상대적으로 후방에 위치하여 동적 압박을 받을 가능성이 적습니다(그림 2). 결과적으로, 늑골쇄골 공간에 영향을 미치는 병리학적 상태는 VTOS를 유발합니다.

신경혈관 다발은 쇄골상 함요에서 쇄골하 함요로 하측외측으로 이어집니다. 상완 신경총 간부는 전방 분지와 후방 분지로 분할되며, 쇄골하 혈관은 제1늑골 외측 경계를 넘어 액와 혈관으로 전환됩니다.58 쇄골하 흉부 출구에서 주요 공간은 소흉근후 공간(그림 1)입니다. 42 이 공간은 상방으로 견봉돌기, 후방으로 제2-4늑골, 전방으로 소흉근(PM)에 의해 경계된다(그림 3).89 이 공간 내에서 신경총 분지들은 재결합하여 외측, 내측, 후측 줄기를 형성하며, 액와동맥의 제2단계는 소흉근(PM) 심부로 계속된다.100 소흉근(PM)은 소흉근 후방 공간을 제어하는 주요 동적 구동력이다.89,91,94

Figure 3.

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Images illustrating the relationship between the brachial plexus and the pectoralis minor within the retropectoralis minor space. (A) Anterior view, with brachial plexus highlighted at the level of the cords. (B) Outlet view of the retropectoralis minor space, again demonstrating proximity of the cords to the undersurface of the pectoralis minor.

소흉근 후방 공간 내 상완 신경총과 소흉근의 관계를 보여주는 이미지.

(A) 전방 관점에서 신경총이 신경다수 수준에서 강조 표시됨.

(B) 소흉근 후방 공간의 출구 관점,

다시 한번 신경다수가 소흉근 하부 표면에 근접해 있음을 보여줌.

The PM originates from the costal cartilage margin of the third through fifth ribs and inserts onto the superomedial aspect of the coracoid, functioning as a dynamic stabilizer of the scapula (Fig. 3).13,61,108 PM abnormalities cause altered scapular kinematics, particularly during repetitive movements with scapular protraction.14 Repetitive movement in forward and downward directions potentiates adaptive changes in the PM in response to scapular dyskinesis.75 Over time, hyperactive or spasming PM shortens and develops contracture, leading to protracted resting scapular position (Fig. 4) and altered scapular contribution to shoulder range of motion.104 Derangement in dynamic scapular external rotation and abduction alters scapular accommodation to shoulder motion, a well-known feature in various shoulder pathologies.18,36,105 Patients with shortened PM exhibit scapular dyskinesia manifesting as decreased scapular external rotation/retraction and posterior tilting of the inferior scapula of over 10o compared with controls (Fig. 4).15 Patients with scapular dyskinesia often receive incorrect diagnoses of instability, as this pathologic motion pattern is challenging to interpret and diagnose.95

소흉근은

제3~5늑골의 늑연골 가장자리에서 기시하여 견갑골의 상내측면에 삽입되며,

견갑골의 동적 안정화 역할을 수행한다(그림 3).13,61,108

소흉근 : 견갑골 앞쪽에서 dynamic stabilizer of the scapula

소흉근 이상은

특히 견갑골 전방 이동을 수반하는 반복적 동작 시 견갑골 운동학 변화를 초래한다. 14

전방 및 하방 방향의 반복적 움직임은

견갑골 운동 장애에 대한 반응으로 소흉근의 적응적 변화를 촉진한다.75

시간이 지남에 따라 과활성화되거나 경련을 일으키는 소흉근은

단축되고 구축을 일으켜 휴식 시 견갑골의 전방 위치(그림 4)와

어깨 가동 범위에 대한 견갑골의 기여도 변화를 초래한다. 104

동적 견갑골 외회전 및 외전 기능의 장애는 견갑골의 어깨 운동 적응을 변화시키며,

이는 다양한 어깨 병리에서 잘 알려진 특징이다.18,36,105

단축된 PM을 가진 환자는 견갑골 운동 장애를 보이며,

이는 대조군에 비해 견갑골 외회전/후퇴 감소 및 하부 견갑골의 10도 이상의 후방 경사로 나타난다(그림 4). 15

견갑골 운동 장애 환자들은

이 병리적 운동 패턴을 해석하고 진단하기 어려워 불안정성으로 잘못 진단받는 경우가 흔하다.95

Figure 4.

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Appearance of scapular protraction in 2 patients. (A) Posterior view with protraction of left scapula, creating posterior elevation and prominence of the inferior angle. (B) Lateral and superior view demonstrating protracted resting position of the left scapula, with prominence of the inferior angle posteriorly.

2명의 환자에서 관찰된 견갑골 전방위(protraction)의 모습. (A) 좌측 견갑골 전방위로 인한 후방 상승 및 하각(inferior angle)의 후방 돌출을 보여주는 후방 관점. (B) 좌측 견갑골의 전방위 휴식 위치를 보여주는 측면 및 상부 관점, 하각의 후방 돌출이 관찰됨.

Loss of coordinated scapular rotation alters the normal harmony of glenohumeral to scapulothoracic motion, known as scapulohumeral rhythm.37,44,71,98 This altered motion, creates chronic compensatory mechanisms, producing impingement from greater tuberosity impaction against the acromion during arm elevation.49 This pathologic cascade is especially preval‎ent and limiting for overhead athletes. McClain et al69 noted protracted resting scapular posture in the dominant arms of overhead vs. nonoverhead athletes, attributed to PM shortening. Other kinematic studies of overhead athletes showed similar results, with the dominant arm assuming protracted and anteriorly tilted superior scapular resting position.80,85 Cools et al27 further found PM shortening in the dominant arms of elite adolescent tennis players. Eval‎uating swimmers and volleyball players, Tate et al99 and Reeser et al,84 respectively, found PM shortening to be a risk factor for symptomatic shoulder pain.

