Shoulder Pain in Patients with Hemiplegia - Physical Therapy

Shoulder Pain in Patients with Hemiplegia : A
Literature Review
Judy Griffin and Gay Reddin
PHYS THER. 1981; 61:1041-1045.
The online version of this article, along with updated information and
services, can be found online at:
http://ptjournal.apta.org/content/61/7/1041
Collections
e-Letters
This article, along with others on similar topics, appears
in the following collection(s):
Hemiplegia/Paraplegia/Quadriplegia
Injuries and Conditions: Shoulder
To submit an e-Letter on this article, click here or click on
"Submit a response" in the right-hand menu under
"Responses" in the online version of this article.
E-mail alerts Sign up here to receive free e-mail alerts
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013

Shoulder Pain in Patients with Hemiplegia
A Literature Review
JUDY GRIFFIN, MS,
and GAY REDDIN, BS
The primary cause of hemiplegic shoulder pain remains elusive, making prevention
and effective management difficult. Several possible causes are discussed,
such as passive exercise, subluxation, and shoulder-hand syndrome. Treatment
considerations and suggestions for clinical research are presented.
Key Words: Hemiplegia, Shoulder joint, Pain.
Shoulder pain is a serious and frequent complication
in patients with hemiplegia. The incidence has
been reported as high as 70 percent 1 and 84 percent 2
in patients suffering from a cerebrovascular accident
(CVA). Complaints of pain usually occur when passive
motion is attempted at the shoulder joint, but in
severe cases the patient has pain at rest. Painful,
limited joint range of motion (ROM) interferes with
use of the limb in functional activities and prevents
the patient's full participation in rehabilitation. 3
Under normal circumstances, pain-sensitive soft
tissue surrounding the glenohumeral joint (GHJ)—
rotator cuff, joint capsule, subacromial bursa, and
biceps brachii tendon—is subject to many stresses.
Gravity provides traction stress, and GHJ flexion and
abduction movements create friction-compression
stress between the humeral head and coracoacromial
liagment. 4 Hemiplegia may produce additional
stresses of paralysis, sensory and perceptual deficits,
and abnormal tone. Cailliet has observed that latent
tendinitis and bursitis symptoms may become activated
during hemiplegia. 5
The primary cause of hemiplegic shoulder pain has
never been identified. However, a variety of causative
agents has been suggested by authorities, including
improper passive movement, spasticity, contractures,
GHJ subluxation, and shoulder-hand syndrome. The
purposes of this article are to review the literature
concerning possible causes of the pain, propose man­
Ms. Griffin is Assistant Professor, The University of Tennessee
Center for the Health Sciences, Department of Physical Therapy,
Memphis, TN, and Research Coordinator for Physical Medicine and
Rehabilitation, St. Francis Hospital, 5959 Park Ave, Memphis, TN
38117 (USA).
Ms. Reddin is Senior Physical Therapist, Stroke Unit and Geriatrics,
Baptist Memorial Hospital—Lamar Unit, 1025 E. H. Crump
Blvd, Memphis, TN 38104.
This article was submitted May 26, 1980, and accepted December
9, 1980.
Volume 61 / Number 7, July 1981
agement considerations, and identify areas needing
clinical research.
LITERATURE REVIEW
Handling Techniques
Handling of the affected arm, during such activities
as exercise, positioning, and transfers, constitutes a
potential strain upon the GHJ. For complete GHJ
abduction to occur without compression of suprahumeral
soft tissue, the scapula must upwardly rotate
and the humeral head must depress and externally
rotate. During passive exercise, if abduction of the
paralyzed shoulder is performed without attention to
this fact, compression trauma to capsule, bursa, or
tendon may result. 4 Persons changing position of the
unconscious patient may inadvertently apply traction
to the flaccid arm, traumatizing periarticular tissue. 3
Also, sensory deficits may facilitate rough handling
of the paralyzed arm by relatives, hospital personnel,
or the patient himself.
