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Posterior Shoulder Instability

Original Editors Petrice Waters, Suzanne Downing, Emily Padgett and Emily Anthony as part of the Texas State University Evidence-based Practice Project

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Definition/Description

Posterior shoulder instability (PSI) exists on a spectrum from asymptomatic laxity to recurrent posterior subluxation or locked posterior dislocation. Symptomatic posterior translation outside an individual’s normal physiologic range defines PSI; asymptomatic translation is considered laxity.[1]

Epidemiology/Aetiology

Posterior shoulder instability (PSI) is relatively uncommon, accounting for approximately 2–10% of all shoulder instability cases in the general population. [2] [3] [4] It is most frequently observed in young, physically active individuals, particularly those engaged in collision sports (e.g. rugby, American football) and overhead activities (e.g. weightlifting, swimming, throwing sports).[3] [5] For this population, the incidence of PSI leading to surgical intervention is much higher, reported to account for up to 24% of shoulder instability cases.[3]

The aetiology of PSI is multifactorial and can be difficult to isolate. Contributing mechanisms include:

  • Macrotrauma: a single significant event such as a blow to the anterior shoulder or a fall on an outstretched arm with the shoulder flexed, adducted, and internally rotated.[3]
  • Microtrauma: repetitive loading in the flexed, adducted, and internally rotated position (e.g. bench pressing, blocking in contact sports), which may lead to gradual capsulolabral or bony injury.[6] [5]
  • Structural factors: posterior labral tears, reverse Bankart lesions, reverse Hill-Sachs defects, and glenoid retroversion are common findings associated with recurrent PSI.[4] [7]
  • Neuromuscular and scapulothoracic dysfunction: winging of the scapula often occurs as the shoulder subluxates during a provocative position and dynamic anatomical movement. Abnormal activation patterns of the scapular stabilisers, or serratus anterior weakness, may reduce dynamic control of the shoulder, although the exact contribution is still under investigation.[5]
  • Volitional instability: some patients can voluntarily sublux their shoulder. In the absence of psychological factors, this may cause symptomatic instability, but surgical management is rarely indicated unless conservative treatment fails.[4]

Only a minority of patients present with a true posterior dislocation requiring reduction. More often, symptoms include recurrent subluxation, posterior shoulder pain, or mechanical symptoms, rather than full dislocation.[2][5]

Clinically Relevant Anatomy

The glenohumeral joint (GHJ), a multi-axial ball and socket joint, is one of the largest and most complex joints in the body. The spherical shaped convex humeral head articulates with the glenoid fossa, an irregular, oval-shaped concave surface, which is an extension of the scapula. Only 25% of the humeral head makes contact with the glenoid fossa at any time, which enables the GHJ to have the greatest range of movement of any joint, however, this leaves it inherently unstable and with the highest incidence of dislocation among the body’s joints.

This joint is surrounded by numerous ligaments and muscles which give it stability. The surrounding capsule may also add some stability with the coracohumeral and glenohumeral ligaments reinforcing the capsule. Other important bones in the shoulder include:

  • The acromion: a bony projection off the scapula
  • The clavicle: which joins the acromion via the acromioclavicular joint and distal sternoclavicular joint to the axial skeleton
  • The coracoid process: a hook-like bony projection from the scapula

The shoulder has several other important structures:

  • The rotator cuff: a collection of 4 muscles originating from the scapula (supraspinatus, infraspinatus, subscapularis and teres minor) which provide dynamic stabilization to the GHJ and allow the wide range of motion.
  • The bursae: there are a number of bursae associated with the shoulder of which the subacromial bursa is the one most likely to become symptomatic with bursitis. It sits between the superior surface of the supraspinatus tendon and the acromion, coracoid and the coracoacromial ligament, extending down over the humeral tendinous attachment of supraspinatus
  • The labrum: a fibrous ring of cartilage which extends up from the glenoid providing stability in the form of a deeper cup for the humeral head to fit into.

