Key Point

• There are seven conditions that can cause or contribute to shoulder impingement syndrome. Understanding the underlying biomechanical pathophysiology and function helps us creatively apply our hands-on assessment and treatment skills.

Shoulder impingement syndrome (SIS) is an extremely common condition of the glenohumeral joint in which impingement/compression of soft tissue occurs between the head of the humerus and the acromion process of the scapula. The soft tissues usually impinged are the distal tendon of the supraspinatus muscle of the rotator cuff group, the subacromial bursa, and/or the long head of the biceps brachii muscle (Image 1). This can lead to rotator cuff degeneration and tearing, subacromial bursitis, and/or damage to the biceps brachii long head tendon. Beyond the importance of knowing about SIS (because it is so prevalent with clients), this condition is incredibly interesting because there are so many causes that raise fascinating questions about biomechanics.

The following seven conditions can cause or contribute to SIS:

1. Rotator cuff weakness
2. Scapular upward rotation musculature weakness
3. Clavicular dysfunction
4. Scapular downward rotation musculature tightness
5. Greater tubercle impingement
6. Shape of the acromion
7. Acromion process bone spur

Let’s take a look at each of these conditions.

1. Rotator Cuff Weakness

The first biomechanical cause of SIS we will discuss is weakness or inhibition of the rotator cuff group (Images 2A and 2B). To understand this, let’s explore the function of the rotator cuff group. Although each rotator cuff muscle has its individual joint action at the glenohumeral joint (i.e., the infraspinatus and teres minor are lateral rotators, the subscapularis is a medial rotator, and the supraspinatus can abduct and flex), the principal function of the rotator cuff group is to stabilize the head of the humerus down into the glenoid fossa of the scapula when a muscle like the deltoid contracts. 

This raises the question of what the deltoid actually does when it contracts. Simplifying its action, we say it abducts the glenohumeral joint. (I say “simplifying” because the anterior deltoid also flexes and medially rotates, the posterior deltoid also extends and laterally rotates, and there are even other considerations we will omit here.) But would an isolated contraction of the deltoid (think of the middle deltoid here) really lift the arm into abduction at the glenohumeral joint? The answer is a resounding no. Abducting the arm requires the distal end of the humerus to lift outward in the frontal plane in an arc-like motion (Image 3). But the line of pull of the deltoid when the body is in anatomic position would pull the humerus straight vertically upward, jamming its head into the acromion process above as seen in Image 4. This means that for the distal humerus to lift up and out, the proximal head has to be stabilized down and into the glenoid fossa. This is the principal function of the rotator cuff group (Image 5). Therefore, if the rotator cuff group is weak, inhibited, or dysfunctional in any way, the head will not be stabilized into the glenoid fossa and would instead lift into the acromion process above, impinging the soft tissue located between. This creates SIS! 

What I find so fascinating about this scenario is that it highlights how the true function of a muscle is often not immediately appreciated. The deltoid, acting on its own, cannot abduct the humerus; it pulls the entire humerus vertically upward. It is only with the synergistic help of the rotator cuff group that true abduction of the humerus is achieved (Image 5).

2. Scapular Upward Rotation Musculature Weakness

Another biomechanical cause of SIS is weakness of upward rotation musculature of the scapula at the scapulocostal/scapulothoracic joint. To understand this, we need to explore two topics: scapulohumeral rhythm and closed-chain/reverse actions at the glenohumeral joint. 

Scapulohumeral rhythm, as its name implies, is the name given to the coordinated rhythm of the scapula and humerus. Whenever the humerus moves, at a certain point the scapula must move with it (the clavicle too). For full range of motion of the arm relative to the trunk, whenever the humerus abducts, the scapula must upwardly rotate (Image 6). This is done specifically to make space for the head of the humerus to orient upward, allowing the arm to abduct 180 degrees relative to the trunk. When the arm abducts to 180 degrees, only 120 degrees of this motion occurs at the glenohumeral joint; the other 60 degrees (fully ¹⁄3 of the movement) is scapular upward rotation at the scapulocostal joint.