Rotator cuff injury has been cited as a cause of
hemiplegic shoulder pain. Using arthrogram studies
with 32 hemiplegic patients, Najenson and associates
found that 40 percent had rupture of the rotator cuff
and that 10 of 11 patients with severe shoulder pain
had rupture of the rotator cuff. 2 None of the patients
had a history of shoulder dysfunction prior to the
onset of hemiplegia. The precipitating cause of the
rotator cuff tear was identified as forced humeral
abduction without external rotation, although other
possible contributing causes such as subluxation and
aging changes in the rotator cuff were mentioned.
"Especially contraindicated, from our point of view,
is the passive abduction performed in the physiotherapy
department by the patients themselves, using
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013
1041

pulleys to produce abduction in the glenohumeral
joint through traction with the unaffected arm. ,,2 Voss
has also stated that the use of overhead pulleys can
produce shoulder pain. 6
Other investigators have implied that physical therapy
may contribute to painful, limited shoulder motion.
In a long-term study of 107 severely disabled
hemiplegic patients receiving physical therapy,
Brocklehurst and associates found that stiff and painful
shoulders were present in 21 patients by two weeks
postonset and had developed in 37 additional patients
by one year postonset. 7 "Disappointingly, painful
limitation of shoulder movement was not affected by
the amount of physiotherapy given or the time at
which it was started." 7 However, there was no control
group for comparison in that study, and the severity
of joint pain and limitation of motion were not described.
Spasticity, Flaccidity, and Contractures
Immediately following an upper motor neuron lesion
such as a CVA, the affected extremities become
flaccid in approximately 90 percent of cases. 8 Flaccidity
usually lasts a short time and is replaced by a
predictable pattern of spasticity within 12 to 18
months. 9 In the shoulder girdle, spasticity develops in
muscle groups producing scapular retraction-depression
and humeral adduction-internal rotation. 9,10
There is wide agreement among experts that such
spasticity interferes with the normal scapulohumeral
rhythm necessary during GHJ abduction; therefore,
passive elevation of the spastic shoulder causes soft
tissue compression and pain if proper attention is not
given to scapular mobilization and humeral external
rotation. 9-11
The presence of spasticity increases the likelihood
of contractures. 12 Once contractures develop, a cycle
is established in which attempts to stretch the contracture
cause pain, generating reflex protective
spasm of the contracted muscles and patient apprehension
and hostility. 11 Consequently, increasingly
greater limitations of passive ROM, reduced active
motion, disuse atrophy, and osteoporosis result. 5
Flaccidity and spasticity have each been named as
the cause of hemiplegic shoulder pain. Tobis states
that the typical clinical picture of hemiplegic shoulder
pain includes flaccid, paralyzed, and atrophic shoulder
musculature, with GHJ subluxation. 13 Conversely,
Bobath states that shoulder pain does not
become a problem until spasticity develops. 14 Other
investigators have noted that hemiplegic patients with
spastic shoulder girdle musculature more frequently
complain of pain than do patients who have flaccidity.
1, 15 The relative incidence of flaccidity versus spasticity
in patients with hemiplegic shoulder pain is not
well documented in the literature.
Subluxation
The incidence of GHJ subluxation has been reported
as high as 81 percent in patients with hemiplegia.
2 Many authorities maintain that such GHJ
malalignment is the main cause of shoulder
pain. 12,13,16,17 However, others discount any relationship
between pain and subluxation. Johnstone states,
"The flaccid or hypotonic hanging shoulder will sublux
but this is not a factor to which any undue concern
ought to be given. ,,9 Bobath maintains that subluxation
is not painful as long as the scapula is mobile, 10
and Mossman suggests that subluxation is harmless
as long as passive ROM is not painful. 12
Although several investigators have reported the
incidence of GHJ subluxation, few have documented
the relationship between pain and subluxation. An
exception is Najenson and associates' classical study
of associations among hemiplegic patients' shoulder
pain, rupture of the rotator cuff, and GHJ subluxation.
