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

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Frozen Shou lderCAROLYN T. WADSWORTH

Widespread use of the label "frozen shoulder" as a diagnosis for any stiff andpainful shoulder condition has led to its becoming a rather meaningless, catchallterm. In addition to confounding both the lay public and health care professionals,this indiscriminate labeling may prevent a patient from receiving appropriatetreatment. In this article, I define frozen shoulder and review its pathologic andetiologic factors, epidemiology, natural history, and diagnosis. I present thisinformation in correlation with an examination process to assist physical thera-pists in identifying suspected cases of frozen shoulder. I also present the currentoptions for treatment, including physical therapy management with physicalagents and exercise.Key Words: Pain, Physical therapy, Shoulder.

Frozen shoulder (FS) is a distinct clinical entity with characteristic clinical and arthrographic findings.1 The purpose ofthis article is to describe the pathologic factors, natura l history,signs, and symptoms of FS that clearly distinguish it fromother disorders that produce shoulder stiffness and pain. Thisinforma tion should assist the clinician in identifying true casesof FS (synonymously termed adhesive capsulitis) and labelingthem appropriately.This article details the various methods of treating FS,although an extensive review of the literature revealed noagreement on any one method. It also summarizes the fewreported studies comparing the efficacy of different treatments, including physical therapy. Finally, it proposes a physical therapy plan ofmanagement, which a therapist monitorsand modifies as a patient's status changes during the naturalcourse of this disorder.HISTORICAL PERSPECTIVE

Painful restriction of shoulder motion is one of the mostcommon and disabling orthopedic disorders for which pa-tients seek treatment.2- 5 The specific type of restriction thatwe recognize today as FS has been reported in medical literature for over 100 years. Duplay referred to FS in 1872 as"scapulohumeral periarthritis," a disorder he believed resultedfrom subacromial bursitis.3,6-9 Pasteur later referred to thesame condition as "tenobursite," which he attributed to bicipital tendinitis.4,9 In 1934, Codman coined the term "frozenshoulder" but used it in association with tendinitis of therotator cuff.7 Although these early practitioners describedsome of the clinical characteristics of FS, they did no t identifyaccurately the site of the pathological cond ition as it is understood today. In 1945, Neviaser introduced the concept ofadhesive capsulitis when he discovered that the capsule wastight, thickened, and stuck to the humerus in such a mannerthat it could be peeled off like "adhesive plaster from theskin."1,4-6,10-14 Current doctrine supports Neviaser's theorythat the capsule is the site of the lesion and lends credence tothe synonymous use of the terms adhesive capsulitis andfrozen shoulder.3,6,8,10,11,14

Definition and PathologyFrozen shoulder typically is referred to as the spontaneousonset of gradually progressive shoulder pain andsevere limitation ofmovement.1,5,7,8,14,15 Features of this pathologic condition include microscopic evidence of chronic capsular in-flammation with fibrosis and perivascular infiltration.3,5,14Although several researchers found no evidence of inflammation, they concurred thatfibrosisexists in the capsule.14,16,17Chronic cases of FS demonstrate constrictive capsulitis, characterized by adhesions of synovial folds; obliteration of thejoint cavity; and a thickened, contracted capsule that eventually becomes fixed to the bone.3,13,18

EtiologyThe etiology of FS remains unknown. Lundberg16 andHelbig et al19 proposed primary and secondary classificationsfor cases that occur spontaneously and for those that resultfrom trauma. The primary, idiopathic cases are the mostcommon and the least understood. An unknown stimulusproduces profound histological changes in the capsule thatare substantially different from changes produced by immobilization or degeneration.9,16,18 Although a single critical stimulus has not been identified, a combination of host andextrinsic factors may precipitate primary FS. For example,the patient is usually between 40 and 60 years old and, basedon the greater incidence of cases occurring bilaterally ratherthan randomly in the general population, probably has aconstitutional predisposition for developing the condition.7,11,14,16 Extrinsic factors may include trauma, immobilization, certain diseases, and faulty body mechanics. 1416In contrast to the primary type of FS, secondary FS com monly develops after a variety of antecedent episodes, suchas central nervous system involvement, upper limb imm obilization, trauma to the arm, pulmonary cancer or infection,myocardial infarction, lengthy duration of intravenous infusion, cervical disk disease, rheumatoid arthritis, or diabetesmellitus.1,3,4,6,8,l0For secondary FS, Quigley hypothesized tha tminor trauma or an episode of inflammation may producepain, which eventually leads to disuse and the classical restriction ofmotion characterizing FS.17 Loyd and Loyd suggested

