Frozen Shoulder Carolyn T Wadsworth PHYS THER. 1986; 66:1878-1883.

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Frozen Shoulder
CAROLYN T. WADSWORTH Widespread use of the label "frozen shoulder" as a diagnosis for any stiff and painful shoulder condition has led to its becoming a rather meaningless, catchall term. In addition to confounding both the lay public and health care professionals, this indiscriminate labeling may prevent a patient from receiving appropriate treatment. In this article, I define frozen shoulder and review its pathologic and etiologic factors, epidemiology, natural history, and diagnosis. I present this information in correlation with an examination process to assist physical therapists in identifying suspected cases of frozen shoulder. I also present the current options for treatment, including physical therapy management with physical agents and exercise. Key Words: Pain, Physical therapy, Shoulder.

Frozen shoulder (FS) is a distinct clinical entity with characteristic clinical and arthrographic findings.1 The purpose of this article is to describe the pathologic factors, natural history, signs, and symptoms of FS that clearly distinguish it from other disorders that produce shoulder stiffness and pain. This information should assist the clinician in identifying true cases of FS (synonymously termed adhesive capsulitis) and labeling them appropriately. This article details the various methods of treating FS, although an extensive review of the literature revealed no agreement on any one method. It also summarizes the few reported studies comparing the efficacy of different treatments, including physical therapy. Finally, it proposes a physical therapy plan of management, which a therapist monitors and modifies as a patient's status changes during the natural course of this disorder. HISTORICAL PERSPECTIVE Painful restriction of shoulder motion is one of the most common and disabling orthopedic disorders for which patients seek treatment.2-5 The specific type of restriction that we recognize today as FS has been reported in medical literature for over 100 years. Duplay referred to FS in 1872 as "scapulohumeral periarthritis," a disorder he believed resulted from subacromial bursitis.3,6-9 Pasteur later referred to the same condition as "tenobursite," which he attributed to bicipital tendinitis.4,9 In 1934, Codman coined the term "frozen shoulder" but used it in association with tendinitis of the rotator cuff.7 Although these early practitioners described some of the clinical characteristics of FS, they did not identify accurately the site of the pathological condition as it is understood today. In 1945, Neviaser introduced the concept of adhesive capsulitis when he discovered that the capsule was tight, thickened, and stuck to the humerus in such a manner that it could be peeled off like "adhesive plaster from the skin."1,4-6,10-14 Current doctrine supports Neviaser's theory that the capsule is the site of the lesion and lends credence to the synonymous use of the terms adhesive capsulitis and frozen shoulder.3,6,8,10,11,14

Definition and Pathology Frozen shoulder typically is referred to as the spontaneous onset of gradually progressive shoulder pain and severe limitation of movement.1,5,7,8,14,15 Features of this pathologic condition include microscopic evidence of chronic capsular inflammation with fibrosis and perivascular infiltration.3,5,14 Although several researchers found no evidence of inflammation, they concurred thatfibrosisexists in the capsule.14,16,17 Chronic cases of FS demonstrate constrictive capsulitis, characterized by adhesions of synovial folds; obliteration of the joint cavity; and a thickened, contracted capsule that eventually becomes fixed to the bone.3,13,18 Etiology The etiology of FS remains unknown. Lundberg16 and Helbig et al19 proposed primary and secondary classifications for cases that occur spontaneously and for those that result from trauma. The primary, idiopathic cases are the most common and the least understood. An unknown stimulus produces profound histological changes in the capsule that are substantially different from changes produced by immobilization or degeneration.9,16,18 Although a single critical stimulus has not been identified, a combination of host and extrinsic factors may precipitate primary FS. For example, the patient is usually between 40 and 60 years old and, based on the greater incidence of cases occurring bilaterally rather than randomly in the general population, probably has a constitutional predisposition for developing the condition.7,11,14,16 Extrinsic factors may include trauma, immobilization, certain diseases, and faulty body mechanics.1416 In contrast to the primary type of FS, secondary FS commonly develops after a variety of antecedent episodes, such as central nervous system involvement, upper limb immobilization, trauma to the arm, pulmonary cancer or infection, myocardial infarction, lengthy duration of intravenous infusion, cervical disk disease, rheumatoid arthritis, or diabetes mellitus.1,3,4,6,8,l0For secondary FS, Quigley hypothesized that minor trauma or an episode of inflammation may produce pain, which eventually leads to disuse and the classical restriction of motion characterizing FS.17 Loyd and Loyd suggested that secondary FS develops when painful spasm limits activity and creates dependency of the arm.1 The exact combination PHYSICAL THERAPY

Ms. Wadsworth is Lecturer, Physical Therapy Education, College of Medicine, The University of Iowa, Iowa City, IA 52242 (USA).

