Can a shoulder become “frozen”? What is frozen? Why doesn’t this shoulder move like it used to move? And how does this cause pain?
There is no doubt – loss of shoulder motion is a common cause of pain. Thus, the first “pillar” of normal shoulder function is maintaining normal range of motion. In fact, this is one of the more prevalent findings upon evaluation of the painful shoulder. And return of motion often corresponds to return of comfort. Again, I am grateful for the lessons I learned about shoulder stiffness from my mentors at the University of Washington.
A regular stretching program is also one of the more important activities to perform to maintain healthy shoulders.
The capsule, the deepest layer of tissue connecting the ball to the socket of the shoulder joint, is the usual source of loss of motion. It encompasses the ligaments of the joint. Normally quite lax during normal motions of the shoulder, it plays little role in holding the ball on the socket during many of our day to day activities (more to come in the “Stability” pillar). Sometimes, only one area of the capsule becomes contracted and tightened. More commonly, the entire capsule can lose its normal laxity. Often we do not understand the cause of the contracture: the condition is “idiopathic”, meaning the cause isn’t known.
This tightening is often associated with a definitive inflammatory component, which leads to the thickening and contracture of the capsule. As such calling it “frozen” is a bit of a misnomer. Another commonly utilized term is “adhesive capsulitis”. This is also not quite right, as adhesions are not present with most cases of frozen shoulder. The process is simply an inflammation that lingers and causes thickening and essential shrinking of the capsule. Pain results from the stretch of inflamed tissue that occurs with use of the arm.
Other conditions present with a tightening of only a part of the capsule. For example, contracture of the “posterior” capsule is an important cause of a condition called shoulder impingement. This occurs when the tight posterior capsule pushes the ball forward and superior on the socket during elevation of the arm, leading to a squeezing the the bursa and rotator cuff against the arch on top of the shoulder (the coracoacromial arch). Dr. Doug Harryman and Dr. Frederick Matsen of the University of Washington published a classic paper in 1990 describing this phenomenon, and it should be known by all shoulder surgeons1. Clinically the diagnosis is made by recognizing a loss of normal internal rotation with arm abducted in the scapular plane, loss of motion reaching up the back, and loss of motion moving into adduction across the body (also known as GIRD, or glenohumeral internal rotation deficiency).

Photo taken from Matsen et al, Practical Evaluation and Management of the Shoulder, 19942
Another important concept to understand as it relates to shoulder mobility is the association between tightness of specific areas of the capsule and reproducible loss of mobility in specific directions. For example, tightness of the inferior capsule leads to loss of elevation of the arm. This is important to understand for a surgeon who wants to release a part of the capsule to improve motion in a specific direction. It is also helpful for a physical therapist looking to optimize treatment for a patient with a stiff shoulder. The following table describes motion that can be attributed to areas of the capsule, moving around the clockface of the shoulder.
| Rotator Interval | External Rotation with the arm at the side (ERS) |
| Anterior Capsule/MGHL | External Rotation in midrange of abduction |
| Antero-inferior capsule (anterior band of the IGHL) | External Rotation in abduction (ERA) |
| Inferior capsule | Forward Elevation (FE) |
| Posteroinferior capsule (posterior band of the IGHL) | Internal Rotation in Abduction (IRA) |
| Posterior capsule | Internal Rotation up the back (IR) |
You will notice that abduction is not included in the table, as it can be a bit less reliable between observers, depending on the rotation of the humerus.
Shoulder stiffness can also result from true scarring or adhesion in a different part of the shoulder. An area known as the humeroscapular motion interface, taught to me by Dr. Matsen and Dr. Kevin Smith in my fellowship training, is an important “joint”. 3-5 cm of gliding between the rotator cuff and proximal humerus with the overlying acromion, coracoacromial ligament, coracoid, and deltoid is normally seen. Normal motion can be limited due to scarring in this tissue plane. Fracture, prior surgery, or other trauma can lead to adhesions in this tissue plane. Isolated release of the capsule will fail to improve motion for these patients. Thus, recognizing a post-traumatic stiff shoulder is important to distinguish from an idiopathic frozen shoulder. Treatment outcomes and expectations are expectedly different, due to the nature of the problem.

Photo taken from Matsen et al, Practical Evaluation and Management of the Shoulder, 1994
Shoulder Stiffness is a major source of dysfunction for patients, and is often readily treated by a program of frequent but gentle stretching: these exercises can often restore the normal laxity of the shoulder capsule. I will delve into more depth about specific types of shoulder stiffness, treatment options, as well as expected outcomes in future posts about shoulder stiffness. But for now, it is time to move on to the next “pillar” of normal shoulder function. STABILITY

2. Matsen, Lippitt, Sidles, Harryman. Practical Evaluation and Management of the Shoulder, 1994.


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