Adhesive Capsulitis in Physical Medicine and Rehabilitation 

Author: André Roy, MD, FRCPC; Chief Editor: Rene Cailliet, MD   more...

 

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.

Epidemiology

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. 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.

Differential Diagnoses

Biceps Rupture Biceps Tendinopathy Brachial Neuritis Cervical Disc Disease Cervical Myofascial Pain Cervical Spondylosis Cervical Sprain and Strain Complex Regional Pain Syndromes Heterotopic Ossification Myelomeningocele Neoplastic Brachial Plexopathy Parkinson Disease Psoriatic Arthritis Rheumatoid Arthritis Rotator Cuff Disease Shoulder and Hemiplegia Thoracic Outlet Syndrome Traumatic Brachial Plexopathy

Laboratory Studies

Whether laboratory investigations should be mandatory in patients presenting with the classic syndrome of idiopathic FS but without symptoms of concomitant systemic rheumatologic, inflammatory, peptic, or metastatic disorders remains unclear.

The scientific literature shows an elevated incidence of diabetes, hyperthyroidism, and hypertriglyceridemia in patients with FS.

o Lequesne and colleagues found that 28% of 60 new patients who presented with idiopathic FS had unsuspected diabetes.[11]

o This association should prompt possible testing of thyroid-stimulating hormone (TSH), serum triglyceride, and fasting blood sugar levels in most patients, particularly those presenting with bilateral disease and patients presenting with FS who are younger than 45 years.

Imaging Studies

Radiologic studies o In general, idiopathic FS is considered a clinical diagnosis that does not require

confirmation with radiologic imaging.o Current radiologic studies do not seem to confer any useful information,

prognostic or otherwise, that changes the way the patient is treated. o For the moment, the principal utility of these tests is in ruling out concomitant

conditions that may influence the treatment of an individual patient. Plain radiography

o All patients presenting with FS should undergo plain radiography of the shoulder, with the acquisition of soft-tissue views of the rotator cuff to rule out a septic or metastatic process.

o A plain radiograph may also show evidence of a large calcification of the rotator cuff in the painful resorptive phase, an avascular necrosis of the humeral head (that is, Milwaukee shoulder), or a Charcot joint.

Gallium nuclear scanning - Patients who are immunocompromised, as well as those who abuse intravenous (IV) drugs, should undergo gallium nuclear scanning to rule out a septic joint.

Arthrography of the glenohumeral joint o Binder and colleagues examined the arthrographic and scintigraphic features of

36 patients who presented with clinically diagnosed FS.[12] They reported no association between uptake on bone scans and arthrographic features (glenohumeral contrast enhancement), and neither finding was useful in predicting the rate or extent of recovery. FS of traumatic onset behaved no differently than did spontaneously arising FS. The authors concluded that arthrography or99m Tc diphosphonate scanning performed at presentation did not contribute to the assessment of a painful, stiff shoulder.

o The present authors share the opinions of Binder and coauthors on this matter.o Of 36 subjects who met strict clinical criteria for FS in the study by Binder and

colleagues (ie, loss of ≥ 50% of glenohumeral PROM in abduction and external rotation), only 50% had a positive arthrogram. Either arthrography had low sensitivity in diagnosing FS, or the expert physicians tended to overdiagnose FS. The fact that a positive arthrogram had no affect on the clinical outcome in this 4-year prospective study suggests that arthrography of the glenohumeral joint is a poorly sensitive test for diagnosing FS, although a positive glenohumeral arthrogram showing the classic signs of FS confirms the diagnosis beyond any doubt.

o A study by Mao and coauthors showed a poor correlation between ROM of the glenohumeral joint and its arthrographic appearance in patients with shoulder pain for 2 months or longer.[13] This result once again showed the limited prognostic usefulness of arthrography of the glenohumeral joint.

o To date, arthrography is used mostly to treat FS, rather than to diagnose the condition.

o The injection of contrast medium into the glenohumeral joint helps to determine its volume and configuration. The normal volume of the joint is 13 mL. In FS, the volume can be reduced to 5-8 mL.