that secondary FS develops when painful spasm limits activityand creates dependency of the arm.1 The exact combinationM s. Wadsworth is Lecturer, Physical Therapy Education, College of M ed icine, TheUniversity of Iowa, Iowa City, IA 52242 (USA).1878 PHYSICAL THERAPY

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of factors that predispose certain persons to develop eitherprimary or secondary FS still eludes us .Epidemiology

The incidence of FS is slightly higher in women than inmen and is somewhat more common in the nondominantarm.7,13,16 This condition mos t frequently affects persons aged40 to 60 years and rarely occurs in persons younger than 40years of age.7,9,14,20,21 About 12% of persons affected developthe condition bilaterally, indicating a constitutional predisposition.9,11,16,18,22 The s ame shoulder rarely is affected s ubsequently.History and Diagno sis

The clinical manifestations of FS, whether primary or secondary, are consis tent. The typical presentation described inthe following paragraphs, therefore, should allow the clinicianto discern accurately true FS from other conditions that renderthe s houlder stiff and painful.The condition's onset is insidious and idiopathic in themajority of cases.1,9,14,21,23 Trauma and other factors that placethe patient at risk as previously described, however, are involved occasionally.* The natural history of FS follows aclassic cycle of "freezing," "frozen," and "thawing."26 Slow,spontaneous recovery of partial or complete function occurswithin one to three years. The initial s everity of the conditionhas no correlation with eventual recovery.19,23The patient's medical history may provide information thatwill enable the examiner to localize the lesion to the gleno-humeral joint. Initially, pain is the predominant feature ofthis disorder. M any patients describe an ons et of acute painthat often worsens during the first weeks or months. Unlikepain associated with many other musculoskeletal disturbances, such as tendinitis and degenerative joint disease, thepain of FS is present during both activity and rest. Patientsfrequently complain of having pain at night and of beingunable to sleep on the affected side, resulting in long-termsleep disturbances.7,10,11,23 As the condition progresses, painduring rest subsides, and discomfort occurs only during movement. Eventually, the pain abates spontaneously, but motionrestriction persists.8,23,26-28Pain is distributed vaguely in the deltoid muscle area. Itoften is worse anteriorly, but the only point of tenderness isover the bicipital groove.4,5 Pain sometimes radiates distallythroughout the C5 dermatome. Some patients also complainof proximal s oreness of the upper back and neck, a symptomprobably attributable to compensatory overuse of shouldergirdle muscles, such as the trapezius, rather than to referredpain from the shoulder. The nature of the pain varies from amild to severe ache.4,9 Arm movement that places the shoulderat the end of its limited range of motion aggravates suchsymptoms.Limitation of shoulder motion frequently is the symptomthat makes the patient seek medical attention. M otion oftenis restricted as early as two to three weeks after onset of thedisorder and continues to decline during the freezing s tage ofthe cycle.7,9 This restriction may impose severe functionallimitations on a patient.A physical examination conducted soon after the onset ofthe condition likely will reveal a patient who is very protective

