Hemiplegic Shoulder Pain

JUDY W. GRIFFIN
This article reviews the literature relevant to the possible causes, prevention,
and treatment of hemiplegic shoulder pain. Shoulder pain and stiffness impede
the rehabilitation of patients with hemiplegia. The cause of this complication is
unknown, but it may be related to the severity of neurological deficits, preexisting
or posthemiplegic soft tissue injury, subluxation, brachial plexus injury, or shoulder-hand syndrome. Shoulder pain may be preventable if risk factors can be
identified and appropriate prophylaxis applied. Resolution of the condition depends on diagnosis and effective treatment at the onset of the symptoms. More
clinical research is needed to clarify the cause of hemiplegic shoulder pain and
to document the efficacy of prophylactic and treatment methods.
Key Words: Cerebrovascular disorders, Hemiplegia, Pain, Physical therapy,
Shoulder.

Shoulder pain and stiffness.are, unfortunately, frequent complications in

hemiplegia. The following clinical picture of hemiplegic shoulder pain (HSP)
has been described by several authorities.1-3 The patient frequently has severe
paralysis; glenohumeral joint (GHJ)
subluxation or edema of the wrist and
hand also may exist. Pain may be localized to the shoulder or can radiate to
include the elbow and hand. Localized
tenderness over the biceps brachii and
supraspinatus tendons frequently is
present. Although pain may be present
at rest, the patient complains of increased pain with attempted passive motion or with a dependent position of the
arm. The most painful and limited
shoulder movement is usually lateral
(external) rotation, which is followed in
severity by abduction.4-6 Pain may intensify at night, interfering with sleep.
Many authorities believe spasticity is
characteristic of the HSP syndrome,7-9
although flaccidity also has been described as the associated state of tone.1
No significant relationship between sex
or hemiplegic side appears to exist.4,10
Duration of hemiplegia appears to be
significantly related to HSP, although
HSP can develop in the early weeks after
stroke. In a longitudinal study of 135
patients, Brocklehurst et al noted that
pain and stiffness were present in 16%
of the patients two weeks after the stroke
and had developed in an additional 27%

Ms. Griffin is Associate Professor, Department of

Rehabilitation Sciences, University of Tennessee,
Memphis, 800 Madison Ave, Memphis, TN 38163
(USA).

1884

after one year.11 Liao et al noted a significant correlation between HSP and
the duration of hemiplegia before physical therapy was begun.4 Studies of patients with HSP have reported an average onset time after the stroke to be two
to three months.4,10,12
Hemiplegic shoulder pain impedes
and prolongs rehabilitation. Pain and
limited shoulder range of motion interfere with self-care activities, impede balance, and create difficulty with transfers
and ambulation. Liao et al found that
patients with HSP demonstrated significantly less motor recovery in the upper
limb and achieved less ambulatory success than comparable patients without
HSP.4 Shoulder pain limits patient ability and desire to participate in social as
well as physical activities, and it contributes to anxiety, frustration, and discouragement. According to Braun et al,
the patient who has pain when he
moves will remain immobile. If he
also has pain at rest, he usually withdraws from any rehabilitation program.13

DEFINITION OF THE PROBLEM

Epidemiological data concerning
HSP have been gathered from patients
enrolled in outpatient or inpatient rehabilitation programs; these patients
inevitably are the most severely physically disabled.11 Thus, the incidence of
HSP essentially is unknown in patients
not participating in rehabilitation programs, in patients with mild physical
disability, or in patients after discharge
from rehabilitation. In the general population of hemiplegic patients enrolled
in rehabilitation programs, incidences of

HSP have been reported at 38%14 and

70%.15 Incidences at the time of patient
admission into rehabilitation programs
have varied from 28%4 to 67%.5 Development of HSP during the rehabilitation phase has been reported,4,5and one
group of investigators noted that 72%
of their patients developed HSP during
rehabilitation.16 Variability in reported
incidences may be a result of patient
differences in duration of hemiplegia
and severity of paralysis, in addition to
differences among investigators in defining HSP.
A major obstacle to determining the
magnitude of the problem is a lack of
an accepted set of diagnostic criteria.
Hemiplegic shoulder pain remains a
nebulous clinical entity, defined differently by each investigator. Pain is an
elusive symptom, defying quantitative
measurement even in patients with intact sensorimotor, cognitive, and communicative faculties. The presence of
pain in hemiplegic patients has been
defined variously as discomfort with
pressure over the supraspinatus or biceps brachii tendons14 or shoulder joint1
and complaint of pain at rest or with
movement.17 Pain has been graded from
moderate to severe, based on its radiation or location.17 Several investigators
reporting on HSP have not defined pain
at all.11,16,18-21
A reduced amplitude of passive shoulder ROM frequently is included as part
of the definition of HSP. Improvement
or worsening of the pain is considered
to be reflected by an increase or decrease
of passive ROM.4-6,22 Differences exist,
however, among investigators in their
descriptions of ROM. Examples include
PHYSICAL THERAPY

percentage of patients who could not

tolerate passive flexion to 90 degrees,14
description of ROM as limited or not
limited,1 and present or absent limitations of passive ROM.11 Some investigators used a rating scale, combining
percentage of limited ROM with the
amount of associated pain.5,6 A few research studies have reported direct goniometric measurements of each shoulder motion.4,22
Diagnosis of HSP typically is accomplished clinically, based on a combination of signs and symptoms. A need
exists, however, for commonly agreed
on diagnostic criteria and methods for
measuring pain and ROM. Otherwise,
the findings of different investigators are
not comparable concerning either the
incidence of HSP or the efficacy of prophylaxis and treatment.
The pathogenesis of HSP remains unclear. Etiologic agents most commonly
mentioned in the literature are subluxation, rotator cuff tears, severe paralysis,
brachial plexus injuries, exacerbation of
preexisting pathological conditions, and
improper exercise or handling of the
paralyzed arm. In more severe cases, a
shoulder-hand syndrome (SHS) may exist. Chronic frozen shoulder also has
been reported as the associated state of
patients with HSP. Comprehensive
long-range studies to identify the cause
of HSP have not been conducted yet.
Many investigators have sought to determine the incidence of single factors
such as subluxation or rotator cuff tears;
some have studied only patients with
HSP, and others have studied the incidence of single factors in a general hemiplegic population.