99m Tc methylene diphosphonate (MDP) bone scanning o Binder and colleagues also examined the utility of nuclear bone scanning in the

diagnosis and treatment of patients with FS. They again found that these studies had little prognostic value, although they were considerably more sensitive, with 92% of the study subjects having a positive scan.

o In general, the problem with bone scans in the practice of musculoskeletal medicine is that they are highly sensitive but not specific. The pilot work by Clunie and colleagues showed that abnormalities on posterior99m Tc MDP shoulder studies of patients with shoulder pain did tend to be specific for FS.[14]

However, this work must be reproduced on a large scale to be considered conclusive.

Other studies - Computed tomography (CT) scanning, CT arthrography, ultrasonography, and magnetic resonance imaging (MRI) are sensitive imaging modalities that depict specific signs for FS. However, use of these modalities is rarely indicated.

Histologic Findings

See Pathophysiology.

Rehabilitation Program

Physical Therapy

Although studies have shown the efficacy of physical therapy, no current evidence has suggested that physical therapy alone improves function in the treatment of FS.[15, 16, 17, 18]

However, physical therapy associated with an intra-articular injection of corticosteroid improves function and ROM more rapidly than does intra-articular corticosteroid injection alone.[15, 19]

Therapeutic exercises

Although many therapeutic exercises are described, few have been evaluated in the treatment of FS. Therapeutic exercises that have been studied include articular stretching and pulley therapy.[20, 21, 22] Passive articular stretching exercises improve ROM. The superiority of supervised versus home exercise programs has yet to be demonstrated.[23]

Manual therapy

Data from 2 studies support the use of manual therapy to improve ROM in the short term. One study showed that passive mobilization in the end-range position of the glenohumeral joint was more effective for improving ROM and function than was passive mobilization in the pain-free zone.[24] However, the overall difference between the interventions was small. In addition, patients appeared to achieve greatest improvement in ROM when treatment was administered early.[25]

In summary, the findings indicated that patients with FS improve with physical therapy regardless of when it is administered after the onset of FS but that they achieve the greatest improvement in their ROM when treatment is administered early.

Physical modalities

Many electroanalgesic and thermoanalgesic modalities are often used in physical therapy. Prospective, randomized, placebo-controlled clinical trials have demonstrated the inefficacy of bipolar interferential electrotherapy, TENS (transcutaneous electrical nerve stimulation) pulsed ultrasound therapy, laser therapy, and magnetotherapy with electromagnetic fields in the treatment of painful shoulder disorders. Indeed, a systematic review of randomized clinical trials has demonstrated that little evidence supports the use of common physiotherapeutic modalities to treat shoulder pain. (Nonetheless, clinical observations suggest that electroanalgesia and heat can provide some temporary relief to patients with severe shoulder pain and that they can do so without side effects.)

In summary, physical therapy alone has not been shown to improve function. However, when associated with an intra-articular corticosteroid injection, physical therapy improves ROM and function more rapidly than does intra-articular corticosteroid injection alone. The effectiveness of physical modalities has not been demonstrated. However, therapeutic exercises and manual therapy do improve ROM (see above).

Given the paucity of evidence supporting the effectiveness of physical therapy, the present authors believe that clinicians should be most conservative in designing a physical therapy program for patients with FS. An intermittently supervised, home-based articular stretching and strength-maintenance program can be combined with manual therapy, the appropriate analgesic medications, and the judicious use of electroanalgesia and warm packs. This approach generally suffices to provide adequate pain relief in most patients while the disease runs its usual, favorable course. (For additional information, see Home Exercises for the Stiff Shoulder, on the University of Washington School of Medicine Web site.