Burkhart et al19 coined “SICK” scapula syndrome (scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement) as a cause of anterior shoulder pain in overhead athletes. This leads to static anteriorly tilted coracoid malposition with tightening, shortening, and tenderness of the PM.12 PM tightening exacerbates scapular malposition, resulting in depression of the anterior acromion and impingement with humeral elevation.41 While debate remains whether PM tightness is causative or a consequence of scapular dyskinesis, there is well-established interplay resulting in clinical manifestations of anterior shoulder pain and functional limitation.57

The progressive PM tightness, shortening, and fibrosis, combined with anterior coracoid tilt, decreases the volume of the retropectoralis minor space.42 As the brachial plexus travels to the axilla and upper arm (Figs. 1 and 3), decreased volume leads to compression of the medial, lateral, and posterior cords and is especially pronounced during overhead activity. Thus, it is by this pathoanatomic cascade that PM tightness creates brachial plexus compression.90

An additional pathology that simultaneously occurs from this cascade is suprascapular nerve (SSN) entrapment and resultant traction injury at the suprascapular notch (Fig. 5). Chronic protracted scapular posture from PM tightness creates anterior tilt of the superior scapula, pulling the coracoid and suprascapular notch relatively anterior. The SSN is tethered at the suprascapular notch upon entering the supraspinatus fossa due to branching supraspinatus innervation and presence of the overlying transverse scapular ligament.38,96 Therefore, scapular protraction creates chronic stretch injury of the SSN, with symptoms of posterosuperior shoulder pain exacerbated by overhead activity, and even atrophy of the supraspinatus and infraspinatus if left untreated.53

견갑골 회전의 조화로운 움직임이 상실되면

견관절 운동과 견갑흉곽 운동 간의 정상적인 조화,

즉 견갑상완 리듬이 깨진다.37,44,71,98

이러한 변형된 움직임은

만성적인 보상 기전을 유발하여 팔을 들어 올릴 때

대결절이 견봉과 충돌하여 충돌 증후군을 일으킨다.49

이 병리적 연쇄 반응은

특히 머리 위로 동작을 하는 운동선수들에게 흔히 나타나며 활동에 제한을 가한다.

McClain 등69은

머리 위로 동작을 하는 운동선수와 그렇지 않은 운동선수를 비교했을 때,

우세 팔에서 견갑골 휴식 자세가 전방으로 연장된 상태를 보인다고 지적했으며,

이는  소흉근(PM)의 단축 때문이라고 설명했습니다.

머리 위로 동작을 하는 운동선수를 대상으로 한 다른 운동학 연구에서도 유사한 결과가 나타났는데, 우세 팔이 전방으로 연장되고 상방으로 기울어진 상부 견갑골 휴식 위치를 취하는 것으로 나타났습니다.80,85 Cools 등27은 엘리트 청소년 테니스 선수의 우세 팔에서도 견갑골 하방근(PM) 단축을 추가로 발견했습니다. 수영 선수와 배구 선수를 평가한 Tate 등99와 Reeser 등84는 각각 견갑골 전방위 단축이 증상이 있는 어깨 통증의 위험 요인임을 발견했습니다.

Burkhart 등19은

오버헤드 운동선수의 전방 어깨 통증 원인으로

“SICK” 견갑골 증후군(견갑골 위치 이상, 하내측 경계 돌출, 쇄골상돌기 통증 및 위치 이상, 견갑골 운동 이상)을 제시했다.

이는 쇄골상돌기의 정적 전방 경사 위치 이상을 초래하며,

이에 따라 쇄골상돌기근의 긴장, 단축 및 압통이 발생한다. 12

PM의 긴장은

견갑골 위치 이상을 악화시켜 전방 견봉의 함몰과 상완골 상승 시 충돌을 유발한다.41

PM 긴장이 원인이 되는지,

아니면 견갑골 운동 장애의 결과인지에 대한 논쟁은 지속되지만,

전방 어깨 통증과 기능적 제한이라는 임상적 증상을 초래하는 상호작용은 잘 확립되어 있다.57

Pectoralis minor syndrome – review of pathoanatomy, diagnosis, and management of the primary cause of neurogenic thoracic outl

Burkhart et al19 coined

“SICK” scapula syndrome (scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement)

as a cause of anterior shoulder pain in overhead athletes

점진적인 소흉근의 긴장, 단축 및 섬유화와 함께 앞쪽 쇄골상돌기의 경사는

소흉근 후방 공간의 부피를 감소시킵니다.42

상완 신경총이 겨드랑이와 상완부로 이동함에 따라(그림 1 및 3), 부피 감소는

내측, 외측 및 후측 신경다발의 압박을 초래하며, 특히 머리 위로 팔을 올리는 동작 시 두드러집니다.

따라서 이 병리해부학적 연쇄 작용을 통해 소흉근 긴장이 상완 신경총 압박을 유발한다.90

이 연쇄 작용과 동시에 발생하는 추가 병리로는

견갑상 신경(SSN)의 견갑상 결절 부위 포획 및 이에 따른 견갑상 결절에서의 견인 손상이 있다(그림 5).

견갑골 전방 경사 증후군으로 인한 만성적인 견갑골 전방 위치는

상부 견갑골의 전방 경사를 유발하여, 쇄골상돌기와 견갑골 상부 홈을 상대적으로 전방으로 당깁니다.

견갑골 상부 홈을 통과하여 상근과다구로 진입하는 상완골 상근 신경은

상근 분지 신경 분포와 상부 횡견갑 인대의 존재로 인해

견갑골 상부 홈에 고정됩니다.38,96

따라서,

견갑골 전방 이동은

상완골두신경의 만성적 신장 손상을 유발하며,

이는 머리 위 동작으로 악화되는 어깨 통증 증상을 동반하고, 치료하지 않을 경우

극상근과 극하근의 위축까지 초래할 수 있다.53

Figure 5.

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Rendering of the suprascapular nerve and the transverse scapular ligament with subtraction of the deltoid, trapezius, rotator cuff muscles, brachial plexus, vasculature, and pectoralis minor. (A) Anterior view. (B) Posterior view. (C) Superior view. Note how the branch innervating the supraspinatus takes a sharp turn meidally in the supraspinatus fossa immediately beyond the transverse scapular ligament (

 indicates transverse scapular ligament).

삼각근, 승모근, 회전근개 근육, 상완 신경총, 혈관, 소흉근을 제거한 상견갑신경과 견갑골 횡인대의 렌더링. (A) 정면도. (B) 후면도. (C) 상부 관점. 견갑상근을 신경 분포하는 가지가 견갑횡인대 바로 너머 견갑상근과에서 내측으로 급격히 꺾이는 모습을 주목하십시오 (

는 견갑횡인대를 나타냄).

