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Adhesive Capsulitis
Updated: Oct 15, 2009
Introduction
Background
Adhesive capsulitis, most commonly referred to as frozen shoulder (FS), is an idiopathic disease with 2 principal characteristics: pain and contracture.
Pain
Shoulder pain associated with FS is progressive and initially felt mostly at night or when the shoulder is moved close to the end of its range of motion (ROM). It can be caused by certain combined movements of the shoulder, such as abduction and external rotation (eg, grooming one's hair, reaching for a seatbelt overhead) or extension and internal rotation (eg, reaching for a back pocket or bra strap). The pain usually progresses to constant pain at rest that is aggravated by all movements of the shoulder and that may be worsened by repetitive movements of the involved upper extremity, psychological stress, exposure to cold or vibration, and changes in the weather. In approximately 90% of patients with FS, this pain usually lasts 1-2 years before subsiding.1
Contracture
The second principal characteristic of FS is progressive loss of passive ROM (PROM) and active ROM (AROM) of the glenohumeral joint in a capsular pattern. That is, the movements are usually restricted to a characteristic pattern, with proportionally greater passive loss of external rotation than of abduction and internal rotation.
In 1934, Codman stated, "This entity [FS] is difficult to define, difficult to treat, and difficult to explain from the point of view of pathology." Codman's statement continues to hold true today.
In 1992, the American Shoulder and Elbow Surgeons Society agreed on the following definition of FS by consensus: a condition of uncertain etiology that is characterized by clinically significant restriction of active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder.
Pathophysiology
Neurologic, surgical, and histologic findings
The pathophysiology of FS continues to be largely mysterious. However, certain consistent neurologic, surgical, and histologic findings in soft-tissue specimens of patients with FS have been identified and appear to be specific to the pathology of FS.
Evaluation of anatomic, histologic, and surgical specimens from subjects affected by idiopathic FS demonstrates that the glenohumeral joint synovial capsule is often involved in this disease process. However, most of the notable loss of ROM is caused by disease in structures outside the synovial capsule glenohumeral joint, such as the coracohumeral ligament, soft tissues in the rotator interval, the subscapularis muscle, and the subacromial bursae.
Most authors do not describe clinically significant capsular adhesions as a predominant finding in the chronic phase of this condition. Instead, pathologic data confirm an active process of hyperplastic fibroplasia and excessive type III collagen secretion that lead to soft-tissue contractures of the aforementioned structures (ie, the coracohumeral ligament, soft tissues of rotator interval, the subscapularis muscle, the subacromial bursae). However, these findings were observed in surgical patients who had severe and late-phase disease and cannot be applied to early phases of the disease.
From the chromosomal, cytochemical, and histologic points of view, the soft-tissue contractures are identical to those seen in a Dupuytren contracture of the hand. These contractures result in the classic progressive loss of ROM of the glenohumeral joint, which affects external rotation and abduction, then flexion, adduction, and extension (in descending order of severity). Despite these histopathologic similarities, the favorable and regressive outcome of adhesive capsulitis differs from the unfavorable and progressive outcome of Dupuytren disease.
Genetic abnormalities
Specific genetic abnormalities have been identified with this condition. In particular, frequent trisomy 7 and trisomy 8 in the fibroblasts were confirmed in cultures of tissue samples obtained from glenohumeral joint capsules resected at the time of surgery for FS. These pathologic findings were observed in studies of tissue specimens that usually were obtained from subjects with chronic FS that did not respond to typical conservative modalities. Little is known about the tissue characteristics of the acute phase of this condition.
Pathophysiologic model and complex regional pain syndrome type 1 versus FS
To date, no robust pathophysiologic model explains the relationship between the principal characteristics of this disease (ie, pain, contracture). Neurologic factors seem to be the principle mediators of the pain, whereas a process resembling fibromatosis causes the contracture, as described in the above text. Why the pain precedes the contracture and why it resolves before the contracture does in most subjects remain unclear. The fact that the pain of FS often precedes stiffening of the joint tends to support the notion that the initial pain probably does not stem from altered mechanics of the glenohumeral joint.
Clinical research suggests the presence of autonomic sympathetic dysfunction in the upper extremities in many patients with isolated idiopathic FS. This dysfunction is not detectable during usual clinical examination. However, various examination techniques, such as 3-phase nuclear technetium-99m (99m Tc) bone thermography, laser Doppler flowmetry, and transcutaneous measurement of oxygen tension, have been used to detect the anomalies found in more than 80% of subjects examined in various studies. The subjects did not have any of the dramatic manifestations of full-blown complex regional pain syndrome type 1 (CRPS1). Studies have shown similar histologic findings in joints affected by CRPS1 and FS.
A broad look at the similarities between FS and CRPS1 with regard to risk factors and the usual clinical course of the disease shows many parallels between the conditions. For example, risk factors common to both conditions are trauma, diabetes, thyroid disease, and dyslipidemia.
The initial, painful phase, without any inflammatory, exudative cellular joint process, lasts for several weeks or months. This phase usually progresses to include the gradual development of connective-tissue contracture. In most patients, the pain and contracture gradually resolve, although in a few individuals, 1 or both persist.
Neurologic mechanisms contributing to the generation and perpetuation of pain in CRPS1 probably also play a role in the pain and disability associated with FS. These mechanisms include peripheral alpha-adrenoreceptor hyperresponsiveness, dorsal-root reflexes (DRRs), central nervous system (CNS) factors, myxoid globular degeneration, and sympathetic autonomic hyperactivity.