Purpose of Paper
A single cause of HSP probably does
not exist; the pathogenesis no doubt is a
complex series of interrelated factors.
Prospective, controlled research is lacking concerning the causes of HSP and
efficacy of treatment. Several studies,
however, have examined the association
of HSP with one or more of the above
potential etiologic factors. One purpose
of this article is to review those studies.
The ultimate value of such a review
would be 1) to identify early after the
stroke the patients who might be at risk
and 2) to describe prophylaxis. Hemiplegic shoulder pain should be viewed
as a largely preventable complication
after stroke. Additional purposes of this
article are to discuss the management of
HSP and to summarize general approaches for further study of HSP.

Volume 66 / Number 12, December 1986

POSSIBLE CAUSES
Neurological Deficits
The reported positive association between HSP and loss of motor functions
is impressive. Patients with slight paresis
rarely complain of shoulder pain,
whereas patients having severe paralysis
frequently develop shoulder problems
during rehabilitation.3 Najenson et al
noted 84% of hemiplegic patients with
severe paralysis had moderate or severe
shoulder pain.17 In a prospective study
of hemiplegic patients, Fugl-Meyer et al
noted joint pain and limited ROM that
developed in patients who initially had
poor motor function.18 In patients having had neurosurgery, the development
of a stiff painful shoulder was found to
be correlated significantly with both the
extent of hemiparesis and impairment
of consciousness.10
The trauma that may be associated
with handling a paralyzed upper limb
can aggravate preexisting conditions
such as arthritis or tendinitis.23 Paralysis
imposes a condition of immobility that
may contribute to the development of
GHJ stiffness. Paralysis also may predispose the affected shoulder to subluxation or traction injury, which secondarily may cause pain.
Abnormal toneeither flaccidity or
spasticityhas been mentioned as an
etiological factor in HSP. Because abnormal tone coexists with deficits in
voluntary motor function, shoulder immobility and, therefore, danger of contractures result. Spasticity tends to be
mentioned more frequently as being associated with HSP, perhaps because
spasticity is the predominant condition
over time in chronic hemiplegia. In a
recent study of patients with cerebrovascular accidents (CVAs) with HSP, 88%
were classified as spastic and 24% flaccid.16 Flaccidity and spasticity will be
included in further sections as they
relate to other possible causative agents.
Other neurological deficits such as
sensory loss, visual field deficits, communication disorders, loss of body image, and sensory-integrative disorders
affect the prognosis for upper limb function.24 These deficits in combination
with motor loss and abnormal muscle
tone may increase the risk of HSP.

Soft Tissue Injury

Influence of preexisting pathological
conditions. The painless excursions of
shoulder flexion and abduction normally decrease with age.25 One factor

contributing to this decreased range is

that of postural changes. The elderly
individual develops increased dorsal kyphosis with resultant downward scapular rotation.25 This position lowers the
coracoacromial arch, causing impingement early in the range of GHJ flexion
or abduction.26 Also contributing to decreased shoulder ROM are the many
degenerative changes in articular surfaces and soft tissue that occur with age.
Such degenerative changes may or may
not have been asymptomatic before the
onset of the hemiplegia.
Degenerative changes of the acromioclavicular joint, glenoid labrum, and articular cartilage of the glenoid fossa appear after the second decade of life,27,28
and hypertrophy of synovial tissue develops by age 30 years.27 Between the
fourth and fifth decades of life, and increasing with age, significant degenerative changes occur in the periarticular
soft tissue: The biceps brachii tendon
thickens and shreds; the rotator cuff,
particularly the supraspinatus muscle,
thins and frays; calcific deposits may
appear in the rotator cuff tendons.27 The
most severe tears in the rotator cuff
occur from ages 60 to 70 years.27 With
the wear and tear of normal use, degenerated areas of the rotator cuff and the
biceps brachii tendon become edematous, and adjacent bursae thicken. The
significant result is reduced space under
the coracoacromial arch, with an increased likelihood of impingement and
pain. Although extensive degenerative
changes can be present without symptoms or an impairment of function, the
additional stress of paralysis can activate
previously asymptomatic abnormalities.2327
Impingement during passive shoulder
flexion and abduction. Impingement of
soft tissue may occur during shoulder
flexion or abduction if the humerus is
compressed against the coracoacromial
arch. Severe impingement can cause rotator cuff ischemia,23 soft tissue injury,
and pain.3 Impingement usually is minimized by two mechanisms: upward rotation of the scapula, which elevates the
coracoacromial arch, and humeral rotation, which alters the position of humeral tubercles in relation to the arch.
Medial rotation must accompany flexion, and lateral rotation must accompany abduction to avoid impingement.2729
In the flaccid paralytic state, the
weight of the unsupported arm can
lower the coracoacromial arch, increasing the danger of impingement during