In that study, 25 of the 26 patients with GHJ
subluxation also had moderate or severe pain. 2 Subluxation
would therefore appear to be strongly associated
with shoulder pain. According to Tobis, the
traction forces present in GHJ subluxation may contribute
to rotator cuff tears. 13 All of Najenson and
associates' 13 hemiplegic patients with documented
rupture of the rotator cuff had GHJ malalignment. 2
The relationship between GHJ subluxation and
abnormal tone is unclear. Miglietta and associates
reported finding no relationship between subluxation
and spasticity. 16 Many authorities suggest that subluxation
is caused by spasticity in muscles that depress
the humerus and downwardly rotate the scapula. 5,10
On the other hand, some evidence exists that spasticity
may actually reduce subluxation; apparently, hyperactive
stretch reflexes can be stimulated by the
weight of the unsupported arm during ambulation,
causing temporary reduction of subluxation. 1819
However, flaccidity may be the characteristic state
during the subluxation process. According to this
viewpoint, gravitational pull unopposed by flaccid
shoulder musculature produces painful and possibly
irreversible overstretching of superior joint capsule
and supraspinatus muscle. 13,16
Subluxation appears to develop in the first few
weeks following hemiplegia. Investigating the relationship
of supraspinatus muscle activity to the onset
of GHJ subluxation, Chaco and Wolf performed
EMG studies on 40 patients at four- and eight-week
intervals after a CVA. 20 All six patients who ultimately
developed subluxation had done so within
four weeks, when the affected arm was flaccid (no
supraspinatus EMG activity). Two of the patients
later developed spasticity but maintained their subluxation.
These investigators concluded that the supraspinatus
muscle began responding to "loading" of
1042 PHYSICAL THERAPY
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013

the dependent arm when spasticity appeared, and
subluxation did not occur. However, if the superior
capsule had been allowed to become overstretched
when the flaccid supraspinatus muscle could not respond
to loading, the GHJ subluxation persisted,
even though spasticity and muscle activity later appeared.
Chaco and Wolf recommended that "... to
avert subluxation of the glenohumeral joint, loading
on the joint should be avoided as long as the affected
limb is flaccid. ,,20 Moskowitz and associates suggested
that support of the flaccid shoulder early in management
can reduce the incidence of subluxation to as
low as 2 to 5 percent. 8
Active Motor Function
Severity of motor disability in hemiplegia is apparently
associated with shoulder pain and subluxation.
Fugl-Meyer and associates found that patients with
poor motor ability in the affected arm tended to
develop joint pain and limited passive motion,
whereas patients who quickly regained motor function
did not. 21 In one study of 222 hemiplegic patients,
the incidence of GHJ malalignment was 66 percent
in patients with complete or severe paralysis but only
16 percent in patients with partial paralysis. 17 Miglietta
and associates reported that 79% of hemiplegic
patients with subluxation had no active shoulder
motion, whereas only 9 percent of patients without
subluxation had such severe paralysis. 16 Whether the
presence of subluxation can actually impede return
of active motion, as has been suggested by Miglietta
and associates, 16 and whether shoulder subluxation
and pain can be reversed if active motion later improves,
cannot be ascertained from available data.