of the involved limb. M otion is guarded, and the arm is heldagainst the body with the shoulder adducted and medially(internally) rotated.9 A patient may prefer wearing a sling tosupport the arm. Protective muscle spasm is a commonfeature. Functional activities (such as dressing or grooming)that require reaching overhead or behind the back may bedifficult or imposs ible because of the pain. Active and passivemovements are difficult to test because of pain and muscleguarding, which may impart an "empty end feel" to the endof the ROM (ie, the patient refuses to allow the joint to bemoved to where resistance is felt by the examiner).If the examiner assesses the patient after the pain hassubsided, then motion restriction will be the most predominant feature. The patient attempts to substitute scapularmovement for glenohumeral movement, producing a characteristic "girdle hunching maneuver." Disuse atrophy maybe evident in the rotator cuff and in the deltoid, biceps brachii,and triceps brachii muscles. Examination of the shouldercomplex reveals an inert tissue (capsular) lesion: Both activeand passive physiological movements may be restricted bypain at the end of the glenohumeral joint's ROM . Resistedmovements in the midrange usually are asymptomatic, however, leading the examiner to conclude that contractile tissuesare not involved. Such testing helps distinguish FS frombicipital and rotator cuff tendinitis, which may have s imilarsigns and symptoms, but they are markedly s ymptomatic withresisted rather than pass ive m ovement.

The limitation of passive ROM found in FS is characteristicof a capsular pattern; that is, lateral (external) rotation islimited more than abduction, which is limited more thanmedial rotation. During maximal capsular restriction, ROMmeasurements for the glenohumeral joint average 45 degreesof lateral rotation,1,17,23 less than 80 degrees of abduction,8,15,17,28 and less than 70 degrees of medial rotation.8,20Capsular contractures limit the range and, thus, produce acapsular end feel. With FS, a painful arc of glenohumeralmotion does not occur.Accessory glenohumeral movements also are limited, particularly anterior and inferior glide and lateral distraction. Areview of the involved anatomical structures will highlight thecorrelation between the anterior and inferior synovial andcapsular adhesions and the respective loss of gliding (Fig. 1).Also, the tightness in the anterior and inferior aspects of thecapsule correlates with the loss of physiological movementsof lateral rotation and abduction, respectively.

Palpation may reveal tenderness over the bicipital groove.The overlying tissues, otherwise, obscure further findings ofjoint capsule involvement. Neurologic testing for sensory andreflex changes is negative with FS unless underlying conditions exist. Because C5 segmental involvement frequentlyrefers symptoms to the shoulder, the therapist routinelyshould examine the cervical area as well. Neurologic testingmay reveal shoulder girdle weakness as a result of disuseatrophy in later stages of the disorder.

Arthrography is the standard diagnostic technique used toconfirm FS.3,919,26 This technique reveals at least a 50% reduction of shoulder joint volume and a box-like appearanceof the joint cavity.9,29 The shoulder joint volume capacity ofpatients with FS is only 5 to 10 mL, compared with 20 to 30mL for healthy shoulders.1,7,9,14,27,30,31 Other findings duringarthrography include a tight, thickened capsule 3,7,10,27; loss ofthe axillary recess, the subcoracoid folds, and the s ubscapularbursa1,3,19,21,16; and the absence of dye in the biceps tendonsheath (Fig. 1).27 Binder et al note that, although arthrography*1,3,8,10,11,14,24,25.tl,6-8,10,11,15,17,27.

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foramen ofWeitbrecht

glenohumeralligamentssubscapularismuscle

anteriorjointcapsule

axillary recess-

tendon of long head bicepsbrachii muscle

_ supraspinatusmuscle

infraspinatus muscleglenoid fossa

-teres minor muscle

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

is useful in the diagnosis of FS, arthrography findings do notindicate the type of onset (primary or secondary) or the rateor extent of recovery.29Radiography is more useful in ruling out other disordersthan in specifically diagnosing FS. Shoulder roentgenogramsof patients with FS, however, commonly reveal conditionssuch as osteoporosis,1,2,10,17,26 degenerative changes,10,29 decreased space between the acromion and humeral head,9,18,29calcium depos its,5,9,17 and cystic changes.9TREATMENTReview