1885

passive elevation of the arm. Spasticity

may increase the likelihood of impingement during GHJ abduction, because
spastic rhomboid muscles fix the scapula in downward rotation, and spastic
adductor-medial rotator muscles prevent lateral humeral rotation.8,23 Spasticity, thus, might contribute to impingement during active and passive GHJ
abduction. Several authorities in stroke
rehabilitation have discussed the importance of reducing tone and adhering to
biomechanical principles during passive
elevation of the spastic shoulder.30-32
Improper passive exercise by health
care professionals, family, or patients
themselves may be a major cause of
shoulder pain in hemiplegic patients.3,8,11,33 Failure to provide upward
scapular rotation and lateral humeral
rotation during passive abduction are
the most frequently mentioned mechanisms of pain. Use of overhead pulleys,
furthermore, has been cited as a cause
of impingement pain17,34 and even rotator cuff rupture.17 No controlled studies,
however, have been conducted in this
area.
Rotator cuff rupture. Partial tears of
the rotator cuff are common after 50 or
60 years of age.27-28 Wear that is secondary to impingement has been cited as a
major contributing factor in rotator cuff
tears.35 A fall or stress causing forcible
abduction without lateral rotation can
convert a partial tear to a complete rupture.36 Degenerative changes, however,
can be so severe that even minor injuries
in nonhemiplegic patients can precipitate a complete tear.27 Patients with rotator cuff rupture have symptoms of
severe pain, especially with passive flexion or abduction; tenderness with palpation at the rupture site; and atrophy
and weakness of the lateral rotator and
the deltoid muscles.27,37
Several arthrographic studies in hemiplegic patients have revealed a high incidence of rotator cuff tears. Ruptures
were found in 33% of hemiplegic patients with painful, stiff shoulders; none
of the patients had a premorbid history
of pathological conditions of the shoulder.38 Examining only patients with severe paralysis, Najenson et al found a
40% incidence of rotator cuff rupture
on the affected side compared with a
16% incidence on the nonaffected
side.17 Najenson et al further associated
pain with rotator cuff rupture and subluxation; all of the 11 patients with severe pain had subluxation, and 10 had
rupture of the rotator cuff.17
1886

The cause of rotator cuff rupture in

hemiplegia has been identified as impingement during passive abduction
above 90 degrees3 and as forced abduction without lateral rotation, especially
with the use of overhead pulleys.17 Rotator cuff rupture also may be facilitated
by prior degenerative changes and by
subluxation,17 trauma during falls,38 and
repeated small traction injuries.39
Adhesive capsulitis. Conversely,
other investigators have noted that adhesive capsular changes, not rotator cuff
ruptures, are the predominant findings
during arthrography of hemiplegic
shoulders. Rizk et al performed arthrographic studies of 30 patients with stiff,
painful shoulders and reported a 77%
incidence of adhesive capsulitis; they
saw no evidence of rotator cuff rupture.12 Hakuno et al, performing arthrography on both affected and unaffected shoulders in 77 randomly selected
hemiplegic patients, found an equal incidence of rotator cuff rupture on affected and unaffected sides (22% and
24%, respectively).40 Hakuno et al further reported that adhesive changes were
noted the most frequently during arthrography. Although adhesive changes
were noted in both paralyzed and nonparalyzed shoulders, 55% of the paralyzed shoulders with adhesions had multiple adhesion sites compared with 4%
of nonparalyzed shoulders. Adhesions
in the GHJ and the subscapularis bursae
were associated significantly with limited GHJ motion; adhesions in the bicipital tendon sleeve were associated significantly with subluxation but not with
ROM restriction.40
The classical clinical picture for adhesive capsulitis41 is strikingly similar to
that described previously for HSP. The
cause of adhesive capsulitis even in nonhemiplegic patients is unknown.27 The
most significantly related factors in development seem to be prolonged immobilization secondary to pain and age
greater than 40 years.27,28,41,42 Pain secondary to impingement may be a precipitating factor.41 DePalma has noted
that the ages of the greatest incidence of
adhesive capsulitis and the most degenerative soft tissue changes are the same
(40 to 60 years).27 Suprascapular neuropathy also has been associated with
frozen shoulder.43
In hemiplegic patients, the development of adhesive capsulitis has been
related to paralysis,10,40 unconsciousness,10 impingement pain,3 and subluxation.20 The precise cause, however, remains obscure.

Glenohumeral joint malalignment. Inferior subluxation of the GHJ appears

more frequently in patients with hemiplegia than in other geriatric patients.
Reviewing radiographs of 300 geriatric
patients, Carpenter and Millard reported a 5% incidence of subluxation;
80% of the subluxations were superior
in the nonhemiplegic patients.44 All 5 of
the hemiplegic patients had inferior subluxation, and 4 of these had bilateral
subluxation. The magnitude of inferior
subluxation on the affected side, however, was much greater than on the unaffected side. Radiographic studies by
other investigators have not demonstrated subluxation on the unaffected
side.245
In hemiplegic patients, without regard
to severity of paralysis or time since the
onset of the hemiplegia, the incidence
of inferior subluxation has been reported variously as 30%,2,40 56%,14 and
64%.20 In patients with severe paralysis,
the reported incidences of subluxation
usually are substantially higher: 66%,2
81%,17and 92%.46
Subluxation appears to develop during the several weeks immediately after
the stroke, when flaccid paralysis prevents normal muscle response to loading.47 Using radiological examinations
of stroke patients within 24 hours of
their admission to the hospital, Smith et
al found 60% of their patients with complete paralysis had GHJ malalignment.48
Some evidence exists that subluxation
may be irreversible after a certain period
of time, regardless of return of active
motion or spasticity in the deltoid and
supraspinatus muscles. Longitudinal
electromyographic studies demonstrated that subluxation developed during the flaccid period and did not occur
after the supraspinatus muscle demonstrated EMG activity in response to
loading. Having developed, however,
the subluxation did not reverse even
when supraspinatus muscle EMG activity became evident.17 Some anecdotal
reports indicate that, in many patients
who have chronic subluxation at rest,
temporary reduction of the subluxation
can occur during ambulation9 or during
voluntary effort.14
Removal of the usual glenohumeral
stabilizing mechanisms described by
Basmajian and Bazant49 permits inferior
displacement of the humeral head in
relation to the glenoid fossa: Specifically, superior tilting of the glenoid fossa
is reversed secondarily to paralysis of
the muscles that rotate the scapula upPHYSICAL THERAPY