Shoulder-Hand Syndrome
Pain in the hemiplegic arm may in some cases be
caused by a reflex neurovascular disorder. A typical
constellation of symptoms, often referred to as the
"shoulder-hand syndrome" or "reflex sympathetic
dystrophy," may materialize after a CVA or a myocardial
infarction and is also known to develop following
external trauma such as peripheral nerve injury
or fracture. 22 The proportion of patients who
may be expected to develop the shoulder-hand syndrome
following CVA has been estimated at 12.5
percent, but the incidence of the undiagnosed condition
may be much larger. 23 The syndrome can occur
in patients whose upper limbs are flaccid and without
contractures. 12
Phases of progression in shoulder-hand syndrome
were originally described by Steinbrocker. 24 Initially,
the main signs are usually edema of wrist, metacarpophalangeal,
and proximal interphalangeal joints
and hot, dry, and red or blotchy skin. The patient
complains of severe pain in the hand or shoulder, or
both, and protectively restricts any movement or sensory
input to the limb. Gradually, muscle atrophy
and trophic changes in skin, connective tissue, and
joints become the major signs, and the hand becomes
cyanotic, cool, and damp. The typical deformity position
assumed by the hand is metacarpophalangeal
joint extension and interphalangeal joint flexion, resembling
the "intrinsic minus hand. , ,5 Symptoms are
presumed to result from reflex stimulation of the
sympathetic nerve supply by an irritative focus or
from interference with autonomic nervous system
control by the cerebral lesion. 25
Although the signs and symptoms of shoulder-hand
syndrome can develop suddenly, they may begin
slowly and insidiously, going unrecognized until
changes are irreversible. Early signs of joint swelling
may be dismissed as dependent edema. Complaints
of severe pain and hyperesthesia and the patient's
refusal to move the wrist, fingers, and shoulder may
be dismissed as emotional lability, depression, or
organic brain syndrome, when in fact the patient's
emotional disorder appeared after, not before, signs
of painful restricted motion. 22 The existence of a
shoulder-hand syndrome in the upper limb is incompatible
with the rehabilitation goals of increased mobility
and function of the upper limb.
Management Considerations
Vigorous painful stretching of the affected shoulder
should be avoided. All persons managing the patient
(including family) should be instructed in proper
handling techniques and in the dangers of pulling on
the affected arm. Prior to, and during, passive or
assistive elevation of the affected shoulder, methods
should be used to reduce spasticity, and attention
should be directed toward scapular mobilization and
humeral external rotation during shoulder abduction.
Techniques for accomplishing such mobilization are
described by Bobath, 10 Johnstone, 9 and Brunnstrom. 11
Because traumatic soft tissue compression can occur
with passive humeral abduction, therapists should
caution against passive abduction greater than 90
degrees and should direct treatment goals toward full
shoulder external rotation and flexion. Shoulder pulleys
do not provide adequate scapular rotation and
humeral external rotation and should not be used as
a means of passive elevation of the affected arm.
All possible efforts should be undertaken to prevent
GHJ subluxation in the first few weeks after onset of
hemiplegia, when the upper limb is flaccid. The most
effective way to prevent subluxation has not yet been
established, although opinions abound in the literature.
Shoulder slings have been condemned for interfering
with body image, immobilizing the arm, reinforcing
flexor tone, impairing postural support, and
Volume 61 / Number 7, July 1981 1043
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013

impeding normal gait. 6 Many question whether slings
prevent subluxation: Friedland states that "there is
no need to support a painfree shoulder in order to
prevent or correct subluxation since the sling does not
prevent, improve, cure or reduce such a deformity." 19
In one study comparing a small group of new hemiplegic
patients using a sling with a control group, no
appreciable difference in GHJ subluxation was found
to exist. 26 Slings other than the traditional type have
been described and alternatives, such as lapboards
and arm rests fitted to the wheelchair, have been
used. 10,12,27 However, the effectiveness of any of these
methods in preventing subluxation has yet to be
established.
