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Frozen Shoulder
Carolyn T Wadsworth
PHYS THER. 1986; 66:1878-1883.
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Anatomy and Physiology: Musculoskeletal System
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Injuries and Conditions: Shoulder
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Frozen Shoulder
CAROLYN T. WADSWORTH
Widespread use of the label "frozen shoulder" as a diagnosis for any stiff and
painful shoulder condition has led to its becoming a rather meaningless, catchall
term. In addition to confounding both the lay public and health care professionals,
this indiscriminate labeling may prevent a patient from receiving appropriate
treatment. In this article, I define frozen shoulder and review its pathologic and
etiologic factors, epidemiology, natural history, and diagnosis. I present this
information in correlation with an examination process to assist physical therapists in identifying suspected cases of frozen shoulder. I also present the current
options for treatment, including physical therapy management with physical
agents and exercise.
Key Words: Pain, Physical therapy, Shoulder.
Frozen shoulder (FS) is a distinct clinical entity with characteristic clinical and arthrographic findings.1 The purpose of
this article is to describe the pathologic factors, natural history,
signs, and symptoms of FS that clearly distinguish it from
other disorders that produce shoulder stiffness and pain. This
information should assist the clinician in identifying true cases
of FS (synonymously termed adhesive capsulitis) and labeling
them appropriately.
This article details the various methods of treating FS,
although an extensive review of the literature revealed no
agreement on any one method. It also summarizes the few
reported studies comparing the efficacy of different treatments, including physical therapy. Finally, it proposes a physical therapy plan of management, which a therapist monitors
and modifies as a patient's status changes during the natural
course of this disorder.
HISTORICAL PERSPECTIVE
Painful restriction of shoulder motion is one of the most
common and disabling orthopedic disorders for which patients seek treatment.2-5 The specific type of restriction that
we recognize today as FS has been reported in medical literature for over 100 years. Duplay referred to FS in 1872 as
"scapulohumeral periarthritis," a disorder he believed resulted
from subacromial bursitis.3,6-9 Pasteur later referred to the
same condition as "tenobursite," which he attributed to bicipital tendinitis.4,9 In 1934, Codman coined the term "frozen
shoulder" but used it in association with tendinitis of the
rotator cuff.7 Although these early practitioners described
some of the clinical characteristics of FS, they did not identify
accurately the site of the pathological condition as it is understood today. In 1945, Neviaser introduced the concept of
adhesive capsulitis when he discovered that the capsule was
tight, thickened, and stuck to the humerus in such a manner
that it could be peeled off like "adhesive plaster from the
skin."1,4-6,10-14 Current doctrine supports Neviaser's theory
that the capsule is the site of the lesion and lends credence to
the synonymous use of the terms adhesive capsulitis and
frozen shoulder.3,6,8,10,11,14
Ms. Wadsworth is Lecturer, Physical Therapy Education, College of Medicine, The University of Iowa, Iowa City, IA 52242 (USA).
Definition and Pathology
Frozen shoulder typically is referred to as the spontaneous
onset of gradually progressive shoulder pain and severe limitation of movement.1,5,7,8,14,15 Features of this pathologic condition include microscopic evidence of chronic capsular inflammation with fibrosis and perivascular infiltration.3,5,14
Although several researchers found no evidence of inflammation, they concurred thatfibrosisexists in the capsule.14,16,17
Chronic cases of FS demonstrate constrictive capsulitis, characterized by adhesions of synovial folds; obliteration of the
joint cavity; and a thickened, contracted capsule that eventually becomes fixed to the bone.3,13,18
Etiology
The etiology of FS remains unknown. Lundberg16 and
Helbig et al19 proposed primary and secondary classifications
for cases that occur spontaneously and for those that result
from trauma. The primary, idiopathic cases are the most
common and the least understood. An unknown stimulus
produces profound histological changes in the capsule that
are substantially different from changes produced by immobilization or degeneration.9,16,18 Although a single critical stimulus has not been identified, a combination of host and
extrinsic factors may precipitate primary FS. For example,
the patient is usually between 40 and 60 years old and, based
on the greater incidence of cases occurring bilaterally rather
than randomly in the general population, probably has a
constitutional predisposition for developing the condition.7,11,14,16 Extrinsic factors may include trauma, immobilization, certain diseases, and faulty body mechanics.1416
In contrast to the primary type of FS, secondary FS commonly develops after a variety of antecedent episodes, such
as central nervous system involvement, upper limb immobilization, trauma to the arm, pulmonary cancer or infection,
myocardial infarction, lengthy duration of intravenous infusion, cervical disk disease, rheumatoid arthritis, or diabetes
mellitus.1,3,4,6,8,l0For secondary FS, Quigley hypothesized that
minor trauma or an episode of inflammation may produce
pain, which eventually leads to disuse and the classical restriction of motion characterizing FS.17 Loyd and Loyd suggested
that secondary FS develops when painful spasm limits activity
and creates dependency of the arm.1 The exact combination
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PHYSICAL THERAPY
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of factors that predispose certain persons to develop either
primary or secondary FS still eludes us.