Sympathetic dysfunction in patients with FS is believed to mediate hyperresponsiveness of peripheral alpha adrenoreceptors in the nerve endings of somatosensory neurons, including various joint nociceptive and proprioceptive fibers of the shoulder. This hyperresponsiveness probably contributes to the pain (allodynia) produced with gentle, passive mobilization of the shoulders observed in patients with FS.
DRRs, involved in previously unknown efferent neuronal activity in the somatic sensory nerves, are said to contribute to the pain of certain neurologically mediated painful conditions. These conditions are related to the release of substance P and of other local-tissue pain-and-inflammation – causing neurotransmitters into the regional tissues.
CNS factors, such as sensitization of wide-dynamic-range interneurons (WDRIs) in the dorsal horn of the spinal cord, may contribute to the allodynia affecting patients with FS.
In healthy subjects, myxoid globular degeneration of the terminal sensory nerve fibers of the glenohumeral joint capsule was particularly important in the fifth and sixth decades of life (when as many as 40% of terminal sensory nerve fibers of the shoulder are in a degenerated state). The importance of this phenomenon in the genesis and perpetuation of FS remains unknown. However, of note, FS is most common in the fifth and sixth decades of life, when such degenerative changes in the terminal nerve fibers of the shoulder joint become prevalent. Destruction of terminal sensory nerve fibers as a result of myxoid globular degeneration may play a role in the apparent dysfunction of the nervous system in FS.
Wohlgethan implicated sympathetic autonomic hyperactivity in the genesis and perpetuation of painful FS in patients with hyperthyroidism.2 Several authors reported an apparently dramatic improvement in the pain and disability of FS in patients whose hyperthyroidism was adequately treated.
Despite the aforementioned similarities, FS should not be considered CRPS1. First, idiopathic FS does not fit the diagnostic criteria for CRPS1 that the International Association for the Study of Pain (IASP) proposed in 1996. Second, the diagnosis of CRPS1 is relatively nonspecific because of the heterogeneous pathologies it encompasses. Further expansion of the diagnosis of CRPS1 to include FS dilutes its meaning and falsely implies that any painful condition associated with anomalies of the autonomic nervous system must be categorized as CRPS. A preferable option is to include neuromodulatory concepts from CRPS research in a pathoetiologic model in which FS is a distinct clinical entity.
Inclusion of the aforementioned neuromodulatory concepts of joint pain into the authors' proposed pathoetiologic model of FS leaves room for the exploration of therapeutic modalities, such as bupivacaine suprascapular nerve blocks, stellate-ganglion blocks, and intra-articular morphine injections, to treat the pain associated with FS.
Ischemia of the soft tissues may link the apparently distinct and separate pathophysiologic entities observed in FS, namely, neurologically mediated pain and fibromatosis-like contracture. The histologic and cytochemical profiles of connective-tissue specimens in patients with FS are identical to those of patients with Dupuytren contracture, a condition whose pathoetiology has been linked to microangiopathy and local tissue ischemia. Pre-existing microvascular disease, often related to hypertriglyceridemia or diabetes in patients with FS, may predispose them to ischemia of the connective tissues of the glenohumeral joint capsule, which itself is subject to the ischemic stresses because of mechanical stress and tension. Furthermore, hypersensitization of peripheral vasomotor alpha-adrenergic receptors and a pain-induced increase in local vasomotor tone also can contribute to ischemia of the local connective tissues of the shoulder.
Resultant regional ischemia of the soft tissues of the shoulder can lead to the local release of free radicals and a platelet-derived growth factor that can initiate a cycle of fibroblastic hyperplasia and excessive deposition of collagen and glycosaminoglycans. The whole process ends with the active development of a tough, thick, fibrous contracture of the connective tissues of the shoulder. In his 1990 review on FS, Hazelman noted that microvascular disease might be the common thread linking FS to diabetes and dyslipidemias.3
In cases of FS occurring after fractures of the humeral head or following rotator cuff tears, the capsular, ligamentous, and tendinous circulation of the local soft tissue may be compromised. This effect may contribute to the aforementioned ischemic mechanisms leading to FS.
Care should be taken to avoid overusing the term FS secondary to shoulder tendonitis. In 1934, Codman described signs of inflammation of the tendon of the long portion of the biceps in cadaveric specimens of FS, giving rise to the still-popular theory that FS is a consequence of an inflammatory process of the tendons of the shoulder. Data from subsequent studies have largely refuted this as a pathophysiologic mechanism for FS, but the idea remains difficult to erase from the minds of clinical practitioners. Inflammation seen in the tendon of the long portion of the biceps in Codman's cadaveric specimens was most likely a late sequela of FS itself, which causes narrowing of the bicipital groove secondary to a retraction of the overlying soft tissues.
Frequency
United States
Shoulder pain is the third most common cause of musculoskeletal disability after low back pain (LBP) and neck pain. The prevalence of FS in the general population is reported to be 2%, with an 11% prevalence in unselected individuals with diabetes. For patients with type I diabetes, the risk of developing FS in their lifetime is approximately 40%.
FS may affect both shoulders, either simultaneously or sequentially, in as many as 16% of patients. The frequency of bilateral FS is higher in subjects with diabetes than in those without diabetes. In 14% of patients, while FS still is active in the initial shoulder, the contralateral shoulder also becomes affected. Contralateral FS usually occurs within 5 years of disease onset. A relapse of FS in the same shoulder is unusual.
FS most frequently occurs in subjects with hyperthyroidism and hypertriglyceridemia. Although various authors report that heart disease, tuberculosis, and many other medical conditions are associated with FS, these associations are largely anecdotal and are not supported in proper, case-controlled studies.