ward and secondarily to the weight of

the unsupported arm; the normal passive restraint mechanism from the
superior capsule and coracohumeral ligament is ineffective secondarily to scapular downward rotation; and the normal
active restraint mechanism of the posterior deltoid and supraspinatus muscle
contractions is inactive secondarily to
the upper motor neuron paralysis. The
gravitational pull on the arm when the
patient is upright creates an unopposed
distracting force with resulting inferior
subluxation of the humeral head23 (Figure). Although the cause of inferior subluxation usually is attributed to paralysis
resulting from CVA, other possible
causes are rotator cuff tear17 and brachial plexus upper trunk injury.23,50
Spasticity also has been mentioned as
contributing to subluxation by positioning the scapula in downward rotation.23,30 The real association between
subluxation and spasticity, however, is
unclear.
How dangerous is subluxation? Several authorities in rehabilitation discount any importance of subluxation,30,32,51 although they offer little
evidence to support their view. Others
believe that subluxation may be a major
cause of HSP because of the resulting
overstretching of the GHJ soft tissue.1,20,46 Passive dependence of the unsupported arm, even in an uninvolved
shoulder, elongates the rotator cuff and
creates ischemia in the biceps brachii
tendon and in the "critical zone" of the
rotator cuff.26,28 Hakuno et al found a
significant correlation between subluxation and arthrographically demonstrated adhesive changes in the bicipital
tendon sleeve.40 Subluxation may cause
traction injury to the upper trunk of the
brachial plexus.50 Ring et al reported
EMG evidence of axillary nerve dysfunction in patients with GHJ subluxation and hypothesized that initial stages
of subluxation may cause axillary nerve
compression.52
The relationship of pain to subluxation is unclear. Some investigators have
reported no correlation between incidences of subluxation and pain.12,14Najenson et al, however, found 93% of
their hemiplegic patients with severe paralysis that was accompanied by moderate or severe pain had subluxation.17
Although subluxation may not be associated with pain in the early stage of
hemiplegia, if subluxation continues
into the chronic spastic stage, the association of pain and limited motion may
be higher.13 A recent study found subVolume 66 / Number 12, December 1986

luxation was associated frequently with

HSP; 85% of the patients with spasticity
had HSP, and subluxation was present
in 67% of these patients.16
Brachial plexus and peripheral nerve
injuries. Electromyographic evidence of
lower motor neuron involvement has
been reported in hemiplegic patients
and is found twice as frequently in the
upper as in the lower limb.23 Brachial
plexus injury may be a source of shoulder pain and a cause of subluxation.
Chino reported 75% of his hemiplegic
patients with subluxation demonstrated

Figure. Basmajian's principle. A) The normal position of the shoulder prevents subluxation because the humeral head cannot
displace laterally out of the upwardly tilted
glenoid fossa (dotted arrow). B) Drooping of
the shoulder in some hemiplegic patients permits subluxation of the humeral head out of
the downwardly tilted glenoid fossa (dotted
arrow). (Reprinted by permission of W. B.
Saunders Co.92)

neuropathic responses in the deltoid and

supraspinatus muscles.50 Kaplan et al
found EMG changes consistent with injury of the upper trunk of the brachial
plexus in five hemiplegic patients with
flaccid paralysis and atrophy of the
shoulder musculature.53 Electromyographic evidence of pressure neuropathy
of the ulnar nerve and brachial plexus
neuropathies was reported by Moskowitz and Porter in eight hemiplegic patients.54 Other investigators have found
no electrophysiological evidence of brachial plexus injuries in hemiplegic patients.12,19,46,47,55

Signs of neuropathy are superimposed

on the hemiplegic paresis. They include
extensive segmental atrophy, an atypical
pattern of return of motor function (ie,
distal before proximal return), and electrophysiological signs.54
All investigators reporting brachial
plexus injuries in hemiplegic patients
identify the probable mechanism of injury as a combination of flaccid paralysis and traction injury. Traction stress is
caused by either lack of support of the
paralyzed flaccid shoulder50,52-54 or pulls
on the flaccid arm by personnel who
move the patient.54,56 Patients who are
unconscious are at the greatest risk of
having traction and pressure neuropathies.56
The occurrence of a brachial plexus
injury can increase rehabilitation time
greatly. The superimposition of a lower
motor neuron injury on the upper motor neuron lesion increases the likelihood for the development of painful
contractures.54 A brachial plexus injury
constitutes a major setback for recovery
of active motion; because of the slow
rate of nerve regeneration, functional
recovery of shoulder movement may be
delayed by 8 to 12 months.53
Shoulder-hand syndrome. This reflex
neurovascular disorder is characterized
by pain and hyperesthesia, edema,
trophic changes, and vasomotor instability. Signs and symptoms vary among
patients, and onset may be dramatic.57
The temporal sequence of signs has been
described by many authorities.58-60Early
manifestations include pain and limited
motion in the shoulder, wrist, and hand;
the most restricted motions are shoulder
lateral rotation and abduction, wrist
dorsiflexion, and flexion of the metacarpophalangeal and proximal interphalangeal joints. Edema is evident in the wrist
and finger joints, with increased skin
temperature, rubor, and hyperhidrosis
or hypohidrosis. As the condition progresses, pain decreases and stiffness predominates. The skin becomes shiny, cyanotic, and hyperhidrotic. Intrinsic
muscle atrophy, nail changes, and thickening of subcutaneous tissue in the finger joints and palmar fascia develop.
Osteoporosis is demonstrable radiographically. The syndrome may last
from months to years.61
Shoulder-hand syndrome is known to
develop after internal lesions such as
CVA, myocardial infarction, cervical osteoarthritis, or spondylosis. The syndrome also develops often after trauma
such as peripheral nerve injury, fracture,
or spinal cord injury.58,59,62 The precise
1887