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of factors that predispose certain persons to develop either primary or secondary FS still eludes us.

Epidemiology
The incidence of FS is slightly higher in women than in men and is somewhat more common in the nondominant arm.7,13,16 This condition most frequently affects persons aged 40 to 60 years and rarely occurs in persons younger than 40 years of age.7,9,14,20,21 About 12% of persons affected develop the condition bilaterally, indicating a constitutional predisposition.9,11,16,18,22 The same shoulder rarely is affected subsequently.

History and Diagnosis

The clinical manifestations of FS, whether primary or secondary, are consistent. The typical presentation described in the following paragraphs, therefore, should allow the clinician to discern accurately true FS from other conditions that render the shoulder stiff and painful. The condition's onset is insidious and idiopathic in the majority of cases.1,9,14,21,23 Trauma and other factors that place the patient at risk as previously described, however, are involved occasionally.* The natural history of FS follows a classic cycle of "freezing," "frozen," and "thawing."26 Slow, spontaneous recovery of partial or complete function occurs within one to three years. The initial severity of the condition has no correlation with eventual recovery.19,23 The patient's medical history may provide information that will enable the examiner to localize the lesion to the glenohumeral joint. Initially, pain is the predominant feature of this disorder. Many patients describe an onset of acute pain that often worsens during the first weeks or months. Unlike pain associated with many other musculoskeletal disturbances, such as tendinitis and degenerative joint disease, the pain of FS is present during both activity and rest. Patients frequently complain of having pain at night and of being unable to sleep on the affected side, resulting in long-term sleep disturbances.7,10,11,23 As the condition progresses, pain during rest subsides, and discomfort occurs only during movement. Eventually, the pain abates spontaneously, but motion restriction persists.8,23,26-28 Pain is distributed vaguely in the deltoid muscle area. It often is worse anteriorly, but the only point of tenderness is over the bicipital groove.4,5 Pain sometimes radiates distally throughout the C5 dermatome. Some patients also complain of proximal soreness of the upper back and neck, a symptom probably attributable to compensatory overuse of shoulder girdle muscles, such as the trapezius, rather than to referred pain from the shoulder. The nature of the pain varies from a mild to severe ache.4,9 Arm movement that places the shoulder at the end of its limited range of motion aggravates such symptoms. Limitation of shoulder motion frequently is the symptom that makes the patient seek medical attention. Motion often is restricted as early as two to three weeks after onset of the disorder and continues to decline during the freezing stage of the cycle.7,9 This restriction may impose severe functional limitations on a patient. A physical examination conducted soon after the onset of the condition likely will reveal a patient who is very protective
*1,3,8,10,11,14,24,25. tl,6-8,10,11,15,17,27.