Although FS is a self-limiting condition, it imposes suchmorbidity and lengthy recovery time that patients and clinicians alike seek treatment interventions. No standard treatment regimen, however, is accepted universally.Analgesics, such as salicylates and codeine compounds,often are used for pain relief.4,9,17 Oral anti-inflammatorymedications also may help to relieve pain and reduce theinflammatory reaction.9,17 M any m edical practitioners preferthe intra-articular injection of s teroids, accom panied by localanalgesics and gentle active motion, in the freezing stage ofFS.1,11,15,21,23 This treatment is reported to reverse the pain andfibrosis of FS.14,21,23 Hollingworth reported that injection of acorticosteroid directly into the anatomical site of the lesionproduced pain relief and at least 50% improvement in ROMin 26% of the cases studied.32 Conversely, Quigley17 andNeviaser3 do not believe that steroids can affect establishedscars, contractures, or adhesions , but Q uigley s tated that theymay reduce pain if administered in conjunction with manipulation. Quigley administered intravenous steroids to 26 patients (3 with bilaterally involved shoulders) whose shoulderswere manipulated under anesthesia; 10 of the shoulders re

gained painless, normal motion; 13 improved; and 6 wereunimproved.17 Weiser injected prednisolone into the shoulderjoints of 100 patients, then passively mobilized the joint andgave the patients a vigorous active home exercise program;78% obtained pain relief, and 61% regained normal function.15 In summary, local corticosteroid injections have beenused with various results but, generally, they produce a greatergain in motion recovery if given repeatedly in several sitesand if used in combination with exercises and heat therapy.14,15,33Infiltration debrisement has been used to improve functionin numerous cases, although the literature does not defineclearly when during the natural history of the condition it isperformed.4,5,8,30 This method consists of forcibly extendingthe joint capsule with the contrast material that is used forarthrographic procedures. Local anesthetics and ROM exercises may be com bined with infiltration debrisement to facilitate restoration o f m otion.For patients with residual motion deficits, manipulationunder anesthesia has been found useful by some.4,8,9,11,19,27While the patient is under general anesthesia, an assistantstabilizes the scapula, and an operator forcibly abducts thehumerus until the capsule tears. Some physicians supplementthe forced abduction with lateral and medial rotation manipulations, but others consider these manipulations too riskybecause of potential humeral fracture. This procedure resultsin freedom of motion by severing adhesions between thecapsule and humeral head and also intracapsular adhesions .27Extravasation of a contrast medium after manipulation readily demonstrates the extent of damage to the capsule.31 Toprevent the ruptured tissues from healing in their former stateof retraction, the arm must be abducted at least 90 degreesfor one to two weeks while the patient is recumbent. Tomaintain ROM , a physical therapist s hould institute an exer-

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rise program within 24 hours of the manipulation.3,17 Bate-man prefers to expose the joint surgically to avoid blindtearing of tissue when performing manipulation.18 M anipulation under anesthesia is not without risk, because tissues aretorn grossly and m ay develop further scarring. M anipulationalso increases the possibility of fractures, dislocation, andbrachial plexus injuries.5,27 Lundberg proposed that manipulation increases the rate of restoration of ROM but does notshorten the duration of the disease; however, intensive physical therapy after manipulation further increases the rate ofrestoration and also shortens the total duration.16Surgery is used as a last resort for patients who do notrespond to more conservative methods or for whom manipulation is contraindicated because of antecedent fracture,dislocation, or os teoporosis.3,4,8,9,17 Such surgery may involvedivision of the subscapularis tendon and the anteroinferiorjoint capsule17 or arthrotomy of the dependent axillary folds .3Few controlled studies that compare the effects of variousforms of physical therapy and medical treatment are reportedin the literature. Of the available studies, the following discuss ion offers s ome useful information. M ost of the studiesdo not provide details, however, regarding the stage of thedisease process, previous treatment, and etiological considerations (primary vs secondary). Selection or grouping of subjects based on these criteria would enhance the validity andreproducibility of the results.Nicholson compared the pain and hypomobility of onegroup, treated with passive joint mobilization and activeexercises, with that of a control group treated with activeexercises alone.25 The mobilization consisted of passive oscillatory movements of one articular surface against its counterpart. Nicholson found that pain decreased s ignificantly in themobilization group and not in controls. All motions (exceptmedial rotation in the control group) increased significantlyin both groups. The only statistically significant difference inmotion gained between groups was the increase in passiveabduction in the mobilization group.25Lee et al compared infrared irradiation plus active andresistive exercises, local injection of hydrocortisone acetateplus active and resistive exercises , and analgesics alone.33 Thegroups receiving exercises demonstrated a significant difference in motion gained (abduction, medial rotation, and lateralrotation) compared w ith the group receiving analgesics only,but no significant difference was s een between those receivingthe injection plus exercise and those receiving infrared irradiation plus exercise.Bulgen et al studied four groups of patients, all of whomperformed pendulum exercises.23 In addition, each groupreceived either intra-articular steroids, M aitland's mobilization, ice packs followed by proprioceptive neuromuscularfacilitation, or no additional treatment. All groups reportedan improvement in pain relief, with best results after fourweeks of treatment. The group that received the steroidsshowed the most marked initial improvement in movement,but no significant difference was seen between groups aftersix months of treatment.