mechanisms triggering SHS are unknown. Tissue injury may serve as a

focus of noxious stimuli, altering central
control of the sympathetic nervous system.58 Immobilization of the limb because of injury, debility, pain, or paralysis may result in decreased sensory input from the limb to the central nervous
system, causing an imbalance in the central neural control of the sympathetic
nervous system.58 Inactivity of muscles
that perform pumping actions in the
hand and the axilla (secondary to paralysis or immobilization) may cause altered circulation and edema.23,27,63,64
In hemiplegia, however, vasomotor
changes may not be related necessarily
to paralysis.51,65 The cerebrovascular lesion may disturb central vasomotor regulation, resulting in arteriolar vasodilation of the upper limb.65 Lesion of the
premotor and anterior motor cortical
regions may cause SHS after a stroke.66
The incidence of SHS among hemiplegic patients is unclear. Ring et al
found no cases in 24 patients followed
one year after a stroke.52 In a retrospective study of 540 hemiplegic patients,
Davis et al reported a 12.5% incidence
of SHS.57 Van Ouwenaller et al found
the incidence of SHS in 215 hemiplegic
patients was 28%.16 Finch and Harvey,
in a prospective study of 20 patients
hospitalized after stroke, reported 50%
developed signs of SHS.67 Of hemiplegic
patients with shoulder pain, the percentage of patients with signs of SHS
has been cited as 36%6 and 32%.16
Davis et al reported that most of their
patients who developed SHS did so two
to four months after the stroke, and they
hypothesized that the incidence was the
least in patients with mild involvement.57 Mossman also reported that the
syndrome was more typical of patients
with little or no voluntary motor ability.51 Two studies comparing hemiplegic
patients with and without SHS, however, reported no difference between
groups in active motor ability or muscle
tone.6,67 Van Ouwenaller et al found a
higher incidence of SHS in patients with
spasticity than in those without.16
Hemiplegic patients with SHS have
been found to be significantly more confused and have greater sensory loss than
other hemiplegic patients; they also have
a higher incidence of subluxation than
other hemiplegic patients.67 Weiss and
Ellis stated that hemiplegic patients with
prior myocardial infarction may be at
special risk for developing SHS.65 Confirming this finding, Finch and Harvey
reported that half of the patients devel-

1888

oping the syndrome had a history of

cardiac abnormalities.67
Thalamic pain. A burning, excruciating pain may involve the face, tongue,
and thorax as well as the affected
limbs.68 Marked proprioceptive loss
usually is present,68 and the patient may
neglect the paretic side except during a
painful episode.69 Peculiar sensations relating to the limb, feelings such as absence, twisting, or changes in size, may
be present. The pain may be constant
but is exacerbated by changes in emotional states, visual or auditory stimuli,
temperature, or cutaneous stimuli.68,69
Vasomotor disturbances may be present
on the affected side, characterized by
cycles of skin coolness, pallor, and hyperhidrosis, alternating with warmth,
rubor, and edema.
A lesion of the lateral thalamus, the
posterior limb of the internal capsule, or
the parietal lobe is believed to be responsible.68,69 The incidence is unknown.
Thalamic pain responds poorly to treatment.70

PROPHYLAXIS AND
TREATMENT
Although cases of HSP may result
directly from CNS lesions, many may
be caused by faulty treatment after the
stroke.71 Careless handling of the paralyzed upper limb at any time after the
onset of hemiplegia can precipitate
shoulder injury and pain. For prophylaxis to be effective, however, it must
begin immediately after the stroke. After
the pain cycle has begun, resultant anxiety, overprotection, and disuse inevitably produce decreased ROM and contractures.23
Treatment of the many varieties of
HSP represents a complex and difficult
problem. The ideal treatment is prevention; the next best management is to
implement a treatment program immediately when the first painful symptoms
appear.

Positioning and Handling of the

Dependent Patient
Education of the patient and everyone
associated with the care of the patient in
the acute period after the stroke is critical to the success of a positioning and
handling program. According to Mulley,
pain in the shoulder is a complex subject that has not yet been approached
systematically, but even in our present
state of ignorance we can prevent
much pain and limitation of movement in the shoulder by careful positioning and handling.33

Adequate support and protection of

the flaccid arm are essential when the
patient is lifted or moved in bed.48,71,72
All persons moving the dependent patient must be instructed concerning the
hazards of pulling on the affected arm.
Methods of upper limb handling when
the patient is moved in bed or is assisted
to a sitting position have been described.30'32'72"74
Positioning for the flaccid limb in bed
also is important, and protocols are discussed in several sources.23,30,32,72,74,75
The typical spasticity pattern of scapular
retraction, neck flexion to the affected
side, shoulder medial rotation and adduction, and elbow-wrist flexion should
be avoided. Pillows can be used to support and elevate the limb to lessen dependent edema of the hand.74,76,77 When
the patient is in the supine position, the
shoulder should be supported in a flexion-abduction-lateral rotation position.71,72 Bohannon et al have described
a method of shoulder positioning in bed
using a device made of foam and Velcro.78 Chino recommended overhead
suspension of the arm in bed.50 When
the patient is sidelying, the affected arm
should be flexed and rotated laterally
with the shoulder girdle protracted.71
Limited sidelying on the affected side
sometimes is recommended.77 When the
patient is sidelying on the unaffected
side, the affected shoulder should be
supported on pillows and not allowed to
lie in horizontal adduction. A horizontally adducted position may exert traction of the suprascapular nerve and
cause HSP.43

Facilitation of Active Motion

Early facilitation of activity in muscle
groups producing protraction and upward rotation of the scapula and flexionabduction of the shoulder is essential.
Methods to inhibit spasticity contributing to scapular retraction and shoulder
adduction and medial rotation likewise
are essential if spasticity is present. A
discussion of these methods is beyond
the scope of this article; descriptions of
facilitation-inhibition programs may be
found in several sources.23,30-32,74,75,79,80
Unfortunately, little controlled research
is available documenting the relative efficacy of these methods.
Electrical stimulation and EMG biofeedback, alone or in combination, have
emerged as promising therapeutic adjuncts in the facilitation of voluntary
motion and the inhibition of spasticity.81-85 Most studies relating to the efficacy of these methods, however, have

PHYSICAL THERAPY

been of distal extremity function, that

is, facilitation of ankle dorsiflexion and
wrist-finger extension. Few studies have
been published relating to the effect of
biofeedback on proximal muscle function. Lee et al found no difference in
the deltoid muscle EMG activity between patients receiving biofeedback
and patients in conventional physical
therapy and placebo groups.86 Inglis et
al, however, found that hemiplegic patients receiving EMG biofeedback and
physical therapy improved more in
shoulder strength and ROM than patients receiving physical therapy alone.87
Patients with proprioceptive impairment may have limited success with biofeedback training,88 although some evidence indicates sensory loss may not
preclude improvement with biofeedback.89 Electrical stimulation and biofeedback may be effective in preventing
or reducing GHJ subluxation, as will be
discussed in the next section.

