Chronic Rotator Cuff Tendinopathy

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, genetic, 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 Sensitization

Central Nervous System Reorganization[edit | edit source]

Rat Hippocampal Neuron.jpg

While structural-oriented treatment may be effective in acute stages of musculoskeletal disorders (MSD), the outcomes are relatively poor in chronic stages. This proposes 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 structures, 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 occurs as a result of the cascades of disruptions.

Understanding maladaptive organizations has great clinical implications. While strength training and endurance training have shown induced angiogenesis in motor cortex and synaptogenesis within spinal cord respectively, skill training 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 reorganization, including sensorimotor training, pain education and postural exercises.

New therapeutic 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 :
TDCS administration.gif
  1. Transcranial direct current stimulation (tDCS)
  2. 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 terminology[14]. Whether it is rotator cuff tendinopathy, subacromial pain syndrome or subacromial impingement syndrome we have to acknowledge the fact that shoulder pain is multifactorial and can be attributed to multiple reasons.

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

Tendon overload/degeneration is likely to be a cause of 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 degeneration/loading are:

  • Vascularity
  • Morphology
  • Mechanical
  • Ageing
  • Genetic

Neovascularization, referring to increased blood supply in tendons causing pain, was evident in the lower limb. Kardouni JR[15] reported increased supraspinatus vascularity. Despite this finding, we still need more studies to confirm neovascularity as a contributing factor to RCT. The less vascularity in shoulder tendons and the difficulty in obtaining diagnostic images similar to lower limb tendons propose challenges to study this factor [3].

Although there is a wide agreement towards adapting the terminology ''Tendinopathy'' instead of '' tendonitis'', inflammation was reported by Dean BJ[16]. Tendon thickening was also present in tendinopathy as a result of abnormal collagen laydown. However, it starts thinning with progressive tendon disease which may lead to tear. But thickening isn't always a sign of tendinopathy as it was evident in overhead athletes and spinal cord injuries[3].

Compression is likely to be the reason of pain in three circumstances[3]:

  • Thicker tendon e.g: overuse or disease
  • Smaller distance between Acromion and Humerus AHD (7-8mm). Normally AHD= 10-15 mm.
  • Occupation ratio: Supraspinatus Tendon:AHD. If the tendon occupies > AHD.

AHD is at its smallest between 0-90°. Therefore pain above 90° is likely to be of other reasons.

For rehabilitation decision making purposes, diagnosing shoulder pain could be classified as following:

  • 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)/ Partial Thickness Tear 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]:


2-Pianful Arc

3-ER resistance(Pain/weakness).

All 3+: +LR of 10.56

All 3-: -LR of 0.17

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

1-Painful Arc

2-Resisted ER (marked weakness)

3-Drop Arm

4-ER lag-massive tear


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



5-Full Can

6-Empty can/Jobe test

ComboTets[23]: 3/5



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]:

1-Drop Arm

2-Painful Arc


All 3 + R/In: + LR of 15.57

All 3 - R/Out: -LR of 0.16


Full video provided by Clinically Relevant

Drop video provided by Clinically Relevant

Hawkins-Kennedy video provided by Clinically Relevant

Neer video provided by Clinically Relevant

Empty video provided by Clinically Relevant


Lift video provided by Clinically Relevant

Scapula[edit | edit source]

In healthy individuals, scapular movement is controlled through balanced activation patterns as follows:

  • Prime Movers
  • Dynamic Stabilizers
  • Postural Muscles

Altered muscle activation patterns in scapula in relation to RCT can be summarized in the following table[28][29][30]:

Hypoactive muscles Hyperactive muscles Hypo or Hyperactive muscles
Lower Trapezius

Middle Trapezius

Serratus Anterior

Pectoralis Minor

Levator Scapula

Upper Trapezius


Since Scapula plays an integral role in bridging shoulder complex to the spine[31], overloading the RC tendons to maintain GH stability is possible.Therefor it is essential to integrate scapular rehabilitation in the RCT management program[3].

When it comes to deciding which scapular-focused exercise to include in the rehabilitation program, clinicians should consider the following[32]:

1- Neuromuscular Coordination and correcting scapular position consciously.

2-Restoring muscle balance rather than strengthening.