Hamer and Kirk contrasted cryotherapy (using wet towelsand crushed ice) with ultrasound among patients who alsoreceived passive and active exercises.22 They found no signif-icant difference between the cryotherapy and ultrasound treatment results, although pain relief and arm m ovement in bothpatient groups improved.Rizk et al compared a group treated by heat modalities,active-assistive exercise, and rhythmic stabilization manipu

lation with a group treated by transcutaneous electrical nervestimulation plus pulley traction in abduction for up to twohours.14 Both groups gained ROM , but the TENS-tractiongroup gained a total of 138 degrees more m otion in all rangescombined than the heat-exercise-manipulation group. Thisgroup also achieved pain-free s leep after four to six weeks oftreatment, compared with the other group in which all patients gained pain-free s leep only after four to six m onths.Objectives

The studies cited have s hown that various forms of exerciseare effective in reducing the motion restriction and pain ofpatients with FS. Physical therapists, as specialists dealingwith exercise and movement dysfunction, play a major rolein restoring function to these persons. After performing thenecessary tests to confirm the diagnosis of FS, ascertain thecurrent s tatus of the condition, and identify causative factors,a physical therapist is prepared to design a treatment program.Each individual case will dictate whether physical therapy isto be used alone or in conjunction with other medical orsurgical treatment.The treatment objective in the early stage of the FS cycle is

to reduce the pain and inflammation. A combination ofexercise and physical modalities helps accomplish this objective. By moving tissues engorged with blood and inflammatory exudate, exercise stimulates circulation and resorption ofdebris. To interrupt the vicious cycle of pain and restrictedmotion, a therapist should instruct a patient to performactivity as vigorous as his condition will allow. 11 Active andactive-assistive exercises such as pedulum, wand, and physiologic ROM should be performed for at least one half-hourthree times a day. Supplementing active exercise, a therapistadministers daily passive physiological exercise (motion in arange that usually is achieved actively) or accessory exercise(motion between joint surfaces, which cannot be achievedactively), or both.34Passive exercise has multiple benefits. Gentle passive m ovement, short of pain and the pathologic limit of motion,reduces pain.35 Theoretically, this pain reduction occurs because of a neuromodulation effect on the mechanoreceptorswithin a join t.34 Often, reflex muscle spasm prevents a patientfrom performing active exercise, whereas a therapist canpassively guide the limb further into the range without eliciting spasm or a stretch reflex. Also, because m any patients arereluctant psychologically to perform regular, appropriate active exercise, passive exercise becomes the treatment ofchoice.20

Pain and inflammation also are reduced by physical agentssuch as iontophoresis and phonophoresis.36 Various ions withanalgesic and anti-inflammatory properties are transmittedinto the tissues to promote resolution of the condition. Theydecrease edema and help minimize the formation of fibrinousexudate, which may become a precursor of adhesions whencombined with imm obilization. Heat therapy modalities andultrasound reduce pain and muscle spasm. Electroacupressureand TENS also are effective in the management of acute andchronic musculoskeletal pain.36