Subluxation
Prevention of subluxation requires
the institution of prophylactic methods
in the first few weeks of flaccid paralysis.46,50 After spasticity or active shoulder
motion, or both, appear, subluxation
seems unlikely to develop.47
Objective documentation of subluxation requires radiographs with the patient in the upright, not supine, position.17,20,46,48 Likewise, the efficacy of
methods for preventing or reducing subluxation should be demonstrated radiographically. Shai et al hypothesized
that earlier radiologic diagnosis of subluxation (ie, before grade I or II changes
are demonstrated) might enable more
effective prevention than if it is delayed.21 In their study, 12 of 14 patients
showing early, positive radiologic signs
of subluxation subsequently developed
a painful shoulder, and 4 developed subluxation. Shai et al suggested that patients showing early radiologic signs of
subluxation might be most likely to benefit from early orthotic intervention.
When the patient is upright, the arm
should be supported and positioned to
prevent unopposed gravitational stress
on the soft tissue of the GHJ. Various
methods have been described for upper
limb positioning in the wheelchair: pillows, a padded arm trough attached to
the wheelchair arm or a lapboard,30,72 or
an overhead wheelchair sling.15,23,72,90
None of these methods has been proven
to be more effective than others in preventing or reducing subluxation.

Volume 66 / Number 12, December 1986

Some support of the flaccid arm is

necessary when the patient is ambulating. The patient with severe perceptual
deficits and denial may need a sling for
protecting the arm against trauma.74 A
multitude of sling types have been described.30,91-96 Elements to be considered
in the choice of slings for particular
patient problems have been summarized.95,96 External support can be discontinued when muscle tone around the
GHJ is adequate to prevent subluxation.91 If needed, a sling should be used
only during ambulation; the sling cannot be allowed to contribute to shoulder
immobilization. An exercise program
always should accompany the use of a
sling.24
Controversy abounds concerning the
use of slings; disadvantages to their use
have been enumerated by many authorities.34,71,94,97 The major purpose of a
sling is to provide an upward force to
maintain the humeral head in the glenoid fossa. Unfortunately, little documentation exists in the form of radiological evidence to indicate which of the
plethora of sling types produces the
most effective reduction. In the only
controlled, longitudinal study on sling
efficacy, Hurd et al found one type of
sling ineffective in preventing subluxation.19 Sodring94 and Rajaram and
Holta98 reported radiographic evidence
of GHJ reduction with two types of
slings; however, no controlled research
study was conducted to demonstrate the
efficacy of subluxation in prophylaxis.
In circumstances when the presence
of subluxation has been determined to
be the primary cause of HSP, use of a
Varney brace has been reported to be
successful; patients became asymptomatic in five to seven days.99 After the
subluxation is reduced and the shoulder
is asymptomatic, an active and passive
exercise program is important to improve and maintain ROM.99
Electrical stimulation of the supraspinatus and deltoid muscles can be used
as an "electrical orthosis" for maintaining the alignment of the GHJ and has
been recommended as an effective substitute for a sling.83 Studies conducted at
Rancho Los Amigos Rehabilitation
Engineering Center reported that patients who were receiving electrical stimulation to the posterior deltoid and
supraspinatus muscles demonstrated radiological evidence of reduced subluxation.100,101 Some evidence existed that
the reduction was maintained after the
stimulation was discontinued.100 No
prospective longitudinal studies could

be located, however, documenting the

efficacy of electrical stimulation for the
treatment of subluxation. (See the article by L. Baker in this issue.)
Electromyographic biofeedback has
been reported to be successful in reducing subluxation,82,85 although little prospective research seems to exist. In a
controlled study on hemiplegic patients
with subluxation, Shahani et al noted
equal effectiveness of an EMG biofeedback program and a "conventional"
physical therapy program in reducing
subluxation; a correlation existed between the decrease in subluxation and
the increase in strength and tone in the
shoulder muscles.102
In a clinical report, Burstein recommended weight bearing on the affected
arm and manual reduction of the subluxation during exercise as effective
methods in relieving HSP.103 Smith presented two case reports describing the
reduction of subluxation and the increase of active abduction using an intensive facilitation program for the supraspinatus, deltoid, and serratus anterior muscles.104

Avoidance of Impingement
During Passive Exercise
Immobilization contributes to loss of
motion, and passive ROM is an essential
prophylactic measure to prevent joint
stiffness and soft tissue contractures.
The effectiveness of passive ROM, however, does not necessarily indicate that
all types of shoulder exercise are beneficial or that a patient who begins to
complain of pain during exercise requires more aggressive exercise therapy.11 Improperly administered passive
exercise can cause impingement, resulting in soft tissue trauma, inflammation,
and pain.3,8,17,34,50 Increased exercise of
the wrong type can contribute to the
development of a stiff, painful shoulder.
All persons performing passive exercise to the flaccid or spastic arm, from
professional staff to family and the patient himself, must be taught the correct
exercise techniques. Certainly, manual
reduction of subluxation, if it exists,
should be accomplished before passively
elevating the arm. Medial or lateral rotation must accompany flexion or abduction, and scapular upward rotation
must accompany either rotation to
avoid soft tissue impingement. Spasticity must be reduced before elevating
the arm more than 90 degrees. Overhead
pulleys provide neither correct humeral
nor correct scapular rotation during pas1889