Occupational Therapy

Patients with severe FS may benefit from a referral to an occupational therapist for assistance and instruction in performing activities of daily living (ADLs). The occupational therapist helps the patient learn how to use adaptive equipment and suggest home and workplace modifications that may be necessary and beneficial for completing professional activities and routine daily tasks (eg, dressing, bathing, grooming). (See also Patient Education.) However, the effectiveness of these interventions has yet to be demonstrated. Researchers who performed a systematic review concluded that evidence supporting the effectiveness of rehabilitation in the workplace is lacking.[26]

Medical Issues/Complications

Certain authors, including the present authors, believe that idiopathic FS should be considered a distinct clinical entity. The prognosis and therapeutic approach for idiopathic FS differ from those of posttraumatic shoulder stiffening resulting from a fracture or a surgical insult to the glenohumeral joint.

Surgical Intervention

Duplay, the first person to describe the syndrome of FS, in 1872, proposed treating this condition with manipulation of the glenohumeral joint, with the patient under general anesthesia. Although some orthopedic surgeons continue to practice this technique, the benefits of this approach have not been demonstrated in controlled clinical trials.

In 1972, Hazelman noted that, in the context of a prospective controlled clinical trial, patients who had been treated with manipulation of the glenohumeral joint fared no better than did patients who received only a series of steroid injections and physical therapy.[27] Data from a long-term prospective study by Binder and colleagues seemed to support the notion that subjects who are treated with vigorous shoulder manipulation fare worse than do those who are not treated at all.[8]

A 2009 study by Jacobs et al also found no evidence that manipulation provides a better treatment outcome in FS.[28] The investigators divided 53 patients suffering from idiopathic FS into 2 groups, with one undergoing shoulder manipulation under anesthetic and the other being treated with intra-articular steroid injections and distension (see Other Treatment). After 2 years of follow-up, the investigators found no statistical difference between outcome measures in the 2 groups.

Various improvements in surgical techniques, such as the advent of controlled capsular release by using arthroscopic access to the anterior glenohumeral joint capsule and the coracohumeral ligament, appear to offer promising treatments. However, the effectiveness of these surgical techniques has yet to be demonstrated in controlled clinical trials.

Considering the favorable prognosis for patients with idiopathic FS, surgical intervention should probably be reserved for rare patients whose condition does not respond to maximal conservative modalities implemented over a sufficient period of time.[29]

Some authors propose early surgical intervention in patients with FS because of the patients' high risk of permanent contracture of the glenohumeral joint. However, this approach remains controversial because patients with diabetes often have recurring pain and contracture in the postoperative rehabilitation phase and because their rate of preoperative complications is generally increased.

Other Treatment

Studies of intra-articular and intrabursal injections, glenohumeral distension arthrography, and nerve blocks have been conducted, as described in the following text.

Intra-articular and intrabursal injections

Intra-articular corticosteroid injections

Intra-articular injections of steroid derivatives are the second most common medical intervention for treating painful joint conditions. (The most common intervention is the administration of nonsteroidal anti-inflammatory drugs [NSAIDs]). The rationale for injection of an intra-articular steroid derivative is to allow direct delivery of a modest dose of concentrated drug with analgesic and anti-inflammatory properties to the targeted site of pathology.[30] Researchers at the Manchester Rheumatology Service investigated the accuracy of a variety of joint injections

that were administered by using anatomic landmarks to the upper and lower extremities. Their study demonstrated inaccurate placement of the drug in 65% of 108 joints injected.

A study by Eustace and colleagues showed results similar to those above, demonstrating that 68% of shoulder injections performed by expert specialist physicians without radiologic guidance failed to hit their target.[31] Overall, when radiologic guidance is not used, the accuracy of these injections is poor. When anatomic landmarks are used, the rate of misplacement is as high as 58% in the glenohumeral joint and as high as 69% in the subacromiodeltoidian bursae. Accuracy of the injection is associated with improved clinical results.[31, 32, 33]

If the rationale for using an intra-articular injection of steroid derivative is to deliver targeted therapy, the target in FS is the glenohumeral joint. The work by Eustace and coauthors suggests that targeted therapy that does not hit its target is not ineffective.[31] In general, however, physicians who are less experienced in joint injection than the expert rheumatologists in that study should avoid injecting shoulders without radiologic guidance. The results of their study are impressive, even for physicians who are experienced in the field of joint injections.