of the involved limb. Motion is guarded, and the arm is held against the body with the shoulder adducted and medially (internally) rotated.9 A patient may prefer wearing a sling to support the arm. Protective muscle spasm is a common feature. Functional activities (such as dressing or grooming) that require reaching overhead or behind the back may be difficult or impossible because of the pain. Active and passive movements are difficult to test because of pain and muscle guarding, which may impart an "empty end feel" to the end of the ROM (ie, the patient refuses to allow the joint to be moved to where resistance is felt by the examiner). If the examiner assesses the patient after the pain has subsided, then motion restriction will be the most predominant feature. The patient attempts to substitute scapular movement for glenohumeral movement, producing a characteristic "girdle hunching maneuver." Disuse atrophy may be evident in the rotator cuff and in the deltoid, biceps brachii, and triceps brachii muscles. Examination of the shoulder complex reveals an inert tissue (capsular) lesion: Both active and passive physiological movements may be restricted by pain at the end of the glenohumeral joint's ROM. Resisted movements in the midrange usually are asymptomatic, however, leading the examiner to conclude that contractile tissues are not involved. Such testing helps distinguish FS from bicipital and rotator cuff tendinitis, which may have similar signs and symptoms, but they are markedly symptomatic with resisted rather than passive movement. The limitation of passive ROM found in FS is characteristic of a capsular pattern; that is, lateral (external) rotation is limited more than abduction, which is limited more than medial rotation. During maximal capsular restriction, ROM measurements for the glenohumeral joint average 45 degrees of lateral rotation,1,17,23 less than 80 degrees of abduction,8,15,17,28 and less than 70 degrees of medial rotation.8,20 Capsular contractures limit the range and, thus, produce a capsular end feel. With FS, a painful arc of glenohumeral motion does not occur. Accessory glenohumeral movements also are limited, particularly anterior and inferior glide and lateral distraction. A review of the involved anatomical structures will highlight the correlation between the anterior and inferior synovial and capsular adhesions and the respective loss of gliding (Fig. 1). Also, the tightness in the anterior and inferior aspects of the capsule correlates with the loss of physiological movements of lateral rotation and abduction, respectively. Palpation may reveal tenderness over the bicipital groove. The overlying tissues, otherwise, obscure further findings of joint capsule involvement. Neurologic testing for sensory and reflex changes is negative with FS unless underlying conditions exist. Because C5 segmental involvement frequently refers symptoms to the shoulder, the therapist routinely should examine the cervical area as well. Neurologic testing may reveal shoulder girdle weakness as a result of disuse atrophy in later stages of the disorder. Arthrography is the standard diagnostic technique used to confirm FS.3,919,26 This technique reveals at least a 50% reduction of shoulder joint volume and a box-like appearance of the joint cavity.9,29 The shoulder joint volume capacity of patients with FS is only 5 to 10 mL, compared with 20 to 30 mL for healthy shoulders.1,7,9,14,27,30,31 Other findings during arthrography include a tight, thickened capsule3,7,10,27; loss of the axillary recess, the subcoracoid folds, and the subscapular bursa1,3,19,21,16; and the absence of dye in the biceps tendon sheath (Fig. 1).27 Binder et al note that, although arthrography 1879

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tendon of long head biceps brachii muscle foramen of Weitbrecht _ supraspinatus muscle

glenohumeral ligaments subscapularis muscle anterior joint capsule infraspinatus muscle glenoid fossa

axillary recess-

-teres minor muscle

Fig. 1. The glenoid cavity with surrounding labrum and fibrous capsule. Adhesions of the anterior capsule and axillary recess limit anterior and inferior glide of the humeral head on the glenoid fossa surface.

is useful in the diagnosis of FS, arthrography findings do not indicate the type of onset (primary or secondary) or the rate or extent of recovery.29 Radiography is more useful in ruling out other disorders than in specifically diagnosing FS. Shoulder roentgenograms of patients with FS, however, commonly reveal conditions such as osteoporosis,1,2,10,17,26 degenerative changes,10,29 decreased space between the acromion and humeral head,9,18,29 calcium deposits,5,9,17 and cystic changes.9

TREATMENT Review
Although FS is a self-limiting condition, it imposes such morbidity and lengthy recovery time that patients and clinicians alike seek treatment interventions. No standard treatment regimen, however, is accepted universally. Analgesics, such as salicylates and codeine compounds, often are used for pain relief.4,9,17 Oral anti-inflammatory medications also may help to relieve pain and reduce the inflammatory reaction.9,17 Many medical practitioners prefer the intra-articular injection of steroids, accompanied by local analgesics and gentle active motion, in the freezing stage of FS.1,11,15,21,23 This treatment is reported to reverse the pain and fibrosis of FS.14,21,23 Hollingworth reported that injection of a corticosteroid directly into the anatomical site of the lesion produced pain relief and at least 50% improvement in ROM in 26% of the cases studied.32 Conversely, Quigley17 and Neviaser3 do not believe that steroids can affect established scars, contractures, or adhesions, but Quigley stated that they may reduce pain if administered in conjunction with manipulation. Quigley administered intravenous steroids to 26 patients (3 with bilaterally involved shoulders) whose shoulders were manipulated under anesthesia; 10 of the shoulders re1880