Inasmuch as degree of paralysis seems related to
GHJ subluxation and pain, therapists should vigorously
employ methods to improve active motion in
the affected shoulder. Such methods are described by
several authorities. 5,9-11 However, a causal relationship
between use of these techniques and improvement
in neuromuscular function has not been documented,
as observed by Friedland. 19
Many authorities believe the most effective treatment
of the shoulder-hand syndrome is a sympathetic
block followed by intensive physical therapy. 22,28 Apparently,
the decreased pain following interruption of
sympathetic function permits increased use of the
limb with resultant increased sensory input from muscle
contraction and joint motion. 28 Success has also
been reported using a combination of corticosteroids
and physical therapy. Davis and associates reported
complete resolution of symptoms within three weeks
in 68 hemiplegic patients with early signs of shoulderhand
syndrome, using a combination of oral steroids,
a sling, and exercise preceded by heat or cold. 23 All
authorities concur that the best response to treatment
occurs when symptoms are recognized and treated
early. The type of physical therapy for shoulder-hand
syndrome described in the literature includes procedures
to overload sensory input and to desensitize,
such as the application of continuous cold or heat
treatments (up to eight hours a day), deep stroking
and kneading massage, and vigorous active and passive
exercise. 29 Any procedures that increase the patient's
pain should be avoided, inasmuch as pain
encourages immobilization. The use of transcutane­
1. Caldwell CB, Wilson DJ, Braun RM: Evaluation and treatment
of the upper extremity in the hemiplegic stroke patient. Clin
Orthop 63:69-93, 1969
2. Najenson T, Yacubovich E, Pikielini S: Rotator cuff injury in
shoulder joints of hemiplegic patients. Scand J Rehabil Med
3:131-137, 1971
3. Rusk H: Rehabilitation Medicine. St. Louis, MO, C.V. Mosby
Co, 1977, pp 601-620
REFERENCES
ous electrical nerve stimulation has been reported
effective in the treatment of reflex sympathetic dystrophy.
30 ' 31
CONCLUSIONS
In patients with hemiplegia, pain and limited shoulder
joint ROM tend to occur together and constitute
a significant problem. Although a blend of factors,
such as contracture, poor motor function, and immobilization,
may be responsible, GHJ subluxation
seems highly suspect as a cause, and all possible
efforts should be made to prevent subluxation when
the limb is flaccid. Forced passive stretching of the
shoulder into abduction can traumatize the rotator
cuff and bursae and is contraindicated, especially if
external rotation is limited or if spasticity is present.
Improper exercise technique and subluxation may
both contribute to the apparently high incidence of
rotator cuff lesions in hemiplegic patients. Shoulderhand
syndrome is treatable if recognized early but
leads to irreversible pathophysiological changes if
unrecognized. Preventive management by therapists
aware of shoulder biomechanics and the deficits sustained
by the hemiplegic patient should help eliminate
the problem of the painful upper extremity.
When pain does occur, a thorough evaluation by the
therapist and early treatment are essential.
Longitudinal studies of patients with hemiplegia
are needed to document the relationship of such
factors as spasticity, GHJ subluxation, painful limited
shoulder ROM, and active motor ability in the affected
upper extremity. Longitudinal studies might
also clarify under what circumstances subluxation
develops and whether it ever resolves. Further clinical
research is needed to identify the most effective means
of preventing GHJ subluxation. Clinical evidence is
needed concerning effectiveness of facilitation methods
in affecting return of active motion. Inasmuch as
some authorities have implied that physical therapy
may be ineffective in preventing and treating hemiplegic
shoulder pain, a controlled study concerning
this question seems indicated. Efforts should be made
to document signs of shoulder-hand syndrome in the
hemiplegic population, determine the real incidence
of this disorder, and identify the most effective early
therapy.
4. Cailliet R: Shoulder Pain. Philadelphia, PA, F.A. Davis Co,
1966, pp 33-58
5. Cailliet R: The Shoulder in Hemiplegia. Philadelphia, PA, F.A.
Davis Co, 1980, pp 89-120
6. Voss D: Should patients with hemiplegia wear a sling? Phys
Ther 49:1030, 1969
7. Brocklehurst JC, Andrews K, Richards B, et al: How much
physical therapy for patients with stroke? Br Med J 1:1307-
1310, 1978
1044 PHYSICAL THERAPY
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013