Eustace's study also puts an interesting twist on the interpretation of data from placebo-controlled clinical trials that failed to demonstrate favorable results with the steroid injection into the shoulder to treat FS. Some investigators did use radiologic guidance, but most employed anatomic landmarks.[15, 34, 35, 36, 37] Because some studies involved radiologic confirmation of location of the injectate, most of the injections may have missed their target. The present authors believe that no conclusions can be drawn from studies using anatomic landmarks, given the inaccuracy of the intervention.

From the current literature, we know that intra-articular corticosteroid injections or distension arthrography with corticosteroids or sodium chloride solution (discussed below) considerably improve FS in the short term. However, in the long term, they are not superior to placebo but they are superior to supervised physical therapy.[15, 38] Whether their effectiveness is the result of distension arthrography, the intra-articular corticosteroid, or their combination is unclear because most studies used corticosteroids.

Intrabursal corticosteroid injections

Many authors have shown that the pathology of FS is in the extra-articular structures, such as the coracohumeral ligament, the interval of the rotator cuff, the subacromial space, and the articular capsule.[39, 40, 41] From a pathophysiologic point of view, a rationale supports the use of corticosteroid injection in the subacromiodeltoidian bursa to treat FS.

A comparison of intra-articular and intrabursal injections with lidocaine alone or with lidocaine and a corticosteroid showed similar decreases in pain and increases in ROM in all groups.[22]

However, a significant short-term decrease in pain was observed in the lidocaine-plus-corticosteroid group compared with the lidocaine-only group. Data from another study supported these findings, showing that patients whose condition did not improve with distension arthrography benefited from an intra-articular bursal injection of corticosteroid.[42]

Because of the inaccuracy of injections given by using anatomic landmarks, the present authors recommend that intra-articular and intrabursal injections should be administered by using fluoroscopic guidance. When the needle is accurately positioned, intra-articular corticosteroid injection and distension arthrography are effective in the short them. However, in the long term,

they are not superior to placebo. This observation is not surprising given the favorable evolution of this disease. An intrabursal injection of corticosteroid can be used as a complementary treatment to intra-articular injection and distension arthrography or as treatment in patients whose condition does not improve with an intra-articular corticosteroid injection or with distension arthrography.

Many issues remain unclear. Factors to be resolved are whether distension is necessary, whether an intra-articular corticosteroid injection without distension (or vice versa) is enough, how many injections are needed, the stage of disease at which injections should be administered, the most effective corticosteroid, and the most effective dosage.

Intra-articular injection of sodium hyaluronate

Sodium hyaluronate has a metabolic effect on the articular cartilage, synovial tissues, and liquid. Few studies on the effect of sodium hyaluronate have been reported.[43, 44, 45] The present authors are aware of only 1 controlled study of the effectiveness of sodium hyaluronate as a sole treatment of FS. At 3 months, sodium hyaluronate was as effective as an intra-articular corticosteroid injection or physical therapy in improving function, but it was less effective than the comparators in improving ROM.[43] Although additional studies are needed before conclusions about efficacy can be drawn, intra-articular injections of sodium hyaluronate may be an alternative treatment for FS, mainly in patients in whom corticosteroid injections are contraindicated.

Glenohumeral distension arthrography

One controlled study showed no benefit to distension arthrography over intra-articular corticosteroid injection without distension.[46] Another controlled study showed a significant increase in ROM and a significant decrease in the use of analgesics after distension arthrography, compared with the use of intra-articular corticosteroid injection alone.[47]

The benefit of performing distension arthrography until the capsule ruptures must be demonstrated.[22, 48]

One uncontrolled study that was designed to examine the optimal number of distension arthrography procedures that should be performed showed that 2 procedures administered within 3 weeks, when combined with home exercises, significantly improved function. However, a third procedure offered no benefit.[49]

Another unknown factor is the stage at which infiltration should be performed. To the authors' knowledge, only 1 uncontrolled study on this question has been completed.[35] The researchers concluded that distension arthrography should be done in the second stage of disease that is not progressing, despite the patient's participation in physical therapy.