Epidemiology
The incidence of FS is slightly higher in women than in
men and is somewhat more common in the nondominant
arm.7,13,16 This condition most frequently affects persons aged
40 to 60 years and rarely occurs in persons younger than 40
years of age.7,9,14,20,21 About 12% of persons affected develop
the condition bilaterally, indicating a constitutional predisposition.9,11,16,18,22 The same shoulder rarely is affected subsequently.
History and Diagnosis
The clinical manifestations of FS, whether primary or secondary, are consistent. The typical presentation described in
the following paragraphs, therefore, should allow the clinician
to discern accurately true FS from other conditions that render
the shoulder stiff and painful.
The condition's onset is insidious and idiopathic in the
majority of cases.1,9,14,21,23 Trauma and other factors that place
the patient at risk as previously described, however, are involved occasionally.* The natural history of FS follows a
classic cycle of "freezing," "frozen," and "thawing."26 Slow,
spontaneous recovery of partial or complete function occurs
within one to three years.† The initial severity of the condition
has no correlation with eventual recovery.19,23
The patient's medical history may provide information that
will enable the examiner to localize the lesion to the glenohumeral joint. Initially, pain is the predominant feature of
this disorder. Many patients describe an onset of acute pain
that often worsens during the first weeks or months. Unlike
pain associated with many other musculoskeletal disturbances, such as tendinitis and degenerative joint disease, the
pain of FS is present during both activity and rest. Patients
frequently complain of having pain at night and of being
unable to sleep on the affected side, resulting in long-term
sleep disturbances.7,10,11,23 As the condition progresses, pain
during rest subsides, and discomfort occurs only during movement. Eventually, the pain abates spontaneously, but motion
restriction persists.8,23,26-28
Pain is distributed vaguely in the deltoid muscle area. It
often is worse anteriorly, but the only point of tenderness is
over the bicipital groove.4,5 Pain sometimes radiates distally
throughout the C5 dermatome. Some patients also complain
of proximal soreness of the upper back and neck, a symptom
probably attributable to compensatory overuse of shoulder
girdle muscles, such as the trapezius, rather than to referred
pain from the shoulder. The nature of the pain varies from a
mild to severe ache.4,9 Arm movement that places the shoulder
at the end of its limited range of motion aggravates such
symptoms.
Limitation of shoulder motion frequently is the symptom
that makes the patient seek medical attention. Motion often
is restricted as early as two to three weeks after onset of the
disorder and continues to decline during the freezing stage of
the cycle.7,9 This restriction may impose severe functional
limitations on a patient.
A physical examination conducted soon after the onset of
the condition likely will reveal a patient who is very protective
*1,3,8,10,11,14,24,25.
tl,6-8,10,11,15,17,27.
of the involved limb. Motion is guarded, and the arm is held
against the body with the shoulder adducted and medially
(internally) rotated.9 A patient may prefer wearing a sling to
support the arm. Protective muscle spasm is a common
feature. Functional activities (such as dressing or grooming)
that require reaching overhead or behind the back may be
difficult or impossible because of the pain. Active and passive
movements are difficult to test because of pain and muscle
guarding, which may impart an "empty end feel" to the end
of the ROM (ie, the patient refuses to allow the joint to be
moved to where resistance is felt by the examiner).