Characteristics/Clinical Presentation

Signs and symptoms for posterior shoulder instability:

  • Posterior shoulder pain, often poorly localized, accompanied by aching or clicking more frequently than reports of actual instability.[3] [4] [8]
  • The arm may be held in internal rotation, giving prominence to the posterior humeral head. Coracoid process can also appear more noticeable.[4]
  • Pain or a sense of instability is often provoked when the arm is placed in forward flexion, adduction, and internal rotation.[3] [8]
  • In overhead athletes, these symptoms commonly arise during follow-through phases of motion such as in tennis or throwing sports.[8]
  • Depending on the history, patients may cite a traumatic event that led to dislocation or reduction, or a more gradual onset from overuse.[3][4] [8]
  • Some individuals are also able to volitionally sublux their shoulder.[4] [9]

Differential Diagnosis

Posterior shoulder instability (PSI) can be difficult to diagnose because its symptoms often overlap with other shoulder pathologies. A structured differential diagnosis is essential to avoid mismanagement.[8][10][11]

  • SLAP Lesions & Rotator Cuff Tears
    • Patients with PSI often present with vague, posteriorly located shoulder pain, which can mimic SLAP tears or rotator cuff pathology.[8][11]
    • Key distinction: PSI symptoms are typically reproduced in forward flexion, adduction, and internal rotation, whereas SLAP/rotator cuff pain may not consistently reproduce instability sensations.
  • Subacromial Impingement
    • Special tests for impingement (e.g., Neer, Hawkins–Kennedy) may provoke pain in PSI because the positions overlap with provocative instability positions.[8]
    • Key distinction: Patients with impingement usually do not test positive on PSI tests such as the Jerk or Kim test.[8]
  • Multidirectional instability (MDI).
    • Multidirectional instability is defined as involuntary, symptomatic shoulder instability in two or more directions.[10][11]
    • Some PSI patients may display a sulcus sign (inferior translation). If the sign is asymptomatic (no pain or instability reported), it may reflect benign laxity rather than true MDI.[10]

Clinical Examination

Upper Quarter Screening

A comprehensive upper quarter examination is essential to rule out referred pain or pathology from adjacent joints (cervical spine, scapulothoracic articulation, elbow).[12]

Observation & Palpation

  • Observation should assess for shoulder asymmetry, muscle atrophy/hypertrophy, abnormal scapular kinematics, and swelling.
  • Palpation may reveal tenderness along the posterior glenohumeral joint line.[13]

Range of Motion (ROM) & Strength Testing

  • Assess active and passive ROM of both shoulders, particularly internal/external rotation, forward flexion, and horizontal adduction.
  • Evaluate rotator cuff and scapular stabilizer strength. Weakness is common, especially in infraspinatus, subscapularis, and lower trapezius.[13]

Instability & Provocative Tests

Use a combination of tests to enhance diagnostic accuracy, as no single test is sufficient.[14]

Test Description Positive Sign Diagnostic Value
Jerk Test[15] Axial load applied during horizontal adduction in 90° abduction and IR. Sharp posterior clunk or pain. Sensitivity: 73%; Specificity: 98%.
Kim Test[16] Posterior-inferior force with diagonal elevation in 90° abduction. Posterior pain or clunk. Sensitivity: 80%; Specificity: 94%.
Posterior Apprehension Test[8][17] Posterior force applied in 90° flexion, adduction, and IR. Apprehension or guarding. Sensitivity: 19.2%; Specificity: 99.2%,
Load & Shift[18] Posterior glide of humeral head in neutral and abducted positions. Excessive translation, pain. Sensitivity: 14%; specificity 100%
Thumb Test[19] Examiner places thumb over posterior GHJ; patient flexes arm. Pain reduction or improved control. Emerging test; under further validation.