Diagnosis

Clinical history and physical examination

Diagnosis of PMS is challenging, with patients experiencing chronic symptoms and often undergoing several surgeries, such as open brachial plexus dissection, scalenectomy, and first rib resection, with variable outcomes due to initial misdiagnosis.42,45 Isolated PMS is frequently seen in teenagers or young adults participating in repetitive upper extremity activities.94 Sports like baseball, softball, swimming, volleyball, gymnastics, tennis, and weightlifting all rely heavily on scapular protraction and retraction and harmonious contraction of PM. These repetitive scapular protraction/retraction activities lead to irritation and compression of the plexus in the retropectoralis minor space when PM pathology exists.89 Young athletes with underlying scapular dyskinesia are at a particular risk for developing PMS.

진단

병력 및 신체 검사

PMS 진단은 어려우며,

환자들은 만성 증상을 경험하고

종종 개방형 상완 신경총 절개술, 사다리꼴근 절제술, 제1늑골 절제술 등

여러 수술을 받지만 초기 오진으로 인해 결과가 다양하다.42,45 

고립성 PMS는

반복적인 상지 활동을 하는 청소년이나 젊은 성인에게서 흔히 관찰된다.94 

야구, 소프트볼, 수영, 배구, 체조, 테니스, 역도 등은

모두 견갑골 전방/후방 이동과 견갑골근(PM)의 조화로운 수축에 크게 의존한다.

이러한 반복적인 견갑골 전후방 이동 활동은 견갑골근 병리가 존재할 경우

소흉근 후방 공간에서 신경총의 자극과 압박을 유발한다.89 

기저 견갑골 운동 장애가 있는 젊은 운동선수들은

특히 PMS 발병 위험이 높다.

Physicians must first distinguish whether symptoms stem from NTOS vs. VTOS, which permits identification of site(s) of compression. As detailed previously, robust anatomic understanding of thoracic outlet and dynamic scapulothoracic motion is crucial to diagnosis. In addition to differentiating NTOS vs. VTOS, some authors such as Sanders and Rao94 view NTOS and PMS as distinct entities despite similar presentations of anterior shoulder pain, intermittent paresthesia, and weakness, particularly during overhead activities. They further acknowledge significant overlap among the conditions, with approximately 75% of NTOS patients also having PMS, although many have PMS alone.94 Based on thoracic outlet anatomy (Figure 1, Figure 2, Figure 3) and scapulothoracic biomechanics, we believe PMS creating compression in the retropectoralis minor space is the prime cause of NTOS. Compression in the supraclavicular thoracic outlet at the scalene triangle and/or costoclavicular space predominantly causes VTOS. Naturally, there are variations or dual sites of compression that can obfuscate diagnosis; however, it is by this fundamental framework of anatomy that we recommend honing one’s differential in patients with suspected thoracic outlet syndrome. Symptoms and signs of PMS are separated into 4 stages (Table II).

의사는

증상이 NTOS(상부 흉곽 출구 증후군)에서 비롯되었는지

VTOS(하부 흉곽 출구 증후군)에서 비롯되었는지 먼저 구분해야 하며,

이를 통해 압박 부위를 확인할 수 있다.

앞서 상세히 설명한 바와 같이, 흉곽 출구와 견갑흉곽 운동의 역학적 움직임에 대한 해부학적 이해가 진단에 매우 중요하다. NTOS와 VTOS를 구분하는 것 외에도, Sanders와 Rao94와 같은 일부 저자들은 전방 어깨 통증, 간헐적 감각 이상, 특히 머리 위로 팔을 올리는 동작 시 발생하는 근력 약화 등 유사한 증상을 보임에도 불구하고 NTOS와 PMS를 별개의 질환으로 간주합니다. 그들은 또한 약 75%의 NTOS 환자가 PMS를 동반하지만, 많은 환자가 PMS만 단독으로 앓는 등 두 질환 간 상당한 중복이 있음을 인정합니다.94 흉부 출구 해부학(그림 1, 그림 2, 그림 3)과 견갑흉부 생체역학에 기반하여, 우리는 소흉근 후방 공간에서 압박을 유발하는 PMS가 NTOS의 주요 원인이라고 믿습니다.

승모근 삼각부 및/또는 늑골쇄골 공간에서 발생하는

쇄골상 흉곽출구 압박이 주로 VTOS를 유발합니다.

당연히 진단이 복잡해질 수 있는 압박 부위의 변이 또는 이중 압박 부위가 존재하지만,

흉곽출구증후군 의심 환자의 감별진단을 정교화하기 위해

이 해부학적 기본 틀을 권장합니다.

PMS의 증상과 징후는 4단계로 구분됩니다(표 II).

Stage 1 patients experience vague anterior shoulder pain, primarily during overhead activity. Mild scapular dyskinesia with subtle increased protraction is present and may be missed without detailed attention to scapular motion. Patients tolerate the physical examination, with pain experienced toward extremes of shoulder forward elevation and abduction. Patients typically have not ceased sport participation. Stage 2 presents with worsening symptoms and more severe pain radiating about the shoulder and upper arm. Tenderness over the coracoid is present. Scapular dyskinesia with asymmetric protraction is more pronounced and noticeable on contralateral comparison. Patients either take hiatus from overhead sport or seek counsel during off-season in the hope of ameliorating symptoms for return. Stage 3 presents with hallmark tertiary issues of suprascapular neuropathy and severe scapular dyskinesia limiting function. As PM shortens and the scapula chronically protracts (Fig. 4), constant traction is placed on the SSN in its fixed location at the suprascapular notch. This exacerbates radiating pain about the posterior shoulder, with subjective or even objective weakness during shoulder motion depending on chronicity. Scapular protraction limits shoulder function, as scapular contribution to total arc of motion is diminished. Severe tenderness is present about the coracoid, along with positive Tinel’s sign. Pain and tenderness are present at the medial scapular border, secondary to dyskinesia precipitating scapulothoracic bursitis at the articulation against the chest wall. Patients have completely ceased sports and often sought eval‎uation with several providers. Stage 4 patients experience severe pain diffusely about the shoulder and periscapular area. There is obvious resting scapular protraction, exacerbated with motion. Severe tenderness and Tinel’s are present over the coracoid, with marked limitation in shoulder function, and atrophy about the infraspinatus. Patients develop compensatory mechanisms to avoid pain exacerbation from the scapular protraction, relying on periscapular stabilizers (trapezius, rhomboids, levator scapulae, and serratus anterior). These muscles contribute to diffuse periscapular pain, adding challenge to the diagnosis. Finally, severe scapular protraction from PM contracture creates chronic anterior stretch of the brachial plexus. From its native relatively posterior position, the plexus is pulled anteriorly in the retropectoralis minor space and throughout the entire thoracic outlet, leading to abutment against the subclavius and anterior scalenes. Resulting tenderness and positive Tinel’s become apparent in the supraclavicular fossa in patients with advanced PMS. Stage 4 presentation can be challenging, as one may examine the patient and confuse this proximal, supraclavicular pain and provocative examination findings as the prime culprit and the distal periscapular and anterior chest pain as secondary effects. However, sound understanding of thoracic outlet anatomy and biomechanics leading to progressive symptomatology ensures correct identification of underlying etiology.