If the examiner assesses the patient after the pain has
subsided, then motion restriction will be the most predominant feature. The patient attempts to substitute scapular
movement for glenohumeral movement, producing a characteristic "girdle hunching maneuver." Disuse atrophy may
be evident in the rotator cuff and in the deltoid, biceps brachii,
and triceps brachii muscles. Examination of the shoulder
complex reveals an inert tissue (capsular) lesion: Both active
and passive physiological movements may be restricted by
pain at the end of the glenohumeral joint's ROM. Resisted
movements in the midrange usually are asymptomatic, however, leading the examiner to conclude that contractile tissues
are not involved. Such testing helps distinguish FS from
bicipital and rotator cuff tendinitis, which may have similar
signs and symptoms, but they are markedly symptomatic with
resisted rather than passive movement.
The limitation of passive ROM found in FS is characteristic
of a capsular pattern; that is, lateral (external) rotation is
limited more than abduction, which is limited more than
medial rotation. During maximal capsular restriction, ROM
measurements for the glenohumeral joint average 45 degrees
of lateral rotation,1,17,23 less than 80 degrees of abduction,8,15,17,28 and less than 70 degrees of medial rotation.8,20
Capsular contractures limit the range and, thus, produce a
capsular end feel. With FS, a painful arc of glenohumeral
motion does not occur.
Accessory glenohumeral movements also are limited, particularly anterior and inferior glide and lateral distraction. A
review of the involved anatomical structures will highlight the
correlation between the anterior and inferior synovial and
capsular adhesions and the respective loss of gliding (Fig. 1).
Also, the tightness in the anterior and inferior aspects of the
capsule correlates with the loss of physiological movements
of lateral rotation and abduction, respectively.
Palpation may reveal tenderness over the bicipital groove.
The overlying tissues, otherwise, obscure further findings of
joint capsule involvement. Neurologic testing for sensory and
reflex changes is negative with FS unless underlying conditions exist. Because C5 segmental involvement frequently
refers symptoms to the shoulder, the therapist routinely
should examine the cervical area as well. Neurologic testing
may reveal shoulder girdle weakness as a result of disuse
atrophy in later stages of the disorder.
Arthrography is the standard diagnostic technique used to
confirm FS.3,919,26 This technique reveals at least a 50% reduction of shoulder joint volume and a box-like appearance
of the joint cavity.9,29 The shoulder joint volume capacity of
patients with FS is only 5 to 10 mL, compared with 20 to 30
mL for healthy shoulders.1,7,9,14,27,30,31 Other findings during
arthrography include a tight, thickened capsule3,7,10,27; loss of
the axillary recess, the subcoracoid folds, and the subscapular
bursa1,3,19,21,16; and the absence of dye in the biceps tendon
sheath (Fig. 1).27 Binder et al note that, although arthrography
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tendon of long head biceps
brachii muscle
foramen of
Weitbrecht
_ supraspinatus
muscle
glenohumeral
ligaments
subscapularis
muscle
infraspinatus muscle
glenoid fossa
anterior
joint
capsule
-teres minor muscle
axillary recess-
Fig. 1. The glenoid cavity with surrounding labrum and fibrous capsule. Adhesions of the anterior capsule and axillary recess limit anterior and
inferior glide of the humeral head on the glenoid fossa surface.
is useful in the diagnosis of FS, arthrography findings do not
indicate the type of onset (primary or secondary) or the rate
or extent of recovery.29
Radiography is more useful in ruling out other disorders
than in specifically diagnosing FS. Shoulder roentgenograms
of patients with FS, however, commonly reveal conditions
such as osteoporosis,1,2,10,17,26 degenerative changes,10,29 decreased space between the acromion and humeral head,9,18,29
calcium deposits,5,9,17 and cystic changes.9
TREATMENT
Review
Although FS is a self-limiting condition, it imposes such
morbidity and lengthy recovery time that patients and clinicians alike seek treatment interventions. No standard treatment regimen, however, is accepted universally.