Most survivors of cerebral vascular accidents (CVAs) that cause hemiplegia develop painful stiffening of their shoulders. However, the painful hemiplegic shoulder has distinct characteristics, which are not discussed in this article.
FS will undoubtedly become increasingly common as the baby-boom generation ages, because this condition most frequently occurs in the fifth and sixth decades of life. Patients who present with an idiopathic FS when they are younger than 40 years should definitely be examined to rule out occult diabetes, hyperthyroidism, hypertriglyceridemia, or concomitant neurologic or systemic rheumatologic disorder affecting the upper extremity.
International
The data reported above are derived from the international literature. No regional variations are recognized in the frequency of occurrence of FS.
Mortality/Morbidity
Shoulder pain is the third most common cause of musculoskeletal disability in the workplace after LBP and neck pain. For more information, see the Musculoskeletal Disorders and Workplace Factors, published by the National Institute for Occupational Safety and Health, on the Centers for Disease Control and Prevention Web site.
The degree of pain and disability caused by idiopathic FS is highly variable and depends on the stage of the disease. Retrospective data tend to show that patients cope well with a painless glenohumeral contracture. Therefore, most disabilities occur during the initial, painful phase and the subsequent, freezing phase.
See also Patient Education.
Race
No racial variation is described in the literature.
Sex
FS affects women more frequently than men, with a female-to-male ratio of about 1.4:1. Menopause is often reported as a cause of FS in women, although Lundberg seems to have ruled out this hypothesis by demonstrating that age is the principal predictor.4 He specifically demonstrated that women with early menopause did not have FS any earlier than their counterparts who undergo late menopause.
Age
To date, the best data available seem to show that FS affects women somewhat earlier than it does men. The mean ages of onset are 52 years for women and 55 years for men, with a standard deviation of 7.
Clinical
History
Clinical phases
The following 3 clinical phases typically characterize FS:
- Phase 1 - The painful phase; the patient describes an insidious onset of predominantly nocturnal pain, usually without a precipitating factor. The pain is not related to activity, although the farthest ROM can increase the pain. As the disease progresses, patients have pain at rest. In this phase, which lasts 2-9 months, ROM is not restricted, and the diagnosis may remain unclear.5,6
- Phase 2 - The frozen, or adhesive, phase; the pain from phase 1 can persist, although it may decrease. Progressive limitation in ROM occurs in a capsular pattern (that is, in all directions). Normal daily activities can be severely affected. Hallmarks of this phase are an inability to move at great amplitude and an inability to move on the affected side. Diagnosis is easier in this phase than in phase 1. Although phase 2 is reported to last 3-9 months, it can persist longer than this.7
- Phase 3 - The thawing, or regressive, phase; pain progressively decreases, and limitations in ROM progressively increase over 12-24 months. Although approximately 40% of patients have slight, persistent limitations in ROM, only 10% have clinically significant long-term functional limitations.8
Trauma
FS can result from clinically significant trauma to the shoulder, cervical radiculopathy, pathology of the brachial plexus, any neurologic insult affecting shoulder function or innervation, or an episode of rotator cuff tendonitis. However, FS usually occurs without any clear precipitating factors. Most patients with FS have no notable history of trauma. Hence, the clinician must remember that this is an idiopathic disease in which the loss of ROM results from a dystrophic pain syndrome combined with contracture caused by an active process resembling fibromatosis.
Although patients often try to recall minor trauma associated with the onset of their shoulder symptoms, careful history taking on the part of the examiner often reveals subtle symptoms, such as night pain or pain and stiffness at the end of ROM, that predated the episode of minor trauma. In most cases, the minor trauma simply makes the patient conscious of the insidious, underlying disease process.
Pain
Patients with FS typically describe a progressive onset of pain over several weeks. Patients usually report that the initial pain was night pain or pain associated with involved movements of the shoulder (eg, combing one's hair, reaching overhead for a seat belt, reaching for one's back pocket). Combing one's hair and reaching overhead for a seat belt require a combined motion of abduction and external rotation, and reaching for one's back pocket requires extension and internal rotation of the shoulder. These combined movements tend to stretch the anterior and posterior glenohumeral capsule, respectively.
The pain of FS then progresses to a constant pain at rest that is often aggravated by any movement of the shoulder, psychological stress, exposure to cold or vibration, and changes in the weather. Patients report worsening of the pain after they engage in activities that require repetitive movements of the affected shoulder.
In about 90% of patients, the pain associated with this condition usually lasts 1-2 years before subsiding. The pain is a prominent feature of the initial phase and of the second (frozen) phase of the disease. During the thawing phase, the pain usually is less intense than it is in the other phases. It is usually felt only if the patient is moving at the end of his/her ROM (particularly in positions of subacromial impingement), if the patient performs repetitive movements of the shoulder, or if the patient is exposed to other important ergonomic stresses of the shoulder.
Physical
In the early phase of FS, the only physical finding may be pain produced at the end of ROMs in the glenohumeral joint, particularly those that stretch the capsule, such as combined abduction and external rotation (such as combing one's hair) or combined extension and internal rotation (such as reaching to scratch one's midback). During the initial, painful stage, FS may not be distinguishable from an inflammatory synovitis affecting the glenohumeral joint or from a painful episode of rotator cuff tendinopathy. In the second, or freezing, stage of the disease, contracture of the glenohumeral joint becomes readily apparent. This stage may occur only several months after the onset of symptoms.