1단계 환자는 주로 머리 위로 팔을 올리는 동작 시 모호한 전방 어깨 통증을 경험합니다. 경미한 견갑골 운동 장애와 미세한 견갑골 전방 돌출 증가가 나타나며, 견갑골 움직임에 대한 세심한 관찰 없이는 놓칠 수 있습니다. 환자는 신체 검사를 견딜 수 있으나, 어깨 전방 상승 및 외전 극한 위치에서 통증을 느낍니다. 환자들은 일반적으로 스포츠 활동을 중단하지 않은 상태입니다.

2단계에서는 증상이 악화되고 어깨와 상완을 따라 더 심한 통증이 방사됩니다. 견봉돌기 부위에 압통이 존재합니다. 비대칭적 전방돌출을 동반한 견갑골 운동 장애가 더 뚜렷해지며, 반대측 비교 시 더욱 두드러집니다. 환자들은 머리 위로 하는 스포츠를 일시 중단하거나, 시즌이 끝난 후 증상 완화를 위해 상담을 받으며 복귀를 희망합니다.

3단계에서는 견갑상신경병증과 기능 제한을 초래하는 심한 견갑골 운동 장애라는 특징적인 3차 문제가 나타난다. 견갑골이 만성적으로 전방으로 돌출되면서(그림 4), 견갑상공에 고정된 위치의 견갑상신경(SSN)에 지속적인 견인력이 가해진다. 이는 만성 정도에 따라 어깨 운동 시 주관적 또는 객관적 쇠약과 함께 후방 어깨 부위의 방사통을 악화시킨다. 견갑골 전방위 운동은 전체 운동 범위에 대한 견갑골 기여도가 감소함에 따라 어깨 기능을 제한합니다. 쇄골상돌기 주변에 심한 압통이 있으며, 티넬 징후도 양성입니다. 견갑골 내측 경계부에도 통증과 압통이 존재하는데, 이는 운동 장애로 인해 흉벽과의 접합부에서 견갑흉막 활액낭염이 유발되기 때문입니다. 환자들은 스포츠 활동을 완전히 중단했으며 종종 여러 의료진에게 진단을 요청합니다.

4단계 환자는 어깨 및 견갑골 주위 부위에 광범위하게 심한 통증을 경험합니다. 휴식 시에도 명백한 견갑골 전방 돌출이 관찰되며, 움직임으로 악화됩니다. 견봉돌기 부위에 심한 압통과 티넬 증상이 나타나며, 어깨 기능이 현저히 제한되고 견갑하근 주변에 위축이 관찰됩니다. 환자들은 견갑골 전방돌출로 인한 통증 악화를 피하기 위해 견갑골 주변 안정근(승모근, 능형근, 견갑거근, 전거근)에 의존하는 보상 기전을 발달시킵니다. 이러한 근육들은 견갑골 주변의 확산성 통증에 기여하여 진단에 어려움을 더합니다.

마지막으로, 견갑골 전방돌출을 유발하는 견갑골 후방근(PM) 수축은 상완신경총의 만성적 전방 신장을 초래한다. 본래 상대적으로 후방에 위치하던 신경총이 소흉근 후방 공간을 거쳐 흉곽출구 전체를 가로지르며 전방으로 당겨져, 쇄골하근 및 전경사근과 접촉하게 된다. 이로 인한 압통과 티넬 증상은 진행된 견갑골 전방돌출증(PMS) 환자에서 쇄골상와에서 뚜렷하게 나타난다. 4단계 증상은 진단이 까다로울 수 있다. 환자를 검사할 때 이 근위부, 쇄골상 통증 및 유발 검사 소견을 주된 원인으로, 원위부 견갑주위 및 전흉부 통증을 이차적 효과로 오인할 수 있기 때문이다. 그러나 진행성 증상을 유발하는 흉곽출구 해부학 및 생체역학에 대한 정확한 이해는 근본적 원인 규명을 보장한다.

Table II.

Four stages of pectoralis minor syndrome.

StageSymptomsClinical signsSport/Activity participation

1	Mild anterior shoulder, upper chest, trapezial pain	Subtle scapular dyskinesia and protraction	Able to participate
2	Moderate to severe pain, with additional radiation about the shoulder and upper arm	Localized tenderness ± Tinel’s over coracoid Noticeable scapular dyskinesia compared to contralateral side	Hiatus from sport
3	Severe diffuse shoulder pain Significant posterior radiation as suprascapular nerve involvement worsens Worsening periscapular pain	Severe tenderness and Tinel’s over coracoid Marked scapular dyskinesia with limited arm elevation Tenderness at medial scapula (scapulothoracic bursitis) Pain limited and/or objective weakness of supra/infraspinatus	Completely ceased
4	Stage 3, plus additional pain over supraclavicular fossa and neck	Stage 3, plus additional tenderness and Tinel’s over supraclavicular fossa	Completely ceased

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Patients with PMS typically lack positive findings to classic provocative thoracic outlet tests, such as rotational neck maneuvers and Adson, Wright, Roos, and Cyriax tests.59,88,92 In fact, these maneuvers were found unreliable, demonstrating high false-positive and false-negative rates.77 The most precise physical findings for PMS are tenderness and positive Tinel’s over the PM insertion at the superomedial.6,90 Pain and neurologic symptoms are often worsened by the elevated arm stress test, positioning the shoulder in extension and varying positions of abduction to reproduce pain through compression of the brachial plexus between the PM and thoracic wall.92