Analgesics, such as salicylates and codeine compounds,
often are used for pain relief.4,9,17 Oral anti-inflammatory
medications also may help to relieve pain and reduce the
inflammatory reaction.9,17 Many medical practitioners prefer
the intra-articular injection of steroids, accompanied by local
analgesics and gentle active motion, in the freezing stage of
FS.1,11,15,21,23 This treatment is reported to reverse the pain and
fibrosis of FS.14,21,23 Hollingworth reported that injection of a
corticosteroid directly into the anatomical site of the lesion
produced pain relief and at least 50% improvement in ROM
in 26% of the cases studied.32 Conversely, Quigley17 and
Neviaser3 do not believe that steroids can affect established
scars, contractures, or adhesions, but Quigley stated that they
may reduce pain if administered in conjunction with manipulation. Quigley administered intravenous steroids to 26 patients (3 with bilaterally involved shoulders) whose shoulders
were manipulated under anesthesia; 10 of the shoulders re-
gained painless, normal motion; 13 improved; and 6 were
unimproved.17 Weiser injected prednisolone into the shoulder
joints of 100 patients, then passively mobilized the joint and
gave the patients a vigorous active home exercise program;
78% obtained pain relief, and 61% regained normal function.15 In summary, local corticosteroid injections have been
used with various results but, generally, they produce a greater
gain in motion recovery if given repeatedly in several sites
and if used in combination with exercises and heat therapy.14,15,33
Infiltration debrisement has been used to improve function
in numerous cases, although the literature does not define
clearly when during the natural history of the condition it is
performed.4,5,8,30 This method consists of forcibly extending
the joint capsule with the contrast material that is used for
arthrographic procedures. Local anesthetics and ROM exercises may be combined with infiltration debrisement to facilitate restoration of motion.
For patients with residual motion deficits, manipulation
under anesthesia has been found useful by some.4,8,9,11,19,27
While the patient is under general anesthesia, an assistant
stabilizes the scapula, and an operator forcibly abducts the
humerus until the capsule tears. Some physicians supplement
the forced abduction with lateral and medial rotation manipulations, but others consider these manipulations too risky
because of potential humeral fracture. This procedure results
in freedom of motion by severing adhesions between the
capsule and humeral head and also intracapsular adhesions.27
Extravasation of a contrast medium after manipulation readily demonstrates the extent of damage to the capsule.31 To
prevent the ruptured tissues from healing in their former state
of retraction, the arm must be abducted at least 90 degrees
for one to two weeks while the patient is recumbent. To
maintain ROM, a physical therapist should institute an exer-
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rise program within 24 hours of the manipulation.3,17 Bateman prefers to expose the joint surgically to avoid blind
tearing of tissue when performing manipulation.18 Manipulation under anesthesia is not without risk, because tissues are
torn grossly and may develop further scarring. Manipulation
also increases the possibility of fractures, dislocation, and
brachial plexus injuries.5,27 Lundberg proposed that manipulation increases the rate of restoration of ROM but does not
shorten the duration of the disease; however, intensive physical therapy after manipulation further increases the rate of
restoration and also shortens the total duration.16
Surgery is used as a last resort for patients who do not
respond to more conservative methods or for whom manipulation is contraindicated because of antecedent fracture,
dislocation, or osteoporosis.3,4,8,9,17 Such surgery may involve
division of the subscapularis tendon and the anteroinferior
joint capsule17 or arthrotomy of the dependent axillary folds.3
Few controlled studies that compare the effects of various
forms of physical therapy and medical treatment are reported
in the literature. Of the available studies, the following discussion offers some useful information. Most of the studies
do not provide details, however, regarding the stage of the
disease process, previous treatment, and etiological considerations (primary vs secondary). Selection or grouping of subjects based on these criteria would enhance the validity and
reproducibility of the results.