Nerve blocks

Suprascapular nerve block

The suprascapular nerve block is a simple procedure but is not well known by most clinicians.

Dangoisse's technique for suprascapular nerve block was modified to render it steroid free and accessible to most physicians who practice musculoskeletal medicine in ambulatory-care facilities and private offices. A 3.75-cm, 25-gauge needle is directed in the plane of the scapula toward the center of the floor of the supraspinous fossa. The needle-insertion point is 2 cm above the bisection point of the upper border of the spine of the scapula. After aspiration is performed to rule out intravascular needle placement, 10 mL of bupivacaine 0.5 is slowly injected into the floor of the supraspinous fossa to fill the fascial contents of this fossa and to produce an indirect suprascapular nerve block. The highly concentrated bupivacaine bathes the suprascapular nerve as it enters the fossa through the suprascapular notch.

Since 1996, thousands of bupivacaine suprascapular nerve blocks have been performed by using the above-described technique. No notable complications, other than vasovagal episodes and tenderness at the site of injection, have occurred. Most specialists in musculoskeletal medicine who treat shoulder pain in an outpatient context can safely and inexpensively perform modified indirect suprascapular nerve blocks without radiologic guidance if they are adequately trained.

A randomized controlled trial was performed to compare the effectiveness of a single suprascapular nerve block with that of series of intra-articular corticosteroid injections given by using anatomic landmarks without fluoroscopic guidance.[50] Pain decreased and ROM increased more rapidly and more completely with the nerve block than they did with the intra-articular injections.

A double-blind, placebo-controlled, randomized trial showed the superiority of 3 bupivacaine suprascapular nerve blocks.[51] At 1 month, a 64% decrease in pain was reported in the bupivacaine group compared with 13% in the placebo group. Although functional improvement was superior with bupivacaine, the difference was not statistically significant. The same authors preformed a double-blind, placebo-controlled, randomized trial larger than the previous study by using the same protocol (unpublished data). They observed no statistically significant difference between bupivacaine and placebo in terms of pain and function.

Some studies have shown the effectiveness of bupivacaine suprascapular nerve blocks to treat chronic tendinopathy of the rotator cuff, as well as to treat painful shoulders in patients with rheumatoid arthritis.[52, 53, 54] However, studies are scant, and the results are contradictory regarding the effectiveness of bupivacaine suprascapular nerve blocks in managing FS. Additional studies are needed before conclusions can be drawn.

Stellate block

An uncontrolled study of the combined effect of electropuncture, stellate block, and suprascapular nerve block showed that the combination improved pain control and increased ROM more than electropuncture or nerve block alone.[55]

Medication Summary

The goal of pharmacologic intervention in FS is uniquely the control of pain in the 2 first stages of the disease because no drug affects the underlying disease process. Medication does not affect the duration of disease or the severity or duration of glenohumeral joint contracture. Most of the time, patients with FS can manage their pain with analgesics, such as acetaminophen, as

needed. However, during the most painful months of the condition, when rest pain and night pain are most bothersome, appropriate use of narcotic agents is warranted.

Pain control should be aimed at relieving pain in the following order of priority:

1. Rest pain and night pain: The preferred agent should be a long-acting, centrally acting agent (eg, calcitonin) or a sustained-release narcotic preparation (eg, low-dose oxycodone HCl [OxyContin]).

2. Activity-related pain: Some physicians advocate the use of short-acting analgesic agents, such as oxycodone, before sessions of physical therapy to improve shoulder mobilization. The authors' opinion is that this regimen should be used with care because of the risk of causing a flare-up after physiotherapeutic mobilization due to an excessively vigorous mobilization session.