This is divided by the subject’s height and multiplied by 100 to determine pectoralis minor index (Fig. 6, A and B). Although simple to measure, there have been challenges establishing normative values and clinically relevant deviations. The medial scapular distance as a measure of scapular protraction is assessed with the patient prone (Fig. 6, C and D).82 Finally, medial scapular angle and scapular protraction height are measured with the patient standing and supine, respectively (Fig. 7). More frequently, PM length and tightness are determined indirectly by assessing scapular position both statically and dynamically, while observing a patient’s scapular motion during simultaneous bilateral arm elevation.50,63,106

PMS 환자는 일반적으로 회전 목 검사 및 애드슨, 라이트, 루스, 시리아크스 검사 등 전형적인 유발성 흉곽출구 검사에서 양성 소견이 부족하다.59,88,92 실제로 이러한 검사들은 높은 위양성률과 위음성률을 보여 신뢰할 수 없는 것으로 판명되었다.77 PMS에 대한 가장 정확한 신체 소견은 상내측부 흉골상부근(PM) 부착부 위의 압통과 티넬 검사 양성 반응이다. 6,90 통증과 신경학적 증상은 상완 신경총을 소흉근과 흉벽 사이에 압박하여 통증을 재현하기 위해 어깨를 신전 및 다양한 외전 위치로 배치하는 팔 들어올리기 스트레스 검사로 종종 악화됩니다.92

이 값을 피험자의 신장으로 나눈 후 100을 곱하여 소흉근 지수를 결정합니다(그림 6, A와 B). 측정법은 간단하나, 기준값 설정과 임상적 의미 있는 편차 규명에는 어려움이 있었다. 견갑골 전방 이동을 측정하는 내측 견갑골 거리는 환자를 엎드린 자세에서 평가한다(그림 6, C와 D).82 마지막으로, 내측 견갑골 각도와 견갑골 전방 이동 높이는 각각 환자를 서 있는 자세와 누운 자세에서 측정한다(그림 7). 더 흔히, PM 길이 및 긴장은 양측 팔을 동시에 들어 올리는 동안 환자의 견갑골 움직임을 관찰하면서 정적 및 동적 상태에서 견갑골 위치를 평가하여 간접적으로 결정됩니다.50,63,106

Figure 6.

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(A) Pectoralis minor length and index. Measure the distance from the medial aspect of the coracoid to the inferior margin of the fourth rib at the sternocostal junction with the patient upright. Pectoralis minor muscle index is calculated by dividing this length by the patient’s height (centimeters) and multiplying by 100. (B) Measurement of the contralateral side should be performed for comparison. (C) Medial scapular distance. This is assessed at the cranial-caudal midpoint of the medial border of the scapula. Dorsum of a patient’s hand is placed on the lumbar spine and a ruler is pressed into the posterior chest wall at the aforementioned midpoint. (D) The vertical distance from the posterior chest wall to the medial scapular border is measured. Assessment of the contralateral side should be performed for comparison.

Figure 7.

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(A) Medial scapular angle. With the patient standing upright, first obtain baseline measurement of the angle subtended between a vertical line and the line along the medial scapular border. (B) Have the patient abduct their arms to 90° and repeat the measurement. Subtract the baseline angle from the 90° abducted measurement to obtain the medial scapular angle. Similarly assess the contralateral side for comparison. (C) Scapular protraction height. With the patient lying supine and relaxed, measure the baseline vertical distance from the table to the posterolateral acromion. (D) Ask the patient to actively protract their scapula (bring their shoulder forward without raising their arm off the table) and again measure the vertical distance. The difference between these values is the scapular protraction height. Similarly, assess the contralateral side for comparison.

Imaging

Patients often present with some workup already completed. At minimum, radiographs of the cervical spine and ipsilateral shoulder are obtained. With PMS, these are often normal. However, they rule out the presence of cervical ribs, congenital enlargement of vertebral transverse processes, apical lung masses representing Pancoast tumor, or prior clavicle fracture with nonunion or malunion.11,25,86 Advanced imaging is frequently utilized, although no specific modality has proven superiority. Magnetic resonance imaging of the brachial plexus eval‎uates possible sites of compression, nerve edema or fibrosis, or pathology along the plexus mimicking PMS, such as space-occupying lesions or nerve sheath tumors.110 The magnetic resonance images are often negative for specific signs of NTOS due to static nature of the test and lack of obvious compressive lesions.17 The shoulder magnetic resonance images may demonstrate separate pathologic findings or potential causes for compression, such as subcoracoid cysts (Fig. 8). Neuromuscular ultrasound permits dynamic eval‎uation of PM during arm abduction in the plane of the body. Compared with unafflicated patients (Fig. 9), those with PMS exhibit posterior indentation of the muscle during arm abduction (Fig. 10), due to shortened and fibrosed PM pressing against the brachial plexus in the shrunken volume of the retropectoralis minor space. Like all ultrasound techniques, there is a user-dependent variability.97 Furthermore, no current standard defines normal vs. abnormal with this dynamic eval‎uation. Vascular workup, including magnetic resonance or computed tomography angiogram, may rule out vascular anomalies prior to surgical treatment. Specific VTOS imaging protocols with arms elevated vs. at the side rule out dynamic elements of vascular.33,94,111

Figure 8.

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Large subcoracoid cyst noted on MRI of the left shoulder in a patient with vague, deep pain about the anterior shoulder and upper chest, worse with repetitive activity. (A) Coronal view, cyst marked with white ∗. (B) Sagittal view, cyst marked with white ∗. Dedicated MRI of the brachial plexus was performed, showing proximity of the subcoracoid cyst to the brachial plexus. (C) Anterior coronal slice, cyst marked with white ∗, plexus marked with white ˆ. (D) Posterior coronal slice, cyst marked with white ∗, coracoid marked with white start, humeral head marked with white downward arrow. The patient was treated with arthroscopic pectoralis minor release, cyst decompression, and brachial plexus neurolysis, with resolution of her symptoms and return to activity. MRI, magnetic resonance imaging.

Figure 9.

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Dynamic ultrasound eval‎uation of the right pectoralis minor during active arm abduction in the plane of the body, in a normal patient without symptoms. (A) Resting adduction with arm at the side. (B) 90o active abduction. (C) 120o active abduction. Note the absence of posterior pectoralis minor muscle indentation. AA, axillary artery; AV, axillary vein; LC, lateral cord; PM, pectoralis minor; PMa, pectoralis major; ∗ indicates coracoid.

Figure 10.