Nicholson compared the pain and hypomobility of one
group, treated with passive joint mobilization and active
exercises, with that of a control group treated with active
exercises alone.25 The mobilization consisted of passive oscillatory movements of one articular surface against its counterpart. Nicholson found that pain decreased significantly in the
mobilization group and not in controls. All motions (except
medial rotation in the control group) increased significantly
in both groups. The only statistically significant difference in
motion gained between groups was the increase in passive
abduction in the mobilization group.25
Lee et al compared infrared irradiation plus active and
resistive exercises, local injection of hydrocortisone acetate
plus active and resistive exercises, and analgesics alone.33 The
groups receiving exercises demonstrated a significant difference in motion gained (abduction, medial rotation, and lateral
rotation) compared with the group receiving analgesics only,
but no significant difference was seen between those receiving
the injection plus exercise and those receiving infrared irradiation plus exercise.
Bulgen et al studied four groups of patients, all of whom
performed pendulum exercises.23 In addition, each group
received either intra-articular steroids, Maitland's mobilization, ice packs followed by proprioceptive neuromuscular
facilitation, or no additional treatment. All groups reported
an improvement in pain relief, with best results after four
weeks of treatment. The group that received the steroids
showed the most marked initial improvement in movement,
but no significant difference was seen between groups after
six months of treatment.
Hamer and Kirk contrasted cryotherapy (using wet towels
and crushed ice) with ultrasound among patients who also
received passive and active exercises.22 They found no significant difference between the cryotherapy and ultrasound treatment results, although pain relief and arm movement in both
patient groups improved.
Rizk et al compared a group treated by heat modalities,
active-assistive exercise, and rhythmic stabilization manipu-
lation with a group treated by transcutaneous electrical nerve
stimulation plus pulley traction in abduction for up to two
hours.14 Both groups gained ROM, but the TENS-traction
group gained a total of 138 degrees more motion in all ranges
combined than the heat-exercise-manipulation group. This
group also achieved pain-free sleep after four to six weeks of
treatment, compared with the other group in which all patients gained pain-free sleep only after four to six months.
Objectives
The studies cited have shown that various forms of exercise
are effective in reducing the motion restriction and pain of
patients with FS. Physical therapists, as specialists dealing
with exercise and movement dysfunction, play a major role
in restoring function to these persons. After performing the
necessary tests to confirm the diagnosis of FS, ascertain the
current status of the condition, and identify causative factors,
a physical therapist is prepared to design a treatment program.
Each individual case will dictate whether physical therapy is
to be used alone or in conjunction with other medical or
surgical treatment.
The treatment objective in the early stage of the FS cycle is
to reduce the pain and inflammation. A combination of
exercise and physical modalities helps accomplish this objective. By moving tissues engorged with blood and inflammatory exudate, exercise stimulates circulation and resorption of
debris. To interrupt the vicious cycle of pain and restricted
motion, a therapist should instruct a patient to perform
activity as vigorous as his condition will allow.11 Active and
active-assistive exercises such as pedulum, wand, and physiologic ROM should be performed for at least one half-hour
three times a day. Supplementing active exercise, a therapist
administers daily passive physiological exercise (motion in a
range that usually is achieved actively) or accessory exercise
(motion between joint surfaces, which cannot be achieved
actively), or both.34
Passive exercise has multiple benefits. Gentle passive movement, short of pain and the pathologic limit of motion,
reduces pain.35 Theoretically, this pain reduction occurs because of a neuromodulation effect on the mechanoreceptors
within a joint.34 Often, reflex muscle spasm prevents a patient
from performing active exercise, whereas a therapist can
passively guide the limb further into the range without eliciting spasm or a stretch reflex. Also, because many patients are
reluctant psychologically to perform regular, appropriate active exercise, passive exercise becomes the treatment of
choice.20
Pain and inflammation also are reduced by physical agents
such as iontophoresis and phonophoresis.36 Various ions with
analgesic and anti-inflammatory properties are transmitted
into the tissues to promote resolution of the condition. They
decrease edema and help minimize the formation of fibrinous
exudate, which may become a precursor of adhesions when
combined with immobilization. Heat therapy modalities and
ultrasound reduce pain and muscle spasm. Electroacupressure
and TENS also are effective in the management of acute and
chronic musculoskeletal pain.36
The emphasis of treatment in the late stage of the FS cycle
deals with movement restriction. A physical therapist again
uses a combination of exercise and physical modalities, which
in this stage are used to restore motion. Muscle stretching by
physiological and accessory movements now is performed at
the limit of the pathologic ROM. Functional use of the arm
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1881
Fig. 2. Gentle cephalad-caudad mobilization, short of pain or motion
restriction, used to treat pain.