3-Integrating functional-specific or sport-specific exercises.

Recommendations for balancing muscle activation patterns[3][30][33]:

  • To address middle and lower trapezius muscles hypoactivity/weakness, it is recommended to add external rotation in different positions e.g. diagonal pattern and with shoulder elevation.
Shoulder ER diagonal.png
Shoulder ER with elevation.png
Shoulder Elevation and ER on ball.png
Forward shoulder elevation.png
  • Elevation Exercises are preferred over isolated protraction when targeting serratus anterior muscle.
  • Adding an external rotation component and/or performing exercises in a lying position with the head resting are suggested for decreasing upper trapezuis hyperactivity.
Shoulder ER in lying position.png
  • Open chain exercises with external rotation has been shown to decrease hyperactivity of pectoralis minor.
  • Overhead exercises or closed chain positions such as overhead retractions, overhead shrugging and wall slide are recommended to decrease levator scapula hyperactivity.

Integrating core and peripheral muscles could be helpful in RCT rehabilitation, considering kinetic chain role of the scapula. Serratus Anterior activation could be targeted by conscious contraction of core abdominal muscles[34] and during high load exercises.

Overhead retractions.png

Proprioception[edit | edit source]

The functional stability paradigm describes the cascade of events following a MS injury leading to prioprioception deficits[35]. Studies investigating joint kinesthesia in individuals with RCT and SPS have challenged this model.

Fyhr C [36] reported no significant difference in active position sense between individuals with shoulder injury and controls. The results were different with regard to passive position sense when the injured shoulder was compared to the contralateral side. Another study found no difference between symptomatic and asymptomatic female workers in joint position sense at different shoulder movements[37]. However, there was enhanced acuity of position sense associated with active internal rotation in symptomatic individuals.

Pain, despite having a negative effect on muscle strength and performance[38], had a positive effect on movement sense. Fatigue was also studied to see the effect it has on proprioception, and found to have no affect on proprioception, movement speed or accuracy[39].

Understanding cortical representations ''neurotags'' might explain the observed enhancement of proprioception[3]. Neurotags have a role in building protective strategies to counteract or minimize the impact of injury and pain on movement control. Proprioception, being one of several variables modulating neurotags, may not be altered in chronic conditions[40].

Although some studies reported enhancement in proprioception, the available evidence is not sufficient to conclude whether proprioception deficits are linked to chronic RCT. Future studies should focus on getting an in-depth insight of the central influence of pain rather than the peripheral effects only. This also should be reflected on clinical practice, in terms of prescribing exercises that address both central and peripheral impairments[3].

Central Sensitization[edit | edit source]

In response to pain, many people develop neuroplastic changes in the peripheral and central nervous systems. Neuroplasticity is associated with functional and chemical changes that induce sensitization rather than habituation. As a result, innocuous stimulus such as touch might be perceived as noxious ''painful'' [3].

Systematic reviews[41][42] reported significant presence of central sensitization(CS) in a subgroup of chronic shoulder pain, but its specific role hasn't yet been investigated sufficiently[43].

Patients with chronic pain could be identified if they are having CS or not using a simple algorithm proposed by Nijs et al [44]. Disproportionate, diffused pain are the most distinguishing criteria of CS. Central Sensitization Inventory and Scoring is also used to detect individuals with CS[3]. Additionally, we can subcategorize individuals with CS-dominance as either persisters or avoiders. Persisters will resume their normal activities after pain subsides, while avoiders will restrict or decrease their level of movement.

Regardless of CS-dominance, pain neuroscience education has been shown to be effective in chronic pain management[45]. In addition, avoiders might benefit from graded exposure to exercises whereas pacing strategies might be helpful for persisters[3].

Meeus et al[45] suggested starting with general exercises, especially if the patient has high levels of pain, then progressing to more specific exercise. General fitness exercises as well as manual therapy have shown analgesic effects in patients with chronic pain syndromes[45] [46].

Conclusion[edit | edit source]

Each patient is unique and it is important to remember that Rotator Cuff Tendinopathy is not caused by only one injury mechanism and that different factors may be involved in each patient.  Every patient should receive a thorough clinical examination and the treatment plan should be based on those findings while considering evidence based treatments for each factor.[3]

References[edit | edit source]

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