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Dynamic ultrasound eval‎uation of the left pectoralis minor during active arm abduction in the plane of the body, in a patient with symptoms of neurogenic thoracic outlet. Note the indentation of the posterior aspect of the pectoralis minor during progressive abduction, as well as the proximity of the axillary vessels and cords compared to the patient in Figure 6, a consequence of decreased volume in the retropectoralis minor space. Arm at side (A), arm in abduction (B), and maximal abduction (C). AA, axillary artery; AV, axillary vein; LC, lateral cord; MC, medial cord; PM, pectoralis minor; PMa, pectoralis major; ∗ indicates coracoid.

Electrophysiologic testing

Electromyography (EMG) and nerve conduction studies (NCSs) are frequently utilized in upper extremity compression syndromes. Nerve compression is quantified as a measured response of latency and amplitude of action potentials. Historically, EMG/NCSs were often normal in the majority of NTOS patients. Recent evidence suggests abnormal NCS response of the medial antebrachial cutaneous nerve may be indicative of PMS, but this is by no means a common finding nor definitive in diagnosis.3,67 One study demonstrated that 40 of 41 patients had at least 1 abnormal finding on EMG/NCSs including latency >2.4ms, latency difference of 0.3 or more between sides, <10 uv amplitudes, and amplitude ratios ≤0.5.67 As previously stated, advanced scapular dyskinesia can further cause suprascapular neuropathy via chronical scapular protraction and stretch at the suprascapular notch. The supraspinatus and infraspinatus can be assessed both clinically (atrophy, weakness, or fasciculations noted on physical examination) and via EMG/NCSs.54 While these studies confirm‎ the presence of neurologic changes, many patients with NTOS from display negative EMG/NCS results. Ultimately, these tests assist in ruling out alternate compressive neuropathy such as carpal or cubital tunnel syndrome, or cervical radiculopathy, but cannot be relied on alone to diagnose NTOS.22,76

Diagnostic injections

Injection of local anesthetic is the gold standard in diagnosing brachial plexus compression syndromes, including PMS. PM injections are performed under ultrasound guidance for accuracy, targeted just deep to PM insertion on the coracoid (Fig. 11). Following injection, the patient is assessed for pain relief,16 deemed successful (positive) if >50% relief of pain or paresthesias is achieved. Positive injections are associated with better outcome after surgical treatment.35,73,94,95 If symptoms are not improved by injection, or if the patient has symptoms localizing to the supraclavicular area, a separate targeted scalene block (Fig. 12) can assess for potential proximal involvement in advanced stage 4 NTOS.16,65,91 Guided scalene injections are also correlated with favorable response to surgical intervention.16,65 In patients with concomitant SSN compression secondary to chronic anterior tilt of the superior scapula (Fig. 5), ultrasound-guided injection targets the suprascapular notch (Fig. 13). Botulinum injections targeted to the scalenes or PM are another option, but these are less effective at predicting surgical outcome compared to anesthetic blocks with or without corticosteroids.65

Figure 11.

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Ultrasound-guided injection of local anesthetic targeted to the pectoralis minor insertion on the coracoid. PMa, pectoralis major; ∗, coracoid; ˆ, pectoralis minor insertion; white upward arrows, needle.

Figure 12.

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Ultrasound-guided injection of local anesthetic targeted to the scalene triangle. AS, anterior scalene; CA, carotid artery; IJ, internal jugular vein; MS, middle scalene; SCM, sternocleidomastoid; white arrows, needle.

Figure 13.

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Ultrasound-guided injection of local anesthetic targeted to the suprascapular notch, demonstrating 2 different injection techniques. (A) Superior approach, with additional Doppler utilization to identify the suprascapular artery (white arrows with split tails demonstrate needle path and infiltration of anesthetic fluid). (B) Posterior approach. SS, supraspinatus; Tr, trapezius; white arrows, needle; white arrowheads, infiltration of fluid in the suprascapular notch.

TreatmentNonoperative management

Initial treatment of PMS is nonoperative, focusing on periscapular muscle stretching and postural retraining. The goal is improving PM length and flexibility while retraining scapular mechanics and scapulohumeral rhythm. To lengthen and stretch PM, the coracoid insertion is moved away from the anterior rib origin.40 Specific techniques are depicted in Figures 14 and 15.19 Additional exercises to retrain scapular kinematics are also incorporated (Figs. 16 and 17). Orthotic bracing (figure-of-eight) is used to counteract chronic scapular protraction by maintaining shoulders in passive retraction (Fig. 18).

Figure 14.

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(A, B) Center spine towel roll stretch. The patient lays supine with rolled towel between the shoulder blades, allowing the shoulders and scapula to drift posteriorly, stretching the anterior shoulders, chest, and pectoralis muscles. (C, D) Corner stretch. The patient stands with contralateral foot forward and arm abducted and externally rotated 90° against the wall. The patient turns their body away from the wall, stretching the pectoralis muscles, anterior shoulder, and chest.

Figure 15.

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(A) Butterfly stretch. The patient lies supine on foam roller or rolled towel between their shoulder blades. (B) Stretch begins with arms extended at the side and progresses via abduction of arms to an overhead position in a controlled fashion. (C, D) Wall wash. The patient pushes a folded towel against the wall, sliding the towel up and forward with scapula protraction in a diagonal motion, and then reversing the motion downwards and in extension using scapular retraction.

Figure 16.

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Scapular retraining exercises performed standing upright with arms in forward elevation and hands pressed against a wall. (A, B) Scapular depression and elevation. (C, D). Scapular retraction and protraction.

Figure 17.

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Scapular stretching exercises. (A, B) Shoulder flexion stretch, performed supine whilst holding a stick in both hands, permitting the normal arm to assist the compromised arm in attaining maximal overhead flexion stretch. (C) External rotation stretch, similarly performed supine to allow contralateral arm to assist with attaining maximal external rotation stretch for the anterior shoulder anatomy. (D) Sleeper stretch, performed in lateral decubitus to stretch the posterior shoulder anatomy.

Figure 18.

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Figure of Eight Brace. The brace combats resting scapular protraction by exerting a constant posterior force on the scapula. This augments postural retraining and relieves compression in the retropecotalis minor space induced by a protracted scapular position.