gained painless, normal motion; 13 improved; and 6 were unimproved.17 Weiser injected prednisolone into the shoulder joints of 100 patients, then passively mobilized the joint and gave the patients a vigorous active home exercise program; 78% obtained pain relief, and 61% regained normal function.15 In summary, local corticosteroid injections have been used with various results but, generally, they produce a greater gain in motion recovery if given repeatedly in several sites and if used in combination with exercises and heat therapy.14,15,33 Infiltration debrisement has been used to improve function in numerous cases, although the literature does not define clearly when during the natural history of the condition it is performed.4,5,8,30 This method consists of forcibly extending the joint capsule with the contrast material that is used for arthrographic procedures. Local anesthetics and ROM exercises may be combined with infiltration debrisement to facilitate restoration of motion. For patients with residual motion deficits, manipulation under anesthesia has been found useful by some.4,8,9,11,19,27 While the patient is under general anesthesia, an assistant stabilizes the scapula, and an operator forcibly abducts the humerus until the capsule tears. Some physicians supplement the forced abduction with lateral and medial rotation manipulations, but others consider these manipulations too risky because of potential humeral fracture. This procedure results in freedom of motion by severing adhesions between the capsule and humeral head and also intracapsular adhesions.27 Extravasation of a contrast medium after manipulation readily demonstrates the extent of damage to the capsule.31 To prevent the ruptured tissues from healing in their former state of retraction, the arm must be abducted at least 90 degrees for one to two weeks while the patient is recumbent. To maintain ROM, a physical therapist should institute an exer-

PHYSICAL THERAPY
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rise program within 24 hours of the manipulation.3,17 Bateman prefers to expose the joint surgically to avoid blind tearing of tissue when performing manipulation.18 Manipulation under anesthesia is not without risk, because tissues are torn grossly and may develop further scarring. Manipulation also increases the possibility of fractures, dislocation, and brachial plexus injuries.5,27 Lundberg proposed that manipulation increases the rate of restoration of ROM but does not shorten the duration of the disease; however, intensive physical therapy after manipulation further increases the rate of restoration and also shortens the total duration.16 Surgery is used as a last resort for patients who do not respond to more conservative methods or for whom manipulation is contraindicated because of antecedent fracture, dislocation, or osteoporosis.3,4,8,9,17 Such surgery may involve division of the subscapularis tendon and the anteroinferior joint capsule17 or arthrotomy of the dependent axillary folds.3 Few controlled studies that compare the effects of various forms of physical therapy and medical treatment are reported in the literature. Of the available studies, the following discussion offers some useful information. Most of the studies do not provide details, however, regarding the stage of the disease process, previous treatment, and etiological considerations (primary vs secondary). Selection or grouping of subjects based on these criteria would enhance the validity and reproducibility of the results. Nicholson compared the pain and hypomobility of one group, treated with passive joint mobilization and active exercises, with that of a control group treated with active exercises alone.25 The mobilization consisted of passive oscillatory movements of one articular surface against its counterpart. Nicholson found that pain decreased significantly in the mobilization group and not in controls. All motions (except medial rotation in the control group) increased significantly in both groups. The only statistically significant difference in motion gained between groups was the increase in passive abduction in the mobilization group.25 Lee et al compared infrared irradiation plus active and resistive exercises, local injection of hydrocortisone acetate plus active and resistive exercises, and analgesics alone.33 The groups receiving exercises demonstrated a significant difference in motion gained (abduction, medial rotation, and lateral rotation) compared with the group receiving analgesics only, but no significant difference was seen between those receiving the injection plus exercise and those receiving infrared irradiation plus exercise. Bulgen et al studied four groups of patients, all of whom performed pendulum exercises.23 In addition, each group received either intra-articular steroids, Maitland's mobilization, ice packs followed by proprioceptive neuromuscular facilitation, or no additional treatment. All groups reported an improvement in pain relief, with best results after four weeks of treatment. The group that received the steroids showed the most marked initial improvement in movement, but no significant difference was seen between groups after six months of treatment. Hamer and Kirk contrasted cryotherapy (using wet towels and crushed ice) with ultrasound among patients who also received passive and active exercises.22 They found no significant difference between the cryotherapy and ultrasound treatment results, although pain relief and arm movement in both patient groups improved. Rizk et al compared a group treated by heat modalities, active-assistive exercise, and rhythmic stabilization manipuVolume 66 / Number 12, December 1986

lation with a group treated by transcutaneous electrical nerve stimulation plus pulley traction in abduction for up to two hours.14 Both groups gained ROM, but the TENS-traction group gained a total of 138 degrees more motion in all ranges combined than the heat-exercise-manipulation group. This group also achieved pain-free sleep after four to six weeks of treatment, compared with the other group in which all patients gained pain-free sleep only after four to six months.