sive elevation and are a likely cause of

impingement.
An important question to be addressed is how much ROM is "enough."
All medical professionals seem "programmed" to take each joint through its
full ROM. As previously noted, complete ROM to a young physical therapist
is not necessarily complete ROM to a
geriatric stroke patient. Perhaps a more
realistic goal is the maintenance of painfree functional ROM in the shoulder.
The affected arm must be pain free to
serve even in an assistive role.38 Functional ROM has been defined as flexion
to 100 degrees, abduction to 90 degrees,
lateral rotation to 30 degrees, and medial rotation to 70 degrees.90
Another aspect to be considered is
whether abduction should be included
in passive exercise, in view of its tendency to cause soft tissue impingement.
Some authorities recommend that abduction should be performed only in the
scapular plane, that is, 30 degrees to 40
degrees from the frontal plane,3,34 because lateral rotation is not required to
prevent impingement.27 Curtailing the
amplitude of passive abduction in exercise programs might preserve functional
ROM and minimize impingement pain.
If impingement during ROM is determined to be the etiological factor in
pain, then the amplitude of passive motion should be kept within the pain-free
range.15 Caldwell et al reported that pain
subsided in 43% of their patients with
HSP when the amplitude of passive
ROM was limited.15
Should the patient begin to complain
of pain during passive ROM, a thorough
evaluation to assess the cause of pain
should be conducted before pain and
stiffness become established.

Diagnosis of Established Painful

Conditions
If a patient has an established painful,
stiff shoulder, the first step in treatment
is the identification of the cause. A carefully detailed medical history is important to determine the prestroke history
of any shoulder pathological conditions
and to identify any known trauma that
occurred after the stroke, such as
falls.23,27 A correct diagnosis of the cause
is essential if the patient is to be helped."
A thorough diagnostic examination of
the neck and shoulder should be conducted to identify cervical spine pathological factors, rotator cuff or biceps
brachii tendinitis, or GHJ or acromioclavicular joint arthritis.42,99 Confirmatory evidence of rotator cuff tears and
1890

adhesive capsulitis can be obtained with

arthrography. Radiographs can rule out
humeral fracture3 and ectopic ossification.105 Electrophysiological studies can
be used to identify brachial plexus injurv. Shoulder-hand syndrome may be
confirmed by a positive response to stellate ganglion block.58

Conservative Management
If subluxation is identified as the causative agent, several treatment methods
exist. Pain and stiffness in a subluxated
shoulder, however, are not necessarily a
result of subluxation.15,102Krempen et al
examined 37 patients with pain and subluxation and found 16 patients had
other, orthopedic causes for the pain."
Conservative orthopedic management of patients with diagnoses of tendinitis, bursitis, and rotator cuff tears is
similar. The goals of treatment are pain
reduction and improvement of ROM.
Symptoms may be reduced with oral
anti-inflammatory agents and analgesics
and injections of lidocaine and steroids
into trigger points, the subacromial bursae, or the joint space.27,28,42,106 As pain
decreases, active, passive, and assistive
exercises are used to improve ROM.
Applications of heat, cold, phonophoresis, and transcutaneous electrical
nerve stimulation may be effective in
relieving pain and encouraging motion.106 Applications of heat, however,
have not been proven to be of particular
benefit in the treatment of HSP. Liao et
al found no significant difference in the
amount of improvement in ROM between patients treated with exercise only
versus those treated with a combination
of heat and exercise therapy; exercise
appeared to be the most effective treatment.4 Thus far, in studies of hemiplegic
patients with unstated etiologic factors
of pain, ultrasound22 and TENS6 have
not been found to decrease pain or to
contribute to increased range of shoulder motion.
If an injury to the upper trunk has
been diagnosed, the brachial plexus
must be protected until regeneration can
occur.53 The shoulder should be splinted
in 45 degrees of abduction, a treatment
similar to that of postsurgical repair of
the upper trunk.107 Care must be taken
to prevent further traction injury until
regeneration occurs. The prognosis for
recovery of function varies widely.23
Although evidence exists that adhesive capsulitis in nonhemiplegic patients
is a self-limited disease resolving in one
to three years, (see the article by C. T.
Wadsworth in this issue), the same does

not appear to be true of hemiplegic adhesive capsulitis.12,42 A vigorous program of ice or heat applications and
active and passive exercises can be combined with anti-inflammatory and analgesic medications, oral corticosteroids,
and muscle relaxants.41 Suprascapular
nerve blocks,108 corticosteroid injections
into trigger points, and stellate ganglion
blocks have been reported to be beneficial.23
Antispasmodic medications may supplement inhibition and relaxation techniques.16 Motor-point blocks of the
trapezius16 and pectoralis major109,110
muscles may aid in controlling spasticity.
In the management of SHS, early recognition is the key to a favorable prognosis; prompt treatment is essential to
prevent permanent disability.58,60,111 An
aggressive exercise program is an essential component of treatment.27,59 Active
muscle contraction and joint movements are important, as are light weightbearing activities. Exercise must be performed within the pain-free range and
frequently for short periods during the
day. Modalities such as heat or ice treatments or TENS may be used to increase
sensory input and reduce pain.28,71,112
Although TENS has been reported as
helpful in the management of reflex
sympathetic dystrophies, no research results appear to be reported on the effectiveness of TENS in hemiplegic SHS.
Aggressive and prompt management
of hand edema is important, because
prolonged edema will precipitate perhaps irreversible hand stiffness.27 Dependent positions of the hand should be
avoided; an elevated position is preferable. Intermittent pneumatic compression may be of value in reducing hand
edeipa,23,90,113 and an elastic glove is
helpful also in controlling edema.71
Systemic administration of corticosteroids for two to three weeks is recommended by several authorities for the
management of SHS.27,59,71 Davis et al
reported a complete resolution of symptoms in 68 hemiplegic patients using
oral steroids in combination with an
intensive rehabilitation program.57 A
sympathetic block followed by intensive
rehabilitation is cited as the most effective treatrnent by Some researchers.58,61,111 Sympathectomy is suggested
in refractory cases.58,59,111
The emotional state of patients with
severe HSP has been described as tense,
hyperresponsive to pain, overemotional,
apathetic, and emotionally dependent.23
Whether such emotional states contribPHYSICAL THERAPY

ute to the development of HSP or

emerge as a result of the pain is unknown.111 In any event, appropriate psychological management is important for
successful treatment.23

