Chronic Rotator Cuff Tendinopathy: Difference between revisions

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Revision as of 16:29, 30 September 2018

Original Editor -Mariam Hashem

Top Contributors - Mariam Hashem, Tarina van der Stockt, Kim Jackson and Wanda van Niekerk  

Introduction[edit | edit source]

Rotator Cuff Tendinopathy is a common condition representing 30-70% of shoulder pain disorders[1]. This condition is more significant after the age of 50 and can be attributed to multiple factors.

Rotator Cuff Tendinopathy has adverse consequences on the quality of life and is associated with long-term disability, retirement and high rates of chronicity (40-50%)[2].

To develop effective management strategies, clinicians need to understand the factors contributing to the development of chronicity. Structural, gentic, biomechanical and psychosocial factors play an integral role in the development of Chronic Rotator Cuff Tendinopathy. Additionally, the following five factors have been discussed in recent literature and therefore should be considered when addressing this condition:

  • Central Nervous System reorganization
  • RC Tendons
  • Scapula
  • Proprioception
  • Central Senstization

Central Nervous System Reorganization[edit | edit source]

Rat Hippocampal Neuron.jpg

While structural-oriented treatment may be effective in acute stages of MSD, the outcomes are relatively poor in chronic stages. This propses a question of what are the reasons beyond the development of chronic pain and disability in Rotator Cuff Tendinopathy? This simply leads us to consider CNS-related factors.

Changes in neuronal structure, organization and properties (Neural plasticity) following MSD can possibly explain altered joint control and persistent pain[3]. Numerous studies have investigated the CNS reorganization associated with different MSD and reported altered perception threshold to sensory stimuli, augmented pain perception and other similar symptoms presented bilaterally and away from the site of injury[4][5][6][7]. A study by Nogomo et al [8] reported cortical reorganization correlating with the magnitude of MS-related pain. Overlap in spatial territory of cortical representation of muscles and alterations in intracortical inhibitory and facilitatory networks were also reported in different studies[9][10]. This supports the hypothesis that structural abnormalities shouldn't always be associated with MS-related symptoms[11].

Selective facilitation of needed muscles and inhibition of others for smooth performance, as well as intermuscular coordination may be disrupted as consequences of CNS reorganization[9][10]. Motor cortical reorganization may persists despite alleviation of pain, leading to modifications in motor strategies to control the affected joint. Eventually, chronicity is likely to occure as a result of the cascades of disruptions.

Understanding maladaptive organizations has great clinical implicaitions. While strength training and endurance training have shown induced angiogenesis in motor cortex and synaptogenesis within spinal cord respectively, skill trianing targets the motor map organization[12]. Rehabilitation strategies should include motor control training in the rehabilitation of chronic RCT[3]. The study of Roy et al [13] features different structural and global approaches to rehabilitate CNS reoganiaztion, including sensorimotor training, pain education and postural exercises.

New therapeuric interventions that aim to modulate neuronal excitability have emerged, however, studies are not sufficient to support their clinical implementation.These include:

  • Non-invasive brain stimulations :
  1. TDCS administration.gif
    Transcranial direct current stimulation (tDCS)
  3. Repetitive transcranial magnetic stimulation (rTMS)
  • Peripheral neuromuscular stimulations:
  1. Peripheral electrical stimulation(PES)
  2. Repetitive peripheral magnetic stimulation(RPMS)

RC Tendons[edit | edit source]

There is a wide debate in the literature regarding shoulder pain terinology. Wether it is a rotator cuff tendinopathy, subacromial pain syndome or subacromial pain impinegemnt syndrome we have to acknowledge the fact the shoulder pain is multifactorial and can be deriven from multiple reasons.

However, in a clinical setting it is better to have objective measures to diffrentiate between rotator cuff tendinopathy and subacromial pain syndrome. This is particularly helpful for rehabilitation decision making[3].

Tendon overload/degenration is likely to be a cause for subacromial pain. Tendons, especially Supraspinatus tendon, also could be compressed mechanically in the subacromial space. However, bony pathologies cannot be attributed as the sole cause of pain. Surgical approaches combined with rehabilitation was found to be no more effective than rehabilitation alone. Therefore, researchers suggest abandoning the ''impingement'' terminology[14].

Intrinsic factors contributing to RC tendons degenration/loading are:

  • Vascularity
  • Morphology
  • Mechanical
  • Ageing
  • Genetic

Neovascularization, refering to increased blood supply in tendon causing pain, was evident in lower limb. The less vascularity in shoulder and the difficulty in obtaining daignostic images similar to lower limb tendons resulted in less studied neovascularity of RC tendinopahty. increased supraspinatus vascularity was reported in a study by Kardouni JR[15]. there is still conflicting results regarding wether neovascularization is evident and could be a contributing fator to developing Chronic RCT[3].