Let’s explore the concept of closed-chain muscle function and apply it to frontal-plane abduction of the humerus at the glenohumeral joint. When the deltoid contracts, it pulls on both of its attachments, the humerus and the scapula. This is a fundamental truth about muscle function that is often not fully appreciated; when a muscle contracts, it pulls equally on both attachments (Image 7). I like to describe this as not just bone A (humerus) being pulled toward bone B (scapula), but bone B (scapula) also being pulled toward bone A (humerus). Both distal and proximal attachments will be pulled toward each other. Looking at contraction of the deltoid, we see that when it pulls the humerus up toward the scapula, it simultaneously pulls the scapula down toward the humerus (Image 8). 

This downward pulling force on the scapula would cause the scapula to downwardly rotate into the head of the humerus, pinching the soft tissue between them, causing SIS. Therefore, to prevent this, we need to stabilize the scapula to stop it from downwardly rotating. This occurs by a simultaneous contraction force of scapular upward rotation musculature. The muscles that can do upward rotation of the scapula are the upper trapezius, lower trapezius, and serratus anterior. With frontal-plane humeral abduction, the most logical choice for nervous system activation would be the upper and lower trapezius because they are in the frontal plane, whereas the serratus anterior is more sagittal-plane in orientation. Image 9 demonstrates the upper trapezius contracting to stabilize the scapula against the pull of the deltoid.

Therefore, using the upper trapezius as our example muscle, if it is dysfunctional in any way, it would not engage properly, thereby not creating the necessary upward rotation force. This would allow scapular downward rotation, predisposing the person to SIS. Why might the upper trapezius be dysfunctional? There are many possible reasons, but a simple one is that it is tight and painful, perhaps with myofascial trigger points. In fact, the most common trigger point in the human body is in the upper trapezius! Therefore, the nervous system, knowing that upper trapezius engagement might create pain, would inhibit its contraction and predispose the person to SIS.

This biomechanical cause of SIS raises our awareness of multiple concepts: scapulohumeral rhythm, reverse/closed-chain muscle function, pain creating neural inhibition or weakness, and the relationship between how massage to alleviate tight musculature and trigger points could functionally strengthen the musculature by facilitating its engagement.

3. Clavicular Dysfunction

As stated, the rhythm of the scapula and humerus also requires a coordinated rhythm of the clavicle. Perhaps instead of scapulohumeral rhythm, the better term for healthy shoulder motion should be claviculoscapulohumeral rhythm. Returning to our example of arm abduction, when the humerus abducts and the scapula upwardly rotates, the clavicle must also elevate and upwardly rotate (Images 10A and 10B). In fact, of the 60 degrees of scapular abduction, 10 degrees of this motion is due to clavicular motion, primarily at the sternoclavicular joint. Therefore, any dysfunction of clavicular movement would impede scapular upward rotation, which in turn would allow for approximation of the humeral head with the acromion, leading toward SIS. 

Further, the acromioclavicular joint also plays a role in clavicular motion and therefore total upward rotation of the scapula. Any dysfunction of the acromioclavicular joint due to injury or overuse could also play a role in SIS. What we see here is that when a client presents with SIS, and we perform our physical exam assessment, we need to widen our focus to include not just the glenohumeral joint itself, but also the sternoclavicular and acromioclavicular joints and all related musculature. 

4. Scapular Downward Rotation Musculature Tightness

Returning to the concept of muscular dysfunction and scapular rotation, if weakness of upward rotation musculature prevents proper scapular upward rotation, then tightness and overly facilitated downward rotation musculature would fight the upward rotation musculature, thereby preventing the upward rotation necessary to preserve the space between the humeral head and acromion process. The principal downward rotator of the scapula is the pectoralis minor, which is often tight and overly facilitated (locked short . . . there are so many terms to employ here!). Indeed, a tight pectoralis minor is integral to the postural distortion pattern known as upper-crossed syndrome, which is so prevalent due to all the time we spend rounded forward, engaging with our digital devices (Images 11A and 11B). 

So, we now see how SIS ties into common postural distortion patterns of everyday life. The upper-crossed syndrome pattern leads us into our next cause of SIS—greater tubercle impingement.

5. Greater Tubercle Impingement

We have discussed how the cause of SIS can result from approximation of the head of the humerus and acromion process. Therefore, the key to preventing SIS is preserving this space. Upon closer examination, we see that the amount of this space changes depending on whether it is the greater or lesser tubercle of the humeral head that is in line with the acromion process above. The greater tubercle is so named because it is larger than the lesser tubercle. So, if the greater tubercle lines up with the acromion process, there is less space between the two bones, and therefore a greater likelihood of approximation and impingement (Images 12A and 12B). 