The emphasis of treatment in the late s tage of the FS cycledeals with movement restriction. A physical therapist againuses a combination of exercise and physical modalities, whichin this stage are used to restore motion. M uscle stretching byphysiological and accessory movements now is performed atthe limit of the pathologic ROM . Functional use of the arm



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

Fig. 3. Caudal glide mobilization, at the end of restricted accessorymotion, used to treat stiffness.is encouraged in activities of daily living. A therapist may useheat to induce relaxation and ultrasound to increase tissueextensibility.36Because the use of passive movement may not be familiarto some, I will elaborate on this aspect oftreatment in boththe early and late stages ofFS. Typically, a patient with FSinitially might have agreater than 50% painful limitation ofactive and passive motion. Aphysical therapist would applyaccessory movem ent in a comfortable joint position, with theaffected arm supported in a loose-packed position (Fig. 2).The therapist administers slow, gentle oscillatory movementsin anterior-posterior and cephalad-caudad directions if theydo not increase pain or induce muscle spasm.35 The therapistreassesses physiological movements after each treatment.When 50% of the range is regained, in abduction for example,then passive physiological abduction motions are begun.35The therapist provides amechanical block to movement shortof the painful, restricted range and continues to use gentle,low-amplitude oscillations.As the condition progresses, the therapist may detect stiff-ness before or concurrently with the onset of pain. Thetherapist then should begin low-amplitude physiological andaccessory oscillations at the limit of the restriction.35 Toincrease abduction, for example, the therapist "takes up theslack" in the shoulder joint capsule with caudal glide andperforms more powerful oscillations at the end of the accessory range (Fig. 3). The therapist uses ventral and dorsalaccessory glides to increase lateral and medial rotation, re-

spectively, and lateral distraction to increase movement ingeneral. If the intense stretching at the end of the rangeproduces soreness, the therapist may help alleviate this byusing larger-amplitude oscillations to end the treatment. Asthe range increases, the therapist uses physiological treatmentmovements to enhance motion further. By assessing the patient's pain response and movement after each technique, thetherapist can determine results and plan subsequent treatments.When designing any treatment program, the therapist al-ways should consider the specific aspects of each individualcase. Different starting positions and combinations of movement may be used to obtain the desired results. For example,a patient with limited lateral rotation will have difficultyabducting his arm. The therapist, therefore, may assist abduction by passively gliding the humeral head inferiorly or anteriorly. In other cases, the therapist may need to stabilize thehumeral head passively to substitute for a weakened rotatorcuff while a patient attempts active or resistive arm movements. As another example of individual adaptation, thetherapist may facilitate some muscles selectively by properhand placement and resistance and by guiding the sequenceand direction of movement. Also, the therapist may addrhythmic stabilizationa simultaneous, isometric contraction of antagonistic muscle groups that produces relaxationand allows mobilization techniques to increase the limit ofmovement.37A strong case exists for prevention because no treatment iseffective consistently. Preventing prolonged immobilizationand avoiding trauma to the shoulder when dealing with otherlimb disorders may bemajor factors in reducing the incidenceof FS .8,9,10,13 Physical therapists should identify high-risk patients such as those with trauma or surgery involving theshoulder or chest, those w ith hemiplegia, and 40- to 60-year-olds undergoing prolonged hospitalization or immobilization.They must make a concerted effort to maintain shouldermotion in these patients by instructing them about upperextremity exercises and cautioning them to avoid furthershoulder trauma. If necessary, therapists should implement amore involved program, such as that described in the preceding paragraphs.CONCLUSION

Frozen shoulder is a discrete clinical diagnosis for painfulrestriction of shoulder motion that results from capsularfibrosis. Its etiology, although unclear, is associated with theinteraction of constitutional and extrinsic factors among patients who, notably, are between 40 and 60 years of age. Stagesof freezing, frozen, and thawing characterize the natural history of FS, and the condition is self-limiting within one tothree years. By applying appropriate treatment techniquesand modalities in a creative and judicious manner, the physical therapist can do much to enhance the speed and degreeof recovery from FS, More controlled studies, however, areneeded comparing the effects of different forms of treatment.REFERENCES