Surgical Management
Surgical release of soft tissue may be
of value if conservative methods have
failed and if shoulder motion has become severely limited and painful.112
Recent improvements in rehabilitation
techniques have decreased the need for
surgical intervention.75 The most frequently described surgical management
involves resection of the subscapularis
and pectoralis major tendons15,114 and
release of the capsule115; insertions of
the latissimus dorsi and teres major
muscles also may be necessary.116,117 Surgical release does not result in improved
ROM without an intensive postoperative program of exercise and splinting to
maintain and increase abduction and
external rotation.15,117
The indications for surgery include
ROM limitation to the point of functional impairment (ie, abduction to 45
degrees and lateral rotation to 15 degrees
or less15), pain of such intensity that it
interferes with skin hygiene114 or prevents participation in rehabilitation,15
and progressively decreasing ROM resulting from increased internal rotator
muscle spasticity.15,109,117 Factors affecting the patient's rehabilitation potential,
such as cognitive awareness, sensory and
perceptual deficits, and communication
disorders, also should be considered.15
Surgery usually is delayed until at least
six months after the stroke when spontaneous recovery is fairly complete.114
Surgery is contraindicated in the presence of etiological factors other than soft
tissue contracture or if postoperative
therapy is unavailable.15 Surgery for
thalamic pain is not indicated.15,118
The reported magnitude of an increase in ROM after surgery is not great.
Caldwell et al reported that the lateral
rotation range was poor, although most
patients regained 90 degrees of abduction; some patients developed active abduction postoperatively that had not
been observed preoperatively.15

immobilizes the limb but increases the

likelihood for traction injury because
the patient cannot protect himself. Increasing age may increase the risk also.
Most patients over 50 years of age have
significant degenerative changes around
the GHJ. Such soft tissue pathological
factors can be exacerbated only by
events accompanyingflaccidparalysis.
The acute period after a stroke appears to be a critical time for the prevention of GHJ soft tissue injuries such as
rotator cuff tears or brachial plexus injuries. Such trauma, which may go unnoticed in the acute period after a
stroke, may cause significant HSP or
functional impairment later in rehabilitation. Education of all personnel handling the flaccid arm is imperative if
prophylaxis of shoulder injury is to be
effective.
Failure to provide support for the flaccid arm when the patient is upright may
allow shoulder subluxation and consequent painful overstretching of soft tissue or nerve injury or both. The deleterious effects of subluxation may be
cumulative. Effective methods for the
prevention of subluxation remain to be
established in a controlled clinical trial,
but electrical stimulation appears
promising.
Immobilization is a key factor contributing to shoulder stiffness in elderly
patients. In patients with hemiplegia,
immobilization is promoted by paralysis, spasticity, and, sometimes, brachial
plexus injury. Pain is another wellknown immobilizing influence. Lack of
passive exercise for the paralyzed shoulder certainly will result in painful contractures. Careless passive exercise techniques without regard to biomechanical
principles may cause impingement.
Thus, improperly administered exercise
may be a cause of trauma, pain, and
further immobilization.
When pain and stiffness begin to develop, a thorough evaluation of the
cause is essential. Conservative management methods may be effective if the
treatment is appropriate for the cause.
Surgical intervention may be indicated
in extreme cases. Early preventive measures, however, remain the key to minimizing the complication of shoulder
pain in patients with hemiplegia.

CONCLUSIONS
Patients at highestriskfor developing
HSP seem to be those with severe upper
limb paralysis, particularly if sensory
loss and mental confusion also exist.
Such a combination of factors not only

Volume 66 / Number 12, December 1986

Need for Clinical Research

Longitudinal studies are needed concerning developments in the shoulder
after hemiplegia. Periodic assessments
of shoulder status, from the onset until

at least one year after the onset of hemiplegia, would add greatly to present
knowledge concerning the evolution of
HSP. Pertinent aspects to be included
in such assessments are active motor
function, sensory status, passive ROM,
amount of pain associated with passive
motion, spasticity, subluxation, and
functional ability of the upper limb.
Cognitive status and age also should be
included. If HSP and limited ROM develop during the longitudinal study,
prompt diagnostic steps to identify the
cause should be instituted. When etiologic factors of the pain can be established, controlled studies of the relative
effectiveness of various treatment methods are essential. The optimum treatment for hemiplegic patients with established diagnoses such as SHS or adhesive
capsulitis currently is unknown.
Knowledge of the effectiveness of
methods for preventing subluxation (ie,
electrical stimulation vs positioning
alone) would be helpful in determining
prophylaxis. Also of clinical importance
are controlled studies to establish the
relative efficacy of methods such as biofeedback, electrical stimulation, and exercise alone in improving proximal control in the hemiplegic shoulder.
The obstacles to clinical research in
the area of HSP may seem formidable:
Hemiplegic patients admitted to rehabilitation settings differ widely in medical history and prestroke shoulder dysfunction; the time since the stroke varies
among patients; and the history of
shoulder trauma after the stroke often is
impossible to ascertain. Such variables
may account for the different responses
to treatment and may make the original
causes of HSP difficult to determine.
Such difficulties might be overcome partially by beginning a longitudinal study
immediately after the stroke and by including significant numbers of patients
in the study. The HSP syndrome represents such a major obstacle to rehabilitation that systematic studies of the
problem are imperative. Controlled research is needed to determine effective
prophylaxis and to document the therapeutic efficacy of treatment.

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