8. Moskowitz H, Goodman CR, Smith E, et al: Hemiplegic
shoulder. NY State J Med 69:548-550, 1969
9. Johnstone M: Restoration of Motor Function in the Stroke
Patient. New York, NY, Churchill Livingstone, Inc. 1978, pp
15-177
10. Bobath B: Adult Hemiplegia: Evaluation and Treatment. London,
England, William Heinemann, 1978, pp 58-134
11. Brunnstrom S: Movement Therapy in Hemiplegia. New York,
NY, Harper & Row, Publishers, Inc. 1970, pp 64-99
12. Mossman PL: A Problem-Oriented Approach to Stroke Rehabilitation.
Springfield, IL, Charles C Thomas, Publisher,
1976, pp 145-152
13. Tobis JS: Problems in rehabilitation of the hemiplegic patient.
NY State J Med 57:1377-1380, 1957
14. Bobath K: Letter to the editor. Phys Ther 52:444-445,1972
15. Dardier E, Reid C: Hemiplegia and painful shoulders (letter
to the editor). Phys Ther 52:1208, 1972
16. Miglietta O, Lewitan A, Rogoff JB: Subluxation of the shoulder
in hemiplegic patients, NY State J Med 59:457-460,
1959
17. Najenson T, Pikielny S: Malalignment of the glenohumeral
joint following hemiplegia: A review of 500 cases. Annals of
Physical Medicine 8:96-99, 1965
18. Taketomi Y: Observations on subluxation of the shoulder
joint in hemiplegia. Phys Ther 55:39-40, 1975
19. Friedland F: Physical therapy. In Licht S (ed): Stroke and its
Rehabilitation. Baltimore, MD, Williams & Williams Co, 1975,
pp 246-248
20. Chaco J, Wolf E: Subluxation of the glenohumeral joint in
hemiplegia. Am J Phys Med 50:139-143, 1971
21. Fugl-Meyer AR, Jaasko L, Norlin V: The post-stroke hemiplegic
patient. Scand J Rehabil Med 7:73-83, 1975
22. Moskowitz E, Bishop HF, Pe H, et al: Post-hemiplegic reflex
sympathetic dystrophy. JAMA 167:836-838, 1958
23. Davis SW, Petrillo CR, Eichberg RD, et al: Shoulder-hand
syndrome in hemiplegic population: A 5-year retrospective
study. Arch Phys Med Rehabil 58:353-356, 1977
24. Steinbrocker O: Shoulder-hand syndrome: Associated painful
homolateral disability of shoulder and hand with swelling
and atrophy of hand. Am J Med 3:402-407, 1947
25. Swan DM: Shoulder-hand syndrome following hemiplegia.
Neurology 4:480-482, 1954
26. Hurd MM, Farrell KH, Waylonis GW: Shoulder sling for hemiplegia:
Friend or foe? Arch Phys Med Rehabil 55:519-522,
1974
27. Zankel HT: Stroke Rehabilitation. Springfield, IL, Charles C
Thomas, Publisher, 1971, pp 138-140
28. Bonica JJ: Causalgia and other reflex sympathetic dystrophies.
Postgrad Med 53:143-148, 1973
29. Johnson EW, Pannozzo AN: Management of shoulder-hand
syndrome. JAMA 195:152-154, 1966
30. Stilz RJ, Carron H, Sanders DB: Reflex sympathetic dystrophy
in a 6 year-old: Successful treatment by transcutaneous
nerve stimulation. Anesth Analg 56:438-443, 1977
31. Richlin DM, Carron H, Rowlingson JC, et al: Reflex sympathetic
dystrophy: Successful treatment by transcutaneous
stimulation. J Pediatr 93:84-86, 1978
Volume 61 / Number 7, July 1981 1045
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013

Cited by
Shoulder Pain in Patients with Hemiplegia : A
Literature Review
Judy Griffin and Gay Reddin
PHYS THER. 1981; 61:1041-1045.
This article has been cited by 7 HighWire-hosted articles:
http://ptjournal.apta.org/content/61/7/1041#otherarticles
Subscription http://ptjournal.apta.org/subscriptions/
Information
Permissions and Reprints http://ptjournal.apta.org/site/misc/terms.xhtml
Information for Authors http://ptjournal.apta.org/site/misc/ifora.xhtml
Downloaded from
http://ptjournal.apta.org/ by guest on March 25, 2013