Attaining the favorable prognosis requires patience on the part of the physician and the patient.

Endocrine metabolic agents

Class Summary

Agents in this class may have analgesic effects.

View full drug information

Calcitonin (Miacalcin, Osteocalcin)

 

Can relieve some back pain associated with adhesive capsulitis. A prospective, randomized study was conducted to compare calcitonin SC for 3 wk with manual therapy and physical therapy with physical therapy alone. Pain decreased more in patients with posttraumatic capsulitis who were receiving calcitonin, manual therapy, and physical therapy than it did in others. The speed of recovery was comparable in both groups.

NSAIDs

Class Summary

Given the absence of histopathologic evidence of capsular inflammation, NSAIDs must be used for their analgesic effects. To our knowledge, no researchers have compared the efficacy of NSAIDs with that of placebo in adhesive capsulitis. Comparisons of the efficacy of different NSAIDs in the treatment of adhesive capsulitis show a positive effect regardless of the NSAID used.

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well; examples are inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

COX-2 – selective NSAIDs are recommended in cases of FS. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than it is with traditional NSAIDs. Ongoing analysis of the cost of preventing GI bleeds will help in further defining the patient populations who are most likely to benefit from COX-2 inhibitors.

Two randomized, controlled studies were conducted to compare oral (PO) corticosteroids with placebo. One study showed an improvement only of night pain at 4 weeks. The other study showed an improvement of pain and function at 3 weeks. Therapeutic effects of PO corticosteroids after these periods have not been demonstrated.

PO corticosteroid therapy is significantly less effective than intra-articular corticosteroid injection in the short term.

Given the systemic adverse effects, one should question the indication for PO corticosteroids in the treatment of FS. Other drugs with fewer adverse effects are available; alternatively, corticosteroids can be administered intra-articularly with fewer adverse effects.

View full drug information

Celecoxib (Celebrex)

 

Inhibits primarily COX-2, an isoenzyme induced during pain and by inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; therefore, GI toxicity may be decreased. Seek the lowest dose for each patient.

Analgesic agents

Class Summary

In rare cases, narcotic analgesia may be needed for adequate pain control if the patient's condition is refractory to the judicious use of bupivacaine or bupivacaine suprascapular nerve blocks or in situations in which these nerve-block procedures and/or steroid injections (which are most often performed with fluoroscopic guidance) are not readily available. When combined with anti-inflammatory agents and physical modalities, analgesics should result in good pain control.

In the occasional patient whose condition does not respond to the aforementioned therapies, the use of a long-acting narcotic agent, such as codeine, morphine sulfate (MS Contin), oxycodone HCl (OxyContin), or hydromorphone, should be considered, along with rescue doses of short-acting drugs every 4-6 hours.

View full drug information

Acetaminophen (Tylenol, Feverall, Tempra, Aspirin Free Anacin)

 

Should be first-line drug of choice. In most patients, 3 g/d suffices to control the pain of FS during all but the most painful months. Narcotics and NSAIDs should be used only if the regular use of acetaminophen 1 g tid fails to adequately control pain. The authors prefer to be conservative and limit the prescription to 75% of the maximal daily dosage because patients may be prone to liver toxicity if they take the maximal dosage for many consecutive months.

View full drug information

Oxycodone (OxyContin, OxyIR, Roxicodone)

 

Indicated for relief of moderate to severe pain.

Further Inpatient Care

In general, treatment and follow-up care for individuals with FS is performed on an outpatient basis; however, for patients who require more aggressive treatment, a short hospitalization may be required.

Pain control and maintenance of ROM are common goals after surgical procedures or glenohumeral manipulations that are performed with the patient under anesthesia.

Further Outpatient Care

The physician and patient together should decide on the most appropriate treatment plan based on the patient's current status and functional goals.

Most patients with FS achieve successful outcomes with conservative care. Outpatient follow-up visits should occur on a regular basis (for example, monthly) so that

the physician can properly monitor the patient's progress and adjust the treatment plan as needed.