Objectives
The studies cited have shown that various forms of exercise are effective in reducing the motion restriction and pain of patients with FS. Physical therapists, as specialists dealing with exercise and movement dysfunction, play a major role in restoring function to these persons. After performing the necessary tests to confirm the diagnosis of FS, ascertain the current status of the condition, and identify causative factors, a physical therapist is prepared to design a treatment program. Each individual case will dictate whether physical therapy is to be used alone or in conjunction with other medical or surgical treatment. The treatment objective in the early stage of the FS cycle is to reduce the pain and inflammation. A combination of exercise and physical modalities helps accomplish this objective. By moving tissues engorged with blood and inflammatory exudate, exercise stimulates circulation and resorption of debris. To interrupt the vicious cycle of pain and restricted motion, a therapist should instruct a patient to perform activity as vigorous as his condition will allow.11 Active and active-assistive exercises such as pedulum, wand, and physiologic ROM should be performed for at least one half-hour three times a day. Supplementing active exercise, a therapist administers daily passive physiological exercise (motion in a range that usually is achieved actively) or accessory exercise (motion between joint surfaces, which cannot be achieved actively), or both.34 Passive exercise has multiple benefits. Gentle passive movement, short of pain and the pathologic limit of motion, reduces pain.35 Theoretically, this pain reduction occurs because of a neuromodulation effect on the mechanoreceptors within a joint.34 Often, reflex muscle spasm prevents a patient from performing active exercise, whereas a therapist can passively guide the limb further into the range without eliciting spasm or a stretch reflex. Also, because many patients are reluctant psychologically to perform regular, appropriate active exercise, passive exercise becomes the treatment of choice.20 Pain and inflammation also are reduced by physical agents such as iontophoresis and phonophoresis.36 Various ions with analgesic and anti-inflammatory properties are transmitted into the tissues to promote resolution of the condition. They decrease edema and help minimize the formation of fibrinous exudate, which may become a precursor of adhesions when combined with immobilization. Heat therapy modalities and ultrasound reduce pain and muscle spasm. Electroacupressure and TENS also are effective in the management of acute and chronic musculoskeletal pain.36 The emphasis of treatment in the late stage of the FS cycle deals with movement restriction. A physical therapist again uses a combination of exercise and physical modalities, which in this stage are used to restore motion. Muscle stretching by physiological and accessory movements now is performed at the limit of the pathologic ROM. Functional use of the arm 1881

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Fig. 2. Gentle cephalad-caudad mobilization, short of pain or motion restriction, used to treat pain.

Fig. 3. Caudal glide mobilization, at the end of restricted accessory motion, used to treat stiffness.

is encouraged in activities of daily living. A therapist may use heat to induce relaxation and ultrasound to increase tissue extensibility.36 Because the use of passive movement may not be familiar to some, I will elaborate on this aspect of treatment in both the early and late stages of FS. Typically, a patient with FS initially might have a greater than 50% painful limitation of active and passive motion. A physical therapist would apply accessory movement in a comfortable joint position, with the affected arm supported in a loose-packed position (Fig. 2). The therapist administers slow, gentle oscillatory movements in anterior-posterior and cephalad-caudad directions if they do not increase pain or induce muscle spasm.35 The therapist reassesses physiological movements after each treatment. When 50% of the range is regained, in abduction for example, then passive physiological abduction motions are begun.35 The therapist provides a mechanical block to movement short of the painful, restricted range and continues to use gentle, low-amplitude oscillations. As the condition progresses, the therapist may detect stiffness before or concurrently with the onset of pain. The therapist then should begin low-amplitude physiological and accessory oscillations at the limit of the restriction.35 To increase abduction, for example, the therapist "takes up the slack" in the shoulder joint capsule with caudal glide and performs more powerful oscillations at the end of the accessory range (Fig. 3). The therapist uses ventral and dorsal accessory glides to increase lateral and medial rotation, re1882