Although there is a wide agreement towards adapting the terminology ''endinopathy'' instead of '' tendenitis'', inflammation was reported by Dean BJ[16]. Tendon thickning was also present in tendinopathy as a result of abnormal collagen laydown. however, it starts thinning with progresive tendon disease whickh may lead to tear[3]. But thickneing isn't always a sign of tendinopathy as it was evident in overhead athletes and spinl cord injuries.

if tendon thickens in the sa space (10-15 mm in healthy individuals) AHD. A smaller AHD was observed (7-8 mm)

Compression is likely to be the reason of pain in three circumstances:

  • Thicker tendon e.g: overuse or disease
  • Smaller AHD (7-8mm)
  • Occupation ratio: Supraspinatus Tendon:AHD. If hte tendon occupies > AHD.

AHD is at its smallest between 0-90° so above 90° is likely to be of another reasons.

RCT could be classified as partial thickness and full thickness tear. Partial thickness tear could be articular, bursal or mid-substance. Full thickness tear could be imagned as a ''hole in the sock'' meaning that there is a tear but it doesn't neccessarily goes to the entire tendon unless it's across the three tendons. there is something still intact

For rehab decision making pruposes, we would consider full thickness tear in a seperate category different from partial thickness tear and subacromial pain syndrome.

  • Subacromial Pain Syndrome:
  1. SPS
  2. Partial Thickness RC tear
  • Full Thickness Rotator Cuff Tear (FT-RCT)

Recommendations for Diagnosis[3][edit | edit source]
Subacromial Pain Syndrome (SPS) Full Thickness Tear (FT-RCT)
Confirm (Rule In): Specifity ≥ 80%. Likelihood ratio ≥ 2.0. Single Tests[17][18][19][20]:

1-Painful Arc

2-Resisted External Rotation (Pain or Weakness)

3-Full can

4- Drop Arm.

Combo Tests[21]:

1-Hawkins

2-Pianful Arc

3-ER resistance.

All 3+: +LR of 10.56

All 3-: -LR of 0.17

Single Test[17][18][19][20]:

1-Painful Arc

2-Resisted ER

3-Drop Arm

4-ER lag-massive tear

5-Atrophy(infraspinatus)

6-IR lag& lift off

7-Belly off-subscapularis

Combo Tests[22]:

1- Age ≥ 65 yo

2-ER marked weakness

3- Night Pain

All 3 + :+LR of 9.84

All 3 - : -LR of 0.54

Screen out (Rule Out) : Senstivity ≥ 80%. LR ≤ 0.5 Single Tests:

1-Painful Arc

2-Resisted ER: Pain or Weakness

3-Hawkins

4-Neer

5-Full Can

6-Empty can

ComboTets[23]: 3/5

1-Hawkins

2-Neer

3-Painful Arc

4-Empty Can

5-ER resistance

If ≥ 3+ /5 : +LR of 2.93

If < 3+ / 5: - LR of 0.34

Single Tests:

1-Resisted ER→marked weakness

2-IR lag and lift off

3-Full Can

4-Empty Can

Combo Tests[21]:

Drop Arm

Painful Arc

ERRT

All 3 + R/In: + LR of 15.57

All 3 - R/Out: -LR of 0.16

Scapula[edit | edit source]

Proprioception[edit | edit source]

Central Senstization[edit | edit source]

References[edit | edit source]