Functional & Symptom Reproduction

  • Ask patients to replicate provocative activities (e.g. pushing, bench pressing, cross-body reaching).
  • Assess for pain, apprehension, instability, or mechanical symptoms.
  • Pain during Jerk Test correlates with poor outcomes in nonoperative treatment.[15]

Outcome Measures

Diagnostics

Appropriate treatment and prevention of recurrence in PSI requires determination of cause, severity, direction, and associated lesions. Imaging is essential to delineate both osseous and soft tissue pathology. Recent reviews emphasise that radiologic evaluation should follow clinical history and physical examination.[20]

  • Plain radiographs
    • Whilst AP and lateral views are often routine, they may appear normal in many PSI patients but may reveal gross glenoid rim damage or humeral head defects.[20]
    • An axillary view or sufficiently oblique view is also highly recommended as it better demonstrates posterior dislocation or subluxation, posterior glenoid rim defects, humeral head position, and posterior joint alignment.[20]
  • Magnetic Resonance Imaging (MRI) / MR Arthrography (MRA)
    • MRA has high sensitivity and specificity for detecting posterior glenoid labral tears: in a recent study, sensitivities of ~ 76–84%, specificity ~ 88% for isolated posterior labral lesions vs arthroscopy as reference standard.[21]
    • MRA (or conventional MRI where appropriate) allows evaluation of labrum, capsulolabral complex, posterior band of inferior glenohumeral ligament, cartilage defects, and concomitant soft tissue lesions.[20][22]
    • MRI helps to guide surgical planning and can influence choice between arthroscopic vs open approaches.[20][22]
  • Computed Tomography (CT / CT Arthrography
    • When radiographs or MRI indicate bony abnormalities (e.g. glenoid rim deficiency, reverse Bankart, or humeral head impaction), CT is superior for precise evaluation of bone morphology, glenoid version, quantification of bone loss.[20]
    • CT arthrography may also delineate labral or chondral tears especially when MRI/MRA is equivocal or contraindicated.[20][23]

Physical Therapy Management

Conservative management is first-line for most patients with posterior shoulder instability (PSI), especially for atraumatic/micro-traumatic PSI and first-time dislocations without large structural defects. A structured, progressive programme that combines motor control, targeted rotator-cuff and scapular strengthening, proprioception and activity-modification produces meaningful improvement for most patients; imaging and surgical interventions are indicated when structural lesions, marked bone loss, or failed conservative care are present.[1][24][25][26]

Conservative Rehabilitation Programme

The program will vary in length for each individual depending on severity of injury and other rehabilitation factors.

Phase 1 — Immediate care / education (days–2 weeks)

  • Goal: pain control, protect healing tissues, education on protective positions and activity modification (avoid flexion + adduction + IR). Reassure and set expectations: structured rehab takes weeks–months.[24][26]
  • Immobilization: after a first-time posterior dislocation, immobilization may be prescribed briefly to allow tissue healing, usually around 3 weeks, though practical durations vary by age and local practice.[27]

Phase 2 — Motor control & low-load activation (weeks 1–6)

  • Focus: retrain correct muscle recruitment before loading. Target: infraspinatus/external rotators, posterior deltoid modulation, serratus anterior, middle/lower trapezius, rhomboids. Start with low-load isometrics and scapular activation (supine → sidelying → standing).[1][26][28]
  • Tools: tactile cueing, manual resistance, low-load bands, visual cues.

Phase 3 — Strength & endurance (weeks 4–12)

Strengthening is the cornerstone of PSI rehabilitation and the muscular stabilizers of the shoulder joint need to be engaged to compensate for the stretched capsule that often occurs with shoulder instability and to promote proprioception of the joint.[29]

  • Rotator cuff (especially the infraspinatus, plus supraspinatus, teres minor, subscapularis).[30][31][32]
  • Scapular stabilizers (middle/lower trapezius, rhomboids, serratus anterior). [30][33]
  • Posterior deltoid to support posterior stability, though overactivation can worsen symptoms if not balanced with cuff activity.[32]
  • Progression: programs should begin with isometric activation, progressing to concentric/eccentric control. Load should be increased gradually, initially introducing closed-chain exercises and dynamic control tasks (e.g., controlled weight-bearing on fists/wall). Use upper-body ergometer (UBE) can be used for safe bilateral dynamic conditioning without excessive joint loading. where appropriate.[24] [34] [35] Manual resistance, bands, weights, and machines can all be used.
  • Aim: build endurance of rotator cuff and scapular muscles and improve functional stability.