spectively, and lateral distraction to increase movement in general. If the intense stretching at the end of the range produces soreness, the therapist may help alleviate this by using larger-amplitude oscillations to end the treatment. As the range increases, the therapist uses physiological treatment movements to enhance motion further. By assessing the patient's pain response and movement after each technique, the therapist can determine results and plan subsequent treatments. When designing any treatment program, the therapist always should consider the specific aspects of each individual case. Different starting positions and combinations of movement may be used to obtain the desired results. For example, a patient with limited lateral rotation will have difficulty abducting his arm. The therapist, therefore, may assist abduction by passively gliding the humeral head inferiorly or anteriorly. In other cases, the therapist may need to stabilize the humeral head passively to substitute for a weakened rotator cuff while a patient attempts active or resistive arm movements. As another example of individual adaptation, the therapist may facilitate some muscles selectively by proper hand placement and resistance and by guiding the sequence and direction of movement. Also, the therapist may add rhythmic stabilizationa simultaneous, isometric contraction of antagonistic muscle groups that produces relaxation and allows mobilization techniques to increase the limit of movement.37 A strong case exists for prevention because no treatment is effective consistently. Preventing prolonged immobilization and avoiding trauma to the shoulder when dealing with other limb disorders may be major factors in reducing the incidence of FS.8,9,10,13 Physical therapists should identify high-risk patients such as those with trauma or surgery involving the shoulder or chest, those with hemiplegia, and 40- to 60-yearolds undergoing prolonged hospitalization or immobilization. They must make a concerted effort to maintain shoulder motion in these patients by instructing them about upper extremity exercises and cautioning them to avoid further shoulder trauma. If necessary, therapists should implement a more involved program, such as that described in the preceding paragraphs. CONCLUSION Frozen shoulder is a discrete clinical diagnosis for painful restriction of shoulder motion that results from capsular fibrosis. Its etiology, although unclear, is associated with the interaction of constitutional and extrinsic factors among patients who, notably, are between 40 and 60 years of age. Stages of freezing, frozen, and thawing characterize the natural history of FS, and the condition is self-limiting within one to three years. By applying appropriate treatment techniques and modalities in a creative and judicious manner, the physical therapist can do much to enhance the speed and degree of recovery from FS, More controlled studies, however, are needed comparing the effects of different forms of treatment.
REFERENCES 1. Loyd JA, Loyd HM: Adhesive capsulitis of the shoulder: Arthrographic diagnosis and treatment. South Med J 76:879-883, 1983 2. Bland JH, Merrit JA, Boushey DR: Painful shoulder. Semin Arthritis Rheum 7:21-47, 1977 3. Neviaser JS: Adhesive capsulitis and the stiff and painful shoulder. Orthop Clin North Am 11:327-333, 1980 4. Post M (ed): The Shoulder: Surgical and Nonsurgical Management. Philadelphia, PA, Lea & Febiger, 1978