As the condition progresses, the clinician should observe progressive limitation of the PROM, characterized by a painful capsular end-feel. The motion affected first and most severely is external rotation, followed by abduction, internal rotation, and flexion. Extension and horizontal adduction tend to be least affected. PROM of the glenohumeral joint progressively worsens over several months and may result in a loss of up to 80% of the normal movement of glenohumeral joint.
In severe cases, evaluation of AROM may show an inverted scapulothoracic motion (that is, motion of the scapula on the thorax). For example, the scapulothoracic joint initiates abduction (followed by the glenohumeral joint) to compensate for the loss of ROM in the glenohumeral joint.
On occasion, a sizable calcification of the rotator cuff in its resorptive phase may cause an acute tendinobursitis that may mimic FS. This type of acute tendinobursitis may be extremely painful, and it may result in an antalgic phenomenon, causing a loss of PROM. The acute and rapidly progressive onset of tendinobursitis over a few hours or days differentiates it from the relatively progressive onset of FS, which occurs over weeks. Another mimic of FS is severe synovitis or arthritis of the glenohumeral joint caused by an underlying primary rheumatologic inflammatory, degenerative, septic, or metastatic process.
Most patients with a painful FS have pain during resisted contraction of all of the rotator cuff tendons, during specific maneuvers designed to detect subacromial impingement (for example, the Hawkins, Neer, and Yocum maneuvers), and during maneuvers designed to detect tendinopathy of the long portion of the biceps (such as the Yergason and Speeds maneuvers). This phenomenon results because the pain generators in FS may include all of the extra-articular and intra-articular soft tissues of the glenohumeral joint and humeroscapular-motion interface (eg, subacromial bursa, rotator cuff, biceps tendon). (See Mechanics of Glenohumeral Arthritis, on the University of Washington School of Medicine Web site.)
In the presence of a clinically significant loss of PROM of the glenohumeral joint in the previously described capsular pattern, the clinician should probably be content with retaining the diagnosis of FS while de-emphasizing the aforementioned maneuvers designed to diagnose other specific, painful soft-tissue disorders affecting the shoulder.
The difficulty of accurately and reliably establishing a specific diagnosis for a painful shoulder condition based on a physician's clinical assessment should not be underestimated, as demonstrated by data from the Netherlands. The rate of interobserver agreement with regard to a diagnostic classification of shoulder disorders based on history taking and physical examination was surprisingly poor. Only moderate agreement was observed overall. The percentage of agreement was 60%, with a Cohen coefficient of 0.45 and a 95% confidence interval (CI) of 0.37-0.54. Agreement was higher than this for patients classified as having a capsular syndrome, with a Cohen coefficient of 0.63 and a 95% CI of 0.50-0.76. Disagreement was most pronounced concerning patients with severe pain, chronic complaints, and bilateral involvement.
Despite the aforementioned limitations, the diagnosis of idiopathic FS syndrome is clinically based on the patient's history and physical findings because of the poor sensitivity and/or specificity of most diagnostic tests used to confirm this condition. However, the literature offers no consensus regarding the clinical diagnostic criteria for FS. The minimal loss of ROM needed to diagnose FS varies among authors. Some suggest a loss of 2 ROMs, whereas others stipulate that the limited range must be present in all motions.4,5,8,9
Concomitant conditions
Careful neurologic examination should be conducted in all patients presenting with signs and symptoms associated with FS. Patients who have a history of smoking should undergo chest radiography with apical views to rule out a Pancoast tumor irritating the brachial plexus, which can cause FS. All patients should receive a thorough neurologic examination of the upper extremities and neck to rule out cervical radiculopathy and brachial plexopathy. Care also should be taken to look for signs of Parkinson disease, because the prevalence of shoulder pain in patients with this treatable condition is 4-5 times that of the healthy population. Furthermore, shoulder pain often is an early manifestation of Parkinson disease, and it sometimes precedes the tremor by many years.10
Proper and complete musculoskeletal and integumentary examination should be performed to rule out concomitant systemic rheumatologic, inflammatory, metastatic, or infectious disorders. Clinicians should also take the time to properly examine the thyroid gland to rule out concomitant hyperthyroidism. Physicians should remain alert to signs of unsuspected diabetes, which may be present in approximately 25% of subjects presenting with FS.
Causes
Early authors pointed to chronic inflammation as the cause of the fibrosis in FS, but objective findings have not supported this suggestion. The absence of crystals, synovial effusion, systemic symptoms, prodromal illness, and serologic markers of autoimmune or reactive arthropathic disease has limited possible theories of an inflammatory process secondary to crystalline, inflammatory, viral, or autoimmune disease.
FS remains a largely idiopathic disorder. The conditions most commonly associated with idiopathic FS are diabetes, hyperthyroidism, hypertriglyceridemia, CVA with upper-extremity paresis, brachial plexus injury, cervical spinal cord injury, and Parkinson disease. The performance of repetitive movements of the upper extremities also is associated with FS.
Anecdotal reports of patients developing FS after a coronary event or following open heart surgery are frequently found in the literature. However, the authors know of no prospective case-control study that has been conducted to confirm this supposition.
Patients who have active glenohumeral synovitis in relation to a systemic inflammatory rheumatologic disorder may develop FS as a complication of this condition. Patients who have undergone surgery to the shoulder area, with postoperative immobilization or with clinically significant pain that causes them to immobilize their shoulder, also are predisposed to develop FS.
More on Adhesive Capsulitis |
 Overview: Adhesive Capsulitis |
| Differential Diagnoses & Workup: Adhesive Capsulitis |
| Treatment & Medication: Adhesive Capsulitis |
| Follow-up: Adhesive Capsulitis |
| References |
| Further Reading |
| Next Page » |
References
Staples MP, Forbes A, Green S, et al. Shoulder-specific disability measures showed acceptable construct validity and responsiveness. J Clin Epidemiol. Aug 13 2009;[Medline].