Phase 4 — Neuromuscular re-education and advanced strengthening (weeks 8–24)

Simply strengthening the rotator cuff muscles may not be enough because PSI patients often demonstrate abnormal recruitment patterns and poor synergy between cuff and scapular stabilizers. [29]

  • Neuromuscular re-education: neuromuscular re-education is an important part of activating scapular and glenohumeral muscles during functional movements. PNF/diagonal patterns, sport-specific movement patterns and perturbation training can be used to restore co-ordinated activation during functional tasks. Emphasis here is needed on quality of movement and progressive exposure to provocative positions under control.[1][26]
  • Biofeedback (EMG/force/visual): EMG biofeedback is often used when abnormal recruitment patterns are evident, and can help focus muscular activity on dynamic stabilizers by retraining activation patterns, particularly by enhancing infraspinatus activity and reducing compensatory posterior deltoid dominance.[1][28] [32] Controlled studies and case series show biofeedback can improve activation patterns and proprioception.[28][32][36]
  • Advanced Strengthening: Strengthening should progress to include full range and diagonal and spiral patterns including PNF patterns.[37] The focus will shift towards high-level strength, power, sport-specific movement control and safe return to sport tasks. Gradual progression is required for resistance, speed and range, including for plyometrics, overhead/throwing drills, contact simulations/ sport specific exercises, particularly in provocative positions as appropriate.[9][38][39]

Recent innovations

  • Neuromuscular electrical stimulation (NMES)– emerging evidence has found enhanced rehab to have early promise for severe functional (voluntary) PSI and may improve muscle activation when combined with exercise.[40]
  • Robotic/EMG-assisted devices and UBE training are being investigated with early findings indicating improvements in muscle control and endurance, but broader clinical outcome results are limited.[41]

When to refer for surgical intervention

Refer earlier if any of the following are present:

  • Recurrent traumatic dislocations
  • Locked or irreducible dislocation
  • Significant functional loss despite high-quality rehab
  • Imaging showing substantial posterior glenoid bone loss or an engaging humeral head defect[25][42]

Medical Management

Whilst first line management is often a conservative approach physiotherapy, surgical intervention may be considered if there is persistent pain/instability after adequate rehab, recurrent dislocations/subluxations, structural lesions (labral tear, bone loss, reverse Hill-Sachs) or if the patient’s functional demands require more definitive restoration.[1] [27] For traumatic posterior dislocation with capsulolabral avulsion, early surgical repair is commonly advocated.[27] The success of surgical intervention depends on the ability to correct the underlying impairment. Therefore, operative treatment may involve more than one procedure to address the factors contributing to the instability.[27] Factors that influence the choice of operative intervention include volitional instability, injury to the shoulder, degree of instability, structural abnormalities, and direction of instabilities.[27]

Volitional Instability

Surgery for purely volitional/psychogenic posterior dislocations is generally contraindicated until psychological drivers are addressed, due to the associated poor outcomes with this group.[43] These dislocations are normally treated with physiotherapy and behavioural/psychological interventions, with surgery reserved only for objectively refractory structural lesions after psychological factors are controlled.[27] Patients without psychological problems usually respond well to a trial of physical therapy that includes pain management, activity modification, and strengthening of the scapulothoracic and rotator cuff muscles.[44][45]

Influence of bone loss on surgery

  • Posterior glenoid bone loss (pGBL) is an important predictor of failure after isolated soft-tissue repair. Multiple recent systematic reviews suggest an increased risk of soft-tissue repair failure as pGBL rises,[46] with some reporting that a 11% posterior glenoid bone loss was associated with around ten times higher risk of failure of arthroscopic posterior labral repair, and 15% bone loss was associated with 25 times higher risk, though these findings are based on a relatively small sample.[47]
  • Glenoid bone augmentation (bone-block) or osteotomy may be considered, rather than isolated capsulolabral repair, when pGBL exceeds the surgeon’s accepted threshold; many groups consider ≥13–20% as an indication to add augmentation, especially in high-demand athletes or recurrent instability.[48]