  1. ↑ Oliva F, Piccirilli E, Bossa M, Via AG, Colombo A, Chillemi C, Gasparre G, Pellicciari L, Franceschetti E, Rugiero C, Scialdoni A. IS Mu. LT-rotator cuff tears guidelines. Muscles, ligaments and tendons journal. 2015 Oct;5(4):227.
  2. ↑ Kuijpers T, van der Windt DA, Boeke AJ, Twisk JW, Vergouwe Y, Bouter LM, van der Heijden GJ. Clinical prediction rules for the prognosis of shoulder pain in general practice. Pain. 2006 Feb 1;120(3):276-85.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 WCPT 2017: Rotator Cuff Tendinopathy (FS-16). [Presentation]. World Confideration for Physical Therapy 2 July 2017. [27 Sep 2018] Available from: https://www.youtube.com/watch?v=driyaw7ALDg
  4. ↑ Wilder-Smith OH, Tassonyi E, Arendt-Nielsen L. Preoperative back pain is associated with diverse manifestations of central neuroplasticity. Pain. 2002 Jun 1;97(3):189-94.
  5. ↑ Jensen R, Kvale A, Baerheim A. Is pain in patellofemoral pain syndrome neuropathic?. The Clinical journal of pain. 2008 Jun 1;24(5):384-94.
  6. ↑ Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. The Journal of Pain. 2009 Sep 1;10(9):895-926.
  7. ↑ Pelletier R, Higgins J, Bourbonnais D. Is neuroplasticity in the central nervous system the missing link to our understanding of chronic musculoskeletal disorders?. BMC musculoskeletal disorders. 2015 Dec;16(1):25.
  8. ↑ Ngomo S, Mercier C, Bouyer LJ, Savoie A, Roy JS. Alterations in central motor representation increase over time in individuals with rotator cuff tendinopathy. Clinical Neurophysiology. 2015 Feb 1;126(2):365-71.
  9. ↑ 9.0 9.1 Schabrun SM, Hodges PW, Vicenzino B, Jones E, Chipchase LS. Novel adaptations in motor cortical maps: the relation to persistent elbow pain. Med Sci Sports Exerc. 2015 Apr 1;47(4):681-90.
  10. ↑ 10.0 10.1 Burns E, Chipchase LS, Schabrun SM. Altered function of intracortical networks in chronic lateral epicondylalgia. European Journal of Pain. 2016 Aug;20(7):1166-75.
  11. ↑ Lewis J, McCreesh K, Roy JS, Ginn K. Rotator cuff tendinopathy: navigating the diagnosis-management conundrum. journal of orthopaedic & sports physical therapy. 2015 Nov;45(11):923-37.
  12. ↑ Adkins DL, Boychuk J, Remple MS, Kleim JA. Motor training induces experience-specific patterns of plasticity across motor cortex and spinal cord. Journal of applied physiology. 2006 Dec;101(6):1776-82.
  13. ↑ Roy JS, Bouyer LJ, Langevin P, Mercier C. Beyond the Joint: The Role of Central Nervous System Reorganizations in Chronic Musculoskeletal Disorders. journal of orthopaedic & sports physical therapy. 2017 Nov;47(11):817-21.
  14. ↑ Cools AM, Michener LA. Shoulder pain: can one label satisfy everyone and everything?.
  15. ↑ Kardouni JR, Seitz AL, Walsworth MK, Michener LA. Neovascularization prevalence in the supraspinatus of patients with rotator cuff tendinopathy. Clinical Journal of Sport Medicine. 2013 Nov 1;23(6):444-9.
  16. ↑ Dean BJ, Gettings P, Dakin SG, Carr AJ. Are inflammatory cells increased in painful human tendinopathy? A systematic review. Br J Sports Med. 2015 Aug 5:bjsports-2015.
  17. ↑ 17.0 17.1 Hermans J, Luime JJ, Meuffels DE, Reijman M, Simel DL, Bierma-Zeinstra SM. Does this patient with shoulder pain have rotator cuff disease?: The Rational Clinical Examination systematic review. Jama. 2013 Aug 28;310(8):837-47.
  18. ↑ 18.0 18.1 Hanchard NC, Lenza M, Handoll HH, Takwoingi Y. Physical tests for shoulder impingements and local lesions of bursa, tendon or labrum that may accompany impingement. The Cochrane database of systematic reviews. 2013 Apr 1.
  19. ↑ 19.0 19.1 Hegedus EJ, Goode AP, Cook CE, Michener L, Myer CA, Myer DM, Wright AA. Which physical examination tests provide clinicians with the most value when examining the shoulder? Update of a systematic review with meta-analysis of individual tests. Br J Sports Med. 2012 Nov 1;46(14):964-78.
  20. ↑ 20.0 20.1 Alqunaee M, Galvin R, Fahey T. Diagnostic accuracy of clinical tests for subacromial impingement syndrome: a systematic review and meta-analysis. Archives of physical medicine and rehabilitation. 2012 Feb 1;93(2):229-36.
  21. ↑ 21.0 21.1 Park HB, Yokota A, Gill HS, El Rassi G, McFarland EG. Diagnostic accuracy of clinical tests for the different degrees of subacromial impingement syndrome. JBJS. 2005 Jul 1;87(7):1446-55.
  22. ↑ Litaker D, Pioro M, Bilbeisi HE, Brems J. Returning to the bedside: using the history and physical examination to identify rotator cuff tears. Journal of the American Geriatrics Society. 2000 Dec;48(12):1633-7.
  23. ↑ Michener LA, Walsworth MK, Doukas WC, Murphy KP. Reliability and diagnostic accuracy of 5 physical examination tests and combination of tests for subacromial impingement. Archives of physical medicine and rehabilitation. 2009 Nov 1;90(11):1898-903.
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