Wohlgethan JR. Frozen shoulder in hyperthyroidism. Arthritis Rheum. Aug 1987;30(8):936-9. [Medline].
Hazleman B. Why is a frozen shoulder frozen?. Br J Rheumatol. Apr 1990;29(2):130. [Medline].
Lundberg BJ. The frozen shoulder. Clinical and radiographical observations. The effect of manipulation under general anesthesia. Structure and glycosaminoglycan content of the joint capsule. Local bone metabolism. Acta Orthop Scand Suppl. 1969;119:1-59. [Medline].
Reeves B. The natural history of the frozen shoulder syndrome. Scand J Rheumatol. 1975;4(4):193-6. [Medline].
Walmsley S, Rivett DA, Osmotherly PG. Adhesive capsulitis: establishing consensus on clinical identifiers for stage 1 using the DELPHI technique. Phys Ther. Sep 2009;89(9):906-17. [Medline].
Ogilvie-Harris DJ, Biggs DJ, Fitsialos DP, et al. The resistant frozen shoulder. Manipulation versus arthroscopic release. Clin Orthop Relat Res. Oct 1995;238-48. [Medline].
Binder AI, Bulgen DY, Hazleman BL, et al. Frozen shoulder: a long-term prospective study. Ann Rheum Dis. Jun 1984;43(3):361-4. [Medline]. [Full Text].
Rizk TE, Pinals RS. Frozen shoulder. Semin Arthritis Rheum. May 1982;11(4):440-52. [Medline].
Sano H, Hatori M, Mineta M, et al. Tumors masked as frozen shoulders: A retrospective analysis. J Shoulder Elbow Surg. Jun 30 2009;[Medline].
Lequesne M, Dang N, Bensasson M, et al. Increased association of diabetes mellitus with capsulitis of the shoulder and shoulder-hand syndrome. Scand J Rheumatol. 1977;6(1):53-6. [Medline].
Binder AI, Bulgen DY, Hazleman BL, et al. Frozen shoulder: an arthrographic and radionuclear scan assessment. Ann Rheum Dis. Jun 1984;43(3):365-9. [Medline]. [Full Text].
Mao CY, Jaw WC, Cheng HC. Frozen shoulder: correlation between the response to physical therapy and follow-up shoulder arthrography. Arch Phys Med Rehabil. Aug 1997;78(8):857-9. [Medline].
Clunie G, Bomanji J, Ell PJ. Technetium-99m-MDP patterns in patients with painful shoulder lesions. J Nucl Med. Sep 1997;38(9):1491-5. [Medline]. [Full Text].
Carette S, Moffet H, Tardif J, et al. Intraarticular corticosteroids, supervised physiotherapy, or a combination of the two in the treatment of adhesive capsulitis of the shoulder: a placebo-controlled trial. Arthritis Rheum. Mar 2003;48(3):829-38. [Medline]. [Full Text].
Green S. Physiotherapy and injection better than injection alone or physiotherapy alone for improving range of motion in adhesive capsulitis. Aust J Physiother. 2003;49(2):145. [Medline].
Jürgel J, Rannama L, Gapeyeva H, et al. Shoulder function in patients with frozen shoulder before and after 4-week rehabilitation. Medicina (Kaunas). 2005;41(1):30-8. [Medline]. [Full Text].
Pajareya K, Chadchavalpanichaya N, Painmanakit S, et al. Effectiveness of physical therapy for patients with adhesive capsulitis: a randomized controlled trial. J Med Assoc Thai. May 2004;87(5):473-80. [Medline].
Griggs SM, Ahn A, Green A. Idiopathic adhesive capsulitis. A prospective functional outcome study of nonoperative treatment. J Bone Joint Surg Am. Oct 2000;82-A(10):1398-407. [Medline].
Rizk TE, Christopher RP, Pinals RS, et al. Adhesive capsulitis (frozen shoulder): a new approach to its management. Arch Phys Med Rehabil. Jan 1983;64(1):29-33. [Medline].
Rizk TE, Gavant ML, Pinals RS. Treatment of adhesive capsulitis (frozen shoulder) with arthrographic capsular distension and rupture. Arch Phys Med Rehabil. Jul 1994;75(7):803-7. [Medline].
Michlovitz SL, Harris BA, Watkins MP. Therapy interventions for improving joint range of motion: A systematic review. J Hand Ther. Apr-Jun 2004;17(2):118-31. [Medline].
Vermeulen HM, Obermann WR, Burger BJ, et al. End-range mobilization techniques in adhesive capsulitis of the shoulder joint: A multiple-subject case report. Phys Ther. Dec 2000;80(12):1204-13. [Medline].
Liaw SC. The effect and timing of physiotherapy on change in range of motion and function in frozen shoulder. Physiother Singapore. Sep 2000;3(3):82-6.
Williams RM, Westmorland MG, Schmuck G, et al. Effectiveness of workplace rehabilitation interventions in the treatment of work-related upper extremity disorders: a systematic review. J Hand Ther. Apr-Jun 2004;17(2):267-73. [Medline].
Hazleman BL. The painful stiff shoulder. Rheumatol Phys Med. Nov 1972;11(8):413-21. [Medline].
Jacobs LG, Smith MG, Khan SA, et al. Manipulation or intra-articular steroids in the management of adhesive capsulitis of the shoulder? A prospective randomized trial. J Shoulder Elbow Surg. May-Jun 2009;18(3):348-53. [Medline].