Surgical Interventions

  • Arthroscopic labral repair: these are keyhole procedures to re-attach torn soft tissues. Good reported outcomes if the bone loss is small. Arthroscopic repair is first-line for soft-tissue lesions in most cases.[39][49]
  • Bone-block/ graft augmentation: this rebuilds the bony rim of the glenoid fossa and is used when moderate to severe bone loss is present, or when prior soft-tissue repair has failed. This procedure has a higher technical demand and more risk of complications.[27][50] All-arthroscopic bone-block reconstructions (iliac crest autograft or allograft) with modern fixations, including metal-free cerclage and suture-tape constructs are increasingly reported with promising short- and mid-term results, but longer-term comparative results versus open bone-block remain limited.[51][52]
  • Posterior glenoid osteotomy: For cases with excessive tilt (“retroversion”) of the glenoid that contribute to instability. This is a complex, specialist surgery and used less commonly.[42][53]
  • Open soft-tissue methods: These are older techniques, largely replaced by minimally invasive (arthroscopic) repair except in salvage or combined with bony procedures.[54]

Reverse Hill-Sachs Lesions Management

  • Small (<20% articular surface, non-engaging): closed reduction and nonoperative management or concomitant posterior labral repair.[55]
  • Engaging or moderate (~20–40%) or symptomatic articular defects: options include modified McLaughlin (transfer of subscapularis/lesser tuberosity into defect), defect-filling (autograft/allograft), or arthroscopic “reverse-remplissage” / subscapularis transfer techniques. Contemporary literature supports arthroscopic modified McLaughlin or reverse-remplissage as effective options in selected patients.[55][56]
  • Large defects (>40%) or chronic locked dislocations: consideration for articular reconstruction (structural grafting) or humeral head reconstruction/arthroplasty depending on patient age and joint degeneration.[57]

Post-Surgical Physical Therapy

Post-surgical rehabilitation does not differ significantly from conservative treatment without surgery. The goals of treatment are the same and treatment includes ROM, neuromuscular re-education/function, and strengthening. Rehabilitation should be time- and criterion-based, protect tissue healing in the early weeks and progressively load the repair as neuromuscular control and strength return.[34] Consult the operative report and the surgeon for procedure-specific precautions (e.g., capsule tensioning, number/location of anchors, bone grafts) before progressing.[38] Use objective criteria (pain, ROM, strength, scapular control, functional tests) rather than time alone to advance phases where possible.[34]

Clinical Bottom Line

Posterior shoulder instability (PSI) is an uncommon but clinically important condition that should be distinguished from other causes of shoulder pain and dysfunction. It may result from microtrauma (repetitive loading) or macrotrauma (acute injury) and often involves a combination of capsulolabral, bony, or muscular contributors. Patients typically present with vague posterior shoulder pain, mechanical symptoms (e.g., clicking), and reproduction of symptoms on instability-specific physical tests. Careful history, targeted examination, and appropriate imaging are essential, as successful management—especially surgical repair—depends on identifying lesion-specific pathology.

Conservative management is the recommended first-line approach, focusing on neuromuscular control, strengthening of dynamic stabilisers, and activity modification. Most patients are treated nonoperatively unless instability follows a traumatic event or symptoms persist despite ≥6 months of structured rehabilitation. When surgery is indicated, outcomes are optimised when procedures are tailored to the identified pathology, and postoperative rehabilitation emphasises gradual restoration of range of motion, followed by strengthening and sport- or work-specific retraining.