Fig. 3. Caudal glide mobilization, at the end of restricted accessory
motion, used to treat stiffness.
is encouraged in activities of daily living. A therapist may use
heat to induce relaxation and ultrasound to increase tissue
extensibility.36
Because the use of passive movement may not be familiar
to some, I will elaborate on this aspect of treatment in both
the early and late stages of FS. Typically, a patient with FS
initially might have a greater than 50% painful limitation of
active and passive motion. A physical therapist would apply
accessory movement in a comfortable joint position, with the
affected arm supported in a loose-packed position (Fig. 2).
The therapist administers slow, gentle oscillatory movements
in anterior-posterior and cephalad-caudad directions if they
do not increase pain or induce muscle spasm.35 The therapist
reassesses physiological movements after each treatment.
When 50% of the range is regained, in abduction for example,
then passive physiological abduction motions are begun.35
The therapist provides a mechanical block to movement short
of the painful, restricted range and continues to use gentle,
low-amplitude oscillations.
As the condition progresses, the therapist may detect stiffness before or concurrently with the onset of pain. The
therapist then should begin low-amplitude physiological and
accessory oscillations at the limit of the restriction.35 To
increase abduction, for example, the therapist "takes up the
slack" in the shoulder joint capsule with caudal glide and
performs more powerful oscillations at the end of the accessory range (Fig. 3). The therapist uses ventral and dorsal
accessory glides to increase lateral and medial rotation, re-
spectively, and lateral distraction to increase movement in
general. If the intense stretching at the end of the range
produces soreness, the therapist may help alleviate this by
using larger-amplitude oscillations to end the treatment. As
the range increases, the therapist uses physiological treatment
movements to enhance motion further. By assessing the patient's pain response and movement after each technique, the
therapist can determine results and plan subsequent treatments.
When designing any treatment program, the therapist always should consider the specific aspects of each individual
case. Different starting positions and combinations of movement may be used to obtain the desired results. For example,
a patient with limited lateral rotation will have difficulty
abducting his arm. The therapist, therefore, may assist abduction by passively gliding the humeral head inferiorly or anteriorly. In other cases, the therapist may need to stabilize the
humeral head passively to substitute for a weakened rotator
cuff while a patient attempts active or resistive arm movements. As another example of individual adaptation, the
therapist may facilitate some muscles selectively by proper
hand placement and resistance and by guiding the sequence
and direction of movement. Also, the therapist may add
rhythmic stabilization—a simultaneous, isometric contraction of antagonistic muscle groups that produces relaxation
and allows mobilization techniques to increase the limit of
movement.37
A strong case exists for prevention because no treatment is
effective consistently. Preventing prolonged immobilization
and avoiding trauma to the shoulder when dealing with other
limb disorders may be major factors in reducing the incidence
of FS.8,9,10,13 Physical therapists should identify high-risk patients such as those with trauma or surgery involving the
shoulder or chest, those with hemiplegia, and 40- to 60-yearolds undergoing prolonged hospitalization or immobilization.
They must make a concerted effort to maintain shoulder
motion in these patients by instructing them about upper
extremity exercises and cautioning them to avoid further
shoulder trauma. If necessary, therapists should implement a
more involved program, such as that described in the preceding paragraphs.
CONCLUSION
Frozen shoulder is a discrete clinical diagnosis for painful
restriction of shoulder motion that results from capsular
fibrosis. Its etiology, although unclear, is associated with the
interaction of constitutional and extrinsic factors among patients who, notably, are between 40 and 60 years of age. Stages
of freezing, frozen, and thawing characterize the natural history of FS, and the condition is self-limiting within one to
three years. By applying appropriate treatment techniques
and modalities in a creative and judicious manner, the physical therapist can do much to enhance the speed and degree
of recovery from FS, More controlled studies, however, are
needed comparing the effects of different forms of treatment.
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Volume 66 / Number 12, December 1986
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1883
Frozen Shoulder
Carolyn T Wadsworth
PHYS THER. 1986; 66:1878-1883.
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