Lorbach O, Anagnostakos K, Scherf C, et al. Nonoperative management of adhesive capsulitis of the shoulder: oral cortisone application versus intra-articular cortisone injections. J Shoulder Elbow Surg. Sep 30 2009;[Medline].
Eustace JA, Brophy DP, Gibney RP, et al. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. Jan 1997;56(1):59-63. [Medline]. [Full Text].
Esenyel CZ, Esenyel M, Yesiltepe R, et al. [The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement syndrome]. Acta Orthop Traumatol Turc. 2003;37(1):41-5. [Medline].
Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. Feb 2004;31(2):308-14. [Medline].
Ryans I, Montgomery A, Galway R, et al. A randomized controlled trial of intra-articular triamcinolone and/or physiotherapy in shoulder capsulitis. Rheumatology (Oxford). Apr 2005;44(4):529-35. [Medline]. [Full Text].
Vad VB, Sakalkale D, Warren RF. The role of capsular distention in adhesive capsulitis. Arch Phys Med Rehabil. Sep 2003;84(9):1290-2. [Medline].
de Jong BA, Dahmen R, Hogeweg JA, et al. Intra-articular triamcinolone acetonide injection in patients with capsulitis of the shoulder: a comparative study of two dose regimens. Clin Rehabil. Jun 1998;12(3):211-5. [Medline].
van der Windt DA, Koes BW, Devillé W, et al. Effectiveness of corticosteroid injections versus physiotherapy for treatment of painful stiff shoulder in primary care: randomised trial. BMJ. Nov 7 1998;317(7168):1292-6. [Medline]. [Full Text].
Buchbinder R, Green S, Forbes A, et al. Arthrographic joint distension with saline and steroid improves function and reduces pain in patients with painful stiff shoulder: results of a randomised, double blind, placebo controlled trial. Ann Rheum Dis. Mar 2004;63(3):302-9. [Medline]. [Full Text].
Bunker TD, Anthony PP. The pathology of frozen shoulder. A Dupuytren-like disease. J Bone Joint Surg Br. 1995;77(5):677-83.
Neer CS 2nd, Satterlee CC, Dalsey RM, et al. The anatomy and potential effects of contracture of the coracohumeral ligament. Clin Orthop. Jul 1992;(280):182-5. [Medline].
Ozaki J, Nakagawa Y, Sakurai G, et al. Recalcitrant chronic adhesive capsulitis of the shoulder. Role of contracture of the coracohumeral ligament and rotator interval in pathogenesis and treatment. J Bone Joint Surg Am. Dec 1989;71(10):1511-5. [Medline].
Andrieu V, Dromer C, Fourcade D, et al. Adhesive capsulitis of the shoulder: therapeutic contribution of subacromial bursography. Rev Rhum Engl Ed. Dec 1998;65(12):771-7. [Medline].
Calis M, Demir H, Ulker S, et al. Is intraarticular sodium hyaluronate injection an alternative treatment in patients with adhesive capsulitis?. Rheumatol Int. Apr 2006;26(6):536-40. [Medline].
Itokazu M, Matsunaga T. Clinical evaluation of high-molecular-weight sodium hyaluronate for the treatment of patients with periarthritis of the shoulder. Clin Ther. Sep-Oct 1995;17(5):946-55. [Medline].
Rovetta G, Monteforte P. Intraarticular injection of sodium hyaluronate plus steroid versus steroid in adhesive capsulitis of the shoulder. Int J Tissue React. 1998;20(4):125-30. [Medline].
Corbeil V, Dussault RG, Leduc BE, et al. [Adhesive capsulitis of the shoulder: a comparative study of arthrography with intra-articular corticotherapy and with or without capsular distension]. Can Assoc Radiol J. Apr 1992;43(2):127-30. [Medline].
Gam AN, Schydlowsky P, Rossel I, et al. Treatment of "frozen shoulder" with distension and glucorticoid compared with glucorticoid alone. A randomised controlled trial. Scand J Rheumatol. 1998;27(6):425-30. [Medline].
Bell S, Coghlan J, Richardson M. Hydrodilatation in the management of shoulder capsulitis. Australas Radiol. Sep 2003;47(3):247-51. [Medline].
Piotte F, Gravel D, Moffet H, et al. Effects of repeated distension arthrographies combined with a home exercise program among adults with idiopathic adhesive capsulitis of the shoulder. Am J Phys Med Rehabil. 2004;83(7):537-46; quiz 547-9.
Jones DS, Chattopadhyay C. Suprascapular nerve block for the treatment of frozen shoulder in primary care: a randomized trial. Br J Gen Pract. Jan 1999;49(438):39-41. [Medline]. [Full Text].
Dahan TH, Fortin L, Pelletier M, et al. Double blind randomized clinical trial examining the efficacy of bupivacaine suprascapular nerve blocks in frozen shoulder. J Rheumatol. Jun 2000;27(6):1464-9. [Medline].
Emery P, Bowman S, Wedderburn L, et al. Suprascapular nerve block for chronic shoulder pain in rheumatoid arthritis. BMJ. Oct 28 1989;299(6707):1079-80. [Medline]. [Full Text].
Gado K, Emery P. Modified suprascapular nerve block with bupivacaine alone effectively controls chronic shoulder pain in patients with rheumatoid arthritis. Ann Rheum Dis. Mar 1993;52(3):215-8. [Medline]. [Full Text].
Shanahan EM, Ahern M, Smith M, et al. Suprascapular nerve block (using bupivacaine and methylprednisolone acetate) in chronic shoulder pain. Ann Rheum Dis. May 2003;62(5):400-6. [Medline]. [Full Text].