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Sadi J, Torchia E, Faber KJ, et al. Posterior Shoulder Instability Classification, Assessment, and Management: An International Delphi Study. J Orthop Sports Phys Ther. 2020;50(7):373-380. doi:10.2519/jospt.2020.9225
  2. ↑ 2.0 2.1 Woodmass, J. M., Lee, J., Wu, I. T., Desai, V. S., Camp, C. L., Dahm, D. L., & Krych, A. J. (2019). Incidence of posterior shoulder instability and trends in surgical reconstruction: a 22-year population-based study. Journal of shoulder and elbow surgery, 28(4), 611–616. https://doi.org/10.1016/j.jse.2018.08.046
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Paksoy A, Akgün D, Lappen S, Moroder P. Diagnosis and treatment of posterior shoulder instability based on the ABC classification. EFORT Open Rev. 2024;9(5):403-412. Published 2024 May 10. doi:10.1530/EOR-24-0025
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Trivellas M, Hoyt B, Bokshan S, Dickens JF, Lau BC. Evolving concepts in the treatment of posterior shoulder instability with glenohumeral bone loss. Ann Jt. 2024;9:28. Published 2024 Jul 12. doi:10.21037/aoj-23-45
  5. ↑ 5.0 5.1 5.2 5.3 Hurley, E. T., Aman, Z. S., Doyle, T. R., Levin, J. M., Jazrawi, L. M., Garrigues, G. E., Namdari, S., Hsu, J. E., Klifto, C. S., Anakwenze, O., Dickens, J. F., & Posterior Shoulder Instability International Consensus Group (2025). Posterior Shoulder Instability, Part I-Diagnosis, Nonoperative Management, and Labral Repair for Posterior Shoulder Instability-An International Expert Delphi Consensus Statement. Arthroscopy : the journal of arthroscopic & related surgery : official publication of the Arthroscopy Association of North America and the International Arthroscopy Association, 41(2), 166–180.e11. https://doi.org/10.1016/j.arthro.2024.04.035
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  10. ↑ 10.0 10.1 10.2 Housset, V., Ho, S. W. L., Lädermann, A., Phua, S. K. A., Hui, S. J., & Nourissat, G. (2024). Multidirectional instability of the shoulder: a systematic review with a novel classification. EFORT open reviews, 9(4), 285–296. https://doi.org/10.1530/EOR-23-0029
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  12. ↑ Borsa PA, Sauers EL, Herling DE. Patterns of glenohumeral joint laxity and stiffness in healthy college-aged men and women. J Athl Train. 2000;35(2):147-53.
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  17. ↑ Bäcker HC, Galle SE, Maniglio M, Rosenwasser MP. Biomechanics of posterior shoulder instability - current knowledge and literature review. World J Orthop. 2018;9(11):245-254. Published 2018 Nov 18. doi:10.5312/wjo.v9.i11.245
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  24. ↑ 24.0 24.1 24.2 Watson, L., Balster, S., Warby, S., Lenssen, R., Hoy, G., Barwood, S., French, J., Kerr, B., Lawrence, S., Ganderton, C., Davis, K., & Pizzari, T. (2024). The efficacy of conservative management of micro-traumatic posterior shoulder instability. JSES international, 9(1), 46–55. https://doi.org/10.1016/j.jseint.2024.09.016
  25. ↑ 25.0 25.1 Paksoy, A., Akgün, D., Lappen, S., & Moroder, P. (2024). Diagnosis and treatment of posterior shoulder instability based on the ABC classification. EFORT open reviews, 9(5), 403–412. https://doi.org/10.1530/EOR-24-0025
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  27. ↑ 27.0 27.1 27.2 27.3 27.4 27.5 27.6 Hachem, A. I., Molina-Creixell, A., Rius, X., Rodriguez-Bascones, K., Cabo Cabo, F. J., Agulló, J. L., & Ruiz-Iban, M. A. (2022). Comprehensive management of posterior shoulder instability: diagnosis, indications, and technique for arthroscopic bone block augmentation. EFORT open reviews, 7(8), 576–586. https://doi.org/10.1530/EOR-22-0009