Various stretching techniques for PM lengthening have been described with mixed results.14,60,82,107 Borstad et al14 compared 3 different techniques and found unilateral self-stretch was superior to supine or sitting manual stretch.39 Other studies found not only PM lengthening but also greater scapular upward rotation and posterior scapular tilting after stretching.60,107 In a cohort of 46 young, active patients, Provencher et al82 found 40 (87%) responded to stretching and scapular retraining with improved scapular positioning, shoulder function, and pain.

Other studies assessing stretching have equivocal results.70,87 Two studies of home exercise programs involving PM stretching did not show differences in PM length or scapular kinematics but did report decreased symptoms and improved function.70,87

Surgical management

For patients with continued symptoms despite scapular-focused and extensive (6 months) nonoperative treatment, surgical management for PM release is appropriate (Fig. 19). For over 50 years, procedures such as the Latarjet and open brachial plexus exploration incorporated release of PM off the coracoid without adverse consequence.4,73 Recently, isolated PM release for recalcitrant PMS causing NTOS has been advocated. Surgical release of PM has been described via open72,82,94,103 and arthroscopic techniques40,54,55 with initial promising results, although most studies only report short-term outcomes.

Figure 19.

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Stepwise treatment for a patient with neurogenic thoracic outlet syndrome. Initial management is conservative, and surgical treatment is reserved for patients failing to improve with therapy and who also demonstrate a positive response (improvement, even transient) to image-guided anesthetic injection. These patients are treated with arthroscopic surgery, often entailing pectoralis minor release. Concomitant suprascapular neurolysis and/or brachial plexus neurolysis are performed based on preoperative work-up as detailed above.

Prior to detailing specific techniques, distinction must be made regarding overall surgical management of NTOS vs. VTOS (Table I). As PM tightness and ensuing scapular dyskinesia are the prime agents causing NTOS, it follows that surgical algorithm for NTOS primarily addresses the PM. Secondary effects of PMS, such as suprascapular neuropathy and proximal brachial plexus compression in long-standing cases, are addressed simultaneously pending diagnostic workup. If SSN entrapment is found, release at the suprascapular notch is performed simultaneously. Similarly, if proximal plexus compression is discovered preoperatively, brachial plexus neurolysis is undertaken.

Surgical management of VTOS follows a similar anatomic framework. Primary cause of VTOS is dynamic compression of subclavian vessels between the clavicle and first rib during scalene muscle contraction.28,43,48 Therefore, first rib resection targets the principal pathoanatomy creating VTOS.101 Additional agents precipitating VTOS include anomalous structures, scalene hypertrophy, or pathology intrinsic to subclavian vessels themselves.23 Akin to addressing secondary factors in NTOS, these supplementary etiologies in VTOS are addressed per preoperative workup with scalenectomy, resection of anomalous anatomy, or vascular reconstruction.64,93 Outcomes of first rib resection are detailed in multiple studies, varying based on underlying diagnosis,10,30,34 surgical approach,1,10,30 and robotic assistance.51 A systematic review analyzing surgical treatment of TOS by Peek et al81 found first rib resection with or without scalenectomy yielded good or excellent results in 90% of VTOS patients. However, in NTOS patients, this resolved symptoms in a less-consistent 58%-89% range. Furthermore, the largest included study by Vemuri et al103 compared isolated PM release vs. PM release combined with first rib resection and scalenectomy. Isolated PM release demonstrated significantly improved DASH score at 3 months compared with the combined group (26.6 vs. 41.5). Peek et al81 reported complication rates stemming from first rib resection with or without scalenectomy of up to 40%, including pneumothorax, hematoma requiring evacuation, neurologic injury, and infection. They concluded the greatest challenge in treating TOS is the diagnosis itself, particularly of NTOS, given that no standard algorithm exists. Another systematic review by Yin et al109 eval‎uated outcomes in TOS patients with and without first rib resection. They found a mean success rate of 76% and 77% for transaxillary and supraclavicular first rib resection, respectively, and 85% for supraclavicular release without first rib resection. They found mean success rate of 76% and 77% for transaxillary and supraclavicular first rib resection, respectively, and 85% for supraclavicular release without first rib resection. Avoiding first rib resection had the highest likelihood of achieving complete symptom relief. Finally, complication rates were approximately twice as high for transaxillary and supraclavicular first rib resection (22.5% and 25.9%, respectively) compared to supraclavicular release without first rib resection (12.6%). Majority of these complications, such as pneumothorax and neurologic injury, did not have permanent sequelae, with rates of less than 1% for permanent plexus injury or death in the rib resection group. Permanent complications did not occur in the group without rib resection. These data suggest that first rib resection offers viable treatment for VTOS but is less reliable and effective for NTOS. As detailed in the vascular surgery literature, Ambrad-Chalea et al5 recognized PMS as a causative factor in patients with residual symptoms after thoracic outlet decompression involving first rib resection and scalenectomy. Sanders et al94 further utilized open transaxillary approach for PM release in 100 patients: 52 with PMS alone and 48 with PMS and additional proximal compression diagnosed using PM and scalene blocks. In the isolated PMS group, they noted 90% good or excellent result compared to 35% in the combined (PMS and scalene compression) group. They noted failure with isolated PM decompression of 8% in the PMS group compared to 46% with both sites involved. Three patients had early wound infections and 15% reported paresthesia on the undersurface of their arm related to injury of the intercostal brachial cutaneous nerve. Vemuri et al103 performed PM tenotomy in 52 patients with isolated PMS, diagnosed via examination of predominantly infraclavicular tenderness.68 They noted 75% of patients exhibited improvement in symptoms and function at 3 months.

In the orthopedic surgery literature, McIntyre72 in 1975 described open release of PM in 10 patients. All patients reported relief of radiating arm pain and return to work within 6 weeks. Three decades later, Provencher et al82 eval‎uated the surgical release of PM in 6 patients who failed conservative management, via mini-open deltopectoral approach. There was significant improvement in pain and shoulder scores, as well as improved scapular motion in all patients. No surgical complications were noted, and all patients returned to full activity.

A recent innovation in shoulder arthroscopy is arthroscopic PM release (Fig. 20). Though technically challenging, Lafosse et al56 have shown this arthroscopic/endoscopic PM release and concomitant brachial plexus neurolysis are possible, reproducible, and safe in skilled hands. Their surgical technique allows for arthroscopic access to the subcoracoid, subdeltoid, and retropectoralis minor space for PM tenotomy off the coracoid. Further proximomedial advancement permits brachial plexus neurolysis and visualization of axillary vessels (Fig. 21).55 Their group performed arthroscopic brachial plexus neurolysis and PM release in 36 patients, with resolution of symptoms and no postoperative complications.54 In another series of arthroscopic PM release, the senior author was involved in a multicenter study examining outcomes of arthroscopic PM release in 21 patients with a mean 19-month follow-up. Overall, 20 of 21 (95%) had substantial relief of their symptoms with no complications at the time of the latest follow-up (unpublished data).