Try the following kinesthetic exercise. Stand up in anatomic position, and maximally medially rotate your arm at the glenohumeral joint (either the left or right side). Now (very slowly, please!) abduct your arm at the glenohumeral joint as far as you can. Does your arm go to a vertical position of 180 degrees of abduction relative to the trunk? Likely the answer is no. Now, staying in this position, maximally laterally rotate your humerus and see if you have greater abduction range of motion and can abduct fully. The answer is probably yes (Images 13A and 13B). 

What is happening here? When the humerus is medially rotated, the greater tubercle lines up with the acromion, decreasing the space and causing approximation and impingement. But with lateral rotation, the greater tubercle moves out of the way, and instead, the lesser tubercle lines up with the acromion, affording the space needed for full abduction without impingement (Images 12A and 12B). So how does this tie into upper-crossed syndrome? It turns out that upper-crossed syndrome involves humeral medial rotation. Therefore, if a person is chronically stuck in humeral medial rotation, whenever they lift their arm into abduction (or flexion for that matter), the greater tubercle will impinge against the acromion, causing SIS. 

This example is fascinating from a biomechanical perspective because it raises our awareness of how the position of a bony landmark can change with changes in joint angle, thereby impacting joint function and predisposing toward pathologic dysfunction. 

6. Shape of Acromion Process

Let’s turn our attention to the acromion process of the scapula. It turns out that the shape of the acromion can vary based on genetics, and that the varying shapes can have an effect on whether the person develops SIS. Images 14A, 14B, and 14C demonstrate the three acromial shapes: flat, curved, and hooked. Of these, the flat acromion affords the most space and is the healthiest; the curved—and to a greater extent, the hooked—closes on the space and predisposes toward SIS. 

7. Acromion Process Bone Spur

Genetics are nature, but nurture can also play a role in the shape of the acromion. The shape of the acromion can effectively change by the formation of a bone spur. There is a principle called Wolff’s Law, which states that the body lays down calcium in response to physical stress. Applying this principle to bone, when a bone is physically stressed, usually due to compression or tension forces (or perhaps physical macrotrauma), the body seeks to fortify it by increasing calcium mass in the trabeculae of the bone. Unfortunately, when the physical forces become excessive (often due to repetitive overuse microtrauma over time), Wolff’s Law goes awry, and calcium is laid on the outer surface margin of the bone. 

This calcium buildup can lead to bone spur formation as part of what is called osteoarthritis/osteoarthrosis, also known as degenerative joint disease. When large enough, a bone spur can then interfere with joint function. In the case of the glenohumeral joint, a bone spur can form in several locations. One common bone spur is along the attachment of the acromioclavicular ligament on the underside of the acromion. Another common bone spur occurs at the deltoid attachment on the acromion and is due to excessive use of the deltoid and/or a chronically tight deltoid (Image 15). In time, a bone spur in the glenohumeral joint can sufficiently decrease the space between the acromion and the head of the humerus, causing SIS. 

What is most interesting here is that when the formation of the bone spur begins, which can easily be seen on an X-ray, it is a sign that the person is repetitively overusing their deltoid and/or that the deltoid is tight at baseline tone, creating excessive tension pulling force on the acromion process. Hopefully, if caught in the early stages of this process, counseling the client about postures and movement patterns that involve deltoid use, as well as massage to loosen the deltoid baseline tone/tension, offers the opportunity to prevent SIS before it progresses to cause irreparable soft-tissue damage. 

Conclusion

My purpose in writing this article is twofold. One purpose is to explore the possible reasons our clients might experience SIS. Understanding the underlying biomechanical pathophysiology equips us to not only assess and treat our clients more effectively but to also counsel them with self-care postures, trigger-point work on therapy balls, exercises, and stretching to help prevent SIS from developing. My second purpose is more fundamental: Learning about and understanding the biomechanics of SIS leads us into incredible biomechanical explorations of kinesiology of how the human body functions. When we start to understand kinesiologic/biomechanical function at this fundamental level, we are empowered to creatively apply our hands-on assessment and treatment skills for any and all musculoskeletal pathologic conditions with which our clients present.