  28. ↑ 28.0 28.1 28.2 Yu IY, Choo YK, Kim MH, Oh JS. The effects of pressure biofeedback training on infraspinatus muscle activity and muscle thickness. J Electromyogr Kinesiol. 2018;39:81-88. doi:10.1016/j.jelekin.2018.01.007
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  30. ↑ 30.0 30.1 Jaggi A, Alexander S. Rehabilitation for Shoulder Instability - Current Approaches. Open Orthop J. 2017;11:957-971. Published 2017 Aug 31. doi:10.2174/1874325001711010957
  31. ↑ Bishop JY, Santiago-Torres JE, Rimmke N, Flanigan DC. Smoking Predisposes to Rotator Cuff Pathology and Shoulder Dysfunction: A Systematic Review. Arthroscopy. 2015;31(8):1598-1605. doi:10.1016/j.arthro.2015.01.026
  32. ↑ 32.0 32.1 32.2 32.3 Lim OB, Kim JA, Song SJ, Cynn HS, Yi CH. Effect of Selective Muscle Training Using Visual EMG Biofeedback on Infraspinatus and Posterior Deltoid. J Hum Kinet. 2014;44:83-90. Published 2014 Dec 30. doi:10.2478/hukin-2014-0113
  33. ↑ McClure PW, Michener LA, Karduna AR. Shoulder function and 3-dimensional scapular kinematics in people with and without shoulder impingement syndrome. Phys Ther. 2006;86(8):1075-1090.
  34. ↑ 34.0 34.1 34.2 Goldenberg BT, Hurley ET, Anavian J, Sanchez G, Millett PJ. Rehabilitation following posterior shoulder stabilization: clinical commentary. Int J Sports Phys Ther. 2021;16(3):861-71.
  35. ↑ Ludewig PM, Borstad JD. Effects of a home exercise programme on shoulder pain and functional status in construction workers. Occup Environ Med. 2003;60(11):841-849. doi:10.1136/oem.60.11.841
  36. ↑ Tannenbaum E, Sekiya JK. Evaluation and management of posterior shoulder instability. Sports Health. 2011;3(3):253-263. doi:10.1177/1941738111400562
  37. ↑ Engle, R. P., & Canner, G. C. (1989). Posterior shoulder instability: approach to rehabilitation. The Journal of orthopaedic and sports physical therapy, 10(12), 1–494.
  38. ↑ 38.0 38.1 Fried JW, Hurley ET, Duenes ML, et al. Return to Play After Arthroscopic Stabilization for Posterior Shoulder Instability-A Systematic Review. Arthrosc Sports Med Rehabil. 2020;3(1):e249-e256. Published 2020 Dec 24. doi:10.1016/j.asmr.2020.08.007
  39. ↑ 39.0 39.1 Gouveia K, Kay J, Memon M, Simunovic N, Bedi A, Ayeni OR. Return to Sport After Surgical Management of Posterior Shoulder Instability: A Systematic Review and Meta-analysis. Am J Sports Med. 2022;50(3):845-857. doi:10.1177/03635465211011161
  40. ↑ Moroder P, Karpinski K, Akgün D, et al. Neuromuscular Electrical Stimulation-Enhanced Physical Therapist Intervention for Functional Posterior Shoulder Instability (Type B1): A Multicenter Randomized Controlled Trial. Phys Ther. 2024;104(1):pzad145. doi:10.1093/ptj/pzad145
  41. ↑ Lavallière M, Tremblay M, Ojardias E, Turpin M, Perrochon A, Rigoard P, Goudman L, Moens M, David R, Billot M. Shoulder Musculoskeletal Disorder Rehabilitation Using a Robotic Device Based on Electromyography (EMG) Biofeedback: A Retrospective Cohort Study. Medicina. 2025; 61(2):272. https://doi.org/10.3390/medicina61020272
  42. ↑ 42.0 42.1 Hurley ET, Aman ZS, Doyle TR, et al. Posterior Shoulder Instability, Part II-Glenoid Bone Grafting, Glenoid Osteotomy, and Rehabilitation/Return to Play-An International Expert Delphi Consensus Statement. Arthroscopy. 2025;41(2):181-195.e7. doi:10.1016/j.arthro.2024.04.034