Figure 20.

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Arthroscopic pectoralis minor release of the right shoulder. (A) View from anterolateral portal with standard 30° arthroscope, demonstrating the coracoacromial ligament (∗) and conjoint tendon (ˆ). (B) View from same portal with 70° arthroscope, demonstrating the classic “T” appearance of the coracoacromial ligament (∗), conjoint tendon (ˆ), and pectoralis minor (downward white arrow) converging on the coracoid process. (C) Release of the pectoralis minor tendon insertion (downward white arrow) off the medial coracoid using electrocautery. Conjoint tendon is also seen in this view (ˆ). (D) Continued release off the coracoid with inferior and medial retraction of the pectoralis minor tendon (downward white arrow). This retraction is routinely noted in patients with pectoralis minor syndrome.

Figure 21.

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Brachial plexus arthroscopic neurolysis following pectoralis minor release (the same patient as Fig. 20). (A) Pectoralis minor completely released (downward white arrow) with classic inferomedial retraction. Retropectoralis minor space is now open. (B) Release of adhesions and areolar tissue in the retropectoralis minor space uncovers the lateral cord of the brachial plexus. (C) Continued proximal release uncovers the axillary artery. Medial cord is partially visualized at the Bottom Right portion of the photo. (D) Further proximal release presents the subclavius muscle on the inferior surface of the clavicle. This is released, completing the infraclavicular release. AA, axillary artery; LC, lateral cord; MC, medial cord; S, subclavius muscle.

In patients with both SSN entrapment and PMS (stages 3 and 4), arthroscopic approach involves complete infraclavicular thoracic outlet release. The SSN release is performed first, followed by PM release, and finally brachial plexus neurolysis proximally to the level of the subclavius muscle. After arthroscopic SSN decompression via release of the transverse scapular ligament (Fig. 22), further medial advancement often displays fibrous bands and adhesions that are released toward the subclavius muscle at the inferior surface of the clavicle. Attention is then turned to the PM release, as depicted in Figure 20. After this is completed, continued superomedial brachial plexus neurolysis is performed by following the plexus cords proximally until the subclavius muscle is encountered on the inferior surface of the clavicle. The subclavius is fully débrided (Fig. 21), along with any residual fibrous bands or adhesions. Once this is complete, the entire infraclavicular thoracic outlet is decompressed.

Figure 22.

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Arthroscopic suprascapular nerve release of the right shoulder (the same patient as Figs. 20 and 21). (A) View from subacromial space via lateral portal and 30o arthroscope, progressing medially following the CA ligament and releasing along the anterior border of the supraspinatus muscle until the transverse scapular ligament is encountered posterior to the coracoid. (B) Needle localization creating superomedial working portal. (C) Arthroscopic scissors introduced through this working portal, releasing transverse scapular ligament. The suprascapular nerve is safely visualized inferior to the ligament. The suprascapular artery runs anterior to posterior over the ligament and is displaced posterior-medial to the scissors to ensure it remains protected. (D) Released suprascapular nerve. CA, carotid artery; TSL, transverse scapular ligament; ∗, indicates suprascapular nerve; ˆ, indicates suprascapular artery.

Postoperative protocol is detailed in Table III. Early range of motion and targeted stretching program begins under therapist guidance, along with use of figure-of-eight brace to reverse protracted resting scapular posture. These protocols involve comprehensive PM stretching, postural retraining, and scapulohumeral rhythm retraining.14,19,60,82,107 Aggressive periscapular muscle strengthening is initiated between 4 and 6 weeks, with most patients returning to overhead activity, including sports, by 3 to 4 months postoperatively. During rehabilitation, strict attention to core, hip, and lower extremity strengthening and coordination is emphasized.40,82

Table 3.

Postoperative protocol after arthroscopic pectoralis minor release.

Weeks 0-2	Phase 1: Immobilization	-Simple sling immediately postoperatively -Transition to Figure-of-Eight brace at the first postoperative visit -Passive and active elbow, wrist, and hand motion
Weeks 2-6	Phase 2: Range of motion and scapula retraining	-Progress from passive to active assisted to active shoulder motion -Periscapular strengthening, retrain scapular kinematics, and pectoralis minor stretching -Continue using Figure-of-Eight brace -Pool therapy encouraged
Weeks 6-12	Phase 3: Strengthening	-Full active/passive shoulder motion -More aggressive strengthening with progression to eccentric strengthening -Continue postural retraining and scapulohumeral rhythm kinematics, continue use of Figure-of-Eight brace
Weeks 12-16	Phase 4: Sport and activity specific	-Continue Phase 3 therapy -Wean use of Figure-of-Eight brace -Gradual return to sport and activity

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Conclusion

PMS and resultant NTOS are challenging entities to recognize, diagnose, and treat. Sound understanding of scapulothoracic mechanics and thoracic outlet anatomy are essential for all providers who treat these patients. Diagnostic workup must be thorough to rule out various etiologies mimicking NTOS. Ultrasound-guided injections are a mainstay of diagnosis and recommended for patients with suspected NTOS prior to invasive treatment. A majority of patients improve with therapy targeted at correcting scapular dyskinesia and stretching of the pectoralis minor. In recalcitrant cases, open or arthroscopic pectoralis minor release yields high rates of success and can be combined with SSN and brachial plexus neurolysis.

Disclaimers:

Funding: No funding was disclosed by the authors.

Conflicts of interest: Michael B. Gottschalk reports being an Acumed consultant and that he recieved institutional support from Arthrex, Acumed, Skeletal Dynamics, Stryker PI research funding. None are relevant to this manuscript. Eric R. Wagner reports receiving consulting fees from Stryker, Wright Medical, Biomet, Acumed, and Osteoremedies and research support from Arthrex, Konica Minolta, Arthrex, and DJO. None are relevant to this manuscript. The other authors, their immediate families, and any research foundation with which they are affiliated have not received any financial payments or other benefits from any commercial entity related to the subject of this article.

Footnotes

Institutional review board approval was not required for this review article.