1 . Loyd JA, Loyd HM: Adhesive capsulitis of the shoulder: Arthrographicdiagnosis and treatment. South Med J 76:879-883, 19832. Bland JH, Merrit J A, Boushey DR: Painful shoulder. Semin Arthritis Rheum7:21-47, 19773. Neviaser JS : Adhesive capsulitis and the stiff and painful shoulder. OrthopClin North Am 1 1: 327-333, 19804. Post M (ed): The Shoulder: Surgical and Nonsurgical Management. Philadelphia, PA, Lea & Febiger, 1 978

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5. S imon WH: S oft t is s u e d is ord ers of th e s h ou ld er : F rozen s h o u ld er , calcif ictendin itis, and bicipital tend initis. Orthop Clin North A m 6:5 21-5 39, 19756. Bruckner FE, Nye CJ: A prospe ctive stud y Of adh esive capsulitis of theshoulder ("frozen shoulder") in a high risk population. Q J Med 50:191-2 0 4 , 19817. Kes s e l L, Bayley I, You n g A: T h e u p p er l imb: T h e froze n s h ou ld e r . Br JH o s p M e d 2 5 : 3 3 4 , 3 3 6 - 3 3 7 , 3 3 9 ; 1 9 8 18. Kozin F : T w o u n iq u e s h ou ld er d is ord ers : Ad h es iv e caps u l itis an d re f lexs ymp ath et ic d ys trop h y s yn d rome. Pos tgrad Med 73:207-210, 214-216;1 9 8 39. R izk T E, Pin als R S : F roz en s h ou ld er . S e min Arth ritis R h eu m 11:440-4 52,1 9 8 210 . Jays on Ml: F rozen s h ou ld er: Ad h es iv e cap s u l it is . Br Med J [C lin R es ]2 8 3 : 1 0 0 5 - 1 0 0 6 , 1 9 8 111 . Kay N R : T h e c l in ica l d iagn os is an d man agemen t of frozen s h ou ld ers .Pract it ion er 2 25:16 4-167 , 198112 . N ev ias er JS : Ad h es iv e cap s u l it is o f th e s h ou ld er: A s tu d y of th e p ath ological findings in periarthritis of the shoulder. J Bone Joint Surg 27:211-222,1 9 4 513 . Neviaser RJ: Painful conditions affecting the shoulder. Clin Orthop 173:63-6 9 , 1 9 8 314 . Rizk TE, Christopher RP, Pinals RS, et al: Adhesive capsulitis (frozens h ou ld er) : A n ew ap p roach to i ts man agemen t . Arch Ph ys Med R eh ab i l6 4 : 2 9 - 3 3 , 1 9 8 315 . Weiser HI: Painful primary frozen shoulder mobilization under local anesth es ia . Arch Ph ys Med R eh ab i l 58:406-408, 197716 . Lu n d b erg BJ: T h e frozen s h ou ld er . Acta Orth op S can d [S u p p l] 119:5-59,196817 . Qu igley T B: C h eck re in s h ou ld er: A typ e of " frozen " s h ou ld er: D iagn os isan d treatmen t b y man ip u lat ion an d AC T H or co rt is on e . C l in Orth op 16 4:4-9, 198218 . Bateman JE: T h e S h ou ld er an d N eck , ed 2 . Ph ilad e lph ia , PA, W B S au n d ersCo . 1 9 7 819 . Helbig B, Wagner P, Dohler R: Mobilization of frozen shoulder undergen era l an aes th es ia . Acta Orth op Be lg 49:267-274, 198320 . Clark GR, Willis LA, Fish WW , et al: Preliminary stud ies in measuring ran geof motion in normal and painful stiff shoulders. Rheumatol Rehabil 14:39-46 , 19752 1 . Weiss JJ, Ting YM: Arthrography-assisted intra-articular injection of steroid s in t reatmen t of ad h es iv e cap s u l it is . Arch P h ys Med R eh abi l 59:2 85-2 8 7 , 1978

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

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