Lin ML, Huang CT, Lin JG, et al. [A comparison between the pain relief effect of electroacupuncture, regional never block and electroacupuncture plus regional never block in frozen shoulder]. Acta Anaesthesiol Sin. Dec 1994;32(4):237-42. [Medline].
Acquaviva P, Schiano A, Harnden P, et al. Algodystrophy: predisposition and pathogenic factors. Results of a multicentric survey concerning 765 cases [in French]. Rev Rhum Mal Osteoartic. Nov 1982;49(11):761-6. [Medline].
Vadeboncoeur. In: Dupuis M, Leclaire R, eds. Algodystrophie: Pathologie Medicale de l'Appareil Locomoteur. Medisem; 1986:562-87.
Amor B, Tallet F, Raichvarg D, et al. [Algodystrophy and metabolic anomalies]. Rev Rhum Mal Osteoartic. Nov 1982;49(11):827-33. [Medline].
Arnold JM, Teasell RW, MacLeod AP, et al. Increased venous alpha-adrenoceptor responsiveness in patients with reflex sympathetic dystrophy. Ann Intern Med. Apr 15 1993;118(8):619-21. [Medline]. [Full Text].
Binder A, Hazleman BL, Parr G, et al. A controlled study of oral prednisolone in frozen shoulder. Br J Rheumatol. Aug 1986;25(3):288-92. [Medline].
Bridgman JF. Periarthritis of the shoulder and diabetes mellitus. Ann Rheum Dis. Jan 1972;31(1):69-71. [Medline]. [Full Text].
Buchbinder R, Hoving JL, Green S, et al. Short course prednisolone for adhesive capsulitis (frozen shoulder or stiff painful shoulder): a randomised, double blind, placebo controlled trial. Ann Rheum Dis. Nov 2004;63(11):1460-9. [Medline].
Bunker TD. Frozen shoulder: unravelling the enigma. Ann R Coll Surg Engl. May 1997;79(3):210-3. [Medline].
Carrillon Y, Noel E, Fantino O, et al. Magnetic resonance imaging findings in idiopathic adhesive capsulitis of the shoulder. Rev Rhum Engl Ed. Apr 1999;66(4):201-6. [Medline].
Chapman EM, Maloof F. Bizarre clinical manifestations of hyperthyroidism. N Engl J Med. Jan 5 1956;254(1):1-5. [Medline].
Clarke GR, Willis LA, Fish WW, et al. Preliminary studies in measuring range of motion in normal and painful stiff shoulders. Rheumatol Rehabil. Feb 1975;14(1):39-46. [Medline].
de Winter AF, Jans MP, Scholten RJ, et al. Diagnostic classification of shoulder disorders: interobserver agreement and determinants of disagreement. Ann Rheum Dis. May 1999;58(5):272-7. [Medline]. [Full Text].
Doury P, Dirheimer Y, Pattin S. Algodystrophy. New York, NY: Springer-Verlag; 1984:87-95.
Doury P, Pattin S, Eulry F, et al. [Algodystrophy of the knee and scanography]. Rev Rhum Mal Osteoartic. Nov 1987;54(11):725-9. [Medline].
Green S, Buchbinder R, Glazier R, et al. Systematic review of randomised controlled trials of interventions for painful shoulder: selection criteria, outcome assessment, and efficacy. BMJ. Jan 31 1998;316(7128):354-60. [Medline]. [Full Text].
Hashimoto T, Hamada T, Nakamura T, et al. Myxoid and globular degeneration of nerves in the shoulder joint. Clin Orthop. Nov 1995;(320):55-64. [Medline].
Janig W. The puzzle of reflex sympathetic dystrophy: mechanisms, hypotheses, open questions. In: Janig W, Stanton-Hicks M, eds. Reflex Sympathetic Dystrophy: A Reappraisal, Progress in Pain Research and Management. vol 6. Seattle, Wash: Int Assoc for the Study of Pain; 1996.
Jeracitano D, Cooper RG, Lyon LJ, et al. Abnormal temperature control suggesting sympathetic dysfunction in the shoulder skin of patients with frozen shoulder. Br J Rheumatol. Aug 1992;31(8):539-42. [Medline].
Jones A, Regan M, Ledingham J, et al. Importance of placement of intra-articular steroid injections. BMJ. Nov 20 1993;307(6915):1329-30. [Medline]. [Full Text].
Joshi GP, McCarroll SM. Intra-articular morphine for the management of frozen shoulder. Anaesthesia. Jul 1992;47(7):627. [Medline].
Koltzenburg M. Afferent mechanisms mediating pain and hyperalgesias in neuralgia. In: Janig W, Stanton-Hicks M, eds. Reflex Sympathetic Dystrophy: A Reappraisal, Progress in Pain Research and Management. vol 6. Seattle, Wash: Int Assoc for the Study of Pain; 1996.
Leclaire R, Bourgouin J. Electromagnetic treatment of shoulder periarthritis: a randomized controlled trial of the efficiency and tolerance of magnetotherapy. Arch Phys Med Rehabil. Apr 1991;72(5):284-7. [Medline].
Mani R, Cooper C, Kidd BL, et al. Use of laser Doppler flowmetry and transcutaneous oxygen tension electrodes to assess local autonomic dysfunction in patients with frozen shoulder. J R Soc Med. Sep 1989;82(9):536-8. [Medline]. [Full Text].
Manton GL, Schweitzer ME, Weishaupt D, et al. Utility of MR arthrography in the diagnosis of adhesive capsulitis. Skeletal Radiol. Jun 2001;30(6):326-30. [Medline].