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5. Simon WH: Soft tissue disorders of the shoulder: Frozen shoulder, calcific tendinitis, and bicipital tendinitis. Orthop Clin North Am 6:521-539, 1975 6. Bruckner FE, Nye CJ: A prospective study Of adhesive capsulitis of the shoulder ("frozen shoulder") in a high risk population. Q J Med 50:191204, 1981 7. Kessel L, Bayley I, Young A: The upper limb: The frozen shoulder. Br J Hosp Med 25:334,336-337, 339; 1981 8. Kozin F: Two unique shoulder disorders: Adhesive capsulitis and reflex sympathetic dystrophy syndrome. Postgrad Med 73:207-210, 214-216; 1983 9. Rizk TE, Pinals RS: Frozen shoulder. Semin Arthritis Rheum 11:440-452, 1982 10. Jayson Ml: Frozen shoulder: Adhesive capsulitis. Br Med J [Clin Res] 283:1005-1006, 1981 11. Kay NR: The clinical diagnosis and management of frozen shoulders. Practitioner 225:164-167, 1981 12. Neviaser JS: Adhesive capsulitis of the shoulder: A study of the pathological findings in periarthritis of the shoulder. J Bone Joint Surg 27:211-222, 1945 13. Neviaser RJ: Painful conditions affecting the shoulder. Clin Orthop 173:6369,1983 14. Rizk TE, Christopher RP, Pinals RS, et al: Adhesive capsulitis (frozen shoulder): A new approach to its management. Arch Phys Med Rehabil 64:29-33, 1983 15. Weiser HI: Painful primary frozen shoulder mobilization under local anesthesia. Arch Phys Med Rehabil 58:406-408, 1977 16. Lundberg BJ: The frozen shoulder. Acta Orthop Scand [Suppl] 119:5-59, 1968 17. Quigley TB: Checkrein shoulder: A type of "frozen" shoulder: Diagnosis and treatment by manipulation and ACTH or cortisone. Clin Orthop 164:49, 1982 18. Bateman JE: The Shoulder and Neck, ed 2. Philadelphia, PA, W B Saunders Co. 1978 19. Helbig B, Wagner P, Dohler R: Mobilization of frozen shoulder under general anaesthesia. Acta Orthop Belg 49:267-274, 1983 20. Clark GR, Willis LA, Fish WW, et al: Preliminary studies in measuring range of motion in normal and painful stiff shoulders. Rheumatol Rehabil 14:3946, 1975 21. Weiss JJ, Ting YM: Arthrography-assisted intra-articular injection of steroids in treatment of adhesive capsulitis. Arch Phys Med Rehabil 59:285287, 1978

22. Hamer J, Kirk JA: Physiotherapy and the frozen shoulder: A comparative trial of ice and ultrasonic therapy. NZ Med J 83:191-192,1976 23 Bulgen DY, Binder Al, Hazleman BL, et al: Frozen shoulder: Prospective clinical study with an evaluation of three treatment regimens. Ann Rheum Dis 43:353-360,1984 24. Ha'eri GB, Maitland A: Arthroscopic findings in the frozen shoulder. J Rheumatol 8:149-152,1981 25. Nicholson GG: The effects of passive joint mobilization on pain and hypomobility associated with adhesive capsulitis of the shoulder. Journal of Orthopaedic and Sports Physical Therapy 6:238-246,1985 26. Reeves B: The natural history of the frozen shoulder syndrome. Scand J Rheumatol 4:193-196, 1975 27. Grey RG: The natural history of "idiopathic" frozen shoulder. J Bone Joint Surg [Am] 60:564, 1978 28. Thomas D, Williams RA, Smith DS: The frozen shoulder: A review of manipulative treatment. Rheumatol Rehabil 19:173-179,1980 29. Binder Al, Bulgen DY, Hazleman BL, et al: Frozen shoulder: An arthrographic and radionuclear scan assessment. Ann Rheum Dis 43:365-369, 1984 30. Gilula LA, Schoenecker PL, Murphy WA: Shoulder arthrography as a treatment modality. American Journal of Roentgenology 131:1047-1048, 1978 31. Tielbeek AV, van Horn JR: Double-contrast arthrography of the shoulder. Diagn Imag Clin Med 52:154-162,1983 32. Hollingworth GR, Ellis RM, Hattersley TS: Comparison of injection techniques for shoulder pain: Results of a double blind, randomized study. Br Med J [Clin Res] 287:1339-1341,1983 33. Lee M, Haq AM, Wright V, et al: Periarthritis of the shoulder: A controlled trial of physiotherapy. Physiotherapy 59:312-315,1973 34. Barak T, Rosen ER, Sofer R: Mobility: Passive orthopaedic manual therapy. In Gould JA, Davies GJ (eds): Orthopaedic and Sports Physical Therapy. St. Louis, MO, C V Mosby Co, 1985, pp 212-227 35. Maitland GD: Treatment of the glenohumeral joint by passive movement. Physiotherapy 69:3-7, 1983 36. Santiesteban AJ: Physical agents and musculoskeletal pain. In Gould JA, Davies GJ (eds): Orthopaedic and Sports Physical Therapy. St. Louis, MO, C V Mosby CO, 1985, pp 199-211 37. Holland TS: Coupling PNF and joint mobilization. In: Voss DE, et al (eds): Proprioceptive Neuromuscular Facilitation, ed 3. Philadelphia, PA, Harper & Row Publishers Inc, 1985, pp 327-329

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