  43. ↑ Frank RM, Romeo AA, Provencher MT. Posterior glenohumeral instability: evidence-based treatment. Journal of the American Academy of Orthopaedic Surgeons 201725610–623. ( 10.5435/JAAOS-D-15-00631)
  44. ↑ Moroder P, Danzinger V, Maziak N, Plachel F, Pauly S, Scheibel M, Minkus M. Characteristics of functional shoulder instability. Journal of Shoulder and Elbow Surgery 20202968–78. ( 10.1016/j.jse.2019.05.025)
  45. ↑ Robinson CM, Aderinto J. Recurrent posterior shoulder instability. J Bone Joint Surg. 2005;87(4):883-892.
  46. ↑ Brown CL, LeVasseur CM, Scott D, Hughes JD, Lin A, Anderst WJ. Best-Fit Circle Missing Area Method Shows Good Accuracy and Interrater Reliability When Assessing Glenoid Bone Loss. Am J Sports Med. 2025;53(9):2060-2065. doi:10.1177/03635465251346838
  47. ↑ Arner JW, Ruzbarsky JJ, Midtgaard K, Peebles L, Bradley JP, Provencher MT. Defining Critical Glenoid Bone Loss in Posterior Shoulder Capsulolabral Repair. Am J Sports Med. 2021;49(8):2013-2019. doi:10.1177/03635465211016804
  48. ↑ Briggs DV, Hurley ET, Warren E Jr, et al. Bone block options for treating glenoid bone loss and glenohumeral instability: A systematic review. Shoulder Elbow. Published online November 3, 2024. doi:10.1177/17585732241293763
  49. ↑ Ralph, J. E., Hurley, E. T., Lunn, K., Levin, J. M., Klifto, C. S., Owens, B. D., Anakwenze, O. A., Lau, B. C., & Dickens, J. F. (2024). Outcomes of arthroscopic stabilization for posterior shoulder instability: a systematic review. Journal of shoulder and elbow surgery, 33(11), 2530–2538. https://doi.org/10.1016/j.jse.2024.04.006
  50. ↑ Boileau P, Hardy MB, McClelland WB Jr, Thélu CE, Schwartz DG. Arthroscopic posterior bone block procedure: a new technique using suture anchor fixation. Arthrosc Tech. 2013;2(4):e473-e477. Published 2013 Nov 8. doi:10.1016/j.eats.2013.07.004
  51. ↑ Hachem AI, Diaz-Apablaza E, Molina-Creixell A, Ruis X, Videla S, Luis Agulló J. Clinical Outcomes and Graft Resorption After Metal-Free Bone Block Suture Tape Cerclage Fixation for Recurrent Anterior Shoulder Instability: A Computed Tomography Analysis. Am J Sports Med. 2024;52(6):1472-1482. doi:10.1177/03635465241236179
  52. ↑ Karkosch RF, Slapar J, Smith T, Wellmann M, Pastor MF, Horstmann H. Recurrent posterior shoulder instability-Long-term results after arthroscopic posterior bone block with capsular reconstruction. J Exp Orthop. 2025;12(1):e70166. Published 2025 Feb 12. doi:10.1002/jeo2.70166
  53. ↑ Evans JP, Handshin S, Bain G. Posterior shoulder instability - A systematic review and meta-analysis of glenoid osteotomy and bone block procedures. JSES Rev Rep Tech. 2025;5(3):506-515. Published 2025 Apr 2. doi:10.1016/j.xrrt.2025.03.004
  54. ↑ Antosh IJ, Tokish JM, Owens BD. Posterior Shoulder Instability. Sports Health. 2016;8(6):520-526. doi:10.1177/1941738116672446
  55. ↑ 55.0 55.1 Rinaldi VG, Coliva F, Favero A, et al. From Diagnosis to Decision-Making: A Systematic Review of the Management of Reverse Hill-Sachs Lesions after Posterior Shoulder Dislocations. J Clin Med. 2024;13(7):2085. Published 2024 Apr 3. doi:10.3390/jcm13072085
  56. ↑ Arauz S, González-Martín D, Quiroga M, Guillén P. Arthroscopic Modified McLaughlin Procedure and Remplissage for Treatment of Simultaneous Reverse Hill-Sachs and Hill-Sachs Lesions. Arthrosc Tech. 2022;11(8):e1473-e1478. Published 2022 Jul 14. doi:10.1016/j.eats.2022.03.038
  57. ↑ van der List JP, Waterman BR. Humeral Head Reconstruction of Reverse 
Hill-Sachs Lesions. Instr Course Lect. 2024;73:559-571.

 

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