The suggested working definition of frozen shoulder is GH joint stiffness resulting from a noncontractile element unless it coexists with a noncontractile lesion. Both active motion and passive motion are painful and restricted. Passive mobility is limited in the capsular pattern, with ER the most limited, followed by ABD and internal rotation (IR). The GH capsular volume is less than 10 mL, and plain radiographic films are normal.


In the United States, the prevalence of frozen shoulder is 2% to 5% of the population, and the condition is more common among women. The affliction also occurs more frequently in the nondominant arm. The condition is most commonly reported between the ages of 40 and 64 years. The cost of treatment for idiopathic adhesive capsulitis in the United States in the year 2000 was estimated to be $7 billion.


Frozen shoulder is a grouping of multiple symptoms. Although not all patients follow the same course, awareness of the typical clinical course of frozen shoulder may be helpful.


Painful or Freezing Phase

The painful or freezing phase, as Reeves describes it, usually lasts 10 to 36 weeks. The patient has a spontaneous onset of shoulder pain, which is often severe and disturbs sleep. The patient often rests the arm and notices a decrease in pain, but an increase in stiffness with rest. At the end of the painful phase, the volume of the GH capsule is significantly reduced.

Stiffening or Frozen Phase

The painful phase is often followed by a stiffening phase. This phase may last 4 to 12 months. The patient has restricted ROM in a characteristic pattern of loss of ER, IR, and ABD.

Thawing Phase

The final phase is described as thawing and is characterized by the gradual recovery of ROM. The thawing phase lasts an average of 5 to 26 months and is reportedly directly related to the length of the painful phase.


Primary frozen shoulder refers to the idiopathic form of a stiff and painful shoulder. The debate on the pathogenesis of idiopathic frozen shoulder continues. Possible causes include immune, inflammatory, biochemical and endocrine abnormalities. Bunker and Anthony, in 1995, reported that only 50 of the 935 shoulders assessed with GH joint restriction could be classified as primary frozen shoulder. In these 50 cases, the loss of motion was caused by the thickening and contracture of the coracohumeral ligament and rotator interval, thus acting as a tight "queen", which prevented ER. These researchers also confirmed a histological similarity between Dupuytren's disease and frozen shoulder. Also in 1995, Bunker and Esler reported an association between hyperlipidemia, frozen shoulder, and Dupuytren's disease. The incidence of frozen shoulder in the diabetic population is 10.8%. In 1993, Janda and Hawkins reported an unfavorable outcome in the frozen shoulder diabetic population after manipulative treatment under anesthesia.


Secondary frozen shoulder can follow a precipitating event or trauma, which can be identified to explain the loss of motion. Examples of such events leading to frozen shoulder include limitations following surgery, soft tissue trauma, and fracture. The three phases of frozen shoulder may not always be

recognizable in the patient with secondary frozen shoulder.

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