Mavrikakis ME, Sfikakis PP, Kontoyannis SA, et al. Clinical and laboratory parameters in adult diabetics with and without calcific shoulder periarthritis. Calcif Tissue Int. Oct 1991;49(4):288-91. [Medline].
Mays KS, North WC, Schnapp M. Stellate ganglion blocks with morphine in sympathetic type pain. J Neurol Neurosurg Psychiatry. 1981;44:189.
Murrell GA. Scientific comment. Basic science of Dupuytren''s disease. Ann Chir Main Memb Super. 1992;11(5):355-61. [Medline].
Musculoskeletal Disorders and Workplace Factors. Cincinnati, OH: Natl Inst Occup Safety and Health; Jul 1997. [Full Text].
Ochoa J, Serra J. Dorsal root reflexes: do they play a role in chronic neuropathic pain patients?. Pain Forum. 4(3):155-7.
Ogilvie-Harris DJ, Myerthall S. The diabetic frozen shoulder: arthroscopic release. Arthroscopy. Feb 1997;13(1):1-8. [Medline].
Oldham BE. Periarthritis of the shoulder associated with thyrotoxicosis. A report of five cases. N Z Med J. Dec 1959;58:766-70. [Medline].
Rizk TE, Pinals RS, Talaiver AS. Corticosteroid injections in adhesive capsulitis: investigation of their value and site. Arch Phys Med Rehabil. Jan 1991;72(1):20-2. [Medline].
Rockwood C, Mattson F III. The stiff shoulder. In: The Shoulder. 2nd ed. Philadelphia, Pa: WB Saunders; 1998:1065-7.
Ryu KN, Lee SW, Rhee YG, et al. Adhesive capsulitis of the shoulder joint: usefulness of dynamic sonography. J Ultrasound Med. Aug 1993;12(8):445-9. [Medline].
Sluka KA, Willis WD, Westlund KN. The role of dorsal root reflexes in neurogenic inflammation. Pain Forum. 1995;4(3):141-9.
Stenlund B, Goldie I, Hagberg M, et al. Shoulder tendinitis and its relation to heavy manual work and exposure to vibration. Scand J Work Environ Health. Feb 1993;19(1):43-9. [Medline].
Subbarao J, Stillwell GK. Reflex sympathetic dystrophy syndrome of the upper extremity: analysis of total outcome of management of 125 cases. Arch Phys Med Rehabil. Nov 1981;62(11):549-54. [Medline].
University of Washington School of Medicine. Home Exercises for the Stiff Shoulder. Available at http://www.orthop.washington.edu/uw/tabID__3376/ItemID__208/mid__10313/Articles/Default.aspx.
van der Heijden GJ, van der Windt DA, de Winter AF. Physiotherapy for patients with soft tissue shoulder disorders: a systematic review of randomised clinical trials. BMJ. Jul 5 1997;315(7099):25-30. [Medline]. [Full Text].
Vecchio PC, Adebajo AO, Chard MD, et al. Thermography of frozen shoulder and rotator cuff tendinitis. Clin Rheumatol. Sep 1992;11(3):382-4. [Medline].
Vermeulen HM, Rozing PM, Obermann WR, et al. Comparison of high-grade and low-grade mobilization techniques in the management of adhesive capsulitis of the shoulder: randomized controlled trial. Phys Ther. Mar 2006;86(3):355-68. [Medline].
Waldburger M, Meier JL, Gobelet C. The frozen shoulder: diagnosis and treatment. Prospective study of 50 cases of adhesive capsulitis. Clin Rheumatol. Sep 1992;11(3):364-8. [Medline].
Widiastuti-Samekto M, Sianturi GP. Frozen shoulder syndrome: comparison of oral route corticosteroid and intra-articular corticosteroid injection. Med J Malaysia. Aug 2004;59(3):312-6. [Medline].
Wilson PR, Phillip AL, Bedder MD, et al. Diagnostic algorithm for complex regional pain symptoms. In: Janig W, Stanton-Hicks M, eds. Reflex Sympathetic Dystrophy: A Reappraisal, Progress in Pain Research and Management. Int Assoc for the Study of Pain; 1996:93-105.
Zanotti RM, Kuhn JE. Arthroscopic capsular release for the stiff shoulder. Description of technique and anatomic considerations. Am J Sports Med. May-Jun 1997;25(3):294-8. [Medline].
Further Reading
Clinical guidelines:
Shoulder (acute & chronic). Work Loss Data Institute - Public For Profit Organization. 2003 (revised 2008 May 28). 217 pages. NGC:006566
Clinical trials:
Arthroscopy and Manipulation vs a Home Therapy Program in the Treatment of Adhesive Capsulitis
Collagenase in the Treatment of Adhesive Capsulitis (Frozen Shoulder)
Correlating Clinical Disease State With Color Doppler Ultrasound
Effects of Intra-articular Versus Subacromial Steroid Injections on Clinical Outcomes in Adhesive Capsulitis
Prevalence of Impaired Glucose Tolerance (IGT) in Patients With Frozen Shoulder
Should the Joint Capsule of the Painful Stiff Shoulder Be Ruptured During Intra-articular Hydraulic Distension?
Keywords
adhesive capsulitis, frozen shoulder, frozen shoulder exercises, frozen shoulder therapy, shoulder physical therapy, glenohumeral joint, frozen shoulder syndrome, frozen shoulder causes, frozen shoulder pain, restrictive periarthritis, Duplay disease, Duplay's disease, scapulohumeral periarthritis, complex regional pain syndrome