See the Treatment section for a discussion of outpatient treatment suggestions.

Deterrence

The best treatment for FS is prevention. Early mobilization of the shoulder is crucial in the early stages of FS syndrome. Individuals who do repetitive activities with their upper extremities at work need to pay

special attention to their posture and to the ergonomics of their workstation in order to prevent FS.

Complications

Complications of FS include constant pain, loss of functional use of the upper extremity, recurrence, and permanent disability of the shoulder.

When patients receive aggressive treatment involving manipulation or surgical intervention, complications may include increased pain, humeral fracture, or neurovascular injury.

Prognosis

The prognosis for patients with FS is generally favorable.

Patient Education

Throughout all stages of the disease process, patient education is an important aspect of treatment for individuals with FS.

o Patients with FS need to take an active part in their treatment programs to achieve the most successful results.

o Physical and occupational therapists are valuable members of the treatment team and generally provide a great deal of patient education as part of therapy.

o Patients should be instructed in a home exercise program to continue working on their ROM and functional abilities.

o Patients at risk or in the early stages of the disease process must be educated about the disease, especially about prevention strategies.

Patients should be advised about the effects of FS and its treatment on their ability to return to work or to resume ADLs.

o For a manual laborer, an episode of unilateral FS may mean prolonged absence from work, usually for at least 1-3 years. A sedentary office worker may be able to continue working throughout the disease process if given adequate tools to cope with the pain of the illness. These tools may include analgesic medication, the judicious use of injections, use of a TENS unit, and appropriate ergonomic adjustments to his/her workstation.

o Patients with severe bilateral FS may find that even basic ADLs are a challenge. The loss of ROM during combined extension and internal rotation may make it difficult or impossible for patients with FS to perform many basic daily tasks (eg, toileting, hygiene, dressing, driving, fastening a seat belt). The loss of the combined movements of abduction and external rotation may render it impossible for patients with FS to groom their hair or reach for their seat belt.

o Patients need to be reminded that improvements in pain and disability after the treatment of FS usually occur over measured months and not over days or weeks. Because 60% of individuals with FS have some permanent residual contracture at the end of the disease process, workers whose tasks require them to move their shoulder to the end of their ROM or to a position of subacromial impingement may have long-term difficulties in resuming their previous job. These individuals may need to adapt their workstations or to change jobs in order to rejoin the workforce. Employees whose job requires repetitive movement of their shoulders or who operate heavy machinery that vibrates may encounter similar difficulties.

For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center and Osteoporosis and Bone Health Center. Also, see eMedicine's patient education article Shoulder and Neck Pain.

Proceed to Clinical Presentation

  Contributor Information and DisclosuresAuthor

André Roy, MD, FRCPC  Consulting Staff, Department of Physiatry, Montreal University Hospital Center and Montreal Rehabilitation Institute André Roy, MD, FRCPC is a member of the following medical societies: American Academy of Physical Medicine and RehabilitationDisclosure: Nothing to disclose.

Coauthor(s)

Thierry HM Dahan, MD, LMCC, CCFP, FRCPC, FABPMR  Head, Pain Rehabilitation Center, Haim Sheba Medical Center, Tel Hashomer, Israel Thierry HM Dahan, MD, LMCC, CCFP, FRCPC, FABPMR is a member of the following medical societies: Royal College of Physicians and Surgeons of CanadaDisclosure: Nothing to disclose.

Specialty Editor Board

Curtis W Slipman, MD  Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine SocietyDisclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment

Patrick M Foye, MD  Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention SocietyDisclosure: Nothing to disclose.

Kelly L Allen, MD  Medical Director, Medevals Disclosure: Nothing to disclose.

Chief Editor

Rene Cailliet, MD  Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association Disclosure: Nothing to disclose.

Additional Contributors

The editors wish to thank Luc Fortin, MD, for his previous contributions to this article.

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